Copilot Exam 4 - Notes Week 7 to 11 Flashcards
(180 cards)
1
Q
Questions
A
Answers
2
Q
What is myocardial ischemia?
A
Reduced blood flow to heart muscle, limiting oxygen supply.
3
Q
What determines myocardial oxygen demand?
A
Heart rate, contractility, wall tension, metabolic activity.
4
Q
What are causes of myocardial ischemia?
A
Atherosclerosis, coronary spasm, thrombosis, embolism, dissection, anemia, hypotension.
5
Q
What are the types of angina?
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Stable: Exertional, relieved by rest. Unstable: Occurs at rest, unpredictable. Prinzmetal’s: Coronary spasm, transient ST elevation.
6
Q
What are ECG changes in angina?
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Stable: ST depression, T wave inversion. Prinzmetal’s: Transient ST elevation. Unstable: Non-specific changes.
7
Q
What is the management of angina?
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Lifestyle (quit smoking, exercise), medications (nitrates, beta-blockers, CCBs, antiplatelets), revascularization (PCI, CABG).
8
Q
What are risk factors for atherosclerosis?
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Smoking, hypertension, hyperlipidemia, diabetes, obesity, age, sex, family history.
9
Q
What is the pathogenesis of atherosclerosis?
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Endothelial injury → Lipid accumulation → Foam cells → Fibrous cap → Plaque formation.
10
Q
What are microscopic features of plaques?
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Lipid core, fibrous cap (collagen, muscle cells), inflammatory cells, neovascularization.
11
Q
Plaque rupture vs. erosion in MI?
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Rupture: Exposes thrombogenic core, occlusive thrombosis. Erosion: Less fibrous disruption, also leads to thrombosis.
12
Q
What are anti-atherosclerotic therapies?
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Lifestyle (diet, exercise, smoking cessation), medications (statins, antihypertensives, antidiabetics).
13
Q
What are types of lipids?
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Triacylglycerols (energy), phospholipids (membranes), cholesterol (hormone precursor).
14
Q
What are types of lipoproteins?
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Chylomicrons, VLDL, LDL, HDL.
15
Q
What is LDL’s role in atherosclerosis?
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Transports cholesterol to tissues; oxidized LDL triggers endothelial damage, foam cell formation.
16
Q
What are apolipoproteins?
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Lipoprotein structural components, receptor ligands (e.g., ApoB-100 for LDL).
17
Q
What is HDL’s protective role?
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Reverse cholesterol transport, anti-inflammatory, antioxidant effects.
18
Q
What are lipid-lowering agents?
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Statins (HMG-CoA reductase inhibitors), ezetimibe (blocks intestinal absorption), PCSK9 inhibitors (increase LDL receptor recycling).
19
Q
What is ischemic heart disease (IHD)?
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Coronary artery narrowing, leading to myocardial ischemia.
20
Q
What are MI risk factors?
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Smoking, hypertension, hyperlipidemia, diabetes, metabolic syndrome.
21
Q
What is MI pathophysiology?
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Plaque rupture → thrombosis → coronary occlusion → myocardial necrosis.
22
Q
What are ECG findings in STEMI vs. NSTEMI?
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NSTEMI: ST depression, T wave inversion. STEMI: ST elevation, new LBBB, later Q waves.
23
Q
What are cardiac biomarkers for MI?
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Troponin I/T (most sensitive), CK-MB (detects reinfarction).
24
Q
What are diagnostic imaging modalities?
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Echocardiogram, cardiac MRI, coronary angiography, CT angiography.
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What are MI medical treatments?
MONA: Morphine, oxygen, nitrates, aspirin. Beta-blockers, anticoagulants, statins.
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What are drug mechanisms in MI management?
Aspirin/clopidogrel (platelet inhibition), nitrates (vasodilation), beta-blockers (↓ oxygen demand), heparin (thrombus prevention).
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What are MI interventions?
PCI (preferred for STEMI), CABG for high-risk cases, thrombolysis if PCI unavailable.
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What are complications of MI?
Arrhythmias (most common early death cause), heart failure, shock, rupture, embolism, ventricular aneurysm, Dressler’s syndrome.
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What are lifestyle modifications post-MI?
Smoking cessation, exercise, healthy diet, weight control, adherence to medications.
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Questions
Answers
31
What embryonic layer forms the heart?
Mesoderm (cardiogenic mesoderm).
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Which cells contribute to heart development?
Neural crest (outflow tract), proepicardial (epicardium, coronary vessels).
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What initiates heart conduction?
SA node develops as pacemaker; AV node, bundle of His, Purkinje fibers follow.
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What forms the atrial septa?
Septum primum grows, leaving foramen primum; foramen secundum forms before closure; septum secundum completes partitioning.
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How does the AV canal partition?
Endocardial cushions grow and fuse, forming right and left AV canals.
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What forms the ventricular septum?
Interventricular septum grows upward; endocardial cushions and bulbus cordis contribute.
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What forms heart valves?
Endocardial cushions remodel and thin into valve leaflets.
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What forms the aorta and arches?
Aortic sac and dorsal aortae; aortic arches remodel into adult arteries.
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What forms coronary arteries?
Epicardium and endothelial cells contribute.
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What forms cranial arteries?
Aortic arches and plexuses in the head region.
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What forms the lymphatic system?
Endothelial sacs arise from veins.
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What veins form early circulation?
Cardinal (embryo drainage), vitelline (yolk sac), umbilical (placental oxygenation).
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What are key fetal circulation features?
Placenta oxygenates blood; foramen ovale and ductus arteriosus bypass lungs.
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What are fetal blood oxygenation levels?
Oxygenated: Umbilical vein. Mixed: Right atrium, ventricle, aorta. Deoxygenated: Umbilical arteries.
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What fetal circulation adaptations exist?
Foramen ovale (RA to LA shunt), ductus venosus (placenta bypass), ductus arteriosus (PA to aorta shunt).
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What changes occur at birth?
Closure of foramen ovale, ductus arteriosus, ductus venosus; umbilical vessels obliterate.
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What causes these changes?
Increased LA pressure closes foramen ovale; oxygen ↑ and ↓ prostaglandins close ductus arteriosus.
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What is a congenital heart defect?
Structural abnormality of the heart present at birth.
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What are left-to-right shunt defects?
PDA, VSD, ASD, PFO (increased pulmonary flow).
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What are right-to-left shunt defects?
Tetralogy of Fallot, transposition of great arteries (cyanosis).
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What causes PDA?
Failure of ductus arteriosus to close; leads to pulmonary overload.
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What is PDA management?
Indomethacin (closure), surgery (if needed).
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What causes TGA?
Aorta and PA switched; survival depends on mixing via shunts.
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What is TGA management?
Prostaglandins (maintain ductus arteriosus), septostomy, surgical correction.
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What causes VSD?
Failure of interventricular septum to close; left-to-right shunting.
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What is VSD management?
Small defects may close spontaneously; larger ones need surgery.
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What causes ASD?
Failure of interatrial septum to close; left-to-right shunting.
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What is ASD management?
Small ASDs may close; larger ones need closure devices or surgery.
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What causes Tetralogy of Fallot?
Four defects: VSD, overriding aorta, pulmonary stenosis, RV hypertrophy.
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What is TOF management?
Surgical repair, possible staged procedures.
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What causes coarctation of the aorta?
Aortic narrowing; leads to hypertension above the narrowing.
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What is coarctation management?
Surgery or balloon angioplasty.
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What are cardiovascular changes in pregnancy?
↑ CO (30-50%), ↑ plasma volume (40-50%), vasodilation, right axis ECG shift.
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What is pre-eclampsia?
Hypertension + proteinuria after 20 weeks; can involve thrombocytopenia, organ dysfunction.
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What are pre-eclampsia risk factors?
Nulliparity, multiple gestation, hypertension, diabetes, obesity.
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What are pre-eclampsia symptoms?
Hypertension, proteinuria, edema, headache, visual disturbances.
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What is pre-eclampsia management?
Monitoring (mild); hospital care, antihypertensives, magnesium sulfate, delivery (severe).
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What complications does pre-eclampsia cause?
Maternal: HELLP, eclampsia, stroke. Fetal: Prematurity, IUGR, stillbirth.
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Questions
Answers
70
What is endocarditis?
Inflammation of the heart's inner lining, primarily affecting valves.
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What are risk factors for endocarditis?
Valvular disease, prosthetic valves, IV drug use, congenital defects, catheters, immune compromise.
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What bacteria commonly cause infective endocarditis?
Staphylococcus aureus, Streptococcus viridans, Enterococci, HACEK group.
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What are the main fungal causes of endocarditis?
Rare, seen in immunocompromised patients or prosthetic valves.
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Describe the pathogenesis of infective endocarditis.
Endothelial damage → platelet-fibrin thrombus → bacterial colonization → vegetation formation.
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What are key symptoms of infective endocarditis?
Fever, new/changing murmur, fatigue, malaise, anorexia, weight loss.
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What embolic events occur in endocarditis?
Stroke, splenic infarct, renal infarct, pulmonary emboli (right-sided IE).
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What immunologic signs appear in endocarditis?
Osler nodes, Janeway lesions, Roth spots, glomerulonephritis.
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What investigations confirm endocarditis?
Blood cultures (≥3 sets), echocardiography (TTE/TEE).
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What lab findings support endocarditis diagnosis?
Elevated ESR, CRP, anemia, leukocytosis.
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What criteria are used to diagnose endocarditis?
Duke Criteria: Blood cultures + echocardiography + minor signs.
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What is the medical treatment for infective endocarditis?
IV antibiotics for 4-6 weeks tailored to organism.
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When is surgery needed in infective endocarditis?
Severe valve dysfunction, high embolic risk, uncontrolled infection.
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What monitoring is needed during endocarditis treatment?
Serial blood cultures, echocardiograms, clinical assessment.
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What are cardiac complications of endocarditis?
Heart failure due to valve destruction.
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What are systemic complications of endocarditis?
Stroke, embolic infarcts, abscess formation, renal failure.
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What is myocarditis?
Inflammation of the heart muscle.
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What causes myocarditis?
Viruses (Coxsackie B, adenovirus, HIV), bacteria, fungi, parasites, autoimmune diseases, toxins.
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What is the pathogenesis of viral myocarditis?
Direct infection of heart cells, immune attack causing damage.
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What are symptoms of myocarditis?
Flu-like symptoms, chest pain, dyspnea, palpitations, syncope, arrhythmias.
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What investigations confirm myocarditis?
ECG (ST/T wave changes), troponin, echocardiography, cardiac MRI, biopsy.
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What are microscopic findings in myocarditis?
Inflammatory infiltrates, myocyte necrosis, edema.
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What is myocarditis management?
Supportive care, HF treatment, arrhythmia management, avoid NSAIDs/alcohol.
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What complications arise from myocarditis?
Dilated cardiomyopathy, arrhythmias, heart failure.
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What is acute pericarditis?
Inflammation of the pericardium.
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What causes pericarditis?
Viral (Coxsackie, adenovirus), bacterial, autoimmune (SLE), uremia, trauma, post-MI.
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What are symptoms of pericarditis?
Pleuritic chest pain relieved by leaning forward, pericardial friction rub.
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What ECG changes occur in pericarditis?
Widespread ST elevation, PR depression.
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What is the treatment for pericarditis?
NSAIDs, colchicine, steroids (if refractory), treat underlying cause.
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What are complications of pericarditis?
Pericardial effusion, cardiac tamponade, constrictive pericarditis.
100
What is acute rheumatic fever?
Autoimmune reaction post-Strep throat, affecting heart, joints, brain, skin.
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What is rheumatic heart disease?
Chronic valve damage from repeated rheumatic fever episodes.
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What is the pathogenesis of rheumatic fever?
Molecular mimicry—antibodies against strep attack heart, joints, brain.
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What are signs of acute rheumatic fever?
Migratory arthritis, carditis, Sydenham's chorea, erythema marginatum, subcutaneous nodules.
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What are major criteria for rheumatic fever diagnosis?
Carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules.
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What are minor criteria for rheumatic fever?
Fever, arthralgia, elevated ESR/CRP, prolonged PR interval.
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What tests confirm recent strep infection in RF?
Throat culture, anti-streptolysin O titers.
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What is the management for rheumatic fever?
Penicillin, aspirin, corticosteroids, long-term antibiotic prophylaxis.
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What are complications of rheumatic fever?
Rheumatic heart disease, heart failure, arrhythmias, stroke.
109
What is myxoma?
Most common primary heart tumor, usually benign.
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What are symptoms of myxoma?
Obstruction (syncope, dyspnea), embolism (stroke, infarcts), systemic (fever, weight loss).
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What is the best test for myxoma?
Echocardiography for visualization.
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What is the treatment for myxoma?
Surgical excision.
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Questions
Answers
114
What is cardiomyopathy?
Disease of the heart muscle impairing its ability to pump blood effectively.
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What are the main types of cardiomyopathy?
Dilated (DCM), Hypertrophic (HCM), Restrictive (RCM), Arrhythmogenic Right Ventricular (ARVC).
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What is dilated cardiomyopathy (DCM)?
Ventricular dilation and impaired systolic function, leading to reduced ejection fraction.
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What causes DCM?
Idiopathic (most common), genetic mutations, infections, toxins (alcohol, drugs), metabolic disorders.
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What are symptoms of DCM?
Heart failure signs: Dyspnea, fatigue, edema, palpitations, syncope.
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What is the primary diagnostic tool for DCM?
Echocardiography: Shows ventricular dilation and reduced ejection fraction.
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What is the treatment for DCM?
Heart failure management: ACE inhibitors, beta-blockers, diuretics, lifestyle modifications, possible device therapy.
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What is hypertrophic cardiomyopathy (HCM)?
Genetic disorder causing unexplained left ventricular hypertrophy.
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What causes HCM?
Autosomal dominant mutations in sarcomere protein genes (e.g., MYH7, MYBPC3).
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What are symptoms of HCM?
Dyspnea, syncope, chest pain, palpitations, sudden cardiac death risk.
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What is the primary diagnostic tool for HCM?
Echocardiography: Shows asymmetric LV hypertrophy (>15mm).
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What is the treatment for HCM?
Beta-blockers, calcium channel blockers, activity restriction, possible surgery (myectomy).
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What is restrictive cardiomyopathy (RCM)?
Stiff ventricular walls impairing diastolic filling, leading to heart failure with preserved ejection fraction.
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What causes RCM?
Infiltrative diseases (amyloidosis, sarcoidosis), fibrosis, radiation therapy.
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What are symptoms of RCM?
Dyspnea, edema, fatigue, signs of diastolic heart failure.
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What is the diagnostic tool for RCM?
Echocardiography: Shows normal/increased ventricular wall thickness with restrictive filling pattern.
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What is the management for RCM?
Supportive treatment, managing underlying cause, diuretics for symptom relief.
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What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?
Genetic disease causing RV myocardium replacement with fibrofatty tissue, leading to arrhythmias.
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What causes ARVC?
Genetic mutations in desmosomal proteins (e.g., PKP2, DSG2).
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What are symptoms of ARVC?
Palpitations, syncope, ventricular tachycardia (often exertion-related).
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What is the primary diagnostic tool for ARVC?
Echocardiography: Shows RV dilation and dysfunction.
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What is the treatment for ARVC?
Beta-blockers, activity restriction, ICD placement for sudden death prevention.
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What is pericardial effusion?
Abnormal fluid accumulation in the pericardial space.
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What are causes of pericardial effusion?
Pericarditis (viral, bacterial), malignancy, trauma, autoimmune diseases, post-MI (Dressler’s syndrome).
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What are symptoms of pericardial effusion?
Dyspnea, chest discomfort, muffled heart sounds, pericardial friction rub.
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What is the diagnostic tool for pericardial effusion?
Echocardiography: Detects fluid in pericardial space.
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What is the treatment for pericardial effusion?
Observation (small effusions), NSAIDs/colchicine, pericardiocentesis (large/symptomatic effusions).
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What is cardiac tamponade?
Life-threatening condition due to rapid/excessive pericardial fluid accumulation, compressing the heart.
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What are symptoms of cardiac tamponade?
Beck’s Triad: Hypotension, muffled heart sounds, jugular venous distension.
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What is the treatment for cardiac tamponade?
Emergency pericardiocentesis to relieve compression.
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What is constrictive pericarditis?
Thickened pericardium restricting ventricular filling, leading to right heart failure signs.
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What are causes of constrictive pericarditis?
Idiopathic, tuberculosis, radiation therapy, cardiac surgery.
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What are symptoms of constrictive pericarditis?
Progressive dyspnea, peripheral edema, ascites, hepatomegaly.
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What is the treatment for constrictive pericarditis?
Definitive treatment: Pericardiectomy.
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Questions
Answers
149
What is peripheral vascular disease (PVD) and acute limb ischemia (ALI)?
PVD affects blood vessels outside the heart and brain; ALI is a sudden drop in limb blood flow, threatening viability.
150
What are causes and symptoms of acute limb ischemia?
Caused by embolism/thrombosis. Symptoms: Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Poikilothermia.
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How is acute limb ischemia diagnosed and managed?
Clinical exam, Doppler ultrasound, angiography. Managed with urgent revascularization (embolectomy, thrombolysis, bypass).
152
What causes chronic limb ischemia, and what are its symptoms?
Atherosclerosis; symptoms include claudication, rest pain, non-healing ulcers, gangrene.
153
How is chronic limb ischemia diagnosed and treated?
ABI, Doppler ultrasound, angiography. Treated with lifestyle changes, medications (antiplatelets), revascularization.
154
What is aortic dissection (AD), and how common is it?
A tear in the inner aortic layer leading to separation of wall layers; rare but life-threatening.
155
What are AD risk factors and the role of cystic medial degeneration?
Hypertension, Marfan syndrome, Ehlers-Danlos, bicuspid aortic valve; medial degeneration weakens aortic wall.
156
What are the Stanford and DeBakey classifications of AD?
Stanford: Type A (ascending aorta), Type B (descending aorta). DeBakey: Type I (extends), Type II (ascending only), Type III (descending).
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What are symptoms of AD?
Sudden severe tearing chest/back pain that may migrate, neurological deficits, limb ischemia.
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How is AD diagnosed and treated?
CT angiography (gold standard). Type A: Surgery; Type B: Blood pressure control, possible surgery.
159
What is an aneurysm and its epidemiology?
Localized vessel dilation; AAA common in older men, often linked to atherosclerosis.
160
How are aneurysms classified?
True (all three wall layers: fusiform/saccular) vs. False (pseudoaneurysm with hematoma).
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What is the pathogenesis of aortic aneurysm?
Arterial wall weakening via atherosclerosis, genetic disorders, infection, or inflammation.
162
What are symptoms and diagnostic tools for aortic aneurysm?
Often asymptomatic; when symptomatic, pulsatile mass, back pain. Diagnosed via ultrasound, CT, MRI.
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How are aneurysms managed?
Small: Monitoring, risk control. Large/symptomatic: Open surgery or EVAR. Ruptured: Emergency repair.
164
What are varicose veins?
Dilated, tortuous superficial veins, often in the legs due to valve failure.
165
What is the pathogenesis and symptoms of varicose veins?
Valve incompetence → reflux → venous hypertension → vein dilation. Symptoms: Visible bulging veins, heaviness, swelling, skin changes.
166
What investigations diagnose varicose veins?
Clinical exam, duplex ultrasound (assesses reflux and rules out DVT).
167
How are varicose veins managed, and what are complications?
Compression stockings, sclerotherapy, endovenous ablation, surgery. Complications: Thrombophlebitis, bleeding, ulcers.
168
What is deep vein thrombosis (DVT)?
Formation of thrombus in deep veins, commonly in the legs.
169
What causes DVT, and what are symptoms?
Virchow’s Triad: Stasis, endothelial injury, hypercoagulability. Symptoms: Unilateral swelling, pain, warmth.
170
What investigations diagnose DVT?
D-dimer (rule out), compression ultrasound (gold standard).
171
How is DVT managed, and what are complications?
Anticoagulation (heparin, LMWH, oral drugs). Complications: PE, post-thrombotic syndrome.
172
What is chronic venous insufficiency (CVI)?
Impaired venous return due to valve dysfunction, causing chronic venous hypertension.
173
What is the pathogenesis and symptoms of CVI?
Venous reflux causes sustained hypertension. Symptoms: Edema, pain, itching, skin changes, ulcers.
174
What investigations diagnose CVI?
Clinical exam, duplex ultrasound (assesses reflux and obstruction).
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How is CVI managed, and what are complications?
Compression therapy, leg elevation, wound care; possible surgery. Complications: Venous ulcers, cellulitis, recurrent DVT.
176
What is vasculitis?
Inflammation of blood vessel walls.
177
What are the types of vasculitis?
Large-vessel (GCA, Takayasu), medium-vessel (PAN, Kawasaki), small-vessel (ANCA-associated, IgA vasculitis).
178
What are the pathogenic mechanisms of vasculitis?
Non-infectious: Immune-mediated (autoantibodies, immune complexes). Infectious: Direct pathogen invasion.
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What are symptoms of vasculitis?
Fever, weight loss, skin rashes, arthralgia, kidney failure, neurological deficits.
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How is vasculitis diagnosed and treated?
Clinical assessment, lab tests (ANCA, CRP), imaging (angiography), biopsy. Treated with immunosuppressants (steroids, cyclophosphamide).
