Vascular Pathology — MCQs

Vascular Pathology Indian Medical PG Practice Questions and MCQs

Question 281: Plaques jaunes are seen in which condition?

A. Syphilis
B. Head injury
C. Endocarditis
D. Atherosclerosis (Correct Answer)

Explanation: ***Head injury*** - **Plaques jaunes**, or yellow plaques, are primarily associated with brain injuries, particularly in areas of **contusion** or **hemorrhage** [1]. - These plaques may represent **lipid-laden macrophages** and indicate areas of *necrosis* and inflammation in the brain [1]. *Endocarditis* - Endocarditis is characterized by **vegetations** on heart valves rather than plaques in the brain. - Symptoms typically include **fever**, **murmurs**, and **embolization**, which do not involve yellow plaques. *Syphilis* - Syphilis may cause *gummatous lesions* but is not associated with yellow plaques in the brain. - Typical findings include **rash** and **ulcerative lesions**, particularly during the secondary stage. *Atherosclerosis* - Atherosclerosis involves **plaque formation** in blood vessels but these are not the same as **plaques jaunes** in neurological contexts. - It is characterized by **cholesterol** deposits and plaque rupture leading to cardiovascular events, not plaques seen in head injuries. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1262-1264.

Question 282: Most supportive laboratory investigation for Henoch-Schönlein purpura is -

A. C-reactive protein (CRP) levels
B. Serum IgA levels (Correct Answer)
C. DTPA scan
D. Renal biopsy

Explanation: ***Serum IgA levels*** - **Henoch-Schönlein purpura (HSP)** is an **IgA vasculitis**, and elevated serum IgA levels are characteristic, although not diagnostic on their own. - The disease involves **IgA deposition** in small blood vessels, particularly in the skin, kidneys, and gastrointestinal tract. *C-reactive protein (CRP) levels* - CRP is a general **marker of inflammation**, which can be elevated in many conditions, including HSP. - It is **not specific to HSP** and does not help differentiate it from other inflammatory disorders. *Renal biopsy* - A renal biopsy can confirm **IgA nephropathy** with characteristic IgA deposition, which often occurs in HSP. - However, it is an **invasive procedure** and not the **most supportive laboratory investigation** for initial diagnosis compared to serum IgA, particularly when considering the broader clinical picture of HSP. *DTPA scan* - A **DTPA (diethylene triamine pentaacetic acid) scan** is a nuclear medicine test used to assess **renal function** and blood flow. - It is used to evaluate **renal complications** but is not a diagnostic tool for HSP itself.

Question 283: The tissue of origin of the Kaposi's sarcoma is

A. Lymphoid
B. Vascular (Correct Answer)
C. Neural
D. Muscular

Explanation: ***Vascular*** - Kaposi's sarcoma originates from the **vascular tissue**, specifically from endothelial cells lining blood vessels [2]. - The lesions are characterized by **angiogenesis**, leading to the formation of vascular tumors with dilated endothelial cell-lined vascular spaces [1]. *Muscular* - Muscular tissue is involved in **voluntary** and **involuntary movements** but is not related to the etiology of Kaposi's sarcoma. - This condition does not arise from **muscle cells** or any muscular components. *Neural* - Neural tissue consists of **neurons** and **glial cells**, which are not implicated in Kaposi's sarcoma. - Kaposi's sarcoma does not originate from any **neural structures** or pathologies. *Lymphoid* - Lymphoid tissue primarily concerns the immune system, particularly the **lymphatic system**, and does not give rise to Kaposi's sarcoma. - This malignancy does not derive from **lymphoid components** like lymphocytes or lymph nodes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 526-527. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 282-283.

Question 284: Obliterative endarteritis in vasa vasorum is seen in -

A. Essential Hypertension
B. Tertiary Syphilis (Correct Answer)
C. Systemic Lupus Erythematosus
D. Pulmonary Tuberculosis

Explanation: ***Tertiary Syphilis*** - **Obliterative endarteritis** of the **vasa vasorum** is a hallmark pathological finding in tertiary syphilis, particularly affecting the **aorta**. - This inflammation and occlusion of the small blood vessels supplying the aorta lead to **ischemic injury** of the aortic wall, causing **aneurysms** and **aortic regurgitation**. *Essential Hypertension* - While hypertension can lead to vascular changes like **arteriolosclerosis** and **hyperplastic arteriolosclerosis**, it does not typically involve obliterative endarteritis of the vasa vasorum. - The vascular damage in essential hypertension is more generalized to smaller arteries and arterioles, not specifically the vasa vasorum. *Systemic Lupus Erythematosus* - SLE is an **autoimmune disease** that can cause **vasculitis**, but the specific pattern of obliterative endarteritis of the vasa vasorum is not characteristic. - Vascular involvement in SLE is diverse, ranging from small vessel vasculitis to accelerated atherosclerosis, but distinct from syphilitic changes. *Pulmonary Tuberculosis* - Tuberculosis is primarily an **infectious granulomatous disease** affecting the lungs and other organs; it does not typically cause obliterative endarteritis of the vasa vasorum. - Although it can cause vascular complications like **aneurysms** (e.g., Rasmussen's aneurysm) due to erosion, the underlying mechanism is not the same as syphilitic changes.

Question 285: Which of the following is a type of small vessel vasculitis?

A. Classical PAN
B. Giant cell arteritis
C. Granulomatosis with polyangiitis (GPA) (Correct Answer)
D. None of the options

Explanation: ***Granulomatosis with polyangiitis (GPA)*** - GPA is a prototypic **ANCA-associated small vessel vasculitis** characterized by necrotizing granulomas and vasculitis [1], [2]. - It commonly involves the **upper and lower respiratory tracts** and the **kidneys** with necrotizing granulomatous inflammation [1], [2]. - Classified as small vessel vasculitis according to the **Chapel Hill Consensus Conference** classification. *Classical PAN* - This refers to **Polyarteritis Nodosa (PAN)**, which is a **medium-sized vessel vasculitis**. - PAN is characterized by multifocal inflammatory and necrotizing lesions of medium-sized muscular arteries, **not small vessels**. *Giant cell arteritis* - **Giant cell arteritis (GCA)** is a **large vessel vasculitis** that primarily affects the aorta and its major branches, particularly the temporal artery [3]. - Symptoms include headache, jaw claudication, and visual disturbances, reflecting the involvement of larger blood vessels [3]. *None of the options* - This option is incorrect because Granulomatosis with polyangiitis (GPA) is a clear example of a small vessel vasculitis. - There is a correct answer among the provided choices. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.

Question 286: Lines of Zahn are LEAST likely to be seen in -

A. Liver
B. Kidney
C. Heart
D. Lung (Correct Answer)

Explanation: ***Lung*** - **Lines of Zahn are LEAST likely in the lungs** because most pulmonary thrombi are actually **emboli that formed elsewhere** (typically in deep leg veins) and then **lodged in pulmonary vessels**. - These pre-formed thrombi developed in **low-flow venous environments** and therefore **lack the characteristic layered appearance** of Lines of Zahn. - Even when thrombi form in situ in pulmonary vessels, the vascular bed characteristics make Lines of Zahn formation less common compared to other sites. *Heart* - **Mural thrombi** in heart chambers (especially post-MI in left ventricle or in atrial fibrillation) commonly show **Lines of Zahn**. - The **high-flow, turbulent environment** with continuous cardiac contractions creates ideal conditions for alternating platelet-fibrin and RBC layer deposition. - These are classic examples of antemortem thrombi with visible Lines of Zahn. *Liver* - **Portal vein thrombosis** and **hepatic vein thrombosis** (Budd-Chiari syndrome) can exhibit **Lines of Zahn**. - Despite being venous, these vessels have **sufficient flow velocity and turbulence** to allow layered thrombus formation. - Lines of Zahn indicate the thrombus formed during life with flowing blood. *Kidney* - **Renal artery thrombosis** and **renal vein thrombosis** frequently show **Lines of Zahn**. - Both arterial and venous renal circulation have adequate flow dynamics for layered thrombus formation. - These represent antemortem thrombi formed in vessels with active blood flow.

Question 287: All of the following are true regarding fibromuscular dysplasia EXCEPT:

A. Medium size vessels are affected
B. Aneurysm may occur
C. Irregular hyperplasia
D. OCPs predispose (Correct Answer)

Explanation: ***OCPs predispose*** - **Oral contraceptive pills (OCPs)** are not identified as a predisposing factor for fibromuscular dysplasia (FMD). FMD is largely considered a sporadic condition with some genetic predisposition, but not linked to OCP use [1]. - While hormonal influences are suspected given its higher prevalence in women, direct causation or exacerbation by OCPs has not been established [1]. *Medium size vessels are affected* - Fibromuscular dysplasia (FMD) predominantly affects **medium-sized arteries**, most commonly the renal and carotid arteries [1]. - This involvement leads to characteristic stenoses, aneurysms, or dissections in those vessels. *Aneurysm may occur* - The abnormal arterial wall architecture in FMD, characterized by alternating areas of stenosis and dilation, can lead to the formation of **aneurysms**. - These aneurysms are usually **intracranial** or within the affected renal and carotid arteries, and represent a significant risk of rupture or dissection. *Irregular hyperplasia* - FMD involves **irregular fibrous or fibromuscular hyperplasia** of the arterial wall layers (intima, media, or adventitia). - This abnormal cellular proliferation and connective tissue deposition result in the characteristic "string of beads" appearance on angiography. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 493-494.

Question 288: Fibrinoid necrosis with neutrophilic infiltration is seen in ?

A. Polyarteritis Nodosa (PAN) (Correct Answer)
B. Giant Cell Arteritis
C. Takayasu Arteritis
D. Wegener's Granulomatosis

Explanation: ***PAN*** - **Fibrinoid necrosis** with **neutrophilic infiltration** is characteristic of Polyarteritis Nodosa (PAN), which primarily affects medium-sized arteries [1]. - The necrosis is often seen in the context of **systemic vasculitis**, where it leads to damage and inflammation of vessel walls [3]. *Takayasu arteritis* - Primarily affects **large vessels** like the aorta and its major branches, typically presenting with **pulselessness** or **claudication**. - It shows **granulomatous inflammation** rather than fibrinoid necrosis with neutrophilic infiltration. *Giant cell arteritis* - Predominantly affects large and medium arteries, especially the **temporal artery**, often leading to headaches and visual disturbances. - It is associated with **giant cells** and lymphocytic infiltration rather than fibrinoid necrosis. *Wegener's granulomatosis* - Characterized by **granulomatous inflammation** and vasculitis affecting small to medium vessels, particularly in the lungs and kidneys. - It does not typically present with **fibrinoid necrosis**; instead, it shows necrotizing granulomas [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 687-688.

Question 289: All are true about non-bacterial thrombotic endocarditis, except?

A. No inflammatory reaction
B. Locally nondestructive
C. Cause emboli
D. Vegetation > 5 mm (Correct Answer)

Explanation: ***Vegetation > 5 mm*** - Non-bacterial thrombotic endocarditis (NBTE) typically features **small vegetations**, often less than 5 mm, associated with conditions like **cancer** or **hypercoagulable states** [1]. - The presence of larger vegetations is more characteristic of **infective endocarditis**, making this statement false regarding NBTE. *Cause emboli* - NBTE is known to cause **embolic phenomena** due to small vegetations that dislodge, leading to **ischemia** in distant organs. - It is associated with conditions such as **adenocarcinoma**, contributing to possible embolic events. *No inflammatory reaction* - Although inflammatory cells are sparse, NBTE can produce a **minimal inflammatory response** in the tissues. - The presence of fibrin deposits and small vegetations has implications for **thrombus formation**, suggesting a mild inflammatory component. *Locally nondestructive* - NBTE vegetations are primarily **nondestructive** to the underlying valves [1], contrasting with infected vegetations that can cause significant **valvular damage**. - However, this characteristic still does not undermine that these vegetations can lead to systemic embolism despite being locally nondestructive. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568.

Question 290: Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?

A. Inflammatory cell infiltration
B. Thick fibrous cap (Correct Answer)
C. Cell debris
D. Smooth muscle cell atrophy

Explanation: ***Smooth muscle cell hypertrophy*** - **Smooth muscle cell hypertrophy** is generally associated with stable plaques and does not typically occur in ruptured atherosclerotic plaques [2]. - At rupture, there is **loss of smooth muscle cells** and thinning of the fibrous cap, leading to plaque instability [2]. *Thin fibrosis cap* - A **thin fibrous cap** is a critical feature of vulnerable plaques, making them prone to rupture [2]. - It indicates a **weakened structure** that can no longer withstand the pressure of the underlying lipid core [2]. *Cell debris* - **Cell debris** is often found at the site of rupture, resulting from the necrosis of foam cells and smooth muscle cells. - This indicates **plaque instability** and contributes to the thrombus formation at the rupture site. *Multiple foam cap* - The presence of **multiple foam cells** reflectsing lipid accumulation in the plaque but does not contribute to the phenomenon of plaque rupture directly. - While foam cells are associated with rupture, a **foam cap** is not a recognized pathological finding at the time of rupture. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 271-272. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 268-270.

Practice by Chapter

Atherosclerosis

Practice Questions

Hypertensive Vascular Disease

Practice Questions

Aneurysms and Dissection

Practice Questions

Vasculitis

Practice Questions

Venous Disease and Thrombosis

Practice Questions

Vascular Tumors

Practice Questions

Varicose Veins and Lymphatics

Practice Questions

Pathology of Vascular Interventions

Practice Questions

Vascular Diseases in Specific Organs

Practice Questions

Congenital Vascular Anomalies

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