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Pharmacology final Flashcards

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1
Q

abciximab (anticoagulant) MOA

A

inhibits GP IIb/IIIa receptor complex, blocks the binding of fibrinogen and VW factor so aggregation does not occur.

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2
Q

acetylcholine (cholinergic agonist direct) MOA

A

acts on nicotinic and muscarinic receptors–constriction of pupils, increases GI motility, bronchodilation, decreases HR, CO, BP, increases salivary, GI and gastric secretion, stimulates intestinal motility

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3
Q

albuterol (b2 agonist) MOA

A

Stimulates beta-2 receptors, bronchodilation

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4
Q

alpha-methyldopa (antihypertensive) MOA

A

binds alpha 2 receptors, lowers BP by causing vasodilation

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5
Q

alteplase (thombolytic) MOA

A

tissue plasminogen activator (tPA), binds fibrin and activates plasminogen that is bound in clot to DISSOLVE clot

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6
Q

aminocaproic acid (antifibrinolytic) MOA

A

inhibits plasminogen, helps keep clots

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7
Q

aspirin (anticoagulant) MOA

A

inhibits TXA2 synthesis, which inactivates enzyme that causes platelet aggregation. inhibits platelet function

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8
Q

atenolol (b1 blocker) MOA

A

blocks b1, decreases BP, antihypertensive

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9
Q

atorvastatin (antihyperlipidemic) MOA

A

inhibits HMG-CoA reductase enzyme so inhibits cholesterol synthesis, causes decrease in cholesterol, causes LDL receptor expression, more LDL removed from body

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10
Q

atropine (anticholinergic)

A

inhibits ach in smooth muscle, decreases CO, inhibits secretion. antimuscarinic

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11
Q

bethanechol (cholingeric agonist) MOA

A

stimulates muscarinic receptors which increases intestine movement and bladder muscle

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12
Q

caffeine (stimulant) MOA

A

inhibits phosphodiesterase which causes cAMP accumulation–> increases Ca2, increases HR,

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13
Q

carvedilol (b1 blocker) MOA

A

blocks beta receptors which causes peripheral vasodilation, reducing BP. Used for hypertension

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14
Q

cefotaxime (antibiotic) MOA

A

cell wall inhibitor, blocks PEP side chain cross-linking process which is part of the synthesis of peptidoglycan; target = transpeptidase enzyme, which is needed to make cell wall

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15
Q

chloramphenicol (antibiotic) MOA

A

protein synthesis inhibtor, binds 50S inhibits peptidyltransferase function of forming peptide bod

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16
Q

cholestyramine (bile acid sequestrant) MOA

A

increases excretion of cholesterol by preventing reabsorption of bile acid and salts in intestine

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17
Q

ciprofloxacin (antibiotic) MOA

A 
MOA = inhibit bacterial DNA synthesis
TARGET = DNA GYRASE & TOPOISOMERASE (relax DNA)
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18
Q

clavulanic acid (antibiotic) MOA

A

beta-lactamase inhibitor, keeps bacteria from breaking down penicillins

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19
Q

clonidine (alpha 2 adrenergic agonist) MOA

A

stimulates alpha 2 receptors, causes vasodilation

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20
Q

clopidogrel (anticoagulant) MOA

A

inhibits binding of ADP to P2Y12 receptor on platelets, inhibits activation of GP IIb/IIIa receptors

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21
Q

cocaine (stimulant) MOA

A

blocks D2 transporters, affects nt uptake/release. more D2 available

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22
Q

diazepam (benzodiazepine) MOA

A

facilitates GABA, cause relaxation, sedation

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23
Q

digoxin (inotropic) MOA

A

Inhibits Na+/K+ ATPase pump, which reduces Na+ from leaving the cell, which increases Ca2+ outside the cell and increases contractility. Increases force of contraction, increasing CO. Used for HF.

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24
Q

diltiazem (ca channel blocker) MOA

A

bind the L-type (ligand) Ca channels of cardiac and smooth muscle, this causes a conformational change and keeps the probability of the channel opening LOW. Calcium is important for muscle contraction

Relax smooth muscle = vasodilation

Negative inotropic effects = decrease contractility
Suppression of cardiac conduction

Vasodilation of coronary arteries and periph arterioles, decreases BP

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25
dobutamine (b1 agonist) MOA
stimulates beta-1 receptors, increases CO, BP and HR, decreases peripheral vascular resistance
26
enoxaparin (antithrombotic) MOA
binds antithrombin III, inhibition of thrombin
27
ephedrine (a/b agonist) MOA
alpha and beta adrenergic agonists, causes release of NE from sympathetic neurons, causes increased HR, BP, CO and increases peripheral resistance
28
epinephrine (a agonist) MOA
alpha-adrenergic effect, increases CO and HR, decreases renal perfusion, decreases peripheral vascular resistance, vasoconstriction
29
erythromycin (antibiotic) MOA
protein synthesis inhibitor MOA = inhibits translocation where ribosome is supposed to shift over one codon, so the ribosome gets stuck. P450 enzyme inhibitors BINDS 50S (large) subunit
30
fluoxetine (SSRI) MOA
selectively inhibits serotonin reuptake, improves mood
31
furosemide (loop diuretic) MOA
inhibits (Na+-K+-2 Cl−) co-transporter in the | thick ascending limb of the loop of Henle
32
gemfibrozil (fibrate antihyperlipidemic) MOA
stimulates lipoprotein lipase activity (lipoprotein lipase hydrolyses chylomicrons and VLDL), increases the clearance of VLDL
33
gentamicin (antibiotic) MOA
protein synthesis inhibitor MOA = acts during initiation, disrupts protein synthesis by causing misreading BIND 30S (small) subunit narrow spectrum
34
heparin (antithrombotic) MOA
binds antithrombin III and creates a conformational change that catalyzes inhibition of thrombin quickly
35
hydrochlorothiazide (thiazide diuretic) MOA
inhibits sodium chloride transport in the distal convoluted tubule. Act to increase excretion of water Result of drug = decreased blood volume, decrease BP
36
imipramine (TCA) MOA
neurotransmitter reuptake inhibiting of NE and serotonin, improves mood
37
insulin (hypoglycemic) MOA
exogenous insulin replaces insulin secretion (Type I) or is a supplement for insufficient insulin (Type II). Insulin inhibits fat breakdown by inhibiting intracellular lipase that would otherwise hydrolyze triglycerides to release fatty acids. Insulin binds to glycoprotein alpha/beta receptors on the surface of the cells
38
isoniazid (antimycobacterial) MOA
MOA = targets P-450 in liver | activated by mycobacterial catalase-peroxidase (KatG), and targets 2 acids in fatty acid synthesis
39
isosorbide dinitrate (antiangina)
relaxes vascular smooth muscle by converting to nitric oxide, which leads to increased cGMP, causing dephosphorylation that results in vascular smooth muscle relaxation. Decreases the workload of the heart. Increases blood supply to the heart muscle, decreases angina sensation vasodilator
40
lisinopril (ACE inihib) MOA
prevents ACE from converting angiotensin I to angiotensin II, preventing vasoconstriction Decrease blood volume, decrease workload Fewest side effects, given first decreases blood volume, lowers BP used for HF
41
lithium (antimanic) MOA
inhibits dopamine receptor postsynaptically, improves mood
42
losartan (ARB) MOA
block the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor found in vascular smooth muscle vasodilator
43
metformin (biguanide) MOA
insulin sensitizer, increases uptake of glucose by cells, decreasing insulin resistance. metformin reduces hepatic gluconeogenesis, slows absorption of sugars so that glucose uptake is improved.
44
methylphenidate (ADHD stimulant) MOA
blocks reuptake of NE and dopamine at presynaptic neurons, stimulates CNS, increases focus and attention
45
metoprolol (b blocker)
Blocks Beta-1 and beta-2, which decreases CO, lowering the HR, increases oxygen consumption to treat angina, hypertension, prevent MI, migraines, hyperthyroidism
46
milrinone (inotropic) MOA
inhibits phosphodiesterase, which increases cAMP intracellularly, which increases contractility of the heart. This can be used for HF
47
niacin (nicotinic acid) MOA
inhibits lipolysis in adipose tissue, decreases circulating fatty acids Decreases VLDL, raises HDL because there are no free fatty acids, which the liver would need in order to make VLDL
48
nicotine (ganglionic blocker) MOA
Acts as agonist at nicotinic ACh receptors, increases HR and respiratory rate, increases CO and BP
49
nitroglycerine (antiangina) MOA
vasodilator relaxes vascular smooth muscle by converting to nitric oxide, which leads to increased cGMP, causing dephosphorylation that results in vascular smooth muscle relaxation. Decreases the workload of the heart. Increases blood supply to the heart muscle by dilating large veins, decreases angina sensation.
50
penicillin G (antibiotic) MOA
cell wall inhibitor ( blocks PEP side chain cross-linking process which is part of the synthesis of peptidoglycan; target = transpeptidase enzyme, which is needed to make cell wall)
51
phenelzine (MAOI) MOA
non selectively inhibits monoamine oxidase, results in increased dopamine, serotonin, epi and NE, improves mood
52
phenobarbital (barbiturate) MOA
anticonvulsant inhibits GABA in the synapses, raises the threshold for seizures, so decreases seizures, or used as sedative hypnotic
53
phenylephrine (a1 agonist) MOA
decongestant, produces systemic vasoconstriction of arteries by stimulate alpha-1 receptors, causes vasoconstriction and decreases edema and increases nasal drainage
54
physostigmine (cholingeric agonist indirect) MOA
inhibits acetylcholinesterase, stimulates muscarinic and nicotinic sites, potentiates cholinergic activity, causes contraction of GI muscles, miosis, lowers HR and BP
55
prazocin (a1 blocker) MOA
antihypertensive, blocks alpha-1 receptor, lowers blood pressure to treat hypertension by decreasing PVR
56
propranolol (b blocker) MOA
Blocks Beta-1 and beta-2, which decreases CO, lowering the HR, increases oxygen consumption to treat angina, hypertension, prevent MI, migraines, hyperthyroidism
57
spironolactone (k sparing diuretic) MOA
antagonist of aldosterone, acting primarily through competitive binding of receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule.
58
succinylcholine (cholinergic antagonist) MOA
depolarizes motor endplate of neural junctions, causes sustained relaxed muscles; paralysis
59
sulfamethoxazole (antibiotic) MOA
folate inhibitor, Folic acid from diet--dihydrofolic acid (DHF) → tetrahydrofolic acid (THF) = needed for amino acid synthesis, purine synthesis, thymidine synthesis MOA = inhibit reduction step converting to THF Co-administered with trimethoprim (Bactrim) = synergy used for MRSA
60
tetracycline (antibiotic) MOA
``` protein synth inhibitor, antibiotic MOA = target 30S subunit and prevents binding of tRNA to mRNA BIND 30S (small) subunit ```
61
trimethaphan (ganglionic blocker) MOA
act on nicotinic receptors of paraSNS and sympathetic autonomic ganglia--blocking ANS output
62
tubocurarine (non depolarizing cholinergic antagonist) MOA
muscle relaxer, inhibits ACh at nicotinic receptors as a nondepolarizing competitive antagonist. Causes skeletal muscle relaxation
63
vancomycin (antibiotic) MOA
cell wall inhibitor, binds to peptidoglycan precursors, preventing polymerization that leads to cross-linking that is needed to make the cell wall in the bacteria--bactericidal.
64
vitamin K (antifibrinolytic) MOA
reverses bleeding from warfarin by attaching an extra carboxyl group to the clotting factor. With each reaction, vitamin K gets oxidized and with vitamin K epoxide reductase, vitamin K is reverted back to the reduced form.
65
warfarin (anticoagulant) MOA
inhibits vitamin K epoxide reductase (cofactor for clotting) which prevents vitamin K from being regenerated, therefore prevents clotting
66
``` what kind of receptors (GPCR or ligand) for: alpha beta muscarinic nicotinic ```
``` alpha = GPCR beta = GPCR muscarinic = GPCR nicotinic = ligand gated ```
67
what 4 things causes faster absorption fo drug?
protonation of weak acid, absence of food in GI, thin membranes, ability to mix with lipids
68
the process by which the amount of drug in body is reduced after administration before entering blood is:
first pass effect
69
what is an indicator of how long the drug will produce effect in body?
half life
70
if the plasma concentration of a drug declines with first order kinetics, this means what?
rate of elimination is constant
71
drugs that dissolve in lipids are __?
hydrophobic
72
Drug A has a high affinity for albumin. Drug B has a high affinity for albumin but is the dose is 100x the binding capacity of drug B. What happens to drug A when B is administered?
the tissue concentration of drug A increases--increased Vd
73
If drug X and Y have the same MOA, but drug X at a dose of 5mg produces the same magnitude of inhibition as 0.5mg of drug Y, this means that drug Y is more or less potent than drug X?
drug Y is 10x more potent than drug X
74
what are 4 details about the ANS?
- neurotransmitter released from presynaptic nerve - para sns activated under non stressful conditions - cholinergic receptors = muscarinic and nicotinic - parasympathomimetic is a drug that produces same effects as activation of para sns
75
What are 4 characteristics of paraSNS stimulation?
- increase in GI motility - bronchoconstriction - contraction of bladder - decrease HR
76
what is a characteristic of SNS stimulation?
inhibits salivation
77
what substance with similar molecular weight and lipid solubility would be absorbed fastest from small intestine (pH 5.4) into plasma (pH 7.4)?
weak acid with pKa 5.4
78
what are 3 SEs of antimuscarinic agent?
dry mouth, tachycardia, urinary retention
79
the potency of a drug is related to its ___ for its receptor
affinity
80
an increase in Vd increases ___
half life
81
will drugs bound to albumin have more/less difficulty getting distributed?
more difficulty
82
drug distribution depends on the unbound drug concentration gradient between ___ and tissue
blood
83
what do antagonists do?
block/inhibit action of agonist drugs
84
what psych drug has ability for high dependence?
phenobarbital
85
what do CNS depressants do to brain activity?
slow neuronal activity, cause relaxation to sedation at low doses, and sleep/anesthesia at high doses
86
in response to low BP the kidneys release __?
renin
87
Ca channel blockers do what?
block Ca2 from entering cell so no contraction
88
ACE inhibitors for HF do what 4 things?
decrease PVR decrease venous tone decrease BP increase CO
89
what HF med relives pulm congestion and periph edema?
diuretics
90
does direct dilation of venous blood vessels cause increased or decreased preload by increasing venous capacitance leading to increased CO?
decreased preload
91
ionotropic drugs cause increase or decrease in force of contractility which caused increased CO?
increase contractility
92
compensatory increases in HR and renin release in HF can be helped by what drug class?
beta blockers | metoprolol
93
what drug is given to treat thromboembolic disease to dissolve clots?
alteplase
94
what are 4 responses to a drop in BP?
activation of B1 receptors activation of a1 receptors increased renin release increased Na+/H20 retention
95
ACE inhibitor (lisinopril) does what 4 things?
decrease sympathetic output increase vasodilation of vasc smooth muscle decrease retention of Na/H20 increase bradykinin levels
96
thrombin catalyzes fibrinogen to ___?
fibrin
97
prostacyclin inhibits what?
platelet aggregation
98
calcium causes activation of what receptors in clotting?
GP IIb/IIIa
99
what is the primary role of chylomicrons?
carry triglycerides from intestine to tissues
100
what 4 things are mechanism affects of atorvastatin? | regarding hmg coa, concentration, ldl receptors, vldl
- inhibit HMG-Coa reductase leading to decrease in cholesterol synthesis - low concentration of cholesterol stimulates synth of LDL receptors - increase in LDL receptors promotes uptake of LDL from blood - low concentrations of cholesterol results in decreased secretion of VLDL
101
clopidogrel, losartan, spironolactone are competitive ___?
competitive antagonists
102
aspirin is special in that it is an ____
enzyme inhibitor
103
all antihypertensive meds cause what AE?
orthostatic hypotension
104
what 2 drugs are given to treat angina?
Ca channel blockers | B blockers

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