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Flashcards in Pharmacology Deck (293):
1

Pramlintide

Amylin analog. MOA = decrease gastric emptying and decrease glucagon. Used for type 1 + type 2 DM.

2

Dopamine MOA

At low doses stimulates D1 receptors in the renal vasculature and tubules, thereby increasing GFR, RBF, and sodium excretion. Big heart in middle of room + normal sized christian is squeezing it/at high doses stimulates beta-1 adrenergic receptors in the heart, thereby increasing cardiac contractility + pulse pressure + systolic BP. Huge air force one plane by the left that monster Christian is driving/at highest doses stimulates alpha-1 receptors in the systemic vasculature.

3

Why do you give dopamine for shock?

To stimulate a1 receptors in the systemic vasculature, causing vasoconstriction.

4

Amiloride vs. amiodarone vs.

Amiloride --> K+ sparing diuretic.
amiodarone --> K channel blocker
amlodipine --> Ca channel blocker

5

Ergotamine

o Code: Elisabeth with Erik backpack/ergotamine. Smoking a huge blunt + walking out of air force one/MOA = partial agonist/antagonist activity at tryptaminergic + dopaminergic + alpha-adrenergic receptors. Feet and arms are gangrenous/SE’s = peripheral vascular ischemia + potentially gangrene.
o Location: /usually used for migraines.

6

How can morphine therapy lead to toxicity?

Morphine is metabolized to active metabolites that accumulate and can cause CNS depression.

7

Drugs contraindicated in CHF

Diltiazem and verapamil.

8

Hydralazine MOA

Smooth muscle relaxant and vasodilator in arteries and arterioles. Exact mechanism unclear.

9

Phenoxybenzamine MOA

Non-selective irreversible alpha blocker

10

labetalol MOA

Mixed alpha/beta adrenergic antagonist

11

What is Vmax proportional to?

Enzyme concentration

12

Relationship of Km to Vmax

Km is enzyme saturation at 1/2Vmax

13

competitive inhibitor vs. noncompetitive inhibitor

FA 236

14

What does a change in y-intercept on Lineweaver-Burk plot indicate?

Increased y-intercept = decreased Vmax since y-axis is the reciprocal of Vmax

15

What does x-intercept represent on lineweaver-Burk plot?

The further to the right (i.e. the closer to zero), the greater the Km and the lower the affinity since x-axis is reciprocal of negative Km.

16

What is slope on Lineweaver-Burk plot?

Km/Vmax

17

How do you differentiate competitive inhibitors from noncompetitive on Lineweaver-Burk plot?

Reversible competitive inhibitors cross each other competitively, whereas noncompetitive inhibitors do not.

18

Competitive inhibitors, reversible
1) resemble substrate?
2) overcome by increased saturation?
3) bind active site?
4) effect on Vmax?
5) effect on Km?
6) potency? efficacy?

1) Yes
2) Yes
3) Yes
4) Unchanged
5) Increased
6) Decreased potency

19

Competitive inhibitors, IRREVERSIBLE
1) resemble substrate?
2) overcome by increased saturation?
3) bind active site?
4) effect on Vmax?
5) effect on Km?
6) potency? efficacy?

1) Yes
2) No
3) Yes
4) Decreased
5) Unchanged
6) Decreased efficacy

20

NONcompetitive inhibitors
1) resemble substrate?
2) overcome by increased saturation?
3) bind active site?
4) effect on Vmax?
5) effect on Km?
6) potency? efficacy?

1) No
2) No
3) No
4) Decreased
5) Unchanged
6) Decreased efficacy

21

What is bioavailability?

Fraction of administered drug reaching systemic circulation unchanged

22

bioavailability of IV dose of drug

100%

23

Why is bioavailability usually less than 100%

Incomplete absorption + first pass metabolism

24

How do liver and kidney disease affect Vd?

Decreased protein binding leads to increased volume of distribution.

25

Drugs that stick to blood compartment characteristics...

Large/charged molecules; plasma protein bound

26

Relative Vd of ECF, tissue, Blood compartments

Blood = low
ECF = medium
All tissues including fat = high

27

Characteristics of drugs that stay in ECF compartment?

Small hydrophilic molecules

28

Characteristics of drugs that stay in fat/tissue compartment?

Small lipophilic molecules, especially if bound to tissue protein.

29

Steady state in a drug with first-order kinetics?

Takes 4-5 lives to reach steady state and 3.3 half lives to reach 90% of steady-state.

30

What happens to maintenance and loading dose with renal or liver disease?

You need need to decrease maintenance dose. Loading dose is usually unchanged.

31

What does time to steady state depend on?

Primarily half life. Independent of dose and dosing frequency.

32

Additive drug interaction?

Effect of substance A and B together is equal to the sum of their individual effects.

33

Example of additive drug interaction

Aspirin + acetaminophen

34

Permissive drug interaction?

Presence of substance A is required for the full effects of substance B.

35

Example of permissive drug interaction?

Cortisol on catecholamine responsiveness

36

synergistic drug interaction?

Effect of substance A and B together is greater than the sum of their individual effects.

37

Classic example of synergistic drug interaction?

Clopidogrel with aspirin

38

tachyphylactic drug interaction?

Acute decrease in response to a drug after initial/repeated administration.

39

classic examples of tachyphylactic drug interactioN?

MDMA and LSD

40

Graph of plasma concentration of drug vs. time with zero-order elimination?

linear

41

Drugs with zero-order elimination?

1) phenytoin
2) ethanol
3) aspirin (at high or toxic concentrations)

42

term for elimination in zero-order elimination?

"Capacity-limited elimination"

43

What is rate of elimination proportional to in first-order clearance?

Directly proportional to drug concentration (constant fraction eliminated per unit time)

44

term for elimination in first-order elimination?

"flow-dependent elimination"

45

Graph of plasma concentration of drug vs. time with first-order elimination?

exponential

46

Difference between ionized drugs and non-ionized in terms of renal clearance?

Ionized species are trapped in urine and cleared quickly. Neutral forms can be reabsorbed.

47

Examples of drugs that are weak acids...

1) phenobarbital
2) methotrexate
3) aspirin

48

Treating overdose for weak acid drugs...

Trapped in basic environments so treat overdose with bicarbonate.

49

Examples of drugs that are weak bases...

1) amphetamines
2) TCAs

50

Treating overdose for weak base drugs...

Trapped in acidic environments so treat with ammonium chloride.

51

Drug metabolism changes with age.

1) Geriatric patients lose phase I metabolism first.
2) More Phase II

52

What is Phase I metabolism?

Reduction, oxidation, hydrolysis with CYP-450 usually yielding slightly polar, water-soluble metabolites.

53

Caveat about drugs after Phase 1 metabolism...

Often still active.

54

What is Phase II metabolism?

Conjugation (MGAS - Methylation, glucuronidation, acetylation, sulfating), usually yields very polar, inactive metabolites (really excreted).

55

Problem with people who are slow acetylators?

They have increased side effects from certain drugs because of decreased rate of Phase II metabolism.

56

What is efficacy proportional to?

Vmax

57

How is potency represented on maximal effect vs. dose graph?

X-axis (EC50), left shift = decreased EC50 = increased potency = decreased drug needed.

58

partial agonist vs. agonist

partial agonists have lower efficacy.

59

effect of competitive antagonist

Shifts curve right (decreased potency, no change in efficacy.

60

effect of NONcompetitive antagonist

Shifts curve down (decreasing efficacy).

61

phenoxybenzamine MOA

noncompetitive antagonist on alpha receptors

62

Therapeutic index?

Difference between TD50 and ED50

63

TD50?

median toxic dose

64

ED50?

median effective dose

65

therapeutic window

Dosage range that can safely and effectively treat disease.

66

How to calculate therapeutic index?

TD50/ED50

67

Drugs with lower therapeutic indexes?

1) Digoxin
2) Lithium
3) theophylline
4) warfarin

68

Implication of drugs with low therapeutic indices?

Frequently require monitoring

69

LD50?

Basically TD50 in animal studies.

70

Caveat about adrenal medulla and sweat glands

Part of sympathetic nervous system but innervated by cholinergic fibers

71

Somatic nervous system structure + neurotransmitter

Voluntary motor nerves synapsing on skeletal muscle and release ACh.

72

Parasympathetic nervous system structure + neurotransmitter

1) Long preganglionics releasing ACh and synapsing on nicotinic receptors
2) short postganglionics releasing ACh and synapsing on muscarinic receptors at target organ

73

What receives sympathetic innervation?

1) sweat glands
2) cardiac and smooth muscle (both PS and S)
3) gland cells (both PS and S)
4) renal vasculature
5) vessels

74

Sympathetic vs. parasympathetic nerve structure

1) In parasympathetic, you have long preganglionics and short postganglionics.
2)

75

Sympathetic pregalgnionics

All release ACh onto Nicotinic receptors.

76

Sweat gland innervation

Sympathetic. ACh on muscarinic receptors.

77

Cardiac and smooth muscle, gland cells, nerve terminals innveration in sympathetic

NE synapsing on adrenergic receDptors

78

Dopamine 1 receptors expressed in...

1) renal vasculature
2) smooth muscle

79

Adrenal meddle neuromuscular transmission

preganglionics release ACh onto nicotinic receptors in the adrenal medulla. Catecholamines are released into blood. NE acts on A1,A2,B1, Epi on A1,A2, B1,B2

80

Structure of nicotinic ACh receptors?

Ligand-gated Na+/K+ channels.

81

Subdivisions of nicotinic receptors and expression

1) Nn (autonomic ganglia + adrenal medulla)
2) Nm (found in NMJ of skeletal muscle)

82

Muscarinic ACh receptor structure

G-protein-coupled receptors that usually act through 2nd messengers.

83

A1 functions

1) vascular smooth muscle contraction
2) Increase pupillary dilator muscle contraction (Mydriasis)
3) increase intestinal and bladder sphincter muscle contraction

84

A2 receptor functions

1) decrease sympathetic (adrenergic) outflow
2) decrease insulin release
3) lipolysis
4) decrease platelet aggregation
5) decrease aqueous humor production

85

B1 receptor functions

1) increase HR
2) increase contractility
3) increase renin release
4) increase lipolysis

86

B2 receptor functions

1) vasodilation
2) bronchodilation
3) increased lipolysis
4) increase insulin release
5) decrease uterine tone (tocolysis)
6) ciliary muscle relaxation
7) increase aqueous humor production

87

beta 3 class

Gs

88

Beta 3 functions

1) increased lipolysis
2) thermogenesis in skeletal muscle

89

M1 functions

1) CNS
2) enteric nervous system

90

M2 class

Gi

91

M2 functions

1) decrease heart rate
2) decrease contractility of atria

92

M3 functions

1) exocrine gland secretions (lacrimal, sweat, salivary, gastric acid)
2) increase gut peristalsis
3) increase bladder contraction
4) bronchoconstriction
5) Increase pupillary sphincter muscle contraction (mitosis)
6) ciliary muscle contraction (accommodation)

93

D1 receptors

Gs

94

D1 functions

1) relax renal vascular smooth muscle

95

D2 receptor

Gi

96

D2 receptor functions

1) modulates transmitter release, especially in brain

97

H1 receptor g protein class

Gq

98

H1 receptor function

1) Increase nasal and bronchial mucus production
2) increase vascular permeability
3) contraction of bronchioles
4) pruritus
5) pain

99

H2 receptor class

Gs

100

H2 receptor function

1) increase gastric acid secretion

101

V1 receptor class

Gq

102

V1 receptor function

Increase vascular smooth muscle contraction

103

V2 receptor class

Gs

104

V2 receptor function

1) ADH

105

Gq pathway

PIP2 (phospholipase C) --> DAG --> PKC
OR
PIP2 (phospholipase C) --> IP3 --> increased calcium concentration --> smooth muscle contraction

106

Gs/Gi pathway

adenylyl cyclase --> ATP to cAMP --> PKA --> increased calcium in heart OR myosin light-chain kinase (smooth muscle)

107

Hemicholinium

enzyme that inhibits choline uptake into neurons

108

vesamicol

enzyme that inhibits ACh uptake into vesicles

109

Metyrosin MOA

inhibits conversion of tyrosine to DOPA

110

Reserpine MOA

inhibits dopamine uptake into vesicles

111

ephedrine cell bio MOA

stimulates release of NE from vesicles

112

Bretylium MOA

Inhibit NE release from vesicles.

113

Guanethidine MOA

Inhibit NE release from vesicles. indirect general agonist + releases stored catecholamines, thus activating alpha and beta receptors

114

How is NE release from sympathetic nerves modulated?

NE regulates itself, by feeding back and acting on presynaptic alpha2 receptors.

115

How do amphetamines get into presynaptic terminal?

NET transporter (NE transporter) (NET)

116

How do amphetamines get into vesicles? What happens after?

VMAT, vesicular monoamine transporter. This displace NE from the vesicles. Once NE reaches a concentration threshold within the presynaptic terminal, the action of NET is reversed, and NE is expelled into the synaptic cleft, contributing to the characteristics and effects of increased NE observed in patients taking amphetamines.

117

Excess tyramine mechanism

It enters presynaptic vesicles and displaces other neurotransmitters (eg, NE) --> increasing amount of active presynaptic neurotransmitters, which diffuse into the synaptic cleft, leading to increased sympathetic simulation and hypertensive crisis.

118

Bethanechol impt pharmacology point

resistant to AChE

119

Bethanechol

direct agonist at bowel and bladder smooth muscle

120

bethanechol uses

1) postoperative ileus
2) neurogenic ileus
3) urinary retention

121

carbachol MOA

direct cholinomimetic

122

carbachol applications

constricts pupil and relives intraocular pressure in open-angle glaucoma (increases aqueous humor outflow)

123

pilocarpine MOA

direct agonist -- contracts ciliary muscle of eye (open-angle glaucoma) + pupillary sphincter (closed-angle glaucoma).

124

pilocarpine impt pharmacology ypoint

resistant to AChe

125

pilocarpine uses

1) potent stimulator of sweat, tears, and saliva.
2) open-angle and closed-angle glaucoma
3) xerostomia (Sjogren's)

126

rivastigmine MOA

indirect, increases ACh

127

galantine MOA

indirect, increases ACh

128

options for AD

1) donepezil
2) galantine
3) rivastigmine

129

How is MG actually diagnosed now?

Anti-AChR Ab (anti-acetylcholine receptor antibody) test.

130

edrophonium MOA

indirect, increases ACh

131

All cholinomimetics can exacerbate...

1) COPD
2) asthma
3) peptic ulcers

132

neostigmine impt pharmacology poitn

Neo CNS = NO CNS penetration

133

neostigmine uses

1) postoperative and neurogenic ileus and urinary retention
2) MG
3) reversal of neuromuscular junction blockade (postop)

134

physostigmine is used for anticholinergic toxicity because...

it crosses BBB into CNS

135

pyridostigmine and CNS

Long acting but does NOT penetrate CNS.

136

organophosphate commonly causing cholinesterase inhibitor .

parathion

137

Why do organophosphates cause poisoning?

They irreversibly inhibit AChE

138

How is pralidoxime affective?

Regenerates AChE if given early.

139

Major concern with untreated cholinesterase inhibitor poisoning...

respiratory failure

140

DUMBBELSS

Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, and Salivation.

141

What does muscarinic antagonism create in the eye?

1) mydriasis
2) cycloplegia

142

cycloplegia

paralysis of ciliary muscle

143

benztropine MOA

muscarinic antagonist in the CNS

144

benztropine uses

1) PD
2) Acute dystonia

145

glycopyrrolate MOA

Muscarinic antagonist targeting GI + respiratory

146

glycopyrrolate uses

1) parenteral: preoperative use to reduce airway secretions
2) oral: drooling + peptic ulcers

147

drug like hyoscyamine

dicyclomine

148

dicyclomine, hyoscyamine uses

Antispasmodics for IBS

149

Ipratropium, tiotropium uses

1) COPD
2) asthma

150

Ipratropium, tiotropium MOA

muscarinic antagonists targeting respiratory system

151

muscarinic antagonists targeting GU system

1) oxybutynin
2) solifenacin
3) tolterodine

152

Atropine affects

1) mydriasis, cycloplegia
2) decrease airway secretions
3) decrease acid secretion in stomach
4) decrease gut motility
5) decrease urgency in cystitis

153

AE's of atropine

1) Hot as a hare
2) Dry as a bone (dry, flushed skin)
3) Red as a beet
4) Blind as a bat
5) Mad as a hatter (disorientation)

rapid pulse + dry mouth + constipation.

154

Atropine AE's/contranidcations

1) urinary retention in men with BPH
2) hyperthermia in infants
3) acute angle-closure glaucoma

155

albuterol vs. salmeterol clinical applications

1) albuterol for acute asthma or COPD
2) salmeterol for long-term asthma or COPD control.

156

Dobutamine primarily targets...

B1 more so than B2, alpha

157

dobutamine uses

1) HF (inotropic more so than chronotropic)
2) cardiac stress testing

158

Dopamine targets...

D1 = D2, then B, then A

159

dopamine uses

1) unstable bradycardia
2) HF
3) shock
4) inotropic AND chronotropic effects at lower doses
5) vasoconstriction at high doses due to alpha effects

160

epinephrine targets primarily

beta more so than alpha

161

isoproterenol uses

1) electrophysiologic evaluation of tachyarrhythmias

162

isoproterenol contraindications

CAD (can worsen ischemia)

163

midodrine MOA

alpha1 agonist

164

norepinephrine uses

1) hypotension
2) septic shock

165

norepinephrine targets

alpha1, then alpha 2, then beta1

166

phenylephrine targets

alpha1 primarily, but also alpha 2

167

phenylephrine uses

1) hypotension (vasoconstrictor)
2) ocular procedures
3) rhinitis (decongestant)

168

what are the indirect sympathomimetics?

1) amphetamine
2) cocaine
3) ephedrine

169

amphetamine MOA

1) Indirect general agonist
2) reuptake inhibitor
3) releases stored catecholamines

170

cocaine MOA

1) indirect general agonist
2) reuptake inhibitor

171

ephedrine MOA

1) indirect general agonist, releases stored catecholamines

172

ephedrine uses

1) nasal decongestion
2) urinary incontinence
3) hypotension

173

isoproterenol affects on BP, HR

vasodilation (via B2) + increased HR through both B1 + reflex activity

174

guanfacine MOA

A2 agonists

175

clonidine, guanfacine uses

1) hypertensive urgency in limited situations
2) ADHD
3) Tourettes

176

Clonidine, guanfacine AE's

1) CNS depression
2) bradycardia
3) hypotension
4) respiratory depression
5) miosis

177

alpha-methyldopa AE's

1) direct coombs positive hemolysis
2) SLE-like syndrome

178

beta blockers used for SVTs?

metoprolol + esmolol

179

beta blocker MOA for use in SVTs?

Decrease AV conduction velocity.

180

beta blocker MOA for use in HTN?

1) decrease cardiac output
2) *decrease renin secretion (beta1 blockade on JGA cells)

181

beta blockers used to decrease mortality in HF?

1) bisoprolol
2) carvedilol
3) metoprolol

182

timolol mechanism in glaucoma?

Decreases secretion of aqueous humor

183

Other BB usage?

Decrease variceal bleeding

184

BB's to use to decrease variceal bleeding?

1) nadolol
2) propranolol

185

beta blocker MOA for use in variceal bleeding?

Decrease hepatic venous pressure gradient and portal HTN.

186

beta blocker AE's

1) erectile dysfunction
2) cardiovascular AE's (bradycardia, AV block, HF)
3) CNS (seizures, sedation, sleep alterations)
4) asthma/COPD exacerbations

187

metoprolol other AE

dyslipidemia

188

What's the deal with using beta blockers in diabetics?

despite concern with masking hypoglycemia, benefits likely outweigh risk so they are indicated.

189

nonselective betablockers

1) nadolol
2) pindolol
3) propranolol
4) timolol

190

nonselective antagonism means what?

B1 = b2 (unlike selective, which primarily target B1) N

191

Nebivolol MOA

Blocks beta1 but stimulates B3, thus activating NO synthase in vasculature

192

tetrodotoxin source

pufferfish

193

tetrodotoxin MOA

Highly potent; binds fast voltage-gated Na+ channels in cardiac/nerve tissue, preventing depolarization.

194

tetrodotoxin symptoms

nausea + diarrhea + paresthesias + weakness + dizziness + loss of reflexes

195

tetrodotoxin treatment

primarily supportive

196

ciguatoxin sources

Reef fish...
1) barracuda
2) snapper
3) moray eel

197

ciguatoxin mechanism

1) OPENs Na+ channels, causing depolarization

198

ciguatoxin presentation

symptoms mimic cholinergic poisoning

199

ciguatoxin poisoning treatment

primarily supportive

200

scombroid poisoning is basically...

histamine poisoning

201

scombroid sources

spoiled dark-meat fish..
1) tuna
2) mahi-mahi
3) mackerel
4) bonito

202

scombroid mechanism

Bacterial histidine decarboxylase converts histidine to histamine

203

What is scombroid poisoning frequently misdiagnosed as?

Fish allergy

204

scombroid poisoning presentation...

anaphylaxis picture...
1) acute burning sensation of mouth
2) flushing of face
3) erythema
4) urticaria
5) itching
6) bronchospasm
7) angioedema
8) hypotension

205

scombroid treatment

Antihistamines. Albuterol + epinephrine if needed.

206

Treatment for amphetamine overdose...

ammonium chloride (amphetamines are basic so you want to acidify the urine)

207

Treatment for antimuscarinic/anticholinergic overdose...

physostigmine + *control hyperthermia

208

Treatment for arsenic overdose...

dimercaprol + succimer

209

Treatment for beta-blocker overdose...

saline + atropine + glucagon

210

Treatment for copper overdose...

penicillamine + trientine

211

Treatment for cyanide overdose...

Nitrite + thiosulfate + hydroxocobalamin

212

Treatment for digitalis overdose...

anti-dig Fab fragments

213

Treatment for gold overdose...

penicillamine + dimercaprol (BAL) + succimer

214

Treatment for heparin overdose...

protamine sulfate

215

Treatment for iron overdose...

deFERoxamine, deFERasirox, deFERipone

216

Treatment for lead overdose...

1) EDTA
2) dimercaprol
3) succimer
4) penicillamine

217

Treatment for amphetamine overdose...

diMERCaprol + succimer

218

Treatment for methanol, ethylene glycol (antifreeze) overdose...

Fomepizole. Also, ethanol or dialysis if fomepizole isn't available.

219

Treatment for opioid overdose...

naloxone

220

Treatment for salicylate overdose...

sodium bicarb (alkalinize urine) + dialysis

221

Drugs associated with coronary vasospasm...

1) cocaine
2) sumatriptan
3) ergot alkaloids

222

Drugs associated with cutaneous flushing...

VANCE
Vancomycin
Adenosine
Niacin
Ca2+ channel blockers
Echinocandins

223

What do you give to prevent dilated cardiomyopathy with anthracyclines (doxorubicin, daunorubicin)?

Dexrazoxane

224

Drugs associated with torsades de pointes

1) 1A + III antiarrhythmics
2) macrolides
3) haloperidol
4) TCA's
5) ondansetron

225

Drugs associated with hot flashes

1) tamoxifen
2) clomiphene

226

Drugs associated with hyperglycemia

1) tacrolimus
2) protease inhibitors
3) niacin
4) HCTZ
5) corticosteroids

227

Drugs associated with hypothyroidism

1) lithium
2) amiodarone
3) sulfonamides

228

Erythromycin AE's

acute cholestatic hepatitis + jaundice

229

Drugs causing diarrhea

1) acamprosate
2) acarbose
3) cholinesterase inhibitors
4) colchicine
5) erythromycin
6) ezetimibe
7) metformin
8) misoprostol
9) Orlistate
10) pramlintide
11) quinidine
12) SSRIs

230

Drugs associated with focal to massive hepatic necrosis...

HAVAc
Halothane
Amanita phalloides
Valproic acid
Acetaminophen

231

drugs associated with hepatitis

Rifampin
Isoniazid
Pyrazinamide
Statins
Fibrates

232

Drugs associated with pancreatitis

Didanosine
Corticosteroids
Alcohol
Valproic acid
Azathioprine
Diuretics (furosemide, HCTZ)

233

Drugs associated with pill-induced esophagitis

1) tetracyclines
2) bisphosphonates
3) potassium chloride

234

How do you minimize pill-induced esophagitis?

good posture + adequate water ingestion

235

Drugs associated with pseudomembranous colitis

Clindamycin
Ampicillin
Cephalosporins

236

Drugs associated with
agranulocytosis

Clozapine
Carbamazepine
propylthiouracil
Methimazole
Colchicine
Ganciclovir

237

Drugs associated with aplastic anemia

Carbamazepine
Methimazole
NSAIDs
Benzene
Chloramphenicol
PTU

238

Drugs associated with direct Coombs-positive hemolytic anemia

1) methyldopa
2) penicillin

239

Drugs associated with hemolysis in G6PD deficiency

Isoniazid
Sulfonamides
Dapsone
Primaquine
Aspirin
Ibuprofen
Nitrofurantoin

240

Drugs associated with megaloblastic anemia

Phenytoin
Methotrexate
Sulfa drugs

241

Drugs associated with thrombosis

1) OCPs
2) hormone replacement therapy

242

Drugs causing gingival hyperplasia

1) phenytoin
2) calcium channel blockers
3) cyclosporine

243

Drugs associated with hyperuricemia

1) pyrazinamide
2) thiazides
3) furosemide
4) niacin
5) cyclosporine

244

Drugs associated with myopathy

Vibrates
Niacin
colchicine
hydroxycloroquine
INF-alpha
penicillamine
statins
GCs

245

Drugs associated with osteoporosis

corticosteroids, heparin

246

Drugs associated with photosensitivity

Sulfonamides
Amiodarone
Tetracyclines
5-FU

247

Drugs associated with Stevens-Johnson syndrome

1) lamotrigine
2) allopurinol
3) sulfa drugs
4) etanercept

248

drugs causing cinchonism

quinidine + quinine

249

Drugs associated with Parkinson-like syndrome

Cogwheel rigidity of ARM
1) antipsychotics
2) reserpine
3) metoclopromide

250

Drugs associated with seizures

1) isoniazid
2) bupropion
3) Imipenem/cilastatin
4) tramadol
5) enflurane

251

Drugs associated with tardive dyskinesia

1) antipsychotics
2) metoclopramide

252

Drugs associated with fanconi syndrome

1) tenofovir
2) ifosfamide

253

Drugs associated with hemorrhagic cystitis?

1) cyclophosphamide
2) ifosfamide

254

Drugs associated with interstitial nephritis?

1) methicillin
2) NSAIDs
3) furosemide

255

Drugs associated with SIADH?

1) carbamazepine
2) cyclophosphamide
3) SSRIs

256

Drugs associated with pulmonary fibrosis?

1) methotrexate
2) nitrofurantoin
3) carmustine
4) bleomycin
5) busulifan
6) amiodarone

257

Drugs with antimuscarinic side effects?

1) TCA's
2) H1-blockers
3) antipsychotics

258

Drugs associated with disulfiram-like reaction?

1) metronidazole
2) certain cephalosporins
3) griseofulvin
4) procarbazine
5) 1st generation sulfonylureas

259

Drugs associated with nephrotoxicity/ototoxicity?

1) aminoglycosides
2) vancomycin
3) loop diuretics
4) cisplatin

260

What can you treat cisplatin toxicity with?

Amifostine

261

CYP 450 inducers

1) *Chronic* alcohol
2) *St. John's wort
3) phenytoin
4) phenobarbital
5) nevi rapine
6) rifampin
7) griseofulvin
8) carbamazepine

262

CYP-450 substrates

1) Anti-epileptics
2) theophylline
3) warfarin
4) OCPs

263

CYP-450 inhibitors

1) acute alcohol abuse
2) ritonavir
3) amiodarone
4) cimetidine/ciprofloxacin
5) ketoconazole
6) sulfonamides
7) isoniazid
8) grapefruit juice
9) quinidine
19) macrolides (*except azithromycin)

264

sulfa allergic reaction presentation...

fever + UTI + SJS + hemolytic anemia + thrombocytopenia + agranulocytosis + urticaria

265

Sulfa drugs

1) sulfonamide antibiotics
2) sulfasalazine
3) probenecid
4) furosemide
5) acetazolamide
6) celecoxib
7) thiazides
8) sulfonylureas

266

-azole suffix means...

ergosterol synthesis inhibitor

267

-cillin means...

peptidoglycan synthesis inhibitor

268

-ivir suffix means...

neuraminidase inhibitor (oseltamivir)

269

-ovir suffix means..

DNA polymerase inhibitor (acyclovir)

270

-ane suffix means

inhalation general anesthetic

271

thioridazine

typical antipsychotic (ends in -azine)

272

-caine means...

local anesthetic

273

-etine means...

SSRI

274

-curium, -curonium

*nondepolarizing paralytic

275

atracurium, vecuronium

non depolarizing paralytics

276

-terol means...

Beta2 agonist

277

prazosin

alpha *1 antagonist

278

-afil means...

PDE-5 inhibitor

279

-dipine means..

dihydropyridine Ca2+ channel blocker

280

-xaban means...

direct factor Xa inhibitors

281

examples of factor Xa inhibitors

1) apixaban
2) edoxaban
3) rivaroxaban

282

-glitazone means...

PPAR-gamma activator

283

Example of PPAR-gamma activator

Rosiglitazone

284

-prost means...

prostaglandin analog

285

-tidine means

H*2 antagonist

286

-tropin means

pituitary hormone

287

-ximab means...

Chimeric monoclonal Ab (eg basiliximab)

288

-zumab means

Humanized monoclonal Ab (daclizumab)

289

daclizumab vs. basiliximab

Basiliximab is a chimeric monoclonal Ab, daclizumab is a monoclonal Ab.

290

ergot alkaloids

bromocriptine + cabergoline

291

nitrosoureas

Carmustine
Lomustine
Semustine
Streptozocin

292

NNRTIs

Delaviridine
Efavirenz
Nevirapine

293

Cholinergic effects

o Code: Coleen: Huge red inflatable car man to left + she’s in a gocart with nitrous boosters (nitric oxide code)/receptors present on endothelial surface of peripheral blood vessels. Binding promotes release of NO, thus producing vasodilation. NO activates guanylate cyclase and increases intracellular cGMP. She’s shitting on a towel + drenched in sweet + crying + salivating saliva everywhere + brady in passenger seat + neon eyes/effects = increase tone of smooth muscle of visceral walls + increase motility and secretion in GI tract, manifesting as nausea + vomiting + abdominal cramps + diarrhea + sweating + lacrimation + decreased contractility of heart + decreased conduction velocity + pupillary constriction (via M3 agonism). /decreased conduction velocity may result in heart block. Fizz cartoon and sally cooper resuscitating colleen + waving fan over her on the left/antidote = physostigmine salicylate + control hyperthermia. Erin in car next to brady/NOTE vasodilation can result in baroreceptor-mediated tachycardia.
o Location: Entryway