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Pharmacology > Toxicities > Flashcards

Toxicities Flashcards

0
Q

PCBs

A

Polychlorinated biphenyls
Co planar configure and can fit into Ah receptor
Co planar-bind Ah receptor with high affinity, mediate many effects through gene transcription
Noncoplanar-not good Ah receptor ligands, initiated by changes in cell signaling

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1
Q

Dioxin

A

Sources: heating of chlorinated organic compounds (agent orange)
Planar, stable, highly lipid soluble
Persistent-slowly eliminated
Causes chloracne
MOA: binds to cytosolic Ah-receptor->translocation to nucleus-> altered gene expression
P450 1A1 liver bio marker

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2
Q

Indole-3,2 carbizole

A

Naturally occurring plant constituent from Brussels sprouts or cauliflower
Converted by acid stomach and binds to Ah receptor

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3
Q

Estrogen receptors

A

Work like Ah receptor
Agonists/antagonists: furanocoumarins (soy), diethylstillbestrol (DES), tamoxifen, RU486
Endocrine disrupters

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4
Q

Saxitoxin, tetrodoxin

A

Block Na channels

Marine toxin

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5
Q

Organic solvents

A

CNS effects
Disorientation, euphoria, unconsciousness, paralysis, convulsion, death
MOA: physical interaction with CNS
Alter membrane fluidity

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6
Q

DDT

A

Insecticide

Interferes with Na channel closing

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7
Q

Organophosphates carbamates

A

Pesticides

Inhibit AChe

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8
Q

Benzene

A

Volatile organic solvent
Hematopoietic toxicity-aplastic anemia, leukemia
Bio activation to epoxide, quinones, t-muconaldehyde

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9
Q

Carbon tetra chloride CCl4

A

Volatile organic solvent
Hepatotoxicity
Metabolic activation

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10
Q

Methanol

A

Volatile organic solvent
Retinal toxicity
Metabolic acidosis
Metabolic activation to Formic acid

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11
Q

N-hexane

A

Volatile organic solvent
Neurotoxicity
Metabolic activation to pyrroles

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12
Q

Ethylene glycol ethers

A

Volatile organic solvent

Reproductive toxicity

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13
Q

Dioxane

A

Volatile organic solvent

Carcinogenesis, respiratory irritant

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14
Q

Ethanol

A

Organic solvent
CNS: Depressant (acute), wernickes Korsakoff’s syndrome (chronic)
Liver: steatosis, hepatitis, collagen deposition (cirrhosis), portal hypertension
GI: gastritis, peptic ulcer
Pancreatitis
Heart: vasodilation, (acute hypothermia), cardiomyopathy, arrhythmias
Endocrine: feminization in males
Cancer: upper GI, liver
Development:FAS
Immune compromise

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15
Q

Carbon monoxide

A

Interference with energy production

Competes with O2 for hemoglobin

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16
Q

Nitrite NO2-

A

Interference with energy production
Oxidizes hemoglobin
Sources:drugs, food preparation (sodium nitrite), well water affects infants due to less ph in stomach killing metabolizing bacteria
Effects: cyanosis (brown blood), hypotension, cardiovascular collapse, abdominal pain, nausea, vomiting, headache, vertigo, altered breathing and heart rates, increased Intraocular pressure, elevated intracranial pressure, coma, nitrosamines formation->Cancer
MOA: oxidize HB-fe to methemoglobin
40% metHb=toxicity
70-80%= death due to hypoxia, vasodilation
Treatment:,maintain circulation and respiration
Transfusion, methylene blue reduces MetHb (fast)

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17
Q

hydrogen sulfide, azide

A

Interference with energy production

Inhibits mitochondrial electron transport

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18
Q

Nitro phenols

A

Interference with energy production

Uncoupled oxidative phosphorylation

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19
Q

Fluoroacetate

A

Interference with energy production

Inhibits Krebs cycle

20
Q

Cyanide (CN-)

A

Interference with energy production
Sources: CN- salts, hydrocyanic acid (jewelry, Metal cleaning, photographic processes), HCN gas fumigant, tampering with drugs, smoke inhalation, cyanogenic compounds, (Laetrile, amygdalin, acetonitrile, proprionitrile, nitropusside metabolism
Toxicity: heart and brain rapid
Headache, anxiety (early), nausea, vomiting, arrythmia, pulmonary edema, coma, convulsion, shock, respiratory failure, death
CN binds to HEME especially cytochrome oxidase in mitochondria blocking transfer of electrons
Brightens blood due to increased O2
Treatment: supportive therapy
Antidotes: sodium nitrite CN binds to metHb
CN reacts with S2O3to form SCN- and SO3 with help from Rhodanese

21
Q

Antidote for GSH depletion

A

N-acetyl cysteine

-SH donors

22
Q

Aflatoxin B1

A

Mycotoxin produced by aspergillus strains-common contaminants of grain, nut crops
Causes acute liver injury and hepatocarcionogenesis
Metabolized/activated by cytochrome p450
Most active metabolite is 8,9 endo-epoxide forms covalent bonds with cellular macromolecules (Proteins and DNA)
Biomarker:ALT

23
Q

Benzo(a)pyrene

A

Bio activated by p450 cytochromes to epoxide metabolite to an electrophile that binds DNA
Leading to mutation and possibly cancer

24
Q

DES

A

Causes vaginal adenocarcinoma

Used in teens

25
Q

Free radicals MOA in lipid bilayer

A

Free radicals abstract H’ from side chains forming a free radical in chain (L’)-initiation
L’ reacts with neighboring lipids forming more L’
Oxygen reacts forming (LOO’)
Propagation of lipid peroxidation
Complex chain reactions occur resulting in destruction of lipid bilayer integrity
E.g. CCL4->CCl3’ , O2’,
OH’ very reactive
Also cause glutathione oxidation, protein oxidation and depletion of NADH

26
Q

Paraquat

A

Forms reactive oxygen species

27
Q

Protection against ROS

A

Superoxide dismutase: O2’ to H2O2 plus Fe2+ and OH’ forms H2O
Glutathione peroxidase: H2O2 to H20
Glutathione reductase: replenishes glutathione peroxidase with H from NADPH
Protein disulfide: replenishes glutathione disulfide
If become compromised more sensitive to
Vit E and C toxicity
Selenium deficiency (Gs peroxidase requires Se)
GSH depletion (malnutrition, fasting)
Genetic abnormalities. (SOD deficiency)

28
Q

Nitrogen dioxide NO2

A

Sources: silos-in incomplete reduction of NO3-
Smogs
Toxicity: bronchiolitis obliterans, silo fillers disease (100 ppm=dangerous 200=fatal)
MOA: direct irritant (HNO3)
Oxidant: lipid peroxidation

29
Q

MPTP

A

Illicit street drug
Selective destruction of dopaminergic neurons
Parkinson’s like syndrome

30
Q

Thalidomide

A

Sedative
Reduction in long bones of limbs-loss of fetal limb buds
Between days 35-50 of pregnancy
Teratogenic

31
Q

Vitamin A

A

Teratogenic

Synthetic retinoids

32
Q

Cocaine

A

Teratogenic

GI, limb and kidney malformations

33
Q

Elemental Mercury Hg0

A

Inhalation
Accumulates in: kidneys
Converted to Hg++ in body
1-2 months for elimination
Causes: corrosive bronchitis, interstitial pneumonitis, thyroid enlargement, hematologic changes, gingivitis, salivation,
CNS:memory loss, excitability, depression, hallucination, tremor, decreased fine motor function (mad hatter)
Treatment: hemodialysis or chelators: cysteine, penicillamine, British antilewisite, succimer (choice)

34
Q

Inorganic mercury Hg++ and HG2++

A

GI absorption
Accumulates in kidneys
Converted to Hg++ in body
1-2 months for elimination
Corrosive in high doses: GI ulceration, bleeding necrosis, shock
Renal failure necrosis of proximal tubules, glomerular injury, neuropathy
Treatment: hemodialysis or chelators: cysteine, penicillamine, British antilewisite, succimer (choice

35
Q

Organic methyl Hg

A

Aquatic microorganism a ingested by fish
GI absorption
Accumulates in brain
Converted to Hg++ in brain
1-2 months for elimination
Neurotoxicity-parsthesia, ataxia, neurasthenia, vision and hearing loss, spasticity, tremor, coma death
Teratogenic: interferes with brain development, seizures
Treatment: hemodialysis or chelators: cysteine, penicillamine, British antilewisite, succimer (choice

36
Q

Lead

A

Sources: soil:leaded gasolines and paints, water: lead pipes, lead paint: children’s toys, clothes and shoes from industrial workers, canned foods, ceramic glazers, moonshine whiskeys, traditional remedies and cosmetics
Absorption: inhalation, most GI absorption
Distributin: initially liver and kidney, 99% to blood, redistribution to bone, placental transfers
Slow elimination: mostly by kidneys, hair and nails: chronic 1-2 months, 20-30 yrs from bone
Diagnosis: blood lead levels indicate recent exposure 30-75 ug/dal mild signs, >70 clear signs, >100 Pb encephalopathy
Children >10 risk for developmental abnormalities
EDTA provocation test estimates body burden indicates need for chelation therapy
Treatment: initially-supportive, prevent further exposures diazepam for seizures, maintain electrolyte balance, mannitol and dexmsthazone for cerebral edema
Chelation therapy: CaNa2EDTA (Im or IV), dimercaprol (IM), D-penicillamine(oral), succimer (oral)

37
Q

Acute lead poisoning signs

A

Metallic taste, nausea, abdominal pain, milky vomit, shock syndrome, parathesia, pain, muscle weakness, anemia, hemoglobinurea, oliguria kidney damage, death, placental transfers

38
Q

Chronic lead poisoning signs

A

CNS more in children, GI more in adults
GI: lead colic anorexia, muscle discomfort, malaise, headache, constipation, metallic taste, severe abdominal pain
Neuromuscular syndrome: lead palsy muscle weakness, fatigue
CNS syndrome: lead encephalopathy ataxia, vertigo, headache insomnia, restlessness, irritability, excitement and confusion, projectile vomiting, visual disturbances, delirium, tonic convulsions, lethargy, coma
Progressive mental retardation in children with BLL >60
Hematological: anemia, inhibition of synthesis of heme, d-ALA in plasma
Renal:proteinuria, hematuria, urine casts, Hyperurecemia with gout
Ashen face, retinal stippling, poor muscle tone and posture, gingival lead line, interference with vit d, hypertension, decreased sperm Count
Death is rare

39
Q

Organic PB poisoning

A

From tetra ethyl in gasoline
Highly lipid soluble
Readily absorbed from skin, lungs, GI tract and crosses BBB
Mainly CNS signs

40
Q

Iron

A

Sources: FeSO4 tablets
Iron overload-idiopathic hemochromatosis excess dietary fe
Frequent blood transfusions
Effects: vomiting, GI ulceration, shock, metabolic acidosis, liver injury, coagulation effects, renal failure
Mechanism: lipid peroxidation leading to organellar damage
Antidote: deferoxamine chelator, ascorbate (increased fe excretion)

41
Q

Carbon monoxide

A

Incomplete combustion of organic fuels
Competes with O2 for binding to heme
210x more affinity than O2 less than 1% in inspired air needed
20%COHb=headache
20-30=irritability, emotional, impaired judgment, defective memory, fatigue
30-40=weakness, vomiting, dizziness, dim vision, confusion, ataxia
40-50=loss of sphincter tone! severe ataxia collapse with exertion
50-60= coma, convulsion, tachycardia, weak pulse, reddish skin
>60=death
Diagnosis: cherry red blood
Delayed neurological disorder: poor concentration, memory loss, cognitive impairment-1 month post exposure
Treatment:O2
Sensitive populations: fetus and coronary artery disease

42
Q

Urushiol

A

Cause type IV hypersensitivity
Catechols found In poison ivy
3-n-pentadecandienyl Catechol most prominent
70% people exposed are sensitized to it

43
Q

Natural latex products

A

Type IV hypersensitivity

Due to chemical additives

44
Q

TDI toluene diisocyanate

A

Causes type I hypersensitivity
Occupational exposure by inhalation in chemical factories resulting in asthmatic reactions
Symptoms persist along time after cessation of exposure

45
Q

Apamin

A

Causes type I hypersensitivity

Attack of the killer bees

46
Q

Sulfites

A

Cause anaphylactoid reactions
Sprayed on restaurant salads, and wine
Sensitive individuals deficient in sulfite oxidase which metabolizes organic sulfate
Cause bronchospasm leading to asthma
Enzyme deficiency and not an immune response

47
Q

Penicillin hypersensitivity

A

.7-8% of patients treated
Anaphylaxis in.01% fatality rate 9%
Forms immunogenic hapten carrier complexes by binding directly to macromolecules in plasma and on cell surfaces

Pharmacology (15 decks)

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