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STEP > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Pramlintide

A

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

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2
Q

Dopamine MOA

A

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.

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3
Q

Why do you give dopamine for shock?

A

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

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4
Q

Amiloride vs. amiodarone vs.

A

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

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5
Q

Ergotamine

A

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.

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6
Q

How can morphine therapy lead to toxicity?

A

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

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7
Q

Drugs contraindicated in CHF

A

Diltiazem and verapamil.

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8
Q

Hydralazine MOA

A

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

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9
Q

Phenoxybenzamine MOA

A

Non-selective irreversible alpha blocker

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10
Q

labetalol MOA

A

Mixed alpha/beta adrenergic antagonist

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11
Q

What is Vmax proportional to?

A

Enzyme concentration

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12
Q

Relationship of Km to Vmax

A

Km is enzyme saturation at 1/2Vmax

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13
Q

competitive inhibitor vs. noncompetitive inhibitor

A

FA 236

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14
Q

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

A

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

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15
Q

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

A

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.

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16
Q

What is slope on Lineweaver-Burk plot?

A

Km/Vmax

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17
Q

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

A

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

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18
Q

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?

A

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

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19
Q

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?

A

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

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20
Q

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?

A

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

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21
Q

What is bioavailability?

A

Fraction of administered drug reaching systemic circulation unchanged

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22
Q

bioavailability of IV dose of drug

A

100%

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23
Q

Why is bioavailability usually less than 100%

A

Incomplete absorption + first pass metabolism

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24
Q

How do liver and kidney disease affect Vd?

A

Decreased protein binding leads to increased volume of distribution.

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25
Q

Drugs that stick to blood compartment characteristics…

A

Large/charged molecules; plasma protein bound

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26
Q

Relative Vd of ECF, tissue, Blood compartments

A

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

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27
Q

Characteristics of drugs that stay in ECF compartment?

A

Small hydrophilic molecules

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28
Q

Characteristics of drugs that stay in fat/tissue compartment?

A

Small lipophilic molecules, especially if bound to tissue protein.

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29
Q

Steady state in a drug with first-order kinetics?

A

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

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30
Q

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

A

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

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31
Q

What does time to steady state depend on?

A

Primarily half life. Independent of dose and dosing frequency.

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32
Q

Additive drug interaction?

A

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

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33
Q

Example of additive drug interaction

A

Aspirin + acetaminophen

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34
Q

Permissive drug interaction?

A

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

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35
Q

Example of permissive drug interaction?

A

Cortisol on catecholamine responsiveness

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36
Q

synergistic drug interaction?

A

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

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37
Q

Classic example of synergistic drug interaction?

A

Clopidogrel with aspirin

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38
Q

tachyphylactic drug interaction?

A

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

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39
Q

classic examples of tachyphylactic drug interactioN?

A

MDMA and LSD

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40
Q

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

A

linear

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41
Q

Drugs with zero-order elimination?

A

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

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42
Q

term for elimination in zero-order elimination?

A

“Capacity-limited elimination”

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43
Q

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

A

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

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44
Q

term for elimination in first-order elimination?

A

“flow-dependent elimination”

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45
Q

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

A

exponential

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46
Q

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

A

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

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47
Q

Examples of drugs that are weak acids…

A

1) phenobarbital
2) methotrexate
3) aspirin

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48
Q

Treating overdose for weak acid drugs…

A

Trapped in basic environments so treat overdose with bicarbonate.

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49
Q

Examples of drugs that are weak bases…

A

1) amphetamines

2) TCAs

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50
Q

Treating overdose for weak base drugs…

A

Trapped in acidic environments so treat with ammonium chloride.

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51
Q

Drug metabolism changes with age.

A

1) Geriatric patients lose phase I metabolism first.

2) More Phase II

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52
Q

What is Phase I metabolism?

A

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

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53
Q

Caveat about drugs after Phase 1 metabolism…

A

Often still active.

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54
Q

What is Phase II metabolism?

A

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

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55
Q

Problem with people who are slow acetylators?

A

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

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56
Q

What is efficacy proportional to?

A

Vmax

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57
Q

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

A

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

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58
Q

partial agonist vs. agonist

A

partial agonists have lower efficacy.

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59
Q

effect of competitive antagonist

A

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

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60
Q

effect of NONcompetitive antagonist

A

Shifts curve down (decreasing efficacy).

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61
Q

phenoxybenzamine MOA

A

noncompetitive antagonist on alpha receptors

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62
Q

Therapeutic index?

A

Difference between TD50 and ED50

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63
Q

TD50?

A

median toxic dose

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64
Q

ED50?

A

median effective dose

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65
Q

therapeutic window

A

Dosage range that can safely and effectively treat disease.

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66
Q

How to calculate therapeutic index?

A

TD50/ED50

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67
Q

Drugs with lower therapeutic indexes?

A

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

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68
Q

Implication of drugs with low therapeutic indices?

A

Frequently require monitoring

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69
Q

LD50?

A

Basically TD50 in animal studies.

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70
Q

Caveat about adrenal medulla and sweat glands

A

Part of sympathetic nervous system but innervated by cholinergic fibers

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71
Q

Somatic nervous system structure + neurotransmitter

A

Voluntary motor nerves synapsing on skeletal muscle and release ACh.

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72
Q

Parasympathetic nervous system structure + neurotransmitter

A

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

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73
Q

What receives sympathetic innervation?

A

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

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74
Q

Sympathetic vs. parasympathetic nerve structure

A

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

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75
Q

Sympathetic pregalgnionics

A

All release ACh onto Nicotinic receptors.

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76
Q

Sweat gland innervation

A

Sympathetic. ACh on muscarinic receptors.

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77
Q

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

A

NE synapsing on adrenergic receDptors

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78
Q

Dopamine 1 receptors expressed in…

A

1) renal vasculature

2) smooth muscle

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79
Q

Adrenal meddle neuromuscular transmission

A

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

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80
Q

Structure of nicotinic ACh receptors?

A

Ligand-gated Na+/K+ channels.

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81
Q

Subdivisions of nicotinic receptors and expression

A

1) Nn (autonomic ganglia + adrenal medulla)

2) Nm (found in NMJ of skeletal muscle)

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82
Q

Muscarinic ACh receptor structure

A

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

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83
Q

A1 functions

A

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

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84
Q

A2 receptor functions

A

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

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85
Q

B1 receptor functions

A

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

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86
Q

B2 receptor functions

A

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

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87
Q

beta 3 class

A

Gs

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88
Q

Beta 3 functions

A

1) increased lipolysis

2) thermogenesis in skeletal muscle

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89
Q

M1 functions

A

1) CNS

2) enteric nervous system

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90
Q

M2 class

A

Gi

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91
Q

M2 functions

A

1) decrease heart rate

2) decrease contractility of atria

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92
Q

M3 functions

A

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)

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93
Q

D1 receptors

A

Gs

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94
Q

D1 functions

A

1) relax renal vascular smooth muscle

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95
Q

D2 receptor

A

Gi

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96
Q

D2 receptor functions

A

1) modulates transmitter release, especially in brain

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97
Q

H1 receptor g protein class

A

Gq

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98
Q

H1 receptor function

A

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

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99
Q

H2 receptor class

A

Gs

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100
Q

H2 receptor function

A

1) increase gastric acid secretion

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101
Q

V1 receptor class

A

Gq

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102
Q

V1 receptor function

A

Increase vascular smooth muscle contraction

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103
Q

V2 receptor class

A

Gs

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104
Q

V2 receptor function

A

1) ADH

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105
Q

Gq pathway

A

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

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106
Q

Gs/Gi pathway

A

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

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107
Q

Hemicholinium

A

enzyme that inhibits choline uptake into neurons

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108
Q

vesamicol

A

enzyme that inhibits ACh uptake into vesicles

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109
Q

Metyrosin MOA

A

inhibits conversion of tyrosine to DOPA

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110
Q

Reserpine MOA

A

inhibits dopamine uptake into vesicles

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111
Q

ephedrine cell bio MOA

A

stimulates release of NE from vesicles

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112
Q

Bretylium MOA

A

Inhibit NE release from vesicles.

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113
Q

Guanethidine MOA

A

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

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114
Q

How is NE release from sympathetic nerves modulated?

A

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

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115
Q

How do amphetamines get into presynaptic terminal?

A

NET transporter (NE transporter) (NET)

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116
Q

How do amphetamines get into vesicles? What happens after?

A

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.

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117
Q

Excess tyramine mechanism

A

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.

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118
Q

Bethanechol impt pharmacology point

A

resistant to AChE

119
Q

Bethanechol

A

direct agonist at bowel and bladder smooth muscle

120
Q

bethanechol uses

A

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

121
Q

carbachol MOA

A

direct cholinomimetic

122
Q

carbachol applications

A

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

123
Q

pilocarpine MOA

A

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

124
Q

pilocarpine impt pharmacology ypoint

A

resistant to AChe

125
Q

pilocarpine uses

A

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

126
Q

rivastigmine MOA

A

indirect, increases ACh

127
Q

galantine MOA

A

indirect, increases ACh

128
Q

options for AD

A

1) donepezil
2) galantine
3) rivastigmine

129
Q

How is MG actually diagnosed now?

A

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

130
Q

edrophonium MOA

A

indirect, increases ACh

131
Q

All cholinomimetics can exacerbate…

A

1) COPD
2) asthma
3) peptic ulcers

132
Q

neostigmine impt pharmacology poitn

A

Neo CNS = NO CNS penetration

133
Q

neostigmine uses

A

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

134
Q

physostigmine is used for anticholinergic toxicity because…

A

it crosses BBB into CNS

135
Q

pyridostigmine and CNS

A

Long acting but does NOT penetrate CNS.

136
Q

organophosphate commonly causing cholinesterase inhibitor .

A

parathion

137
Q

Why do organophosphates cause poisoning?

A

They irreversibly inhibit AChE

138
Q

How is pralidoxime affective?

A

Regenerates AChE if given early.

139
Q

Major concern with untreated cholinesterase inhibitor poisoning…

A

respiratory failure

140
Q

DUMBBELSS

A

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

141
Q

What does muscarinic antagonism create in the eye?

A

1) mydriasis

2) cycloplegia

142
Q

cycloplegia

A

paralysis of ciliary muscle

143
Q

benztropine MOA

A

muscarinic antagonist in the CNS

144
Q

benztropine uses

A

1) PD

2) Acute dystonia

145
Q

glycopyrrolate MOA

A

Muscarinic antagonist targeting GI + respiratory

146
Q

glycopyrrolate uses

A

1) parenteral: preoperative use to reduce airway secretions

2) oral: drooling + peptic ulcers

147
Q

drug like hyoscyamine

A

dicyclomine

148
Q

dicyclomine, hyoscyamine uses

A

Antispasmodics for IBS

149
Q

Ipratropium, tiotropium uses

A

1) COPD

2) asthma

150
Q

Ipratropium, tiotropium MOA

A

muscarinic antagonists targeting respiratory system

151
Q

muscarinic antagonists targeting GU system

A

1) oxybutynin
2) solifenacin
3) tolterodine

152
Q

Atropine affects

A

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

153
Q

AE’s of atropine

A

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
Q

Atropine AE’s/contranidcations

A

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

155
Q

albuterol vs. salmeterol clinical applications

A

1) albuterol for acute asthma or COPD

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

156
Q

Dobutamine primarily targets…

A

B1 more so than B2, alpha

157
Q

dobutamine uses

A

1) HF (inotropic more so than chronotropic)

2) cardiac stress testing

158
Q

Dopamine targets…

A

D1 = D2, then B, then A

159
Q

dopamine uses

A

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
Q

epinephrine targets primarily

A

beta more so than alpha

161
Q

isoproterenol uses

A

1) electrophysiologic evaluation of tachyarrhythmias

162
Q

isoproterenol contraindications

A

CAD (can worsen ischemia)

163
Q

midodrine MOA

A

alpha1 agonist

164
Q

norepinephrine uses

A

1) hypotension

2) septic shock

165
Q

norepinephrine targets

A

alpha1, then alpha 2, then beta1

166
Q

phenylephrine targets

A

alpha1 primarily, but also alpha 2

167
Q

phenylephrine uses

A

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

168
Q

what are the indirect sympathomimetics?

A

1) amphetamine
2) cocaine
3) ephedrine

169
Q

amphetamine MOA

A

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

170
Q

cocaine MOA

A

1) indirect general agonist

2) reuptake inhibitor

171
Q

ephedrine MOA

A

1) indirect general agonist, releases stored catecholamines

172
Q

ephedrine uses

A

1) nasal decongestion
2) urinary incontinence
3) hypotension

173
Q

isoproterenol affects on BP, HR

A

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

174
Q

guanfacine MOA

A

A2 agonists

175
Q

clonidine, guanfacine uses

A

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

176
Q

Clonidine, guanfacine AE’s

A

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

177
Q

alpha-methyldopa AE’s

A

1) direct coombs positive hemolysis

2) SLE-like syndrome

178
Q

beta blockers used for SVTs?

A

metoprolol + esmolol

179
Q

beta blocker MOA for use in SVTs?

A

Decrease AV conduction velocity.

180
Q

beta blocker MOA for use in HTN?

A

1) decrease cardiac output

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

181
Q

beta blockers used to decrease mortality in HF?

A

1) bisoprolol
2) carvedilol
3) metoprolol

182
Q

timolol mechanism in glaucoma?

A

Decreases secretion of aqueous humor

183
Q

Other BB usage?

A

Decrease variceal bleeding

184
Q

BB’s to use to decrease variceal bleeding?

A

1) nadolol

2) propranolol

185
Q

beta blocker MOA for use in variceal bleeding?

A

Decrease hepatic venous pressure gradient and portal HTN.

186
Q

beta blocker AE’s

A

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

187
Q

metoprolol other AE

A

dyslipidemia

188
Q

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

A

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

189
Q

nonselective betablockers

A

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

190
Q

nonselective antagonism means what?

A

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

191
Q

Nebivolol MOA

A

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

192
Q

tetrodotoxin source

A

pufferfish

193
Q

tetrodotoxin MOA

A

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

194
Q

tetrodotoxin symptoms

A

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

195
Q

tetrodotoxin treatment

A

primarily supportive

196
Q

ciguatoxin sources

A

Reef fish…

1) barracuda
2) snapper
3) moray eel

197
Q

ciguatoxin mechanism

A

1) OPENs Na+ channels, causing depolarization

198
Q

ciguatoxin presentation

A

symptoms mimic cholinergic poisoning

199
Q

ciguatoxin poisoning treatment

A

primarily supportive

200
Q

scombroid poisoning is basically…

A

histamine poisoning

201
Q

scombroid sources

A

spoiled dark-meat fish..

1) tuna
2) mahi-mahi
3) mackerel
4) bonito

202
Q

scombroid mechanism

A

Bacterial histidine decarboxylase converts histidine to histamine

203
Q

What is scombroid poisoning frequently misdiagnosed as?

A

Fish allergy

204
Q

scombroid poisoning presentation…

A

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
Q

scombroid treatment

A

Antihistamines. Albuterol + epinephrine if needed.

206
Q

Treatment for amphetamine overdose…

A

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

207
Q

Treatment for antimuscarinic/anticholinergic overdose…

A

physostigmine + *control hyperthermia

208
Q

Treatment for arsenic overdose…

A

dimercaprol + succimer

209
Q

Treatment for beta-blocker overdose…

A

saline + atropine + glucagon

210
Q

Treatment for copper overdose…

A

penicillamine + trientine

211
Q

Treatment for cyanide overdose…

A

Nitrite + thiosulfate + hydroxocobalamin

212
Q

Treatment for digitalis overdose…

A

anti-dig Fab fragments

213
Q

Treatment for gold overdose…

A

penicillamine + dimercaprol (BAL) + succimer

214
Q

Treatment for heparin overdose…

A

protamine sulfate

215
Q

Treatment for iron overdose…

A

deFERoxamine, deFERasirox, deFERipone

216
Q

Treatment for lead overdose…

A

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

217
Q

Treatment for amphetamine overdose…

A

diMERCaprol + succimer

218
Q

Treatment for methanol, ethylene glycol (antifreeze) overdose…

A

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

219
Q

Treatment for opioid overdose…

A

naloxone

220
Q

Treatment for salicylate overdose…

A

sodium bicarb (alkalinize urine) + dialysis

221
Q

Drugs associated with coronary vasospasm…

A

1) cocaine
2) sumatriptan
3) ergot alkaloids

222
Q

Drugs associated with cutaneous flushing…

A 
VANCE
Vancomycin
Adenosine
Niacin
Ca2+ channel blockers
Echinocandins
223
Q

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

A

Dexrazoxane

224
Q

Drugs associated with torsades de pointes

A

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

225
Q

Drugs associated with hot flashes

A

1) tamoxifen

2) clomiphene

226
Q

Drugs associated with hyperglycemia

A

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

227
Q

Drugs associated with hypothyroidism

A

1) lithium
2) amiodarone
3) sulfonamides

228
Q

Erythromycin AE’s

A

acute cholestatic hepatitis + jaundice

229
Q

Drugs causing diarrhea

A

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
Q

Drugs associated with focal to massive hepatic necrosis…

A 
HAVAc
Halothane
Amanita phalloides 
Valproic acid
Acetaminophen
231
Q

drugs associated with hepatitis

A 
Rifampin
Isoniazid
Pyrazinamide
Statins
Fibrates
232
Q

Drugs associated with pancreatitis

A 
Didanosine
Corticosteroids
Alcohol
Valproic acid
Azathioprine
Diuretics (furosemide, HCTZ)
233
Q

Drugs associated with pill-induced esophagitis

A

1) tetracyclines
2) bisphosphonates
3) potassium chloride

234
Q

How do you minimize pill-induced esophagitis?

A

good posture + adequate water ingestion

235
Q

Drugs associated with pseudomembranous colitis

A

Clindamycin
Ampicillin
Cephalosporins

236
Q

Drugs associated with

agranulocytosis

A 
Clozapine
Carbamazepine
propylthiouracil
Methimazole
Colchicine
Ganciclovir
237
Q

Drugs associated with aplastic anemia

A 
Carbamazepine
Methimazole
NSAIDs
Benzene
Chloramphenicol
PTU
238
Q

Drugs associated with direct Coombs-positive hemolytic anemia

A

1) methyldopa

2) penicillin

239
Q

Drugs associated with hemolysis in G6PD deficiency

A 
Isoniazid
Sulfonamides
Dapsone
Primaquine
Aspirin
Ibuprofen
Nitrofurantoin
240
Q

Drugs associated with megaloblastic anemia

A

Phenytoin
Methotrexate
Sulfa drugs

241
Q

Drugs associated with thrombosis

A

1) OCPs

2) hormone replacement therapy

242
Q

Drugs causing gingival hyperplasia

A

1) phenytoin
2) calcium channel blockers
3) cyclosporine

243
Q

Drugs associated with hyperuricemia

A

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

244
Q

Drugs associated with myopathy

A 
Vibrates
Niacin
colchicine
hydroxycloroquine
INF-alpha
penicillamine
statins
GCs
245
Q

Drugs associated with osteoporosis

A

corticosteroids, heparin

246
Q

Drugs associated with photosensitivity

A

Sulfonamides
Amiodarone
Tetracyclines
5-FU

247
Q

Drugs associated with Stevens-Johnson syndrome

A

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

248
Q

drugs causing cinchonism

A

quinidine + quinine

249
Q

Drugs associated with Parkinson-like syndrome

A

Cogwheel rigidity of ARM

1) antipsychotics
2) reserpine
3) metoclopromide

250
Q

Drugs associated with seizures

A

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

251
Q

Drugs associated with tardive dyskinesia

A

1) antipsychotics

2) metoclopramide

252
Q

Drugs associated with fanconi syndrome

A

1) tenofovir

2) ifosfamide

253
Q

Drugs associated with hemorrhagic cystitis?

A

1) cyclophosphamide

2) ifosfamide

254
Q

Drugs associated with interstitial nephritis?

A

1) methicillin
2) NSAIDs
3) furosemide

255
Q

Drugs associated with SIADH?

A

1) carbamazepine
2) cyclophosphamide
3) SSRIs

256
Q

Drugs associated with pulmonary fibrosis?

A

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

257
Q

Drugs with antimuscarinic side effects?

A

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

258
Q

Drugs associated with disulfiram-like reaction?

A

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

259
Q

Drugs associated with nephrotoxicity/ototoxicity?

A

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

260
Q

What can you treat cisplatin toxicity with?

A

Amifostine

261
Q

CYP 450 inducers

A

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

262
Q

CYP-450 substrates

A

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

263
Q

CYP-450 inhibitors

A

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
Q

sulfa allergic reaction presentation…

A

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

265
Q

Sulfa drugs

A

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

266
Q

-azole suffix means…

A

ergosterol synthesis inhibitor

267
Q

-cillin means…

A

peptidoglycan synthesis inhibitor

268
Q

-ivir suffix means…

A

neuraminidase inhibitor (oseltamivir)

269
Q

-ovir suffix means..

A

DNA polymerase inhibitor (acyclovir)

270
Q

-ane suffix means

A

inhalation general anesthetic

271
Q

thioridazine

A

typical antipsychotic (ends in -azine)

272
Q

-caine means…

A

local anesthetic

273
Q

-etine means…

A

SSRI

274
Q

-curium, -curonium

A

*nondepolarizing paralytic

275
Q

atracurium, vecuronium

A

non depolarizing paralytics

276
Q

-terol means…

A

Beta2 agonist

277
Q

prazosin

A

alpha *1 antagonist

278
Q

-afil means…

A

PDE-5 inhibitor

279
Q

-dipine means..

A

dihydropyridine Ca2+ channel blocker

280
Q

-xaban means…

A

direct factor Xa inhibitors

281
Q

examples of factor Xa inhibitors

A

1) apixaban
2) edoxaban
3) rivaroxaban

282
Q

-glitazone means…

A

PPAR-gamma activator

283
Q

Example of PPAR-gamma activator

A

Rosiglitazone

284
Q

-prost means…

A

prostaglandin analog

285
Q

-tidine means

A

H*2 antagonist

286
Q

-tropin means

A

pituitary hormone

287
Q

-ximab means…

A

Chimeric monoclonal Ab (eg basiliximab)

288
Q

-zumab means

A

Humanized monoclonal Ab (daclizumab)

289
Q

daclizumab vs. basiliximab

A

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

290
Q

ergot alkaloids

A

bromocriptine + cabergoline

291
Q

nitrosoureas

A

Carmustine
Lomustine
Semustine
Streptozocin

292
Q

NNRTIs

A

Delaviridine
Efavirenz
Nevirapine

293
Q

Cholinergic effects

A

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

STEP (85 decks)

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