all CRR drugs Flashcards
abciximab (reopro)
glycoprotein IIb/IIIa antagonist
blocks GPIIb/IIIa receptor on platelets to bind vWF or fibrinogen therefore reduces platelet aggregation and clotting
other examples of glycoprotein IIb/IIIa antagonists: eptifibatide, tirofiban
aspirin
NSAID- nonsteroidal anti-inflammatroy drug
acetylsalycic acid
irreversibly inhibits COX (inhibits activation/secretion step of platelet plug formation), reduces clotting
NSAIDs
NSAID- nonsteroidal anti-inflammatroy drug
competitive inhibitors for COX (therefore reduce platelet aggregation and clotting)
reversible: ibuprofen, acetaminophin, indomethacin
irreversible: aspririn
ADP receptor (PY12) antagonists
irreversibly blocks ADP receptor on platelet therefore reduce platelet aggregation and platelet plug formation
ex. plavix (clopidogrel)
plavix (clopidogrel)
ADP receptor (PY12) antagonist irreversibly blocks ADP receptor on platelet therefore reduce platelet aggregation and platelet plug formation
glycoprotein IIb/IIIa antagonist
blocks GP IIb/IIIa receptor on platelets therefore reducing platelet aggregation and platelet plug formation
Reopro (abciximab, eptifiatide, tirofiban)
vorapaxar
blocks thrombin receptor (PAR-1) on platelets, reduces platelet plug formation and clotting
heparin
increases antithrombin III activity in inhibiting factor X and thrombin
reduces coagulation
warfarin
inhibits vitamin K synthesis therefore inhibiting vitamin K dependent factors in coagulation: X, IX, XII, II, protein Ca, and protein S
direct thrombin inhibitors
anticoagulants
bivalirudin (angiomax)
dabigatran (pradaxa)
apixaban (eliquis)
bivalirudin (angiomax)
inhibits thrombin
anticoagulant
dabigatran (pradaxa)
inhibits thrombin
anticoagulant
apixaban (eliquis)
inhibits factor Xa
anticoagulant
voxelotor
blocks the polymerization of hemoglobin in SCD and beta thalassemias
5-azacytidine
removes methylation on CpGs islands of gamma globin genes (normally repress gamma globin expression) in order to promote HbF expression
hydroxyurea
promotes gamma globin expression, therefore HbF expression
Endari
increases NADH in RBC to promote glutathione reduction
Thiopental
high lipid coefficient which allows it to rapidly enter the brain
induces rapid anesthesia
also leaves the brain rapidly so short duration of action
Inducers of CYP450 enzymes
enhance CYP450 activity which increases the rate at which they metabolize drugs, excrete drugs more quickly
ex. phenobarbital, rifampin, carbamazepine, cruciferous vegetables, smoking
inhibitors of CYP450 enzymes
inhibit CYP450 enzymes from metabolizing drugs, drug build up in the body, increases response to drug
ex. omeprazole, eeythromycin, grapefruit juice, cumin,
MAOIs
inhibitors of MAO which normally breaks down catecholamines and serotonin, allows build up of these neurotransmitters increasing the post synaptic stimulation
disulfiram
inhibits aldehyde dehydrogenase (breaks down aldehyde, by product of alcohol metabolism
causes aldehyde build up when person drinks alcohol–> ill with vommitting, sweat, etc
naltrexone
k and m opiod receptor antagonist
reduces cravings for alcohol bc decreases alcohol activation of dopamine reward pathway
acamprosate
antagonist of NMDA receptors thus reducings the activity of glutamate in the CNS and reduces cravings for alcohol
isoproterenol
beta agonist: increases heart rate, increase contraction force, increases conduction velocity, dilates blood vessels
epinephrine
mixed alpha, beta agonist: primarily a beta receptor agonsit at low doses and an alpha agonist at high doses
used clinically as:
with local anestetic bc local vasoconstriction will localize action of the anesthetic
local hemostatic (control bleeding during surgery)
increase cardiac activity after cardiac arrest
treat allergic reaction by counter acting hypotention from histamines, counters constriction of airways (beta 2 broncho dilation)
norepinephrine
catecholamine
primarily alpha receptor agonist
used clinically as:
pressor agent to block system hypotension
nonselective beta agonist
increase intropic and chronotropic effects and cause some vasodilation
ex. isoproterenol
beta 1 selective agonist
inotropic/cardioselective effects, increase myocardial oxygen demand
ex. dobutamine
beta 2 selective agonist
bronchodilation
ex. salbutamol, terbutaline, elbuterol, arformoterol tartarate
non selective beta blocker
decrease HR, CF, and CO
effects are more substantial as sympathetic tone increases
reflex from decreased BP causes a temporary rise in BP
can have bronchodilation effects so bad for pulmonary compromised patients
also blocks renin secretion in kidney –> vasodilation
ex. propranolol
beta 1 selective blocker
cardioselectively increase HR, CF, and CO, do NOT cause a decrease in bronchoconstriction like non selective so these are safer to use with pulmonary compromised patients
also blocks renin secretion in kidney –> vasodilation
ex. metoprolol, esmolol, atenolol, nadolol
beta 2 selective blocker
inhibits bronchodilation –> bronchoconstriction
alpha receptor blocker
decreases peripheral resistance
used to treat hypertension without effecting heart rate, renal blood flow, or GFR
ex. prazosin, terazosin, doxazosin, phenoxybenzamine
muscarininc agonist
stimulates effect of PNS
direct: ex. pilocarpine, carbachol
indirect: inhibits AChE ex. neostigmine, physostigmine, organophosphate
muscarininc antagonsit
inhibit response from PNS
ex. atropine, ipratropium
isoproterenol
nonselective beta agonist
dobutamine
beta 1 selective agonist
salbutamol
beta 2 selective agonist
terbutaline
beta 2 selective agonist
albuterol
beta 2 selective agonist
arformoterol tartrate
beta 2 selective agonist
propranolol
nonselective beta blocker
metoprolol
beta 1 selective blocker
atenolol
beta 1 selective blocker
esmolol
beta 1 selective blocker
nadolol
beta 1 selective blocker
prazosin
alpha receptor blocker
terazosin
alpha receptor blocker