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Decontamination/Elimination/Antidotes Flashcards

1
Q

What is decontamination?

A

stop ongoing exposure
-no longer in direct contact with the patient
to prevent absorption and thereby minimize systemic toxicity
decrease the possibility of transfer of the toxic substance

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2
Q

What are the principles of GI decontamination?

A

if a patient is already symptomatic, it means absorption has occurred and decontamination is unlikely to be benefit
-its efficacy decreases with time
prioritize airway protection and provide symptomatic and supportive care
risk vs benefit of GI decontamination is largely dependent on severity of potential toxicity

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3
Q

What is activated charcoals absorptivity attributed to?

A

its highly porous structure

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4
Q

What happens when toxicant and activated charcoal form a complex?

A

not systemically absorbed; therefore toxicant removed with AC upon bowel movement

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5
Q

Describe AC preparation.

A

derived from various organic materials
-e.g. coconut shells or peat
activated by heating at 600-900 C, then washing with inorganic acids and drying
creates highly developed internal pore structure
-small particle size with large surface area make it very adsorptive
allows for the adsorption of drugs and toxins through weak intermolecular forces
AC becomes less effective with use and have to be recharged or replaced

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6
Q

What are examples of agents that adsorb to AC?

A

acetaminophen
amitriptyline
amphetamines
chlordiazepoxide
cimetidine
codeine
diazepam
digoxin
salicylates

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6
Q

What are examples of agents that do not adsorb to AC?

A

boric acid
cyanide
ethanol
ethylene glycol
iron
lithium
malathion
methanol
petroleum distillates

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7
Q

What is sometimes added to AC to increase palatability?

A

sorbitol (sugar alcohol)

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8
Q

What is the dose of AC if the amount of toxicant ingested is known?

A

10-40x the dose of toxicant

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9
Q

When is AC more likely to reduce poison absorption?

A

if it is administered within 1 hour of ingestion
insufficient data to support or exclude the use of AC when more than 1 hour has passed since ingestion

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10
Q

When do we start AC method?

A

within 1 hour of ingestion (if feasible) but consider:
-bezoars
-MR products
-toxicants or co-ingestants that reduce GI motility/gastric emptying rate
-effect of volume ingested on gastric emptying rate
the above have benefits well beyond 1 hour

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11
Q

What are factors that increase AC appropriateness?

A

serious toxicity anticipated, no antidote
recent ingestion
alert, cooperative, intact airway
favourable stoichiometry
MR product
known to adsorb
no ileus/intestinal obstruction
opioids (can be given 2-3 hours after ingestion)

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12
Q

What are contraindications to AC?

A

toxicant known not to adsorb
unprotected airway (unconscious or trauma)
ingestion of hydrocarbons - risk of aspiration
risk of GI perforation (has ulcer, surgery, caustic agent)
endoscopy will be required (ex. corrosive)

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13
Q

What are examples of caustic agents?

A

drain cleaners
detergents
strong acids or alkali

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14
Q

What are complications of AC?

A

emesis
constipation/diarrhea
pulmonary aspiration
black stool/tongue/mucous membranes
pts with pre-existing motility disorders might be at greater risk

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15
Q

When is orogastric lavage considered?

A

ingested a potentially life-threatening amount of a poison and the procedure can be undertaken within 60 minutes of ingestion

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16
Q

What are practical indications for orogastric lavage?

A

toxicant likely to be life-threatening
OR obvious signs and symptoms of life-threatening toxicity
AND reason to believe significant amount in stomach
AND AC not an option
AND no spontaneous emesis
OR no highly effective antidote or alternative therapies pose high risk

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17
Q

What is whole bowel irrigation?

A

introduction of large amounts of fluid into GIT to expel intraluminary contents
rationale: cleanses bowel with large amounts of PEG solution to minimize drug absorption and expel intraluminal contents out of GIT; does not cause net change in ions, therefore no electrolyte imbalances

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18
Q

What are situations where WBI is an option?

A

expediting GI luminal clearance of:
-SR preparations
-toxic heavy metals
-packets of illicit drugs smuggled within the body

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19
Q

What is the evidence for WBI?

A

reported effective:
-decrease lithium concentrations
-98% success in body packers
-not effective for rapidly absorbed drugs
-may reduce hospital time, if successful

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20
Q

What are contraindications to WBI?

A

unprotected or compromised airways
GI compromises/hemorrhage
hemodynamically unstable
persistent vomiting
suspected leakage from drug packets or bowel obstruction or perforation

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21
Q

What are complications of WBI?

A

nausea/vomiting
abdominal cramping/bloating
aspiration/acute respiratory distress syndrome
hypo/hypernatremia
interreference with AC

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22
Q

What are some “other” methods of decontamination?

A

surgical removal
misc adsorbents
-Kayexalate
-cholestyramine

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23
Q

What is elimination?

A

enhances the removal of a toxicant that has already been systemically absorbed
removal from blood, therefore related to distribution or redistribution from tissues

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24
When wont elimination methods have much effect?
if distribution is large Vd > 1 L/kg considered large because it indicates that only a small portion of the total dose is in the plasma
25
What are the two types of elimination methods?
intracorporeal (occurring inside the body) extracorporeal (occurring outside the body)
26
What is an example of an intracorporeal elimination method?
multiple dose activated charcoal
27
What are examples of extracorporeal elimination methods?
hemodialysis hemofiltration hemoperfusion
28
When does MDAC decrease absorption to tissues?
large amounts of xenobiotics are ingested, and dissolution is delayed (bezoars, SR, impaired GI motility) when reabsorption can be prevented by lowering the concentration of free toxic substance in the intestinal lumen
29
How does MDAC work?
repeated administration of oral AC to enhance elimination to enhance elimination of drugs already absorbed into the body by functioning as an adsorbent "sink" at several sites in the gut
30
What is the dose for MDAC?
optimum dose unknown dose and administration interval tailored to: -amount and dosage form of xenobiotic ingested; severity of overdose; whether the patient is vomiting; potential lethality of xenobiotic; and tolerability
31
Which drugs have enhanced elimination from MDAC?
carbamazepine dapsone phenobarbital quinine theophylline
32
What are contraindications to MDAC?
patients with unprotected airways if use is likely to increase risk and severity of aspiration when threat of GI perforation or hemorrhage is high when endoscopy is likely to be attempted intestinal obstruction when activated charcoal is known to not meaningfully adsorb the ingested toxin if decreased peristalsis is likely to occur from the substance ingested
33
What are complications of MDAC?
constipation bowel obstruction emesis/aspiration rectal ulcer/hemorrhage reduction of therapeutically used xenobiotic
34
What are indications for MDAC?
life-threatening amount of CBZ, dapsone, phenobarbital, quinine, or theophylline drugs with long t1/2, small Vd (<1L/kg), and those that undergo enterohepatic recirculation
35
Differentiate hemodialysis, hemofiltration, hemoperfusion, and hemodiafiltration.
hemodialysis: -uses diffusion through a concentration gradient hemofiltration: -uses convection through a pressure gradient -removes larger molecules hemoperfusion: -blood passes through adsorbent substance -even larger molecules -plasma removed, treated, and returned to body hemodiafiltration: -combines hemodialysis and hemofiltration
36
What are complications of hemodialysis?
hypotension osmolar imbalance hypoxemia bleeding (have to anticoagulate) rebound levels air embolism
37
What must be the route of elimination for a drug if urine alkalinization is used?
kidneys
38
What is the mechanism of action of urine alkalinization?
ion trapping -ionized drugs cannot cross lipid bilayer helps clear weak acids by trapping the xenobiotics in the tubular lumen and not allowing it to be passively reabsorbed into the bloodstream
39
Which drugs are used for alkalinization and acidification?
alkalinization: sodium bicarbonate acidification: ascorbic acid *done through IV*
40
What are contraindications to urine alkalinization?
established/incipient renal failure pre-existing heart failure (would be better suited for hemodialysis)
41
What are complications of urine alkalinization?
alkalemia hypokalemia hypernatremia fluid overload hypocalcemia alkalotic tetany and hyperexcitability of nerves and muscles
42
When is urine alkalinization considered 1st line?
patients with moderately severe salicylate poisoning who do not meet criteria for hemodialysis
43
What are antidotes?
neutralize or counteract the toxin prevents the development of, or reverses the signs and symptoms of toxicity specifically counteracts the poison beyond a more general decontamination/elimination strategy
44
Are there lots of antidotes available?
few antidotes available
45
What must be done after treatment with an antidote?
patient must be monitored until toxic effects abate in absence of antidote
46
What are the types of antidotes?
receptor antagonists -ex: atropine, vitamin K chemical/chelator -forms compound of lesser toxicity that is removed -ex: deferoxamine, digoxin-specific antibody fragments, idarucizumab dispositional -alters toxicants ADME -ex: ethanol, fomepizole unclassified -ex: intralipid
47
What is the use of atropine?
toxicity caused by acetyl-cholinesterase inhibitors -donepezil, rivastigmine pesticides -organophosphates, carbametes clitocybe or inocybe mushrooms sometimes for digitalis through indirect MOA
48
What is the MOA of atropine?
competitive antagonist of acetylcholine common binding site on muscarinic receptors but nicotinic receptors
49
What is the use of atropine in surgery?
reduce saliva and fluid in the respiratory tract during surgery
50
What is the reversal for atropine?
physostigmine
51
What are precautions against atropine?
tachyarrhythmias, CHF, CAD, hyperthyroid obstructive diseases of GIT
52
What is the use of deferoxamine?
used in iron/aluminum toxicity
53
What is the MOA of deferoxamine?
acts as a chelator and binds free Fe to form ferrioxamine, which is renally excreted (brown urine results)
54
What is severe iron toxicity?
serum levels > 90 umol/L clinical signs of significant toxicity
55
What should deferoxamine be accompanied with?
GI decontamination and supportive measures
56
What are complications of deferoxamine?
rapid IV admin can cause flushing, urticaria, hypotension, shock Fe-ferrioxamine complex: hypotension, accumulation if renal disease, reddish urine -may need hemodialysis if renal impairment to remove complex
57
What is the use of DigiFab?
used in severe, life-threatening digoxin toxicity
58
What is the MOA of DigiFab?
antibody fragments bind to digoxin = renally excreted
59
How many vials of DigiFab are needed for acute toxicity? What about chronic toxicity?
acute: 10 chronic: 6
60
What are complications of DigiFab?
very few -monitor for deterioration of cardiac function -hypokalemia no contraindications
61
What is the brand name of idarucizumab?
Praxbind
62
What is the use of Praxbind?
reversing dabigatran-induced anticoagulation
63
What is the MOA of Praxbind?
antibody fragments bind to dabigatran complex renally excreted
64
What are precautions to Praxbind?
thrombosis hypersensitivity hereditary fructose intolerance -idarucizumab contains 4g sorbitol as excipient
65
What is the MOA of ethanol?
competitively blocks the formation of toxic metabolites in toxic alcohol ingestion by having a higher affinity for ADH
66
What is the application of ethanol?
methanol and ethylene glycol ingestion -now regarded as second choice antidote in countries that have access to fomepizole
67
What is the lethal dose of ethylene glycol?
1.4 ml/kg
68
What is the lethal dose of methanol?
1-2 ml/kg
69
How are toxic alcohols metabolized?
by ADH and ALDH --> toxic organic acids (no rapid elimination pathway = accumulation) --> metabolic acidosis
70
How much higher is the affinity of ethanol for ADH compared to methanol?
15.5 x
71
What is the metabolite of methanol that results in toxicity?
formic acid and formaldehyde
72
What is the mechanism of ethylene glycol toxicity?
ethylene glycol is metabolized to ketoadipate and glycine using thiamine and pyridoxine as cofactors
73
How much higher is the affinity of ethanol for ADH compared to ethylene glycol?
67 x
74
When might hemodialysis need to be used for methanol or ethylene glycol toxicity after ADH has been blocked?
degree of end-organ damage has occurred how well the body can eliminate the parent compound by itself to extent to which toxic metabolites are already present
75
What are the complications of ethanol?
CNS depression toxicities: hepatitis, pancreatitis, hypoglycemia, dehydration
76
What is the preferred alternative to ethanol?
fomepizole
77
What is the use of fomepizole?
treat ethylene glycol or methanol poisoning
78
What is the preferred antidote for methanol and ethylene glycol toxicity?
fomepizole
79
What is the MOA of fomepizole?
complete inhibition of ADH even greater affinity to ADH than ethanol (80,000x greater than methanol/ethylene glycol, 8,000x greater than ethanol)
80
What is the use of intravenous lipid emulsion (Intralipid)?
current recommended treatment for local anesthetic systemic toxicity
81
What are precautions to Intralipid?
allergies -soy, eggs medical conditions -ARDS, pancreatitis, fat metabolism disorder
82
What are the toxicant properties that make use of Intralipid more successful?
lipophilic cardiotoxic
83
What is the MOA of Intralipid?
modulation of intracellular metabolism -ILE overcomes blocked or inhibited enzymes by providing fatty acids as energy source for myocytes lipid sink -lipophilic drugs have high Vd, ILE expands the plasma lipid phase allowing toxicant to move from tissue to plasma lipid phase activation of ion channels -either or both Ca2+ or Na+ channels of mycotes -increased intracellular Ca2+ = improved contractility
84
What are complications of Intralipid?
pancreatitis fat emboli syndrome lipemic serum decreases effect of other therapies?

PHAR324 (11 decks)

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