Atherosclerosis — MCQs
Plaques jaunes are seen in which condition?
Following are the risk factors of atherosclerosis, except?
Which of the following is a non- modifiable risk factor for CHD -
Primordial prevention in myocardial infarction is all except -
Fibrinoid necrosis with neutrophilic infiltration is seen in ?
Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
Which of the following is not a symptom of carotid atherosclerosis?
Which of the following factors play a major role in the initiation of thrombus formation?
Which cell acts as the primary effector cell in type IV (delayed-type) hypersensitivity reactions?
An athlete collapsed suddenly during exercise and died on the field. Postmortem heart is shown in the figure. There is family history of heart disease. What is the diagnosis?
Atherosclerosis Indian Medical PG Practice Questions and MCQs
Question 1: 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 2: Following are the risk factors of atherosclerosis, except?
- A. Diabetes
- B. Regular moderate exercise (Correct Answer)
- C. Obesity
- D. Hypertension
Explanation: ***Obesity*** - Obesity is considered a **modifiable risk factor** for atherosclerosis as it can be addressed through lifestyle changes like diet and exercise. [2] - It is associated with increased levels of **LDL cholesterol** and other metabolic disturbances that contribute to vascular disease. [5] *Hypertension* - Hypertension is also a **modifiable risk factor** and can be managed through medication and lifestyle changes. [4] - Elevated blood pressure contributes to **endothelial damage** and atherosclerosis progression. [1] *Diabetes* - Diabetes is a significant **modifiable risk factor** as it can worsen atherosclerosis through high blood sugar levels damaging blood vessels. [4] - Management of diabetes through diet, exercise, and medication can significantly reduce cardiovascular risk. [3] *Physical inactivity* - Physical inactivity is a **modifiable risk factor** as regular exercise can improve cardiovascular health and lower atherosclerosis risk. - Increased physical activity helps maintain a healthy weight and reduces **blood pressure** and blood sugar levels.
Question 3: Which of the following is a non- modifiable risk factor for CHD -
- A. Diabetes
- B. Smoking
- C. Hypertension
- D. Old age (Correct Answer)
Explanation: Old age - Age is a **non-modifiable risk factor** for Coronary Heart Disease (CHD) because it is an inherent biological process that cannot be changed [3]. - The risk of developing CHD **increases with age** due to cumulative exposure to other risk factors and natural wear and tear on the cardiovascular system [3]. *Diabetes* - Diabetes is a **modifiable risk factor** for CHD because it can be managed and controlled through lifestyle changes, medication, and regular monitoring [2]. - **Poorly controlled diabetes** significantly increases the risk of heart disease by damaging blood vessels and promoting atherosclerosis. *Smoking* - Smoking is a highly **modifiable risk factor** for CHD as it can be completely stopped [1], [2]. - **Cessation of smoking** significantly reduces the risk of heart attack and stroke over time [1]. *Hypertension* - Hypertension is a **modifiable risk factor** for CHD because blood pressure can be lowered through lifestyle interventions, such as diet and exercise, and pharmacotherapy [2]. - **Uncontrolled high blood pressure** places increased stress on the heart and blood vessels, accelerating the development of atherosclerosis [1].
Question 4: Primordial prevention in myocardial infarction is all except -
- A. Change in life style
- B. Change in Nutritional habits
- C. Maintenance of normal body weight
- D. Screening for hypertension (Correct Answer)
Explanation: ***Screening for hypertension*** - **Screening for hypertension** falls under **primary prevention**, as it aims to detect and treat a risk factor in individuals who have already developed a predisposition to the disease. - **Primordial prevention** focuses on preventing the development of risk factors themselves, rather than detecting them once they've emerged. *Change in life style* - **Lifestyle changes** such as promoting regular physical activity and avoiding smoking are key components of **primordial prevention**, preventing the development of risk factors like obesity and hypertension. - These interventions aim to stop risk factors from even appearing in healthy populations. *Change in Nutritional habits* - Promoting **healthy nutritional habits** from an early age is a fundamental strategy in **primordial prevention**, aiming to prevent the development of conditions like obesity and hyperlipidemia. - This proactive approach seeks to establish healthy patterns before disease risk factors take hold. *Maintenance of normal body weight* - Encouraging and supporting the **maintenance of normal body weight** in the general population is a classic example of **primordial prevention**. - This prevents the emergence of obesity, a major risk factor for cardiovascular diseases like myocardial infarction.
Question 5: 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 6: 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.
Question 7: Which of the following is not a symptom of carotid atherosclerosis?
- A. Contralateral body TIA
- B. Ipsilateral retinal infarction
- C. Ipsilateral amaurosis fugax
- D. Contralateral retinal infarction (Correct Answer)
Explanation: ***Contralateral retinal infarction*** - Retinal infarction, or **ocular stroke**, specifically affects the **ipsilateral eye** (the eye on the same side as the affected carotid artery), as the ophthalmic artery branches off the internal carotid artery. - A contralateral retinal infarction would imply the blockage is in the opposite carotid artery or a different circulatory issue. *Ipsilateral retinal infarction* - This is a direct consequence of **carotid stenosis**, as emboli from the carotid artery can travel up the **ophthalmic artery** to cause infarction in the retina of the same-sided eye. - Presents as sudden, painless **loss of vision** in one eye, often in a specific field. *Contralateral body TIA* - **Transient ischemic attacks (TIAs)** resulting from carotid atherosclerosis typically cause neurological deficits on the **contralateral side of the body** due to the decussation of motor and sensory pathways in the brain. - Symptoms like temporary weakness, numbness, or speech difficulties on the opposite side of the body are characteristic. *Ipsilateral amaurosis fugax* - **Amaurosis fugax** is a classic symptom of carotid atherosclerosis, characterized by a **transient monocular vision loss** (often described as a curtain coming down) in the eye on the *same side* as the affected carotid artery. - This occurs due to **retinal emboli** originating from the carotid plaque.
Question 8: Which of the following factors play a major role in the initiation of thrombus formation?
- A. Vasoconstriction
- B. Coagulation cascade activation
- C. Platelets activation
- D. Endothelial injury (Correct Answer)
Explanation: ***Endothelial injury*** - **Endothelial injury** is a critical initiating factor in thrombus formation, leading to platelet adhesion and activation [1]. - Damage to the endothelium exposes the underlying **collagen** and **tissue factor**, which promote hemostasis and coagulation [2,3,5]. *Vasoconstriction* - While vasoconstriction can reduce blood flow and helps in minimizing blood loss, it is not a direct initiator of thrombus formation. - It primarily acts as a response to injury rather than a trigger for the **clotting mechanism**. *Coagulation cascade activation* - Activation of the coagulation cascade occurs after endothelial injury and is part of the clotting process, not the initiation [2]. - It involves various factors like fibrinogen and prothrombin but is secondary to the initial endothelial damage. *Platelets activation* - Platelet activation is a response to the exposed collagen due to endothelial injury and is not the initial trigger of thrombus formation [3,4,5]. - It occurs as a subsequent step once the endothelial injury has taken place, facilitating plug formation [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 132-133. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 126-128. [3] 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. 142-143. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-582. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128.
Question 9: Which cell acts as the primary effector cell in type IV (delayed-type) hypersensitivity reactions?
- A. Neutrophil
- B. Dendritic cell
- C. Macrophage (Correct Answer)
- D. Cytotoxic T cell
Explanation: ***Macrophage*** - **Macrophages** are the **principal effector cells** in type IV hypersensitivity reactions, responsible for the characteristic tissue damage and inflammation [1]. - They are activated by **IFN-γ and other cytokines** released by sensitized CD4+ Th1 cells upon antigen re-exposure [2]. - Activated macrophages release **inflammatory mediators, lysosomal enzymes, and reactive oxygen species** that cause tissue damage [3]. - They are central to **granuloma formation** (e.g., tuberculosis, sarcoidosis) and the classic tuberculin skin test reaction [1]. *Neutrophil* - **Neutrophils** are the hallmark of acute inflammation and type III hypersensitivity (immune complex reactions). - While neutrophils can be recruited in some type IV reactions (subtype IVd), they are **not the defining effector cells** of classic delayed-type hypersensitivity [1]. *Dendritic cell* - **Dendritic cells** function as **antigen-presenting cells (APCs)** in the sensitization/afferent phase [1]. - They capture and present antigens to naive T cells but do **not serve as effector cells** causing tissue damage in the efferent phase. *Cytotoxic T cell* - **CD8+ cytotoxic T cells** are involved in a specific subtype of type IV hypersensitivity (type IVc) where they directly kill antigen-bearing target cells. - However, in **classic delayed-type hypersensitivity** (type IVa, e.g., tuberculin reaction, contact dermatitis), **macrophages are the predominant effector cells** mediating tissue damage through inflammatory mediators rather than direct cytotoxicity [1]. **Note:** Type IV hypersensitivity is T cell-mediated, with CD4+ Th1 cells initiating the response, but macrophages execute the effector function as the primary tissue-damaging cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.
Question 10: An athlete collapsed suddenly during exercise and died on the field. Postmortem heart is shown in the figure. There is family history of heart disease. What is the diagnosis?
- A. Hypertrophic cardiomyopathy (Correct Answer)
- B. Mitral regurgitation
- C. Mitral stenosis
- D. Aortic stenosis with left ventricular hypertrophy
Explanation: ***Hypertrophic cardiomyopathy*** - **Sudden cardiac death** in young athletes, especially with a family history, is a classic presentation of **hypertrophic cardiomyopathy (HCM)** [2][3]. - Postmortem examination typically reveals **asymmetric septal hypertrophy** and **myocardial fiber disarray**, which are characteristic of HCM [1]. *Mitral regurgitation* - While mitral regurgitation can lead to heart failure, it is less commonly associated with **sudden death in athletes** without prior symptoms. - The primary finding would be **valvular abnormalities** and **left atrial/ventricular dilation**, not typically isolated hypertrophy. *Mitral stenosis* - Mitral stenosis primarily causes **left atrial enlargement** and **pulmonary hypertension**, leading to symptoms like dyspnea and fatigue. - It is not a common cause of **sudden cardiac death** in athletes and would not typically present with the gross hypertrophy seen in HCM. *Aortic stenosis with left ventricular hypertrophy* - Aortic stenosis can cause **left ventricular hypertrophy** due to increased pressure overload. - However, sudden death in athletes due to aortic stenosis is less common than HCM, and the hypertrophy in aortic stenosis is typically **concentric** and symmetrical, unlike the asymmetric hypertrophy often seen in HCM [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 577-578. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 576-577. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 303-304.
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