Respiratory difficulties, difficulty in swallowing, persistent cough, pain, cardiac disease, and rupture.
Hypertension.
Platelet-derived factors and thrombin are major contributors to vascular pathology.
A local or systemic immune response.
Hemodynamic disturbances and hypercholesterolemia.
Heart failure secondary to aortic valvular incompetence.
Fever, myalgia, arthralgia, and malaise.
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.
Polyarteritis nodosa, which involves immune complex deposition of HBsAg and anti-HBsAg.
The accumulation of cholesterol crystals and free fatty acids in macrophages.
Kidneys, heart, liver, and gastrointestinal tract (GIT) in descending order of frequency.
IV immunoglobulin therapy and aspirin.
Ehlers-Danlos Syndrome causes weak vessel walls due to defective type III collagen synthesis.
Cigarette smoking.
Inflammation is present during all stages of atherogenesis and is linked to plaque formation and rupture.
A general term for vessel wall inflammation.
Atherosclerosis is a chronic inflammatory and healing response of the arterial wall to endothelial injury.
The internal elastic lamina.
Intimal smooth muscle cells proliferation and ECM deposition.
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.
Loose connective tissue containing nerve fibers and the vasa vasorum.
They upregulate the expression or release of PR3 and MPO.
Corticosteroids and Cyclophosphamides.
By inducing vascular contraction, stimulating aldosterone secretion, and increasing tubular sodium resorption.
Palpable purpura, GI bleeding, renal disease, and myocardial involvement leading to cardiomyopathy.
The formation of new blood vessels at the periphery of the lesion.
Diabetes mellitus.
Increased LDL cholesterol levels, decreased HDL cholesterol levels, and increased levels of abnormal lipoprotein a.
They may aggregate or be oxidized by free radicals.
Arteries have several well-organized concentric layers of smooth muscle cells, while veins have smooth muscle cells arranged haphazardly.
Circulating antibodies present in patients with vasculitis that react with neutrophil cytoplasmic antigens.
Thin-walled channels lined by specialized endothelium.
A balance between vasoconstrictors (e.g., angiotensin II, catecholamine, endothelin) and vasodilators (e.g., kinins, prostaglandins, NO).
Marfan syndrome involves defects in fibrillin that lead to aberrant TGF-β activity, weakening elastic tissues and contributing to aneurysm formation.
Red-brown.
Intimal thickening, medial granulomatous inflammation, T cell and macrophage infiltrate, multinucleated giant cells.
Thrombi that can embolize to produce microinfarct.
At ostia of exiting vessels, branch points, and along the posterior wall of the abdominal aorta.
To accommodate pulsatile flow and higher blood pressure.
By increasing local ROS production.
Veins have large diameters, larger lumens, and thinner, less-organized walls.
High elastin content in the media.
PDGF (Platelet-Derived Growth Factor).
Arterioles.
HDL likely helps clear cholesterol from these accumulations.
Lipid-filled foamy macrophages.
Mutations in the TGF-β receptors lead to defective synthesis of elastin and collagens I and III, causing aneurysms.
By releasing granule contents and reactive oxygen species (ROS).
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.
Insulin resistance, hypertension (HTN), dyslipidemia, hypercoagulability, and a proinflammatory state.
Diabetes Mellitus and hypothyroidism.
About 2/3 of the circulating blood.
An arterial dissection arises when blood enters a defect in the arterial wall and tunnels between its layers.
Polyangiitis.
Intimal thickening and lipid accumulation, which together form plaques.
They are patchy, usually involving only a portion of any given arterial wall and are rarely circumferential, appearing as eccentric.
MMPs degrade virtually all components of the ECM, contributing to aneurysm development.
Unknown, but a variety of infectious agents (mostly viral) have been implicated.
AAAs most commonly form in the abdominal aorta and common iliac arteries as a consequence of atherosclerosis.
Multiple small changes in renal sodium hemostasis or vessel wall tone or structure.
Primary hyperaldosteronism.
It doubles the risk.
Premature vascular disease.
Narrowing (stenosis) or complete obstruction of vessel lumina, and weakening of vessel walls leading to dilation or rupture.
Genetic defects in lipoprotein uptake and metabolism.
Endothelial cells, smooth muscle cells, and a variety of ECM (e.g., collagen, elastin, GAGs).
Cardiac output and peripheral vascular resistance.
Filling pressure, regulated via sodium homeostasis and its effect on blood volume.
Hyperlipidemia, hyperglycemia, hypertension, and other influences.
An increase in blood flow induces vasoconstriction to prevent hyperperfusion.
Approximately the diameter of an RBC (7-8 μm).
Hemoptysis, hematuria, proteinuria, bowel pain or bleeding, muscle pain or weakness, and palpable cutaneous purpura.
Into proximal lesions (Type A) and distal lesions (Type B).
Endothelial injury.
Ulcerations, infarcts, ischemic atrophy, or hemorrhages.
Resistance of fluid flow is inversely proportional to the fourth power of the diameter.
Microscopic polyangiitis and Churg-Strauss syndrome.
Developmental or Berry Aneurysm, Arteriovenous fistula, and Fibromuscular Dysplasia.
Defects in immune regulation, such as in Kawasaki disease.
Temporal arteries, but also vertebral and ophthalmic arteries.
Volume expansion in the atrial and ventricular myocardium.
A specialized lining for blood vessels.
The process by which endothelial cells respond to various stimuli by adjusting their steady-state functions and expressing inducible properties.
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.
Similar throughout the cardiovascular system.
Vasculitis seen in systemic immunologic disorders like SLE, associated with autoantibody production and immune complex deposition.
The α and β-adrenergic systems.
An acute febrile illness of infancy and childhood, leading cause of acquired heart disease in children.
To return interstitial tissue fluid and inflammatory cells to the bloodstream.
Elastic (large) arteries, muscular (medium) arteries, and small arteries.
Because functionally useful oxygen diffusion is limited to only 100 μm.
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.
Dense transmural inflammatory infiltrate, T4 delayed type hypersensitivity reaction, and formation of autoantibodies to endothelial and smooth muscle cells.
Aortic arch and its branches, with pulmonary arteries involved in half of the cases.
Irregular thickening of the vessel wall with intimal hyperplasia, adventitial mononuclear infiltrates, granulomatous inflammation.
Hypertension, although other causes like Marfan and Loeys-Dietz syndromes are recognized.
Blood separates the laminar planes of the media to form a blood-filled channel within the aortic walls.
Vascular pathology.
Cholesterol and cholesterol esters.
Drugs that act as haptens by binding to serum proteins or vessel wall constituents, such as penicillin.
It involves small to medium-sized arteries and can lead to aneurysms due to weakened arterial walls.
They become less compliant and tend to raise systolic pressure.
Neutrophil primary granules, monocyte lysosomes, and endothelial cells.
Arterial walls constantly remodel by synthesizing, degrading, and repairing damage to their extracellular matrix (ECM).
A necrotizing vasculitis affecting capillaries, small arterioles, and venules.
An aneurysm that occurs in cerebral vessels and can cause fatal intracerebral hemorrhage when ruptured.
Direct connections between arteries and veins that bypass the intervening capillary bed.
Focal irregular thickening in medium and large muscular arteries, including renal, carotid, splanchnic, and vertebral vessels.
Facial pain or headache, most intense along the course of the superficial temporal arteries.
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.
Infectious vasculitis and non-infectious vasculitis.
Small muscle arteries and arterioles.
Foam cells are macrophages that have accumulated modified LDL which they cannot degrade.
Stroke volume and heart rate.
Venous valves.
A fusiform aneurysm is a diffuse, circumferential dilation of a long vascular segment, varying in diameter and length.
Conjunctival and oral erythema, edema of hands and feet, erythema of palms and soles, desquamative rash, and cervical lymph node enlargement.
By filtering plasma and reabsorbing sodium to maintain total body sodium levels.
Low BP in the afferent arterioles, elevated levels of circulating catecholamine, and low sodium levels in the DCT.
Plasma angiotensinogen.
It increases sodium and water resorption in the DCT, which increases blood volume.
A string of beads appearance.
The risk of rupture for an aneurysm larger than 6 cm is 25%.
Inflammatory AAAs are characterized by abundant lymphoplasmacytic inflammation, many macrophages, and dense periaortic scarring. They account for 5-10% of all AAAs.
Collagen, elastin, and proteoglycans, and they can elaborate growth factors and cytokines.
30%.
Partial or total thrombosis superimposed on a disrupted plaque is a central factor in acute coronary syndromes.
Smooth muscle with thickened, reduplicated basement membrane.
Inadequate organ perfusion, tissue dysfunction, or death.
Men aged 40-60 years with antecedent hypertension and younger adults with connective tissue abnormalities.
Sudden onset of excruciating pain, cardiac tamponade, aortic insufficiency, and vascular obstruction.
Stressful lifestyle (Type A personality), lack of exercise, and obesity.
Elastic and muscular arteries.
A single layer of endothelial cells sitting on a basement membrane underlain by a thin layer of ECM.
At the level of the arterioles by neural and hormonal inputs.
Induced by drugs or cross-reactive microbial antigens.
They are white-yellow and encroach on the lumen of the artery.
1. Smooth muscle cells, macrophages, and T cells; 2. ECM (collagen, elastic fibers, proteoglycans); 3. Intracellular and extracellular matrix.
Thrombosis, which may partially or completely occlude the lumen.
An alteration in the endothelial phenotype that is often both proinflammatory and prothrombogenic.
Vasoconstriction and vasodilation in response to physiologic or pharmacologic stimuli.
Renal arterial involvement.
They can lead to an increase in peripheral resistance.
Genetics, age, and gender.
Underlying renal or adrenal disease, or other identifiable causes.
Because they have less rigid walls.
Microbes and tumor cells.
Vitamin C deficiency in scurvy causes altered collagen cross-linking, weakening the vascular wall.
High-output cardiac failure.
Prostaglandin and NO.
Most AAAs are asymptomatic and discovered incidentally as an abdominal mass. They can rupture, obstruct vessels, cause embolism, or impinge on adjacent structures.
In small arteries, atherosclerotic plaques can gradually occlude vessel lumina, compromise blood flow, and cause ischemic injury.
A localized abnormal dilation of a blood vessel or the heart that may be congenital or acquired.
Plasma protein leakage across the injured endothelial cell and increased matrix synthesis of smooth muscle.
Premenopausal women are protected against atherosclerosis compared to age-matched men, possibly due to the favorable influence of estrogen.
Elevated levels of LDL and decreased levels of HDL can initiate lesion development.
Half of the patients die of ischemic heart disease or congestive heart failure, and another third die of stroke.
Giant Cell (Temporal) Arteritis.
Atherosclerosis and hypertension are the two most important causes of aortic aneurysms.
Activated T cells and monocytes/macrophages.
Corticosteroids or Anti-TNF therapy.
Plaque rupture that discharges atherosclerotic debris into the bloodstream, producing microemboli.
Large, elastic arteries (Aorta, carotid) and large, medium, muscular arteries (Coronary, popliteal).
Rupture/Fissuring, erosion/ulceration, and hemorrhage into atheroma.
Corticosteroids and Cyclophosphamide.
Hardening of the arteries.
Small arteries and arterioles.
Hyperlipidemia, hypertension, smoking, diabetes, and physical inactivity.
Endothelial cells.
90-95%.
A small vessel necrotizing vasculitis associated with asthma, allergic rhinitis, lung infiltrates, peripheral hypereosinophilia, and extravascular necrotizing granuloma.
Renovascular hypertension.
Maintaining a non-thrombogenic surface, modulating medial smooth muscle tone, metabolizing hormones, regulating inflammation, and affecting growth of other cell types.
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.
A systemic vasculitis of small or medium-sized muscular arteries, typically involving renal and visceral vessels but sparing the pulmonary circulation.
At a higher blood pressure, enough additional sodium is excreted by the kidneys to equal intake and prevent further fluid retention.
Homogenous pink hyaline thickening of arterioles associated with luminal narrowing.
A condition characterized by 'gruel hardening' and is the most frequent and clinically important pattern of arteriosclerosis.
Endothelial cell dysfunction or loss.
A T-cell mediated immune response against vessel wall antigens, driving pro-inflammatory cytokine production.
Segmental fibrinoid necrosis of the media and focal transmural necrotizing lesions, with infiltrating neutrophils.
Surgery, including bypass, grafts, and stents, is the treatment for an aneurysm larger than 5 cm.
Fatigue, weight loss, fever, claudication of legs, pulmonary hypertension, myocardial infarction, systemic hypertension.
Increase systemic BP or induce local vasoconstriction, thereby increasing physical stress.
People aged 50 and above.
Systolic pressure of more than 200 mmHg and diastolic pressure of more than 120 mmHg.
They inhibit sodium resorption in the DCT, leading to Na excretion and diuresis, and induce systemic vasodilation.
A granulomatous vasculitis of medium and larger arteries characterized by ocular disturbances and weakening of pulses in the upper extremities.
They play an important role in normal vascular repair and pathologic processes such as atherosclerosis.
A mycotic AAA is an aneurysm that has become infected by circulating microorganisms, leading to suppuration and potential rapid dilation or rupture.
Ischemia and infarction of affected tissues and organs, hypertension, bloody stools, abdominal pain, muscle aches, peripheral neuritis.
Reduced renal sodium excretion in the presence of normal arterial pressure.
Compromise lumen size and potentiate plaque disruption by increasing local mechanical forces.
Calcification of the walls of muscular arteries, typically involving the internal elastic membrane.
Intimal thickening.
End-organ damage and increased risk of atherosclerosis.
Cardiac Output = Heart Rate (HR) x Stroke Volume (SV).
Rupture, ulceration, or erosion; hemorrhage into a plaque; atheroembolism; aneurysm formation.
Renal artery stenosis leading to decreased GFR and pressure in the afferent arteriole, inducing renin secretion.
It accelerates atherogenesis and causes degenerative changes in the walls of large and medium arteries, leading to aortic dissection and cerebrovascular hemorrhage.
Fibrinoid deposits and vessel wall necrosis, particularly in the kidneys.
Induced pressure or ischemic atrophy of the underlying media, with loss of elasticity of tissue causing weakness and potential rupture.
Myocardial infarction, cerebral infarction (stroke), aortic aneurysm, peripheral vascular disease (ischemia - gangrene).
Genetic factors influence blood pressure regulation.
Stress, obesity, smoking, physical inactivity, and heavy salt consumption.
Diffuse impairment of renal blood supply and glomerular scarring.
Migrate into the intima and synthesize extracellular matrix.
It increases with age and is higher among African Americans.
Blood Pressure (BP) = Cardiac Output (CO) x Peripheral Resistance.
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.
Increased fluid volume, increased cardiac output, and peripheral vascular resistance.
A defect in the vascular wall leading to extravascular hematoma that freely communicates with the intravascular space.
Concentric laminated (onion-skin) thickening of the vessel walls with luminal narrowing.
An aneurysm involving an attenuated but intact arterial wall or thinned ventricular wall of the heart.
Hyaline arteriosclerosis, with hyperglycemia-induced endothelial dysfunction as the underlying etiology.
Arteriolosclerosis, Mönckeberg medial sclerosis, and atherosclerosis.
Hyaline and hyperplastic.
The incidence of myocardial infarction increases fivefold between ages 40 and 60.
Chronic hypertension.
Cardiac hypertrophy, heart failure, multi-infarct dementia, aortic dissection, and renal failure.
Hyaline arteriosclerosis and hyperplastic arteriosclerosis.
It is the most important independent risk factor for atherosclerosis.
From adjacent uninjured areas or derived from circulating precursors.
Rapidly rising blood pressure that can lead to death within 1 to 2 years if untreated.
Sustained diastolic pressure above 89 mmHg or sustained systolic pressure above 139 mmHg.
Stroke Volume (SV) = End Diastolic Volume - End Systolic Volume.
