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PATHOLOGY FINAL TEST - Complete Answers & Explanations

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FINAL TEST (University of East Sarajevo, Faculty of Medicine in Foca)

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Q1. Which of the following terms is a "group name" for changes...

• A. Atherosclerosis - specific type: large-artery intimal lipid plaque disease
• B. Arteriolosclerosis - specific type: small artery/arteriole wall thickening
• C. Arteriosclerosis ✅ - the broad group name encompassing all forms of arterial hardening/thickening
• D. Monckeberg's medial calcific sclerosis - specific type: calcification of tunica media in medium arteries

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Q2. Obliterative endarteritis is caused by (1):

• A. Malignant hypertension - causes fibrinoid necrosis of arterioles/hyperplastic arteriolosclerosis
• B. HIV virus - causes vasculitis but not the classic obliterative endarteritis pattern
• C. Treponema pallidum ✅ - syphilis causes endarteritis obliterans (proliferation of endothelial cells obliterating the lumen) - a hallmark of syphilitic vasculitis
• D. Thorotrast - causes hepatic angiosarcoma (radioactive contrast)
• E. ANCA - causes necrotizing vasculitis (Wegener's, microscopic polyangiitis)

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Q3. Which syndrome/phenomenon is caused by scleroderma and systemic lupus erythematosus? (1)

• A. Reye's syndrome - mitochondrial dysfunction in children, associated with aspirin + viral illness
• B. Raynaud's phenomenon ✅ - episodic vasospasm of digits (pallor → cyanosis → redness); hallmark of both scleroderma and SLE
• C. Paraneoplastic syndrome - caused by tumors, not autoimmune connective tissue disease
• D. Sjögren's syndrome - a separate autoimmune disease itself (dry eyes/mouth)
• E. Eisenmenger's syndrome - pulmonary hypertension due to left-to-right shunt reversal

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Q4. "Jet" lesions occur in (1):

• A. Left atrium - mitral stenosis causes left atrial changes
• B. Left ventricle - aortic regurgitation jet lesions can occur here but not the classic description
• C. Right atrium ✅ - in tricuspid regurgitation, the high-velocity regurgitant jet strikes the right atrial endocardium, creating jet lesions (MacCallum's patch equivalent). Also seen in ventricular septal defect where jet hits right ventricular wall
• D. Right ventricle - possible but less classic
• E. Foramen ovale - not the classic site

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Q5. Which lymphoma forms "lymphoepithelial lesions"? (1)

• A. Follicular lymphoma - nodular growth pattern, bcl-2 rearrangement
• B. Burkitt lymphoma - high-grade B-cell, starry-sky pattern, c-MYC translocation
• C. Mantle cell lymphoma - t(11;14), cyclin D1 overexpression
• D. Extranodal marginal zone B-cell lymphoma (MALT lymphoma) ✅ - invades glandular epithelium to form lymphoepithelial lesions; associated with H. pylori (stomach), Sjögren's (salivary glands), Hashimoto's (thyroid)
• E. Mycosis fungoides - cutaneous T-cell lymphoma (Pautrier microabscesses)

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Q6. Malignant thymoma is (1):

• A. Squamous cell carcinoma ✅ - malignant thymoma is classified as thymic carcinoma; most common histological type is squamous cell carcinoma
• B. B-cell lymphoma - lymphomas of the thymus are separate entities (thymic B-cell lymphoma)
• C. T-cell lymphoma - precursor T-cell lymphoblastic lymphoma can arise in thymus
• D. Adenocarcinoma - rare in thymus
• E. Histiocytosis X - Langerhans cell histiocytosis, a different disease

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Q7. Which cells play the most important role in the pathogenesis of ARDS? (1)

• A. Mast cells - key in Type I hypersensitivity/allergy
• B. Eosinophilic granulocytes - key in allergic conditions and parasitic infections
• C. T lymphocytes - key in chronic inflammation and cell-mediated immunity
• D. Neutrophilic granulocytes ✅ - in ARDS (Acute Respiratory Distress Syndrome), activated neutrophils sequester in pulmonary capillaries, release proteases, ROS, and pro-inflammatory mediators, destroying the alveolar-capillary membrane causing diffuse alveolar damage
• E. B lymphocytes - key in antibody-mediated immunity

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Q8. Schaumann bodies are present in (1):

• A. Syphilis - obliterative endarteritis, plasma cell infiltrate
• B. Alzheimer's disease - amyloid plaques, neurofibrillary tangles
• C. Rheumatic fever - Aschoff bodies (not Schaumann bodies)
• D. Sarcoidosis ✅ - Schaumann bodies (laminated calcified concentric structures) are found inside giant cells within sarcoid granulomas. Also present: asteroid bodies
• E. Alcoholic liver disease - Mallory-Denk bodies (keratin aggregates)

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Q9. Nasopharyngeal carcinoma is caused by (1):

• A. Beta-hemolytic streptococcus - causes pharyngitis, rheumatic fever
• B. HIV - associated with certain lymphomas (EBV co-factor), Kaposi sarcoma
• C. CMV - causes mononucleosis-like illness, retinitis in immunocompromised
• D. HPV - causes cervical carcinoma, oropharyngeal cancer (base of tongue/tonsil), NOT nasopharynx
• E. EBV (Epstein-Barr virus) ✅ - strongly associated with nasopharyngeal carcinoma (especially undifferentiated type). Also causes Burkitt lymphoma and Hodgkin's lymphoma (EBV+)

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Q10. Red hepatization is seen in (1):

• A. Community-acquired atypical pneumonia - interstitial pattern, no hepatization
• B. Necrotizing pneumonia - causes cavitation, distinct from hepatization
• C. Aspiration pneumonia - lower lobe, dependent zones
• D. Nosocomial pneumonia - hospital acquired
• E. Community-acquired pneumonia ✅ - Lobar pneumonia (typically pneumococcal) classically goes through: Congestion → Red hepatization → Gray hepatization → Resolution. Red hepatization = alveoli filled with RBCs, fibrin, and neutrophils

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Q11. Which of the following is NOT a feature of malignant tumors? (2)

• A. Poor cell cohesion - IS a feature of malignant tumors (allows invasion/metastasis)
• B. Expansive growth pattern ✅ - is a feature of BENIGN tumors (they push/compress surrounding tissue rather than infiltrate). Malignant tumors grow invasively.
• C. Cellular atypia - IS a feature of malignancy
• D. High number of mitotic cells - IS a feature of malignancy
• E. Lack of tumor capsule - IS a feature of malignancy

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Q12. Bleeding tendency, incomplete formation of osteoid matrix, and delayed wound healing are consequences of deficiency in (1):

• A. Alpha-1-antitrypsin - deficiency causes emphysema and liver disease
• B. Vitamin C (Ascorbic acid) ✅ - Scurvy: Vit C is essential for collagen hydroxylation (proline/lysine hydroxylase). Deficiency causes defective collagen → bleeding (perifollicular hemorrhages, gingival bleeding), poor wound healing, and defective osteoid matrix formation
• C. One X chromosome (karyotype 45,X0) - Turner syndrome
• D. Vitamin D - causes rickets/osteomalacia (defective mineralization)
• E. Vitamin A - deficiency causes night blindness, xerophthalmia, squamous metaplasia

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Q13. Tumor stage T3N2M0 according to the TNM system means (1):

• T3 = large/locally advanced primary tumor
• N2 = multiple/bilateral regional lymph node metastases
• M0 = no distant metastases
• A. Small primary, few regional LN metas, no distant - would be T1N1M0
• B. ✅ Large primary + few regional LN metas, no distant
• C. Very large primary, few regional LN metas, no distant - closer but N2 implies more nodes
• D. Malignant unknown primary, with LN metas, no distant - would be TxN+M0
• E. Relatively large primary, multiple LN metas AND one distant - would require M1

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Q14. Which of the following diseases do NOT have an autoimmune character? (1)

• A. Systemic lupus erythematosus - autoimmune (anti-dsDNA, anti-Sm antibodies)
• B. Gout ✅ - metabolic disease (uric acid crystal deposition); not autoimmune
• C. Insulin-dependent diabetes mellitus (Type 1) - autoimmune destruction of beta cells
• D. Hashimoto thyroiditis - autoimmune (anti-TPO, anti-thyroglobulin)
• E. Rheumatoid arthritis - autoimmune (anti-CCP, RF)

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Q15. Chagas disease causes (1):

• A. Mallory-Weiss syndrome - esophageal mucosal tear from vomiting
• B. Mikulicz syndrome - bilateral salivary/lacrimal gland enlargement
• C. Hirschsprung disease - congenital absence of ganglion cells
• D. Pseudomembranous enterocolitis - C. difficile toxin
• E. Angiodysplasia - vascular malformations of GI tract

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QUIZ II (Special Pathology) Questions (Pages 5 & 13)

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Q1. Which blood vessels have elastic fibers interspersed with muscle cells in the media layer?

• a) Inferior vena cava - vein, predominantly smooth muscle and collagen
• b) Iliac arteries ✅ - muscular arteries (medium-sized) have a tunica media containing both smooth muscle AND elastic fibers interspersed = "mixed" (musculo-elastic) type
• c) Renal artery - similar muscular artery
• d) Capillaries - only endothelium + basement membrane, no media
• e) Superior vena cava - vein structure

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Q2. Diffusion of oxygen and nutrients in the capillary network is ineffective at a distance of (1):

• Oxygen diffuses effectively up to ~100 μm from capillaries. Beyond this distance, cells become hypoxic.
• a) 50 μm - too short
• b) 200 μm - too far
• c) 300 μm - too far
• d) 100 μm ✅ - the effective diffusion distance limit
• e) 6 μm - capillary wall thickness only

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Q3. Morphological changes in atherosclerotic plaques that are NOT clinically significant are (1):

• a) Rupture - clinically significant: triggers thrombosis → MI/stroke
• b) Ulceration - clinically significant: thrombosis, embolization
• c) Erosion of the intimal surface ✅ - superficial/minor erosion without deep plaque disruption is less clinically significant compared to full rupture
• d) Hemorrhage into the plaque - clinically significant: rapid plaque growth
• e) Formation of angiosarcoma - rare, but significant

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Q4. Features of Takayasu arteritis are (1):

• a) Granulomatous vasculitis of medium and small arteries - Takayasu affects large arteries (aorta and branches)
• b) Visual disturbances ✅ - occur due to involvement of carotid/vertebral arteries
• c) Tingling and claudication in the lower limbs ✅ - subclavian/aortic involvement causes upper/lower limb ischemia
• d) Increased pulse in the upper limbs - actually DECREASED/absent pulse ("pulseless disease")
• e) Vomiting - not a feature

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Q5. Kaposi's sarcoma arises (1):

• Kaposi sarcoma arises in states of immunosuppression (HIV/AIDS - CD4+ T-cell depletion, post-transplant)
• It is of vascular/lymphatic endothelial origin
• c) In states of B-cell immunosuppression - more accurately it is T-cell (CD4+) immunosuppression
• e) In the leptomeninges - not correct

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Q6. Myocardial infarction is recognized after 24 to 48 hours as an area (1):

• After 24-48 hours, the infarcted myocardium becomes a pale/white-yellow area that is firm (coagulative necrosis with beginning organization)
• a) Yellow and soft - describes later stage (days 3-7, liquefactive changes/softening)
• b) White and firm in consistency ✅ - 24-48 hours: coagulative necrosis, pale/white, firm
• c) Red-blue area due to trapped blood stasis - early congestion phase (first few hours)
• d) Red-blue area due to cardiac rupture - complication around day 5-7
• e) Green and soft - not a valid stage description

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Q7. In dilated cardiomyopathy, ineffective cardiac contraction is (1):

• Normal ejection fraction is 55-70%. In dilated cardiomyopathy (DCM), the ejection fraction is severely reduced.
• a) Greater than 25% - too nonspecific
• b) Less than 5% - incompatible with life
• c) Less than 1% - incompatible with life
• d) Less than 25% ✅ - DCM typically presents with EF < 40%, often < 25% in severe disease
• e) Greater than 10% - too broad

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Q8. Morphological features of chronic nonspecific lymphadenitis are (1):

• a) Granulomas without necrosis - sarcoid-type granulomatous lymphadenitis
• b) Presence of giant cells - granulomatous inflammation
• c) Paracortical hypoplasia - atrophy, not characteristic of reactive lymphadenitis
• d) Sinus histiocytosis ✅ - distension of lymph sinuses by histiocytes; a common feature of chronic nonspecific reactive lymphadenitis (especially in lymph nodes draining cancers)
• e) Granulomas with necrosis - caseating granulomas = TB

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Q9. Waldenström's macroglobulinemia is characterized by high concentration of (1):

• a) IgM ✅ - Waldenström's macroglobulinemia is a lymphoplasmacytic lymphoma that secretes monoclonal IgM. The large IgM pentamers cause hyperviscosity syndrome (visual disturbances, bleeding, neurological symptoms)
• b) IgE - elevated in allergic/parasitic conditions
• c) IgA - elevated in IgA myeloma or IgA nephropathy
• d) IgD - rare myeloma subtype
• e) IgF - does not exist

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Additional Test Questions (Pages 7 & 12 - different test)

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Q16. Stages of pneumonia development are (3):

• a) Congestion ✅, b) Red hepatization ✅, c) Gray hepatization ✅, d) Resolution ✅
• e) Ossification - not a normal stage

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Q17. A precancerous lesion in the lungs is (1):

• a) Lobar pneumonia - inflammatory, not precancerous
• b) Hemosiderosis - iron deposition, not precancerous
• c) Squamous metaplasia - adaptive change; itself not precancerous unless dysplastic
• d) Pneumocyte hyperplasia - reactive
• e) Squamous epithelial dysplasia ✅ - the precancerous lesion for squamous cell carcinoma of the lung (progression: metaplasia → dysplasia → carcinoma in situ → invasive carcinoma)

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Q18. Microscopically, papillary renal carcinoma (1):

• a) Forms only micropapillae ✅ - papillary RCC has true papillary architecture with fibrovascular cores
• b) The central part of papillae corresponds to fibrovascular core ✅ - this is actually correct
• c) Papillary surfaces are covered with normal urothelium - NO, covered with tumor cells (cuboidal/columnar)
• d) Does not occur in ureters - correct, it's a renal parenchymal tumor
• e) Does not occur in the urinary bladder - correct

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Q19. The presence of well-defined, developed pancreatic tissue in the gastric submucosa is an example of (1):

• a) Hamartoma - disorganized but native tissue elements in their normal location
• b) Teratoma - all 3 germ layers, typically in gonads
• c) Choristoma ✅ - normal tissue (pancreatic tissue) in an ABNORMAL LOCATION (gastric wall). This is heterotopic pancreatic tissue = choristoma (ectopic/heterotopic rest)
• d) Adenoma - benign epithelial neoplasm
• e) Papilloma - benign papillary epithelial neoplasm

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Q20. Mark what is NOT a risk factor for the intestinal type of gastric carcinoma (1):

• a) Chronic gastritis with intestinal metaplasia ✅ - IS a risk factor
• b) Pernicious anemia ✅ - This IS actually a risk factor (autoimmune gastritis causes atrophy → intestinal metaplasia → dysplasia). So the NOT-a-risk-factor answer would be something else.
• c) Occupational exposure to β-naphthylamine ✅ - this is a risk factor for BLADDER cancer, NOT gastric cancer. This is the correct answer for "NOT a risk factor" ✅
• d) H. pylori infection ✅ - major risk factor for intestinal type gastric carcinoma
• e) Diet rich in nitrite precursors ✅ - risk factor

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Q21. Mark the statements that are NOT correct (1):

• a) Prostate, breast, kidney, lung carcinomas often metastasize to bone ✅ - TRUE
• b) The axial skeleton is LESS frequently a site of metastasis than distal extremities - FALSE ✅. The axial skeleton (spine, pelvis, ribs, skull, proximal femur) is MORE commonly involved in bone metastases
• c) Rhabdomyosarcoma, neuroblastoma, Wilms tumor are most common solid malignant tumors in children ✅ - TRUE
• d) Metastases are the most common malignant bone tumors ✅ - TRUE
• e) Metastases may appear radiographically as lytic or sclerotic lesions ✅ - TRUE

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Q22. What is NOT a cause of hemosiderosis? (1):

• A. Decreased iron utilization ✅ - NOT a cause; hemosiderosis results from iron EXCESS/overload, not reduced utilization per se (though it can accompany conditions)
• B. Increased iron absorption from food - IS a cause (hereditary hemochromatosis)
• C. Frequent blood transfusions - IS a cause (transfusional hemosiderosis)
• D. Hemolytic anemia - IS a cause (excess RBC breakdown releases iron)
• E. Prolonged work in iron ore mines - IS a cause (exogenous iron inhalation/ingestion)

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Q23. Hydatidiform mole is a (1):

• A. Inflammatory lesion - no, it's a trophoblastic proliferation
• B. Metaplastic change - no
• C. Tumor - technically a gestational trophoblastic disease; complete mole has 46,XX (androgenetic)
• D. Pseudotumor ✅ - hydatidiform mole is considered a pseudotumor (abnormal but non-neoplastic proliferation of trophoblastic tissue); it mimics a tumor but represents abnormal conception
• E. Pseudocystic lesion - no

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Q24. Which tumor causes Meigs syndrome? (1):

• A. Dysgerminoma - germ cell tumor, no Meigs association
• B. Granulosa-theca cell tumor - sex cord tumor, causes estrogen excess
• C. Mucinous adenocarcinoma of the appendix - causes pseudomyxoma peritonei
• D. Thecoma-fibroma ✅ - Meigs syndrome = ovarian fibroma + ascites + right-sided pleural effusion. Caused by fibroma (or thecoma-fibroma). Benign tumor that paradoxically causes fluid accumulation.
• E. Sertoli-Leydig cell tumor - androgen-producing, causes virilization

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Q25. Apocrine metaplasia is a (1):

• A. Benign change ✅ - apocrine metaplasia (change of ductal epithelium to apocrine-type cells) in the breast is a benign, non-proliferative change with NO increased cancer risk
• B. Precancerous change - incorrect; it is NOT premalignant
• C. Malignant change - incorrect

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Q26. Lisch nodules are associated with (1):

• A. Tuberous sclerosis - causes hamartomas, "ash leaf" spots, subependymal nodules
• B. Neurofibromatosis type 1 (NF1/von Recklinghausen) ✅ - Lisch nodules are melanocytic hamartomas of the iris; pathognomonic for NF1 (along with café-au-lait spots and neurofibromas)
• C. Neurofibromatosis type 2 - causes bilateral acoustic neuromas (vestibular schwannomas)
• D. Von Hippel-Lindau disease - hemangioblastomas, renal cell carcinoma, pheochromocytoma
• E. Neurilemmoma (Schwannoma) - benign nerve sheath tumor

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Q27. The Gleason system is used for grading (1):

• A. Chronic bronchitis - graded by clinical criteria, not Gleason
• B. Renal adenocarcinoma - uses Fuhrman/ISUP grade
• C. Prostate adenocarcinoma ✅ - Gleason scoring grades prostate cancer 1-5 based on glandular architecture; two most prevalent patterns summed = Gleason score (e.g., 3+4=7). Determines prognosis and treatment.
• D. Asthma - not graded by Gleason
• E. Adrenal cortex carcinoma - uses Weiss criteria for grading

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Additional Test Questions (Pages 15-18 - Colloquium II, Systemic Pathology)

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Q1. Most common cause of myocardial infarction:

• a) Coronary artery embolism - rare cause (~5%)
• b) Coronary artery vasospasm - Prinzmetal angina, rare cause of MI
• c) Coronary artery thrombosis ✅ - >90% of MIs result from thrombosis superimposed on a ruptured/eroded atherosclerotic plaque
• d) Aortic dissection - can compromise coronary ostia but rare MI cause
• e) Viral myocarditis - causes cardiomyopathy, not typical MI

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Q2. Glomerular disease most commonly associated with nephrotic syndrome in adults:

• a) Minimal change disease - most common in CHILDREN
• b) Focal segmental glomerulosclerosis (FSGS) - most common cause of nephrotic syndrome in Black adults
• c) Membranous nephropathy ✅ - most common cause of nephrotic syndrome in WHITE adults; "spike and dome" on EM; anti-PLA2R antibodies
• d) IgA nephropathy - most common glomerulonephritis worldwide; presents as nephrITIC (hematuria)
• e) Post-streptococcal GN - nephritic syndrome, not nephrotic

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Q3. Common feature of chronic inflammation:

• a) Neutrophilic infiltration - feature of ACUTE inflammation
• b) Caseous necrosis - specific to granulomatous (TB) inflammation
• c) Granulation tissue formation ✅ - chronic inflammation is characterized by: mononuclear cell infiltrate (lymphocytes, macrophages, plasma cells), tissue destruction, and repair with granulation tissue/fibrosis/angiogenesis
• d) Edema - more prominent in acute inflammation
• e) Fibrin deposition - acute phase feature

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Q4. Most common site for atherosclerotic plaque formation:

• a) Pulmonary artery - atherosclerosis rarely affects pulmonary vessels
• b) Abdominal aorta ✅ - most severely affected site; especially below the renal arteries. Also: coronary arteries, carotid bifurcation, and popliteal arteries are high-risk areas
• c) Renal artery - affected but less common
• d) Portal vein - vein, not affected by atherosclerosis
• e) Subclavian vein - vein, not affected

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Q5. Which tumor is associated with Reed-Sternberg cells?

• a) Non-Hodgkin lymphoma - no Reed-Sternberg cells; different cell types
• b) Multiple myeloma - plasma cell neoplasm, myeloma cells not RS cells
• c) Hodgkin lymphoma ✅ - Reed-Sternberg cells are the pathognomonic giant cells of Hodgkin lymphoma; large binucleated/bilobed cells with prominent "owl-eye" nucleoli; CD15+, CD30+
• d) Chronic lymphocytic leukemia - small B lymphocytes, CD5+
• e) Burkitt lymphoma - high-grade B-cell, c-MYC translocation, starry sky

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Q6. Bacterial infection most commonly associated with peptic ulcer disease:

• a) E. coli - causes UTIs, diarrhea, not PUD
• b) Helicobacter pylori ✅ - present in ~95% of duodenal ulcers and ~70% of gastric ulcers; urease-producing, survives in gastric mucus; causes chronic gastritis → ulceration
• c) Streptococcus pyogenes - causes pharyngitis, cellulitis
• d) Salmonella typhi - typhoid fever
• e) Clostridium difficile - pseudomembranous colitis

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Q7. Most common primary malignancy of the liver:

• a) Hepatocellular carcinoma (HCC) ✅ - most common primary liver cancer; associated with cirrhosis, HBV, HCV, aflatoxin, alcohol; AFP elevated
• b) Metastatic adenocarcinoma - most common OVERALL liver malignancy (metastasis > primary), but not a PRIMARY malignancy
• c) Angiosarcoma - rare; associated with vinyl chloride, arsenic, Thorotrast
• d) Hepatoblastoma - most common in young children
• e) Cholangiocarcinoma - bile duct origin; second most common PRIMARY liver cancer

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Q8. Common complication of chronic hypertension:

• a) Renal cell carcinoma - no association with hypertension
• b) Nephrotic syndrome - caused by glomerular disease, not directly by HTN
• c) Hyaline arteriolosclerosis ✅ - long-standing benign hypertension → hyaline deposits in arteriolar walls → nephrosclerosis (benign nephrosclerosis). Arterioles develop homogeneous pink hyaline deposits
• d) Acute tubular necrosis - caused by ischemia or nephrotoxins
• e) Hydronephrosis - caused by urinary obstruction

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Q9. Colitis caused by Clostridium difficile proceeds in the form of:

• a) Interstitial colitis - not the C. diff pattern
• b) Pseudomembranous inflammation ✅ - C. difficile toxins A & B cause mucosal necrosis with formation of pseudomembranes (fibrin, necrotic debris, inflammatory cells) adherent to the colon wall = pseudomembranous colitis
• c) Granulomatous inflammation - Crohn's disease
• d) Gangrenous inflammation - ischemic colitis/volvulus
• e) Ulcerative colitis - a different disease entity

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Q10. Prostate carcinoma most frequently metastasizes to:

• a) Brain - uncommon
• b) Lungs - less common than bone
• c) Liver - can occur but less common than bone
• d) Bones ✅ - prostate carcinoma has a strong predilection for bone metastases (especially axial skeleton - vertebrae, pelvis, ribs). These are characteristically OSTEOBLASTIC (sclerotic/blastic) metastases = increased bone density on X-ray
• e) Adrenal glands - less common

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Q11. What is cervical erosion?

• a) Bacterial lesion - not caused by bacteria per se
• b) Traumatic lesion - not the definition
• c) Area with keratinized stratified squamous epithelium - this is normal ectocervical epithelium
• d) Presence of endocervical mucosa on the ectocervix ✅ - cervical erosion (ectropion) = eversion of the endocervical columnar epithelium onto the ectocervix; appears red/raw. Common in pregnancy, OCP use. The columnar epithelium of the endocervix is visible on the ectocervix.
• e) Papillary epithelial hyperplasia - not the definition

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Q12. Hyaline membrane disease in newborns occurs due to:

• a) Atelectasis - a CONSEQUENCE of surfactant deficiency, not the cause
• b) Surfactant deficiency ✅ - Hyaline membrane disease (Neonatal Respiratory Distress Syndrome) is caused by deficiency of surfactant (especially in premature infants < 37 weeks). Surfactant (mainly phosphatidylcholine/dipalmitoyl phosphatidylcholine, produced by type II pneumocytes) reduces surface tension. Without it → alveolar collapse → hyaline membranes form (fibrin + necrotic type II pneumocytes)
• c) Oxygen inhalation - oxygen toxicity is a separate problem
• d) Aspiration of amniotic fluid - aspiration pneumonia, different disease
• e) Pulmonary hemorrhage - consequence, not cause

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Q13. Appearance of a cirrhotic liver:

• a) Small and flabby - incorrect; cirrhotic liver is firm (fibrotic)
• b) Enlarged and flabby - enlarged/flabby = fatty liver (steatosis)
• c) Normal size and firm consistency - possible in early cirrhosis
• d) Firm and nodular appearance ✅ - cirrhotic liver: small (shrunken in end-stage), firm (due to fibrosis), nodular surface (regenerative nodules surrounded by fibrous bands). Classic appearance.
• e) Edematous and yellowish - more like acute hepatic failure/steatosis

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Q28. Which statement about granulomatous inflammation is NOT correct? (1)

• A. Granulomatous inflammation may lead to fibrosis and organ dysfunction ✅ - TRUE (e.g., pulmonary fibrosis in sarcoidosis/TB)
• B. Prolonged T-cell stimulation by microorganisms induces cytokine activation with granuloma formation ✅ - TRUE (IFN-γ from T-cells activates macrophages to form epithelioid cells)
• C. Granulomatous inflammation may occur in response to inert foreign bodies ✅ - TRUE (sutures, talc, silica → foreign body granulomas)
• D. Granulomas ALWAYS contain multinucleated giant cells ✅ NOT CORRECT - some granulomas (especially early or small ones) may lack giant cells. Giant cells are common but not universal.
• E. Central necrosis often develops within granulomas ✅ - TRUE in infectious granulomas (TB = caseous necrosis)

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Q29. What are the main categories of amyloidosis? (3):

• A. Hereditary amyloidoses ✅ - e.g., familial amyloid polyneuropathy (transthyretin mutations)
• B. Localized amyloidoses ✅ - deposits confined to one organ (e.g., AL amyloid in Alzheimer's plaques [Aβ], islet amyloid in Type 2 DM [IAPP])
• C. Systemic (generalized) amyloidosis ✅ - involves multiple organs (AL type in myeloma, AA type in chronic inflammation)
• D. Transthyretin amyloidosis - a specific TYPE within hereditary/systemic, not a main category
• E. AL protein amyloidosis - a specific TYPE within systemic, not a main category

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Q30. "Contraction band necrosis" occurs in (1):

• A. Myasthenia gravis - neuromuscular junction autoimmune disease
• B. Duchenne muscular dystrophy - dystrophin deficiency, causes muscle fiber necrosis but not contraction bands
• C. Myocardial infarction ✅ - contraction band necrosis (hypercontraction necrosis) occurs when previously ischemic myocardium is suddenly reperfused (reperfusion injury). Ca²⁺ floods into cells → hypercontracted sarcomeres → eosinophilic transverse "contraction bands" across muscle fibers. Also seen in catecholamine-induced myocardial injury (pheochromocytoma).
• D. Lambert-Eaton syndrome - paraneoplastic neuromuscular disease
• E. Botryoid sarcoma - rhabdomyosarcoma variant in children

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Q16. Tropheryma whipplei causes (1):

• A. Gallbladder colonization - not the disease caused
• B. Pseudomembranous colitis - C. difficile
• C. Ulcerative colitis - idiopathic IBD
• D. Malabsorption syndrome ✅ - Whipple's disease: T. whipplei infects macrophages in small intestinal lamina propria → PAS-positive macrophages stuffed with bacteria → villous blunting → malabsorption, weight loss, diarrhea, arthralgias
• E. Crohn's disease - idiopathic IBD

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Q17. "Ground-glass nuclei" of hepatocytes are seen in (1):

• A. Autoimmune hepatitis - plasma cell infiltrate, rosette formation
• B. Alcoholic liver disease - Mallory-Denk bodies, steatosis, ballooning degeneration
• C. Viral hepatitis (HBV) ✅ - "ground-glass hepatocytes" are pathognomonic for chronic HBV infection. The ground-glass appearance results from accumulation of HBsAg (surface antigen) in smooth ER. HBsAg-positive cells appear pale with finely granular cytoplasm.
• D. Wilson disease - copper deposition, Kayser-Fleischer rings
• E. Hepatocellular carcinoma - various features but not ground-glass nuclei specifically

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Q18. Characteristic of chronic inflammation (1):

• A. Replacement of damaged cells with normal tissue - this is regeneration (resolution), not inflammation per se
• B. Removal of cells and mediators of acute inflammation - resolution, not characterization of chronic
• C. Pus formation - acute inflammation (neutrophilic)
• D. Polymorphonuclear inflammatory infiltrate - acute inflammation
• E. Angiogenesis ✅ - chronic inflammation is characterized by mononuclear cell infiltrate, tissue destruction, and attempted repair including angiogenesis (new blood vessel formation) and fibrosis

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Q19. Primary effects of histamine and serotonin as inflammatory mediators (1):

• A. Activation of neutrophils - done by C5a, LTB4, IL-8
• B. Chemotaxis - done by C5a, LTB4, bacterial products
• C. Cytotoxicity with free radicals - done by macrophages/neutrophils
• D. Leukocyte activation - done by cytokines (IL-1, TNF)
• E. Vasodilation and increased vascular permeability ✅ - histamine (from mast cells/basophils/platelets) and serotonin (from platelets) cause immediate transient vasodilation + increased vascular permeability (endothelial cell contraction, gap formation) in the IMMEDIATE phase of acute inflammation

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Q20. Pyknosis, karyorrhexis, and karyolysis represent changes in the cell that occur in (1):

• A. Hydropic degeneration - cell swelling, vacuolation, reversible
• B. Apoptosis - has chromatin condensation and cell fragmentation, but karyolysis is not typical; apoptosis has pyknosis and karyorrhexis but not karyolysis
• C. Dysplasia - abnormal growth, nuclear changes but not these specific ones
• D. Necrosis ✅ - these are the three sequential nuclear changes in necrosis:
  • Pyknosis: nuclear shrinkage, chromatin condensation (dark)
  • Karyorrhexis: nuclear fragmentation
  • Karyolysis: nuclear dissolution/fading (DNases digest chromatin)
• E. Mitosis - has condensed chromosomes but is a normal cell division process

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Q21. What type of disease when antibodies act at the receptor level, inhibiting neurotransmitter binding? (2)

• A. Type II hypersensitivity ✅ - antibody-mediated hypersensitivity. When antibodies block receptors (e.g., anti-acetylcholine receptor in Myasthenia Gravis, anti-TSH receptor in Graves' disease), this is Type II hypersensitivity. Graves' = stimulatory Type II; MG = blocking Type II.
• B. Type I hypersensitivity - IgE-mediated, anaphylaxis/allergy
• C. Type III hypersensitivity - immune complex deposition (SLE, post-streptococcal GN)
• D. Autoimmune disease - correct but less specific than Type II
• E. Type IV hypersensitivity - T-cell mediated (delayed-type), contact dermatitis, TB

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Q22 (from page 8). Mark the incorrect statement about testicular germ cell neoplasia (1):

• a) Germ cell tumors of testis originate from intratubular germ cell neoplasia ✅ TRUE
• b) Seminomas are histologically identical to dysgerminomas and extragonadal germinomas ✅ TRUE
• c) Most testicular tumors arise from Sertoli and Leydig cells - FALSE ✅ - most testicular tumors (95%) arise from GERM CELLS, not Sertoli/Leydig cells
• d) Testicular teratomas are more common in cryptorchidism ✅ TRUE
• e) Adult testicular teratomas often contain elements of malignant germ cell tumors ✅ TRUE (unlike in children where teratomas are benign)

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Q24. Granulomatous but non-tuberculous orchitis is often associated with (1):

• a) Testicular seminoma - germ cell tumor, not orchitis
• b) Acute prostatitis - different organ
• c) Glomerulonephritis - kidney disease
• d) Testicular trauma - traumatic, not granulomatous
• e) Syphilis ✅ - syphilitic orchitis is a granulomatous inflammation (gumma formation); tertiary syphilis can cause testicular gummas. Also mumps can cause orchitis but it's not granulomatous.

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Q25. Brenner tumor often produces (1):

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Q26. Most common CNS tumor in childhood (1):

• a) Meningioma - most common in adults, not children
• b) Schwannoma - peripheral nerve sheath, adults
• c) Meningiosarcoma - rare malignant meningioma
• d) Medulloblastoma ✅ - most common malignant brain tumor in children; arises in the cerebellum (posterior fossa); PNET (primitive neuroectodermal tumor); highly radiosensitive; "small blue cell tumor"
• e) Ependymoma - second most common pediatric CNS tumor; arises from ependymal cells lining ventricles

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Q27. Significant feature of allergic nasal polyps (1):

• a) Presence of lymphocyte infiltrate - nonspecific chronic inflammation
• b) Presence of macrophage infiltrate - chronic inflammation, not specific to allergy
• c) Presence of eosinophilic granulocyte infiltrate ✅ - allergic nasal polyps characteristically show a dense eosinophilic infiltrate, edematous stroma, thickened basement membrane; driven by IgE-mediated (Type I) hypersensitivity and IL-5 (eosinophil growth factor)
• d) Absence of eosinophilic granulocyte infiltrate - WRONG
• e) Presence of plasma cell infiltrate - more characteristic of chronic infectious polyps

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Q28 (page 9). Which disease is characteristically associated with bruising and joint bleeding after minor trauma (1):

• a) Thrombotic microangiopathy - causes thrombocytopenia, microangiopathic hemolytic anemia
• b) Autoimmune hemolytic anemia - red cell destruction, anemia not bleeding
• c) Hemophilia A and B ✅ - Factor VIII (Hemophilia A) and Factor IX (Hemophilia B) deficiencies; X-linked recessive; hallmarks: hemarthroses (joint bleeding), muscle hematomas, easy bruising after minor trauma; normal platelet count, prolonged aPTT
• d) Hodgkin lymphoma - lymphoma, no primary hemostatic defect
• e) Malaria - thrombocytopenia can occur but not the classic joint bleeding pattern

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Q29. A round mucosal defect 3 cm in diameter, with sharp edges and clean base located at the lesser curvature of the stomach is most likely (1):

• a) Ulcerated gastric adenocarcinoma - irregular, heaped-up/raised edges, necrotic base
• b) Acute gastric ulcer ("stress ulcer") - typically multiple, shallow, not rounded with clean base
• c) Diffuse gastric adenocarcinoma - linitis plastica, not focal ulcer
• d) Krukenberg tumor - ovarian metastasis from gastric cancer
• e) Peptic gastric ulcer ✅ - classic description: round/oval, punched-out edges, clean base (granulation tissue), located at lesser curvature (most common site); H. pylori or NSAID-associated

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Q30. Most common cause of primary hyperparathyroidism (1):

• a) Primary hyperplasia of parathyroid glands - causes ~15-20% of primary HPT (all 4 glands involved)
• b) Hypothalamic neoplasms - don't affect parathyroid
• c) Parathyroid adenoma ✅ - accounts for ~80-85% of primary hyperparathyroidism; usually single benign adenoma of one parathyroid gland; causes hypercalcemia, kidney stones, bone disease
• d) Parathyroid carcinoma - very rare (<1%)
• e) Renal insufficiency - causes SECONDARY hyperparathyroidism (reactive, due to low calcium)

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Additional Questions (Pages 16-17, Colloquium II cont.)

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Q10 (occupational): Most common chronic occupational disease in the world (1):

• a) Asbestosis - important but not #1
• b) Silicosis ✅ - silicosis is the most common occupational lung disease worldwide (inhalation of crystalline silica → silicotic nodules, progressive massive fibrosis)
• c) Anthracosis - coal dust, most common pneumoconiosis by volume in coal miners
• d) Byssinosis - cotton dust
• e) Plumbism - lead poisoning

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Q11. Which is not a modifiable risk factor for atherosclerosis (1):

• a) Hyperlipidemia - modifiable ✅
• b) Hypertension - modifiable ✅
• c) Cigarette smoking - modifiable ✅
• d) Diabetes mellitus - modifiable (controllable) ✅
• e) Malignant melanoma ✅ - NOT a risk factor for atherosclerosis at all. Non-modifiable risk factors include age, sex, family history, genetics.

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Q12. Pyogenic granuloma (1):

• a) Resembles exuberant young granulation tissue ✅ TRUE - pyogenic granuloma = lobular capillary hemangioma; resembles granulation tissue histologically
• b) Occurs on the extremities - mostly occurs on gingiva, lips, fingers, and skin
• c) Cannot undergo fibrosis - it CAN involute/fibrosis
• d) Cannot regress - it CAN regress
• e) Does not occur on the gingiva - FALSE, gingiva is a very COMMON site

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Q13. Irreversible damage and coagulative necrosis occur if prolonged ischemia lasts (1):

• a) 15 minutes - too short; reversible injury occurs up to ~20-30 min in myocardium
• b) 50 minutes - beyond the threshold
• c) 20 to 40 minutes ✅ - in cardiac muscle, irreversible injury begins after ~20-30 minutes of sustained ischemia. Coagulative necrosis (preservation of cell outline, loss of nuclei) follows
• d) 5 minutes - too short
• e) 1 minute - too short

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Q14. Cardiac myxomas are (1):

• a) Sessile or pedunculated tumors ✅ - TRUE (usually pedunculated)
• b) Located in the region of the fossa ovalis on the atrial septum ✅ - most common cardiac tumor in adults; 75% in LEFT atrium, typically attached to the atrial septum near the fossa ovalis by a stalk
• c) Composed of giant pleomorphic cells - NO; composed of scattered stellate/polygonal "lepidic" cells in myxoid stroma
• d) Myxomatous cells mixed with squamous cells - NO
• e) Myxomatous cells mixed with rhabdoid cells - NO

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Q15. Lacunar cells (1):

• a) Are not a variant of Reed-Sternberg cells - FALSE; lacunar cells ARE a variant of RS cells seen in Nodular Sclerosis Hodgkin lymphoma
• b) Have a multilobulated nucleus with small nucleoli ✅ - lacunar cells have multilobulated nuclei; in formalin fixation the cytoplasm retracts creating a "lacuna"
• c) Have scant cytoplasm - they actually have abundant pale cytoplasm (which retracts in formalin)
• d) Due to fixation, cytoplasm is lost giving the impression of being in a lacuna ✅ - this is the CORRECT explanation; in formalin-fixed tissue the cytoplasm of lacunar cells retracts, making them appear to sit in clear spaces (lacunae)
• e) Contain keratin in the cytoplasm - NO

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Q16. Basic lesion in luetic (syphilitic) mesaortitis is found in the:

• a) Intima - intima involvement is secondary
• b) Media - medial destruction (smooth muscle/elastic fiber loss) leads to aneurysm but the PRIMARY lesion starts elsewhere
• c) Adventitia ✅ - syphilitic aortitis (luetic mesaortitis): inflammation begins in the ADVENTITIA via vasa vasorum (obliterative endarteritis of vasa vasorum) → ischemia of the media → smooth muscle and elastic tissue destruction → aneurysm formation. The adventitia shows perivascular plasma cell infiltrate.
• d) Vasa vasorum ✅ - technically the inflammation starts in the vasa vasorum
• e) Endothelium - not the primary site

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Q17. Benign nephrosclerosis results from:

• a) Kidney trauma - causes contusions, not nephrosclerosis
• b) Renal infarction - focal ischemic necrosis
• c) Long-standing benign hypertension ✅ - benign nephrosclerosis = hyaline arteriolosclerosis of renal arterioles, causing progressive ischemic atrophy → small, granular-surfaced kidneys with cortical thinning
• d) Long-standing diabetes mellitus - causes diabetic nephropathy (Kimmelstiel-Wilson nodules, diffuse mesangial sclerosis)
• e) Chronic glomerulonephritis - different mechanism (immune-mediated)

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Q18. Which is NOT characteristic of Buerger's disease (Thromboangiitis obliterans)?

• a) Most often affects lower limb arteries ✅ - TRUE (and upper limb arteries too)
• b) Affects both sexes equally - FALSE ✅ - Buerger's predominantly affects YOUNG MALE SMOKERS; male > female strongly
• c) Thrombosis in affected arteries ✅ - TRUE feature
• d) Accompanying phlebitis-like changes in veins ✅ - TRUE (migratory superficial thrombophlebitis)
• e) Early manifestations include cold-induced Raynaud phenomenon ✅ - TRUE early feature

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Q19. Pleomorphic adenoma is a tumor of the:

• a) Salivary glands ✅ - pleomorphic adenoma (mixed salivary gland tumor) is the most common salivary gland tumor; usually in the PAROTID gland. Contains epithelial and myoepithelial cells in a myxochondroid stroma; "pleomorphic" refers to histological diversity not nuclear pleomorphism
• b) Stomach - gastric tumors are adenocarcinomas/GISTs
• c) Liver - hepatocellular carcinoma, hemangioma
• d) Kidneys - renal cell carcinoma
• e) Adrenal glands - pheochromocytoma, adenoma

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Q20. Nodular fasciitis is:

• a) A variant of nodular sclerosis - nodular sclerosis is a Hodgkin's subtype
• b) Benign fibroblastic proliferation ✅ - nodular fasciitis is a BENIGN, self-limited, reactive proliferation of fibroblasts/myofibroblasts; often in subcutaneous tissue of the forearm; can mimic a sarcoma histologically ("pseudosarcoma"); important not to over-diagnose as malignant
• c) Granulomatous inflammation - no granulomas
• d) Malignant tumor of fibrous tissue - benign, not malignant
• e) Post-traumatic pseudotumor - it may be reactive/post-traumatic but is more precisely a benign fibroblastic proliferation

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Q21. Choose the correct statement about microglia:

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Summary Answer Key: 1-C | 2-C | 3-B | 4-C | 5-D | 6-A | 7-D | 8-D | 9-E | 10-E | 11-B | 12-B | 13-B | 14-B | 15-C | 16-D | 17-C | 18-E | 19-C | 20-C | 21-B | 22-A | 23-D | 24-D | 25-A | 26-B | 27-C | 28-D | 29-A,B,C | 30-C