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NBDE II > PHARMACOLOGY part 1 > Flashcards

PHARMACOLOGY part 1 Flashcards

1
Q

the following suffix is indicative of what corresponding drug class?
“caine”

A

local anesthetic

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2
Q

the following suffix is indicative of what corresponding drug class?
“coxib”

A

cyclooxygenase (COX)-2 inhibitors

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3
Q

the following suffix is indicative of what corresponding drug class?
“dipine”

A

dihydropyridine calcium channel blockers

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4
Q

the following suffix is indicative of what corresponding drug class?
“dronate”

A

bisphosphonates

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5
Q

the following suffix is indicative of what corresponding drug class?
“fungin”

A

glucan synthesis inhibitor, antifungal

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6
Q

the following suffix is indicative of what corresponding drug class?
“gliptin”

A

dipeptidyl peptidase-4 inhibitor drug for type 2 diabetes

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7
Q

the following suffix is indicative of what corresponding drug class?
“glitazone”

A

peroxisome proliferator activated receptor gamma activator for type 2 diabetes

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8
Q

the following suffix is indicative of what corresponding drug class?
“grel”

A

P2Y12 adenosine diphosphate receptor inhibitor in platelets

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9
Q

the following suffix is indicative of what corresponding drug class?
“olol”

A

beta adrenergic receptor blockers

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10
Q

the following suffix is indicative of what corresponding drug class?
“ilol” or “alol”

A

beta adrenergic receptor blocker that also blocks alpha1 adrenergic receptors

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11
Q

the following suffix is indicative of what corresponding drug class?
“mab”

A

monoclonal antibodies

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12
Q

the following suffix is indicative of what corresponding drug class?
“onium” or “urium”

A

quaternary ammonium compounds, usually competitive, peripherally acting skeletal muscle relaxers

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13
Q

the following suffix is indicative of what corresponding drug class?
“osin”

A

alpha1 adrenergic receptor blockers

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14
Q

the following suffix is indicative of what corresponding drug class?
“oxacin”

A

fluoroquinolone antibacterial

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15
Q

the following suffix is indicative of what corresponding drug class?
“parin”

A

heparin or low-molecular-weight heparin

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16
Q

the following suffix is indicative of what corresponding drug class?
“prazole”

A

proton pump inhibitor

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17
Q

the following suffix is indicative of what corresponding drug class?
“penem”

A

carbapenem beta lactam antibacterial

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18
Q

the following suffix is indicative of what corresponding drug class?
“pril” or “prilat”

A

angiotensin-converting enzyme (ACE) inhibitors

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19
Q

the following suffix is indicative of what corresponding drug class?
“sartan”

A

angiotensin II receptor blockers

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20
Q

the following suffix is indicative of what corresponding drug class?
“statin”

A

3-hydroxy-3-methylglutaryl coenzyme A (HMG-COA) reductase inhibitor antilipid drugs

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21
Q

the following suffix is indicative of what corresponding drug class?
“teplase”

A

tissue plasminogen activator drug

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22
Q

the following suffix is indicative of what corresponding drug class?
“ triptan”

A

serotonin 5-HT agonist antimigraine drugs

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23
Q

___ is the maximal effect of a drug

A

intrinsic acvitity

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24
Q

___ is the effect of a drug as a function of level of binding to its receptor

A

efficacy

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25
Q

___ is a term that refers to the attractiveness of a drug to its receptor

A
  • affinity
  • measured by the dissociation constant (Kd)
  • lower Kd corresponds to higher affinity
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26
Q

___ is the response to a drug over a given range of concentrations

A

potency

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27
Q

___ is the study of what the body does to the drug

A

pharmacokinetics

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28
Q

if a drug is made active by metabolism, it is called a ___

A

prodrug

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29
Q

what are examples of phase I reactions?

A

oxidation, reduction, and hydrolysis

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30
Q

what are examples of phase II reactions?

A

conjugation, in which a chemical substituent is added to the drug

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31
Q

most metabolism of drugs occurs in which organ?

A

liver

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32
Q

excretion of drugs usually occurs in what organ?

A

the kidney, especially for more soluble drugs

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33
Q

___ refers to the elimination of a constant amount of drug eliminated regardless of dose

A

zero-order elimination kinetics

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34
Q

___ is the most common type of elimination kinetics, in which a constant percentage of remaining drug is eliminated

A

first-order elimination kinetics

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35
Q

between zero-order and first-order kinetics, the risk of accumulation is usually greater for which one?

A

zero-order kinetics

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36
Q

the most common form of drug-drug interaction is one drug affecting the ___ of another drug

A

metabolism

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37
Q

describe the drug-drug interaction between the following drugs commonly used in dentistry:

  • aspirin
  • anticoagulants
A

increased bleeding tendency

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38
Q

___ describes an adverse drug reaction that is due to a genetic change usually involving a change in enzyme activity

A

idiosyncratic reaction

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39
Q

what is the idiosyncratic response to the following genetic abnormality and involved drug:

  • altered muscle calcium homeostasis
  • volatile inhalation anesthetics, succinylcholine
A

malignant hyperthermia

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40
Q

what is the idiosyncratic response to the following genetic abnormality and involved drug:

  • prolonged Q-T interval
  • some antipsychotics and antiarrhythmics
A

torsades de pointes

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41
Q

all nerve pathways originate from the CNS; the sympathetics from ___ outflow, and the parasympathetics from ___ outflow

A
  • thoracolumbar

- cranial-sacral

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42
Q

the adrenal medulla secretes which two hormones?

A
  • epinephrine and norepinephrine

- there is no ganglion here, but the ACh receptors are ganglionic nicotinic in type

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43
Q

what is the sympathetic response of salivary glands? what about the parasympathetic response?

A
  • sympathetic response is a viscous secretion, amylase secretion
  • parasympathetic response is a more profuse, watery secretion
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44
Q

what is the main use for the following adrenergic agonists?

  • epinephrine
  • norepinephrine
A
  • epinephrine: reverse anaphylaxis, vasoconstriction, bronchodilation
  • norepinephrine: vasoconstriction
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45
Q

what are alpha-1 blockers used to for?

A

to treat hypertension, heart failure, and benign prostate hypertrophy

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46
Q

what are the adverse effects of alpha-1 blockers?

A

hypotension (especially first-dose effect), fluid retention, dry mouth, and nasal stuffiness

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47
Q

which adrenergic neuron blockers indirectly reduce granule content of NE but increase it in the cytoplasmic pool of adrenergic neurons?

A

MAO inhibitors, such as pargyline and tranylcypromine

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48
Q

which medication is used in dentistry to reverse soft tissue anesthesia more quickly after procedures involving a local anesthetic with a vasoconstrictor?

A
  • phentolamine (oraverse)

- nonselective alpha-adrenergic receptor blocker (alpha 1 and 2)

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49
Q

beta blockers increase the ___ response to epinephrine, but reduce the ___ resulting from epinephrine

A
  • vasoconstrictor response

- tachycardia

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50
Q

what is the use for the following cholinergic receptor agonists:

  • pilocarpine
  • cevimeline
A
  • pilocarpine: treat glaucoma and stimulate salivary flow

- cevimeline: stimulate salivary flow

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51
Q

what is the use for the following cholinesterase inhibitors:

  • physostigmine
  • pyridostigmine
A
  • physostigmine: glaucoma, antidote for atripine

- pyridostigmine: treat myasthenia gravis

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52
Q

what is the use for the following cholinesterase inhibitors:

  • tacrine
  • donepezil
A

both: treat alzheimer’s disease

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53
Q

what is the use for the following cholinesterase inhibitors:

  • galantamine
  • rivastigmine
A

both: treat alzheimer’s disease

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54
Q

what is the use for the following cholinesterase inhibitors:

  • sarin
  • soman
A

both: nerve gas

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55
Q

___ is used to reactivate acetylcholinesterase after irreversible inhibition by an organophosphate (echothiophate, isoflurophate, sarin, soman)

A

pralidoxime

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56
Q

what are the uses for the following antimuscarinic drugs?

  • atropine
  • scopolamine
A
  • atropine: prototype, to reduce salivary flow, for antivagal effect during surgery, antidote for physostigmine
  • scopolamine: prototype, for motion sickness
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57
Q

what is the dose of atropine for reducing salivary flow?

A

oral administration is 0.5mg (adult dose)

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58
Q

what are the contraindications for antimuscarinic drugs?

A
  • narrow-angle glaucoma
  • prostate hypertrophy
  • paralytic ileus
  • tachycardia
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59
Q

what are skeletal neuromuscular blockers used for?

A

during surgery for relaxing skeletal muscle, for endotracheal intubation, and for treatment of tetanus

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60
Q

what are examples of curare-type neuromuscular junction blockers?

A

d-tubocurarine, pancuronium, atracurium, vecuronium, pipecuronium, rocuronium, doxacurium, mivacurium

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61
Q

which skeletal neuromuscular junction blocker relaxes skeletal muscle without blocking nicotinic receptors?

A

dantrolene

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62
Q

botulinum toxin A (botox) is a skeletal neuromuscular junction blocker that prevents the release of ___ from neurons

A

ACh

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63
Q

what are the uses of botulinum toxin A?

A
  • ophthalmology to relax extraocular muscles
  • muscle dystonias
  • remove wrinkles
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64
Q

which local anesthetics are esters?

A

procaine, tetracaine, and cocaine

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65
Q

which local anesthetics are amides?

A

lidocaine, mepivacaine, bupivacaine, prilocaine, and dibucaine

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66
Q

where are ester local anesthetics metabolized?

A

plasma, by esterases

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67
Q

where are amide local anesthetics metabolized?

A

liber

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68
Q

which class of drugs has the most consistency in structure?

A
  • local anesthetics
  • they are either esters or amides, and differ only in their structure in the intermediate chain (either ester or amide) that connects the aromatic group to the secondary or tertiary amino terminus
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69
Q

what are the toxic reactions to local anesthetics due to?

A

either high systemic levels of LA in general (cardiovascular collapse due to myocardial depression, hypotensive shock), or to a specific agent (such as prilocaine, which causes methemoglobinemia)

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70
Q

what is the mechanism of action of local anesthetics?

A

they prevent the generation of nerve impulses by interfering with sodium transport into the neuron

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71
Q

in terms of absorption of local anesthetics, which form penetrates tissue membranes?

A
  • the non-ionized (free base) form

- once inside the neuron, only the ionized form is effective

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72
Q

describe the pH of inflamed tissue and how that affects absorption of local anesthetics

A

inflamed tissue has a lower than normal pH, which decreases the amount of non-ionized form available to penetrate

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73
Q

which local anesthetics have a short duration of action?

A

procaine

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74
Q

which local anesthetics have a moderate duration of action?

A

prilocaine, mepivacaine, and lidocaine

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75
Q

which local anesthetics have a long duration of action?

A

bupivacaine, tetracaine, and etidocaine

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76
Q

initially, local anesthetics inhibit ___ neurons, which results in CNS ___, which can proceed to ___. at higher doses, they inhibit both ___ and ___ neurons, leading to a generalized state of CNS ___, which can result in ___ and ___

A
  • central inhibitory
  • stimulation
  • convulsions
  • inhibitory and excitatory
  • depression
  • respiratory depression and death
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77
Q

in toxic doses, local anesthetics depress ___ and ___

A

membrane excitability and conduction velocity

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78
Q

which is the only local anesthetic that predictably produces vasoconstriction?

A

cocaine

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79
Q

which is the only local anesthetic to block the reuptake of NE into adrenergic neurons, and thus potentiate the NE that has been released from nerve endings?

80
Q

describe onset of action of local anesthetics in terms of nerve size

A
  • the theory states that there is a size dependent critical length of anesthetic exposure necessary to block a given nerve
  • small fibers will be blocked first because the anesthetic concentration needed for the critical length in a small fiber will be reached faster than the critical length in a larger fiber
  • you need to block 3 nodes of ranvier, and they are farther apart in larger fibers than they are in smaller fibers
81
Q

what is the AHA limit of local anesthetic for a patient who is cardiovascularly compromised?

A

0.04mg, compared to 0.2mg in the healthy patient

82
Q

of penicillin V and penicillin G, which is more sensitive to acid degradation in the stomach and thus is usually injected rather than taken orally?

A

penicillin G

83
Q

which penicillin has the best gram-negative spectrum?

A

ampicillin

84
Q

which drugs are cross-allergenic with penicillin?

A
  • most usually asked about ones are cephalosporins and ampicillin
  • erythromycin is not cross-allergenic
85
Q

which penicillin is useful against penicillinase-producing bugs such as staphylococcus?

A

dicloxacillin

86
Q

which penicillin is specific for pseudomonas infections?

A

an extended spectrum such as carbenicillin

87
Q

which combination of agents should be used prophylactically for patients with heart valve to prevent bacterial endocarditis?

A
  • ampicillin and gentamycin (combinations are no longer used)
  • keflex 2g (4x500mg), PO 1 hr before treatment. number of tablets dispensed depends on number of appointments
88
Q

what is the first choice prophylactic regimen for subacute bacterial endocarditis if a patient is not allergic to penicillin?

A
  • amoxicillin 2g (4x500mg), PO 1 hr before treatment. number of tablets dispensed depends on number of appointments
  • children dose is 50mg/kg 1 hr before appointment
89
Q

what is the first choice prophylactic regimen for subacute bacterial endocarditis if a patient is allergic to penicillin?

A

-clindamycin 600mg (4x150mg), PO 1 hr before appointment. number of tablets dispensed depends on number of appointments

90
Q

what is the non-oral prophylactic regimen for subacute bacterial endocarditis?

A
  • ampicillin IV/IM 2g, 1/2 hr before appointment (children: 50mg/kg)
  • clindamycin (for PCN-allergic) 600mg IV 1/2 hr before appointment (children: 20mg/kg)
91
Q

for the following list of cardiovascular conditions, which requires prophylaxis?
prosthetic valves, previous endocarditis, cardiac pacemakers, rheumatic fever without valvular dysfunction, mitral valve prolapse without valvular regurgitation, pulmonary shunts

A

-required: proshetic valves, previous endocarditis, and pulmonary shunts

92
Q

for the following list of dental procedures, which requires prophylaxis in a patient with a risk of infective endocarditis or prosthetic joint infection?
extractions, restorative procedures, intracanal endodontic treatment, periodontal surgery, implants, taking of impressions

A

-required: extractions, periodontal surgery, implants (rule of thumb is anything that includes gingival manipulation or mucosal incision

93
Q

what is the prescription regimen for treating an infection?

A
  • penicillin VK 250-500mg, dispense 30, take 2 tablets at once, then 1 tab every 6 hrs until gone (7 days) some sources do not indicate loading dose, so dispense 28, take 1 Q6H until gone (kids less than 12 yrs: 20-50mg/kg QID)
  • clindamycin 150-300mg, dispense 21, take 1 capsule every 8 hrs until gone (7 days), (kids: 8-12mg/kg TID or QID)
  • amoxicillin 500mg, dispense 21, take 1 capsule every 8 hrs until gone (7 days), (kids under 20kg: 20-40 mg/kg TID)
94
Q

what is the mechanism of action of penicillins?

A
  • bactericidal

- kill rapidly growing cells by inhibiting cell wall synthesis

95
Q

what is the mechanism of action of tetracycline?

A
  • bacteriostatic

- limit population growth (do not kill bugs) by interfering with protein synthesis on bacterial ribosomes

96
Q

what is the mechanism of action of nystatin?

A
  • antifungal

- binds to ergosterol in the fungal cell wall to weaken the wall

97
Q

what is the mechanism of action of sulfonamides?

A
  • bacteriostatic

- compete with PABA in folic acid synthesis, thus resulting in folic acid deficiency

98
Q

what are symptoms seen during allergic reactions to penicillins?

A

dermatitis, stomatitis, bronchoconstriction, and cardiovascular collapse

99
Q

what agent produces GI upset and pseudomembranous colitis?

A

clindamycin

100
Q

which agents are most likely or least likely to cause superinfection?

A
  • most likely: broad spectrum agents such as tetracyclines

- least likely: narrow spectrum agents such as penicillin G

101
Q

aplastic anemia is associated with which agent?

A

chloramphenicol

102
Q

toxic levels of tetracycline are associated with what?

A

liver damage or hepatotoxicity, especially in pregnant patients with history of renal disease

103
Q

which agent is associated with allergic cholestatic hepatitis?

A

erythromycin estolate

104
Q

what is the drug-drug interaction for tetracycline and penicillin?

A
  • cidal-static interaction

- cancel each other out due to opposing mechanisms of action

105
Q

what is the drug-drug interaction for probenacid and penicillin

A

probenacid alters the rate of renal clearance of penicillin

106
Q

what is the drug-drug interaction for tetracyclines and antacids?

A

effectiveness of tetracyclines is reduced by concurrent ingestion of antacids or dairy products

107
Q

what is the drug-drug interaction for broad spectrum antibiotics and coumarin anticoagulants?

A

broad spectrum antibiotics enhance the action of coumarin anticoagulants (vitamin K antagonists, include coumadin/warfarin) because of the reduction of vitamin K sources

108
Q

what is the drug-drug interaction for antibiotics such as ampicillin and oral contraceptives?

A

antibiotics such as ampicillin decrease the effectiveness of oral contraceptives due to suppression of normal GI flora involved in the recycling of active steroids from bile conjugates, leading to more rapid excretion of the steroids from the body

109
Q

what is the drug-drug interaction for macrolides such as erythromycin and drugs such as seldane and digoxin?

A

macrolides inhibit the metabolism of seldane and digoxin

110
Q

what is acyclovir used for?

A

an antiviral used for various forms of herpes

111
Q

what are fluconazole and ketoconazole used for?

A

systemic-acting antifungals useful for treating candidiasis

112
Q

cephalosporins (like cephalexin) are chemically related to which agent?

A
  • penicillins

- therefore, cephalosporins share the relatively nontoxic nature of penicillins

113
Q

___ is considered an “extended spectrum” form of penicillin, and is not penicillinase resistant

A

ampicillin

114
Q

what antibiotic is useful for treating bone infections such as osteomyelitis?

A

clindamycin

115
Q

what antibiotic is able to achieve a higher concentration in gingival fluid than in serum?

A

tetracycline

116
Q

which antibiotic can damage the eighth nerve, affecting both balance and hearing?

A

streptomycin

117
Q

T or F:

other than allergic reactions, penicillins are extremely safe, with no effect on the liver

118
Q

___ is an antifungal agent that produces such adverse side effects as nephrotoxicity and hypokalemia, but not liver toxicity

A

amphotericin B

119
Q

is gentamicin broad or narrow spectrum?

120
Q

is tetracycline broad or narrow spectrum?

121
Q

is penicillin G broad or narrow spectrum?

122
Q

is streptomycin broad or narrow spectrum?

123
Q

is chloramphenicol broad or narrow spectrum?

124
Q

tetracyclines are broad spectrum antibiotics effective against which bacteria?

A

gram positive and gram negative cocci and bacilli

125
Q

compare the spectrum of activity of clindamycin, erythromycin, vancomycin, and tetracycline

A

clindamycin has a spectrum of activity similar to erythromycin and vancomycin, which is less than that of the tetracyclines, mainly affecting gram positive microogranisms

126
Q

compare 1st generation cephalosporins to 3rd generation cephalosporins

A

1st generation are effective against both gram negative and gram positive organisms, but 3rd generation ones have increased activity against gram negative but greatly decreased activity against gram positive microorganisms

127
Q

T or F:

tetracyclines are the drug of choice for prophylaxis against infective endocarditis

A
  • false
  • this is due to streptococcal infection (15-20% of group A streptococci are resistant to tetracyclines, but none are resistant to penicillin or erythromycin
128
Q

why will patients with renal disease show high blood levels of penicillin?

A
  • penicillin is metabolized in the liver, but it rapidly disappears from the blood due to rapid clearance by the kidneys
  • 90% is excreted by tubular secretion
  • similarly, probenicid (a uricosuric agent which tends to enhance the excretion of uric acid by reducing renal tubular transport mechanisms) reduces the renal clearance of penicillins
129
Q

what is the erythromycin-seldane potentially lethal interaction?

A
  • erythromycin blocks the metabolism of seldane to its antihistamine metabolite (it stays unmetabolized and causes cardiac arrythmias)
  • erythromycin decreases the metabolism of many useful drugs, including digoxin
130
Q

which classes of drugs are used to treat hypertension?

A
  • duretics (furosemide)
  • beta blockers (propranolol, or cardioselective beta blocker metoprolol or atenolol)
  • alpha-1 blocker (prazosin)
  • centrally acting adrenergic drugs (methyldopa or clonidine)
  • neuronal blockers (guanethidine, reserved for severe hypertension)
  • angiotensin converting enzyme inhibitors (captopril, lisinopril)
131
Q

which drugs are used to treat angina?

A

nitroglycerin, sometimes propranolol, calcium channel blockers like verapamil

132
Q

which drugs are used to treat ventricular arrhythmias?

133
Q

which drugs are used to reverse digitalis induced arrhythmias?

134
Q

which drug is used to treat supraventricular tachyarrhythmias and atrial fibrillation?

135
Q

which drug is used to treat supraventricular tachyarrhythmias, paroxymal tachycardia, and atrial fibrillation?

136
Q

which drug is used to treat atrial fibrillation and paroxysmal tachycardia?

A

digitalis (verapamil will treat these as well, in addition to supraventricular tachyarrhythmias)

137
Q

which type of arrhythmia is propranolol used to treat?

A

paroxysmal tachycardia

138
Q

which drugs are used to treat congestive heart failure?

A
  • glycosides such as digitalis and digoxin

- ACE inhibitors such as captopril

139
Q

which cardiac problem is described as an irregularity in heart beat?

A

arrhythmia

140
Q

what is the mechanism of action of antiarrhythmics?

A
  • type 1A agents such as quinidine: acts by increasing the refractory period of cardiac muscle
  • type 1B agents such as lidocaine decrease cardiac excitability
  • when digitalis is used for atrial fibrillation, it acts by decreasing the rate of A-V conduction
141
Q

which cardiac problem is described as insufficient oxygen to meet demands of the myocardium?

142
Q

what is the mechanism of action of antiangina drugs?

A
  • nitroglycerin increases oxygen supply to the heart by a direct vasodilatory action on the smooth muscle in coronary arteries
  • propranolol reduces oxygen demand by preventing chronotropic responses to endogenous epinephrine, emotions, and exercise
  • calcium channel blockers decrease oxygen demand by reducing afterload by reducing peripheral resistance via vasodilation
143
Q

most antihypertensive drugs have the ultimate effect of reducing ___ via ___

A

peripheral resistance via vasodilation

144
Q

what is the mechanism of action of ACE inhibitors used as antihypertensives?

A
  • captopril blocks the enzyme which converts angiotensin I to angiotensin II
  • the latter is a potent vasoconstrictor (administration of angiotensin will result in an elevation of blood pressure)
145
Q

what is the mechanism of action of the following adrenergic agents:
prazosin and methyldopa

A
  • prazosin: selevtive alpha-1 blocker, inhibits binding of nerve induced release of NE, resulting in vasodilation
  • methyldopa: acts centrally as a false neurotransmitter stimulating alpha receptors to reduce sympathetic outflow, resulting in vasodilation
146
Q

what is the mechanism of action of the following adrenergic agents:
clonidine, propranolol, and metoprolol

A
  • clonidine: selective agonist stimulates alpha-2 receptors in the CNS to reduce sympathetic outflow to peripheral vessels, resulting in vasodilation
  • propranolol: nonselective beta blocker reduces cardiac output and inhibits renin secretion
  • metoprolol: selective beta-1 blocker, reduces cardiac output
147
Q

what is the mechanism of action of diuretics? what are 3 examples?

A
  • decrease the renal absorption of sodium, thus resulting in fluid loss and a reduction in blood volume
  • thiazides (chlorothiazide), high-ceiling or loop acting (furosemide), and potassium sparing (spironolactone)
148
Q

what is the mechanism of action of congestive heart failure drugs (cardiac glycosides like digitalis or digitoxin)?

A
  • positive inotropic effect increases the force of contraction of the myocardium
  • this is achieved by inhibition of Na+, K+ ATPase leading to increased calcium influx
  • digitalis therapy reduces the compensatory changes that are associated with congestive heart failure such as increased heart size, rate, edema, etc
149
Q

how does hydralazine reduce hypertension?

A

has a direct action on vascular smooth muscle to cause vasodilation

150
Q

aside from blocking beta-1 receptors, blocking of ___ release is thought to be the other mechanism whereby beta-blockers alter hypertension

151
Q

which loop or high-ceiling diuretic is associated with deafness?

A

ethacrynic acid

152
Q

which diuretic causes potassium loss (hypokalemia)?

A

chlorothiazide

153
Q

what is the mechanism of action of the analgesic effects of NSAIDs?

A

aspirin inhibits the synthesis of prostaglandins

154
Q

what is the mechanism of action of the antipyretic (reduce fever) effects of NSAIDs?

A

aspirin inhibits prostaglandin synthesis in the hypothalamic temperature regulation center

155
Q

what is the mechanism of action of the bleeding time effects of NSAIDs?

A

inhibits synthesis of thromboxane A2, preventing platelet synthesis

156
Q

what are the therapeutic effects of aspirin (NSAID)?

A

pain relief, antipyretic (anti-fever) effects, antirheumatic, and anti-inflammatory effects

157
Q

what are the adverse or toxic effects of aspirin (NSAID)?

A

occult bleeding from the GI tract, tinnitus, nausea and vomiting, acid-base disturbance or metabolic acidosis, decreased tubular reabsorption of uric acid, salicylism, delirium, and hyperventilation

158
Q

what is the difference between aspirin and acetaminophen?

A

acetaminophen lacks anti-inflammatory activity, is hepatotoxic, and does not cause GI upset

159
Q

what is the difference between aspirin and other anti-inflammatories like prednisone, hydrocortisone, and triamcinolone?

A

prednisode, hydrocortisone, and triamcinolone are steroids and do not act primarily on prostaglandin inhibition

160
Q

what is the difference between aspirin and ibuprofen?

A

ibuprofen causes much less GI irritation

161
Q

which NSAID has a longer half-life than aspirin, acetaminophen, and ibuprofen?

A

diflunisal (dolobid)

162
Q

what are the toxic effects of acetaminophen?

A
  • liver toxicity/necrosis, especially when combined with alcohol or taken in excess of 4g/day
  • renal necrosis as well
163
Q

what is the drug of choice for a feverish child?

A

acetaminophen

164
Q

why should aspirin be avoided for a feverish child?

A

increased risk of reye’s syndrome

165
Q

what is the mechanism of action of heparin?

A

inhibits thrombin and prevents formation of the fibrin network

166
Q

what is the mechanism of action of coumarin?

A

inhibits GI absorption of vitamin K and prevents synthesis of blood clotting factors

167
Q

what is the mechanism of action of corticosteroids, like triamcinolone?

A

inhibits phospholipase A2

168
Q

NSAIDs cause gastric irritation and bleeding due to their effects on ___ synthesis in the ___

A

prostaglandin synthesis in the mucosal wall of the gut

169
Q

what is phenytoin?

A

an anticonvulsant, with the major side effect of gingival hyperplasia

170
Q

which NSAID causes so much GI irritation that its use is limited in humans?

A

indomethacin

171
Q

what are the effects aspirin has on body temperature?

A

it only lowers body temperature in the presence of a fever (no effect on body temp in the non-feverish patient)

172
Q

suppression of the cough reflex is a major therapeutic use of which drugs?

A

narcotic opiates such as codeine

173
Q

what are two common mixed-agonist-antagonists (MAA)?

A

pentazocine and nalbuphine

174
Q

___ is an antagonist used to treat overdose

175
Q

___ is used in detoxification of morphine addicts

176
Q

what are the effects of morphine?

A

produces respiratory depression, euphoria, sedation, dysphoria, analgesia, constipation, and urinary retention

177
Q

what does overdose of morphine cause?

A

coma, miosis, and respiratory depression

178
Q

in morphine overdose, what is the mechanism of respiratory depression?

A

loss of sensitivity of the medullary respiratory center to carbon dioxide

179
Q

describe the use of narcotics for the treatment of diarrhea

A

-OTC narcotics in the form of paregoric (tincture of opium) and lomotil (loperamide) act on receptors in the gut to produce constipation

180
Q

what are the only class of drugs that suppress the cough reflex?

A

opioids (codeine and meperidine - codeine is better)

181
Q

what are the two hallmark opioid overdose effects?

A

miosis (pinpoint pupils) and respiratory depression

182
Q

which of the following are agonists only, and which are antagonists only?
codeine, methadone, naloxone, meperidine

A
  • agonists: codeine, methadone, and meperidine

- antagonists: naloxone

183
Q

why is withdrawal of methadone less severe than with morphine?

A

because methadone has a much longer half-life

184
Q

what are 3 competitive muscarinic receptor blockers that are sometimes used to control salivary secretions?

A

atropine, scopolamine, and propantheline

185
Q

what is the mechanism of action of atropine?

A

blocks vagal reflexive control of heart rate, resulting in tachycardia

186
Q

describe physostigmine and neostigmine

A
  • both are reversible anticholinesterases sometimes used in the treatment of xerostomia
  • physostigmine acts both centrally and peripherally
  • neostigmine only peripherally, but also has some direct ACh-like activity at the neuromuscular junction, in addition to prolonging the activity of endogenous ACh
187
Q

what are 2 direct acting cholinergic agonists sometimes used for xerostomia?

A

pilocarpine and methacholine

188
Q

___ and ___ irreversibly inhibit cholinesterase

A

organophosphates and insecticides

189
Q

___ is an enzyme regenerator used in organophosphate toxicity

A

pralidoxime

190
Q

___ is a depolarizing neuromuscular junction blocker, subject to rapid inactivation by plasma pseudocholinesterase; it is used to prevent laryngospasm

A

succinylcholine

191
Q

___ is a non-depolarizing neuromuscular junction blocker

A

d-tubocurarine

192
Q

___ and ___ are ganglionic blockers that produce orthostatic hypertension

A

mecamylamine and hexamethonium

193
Q

what are cholinergic crisis symptoms? how is it treated?

A
  • bradycardia, lacrimation, salivation, voluntary muscle weakness, diarrhea, and bronchoconstriction
  • treat with atropine
194
Q

what are the signs of scopolamine overdose? how is it treated?

A
  • disorientation, confusion, hallucinations, burning dry mouth, and hyperthermia
  • treat with physostigmine
195
Q

how does atropine cause tachycardia?

A

blocks vagal reflexive control of heart rate

NBDE II (35 decks)

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