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x M2T4 Pharm (GI, CT/MSK) > GI: Toxicology > Flashcards

GI: Toxicology Flashcards

1
Q

FYI. On the exam, there will be 3 Qs on this material, concerning cases of poisoning by the agents on the flip side of this card. Did not make FCs on benzene/toluene, organophosphates that are not on this list)

A

Carbon monoxide

Organophosphate (carbamyl/malathion/parathion)

Iron

Lead

Arsenic

Acetaminophen

Aspirin

Benzodiazepines

Methanol, ethylene glycol

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2
Q

What is the range of the LD50 for various chemicals?

A

Bottom line is that the LD50 for chemicals covers a very wide range (9 orders of mag). Extreme ends of the lethal range: botulinum toxin is lethal at 0.00001 mg/kg, ethyl alcohol is not lethal until 10,000 mg/kg.

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3
Q

what is a chelator for lead with EDTA, arsenic, and mercury?

A

dimercaprol

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4
Q

what is a chelator for lead?

A

EDTA calcium or disodium

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5
Q

what is a chelator for acute arsenic, mercury or lead?

A

unithiol

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6
Q

what is a chelator for lead (kids & adults), mercury and arsenic?

A

succimer

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7
Q

what is a chelator for iron?

A

deferoxamine and deferasirox

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8
Q

what is a chelator for copper, adjunct for arsenic, gold, lead?

A

penicillamine

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9
Q

what is an antidote to acetaminophen?

A

N-acetylcysteine (NAC) give activated charcoal if within 1-2 h of ingestion

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10
Q

what is an antidote to gastric absorption?

A

activated charcoal

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11
Q

what is an antidote to benzodiazapines?

A

flumazenil

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12
Q

what is an antidote to methanol and ethylene glycol?

A

fomepizole

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13
Q

very big picture: the 10 drugs for this lecture are members of what two classes?

A

chelators and antidotes

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14
Q

define bioaccumulation

A

increasing concentration of a substance in the env’t, leading to accumulation in biol tissues. ex: a fish eats lots of little fish that all have a tiny bit of mercury in them, and the big fish ends up with a LOT of mercury in its tissues since it never goes away

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15
Q

define biomagnification

A

the fold increase in concentration of a substance in the food chain, resulting from bioaccumulation

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16
Q

define an endocrine disruptor

A

chemical in the env’t with endocrine effects: possible infertility, repro cancer, birth defects.

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17
Q

define environmental toxicology

A

environmental exposure to chemicals, regulated by the EPA

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18
Q

define acceptable daily intake (ADI)

A

daily intake of chemical, which over lifetime appears to carry no risk

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19
Q

define occupational toxicology

A

exposure of workers to chemicals at workplace: regulated by OSHA

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20
Q

define threshold limit value (TLV)

A

used for occupational control. exposure limit to an agent for a defined period of time. (shorter time = higher level allowed)

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21
Q

Carbon monoxide: what it is? what does it do in the body?

A
  • odorless, colorless gas
  • competes with O2 for hemoglobin (has a 200x greater affinity). affinity for fetal Hg even higher
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22
Q

Carbon monoxide: treatment? how do we detect it in the body?

A

tx: 100% O2, hyperbaric O2
- cannot use regular pulse ox, use a CO-oximeter to determine carboxyhemoglobin (COHb) levels

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23
Q

Sx of CO poisoning with 10% COHb, 40-50% COHb, 60-70% COHb?

A

10%: headache, dizziness

40-50%: nausea, convulsions, tachy

60-70%+: resp arrest, death

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24
Q

what are some cholinesterase inhibitors?

A

(pesticides)

Carbamates - carbaryl

Organophosphates - malathion, parathion

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25
Q

Cholinesterase inhibitors: what effect do they have in the body?

A
  • Muscarinic and nicotinic activators
  • SLUDGE (meaning of this is on a separate card)
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26
Q

Cholinesterase inhibitors: treatment?

A
  • atropine to block receptor activation
  • pralidoxime to regenerate cholinesterase
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27
Q

what does SLUDGE stand for? what is it associated with?

A
  • Salivation, lacrimation, urination, defecation, GI upset, emesis
  • symptoms of muscarinic and nicotinic receptor activation, possibly by a pesticide
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28
Q

what is Agent Orange?

A

Herbicide used in Vietnam War. associated with chronic disease

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29
Q

Common sources of CO?

A
  • car exhaust
  • spills from appliances
  • building fires
  • forklifts, snowblowers
  • generators, heaters (boiler room malfunction!)
  • zambonis (ice rinks)
  • CO is the main indoor pollutant causing headaches
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30
Q

what is a baseline level for blood COHb in a non-smoker? what is the half life for CO?

A

baseline = 1-3%

half life = 5 h

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31
Q

What are some general clues that a person may have CO poisoning?

A
  • more than one person affected
  • pets affected
  • relation of sx to use of combustion appliances
  • exposure to tobacco smoke, volatile organics
32
Q

acute lead poisoning: cause? sx?

A

acute poisoning is rare: occurs when kids eat paint chips.

abdominal colic, CNS changes.

33
Q

chronic lead poisoning: cause? sx? sx particularly seen in children?

A
  • environmental toxin, seen in low SES pts with older housing
  • peripheral neuropathy (wrist drop), anorexia, anemia, tremior, GI. may see lead line on gums
  • kids: growth delay, neuro deficits, dev delay
34
Q

chronic lead poisoning: appearance on blood smear?

A

basophilic stippling of RBCs

35
Q

lead poisoning: preferred chelator for kids?

A

oral succimer

36
Q

acute arsenic poisoning: symptoms?

A

severe GI discomfort, rice water stools, vomiting, capillary damage with dehyd and shock (sim to cholera, typhoid)

37
Q

chronic arsenic poisoning: symptoms?

A

skin changes, hair loss, bone marrow depression, anemia, nausea, GI disturbance

38
Q

what are Mee’s lines? what do they indicate?

A

transverse white lines running across the nail, shape of the nail moon.

arsenic poisoning

39
Q

arsenic: source of chronic poisoning?

A

environmental: ground water, soil

40
Q

acute mercury poisoning: sx?

A

chest pain, SOB, n/v, kidney damage, gastroenteritis, CNS damage

41
Q

chronic mercury poisoning: sx?

A

sore gums/teeth, GI disturbance, neuro and beh changes.

remember the ‘mad hatters’ in 18th c who had mercury pois from processing felt

42
Q

mercury poisoning: tx?

A

chelation with succimer or dimercaprol (IM)

43
Q

acute mercury poisoning: sources?

A

from inorganic mercury: salts and metallic.

occupational, dental labs, wood preservatives, insecticides, batteries.

44
Q

organic mercury is used as what? more or less toxic than inorganic (salt/metallic mercury)?

A
  • anti-fungal. will bioaccumulate
  • MORE toxic than inorganic mercury
  • highly toxic to fetuses
45
Q

iron poisoning: source?

A

too many iron supplement pills, prenatal vits

accidental OD by child

46
Q

iron overdose: sx?

A

vomiting, GI bleed, lethargy, grey cyanosis. may progress to GI necrosis, pneumonitis, jaundice, seiz, coma

47
Q

iron OD: what is the chelating agent of choice?

A

deFERoxamine.

48
Q

Iron OD: tx with gastric lavage with charcoal?

A

charcoal does not bind iron. if within 60 min, use gastric lavage. if longer than 60 min, use whole bowel irrigation

49
Q

chelators: what is their overall mechanism?

A

form a cage around a metal ion, sequestering it and preventing binding to cells. promotes excretion. cannot reverse damage, only prevent further damage.

50
Q

Bidentate v polydentate: what’s the difference?

A

refers to the # of electronegative groups a chelator has available to complex with cationic metal ions

51
Q

of the chelators, which are bidentate? polydentate?

A

Bidentate are Succimer, Penicillamine, Unithiol, Dimercaprol (SPUD)

Polydentate are EDTA and deferoxamine

52
Q

regardless of suspected poison, what is initial treatment for a poisoned patient?

A

ABCD: airway, breathing, circ, DEXTROSE if altered mental status

53
Q

Organophosphate poisoning (cholinesterase inh): eye findings? skin findings? abdominal findings? (not in SLUDGE)

A

miosis (constricted pupil)

excessive sweating

hyperactive bowel

54
Q

what type of decontamination is currently favored? (emesis, lavage, charcoal, laxatives)?

A
  • emesis and lavage used less now: emesis increases exposure to toxin
  • charcoal currently favored. large surface area, absorbs toxin.
  • laxatives may help toxin exit body quickly. no hard evidence. whole bowel irrigation may help after ingestion of iron tablets, (+ other things)
55
Q

what will charcoal NOT bind?

A

iron, lithium, potassium binds alcohols and cyanide poorly

56
Q

how does N-acetylcysteine work as an antidote? antidote for what? when to give? what labs to follow?

A
  • acetaminophen.
  • acts as a glutathione substitute, binds hepatotoxic metabolite as it is made. also replenishes glutathione reserve, preventing formation of metabolite
  • give within 8-10 h (as soon as possible)
  • follow LFTs and serum drug levels
57
Q

aspirin toxicity: what will be the course? what is treatment & how does it work? treatment for severe cases?

A
  • resp alkalosis followed by metabolic acidosis
  • IV sodium bicarb alkalizes urine and promotes salicylate excretion
  • severe: hemodialysis
58
Q

cholinesterase inhibitors: tx? mechanism?

A

Atropine: competes for muscarinic receptors

Pralidoxime (2-PAM) can regenerate cholinesterase activity

59
Q

treatment for benzodiazepine OD? mechanism?

A
  • flumazenil
  • blocks site of benzo action.
60
Q

treatment for methanol/ethylene glycol toxicity? mechanism?

A
  • fomepizole
  • competes for alcohol dehydrogenase, thus reduces production of toxic metabolites
61
Q

methanol poisoning causes what sx (eyes)?

A

severe vision disturbances

62
Q

acetominophen OD: how does it cause liver necrosis?

A

normal metabolism is saturated, so acetaminophen is metabolized in liver to a toxic metabolite. the metabolite binds to proteins and the lipid bilayer of hepatocytes; yields hepatic injury and centrilobular liver necrosis.

63
Q

what is one of the most common pharmaceuticals seen in both intentional and accidental poisoning?

A

acetaminophen

64
Q

urinary pH manipulation: urinary alkalinazation is useful in what kind of OD?

A

salicylate (aspirin)

65
Q

salicylates: what do they cause, metabolically?

A

uncoupling of oxidative phosphorylation.

results in incr O2 consumption, incr CO production, incr glycolysis, incr lipolysis. –>resp alkalosis and met acidosis –>incr anion gap due to accumulated lactate

66
Q

clinical picture of salicylate OD?

A
  • hyperpnea (deep, quick breaths)
  • hyperthermia
  • GI hemorrhage
  • N/V
  • ototoxicity
67
Q

tx for aspirin/salicylate OD?

A
  • gastric lavage up to 60 min
  • activated charcoal after 60 min -bicarb to alkalinize urine, incr salicylate excr, correct acidosis
  • hemodialysis to remove salicylate, restore fluids
68
Q

aspirin/salicylate OD - when might you consider whole bowel irrigation?

A

if large mass of enteric coated pills were ingested

69
Q

5yo in ER in December. Confused, headaches, lethargy, joint aches, nausea. HR 120, HP 130/85, RR 25. Mom also has headache. Moved to old building 6 mo ago. What is the likely toxin? what test should we do?

A
  • CO
  • test carboxyhemoglobin level
  • older apt suggests lead
  • shared symptoms of both mother and daughter suggests CO
70
Q

crop duster in ER with weakness, sweating, wheezing, abd cramps, diarrhea, miosis, bradycardia, muscle twitches. what is he poisoned with? how do we treat his weakness, labored breathing?

A
  • malathion (organophosphate)
  • SLUDGE sx

-treat with atropine (block receptor binding), pralidoxime (reactivate AChE)

71
Q

3yo in ER, vomiting (some blood), abdominal pain. non bloody diarrhea, listless. HR 170, RR 28, BP 98/58. Dry mucous membranes. low serum bicarb. what is toxin?

A

Iron, from mom’s prenatal vitamins. for a small child, only 4 pills could be toxic

72
Q

Iron OD 3 hrs ago, has been vomiting: best treatment is whole bowel lavage, gastric lavage, activated charcoal, or ipecac?

A

whole bowel irrigation with polyethylene glycol solution too late for lavage, charcoal doesn’t bind iron well, more vomiting will not help

73
Q

chelating agent for iron overdose?

A

deferoxamine - chelates iron, but poorly binds other trace metals

74
Q

42 yo, ingested 30 pain pills yesterday. (taken to ER and was treated). Today she re-presents with RUQ pain, elevated AST and ALT. what is best antidote?

A

-NAC. acetaminophen OD: accumulation of a metabolite. NAC replenishes glutathione reserves, preventing this

75
Q

74 yo women with confusion, fever, hearing loss over past 2 days. takes OTC aspirin for her osteoarthritis. best treatment?

A

activated charcoal, IV fluids, urine alkalization. ingestion was chronic so gastric lavage will not help a lot. activated charcoal is especially indicated for enteric-coated drugs. raising the pH of urine can incr aspirin excretion by 10x

x M2T4 Pharm (GI, CT/MSK) (6 decks)

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