Toxicology Flashcards
LPT for OD
Bring all pills
Call poison control
OD; ask
Poison; What, when, how much, why,
Reduction of absorption
Ipecec - rarely used
Gastric lavage (stomach pump)
Activated charcoal
Cathartics enhance elimination, whole bowel irrigation
The 4 anticholinergics
Antihistamine, psychotic, depressant, parkinsonian
Red, dry, blind, mad, hot
Flushing, dry skin and membranes, mydriasis (dilation), fever, altered LOC, tachycardia
TCA names -ine
Amitriptyline (elavil), amoxapine (asendin), clomipramine (anafranil), doexpin (sinequan)
Pharmacologic properties of TCA
Inhibits reuptake of norepi and reotonin Antichol actions Alpha-adrenergic blockade Inhibit potassium in heart Inhibits sodium in brain and heart
TCA on the heart
Block fast sodium - QRS prolongation, tall R wave in aVR)
Inhibits K+ channels (QTc prolongation, direct myocardial depression)
M1, H1 and A1 blockade as well
QRS > 100ms predictive of seizures
QRS > 160ms predictive of ventricular arrhythmias
ECG features of sodium channel blockade
IVCD Terminal R wave > 3mm in aVR R/S ratio >0.7 in aVR Sinus tach due to M1 blockade Heart blocks
TX of TCA OD
40mL/kg fluid Cardiotoxicity - bicarb 1mEq/kg (refractory hypotension or QRS >0.10 or ventricular dysrhythmia) Benzos for seizures 2g mag in 50mL over 5 if needed Norepi for pressors Avoid a
Activated charcoal
Charcoaid
Class absorbent
Contras - need an OG/NG if altered, don’t give if corrosive agent (vomit) 1g/kg for everyone
Antiarrhythmics in TCA
Avoid Ia and IC, beta blockers and ami as these may all worsen hypotension or conduction abnormalities
LITFL says lido after bicarb and hyperventilation, tins says no evidence of this
Overdrive pacing or isoprotenolol in tins…maybe
Things that cause cholinergic tox
Nictotine, muscarine mushrooms, neostigmine, cevimeline, organophosphates
S&S of chol tox
BM SLUDGE Bradycardia/bronchospasm/bronchorrhea Miosis Salivation Lacrimation Urination Defecation GI upset Emesis Miosis
Cholinergic toxicity MOA
Cholinesterase inhibitors have high affinity for ACHe which metabolizes ACh.
TX for chol tox (SLUDGEM)
Decontamination Assisted resps Monitor for torsades Atropine 2mg IV/IO q 5 until reversal Avoid succs (prolonged paralysis) Pulmonary edema 2-PAM
Pralidoxime hydrochloride
2-PAM. Regenerates ACHe activity, must be given early
Metabolic considerations
Rhado/renal failure
Stim OD protocol
Cool 12lead 5IV midaz 2.5 q 5 max 20 10IM midaz 5mg q 10 max 20 Bicarb for QRS widening 1mEq/kg q 5 ma 2 mEq Refractory chest pain treat ACS
Beta blocker theory for stim OD
Unopposed alpha because if B2 is blocked (peripheral vasodilation) and A1 still stimulated you get sky high BP
(propanolol is non selective B)
Metoprolol (selective B1) or Isoprotenolol (blocks alpha and beta) can be given according to LITFL.
Tins says you can give
Tins antipyschotics
Haloperidol may decrease seizure threshold, contribute to hyperthermia, and increase QT prolongation. Still give, but after beta blockers
Anxiolytics OD presentation
Benzos/barbs
Decreased LOC, delirium, slurred speech, combative, resp depression, hypotension, bradycardia, diaphoresis, hypothermia, nystagmus
Barbs and bicarb
Alkalization of urine enhances elimination of phenobarb by ion trapping. Just used for long acting barbs
Zero order kinetics
A set amount of drug is eliminated per unit of time
Happens to salicylates after liver is saturated, the kidneys become primary route of excretion at this point
Salicylate tox and alkalinization
Serum alkalinization used to keep drug in plasma and out of tissue
Urinary pH above 7.5 keeps ASA from being reabsorbed
pH salicylate tox
Direct stimulation of resp center causes tachypnea, hypernea and resp alkalosis
Inhibition of metabolism produces acidosis that overwhelms alkalosis and may create late resp acidosis (coingestion of other drugs may cancel resp center stimulation)
Salicylate tox sugars
Initial mobilization of glycogen stores causing hyperglycemia but inhibits gluconeogensis so pts are often normoglycemic (tins says hypoglycemia is rare)
Profound decrease in brain glucose despite normal serum glucose meaning.
Salicylate lungs
Can cause noncardiogenic pulmonary edema - may also cause cerebral edema
Salilcylate GI
Corrosive injury of GI with abdo pain N/V and occasionaly hematemsis with volume loss, metabolic alkalosis and hypokalemia
Salicylate OD tx
ABCs, fluid, control hyperthermia, sugar for sugars benzos for seizures and maybe bicarb
Activated charcoal within 60 minutes
Beta blocker TXs
Fluid, pacing, epi or dope, glucagon and CaCl as beta blockers inhibit calcium entr
Common CCB
Verpamil (isoptin) Nifedipine (adalat) Diltiazem (cardizem)
4 cardio effects of CCB
Negative ino chrono and dromotropy plus vasodilation
S&S CCB OD
Hypotension, bradycardia, heart block
Altered LOC/seizures
Hyperglycemia
MOA CCBs
Bind to L-type calcium channel causing it to favour closed state and decreasing Ca2+ entry during phase 2.
Verapamil at high concentration occupies and completely blocks channel
3 classes of CCB
phenylalkylamines (verapamil and gallopamil)
benzothiazepines (diltiazem)
Dihydropyridines (nifedipine, amlodipine)
TX of CCB
CaCl, insulin, TCP, glucagon (N/V) pressors of epi or dope
Dig presentation
Headache, irritability, psychosis, yellow-greenish vision, anorexia, N/V, palpitations, syncope, dyspnea, atrial tachycardia with block, junctional tachy ectopy
Tachyarrhythmias and heart blocks
Dig Tox TX
12-lead, fluid, TCP/atropine, hyperK+ tx with digibind THEN calcium
Digibind dose
400mg IV over 15 minutes
800mg IVP if in arrest
Ethylene glycol
Antifreeze, can produce intox, severe toxicity
Methanol
Primary in windshield fluid
Methanol/ethylene glycol MOA
Metabolized by same enzyme as ETOH - dehydrogenase, but into toxic by-products that lead to severe multi-system toxicity
Ethylene glycol metabolites
glycolic acid, glyoxylic acid, oxalic acid, lactic acid
Methanol metabolites
formic acid and lactic acid
Methanol/ethylene S*S
May just show as intox for first 6 hours
Both produce severe metabolic acidosis with elevated anion gap and osmolar gaps
Ethanol as tx
Competitive substrate for enzyme alcohol dehydrogenase
Pyridoxine (vit B6) - cofactor in enzymatic breakdown of glyoxylic acid into non-toxic by products
Folic acid - enzyme cofactor
B1(thiamine) 100mg IV/IM - cofactor in enzymatic breakdown glyoxylic acid
MDMA
Jaw clenching, teeth grinding, scratching, nystagmus, dilated pupils, tachycardia, HTN, hyperthermia, sensation of chills, elevated temp, severe dehydration with hyponatremia, decreased LOC, coma, seizure, death, DIC, malignant hyperthermia
TX with fluids and cooling
Hydrocarbons
Kerosene, gasoline, lighter fluid, turpentine, mineral oil, petroleum jelly, paraffin wax
Hydrocarbons S*S
Euphoria, anxiety, choking/gagging/coughing, N/V/D upsetstomach pepto bismal hypoglycemia
