Toxicology Flashcards
(28 cards)
Toxins causing Bradycardia
PACED: Propranolol (BetaBs), Poppies (Opioids), Physostigmine, Propoxyphene, Anticholinesterase drugs, Antiarrhythmics, Clonidine, CCBs, Ethanol/Alcohols, Digoxin, Digitalis
Toxins causing Tachycardia
FAST: Free base cocaine, Freon, Anticholinergics, Antihistamines, Antipsychotic amphetamines, Alcohol WITHDRAWAL, Sympathomimetics, Solvents, Strychnine, Theophylline, TCAs, Thyroid hormones
Toxins causing Hypothermia
COOLS: Carbon monoxide, Opioids, Oral hypoglycemics, Insulin, Liquor, Sedative-hypnotics
Toxins causing Hyperthermia
NASA: Neuroleptic malignant syndrome, Nicotine, Antihistamines, Alcohol withdrawal, Salicylates, Sympathomimetics, Serotonin Syndrome, Anticholinergics, Antidepressants, Antipsychotics
Toxins causing Hypotension
CRASH: Clonidine, CCBs, Rodenticides (Arsenic, Cyanide), Antidepressants, Amiophylline, Antihypertensives, Sedative-hypnotics, Heroin (Opioids)
Toxins causing Hypertension
CT SCAN: Cocaine, Thyroid supplements, Sympathomimetics, Caffeine, Anticholinergics, Amphetamines, Nicotine
Toxins causing Tachypnea
PANT: Phencyclidine (PCP), Pneumonitis, Phosgene, Paraquat, ASA, Nerve Agents, Noncardiogenic pulmonary edema, Toxin-induced metabolic acidosis
Toxins causing Bradypnea
SLOW: Sedative-hypnotics, Liquor, Opioids, Weed
In salicylate overdose, what does acidemia signify?
Loss of respiratory compensation (first sign is tachypnea), and acceleration of the toxicity (acid to the CNS)
Sources of salicylate
Aspirin (acetylsalicylic acid), Topical salicylates, Analgesic balms, Oil of wintergreen, Willow bark, Alka Seltzer, Bismuth subsalicylate
Progression of Acid-Base Disturbance and Toxicity in Acute ASA OD.
Early (0-4 hours): 20-60mg/dL, Respiratory alkalosis with alkalemia, GI distress, Mild-mod hyperpnea, Tinnitus, Lethargy.
Moderate (2-12 hours): 50-90mg/dL, Respiratory alkalosis + Metabolic acidosis with alkalemia or neutral pH, Severe hyperpnea, Lethargy or Agitation, Hyperthermia.
Severe (6-24 hours): >80mg/dL, Respiratory alkalosis or acidosis + Metabolic acidosis with acidemia, Severe hyperpnea, Coma or Acute Delirium, Hyperthermia, Pulmonary or Cerebral edema, Seizure, Cardiovascular collapse.
Salicylate toxicity causes what metabolic issues?
Interferes with aerobic metabolism, Uncoupling of mitochondrial oxidative phosphorylation, Inhibition of Krebs cycle = increased pyruvic acid -> lactic acid, Increased lipid metabolism -> ketone bodies, Increased metabolic rate, temperature, tissue CO2 and O2 consumption, Tissue glycolysis = hypoglycemia, Ineffective anaerobic metabolism = decreased ATP production, Energy lost as heat = hyperthermia.
How does ASA toxicity lead to hypokalemia?
- Vomiting 2/2 stimulation of medullary chemoreceptor trigger zone.
- Increased renal excretion of K, Na, HCO3 2/2 compensation to resp alkalosis + ASA-induced increased permeability of renal tubules losing more K.
- Inhibition of active transport system 2/2 uncoupling of oxidation phosphorylation.
Risk factors for salicylate-induced pulmonary edema
Age > 30, Chronic smoking, Chronic ASA ingestion, Metabolic acidosis, Neurologic symptoms, ASA > 80mg/dL, Large AGMA, Hypokalemia, Low pCO2.
Two salicylate effects on CNS
- Cerebral Edema = increased energy requirements, acidemia, direct cellular toxicity.
- Neuroglycopenia = consumption of glucose in brain may be faster than supply (even with normal serum glucose). One or both of above can cause AMS, seizure, coma.
How does ASA toxicity affect bleeding?
Therapeutic dose = increased bleed risk via irreversible inhibition of PLT COX. Overdose = vitamin K epoxide reductase is inhibited (similar to warfarin). Acquired coagulopathy prolongs prothrombin time, associated with increased risk of clinically significant bleeding.
How are the elderly predisposed to salicylate toxicity from chronic therapeutic ingestions?
Decreased liver blood flow limits biotransformation of salicylate, Decreased renal function reduces salicylate clearance, Decreased albumin binding = increased free salicylate entering cells and passing through blood-brain barrier.
Clinical features of salicylate toxicity?
GI upset, Tachypnea and respiratory alkalosis, Tinnitus & hearing disturbances (concentration-dependent reversible ototoxicity), Diaphoresis, AGMA, Hyperthermia, Coagulopathy, Cerebral edema, Pulmonary edema, Cardiovascular collapse, Death.
DDx for Salicylism
Salicylism, Sepsis, CNS infection, Withdrawal syndromes, Alcoholic ketoacidosis, Diabetic ketoacidosis.
Toxins causing AGMA
ASA, Colchicine, Iron, Isoniazid, Methanol, Ethylene glycol, Metformin, Cyanide.
Toxins causing tinnitus
ASA, Aminoglycosides, Loop diuretics, Opioids, Methotrexate, Cisplatin, Quinine.
Is activated charcoal useful for ASA overdose?
Yes. Can use MDAC as well. 25-50g NG q2-4h x 2-4 doses. For acute ingestions. NOT chronic.
Main treatment objectives in ASA toxicity?
- Correct fluid deficits and acid-base abnormalities.
- Increase excretion.
Treatment of Acute Salicylate Toxicity
Consider MD activated charcoal, 25g q2-4h x2-4 doses, Treat dehydration, urine output 2-3ml/kg/hr, Correct K depletion with goal serum 4.5-5.0, Alkalinize urine, goal pH 7.5-8.0, serum goal pH 7.55, NaHCO3 150mEq = 3amps, in D5W 1L, with KCl 40mEq @ 2-3ml/kg/hr, Dextrose 0.5-1.0g/kg IV for any CNS abnormalities, Hemodialysis if criteria met = AMS, coma, seizure, respiratory failure, pulmonary edema, serum pH <7.2, renal failure, hepatic failure, rapidly rising salicylate level, failure of urine alkalinization, ASA >100mg/dL in acute OD, ASA >40mg/dL in chronic OD.
