KC Tox Flashcards

Question

How do you calculate anion gap

Answer 1

Na - (HCO3 + HCL) Elevated if >12

Answer 2

Loss of bicarb (diarrhea, renal tubular acidosis) Gain of chloride (ammonia, calcium chloride) HARDUP Hyperalimentation Acetazolamide RTA Diarrhea Ureteroenterostomy Pancreatoenterosomites

Answer 3

Killer Cs Cyanide, colchicine, calcium channel blockers, cyclic antidepressants, cardio glycosides, cyclopeptide mushrooms (amanita phalloides), cocaine, cicutoxin, salicylates

Answer 4

PHAILS Pesticides, hydrocarbons, heavy metals, acid/alkalis, iron, lithium, solvents

Answer 5

ABCDQ (drugs with significant enterohepatic circulation) Aminophylline/theophylline Barbiturates Carbamazepine, concretion forming drugs ex. Salicylates Dapsone Quinine

Answer 6

Salicylates, methotrexate, phenobarbital

Answer 7

Lipid sink Enhance cardiac metabolism of free fatty acids

Answer 8

Refractory beta blocker overdose, calcium channel blocker overdose, bupropion, cocaine toxicity

Answer 9

Acetaminophen = N-acetylcysteine Methanol/ethylene glycol = fomepizole Organophosphates = atropine/pralidoxime Iron = deferoxamine Arsenic = Dimercaprol (BAL) Isoniazid = pyridoxine

Answer 10

2*Na + BUN + glucose

Answer 11

ethylene glycol, methanol, acetone, mannitol, polyethylene glycol (IV lorazepam), ketosis (diabetic, alcoholic), renal failure, multi-organ failure, IVIG, pseudohyponatremia, uremia

Answer 12

Type A: poor perfusion: sepsis, mesenteric ischemic, hemorrhage Type B: no hypoperfusion - Metformin, DKA - Seizure - Alcohol: liver dysfunction, alcoholic ketosis, toxic alcohols - Mitochondrial defects - Drug s/e: Ventolin, propofol - Tox: salicylate poisoning, carbon monoxide, cyanide, massive Tylenol

Answer 13

CHIPES: Calcium carbonate, heavy metals (Fe), iodized toxins (thyroxine), packer/potassium/psychotropics, enteric coated pills (ASA, slow K), solvents (halogenated hydrocarbons)

Answer 14

orogastric lavage, charcoal, whole bowel irrigation

Answer 15

1g/kg PO (usually 50g) or 10g AC per 1g of toxin in a single dose

Answer 16

PEG 100ml/hr titrated up to 1-2L/hr until rectal effluent is clear | You are 100-1000% going to shit your pants

Answer 17

metals (potassium, magnesium, sodium) as these can ignite on contact with water

Answer 18

Urine alkalinization, MDAC, dialysis

Answer 19

loading dose (10:1) followed by 50% of initial dose every 4-6 hours for 24 hours

Answer 20

TCAs, type 1a and 1c antidysrhythmic, cocaine, diphenhydramine

Answer 21

Oral hypoglycemic agents, sulfonylureas, insulin Beta blockers, isoniazid, salicylates, ethanol

Answer 22

ABC GET MOM A - ASA B - BBs C - CCBs, clonidine, cardiac glycosides, colchicine, camphor G - glucose lowering (sulfonylureas) E - EG T - TCAs, Theophylline M - methanol O - opioids M - MAOIs, metals (iron, lead)

Answer 23

agranulocytosis, leukoencephalopathy, cutaneous vasculitides

Answer 24

methanol, ethylene glycol, diabetic ketoacidosis, alcoholic ketoacidosis, uremia, septic shock, multiorgan failure

Answer 25

1 - acute neurologic stage, 30 min - 12 hours 2 - cardiopulmonary stage, 12 - 24 hours 3 - renal stage, 24 - 72 hours 4 - delayed neurologic stage, bulbar palsy, 5 - 20 days

Answer 26

- Glycolic acid - Glyoxylic acid - Oxalic acid

Answer 27

- Sodium bicarbonate: Correcting metabolic acid may increase urinary excretion of EG and delay calcium oxalate- induced AKI - Fomepizole/Ethanol: ADH blockade prevents metabolism of EG into toxic metabolites - Dialysis: Removal of EG in the setting of acidosis (pH < 7.3)/renal failure/serum EG level > 8.1 mmol/L (level taken from Toxinz)

Answer 28

1) Pyridoxine 2) Thiamine

Answer 29

Albumin corrected anion gap = anion gap +2.5*(normal albumin-measured albumin) Albumin is a negative charged protein. AG will be lowered in the presence of hypoalbuminemia, thereby masking an elevated AG - a normal AG may actually represent a metabolic acidosis

Answer 30

12 Normal gap 6-14, elevated if >12

Answer 31

Osmolar gap = measured serum osmolarity – calculated serum osmolarity Calculated serum osmolarity = 2*Na + Glucose + BUN + 1.2*EtOH

Answer 32

Delta gap = (change in anion gap) - (change in bicarb) Delta gap = (AG-12)-(24-HCO3-) Determines if the anion gap is accounted for by the change in Bicarb Positive delta gap = delta AG > delta bicarb = metabolic acidosis + metabolic alkalosis No delta gap = delta AG = delta bicarb = pure AGMA Negative delta gap = delta AG < delta bicarb = AGMA + non anion gap metabolic acidosis

Answer 33

PaCO2 = (1.5*serum HCO3-) + (8 +/- 2) Used to calculate the expected arterial PCO2 for the serum bicarbonate level Tells us if there is a mixed picture

Answer 34

Methanol and ethylene glycol

Answer 35

1) Contained in windshield wiper fluid, de-icing products, paint removers, antifreeze, camping stove fluid 2) Methanol -> formaldehyde -> formic acid 3) Neurologic symptoms including optic neuritis, parkinsonism, ataxia, confusion 4) Labs show elevated osmolar gap and acidosis 5) Treated with fomepizole, folic acid 50mg, dialysis

Answer 36

1) Found in radiator fluid, antifreeze, metal cleaners 2) Ethylene glycol -> glycolaldehyde -> glycolic acid -> oxalic acid 3) Stage 1 CNS, mimics alcohol intoxication. Stage 2 cardiopulmonary with myocardial dysfunction. Stage 3 renal failure with ATN from calcium oxalate crystals. Stage 4 late neurological sequelae i.e. bulbar palsy 4) Labs show elevated osmolar gap and acidosis. Typically high lactate. Hypocalcemia with calcium oxalate in the urine 5) Treated with fomepizole, pyridoxine 100mg, thiamine 100mg, dialysis

Answer 37

1) Found in rubbing alcohol, hand sanitizer 2) Isopropyl alcohol -> acetone -> acetol 3) Intoxication, more prolonged than EtOH, fruit odor on breath 4) Ketosis and elevated osmolar gap without acidosis 5) Supportive care. No fomepizole as the metabolite is no more toxic than isopropyl alcohol itself. Fomepizole will only prolong CNS depression

Answer 38

5.5 mmol/hr

Answer 39

1) correction of acidosis 2) inhibition of the production of toxic metabolites 3) elimination of parent alcohol and its toxic metabolites

Answer 40

No; quickly absorbed

Answer 41

Methanol concentration > 6.2 mmol/L,> 3.2 for ethylene glycol Hx of methanol or EG ingestion with an osmol gap >10 Suspected methanol or EG ingestion with at least 2 of: pH <7.3, Co2 level <20, urinary oxalate crystals present, osmolar gap >10

Answer 42

15mg/kg over 30 mins, then 10mg/kg over 30 mins q12 for the first 48 hours (x 4 doses) then 15 mg/kg q 12

Answer 43

[Rosens]: significant acid-base disturbances, end organ toxicity (coma, seizure, visual disturbances), renal failure, methanol >15.6 mmol/L, ethylene glycol >8.0 [Extrip]: impaired kidney function, coma, seizures, new vision deficits, blood pH <7.15, persistent metabolic acidosis despite adequate support measures and antidotes, anion gap >24, methanol >21.8 with fomepizole or >15.6 without fomepizole

Answer 44

Wernicke-Korsakoff syndrome Treatment: Thiamine and magnesium repletion

Answer 45

Stroke Hepatic encephalopathy Encephalitis Intox Brain tumour Dementia

Answer 46

- AST/ALT ratio > 2 – MOST SPECIFIC TO ALCOHOL

Answer 47

Classic triad: - Altered mental status - Oculomotor dysfunction - Gait ataxia

Answer 48

- Nausea or vomiting - Tremor - Paroxysmal sweats - Anxiety - Tactile disturbances - Auditory disturbances - Visual disturbances - Headache - Agitation - Orientation and clouding of sensorium

Answer 49

1. Withdrawal (alcohol or drugs) 2. Neuro Exacerbation of idiopathic or post-traumatic seizures 3. Infectious (meningitis, encephalitis, brain abscess) 4.Trauma (intracranial hemorrhage) 5. Metabolic (hypoglycemia, hyponatremia (Beer potomania), hypernatremia, hypocalcemia, hepatic failure)

Answer 50

1. benzo: ativan, diazepam (1mg ativan = 5mg diazepam), switch to other agent after 400mg 2. propofol 3. phenobarb 4. dexmedetomidine (for refractory) 5. ketamine (for refractory) 6. Thiamine (+magnesium)

Answer 51

AG: [Na+] - ([Cl−] + [HCO − ]) Delta gap = (change in anion gap) - (change in bicarbonate) ... (Anion gap - 12) - (24 - bicarbonate)

Answer 52

- Alcoholic/starvation ketoacidosis - Diabetic ketoacidosis - Ethylene glycol toxicity - Methanol toxicity

Answer 53

1 - Long-standing ethanol user abruptly stops drinking (acute starvation on top of malnutrition) 2 - Ketones are generated (ketogenesis blocked by drinking) and accumulation of β-hydroxybutyrate and the inhibition of gluconeogenesis

Answer 54

- Fluids (D5NS) - Thiamine - Electrolyte replacement - Correction of acidosis (should correct with above)

Answer 55

Insulin - down Ketones - up Catecholamines - up Lipolysis - up

Answer 56

Alcohol by AHD -> alcohol dehydrogenase -> acetaldehyde -> acetyl coenzyme A _ CO2 + H20 (acetate)

Answer 57

Decrease in GABA with the cessation of alcohol. Low GABA and high glutamate cause CNS excitation

Answer 58

Stage 1 (12-18hrs onset): shakes, sweating, agitation, anorexia, anxiety Stage 2 (12-24): seizures Stage 3 (12-24, often later): hallucinations Stage 4: (3-5 days): delirium tremens

Answer 59

Life threatening form of alcohol withdrawal characterized by altered sensorium (confusion, delusions) + autonomic hyperactivity (fever, tachycardia, hypertension)

Answer 60

Diazepam 10-20mg PO or IV q15 until tachycardia is resolved and patient is comfortable. Phenobarbitals 5-10mg/kg (~65mg, can double each dose) as a second line agent Alternatives would be to follow the CIWA protocol and give benzos if score >10

Answer 61

Naltrexone, gabapentin, disulfiram, acamprosate

Answer 62

Neurological: withdrawal seizures, polyneuropathy, tremor, cerebellar dysfunction, ataxia, Wernicke's, Korsakoff Cardiovascular: increased HR/HTN, contribute to CAD and arrhythmias ex. Holiday heart Resp: increased pneumonia, often concurrent smoking GI: esophagitis, GERD, GI bleeding from varices, alcoholic hepatitis (AST/ALT >2), cirrhosis, pancreatitis ID: immunosuppression Heme: anemia, leukopenia, thrombocytopenia Metabolic: hypoglycemia (likely due to starvation and depletion of liver glycogen stores) electrolyte deficiencies

Answer 63

desire to cut back, annoyed when people ask, guilty about drinking, eye opener in the morning

Answer 64

2023 Canadian guidelines 0 - health benefits, sleep benefits 1-2 - likely avoid harms 3-6 - increase CA risk (breast and colon) >7 - increase MI and stroke risk Don’t have more than 2 on one day per week 0 in pregnancy

Answer 65

Screening, brief intervention, referral to treatment

Answer 66

Stage 1 = Pre – Injury (<24hrs – 36hrs) Asymptomatic Possible N/V/Abdo Pain Stage 2 = Liver Injury (8 – 36hrs) N/V/Abdo Pain Elevated AST/ALT Stage 3 = Maximal Liver Injury (2-4 days) Fulminant hepatic failure (enceph / coagulopathy / acidosis etc) Stage 4 = Recovery (> 4 days) Death or recovery

Answer 67

Kings College criteria: pH < 7.30 INR > 6.5 (PT > 100 sec) Creatinine 300 µmol/L Grade III or IV hepatic encephalopathy

Answer 68

- IV crystalloid resuscitation - IV NAC - Intubation - Consult transplant service - Consult nephrology service regarding hemodialysis - Regular monitoring of CBC/INR/PTT/VBG/glucose/LFT

Answer 69

For delayed, chronic, or supratherapeutic toxicity, NAC therapy should continue until acetaminophen is undetectable in the serum (<10 mcg/mL) AND: - Any signs of liver injury have resolved (ie, encephalopathy has cleared, normalization of the coagulation profile, resolution of metabolic acidosis) - AST is less than 1000 IU/L with demonstration of a downward trend

Answer 70

Decreases rates of cerebral edema, hypotension and death

Answer 71

Glucuronidation (50% range 40-67%) Sulfation (30% range 20-46%) CYP (~10%); this is what produces NAPQI Direct Renal Clearance (~10%)

Answer 72

Decrease toxic / free NAPQI Glutathione precursor Glutathione substitute Direct reduction of NAPQI-APAP Increase Sulfation route Free radical scavenger Hepatocyte stabilizing effect

Answer 73

Reference graph plotting serum APAP level and time in hours. At 4h - levels greater than 1000 umol/L toxic 8h - greater than 500 12h - greater than 250 Not to be used in chronic ingestions, extended release preparations, co-ingestions etc.

Answer 74

False - CYP inducer is busy so less NAPQI is produced True - more NAPQI is produced

Answer 75

False (CYP450 inhibitor) True

Answer 76

>500mg/kg or >50gm or acetaminophen ingestion + rapid onset of lactic acidosis, hyperthermia, hyperglycemia, altered mental status

Answer 77

chronic use, chronic EtOH, pre-existing liver disease, malnourished, other CYP meds (ex. Rifampin, phenobarbital, phenytoin)

Answer 78

4 hours after ingestion and q4 hours until peaked

Answer 79

200mg/kg or ~ 10-12g [OPC]

Answer 80

Acetaminophen level about the treatment line, chronic acetaminophen toxicity with signs of toxicity (clinical symptoms, elevated AST x2 limits, elevated APAP), clinical suspicion for massive ingestion, unable to get APAP level back within 8 hours of ingestion, acetaminophen ingestion + elevated liver enzymes

Answer 81

Will vary based on local poison control protocol 3% NAC 60mg/kg/hr for 4 hours + 6mg/kg/hr (max 600mg/hr) until stopping criteria reached

Answer 82

Tylenol level is undetectable AND N-acetylcysteine has been given for at least 12 hours AND AST/ALT <100 and falling and INR <2

Answer 83

APAP >1000mg/L or 6620 umol/L without NAC APAP >700mg/L or 4630 umol/L with altered mental status, acidosis, elevated lactate and without NAC APAP >900mg/L or 5960 umol/L with altered mental status, acidosis, elevated lactate with NAC

Answer 84

Decreased liver blood flow limits biotransformation of salicylate Decreased renal function reduces salicylate clearance Chronic ingestion decreases albumin binding, increasing the free salicylate that can enter the cell, and allows salicylates more time to pass through the blood-brain barrier.

Answer 85

Falling concentration may reflect redistribution rather than clearance

Answer 86

ASA, oil of wintergreen methyl cold products, bismuth (pepto bismol)

Answer 87

200mg/kg or ASA 10-30g

Answer 88

Tachypnea, hyperpnea, hyperthermia Resp: pulmonary edema GI: Abdo pain, nausea/vomiting Neuro: altered mental status, irritability, ototoxicity Heme: coagulopathy

Answer 89

Respiratory alkalosis 0-4 hrs - tachypnea from stimulation of the medulla. Neutral 2-12 hours - metabolic acidosis from uncoupling of oxidative phosphorylation + metabolic alkalosis from vomiting Metabolic acidosis 6-12 hours - respiratory acidosis if preterminal due to respiratory muscle fatigue

Answer 90

serum levels may underestimate the severity of the intoxication because salicylate has already accumulated in the brain

Answer 91

1. GI decontamination 2. IV fluids 3. Urine alkalinization 4. Glucose supplementation 5. Potassium correction 6. Dialysis if refractory

Answer 92

1-2 mEq/kg bicarb bolus then bicarb drip (3 amps of sodium bicarb in 1L D5 with 40mEq at 2.5*maintenance) Target urine pH 7.5-8.0 and serum pH of 7.55

Answer 93

Acute ASA level >3.5 [OPC] Chronic ASA level >2.9 ASA ingestion + clinical symptoms

Answer 94

Salicylate are acidic and readily ionize in an alkali environment Only the non ionized state can traverse cell membrane and cause toxicity. The non ionized state is the one that causes clinical harm Once ionized in the urine they are ’trapped’ there Alkaline urine traps the salicylate on and increased excretion Reduces reabsorption of salicylate molecules and encourages secretions down a concentration gradient

Answer 95

Salicylate >7.2 mmol/L or >6.5 mmol/L in the presence of impaired kidney function Salicylate toxicity + altered mental status, hypoxia, Failure of standard therapy (ex. urine alkalinization) In general, lower threshold for chronic ingestions

Answer 96

Caution as it is difficult to match the patient's ventilation. If intubation is necessary: - VBG beforehand - Bicarb boluses before hand - Intubation without paralysis - Bag during the apneic period - Match pt's pre intubation RR on the vent

Answer 97

Anticholinergic ingestions antagonize the muscarinic receptors (ex. Salivary glands, SA node, pupils, skin) Do not affect the nicotinic receptors at the neuromuscular junction

Answer 98

Diphenhydramine, toxic at >2.5mg/kg, also act as a sodium channel blocker TCAs, toxic at >2,5mg/kg, also act as a sodium channel blocker Antihistamines Antipsychotics Antiparkinsonian agents ex. Cogentin Atropine, scopolamine, glycopyrrolate Antiemetics dimenhydrinate Jimson weed, belladonna, amanita mushrooms

Answer 99

"Dry as a bone (dry mucous membranes, decreased motility, urinary retention, dry skin), hot as a hare, red as a beet, mad as a hatter, blind as a bat (mydriasis)" Tachycardic, hypertensive, hyperthermic Warm, dry skin Large pupils Delirium, agitation, hallucinations, picking gestures, myoclonus

Answer 100

Physostigmine 0.5-2mg IV slow bolus over 5 mins [OPC] [1-2mg IV in Rosens]

Answer 101

Acetylcholinesterase inhibitor, allowing for acetylcholine accumulation and competition with the antimuscarinic blocking agents. Crosses the blood brain barrier so can reverse the central and peripheral anti-muscarinic effects

Answer 102

wide QRS, narrow angle glaucoma, bradycardia or heart block, seizures, salicylate allergy, ileus, urinary retention, asthma Will worsen any existing cholinergic symptoms

Answer 103

The mnemonic FINISH summarizes the symptoms of antidepressant discontinuation syndrome: Flu-like symptoms (lethargy, fatigue, headache, achiness, sweating), Insomnia (with vivid dreams or nightmares), Nausea (sometimes vomiting), Imbalance (dizziness, vertigo, light-headedness), Sensory disturbances (“burning,” “tingling,” “electric-like” or “shock-like” sensations) and Hyperarousal (anxiety, irritability, agitation, aggression, mania, jerkiness).

Answer 104

7 mechanisms - Na channel blockade (wide QRS) - K Efflux blockade (prolonged QT) - Alpha 1 blockage (hypotension) - Amine reuptake inhibition (norepinephrine, serotonin - serotonin syndrome) - Anticholinergic (muscarinic - hot as a hair, mad as a hatter) - Antihistamine (sedation, altered LOC) - Indirect GABA antagonism (CNS, seizure)

Answer 105

- Benzodiazepine - Sodium bicarbonate - Phenobarbital/Propofol - Intralipid

Answer 106

- Prolonged QT - Delayed Seizures - Ventricular Tachycardia - Serotonin Syndrome

Answer 107

Cyproheptadine

Answer 108

Cooling IVF Benzos Bicarb + potassium Hypertonic saline Lidocaine Intralipid Propofol | Two alternatives to Bicarb, one extra that goes with bicarb

Answer 109

SSRIs: escitalopram, citalopram, fluoxetine, paroxetine, sertraline SNRIs: Duloxetine, venlafaxine TCA: amitriptyline MAOIs: Selegiline, Rasagiline Metoclopramide, Linezolid, Tramadol Cocaine, NMDA, LSD, St. John's wort

Answer 110

In the setting of exposure to a known serotonergic agent, serotonin syndrome can be diagnosed in the presence of any of: Spontaneous clonus Inducible clonus AND agitation/diaphoresis Ocular clonus AND agitation/diaphoresis Tremor and hyperreflexia Elevated temp AND ocular or inducible clonus | SETH - vowels in the middle

Answer 111

Triad of symptoms - Psychiatric - confusion, altered LOC, agitation, restlessness - Autonomic - increased BP, HR, nausea, vomiting, sweating, hyperthermia - Neurologic - tremor, myoclonus, hyperreflexia, ocular flutter

Answer 112

Similar presentations Risk of more serious overdose with more cardiac complications (prolonged Qtc and prolonged QRS) with an SNRI overdose

Answer 113

Prolonged QRS, R/S ratio >0.7, R wave >3mm R bundle branch block, Brugada pattern, rightward access Prolonged QTC Tachycardia

Answer 114

Sodium bicarbonate for wide QRS Correction of acidemia target pH 7.50-7.55 Benzos for agitation or seizures Fluid for hypotension Activated charcoal if within 2 hours

Answer 115

Hypertonic saline (100ml bolus of 3%) if cannot give bicarb due to alkalemia or hypernatremia Lidocaine 1 mg/kg; also acts a sodium channel blocker so will compete with TCA Intralipid if cardiac arrest Magnesium for prolonged Qtc

Answer 116

Wide QRS is due to blockage of potassium channel and cardiac gap junction; NOT sodium channels

Answer 117

1. Drug food interactions/hypertensive crisis - Dietary tyramine in cheese, pickles, alcohol, soy sauce, sausage - Tyramine is a sympathomimetic amine that is usually broken down by MAO - When MAO A is inhibited tyramine is systemically absorbed causing the release of norepinephrine and serotonin, leading to a hypertensive crisis - Tyramine syndrome presents as headache, hypertension, flushing, diaphoresis 2. Drug interactions (amphetamines, phenylephrine/ephedrine) 3. Overdose

Answer 118

TCA Type 1a antiarrhythmic: quinidine, procainamide Type Ic antiarrhythmic: flecainide Cocaine Antimalarial: chloroquine Anesthetic Other: propranolol, carbamazepine, quinine, certain antipsychotics, gravol, phenytoin (don’t use in Na block-induced seizures)

Answer 119

- Atrial fibrillation with slow, regular ventricular rate (AV dissociation) - Nonparoxysmal junctional tachycardia (rate 70 to 130 beats/min) - Atrial tachycardia with block (atrial rate usually 150 to 200 beats/min) - Bidirectional ventricular tachycardia

Answer 120

Digibind Temporize bradycardia with atropine Watch the K+ (helps guide acute Fab treatment or chronic OD’s need repletion) Correct the Mg+ Temporizing measures while waiting for DigiFab: Consider pacing and cardioversion (avoid if possible!) Consider Phenytoin or lidocaine for tachydysrhythmias Caution with calcium (theoretical risk of stone heart)

Answer 121

History: Other cardiac toxic drug ingestion – CCB, BB, TCA with shock Acute ingestion > 10 mg plus clinical toxicity Ingestion of plant containing cardioactive steroids plus dysrhythmias Physical: Too fast and deadly: unstable ventricular dysrhythmias (not PVCs) Too slow and deadly: unstable dysrhythmias (hemodynamic compromise) such as symptomatic sinus bradycardia, or second- or third-degree heart block unresponsive to atropine. Cardiac arrest Labs: Serum potassium level above 5.0 mEq/L (acute ingestion) Acute steady state > 12 nmol/L and one clinical sign or chronic >7 nmol/L Any serum level > 19 nmol/L (this is not a steady state level, will change after drug distributes)

Answer 122

Benzodiazepines EtOH Cannabis Cardioactive steroids BB CCB Opioids Hypoglycemics ...

Answer 123

Clonidine BB CCB Digoxin

Answer 124

IV fluids → increase preload Atropine → anticholinergic, increases firing through SA and AV node Calcium → replaced depleted intracellular calcium High dose insulin + glucose → provides substrate to heart, may be inotropic

Answer 125

Paralyzes the Na/K/ATP pump. Potassium cannot enter the cells, conduction is depressed through the AV node creating AV blocks/bradyarrhythmias, and Purkinje fibres are more sensitive to electrical stimulation creating enhanced automaticity Also why you get hyperkalemia - none of the K can get into cells just sits outside can be over 10

Answer 126

General: weakness, fatigue, malaise GI: nausea and vomiting, abdominal pain, diarrhea Optho: blurry or snowy vision, photophobia, visual changes to colour Neurologic: dizziness, headache, confusion, hallucinations, parasthesias, seizures Cardiac: bradyarrhythmia, tachyarrhythmia, PVCs

Answer 127

Drug-drug interactions (antibiotics, diuretics, other cardiac meds), declining renal function, electrolyte imbalance, hypothyroidism, elderly, female patient

Answer 128

1) Serum dig level *5.6 L/kg *kg /1000 2) # of vials = [(PO digoxin in mg)*0.8]*2 - 1 vial brings down the dig level by 0.5 mg

Answer 129

B1: myocardium, kidney, eye - increases inotropy, chronotropy, renin release, aqueous humour production B2: bronchial and visceral smooth muscle - increases bronchodilator, vasodilation

Answer 130

A-M cardioselective block B1 ex. Atenolol, metoprolol N-Z nonspecific B1 and B2 (can cause bronchospasm in asthmatics) ex. Nadolol, propranolol Olol - pure beta blocker Vowel -lol alpha and beta blocker ex. Labetalol

Answer 131

Supportive care: IVF GI decontamination if large overdose Atropine 1mg IV Calcium supplementation Treatment: Glucagon 5-10mg IV bolus High dose insulin - 0.5-1U/kg IV bolus then 1-10 U/kg/hr titrate to effect - 1g/kg IV D50 bolus then 0.5-1g/kg/hr of glucose Salvage: Intralipid 1.5ml/kg bolus then 0.025 ml/kg/min infusion Dialysis if applicable Circulatory support LVAD, ECMO, IAMP

Answer 132

SATAN - sotalol, atenolol, timolol, acebutolol, nadolol

Answer 133

Propranolol: most toxic due to lipophilic nature, allows it to penetrate the CNS resulting in seizures

Answer 134

Membrane stabilizing: can result in sodium channel inhibition and wide QRS ex. Propranolol, acebutolol, nadolol

Answer 135

Sotalol, Acebutolol: can resulted in prolonged QT + TdP

Answer 136

Supportive care: IVF (caution due to increased risk of pulmonary edema) GI decontamination if large overdose Atropine 1mg IV Calcium supplementation Treatment: High dose insulin - 0.5-1U/kg IV bolus then 1-10 U/kg/hr titrate to effect - 1g/kg IV D50 bolus then 0.5-1g/kg/hr of glucose Pressors Salvage: Intralipid 1.5ml/kg bolus then 0.025 ml/kg/min infusion Methylene blue 1-2mg/kg bolus Circulatory support LVAD, ECMO, IAMP

Answer 137

Glucose Hyperglycemia -> CCB Hypoglycemia -> BB

Answer 138

- Irrigation with copious amounts of water for at least 15-30 minutes - Removal of blisters, as necrotic tissue may harbour fluoride ions - Clothing removal

Answer 139

- Topical calcium gluconate gel, which can be made by mixing 3.5 g of calcium gluconate powder in 150 ml of water-soluble lubricant (e.g. K-Y jelly) and secured with an occlusive cover - Infiltration of subcutaneous calcium gluconate for deeper burns (note: this is painful, so consider a regional nerve block) - Intravenous calcium gluconate - Intra-arterial calcium gluconate Pain control

Answer 140

Hypocalcemia hypomagnesemia hyperkalemia

Answer 141

Inhalation and skin exposure to 70% hydrofluoric acid can result in pulmonary edema and death within 2 hours. However, delayed pneumonitis and adult respiratory distress syndrome can also occur, and they can be present for months. Pneumonitis can be severe and require ventilatory support.

Answer 142

Secure IV access/crystalloid resuscitation as indicated • Secure airway/intubate • Pain management • Consult surgical service as indicated • Antibiotics if suspected/confirmed perforation • Consult poison centre • consider careful nasogastric aspiration if ingestion within 30-45 mins, other forms of GI decontamination/charcoal contraindicated • Monitoring in ICU

Answer 143

• Scope (12-24h post ingestion) • Barium • CT

Answer 144

• - Renal failure • - Hepatic failure • - Hemolysis • - DIC • - Metabolic acidosis Metabolic acidosis, renal and liver crap out, then blood says screw this and taps out

Answer 145

• - Burns, pneumonitis, esophageal perforation • - Hypocalcemia (calcium scavenged by free fluoride ions) • - Hypomagnesaemia (magnesium scavenged by free fluoride ions) • - Hyperkalemia (per Rosen's 9, due to inhibition of sodium-potassium ATPase and cellular destruction

Answer 146

pH: injury increases with pH <3 or >11 Concentration, volume, viscosity Duration of contact: greater with crystals/solid particles than liquids Presence of food in stomach

Answer 147

Phase 1 - initial necrosis occurs, with invasion by bacteria and leukocytes Phase 2 - vascular thrombosis Phase 3 - superficial layers of injured tissue begin to slough, lowering the tensile strength of the healing tissue and potentially risking delayed perforation Phase 4 - granulation tissue forms, collagen is deposit, strictures may form

Answer 148

Similar to a burn - Grade 1 - edema and hyperemia - Grade 2 - superficial ulcers, whitish membranes, friability, hemorrhage - Grade 2a - non circumferential - Grade 2b - nearly circumferential - Grade 3 - transmittal involvement with deep tissue injury, necrotic mucosa, frank perforation of the stomach or esophagus. 90% result in strictures

Answer 149

12 to 24 hours, endoscopy too soon is more likely to miss injury and too late is more likely to cause perforation

Answer 150

Cause liquefaction necrosis Generally easily penetrates tissues leading to protein denaturation, liquid saponification, and liquefaction necrosis. Minimal pain on ingestion so self harm tends to be more serious

Answer 151

- Cocaine - Amphetamines - MDMA/ecstasy - Methamphetamine/crystal meth - Ephedrine - Khat - Bath salts

Answer 152

DIMES Drugs Amphetamines, cocaine, caffeine, anticholinergics, lithium, ASA OD, EtOH withdrawal, DRESS syndrome, synthroid OD Infectious Meningitis, Encephalitis Metabolic Thyrotoxicosis, Hyperammonemia, Hypoglycemia, Hypoxia, Uremia Environmental Heat stroke Structural Hemorrhage, mass, stroke, trauma

Answer 153

DIMES Drugs Amphetamines, cocaine, caffeine, anticholinergics, lithium, ASA OD, EtOH withdrawal, DRESS syndrome, Synthroid OD Infectious Meningitis, Encephalitis Metabolic Thyrotoxicosis, Hyperammonemia, Hypoglycemia, Hypoxia, Uremia Environmental Heat stroke Structural Hemorrhage, mass, stroke, trauma

Answer 154

i. SSRIs ii. SNRIs iii. MAOi iv. TCA v. Dextromethorphan vi. Amphetamines vii. Lithium viii. Cocaine ix. Meperidine x. LSD xi. Buspirone xii. Ecstasy

Answer 155

Cyproheptadine

Answer 156

- Laxatives - Whole bowel irrigation (PEG)

Answer 157

Urine drug screen

Answer 158

Phentolamine (acute cocaine hypertension) Laparoscopic removal of packets

Answer 159

i. Serotonin syndrome ii. Neuroleptic malignant syndrome

Answer 160

CK, WBC, LFTs, VBG, lactate, Creatinine, electrolytes, coags, serum catecholamines

Answer 161

Stop offending agent Benzos IV fluids Cyproheptadine for severe cases

Answer 162

atherosclerosis, platelet aggregation, vasospasm, demand ischemia, LVH, dissection

Answer 163

agranulocytosis, thrombosis, ulcers esp. on the ear

Answer 164

Benzos, phentolamine 1mg q3min, IV nitro, hydralazine Avoid beta blockers due to unopposed alpha activity

Answer 165

Increased free water retention (affects release of vasopressin, SIADH) Increased free water consumption

Answer 166

ASA, DAPT Should be treated as ACS if meeting criteria as a significant number of cocaine users end up having angiographically significant disease

Answer 167

Plant derived alkaloids ex. Theophylline, caffeine

Answer 168

Zofran Haldol Gravol Metoclopramide Seroquel Risperidone Ativan

Answer 169

Hot shower/bath Capsaicin cream Stop smoking PO fluids

Answer 170

THC and CBD

Answer 171

Warfarin (increases INR) Fluoxetine (serotonin syndrome) Glyburide Acetaminophen (increased hepatoxicity) NSAIDs (less GI bleeding) Indinovir (reduces effectiveness) Verapamil (decreases activity)

Answer 172

LSD 'Natural' morning glory seeds, nutmeg, jimson weed, amanita muscaria mushrooms, buff toad, Mescaline, Salvia, THC/marijuana, peyote, Kratom

Answer 173

Ferrous gluconate 12%, ferrous sulfate 20%, ferrous fumarate 33%

Answer 174

<20 mg/kg benign 20-40mg/kg if asymptomatic likely benign >40mg/kg mild to moderate toxicity; needs referral >60mg/kg is considered severe

Answer 175

1: GI stage <6 hours - sx from direct caustic effects of iron, causes vomiting, abdominal pain, GI bleeding 2: Latent 6-24 hours - resolution of gastric symptoms, may be asymptomatic. May start developing systemic symptoms due to ongoing cellular toxicity and organ damage 3: Systemic 12-24 hours - return of GI symptoms, systemic symptoms including coagulopathy, lethargy, cardiovascular collapse, metabolic acidosis 4: Hepatic 2-5 days - fulminant liver failure 5: Obstructive 3-6 weeks - pyloric or bowel scarring, obstruction, gastric outlet obstruction

Answer 176

Rosens: <30 micromol/L mild, >60 micromol/L moderate , >90 micromol/dL considered severe

Answer 177

Whole bowel irrigation (iron can clump and form bezoars) Activated charcoal does not bind

Answer 178

Deferoxamine 15mg/kg/hr IV x 24 hours, repeated up to 6 g in the fist 24 hours S/E include hypotension, anaphylactoid reactions, ARDS, yersinia enterocolitis, oto and visual toxicity, vin rose urine

Answer 179

CNS: Encephalopathy, seizures, ataxia, HA, mood disturbances, peripheral neuropathy, absent DTR - due to segmental demyelination of degeneration of motor axons, decreased IQ Resp: acute lung injury and pulmonary edema if acute inhalation GI: Abdo pain, constipation, hepatitis, diarrhea Renal: ATN, nephritis, HTN, gout Heme: hemolytic anemia

Answer 180

Lead levels >70 ug/dL or >45 with clinical toxicity Chelation via succimer 10mg/kg q 8 PO x 5 days then 10mg/kg q 12 PO for mild cases Chelation via dimercaprol BAL 4mg/kg IM Q4H for 5 days for severe cases

Answer 181

Peanut allergy

Answer 182

Serum >90 (or >60 + systemically unwell), systemic toxicity, metabolic acidosis

Answer 183

Inorganic arsenic and arsine gas is toxic Elemental arsenic is poorly absorbed and non toxic, organic arsenic (in shellfish) is also non toxic

Answer 184

GI: nausea, vomiting, diarrhea (rice water), abdominal pain, jaundice, pancreatitis, hepatosplenomegaly Neuro: encephalopathy with seizures and coma, sensorimotor neuropathy (appears after months) Resp: Respiratory failure, ARDS, pulmonary edema Cardiac: dysrhythmias, prolonged Qt, Torsade's Renal: proteinuria, hematuria, oliguria, renal failure Derm: characteristic Aldrich-Mees lines (appears after months)

Answer 185

Intramuscular BAL is the preferred chelator Succimer can be given orally but is limited due to gastroenteritis symptoms Chelation is not useful for arsine gas exposures (needs hemodialysis and plasma exchange)

Answer 186

Organic: may be absorbed through the skin in chronic exposures Inorganic (mercury salts): caustic with oral ingestion Elemental (ex. Thermometers): volatile at room temperature, may deposit in the lungs. Poorly absorbed from the GI tract and poses no risk

Answer 187

Resp: tachypnea, wheezing, respiratory distress, burning sensation, pneumonitis, ARDS (esp. if inhalation or aspirated) CNS: Altered mental status, tremors, visual field changes, hearing loss, hyperreflexia GI: gastroenteritis, anemia, elevated in liver enzymes, abdo pain (especially if ingested) Renal: renal tubular necrosis

Answer 188

Aliphatic (straight chain): ex. Petroleum Aromatic (ring) ex. Solvents, toluene Halogenated (side chain) ex. Chloroform Terpene ex. turpentine

Answer 189

Camphor: neurotoxicity and seizures Halogenated: dysrhythmias and hepatotoxicity Aromatic: bone marrow suppression and leukemia Toluene: renal tubular acidosis Benzene: bone marrow toxicity ## Footnote Camphor = crazy, halogenated haptotoxic, aromatic anemia, toulene tubular, beneze bone marrow

Answer 190

Viscosity: lower viscosity = more toxic Volatility: higher volatility = more toxic Surface tension: lower surface tension = more toxic Chemical side chains: may produce their own symptoms ex. Arsenic Lipophilicity: more toxic if can cross BBB

Answer 191

Chemical pneumonitis, destruction of surfactant, atelectasis, bronchospasms, hypoxia (due to volatility), hyaline membrane formation, interstitial inflammation

Answer 192

Cardiac arrhythmias CNS depression, coma Hepatotoxicity Renal tubular acidosis Direct chemical burns, angioedema

Answer 193

No; GI effects less toxic than respiratory effect

Answer 194

1) asymptomatic after 6 hours 2) normal CXR

Answer 195

Avoidance of epinephrine Vasopressin and phenylephrine as preferred pressors Esmolol (beta blockers) for ventricular dysrhythmias

Answer 196

Symptoms: headache, nausea, vomiting, dizziness, myalgia, and confusion Presents with: altered mental status, including coma and seizures; extremely abnormal vital signs, including hypotension and cardiac arrest; and metabolic acidosis

Answer 197

Half life on room air is 5 h. NRB: 60-90mins HBO at 3ATA: 30min so: Room air: 10 hour NRB: 2 hour HBO: 1 Hour

Answer 198

Co-oximetry VBG Lactate Beta HCG CBC Electrolyte panel

Answer 199

o COHgb > 25% in adult o COHgb > 15% in pregnant patient, child Elevation in CO plus: - Associated Hemodynamic instability: MI, Arrhythmias - Associated Neurologic impairment: SZ, Coma o Decompression sickness I, II o Arterial Gas embolism o Increased wound healing (ex. Malignant Otitis externa) o Hydrogen peroxide ingestion

Answer 200

Focal deficits Seizures Memory deficits Personality changes Apathy

Answer 201

Extremes of age LOC

Answer 202

Bind de-oxyhemoglobin, preventing binding of O2 Shift Hbg-SpO2 curve to LEFT, impairing release of O2 in tissue Inhibits cytochrome complex leading to anaerobic metabolism Inhibits oxidative phosphorylation Binds myoglobin causing atraumatic rhabdo Generation of free radicals leading to inflammatory cascade Release of excitatory neurotransmitters Vasodilation and myocardial depression Lipid peroxidation

Answer 203

i) Simple asphyxiants: CO2; methane; nitrogen gas; nitrous oxide; noble gases (tachycardia, dyspnea, AMS) ii) Upper A/W irritants: Ammonia, Chloramine, Hydrogen chloride, Sulfur dioxide (lacrimation, cough) - these have high water solubility iii) Lower A/W irritants: Phosgene, nitric oxide (resp failure, ARDS - these have low water solubility iv) Cellular toxins: CO, CN, HS (seizures, coma)

Answer 204

Carbon monoxide

Answer 205

- CO - huffing/bagging/sniffing - other ingestion? - heat stroke? - based on this stem, hard to say what specifically they were looking for from the "hot and altered" list

Answer 206

- prolonged immobilization - hyperthermia - illicit drugs - CO (binds myoglobin and causes atraumatic rhabdo, pg 2041) - seizures

Answer 207

Hydrogen sulfide Pulmonary irritant, cellular asphyxiant, shifts curve to right Supportive, remove from source In severe cases can use sodium nitrite from cyanide kit

Answer 208

Increased production - Type A: poor perfusion: sepsis, mesenteric ischemic - Type B: no hypoperfusion - DKA, metformin - Seizure - Alcohol: liver dysfunction, alcoholic ketosis, toxic alcohols - Leukemia, lymphoma - Inborn errors of metabolism - Drug s/e: Ventolin, propofol - Tox: salicylate poisoning, carbon monoxide, cyanide, massive Tylenol Poor clearance: liver disease, renal disease

Answer 209

1. Asphyxiants (simple and chemical); cause damage through displacement of oxygen or direct chemical injury 2. Pulmonary irritants; cause damage through the destruction of the mucosal barrier of the respiratory tract, leading to inflammation

Answer 210

carbon monoxide, carbon dioxide, methane (natural gas), nitrogen (mines, scuba), nitrous oxide (inhalant of abuse), helium, neon

Answer 211

21%: None 16-12%: tachypnea, hyperpnea, tachycardia, reduced attention and alertness, headache - Dyspnea is not an early finding because hypoxemia is not as potent a stimulus to the respiratory centre as hypercarbia and acidemia 14-10% altered judgement, incoordination, muscular fatigue, cyanosis 10-6%: nausea/vomiting, lethargy, air hunger, severe incoordination - Lethargy starts as FiO2 falls below 10% <6: gasping, seizure, coma, cherry red skin (terminal)

Answer 212

Ammonia (fertilizer, combustion), hydrogen chloride (industrial), sulfur dioxide (photochemical smog)

Answer 213

Supportive care Beta agonist for bronchospasm

Answer 214

Nebulized 2% sodium bicarb solution for patients exposed to chlorine

Answer 215

Inhibits oxidative metabolism in the electron transport chain -> depletes ATP -> cellular hypoxia and death -> anaerobic metabolism (high lactate). No effect on hemoglobin

Answer 216

1. Anion gap metabolic acidosis 2. Elevated lactate 3. Elevated cyanide level 4. Similar PO2 levels between arterial and venous gas

Answer 217

1. Hydroxycobalamin 5g IV 2. Sodium thiosulfate 12.5g IV 3. Sodium nitrite 10mls 4. Amyl nitrite

Answer 218

Methemoglobinemia

Answer 219

Mild 5-10% - headache, nausea, dizziness, myalgia, and confusion. Consider if there is a group of people with a similar symptom Mod 10-30% - headache, weakness, dizziness, dyspnea, irritability, N/V, impaired judgement Severe 30-50% - coma, seizure death

Answer 220

All normal

Answer 221

Oxygen, hyperbarics if severe

Answer 222

Left (difficulty unloading O2): decreased temp, decreased 2-3 DPG, decreased H+ (alkalotic), CO Right (easier to unload O2): increased temp, increased 2-3 DPG, acidosis

Answer 223

- Urine lytes for nephrogenic DI - Thyroid function studies ** big increased risk of severe neurotox in hypothyroid - Creatinine (renal impairment) - Beta? - Tox screen

Answer 224

- Fluid resus (NaCl) - ECTR

Answer 225

CHECK QUESTION. WAS IT REALLY DM THEY ASKED ABOUT? Regardless, NMS and serotonin syndrome could result.

Answer 226

Whole bowel irrigation NG, 2L PEG per hour until effluent is clear *** Rosen's very clearly does not endorse WBI, but 2016 paper by Dr. Gosselin does.

Answer 227

NMS - antipsychotics MH - volatile agents, succinylcholine SS - SSRIs, MAOIs, lithium, dextromethorphan, meperidine, tramadol

Answer 228

False not metabolized, excreted renally 95% unchanged

Answer 229

Tremors Clonus Hyperreflexia Somnolence Extrapyramidal symptoms Coma Seizures

Answer 230

Bradycardia Junctional rhythm / AV blockade ST changes QT prolongation Flattened or inverted T-waves Brugada pattern on ECG Ischemic changes on ECG

Answer 231

BZD, carbamazepine, diuretics, ACEi, ARB, NSAIDs

Answer 232

Diabetes insipidus, hypothyroid, hypercalcemia, hyperparathyroidism

Answer 233

Acute: more GI symptoms predominate ex. Nausea, vomiting, diarrhea Chronic: more neuro symptoms; these patients are already saturated

Answer 234

Acute >4.0 mEq and chronic >2.5 [Rosens] - >4.0 and impaired kidney function [ExTrip - no specific chronic level] - Can consider at low levels if symptomatic Severely symptomatic Renal impairment Unable to tolerate fluid hydration

Answer 235

Dystonia will usually respond within 30 minutes to diphenhydramine 25 to 50 mg or benztropine 1 to 2 mg intravenously, intramuscularly, or orally. Lorazepam 1 to 2 mg IV may also be effective in patients who do not respond within 1 hour to diphenhydramine or benztropine.

Answer 236

Extrapyramidal: akathisias, parkinsonism, NMS, tardive dyskinesia Prolonged QtC

Answer 237

Prolonged Qtc

Answer 238

Dopamine + TCA list Dopamine (main effect) Muscarinic (anticholinergic symptoms) Histamine (sedation) Alpha (vasodilation) Sodium channel (wide QRS) Potassium channel (prolonged Qtc) Gaba (leads to seizures Serotonin

Answer 239

First: Dopamine >serotonin, higher incidence of EPS, more sedating ex. loxapine, haloperidol Second: Serotonin >dopamine, lower incidence of EPS, less sedating but more metabolic side effects, treats positive and negative symptoms ex. Clozapine, quetiapine, olanzapine, aripiprazole

Answer 240

Rapid dose escalation, cumulative drug dosage, high potency antipsychotics, prior brain injury, poorly controlled extrapyramidal symptoms, previous episodes of NMS

Answer 241

FARM Fever, autonomic dysfunction, rigidity with rhabdomyolysis and CK>1000, mental status changes

Answer 242

NMS: patient rigid, always has a fever, diminished reflexes, can occur at any time SS: no rigidity, fever late sign, hyperreflexia, temporally related to acute overdose

Answer 243

Serotonin syndrome Hypertonicity Myoclonus Seizures Apnea

Answer 244

- Yawning - Piloerection - CNS excitation (e.g. restlessness, agitation, dysphoria, insomnia) - Tachypnea - Mydriasis - Tachycardia - Hypertension - Nausea - Vomiting - Diarrhea - Abdominal cramps - Myalgias

Answer 245

- Suboxone or methadone - IV fluids - Clonidine (for tachycardia, hypertension, sweating, anxiety, restlessness) - Ondansetron (for nausea/vomiting)

Answer 246

Potential precipitation of withdrawal symptoms due to suboxone containing naloxone, which has little to no activity when administered sublingually

Answer 247

Alpha 2 -agonist, can be used to suppress sympathetic hyperactivity and shorten the duration of withdrawal.

Answer 248

11 items Tachycardia Chills/flushing, mydriasis, bone and joint aches, runny nose, GI upset, tremor, yawning, goosebumps Restlessness, anxiety

Answer 249

Suboxone is a partial opioid agonist with high affinity Provides some stimulation at the opioid receptors preventing symptoms of withdrawal Precipitated withdrawal occurs when suboxone is given while there is still native opioid in the system. The high affinity suboxone displaces the existing opioid. The suboxone is a less potent stimulator of the receptor, so overall the patient feels profound withdrawal

Answer 250

Nothing if ingested orally Deactivates the suboxone if given IV

Answer 251

Generally 0.4 (can range 0.04-4mg) target to RR>10 If multiple doses are needed an infusion can be started at 1/3 of the wake up dose

Answer 252

S = Salivation L = Lacrimation U = Urinary incontinence D = Diarrhea/Diaphoresis G = Gastrointestinal cramps E = Emesis (Killer) Bs: Bradycardia/bronchorrhea/bronchospasm

Answer 253

(1) Decontamination (2) Supportive care with an emphasis on respiratory stabilization (3) Reversal of acetylcholine excess (atropine) (4) Reversal of toxin binding at receptor sites on the cholinesterase molecule (2-PAM)

Answer 254

Atropine, 2-PAM

Answer 255

Compounds bind to acetylcholinesterase, inhibiting the break down of acetylcholine and causing a cholinergic crisis

Answer 256

Muscarinic: SLUDGE DUMBELLS - salivation, lacrimination, urinary incontinence, defecation, GI upset, emesis, diaphoresis, urination, bronchorrhea/bradycardia/bronchospasm, excitation, lacrimination, lethargy, salivation Nicotinic: MATCH - muscle fasciculations, adrenergic stimulation, tachycardia, cramping, hypertension; may eventually lead to paralysis with prolonged stimulation

Answer 257

Occurs when an agent forms an irreversible bond with the acetylcholinesterase leading to prolonged effects. Occurs with organophosphates but not carbamates

Answer 258

Decontamination: dermal absorption is contributory; remove clothes and flush skin. GI decontamination is often not helpful Supportive care: suctioning, correction of electrolytes

Answer 259

Atropine 1mg doubling q5 mins until secretions dry up, with infusion of 10-20% of the cumulative dose over an hour Pralidoxime 1mg bolus (limited evidence)

Answer 260

1. Highly lipid soluble and absorbed dermally. Can result in seizures, neurologic sx, risk of V tachy due to myocardial sensitization to catecholamines. Needs decontamination, betablockers for arrhythmias 2. Presents like sympathomimetic toxidrome: hyperthermia, tachycardia, diaphoresis, agitation, rhabdo, yellowing of skin, hypoglycemia (used as weight loss medication) 3. Diffuse fasciculations can lead to rhabdo, hyperthermia, hypermetabolic state 4. Risk of pulmonary injury, concentrates in the lung with toxicity through oxygen free radicals, avoid excessive oxygen, common agent of suicide 5. Allergic like reaction; dermatitis, wheezing, vomiting 6. Poorly absorbed dermally, absorbed through GI tract

Answer 261

<2 do not use >2 10% DEET >30% DEET can result in seizures

Answer 262

Anticoagulants: 90% of all exposures, managed with RBCs, transfusion, PCC, vitamin K Non anticoagulants: uncouple oxidative phosphorylation ex. Arsenic, barium, phosphorus

Answer 263

White mushroom with a ring at the bottom and veil on the stalk Sx include severe liver toxicity, renal toxicity, GI symptoms Decontamination and supportive care, can consider NAC, needs serial monitoring of liver enzymes

Answer 264

Brown ribbed mushroom, looks similar to true morel Sx include refractory seizures due to the inhibitory effects on pyridoxine. May also cause hepatotoxicity and methemoglobinemia Seizures managed with IV pyridoxine 5g

Answer 265

1. Hallucinogenic 2. Hallucinogenic 3. Renal failure 4. Cholinergic toxidrome 5. Disulfram reaction

Answer 266

Amanita phalloides, gyromitrin

Answer 267

1. Anticholinergic toxidrome 2. Contains colchicine; GI symptoms -> multi organ failure -> sepsis 3. Cardiac glycosides, like digoxin toxicity 4. Intractable and life threatening seizures 5. Nicotinic/cholinergic poisoning 6. Vomiting, mucosal and airway edema 7. Ricin if chewed 8. Sodium channel blockage can lead to arrhythmia and cardiac arrest 9. Sodium channel blockage can lead to arrhythmia and cardiac arrest

Answer 268

Benzos, barbiturates, GHB, chloral hydrate, rohypnol, zopiclone

Answer 269

Co-ingestions (esp. those suspected at lowering seizure threshold) Chronic benzos use Seizure Ongoing withdrawal Hypersensitivity to flumazenil or benzos Muscular blockage

Answer 270

Pear odor, CNS depression, arrhythmias

Answer 271

Insulin, sulfonylureas (ex. Glicizide, glyburide), meglitindes

Answer 272

Octreotide; inhibits insulin release

Answer 273

How often have you had a drink of alcohol in the past year? (Monthly, 2x a month, 2x a week, 4x a week) If you were drinking in the past year, how many drinks did you have on a typical day? )0,3,5,7,10) How often did you have 6 or more drinks in the past year? Never, monthly, weekly daily)

KC Tox Flashcards

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