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Pharmacology Basic Principles > Toxicology > Flashcards

Toxicology Flashcards

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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
Penicillamine
Binds Mercury. S and Amine group
26
Carbon Monoxide
Affect brain and heart. Symptoms - headache, weakness, nausea/vomiting, unconsciousness, death
27
CO treatment
Remove exposure, re-institute respiration with pure O2 in severe cases
28
Cyanide
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
Cyanide treatment
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
Methanol
Alcohol dehydrogenase converts methanol to formaldehyde. Aldehyde dehydrogenase converts formaldehyde to formic acid. Symptoms are similar to ethanol with increased vision symptoms
31
Treatment of methanol
Treat the acidosis. Paradoxically, give ethanol to saturate the alcohol dehydrogenase
32
Ethylene glycol
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
Ethylene glycol treatment
Gastric levage, sodium bicarbonate for acidosis, ethanol slows metabolism, hemodialysis for kidney
34
Acetaminophen
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
APAP treatment
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
Vitamin Poisoning
Major cause of poisoning in children under 5. Magadose is 10x RDA. toxicity from fat-soluble vitamins most commonly (A and D)
37
Chlorinated Hydrocarbon Insecticides
Fat soluble, low molecular weight. DDT, cyclodiens and hydrocarbone. Rapid repetitive neuronal firing - interferes with inactivation of sodium channels
38
DDT
Hydrophobic builds up in adipose tissue, poor biodegradability, persistent, crosses BBB and placenta.
39
Treatment of acute DDT poisoning
Supportive only. Note: survival of acute phase, may still experience increased risk of cancer
40
Symptoms of acute DDT poisoning
Nausea and vomiting, neurological hypersensitivity, respiratory failure and death.
41
Organophosphorous Insecticides
Phosphate esters, phosphothiol groups, highly toxic, inhibit acetylcholine esterase by phosphorylating enzyme
42
Symptoms of acute Organophosphate poisoning
autonomic and somatic effects
43
Carbamate insecticides
Highly to moderately toxic, inactivates acetylcholine esterase reversibly. They do not persist in environment or bioaccumulate
44
Herbicides
Do not accumulate in animals, only slowly metabolized but readily excreted in urine, mechanism of toxicity largely unknown
45
Bipyridyl herbicides
Paraquat - primary sites of damage are lung, liver, kidney. Proliferation of lung fibroblast, redox cycling and oxidative stress
46
Polycholorinated biphenyls
PCBs, environmental pollutants, very lipophilic, stable, poorly metabolized, bioaccumulates
47
Drug interactions
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
Interactions due to alcohol
Chronic use cause some CYP450 induction in liver, may increase of decrease drug effects, competitve substrate for some p450s. CNS interactions
49
Interactions due to caffeine
Inducer and substrate for microsomal drug metabolizing enzymes. Risk with benzodiazepines, oral contraceptives, cimetidine, MAOI, phenothiazines, thephylline
50
Interactions due to tobacco
Some drug metabolizing enzymes induced, decrease effects of acetaminophen, anti-depressants, benzodiazapine, cimetidine, oral contraceptives, estrogens, insulin, propranolol, theophylline
51
Toxicity and elderly patients
altered physiology, drug metabolism and polypharmacy. Changes in ADME, adjust dose monitor progress, individualize therapy, consider benefit to risk ratio.
52
Bioactivation of xenobiotics to stable but toxic metabolites
Cyanide and Carbon Monoxide
53
Biotransformation of xenobiotics to reactive, electrophilic metabolites
Acetaminophen, bromobenzene, benzo(a)pyrene, 2-acetylaminofluorene, N-dimethylnitrosamines, trichloroethylene
54
Biotransformation of xenobiotics to free radicals
Carbon tetrachloride
55
Formation of reduced oxygen metabolites
Paraquat, quinones
56
Metabolic derangements associated with xenobiotic transformation
Galactosamines, ethionine, fructose, fluroacetate
57
Dicloromethane
Carbon monoxide (from CYP450, then glutathione metabolism, then formaldehyde dehydrogenase)
58
Acetonitrile
Cyanide (from CYP450, then rhodanese) unstable intermediate
59
Hard nucleophiles
High electronegativity, low polarizability, difficult to oxidize. Ex. Amino groups, oxygen-containing functional groups in DNA and protein
60
Soft nucleophiles
Low electronegaticity, high polarizability, easy to oxidize. Ex. Thiol group of GSH and cystein. Protein sulfhydryl group
61
Hard Electrophiles
High positive charge, small size, lacks unshared electrons in valence shell, Ex. Alkyl carbonium ion
62
Soft electrophiles
low positive charges, relatively larges size, unshared electrons in valence shell. Michael acceptors. Beta-unstaturated carbonyl compound
63
Reactions of free radicals
Initiation, propagation (injury) and termination. Ex. Tetrachloride (CYP450) or reactive oxygen intermediates
64
Paraquat
Herbicide - redox cycle, keeps releasing superoxide - lung fibrosis
65
Menadione
Quinone (similar to vit. K) NADPH consumed to create semiquinone, releasing superoxide forming hydroquinone. Cycle starts again
66
Galactosamine
UTP depletion
67
Ethionine
ATP depletion from s-adenosylethionine
68
Fructose
ATP depletion from fructose 1-P
69
Fluroacetate
fluroacetyl-coA inhibits aconitase leading to cytotoxicity

Pharmacology Basic Principles (11 decks)

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