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
doxazosin
alphareceptor blocker
pilocarpine
direct muscarinic agonist
carbachol
direct muscarinic agonist
neostigmine
indirect muscarinic agonist
physostigmine
indirect muscarininc agonist
organophosphate
indirect muscarininc agonist
atropine
muscarininc antagonist
ipratropium
muscarininc antagonist
class I antiarrhythmic drugs
sodium channel blockers
slow phase 0, work better on cells rapidly depolarizing
1A: slow 0, prolong action potential (ex. procainamide)
1B: shorten phase 3 ex. lidocane
1C: slow phase 0 ex. flecainide
treat re-entrant arrhythmias (mainly 1A), tachyarrythmias, and abnormal automacity
procainamide
type IA antiarrythmic drug
slows phase 0 and prolongs action potential by blocking sodium channels
lidocane
type 1B antiarrhythmic drug
shortens phase 3 by blocking sodium channels
flecainide
type 1C antiarrhythmia drug
slows phase 0 by blocking sodium channels
class II antiarrhythmic drugs
beta blockers
decrease HR, CF, and CO
effectiveness increases as sympathetic tone increases
treat tachyarrhytmias secondary to sympathoadrenal discharge, distubance of aytomaticity and re-entry
ex. non selective: propanolol, B1 selective: metoprolol, atenolol, nadolol, esmolol
class III antiarrhythmic drugs
potassium channel blockers
prolong phase 3 which increases effective refactory period, depolarization
treat supraventricular and or ventricullar tachy
ex. amiodarone, sotalol
amiodarone
class III/potassium channel blocker treat tachycardia
sotalol
class III/potassium channel blocker treat tachy
class IV antiarrhymic
calcium channel blocker
especially affects AV node (ca++ dependent) to decrease phase 4 which prolongs effecticve refractory period
decreases normal and abnormal automaticity
treat supraventricular arrhythmias, AV reentry and ectopic stimulation
ex. verapamil and diltiazem
verapamil
class IV/ calcium channel blocker treat supraventricular arrhythmias, AV re entry and ectopic stimulation
class V antiarrhymic
misc.
ex. digoxin, atropine, epi, iso, adenosine
digoxin
increase calcium which increases force of contraction
enhances pNS at nodal areas which decreases SA and AV automaticity but mainly affects AV
atropine
musc. blocker, treats bradycardia and sinus arrest secondary to PNS stimulation
adenosine
receptors at SA and AV
inhibits adenylyl cyclase –> decreased calcium and increased potassium, thereofre decreasing conduction, prolonging ERP and decreasing AV automaticity
treats paroxysmal supraventricular tachycardia
ACEI
angiotensin converting enzyme inhibitors
AT I is not turned into AT II, so blocks the vasoconstriction ATII usually produces in arteries and venules
decreases cardiac load and arterial pressure
ex. captopril, enalapril, lisinopril
good for young people and European people who have normal or high plasma renin
captopril
ACEI
short duration of action
treat HTN by lowering BP
enalapril
ACEI
long duration
treat HTN
lisinopril
ACEI
long duration
treat HTN
ARB
angiotensin II receptor blocker/angiotensin I antagonist
blocks receptor ATII binds to (ATI)
blocks inflow of calcium and therefore block vasoconstriction
works well in kidney and brain
ex. losartan, valsartan, irbesartan, candesartan
works well in young people and european people with high plasma renin
losartan
ARB
candesartan
ARB
valsartan
ARB
Irbesartan
ARB
Ca+ channel antagonists
block influx of calcium thus inducing vasodilation
ex. nifedipine, amlodipin, verapramil, dilitiazem
good for older people and people with low plasma renin
nifedipine
Ca+ channel antagonist
vasodilation
amlodipine
Ca+ channel antagonist
vasodilation
verapramil
Ca+ channel antagonsit
vasodilation
dilitiazem
Ca+ channel antagonist
vasodilation
HCTZ
thiazide diuretic
lopressor HCT
metoprolol and HCTZ
beta blocker and thiazide diuretic
HYZAAR
losartan + HCTZ
ARB and thiazide diuretic
vaseretic
enalapril + HCT
ACEI and thiazide diuretic
renin inhibitors
blocks ATI –> ATII
vasodilation
ex. aliskiren
aliskiren
renin inhibitor
vasodilation
phenoxybenzamine
non selective alpha receptor antagonist
binds irreversibly and only used during removal of phaeochromocytoma removal (adrenal gland tumor) since the tumor could release catecholamines when moved
aldosterone antagonist
blocks Na and H2O reabsorption in kidney and potassium excretion thus decreases BP while sparing potassium
ex. spironolactone
spironolactone
aldosterone antagonist
potassium sparing diuretic
potassium channel activator
opens KATP channel causing hyperpolarization of cells and decreasing activity of calcium channels and calcium influx thus induces vasodilation
ex. minoxidil
minoxidil
potassium channel activator
vasodilator
last resort for severe HTN because very potent and long duration
endothelin receptor antagonist
blocks endothelin induced vasoconstriction
ex. bosentan
bosentan
blocks both ETA and ETB receptors of endothelin
vasodilation
alpha methyldopa
sympatholytic
decreases BP without affecting the kidney
safe to use in kidney compromised patients and during pregnancy
hydralazine
acts on arteries by unkown mechanism to decrease blood pressure
can cause tachycardia and increased cardiac output
only used short term for severe hypertension during pregnancy
Nitric Oxide
activates guanylyl cylcase to increase cGMP to alter PKG, cyclic nucleotide phosphodiesterase, and ion channels in order to decrease/block Ca++ channels and stop constriction
vasodilation
ex. nitroprusside
sacubitril
blocks neprilysin
neprilysin cleaves ANP, BNP, and CNP which usually induce vasoconstriction but also degrades ATII which usualy induce vasoconstriction
using ACEI with neprilysin will block increased ATII and result in only vasodilation
nitroprusside
NO
vasodilation
entresto
valsartan + sacubitril
ACEI and sacubitril (degrades neprilysin)
acetazolamide
inhibits carbonic andhydrase which normally breaks down HCO3 into CO2 and H2O
results in decreases H2O and Na+ absorptopn and alkaline urine (HCO3 is excreted and not absorbed)
osmotic diuretics
inhibit reabsorption of solute and water by altering the osmotic forces along the nephron in the proximal tubule
makes the lumen of tubule very concrentrated so water does not leave the lumen
ex. mannitol, glyverin, isosorbide, and urea
mannitol
osmotic diuretic
decreases H2O and solute reabsorption in proximal tubule
carbonic anhydrase inhibitors
inhibits carbonic anhydrase which decreases bicarb break down which decreases CO2 and H2O absorption which decreases H+ leaving cell via H/Na transporter leading to decreased Na+ reabsorption
results in decreases H2O and Na absorption and alkaline urine
ex. acetazolamide
loop diuretics
inhibit Na,2Cl, K symporter in loop of henle
decreases Na reabsorption and H2O reabsorption
risk of hypokalemia
ex. furosemide, ethocrynic (etharcinic) acid, bumetanide, torsemide
furosemide
loop diuretic
ethocrynic (etharcinic) acid
loop diuretic
bumetanide
loop diuretic
torsemide
loop diuretic
thiazide diuretics
block Na/Cl symporter in distal convoluted tubule
decreasing Na+ absorption and H2O absorption
risk of hypokalemia
ex. HCTZ, chlorthalidone, indapamide, metolazone
HCTZ
thiazide diuretic
chlorthalidone
thiazide diuretic
indapamide
thiazide diuretic
metolazone
thiazide diuretic
potassium sparing diuretics
inhibit either Na+ channel (ENAC) or aldosterone action in the principal cells which decreases the amount of K+ secretion and excretion
only has small volume changes
ex. Na+ channel inhibitors: amiloride, triamterene
ex. aldosterone antagonist: spironolactone, eplerenone
spironolactone
potassium sparing diuretic that acts on aldosterone
eplerenone
potassium sparing diuretic that acts on aldosterone
amiloride
potassium sparing diuretic that acts on ENAC
triamteren
potassium sparing diuretic that acts on ENAC
