Cardiac Pathology — MCQs
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A 10-year-old girl develops subcutaneous nodules over the skin of her arms and torso 3 weeks after a bout of acute pharyngitis. She manifests choreiform movements and begins to complain of pain in her knees and hips, particularly with movement. A friction rub is heard on auscultation of her chest. An abnormality detected by which of the following serum laboratory findings is most characteristic of the disease affecting this girl?
What is the most common tumor of the heart?
What is the first enzyme to be elevated in myocardial infarction?
Histopathological examination (HPE) of mitral valve in mitral valve prolapse syndrome (MVPS) typically shows which of the following types of degeneration?
What is the most common tumor of the heart?
A young asymptomatic female is observed to have a midsystolic click on routine examination. Which valvular change is most likely responsible?
Atrial myxoma is associated with elevated serum levels of which interleukin?
SLE is characterized by vegetations on the mitral and tricuspid valves. These vegetations are known as:
A 20-year-old male patient collapses and dies suddenly while jogging. Autopsy reveals significant left ventricular hypertrophy predominantly affecting the septum, with no valvular abnormalities. The patient's family history is significant for an uncle who died suddenly at the age of 20 years. Assuming this patient died of an inherited condition, what is the most likely finding on gross examination of the heart?
In Rheumatic fever, fibrinoid necrosis occurs in which of the following structures?
Cardiac Pathology Indian Medical PG Practice Questions and MCQs
Question 151: A 10-year-old girl develops subcutaneous nodules over the skin of her arms and torso 3 weeks after a bout of acute pharyngitis. She manifests choreiform movements and begins to complain of pain in her knees and hips, particularly with movement. A friction rub is heard on auscultation of her chest. An abnormality detected by which of the following serum laboratory findings is most characteristic of the disease affecting this girl?
- A. Anti-streptolysin O antibody titer (Correct Answer)
- B. Antinuclear antibody titer
- C. Creatinine level
- D. Rapid plasma reagin test
Explanation: The clinical presentation describes a classic case of **Acute Rheumatic Fever (ARF)**, a multisystem inflammatory disease following a Group A Streptococcal (GAS) pharyngitis. [1] ### **Explanation of the Correct Answer** The patient exhibits several **Jones Criteria**: Subcutaneous nodules, Sydenham chorea, migratory polyarthritis (knee/hip pain), and carditis (friction rub indicating pericarditis). ARF is a type II hypersensitivity reaction caused by **molecular mimicry**, where antibodies against the streptococcal M-protein cross-react with self-antigens in the heart, joints, and brain [1]. To diagnose ARF, evidence of a preceding GAS infection is mandatory. The **Anti-streptolysin O (ASO) titer** is the most common serological test used to confirm this recent infection. ### **Why Other Options are Incorrect** * **B. Antinuclear antibody (ANA) titer:** Used to screen for Systemic Lupus Erythematosus (SLE). While SLE can cause arthritis and serositis, it does not typically follow pharyngitis or present with chorea [3]. * **C. Creatinine level:** A marker of renal function. While Post-Streptococcal Glomerulonephritis (PSGN) follows GAS infection, it presents with hematuria and hypertension, not chorea or friction rubs [2]. * **D. Rapid plasma reagin (RPR):** A screening test for Syphilis. Syphilis does not present with this constellation of acute inflammatory symptoms in a child. ### **High-Yield NEET-PG Pearls** * **Jones Criteria (Major):** **J**oints (Polyarthritis), **O** (Carditis), **N**odules (Subcutaneous), **E**rythema marginatum, **S**ydenham chorea. * **Pathognomonic Feature:** **Aschoff bodies** (granulomatous foci with fibrinoid necrosis) containing **Anitschkow cells** ("caterpillar cells" with condensed chromatin) [1]. * **Most Common Valve Affected:** Mitral valve (Mitral regurgitation in acute phase; Mitral stenosis in chronic phase). * **Prophylaxis:** Penicillin is the drug of choice to prevent recurrent attacks and chronic valvular heart disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 914-915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 232-233.
Question 152: What is the most common tumor of the heart?
- A. Myxoma (Correct Answer)
- B. Rhabdomyosarcoma
- C. Fibroma
- D. Leiomyosarcoma
Explanation: **Explanation:** The most common primary tumor of the heart in adults is the **Myxoma** [1]. While metastatic tumors (from lung, breast, or melanoma) are technically more common than primary cardiac tumors, among primary tumors, Myxoma accounts for approximately 50%. **Why Myxoma is correct:** Myxomas are benign mesenchymal tumors [1]. About 75-80% occur in the **left atrium**, typically attached to the interatrial septum near the fossa ovalis [2]. They often present with a "tumor plop" sound on auscultation and can cause "ball-valve" obstruction of the mitral valve, mimicking mitral stenosis [2]. Histologically, they are characterized by stellate "myxoma cells" in a mucopolysaccharide stroma [2]. **Why other options are incorrect:** * **Rhabdomyosarcoma:** This is the most common primary **malignant** cardiac tumor in adults, but it is far less frequent than the benign myxoma. * **Fibroma:** These are benign connective tissue tumors, much rarer than myxomas, and are typically seen in the pediatric population (often associated with Gorlin syndrome). * **Leiomyosarcoma:** A rare malignant tumor of smooth muscle origin; it is not a common primary cardiac neoplasm. **High-Yield Clinical Pearls for NEET-PG:** * **Most common primary tumor in children:** Rhabdomyoma (strongly associated with Tuberous Sclerosis) [1]. * **Carney Complex:** An autosomal dominant syndrome featuring multiple cardiac myxomas, skin pigmentation (lentigines), and endocrine overactivity. * **Positional Symptoms:** Myxoma symptoms often change with body position due to the mobile nature of the pedunculated mass [2]. * **Most common site for metastases:** Pericardium (presenting as hemorrhagic pericardial effusion). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 304-306. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 583-584.
Question 153: What is the first enzyme to be elevated in myocardial infarction?
- A. CPK-MB
- B. LDH
- C. Myoglobin (Correct Answer)
- D. Troponin-I
Explanation: **Explanation:** In the setting of acute myocardial infarction (AMI), the timing of cardiac biomarker release depends on the molecule's size and solubility. **Myoglobin** is a small heme protein found in cardiac and skeletal muscle. Due to its low molecular weight, it is released rapidly into the bloodstream following myocyte necrosis, making it the **earliest marker** to rise. * **Why Myoglobin is correct:** It begins to rise within **1–2 hours** of onset, peaks at 6–9 hours, and returns to baseline within 24 hours. While highly sensitive for early diagnosis, it lacks specificity as it also rises in skeletal muscle injury. **Analysis of Incorrect Options:** * **CPK-MB (Creatine Kinase-MB):** This isoenzyme is more specific to the heart than total CK [1]. It begins to rise at **4–6 hours**, peaks at 24 hours, and returns to normal in 48–72 hours [1]. It is the gold standard for detecting **re-infarction**. * **Troponin-I:** These are the most specific markers for myocardial injury. They begin to rise at **3–6 hours** (similar to CPK-MB), peak at 12–24 hours, and remain elevated for 7–10 days. * **LDH (Lactate Dehydrogenase):** This is a late marker. It begins to rise at **12–24 hours**, peaks at 2–3 days, and can stay elevated for up to 14 days [1], [2]. **NEET-PG High-Yield Pearls:** 1. **Earliest Marker:** Myoglobin. 2. **Most Specific Marker:** Cardiac Troponins (I and T). 3. **Marker for Re-infarction:** CPK-MB (due to its short half-life) [1]. 4. **Late Marker:** LDH (useful for patients presenting days after the event) [2]. 5. **Troponin T** stays elevated longer (up to 14 days) than Troponin I. **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. 255-256. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554.
Question 154: Histopathological examination (HPE) of mitral valve in mitral valve prolapse syndrome (MVPS) typically shows which of the following types of degeneration?
- A. Hyaline degeneration
- B. Elastic degeneration
- C. Myxomatous degeneration (Correct Answer)
- D. Fibrinoid necrosis
Explanation: **Explanation:** **Mitral Valve Prolapse (MVP)**, also known as Barlow syndrome, is characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. [1] **Why Myxomatous Degeneration is Correct:** The hallmark histopathological feature of MVP is **myxomatous degeneration**. This involves the marked thickening of the **spongiosa layer** of the valve due to the deposition of mucoid (glycosaminoglycan) material. This process weakens the structural integrity of the valve’s fibrosa layer, leading to the characteristic "billowing" or "floppy" appearance of the leaflets. Under the microscope, this appears as an accumulation of loose, ground substance that stains positively with Alcian blue. Abnormal matrix synthesis and turnover result in myxomatous degeneration and insufficiency. [1] **Analysis of Incorrect Options:** * **A. Hyaline degeneration:** This refers to a non-specific, glassy, pink appearance on H&E stain (e.g., in vascular walls due to hypertension). It is not the primary process in MVP. * **B. Elastic degeneration:** While elastic fibers may be fragmented in MVP, the primary pathological process is the expansion of the myxomatous spongiosa, not a specific "elastic degeneration." * **C. Fibrinoid necrosis:** This is a pattern of cell death characterized by the leakage of fibrin into vessel walls, typically seen in immune-mediated vasculitis or malignant hypertension, not in degenerative valvular disease. **NEET-PG High-Yield Pearls:** * **Clinical Sign:** Characterized by a **mid-systolic click** followed by a late systolic murmur. * **Associations:** Frequently associated with connective tissue disorders like **Marfan Syndrome** (mutation in Fibrillin-1). * **Complications:** Most patients are asymptomatic, but it can lead to infective endocarditis, mitral regurgitation, or sudden cardiac death (rare). * **Gross Appearance:** "Hooding" or "Ballooning" of the leaflets with elongated, thinned chordae tendineae. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 572.
Question 155: What is the most common tumor of the heart?
- A. Myxoma
- B. Secondaries (metastatic tumors) (Correct Answer)
- C. Papillary fibroelastoma
- D. Rhabdomyomas
Explanation: **Explanation:** In cardiac pathology, the most important distinction to make is between primary and secondary tumors. **1. Why "Secondaries" is correct:** Metastatic (secondary) tumors are significantly more common than primary tumors of the heart, occurring approximately **20 to 40 times more frequently**. The most common sources of cardiac metastases are cancers of the lung, breast, melanomas, and lymphomas [1]. These reach the heart via hematogenous spread, lymphatic spread, or direct extension [1]. **2. Analysis of Incorrect Options:** * **A. Myxoma:** This is the most common **primary** tumor of the heart in **adults** [2]. It is typically a benign, gelatinous mass found in the left atrium (75% of cases) [3]. * **C. Papillary fibroelastoma:** These are small, sea-anemone-like benign tumors usually found on cardiac valves. While they are the most common primary tumor of the cardiac valves, they are not the most common overall. * **D. Rhabdomyomas:** These are the most common **primary** cardiac tumors in **infants and children** [3]. They are highly associated with **Tuberous Sclerosis** and often regress spontaneously. **Clinical Pearls for NEET-PG:** * **Most common primary tumor (Adults):** Myxoma ("Ball-valve" obstruction, mid-diastolic murmur) [2]. * **Most common primary tumor (Children):** Rhabdomyoma (Spider cells on histology) [3]. * **Most common primary malignant tumor:** Angiosarcoma (usually in the right atrium). * **Kussmaul sign:** Can be seen in cases of metastatic involvement causing restrictive cardiomyopathy or pericardial effusion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 584-586. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 582-584. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 304-306.
Question 156: A young asymptomatic female is observed to have a midsystolic click on routine examination. Which valvular change is most likely responsible?
- A. Myxomatous degeneration (Correct Answer)
- B. Aschoff bodies
- C. Calcific degeneration
- D. Ruptured chordae tendinae
Explanation: **Explanation:** The clinical presentation of a **midsystolic click** in a young, asymptomatic female is the classic hallmark of **Mitral Valve Prolapse (MVP)**, also known as Barlow Syndrome [1]. **1. Why Myxomatous Degeneration is Correct:** The underlying pathology in MVP is **myxomatous degeneration** of the mitral valve leaflets. This involves the pathological accumulation of dermatan sulfate (glycosaminoglycans) within the *stratum spongiosa* of the valve. This weakens the fibrosa layer, making the leaflets enlarged, redundant, and "floppy." During systole, as the left ventricle contracts, these floppy leaflets balloon (prolapse) back into the left atrium [1]. The sudden tensing of the redundant leaflets and chordae tendineae during this prolapse creates the characteristic **midsystolic click** [1]. **2. Analysis of Incorrect Options:** * **Aschoff Bodies:** These are pathognomonic microscopic foci of fibrinoid necrosis found in **Acute Rheumatic Carditis**. Rheumatic heart disease typically presents with mitral stenosis, not a systolic click [3]. * **Calcific Degeneration:** This is the most common cause of **Aortic Stenosis** in the elderly [2]. It results from chronic "wear and tear" and leads to a harsh systolic ejection murmur, not a click. * **Ruptured Chordae Tendineae:** While this can be a complication of severe MVP or MI, it typically results in **acute mitral regurgitation**, presenting with a holosystolic murmur and sudden heart failure, rather than an isolated asymptomatic click [1]. **NEET-PG High-Yield Pearls:** * **Most common** cause of isolated mitral regurgitation requiring surgery [1]. * **Associations:** Often associated with connective tissue disorders like **Marfan Syndrome** or Ehlers-Danlos Syndrome. * **Auscultation:** Midsystolic click followed by a late systolic murmur. * **Dynamic Auscultation:** The click occurs **earlier** (closer to S1) with maneuvers that decrease preload (e.g., Standing, Valsalva). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 564-566. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 563-564. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 293-294.
Question 157: Atrial myxoma is associated with elevated serum levels of which interleukin?
- A. IL-1
- B. IL-4
- C. IL-6 (Correct Answer)
- D. None of the above
Explanation: **Explanation:** **Atrial Myxoma** is the most common primary cardiac tumor in adults [1][2]. The correct answer is **IL-6 (Interleukin-6)** because these tumor cells characteristically produce and secrete high levels of this pro-inflammatory cytokine. 1. **Why IL-6 is correct:** The systemic manifestations of atrial myxoma (fever, weight loss, malaise, and arthralgia) are often referred to as "constitutional symptoms." These are directly mediated by the overproduction of **IL-6**. Furthermore, IL-6 stimulates the liver to produce acute-phase reactants, leading to an elevated Erythrocyte Sedimentation Rate (ESR) and C-reactive protein (CRP), which are classic laboratory findings in these patients. 2. **Why other options are incorrect:** * **IL-1:** While IL-1 is a potent pyrogen (fever-inducer), it is primarily produced by macrophages and is not the specific biochemical marker associated with the secretory activity of myxoma cells. * **IL-4:** This is a Th2-related cytokine involved in B-cell differentiation and IgE production; it plays no role in the pathogenesis or systemic features of cardiac myxomas. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** 75–80% occur in the **Left Atrium** (usually attached to the fossa ovalis) [1]. * **Auscultation:** Characterized by a **"Tumor Plop"** (a diastolic sound heard as the pedunculated mass swings through the mitral valve) [1]. * **Histology:** Features **Stellate (Myxoma) cells** embedded in a loose, acid mucopolysaccharide (myxoid) stroma [1]. * **Complications:** Systemic embolization (e.g., stroke) and "ball-valve" obstruction of the mitral orifice [1][2]. * **Carney Complex:** An autosomal dominant syndrome (PRKAR1A mutation) featuring cardiac myxomas, skin pigmentation (lentigines), and endocrine overactivity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 583-584. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 304-306.
Question 158: SLE is characterized by vegetations on the mitral and tricuspid valves. These vegetations are known as:
- A. Salmon patch
- B. Libman-Sacks endocarditis (Correct Answer)
- C. Janeway lesions
- D. Osler nodes
Explanation: **Libman-Sacks Endocarditis (LSE)** is the characteristic cardiac manifestation of Systemic Lupus Erythematosus (SLE) [1][2]. These vegetations are unique because they are **sterile (non-bacterial)** and can occur on **both sides of the valve leaflets** (superior and inferior surfaces), as well as on the chordae tendineae and endocardial surfaces [1][3]. They are typically small, single or multiple, pinkish, and warty (verrucous) [1]. Pathologically, they represent an intense local inflammatory response followed by fibrinoid necrosis. **Analysis of Incorrect Options:** * **A. Salmon patch:** This refers to a "stork bite" or nevus simplex, a common capillary vascular malformation seen in newborns, usually on the forehead or nape of the neck. * **C. Janeway lesions:** These are small, **painless**, erythematous macules on the palms or soles. They are a peripheral manifestation of **Infective Endocarditis (IE)** [2] caused by septic emboli. * **D. Osler nodes:** These are **painful**, tender, raised nodules found on the pads of fingers and toes. They are also seen in **Infective Endocarditis** and are caused by immune complex deposition (Type III hypersensitivity). **High-Yield NEET-PG Pearls:** * **Location:** While LSE can affect any valve, the **Mitral valve** is most commonly involved [1][3]. * **Key Feature:** LSE vegetations are "undersurface" or "bidirectional," unlike Rheumatic Heart Disease (verrucae along lines of closure) or Infective Endocarditis (large, friable vegetations) [2][3]. * **Association:** LSE is strongly associated with **Antiphospholipid Antibody Syndrome (APS)**. * **Complication:** Though sterile, these vegetations can lead to valve scarring (regurgitation) or serve as a nidus for secondary bacterial endocarditis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 570. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 232-233.
Question 159: A 20-year-old male patient collapses and dies suddenly while jogging. Autopsy reveals significant left ventricular hypertrophy predominantly affecting the septum, with no valvular abnormalities. The patient's family history is significant for an uncle who died suddenly at the age of 20 years. Assuming this patient died of an inherited condition, what is the most likely finding on gross examination of the heart?
- A. Dilated cardiomyopathy
- B. Restrictive cardiomyopathy
- C. Aortic dissection
- D. Hypertrophic cardiomyopathy (Correct Answer)
Explanation: **Explanation:** The clinical presentation describes a classic case of **Hypertrophic Cardiomyopathy (HCM)** [1]. HCM is the most common cause of sudden cardiac death (SCD) in young athletes [2]. **Why the correct answer is right:** HCM is characterized by **asymmetric septal hypertrophy** (disproportionate thickening of the interventricular septum compared to the free wall) without a secondary cause like hypertension or aortic stenosis [1]. It is an autosomal dominant condition, most commonly due to mutations in genes encoding sarcomeric proteins (e.g., **Beta-myosin heavy chain** or **Myosin-binding protein C**). The sudden death is typically caused by ventricular arrhythmias or outflow tract obstruction (HOCM) [1]. **Why incorrect options are wrong:** * **A. Dilated cardiomyopathy:** Characterized by four-chamber dilation and impaired systolic function [3]. While it can be familial, it does not typically present with isolated septal hypertrophy. * **B. Restrictive cardiomyopathy:** Characterized by stiff, non-compliant ventricles (often due to amyloidosis or sarcoidosis) with normal wall thickness and dilated atria. * **C. Aortic dissection:** Usually associated with Marfan syndrome or long-standing hypertension. While it causes sudden death, it involves a tear in the aortic intima, not primary septal hypertrophy. **High-Yield NEET-PG Pearls:** * **Histology:** Look for **myocyte disarray**, interstitial fibrosis, and hypertrophied myocytes [1]. * **Pathophysiology:** Systolic Anterior Motion (**SAM**) of the mitral valve can lead to Left Ventricular Outflow Tract (LVOT) obstruction [1]. * **Genetics:** Most common mutation is **$\beta$-myosin heavy chain**. * **Murmur:** Harsh systolic ejection murmur that **increases** with Valsalva or standing (decreased preload) and **decreases** with squatting. **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. 559-560. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 576.
Question 160: In Rheumatic fever, fibrinoid necrosis occurs in which of the following structures?
- A. Myocardium
- B. Collagen (Correct Answer)
- C. Pericardium
- D. Endocardium
Explanation: ### Explanation **Correct Answer: B. Collagen** Rheumatic Fever (RF) is a multisystem inflammatory disease following a Group A Streptococcal infection. The hallmark of RF is the **Aschoff body**, which represents a focus of T cells, plasma cells, and activated macrophages (Anitschkow cells) [1]. The fundamental pathological process in these lesions is **fibrinoid necrosis of the connective tissue (collagen)** [1]. During the early phase of RF, the connective tissue undergoes "mucoid degeneration" followed by the deposition of eosinophilic, proteinaceous material that resembles fibrin. This fibrinoid necrosis specifically targets the **interstitial collagen fibers** within the heart and other connective tissues throughout the body [1]. **Analysis of Incorrect Options:** * **A. Myocardium:** While the myocardium is the most common site for Aschoff bodies (interstitial myocarditis), the necrosis does not occur within the myocytes themselves. Instead, it occurs in the **interstitial collagen** between the muscle fibers [1]. * **C. Pericardium:** RF causes "bread and butter" pericarditis (fibrinous pericarditis) [2]. While fibrin is deposited on the surface, the characteristic fibrinoid necrosis of collagen is a feature of the granulomatous Aschoff body, primarily found in the interstitium. * **D. Endocardium:** Endocardial involvement leads to valvulitis and Verrucae. While the underlying pathology involves collagen damage, the specific pathological description of "fibrinoid necrosis" in RF textbooks specifically refers to the alteration of collagenous connective tissue. **NEET-PG High-Yield Pearls:** * **Anitschkow Cells:** Pathognomonic "caterpillar cells" (activated macrophages with condensed chromatin) found in Aschoff bodies [1]. * **Pancarditis:** RF affects all three layers, but **Myocarditis** is the most common cause of death in the acute phase. * **McCallum Patch:** A map-like area of subendocardial thickening, usually in the **posterior wall of the left atrium**, caused by regurgitant jets. * **Jones Criteria:** Used for clinical diagnosis (Major: Joint, Carditis, Nodules, Erythema marginatum, Sydenham chorea). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 566-567. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 101-103.
Practice by Chapter
Congenital Heart Disease
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Ischemic Heart Disease
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Hypertensive Heart Disease
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Valvular Heart Disease
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Myocarditis and Cardiomyopathies
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Pericardial Disease
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Cardiac Tumors
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Heart Failure Pathophysiology
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Cardiac Transplantation Pathology
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Endocarditis
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