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Block 7 Week 3 > Buxton toxicology > Flashcards

Buxton toxicology Flashcards

1
Q

What is poison?

A

all substances are poisons,

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2
Q

What is the science of the adverse effects of chemicals on the living organism?

A

decriptive toxicologist
mechanistic toxicologist
regulatory toxicologist

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3
Q

What are adverse effects?

A

Any change from an organism’s norma state

dependent upon the concentration of active compound at the target site for sufficient time.

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4
Q

What is a toxicant (poison)?

A

any agent capable of producing a deleterious response in a biological system

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5
Q

What are regulatory agencies for toxicology?

A

FDA
EPA
OSHA
CPSC

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6
Q

What is EPA for?

A

pesticides and environmental chemicals

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7
Q

What is OSHA for?

A

Workplace exposures

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8
Q

What is CPSC?

A

for consumer product safety commission

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9
Q

What is this:
Medicolegal aspects of chemical/drug exposures
Cause and circumstances of death

A

Forensic toxicology

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10
Q

What is this:
Treatment of patients exposed to toxicants
Development of diagnostic tests and treatments

A

Clinical toxicology

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11
Q

What is this:

Testing of drugs under specified conditions in animal organ systems looking for toxicity (FUNCTIONAL CHANGES)

A

safety pharmacology

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12
Q

As with therapeutic use of chemicals, toxicology references the understanding of the toxic effects of chemicals to (blank) or (blank)

A

concentration: effect
dose: response

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13
Q

What is a dose?

A

the amoutn of toxin entering the body

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14
Q

What is the dose dependent upon?

A 
The environmental concentration
Properties of the toxin
Pathway of exposure
Duration of exposure
Frequency of exposure
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15
Q

(blank) is all or none

(blank) is some on a scae

A

quantal

graded

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16
Q

In an individual you will have a dose response that is (blank)

A

graded

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17
Q

In a population you will have a dose response that is (blank)

A

quantal

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18
Q

Classically, a quantal dose (concentration) response (effect) is used to determine the (blank)

A

lethal dose

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19
Q

T or F

The dose makes the poison

A

T

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20
Q

What is ED50?

A

Median effective dose 50; the dose at which 50 percent of the pop or sample manifests a given effect; used with quantal d/r curves

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21
Q

What is TD50?

A

Median toxic dose 50- dose at which 50 percent of the popuation manifests a given toxic effect

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22
Q

What is LD50?

A

Median toxic dose 50- dose which kills 50 percent of the subjects (animal studies)

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23
Q

What is this:

LD50/ ED50

A

Therapeutic index

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24
Q

What is the margin of safety for drugs?

A

LD1/ED99

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25
Q

What is the margin of safety for toxins?

A

NOAEL/exposure- no observed adverse effect level (just shows where the death limit)

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26
Q

What is the most useful tool for figuring out margin of safety?

A

MABEL “minimal anticipated biological effect level”

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27
Q

What are the 2 ways you can find the therapeutic index?

A

TD50/ED50 or LD50/ED50

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28
Q

THe higher the (blank) the better the drug

A

Therapeutic index (TI)

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29
Q

TI will vary from (Blank) such as antineoplastic drugs to greater than (blank) such as penicillin

A

1

1000

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30
Q

Drugs acting on the same receptor or enzyme system often have the same (blank)

A

TI

e.g 50 mg of hydrochlorothiazide equates to 2.5 mg of indapamide

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31
Q

Some chemicals have both therapeutic and toxic effects such as (blank)

A

vitamin A

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32
Q

WHat happens if you have too low of a dose of vit A?

A

blindness, dry skin, increased infections

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33
Q

WHat happens if you have too high of a dose of vit A?

A

anorexia, anemia, nose bleeds, muscle and joint pain

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34
Q

(blank) is a group of unsaturated nutritional hydrocarbons that includes retinol, retinal, retinoic acid, and beta carotene

A

Vitamin A

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35
Q

What does Vit A do?

A

as retinoic acid regulates gene transcription at RXR receptors

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36
Q

What is the adequate intake for Vit A?

A

3 mg/day for adults

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37
Q

What has a very high lethal dose?

A

ethyl alcohol

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38
Q

What has a very low lethal dose?

A

botulinim toxin

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39
Q

What are the routes and sites of exposure?

A

ingestion (GI tract)
Ihalation (lungs)
Dermal/topical (skin)
injection (intravenous, intramuscular, intraperitoneal)

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40
Q

in order what are the most effective to least effect routes of exposure.

A

IV> inhale> ip> im> ingest> topical

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41
Q

What is acute exposure?

A

less than 24 hr usually a single exposure

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42
Q

What is subacute exposure?

A

about 1 month repeated dosese

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43
Q

What is subchronic exposures?

A

1-3 months in repeated doses

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44
Q

What is chronic exposure?

A

greater than 3 months repeated doses

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45
Q

Over time what can happen to the drug if you are chronically using it?

A

the amount of chemical can build up and redistribute or it can overwhelm repair and removal mechanisms

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46
Q

Once a living organism has been exposed to a toxicant, the compound must get into the body and to its target site in an (Blank) in order to cause adverse effect

A

active

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47
Q

What are the bodies defenses?

A
  • membrane barriers (passive and facilitate diffusion, active transport)
  • biotransformation enzymes, antioxidants
  • elimination mechanisms
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48
Q

What is this:

absorption through GI tract stomach (acids), small intestine (long contact time, large surface area - villi)

A

ingestion

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49
Q

What is this:
readily absorb gases into the blood stream via the alveoli. (Large alveolar surface, high blood flow, and proximity of blood to alveolar air)

A

inhalation

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50
Q

What is 1st pass effect?

A

liver detoxifies and reduces amount of drug

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51
Q

What is this:

absorption through epidermis (stratum corneum), then dermis; site and condition of skin

A

percutaneous absorption

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52
Q

What is this:

blood carriers the agent to and from its site of action, storage depots, organ transformation and organs of elimination

A

distribution

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53
Q

What is the rate of distribution dependent on?

A

blood flow and characteristic of toxicant (affinity for the tissue, and the partition coefficient)

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54
Q

T or F

distribution maychange over time

A

T

depo storage of toxicant in fat

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55
Q

What wil store in fat?

How can you get rapid release of these drugs?

A

very lipophylic compounds (DDT)

Rapid mobilization of the fat (starvation)

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56
Q

What drugs will deposit in bone?

A

chemicals analogous to calcium-fluoride, lead, strontium

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57
Q

Whats messed up about drugs that bind to plasma proteins?

A

they displace endogenous compounds and only free is available for adverse effects or excretion

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58
Q

Why is the liver a target organ?

A

it has high blood flow and participates in oxidative reactions

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59
Q

Why is the kidney a target organ?

A

high blood flow, concentrates chemials

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60
Q

Why is the lung a target organ?

A

high blood flow, site of exposure

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61
Q

Why are neurons a target organ?

A

oxygen dependent and causes irreversible damage

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62
Q

Why is the myocardium a target organ?

A

cuz it is oxygen dependent

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63
Q

Why is the bone marrow, intestinal mucosa a target organ?

A

rapidly dividing cells

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64
Q

Where can adverse effects occur?

A

at the level of molecule, cell, organ or organism

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65
Q

TOxins interact with ….?

A

proteins, lipids, RNA, DNA

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66
Q

What do toxins interfere with?

A 
receptor-ligand binding
membrane function
cellular energy production
alters membrane ion channels
perturb homeostasis (Ca2+)
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67
Q

What is filtered by the kidney and excreted in the urine?

A

water soluble products

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68
Q

What are exhaled?

A

volatile compounds

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69
Q

Compounds can be excreted by the liver and excreted into the (blank) which will drain into the small intestine and is eliminated in feces

A

bile

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70
Q

What are the ways you can get excretion?

A

milk, sweat, saliva, bile, feces, exhalation, urine

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71
Q

What is the primary objective of metabolism?

A

to make chemical agents more water soluble and easier to excrete

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72
Q

What will metabolism do?

A

decrease lipid solubility
decrease amount at target
increase ionization
increase excretion rate=decreased toxicity

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73
Q

What is this:

biotransformation can result in the formation of reactive metabolites

A

bioactivation

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74
Q

What is the major mechanism for activating or terminating the biological activity of chemicals?

A

metabolism

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75
Q

Metabolism is frequently the single most important determinant of the (blank) and (blank) of the pharmacological response to a chemical

A

duration and intensity

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76
Q

Where does biotransformation occur?

A

in liver, kidney, lung, GI and other organs

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77
Q

What is paraoxin?

A

a parasympathomimetic; acetylcholinesterase inhibitor.

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78
Q

What is an organophosphate active metabolite of the insecticide parathion?

A

paraxon

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79
Q

What are the key organs in biotransformation?

A

Liver (high), lung, kidney, intestine (medium), others (low)

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80
Q

What is phase I of biotransformation?

A

make the toxicant more water soluble

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81
Q

What is phase II of biotransformation?

A

Links with soluble endogenous agent (conjugation)

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82
Q

What does pharmacogenomics and toxicogenomics do?

A

identifiy subsets of people at risk for toxicity to chemicals or drugs

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83
Q

Who can get underdeveloped biotransformation enzymes and it will result in gray baby syndrome?

A

premature infants and infants 6-12 months who get chloramphenicol

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84
Q

Why can infants have decreased drug affects compared to adults?

A

they have greater percentage of water than humans so allows for dilution of drug

85
Q

What leads to greater absorption of heavy metals?

A

stomach is less acidic and periods between stomach emptying are longer

86
Q

WHen is the most sensitive period of the fetus?

A

3-8 weeks

87
Q

What is an enzyme responsible for acetylating and detoxifying many chemicals including aryl amines?

A

N-aceytlytransferase

88
Q

Who has slow acetylation (due to lack of n acetyltransferase)?

A

jews, scandanavans, N. African caucasians

89
Q

Who are fast acetylators?

A

Inuit and japanese

90
Q

Whats scary about slow acetylators?

A

greater rates of bladder cancer

91
Q

What is this:

Enzyme responsible for S-methylation of some anticancer drugs used in chemotherapy (azathiopurine and 6-mercaptopurine)

A

Thiopurine S-methyltransferase (TPMT)

92
Q

People with (high/low) TPMT levels respond poorly to chemo, since htey conjugate the drugs before they can act (need high dose).

A

high

93
Q

If you have low TPMT can you use chemo?

A

no, it will be toxic to them

94
Q

Why are the elderly suscpetible to drug toxicity?

A
  • imparied renal/respiratory function
  • inefficient metabolizers
  • more fat
  • lower water content
  • lower cardiac output/perfusion
  • low albumin
95
Q

What is bioactivation?

A

compounds to reactive metabolites

96
Q

What is this:

colorless, tasteless, odorless-0.1ppm in aire but reaches 100 ppm in heavy traffic.

A

CO

97
Q

(blank) is formed which does not carry oxygen and decreased O2 transfer of O2-heamoglobin

A

Carboxyhemoglobin

98
Q

Cigarette smokers have (blank) saturation of Hb by CO.

A

5-10%

99
Q

What are the effects of hypoxia?

A

headache, confusions, vision changes, tachypnea, tachycardia, coma, respiratory failure, death

100
Q

How do you treat CO?

A

removal of CO and treatment of O2

101
Q

What is SO2?

A

colorless product of fossil fuel combustion, should be 0 ppm; expsoures NOT TO EXCEED 2 ppm

102
Q

What does SO2 do to they body?

A

Forms acid (H2SO4) on moist membranes-irritant in eyes, mucous membranes, skin (has signif toxicity in the lungs-causes bronchiolar constriction and bronchospasm at great exposure levels

103
Q

What amount of SO2 results in bronchiolar constriction and bronchospasm?

A

5 ppm

104
Q

How do you treat SO2?

A

supportive respiratory care

105
Q

What is NO2?

A

brownish colored gas associated with fires and is a product of fermentation ang given off in large amounts in gran silos (silo-fillers disease)

106
Q

What is considered too much exposures of NO2?

A

3 ppm

107
Q

What does NO2 toxicity cause?

A

deep lung irritation- irritating to eyes and nose. has signif toxicity in the lung-pulmonary edema.

108
Q

Exposure to NO2 in high levels for even short periods can cause (blank), (blank), and (blnk)

A

pulmonary lesions, pulmonary edema, death

109
Q

How do you treat NO2?

A

supportive respiratory care, use of antibiotics and bronchodilators

110
Q

What is O3?

A

ozone is a bluish gas that is the product of electrical equipment and generators of ozone use in water purification

111
Q

Exposures of O3 should not exceed (blanK)

A

0.5 ppm

112
Q

What does O3 toxicity do?

A

deep lung irritante-irritates eyes and nose -signif toxicity in lung -pulmonary edema
causes airway inflammation and hyper-responsiveness**

113
Q

What is the treatment of O3?

A

respiratory care, use of antibiotics and bronchodilators

114
Q

Cholinesterase inhibitors include so called (blank) agents

A

nerve gas (VX, sarin, and soman)

115
Q

What are the symptoms of organosphate and carbamate insecticide poisoning?

A

DUMBELS (Diarrhea, Urination, Miosis, B(bradycardia); Excitation with muscle fasciculation, anxiety, seizures, Lacrimation, and Seizures)

116
Q

How do you diagnose organophosphate and carbamate insecticide poisoning?

A

with low plasma or RBC cholinesterase level

117
Q

Organophsphates bind (blank), whereas carbamates are (blank) inhibitors

A

irreversibly

reversible

118
Q

How are organosphostates and carbamate insecticides absorbed?

A

from skin, GI tract and respiratory tract

119
Q

What is parathione?

A

an organosphosphate insecticide

120
Q

How does parathione work?

A

if ingested or absorbed, it is converted to paraoxone, an inhibitor of cholinesterase
delayed toxicity*

121
Q

How do you treat insecticide poisoning?

A 
atropine IV to reverse the muscarinic effects (continue until wheezing and bronchorrhea are gone)
OR
Pralidoxime (i.v.) 2-Pam to reverese the effect of organophosphates at all sites (early, within 24 hours)
122
Q

How does pralidoxime work?

A

chemical phosphorylation reverese the AChE enzyme

123
Q

What is the leading cause of toxic drug ingestions in the US?

A

acetaminophen (can lead to hepatic toxicity and death w/ greater than 150mg/kg)

124
Q

Acetaminophen is metabolized to a toxic intermediate that can deplete (blank). In infants and adults, this can lead to liver damage. Adults are better at making the metabolite.

A

hepatic glutathione

125
Q

What is the treatment for acetaminophen poisoning?

A

oral activated charcoal (w/in 2-3 hr of ingestion)
oral N-acetylcysteine (NAC)
Acetadote (IV n-acetylcysteine) administered IV within 8-10 hrs after ingestion

126
Q

When can you stop giving NAC in acetaminophen poisoning?

A

if no evident liver injury after 6 hours after ingestion

127
Q

T or F

Most toxins do not have specific antidotes

A

T

128
Q

What is the generic name for NAC for acetaminophen poisoning?

A

Mucomyst

129
Q

When should you not induce emesis with ipecac?

A

for strong acids, or alkali petrol or stimulants

130
Q

What is the most important treatment for poisons?

A

activated charcoal

131
Q

What are ways to treat poisons?

A 
Dialysis
urinary excretion (alkalinization)
activated charcoal
gastric lavage
emesis (ipecac)
132
Q

What is the antidote for organophosphate?

A

quaternary ammonium oxime (2-PAM) (to reconstitute cholinesterase activity)

133
Q

What is the antidote for formaldehyde poisoning?

A

ammonia ( to form hexamethylenetetramine)

134
Q

What is the antidote for mercury poisoning?

A

formaldehyde sulfoxylate

135
Q

What is the antidote for ferrous ion poisoning?

A

sodium bicarbonate (to convert it to ferrous carbonate)

136
Q

What are the causes of heavy metal poisonings?

A

lead
arsenic
mercury
iron

137
Q

What is this:
Widely used in manufacturing; [ex. batteries; glass; as an additive to corrosion-resistant paints, binder in plastics, hair dyes]
Children susceptible to inhalation of paint dust, oral contamination by paint chips
Exposure to certain ceramic glazes and gasoline both contact and air pollutant

A

Lead

138
Q

Why is lead sucky?

A

intereres with protein function where carboxy phosphate and sulfhydryl binding occurs and where calcium, zinc, and iron binding are important

139
Q

What is the result of lead poisoning?

A

wide spread dysfuntion;
low level in children-> decreased development and mental retardation. Peripheral neuropathy, nephrotoxicity, anemia
(multi-system effects)

140
Q

Pb both inhaled and ingested binds to (blank) and is deposited in bone/

A

erythrocytes

141
Q

How can you detect lead?

A

blood and urine and with imaging

142
Q

How do you treat lead poisoning?

A

w/ metal chelators such as calcium EDTA and dimercaprol (to enhance Pb excretion)

143
Q

What are the chelators used to treat heavy metals?

A 
Dimercaprol
Succimer
EDTA
Penicillamine
Deferoxamine
144
Q

What is penicillamine used for?

A

copper poisoning

145
Q

What is deferoxamine used for?

A

iron poisoning

146
Q

How do you often get methanol intoxication?

A

as a result of its use as an ethanol substitute (30-200ml is lethal)

147
Q

Why is methanol bad?

A

metabolized to ADH to formaldehyde-> metabolized to formic acid by aldehyde dehyrogenase-> formate and formate/formic acid causes acidosis and blindness

148
Q

Toxicity for methanol is delayed (blank) hours

A

6-30

metabolism is slow 1/10th that of ethanol

149
Q

How do you treat methanol intoxication?

A

Supportive measures, airways etc.

  • bicarb (for acidosis)
  • administer fomepizole to block the alcohol dehydrognase (also used in ethylene glycol poisoning)
  • folic acid (to breakdown formic acid)
150
Q

What is TOCP?

A

an organophosphate found in boot leggers drinks that was a neurotoxin and created paralysis

151
Q

What is dioxin?

A

mutagen that is toxic and concentration in fat and thymus

152
Q

What are the effects of dioxin?

A

Acute: eye, skin, and mucous membrae irritation, nausea, vomiting and muscle pain

After a few weeks:polyneurpathies, sensory impairment, lower extremity weakness, motor problems,

153
Q

Is there an antidote for dioxin?

A

no but you can use olestra to promote elimination decreased half-life from 7 years to 1-2 years

154
Q

What is a more common name for dioxin?

A

agent orange

155
Q

What substance is most commonly involved in human poison exposure?
least likely?

A

analgesics

chemicals

156
Q

What substance causes the largest number of deaths?

Least?

A

analgesics

pesticides

157
Q

Benzes exposure is linked with (blanK0

A

leukemia and aplastic anemia

158
Q

Mercury interferes with (blank)

A

development

159
Q

What are some known carcinogens?

A 
aflatoxins
alcohol
analgesics w/ phenacetin
cyclosporin A
tobacco smoke
estrogens, steroidal
160
Q

Initial management of the poisoned patient begins with the (blank).
Then use (blank)
Then (blank)

A

ABC’s.
ACLS algorithms
consider bioavailability and H and P

161
Q

Besides the usual vitals what else should you get from the patient?

A

blood glucose

162
Q

(blank) are key to your initial managament of the patient

A

vitals

163
Q

If you smell bitter almonds what is the poison?

A

cyanide

164
Q

If you smell mothballs what is the poison?

A

camphor

165
Q

If you smell garlic what is the poison?

A

organophosphates, arsenic

166
Q

If you smell peanuts what is the poison?

A

rodenticide

167
Q

If you smell carrots what is the poison?

A

water hemlock

168
Q

If you smell rotten eggs what is the poison?

A

sulfur dioxide, HS

169
Q

If you smell wintergreen what is the poison?

A

methyl salicylates

170
Q

If you smell gasoline what is the poison?

A

hydrocarbons

171
Q

If you smell fruity what is the poison?

A

DKA, isopropanol

172
Q

If you smell pears, what is the poison?

A

chloral hydrate

173
Q

The most commonly reported poison?

A

analgesics

174
Q

The least commony reported poison?

A

alcohol

175
Q

The most commonly associated posion with death?

A

analgesics

176
Q

What poison is least associated with death?

A

hydrocarbons

177
Q

What is the number one poisonous killer?

A

carbon monoxide

178
Q

Why do you want to get an EKG?

A

look for conduction delay and ischemia

179
Q

Why do you want to get CMP?

A

to calculate anion gap and osmolality

180
Q

Why do you want to check tylenol and aspirin levels?

A

frequency of abuse and co-ingestionn

181
Q

What do serum volatiles tell you?

A

quantitative amounts of alcohols (for people with altered mental state of unknown etilogy)

182
Q

WHy check the urine?

A

screening (rarely changes management)

183
Q

What check the blood?

A

for quantitative info regarding spec. ingestants

184
Q

What is the coma cocktail and what is it for?

A

Dextrose, Narcan, Thiamine
cuz the three most likely reasons for being unconscious in the ER are:
ketoacidosis (diabetes)-> dextrose
Opoid overdes-narcan
Too much alcohol (thiamine deficiency)-> thiamine (malnourished)

185
Q

When do you give flumazenil?

A

For people who we overdose with benzos

186
Q

Do we still use ipecac?

A

no!!

187
Q

What do you use to manage GI decontamination?

A

gastric lavage: use with “moderate to severe overdoses” within an hour of ingestion
variable outcome*
Activated charcoal

188
Q

When should you not give lavage?

A

contraindicated with ingestion of corrosives

189
Q

Which is better gastric lavage or charcoal?

A

charcoal (used within an hour of ingestions)

190
Q

What is the dose for charcoal?

A

1g/kg or 10: 1 ration of charcoal to poison

191
Q

When do you give cathartics?

A

with charcoal to enhance elimination

192
Q

When should you use whole bowel irrigation?

A
  • for things not absorbed by charcoal

- used for body stuffer/packers

193
Q

What is the antidote to anticholinergics?

A

physostigmine

194
Q

What is the antidote for anticholinergics?

A

physostigmine

195
Q

What is the antidote for arsenic/lead?

A

BAL chelation

196
Q

What is the antidote for beta-blockers?

A

glucagon

197
Q

What is the antidote for benzos

A

flumazenil

198
Q

What is the antidote for CO?

A

O2, HBO

199
Q

What is the antidote for cyanide?

A

Nitrites

200
Q

What is the antidote for digoxin?

A

digibind

201
Q

What is the antidote for ethylene glycol/methano?

A

fomepizole/ethanol

202
Q

What is the antidote for iron?

A

deferoxamine

203
Q

What is the antidote for INH?

A

B6/pyridoxine

204
Q

What is the antidote for Lead/mercury?

A

succimer/DMSA

205
Q

What is the antidote for methemoglobinia?

A

methylene blue

206
Q

What is the antidote for opoids?

A

naloxone

207
Q

What is the antidote for organophosphates?

A

atropine

208
Q

What is the antidote for Tricyclic Antidepressants’s?

A

sodium bicarbonate

Block 7 Week 3 (4 decks)

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