Trachte Rx Flashcards
Paragyline
MAOI
a1
b1
increase BP
Cocaine
- axoplasmic pump = block reuptake NE
a1
b1
increase BP
Imipramine
TCA
- axoplasmic pump = block reuptake NE
a1
b1
increase BP
Tyramine
reverse axoplasmic transporter = increase release NE
a1
b1
increase BP
Amphetamine
reverse axoplasmic transporter = increase release NE
a1
b1
increase BP
Ephedrine
reverse axoplasmic transporter = increase release NE
a1
b1
increase BP
Reserpine
- granular pump = decrease accumulation NE = deplete NE
decrease BP
Guanethidine
induce NE release = deplete NE stores
decrease BP
Guanadrel
induce NE = release = deplete NE stores
decrease BP
Epinephrine
a1 VASOCNX
a2
b1
b2
increase BP
Norepinephrine
a1 VASOCNX
a2
b1
increase BP
Isoproterenol
b1
b2 RELAX SM
decrease BP
Phenylephrine
a1 VASOCNX
increase BP
Clonidine
a2 inhibit neural NE release
decrease BP
Alpha methyl Dopa
a2 inhibit neural NE release
decrease BP
antihypertensive safe for pregnancy
Guanabenz
a2 inhibit neural NE release
decrease BP
Dobutamine
b1 INCREASE HR AND FORCE
increase BP
Albuterol
b2 RELAX SM
some b1
decrease BP
bronchodilation
Metaproterenol
b2 RELAX SM
some b1
decrease BP
bronchodilation
Salmeterol
b2 RELAX SM
some b1
decrease BP
bronchodilation
Ritodrine
b2 RELAX SM
decrease BP
delay labor
Tertbutaline
b2 RELAX SM
decrease BP
delay labor
TPR =
8Lv/nr^4
r^4 is only variable
Terazosin
a1 ANTAGONIST
decrease vasocnx
decrease BP
Propanolol
nonspecific b blocker
block b1: decrease HR and contractility
block b2: decrease bronchodilation (not as important)
decrease BP
Metoprolol
b1 antagonist
b1 blocker
block b1: decrease HR and contractility
decrease BP
*specific to b1 = specific to heart
Atenolol
b1 antagonist
b1 blocker
block b1: decrease HR and contractility
decrease BP
*specific to b1 = specific to heart
a1
vascular SM contractility
VASOCONSTRICTION
b1
1 heart = b1
increase HR and contractility
a2
don’t need to care about it
inhibit neural NE release
b2
2 lungs = b2
vascular SM relaxation
VASODILATION
BRONCHODILATION
decreased uterine tone
Ceftriaxone
3rd gen cephalosporin
CELL WALL INHIBITOR
blocks transpeptidation fo peptidoglycan in bacterial cell walls
Tx: MSSA, strep, some gram (-)
Vancomycin
CELL WALL INHIBITOR
binds D-ala-D-alanine to prevent transglycosylation
Tx: MRSA, broad gram (+)
Empiric treatment of infectious endocarditis (according to PBL)
ceftriaxone and vancomycin
Penicillin G
CELL WALL INHIBITOR
beta-lactam
binds pbp and blocks transpeptidation of peptidoglycan in bacterial cell walls
Tx: some gram (+), basically strep
Treatment of most common cause of subacute IE
penicillin G
strep viridans = gram (+)
Amoxicillin
CELL WALL INHIBITOR
AMINO-beta-lactam
binds pbp and blocks transpeptidation of peptidoglycan in bacterial cell walls
Tx: some gram (+) = mainly strep, some gram (-)
can still be inactivated by beta-lactamases, so give with clavulanate
Clavulanate
beta-lactamase resistant
Alteplase
t-PA
tissue plasminogen activator: converts plasminogen to plasmin –> break down fibrin clots
Tx: non-hemorrhagic stroke or clot (emboli or thrombi)
CONTRAINDICATED IN ENDOCARDIDITS
Morphine
OPIOD PAIN RELEIVER/ANALGESIC
acts on mu receptors in three locations:
- presynatpic nociception pathway (blocks calcium pump –> blocks vesicle release)
- postsynatpic nociception pathway (increases K permeability –> blocks depolarization)
- presynatpic descending inhibitory pathway (blocks GABA release –> allos inhibior neuron firing and blocking nociception pathway)
Nitroglycerin
VENOdilator
forms free radical NO -> activates guanylyl cyclase –> incrase cGMP –> increase MLC phosphatase –> increase MLC dephosphorylation –> SM relaxation –> VEINS vasodilate –> decreased blood returning to heart –> decrease preload
Tx: decrease myocardial activity and oxygen demand –> decrease ischemic damage
Clopidogrel
ANTI-COAGULANT
INHIBITS PLATELET ACTIVATION
blocks ADP receptors on platelets –> inhibits platelet activation
Tx: post MI anticoagulation therapy
Heparin
ANTI-COAGULANT
INHIBITS FIBRIN FORMATION
increases activity of antithrombin III –> Inhibits thrombin –> blocks conversion of fibrinogen to fibrin = NO CLOT
Tx: post MI anticoagulation therapy
Eptifibatide
ANTI-COAGULANT
INHIBITS PLATELET AGGREGATION
binds GPIIb/IIIa receptor on activated platelets –> inhibits binding of fibrinogen –> block initiatino of coagulation cascade post-platelet plug
Tx: post MI anticoagulation therapy
Aspirin
ANTI-COAGULANT
INHIBITS PLATELET AGGREGATION
irreversibly inhibits COX1/2 –> blocks production of TXA2 –> inhibits platelet aggregation
Tx: used IMMEDIATELY upon suspected MI UNLESS patient recently took aspirin
Statins
INHIBIT CHOLESTEROL SYNTHESIS
inhibit HMG-CoA reductase
reduces plaque formation in vessels
Tx: dyslipidemia –> decrase atherosclerosis and risk of CAD
ACE inhibitors
angiotensin converting enzyme inhibitor
SUPPRESSES RAAS system
suppresses RAAS system by inhibitng conversion of angiotensin I to angiotensin II –> decreased aldosterone release –> decreased Na reabsorption in kidney –> DECREASED BLOOD VOLUME AND PRELOAD
DECREASED VASOCNX –> DECREASED AFTERLOAD
Tx: post MI management, chronic CHF management
Lisinopril
ACE inhibitor
suppresses RAAS system –> dec aldosterone –> DECREASE BLOOD VOLUME AND PRELOAD
DECREASED VASOCNX –> DECREASED AFTERLOAD
Tx: post MI, chronic CHF
Enalapril
ACE inhibitor
suppresses RAAS system –> dec aldosterone –> decreased Na reabsorption in kidney –> DECREASED BLOOD VOLUME –> DECREASED PRELOAD
DECREASED VASOCNX –> DECREASED AFTERLOAD
Tx: post MI, chronic CHF
Beta-blockers
block b1 receptors: MAIN ACTIVITY ON HEART:
DECREASE HR AND CONTRACTILITY
decrease myocaridal oxygen demand
decrease BP
Tx: MI to reduce ischemia, post MI, chronic CHF
*contraindicated in acute CHF (need to preserve heart function and complete diuresis first)
Metoprolol
specific b1 blocker: block b1 receptors: MAIN ACTIVITY ON HEART:
DECREASE HR AND CONTRACTILITY
decrease myocaridal oxygen demand
decrease BP
Tx: MI to reduce ischemia, post MI, chronic CHF
Propranolol
nonspecific beta blocker (blocks b1 and b2)
block b1 receptors: MAIN ACTIVITY ON HEART:
DECREASE HR AND CONTRACTILITY
decrease myocaridal oxygen demand
decrease BP
Tx: MI to reduce ischemia, post MI, chronic CHF
Isosorbide dinitrate
same mech as NO
NO –> binds SM –> G-protein coupled receptor –> activates guanyly cyclase –> increase cGMP –> decrease intracellular Ca –> relaxes SM –> VENOdilator –> decrases preload
*longer half-life than NO (60-90 min)
Hydralazine
increases NO synthesis in endothelium –> NO –> binds SM –> g-protein coupled receptor –> incrase cGMP –> dec intracell Ca –> relaxes SM –> VENOdilator –> decreases preload
*HIGHER SELECTIVITY FOR ARTERIOLES = decrease afterload
Aldosterone Receptor Blockers
ARBs
Block aldosterone action –> decrease Na reabsorption in kidney –> DECREASES BLOOD VOLUME –> DECREASES PRELOAD
*causes an increase in aldosterone and renin plasma concentration = INHIBITION OF NEGATIVE FEEDBACK
Eplerenone
ARB
block aldosterone –> decrease BV –> decreases preload
Spirinolactone
ARB
blocks aldosterone –> decrease BV –> decreases preload
Digoxin
Inhibits Na/K/ATPase
POSITIVE INOTROPE: increases CONTRACTILITY
NEGATIVE CHRONOTROPE: decreases HR