Week 1 - Atherosclerosis & HTN
Terms in this set (63)
intima (endothelium), media (smooth muscle), adventitia (supporting layer)
What are the layers of a blood vessel?
aorta, innominate, common carotid, subclavian, pulmonary
What are 5 examples of elastic arteries?
radial, femoral, coronary, cerebral
What are 4 examples of muscular arteries?
media, external and internal elastic lamina
elastic arteries have numerous layers of elastin in the tunica _____layer. while muscular arteries possess ____and____layers
control permeability, anti-inflammatory, prevent thrombosis via vasodilation and anti-anthrombotic mediators (but promotes thrombosis when required)
What are 3 normal functions of endothelium?
important integrin for assisting in migration of WBC through wall of blood vessel
______on the endothelium activates antithrombin which binds IIa, IXa, Xa, XIa, and XII
prostacyclin, nitric oxide
_____&____are released by endothelium to inhibit platelet aggregation and promote vasodilation
thrombin activates protein C by binding to _______on the endothelium
von Willebrand factor, tissue factor
to promote thrombosis, endothelial cells produce ____which promotes platelet adhesion and activates Factor V along with _____for activating the extrinsic clotting cascade
the substance _____produced by the endothelial cells promotes vasoconstriction
when damaged, smooth muscle cells migrate into the tunica ___layer where they can proliferate and produce ____allowing for thickening of the vessel wall
arteriosclerosis characterized by irregularly distributed lipid deposits in the intima of *
large and medium-sized arteries
* (e.g., aorta and carotid and coronary arteries); such deposits are associated with fibrosis and calcification
list two types of arteriosclerosis
endothelium becomes dysfunctional
* allowing LDL to enter intima, become oxidized and accumulate and through the interaction of mediators (macrophages, smooth muscle) plaque increases in size leading to lipid deposition, fibrosis, and complications
Describe the process of atherosclerosis
hypertensive stress, diabetes mellitus, hyperhomocysteinemia, tobacco use
damage to the endothelium is the key step in atherosclerosis, what disorders can lead to this damage?
damage to endothelium, migration of smooth muscles from media to intima
What are the 2 critical steps in development of an atherosclerotic plaque?
endothelial, smooth muscle, macrophages, T lymphocytes
What 4 cell types are involved in the process of atherosclerosis?
engulf oxidized LDL forming foam cells and produce cytokines to promote ECM deposition (PDF, FGF, TNF, IL-1, IFN-alpha, TGF-beta) and release IL-1 and TNF to stimulate endothelial cells to produce PAF, tissue factor, and plasminogen activator inhibitor
What is the role of macrophages in atherosclerosis?
cholesterol and TAGs are absorbed from intestine and packaged In chylomicrons for transport, they acquire ApoCII (activates lipoprotein lipase) and ApoE (for liver entry) from HDL, then lipoprotein lipase removes TAGs from chylomicron to form remnant
Explain the ApoB48 (exogenous pathway) of lipoproteins
chylomicrons with VLDL are secreted from liver and acquire ApoCII and E from HDL, lipoprotein lipase removes TAGs and the ApoCII and E are transfered back to HDL forming IDL which is taken up by liver or converted to LDL by hepatic lipoprotein lipase and provides cholesterol to peripheral tissues
explain the ApoB100 (endogenous pathway) of lipoproteins
LDL receptor mutation preventing LDL from entering peripheral tissue leading to elevated LDL
explain the mechanism of familial hypercholesterolemia
lipoprotein (a) is an LDL-like particle to which ____is attached. It is homologous to _____, thus the body may try to use it to generate plasmin leading to inhibition of clot lysis
dyslipidemia, tobacco use, HTN, diabetes mellitus, sedentary; age, male sex, hereditary
What are the modifiable risk factors for atherosclerosis? non-modifiable?
oxidized LDL stays in the intima and can no longer diffuse in and out, endothelial dysfunction, increased platelet adhesion, stimulation of sympathetic nervous system
What are 4 effects of tobacco use on the vasculature?
fatty streaks (raised line of foam cells in intima), intimal cell mass (thickened intima at vessel branch points)
what are 2 precursor lesions for atherosclerosis?
smooth muscle; TNF-alpha, IL-1, TGF-beta, PDGF
_____cells migrating into intima allow for transition from fatty streak to an atheromatous plaque. This is promoted by cytokines, ____, ____, and ___along with _____.
endothelial dysfunction, accumulation of oxidized LDL engulfed by macrophages forming foam cells, smooth muscle cell migration, neovascularization, dystrophic calcification of plaque, thrombosis
What changes occur with atherosclerosis?
stable: thick fibrous cap with small amount of lipid; vulnerable: thin fibrous cap with large amount of lipid and inflammatory cells
contrast a stable versus vulnerable atherosclerotic plaque
_____produced by T-lymphocytes inhibits the activity of smooth muscle cells preventing the building up of a fibrous cap, additionally via interactions with ____on foam cells T cells can activate foam cells leading to MMP activity to break down the fibrous cap
hypoxia-ischemia (stenosis, ulceration, etc), aneurysm, embolism, PAD
What are 4 general complications of atherosclerosis?
local anemia due to mechanical obstruction of the blood supply
an area of necrosis resulting from a sudden insufficiency of arterial or venous blood supply
femoral-popliteal, peripheral arterial disease
calf claudication is indicative of ______ disease, a type of ______
aortoilliac disease (leriche's syndrome), peripheral arterial disease
Discomfort in thigh, hip, buttock associated with impotence indicates ______ , a type of ______
compare SBP in upper/lower extremities, ABI, to localize: Doppler ultrasound, MRI, CTA
What tests can be done for a diagnosis of PAD?
0.9, 0.5-0.8, 0.5
ABI <___is indicative of PAD, when claudication is present it is normally between ____-____. Patients may have resting pain when <___.
C-reactive protein, lipoprotein(a), ApoA-I, ApoB, LDL-C, HDL-C
What lab results may be useful in assessing a patient for atherosclerosis?
contractility, venous return (affected by blood volume and venous tone)
What are the determinants of stroke volume?
circulating regulators (angiotensin II, catecholamines), innervation (alpha1, Beta2 decrease), blood viscosity (hematocrit), local regulators (NO, prostaglandins, adenosine, H+ all decrease, endothelin increase)
What are the determinants of peripheral resistance? (unless noted, these increase resistance)
angiotensin from the liver is converted to angiotensin I via renin from the kidney, angiotensin I to angiotensin II via ACE leading to vasoconstriction and increased aldosterone for Na+ reabsorption
Describe the MOA of the RAAS
essential hypertension that runs a relatively long and symptomless course
hypertension without pre-existing renal disease or known cause
severe hypertension that runs a rapid course, causing necrosis of arteriolar walls in kidney, retina, etc
according to the CDC____% of adults have HTN, and of those ____% have uncontrolled HTN
120-139/80-89; 140-159/90-99; >160/>100
What is the classification of preHTN? Stage 1 HTN? Stage 2 HTN?
HTN causes damage to ________.
elevated blood pressure, organ damage
Most often essential HTN is asymptomatic, but what is a primary sign? secondary?
headache, blurred vision, confusion, somnolence, coma, angina; retinal hemorrhage, exudate, papilledema; fibrinoid necrosis,
, pulmonary edema
What are 6 common symptoms of malignant HTN (hypertensive crisis)? 3 signs? 3 pathologic findings?
chronic renal disease, primary aldosteronism, renovascular, pheochromocytoma, coarctation of aorta, Cushing syndrome
What are some causes of secondary HTN?
initial evaluation identifies cause for HTN, HTN is severe and refractory to treatment
In what situations should you look for secondary HTN as the cause of a patient's HTN?
hyaline arteriosclerosis, glomerulonephritis
What 2 pathologic findings would you look for in chronic renal disease?
low potassium; adrenal adenoma secreting aldosterone
What is the major sign of primary aldosteronism? What pathologic finding would you expect?
atrophy of ipsilateral kidney, nephrosclerosis of contralateral kidney; fibromuscular dysplasia in younger women
What pathologic findings would you expect in an individual with renovascular HTN?
episodic HTN; palpitations, sweating, headache, tachycardia
What is the major sign of pheocromocytoma? What additional symptoms are present?
BP > in arms than legs, midsystolic murmur; stenosis of aorta at or distal to ligamentum arteriosum, bicuspid aortic valve (25%)
What are 2 signs of aortic coarctation? What pathologic findings would you expect to see?
change of PMI, sustained apical impulse, S4; predisposition to cardiac dysrhythmias, sudden death
What are 3 signs of cardiac hypertrophy? What are possible complications?
acute: aortic dissection, intracerebral hemorrhage, HTN crisis; chronic: cardiac hypertrophy, chronic renal failure, atherosclerosis
What are 3 acute complications of HTN? 3 of chronic?
tearing of the aortic intima away from the media, with a false lumen produced that fills with blood
HTN, cocaine and methamphetamine, Marfan, bicuspid aortic valve
What are 5 risk factors for aortic dissection?
Type A aortic dissections are more deadly as they involve the ____aorta, while Type B involve the ____aorta
SBP >200 or DBP >120; aortic dissection, HTN after CABG, acute MI
What are the classifications for acute severe HTN? What are some common causes?
Monckbergs medial calcification
disease resulting in calcification of media in the arteries of the forearm more commonly found in older males
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