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pharm > sepsis, HTN, CHF, angina > Flashcards

sepsis, HTN, CHF, angina Flashcards

1
Q

intra-abdominal infection treatment

A

cefazolin or ceftriaxone or tobramycin + metronidazole (E. coli and B. frag.)

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2
Q

metronidazole MOA

A

MOA: disrupt nucleic acid synthesis via free radical release

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3
Q

metronidazole ADME

A

prodrug activated by microbes

oral absorption; excellent penetration and well tolerated

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4
Q

metronidazole use

A

Gr- anaerobes (B. frag)

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5
Q

Dopamine MOA

A

low dose - beta 1 and beta 2 agonist; D1 agonist (increase contractility, HR, and vasodilate renal arteries)
high dose - beta 1, beta 2, and alpha 1 agonist

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6
Q

Dobutamine MOA

A

beta 1 agonist, moderate beta 2 agonist (increase contractility, HR)

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7
Q

epinephrine MOA and use

A

low dose - beta 1, beta 2 agonist
high dose - beta 1, alpha 1 agonist
use: cardiac arrest

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8
Q

norepinephrine MOA

A

beta 1 and alpha 1 agonist

use: septic hypotension

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9
Q

vasopressin (ADH, AVP) MOA

A

V1 - vasoconstrict
V2 - increase renal water reabsorption
alpha 1 - vasoconstrict

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10
Q

-thiazides and chlorthalidone MOA

A

inhibit Na+ transporters in distal tubule -> decreased H2O reabsorption

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11
Q

-thiazides and chlorthalidone use

A

first line in HTN treatment, esp. blacks

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12
Q

-thiazides and chlorthalidone ADME

A

enhance efficacy of virtually all other HTN medications

distal tubule -> least potent

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13
Q

-thiazides and chlorthalidone AE’s

A

low: Mg, Na, K
high: Ca, uric acid, cholesterol
postural hypotension, decreased glucose tolerance

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14
Q 
drug suffix for: 
ACE-I
ARB
alpha 1 blocker
beta blocker
distal diuretic
vasodilatory CCBs
A 
ACE = -pril
ARB = -sartan
alpha 1 antagonist = -osin
beta blocker = -olol
distal diuretic = -thiazide
vasodilatory CCB = -dipine
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15
Q

ACE-I and ARB MOA:

A

ACE-I = block conversion of angiotensin I to angiotensin II by Angiotensin Converting Enzyme
ARB = aldosterone receptor blocker
-> decrease SVR, blood volume, SNS effects, cardiac and vascular hypertrophy, and bradykinin breakdown

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16
Q

ACE-I and ARB AE’s

A

hypotension, high K, birth defects, decreased renal function

ACE-I: cough, angioedema (due to bradykinin buildup)

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17
Q

ACE-I and ARB use:

A

CKD

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18
Q

CCB’s MOA

A

verapamil, diltiazem: inhibit Ca++ entry in cardiac muscle -> decrease contractility and HR
-dipines: inhibit Ca++ entry in smooth muscle -> vasodilate

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19
Q

CCB use:

A

first line for HTN

prevention of variant angina

20
Q

CCB AE’s

A

cardiac depression: cardiac arrest, bradycardia, AV block, heart failure; more likely if given with a beta blocker
minor: flushing, dizziness, nausea, edema, constipation (esp. with verapamil)

21
Q

beta blockers MOA

A

metoprolol, atenolol: beta 1 selective blockade
carvedilol, labetalol: non-selective beta blockade and alpha 1 blocade
-> decrease contractility, HR by blocking SNS
-> decrease BP by inhibiting renin release via blocking receptors on juxtaglomerular cells

22
Q

alpha 1 blockers MOA

A

vasodilate

23
Q

alpha 2 agonists MOA

A

stimulate alpha 2 autoreceptors -> negative feedback and decreased NE release -> vasodilation
decreased PVR via stimulation in CNS vasomotor center
analgesia via stimulation of dorsal horn spinal cord receptors

24
Q

alpha 2 agonists agents

A

methyldopa, clonidine

25
Q

nitroprusside MOA and AEs

A

vasodilation via NO group

nausea, vomiting, muscle twitching, cyanide toxicity

26
Q

Hydralazine MOA

A

K+ channel agonist -> hyperpolarization and constriction blockage -> vasodilate

27
Q

hydralazine use

A

eclampsia (HTN emergency in pregnancy)

28
Q

hydralazine AE

A

tachycardia, flushing, HA, vomiting, angina, aggrevation

29
Q 
drugs to avoid in this condition:
gout
asthma
heart block
heart failure
hyperkalemia
pregnancy
A 
diuretic
beta blocker
beta blocker, CCB
CCB
ACE-I, ARB
ACE-I, ARB
30
Q

digitalis (digoxin, cardiac glycosides) MOA

A

inhibit Na/K ATPase -> decreased Na/Ca exchange -> Ca buildup and increased contractility and HR

31
Q

digoxin use

A 
increased contractility (CHF)
arrhythmias due to low HR and slow AV nodal conduction
32
Q

cardiac glycoside t1/2

A

40 hours - give every 24-48 hours

33
Q

digoxin AE’s

A

nausea, vomiting, bradycardia, AV block and other arrhythmias
cardiac AE’s increase with hypokalemia
antidote: Digoxin Immune FAB (digiband)

34
Q

PDE-3 inhibitors MOA

A

inhibit phosphodiesterase-3 which degrades cAMP -> increase cAMP levels -> increase contractility and vasodilation

35
Q

PDE-3 agents

A

milrinone, inamrinone

36
Q

PDE-3 administration

A

constant IV infusion

37
Q

lusitropy

A

beta 1 agonist effect

increased diastolic relaxation so that EDV can be maintained even as HR increases

38
Q

spironolactone MOA

A

aldosterone antagonist

39
Q 
effects on FS curve of:
oral nitrates, loop diuretics
ACE / ARB
fluids (saline)
digoxin
A

shift leftward along same curve (decrease LV filling pressure for a given SV curve)
shift leftward and upward to a new curve (decrease LV filling pressure and increase SV)
shift rightward along the same curve (increase SV and LV filling pressure)
shift upward to a new curve (increase SV for a given LV filling pressure)

40
Q

nitrates agents

A

nitroglycerin, isosorbide mononitrate (dinitrate)

41
Q

nitrate MOA

A

activation of guanylyl cyclase -> increased cGMP -> dephosphorylation of myosin light chain -> venodilation

42
Q

nitrate use:

A

acute angina symptoms

43
Q

nitrate AE’s

A

orthostatic hypotension, tachycardia, HA, tolerance

44
Q

nitrate contraindications

A

elevated intracranial pressure

PDE-5 inhibitor (viagra)

45
Q

beta blocker AE’s

A

bradycardia, CNS effects (depression, mood changes, dizziness, lethargy)

46
Q

beta blocker contraindications

A

vasospastic disease or asthma
severe bradycardia
AV block or ventricular block

47
Q

ACE / ARB contraindications

A

pregnancy

hyperkalemia

pharm (8 decks)

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