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tsomkapQ > Kaplan High Yield Pharm > Flashcards

Kaplan High Yield Pharm Flashcards

1
Q

What is Vmax?

A

Vmax is the maximum velocity for a given amount of enzyme

-Proportional to enzyme concentration

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2
Q

What is the Michaelis constant (Km)?

A

Km is the substrate concentration required to reach half Vmax
Km = 1/affinity

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3
Q

What does a high Km mean?

A

A high Km means low affinity (opposite for low Km)

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4
Q

What is the equation for the intersection of the Y-axis on a Lineweaver-Burk plot?

A

Intersection of the Y-axis = 1/Vmax

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5
Q

What is the equation for the intersection of the X-axis on a Lineweaver-Burk plot?

A

Intersection of the X-axis = -1/Km

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6
Q

What are the characteristics of a competitive inhibitor?

A
  • Resemble substrate, bind at active site
  • Increasing substrate concentration can overcome inhibition
  • Decrease potency
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7
Q

What is the effect on Vmax and Km by a competitive inhibitor?

A

No effect on Vmax

Increases Km

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8
Q

What are the characteristics of non-competitive inhibitors?

A
  • Bind to allosteric site, not near active site
  • Cannot be overcome with increased substrate concentration
  • Decrease efficacy
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9
Q

What is the effect on Vmax and Km by a non-competitive inhibitor?

A

Decreases Vmax

No effect on Km

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10
Q

Do the Lineweaver-Burk plots of competitive or non-competitive inhibitors cross with the Lineweaver-Burk plot with no inhibitor?

A

The Lineweaver-Burk plot of a competitive inhibitor crosses the Lineweaver-Burk plot with no inhibitor

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11
Q

What is the equation for volume of distribution (Vd)?

A

Vd = total amount of drug in body/conc. of drug in plasma

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12
Q

A low Vd (4-8 L) means the drug is mostly contained in?

A

Blood

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13
Q

A medium Vd (12-14L) means the drug is mostly contained in?

A

Extracellular fluid

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14
Q

A high Vd (> total body water) means the drug is?

A

Distributed in all tissues, non-fluid compartments (fat)

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15
Q

What is the effect of hepatic disease on the Vd of plasma protein bound drugs?

A

Decreased synthesis of plasma proteins -> Drugs diffuse into body tissues, effectively increasing the drug’s Vd

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16
Q

What is the effect of renal disease on the Vd of plasma protein bound drugs?

A

Plasma proteins (and bound drugs) are excreted in the urine

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17
Q

What is the equation for drug clearance?

A

Drug clearance = Rate of drug elim./plasma drug conc.

Vd x Ke

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18
Q

When is renal clearance equal to GFR?

A

When there is no reabsorption, secretion, or plasma protein binding

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19
Q

What 2 substances are used to estimate the GFR?

A

Inulin and creatinine

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20
Q

What is the equation for the clearance of protein bound drugs (not cleared)?

A

Clearance = free fraction x GFR

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21
Q

What is the half life equation?

A

T1/2 = (.7 x Vd)/clearance

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22
Q

How many half lives does it take to reach steady state with continuous infusion?

A

Steady state is reached in 4-5 half lives with continuous infusion

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23
Q

What is a loading dose?

A
  • Large initial dose given to fill up Vd

- Can increase plasma concentration in less than 4-5 half lives

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24
Q

What is the equation for loading dose?

A

LD = (Vd x Cp)/F

Cp=blood plasma conc.
F=bioavailability

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25
Q

What is a maintenance dose?

A
  • A dose given to maintain constant blood plasma levels

- Lowered if hepatic/renal function is impaired

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26
Q

What is the equation for maintenance dose?

A

MD = (Cl x Cp)/F

Cl = clearance

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27
Q

What is bioavailability (F)?

A
  • Fraction of administered drug that reaches systemic circulation
  • Some drugs fail to be absorbed, or are metabolized before reaching circulation
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28
Q

What is the bioavailability of an IV infusion?

A

F = 1 for IV infusion

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29
Q

What is zero order elimination?

A

Constant amount of drug eliminated with time

Example: 100 mg -> 90 mg -> 80 mg…10 mg being eliminated per hr

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30
Q

What are substances that exhibit zero order elimination?

A

Phenytoin, aspirin, ethanol

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31
Q

What is first order elimination?

A
  • Constant fraction of drug eliminated with time
  • Most drugs follow first order kinetics
  • Example: 100 mg -> 50 mg -> 25 mg…elimination of half concentration per hour
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32
Q

Explain the renal excretion of ionized and non-ionized substances

A
  • Both ionized forms and non-ionized forms are filtered
  • Only non-ionized forms are actively secreted or reabsorbed
  • Ionized forms of drug are trapped in the filtrate
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33
Q

What are some examples of drugs that are weak acids?

A

Barbiturates, methotrexate, aspirin

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34
Q

How would you increase the elimination of a weak acid to save a patient from an overdose?

A

Give them base (HCO3-) -> alkalinize the urine (opposite for a weak base -> give NH4Cl)

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35
Q

What is an example of a drug that is a weak base?

A

Amphetamines

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36
Q

What is biotransformation?

A

Conversion of lipid soluble drugs into water soluble metabolites in the liver -> increases renal excretion
-Two forms of drug metabolism-phase 1 and 2

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37
Q

What is phase 1 drug metabolism?

A

Oxidation, reduction, and hydrolysis of drugs by cytochrome P450 enzymes

  • Located in the smooth endoplasmic reticulum of the liver
  • Require O2 and NADP
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38
Q

Name the drugs that are cytochrome P450 inducers (9)

-What is the acronym?

A

QRBPSGGCC

  • Quinidine
  • Barbiturates
  • Phenytoin
  • St. John’s Wort
  • Rifampin
  • Griseofulvin
  • Glucocorticoids
  • Carbamazepine
  • Chronic alcohol use
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39
Q

Name the drugs that are cytochrome P450 inhibitors (10)

-What is the acronym?

A

HIS COCK MR G

  • HIV protease inhibitors
  • Isoniazid (INH)
  • Sulfonamides
  • Cimetidine
  • Omeprazole
  • Chloramphenicol
  • Ketoconazole
  • Macrolides
  • Ritonavir
  • Grapefruit juice
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40
Q

What are the non-cytochrome P450 enzyme phase 1 metabolism mechanisms?

A
  • Hydrolysis (addition of H2O to drugs to assist metabolism, esterase/amidase)
  • Monoamine oxidase
  • Alcohol metabolism
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41
Q

What are the endogenous amines metabolized by MAO?

A

Dopamine, NE, and serotonin

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42
Q

What is the exogenous amine metabolized by MAO?

A

Tyramine

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43
Q

What is phase 2 metabolism?

A

Conjugation of functional groups to a drug via transferase enzymes

  • Converts polar molecules to inactive molecules -> increase renal excretion
  • Mechanisms of metabolism include - acetylation, glucuronidation, sulfation, methylation, and glutathione conjugation
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44
Q

What is potency?

A
  • Measure of how much drug is required to give desired effect
  • Typically expressed as EC50 - concentration that gives 50% of max response
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45
Q

What is efficacy?

A

Maximal effect that a drug can produce

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46
Q

See graphs on slides 17 and 18

A

…

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47
Q

What is a full agonist?

A

With receptor saturation, drug can reach full efficacy

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48
Q

What is a partial agonist?

A

Acts at the same site as agonist, but lower EFFICACY

-Can have higher or lower potency than agonist

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49
Q

What are physiologic antagonists?

A

Substrate that produces opposite effect of an agonist, but acts through different receptor/pathway

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50
Q

What is therapeutic index?

A
  • Measure of drug safety

- Higher therapeutic index indicates safer drug

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51
Q

What is the equation for therapeutic index?

A

TI = LD50/ED50

-See graph on slide 20

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52
Q

Draw out the diagram on slide 22

A

…

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53
Q

What is a nicotinic Ach receptor (nAchr) and what are the different types?

A

Ligand gated Na/K channels

  • Nn-autonomic
  • Nm-somatic muscular (neuromuscular junction)
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54
Q

The cAMP system for GPCRs includes receptors for?

A
  • Catecholamines beta1, beta2 (Gs), and alpha2 (Gi)
  • Ach M2 (Gi)
  • Glucagon (Gs)
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55
Q

The PIP2 system for GPCRs includes receptors for?

A

ALL are Gq

  • Catecholamines alpha1
  • Ach M1-M3
  • Angiotensin II
  • Vasopressin
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56
Q

Study the rest of slide 24 and 25

A

…

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57
Q

What are 3 examples of drugs that act at the cholinergic nerve terminal?

A
  • Hemicholinium
  • Botulinum toxin
  • Vesamicol
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58
Q

What is the MOA of hemicholinium?

A

Inhibits choline uptake into nerve terminal -> decreases Ach production

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59
Q

What is the MOA of botulinum toxin?

A

Inhibits the release of Ach containing vesicles from the nerve terminal

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60
Q

What is the MOA of vesamicol?

A

Stops the conversion of acetyl CoA to Ach by inhibiting choline acetyl transferase

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61
Q

What are some examples of drugs that act at the adrenergic nerve terminal?

A
  • Metyrosine
  • Reserpine
  • Cocaine, TCAs, and amphetamines
  • Guanethidine
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62
Q

What is the MOA of metyrosine?

A

Inhibits the conversion of tyrosine to Dopa by inhibiting tyrosine hydroxylase

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63
Q

What is the MOA of reserpine?

A

Blocks the uptake of NE into vesicles

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64
Q

What is the dual action MOA for amphetamines?

A
  • Directly block the reuptake of NE

- Increase the release of NE into the synapse

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65
Q

What is the MOA of cocaine and TCAs?

A

Directly block the reuptake of NE

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66
Q

What is the MOA of guanethidine?

A

Blocks the release of NE into the synapse

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67
Q

What are examples of cholinomimetics (parasympathomimetics)?

A
  • Bethanechol
  • Carbachol
  • Pilocarpine
  • Methacholine
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68
Q

What is bethanechol?

A
  • Muscarinic agonist
  • Longer acting than Ach (resistant to acetylcholinesterase)
  • Tx of ileus and urinary retention (Bowels and bladder)
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69
Q

What is carbachol?

A
  • Muscarinic/nicotinic agonist
  • Also resistant to acetylcholinesterase
  • Applied to eye to cause contraction of ciliary muscle, relief to open angle glaucoma, also constricts pupil
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70
Q

What is pilocarpine?

A
  • Muscarinic agonist
  • Stimulates tears, sweat, saliva
  • Constricts pupil and ciliary muscle
  • Also used for acute glaucoma
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71
Q

What is methacholine?

A
  • Muscarinic agonist
  • Causes bronchoconstriction when inhaled
  • Used for asthma challenge test
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72
Q

What are examples of anticholinesterases (indirect cholinomimetics)?

A
  • Neostigmine
  • Pyridostigmine
  • Edrophonium
  • Physostigmine
  • Echothiophate
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73
Q

What is neostigmine?

A
  • Quaternary amine-acts on peripheral nervous system (no entry into CNS)
  • Tx of ileus, urinary retention, and myasthenia gravis
  • Post-operative reversal of neuromuscular junction blockade
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74
Q

What is pyridostigmine?

A
  • Quaternary amine-acts on peripheral nervous system (no entry into CNS)
  • Treatment of myasthenia gravis
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75
Q

What is edrophonium?

A
  • Very short acting (10-20 mins)

- Diagnosis of myasthenia gravis

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76
Q

What is physostigmine?

A
  • Tertiary amine (can enter CNS)

- Tx of glaucoma, antidote for atropine toxicity

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77
Q

Echothiophate is used for the tx of?

A

Glaucoma

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78
Q

What are the symptoms for cholinesterase inhibitor poisoning (high systemic Ach)? What is the acronym?

A

DUMBBELSS

  • Diarrhea
  • Urination
  • Miosis
  • Bronchoconstriction
  • Bradycardia
  • Excitation (skeletal muscle and CNS)
  • Lacrimation
  • Salivation
  • Sweating
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79
Q

What is the treatment for cholinesterase inhibitor poisoning (high systemic Ach)?

A
  • Atropine (muscarinic antagonist)

- Pralidoxime (2PAM) (regenerates cholinesterase)

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80
Q

What is the classic example of a muscarinic receptor antagonist?

81
Q

What is atropine?

A
  • Muscarinic receptor antagonist
  • Tertiary amine-can enter the CNS
  • Effects-the opposite of DUMBBELSS
82
Q

What are the clinical uses of atropine?

A
  • Antispasmodic
  • Antisecretory
  • Management of AchE inhibitor OD
  • Antidiarrheal
  • Ophthamology (but long action)
83
Q

What is tropicamide used for clinically?

A

Ophthamology (topical)

84
Q

What is ipratropium used for clinically?

A

Asthma and COPD (inhalational)

-No CNS entry, no change in mucous viscosity

85
Q

What is scopolamine used for clinically?

A

Tx of motion sickness

-causes sedation and short term memory block

86
Q

What are benztropine and trihexyphenidyl used for?

A
  • Lipid-soluble (CNS entry)

- Used in parkinsonism and in acute extrapyramidal symptoms induced by antipsychotics

87
Q

What are the direct sympathomimetics?

A
  • Epi and NE
  • Isoproterenol
  • Dopamine
  • Dobutamine
  • Ritodrine
  • Metaproterenol
  • Albuterol
  • Salmeterol
  • Terbutaline
88
Q

What is the function of epinephrine?

A
  • Alpha and beta agonist (a1=a2, b1=b2)

- Low doses selective for B1 receptors

89
Q

What is the clinical use of epi?

A
  • Tx for anaphylaxis, open angle glaucoma, asthma hypotension
  • Prolongs the effect of local anesthesia
90
Q

What are the adverse effects of epi?

A

Increased systolic blood pressure and decreased diastolic blood->Widened pulse pressure

91
Q

What is the function of NE?

A

Mainly an alpha receptor agonist but has some beta receptor activity (a1=a2, b1>b2)

92
Q

What is the clinical use of norepi?

A

Tx of hypotension

93
Q

What are the adverse effects of NE?

A
  • Splanchnic vasoconstriction (can cause bowel ischemia) and decreased renal perfusion
  • Increased systolic blood pressure and diastolic blood pressure -> little/no change in pulse pressure
  • Reflexive decrease in HR
94
Q

What is isoproterenol?

A
  • B1B2 agonist
  • Tx for AV conduction block
  • Decreases diastolic BP (induces a reflexive increase in HR)
95
Q

What is dopamine?

A
  • D1=D2 > beta > alpha
  • Inotropic and chronotropic
  • Treatment for shock, especially with heart failure
96
Q

What is dobutamine?

A
  • B1>B2 agonist
  • Inotropic
  • Tx of heart failure
  • Used in cardiac stress test
97
Q

What is ritodrine?

A
  • B2 agonist

- Reduces premature uterine contractions

98
Q

What are the selective B2 agonists (B2>B1)?

A
  • Metaproterenol-short-acting
  • Albuterol-short-acting
  • Salmeterol-long-acting
  • Terbutaline
99
Q

Name the indirect sympathomimetics

A

Amphetamine, ephedrine, cocaine, tyramine

100
Q

What is amphetamine?

A
  • Induces catecholamine release from terminals

- Tx for narcolepsy, obesity, and ADHD

101
Q

What is ephedrine?

A
  • Induces catecholamine release

- Tx for nasal congestion, urinary incontinence, and hypotension

102
Q

What is cocaine?

A
  • Inhibits reuptake of catecholamines

- Causes vasoconstriction, local anesthetic

103
Q

What is tyramine?

A
  • Similar mechanism to amphetamines, cleared by MAO
  • MAO inhibitors can cause HTN, especially with tyramine (breakdown product of tyrosine)-rich foods such as wine and cheese
104
Q

What are the sympathoplegics?

A
  • Clonidine

- alpha-methyldopa

105
Q

What is clonidine?

A

Agonist of central alpha2-adrenergic receptors which decrease sympathetic outflow

106
Q

What is alpha-methyldopa?

A

Used to treat HTN by decreasing sympathetic tone

107
Q

Both clonidine and alpha-methyldopa are used to tx?

A

HTN that is resistant to other tx

108
Q

What are the non-selective alpha (a1 and a2) blockers?

A
  • Phenoxybenzamine

- Phentolamine

109
Q

What is phenoxybenzamine?

A
  • Non-selective and irreversible

- Tx of pheochromocytoma, Raynaud’s syndrome

110
Q

What is important to know when giving alpha blockers for the tx of pheochromocytoma?

A

Give the alpha blockers before removal of pheo tumors to prevent excessive catecholamines from spilling into circulation

111
Q

What is phentolamine?

A
  • Non-selective and reversible

- Tx of pheo and Raynaud’s syndrome

112
Q

What are the alpha1-selective blockers?

A
  • Prazosin
  • Terazosin
  • Doxazosin
113
Q

What are the alpha1 selective blockers used for?

A
  • Tx of HTN, urinary retention (BPH)

- May cause orthostatic hypotension (usually taken at bedtime)

114
Q

Which alpha1 selective blocker is the longest acting?

115
Q

What is the alpha2-selective alpha blocker?

A

Mirtazapine

116
Q

What is mirtazapine used for?

A
  • Tx of depression

- Can cause sedation, increased serum cholesterol, and increased appetite

117
Q

What are the non-selective (b1 and b2) beta blockers?

A
  • Propanolol
  • Timolol
  • Nadolol
  • Pindolol
118
Q

What is propanolol used for?

119
Q

What is timolol used for?

120
Q

What are the beta1 selective beta blockers?

A
  • Metoprolol
  • Atenolol
  • Betaxolol
  • Esmolol
121
Q

Which of the beta1-selective beta blockers is very short acting?

122
Q

What are the mixed alpha and beta blockers?

A
  • Carvedilol

- Labetalol

123
Q

What are the partial beta-agonists?

A
  • Pindolol

- Acebutolol

124
Q

When used for HTN use of beta blockers results in?

A
  • Decreased CO

- Decreased renin production (beta1-blockade of JG cells)

125
Q

When used for angina use of beta blockers results in?

A
  • Decreased HR
  • Decreased inotropy
  • Decreased myocardial O2 consumption
126
Q

When used for myocardial infarction use of beta blockers results in?

A

decreased mortality

127
Q

Which beta blockers are used for sinus ventricular tachycardia (SVT)?

A

Propanolol/esmolol -> decrease AV conduction

128
Q

When used for HF use of beta blockers results in?

A

Slows the progression of CHF (decreases cardiac demand)

129
Q

What are the side effects of beta blockers?

A
  • Exacerbation of asthma
  • Impotence
  • Bradycardia
  • AV blockade
  • Sedation
  • Decreased glucagon secretion -> Hypoglycemia in diabetics
130
Q

What is the antidote used to treat acetaminophen toxicity?

A

N-acetylcysteine

131
Q

What is the antidote for salicylate toxicity?

A

Sodium bicarbonate (alkalinize the urine), dialysis for severe cases

132
Q

What is the antidote for anticholinesterases/organophosphate (insecticides) poisoning?

A

Atropine and pralidoxime (2-PAM)

133
Q

What is the antidote for anticholinergics toxicity?

A

Physostigmine

134
Q

What is the antidote for beta blocker toxicity?

A

Glucagon (to increase inotropy and chronotropy of the heart)

135
Q

What is the antidote for digitalis toxicity?

A
  • Anti-digitalis Fab fragments

- Normalize serum electrolytes, especially K, then lidocaine, magnesium

136
Q

What is the antidote for iron toxicity?

A

Deferoxamine

137
Q

What are the antidotes for lead poisoning?

A

Ca-EDTA (chelator), dimercaprol, succimer, penicillamine

138
Q

What is the antidote for arsenic, mercury, or gold poisoning?

A

Dimercaprol, succimer

139
Q

What is the antidote for copper, arsenic, or gold poisoning?

A

Penicillamine

140
Q

What is the antidote for cyanide poisoning?

A

Nitrite, hydroxycobalamin, thiosulfate

141
Q

What is the antidote for methemoglobin?

A

Methylene blue, vitamin C

142
Q

What is the antidote for carbon monoxide poisoning?

A

100% O2 (hyperbaric chamber)

143
Q

What is the clinical presentation of methanol poisoning?

144
Q

What is the clinical presentation of ethylene glycol?

A

Nephrotoxicity -> acute renal failure

145
Q

What is the antidote for methanol/ethylene glycol poisoning?

A

Ethanol, fomepizol

146
Q

What are the antidotes for opioid overdose and what is the MOA of each?

A

Naloxone-Competitive antagonist

Naltrexone-Receptor antagonist

147
Q

What is the antidote for benzodiazepine toxicity?

A

Flumazenil

148
Q

What is the antidote for TCA toxicity?

A
  • NaHCO3 (IV alkalinization)

- Adjunctively treat for seizure, hyperthermia, and arrhythmia

149
Q

What is the antidote for heparin toxicity?

150
Q

What are the antidotes for warfarin (coumadin) toxicity?

A
  • Vitamin K

- Fresh frozen plasma-used for acute warfarin toxicity (restore 1972CS)

151
Q

What is the antidote for tPA, streptokinase toxicity?

A

Aminocaproic acid

152
Q

What is the antidote for theophylline?

A

beta-blocker

153
Q

Atropine-like (anti-cholinergic) symptoms can be caused by what agents?

A
  • TCAs

- Anti-histamines

154
Q

Dilated cardiomyopathy can be caused by what agents?

A

Doxorubicin, daunorubicin

155
Q

Coronary vasospasm can be caused by what agents?

A
  • Cocaine

- Sumatriptan

156
Q

Cutaneous flushing can be caused by what agents?

A

VANC

  • Vancomycin
  • Adenosine
  • Niacin
  • Ca channel blockers
157
Q

The cutaenous flushing that can be caused by vancomycin is known as?

A

Red man syndrome

158
Q

Torsades de pointes can be caused by what agents?

A
  • Class III (sotalol)
  • Class Ia (quinidine)
  • Cisapride (removed from market d/t arrhythmias)
  • Tx with Mg
159
Q

Agranulocytosis can be caused by what agents?

A
  • Clozapine
  • Carbamazepine
  • Colchicine
  • Propylthiouracil
  • Dapsone
  • Methimazole
160
Q

Aplastic anemia can be caused by what agents?

A
  • Chloramphenicol
  • Benzene
  • NSAIDs
  • Falbamate
161
Q

Hemolytic anemia (Coombs-positive) can be caused by what agent?

A

Methyldopa

162
Q

Gray baby syndrome can be caused by what agent?

A

Chloramphenicol

163
Q

G6PD hemolytic anemia can be caused by what agents?

A
  • Isoniazid (INH)
  • Sulfa drugs
  • Aspirin
  • Ibuprofen
  • Nitrofurantoin
  • Primaquin
164
Q

Megaloblastic anemia (hypersegmented neutrophils) can be caused by what agents?

A
  • Methotrexate
  • Sulfa drugs
  • Phenytoin
165
Q

Thrombosis can be caused by what agents?

A

Oral contraceptives (higher risk with smoking)

166
Q

Cough can be caused by what agent?

A

ACE-inhibitors (use ARBs instead)

167
Q

Pulmonary fibrosis can be caused by what agents?

A
  • Bleomycin
  • Amiodarone
  • Busulfan
168
Q

Hepatitis can be caused by what agent?

A

Isoniazid (INH)

169
Q

Cholestatic hepatitis can be caused by what agents?

A

Macrolide abx (azithromycin, clarithromycin)

170
Q

Hepatic necrosis can be caused by what agents?

A
  • Halothane
  • Valproate
  • Acetaminophen
  • Amanita phalloides (mushroom)
171
Q

Pseudomembranous colitis (C. difficile) can be caused by what agents?

A
  • Clindamycin
  • Ampicillin
  • Cephalosporins
172
Q

Pancreatitis can be caused by what agents?

A
  • Azathioprine
  • Sulfonamides
  • Valproate
  • Methyldopa
  • Furosemide
  • Corticosteroids
173
Q

Adrenocortical insufficiency can be caused by what agents?

A
  • Glucocorticoid withdrawal

- Etomidate

174
Q

Gynecomastia can be caused by what agents?

A
  • Spironolactone
  • Digitalis
  • Cimetidine
  • Alcohol
  • Estrogens
  • Ketoconazole
175
Q

Hot flashes can be caused by what agents?

A
  • Tamoxifen

- Clomiphene

176
Q

Hypothyroidism can be caused by what agents?

A
  • Lithium

- Amiodarone

177
Q

Gingival hyperplasia can be caused by what agent?

178
Q

Gout can be caused by what agents?

A
  • Furosemide

- Thiazides

179
Q

Osteoporosis can be caused by what agents?

A
  • Corticosteroids

- Heparin

180
Q

Photosensitivity can be caused by what agents?

A
  • Fluoroquinolones
  • Amiodarone
  • Tetracyclines
  • Sulfonamides
181
Q

Rash (Stevens-Johnson syndrome) can be caused by what agents?

A
  • Carbamazepine
  • Allopurinol
  • Penicillin
  • Sulfa drugs
182
Q

Lupus-like syndrome can be caused by what agents?

A
  • Hydralazine
  • INH
  • Procainamide
  • Phenytoin
183
Q

Tendon rupture (achilles) can be caused by what agent?

A

Fluoroquinolones

184
Q

Fanconi’s syndrome can be caused by what agent?

A

Tetracyline (expired)

185
Q

Interstitial nephritis can be caused by what agents?

A
  • Methicillin

- NSAIDs

186
Q

Hemorrhagic cystitis can be caused by what agent?

A

Cyclophosphamide

187
Q

Cinchonism can be caused by what agents?

A
  • Quinidine

- Quinine

188
Q

Diabetes insipidus can be caused by what agents?

A
  • Lithium

- Demeclocycline

189
Q

Seizures can be caused by what agents?

A
  • Buproprion
  • Imipenem/cilastatin
  • INH
190
Q

Parkinson-like syndrome can be caused by what agents?

A
  • Haloperidol
  • Chlorpromazine
  • Reserpine
  • Metoclopramide
191
Q

Tardive dyskinesia can be caused by what agents?

A

Typical antipsychotics

192
Q

Disulfiram-like reaction (acute sensitivity to alcohol) can be caused by what agents?

A
  • Metronidazole
  • Procarbazine
  • Sulfonylureas
  • Cephalosporins
193
Q

Nephrotoxicity/neurotoxicity can be caused by what agents?

A

Polymxyins

194
Q

Nephrotoxicity/ototoxicity can be caused by what agents?

A
  • Aminoglycosides
  • Vancomycin
  • Loop diuretics
  • Cisplatin
195
Q

Review slide 58

196
Q

List the sulfa drugs (any drugs that contain a sulfonamide group)
-Allergies to these drugs are common

A
  • Sulfonamide abx
  • TMP-SMX
  • Acetazolamide
  • Furosemide
  • Thiazides
  • Sulfsalazine
  • Celecoxib
  • Probenecid
197
Q

What are the symptoms of a reaction to sulfa drugs?

A
  • Pruritic rash
  • Fever
  • Stevens-Johnson syndrome
  • Hemolytic anemia
  • Thrombocytopenia
  • Agranulocytosis
  • Urticaria (hives)
198
Q

Common drug suffixes-MEMORIZE

tsomkapQ (117 decks)

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