Lyrics · 完整歌詞
Cholesterol gallstone formation reflects three interacting processes: biliary supersaturation,
crystal nucleation and impaired gallbladder emptying.
Cholesterol stones make up about three quarters and are radiolucent.
Ursodeoxycholic acid dissolves only small radiolucent cholesterol stones in patients too frail for surgery.
Once formed, a stone is named by where it lodges.
Held in the gallbladder, it causes colic under six hours without fever.
Wedged in the cystic duct, it causes cholecystitis: pain beyond six hours,
fever and Murphy's sign.
The inspiratory arrest occurs as the descending diaphragm presses the inflamed gallbladder
onto the examiner's fingers.
Ultrasound comes first, showing a wall over three millimetres and pericholecystic fluid;
HIDA is most specific, and laparoscopic cholecystectomy follows within 72 hours.
Acalculous cholecystitis, from stasis and ischaemia,
stalks the ventilated patient on parenteral nutrition.
Lodged in the common duct,
the stone raises alkaline phosphatase and GGT and yellows the skin.
Add bacteria and cholangitis follows: Charcot's triad is pain, fever and jaundice,
never a palpable gallbladder.
Shock and confusion complete Reynolds' pentad;
antibiotics and fluid merely bridge to urgent endoscopic drainage.
Morphine tightens the sphincter of Oddi, so an anti-inflammatory eases biliary pain.
Cholesterol gallstone formation reflects three interacting processes: biliary supersaturation,
crystal nucleation and impaired gallbladder emptying.
Lodged at the ampulla, the stone triggers pancreatitis:
trypsinogen activates within the gland, autodigestion follows,
and cytokines produce systemic inflammation and third-space fluid loss.
Diagnosis needs two of three: typical pain,
lipase above three times the upper limit, and consistent imaging;
stones and alcohol cause about 80 per cent.
BISAP counts urea over 25, impaired mentation, SIRS,
age over 60 and pleural effusion;
a haematocrit above 44 per cent betrays haemoconcentration.
Fluid comes first, antibiotics wait for infected necrosis,
and ERCP is reserved for cholangitis or persistent obstruction.
Saponification of fat consumes calcium.
When the gland burns out, insulin and glucagon fail together,
so type 3c diabetes fears hypoglycaemia, not ketoacidosis.
Fat and amino acids in the duodenum release cholecystokinin from I cells,
which contracts the gallbladder and relaxes the sphincter of Oddi.
Acid releases secretin from S cells, summoning bicarbonate and inhibiting gastric acid.
Embryology adds a trap:
the gallbladder is foregut endoderm from the hepatic diverticulum,
whereas the spleen is dorsal mesogastric mesenchyme.
The pancreatic head drains to the superior mesenteric vein,
which joins the splenic vein to form the portal vein.
That portal vein is the hub of cirrhosis.
Injury turns stellate cells into myofibroblasts under TGF-beta;
collagen and regenerating nodules squeeze the sinusoids and resistance climbs.
Varices open along the left gastric to azygos route.
Ascites with a serum-ascites albumin gradient of at least 1.1 g/dL is portal;
an ascitic neutrophil count of 250 or more declares peritonitis.
Primary prophylaxis needs a non-selective beta-blocker:
beta-1 blockade lowers output while beta-2 blockade constricts the splanchnic bed.
Hepatitis C becomes chronic in 75 to 85 per cent;
hepatitis B in over 90 per cent of neonates
yet under 5 per cent of adults.
Primary sclerosing cholangitis carries a 10 to 15 per cent lifetime risk of cholangiocarcinoma.
Cholesterol gallstone formation reflects three interacting processes: biliary supersaturation,
crystal nucleation and impaired gallbladder emptying.