Pharm Flashcards

1
Q

Bethanechol - MoA

A

Cholinomimetic - activates bladder and bowel smooth muscle; resistant to AChE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Carbachol - clinical use

A

constricts pupil and relieves intraocular pressure in glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Carbachol - MoA

A

Cholinomimetic - binds ACh receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Methacholine - Clinical use

A

challenge test for asthma diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Methacholine - MoA

A

cholinomimetic - stimulates muscarinic receptors in airway causing bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pilocarpine - clinical use

A

stimulator of sweat, tears, and saliva

treats open angle and closed angle glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pilocarpine - MoA

A

Cholinomimetic - contracts ciliary muscle of eye (open-angle glaucoma), contracts pupillary sphincter (closed-angle glaucoma); resistant to AChE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Rivastigmine/Donepezil - clinical use

A

alzheimer disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Rivistigmine/Donepezil - MoA

A

Anti-cholinesterase - increases ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Edrophonium - clinical use/MoA

A

diagnosis of myasthenia gravis (improves symptoms by increasing ACh in synapse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Neostigmine - clinical use

A

Post-op and neurgenic ileus and urinary retention; myasthenia gravis, reversal of NMJ blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Neostigmine - MoA

A

Anti-AChE - increases ACh

No CNS penetration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Physostigmine - clinical use

A

anticholinergic toxicity (atropine overdose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Physostigmine - MoA

A

anti-AChE - increases ACh

Crosses BBB - CNS activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pyridostigmine - clinical use

A

myasthenia gravis - long acting, increases muscle strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pyridostigmine - MoA

A

anti-AChE - increases ACh

Does NOT penetrate CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cholinomimetic agents - contraindications

A

exacerbation of COPD, asthma, and peptic ulcers in susceptible patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cholinesterase inhibitor poisoning

A

Organophosphates - irreversibly inhibit AChE

DUMBBELSS - diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle and CNS, lacrimation, sweating, salivation

Antidote - Atropine + Pralidoxime (given early - regenerates AChE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Atropine - clinical use

A

treat bradycardia and for ophthalmic applications (produces mydriasis and cycloplegia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Atropine - MoA and effects

A
Muscarinic antagonist:
Eye - pupil dilations and cycloplegia
Airway - decreases secretions
Stomach - decreases acid secretion
Gut - decreases motility
Bladder - decreases urgency (cystitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Atropine toxicity

A
Atropine Man - HOT as a hare (inc body temp due to dec sweating)
DRY as a bone (dry mouth, dry skin)
RED as a beet (flushed skin)
BLIND as a bat (cycloplegia)
MAD as a hatter (disorientation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Benzotropine - clinical use

A

Parkinson disease, acute dystonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Benzotropine - MoA

A

muscarinic antagonist (CNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Glycopyrrolate - clinical use

A

parental: preop use to reduce airway secretions
Oral: decrease drooling, peptic ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Glycopyrrolate - MoA

A

Muscarinic antagonist - GI/Respiratory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hyocyamine/dicyclomine - clinical use

A

antispasmodics for IBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hyoscyamine/dicyclomine - MoA

A

muscarinic antagonist - GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

ipratropium/tiotroprium - clinical use

A

COPD and asthma relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ipratropium/tiotropium - MoA

A

muscarinic antagonist - Respiratory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

solifenacin/tolterodine - clinical use

A

reduce bladder spasms and urge urinary incontinence - overactive bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

solifenacin/tolterodine - MoA

A

muscarinic antagonists - genitourinary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

scopolamine - clinical use

A

motion sickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

scopolamine - MoA

A

muscarinic antagonist - CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Albuterol/Salmeterol - clinical use

A

Albuterol - acute asthma

Salmeterol - long-term asthma/COPD control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Albuterol/Salmeterol - MoA

A

sympathomimetic - B2>B1 adrenergic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Dobutamine - clinical use

A

heart failure (inotropic>chronotropic), cardiac stress testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

dobutamine - MoA

A

sympathomimetic - B1>B2,alpha adrenergic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Dopamine - clinical use

A

unstable bradycardia, HF, shock

inotropic and chronotropic alpha effects predominate at high dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

dopamine - MoA

A

sympathomimetic - D1=D2> beta > alpha adrenergic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Epinephrine - clinical use

A

anaphylaxis, asthma, open-angle glaucoma

alpha effects predominate at high dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

epinephrine - MoA

A

sympathomimetic - beta > alpha adrenergic agonist

much stronger effect at B2-receptor than norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

isoproterenol - clinical use

A

electrophysiologic eval of tachycardia; can worsen ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

isoproterenol - MoA

A

sympathomimetic - B1 = B2 adrenergic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

norepinephrine - clinical use

A

hypotension (decreases renal perfusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

norepinephrine - MoA

A

sympathomimetic - alpha1 > alpha 2 > B1 adrenergic agonist

Significantly weaker at B2 than epinepherine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Phenylephrine - clinical use

A

Hypotension (vasoconstrictor); ocular procedures (mydriatic); rhinitis (decongestant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Phenylephrine - MoA

A

sympathomimetic - alpha 1 > alpha 2 adrenergic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

amphetamine - clinical use

A

narcolepsy, obesity, ADHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

amphetamine - MoA

A

indirect sympathomimetic general agonist
reuptake inhibitor
releases stored catecholamines

“turns on the faucet and blocks the drain”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

cocaine - clinical use

A

vasoconstriction and local anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

cocaine - MoA

A
indirect sympathomimetic - general agonist
reuptake inhibitor (blocks the drain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

cocaine - contraindications

A

do not give beta-blockers when suspected cocaine intoxications - can lead to unopposed alpha 1 activations -> extreme hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

ephedrine - clinical use

A

nasal decongestion, urinary incontinence, hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

ephedrine - MoA

A

indirect sympathomimetic - general agonist

releases stored catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Clonidine - clinical use

A

hypertensive urgency, does not decrease renal blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Clonidine - MoA

A

sympatholytic - alpha 2 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Clonidine - toxicity

A

CNS depression, bradycardia, hypotension, respiratory depression, miosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

methyldopa - clinical use

A

HTN in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

methyldopa - MoA

A

sympatholytic - alpha 2 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Methyldopa - toxicity

A

SLE-like syndrome, direct Coombs + hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Bethanechol - clinical use

A

postop ileus, neurogenic ileus, urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Phenoxybenzamine - clinical use

A

pheochromocytoma (preoperatively) to prevent catecholamine crisis (hypertension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

phenoxybenzamine - MoA

A

alpha blocker (irreversible)

side effects - orthostatic hypotension and reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Phentolamine - MoA

A

alpha blocker (reversible)

side effects - orthostatic hypotension and reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Phentolamine - clinical use

A

give to patients on MAI inhibitors who eat tyrosine rich foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Mirtazapine - clinical use

A

anti-depressant

side effects - sedation, increased serum cholesterol, increased appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Mirtazapine - MoA

A

alpha 2 selective blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Prazosin, terazosin, doxazosin, tamsulosin (-osin) - MoA

A

Selective alpha 1 blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Prazosin, terazosin, doxazosin, tamsulosin (-osin) - clinical use

A

urinary symptoms of BPH, PTSD (prazosin)
hypertension (NOT tamsulosin)

side effects - first dose orthostatic hypotension, dizziness, headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Beta blocker effects - Angina

A

decrease heart rate and contractility, resulting in decreased O2 consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Beta blocker effects - MI

A

decrease mortality (metoprolol, carvedilol, bisoprolol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

beta blocker effects - SVT

A

decrease AV conduction velocity - class II antiarrhythmics (esmolol and metoprolol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Beta blocker effects - hypertension

A

decrease CO, decrease renin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Beta blocker effects - HF

A

decrease mortality in chronic HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Beta blocker effects - glaucoma

A

Timolol - decreases secretion of aqueous humor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Beta blocker - toxicity

A

impotence, cardiovascular adverse effects (bradycardia, AV block, HF), CNS effects (seizures, sedation, sleep alterations), dyslipidemia (metoprolol), asthma/COPD exacerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

B1 selective antagonists (B1>B2)

A

acebutolol, atenolol, esmolol, metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Non-selective Beta antagonists

A

pindolol (partial agonist), propranolol, timolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Non-selective alpha and beta antagonists

A

carvediol and labetalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Antihypertensive therapy - primary HTN

A

thiazide diuretics, ACE-I, ARBs, dihydropyridine calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

antihypertensive therapy - HTN w/ HF

A

diuretics, ACE-I/ARBs, beta-blockers, aldosterone agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

antihypertensive therapy - diabetics

A

ACE-I, ARBs - protective against diabetic nephropathy

Calcium channel blockers, thiazide diuretics, beta-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

antihypertensive therapy - pregnancy

A

methyldopa (alpha-agonist), hydralazine, labetalol, nifedipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Dihydropyridine calcium channel blockers - clinical use

A

(Amlodipine)

HTN, Angina (including Prinzmetal), Raynaud phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Dihydropyridine calcium channel blockers - MoA

A

(Amlodipine)
block voltage dependent calcium channels - decreased intracellular calcium - decreased muscle contractility (vascular smooth muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Dihydropyridine calcium channel blockers - toxicity

A

(amlodipine)

reflex tachycardia, gingival hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

non-dihydropyridine calcium channel blockers - MoA

A

Diltiazem and verapamil

block voltage dependent calcium channels - decreased intracellular calcium - decreased muscle contractility (heart) - decreases CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

non-dihydropyridine calcium channel blockers - clinical use

A

diltiazem and verapamil

HTN, angina, atrial fibrillation/flutter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

non-dihydropyridine calcium channel blockers - toxicity

A

verapamil - hyperprolactinemia, constipation, AV block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

hydralazine - clinical use

A

severe HTN, HF

safe during pregnancy; administer w/ beta blocker to prevent reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

hydralazine - MoA

A

increases cGMP - smooth muscle relaxation

vasodilates arterioles > veins

decreases afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

hydralazine - toxicity

A

compensatory tachycardia (contraindicated in angina, CAD), fluid retention, headache, angina

Lupus-like syndrome in slow-acetylators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Nitroprusside - clinical use

A

hypertensive emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Nitroprusside - MoA

A

increases cGMP via direct release of NO - dilation of arterioles and veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Nitroprusside - toxicity

A

cyanide toxicity - releases cyanide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Fenoldopam - clinical use

A

hypertensive emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Fenoldopam - MoA

A

dopamine D1 receptor agonist - coronary, peripheral, renal, and splanchnic vasodilation

decreases BP, increases natriuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Nitrates - nitroglycerin, isosorbide dinitrate and mononitrate

MoA

A

vasodilate by increasing NO in vascular smooth muscle - increased cGMP and smooth muscle relaxation

dilate veins&raquo_space; arterioles - decreases preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Nitrates - nitroglycerin, isosorbide dinitrate and mononitrate
Clinical use

A

angina, acute coronary syndrome, pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Nitrates - nitroglycerin, isosorbide dinitrate and mononitrate
toxicity

A

reflex tachycardia (treat with beta blockers), hypotension, flushing, headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

HMG-CoA reductase inhibitors (statins) - MoA

A

inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

HMG-CoA reductase inhibitors (statins) - lipid profile effects

A

decrease LDL&raquo_space;> TG = VLDL

increase HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

HMG-CoA reductase inhibitors (statins) - toxicity

A

hepatotoxic - increased LFT

myopathy when used with fibrates or niacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Bile acid resins (cholestyramine) - MoA

A

prevent intestinal reabsorption of bile acids - liver uses cholesterol to produce new bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Bile acid resins (cholestyramine) - lipid profile effects

A

decreases LDL

slightly increases HDL and TG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Bile acid resins (cholestyramine) - toxicity

A

GI upset, decreased absorption of other drugs and fat-soluble vitamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Ezetimibe - MoA

A

prevents cholesterol absorption at the small intestine brush border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Ezetimibe - lipid profile effects

A

decreases LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Ezetimibe - toxicity

A

rarely increases LFT, diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Fibrates (gemfibrozil) - MoA

A

upregulate LPL - increase TG clearance

Active PPAR-alpha to induce HDL synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Fibrates (gemfibrozil) - lipid profile effect

A

decrease TG»>LDL, increase HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Fibrates (gemfibrozil) - toxicity

A

myopathy (inc risk w/ statins)

cholesterol gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Niacin (B3) - lipid profile effect

A

decreases LDL>TG

increases HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Niacin (B3) - MoA (lipids)

A

inhibits lipolysis in adipose tissue; reduces hepatice VLDL synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Niacin (B3) - toxicity (lipid-lowering agent)

A

red, flushed face (due to inc PG) - decreased by taking NSAIDS
hyperglycemia, hyperuricemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Cardiac glycosides (digoxin) - MoA

A

inotrope
directly inhibits sodium-potassium ATPase - indirectly inhibits sodium-calcium exchange - increases intracellular calcium - + inotropy

Indirect - stimulates vagus nerve - decreases HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Cardiac glycosides (digoxin) - clinical use

A

HF, atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Cardiac glycosides (digoxin) - toxicity

A

cholinergic - nausea, vomiting, diarrhea, blurry vision, arrhythmias, AV block

hyperkalemia - poor prognosis

Factors increasing toxicity - renal failure, hypokalemia, verapamil, amiodarone, quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Cardiac glycosides (digoxin) - antidote

A

slowly normalize potassium, cardiac pacer, anti-digoxin Fab fragments, magnesium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Quinidine - MoA

A

Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
increases APD and ERP in ventricular AP (decreases slope of phase 0)
increases QT interval (prolongs repolarization - phase 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Procainamide - MoA

A

Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
increases APD and ERP in ventricular AP (decreases slope of phase 0)
increases QT interval (prolongs repolarization - phase 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Disopyramide - MoA

A

Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)
increases APD and ERP in ventricular AP (decreases slope of phase 0)
increases QT interval (prolongs repolarization - phase 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Quinidine - clinical use

A

Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)

atrial and ventricular arrythmias, re-entrant and ectopic SVT and VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Procainamide - clinical use

A

Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)

atrial and ventricular arrythmias, re-entrant and ectopic SVT and VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Disopyramide - clinical use

A

Class IA antiarrhythmic - blocks open/active sodium channels (phase 0)

atrial and ventricular arrythmias, re-entrant and ectopic SVT and VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Quinidine - toxicity

A

Cinchonism (headache and tinnitus)
thrombocytopenia
torsades de pointes due to long QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Procainamide - toxicity

A

Reversible SLE - like symptoms (slow acetylators)
thrombocytopenia
torsades de pointes due to long QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Disopryamide - toxicity

A

Heart failure
thrombocytopenia
torsades de pointes due to long QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Lidocaine - MoA

A

Class IB antiarrhythmic - blocks inactive sodium channels (phase 0)

decrease slope of phase 0 and shorten AP duration
preferentially affect ischemic or depolarized purkinje and ventricular tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Mexiletine - MoA

A

Class IB antiarrhythmic - blocks inactive sodium channels (phase 0)

decrease slope of phase 0 and shorten AP duration
preferentially affect ischemic or depolarized purkinje and ventricular tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Lidocaine - clinical use

A

acute ventricular arrhythmias (post-MI)

digitalis induced arrythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Mexiletine - clinical use

A

acute ventricular arrhythmias (post-MI)

digitalis induced arrythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Lidocaine - toxicity

A

least cardiotoxic antiarrhythmics

CNS stimulation - seizures; CNS depression; CV depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Mexiletine - toxicity

A

least cardiotoxic antiarrhythmics

CNS stimulation - seizures; CNS depression; CV depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

flecainide - MoA

A

Class IC antiarrhythmic - blocks fast sodium channels (phase 0)

decreases slope of phase 0, significantly prolongs ERP in AV node and accessory bypass tracks
No effect of ERP in purkinje and ventricles; minimal effect on AP duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Propafenone - MoA

A

Class IC antiarrhythmic - blocks fast sodium channels (phase 0)

decreases slope of phase 0, significantly prolongs ERP in AV node and accessory bypass tracks
No effect of ERP in purkinje and ventricles; minimal effect on AP duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Flecainide - clinical use

A

SVTs, including atrial fibrillation

last resort in refractory VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Propafenone - clinical use

A

SVTs, including atrial fibrillation

last resort in refractory VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Flecainide - toxicity

A

pro-arrhythmic (post-MI) - sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Propafenone - toxicity

A

pro-arrhythmic (post-MI) - sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Class II antiarrhythmics

A

Beta blockers!
Esmolol (cardioselective)
metoprolol, propranolol, atenolol, timolol, carvedilol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Class II antiarrhythmics - MoA

A

Beta blockers
decrease SA and AV nodal activity by decreasing cAMP and calcium currents

suppress abnormal pacemaker activity by decreasing slope of phase 4 (prolonged depolarization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Class II antiarrhythmics - clinical use

A

SVT, ventricular rate control in atrial flutter and atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Class II antiarrhythmics - toxicity

A

impotence, exacerbation of COPD/asthma, CV effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alteration)

may mask symptoms of hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Amiodarone - MoA

A

Antiarrhythmics - Class III (mimics I,II,III,IV) - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Ibutilide - MoA

A

Antiarrhythmics - Class III - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Sotalol - MoA

A

Antiarrhythmics - Class III - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Dofetilide - MoA

A

Antiarrhythmics - Class III - potassium channel blocker - slows phase 3 - prolongs repolarization
increases AP duration, increases ERP, increases QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Amiodarone - clinical use

A

atrial fibrilation, atrial flutter, VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Sotalol - clinical use

A

atrial fibrilation, atrial flutter, VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Ibutilide - clinical use

A

atrial fibrilation, atrial flutter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Dofetilide - clinical use

A

atrial fibrilation, atrial flutter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Amiodarone - toxicity

A

pulmonary fibrosis (check PFTs)
hepatotoxicity (check LFTs)
hyperthyroidism (Check TFTs)
acts as hapten - blue/grey skin deposits - photodermatitis
neurologic effects
constipation
CV effects - bradycardia, heart block, HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Class IV antiarrhythmics

A

verapamil, diltiazem
calcium channel blockers - block slow calcium channels - slow rise of AP (phase 0) and prolong repolarization (phase 3)

decrease conduction velocity, increase ERP, increase PR
prevent nodal arrhythmias, rate control in atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Adenosine

A

antiarrhythmic - increases potassium efflux - hyperpolarizes the cell and decreases intracellular calcium (Gi coupled - decreases cAMP)

diagnose/abolish SVT

Very short acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Aspart, glulisine, lispro - MoA

A

rapid acting insulin - bind insulin receptor (tyrosine kinase)
Liver: increases glucose stored as glycogen
Muscle: increases glycogen, protein synthesis; increases potassium uptake
Fat: increases TG storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Detemir, glargine - MoA

A

long acting insulin - bind insulin receptor (tyrosine kinase)
Liver: increases glucose stored as glycogen
Muscle: increases glycogen, protein synthesis; increases potassium uptake
Fat: increases TG storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Metformin - MoA

A

biguanide - mechanism unknown
increases glycolysis, peripheral glucose uptake (insulin sensitivity)
decreases gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Metformin - clinical use

A

oral - first line therapy for T2DM
cause modest weight loss

can be used in pts w/o islet cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Metformin - toxicity

A

GI upset, lactic acidosis (contraindicated in renal insufficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Chlorpropamide, tolbutamide - MoA

A

first gen sulfonylureas

close potassium channel in beta-cell membrane - cell depolarizes - insulin release via calcium influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Chlorpropamide, tolbutamide - clinical use

A

first gen sulfonylureas

stimulate release of endogenous insulin in T2DM.
Requires some islet cell function to work (not for T1DM).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Chlorpropamide, tolbutamide - toxicities

A

first gen sulfonylureas

risk of hypoglycemia (renal failure)
disulfiram-like effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Glimepiride, glipizide, glyburide - MoA

A

2nd gen sulfonylureas

close potassium channel in beta-cell membrane - cell depolarizes - insulin release via calcium influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Glimepiride, glipizide, glyburide - clinical use

A

2nd gen sulfonylureas

stimulate release of endogenous insulin in T2DM.
Requires some islet cell function to work (not for T1DM).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Glimepiride, glipizide, glyburide - toxicity

A

2nd gen sulfonylureas

risk of hypoglycemia (renal failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Pioglitazone, rosiglitazone - MoA

A

Glitazones/thiazolidinediones

increase insulin sensitivity in peripheral tissue
binds to PPAR-gamma nuclear transcription regulator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Pioglitazone, rosiglitazone - clinical use

A

Glitazones/thiazolidinediones

mono- or combined therapy for T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Pioglitazone, rosiglitazone - toxicity

A

Glitazones/thiazolidinediones

weight gain, edema
hepatotoxicity, HF, increased risk of fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

exenatide, liraglutide - clinical use/MoA

A

GLP-1 analogs - T2DM

increase insulin
decrease glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

exenatide, liraglutide - toxicity

A

GLP-1 analogs - T2DM

nausea, vomiting, pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

linagliptin, saxagliptin, sitagliptin - clinical use/MoA

A

DPP-4 inhibitors - T2DM

increase insulin
decrease glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

linagliptin, saxagliptin, sitagliptin - toxicity

A

DPP-4 inhibitors

mild urinary or respiratory infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

pramlintide - clinical use/MoA

A

amylin analogs - T2DM, T1DM

decrease gastric emptying
decrease glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

pramlintide - toxicity

A

hypoglycemia, nausea, diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

canagliflozin - clinical use/MoA

A

SGLT-2 inhibitors - Type 2 DM

block reabsorption of glucose in PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

canagliflozin - toxicity

A

SGLT-2 inhibitors

glucosuria, UTIs, vaginal yeast infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

acarbose, miglitol - clinical use, MoA

A

alpha-glucosidase inhibitors - T2DM

delayed carbohydrate hydrolysis and glucose absorption - decreased postprandial hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

propylthiouracil - MoA/clinical use

A

block thyroid peroxidase, inhibiting the oxidation of iodide and then organification (coupling) or iodine - inhibition of thyroid hormone synthesis
Blocks 5-deiodinase - decreases peripheral conversion of T4 to T3

hyperthyroidism; can be used in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

methimazole - MoA/clinical use

A

block thyroid peroxidase, inhibiting the oxidation of iodide and then organification (coupling) or iodine - inhibition of thyroid hormone synthesis

Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

propylthiouracil - toxicity

A

skin rash, agranulocytosis, aplastic anemia, hepatotoxicity

182
Q

methimazole - toxicity

A

skin rash, agranulocytosis, aplastic anemia

can cause aplastic crisis - teratogenic

183
Q

Levothyroxine, triiodothyronine - MoA

A

thyroid hormone replacement

184
Q

Levothyroxine, triiodothyronine - toxicity

A

tachycardia, heat intolerance, tremors, arrhythmias

185
Q

ADH antagonists - clinical use

A

SIADH, block action of ADH and V2-receptor

186
Q

desmopressin

A

central DI

187
Q

oxytocin - clinical use

A

stimulates labor, uterine contractions, milk let-down

controls uterine hemorrhage

188
Q

somatostatin (otreotide) - clinical use

A

acromegaly, carcinoid syndrome, gastinoma, glocagonoma, esophageal varices

189
Q

Demeclocycline - MoA

A

ADH antagonist

190
Q

Demeclocycline - clinical use

A

SIADH

191
Q

Demeclocycline - toxicity

A

nephrogenic DI, photosensitivity, abnormalities in bones and teeth

192
Q

glucocorticoids - MoA

A

metabolic, catabolic, anti-inflammatory, immunosuppressive effects mediated by glucocorticoid response elements, inhibition of phospholipase A2, inhibition of transcription factors (NF-KB)

193
Q

glucocorticoids - clinical use

A

Addison disease
inflammation
immunosuppression
asthma

194
Q

glucocorticoids - toxicity

A
iatrogenic cushing syndrome
adrenal insufficiency (with abrupt stop)
195
Q

Cinacalcet - MoA

A

sensitizes calcium sensing receptor in PTH glands to circulating calcium - decreases PTH

196
Q

Cinacalcet - clinical use

A

hypercalcemia due to primary or secondary hyperparathyroidism

197
Q

Cinacalcet - toxicity

A

hypocalcemia

198
Q

valproic acid - clinical use

A

all types of seizures except status epilepticus
bipolar disorder
myoclonic seizures

199
Q

valproic acid - toxicity

A

GI, rare but fatal liver toxicity (measure LFTs), neural tube defects, tremor, weight gain

200
Q

gabapentin - MoA

A

inhibits high voltage gated calcium channels

GABA analog

201
Q

gabapentin - clinical uses

A

simple and complex seizures
postherpetic neuralgia
peripheral neuropathy

202
Q

phenobarbital (seizure) - MoA

A

increases GABAa action

203
Q

phenobarbital (seizure) - clinical use

A

simple, complex, tonic-clonic seizures

first line in neonates

204
Q

phenobarbital (seizure) - toxicity

A

sedation, tolerance, dependance, cardirespiratory depression

induces CYP450

205
Q

topiramate - MoA

A

blocks sodium channels, increases GABA action

206
Q

topiramate - clinical use

A

simple, complex, tonic-clonic seizures

migraine prevention

207
Q

topiramate - toxicity

A

sedation, metal dulling, kidney stones, weight loss

208
Q

Lamotrigine - MoA

A

blocks voltage gated sodium channels

209
Q

Lamotrigine - clinical use

A

all seizure types except status epilepticus

210
Q

Lamotrigine - toxicity

A

Stevens-Johnson syndrome (titrated slowly)

211
Q

levetiracetam - MoA

A

unknown - may modulate GABA and glutamate release

212
Q

levetiracetam - clinical use

A

simple, complex, tonic-clonic seizures

213
Q

Tiagabine - MoA

A

increases GABA by inhibiting reuptake

214
Q

Tiagabine - clinical use

A

simple and complex seizures

215
Q

Vigabatrin - MoA

A

increases GABA by irreversibly inhibiting GABA transaminase

216
Q

Vigabatrin - clinical use

A

simple and complex seizures

217
Q

Barbiturates (general) - MoA

A

Phenobarbitol, pentobarbitol, thiopental, secobarbital

facilitate GABAa action by increasing DURATION of chloride channel opening - decreases neuronal firing

218
Q

Barbiturates (general) - clinical use

A

sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)

219
Q

Barbiturates (general) - toxicity

A

respiratory and CV depression
CNS depression
induces CYP450
contraindicated in porphyria

220
Q

benzodiazepines (general) - MoA

A

facilitate GABAa action by increasing FREQUENCY of chloride channel opening.
decrease REM sleep
most have long half-life and active metabolites

221
Q

short-acting benzodiazepines

A

alprazolam, triazolam, oxazepam, midazolam

higher addictive potential

222
Q

benzodiazepines - clinical use

A

anxiety, spasticity, status epilepticus (lorazepam/diazepam), alcohol detox (DTs), night terrors, sleepwalking, general anesthetic, hypnotic

223
Q

benzodiazepines - toxicity

A

daytime drowsiness assoc w/ ataxia and falls

dependence, additive CNS depression w/ EtOH

Treat OD with flumazenil

224
Q

Zolpidem, Zaleplon, Eszoplicone - MoA

A

non-benzo hypnotics

act via BZ1 subtype of GABA receptor

225
Q

Zolpidem, Zaleplon, Eszoplicone - clinical use

A

insomnia

226
Q

Zolpidem, Zaleplon, Eszoplicone - toxicity

A

ataxia, headache, confusion
decreased dependence
short duration (rapid liver metabolism)

227
Q

Malignant hyperthermia

A

due to inhaled anesthetics + succinylcholine = fever and sever muscle contractions

antidote = dantrolene

228
Q

Thiopental - IV anesthetic

A

high potency, high lipid solubility, rapid entry into brain and rapid redistribution to muscle/fat

decreases cerebral blood flow

229
Q

Midazolam - IV anesthetic

A

benzo - short-acting

may cause severe post-op respiratory depression and decreased BP (treat w/ flumazenil); anterograde amnesia

230
Q

Ketamine (anesthetic)

A

IV arylcyclohexylamine - PCP analog that acts as dissociative anesthetic

blocks NMDA receptors

increases cerebral blood flow

231
Q

Propofol (anesthetic)

A

IV - used in ICU for sedation
Potentiates GABAa

rapid induction, good for short procedures
less post-op nausea than thiopental

232
Q

local anesthetics (esters and amides) - MoA

A

block sodium channels by binding receptors on inner portion of channel - prefer activated channels, so most effective in rapidly firing neurons

pain>temp>touch>pressure

small myelinated > small unmyelinated > large myelinated > large unmyelinated

233
Q

succinylcholine - MoA

A

depolarizing neuromuscular block

strong ACh receptor agonist - produces sustained depolarization and prevents muscle contraction

selective for motor (nicotinic) receptors

234
Q

succinylcholine - phase I blockade

A

prolonged depolarization - no antidote

potentiated by cholinesterase inhibitors

235
Q

succinylcholine - phase II blockade

A

repolarized but blocked - ACh receptors are available but desensitized
antidote is cholinesterase inhibitors

236
Q

succinylcholine - toxicity

A

hypercalcemia, hyperkalemia, malignant hyperthermia

237
Q

Tubocurarine, atracurium, pancuronium, etc

A

non-depolarizing neuromuscular blocking drugs
competitive ACh antagonists

reverse blockage with neostigmine (give w/ atropine to prevent muscarinic effects), edrophonium, and cholinesterase inhibitors

238
Q

Dantrolene - MoA

A

prevents release of calcium from SR of skeletal muscle

239
Q

Dantrolene - clinical use

A

malignant hyperthermia and neuroleptic malignant syndrome (antipsychotics)

240
Q

Baclofen - MoA

A

activates GABA B receptors at spinal cord - induces skeletal muscle relaxation

241
Q

Baclofen -CLINICAL USE

A

back pain/muscle spasms

242
Q

cyclobenzaprine - MoA

A

centrally affecting skeletal muscle relaxant

structurally similar to TCAs - similar anticholinergic side effects

243
Q

cyclobenzaprine - clinical use

A

muscle spasms

244
Q

L-Dopa - MoA

A

increases level of dopamine in brain (dopamine precursor)

crosses BBB and is converted by dopa decarboxylase to dopamine

245
Q

Carbidopa - MoA

A

peripheral Dopa Decarboxylase inhibitor - allows more L-Dopa to enter CNS and limits peripheral side effects

246
Q

L-Dopa - toxicity

A

arrhythmias from increased peripheral formation of catecholamines
long term - dyskinesias following administration, akinesia between doses (“on/off” phenomenon)

247
Q

Selegine - MoA

A

selectively inhibits MAO-B increasing the availability of dopamine

248
Q

selegiline - clinical use

A

adjunctive to L-Dopa in parkinson; may enhance adverse effects of L-Dopa

249
Q

Tolcapone/Entacapone - MoA

A

COMT inhibitors - block peripheral conversion of L-Dopa to 3-O-methyldopa

Tolcapone - also central COMT inhibitor and blocks conversion of dopamine to 3-MT in CNS

250
Q

Bromocriptine - MoA

A

dopamine agonist (ergot) (parkinson disease)

251
Q

pramipexole, ropinirole - MoA

A

dopamine agonist (non-ergot) (parkinson disease)

252
Q

Amantadine - MoA

A

increases dopamine release and inhibits reuptake
(Parkinson disease)

also used as antiviral - influenze and rubella

253
Q

Benzotropine - MoA

A

antimuscarinic that improves tremor and rigidity in parkinson disease
curbs excess cholinergic activity

254
Q

Memantine

A

NMDA receptor antagonist - helps prevent excitotoxicity (mediated by calcium)

Alzheimer Disease

dizziness, confusion, hallucinations

255
Q

Tetrabenazine and reserpine - MoA/clinical use

A

inhibit vesicular monoamine transporter (VMAT) - limits dopamine packaging and release - decrease dopamine availability

Huntington disease

256
Q

Haloperidol - MoA/clinical use

A

D2 receptor antagonist - Huntington

257
Q

Sumatriptan - MoA

A

5-HT-1B/1D agonists
inhibit trigeminal nerve activation
prevent vasopeptide release
induce vasonstiction

258
Q

Sumatriptan - toxicity

A

coronary vasospasm - contraindicated in Prinzmetal angina or CAD
mild paresthesia

259
Q

leuprolide - MoA

A

GnRH analog

pulsatile = agonist; continuous = antagonist

260
Q

leuprolide - clinical use

A

pulsatile - infertility

continuous - prostate cancer, uterine fibroids, precocious puberty

261
Q

estrogens (ethinyl estradiol, DES, mestranol) - clinical use

A

hypogonadism or ovarian failure, menstrual abnormalities, HRT

men - androgen-dependent prostate cancer

262
Q

clomiphene - MoA

A

selective estrogen receptor modulator
antagonist at estrogen receptors in hypothalamus - prevents normal feedback inhibition and increases the release of LH and FSH from pituitary, stimulating ovulation

263
Q

clomiphene - clinical use

A

stimulates ovulation - infertility due to anovulation

264
Q

tamoxifen - MoA

A

selective estrogen receptor modulator - antagonist at breast; agonist at bone/uterus

265
Q

tamoxifen - clinical use

A

treat/prevent recurrence of ER/PR + breast cancer

266
Q

raloxifene - MoA

A

selective estrogen receptor modulator - antagonist at breast/uterus; agonist at bone

267
Q

raloxifene - clinical use

A

osteoporosis

268
Q

anastrozole/exemestane - MoA

A

aromatase inhibitors

269
Q

anastrozole/exemestane - clinical use

A

ER + breast cancer in post-menopausal women

270
Q

progestin - MoA

A

bind progesterone receptors - decrease growth and increase vascularization of endometrium

271
Q

progestin - clinical use

A

oral contraceptives, endometrial cancer, abnormal uterine bleeding

272
Q

mifepristone - MoA

A

competitive inhibitor of progestins at progesterone receptors

273
Q

mifepristone - clinical use

A

termination of pregnancy (co-admin w/ misoprotol - PGE1)

274
Q

oral contraceptives

A

estrogen and progestins inhibit LH/FSH - prevents estrogen surge - prevents LH surge - no ovulation

progestins - thicken cervical mucus and inhibit endometrial proliferation

275
Q

terbutaline, ritodrine - MoA

A

B2 agonists that relax the uterus

276
Q

terbutaline, ritodrine - clinical use

A

decrease contraction frequency in women during labor

277
Q

danazol - MoA

A

synthetic androgen that acts as partial agonist at androgen receptors

278
Q

danazol - clinical use

A

endometriosis, hereditary angioedema

279
Q

testosterone, methyltestosterone - MoA

A

agonists at all androgen receptors

280
Q

testosterone, methyltestosterone - clinical use

A

hypogonadism, promotes development of secondary sex characteristics, stimulates anabolism to promote recovery (post-burn/injury)

281
Q

Finasteride - MoA

A

5a-reductase inhibitor

282
Q

Finasteride - clinical use

A

male pattern baldness, BPH

283
Q

flutamide - MoA

A

nonsteroidal competitive inhibitor at androgen receptors

284
Q

flutamide - clinical use

A

prostate carcinoma

285
Q

ketoconazole - MoA

A

inhibits 17,20-desmolase - inhibits steroid synthesis

286
Q

ketoconazole - clinical use

A

PCOS - reduction of androgen symptoms

can cause gynecomastia and amenorrhea

287
Q

spironolactone - clinical use

A

PCOS - reduction of androgen symptoms

can cause gynecomastia and amenorrhea

288
Q

spironolactone - MoA

A

inhibits steroid binding, 17a-hydroxylase, and 17,20-desmolase

289
Q

tamsulosin - MoA

A

alpha-1 agonist - selective for alpha 1A,D receptors in prostate

inhibits smooth muscle contraction

290
Q

tamsulosin - clinical use

A

BPH

291
Q

sildenafil, vardenafil, tadalafil - MoA

A

inhibit PDE-5 - increases cGMP, smooth muscle relaxation in corpus cavernosum

increases blood flow and penile erection

292
Q

sildenafil, vardenafil, tadalafil - toxicity

A

headache, flushing, dyspepsia, cyanopsia

life-threatening hypotension in pts taking nitrates

293
Q

minoxidil - MoA

A

direct arteriolar vasodilator

294
Q

minoxidil - clinical use

A

androgenetic alopecia; severe refractory hypertension

295
Q

Burkitt Lymphoma

A

increased C-myc activity

t(8,14)

296
Q

CML

A

BCR-ABL translocation (9,22)

increased tyrosine kinase activity

297
Q

Heparin - MoA

A

activator of antithrombin - decreases thrombin and factor Xa

short halflife

298
Q

Heparin - clinical use

A

immediate anti-coag for PE, acute coronary syndrome, MI, DVT

use during pregnancy (does NOT cross placenta)

Monitor with PTT

299
Q

Heparin - toxicity

A

bleeding, HIT, osteoporosis, drug-drug interactions

Rapid reversal - protamine sulfate (negatively charged - binds positively charged heparin molecules)

300
Q

Heparin - LMWH

A

enoxaprarin, dalteparin - act more on factor Xa
better bioavailability, longer half-life
can be administered subcutaneously w/o lab monitoring
Not easily reversible

301
Q

Fondaparinux

A

direct Xa inhibitor

302
Q

Heparin-induced thrombocytopenia

A

development of IgG antibodies against heparin-bound platelet factor 4 (PF4)

antibody-heparin-PF4 complex activates platelets - thrombosis and thrombocytopenia

STOP heparin, do NOT give coumadin

303
Q

argatroban, bivalirudin, dabigatran

A

direct thrombin inhibitors - use in pts with HIT

304
Q

Warfarin - MoA

A

interferes with gamma carboxylation of Vit-K dependent clotting factors (2,7,9,10,S,C)

increases PT

305
Q

warfarin - clinical use

A

chronic anti-coagulation
cannot use in pregnant women
follow PT/INR

306
Q

Warfarin - toxicity

A

bleeding, teratogen, skin/tissue necrosis, drug-drug interactions

early transient hypercoag - small vessel microthrombi (necrosis)
VitK - reversal
rapid reversal - fresh frozen plasma

307
Q

Apixaban, rivaroxaban - MoA

A

direct factor Xa inhibitors

308
Q

Apixaban, rivaroxaban - clinical use

A

treat/prophylax - DVT, PE, stroke (in pts with a.fib)

309
Q

Apixaban, rivaroxaban - toxicity

A

bleeding - no reversal agents

310
Q

Thrombolytics - MoA

A

alteplase, reteplase, streptokinase, tenecteplase

directly or indirectly aid conversion of plasminogen to plasmin
plasmin cleaves thrombin and fibrin clots
increase PT and PTT, no change in platelet counts

311
Q

thrombolytics - clinical use

A

alteplase, reteplase, streptokinase, tenecteplase

early MA, early ischemic stroke, severe PE

312
Q

thrombolytics - toxicity

A

alteplase, reteplase, streptokinase, tenecteplase

bleeding - contraindicated in pts w/ bleeding, history of intracranial bleed, recent surgery, severe HTN
treat toxicity w/ aminocaproic acid (inhibits fibrinolysis)

313
Q

Aspirin - MoA

A

irreversibly inhibits COX-1 and COX-2 by covalent acetylation
increase bleeding time, decrease TXA2 and prostaglandins
no effect on PT and PTT

314
Q

Aspirin - clinical use

A

antipyretic, analgesic, anti-inflammatory, anti-platelet

315
Q

aspirin - toxicity

A

gastic ulceration, tinnitus (CN VIII), acute renal failure (chronic use), interstitial nephritis, upper GI bleeding

OD - initially causes hyperventilation and respiratory alkalosis, transitions to metabolic mixed acidosis-respiratory alkalosis

316
Q

ADP receptor inhibitors - MoA

A

clopidogrel, prasugrel, ticagrelor (reversible), ticlopidine

inhibit platelet aggregation by irreversibly blocking ADP receptors
prevents expression of GP IIb/IIIa on platelet surface

317
Q

ADP receptor inhibitors - clinical use

A

acute coronary syndrome, coronary stenting
decrease incidence or recurrence of thrombotic stroke

clopidogrel, prasugrel, ticagrelor (reversible), ticlopidine

318
Q

ADP receptor inhibitor - toxicity

A

clopidogrel, prasugrel, ticagrelor (reversible), ticlopidine

neutropenia - ticlopidine!
TTP

319
Q

Cilostazol, dipyridamole - MoA

A

phosphodiesterase III inhibitor - increases cAMP in platelets resulting in inhibition of aggregation

vasodilators

320
Q

Cilostazol, dipyridamole - clinical use

A

intermittent claudication, coronary vasodilation, prevention of stroke/TIA, angina prophylaxis

321
Q

Cilostazol, dipyridamole - toxicity

A

nausea, headache, flushing, hypotension, abdominal pain

322
Q

GP IIb/IIIa inhibitors - MoA

A

abciximab, eptifibatide, tirofiban

bind GP IIb/IIIa on activated platelets and prevent aggregation

323
Q

GP IIb/IIIa inhibitors - clinical use

A

unstable angina, percutaneous transluminal coronary angioplasty

abciximab, eptifibatide, tirofiban

324
Q

GP IIb/IIIa inhibitors - toxicity

A

abciximab, eptifibatide, tirofiban

bleeding, thrombocytopenia

325
Q

meningitis in newborns

A

group B strep (gram + cocci, beta-hemolytic, catalase -, bacitracin resistant)
E. coli (gram - rods, lactose fermenter, metallic green on EBM)
listeria (gram + rods, tumbling motility)

326
Q

meningitis in children (6mo-6yrs)

A

S. pneumo (lancet shaped diplococci, gram+, alpha hemolytic, bile soluble)
N. meningitidis (gram - diplococci, ferments maltose)
H.influenzae B (gram - coccoid rods, grow on chocolate agar or w/s.aureus)
Enteroviruses

327
Q

meningitis - adults (6 yrs-60yrs)

A

S.pneumo (lancet shaped diplococci, gram+, alpha hemolytic, bile soluble)
N. meningitidis - #1 in teens (gram - diplococci, ferments maltose)
Enterovirus
HSV

328
Q

meningitis - 60+ yrs

A

S.pneumo (lancet shaped diplococci, gram+, alpha hemolytic, bile soluble)
gram negative rods
listeria (gram + rods, tumbling motility)

329
Q

methylphenidate, dextrophetamine, methamphetaine - MoA

A

CNS stimulants - increases catecholamines in the synaptic cleft, especially NE and dopamine

330
Q

methylphenidate, dextrophetamine, methamphetaine - clinical use

A

ADHD, narcolepsy, appetite control

331
Q

Antipsychotics - neuroleptics - MoA

A

haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine (haloperidol + -azines)

block D2 receptors - increases cAMP

332
Q

antipsychotics - neuroleptics - clinical use

A

schizophrenia, psychosis, acute mania, Tourette syndrome, huntington

333
Q

anti-psychotics - neuroleptics - toxicity

A

High potency (Trifluoperazine, fluphenazine, haloperidol) - neurologic side effects (extrapyramidal symptoms)

Low potency (chlorpromazine, thioridazine) - non-neuro side effects (anticholinergic, antihistamine, alpha 1 blockade effects)

chlorpromazine - corneal deposits
thioridazine - retinal deposits
Haloperidol - NMS, tardive dyskinesia

334
Q

neuroleptic malignant syndrome

A

rigidity, myoglobinuria, autonomic instability, hyperpyrexia

“FEVER - Fever, Encephalopathy, Vitals unstable, Enzymes elevated, Rigidity”

treat w/ dantrolene, D2 agonists

335
Q

tardive dyskinesia

A

oral-facial movements - long term antipsychotic use ( 4 mo)

336
Q

extrapyramidal system effects

A

treat with benztropine or diphenhydramine

4 hr - acute dystonia (muscle spasm, stiffness, oculogyric crisis)
4 day - akathisia (restlessness)
4 weeks - bradykinesia (parkinsonism)
4 months - tardive dyskinesia

337
Q

atypical antipsychotics

A

olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone - atypical for Old CLOZets to Quietly RISPER from A to Z

338
Q

atypical antipsychotics - MoA

A

olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

not completely understood - varied effects on 5-HT2, dopamine, and alpha and H1 receptors

339
Q

atypical antipsychotics - clinical use

A

olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

schizophrenia - positive and negative symptoms
bipolar, OCD, anxiety, depression, mania, tourette

340
Q

atypical antipsychotics - toxicity

A

olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone

fevers EPS and anticholinergic effects that neuroleptics; all prolong QT interval

Olanzapine/clozapine - significant weight gain
Clozapine - agranulocytosis (weekly WCB monitoring)
Risperidone - increase prolactin - decreases GnRH, LH, FSH - irregular menstruation

341
Q

Lithium - clinical use

A

mood stabilizer for bipolar
blocks relapse and acute manic events

treats SIADH

342
Q

Lithium - toxicity

A

LMNOP - Movement (tremor), Nephrogenic DI, hypOthyroidism, Pregnancy problems

causes Epstein’s anomaly in newborns if taken during pregnancy

excreted by kidneys - reabsorbed in PCT with Na+; Thiazide use can cause lithium toxicity

343
Q

Buspirone - MoA

A

stimulates 5-HT1A receptors

344
Q

Buspirone - clinical use

A

GAD
does not cause sedation, tolerance, addiction

takes 1-2 weeks for effect
does NOT interact with alcohol

345
Q

SSRIs

A

Fluoxetine, paroxetine, sertraline, citalopram

346
Q

SSRI - MoA

A

Fluoxetine, paroxetine, sertraline, citalopram

5-HT specific reuptake inhibitors

takes 4-8 wks for effect

347
Q

SSRI - clinical use

A

Fluoxetine, paroxetine, sertraline, citalopram

depression, GAD, panic disorder, OCD, bulimia, social phobias, PTSD

348
Q

SSRI - toxicity

A

Fluoxetine, paroxetine, sertraline, citalopram

fever than TCAs
GI distress, SIADH, sexual dysfunction
serotonin syndrome - w/ any drug that increases 5-HT

349
Q

serotonin syndrome

A

hyperthermia, confusion, myoclonus, CV instability, flushing, diarrhea, seizures

treat w/ cyproheptadine (5-HT2 receptor antagonist)

350
Q

SNRIs

A

venalfaxine, duloxetine

351
Q

SNRIs - MoA

A

venalfaxine, duloxetine

inhibit 5-HT and NE reuptake

352
Q

SNRIs - clinical use

A

depression

venalfaxine - GAD, panic disorder, PTSD
duloxetine - peripheral diabetic neuropathy

353
Q

SNRIs - toxicity

A

venalfaxine, duloxetine

increased BP, stimulant effects, sedation, nausea

354
Q

TCAs

A

amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

355
Q

TCAs - MoA

A

amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

block reuptake of NE and 5-HTq

356
Q

TCAs - clinical use

A

amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

depression, OCD (clomipramine), peripheral neuropathy, chronic pain, migraine prophylaxis

357
Q

TCAs - toxicity

A

amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine

Tri-C: Convulsions, Coma, Cardiotoxicity (arrhythmia due to inhibiting Na+ channel conduction) - use NaHCO3 to prevent arrhythmias

respiratory depression, hyperpyrexia, confusion and hallucinations in elderly due to anticholinergic effects

sedation, alpha 1 block (postural hypotension), atropine-like effects (amitriptyline > nortriptyline), prolong QT

358
Q

MAO-I

A

Tranylcypromine, phenelzine, isocarboxazid, selegiline (selective MAO-B)

359
Q

MAO-I - MoA

A

Tranylcypromine, phenelzine, isocarboxazid, selegiline (selective MAO-B)

increase amine neurotransmitters (NE, 5-HT, dopamine)

360
Q

MAO-I - clinical use

A

Tranylcypromine, phenelzine, isocarboxazid, selegiline (selective MAO-B)

atypical depression, anxiety

361
Q

MAO-I toxicity

A

Tranylcypromine, phenelzine, isocarboxazid, selegiline (selective MAO-B)

hypertensive crisis (w/ ingestion of tyramine) CNS stimulation

contraindicated w/ SSRIs, TCAs, St. John’s wort, meperidine, dextromethorphan - prevent serotonin syndrome

362
Q

bupropion - MoA

A

atypical antidepressant
smoking cessation
increase NE and dopamine (unknown mechanism)

363
Q

bupropion - toxicity

A

stimulant effect (structurally similar), headache, seizures in anorexic/bulimic pts, no sexual side effects

364
Q

Mirtazapine- MoA

A

alpha 2 antagonist - increases release of 5-HT and NE
potent 5-HT2 and 5-HT3 receptor antagonist

atypical antidepressants

365
Q

mirtazapine - toxicity

A

sedation, increased appetite, weight gain, dry mouth

366
Q

trazodone - MoA

A

blocks 5-HT2 and alpha 1 receptors

367
Q

trazodone - clinical use

A

atypical antidepressant - primarily for insomnia (high dose for anti-depressive effect)

368
Q

trazadone - toxicity

A

sedation, nausea, priapism (trazaBONE), postural hypotension

369
Q

Cluster A personality disorders

A

“Weird” - odd or eccentric, inability to develop meaningful social relationships, no psychosis, genetic association with schizophrenia

Paranoid “Accusatory”
Schizoid “Aloof”
Schizotypal “awkward”

370
Q

pervasive distrust and suspiciousness; projection is major defense mechanism

A

paranoid personality disorder (cluster A)

371
Q

voluntary social withdrawal, limited emotional expression, content with social isolation

A

schizoid personality disorder - cluster A

372
Q

eccentric appearance, odd beliefs/magical thinking, interpersonal awkwardness

A

schizotypal personality disorder - cluster A

373
Q

cluster B personality disorders

A

dramatic, emotional, erratic
generic association with mood disorders and substance abuse

“Wild” (Bad to the Bone)
Antisocial, borderline, histrionic, narcissitic

374
Q

disregard for and violation of the rights of others, criminality, impulsivity

A

antisocial PD - cluster B

M»F; must be >18 w/ history of conduct disorder

375
Q

unstable mood and interpersonal relationships, impulsivity, self-mutilation, boredom, sense of emptiness

A

borderline PD - cluster B

F»M

splitting = major defense mechanism

376
Q

excessive emotionality and excitability, attention seeking, sexually provocative, overly concerned with apperance

A

histrionic PD - cluster B

377
Q

grandiosity, sense of entitlement, lacks empathy and requires excessive admiration, often demands the best and reacts to criticism with rage

A

narcissistic PD - cluster B

378
Q

cluster C personality disorders

A

“worried” anxious or fearful; genetic association with anxiety disorders
Cowardly - avoidant
compulsive - Obsessive-compulsive
clingy - dependent

379
Q

hypersensitive to rejection, socially inhibited, timid, feelings of inadequacy, desires relationships with others

A

avoidant PD - cluster C

380
Q

preoccupation with order, perfectionism and control; ego-syntonic

A

obsessive-compulsive PD - cluster C

381
Q

submissive and clingy, excessive need to be taken care of, low self-confidence

A

dependent PD - cluster C

often stuck in abusive relationships

382
Q

alcohol intoxication

A

emotional lability, slurred speech, ataxia, coma, blackouts
serum GGT - sensitive indicator of alcohol use
AST&raquo_space; ALT

383
Q

Alcohol withdrawal

A

tremor, tachycardia, HTN, malaise, nausea, DTs

384
Q

Delirium tremens

A

life threatening alcohol withdrawal that peaks 2-4 days after last drink
autonomic hyperactivity (tachycardia, tremors, anxiety, seizures)
5-15% mortality rate

treat w/ benzos

alcoholic hallucinations - 12-18 hrs after last drinks

385
Q

opioid intoxication

A

euphoria, respiratory and CNS depression, decreased gag reflex, pinpoint pupils, seizures (OD)

treat w/ naloxone or naltrexone

386
Q

opioid withdrawal

A

sweating, dilated pupils, piloerection, fever, rhinorrhea, diarrhea, yawing, nausea, cramps

treat w/ long-term support, buprenorphine, methadone

387
Q

barbiturate - intoxication

A

low safety margin - marked respiratory depression

treat by managing symptoms (increase BP, assist respiration)

388
Q

barbiturate withdrawal

A

delirium, life-threatening CV collapse

389
Q

benzos - intoxication

A

greater safety margin than barbiturates

ataxia, minor respiratory depression

treat with flumazenil

390
Q

benzos withdrawal

A

sleep disturbance, depression, rebound anxiety, seizure

391
Q

amphetamine intoxication

A

euphoria, grandiosity, pupillary dilation, agitation, insomnia, arrhythmias, tachycardia, anxiety

392
Q

amphetamine withdrawal

A

anhedonia, increased appetite, hypersomnolence, existential crisis

post-use crash: depression, lethargy, weight gain, headache

393
Q

cocaine intoxication

A

impaired judgement, pupillary dilation, hallicinations, paranoid ideations, angina, sudden cardiac death

treatment: alpha blockers, benzos (NOT beta blockers)

394
Q

cocaine withdrawal

A

hypersomnolence, malaise, severe craving, depression/suicidality

post-use crash: depression, lethargy, weight gain, headache

395
Q

caffeine intoxicatoin

A

restlessness, increased diuresis, muscle twitching

396
Q

caffeine withdrawal

A

lack of concentration, headache

397
Q

nicotine intoxication

A

restlessness

398
Q

nicotine withdrawal

A

irritability, anxiety, craving

treatment: nicotine patches/gum/etc, bupropion, varenicline

399
Q

varenicline

A

partial nicotinic receptor agonist - decreases nicotine w/d symptoms and decreases reward from nicotine

400
Q

PCP intoxication

A

belligerence, impulsivity, fever, psychomotor agitation, analgesia, vertical and horizontal nystagmus, tachycardia, homicidality, psychosis, delirium, seizures

treatment: benzos, rapid-acting anti-psychotic

401
Q

PCP withdrawal

A

depression, anxiety, irritability, restlessness, anergia, disturbances of thought and sleep

402
Q

LSD intoxication

A

perceptual distortion, depersonalization, anxiety, paranoia, psychosis, flashbacks

403
Q

Marijuana intoxication

A

euphoria, anxiety, paranoid delusions, perception of slowed time, impaired judgement, social withdrawal, increased appetite, dry mouth, conjunctival injections, hallucinations

404
Q

marijuana withdrawal

A

irritability, depression, insomnia, nausea, anorexia

peak w/in 48 hrs (may last 5-7 days)

405
Q

methadone

A

long-acting oral opiate for heroin detox and maintenance

406
Q

naloxone

A

antagonist - must be injected (not orally bioavailable)

407
Q

buprenorphine

A

opiate partial agonist

408
Q

naltrexone

A

long-acting opiate antagonist used for relapse prevention once detoxed from heroin

409
Q

HIV therapy

A

HAART
2 nucleoside reverse transcriptase inhibitors + 1 protease inhibitor OR integrase inhibitor OR non-nucleoside reverse transcriptase inhibitor

410
Q

protease inhibitors

A

-navir (Navir tease a protease)

atazanavir
darunavir
fosamprenavir
indinavir
lopinavir
ritonavir
saquinavir
411
Q

protease inhibitors - MoA

A

-navir

assembly of virons depends on viral protease (pol gene) - PI prevents maturation of new viruses

412
Q

protease inhibitors - toxicity

A

hyperglycemia, GI intoleraqnce, lipodystrophy

indinavir - nephrotoxicity, hematuria

contraindicated w/ rifampin (CYP inducer)

413
Q

nucleoside reverse transcriptase inhibitors

A
abacavir
didanosine
emtricitabine
lamivudine
stavudine
tenofir
zidovudine
414
Q

nucleoside reverse transcriptase inhibitors - MoA

A

competitively inhibit nucleotide binding to reverse transcriptase and terminate DNA chain

all need to be phosphorylated to be active EXCEPT tenofovir
zidovudine - general prophylaxis and during pregnancy

415
Q

Nucleoside reverse transcriptase inhibitors - toxicity

A
bone marrow suppression (reversed with G-CSF and EPO)
peripheral neuropathy
lactic acidosis (except tenofovir)
anemia (zidovudine)
pancreatitis (didanosine)
416
Q

non-nucleoside reverse transcriptase inhibitors

A

delvirdine
efavirenz
nevirapine

417
Q

non-nucleoside reverse transcriptase inhibitors - MoA

A

bind to reverse transcriptase in a different site from NRTIs

do not require phosphorylation

418
Q

non-nucleoside reverse transcriptase inhibitors - toxicity

A

rash, hepatotoxicity
vivid dreams - efavirenz
only use nevirapine in pregnancy

419
Q

raltegravir - MoA

A

integrase inhibitors - inhibits HIV genome integration into host chromosome by reversibly inhibiting HIV integrase

420
Q

raltegravir - toxicity

A

integrase inhibitor

increases creatine kinase

421
Q

enfuvirtide - MoA

A

fusion inhibitor - binds gp41, inhibiting viral cell entry

causes skin reaction at injection site

422
Q

maraviroc - MoA

A

fusion inhibitor - binds CCR5 in surface of T cells/monocytes
inhibits interaction with gp120

423
Q

H2 blockers (GI) - MoA

A

cimetidine, ranitidine, famotidine, nizatidine

reversible block of H2 receptors - decrease H+ secretion by parietal cells

424
Q

H2 blockers (GI) - clinical use

A

cimetidine, ranitidine, famotidine, nizatidine

peptic ulcer, gastritis, mild esophageal reflux, zollinger-ellison

425
Q

H2 blocker (GI) - toxicity

A

cimetidine, ranitidine, famotidine, nizatidine

cimetidine - inhibits CYP450; antiandrogenic effects, crossed BBB and placenta

cimetidine and ranitidine - decrease renal excretion of creatinine

426
Q

proton pump inhibitors - MoA

A

omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

irreversible inhibit H+/K+ ATPase in parietal cells

427
Q

PPI - clinical use

A

omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

peptic ulcer, gastritis, esophageal reflux, zollinger-ellison

428
Q

PPI - toxicity

A

omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

C.diff infection, pneumonia
decreased serum Mg with longterm use

429
Q

bismuth, sucralfate - MoA

A

binds to ulcer base - physical protection; allows HCO3 to reestablish pH gradient in mucosa

430
Q

bismuth, sucralfate - clinical use

A

ulcer healing, travelers diarrhea

431
Q

misoprostol - MoA

A

PGE1 analog - increases production and secretion of gastric mucous barrier (mucus and bicarb)
decreases acid production

432
Q

misoprostol - clinical use

A

prevention of NSAID inducted peptic ulcers
maintain PDA

induction of labor (off label); abortifacient

433
Q

misoprostol - toxicity

A

diarrhea

434
Q

octreotide - MoA

A

long acting somatostatin analog, prohibits actions of splanchnic vasodilatory hormones

435
Q

octreotide - clinical use

A

acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors

436
Q

octreotide - toxicity

A

nausea, cramps, steatorrhea

437
Q

antacids - MoA

A

neutralize protons in gut

alter gastric and urinary pH; delay gastric emptying

438
Q

antacids - toxicity

A

all can cause hypokalemia

Aluminum hydroxide - constipation, hypophosphatemia, prox. muscle weakness, osteodystrophy, seizures

Calcium carbonate - hypercalcemia, rebound acid, chelates other drugs (tetracycline)

Magnesium hydroxide - diarrhea, hyporeflexia, hypotension, cardiac arrest

439
Q

sulfasalazine - MoA

A

combo of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)

activated by colonic bacteria

440
Q

sulfasalazine - clinical use

A

Ulcerative colitis, Crohn disease (colitis component)

441
Q

sulfasalazine - toxicity

A

malaise, nausea, sulfonamide toxicity, reversible oligospermia

442
Q

odansetron - MoA

A

5-HT3 antagonist, decreases vagal stimulation

powerful anti-emetic (central acting)

443
Q

odansetron - clinical use

A

post-op and cancer anti-emetic

444
Q

odansetron - toxicity

A

headache, constipation, prolonged QT interval

445
Q

metoclopramide - MoA

A

D2 receptor antagonist
increases resting tone, contractility, LES tone, motility

does NOT influence colon transport time

446
Q

metoclopramine - clinical use

A

diabetic and post-op gastroparesis, anti-emetic

447
Q

metoclopramine - toxicity

A

parkinsonian effects, tardive dyskinesia

restlessness, fatigue, drowsiness, depression, diarrhea

448
Q

orlistat - MoA

A

inhibits gastric and pancreatic lipase - decrease breakdown/absorption of dietary fats

449
Q

orlistat - clinical use

A

weight loss

450
Q

orlistat - toxicity

A

steatorrhea, decreased absorption of fat soluble vitamins