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1. veins low elasticity; little ECM/smooth muscle; assisted return of
blood to the heart - thrombosis
2. return veins are responsible of the ______ of blood to the heart;
velocity without pressure
3. capillaries no elasticity; low barrier to tissue - inflammation, edema
4. exchange capillaries allow for ________, new blood comes into veins
after BP has been decreased
5. arteries highly elastic; abundant ECM and smooth muscle; sustains
BP - artherosclerosis, aneurysm
6. transport arteries are responsible for _________ of blood to tissues
via mechanisms of pressure, velocity, and volume
7. arteries, veins can elastically respond to pressure changes in the heart allow
blow flow to return via veins
8. collagen elasticity/elastic recoil physiological feature in connective tissue (some muscles -
arteries) that allows a being to "spring"/jump high (ie. kan-
garoos)
9. open valves into muscles to how are jumping spiders able to jump?
release pressure and extend
joints (hydraulics)
10. pressure differential, laminar physcial factors of BP and flow
flow, resistance, gravity
11. r^4 Poiseuille-Hagen equation variable which blood flow is pro-
portional to
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12. less resistance to flow, higher a greater r^4 would indicate?
blood flow
13. distance from heart, height, pressure differential, laminar flow, resistance, gravity (phys-
side/structure of blood vessel ical factors of blood pressure and flow) are influenced by:
14. high, low pressure in arteries is _____, while pressure in veins is _____
15. collagen, muscle velocity and pressure are directed by what tissue?
16. muscle vasoconstriction/dilation are directed by what?
17. Hypertension (HTN) A condition where BP increases > 140/90 mm Hg
18. hypertrophy, cardiac failure, in- pathological consequences of hypertension on the heart:
farction
19. intra-cerebral hemorrhage, in- pathological consequences of hypertension on the brain
farction
20. ischemia, chronic renal failure, pathological consequences of hypertension on the kidney
infarction
21. filtration the kidneys require blood for _______
22. atheroma, aneurysm, dissec- pathological consequences of hypertension on the blood
tion vessels
23. cardiac output x peripheral re- Blood Pressure = _____ x _________.
sistance
24. alpha (constrictor) and beta neural factors that stimulate adrenergic receptors for periph-
(dilator) adrenergic eral resistance in SNS and PNS
25. amount of blood volume in cardiac output is affected by:
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NA+, mineralcorticoids, atrial
natriuertic peptide
26. HR, contractility cardiac factors that affect cardiac output
27. primary (essential, idiopathic) hypertension induced by environmental factors - obesity,
hypertension sedentary lifestyle, insulin resistance, genetic influence, high
alcohol intake, high sodium intake, low potassium intake,
stress
28. "monogenic" influence, prima- hypertension due to mendelian inheritance - single gene
ry hypertension disorders in renin, aldosterone synthesis, sodium transport:
Liddle's syndrome; familial HTN
29. secondary hypertension hypertension from an identified disorder that causes
BP to become elevated - reno-vascular disease/failure,
artherosclerosis, pheochromocytoma, endocrine disorders
(hyperaldosteronism, hyperthyroidism, Cushings)
30. Benign hypertension hypertension where there is a chronic alteration in physio-
logical regulation of blood pressure
31. accelerated (malignant) hyper- hypertension which occurs from a rise to > 200/120, renal
tension failure, retinal hemorrhage
32. Artherosclerosis (heart, If an individual has HTN they are at risk for what other
brain, kidneys), CAD/MI, cardiovascular conditions?
stroke/aneurysm
33. renin-angiotensin-aldosterone Genetic (gene defects in NA and aldosterone secretion ie.
axis, Cardiac output and diabetes), Physiological (impairment of NA/H2O secretion
natiuretic system, peripheral ie. increased blood volume), Environmental (smoking, stress,
resistance NA intake, obesity), and Vascular (intimal thickening, athero-
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sclerosis, thrombosis, vasoconstriction) pathogenesis factors
of HTN alter what pathways to increase blood pressure?
34. tunica intima: endothelial cells vascular cellular element responsible for: semi-permeable
barrier, hemo-stasis and thrombosis, vaso-active hormones,
cytokines, growth hormones, inflammatory and coagulation
reactions
35. SMC migration and de-differ- response from the tunica intima when endothelial injury
entiation occurs
36. intimal hyperplasia (thicken- Outcomes of SMC effects in tunica intima in response to cell
ing), healing w/ little remodel- injury
ing, atheroma, HTN, aneurysm
37. internal elastic layer Layer allowing expansion in arteries between the tunica in-
tima and the media
38. Tunica media: smooth muscle vascular cellular element responsible for: vasoconstric-
cells, ECM tion/vasodilation, migration and remodeling in response to
injury
39. external elastic lamina Layer between tunica media and externa.
40. Tunica adventitia (extrema): vascular cellular element responsible for: Collagen
ECM