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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
Cholinesterase inhibitors: what effect do they have in the body?
- Muscarinic and nicotinic activators - SLUDGE (meaning of this is on a separate card)
26
Cholinesterase inhibitors: treatment?
- atropine to block receptor activation - pralidoxime to regenerate cholinesterase
27
what does SLUDGE stand for? what is it associated with?
- Salivation, lacrimation, urination, defecation, GI upset, emesis - symptoms of muscarinic and nicotinic receptor activation, possibly by a pesticide
28
what is Agent Orange?
Herbicide used in Vietnam War. associated with chronic disease
29
Common sources of CO?
- 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
30
what is a baseline level for blood COHb in a non-smoker? what is the half life for CO?
baseline = 1-3% half life = 5 h
31
What are some general clues that a person may have CO poisoning?
- more than one person affected - pets affected - relation of sx to use of combustion appliances - exposure to tobacco smoke, volatile organics
32
acute lead poisoning: cause? sx?
acute poisoning is rare: occurs when kids eat paint chips. abdominal colic, CNS changes.
33
chronic lead poisoning: cause? sx? sx particularly seen in children?
- 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
chronic lead poisoning: appearance on blood smear?
basophilic stippling of RBCs
35
lead poisoning: preferred chelator for kids?
oral succimer
36
acute arsenic poisoning: symptoms?
severe GI discomfort, rice water stools, vomiting, capillary damage with dehyd and shock (sim to cholera, typhoid)
37
chronic arsenic poisoning: symptoms?
skin changes, hair loss, bone marrow depression, anemia, nausea, GI disturbance
38
what are Mee's lines? what do they indicate?
transverse white lines running across the nail, shape of the nail moon. arsenic poisoning
39
arsenic: source of chronic poisoning?
environmental: ground water, soil
40
acute mercury poisoning: sx?
chest pain, SOB, n/v, kidney damage, gastroenteritis, CNS damage
41
chronic mercury poisoning: sx?
sore gums/teeth, GI disturbance, neuro and beh changes. remember the 'mad hatters' in 18th c who had mercury pois from processing felt
42
mercury poisoning: tx?
chelation with succimer or dimercaprol (IM)
43
acute mercury poisoning: sources?
from inorganic mercury: salts and metallic. occupational, dental labs, wood preservatives, insecticides, batteries.
44
organic mercury is used as what? more or less toxic than inorganic (salt/metallic mercury)?
- anti-fungal. will bioaccumulate - MORE toxic than inorganic mercury - highly toxic to fetuses
45
iron poisoning: source?
too many iron supplement pills, prenatal vits accidental OD by child
46
iron overdose: sx?
vomiting, GI bleed, lethargy, grey cyanosis. may progress to GI necrosis, pneumonitis, jaundice, seiz, coma
47
iron OD: what is the chelating agent of choice?
deFERoxamine.
48
Iron OD: tx with gastric lavage with charcoal?
charcoal does not bind iron. if within 60 min, use gastric lavage. if longer than 60 min, use whole bowel irrigation
49
chelators: what is their overall mechanism?
form a cage around a metal ion, sequestering it and preventing binding to cells. promotes excretion. cannot reverse damage, only prevent further damage.
50
Bidentate v polydentate: what's the difference?
refers to the # of electronegative groups a chelator has available to complex with cationic metal ions
51
of the chelators, which are bidentate? polydentate?
Bidentate are Succimer, Penicillamine, Unithiol, Dimercaprol (SPUD) Polydentate are EDTA and deferoxamine
52
regardless of suspected poison, what is initial treatment for a poisoned patient?
ABCD: airway, breathing, circ, DEXTROSE if altered mental status
53
Organophosphate poisoning (cholinesterase inh): eye findings? skin findings? abdominal findings? (not in SLUDGE)
miosis (constricted pupil) excessive sweating hyperactive bowel
54
what type of decontamination is currently favored? (emesis, lavage, charcoal, laxatives)?
- 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
what will charcoal NOT bind?
iron, lithium, potassium binds alcohols and cyanide poorly
56
how does N-acetylcysteine work as an antidote? antidote for what? when to give? what labs to follow?
- 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
aspirin toxicity: what will be the course? what is treatment & how does it work? treatment for severe cases?
- resp alkalosis followed by metabolic acidosis - IV sodium bicarb alkalizes urine and promotes salicylate excretion - severe: hemodialysis
58
cholinesterase inhibitors: tx? mechanism?
Atropine: competes for muscarinic receptors Pralidoxime (2-PAM) can regenerate cholinesterase activity
59
treatment for benzodiazepine OD? mechanism?
- flumazenil - blocks site of benzo action.
60
treatment for methanol/ethylene glycol toxicity? mechanism?
- fomepizole - competes for alcohol dehydrogenase, thus reduces production of toxic metabolites
61
methanol poisoning causes what sx (eyes)?
severe vision disturbances
62
acetominophen OD: how does it cause liver necrosis?
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
what is one of the most common pharmaceuticals seen in both intentional and accidental poisoning?
acetaminophen
64
urinary pH manipulation: urinary alkalinazation is useful in what kind of OD?
salicylate (aspirin)
65
salicylates: what do they cause, metabolically?
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
clinical picture of salicylate OD?
- hyperpnea (deep, quick breaths) - hyperthermia - GI hemorrhage - N/V - ototoxicity
67
tx for aspirin/salicylate OD?
- 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
aspirin/salicylate OD - when might you consider whole bowel irrigation?
if large mass of enteric coated pills were ingested
69
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?
- CO - test carboxyhemoglobin level - older apt suggests lead - shared symptoms of both mother and daughter suggests CO
70
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?
- malathion (organophosphate) - SLUDGE sx -treat with atropine (block receptor binding), pralidoxime (reactivate AChE)
71
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?
Iron, from mom's prenatal vitamins. for a small child, only 4 pills could be toxic
72
Iron OD 3 hrs ago, has been vomiting: best treatment is whole bowel lavage, gastric lavage, activated charcoal, or ipecac?
whole bowel irrigation with polyethylene glycol solution too late for lavage, charcoal doesn't bind iron well, more vomiting will not help
73
chelating agent for iron overdose?
deferoxamine - chelates iron, but poorly binds other trace metals
74
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?
-NAC. acetaminophen OD: accumulation of a metabolite. NAC replenishes glutathione reserves, preventing this
75
74 yo women with confusion, fever, hearing loss over past 2 days. takes OTC aspirin for her osteoarthritis. best treatment?
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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