Toxicology Flashcards
Acetaminophen toxicity
nausea
hepatic failure
max therapeutic dose (4g in 24 hours for an adult)
toxicity at >10-12 g (adult)
Treat with PO or IV N-acetylcysteine (also used in renal protection and CF)
Stages of acetaminophen toxicity
Stage I: (30min-24hrs)- n/v, diaphoresis, pallor, lethargy, malaise
Stage II: (24-72hrs)- elevated LFT, PT, tbili, RUQ pain and tenderness
Stage III: (72-96hrs)- peak LFT elevation, jaundice, hepatic encephalopathy, bleeding, +/- acute renal failure, possible multisystem organ failure, leading to death
Stage 4:3 days- 2 weeks- recovery
Anticholinergic toxicity
Hot as a hare dry as a bone red as a beet blind as a bat mad as a hatter bloated as a toad tachycardia decreased or absent bowel sounds antidote: physostigmine
Benzodiazepine toxicity
sedation
respiratory depression
Treatment: flumazenil
Beta blocker toxicity, CCB toxicity
bradycardia
hypotension
hypoglycemia
pulmonary edema
Treatment: fluids, atropine, glucagon which activates adenylate cyclase there by increasing calcium
give calcium to increase HR and contractility
insulin and glucose (beta blockers interferes with myocyte metabolism and inhibits insulin release, so administering these gives energy to organs)
cocaine toxicity
tachycardia agitation mydriasis HTN cardiac arrest hemorrhagic stroke
treatment:
supportive care, benzodiazepines, alpha- blockers
cyanide toxicity characteristics and treatment
tachycardia, htn, flushing, tachypnea leading to obtundation, coma, death
almond- scented breath (in 60% of the population)
late findings: bradycardia, hypotension, bradypnea, cyanosis, hepatic necrosis, renal failure
delayed- onset Parkinsonism in survivors of severe poisoning (basal ganglia is sensative to cyanide)
Tx: ABC, high-flow oxygen regardless of pulse-ox readings. mouth-to-mouth resuscitation is contraindicated here due to risk of provider exposure
if oral ingestion, one dose of activated charcoal
Sodium thiosulfate (sulfure donor that facilitates conversion of cyanide to thiocyanate, which is renally excreted)
Hydroxocobalamin (B12 precursor), directly binds cyanide to form cyanocobalamin, which is less toxic and excreted in the urine
Causes reddish discoloration of the skin, mucous membranes, and urine
Generally preferred over nitrate- induced methemoglobinemia, which can be lethal
Amyl nitrate and sodium nitrate
induce methemoglobin production, which binds cyanide to form cyanomethemoglobin. Goal methemoglobin level is 20-30%, but this is lethal in children and anemic patients. Contraindicated in patients with carboxyhemoglobinemia (usually from smoke inhalation)
Although methemoglobinemia can be reversed with methylene blue, this should be avoided in cyanide- poisoned patients because it will release free cyanide
Works well in conjunction with sodium thosulfate
Digoxin toxicity
Nonspecific symptoms: fatigue, blurred vision, change in color vision (eg yellow vision), anorexia, nausea, vomiting, diarrhea, abdominal pain, headache, dissiness, confusion, delirium
characteristic EKG changes:
-prolonged PR interval, “scooping” of ST segments- seen at therapeutic levels
- bradycardia- frequent vital sign abnormality
- PVCs are most common findings on EKG
- atrial tachycardia with AV block (4:1 or 6:1)- less common
Hyperkalemia indicates the severity of the digoxin toxicity (it inhibits the Na-K ATPase), look for elevated serum digoxin levels as well
What is the treatment for digoxin toxicity?
Activated charcoal in repeated doses
Digoxin Ab fragments if one of the following is present:
-hemodynamic instability
-life-threatening arrhythmia or severe bradycardia (even if responsive to atropice)
-plasma potassium level>5 mEq/L in an acute overdose
-plasma digoxin level>10ng/mL
-ingestion of >10mg of digoxin in adults or >4mg in children
-presence of a digoxin toxic rhythm in the setting of an elevated digoxin level
Treat hyperkalemia only if it is causing EKG disturbances and avoid calcium, which can worsen intracellular hyperkalemia in these particular patients
If bradycardia, atropine
ACLS if needed
Heparin toxicity
excessive bleeding
easy bruising
gross hematuria
treatment: protamine sulfate
Isoniazid
peripheral neuropathy
hepatotoxicity
treatment: B6
Isopropyl alcohol
decreased consciousness, nausea, abdominal pain, treatment
treatment: supportive care
Methanol (wood alcohol), used in antifreeze
amounts as small as 10mL can cause permanent blindness
Ethylene glycol (also in antifreeze), sweet- tasting
vomiting, hyperventilation, dizziness, slurred speech, metabolic acidosis, acute kidney failure
elevated anion gap
Treatment for methanol or ethylene glycol toxicity
ABC
NG tube gastric aspiration if ingestion of a large amount within the last 60 minutes (rare)
Sodium bicarbonate to correct acidosis and limit penetration of toxic metabolites into tissues (such as retina)
inhibit the alcohol dehydrogenase enzyme with fomepizole or ethanol
- fomepizole- preferred drug
- ethanol- if fomepizole is unavailable, dose to serum level of 100mg/dL
dialysis if severe acidosis or organ damage (vision changes or renal failure)
folic acid, thiamine, and pyridoxine supplementation to optimize elimination pathways
