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pharm unit 4 > physiology of the heart > Flashcards

physiology of the heart Flashcards

1
Q

what is a U wave

A

this is purkinje repolarization after the T wave. due to hypokalemia

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2
Q

J wave

A

this is a separate wave within the ST segment that has to due with hypothermia or hypocalcemia.

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3
Q

when to use thiazides

A

moderate to mild HTN. since they are in the middle for potentcy

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4
Q

when to use loops

A

HTN crisis, CHF, cirrhosis, renal dysfucntion

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5
Q

what to watch out for with diuretics

A

HSR to thiazides, volume depletion, hypokalemia, hypomagnesemia, glucose intolerance, lipid profile, ototoxic, erectile dysfunction,

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6
Q

caution for potassium sparing

A

gynecomastia in men, breast pain, menstrual irregularities, hyperkalemia. do not use in renal failure, diabetes, or when using ACEi and ARBs.

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7
Q

list of potassium sparing diuretics

A

amiloride, triemterine, spironolactone.

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8
Q

mechanism of ACEi

A

blocks ACE from converting angiotensin I to angiotensin II also inhibits the breakdown of bradykinin.

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9
Q

mechanism for ARBS

A

inhibits angiotensin II from binding to its receptor and stops the release of aldosterone and vasodilator

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10
Q

side effects of ACEi and ARBs

A

cough (not ARBs), hypotension, decreased renal function, angioedema.

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11
Q

when are ACEi and ARBs contraindicatred

A

renal artery stenosis, hyperkalemia, caution in renal failure, pregnancy

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12
Q

what else do ACEi and ARBs do?

A

benefit chronic renal failure (NOT ACUTE) congestive HF, LV remodeling, LVH, may even reduce risk of diabetes.

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13
Q

what do CCBs do?

A

they inhibit the Ca influx for vascular sooth muscle thus decrease TPR.

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14
Q

what are the two classes of CCBs

A

dihyropyridines and non dipine

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15
Q

what are the two dipine used

A

amlodipine and nifedipine

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16
Q

what are the two nondipines

A

diltiazem and verapamil

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17
Q

what else to CCB do?

A

good for raynauds, antianginal

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18
Q

when treating angina with dipine what do we watch out for?

A

reflex tachy and worsening angina

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19
Q

what is the main reason to use a beta blocker for HTN

A

to reduce cardiac output.

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20
Q

what secondary reasons do we use b blockers for

A

to decrease the release of renin

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21
Q

side effects for beta blockers

A

decreased exercise tolerance, bronchospasm, bradycardia, CHF due to negative inotropy, mask symptoms of hypoglycemia, depression, worsening PVD

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22
Q

why use metoprolol and atenolol

A

because they have cardiogenic selectivity and not broncho interference. if asthma and need a beta blocker use a selective like metoprolol and atenolol

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23
Q

why use carvedilol, esmolol and labetolol

A

these are used for HTN urgency or acute coronary syndromes. because they have additional sympathomimetic activity and can drastically lower BP.

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24
Q

what is the main use for esmolol

A

AV nodal blocking. it is unique due to its short half life.

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25
Q

alpha blockers mechanism

A

reduces vascular resistance.

26
Q

aphla blockers examples

A

terazosin and doxazosin

27
Q

SE of alpha blockers

A

orthostatic hypertension, fkuid retention, worse angina

28
Q

even though they are clearly outdated, why use alpha blockers at all

A

because they can aid in BPH

29
Q

examples of systemic vasodilators

A

hydralazine and minoxidil

30
Q

mechanism of hydralazine and minoxidil

A

they are vasodilators by relaxing smooth muscle of arterioles

31
Q

when to use hydralazine and minoxidil

A

in CHF and HTN. also used in refractory HTN.

32
Q

central acting sympathoplegic

A

these are alpha 2 agonists that reduce sympathetic outflow from the brainstem. the decreased sympathetic tone also reduces release of renin

33
Q

examples of central sympathp

A

clonidine, methyldopa, guanabenz

34
Q

when to use methyl dopa

A

during pregnancy

35
Q

SE of the central acting

A

sedation, dry mouth, rebound HTN. fatigue, orthostatic hypotension, depression.

36
Q

what are ganglion blockers

A

adrenergic neuron blocking agents. pharma sympathectomy.

37
Q

examples of ganglion blockers? 2

A

guanethidine and reserpine.

38
Q

SE of the ganglion blockers

A

sedation, parkinson, mental status changes

39
Q

aspirin uses

A

CAD.

40
Q

what is aspirin mechanism

A

irreversible inhibition of COX enzymes. blocking prostaglandin and thromboxane synthesis

41
Q

ticlopidine what is it and when to use it?

A

this an alternative to aspirin for treating CAD. it is a thienopyridine derivative that inhibits platelet aggregation by ADP. decreases fibrinogen and thus blood viscosity

42
Q

SE of ticlopidine

A

neutropenia and TTP

43
Q

clopidogrel what is it and when to use it

A

alternative to aspirin, it is a thienopyridine derivative with a greater anitthrombotic activity than ticlopidine. selectively inhbits the ADP platelet receptor.

44
Q

prasugrel what is it and when

A

this is another anti platelet alternative to aspirin. same family.

45
Q

who can we use prasugrel on?

A

<75 years of age, greater than 60kg, no history of stroke of TIA

46
Q

dipyridamole

A

pyrimido-pyrimidine derivative. increases cAMP inhibits PDE, activates adenylyl cyclase limited use due to exercise induced ischemia

47
Q

cilostazol

A

another alternative to aspirin for anti platelet. quinilone derivative that inhibits PDE. increases cAMP leading to inhibition of platelet aggregation.

48
Q

which beta blockers do we use in CAD

A

beta 1 selective or cardioselective

49
Q

which are beta 1 selective

A

metoprolol, atenolol, bisoprolol

50
Q

when not to use Beta blockers

A

bradycardia, AV block, sick sinus syndrome, unstable LVF, asthma, severe depression, peripheral vascular disease.

51
Q

SE of beta

A

sedation, fatigue, decreased exercise tolerance. lethargy, insomnia, claudication worse, impotence

52
Q

contra for nitrates

A

hypotension, aortic stenosis, hypertrophic cardiomyopathy, use of PDE to treat erectile dysfunction

53
Q

SE to nitrates

A

tolerance. HA, hypotension.

54
Q

digoxin when to use it

A

use for HF. it stimulates the heart.

55
Q

what is the mechanism for digoxin

A

it inhibits the Na/k ATPase. this allows for calcium to come into the heart cell giving the heart an increased force of contraction due to the calcium.

56
Q

what does digoxin do for the heart in CHF?

A

it increases CO, LVEF, exercise tolerance, natriuresis, vagal tone, and decreases LVEDP, NE, RAAS, and neural-hormonal activity.

57
Q

why is use of digoxin waining

A

due to the narrow therapeutic window. can be toxic and proarrhthmigenic

58
Q

what is dobutamine and when do we use it

A

we use it in heart failure. it is a direct beta agonist

59
Q

what are the downfalls od dobutamine

A

tolerance develops within 48 hrs.

60
Q

what is milrinone and when do we use it

A

it is a PDEi that increases contractility and relaxation. we use it in HF. there is no tolerance up to 72 hours.

pharm unit 4 (4 decks)

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