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NUR 303 UMaine Exam 3 Guide With Complete Solution $11.99
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NUR 303 UMaine Exam 3 Guide
With Complete Solution

Endothelium-ANS active tissue, in arteries, not veins, control passage of
WBCs in and out of blood stream

nitric oxide-ANS secreted by endothelium, vessel vasodilation

endothelin-ANS secreted by endothelium, vessel contraction

VEGF's (vascular endothelian growth factors)-ANS secreted by endothelium,
growth of new blood vessels

Thromboxane A2-ANS secreted by endothelium, activates clotting

von Willebrand factor-ANS secreted by endothelium, activates clotting

prostacyclin - produced by endothelium; inhibits clotting

blood pressure determined by - flow and resistance; reflection of arterial
pressures

lumen - inside vessel

baroreceptors - neural regulation; regulates BP; in walls of carotid artery and
aortic arch

RAAS - Renin-Angiotension-Aldosterone System ANSWER Renin
produced/stored in kidneys, nephrons in kidneys sensitive to change in BP
and either increase or decreases renin levels. Causes angiotensin I =>
angiotensin II (potent vasoconstrictor), & release of aldosterone to retain Na
and H2O (in kidneys)- both INCREASE BP. *FEEDBACK LOOP*

,catecholamines - ANSWER norepinephrine & epinephrine

norepinephrine & epinephrine - ANSWER released from adrenal medulla;
alpha receptors, beta 2, beta 1 increase HR

Antidiuetic Horome - ADH-vasopressin - ANSWER released form posterior
pituitary; responds to decrease in BP/ volume & increased plasma osmolality;
ADH reabsorbs water in renal tubules

Atrial Natriuretic Peptide (ANP)-peptide released from atrium when cells
sense too much circulating fluid; acts on kidneys to increase Na excretion in
order to reduce volume

Brain Natriuretic Peptide (BNP)-peptide released from ventricles when cells
sense too much circulating fluid; acts on kidneys to increase Na excretion in
order to reduce volume

perfusion-passage of blood through a vessel

ischemia - ANSWER decreased blood supply to organ/ thereby reducing
oxygen, waste removal, nutrients

occlusion - ANSWER blockage

infarction - ANSWER death to cells

vasoconstriction - ANSWER narrowing of blood vessels

vasodilation - ANSWER widening of blood vessels

hyperlipidemia - ANSWER high levels of lipids in blood- mainly cholesterol
and triglyceride; increases risk for many chronic diseases-mainly CV disease

lipids - ANSWER needed for cellular stability and come from diet and liver
production

,low density lipoproteins (LDLs) - ANSWER carry fat to cells of body including
endothelium; "bad," normal <100 mg/dL

high density lipoproteins (HDLs) - ANSWER transports fats and cholesterol
away from cells to liver to be excreted, "good," >60 mg/dL; low levels are
risk

triglycerides - ANSWER ideal less than 150 mg/dL

foam cells - ANSWER macrophages that accumulate LDL when attracted to
site of endothelial injury; form plaque; release growth factor

dyslipidemia - ANSWER asymptomatic until develops into other diseases; Dx-
cholesterol screening & lipid panels; Tx- diet, exercise

hypertension - ANSWER (140-159/90-99) prolonged elevation of BP; high
sheering force in arteries; excessive cardiac workload due to increased
afterload and vasoconstriction; sign heart is being overworked

normal BP - ANSWER 120/80

prehypertension - ANSWER 120-139/80-89

non-modifiable risk factors hypertension - ANSWER advancing age, ethnicity,
family Hx

modifiable risk factors hypertension - ANSWER overweight/obese, phsyically
inactive, tobacco, high-Na, low potassium, low Vit D, alcohol

primary hypertension - ANSWER most common form (90-95%); develops
gradually over time

secondary hypertension - ANSWER more sudden and severe; side effect of
another disease (renal artery stenosis, adrenal gland tumors, certain

, congenital heart defects)

Hypertension presentation ANSWER "silent killer," fatigue, headache,
malaise, dizziness associated with atherosclerosis, aneurysms, heart failure,
renal damage, loss of vision, metabolic syndrome, memory impairment




atherosclerosis - ANSWER chronic inflammatory disease of the arterial
system; abnormal thickening and hardening of vessel walls; damage from
hypertension, elevated LDL, infection; smooth muscle cells and collagen
fibers migrate to tunica intima; lesions develop on vessel wall and calcify
over time; LARGE CONTRIBUTOR of heart disease

-leads to obstruction, platelet aggregation, vasodilatory capability decreases
(hardening) and increase fragility




complications of atherosclerosis - ANSWER peripheral vascular disease,
coronary artery disease (ischemic heart disease), thrombi, hypertension,
stroke




risk factors atherosclerosis - ANSWER non-modifiable: male >45, female> 55
(post-menopausal), African-American, genetic

modifiable: excess Na and sat fat, lack of exercise, BMI >30, triglycerides
>150 mg/dL, smoking, stress- over activation of RAAS, HTN




Dx atherosclerosis - ANSWER identify contributing factors, lipid panel,

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