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Toxicology Flashcards

1
Q

What is the difference between a toxin and toxicant?

A

Toxin - natural, toxicant - man made

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2
Q

Bioaccumulation

A

The accumulation of a substance within tissues of an organism (distribution exceeds elimination)

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3
Q

Biomagnification

A

Process whereby concentration of a substance increases as the substance moves up the food chain

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4
Q

How is therapeutic index calculated?

A

LD50/ED50 (lethal dose over effective dose)

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5
Q

Categories for dosing (time of exposure) in toxicology

A

Acute lt 24 hr, Subacute repeated exposure for 1 month or less, Subchronic repeated exposure for 1 to 3 months, Chronic more than 3 months

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6
Q

When analyzing a toxicants dose-response curve, does a steeper line imply less certainty or more certainty about the toxicants effects?

A

More certainty (a perfectly vertical line would mean the entire population has the same response)

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7
Q

When analyzing a toxicants dose-response curve, is the curve with a steeper slope or shallower slope considered more toxic (assuming the same LD50)?

A

Shallower slope (will show more problems at low dose)

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8
Q

What toxicant caused problems during World War II and why was this surprising?

A

Diethylene glycol. Sulfanilamide (antibiotic) was put in diethylene glycol, which was not known to be toxic because it has a shallow (unpredictable) dose-response curve

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9
Q

What compound was accidentally released in Bhopal, India in 1984?

A

Methyl isocyanate

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10
Q

What five pollutants account for 98% of outdoor air pollution

A

Sulfar dioxide (SO2), Particulate matter (PM), Nitrogen Dioxide (NO2), Carbon Monoxide (CO) and Volatile Organic Compounds

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11
Q

Which outdoor pollutants are reducing

A

Sulfur dioxide (SO2) and smoke

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12
Q

What outdoor poullutants are oxidizing?

A

Hydrocarbons, nitrogen oxides, secondary photochemical oxidants (e.g. ozone)

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13
Q

Effects of SO2 exposure

A

Pulmonary irritant, upper airway mucus secretion, bronchoconstriction, thickening of mucus layer in trachea

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14
Q

Effects of particulate matter exposure

A

Chronic pulmonary inflammatory conditions and cancers. Mesothelioma (asbestos), pneumoconiosis (blakc lung), aluminosis (Shavers disease, bauxite lung), Byssinosis (cotton dust), Berylliosis (berrylium)

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15
Q

What is the relationship between particulate size and deposition in the lung

A

Smaller particulate size, deposition deeper into the lung

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16
Q

Effects of exposure to oxides of nitrogen

A

Deep lung irritation, increased respiratory frequency, decreased compliance

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17
Q

Effects of exposure to ozone

A

Lung irritation, pulmonary edema (mostly lower respiratory tract), cough, chest tightness, dryness of throat. Long term - chronic bronchitis, fibrosis, emphysematous changes

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18
Q

What is the environmental agent responsible for the most deaths each year?

A

Carbon monoxide

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19
Q

What is a normal reading for COHb

A

lt 5% in non-smokers, up to 15% in smokers

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20
Q

Effects of a low level of carbon monoxide poisoning (10-20% COHb)

A

Headache, cutaneous blood vessel dilation

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21
Q

Effects of a medium level of carbon monoxide poisoning (20-40% COHb)

A

Significant headache, dizziness, nausea, vomiting, collapse, potential death

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22
Q

Effects of a high level of carbon monoxide poisoning (above 40% COHb)

A

Syncope, Cheyne-Stokes respiration, Convulsions, Decreased CV function, coma, death

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23
Q

What is the apperance of a patient who has carbon monoxide poisining?

A

Bright pink skin (due to cherry-red color of COHb)

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24
Q

What occurs within 2-3 weeks of CO poisoning?

A

Neurologic deterioration (can also get atherosclerotic disease)

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25
Q

Treatment for CO poisoning

A

100% oxygen (and hyperbaric oxygen therapy, which is somewhat controversial)

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26
Q

Common signs and symptoms for Sick Building syndrome

A

Eye nose and throat irritation, headaches, fatigue, reduced attention span, irritability, nasal congestion, difficulty breathing, nosebleeds, dry skin, nausea

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27
Q

Common signs and symptoms from solvent exposure

A

CNS depression (headache, dizziness, anesthesia, asphyxiation, respiratory depression, coma, death). Chronic - cirrhosis and carinogenesis

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28
Q

Effects of exposure to halogenated aliphatic hydrocarbons

A

Acute - CNS depression and adverse cardiac effects (arrhythmias). Chronic - liver problems, cancer, impaired memory, neuropathies, renal issues

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29
Q

Three toxic halogenated aliphatic hydrocarbons

A

Carbon tetrachloride, chloroform, trichloroethylene

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30
Q

Effects of exposure to aromatic hydrocarbons

A

Variable, mainly CNS depression, sometimes hematopoietic disturbances (benzene, chronic)

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31
Q

Effects of exposure to polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs)

A

Dermatologic effects (chloracne, erythema, hyperkeratosis), elevated triglycerides, long-term liver problems

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32
Q

Effects of endocrine disruptors (such as Diethylstilbestrol (DES))

A

Genital tract anomalies, clear cell adenocarinoma, epidydmal cysts, hypotrophic testes, low ejaculatory volume, poor semen quality

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33
Q

Define TLVs, TWA, STEL, TLV-C, and BEI

A

Threshold limit values, Time-Weighted Average (allowed time of exposure), Short-Term Exposure Limit, Threshold Limit Value Ceiling, Biological Exposure Index (normal measured biological value)

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34
Q

What class of drugs are chemical insectisides in use today?

A

Neurotoxicants

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35
Q

What class of pesticides are no longer used in the west, but still used in third world, and give a few examples

A

Organochlorine compounds, DDT, Chlordane, Lindane

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36
Q

Effects of DDT exposure

A

Acute - paresthesia, ataxia, CNS disturbances, fatigue, tremor. Chronic - weight loss, mild anemia, muscular weakness, EEG changes, hyperexcitability

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37
Q

Effects of cyclodiene (e.g. chlordane) exposure

A

Acute - dizziness, headache, nausea, vomiting, hyperreflexia, myoclonus, convulsions. Chronic - same as acute, psychological disturbances, EEG changes

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38
Q

Effects of chlorinated benezenes exposure (e.g. lindane)

A

Acute - same as DDT (paresthesia, ataxia, CNS disturbances, fatigue, tremor), and seizures

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39
Q

Mechanism of DDT-type pesticides

A

Alteration of Na and K transport across axonal membranes. Increased negative afterpotential, prolonged APs, repetitive firing, spontaneous firing

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40
Q

Mechanism of action of Cyclodienes (e.g. chlordane)

A

Antagonists for GABA receptors, partial repolarization of the neuron and a state of uncontrolled excitation

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41
Q

What pesticides replaced organochlorines and how do they work?

A

Organophosphates and Carbamates. They inhibit acetylcholinesterase

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42
Q

For the pesticides that replaced organochlorides, which is fast (reversible) and which is slow (irreversible)

A

Organophosphates react irreversibly w/ body, Carbamates react reversibly

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43
Q

Treatment for exposure to organophosphates or carbamate pesticides and give restrictions

A

Atropine, and/or Pralidoxime (2-PAM). 2-PAM will not work with all Organophosphates (OPs), and will not work long after OP exposure

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44
Q

What is contraindicated in carbamate poisoning?

A

Oxime antidotes

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45
Q

Effects of pyrethroid insectiside exposure

A

Cutaneous paresthesias, dizziness, burning, itching, tingling of skin. Ingestion - epigastric pain, nauesea, vomiting, headache, blurred vision, parasthesia, palpitations, muscle fasciculations, disturbances of consciousness, convulsions

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46
Q

Types of pyrethroid pesticides and differences between them

A

Type I lack an alpha-cyano group as opposed to Type II

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47
Q

Mechanism of pyrethroid pesticides

A

Modify gating kinetics of Na channels, resulting in hyperexcitable states

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48
Q

Which type of pyrethroids are longer acting

A

Type II

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49
Q

At what COHb point does death occur

A

Usually around 50% (can be as low as around 25-30%)

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50
Q

Effects of exposure to chlorphenoxy herbicides

A

Persistent chloracne, skin, eye and respiratory tract irritation, dizziness, headache, severe muscle pain in thorax, shoulders and extremities, fatigue, decreased libido, dyspnea, irritability, intolerance to cold

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51
Q

What class are paraquat and diquat in?

A

Bipyridyl herbicides

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52
Q

What are the long term effects of bipyridyls (e.g. paraquat and diquat)

A

Pulmonary toxicity, death (3-4 weeks)

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53
Q

Treament for paraquat/diquat exposure

A

Gastric lavage, Fuller’s earth (Kaolin), hemoperfusion

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54
Q

Types of fungicides

A

Hexachlorobenzene (HCB), phthalimides, dithiocarbamates

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55
Q

Two widely used fumigants

A

Phosphine, Ethylene dibromide/dibromochloropropane

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56
Q

Most common rodenticides and the effects of each

A

Zinc phosphide (necrosis of GI tract, liver/kidney damage), Fluoroacetate (intereferes with Krebs ycle by inhibition of aconitase), Anticoagulants (hemorrhage by antagonizing vitamin K)

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57
Q

What do aromatic hydrocarbons cause?

A

Leukemia

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58
Q

Essential trace elements

A

Metals which we require to live (e.g. need chromium in +3 state to regulate glucose)

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59
Q

Proteins that help with transport, storage, and elimination of metals

A

Metallothioneins (Cd, Cu, Hg, Ag, Zn), Transferrin (Fe, Al, Mn), Ferritin (Fe, Cd, Zn, Be, Al), and Ceruloplasmin (Cu)

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60
Q

Chronic exposure to cadmium causes increased concentrations of what in urine?

A

B-2 microglobulin

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61
Q

What can be a side effect of chelation therapy

A

Deficiency of essential trace elements (because chelators are usually not specific for a given metal)

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62
Q

Toxicity of various forms of arsenic

A

Organic arsenicals less than As5+ less than As3+ less than Arsine

63
Q

Selective toxicity

A

The property of a toxicant (e.g. pesticides) that they kill the intended organism but do not affect others (e.g. us)

64
Q

Long term sequelae of arsenic exposure

A

Lung, skin, bladder cancers

65
Q

Mechanisms of Arsenic

A

Uncouple Ox Phos (5+), Bind with Sulfhydrl (3+), Interact with hemoglobin to cause hemolysis (Arsine gas)

66
Q

Treatment for arsenic poisoning

A

Severe cases - chelation with dimercaprol (BAL) or succimer (chelation ineffective for arsine gas exposure)

67
Q

How do we monitor patients exposed to arsenic?

A

Blood and urine arsenic concentrations and hair/nail analysis

68
Q

Mee’s lines

A

Transverse white deposits of arsenic on the nails

69
Q

What class of symptoms are characteristic of posoning with arsenic (arsnicals or arsine gas)?

A

GI Disturbances (projectile vomiting, diarrhea)

70
Q

Common sources of cadmium exposure

A

Shellfish, fish from polluted water

71
Q

Smoking a pack a day doubles one’s body burden of what metal?

A

Cadmium

72
Q

Cadmium exposure is correlated with what long term sequelae?

A

Lung and prostate cancers

73
Q

Principally what organs does cadmium end up in?

A

Lungs (absorbed from air), Kidney, Liver. Most cadmium in GI tract gets excreted in feces

74
Q

In what form is cadmium found in the blood?

A

In blood cells bound to metallothionein

75
Q

What is the mechanism of action of cadmium

A

Interaction with functional macromolecules

76
Q

Effects of cadmium exposure (chronic)

A

Renal problems, chronic pulmonary dysfunction, osteopenia-osteomalacia, yellow teeth lines

77
Q

Treatment for cadmium exposure

A

Vitamin D once osteomalacia evident, chelation controversial, EDTA salts?

78
Q

Biomarkers of effect for cadmium

A

Renal function related proteins: B-2 microglobulin, retinol-binding protein (RBP), N-acetyl-B-D-glucosaminidase (NAG). These are not SPECIFIC for cadmium

79
Q

Typical means of exposure to lead

A

Food, also environmental sources (lead paint, etc)

80
Q

Why is speciating arsenic tests important?

A

The patient may be exposed to organic arsenicals (e.g. from lobster) which is ok, but without speciation it can return a general high As level

81
Q

What are rice water stools a symptom of?

A

Arsenic poisoning

82
Q

Why are children more at risk for lead poisoning?

A

They have a much higher absorption percentage (up to 40%)

83
Q

In what form is lead found in the blood?

A

Bound to hemoglobin

84
Q

Main target organs for lead toxicity

A

Kidney, liver, brain. Also heavy deposition in long bones

85
Q

Does lead cross the placenta?

A

Yes

86
Q

Mechanism of action of lead

A

Binds sulfhydryl groups, interfering with many important enzymes (ALA-D, Ferrocheletase, others), also affect DNA transcription factors and calcium-related activity

87
Q

Effects of acute lead poisoning

A

GI disturbances, CNS effects (paresthesias, pain, muscle weakness), and renal damage. Death in 1-2 days

88
Q

Effects of chronic lead poisoning (plumbism)

A

CNS - ataxia, falling, headache, clumsiness, iritability, confusion, visual disturbances, delirium, convulsions, coma, MR, EEG changes, seizures, cerebral palsy. Neuromuscular - muscle weakness, fatigue. Heamtologic - basophilic stipling in RBCs, hypochromic microcytic anemia. Other - renal tubular disorder, nephropathy, ashen color of face, lead-lines along gums, reproductive problems

89
Q

Which form of lead crosses the BBB particularly well?

A

Organic lead (tetraethyl- and tetramethyl- forms are lipid soluble)

90
Q

Treatment for lead poisoning

A

Chelation with CaNa2EDTA or dimercaprol (BAL) and D-penicillamine

91
Q

For which types of lead poisoning is chelation therapy used?

A

Inorganic lead. Do not use chelation for organic lead exposures

92
Q

Useful biomarkers for lead exposure

A

Zinc protoporphyrin (ZPP) and free protoporphyrin (FEP) in blood, ALA in blood and urine

93
Q

How do you measure lead in organic vs inorganic exposures?

A

Organic - urine lead, Inorganic - whole blood lead

94
Q

Why are ALA and ZPP not good biomarkers for ORGANIC lead exposure?

A

Because organic lead compounds do not affect heme synthesis

95
Q

At what blood level of lead is treatment recommeded to begin (retesting, lead prevention activities)

A

Above 10 mcg/dL

96
Q

At what blood level of lead should chelation first be considered?

A

Above 20 mcg/dL. Recommended above 45 mcg/DL

97
Q

Most common sources of exposure to mecury

A

Contaminated food (e.g. fish)

98
Q

Three toxic forms of mercury

A

Elemental, inorganic and organic mercurials

99
Q

Mechanism of action of mercury

A

Bonds with sulfur (e.g. Sulfhydryl groups)

100
Q

Absorption and transport of elemental mercury

A

Not well absorbed (skin or GI), transported by RBCs

101
Q

Where does elemental mercury tend to end up in the body?

A

Lungs, fistulas, diverticula, brain. Does cross BBB

102
Q

Effects of acute exposure to elemental mercury

A

GI distrubances, metallic taste in mouth, cough, chest tightness, pulmonary toxicity (residual fibrosis)

103
Q

Effects of chronic exposure to elemental mercury

A

Asthenic vegetative syndrome (micromercurialism) - neurasthenia, gingivitis, thyroid disturbance (e.g. goiter), tremor, psychological changes, perspiration, erethism (blushing)

104
Q

Classic triad of mercury vapor exposure

A

Excitability, tremors, gingivitis

105
Q

Absorption and transport of inorganic salts of mercury

A

Some GI, some skin. Transported by RBCs and plasma. Generally does not cross BBB

106
Q

In what organs do inorganic salts of mercury end up?

A

Kidney, liver

107
Q

Acrodynia

A

An idiosyncratic reaction to chronic mercury - erythema, photophobia, diaphoresis, anorexia, tachycardia, irritability, milarial rash

108
Q

Absorption and transport of organic mercurials

A

Oral, skin, inhalation. Transported by RBCs, does cross BBB

109
Q

Organs in which organic mercurials tend to end up

A

Liver, kidney, brain, hair, and epidermis

110
Q

What type of mercury is subject to enterohepatic recirculation?

A

Organic mercurials

111
Q

Most toxic form of organic mercurials and their effects?

A

Alkyl mercurials (used as fungicides) - paresthesia, ataxia, neurasthenia, vision and hearin loss, tremor, spasticity, coma, death

112
Q

Treatment for mercury exposure

A

Chelation with BAL, D-penicillamine (do not use BAL with organic mercury)

113
Q

In what case of mercury exposure should chelation not be used?

A

Organic mercurials (may redistribute the mercury). In these cases use N-acetylcysteine or cysteine followed by succimer

114
Q

Absorption of Thallium

A

Oral, inhalation, derm

115
Q

Where is most of the absorbed thallium in the body found?

A

The kidneys

116
Q

What is the mechanism of action of thallium?

A

Mimics potassium ions, uncouples Ox Phos, affects protein synthesis, and interferes with several enzymes

117
Q

Effects of acute thallium poisoning

A

Gastroenteritis, convulsions, confusion, collapse, neuropathy

118
Q

Effects of chronic thallium poisoning

A

Non-descript ill health, paresthesias, neuropathies, loss of hair, Mee’s lines

119
Q

Chronic poisoning with what metal is often misdiagnosed sa Guillain-Barre syndrome?

A

Thallium

120
Q

Treatment for thallium poisoning

A

Gastric lavage, emesis, Prussian blue. Chelation is ineffective and may redistribute Thallium

121
Q

What proportion of poisonings and fatalities involve children under age 6?

A

Half of poisonings, 3% of fatalities

122
Q

What is implied about a drug by a large or small Vd?

A

Large Vd - Lipophilic, Small Vd - Lipophobic

123
Q

What general effect do most toxins result in?

A

CNS depression leading to obtundation or coma

124
Q

How do patients who die from poisoning typically die?

A

From airway obstruction by flaccid tongue, aspiration of gastric contents, or respiratory arrest

125
Q

Examples of cardiotoxic drugs

A

Ephedrine, amphetamines, cocaine, tricyclics, digitalis

126
Q

Some drugs that cause cellular hypoxia

A

Cyanide, hydrogen sulfide, carbon monoxide

127
Q

Some drugs that cause seizures

A

Tricyclics, isoniazid (INH), diphenhydramine, antipsychotics, cocaine, amphetamines

128
Q

What does the coma cocktail do?

A

Reverse depressed mental status and respiratory rate

129
Q

What is in the present day coma cocktail?

A

Oxygen, dextrose, naloxone (narcan), and thiamine

130
Q

Why is dextrose part of the coma cocktail?

A

In case the patient is hypoglycemic (a common cause of altered mental status)

131
Q

What does naloxone (narcan) do?

A

It is an opioid antagonist that reverses respiratory and CNS depression due to opioids

132
Q

What is the relationship between naloxone half life and half life of many opioids?

A

Naloxone has a much shorter half life (may require more naloxone)

133
Q

What might naloxone administration result in and what is the result of this?

A

Catecholamine surge, can lead to cardiac sensitization and dysrhytmias

134
Q

Why is thiamine part of the coma cocktail?

A

In case the patient is malnourished or alcoholic (Wernicke’s, Korsakoff’s)

135
Q

Signs and symptoms of Wernicke’s

A

Depressed mental status, ataxia, nystagmus, opthalmoplegia

136
Q

Signs and symptoms of Korsakoff’s

A

Short-term memory loss, confabulation

137
Q

What are the only lab tests required for most poisoned patients?

A

Acetaminophen level, ECG and SMA7

138
Q

What does the ECG pickup in the case of poisoned patients?

A

Evidence of Na channel blockade from medications like tricyclics, atypical antipsychotics and Type I antidysrhytmics

139
Q

What does the SMA7 lab test identify in the poisoned patient?

A

Xenobiotics that cause anion gap metabolic acidosis

140
Q

Give the calculation for anion gap

A

(Na + K) - (HCO3 + Cl)

141
Q

What is the normal anion gap?

A

12-16 meq/L

142
Q

Three poisons that are suggested by a negative anion gap

A

Bromism, Lithium, paraproteins

143
Q

Common causes of anion gap metabolic acidosis

A

Methanol, uremia, DKA, paraldehyde, iron, isoniazid, lactic acidosis, ethylene glycol, salicylates

144
Q

Give the calculation for osmolar gap

A

Measured serum osmolality (blood test) - calculated osmolarity

145
Q

Give the calculation for calculated osmolarity

A

2 x Na + Glucose/18 + BUN/2.8 + ETOH/4.6

146
Q

What are the normal measured osmolality and osmolar gap?

A

Osmolality: 280-290 mosm/L and mosmolar gap: 0-15 mosm/L

147
Q

What substances cause an elevated osmolar gap?

A

Ethanol, ethylene glycol, methanol, isopropanol

148
Q

What is the single most useless test the physician can order on a poisoned patient?

A

Urine drug screen

149
Q

The two primary mechanisms for removing toxins

A

Orogastric lavage and activated charcoal

150
Q

Orogastric lavage should be considered in patients who present within one hour and ingested one of these substances

A

calcium channel blockers, beta blockers, tricyclics, antineoplastic agents, colchicine, paraquat/diquat, pdophyllin

151
Q

What seriously toxic substances are not absorbed by activated charcoal?

A

Cyanide salts, potassium supplements, metals, and alcohols

152
Q

What proportion of gastric contents can orogastric lavage remove?

A

40% at most

153
Q

What is a risk of administering activated charcoal by NG tube?

A

Aspiration

Pharmacology (16 decks)

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