sepsis, HTN, CHF, angina Flashcards

(47 cards)

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

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
nitroprusside MOA and AEs
vasodilation via NO group | nausea, vomiting, muscle twitching, cyanide toxicity
26
Hydralazine MOA
K+ channel agonist -> hyperpolarization and constriction blockage -> vasodilate
27
hydralazine use
eclampsia (HTN emergency in pregnancy)
28
hydralazine AE
tachycardia, flushing, HA, vomiting, angina, aggrevation
29
``` drugs to avoid in this condition: gout asthma heart block heart failure hyperkalemia pregnancy ```
``` diuretic beta blocker beta blocker, CCB CCB ACE-I, ARB ACE-I, ARB ```
30
digitalis (digoxin, cardiac glycosides) MOA
inhibit Na/K ATPase -> decreased Na/Ca exchange -> Ca buildup and increased contractility and HR
31
digoxin use
``` increased contractility (CHF) arrhythmias due to low HR and slow AV nodal conduction ```
32
cardiac glycoside t1/2
40 hours - give every 24-48 hours
33
digoxin AE's
nausea, vomiting, bradycardia, AV block and other arrhythmias cardiac AE's increase with hypokalemia antidote: Digoxin Immune FAB (digiband)
34
PDE-3 inhibitors MOA
inhibit phosphodiesterase-3 which degrades cAMP -> increase cAMP levels -> increase contractility and vasodilation
35
PDE-3 agents
milrinone, inamrinone
36
PDE-3 administration
constant IV infusion
37
lusitropy
beta 1 agonist effect | increased diastolic relaxation so that EDV can be maintained even as HR increases
38
spironolactone MOA
aldosterone antagonist
39
``` effects on FS curve of: oral nitrates, loop diuretics ACE / ARB fluids (saline) digoxin ```
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
nitrates agents
nitroglycerin, isosorbide mononitrate (dinitrate)
41
nitrate MOA
activation of guanylyl cyclase -> increased cGMP -> dephosphorylation of myosin light chain -> venodilation
42
nitrate use:
acute angina symptoms
43
nitrate AE's
orthostatic hypotension, tachycardia, HA, tolerance
44
nitrate contraindications
elevated intracranial pressure | PDE-5 inhibitor (viagra)
45
beta blocker AE's
bradycardia, CNS effects (depression, mood changes, dizziness, lethargy)
46
beta blocker contraindications
vasospastic disease or asthma severe bradycardia AV block or ventricular block
47
ACE / ARB contraindications
pregnancy | hyperkalemia