EXPLANATIONS OF (MOST) ANSWERS TO 2002 GI TEST

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Brought to you by Aganga, Farrell, Kamel, Marcovici, Miloushev,Park, Rougas, Saal,
Wan, and C-Lo & the Gang, who make no claims to accuracy or originality but do claim
(and justly so) that Andre the seal should be allowed to eat all the River Leven salmon he
wants.

Q1.
This is a slide of hepatocellular carcinoma, most common primary malignant tumor of
liver (HCC). Risk factors for HCC: 70% have underlying cirrhosis- especially from
HBV, HCV. Also risk if cirrhosis from EtOH or hereditary hemochromatosis. Aflatoxin
exposure is another risk factor, as is repeated necrosis, inflammation and regeneration.
The answer is (C): CEA is elevated in colon cancer, not HCC. Q2.
This is a slide of hereditary hemochromatosis (HHC) (autosomal recessive). (A) is
referring to (non hereditary) hemochromatosis which results from too many transfusions
and deposition of Fe in parenchyma of many organs. In HHC, there is deposition of iron
in tissues, especially the liver, heart, panc. islets, joints (hence the nickname Bronze
diabetes.) Yes, test for the 2 mutations on HFE gene associated with HHC: C28Y and
H63D. Homozygous C28Y and heterozygous C28Y/H63D are expressed clinically. The
wild type gene codes for a gate keeper that allows only minimal Fe to be absorbed from
small intestine. Mutate it, and too much Fe is absorbed (answer B). Ferritin is high (C)
(patient is trying to store the excess Fe) and transferrin is saturated above 45% (D). Yes,
cirrhosis may develop if untreated (E).

Q3.
Microscopic feature of the portal tract in: -chronic hepatitis from AAT deficiency: look for the purple-red PAS+ globules-
pretty distinctive actually.
-chronic HCV: dense lymphoid aggregate in the region of the portal tract,
especially around the bile duct. Not as dramatic as acute hepatitis.
-Choledocholithiasis (stones in common bile duct): obstruction of a large bile
duct. Look for: EDEMA, PMNs, bile ductular PROLIFERATION. Say it ten
times fast.
-advanced alcoholic liver dz: effects of EtOH progress from fatty liver
(steatosis) to steatohepatitis to cirrhosis (and possibly to HCC). In steatosis, you
see the macrovesicular fatty cells, with the nuclei smooshed off to the side. In
steatohepatitis, its worse: Mallory Bodies, PMNs, fibrosis. By cirrhosis, its the
fibrosis surrounding architecturally abnormal regenerative nodules.
-schistosomiasis: look for the little bugger walled off by a granuloma- this is in
the portal tract- causing pipestem fibrosis and portal HTN.
Q4.
Seems that this is a slide of cirrhosis. We know that HAV doesnt lead to cirrhosis- its a
self-limited disease. Only HBV, HCV, HDV of the hepatitititis lead to cirrhosis. (B) yes,
serum liver tests (AST, ALT) are high in cirrhosis- they are leaked from hepatocyte cytoplasm with cell destruction. (C) Esophageal varices are a complication of portal
HTN, which is associated with cirrhosis. (D) Yes, cirrhosis predisposes to HCC (70% of
HCC have cirrhosis underlying). (E) Steatohepatitis can progress to cirrhosis, and thence
to HCC (for example, remember the progression in EtOH: fatty liver to steatohepatitis to
cirrhosis to HCC).


Q5.
Patient with diarrhea and malnutrition is a classic presentation of Celiac Disease (might
also expect to find some nutrient deficiencies). Remember that more people actually
have silent Celiac, with anemia, osteoporosis, susceptibility to other autoimmune
diseases, malignancy (especially T lymphomas and carcinomas), but no gi symptoms,
despite having the same gi pathology as the classic presenters. In silent cases, the gi
histology normalizes and the systemic symptoms improve on the gluten-free diet. Celiac
Disease histo: totally flat villi (they have atrophied), lymphocytes in the epithelia, crypt
hyperplasia. Yes, remove gluten, the cause of the T-cell-provoked inflammation (B).
(A) I dont know what they are after here, but there is no reason to associate a thrombus
with this presentation. (C) is a slide of Giardiasis, from old friend Giardia lamblia, the
intestinal amoeba. Treat with metronidazole. (D) if you found a carcinoid in the SI, yes,
look elsewhere also, seems prudent. Prescribe multivitamin supplements if problem with
absorption (E).

Q6.
Slide of GERD. Histologically, GERD has 4 features- B.I.L.E.: Basal cell hyperplasia,
Inflammatory infiltrate, Long papillae, Eosinophils. GERD is experienced as heartburn
(A). Complications include ulceration, bleeding (B), stricture, Barretts (intestinal
metaplasia) (C). Most patients with severe reflux esophagitis do have sliding hiatal
hernia (D) (though most with hernia dont have esophagitis). NO VARICES IN GERD-
think portal HTN.

Q7.
Colon bleed resection: Hyperplastic epithelium would make rugae/thick epithelium, not
bleeds. All the other lesions could rupture/bleed.

Q8.
Steatohep: Fatty liver plus centrilobular fibrosis. Causes are usually alcohol.
Alc aldehyde acetate. Aldehyde causes lipid peroxidation problems. Endotoxin can
poison the hepatocytes with same result. Mallary bodies are intermediate filaments that
clump due to aldeyhyde. Ito cells are the cause of fibrosis, which the aldehyde stimulates
(via cytokines).

Note: copper is a diffuse metabolic problem. May lead to cirrosis.

Q9.
Nutmeg liver (centrilobular congestion) is Lefkos favorite. Its due to blood back up into
CV, usually right heart failure.
Q10.
Bile duct damage and endothelial damage together should signal you to think its immune
mediated, since both have MHC 2 on surface.

Q11.
Ground glass is all you need for this one. Ground glass=Hep B (chronic). Remember that
the other signs are possible with other forms of cirrhosis.

Q12.
So, its not clear from the question stem that he has active hep-B AGAIN now, but you
have to assume he does, since all but one of signs present are active new Hep B. So,
choose the one that is not like the other (Hep Bs-AB). Apparently he has not mounted a
new response to this Hep B infection yet.

BACKGROUND FOR Qs 13-16.
13-16 based on case history: 28y.o. man has UC, onset at age 22. UC has been stable on
medication for several years, but at checkup MD noticed jaundice. Dx: primary
sclerosing cholangitis (PSC).

PSC is a cause of cholestasis classified as a bile duct disease. This is a disease that can
affect both large and small vessels of the biliary tract, as opposed to primary biliary
cirrhosis (PBC), which is an autoimmune disease with specific effects on the small
intrahepatic bile ducts only. PBC is characterized by segmental destruction of
intrahepatic bile ducts by plasma cells and lymphocytes, resulting in bile duct epithelial
damage/inflammation, and eventual loss of the bile ducts. This is called chronic non-
supporative destructive cholangitis (CNSDC) and is mostly seen in middle-aged or young
women, often asymptomatic or presenting only with pruritis until late in the game. Both
PSC and PBC ultimately lead to bridging fibrosis and biliary cirrhosis, the sequellae of
any chronic bile duct obstruction, but it takes a lot longer to reach this point in PBC
because there is so much reserve of unaffected intrahepatic bile ducts in the liver. Note
that although this patient does not have pruritis, pruritis would often be among the
presenting symptoms in PBC, and it is thought to have something to do with bile acid
deposition in the skin and its effects on opioid receptor pathways.

With PSC and all diseases of large bile duct obstruction, expect to see: cholestasis,
edema, bile ductular proliferation, PMN infiltration, feathery degeneration in liver cells
containing bile, due to the leaching action of retained bile salts. Bile infarcts, extravasates
and lakes are all virtually pathognomonic of large bile duct obstruction. Unrelieved
obstruction leads to portal fibrosis and ultimately bridging fibrosis nodular
regeneration biliary cirrhosis. Also common to all types of large bile duct obstructive
cholestasis: stagnant bile = ascending infection (cholangitis). Typical organism: E. coli,
which can lead to liver abcess if it seeds the liver parenchyma, often in the
subdiaphragmatic region of the liver.
Specific to PSC: this is a chronic fibrosing disorder associated with IBD (more UC than
CD) in 75% of cases. 80% of patients have positive serum p-ANCA tests. unknown
cause. In PSC, ducts become surrounded by onion skin fibrosis (dense, concentric) and
the characteristic cholangiogram shows strictures and dilatations (beading and
structuring). Disease often affects young adults and is a major indication for liver
transplantation.

Q13.
Most significant abnormalities in serum liver tests: a) elevated AST and ALT: (p. 19): ALT is present in hepatocyte cytosol, catalyzes transamination between amino and alpha-keto acids, is specific for hepatocytes,
and serum conc. Is elevated when hepatocytes are damaged. AST, by comparison,
is present in hepatocyte mitochondria and cytosol as well as heart and skeletal
muscle, so it is not as specific for hepatocyte damage/liver disease. In this case,
the elevated AST and ALT tell you something is wrong in the liver that is causing
hepatocyte destruction, but that is basically all it tells you. Note: in steatohepatitis,
AST and ALT are both elevated but AST>> ALT. Compare to viral hepatitis in
which AST and ALT are elevated and similar in number. b) elevated bili and alk phos. This goes with the classic labs for cholestasis, which would also tend to include elevated bile acids, phosphatase, and cholesterol, all of
which are normally excreted in bile. Getting the simpler one out of the way first,
alk phos is found near microvilli of bile canaliculi as well as in bone and placenta.
Serum activity is elevated in intrahepatic cholestasis, extrahepatic biliary
obstruction, or invasion of the liver (tumor, mycobacteria), or of course, in bone
disease. For an incredibly detailed account of causes of elevated bili, see pages
13-18 of the syllabus. For the purposes of this question, well stick to the reason
elevated bili in PSC. PSC is biliary tree obstruction. The conjugation process is
not affected, but the flow of conjugated bilirubin, in bile, from the hepatocytes to
the common bile duct, or into the intestines from the common bile duct, is
obstructed. This leads to a buildup of mostly conjugated bilirubin, which is water
soluble and exists unbound in the blood. It builds up in the blood because it
cannot be secreted via bile into the intestines. Failure of bilirubin secretion into
the intestines through the common bile duct is is the cause of acholic (pale) stool
seen in PSC and all cases of cholestasis caused by biliary tree obstruction.
Normally, bilirubin is hydrolyzed, deconjugated, and reduced into a colorless
tetrapyrrole called urobilinogen in the colon. 20% of urobilinogen is subsequently
taken up by the liver via portal circulation. The rest is either peed out or oxidized
to urobilin, which gives normal stool its brown color. Note that conjugated bili
can be peed out because it is water soluble and therefore, filtered in the kidney (as
opposed to unconjugated bili, which is not water soluble, is almost always
protein-bound in serum, and is never found in the urine). Going along with this is
the fact that you can also see dark-colored urine if there is sufficient
hyperbilirubinemia. Note also that as liver disease progresses, hepatocytes may
release unconjugated bilirubin when they die, which would cause mildly elevated
serum Unconjugated bili. c) high total protein and low albumin. Albumin is synthesized in hepatocytes and secreted into blood. Its half-life is 20 days. Hypoalbuminemia occurs with hepatic
synthetic dysfunction in chronic liver disease, especially advanced cirrhosis.
However it is not specific for liver disease as it can also be seen in renal, heart,
and other GI diseases. I havent been able to figure out when you would see this
combination. d) increased LDH I really dont know what this would tell you but Im pretty sure its not relevant to liver disease. e) elevated bili alone. Elevated bili alone is not specific enough to make a definitive diagnosis as it could be caused by, at the least:
Q14.
Which test would have led to the most definitive diagnosis of PSC? a) Cholangiography: youd see the classic beading and structuring (dilatations and strictures) of the affected extrahepatic and intrahepatic bile ducts. Better than
biopsy because its more sensitive (I think this is correct use of the word). b) serum liver tests: This answer choice really doesnt mean very much so Im going to ignore it. c) abdominal ultrasound: US is best for visualizing gross obstructions like gallstones, dilated bile ducts, intrahepatic and extrahepatic masses. It can also be
used with Doppler to examine hepatic blood flow to look for causes of portal
HTN. I guess it might show PSC since it can show dilatations, but I guess thats
not enough to make it the most definitive test! d) liver biopsy if you saw onion skin fibrosis on liver biopsy, youd know you had PSC. But you dont always see onion skin fibrosis and you do pretty much always
see beading and structuring on cholangiography (see above), which makes liver
biopsy specific but not sensitive (again, this is a strech back to epi so Im sorry if
its not correct). This answer choice was probably meant to trigger you to think of
PBC, in which the classic biopsy evidence is the florid bile duct lesion. e) serum AMA this would be more diagnostic of autoimmune hepatitis or PBC (question 16d and p. 42 in syllabus), but there is serum AMA in other
autoimmune diseases as well.
Q15.
Liver biopsy, if diagnostic, would have shown: a) fatty change: fatty change is the presence of lipid vacuoles, either large or small, within hepatocytes. This is not seen in PSC. Fatty change develops because of
abnormal lipid and lipoprotein metabolism, as seen in alcohol ingestion, obesity,
diabetes, corticosteroid use, and (less commonly): Reyes syndrome, tetracycline
toxicity, acute fatty liver of pregnancy, toxicity of nucleoside analogues and
valproic acid (used for seizure disorders). Fatty liver is associated with
inflammation and fibrosis in steatohepatitis, which may lead to cirrhosis. b) damage to bile ducts by plasma cells, lymphocytes and granulomas: This suggests chronic autoimmune hepatitis (see #17) or PBC. c) steatohepatitis: progression of fatty change/fatty liver marked by large fat droplets and Mallory bodies (aggregates of intermediate filaments) within hepatocytes causing ballooning, as well as PMN infiltration/inflammation and fibrosis
surrounding the central vein and in the perisinusoidal region. It is usually caused
by alcoholic hepatitis that gets worse, but can also be caused by nonalcoholic
steatohepatitis (NASH): obesity, diabetes, jejunoileal bypass, and drugs such as
amiodarone, tamoxifen, nifedipine. Alcoholic hepatitis usually refers to the
syndrome of nausea, vomiting, fever, abdominal pain, jaundice and peripheral
leukocytosis which is associated with steatohepatitis. d) cholestasis with periductal concentric onion skin fibrosis this is clearly the answer, based on the introductory information above regarding PSC. e) pure intracanalicular cholestasis: this would be seen in drug-induced jaundice or the jaundice associated with gram-negative septicemia. (p. 10) It seems to me it
would also be seen in PBC, which only affects intrahepatic bile ducts, but Im not
positive about that. Maybe intracanalicular cholestasis does not mean (as I
believe) that intrahepatic bile ducts of clogged with bilirubin. (?)
Q16.
Which serum test would most likely have been positive? a) ANA (anti-nuclear antibodies): seen in autoimmune hepatitis type I (see question 17) b) ASMA (anti-smooth muscle antibodies): seen in autoimmune hepatitis type I (see question 17) c) Anti-LKM (anti-liver-kidney microsome antibodies) (seen in autoimmune hepatitis type II, which is the type that is most commonly seen in children 2-14
y.o. and is rare in the US. d) AMA (anti-mitochondrial antibodies): positive in PBC: these antibodies are directed against autoantigens in the 2-oxo-acid dehydrogenase complex (2-
OADC) on the inner mitochondrial membrane, most commonly on the E2 subunit
of the pyruvate dehydrogenase complex (PDC-E2). This disease is associated
with a T-cell response to the autoantigens, probably displayed on MHCII, in
addition to synthesis of AMA. The immune attack creates the classic florid bile
duct lesion , which is diagnostic on liver biopsy. In this lesion, we see a bile duct
within a portal tract infiltrated by lymphocytes, plasma cells and eosinophils with
degeneration of some or all bile duct epithelial cells and sometimes granulomas.
This disease progresses through four stages of biliary damage and fibrosis,
ultimately leading to biliary cirrhosis. PBC is associated with other immunologic
disorders (Sjogrens, Raynauds, Hashimotos thyroiditis, arthropathies, celiac
disease). most common complications = pruritis, fatigue, and
symptoms/complications of osteoporosis. e) p-ANCA (perinuclear anti-neutrophil cytoplasmic antibodies) ) again, see intro. information at beginning, but to get to the point: we dont know why
this is the case, it just is. know it.

While were on the topic, might as well add that type III AIH occurs in adults
with antibodies to soluble liver antigen (anti-SLA), and that the antigenic material
is on hepatocellular cytokeratins 8 and 18. Q17-21 are matching: answer choices: a) Kayser-Fleisher rings: Ring of brown pigment at the corneal margin (Descemets membrane), seen as part of the Wilsons disease triad. the other parts are basal
ganglia degeneration and liver damage. Wilsons disease is autosomal recessive, a
copper storage disease in which mutations in Gene ATP7B on chromosome 13
lead to the production of a dysfunctional copport transport ATPase that normally
traffics copper for excretion via canaliculi, by a route from lysosomes to the trans
Golgi network of hepatocytes. Also seen: low serum ceruloplasmin. neurologic,
psychiatric, ophthalmologic, hepatic or hemolytic clinical presentation.
Treatment: penicillamine or other copper-chelating agents. b) Mallory bodies and fat: clumped eosinophilic aggregates of intermediate filaments composed of cytokeratin and located within the cytoplasm of
hepatocytes. Characteristically seen in steatohepatitis due to alcohol abuse,
chronic hepatitis C (50% of people with HCV have fatty liver, but Im not
positive that this always includes Mallory bodies, although I think it does), and
corticosteroid use as well as in NASH (nonalcoholic steatohepatitis: obesity,
diabetes, jejunoileal bypass, amiodarone, tamoxifen, nifedipine). c) Portal tract granulomas characteristic of schistosomiasis granulomas form around ova. Could also be from drug-related hypersensitivity reaction
(allopurinol, phenylbutazone) and also possibly from PBC (granulomas
sometimes form around the antigenic remains of the epithelium). d) Abundant portal tract plasma cells and interface hepatitis: interface hepatitis is portal and periportal lymphocytic and plasma cell infiltration associated with
apoptosis of the hepatocytes that make up the limiting plate (immediately
surrounding the portal tract). It is inflammatory erosion of the limiting plate by
portal tract inflammation, and it is seen in chronic hepatitis. AKA piecemeal
necrosis. If plasma cells are present, we are thinking autoimmune hepatitis
rather than viral hepatitis. If there are eosinophils there, we might be mre likely to
think PBC e) Portal tract lymphoid aggregates classic for chronic hepatitis C. This is also described as follicles in portal tracts. Fatty liver, bile duct damage (leukocytes and
duct disarray) can also be seen in chronic HCV.
Q17.
Autoimmune hepatitis (AIH) D (abundant portal tract plasma cells and interface
hepatitis) In AIH, the liver is the target of cell-mediated attack by plasma cells and
lymphocytes (as opposed to just lymphocytes in viral hepatitis), with great risk of
progression to cirrhosis if untreated. It usually occurs in the setting of other autoimmune
diseases, so dx. Is based on the following, IN ADDITION TO CHRONIC LIVER
DISEASE: a) serum autoantibodies (antibody helps determine type of AIH)
b) hypergammaglobulinemia
c) concurrent immunologic disorders (autoimmune thyroiditis, rheumatoid arthritis, etc) d) HLA positivity for A1, A8, DR3 or DR4
e) Responsiveness to corticosteroids Notable pathology includes: Liver biopsy: evidence of chronic hepatitis with interface
hepatitis and liver cell rosettes (clusters of peripheral hepatocytes organized into
regenerative structures). Cirrhosis may develop. There are three types of AIH (I, II, III). I
is most common and in the US, type I is the 2 nd most common form of chronic hepatitis after viral. Summary of types:
I: 71% of occurance is in young women with serum anti-smooth muscle antibodies (anti-SMA), anti-nuclear antibodies (ANA), or both. Can present as acute
hepatitis but also presents with hypoalbumenemia and features of portal HTN
(thrombocytopenia, ascites, varices). Transaminases often increased to 500-1000.
II: seen mostly in children ages 2-14. Presents with elevated antibodies to liver/kidney microsomes (anti-LKM) and is rare in the US.
III: occurs in adults with antibodies to soluble liver antigen (anti-SLA), the antigenic material being on hepatocellular cytokeratins 8 and 18.

Once diagnosis of AIH is established, treatment = corticosteroids.

Q18.
Schistosomiasis C example of the pre-sinusoidal variety of intrahepatic portal
hypertension, characterized by lesions in the portal tracts such as fibrosis, granulomas or
obstruction of the portal vein branches. There are many, many terrible consequences of
portal hypertension, regardless of whether it is secondary to schistosomiasis or another
cause (other causes include: PREHAPATIC: thrombosis of portal or splenic vein.
INTRAHEPATIC/SINUSOIDAL: blockage of sinusoids as in cirrhotic nodules,
perisinusoidal fibrosis in steatohepatitis. INTRAHEPATIC/POST-SINUSOIDAL:
obstruction in central veins (veno-occlusive disease/bush tea). POST-HEPATIC:
obstruction within hepatic veins of IVC (thrombosis, congenital web of IVC). Sequellae
of portal HTN include: 1) life threatening esophageal varices, middle/inferior
hemorrhoidal varices, para-umbilical veins/caput medusae


Q31.
a) Vocal cord polyps: relatively frequently seen
usually present as hoarseness often found in people with a history of voice abuse They are NOT tumors, and have no known relationship to carcinoma. a) Laryngeal papillomas: usually seen in young people (unlike nasal papillomas) look like raised, granular lesions, with a broader base than polyps often affect both vocal cords
associated with HPV recur frequently, and usually regress with time malignant change is rare. b) Carcinoma of the larynx: often associated with a history of heavy smoking when tumor affects the vocal cords or vocal apparatus, causes persistent hoarseness can occur in supra-glottic region (above vocal cords), and may involve the epiglottis, aryepiglottic fold, and pyriform sinus supraglottic tumors can grow large before the vocal apparatus is affected and hoarseness occursmore likely to present as dysphagia c) see c
d) Small, in-situ or minimally invasive carcinoma limited to TRUE vocal cord: usually, cord is movable and not fixed do not metastasize; poor lymphatic supply
produce hoarseness early in course can usually be treated with radiation therapy alone carcinomas involving other parts of the larynx are usually large when discovered, and usually require a total laryngectomy
Q32.
Anatomic extent of tumor is the most important predictor of outcome in colon cancer.
The main parameters are 1) depth of invasion
2) lymph node involvement
3) metastasis There are a number of ways to stage colonic adenocarcinoma, including TNM, Dukes,
and Astler-Coller. a) Degree of differentiation is prognostic in most cancers.
b) Extent of invasion into bowel walla tumor in the colon is not considered invasive unless it invades into the submucosa. Extent of invasion is a
major predictor of outcome. c) Presence of tumor within a vein would, I guess, signify invasion into other organs and structures. Plus, it might be a sign of hematogenous
dissemination? d) This is the N part of TNM staging.
e) Adenomatous epithelium is often coexistent with adenocarcinoma
Q33. a) this seems true, although I couldnt find it in the syllabus
b) a tumor in the colon is not considered invasive unless it invades into the submucosa. Extent of invasion is a major predictor of outcome c) the bigger the polyp, the bigger the chance of cancer
d) screening for and removal of adenomas causes a decreased incidence of carcinoma e) not true. Adenomatous polyps (neoplastic) and hyperplastic polyps (nonneoplastic) can look very similar through the ass-cam.
Q34. a) tumors of the small intestine account for only 3-6% of GI tumors primary adenocarcinomas are rare, and are found most commonly in the duodenum, especially near the ampulla of Vater; less often in the jejunum;
and least often in the ileum are rarely in the first portion of the duodenum
can be annular (constricting) or polypoid b) See a
c) Carcinoid tumors: 50% are found in appendix; less often they are found in small intestine, rectum, lung, stomach in the small intestine, 80% of carcinoids are found in the ileum; less often in jejunum or duodenum are endocrine neoplasms of the GI tract intussusception and/or bleeding rarely seen uncommonly, tumor may slowly invade muscularis and extend to peritoneal surface and into mesentery, causing serosal adhesions and
mesenteric contraction; this may lead to angulation kinking of the bowel. have a better prognosis than adenocarcinomas d) anyone, bening or malignant, who messes with the ampulla of Vater could block up bile flow and cause some of that obstructive jaundice e) Obstruction and bleeding are two important patterns of small intestinal tumor presentation. Adenocarcinomas of the jejunum and ileum are most often annular,
constricting lesions which gradually narrow the lumen. Although it doesnt say
this anywhere, I guess obstructive symptoms happen later in their development
than bleeding, since c is the obvious wrong answer here.
BONUS FUN FACT: intestinal tumors can cause sudden onset of obstructive symptoms
when they cause intussusception (telescoping). This can be caused by all small intestine
tumors EXCEPT Adenocarcinoma Carcinoid Lymphoma
Q35. a) this is true. Usually asymptomatic.
b) NAY. see 34 c
c) see 34 c
d) see 34 c
e) see 34 c
Q36.
does anyone know where they talk about diverticulosis in the syllabus? I couldnt find it,
so heres what I know, courtesy of Pathology Secrets. The opportunity to repeatedly use
the words fecalith and outpouching is driving me out of my mind with pleasure.
Diverticulosis: tends to be a disease of old age pulsion divertiocula in colon are outpouchings of mucosa and submucosa through the muscular layer of intestine. Frequently due to
increased pressure in large intestine related to straining during defecation. They are usually multiple and usually at the points of entry of the arteries through muscularis 80% appear in sigmoid colon. Diverticulitis: inflammation of intestinal wall altered by diverticula results from bacterial entry through ulceration of herniated mucosa caused by fecaliths or circulatory disturbance signs/symptoms: pain, change in bowel movement, hemorrhage; inflammation can lead to fever, leukocytosis; area is sensitive to palpation complications: pericolonic abscess, pericolonic fibrosis, peritonitis, colonic stenosis or obstrcution a) no. 80% sigmoid, Jack
b) ok
c) yes, that fecalith can get right in that outpouching and make some trouble
d) thats what they can do
e) I have no idea about this. It is apparently true.
Q37.
E. Acid-fast bacilli indicate the presence of mycobacteria.
A. Granulomas are seen in both TB and Crohns disease.
B. Fistulas are formed in Crohns by extension of mucosal ulcers through the bowel wall. These can also be seen in TB, although TB colitis is rare these
days. C. See B.
D. Crypt abscesses are seen in Crohnsthey are defined as the presence of neutrophils in a crypt lumen. These are also seen in ulcerative colitis and
infectious colitiseg, TB.
Q38.
D. Celiac patients have a 10-20% chance of developing lymphomas.
B. Tropical sprue has no association with celiac disease; it may be caused by bacterial infection or a folate and/or cobalamin deficiency. C. Celiac patients have a 10-20% chance of developing GI and breast carcinomas, but these are not squamous cell carcinomas. D. No association with TB.
E. No association with carcinoid, only with carcinoma.
Q39.
C. No intraepithelial eosinophilia in celiac diseaseceliac is T-cell mediated.
E. Villous atrophyyes.
F. Crypt hypertrophyyes.
D. Plasma cells in lamina propriayes. These are not thought to cause damage, but their antibodies may provide a useful marker for the disease. E. The surface epithelium becomes cuboidal rather than columnar.
Q40.
E. Different drugs for different bugs, eh?
G. Neither is associated with esophageal cancer.
H. Neither produces fistulas.
I. True, but does not seem all that important.
J. See E.
Q41.
A. B12 is absorbed in the ileum.
K. Protein is absorbed in the proximal jejunum (see p. 132 of syllabus).
L. Presumably, fistulas could form anywhere in the small or large intestine.
M. Watery diarrhea can occur with damage to other segments of the guteg, jejunal injury in celiac disease. N. Fever could also be due to infectious colitis, etc.
Q42.
D. UC is primarily a mucosal disease; CD shows transmural involvement.
O. Seen in both, but crypt abscesses are more numerous in UC.
P. Seen in both.
Q. Seen in both.
E. Seen in both, but crypt distortion is more marked in UC.

Q43.
e) H. Pylori does not invade blood vessels. It attaches to surface epithelium- postulated
that it attaches to sialic acid residues on glycoproteins on the gastric epithelial surface.
Inflammatory response to H. Pylori infection damages the mucosal layer, allowing acid to
reach the surface epithelium. Bacterial cytotoxins have also been found VacA (causes
vacuolization of eukaryotes) that may directly damage surface epithelium.

Q44.
c) In the terminal ileum, bile salts are reabsorbed by Na/ Bile co transporters. Pts with
resected ileum cant absorb bile acids. Bile acids reach Colon, gets decongugated by
bacteria renders them more lipids soluble and inserts into plasma membrane of the
intestinal epithelium activates Phospholipases leading to secretion.

Q45.
d) Congenital sodium secretory diarrhea- defect with apical Na/H exchanger. Cant
pump out protons into lumen in exchange for Na, so stool has high [Na] and high pH.
Non anion gap metabolic acidosis occurs due to the loss of bicarb from the diarrhea.
Also, the Na/H exchanger defect leads to the inability to pump out the protons generated
in the intestinal cell, along with the inability to generate bicarb and pump it into the
blood. Congenital Chloride Diarrhea results into a metabolic alkalosis bicarb
accumulation, due to the inability to pump out Bicarb in exchange for chloride. The other congenital diarrheas would result in non-anion gap metabolic acidosis but not such a high
stool [Na].

Q46.
b) Cholera releases the AB toxin. The 5 identical B subunits bind to a GM ganglioside in
the intestinal brush border membrane. Undergoes endocytosis, A subunit then activates
constitutively activates the alpha subunit of Gs increases AC activity increases
cAMP opens the apical Cl Channels intestinal Cl secretion. Cholera toxin also
inhibits Na/H and Cl/HCO3 exchangers preventing the absorption of Na and Cl.

Q47.
d) Oral rehydration solution with Na, Cl, and a glucose polymer; 260 mosm/L.
Cholera toxin promotes active Cl secretion and prevent absorption of Na and Cl. (block
Na/H and Cl/HCO3 exchangers). Giving Na/Cl solution will just increase diarrheal
volume because you cant absorb the salt. However, Cholera doesnt inhibit the
Glucose/Na co transporter, so giving Glucose will result in absorption of Na with water
following. Giving a equimolar Na/Cl and Glucose will only rehydrate the Pt, it will not
decrease diarrheal volume, unless the amount of glucose in the solution was more than
the salt. However, in severely dehydrate pt, giving a hyperosmolar solution of Na/Cl and
glucose will result in rapid water flow into the gut lumen. Glucose polymers will result in
net absorption of fluid without increased osmolarity because the rate of hydrolysis of
oligosaccharides is less than the rate of glucose absorption.

Q49.
A friend of mine's favorite pick-up line used to be "Funny how it's 'Gonna give you every
inch of my love' when England's on the metric system." Eventually he tried in London
and learned that England is not on the metric system. The reason I bring this up is that
expressions like "He has lost about 5 pounds" make you realize why British people, or
American people portraying British people in movies, use silly alternative words like
"stone" for weight. And that we should all be on the metric system, though none of us
should say "sontimeter," which they do in UK. Anyway.
35-yr-old male with esophagitis due to GERD, cramps, WATERY diarrhea, weight loss,
steatorrhea, positive glucose hydrogen breath test, normal barium study.
a) Acquired lactase deficiency. [Note: in the syllabus, lactase deficiency equals lactose
intolerance.] Most common cause of selective carbohydrate malabsorption. Most non-
Europeans lose lactase activity by age 5; hence "acquired" is normal, particularly if you
think drinking mucous from a veiny gland on the underside of a different species is nasty,
which it is. If you lack lactase at birth you have congenital lactase deficiency instead of
acquired. ALD will give you diarrhea (WATERY, since lactose is osmotic), gas, and
bloating. ALD is tested by administering lactose and looking for symptoms -- or, if
you're at Columbia, giving a lactose-specific breath hydrogen test. Regarding hydrogen
tests the syllabus says (on pg 130) "see Table 3," so you'll find info about it on Table 7.
The important things seem to be that 1) this patient had a GLUCOSE-specific hydrogen
test, 2) 35 is late (though not impossible) to hit ALD, and 3) having been told about the
GERD and esophagitis, you shouldn't really be looking this far out for an answer. b) Crohn's Disease. Crohn's can cause esophagitis, but since you're told that his
esophagitis is from GERD, this would be a coincidence. Crohn's skews slightly younger
than this (peak 15-25), and gives EXUDATIVE vs. secretory diarrhea. (You know -- the
dry kind.) In fact, the only thing that gives secretory diarrhea that isn't an infectious
agent is vasoactive intestinal peptide (from carcinoids and pancreatic islet cell tumors);
REM VIP is a VIP. (The reverse is not true -- infectious agents CAN cause exudative
diarrhea, eg in shigellosis.)
Note that fat malabsorption usually occurs when >100 cm of ileum are diseased or
resected (which can happen in Crohn's).
c) Giardiasis. Small feces-water vectored protozoa (rem trophozoites) that attach to the
duodenum and proximal jejunum, giving malabsorption and diarrhea, giving
malabsorptive diarrhea. I think the point with this one is that the patient is unlikely to
have gotten it in the US (outside of Cincinnatti).
d) Enterokinase "I don't appear in the Merriam-Webster Medical Dictionary, let alone the
index of Robbins" deficiency. Enterokinase is better (not saying much) known as
congenital enteropeptidase deficiency. Enteropeptidase is a brush border protein that
activates trypsinogen to trypsin in the lumen. Lack of it causes (a rare) protein
malabsorption. It is very serious and ONLY SEEN IN INFANTS, in whom it causes
diarrhea, growth retardation, and hypoproteinemic edema.
e) Small intestine bacterial growth. The correct answer; note that this CAN occur in
Crohn's. Aka blind loop syndrome. Bacteria do not normally penetrate the intact
squamous epithelium, but they can invade ulcerated mucosa damaged by GERD; this
type of bacterial infection accounts for 15-20% of infectious esophagitis. (Vs chemical
esoph or esoph resulting from other disease.)
The reason bacterial overgrowth causes steatorrhea is that the abnormal bacteria in the
lumen (normally the bowel has only small numbers of Gram-positive aerobes or
faculative anaerobes) deconjugate and hyrdoxylate bile salts, allowing them to be rapidly
reabsorbed across the epithelium of the proximal gut. If bile salt concentration falls
below the CMC (critical micelle concentration) -- you've got steatorrhea!
Note that bile salts can also be bound or precipitated by other conditions (eg ZE
syndrome, which in deference to anti-France sentiment is now known as THE syndrome),
and that bacterial overgrowth can be caused by any condition that results in local stasis or
recirculation of luminal contents (diverticula, fistula from Crohn's, etc.).

Q50.
Cobalamin deficiency is relatively common (100 cases/yr seen at Columbia), so just
because I'd never heard of it until 30 seconds ago is no excuse to get this question wrong.
It causes a disturbance in DNA synthesis resulting in magaloblastic bone marrow, a high
MCV with or without anemia, low platelet and granulocyte counts (if severe), and macro-
ovalocytes and hypersegmented neutrophils. Also glossitis and neurological features,
though patients tend to have only some of these symptoms. Cobalamin = Vitamin B12.
It is (almost) exclusively found in animal products, but even among vegetarians is very
rare in industrialized countries, since 1) it is ubiquitous is animal products, 2) it takes 2-
12 years to deplete, and 3) it gets reabsorbed from bile in the absence of GI disease. It is
seen among vegetarians in India. a) COBALAMIN DEFICIENCY IS USUALLY DUE TO MALABSORPTION, NOT
DIETARY LACK.
b) Intrinsic factor deficiency. Intrinsic factor (a protein from parietal cells, which also
make HCl) binds Cbl, facilitating uptake in the ileum. Pts who lack IF (or
transcobalamin II, another binding protein) WILL develop cobalamin deficiency, and
THE MOST COMMON CAUSE OF COBALAMIN DEFICIENCY IS LACK OF
INTRINSIC FACTOR, which tends to occur from diseases causing secretion failure (eg
from pernicious anemia, aka B12 deficiency; see end of this question), total or partial
gastrectomy, or childhood genetic error. Pernicious anemia, in turn, is most often caused
by chronic atrophic gastritis, 90% of patients for which are middle-aged or elderly (or
both).
That makes this a pretty gnarly question, if you ask me, since answer b is the most like
cause of answer a.
c) Bacterial overgrowth CAN cause Cbl deficiency, since colonic-type bacteria in the
small intestine utilize Cbl. (Incidentally, they also PRODUCE folic acid, leading to
elevated serum folat levels.) Deficiency of Cbl (or folate) can also CAUSE bacterial
overgrowth. But it's just not as common as answer a.
d) Tropical sprue brings together many of the themes of this question, in that most
patients show bacterial overgrowth, it causes megaloblastic anemia from deficiency of
cobalamin or folate or both. The big paragraph about it on page 134 is my favorite in the
syllabus. Like you care.
Tropical sprue, which gives only partial villous atrophy, is common in some tropical
countries but rare in others. No specific causative organism has been identified, but it
typically responds to antibiotics (REM use Tetracycline for Tropical sprue). The
megaloblastic anemia that is its most common presentation is usually associated with
chronic diarrhea.
[As a refresher, MEGALOBLASTIC ANEMIA is a DNA synthesis impairment that
monkeys with RBCs. It comes in two flavors: pernicious anemia (ie B12 deficiency;
usually an absorption problem) and folate deficiency (usually a nutritional deficiency).
REM B12 is the one that gives Brain problems, Folate deficiency is the one that is Faster
(B12 stores last 2-12 years).]
e) See above.

Q51.
Inflammatory bowel disease encompasses both Crohn's and ulcerative colitis; in up to
20% of cases (I think slides review guy sed slightly lower) IBD can't be identified as one
or the other. Briefly, Crohn's and UC are similar in that they have unknown etiology and
pathogenesis, the same basic pathology (inflammation of the colon), peak incidence in
the same age group (15-25), susceptibility to genetic predisposition, and can show
extraintestinal manifestions such as arthritis, eye lesions, PSC, and skin lesions. There
are also a number of differences between them, including (to choose a few) that Crohn's
can be transmural while UC is limited to mucosa, that Crohn's ulcerates while UC does
not, that the carcinoma risk of Crohn's is only 1% while UC is 10%, and that Crohn's is
patchy with skipped areas and usually involves the ileum and right-sided colon whereas
UC is diffuse and predominately involves the left-sided colon. a) This is a trick answer, since HUMAN IBD is idiopathic but known luminal bacteria
ARE involved in animal models, you humanocentric jerk.
b) Another animal research answer. Oops, I accidentally filed it under "Who gives a
shit?" Speaking of excrement (and we do seem to be doing that), kudos to C-Lo (the
individual, not the dance craze or meteorological phenomenon) for catching the bad
Augean stables joke on pg 566 of Robbins.
c) This answer is what I get for being a smartass, since even if you assume that
"individuals" refers to human individuals, it's still boring. Also true, apparently -- for UC
as well as Crohn's.
d) This can be assumed from the fact that Crohn's shows NEUTROPHILS and
GRANULOMAS while UC shows MONONUCLEAR INFILTRATES. (Note however
that UC can show neutrophils within the crypt abscesses that appear in both Crohn's and
UC. This is discussed elsewhere on this test.)
e) Ie, "Even we couldn't think of another animal question."

Q52.
Celiac disease, aka celiac sprue, nontropical sprue, or GLUTEN-SENSITIVE
ENTEROPATHY (GSE) presents in the form of a malabsorption syndrome. It causes
shortening or subtotal atrophy of villi, elongation of crypts, diarrhea or steatorrha, weight
loss/stunted growth in children, and various deficiencies. Exact pathogenesis is not
proven (golden words), but:
-- there's a genetic link, with higher prevalence in Northern Ireland and 95% of patients
inheriting a pair of genes in the DQ (REM Dairy Queen) subregion of the HLA-D region
of the MHC (although 25% of normal population also has this gene)
-- Type I diabetes and autoimmune thyroid disease raise the risk
-- 90% of patients have antibodies to GLIADEN, the alcohol-suluble fraction of
GLUTEN present in WHEAT, and a gluten-free diet relieves the symptoms in majority of
patients
-- the immune system could play a pathogenic role, with the DQ2 molecule presenting
peptides to CD4 T cells
-- traditionally biopsy was essential for diagnosis, but now with have anti-endomysial
antibodies tests (EMAs), including a particularly sensitive and specific one for tissue
transglutaminiase (tTG)
-- there's a biphasic peak age curve: childhood then 5th/6th decades
-- Celiac patients have a 10-20% incidence of GI malignancies
a) Severe disease presents with diarrhea, weight loss, and deficiency of bowel nutrients.
Milder disease, involving only the proximal bowel, can present with vitamin or mineral
deficiencies (eg microcytic anemia due to iron malabsorption, bone disease due to
calcium malabsorption) WITHOUT diarrhea.
b) As mentioned above, the most sensitive and specific blood test for celiac desease is
EMA, particularly the subtype that tests for tTG antibodies. Insert cheap egophony joke
here.
c) This is counter-intuitive, so go with your gut instinct and then do the opposite. You
can lose vitamins A, D, E, and K in celiac disease. You can lose iron and calcium. But
no one seems to mention B12, and question says "common." Note tropical sprue among
others does cause B12 loss; see Q50. d) Majority do improve.
e) Issue is gliadins in gluten in wheat.

Q53.
This a question about gastric bypass. If you remember that gastric bypass is commonly
called "stomach stapling" you will not the stapled line on the picture, past which the food
cannot go. So another way of asking this question would be, "What does the stomach do,
and what would happen if it didn't?" Another thing that would be helpful to bear in mind
is that this is a relatively common procedure, so you would hope it's not too debilitating.
a) Since bypass is after the ampulla of vater, pancreatic enzymes should not be affected.
b) "The stomach serves at least three functions: (1) a reservoir for food; (2) fractionates
food into tiny particles (chyme) ready for digestion and absorption. (3) delivers chyme to
the duodenum at a rate controlled to provide efficient digestion and absorption." (Pg 97)
c) Bile salts don't come from the stomach. They come from the neck.
d) Bile salt wasting. This is a slightly more subtle option, since you may recall that
acidification of the intenstinal lumen can cause bile salts to precipitate, eg in ZE
syndrome (see Q49). However, not only would you expect stomach resection to lead to
alkalinization instead, the acidification is the result of pancreatic problems, not the
stomach.
e) Chylomicrons also come from the neck.

Q54.
Another way they could have phrased this question would be "Screw you!" I mean,
regardless of whether you support Andre the Seal, if you signed up for "medical" school
this question is going to annoy you. So get ready for more non-human-relevant CRAP, ie
pages 69 and 70 of the "syllabus."
The triangular graph that appears four times demonstrates that bile gets supersaturated
when the cholesterol is high and either bile salts or lecithin is low. But apparently the
donkey is you, since the lecithin axis hasn't been documented in humans.
a) Demonstrated ... in humans!
b) Same.
c) Chronic hemolysis. This is the sucker answer, since it doesn't appear on the "Factors
Favoring Cholesterol Gallstone Formation" table or, as far as I can tell, in the chapter.
(Cheer up! Page 65 of the chapter DOES contain a ratio of bile salts that adds up to
113%!) The point is that the so-called "cholesterol stones" that make up 75% of U.S.
gallstones (as opposed to the other 49%, probably) are rarely pure cholesterol --
definitionally they only need to be 50%. So there's bilirubin in them.
d) Syllabus: "During normal fasting, when much of the bile salt pool is sequestered in
the gallbladder, the solubility of cholesterol in newly formed bile has been shown to be
significantly decreased." And: "Stasis of gallbladder bile, as occurs during prolonged
total parenteral nutrition, or during pregnancy, may promote gallstone formation by
favoring nucleation."
e) Good luck, donkey.

Q55.
This patient has "The Four F's": Female
Forty+
Fertile (multiparous)
Fat
Flatulent (intestinal disease or malabsorbtion -- don't look at me like that, I didn't make
this mnemonic up)
Familial, including high prevalence in some ethnic groups, eg Native Americans.
Most stones in the U.S. are 50% or more cholesterol; the rest are mostly pigmentary
bilitrubin. See Q54 for more, if you want.

Q56.
The key to this question is the word "clammy." In fact that's the answer to a lot of
questions when you think about it.
Amylase is a sensitive marker of PANCREATITIS, especially if the elevation is 4x
normal (25-125U/L); it appears within hours of a pancreatic injury. It is not very
specific, rising in 30% of cardiac surgery patients (in whom it comes from the salivary
gland) and extrauterine pregnancy (from the fallopian tubes). The perforated duodenal
ulcer is probably affecting the pancreas, but I don't really know what the deal is with the
kidneys. Anyway, amylase doesn't seem to rise due to gallbladder problems.

Q57.
Alcohol is listed in the "syllabus" under "non-factors," along with diet, stressful life,
personality, alcohol, coffee, and corticosteroids (which do delay healing). Sez Robbins:
"Alcohol has not been proved to directly cause peptic ulceration, but alcoholic cirrhosis is
associated with increased incidence of peptic ulcers."
Positive risk factors are H pylori, NSAIDS, hypOtension (which is helpfully called
"stress ulcer"), family history, and associated diseases such as gastromas et al.

Q58.
a) Prostaglandins 1) stim HCO3 secretion, 2) stim mucus (you don't even know us!)
secretion, and 3) inhibit acid secretion.
b) Blood flowing through mucosal capillaries buffers and carries away protons back-
diffusing from the lumen, hence protects by increasing.
c) Normally tthe gastric and duodenal epithelium turn over every 4-6 days. This is the
origin of the expression about one's "stomach turning over." Conditions that slow
turnover, eg chemo or uremia, predispose to ulcer development or failure to heal.
d) The gastric mucosal barrier has relatively HIGH resistance to ion diffusion. This
prevents HCl back-diffusion, and is also why you don't absorb much from the stomach.
e) NSAIDs inhibit prostaglandin synthesis, hence are ulcerogenic. Sez syllabus: "about
25% of patients taking NSAIDS chronically develop peptic ulcers and about 30% of
cases of upper GI bleeding are due to NSAIDS." So put THAT in your list of statistics
that aren't actually comparative and smoke it.

Q59.
Which of the following statements regarding tropical sprue is true? A) Not true. Serum folate, if anything, would be low due to malabsorption from the
jejunum. However, there can be a deficiency of folate or cobalamin, or both, in the gut,
and treatment of tropical sprue with these vitamins can substantially reverse the
symptoms of this disease.
B) Not true. While the single specific causative organism has not been identified, jejunal
bacterial overgrowth with a number of organisms is found in tropical sprue. These bugs
produce enterotoxins which are believed to affect gut function and structure.
C) Yes this is the correct answer. There is cobalamin deficiency in the gut, presumably
because it is being utilized by the bacterial overgrowths. Part I Shilling (without Intrinsic
Factor) and Part II (with IF) will both be low because the malabsorption if radio-labeled
cobalamin is not due to a failure of absorption, rather it is being used up by the bacteria
before the gut mucosa has a chance to absorb it.
D) Not true. Cassava is a root from which the starch can be ground into a flour and used
as a gluten-free substitute. This is an important food that does not cause an immune
response in people with celiac disease (aka celiac sprue, nontropical sprue, gluten-
sensitive enteropathy).

Q60.
Which of the following statements is incorrect?
A) Incorrect. First, this answer choice is too absolute. Gastric erosions can occur
anywhere, but most commonly in the antrum.
B) Yes. A badly worded answer, in my opinion, but technically can be stretched to be
true. Duodenal ulcers almost always occur coincident with H. pylori infection, which
live only on gastric epithelium (receptors bind to specific sialic acid residues on the
glycoproteins on the epithelial surface), but ulcerate in the duodenum after gastric
metaplasia in the duodenum (from increased gastric acid secretion and duodenitis
secondary to H. pylori-induced postprandial gastrin release). So these ulcers occur where
there is gastic epithelial metaplasia in an otherwise duodenal mucosa background.
C) Yes. Bile acids and alcohol can also damage mucosa, but neither has been found to be
a factor in the incidence of peptic ulcer disease.
D) Yes. As stated in the explanation to B). All ulcers related to H. pylori infection
outside of the stomach exist only within ectopic gastric epithelial metaplasia.
E) Yes. Acid secretions are important in the formation of ulcers when normal mucosal
barrier functions fail (such as: mucosa blood flow with buffering HCO3-, mucosa cell
proliferation, high viscosity mucus gel with standing pH that coats the epithelium,
HCO3- secretion that maintains this standing mucus pH, and prostaglandins that
stimulate HCO3- and mucus secretion and inhibit acid secretion).

Q61.
Which of the following statements regarding H. pylori infection is incorrect?
A) Correct, sort of. H. pylori is only found where gastric epithelium is found, which can
also be found in the esophagus, duodenum, and Meckels diverticlum due to abnormal
epithelial metaplasia.
B) Correct, sort of. H. pylori infection is commonly treated with 2 antibiotics
(clarithromycin and amoxicillin, or replacing one of the two with metronidazole)
combined with a proton pump inhibitor (omeprazole, lansoprazole, or rabeprazol) = 3 agents, not necessarily 3 antibiotics. There are also 2 drug treatments and 4 drug
treatments which have better compliance and effectiveness, respectively. Also to note,
metronidazole-resistance is increasing.
C) Incorrect. H. pylori can survive in the gastric environment because of its
microaerophilic metabolism (survive under mucus gel), its ability to bind to gastric
epithelium to resist peristalsis, and its urease which enables them to generate NH3 to
raise the pH of their immediate environment. They also have a superoxide dismutase and
catalase which may protect them from phagocyte-released oxygen free radicals.
Carbonic anhydrase is used by parietal cells for reciprocal HCO3- release into the blood
for each proton pumped into the gastric lumen.
D) Correct. Chronic peptic ulcers, particularly gastric ulcers, can be pre-cancerous.
Furthermore, a symptom-free symbiosis between H. pylori and host can be established in
some patients and persist for decades and can lead to gastric lymphoma in a very small
number of cases.
E) Correct. The majority of duodenal ulcers are associated with gastic epithelial
metaplasia and H. pylori infection. However, quite unexpectedly, only some gastric
ulcers are associated with H. pylori infection. GUs are more often associated with
NSAID use.

Q62.
The earliest abnormality found in experimental animal models of acute pancreatitis
is:
A) True. This is tidbit of minutiae is highlighted in bold italics on page 77 of the
syllabus. So remember it.
B) No. Rather, it is known that the synthesis of zymogen granules is normal in acute
pancreatitis (thus zymogen granules should be present), but that trypsinogen is converted
to active trypsin with subsequent autodigestion of the pancreas. Anyways, this answer
isnt the earliest abnormality.
C) No. I think with autodigestion of the acinar cell, the mitochondria do swell and the
ER is damaged. But again, this is not the earliest abnormality.
D) No. I think this is a true statement for acute pancreatitis, as the proteins and other
cellular debris from autodigested have to go somewhere. But it is definitely true for
CHRONIC pancreatitis, where protein-rich fluid in the small ductules is the earliest
detectable change.
E) No. This answer is true in connection with CHRONIC pancreatitis, although there it
is a late complication not an early one.

Q63.
All of the following are characteristic of acquired lactase deficiency except:
A) True. A lactase deficiency means just that, a deficiency of lactase, usually at the
mRNA and protein levels and thus a low enzyme activity too. However, in a small
number of patients the defect is in transport and glycosylation of lactase.
B) True. The malabsorbed lactose sugar remains in the gut lumen where it is osmotically
active and draws water and electrolytes into the lumen (watery stool). In the colon, the
sugars are metabolized by bacteria to short chain fatty acids (cause low stool pH), and CO2 and H2 (cause bloating and gas). This is true for the acquired and congenital
deficiencies.
C) True. Lactase deficiency commonly has the GI symptoms of diarrhea, gas, and
bloating see B) above.
D) True. See B) above.
E) False. Mucosal architecture is not changed in any of the brush border
oligosaccharidase (lactase, maltase, sucrase-isomaltase) deficiencies or transport protein
abnormalities (glucose and galactose by SGLT1=Na-dependent cotransporter or fructose
by GLUT5=facilitative glucose transporter). Also, fat and protein absorption are also
normal in these disorders.

Q64.
Which of the following statements regarding small intestinal bacterial overgrowth is
true?
A) True. AKA blind loop syndrome where a primarily colonic flora is established in
the small intestine due to local stasis of recirculation of luminal contents (ie afferent loop
dysfunction following gastrojejunostomy, jejunal diverticula, stricture, or enterocolonic
fistula associated with Crohns disease, or motor abnormalities as in scleroderma or
diabetes). In these states, bile salts are deconjugated and hydroxylated in the jejunum by
bacteria, and in this form the salts can be rapidly reabsorbed across the epithelium of the
proximal gut. This decreases the bile salt concentration which if it falls below the critical
micellar concentration (CMC), will result in fat malabsorption.
B) False. Colonic-type bacteria do not affect pancreatic lipases. However, colonic-type
bacteria can damage brush border oligosaccharidases leading to carbohydrate
malabsorption.
C) False. As explained in B) above, sugar absorption is often affected by small intenstine
bacterial overgrowths.
D) False. As explained in A) above, if the bile salt concentration falls below the CMC,
then there will be some fat malabsorption (fat absorption does not necessarily require
micelle formation, therefore bile salt resorption-related fat malabsorption is not as bad as
pancreatic lipase insufficiency), and considerable fat-soluble vitamin (A, D, E, K)
malabsorption which requires miscelle formation. Patients impaired miscelle formation
present with steatorrhea and clinical manifestations of fat-soluble vitamin deficiency, and
sometimes watery diarrhea.
E) False. Well, technically the cobalamin (water-soluble and AKA vitamin B12)
absorption machinery is normal (I think), but there isnt much cobalamin substrate there
to absorb. Colonic-type bacteria in the small intestine (especially the anaerobes) use up
cobalamin and produce folate, resulting in cobalamin deficiency and normal or elevated
folate serum levels. Cobalamin deficiencies can also be caused by dietary deficiencies
(rare, since its found in all animal products) and malabsorption due to lack of intrinsic
factor (which binds cobalamin and the complex is taken up by ileal cells via a receptor-
mediated mechanism). Pernicious anemia is the most frequent cause of lack of IF (rarely
by hereditary deficit of IF secretion, more commonly pernicious anemia is caused by
chronic atrophic gastritis). Adult-onset pernicious anemia is thought to be a familial
autoimmune disorder characterized by autoantibodies to IF (50% of patients with
cobalamin malabsorption) and to parietal cells (90%). Food-cobalamin malabsorption is caused by a lack of gastric acid required to free cobalamin from proteins in food. The
fish tapeworm Diphyllobothrium latum also consumes cobalamin and can cause a
deficiency. Inflammation or infiltrative disease of the ileum (sprue, ileitis) can also
interfere with absorption and lead to deficiency. Abnormal IF, abnormal receptor that
binds the IF-cobalamin complex, abnormal or lack of transcobalamin II (plasma protein
that delivers cobalamin to tissues) can all lead to cobalamin deficiency states. Finally,
nitrous oxide abuse inactivates cobalamin and can give symptoms of cobalamin
deficiency (crazy dentists). The causes of cobalamin deficiency can be teased out with
the Shilling test (see table 3, page 140 and the other tables that follow). The symptoms of
cobalamin deficiency can be any combination of red cell macrocytosis, anemia, glossitis,
and nervous system damage.

Q65.
Answer is C
In long-standing cirrhosis, the hepatic sinsuoidal endothelium loses its porosity, a
process called capillarization. p. 53 syllabus. (addresses answer a)
In cirrhosis, types I and III collagen and other components of the extracellular matrix are
deposited in all portions of the lobule and sinusoidal endothelial cells lose their
fenestrations. p. 599 Robbins (addresses answers b and e)
couldnt find anything about the increased sensitivity to vasoconstrictors or NO
production.

Q66.
Answer is D
underfill theory see pp53-54. states that renal sodium retenion is secondary to ascites
formation. As the ascites form, the effective vascular volume decreases which leads to
the releas of hormonal and neural factors which induce renal tubules to reabsorb more
sodium.

Q67.
Answer is D.
The increased intrahepatic portal hypertension leads to an increase in the amount of fluid
that extravasates from the sinusoids and into the space of Disse and enters the hepatic
lymphatics. The endothelial lining in the hepatic sinusoids is highly permeable to protein no protein oncotic pressure. But as portal pressure increases, there is not only increased extravasation of fluid from hepatic lymphatics into the peritoneal space but
fluid also begins to extravasate out of the splanchnic capillaries into the peritoneal space.
This fluid is protein free b/c the splanchnic capillaries possess a tight endothelium which
is impermeable to proteins. Ultimately, the protein concentration of the plasma will be
greater than that of the ascitic fluid. (see p. 53 of syllabus)

Q68.
Answer is B.
see p. 57-60 of syllabus. A variety of animal experiments point to an increase in
GABA-ergic tone in HE. Also, the BzR modulates channel activation by GABA. Its occupation by and agonist increases the frequency of channel openings and increases the
affinity of the GABA receptor for GABA. The result is greater post-synaptic inhibition.
The EEG changes are nonspecific see a generalized slowing, aberrant rhythms and
decreased wave amplitude.

Q69.
Answer is D.
Although the question gives us a red herring with Iranian Jewish, this is not a case of
Dubin-Johnson syndrome. If it were, we would see conjugated hyperbilirubinemia, but
instead, we see unconjugated (indirect) bilirubin levels elevated. In Gilberts disease,
there is an elevation fo serum unconjugated bilirubin. The liver is otherwise unimpaired
and there are no clinical consequences. Gilberts disease is caused by an combination of
decreased bilirubin uptake by liver cells and decreased activity of UGT1. Gilberts
disease is exacerbated by stress, fasting, and infection. If the patient had hepatitis, we
would see elevations in AST and ALT.

Q70.
Again, if this were a case of acute hepatitis, we would most likely see janudice. The Anti-
HBc just tells us she has had hep B but not that it is currently a problem. She clearly
drinks enough to cause alcoholic liver disease and this is what she has. Could be due to a
recent heavy bout see p. 614 in robbins.

Q71.
[A]
I am assuming that the question wants us to assume that the
bilirubin and the radioactive carbon were both used for hemoglobin
synthesis <which doesnt really make any sense but oh well>. In in
effective erythropoiesis one expects at least two peaks...one or
more when the red blood cells are being destroyed prematurely in
the bone marrow [so Peak 1 at day 10], and the second peak when the
RBCs that made it out of the bone marrow finally expire 120 days
later.
The other disorders shouldnrt really cause a peak but more of a
build up and flattening of the graph at a maximum since in B - E
one has bile build up in the blood that has no means of excretion
except a little via the urine. In ineffective erythropoesis the the
clearance of the bilirubin is fine its just that its production is
greater than its excretion. This is all my hypothesis...then again
this may all just be bullshit.

Q72.
[C]
Bilirubin derives from the metabolism of Hememoglobin. In the
reticuloendothelial system especially in the spleen, Old RBCs
(usually on their 120 day birthday) get destroyed. The hemoglobin
is catabolized to form an Fe2+ ion, a carbon monoxide molecule, and a linear molecule called BILIVERDIN. Biliverdin is then reduced by
biliverdin reductase to from (unconjugated) Bilirubin which is then
transported into the blood, bound to albumin (as it is insoluble)
and transported to the hepatocytes where they are transported into
the liver for conjugation to glucoronides.

Q73.
[B]
Scleroderma is a potential cause of Gastro esophageal reflux
disease. It is a systemic autoimmune disease that also affects
visceral organs. Its effects on the LES results in a reduction in
its basal tone thus lowering the LES pressure. The decreased LES
can result in Gastro esophageal reflux which clinically presents as
Heart Burn.

Q74.
[A]
Achalasia is the persistent contraction of the LES and absence of
esophageal peristalsis leading to dilation of the esophagus. It is
caused by a loss of ganglion cells in the myenteric plexus which
leads to the progressive dilation of the esophagus. The myenteric
plexus may also be destroyed in Chaga's disease caused by
Trypanosoma Cruzi. Is characterized clinically by difficulty
swallowing. So options B, C, and D involving peristalsis are wrong.

Q75.
[B]
ok, this is not a great question. GERD is associated with an
increased risk of Barrett esophagus (defined as columnar metaplasia
of the lower esophageal squamous epithelium). The LES pressure may
also be decreased (eg scleroderma), Some individuals develop
strictures; is often precipitated by assuming the recumbent
position; is associated with excessive alcohol use; pregnancy
(increased abdominal pressure).

Q76.
[D]
True Esophageal dysphagia is usually described as food sticking in
the chest as in the case of mechanical obstruction of the esophagus
or a motility disorder (eg. achalasia or esophageal strictures).
Compare this to Oropharyngeal dysphagia [syllabus pg 93].

Q83.
Enterokinase (enteropeptidase) deficiency is associated with impaired protein
absorption (C) in infants. Enterokinase is a brush-border protein released into the
intestinal lumen responsible for initially converting trypsinogen to trypsin. Trypsin then activates more peptidases. The disease manifests in infants with diarrhea, growth
retardation, and hypoproteinemic edema. Contrast with Cystinuria (cysteine uptake
defect) and Hartnup disease (defect in neutral aa uptake) which do not cause protein
malabsorption.


Pharm :

Q84.
Misoprostol is recommended for preventing Gastric Ulcers in patients on chronic
NSAID therapy. NSAIDS block prostagladin synthesis. Prostaglandins (E2 and I2)
decrease acid secretion in the stomach. Misoprostol is a synthetic PGE1 derivative, and
can be used to prevent gastric ulcers in chronic NSAID users. It binds EP3 receptors (like
E2 and I2 apparently). There is also a small effect on superficial epithelial cells, where
prostaglandins increase mucin and HCO3- production.

Q85.
Omperazole is an (H+/K+ ATPase) proton pump inhibitor, and hence blocks H+
secretion by parietal cells. In addition to antibiotics (for H. pylori), it is used to heal
duodenal ulcers. Its not a pain medication, however, has high rates of duodenal ulcer
healing. Hence (A) should be correct, and (B) incorrect.

Q86.
Acid secretion by parietal cells is stimulated by vagal tone, histamine binding to H2
parietal cell receptors, gastrin . Acid secretion is inhibited by H2 blockers (like
Cimetadine) and prostaglandins binding to prostaglandin receptors. All of the statements
listed are correct so the answer is all of the above (E).

Q87.
Pirenzipine is a muscarinic blocker and hence has atropine like effects. The muscarinic
blockers can inhibit H+ secretion by parietal cells, due to vagal like block (A). They can
also delay gastric emptying time and allow antacids to work longer (B). Hence the
answer is A & B == (C).

Q88.
Sucralfate is a non-absorbable aluminum salt of sucrose octasulfate. It is not an anti-
coagulant. It has high affinity for ulcerated mucosa and forms a polysacchride like
polymer gel (D). Also, in acid environment it complexes with proteins and inhibits
digestion by pepsin. Hence it protects the mucosa from pepsin and acid, promoting
healing of acute ulcers due to ethanol or aspirin.

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