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STEP1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

How does Km relate to affinity?

A

they are inversely related

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2
Q

A sigmoidal Michaelis-Menten curve is indicative of what receptor characteristic?

A

cooperative binding

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3
Q

How are Km and Vmax derived from a Lineweaver-Burk plot?

A
  • the y-intercept equals 1/Vmax
  • the x-intercept equals 1/-Km
  • the slope = Km/Vmax
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4
Q

How do competitive and non-competitive inhibitors affect the Lineweaver-Burk plot for w given ligand-receptor relationship?

A
  • a competitive inhibitor affects Km only, so the x-intercept shifts more positive
  • a noncompetitive inhibitor affects Vmax without affecting Km, so the y-intercept shifts more positive
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5
Q

How does a competitive inhibitor impact Km and Vmax? Potency and efficacy?

A

it will increase Km (lower affinity) without affecting Vmax, as such it has lowered the potency without lower the efficacy

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6
Q

How does a noncompetitive inhibitor impact Km and Vmax? Potency and efficacy?

A

it will lower Vmax without affecting Km, as such it lowers efficacy without affecting potency

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7
Q

How is bioavailability calculated?

A

F = AUC(oral)/AUC(iv)

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8
Q

How is Vd calculated and interpreted?

A
  • Vd = (total amount of drug in body)/(plasma drug concentration)
  • when Vd = 0.45 it has been distributed in plasma
  • when Vd = 0.2 it has been distributed in ECF
  • when Vd = 0.6 it has been distributed in TBW
  • when Vd > 0.7 it has been distributed in tissue
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9
Q

How does liver disease affect Vd?

A

it often increases Vd because it lowers the amount of protein-bound drug, increasing the free fraction

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10
Q

How do we define clearance?

A

the volume of plasma cleared of drug per unit time

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11
Q

How is clearance calculated?

A

CL = (rate of elimination)/(plasma drug concentration) = Vd x K(el)

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12
Q

Give two equations for calculating K(el).

A

K(el) = CL/Vd = 0.7/(half life)

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13
Q

How long does it take for a drug to reach a new steady state?

A

roughly 4-5 half lives

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14
Q

How is a loading dose calculated?

A

LD = (desired plasma concentration)(Vd)/(F)

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15
Q

How is a maintenance dose calculated?

A

MD = (desired plasma concentration x CL x dosing interval)/F

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16
Q

How do liver and kidney disease affect the required maintenance and loading dose?

A
  • they often decrease the maintenance dose (because CL is reduced)
  • the loading dose is usually unchanged
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17
Q

What is a permissive drug interaction?

A

one in which the presence of drug A is required for the full effects of substance B

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18
Q

What is a tachyphylactic drug interaction? Give an example.

A

one in which there is an acute decrease in response to a drug after initial/repeated administration (e.g. MDMA depletes NT stores and so there is an acute decrease in response)

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19
Q

How does zero-order kinetics compare to first-order kinetics?

A

drugs that experience zero-order kinetics are cleared at a constant amount per time (independent of drug concentration) while drugs that experience first-order kinetics are cleared at a constant fraction per time (dependent of drug concentration)

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20
Q

What three drugs classically experience zero-order kinetics?

A
  • ethanol
  • phenytoin (at high concentrations)
  • aspirin (at high concentrations)
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21
Q

How can you treat an overdose of a drug that is a weak acid?

A

you can alkalinize the urine with bicarbonate to trap the drug in urine and promote elimination of the drug

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22
Q

Drugs that are weak bases become trapped in what environment?

A

a pH more acidic than their pKa, under which circumstance they become deprotonate and trapped in their ionized form

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23
Q

What reactions constitute phase I and phase II drug metabolism?

A
  • phase I: oxidation, reduction, hydrolysis

- phase II: methylation, glucuronidation, acetylation, sulfation, glutathione conjugation

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24
Q

What changes in phase I and II drug metabolism pathways do geriatric patients experience?

A

they typically lose phase I reactions first

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25
Q

What are the efficacy and potency of a drug?

A
  • potency: amount of drug needed for a given effect (i.e. ability to bind the receptor), defined by EC50
  • efficacy: maximal effect a drug can produce (i.e. ability to active the receptor once bound), defined by Vmax
  • e.g. a HTN med that reduces BP by only 5 mmHg but at a very low dose has high potency but low efficacy
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26
Q

How are therapeutic index and margin of safety calculated?

A
  • TI = LD50/ED50

- MoS = LD1/ED99

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27
Q

Where are most nicotinic receptors found in the PNS?

A
  • at the ganglionic synapse of both the SNS and PNS
  • at the adrenal medulla
  • at the neuromuscular junction
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28
Q

Describe the basic anatomy of the SNS and PNS.

A
  • the PNS has craniosacral outputs with long pre-ganglionic fibers and short post-synaptic fibers
  • the SNS has thoracolumbar outputs with short pre-ganglionic fibers synapsing on long post-synaptic fibers in paravertebral chain ganglia
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29
Q

How are the two types of sweat glands innervated?

A
  • eccrine (thermoregulatory) receive input from the SNS but express muscarinic receptors
  • apocrine receive input from the SNS and express a1 receptors
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30
Q

What is the basic structure of nicotinic and muscarinic receptors?

A
  • nicotinic are ligand-gated Na/K channels

- muscarinic are GPCRs

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31
Q

a1, a2, and B receptors are linked to what second messenger cascades?

A
  • a1: Gq
  • a2: Gi
  • B: Gs
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32
Q

M1, M2, and M3 receptors are linked to what second messenger cascades?

A
  • M1: Gq
  • M2: Gi
  • M3: Gq
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33
Q

D1 and D2 receptors are linked to what second messenger cascades?

A
  • D1: Gs

- D2: Gi

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34
Q

H1 and H2 receptors are linked to what second messenger cascades?

A

H1: q
H2: s

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35
Q

V1 and V2 receptors are linked to what second messenger cascades?

A

V1: Gq
V2: Gs

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36
Q

Describe the Gq signal cascade.

A
  • Gq activates PLC, which then cleaves PIP2, forming IP3 and DAG
  • DAG activates PKC
  • IP3 serves to increase intracellular calcium
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37
Q

a1 receptors are tied to which second messenger system and mediate what effects?

A
  • tied to Gq
  • promote vascular smooth muscle contraction (increase TPR) , contraction of the pupillary dilator muscle (mydriasis), and contraction of intestinal as well as bladder sphincter muscles to inhibit evacuation
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38
Q

a2 receptors are tied to which second messenger system and mediate what effects?

A
  • tied to Gi

- expressed on the presynaptic terminal and mediate auto-inhibition to reduce the release of NT

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39
Q

B1 receptors are tied to which second messenger system and mediate what effects?

A
  • tied to Gs

- mediate an increase in HR, inotropy, renin release, and lipolysis

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40
Q

B2 receptors are tied to which second messenger system and mediate what effects?

A
  • tied to Gs
  • stimulation vasodilation in the lungs and skeletal muscle, bronchodilation, lipolysis, insulin release, uterine relaxation, bladder relaxation, ciliary muscle relaxation, and aqueous humor production
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41
Q

Describe the ANS innervation of the eye.

A
  • a receptors are expressed by the pupillary dilator muscle and mediate mydriasis
  • B receptors are expressed by the secretory epithelium and activation promotes production of aqueous humor
  • muscarinic receptors are expressed by the ciliary muscle and pupillary sphincter muscle; activation promotes accommodation of the lens for near vision, drainage of aqueous humor through the canal of Schlemm, and constriction of the pupil (miosis)
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42
Q

M1 receptors are tied to which second messenger system and mediate what effects?

A
  • tied to Gq

- function in the CNS and enteric nervous system

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43
Q

M2 receptors are tied to which second messenger system and mediate what effects?

A
  • tied to Gi

- decreases heart rate and contractility of the atria

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44
Q

How does activation of B1 receptors affect ion currents in the heart?

A
  • increases funny sodium current
  • increases L-type calcium current
  • increases potassium current
  • no effect on sodium current (QRS complex unchanged)
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45
Q

How does activation of muscarinic receptors affect ion currents in the heart?

A
  • decreases funny sodium current

- decreases L-type calcium current

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46
Q

M3 receptors are tied to which second messenger system and mediate what effects?

A
  • tied to Gq
  • promote glandular secretions, gut peristalsis, bladder contraction, bronchoconstriction, mitosis, and lens accommodation
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47
Q

H1 and H2 histamine receptors mediate what effects?

A
  • H1 mediates mucus production, urticaria, pruritis, pain, bronchoconstriction, and an increase in vascular permeability
  • H2 is primarily responsible for increasing gastric acid secretion
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48
Q

Describe monoamine biosynthesis.

A
  • tyrosine is converted to DOPA by tyrosine hydroxylase
  • DOPA is converted to DA by DOPA decarboxylase
  • DA is packaged into vesicles by VMAT
  • in the vesicle, DA is converted to NE by DA-B-hydroxylase
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49
Q

How are monoamines cleared from the synaptic cleft?

A

reuptake

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50
Q

How is acetylcholine cleared from the synaptic cleft?

A

AChE

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51
Q

Describe acetylcholine biosynthesis.

A
  • acetyl-CoA from the mitochondria is combined with choline recycled from the synaptic cleft in a reaction catalyzed by ChAT
  • acetylcholine is then packaged into vesicles by VAT
  • in the synaptic cleft, it is degraded by AChE and choline is recycled
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52
Q

What is tyramine?

A
  • an indirect sympathomimetic
  • enters presynaptic vesicles and displaces monoamines, which subsequently diffuse freely into the synaptic cleft, stimulating post-synaptic receptors
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53
Q

What is hemicholinium?

A

an indirect ACh antagonist that inhibits reuptake of choline by the presynaptic terminal, thereby reducing it’s release

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54
Q

What is vesamicol?

A

an indirect ACh antagonist that inhibits VAT, so ACh stays in the intracellular space where it is degraded rather than released

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55
Q

How does botulinum toxin affect autonomics?

A

it inhibits the release of ACh

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56
Q

What is metyrosine?

A

an indirect sympatholytic drug that inhibits tyrosine hydroxylase and monoamine synthesis

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57
Q

What is reserpine?

A

an indirect sympatholytic drug that inhibits VMAT and packaging of monoamines

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58
Q

What is bethanechol? What are it’s uses?

A
  • a choline ester and muscarinic agonist resistant to AChE

- used to activate the bowel and bladder in those with post-op ileum, neurogenic ileum, or urinary retention

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59
Q

What is carbachol?

A

a choline ester and muscarinic agonist

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60
Q

What is pilocarpine? What are it’s primary uses?

A
  • a muscarinic alkaloid that is a potent stimulator of sweat, tears, and saliva
  • used to treat glaucoma and xerostomia (Sjogren syndrome)
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61
Q

What is donepezil? What are it’s uses?

A

it inhibits AChE and is an indirect cholinomimetic used in the treatment of Alzheimer’s

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62
Q

What is galantamine? What are it’s uses?

A

it inhibits AChE and is an indirect cholinomimetic used in the treatment of Alzheimer’s

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63
Q

What is tacrine?

A

it inhibits AChE and is an indirect cholinomimetic

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64
Q

What is edrophoium? What are it’s uses?

A

it is an AChE inhibitor with a very short half life, primarily used to diagnose myasthenia gravis

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65
Q

What is neostigmine?

A

it is an AChE inhibitor without any CNS activity

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66
Q

What is physostigmine and what are it’s uses?

A
  • it is an AChE inhibitor
  • crosses the BBB
  • used to treat anticholinergic toxicity (atropine poisoning)
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67
Q

What is pyridostigmine and what are it’s uses?

A
  • it is an AChE inhibitor
  • does not penetrate the BBB
  • used to treat myasthenia gravis
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68
Q

Cholinomimetics are likely to exacerbate what three conditions?

A

COPD, asthma, and peptic ulcers

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69
Q

Organophosphate Poisoning

A
  • organophosphates are AChE inhibitors that experience an “aging” effect and are essentially irreversible inhibitors
  • presents with diarrhea, urination, mitosis, bronchospasm, bradycardia, excitation of skeletal muscle, lacrimation, eccrine sweating, and salivation
  • primary risk is that it creates a depolarizing blockade at the NMJ of the diaphragm and leads to respiratory failure
  • treat with atropine and pralidoxime
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70
Q

What is pralidoxime?

A
  • a partial AChE inhibitor with very strong affinity

- used to treat organophosphate poisoning if caught early enough

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71
Q

What is atropine?

A

a tertiary amine (crosses BBB) muscarinic antagonist

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72
Q

What is homatropine?

A

a tertiary amine (crosses BBB) muscarinic antagonist

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73
Q

What is tropicamide?

A

a tertiary amine (crosses BBB) muscarinic antagonist

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74
Q

What is benzotropine? What is it’s primary clinical use?

A
  • a tertiary amine (crosses BBB) muscarinic antagonist

- used to treat Parkinson disease (“park my benz”) and acute dystonia

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75
Q

What is glycopyrrolate? What are it’s primary clinical uses?

A
  • a tertiary amine (crosses BBB) muscarinic antagonist

- used parenterally to reduce airway secretions preoperatively and orally to prevent drooling and peptic ulcers

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76
Q

What is hyoscyamine and what is it’s primary clinical use?

A
  • a muscarinic antagonist

- used as an antispasmodic to treat IBS

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77
Q

What is dicyclomine and what is it’s primary clinical use?

A
  • a tertiary amine muscarinic antagonist

- used as an antispasmodic to treat IBS

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78
Q

What is ipratropium and what is it’s primary clinical use?

A
  • a quaternary amine muscarinic antagonist

- used to treat COPD and asthma

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79
Q

What is tiotropium and what is it’s primary clinical use?

A
  • a quaternary amine muscarinic antagonist

- used to treat COPD and asthma

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80
Q

What is oxybutynin?

A

a tertiary amine muscarinic antagonist

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81
Q

What is solifenacin?

A

a tertiary amine muscarinic antagonist

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82
Q

What is tolterodine? What is it’s primary clinical use?

A
  • a tertiary amine muscarinic antagonist with specificity for M3 receptors in the GU system
  • used to reduce bladder spasms and urge incontinence
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83
Q

What is scopolamine? What is it’s primary clinical use?

A

a tertiary amine muscarinic antagonist used to treat motion sickness

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84
Q

Describe the effects of atropine poisoning.

A

“hot as a hare, dry as a bone, red as a beet, blind as a bat, and mad as a hatter”

  • reduces sweating so temp rises and skin is dry and flush
  • cycloplegia and acute angle-closure glaucoma
  • constipation and urinary retention
  • disorientation
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85
Q

What is jimson weed?

A

a herb/plant that causes mydriasis (known as “gardener’s pupil”) because it contains an alkaloid that is a muscarinic antagonist

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86
Q

What is albuterol?

A

an inhaled B2 agonist used to treat asthma

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87
Q

What is salmeterol?

A

a long-acting oral B2 agonist used to control asthma

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88
Q

What is formoterol?

A

a long-acting oral B2 agonist used to control asthma

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89
Q

What is terbutaline?

A

a B2 agonist

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90
Q

What is dobutamine?

A

a selective B1 agonist

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91
Q

Dopamine will activate what adrenergic receptors?

A

it has a greater affinity for B1 receptors than a1, but at high doses will activate both

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92
Q

What is the selectivity of epinephrine?

A

it activates all adrenergic receptors

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93
Q

What is the selectivity of norepinephrine?

A

it activates a1, a2, and B1

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94
Q

What is the selectivity of isoproterenol?

A

B1 and B2

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95
Q

What is midodrine?

A

an a1 agonist

96
Q

What effect does D1 receptor activation have in the ANS?

A

it relaxes renal vascular smooth muscle

97
Q

What is fenoldopam? Explain it’s ANS effects and uses.

A
  • it is a D1 agonist
  • D1 receptors mediate relaxation of renal vascular smooth muscle
  • therefore, it is used to treat post-op hypertension and hypertensive crisis and is used to promote natriuresis
98
Q

What is the selectivity of phenylephrine?

A

a1 receptors

99
Q

How do amphetamines elicit a sympathomimetic activity?

A
  • they use the NET to enter the presynaptic terminal where they are packaged into the secretory vesicles by VMAT
  • this displaces NE from the vesicles and concentrations build in the presynaptic terminal
  • eventually the concentration rises significantly to reverse the action of NET and NE is expelled into the synaptic cleft
100
Q

Amphetamines are used to treat what medical conditions?

A
  • narcolepsy
  • obesity
  • ADHD
101
Q

What ANS drug class is contraindicated when you suspect cocaine use?

A

never give a beta blocker because this can lead to unopposed a1 vasoconstriction and extreme hypertension

102
Q

What is ephedrine? What are it’s primary uses?

A

it is an indirect sympathomimetic that releases stored catecholamines and serves as a nasal decongestant, treatment for urinary incontinence, and hypotensive therapy

103
Q

How does NE affect TPR, blood pressure, and HR?

A
  • unopposed a1 activity increases TPR, which increases diastolic pressure
  • B1 activity increases inotropy and pulse pressure, raising systolic pressure
  • the net effect is an increase in MAP, which is met by a reflex bradycardia
104
Q

How does epinephrine affect TPR, blood pressure, and HR?

A
  • B2 vasodilation outweighs a1 vasoconstriction and there is a net decrease in TPR, which decreases diastolic pressure
  • B1 activity increases inotropy and pulse pressure, raising systolic pressure
  • the net effect is a slight increase in MAP that isn’t sufficient to induce a reflex bradycardia; instead B1 activity produces a chronotropic effect
105
Q

How does isoproterenol affect TPR, blood pressure, and HR?

A
  • B2 vasodilation creates a significant drop in TPR and diastolic pressure
  • B1 activity increases inotropy and pulse pressure
  • the net effect is a drop in MAP, which induces a reflex tachycardia
  • this tachycardia is also exacerbated by the chronotropic effects of B1
106
Q

List three a2 agonists?

A
  • clonidine
  • guanfacine
  • a-methyldopa
107
Q

What is a-methyldopa? What is it’s primary clinical use? What are it’s major adverse effects?

A
  • it is an a2 agonist (sympatholytic)
  • it is used to treat hypertension during pregnancy
  • it may produce a hemolysis and an SLE-like syndrome
108
Q

What are the primary clinical uses of clonidine and guanfacine? What are their major adverse effects?

A
  • ADHD, Tourette syndrome, hypertensive urgency

- may leads to CNS depression, bradycardia, hypotension, respiratory depression, and miosis

109
Q

What is phenoxybenzamine? What is it’s primary clinical use? What are it’s likely side effects?

A
  • it is an irreversible, non-selective a-adrenergic receptor blocker
  • it is used in the preoperative treatment of pheochromocytomas
  • it may produce orthostatic hypotension and reflex tachycardia
110
Q

What is phentolamine? What is it’s primary clinical use? What are it’s likely side effects?

A
  • it is a reversible, non-selective a-adrenergic receptor blocker
  • it is administered to those on MAO inhibitors who eat tyramine-containing foods
  • it may produce orthostatic hypotension and reflex tachycardia
111
Q

List four a1-selective antagonists? What are their primary clinical uses? What are their likely side effects?

A
  • prazosin, terazosin, doxazosin, tamsulosin
  • used to treat the urinary retention of BPH plus prazosin is used to treat PTSD and all are used to treat hypertension except tamsulosin
  • often cause orthostatic hypotension, dizziness, and headache with the first dose
112
Q

What is mirtazapine? What is it’s primary clinical use and it’s most likely side effects?

A
  • it is an a2-selective antagonist
  • used to treat depression
  • may produce sedation, hypercholesteremia, and an increase in appetite
113
Q

What is yohimbe?

A

an a2-selective antagonist

114
Q

Which beta blockers are also used as class II anti-arrhythmics?

A

metoprolol and esmolol

115
Q

Which beta blocker is typically used to treat glaucoma?

A

timolol

116
Q

Which group of ANS drugs are used to treat variceal bleeding? How?

A
  • beta blockers, specifically nadolol and propanolol

- they decrease the hepatic venous pressure and portal hypertension

117
Q

Name 7 applications for beta blockers.

A
  • angina pectoris
  • reduce the mortality of MI
  • anti-arrhythmics
  • hypertension
  • heart failure
  • glaucoma
  • vatical bleeding
118
Q

Beta-blockers have what side effects?

A
  • erectile dysfunction
  • bradycardia, AV block, exacerbation of HF
  • seizures, sedation, sleep alterations
  • dyslipidemia
  • exacerbation of asthma or COPD
119
Q

What role do beta-blockers play in the treatment of heart failure?

A

they are only used to treat acute heart failure because in the long-term they exacerbate the HF and increase mortality

120
Q

Which beta-blockers are B1 selective?

A

mostly those in the first half of the alphabet

  • acebutolol
  • atenolol
  • betaxolol
  • bisprolol
  • esmolol
  • metoprolol
121
Q

What is labetalol?

A

an a1, B1, B2 antagonist

122
Q

Wha tis carvedilol?

A

an a1, B1, B2 antagonsit

123
Q

How are antagonists of a1, B1, and B2 named?

A

they have the a modified beta-blocker suffix (e.g. labetalol, carvedilol)

124
Q

Which beta-blockers also have partial agonist activity?

A

acebutolol, pindolol, carteolol, penbutolol

125
Q

What is unique about nebivolol compared to other beta blockers?

A

it blocks B1 and B2 activity to reduce cardiac work load but also activates B3 receptors to activate NOS and improve coronary blood flow (i.e. it is a beta blocker with vasodilative effects)

126
Q

Tetrodotoxin Poisoning

A
  • a toxin from pufferfish
  • binds fast voltage-gated sodium channels in cardiac and nerve tissue, preventing depolarization
  • presents with nausea, diarrhea, paresthesia, weakness, dizziness, and loss of reflexes
  • treatment is supportive
127
Q

Ciguatoxin Poisoning

A
  • a toxin from reef fish (e.g. barracuda, snapper, and moray eel)
  • opens sodium channels and causes depolarization
  • mimics cholinergic poisoning
  • treatment is supportive
128
Q

Scombroid Poisoning

A
  • a result of eating spoiled dark-meat fish such as tuna, mahi-mahi, mackerel, or bonito
  • bacterial histidine decarboxylase converts histidine to histamine, which is the mediator of this effect
  • mimics anaphylaxis and is frequently misdiagnosed as a fish allergy
  • treat with anti-histamines, albuterol, and epinephrine as severity dictates
129
Q

How is acetaminophen toxicity treated?

A

N-acetylcysteine to replenish glutathione

130
Q

How is amphetamine toxicity treated?

A

NH4Cl to acidify urine

131
Q

How is antimuscarinic toxicity treated?

A

Physostigmine and control of hyperthermia

132
Q

How is arsenic toxicity treated?

A

Dimercaprol, succimer

133
Q

How is benzodiazepine toxicity treated?

A

flumazenil

134
Q

How is beta-blocker toxicity treated?

A

saline, atropine, and glucagon

135
Q

How is copper toxicity treated?

A

penicillamine, trientine

136
Q

How is cyanide toxicity treated?

A

nitrite + thiosulfate, hydroxocobalamin

137
Q

How is digitalis toxicity treated?

A

anti-dig antibodies

138
Q

How is gold toxicity treated?

A

penicillamine, dimercaprol, succimer

139
Q

How is iron toxicity treated?

A

deferoxamine, deferasirox, deferiprone

140
Q

How is lead toxicity treated?

A

EDTA, dimercaprol, succimer, penicillamine

141
Q

How is mercury toxicity treated?

A

dimercaprol, succimer

142
Q

How is methanol toxicity treated?

A

femepizole is preferred to ethanol and dialysis

143
Q

How is opioids toxicity treated?

A

naloxone

144
Q

How is salicylate toxicity treated?

A

sodium bicarb to alkalinize urine

145
Q

How is TCA toxicity treated?

A

sodium bicarb to alkalinize urine

146
Q

What is succimer?

A

a drug used to treat heavy metal poisoning

147
Q

What is dimercaprol?

A

a drug used to treat heavy metal poisoning

148
Q

Which drug ends in the suffix “-azole”?

A

ergosterol synthesis inhibitor (e.g. ketoconazole)

149
Q

Which drug ends in the suffix “-bendazole”?

A

anti-parasitics/anti-helminthics

150
Q

Which drug ends in the suffix “-cillin”?

A

peptidoglycan synthesis inhibitors

151
Q

Which drug ends in the suffix “-cycline”?

A

protein synthesis inhibitors (e.g. tetracycline)

152
Q

Which drug ends in the suffix “-ivir”?

A

neuraminidase inhibitors

153
Q

Which drug ends in the suffix “-navir”?

A

protease inhibitors (e.g. ritonavir)

154
Q

Which drug ends in the suffix “-ovir”?

A

DNA polymerase inhibitor (e.g. acyclovir)

155
Q

Which drug ends in the suffix “-thromycin”?

A

macrolide antibiotics

156
Q

Which drug ends in the suffix “-ane”?

A

inhalation general anesthetic

157
Q

Which drug ends in the suffix “-azine”?

A

typical antipsychotic

158
Q

Which drug ends in the suffix “-barbital”?

A

barbiturate

159
Q

Which drug ends in the suffix “-caine”?

A

local anesthetic

160
Q

Which drug ends in the suffix “-etine”?

A

SSRI

161
Q

Which drug ends in the suffix “-ipramine”?

A

TCA

162
Q

Which drug ends in the suffix “-triptyline”?

A

TCA

163
Q

Which drug ends in the suffix “-triptan”?

A

5-HT(1B/1D) agonists

164
Q

Which drug ends in the suffix “-zepam”?

A

benzodiazepines

165
Q

Which drug ends in the suffix “-zolam”?

A

benzodiazepines

166
Q

Which drug ends in the suffix “-chol”?

A

cholinergic agonist

167
Q

Which drug ends in the suffix “-curium”?

A

non-depolarizing paralytic

168
Q

Which drug ends in the suffix “-curonium”?

A

non-depolarizing paralytic

169
Q

Which drug ends in the suffix “-olol”?

A

beta-blocker

170
Q

Which drug ends in the suffix “-stigmine”?

A

AChE inhibitors

171
Q

Which drug ends in the suffix “-terol”?

A

beta2-agonist

172
Q

Which drug ends in the suffix “-zosin”?

A

alpha1-antagonist

173
Q

Which drug ends in the suffix “-afil”?

A

PDE-5 inhibitors (e.g. sildenafil)

174
Q

Which drug ends in the suffix “-dipine”?

A

dihydropyridine calcium channel blocker

175
Q

Which drug ends in the suffix “-pril”?

A

ACE inhibitor

176
Q

Which drug ends in the suffix “-sartan”?

A

angiotensin II receptor antagonist

177
Q

Which drug ends in the suffix “-statin”?

A

HMG-CoA reductase inhibitors

178
Q

Which drug ends in the suffix “-xaban”?

A

direct factor Xa inhibitors

179
Q

Which drug ends in the suffix “-dronate”?

A

bisphosphonate

180
Q

Which drug ends in the suffix “-glitazone”?

A

PPARy activator (e.g. rosiglitazone)

181
Q

Which drug ends in the suffix “-prazole”?

A

proton pump inhibitor

182
Q

Which drug ends in the suffix “-prost”?

A

prostaglandin analog

183
Q

Which drug ends in the suffix “-tidine”?

A

H2-antagonist

184
Q

Which drug ends in the suffix “-tropin”?

A

pituitary hormone (e.g. somatotropin)

185
Q

Which drug ends in the suffix “-ximab”?

A

chimeric monoclonal antibody

186
Q

Which drug ends in the suffix “-zumab”?

A

humanized monoclonal antibody

187
Q

Which drugs are known to cause coronary vasospasm?

A
  • cocaine
  • sumatriptan
  • ergot alkaloids
188
Q

Which drugs are known to cause cutaneous flushing?

A

VANCE

  • vancomycin
  • adenosine
  • niacin
  • calcium channel blockers
  • echinocandins
189
Q

Which drugs are known to cause dilated cardiomyopathy?

A

anthracyclines (doxorubicin, daunoribicin)

190
Q

Which drugs are known to cause torsades de pointes?

A

ABCDE

  • anti-Arrhythmics (IA and III)
  • anti-Biotics
  • anti-Cycotics
  • anti-Depressants
  • anti-Emetics
191
Q

What can be used to prevent dilated cardiomyopathy in those taking an anthracycline like doxorubicin?

A

dexrazoxane

192
Q

Which drugs are known to cause hot flashes?

A

tamoxifen and clomiphene

193
Q

Which drugs are known to cause hyperglycemia?

A

Taking Pills Necessitates Having blood Checked

  • tacrolimus
  • protease inhibitors
  • niacin
  • HCTZ
  • corticosteroids
194
Q

Which drugs are known to cause hypothyroidism?

A

lithium, amiodarone, sulfonamides

195
Q

Which drugs are known to cause acute cholestatic hepatitis and jaundice?

A

erythromycin

196
Q

Which drugs are known to cause hepatic necrosis?

A

HAVAc

  • Halothane
  • Amanita phalloides (death cap mushroom)
  • Valproic acid
  • Acetaminophen
197
Q

Which drugs are known to cause hepatitis?

A

rifampin, isoniazid, pyrazinamide, statins, fibrates

198
Q

Which drugs are known to cause pancreatitis?

A

Drugs Causing A Violent Abdominal Distress

  • Didanosine
  • Corticosteroids
  • Alcohol
  • Valproic Acid
  • Azathioprine
  • Diuretics
199
Q

Which drugs are known to cause pill-induced esophagitis?

A
  • bisphosphonates
  • tetracyclines
  • potassium chloride
200
Q

Which drugs are known to cause pseudomembrane colitis?

A

clindamycin, ampicillin, cephalosporins

201
Q

How can pill-induced esophagitis be minimized?

A

adequate water ingestion and maintaining an upright posture after taking the medication

202
Q

Which drugs are known to cause agranulocytosis?

A

Can Cause Pretty Major Collapse of Granulocytes

  • Clozapine
  • Carbamazepine
  • Propylthiouracil
  • Methimazole
  • Colchicine
  • Canciclovir
203
Q

Which drugs are known to cause aplastic anemia?

A

Can’t Make New Blood Cells Properly

  • Carbamazepine
  • Methimazole
  • NSAIDs
  • Benzene
  • Chloramphenicol
  • Propylthiouracil
204
Q

Which drugs are known to cause direct coombs-positive hemolytic anemia?

A

methyldopa, penicillin

205
Q

Which drugs are known to cause gray baby syndrome?

A

chloramphenicol

206
Q

Which drugs are known to cause hemolysis in G6PD deficiency?

A

hemolysis IS D PAIN

  • Isoniazid
  • Sulfonamides
  • Dapsone
  • Primaquine
  • Aspirin
  • Ibuprofen
  • Nitrofurantoin
207
Q

Which drugs are known to cause megaloblastic anemia?

A

having a blast with PMS

  • Phenytoin
  • Methotrexate
  • Sulfa Drugs
208
Q

Which drugs are known to cause thrombotic complications?

A

OCPs and hormone replacement therapy

209
Q

Which drugs are known to cause fat redistribution?

A

protease inhibitors and glucocorticoids

210
Q

Which drugs are known to cause gingival hyperplasia?

A

phenytoin, calcium channel blockers, cyclosporine

211
Q

Which drugs are known to cause hyperuricemia?

A

Painful Tophi and Feet Need Care

  • Pyrazinamide
  • Thiazides
  • Furosemide
  • Niacin
  • Cyclosporine
212
Q

Which drugs are known to cause myopathy?

A

fibrates, niacin, colchicine, hydroxychloroquine, IFNa, penicillamine, statins, glucocorticoids

213
Q

Which drugs are known to cause osteoporosis?

A

corticosteroids and heparin

214
Q

Which drugs are known to cause photosensitivity?

A

SAT For photo

  • sulfonamides
  • amiodarone
  • tetracyclines
  • 5-FU
215
Q

Which drugs are known to cause Stevens-Johnson syndrome?

A

Steven Johnson has Epileptic ALLergy to SULFA drugs and PENICILLIN

  • anti-epileptics
  • allopurinol
  • sulfa drugs
  • penicillin
216
Q

Which drugs are known to cause an SLE-like syndrome?

A

SHIPPE

  • sulfa drugs
  • hydralazine
  • isoniazid
  • procainamide
  • phenytoin
  • etanercept
217
Q

Which drugs are known to cause teeth discoloration?

A

tetracyclines

218
Q

Which drugs are known to cause tendonitis, tendon rupture, and cartilage damage?

A

fluoroquinolones

219
Q

Which drugs are known to cause cinchonism?

A

quinidine and quinine

220
Q

Which drugs are known to cause a Parkinson-like syndrome?

A

ARM

  • antipsychotics
  • reserpine
  • metoclopramide
221
Q

Which drugs are known to cause seizures?

A

I BITE

  • isoniazid
  • bupropion
  • imipenem
  • tramadol
  • enflurane
222
Q

Which drugs are known to cause tardive dyskinesia?

A

antipsychotics and metoclopramide

223
Q

Which drugs are known to cause diabetes insipidus?

A

lithium nad demeclocycline

224
Q

Which drugs are known to cause Fanconi syndrome?

A

tenofovir and ifosfamide

225
Q

Which drugs are known to cause hemorrhagic cystitis?

A

cyclophosphamide and ifosfamide

226
Q

Which drugs are known to cause interstitial nephritis?

A

methicillin, NSAIDs, and furosemide

227
Q

Which drugs are known to cause SIADH?

A

carbamazepine, cyclophosphamide, and SSRIs

228
Q

Which drugs are known to cause a dry cough?

A

ACE inhibitors

229
Q

Which drugs are known to cause pulmonary fibrosis?

A

My Nose Cannot Breathe Bad Air

  • methotrexate
  • nitrofurantoin
  • carmustine
  • bleomycin
  • busulfan
  • amiodarone
230
Q

Which drugs are known to cause a nephrotoxicity or ototoxicity?

A
  • aminoglycosides
  • vancomycin
  • loop diuretics
  • cisplatin
231
Q

How is cisplatin ototoxicity treated?

A

amifostine

232
Q

Which drugs cause a disulfiram-like reaction?

A
  • metronidazole
  • certain cephalosporins
  • griseofulvin
  • procarbazine
  • first gen sulfonylureas
233
Q

Which drugs are classic CYP inducers?

A

CHRONIC ALCOHOLics STeal Phen-Phen and Never Refuse GReasy CARBs

  • chronic alcohol
  • st. john’s wort
  • phenytoin
  • phenobarbital
  • nevirapine
  • rifampin
  • griseofulvin
  • carbamazepine
234
Q

Which drugs are classic CYP substrates?

A

We Always Train Outdoors

  • warfarin
  • anti-epileptics
  • theophylline
  • OCPs
235
Q

Which drugs are classic CYP inhibitors?

A

AAA RACKS IN GQ Magazine

  • acute alcohol abuse
  • ritonavir
  • amiodarone
  • cimetidine/ciprofloxacin
  • ketoconazole
  • sulfonamides
  • isoniazid
  • grapefruit juice
  • quinidine
  • macrolides (except azithromycin)
236
Q

Which drugs are sulfa drugs?

A

Scary Sulfa Pharm FACTS

  • sulfonamides
  • sulfasalazine
  • probenecid
  • furosemide
  • acetazolamide
  • celecoxib
  • thiazides
  • sulfonylureas
237
Q

How does a sulfa drug reaction present?

A

may develop fever, UTI, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria

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