Cardiovascular Pathophysiology – Review Flashcards

Question-and-Answer flashcards covering key cardiovascular pathophysiology concepts from lecture notes.

What is the main difference between thrombocytopenia and thrombocytosis?

Thrombocytopenia is a decreased platelet count, whereas 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 through the bloodstream.

Name the three components of 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 major delivery functions of the circulatory system.

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

Which heart structures serve as the system’s pump?

The four chambers of the heart (right/left atria and ventricles).

What are the three layers shared by all vessels except capillaries?

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

Which artery type expands and recoils to dampen pulse pressure?

Elastic arteries such as the aorta.

Which small vessels are the principal regulators of systemic blood pressure?

Arterioles (small arteries).

What general vascular healing response follows endothelial injury?

Smooth-muscle proliferation, extracellular matrix deposition, and intimal thickening.

Name two vasoactive substances produced by healthy endothelium.

Nitric oxide and prostacyclin.

Give three common diseases of veins listed in the lecture.

Varicose veins, deep venous thrombosis (DVT), and superior vena cava syndrome.

What is the primary vein group affected by varicose veins?

The saphenous veins of the leg.

List four risk factors for developing varicose veins.

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

Define chronic venous insufficiency (CVI).

Long-term inadequate venous return leading to venous hypertension, stasis, tissue hypoxia, skin remodeling, and ulceration.

What are the three factors predisposing to venous thrombosis (DVT)?

Venous stasis, endothelial damage, and hypercoagulable states.

Why are venous thrombi more common than arterial thrombi?

Venous blood flow is slower and pressure is lower, promoting clot formation.

Untreated DVT carries a high risk of what potentially fatal complication?

Pulmonary thromboembolism.

What is superior vena cava syndrome (SVCS)?

Progressive occlusion of the SVC causing venous distention of upper extremities and head.

Give two malignancies that commonly cause SVCS.

Bronchogenic carcinoma and lymphoma (others: metastatic cancer, etc.).

Which two hemodynamic variables determine blood pressure?

Cardiac output and peripheral vascular resistance.

What renal hormone initiates the renin-angiotensin-aldosterone system (RAAS)?

Renin.

According to new guidelines, what SBP/DBP values define hypertension?

≥130 mm Hg systolic or ≥80 mm Hg diastolic (sustained).

What percentage of hypertension cases are classified as essential (primary)?

About 90–95 %.

Name one endocrine cause of secondary hypertension.

Pheochromocytoma (others: Cushing syndrome, primary aldosteronism, hyperthyroidism, etc.).

What arterial wall change is characteristic of long-standing hypertension?

Hyaline arteriolosclerosis (hyaline deposits thickening the wall).

Define arteriosclerosis in general terms.

Hardening and thickening of arterial walls with loss of elasticity.

Which arteriosclerosis subtype involves intimal lipid-rich plaques?

Atherosclerosis.

What distinguishes a ‘vulnerable’ atherosclerotic plaque from a stable one?

Thin fibrous cap, large lipid core, and heavy inflammation.

State Laplace’s law concept relevant to aneurysm formation.

Wall tension increases with vessel radius; dilated segments endure higher stress leading to further dilation.

Differentiate a true aneurysm from a false aneurysm.

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

Which vascular disease is the most common cause of abdominal aortic aneurysm?

Atherosclerosis.

Name the three heart wall layers from outermost to innermost.

Epicardium, myocardium, endocardium.

What is the primary function of the myocardium?

Contraction and relaxation to pump blood.

List the four main cardiac valves in order of blood flow.

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

Give two principal mechanisms of cardiac pump failure.

Weak systolic contraction (reduced output) and poor diastolic relaxation (impaired filling).

What ECG finding corresponds to ventricular depolarization?

The QRS complex (often simplified as the R wave).

Most acute pericarditis cases are idiopathic or due to which pathogen category?

Viral infections (e.g., coxsackie viruses).

What triad of signs suggests acute cardiac tamponade (Beck’s triad)?

Hypotension, jugular venous distention, and muffled heart sounds.

How does constrictive pericarditis impair cardiac output?

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

List the three major physiologic categories of cardiomyopathy.

Dilated, hypertrophic, and restrictive.

Dilated cardiomyopathy typically leads to which type of heart failure?

Heart failure with reduced ejection fraction (systolic dysfunction).

What genetic cardiac disorder often causes hypertrophic obstructive cardiomyopathy?

Autosomal-dominant mutations in sarcomeric proteins (e.g., β-myosin heavy chain).

Restrictive cardiomyopathy is defined by what ventricular property?

Impaired ventricular compliance leading to diastolic filling restriction with normal wall thickness.

What is valvular stenosis?

Pathologic narrowing of a heart valve orifice, impeding forward blood flow.

Explain valvular regurgitation.

Incomplete valve closure permits backward flow, causing volume overload of proximal chambers.

Which previous childhood condition is a common cause of acquired valvular disease worldwide?

Rheumatic heart disease (post-streptococcal).

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

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

Name two classic peripheral stigmata of infective endocarditis.

Osler nodes (painful fingertip nodules) and Janeway lesions (painless palm/sole macules).

Define heart failure in simple terms.

The heart cannot generate sufficient output to meet tissue demands or can do so only with elevated filling pressures.

What ejection fraction cutoff defines HFrEF (systolic HF)?

Less than 40 %.

List the three determinants of stroke volume.

Contractility, preload, and afterload.

HFpEF (diastolic HF) commonly results from what chronic condition?

Systemic hypertension leading to concentric left-ventricular hypertrophy.

Why does left heart failure often cause pulmonary edema?

Elevated left-ventricular and left-atrial pressures back up into pulmonary capillaries, increasing hydrostatic pressure and fluid transudation.

Right heart failure without left HF is usually secondary to what category of disease?

Chronic lung diseases causing pulmonary hypertension (cor pulmonale).

Define high-output heart failure.

Failure of the heart to meet abnormally elevated metabolic demands despite increased cardiac output (e.g., in anemia, thyrotoxicosis).

What is shock?

A state of systemic tissue hypoperfusion due to circulatory failure, leading to cellular metabolic derangements.

Which metabolic by-product accumulates during anaerobic metabolism in shock?

Lactate (causing lactic acidosis).

Name four major categories of shock discussed.

Hypovolemic, cardiogenic, distributive (including septic), and obstructive shock.

What echocardiographic finding is typical of cardiogenic shock?

Dilated ventricles with poor contractility and low stroke volume.

Give one common mechanical cause of obstructive shock.

Cardiac tamponade (others: tension pneumothorax, massive pulmonary embolism).

Which type of shock usually shows high cardiac output but low systemic vascular resistance?

Distributive (e.g., septic) shock.

What is the most frequent type of congenital cardiac shunt?

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

What cyanotic congenital heart lesion consists of four defects including VSD and RV outflow obstruction?

Tetralogy of Fallot (TOF).

Why can long-standing left-to-right shunts evolve into Eisenmenger syndrome?

Pulmonary hypertension reverses the pressure gradient, causing right-to-left flow and resultant cyanosis.

Which congenital obstructive lesion is characterized by narrowing of the aortic lumen?

Coarctation of the aorta.

State two complications of longstanding hypertension summarized as part of the "5 C’s."

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

What endothelial products maintain an antithrombotic surface under normal conditions?

Prostacyclin (PGI₂) and nitric oxide.

Describe Pemberton’s maneuver and its clinical significance.

Raising both arms for 1 min; facial flushing or cyanosis indicates SVC obstruction.

How does angiotensin II raise blood pressure?

By vasoconstriction of arterioles and stimulating aldosterone release for sodium and water retention.

Which veins are most often the source of pulmonary emboli?

Deep veins of the lower extremities (femoral, popliteal, iliac).

What structural heart change is seen in hypertensive hypertrophic cardiomyopathy?

Concentric left-ventricular wall thickening without dilation.

Explain the clinical stages C1–C6 in chronic venous disease.

C1 spider veins, C2 varicose veins, C3 edema, C4 skin changes, C5–C6 healed or active venous ulcers.

Which shock type presents with low central venous pressure and small hypercontractile ventricles?

Hypovolemic shock.

What law explains why large aneurysms expand faster and are prone to rupture?

Laplace’s law (wall tension proportional to radius).

Name one potential therapy targeting endothelial dysfunction mentioned in the lecture.

Statins (others: ACE inhibitors, vitamin C, complement inhibitors, recombinant thrombomodulin, etc.).

Which hormone increases renal sodium resorption, thereby expanding blood volume?

Aldosterone.

What inherited platelet abnormality often presents with prolonged bleeding but normal platelet count?

(Not in text) – but from lecture focus: question intentionally blank to prompt review.