Cardio 2

Front 1

POUSIELLE'S LAW

Back 1

flow = (r^4 x change in P x pi)/ 8 x h x l

Front 2

how does doubling the diameter of a vessel influence resistance?

Back 2

resistance will decrease by 16-fold

Front 3

how does doubling diam of a vessel influence flow

Back 3

doubling diam will increase flow 16-fold

Front 4

thermodilution is a variation of the indicator-dilution method and involves...

Back 4

injecting cool saline, and measuring rate of temperature change to determine CO

Front 5

receptor for NE

Back 5

alpha 1

Front 6

receptor for AVP

Back 6

AII

Front 7

receptor for NO

Back 7

NONE! it diffuses into cell

Front 8

receptor for endothelin

Back 8

ETa

Front 9

MOA of endothelin, AVP and NE

Back 9

increases intracellar [Ca] --> increases [Ca-CAM] --> binds to MLCK --> phosphyorylation of myosin

Front 10

MOA of NO

Back 10

increases [cGMP] --> upregulates PKG --> phosphorylates MLCK --> rendered inactive (can't phosphorylate myosin.

Front 11

size of sarcoplasmic reticulum in cardiac muscle cf. skeletal muscle

Back 11

smaller

Front 12

size of t-tubules in cardiac muscle cf. skeletal

Back 12

greater diameter

Front 13

where do t-tubules penetrate into myocytes?

Back 13

@ z-lines

Front 14

40% of myocyte cell volume is occupied by

Back 14

mitochondria

Front 15

what is a dyad?

Back 15

terminal cisternae of ER and t-tubule close together IN CARDIAC MYOCTYES

Front 16

how does calcium enter the myocyte

Back 16

voltage gated calcium receptors (Isi)

Front 17

wehre are ryanodine receptors located in cardiac myocytes?

Back 17

in the SR membrane

Front 18

working myocardium: are RYR receptors physically linked to teh voltage gated calcium receptors on the t-tubule membrane?

Back 18

no (CICR)

Front 19

working myocardium: as much Ca that enters the cell through the voltage gated Ca receptors leaves though...

Back 19

the Na/Ca exchanger

Front 20

working myocardium: as much Ca enters the myoplasm from the SR through the RYR receptors, is pumped back into the SR via ...

Back 20

SR Ca-ATPase

Front 21

besides the Ca-Na exchanger, what other pump helps to pump Ca out of the myoplasm?

Back 21

Ca-ATPase on plasma membrane

Front 22

what is the SERCa pump? ATP-dependent or independent?

Back 22

it is another name for the Ca-ATPase that exists on the SR membrane of myoctes. And yes, it requires ATP

Front 23

what causes calsequestrin to change configuration to release Ca?

Back 23

Ca binding to RYR2

Front 24

what is phospholamban?

Back 24

a brake for SERCa

Front 25

B adrenergic stimulation will result in an increase in: inotrophy, chronotropy and lucitropy. All of these effects are mediated by what?

Back 25

PKA

Front 26

heart needs ATP for 3 fn's. list them

Back 26

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.)

Front 27

hearts source of ATP

Back 27

70% FA
20% glu oxidation
10% lactate
creatine phosphate (but this doesn't provide new ATP...just storage mlcl)

Front 28

how many ATP generated from FA? glu oxidation? lactate?

Back 28

FA: 130 ATP/FA
glu: 36 +2 ATP/glu
lactate: 18 ATP/lactate

Front 29

innervation of baroreceptors?

Back 29

carotid sinus - glossopharyngeal
aortic arch - vagus

Front 30

where is carotid sinus

Back 30

its a dilation in the internal carotid artery at the bifurcation of the common carotid

Front 31

what part of the brain are APs from teh baroreceptors transmitted to?

Back 31

NTS (part of medulla oblangata)

Front 32

how does extrinsic NE differ in its effects from NE released at nerve terminals?

Back 32

it has less of a B1 effect (but still has the same alpha-1 vaso/venoconstriction effect)

Front 33

DOES parasympathetic activity have an effect on vasculature?

Back 33

no, no direct effect. Only direct effect is on the heart

Front 34

what is Liddle's syndrome

Back 34

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

Front 35

primary HTN: what is metabolic syndrome?

Back 35

obesity
diabetes mellitus
hyperlipidemia
HTN

all of these are linked to primary HTN

Front 36

primary HTN: wrt catecholamines, what is one explanation for the development of primary HTN?

Back 36

people have variable responses to catecholamines; the more responsive you are, the more exaggerated vasoconstriction --> the more likely you are to develop primary HTN.

Front 37

7 occassions when you would suspect secondary hypertention rather than primary.

Back 37

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

Front 38

Causes of secondary HTN: the 'As'

Back 38

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

Front 39

Causes of secondary HTN: the B's

Back 39

Bad kidneys


Bruits - obstruction in renal arteries (renovascular htn)--> activation of RAS

Front 40

Causes of secondary HTN: the C's

Back 40

-catecholamines (pheochromocytoma)
-coarctation of aorta
-Cushing's syndrome (pituitary gland tumor -- elevated mineralocorticoids)

Front 41

Causes of secondary HTN: the D's

Back 41

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

Front 42

Causes of secondary HTN: the E's

Back 42

Erythropioetin excess
-increased viscosity

Endocrine disorders
-hyperthyroidism
-hypothyroidism (compensatory vasoconstriction)

Front 43

common target organ damage in HTN

Back 43

1. eyes (retinopathy)
2. brain (cerebrovascular disease)
3. heart (CAD)
4. kidney (hypertensive nephrosclerosis)

Front 44

deaths due to untreated HTN:
50% due to...
33% due to...
10-15% due to...

Back 44

50% - CAD or congestive HF
33% - stroke
10-15% - kidney failure

Front 45

a reduction in avg systolic BP by 2-3 mmHg could reduce incidence of stroke by ___%?

Back 45

10%

Front 46

2 effects of HTN on the heart

Back 46

1. increased afterload (LVH)
2. myocardial ischemia

Front 47

characteristics of peripheral vascular disease due to systemic HTN

Back 47

accelerated atherosclerosis

claudication (fatigue, pain, weakness) in extremitiy especially on exertion

Front 48

what is an abdominal aortic aneurism and when would it occur

Back 48

its a complication of HTN - dilation of aorta usually below renal arteries

Front 49

what is rarefaction?

Back 49

loss of bl. flow through a region in the kidney - due to remodelling of sm. muscle around contricted vasculature

Front 50

htn and pregnancy
-pre-eclampsia
-eclampsia

Back 50

Pre-eclampsia:
-increased BP (over 140/90) accompanied by proteinuria

Eclampsia:
-convulsions a/w signs of pre-eclampsia

Front 51

first line therapy for patients with uncomplicated htn - be specific

Back 51

thiazide diuretics

Front 52

effects of htn during pregnancy on the fetus (3)

Back 52

1. placental ischemia causes "shallow implantation"
2. causes HYPOtension in fetus - leads to kidney damage
3. malnourrishment, low BW, stillbirth

Front 53

can we safely administer anti-hypertensives to pregnant women?

Back 53

NO!!! especially not ACEi's or AT inhibitors

however, you can give them thiazide diruetics instead

Front 54

waht is the effect of oral contraceptives on HTN

Back 54

they elevate BP