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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
Q

dobutamine (b1 agonist) MOA

A

stimulates beta-1 receptors, increases CO, BP and HR, decreases peripheral vascular resistance

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26
Q

enoxaparin (antithrombotic) MOA

A

binds antithrombin III, inhibition of thrombin

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27
Q

ephedrine (a/b agonist) MOA

A

alpha and beta adrenergic agonists, causes release of NE from sympathetic neurons, causes increased HR, BP, CO and increases peripheral resistance

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28
Q

epinephrine (a agonist) MOA

A

alpha-adrenergic effect, increases CO and HR, decreases renal perfusion, decreases peripheral vascular resistance, vasoconstriction

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29
Q

erythromycin (antibiotic) MOA

A

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

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30
Q

fluoxetine (SSRI) MOA

A

selectively inhibits serotonin reuptake, improves mood

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31
Q

furosemide (loop diuretic) MOA

A

inhibits (Na+-K+-2 Cl−) co-transporter in the

thick ascending limb of the loop of Henle

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32
Q

gemfibrozil (fibrate antihyperlipidemic) MOA

A

stimulates lipoprotein lipase activity (lipoprotein lipase hydrolyses chylomicrons and VLDL), increases the clearance of VLDL

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33
Q

gentamicin (antibiotic) MOA

A

protein synthesis inhibitor
MOA = acts during initiation, disrupts protein synthesis by causing misreading
BIND 30S (small) subunit
narrow spectrum

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34
Q

heparin (antithrombotic) MOA

A

binds antithrombin III and creates a conformational change that catalyzes inhibition of thrombin quickly

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35
Q

hydrochlorothiazide (thiazide diuretic) MOA

A

inhibits sodium chloride transport in the distal convoluted tubule.

Act to increase excretion of water
Result of drug = decreased blood volume, decrease BP

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36
Q

imipramine (TCA) MOA

A

neurotransmitter reuptake inhibiting of NE and serotonin, improves mood

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37
Q

insulin (hypoglycemic) MOA

A

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

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38
Q

isoniazid (antimycobacterial) MOA

A

MOA = targets P-450 in liver

activated by mycobacterial catalase-peroxidase (KatG), and targets 2 acids in fatty acid synthesis

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39
Q

isosorbide dinitrate (antiangina)

A

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

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40
Q

lisinopril (ACE inihib) MOA

A

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

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41
Q

lithium (antimanic) MOA

A

inhibits dopamine receptor postsynaptically, improves mood

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42
Q

losartan (ARB) MOA

A

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
Q

metformin (biguanide) MOA

A

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
Q

methylphenidate (ADHD stimulant) MOA

A

blocks reuptake of NE and dopamine at presynaptic neurons, stimulates CNS, increases focus and attention

45
Q

metoprolol (b blocker)

A

Blocks Beta-1 and beta-2, which decreases CO, lowering the HR, increases oxygen consumption to treat angina, hypertension, prevent MI, migraines, hyperthyroidism

46
Q

milrinone (inotropic) MOA

A

inhibits phosphodiesterase, which increases cAMP intracellularly, which increases contractility of the heart. This can be used for HF

47
Q

niacin (nicotinic acid) MOA

A

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
Q

nicotine (ganglionic blocker) MOA

A

Acts as agonist at nicotinic ACh receptors, increases HR and respiratory rate, increases CO and BP

49
Q

nitroglycerine (antiangina) MOA

A

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
Q

penicillin G (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)

51
Q

phenelzine (MAOI) MOA

A

non selectively inhibits monoamine oxidase, results in increased dopamine, serotonin, epi and NE, improves mood

52
Q

phenobarbital (barbiturate) MOA

A

anticonvulsant inhibits GABA in the synapses, raises the threshold for seizures, so decreases seizures, or used as sedative hypnotic

53
Q

phenylephrine (a1 agonist) MOA

A

decongestant, produces systemic vasoconstriction of arteries by stimulate alpha-1 receptors, causes vasoconstriction and decreases edema and increases nasal drainage

54
Q

physostigmine (cholingeric agonist indirect) MOA

A

inhibits acetylcholinesterase, stimulates muscarinic and nicotinic sites, potentiates cholinergic activity, causes contraction of GI muscles, miosis, lowers HR and BP

55
Q

prazocin (a1 blocker) MOA

A

antihypertensive, blocks alpha-1 receptor, lowers blood pressure to treat hypertension by decreasing PVR

56
Q

propranolol (b blocker) MOA

A

Blocks Beta-1 and beta-2, which decreases CO, lowering the HR, increases oxygen consumption to treat angina, hypertension, prevent MI, migraines, hyperthyroidism

57
Q

spironolactone (k sparing diuretic) MOA

A

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
Q

succinylcholine (cholinergic antagonist) MOA

A

depolarizes motor endplate of neural junctions, causes sustained relaxed muscles; paralysis

59
Q

sulfamethoxazole (antibiotic) MOA

A

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
Q

tetracycline (antibiotic) MOA

A 
protein synth inhibitor, antibiotic
MOA = target 30S subunit and prevents binding of tRNA to  mRNA
BIND 30S (small) subunit
61
Q

trimethaphan (ganglionic blocker) MOA

A

act on nicotinic receptors of paraSNS and sympathetic autonomic ganglia–blocking ANS output

62
Q

tubocurarine (non depolarizing cholinergic antagonist) MOA

A

muscle relaxer, inhibits ACh at nicotinic receptors as a nondepolarizing competitive antagonist. Causes skeletal muscle relaxation

63
Q

vancomycin (antibiotic) MOA

A

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
Q

vitamin K (antifibrinolytic) MOA

A

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
Q

warfarin (anticoagulant) MOA

A

inhibits vitamin K epoxide reductase (cofactor for clotting) which prevents vitamin K from being regenerated, therefore prevents clotting

66
Q 
what kind of receptors (GPCR or ligand) for: 
alpha 
beta
muscarinic
nicotinic
A 
alpha = GPCR
beta = GPCR
muscarinic = GPCR
nicotinic = ligand gated
67
Q

what 4 things causes faster absorption fo drug?

A

protonation of weak acid, absence of food in GI, thin membranes, ability to mix with lipids

68
Q

the process by which the amount of drug in body is reduced after administration before entering blood is:

A

first pass effect

69
Q

what is an indicator of how long the drug will produce effect in body?

A

half life

70
Q

if the plasma concentration of a drug declines with first order kinetics, this means what?

A

rate of elimination is constant

71
Q

drugs that dissolve in lipids are __?

A

hydrophobic

72
Q

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?

A

the tissue concentration of drug A increases–increased Vd

73
Q

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?

A

drug Y is 10x more potent than drug X

74
Q

what are 4 details about the ANS?

A
  • 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
Q

What are 4 characteristics of paraSNS stimulation?

A
  • increase in GI motility
  • bronchoconstriction
  • contraction of bladder
  • decrease HR
76
Q

what is a characteristic of SNS stimulation?

A

inhibits salivation

77
Q

what substance with similar molecular weight and lipid solubility would be absorbed fastest from small intestine (pH 5.4) into plasma (pH 7.4)?

A

weak acid with pKa 5.4

78
Q

what are 3 SEs of antimuscarinic agent?

A

dry mouth, tachycardia, urinary retention

79
Q

the potency of a drug is related to its ___ for its receptor

A

affinity

80
Q

an increase in Vd increases ___

A

half life

81
Q

will drugs bound to albumin have more/less difficulty getting distributed?

A

more difficulty

82
Q

drug distribution depends on the unbound drug concentration gradient between ___ and tissue

A

blood

83
Q

what do antagonists do?

A

block/inhibit action of agonist drugs

84
Q

what psych drug has ability for high dependence?

A

phenobarbital

85
Q

what do CNS depressants do to brain activity?

A

slow neuronal activity, cause relaxation to sedation at low doses, and sleep/anesthesia at high doses

86
Q

in response to low BP the kidneys release __?

A

renin

87
Q

Ca channel blockers do what?

A

block Ca2 from entering cell so no contraction

88
Q

ACE inhibitors for HF do what 4 things?

A

decrease PVR
decrease venous tone
decrease BP
increase CO

89
Q

what HF med relives pulm congestion and periph edema?

A

diuretics

90
Q

does direct dilation of venous blood vessels cause increased or decreased preload by increasing venous capacitance leading to increased CO?

A

decreased preload

91
Q

ionotropic drugs cause increase or decrease in force of contractility which caused increased CO?

A

increase contractility

92
Q

compensatory increases in HR and renin release in HF can be helped by what drug class?

A

beta blockers

metoprolol

93
Q

what drug is given to treat thromboembolic disease to dissolve clots?

A

alteplase

94
Q

what are 4 responses to a drop in BP?

A

activation of B1 receptors
activation of a1 receptors
increased renin release
increased Na+/H20 retention

95
Q

ACE inhibitor (lisinopril) does what 4 things?

A

decrease sympathetic output
increase vasodilation of vasc smooth muscle
decrease retention of Na/H20
increase bradykinin levels

96
Q

thrombin catalyzes fibrinogen to ___?

A

fibrin

97
Q

prostacyclin inhibits what?

A

platelet aggregation

98
Q

calcium causes activation of what receptors in clotting?

A

GP IIb/IIIa

99
Q

what is the primary role of chylomicrons?

A

carry triglycerides from intestine to tissues

100
Q

what 4 things are mechanism affects of atorvastatin?

regarding hmg coa, concentration, ldl receptors, vldl

A
  • 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
Q

clopidogrel, losartan, spironolactone are competitive ___?

A

competitive antagonists

102
Q

aspirin is special in that it is an ____

A

enzyme inhibitor

103
Q

all antihypertensive meds cause what AE?

A

orthostatic hypotension

104
Q

what 2 drugs are given to treat angina?

A

Ca channel blockers

B blockers

Nursing (7 decks)

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