Toxicology Flashcards

Question

Snake Bite Mx

Answer 1

First Aid Pressure bandage + Immobilisation Take to facility with antivenom + 24h lab service Initial Ix * Clinical exam * Iv access x 2 * Consider VDK * Bloods - G+S, FBC, EUC, LFTS, coags inc Fibrinogen, CK Ongoing Monitoring * Features of envenomation or multiple bites or severe envenomation - give one vial of polyvalent or monovalent anti-venom * If no features of envenomation clinically or on labs: * Rpt clinical assessment * Rpt bloods 1hr after removal of PIB * 6 and 12 hours post bite, before considering discharge -vast majority of cases of severe envenoming are likely to be detected with repeat assessment over 12 hours

Answer 2

Early onset toxicity * Calcium channel blockers / clonidine * Amphetamines/ Ecstacy / ICE / Cocaine * Na channel blockers - propanolol, KILL * TCA - amitriptyline, dothiepin * Opioids / methadone * Theophylline * Sulphonlyureas Others include: * Benzodiazepines * Olanzapine/clozapine * Hydroxychloroquine Delayed onset * SR CCBs * SR opioids/methadone * Sulfonylureas

Answer 3

Toxic alcohols - EG, Methanol Hydrocarbons * Petrol, turpentine, kerosene Essential oils - Eucalyptus, tea tree oils Organophosphates Carbamate insectcides Paraquaat Caustic - NaOH Camphor - mothballs Napthalene - mothballs Strychnine - rat pesticide Oil of wintergreen (1ml = 1.4g aspirin)

Answer 4

**Aliphatic** - eucalyptus, essential oils **Aromatic** - benzene, toluene **Halogenated** - carbon tetrachloride, mehtylene chloride, chloroform **Alkane** - propane, butane Toxicity Oral - GI irritation, high risk aspiration Inhalation - Dermal - dermatitis, chemical burns Clinical features: Resp - cough, inc RR, SOB, wheeze, low sats Prolonged inhalation → asphyxia CNS - euphoria, CNS depression, seizures Renal - acute - HAGMA, chronic - RTA (NAGMA) and low K+ Hepatic - halogenated hydrocarbons CVS - palpitations, Porlonged QT, arrhythmia, sudden sniffing death sydrome (rare) Metabolic - toluene causes NAGMA (RTA), HAGMA, hypoK Mx Supportive Decontaminate - remove clothing Seizures - BZ Aspiration pneumonitis - O2, bronchodilators, NIV or I+V - No role for ABx or steroids Cardiotoxicity - more likely with inhalation - Prolonged QT - correct electrolyte disturbances - Consider short active BB (esmolol or metoprolol) for refractory VT - Cardiac arrest - adrenaline may worsen myocardial sensitisation Hepatotoxicity - NAC may be hepatoprotective - clove oil, halogentated hydrocarbons Disposition Normal CXR + Asx D/C after 6 hours Consider MH assessment

Answer 5

**Toxic dose** MILD 150-300mg/kg Severe \>300mg/kg Death \>500mg/kg **Clinical presentation:** * GI - N/V/dyspepsia (GI distress) * Metabolic - resp alkalosis then met acidosis, hypoglycaemia, Hypokalaemia * CNS - tinnitus, agiation, seizures, cerebral oedema * Other - APO, renal failure, hepatic failure Mx 1. Start urinary alkalinization 2. Correct hypovolemia o Urine output 2-3 mL/kg/hr 3. Keep [K] \>4.5 mM, correct any hypomagnesemia - **Correct electrolytes before bicarb or intubation** 4. Give glucose for any CNS changes 5. Haemodialysis Endpoints Resolution of clinical features, acid base status, BSL and K+ Decreasing ASA levels - serial

Answer 6

Topical Oil of wintergreen Willow Bark Bismuth salicylate

Answer 7

Uncoupling of mitochondrial oxidative phosphorylation - Metabolic rate increase → metabolic acidosis - Tissue glycolysis → hypoglycemia and ketosis * NB Only un-ionized particles can cross the BBB and accumulate in the CNS and other tissues. * Because salicylic acid has a pKa of 3.5, the majority of salicylate is ionized and unable to enter tissue at the physiologic pH of 7.4. * However, as serum pH decreases, more particles become un-ionized and cross the BBB / enter tissues Clinical manifestations * Seizures, coma, death * Cerebral oedema * Neuroglycopaenia * Direct nephrotoxicity * Salicylate induced pulmonary oedema * Tinnitus

Answer 8

* * Serum salicylate levels: o >7.2 mmol/L) in acute o > 6.5 mmol/L + ARF **Severe toxicity**: * Altered mental status, including coma, seizure(s) * Renal or hepatic failure * Pulmonary oedema * Severe acid-base imbalance (pH <7.2) * Rapidly rising serum salicylate level * Failure to respond to decontamination or urinary alkalinisation

Answer 9

1. Respiratory alkalosis - direct stimulation of the medullary respiratory centre 2. Metabolic acidosis - multifactorial o Loss of bicarb - renal o ASA itself that is a weak acid o Impaired Kreb cycle -> increasing lactate and ketones o Impaired ability to excrete acids in urine 3. Respiratory acidosis - from cerebral toxicity, neuroglycopenia, salicylate induced pulmonary oedema 4. Metabolic alkalosis from GI losses

Answer 10

Total vs ELEMENTAL * Ingesting \<20mg/kg no symptoms * Mild/moderate toxicity: 20-60 mg/kg * Severe: \> 60mg/kg * Potentially lethal \> 120mg/kg * **LD50 (50% mortality) = 200-250 mg/kg** *** Children - 130mg can cause sig effects** Toxic mechanism * **Direct GI caustic injury** * **Uncoupling oxidative phosphorylation in heart/ CNS / liver** STAGES - see flashcard Ix AXR - confirm or quantify ingestion Iron level 4-6hrs Mx Supportive - replace fluid losses, anti-emetic Specific: - Polyethylene glycol - whole bowel irrigation - AC - does not bind iron **- Antidote - desferrioxamine** - Systemic toxicity - Iron level \>90 umol/L (500 mcg/dL) Disposition * Children \< 40mg/kg + Asx can be managed from home * Adults \< 60mg/kg + Asx at 6hrs, d/c * Sx - WBI * Systemic toxicity - IV chelation + ICU * Consider endoscopic removal for large ingestions

Answer 11

Indications: - Systemic toxicity - Fe levels \> 90 umol/L or 500mcg/dL Mech - binding of iron to make ferrioxamine, excreted in urine. Turns urine vin-rose colour Infusion - 15-35mg/kg/hr for 24hrs Adverse effects: 1. Rash at infusion site 2. Hypotension 3. Anaphylactoid rxn 4. ARDS 5. Yersinia sepsis

Answer 12

Killer B's = bronchorrhoea, bronchospasm, bradycardia **MUSCARINIC** Diarrhoea Urination Miosis Bronchhorrhoea Bronchospasm Emesis Lacrimation Salivation **NICOTINIC** Mydriasis Tachycardia Weakness Tremors Fasciculations Seizures Somnolence

Answer 13

OP exposure results in MOD, Resp muscle weakness and bronchorrhoea -> death Organophosphates: Chlorpyrifos, Fenthion, Malathion, Parathion Carbamates: Aldicarb, Carbofurna, Carbosulfan Clinical features Time of onset of toxicity - variable Early death due to excessive resp secretions and T2RF from muscle paralysis Sx Muscarinic - killer B's, DUMBELLS Nicotinic - MTWTFS Mx DO NOT delay resus with decontamination PPE - contact precautions Resus - HF O2 - IVF for Hypotension + bradycardia - Seizures - Resp failure - bronchorrhoea / bronchospasm Antidotes - **Atropine** - 1.2mg for adults, double dose q5min - Infusion at 10-20% total dose per hour - kids = 50mcg/kg - End point = drying of secretions, resolution of hypotension or dvpt of ACh toxicity - Pralidoxime - D/W tox as not effective for all OPs - works better for chlorpyrifos, diazinon) - 2g for adults over 15 mins - infusion at 500mg/hr - kids = 25-50mg/kg, then infusion 10-20mg/kg/hr - End point = unlikely effective \> 24hrs Complications Anticholinergic delirium

Answer 14

ACUTE - Muscarinic - killer B's, DUMBBELS - Nicotinic - fasciculation, tremor, weakenss, resp muscle paralysis, tachycardia, hypertension - CNS - agitation, coma, seizures - Resp - cholinergic syndrome, chemical pneumonitis if hydrocarbon solvent aspiration INTERMEDIATE D2-4 - delayed onset paralysis DELAYED NEUROTOXICITY 1-5 weeks - delayed neuropathy CHRONIC ORGANOPHOSPHATE NEUROPSYCH DISORDER Follows acute intoxication or chronic low level exposure

Answer 15

**INDICATIONS** * Hyperkalaemia * Treatment of sodium channel blocker overdose (e.g. tricyclic overdose) * Urinary alkalinisation (salicylate poisoning) * Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses) Controversial * Cardiac arrest (in prolonged resuscitation + documented severe metabolic acidosis) * Diabetic ketoacidosis (very rarely, perhaps if shocked and pH \< 6.8) * Severe pulmonary hypertension with RVF to optimize RV function * Severe ischemic heart disease where lactic acidosis is thought to be an arrhythmogenic risk **ADVERSE EFFECTS** * hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) * hyperosmolality (cause arterial vasodilation and hypotension) * volume overload * rebound or ‘overshoot’ alkalosis * hypokalaemia * ionised hypocalcaemia * CSF acidosis * hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) * severe tissue necrosis if extravasation takes place * bicarbonate increases lactate production by: — increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis — shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues

Answer 16

**O**rganosphosphates, **O**ral hypoglycaemics **T**CAs **I**nsulin, isoniazid **S**ympathomimetics, salicylates **C**yanide, CO, cocaine, camphor, chlorinated hydrocarbons **A**mphetamines, anticholinergics **M**ethanol, methylxanthines **P**ropanolo, PCPs **B**enzo withdrawal, botanicals, bupropion **E**TOH withdrawal, EG **L**ithium, lignocaine **L**ead

Answer 17

* pH < **7.3** * Lactate > **3**.0 mmol/L after resus * INR > 6.5 * Creat > **3**00 umol/L or oliguria * Grade **III** or IV encephalopathy * PO4 \> 1.2 mmol/L at 48-96 hrs Other considerations (Not part of criteria) * Oliguria * Hypotension despite IVF resus * Hypoglycaemia * Severe thrombocytopaenia * Altered mental state with no other sedative co-ingestions

Answer 18

Acids = coagulative necrosis Alkalis = liquefactive necrosis \>60ml HCl can be fatal = \> metabolic acidosis, multiorgan failure and perforation Hx Timing, concentration, volume, viscosity, pH, duration contact, ingested w/ food Ax Oral pain, AP, vomiting, drooling common CP, wheezing, cough, resp distress, horseness, odynophagia, dysphagia, stridor and dysphonia Decontamination Not useful Dispo Asx = obs for 6 hrs and then psych Sx - below Ix VBG IV ABx for perforation CXR - erect CT Endoscopy betw/ **12-24hrs** **NO NGT until after OGD**

Answer 19

Early * Metabolic acidosis * Electrolyte disturbances * Dysrrhythmias * Airway compromise * GI perforation Subacute * Strictures Late * Oesophageal cancer

Answer 20

Hb containing Ferric (Fe3+), not ferrous iron (Fe2+) Drugs/Toxins cause MetHb * Congenital - Hb M, NADH depedent Met Hb reductase deficiency * Acquired * Nitrites, (nitrates) * Aniline dyes - inks, paints, varnish * LA agents - prilocaine, procaine * Abx - sulfonamides, dapsone * Phenytoin * Quinones - chloroquine, primaquine * Toxins - propanil (herbicide) Presentation Cyanosis (Sats ~85%) not responding to O2 therapy Signs and symptoms of hypoxia Chocolate brown blood Diagnosis with VBG - MetHb * \<15% - nil Sx * 15% - Cyanosis * 30% - Resp distress, SOB, tachycardia * \>60% - Resp distress, seizures, confusion, arrhytmias, hypotension * \>70% - lethal Mx * Supportive / resuscitative care * Consider charcoal if recent ingestion * **Methylene blue 1mg/kg over 5min** * Up to 2mg/kg, rpt q30-60 mins * **CI in G6PD def** * Hyperbaric oxygen therpay * Exchange transfusion

Answer 21

CN binds to Fe3+ ion → anaerobic metabolism → **severe lactic acidosis** **1mg/kg of cyanide salt = potentiall lethal** Sources * House fires +/- CO poisoning * Industry - mining, plastics * Plants - amygdalin * Medical - Nitroprusside * Chemical warefare Clinical Features * Mild tox * Headache, vomiting, tachycardia, dizzy, SOB * Mod-severe tox * Collapse, seizures, resp distress, confusion, severe met acidosis, CVS collapse, arrhythmias, death Bloods levels * Consider if VBG - sats \> 90% - unable to use O2 at tissue level * Correlation between lactate levels and toxicity * \> 10mmol/l indicates severe poisoning * CN levels * \>20 - symptomatic * \>40 - potentially toxic * \>100 - lethal Mx * Supportive/resus care * Airway - HF O2, I+V * Hypotension - IVF bolus * Decon * HCN = gas = no role * 50g AC for CN salts \< 2hrs * Antidotes * Mod - Severe tox = Hydroxycobalamin + Na thiosulfate * Hydroxycobalamin * 5mg IV in 200mls Saline over 15 mins * Up to 15mg * Sodium thiosulfate * 12.5 IV over 10 mins * Dicobalt edetate * 300mg IV over 1 min + 50% dextrose * End points * Improved LOC * Haemodynamic stability * Resolution metabolic acidosis * Dispo * ASx - monitor 6 hours * Severe poisoning - ICU

Answer 22

Sources * Fires, exhaust fumes, machinery closed spaces * Smoking - hookah (30%), smoking 10-15%) Vulnerable tissues - CNS, CVS, foetus Clinical Features * General - weak, N+V, headcahe, cherry red * CNS - dizzy, ataxia, confusion, coma * CVS - ST, AF, PVCs, ventricular arrythmias, MI * Severe - ARF, rhabdomyolysis, hepatic injury * Delayed neurologic sequelae * Impaire judgement, memory, concentration, dementia Mx * Supportive / resus * NRB O2 or I+V with 100% O2 for 6 hrs * Hypotension Rx * HBO * COHb > 25% or 15% pregnancy * End point - COHb \< 5%

Answer 23

Acute toxicity presents with GI symptoms progressing to life-threatening arrhythmias and CV collapse **Lethal ingestion:** >10mg ingested Serum digoxin level > 15nmol/L K > 5.5mmol/l KIDS > 75mcg/kg Progression 2-4h - GI symptoms 6h - peak serum 8-12hrs - CV collapse Clinical features: GI CVS - increased automaticity (VEBs, bigeminy, VT), bradydysrrhythmias (Slow AF, AV block), hypotension CNS - lethargy, delirium, confusion Mx * Decontamination * AC if < 2hrs OR < 4hrs massive ingestion * Arrhythmias * Brady - atropine, adrenaline, pacing * Tachy - MgSO4 or lignocaine 100mg slow IV push * Hyperkalaemia * Consider calcium **only** with ECG changes + severe hyperK+ * Antidote * Digibind (see flashcard)

Answer 24

At risk Elderly with multiple co-morbidties Meds affecting K+ homeostasis CVS drugs - BB, CCB Poor cardiac and renal function Clinical features Those of acute toxicity Visual - dec VA, yellow halos

Answer 25

INDICATIONS * Cardiac arrest * Ventricular arrhythmias * High degree AV block * Acute : [Digoxin] >15nmol/L * Chronic: [Digoxin] > 3ng/mL * K+ > 5.0mmol/l * Acute K+ \> 5.5 assoc 100% mortality Cardiac arrest ACUTE: 5 vials IV push, rpt q5-10min CHRONIC: 2 vials IV push, rpt q5-10min Non-arrested pt 1-2 vials in 100ml 0.9% saline over 30mins ENDPOINT Resolution of cardiotoxicity + GI symptoms

Answer 26

Effect * Downsloping ST depression with a characteristic “reverse tick” * Flattened, inverted, or biphasic [T waves](https://litfl.com/t-wave-ecg-library/) * Shortened [QT interval](https://litfl.com/qt-interval-ecg-library/) Toxicity * SVT (inc automaticity) * Slow ventricular response (vagal tone) * [Frequent PVCs](https://litfl.com/premature-ventricular-complex-pvc-ecg-library/) (the most common abnormality), including ventricular bigeminy and trigeminy * [Sinus bradycardia](https://litfl.com/sinus-bradycardia-ecg-library/) * Slow [Atrial Fibrillation](https://litfl.com/atrial-fibrillation-ecg-library/) * Any AV block * *Regularised AF* = AF with complete heart block and a junctional or ventricular escape rhythm * [Ventricular tachycardia](https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/), including polymorphic and **bidirectional VT**

Answer 27

Reversible inhibition of Na-K-ATPase pump, inhibiting Na-Ca exchange →** increased intracellular Ca → inc myocardial inotropy / extracellular K+** Toxic doses → after depolarisations → inc risk of **arrhythmias** and shortened refractory period → **increased automaticity** **Inc parasymp tone** → SA/AV nodal block

Answer 28

Significant OD produces rapid onset CVS and CNS toxicity Clinical toxicitiy worse with acidosis >5-10mg/kg - Tachycardia, mild CNS depression, agitation, mydriasis >10mg/kg - Anticholinergic features >20mg/kg - Seizures, coma, hypotension, arrhythmias and death ECG R wave in aVR >3mm - most specific Sinus tachycardia, increased QRS and QT intervals QRS > 120ms inc risk seizures, > 160 inc risk ven arrhythmias Mx Mainstay is supportive care with intubation and hyperventilation, IV NaHCO3, BZ for seizures and ALS for ventricular arrhythmias Resus - Seizures - BZs and NaHCO3 if not responding ot benzos - Hypotension - IVF + inotropes - Na Channel blockade - NAHCO3 - Recurrent ventricular arrhymthmias - adrenaline and lignocaine 100mg when pH > 7.5 and then ECMO referral Decontamination - AC if < 1hr post ingestion or after I+V

Answer 29

Found: wheel cleaner, glass etching, cement/brick cleaner Any concentration + > 5% TBSA = risk systemic fluorosis >50% concentration + 1% TBSA = risk of systemic fluorosis INH - irritation -> pneumonitis -> ARDS PO - GI corrosion, hypo Mg, hypo Ca, hyper K, inc QTc -> arrhytmias / cardiac arrest, seizures Ocular - pain, erosion, tissue damage Mx * Decontamination - remove clothes, wash skin, irrigate eyes 20 mins * Ingestion / systemic features * Correct electrolytes * Ca gluconate 10% 30mls * MgSO4 * Aggressive K+ Mx * Cardiac arrest - Ca + Mg every 5mins * Dermal * Ca gluconate gel * SC or regional infiltration * Intra-arterial infusion for limb exposure * Inhalational * 1ml Ca gluconate in 3ml saline nebulised

Answer 30

> 0.1mg/kg potential toxicity and death > 0.8mg/kg -> MOF + death Clinical * 0-24h - GI Sx, dehydration, ARF + leucocytosis * 24-72h - CV collapse, BM failure, ARF, Liver failure, cerebral oedema, rhabdomyolysis, Low K, Ca, Mg * >1week - leucocytosis, alopecia, neuropathy, myopathy Mx 1. Offer AC to all and may need ETT to facilitate this 2. Replace IV fluid losses 3. Electrolyte replacement 4. Enhanced elimination a. MDAC b. HD for acid-base (does not eliminate colchicine)

Answer 31

Most lethal envenoming creature in the world Death within 20-30 mins if severe envenomation Toxinology Envenomnation caused by microscopic stinging capsules called nematocysts Major stings > 50% limb involvement Children more likely to incur severe envenomation given smaller BSA Clinical Local - pain, dermal lesions (whip like whelts), lymphadenopathy Systemic - CNS - HA, confusion, seizures, coma - CVS - hyper/hypotension, arrhythmias, cardiac arrest - Resp - Resp arrest - MSK / skin rxns Ix Bloods - inc CK and troponin ECG CXR for resp symptoms Mx Cardiac arrest Mx First aid - **Vinegar** prevents further discharge from nematocysts - Washwound with **salt** water (fresh water causes discharge from nematocysts) - Ice packs - Removal of tentacles - Analgesia - opioids - MgSO4 Antivenom inidcated for collapse, hypotension, arrhythmias, cardiac arrest - 6 vials for cardiac arrest - 3 vials for cardiac arrhythmias Dispo Asx and no local pain for 2 hrs can be D/C ICU for others ## Footnote NB **Portuguese Man O War** - Physalia physalis - Severe local pain but no fatal enveonmations. NO Vinegar as it increases nematocyst discharge, otherwise Mx same.

Answer 32

Inhabits northern Autralia from WA (Geraldton) to QLD (Mackay) Deaths occur from catecholamine surge rather then venom itself Clinical feature Local - initial sting not felt, pain dvps at 20-30 mins, resolves 6-12 hours Local - rsah Irukandji Syndrome - N/V/MSK pain - Hyperadrenergic response - Anxiety, dysphoria, HTN, tachycardia, - Rare: ICH, Cariogenic shock, APO Ix ECG Bloods - CK, trop Echo for trop rise Mx Vinegar - not great evidence Analgesia - opioids, MgSO4 HTN Mx - BZ, Clonidine Dispo 6hr obs - if well and Asx D/C Any cardiac involvement HDU/ICU

Answer 33

Shallow coastal waters of Australia Lethal antivenom -> rapid paralysis Toxinology Tetrodotoxin in saliva of BRO bite - venom introduced from beak, not tentacles Clincal Features Collapse and paralysis after seemingly monior bite = CLASSIC Local - bite site painless Neurotoxicity = RAPID, PROGRESSIVE, SYMMETRICAL, DESCENDING - Early = numbness, paraesthesia tonuge/lips - Progressing = Bulbar Sx = Ptosis, diplopia, swallowing difficulty - UnRx = paralysis, T2RF -> hypoxic arrest Mx Paralysis resolves spontaneously within 24 hours ABC - I+V PBI IVF/inotropes for hypotension ADT NO antivenom

Answer 34

Lithium toxicity comes in a three flavors: acute, chronic and acute on chronic. Each form will have a different presentation as well as management. Lithium levels are often unreliable in terms of guiding management and must be taken in context with symptoms and time of ingestion (in acute overdose). IV fluids are a cornerstone of management as increasing intravascular volume and increasing renal elimination are critical. Hemodialysis is indicated for a lithium level > 5 mEq/L or a level > 4 mEq/L in a patient with renal failure. However, dialysis decisions should be made in conjunction with a toxicologist. Two forms of lithium Standard release peak 1-2 hours Extended release peak 4 hours Toxicokinetics 95% renal excretion Increased lithium levels often result outside of overdose when the patient takes a kidney hit (infection/medications) and GFR goes down. Toxidrome: Mild toxicity - N/V/D, AP, hyperreflexia, tremor, agitation, muscle weakness Mod toxicity - stupor, rigidity, hypertonia, hypotension Severe toxicity - ataxia, confusion, somnolence, myoclonus, coma, convulsions Chronic Li toxicity – can develop nephrogenic DI Pearl: make sure you don’t send a lithium level in a lithium salt tube – typically a green top in the US Management Decon: no role for AC, but conisider WBI ingestions > 50g SR and < 4hrs **IV fluids** aiming for 2-3ml/kg Cease nephrotoxic meds - NSAIDs, ARBs, ACEi, diuretics Monitor electrolytes and fluid balance Dialysis - D/w toxicologist: - Neuro Sx or Dysrrhytmias **regardless** of [Li] - Lithium >4 mmol/l + renal impairment - Lithium >5 mmol/l and rising - End point = [Li] < 1 mmol/l

Answer 35

Snake bites < 4hrs presentation Broad 15cm bandage over bite site covering entire limb using smae pressure as for sprained ankle Immobilise limb and then patient for banddage to be effective The pressure bandage should only be removed if either: 1. Antivenom therapy has started 2. Clinical and Bloods confirm no systemic envenoming

Answer 36

Key Ix Coags - INR, PT, aPTT, D-dimer, fibronigen FBC - RBC feagmentation UEC, LFTs LDH CK Urinalyis - detect myoglobinuria Antivenom: Rpt above Ix at 6 and 12 hours post Rpt every 24 hrs until resoled NO Antivenom: 1 hour after removal of PIB, then 6 and 12 hrs post bite Coags - INR, APTT CK

Answer 37

Amanita phylloides One mushroom can kill Heat stable - not inactivated by cooking Clinical Presantation 0-5 h - ASx 5-24h - N/V/D/AP, mild LFT inc, ARF 1-7d - Fulminant Hepatic Failure, ARF, Encephalopathy and death Mx Discuss all cases w/ TOx Support - IVF gor GI losses Decon - charcoal may benefit up to 72 hrs Antidotes - NAC, SIlibinin (some benefit from rifampicin or benpen) Liver transplant - D/W Tx if ALT > 250 Dispo - if ASx 24 hrs post w/ normal bloods then D/C

Answer 38

Rapid onset of hepatic synthetic failure + encepaholopathy Causes Drugs - Paracetamol, NSAIDS, amanita, ABx, dapsone, halothane Alcohol Viruses - EBV, CMV< HIV, Hep B/C, HSV Extras - Obstetric - HELLP, acute fattyl iver of pregnancy - Autoimmune - a1-antitrypsin - Vascular - Budd-Chiari Sepsis Ix FBC, UEC. LFTs, CMP Hepatitis, HIV, EBV, CMV screen Bloods cultures Urine Drug screen ANA, SMA Serum protein electrophoresis Serum copper, caeruloplasmin Mx Supportive - A - intubate if encephalopathic - B - ventilation, may have pleural effusions - C - IVF and Na+ restriction + diuretics - D - BGL monitoring - E - nutrition, correct electrolyte imbalances Antidotes Liver Transplant Paracetamol - pH < 7.3 / INR > 6.5 **OR** Cr > 200 **OR** > gd III encephalopathy Complications Cerebreal oedema Coagulopathy GIH Renal failure Hypoglycaemia Electrolyte abN Resp failure: impaired ventilation, coma, pl effusions, ARDS, aspiration, sepsis

Answer 39

Potent SNRI OD can be fatal - seizures / CVS toxicity in large OD Risk <3g ~ 10% seizure risk >3g ~ 30% risk of seizures >4.5g = 100% risk seizures >7g - Hypotension and LV dysfunction Clinical Features of serotonin toxicity, usually prominent if other serotinergic drug Seizures - may be delayed up to 16hrs, preceded by agitation, tachycardia and tremor NO Coma Hypotension and LV dysnfunction after large OD Resolves in 24hrs Mx Benzo for agitation / tachycardia / tremor and seizures Temp Mx IVF for hypotension +/- inotropes Decon: AC 50g for >4.5g ingestions within 2 hrs presentation Elim: WBI if > 8g ingestion Dispo: < 2g D/C after 8 hours > 2g 16-24 hrs observation

Answer 40

Mx PIB Antivenom TIG

Answer 41

Toxicity dose dependent and can be delayed NB Coma not a feature so consider other causes Risk Seizures all ingestions> 5g Serotonin toxicity > 5g or other serotoniergic agents CVS - rare unless > 8g - LV dysfunction => hypotension and tachyarrhythmias Other - mydriasis, sweating, agitation, clonus Mx Early intubation > 8g ingestion Decon - >2g and alert <2 hrs of presentation Seizure Mx Serotonin toxicity Mx Cardiotoxicity Mx - IVF +/- inotropic support Dispo < 2g - 8 hrs obs 2-5g - 16 hours obs >5g - 24hrs cardiac monitoring >8g - Early ETT and ICU

Answer 42

Body** packing** well-planned ingestion of wrapped drugs for the purpose of trafficking. Body **stuffing** hurried swallowing of either poorly packaged or unpackaged drugs to avoid prosecution. Drug **pushing** is the hurried placement of poorly packaged or unpackaged drugs into the rectum, vagina, or other orifices to avoid arrest or for resale at a later time.

Answer 43

One mishroom can kill Symptoms > 6hours associated with more serious toxicity Presentation 0-5 hrs - Asx 6-24 hrs - N/V/AP/mild elevation liver and renal dysfunction 1-7 d - Fulminant heptic failure, renal failure, encephalopathy and death Mx Supportive - IVF, correct GI losses Early decontamination - AC BZ for seizures ACh Sx - atropine Antidote - NAC, Silibilin, penicillin G or rifampicin (if penicillin not avilaiable) Adjuncts - cimetidine, pyridoxine,

Answer 44

CI Unknown time of ingestion < 4hrs since ingestion >24hrs since ingestion Chronic ingestions Co-ingestions that affect gut motility

Answer 45

Sinus tachycardia Terminal RAD - R wave > 3mm in aVR Wide QRS > 120ms - 50% risk seizures, >160ms seizures imminent Drugs causing Na Channel Blockade TCAs Type Ia AR - procainamide, quinidine Type Ic AR - flecainide LAs - lignocaine, bupivicaine, ropivicaine BB - propanolol Anti-epileptics - carbamazepine, phenytoin Antihistamines - chlorpheniramine Anti-malarials - chloroquine, quinine, hydroxychloroquine Antipsych - thioidazine Muscle relaxants - orphenadrine Misc - cocaine, tramadol

Toxicology Flashcards

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