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Pharm > CV Pharm > Flashcards

CV Pharm Flashcards

1
Q

contrast hypertensive urgency & hypertensive emergency

A

hypertensive urgency has NO associated acute end organ damage, vs. hypertensive emergency which does

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2
Q

what is the term for both hypertensive urgencies & emergencies?

A

hypertensive crisis

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3
Q

term for: when bp is uncontrolled depite the use of 3+ antihypertensive drugs, one of which is a diuretic

A

resistant HTN

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4
Q

risk factors for resistance HTN?

A

older age, obesity, chronic kidney disease, diabetes, obstructive sleep apnea, high salt diet, Af Am race, females (post menopause)

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5
Q

common causes of secondary HTN?

A

renal parenchymal disease, obstructive sleep apnea, renal artery stenosis, primary aldosteronism

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6
Q

ppl with resistance HTN are expected to have high or low fluid levels?

A

expect to be fluid overloaded

inadequate diuretic use is top cause of tx resistance

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7
Q

what is the preferred diuretic for Resistant HTN?

A

chlorthalidone

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8
Q

which drugs can be used to tx HTN in pregnancy?

A

Methyl dopa, labetalol, nifedipine, hydralazine, metoprolol

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9
Q

what is the safest antihypertensive drug for pregnant women?

A

methyldopa

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10
Q

what antihypertensives need to be avoided in pregnant women?

A

diuretics, atenolol, nitroprusside,

ACE inhibitors, angiotensin receptor antagonists

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11
Q

what is anginal pain caused by?

A

release of bradykinin & adenosine onto nociceptive afferents

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12
Q

downside of using organic nitrates?

A

can only be used in acute setting–>tolerance develops early

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13
Q

how to combat nitrate tolerance

A

use dosing regimens that allow for nitrate free of low nitrate concentration for several hrs/day
during window without nitrate, can cover with other drugs (beta blockers, vasodilators, etc)

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14
Q

the ability for a cell to initiate an AP

A

automaticity

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15
Q

the ability of a cell to receive and transmit an AP

A

conductivity

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16
Q

the ability of a cell to receive and transmit an AO

A

dromotropism

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17
Q

what maintains the plateau of the AP?

A

the late INa channels

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18
Q

the ERP/APD ratio is important for what?

A

propagation of abnormal impulses

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19
Q

lower ERP/APD ratio indicates what?

A

it will be easier for tissue to be depolarized by abnormal imppulses

20
Q

what are some things that could create marked prolongatino of the cardiac AP?

A

slow HR, hypokalemia

21
Q

what cell type are early after depolarizatios most readily induced?

A

purkinje cells

22
Q

what do early after repolaizations result in?

A

torsade de pointe

23
Q

delayed after-depolarization occurs under what sort of conditions?

A

Ca overload

ie. MI, adrenergic stress, digitalis intox, HF

24
Q

what happens in delayed after depolarization?

A

if DAD reaches threshold, a secondary triggered beat or beats may occur
normal upstroke followed by abnormal depolarization * secondary upstroke

25
Q

what is teh most common cause of paroxysmal regular narrow complex tachy?

A

AV nodal reentrant tachycardia (AVNRT)

26
Q

what class of antiarrhytmics is good for use in digitalis & MI induced arryhtmia?

A

class 1b

27
Q

why is there an early reoccurence of arryhtmias after amiodarone is discontinued?

A

all tissues are saturated, there is a rapid redistribution out of the myocardium–>responsible for early reoccurrence

28
Q

is binding to L-type Ca channel alpha subunit by Ca-channel blockers a complete blockage?

A

no, it is an incomplete blockage

29
Q

what is the most metabolically active section of the nephron?

A
  1. proximal convoluted tubule

2. thick ascending limb (2nd most)

30
Q

why is cirrhosis a contraindication for use of acetazolamide?

A

induced alkalinizatino of urine will decr urinary excretion of NH4–>may contribute to hyperammonemia, hepatic encephalopathy

31
Q

role of thizaides in tx of nephrogenic diabetes insipidis?

A
  1. incr renal Na reabsorption
  2. recovery of Aquaporin 2 abundance
  3. recovery of NCC, ENaC
32
Q

how does spironolactone prevent LV remodeling & cardiac fibrosis?

A

inhibits MMP, inhibits protein kinase C

33
Q

how does spirinolactone prevent sudden cardiac death?

A

improve HR variability, reduce QT dispersion, reduce early morning risk in HR in HF patients, prevents hypokalemia

34
Q

what are the hemodynamic effects of spirinolactone?

A

bp reduction

modest diuresis, natriuresis

35
Q

what are the vascular effects of spirinolactone?

A 
decr vascular NADPH oxidase activity
reduce the generation of reactive oxygen species 
reverse endothelial dysfunction
increase nitric oxide bioactivity
retard the thrombotic response to injury
36
Q

what are the best agents to use in ppl with previous MI (to prevent risk of sudden cardiac death?

A

beta blockers

37
Q

what is anginal pain mostly due to?

A

release of bradykinind + adenosine onto nocioceptive afferents

38
Q

anginal pain

A

rest or unstable angina

39
Q

anginal pain >30 min, shortness of breath, weakness, N/V

A

acute MI

40
Q

GTN & ISDN are prescribed as what sort of tx for angina?

A

prophylactic tx

41
Q

which of the organic nitrates has a phasic release formulation?

A

ISMN

42
Q

how to calculate CO?

A

SV x HR

43
Q

frank starling mechanism

A

greater preload = greater contractility

44
Q

describe anrep

A

if you incr the afterload acutely, can trigger incr in contractilty

45
Q

describe bowditch

A

relationship b/w hr & contractility

46
Q

how to calculate corrected QT interval?

A

QT/sq root of R to R interval

Pharm (20 decks)

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