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Pharmacy > Toxicology > Flashcards

Toxicology Flashcards

0
Q

Most toxic substance

A

1) botulinus toxin

2) dioxin

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1
Q

Toxin

A

Toxic substance of bacterial, plant, animal

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2
Q

Organophosphate/carbamate

A

Anticholinergic

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3
Q

Toxic parent compound

A

Lead, carbon monoxide

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4
Q

Toxic metabolite

A

Carbon tetrachloride - phosgene

Ethylene glycol - oxalic acid

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5
Q

Reactive oxygen/nitrogen species

A

Pesticides

Oxygen radical, hydrogen peroxide, hydroxy radical, lipid perixidation

Oxidative stress if imbalance with radicals and antioxidant imbalance

Alzheimer’s, Parkinson’s, cancer, cardio

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6
Q

Radical detoxication

A 
Oxygen radical SOD to H2O2
Glutathione peroxidase (GPO) to water with the help of glutathione
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7
Q

FDA

A

Federal food drug and cosmetics act

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8
Q

Environmental protection agency

A

Pesticides

Toxic control act

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9
Q

OSHA

CPSC

A

Occupational safety

Consumer product safety

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10
Q

Increases death by 1/million

A

Smoking
Living in a city - air pollution
Peanut butter
Charbroiled steaks

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11
Q

4 step Risk assessment

A

Hazard identification
Dose-response
Exposure
Risk characterization in exposed population

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12
Q

Saccharine

A

Artificial sweetener

Bladder tumors

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13
Q

Pre clinical tests

A

Animal tests for safety and efficacy

Acute toxicology - high dose, LD50
subchronic toxicity - adverse effects
carcinogenicity

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14
Q

Therapeutic index

A

LD50/ED50

10 is ideal

You want high lethal dose, low effective dose

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15
Q

Food additive no effect dose

A

100 times human consumption level

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16
Q

Phase 1 clinical trial

A

Toxicity profile in healthy volunteers

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17
Q

Phase 2 clinical trial

A

Safety and efficacy in patients

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18
Q

Phase 3 clinical trial

A

Establish dose-range and form

Larger number of patients hundreds

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19
Q

Phase 4 clinical trial

A

Post-market safety

Collections of additional data

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20
Q

Drug development facts

A

Cost >1 billion

12 years

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21
Q

Insecticides

A

Parathion
Carbaryl
DDT
Pyrethrum

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22
Q

Parathion

A

Most toxic organophosphate, activated to paraoxon by CYP

ACh accumulation at receptor sites via AChE blockage

Phosphate (binds to esteric site) can’t be rescued if ethyl groups are cleaved.

Increased cholinergic tone. SLUD
Salivation, lacrimation, urination, diarrhea

Chronic: sensory and motor neurotoxicity

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23
Q

ACh on nicotinic

A

Nm: striated muscle, cramps, weakness
Nn: tachycardia

Anxiety, insomnia, respiratory depression

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24
Q

Parathion treatment

A

Atropine followed by 2-PAM
Atropine for ACh symptoms
2-PAM binds to anionic site to cleave off phosphate group and rescue AChE

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25
Q

Carbamate

A

Less toxic than organophosphate

Like parathion but rapidly reversible

Treat with atropine only for symptoms
2-PAM may inhibit anionic site. AChE will be restored naturally over time

Pesticide but also used clinically for myasthenia gravis and glaucoma (relieve intraocular pressure) - physostigmine

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26
Q

DDT

A

Wide margin of safety between pests and humans

Toxic to fish, food chain, bald eagle shells thin through low estrogen, low Ca

More negative neuron membrane after causing prolonged action potential and repeated firing

Can cause breast cancer

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27
Q

DDT treatment

A

Anticonvulsant, diazepam

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28
Q

Pyrethrum

A

Active ingredient: Pyrethrin I most active

Affects action potential like DDT (CL- transport)

Neuron toxicity: convulsions, ataxia

Increases metabolism in mammals

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29
Q

Herbicides

A

Most active ingredients out of all pesticides

2,4 Dichlorophenoxy acetic acid

2,4,5 trichlorophenoxy acetic acid - banned b/c of carcinogenicity

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30
Q

2,4-D

A

Membrane damage
Interfere with acetyl CoA in metabolism
Uncoupling of oxidative phosphorylation
Less ATP produced

Treat with bicarbonate iv to alkinalize urine and ionize 2,4-D for excretion

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31
Q

2,4,5-T

A

Vietnamese population: birth defects

Toxic due to tetrachlorodibenzodioxin (TCDD)

Carcinogenic

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32
Q

Pentachlorophenol

A

Fungicide

Elevated body temperature

Mechanism: decreased H+ permeability
Short circuiting of ATP synthesis
Increased metabolic rate
Excessive heat generation

Treatment: cholestyramine

33
Q

Rodenticide

A

Warfarin - teratogenic
Brodifacoum

Bleeding gums, bloody urine, hematoma

Warfarin weakens capillary walls causing hemorrhage and unable to clot by inhibiting vitamin K reductase

Treat with vitamin K

34
Q

Cyanide

A

Fumigant, causes hypoxia, respiratory arrest
Bitter almond breath diagnostic

High affinity for Fe3+ on Cyt. Oxidase
Blocks oxygen utilization and inhibits cellular respiration, decreases ATP, and cell death

Can cause heart and brain damage

35
Q

Cyanide treatment

A

1)Na-nitrite: methylHb(Fe3+) formation frees Cyt. Oxidase

Na-thiosulfate : frees MetHb(FeCN) and excretes SCN in urine

100% O2: maximizes recovery

36
Q

Solvent toxicity factors

A

Low surface tension - spreading
Low viscosity - reaching distal airways
High volatility- vaporized & available for absorption
Lipid solubility- facilitation of absorption
Solvent - dissolution of membranes

37
Q

Carbon tetrachloride (solvent)

A

Parent and metabolite are toxic

CCl3 radical leading to lipid peroxidation

Phosgene - covalent bonding to proteins and lipids
Stage 1: CNS, respiratory depression
Stage 2: hepatic damage
Stage 3: renal effects
Chronic toxicity: cirrhosis, liver cancer

Treatment - dialysis to remove metabolite

38
Q

Methanol

A

Paint, varnish, aspartame in diet drinks

Metabolized by alcohol dehydrogenase

Hangs around more than ethanol (lower affinity for ADH)

Formaldehyde to formate acidosis toxicity

Diagnostic: urine has formaldehyde odor

39
Q

Methanol treatment

A 
Gastric lavage (remove unabsorbed toxin)
Bicarbonate - neutralize acid formate 
Hemodialysis - clean blood
Ethanol - competitive antagonist 
4-Methyl Pyrazole (fomepizole) inhibits ADH and slows metabolism to formaldehyde
40
Q

Ethylene Glycol

A

Forms oxalic acid and calcium oxalate crystals via ADH and GDH

Stage 1: NV, CNS depression, inebriation 
Stage 2 (most deadly) 12 hours: Ca-oxalate deposits in blood vessels, lungs, myocardium, CNS meninges causing tachycardia, CHF, pulmonary edema, hypocalcemia

Stage 3: renal tubular necrosis and oliguria from Ca-oxalate deposits

41
Q

Ethylene glycol treatment

A

Drunkard w/o alcoholic breath

Gastric lavage
Fluids
Bicarbonate for acidosis
Ca-gluconate: to replace Ca deficiency

Competitive ADH inhibitor - ethanol, fomepizole

42
Q

Propylene glycol

A

GRAS food additive

43
Q

Benzene

A

Most toxic component in gasoline

Converts to phenol and phenoxyl radical leading to oxidative stress and bone marrow suppression

No antidote, only supportive care

Chronic: CNS effects, carcinogen, bone marrow cell production

Leukemia: chemotherapy
Aplastic anemia: bone marrow transplant

44
Q

Metal toxicity mechanisms

A 
Adventitious bind
Oxidative stress
Enzyme inhibition - arsenic to sulfur
DNA damage 
Gene expression

Inhalation, poor GI absorption

45
Q

Mercury

A

Dental amalgam, dental fillings, HgCl2
Thiomersal vaccines, Fish CH3Hg

Hg2+ has less absorption and cannot reach brain b/c of ion

In brain catalase converts Hg to toxic Hg2+

Neurotoxicity binds to BBB

Ionized excreted in the urine

Acute NVD via GI inflammation
Chronic mad hatter, renal damage, ataxia

46
Q

Mechanism of mercury nephrotoxicity

A

Hg to SH groups of membrane proteins

Damage to glomerulus membrane

Causing glomerular nephritis and proximal tubular necrosis

47
Q

USA Mercury

A

Salt water fish
New England

Pregnant women limit fish to once a week

Hair can tell history of exposure 1cm/month

48
Q

Mercury treatment

A

Hg/Hg2+ : N-acetylpenicillamine to urine

CH3Hg : polythiol resin to feces or NAP

49
Q

Lead (Pb2+)

A

Paint

Ultimately distributed to bones with a 32 year half-life

Inhibits heme biosynthesis (anemia), form lead-protein complexed in renal tubular cells, compete w/ calcium in bones

Chronic: brain damage in children

50
Q

Lead treatment

A

Children: DMSA (metal chelation)

Adults: Ca, Na2-EDTA, replaces lead with calcium

51
Q

Cadmium (Cd2+)

Ouch ouch

A

Inhalation, poor Gi absorption
Binds to metallothionein - t1/2 30 years
Damages kidney, VitD production

Chronic: lung cancer, renal dysfunction, breast cancer, osteomalacia, Ca deficiency

Treat osteomalacia with VitD

No effective chelating agent

52
Q

Arsenic gas
Arsenite (3+)
Arsenate (5+)
Mono/dimethyl-arsenates

A

Short half life liver/kidney

Arsenate-arsenite-monomethyl-dimethyl-trimethylarsenate: causing oxidative damage

Acute: Arsenate 5+ mimics phosphate during glycolysis and causes uncoupled oxidative phosphorylation. No ATP produced

As3+ binds to SH groups on enzymes and inhibits pyruvate metabolism and decreases mitochondrial respiration ATP

Chronic: lipid peroxidation to cell death

53
Q

Arsenic treatment

A

Breath has garlic odor

Multiple organ damage, anemia, cancer

Hemodialysis
Glucocorticoids
BAL, DMSA chelating agents
Pencillamine

54
Q

Pulmonary toxicants

A

Small particles reach alveoli

Heavy particles get deposited in upper respiratory tract

Type 1 alveoli small cytoplasm, efficient gas exchange

55
Q

Lung fibrosis

A

Inflammation leading to excess collagen to alveolar ducts

Lungs become stiff and smaller

56
Q

Emphysema

A

Opposite of fibrosis

Type 1 alveolar cells destroyed and lose efficient gas exchange

Lungs become large, too compliant, and hyper inflated

Inefficient O2 CO2 gas exchange

57
Q

Air pollution

A

60% automobiles

52% carbon monoxide (most abundant)

Smog = stagnant air

Sulfur dioxide to H2SO4 acid rain

Asthmatics most sensitive

58
Q

H2SO4 / SO2

A

H2SO4More airway resistance, more clearance
Smaller particles more toxic

Acts on bronchial smooth muscle
Histamine release causing bronchial constriction

Chronic bronchitis: thickening of mucous layer
Gland hypertrophy

59
Q

Metal chelating agents

A

For treatment

2 SH: DMSA, BAL, DMPS

SH & COOH: pencillamine, N-acetyl pencillamine

60
Q

Nitrogen dioxide

A

Photochemical pollutant

Breaks down ozone UV protection

NO2 automobile exhaust

Pulmonary irritation
Lipid peroxidation
Damage to type 1 cells (emphysema)
Loss of celia, susceptible to infection

61
Q

Formaldehyde

A

Irritant, automobile exhaust

Chronic: runny nose, sore throat, cough, headache

62
Q

Ozone

A

Airline crew exposed

Dry throat, pulmonary irritation
Smog: limit outdoor activities and exertion

Chronic: O3 forms H2O2 lipid peroxidation, necrosis of type 1 cells-emphysema
Can cause compensatory fibrosis by increased collagen synthesis

63
Q

Carbon monoxide

A

Heavy traffic, fires

Acute NV, afib, convulsions
Delayed neuropsych impairment, CVD

CO mechanism

1) reduced O2 in air for absorption
2) reduced O2 carrying capacity by Hb when bound by CO
3) reduced dissociation of O2 from COHb due to conformation change
4) reduced O2 transport in muscle/tissues
5) cytochrome-CO complexes lead to cellular hypoxia and lack cellular respiration

64
Q

Carbon monoxide treatment

A

Diagnosis- Cyanic blue (CO-myo) when alive
Cherry red blood when dead

More toxic in high altitude (low air pressure), high ventilation (exercise), children

Treat 100% oxygen to dissociate COHb
Faster in hyperbaric chamber

65
Q

Radon

A

Indoor air, basement

Chronic: lung, stomach cancer

Forms radioactive decay products (polonium)
Oxidative damage of nucleic acids and protein

ends at stable Pb lead

Seal basement, increase ventilation

66
Q

Asbestos

A

Insulation

Lung cancer forms inside the lung

Pleural plaques scar and thicken lung walls
(Asbestosis) Progresses to Pleural mesothelioma outside lung lining

1) interaction with macromolecules
2) reactive oxygen species
3) inflammation

67
Q

Treatment of malignant pleural mesothelioma

A

Surgery
Radiation

Pemetrexed antifolate
Cisplatin

68
Q

Predifferentiation period

A

Up to day 17

Prenatal lethality if embryo unable to implant

69
Q

Organogenesis period

A

Day 18-56

High susceptibility to teratogenesis

70
Q

Histogenesis period

A

Day 50-90

Resistant to teratogenesis
growth retardation

71
Q

Human development defects

A

20% genetic

5% drugs/chemicals

72
Q

Teratogens

A

Thalidomide
Tobacco smoke
EtOH
Diethylstilbestrol

73
Q

Thalidomide

A

Short/absent limbs

Sensitive 5-7 weeks

More toxic in humans than rabbits and mice

1) signal transduction interference
2) oxidative stress
3) intercalation with DNA in GC region
4) interfere with angiogenesis

74
Q

Tobacco smoke

A

Cleft lip or palate
Low birth weight, slow growth
Learning disorders

300% sudden infant death syndrome

CO - hypoxia
HCN- cellular hypoxia (no respiration)
Cadmium - zinc deficiency
Nicotine- tachycardia

75
Q

Ethyl alcohol

EtOH

A

Fetal alcohol syndrome
No threshold, one single drink can harm

Facial abnormalities
Growth retardation
Mental retardation neuro defect

Acetaldehyde decreases cell division and cell migration

76
Q

Diethylstilbestrol

A

Synthetic steroidal estrogen
Indications: prostatic and breast cancer

No major malformations in infants

Post menopause mother 14x endometrial cancer

Boys - testicular defects, sperm abnormalities boys can reproduce healthy sperm
Girls - vaginal adenosis, adenocarcinoma
Risk of breast cancer after age 40

More age more egg exposure to DES

77
Q

Reproductive study I

Single generation Toxicity study in rats
Drugs of short duration

A

For fertility and reproductive performance

Exposed prior to mating

Number of pregnancies and live fetuses

78
Q

Reproductive study II

A

Perinatal - birth
Postnatal - after birth

Mid-gestation to lactation

Look for physical development
Behavioral effects

79
Q

Reproductive Study III

A

Embryolethality
Teratology

Number of dead fetuses
Malformations in live fetuses

80
Q

Multigeneration study

A

Required for:

1) drugs intended for chronic use
2) food additives & pesticides

Purpose:

1) transplacental carcinogenesis
2) germ cell mutations

Exposure throughout 2nd 3rd mating

Look for cancer, malformations, defects

81
Q

Lipid peroxide

A

Cell degradation

Disrup lipid membrane I

Pharmacy (63 decks)

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