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X Pharmacology > Exam 1 Drugs > Flashcards

Exam 1 Drugs Flashcards

1
Q

What disease is copper toxicity associated with?

A

Wilson’s disease, body cannot eliminate copper and accumulates in tissue

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2
Q

Dimercaprol (BAL in Oil)

A

Chelator of arsenic mainly (also gold, mercury and acute lead)

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3
Q

Penicillamine (Cuprimine)

A

Chelator for copper poisoning

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4
Q

Deferoxamine (Desferal)

A

Chelator for iron poisoning

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5
Q

Calcium disodium edetate (Calcium Disodium Versenate)

A

Chelator for lead poisoning

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6
Q

What targets GPCRs?

A

CNS and autonomic drugs, cardiovascular drugs

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7
Q

What targets voltage-gated ion channels?

A

Local anesthetics, anticonvulsants (hydrophobic interactions because lipid soluble)

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8
Q

What targets ligand-gated ion channels?

A

Nicotine, benzodiazepenes

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9
Q

What targets intracellular receptors?

A

Corticosteroids, sex steroids, hormones (lipid soluble ligands)

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10
Q

What targets enzymes?

A

MAO inhibitors, cholinesterase inhibitors (covalent binding)

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11
Q

What targets transport proteins (DAT, SERT)?

A

Antidepressants

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12
Q

What targets nucleic acids?

A

Anticancer and antiviral drugs

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13
Q

Warfarin

A

Small therapeutic index (much riskier)

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14
Q

Penicillin

A

Large therapeutic index (much safer drug)

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15
Q

Aspirin

A

Participates in irreversible covalent binding

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16
Q

Epinephrine and histamine (what else does epinephrine do on its own?)

A

Physiological/functional antagonism can reverse a fall in blood pressure produced by histamine with epinephrine, both stimulate Gs and activate cAMP, epi can also stimulate Gi and inhibit cAMP

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17
Q

Phenobarbitol/barbiturates

A

Acts on GABA receptor to increase Cl- flow into the cell (synergism with ethanol)

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18
Q

Ethanol

A

Acts on GABA receptor to increase Cl- flow into the cell (synergism with barbiturates)

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19
Q

Drugs that are an example of pharmacokinetic tolerance

A

Barbiturates, ethanol, warfarin

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20
Q

What are 2 drugs that exhibit synergism on the depression of the CNS?

A

Diazepam plus ethanol

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21
Q

What is the relationship between warfarin and phenytoin?

A

These drugs compete for the same plasma binding sites so the dose of warfarin must be decreased in patients that take phenytoin (an anticonvulsant)

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22
Q

What is the overextension-type toxicity of aspirin, warfarin and heparin?

A

Hemorrhage

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23
Q

What is the organ directed toxicity of acetaminophen?

A

Hepatotoxicity

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24
Q

What are the organ directed toxic affects of warfarin?

A

Teratogenic affects so the placenta and therefore the baby are affected

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25
Q

What is the effect of succinylcholine on patients with abnormal serum cholinesterase?

A

It is used to paralyze the muscles and it will cause a much longer recovery time of the paralysis (deficiency of metabolic enzymes leading to enhanced drug effects)

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26
Q

Codeine

A

Very weak analgesic so it must be metabolized to morphine, this metabolism is mediated by CYP450 2D6 (so if patient has a deficiency in this then they will not have the pain relief)

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27
Q

Where is aspirin absorbed?

A

In the stomach (weak acid)

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28
Q

Describe the mechanism of elimination of ethanol

A

Zero-order elimination where a constant amount is eliminated over time

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29
Q

Metabolites of diazepam

A

Nordiazepam (active) and oxazepam (mildly toxic), cleared very slowly

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30
Q

Metabolites of acetaminophen

A

N-acetyl-p-benzo-quinone imine (toxic)

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31
Q

How does ethanol affect acetaminophen?

A

It induces acetaminophen metabolism through CYP2E1 which increases the amount of drug in the toxic pathway

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32
Q

Isoniazid metabolism

A

Phase II (acetylation by n-acetylcysteine) occurs before Phase I (hydrolysis) and this results in toxic metabolites due to the acetylation of toxic metabolites, involved with n-acetyl transferase (phase II)

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33
Q

Mechanism of toxicity of nicotine

A

Interference with receptor-ligand interactions

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34
Q

Mechanism of toxicity of local anesthetics

A

Interference with membrane function

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35
Q

Mechanism of toxicity of MPTP

A

Toxicity from selective cell loss

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36
Q

Mechanism of toxicity of carcinogens

A

Non-lethal alterations in somatic cells

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37
Q

Mechanism of toxicity of dioxins

A

Interference with cellular TFs

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38
Q

Mechanism of toxicity of acetaminophen

A

Induction of programmed cell death

39
Q

What compounds bind directly to cellular components leading to cell death?

A

CO, cyanide and lead

40
Q

What compound undergoes redox cycling in presence of O2 to form ROS

A

Paraquat

41
Q

What does activated charcoal do?

A

Adsorbs many toxins as a treatment of acute poisoning

42
Q

What does ammonium chloride do?

A

Acidifies urine (bases) to enhance elimination

43
Q

What does sodium bicarbonate do?

A

Alkalinizes urine (acids) to enhance elimination

44
Q

Acetylcysteine

A

Used in acetaminophen poisoning to inactivate toxins

45
Q

Atropine

A

Antidote for cholinesterase inhibitor poisons (OPs)

46
Q

Cyanide antidote examples

A

Sodium nitrite, Na thiosulfate, amyl nitrite

47
Q

Ethanol as a poison treatment

A

Used in methanol or ethylene glycol poisoning

48
Q

Fomepizole

A

Antidote used in ethylene glycol poisoning

49
Q

Bleach mechanism of poisoning (NO)

A

Causes oxidative stress with symptoms of severe irritation, hypotension, delirium or coma

50
Q

Treatment of bleach poisoning

A

Remove from skin by flooding with water and then used milk, melted ice cream or beaten eggs

51
Q

Ethylene glycol mechanism of poisoning

A

Converted to oxalic acid by alcohol dehydrogenase, which alters calcium homeostasis and causes CNS depression and kidney damage due to calcium oxalate crystals

52
Q

Treatment of ethylene glycol poisoning

A

Gastric lavage, give ethanol IV as antidote or fomepizole

53
Q

Botulinus toxin mechanism of poisoning

A

Inhibits release of Ach and causes vomiting, double vision and muscular paralysis

54
Q

Treatment of botulinus toxin poisoning

A

Emesis/lavage/cathartic, draw blood to measure toxin concentration and give equine trivalent antitoxin (ABE)

55
Q

Mechanism of organophosphate (parathion, malathion) poisoning

A

Irreversible cholinesterase inhibitors (because bind biomolecules)

56
Q

Main symptoms of organophosphate poisoning

A

SLUD (salivation, lacrimation, urination and defecation)

57
Q

Treatment of organophosphate poisoning

A

Atropine to block cholinergic effects, gastric lavage or emesis if recent ingestion, 2-PAM to reactivate acetylcholinesterase enzyme

58
Q

Mechanism of organochlorine pesticide poisoning (DDT, dieldrin)

A

Bioaccumulation and interfere with inactivation of sodium channels to enhance neuron excitability causing rapid repetitive firing causing twitches/convulsions

59
Q

Mechanism of chlorophenoxy compound poisoning

A

Need high doses to produce toxicity, agonist for aryl hydrocarbon receptor and induces gene expression

60
Q

Mechanism of paraquat poisoning (NO)

A

Causes oxidative stress because it undergoes redox cycling and causes oxidative injury to the lungs

61
Q

Treatment for paraquat poisoning

A

Lavage, cathartics, charcoal and prolonged observation

62
Q

Mechanism of carbon tetrachloride (chloroform)

A

Metabolized by CYP450 to free radicals and the free-radical induced lipid peroxidation causes increase in intracellular Ca2+ leading to apoptotic death

63
Q

Mechanism of mineral acids

A

Oxidative stress

64
Q

Treatment for mineral acid poisoning

A

DO NOT USE GASTRIC LAVAGE OR EMETIC COMPOUDS, dilute with water and reduce pain, non-specific antidote is milk of magnesia

65
Q

Mechanism of arsenic poisoning

A

Binds SH groups on metabolic enzymes, increases oxidative stress and alters gene expression

66
Q

Symptoms of acute poisoning of arsenic

A

GI effects, CNS effects, ventricular arrhythmias, kidney tubular damage

67
Q

Symptoms of chronic arsenic poisoning

A

Polyneuritis, nephritis, cardiac failure, cirrhosis of liver

68
Q

Treatment for arsenic poisoning

A

Lavage/emesis and Dimercaprol

69
Q

Treatment for lead poisoning

A

Chelation (edetate calcium disodium), forms organic lead which is likely to cross BBB (not as toxic to body but will affect brain)

70
Q

Mechanism of iron poisoning (NO)

A

Oxidative injury

71
Q

Treatment for iron poisoning

A

Lavage only within first hour, administer deferoxamine orally and parenterally

72
Q

Mechanism of copper poisoning

A

Redox cycles, increases oxidative stress

73
Q

Kayser-Fleischer rings

A

Copper deposits in the cornea seen in copper poisoning

74
Q

Mechanism of asbestos poisoning

A

Redox cycles, increases oxidative stress, chronic inflammatory action, can increase delivery and activation of carcinogenic chemicals

75
Q

What color is carboxyhemoglobin?

A

Cherry red

76
Q

Mechanism of CO poisoning

A

CO has greater affinity than O2 for hemoglobin and forms carboxyhemoglobin, impairs ability of oxyhemoglobin to transport O2

77
Q

Mechanism of cyanide poisoning

A

Complexes with ferric ion of cytochrome oxidase, produces cellular anoxia by inhibiting oxygen utilization in the mitochondria

78
Q

Treatment for cyanide poisoning

A

Cyanide antidote (administer sodium nitrite or amyl nitrite), sodium thiosulfate is given after nitrite administration, rhodanese and then respiration with 100% O2

79
Q

What is the mechanism of the cyanide antidote?

A

Induces methemoglobinnemia which binds free CN-

80
Q

What is rhodanese?

A

Mitochondrial enzyme that converts CN- to SCN

81
Q

Inducer of CYP450

A

Ethanol

82
Q

Codeine and aspirin

A

Summation effect on pain

83
Q

Tachyphylaxis

A

Rapid development of tolerance as seen in amphetamines

84
Q

Example of synergism

A

Depression of CNS by diazepam and ethanole

85
Q

Overextension toxicity of sedative hypnotics

A

Excessive CNS depression

86
Q

Common drugs that produce hypersensitivity reactions

A

Penicillin/heparin (highly charged) or isoniazid/hydralazine in slow acetylators (long half life)

87
Q

Drugs with a low volume of distribution

A

Heparin/warfarin

88
Q

Drugs with a high volume of distribution

A

Acetaminophen/propranolol

89
Q

Reductive Phase I reaction affecting Warfarin

A

Inactivated by CYP2A6

90
Q

Effect of functional 2D6 genes on nortryiptyline metabolism

A

Lower number of genes leads to higher plasma concentration of the drug

91
Q

What does Fluoxetine (Prozac) inhibit?

A

CYP2D6 (codeine or oxycodone)

92
Q

Relationship between Abacavir and HLA

A

HLA is involved in hypersensitivity reactions like SJS, pts with HLA-B*5701 variant are much more likely to be hypersensitive to abacavir (which is an anticonvulsant)

93
Q

Drugs used for oxidation defect of CYP2D6

A

Codeine, debrisoquin (antihypertensive) and nortriptyline (antidepressant)

X Pharmacology (1 decks)

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