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Pharmacology Basic Principles > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Routes of entry

A

oral, inhalation, parenteral (IV), dermal

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2
Q

Most frequent pediatric emergency

A

poisoning

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3
Q

Acute exposure

A

A single exposure or multiple exposures over a 24 hr period

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4
Q

Subacute exposure

A

Multiple exposures over a 24 hr - 3 mo. period

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5
Q

Chronic exposure

A

Multiple exposures over a 3 mo. or longer period

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6
Q

Zero order rate constant

A

Ke = (Ao - A)/t

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7
Q

Many toxic agents exhibit clearance saturation

A

Alcohol quickly saturates to zero order clearance. Salicylate at levels above 1 gram exhibits zero order clearance. That’s only 3 asprin

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8
Q

Heavy Metal

A

Long lasting in environment, not metabolized, may persist in the body for long periods of time. combine with essential amino acid residues on enzymes

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9
Q

Acute inorganic lead poisoning

A

Severe GI distress, CNS abnormalities, difficult diagnosis - can mimic appendicitis, peptic ulcer, pancreatitis, etc.

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10
Q

Diagnostic tests for Pb

A

Blood and urine analysis for Pb, also can check urine for delta-ALA and coproporphyrin III because the heme pathway is inhibited by lead

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11
Q

Treatment for Pb poisoning

A

Prevent further exposure, support - seizures, cerebral edema. Initiate chelation therapy - dimercaprol, edtate Ca disodium, D-penicillamine

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12
Q

Pb Pharmacokinetics

A

Distribution to soft tissues (kidney and liver), redistribution to bones, teeth and hair. Half-life of Pb in blood: 1-2 mo. Bone: 20 years. Excretion in urine and feces

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13
Q

Chronic inorganic Pb poisoning

A

weakness, anorexia, nervousness, tremor, weight loss, headache, GI distress. Wrist drop extensor weakness without sensory loss.

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14
Q

Organic Pb poisoning

A

Acute CNS, rapid progression to hallucinations, insomnia, headache and irritability. Usually caused by tetraethyl or tetramethyl Pb in gasoline

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15
Q

Mercury poisoning

A

Element poorly absorbed by GI, but better with inhalation, organic forms more readily absorbed, retained in kidney and brain

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16
Q

Acute mercury intoxication

A

Inhalation leads to chest pain, shortness of breath, nausea/vomiting, kidney damage, gingivitis, muscle tremor, psychopathology.

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17
Q

Biochemical effects of mercury

A

React with sulfhydryls as a corrosive, proteins precipitate. Methylmercury readily accumulates in cells

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18
Q

Treatment of mercury poisoning

A

Remove exposure, chelation therapy may use oral penicillamine and monitor removal

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19
Q

Arsenic

A

As3+ sulfhydryl reagent inhibiting SH-sensitive enzymes like the pyruvate dehydrogenase system. As5+ uncouples mitochondrial oxidative phosphorylation

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20
Q

Cadmium

A

Long half-life, no treatment

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21
Q

Heavy metal antagonists

A

Chlelating agents - 2 or more electronegative groups, coordinate covalent bonds with cationic metal atoms. Shares electrons - Think N, S, and O.

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22
Q

Effectiveness of Heavy metal antagonist depends on

A

Affinity for heavy metal compared to essential body metals. Chelator distribution. Ability to mobilize metal. Water solubility. Resistance to metabolism. Readily excreted with little-to-no dissociation from heavy metal. Chelator-metal complex should be less toxic than free metal. Oral administration. Low inherent toxicity.

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23
Q

Dimercaperol

A

2 SH groups, 1 OH group. Lots of side effects. Not to be used with cadmium - enhances accumulation

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24
Q

EDTA

A

Binds lead, hexavalent binding via Oxygen group with iron

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25
Q

Penicillamine

A

Binds Mercury. S and Amine group

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26
Q

Carbon Monoxide

A

Affect brain and heart. Symptoms - headache, weakness, nausea/vomiting, unconsciousness, death

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27
Q

CO treatment

A

Remove exposure, re-institute respiration with pure O2 in severe cases

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28
Q

Cyanide

A

Fatal dose - 50-200 mg depending on route of administration and compound used. Symptoms: giddiness, headache, palpitations, N>V ataxia, convulsions, coma, and death

29
Q

Cyanide treatment

A

CN binds Fe3+ in cytochrome oxidase. Administer sodium nitrite or amyl nitrite which reacts with Hemoglobin, iron in F(III) state which CN then binds instead of cytochrome

30
Q

Methanol

A

Alcohol dehydrogenase converts methanol to formaldehyde. Aldehyde dehydrogenase converts formaldehyde to formic acid. Symptoms are similar to ethanol with increased vision symptoms

31
Q

Treatment of methanol

A

Treat the acidosis. Paradoxically, give ethanol to saturate the alcohol dehydrogenase

32
Q

Ethylene glycol

A

Antifreeze. Patient appears drunk due to neurological involvement, tachycardia, mild hypertension, heart failure, pulmonary edema, renal failure, acute tubular necrosis. Causes formic acidosis and oxalic acidosis. Oxolate stones - renal damage

33
Q

Ethylene glycol treatment

A

Gastric levage, sodium bicarbonate for acidosis, ethanol slows metabolism, hemodialysis for kidney

34
Q

Acetaminophen

A

Toxic dose - 25 g, CYP450 metabolism leads to reactive APAP which binds macromolecules in liver leading to hepatocyte death. (remember Acetaminophen is harmless when glucuronated or sulfonated)

35
Q

APAP treatment

A

And SH compounds to replenish hepatic GSH and acts as an alternate binding target for activated APAP. Example: N-acetylcystein and must be given as quickly as possible

36
Q

Vitamin Poisoning

A

Major cause of poisoning in children under 5. Magadose is 10x RDA. toxicity from fat-soluble vitamins most commonly (A and D)

37
Q

Chlorinated Hydrocarbon Insecticides

A

Fat soluble, low molecular weight. DDT, cyclodiens and hydrocarbone. Rapid repetitive neuronal firing - interferes with inactivation of sodium channels

38
Q

DDT

A

Hydrophobic builds up in adipose tissue, poor biodegradability, persistent, crosses BBB and placenta.

39
Q

Treatment of acute DDT poisoning

A

Supportive only. Note: survival of acute phase, may still experience increased risk of cancer

40
Q

Symptoms of acute DDT poisoning

A

Nausea and vomiting, neurological hypersensitivity, respiratory failure and death.

41
Q

Organophosphorous Insecticides

A

Phosphate esters, phosphothiol groups, highly toxic, inhibit acetylcholine esterase by phosphorylating enzyme

42
Q

Symptoms of acute Organophosphate poisoning

A

autonomic and somatic effects

43
Q

Carbamate insecticides

A

Highly to moderately toxic, inactivates acetylcholine esterase reversibly. They do not persist in environment or bioaccumulate

44
Q

Herbicides

A

Do not accumulate in animals, only slowly metabolized but readily excreted in urine, mechanism of toxicity largely unknown

45
Q

Bipyridyl herbicides

A

Paraquat - primary sites of damage are lung, liver, kidney. Proliferation of lung fibroblast, redox cycling and oxidative stress

46
Q

Polycholorinated biphenyls

A

PCBs, environmental pollutants, very lipophilic, stable, poorly metabolized, bioaccumulates

47
Q

Drug interactions

A

Very important when margin of safety is small and when patient is taking multiple drugs. May be caused by multiple mechanisms - physical binding, metabolism inducement or inhibition, plasma protein displacemtne

48
Q

Interactions due to alcohol

A

Chronic use cause some CYP450 induction in liver, may increase of decrease drug effects, competitve substrate for some p450s. CNS interactions

49
Q

Interactions due to caffeine

A

Inducer and substrate for microsomal drug metabolizing enzymes. Risk with benzodiazepines, oral contraceptives, cimetidine, MAOI, phenothiazines, thephylline

50
Q

Interactions due to tobacco

A

Some drug metabolizing enzymes induced, decrease effects of acetaminophen, anti-depressants, benzodiazapine, cimetidine, oral contraceptives, estrogens, insulin, propranolol, theophylline

51
Q

Toxicity and elderly patients

A

altered physiology, drug metabolism and polypharmacy. Changes in ADME, adjust dose monitor progress, individualize therapy, consider benefit to risk ratio.

52
Q

Bioactivation of xenobiotics to stable but toxic metabolites

A

Cyanide and Carbon Monoxide

53
Q

Biotransformation of xenobiotics to reactive, electrophilic metabolites

A

Acetaminophen, bromobenzene, benzo(a)pyrene, 2-acetylaminofluorene, N-dimethylnitrosamines, trichloroethylene

54
Q

Biotransformation of xenobiotics to free radicals

A

Carbon tetrachloride

55
Q

Formation of reduced oxygen metabolites

A

Paraquat, quinones

56
Q

Metabolic derangements associated with xenobiotic transformation

A

Galactosamines, ethionine, fructose, fluroacetate

57
Q

Dicloromethane

A

Carbon monoxide (from CYP450, then glutathione metabolism, then formaldehyde dehydrogenase)

58
Q

Acetonitrile

A

Cyanide (from CYP450, then rhodanese) unstable intermediate

59
Q

Hard nucleophiles

A

High electronegativity, low polarizability, difficult to oxidize. Ex. Amino groups, oxygen-containing functional groups in DNA and protein

60
Q

Soft nucleophiles

A

Low electronegaticity, high polarizability, easy to oxidize. Ex. Thiol group of GSH and cystein. Protein sulfhydryl group

61
Q

Hard Electrophiles

A

High positive charge, small size, lacks unshared electrons in valence shell, Ex. Alkyl carbonium ion

62
Q

Soft electrophiles

A

low positive charges, relatively larges size, unshared electrons in valence shell. Michael acceptors. Beta-unstaturated carbonyl compound

63
Q

Reactions of free radicals

A

Initiation, propagation (injury) and termination. Ex. Tetrachloride (CYP450) or reactive oxygen intermediates

64
Q

Paraquat

A

Herbicide - redox cycle, keeps releasing superoxide - lung fibrosis

65
Q

Menadione

A

Quinone (similar to vit. K) NADPH consumed to create semiquinone, releasing superoxide forming hydroquinone. Cycle starts again

66
Q

Galactosamine

A

UTP depletion

67
Q

Ethionine

A

ATP depletion from s-adenosylethionine

68
Q

Fructose

A

ATP depletion from fructose 1-P

69
Q

Fluroacetate

A

fluroacetyl-coA inhibits aconitase leading to cytotoxicity

Pharmacology Basic Principles (11 decks)

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