Blood Vessels Generated

Why do arteries have thicker walls than veins?

Because they withstand pulsatile high pressure from the heart.

What happens to arterial structure as arteries get smaller?

Wall thickness decreases but wall-to-lumen ratio increases.

Which vessels are targeted in atherosclerosis?

Elastic and muscular arteries.

Which vessels are targeted in hypertension?

Small muscular arteries and arterioles.

Which vessels are targeted in vasculitides?

Specific vessel calibers depending on the vasculitis type.

What do endothelial cells line?

The lumens of all blood vessels.

Endothelial cells rest on what structure?

A basement membrane.

What specialization of endothelial cells is found in the CNS?

Tight junctions forming the blood-brain barrier.

Where are fenestrated endothelial cells found?

Liver sinusoids and renal glomeruli.

What are the antithrombotic roles of endothelial cells?

Provide non-thrombogenic surface, secrete anticoagulants, and produce fibrinolytics.

Name two vasodilators produced by endothelial cells.

Nitric oxide and prostacyclin.

Name two vasoconstrictors produced by endothelial cells.

Endothelin and angiotensin II.

What triggers endothelial activation?

Inflammatory, immune, metabolic, hemodynamic, or hypoxic stimuli.

What changes occur during endothelial activation?

Increased adhesion molecules, cytokines, MHC, procoagulant activity.

What is endothelial dysfunction?

A shift to a pro-inflammatory, pro-thrombotic, vasoconstrictive phenotype.

What are the primary functions of vascular smooth muscle cells?

Regulate vasoconstriction/vasodilation and maintain structural support.

What ECM components do smooth muscle cells produce?

Elastin, collagen, and glycosaminoglycans.

Where are smooth muscle cells most abundant?

In the media of arteries and veins.

What happens when smooth muscle cells become activated?

They proliferate, migrate to the intima, and synthesize extracellular matrix.

What composes the tunica intima?

Endothelium, basement membrane, and thin extracellular matrix.

What structure separates the intima from the media?

The internal elastic lamina.

What composes the tunica media?

Smooth muscle cells and elastic fibers, varying by vessel type.

What composes the tunica adventitia?

Loose connective tissue, nerve fibers, and vasa vasorum.

Which vessels contain vasa vasorum?

Large and medium arteries and veins.

What is the role of the vasa vasorum?

Supply oxygen and nutrients to the outer media.

What structural feature distinguishes elastic arteries?

Multiple concentric elastin layers.

What is the functional role of elastic arteries?

Store and release energy to maintain continuous blood flow.

What happens to elastic arteries with aging?

Loss of elasticity, increased systolic pressure, and arterial dilation.

What distinguishes muscular arteries?

A media dominated by smooth muscle cells.

What regulates muscular artery tone?

Autonomic signals and local metabolic factors.

Why are arterioles the main resistance vessels?

Small changes in diameter dramatically alter resistance.

What is the relationship between resistance and diameter?

Resistance ∝ 1 / diameter⁴.

What is the typical capillary diameter?

About 5 micrometers.

What cells help stabilize capillaries?

Pericytes.

Why is blood flow slow in capillaries?

Large total cross-sectional area.

Why must metabolically active tissues have dense capillary networks?

Oxygen can only diffuse

Why do veins have thin walls and large lumens?

They operate under low pressure and function as blood reservoirs.

What proportion of total blood volume is in veins?

About two-thirds.

What is the function of venous valves?

Prevent backflow, especially in extremities.

What vessels are the primary site of leukocyte extravasation?

Postcapillary venules.

What do lymphatics drain?

Interstitial fluid and return it to venous circulation.

What role do lymphatics play in immunity?

Transport antigen-bearing cells to lymph nodes.

What role do lymphatics play in disease spread?

Provide pathways for tumor and microbial dissemination.

What triggers intimal thickening?

Endothelial injury or dysfunction.

What cells migrate into the intima during intimal thickening?

Smooth muscle cells.

What do smooth muscle cells do once inside the intima?

Proliferate and produce extracellular matrix.

What is the neointima composed of?

Proliferating smooth muscle cells and extracellular matrix.

What is the clinical significance of intimal thickening?

Occurs in atherosclerosis, restenosis, graft stenosis, vasculitis, and transplant vasculopathy.

What proportion of hypertension is essential (idiopathic)?

90–95%.

What proportion of hypertension is secondary?

5–10%.

What major cardiovascular conditions are associated with chronic hypertension?

Left ventricular hypertrophy, heart failure, stroke, aortic dissection, and chronic kidney disease.

What defines malignant hypertension?

Blood pressure over 180 systolic or 120 diastolic with acute organ damage.

What are signs of malignant hypertension?

Retinal hemorrhages, exudates, papilledema, and acute renal failure.

What is the equation for blood pressure regulation?

BP = cardiac output × peripheral resistance.

What determines cardiac output?

Stroke volume and heart rate.

What regulates stroke volume?

Sodium balance, contractility, and blood volume.

Where is peripheral resistance mainly regulated?

At the level of arterioles.

Name major vasoconstrictors influencing peripheral resistance.

Angiotensin II, catecholamines, endothelin.

Name major vasodilators influencing peripheral resistance.

Kinins, prostaglandins, nitric oxide.

How much plasma sodium does the kidney reabsorb daily?

About 99.5% of filtered sodium.

What hormones promote natriuresis?

ANP and BNP.

What stimulates renin release?

Low afferent arteriole pressure, sympathetic activity, or low distal tubular sodium.

What does angiotensin II do?

Vasoconstricts, increases aldosterone, and increases sodium reabsorption.

What environmental factors contribute to essential hypertension?

High salt, stress, obesity, smoking, inactivity.

What effect does hypertension have on large arteries?

Accelerated atherosclerosis and medial degeneration.

What is hyaline arteriolosclerosis?

Pink, homogeneous thickening of arterioles due to plasma protein leakage and SMC ECM production.

What conditions worsen hyaline arteriolosclerosis?

Hypertension and diabetes.

What organ is most affected by hyaline arteriolosclerosis?

The kidney, leading to nephrosclerosis.

What is hyperplastic arteriolosclerosis?

Concentric “onion-skin” thickening of arterioles.

What causes hyperplastic arteriolosclerosis?

Severe or malignant hypertension.

What additional lesion may accompany hyperplastic arteriolosclerosis in malignant hypertension?

Fibrinoid necrosis.

What is necrotizing arteriolitis?

Acute fibrinoid necrosis of arterioles with inflammation.

Which condition is most associated with necrotizing arteriolitis?

Malignant hypertension.

What is arteriosclerosis?

Hardening of arteries due to wall thickening and loss of elasticity.

What vessels are affected in arteriolosclerosis?

Small arteries and arterioles.

What are the two types of arteriolosclerosis?

Hyaline and hyperplastic.

What is the consequence of arteriolosclerosis?

Downstream ischemia.

What is Mönckeberg medial sclerosis?

Calcification of the media of muscular arteries without lumen narrowing.

At what age is Mönckeberg sclerosis most common?

Adults over 50.

Does Mönckeberg sclerosis usually cause clinical symptoms?

No, it is usually insignificant.

What is fibromuscular intimal hyperplasia?

Intimal thickening in muscular arteries larger than arterioles.

What can cause fibromuscular intimal hyperplasia?

Inflammation from healed arteritis, transplant vasculopathy, or mechanical injury such as angioplasty or stents.

What major condition can fibromuscular intimal hyperplasia cause?

Significant stenosis of arteries.

What is the most clinically significant form of arteriosclerosis?

Atherosclerosis.

What type of lesions does atherosclerosis form?

Intimal plaques or atheromas.

What are the three major components of an atherosclerotic plaque?

Fibrous cap, necrotic core, and shoulder region.

What does the fibrous cap contain?

Smooth muscle cells and dense collagen.

What does the necrotic core contain?

Lipid debris, cholesterol crystals, foam cells, and necrotic tissue.

What cells are abundant in the shoulder of an atheroma?

Macrophages and T lymphocytes.

What are fatty streaks composed of?

Lipid-filled foam cells.

Do all fatty streaks progress to plaques?

No.

Where do atherosclerotic plaques form most commonly?

Abdominal aorta and iliac arteries, followed by coronary arteries.

What arteries are relatively spared from atherosclerosis?

Upper extremity arteries and mesenteric/renal arteries (except at ostia).

What is a vulnerable plaque?

A plaque with a thin fibrous cap and large lipid core prone to rupture.

What are major complications of atherosclerotic plaques?

Thrombosis, embolization, aneurysm formation, and stenosis.

What happens when a plaque ruptures?

Thrombogenic core is exposed leading to acute thrombosis.

What is atheroembolism?

Dislodged fragments of plaque traveling downstream.

What happens in plaque erosion?

Endothelium is lost and subendothelial basement membrane is exposed, causing thrombosis.

What causes aneurysm formation in atherosclerosis?

Destruction of the media from ischemia and elastin loss.

What defines a true aneurysm?

Dilation involving all layers of the vessel wall.