Cardiovascular Pathophysiology – Exam Review

70 question-and-answer flashcards summarizing core concepts from the cardiovascular pathophysiology lecture, covering vascular biology, hemodynamics, hypertension, atherosclerosis, aneurysms, pericardial and myocardial disorders, valvular disease, heart failure, shock, and congenital heart defects.

What is the difference between thrombocytopenia and thrombocytosis?

Thrombocytopenia is a decrease in circulating platelets, whereas thrombocytosis is an abnormally elevated 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 through the bloodstream.

Name the three elements of Virchow’s Triad.

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

What does the acronym DIC stand for?

Disseminated Intravascular Coagulation.

State two primary functions of the circulatory system.

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

List the three layers shared by all blood vessels except capillaries.

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

What are the three functional types of arteries?

Elastic arteries (e.g., aorta) for cushioning and recoil, muscular arteries (e.g., coronaries) for distribution, and small arteries/arterioles for pressure regulation.

Give two common stimuli for endothelial activation.

Cytokines (e.g., TNF-α) and disturbed/turbulent blood flow.

What vascular consequence can excessive intimal thickening produce?

Luminal stenosis leading to vascular obstruction.

List three key homeostatic functions of normal endothelial cells.

Maintaining a permeability barrier, regulating coagulation/inflammation, and producing vasoactive substances (e.g., NO, prostacyclin).

Define a varicose vein.

A dilated, tortuous, palpable superficial vein produced by chronic venous blood pooling.

Name four risk factors for developing varicose veins.

Age, female sex, obesity, pregnancy (others: family history, DVT, prior leg injury).

What is chronic venous insufficiency (CVI)?

Long-standing inadequate venous return causing venous hypertension, stasis, hypoxia, skin remodeling, and possible ulceration.

List the three major factors that promote deep venous thrombosis (DVT).

Venous stasis, endothelial damage, and hypercoagulable states.

Define superior vena cava syndrome (SVCS).

Progressive obstruction of the SVC leading to venous distention of the head, neck, and upper extremities.

What clinical sign is elicited by Pemberton’s maneuver?

Facial flushing or cyanosis and dyspnea on arm elevation, indicating SVC obstruction.

Blood pressure is the product of which two primary variables?

Cardiac output and peripheral vascular resistance.

Describe the role of renin in blood-pressure regulation.

Renin converts angiotensinogen to angiotensin I, ultimately forming angiotensin II, which raises vascular tone and stimulates aldosterone-mediated sodium retention.

According to current guidelines, what blood-pressure value defines hypertension?

A sustained systolic ≥130 mm Hg or diastolic ≥80 mm Hg.

Approximately what percentage of hypertension cases are essential (primary)?

About 90–95 %.

Name two physiologic changes that sustain established hypertension.

Increased blood volume and increased peripheral resistance.

What histologic change is typically seen in small arteries of hypertensive patients?

Hyaline arteriolosclerosis (hyaline thickening of vessel walls).

Identify the three major patterns of arteriosclerosis.

Arteriolosclerosis, Mönckeberg medial sclerosis, and atherosclerosis.

What are the basic components of an atherosclerotic plaque?

Fibrous cap (smooth muscle & collagen) overlying a lipid-rich necrotic core with inflammatory cells.

Contrast stable and vulnerable atherosclerotic plaques.

Stable plaques have thick fibrous caps and small lipid cores; vulnerable plaques have thin caps, large lipid cores, and heavy inflammation, predisposing to rupture.

Define an aneurysm.

Localized, permanent dilation of a vessel wall or cardiac chamber.

Differentiate true from false aneurysms.

True aneurysms involve all three arterial wall layers; false (pseudo) aneurysms are contained ruptures with blood outside the vessel wall communicating with the lumen.

What is the most common underlying cause of arterial aneurysms?

Atherosclerosis, which weakens the media by destroying elastic tissue and provoking inflammation.

Which aortic segments most commonly develop aneurysms?

Abdominal and thoracic aorta.

Name the three layers of the heart wall.

Epicardium, myocardium, and endocardium.

List the four major cardiac valves.

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

State six principal mechanisms that can lead to cardiovascular dysfunction.

Pump failure, flow obstruction, regurgitant flow, shunted flow, conduction disorders, and rupture of heart/vessels.

What is the most frequent cause of acute pericarditis?

Idiopathic or viral infection (e.g., Coxsackie viruses).

Name two potential sequelae of acute pericarditis.

Recurrent pericarditis, constrictive pericarditis, or cardiac tamponade.

List the three signs of Beck’s triad for cardiac tamponade.

Hypotension, jugular venous distention, and muffled heart sounds.

How does constrictive pericarditis impair cardiac output?

Fibrotic, often calcified pericardium encases the heart, restricting diastolic filling and reducing stroke volume.

Name the three morphologic classes of cardiomyopathy.

Dilated, hypertrophic, and restrictive cardiomyopathy.

Give two characteristic features of dilated cardiomyopathy.

Ventricular dilation with impaired systolic function (reduced EF) leading to heart failure.

What anatomic change defines hypertrophic obstructive cardiomyopathy?

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

What is the hallmark of restrictive cardiomyopathy?

Rigid, noncompliant ventricles with impaired diastolic filling despite normal wall thickness and systolic function.

Define valvular stenosis.

A narrowed, stiff valve orifice impeding forward blood flow and creating pressure overload in the proximal chamber.

What is valvular regurgitation?

Failure of valve leaflets to close completely, causing backward flow and volume overload of the affected chambers.

What is infective endocarditis?

Microbial infection and inflammation of the endocardial surface, most often involving heart valves.

Which bacteria account for the majority of infective endocarditis cases?

Streptococci, staphylococci, and enterococci.

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

Endocardial damage with sterile thrombus, bloodstream seeding by microorganisms, and formation of infected vegetations.

Differentiate Osler nodes from Janeway lesions.

Osler nodes are painful, immunologic nodules on finger/toe tips; Janeway lesions are painless, septic embolic macules on palms/soles.

Provide a concise definition of heart failure.

Inability of the heart to supply adequate cardiac output and/or elevated left-ventricular filling pressures leading to tissue hypoperfusion or pulmonary congestion.

What ejection-fraction threshold defines HFrEF (systolic failure)?

Left-ventricular ejection fraction less than 40 %.

Name the three determinants of stroke volume.

Contractility, preload, and afterload.

Describe heart failure with preserved ejection fraction (HFpEF).

Left-sided heart failure characterized by pulmonary congestion and diastolic dysfunction despite normal EF and stroke volume.

Explain how left heart failure can precipitate right heart failure.

Elevated left-sided pressures transmit to pulmonary circulation, increasing pulmonary resistance and overloading the right ventricle.

Define high-output heart failure and give two causes.

Inability to meet metabolic demands despite increased cardiac output; caused by conditions like anemia, septicemia, hyperthyroidism, or beriberi.

What is the fundamental definition of shock?

A state of circulatory failure leading to inadequate tissue perfusion and impaired cellular metabolism.

Name two key cellular consequences of anaerobic metabolism during shock.

Lactate accumulation causing metabolic acidosis and depletion of ATP leading to Na⁺/K⁺ pump failure and cellular edema.

List the four major clinical types of shock.

Cardiogenic, hypovolemic, distributive (e.g., septic, anaphylactic), and obstructive shock.

Give two common left-to-right congenital shunts.

Atrial septal defect (ASD) and ventricular septal defect (VSD) (also patent ductus arteriosus).

What is Eisenmenger syndrome?

Reversal of a long-standing left-to-right shunt to right-to-left due to pulmonary hypertension, resulting in cyanosis.

Identify two classic right-to-left shunt lesions.

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

Give one example of an obstructive congenital heart defect.

Coarctation of the aorta.

How does valve damage lead to varicose veins?

Damaged valves allow reflux, increasing venous pressure and causing progressive dilation and tortuosity.

Why are venous thrombi more common than arterial thrombi?

Lower flow velocity and pressure in veins promote stasis and clot formation.

What is the principal clinical danger of untreated DVT?

Thromboembolization to the pulmonary arteries (pulmonary embolism).

State the percentage of hypertension cases that are secondary to identifiable causes.

Roughly 5–10 % of cases are secondary hypertension.

List the ‘5 C’s’ complications of chronic hypertension.

Coronary artery disease, chronic renal failure, congestive heart failure, cardiac arrest, and cerebrovascular accident (stroke).

Name the three elements signaling smooth-muscle recruitment after vascular injury.

Mediators from endothelial cells, platelets, and macrophages (plus coagulation-complement factors).

What are the three most basic endothelial functions?

Barrier integrity, modulation of hemostasis/inflammation, and release of vasodilators/vasoconstrictors.

Where do most true aneurysms form, and why is this location vulnerable?

Thoracic or abdominal aorta because constant hemodynamic stress and sparse vasa vasorum promote medial weakening.

Which blood-vessel layer provides most of the contractile strength?

The tunica media (smooth-muscle layer).

Name two vasoactive substances released by endothelial cells that cause vasodilation.

Nitric oxide (NO) and prostacyclin (PGI₂).