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MWU Pharmacology II > Lecture 15 / 16: Toxicology > Flashcards

Lecture 15 / 16: Toxicology Flashcards

1
Q

What are the 5 main classes of Toxins?

A
  1. Insectisides
  2. Alcohols
  3. Metals
  4. Gases
  5. Dust and Others
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2
Q

Name an insectiside

A

Oganophosphate insecticide/nerve agents

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3
Q

Name some toxic alcohols

A

Methanol
Ethylene glycol

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4
Q

Toxic Metals

A

Lead
Arsenic
Methylmercury

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5
Q

Toxic Gases

A

Carbon Monoxide
Cyanide

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6
Q

Toxic Dust and Others

A

PCBs and Dioxin

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7
Q

Name 4 non-specific antidotes

A
  1. Activated Charcoal
  2. Liqui-Char
  3. Polyethylene glycol - PEG350
  4. GlycoLax, Miralax
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8
Q

Name 3 specific antidotes

A

Fomepizole
Hydroxocobalamin
Pralidoxime

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9
Q

Name 2 Metal Chelators

A

EDTA, Succimer

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10
Q

Define LD50. What does it measure?

A

lethal dose 50” dosage of a chemical that is needed to produce death in 50% of treated animals

Measure of acute toxicity, carcinogenic and teratogenic effects not accounted for

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11
Q

LC50

A

lethal concentration 50” same as LD50 but applies to exposure to gasses (inhalation or dermal
exposure).

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12
Q

NOAEL

A

“No Observed Adverse Effect Level” highest dose that does not produce a statistically significant toxic effect, subchronic (90 days) animals studies

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13
Q

RfD

A

Reference dose” - estimate of the daily exposure to an agent that is assumed to have no adverse health impact on the human population.

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14
Q

Name 5 Common Toxic Syndromes

A
  1. Anticholinergic Syndromes (atropine)
  2. Sympathomimetic Syndromes (Cocaine)
  3. Opiates (Heroin)
  4. Non-Opiates (alcohol)
  5. Cholinergic Syndromes (Insectisides)
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15
Q

Name some signs of Anticholinergic Syndromes (6)

A

Troubled Little Delinquents Enjoy Using Atropine
* Tachycardia
* Little change in BP
* Dry flushed hot skin
* Elevated temp.
* urinary retention
* agitated delirium

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16
Q

Common causes of anticholinergic syndrome (6)

A
  • atropine
  • scopolamine
  • antihistamines
  • anti-Parkinsons
  • anti-psychotics
  • plants
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17
Q

Treatment for anticholinergic syndrome

A

Physostigmine

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18
Q

Signs of Sympathomimetic Syndromes

A

Methamphetamines Probably Dont Help Students Take Diagnostic Tests

  1. Mydriasis
  2. Paranoia
  3. Diaphoresis
  4. Hypertension
  5. Seizures
  6. Tachycardia
  7. Delirium
  8. Temperature - elevated
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19
Q

Common Causes of Sympathomimetic Syndrome

A
  1. Cocaine
  2. Amphetamine
  3. OTC decongestants (ephedrine)
  4. Caffeine
  5. Theophylline
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20
Q

Sympathomimetic Syndrome Treatments

A
  1. Benzodiazepines for seizures
  2. Lidocaine for tachycardia and Ventricular Fibrillation
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21
Q

Signs and symptoms of opiate poisoning (7)

A

Hypotension, bradycardia, coma, respiratory depression, miosis, hyporeflexia, CNS depression

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22
Q

Common causes of opiate poisoning

A

Narcotics

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23
Q

Treatment of opiate poisoning

A

Symptomatic treatment and specific

antidotes as appropriate (naloxone; Narcan)

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24
Q

Common causes of non-opiate related poisoning

A

Barbiturates, benzodiazepines,
other sedatives, ethanol

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25
Q

Signs of non-opiate related poisoning

A

Hypotension, bradycardia, coma, respiratory depression, miosis, hyporeflexia, CNS depression

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26
Q

Treatment of non-opiate poisoning

A

Symptomatic treatment

specific antidotes as appropriate (flumazenil - benzo antagonist), IV saline

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27
Q

Identify signs of Cholinergic syndromes

A

Concert Conductors Make Music (1st 4)
1. Confusion
2. CNS depression
3. Muscle Twitching-weakness / paralysis
4. Miosis
5. Salivation
6. Lacrimation
7. Urination
8. Defecation
SLUD (last 4)

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28
Q

Common causes of cholinergic syndromes (5)

A

Organophosphate, carbamate insecticides, physostigmine, edrophonium, mushrooms

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29
Q

What are some treatments for Cholinergic syndrome?

A

atropine
Pralidoxime (2-PAM) for organophosphates only

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30
Q

Principles of Non-Specific Treatment: How do you determine nature of the poison?

A

toxic syndrome, history,
lab tests, poison control center

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31
Q

Activated Charcoal

A

Non-specific Treatment

non-specific chelator, limits drug absorption, not as efficacious if drug is rapidly absorbed

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32
Q

Gastric Lavage

A

Non-specific Treatment

recent ingestion of caustic liquids: not as useful for removal of pills or pill fragments

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33
Q

Syrup of Ipecac

A

Used only in rare occasions
Exposure < 30 min, ingestion of massive drug dose (100-150 aspirin tablets)

34
Q

Whole bowel irrigation - when to use

A

Non specific treatment
Non-absorbable polyethylene glycol (PEG-350)

Used with large ingestion of drugs poorly absorbed by activated charcoal (Fe, Li)

35
Q

Name some organophosphates and some key facts.

what do they inhibit / reversible / irreversible

A

methyl parathion, VX nerve agent and
carbamates

Acetylcholine Esterase Inhibitors

irreversible—organophosphates (2-PAM can “reverse”)

reversible—-carbamates

36
Q

Organophosphate Signs and Symptoms

A

headache, nausea, dizziness
cholinergic complaints —-SLUD

37
Q

Organophosphate Mechanism

A

extremely toxic—respiratory failure due to diaphragm muscle paralysis, central depression of respiratory centers in CNS and bronchoconstriction

38
Q

Organophosphate Treatment

A

Treatment: ◼ atropine for both carbamates and organophosphates
◼ Pralidoxime (2-PAM) for organophospate

39
Q

VX nerve agent

A

Cholinergic

Colorless, odorless fast-acting chemical weapon

40
Q

Sources of Methanol Poisoning

A

◼ windshield washer solvent for cars
◼ mixed solvents (paint removers)
◼ hand sanitizer during COVID pandemic

41
Q

Methanol poisoning signs and symptoms

A

CNS depression like ethanol

42
Q

Methanol Metabolic Mechanism of toxicity

A

metabolized to formaldehyde by alcohol dehydrogenase and formate by (aldehyde dehdydrogenase) – blindness, metabolic acidosis

43
Q

Methanol Treatment

A

◼Metabolic acidosis with Na bicarbonate IV
◼Folic acid B vit. complex, converts formate to CO2 and H2O

ADH inhibitors
◼Fomepizole (Antizol®)
◼Ethanol

44
Q

Sources of ethylene glycol poisoning

A

found in auto antifreeze (95%)–other industrial solvents

45
Q

Ethylene glycol signs and symptoms

A

◼ CNS depression like ethanol
◼ metabolized —eventually to oxalic acid
◼** hypocalcemic tetany and oxalicaciduria –crystals **

46
Q

Ethylene Glycol Treatment

A

◼Hypocalcemia treat with Ca2+ IV

◼Pyridoxine, folate, thiamine – cofactors for eth. glyc. metabolism

ADH inhibitors
◼ Fomepizole (Antizol ®)
◼ Ethanol

47
Q

Sources of Lead Poisoning

A

consuming contaminated food prepared with lead cooking utensils, lead-soldered food cans

ingestion of lead paint chips and inhalation of lead dust are major lead sources.

10-20% of exposure due to contaminated drinking water (lead pipes)

Toys made in other countries have lead contaminated paint

Lead in gasoline

Occupational exposure

48
Q

Signs and Symptoms of Lead poisoning: Blood / PNS / CNS

A

Blood - hypochromic microcytic anemia
PNS - weak wrist and ankle extensor muscles
CNS - lead encephalopathy w/ delirium, hallucinations and convulsions - can be fatal

49
Q

Signs and Symptoms of Lead poisoning: GI / Kidney / Reproductive

A

GI- more common in long term exposures; colic loss of appetite
Kidney - increased uric acid (gout)
Reproductive - stillbirths in women; altered sperm

50
Q

Lead poisoning mechanism. What does it inhibit?

A

Unknown, possible molecular mimicry occurs and Pb replaces Ca, Zn, Mg normally found in enzymes, proteins, bone mineral, etc…

Inhibits hemoglobin synthesis - resulting in a build up of hemoglobin precursors in red blood cells

51
Q

Lead poisoning treatment

1st line drug, 2nd, cerebral edema

A

Find lead source and remove patient
For severe cases (≥ 45 µg/dl in children, ≥ 50 µg/dl in adults), metal chelators are given (succimer is first line drug)

EDTA is second line drug

Dexamethasome is given for cerebral edema

52
Q

Lead: Children v. Adults

absorption, blood brain barrier, IQ

A
  • Children absorb 40% of ingested lead, adults 10%
  • Pb deteriorates blood brain barrier, more so in children who may not have fully formed BBB
  • Childhood Pb exposure is associated with lower IQ, ADHD, aggressive behavior and juvenile delinquency
53
Q

Arsenic: Which forms are the most toxic and least toxic

A

several forms exist with varying degree of toxicity

elemental forms are the most toxic (e.g. trivalent or pentavalent).

Organic arsenicals are considered least toxic and occur naturally in seafood.

54
Q

Sources of Arsenic Poisoning

A

◼ contaminant of coal, metal ores, rural/municipal water
supplies in US but especially in Bangladesh
◼ industrial workers in semiconductor industry at risk

55
Q

Signs and Symptoms of Acute Arsenic Poisoning:
GI
Odor
Vessels
What happens if patient survives

A

◼ violent nausea, laryngitis, bronchitis, hemorrhagic gastroenteritis (rice water diarrhea)
◼ garlic odor on breath
◼ capillary damage–dehydration, shock, death
◼ if patient survives– sensory neuropathy follows

56
Q

Chronic Arsenic Intoxication: Signs and Symptoms

dermal, cutaneous, bone marrow, liver, cancer

A

Chronic intoxication:—more common and insidious

◼ can be few symptoms until irreversible injury
◼ dermal manifestations —hyperkeratosis, exfoliative dermatitis, vesicular lesions on feet, peripheral neuropathy
◼ cutaneous vasodilation —”Milk and Roses” complexion
◼bone marrow depression, fatty liver degeneration—death
◼Increased risk of cancers

57
Q

Arsenic Mechanims - what group does it bind to?

A

High affinity for –SH groups on proteins

Likely causes severe oxidative stress and disrupt protein function by binding to –SH containing amino acids

58
Q

Arsenic Treatment

A

◼The metal chelator Dimercaprol (BAL) – British Antilewisite given IM

59
Q

Source of Arsine Gas

A

Only occurs in miners; gas formed when acid touches arsenic metal

60
Q

Signs and Symptoms of Arsine Gas
Low dose?

A

◼ produces rapid hemolysis and death
◼ low dose produces partially reversible kidney damage

61
Q

Arsine Gas Poisoning Treatment

A

◼ NO Antidote—-supportive therapy only

62
Q

Methylmercury toxicity

A

several forms of mercury exist with varying degrees of toxicity.

organic forms are more toxic, specifically methylmercury

Inorganic and elemental forms of mercury tend to be poorly absorbed.

Methylmercury is highly absorbed from GI tract and readily passes blood brain barrier

63
Q

Sources of mercury poisoning

A

◼ Hgo (metallic/elemental mercury) metal in dental labs, old thermometers, gold mining
◼ HgCl2, Hg2Cl2 (inorganic salts) used as preservatives, insecticides
◼ HgNO3 in making felt hats (Mad Hatter’s Disease 1800’s)
◼ Methlymercury –** consumption of contaminated fish and
grain fungicide**; ethylmercury – thimerosal an antibacterial
antifungal agent in multi-dose vaccine vials

64
Q

Organic Mercury Signs and Symptoms (6)

A

All irreversible:

  • Loss of balance
  • ataxia
  • sensory defects
  • loss of visual field
  • deafness
  • dysarthria
65
Q

Organic mercury mechanism

A

Unknown, shown to increase intracellular calcium and bind to metallothionein

66
Q

Mercury: Special Dietary Considerations

A

Consumption of predatory fish (swordfish, shark) should be limited to one serving per week

Women who are nursing or pregnant need to avoid eating predatory fish

Canned tuna is considered safe however the MeHg levels depend on many variables

67
Q

Metal-Chelators: Effect, when is it used, is it effective in chronic cases?

A

Chelators bind metals → excreted from body
Only used in patients with severely elevated metal levels or toxicity

Chronic metal accumulation occurs over a life time, can accumulate significant amounts of metal stored in bone and other tissue.

Chelation therapy only reduces readily accessible pool of metal

After therapy, blood metal levels can rebound

68
Q

Edetate Calcium (EDTA):
1. Type
2. Route and what for
3. Toxicity

A
  1. Metal Chelator
  2. Given IV or IM for severe lead poisoning
  3. Toxic to kidney at high dose
69
Q

EDTA Side-Effects

A

Chills, fever, nausea, vomiting, allergies

70
Q

Succimer:
1. Type
2. Effectiveness for lead
3. Side effects
4. Other possible metals

A
  1. First orally effective chelator
  2. More rapidly effective than EDTA for lead
  3. GI distress, rash, diarrhea, increase in serum transaminases
  4. Studies suggest it may also be useful for arsenic and mercury —Important chelator
71
Q

Carbon Monoxide: Physical characteristics and sources

A

Colorless, odorless, tasteless, nonirritating, ubiquitous

Sources: any burning or combustion process will generate CO

72
Q

CO poisoning signs and symptoms

A

organs with greatest O2 demand will show signs of exposure first

headache, dizziness and increased heart rate

73
Q

CO poisoning mechanism

A
  • out competes oxygen binding to hemoglobin, 220 greater affinity than oxygen
  • when bound to one of the four oxygen binding sites on hemoglobin forms carboxyhemoglobin
  • Carboxyhemoglobin reduces the ability of oxygen to dissociate from hemoglobin and be delivered to the deep tissues needing oxygen.
74
Q

CO poisoning treatment

A

remove from CO, then hyperbaric O2

75
Q

Chronic CO exposure

A

possible cardiovascular problems

76
Q

Cyanide Gas sources

A

present in smoke (burning of plastics, wool), industrial exposure (plastics and metal plating), chemical warfare agent

77
Q

Cyanide Gas Poisoning Signs and Symptoms

A

“bitter almond” breath, headache, nausea, tachypnea, apnea, loss of consciousness, seizures and coma

78
Q

Cyanide Gas Poisoning: Mechanism

A

binds to cytochrome oxidase resulting in inhibition of electron transport chain and the ability of the cell to utilize oxygen in producing ATP

79
Q

Cyanide treatment

A

2 ways to Treat:
* Cyanokit is first line with a 2- step method used as a backup
* Cyanide + Hydroxocobalamin (Cyanokit®) → cyanocobalamin
(vitamin B12)
* Older method 2 steps: can not be given with CO inhalation
1. Na nitrite → methemoglobin + cyanide → cyanomethemoglobin
2. cyanomethemoglobin + Na thiosulfate → thiocynate (urine)

80
Q

PCB’s and Dioxin: Sources

A

Flame retardants, plasticizers, insulating material in electric transformers

Recent finding that farm raised Salmon had higher PCB content than wild Salmon

Environmentally stable, still present even though use curtailed in 1970s

81
Q

PCB/s and Dioxin: Signs and Symptoms

A

dermal acne-like eruptions
called chloracne, nausea, headache, vomiting

82
Q

Treatment for Dioxin poisoning

A

None

MWU Pharmacology II (8 decks)

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