sepsis, HTN, CHF, angina Flashcards
intra-abdominal infection treatment
cefazolin or ceftriaxone or tobramycin + metronidazole (E. coli and B. frag.)
metronidazole MOA
MOA: disrupt nucleic acid synthesis via free radical release
metronidazole ADME
prodrug activated by microbes
oral absorption; excellent penetration and well tolerated
metronidazole use
Gr- anaerobes (B. frag)
Dopamine MOA
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
Dobutamine MOA
beta 1 agonist, moderate beta 2 agonist (increase contractility, HR)
epinephrine MOA and use
low dose - beta 1, beta 2 agonist
high dose - beta 1, alpha 1 agonist
use: cardiac arrest
norepinephrine MOA
beta 1 and alpha 1 agonist
use: septic hypotension
vasopressin (ADH, AVP) MOA
V1 - vasoconstrict
V2 - increase renal water reabsorption
alpha 1 - vasoconstrict
-thiazides and chlorthalidone MOA
inhibit Na+ transporters in distal tubule -> decreased H2O reabsorption
-thiazides and chlorthalidone use
first line in HTN treatment, esp. blacks
-thiazides and chlorthalidone ADME
enhance efficacy of virtually all other HTN medications
distal tubule -> least potent
-thiazides and chlorthalidone AE’s
low: Mg, Na, K
high: Ca, uric acid, cholesterol
postural hypotension, decreased glucose tolerance
drug suffix for: ACE-I ARB alpha 1 blocker beta blocker distal diuretic vasodilatory CCBs
ACE = -pril ARB = -sartan alpha 1 antagonist = -osin beta blocker = -olol distal diuretic = -thiazide vasodilatory CCB = -dipine
ACE-I and ARB MOA:
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
ACE-I and ARB AE’s
hypotension, high K, birth defects, decreased renal function
ACE-I: cough, angioedema (due to bradykinin buildup)
ACE-I and ARB use:
CKD
CCB’s MOA
verapamil, diltiazem: inhibit Ca++ entry in cardiac muscle -> decrease contractility and HR
-dipines: inhibit Ca++ entry in smooth muscle -> vasodilate
CCB use:
first line for HTN
prevention of variant angina
CCB AE’s
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)
beta blockers MOA
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
alpha 1 blockers MOA
vasodilate
alpha 2 agonists MOA
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
alpha 2 agonists agents
methyldopa, clonidine
nitroprusside MOA and AEs
vasodilation via NO group
nausea, vomiting, muscle twitching, cyanide toxicity
Hydralazine MOA
K+ channel agonist -> hyperpolarization and constriction blockage -> vasodilate
hydralazine use
eclampsia (HTN emergency in pregnancy)
hydralazine AE
tachycardia, flushing, HA, vomiting, angina, aggrevation
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
digitalis (digoxin, cardiac glycosides) MOA
inhibit Na/K ATPase -> decreased Na/Ca exchange -> Ca buildup and increased contractility and HR
digoxin use
increased contractility (CHF) arrhythmias due to low HR and slow AV nodal conduction
cardiac glycoside t1/2
40 hours - give every 24-48 hours
digoxin AE’s
nausea, vomiting, bradycardia, AV block and other arrhythmias
cardiac AE’s increase with hypokalemia
antidote: Digoxin Immune FAB (digiband)
PDE-3 inhibitors MOA
inhibit phosphodiesterase-3 which degrades cAMP -> increase cAMP levels -> increase contractility and vasodilation
PDE-3 agents
milrinone, inamrinone
PDE-3 administration
constant IV infusion
lusitropy
beta 1 agonist effect
increased diastolic relaxation so that EDV can be maintained even as HR increases
spironolactone MOA
aldosterone antagonist
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)
nitrates agents
nitroglycerin, isosorbide mononitrate (dinitrate)
nitrate MOA
activation of guanylyl cyclase -> increased cGMP -> dephosphorylation of myosin light chain -> venodilation
nitrate use:
acute angina symptoms
nitrate AE’s
orthostatic hypotension, tachycardia, HA, tolerance
nitrate contraindications
elevated intracranial pressure
PDE-5 inhibitor (viagra)
beta blocker AE’s
bradycardia, CNS effects (depression, mood changes, dizziness, lethargy)
beta blocker contraindications
vasospastic disease or asthma
severe bradycardia
AV block or ventricular block
ACE / ARB contraindications
pregnancy
hyperkalemia
