Blood Vessels 1 (Daenerys)

Hypertension, although other causes like Marfan and Loeys-Dietz syndromes are recognized.

Cigarette smoking.

Respiratory difficulties, difficulty in swallowing, persistent cough, pain, cardiac disease, and rupture.

It doubles the risk.

Heart failure secondary to aortic valvular incompetence.

Diabetes mellitus.

Blood separates the laminar planes of the media to form a blood-filled channel within the aortic walls.

Inflammation is present during all stages of atherogenesis and is linked to plaque formation and rupture.

Men aged 40-60 years with antecedent hypertension and younger adults with connective tissue abnormalities.

CRP (C-reactive protein) is one of the simplest and most sensitive independent markers of risk for MI, stroke, peripheral artery disease, and sudden cardiac death.

Hypertension.

Premature vascular disease.

Sudden onset of excruciating pain, cardiac tamponade, aortic insufficiency, and vascular obstruction.

Insulin resistance, hypertension (HTN), dyslipidemia, hypercoagulability, and a proinflammatory state.

Into proximal lesions (Type A) and distal lesions (Type B).

Lipoprotein a is an altered form of LDL that contains the apolipoprotein B-100 portion of LDL linked to apolipoprotein A, and it is associated with coronary and cerebrovascular disease.

Vascular pathology.

A general term for vessel wall inflammation.

At ostia of exiting vessels, branch points, and along the posterior wall of the abdominal aorta.

Platelet-derived factors and thrombin are major contributors to vascular pathology.

Narrowing (stenosis) or complete obstruction of vessel lumina, and weakening of vessel walls leading to dilation or rupture.

Fever, myalgia, arthralgia, and malaise.

Increased LDL cholesterol levels, decreased HDL cholesterol levels, and increased levels of abnormal lipoprotein a.

Stressful lifestyle (Type A personality), lack of exercise, and obesity.

Similar throughout the cardiovascular system.

Infectious vasculitis and non-infectious vasculitis.

Cholesterol and cholesterol esters.

Atherosclerosis is a chronic inflammatory and healing response of the arterial wall to endothelial injury.

To accommodate pulsatile flow and higher blood pressure.

A local or systemic immune response.

Genetic defects in lipoprotein uptake and metabolism.

Endothelial injury and dysfunction, accumulation of lipoproteins, monocyte adhesion and transformation to macrophages and foam cells, platelet adhesion, factor release inducing smooth muscle cell recruitment, SMC proliferation, ECM production, T cell recruitment, and lipid accumulation.

Elastic and muscular arteries.

Vasculitis seen in systemic immunologic disorders like SLE, associated with autoantibody production and immune complex deposition.

Diabetes Mellitus and hypothyroidism.

Endothelial injury.

Small muscle arteries and arterioles.

Drugs that act as haptens by binding to serum proteins or vessel wall constituents, such as penicillin.

By increasing local ROS production.

Hemodynamic disturbances and hypercholesterolemia.

Endothelial cells, smooth muscle cells, and a variety of ECM (e.g., collagen, elastin, GAGs).

Polyarteritis nodosa, which involves immune complex deposition of HBsAg and anti-HBsAg.

They may aggregate or be oxidized by free radicals.

A single layer of endothelial cells sitting on a basement membrane underlain by a thin layer of ECM.

Foam cells are macrophages that have accumulated modified LDL which they cannot degrade.

The internal elastic lamina.

Veins have large diameters, larger lumens, and thinner, less-organized walls.

Cardiac output and peripheral vascular resistance.

The accumulation of cholesterol crystals and free fatty acids in macrophages.

Arteries have several well-organized concentric layers of smooth muscle cells, while veins have smooth muscle cells arranged haphazardly.

About 2/3 of the circulating blood.

Stroke volume and heart rate.

It involves small to medium-sized arteries and can lead to aneurysms due to weakened arterial walls.

Intimal smooth muscle cells proliferation and ECM deposition.

High elastin content in the media.

Because they have less rigid walls.

Filling pressure, regulated via sodium homeostasis and its effect on blood volume.

Kidneys, heart, liver, and gastrointestinal tract (GIT) in descending order of frequency.

Circulating antibodies present in patients with vasculitis that react with neutrophil cytoplasmic antigens.

An arterial dissection arises when blood enters a defect in the arterial wall and tunnels between its layers.

They become less compliant and tend to raise systolic pressure.

PDGF (Platelet-Derived Growth Factor).

The α and β-adrenergic systems.

Venous valves.

Ulcerations, infarcts, ischemic atrophy, or hemorrhages.

Neutrophil primary granules, monocyte lysosomes, and endothelial cells.

A saccular aneurysm is a spherical outpouching involving only a portion of the vessel wall, varying from 5 to 20 cm in diameter, and often contains a thrombus.

Arterioles.

Hyperlipidemia, hyperglycemia, hypertension, and other influences.

At the level of the arterioles by neural and hormonal inputs.

Thin-walled channels lined by specialized endothelium.

An acute febrile illness of infancy and childhood, leading cause of acquired heart disease in children.

Polyangiitis.

A fusiform aneurysm is a diffuse, circumferential dilation of a long vascular segment, varying in diameter and length.

Resistance of fluid flow is inversely proportional to the fourth power of the diameter.

HDL likely helps clear cholesterol from these accumulations.

A balance between vasoconstrictors (e.g., angiotensin II, catecholamine, endothelin) and vasodilators (e.g., kinins, prostaglandins, NO).

To return interstitial tissue fluid and inflammatory cells to the bloodstream.

Conjunctival and oral erythema, edema of hands and feet, erythema of palms and soles, desquamative rash, and cervical lymph node enlargement.

Microscopic polyangiitis and Churg-Strauss syndrome.

Arterial walls constantly remodel by synthesizing, degrading, and repairing damage to their extracellular matrix (ECM).

Loose connective tissue containing nerve fibers and the vasa vasorum.

Lipid-filled foamy macrophages.

An increase in blood flow induces vasoconstriction to prevent hyperperfusion.

Microbes and tumor cells.

IV immunoglobulin therapy and aspirin.

Induced by drugs or cross-reactive microbial antigens.

Marfan syndrome involves defects in fibrillin that lead to aberrant TGF-β activity, weakening elastic tissues and contributing to aneurysm formation.

Elastic (large) arteries, muscular (medium) arteries, and small arteries.

Intimal thickening and lipid accumulation, which together form plaques.

By filtering plasma and reabsorbing sodium to maintain total body sodium levels.

Developmental or Berry Aneurysm, Arteriovenous fistula, and Fibromuscular Dysplasia.

A necrotizing vasculitis affecting capillaries, small arterioles, and venules.

They upregulate the expression or release of PR3 and MPO.

Mutations in the TGF-β receptors lead to defective synthesis of elastin and collagens I and III, causing aneurysms.

Approximately the diameter of an RBC (7-8 μm).

They are white-yellow and encroach on the lumen of the artery.

Low BP in the afferent arterioles, elevated levels of circulating catecholamine, and low sodium levels in the DCT.

An aneurysm that occurs in cerebral vessels and can cause fatal intracerebral hemorrhage when ruptured.

By releasing granule contents and reactive oxygen species (ROS).

Hemoptysis, hematuria, proteinuria, bowel pain or bleeding, muscle pain or weakness, and palpable cutaneous purpura.

Ehlers-Danlos Syndrome causes weak vessel walls due to defective type III collagen synthesis.

Because functionally useful oxygen diffusion is limited to only 100 μm.

Red-brown.

Plasma angiotensinogen.

Defects in immune regulation, such as in Kawasaki disease.

Direct connections between arteries and veins that bypass the intervening capillary bed.

Corticosteroids and Cyclophosphamides.

Vitamin C deficiency in scurvy causes altered collagen cross-linking, weakening the vascular wall.

They are patchy, usually involving only a portion of any given arterial wall and are rarely circumferential, appearing as eccentric.

By inducing vascular contraction, stimulating aldosterone secretion, and increasing tubular sodium resorption.

Giant Cell (Temporal) Arteritis.

High-output cardiac failure.

A small vessel necrotizing vasculitis associated with asthma, allergic rhinitis, lung infiltrates, peripheral hypereosinophilia, and extravascular necrotizing granuloma.

MMPs degrade virtually all components of the ECM, contributing to aneurysm development.

It increases sodium and water resorption in the DCT, which increases blood volume.

Temporal arteries, but also vertebral and ophthalmic arteries.

Focal irregular thickening in medium and large muscular arteries, including renal, carotid, splanchnic, and vertebral vessels.

Palpable purpura, GI bleeding, renal disease, and myocardial involvement leading to cardiomyopathy.

Atherosclerosis and hypertension are the two most important causes of aortic aneurysms.

A T-cell mediated immune response against vessel wall antigens, driving pro-inflammatory cytokine production.

Prostaglandin and NO.

Renovascular hypertension.

1. Smooth muscle cells, macrophages, and T cells; 2. ECM (collagen, elastic fibers, proteoglycans); 3. Intracellular and extracellular matrix.

Unknown, but a variety of infectious agents (mostly viral) have been implicated.

A mycotic aneurysm is caused by an infection, which can originate from a septic embolus, extension of an adjacent suppurative process, or circulating organisms directly infecting the arterial wall.

A string of beads appearance.

Volume expansion in the atrial and ventricular myocardium.

Facial pain or headache, most intense along the course of the superficial temporal arteries.

The formation of new blood vessels at the periphery of the lesion.

Activated T cells and monocytes/macrophages.

AAAs most commonly form in the abdominal aorta and common iliac arteries as a consequence of atherosclerosis.

A specialized lining for blood vessels.

They inhibit sodium resorption in the DCT, leading to Na excretion and diuresis, and induce systemic vasodilation.

Rupture, ulceration, or erosion; hemorrhage into a plaque; atheroembolism; aneurysm formation.

Corticosteroids or Anti-TNF therapy.

Segmental fibrinoid necrosis of the media and focal transmural necrotizing lesions, with infiltrating neutrophils.

Most AAAs are asymptomatic and discovered incidentally as an abdominal mass. They can rupture, obstruct vessels, cause embolism, or impinge on adjacent structures.

Maintaining a non-thrombogenic surface, modulating medial smooth muscle tone, metabolizing hormones, regulating inflammation, and affecting growth of other cell types.

Thrombosis, which may partially or completely occlude the lumen.

Multiple small changes in renal sodium hemostasis or vessel wall tone or structure.

Intimal thickening, medial granulomatous inflammation, T cell and macrophage infiltrate, multinucleated giant cells.

Dense transmural inflammatory infiltrate, T4 delayed type hypersensitivity reaction, and formation of autoantibodies to endothelial and smooth muscle cells.

The risk of rupture for an aneurysm larger than 6 cm is 25%.

A granulomatous vasculitis of medium and larger arteries characterized by ocular disturbances and weakening of pulses in the upper extremities.

The process by which endothelial cells respond to various stimuli by adjusting their steady-state functions and expressing inducible properties.

Renal artery stenosis leading to decreased GFR and pressure in the afferent arteriole, inducing renin secretion.

Plaque rupture that discharges atherosclerotic debris into the bloodstream, producing microemboli.

Surgery, including bypass, grafts, and stents, is the treatment for an aneurysm larger than 5 cm.

An alteration in the endothelial phenotype that is often both proinflammatory and prothrombogenic.

Primary hyperaldosteronism.

Induced pressure or ischemic atrophy of the underlying media, with loss of elasticity of tissue causing weakness and potential rupture.

Aortic arch and its branches, with pulmonary arteries involved in half of the cases.

Inflammatory AAAs are characterized by abundant lymphoplasmacytic inflammation, many macrophages, and dense periaortic scarring. They account for 5-10% of all AAAs.

Large, elastic arteries (Aorta, carotid) and large, medium, muscular arteries (Coronary, popliteal).

They play an important role in normal vascular repair and pathologic processes such as atherosclerosis.

A severe form of salt-sensitive hypertension caused by a gain-of-function mutation in the epithelial sodium channel protein (ENaC) that increases DCT sodium resorption.

Fatigue, weight loss, fever, claudication of legs, pulmonary hypertension, myocardial infarction, systemic hypertension.

IgG4-related disease is marked by high plasma levels of IgG4 and tissue fibrosis with frequent infiltration of IgG4-plasma cells, affecting various tissues including the pancreas, biliary system, and salivary glands.

Myocardial infarction, cerebral infarction (stroke), aortic aneurysm, peripheral vascular disease (ischemia - gangrene).

Irregular thickening of the vessel wall with intimal hyperplasia, adventitial mononuclear infiltrates, granulomatous inflammation.

Collagen, elastin, and proteoglycans, and they can elaborate growth factors and cytokines.

A mycotic AAA is an aneurysm that has become infected by circulating microorganisms, leading to suppuration and potential rapid dilation or rupture.

In small arteries, atherosclerotic plaques can gradually occlude vessel lumina, compromise blood flow, and cause ischemic injury.

A systemic vasculitis of small or medium-sized muscular arteries, typically involving renal and visceral vessels but sparing the pulmonary circulation.

Vasoconstriction and vasodilation in response to physiologic or pharmacologic stimuli.

The stage at which the occlusion is sufficiently severe to produce tissue ischemia, typically occurring when the occlusion produces a 70% decrease in the luminal cross-sectional area.

30%.

Rupture/Fissuring, erosion/ulceration, and hemorrhage into atheroma.

Ischemia and infarction of affected tissues and organs, hypertension, bloody stools, abdominal pain, muscle aches, peripheral neuritis.

Increase systemic BP or induce local vasoconstriction, thereby increasing physical stress.

Renal arterial involvement.

Genetic factors influence blood pressure regulation.

Partial or total thrombosis superimposed on a disrupted plaque is a central factor in acute coronary syndromes.

Corticosteroids and Cyclophosphamide.

Reduced renal sodium excretion in the presence of normal arterial pressure.

Thrombi that can embolize to produce microinfarct.

Increased fluid volume, increased cardiac output, and peripheral vascular resistance.

Compromise lumen size and potentiate plaque disruption by increasing local mechanical forces.

At a higher blood pressure, enough additional sodium is excreted by the kidneys to equal intake and prevent further fluid retention.

A localized abnormal dilation of a blood vessel or the heart that may be congenital or acquired.

They can lead to an increase in peripheral resistance.

An aneurysm involving an attenuated but intact arterial wall or thinned ventricular wall of the heart.

Stress, obesity, smoking, physical inactivity, and heavy salt consumption.

A defect in the vascular wall leading to extravascular hematoma that freely communicates with the intravascular space.

It accelerates atherogenesis and causes degenerative changes in the walls of large and medium arteries, leading to aortic dissection and cerebrovascular hemorrhage.

Hyaline arteriosclerosis and hyperplastic arteriosclerosis.

Homogenous pink hyaline thickening of arterioles associated with luminal narrowing.

Plasma protein leakage across the injured endothelial cell and increased matrix synthesis of smooth muscle.

Hyaline arteriosclerosis, with hyperglycemia-induced endothelial dysfunction as the underlying etiology.

Diffuse impairment of renal blood supply and glomerular scarring.

Concentric laminated (onion-skin) thickening of the vessel walls with luminal narrowing.

Smooth muscle with thickened, reduplicated basement membrane.

Fibrinoid deposits and vessel wall necrosis, particularly in the kidneys.

Hardening of the arteries.

Arteriolosclerosis, Mönckeberg medial sclerosis, and atherosclerosis.

Small arteries and arterioles.

Hyaline and hyperplastic.

Calcification of the walls of muscular arteries, typically involving the internal elastic membrane.

People aged 50 and above.