Far Eastern University – Nicanor Reyes Medical Foundation
PATHO BCA: RBC, GI, LIVER AND HEPATOBILIARY SYTEM
Ivy Marie M. Viola-Cruz, MD, DPSP
1. 1. An 8-month old female was brought in for consult due to
progressive abdominal enlargement. Upon PE, she was noted
to be pale. Hepatosplenomegaly, frontal & parietal bossing
were likewise noted. Laboratory work up showed hgb of 5
g/dL and markedly hypochromic erythrocytes with marked
anisocytosis and poikilocytosis. What is the possible
genotype of the patient?
a. -/𝛂 𝛂/𝛂
b. -/- 𝛂/𝛂
c. 𝛃+/𝛃
d. 𝛃+ /𝛃o
2. 2. A 40-year-old G3P2 39 weeks AOG was admitted for
elective repeat caesarean section. She is hypertensive & is
maintained on methyldopa 500 mg BID since 24th week
AOG. Lab workup showed microcytic hypochromic anemia,
hgb 8.0 g/ dL, reticulocyte production index of 2.9. A healthy
female newborn with Apgar scores of 9 and 10 at the 1st &
5th minutes, respectively, was delivered. The neonate also
had unremarkable PE findings. A few hours after delivery, the
mother’s hemoglobin level decreased to 7 g/dL. No signs of
hemorrhage from the surgical field was noted. The
hemoglobin further decreased to 6 g/dL after 2 days. The
mother and neonate’s blood type were both “O” positive.
What type of antibody could have caused the patient’s
condition?
a. IgD
b. IgG
c. IgM
d. IgE
RATIO: The patient has warm antibody type immunohemolytic
anemia which is likely caused by methyldopa (tolerance- breaking
drug). Warm antibody type IHA is caused by IgG & IgA (less
common).
PATHOLOGY BCA: RBC, GI, LIVER, AND
HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ)
3. Which of these condition/s confer/s protection against
malarial infection?
a. G6PD Deficiency
b. Sickle Cell Disease
c. Thalassemia
d. A and B only
e. B and C only
f. All of the above
RATIO: Two variants, G6PD- & G6PD Mediterranean have high
frequencies in American blacks and Middle easterns, respectively.
They are believed to stem from a protective effect against
Plasmodium falciparum malaria. p.634
• In certain populations in Africa, the prevalence of
heterozygosity is as high as 30%. This high frequency
stems from protection afforded by HbS against
falciparum malaria. Population studies have shown that
the sickle cell hemoglobin mutation has arisen
independently at least 6x in areas in which falciparum
malaria is endemic. p.635
• Thalassemia syndromes are endemic in the
Mediterranean basin, as well as the Middle East, tropical
Africa, the Indian subcontinent, and Asia, and in
aggregate are among the most common inherited
disorders of humans. As with sickle cell disease & other
common inherited red cell disorders, their prevalence
seems to be explained by protection they afford
heterozygous carriers against malaria. p.638
4. 4. A 9 year old boy was brought for consult due to yellowish
discoloration of the skin associated with abdominal
enlargement. Upon PE, he was also noted to have pale
palpebral conjunctivae. Laboratory workup showed
decreased hemoglobin levels, hyperchromatic RBCs
lacking the central pallor, polychromatophilic RBCs, low
platelet count and splenomegaly. Anemia in this patient can
be corrected by:
a. Iron supplementation
b. Frequent blood transfusion
c. Splenectomy
d. Hematopoietic Stem Cell Transplantation
RATIO: The symptoms presented by the patient are consistent
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 with Hereditary Spherocytosis. Mutations most commonly affect
ankyrin, band 3, spectrin, or band 4.2, which are proteins involved
in stabilizing the lipid bilayer. In effect, as RBCs age, they shed
fragments of the plasma membrane and they assume the smallest
possible diameter for a given volume (sphere). Because of the
spherical shape & reduced deformability, they are trapped in
splenic cords and become easy prey to macrophages.
Splenectomy proves to be of benefit in correcting the anemia.
However, spherocytes in the peripheral blood persist. p.632-633
5. A 13-year-old female was brought in for consult due to pallor
and tea-colored urine. She sought consult 3 days ago
complaining of dysuria and was given nitrofurantion.
Laboratory workup showed normocytic anemia, elevated
bilirubin and peripheral blood smear showed Heinz bodies &
bite cells. What is the mechanism of hemolysis?
a. Enzyme deficiency
b. Structurally abnormal globins
c. Antibody-mediated destruction
d. Acquired genetic defects
RATIO: The patient had and episode of hemolysis due to exposure
to an oxidant drug (nitrofurantoin).
• Heinz bodies are dark inclusions within red cells which
are from denatured globin chains. As the RBCs with
Heinz bodies pass through the splenic cords,
macrophages pluck out the Heinz bodies giving rise to
spherocytes & bit cells. p.634
6. A 25-year-old female came in for consult due to
undocumented fever, cough and chest pain. History revealed
a hereditary hematologic condition. Chest x-ray showed
pulmonary infiltrates. Peripheral blood smear showed RBCs
with a holly-leaf shape and some having round, dark purple
inclusions which are peripherally located. The genetic basis
of the patient’s hematologic condition is a point mutation in
the 6th codon of 𝛃-globin leading to replacement of:
a. glutamine with valine
b. glutamine with lysine
c. valine with glutamine
d. lysine with glutamine
RATIO: The patient’s presentation is consistent with Acute chest
syndrome seen in patients with sickle cell disease. It is a
dangerous type of vaso-occlusive crisis involving the lungs.
• Sickle cell disease is caused by a point mutation in the
6th codon of B-globin that leads to the replacement of a
glutamate residue with a valine residue. p.635
7. Which of the following features differentiate anemia due to
vitamin B12 deficiency from folic acid deficiency?
a. Increased homocysteine level
b. Presence of neurologic changes
PATHOLOGY BCA: RBC, GI, LIVER, AND
HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ)
c. Nuclear hypersegmentation of neutrophils
d. Marrow hyperplasia
RATIO: The megaloblastic anemia that results from a deficiency of
folic acid is identical to that encountered in vitamin B12
deficiency. Thus, the diagnosis of folate deficiency can be made
only by demonstration of decreased folate levels in the serum or
red cells. As in vitamin B12 deficiency, serum homocysteine levels
are increased, but methylmalonate concentrations are normal.
Importantly, neurologic changes do not occur. p.634
8. This is an unusual form of disseminated intravacular
coagulation which occurs in patients with giant
hemangiomas, wherein thrombi form within the neoplasm
because of stasis and recurrent trauma to fragile blood
vessels.
a. Gaisbock syndrome
b. Kasabach-Merritt Syndrome
c. Waterhouse-Friderichsen Syndrome
d. Bernard-Soulier Syndrome
RATIO: Gaisbock syndrome - obscure condition of unknown
etiology wherein affected individuals are usually hypertensive,
obese and anxious; aka stress polycythemia p.656
• KASABACH-MERRITT SYNDROME - p.664
• Waterhouse-Friderichsen syndrome - massive adrenal
hemorrhages in meningococcemia p.664
• Bernard Soulier syndrome - inherited deficiency of the
platelet membrane glycoprotein complex Ib-IX p.660
9. A 50-year-old female presents with joint pains, purpuric rash
in her lower extremities, colicky abdominal pain. She
reported a recent history of upper respiratory tract infection
for which she was prescribed with unrecalled antibiotics.
Urinalysis showed microscopic hematuria. The pathogenesis
of this disease is:
a. Mutations in genes regulating TGF-B signaling
b. Accumulation and deposition of abnormal protein
c. Deposition of circulating immune complexes
d. Defective collagen synthesis
RATIO: The patient’s clinical manifestation is consistent with
Henoch-Schonlein purpura. It is a systemic immune disorder of
unknown cause characterized by a purpuric rash, colicky
abdominal pain, polyarthralgia, and acute glomerulonephritis. All
these changes result from the deposition of circulating immune
complexes within the vessels throughout the body and within the
glomerular and mesangial regions. p.657
10. Deficiency with ADAMTS13 is associated with
a. Hemolytic Uremic Syndrome
typical” HUS - strongly associated with gastroenteritis
caused by E. coli O157:H7
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 “atypical” HUS - associated with defects in complement
factor H, membrane cofactor protein (CD46), or factor I,
three proteins that normally act to prevent excessive
activation of the alternate C’ pathway.
b. Immune Thrombocytopenic Purpura - caused by
autoantibodies to platelets
c. Glazmann Thrombasthenia - defective platelet
aggregation due to deficiency or dysfunction of
glycoproetin IIb-IIIa
d. Thrombotic Thrombocytopenic Purpura - deficiency in
plasma enzyme ADAMTS13 aka vWF metalloproteinase
which normally degrades very high molecular weight
multimers of vWF. In its absence, these multimers
accumulate in plasma & tend to promote platelet
activation & aggregation.
11. A 50-year-old male who underwent partial hepatectomy and
had thrombocytopenia was transfused with 6 units of
platelet concentrate. During transfusion, he suddenly
developed difficulty of breathing. His BP dropped to 80/50, T
38.1C and O2 saturation of 88%. What is the cause of the
patient’s condition?
a. IgM antibodies against donor red cells
b. IgA deficiency
c. Antibodies against MHC class I antigens
d. Bacterial contamination
RATIO: The patient developed Transfusion-Related Acute Lung
Injury (TRALI) which is a severe, frequently fatal complication
wherein factors in a transfused blood product trigger activation
of neutrophils in the lung microvasculature. Antibodies in the
transfused blood product recognize antigens expressed on
neutrophils. The most common antibodies associated with TRALI
are those that bind major histocompatibility complex antigens,
particularly MHC class I antigens. p.666
12. A 3-year-old boy was brought to the ER for persistent
bleeding of a lacerated wound in his mouth incurred after a
fall about 5 hours ago. He is currently given antibiotics for
otitis media. There was no history of hematomas or bruising.
There is also no known of family history of bleeding
disorders. PE revealed 2 small lacerations in the oral mucosa.
Laboratory results showed normal platelet counts, normal PT
and slightly prolonged PTT. What is the most likely diagnosis?
a. Hemophilia A
b. Hemophilia B
c. Von Willebrand Disease
d. Drug-Induced Thrombocytopenia
RATIO: Von Willebrand disease presents with mild bleeding
tendency. The most common presenting symptoms are
spontaneous bleeding from mucous membranes, excessive
bleeding from wounds, or menorrhagia.
PATHOLOGY BCA: RBC, GI, LIVER, AND
HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ)
• Patients with VWD have defects in platelet function
despite a normal platelet count. vWF stabilizes factor
VIII, a deficiency of vWF gives rise to a secondary
decrease in factor VIII levels which may be reflected as
prolongation of PTT. p.662
13. All are characteristic features of Plummer-Vinson syndrome,
except:
a. Glossitis
b. Cheilosis
c. Iron deficiency anemia
d. Esophageal rings
RATIO: In the upper esophagus, webs may be accompanied by
iron deficiency anemia, glossitis, & cheilosis as part of the
Paterson-Brown-Kelly or Plummer-Vinson syndrome. p. 753
14. All of these serve as risk factors for developing esophageal
adenocarcinoma, EXCEPT
a. Helicobacter pylori infection
b. Smoking
c. Radiation exposure
d. Gastroesophageal reflux
RATIO: Some serotypes of H. pylori are associated with decreased
risk of esophageal adenocarcinoma, because they cause gastric
atrophy which in turn leads to reduced acid secretion and reflux,
and reduced incidence of Barrett esophagus. Thus, reduced rates
of H. pylori infection may also be a factor in the increasing
incidence of esophageal adenocarcinoma. p.758
15. A 28-year-old male African who is fond of consuming mursik
developed difficulty of swallowing. An exophytic mass was
noted in the esophagus. Biopsy revealed a malignant
neoplasm composed of nests of tumor cells with abundant
eosinophilic cytoplasm and large nuclei. This tumor is most
commonly located at the of the esophagus
a. Proximal third
b. Middle third
c. Distal third
d. No specific predilection
RATIO: The patient has esophageal squamous cell carcinoma. Risk
factors include alcohol & tobacco use, poverty, caustic
esophageal injury, achalasia, tylosis, Plummer-Vinson syndrome,
diets deficient in fruits or vegetables, and frequent consumption
of very hot beverages. Previous radiation to the mediastinum also
predisposes to the development of esophageas carcinoma.
• A pocket of extremely high esophageal SCCA incidence
in western Kenya includes patients younger than 30
years old and has been linked to consumption of a
traditional fermented milk, termed mursik, which
contains the carcinogen acetaldehyde.
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 • Half of SCCA occur in the middle 3rd of the esophagus,
in contrast to adenocarcinomas which usually occur in
the distal 3rd. p.758-760

16. A 30-year-old female patient sought consult due to

generalized dull headaches of moderate intensity which was
worse in the morning. Other symptoms reported by the
patient include blurring of vision and sharp epigastric pain.
Cranial CT scan revealed a spherical, dural-based mass in the
frontal region, most likely a meningioma. The epigastric pain
felt by the patient is due to
a. Stress ulcers - most common in individuals with shock,
sepsis or severe trauma
b. Cushing ulcers - ulcers that arise in persons with
intracranial disease; high incidence of perforation
c. Curling ulcers - associated with severe burns or trauma;
occurs in the proximal duodenum p.762
19. A 60-year-old female who was previously diagnosed with
17. A 73-year-old female was brought for consult due to pallor
Hashimoto’s thryoiditis came in for consult due to tingling
and easy fatigability. CBC showed low hemoglobin and
sensation and numbness in her distal extremities. Upon PE,
decreased RBC count. Fecal occult blood test was positive.
she was noted to have pallor and a smooth, beefy
She underwent endoscopy which revealed a characteristic
red tongue. Serologic tests reveal the presence of
“watermelon stomach”. This condition is called:
autoantibodies against H+,K+-ATPase. What do you expect
a. Autoimmune gastritis
to see in the gastric biopsy of this patient?
b. Dieulafoy lesion
a. Diffuse mucosal damage of the oxyntic mucosa within
c. Helicobacter pylori gastritis
the body and fundus. (AUTOIMMUNE GASTRITIS)
d. Gastric antral vascular ectasia
b. Dense infiltrates of eosinophils in the mucosa and
muscularis layers of the antral and pyloric regions.
RATIO: GAVE is responsible for 4% of nan-variceal upper
(EOSINOPHILIC GASTRITIS)
gastrointestinal bleeding. It can be recognized endoscopically as
c. Moderate edema and slight vascular congestion in the
longitudinal stripes of edematous erythematous mucosa that
lamina propria with intact surface epithelium and
alternate with less severely injured, paler mucosa & is sometimes
foveolar cell hyperplasia. (GASTROPATHY & ACUTE
referred to as watermelon stomach. The erythematous stripes
GASTRITIS)
are created by ectatic mucosal vessels. Histologically, the antral
d. Granulation tissue filtrated with mononuclear
mucosa shows reactive gastropathy with dilated capillaries
leukocytes and fibrous scar. (PEPTIC ULCERS)
containing fibrin thrombi. p.762-763
20. Familial gastric cancers are associated with mutations in
18. All are characteristics of Helicobacter pylori gastritis, EXCEPT:
a. APC
a. Multifocal disease is associated with an increased risk
b. CDKN2A
of gastric adenocarcinoma.
c. B-catenin
b. H. pylori organisms are most often found in the antrum.
d. CDH1
c. Gastrin production is usually increased.
d. Inflammatory infiltrates consist of neutrophils &
RATIO: FAMILIAL GASTRIC CANCER is strongly associated with
subepithelial plasma cells.
germline loss-of-function mutations in the tumor suppressor
gene CDH1, which encodes the cell adhesion protein E- cadherin.
• Loss-of-function mutations in CDH1 are also present in
~50% of SPORADIC DIFFUSE GASTRIC TUMORS.
• SPORADIC INTESTINAL TYPE GASTRIC CANCERS are
strongly associated with mutations that result in
increased signaling via the Wnt pathway. These include
loss-of-function mutations in the APC tumor suppressor
gene & gain-of-function mutation in the gene encoding

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HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ) AD ASTRA PER ASPERA
 B-catenin. d. Inflammation of the mucosa and superficial submucosa
• Mutation of TP53 is also found in the majority of
SPORADIC GASTRIC CANCERS of both diffuse and
intestinal types. p.771

21. Carney triad is comprised of which of the following?

1. Pulmonary chondroma 3. Gastric GIST
2. Atrial myxoma 4. Paraganglioma
a. 1, 2 and 3
b. 1, 3 and 4
c. 2, 3 and 4
d. 1, 2 and 4

RATIO: Of the uncommon Gastrointestinal Stromal Tumors in

children, some are related to the Carney triad, a nonhereditary
syndrome of unknown etiology seen primarily in young females
that includes gastric GIST, paraganglioma, and pulmonary
chondroma. p.775

22. A caucasian male who complains of chronic diarrhea

underwent endoscopy with small intestinal biopsy.
Microscopic findings revealed dense accumulation of foamy
macrophages in the lamina propria. Macrophages contain
PAS-positive, diastase resistant granules. AFB staining
showed a negative result. What is the causative agent?
a. Clostridium difficile - pseudomembranes; surface
epithelium is denuded, superficial lamina propria
contains a dense infiltrate of neutrophils & occasional
fibrin thrombi within capillaries. Damaged crypts are
distended by a mucopurulent exudate that forms an
eruption reminiscent of a volcano.
b. Salmonella enterica - Peyers patches in the terminal
ileum enlarge into sharply delineated, plateau-like
elevations. Neutrophils accumulate in the superficial
lamina propria & macrophages containing bacteria, red
cells & nuclear debri mix with lymphocytes & plasma
cells in the lamina propria. Oval ulcers in the mucosa
oriented along the axis of the ileum that may perforate.
c. Yersinia enterocolitica - regional lymph node & Peyer 24. A colonic polyp was described to have an arborizing pattern
patch hyperplasia & bowel wall thickening. The mucosa of connective tissue, smooth muscle, lamina propria & glands
may become hemorrhagic & aphthous-like erosions & lined by normal-appearing intestinal epithelium.
ulcers may develop along with neutrophil infiltrates & a. Juvenile Polyp - dilated glands filled with mucin and
granulomas. inflammatory debri. The remainder is composed of
d. Tropheryma whippelii - Microscopic findings revealed lamina propria expanded by mixed inflammatory
dense accumulation of foamy macrophages in the infiltrates. The muscularis mucosae may be normal or
lamina propria. Macrophages contain PAS-positive, attenuated.
diastase resistant granules. AFB staining showed a b. Inflammatory Polyp - mixed inflammatory infiltrates,
negative result. erosion, and epithelial hyperplasia together with
lamina propria fibromuscular hyperplasia.
23. Features of ulcerative colitis, EXCEPT: c. Peutz-Jeghers Polyp
a. Fibrosing strictures d. Sessile Serrated Adenoma - serrated architecture
b. Skip lesions throughout the full length of the glands; lack typical
c. Broad-based ulcers cytologic features of dysplasia that are present in other

PATHOLOGY BCA: RBC, GI, LIVER, AND VISION 20|20

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HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ) AD ASTRA PER ASPERA
 adenomas.
25. What is the most important characteristic of colorectal
adenoma that correlates with the risk of malignancy?
a. Location
b. Size
c. Degree of epithelial stratification
d. Intensity of inflammation
RATIO: Although most colorectal adenomas are benign lesions, a
small proportion may harbor invasive cancer at the time of
detection. Size is the most important characteristic that
correlates with the risk of malignancy. p.808
26. Majority of sporadic colorectal adenocarcinomas have early
mutations in this gene, which is a negative regulator of B-
catenin.
a. MSH2
b. MLH1
c. BRAF
d. APC
27. A 25-year-old female was brought in the emergency
department due to a 3-day history of nausea and vomiting.
A few hours prior to consult, she also complained of
abdominal pain. Physical examination revealed generalized
jaundice and right upper quadrant abdominal tenderness. It
was later on discovered that she intentionally took 50
paracetamol tablets prior to the appearance of symptoms.
Which of the following is expected in the patient’s liver
biopsy?
a. Presence mixed inflammatory infiltrates in portal tracts
b. Fibrous septae linking portal tracts with each other and
with central veins
c. Hepatocytes containing large, round, clear vacuoles
within the cytoplasm
d. Widespread hepatocyte necrosis
RATIO: The patient is presenting with acute liver failure which
usually displays massive hepatic necrosis with broad regions of
parenchymal loss surrounding islands of regenerating
hepatocytes. Toxic injuries such as acetaminophen overdoses
usually take place within hours to days, too brief a period to allow
time for scar formation or regeneration. p.825-826
PATHOLOGY BCA: RBC, GI, LIVER, AND
HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ)
28. The dominant intrahepatic cause of portal hypertension is:
a. Massive fatty change
b. Schistosomiasis
c. Cirrhosis
d. Hepatocellular carcinoma
RATIO: The dominant intrahepatic cause is cirrhosis, accounting
for most cases of portal hypertension. Far less frequent causes
are schistosomiasis, massive fatty change, diffuse fibrosing
granulomatous disease (sarcoidosis) & diseases affecting portal
microcirculation such as nodular regenerative hyperplasia.
29. A 50-year old male came in for consult due intermittent
appearance of fever, joint pains, abdominal pains and urine
for the past 2 years. Serologic testing result revealed (-)
HBsAg, (+) Anti-HBs, (+) HCV RNA. Which of the following
is/are possible histopathologic finding/s in the liver biopsy?
a. Lymhpoid follicles
b. Steatosis
c. Ground glass hepatocytes
d. A and B only
e. All of the above
RATIO: Morphologic changes in acute and chronic viral hepatitis
are shared among the hepatotropic viruses and can be mimicked
by drug reactions or autoimmune hepatitis.
• Characteristic morphologic features:
• Hepatitis A - mononuclear inflammatory cells
rich in PLASMA CELLS
• Hepatitis B - ground glass hepatocytes (cells
with ER swollen by HBsAg) - diagnostic
hallmark
• Hepatitis C - lymphoid aggregates or fully
formed lymphoid follicles; genotype 3 shows
fatty change of scattered hepatocytes
30. Persistence of which of these markers indicate continued
viral replication, infectivity & probably progression to chronic
hepatitis?
a. HBV-DNA
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 b. DNA polymerase
c. HBcAg
d. HBeAg
RATIO: HBeAg, HBV-DNA & DNA polymerase appear in the serum
soon after HBsAg & all signify active viral replication.
• Persistence of HBeAg is an important indicator of
continued viral replication, infectivity and probable
progression to chronic hepatitis. p.833
31. Mallory-Denk bodies can be seen in which of the following
conditions?
a. Alcoholic liver disease
b. Wilson disease
c. Large bile duct obstruction
d. A and B only
e. All of the above
RATIO: Mallory-Denk bodies are usually present as clumped,
amorphous, eosinophilic material in ballooned hepatocytes. They
are made up of tangled skeins of intermediate filaments such as
keratin 8 & 18 in complex with other proteins such as ubiquitin.
These are a characteristic BUT NOT SPECIFIC feature of alcoholic
liver disease, since they are also present in NAFLD & periportal
distributions in Wilson disease and chronic biliary tract diseases.
p.843
32. An individual who has an HFE gene mutation may present
with all of the following clinical features, EXCEPT:
a. Skin pigmentation in sun exposed areas
b. Diabetes mellitus
c. Kayser-Fleischer rings
d. Cardiac dysfunction
RATIO: Hereditary Hemochromatosis
• mutation in HFE gene
• Iron accumulation
• hepatomegaly, abdominal pain, abnormal skin
pigmentation (esp in sun- exposed areas), deranged
glucose homeostasis or DM due to destruction of
pancreatic islets, cardiac dysfunction (arrhythmias,
cardiomyopathy) & atypical arthritis
Wilson disease
• mutation in ATP7B
• Copper accumulation
• Acute or chronic liver disease, neurologic involvment
presenting as movement disorders or rigid dystonia,
psychiatric symptoms, hemolytic anemia
33. All of the following are changes seen in alcoholic liver
disease, EXCEPT:
a. Hepatocytes with swelling and necrosis.
b. Ballooned hepatocytes containing Mallory-Denk
PATHOLOGY BCA: RBC, GI, LIVER, AND
HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ)
bodies.
c. Fibrous scars surrounding individual or small clusters of
hepatocytes.
d. Accumulation of mononuclear cells around
degenerating hepatocytes.
RATIO: Alcoholic Hepatitis is characterized by hepatocyte swelling
and necrosis, Mallory-Denk bodies and neutrophilic reaction.
Alcoholic steatofibrosis begins with sclerosis of central veins
spreading outward, encircling individual or small clusters of
hepatocytes in a chickenwire pattern. With continuous alcohol
use, the scarring leads to a classic micronodular or Laennec
cirrhosis. p.843
34. This disease is caused by absent UGT1A1 activity and is
associated with unconjugated hyperbilirubinemia.
a. Crigler-Najjar syndrome type I
b. Gilbert syndrome
c. Crigler-Najjar syndrome type II
d. Dubin-Johnson syndrome
35. A liver biopsy showed inflammation of large ducts and
circumferential “onion skin” fibrosis of the smaller ducts.
a. Primary hepatolithiasis - pigmented calcium
bilirubinate stones in distended intrahepatic bile ducts.
Ducts show chronic inflammation, mural fibrosis, and
peribiliary gland hyperplasia in the absence of
extrahepatic duct obstruction.
b. Primary sclerosing cholangitis
c. Primary biliary cirrhosis - interlobular bile ducts are
actively destroyed by lymphoplasmacytic inflammation
with or without granulomas.
d. Biliary atresia - inflammation and fibrosing stricture of
the hepatic or common bile ducts
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 RATIO: PREECLAMPSIA is characterized by maternal
hypertension, proteinuria, peripheral edema and coagulation
abdnormalities.
• When hyperreflexia and convulsions occur, the
condition is called ECLAMPSIA

39. A 30-year-old male patient underwent excision biopsy of a

hepatic mass which grossly appears tan-yellow with a central
gray-white stellate scar. The lesion is most likely a
a. Hepatocellular adenoma
b. Focal nodular hyperplasia
c. Hepatocellular carcinoma
d. Angiosarcoma
36. Classic triad of Budd-Chiari syndrome, except:
a. Jaundice
RATIO: FNH appears as a well-demarcated but poorly
b. Liver enlargement
encapsulated nodule. The lesion is generally lighter than the
c. Pain
surrounding liver and is sometimes yellow indicating steatosis.
d. Ascites
Typically, there is a CENTRAL GRAY WHITE, DEPRESSED STELLATE
SCAR from which fibrous septa radiate to the periphery.
RATIO: The obstruction of two or more major hepatic veins
• The central scar contains large vessels, usually arterial,
produces liver enlargement, pain and ascites, a condition known
that typically show fibromuscular hyperplasia with
as Budd-Chiari syndrome. p.863
eccentric or concentric narrowing of the lumen. p.867
37. Kasai procedure is warranted in a patient who presents with
40. What is the most common malignancy of the liver?
this histomorphologic findings in a liver biopsy.
a. Angiosarcoma
a. Inflammation and fibrosing stricture of the hepatic or
b. Hepatocellular carcinoma
common bile ducts.
c. Cholangiocarcinoma
b. Hepatic lobular disarray with focal liver cell apoptosis
d. Metastatic neoplasm
and necrosis, giant-cell transformation, prominent
hepatocellular and canalicular cholestasis and mild
RATIO: Malignant tumors in the liver can be primary or
mononuclear portal inflammation.
metastatic. Most primary liver cancers arise from hepatocytes
c. Acute and chronic inflammation of large ducts with
and are termed hepatocellular carcinoma. Much less common are
minimal inflammation and circumferential “onion
carcinomas of bile duct origin, cholangiocarcinomas. p.869
skin” fibrosis of small ducts.
• Involvement of the liver by metastastic malignancy is far
d. Pigmented calcium bilirubinate stones in distended
more common than primary hepatic neoplasia. p. 875
intrahepatic bile ducts.

41. This is associated with increased incidence of associated

RATIO: Salient features of biliary atresia include inflammation and
cancer.
fibrosing stricture of the hepatic and common bile ducts. There is
a. Hydrops of the gallbladder
considerable variability in the anatomy of biliary atresia. When
b. Porcelain gallbladder
the disease is limited to the common duct (type I) or right and/or
c. Xanthogranulomatous cholecystitis
left hepatic bile ducts (type Ii), the disease is surgically correctable
d. Gangrenous cholecystitis
(Kasai procedure). Unfortunately, 90% of patients have type III
biliary atresia in which there is also obstruction of bile ducts at or
RATIO: Excessive dystrophic calcification within the gallbladder
above the porta hepatis. These cases are not correctable, since
wall may yield a porcelain gallbladder, notable for a markedly
there are no patent bile ducts amenable to surgical anastomosis.
increased incidence of associated cancer. p.879
p.857-858

38. All of the following are features of preeclampsia, EXCEPT:

a. BP = 160/100
b. Knee jerk reflex ++++
c. Platelet count = 110 x 109/L
d. Urine Protein ++
Notes from Lecture PPT only.

PATHOLOGY BCA: RBC, GI, LIVER, AND VISION 20|20

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HEPATOBILIARY SYSTEM (DR. VIOLA-CRUZ) AD ASTRA PER ASPERA