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54 Cards in this Set

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POUSIELLE'S LAW
flow = (r^4 x change in P x pi)/ 8 x h x l
how does doubling the diameter of a vessel influence resistance?
resistance will decrease by 16-fold
how does doubling diam of a vessel influence flow
doubling diam will increase flow 16-fold
thermodilution is a variation of the indicator-dilution method and involves...
injecting cool saline, and measuring rate of temperature change to determine CO
receptor for NE
alpha 1
receptor for AVP
AII
receptor for NO
NONE! it diffuses into cell
receptor for endothelin
ETa
MOA of endothelin, AVP and NE
increases intracellar [Ca] --> increases [Ca-CAM] --> binds to MLCK --> phosphyorylation of myosin
MOA of NO
increases [cGMP] --> upregulates PKG --> phosphorylates MLCK --> rendered inactive (can't phosphorylate myosin.
size of sarcoplasmic reticulum in cardiac muscle cf. skeletal muscle
smaller
size of t-tubules in cardiac muscle cf. skeletal
greater diameter
where do t-tubules penetrate into myocytes?
@ z-lines
40% of myocyte cell volume is occupied by
mitochondria
what is a dyad?
terminal cisternae of ER and t-tubule close together IN CARDIAC MYOCTYES
how does calcium enter the myocyte
voltage gated calcium receptors (Isi)
wehre are ryanodine receptors located in cardiac myocytes?
in the SR membrane
working myocardium: are RYR receptors physically linked to teh voltage gated calcium receptors on the t-tubule membrane?
no (CICR)
working myocardium: as much Ca that enters the cell through the voltage gated Ca receptors leaves though...
the Na/Ca exchanger
working myocardium: as much Ca enters the myoplasm from the SR through the RYR receptors, is pumped back into the SR via ...
SR Ca-ATPase
besides the Ca-Na exchanger, what other pump helps to pump Ca out of the myoplasm?
Ca-ATPase on plasma membrane
what is the SERCa pump? ATP-dependent or independent?
it is another name for the Ca-ATPase that exists on the SR membrane of myoctes. And yes, it requires ATP
what causes calsequestrin to change configuration to release Ca?
Ca binding to RYR2
what is phospholamban?
a brake for SERCa
B adrenergic stimulation will result in an increase in: inotrophy, chronotropy and lucitropy. All of these effects are mediated by what?
PKA
heart needs ATP for 3 fn's. list them
1. fuel for Ca-ATPase on SR membrane and sarcoplasm
2. fuel for actinmyosin ATPase (contraction)
3. other cellular processes ( ionic gradients e.g. Na/K ATPase, etc.)
hearts source of ATP
70% FA
20% glu oxidation
10% lactate
creatine phosphate (but this doesn't provide new ATP...just storage mlcl)
how many ATP generated from FA? glu oxidation? lactate?
FA: 130 ATP/FA
glu: 36 +2 ATP/glu
lactate: 18 ATP/lactate
innervation of baroreceptors?
carotid sinus - glossopharyngeal
aortic arch - vagus
where is carotid sinus
its a dilation in the internal carotid artery at the bifurcation of the common carotid
what part of the brain are APs from teh baroreceptors transmitted to?
NTS (part of medulla oblangata)
how does extrinsic NE differ in its effects from NE released at nerve terminals?
it has less of a B1 effect (but still has the same alpha-1 vaso/venoconstriction effect)
DOES parasympathetic activity have an effect on vasculature?
no, no direct effect. Only direct effect is on the heart
what is Liddle's syndrome
a genetic syndrome in which mutations in the genes encoding for the subunits on the renal tubular sodium channels leads to increased sodium retention; one of the explanations for primary HTN
primary HTN: what is metabolic syndrome?
obesity
diabetes mellitus
hyperlipidemia
HTN

all of these are linked to primary HTN
primary HTN: wrt catecholamines, what is one explanation for the development of primary HTN?
people have variable responses to catecholamines; the more responsive you are, the more exaggerated vasoconstriction --> the more likely you are to develop primary HTN.
7 occassions when you would suspect secondary hypertention rather than primary.
1. extremes of age < 20 >50
2. unexpected target organ damage
3. occurs abruptly
4. response to therapy is atypical
5. renal failure is present
6. hypercalcemia
7. hypokalemia
Causes of secondary HTN: the 'As'
Accuracy of diagnosis (cuff size, 30 sec b/w measurements, both arms measurement, palpate max systolic BP before auscultation, don't rapidly deflate)

Aldosteronism

Obstructive sleep Apnea - hypoxemia and reflux vasoconstriction
Causes of secondary HTN: the B's
Bad kidneys


Bruits - obstruction in renal arteries (renovascular htn)--> activation of RAS
Causes of secondary HTN: the C's
-catecholamines (pheochromocytoma)
-coarctation of aorta
-Cushing's syndrome (pituitary gland tumor -- elevated mineralocorticoids)
Causes of secondary HTN: the D's
DRUGS
percription:
a. NSAIDs
b. corticosteroids
c. oral contraceptives with hi estradiol

non-perscription:
a. nicotine
b. herbals (ephedra)
c. methamphetamines and cocaine

DIET
a. hi caffeine
b. hi salt
c. hi EtOH
Causes of secondary HTN: the E's
Erythropioetin excess
-increased viscosity

Endocrine disorders
-hyperthyroidism
-hypothyroidism (compensatory vasoconstriction)
common target organ damage in HTN
1. eyes (retinopathy)
2. brain (cerebrovascular disease)
3. heart (CAD)
4. kidney (hypertensive nephrosclerosis)
deaths due to untreated HTN:
50% due to...
33% due to...
10-15% due to...
50% - CAD or congestive HF
33% - stroke
10-15% - kidney failure
a reduction in avg systolic BP by 2-3 mmHg could reduce incidence of stroke by ___%?
10%
2 effects of HTN on the heart
1. increased afterload (LVH)
2. myocardial ischemia
characteristics of peripheral vascular disease due to systemic HTN
accelerated atherosclerosis

claudication (fatigue, pain, weakness) in extremitiy especially on exertion
what is an abdominal aortic aneurism and when would it occur
its a complication of HTN - dilation of aorta usually below renal arteries
what is rarefaction?
loss of bl. flow through a region in the kidney - due to remodelling of sm. muscle around contricted vasculature
htn and pregnancy
-pre-eclampsia
-eclampsia
Pre-eclampsia:
-increased BP (over 140/90) accompanied by proteinuria

Eclampsia:
-convulsions a/w signs of pre-eclampsia
first line therapy for patients with uncomplicated htn - be specific
thiazide diuretics
effects of htn during pregnancy on the fetus (3)
1. placental ischemia causes "shallow implantation"
2. causes HYPOtension in fetus - leads to kidney damage
3. malnourrishment, low BW, stillbirth
can we safely administer anti-hypertensives to pregnant women?
NO!!! especially not ACEi's or AT inhibitors

however, you can give them thiazide diruetics instead
waht is the effect of oral contraceptives on HTN
they elevate BP