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Colorectal carcinogenesis often unfolds over years,
creating opportunities for prevention before invasive disease develops.
Normal mucosa becomes an adenoma when APC is inactivated,
advances when KRAS mutates,
and turns malignant only after TP53 and SMAD4 fail.
Accumulating these events takes five to ten years, sometimes fifteen,
which is why removing adenomas at colonoscopy prevents cancer.
Two faster lanes exist.
The serrated pathway runs through BRAF and microsatellite instability.
In Lynch syndrome,
defective mismatch repair drives a few adenomas rapidly to cancer,
usually right-sided and often paired with endometrial cancer.
Peutz-Jeghers syndrome, from STK11, brings hamartomas and mucocutaneous pigmentation,
while familial adenomatous polyposis, from APC, carpets the colon with adenomas.
Obesity and inactivity increase risk rather than reduce it.
Stage directs treatment.
Node-positive stage III colon cancer receives adjuvant FOLFOX or CAPOX,
oxaliplatin with a fluoropyrimidine, and no targeted agent.
Targeted therapy belongs to metastatic stage IV disease: bevacizumab broadly,
and cetuximab
or panitumumab only for RAS wild-type tumours of the left colon
and rectum.
The rectum sits in the pelvis and recurs locally more often,
so locally advanced rectal cancer receives neoadjuvant chemoradiotherapy, then total mesorectal excision,
then adjuvant chemotherapy.
TME follows the embryological plane of the mesorectal fascia,
removing the mesorectum intact while sparing the hypogastric and pelvic splanchnic nerves.
Sexual and bladder function are consequently not worsened.
Laparoscopic resection matches open surgery oncologically,
as the COLOR and COST trials showed,
with faster recovery and unchanged mortality.
Colorectal carcinogenesis often unfolds over years,
creating opportunities for prevention before invasive disease develops.
The dentate line divides the anal canal into two worlds,
because endoderm meets ectoderm there.
Above it the epithelium is columnar
and the superior rectal artery arrives from the inferior mesenteric.
Venous blood returns to the portal system, innervation is autonomic and painless,
lymph drains to internal iliac nodes, and haemorrhoids are internal.
Below it the epithelium is squamous
and the inferior rectal artery arises from the internal pudendal.
Blood returns to the inferior vena cava,
the pudendal nerve from S2 to S4 makes every lesion painful,
lymph drains to superficial inguinal nodes, and haemorrhoids are external.
Portal hypertension distends the anastomosis between the two systems.
The middle rectal artery comes from the internal iliac,
not the inferior mesenteric, whose branches are the left colic,
sigmoid and superior rectal arteries.
The sigmoid perforates more than any other segment,
not because its wall is thin but because diverticula are common
and its calibre is small.
By Laplace's law wall tension equals pressure multiplied by radius,
so a narrow lumen needs higher pressure to generate the same tension,
and thin-walled diverticula give way first.
Hinchey grades the consequences: a pericolic abscess is treated with antibiotics,
a pelvic abscess with antibiotics and CT-guided drainage,
and purulent or faecal peritonitis with emergency surgery.
A colovesical fistula is repaired electively,
and chronic anaemia is never an emergency indication.
Colorectal carcinogenesis often unfolds over years,
creating opportunities for prevention before invasive disease develops.