Test 3 Flashcards

1
Q

How does bradykinin produce vasodilation?

A

Stimulate the release of NO and prastacyclins for potent vasodilation

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2
Q

Which is the main mineralcorticoid?

A

Aldosterone

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3
Q

Which is the post potent vasocontrictor?

A

Angiotension II

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4
Q

Endogenous vasoconstrictor?

A

Endothelin 1

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5
Q

What does ADH cause?

A

Only H20 retention. No Na retention

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6
Q

How does spironolactone affect K and Na levels?

A

K retention and Na excretion

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7
Q

What does aldosterone do?

A

Na retention that leads to concomitant H20 retention
Also does K excretion

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8
Q

Explain how NO causes smooth muscle relaxation?

A

NO combines with the heme group of soluble gunaylyl cyclase which converts GTP to cGMP which leads to vasodilation

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9
Q

What two types of meds might you need to add with hydralazine?

A

beta blocker and diuretic (hydrochlorothiazide) to counteract the compensatory tachycardia and water retention.

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10
Q

clinical results of B2 stimulation?

A

smooth muscle relaxation. I.e. lungs and vascular smooth muscle

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11
Q

How do ACE-I affect renin levels?

A

increase it

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12
Q

What does Aliskiren (tekturna) do?

A

reduce plasma renin activity by 50-80%. Can increase renin levels up to 10x.

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13
Q

Are ACE-I safe in a pt with ischemic heart disease?

A

yes because they don’t cause reflex sympathetic activation.

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14
Q

How do ACE-I affect pt with CKD?

A

diminish proteinuria and stabilize renal function.

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15
Q

How do ACE-I affect DM incidence in patients with high cardiovascular risk?

A

reduce incidence of DM

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16
Q

Are ACE-I venous or arterial?

A

both

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17
Q

How much do ACE-I decrease BP?

A

less than 10mmHg

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18
Q

What meds should you avoid with ACE-I?

A

NSAIDs - block bradykinin mediated vasodilation
K supplements. Lead to hyperkalemia
K sparing diuretics.

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19
Q

clinical effects of NO?

A

relax vascular smooth muscle
inhibit platlet aggregation
inhibit leukocyte-endothelial interactions
directly prevent Na and H2O reabsorption in the kidneys

20
Q

Name a phenylalkylamine

A

verapamil

21
Q

name a benzothiazepine

A

diltiazem

22
Q

Do CCB have high or low first pass effect?

A

high

23
Q

Is orthostatic hypotension a concern in CCB?

A

Not as much as it is with nitrates.

24
Q

Which CCB has greatest affinity for cerebral vascular bed?

A

Nicardipine

25
Q

Verapamil increases levels of what other medication>

A

Digoxin

26
Q

How do alpha 2 receptors work in neurons?

A

inhibit adenylyl cyclase activity, which decreases ca ions influx into cell which decreases exocytosis of vessicle containing NE.

Also decrease cAMP???

27
Q

Name the newer relatively selective alpha 1 antagonists

A

Prazosin
Terazosin
Doxazosin
Trimazosin

28
Q

Name the older non selective alpha blockers

A

phentolamine
phenoxybenzamine

29
Q

Describe how alpha 1 receptors in smooth muscle work

A

Gq linked proteins that activate smooth muscle contraction through IP3 pathway and increased Ca

30
Q

Describe how alpha 2 receptors in smooth muscle cause contraction?

A

alpha 2 are Gi proteins and binding decreases intracellular cAMP > smooth muscle contraction

31
Q

do alpha blockers affect arteries or veins more?

A

arteries because arteries are under greater sympathetic tone

32
Q

Which alpha blockers cause more more reflex tachycardia?

A

non selective alpha blockers

33
Q

How do beta agonists work in the vascular smooth muscle?

A

ATP > cAMP > de-phosphorylation of myosin light chain kinase.

34
Q

How do beta agonists work in the heart?

A

beta receptor stimulates adenylyl cyclase which converts ATP to cAMP. cAMP activates PKA which stimulates Ca influx into cell which causes increased contraction.

35
Q

What three things make up myocardial oxygen demand?

A

wall tension
heart rate
contractility

36
Q

4 ways we can relax vascuar smooth muscle?

A

decrease intracellular calcium
increase cGMP
increase cAMP
hyper polarize (stabilize) cell membrane

37
Q

explain the role of calcium as it relates to myosin light chain?

A

calcium combines with calmodulin complex and activates the enzyme myosin light chain kinase which is what phosphorylates myosin light chains. Once phophorylated, MLCs can couple with actin to produce contraction.

38
Q

how do beta blockers affect L type calcium chanels in vascular cardiac cells?

A

they block cAMP from activating PKA to phosphorylate the Ca chanel which would cause an increase in calcium influx. so we end up with less calcium influx

39
Q

How does cAMP cause smooth muscle relaxation?

A

phosphorylates (inactivates) myosin light chain kinase

40
Q

how does cGMP cause vascular smooth muscle relaxation?

A

it dephosphorylates (inactivates) myosin light chain

41
Q

What is stongest predictor of ischemia under GA?

A

tachycardia

42
Q

Number 1 treatment for effort angina?

A

beta blockers

43
Q

What increases with the use of a PDE inhibitor?

A

cGMP

44
Q

Explain how NTG is processed by the body

A

denitrated by enzymes glutathiube S-transferase and mitochondrial aldehyde dehydrogenase

45
Q

do you get tachypylaxis with nitro vasodilators?

A

yes