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Pharm > Midterm > Flashcards

Midterm Flashcards

1
Q

1st generation H1 antagonist anticholinergic adverse effects

A

dry mouth, blurred vision, urinary retention, impotence

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2
Q

1st generation H1 antagonist cardiovascular adverse effects

A

tachycardia, prolonged QTc, heart blocks, arrhythmias

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3
Q

1st generation H1 antagonist CNS adverse effects

A

somnolence, diminished alertness, slowed reaction time, impaired cognitive function (take in PM)

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4
Q

4 concepts of pharmacodynamics

A

absorption, distribution, biotransformation, elimination

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5
Q

Additive effects

A

1+1=2 summation of drugs taken concurrently (same receptor)

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6
Q

Antagonistic effects

A

1+1=0 one drug cancels/blocks effects of another

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7
Q

Antagonistic effects

A

1+1=0 one drug cancels/blocks effects of another

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8
Q

Are NSAIDs highly protein bound?

A

yes

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9
Q

Benadryl is prescribed as:

A

antiemetic, sedative, antipruritic

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10
Q

Benefits of benzos

A

less risk of tolerance and abuse, large margin of safety

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11
Q

Benzos are used for:

A

antianxiety, sedatives, anticonvulsants, muscle relaxants

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12
Q

Binding of glutamate to NMDA receptors allows

A

influx of Na and Ca

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13
Q

Cardiovascular Adverse Effects of NSAIDs

A

HTN, HF exacerbation, thrombotic events

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14
Q

Clearance

A

volume of plasma cleared of drug per unit time

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15
Q

Clinical uses for SSRIs

A

depression, panic disorders, OCD, PTSD, social phobias

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16
Q

Clonidine

A

selective partial alpha 2 agonist

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17
Q

CNS adverse effects of NSAIDs

A

headache, aseptic meningitis, hearing disturbances

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18
Q

conjugation

A

makes lipid soluble drugs water soluble (with glucoronic acid)

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19
Q

conjugation leads to:

A

a more polar compound that is more highly ionized at physiologic pH and therefore more easily extractable by the kidney via glomerular filtration

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20
Q

Consideration of patient taking lithium and anesthesia

A

decreased anesthetic requirements- may delay CNS recovery from barbiturates, response to NMBs may be prolonged

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21
Q

contraindication of benzo use for anxiety

A

history of alcohol or other substance abuse

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22
Q

Corticosteroids

A

naturally occurring from adrenal glands (hydrocortisone)

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23
Q

dermatologic adverse effects of NSAIDs

A

urticaria, rash, erythema multiforme

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24
Q

Does succinylcholine affect CP450?

A

no

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25
Q

Dosage of benzos for generalized anxiety

A

low dose, 2-5 mg (diazepam) up to 3 times daily

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26
Q

Effects of clonidine

A

antihypertensive, potentiate analgesic effects post-op induced by LA

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27
Q

End products of biotransformation are…

A

usually inactive and water soluble (easier excretion)

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28
Q

example of microsomal enzymes

A

cytochrome P450

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29
Q

Examples of 1st generation H1 antagonists

A

benadryl, chlorpheniramine, atarax

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30
Q

Examples of drugs that undergo zero order kinetics

A

alcohol, phenytoin (dilantin)

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31
Q

Examples of drugs that undergo zero order kinetics

A

alcohol, phenytoin (dilantin), fluoxetine, salicylates

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32
Q

Examples of H2 receptor antagonists

A

ranitidine, famotidine, nizatidine, cimeditine

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33
Q

Examples of MAOIs

A

phenelzine, tranylcypromine, isocarboxazid

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34
Q

Examples of SSRIs

A

fluoxetine, paroxetine, sertraline, fluvoxamine, citalopram, escitalopram

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35
Q

First Order Kinetics

A

constant FRACTION of drug eliminated/unit time

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36
Q

First pass effect

A

drugs absorbed through GI tract enter portal venous blood and pass through liver before entering systemic circulation

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37
Q

GABA anion

A

chloride

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38
Q

GI adverse effects of NSAIDs

A

gastrophy, gastric bleeding, esophageal disease, pancreatitis

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39
Q

Goal lithium plasma concentration

A

1.0-1.2 mEq/L

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40
Q

GU adverse effects of NSAIDs

A

renal insufficiency (use with caution with renal disease), Na/fluid retention, papillary necrosis, interstitial nephritis

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41
Q

Half life

A

period of time required for the concentration/amount of drug to be reduced by half

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42
Q

hematologic adverse effects of NSAIDS

A

increased risk of intraop bleeding (platelet inhibition/dysfunction)

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43
Q

Hepatic clearance depends on

A

hepatic blood flow and hepatic extraction ratio

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44
Q

hepatic extraction ratio

A

drug removed from blood- limited by enzyme activity

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45
Q

How do benzos work?

A

facilitating actions of GABA (y-aminobutyric acid)- major inhibitory NT of nervous system

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46
Q

How long does it take for lithium to be effective?

A

several weeks

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47
Q

hydrolysis

A

split apart with water

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48
Q

In 1st order kinetics, rate of drug elimination is ? to drug plasma concentration

A

proportional (rate increases as drug concentration increases)

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49
Q

In order to be eliminated by the kidneys, can the drug still be bound to proteins?

A

no- must be non protein bound to cross into glomerular filtrate

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50
Q

In zero order kinetics, the rate of drug elimination is ? of drug plasma concentration

A

independent (rate does not increase as drug concentration increases)

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51
Q

ionized

A

charged, not lipid soluble

52
Q

Lithium plasma concentrations should be drawn no sooner than ? after dosage change

A

5 days (unless toxicity suspected)

53
Q

Mechanism of action of glucocorticoids

A

decrease production of inflammatory mediators (alter pain perception), inhibition of phospholipase A2, glucocorticoid receptor activation

54
Q

Mild lithium toxicity

A

1-1.5 mEq/L lethargy, irritability, weakness, tremor, slurred speech, nausea

55
Q

Moderate lithium toxicity

A

1.6-2.5 mEq/L confusion, drowsiness, restlessness, unsteady gait, coarse tremor, dysarthria, fasciculations, vomiting

56
Q

Molecular size

A

the smaller, the better it crosses membrane

57
Q

Most common side effects of lithium:

A

polydipsia, polyuria, hypothyroidism, tremor

58
Q

nonionized

A

no charge, lipid soluble - usually pharmacologically active

59
Q

Nonionized vs ionized, lipid or water soluble?

A

nonionized= lipophilic (easier to get in) ionized= hydrophilic

60
Q

NSAIDs

A

ASA and COX inhibitors

61
Q

NSAIDs should be used with caution with…

A

renal and liver disease

62
Q

Oxidation

A

lose electron, gain oxygen

63
Q

pharmacologic interactions (NSAIDs)

A

displace albumin bound drugs and can potentiate effects (warfarin)

64
Q

phase 1 reactions

A

oxidation, reduction, hydrolysis

65
Q

phase 2 reaction

A

conjugate

66
Q

Phase 2 reactions- a drug or metabolite is conjugated with an endogenous substrate such as…

A

glucuronic, sulfonic, or acetic acid

67
Q

Phases of 1st order kinetics

A

alpha- initial rapid decline in concentration (redistribution) beta- elimination of drug central compartment

68
Q

Plasma proteins and what they bind to

A

-albumin- acidic -alpha 1 glycoprotein- basic beta globulin- basic

69
Q

Plasma proteins and what they bind to

A

-albumin- acidic -alpha 1 glycoprotein- basic beta globulin- basic

70
Q

Prohibited drugs for MAOIs

A

cyclic antidepressants, fluoxetine, cold/allergy medications, nasal decongestants, sympathomimetic drugs, opioids (ESPECIALLY MEPERIDINE)

71
Q

Protein binding

A

-if drug is protein bound, it is not available for site of action -bind is usually weak -protein binding prevents meds from leaving bloodstream to site of action

72
Q

Protein binding and lipid solubility are ? proportional

A

directly

73
Q

Re-distribution

A

alpha phase of the two compartment model- initial rapid decline in plasma concentration (redistribution of drug from central to peripheral compartment)

74
Q

Reduction

A

electron gain

75
Q

respiratory adverse effects of NSAIDs

A

nasal polyps, rhinitis, dyspnea, bronchospasm, angioedema, asthma exacerbation

76
Q

Samter’s triad

A

where an individual has asthma, sinus inflammation with recurring polyps, and sensitivity to ASA and other NSAIDs (severe reaction- upper and lower respiratory symptoms)

77
Q

SE of Trazodone

A

nausea and vomiting, sedation, orthostatic hypotension

78
Q

Severe lithium toxicity

A

>2.5 mEq/L coma, delirium, ataxia, extrapyrimidal symptoms, seizures, impaired renal function

79
Q

skeletal adverse effects of NSAIDs

A

inhibit bone growth/healing/formation

80
Q

Synergistic effects

A

1+1=3 effect of drug is enhanced by another (different receptors)

81
Q

Tachyphylaxis

A

rapid decrease in response to repeated doses over a short period of time- see this with ephidrine boluses

82
Q

Trazodone

A

SSRI- used for depression and insomnia

83
Q

trazodone considerations

A

should not be taken with MAOIs, has brief half life

84
Q

Use of clonidine reduces the need for what?

A

opioids

85
Q

Use of glucocorticoids (steroids)

A

reduce inflammation (most powerful steroid)

86
Q

vessel intermediate compartment

A

muscle, fat, skin

87
Q

Vessel poor compartment

A

bone, ligament, cartilage

88
Q

Vessel rich compartment

A

brain, heart, liver, kidney, endocrine glands -receive 75% of cardiac output

89
Q

volume distribution of NSAIDs is?

A

low

90
Q

What % of protein binding is considered highly protein bound?

A

>90%

91
Q

What are H1 antagonists used for?

A

allergic rhinoconjuctivitis, protection against bronchospasm, pruritis, acute anaphylaxis

92
Q

What are H2 antagonists used for?

A

inhibition of H2 receptor mediated gastric acid secretion

93
Q

What are some conditions that decrease plasma proteins?

A

renal failure, liver failure, malignancies, trauma, infection, malnutrition

94
Q

What can caused increased reabsorption of lithium?

A

sodium depletion (dehydration)- sodium restriction/wasting

95
Q

What cases are clonidine commonly used for?

A

labor epidural- no effects on fetal HR, etc.

96
Q

What disorder is lithium used for?

A

bipolar disorder

97
Q

what do NSAIDs inhibit?

A

biosynthesis of prostaglandin

98
Q

What do phase 1 reactions do?

A

converts drug into polar metabolites

99
Q

What do phase 2 reactions do?

A

couple/conjugate drug into polar end product

100
Q

What do SSRIs do?

A

block reuptake of serotonin

101
Q

What do we use for skeletal muscle rigidity associated with MAOIs?

A

dantrolene

102
Q

What does lithium do to the neurons?

A

depletes second messengers, dampens signal transmission

103
Q

What drugs should patients avoid while on lithium?

A

NSAIDs and diuretics (increases plasma levels)

104
Q

What foods should be avoided when taking MAOIs?

A

cheese, liver, fava beans, avocados, chianti wine

105
Q

What happens if a patient has a reduction in plasma proteins?

A

highly protein bound drugs will have a greater clinical effect (more circulating drug available)- but rate of elimination will also increase

106
Q

What increases half time of lithium?

A

renal disease, old age

107
Q

What is a ligand?

A

drug or neurotransmitter

108
Q

What is a safer alternative to NSAIDs in the perioperative setting?

A

coxibs (less platelet dysfunction and GI toxicity)

109
Q

What is another route that clonidine is administered?

A

Epidurally- prolongs sensory and motor blocks

110
Q

What is the largest compartment in the compartment model?

A

vessel poor

111
Q

What is the ligand for NMDA receptors?

A

glutamate

112
Q

What route is most subject to the first pass effect?

A

oral

113
Q

What tricyclic antidepressants are good for chronic pain like fibromyalgia?

A

amitriptyline, imipramine

114
Q

When should lithium levels be drawn?

A

10-12 hours after last oral dose

115
Q

Where are hepatic microsomal enzymes located?

A

smooth endoplasmic reticulum

116
Q

Which drug has a black box warning for prolonged QTc and torsades?

A

droperidol

117
Q

Which route may or may not be subject to the first pass effect?

A

rectal

118
Q

Which routes completely bypasses the first pass effect?

A

IV, topical (including buccal), sublingual

119
Q

Zero order kinetics

A

constant AMOUNT of drug eliminated per unit time (once you saturate enzymes, eliminated at constant rate)

120
Q

Half life table

A
121
Q

First order vs zero order graph

A
122
Q

4 Types of target proteins

A

receptors, ion channels, enzymes, carrier molecules (transporters)

123
Q

Specificity

A

specific for that receptor (will key fit into lock)

124
Q

Affinity

A

how well/avidly drug binds to receptor

125
Q

Intrinsic activity

A

magnitude of the effect of the drug once it is bound (how well the key turns)

Pharm (5 decks)

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