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NUR 303 UMaine Exam 3 Guide With Complete Solution
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NUR 303 UMaine Exam 3 GuideWith 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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