toxicology Flashcards

Question

approach to the posisoned pt

Answer 1

-decontaminate- protect urself -airways/breathing- intubate as needed -> monitor O2 and ETCO2 -circulation- hypotension -> IV fluids, pacers, vasopressors PRN -EKG- wide QRS -> sodium bicarb; long QT -> give magnesium -disability: -GCS, pupil check, 4 extremity movement, check glucose -neuro depression- consider naloxone, glucose, thiamine -seizure- POC glucose, benzos -counter C collar -exposure- hyperthermic or agitated- benzos, cooling

Answer 2

-There are TOO many drugs! -Impossible to have a drug-by-drug approach -Classify most drugs by TOXIDROME (pattern of symptoms) -Sympathomimetics -Anticholinergics -Cholinergics -Opioids -Sedative-hypnotics -Classifying toxidromes rely on looking at: Eyes, Skin, Secretions, Vital signs

Answer 3

-Caused most often by: -Cocaine -Amphetamines (including MDMA – ecstasy) -PCP -“Bath salts” -Caffeine -Pseudoephedrine -Diet pills -Methylphenidate -CNS excitation: Hyperactivity, agitation, paranoia/psychosis, HTN, hyperthermia!!, tachycardia, tachypnea, dilated pupils, diaphoresis, coronary vasospasm -Lab testing can include: -POC glucose, CBC, CMP, Troponin, BNP, CPK, U/A, Urine toxicology screening, ECG -Imaging can include: -CXR -KUB (suspected body packer) -head CT (if AMS)

Answer 4

-mostly supportive, no specific antidotes -Decrease external stimulation (dim room lights), active cooling, IV fluids -!!Benzodiazepines for agitation, HTN and seizures -!!Beta-blockers are (theoretically?) contraindicated in amphetamine and cocaine use due to unopposed alpha stimulation which can cause worsening hypertension, ischemia, and vasoconstriction -Labetolol has alpha/beta mixed properties

Answer 5

-Overdose has a high mortality rate -Can be snorted, swallowed, injected, smoked -Half life about 1 hour -Causes alpha and beta stimulation -> increased myocardial oxygen demand and vasoconstriction for hours after use -Common to have co-ingestions (alcohol) -Common to have neuropsychiatric and social problems: Bipolar disease, schizophrenia, other drug abuse, HIV, homelessness, uninsured -Injections can be associated with: PTX, thrombosis, pseudoaneurysms of central vessels, AV fistulas, abscesses, thrombophlebitis, tetanus, necrosis -Cocaine associations: abruptio placentae, prematurity, status epilepticus, CVA, MI, rhabdomyolysis

Answer 6

-Common causes: Antihistamines! (diphenhydramine/Benadryl), antidepressants (TCAs), anti-psychotics -Also atropine, phenothiazines, anti-parkinsonian drugs, scopolamine, Jimsonweed -!“Blind as a bat, mad as a hatter, red as beet, dry as a bone, hot as Hades” -Blurry vision, delirium, flushed skin!, dry skin, hyperthermia -Others: mydriasis (dilated pupils!), hypoactive bowel sounds, urinary retention, confusion, agitation, delirium, seizures -ECG: sinus tachy (common), wide complex tachycardias, ventricular dysrhythmias, torsades de pointes -Wide QRS >100msec, terminal R wave , right axis deviation -Treat QRS complex widening with sodium bicarb

Answer 7

-!Mainly supportive: Fluids & cooling -!Mainstay of treatment: Benzodiazepines!* -Consider physostigmine!! for refractory symptoms of seizures, hyperthermia, dysrhythmias -> Contraindicated in heart block and TCA overdose -ECG management: -Ventricular dysrhythmias: lidocaine, amiodarone -Torsades de pointes: Magnesium -Wide complex tachycardia: Sodium bicarb!

Answer 8

-Were a leading cause of pharmacologic self poisoning -Now decreased since SSRIs are more common for depression tx -Examples: Amitriptyline, nortriptyline, cyclobenzaprine -Inhibits reuptake of norepinephrine and serotonin, sodium channel blockade, antagonizes histamine, muscuarinic, alpha 1, sodium channel, potassium channel, GABA receptors -Blood or urine TCA ->5mg/kg – average toxic dose ->10-20mg/kg severe poisoning -!!3 C’s = Cardiac abnormalities, Convulsions, Coma -Anticholinergic effects: flushed skin, dry mouth, mydriasis, decrease bowel sounds, urinary retention -CNS effects: drowsiness, confusion, ataxia, delirium, ↓ LOC, seizures -CV effects: hypotension, tachycardia, wide QRS, V-tach, torsade's -!!!!ECG is the most useful in determining severity

Answer 9

-!Sinus tachycardia -!Widened QRS >100ms (seizures) -Prolonged QT -!!Wide terminal R wave in aVR -Hypotension

Answer 10

-!!ABCs: Cardiac monitor, IV access, oxygen -Patients often need intubation! due to ↓ LOC -NG tube  activated charcoal! -Focused therapy: -ECG changes (QRS>100msec, ventricular dysrhythmias) -!!*Sodium bicarb IV bolus 1-2meq/kg bolus -> infusion! -> lidocaine! if refractory + arrythmia -!!Treat !hypotension with crystalloids! + norepinephrine (reverse a1-receptor blockade) -!!Treat seizures (GABA-A inhibition) with benzos! e.g. diazepam, phenobarbital -> physostigmine! if refractory

Answer 11

-The counterpart to anti-cholinergics, this is mostly parasympathetic -Causes: !Organophosphate poisoning (insecticides)!, chemical warfare agents (nerve gas like sarin) -!!!“Killer Bs”: Bradycardia, Bronchospasm, and Bronchorrhea -Muscle weakness, fasciculations, respiratory failure, wheezing -people that work with chemicals or landscapers (insecticides) -VERY WET PTS = CHOLINERGICS

Answer 12

-SLUDGE: -Secretions / Salivation -Lacrimation -Urination -Defecation/diarrhea -GI dysmotility -Emesis -DUMBBELLS: -Diaphoresis -Urination -Miosis -Bradycardia -Emesis -Lacrimation -Lethargy -Salivation -NICTOINIC EFFECTS: -fasciculations -muscle weakness -paralysis

Answer 13

-!Decontamination, use PPE -ABCs and elevate the head of the bed -Antidotes: ATROPINE! and 2-PAM (PRALIDOXIME)! -Atropine will reduce muscarinic effects. -Keep giving 2-5 mg q 5-10 min until !secretions are dry! -Increases heart rate -Pralidoxime or 2-PAM will reverse the muscle paralysis and fasciculations -2g IV followed by 24 hour infusion

Answer 14

-Death by apnea! -pinpoint pupils + not breathing = opioids -Symptoms: *Respiratory depression*, miosis, lethargy, hypotension, coma, noncardiogenic pulmonary edema, nausea/vomiting in opioid naïve patients, ileus -Most universally cause miosis, however some can cause agitation and dilated pupils such as dilaudid, Demerol, diphenoxylate -Causes: morphine, heroin, fentanyl, Demerol, codeine, diphenoxylate (Lomotil), propoxyphene (Darvon), hydrocodone (Vicodin), Percocet (careful of Tylenol addition), etc. -Caution: Clonidine can mimic opioid overdose (causes pinpoint pupils and hypoventilation) which is also reversed with high dose naloxone (10mg)

Answer 15

-Physical exam: -Pinpoint pupils, lethargy, RR<12 breaths/min -Look for circumstantial evidence of opioid use: needle marks, drug paraphernalia (undress), tourniquets, fentanyl patches (mucus membranes), witnesses -Urine drug screen can be positive 2-4 days after single use -Acute opioid OD treatment: NALOXONE (opioid antagonist) 0.4 to 2 mg -Intranasal (NARCAN): 1mg each nostril (total 2mg) -IV start with 0.4mg if mild-moderate depression, 2mg if apneic -May repeat doses every 2 to 3 minutes up to 10mg due to opioid long half life -Can start IV infusion in long acting opioids or body packers -May cause an ALI that resolves within 24 hours

Answer 16

-Withdrawal: abrupt discontinuation of opioids or naloxone use: -“Cold turkey” symptoms begin ~6 hours after last dose, peaks on day 3, resolves by day 6 -Anxiety, tremors, irritability -Nausea, vomiting, diarrhea -Cramping -Yawning -Rhinorrhea -Piloerection -Symptoms are uncomfortable but rarely fatal

Answer 17

-Sedation and somnolence are the hallmark findings -Loss of airway protective reflexes in severe cases -Causes: Benzodiazepines, barbiturates, melatonin, Z drugs

Answer 18

-Not so common anymore -Treats anxiety, insomnia, seizures -Phenobarbital, pentobarbital -Miosis, hypotension, CNS depression -!Cutaneous bullae = bad prognosis -Renally excreted and dialyzable: -Treatment: Lavage, charcoal, urine alkalinization if long acting, hemodialysis

Answer 19

-Quite common -Lorazepam (Ativan), alprazolam (Xanax), diazepam (valium), chlordiazepoxide (Librium) -Date rape drug Rohypnol -Respiratory depression, ataxia, hypotension, hypothermia, coma -THIS IS ALL YOU NEED TO KNOW: -Treatment: Supportive mostly -!!!!!!bc you cant die from overdose but you can from withdrawal -Can give antidote Flumazenil!!, but benzo withdrawal is more life-threatening than overdose (can cause seizures and death, esp in chronic overuse)

Answer 20

-killer bees

Answer 21

-Toxic metabolites produced by alcohol dehydrogenase which can be inhibited by ethanol or fomepizole. These all cause inebriation. -Consider toxic alcohol if there is an unexplained anion gap or ↑ osmolar gap -Methanol and Ethylene glycol will produce an anion gap. Isopropyl alcohol will NOT.

Answer 22

-This may be the only clue in an isopropyl alcohol ingestion -!!!Osmolal Gap = measured osmolarity – calculated osmolarity -Measured is given to you on a BMP -Calculated = (2 Na) + (BUN/2.8)+ (Glu/18) + (ETOH/4.6) -IF GAP IS >10 consider: -Toxic alcohols: Isopropyl alcohol, methanol, ethylene glycol -Ethanol -Mannitol -DKA/HHS -Drunk + Anion gap metabolic acidosis + osmolol gap = ethylene glycol or methanol poisoning Drunk + osmol gap = isopropyl

Answer 23

-Sources: paint thinner, car window washing solvent, wood alcohol, gas tank additive -Methanol itself is nontoxic, but alcohol dehydrogenase forms the toxic metabolite -Formaldehyde -> broken down by the formaldehyde dehydrogenase into -> formic acid -!!!!!!!Anion gap metabolic acidosis + increased osmolal gap -Symptoms are often delayed 12-18 hours: !Blindness from disc hyperemia!, seizures, resp failure, N/S, pancreatitis, visual changes, ataxia, AMS -Treatment: -!!Fomepizole (4-methylpyrazole) (antizol) -An alcohol dehydrogenase inhibitor -Allows methanol to be excreted intact via the kidneys without being broken down into its toxic metabolites -Usually, a temporizing measure until you can get dialysis -!Ethanol -Occupies alcohol dehydrogenase to limit breakdown of methanol into its toxic metabolites -Ethanol is preferentially metabolized by alcohol dehydrogenase over methanol and ethylene glycol -!!Dialysis and bicarbonate if severe acidosis refractory to 4-MP or ethanol therapy

Answer 24

-Ingestion of antifreeze, moonshine, paints, solvents, windshield wiper fluid -Ethylene glycol metabolizes into oxalic acid -> combines with calcium -> forms calcium oxalate crystals! -> acidosis and kidney injury -!!Intox + CNS depression, heart failure/pulm edema, ATN+anuria -Labs: !Anion gap acidosis, increased osmolar gap!, hypocalcemia, renal failure, hematuria -Wood’s lamp might show green glowing urine, d/t calcium oxalate crystals -Treatment: -FOMEPIZOLE loading dose of 15 mg/kg IV -Fomepizole inhibits alcohol dehydrogenase activity -HEMODIALYSIS if severe -THIAMINE 10 mg IV & PYRIDOXINE 50 mg IV -Both are consumed in the metabolism of ethylene glycol and need supplementation

Answer 25

-"Rubbing alcohol" (mouthwash, ginseng shots, NyQuil) -CNS depression greater than ethanol -Metabolism: in liver >50% metabolized to acetone -!!Hallmark: Normal anion gap, increased osmolar gap , Ketosis with normal glucose, -Hemorrhagic gastritis, pulmonary edema, hypoglycemia -Severe hypotension -Supportive care, don’t give alcohol. -Hemodialysis (if severe)

Answer 26

-NOT A TOXIC ALCOHOL -Found in: Wines, spirits, beers, mouthwash, cologne, perfume -CNS depressant = Downregulates GABA and upregulates NMDA -Many presentations: -Intoxication -Withdrawal -Physical changes: liver disease, varices, SBP, cirrhosis, trauma! -Intoxication: 80-100mg/dL (0.08 - 0.100 g/dL) -!!Supportive care management -Always search for other causes of AMS in the intoxicated patient -Check blood glucose -Consider CT head and c-spine -Look for fractures or other trauma -Look for other evidence of drug use -Evaluate for electrolyte abnormalities -Ethanol serum level, ammonia levels, CBC, BMP+LFTs, VBG, CPK, consider levels for other drugs such as Tylenol or salicylates

Answer 27

-Chronic alcoholism can result in B1 (thiamine) deficiency due to poor nutritional intake, causing Wernicke’s encephalopathy -Tachycardia, tremors, hypertension, agitation, Hallucinations, Seizures, Delirium tremens -Classic triad -1. Oculomotor abnormalities (CN VI palsy, nystagmus) -2. Ataxia -3. Global confusion -Treatment: IV thiamine 500mg q8hours for 3 days -Followed by 250mg daily for 3-5 more days

Answer 28

-Alcohol, barbiturates, benzodiazepines -CNS depressants -Abuse, dependence, and acquired tolerance -Drug intake abruptly stopped = withdrawal symptoms -Withdrawal will cause CNS hyperexcitation! -Tachycardia, hypertension, agitation, diarrhea, mydriasis, insomnia, cramps, diaphoresis, piloerection -Treatment: benzodiazepines, clonidine -Overdose with benzos, booze and barbs is rarely life threatening unless associated with co-ingestion of other CNS depressants such as alcohol, opioids, barbiturates, first-generation antihistamines

Answer 29

-Clinical institute for withdrawal assessment (alcohol, revised) -Validated scoring tool for alcohol withdrawal -Done hourly -Asks about various areas including !nausea, vomiting, anxiety, tremors, hallucinations ! -High scores = severe withdrawal

Answer 30

-6-12 hrs: early uncomplicated withdrawal -> minor sx- anxiety, tremors, insomnia -12-24hrs: alcohol hallucinosis -> hallucinations (tactile > auditory or visual in 7%) -24-48hrs: alcohol withdrawal seizures -> generalized tonic-clonic convulsions -48-72hrs: delirium tremens -> !disorientation/confusion!, hallucinations, hyperthermia, tachycardia, mortality 5%

Answer 31

-Ask- WHY did they stop drinking? -Tremulous, anxious, agitated -!Intention hand tremor, that is constant and does not fatigue -Tongue fasciculations are more sensitive -Early as 6 hours, Peaks at 24-36 hours, resolves at 2-3 days -Treatment: -Benzodiazepines -Assess readiness for rehab -Reassess with CIWA score -<8 can be managed outpatient

Answer 32

-1-48 hours after decrease/cessation of alcohol consumption -Usually 1-6 seizure episodes -Generalized tonic-clonic w/ shorter post-ictal time (few minutes) -Prolonged seizures, localizing findings, focal seizure, or status epilepticus – look for other cause!!! -Low threshold to scan, and look for other trauma -Usually chronic alcoholics (not binge drinkers) -Treat with benzos! to reduce recurrent AWDS -No role for antiepileptics unless hx of epilepsy -Differentials for new onset seizures!: -Head trauma -Intracranial bleed -Metabolic derangement -Acute poisoning -Epilepsy -CNS infection

Answer 33

-Late occurrence: 2-4 days after stopping/decreasing alcohol -1-15% mortality rate -Symptom complex: -!!Must have disturbance in CONCIOUSNESS or COGNITION -(if they are awake and alert its not DT) -Accompanied by tremor, agitation, delusions, hallucinations, fever, tachycardia, diaphoresis, seizures, hyperreflexia -Respiratory alkalosis from hyperventilation -Hypovolemia common -Hypokalemia and hypomagnesemia common

Answer 34

-R/O other causes of AMS -head bleed, infxn, GIB, Liver dz, neuro -General measures (can be applied to any alcoholic): -IVF -Thiamine 100mg IV -Multivitamin PO/IV -Magnesium 2-4g IV -Dextrose if needed -1st line medical option: Benzodiazepines!! (used for all alcohol withdrawals) -GABA agonist -> sedates the patient -!!Valium (diazepam) - Fastest onset 1-5 minutes, 5-10mg IV diazepam -!Ativan (lorazepam) -!Versed (midazolam) -!Librium (chlordiazepoxide)- PO only, 50-100mg, slow onset and long half life, ideal for outpatient setting -Phenobarbital: Barbiturate for benzo-resistant alcohol withdrawal -Propofol is preferred induction agent if intubating -For severe withdrawals, titrate the benzodiazepines to achieve a state of sedation with arousability to minimal stimulation

Answer 35

-!Alcohol + Antabuse (disulfiram) -!Alcohol + metronidazole (flagyl) -Flushed face, neck, trunk -Marked diaphoresis -Nausea, vomiting, headache -Severe reactions: -Hypotension -Seizures -Dysrhythmias

Answer 36

-!Toxic dose: Single ingestion >150mg/kg -Mechanism: -Hepatic metabolism via CYP450 to NAPQI --> highly toxic free radical that causes damages liver -In normal doses, NAPQI combines with thiols to produce non-toxic metabolites -In overdoses, thiol stores are depleted, and NAPQI accumulates -Predisposing factors: chronic alcohol use, malnutrition, older age, meds that utilize the CYP450 pathway (anticonvulsants, anti-TB meds)

Answer 37

-stage 1- first 24hrs -> N/V, abdominal pain -stage 2- 24-48hrs, GI sx resolve (asymptomatic), hepatic/renal dysfunction begins (high AST/ALT bilirubin INR) -stage 3- 3-4 days, LFTs peak, coagulopathy, renal failure, hepatic failure, encephalopathy, sepsis, coma, death -stage 4: 4 days-2wks, recovery phase for those who survive stage 3

Answer 38

-Serum Studies -!LFTs (serial) -Coagulation profile (PT/PTT/INR) -CBC baseline and calculate anion gap acidosis -ABG/VBG to confirm acidosis levels -Renal study -APAP LEVEL -Serum concentration >140u/mL 4 hours after ingestion is considered TOXIC and treatment with NAC should be initiated