Tumors of the Colon Polyps, tumors, caners
MC polyp in entire GI = hyperplastic polyp – it is a little nubbin – aka hemartomas (therefore not
neoplastic), usually in sigmoid colon.
Tubular adenoma: looks like a strawberry on stick, therefore has a stalk with strawberry, which
is the precursor lesion for colon cancer.
Juvenile Polyp: Slide: coming out of child’s butt – kid with polyp in rectum; all juvenile polyps
located in the rectum and are hamartomas (no precancerous).
Lets say it is an adult and the polyp is sticking out (a reddish mass) – dx? Internal hemorrhoids.
Rule: internal hemorrhoids bleed, external hemorrhoids thrombose. Therefore, when you
have blood coating the stool, it is internal hemorrhoid. Internal hemorrhoids are NOT painful,
but they do prolapse.
Adult with something reddish sticking out of their butt = prolapsed internal hemorrhoid.
Internal hemorrhoids bleed and painless, while external thrombose and are painful.
Sessile Polyp (villous adenoma) – looks like the villous surface of the small intestine (hence
name villous adenoma); these are lil finger-like excrenses of the small intestine, hence the name
villous adenoma. These have the greatest malignant potential, and are usually in the rectal
sigmoid. B/c they are villous/finger like they have a lot of mucous coating the stool; mucous
secreting villous. They have a 50% chance of becoming malignant. So, tubular adenomas are
precursors for cancer (size determines malignant potential – if they are above 2 sonometers,
they are very dangerous) and villous adenomas lead to cancer, too.
Familial polyposis – need to have over 100 polyps to have familial polyposis. This dz is
autosomal dominant, uses APC suppressor gene, ras, and p53; APC is the major one. Will
always get cancer in them, usually between 35-40. Therefore, will need to prophylactically
remove the bowel. The autosomal dominant dz is famous for late manifestations, penetrance,
and variable expressivity (as are all other AD dz’s). This means that they will not be born with
polyps at birth (they start developing btwn the ages of 10-20; in ADPKD, they do not have cysts
are birth, they start developing btwn 10-20; in Huntington’s chorea, do not have chorea at birth,
but around 35-40 years, and they have late manifestations.
Affected colon has polyps and brain tumors = Turcot syndrome (like turban) – therefore, you
have a polyposis syndrome with brain tumor; this dz is auto rec (not dominant).
Gardner’s syndrome: Have multiple polyps in there, plus b9 salt tissue tumors: desmoids and
osteomas in the jaw.
Along with auput tumors. All carcinoid tumors are malignant, but have low grade potential. A lot of
it depends on their size and if they are going to mets. Depends on their size in sonometers – if they
are greater than 2 sonometers they have the ability to mets. MC location for carcinoid tumor = tip
of the appendix – have a bright yellow color, but they are NEVER the cause of carcinoid syndrome –
why? B/c the tip of the appendix will never be greater than 2 sonometers. So, where is the MC
location of carcinoid tumor that CAN be associated with carcinoid syndrome? Terminal Ileum –
they are always greater than 2 sonometers. What do all carcinoid tumors make? Serotonin. B/c the appendix and terminal ileum are drained by the portal vein, the serotonin made goes to the
portal vein, goes to the hepatocyte, is metabolized into 5 hydroxyactoactitic (?) acid and is pee’d
out; therefore it is not in the bloodstream. Therefore, there are no signs of flushing and diarrhea
b/c there is no contact with the systemic circulations. However, if you mets to the liver, then those
metastatic nodules that are making serotonin can dump some of it into the hepatic vein tributaries.
This does have access to the systemic circulation b/c goes to IVC to Right side heart, and this is why
you get right sided lesions – “TIPS” = tricuspid insuff and pulmonic stenosis. Serotonin is a
vasodilator in some cases, but a vasoconstrictor in other cases. However, in terms of serotonin
syndrome, it’s a vasodilator that causes flushing (which is the MC symptom of carcinoid), followed
by diarrhea (2 MC). If it has access to systemic circulation, it has high levels of 5
hydroxyacetoacitic (?) acid, which is the screening test of choice b/c it is the metabolite of serotonin.
So, b/c making and LOSING a lot of serotonin, what aa can be deficient? Tryptophan is def,
therefore the vitamin Niacin is def, therefore can have pellagra. You using up all the Tryptophan
and making serotonin instead of niacin.
Neurosecretory granules on EM – colon cancer; left side obstructs, right side bleeds.
This is easy to understand b/c the left colon has a smaller diameter than the right. So, when the
cancer develops in the left colon and wants to form a polyp, it goes around – annular (napkin ring),
and produces constriction. Open bowel in left colon, see one edge of the cancer on each side of the
bowel and bowel is constricted – have signs of obstruction (left side obstructs, right side bleeds).
In the right colon, b/c of there is a bigger diameter; it has a bigger chance of going out and forming a
polyp. Therefore, it is sitting in the stool, leading to a bleed (therefore left side obstructs, right side
So, which is side is more likely to have Fe def? Right sided lesion.
Which is more likely to have alteration in bowel habits (constipation/diarrhea)? Left sided.
Tumor marker for colon cancer = CEA (carcinoembryonic Ag). Not used to dx colon cancer, but
used to follow it for REOCCURRENCE. MCC relates to diet (lack of fiber in stool – therefore, more
fiber you have, the less chance of colon cancer b/c you are getting rid of lipocolic acid). Age is also a
risk factor (pts over 50); smoking is a risk factor that is assoc with colon cancer. Polyposis coli
syndromes also have an association (familial polyposis, Gardner’s syndrome, turcot’s syndrome)
NOT Peutz Jeghers, hyperplastic polyps, or juvenile polyps).
Diseases of the Appendix: Appendicitis
Covered with pus; MCC appendicitis in adults = fecalith = impacted stool. So when you impact stool
it presses on the sides of the appendix, and leads to ischemia, then get a breakdown of the mucosa,
E. coli gets in there and acute appendicitis occurs. This is the SAME mech for diverticulitis (the
diverticular sacs also get fecaliths in them and the same exact thing happens – the pathogenesis of
acute diverticulitis and acute appendicitis is exactly the same). So, fecalith, ischemia along the wall,
inflammation, E coli. Another analogy: acute cholecystitis – except it is not a fecalith, but is a stone in the cystic duct
pushes on the side, leads to ischemia, acute cholecystitis, E coli. So, the