MCQ: Here are all 40 questions rewritten with even A/B/C/D

40 clinical MCQs in Uncategorized. A 55-year-old obese woman develops painful, dilated, tortuous veins in her lower legs afte

Questions, Answers & Explanations

  1. Q1. A 55-year-old obese woman develops painful, dilated, tortuous veins in her lower legs after three pregnancies. What is the primary mechanism of their development?

    Answer: Prolonged increased intraluminal pressure causing venous wall weakening and valve incompetence

    Explanation: Varicose veins result from prolonged elevated intraluminal pressure causing progressive venous wall dilation and valve incompetence — worsened by obesity and pregnancy compressing the IVC.

  2. Q2. A patient with longstanding varicose veins develops brownish discolouration and a non-healing ulcer above the medial malleolus. What is the correct term and mechanism for the skin discolouration?

    Answer: Erythema nodosum from immune complex deposition in venous endothelium

    Explanation: Stasis dermatitis (brawny induration) results from chronic venous congestion → extravasation of RBCs → haemolysis → haemosiderin deposition → brawny discolouration and fibrosis.

  3. Q3. A 45-year-old male with pancreatic cancer develops painful superficial thrombophlebitis in his right leg, which resolves, then recurs in his left arm two weeks later. What eponym describes this phenomenon and its mechanism?

    Answer: Trousseau syndrome — migratory thrombophlebitis from occult visceral malignancy secreting procoagulant factors

    Explanation: Trousseau syndrome is migratory thrombophlebitis classically associated with occult visceral malignancy. Tumours (especially pancreatic and GI) secrete tissue factor and mucins that activate coagulation.

  4. Q4. Which statement correctly distinguishes superficial varicose veins from deep vein thrombosis regarding pulmonary embolism risk?

    Answer: DVT is the major source of PE; embolism from superficial varicose veins is very rare

    Explanation: Embolism from superficial varicose veins is very rare. DVT — particularly in popliteal, femoral, and iliac veins — is the major source of potentially fatal pulmonary embolism.

  5. Q5. A 30-year-old woman has painful red streaks running from a wound on her finger toward her axilla with tender enlarged nodes. Which outcome is most feared if she is not treated urgently?

    Answer: Bacteraemia and sepsis if bacteria escape the draining lymph nodes into the venous circulation

    Explanation: Lymphangitis (most commonly Group A Streptococcus) tracks bacteria through lymphatics. If not contained within draining nodes, bacteria enter the venous circulation causing bacteraemia and potentially fatal sepsis.

  6. Q6. A 40-year-old woman who had a left radical mastectomy 8 years ago has a massively swollen, firm, fibrotic left arm with peau d'orange skin changes. Which condition explains this and what long-term complication is associated?

    Answer: Secondary lymphoedema from surgical lymphatic disruption; associated with lymphangiosarcoma

    Explanation: Surgical severing of axillary lymphatics causes secondary lymphoedema. Chronic post-mastectomy lymphoedema carries a risk of lymphangiosarcoma (Stewart-Treves syndrome) developing in the affected arm.

  7. Q7. Hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu disease) is autosomal dominant. What genes are mutated and what pathway do they affect?

    Answer: ENG (endoglin) or ACVRL1/ALK1 genes — components of the TGF-β signalling pathway in endothelial cells

    Explanation: Osler-Weber-Rendu disease is caused by mutations in ENG or ACVRL1/ALK1 genes, both encoding components of the TGF-β signalling pathway in endothelial cells, leading to widespread telangiectasias present from birth.

  8. Q8. A child has a bright red raised patch on the forehead that grows rapidly in the first 3 months, then fades progressively. By age 7 the lesion is gone. What is this lesion?

    Answer: Juvenile (strawberry) hemangioma — grows rapidly then completely regresses by age 7 in most cases

    Explanation: Juvenile hemangiomas occur in 1 in 200 births, grow rapidly for a few months, then fade and completely regress by age 7 in most cases — parents should be reassured.

  9. Q9. A port wine stain in the distribution of the trigeminal nerve is found in a child with seizures, intellectual disability, and skull "tram-track" calcifications. What underlying mutation causes this syndrome?

    Answer: Somatic GNAQ missense mutation in the Gα subunit causing constitutive signalling

    Explanation: Sturge-Weber syndrome (port wine stain + leptomeningeal angiomas + seizures + intellectual disability) is caused by a somatic GNAQ missense mutation occurring early in development — not inherited.

  10. Q10. A 35-year-old male has a 2 cm vascular lesion in his liver found incidentally. Biopsy shows large dilated cavernous blood-filled spaces with intravascular thrombi and dystrophic calcification. What is most accurate about this lesion?

    Answer: It is a cavernous hemangioma — infiltrative, does not regress, and should never be biopsied percutaneously

    Explanation: Cavernous hemangiomas are infiltrative, do not regress, and can be difficult to distinguish from malignancy on imaging. Percutaneous biopsy risks fatal haemorrhage — diagnosis is usually made radiologically.

  11. Q11. A child has a soft fluctuant 8 cm mass in the left neck at birth. Histology shows massively dilated lymphatic spaces lined by endothelium with indistinct margins. What is the diagnosis and its key association?

    Answer: Cavernous lymphangioma (cystic hygroma) — strongly associated with Turner syndrome (45,X)

    Explanation: Cystic hygromas are cavernous lymphangiomas with indistinct unencapsulated margins in the neck/axilla. They are strongly associated with Turner syndrome and difficult to resect completely due to poor margins.

  12. Q12. A patient presents with an exquisitely painful small lesion under his thumbnail. Excision reveals a tumour composed of modified smooth muscle cells surrounding arteriovenous channels. What is the cell of origin and key distinguishing feature?

    Answer: Glomus tumour — modified smooth muscle cells of glomus bodies; NOT endothelial; excision curative

    Explanation: Glomus tumours arise from modified smooth muscle cells (NOT endothelial) of glomus bodies. They are exquisitely painful, found under fingernails, and are completely cured by excision.

  13. Q13. A 32-year-old HIV-positive male with CD4 count of 45 develops red papules on his skin. Biopsy shows capillary proliferation with epithelioid endothelial cells, scattered neutrophils, and granular eosinophilic material. Warthin-Starry silver stain reveals bacilli. What is the diagnosis and the causative organism?

    Answer: Bacillary angiomatosis — Bartonella species causing vascular proliferation in immunocompromised hosts

    Explanation: Bacillary angiomatosis is caused by Bartonella species (B. henselae or B. quintana) in immunocompromised patients. Warthin-Starry stain reveals the causative bacteria — distinguishing it critically from Kaposi sarcoma.

  14. Q14. Bartonella henselae causes different diseases depending on immune status. Which statement correctly describes this difference?

    Answer: henselae causes cat-scratch disease in immunocompetent and bacillary angiomatosis in immunocompromised

    Explanation: B. henselae (reservoir: domestic cats) causes self-limiting necrotising granulomatous lymphadenopathy (cat-scratch disease) in immunocompetent hosts, but vascular proliferative bacillary angiomatosis in immunocompromised patients.

  15. Q15. Which virus causes Kaposi sarcoma and through what molecular mechanism does latent infection promote tumour growth?

    Answer: HHV8 — viral cyclin D homologue disrupts cell cycle controls and viral proteins inhibit p53

    Explanation: HHV8 (KSHV) causes KS. During latent infection, a viral cyclin D homologue disrupts cell cycle checkpoints and viral proteins inhibit p53, providing infected cells with growth and survival advantages.

  16. Q16. A 70-year-old man of Ashkenazic Jewish descent has slowly progressive red-purple nodular lesions on both ankles present for 10 years. He is HIV-negative. What form of Kaposi sarcoma does he have?

    Answer: Classic KS — older Mediterranean/Eastern European men; indolent; localised to skin; excellent prognosis

    Explanation: Classic KS affects older men of Mediterranean, Middle Eastern, or Eastern European descent. It is NOT HIV-associated, runs an indolent course, and typically remains confined to the skin.

  17. Q17. A prepubertal child in sub-Saharan Africa has Kaposi sarcoma with extensive lymph node and visceral involvement. What is the expected prognosis?

    Answer: Poor — nearly 100% mortality within 3 years for this severe endemic African form in children

    Explanation: The severe endemic African KS in prepubertal children with lymph node and visceral involvement carries nearly 100% mortality within 3 years — one of the most aggressive forms of KS.

  18. Q18. A renal transplant patient on tacrolimus develops Kaposi sarcoma with mucosal and visceral involvement. What is the most appropriate first management step?

    Answer: Reduce or withdraw immunosuppression, accepting the risk of allograft rejection

    Explanation: Transplant-associated KS is driven by T-cell immunosuppression. The first step is reducing or withdrawing immunosuppression — lesions may regress spontaneously, though organ rejection is a risk.

  19. Q19. The three progressive morphologic stages of Kaposi sarcoma are patch, plaque, and nodule. What does the nodular stage specifically herald?

    Answer: Lymph node and visceral involvement signalling progression from localised to systemic disease

    Explanation: The nodular stage — sheets of plump spindle cells with slitlike vascular spaces — heralds lymph node and visceral involvement, marking progression to systemic disease.

  20. Q20. A 62-year-old woman develops a rapidly growing fleshy scalp mass with blurring margins. Biopsy shows atypical endothelial cells forming poorly organised vascular channels. CD31 is positive. What is the diagnosis and prognosis?

    Answer: Angiosarcoma — malignant endothelial neoplasm; 5-year survival approximately 30%

    Explanation: Angiosarcoma is a malignant endothelial neoplasm confirmed by CD31 positivity. It is locally invasive, readily metastasises, and carries an approximately 30% 5-year survival.

  21. Q21. Hepatic angiosarcoma is specifically associated with three carcinogenic exposures with long latency periods. Which combination is correct?

    Answer: Arsenic, Thorotrast (radioactive contrast agent), and polyvinyl chloride

    Explanation: Hepatic angiosarcoma is specifically linked to arsenic (pesticides), Thorotrast (formerly used radioactive contrast agent, now banned), and polyvinyl chloride (PVC) — all with characteristically long latency periods of 15–40 years.

  22. Q22. A 55-year-old woman develops a new lesion in her right arm 6 years after right mastectomy and axillary clearance. Her arm has been massively swollen since surgery. Biopsy reveals malignant endothelial cells (CD31 positive). What is the diagnosis?

    Answer: Lymphangiosarcoma (Stewart-Treves syndrome) arising in chronic post-mastectomy lymphoedema

    Explanation: Post-mastectomy lymphangiosarcoma (Stewart-Treves syndrome) arises in the chronically lymphoedematous arm years after radical mastectomy — a well-recognised complication of secondary lymphoedema.

  23. Q23. Spider telangiectasias are most commonly associated with which clinical states and what is their distinguishing physical examination feature?

    Answer: Hyperestrogenic states (pregnancy, cirrhosis); they are pulsatile and blanch with direct pressure

    Explanation: Spider telangiectasias are associated with hyperestrogenic states. Composed of dilated subcutaneous arterioles, they are characteristically pulsatile and blanch completely with direct pressure.

  24. Q24. A patient with Osler-Weber-Rendu disease presents with recurrent severe nosebleeds and bloody stools. What is the mechanism of bleeding?

    Answer: Spontaneous rupture of widely distributed telangiectasias — malformations of dilated capillaries and venules

    Explanation: In Osler-Weber-Rendu disease, telangiectasias (malformations of dilated capillaries and venules present from birth) are widely distributed including throughout the GI tract and nasopharynx, and can spontaneously rupture.

  25. Q25. A 3-year-old boy has a large vascular mass overlying his sacrum, associated with high-output cardiac failure. Biopsy shows mature vascular channels of arterial and venous type bypassing the capillary bed. What is the diagnosis?

    Answer: Arteriovenous malformation (AVM) — high-flow shunting causing cardiac strain

    Explanation: Arteriovenous malformations (AVMs) are direct connections between arteries and veins bypassing the capillary bed. Large AVMs (e.g., in sacrum, brain) cause significant high-output cardiac failure due to shunting.

  26. Q26. A patient with atherosclerosis has a blood pressure reading of 160/90 mmHg. Which statement about isolated systolic hypertension in the elderly is correct?

    Explanation: Isolated systolic hypertension (systolic BP ≥140 mmHg, diastolic BP <90 mmHg) is common in the elderly due to decreased compliance (stiffness) of the aorta and large arteries with age.

  27. Q27. What is the most common cause of sustained hypertension?

    Answer: Pheochromocytoma

    Explanation: Essential (idiopathic) hypertension, without an identifiable secondary cause, accounts for 90-95% of all cases of hypertension.

  28. Q28. Renal artery stenosis causes hypertension primarily through which mechanism?

    Answer: Activation of the renin-angiotensin-aldosterone system (RAAS) due to reduced renal perfusion

    Explanation: Renal artery stenosis reduces blood flow to the juxtaglomerular apparatus, which stimulates renin release, activating the RAAS and causing hypertension. This is secondary hypertension.

  29. Q29. Which of the following is NOT typically considered a potential complication of hypertension?

    Answer: Hypertrophic cardiomyopathy (non-obstructive type)

    Explanation: Hypertrophic cardiomyopathy (HCM) is a primary genetic myocardial disorder, distinct from the left ventricular hypertrophy (LVH) that can result from chronic hypertension. LVH is a common complication of hypertension.

  30. Q30. What is the primary mechanism by which chronic lymphatic obstruction, such as in filariasis, leads to lymphoedema?

    Answer: Elevated hydrostatic pressure in distal lymphatic channels causing oedema and eventual fibrosis

    Explanation: Filariasis (Wuchereria bancrofti) obstructs lymphatic channels → distal hydrostatic pressure rises → chronic oedema → progressive fibrosis → brawny induration. It is the most common worldwide cause of massive lymphoedema.

  31. Q31. A woman develops chylous ascites after surgery for ovarian cancer. What does the presence of chylous (milky) fluid specifically indicate?

    Answer: Rupture of dilated lymphatics from obstruction allowing lymph to accumulate in the abdomen

    Explanation: Chylous ascites results from rupture of dilated lymphatics caused by obstruction (tumour, surgery) — allowing lymph to accumulate in the peritoneal cavity. The milky appearance reflects its high lipid content.

  32. Q32. Malignant vascular tumours require immunohistochemistry to confirm their endothelial cell origin. Which markers confirm endothelial derivation?

    Answer: CD31 and von Willebrand factor — endothelial cell-specific markers confirming vascular origin

    Explanation: CD31 (PECAM-1) and von Willebrand factor (Factor VIII-related antigen) are endothelial cell-specific markers used to confirm endothelial origin of malignant vascular tumours, including angiosarcoma.

  33. Q33. An intermediate-grade vascular neoplasm — epithelioid hemangioendothelioma — is found around a medium-sized vein. What is its expected clinical behaviour?

    Answer: Variable — most cured by excision, but up to 40% recur and 20–30% eventually metastasise

    Explanation: EHE has variable, intermediate behaviour: most are cured by excision, but up to 40% recur, 20–30% eventually metastasise, and ~15% of patients die of their disease.

  34. Q34. Port wine stain differs from other forms of nevus flammeus in which important way?

    Answer: Port wine stains grow during childhood, progressively thicken the overlying skin, and persist permanently

    Explanation: Unlike most nevus flammeus birthmarks that regress, port wine stains grow progressively during childhood, thicken the overlying skin, and persist indefinitely — requiring laser treatment if clinically significant.

  35. Q35. A 60-year-old male develops an enlarging right upper arm mass with CD31-positive malignant cells on biopsy, arising in an arm that has been chronically swollen since right mastectomy 10 years ago. Which aetiology does this represent?

    Answer: Lymphangiosarcoma from chronic post-mastectomy lymphoedema (Stewart-Treves syndrome)

    Explanation: Angiosarcoma (lymphangiosarcoma/Stewart-Treves) arising in the ipsilateral arm after mastectomy and chronic lymphoedema is a classic, well-recognised aetiology — both radiation and lymphatic obstruction contribute.

  36. Q36. Large-bore synthetic vascular grafts (≥12 mm) function well in high-flow aortic positions. Why do small-diameter synthetic grafts (≤8 mm) generally fail?

    Answer: Small-bore grafts fail primarily from early thrombosis and late anastomotic intimal hyperplasia

    Explanation: Small-diameter synthetic grafts fail due to early thrombosis and late intimal hyperplasia developing at the anastomotic junction — the reason autologous vessels (saphenous vein, IMA) are preferred for small-bore bypass.

  37. Q37. The mechanisms by which saphenous vein grafts fail over 10 years include three distinct sequential processes. Which combination correctly identifies all three?

    Answer: Early thrombosis, intimal thickening (months–years), and accelerated vein graft atherosclerosis

    Explanation: Saphenous vein graft failure occurs through three sequential mechanisms: early thrombosis, later SMC-driven intimal thickening (months–years post-op), and eventual accelerated atherosclerosis — sometimes with plaque rupture.

  38. Q38. Milroy disease is a form of primary lymphoedema. What distinguishes it from secondary lymphoedema?

    Answer: Milroy disease is heredofamilial congenital lymphoedema from hereditary lymphatic agenesis or hypoplasia

    Explanation: Milroy disease (heredofamilial congenital lymphoedema) is caused by hereditary lymphatic agenesis or hypoplasia — present from birth and unrelated to any external acquired cause.

  39. Q39. AIDS-associated Kaposi sarcoma has declined by more than 80% since ART. How much more common does it remain in HIV-infected individuals compared to the general population?

    Answer: 1000-fold more common, even with ART lowering the absolute incidence substantially

    Explanation: AIDS-associated KS remains 1000-fold more common than in the general population and 300-fold more common than in transplant recipients — despite the 80% reduction in incidence achieved with antiretroviral therapy.

  40. Q40. A child has a rapidly growing pedunculated red gingival mass. His mother is 6 months pregnant and has an identical lesion. Biopsy shows immature vascular proliferation resembling granulation tissue. What is the correct diagnosis and management?

    Answer: Pyogenic granuloma — benign; may regress, fibrose, or become a peripheral ossifying fibroma; treat by excision

    Explanation: Pyogenic granulomas are benign vascular proliferations common in pregnant women (granuloma gravidarum) and children. Despite rapid growth, they are benign and managed by complete excision. Recurrence is possible.

View on OmpathStudy