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Cardiovascular Flashcards

1
Q

What is the definition of cardiomyopathy? What are the types of cardiomyopathy and give a cause for each. What are the potential pathologic consequences of dilated cardiomyopathy?

A
  1. Cardiomyopathy is
    - Disease of the myocardium
    - Ventricular hypertrophy or dilatation
    - Mechanical and/or electrical dysfunction
  2. Types of cardiomyopathy
    - Dilated: Congenital, toxins (alcohol), myocarditis, pregnancy
    - Hypertrophic: 75% congenital (HOCM), HTN
    - Restrictive: Amyloidosis, sarcoidosis
  3. Pathologic consequences of dilated cardiomyopathy
    - Valvular dysfunction
    - Atrial fibrillation
    - Arrhythmia
    - Mural thrombus
    - Embolus
    - Death
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2
Q

What are the causes of acquired cardiomyopathy? How do dilated and hypertrophic cardiomyopathy differ?

A
  1. Causes of acquired cardiomyopathy
    - Infections: Viral, bacterial myocarditis
    - Infiltrative: Amyloidosis, sarcoidosis
    - Immunologic: Autoimmune myocarditis
    - Metabolic: Hyperthyroidism
    - Toxins: ETOH
    - IHD, HTN, valvular disease
  2. Dilated vs hypertrophic cardiomyopathy
    - Dilated: Cardiac dilatation, low LVEF, systolic dysfunction
    - Hypertrophic: Myocardium hypertrophy, normal/high LVEF, diastolic dysfunction
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3
Q

What are the characteristics of hypertrophic cardiomyopathy? What are the complications of HCM?

A
  1. Hypertrophic cardiomyopathy
    - Myocardial hypertrophy with no ventricular dilatation
    - Asymmetrical septal thickening
    - Diastolic dysfunction
    - Normal/high LVEF
  2. Complications of HCM
    - Valvular dysfunction
    - Mural thrombus/embolus
    - Arrhythmia
    - Atrial fibrillation
    - Cardiac failure
    - Death
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4
Q

What are the pathological features of hypertrophic cardiomyopathy?

A
  1. Macroscopic features
    - Myocardium hypertrophy without ventricular dilatation
    - Asymmetrical septal wall thickening
    - LV outflow obstruction
  2. Microscopic features
    - Myocytes hypertrophy
    - Disarray of myocytes
    - Interstitial fibrosis
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5
Q

What factors are thought to contribute to essential HTN? What are the long term consequences of essential HTN? Describe the malignant features of malignant HTN.

A
  1. Factors leading to essential HTN
    - Genetic: Familial -> multi-foci gene interactions
    - Vasoconstrictive influences -> Peripheral vasoconstriction
    - Environmental: Obesity, stress, increased salt intake
  2. Complications of HTN
    - Retinopathy
    - CVA
    - Coronary artery disease/IHD
    - Cardiac hypertrophy
    - Cardiac failure
    - Aortic dissection
    - CKD/renal failure
  3. Malignant HTN presents with SBP > 200, DBP > 120
    - Encephalopathy
    - Delirium
    - Retinal hemorrhage
    - Papillaoedema
    - Angina
    - Renal impairment/renal failure
    - Death if untreated
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6
Q

What is cor pulmonale? What are the common causes of cor pulmonale? What are the major morphological features of cor pulmonale?

A
  1. Cor pulmonale is R heart failure
    - Not caused by L heart failure
    - Caused by underlying lung disease with pulmonary hypertension
  2. All causes lead to pulmonary hypertension
    - Disease of lung parenchyma: COPD, interstitial fibrosis, bronchiectasis
    - Disease of lung vessels: Acute PE, primary pulmonary HTN, vasculitis
    - Disease causing pulmonary arterial constriction: Chronic sleep apnea, altitude sickness, metabolic acidosis, hypoxaemia
    - Diseases affecting chest movement: Neuromuscular disease, marked obesity
  3. Morphological features of cor pulmonale
    - Respiratory: Pulmonary hypertension, minimal pulmonary congestion
    - CVS: R ventricular hypertrophy/dilatation, leftward bulging of septum
    - Liver: Congestive liver/nutmeg liver -> centrilobular necrosis
    - Spleen: Congestive splenomegaly
    - Peripheral edema
    - Pleural, pericardial, peritoneal effusions
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7
Q

What is heart failure? Please classify the types of heart failure. What are the clinical features of heart failure?

A
  1. Heart failure is heart disease where there is
    - Mechanical pump failure
    - Inability to maintain sufficient cardiac output to meet body’s metabolic demands
  2. Types of heart failure
    - L heart failure: IHD, valvular disease, rheumatic fever, HTN
    - R heart failure: L heart failure, cor pulmonale/pulmonary HTN
    - Systolic dysfunction/Contractility dysfunction: IHD, valvular disease, dilated cardiomyopathy
    - Diastolic dysfunction/Filling dysfunction: LV hypertrophy, HOCM, pericarditis, amyloidosis
    - Others: Arrhythmia, outflow obstruction
  3. Clinical features of heart failure
    - CVS: 3rd heart sound, murmurs, displaced apex beat, raised JVP
    - Respiratory: Pulmonary edema, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pleural effusion
    - Liver: Congestive hepatomegaly, cirrhosis
    - Spleen: Congestive splenomegaly
    - Renal: Renal impairment, activation of renin-angiotensin system
    - Peripheral edema
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8
Q

What are the major causes of heart failure? What pathological processes can occur in the myocardium in heart failure? What are the pathological changes in the liver caused by heart failure?

A
  1. Major causes of heart failure
    - IHD
    - Valvular heart disease
    - HTN
    - Cardiomyopathy
    - Fluid overload
  2. Pathological process that occurs in heart failure
    - Myocyte hypertrophy
    - Ischaemia/infarction
    - Calcification
    - Interstitial fibrosis
  3. Nutmeg liver in heart failure with
    - Centrilobular necrosis -> From central hypoxia
    - Centrilobular fibrosis -> From long standing RHF
    - Cardiac cirrhosis in extreme cases
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9
Q

What are the systemic and local factors that lead to atherosclerosis? Which arteries are most often affected by atherosclerosis? How does an atherosclerotic plaque suddenly cause symptoms?

A
  1. Factors leading to atherosclerosis
    - Systemic factors: HTN, hyperlipidaemia, smoking, obesity
    - Local factors: Endothelial dysfunction due to hemodynamic disturbances -> Turbulent blood flow at arterial branch points + Hyperlipidaemia -> Increases susceptibility of atherosclerosis at area
  2. Arteries affected
    - Lower abdominal aorta
    - Coronary arteries
    - Popliteal artery
    - Internal carotid artery
    - Arteries of circle of Willis
    - Lower limb arteries > Upper limb arteries
  3. Atherosclerotic plaques can
    - Rupture, erode, ulcerate -> Exposes endothelium -> Formation of thrombus -> Distal ischaemia
    - Ruptured plaque can cause microemboli -> Ischaemia of small vessels/microcirculation ischaemia
    - Haemorrhage into plaque -> Burst fibrous cap -> Occlusion of vessel
    - Disrupt arterial wall -> Formation of aortic aneurysm
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10
Q

Describe the differences between stable and unstable atherosclerotic plaque. What are the consequences of atherosclerotic plaque? Outline the steps in pathogenesis of atherosclerosis. Draw a typical atheromatous plaque

A
  1. Stable vs unstable plaque
    - Stable plaque: Thick fibrous cap, small atheromatous core, minimal inflammation
    - Unstable plaque: Thin fibrous cap, large atheromatous core, increased inflammation, prone to rupture
  2. Consequences of atherosclerotic plaque
    - Rupture, erosion, ulceration -> Thrombus formation
    - Embolism of ruptured plaque
    - Hemorrhage into plaque -> Occlusion
    - Arterial wall disruption -> Aortic aneurysm
  3. Pathogenesis of atherosclerosis
    - Endothelial injury or dysfunction
    - Lipoprotein accumulation in vessel wall
    - Monocytes adhere, migrate into intima and transform into foam cells and macrophages
    - Platelets adhere
    - Smooth muscle cells migrate from media into intima
    - Smooth muscle cells proliferate
    - Further lipid accumulation in intima
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11
Q

What are the pathological consequences of aortic stenosis? What are the likely causes of aortic stenosis? What clinical signs may differentiate calcific aortic stenosis from rheumatic aortic stenosis?

A
  1. Pathological consequences of aortic stenosis
    - Concentric LV hypertrophy
    - LV outflow obstruction
    - Cardiac failure -> Diastolic or systolic
    - Myocardial ischaemic without coronary artery disease
  2. Causes of aortic stenosis
    - Calcific/degenerative
    - Bicuspid valve
    - Rheumatic heart disease
  3. Calcific aortic stenosis vs rheumatic aortic stenosis
    - Rheumatic aortic stenosis usually involves more than 1 valve
    - Presence of MV involvement
    - Presence of aortic regurgitation
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12
Q

What are the predisposing factors for calcific aortic stenosis? What are the clinical consequences of aortic stenosis? What are the potential complications of a congenital bicuspid aortic valve? What is calcific aortic stenosis?

A
  1. Predisposing factors for calcific aortic stenosis
    - Age
    + Normal valves: 70 - 90yo
    + Bicuspid valves: 50 - 70yo
    - Congenital bicuspid valves
    - HTN
    - Hyperlipidaemia
    - Wear and tear
    - Chronic injury
  2. Clinical consequences of AS
    - Gradual LV outflow obstruction
    - Myocardial ischaemia or angina without coronary artery disease
    - Cardiac failure -> Systolic or diastolic
    - Syncope
  3. Complications of congenital bicuspid aortic valve
    - Calcification
    - Stenosis
    - Regurgitation
    - Infective endocarditis
    - Aortic dilatation
    - Aortic dissection
  4. Calcific aortic stenosis
    - Normal wear and tear of aortic valve
    - Heap of calcified mass on cusps of aortic valve -> Slowly protrudes into outflow tract -> Reduces functional valve area
    - Can affect both normal and bicuspid valve
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13
Q

What factors predispose to infective endocarditis? Which organisms commonly cause infective endocarditis? What are the complications of infective endocarditis?

A
  1. Predisposing factors for IE
    - Cardiac factors: Congenital bicuspid valve, calcific aortic valve, mitral valve prolapse, prosthetic valve, rheumatic heart disease
    - Systemic factors: Immunocompromised, IVDU, bacteraemia
  2. Organisms causing IE
    - Staph aureus
    - Strep viridans
    - Staph epidermidis
    - Enterococci
    - HÁČEK = Haemophilus, actinobacter, cardiobacterium, eikenella, kingella
  3. Complications of IE
    - Local: Valve destruction, abscess formation
    - Systemic: Septic emboli (brain, lungs, kidney, spleen), mycotic aneurysm, embolic phenomena (Roth spots, Janeway lesion)
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14
Q

How is hypertension classified? What are the causes of secondary hypertension? What are the criteria for systemic hypertensive heart disease? What are the gross morphology findings in systemic hypertensive heart disease? What are the pathological consequences?

A
  1. Hypertension can be classified into
    - Primary/Essential
    - Secondary
  2. Causes of secondary HTN
    - Renal: Renal artery stenosis, polycystic kidney disease
    - CVS: Coarctation of aorta
    - Endocrine: Hyperthyroidism, phaeochromocytoma, Cushing’s syndrome
    - Neurological: Intracranial HTN, sleep apnea
    - Psychological: Stress, surgery, pain
  3. Criteria for systemic hypertensive heart disease
    - Systemic hypertension
    - Concentric LV hypertrophy
    - No other cause present
  4. Gross morphology in systemic hypertensive heart disease
    - LV hypertrophy
    - L atrium enlargement
    - NO dilatation
    - Increased weight of heart
  5. Pathological consequences of systemic hypertensive heart disease
    - LV hypertrophy
    - Cardiac failure
    - Diastolic dysfunction
    - Atrial fibrillation
    - Sudden cardiac death
    - Arrhythmia
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15
Q

Describe the pathogenesis of myocardial infarction secondary to atherosclerosis. What are the complications of myocardial infarct? What are the main cardiac rupture syndromes? What changes occur in cardiac remodelling? What systemic factors affect infarct healing? Describe the time course of myocardial injury after acute coronary occlusion. What are the potential complications post-reperfusion?

A
  1. Pathogenesis of myocardial infarct
    - Acute plaque changes -> Rupture, erosion, ulceration, hemorrhage
    - Thrombus formation -> Platelet aggregation and activation of clotting cascade
    - Vasoconstriction
    - Vessel occlusion -> Reduce tissue perfusion -> Ischaemia
  2. Complications of myocardial infarct
    - Early
    + Cardiac dysfunction -> LVF, RVF, APO
    + Arrhythmias
    + Extension of infarct
    - Late
    + Papillary muscle rupture
    + Mural thrombus
    + Pericarditis/Dressler syndrome
    + Valvular heart disease
    + Ventricular aneurysm
  3. Cardiac rupture syndrome
    - Ventricular free wall rupture -> Pericardial effusion, tamponade -> Most common Day 1 - 10 post-MI
    - Septal wall rupture -> VSD
    - Papillary muscle rupture -> Severe MR
  4. Ventricular remodelling post-MI
    - Hypertrophy and dilatation -> Increased O2 demand -> Ischaemia, cardiac failure -> Scar formation -> Stiffening
  5. Systemic factors affecting infarct healing
    - Circulation: Arterial and venous
    - Nutritional status: Malnutrition, Vitamin C
    - Metabolic: Diabetes
    - Hormonal: Glucocorticoids
  6. Time course of myocardial injury
    A. Reversible
    - Immediate: Cessation of aerobic metabolism and reduced ATP production
    - 1-2mins: Loss of contractility
    - Mins: Ultrastructural changes -> Cell and mitochondria swelling
    - 10 - 40mins: ATP depletion
    B. Irreversible > 30-40mins
    - Myocyte necrosis
    - Subendothelial progressing to transendothelial infarct
    - 1hr: Microvascular injury
    - 2-4hrs: Extensive tissue necrosis
  7. Post-reperfusion
    - Early: No damage
    - Re-perfusion injury due to generation of oxygen free radicals
    - Further damage to myocytes
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16
Q

Describe the characteristic clinical features of pericarditis. What are the causes of pericarditis? What types of pericardial fluid exudate occur?

A
  1. Clinical features of pericarditis
    - Pleuritic chest pain
    - Pericardial friction rub
    - Signs of heart failure in severe pericarditis
    - Constrictive pericarditis: Muffled heart sound, raised JVP, peripheral edema
  2. Causes of pericarditis
    - Infection: Viral, bacterial, TB, fungal
    - Immunological: SLE, rheumatic fever
    - Trauma
    - Post-myocardial infarction
    - Constrictive pericarditis: Amyloidosis, sarcoidosis
  3. Pericardial fluid
    - Serous fluid: Viral infection, non-infectious cause
    - Fibrinous fluid: Post-MI, trauma, surgery
    - Suppurative fluid: Post-bacterial infection
    - Caseous fluid: TB
    - Hemorrhagic

Pathology (17 decks)

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