CVS Week 9 TLO

Question 2

Define endocarditis.

Answer 2

Inflammation of the endocardium, primarily involving the heart valves.

Question 3

What are the risk factors for endocarditis?

Answer 3

Pre-existing valvular heart disease (e.g., rheumatic heart disease, bicuspid aortic valve)[cite: 1]. Prosthetic heart valves[cite: 1]. Intravenous drug use (IVDU)[cite: 1]. Congenital heart disease[cite: 1]. Indwelling catheters or other foreign bodies[cite: 1]. Compromised immune system[cite: 1].

Question 4

Enumerate the bacterial etiologic agents of infective endocarditis (IE).

Answer 4

Staphylococcus aureus (common in IVDU, prosthetic valves, acute IE)[cite: 1]. Viridans group streptococci (common in native valve IE, especially after dental procedures)[cite: 1]. Enterococci[cite: 1]. HACEK group (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella)[cite: 2].

Question 5

What is the role of fungi as an etiologic agent in infective endocarditis?

Answer 5

Less common, but can occur in immunocompromised patients or with prosthetic valves[cite: 1].

Question 6

Describe the pathogenesis of infective endocarditis (IE).

Answer 6

Starts with endothelial damage to a valve, often due to turbulent blood flow[cite: 1]. Formation of a sterile platelet-fibrin thrombus (non-bacterial thrombotic endocarditis - NBTE) on the damaged valve[cite: 1]. Bacteremia occurs, and bacteria adhere to the NBTE[cite: 1]. Bacterial proliferation within the thrombus, forming vegetations composed of fibrin, platelets, inflammatory cells, and microorganisms[cite: 1]. Vegetations can grow, leading to valve destruction, embolization, or persistent infection[cite: 1].

Question 7

What are the most common clinical manifestations of infective endocarditis (IE)?

Answer 7

Fever [cite: 2] and a new or changing heart murmur[cite: 2].

Question 8

List non-specific clinical manifestations of infective endocarditis (IE).

Answer 8

Fatigue[cite: 2], malaise[cite: 2], anorexia[cite: 2], weight loss[cite: 2].

Question 9

Describe embolic phenomena associated with infective endocarditis (IE).

Answer 9

Systemic emboli (e.g., stroke, splenic infarct, renal infarct)[cite: 1]. Pulmonary emboli (if right-sided IE)[cite: 1].

Question 10

Describe immunologic phenomena associated with infective endocarditis (IE).

Answer 10

Osler nodes (tender, red nodules on fingertips/toes)[cite: 2]. Janeway lesions (non-tender, hemorrhagic macules on palms/soles)[cite: 2]. Roth spots (retinal hemorrhages with pale centers)[cite: 2]. Glomerulonephritis[cite: 1].

Question 11

What are the crucial investigations for diagnosing endocarditis?

Answer 11

Blood Cultures (at least 3 sets from different sites)[cite: 2]. Echocardiography, including Transthoracic echocardiogram (TTE) for initial imaging, and Transesophageal echocardiogram (TEE) which is more sensitive for detecting vegetations, abscesses, and valvular damage[cite: 2].

Question 12

What laboratory findings are associated with endocarditis?

Answer 12

Elevated ESR, C-reactive protein (CRP), anemia, leukocytosis[cite: 2].

Question 13

What diagnostic criteria are used for endocarditis?

Answer 13

Duke Criteria, which combine major (blood cultures, echocardiographic findings of vegetations) and minor criteria (fever, predisposing factors, vascular/immunologic phenomena)[cite: 2].

Question 14

Outline the medical management of infective endocarditis (IE).

Answer 14

Prolonged course of intravenous antibiotics (4-6 weeks), tailored to the causative organism and sensitivities[cite: 2].

Question 15

When is surgery indicated in the management of infective endocarditis (IE)?

Answer 15

For severe valvular dysfunction[cite: 1, 2], intractable infection[cite: 2], large vegetations with high embolic risk[cite: 2], or heart failure[cite: 1, 2].

Question 16

What monitoring is required during the management of infective endocarditis (IE)?

Answer 16

Regular blood cultures[cite: 2], echocardiograms[cite: 2], and clinical assessment[cite: 2].

Question 17

What are the major cardiac complications of infective endocarditis (IE)?

Answer 17

Heart Failure due to severe valvular regurgitation or obstruction[cite: 1].

Question 18

List systemic complications of infective endocarditis (IE).

Answer 18

Systemic Embolism (Stroke, splenic/renal infarcts, mycotic aneurysms)[cite: 1]. Perivalvular Extension (abscess formation, fistulas)[cite: 2]. Renal Failure (due to glomerulonephritis or emboli)[cite: 1].

Question 19

Discuss the prognosis of infective endocarditis (IE).

Answer 19

Variable, depends on the causative organism, extent of valvular damage, presence of complications, and promptness of treatment[cite: 2]. High mortality if untreated or with severe complications[cite: 2].

Question 20

Enumerate the most common etiologic agents of myocarditis.

Answer 20

Viral agents, such as Coxsackievirus B, adenovirus, parvovirus B19, influenza, enteroviruses, and HIV.

Question 21

List other categories of etiologic agents for myocarditis.

Answer 21

Bacterial (e.g., Diphtheria, Lyme disease, Streptococcus). Fungal (e.g., Candida, Aspergillus). Parasitic (e.g., Trypanosoma cruzi - Chagas disease). Autoimmune diseases (e.g., Systemic lupus erythematosus, sarcoidosis). Toxins/Drugs (e.g., alcohol, cocaine, chemotherapy agents).

Question 22

Describe the pathogenesis of viral myocarditis.

Answer 22

Direct viral infection of cardiomyocytes. Immune-mediated damage: Viral antigens trigger an immune response that mistakenly attacks cardiac muscle cells. Myocyte necrosis and inflammation lead to impaired cardiac function.

Question 23

What are the common clinical manifestations of myocarditis?

Answer 23

Highly variable, from asymptomatic to severe heart failure or sudden cardiac death. Flu-like symptoms (fever, myalgia, fatigue) often precede cardiac symptoms. Cardiac symptoms include chest pain (mimicking MI), dyspnea, palpitations, syncope, and symptoms of heart failure (e.g., edema, orthopnea). Arrhythmias (atrial or ventricular, heart block) may also occur.

Question 24

What are the key investigations for myocarditis?

Answer 24

ECG (non-specific changes, ST-T wave abnormalities, arrhythmias, conduction blocks). Cardiac Biomarkers (elevated troponin). Echocardiography (assess ventricular function, wall motion abnormalities, chamber dilation). Cardiac MRI (highly sensitive for detecting myocardial inflammation, edema, and fibrosis). Endomyocardial Biopsy (gold standard for definitive diagnosis, but invasive).

Question 25

What are the Dallas Criteria for the biopsy diagnosis of myocarditis?

Answer 25

"Myocardial inflammatory infiltrate with associated myocyte necrosis not typical of ischemic damage".

Question 26

Describe the microscopic features of myocarditis.

Answer 26

Inflammatory infiltrates (lymphocytes, macrophages, eosinophils depending on cause), myocyte necrosis, edema.

Question 27

Outline the management of myocarditis.

Answer 27

Supportive care: Rest, monitoring, treatment of heart failure symptoms (diuretics, ACE inhibitors, beta-blockers). Immunosuppression may be considered in specific autoimmune forms, but generally not for viral myocarditis. Arrhythmia management (antiarrhythmic drugs, pacemakers if severe heart block). Avoid NSAIDs (can worsen inflammation) and alcohol.

Question 28

What are the complications of myocarditis?

Answer 28

Dilated Cardiomyopathy (chronic inflammation can lead to progressive ventricular dilation and systolic dysfunction). Arrhythmias (persistent arrhythmias, sudden cardiac death). Heart Failure (acute or chronic).

Question 29

Discuss the prognosis of myocarditis.

Answer 29

Highly variable. Many cases resolve spontaneously, but some progress to chronic heart failure or require transplantation.

Question 30

Define acute pericarditis.

Answer 30

Inflammation of the pericardium (the sac surrounding the heart).

Question 31

Enumerate the causes of pericarditis.

Answer 31

Infectious: Viral (most common, e.g., Coxsackievirus, adenovirus), bacterial, fungal, TB. Autoimmune/Inflammatory: SLE, rheumatoid arthritis, Dressler's syndrome (post-MI). Uremia (in kidney failure). Neoplastic (metastatic cancer). Trauma/Surgery (post-cardiac surgery). Idiopathic (no identifiable cause, common).

Question 32

Describe the clinical manifestations of acute pericarditis.

Answer 32

Chest Pain: Pleuritic (sharp, stabbing, worsens with inspiration and cough), typically relieved by leaning forward and worse when lying flat. Pericardial Friction Rub: A high-pitched, scratchy sound heard on auscultation, often triphasic. Fever (common). Dyspnea (may occur due to pain or large effusion).

Question 33

How does the chest pain of acute pericarditis compare to that of pulmonary embolism and myocardial infarction?

Answer 33

Pericarditis: Pleuritic, sharp, stabbing; relieved by leaning forward; worse with inspiration. Pulmonary Embolism: Pleuritic, sudden onset, sharp; worse with inspiration. Myocardial Infarction: Crushing, oppressive, substernal; often radiates to arm/jaw; not pleuritic; not relieved by leaning forward.

Question 34

How do auscultation findings differ in acute pericarditis, pulmonary embolism, and myocardial infarction?

Answer 34

Pericarditis: Pericardial friction rub. Pulmonary Embolism: Normal lung sounds or crackles. Myocardial Infarction: S3/S4 gallop, new murmur.

Question 35

What are the characteristic ECG changes in acute pericarditis compared to pulmonary embolism and myocardial infarction?

Answer 35

Pericarditis: Widespread ST-segment elevation (concave up), PR depression. Pulmonary Embolism: S1Q3T3 pattern, tachycardia, T-wave inversion. Myocardial Infarction: ST-segment elevation (convex up, localized), Q waves, T-wave inversion.

Question 36

Compare the associated symptoms of acute pericarditis, pulmonary embolism, and myocardial infarction.

Answer 36

Pericarditis: Fever, malaise. Pulmonary Embolism: Dyspnea, tachypnea, cough, hemoptysis, syncope. Myocardial Infarction: Diaphoresis, nausea, vomiting, dyspnea.

Question 37

How do cardiac biomarkers differ in acute pericarditis, pulmonary embolism, and myocardial infarction?

Answer 37

Pericarditis: May be mildly elevated (from epicardial inflammation). Pulmonary Embolism: Usually normal. Myocardial Infarction: Significantly elevated (Troponin, CK-MB).

Question 38

What investigations are used for diagnosing pericarditis and what are their diagnostic findings?

Answer 38

ECG: Widespread ST-segment elevation (concave upwards), PR-segment depression (especially in limb leads and V2-V6). Echocardiography: Assess for pericardial effusion, cardiac tamponade. Chest X-ray: May show cardiomegaly if a large effusion is present ("water bottle" sign). Laboratory findings: Elevated inflammatory markers (ESR, CRP), may have elevated troponin (due to associated myocardial inflammation).

Question 39

Outline the management of pericarditis.

Answer 39

Pain Relief: NSAIDs (e.g., ibuprofen, indomethacin) are first-line. Colchicine: Often added to NSAIDs to reduce recurrence. Corticosteroids: Used for refractory cases or specific etiologies (e.g., autoimmune), but generally avoided initially due to recurrence risk. Treat underlying cause (e.g., antibiotics for bacterial, dialysis for uremic).

Question 40

What are the complications of pericarditis?

Answer 40

Pericardial Effusion (fluid accumulation in the pericardial space). Cardiac Tamponade (life-threatening compression of the heart due to rapid or large pericardial effusion). Recurrent Pericarditis (episodes of pericarditis after an initial event). Constrictive Pericarditis (rare, chronic complication where the pericardium thickens and stiffens).

Question 41

Discuss the prognosis of pericarditis.

Answer 41

Most cases of acute viral/idiopathic pericarditis resolve spontaneously. Recurrence is common. Constrictive pericarditis is a serious long-term complication.

Question 42

Define Acute Rheumatic Fever (ARF) and Rheumatic Heart Disease (RHD).

Answer 42

Acute Rheumatic Fever (ARF): An acute, inflammatory disease that may develop after an infection with Group A Streptococcus (GAS), typically pharyngitis. It can affect the heart, joints, brain, and skin. Rheumatic Heart Disease (RHD): A chronic condition resulting from permanent cardiac damage, especially to the heart valves, following one or more episodes of ARF[cite: 1].

Question 43

Discuss the etiology and pathogenesis of Rheumatic Fever (RF).

Answer 43

Etiology: Caused by an autoimmune reaction to Group A Streptococcus pyogenes (GAS) pharyngeal infection (strep throat). Pathogenesis: Involves "molecular mimicry." Antibodies produced against GAS M proteins cross-react with similar antigens in human tissues (heart, joints, brain), leading to inflammation and damage[cite: 1].

Question 44

Describe the morphological features in acute Rheumatic Fever (RF).

Answer 44

Heart: Pancarditis (inflammation of all layers: endocardium, myocardium, pericardium)[cite: 1]. Characteristic Aschoff bodies (fibrinoid necrosis surrounded by inflammatory cells, including Anitschkow cells/caterpillar cells) in the myocardium[cite: 1]. Valvulitis leads to valve leaflet swelling and small vegetations (verrucae) along the lines of closure[cite: 1]. Joints: Migratory polyarthritis. Skin: Erythema marginatum. Brain: Sydenham chorea.

Question 45

Describe the morphological features in Rheumatic Heart Disease (RHD).

Answer 45

Chronic valve damage: Fibrosis, thickening, and calcification of valve leaflets, often leading to stenosis (narrowing) or regurgitation (leakage)[cite: 1]. The mitral valve is most commonly affected, followed by the aortic valve[cite: 1].

Question 46

What are the clinical manifestations of Acute Rheumatic Fever (ARF)?

Answer 46

Arthritis: Migratory polyarthritis of large joints (most common, ~75%). Carditis: Inflammation of the heart, leading to murmurs, pericarditis, or heart failure. Chorea (Sydenham's chorea): Involuntary, purposeless movements. Erythema marginatum: Non-pruritic, erythematous rash with clear centers. Subcutaneous nodules: Firm, painless nodules over bony prominences.

Question 47

What are the clinical manifestations of Rheumatic Heart Disease (RHD)?

Answer 47

Symptoms related to chronic valve dysfunction (e.g., dyspnea, fatigue, palpitations, signs of heart failure) developing years after the acute illness.

Question 48

Enumerate the Major Criteria of Jones Criteria for the diagnosis of Rheumatic Fever (RF).

Answer 48

Carditis, Polyarthritis (migratory), Chorea (Sydenham), Erythema marginatum, Subcutaneous nodules.

Question 49

Enumerate the Minor Criteria of Jones Criteria for the diagnosis of Rheumatic Fever (RF).

Answer 49

Fever, Arthralgia (joint pain), Elevated acute phase reactants (ESR, CRP), Prolonged PR interval on ECG.

Question 50

What evidence of recent GAS infection is required for the diagnosis of Rheumatic Fever (RF)?

Answer 50

Positive throat culture or rapid strep test, elevated anti-streptolysin O (ASO) titer, or anti-DNase B titer.

Question 51

What is required for the diagnosis of Rheumatic Fever (RF) using Jones Criteria?

Answer 51

2 Major criteria OR 1 Major and 2 Minor criteria, PLUS evidence of recent GAS infection.

Question 52

Outline the management of Rheumatic Fever (RF).

Answer 52

Antibiotics: Penicillin to eradicate GAS infection (even if throat culture negative). Anti-inflammatory agents: Aspirin (for arthritis and fever), corticosteroids (for severe carditis). Supportive care: Rest, management of heart failure if present. Secondary Prophylaxis: Long-term antibiotics (usually penicillin) to prevent recurrent GAS infections and subsequent RF episodes. Duration depends on severity of initial RF and presence of carditis.

Question 53

What are the complications of Rheumatic Fever (RF)?

Answer 53

Rheumatic Heart Disease (RHD) [cite: 1] (chronic valvular heart disease: mitral stenosis/regurgitation, aortic stenosis/regurgitation)[cite: 1]. Heart Failure (due to severe valvular dysfunction). Arrhythmias (especially atrial fibrillation in chronic RHD). Stroke (due to emboli from atrial fibrillation or valvular vegetations).

Question 54

Discuss the prognosis of Rheumatic Fever (RF).

Answer 54

Acute RF usually resolves, but recurrence is a major concern. The prognosis of RHD depends on the severity of valvular damage and response to management.

Question 55

Discuss the origin and morphological features of myxoma.

Answer 55

Origin: Most common primary tumor of the heart in adults[cite: 1]. Typically benign[cite: 1]. Arises from multipotent mesenchymal cells[cite: 1]. Location: Over 80% are in the left atrium, followed by the right atrium[cite: 1]. Morphology: Often pedunculated (stalked) and mobile, attached to the interatrial septum near the foramen ovale[cite: 1]. Gelatinous, soft, often lobulated, glistening appearance[cite: 1]. Can range in size from small to several centimeters.

Question 56

Describe the clinical features of myxoma.

Answer 56

Highly variable, often mimics other cardiac conditions. Cardiac symptoms (most common): "Ball-valve" obstruction (intermittent obstruction of the mitral or tricuspid valve orifice, leading to syncopal episodes, dyspnea, or orthopnea, often positional)[cite: 1]. Murmur: Varies with position, can be mistaken for mitral stenosis[cite: 1]. Heart failure symptoms. Embolic phenomena: Fragments of the tumor can embolize systemically (e.g., stroke, splenic infarct, renal infarct)[cite: 1]. Constitutional symptoms: Fever, malaise, weight loss, arthralgia, fatigue (due to cytokine release).

Question 57

What are the key diagnostic tools for myxoma?

Answer 57

Echocardiography (definitive diagnostic tool, allowing visualization of the tumor, its attachment, size, and mobility, as well as its impact on valve function). Cardiac MRI/CT (can also be used for detailed imaging). Laboratory findings: Elevated ESR, CRP, anemia (non-specific).

Question 58

What are the treatment options and prognosis for myxoma?

Answer 58

Treatment: Surgical excision is the definitive treatment. The tumor is usually removed with its stalk and a portion of the attached septum. Prognosis: Excellent post-surgical prognosis if completely resected, but recurrence is possible (especially with incomplete resection or in familial cases). Untreated, it can lead to severe complications or sudden death.

Question 59

Describe familial myxomas and list the components of Carney Complex.

Answer 59

Familial Myxomas: Occur in a small percentage of cases, often multiple, recur more frequently. Carney Complex: An autosomal dominant syndrome associated with familial myxomas. Components: Cardiac myxomas (often multiple), skin myxomas, pigmented skin lesions (lentigines), primary pigmented nodular adrenocortical disease (leading to Cushing syndrome), pituitary adenomas, schwannomas, and testicular tumors.