Cardiovascular Pathophysiology Lecture – Practice Flashcards

A comprehensive set of question-and-answer flashcards covering the main cardiovascular pathophysiology topics discussed in the lecture transcript.

What is the key difference between thrombocytopenia and thrombocytosis?

Thrombocytopenia is a decreased platelet count; thrombocytosis is an increased platelet count.

How does a thrombus differ from an embolus?

A thrombus is a clot attached to the vessel wall; an embolus is a detached intravascular mass that travels and can lodge elsewhere.

What three factors make up Virchow’s triad?

Endothelial injury, abnormal blood flow (stasis or turbulence), and hypercoagulability.

What does the abbreviation “DIC” stand for?

Disseminated Intravascular Coagulation.

List two primary transport functions of the circulatory system.

Delivery of oxygen/nutrients/hormones and removal of metabolic waste products.

Name the three histologic layers common to arteries and veins.

Intima (endothelium), media (smooth muscle), and adventitia (connective tissue).

Which vessel type contains only endothelium and a basement membrane?

Capillaries.

Give one example each of an elastic artery and a muscular artery.

Elastic: aorta; Muscular: coronary artery.

State two major stimuli that can activate endothelial cells.

Pro-inflammatory cytokines and turbulent blood flow.

Mention two normal homeostatic functions of endothelial cells.

Maintain a permeability barrier and regulate coagulation/inflammation.

What pathologic consequence can excessive intimal thickening produce?

Luminal stenosis and vascular obstruction.

Define a varicose vein.

A superficial vein that has become distended, tortuous, and palpable due to pooled blood.

List four risk factors for varicose veins.

Age, female sex, pregnancy, and deep venous thrombosis (others: obesity, family history, previous leg injury).

What is chronic venous insufficiency (CVI)?

Long-standing inadequate venous return leading to venous hypertension, tissue hypoxia, skin changes, and ulceration.

Name the three major promoters of venous thrombosis (DVT).

Venous stasis, endothelial damage, and hypercoagulable states.

Why are untreated DVTs dangerous?

They can embolize to the lungs, causing pulmonary thromboembolism.

Define superior vena cava syndrome (SVCS).

Progressive obstruction of the SVC causing venous congestion of the head, neck, and upper extremities.

Give two common causes of SVCS.

Bronchogenic carcinoma and lymphoma (others: metastases, tuberculosis, mediastinal fibrosis).

What does a positive Pemberton maneuver suggest?

Obstruction of the superior vena cava (facial flushing or dyspnea when arms are raised).

Blood pressure (BP) equals cardiac output multiplied by .

Peripheral vascular resistance.

Outline the renin-angiotensin-aldosterone cascade starting with renin.

Renin converts angiotensinogen → angiotensin I → (ACE) → angiotensin II → vasoconstriction and aldosterone release → sodium/water retention.

Provide the new diagnostic threshold for systemic hypertension.

Sustained BP ≥130/80 mm Hg.

What percentage of hypertension cases are essential (primary)?

Approximately 90–95 %.

Name two typical histologic changes in small arteries caused by chronic hypertension.

Hyaline arteriolosclerosis and smooth-muscle hyperplasia with basement-membrane duplication (hyperplastic).

List the “5 C’s” major complications of hypertension.

Coronary artery disease, Chronic renal failure, Congestive heart failure, Cardiac arrest, Cerebrovascular accident.

Define arteriosclerosis in general terms.

Hardening and thickening of arterial walls with loss of elasticity.

Which arteriosclerosis subtype is usually clinically silent but shows medial calcification in muscular arteries?

Mönckeberg medial sclerosis.

Describe the basic composition of an atherosclerotic plaque.

Fibrous cap of smooth muscle and collagen over a lipid-rich necrotic core with inflammatory cells.

Give two morphologic features of a vulnerable plaque.

Thin fibrous cap and large lipid core with intense inflammation.

Differentiate a true aneurysm from a false aneurysm.

True aneurysm involves dilation of all three vessel wall layers; a false aneurysm is a contained rupture with extravascular hematoma communicating with the lumen.

Which shapes describe most true aneurysms?

Fusiform and circumferential.

State the most common arterial sites for aneurysm formation.

Thoracic and abdominal aorta.

Name the four chambers of the heart.

Right atrium, right ventricle, left atrium, and left ventricle.

Identify the four principal heart valves in normal blood flow sequence.

Tricuspid, pulmonary, mitral (bicuspid), and aortic valves.

List the three layers of the heart wall.

Epicardium, myocardium, and endocardium.

What are the two layers of the pericardium?

Fibrous pericardium and serous (visceral) pericardium.

Name one of the six principal mechanisms that can lead to cardiac dysfunction.

Pump failure (others: flow obstruction, regurgitant flow, shunted flow, conduction disorders, rupture).

Give two common infectious causes of acute pericarditis.

Coxsackievirus and influenza virus (others: HIV, hepatitis, mumps, etc.).

List two possible sequelae of acute pericarditis.

Recurrent pericarditis, pericardial constriction, or cardiac tamponade.

What triad of findings characterizes acute cardiac tamponade (Beck’s triad)?

Hypotension, jugular venous distension, and muffled heart sounds.

How does constrictive pericarditis impair cardiac output?

Fibrotic, often calcified pericardium forms a rigid shell compressing the heart, limiting diastolic filling.

Into which three physiologic categories are cardiomyopathies grouped?

Dilated, hypertrophic, and restrictive.

State one common non-genetic cause of dilated cardiomyopathy.

Chronic alcohol abuse, ischemic heart disease, valvular disease, diabetes, etc.

Describe the key pathologic feature of hypertrophic obstructive cardiomyopathy.

Asymmetric septal hypertrophy causing dynamic obstruction of the left ventricular outflow tract.

What triggers hypertensive or valvular hypertrophic cardiomyopathy?

Increased resistance to ventricular ejection from hypertension or aortic valve stenosis.

How does restrictive cardiomyopathy affect ventricular filling?

Rigid myocardium resists diastolic filling, raising diastolic pressures with normal wall thickness and systolic function.

Define valvular stenosis.

A pathologically narrowed valve orifice that obstructs forward blood flow.

What is valvular regurgitation?

Failure of a valve to close completely, allowing backward flow of blood.

Infective endocarditis most often involves infection of which cardiac layer?

The endocardium, particularly heart valves.

Name the three most common bacterial genera causing infective endocarditis.

Streptococci, Staphylococci, and Enterococci.

List the three critical steps in the pathogenesis of infective endocarditis.

Endocardial damage, adherence of circulating microorganisms, and formation of vegetations.

Differentiate Osler nodes from Janeway lesions.

Osler nodes: painful fingertip/toe nodules (immune complex); Janeway lesions: painless erythematous macules on palms/soles (septic emboli).

Provide a concise definition of heart failure.

Inability of the heart to supply sufficient cardiac output or normal filling pressures to meet tissue metabolic needs.

What ejection fraction defines heart failure with reduced EF (HFrEF)?

Less than 40 %.

Give the three major determinants of stroke volume.

Contractility, preload, and afterload.

What are two common etiologies of heart failure with preserved EF (HFpEF)?

Hypertension-induced myocardial hypertrophy and ischemia-related ventricular remodeling.

Why does left heart failure often lead to right heart failure?

Elevated left-sided pressures transmit to pulmonary circulation, increasing right ventricular afterload and causing right ventricular failure.

List two major causes of isolated right heart failure (cor pulmonale).

Chronic obstructive pulmonary disease (COPD) and cystic fibrosis (also ARDS, diffuse hypoxic lung disease).

Define high-output heart failure.

State in which cardiac output is elevated yet still insufficient to meet increased tissue metabolic demands (e.g., anemia, hyperthyroidism).

What is the basic definition of shock?

Widespread failure of the circulatory system to perfuse tissues adequately, causing cellular metabolism impairment.

Name two key biochemical consequences of cellular hypoxia in shock.

Switch to anaerobic metabolism (lactic acidosis) and depletion of ATP.

Identify the four major clinical categories of shock.

Obstructive, distributive, cardiogenic, and hypovolemic shock.

What type of shock is caused by severe vasodilation and inflammatory mediator release?

Distributive shock (e.g., septic shock).

Provide one echocardiographic feature typical of hypovolemic shock.

Small cardiac chambers with normal or hyperdynamic contractility.

What is the most common pattern of congenital cardiac shunting?

Left-to-right shunt (e.g., ASD, VSD, PDA).

What syndrome describes reversal of a chronic left-to-right shunt leading to cyanosis?

Eisenmenger syndrome.

Name two classic cyanotic right-to-left shunt lesions.

Tetralogy of Fallot (TOF) and transposition of the great arteries (TGA).

Which obstructive congenital lesion involves narrowing of the aorta?

Coarctation of the aorta.