Must-know review

• Correct answers: atrophy = smaller and fewer; hypertrophy = bulk up; hyperplasia = make more; metaplasia = change identity.
• Trap one: "atrophy only shrinks cells, number unchanged" — omits the apoptosis step; wrong.
• Trap two: BPH may be spelled out as "benign prostatic hypertrophy," but in essence it is hyperplasia, not hypertrophy.
• Trap three: classifying an enlarging myocardium as "hyperplasia" — cardiac myocytes do not divide; they can only hypertrophy.

• Barrett esophagus = squamous→columnar (with goblet cells) = metaplasia = pre-malignant lesion for adenocarcinoma.
• The smoker's airway = ciliated columnar→squamous (hardier, but mucus clearance is lost).
• Trap one: bladder "transitional→transitional" is regeneration, not metaplasia (the same type does not count).
• Trap two: metaplasia = a reversible change of identity; dysplasia is where the pre-cancerous process truly begins.
• Trap three: calling Barrett "hyperplasia" is an error that simply gives the mark away.

• Reversible = cellular swelling, nucleus intact; irreversible = pyknosis → karyorrhexis → karyolysis (karyorrhexis is the marker).
• Apoptosis: membrane intact, no inflammation, DNA laddered; necrosis: membrane ruptured, inflammation, DNA randomly fragmented.
• Intrinsic = cytochrome c → caspase-9; extrinsic = Fas/TNFR → caspase-8; both end at caspase-3.
• Trap one: treating "cellular swelling" as irreversible — it is still in the reversible stage.
• Trap two: assigning caspase-8 to the mitochondrial pathway — backwards.
• Trap three: does apoptosis provoke inflammation? The apoptotic membrane stays intact — it does not.

• Steatosis = TG; xanthoma foam cells = cholesterol; lipofuscin = aging; hemosiderin = hemorrhage/iron deposition, Prussian blue positive.
• Strongest regenerative capacity = liver (a stable cell); neurons, cardiac muscle, skeletal muscle = permanent cells, no regeneration.
• Trap one: fatty liver stores cholesterol? Wrong — it is TG.
• Trap two: foam cells store TG? Wrong — it is cholesterol.
• Trap three: the liver is made of labile cells? Wrong — it is the stable cell with the strongest regenerative power.

• Acute protagonist = neutrophils + edema; chronic protagonists = lymphocytes/plasma cells/macrophages + fibrosis.
• Exudate = ↑permeability (>1.020); transudate = pressure (<1.012).
• Trap 1: filing edema under "chronic" — wrong; it is the signature of acute inflammation.
• Trap 2: calling appendicitis chronic (judging by the "-itis" alone) — appendicitis is acute, with a massive neutrophilic infiltrate.
• Trap 3: does a heart-failure pleural effusion count as an exudate? Wrong — it is a transudate.

• Histamine = opens vessels and builds edema; it is not a chemoattractant.
• Neutrophil chemotaxis = LTB4 and C5a (complement).
• PG/bradykinin = pain; TNF/IL-1 = systemic fever.
• Trap 1: pairing histamine with chemotaxis — a mismatch.
• Trap 2: treating LTC4/D4/E4 as chemoattractants — their job is bronchoconstriction.
• Trap 3: crediting fever to histamine — fever is the business of TNF/IL-1.

• Acute protagonist = neutrophils; chronic protagonists = lymphocytes/plasma cells/macrophages.
• Edema belongs to the acute phase (the common wrong option with the "lowest" relevance to chronic inflammation).
• Exudate = ↑vascular permeability; transudate = a pressure problem.
• Histamine opens vessels (not chemotaxis); LTB4/C5a are the true neutrophil chemoattractants; TNF/IL-1 govern systemic fever.
• Granulation tissue = new tissue of repair (fibroblasts + new capillaries + inflammatory cells); granuloma = a pattern of chronic inflammation (epithelioid + multinucleated giant cells).
• UC: mucosa (at most the superficial submucosa), no granulomas; Crohn's: transmural, with granulomas.
• Fibrinoid necrosis is most common in vasculitis; infectious small-vessel vasculitis = syphilis/typhus/ecthyma gangrenosum.
• The Anitschkow cell within the Aschoff body is the specific cell of rheumatic carditis (if asked for the characteristic lesion, answer the Aschoff body).
• Repair sequence: hemostasis → inflammation → proliferation (granulation tissue/epithelium/collagen) → remodeling (type III → I).
• Healing by secondary intention needs abundant granulation tissue and myofibroblast contraction.
• Traps: the main component of a mature scar is type I, not type III; appendicitis is acute; does UC have granulomas? No.

• Source = the deep veins of the lower limb (popliteal and above); superficial varicosities are not the main source.
• Most PEs do not infarct (dual blood supply); infarction occurs only with coexisting left-heart failure.
• Most common ECG finding = sinus tachycardia; S1Q3T3 is classic but uncommon.
• Stable = CTPA; D-dimer is for exclusion, not diagnosis.
• Trap 1: treating a raised D-dimer as "confirming the diagnosis" — wrong; it is sensitive, not specific.
• Trap 2: the pleural effusion of pulmonary infarction is a transudate? Wrong — it is an inflammatory exudate.
• Trap 3: assuming the saddle embolus is common — it is the rare but lethal sudden-death form.

• Virchow's triad = endothelial injury / stasis / hypercoagulability; arterial white thrombus (platelets + fibrin) vs venous red thrombus (RBC + fibrin).
• Most common source of fatal PE = the "deep" veins of the lower limb; most PEs do not infarct (dual blood supply), true infarction only with coexisting left-heart failure; saddle embolus → acute right-heart failure and sudden death.
• Most common ECG finding in PE = sinus tachycardia; the classic S1Q3T3 is uncommon; if stable, CTPA first; D-dimer is used to "rule out" low-risk patients.
• Pleural effusion of pulmonary infarction = inflammatory exudate; chylothorax = milky white, TG > 110 (thoracic duct leak); elephantiasis and postoperative edema = lymphatic obstruction.
• Infarct types: white = heart, kidney, spleen (single blood supply); red = lung, bowel (dual blood supply), venous occlusion, reperfusion.
• Ischemia-reperfusion injury = a second injury by oxygen free radicals.
• Abdominal aortic aneurysm = atherosclerosis (below the renal arteries); thoracic aortic aneurysm = syphilis (do not confuse the locations).
• Endothelin = the most potent vasoconstrictor; NO is its antagonist.
• TTP: ADAMTS13 deficiency → large vWF → platelets glued into microthrombi; plasma exchange first, no platelet transfusion; HUS leans renal, EHEC O157:H7, children; DIC has prolonged coagulation times and D-dimer↑.
• Traps: transfusing platelets in TTP = fuel on the fire; AAA is caused by syphilis? Wrong (syphilis takes the thoracic aorta); the most potent vasoconstrictor is NO? Wrong (NO dilates; the strongest constrictor is endothelin).

• Oncogene: one copy suffices, dominant (RAS/MYC/BRAF/HER2/ABL); suppressor needs two hits (TP53/RB/APC/p16/BRCA).
• BRAF V600E = melanoma / papillary thyroid / colorectal / hairy cell leukemia; uncommon in breast cancer (a frequent reverse question).
• Aflatoxin B1 → TP53 → hepatocellular carcinoma; p16 is usually silenced by promoter methylation.
• Most common in hematopoietic tumors = translocation (CML BCR-ABL, Burkitt MYC); low-grade osteosarcoma = CDK4/MDM2 amplification on chromosome 12 (not MYC).
• Least associated with EBV = cervical cancer (caused by HPV).
• Benign vs malignant rests on metastasis / invasion / infiltration; a pancreatic neuroendocrine tumor with marked pleomorphism may still be benign.
• Staging (TNM) usually outweighs grading for prognosis; nomenclature trap: lymphoma/melanoma/seminoma/glioma are malignant.
• OI = type I collagen (COL1A1/2) + blue sclerae; EDS may be dominant or recessive (trap).
• Wilson = ATP7B (not ATP8A/7A), K-F ring, ceruloplasmin↓; treat with trientine/zinc.
• Hemochromatosis = HFE (C282Y), bronze diabetes, adult onset, phlebotomy.
• 22q11.2 is mostly de novo; dysgenesis of the 3rd and 4th pharyngeal pouches → absent thymus/parathyroids → CATCH-22 (hypocalcemia, T-cell deficiency, conotruncal defects).
• Pellagra 3 D's = dermatitis / diarrhea / dementia; diverticulitis does not count.
• Lead poisoning, three targets = blood (basophilic stippling, anemia) / nerve (wrist drop) / kidney (gout-like arthritis, lead line, abdominal colic); less common = dilated cardiomyopathy.
• Trap collection: low-grade osteosarcoma = MYC? Wrong — CDK4/MDM2; cervical cancer = EBV? Wrong — HPV; EDS always dominant? Wrong — either; Wilson = ATP7A? Wrong — ATP7B (7A is Menkes); cardiomyopathy common in lead poisoning? Wrong — atypical.

• If you have not seen the patient, you cannot issue a certificate that assesses current condition (Physicians Act §11); the exception is approved telemedicine for mountainous, offshore-island, remote, or urgent circumstances.
• Consent (parental, legal) vs Assent (the child's agreement): when a procedure offers no therapeutic benefit and is invasive, both are required; a child's behavioral refusal should be met by bringing in a child-friendly team to communicate, not force, not going straight to court.
• Prenatal abnormality: provide information + confirm the diagnosis + respect autonomy, do not counsel abortion.
• A colleague reported for a missed diagnosis: explain the technical limitations of the examination, neither admit fault on their behalf nor evade the question.
• In ethics options, eliminate any choice involving "pressure, concealment, coercion, or admitting fault on someone else's behalf."
• Traps: (1) assuming "the parents consented = the child consented too" (for a no-benefit, invasive procedure like bone marrow donation, assent cannot be skipped); (2) assuming telemedicine "waives examination" (it changes the method, not the requirement); (3) treating "going straight to court" as the next step after a child's refusal (a child-friendly team and psychologist should be brought in first).

• Simple febrile seizure = generalized, <15 minutes, no recurrence within 24h; no routine EEG/imaging/lumbar puncture needed (clinical diagnosis). Described as "focal" is always wrong (that is the complex type).
• First line for anaphylaxis = IM epinephrine 0.01 mg/kg (1:1000 preparation), into the vastus lateralis on the lateral thigh; ceiling of 0.3 mg in children, repeatable every 5–15 minutes; antihistamines/corticosteroids are adjuncts, not substitutes.
• Burn: blisters + extreme pain = second-degree; third-degree is painless (nerve destruction) and is actually worse.
• Pediatric blood loss: hypotension appears only after 30–45% (not 20%) is lost; early on, watch heart rate, CRT, extremities, and urine output.
• 8% dehydration = moderate, with blood pressure usually still normal — not mild.
• Abusive head trauma triad = retinal hemorrhage + intracranial hemorrhage + cerebral edema + no matching history of trauma; retinal hemorrhage is the single most decisive point differentiating it from meningitis/vascular malformation.
• A scenario that does NOT meet child-abuse reporting criteria: a single hand fracture in a child over 2 years old with a matching mechanism (a common accident).
• Traps: (1) describing a simple febrile seizure as "focal convulsions" (that is the complex type); (2) giving an antihistamine first for suspected anaphylaxis and adding epinephrine only after it fails to work (wrong sequence, potentially fatal); (3) using iodine-containing amiodarone for rate control as if feeding a substrate (that trap belongs to the endocrine chapter; this chapter's counterpart trap is misjudging "8% dehydration with normal blood pressure" as mild); (4) attributing infant intracranial hemorrhage plus retinal hemorrhage to "vascular malformation" (vascular malformation cannot explain retinal hemorrhage).

• Vibrio vulnificus: fisherman/raw seafood ingestion + seawater exposure + cirrhosis (free iron) + hemorrhagic bullae → ceftriaxone + doxycycline, with debridement when necessary. The decoy is "Streptococcus, give penicillin."
• Occult spinal dysraphism: midline skin abnormalities such as a hair tuft (faun tail), a deep dermal sinus (>2.5 cm), a lipoma, or a hemangioma → spinal ultrasound first in neonates, MRI (gold standard) afterward or when suspicion is high; least appropriate = observe if asymptomatic.
• High-altitude acclimatization: respiration↑, heart rate↑, blood pressure↑, venous tone↑, EPO/RBC↑, 2,3-DPG↑; the trap phrase is "a fall in venous tone" (wrong direction).
• Cerebral palsy (CP): prenatal factors predominate; perinatal asphyxia accounts for only 10–20%; the most common subtype = spastic; prematurity + PVL → spastic diplegia; CP from perinatal asphyxia is the least in need of karyotype analysis.
• ADHD (attention-deficit/hyperactivity disorder): heritability of about 70–80% (highly heritable), polygenic (DRD4, DAT1 (SLC6A3)); mechanism = insufficient prefrontal-striatal dopamine/norepinephrine signaling.
• Traps: (1) thinking "Streptococcus, give penicillin" first for hemorrhagic bullae + cirrhosis (ignoring the signature of Vibrio); (2) "just observe" a midline hair tuft in an infant (by the time leg weakness appears, it is irreversible); (3) mistaking "a fall in venous tone" for a compensatory response in high-altitude acclimatization (the direction is reversed — acclimatization presses every accelerator down); (4) attributing all CP to birth asphyxia and then ordering a karyotype anyway (prenatal factors are the majority, and CP from perinatal asphyxia is the least in need of karyotype analysis); (5) describing ADHD as "unrelated to genetics, purely environmental" (heritability is about 75%).

• Feeding: solids from 4–6 months + prioritize iron (fetal iron stores are depleted); no honey before age 1 (Clostridium botulinum spores), no skim milk before age 2, table rules only after age 3; protein under age 1 should be predominantly animal-derived (not "plant protein over two-thirds").
• Exclusively breastfed infants: 400 IU of vitamin D daily (to prevent nutritional rickets).
• Iron is absorbed in the duodenum/proximal jejunum; B12 in the terminal ileum + requires intrinsic factor; misplacing iron in the terminal ileum is the classic trap.
• Reflexes: the Moro and other primitive reflexes are "present at birth and should disappear by 3–6 months"; the parachute reflex "does not appear until 6–9 months and never disappears"; a primitive reflex that should disappear but does not suggests a central lesion.
• Menarche: no menarche at 13 but secondary sexual characteristics are developing = normal range, least in need of a workup; the real thresholds for workup are no menarche past 15, no menarche >3 years after breast development, or no secondary sexual characteristics at 13.
• Traps: (1) placing iron's absorption site in the "terminal ileum" (that belongs to B12; iron is upstream); (2) listing the parachute reflex as a "newborn primitive reflex" or as something that "disappears with age" (it appears late and lasts a lifetime); (3) rushing to check FSH/LH/karyotype for no menarche at 13 (as long as Tanner stage II or beyond is progressing, this calls for waiting, not alarm); (4) stipulating that plant protein should exceed two-thirds under age 1 (a false statement — animal milk protein should predominate); (5) assuming exclusive breast milk is "complete nutrition" that needs no vitamin D supplementation.

• IEM (inborn errors of metabolism) is AR by default; the must-know exception: OTC deficiency is X-linked; mitochondrial inheritance follows only the maternal line — a father transmits it to none of his children.
• Congenital adrenal hyperplasia (CAH) = AR, 21-hydroxylase (CYP21A2) deficiency → cortisol/aldosterone↓ → ACTH↑ → adrenal hyperplasia + diversion into androgen synthesis → virilization of female infants + a neonatal salt-wasting crisis.
• OTC deficiency biochemical fingerprint: ammonia↑, citrulline↓, BUN↓, orotic acid↑ (upstream carbamoyl phosphate overflowing into the pyrimidine pathway); differentiate from CPS1 deficiency by orotic acid.
• Acute hyperammonemia: restrict protein + nitrogen-scavenging agents (sodium benzoate/phenylacetate) + arginine + dialysis when necessary.
• X-linked hypophosphatemic rickets: PHEX mutation → FGF-23↑ → renal phosphate wasting; treat with phosphate + active vitamin D (calcitriol) and the newer agent burosumab; this is not vitamin D deficiency.
• Turner syndrome (45,X) = the strongest evidence base for GH, covered by National Health Insurance; central precocious puberty is treated with a GnRH agonist, not GH.
• Bardet-Biedl syndrome (BBS): obesity + postaxial polydactyly + retinitis pigmentosa + intellectual disability + gonadal/renal abnormalities (a ciliopathy).
• Synthetic (recombinant) GH does not cause CJD (only pre-1985 cadaveric-extracted GH carried that risk).
• CP from perinatal asphyxia is the least in need of a karyotype (an acquired brain injury, not a chromosomal abnormality, unlike a chromosomal disorder such as Down syndrome, trisomy 21).
• Traps: (1) treating every urea cycle disorder as AR when calculating inheritance risk (OTC is the must-know X-linked exception); (2) failing to distinguish OTC from CPS1 deficiency by neglecting orotic acid (elevated in OTC, normal or low in CPS1); (3) treating X-linked hypophosphatemic rickets as "vitamin D deficiency" and loading up on vitamin D (what's leaking is phosphate — treat with phosphate plus calcitriol); (4) mistakenly choosing growth hormone treatment for precocious puberty (that is the territory of the GnRH agonist); (5) listing CJD as a side effect of synthetic GH (that is a historical risk of pre-1985 cadaveric-extracted GH).

• Passive immunization: antibody ready-made → immediate onset, no memory, fades within weeks to months; examples: HBIG, tetanus immunoglobulin (TIG), placentally transferred IgG, breast-milk sIgA.
• Active immunization: antigen triggers the host's own response → slow onset, but with memory and long-term protection.
• Post-exposure prophylaxis often requires both together: passive immunization covers "now," active immunization covers "the future."
• Trap: treating "given immunoglobulin" as equivalent to "vaccinated" — exactly backward; immunoglobulin leaves no memory, and it will interfere with a subsequent live attenuated vaccine (see Chapter 7).

• Live attenuated: replicates → humoral + cellular immunity, few doses, no adjuvant needed; contraindicated in severe immunocompromise and pregnancy.
• Inactivated / subunit / toxoid: does not replicate → predominantly humoral immunity, needs multiple doses + boosters, needs an adjuvant; relatively safe in the immunocompromised and pregnant.
• Aluminum salt adjuvant mechanism = antigen depot effect + activation of the NLRP3 inflammasome, manufacturing a danger signal; local redness and swelling is the adjuvant at work, not a contraindication.
• Conjugate vaccine: the polysaccharide is a T-cell independent antigen → poor response and no memory under age two; once linked to a protein carrier (CRM197 / tetanus toxoid), it becomes T-cell dependent → IgG + memory B cells + reduced carriage.
• The pure polysaccharide vaccine (PPSV23) is not used under age two; PCV13 is the one used in infants and young children.
• Traps: ① treating "local redness and swelling" as a contraindication to the next dose; ② assuming a live attenuated vaccine also needs an adjuvant; ③ assuming a polysaccharide vaccine can substitute for a conjugate vaccine in infants.

• Hepatitis B infection during the newborn period → about 90% become chronic carriers (versus only 5–10% for adults) — this is the immune-tolerance phenomenon of "the earlier the infection, the worse the outcome."
• For a newborn of an HBsAg-positive mother: one dose of HBIG (passive) plus dose 1 of the hepatitis B vaccine (active), as soon as possible within 24 hours of birth, given at different injection sites.
• In Taiwan, starting July 1, 2019, publicly funded HBIG was extended to newborns of all HBsAg-positive mothers (no longer restricted to e-antigen-positive mothers).
• The routine hepatitis B vaccine series is 3 doses: within 24 hours of birth, at 1 month, and at 6 months.
• Follow-up: check HBsAg and anti-HBs at 12 months of age.
• Traps: ① assuming HBIG can substitute for the vaccine (immunoglobulin leaves no memory and is gone within months); ② assuming the two injections will neutralize each other and so must be given on separate days (they must be given the same day, at different sites); ③ assuming an e-antigen-negative mother's newborn does not need HBIG (eligibility was expanded starting July 2019).

• Within 24 hours of birth: hepatitis B dose 1 (plus HBIG if the mother is HBsAg-positive); at 1 month, dose 2; at 6 months, dose 3.
• BCG: at 5 months (recommended window 5–8 months), 1 dose; adjusted from "after 24 hours of birth" starting January 1, 2016, for the purpose of reducing osteitis/osteomyelitis; earlier vaccination requires body weight ≥2,500 g.
• Pentavalent vaccine (DTaP-Hib-IPV): 4 doses at 2, 4, 6, and 18 months; then 1 dose of the quadrivalent vaccine (DTaP-IPV) from age 5 to before starting elementary school.
• PCV13: 3 doses, at 2, 4, and 12–15 months.
• MMR: 2 doses, at 12 months and from age 5 to before starting elementary school; varicella: 1 dose at 12 months.
• Live attenuated chimeric Japanese encephalitis vaccine: 2 doses, at 15 and 27 months (replaced the inactivated mouse-brain vaccine starting May 22, 2017).
• Hepatitis A: 2 doses, at 18 and 27 months (schedule adjusted starting January 1, 2025; added to the routine schedule starting 2018).
• Influenza: from 6 months of age; 2 doses 4 weeks apart for a first-time recipient under 8, 1 dose for a first-time recipient 9 or older, then 1 dose annually.
• HPV: 2 doses of the 9-valent vaccine, publicly funded for junior-high (currently 8th-grade) boys and girls; girls covered starting December 2018, extended to boys starting the 2025 academic year.
• Rotavirus: added to the publicly funded schedule starting January 1, 2027; no earlier than 6 weeks, no later than 8 months of age.
• Tdap in pregnancy: at 28–36 weeks of every pregnancy; currently a self-funded recommendation in Taiwan; the mechanism is bulk placental transfer of IgG via FcRn in the third trimester.
• Traps: ① still answering "BCG given after 24 hours of birth" (the old rule); ② still answering "Japanese encephalitis given as 4 doses of a mouse-brain vaccine" (now changed to 2 doses of live vaccine); ③ answering "12–15 months" for hepatitis A (changed to 18 and 27 months starting 2025); ④ treating Tdap in pregnancy as a publicly funded item in Taiwan; ⑤ forgetting that influenza requires "2 doses for a first-time recipient under 8."

• Herd immunity threshold = 1 − 1/R₀; the larger R₀, the higher the threshold.
• Measles R₀ ≈ 12–18 → threshold about 92–95% (the highest of all, and the sentinel for slipping vaccination rates); mumps/rubella/polio R₀ ≈ 5–7 → about 80–86%.
• R_eff = R₀ × (1 − p); only when R_eff < 1 does an outbreak burn out.
• Two assumptions: uniform population mixing (clustering of vaccine refusers → local outbreaks) and 100% vaccine efficacy; factoring in VE, the required vaccination rate becomes (1 − 1/R₀) ÷ VE.
• The purpose of MMR dose 2 is to rescue those for whom dose 1 failed immunologically — not to "boost" antibody after it has waned.
• Traps: ① memorizing the threshold as a fixed "95%" without knowing it is derived from R₀; ② assuming that meeting the national vaccination target rules out cluster outbreaks (ignoring the clustering effect).

• There are only three genuine reasons for a contraindication: ① anaphylaxis to a component or a previous dose (absolute contraindication); ② a live attenuated vaccine meeting severe immunocompromise or pregnancy; ③ moderate-to-severe acute illness (deferred, not permanent).
• False contraindications (may be vaccinated): mild upper respiratory infection, low-grade fever, currently on antibiotics, a local reaction to a previous dose, preterm infant (by actual age), breastfeeding, family history (seizures, allergy, sudden infant death), egg allergy for the influenza vaccine, a pregnant or immunocompromised person in the household.
• The allergen source in MMR is gelatin and neomycin, not egg; the vaccine genuinely associated with egg is the yellow fever vaccine.
• Unexplained encephalopathy within 7 days of a previous DTaP dose → switch subsequently to a formulation without the pertussis component.
• Traps: ① treating "runny nose, low-grade fever" as a contraindication and sending the child home (a missed opportunity); ② treating "egg allergy" as a contraindication to the influenza vaccine; ③ delaying a preterm infant's vaccination using corrected age (should be actual postnatal age); ④ treating family history as a personal contraindication.

• Injected live attenuated vaccines (MMR, varicella): avoid any antibody-containing blood product for at least 2 weeks after vaccination; if one was given first, wait 3–11 months (depending on the product and dose) before vaccinating.
• The nature of the interference is immunization failure (the vaccine virus is neutralized and cannot replicate), not a safety problem.
• Unaffected cases: every inactivated vaccine, every oral live vaccine (rotavirus, oral polio, oral typhoid — which replicate locally in the intestinal mucosa), and HBIG given together with the hepatitis B vaccine.
• Trap: mistakenly answering that "immunoglobulin + live vaccine" is "dangerous" (the correct reason is that it becomes ineffective); or assuming the oral rotavirus vaccine also needs a three-to-eleven-month wait.

• Local redness, swelling, heat, and pain = normal immune activation caused by the adjuvant and antigen, resolving in 1–2 days; not a contraindication to the next dose.
• Timeline differentiation: fever from an inactivated vaccine occurs mostly within 24–48 hours; MMR's fever and rash occur at 7–10 days (the vaccine virus must replicate first). A fever the day after MMR is, more often than not, not caused by the vaccine.
• MMRV as dose 1 at 12–23 months carries roughly twice the febrile-seizure risk of giving MMR + varicella separately → separate administration is recommended at this age.
• BCG: local ulceration and scarring is the expected reaction; lymphadenitis is the most common finding, usually resolving on its own — no routine anti-tuberculosis drugs, and incision and drainage is not recommended; osteitis/osteomyelitis and disseminated BCG disease point to a host immune deficiency (Taiwan surveillance found osteitis/osteomyelitis at about 30.1 per million vaccinees).
• Arthus reaction: tetanus/diphtheria toxoid boosters given too frequently → type III hypersensitivity with immune complex deposition, producing extensive, deep, painful swelling 4–12 hours after vaccination; the management is to lengthen the booster interval (to at least 10 years), not to stop vaccinating permanently.
• RotaShield: approved in 1998, suspended in July 1999, withdrawn from the market in October; attributable risk about 1 case of intussusception per 10,000 vaccinees, occurring mostly within 3–14 days after dose 1; the mechanism is Peyer's patch hyperplasia forming a lead point.
• The current RotaTeq / Rotarix carry a residual risk of about 1–1.5 cases per 100,000; Taiwan's vaccination window is 6 weeks to 8 months.
• Traps: ① treating a local reaction as a contraindication; ② attributing a fever the day after MMR to the vaccine; ③ operating to drain BCG lymphadenitis; ④ mistaking an Arthus reaction for anaphylaxis and stopping vaccination permanently; ⑤ applying RotaShield's risk figures to the current rotavirus vaccines.

• Legal basis: Article 30 of the Communicable Disease Control Act; the right to claim is extinguished 2 years from the day the injury became known, or 5 years from the day it occurred.
• Funding: collected from the manufacturer/importer when the vaccine passes inspection, funding the Vaccine Injury Compensation Fund (a no-fault system — there is no need to first prove fault on the part of the manufacturer or physician).
• Review committee (VICP): 19–25 members, of whom legal experts and impartial public members together make up ≥ 1/3.
• Three causation categories: related, undetermined, unrelated; "undetermined" can still receive compensation — the single most frequently tested point.
• Four types of payment: death, disability, severe illness, other adverse reactions; funeral expenses and medical examination fees may also be subsidized.
• Traps: ① assuming causation must be proven to receive compensation (that is the logic of tort litigation); ② assuming the compensation funds come from national health insurance or from physicians; ③ misremembering the three categories as "related / cannot be ruled out / unrelated" — the statutory term is undetermined.

• Wakefield's 1998 paper in The Lancet: 12 cases, no control group; later confirmed to involve falsified medical records + conflicts of interest (funding from a lawyer, a competing patent); retracted by The Lancet in February 2010, struck off by the GMC that May. Cohort studies of millions of people across multiple countries consistently reject any association between MMR and autism.
• Japan's HPV vaccine incident: proactive recommendation suspended in June 2013 (the vaccine was not taken off the market and remained in the routine schedule) → vaccination rate collapsed from about 70% to <1%, lasting nearly 9 years → reinstatement decided in November 2021, formally resumed with a catch-up program in April 2022.
• What is most commonly seen at a mass vaccination site is not a vaccine adverse reaction, but fainting (vasovagal syncope) and mass psychogenic reactions → arranging a rest-and-observation period after vaccination is the key design feature.
• Taiwan's response: active surveillance + public statistics, no-fault compensation (paying out even when undetermined), school-based mass immunization paired with health education and consent forms, and public funding extended to junior-high-school boys and girls alike.
• Traps: ① assuming Japan "took the HPV vaccine off the market" (it only suspended the proactive recommendation; the vaccine remained in the routine immunization program); ② assuming vaccination rates automatically recover once a retraction is issued (rebuilding trust is far slower than destroying it); ③ mistaking fainting at a vaccination site for a serious vaccine adverse reaction.

• Sampling timing: at 48 hours after birth (feeding must already have occurred); a small quantity of heel blood + filter-paper card + tandem mass spectrometry.
• Drawing blood too early goes wrong in two directions: a false negative for PKU (phenylalanine has not yet accumulated) and a false positive for congenital hypothyroidism (the physiological TSH surge).
• Taiwan's history: 5 items (1985) → 11 items (July 2006) → 21 items starting October 1, 2019; subsidy of NT$200 per case in general, NT$550 for low-income households / resource-poor areas.
• The original 5 items: congenital hypothyroidism, phenylketonuria, homocystinuria, galactosemia, G6PD deficiency.
• A positive screen is not a diagnosis; the next step is a recall for confirmatory testing, not immediate treatment or a diagnosis given directly. Screening deliberately favors high sensitivity over specificity.
• Principle for including an item: causes irreversible harm before symptoms appear + a reliable test exists + an effective treatment exists; a disease with no treatment should not be placed in a screening program.
• Traps: ① drawing blood immediately after birth (produces false negatives/false positives); ② treating a positive screen as a confirmed diagnosis and proceeding straight to treatment or telling the family; ③ assuming the 21 items include Pompe disease, Fabry disease, or mucopolysaccharidosis — those are self-funded add-on items, not part of the publicly funded 21.

• Congenital hearing loss occurs in about 1–2 / 1,000 newborns; appearance is normal during the newborn period, so it cannot be found without screening.
• The 1-3-6 rule: screening within 1 month, diagnosis within 3 months, intervention before 6 months; the reason is the critical period of the auditory cortex and cross-modal plasticity — miss it, and language development can never be caught back up.
• Taiwan: universal subsidy starting March 15, 2012, covering newborns born on or after that date, registered as residents, and under 3 months of age, at NT$700 per case; the initial screen is performed 24–60 hours after birth.
• Method: aABR or OAE.
• Trap: treating "failed the initial screen" as a confirmed diagnosis of hearing loss (rescreening and confirmatory diagnosis are still required); or assuming that a baby who "startles at sound" must have normal hearing (a unilateral or moderate-to-severe hearing loss can still produce a startle response).

• Child Preventive Health Care (free health check): under age 7; increased from 7 to 9 visits starting July 1, 2026 ("7+2") — added at 4–6 / 6–12 months and ages 3–5 / 5–7; content includes growth assessment, physical exam, developmental assessment, and health education; only the registration fee is required, bringing the NHI card + Children's Health Handbook.
• Child Development Screening: added starting July 1, 2024, offering 6 rounds total under age 7 (6–10 months, 10 months–1 year 6 months, 1 year 6 months–2 years, 2–3 years, 3–5 years, 5 years to under 7 years); assesses four domains — gross motor, fine motor, language and cognition, social skills.
• The two run in parallel; neither replaces the other; the golden window for treating developmental delay is before age 3.
• Trap: conflating "developmental screening" with "the preventive health check," or answering "7 visits" (it became 9 starting July 2026).

• Taiwan's Children's Health Handbook has used the WHO child growth standards since 2009 (ages 0–5), extended with local research data for ages 5–7; the curve has five lines at 3%, 15%, 50%, 85%, and 97%, with the 3rd–97th percentile as the general normal range.
• The WHO standard represents "what a child should grow to look like under good conditions" (a prescriptive standard), not the current distribution of a population (a descriptive reference).
• The core of interpretation is trajectory, not position: a downward crossing of two major percentile lines is the real warning sign; a small child growing steadily along one line is normal.
• Order of deviation: nutritional → weight first, height second, head circumference last; head circumference deviating first → central nervous system / congenital; height and weight proportionately low + slow growth velocity → endocrine (growth hormone, thyroid) or genetic (such as Turner syndrome).
• Developmental screening tools (PEDS, the Children's Health Handbook developmental continuum, DDST, and so on) are used only to identify children who need further evaluation, never to render a diagnosis.
• Traps: ① judging "short stature" from the percentile number alone; ② ignoring growth velocity and trajectory; ③ treating the result of a developmental screening tool as a diagnosis.

• The pigment in micronodular hyperplasia is lipofuscin, not melanin.
• Exogenous cortisol → ACTH suppressed → cortical atrophy (not hyperplasia).
• Sorting Cushing syndrome: most common overall = exogenous steroids; most common endogenous cause = Cushing disease (pituitary ACTH adenoma); most common ACTH-independent cause = adrenal cortical adenoma.

• Etiology: meningococcal sepsis → DIC → bilateral adrenal hemorrhage → adrenal crisis.
• Direction of hemorrhage: medulla → cortex (inside-out); the trap answer reverses this.

• S100(+) = sustentacular cells; chief cells are chromogranin/synaptophysin(+). Do not reverse them.
• First-choice biochemistry: metanephrines; histological arrangement: Zellballen.
• Drug order: α-blocker first, then β-blocker (giving β first risks a hypertensive crisis).
• Roughly 30–40% hereditary, linked to MEN2/VHL/NF1/SDHx.

• Most common cause of pituitary hyperfunction = anterior pituitary adenoma; most common functional type = prolactinoma.
• Macroadenomas can be complicated by pituitary apoplexy and can compress the optic chiasm to cause bitemporal hemianopsia.
• Craniopharyngioma = suprasellar cystic mass, keratinized squamous epithelium, motor-oil-like cyst fluid, calcification, Rathke pouch remnant.
• T1DM = insulitis (immune attack); T2DM = IAPP/amyloid (protein clogging).

• Hypothyroidism causes weight gain (metabolism↓); hyperthyroidism causes weight loss.
• The key to sick euthyroid = rT3↑, T3↓; do not force-feed thyroid hormone.
• Primary hypothyroidism (TSH↑/T4↓) does not need a pituitary MRI; a central problem cannot be distinguished by TSH alone — FT4 must be added.
• Hashimoto's = TPO; Graves' = TRAb. Graves' ophthalmopathy has no direct correlation with the level of thyroid function.
• Pretibial myxedema = non-pitting.

• Gold standard for preoperative benign/malignant distinction = FNAC (not confirmed by ultrasound / scintigraphy).
• Most common = papillary carcinoma (80–85%, lymphatic metastasis); follicular carcinoma spreads hematogenously and is hard to diagnose by FNA.
• Follow thyroglobulin for well-differentiated cancer; follow calcitonin + CEA for medullary carcinoma, linked to MEN2.
• Most important risk factor = history of head-and-neck radiation exposure.

• Storm combination: PTU + propranolol + iodine solution (1 hour after the ATD) + hydrocortisone.
• Iodine solution must not be given before the ATD; storm with atrial fibrillation contraindicates amiodarone (contains iodine).
• ATD with fever + sore throat → check WBC/ANC first to rule out agranulocytosis.
• "Radiotherapy" for hyperthyroidism = RAI (¹³¹I), not stereotactic radiation.
• Myxedema coma: IV levothyroxine + give hydrocortisone first.

• Initial serum potassium in DKA = normal or elevated (total body potassium is deficient); it only falls after insulin is given — when K⁺ <3.3, replace potassium first and hold insulin.
• Acid-base status in DKA = metabolic acidosis + respiratory compensation (Kussmaul hyperventilation), not respiratory acidosis.
• HHS: glucose >600, osmolarity >320; serum sodium is not a reliable indicator of dehydration and requires correction.
• Management = fluids first → check potassium → low-dose continuous IV insulin; oral drugs must not be substituted.
• Bicarbonate is considered only when pH < 6.9.

• Metformin: very rarely causes hypoglycemia, long-term use causes B12 deficiency, held before contrast studies to prevent lactic acidosis.
• Weight loss = SGLT-2i / GLP-1 RA; DPP-4i is weight-neutral. Thiazides raise blood glucose and do not cause hypoglycemia.
• Early diabetic nephropathy = microalbuminuria (creatinine still normal); gold standard for foot osteomyelitis = bone biopsy.
• HbA1c target in the elderly: relaxed to <8.0–8.5%.
• Leading cause of fasting hypoglycemia = glucose-lowering drugs; insulinoma vs. exogenous insulin is distinguished by C-peptide (endogenous↑, exogenous↓).
• Pompe disease = GAA deficiency, newborn screening + ERT.

• Screening = IGF-1 (GH is pulsatile; a single normal measurement cannot rule it out); diagnosis = GH not suppressed after OGTT; localization = MRI.
• First-choice treatment: transsphenoidal surgery; first-choice drug: somatostatin analog; leading cause of death = cardiovascular.
• Prolactinoma is the only pituitary adenoma for which medication is preferred (cabergoline first-choice); high PRL is not always a tumor (stalk effect).

• Water deprivation cannot distinguish CDI/NDI; after desmopressin, urine osmolarity↑ = CDI, no rise = NDI.
• Most common drug cause of NDI = lithium.
• ADH is mainly regulated by plasma osmolarity; SIADH = excess ADH → hyponatremia (the opposite of DI).
• Lymphocytic hypophysitis: postpartum women, MRI shows gland enlargement (not an empty sella).

• Mechanism: postpartum hemorrhage → ischemic necrosis of the anterior lobe; the posterior lobe is spared → diabetes insipidus is uncommon (a trap).
• First to appear = inability to lactate (PRL is lost earliest).
• In acute decompensation, replace steroid first, then thyroid hormone.

• Hypogonadism: FSH/LH high = primary (including postmenopause); low = secondary (Sheehan, Kallmann). FSH is elevated after menopause.
• MEN 1 = 3 P's (Pituitary/Parathyroid/Pancreas, MEN1 gene).
• MTC + pheochromocytoma belong to MEN 2 (RET gene), not MEN 1.

• Metabolic syndrome = high TG + low HDL + hypertension + high glucose + abdominal obesity, 3 of 5, does not include high LDL (the core is insulin resistance; LDL undergoes a qualitative, not quantitative, change).
• Taiwan waist circumference: men ≥ 90, women ≥ 80; obesity = BMI ≥ 27 (overweight 24–26.9); BMI 25.7 = overweight, not obese.
• In obesity: leptin↑ (resistance), adiponectin↓.
• Statins = inhibit HMG-CoA reductase (not oxidase), cardiovascular first-choice; fibrates promote gallstones; niacin flushing is PG-mediated and preventable with aspirin.
• Prava/rosuva are unaffected by grapefruit juice; lova/simva/atorva are affected.
• PCSK9 loss-of-function mutation → LDL decreases (protective); the inhibitor produces the largest reduction.
• DPP-4i (sitagliptin) is weight-neutral and not approved for weight loss; GLP-1 RA is first-choice for weight loss, with tirzepatide producing the largest effect.
• Weight-loss surgery = BMI ≥ 40 or ≥ 35 with comorbidity; lowers mortality, induces remission of diabetes.
• Anorexia nervosa: hypotension, hypoglycemia, elevated cortisol, constipation (not diarrhea).

• Primary hyperparathyroidism = high calcium, low phosphate, high chloride (hyperchloremic acidosis, Cl/P > 33); in malignancy-associated hypercalcemia (PTHrP), true PTH is instead suppressed.
• FHH closely mimics PHPT (PTH normal/mildly elevated) but has low urinary calcium (Ca/Cr clearance < 0.01), is benign, and needs no surgery; CKD → secondary hyperparathyroidism (low/normal Ca, high P); autonomy → tertiary (flips to high Ca).
• Hypercalcemia = neuromuscular depression (weakness, constipation, lethargy); hypocalcemia = neuromuscular excitation (paresthesia, tetany, Chvostek/Trousseau).
• NS hydration is first-line for hypercalcemic emergencies; thiazides are forbidden; bisphosphonate treats the root cause but is slow, calcitonin is fast but brief (often combined).
• Hypocalcemia evaluation order: albumin → PTH → Mg; if Mg is low, replace Mg first, or calcium repletion will fail; 1,25D is not first-line.
• Corrected Ca = measured Ca + 0.8 × (4 − albumin); alkalosis lowers ionized calcium.
• ECG: hypocalcemia prolongs QTc, hypercalcemia shortens QTc.
• Osteoporosis: DXA T-score ≤ −2.5; antiresorptive vs. anabolic (teriparatide is a bone-forming agent, as are abaloparatide and romosozumab); antiresorptive agents are for "preventing recurrence," not acute pain control.
• Traps: PHPT is not high phosphate/low chloride (that is backward); hypercalcemia does not cause paresthesia or cramps; do not give bisphosphonate first in an emergency (too slow); correct for low albumin before anything else; teriparatide builds bone precisely because it is given intermittently; if calcium repletion fails, check magnesium first.

• Any amenorrhea: test for pregnancy first; secondary = ≥ 3 months without a period, primary = no menarche by age 15.
• LH→theca cell (androgens), FSH→granulosa cell (aromatized to E2); the hCG receptor is on the cell membrane; pulsatile GnRH drives both FSH and LH, while continuous administration instead suppresses.
• Estrogen at low concentration gives negative feedback; at high, sustained concentration (≥48h) gives positive feedback → LH surge (the only positive feedback in the whole cycle); the luteal phase is fixed at about 14 days.
• The Rotterdam criteria for PCOS do not include obesity/insulin resistance; obesity with no fertility desire → weight loss first; letrozole is first-line for ovulation induction; follicle threshold is classically ≥12, ≥20 per ovary under the updated guidelines, volume ≥10 mL.
• "Breasts, no hair" = CAIS (46,XY); "breasts and hair, no uterus" = MRKH (46,XX, check the kidneys); no breasts → check FSH: high = Turner, low = Kallmann (anosmia).
• Müllerian duct anomalies require renal/urinary tract screening; the ovaries are not of Müllerian origin; never induce a withdrawal bleed in vaginal agenesis; septate uterus = the most common structural cause of recurrent miscarriage.
• HRT: add progesterone if the uterus is present, estrogen alone if it is not; FIGO Type 0 fibroids → hysteroscopy first-line; GnRH agonists only preoperatively for ≤6 months; danazol is non-standard.
• PMB is most commonly caused by endometrial atrophy, but endometrial cancer must always be excluded first; hydrosalpinx does not cause uterine bleeding.
• In CAH (21-OH deficiency), the female infant's uterus and ovaries are normal — only the external genitalia are virilized; pubic hair is the hair most sensitive to androgen.

• Lipid-soluble hormones (steroids, T4, 1,25-DHCC) use nuclear receptors; water-soluble hormones (peptides, amines, epinephrine) use membrane receptors; T4 is the lipid-solubility trap question.
• The adrenal medulla is stimulated by "preganglionic" sympathetic neurons (not postganglionic) to secrete epinephrine (about 80%).
• Cortisol peaks in the early morning, promotes erythropoiesis, and promotes bone resorption (the hormone least likely to increase bone mass); ACTH → PKA (not PKC); StAR transports cholesterol into mitochondria = the rate-limiting step; DHEA is regulated by ACTH (not LH).
• Hyperkalemia "directly" stimulates the zona glomerulosa to secrete aldosterone.
• Primary hyperaldosteronism: hypertension + hypokalemia + metabolic alkalosis + low renin; hypokalemia → insulin↓ → glucose intolerance.
• TSH is the most sensitive (early) marker, free T4 is best for confirming hypothyroidism; thyroid hormone binds a nuclear receptor; hypothyroidism → PRL↑ → galactorrhea and amenorrhea.
• β-cell GLUT2 senses blood glucose (board convention; human β cells mainly use GLUT1); Ca²⁺↑ triggers exocytosis; insulin's acute action does not include protein synthesis (which occurs hours later); sulfonylureas close the K⁺-ATP channel.
• Parathyroidectomy → serum calcium↓, serum phosphate↑ (one falls and one rises, not both falling).
• LH→Leydig cell→testosterone; FSH→Sertoli cell→sperm+inhibin; oxytocin is synthesized by the hypothalamus and released by the posterior lobe.
• Klinefelter (47,XXY): testosterone↓ → LH and FSH "rise"; 21-OH deficiency → 17-OHP↑↑ + salt-wasting (11-OH deficiency instead causes hypertension).
• GH signals through JAK2/STAT5, mediates growth via IGF-1, peaks during nocturnal deep sleep, and is stimulated by hypoglycemia; before closure = gigantism, after closure = acromegaly; diagnosed by failure of GH suppression after an OGTT. Ghrelin is the only gastrointestinal hormone that stimulates appetite.

• PTC nuclear features: ground-glass nuclei, nuclear grooves, intranuclear pseudoinclusions + psammoma bodies; prominent nucleoli are not PTC; BRAF V600E; tracked with thyroglobulin.
• FTC vs. follicular adenoma is distinguished by capsular/vascular invasion — FNA cannot tell them apart.
• MTC: C cell, secretes calcitonin, stromal amyloid, 25% associated with MEN2 (RET germline), radioactive iodine ineffective; MEN2A = MTC + pheochromocytoma + parathyroid hyperplasia, MEN2B = MTC + pheochromocytoma + mucosal neuromas (no parathyroid disease); pheochromocytoma must be excluded before thyroid surgery.
• Parathyroid: primary = single adenoma (high Ca, low P, high PTH); secondary = CKD (low/normal Ca, high P, high PTH); tertiary = autonomy (flips to high Ca); in malignancy-associated hypercalcemia, PTH is suppressed.
• Thymoma is associated with myasthenia gravis; the most common histologic type of thymic carcinoma = SCC; anterior mediastinum's 4 T's.
• Most common benign salivary gland tumor = pleomorphic adenoma (has a chondroid component); most common malignant = mucoepidermoid carcinoma (not SCC); Warthin = oncocytic + lymphoid stroma, no cartilage, associated with smoking; adenoid cystic carcinoma = perineural invasion + cribriform pattern.
• Oral erythroplakia's malignant transformation risk ~50% ≫ leukoplakia's ~5% (more urgently warrants biopsy).
• Nasopharyngeal carcinoma = EBV; oropharyngeal carcinoma = HPV-16 (p16+, better prognosis); nasopharyngeal angiofibroma = adolescent males, posterolateral wall, androgen-dependent, prone to massive hemorrhage; Schneiderian papilloma = HPV 6/11, recurs easily with incomplete resection.
• Keratoconus's main pathology = corneal stromal thinning; the iris type of ocular melanoma progresses slowly, with a relatively better prognosis.

• Cyclosporine/tacrolimus inhibit calcineurin → ↓IL-2; sirolimus inhibits mTOR (can be combined with CsA, not a contraindication); CsA signature = nephrotoxicity + gingival hyperplasia, tacrolimus = new-onset diabetes.
• The most common side effect of long-term glucocorticoids = osteoporosis; peptic ulcer disease is a contraindication; must never be stopped abruptly; acts on intracellular nuclear receptors, inducing lipocortin → inhibiting phospholipase A2.
• Methimazole is first-line for hyperthyroidism; PTU is used for thyroid storm/the first trimester (PTU additionally inhibits peripheral T4→T3).
• Alendronate (a bisphosphonate) inhibits osteoclasts; teriparatide is an anabolic (bone-forming) agent, as are abaloparatide and romosozumab; vitamin D3 is contraindicated in hypercalcemia; danazol does not improve osteoporosis.
• Raloxifene/clomiphene/tamoxifen are all SERMs with differing tissue selectivity; tamoxifen increases endometrial cancer risk, raloxifene has no uterine stimulation.
• Diabetes: oral hypoglycemics cannot be used in T1DM; SU/meglitinides cause hypoglycemia; repaglinide is safe in renal insufficiency (biliary excretion); metformin + alcohol → lactic acidosis; the GLP-1 agonist liraglutide must be injected (oral semaglutide is now available); SGLT2i is now standard therapy for heart failure and chronic kidney disease — stop preoperatively to prevent euglycemic DKA.
• Laron syndrome is treated with mecasermin (IGF-1), not GH; acromegaly contraindicates GH — use octreotide instead; GH signals through JAK/STAT (not a GPCR); octreotide worsens constipation.
• EPO signals through JAK2/STAT5 (not ERK) and is contraindicated in poorly controlled hypertension; romiplostim/eltrombopag = TPO receptor (not G-CSF); desmopressin is procoagulant → releases Factor VIII + vWF.
• Misoprostol = a PGE1 analog (not PGF2α); tolvaptan = a V2 antagonist for hyponatremia (SIADH); cinacalcet = a calcimimetic that sensitizes the CaSR → ↓PTH, ↓serum calcium.
• IFN-γ → chronic granulomatous disease; IFN-β → multiple sclerosis (do not confuse them); bromocriptine = D2 agonist → ↓prolactin.

• A mask only blocks droplets/aerosols; blood, vector-borne, and foodborne/waterborne routes are not on its path — no amount of wearing helps.
• Giardia/Cryptosporidium are chlorine-resistant; only filtration removes them.
• Surveillance pyramid: most infections at the base, fewest confirmed cases at the apex — reverse the order and it's wrong.
• The incubation period tracks symptoms, the latent period tracks infectiousness, the serial interval tracks two people.
• R₀ is the intrinsic transmissibility with "no immunity, no intervention"; herd-immunity threshold = 1 − 1/R₀.
• Foodborne illness ≥ 2 people; botulism/chemical poisoning 1 person; HIV/AIDS target 95-95-95; Category I notifiable disease reported within 24 h.
• Hexavalent chromium → nasal septal perforation; newspaper press workers are not high-risk for pneumoconiosis.
• TWA's denominator is the sum of actual time, not 8 hours.
• Greenhouse gases do not include NH₃; HACCP's "chicken cooked thoroughly" = CCP; acrylamide comes from the Maillard reaction in starch at high temperature.

• SCT is at the interpersonal level, core construct self-efficacy; HBM is at the individual level, with constructs susceptibility/severity/benefits/barriers/cues to action.
• In TTM, precontemplation calls for "consciousness raising" first — don't rush to teach techniques; contemplation vs. preparation differs on "whether a concrete action has been taken."
• Multi-system + emotional + social stress → the biopsychosocial model.
• The Family APGAR's theoretical foundation = systems theory (not the biopsychosocial model); don't confuse it with the neonatal Apgar.
• Referral = coordination; handling multiple things in one visit = comprehensiveness; the two are most easily swapped.
• Target heart rate at age 70 ≈ 90–105; exercise volume can be accumulated in bouts.
• The Healthy City is a process, not an outcome; a first-time drug-use offender may receive observation/rehabilitation, not automatic prosecution.
• Nonverbal communication ≈ 60–80%; crossed arms = defensiveness; Hall's three thresholds 45/120/360; examination enters the intimate zone.

• Exposure first, then disease = cohort; disease first, then retrospective exposure = case-control; simultaneous = cross-sectional; group as the unit = ecological (prone to ecological fallacy).
• Case-control calculates OR; under the rare-disease assumption, OR ≈ RR; for a common disease, OR overestimates.
• Confounding must be removed; effect modification must be reported; the purpose of matching = controlling confounding (not increasing heterogeneity).
• Case-control fears recall bias; cohort fears loss to follow-up; screening fears lead-time bias.
• Three or more continuous groups → ANOVA; 1:1 matched 2×2 → McNemar's test; expected count < 5 → Fisher's exact test.
• If the CI covers the null value, it's not significant; null for a ratio = 1, null for a difference = 0.
• Type I is α, false positive; Type II is β, false negative; power = 1 − β; too small a sample → Type II error.
• Random error is erratic, systematic error is skewed; use the median for skewed data; use SD to describe spread; pooling different populations introduces confounding bias.
• Highest level of evidence = RCT; Hill's one indispensable criterion = temporality.

• Sn/Sp/LR are unaffected by prevalence; PPV/NPV are affected by prevalence (prevalence↓ → PPV↓ → FDR↑).
• The metrics most meaningful to clinical practice = PPV/NPV; LR+ > 10 strongly rules in, LR− < 0.1 strongly rules out.
• Raising the threshold → Sp↑, Sn↓; parallel testing → Sn↑; serial testing → Sp↑.
• Screening biases: lead-time, length-time, overdiagnosis → should instead look at disease-specific mortality.
• Screening belongs to secondary prevention / the third stage; a disease must be treatable before it should be screened for.
• Judge treatment benefit by ARR/NNT (NNT = 1/ARR), not the exaggeration-prone RRR.
• Meta-analysis = Level I / Grade A; PICO's I is the intervention.
• USPSTF Grade A: pre-pregnancy folate 0.4–0.8 mg/day; STI prevention (Grade B; intensive in 2014, behavioral counseling in 2020) with intensive counseling.
• A 15-year-old girl does not receive the zoster vaccine (it is for age ≥ 50).

• Health-insurance DNA = mandatory enrollment + a single government-run payer; capitation is most economical, FFS is most prone to overtreatment; the global budget is a supply-side control.
• SID belongs to the supply side, moral hazard to the demand side; the demand-side countermeasure is co-payment.
• In BSC, financial is lagging; learning-and-growth/internal process are leading; SWOT's O is Opportunities.
• The WHO Healthy City health-category indicators do not include the abortion rate; the Pharmaceutical Affairs Act's "drugs" include medical devices.
• Shock: flat jugular veins → hypovolemic; distended → cardiogenic/obstructive; Beck's triad → cardiac tamponade.
• Septic shock's vasopressor of choice is norepinephrine; anaphylaxis's first line is IM epinephrine.
• Parkland counts only second- and third-degree burns, half the volume in the first 8 h, counted from the time of injury.
• BAC 0.30 causes light coma; only > 0.40 is potentially fatal.
• The mechanism of referred pain = convergence at the same spinal segment; using it in reverse to localize a viscus is wrong.
• The most common primary headache = tension-type; a thunderclap headache first rules out SAH; MOH is managed by withdrawal.
• Lymphedema: emollients are not contraindicated; for typhoons, the recovery phase exceeds the acute phase; earthquake casualties cluster within hours of the event.
• Chemical disaster: hot zone rescues, warm zone decontaminates, cold zone triages.

• Delirium: dementia is the single most important predisposing factor; incidence in hospitalized older adults is 14–56%; BZDs/restraint/anticholinergics worsen it.
• The one parameter that does not decline with aging = serum insulin.
• MMSE assesses cognition; self-medication = IADL; TUG assesses fall risk.
• The five Fried criteria: thin, tired, weak grip, slow gait, sedentary — cognition is not one of them.
• High risk for hypothermia does not include healthy adults aged 30–50; altered mental status in an older adult is not caused by hypolipidemia; malnutrition risk does not include drinking soda.
• The goal of hospice care = symptom relief and a good death; first-line for dyspnea is low-dose morphine; first-line for delirium is haloperidol; opioids must always be co-prescribed with a laxative.
• Hospice Palliative Care Act vs. Patient Right to Autonomy Act: the latter extends to five categories and allows refusal of artificial nutrition; dementia must be extremely severe.
• DNR priority: self > pre-signed declaration/proxy > spouse > children > parents > siblings > grandparents; adult children take priority over parents.
• Withdrawing life support is legal; euthanasia is illegal; the WMA's 2019 declaration opposes euthanasia and supports informed refusal of life-sustaining treatment.

• The four principles have equal standing, with no fixed order (prima facie); justice = distributive justice.
• When family asks for concealment → decline on the basis of autonomy; therapeutic privilege has a very high threshold and cannot be invoked merely because the family asks.
• Informed consent must include alternative treatment options and the consequences of forgoing treatment; coercion violates voluntariness.
• Nuremberg = the starting point of voluntary consent; Helsinki = subject welfare comes first; Belmont = the three principles; the Declaration of Lisbon belongs to patient rights, not research ethics.
• Under a dependent relationship, informed consent must be obtained by an independent, qualified individual; an impartial witness is not enough.
• Vulnerable populations include the embryo but not the healthy older adult alone; the corresponding author is determined by actual contribution, not by position.
• Clinical trial records are retained permanently (even if the subject is a child).
• Mandatory public health policy must satisfy the principle of proportionality; secondhand smoke exceeds pure autonomy and permits intervention.
• A known surgical complication = no-fault harm; a Phase II trial tests preliminary efficacy + dosing, and later stages often include a control.
• Reporting: for vulnerable persons, mandatory reporting to the competent authority within 24 hours; for adult sexual assault, reporting to the competent authority is a duty, but evidence collection and reporting to police respect the individual's own wishes.
• Confidentiality may be promised externally; the medical record must be charted truthfully; the paper record belongs to the hospital, and the patient may request copies.
• Teaching clerkships require prior notice and consent; unauthorized access to an unrelated record is itself a violation; Medical Care Act Article 106 on obstructing medical practice = a non-complaint offense.

• The central thesis of patient safety: errors originate in the system, not the individual; the Swiss cheese model = an accident occurs when the holes across multiple layers of defense align.
• A critical value is defined by "time," not "magnitude": without immediate action, death or irreversible harm may occur within hours. Thresholds are set by each institution.
• The three elements of the critical-value closed loop: notify the person who can give the order personally → read-back → document the time/recipient/response. Posting in a group chat or leaving a message with a clerk does not count as delivery.
• Both major quality metrics in the laboratory are time-based: turnaround time (TAT) and the critical-value notification interval. The Joint Commission's NPSG.02.03.01, 2005.
• SBAR = a format for the speaker (forcing out the A assessment and R recommendation; originated on nuclear submarines → Kaiser Permanente); I-PASS = a handoff protocol that includes a closed loop (the key is the final synthesis by receiver).
• Responsibility after a handoff does not vanish — it splits: the one handing off is responsible for "speaking clearly," the one taking over is responsible for "acting reasonably"; the only evidence is the medical record.
• Medical Care Act Article 68: Paragraph 1 requires personal documentation plus a signature or stamp with the date; Paragraph 3 requires a verbal order to be followed by a written record within 24 hours.
• The mechanism behind the surgical safety checklist's effectiveness: converting a default assumption into a spoken declaration, creating a legitimate moment to speak, and using team self-introduction to break down hierarchy — not "helping people remember."
• Three checkpoints: sign in before anesthesia induction (patient awake) / time out before incision (whole team pauses) / sign out before leaving the room; WHO 2008, 19 items, the 2009 study showed mortality 1.5%→0.8% and complications 11%→7%.
• The site marking is made by the operating surgeon at the incision site with the patient awake and participating; a discordant count → recount, search, intraoperative X-ray if needed — never close the wound outright.
• Signing a checklist after the fact = ineffective; the active ingredient is verbal execution. Wrong-site/wrong-patient surgery and retained foreign objects = never events.
• What accrediting bodies sell is "whether you are eligible to be paid": TJC 1951 (deemed status), JCI 1998, JCT 1999.
• Reporting systems vs. accreditation run on opposite logic: reporting is anonymous, voluntary, confidential, non-punitive, and oriented toward shared learning (the TPR, 2003); accreditation is named and holds people accountable. The second victim is the healthcare worker involved.

• The four axes of healthcare-associated infection: VAP, SSI, CLABSI, CAUTI.
• CLABSI's three routes of invasion → three corresponding countermeasures: maximal sterile barrier precautions + chlorhexidine (at insertion), daily dressing inspection (the external surface), and scrub the hub (the internal lumen).
• Site: the femoral vein has the highest infection rate (proximity to the perineum plus friction from hip flexion); the subclavian vein has the lowest infection rate but a higher risk of pneumothorax — this is a trade-off, not a ranking.
• The single strongest intervention is "assessing daily whether this line is still needed"; the real variable in Pronovost's Michigan program (2006, NEJM) was authorizing nurses to halt the procedure.
• CAUTI: the biofilm shields bacteria from antibiotics and immune defenses; duration of catheterization is the strongest single risk factor; the only effective intervention = don't place it, remove it early.
• Asymptomatic bacteriuria is not treated, with the only exceptions being pregnant women and before a procedure likely to cause bleeding of the urinary tract mucosa.
• Catheter-tip culture cannot diagnose CAUTI; when in doubt, replace the catheter first, then obtain a specimen.
• Routine catheter changes, bladder irrigation, and prophylactic antibiotics are all ineffective; the drainage bag must be below the bladder, off the floor, and part of a closed system.
• Large trials of antimicrobial-coated catheters do not support routine use — "doing nothing" is the correct answer.
• In the U.S., starting October 1, 2008, CMS stopped providing additional payment for hospital-acquired conditions such as CLABSI/CAUTI arising during a hospital stay (stemming from the Deficit Reduction Act of 2005): using money to turn infection from a cost center into a matter of revenue protection.

• The gold standard for pain assessment is patient self-report; objective indicators are only substitutes. Vital signs cannot replace a pain assessment.
• Scales fall into two classes: self-report (NRS, VAS, VRS, Wong-Baker FACES) and behavioral observation (FLACC, PAINAD, CPOT/BPS).
• Wong-Baker is a self-report tool, for roughly age 3 and up, and the patient points to it himself — the tool most often mistaken for an observational scale.
• FLACC ≈ 2 months–7 years; PAINAD is for advanced dementia; use CPOT/BPS for intubated, sedated patients.
• The generally accepted threshold for a clinically meaningful improvement is an NRS decrease of ≥ 2 points or ≥ 30%.
• A complete pain assessment covers more than intensity alone: location, quality, temporal pattern, aggravating and relieving factors, and functional impact (can the patient sleep, can he walk). Recording only a single number is the most common quality defect.
• The "fifth vital sign" movement: proposed by the American Pain Society in the 1990s → adopted by the Veterans Health system in 1999 → the Joint Commission's 2001 pain management standards; its causal relationship to the opioid crisis remains contested and cannot be asserted outright, and the field has since shifted toward functional improvement and multimodal analgesia.

• Communication: SPIKES = Setting up, Perception (ask first), Invitation, Knowledge (warning shot + small pieces + jargon-free), Emotions (emotion before information), Strategy; the order comes from cognitive load and cannot be reordered.
• Companion tools: ask-tell-ask, NURSE; never say "there's nothing more we can do"; silence is a tool; answer prognosis questions with a range.
• Informed consent vs. SDM: the former is one-way disclosure followed by authorization (a recommendation already exists); the latter applies when multiple reasonable options exist and their relative merit depends on the patient's values and preferences. Taiwan has promoted SDM since 2016.
• Children and adolescents: legal consent rests with the guardian, but the child's assent should still be obtained.
• Medical records: of SOAP's four columns, A (Assessment) is the most valuable, since it is the only place the reasoning process is documented; undocumented ≈ never done.
• Article 68 of the Medical Care Act: ① personal recording + signature/seal + dated by year, month, day; ② any addition or deletion must be signed/sealed and dated at the point of change, struck through with a line, never obliterated; ③ a verbal order must be followed by a written record within 24 hours.
• Lawful correction = a line struck through + the original text still legible + an annotation + a signed date; correction fluid, torn-out pages, or after-the-fact backfilling = falsification and tampering.
• Risks of the electronic record: note bloat and copy-forward give errors the false credibility of having been "confirmed every day"; the audit trail must never be falsified. Patients can access records in real time (Taiwan's My Health Bank, since 2014), and derogatory phrasing shapes subsequent care.
• Death certificate: Article 11-1 of the Physicians' Act — may not be issued without personally examining the body; Article 76 of the Medical Care Act — may not be refused without cause, the cause of death must be handled with the utmost care, and a death that is not natural or suspected not to be natural must be reported to the prosecutorial authority for inquest; Article 16 of the Physicians' Act carries the same intent.
• Administrative inquest (natural disease/natural death, physician, issues the death certificate) vs. judicial inquest (not natural or suspected not to be, prosecutor accompanied by a forensic physician, issues the inquest certificate). The test is whether a non-natural death can be ruled out.
• The cause-of-death section is a causal chain; the bottom-most line is the underlying cause of death, and it is this single line that ICD cause-of-death statistics code.
• "Cardiopulmonary failure / respiratory failure / cardiac arrest / multi-organ failure" are modes of dying, not acceptable underlying causes of death; an external cause must state the mechanism and circumstances of injury.

• MHC: I → HLA-A/B/C, all nucleated cells, presents endogenous antigen, to CD8; II → HLA-DR/DP/DQ, APCs, exogenous, to CD4 (8×1, 4×2).
• Orbital floor blow-out → inferior rectus entrapment → cannot look up (do not mistakenly pick the superior rectus).
• Septal hematoma → immediate incision and drainage (otherwise cartilage necrosis, saddle nose); the cartilage eats only by clinging to its membrane.
• Cyclosporin/Tacrolimus = calcineurin inhibitors → inhibit IL-2; shared nephrotoxicity, grapefruit-juice interaction; first choice for acute rejection is high-dose steroid pulse (not a change of drug).
• Most common melanoma = SSM (superficial spreading); biopsy by complete excision.
• Pressure ulcers: ischium 60 mmHg, sustained >1 hour is irreversible; turn every 2 hours in bed, every 15 minutes when seated.
• Supreme principle of clinical trials: participant rights, safety and well-being first, overriding scientific/social interests.

• NHI launched on 1995/3/1, integrating the medical benefits of the thirteen existing social insurance schemes; single insurer = the National Health Insurance Administration (NHIA).
• The reason for mandatory enrollment is to prevent adverse selection; the reason for a single insurer is to prevent risk selection.
• Premiums are split three ways: employee 30% / employer 60% / government 10%; employers and the self-employed pay 100% themselves; Category 2 and the Category 6 regional population pay 60% themselves; Category 5 low-income households are fully covered by the government.
• General premium = insured amount × rate × contribution ratio × (self + dependents, dependents counted up to 3); current rate 5.17%, statutory cap 6%.
• Second-generation NHI implemented 2013/1/1; supplementary premium rate 2.11%, six withholding items: bonuses (above 4 times the insured amount), part-time salary (at or above the basic wage), professional practice, dividends, interest, rent (single payment of NT$20,000 or more), cap per payment NT$10 million → because of the cap, the supplementary premium is regressive.
• The employer-side supplementary premium is charged on "the difference between total salaries and total insured amounts," to prevent under-reporting.
• The theoretical basis of copayment is moral hazard; its downside cost is suppressing necessary care among the vulnerable.
• Inpatient copayment: acute ward 10% within 30 days, 20% for days 31–60, 30% from day 61 (the longer the stay, the heavier the out-of-pocket share — the incentive is to push transfers out).
• New scheme of 2023/7/1: emergency copayment NT$750 at medical centers, NT$400 at regional hospitals; the outpatient-drug cap at medical centers / regional hospitals raised to NT$300.
• Exempt from copayment: catastrophic illness, childbirth, mountain and offshore-island areas, low-income households, veterans, children under 3, occupational injury or illness, tuberculosis.

• Fee-for-service (FFS) incentive = do more, get more → supplier-induced demand → runaway costs.
• Global budget payment system: set the total first, then allocate; payment per point = sector global budget ÷ sector total claimed points → floating point value.
• Implementation sequence: dental 1998/7 → Chinese medicine 2000/7 → Western-medicine primary care 2001/7 → hospitals 2002/7 (full implementation).
• Taiwan uses an expenditure cap (not an expenditure target) → the risk of excess volume is borne by providers through point-value dilution.
• Point value < 1 = point-value dilution / discount; collective volume-pushing is a prisoner's dilemma, and self-discipline is game-theoretically unstable.
• Tw-DRG: phase one 2010/1, 164 groups; phase two 2014/7, 254 groups; phase three postponed.
• The larger the settlement unit (FFS → per diem → DRG → capitation), the stronger the incentive to economize, and the stronger the incentive for risk selection.
• DRG side effects: cream skimming, diagnostic upcoding (DRG creep), premature discharge and readmission; mitigated by exclusion clauses and outlier add-on payments (80% of costs above the upper threshold).
• P4P (pay-for-performance) piloted since 2001/11; pitfalls are indicator selection bias, patient selection due to inadequate risk adjustment, and the ceiling effect.

• Drug-price gap = NHI reimbursement price − the institution's actual purchase price; it is a lawful negotiated margin, and "drug-price black hole" is a misnomer.
• Drug price survey → lower reimbursement prices based on actual transaction prices; the side effect is low-margin old drugs leaving the market → drug shortages.
• Drug Expenditure Target (DET): if the annual drug-spending target is exceeded, a price adjustment is triggered the following year to recover the overspend.
• Marketing authorization (TFDA) ≠ reimbursement (NHIA): the former asks about safety and efficacy, the latter about cost-effectiveness.
• Coverage-assessment tools: HTA (health technology assessment), ICER (incremental cost-effectiveness ratio), QALY (quality-adjusted life year).
• Drug Benefit Items and Reimbursement Schedule Joint Committee: members include payers, the medical profession, the pharmacy profession, experts, and relevant agencies (patient groups may only be invited to express views), with public deliberations → the concrete institution behind second-generation NHI's "broader participation, information transparency."
• Intermediate options: temporary reimbursement, conditional reimbursement (restricted indications / prior authorization), risk-sharing agreements — used to share financial risk when the evidence is uncertain.

• Article 88 of the Medical Care Act authorizes dividing medical care regions, establishing tiered care, and drawing up the healthcare network plan.
• The country is divided into 6 primary medical regions (Taipei, Northern, Central, Southern, Kaohsiung-Pingtung, Eastern) / 17 secondary medical regions / 50 sub-regions.
• Hospital emergency capability grading (under the Emergency Medical Services Act): advanced, intermediate, general; prehospital triage goes by "can handle," not "closest."
• Basic outpatient copayment (since 2017/4/15; unchanged by the 2023 reform): medical center NT$170 with referral / NT$420 without; regional hospital 100/240; district hospital 50/80; clinic 50.
• The design intent of the price gap = using price to buy sequence, pushing patients toward primary care; clinics charge NT$50 with or without a referral.
• Family Physician Integrated Care Program (piloted 2003/3): primary-care clinics join with partner hospitals to form community healthcare groups.
• Core attributes of family medicine: accessibility, continuity, comprehensiveness, coordination — the success or failure of tiered care depends on whether primary care is strong enough.

• NHI = medical care (low probability, high cost — suited to insurance); LTC = daily-living support (high probability, long duration — tax-financed).
• LTC 2.0 has been rolled out since 2017; the "four envelopes" payment scheme took effect in January 2018; from 2026 it continues under LTC 3.0 (2026–2035), with the four-envelope framework retained.
• The four envelopes: ① care and professional services (copayment cap 16%), ② transportation (30%, Level 4 and above only), ③ assistive devices and home accessibility (30%, NT$40,000 every 3 years, or NT$60,000 under the Group 2 option from July 2026), ④ respite services (16%).
• The beneficiary of respite services is the "caregiver," not the disabled person.
• LTC need level (CMS) 1–8; Level 1 receives no benefits; eligibility to apply starts at Level 2; transportation requires Level 4 or above.
• ABC model: A Community Integrated Service Center (planning and linking) / B Composite Service Center (delivering services) / C Neighborhood LTC Station (nearby temporary care, communal meals, delaying disability); the goal is aging in place.
• Funding = Long-Term Care Services Development Fund: added revenue from the three-bracket progressive estate and gift tax (10/15/20%) + added revenue from the tobacco tax increase + Tobacco Health and Welfare Surcharge + consolidated housing and land tax + government budget appropriations → tax-financed, not insurance-financed.
• The dividing line: acute medical care and post-acute care (PAC) belong to NHI; home care services, day care, and respite belong to LTC.

• NHI is pay-as-you-go; the root of its financial problem is population structure (shrinking payers, expanding users), not simply a management problem.
• The reserve should be maintained at the equivalent of 1–3 months of insurance benefit expenditure (National Health Insurance Act Article 78); below 1 month, the insurer must draft a benefit-scope adjustment proposal for the committee under Article 26.
• Premium-rate adjustment procedure: review and agreement by the National Health Insurance Committee → MOHW → approval by the Executive Yuan; statutory cap 6%.
• Current general premium rate 5.17%, supplementary premium rate 2.11% (since 2021/1/1).
• Actuarial requirement: at least once every 5 years, each projection covering 25 years (Article 25).
• The three main thrusts of 2G-NHI: broadening the premium base (supplementary premium), broadening participation (National Health Insurance Committee), transparency (opening the Joint Drafting Meetings).
• 2G-NHI's unfinished business = premium base still mainly wages, total household income not adopted; this is the core of subsequent reform discussions.

• The NHI IC card fully replaced the paper card from 2004/1/1; its significance is "voucher → interface," enabling data to be linked across hospitals and clinics.
• NHI MediCloud System (PharmaCloud): tackles duplicate medications, duplicate tests, and drug interactions; it is a form of clinical decision support.
• Order of dispute remedies: NHI dispute review → administrative appeal → administrative litigation (review is a prerequisite procedure; you may not go straight to court).
• Scope of dispute review: premiums (insured amount, premium calculation), benefits, payment and deduction of medical expense claims, etc.
• Constitutional Court Judgment 111-Hsien-Pan-13 (2022/8/12): the entities, purposes, requirements, scope, methods, and oversight mechanisms for use of NHI data beyond its original purpose lack clear provisions, violating legal reservation and the right to informational privacy; no independent personal data oversight mechanism; no opt-out mechanism for data subjects; follow-up law = the National Health Insurance Data Management Act (promulgated 2025/12/19, in force 2026/8/10, opt-out right written in; the independent data-protection commission's organic act still pending as of 2026-09); amendment originally ordered within 3 years.
• Core concept: de-identification is a technical safeguard; clear legal authorization, independent oversight, and the right to opt out are institutional safeguards — neither can substitute for the other.

• Physician certificate (issued centrally, qualification) ≠ practice license (issued locally, practice registration, renewed every 6 years); practice limited to one location.
• Continuing education: physicians 120 points per 6 years, of which the professional quality/ethics/regulations categories must total at least 12 points, counted up to 24 (the old pre-2013 rule was 180 and 18 points; must include infection control and gender issues); the same as other practitioner-level medical personnel, i.e. 120/12 points.
• Physicians Act Article 21 = the physician's personal duty to rescue; Medical Care Act Article 60 = the institution's duty to provide emergency care.
• Physicians Act Article 11: no treatment, prescribing, or diagnostic certificate without personal examination; exception = mountain areas, offshore islands, remote areas, or special urgent circumstances. Telemedicine does not waive the duty to examine.
• Discipline from lightest to heaviest: warning → additional continuing education/clinical training → restriction of scope of practice or suspension for 1 month to 1 year → revocation of practice license → revocation of physician certificate.
• Institution classification: wards admitting inpatients = hospital, outpatient only = clinic (clinics limited to 9 observation beds; a teaching hospital is an accreditation status, not a type); the juridical-person forms are medical foundations/medical associations.
• Medical advertising uses a positive list; non-medical institutions may not engage in medical advertising; implying or alluding is deemed medical advertising; academic publications and health education without solicitation do not count.
• Medical record retention: at least 7 years; minors until 7 years after adulthood; human-trial records kept permanently.
• Medical Care Act Article 82: civil liability is limited to "intent" or "breach of the duty of care necessary in medicine together with exceeding reasonable clinical professional discretion," and criminal liability covers only negligent death or injury under the same two conditions (promulgated January 2018); both are judged by the medical customs, standards, facilities, working conditions, and urgency at that time and place.
• Medical practice = "deciding," done personally by the physician; medical auxiliary acts = "executing," done by nurses under a physician's direction (11 announced items, e.g., assisting with invasive examinations and procedures, assisting with drug administration, monitoring vital signs; vaccination also counts). Nurses' independent practice consists of only three areas: assessment, preventive health care measures, guidance and counseling.
• Emergency Medical Services Act: EMTs are EMT-1/EMT-2/EMTP; hospital emergency care capability is classified as advanced/intermediate/general; public places must have AEDs; rescue by people other than emergency personnel is covered by the necessity exemption (Good Samaritan clause).

• Medical Accident Prevention and Dispute Resolution Act: promulgated June 22, 2022 (ROC 111), in effect January 1, 2024 (ROC 113). Three principles = immediate care, mediation first, prevention to improve quality.
• Explanation-and-care team: explain and communicate within 5 working days starting from the day after the accident; hospitals with 99 beds or fewer, and clinics, may delegate this to professional staff/institutions.
• Apologies are not evidence: expressions of regret, apologies, or similar statements during the care process may not be used as evidence in litigation or as a basis for a judgment.
• Mediation first: without mediation, no directly filing a civil suit; criminal cases shall be referred to mediation; handled by the county/city medical dispute mediation committee, which may request a medical dispute assessment.
• Reporting and RCA: major accidents must be reported and undergo root cause analysis; reported and analyzed data may not be used as judicial evidence. The spirit is systems thinking (the Swiss cheese model) — don't ask who was wrong; ask why the system allowed it.
• Childbirth Accident Emergency Relief Act: promulgated ROC 104 (2015), in effect June 30, ROC 105 (2016); four principles = no blame, no fault, timely relief, error correction and improvement; the forerunner of the Medical Accident Act.
• International comparison: New Zealand's ACC no-fault compensation (since 1974) replaces personal-injury litigation; the U.S. EMTALA (1986) deals with access, not compensation — don't mix them up.
• Trap: the Medical Accident Act does not exempt physicians from liability and does not ban litigation; what it changes is the order of procedures and the admissibility of evidence.

• Hospice Palliative Care Act (2000): applies only to terminal patients (diagnosed by two physicians); may refuse CPR and life-sustaining treatment, not including artificial nutrition; if the patient is comatose, the closest relative's letter of consent (order: spouse → adult children and grandchildren → parents → siblings → grandparents → …).
• Patient Right to Autonomy Act: promulgated ROC 105, in effect ROC 108 (2019), Asia's first dedicated patient-centered law. The first in line to be informed is the patient personally.
• AD requirements: aged 18 or older with full legal capacity → go through ACP (must include at least one relative within the second degree; the team includes a physician + nurse + psychologist or social worker) → sign the AD → annotate it on the NHI card.
• Five clinical conditions: terminal illness, irreversible coma, permanent vegetative state, very severe dementia, and announced conditions of unbearable suffering with no solution; confirmation by two specialist physicians + two palliative care team consultations.
• The Patient Right to Autonomy Act allows refusing life-sustaining treatment + artificial nutrition and hydration (the step the Hospice Act cannot take).
• Patient Right to Autonomy Act ≠ euthanasia: what it permits is refusal/withdrawal, not actively causing death; Taiwan has not legalized euthanasia.
• Brain death determination: prerequisites (deep coma, ventilator dependence, established cause) + exclusion of reversible factors → observe 12 hours (drug intoxication: past the half-life, then another 12 hours; unknown drug: at least 72 hours) → all brainstem reflexes absent → apnea test (PaCO₂ ≥ 60 mmHg) → two determinations, 4 hours apart; determining physicians may not be members of the transplant team.
• Source of organs: Taiwan uses explicit consent (opt-in), which can be annotated on the NHI card; Spain uses presumed consent (opt-out) + transplant coordinators.
• Living donation: the donor must be an adult (the statute says age 20 or older; from 18, only part of the liver may be donated, to relatives within the fifth degree); recipients limited to blood relatives within the fifth degree or a spouse; a spouse must be married 2 years or more or have a child together; buying and selling prohibited.
• Allocation priority: if a spouse or a blood relative within the third degree was once a deceased donor, the candidate has allocation priority.

• The logic of the five categories = the intensity of the state's response; reporting deadlines: Categories I, II, and V within 24 hours, Category III within one week, Category IV per announcement, varying by disease (mostly one week; some 24 hours; Creutzfeldt–Jakob disease one month). COVID-19 has been moved from Category V to Category IV.
• Isolation = people already sick; quarantine = exposed but not yet sick. Category I shall be compulsorily isolated; Categories II and III may, when necessary, be compulsorily isolated.
• Requisition (Article 54) must take place while the command center is in operation, with appropriate compensation; the legal basis of the Central Epidemic Command Center is Article 17, and it is established with the approval of the Executive Yuan.
• Dengue: *Aedes aegypti*/*Aedes albopictus*, daytime biting, standing water in artificial containers; secondary infection with a different serotype → ADE → hemorrhagic fever/shock; 24–48 hours after defervescence is the danger period; no NSAIDs/aspirin.
• Japanese encephalitis: *Culex tritaeniorhynchus* and other *Culex* mosquitoes (not *Aedes*); pigs are amplifying hosts, humans are dead-end hosts, no human-to-human transmission; about 1 in 300 develop disease; vaccine dose 1 at 15 months, dose 2 twelve months later.
• Scrub typhus: *Orientia tsutsugamushi*, bite of chigger larvae, eschar in clothing folds; drug of choice doxycycline, β-lactams ineffective (obligate intracellular).
• Hantavirus: inhalation of aerosolized rodent urine and feces; never dry-sweep during cleanup — wet and disinfect first; HFRS (fever + bleeding + renal failure) / HPS (pulmonary edema).
• Rabies: Category I; retrograde axonal transport, incubation 1–3 months and shorter the closer the bite is to the brain; Negri body; ferret-badgers in 2013 made Taiwan an affected area again. PEP = wash with soap for 15 minutes → don't suture → HRIG infiltrated around the wound + vaccine on days 0/3/7/14/28; previously fully vaccinated: only 2 boosters, no HRIG.
• Tuberculosis: DOTS — into the hand, into the mouth, leave after it's swallowed; 2 months HRZE + 4 months HR; LTBI via IGRA (unaffected by BCG); MDR-TB is Category II.
• HIV: the dedicated law guarantees anonymous screening and non-discrimination; people with HIV must disclose when seeking care; prenatal screening of pregnant women + prevention of vertical transmission (no breastfeeding); PrEP / PEP (within 72 hours, for 28 days) / U=U.
• Enterovirus: EV71 is the most neuroinvasive; severe-disease warning signs = lethargy, altered consciousness, poor activity, limb weakness, myoclonic jerks, persistent vomiting, tachypnea or tachycardia; the path is brainstem encephalitis → neurogenic pulmonary edema → cardiopulmonary failure; alcohol is ineffective (non-enveloped) — use chlorine bleach.
• Measles: R₀ 12–18, airborne, negative pressure required; 3 Cs + Koplik spots (the only pathognomonic sign); rash spreads downward from the hairline behind the ears; infectious from 4 days before to 4 days after rash onset; post-exposure MMR within 72 hours or immune globulin within 6 days; among complications, pneumonia is the most common cause of death, with SSPE as a late complication.
• Pertussis: the catarrhal stage is the most contagious; infants may present with apnea alone; treat with macrolides; Tdap at weeks 28–36 of every pregnancy (better than cocooning).
• IPD: isolated from a sterile site; asplenia / under age 2 / 65 and older at high risk; conjugate (PCV13) → T-cell dependent → memory, hence used in young children; pure polysaccharide (PPV23) → T-cell independent, poor response under age 2.

• In 1984 Taiwan became the first country in the world to launch a nationwide neonatal hepatitis B vaccination program; the main route of transmission is mother-to-child vertical transmission, and the younger the age at infection, the higher the chronic carrier rate, so dose 1 must be given within 24 hours of birth; infants of HBsAg-positive mothers (regardless of e-antigen status since July 2019) also receive HBIG (active + passive immunization, at different sites). Results: childhood HBsAg carrier rate fell below 1% and childhood hepatocellular carcinoma incidence declined — the first vaccine in history proven to prevent cancer.
• Key ages in the schedule: within 24 hours, HepB dose 1; 2 months, pentavalent + PCV13; 5 months, BCG; 6 months, first influenza dose; 12 months, MMR + varicella + PCV13 booster; 15 months, JE dose 1; 18 months, pentavalent dose 4 + HepA dose 1; 27 months, JE dose 2 + HepA dose 2; before elementary school, DTaP-IPV + MMR dose 2; publicly funded HPV for junior-high students (boys included since September 2025).
• The reason BCG was postponed to 5 months was reports of BCG osteitis — the immunization schedule is a living document that safety data can rewrite.
• The Japanese encephalitis vaccine switched from mouse-brain-derived inactivated to cell-culture live attenuated chimeric vaccine (schedule simplified to 2 doses).
• Publicly funded vs. self-paid criterion = disease burden × cost-effectiveness × herd-immunity externality × safety and supply; recommendations come from ACIP. "Universal vaccination is always in the public interest" is a false statement.
• Vaccine Injury Compensation Fund: legal basis is Article 30 of the *Communicable Disease Control Act*; funded by levies paid by vaccine manufacturers/importers per dose passing inspection; total fund NT$150 million–NT$400 million; decisions are made by the VICP review panel (medical + legal experts + impartial members of the public), with outcomes classified as related / cannot be determined / unrelated, and the first two are compensated.
• The underlying spirit: not fault-based liability, but the socialization of risk — herd immunity is a public good, so injury should not be borne by the individual alone.
• International comparison: the US 1986 National Childhood Vaccine Injury Act; a companion 1987 law levies an excise tax, since 1997 US$0.75 per dose per disease prevented, paid into a trust fund, handled through the Vaccine Court and the Vaccine Injury Table.

• The *Prevention of Rare Diseases and Orphan Drug Act* was promulgated on February 9, 2000 (ROC year 89); Taiwan was the fifth jurisdiction in the world to enact a dedicated rare-disease law (after the US, Japan, Australia, and the EU).
• What makes it special: it covers both "prevention and control" (newborn screening, genetic counseling, prenatal testing and genetic diagnosis, reporting and registry, reproductive support) and "drugs" (supply, special approval for manufacture or import, market exclusivity, National Health Insurance reimbursement); the US 1983 *Orphan Drug Act* deals only with drug-market incentives (market exclusivity, tax credits, fee waivers).
• Governing body: the Review Committee on Rare Diseases and Orphan Drugs; recognition of a rare disease uses prevalence as its core criterion.
• Newborn screening: fully expanded to 21 conditions from October 2019 (ROC year 108); 22 with SMA and a fully subsidized test fee from July 2026; heel-prick blood collected at 48 hours of age; the subsidy is NT$200 per case in general before July 2026, and NT$550 for low-income households and areas lacking medical resources.
• The 21 publicly funded conditions (Pompe disease, Fabry disease, and SCID are self-paid add-ons, not among them) include: CHT, CAH, PKU, homocystinuria, MSUD, citrullinemia types I/II, galactosemia, G6PD deficiency (favism), MCAD, VLCAD, primary carnitine deficiency, CPT I/II, early-onset GA II, the organic acidemias (including HMG-CoA lyase and holocarboxylase synthetase deficiencies), and others.
• The technical reason the panel could expand = tandem mass spectrometry (MS/MS) drives the marginal cost of each added condition toward zero; the real threshold is Wilson & Jungner's "Is there an accepted treatment?"
• Newborn screening is secondary prevention; a positive screen ≠ a diagnosis — recall for repeat testing and confirmatory diagnostic testing is required (the design prioritizes high sensitivity).

• The Occupational Safety and Health Act (renamed in ROC year 102 [2013] from the Labor Safety and Health Act) extends its scope to "workers" in all industries (including the self-employed).
• General health exam: under 40 every 5 years, 40–64 every 3 years, 65 and over every year; special health exam: for operations with special health hazards, once a year.
• Graded management of special health exams: Level 1 = not abnormal; Level 2 = abnormal but unrelated to work; Level 3 = abnormal but work-relatedness uncertain → refer to an occupational medicine specialist; Level 4 = abnormal and work-related → immediate hazard control.
• Five criteria for recognizing occupational disease: evidence of disease, evidence of exposure, plausible temporal sequence, support from the literature and a dose–response relationship, exclusion of non-occupational causes. Pneumoconiosis latency is 10–30 years; onset after retirement still counts as occupational disease.
• Labor Occupational Accident Insurance and Protection Act: promulgated in ROC year 110, in force May 1, 2022 (ROC year 111); occupational accident insurance becomes a standalone insurance under its own act; compulsory coverage from the first day of employment regardless of employer size; establishes the occupational injury and disease diagnosis and treatment network and triple rehabilitation — medical / social / vocational.
• Overwork recognition (guideline on work-related cerebrovascular and cardiac diseases): > 100 hours of overtime in the 1 month before onset, or a monthly average > 80 hours over the preceding 2–6 months → very strong association; monthly average 45–80 hours, the longer the stronger; < 45 hours, weak. It is an administrative guideline, not a law.
• Noise-induced hearing loss: basal-turn outer hair cells damaged first → 4000 Hz notch; sensorineural, bilateral, irreversible; 85 dBA triggers a hearing conservation program, 90 dBA is the permissible limit, 5-dB exchange rate.
• Silicosis = upper lobes + eggshell calcification + increased TB risk; asbestosis = lower lobes + pleural plaques + mesothelioma; asbestos × smoking is multiplicative for lung cancer, not for mesothelioma.
• Lead poisoning: inhibits ALAD and ferrochelatase → microcytic anemia + basophilic stippling + elevated ZPP/δ-ALA; wrist drop (predominantly motor), Burton's line, lead colic, saturnine gout; monitor with blood lead; remove the exposure first, then chelate.
• HAVS: localized vibration → endothelial injury and sympathetic over-reaction → vibration white finger (pallor → cyanosis → rubor); the distinction from primary Raynaud's disease lies in the exposure history.
• Occupational skin disease: ICD (non-immunologic, can occur on first contact, dose-related, about 80%) vs ACD (type IV delayed hypersensitivity, requires sensitization, 24–72 hours, patch test).
• RCA Taoyuan plant (1970–1992, trichloroethylene/tetrachloroethylene): with exposure records lost, the court adopted population-level epidemiological inference — a real-life case of temporality, the Hill criteria, and the burden of proof.

• The new ICF system took effect on July 11, 2012 (ROC year 101): classification changed from 16 categories to eight major systems; assessment by a medical + social-work team with an added evaluation of activity/participation and environmental factors; disability handbook → disability certificate + needs assessment.
• The core idea of the ICF: from the ICIDH's one-way linear model (impairment → disability → handicap) to an interactive model — disability results from a mismatch between person and environment, and environmental factors can either worsen or eliminate disability.
• Order of the eight systems: nervous & mental/psychological → eye/ear, senses & pain → voice & speech → circulatory, hematopoietic, immune & respiratory → digestive, metabolic & endocrine → urinary & reproductive → neuromusculoskeletal movement → skin.
• The Indigenous Peoples Health Act was promulgated on June 21, 2023 (ROC year 112), Taiwan's first health law for a specific population group; key points = dedicated unit, adequate budget, regular surveys and a database, training Indigenous healthcare professionals, traditional medical and healthcare knowledge, and members with Indigenous status must make up no fewer than one-half of the policy council.
• Indigenous vs national-average life-expectancy gap: 8.17 years in 2017 → 6.19 years in 2022. The cause is SDOH, not ethnic constitution.
• IDS (Medical Benefit Improvement Plan for Mountainous and Offshore-Island Areas): a bundled/capitation-like contract giving one hospital the care of a whole township; principle = the larger the settlement unit, the stronger the incentive to prevent and economize (FFS < per diem < DRG < capitation).
• Accessibility ≠ availability: NHI solved "can you afford it"; IDS solves "is anyone coming." The telemedicine exception in Article 11 of the Physicians Act exists precisely to patch a market failure.
• Blackfoot disease: chronic exposure to inorganic arsenic in deep-well water on the Chiayi–Tainan coast → peripheral arterial occlusive gangrene + skin cancer (Bowen's disease [SCC in situ], SCC, BCC; arsenical keratosis is precancerous), bladder cancer, lung cancer, liver cancer + raindrop pigmentation changes; the cure was tap water (environmental intervention), not drugs; WHO drinking-water arsenic guideline value 10 μg/L.

• Tobacco Hazards Prevention Act: amended and promulgated February 15, 2023 (ROC year 112), in force March 22. Seven key points: total ban on tobacco-like products (e-cigarettes), designated tobacco products (including heated tobacco) must pass a health risk assessment review, minimum smoking age raised to 20, warning graphics 35% → 50% (in force March 22, 2024), expanded smoke-free places (universities, kindergartens, infant care centers, and home-based childcare, including outdoors; bars and nightclubs indoors), heavier penalties, and a statutory definition of tobacco-like products.
• The difference between the e-cigarette total ban and the heated-tobacco review system lies in whether the product contains tobacco (tobacco-like product vs tobacco product); heated tobacco that has not passed review is illegal in Taiwan.
• MPOWER: Monitor/Protect/Offer/Warn/Enforce/Raise; the single most cost-effective measure is raising tobacco prices. Health and welfare surcharge on tobacco products = user pays + earmarking, feeding the NHI safety reserve and cancer prevention and screening.
• Cessation drugs: NRT, varenicline (α4β2 partial agonist), bupropion.
• Drunk driving: administrative penalty 0.15 mg/L (blood 0.03%); criminal offense of driving while unable to drive safely 0.25 mg/L (blood 0.05%).
• ALDH2 deficiency (about 30–50% of East Asians) → acetaldehyde accumulation → flushing and palpitations; acetaldehyde is a Group 1 carcinogen → sharply raised risk of esophageal squamous cell carcinoma. "Flushing when you drink" is a clearance defect, not low tolerance.
• Withdrawal: delirium tremens usually 48–96 hours after the last drink, first-line benzodiazepine; thiamine before glucose (to prevent Wernicke).
• The areca nut itself (without betel inflorescence or tobacco) is an IARC Group 1 carcinogen; arecoline and its nitrosated derivatives are genotoxic. Precancerous lesions: leukoplakia (most common), erythroplakia (highest malignant transformation rate), oral submucous fibrosis (most specific to betel quid; hallmark is restricted mouth opening). Tobacco + alcohol + betel quid act multiplicatively.
• Target populations for the four cancer screenings + lung cancer: cervical (ages 25–29 every 3 years; 30 and over annually; HPV test added at ages 35/45/65), breast (ages 40–74, every 2 years), colorectal (ages 45–74; ages 40–44 with a family history, every 2 years, FIT), oral (aged 30+ who chew betel quid or smoke; Indigenous people aged 18+ who chew betel quid, every 2 years), lung LDCT (ages 50–74 with ≥20 pack-years and currently smoking or quit less than 15 years ago; family history: women 40–74, men 45–74, every 2 years).
• Timeline: lung-cancer LDCT launched July 1, 2022 (ROC year 111); 2025 (ROC year 114) was an expansion (not the launch year).
• The three big screening biases: lead-time bias (earlier diagnosis falsely lengthens survival time), length-time bias (tends to catch slow-growing tumors), and overdiagnosis. The only reliable evidence of benefit is a fall in disease-specific mortality in randomized trials, not five-year survival.

• Mental Health Act: amended and promulgated December 14, 2022 (ROC year 111), in force December 14, 2024 (ROC year 113); the part transferring compulsory admission to court rulings had a separate effective date because of the judicial infrastructure it needs and has been in force since August 1 (August 2026, ROC year 115).
• The court uses a lay-assessor system: judge + lay assessor who is a psychiatric specialist + patient-rights advocacy group representative, deciding by majority opinion. Constitutional basis = judicial reservation for personal liberty.
• Time limits: court-ordered compulsory admission may not exceed 60 days; extension must be petitioned 14 days before expiry, only once, and may not exceed 60 days.
• Patient-rights groups may monitor cases of compulsory admission, compulsory community treatment, and emergency placement, and may petition the court for termination; severe patients or their protectors may also petition for termination, and petitions and appeals are exempt from court fees.
• Definition of "severe patient": bizarre thoughts and strange behavior detached from reality, rendering the patient unable to manage their own affairs (2007 wording; current Article 3 says a mental state detached from reality), as diagnosed and determined by a specialist physician. Diagnosis ≠ grounds for compulsion; requirements for compulsion = severe patient + risk of harm to self or others + need for full-time admission yet refusal.
• Emergency placement is a short-term measure (7 days) before compulsory admission, accompanied by a compulsory assessment; compulsory community treatment is a less intrusive middle option (medication, blood-level testing, alcohol/drug screening, etc.) embodying the principle of proportionality.
• Community support and reasonable accommodation written into law, strengthening community mental health centers and cross-agency collaboration — using compulsion less presupposes that the community has something to offer.
• Suicide Prevention Act: reporting and follow-up care; media guidelines to avoid the Werther effect and promote the Papageno effect.

• Asbestos = lower lobes + pleural plaques + mesothelioma + lung epithelial carcinoma; pulmonary lymphoma is the exception.
• Silicosis = upper lobes + eggshell calcification + increased tuberculosis (TB) risk.
• Asbestos bodies are mostly found in normal lung parenchyma — not diagnostic of mesothelioma.
• Traps: ① assigning asbestos to the "upper lobes"; ② naming "pulmonary lymphoma" as the asbestos-related cancer; ③ describing silicosis as "lower lobe, decreased TB risk."

• Adenocarcinoma = peripheral + EGFR; squamous cell = central + smoking + keratinization + PTHrP-driven hypercalcemia; small cell carcinoma (SCLC) = central + neuroendocrine + paraneoplastic, not surgical.
• SCLC's paraneoplastic repertoire: SIADH, Cushing syndrome, Lambert-Eaton (LEMS).
• Traps: ① mistaking "a non-smoking Asian woman with a peripheral mass" for squamous cell; ② attributing hypercalcemia to SCLC (it is actually PTHrP from squamous cell); ③ describing SCLC as "primarily surgical."

• Emphysema = neutrophil/macrophage elastase destroying elastic fibers; α1-AT deficiency → panacinar, lower lobes.
• The ordinary smoker = centriacinar, upper lobes.
• Asthmatic smooth muscle = hypertrophy, not atrophy.
• Traps: ① describing asthmatic smooth muscle as atrophic; ② assigning α1-AT deficiency to "upper-lobe centriacinar"; ③ attributing the enzyme source in emphysema to "lymphocytes/eosinophils" (it is actually neutrophils + macrophages).

• Anterior mediastinum = 4 T's (thymoma, teratoma, lymphoma, thyroid); posterior mediastinum = neurogenic tumors.
• Pericardial tamponade does "not" cause secondary PAH (external compression; PVR has not risen).
• Inspiratory stridor = upper-airway (extrathoracic) obstruction; expiratory wheeze = lower-airway (intrathoracic); biphasic = fixed obstruction.
• Traps: ① listing pericardial tamponade as a "cause of secondary PAH"; ② reflexively giving SABA for inspiratory stridor (the airway needs protecting instead); ③ naming the posterior mediastinum as the classic site for thymoma.

• ① FEV₁/FVC < 0.70 = obstruction; ② TLC < 80% = restriction (FVC alone cannot be used); ③ DLCO localizes further.
• Obstruction + DLCO↓ = emphysema; obstruction + normal DLCO = asthma.
• Restriction + DLCO↓ = pulmonary fibrosis; restriction + normal DLCO + ↓MIP = neuromuscular disease.
• Positive BD test = FEV₁ or FVC ↑ ≥ 12% and ≥ 200 mL (both conditions required).
• Traps: ① using FVC alone to call restriction (TLC is mandatory); ② remembering only the 12% for a positive BD test and forgetting the 200 mL; ③ misclassifying a patient with chest wall deformity as pulmonary fibrosis (a normal DLCO rules it out).

• Diagnosis = post-BD FEV₁/FVC < 0.70; GOLD 1–4 grades severity, but initial therapy follows ABE (symptoms + exacerbation history) — group E starts on LABA+LAMA immediately.
• Inflammation includes CD8⁺ T lymphocytes and, in some patients, eosinophils; Eos ≥ 300/μL predicts a good ICS response.
• Pulmonary rehabilitation has strong evidence; IV theophylline has weak evidence and is not routine.
• AECOPD: inhaled SABA+SAMA, systemic steroids for 5 days, antibiotics when indicated, NIPPV, SpO₂ 88–92%.
• HRCT can diagnose bronchiectasis (signet ring sign).
• Traps: ① "give chronically hypercapnic COPD patients all the oxygen they want" (causes CO₂ retention); ② "COPD inflammation is only neutrophils" (misses CD8 + eosinophils); ③ "pulmonary rehabilitation has limited benefit" (its evidence is actually the strongest).

• Positive reversibility = FEV₁ ↑ ≥ 12% and ≥ 200 mL (both conditions at once).
• Mechanistic chain = TSLP/IL-25/IL-33 → ILC2/Th2 → IL-5 (eosinophils)/IL-4·13 (IgE, AHR) → FeNO↑; this is Th2.
• Every adult regimen must include ICS; SABA is never used alone; the step-up answer is almost always adding regular LABA.
• Step-down requires ≥ 3 months of stability.
• Pregnancy, anesthesia, AERD, and ABPA are mostly not contraindications — ABPA's primary treatment is actually oral corticosteroids.
• Traps: ① writing IL-12/IL-10 into the asthma mechanism (they are actually anti-inflammatory); ② calling ICS in pregnant asthma a contraindication; ③ treating rising SABA use as "step-up therapy" (it is actually worsening control).

• The key distinction among the three types = whether respiratory effort is present: OSA present, CSA absent, OHS present and often coexisting with OSA.
• AHI thresholds: ≥ 5 with symptoms, ≥ 15 without; severity cutoffs: 15 and 30.
• BMI is a risk factor, not a severity index.
• OHS = obesity + awake PaCO₂ ≥ 45 + other causes excluded; treatment is NIV/CPAP + weight loss.
• CPAP is first-line for moderate-to-severe OSA; OSA is a treatable cause of secondary/resistant hypertension.
• Traps: ① judging OSA severity by BMI (should use AHI/ODI/nadir SpO₂); ② "OSA always needs AHI > 15" (≥ 5 suffices with symptoms); ③ jumping straight to COPD for obesity + hypercapnia (think OHS first).

• Classify by PaCO₂ first: myasthenia gravis + CO₂↑ = type 2 pump failure.
• NIPPV contraindications = coma/shock/copious secretions; a high PaCO₂ is not a contraindication — it is the indication.
• ARDS = a leak (PAWP ≤ 18, per the older 1994 AECC criteria); cardiogenic edema = a flood (PAWP > 18).
• ARDS treatment = tidal volume 6 mL/kg, plateau pressure < 30, PEEP, prone positioning when needed.
• Hypoxemia with a normal CXR = PE, shunt, hepatopulmonary syndrome, asthma (pulmonary edema does not belong here).
• Traps: ① listing a high PaCO₂ as a NIPPV contraindication (it is actually the indication); ② reversing the PAWP cutoffs (ARDS ≤ 18); ③ using a high tidal volume in ARDS (it must be 6 mL/kg predicted body weight, not actual body weight).

• The triad: ↓fremitus + dull = effusion; ↓fremitus + hyperresonance = pneumothorax; ↑fremitus + dull = consolidation.
• Light's criteria: any one positive criterion means exudate (protein ratio > 0.5 / LDH ratio > 0.6 / LDH > 2/3 of the upper limit).
• Empyema drainage (older textbook ranking; current guidelines: pH discriminates best, glucose cutoff 60): glucose < 40 is the strongest indicator, followed by pH < 7.2.
• Chylothorax = TG > 110; hemothorax = effusion Hct > 50% of peripheral Hct; tuberculous effusion = lymphocyte-predominant + ADA > 40.
• Tension pneumothorax = a clinical diagnosis; needle decompression is immediate and does not wait for imaging.
• Ultrasound cannot detect mediastinal/hilar lymph nodes.
• Traps: ① mistaking bronchial breath sounds heard peripherally for effusion (it is actually consolidation); ② judging chylothorax by cholesterol (use TG instead); ③ ordering an X-ray before treating tension pneumothorax (a fatal delay).

• Cause of death = cardiogenic shock from right-heart failure (classified as obstructive shock; not hypoxemic respiratory failure).
• D-dimer is a rule-out tool, not a diagnostic one; diagnosis = CTPA.
• High risk (hypotension) = systemic thrombolysis with tPA; intermediate/low risk relies mainly on anticoagulation.
• Unprovoked PE carries the highest recurrence risk and needs long-term anticoagulation; provoked PE needs about 3 months.
• Top priority in anaphylactic shock = IM epinephrine into the lateral thigh (not steroids/antihistamines).
• Wells does not include plain chest pain.
• Traps: ① treating a positive D-dimer as diagnostic; ② giving steroids/antihistamines before epinephrine in anaphylactic shock; ③ writing the cause of death in PE as hypoxemic respiratory failure.

• VAP head-of-bed = 30–45 degrees (60 degrees is wrong).
• Supine aspiration lung abscess = RUL posterior segment + superior segments of the lower lobes; the right middle lobe/lingula are not favored sites.
• Aspiration risk factors = impaired swallowing/esophageal motility (scleroderma, Parkinson disease); not pulmonary fibrosis, not asplenia.
• Bronchiectasis imaging = tram-track/signet-ring sign, favoring both lower lobes.
• Diffuse bronchiectasis = PCD/CF/hypogammaglobulinemia/ABPA; pulmonary sequestration is a focal cause.
• Rib fracture in the elderly → pneumonia: prevented by analgesia + chest physiotherapy, not reflexive antibiotics.
• Bronchial breath sounds heard over a peripheral lung field = consolidation (not effusion or pneumothorax).
• Traps: ① a 60-degree head-of-bed for VAP prevention; ② treating pulmonary fibrosis/asplenia as aspiration-pneumonia risk factors; ③ treating pulmonary sequestration as a cause of diffuse bronchiectasis.

• SCLC paraneoplastic syndromes: SIADH, ectopic ACTH (Cushing), Lambert-Eaton; squamous cell paraneoplastic syndrome: PTHrP-mediated hypercalcemia.
• Adenocarcinoma = peripheral + nonsmoker/female + EGFR/ALK; lepidic subtype has the best prognosis, micropapillary/solid the worst.
• Horner's syndrome = cervical sympathetic chain (not the phrenic nerve); diaphragmatic paralysis = phrenic nerve; hoarseness = recurrent laryngeal nerve.
• For an apical lesion, choose the lordotic view; monophonic wheeze most commonly = lung cancer; clubbing + HOA most commonly = bronchogenic carcinoma.
• Absolute contraindications to curative resection of NSCLC = SVC syndrome, malignant pleural/pericardial effusion, N3 contralateral mediastinal nodes, M1; FEV1 > 1 L, N1 disease, and stable angina are NOT absolute contraindications.
• First-line therapy for extensive-stage SCLC = systemic chemotherapy (etoposide + platinum), often with immunotherapy added; mild SVC compression does not require emergent radiotherapy.
• A 50-year-old with chronic cough plus a mass on chest film — rule out lung cancer first.
• Traps: ① Writing SCLC as "secreting PTHrP causing hypercalcemia" (that's squamous cell carcinoma); ② Misreading Horner's syndrome as diaphragmatic paralysis; ③ Listing FEV1 > 1 L as an absolute surgical contraindication.

Lung cancer essentials

• Reactivation TB favors the upper lung zones, because oxygen tension is highest there and the tubercle bacillus is an obligate aerobe.
• LTBI: TST or IGRA; not contagious; roughly 10% lifetime progression; treatment cuts it by 60–90%; cannot distinguish latent vs. active.
• Tuberculous pleural effusion = delayed-type hypersensitivity (type IV); lymphocytes >50%, mesothelial cells <5%, ADA ≥40.
• RIPE: INH neuropathy requires added B6; rifampin stains fluids orange-red plus enzyme induction; PZA raises uric acid; ethambutol causes optic neuritis.
• Monitoring: liver function + CBC; CK not required routinely.
• Liver enzymes <3× normal, asymptomatic → continue; >3× with symptoms or >5× → stop.
• Resistance genes: rpoB→RIF, katG/inhA→INH, pncA→PZA, embB→EMB; MDR = simultaneous resistance to INH+RIF.
• BCG gives poor protection against adult-type reactivation TB and cannot replace N95 respirators and negative-pressure isolation.
• Traps: ① Treating latent infection as contagious and isolating the patient; ② Ordering CK to monitor RIPE therapy (unnecessary); ③ Writing MDR as "resistant to INH alone" (both INH and RIF must be resistant).

Tuberculosis essentials

• Restrictive-pattern formula: FEV1/FVC normal or ↑ + TLC/FVC↓ + DLco↓; chest wall deformity has a normal DLco, which rules it out.
• Sarcoidosis's three pillars: non-caseating granulomas, BAL CD4/CD8↑, corticosteroid treatment; hypercalcemia comes from macrophage 1α-hydroxylase (not ACE); Löfgren syndrome carries the best prognosis; asymptomatic stage I often remits spontaneously.
• IPF = UIP (honeycombing) = steroid-unresponsive = pirfenidone/nintedanib; NSIP responds to corticosteroids.
• Hypersensitivity pneumonitis = organic antigen; pneumoconiosis = inorganic dust; prevention hierarchy engineering controls > administrative controls > PPE.
• Eosinophilic pneumonia: BAL eosinophils >25% is diagnostic; NSAIDs are a common trigger.
• Traps: ① Writing sarcoidosis hypercalcemia as ACE-driven (it's actually macrophage 1α-hydroxylase); ② Prescribing corticosteroids for IPF (ineffective); ③ Writing CD4/CD8 as decreased (it's actually elevated).

ILD essentials

• Inspiratory stridor = upper airway; expiratory wheezing = lower airway.
• Steeple sign = croup (subglottic, parainfluenza, single-dose dexamethasone); thumb sign = epiglottitis (Hib, no tongue depression); bronchiolitis = RSV, <2 years old, SABA ineffective.
• Asthma under age 5 relies on history (pulmonary function testing impossible, IgE cannot confirm diagnosis); ICS is the most effective controller; LTRA is less effective than ICS.
• Mediastinal widening at age 2, most commonly = normal thymus.
• Allergy prevention: no routine probiotics; early introduction of complementary foods (including peanut) from 4–6 months lowers allergy risk.
• Traps: ① Swapping steeple and thumb signs; ② Directly depressing the tongue to examine epiglottitis (can be fatal); ③ Reflexively recommending delayed introduction of complementary foods (early introduction is actually correct).

Pediatric acute airway disease

• Spastic = bilateral UMN; flaccid = LMN; ataxic = cerebellum (scanning speech); dysarthria is a muscular execution problem, distinct from aphasia.
• Total glossectomy (oral phase) → chin-up (gravity-assisted); use chin-tuck to prevent aspiration; patients without a tongue cannot use Masako.
• Absolute contraindications to cardiac rehabilitation = acute pericarditis/myocarditis, unstable angina, uncontrolled arrhythmia; a stabilized MI, post-CABG/PCI are indications.
• MVO₂ ≈ double product = heart rate × systolic blood pressure.
• Pulmonary rehabilitation: drain with the affected side up; expectorants should be used actively; active respiratory distress is an indication.
• Traps: ① Choosing chin-tuck or Masako for total glossectomy (both require a tongue to propel the bolus); ② Listing a stabilized acute MI as a contraindication (it's an indication); ③ Draining with the healthy side up (the affected side should be up).

Rehabilitation essentials

• RQ: carbohydrate 1.0 (highest), protein 0.8, fat 0.7.
• CO = diffusion-limited (clinically measured as DLco); N₂O = perfusion-limited; normal O₂ and CO₂ = perfusion-limited, O₂ shifts to diffusion-limited during exercise or fibrosis.
• Anemia: PaO₂ and SaO₂ normal, Hb↓, oxygen content↓; CO poisoning: PaO₂ normal but SaO₂↓, pulse oximetry may be falsely normal.
• A shunt cannot be corrected even with 100% oxygen; V/Q mismatch and diffusion impairment can be corrected with supplemental oxygen.
• Chloride shift: HCO₃⁻ out, Cl⁻ in, AE1 is an exchanger (not a cotransporter).
• During forced exhalation, intrapleural pressure can turn positive → dynamic compression, effort-independent.
• Surfactant comes from type II alveolar cells; glucocorticoids mature the fetal lung; the most sensitive cough-reflex trigger = the carina.
• Traps: ① Assuming anemia always means low PaO₂ (it's actually normal); ② Relying on pulse oximetry for CO poisoning (falsely normal); ③ Writing AE1 as a cotransporter.

Gas exchange physics

• OSA = respiratory effort persists; CSA = respiratory effort is absent. OSA occurs in both NREM and REM sleep.
• Gold-standard diagnosis = PSG; severity by AHI (>30 severe); HSAT is a screening tool, not diagnostic.
• Risk factors: obesity, tonsillar hypertrophy, male sex, alcohol, supine sleep, micrognathia; mandibular prognathism is NOT one; hypertension is a consequence or comorbidity.
• First-line treatment = CPAP; first-line in children = tonsillectomy.
• DSPS (adolescents) has a delayed phase, treated with morning light exposure + evening melatonin; nighttime light exposure is the wrong treatment. ASPS (elderly) has an advanced phase.
• Traps: ① Treating hypertension as an OSA risk factor (it's actually a consequence); ② Treating mandibular prognathism as a risk factor (it actually enlarges the airway); ③ Using nighttime light exposure for DSPS (it delays the phase further).

Sleep breathing and circadian rhythm

• Appendix = simple columnar with goblet cells (not stratified squamous); esophagus = nonkeratinized stratified squamous; alveoli = type I simple squamous.
• Parietal cell acid secretion: H⁺/K⁺-ATPase pumps H⁺; HCl forms in the lumen of the intracellular canaliculi.
• The brachial artery is muscular type; the aorta and pulmonary trunk are elastic type.
• Liver: Zone 3 dies first (around the central vein); Zone 1 regenerates first (around the portal tract).
• Purkinje fibers = specialized cardiac myocytes; albumin comes from hepatocytes; alveolar macrophages cannot digest TB; CF = CFTR, autosomal recessive; mitochondria = double membrane.

Histology essentials

• Stanford A = ascending aorta involved = emergency surgery; B = descending aorta only = medical therapy. DeBakey II involves the ascending aorta only (not the arch).
• Diagnosis = CT angiography (TEE if unstable); IMH has no false-lumen flow; a normal X-ray cannot rule it out.
• β-blocker first, then vasodilator (reversing the order causes reflex tachycardia and worsens the dissection); target HR<60, SBP 100–120.
• Type A with malperfusion carries a markedly worse prognosis; complicated type B → TEVAR preferred.
• AAA surgical threshold = ≥5.5 cm; Marfan = FBN1, autosomal dominant; mycotic aneurysm = bacterial (not fungal).
• The IABP balloon sits in the descending aorta, 2 cm distal to the left subclavian; CSF drainage benefits both open surgery and TEVAR; OPCAB shows no clear advantage.
• Traps: ① Giving nitroprusside before the β-blocker (reversing the order worsens the dissection); ② Writing DeBakey II as "including the aortic arch"; ③ Mistaking a mycotic aneurysm for a fungal infection.

Aortic dissection

• ABI < 0.9 = PAD; > 1.3 is falsely normal from calcification — switch to toe-brachial.
• Fontaine: I asymptomatic → II claudication → III rest pain → IV tissue loss; III/IV = CLI.
• First line for claudication: smoking cessation + the three highs + antiplatelet therapy + supervised exercise + cilostazol; don't rush to bypass.
• Traps: ① Writing ABI > 1.3 as "healthier" (it's actually calcification); ② Scheduling bypass the moment you see claudication (exercise and medication come first); ③ Writing cilostazol as an antiplatelet agent (it's actually a PDE inhibitor).

• The 6 P's; the most common cause = cardiac embolism (atrial fibrillation).
• Differentiation: embolism is sudden with a normal contralateral pulse; thrombosis occurs on old PAD with milder symptoms.
• Reperfusion: hyperkalemia, CK↑, myoglobinuria, acidosis, compartment syndrome; NOT hypercalcemia (early hypocalcemia instead).
• Traps: ① Picking "hypercalcemia" for reperfusion; ② Writing the contralateral pulse in atrial-fibrillation embolism as weak (it's normal); ③ Treating an acute embolism as in-situ thrombosis and just anticoagulating (embolectomy is needed).

• Virchow's triad: stagnant flow, vessel injury, thickened blood.
• May-Thurner syndrome = the cause (right iliac artery compressing the left iliac vein, causing an isolated left-sided iliofemoral DVT), not a complication.
• Diagnostic pathway: Wells score → D-dimer (negative excludes) → compression ultrasound (first-line for confirmation, >95%).
• Treatment: anticoagulation leads; extensive disease/phlegmasia adds thrombolysis or thrombectomy; an IVC filter is for contraindication to or failure of anticoagulation; placing a filter in a chronically, completely occluded IVC is useless.
• D-dimer NPV >95% (up to 99%) — "<90%" is the trap answer.
• Traps: ① Writing May-Thurner syndrome as a complication of DVT (it's actually the cause); ② Placing a filter in a completely occluded IVC (useless); ③ D-dimer NPV listed as <90%.

• First choice for infrapopliteal bypass = autologous great saphenous vein; PTFE is not first-line.
• TOS: young women, mostly neurogenic type, Adson/Halsted/Wright tests (breath test is not valid).
• Carotid stenosis classically at the origin of the ICA; traumatic CCF is high-flow, first-line = endovascular embolization.
• Hemangiomas involute at 5–7 years (not before age 1); use propranolol when treatment is needed; AVM is high-flow → embolization (not sclerotherapy).
• Pectus excavatum: Haller index > 3.25; Nuss procedure at 6–14 years; bar left in place 2–3 years.
• Traps: ① Hemangiomas involuting before age 1 (it's actually 5–7 years); ② Injecting sclerosant into an AVM (high flow causes reflux); ③ Operating on pectus excavatum before age 3 (prone to recurrence).

• Triad = wall breaks (free wall), septum breaks (VSD), rope snaps (papillary muscle); AR is not included.
• IABP-SHOCK II: no survival benefit in cardiogenic shock; but VSD / acute MR still require an IABP bridge.
• IABP contraindications: moderate-to-severe AR, aortic dissection, severe PAD.
• CABG under shock favors on-pump; off-pump is not mandatory.
• Emergency life-saving care carries the presumed consent exception.
• Traps: ① listing AR as a mechanical complication of AMI; ② stating IABP "improves survival" in cardiogenic shock; ③ forcing off-pump CABG onto AMI + shock.

• The four immediately lethal injuries: tension pneumothorax / open pneumothorax / massive hemothorax / cardiac tamponade.
• Tension pneumothorax vs. cardiac tamponade → check whether breath sounds are symmetric; both share jugular venous distension and hypotension (not useful for distinguishing them).
• Thoracotomy thresholds: >1,500 mL or >200 mL/hr × 3–4 hr or instability; stable at 500 mL means no thoracotomy needed.
• Subcutaneous / mediastinal emphysema → check the esophagus and trachea; Boerhaave syndrome requires surgery, and a delay >24 hours carries 50–70% mortality.
• The most common EA/TEF is Gross type C (85%); stabilize and screen for VACTERL (cardiac) first → elective surgery.
• Anterior mediastinum — the 4 T's; thymoma is treated primarily with surgery, staged by Masaoka; 30–50% of thymoma patients have concurrent MG, but only 10–15% in reverse.
• Seminoma does not secrete AFP; AFP↑ → NSGCT.
• Barrett esophagus = intestinal metaplasia → adenocarcinoma (not squamous cell carcinoma); Nissen = 360° (not partial); first-line GERD therapy is PPI.
• Chylothorax: TG >110, lymphocyte-predominant, ligated via right thoracotomy.
• Traps: ① waiting for an X-ray before treating tension pneumothorax (a fatal delay); ② labeling Nissen a partial wrap; ③ calling Barrett's malignancy squamous cell carcinoma (it is actually adenocarcinoma).

• Squamous cell carcinoma: central, cavitating, sputum-positive, PTHrP hypercalcemia; adenocarcinoma: peripheral, high brain metastasis rate, EGFR/ALK.
• SCLC metastasizes widely early, is treated mainly with chemotherapy, and carries many paraneoplastic syndromes.
• Preoperative (older cutoffs; ACCP 2013: ppoFEV1 and ppoDLCO both above 60% = low risk, either below 30% → cardiopulmonary exercise testing): FEV1 > 80%; ppo-FEV1 > 40% (< 30% is high risk); DLCO < 50% → add VO₂max; resecting the right middle lobe has the least impact.
• In COPD, FEV1/FVC falls (it does not rise).
• Screening = LDCT (NLST); PET-CT = staging (don't mix them up).
• Traps: ① using PET-CT to screen for lung cancer; ② writing COPD's FEV1/FVC as rising; ③ feeling safe to operate at a ppo-FEV1 of 50% (it is already high risk below 40%).

• Venous cannula in the SVC/IVC, arterial cannula in the ascending aorta; no cannula in the pulmonary artery.
• Hypothermia → lower flow; using 2.4 at 20°C is too high (that's the normothermic value) — the actual figure is about 1.0–1.5.
• CPB inevitably triggers SIRS (complement + coagulation + white cells); "no SIRS" is wrong.
• Duration is limited: the longer it runs, the more coagulopathy, embolism, and organ injury (<6 hours).
• Full-course heparinization (ACT > 400–480 seconds), reversed at the end with protamine; myocardial protection relies on cross-clamp + high-potassium cardioplegia.
• Traps: ① treating a pulmonary artery cannula as venous drainage (it's actually SVC/IVC); ② running 2.4 flat-out at 20°C (loses the benefit of cooling); ③ stating "CPB does not trigger SIRS."

• The costal margin is formed by the 7th–10th costal cartilages; true ribs 1–7, false ribs 8–10, floating ribs 11–12.
• VAN runs in the costal groove along the inferior rib border; needle entry is along the superior rib border; the brachiocephalic trunk gives off no intercostal arteries; the lateral cutaneous branch emerges at the midaxillary line.
• In the left hilum, the PA sits highest; in the right hilum, the bronchus sits highest.
• Anterior to the transverse pericardial sinus = the ascending aorta + pulmonary trunk; the only direct branches of the ascending aorta = the coronary arteries.
• The right phrenic nerve runs lateral to the SVC; the right recurrent laryngeal nerve loops the right subclavian artery, the left loops the aortic arch.
• Pulmonary valve auscultation = left 2nd intercostal space (auscultation site); anatomic projection = left 3rd costal cartilage — don't confuse the two.
• Traps: ① inserting the needle along the inferior rib border (injures the VAN); ② treating the brachiocephalic trunk as a source of intercostal arteries; ③ writing the pulmonary valve's anatomic projection as its auscultation site.

• Posterior cord = master of extension (axillary, radial, thoracodorsal); the thoracodorsal nerve supplies latissimus dorsi (not subscapular / long thoracic).
• Erb (upper trunk C5–C6) = waiter's tip hand; Klumpke (lower trunk C8–T1) = claw hand ± Horner.
• Surgical neck → axillary nerve (numb regimental badge area, cannot abduct); mid-shaft humerus → radial nerve (+ profunda brachii) → wrist drop; supracondylar → AIN (cannot make the OK sign) + brachial artery; wrist → median (ape hand, thenar wasting, sensation of the lateral three and a half digits); medial epicondyle → ulnar nerve claw hand.
• Winged scapula = long thoracic nerve (serratus anterior), not the accessory nerve.
• Radial tuberosity—biceps brachii, ulnar tuberosity—brachialis; the terminal branch of the musculocutaneous nerve = lateral antebrachial cutaneous nerve.
• C6 thumb, C7 middle finger, C8 little finger.
• Traps: winged scapula ≠ accessory nerve (that is shrugging); swapping Erb and Klumpke; writing the terminal branch of the musculocutaneous nerve as the "medial" cutaneous nerve; reversing the muscles that attach to the radial and ulnar tuberosities.

• Anterior compartment dorsiflexes (deep fibular), lateral everts (superficial fibular), posterior plantarflexes (tibial); femoral = knee extension, obturator = adduction.
• Common fibular nerve (fibular neck) = foot drop, steppage gait (the most easily injured nerve of the lower limb); tibial nerve = cannot rise onto tiptoe; superior gluteal nerve (gluteus medius) = Trendelenburg.
• The ITB is fed by the tensor fasciae latae + gluteus maximus and inserts on Gerdy's tubercle; runner's knee = friction over the lateral femoral epicondyle.
• O'Donoghue triad = MCL + medial meniscus + ACL (the MCL is joined to the medial meniscus, not the lateral).
• The patellar ligament inserts on the tibial tuberosity (Osgood-Schlatter).
• Bleeding from the lateral plantar artery: compress the posterior tibial artery at the tarsal tunnel; cardiac catheterization (in anatomy questions; radial access now dominates clinically) prefers the femoral artery; deep plantar arch = anastomosis of the deep branch of the dorsalis pedis + lateral plantar artery.
• Sural nerve pairs with the small saphenous and covers the small toe; the saphenous nerve pairs with the great saphenous and covers the medial side.
• Traps: choosing the tibial nerve for the fibular neck (the tibial is the tiptoe nerve); choosing the lateral meniscus for the unhappy triad; pressing the dorsalis pedis for lateral plantar artery bleeding (the wrong upstream vessel); writing the anterior tibial trunk for the deep plantar arch (the correct answer is the deep branch of the dorsalis pedis).

• Direction: proximal→distal, gross→fine (determined by the sequence of myelination plus the size of the cortical map).
• Earliest gross-motor milestone = rolling over (about 4 months); fine motor at 12 months = mature pincer grasp (fingertip-to-fingertip pinch); stacking 2 blocks = 15–18 months.
• Traps: ① moving block stacking forward to 12 months (wrong); ② naming sitting unsupported as the earliest gross-motor milestone (6 months, later than rolling over); ③ giving "places a small object into a cup" as the 12-month fine-motor marker (that belongs to the immature stage at 9–10 months).

• The basis of medical decision-making = the patient's best interest, not the interests of the National Health Insurance/hospital/physician.
• Domestic violence is subject to mandatory reporting (medical personnel are the obligated reporters), and the patient's refusal does not exempt them.
• Traps: ① taking "saving National Health Insurance expenditure" as the basis for a decision (wrong); ② taking "the family objects" as a reason not to report (wrong — the family member may be the very perpetrator); ③ taking "wait for the patient's consent before reporting" as a lawful option (wrong — the law bypasses the chain of consent).

• 7% → aging; 14% → aged; 20% → super-aged. Mnemonic: "7 aging, 14 aged, 20 super" (original chant "7 化, 14 齡, 20 超").
• Traps: ① labeling 14% as "super-aged" (wrong — that is 20%); ② computing 7% as a share of "the total population" while forgetting the restriction to those aged 65 and above; ③ swapping the names "aged society" and "aging society" (one character apart — 化 — and 7 percentage points apart).

• GBS = post-infectious autoimmune demyelination (molecular mimicry attacking Schwann cell myelin), distal→proximal ascending symmetric weakness, loss of reflexes, CSF albuminocytologic dissociation.
• CMT = hereditary, chronic, distal atrophy (stork legs, pes cavus, foot drop), CMT1 affects myelin → NCV ↓; pain is atypical.
• Traps: ① writing the direction of GBS paralysis as "from the trunk downward" (wrong — it is from the bottom up); ② stuffing "severe pain" into the typical features of CMT (wrong — CMT is atrophy, not pain); ③ writing the CSF in GBS as "both cells and protein elevated" (wrong — protein elevated with a normal cell count is correct).

• Strongest overall and for rotation/lateral bending = halo vest (skull pins lock the halo ring + thoracic vest).
• SOMI = good flexion control (especially the lower segments, C1–C5), poor for extension/lateral bending (its selling point is flexion, not lateral bending/rotation).
• Traps: ① treating the SOMI as the strongest for rotation control (wrong — that is the halo); ② treating the soft collar as usable for an unstable cervical fracture (wrong — it is only a reminder); ③ treating the Philadelphia collar as able to block rotation (wrong — it blocks only flexion-extension).

• Principle: work against the contracture (scar contraction pulls the joint toward flexion/adduction, so position it in abduction/extension to counteract this).
• Axilla = abduction to about 90° (airplane splint); neck = extended; hand = safe position (MCP flexed, IP extended, thumb abducted).
• Traps: ① taking the "comfortable position" as the principle of positioning (wrong — comfort = the contracture direction); ② positioning the axilla in adduction against the trunk (wrong); ③ describing the safe position of the hand as "fully straight or a clenched fist" (wrong — the MCP joints must be flexed).

• Cervical orthoses: strongest in all directions = halo vest (locked with skull pins); the SOMI is strong in flexion (especially the lower segments, C1–C5), poor for lateral bending/rotation.
• Burn positioning: work against the contracture, axilla abducted to about 90° (airplane splint); hand = safe position (MCP flexed, IP extended).
• Amputation prostheses: early intervention (IPOP/soft residual-limb sock), no need to wait for complete healing; PTB weight-bearing (exam answer; the main load also falls on the medial tibial flare) = patellar tendon, medial femoral condyle; avoid the tibial crest and fibular head (common peroneal nerve).
• An AFO cannot completely eliminate subtalar joint motion; wheelchair camber: lateral stability/hand protection are advantages, uneven tire wear is a disadvantage.
• FES for foot drop stimulates the deep peroneal nerve → dorsiflexors (tibialis anterior), not the tibial nerve (that produces plantarflexion).
• Traps: ① treating IPOP as "usable only after healing" (wrong — it is early intervention); ② listing the tibial crest as a PTB weight-bearing area (wrong — that is a bony prominence); ③ describing FES as "stimulating the tibial nerve to lift the foot" (wrong — stimulating the tibial nerve causes plantarflexion and the foot droops further); ④ listing camber's "uneven wear" as an advantage (wrong — it is a physical price).

• Ulnar nerve = claw hand (most conspicuous in the ring/little fingers, lumbricals paralyzed); ulnar paradox: a distal lesion produces more pronounced clawing (FDP preserved).
• Median nerve = ape hand (thenar atrophy, loss of opposition); CTS is the most common cause.
• Radial nerve = wrist drop (midshaft humerus fracture, Saturday night palsy).
• Traps: ① describing the claw as "uniform across all five fingers" (wrong — the ring/little fingers are most conspicuous); ② labeling an ulnar nerve lesion at the elbow as "the most severe clawing" (wrong — it is actually milder, the paradox); ③ attributing wrist drop to a median nerve injury (wrong — the median nerve gives the ape hand).

• Night/rest pain, no relief lying flat, progressive → tumor/infection (continuous irritation by inflammatory mediators, which does not stop with rest).
• Saddle anesthesia + bowel and bladder incontinence + bilateral lower-limb weakness = cauda equina syndrome, a surgical emergency (MRI + decompression within 48 hours).
• Traps: ① treating "worse with activity, relieved by rest" as a red flag (wrong — this is classic mechanical pain); ② stating that rheumatoid arthritis (RA) favors the lumbar spine (wrong — RA favors the small joints); ③ contemplating physical therapy first when signs of cauda equina compression appear (wrong — MRI and surgery come first).

• Claw hand = ulnar nerve (lumbricals paralyzed, most conspicuous in the ring/little fingers); ulnar paradox = a distal lesion produces more pronounced clawing (FDP preserved).
• Low back pain red flags: night/rest pain → tumor/infection; cauda equina = surgical emergency.
• Osgood-Schlatter = tibial tuberosity apophysis (adolescent boys, self-limiting); RA does not typically involve the lumbar spine.
• First-choice study for NMJ disease = RNS (MG decrements, Lambert-Eaton increments).
• Heat therapy most readily causes contact burns in patients with sensory deficits; contraindications to ultrasound/TENS include pacemaker, growth plate, pregnancy and malignancy.
• Traps: ① treating NCS as the first choice for NMJ disease (wrong — RNS is); ② placing tennis elbow at the medial epicondyle (wrong — lateral epicondyle; the medial epicondyle is golfer's elbow); ③ applying heat therapy over an area of sensory loss (wrong — most prone to burns); ④ describing Osgood-Schlatter as a patellar lesion (wrong — the lesion is at the tibial tuberosity).

• Location decides fate: perimembranous (most common, ~70%), subarterial/supracristal (East Asians, prone to AR), inlet (AVSD spectrum, Down syndrome), muscular (self-closing, "Swiss cheese").
• "VSD + AR" → subarterial (type I): the hole sits beneath the aortic valve; Venturi suction pulls down the right coronary cusp → prolapse → AR — AR itself is an indication for surgery.
• Closure rates: muscular highest; perimembranous ~47–57%, higher when small; inlet/subarterial do not self-close.
• Surgical threshold: Qp:Qs > 2:1 (the classic exam cutoff — pulmonary flow at least double systemic), refractory heart failure, early pulmonary hypertension, failure to thrive; observe if Qp:Qs < 2:1. <!-- Note: 2018 AHA/ACC adult CHD guidelines allow repair from Qp:Qs ≥ 1.5 with LV volume load and acceptable PVR; for the licensing exam answer >2:1. -->
• The volume load lands on the left heart (LA + LV dilate) — the key contrast with ASD (right-heart dilation). Do not reverse them.
• Traps: ① picking perimembranous for VSD + AR → wrong, choose subarterial; ② assigning the volume load to the right heart → that is ASD; ③ believing muscular is rarer than perimembranous at closing → muscular has the highest closure rate.

• Signature sound = wide, fixed splitting of S2; mechanism: continuous left→right feeding keeps right-heart filling constantly high → P2 closes late all year, never merging with expiration.
• ASD dilates the right heart (LV spared); it is VSD that dilates the left — never reverse.
• Type pairings (location decides neighbors): secundum (fossa ovalis) most common; primum → MR (the cleft sits beside the mitral valve); sinus venosus → PAPVR (right at the pulmonary vein doorway); coronary sinus type rare.
• The murmur quartet: fixed S2, left second-interspace ESM (relative PS), tricuspid mid-diastolic murmur (relative TS), and no loud split S1 (trap option).
• A large ASD can also reach Eisenmenger — but far more slowly than VSD/PDA (small pressure gradient, slow progression).
• Traps: ① attributing fixed splitting to VSD → wrong; ② putting the volume load on the left heart → that is VSD; ③ pairing sinus venosus with MR → MR belongs to ostium primum; sinus venosus goes with PAPVR.

• All four pulmonary veins drain to the wrong side; mixing via PFO/ASD is obligatory → cyanosis.
• Types: supracardiac most common; infracardiac most obstruction-prone.
• Surgery: reconnect to the LA + ligate the vertical vein; preserving the vertical vein is the wrong move (exam answer; some centers leave it open temporarily when the left heart is small).

• Decision logic: choose the option that grows with the child.
• First: balloon valvuloplasty; then the Ross procedure (autologous pulmonary valve).
• A mechanical valve is the worst option: no growth + anticoagulation risk.

• Unstable → synchronized cardioversion 0.5–1 J/kg; stable → vagal maneuvers → adenosine 0.1 mg/kg.
• It is synchronized cardioversion, not defibrillation.
• Pediatric infective endocarditis is caused mainly by viridans streptococci / S. aureus; pneumococcus is uncommon (its territory is pneumonia, bacteremia, meningitis).
• Highest-risk IE groups (prophylaxis indicated): prosthetic valves/material, previous IE, unrepaired cyanotic CHD / surgical shunts / first 6 months after repair or residual defect, transplant valvulopathy; rheumatic heart disease and MVP were removed in 2007; age < 1 year is not itself a criterion.

• Upper-limb hypertension + lower-limb hypotension + weak/delayed femorals; X-ray shows inferior rib notching and the figure-3 sign.
• Male > female (~2:1); associated with Turner syndrome and bicuspid aortic valve (most common association, 50–85%).
• Traps: "superior-border" notching, "female-predominant," and filing CoA under cyanotic disease — all wrong.

• The tetrad PROVe, each letter earning its place: PS (sets cyanosis severity — it fixes the pulmonary-side resistance), RVH (compensatory consequence, not cause), Overriding aorta (gives RV blood a shortcut into the aorta), VSD (a large hole equalizing ventricular pressures so that blood obeys resistance alone).
• Cyanosis timing follows PS severity (right→left shunt): severe PS/pulmonary atresia → neonatal cyanosis; mild PS → "pink tet," acyanotic at birth, progressing over months. Never write "cyanotic from birth" as a blanket rule. X-ray: boot-shaped heart (RVH tips the apex upward), oligemic lung fields.
• Tet spell: the core is a sudden ↓SVR → the balance tips systemic → blood bypasses the lungs; every treatment reverses it — squatting/knee-chest (compress femorals, instantly ↑SVR), oxygen (↓pulmonary resistance), morphine (↓catecholamines, eases infundibular spasm), fluids (support the RV), phenylephrine (pure α — pharmacological squatting).
• The logic is the inverse of adult hypertension management — here you *raise* SVR.
• Traps: ① antihypertensives during a tet spell → lethal, wrong direction; ② pairing the boot-shaped heart with pulmonary plethora → reversed, TOF lungs are oligemic; ③ calling RVH the cause → RVH is the long-term *consequence* of PS load.

• Murmur: continuous machinery murmur below the left clavicle (systole + diastole); bounding pulses, wide pulse pressure.
• Imaging: a tubular channel between main PA and descending aorta (not a focal bulge, not a pinched lumen).
• Drug directions: PGE₁ keeps it open (duct-dependent lesions); indomethacin/ibuprofen closes it (preterm) — reverse them and someone dies.
• d-TGA: continuous PGE₁ to hold the PDA, ASO within 2 weeks; Rashkind septostomy when needed.

• The cellular chain: large L→R shunt → abnormal shear → endothelial dysfunction (NO/PGI₂↓, ET-1↑) → medial smooth-muscle hypertrophy → intimal fibroproliferation → plexiform lesions → PVR↑↑ irreversible → shunt reverses R→L → cyanosis, clubbing, secondary erythrocytosis.
• Lesions that can get there: VSD, PDA, truncus arteriosus, large ASD/AVSD (all L→R); VSD/PDA fastest, ASD slowest.
• Once established, never close the defect — the RV loses its only vent; afterload has no exit → acute right-heart failure and death.
• Remaining treatment: vasodilators (bosentan, sildenafil) for palliation, ultimately heart–lung transplant; avoid pregnancy, dehydration, altitude.
• Unrepaired cyanotic disease → highest IE risk, prophylaxis required.
• Traps: ① closing the VSD in Eisenmenger → lethal error; ② believing vasodilators cure → palliation only; ③ believing ASD never reaches Eisenmenger → large ASDs do, just slowly.

• Too much lung flow → PA banding (tie it down); too little → BT shunt (pipe it in) — never reverse.
• Valved RV–PA conduit for truncus arteriosus and pulmonary atresia + VSD.
• d-TGA: PGE₁ holds the PDA + ASO within 2 weeks; delay deconditions the LV.
• Single-ventricle physiology (post-Glenn): never leave a systemic–pulmonary shunt in place — two roads flood the lungs, overload the ventricle, and shorten survival.
• Pulmonary artery sling = obstructive (a vascular ring), not cyanotic — do not misfile it.
• After Eisenmenger, never close the defect; vasodilators palliate, transplant is the endgame.

• Laplace reasoning: wall tension ∝ radius × pressure → bigger, higher, faster = operate sooner.
• Thresholds: ascending TAA ≥ 5.5 cm; AAA men ≥ 5.5 / women ≥ 5.0; connective-tissue disease (Marfan, Loeys-Dietz) / bicuspid valve lowered to 4.5–5.0; growth > 0.5–1 cm/yr or symptoms also operate.
• Small TAA (4 cm) → annual CT surveillance; CT, not TTE (echo cannot see the distal descending aorta — tool trap).
• AAA: infrarenal, atherosclerotic type mostly > 4 cm; old male smoker = the risk trio; screen men 65–75 with smoking history once by ultrasound.
• Rupture triad: abd/back pain + hypotension + pulsatile mass → straight to the OR, no CT.
• Traps: ① 4 cm TAA followed by TTE → CT; ② asymptomatic 5.2 cm AAA in a man "observe" → male threshold is 5.5, female 5.0; ③ Marfan AAA at 4.6 cm observed → connective-tissue threshold is 4.5–5.0; ④ believing AAA is usually < 4 cm → atherosclerotic ones are mostly > 4 cm.

• The AAS spectrum = dissection (intimal flap, double lumen), IMH (crescentic wall thickening, no flap), PAU (deep penetrating crater); shared picture: abrupt tearing chest/back pain, asymmetric pulses, large inter-arm BP gap; CTA is the first-line diagnosis.
• Risk factors (brittle wall + high pressure): hypertension (most common), Marfan/Ehlers-Danlos, bicuspid valve, pregnancy (third trimester), cocaine, trauma, aortitis; sick sinus syndrome is unrelated (rhythm problem — trap option).
• Stanford A (ascending involved) → emergency surgery (tamponade, acute AR, coronary ostium); Stanford B (descending only) → medical BP + rate control first, intervene only for complications (organ ischemia, expansion, rupture).
• The BP iron rule: the core quantity is dP/dt, not pressure alone. β-blocker first (esmolol, labetalol), rate to 60, dP/dt down, vasodilator only afterward; nitroprusside alone → reflex tachycardia → dP/dt up → tear extends.
• Targets: SBP 100–120, MAP < 65–70.
• Traps: ① nitroprusside first for tearing pain → worsens it; ② sick sinus syndrome as a dissection risk factor → unrelated; ③ Stanford B straight to the OR regardless of symptoms → uncomplicated goes medical first; ④ 4 cm TAA followed by TTE → CT, echo can't see the distal descending aorta.

• Bruit = turbulence at a stenosis (carotid / renal artery); shunt = continuous machinery murmur (AVM, fistula) — different mechanisms, never swap.
• Orthostatic hypotension = within 3 minutes of standing, SBP↓ ≥ 20 or DBP↓ ≥ 10; the trap writes 15/5.
• Neurogenic: pressure falls, rate does not rise; hypovolemic: pressure falls, rate rises > 15–20 bpm.
• Three causal families: autonomic failure, hypovolemia, drugs.

• Mechanism: valve failure → reflux → venous hypertension → edema, pigmentation, venous ulcer.
• Venous ulcer: medial malleolus, relieved by elevation; arterial ulcer: toes/heel, worse on elevation (no inflow).
• First-line diagnosis: venous duplex ultrasonography (anatomy + reflux).
• Risk factors: family history, female sex, pregnancy, prolonged standing, obesity, HRT/OCP — HRT/OCP raise risk, never protect.
• Primary disease = superficial great saphenous; deep involvement is usually post-thrombotic after DVT.

• Compressions: 100–120/min, 5–6 cm deep, full recoil, minimal interruption, no over-ventilation (adults 8–10 breaths/min).
• ETCO₂: live gauge of compression effectiveness; < 10 mmHg = ineffective; sudden surge → ROSC.
• Ventilation and compression must balance; over-ventilation = high intrathoracic pressure, blocked venous return, output ↓.

• Unstable (any of: hypotension / altered consciousness / ischemic chest pain / acute HF / shock) → immediate synchronized cardioversion; pulseless VT/VF → defibrillation.
• Stable SVT → vagal → adenosine → verapamil/β-blocker; normal pressure is never shocked outright.
• Stable SVT does not get amiodarone first; adenosine — ultra-short half-life, selective AV-node block — is safe and doubles as diagnosis.

• Chain: K-wasting diuretics → low K/Mg → delayed ventricular repolarization, long QT → EADs at the repolarization tail → premature beat lands on the T-wave peak (R-on-T) → polymorphic VT twisting around the baseline.
• First line: IV magnesium sulfate 2 g push (even with normal Mg; it stabilizes L-type Ca channels, suppresses EADs); replete K to a target > 4.0.
• Refractory: isoproterenol / overdrive pacing at 100–120 bpm — shorter RR → proportionally shorter QT → narrower vulnerable window; pacing at 70 bpm is useless.
• Avoid all QT-prolongers: Ia (quinidine, procainamide), III (sotalol, amiodarone), macrolides, antipsychotics, ondansetron — fuel on the fire.
• Pulseless TdP → defibrillation.
• Traps: ① amiodarone for TdP → itself prolongs the QT; ② withholding Mg because levels are normal → first line regardless; ③ slow pacing (70 bpm) → useless, 100–120 squeezes the QT.

• Threshold: men ≥ 2, women ≥ 3; non-valvular AF → DOAC first (apixaban, rivaroxaban, edoxaban, dabigatran) — short half-life, no INR checks, less bleeding (especially intracranial).
• Scoring: C (CHF) 1 + H (HTN) 1 + A₂ (≥75) 2 + D (DM) 1 + S₂ (stroke/TIA) 2 + V (MI/PAD/aortic plaque) 1 + A (65–74) 1 + Sc (female) 1.
• Worked example (76-year-old woman + HTN + DM) = A₂(2)+H(1)+D(1)+Sc(1) = 5; dropping A₂ or Sc is the classic lost point.
• New guidelines ban aspirin monotherapy for AF stroke prevention (weak protection, undiminished bleeding).
• Rheumatic MS / mechanical valve AF = warfarin, mandatory — no DOAC (mechanical valves failed in RE-ALIGN; rheumatic MS never approved).
• Traps: ① aspirin alone for the 76-year-old → violates current guidelines; ② apixaban on a mechanical valve → contraindicated; ③ forgetting the female +1; ④ scoring A₂ as 1; ⑤ "rate control is enough, skip anticoagulation" → stroke is the real killer.

• AV node = vagal suppression + sympathetic excitation + RCA supply (hence inferior MI involvement).
• Causes AV block: excess vagal tone, inferior MI, hyperkalemia, β-blocker/CCB/digoxin.
• Does not: hyperthyroidism (sinus tach/AF instead), α-blockers (unrelated to bradycardia).
• Transplanted heart: atropine useless (denervated); use catecholamines / pacing.

• Seven steps: rhythm → rate → axis → P → PR → QRS → ST/T/QT.
• Mobitz I (Wenckebach): PR stretches then drops, within the node, mostly benign.
• Mobitz II: PR fixed, sudden drop, below the His, usually paced.
• Third degree: P and QRS fully dissociated, bradycardic, syncopal → permanent pacemaker.

• Long: low K / low Ca / low Mg, Ia/III antiarrhythmics, macrolides, antipsychotics, ondansetron, hypothyroidism, LQTS, hypothermia.
• Short: hypercalcemia, hyperthyroidism (not long — the classic reversal), digoxin effect, SQTS.
• The long QT's endgame = TdP; the cure is IV Mg, not more antiarrhythmics.

• Delta wave = WPW; Osborn J wave = hypothermia < 32°C; Epsilon wave = ARVC; electrical alternans = tamponade; prominent U = hypokalemia.
• Brugada = V1–V3 ST elevation, pseudo-RBBB; Wellens = critical proximal LAD, no stress test; de Winter = acute proximal LAD occlusion, STEMI-equivalent.
• AC beats DC at triggering VF (lands in the vulnerable window).
• Tl-201 = K⁺ analog + Na-K pump active transport; redistribution = ischemia (viable), fixed defect = infarct.
• The useless syncope test = pulmonary function testing.

• Fork on ST → troponin: STEMI (total occlusion, red thrombus) → immediate primary PCI, door-to-balloon < 90 min / lytics within 30 min without a lab; NSTEMI (subtotal, white thrombus, troponin ↑) → by risk tier (very high < 2 h; GRACE > 140 high < 24 h; intermediate < 72 h); UA (normal troponin) → antithrombotics + stratification.
• STEMI iron law: ECG diagnosis activates PCI — no waiting for enzymes; oxygen only if SpO₂ < 90% (routine O₂ is useless, possibly harmful).
• Platelet three-step: adhesion (vWF–GPIb) → activation (ADP, TXA₂, shape change) → aggregation (GP IIb/IIIa conformational change, fibrinogen bridging two platelets).
• Four antiplatelet mechanisms (four stations): irreversible COX-1 (aspirin, lifelong) / P2Y12 antagonists (clopidogrel, prasugrel, ticagrelor) / GP IIb/IIIa antagonists (abciximab, eptifibatide, tirofiban — the finish line) / PAR-1 antagonist (vorapaxar, thrombin-mediated activation).
• Stable CAD: COURAGE/BARI 2D/ISCHEMIA — PCI helps symptoms, not MI/death; hard outcomes belong to ACS.
• Traps: ① STEMI held for enzyme results → muscle wasted; ② routine 100% oxygen → only below SpO₂ 90%; ③ pasting stable-CAD PCI conclusions onto ACS → never mix; ④ GP IIb/IIIa receptors binding each other directly → fibrinogen must bridge.

• Chain: inferior MI (RCA) hits the RV → thin-walled passive pump, steep Frank-Starling slope → preload lost, output collapses → left preload starved → hypotension/shock.
• Four-part cluster: inferior STEMI + hypotension + JVD + clear lungs (no crackles); V4R ST elevation ≥ 1 mm confirms.
• First move = rapid fluids, 1–2 L saline (preload back, RV filling held).
• Absolute contraindications = nitrates (all routes) / morphine / diuretics — every preload-cutter severs the lifeline.
• Fluids fail → dobutamine, IABP; definitive = RCA PCI.
• Traps: ① treating inferior STEMI + hypotension like left failure with nitro/morphine/lasix → lethal; ② never hooking up V4R → missed diagnosis; ③ pairing JVD with "pulmonary edema" → RV MI's signature is JVD *with clear lungs.*

• Very high < 2 h; high (GRACE > 140) < 24 h; intermediate < 72 h; low — elective.
• Not every NSTEMI gets PCI within 12 hours.
• Post-sheath bradycardia + hypotension = vasovagal → atropine + fluids.
• Stress-test contraindications: symptomatic severe AS is absolute; asymptomatic AS is not.

• Physiologic (widens on inspiration); Wide = P2 delayed (PS/RBBB); Fixed = ASD; Paradoxical = A2 delayed (severe AS/LBBB); single S2 = severe AS/Eisenmenger.
• The paradoxical key is a delayed A2, not the mitral valve.

• MS + pregnancy: volume ↑ + rate ↑ → gradient spikes → pulmonary edema; decompensation typically mid-to-late.
• Management: β-blocker rate control, salt restriction, balloon valvuloplasty.
• Pregnancy: ACEI/ARB forbidden; high-risk pre-eclampsia gets low-dose aspirin; GDM uses insulin; mechanical valves switch to LMWH in the first trimester.

• AR's three doors (any one → surgery): ① symptoms (any EF) ② reduced EF (old < 50%, 2020 AHA/ACC ≤ 55%) ③ LVESD > 50 mm (or LVESDi > 25 mm/m²); example: asymptomatic, normal EF, LVESD 30 mm → below threshold, follow (decoys say "operate").
• AS: any of the big three (angina/syncope/failure), or asymptomatic EF < 50% → replace; drugs don't change the course; prognosis in years/months (never just observe); TAVR now reaches intermediate/low risk (PARTNER 3, Evolut Low Risk).
• MS + AF + embolism → warfarin, Class I + optional Maze procedure at surgery.
• Ross procedure (autologous pulmonary valve to aortic seat + homograft rebuild): for the young, children, childbearing women (no anticoagulation, growth, pregnancy); not for the elderly (bioprosthesis achieves anticoagulation-freedom without the two-valve gamble).
• Mechanical < 50 leaning (durable, no reoperation); bioprosthetic > 65 (aortic)/> 70 (mitral) leaning; mechanical = warfarin only, DOAC contraindicated (RE-ALIGN failure); INR target 2.5–3.5 by valve type.
• Triangle of Koch (coronary sinus os, septal leaflet attachment, tendon of Todaro) — apex = AV node; deep tricuspid stitches → complete AV block ("no conduction worry in tricuspid surgery" is false).
• Traps: ① replacing an asymptomatic AR at LVESD 30 mm → below threshold; ② observing severe symptomatic AS on meds → drugs never change the course; ③ DOAC on a mechanical valve "to skip INR checks" → contraindicated; ④ Ross in the elderly → population reversed; ⑤ DOAC for embolized MS + AF → rheumatic disease takes warfarin.

• Commonest cause = idiopathic/viral (coxsackie by name); commonest symptom = chest pain.
• Pain eases leaning forward, worsens supine; friction rub = high-pitched scratch, clearest leaning forward at end-expiration, disappears as effusion grows (calling it low-pitched is the trap).
• ECG: diffuse ST elevation + PR depression (the fingerprint); four stages: ST up → baseline → T inversion → recovery.
• First line: NSAID (or aspirin) + colchicine (colchicine's recurrence cut is the core); steroids not first line — autoimmune, uremic, or refractory only.

• Beck's triad = hypotension + JVD + muffled sounds (no Kussmaul, no rub).
• Pulsus paradoxus (inspiratory SBP↓ > 10 mmHg) = tamponade's signature; uncommon in constriction.
• Kussmaul sign (JVP rises on inspiration) = constriction, RV infarct, severe TR — never tamponade (the high-frequency trap).
• Y descent: blunted in tamponade; steep and deep in constriction.
• Constriction cath = dip-and-plateau (square root), RV systolic < 50 mmHg (vs pulmonary hypertension).
• Management: tamponade → pericardiocentesis; constriction → pericardiectomy. Diuretics may decongest constriction — never in tamponade.

• Mechanism = MYH7 (commonest, β-myosin heavy chain) / MYBPC3 sarcomere mutations (AD) → asymmetric septal hypertrophy → systolic flow through a narrowed LVOT → Venturi effect sucks the anterior mitral leaflet septum-ward (SAM) → LVOT obstruction + MR (a leaflet pulled away cannot close).
• Pathology: myofiber disarray + interstitial fibrosis (DCM: stretched but orderly).
• Murmur dynamics: "emptier is tighter" — Valsalva strain / standing / nitrates → preload ↓ → small chamber → louder; squat / leg raise / handgrip → loads ↑ → softer (the exact inverse of AS).
• Treatment iron law = guard the loads and the rate: first-line β-blocker (slow, long diastole, less suction) or verapamil; no aggressive diuretics, no nitrates, no digoxin (all three empty the chamber). Severe obstruction: alcohol septal ablation / myectomy; the new agent mavacamten is a myosin inhibitor built for obstructive disease.
• ~3–8.5% (usually cited 3–5%, < 10%) burn out into DCM physiology; LVH emerges in adolescence (not at birth); SCD high-risk (family SCD, unexplained syncope, NSVT, wall ≥ 30 mm, flat exercise BP) → ICD.
• Traps: ① swollen legs → furosemide (+ nitrate + digoxin) → triple landmine; ② applying AS dynamics (louder on squatting) → reversed; ③ hypertrophy visible from birth → adolescence; ④ digoxin for "more squeeze" → harder suction, worse obstruction.

• Commonest primary cardiac tumor (benign); primaries ~75% benign; > 75% sit at the left atrial septum near the fossa ovalis.
• Clinical triad: embolism, obstruction (MS-like, positional, tumor plop), systemic symptoms (fever, weight ↓, ESR ↑ — mimics endocarditis).
• Female:male ≈ 2:1; some link to Carney complex.
• Diagnosis: echocardiography first (not CT); treatment = surgical excision (never anticoagulation alone once embolic).
• Childhood champion = rhabdomyoma (tuberous sclerosis) — never confuse with the adult myxoma.

• The four: DCM weak-pump balloon / HCM stiff self-plug / RCM stiff-but-normal-size (stuffed) / ARVC fat-replaced RV firing wild.
• DCM causes = alcohol, doxorubicin (dose-dependent), TTN mutations (commonest single-gene), viral myocarditis, peripartum (within 1 month post-delivery; Black women, twins, advanced age); histology "stretched but orderly" + fibrosis, no disarray.
• HCM hallmark = myofiber disarray (absent in DCM); ARVC biopsy = RV muscle replaced by fat/fibrosis (desmosome mutations).
• Cardiac amyloid = a leading RCM cause; thick walls + low ECG voltage (the mismatch fingerprint — amyloid fills space but conducts nothing); ATTR (elderly men or hereditary; carpal tunnel/macroglossia clues) → tafamidis; AL (plasma-cell light chains) → chemo ± auto-SCT; ultrastructure = non-branching 7.5–10 nm fibrils, Congo red apple-green birefringence.
• MI timeline: 0–4 h no light-microscope change, arrhythmia; 4–24 h coagulation necrosis + contraction bands; 1–3 d neutrophils + fibrinous pericarditis; 3–7 d macrophages, weakest wall → the three ruptures (free wall/tamponade, septum/acute VSD, papillary/acute MR); 1–2 wk granulation; > 2 wk collagen scar, Dressler, persistent ST → true aneurysm.
• Degenerative vs rheumatic: commissural fusion = rheumatic (commonest MS cause), "fish-mouth" valve, acute Aschoff body with central fibrinoid necrosis ringed by Anitschkow cells (owl-eye nuclei); nodular calcification, no fusion = degenerative (commonest elderly AS cause).
• Traps: ① thick walls auto-filed as HCM → elderly low-voltage should scream amyloid; ② DCM paired with disarray → that is HCM; ③ elderly MS labeled "nodular calcification" → MS is mostly rheumatic, fused commissures; ④ rupture on day 2 → the peak is days 3–5; ⑤ aneurysm's ST elevation read as re-infarction → chronic scar behavior.

• Classes: HFrEF EF < 40 / HFmrEF 41–49 / HFpEF ≥ 50; NYHA I–IV moves with therapy — 10 trips down to 5, fine at rest = Class II (mis-filed as III).
• Four pillars (survival) = ① ARNI (beats ACEI/ARB) ② β-blocker (Car-Bi-Met only: carvedilol/bisoprolol/metoprolol succinate; propranolol has no evidence) ③ MRA (spironolactone/eplerenone) ④ SGLT2i (dapagliflozin/empagliflozin, diabetes or not).
• Symptom-only (no survival): diuretics (furosemide), digoxin, hydralazine + nitrate (intolerance substitute), ivabradine (rate still > 70).
• Contraindicated: non-DHP CCB (verapamil, diltiazem) in HFrEF (strong negative inotropy); propranolol has no HFrEF survival data.
• BNP traps: obesity reads low (adipocyte NPR-C clearance; BNP 100 excludes nothing in the obese); renal failure, age, female, AF read high; ARNI raises BNP (unreliable) while NT-proBNP stays honest — track NT-proBNP.
• Among signs, the RV heave adds least to a left-failure/valve diagnosis (downstream consequence only).
• Traps: ① verapamil for HFrEF rate → banned, β-blocker instead; ② BNP rising on ARNI → not deterioration, sacubitril blocked degradation; ③ propranolol counted in GDMT → excluded; ④ digoxin counted as survival drug → symptoms/admissions only.

• Anticoagulants: UFH/LMWH/fondaparinux act through AT-III — indirect (UFH hits Xa + IIa, monitor aPTT; LMWH mostly Xa; fondaparinux pure Xa); -xabans directly inhibit Xa, dabigatran directly inhibits IIa; warfarin blocks the vitamin K cycle (II/VII/IX/X, proteins C/S), initially procoagulant — bridge with heparin; DOACs banned at mechanical valves and severe MS.
• Antiplatelets: aspirin irreversibly inhibits COX-1; P2Y12 antagonists (clopidogrel/prasugrel/ticagrelor); abciximab GP IIb/IIIa (final pathway); vorapaxar PAR-1.
• Antihypertensives by site: diuretics, β, CCB, ACEI/ARB, ARNI, α, central clonidine, direct hydralazine, mineralocorticoid antagonists.
• Natriuretic system: ANP/BNP → NPR-A → cGMP ↑ → diurese/dilate; neprilysin degrades them; sacubitril inhibits neprilysin (ARNI); nesiritide is recombinant BNP — neither is an inotrope.
• Inotropes ride cAMP (dobutamine β₁, milrinone PDE3); NO/nitrates ride cGMP (never cAMP).
• Ductus: ibuprofen closes the PDA (preterm); PGE₁ keeps it open (cyanotic disease).

• Transplant = last resort; contraindications: surgically correctable congenital disease, irreversible pulmonary hypertension (PVR > 5 WU, TPG > 15), active infection/malignancy, severe irreversible other-organ failure, inability to comply with immunosuppression.
• Irreversible pulmonary hypertension → consider heart-lung transplant.
• End-stage alternatives: LVAD (BTT or destination therapy); acute cardiogenic shock bridges = IABP/ECMO.
• IABP: inflate in diastole → coronary perfusion ↑; deflate before systole → afterload ↓. Contraindications: AR, aortic dissection.
• STITCH: both arms improved symptoms equally; SVR added nothing, survival unchanged (smaller volume ≠ longer life; primary endpoint 59% vs 58%, ESVI −19% vs −6%); the core of failure therapy remains GDMT.
• Primary cardiac tumors ~75% benign, myxoma first (adult, left atrial septum); metastases far outnumber primaries; malignant = angiosarcoma, lymphoma; children = rhabdomyoma (tuberous sclerosis).

• Chylomicron: gut → exogenous TG → periphery; apoB-48; LPL hydrolysis.
• VLDL: liver → endogenous TG → periphery; apoB-100; LPL hydrolysis.
• LDL: from IDL, delivers cholesterol outbound; apoB-100; cleared by LDL receptors.
• HDL: liver/gut → collects peripheral cholesterol → back to liver (reverse transport); apoA-I; LCAT esterification.
• Trap: LPL splits TG ≠ LCAT locks cholesterol.

• At any xanthoma ask the lipid first: eruptive = extreme TG; tendon = extreme LDL (FH); palmar = Type III (apoE2/E2).
• Above TG 1,000 the killer is acute pancreatitis, not CAD.
• Commonest primary hyperlipidemia = Type IV (VLDL up, TG up).
• I and V: LPL/apoC-II defects, extreme TG → pancreatitis, no atherosclerosis.
• Eruptive ≠ tendon — the exam's favorite swap.

• Four statin indications: established ASCVD; LDL ≥ 190 (suspect FH); DM 40–75 with LDL 70–189; 10-year risk ≥ 7.5%.
• Intensity = percent drop: high ≥ 50% (atorvastatin 40–80, rosuvastatin 20–40), moderate 30–49%; never absolute mg.
• LDL targets: very-high-risk < 55 (ESC), high-risk < 70; quoting < 100 is obsolete.
• High LDL → statin base; TG > 500 → fibrate first, pancreatitis before CAD.
• Statin mechanism = HMG-CoA reductase inhibition (not oxidase, not direct LDL binding); myopathy's leading mechanism = mevalonate → CoQ10 drained → mitochondrial failure.
• Grapefruit trap: inhibits CYP3A4 → simvastatin/lovastatin/atorvastatin levels climb → myopathy; pravastatin, rosuvastatin unaffected.
• PCSK9 = the LDL-receptor demolition crew: high activity → fewer receptors → higher LDL; LOF mutants live low-LDL and protected; the inhibitors (evolocumab/alirocumab) mimic LOF — the largest LDL drops of any class.
• Bile-acid resins banned in high TG (they raise it); niacin flush is PGD2, aspirin prevents.
• Traps: ① "PCSK9 LOF raises LDL" → reversed, it lowers; ② LDL < 100 as the very-high-risk target → obsolete; ③ TG 2,000 treated first with a statin → fibrate first, pancreatitis is the clock.

• ACC/AHA 2017: Stage 1 ≥ 130/80, Stage 2 ≥ 140/90.
• ESC/ESH: diagnostic line still ≥ 140/90 (2018/2023/2024 unchanged). <!-- Note: 2024 ESC adds an "Elevated BP" middle band (120–139/70–89) with an SBP 120–129 treatment target for the high-risk; 2025 ACC/AHA keeps the 2017 cutoffs (changing PREVENT risk assessment and strategy, not the diagnostic line). -->
• Taiwan 2022: home BP ≥ 130/80 = hypertension.
• Diagnosis: multiple days, or home/ambulatory BP; the white-coat effect is excluded at home.

• Primary ≈ 95%; secondary clues = young, abrupt, resistant, low K, nocturia, paroxysms, Cushingoid, arm > leg pressure.
• Low K + hypertension → primary aldosteronism (ARR screen).
• Paroxysmal headache and sweats → pheochromocytoma (metanephrines).
• Old diabetic smoker + creatinine jump on ACEI → renal artery stenosis.
• Snoring, obese, sleepy by day → OSA.
• Trap: hyperlipidemia is a risk factor, never a secondary cause.

• Most settings: renoprotective, afterload down, proteinuria down, heart-failure mortality down (diabetic nephropathy, CHF, HFrEF).
• Bilateral renal artery stenosis bans ACEI/ARB — mechanism: GFR is propped by AngII squeezing the efferent arteriole; remove AngII → efferent dilates, intraglomerular pressure collapses → creatinine leaps.
• Side-effect directions: potassium up (AngII blocked → aldosterone ↓ → potassium kept) — hyperkalemia is the contraindication, hypokalemia is not; dry cough (bradykinin); angioedema (rare, lethal); banned in pregnancy (fetal renal dysgenesis, oligohydramnios, calvarial hypoplasia).
• Unilateral RAS usually tolerates the drug (the healthy kidney compensates); bilateral is the absolute ban.
• Traps: ① creatinine 1.3 → 2.6 on ACEI called drug-induced AKI → it unmasked bilateral RAS; ② hypokalemia listed as an ACEI contraindication → reversed, it is hyperkalemia; ③ ACEI in pregnancy → teratogenic; ④ banning unilateral RAS too → only bilateral.

• Definition: BP > 180/120 + acute target-organ damage (encephalopathy, hemorrhagic/ischemic stroke, ACS, pulmonary edema, dissection, pre-eclampsia/eclampsia, acute AKI).
• Treatment: IV labetalol (α+β, single-agent capable), nicardipine, clevidipine, nitroprusside (cyanide on prolonged use) — titratable.
• Speed iron rule: MAP ≤ 25% down in hour one, ~160/100 by 2–6 h, target by 24–48 h; dissection excepted — SBP 100–120 fast.
• Why not slam: chronic hypertension shifted cerebral autoregulation upward — a plunge means cerebral hypoperfusion, ischemia.
• Urgency (extreme BP, no acute damage) → oral, gradual; no IV demolition.
• Pregnancy: labetalol / nifedipine / methyldopa; ACEI/ARB absolutely banned (renal dysgenesis, oligohydramnios, calvarial defects).
• Traps: ① IV nitroprusside for the asymptomatic 200/118 → urgency over-treated as emergency; ② halving MAP at once in an emergency → cerebral ischemia; ③ ACEI in pregnancy → teratogenic; ④ sick sinus or hyperlipidemia listed as emergency criteria → not on the organ list.

• Q = ΔP / R; R ∝ ηL/r⁴ → Q ∝ r⁴.
• Radius doubled → flow ×16 (not diameter, not squared).
• Viscosity ↑ (polycythemia) → Q ↓.
• MAP = CO × TPR; MAP ≈ DBP + ⅓ pulse pressure (not the plain average).
• Vasoconstriction dominates resistance — the fourth power at work.

• CO = HR × SV; SV runs on preload, afterload, contractility.
• Frank-Starling: preload ↑ → SV ↑ (rolls over past the ceiling).
• Pressure overload (AS, HTN) → concentric hypertrophy; volume overload (AR, MR) → eccentric, dilated.
• Chronic AR compensation = RAAS on → volume ↑ → Frank-Starling; decoy = salt-dumping/ANP (reversed).
• MAP ≈ DBP + ⅓ pulse pressure.

• Sensors: carotid sinus (CN IX), aortic arch (CN X).
• Center: medullary NTS (not the thalamus).
• Pressure ↑ → firing ↑ → parasympathetic ↑ / sympathetic ↓ → dilation, HR ↓, SV ↓ → pressure down.
• Orthostatic hypotension: within 3 min, SBP↓ ≥ 20 or DBP↓ ≥ 10 ("20/10, 3 minutes").

• Fibrous pericardium = pleuropericardial membranes + septum transversum fused; the membranes smuggled in the phrenic nerve + common cardinal vein.
• Serous parietal = somatic mesoderm; visceral (epicardium) = splanchnic mesoderm.
• Purkinje fibers = specialized cardiomyocytes (never neuronal).

• 10-year patency ranking: LIMA-LAD (> 90%) ≫ RIMA > radial > SVG (~50–60%); femoral unsuitable (wide, short, limb ischemia, far from field).
• Why arteries beat veins: endothelium continuously secreting NO + PGI₂ (antithrombotic, anti-proliferative), elastic media holding arterial pressure; a vein in arterial circulation runs "early intimal hyperplasia → late graft atherosclerosis."
• LIMA→LAD = the golden pairing, Class I; the IMA endothelium resists atherosclerosis best of all conduits.
• Radial as second conduit (2021 ACC/AHA Class I over SVG); requires target stenosis ≥ 70–90% (else it competes with native flow and closes), spasm-prone — CCB prophylaxis.
• BIMA cautions: poorly controlled DM (high HbA1c), obesity, advanced age, chronic steroids, renal failure (sternal supply halved → deep sternal wound infection, mediastinitis); inhaler-treated COPD is not a contraindication (standing decoy).
• Off-pump vs on-pump: ROOBY and CORONARY show equivalent long-term patency and survival; "off-pump patency is better" is the planted falsehood.
• Emergency CABG indications: STEMI mechanical complications (papillary rupture, septal perforation, free-wall rupture), acute left main unsuitable for PCI, failed PCI, cardiogenic shock + multivessel disease; life before washout (bleeding is replaceable, myocardium is not).
• Digoxin improves symptoms, never mortality; mortality belongs to the four GDMT pillars (ACEI/ARNI, β-blocker, MRA, SGLT2i).
• Traps: ① ranking SVG above LIMA-LAD; ② COPD inhalers as a BIMA contraindication; ③ off-pump as patency-superior; ④ delaying emergency CABG for ticagrelor washout → time is muscle; ⑤ counting digoxin among the survival pillars → it is not.

• MHC class I × 8, class II × 4; class III encodes complement/TNF and takes no part in presentation; neutrophils are not major APCs.
• Two-signal model: missing signal 2 → anergy (not activation); CD3 = ITAM, ITIM = KIR/PD-1 (CTLA-4 lacks a classic ITIM).
• The CTL's three weapons: perforin + granzyme + FasL; IFN-γ is not a direct killing mediator; ADCC belongs to NK cells/Fc receptors, not CD8.
• AIRE → medullary negative selection against peripheral tissue antigen → APECED; class I/TAP deficiency → CD8↓; class II (BLS-II, CIITA/RFX) → CD4↓.
• RLRs recognize RNA, cGAS recognizes DNA, NLRP3 → IL-1β; IFN-α is a cytokine, belongs to innate immunity, and is secreted by pDCs/infected cells.
• Complement converges on C3: C3b is an opsonin, C5a is a chemoattractant and anaphylatoxin; C5-9 deficiency = recurrent Neisseria; C1-INH deficiency = HAE; CD59 blocks the MAC.
• NK cells = missing-self; M cells only sample and transport.
• V(D)J (RAG+TdT, antigen-independent) → SHM/CSR (AID, germinal center); SHM acts only on the variable region; CSR adds no diversity.
• IgM: primary response/pentamer/strongest complement activation; IgG crosses the placenta; secretory IgA = 2 IgA + J chain (plasma cell) + secretory component (epithelium); IgA switching needs IL-10/TGF-β; IgG subclasses differ in Fc-receptor affinity.
• TI antigens (polysaccharides) elicit a poor response under age 2 → conjugation converts them to TD.
• Hyper-IgE/Job syndrome (STAT3) → Th17↓ → cold abscesses from Candida + Staphylococcus.

• Working backward from the infection fingerprint: antibody deficiency→enteroviruses/encapsulated organisms; T-cell deficiency→viruses/fungi/live vaccines are fatal; phagocyte deficiency→catalase-positive organisms; C5-9 deficiency→Neisseria meningitidis.
• Gene pairings: X-linked agammaglobulinemia (XLA)=BTK, Hyper-IgM=CD40L/AID, Wiskott-Aldrich (WAS)=WASp (not NF-κB), NEMO=NF-κB, ataxia-telangiectasia (AT)=ATM, DiGeorge=22q11, Hyper-IgE/Job=STAT3, chronic granulomatous disease (CGD)=NADPH oxidase, Mendelian susceptibility to mycobacterial disease (MSMD)=IFN-γR.
• Positive-selection defects: MHC class II→CD4↓; MHC class I/TAP→CD8↓.
• Severe combined immunodeficiency (SCID) is an absolute contraindication to live vaccines; X-linked SCID=IL-2Rγc (T⁻B⁺NK⁻); adenosine deaminase deficiency (ADA) (T⁻B⁻NK⁻).
• In chronic HIV, CTLs/antibodies are produced but their function fails; CD4<200→AIDS.
• Vaccines: polysaccharide=T-independent (TI), conjugate=T-dependent (TD); give conjugate vaccines under age 2; mucosal immunity requires an oral/mucosal route; pertussis=acellular (aP); poliovirus's only host=humans; HPV-16/18≈70% of cervical cancer; measles has a high R0, herd immunity≈95%.
• Transplant: hyperacute=preformed antibody; acute=T cells; chronic=vascular disease; the mixed lymphocyte reaction (MLR) does not reduce graft-versus-host disease (GVHD) — it activates T cells instead.
• Tumor: three phases of editing=elimination/equilibrium/escape (pruning, not shrinking); CTLA-4 on the T cell, PD-L1 on the tumor; trastuzumab→HER2; tyrosinase=a melanoma TAA.
• Tolerance: Treg=CD4⁺CD25⁺/FoxP3, not cytotoxic; FoxP3→IPEX; IL-10→inflammatory bowel disease (IBD); CTLA-4/FasL→autoimmunity.
• SLE: anti-dsDNA → TLR-9 → IFN-α; type 1 diabetes (T1DM) is cell-mediated and does not rely on IgG crossing the placenta; CD23 is not central to tolerance.
• Traps: writing WAS as NF-κB (it is actually the WASp cytoskeleton); using the MLR to reduce GVHD (it activates T cells instead); placing CTLA-4 on the tumor (it is actually on the T cell); claiming 60% coverage is enough for measles herd immunity (it needs ≈95%); claiming a T1DM mother's IgG crosses the placenta to transmit diabetes to her baby (it is cell-mediated and is not transmitted); claiming SCID patients can receive BCG (an absolute contraindication).

• Gell-Coombs types 1234 = IgE / cytotoxic IgG / immune complex / T cell; Graves' disease and myasthenia gravis belong to the receptor-mediated subtype of Type II; only Type IV does not depend on antibody.
• The complete Type I chain: sensitization (Th2→IgE) → binds FcεRI → cross-linking on re-exposure → degranulation (histamine + LTC4/D4) → immediate reaction + a late-phase reaction 4–8h later as IL-5 recruits eosinophils.
• The hygiene hypothesis = excessive cleanliness/antibiotics → a Th2 skew → allergy↑; the dust mite is visible under a light microscope.
• Anaphylaxis = epinephrine 0.3–0.5 mg IM into the thigh; antihistamines/corticosteroids are not life-saving drugs; hereditary angioedema (HAE) works through bradykinin, and antihistamines are ineffective.
• First line for chronic urticaria = a second-generation antihistamine (desloratadine); the step-up ladder: quadruple the dose → omalizumab → cyclosporine.
• Rheumatic fever: group A Streptococcus (Streptococcus pyogenes), an interval of 2–4 weeks, JONES, carditis is the most severe finding, erythema marginatum <5%; long-term penicillin prevents recurrence.
• Gynecology: bacterial vaginosis (BV, fishy odor + clue cells) / candidiasis (Candida albicans, curd-like discharge + itching) / trichomoniasis (Trichomonas vaginalis, green frothy discharge + strawberry cervix, an STI requiring the partner to be treated); pelvic inflammatory disease (PID) shows cervical motion tenderness, Fitz-Hugh-Curtis syndrome; ASB in pregnancy ≥10⁵ must always be treated (30–40% progress to pyelonephritis).
• Malaria: malignant malaria (P. falciparum) has an irregular, most lethal course (cytoadherence, blackwater fever); vivax malaria (P. vivax)/ovale malaria (P. ovale) carry a hypnozoite, requiring added primaquine (check G6PD); malariae malaria (P. malariae) carries immune-complex nephritis; IV artesunate is first-line for severe malaria.
• Amoebae: E. histolytica, 4 nuclei, pathogenic; Entamoeba coli, 8 nuclei, the largest, non-pathogenic; Acanthamoeba keratitis = contact lenses + tap water.
• Trematodes: schistosomes penetrate the skin with no metacercarial stage; other flukes are ingested as metacercariae; a snail is the shared first intermediate host; S. japonicum has the highest egg output/the worst Katayama fever; S. haematobium→bladder squamous cell carcinoma; the liver fluke (Clonorchis)→cholangiocarcinoma; the lung fluke (Paragonimus)→can reach the brain; the giant intestinal fluke (Fasciolopsis) stays confined to the small intestine; Fasciola→halzoun syndrome→triclabendazole; praziquantel for the rest.
• Traps: writing Graves' disease as Type I (it is actually the receptor-mediated subtype of Type II); writing the first line for anaphylaxis as IV or subcutaneous (it must be IM); giving HAE an antihistamine (ineffective; C1-INH/icatibant is required); writing rheumatic fever as group B or a 3-month interval (it is actually group A, 2–4 weeks); leaving asymptomatic bacteriuria in pregnancy untreated (it must always be treated); writing vivax as having no hypnozoite (it actually does, requiring primaquine to clear the liver).

• Structure: the scolex uses suckers and hooks to anchor to the gut; each proglottid is hermaphroditic and reproduces sexually; there is no digestive tract, and absorption occurs through the tegument.
• The fork: eat the larva (meat) → the human is the definitive host, intestinal taeniasis; eat the egg → the human is the intermediate host, a tissue lesion.
• The pork tapeworm is the only one with a dual identity: eating meat grows an adult worm in the gut, eating eggs grows a cyst in the brain (neurocysticercosis).
• The fish tapeworm competes for B12 → megaloblastic anemia; Echinococcus = ingesting eggs (from dog feces), forming a hepatic/pulmonary hydatid cyst — aspiration is forbidden.
• H. nana is the only tapeworm needing no intermediate host and can autoinfect; the dog flea tapeworm is transmitted via the flea.
• Treatment: praziquantel for intestinal tapeworms; albendazole for Echinococcus and neurocysticercosis (combined with corticosteroids).

• Roundworm/hookworm larvae migrate through the lungs (Löffler syndrome); pinworm is diagnosed by the morning tape test; heavy whipworm infection causes rectal prolapse; hookworm penetrates the skin and causes iron-deficiency anemia.
• Strongyloides stercoralis: can autoinfect; immunosuppression→dissemination + gram-negative sepsis; eosinophils may not rise; ivermectin is first-line.
• Angiostrongylus cantonensis: eating raw snails/slugs/greens→eosinophilic meningitis; the human is an accidental host, the definitive host is the rat.
• Trichinella: adult in the gut, larva encysted in striated muscle; periorbital edema + high eosinophils; confirmed by muscle biopsy, stool is useless.
• Onchocerca volvulus: transmitted by the blackfly→river blindness + subcutaneous nodules; does not cause pulmonary nodules; diagnosed by skin snip; ivermectin.
• Capillaria philippinensis: eating raw fish containing the larva (not the egg); Gnathostoma: migratory subcutaneous/periorbital swellings.

• Three broad classes: flyers (flies, sandflies, blackflies, mosquitoes) mostly transmit protozoa/filariae/viruses; crawlers, ticks and mites, mostly transmit rickettsiae/spirochetes; lice and fleas transmit typhus/plague.
• Tsetse fly → Africa, T. brucei, sleeping sickness (by bite); kissing bug → the Americas, T. cruzi, Chagas disease (by fecal contamination).
• Sandfly→kala-azar; blackfly→river blindness; chigger mite, larval stage→scrub typhus with an eschar.
• The hard tick Ixodes, one vector many diseases: Babesia + Lyme disease + Anaplasma co-infection.
• Division of labor among the three mosquitoes: Anopheles for malaria; Aedes (day-biting) for dengue/yellow fever/Zika/chikungunya; Culex for Japanese encephalitis + Wuchereria bancrofti.
• Name check: kala-azar (sandfly/Leishmania) ≠ blackwater fever (a complication of malignant malaria) ≠ the Black Death (rat flea/plague).

• SLE blood counts show "all three lineages falling" (hemolytic anemia, leukopenia, thrombocytopenia); C3/C4 fall during the active phase.
• ANA screens (sensitive); dsDNA tracks the course/nephritis; Sm is the most specific but does not change. Ro/La→neonatal lupus with heart block; histone→drug-induced lupus.
• JIA: onset <16 years, arthritis ≥6 weeks; subtyping looks at the joint count within the first 6 months (don't confuse the two "sixes").
• Oligoarthritis (ANA+) → chronic, asymptomatic anterior uveitis (requires follow-up); enthesitis-related (B27) → acute, symptomatic uveitis.
• Still disease: spiking fever + salmon-colored rash + MAS; anti-IL-6/IL-1 is first-line.
• Omalizumab is an anti-IgE agent and is unrelated to JIA — a distractor option.

• Live attenuated vaccines (oral rotavirus, intradermal BCG, subcutaneous varicella, subcutaneous MMR) are contraindicated in pregnancy and severe immunodeficiency.
• Two injectable live vaccines, if not given the same day, need at least a 4-week interval; inactivated vaccines carry no such restriction. Defer live vaccines for several months after recent IVIG/transfusion.
• Kawasaki disease = fever ≥5 days + CRASH ≥4 features; desquamation occurs in the 2–3-week convalescent period; IVIG + high-dose aspirin given within 10 days.
• Mycoplasma pneumonia: no cell wall→ macrolide; diagnosis relies on cold agglutinins/IgM/PCR.

• Graves' = TRAb (stimulating) → hyperthyroidism + exophthalmos; pathology is follicular hyperplasia + scalloping.
• Hashimoto's = anti-TPO/Tg (destructive) → hypothyroidism; pathology is lymphocytic infiltration + germinal centers + Hürthle cells.
• Distinguish Graves' by looking at the whole combination (hyperthyroidism + exophthalmos + TRAb), not lymphocytic infiltration alone.
• Behçet's: HLA-B51; three cardinal features — oral/genital/ocular; anterior uveitis is the most common (traditional teaching; cohort studies find panuveitis most common; ≠ the most severe); pathergy test.
• Healthy people are often ANA-positive (about 20–30% at 1:40, about 5% at 1:160); specificity is not 90%; anti-histone → drug-induced lupus.

• DNA general rule: double-stranded, replicates in the nucleus; exceptions: Parvo single-stranded, Poxvirus in the cytoplasm, HBV reverse transcription.
• Nonenveloped mnemonic "bare PPPA": Parvo/Papilloma/Polyoma/Adeno.
• Oncogenesis: HPV E6→p53, E7→pRb; SV40 large T→p53+pRb, small t→PP2A; adenovirus E1A/E1B; HHV-8→Kaposi; JC→oligodendrocytes, PML.
• Hepatitis nucleic acid: only B is DNA; HCV most prone to chronicity (~80%); HEV high fatality in pregnancy; HDV borrows HBsAg for its envelope.
• Negative-sense/dsRNA must carry its own RdRp; enfuvirtide is a peptide fusion inhibitor (gp41, subcutaneous).
• Influenza: HA for attachment, NA for release; oseltamivir inhibits NA; shift = reassortment pandemic, drift = point-mutation seasonal.
• LAIV restricted to healthy people aged 2–49; rabies→Negri bodies; EV71 death = brainstem encephalitis; rubella diagnosed by serum/PCR.

• Five targets: cell wall, 30S, 50S, DNA/RNA, folate synthesis; four resistance mechanisms: enzymatic degradation, target alteration, uptake/efflux, metabolic bypass.
• MRSA = PBP2a target alteration (β-lactamase inhibitors ineffective); VRE = D-Ala-D-Lac (both vancomycin and dalbavancin ineffective).
• Class B β-lactamase = metalloenzyme (Zn²⁺) that hydrolyzes carbapenems (NDM/IMP/VIM), unaffected by clavulanate.
• β-lactamase inhibitors themselves (except sulbactam, which is active on its own against Acinetobacter) have almost no bactericidal activity; they only protect the β-lactam.
• FQ resistance = GyrA/ParC mutation; sulfonamides strike folate synthesis (unrelated to PBP); linezolid = 50S initiation complex.
• Tuberculosis HRZE: INH → peripheral neuropathy (supplement B6); rifampin → orange-red fluids + CYP induction; pyrazinamide → hyperuricemia; ethambutol → optic neuritis/red-green color blindness.

• Three routes of horizontal transfer: transformation/transduction/conjugation (pilus transfers a plasmid, the main resistance route).
• Plasmid = circular dsDNA, replicates independently, found in both G+ and G−.
• Nonsense → a stop codon that truncates the protein; silent leaves the amino acid unchanged; missense swaps the amino acid.
• The lac operon = catabolite repression + lactose induction, dual control, unrelated to quorum sensing.
• Diphtheria toxin A → ADP-ribosylates EF-2; cholera→Gs/cAMP↑; Shiga→cleaves 28S rRNA.
• Tuberculosis: blocks phagosome-lysosome fusion; mycolic acid→acid-fast; high GC; membrane has no sterols; immunity is Th1.
• Prions contain no nucleic acid → UV is ineffective; routine autoclaving is not enough.
• Gram-negative: thin peptidoglycan, stains red, binary fission; LPS = O antigen + core + lipid A; O=LPS, H=flagellum, K=capsule; porins sit in the outer membrane.
• Kanagawa (+) = produces TDH; plague = flea regurgitation (not vomiting); Legionella is cleared by cell-mediated immunity.

• Catalase sorts staph from strep; only coagulase can distinguish S. aureus vs. S. epidermidis (catalase cannot).
• Group A S. pyogenes: bacitracin-sensitive, PYR(+); group B S. agalactiae: bacitracin-resistant, CAMP(+), hippurate(+), neonatal meningitis.
• S. saprophyticus: novobiocin-resistant, UTI in young women.
• Coagulase forms fibrin; staphylokinase dissolves fibrin (opposite directions).
• Protein A binds the IgG Fc portion, blocking opsonophagocytosis; TSST-1 is a superantigen.

• Diphtheria: humans are the sole host; the toxin gene sits on bacteriophage β (not a plasmid); ADP-ribosylates EF-2.
• Anthrax: PA + EF + LF; EF is a calmodulin-dependent adenylate cyclase; three forms = cutaneous/inhalational/gastrointestinal (CDC also lists injection anthrax), no muscle-necrosis form.
• Listeria: facultative intracellular, still grows at 4°C, tumbles at 25°C, polymerizes actin via ActA to move between cells.
• Pneumococcal vaccine = capsular polysaccharide (PCV is a conjugate vaccine), not a surface protein.
• STa/STb → ETEC; EF → anthrax (do not assign to S. aureus).

• Mucor = non-septate, broad, 90° right angle; Aspergillus = septate, 45° acute angle.
• Coccidioides turns into a spherule containing endospores in tissue, not a yeast.
• Malassezia culture requires olive oil; C. glabrata forms no hyphae; C. neoformans appears coffee-brown on birdseed agar; C. gattii infects immunocompetent hosts with more severe disease.
• Epidermophyton has no microconidia; Microsporum is rich in macroconidia; Trichophyton is rich in microconidia.
• Polyene = binds ergosterol directly and punches holes; azole/terbinafine = inhibit ergosterol synthesis; echinocandin = inhibits cell-wall β-glucan.
• Pneumocystis lacks ergosterol → amphotericin/azole ineffective; treat with TMP-SMX.

• Six-step chain: gp120 binds CD4 → gp41 binds CCR5/CXCR4 → membrane fusion → reverse transcription + integration → chronic viremia exhausts CD4 → CD4<200 enters AIDS.
• gp120 binds CD4 plus a coreceptor (R5/CCR5 or X4/CXCR4), and gp41 mediates membrane fusion; CCR5 Δ32 confers resistance to R5.
• CD4 < 200 → Pneumocystis pneumonia (PJP); < 100 → Toxoplasma/Cryptococcus; < 50 → cytomegalovirus (CMV)/Mycobacterium avium complex (MAC).
• AIDS-defining conditions include Kaposi sarcoma, non-Hodgkin lymphoma (NHL, including Burkitt/primary CNS lymphoma), and invasive cervical cancer; Hodgkin lymphoma does not count.
• Diagnosis: enzyme immunoassay (EIA) screening → must be confirmed by Western blot or antibody differentiation; the acute phase uses HIV RNA or p24 antigen.
• Vertical transmission: 25–30% untreated; < 1% with complete cART and undetectable virus (U=U).
• TB/HIV: CD4 < 50 → start ART within 2 weeks of anti-TB therapy; ≥ 50 → within 2–8 weeks; TB meningitis deferred to 4–8 weeks (starting early raises mortality instead).
• Protease inhibitors (PIs) cannot be combined with rifampin (CYP3A4 induction) → switch to rifabutin or nine months of isoniazid.
• Traps: treating a positive EIA as diagnostic (Western blot is required); waiting for antibody positivity in the acute phase (RNA/p24 is required); calling CD4<200 an early infection (it is already AIDS); listing Hodgkin lymphoma as AIDS-defining (it is not — only NHL is); starting ART early for TB meningitis just because CD4 is low (it must be deferred 4–8 weeks); prescribing rifampin for latent TB in a patient on a PI (it suppresses the PI's concentration).

• Sepsis five-step chain: PAMP/DAMP → TLR/PRR → massive cytokines (TNF-α/IL-1/IL-6) → systemic vasodilation + ↑permeability → distributive shock + lactate accumulation.
• Sepsis-3: sepsis = infection + organ failure; septic shock = vasopressor to maintain MAP≥65 + lactate>2.
• Cytokine storm = TNF-α/IL-1/IL-6; IL-5 belongs to allergy/eosinophils (distractor).
• 1-hour bundle: lactate → blood cultures → antibiotics within 1h → crystalloid 30 mL/kg → vasopressor.
• First-line vasopressor = norepinephrine; bicarbonate is not a priority (reserved for pH<7.2).
• Spontaneous bacterial peritonitis (SBP) main cause = G(−) enteric organisms (not G(+)); cellulitis tissue culture positivity 20–30% (not 70%).
• Traps: using SIRS as the sepsis standard (already retired); giving sodium bicarbonate first to suppress the acidosis (the real fix is fluids + antibiotics); skipping cultures before antibiotics; writing SBP as predominantly G(+); claiming cellulitis tissue-culture positivity >70%; calling vancomycin the first-line "pressor" for sepsis (the first-line vasopressor is norepinephrine).

• Mechanism: endothelial injury → sterile thrombus (NBTE) → bacteremic colonization → vegetation; course 4–6 weeks IV (a vegetation has no blood supply).
• Pairings: after dental work = viridans streptococci; tricuspid valve in IVDU = Staphylococcus aureus; early prosthetic valve = S. epidermidis; S. gallolyticus → look for colon cancer; culture-negative → think HACEK/Q fever/Bartonella.
• Duke major criteria number only two: typical-organism bacteremia + endocardial involvement (modified Duke; the 2023 Duke-ISCVID adds intraoperative findings); fever, Janeway lesions, and Osler nodes are all minor.
• Osler is painful (immune), Janeway is painless (embolism); TTE comes first, TEE is first-line for a prosthetic valve.
• Three major surgical indications: heart failure, uncontrollable infection (bacteremia ≥7–10 days), and prevention of embolism; fever in the first 3 days is not a surgical indication.
• Prophylaxis narrowed to: prosthetic valve/prior IE/cyanotic congenital heart disease + a dental procedure that breaches the mucosa; stop 6 months after complete repair; mitral valve prolapse (MVP)/atrial septal defect (ASD)/gastrointestinal or genitourinary procedures do not routinely need prophylaxis.
• Traps: treating Osler/Janeway as major (they are minor); listing ASD as high-risk for IE (no jet lesion, so risk is actually low); treating IE with a 4-week oral course (it must be 4–6 weeks IV); requiring dental prophylaxis for simple MVP (not needed); operating just because fever persists at 3 days (the surgical threshold is ≥7–10 days).

• Southeast Asia + diabetes + pulmonary infiltrates + splenic abscess + safety-pin appearance → melioidosis; intensive phase ceftazidime/meropenem → eradication phase TMP-SMX for 3–6 months.
• Pneumonia after a cruise + diarrhea + altered mentation + hyponatremia → Legionella.
• Wading through water + rat urine + conjunctival injection → Leptospira (contact, not mosquito-borne).
• Traveler's diarrhea: bismuth is contraindicated in children; azithromycin is first-line in Southeast Asia (safe in pregnancy).
• Suspected influenza in pregnancy → oseltamivir, must not be delayed; the common cold = rhinovirus.
• Jarisch-Herxheimer reaction 50–90%, self-limited, do not stop treatment; treatment remains benzathine penicillin G.

• FUO = >38.3°C, ≥3 weeks, cause not found; three major categories = infection/tumor/autoimmune; do not fire antibiotics blindly first.
• EBV triad = fever + pharyngitis + posterior cervical lymphadenopathy; incubation 30–50 days; ampicillin causes a rash; avoid contact sports with splenomegaly; CMV has a negative heterophile antibody.
• Ludwig's angina = lower-molar dental source, bilateral submandibular swelling, tongue base obstructs the airway; secure the airway first.
• Rhino-cerebral fungal infection (DKA): Mucor non-septate/right-angle; Aspergillus septate/acute-angle; treatment = debridement + amphotericin B.
• Osteomyelitis: predominantly S. aureus; X-ray first, MRI most sensitive; biopsy culture is the gold standard.

• CSF: low glucose → bacterial/tuberculous/fungal; normal glucose → viral; protein is high in all — differentiate by predominant cell type plus glucose.
• Listeria = G(+) bacillus; ampicillin is first-line, cephalosporins do not cover it; vancomycin/ciprofloxacin perform poorly.
• High-risk groups (neonate/>50/pregnant/immunocompromised): standard regimen + ampicillin.
• Dexamethasone before the first dose reduces hearing loss from pneumococcal disease.
• Cryptococcal three phases: induction with ampho+5FC ≥2 weeks, consolidation with fluconazole for 8 weeks, maintenance for ≥1 year; total >12 weeks.
• Tuberculous meningitis: culture is the gold standard; PCR is an adjunct and has not replaced it.
• Suspected HSV encephalitis → give acyclovir immediately; PCR can remain positive for several days of treatment.

• Three axes: device + positioning + resistant organisms; ventilator-associated pneumonia (VAP) prevention = head of bed elevated 30–45°, sedation vacation, oral chlorhexidine.
• Sucralfate does not raise gastric pH and does not increase VAP risk (vs. H2 blockers/PPIs).
• Alcohol rub fails for visibly soiled hands and after Clostridioides difficile–associated diarrhea (CDAD) → soap and water.
• Febrile neutropenia first-line = cefepime/pip-tazo/carbapenem (covering Pseudomonas aeruginosa); vancomycin is not first-line.
• Methicillin-resistant Staphylococcus aureus (MRSA) is resistant to all β-lactams (except ceftaroline); first-line is vancomycin; do not use daptomycin for pneumonia (inactivated by surfactant).
• No renal adjustment needed: metronidazole, azithromycin, ceftriaxone, moxifloxacin, linezolid, clindamycin, doxycycline.
• Chelation: tetracycline/fluoroquinolone vs. Ca/Mg/Al/Fe → separate dosing by 2 hours.
• Viral URI: purulent discharge is not evidence of bacterial infection; asymptomatic bacteriuria (except pregnancy, before urologic surgery) is not treated.
• Needlestick HIV PEP: best <2 hours, 72-hour cutoff → go to the emergency department that same night.
• Traps: alcohol rub alone after CDAD (soap and water is required); giving vancomycin first for febrile neutropenia (an antipseudomonal agent must come first); using daptomycin for pneumonia (inactivated by pulmonary surfactant); adding a β-lactamase inhibitor to kill MRSA (ineffective — the target has changed, it is not being cleaved by an enzyme); delaying a needlestick to the next day (PEP must start that same night).

• Fever = upper urinary tract/pyelonephritis; simple cystitis has no fever; most common organism = E. coli.
• Cervical spinal injury = spastic UMN; flaccid LMN requires injury at S2-S4 or lower.
• Imaging for recurrent infant UTI: ultrasound first → VCUG to rule out VUR; UPJ obstruction → pyeloplasty (not reimplantation).
• IC = no bacteria, no pyuria; the main cause of unresolved bacteriuria = resistance; think glomerular first for hematuria in children (once UTI is excluded).
• Terminal complement C5-C9 deficiency → recurrent Neisseria infection (check CH50, vaccinate against meningococcus).
• Organophosphates = DUMBELS (increased secretions, miosis); treatment = atropine + pralidoxime; physostigmine is contraindicated.
• Thunderclap headache + neck stiffness + loss of consciousness → SAH; non-contrast CT first-line → if negative but suspicion is high, do an LP for xanthochromia.
• Vertebral osteomyelitis favors the lumbar spine, is usually S. aureus, and MRI is first-line.

• Only two absolute contraindications: active infection (e.g., open pulmonary TB) and active malignancy; stable HIV, cancer cured for five years, and age >70 are all relative.
• Three great sensitizing factors: transfusion, pregnancy, previous transplant → PRA↑; eosinophilia is not a sensitizing factor.
• A positive cross-match = transplantation is absolutely forbidden; ABO incompatibility can be managed with desensitization (plasmapheresis + rituximab + IVIG) — it is not an absolute contraindication.
• Best timing: pre-emptive transplantation, before dialysis begins; living donation is superior to deceased donation.
• Native nephrectomy indicated for: symptomatic polycystic kidneys, recurrent pyelonephritis, renal cancer, refractory hypertension/proteinuria; controllable hypertension does not require removal.
• Post-transplant recurrence: high for FSGS and DDD; a minority of SLE also recurs (do not memorize it as "never").

• Asthma is Type I (IgE); epinephrine is the drug of first choice for systemic anaphylaxis (not antihistamines/steroids).
• SLE's five-step chain: complement deficiency (C1q/C3/C4) → failed clearance of apoptotic cells → self nuclear antigens exposed → autoantibodies form immune complexes → deposition activates complement and causes tissue injury (C3/C4 fall from consumption).
• SLE = immune complex (Type III); vascular fibrinoid necrosis, Libman-Sacks bilateral-surface vegetations (mitral valve), wire-loop lesions belong to diffuse proliferative (Class IV).
• Dense deposit disease (DDD): C3↓, factor B↓, C1 normal; C3 nephritic factor (C3NeF) stabilizes C3 convertase (not inhibits it).
• Immune thrombocytopenic purpura (ITP): anti-GPIIb/IIIa, bone marrow megakaryocytes increased, favors women of childbearing age.
• IgG4-related disease (IgG4-RD) — the least likely finding: neutrophilic infiltrate.
• Myasthenia gravis (MG), thymus: follicular hyperplasia is most common; only about 15% is thymoma.
• Traps: SLE active phase "C3/C4 rise" (actually fall from consumption); lupus nephritis deposit written as anti-GBM (actually an immune complex); wire-loop filed under Class V membranous (actually Class IV diffuse proliferative); DDD with "C1 also low" (only the alternative pathway burns; C1/C4 are normal); ITP "megakaryocytes decreased" (actually compensatorily increased); MG "usually thymoma" (follicular hyperplasia is actually the most common).

• VZV reactivation: blisters along a single unilateral dermatome, not crossing the midline; antiviral therapy within 72 hours.
• Erythrasma = bacterial (Corynebacterium), coral-red fluorescence (coproporphyrin III), treated with an antibiotic (first choice; topical azoles also work).
• Tinea versicolor: yellow-green/gold; tinea capitis: green; erythrasma: coral-red; vitiligo: bright white (no infection).
• Scabies confirmation: microscopy showing mite/eggs/fecal pellets, any one suffices; first choice permethrin; lindane is neurotoxic, contraindicated in pregnancy and children; first-infection incubation 4–6 weeks.
• Warts = HPV (not S. aureus); most common opportunistic fungus in immunocompromise = Candida.

• Anti-dsDNA, anti-Sm = specific for SLE; anti-SSB/La = most specific for Sjögren (SSA/Ro is not specific).
• DILE = anti-histone (+), dsDNA (−), complement normal, little renal involvement, resolves with withdrawal; drug mnemonic HIP (hydralazine, isoniazid, procainamide).
• DLE → SLE progression rate only about 5%; SLE's cutaneous ACR items = malar rash, photosensitivity, discoid rash, oral ulcers (urticaria does not count).
• Systemic sclerosis = Raynaud (>90%), skin sclerosis, ANA (+); heliotrope is dermatomyositis, not sclerosis.
• Sclerosis skin sclerosis (mainly localized scleroderma; systemic sclerosis skin → MTX or MMF first) → UVA1 phototherapy; digital ulcers → vasodilator (not a topical steroid).

• First question: does the split lie within the epidermis (pemphigus) or beneath it (pemphigoid)?
• Pemphigus: Nikolsky positive, flaccid, DIF intercellular chicken-wire; pemphigoid: Nikolsky negative, tense, DIF linear basement membrane.
• PV, anti-Dsg3 → oral mucosa affected first, suprabasal split, tombstoning; PF, anti-Dsg1 only → most superficial layer, no mucosal involvement.
• BP vs. EBA: indistinguishable on H&E; salt-split DIF — BP's antibody stains the roof, EBA's the floor.
• Gottron papules (violaceous papules over the dorsal finger joints) are pathognomonic for dermatomyositis; heliotrope is highly suggestive but not pathognomonic; dermatomyositis is often pruritic and is associated with malignancy.

• CSF triad: low glucose + neutrophils = bacterial; normal glucose + lymphocytes = viral; low glucose + lymphocytes + high protein = tuberculous/fungal.
• Management: blood cultures → antibiotics immediately (+ dexamethasone) → then CT/LP; never delay for cultures.
• Empiric therapy in adults: ceftriaxone + vancomycin; add ampicillin (for Listeria) if >50 or immunocompromised; neonates: ampicillin + cefotaxime.
• HSV encephalitis: anterior temporal hemorrhagic necrosis; start acyclovir on suspicion alone; EEG = PLEDs.
• Neurosyphilis: serum treponemal (+) + CSF VDRL (+); IV penicillin.
• Tuberculous meningitis should have steroids added (not contraindicated). The Cushing reflex is a slow heart rate (not fast).
• vCJD: young, linked to beef, psychiatric symptoms come first; CJD's EEG = PSWC ≈ 1 Hz triphasic waves.

• Central = oligodendrocyte (MS/NMOSD/MOGAD/CPM); peripheral = Schwann cell (GBS/CIDP).
• NMOSD = anti-AQP4 (attacking astrocyte AQP4), LETM ≥3 segments, female:male 9:1, often coexists with other autoimmune disease; thymoma belongs to MG, not NMOSD. MOGAD = anti-MOG.
• MS: incidence↑ at high latitude, female:male 2:1; CSF protein <100, usually <50; oligoclonal bands (+) (serum negative).
• GBS: post-infectious autoimmunity, ascending symmetric weakness + areflexia, CSF albuminocytologic dissociation; treatment IVIG/plasmapheresis, steroids do not work.
• CPM: hyponatremia corrected >8–10 mEq/L/24h → onset only after 1–5 days.
• SCD (B12): knee-jerk↑, ankle-jerk↓, pain/temperature sensation normal, vibration sense lost, plus a history of veganism.

• Calcium oxalate: do not restrict dietary calcium (restricting it actually raises urinary oxalate↑); only uric acid and cystine stones can be dissolved by alkalinizing the urine.
• Uric acid stones: radiolucent, acidic urine; treatment alkalinize urine + allopurinol; probenecid/benzbromarone are contraindicated (uricosurics worsen the stone).
• Struvite = urease-producing bacteria (Proteus), staghorn calculus; E. coli, 75–85%, is the most common cause of community-acquired UTI.
• ASB is treated only in pregnancy and before urologic surgery; not treated in the elderly, diabetics, or catheterized patients.
• Obstruction + infection = a surgical emergency: emergency double-J stent or PCN + antibiotics; antibiotics alone are not enough.
• Ureteral stones: first choice URS (superior to ESWL); <5–6 mm can be managed conservatively.
• Reflux nephropathy = asymmetric atrophy + irregular contour; calling it "symmetric" is wrong.

• Omalizumab binds IgE's Fc-epsilon segment → allergic asthma, chronic spontaneous urticaria, peanut allergy.
• Abatacept = CTLA-4-Ig, occupies B7 to block CD28's second signal; not a TNF antagonist.
• Etanercept = TNF-receptor fusion protein (decoy); infliximab/adalimumab = anti-TNF monoclonal antibodies.
• -mab/-cept are injected; -tinib (JAK) is oral; RA's first-choice conventional DMARD = methotrexate.
• Every TNF inhibitor requires screening for LTBI and HBV before starting; may trigger demyelination and DILE.
• Cyclosporine/tacrolimus → calcineurin → IL-2↓; sirolimus → mTOR, lowest nephrotoxicity.
• Echinacea is immune-enhancing (not suppressive), an adjunct for upper respiratory tract infection.

• Sort the target first: cell wall/30S/50S/DNA gyrase/RNA polymerase/folate/cell membrane.
• Amoxicillin resistance = β-lactamase hydrolysis (countered by adding clavulanate); PBP mutation = MRSA.
• Imipenem must be paired with cilastatin (a DHP-I inhibitor that protects the drug).
• Cefepime + amikacin act synergistically (breaching the wall to let the drug penetrate); aminoglycosides are concentration-dependent (once-daily, high-dose), β-lactams are time-dependent; aminoglycosides are naturally resistant against anaerobes, toxicity = renal + ototoxic.
• Sulfonamide selectivity: the human body does not make its own folate, taking it from food instead; side effects — SJS/G6PD hemolysis/kernicterus.
• Acyclovir is a prodrug requiring viral TK; has no effect on latent infection; TK mutation = resistance.
• Oseltamivir is not used for HIV (that's the influenza drug); tenofovir is less effective against adefovir-resistant strains.
• Polyenes bind ergosterol directly; azoles inhibit the synthesis of ergosterol.

• Light's criteria: protein ratio >0.5, LDH ratio >0.6, LDH > 2/3 the upper limit of normal — any one makes it an exudate.
• Malignant effusion, overall most common = lung adenocarcinoma; in women = breast cancer; for recurrent effusion, first choice talc pleurodesis (the best option, not the worst; an indwelling pleural catheter is also first-line when the lung is expandable).
• Parapneumonic effusion pH <7.2 = a chest tube is required; antibiotics alone are insufficient. S. aureus bacteremia can spread to the lung hematogenously and cause multiple abscesses.
• Aspergilloma with hemoptysis: surgery is the first choice (antifungals penetrate poorly); mechanism = colonization inside an old tuberculous cavity.
• Bronchogenic cyst, CPAM, and sequestration favor resection even when asymptomatic; CPAM carries malignant potential.
• Pancoast→Horner (ptosis + miosis + anhidrosis); superior mediastinum→SVC syndrome; pseudopolycythemia = dehydration, unrelated to the thorax.
• Sarcoidosis = non-caseating; TB = caseating; sarcoidosis involves the lung in >90% of cases.

• A new bone lesion in a patient >40 should first suggest metastasis (breast/lung/thyroid/kidney/prostate); prostate cancer is blastic.
• Osteosarcoma: ages 10–20, metaphysis around the knee, nighttime pain, sunburst/Codman triangle, ALP↑; ~15–20% already have lung metastasis at diagnosis.
• Osteoid osteoma: diaphysis, nighttime pain, markedly relieved by NSAIDs; osteoblastoma responds poorly to NSAIDs and requires surgery.
• Osteochondroma on a flat bone carries a higher risk of malignant transformation; MHE is autosomal dominant with high penetrance.
• Chondrosarcoma grading requires all three together (clinical + radiologic + pathologic).
• Diabetic foot osteomyelitis: X-ray lags 2–3 weeks; MRI is most sensitive; a normal early X-ray cannot rule it out.
• Paget's disease: both resorption and formation are ↑, mosaic cement lines, ALP↑; treatment bisphosphonate (not PTH).
• Fibrous dysplasia: blood tests are usually normal; ground-glass appearance.
• Sacral pain after pelvic radiotherapy + the Honda sign = an insufficiency fracture, not metastasis/recurrence.

• Category 2 notifiable communicable disease, reported within 24 hours; four serotypes, a second infection with a different serotype causes severe disease via ADE.
• Aedes aegypti: south of Budai, Chiayi, indoors, prefers human blood, bites multiple people → the primary vector in the south; Aedes albopictus: island-wide below 1,500 m, outdoors, lower transmission efficiency.
• The 24–48 hours around defervescence is the warning period for plasma leakage, not the recovery period.
• Warning signs: abdominal pain, persistent vomiting, fluid accumulation, mucosal bleeding, lethargy/restlessness, hepatomegaly >2 cm, hematocrit↑ + platelets↓.
• Diagnosis: within 5 days, NS1/RT-PCR; after 5 days, IgM/IgG.
• Treatment: fluids + acetaminophen; aspirin/NSAIDs contraindicated; the core of prevention is eliminating man-made standing-water breeding sites.
• In 2015 the nation's locally acquired cases exceeded 43,000 (the most severe on record); Tainan saw another large outbreak in 2023.

• Category 3 notifiable communicable disease, reported within one week; a Flavivirus.
• Culex tritaeniorhynchus is the main vector, breeding in rice paddies and irrigation ditches; active at dusk and dawn.
• Pig = amplifying host; human = dead-end host, no person-to-person spread.
• Epidemic season May–October, peaking June–July; encephalitis may show an extrapyramidal syndrome.
• Current vaccine: cell-culture-derived live attenuated chimeric vaccine (17D backbone + SA14-14-2's prM/E), first dose at 15 months, second dose 12 months later; contraindicated in pregnancy and severe immunocompromise.

• The 1998 epidemic: 405 severe cases, 78 deaths, a 19.3% case-fatality rate among severe cases; it led to the establishment of the Centers for Disease Control in 1999.
• Fatal mechanism = brainstem encephalitis → neurogenic pulmonary edema/cardiopulmonary failure (not dehydration, not latent infection).
• Four prodromal signs of severe disease: myoclonic jerk during sleep, persistent vomiting, tachypnea or tachycardia, lethargy and poor activity/limb weakness.
• From prodrome to severe disease, the window can be as short as 8–12 hours → send to a major hospital immediately if any one sign appears.
• A non-enveloped virus → alcohol hand rub works poorly; requires soap-and-water scrubbing + chlorine-based bleach for environmental disinfection.
• Enterovirus infection with severe complications = Category 3, reported within one week.

• Reporting is a statutory duty: the deadline is counted in hours, and the middle of the night and holidays count the same; report on suspicion, do not wait for culture.
• Categories 1, 2, and 5: 24 hours; Category 3: one week; Category 4: as announced (mostly 24 hours; Creutzfeldt-Jakob disease: 1 month).
• Rabies = Category 1; dengue, Hantavirus, both forms of dysentery = Category 2; tuberculosis, Japanese encephalitis, severe enterovirus disease, HIV = Category 3; scrub typhus, melioidosis, leptospirosis, Q fever, invasive pneumococcal disease = Category 4.
• Scrub typhus: east coast and outlying islands, bitten by the mite's larval stage, eschar hidden under clothing, doxycycline is first choice at every age.
• Leptospirosis: after flooding, rat urine, calf pain + conjunctival suffusion, Weil's disease = jaundice + renal failure + hemorrhage.
• Melioidosis: after typhoon rains, diabetes is the highest risk, safety-pin morphology, ceftazidime/meropenem → TMP-SMX for 3–6 months.
• Q fever: aerosol from cattle/sheep parturition, occupational exposure, one cause of culture-negative endocarditis.
• Rabies PEP: soap and copious water for ≥15 minutes, plus vaccine, plus (for the previously unvaccinated) HRIG infiltrated around the wound; the wound should not be sutured immediately; there is no "wait and see" option.
• Invasive pneumococcal disease = isolation of the organism from a sterile site (a positive sputum culture does not count); asplenia is high risk.

• Ordinary tuberculosis = Category 3, reported within one week; multidrug-resistant tuberculosis (MDR-TB) = Category 2, reported within 24 hours.
• Taiwan's incidence fell from about 73 per 100,000 in 2005 to about 25 per 100,000 in 2025, with new cases at 5,742, dropping below six thousand for the first time; target is elimination by 2035.
• MDR-TB is selected for by an interrupted course, not by the patient's constitution; so the core of control is DOTS (directly observed therapy).
• Latent tuberculosis infection (LTBI) causes no disease, is not contagious, and comes with a normal X-ray; roughly a 10% lifetime risk of progression, higher in the immunocompromised.
• BCG interferes with the TST (false positives) but not with IGRA (ESAT-6/CFP-10 come from the RD1 region deleted from BCG).
• Taiwan's current LTBI regimens: 3HP (once weekly, 12 doses total), 3HR, 4R, 9H, plus 1HP and 6H; the shorter the course, the higher the completion rate.

• HIV infection = Category 3, reported within one week; anonymous screening is designed to lower the psychological barrier of identity exposure.
• U=U: regular treatment that brings the viral load to undetectable means no sexual transmission → treatment is prevention.
• PrEP publicly funded groups (current Taiwan policy): the spouse or sexual partner of a person with HIV (women prioritized); citizens 35 or younger at high risk; those in chemsex addiction treatment and sex workers are exempt from the age limit.
• HIV-negative status must be confirmed before prescribing PrEP; using it by mistake during the window period → induces drug resistance; the acute phase relies on HIV RNA/p24.
• PEP = within 72 hours after exposure, 4-week course (a needlestick is an emergency — handle it that same night).

• Taiwan was once a hepatitis B high-prevalence region, with mother-to-child vertical transmission as the dominant route.
• The younger the age at infection, the higher the chronicity rate (about 90% in infancy) → so the interception point is the first vaccine dose within 24 hours of birth (plus HBIG if the mother is e-antigen-positive).
• Starting July 1984 for newborns of carrier mothers, expanded to all newborns in July 1986 — the world's first program of its kind; the pediatric carrier rate fell from about 10% to under 1%, and childhood hepatocellular carcinoma dropped sharply (1997, *NEJM*).
• Hepatitis D borrows HBsAg as its envelope → the hepatitis B vaccine simultaneously prevents hepatitis D.
• No vaccine exists for hepatitis C (E1/E2 are highly variable); DAA course 8–12 weeks, cure rate near 99%.
• Taiwan added DAAs to National Health Insurance in 2017 and removed the liver-fibrosis threshold for full reimbursement starting January 2019; reached the WHO elimination target ahead of schedule in 2025.
• Acute viral hepatitis B, C, D, and E are all Category 3 notifiable diseases, reported within one week.

• Resistance = a product of selective pressure; the hospital = a three-in-one breeding ground of high antibiotic density + weak host + invasive catheters.
• CRAB: Taiwan's medical center ICU resistance rate rose from 59.6% in 2008 to 70.6% in the third quarter of 2017; mechanism = OXA-type carbapenemase + porin loss + efflux pumps; desiccation-tolerant, survives weeks on surfaces → environmental cleaning and contact precautions matter equally.
• MRSA = a target change via mecA/PBP2a, unaffected by β-lactamase inhibitors; CA-MRSA carries PVL, causing skin abscesses and necrotizing pneumonia.
• CRE: KPC (class A) and NDM/IMP/VIM (class B metallo-enzymes, zinc-dependent, unaffected by clavulanate).
• ASP's four D's: right Drug/Dose/De-escalation/Duration; strategy = prospective audit and feedback + preauthorization; Taiwan adds National Health Insurance reimbursement rules as an extra lever.
• The four HAI categories = VAP/CAUTI/CLABSI/SSI; shared structure = tube + time + host, with biofilm defeating the drugs → daily assessment and early removal is the common closing line of every bundle.
• CLABSI bundle: hand hygiene, maximal sterile barrier precautions, chlorhexidine, avoid the femoral vein, scrub the hub. CAUTI bundle: insert only with an indication, closed drainage, collection bag below the bladder and off the floor, remove as early as possible.
• The five moments for hand hygiene: before touching a patient, before an aseptic procedure (protects the patient); after body-fluid exposure, after touching a patient, after touching the environment (protects you and the next patient).
• Three transmission-based precaution routes: contact (MRSA/CRAB/*C. difficile*); droplet (influenza, pertussis, meningococcus) → surgical mask; airborne (tuberculosis, measles, varicella) → negative-pressure isolation room + N95. Measles and varicella are airborne, not droplet (a high-frequency trap).
• SARS, 2003: the Heping Hospital lockdown exposed the errors of collapsed in-hospital infection control and "isolation that became congregation"; it gave rise to revision of the Communicable Disease Control Act, a negative-pressure ward network, infection control audits, fever screening, and the TOCC intake routine.
• COVID-19: the mask name-based rationing system replaced price competition with quota sales through the National Health Insurance card; now classified as Category 4 notifiable disease "COVID-19 with severe complications."

• Sequence: TSH → ultrasound → (risk-based) FNA; only a low TSH triggers a radionuclide scan to rule out a hot nodule.
• PET, CA markers, physical exam alone, and proceeding straight to surgery are all common wrong answers.
• Bethesda III/IV is the gray zone requiring molecular testing or lobectomy; V/VI go straight to surgery.
• Papillary (most common, lymphatic), follicular (hematogenous, hard to confirm by FNA), medullary (calcitonin, MEN2), anaplastic (dismal prognosis).
• Differentiated cancer is followed with Tg; medullary cancer with calcitonin plus CEA; the most important risk factor = history of head and neck radiation.

Thyroid nodule evaluation

• Storm regimen: PTU + propranolol + hydrocortisone + iodine (1 hour after the ATD).
• Iodine must never precede the ATD; amiodarone (iodine-containing) is contraindicated; fever + sore throat on an ATD → check WBC/ANC to rule out agranulocytosis.
• First-line for routine hyperthyroidism: methimazole; PTU is preferred only in storm and the first trimester of pregnancy.
• Total thyroidectomy raises complication risk (not lowers it): hypoparathyroidism (postoperative perioral numbness, Chvostek/Trousseau signs), RLN injury (bilateral = airway obstruction).

Thyroid storm and total thyroidectomy

• Mass in age <40/pregnancy/lactation → ultrasound; mammography primary at ≥40.
• CA15-3 cannot diagnose breast cancer (used only to monitor metastasis); a normal exam does not stop follow-up; proceeding straight to surgery or relying on PET alone are both wrong.
• Chemotherapy decision factors: size, nodal status, ER/PR/HER2, Ki-67/grade; tumor location is not a decision factor.
• Medial upper-arm numbness after axillary clearance = intercostobrachial n.; winged scapula = long thoracic n.
• Absence of skin dimpling cannot rule out breast cancer (high PPV ≠ high sensitivity).
• Pituitary apoplexy: severe headache + bitemporal hemianopsia + acute hypopituitarism → steroids first ± decompressive surgery.

Breast masses and pituitary apoplexy

• Classification: sleeve/AGB/VBG = purely restrictive; RYGB = restrictive + malabsorptive; BPD/DS = strongly malabsorptive (not purely restrictive).
• Most common = sleeve; RYGB is first-line for severe GERD; target population = type 2 diabetes (not type 1).
• Indications: BMI ≥ 40, or ≥ 35 + comorbidity (2022 guideline: recommended at ≥ 35) (threshold can drop to ≥30 for poorly controlled T2DM); psychiatric evaluation is mandatory — "decided at a family meeting" and "no psychiatric evaluation needed" are both wrong.
• The mechanism is not purely mechanical: GLP-1↑, PYY↑, ghrelin↓; glycemic improvement often precedes weight loss.
• Complications: early leak (often requires surgery), nutritional deficiency (worst with malabsorptive procedures), dumping, gallstones.

Bariatric surgery

• Incarcerated vs strangulated: incarcerated is irreducible but blood flow is still intact; strangulated has interrupted blood flow with tissue death — emergency.
• Direct vs indirect (relative to the inferior epigastric artery): direct is medial, indirect is lateral; femoral hernia is below the inguinal ligament, more common in women, highest incarceration rate.
• Standard repair = tension-free Lichtenstein mesh; bowel obstruction plus a groin mass in an elderly patient = incarcerated hernia.
• TAPP has more space, TEP is tight; preperitoneal repair must not ligate the lateral femoral cutaneous nerve (meralgia paresthetica); avoid placing tacks in the "triangle of doom/pain."
• Elective repair after MI is delayed ≥6 months (current ACC/AHA: ≥60 days); most common short-term postoperative complication = pain; SILS umbilical fascia = absorbable suture.
• When a patient requests treatment outside the indication (e.g., albumin) → decline professionally after thorough discussion.

Hernias

• Sequence: APC → KRAS → TP53/SMAD4; adenoma to carcinoma takes about 5–10 years (10–15 years); "1–2 years" is always wrong.
• Two fast lanes: serrated (BRAF/MSI), Lynch (MMR deficiency).
• Risk: age, low-fiber diet high in red meat, family history, IBD, obesity/sedentary lifestyle (increases, not decreases), smoking and alcohol.

Colorectal cancer mechanism and risk

• Stage III colon cancer: FOLFOX/CAPOX adjuvant chemotherapy, no targeted therapy added.
• Stage IV: chemotherapy plus targeted therapy (bevacizumab; cetuximab/panitumumab restricted to RAS wild-type, left-sided).
• Locally advanced rectal cancer: neoadjuvant chemoradiation → TME → adjuvant chemotherapy.
• TME protects the autonomic nerves → sexual dysfunction does not increase; laparoscopic vs open surgery: comparable oncologic outcomes, faster recovery.
• Hereditary syndromes: PJS = STK11, hamartomas plus mucocutaneous pigmentation; FAP = APC, carpeted with adenomas; Lynch = MMR, fewer polyps but fast, MSI-high, predominantly right-sided.

Staged treatment and surgery

• The levator ani = puborectalis + pubococcygeus + iliococcygeus; the piriformis/gluteus maximus are not included.
• Above the dentate line: columnar/transitional epithelium, IMA → portal vein, autonomic nerves (painless), internal iliac nodes, internal hemorrhoids.
• Below the dentate line: squamous epithelium, internal pudendal → IVC, pudendal n. S2–S4 (painful), superficial inguinal nodes, external hemorrhoids.
• The middle rectal artery = the internal iliac artery (not the IMA); IMA branches = left colic/sigmoid/superior rectal.
• The sigmoid colon's propensity to perforate = diverticula + small diameter → high intraluminal pressure by Laplace's law, not a thinner bowel wall.

Anal canal anatomy

• ACS: bladder pressure (not a nasogastric tube); sustained IAP ≥12 = IAH; >20 plus organ dysfunction = ACS; CVP is falsely elevated, has a clear effect on breathing, heart rate rises reflexively, renal blood flow↓ → oliguria; definitive treatment = decompressive laparotomy.
• UGIB vs LGIB divided by the ligament of Treitz; LGIB includes the jejunum (traditional; now termed small-bowel bleeding); about 80% stops spontaneously.
• Free air under the diaphragm on an upright film, most common cause = perforated peptic ulcer (not cholecystitis/pneumothorax/liver abscess).

Three questions in the acute abdomen

• Diverticulitis favors the sigmoid colon; Hinchey III/IV → emergency surgery; a colovesical fistula = elective surgery; a small abscess can be managed with CT-guided drainage; chronic anemia is not an indication for emergency surgery.
• UC: mucosal, continuous, rectum upward, can show backwash ileitis, more often associated with PSC, flares with smoking cessation.
• Crohn's: transmural, skip pattern, mouth to anus, fistulas/perianal disease, worsened by smoking.
• Free air under the diaphragm = perforated peptic ulcer is the most common cause.

Diverticular disease, IBD, and perforation

• Double-bubble + bilious vomiting = duodenal atresia (~30% associated with Down syndrome); single bubble + projectile bile-free vomiting + olive-shaped mass + hypochloremic, hypokalemic alkalosis = hypertrophic pyloric stenosis.
• Bile is the watershed: bilious vomiting = obstruction below the ampulla.
• Gastroschisis: beside the umbilicus, no membrane, few associated anomalies; omphalocele: at the midline, has a membrane, about 50% associated anomalies.

Neonatal gastrointestinal obstruction plus abdominal wall defects

• NEC: prematurity + ischemia + feeding → pneumatosis intestinalis; usually conservative (NPO, decompression, antibiotics, fluids), free air (perforation) is what mandates surgery; portal venous gas = severe disease.
• Thyroglossal duct cyst = midline, moves with swallowing, Sistrunk procedure; branchial cleft cyst = anterior border of the SCM; cystic hygroma = transilluminates in the posterior neck.
• A supraclavicular lymph node → highly suspicious for malignancy, biopsy; cervical teratoma is extremely rare.
• Neonatal teratoma favors = the sacrococcygeal region (40–70%); early diagnosis and early surgery give a better prognosis; excising the coccyx reduces recurrence.

NEC/neck masses/teratoma

• Monkey bite → herpes B virus → acyclovir/valacyclovir (antiviral); fatality rate about 80%; irrigate the wound copiously for ≥15 minutes.
• Dog/cat/human bite → Pasteurella/Eikenella → Augmentin.
• Seawater/fish spine → Vibrio vulnificus → fluoroquinolone + a third-generation cephalosporin; freshwater → Aeromonas → fluoroquinolone.
• Common to all: debridement, delayed closure in most cases, tetanus booster, rabies risk assessment.

Bite wounds

• Logic: never go complex when simple will do; exposed bare bone/tendon/hardware → a flap is mandatory, a skin graft is not an option.
• Skin grafts: FTSG, thick dermis → least contracture; STSG, thin → most contracture; the three chief causes of failure = shear, hematoma, infection.
• Mathes-Nahai: I gastrocnemius, II soleus, III gluteus maximus/rectus abdominis, IV sartorius (no free flap), V latissimus dorsi/pectoralis major.
• The pectoralis major's vascular pedicle = the thoracoacromial artery (not the internal mammary); the radial forearm flap = fasciocutaneous type B.
• Microsurgery = large defects, free tissue transfer, vascular/nerve repair; "small area" is always wrong.
• Ischemia: muscle warm ischemia 1–2 hours, skin 4–6 hours; digit warm ischemia ≤12 hours/cold 24 hours; limb warm ischemia ≤6 hours; when cooling, never immerse directly in ice.
• Digit replantation: thumb, young children, multiple digits, distal amputations — replant aggressively; a single non-thumb digit with multi-level amputation is a relative contraindication.
• The advantage of a perforator flap = preserving donor-site muscle function (do not mistake this for a disadvantage).
• Glomus tumor = subungual, pinpoint pain, cold sensitivity, point tenderness.
• Stage 4 pressure ulcer → debridement plus a local muscle flap (not a skin graft).

The reconstructive ladder

• Laser = selective photothermolysis; CO2/Er:YAG → water; PDL → oxyhemoglobin; ruby/alexandrite → melanin/tattoo pigment.
• Residual fine lines after a facelift = fractional CO2 (ablative).
• Z-plasty angle–lengthening: 30/45/60/75/90° → 25/50/75/100/120%; 60° is the most commonly used.
• RSTLs run perpendicular to the direction of muscle contraction and parallel to the dynamic wrinkles; on the lip, perpendicular to the vermilion border.
• Lidocaine: ordinary 4–5 mg/kg, 7 mg/kg with epinephrine, tumescent technique up to 35 mg/kg.
• Syndactyly most commonly involves the middle and ring fingers; the first allogeneic face transplant: France, 2005.

The finer points of plastic surgery

• Crohn's = skip lesions, transmural, granulomas, fistulas, worsened by smoking; UC = continuous, superficial, no granulomas, thin bowel wall, curable.
• A thick bowel wall = Crohn's (a trap answer choosing UC as thickened is wrong); the focus of cancer surveillance = UC.
• 5-ASA is used in UC, no longer used in Crohn's; moderate-to-severe Crohn's favors early top-down biologics.
• Asian IBD incidence is lower than in Europe and North America.
• Short bowel diet: MCT preferred (absorbed directly into the portal vein); B12 must be supplemented after terminal ileum resection; preserving the ileocecal valve is key to prognosis.
• Traps: "smoking worsens UC" (reversed — UC paradoxically flares after smoking cessation) / "Crohn's is continuous" (reversed — skip lesions are correct) / "5-ASA for Crohn's maintenance" (obsolete).

• The SMA supplies through the proximal two-thirds of the transverse colon; the IMA takes over through the upper rectum, with its terminal branch = the superior rectal artery.
• Watershed zones = the splenic flexure and the rectosigmoid junction, the favored sites for ischemic colitis.
• Left lower quadrant pain plus bloody stool after AAA repair = ischemic colitis (IMA injury).
• The internal pudendal/gluteal/vesical arteries belong to the internal iliac artery, not branches of the IMA.
• The most common cause of small bowel bleeding = angiodysplasia.
• NEC occurs mainly in preterm infants but can affect term infants too; favors the ileocecal region; thrombocytopenia; perforation with free air requires surgery.

• The most common cause of adult bowel obstruction = postoperative adhesions; the most common electrolyte abnormality in paralytic ileus = hypokalemia.
• For pediatric intussusception, enema reduction is first-line (successful in most cases); surgery is reserved for perforation/failed reduction.
• The four steps of the Ladd procedure: counterclockwise detorsion → division of Ladd's bands → widening the base of the mesentery → appendectomy.
• Gastroschisis: no membrane + jejunoileal atresia; omphalocele: has a membrane + cardiac/chromosomal anomalies.
• The most common primary malignant small bowel tumor (per the licensing exam) = adenocarcinoma, favoring the duodenum; GIST is "the most common mesenchymal tumor," not the most common malignant tumor.
• The key factors in short bowel syndrome = the amount of ileum resected, the ileocecal valve; smoking is a risk factor in Crohn's disease.

• Grade I–III internal hemorrhoids: ligation; a thrombosed external hemorrhoid: excise <72h, manage conservatively >72h.
• The standard Goodsall's rule = curved posteriorly, straight anteriorly (posterior curves to 6 o'clock, anterior runs straight); if the official key states "posterior runs straight to the corresponding clock position," answer per the official key.
• Parks type 2 = transsphincteric.
• A fissure is located at the posterior midline; the triad = a posterior wound + bright red blood + a sentinel skin tag.
• 80–90% of acute fissures heal with conservative treatment; LIS is reserved for refractory cases.

• H. pylori: 1994 IARC Group I; strongly linked to both gastric cancer and MALToma.
• Among gastric polyps, only the adenomatous type is removed; the others are mostly benign.
• Gastric cancer diagnosis = endoscopy + biopsy; CT is a staging tool.
• EGC = confined to the mucosa or submucosa, regardless of nodal metastasis; only invasion through the submucosa counts as advanced.
• Indications for ulcer surgery = perforation, bleeding, obstruction, refractory to treatment; H. pylori infection alone is not a reason for surgery.
• The parietal cell is eosinophilic (mitochondria-rich) and secretes intrinsic factor.
• Advanced gastric cancer = adequate margins plus D2 lymphadenectomy.

• HCC imaging = arterial-phase wash-in, delayed-phase washout, no biopsy needed; a normal AFP does not exclude HCC.
• The classic paraneoplastic presentation = hypoglycemia plus erythrocytosis; hypercalcemia is comparatively rare.
• Child-Pugh's five components (A/B/C/D/E): A=5–6, B=7–9, C=10–15; a score of 6 belongs to class A.
• Insulinoma is the most common, about 90% benign; gastrinoma is mostly malignant.
• Acute pancreatitis = hypocalcemia (fat saponification).
• Calot's triangle = the cystic duct, the common hepatic duct, the inferior border of the liver; the right portal vein is not a boundary.
• Calculous cholecystitis = early laparoscopy (within 72h) is the standard, not a contraindication.
• The most common source of pyogenic liver abscess = biliary infection (in Taiwan mostly cryptogenic Klebsiella, can cause endophthalmitis).
• The most valuable preoperative test for biliary atresia (confirmatory gold standard: intraoperative cholangiography) = liver biopsy; the Kasai procedure must be done within 60 days.

• CO2 pneumoperitoneum is the standard, giving a uniform, wide field; the gasless retractor is inferior.
• Pneumoperitoneum side effects = ↑airway pressure, ↓venous return, CO2 retention and acidosis; pressure 12–15 mmHg.
• Trocars avoid crossing hands (fulcrum effect).
• Splenectomy in portal hypertension = high bleeding risk; simulation training builds depth perception and hand-eye coordination.
• General surgery basics = gallbladder, hernia, appendix; hysterectomy belongs to gynecology.

• Class IV = delayed primary closure or healing by secondary intention; primary closure = deep abscess.
• Clean wound SSI = 1–5%, not 0.1–0.3%.
• Prophylactic antibiotics within 60 minutes before incision; vancomycin/FQ within 120 minutes; redosing after 2 half-lives or blood loss > 1500 mL; stopped 24 hours after surgery.
• Antibiotics cannot prevent CRBSI/UTI; rely on sterile insertion and early catheter removal.
• Proliferative-phase fibroblasts migrate in from local tissue, not delivered by blood.

• Early dumping (15–30 min) = osmotic + vasomotor reaction; late (1–3 hr) = hypoglycemia.
• Earliest ECG sign of hyperkalemia = tall peaked T wave; first step in resuscitation = IV calcium to stabilize the membrane; sequence is "stabilize, shift, remove."
• Kayexalate is slowest, not the first step.
• Warfarin held 5 days, INR < 1.5; high thrombotic risk → LMWH bridging; clopidogrel 5–7 days; DOAC 2–3 days.

• DFSP is locally aggressive but rarely metastatic — wide excision/Mohs, no lymph node dissection needed; MFH and angiosarcoma are both high-grade and can metastasize.
• Kaposi sarcoma pathogen = HHV-8; Bence Jones protein belongs to multiple myeloma.
• Giant CMN (over 40 cm) can coexist with leptomeningeal melanocytosis, diagnosed by MRI.
• Choroid plexus tumor is in the fourth ventricle in adults; meningioma arises from arachnoid cap cells; sudden deterioration of a brain abscess = rupture into the ventricle.
• NPH = Wet, Wacky, Wobbly (no tremor); gait is earliest to appear and first to improve.
• Vessel responsible for trigeminal neuralgia = SCA; first-line for refractory temporal lobe epilepsy = anterior temporal lobectomy.

• Four principles = autonomy, beneficence, non-maleficence, justice; pathway = capacity → advance directive → emergency.
• A legal proxy takes priority over family and need not be a relative; an emergency with no proxy = implied consent to save the life first.
• HIV is reported to the health authority; the spouse may not be told directly; Tarasoff = minimum necessary disclosure.
• A surgical error = commission; regardless of negligence, disclose honestly.
• AD applies to terminal/irreversible/vegetative state/extremely severe dementia/announced unbearable suffering; acute traumatic coma does not apply → saving the life comes first.
• Organ allocation = equity + no buying or selling; "affects national health insurance" is a distractor.

• Domestic violence/child protection/sexual assault: a statutory duty of healthcare workers, must be reported within 24 hours at the latest; not the police's duty alone.
• HIV's four layers: confidentiality is the default; the partner is told only with consent, without consent, report to the health authority first; HIV is a notifiable disease, the physician must report it; concealment causing infection carries criminal liability.
• Conflict-of-interest distractor = patient privacy (irrelevant, eliminate it).
• Industry code: academic time ≥ 2/3; the only payment allowed is a lecture honorarium; gift certificates = money, may not be accepted.

Reporting, confidentiality, industry ties

• Three elements: decision-making capacity + adequate disclosure + voluntariness; missing any one invalidates it.
• A capacitated adult refusing life support / withholding disclosure from parents / refusing admission: respect autonomy, process an AMA discharge and document the chart; neither force them to stay nor simply let them leave unrecorded.
• Three conditions of implied consent: cannot express a choice + no legal proxy + withholding treatment would endanger life; reasonable resuscitation time for an unidentified comatose patient is 30 minutes to 1 hour.
• A prior refusal of an elective procedure ≠ a refusal covering a sudden emergency loss of consciousness; treat in an emergency regardless.
• Manipulation = selective exaggeration/concealment plus family pressure, undermining voluntariness.

Informed consent and emergency implied consent

• Medical Care Act Articles 63/64: only the physician may explain; the audience for the explanation is flexible; treatment may proceed directly in an emergency.
• Surrogacy: adult children rank equally, no eldest-child priority, no majority vote, paying does not confer priority; divided opinions → consensus through a family meeting.
• Hospice Palliative Care Act = terminal patients, nearest relatives may sign a DNR in order of priority; Patient Right to Autonomy Act = five conditions + ACP + AD, the AD cannot be signed by the family on the patient's behalf.
• Scarce resources: the principle of utility = priority to the better prognosis (not age, not first-come-first-served).
• A medical record addendum must be dated, or a court may refuse to accept it as evidence.

Informed consent and resource allocation

• Pathophysiology: obstruction → ischemia → necrosis → perforation; fecalith is most common (lymphoid hyperplasia in children, tumor in the elderly).
• Classic migratory pain (periumbilical → right lower quadrant) plus McBurney's point tenderness is the diagnostic eye.
• Imaging: ultrasound is first-line in children/pregnant women/young women (>6 mm, target sign); CT is the gold standard in adults; X-ray cannot confirm the diagnosis.
• Psoas = retrocecal; Obturator = pelvic; Rovsing = peritoneal irritation.
• Treatment: laparoscopy is first-line; 25–40% still need surgery within a year after antibiotic therapy; an abscess can be drained.
• Most common postoperative complication = SSI (10–20% with perforation); think tumor in the elderly.

Appendicitis

• Level IA = both anterior digastric bellies + hyoid (spanning the midline) (submental); IB = contains the submandibular gland.
• Salivary gland: most common overall = pleomorphic adenoma (benign); most common malignant = mucoepidermoid carcinoma; ACC: perineural invasion, late lung metastasis.
• ACC's three histologic patterns, by prognosis: tubular best > cribriform > solid worst.
• OSCC AJCC 8th: DOI >10 mm alone makes T3 (on par with >4 cm); N2b = multiple ipsilateral nodes ≤6 cm, no ENE.
• The goal of orthognathic surgery = Angle Class I (not II or III).

Neck and oral cancer

• Blunt trauma most often injures the spleen (liver next); penetrating/gunshot injury most often injures the small bowel; stab wounds most often hit the liver.
• FAST is highly specific but only moderately sensitive (a negative result cannot rule out injury); CT = the gold standard (first choice for a stable patient).
• Unstable + positive FAST → straight to laparotomy; do not wait for CT.
• Neck: Zone II (cricoid cartilage → angle of mandible) is easiest to operate on; hard signs always mean exploration, otherwise no-zone + CTA.
• L1 Chance fracture → duodenal injury.
• Pregnancy: left lateral decubitus; secretion pH ≥ 6.5 = ruptured membranes; pelvic exam contraindicated if placenta previa is suspected; CT may be done when necessary.
• AAST liver injury has six grades.
• Mafenide: strong penetration + metabolic acidosis + pain; SSD has weak penetration and is painless.
• Burn infection: early G(+), later G(-); no routine prophylactic antibiotics.

Trauma

• Infant direct hyperbilirubinemia + pale stool + tea-colored urine = a surgical emergency; Kasai surgery after 60 days in biliary atresia carries a worse prognosis; Alagille = JAG1 + paucity of bile ducts + butterfly vertebrae + pulmonary artery stenosis + posterior embryotoxon.
• For diarrhea, check the response to fasting first: secretory persists during fasting, osmotic improves with fasting; congenital chloride diarrhea (SLC26A3) = secretory + alkalosis + hypochloremia (the direction is a common reversal trap).
• Low potassium + alkalosis + low urinary calcium + low serum magnesium = Gitelman; high urinary calcium = Bartter; hypertension = Liddle.
• Main cause of gallbladder hydrops = Kawasaki disease (CF is atypical); bloody stool in an exclusively breastfed infant = maternal cow's milk protein; enema reduction is first-line for intussusception; for constipation, stool in the rectum is not a red flag.
• Mild-to-moderate VUR is managed conservatively first, with prophylactic antibiotics, not immediate surgery.

Infant digestion and electrolytes

• Sequence: ABC + fluids + airway protection → endoscopy once stable; do not perform colonoscopy in the acute phase; β-blockers are contraindicated in the acute phase (for prevention, not hemostasis).
• Esophageal variceal combination: octreotide/terlipressin + IV ceftriaxone + EVL; for refractory cases, bridge with an SB balloon, then TIPS.
• Hb can be normal at the very start of massive acute bleeding (hemodilution has not yet occurred); judge blood loss by hemodynamics.
• Forrest: Ia highest at 55%, III lowest at 2–5%; high-risk patients get endoscopy + 72-hour high-dose PPI.
• Mesenteric ischemia clue: AF/cardiac catheterization + severe pain with a soft abdomen; add flow, don't constrict vessels; vasoconstrictors are contraindicated; early vascular reconstruction.

GI bleeding

• IBS essence = gut–brain axis dysregulation + visceral hypersensitivity; about 80% of moderate-to-severe cases are women; Rome IV = abdominal pain ≥1 day/week + ≥2 defecation-related items.
• Fecal calprotectin = an IBD marker (not elevated in IBS); fecal occult blood/white cells should be negative in IBS, and a positive result means ruling out IBD/cancer.
• Tenesmus ≠ a definitive indicator of rectal tumor.
• Chronic alcohol use = secretory diarrhea; bowel sounds in mechanical obstruction go hyperactive first, then absent.
• B12 deficiency = neuropathy + megaloblastic anemia (not tetany; tetany comes from low Ca/Mg).
• In an older child with intussusception, a lead point must be sought.

IBS and diarrhea

• Psoas = retrocecal appendix; Obturator = pelvic; Murphy = halts on inspiration (not expiration); Grey Turner = flank bruising; Cullen = periumbilical bruising.
• B12 and bile acids are absorbed in the terminal ileum; iron and calcium in the duodenum/upper jejunum; resecting the duodenum does not affect B12.
• Fat-soluble vitamins = A, D, E, K.
• Hemorrhoids: grade three reduces manually, grade four cannot be reduced (don't reverse these).
• Diverticular disease: CT is first-line, smoking is a risk factor, mesalazine reduces symptomatic recurrence.
• Esophageal indentation: the aortic arch is on the left side.

Signs of the acute abdomen and the small bowel map

• ALF definition = no chronic liver disease + INR ≥ 1.5 + encephalopathy (< 26 weeks); neither condition may be missing.
• Severity is judged by PT/INR + bilirubin + encephalopathy; ammonia does not track in parallel, and ALT paradoxically falls in the end stage — neither should be judged alone.
• Etiology: acetaminophen is most common worldwide (antidote NAC); HBV predominates in Taiwan; Wilson's disease = young + KF ring + negative viral markers.
• Treatment: find the cause, prevent cerebral edema, no routine prophylactic FFP; King's College criteria → liver transplantation.
• Wilson's labs: ceruloplasmin ↓, free copper ↑, urinary copper ↑ (direction is a common reversal trap); treatment is D-penicillamine/trientine/zinc.
• ACLF (acute decompensation of chronic liver disease) differs from ALF, with different management and prognosis.
• Traps: ALT falling means improvement (backwards — it may mean the hepatocytes have all died) / ammonia level equals the severity of encephalopathy (not parallel) / Wilson's urinary copper should be low (backwards — it is elevated).

Acute liver failure and Wilson's disease

• SBO's most common cause = adhesions; LBO's most common cause = colorectal cancer (volvulus second).
• Mechanical SBO does not raise amylase; a rise should suggest strangulation or pancreatitis.
• Simple SBO is managed conservatively first (NPO + NG + IV fluid); surgery only for signs of strangulation.
• The sigmoid colon is where volvulus favors, with bird-beak on CT; endoscopic decompression is first-line.
• Rovsing's sign = pressing the left lower quadrant elicits right lower quadrant pain; appendicitis's "periumbilical first, right lower quadrant later" is migratory pain.

• DU: pain when fasting, relieved by eating; GU: pain after eating, requires biopsy.
• Stop the PPI two weeks before UBT; wait four weeks after eradication before retesting.
• GERD has no causal link to H. pylori; H. pylori connects to peptic ulcer, gastric adenocarcinoma (intestinal type), and MALT lymphoma.
• The sliding hiatal hernia is the most common type (about 95%); the paraesophageal type is less common but carries a risk of strangulation.
• Afferent loop syndrome = postprandial bloating and pain, relieved after vomiting bile, elevated MCV; dumping syndrome's most common trigger = high carbohydrate intake, with the late phase = reactive hypoglycemia.
• Type A gastritis = body of the stomach + autoimmune (B12 deficiency); Type B = antrum + H. pylori.
• Parietal cells are rich in mitochondria; eradicating H. pylori after early gastric cancer resection lowers metachronous gastric cancer recurrence.

• PBC = women, AMA(+), granulomatous destruction of intrahepatic small bile ducts, UDCA; PSC = men, onion-skin fibrosis, beaded bile ducts, associated IBD, high risk of cholangiocarcinoma.
• MCN = ovarian-type stroma; IPMN communicates with the pancreatic duct; SPN favors young women (not men).
• FAP = APC mutation, with polyps appearing only at puberty and nearly 100% malignant transformation.
• AAC risk factors = trauma / major surgery / fasting / burns / TPN (sepsis is also a risk factor; alcohol is not).
• Pseudomembranous colitis relies on toxin testing, not culture; treatment is oral vancomycin or fidaxomicin.
• Intestinal-type gastric cancer ↔ H. pylori; diffuse type ↔ CDH1 / signet-ring cells.
• Fundic gland polyps ↔ long-term PPI use.

• CD = transmural / skip lesions / fistula and stricture / ASCA(+); UC = mucosal / continuous / bloody stool / p-ANCA(+).
• Smoking worsens CD and protects against UC; appendectomy protects against UC; oral contraceptives increase CD risk (a direction often reversed on exams).
• Corticosteroids can induce but must never maintain; 5-ASA is the mainstay for UC maintenance; anti-TNF is the mainstay for moderate-to-severe CD, promoting fistula healing and reducing surgery.
• Bowel rest + TPN for inducing CD remission ≈ corticosteroids (older data; current: bowel rest is unnecessary, exclusive enteral nutrition is first-line in children, and TPN is only for those who cannot be fed enterally); when CD drug therapy fails, the next step = step up to a biologic, not surgery.
• Toxic megacolon = transverse colon > 6 cm + systemic toxicity; anticholinergics and antidiarrheal agents are contraindicated.

• HCV is most likely to become chronic (75–85%); neonatal HBV chronicity >90%; 95% of adults with acute hepatitis B recover, <5% become chronic, and nucleos(t)ide analogs do not shorten the course.
• Progression factors in chronic hepatitis C: male sex / heavy alcohol use / infection after age 30 / HIV or HBV coinfection (not female sex).
• The course of HBV is determined by host immunity and age at infection, not viral genotype.
• Primary prophylaxis against varices = a nonselective β-blocker.
• Hepatic encephalopathy: lactulose + rifaximin.
• Fatty liver on CT: liver density < spleen; in pregnancy, ALP↑ while AST/ALT do not rise.
• Cholangiocarcinoma risk = PSC; AMA(+) = PBC.

• Diagnosis requires two of three criteria, with lipase/amylase > 3 times normal.
• The most important initial treatment = aggressive IV fluid resuscitation (current: early, moderate goal-directed fluids — WATERFALL 2022); antibiotics are not routine; ERCP is urgent only with concurrent cholangitis/obstruction.
• BISAP's P = pleural effusion; Hct > 44% on admission suggests severe disease.
• The imaging of choice for acute pancreatitis = abdominal CT; a barium esophagram is entirely inappropriate (current practice: ultrasound on admission, CT only for an unclear diagnosis or no improvement at 48–72 h).
• Serum calcium in acute pancreatitis is low (consumed by fat saponification); type 3c diabetes fears hypoglycemia, not DKA.
• Pancreatic cancer's resectability rate is 15–20%; R1 resection occurs in about 30%; postoperative FOLFIRINOX/gemcitabine is the standard of care.
• Traps: giving prophylactic antibiotics for pancreatitis (not routine) / rushing to ERCP whenever lipase rises (reserved for cholangitis or obstruction) / claiming type 3c DM is prone to ketoacidosis (backwards — it is in fact less prone).

• T2 = invades the muscularis propria; N2 = ≥4 nodes; T2N2M0 = Stage III.
• Stage II/III rectal cancer: preoperative CCRT for downstaging; cetuximab is effective only in RAS wild-type disease; CRC's most common recurrence = distant metastasis.
• Lynch = MMR, proximal adenomas, early age of diagnosis; Peutz-Jeghers = STK11, hamartomas; Turcot pairs with brain tumor, Gardner pairs with osteoma.
• Sessile (broad-based) polyps are more invasive than pedunculated (stalked) ones.
• Intestinal-type gastric cancer favors the antrum/body; diffuse type can arise anywhere in the stomach, with no specific site.
• H. pylori shows the weakest association with esophageal adenocarcinoma (even protective).
• Early HCC (BCLC 0/A) = surgical resection / RFA / liver transplantation; TACE is palliation for intermediate-stage disease.

• Morphine is contraindicated for biliary pain (constricts the sphincter of Oddi); choose meperidine or an NSAID (the exam answer; NSAIDs are now first-line and meperidine is largely avoided).
• Charcot's triad = pain, fever, jaundice (does not include gallbladder enlargement); add shock plus altered mental status = Reynolds' pentad → emergency ERCP.
• Acalculous cholecystitis favors ICU/TPN/trauma/burn patients; "cholecystitis must involve a stone" is wrong.
• UDCA dissolves only small, radiolucent, pure cholesterol stones, used in patients at high surgical risk.
• PSC = the strongest risk factor for cholangiocarcinoma.
• Imaging questions: Rokitansky-Aschoff sinuses + comet-tail artifact = adenomyomatosis; tubular hyperechoic structures + reverberation artifact = pneumobilia.
• Traps: giving morphine for biliary colic (contraindicated — constricts the sphincter of Oddi and raises biliary pressure) / including gallbladder enlargement in Charcot's triad (it is not included) / delaying ERCP to the next day in cholangitis (a fatal delay — it must be done urgently).

• Muscle lacks G-6-Pase, so it cannot release glucose into the blood; gluconeogenesis occurs mainly in the liver.
• Ethanol and even-chain fatty acids are not substrates for gluconeogenesis; glycerol, lactate, glucogenic amino acids, and propionyl-CoA are.
• F-2,6-BP = the master switch of glycolysis/gluconeogenesis: up → glycolysis, down → gluconeogenesis.
• Glycolysis's rate-limiting enzyme = PFK-1; gluconeogenesis's = F-1,6-BPase; the PPP's = G6PD.
• Anaerobic glycolysis → 2 ATP + lactate (in humans; only yeast proceeds to ethanol).
• The three ketone bodies: acetoacetate, β-OH-butyrate, acetone (α-KG is not one).
• Oxidation at C-1 = gluconic acid.

• Saliva: both sympathetic and parasympathetic are stimulatory (the opposite of the rest of the gut).
• Fat entering the duodenum = the strongest signal for inhibiting gastric emptying.
• About 90% of serotonin comes from gut EC cells; the vomiting center is in the medulla.
• Gastrin has the strongest trophic effect; CCK governs pancreatic enzymes/gallbladder; secretin inhibits gastric acid and promotes HCO₃⁻; GIP is an incretin.
• Fatty acids <12C travel by the portal vein; long-chain fatty acids travel by the lacteals/lymphatics.
• ENS = myenteric plexus + submucosal plexus + ICC; the nodose ganglion does not belong to the ENS.
• Intrinsic factor is secreted by parietal cells; B12 is absorbed in the terminal ileum.
• Somatostatin (D cell) = the universal inhibitor.

• The spleen = mesenchyme (dorsal mesogastrium), not foregut endoderm; the gallbladder is the true foregut derivative (hepatic diverticulum).
• Sertoli → MIS → Müllerian regression; Leydig → testosterone → Wolffian differentiation.
• Ureter / renal pelvis / collecting ducts / trigone = mesonephric duct; nephron = metanephric mesenchyme.
• The umbilical vein → the ligamentum teres hepatis.
• Prostate ↔ Skene's glands; Cowper's ↔ Bartholin's.
• The secondary spermatocyte = n, 2C (not 1C).

• Pancreatic head veins → SMV (not the splenic vein); SMV + splenic vein → portal vein; IMV → splenic vein.
• Above and below the pectinate line: above = portal / painless / internal iliac lymphatics (internal hemorrhoids); below = systemic / painful / inguinal lymphatics (external hemorrhoids).
• The lateral end of the inguinal ligament attaches to the ASIS; the conjoint tendon = internal oblique + transversus abdominis.
• An indirect hernia runs lateral to the inferior epigastric artery; a direct hernia runs medial to it (Hesselbach's triangle).
• The pelvic inlet includes the pecten pubis (where fractures favor); the ischial spine belongs to the outlet.
• The levator ani relaxes during defecation (it does not contract).
• The perineal membrane = the superior boundary of the superficial perineal pouch.
• The cisterna chyli = the intestinal trunk + the left/right lumbar trunks, draining via the thoracic duct into the left venous angle.

• Double-stranded DNA: A=T, G=C; A+G (purines) = T+C (pyrimidines) = 50%.
• Calculation formula: given T=31% → A=31%, the remaining 38% is split between G and C → C=G=19% (not 31%).
• B-DNA = right-handed, 10 bp/turn, base-pair rise of 3.4 Å (the predominant physiological conformation).
• A-DNA = right-handed, 11 bp/turn, 2.6 Å (dehydrated conditions, RNA-DNA hybrids).
• Z-DNA = left-handed, 12 bp/turn, 3.7 Å (alternating GC sequences, transcriptionally active regions).
• Traps: ① B-DNA listed as 3.6 Å (wrong — it is 3.4); ② B-DNA called left-handed (wrong — left-handed is Z); ③ T=31% leads you to write C as 31% too (wrong — it is 19%).

• The primer in DNA replication is RNA (synthesized by primase, not DNA).
• AZT mechanism = chain termination from the missing 3'-OH; target = HIV reverse transcriptase.
• Proofreading activity = Pol III's 3'→5' exonuclease (Taq lacks this activity → low fidelity).
• Primer removal = Pol I's 5'→3' exonuclease; sealing the nick = DNA ligase (not a polymerase).
• The lagging strand is made of Okazaki fragments; once the primer is excised, the gap is filled in and sealed.
• Traps: ① listing the AZT target as protease/RNase H/host polymerase (wrong — it is reverse transcriptase); ② listing nick-sealing as polymerase/helicase (wrong — it is ligase); ③ listing the proofreading direction as 5'→3' (wrong — it is 3'→5').

• BER: DNA glycosylase excises the abnormal base (deamination, oxidation, uracil) → AP endonuclease.
• NER: handles large distorting lesions such as UV pyrimidine dimers; deficiency = XP (xeroderma pigmentosum).
• MMR: post-replication mismatches; MutS recognizes, MutH nicks the unmethylated new strand; deficiency = Lynch syndrome / HNPCC.
• SOS: RecA activation → LexA autocleavage (the one being cleaved) → repair genes are derepressed.
• Traps: ① listing DNA glycosylase under MMR (wrong — it belongs to BER alone); ② assigning UV dimers to BER (wrong — they need NER); ③ naming UvrA or RecA as the one broken down in SOS (wrong — it is LexA).

• Three steps: 95 / 50–65 / 72°C (denaturation / annealing / extension).
• Main reason for using Taq = heat resistance (*E. coli* Pol is inactivated at 95°C); Taq's lack of proofreading is a side effect.
• One primer pair → one specific segment; multiple sites require multiplex PCR.
• Traps: ① listing the main reason as "Taq has high fidelity" (wrong — it is actually low); ② claiming one primer pair can amplify multiple regions (wrong — only one segment); ③ listing the polymerase used in PCR as *E. coli* Pol (wrong — it would be heat-inactivated).

• Genomic library = restriction enzyme + ligase (no reverse transcriptase needed; contains introns).
• cDNA library = reverse transcriptase + ligase (no introns; allows eukaryotic protein expression in prokaryotes).
• RFLP is used for paternity testing, linkage analysis, and DNA fingerprinting (not for building a cDNA library).
• Largest vector = YAC (contains an origin of replication, telomere, and centromere).
• Type II restriction enzymes recognize palindromic sequences; transformation = CaCl₂ + 42°C heat shock; site-directed mutagenesis needs no reverse transcriptase.
• The three blots: Southern = DNA, Northern = RNA, Western = protein (using antibodies).
• Traps: ① adding reverse transcriptase to a genomic library (wrong — not needed); ② using RFLP to build a cDNA library (wrong — unrelated); ③ describing transformation as "low-voltage electrophoresis" (wrong — it is heat shock or electroporation).

• lac = inducible: fully on only when no glucose (glucose low, cAMP↑, CAP-cAMP activation) and lactose is present (repressor released) → lacZYA is transcribed.
• lacZ = β-gal, lacY = permease, lacA = transacetylase, lacI = repressor.
• trp = repressible: Trp high → termination, Trp low → continuation; the mechanism is a switch in mRNA secondary structure (terminator vs. antiterminator), not the leader peptide acting directly on RNA pol.
• Traps: ① assuming lactose alone turns it fully on (wrong — glucose must also be low); ② assuming Trp high leads to continuation (wrong — it leads to termination); ③ swapping lacZ/lacY (wrong — Z is β-gal).

• The main reason housekeeping-gene expression levels differ = the promoter's affinity for RNA pol (not degradation rate).
• The direct binder of the enhancer = the activator (a transcription factor); the coactivator is a bridge, and TBP binds TATA.
• Traps: ① attributing enhancer binding to coactivator/TBP (wrong — it is the activator); ② attributing expression-level differences to degradation rate (wrong — it is promoter strength).

• DNA methylation: DNMT acts on CpG (not TATA / CAAT / telomere) → transcriptional repression.
• HAT acetylation → loosens → activation; HDAC deacetylation → condenses → repression.
• Mediates dimerization = leucine zipper; main DNA-binding motif = zinc finger; homeotic genes contain a homeodomain and, expressed late, determine "segment structure".
• Traps: ① listing the methylation hotspot as TATA/CAAT/telomere (wrong — it is CpG); ② listing zinc finger or β-barrel as mediating the dimer (wrong — it is the leucine zipper); ③ pairing homeotic genes with "specific organs" (wrong — it is "body segments").

• NAD⁺ structure: two nucleotides + a pyrophosphate bridge; the hydrogen-accepting site = nicotinamide C4, accepting a hydride; the reduced form is NADH.
• NADP⁺ vs. NAD⁺: the only difference is one extra phosphate on the 2'-position of the ribose at the adenine end.
• NADH is routed toward catabolism (energy production); NADPH is routed toward biosynthesis and antioxidant defense.
• Vitamin sources: NAD/NADP ← B3 niacin; FAD/FMN ← B2 riboflavin.
• Quick reference for other coenzymes: B1 = TPP (oxidative decarboxylation), B5 = CoA (acyl transfer), B6 = PLP (transamination/decarboxylation), B7 biotin = carboxylation (requires CO₂ + ATP), B9 = THF (one-carbon transfer), B12 = cobalamin (methyl transfer/isomerization).
• Traps: ① writing NADH₂ (wrong — it is NADH; FADH₂ is the one with two H's); ② listing NAD as coming from B2 (wrong — it is B3); ③ routing NADPH toward catabolic energy production (wrong — it goes toward biosynthesis and antioxidant defense).

• Histones carry a positive charge (rich in Lys/Arg) → they grip the negatively charged DNA electrostatically (not covalently or hydrophobically).
• Hierarchy: DNA → nucleosome (8 histones) → 30 nm fiber (with H1's help) → chromosome.
• The protein-coding fraction of the human genome = about 1.5–2% (not >40%).
• Traps: ① describing the histone-DNA interaction as covalent/hydrophobic (wrong — it is electrostatic); ② listing the coding fraction as 40% (wrong — it is 1.5–2%); ③ pairing the nucleosome with H1 (wrong — H1 assists in forming the 30 nm fiber).

• Homologous recombination = requires homology (meiosis, double-strand break repair).
• Site-specific recombination = requires no homology; V(D)J belongs here, RAG1/2 recognize the RSS.
• Transposition/viral integration = requires no homology; after retroviral integration, the LTR is duplicated at both ends (gag/pol/env occur only once).
• V–J occurs in DNA, J–C occurs via RNA splicing.
• Traps: ① listing V(D)J as homologous recombination (wrong — it is site-specific); ② claiming gag/pol/env are also duplicated after integration (wrong — only the LTR is); ③ claiming J–C is also DNA recombination (wrong — it is RNA splicing).

• Sickle cell disease: β-globin Glu→Val point mutation (qualitative); β/α-thalassemia: reduced/absent chain synthesis (quantitative).
• Telomere sequence = repeating TTAGGG; the single-stranded overhang forms a four-stranded G-quadruplex (not three- or five-stranded).
• Telomerase shows high activity in stem/germ/cancer cells.
• Terminally differentiated cells exit the cycle → G0 phase; the cycle = G1→S→G2→M.
• Traps: ① describing sickle cell as "too little chain made" (wrong — it is a wrong substitution); ② listing the G-quadruplex as three- or five-stranded (wrong — it is four-stranded); ③ saying differentiated cells arrest in G1 (wrong — it is G0).

• HGPRT deficiency = Lesch-Nyhan: salvage blocked, uric acid↑, intellectual disability, self-mutilation; de novo synthesis is intact and even accelerated.
• APRT deficiency = adenine is oxidized by XO into 2,8-DHA → kidney stones.
• Overactive PRPP synthetase = de novo synthesis↑ → uric acid↑ → gout.
• Xanthine has no salvage enzyme and can only be oxidized by XO into uric acid.
• Allopurinol/febuxostat inhibit XO; an acute flare is treated with NSAIDs/colchicine/steroids, never started with a urate-lowering drug.
• Traps: ① describing Lesch-Nyhan as "de novo broken" (wrong — salvage is broken, and de novo actually accelerates); ② claiming xanthine can also be salvaged (wrong — no enzyme exists for it); ③ giving allopurinol first in acute gout (wrong — it would provoke a flare).

• Orotic aciduria (part of the same family of metabolic defects as galactosemia) = UMP synthase deficiency; supplementing uridine bypasses the defect and provides feedback to suppress orotic acid; it does not improve with folate/B12.
• dUMP→dTMP is carried out by thymidylate synthase (methyl donor = 5,10-methylene-THF); 5-FU inhibits thymidylate synthase, methotrexate inhibits DHFR.
• The difference between thymine and uracil = one extra methyl group at the 5-position.
• 5-methylcytosine deaminates → thymine (mutational hotspot); cytosine→uracil; adenine→hypoxanthine; guanine→xanthine.
• End products: purines → uric acid; pyrimidines → β-alanine / β-aminoisobutyric acid.
• Traps: ① supplementing thymine or adenosine for orotic aciduria (wrong — it should be uridine); ② claiming 5-mC deaminates to uracil (wrong — it becomes thymine); ③ listing uric acid as a pyrimidine breakdown product (wrong — uric acid comes from purines).

• PDH = 3 enzymes, 5 coenzymes (TPP, lipoic acid, CoA, FAD, NAD⁺); biotin/CoQ are neither. B1 deficiency → Wernicke-Korsakoff syndrome, beriberi.
• One turn of the TCA cycle: 2 CO₂, 3 NADH, 1 FADH₂, 1 GTP; net OAA consumption = 0; rate-limiting enzyme = isocitrate DH.
• Substrate-level phosphorylation = occurs in both the cytosol and the mitochondrion; oxidative phosphorylation = only at the inner mitochondrial membrane.
• Electron pathway: I → CoQ → III → Cyt c → IV → O₂; the one that hands off directly to O₂ = Complex IV; FADH₂ enters at II.
• Pumping H⁺: matrix → intermembrane space (I, III, IV); ATP yield = NADH 2.5 / FADH₂ 1.5.
• Inhibitors (oxygen consumption↓): rotenone (I), antimycin A (III), CN⁻/CO/H₂S/azide (IV), oligomycin (V).
• Uncouplers (oxygen consumption↑, heat production↑, ATP↓): 2,4-DNP, aspirin overdose, UCP1.
• Clearing H₂O₂ = glutathione peroxidase; reductase uses NADPH to recharge GSH.
• Acetyl-CoA: a high-energy thioester bond.
• Traps: ① listing biotin or CoQ among the PDH coenzymes (wrong — neither is); ② claiming cyanide blocks Complex I (wrong — it is IV); ③ saying 2,4-DNP decreases oxygen consumption (wrong — it rises instead).

• Fed = insulin-dominant (storage); fasting = glucagon-dominant (mobilization, lipolysis, ketogenesis).
• Low-carbohydrate, high-protein → β-oxidation↑ → ketone bodies↑ → high-anion-gap metabolic acidosis (not alkalosis); urea↑; fat↓.
• β-OHB is the most abundant; the nitroprusside strip cannot detect β-OHB (urine ketones may be falsely negative).
• The liver makes but does not use ketone bodies (lacking SCOT/thiophorase); ketone bodies serve the brain, heart, and muscle.
• HIF-1↑ → PDK1↑ → PDH↓ → glycolysis, ROS↓ (decreased) (one of the Warburg mechanisms).
• N-glycosylation attaches to Asn (amide nitrogen), consensus Asn-X-Ser/Thr (X≠Pro), initiated by GlcNAc, in the ER; O-glycosylation attaches to Ser/Thr (hydroxyl), initiated by GalNAc, in the Golgi.
• Cysteine is not a standard glycosylation site.
• Traps: ① describing a low-carb, high-protein diet as causing alkalosis/decreased urea (wrong — it is acidosis/increased urea); ② ruling out DKA on a negative strip (wrong — β-OHB cannot be detected); ③ saying HIF-1 activation leaves ROS unchanged (wrong — it decreases).

• Oncogene: gain-of-function, dominant (one allele is enough for disease). Metaphor = gas pedal stuck to the floor.
• Tumor suppressor: loss-of-function, recessive, two-hit (RB is the prototype; LOH achieves the second hit).
• DNA repair gene: a mutator, usually also two-hit.
• Exception: TP53's dominant-negative effect lets Li-Fraumeni show a clear cancer increase with a single germline mutation; some suppressors also show haploinsufficiency.
• "The most commonly mutated tumor suppressor" = TP53, not RB.
• Traps: ① listing oncogenes as recessive (wrong — they are dominant); ② claiming RB is also dominant-negative (wrong — that is TP53); ③ listing RB as the most commonly mutated (wrong — it is TP53).

• Lynch (HNPCC) = MMR mutation (MLH1/MSH2/MSH6/PMS2) → MSI-high.
• Favors the right colon + endometrial cancer; often <50 years old; does not arise through a large number of polyps.
• FAP = APC (a suppressor), covered with polyps.
• Screening uses the Amsterdam/Bethesda criteria; diagnosis relies on MSI testing + genetics.
• MSI-high / dMMR → respond well to anti-PD-1 (pembrolizumab) (a frequent, newer test point).
• Traps: ① listing Lynch as APC (wrong — it is MMR); ② describing Lynch as a field of polyps (wrong — that is FAP); ③ saying Lynch favors the left colon (wrong — it is the right).

• KRAS mutation → anti-EGFR ineffective (a frequent, high-stakes question).
• BRCA1/2 → PARP inhibitor (synthetic lethality).
• Burkitt = MYC t(8;14); CML = BCR-ABL t(9;22).
• "The most commonly mutated tumor suppressor" = TP53.
• Traps: ① giving cetuximab despite a KRAS mutation (wrong — it is ineffective); ② listing Burkitt as t(9;22) (wrong — it is t(8;14)); ③ pairing BRCA with an EGFR inhibitor (wrong — it pairs with a PARP inhibitor).

• B1 (TPP) → PDH, α-KGDH; deficiency = beriberi, Wernicke-Korsakoff syndrome. In patients with alcohol use disorder, give thiamine before glucose.
• B3 (NAD/NADP): the 3 D's of pellagra; Hartnup disease / carcinoid / INH can all cause pellagra-like presentations.
• B5 (CoA) comes from pantothenic acid, not folate (a frequent trap).
• B6 (PLP): transamination, decarboxylation; coenzyme for ALA synthase → sideroblastic anemia; INH causes deficiency.
• B7 (biotin): carboxylation; avidin in raw egg white binds biotin and causes deficiency.
• Vitamin C: hydroxylates collagen (scurvy), reduces iron; it is not merely an antioxidant.
• Traps: ① listing CoA as coming from folate (wrong — it is pantothenic acid, B5); ② claiming INH causes B12 deficiency (wrong — it is B6); ③ giving glucose before thiamine in alcohol use disorder (wrong — the order is reversed).

• B12 deficiency = MMA↑ + Hcy↑ + neurological deficit; folate deficiency = only Hcy↑, no neurological symptoms.
• Folate alone must not be used: it corrects the anemia while worsening the neuropathy.
• Pernicious anemia = autoimmune destruction of gastric parietal cells → IF deficiency → poor B12 absorption.
• The structural metal of B12 = cobalt (Co); active forms = methyl-/adenosylcobalamin.
• CoA comes from pantothenic acid (B5), not folate (a frequent, high-stakes question).
• The zinc finger = Cys+His coordinating zinc; do not confuse it with the leucine zipper.
• Traps: ① treating B12 deficiency with folate alone (wrong — it worsens the neuropathy); ② listing the B12 metal as iron or magnesium (wrong — it is cobalt); ③ claiming folate deficiency also raises MMA (wrong — only B12 deficiency does).

• Transamination → deamination → ammonia disposal; blood ammonia transport = glutamine (whole body/brain) + alanine (muscle, Cahill cycle).
• The urea cycle's two nitrogen sources: free NH₄⁺ (via CPS-I) + aspartate.
• Final products = urea + fumarate; fumarate enters the TCA cycle.
• CPS-I is the rate-limiting enzyme, requiring activation by NAG; the first 2 steps occur in the mitochondrion, the last 3 in the cytosol.
• OTC deficiency (X-linked, most common) → hyperammonemia + orotic aciduria.
• Traps: ① calling the final products urea + OAA (wrong — it is fumarate); ② claiming both nitrogens come from NH₄⁺ (wrong — the second is aspartate); ③ claiming all six steps occur in the cytosol (wrong — the first two occur in the mitochondrion).

• PKU: PAH or BH4 deficiency; Tyr becomes essential; avoid aspartame; the BH4 variant also disrupts neurotransmitters.
• Homocystinuria: CBS (requires B6) deficiency; downward lens dislocation (Marfan: upward); some patients respond to high-dose B6.
• MSUD: deficiency of branched-chain α-ketoacid dehydrogenase (requires B1).
• Albinism = tyrosinase; alkaptonuria = homogentisate oxidase; PKU = PAH — do not confuse the three.
• GSH = γ-Glu–Cys–Gly (γ bond); creatine = Gly + Arg + Met (SAM supplies the methyl group).
• OI (osteogenesis imperfecta) = type I collagen mutation, usually a glycine substitution.
• Traps: ① calling the PKU deficiency tyrosinase (wrong — that is albinism); ② homocystinuria dislocating the lens upward (wrong — it is downward; Marfan is upward); ③ GSH as α-Glu-Cys-Gly (wrong — it is a γ bond).

• Rate-limiting step of fatty acid synthesis = ACC (→ malonyl-CoA, requires biotin); rate-limiting step of cholesterol synthesis = HMG-CoA reductase.
• Synthesis in the cytosol, oxidation in the mitochondrion; malonyl-CoA also inhibits CPT-I (the gate to β-oxidation).
• Odd-chain fatty acid → propionyl-CoA → (B12) → succinyl-CoA; B12 deficiency → MMA↑.
• COX substrate = arachidonate (C20:4), not a saturated fatty acid; aspirin does not affect cholesterol synthesis.
• Cardiolipin is in the inner mitochondrial membrane; integral membrane proteins require detergent extraction; PAF = alkyl-ether, plasmalogen = vinyl-ether.
• Lipoproteins: HDL performs reverse transport (esterification by LCAT); LDL travels via the LDL receptor (defective in FH).
• Traps: ① aspirin lowering cholesterol (wrong — it acts on COX); ② naming palmitate as the COX substrate (wrong — it is arachidonate); ③ placing cardiolipin in the plasma membrane (wrong — it is in the inner mitochondrial membrane).

• Lipid-soluble → receptor inside, slow and long-lasting; water-soluble → receptor on the membrane, fast and brief. Hsp90 binds the ligand-binding domain, not the DNA-binding domain.
• Gs/Gi/Gq downstream: cAMP↑ / cAMP↓ / IP3 + DAG.
• Cholera = locks Gsα on (inhibits GTPase); pertussis = locks Giα off (cannot bind GTP); both raise cAMP↑.
• Insulin MAPK sequence: IRS-1 → Grb2-Sos → Ras → Raf → MEK → ERK.
• ANP = membrane-bound GC → cGMP; JAK-STAT = IL, GH, EPO, leptin, IFN.
• The β receptor does not directly activate Ras (Ras belongs to the RTK pathway).
• Cyclin is the regulatory subunit and does not catalyze directly; CDK is the catalyst.
• Traps: ① Hsp90 binding the DNA-binding domain (wrong — it is the ligand-binding domain); ② cholera and pertussis modifying the same G protein (wrong — Gs vs. Gi); ③ MEK downstream of ERK (wrong — it is upstream).

• Pol I → large rRNA / Pol II → pre-mRNA / Pol III → tRNA + 5S rRNA; α-amanitin: Pol II most sensitive, Pol I insensitive.
• Prokaryotes have only one RNA polymerase; mammals have no Pol IV (a trap).
• The three major mRNA modifications occur entirely in the nucleus, co-transcriptionally; 3′ processing = polyadenylation, not phosphorylation; signal = AAUAAA.
• Group I = exogenous G 3′-OH; group II and the spliceosome = internal A 2′-OH (lariat).
• The 3′ end of every tRNA = -CCA-OH.
• Traps: ① Pol I being most sensitive to amanitin (wrong — it is Pol II); ② calling 3′ processing phosphorylation (wrong — it is poly(A)); ③ group I using an internal A (wrong — it uses an exogenous G).

• Initiator tRNA: prokaryotes fMet, eukaryotes Met; the small subunit binds mRNA first, the large subunit last.
• The SD sequence pairs with the 3′ end of 16S rRNA (prokaryotes); eukaryotes use cap → scanning.
• Peptide bond catalysis = 23S rRNA (a ribozyme); polypeptide N→C, mRNA 5′→3′.
• Ampicillin hits the cell wall, not the ribosome (a trap); 30S = aminoglycoside/tetracycline; 50S = chloramphenicol/macrolide.
• Iron deficiency → HRI → eIF2α phosphorylation → global translation shutdown.
• Calculation: (bp/3) − 1 = aa; aa × 110 ≈ Da.
• Gly-Pro → β-turn; the disulfide bond belongs to tertiary structure, the α-helix relies on hydrogen bonds.
• Codon-anticodon = hydrogen bonds, not covalent.
• Traps: ① ampicillin hitting the ribosome (wrong — it hits the cell wall); ② eukaryotic initiation using fMet (wrong — it is Met); ③ the peptide bond being catalyzed by a protein enzyme (wrong — it is 23S rRNA).

• When [S] ≪ Km, the rate constant = kcat/Km (second-order rate constant; Vmax/Km = kcat/Km × [E]t), not kcat.
• LB plots for the three inhibition types: competitive shares the y-intercept / noncompetitive shares the x-intercept / uncompetitive runs parallel; competitive: Km↑, Vmax unchanged; uncompetitive: Km↓, Vmax↓.
• A280 = Trp > Tyr > Phe; non-aromatic residues do not absorb; A280 is for quantification only, not identification.
• The disulfide bond belongs to tertiary structure, the only covalent bond; the α-helix relies purely on backbone hydrogen bonds (i↔i+4).
• SDS-PAGE measures molecular weight and destroys activity; IEF measures pI; in gel filtration, large molecules elute first — it cannot identify a protein's identity.
• Irreversible inhibition (aspirin acetylating COX, organophosphates inhibiting AChE) causes covalent inactivation, which kinetically resembles a drop in [E].
• Traps: ① answering kcat when [S] ≪ Km (wrong — it is kcat/Km); ② Asn also absorbing at 280 (wrong — it has no aromatic ring); ③ using IEF to measure molecular weight (wrong — IEF measures pI).

• First trimester = low PAPP-A + high free β-hCG + thick NT.
• Second-trimester quad test = low AFP, low uE3, high hCG, high inhibin A (two low, two high).
• uE3, AFP, and inhibin A are not first-trimester markers — a common trap.
• Edwards syndrome (18) = triple-low; open NTD = AFP elevated in isolation.
• NIPT is a screening test; diagnosis rests on amniocentesis or CVS.

• NST reactive = ≥ 2 accelerations within 20 minutes, each ≥ 15 bpm and lasting ≥ 15 seconds (at ≥ 32 weeks).
• Late/early decelerations belong to the CST, not the NST.
• BPP: each item scores only 0 or 2; breathing ≥ 30 seconds within 30 minutes = 2 points; total score ≤ 4 requires intervention.
• The worst umbilical artery Doppler finding = REDV (reversed), not AEDV.
• TTTS: the donor is small, oligohydramniotic, and anemic; the recipient is large, polyhydramniotic, and polycythemic.
• Folic acid started 4 weeks before conception cuts NTD risk by ~70%; open NTD = AFP elevated in isolation.
• The Kleihauer-Betke test estimates fetomaternal hemorrhage volume, which sets the anti-D dose.
• GBS gets penicillin intrapartum — not early treatment the moment the screen turns positive.

• Core mechanism = impaired trophoblast invasion → placental ischemia → sFlt-1 ↑, PlGF ↓ → endothelial dysfunction.
• The classic triad = hypertension + proteinuria + edema (current: edema is not a diagnostic criterion); elevated blood glucose does not count (that is GDM).
• Severe = blood pressure ≥ 160/110, PLT < 100,000, liver/kidney/lung/neurologic damage; the amount of proteinuria is not a severity marker.
• MgSO4 = seizure prevention (not an antihypertensive); toxicity begins with loss of deep tendon reflexes, antidote calcium gluconate.
• Acute blood pressure control = hydralazine / labetalol / nifedipine; postpartum hemostasis = oxytocin.
• Methergine is contraindicated in preeclampsia (vasoconstriction).
• Management of severe preeclampsia = immediate admission + evaluation for delivery; outpatient follow-up alone is not acceptable.
• The complication most increased in obese pregnant women = GDM (3–7 fold, higher than preeclampsia's 2–4 fold).
• Risk factors for pulmonary edema = preeclampsia / sepsis / tocolytics; GDM is not one of them.
• First-choice medication for GDM in pregnancy = insulin; diet control must not be forgotten.
• Treating 100 mg of proteinuria as severe (it does not even reach the 300 mg diagnostic threshold).
• Mistaking MgSO4 for an antihypertensive.
• Using methergine for postpartum hemostasis in preeclampsia (blood pressure spikes).
• Choosing preeclampsia as the top complication in an obese pregnant woman (it should be GDM).

Traps:

• Late period + lower abdominal pain + bleeding → test for pregnancy first to rule out a ruptured ectopic.
• Incomplete abortion = open cervical os + retained tissue → D&C.
• MTX and salpingostomy carry a similar risk of repeat ectopic pregnancy (MTX is not higher).
• Painless, bright-red bleeding = previa (ultrasound, no digital exam); pain plus a rigid uterus = abruption (guard against DIC).
• Shoulder dystocia: McRoberts plus suprapubic pressure is first-line; fundal pressure is forbidden.
• The most common cause of PPH = uterine atony (the Tone in the 4 T's); its most common cause = overdistension (twin pregnancy); first-line oxytocin.
• Ergot is contraindicated in preeclampsia; PGF2α (carboprost) is contraindicated in asthma.
• The earliest sign of hemorrhage = tachycardia (not hypotension).
• Active management of the third stage = oxytocin + controlled cord traction + massage (WHO 2012: massage replaced by uterine tone assessment); does not include manual extraction of the placenta.
• Chorioamnionitis → antibiotics + prompt delivery; tocolytics are forbidden.

Traps: using fundal pressure for shoulder dystocia, using ergot for PPH in preeclampsia, using carboprost in asthma, treating hypotension as the earliest sign of hemorrhage, blaming atony on previa/abruption, and giving tocolytics after infection is confirmed.

• Nullipara = para 0; a miscarriage (< 20 weeks) does not count toward para; a twin delivery is +1 para but Living +2.
• Fundal height reaches the umbilicus at 20 weeks; after 20 weeks, fundal height (cm) ≈ gestational age in weeks.
• Amniotic fluid pH 7.0–7.5 (alkaline): Nitrazine turns blue plus ferning; vaginal secretions pH 4.5–5.5 (acidic); blood, semen, and BV can cause false positives.
• First-stage active phase with ≥ 4–6 hours of no progress = arrest; third stage > 30 minutes = retained placenta.
• Station 0 = engaged; operative delivery requires station ≥ +2.
• Perineal laceration third degree = includes the anal sphincter (memorize the cumulative order).
• Prolactin makes the milk, oxytocin ejects it (the most frequently reversed trap).
• The contraindication to VBAC is a classical vertical incision; epidural analgesia is not a contraindication.
• Protection of vulnerable research populations = limited capacity for autonomous consent, not small numbers.

Traps: counting para as the number of pregnancies, using fundal pressure for shoulder dystocia (see Chapter 3), swapping prolactin and oxytocin, and mistakenly believing VBAC forbids epidural analgesia.

• Apgar assesses the response to resuscitation and is never used to decide whether to start resuscitation; a heart rate of 75 = 1 point, cyanosis all over = 0 points.
• NRP: heart rate < 100 with no breathing → PPV for 30 seconds first; only if still < 60 add compressions (3:1); if still < 60, give adrenaline. Starting compressions without first giving PPV is wrong.
• The core of neonatal resuscitation = ventilation (the reverse of the adult approach).
• Physiologic weight loss ≤ 10%; recovers by day 7–10; anything more is abnormal.
• Acrocyanosis is normal; central cyanosis requires cardiopulmonary evaluation.
• IDM = hypoglycemia within 24 hours, hypocalcemia, hypomagnesemia, polycythemia, macrosomia; not hyperglycemia.
• Nuchal rigidity is the least reliable sign of neonatal meningitis; a bulging fontanelle is the reliable one; GBS = a gram-positive coccus, ascending from the birth canal.
• Breast milk jaundice = unconjugated → phototherapy only above the threshold; MRCP is not needed.

Traps: judging a newborn by adult-style nuchal rigidity, treating an 11% weight loss as normal, jumping straight to chest compressions at heart rate < 100, writing hypercalcemia for IDM, and ordering an MRCP for breast milk jaundice.

• Epididymis = pseudostratified columnar + stereocilia (immotile); fallopian tube = simple columnar + true cilia (motile).
• Ectocervix = non-keratinized stratified squamous epithelium; the SCJ = the favored site of cervical cancer.
• Spermiogenesis = the remodeling of a spermatid into a sperm, with no division; spermatogenesis is the one that includes meiosis.
• The zona pellucida = first appears at the primary follicle (absent in the primordial follicle).
• Semen: seminal vesicle fructose 60%, prostate PSA 30%; the corpus cavernosum contributes nothing.
• The skin of the penile shaft has no subcutaneous fat.
• Seminiferous tubule: Leydig cells secrete testosterone (outside the tubule); myoid cells secrete nothing; Sertoli cells form the blood-testis barrier.
• The myometrium's middle layer is thickest; during pregnancy it undergoes hypertrophy plus hyperplasia.

Traps: writing "true cilia" for the epididymis, saying the primordial follicle already has a zona pellucida, listing the corpus cavernosum as a source of semen, answering that myoid cells secrete testosterone, and writing that the outer layer of the myometrium is thickest.

• hCG comes from the syncytiotrophoblast (not the corpus luteum, not the decidua, not the pituitary).
• The action of hCG = rescuing the corpus luteum → progesterone sustains the pregnancy (not a direct effect of hCG itself).
• The outermost layer of the villi is always syncytiotrophoblast.
• Capillaries appear only at the tertiary villus stage; secondary villi go only as far as connective tissue.
• The placental barrier thins as pregnancy advances (as the cytotrophoblast regresses).
• The decidua arises from the maternal endometrium.

Traps: saying the corpus luteum secretes hCG, saying secondary villi already have blood vessels, writing the outermost layer as cytotrophoblast, or counting the decidua as fetal tissue.

• The three evaluation axes: male semen, HSG, ovulation; check the man's semen first, image the tubes with HSG, assess ovulation with luteal-phase progesterone.
• Most uterine fibroids are not the primary cause of infertility; only submucosal fibroids directly impair implantation.
• The LH surge threshold = E2 ≥ 200 pg/mL sustained for > 50 hours; not a progesterone value.
• Clomiphene is ineffective in hypothalamic-pituitary failure; the next step after clomiphene resistance = metformin / letrozole / gonadotropin, not a dopamine agonist.
• Letrozole = first-line ovulation induction in PCOS (higher live-birth rate than clomiphene).
• PCOS = insulin resistance → SHBG↓ → free androgen↑, anovulation, unopposed endometrial thickening.
• The first step for azoospermia = repeat the semen analysis, not immediate treatment.
• ART: only IUI skips egg retrieval.
• Meiosis II is completed after fertilization, not at ovulation.
• COC contraindications: smoking > 35 years old, VTE, migraine with aura.

Traps: choosing a dopamine agonist for clomiphene resistance, assuming any fibroid is the cause of infertility, placing completion of meiosis II at ovulation, or mistakenly remembering the LH surge threshold as a progesterone value.

• Body pairings: Schiller-Duval = yolk sac tumor (AFP); Call-Exner = granulosa cell tumor; abundant psammoma bodies = serous tumor, well differentiated; dysgerminoma = large cells, pale cytoplasm, prominent nucleoli.
• Endometrioid ovarian carcinoma often coexists with endometrial cancer; clear cell carcinoma is linked to endometriosis and is uniformly grade 3.
• Cervical cancer FIGO staging: invasion of the lower 1/3 of the vagina = IIIa; parametrial involvement = IIb; ureteral obstruction / hydronephrosis = IIIb; lymph node metastasis = IIIc (c1 pelvic, c2 para-aortic, added in 2018).
• CIN2 / CIN3 → conization / LEEP; CIN1 → observation; the HPV vaccine has no therapeutic effect.
• Postmenopausal bleeding → history + pelvic exam + TVS → endometrial sampling; do not go straight to hysterectomy or estrogen.
• Choriocarcinoma most often metastasizes to the lung; brain metastasis is assessed by CSF/serum hCG ≥ 1:60; high-risk disease uses EMA-CO.
• Avoid monopolar electrocautery when transecting the IP ligament (risk of ureteral injury).

Traps: ruling out IIIa because "there is no parametrial invasion" (lower 1/3 vaginal involvement already upstages it), simply observing CIN2, giving estrogen to work up postmenopausal bleeding, or reading a 1:100 ratio as evidence of brain metastasis.

• Dysgerminoma typically occurs at ages 10–30, marker LDH, radiosensitive; ovarian malignancy under age 10 is mostly the yolk sac tumor (AFP + Schiller-Duval bodies).
• Complete mole: 46,XX, sky-high hCG, 15–20% malignant transformation; partial mole: triploid, 1–5% malignant transformation.
• Ectopic pregnancy: 95% occur in the fallopian tube (ampulla most common).
• Mammary Paget disease ≈ almost always an underlying breast cancer; extramammary Paget disease usually has no underlying invasive cancer.
• BPH = transition zone + combined epithelial and stromal hyperplasia (prostate cancer arises in the peripheral zone).
• Cryptorchidism most often arrests in the inguinal canal, raising the risk of seminoma.
• Site of onset in orchitis: tuberculosis / gonorrhea / E. coli start in the epididymis; syphilis / mumps start in the testis.
• The adult granulosa cell tumor = low-grade malignant, can recur late, secretes estrogen, Call-Exner bodies.

Traps: answering "dysgerminoma" for a child (it should be yolk sac tumor), calling the adult granulosa cell tumor benign, assuming extramammary Paget disease carries invasive cancer the way mammary Paget disease does, saying tuberculosis strikes the testis first, or describing BPH as simple epithelial hyperplasia.

• The three mechanisms of high intra-abdominal pressure in laparoscopy = CO2 absorption (hypercarbia) + compression of the inferior vena cava (hypotension) + CO2 embolism.
• Least related to the pneumoperitoneum = hyperglycemia (a spot-the-exception test point).
• Abortion in a minor = written consent from a legal guardian.
• A forged consent form = void from the outset; lawful consent must be obtained to cure it; good intentions cannot bypass the procedure.

• Facilitated diffusion = down the gradient, requires a membrane protein, consumes no ATP, saturable; simple diffusion has no ceiling.
• Primary hydrolyzes ATP directly; secondary borrows the Na⁺ gradient; the wellspring of it all is the Na⁺-K⁺ ATPase (3 Na⁺ out, 2 K⁺ in, electrogenic; inhibited by ouabain/digoxin).
• H⁺-K⁺ ATPase (parietal cell) = the body's largest ionic concentration gradient (on the order of a million-fold).
• For secondary active transport, whether "this ion moves down or against" depends on locking onto the ion the question asks about (SGLT: Na⁺ down, glucose against).
• Resting Vm lies closest to E_K (≈ −90 mV); opening Na⁺ channels moves it toward +60, opening K⁺ channels toward −90.
• Hypertonic > 300, isotonic = 0.9% NaCl; 5% dextrose ends up hypotonic (trap).
• Traps: picking Na⁺-K⁺ for the largest ionic gradient; labeling secondary active transport as consuming ATP directly; assuming cells swell in a hypertonic solution; treating 5% dextrose as isotonic over the long run.

• Hypothalamic set point: anterior for heat loss, posterior for heat production; damage drives each in the opposite direction.
• Fever (PGE₂ raises the set point): antipyretics are effective; heat stroke (set point normal, heat dissipation fails): use physical cooling, antipyretics are ineffective.
• The first few seconds of exercise = creatine phosphate; 10 seconds to 2 minutes = anaerobic glycolysis (lactate produced); > 2 minutes = aerobic.
• Pernicious anemia = intrinsic factor deficiency → B12 malabsorption → megaloblastic anemia + subacute combined degeneration; replace B12, never folate alone (it masks the neuropathy); folate deficiency causes no neurological symptoms.
• Traps: antipyretics mistakenly given for heat stroke; aerobic metabolism chosen for the first few seconds; folate alone masking the neuropathy.

• Adrenal medulla = a specialized postganglionic neuron, so it is innervated by preganglionic sympathetic fibers + ACh, not postganglionic + NE. Trap: choosing "postganglionic + NE" pastes ordinary sympathetic wiring onto the medulla.
• Cortisol: suppresses white cells (eosinophils/lymphocytes↓), stimulates RBCs, suppresses bone, and produces a pseudo-rise in neutrophils (demargination); its permissive effect enables α-mediated vasoconstriction — Addison crisis → hypotension. Trap: extending "suppresses white cells" to RBCs, writing "increases bone mass," or forgetting that the neutrophil rise is pseudo.
• The β cell uses GLUT2 (high Km, non-saturable); the signaling chain is ATP↑ → K_ATP closes → depolarization → Ca²⁺ influx → insulin exocytosis. Sulfonylureas close K_ATP directly. Trap: writing GLUT4 or a GPCR.
• Insulin within seconds: GLUT4 translocation, K⁺/amino acids entering the cell, Na⁺/K⁺-ATPase activation (= the hyperkalemia rescue mechanism); protein synthesis takes hours, not an acute effect. Trap: treating "protein synthesis" as a seconds-scale acute effect.
• Steroids/thyroid hormone = lipid-soluble, intracellular receptors; peptides/catecholamines = water-soluble, membrane receptors; insulin = RTK (not cAMP). Trap: labeling cortisol as a membrane receptor, or insulin as cAMP.
• The antrum's appearance = secondary follicle; the cumulus oophorus appears only at the Graafian stage; an unrescued corpus luteum lasts ≈14 days. Trap: slotting the cumulus oophorus into the primary follicle.

• O₂ content = (1.34 × Hb × SaO₂) + dissolved O₂; anemia: PaO₂/SaO₂ normal, only Hb↓; CO poisoning: PaO₂ normal, SaO₂↓, oximeter falsely normal. Trap: misjudging anemia as PaO₂↓, or trusting a normal SpO₂ in CO poisoning.
• A–a gradient: normal → hypoventilation or high altitude (correctable with pure O₂); elevated and uncorrectable with pure O₂ = shunt. Trap: misclassifying oxygen-refractory hypoxia as V/Q mismatch.
• CO is always diffusion-limited, N₂O is always perfusion-limited; CO₂ travels in three forms: HCO₃⁻≈70% > carbamino-Hb≈23% > dissolved 7%; the chloride shift runs both ways (AE1 is an exchanger, not a cotransporter). Trap: reversing the direction of HCO₃⁻ at the tissue end, or mistaking AE1 for a cotransporter.
• During forced expiration, intrapleural pressure can turn positive → dynamic compression downstream of the equal pressure point; RQ: carbohydrate 1.0 > protein 0.8 > fat 0.7. Trap: writing "intrapleural pressure is always negative."
• Surfactant = secreted by type II cells, built from DPPC; the cough reflex's most sensitive point = the carina. Trap: choosing type I cells or the larynx.
• Poiseuille: Q ∝ r⁴; doubling the radius multiplies flow ×16 and drops resistance to 1/16 (tuning the radius is the most efficient lever). Trap: calculating it as ×2 or ×4.
• Compensation in valve disease: AR = volume expansion, Frank-Starling, eccentric hypertrophy; AS = concentric hypertrophy; AR never takes the ANP↑/natriuresis↑ route (that runs the opposite direction). Trap: choosing ANP↑ as AR's compensation.
• Papillary muscle/chordae = prevent the valve from prolapsing into the atrium, not open it.
• Baroreflex relay station = the NTS in the medulla (not the thalamus); baroreceptor firing↑ = blood pressure is high → the reflex response lowers it. Trap: choosing the thalamus, or equating firing↑ with raising pressure.
• Coronary arteries fill during diastole; tachycardia shortens diastole → ischemia; a β-blocker both lowers oxygen demand and lengthens perfusion time.
• The main driver of endurance training's oxygen-carrying gain = EPO↑ → RBC↑ (not vital capacity, not 2,3-DPG); vWF = endothelium + megakaryocytes (not smooth muscle). Trap: attributing vWF production to smooth muscle.

• Referred pain converges in the spinal cord (not the medulla/thalamus); gallbladder/diaphragm → right shoulder (C3–C5, phrenic nerve) — do not write left shoulder. Trap: placing the convergence point in the medulla, or writing gallbladder-referred pain as left shoulder.
• Skeletal muscle = DHPR (senses voltage) → RyR1 (releases calcium) → troponin-C, independent of extracellular calcium; smooth muscle = Ca-calmodulin → MLCK phosphorylates MLC, relaxation via MLCP, no troponin; the latch state lets smooth muscle sustain tension at extremely low energy cost. Trap: writing that DHPR releases calcium directly, or that skeletal muscle needs extracellular calcium.
• The NMJ end-plate = nicotinic (not muscarinic).
• Planning a voluntary movement = basal ganglia + cerebellum + cortex (never the cortex alone); a cerebellar lesion produces ipsilateral ataxia (two crossings = no crossing). Trap: choosing "the cortex alone."
• Taste = CN VII / IX / X; CN V carries the tongue's general sensation (touch, temperature, pain), not taste. Trap: mistaking the trigeminal nerve for a taste nerve.
• The auditory receptor = the organ of Corti in the inner ear (not the middle ear).
• Nasal fibers cross, temporal fibers do not; central compression of the optic chiasm → bitemporal hemianopia (pituitary macroadenoma, craniopharyngioma). Trap: writing "all fibers cross," or choosing homonymous hemianopia.

• Four kinds of membrane transport: simple diffusion, facilitated diffusion (with the gradient, needs a carrier, no ATP), primary active (against the gradient, direct ATP), secondary active (borrows the sodium gradient). Trap: describing SGLT as "active transport that spends ATP directly."
• Na⁺-K⁺ ATPase = electrogenic, 3 out, 2 in; the body's largest gradient = H⁺-K⁺ ATPase (gastric acid, ~10⁶-fold). Trap: choosing the Na⁺-K⁺ ATPase as the largest gradient, or reversing the 3:2 ratio.
• The parietal cell's three acid-secretion pathways: ACh + gastrin + histamine; an H₂ blocker blocks one pathway, a PPI blocks the final shared exit (the strongest option).
• Opening a given channel → the membrane potential drifts toward that ion's equilibrium potential; a hypertonic solution → red cells crenate (not swell). Trap: misjudging a hypertonic solution as causing swelling, or treating opening a Cl⁻ channel and opening a K⁺ channel as pulling in the same direction.
• IP₃R releases calcium, SERCA recaptures it (opposite directions). Trap: describing SERCA as releasing calcium.
• Saliva = both sympathetic and parasympathetic input stimulate secretion (parasympathetic gives copious and thin, sympathetic gives scant and thick); saliva is hypotonic. Trap: writing "the sympathetic system inhibits salivation."
• The strongest brake on gastric emptying = fat entering the duodenum (via CCK); gastric distension promotes emptying instead. Trap: choosing gastric distension as the brake.
• The four major gastrointestinal hormones: gastrin = acid + growth, CCK = bile + enzymes, secretin = neutralization, GIP = boosts insulin; GIP + GLP-1 = the two major incretins. Trap: swapping the functions of CCK and gastrin.
• The nodose ganglion ≠ the ENS (it is a vagal sensory ganglion); 90% of 5-HT comes from gut EC cells; the vomiting center sits in the medulla. Trap: filing the nodose ganglion under the ENS, or writing that 5-HT is mainly secreted by the brain.
• Long chains travel by lymph (as chylomicrons), short chains travel by portal vein; bile salts are reabsorbed at the terminal ileum. Trap: describing short chains as traveling by lymph.

• GFR = P_GC − (P_BS + π_GC); urinary obstruction → P_BS↑ → GFR↓; Ang II constricts the efferent arteriole to prop up GFR → an ACEI/ARB causes GFR to collapse in renal artery stenosis. Trap: reversing the efferent and afferent chains.
• Autoregulation: the myogenic reflex + tubuloglomerular feedback (macula densa → adenosine); stable across MAP 80–180. Trap: remembering only nerves/hormones and forgetting the macula densa.
• Glucose reabsorption occurs only in the PCT; NKCC2 is in the TAL (where loop diuretics act), NCC is in the DCT (where thiazides act); loop diuretics waste calcium, thiazides spare calcium. Trap: reversing the calcium direction of loop diuretics and thiazides.
• A low-protein diet → urea↓ → a weaker medullary gradient → concentrating capacity↓ (never enhanced). Trap: writing that a low-protein diet enhances concentration.
• AQP2 is translocated via ADH/V2/cAMP/PKA; AQP1 in the PCT/descending limb stays permanently open; every AQP = passive. Trap: writing that AQP1 is regulated by ADH, or treating an AQP as active transport.
• Aldosterone escape = only the sodium-retaining half escapes; K⁺/H⁺ excretion never escapes (so primary hyperaldosteronism keeps its persistent low K⁺ and metabolic alkalosis). Trap: assuming the escape includes potassium excretion.
• Renal compensation in DKA = reabsorbing almost all filtered HCO₃⁻ (none extra appears in urine) + Kussmaul breathing. Trap: writing that HCO₃⁻ is excreted into the urine in large amounts.
• The temperature center = the hypothalamus (anterior for heat loss, posterior for heat production); fever = the set point shifts up, heatstroke = regulation itself fails; NSAIDs/acetaminophen break a fever by inhibiting PGE₂. Trap: choosing the premotor cortex, or using antipyretics for heatstroke.
• The fueling sequence: stored ATP (seconds) → CP via creatine kinase (roughly 10–15 seconds) → anaerobic glycolysis (minutes) → aerobic metabolism (>2 minutes). Trap: attributing the first few seconds to glycolysis.
• Pernicious anemia = autoimmune process → intrinsic factor↓ → B₁₂↓; presentation: megaloblastic anemia + subacute combined degeneration (SCD) + atrophic gastritis; MMA↑ identifies B₁₂ deficiency; treatment = B₁₂ injection; folate only masks it. Trap: giving folate and assuming the correction is complete.

• BCC = most common, almost never metastasizes to viscera, best prognosis; high risk (morpheaform, perineural invasion, H-zone, recurrent) → Mohs surgery.
• AK progresses to SCC (not melanoma); SCC spreads via regional lymphatics.
• Melanoma prognosis is determined first by Breslow thickness; BRAF V600E-positive tumors can be treated with BRAF+MEK inhibitors; the most common subtype in Taiwan = acral lentiginous (lower BRAF mutation rate).
• Hutchinson's sign = subungual pigment extending onto the proximal nail fold, a red flag for subungual melanoma.
• Port-wine stain = benign vascular malformation, not a tumor; Sturge-Weber is associated with leptomeningeal angioma, glaucoma, and seizures.
• Keratoacanthoma = rapid growth over weeks on the face, crater-shaped; histology resembles SCC but behavior leans benign.
• NF-1 café-au-lait spots: > 5 mm in children, > 15 mm in adults (not 30 mm).
• Traps: describing BCC as "readily metastatic," describing melanoma as "good prognosis," saying AK turns into melanoma, listing port-wine stain among malignant tumors, rewriting the NF-1 threshold as 30 mm, and assuming acral melanoma always carries a BRAF mutation — all are common exam-killers.

• Sarcoidosis = cutaneous granuloma + bilateral hilar adenopathy; ACE↑, hypercalcemia/hypercalciuria; the Löfgren triad has a good prognosis; erythema nodosum is an accompanying feature, not histologically a granuloma.
• Scleredema diabeticorum: symmetric, asymptomatic induration of the upper back / nape / shoulders, with obesity plus poorly controlled T2DM; begins centrally on the trunk, no Raynaud phenomenon, no autoantibodies (contrast scleroderma, which begins acrally).
• Necrobiosis lipoidica = yellow-brown atrophic pretibial plaque (diabetes); acanthosis nigricans = insulin resistance / visceral malignancy (if sudden onset).
• Atopic dermatitis = Th2, eosinophils↑, IgE↑, flexor surfaces, filaggrin barrier defect; it is eosinophils that rise (not neutrophils); new treatment dupilumab (anti-IL-4Rα).
• Psoriasis = Th17/IL-23, extensor surfaces, thick silvery scale, Auspitz sign, Koebner phenomenon, nail pitting; avoid oral corticosteroids (abrupt withdrawal → pustular psoriasis); beta-blockers, lithium, and antimalarials can trigger it.
• Pityriasis alba: hypopigmented, finely scaling patches on the face of atopic children, benign, improves with age.
• Lower-leg pigment change + varicose veins = stasis dermatitis (venous), not PAOD (arterial).
• Asteatotic eczema management: moisturizer is king; avoid hot water/soap/excessive bathing (the "least appropriate" answer choice is usually "soak in a hot bath").
• Traps: treating erythema nodosum as sarcoidosis's granulomatous lesion itself (it is only an accompanying feature); reversing the flexor/extensor distribution of eczema and psoriasis; writing the elevated cell type in atopic dermatitis as neutrophils; giving psoriasis oral corticosteroids that rebound into the pustular form on withdrawal; describing scleredema as beginning acrally (that is scleroderma).

• Oral isotretinoin's absolute contraindication = pregnancy (a potent teratogen); adverse effects mucosal dryness, elevated triglycerides, elevated liver enzymes; contraindicated with tetracycline (pseudotumor cerebri).
• Acne should never be treated with oral antibiotic monotherapy (prone to resistance); it must be paired with benzoyl peroxide / a retinoid.
• Androgenetic alopecia = DHT-driven follicular miniaturization, gradual, non-scarring; not "sudden, massive shedding"; treated with minoxidil + finasteride.
• Hidradenitis suppurativa (HS) is fundamentally = follicular occlusion, not a simple bacterial infection; female > male, favors apocrine-bearing areas; adalimumab (anti-TNF-α) was the first approved biologic.
• Hirsutism (androgen-related, androgen-dependent sites in women) ≠ hypertrichosis (androgen-unrelated, any site); swapping the two is a common trap.
• Traps: combining isotretinoin with tetracycline, precipitating pseudotumor cerebri; treating acne with oral antibiotic monotherapy and breeding resistance; describing androgenetic alopecia as "sudden, massive shedding" (that is telogen effluvium); treating HS as a simple bacterial infection with prolonged antibiotics; swapping the definitions of hirsutism and hypertrichosis.