Vascular Pathology — MCQs

Vascular Pathology Indian Medical PG Practice Questions and MCQs

Question 81: What is the most important modifiable risk factor for atherosclerosis?

A. Hyperlipidemia
B. Diabetes mellitus
C. Cigarette Smoking (Correct Answer)
D. Hypertension

Explanation: Atherosclerosis is a chronic inflammatory response of the arterial wall to endothelial injury. While multiple risk factors contribute to its development, they are categorized into non-modifiable (age, gender, genetics) and modifiable factors. **Why Cigarette Smoking is the Correct Answer:** In the context of NEET-PG and standard pathology (Robbins), **Cigarette Smoking** is considered the most potent and clinically significant modifiable risk factor, particularly for the development of atherosclerosis in the coronary arteries and the abdominal aorta. It acts by inducing endothelial dysfunction [1], increasing oxidative stress (free radical production), and promoting a pro-thrombotic state. In many epidemiological studies, it is cited as the single most preventable cause of atherosclerotic cardiovascular disease. **Analysis of Incorrect Options:** * **Hyperlipidemia (specifically Hypercholesterolemia):** This is a major risk factor and is often considered the *sufficient* factor to induce lesions even in the absence of others [1]. However, in terms of overall modifiable impact on public health and synergy with other factors, smoking often takes precedence in clinical questioning. * **Hypertension:** This is a major risk factor that primarily increases the risk of Left Ventricular Hypertrophy and Stroke. While it accelerates atherosclerosis, it is statistically less potent than smoking or hyperlipidemia for coronary artery disease. * **Diabetes mellitus:** DM induces hypercholesterolemia and significantly increases the risk of atherosclerosis (making it equivalent to a "cardiovascular risk equivalent") [1], but it is often categorized as a metabolic contributor rather than the primary modifiable behavioral factor. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site for atherosclerosis:** Abdominal aorta > Coronary artery > Popliteal artery > Internal carotid artery. * **Earliest lesion:** Fatty streaks (can be seen in infants). * **Characteristic Cell:** The "Foam Cell" (macrophages that have ingested oxidized LDL). * **Protective Factor:** High levels of HDL ("Good cholesterol") are inversely related to risk [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 500-504.

Question 82: A 40-year-old female patient complains of breathlessness. She was operated for a femur fracture and is in her third trimester of pregnancy. Which type of embolism is most probably present in this patient?

A. Fat embolism (Correct Answer)
B. Air embolism
C. Amniotic fluid embolism
D. Cholesterol embolism

Explanation: ### Explanation The correct answer is **Fat Embolism (Option A)**. **Why it is correct:** The clinical hallmark for fat embolism is a **long bone fracture** (like the femur) [1]. When a bone is fractured, the fatty marrow is released into the ruptured marrow sinusoids and travels to the lungs [1]. While the patient is in her third trimester (a risk for amniotic fluid embolism), the **femur fracture** is the most specific and classic trigger provided in the clinical vignette. Fat Embolism Syndrome typically presents with a triad of dyspnea (breathlessness), neurological symptoms, and a petechial rash. **Why the other options are incorrect:** * **B. Air Embolism:** Usually occurs due to obstetric procedures, chest wall injuries, or improper decompression (caisson disease) [2]. It requires a significant volume of air (typically >100ml) to be clinically symptomatic. * **C. Amniotic Fluid Embolism:** While the patient is pregnant, this is a rare, catastrophic complication of labor or the immediate postpartum period caused by the entry of amniotic fluid into maternal circulation [2]. It presents with sudden severe shock, DIC, and seizures, rather than being linked to a fracture. * **D. Cholesterol Embolism:** This occurs due to the erosion of atheromatous plaques, usually following invasive vascular procedures (like angiography) in elderly patients with atherosclerosis. It typically affects the kidneys or skin ("blue toe syndrome"). **NEET-PG High-Yield Pearls:** * **Classic Triad:** Dyspnea, Petechiae (often on the conjunctiva/axilla), and Mental confusion. * **Stain of choice:** **Sudan Black** or **Oil Red O** on frozen sections (fat is washed away in routine paraffin processing). * **Mechanical vs. Biochemical Theory:** Mechanical obstruction by fat globules is followed by biochemical injury where free fatty acids cause endothelial damage and ARDS. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 146-147. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 323-324.

Question 83: What is the major change occurring in blood vessels in hypertension?

A. Atherosclerosis
B. Hyaline arteriosclerosis
C. Multiple small aneurysms
D. Fibrinoid necrosis (Correct Answer)

Explanation: **Explanation:** The question focuses on the hallmark pathological changes associated with **Malignant (Accelerated) Hypertension**. **1. Why Fibrinoid Necrosis is Correct:** In malignant hypertension (systolic >200 mmHg, diastolic >120 mmHg), the sudden, severe rise in blood pressure causes acute hemodynamic injury to the endothelial cells. This leads to the leakage of plasma proteins (including fibrin) into the vessel wall [2]. The accumulation of these proteins, combined with the death of smooth muscle cells, creates a bright pink, smudgy appearance under H&E staining known as **fibrinoid necrosis** [1]. This is typically seen in the arterioles of the kidneys. **2. Why the other options are incorrect:** * **Atherosclerosis:** This affects **large and medium-sized elastic and muscular arteries** (e.g., aorta, coronary arteries). While hypertension is a risk factor, atherosclerosis is a chronic inflammatory process involving lipid deposition, not a direct acute hypertensive change. * **Hyaline Arteriosclerosis:** This is the hallmark of **Benign Hypertension** and diabetes mellitus [3]. It involves the leakage of plasma components across the endothelium, resulting in a homogenous, pink thickening of the arteriolar wall, but without the acute cell death (necrosis) seen in malignant cases [1]. * **Multiple Small Aneurysms:** Specifically known as **Charcot-Bouchard aneurysms**, these occur in the small penetrating arteries of the brain (e.g., lenticulostriate arteries) due to chronic hypertension. While important, they are a complication rather than the primary vascular wall change. **High-Yield Clinical Pearls for NEET-PG:** * **Malignant Hypertension:** Look for "Fibrinoid necrosis" and **"Onion-skinning"** (Hyperplastic arteriolitis) [1]. * **Benign Hypertension:** Look for "Hyaline arteriosclerosis" [1]. * **Kidney Findings:** Malignant hypertension leads to **"Flea-bitten kidney"** (pinpoint hemorrhages), whereas benign hypertension leads to "Benign Nephrosclerosis" (granular surface). * **Key Site:** The afferent arterioles of the kidney are the most characteristic site for these changes [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 277-278. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 541-542.

Question 84: Saddle embolus causes sudden death by blocking which arteries?

A. Coronary arteries
B. Cerebral arteries
C. Pulmonary arteries (Correct Answer)
D. Renal arteries

Explanation: **Explanation:** A **Saddle Embolus** refers to a large blood clot that lodges at the **bifurcation of the main pulmonary artery**, extending into both the right and left pulmonary arteries [1]. **Why Pulmonary Arteries is Correct:** The term "saddle" describes the shape of the thrombus as it straddles the bifurcation [2]. This massive pulmonary embolism (PE) causes sudden death by obstructing more than 60% of the pulmonary circulation. This leads to **acute right heart failure (Cor Pulmonale)** and a sudden drop in cardiac output (obstructive shock), as blood cannot reach the left side of the heart for systemic distribution [1]. **Why Other Options are Incorrect:** * **Coronary Arteries:** Blockage here causes Myocardial Infarction. While fatal, these are small-caliber vessels where a large "saddle" thrombus cannot physically lodge. * **Cerebral Arteries:** Blockage leads to Ischemic Stroke. These emboli are typically small (e.g., from the carotid or heart valves) and cannot bridge a major bifurcation in the manner of a saddle embolus [2]. * **Renal Arteries:** Emboli here cause renal infarction, which typically presents with flank pain and hematuria rather than sudden death. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** >95% of pulmonary emboli originate from **Deep Vein Thrombosis (DVT)** of the lower limbs (proximal veins like popliteal, femoral, or iliac) [2]. * **Pathophysiology:** Sudden death in saddle embolus is due to **Electromechanical Dissociation (EMD)** or Pulseless Electrical Activity (PEA). * **Lines of Zahn:** These are characteristic laminations (pale platelet/fibrin layers alternating with red cell layers) found in thrombi formed in flowing blood, helping to distinguish a pre-mortem clot from a post-mortem "currant jelly" clot. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 144-145. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 137-138.

Question 85: What are the most common vessels involved in cutaneous vasculitis?

A. Arteries
B. Arterioles
C. Capillaries
D. Post-capillary venules (Correct Answer)

Explanation: **Explanation:** Cutaneous vasculitis, specifically **Cutaneous Small Vessel Vasculitis (CSVV)** or leukocytoclastic vasculitis, primarily affects the **post-capillary venules** [1][3]. **Why Post-capillary Venules?** The underlying mechanism is typically a **Type III Hypersensitivity reaction**. Circulating antigen-antibody (immune) complexes deposit in the vessel walls [2]. Post-capillary venules are the preferred site for this deposition because: 1. **Low Flow/Pressure:** Blood flow is slowest here, allowing complexes to settle. 2. **Endothelial Gaps:** These vessels have thinner walls and more "leaky" junctions compared to arterioles, facilitating the migration of inflammatory cells (neutrophils) and the extravasation of red blood cells (leading to palpable purpura). **Analysis of Incorrect Options:** * **Arteries (A):** Involved in large-vessel (e.g., Giant Cell Arteritis) or medium-vessel vasculitis (e.g., Polyarteritis Nodosa) [1]. These are located deeper in the dermis or subcutis and are not the primary site for common cutaneous eruptions. * **Arterioles (B):** While they can be involved in systemic vasculitides, they have a thicker muscular coat and higher intraluminal pressure, making them less susceptible to immune complex deposition than venules. * **Capillaries (C):** Although capillaries can be involved, the classic histopathological hallmark of leukocytoclastic vasculitis is centered on the post-capillary venules of the superficial dermis [1]. **NEET-PG High-Yield Pearls:** * **Clinical Hallmark:** The classic presentation is **palpable purpura**, usually on dependent areas like the lower legs [3]. * **Histopathology:** Look for **Leukocytoclasis** (nuclear dust from neutrophils), fibrinoid necrosis of the vessel wall, and RBC extravasation [1][3]. * **Most Common Cause:** Often idiopathic, but frequently triggered by drugs (NSAIDs, Penicillin) or infections (Hepatitis B/C) [3]. * **Henoch-Schönlein Purpura (HSP):** A specific type of small vessel vasculitis characterized by **IgA** immune complex deposition. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 279-280.

Question 86: Which of the following acquired conditions is low risk for thrombosis?

A. Heparin-induced thrombocytopenia
B. Oral contraceptive use (Correct Answer)
C. Antiphospholipid antibody syndrome
D. Myocardial infarction

Explanation: This question tests the ability to stratify risk factors for thrombosis according to **Virchow’s Triad**. Acquired (secondary) risk factors for thrombosis are categorized into **High Risk** and **Lower Risk** based on their clinical potency [2]. ### **Explanation of the Correct Answer** **B. Oral contraceptive use:** While estrogen in OCPs increases the hepatic synthesis of coagulation factors (II, VII, IX, X) and decreases antithrombin III, it is classified as a **Lower Risk** (or minor) condition for thrombosis compared to the other options [1]. Other lower-risk conditions include pregnancy, obesity, and prolonged immobilization (e.g., long-distance flights). ### **Analysis of Incorrect Options (High-Risk Conditions)** * **A. Heparin-induced thrombocytopenia (HIT):** This is a **High-Risk** prothrombotic state. It involves the formation of antibodies against the Heparin-PF4 complex, leading to massive platelet activation and consumption, paradoxically causing widespread venous and arterial thrombosis despite a low platelet count. * **C. Antiphospholipid antibody syndrome (APS):** This is a **High-Risk** autoimmune condition. Antibodies (like Lupus Anticoagulant) interfere with phospholipids, causing recurrent vascular thrombosis and pregnancy losses. * **D. Myocardial infarction:** This is a **High-Risk** condition for mural thrombi. The combination of endocardial injury and dyskinetic/akinetic wall motion (stasis) creates a highly thrombogenic environment. ### **High-Yield NEET-PG Pearls** * **High-Risk Acquired Factors:** Prolonged bed rest, MI, Tissue injury (surgery/fracture), Cancer, HIT, and APS. * **Genetic (Primary) Risk Factors:** Factor V Leiden mutation (most common), Prothrombin G20210A mutation, and Antithrombin III deficiency [2]. * **The "Triad":** Remember that **Endothelial Injury** is the most important factor for arterial thrombosis, while **Stasis** is the primary driver for venous thrombosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 428-430. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134.

Question 87: Ischemic heart disease is the usual sequel to:

A. Abdominal aortic aneurysm
B. Rheumatic fever
C. Varicose veins
D. Atherosclerosis (Correct Answer)

Explanation: **Explanation:** **Correct Answer: D. Atherosclerosis** Ischemic Heart Disease (IHD) is a condition characterized by an imbalance between myocardial oxygen supply and demand [3]. The most common underlying cause (in >90% of cases) is **Atherosclerosis** of the epicardial coronary arteries [1]. This chronic inflammatory process leads to the formation of atheromatous plaques, which cause luminal narrowing (stable angina) or acute plaque rupture with thrombosis (Acute Coronary Syndromes/Myocardial Infarction) [2], [4]. **Why the other options are incorrect:** * **A. Abdominal Aortic Aneurysm (AAA):** While AAA shares the same risk factor (atherosclerosis), it is a structural dilation of the aorta [1]. It does not directly cause IHD, though patients with AAA often have concurrent coronary artery disease. * **B. Rheumatic Fever:** This is an autoimmune sequela of Group A Streptococcal infection. It primarily causes **valvular heart disease** (most commonly Mitral Stenosis) rather than ischemic disease of the myocardium. * **C. Varicose Veins:** These are dilated, tortuous superficial veins, usually in the lower limbs, caused by venous hypertension and valvular incompetence. They have no pathophysiological link to coronary artery ischemia. **High-Yield Clinical Pearls for NEET-PG:** * **Critical Stenosis:** IHD symptoms typically manifest when there is >70% reduction in the cross-sectional area of a coronary artery. * **Most Common Site:** The **Left Anterior Descending (LAD)** artery is the most common site of clinically significant atherosclerosis ("The Widow Maker"). * **Risk Factors:** Modifiable risk factors like hyperlipidemia, hypertension, and smoking are the primary drivers of the "Response to Injury" hypothesis of atherosclerosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 507-508. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 499-500. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 558. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 271-272.

Question 88: Which of the following is the least common site of atherosclerotic lesions?

A. Aortic bifurcation
B. Pulmonary arterial trunk (Correct Answer)
C. Common carotid artery
D. Middle cerebral artery

Explanation: **Explanation:** Atherosclerosis is a disease of high-pressure systems. The primary driver for the development of atheromatous plaques is **endothelial injury** caused by hemodynamic stress (hypertension) and biochemical factors [1]. **Why Pulmonary Arterial Trunk is correct:** The pulmonary circulation is a **low-pressure system** (normal systolic pressure ~25 mmHg). Because the shear stress on the endothelium is significantly lower than in the systemic circulation, the pulmonary trunk is generally protected from atherosclerosis. It only develops significant lesions in the setting of **Pulmonary Hypertension**, where pressures rise enough to cause endothelial damage [2]. **Analysis of Incorrect Options:** * **A. Aortic Bifurcation:** This is one of the **most common** sites. Atherosclerosis preferentially involves areas of turbulent flow and "branch points." The bifurcation of the abdominal aorta is a classic site for severe plaque formation [1]. * **C. Common Carotid Artery:** Specifically the carotid bifurcation, this is a high-frequency site for plaque development, often leading to transient ischemic attacks (TIAs) or strokes. * **D. Middle Cerebral Artery:** While smaller than the aorta, the Circle of Willis and its major branches (like the MCA) are frequent sites for atherosclerosis, particularly in patients with chronic hypertension or diabetes. **High-Yield Facts for NEET-PG:** * **Order of Frequency of Atherosclerosis:** Abdominal Aorta > Coronary Arteries > Popliteal Arteries > Internal Carotid Arteries > Circle of Willis. * **Vessels Spared:** Atherosclerosis typically **spares** the upper extremity arteries, mesenteric arteries (except at their ostia), and the pulmonary trunk (unless hypertensive). * **Key Risk Factor:** Hyperlipidemia (specifically high LDL) is the most significant independent risk factor for initiating the "Response to Injury" hypothesis of atherosclerosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 499-506. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 144-145.

Question 89: Hyaline atherosclerosis is seen in which of the following conditions?

A. Benign hypertension (Correct Answer)
B. Chronic hypertension
C. Diabetic nephropathy
D. Analgesic nephropathy

Explanation: **Explanation:** **Hyaline arteriolosclerosis** is a characteristic vascular lesion characterized by homogeneous, pink, hyaline thickening of the arteriolar walls with associated luminal narrowing [1], [3]. **1. Why Benign Hypertension is correct:** In **benign hypertension**, the chronic hemodynamic stress causes plasma components to leak across the vascular endothelium (**extravasation**) [1], [3]. This, combined with increased smooth muscle cell matrix synthesis, results in the deposition of hyaline material. This process is a hallmark of long-standing, non-accelerated (benign) systemic hypertension [2]. **2. Analysis of other options:** * **Chronic Hypertension:** While hyaline changes occur in chronic cases [1], "Benign Hypertension" is the more specific pathological term used in standard textbooks (like Robbins) to differentiate it from the "Hyperplastic" changes seen in malignant hypertension [2], [3]. * **Diabetic Nephropathy:** While hyaline arteriolosclerosis is a classic finding in diabetes (due to non-enzymatic glycosylation of proteins), it typically affects **both afferent and efferent arterioles** [3]. However, in the context of standard pathology questions, it is most classically linked to benign hypertension as the primary etiology. * **Analgesic Nephropathy:** This condition primarily involves **renal papillary necrosis** and chronic interstitial nephritis, not primary hyaline vascular changes. **3. NEET-PG High-Yield Pearls:** * **Hyaline Arteriolosclerosis:** Seen in Benign Hypertension and Diabetes Mellitus [3]. * **Hyperplastic Arteriolosclerosis:** Seen in **Malignant Hypertension** (BP >200/120 mmHg) [3], [4]. It shows a characteristic **"onion-skin"** appearance due to concentric laminated thickening of the wall [4]. * **Monckeberg Medial Sclerosis:** Calcification of the media of medium-sized muscular arteries; does *not* narrow the lumen (clinically insignificant). * **Key Histology:** Hyaline change appears as "smudgy" eosinophilic material on H&E stain. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 541-542. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945.

Question 90: In malignant hypertension, hyperplastic arteriosclerosis is seen in all of the following except?

A. Heart (Correct Answer)
B. Kidney
C. Pericardial fat
D. Peripancreatic fat

Explanation: **Explanation:** **Hyperplastic arteriolosclerosis** is the hallmark vascular lesion of **malignant hypertension** (systolic >200 mmHg, diastolic >120 mmHg) [4]. It is characterized by "onion-skin" concentric laminations of smooth muscle cells and basement membrane thickening, leading to luminal narrowing [1]. **Why Heart is the Correct Answer:** While malignant hypertension causes significant damage to the heart (resulting in Left Ventricular Hypertrophy and potential heart failure), the characteristic **hyperplastic arteriolosclerosis is notably absent in the heart.** The intramyocardial arterioles do not typically show these changes; instead, the heart suffers from the systemic hemodynamic effects of the pressure overload rather than the specific morphological arteriolar lesion [3]. **Analysis of Incorrect Options:** * **Kidney:** This is the most common site [2]. It leads to "flea-bitten kidney" due to petechial hemorrhages and can progress to necrotizing arteriolitis (fibrinoid necrosis) [1]. * **Peripancreatic and Pericardial Fat:** These are classic locations where hyperplastic changes are frequently identified during histopathological examination in cases of systemic malignant hypertension. Other common sites include the gallbladder and intestines. **NEET-PG High-Yield Pearls:** 1. **Two types of Arteriolosclerosis:** * **Hyaline:** Seen in benign hypertension and Diabetes Mellitus (due to plasma protein leakage). * **Hyperplastic:** Seen in malignant hypertension (onion-skin appearance) [1]. 2. **Fibrinoid Necrosis:** If the hypertension is severe enough, hyperplastic changes are accompanied by necrotizing arteriolitis, especially in the renal arterioles [1]. 3. **Flea-bitten Kidney:** Gross appearance in malignant hypertension due to rupture of arterioles/capillaries. (Differential: PSGN, Infective Endocarditis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 276-277. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 277-278. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 495-496.

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

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free