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PMCOL 343 > 6-cardio > Flashcards

6-cardio Flashcards

1
Q

why can diuretics be good for heart failure (3)

A

relieve oedema and work load on heart, may have vasodilatory action

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2
Q

what kind of diuretics are thiazides

A

loop diuretics (high ceiling)

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3
Q

what is an example of a thiazide

A

furosemide

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4
Q

how does furosemide work

A

causes K+ loss

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5
Q

what is spironolactone

A

K+ sparing diuretic

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6
Q

how does spironolactone work

A

aldosterone antagonist

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7
Q

where is aldosterone released from

A

adrenal cortex

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8
Q

what does aldosterone release do to K+

A

increase loss

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9
Q

what does aldosterone release do to Na+

A

increase retention

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10
Q

what does aldosterone release do to H2O

A

increase retention

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11
Q

what does spironolactone do to K+

A

increase retention

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12
Q

what does spironolactone do to Na+

A

increase loss

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13
Q

what does spironolactone do to H2O

A

increase loss

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14
Q

what do vasodilators do to preload in healthy subjects

A

decrease

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15
Q

what do vasodilators do to cardiac output in healthy subjects(and how)

A

decrease bc decreased preload (frank starling)

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16
Q

what do vasodilators do to veins(in healthy subject)

A

dilates

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17
Q

what do vasodilators do to arterioles(in healthy subject)

A

dilates

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18
Q

what do vasodilators do to arterial pressure(in healthy subject)

A

decrease

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19
Q

what do vasodilators do to afterload (in healthy subject)

A

decrease

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20
Q

what happens to BP with decreased cardiac output and arterial pressure (in healthy subject)

A

there is a decrease in BP

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21
Q

what happens to HR with decreased cardiac output and arterial pressure (in healthy subject)

A

increase (low BP causes BR receptor reflex)

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22
Q

what is the net effect on BP and HR with vasodilators (in healthy subject)

A

hypotension and tachycardia

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23
Q

why does afterload increase during heart failure

A

compensatory sympathetic reflexes + increased angiotension = arteriolar constriction

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24
Q

what does high afterload do to output of a failing heart

A

it may limit output

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25
Q

why can cardiac output increase with vasodilatory agents with CHF patients (compared to healthy patients)

A

less afterload so the heart will have an easier time pumping out blood

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26
Q

what happens do BP and HR with vasodilators in CHF patients + why

A

they dont fall and no reflex tachycardia

because reduced peripheral resistance is balanced out by increased cardiac output

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27
Q

where is angiotensinogen released

A

liver

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28
Q

where is renin released

A

kidneys

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29
Q

where does angiotensin converting enzyme come from

A

lungs

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30
Q

what does ACE do

A

convers angiotensin 1 into angiotensin2

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31
Q

what does renin do

A

converts angiotensinogen into andgiotension 1

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32
Q

what does angiotension do to vessels

A

vasoconstrict

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33
Q

what does angiotension do to aldosterone release

A

increase

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34
Q

where is aldosterone released from

A

adrenal cortex

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35
Q

what does what does angiotension do to K+

A

increase loss

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36
Q

what does angiotension do to Na+

A

increase retention

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37
Q

what does angiotension do to H2O

A

increase retention

38
Q

what are 4 main effects of ACE inhibibots (vessels and molecules)

A

vasodilation
K+ retention
H2O land Na+ loss

39
Q

what do ACE inhibitors do to angiotensin 2 formation

A

inhibit

40
Q

what does angiotension 2 do to bradykinin

A

prevents its catabolism

41
Q

what is the role of bradykinin

A

potent activator of NO release from endothelium

42
Q

what does bradykinin in lungs do

A

causes the dry cough that is a side effect of ACE inhibitors

43
Q

what causes the dry cough with ACE inhibitors

A

they prevent breakdown of bradykinin which causes dry cough when acting in lungs

44
Q

besides the cough, what are other bad side effects of ACE inhibitors

A

makes things taste weird

45
Q

what are 2 ACE inhibitor drug names

A

enalapril and captopril

46
Q

what do enalapril and captopril do in general

A

stop AG2 synthesis

47
Q

what do enalapril and captopril do to afterload

A

decrease

48
Q

what do enalapril and captopril do to preload

A

decrease

49
Q

how can what do enalapril and captopril help with oedema

A

they increase Na+ and H2O loss (inhibits aldosterone)

50
Q

what happens to cardiac output in heart failure

A

decrease

51
Q

what happens to venous return in heart failure

A

decrease

52
Q

what are 2 drugs classes that are often combined to dreat CHF

A

ACE inhibitor and diuretic

53
Q

why is it good to use low doses of both ACE inhibitor and diuretic instead of a high dose of 1

A

you get additive therapeutic effects and less side effects (sometimes side effects cancel out)

54
Q

which side effects cancel out with ACE inhibitor and diuretic (which diuretics)

A

thiazide diuretics promore K+ loss and ACE inhibitors promote K+ retention

55
Q

what is losartan (2 things)

A

vasodilator

angiotension receptor antagonist

56
Q

what are amrinone and milrinone (3) +What do they do to vessels and heart

A

phosphoriesterase inhibitors

vasodilate and stimulate heart

57
Q

what do amrinone and milrinon do to contraction of heart

A

increase

58
Q

what do amrinone and milrinon do to contraction of vascular smooth muscle

A

reduce

59
Q

how do beta agonists work on cardiac muscle stimulation

A

cAMP, PKA, increase Ca++ through L type

60
Q

if B1 agonist stimulate heart and B2 relax vascular smooth muscle but both are Gs, how does this work?

A

there are different contractile mechanisms of smooth and cardiac muscle

61
Q

is myocin light chain kinase in heart

A

no

62
Q

is myosin light chain kinase in vascular smooth muscle

A

yes

63
Q

how do B2 agonists cause vascular smooth muscle relaxation

A

elevated cAMP inactivates MLCK by phosphorylating it so then it cant contract

64
Q

what are dobutamine and dopamine (mechanism of action)

A

beta1 agonists

65
Q

why can beta blockers be used for chronic failure (dobutamine and dopamine (b1 agonists) are also used)?

A

it can help calm down the crazy sympathetic outflow

66
Q

what are 4 beneficial effects of beta blockers and CHF

A
  • attenuation of adverse effects of high [NA]
  • decreased HR
  • inhibit mitogenic activity of catecholamines
  • lower afterload by reducing renin release
67
Q

why is it good that beta blockers inhibit mitogenic activity of catecholamines

A

because sometimes the vessels grow in the wrong areas and stuff which is bad

68
Q

what receptors does carvedilol target

A

beta 1
beta 2
alpha 1

all block

69
Q

what is the benefit of carvedilol over beta blockers

A

it also lowers afterload (because it blocks alpha1)

70
Q

what are 4 therapeutic approaches to high BP

A
  • diuretics
  • sympatholytic agents
  • direct vasodilators
  • ACE inhibitors (or any drug that can block production or action of angiotensin)
71
Q

what do diuretics do to vessels (sometimes)

A

can vasodilate

72
Q

what does depletion of Na+ from diuretics do to blood vessels stiffness

A

help reduce it

73
Q

what do thiazides to in the kidney (mechanism of action in nephron)

A

inhibit NaCl reabsorption by distal convoluted tubule

74
Q

what is metoprolol

A

b1 selective antagonist

75
Q

why can metoprolol be better than propranolol

A

acute vasodilatory action from b2 receptors may reduce effectiveness ( you dont wanna block those )

76
Q

what are 4 main things that beta blockers do (MECHANISM)

A
  • inhibit renin release
  • inhibit presynaptic Beta that usually increase NA release
  • reduce sympathetic outflow (possible actions in CNS)
  • slows HR during exercise and stress
77
Q

is it better to work on the angiotensin or adrenergic system to change BP

A

angiotensin system is connected just to BP while the adrenergic is more linked throughout the whole body (so angiotensin is better)

78
Q

what class is hydralazine is

A

vasodilator

79
Q

what does hydralazine do (3)

A

arteriolar vasodilation, lowers BP and reflex tachycardia

80
Q

what do you usually combine with hydralazine and why

A

beta blocker to help prevent the reflex tachycardia

81
Q

what is nitroprusside (how and when is it used)

A

powerful arteriolar and venous vasodilator used in hypertension emergencies

82
Q

what are 6 types of vasodilators

A 
hydralazine
nitroprusside
verapamil
nifedipine
dihydropyridines
ca channel blockers
83
Q

are ca channel blockers vasodilators

A

yes

84
Q

what are 3 agents that block the production / agent of angiotensin

A

captopril
enalapril
losartan

85
Q

what is captopril

A

ACE inhibitor

86
Q

what is enalapril

A

ACE inhibitor

87
Q

what is losartan

A

angiontensin receptor blocker

88
Q

does captopril make the dry cough

A

yes

89
Q

does enalapril make the dry cough

A

yes

90
Q

does losartan make the dry cough

A

no

PMCOL 343 (31 decks)

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