-
abciximab
- platelet inhibitor
- binds between glycoprotein receptors
-
acetylcholine
cholinergic agonist-direct
-
albuterol
- beta2-adrenergic agonist
- vasodilation, bronchodilation (asthma)
-
alpha-methyldopa
alpha2-adrenergic agonist
-
aminocarproic acid
- treatment of bleeding
- promotes clot formation, prevents plasmin formation
-
aspirin
- platelet inhibitor
- inhibits prostaglanind formation
-
atenolol
- beta1-blocker
- used to treat cardiovascular diseases (angina, hypertension)
-
atorvastatin
- HMG-CoA reductase inhibitor
- inhibits synthesis of chol
-
atropine
- antimuscarinic
- cholinergic antagonist
-
beclomethasone
choinergic agonist-direct
-
bethanechol
cholinergic agonist-direct
-
-
cefotaxime
- inhibitor of cell wall synthesis
- inhibits peptidoglycan strands
-
chloramphenicol
protein synthesis inhibitors
-
cholestyramine
- bile acid sequestrant
- increases excretion of cholesterol thru feces
-
cimetidine
H2-histamine blocker
-
ciprofloxacin
inhibitors of DNA gyrase
-
clonidine
- alpha2-adreneric agonist
- presynaptic receptor (inhibits further NE release)
-
clozapine
neuroleptics, atypical
-
dextromethophan
cough suppressant
-
diazepam
- benzodiazepines
- decreases excitability of certain areas of spinal cord and brain
-
digoxin
- ionotropic agents
- digitalis
-
diphenhydramine
antihistamines
-
dobutamine
- beta1-adrenergic agonist
- used to stimulate the heart
-
enalapril
- ACE inhibitors
- will reduce afterload of heart (increasing cardiac output)
- decreases preload (reduces peripheral edema)
-
ephedrine
adrenergic agonist
-
epinephrine
adrenergic agonist
-
gemfibrozil
- fibric acid agents
- stimulate lipoprotein lipase activity (hydrolyzes TGs)
-
erythromycin
- protein synthesis inhibitors
- binds to 50s, inhibits translocation
-
gentamicin
- inhibitor of protein synthesis
- binds to 30s and distorts structure, thus inhibiting protein synthesis
- narrow spectrum
-
glipizide
oral hypoglycemic
-
heparin
- anticoagulants
- changes anti-thrombin III to interact with clotting factor
-
hydralazine
direct vasodilators
-
hydrochlorothiazide
- diuretics
- lowers plasma volume and decreases workload of heart
-
imipramine
- TCAs (antidepressants)
- drugs cause increase in neurtoransmitter NE and 5-HT
-
-
lithium salts
antimanics (bipolar)
-
losartan
- ARBs
- angiotensin I receptor blocker
-
methylphenidate
CNS stimulants
-
metoprolol
- beta-blocker
- prevent sympathetic compensatory response
-
milrinone
- ionotropic agents
- phosphodiesterase inhibitor
-
niacin
- antihyperlipidemia
- decreases VLDL levels and most potent at raising HDL
-
nicotine
ganglionic blockers
-
-
nitroglycerin
organic nitrate
-
omeprazole
proton pump inhibitor
-
oxymetazoline
alpha-adrenergic agonist (nasal decongestant)
-
penicillin G
- inhibitor of cell wall synthesis
- acts by attaching to the PBP at the active site
- prevents cross-link (making a non-functionable cell wall)
-
-
phenobarbital
- barbiturates
- increases GABA effects
-
phenylephrine
- alpha1-adrenergic agonist
- vasoconstriction (decrease b.p without affecting the heart)
-
physostigmine
- cholinergic agonist-indirect
- hypotension, bradycardia
-
prazosin
- alpha1-blocker
- used clinically to treat hypertension
-
sulfisoxazole
folic acid antagonist
-
propranolol
- beta-blocker
- used to treat cardiovascular diseases (angina, hypertension)
-
-
streptokinase
- thrombolytics
- breaks clots, forms complex with plasminogen
-
succinylcholine
depolarizing cholinergic antagonist
-
tetracycline
- protein synthesis inhibitors
- inhibit formation of protein synthesis by inhibiting tRNA
-
ticlopidine
- platelet inhibitors
- ADP inhibitor
-
trimethaphan
ganglionic blockers
-
tubocurarine
non-depolarizing cholinergic antagonist
-
vancomycin
- inhibitors of cell wall synthesis
- targets cell wall, interferes with cell membrane synthesis
-
vitamin K
treatment of bleeding
-
warfarin
- anticoagulants
- wont synthesize clotting factors
-
sedatives
hypnotics
tranquilizers
- CNS depressant
- induces sleep
- produce a calming effect
-
Treating depression
drugs cause increase in neurotransmitter NE and 5-HT
-
Mechanism of actions- SSRIs
- selective serotonin reuptake inhibitors
- inhibits reuptake of 5-HT
-
Mechanism of action TCA's
inhibit reuptake of NE and 5-HT
-
Mechanism of action- MAOIs
MAO breaks down the neurotransmitters NE, epinephrine, DA, and 5-HT (inhibits break down of N.Ts)
-
Hemostasis
the process of stopping blood flow
-
singals from undamaged tissue (2 molecules)
- prostacyclin
- nitric oxide
- inhibit platelet aggregation by formation of cAMP
-
receptors on platelets bind:
- thromnin
- thromboxanes
- exposed collagen
-
molecules released from granules taht promote platelet activation
TXA2, ADP, 5-HT, thrombin
-
What is happening to the platelet which is part of the activation process
change shape- release ADP, TXA2, 5-HT
-
What do you call the aggregation of activated platelets at teh site of injury?
hemolytic plug (primary plug)
-
What initiates the coagulation cascade
tissue facator expression (activated endothelial cells)
-
The activation of what molecule is the culmination of the coagulation cascade?
thrombin
-
What protein polymerizes and cross-links around the site of injury and found in the definitive (secondary) hemostatic plug
fibrin
-
What molecules are considered natural anticoagulants, limiting the size of the plug
PGI2, t-PA, nitric oxide, prostacyclin
-
effects of blocking calcium channels
- relaxation of smooth muscle (vasodilation)
- negative ionotropic effects on heart (decreases force of contraction)
- suppression of cardiac conduction
-
Goal of drug therapy for asthma and COPD
terminate acute bronchopasms and reduce frequency of attacks
-
Antibiotics goal of therapy
- disrupt the life cycle of the invading microorganism
- bacteriocidal
- bacteriostatic
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