Toxicology Flashcards

Question

What is the routine lab-test for intoxicated patients?

Answer 1

1. ABGs 2. complete blood cell count 3. serum electrolyte 4. glucose levels 5. chemical screen with hepatic and renal function studies 6. serum osmolarity may be helpful if poisoning with methanol, ethylene glycol or isopropanol is suspected.

Answer 2

If you suspect: 1. aspiration 2. coma 3. ingestion of substances that may cause non-cardiogenic pulmonary edema

Answer 3

Monitor blood lvls of the substance and be sure that levels are sustainly decreasing, a sudden increase could be a sign of reexposure (rupture of unremoved hidden drug pouch in the GI)

Answer 4

1. A syrup that can induce vomiting by irritating GI mucosae and stimulate chemotrigger zone of the brain 2. May be used to remove ingested poisons/drugs 3. 30ml for adults, 15ml for children 4. Most common side effect is vomiting lasting \>60 min (although prolonged vomiting could also be caused by the toxin)

Answer 5

1. ingestions with potential for change in mental status 2. active or prior vomiting 3. corrosives and volatile poisons 4. heart disease patients 5. pregnant women 6. toxin with more pulmonary than GI toxicity 7. ingestion of toxins with potential for seizures (aspiration pneumonia)

Answer 6

Only indication for Ipecac use at home is if there would be a delay of 1 h or more before a patient (adult) could get to an Emergency Department (and even then, only if it could be administered within 30-90 min after the ingestion) Home-use of ipecac in pediatric patients is not recommended!

Answer 7

* Must be done within 1h of ingestion * If the drug contains on of the following: 1. hydrocarbon 2. benzene 3. toluene, camphor 4. halogenated hydrocarbons 5. pesticides 6. heavy metals * If the drug is liquid: more than 4ml/kg has to be ingested

Answer 8

* A type of Gastric Emptying procedure * Flexible tube is inserted through the nose into the stomach * Size: \> 36 French for adults or 22-24 French for children * Used for retrieving tablet fragments

Answer 9

1. Before nose insertion, measure from chin to xiphoid and confirm with air insufflation 2. Because lavage sometimes forces substances farther into the GI tract, a 25g dose of charcoal is instilled through the tube first 3. Lavage continues until the withdrawn fluids appear free of the substance (usually 500 - 3000ml), while small aliquits of lavage fluid are repeatadly introduced into the stomach by gravity 4. After lavage, give a 2nd dose of 25g charcoal

Answer 10

1. no patient’s agreement 2. large pills 3. nontoxic ingestion 4. non-life threatening 5. most hydrocarbons 6. airway integrity not secured 7. drug is more toxic to lung than GI

Answer 11

1. Given when multiple or unknown substances have been ingested 2. Absorbs most toxins because of its molecular configuration 3. Given at doses of 1-2g/kg, repeat with 4-6h interval 4. Given in fluid solution (e.g in a slurry or soft drink) 5. Given trough gastric tube in unconcious patients 6.

Answer 12

Substances that undergo enterohepatic recirculation 1. phenobarbital 2. carbamazepine SR 3. aspirin (enterocoated tablets) 4. theophylline SR 5. other Sustained-Release products

Answer 13

The typical substances that we prefer Gastric Lavage for: 1. cyanide 2. mineral acids 3. caustic 4. organic solvents 5. iron 6. ethanol 7. methanol 8. lithium

Answer 14

1. decreased O2 2. nausea/ vomiting 3. epistaxis 4. insertion into trachea 5. aspiration 6. fluid and elctrolyte abnormalities 7. small bowel obstruction 8. pneumonia

Answer 15

1. Substance that accelerates defecation 2. Consist of either 70% sorbitol 1g/kg or 10 magnesium citrate 3. Often given with activated charcoal 4. Typically used in WBI (whole bowel irrigation)

Answer 16

* A commercially prepared solution of polyethylene glycol (PEG glycol) (which is nonabsorbable) and electrolytes is given at a rate of 1-2 L/h until the rectal effluent is clear * Usually given through gastric tube * Benefits of WBI are uncertain, may help for SR drug intox

Answer 17

A method of eliminating weak acids by giving a solution of Dextrose, NaHCO3 and KCl

Answer 18

Removing toxin by hemodialysis or hemoperfusion

Answer 19

**All of the** following must be present: 1. Exposition to toxic drug 2. Drug must be readily eliminated by ECT 3. Evidence of toxicity either (biochemical or clinical sympt) 4. Lack of alternative life saving treatments (antidote)

Answer 20

1. Deteriorating condition despite optimal therapy 2. Problems with renal or hepatic metabolism

Answer 21

1. Ethylene glycol 2. Lithium 3. Methanol 4. Salicylates 5. Theophylline 6. VPA 7. Phenobarbital

Answer 22

If the poison... 1. Is a large or charged 2. Has a large volume of distribution 3. Is stored in fatty tissue 4. Is extensively bound to protein

Answer 23

When the liver/kidneys are damaged and need time for recovery/transplantation

Answer 24

It consists of a filter made of activated charcoal in the dialysis circuit (might help in filtrating large or protein-bound toxins)

Answer 25

N-Acetylcysteine

Answer 26

Physostigmine

Answer 27

Flumazenil

Answer 28

1. Ca IV 2. Insulin with IV glucose

Answer 29

1. Atropine 2. Pralidoxime

Answer 30

1. Atropine 2. Pralidoxime

Answer 31

Specific Fab fragments

Answer 32

1. Ethanol 2. Fomepizole

Answer 33

1. Fomepizole 2. Ethanol (if fomepizol is unavailable)

Answer 34

Chelating drugs

Answer 35

Deferoxamine

Answer 36

Pyridoxine (vitamin B6)

Answer 37

1. Aniline dyes 2. Some local anesthetics 3. Nitrates 4. Nitrites 5. Phenacetin 6. Sulfonamides

Answer 38

Methylene blue

Answer 39

1. Hydroxocobalamin 2. Cyanide antidote kit (includes amyl nitrate, Na nitrite, and Na thiosulfate)

Answer 40

First try giving 2mg Naloxone, if it still persists do endotracheal intubation with slow-infusing Naloxone perfusion

Answer 41

1. FIRST give 100mg thiamine 2. Then give 50ml of 50% Dextrose solution

Answer 42

Norepinephrine 0.5-1mg/min (if the hypotension is refractory, consider other vasopressors)

Answer 43

* Cardiac Pacing For Torsades de Pointes we can give Magnesium Sulfate 1-2g IV

Answer 44

1. Benzodiazepines first 2. Phenobarbital or phenytoin if benzo doesn't work

Answer 45

Ocurrs due to metabolism by p450 (mainly CYP2E1) to the hepatotoxic substance **NAPQI** --\> GSH depletion, oxidative stress and mitochondrial dysfunction

Answer 46

Used for estimation of the likelihood of hepatic injury due to acetaminophen toxicity for patients with a single ingestion at a known time

Answer 47

Decreased NAPQI due to ethanol being a competitive substrate of CYP2E1

Answer 48

Increased NAPQI due to long ethanol abuse will over time increase number and action of CYP2E1 enzyme

Answer 49

1. First 24 hours of ingestion 2. Characterized by the non-specific symptoms of nausea, vomiting, malaise, lethargy and diaphoresis 3. AST and ALT are usually normal

Answer 50

1. 24 to 72 hours 2. Characterized by resolution of stage I symptoms 3. Elevations of AST and ALT typically begin to occur 4. In severe cases:hepatomegaly (with right-upper quadrant pain), jaundice and coagulopathy 5. 1∼2% of patients may also experience renal failure

Answer 51

1. 72 to 96 hours after ingestion 2. Return of stage I symptoms 3. AST and ALT elevations 4. Maximal liver injury (jaundice, encephalopathy, coagulopathy and lactic acidosis) 5. Renal failure, and on rare occasions pancreatitis 6. Prolonged prothrombin time

Answer 52

Increase lactic acid in two ways (two-hit increase): 1. NAPQI causes hypoxia in hepatic cells --\> increased lactic acid 2. NAPQI-induced hypoxia in hepatic cells --\> decreased lactic acid metabolism --\> even more lactic acid buildup!

Answer 53

* 96 hours after stage 3 (1-2 weeks from time of ingestion) * May last longer depen ding on severity

Answer 54

\> 7.5g of acetaminophen is toxic

Answer 55

If acetylcysteine is not accessible, give activated charcoal 1g/kg within 4 hours of poison ingestion

Answer 56

1. Acetaminophen lvl above "treatment" line on the nomogram chart 2. Single ingestion of greater than 150 mg/kg (7.5 g total dose regardless of weight) 3. Unknown time of ingestion and a serum acetaminophen concentration \>10 mcg/mL (66 micromole/L) 4. Patient with a history of acetaminophen ingestion and any evidence of liver injury 5. Patients with delayed presentation (\>24 hours after ingestion) + evidence of liver injury or history of previous acetaminophen overdose

Answer 57

1. Administer initial loading dose of 150 mg/kg IV for 1 hour 2. Next, administer a 12.5 mg/kg/h IV for 4 hours 3. Finally, administer 6.25 mg/kg/h for 16 hours

Answer 58

1. Loading dose of 140 mg/kg 2. Then 70 mg/kg every 4 hours (total dose of 17 times)

Answer 59

* Non-IgE mediated anaphylaxis (when given IV) * Vomiting (when given oral)

Answer 60

1. Choose IV acetylcystein regimen (improves hepatic microcirculatory function) 2. Continued until patient recieves transplant or [encephalopathy is resolved and INR \<2] 3. Additional supportive therapies are also started

Answer 61

1. Inhibition of COX 1 and 2 decreased synthesis of prostaglandins, prostacyclin and thromboxanes --\> platelet dysfunction and gastric mucosal injury 2. Stimulation of the chemoreceptor trigger zone in the medulla causes nausea and vomiting 3. Activation of the respiratory center of the medulla results in hyperventilation and respiratory alkalosis 4. Interference with cellular metabolism (eg, Krebs cycle, oxidative phosphorylation) leads to metabolic acidosis

Answer 62

1. Binding to protein (90% of normal dose bind to protein) 2. Hepatic metabolism

Answer 63

As aspirin lvl rises, the body runs out of enough proteins to bind the aspirin (salisylate) and hepatic metabolism can't keep up with the large amounts --\> elimination becomes dependent upon (slow) renal excretion --\> aspirin half-life increase from 2-4h to 30h!

Answer 64

1. First symptoms present within 1-2h after ingestion 2. Early symptoms include hyperpnea (earliest), tinnitus, vertigo, nausea, vomiting and diarrhea 3. Afterwards if the overdose is severe, another set of symptoms including altered mental status, hyperpyrexia, noncardiac pulmonary edema, and coma 4. Most patient also have either respiratory-alkalosis or a mix of respiratory-alkalosis and metabolic-acidosis

Answer 65

* Therapeutic range: 10 to 30 mg/dL * Fatal dose: 10-30g/dL First signs of intoxication appear as early as 40-50mg/dL

Answer 66

1. Salicylate is directly toxic to the CNS 2. Overdose may cause neuroglycopenia 3. Overdose may cause cerebral edema

Answer 67

Salicylate-induced noncardiogenic pulmonary edema

Answer 68

* Salicylate directly effects the respiratory center --\> hyperpnea --\> respiratory alkalosis * Cell-damage and glycopnea induced by overdose cause buildup of acids (lactic and ketoacids) --\> metabolic-acidosis

Answer 69

1. The molecular design of Salisylic Acid consists of a deprotonated (charged) and protonated (uncharged) form 2. The uncharged form can cross lipid barriers meaning it can cross the blood-brain barrier and epithelium of renal tubule 3. The lipid soluability means low doses are enough for a cns buildup as it can easyly get reabsorbed in renal collecting tubule and move towards the brain and affect it

Answer 70

By giving sodium bicarbonate (NaCOH₃ ): Increasing the systemic pH increases the charged/uncharged ratio of salisylic acid, more uncharged means less lipid soluability (less cross blood-brain, and less are reabsorbed in the renals) 1. Initial dose of NaCOH₃ 1-2mEq/kg IV 2. Then: 100-150 mEq NaCOH₃ in 1L 5% dextrose solution 3. Keep going until Serum Salicylate \<40mEq/kg * Give Potassium even if patient doesn't have hypokalemia as alkanization will further decrease serum potassium

Answer 71

1. Serum Salicylate lvl - \>40 mg/dL (2.9 mmol/L) 2. Serum Creatinine lvl - (aspirin is excreted through kidneys) 3. Serum potasium - chance of hypokalemia 4. Prothrombin time - overdose may cause hepatotoxicity --\> interfere with Vit K metabolism 5. Serum Lactate - Salicylates uncouple oxidative phosphorylation --\> increased anaerobic metabolism 6. Anion gap - often elevated with overdose

Answer 72

1. ABCDE (stabilize!) 2. Tracheal intubation ONLY IF NECESSARY (patient has respiratory alkalosis to manage the low pH and we must try to not disturb this natural management) 3. If hypotensive give fluids, unless patient has cerebral edema or pulmonary edema 4. Activated Charcoal within two hours of ingestion (1g/kg, 50g total dose) 5. Give glucose solution despite normal blood glucose (as **cerebral** glucose lvls are often low)

Answer 73

Yes! Respiratory alkalosis is not a contraindication of treatment, just keep serum pH \<7.6

Answer 74

No, urinary flow is not beneficial to remove salicylate unless the pH is normal or high (when it's low, most salicylate gets reabsorbed), give more NaHCO₃

Answer 75

Patient has one or more of the following: 1. Altered mental status 2. Pulmonary edema due to respiratory distress 3. Cerebral edema 4. Acute or chronic kidney injury 5. Fluid overload that prevents HCO₃ administration 6. Very high serum salicylate (\>90mg/dL) 7. Severe acidemia (pH \<7.2)

Answer 76

NSAIDs prevent COX-mediated production of prostaglandins and thromboxanes but not leukotrienes and other eicosanoids (while Aspirin does!)

Answer 77

COX-1: Expressed in most tissues and regulates basal cellular homeostasis (platelet function, gastric mucosal integrity, and regulation of renal blood flow) Cox-2: Regulates inflammatory cytokines and pain

Answer 78

1. They are weak acids 2. Peak serum lvl within 1-2h, overdose ight cause delay of 3-4h 3. 99% becomes protein-bound, and 1% is free (ratio changes during overdose, too few proteins to bind it all) 4. Metabolised in the liver, then excreted through the kidneys 5. Half life differ based on type (either over or under 8h)

Answer 79

1. Ibuprofen 2. Indomethacin 3. Ketorolac 4. Diclofenac

Answer 80

1. Naproxen (shortest of them) 2. Oxaprozin 3. Piroxicam) 4. Phenylbutazone (longest of them)

Answer 81

\> 100mg/kg (except mefenamic acid and phenylbutazone) Most common symptoms include: 1. Nausea and vomiting 2. Drowsiness 3. Blurred Vision 4. Dizziness (at this lvl, very few show severe harm or need treatment)

Answer 82

Aspirin and acetaminophen! People often mistake them for being NSAIDs and initial overdose-symptoms may be similar.

Answer 83

Severe toxicity at ingestion \>400mg/kg Symptoms: 1. Anaphylaxis (especially in asthma & urticaria patients) 2. Increased anion gap 3. Lactic acidosis and weak-acidic metabolites 4. Cardiac Dysrythmias (due to acidosis) 5. Electrolyte disturbance (due to acidosis) 6. Seizures and mental status change (due to acidosis) 7. Acute renal failure/necrosis (very rare) 8. Hypotension/cardiovascular collapse (ibuprofen) 9. Anemia or agranulocytosis (phenylbutazone and indomethacin)

Answer 84

1. Rule out aspirin and acetaminophen ingestion (check blood levels!) 2. CBC and Hb lvls (in case of NSAID-induced bleeding) 3. Renal function test in severe cases 4. Routine ABG if mental status changes (rule out acidosis) Serum NSAID lvl is of no value, we monitor symptoms rather than NSAID blood lvl, as even high doses might not cause as severe symptoms as mentioned above

Answer 85

1. ABCDE first 2. Activated Charcoal within 2h of ingestion 3. Correction of metabolic acidosis 4. Crystalloid in case of hypotension 5. Benzodiazepines in case of seizures 6. External warming in case of hypothermia \*Extracorporeal removal is ineffective due to high protein binding

Answer 86

1. Calcium Channel Blockers 2. Mainly affect smooth muscle 3. May cause reflex-tachycardia (due to smooth muscle relaxation causing hypotension)

Answer 87

1. Amlodipine 2. Felodipine 3. Nicardipine 4. Nifedipine

Answer 88

1. Calcium Channel Blockers 2. Affects myocardial muscle and smooth muscle 3. Cause myocardial depression and decreased electrical activity

Answer 89

1. Diltiazem 2. Verapamil

Answer 90

1. At high doses, can block sodium channels --\> QRS prolongation 2. Often affect pancreas --\> decreased insulin release --\> hyperglycemia

Answer 91

1. Hypotension (the main sign of both types) 2. Bradycardia (in nondehydropyridines + nifedipine) 3. Reflex-tachycardia (only in dehydropyridines) 4. Jugular venous distention and respiratory crackles (and other clinical signs heart failure)

Answer 92

1. Antidotes 2. Decontamination therapy 3. Adrenergic agents 4. High-dose Insulin Euglycemia Therapy (HIET) 5. Invasive therapy 6. Intralipid therapy

Answer 93

1. Calcium salts: * Calcium chloride 10-20ml 10% solution over 10 min * Calcium gluconate 30-60ml 10% solution (both can also be repeated once and given continuously) 2. Glucagon: 5mg IV (can be repeated twice with 10 min interval)

Answer 94

Give a combination of the following: 1. 50g Activated Charcoal 2. IV fluids 3. Atropine 1mg IV (can be repeated until total 3mg)

Answer 95

Give vasopressors, especially adrenergic agents (norepinephrine, dopamine etc...)

Answer 96

Give the following combination (insulin-glucose): 1. Insulin bolus 1 U/kg IV. then continuous 0.5–1 U/kg/h 2. Dextrose 25-50g bolus, then continous 0.5g/kg/h

Answer 97

1. Transvenous pacing 2. Intraaortic balloon pump 3. Cardiopulmonary bypass 4. Extracorporeal membrane oxygenation

Answer 98

20% Lipid emulsion is given bolus of 1.5ml/kg, then continous 0.25ml/kg/min Helps in three ways: 1. Makes an intravascular fatty compartment that absorbs some of the CCB 2. The free fatty acids are an alternative energy source for myocardial cells 3. The triglycerides prolong myocardial calcium channel opening --\> increased myocardial Ca²⁺ concentration

Answer 99

B₁: Found in heart muscle, activation causes: 1. Increased HR and contractility 2. Increased AV conduction 3. Decreased Av-node refractory period B₂: Found in heart, but mostly in bronchial and vascular smooth muscle. Activation causes: 1. Vasodilation 2. Bronchodilation B₃: Found in the heart and adipose tissue, activation causes: 1. Reduced cardiac contraction 2. Catecholamine-induced thermogenesis

Answer 100

1. Bronchoconstriction 2. Decreased gluconeogenesis 3. Decreased insulin release

Answer 101

1. Decreased myocardial contractility 2. Decreased automaticity in pacemaker cells 3. Decreased AV-node conduction

Answer 102

Occur within 2-6h, but can take upto 24h in SR types and sotalol 1. Bradycardia 2. Hypotension 3. Mental status change and seizures (specially in hypotension) 4. Bronchospasm 5. Hypoglycemia

Answer 103

1. PR prolongation (due to decreased AV-node conduction) 2. RR prolongation (due to bradycardia) 3. QRS prolongation (due to overall decreased conduction) 4. Significant QTc prolongation (sotalol antiarrythmatic effect)

Answer 104

Glucagon IV 5mg over 1min, if no increase in pulse or BP after 10-15min, give 2nd bolus of 2-5mg over 1h (Atropine and isoprotenerol might also help, but are inconsistent)

Answer 105

Because glucagon receptors activate the same secondary messenger system as B-receptors

Answer 106

1. Secure the airways 2. Give ALS if necessary 3. Establish IV access and heart monitoring 4. Isotonic fluid to correct hypotension 5. Treat bradycardia with Atropine 0.5-1mg IV every 3-5min, total dose of 0.03mg/kg 6. IV glucagon treatment protocol (main antidote) 7. NaHCO₃ or Magnesium in case of arrythmia 8. IV calcium salts 9. Vasopressors 10. HIET 11. Lipid Emulsion Therapy

Answer 107

1. Calcium chloride IV 10ml of 10% solution through CVK 2. Calcium gluconate 30ml of 10% solution through PVK

Answer 108

Myocardial cell benefits due to the insulin: 1. increased glucose and lactate uptake by myocardial cells 2. improved myocardial function without increased O₂ demand 3. increased pyruvate dehydrogenase activity --\> increased myocardial lactate oxidation --\> better Ca²⁺ handling Myocardial cell benefits due to the glucose: 1. Increased myocardial SR-ATPase activity 2. Increased cytoplasmatic Ca²⁺ concentration 3. Incrased Ca²⁺ entrance into mitochondria & sarcolemma

Answer 109

1. Hypoglycaemia 2. Hypokalaemia 3. Hypomagnesaemia 4. Hypophosphataemia

Answer 110

Increases intracellular Ca² concentration in myocardial cells. Happens due to Digoxin inhibiting Na-K ATPase --\> inhibition of Na-Ca symporter --\> more intracellular calcium

Answer 111

1. Renal impairment (cause it's excreted in urine) 2. Acid–base disturbances 3. Hypokalaemia 4. Hypomagnesaemia 5. Hypercalcaemia 6. Myocardial ischaemia 7. Hypoxaemia

Answer 112

1. Lethargy 2. Confusion 3. GI symptoms 4. Visual symptoms 5. Cardiac arrythmias (might be deadly)

Answer 113

Reverse ticks: downsloping ST depression

Answer 114

1. Premature Ventricular Contractions (PVCs) 2. Sinus bradycardia 3. Overall decreased conduction

Answer 115

Digoxin-spesific antibody fragments

Answer 116

1. Life-threatening arrhythmia 2. Cardiac arrest 3. Potassium \>5.0 mmol/L 4. Acute ingestion of \>10 mg in adults or \>4 mg in children 5. Evidence of end-organ dysfunction 6. Moderate to severe gastrointestinal symptoms 7. Serum digoxin concentration \>12 nanogram/mL 8. Significant clinical features of digoxin toxicity with serum digoxin concentration \>1.6 nanogram/mL. These indications are needed because the treatment is very expensive, not because of side-effects

Answer 117

Different protocols exist, based on what info we have 1. Known Digoxin concentration: number of ampuoles = (serum digoxin ng/mL x bodyweight (kg)) / 100 2. Known amount ingested: number of ampuoles = amount ingested x 2 x 0.7 3. Uknown data about patient: 5 ampuoles if haemodynamically stable, or 10 if unstable

Answer 118

1. Activated Charcoal within 2h of ingestion 2. Lignocaine for tachyarrythmias 3. Atropine for bradyarrythmias 4. Give oral or IV potassium if patient has hypokalemia 5. In case of cardiac arrest, ALS given for at least 30min after giving digoxin-spesific antibody fragments

Answer 119

1. Aliphatic hydrocarbons: carbons connected by a single, double or tripple bond 2. Aromatic hydrocarbons: cyclic compunds, containing a benzene ring 3. Halogenated hydrocarbons: containing fluoride, chloride or bromide 4. Terpenes: derived from isopren (natural gum substance)

Answer 120

1. Nonintentional-nonoccupational (ie. children unintentionally drinking open bottles they find) 2. Recreational (for getting high) 3. Occupational exposure (inhaling vapor at work) 4. Intentional (for suicide)

Answer 121

1. Volatility - the ability to vaporize or to exist in a gaseous form (more votality = easier absorption) 2. Surface tension – the adherence of molecules along a liquid surface (low surface tension = more spread in the body) 3. Viscosity – the resistance to flow through an orifice (low viscosity = easier flow into the body)

Answer 122

CHAMP * C: Camphor * H: Halogenated * A: Aromatic * M: Metal additives * P: Pesticides

Answer 123

* Most commonly seen with aromatic and halogenated * When ingested, most toxic types are aliphatic with toxic additives (ie. metals, camphor etc...) * When ingested, mainly determined by votality and absorption within the GI * Symptoms: 1. Myocardial sensitization --\> arrythmias 2. CNS depression and seizures 3. Hepatic and renal tubular necrosis

Answer 124

1. Pulmonary aspiration (the most common) 2. Hydrocarbon pneumonitis (type 2 pneumocyte injury) 3. Histological changes of lung tissue (inflammation, hemorrhage, necrosis etc...)

Answer 125

1. Direct injury to the brain: many HCs are liophilic and cross blood-brain barrier 2. Indirect injury to the brain: due to hypoxia or asphyxiation after inhaling HCs

Answer 126

1. Leukoencephalopathy 2. Peripheral neuropathy 3. Blurred vision 4. Sensory impairment 5. Muscle atrophy 6. Parkinsonism + Hypercarbia: happens in individuals "bagging" HCs for recreational use

Answer 127

Mainly the chlorinated hydrocarbons (halogenated) * Hydrocarbon metabolites and free radicals made during hydrocarbon metabolism attach to hepatic structures --\> lipid peroxidation response --\> hepatic necrosis * Example: Methylene chloride is metabolised in the liver into CO (although not as toxic as inhaling CO in the air)

Answer 128

1. Cardiovascular: sensitization to cathecholamines --\> tachydysrhytmias --\> syncope or death 2. Hematologic: Aplastic anemia, multiple myeloma, acute myelogenous leukemia, hemolysis 3. GI: Irritation of GI mucosae --\> vomiting, diarrhoea, burning sensation 4. Renal: Due to repeated aromatic toluene exposure --\> renal tubular acidosis

Answer 129

1. Respiratory symptoms: cougching, wheezing, tachypnea, dyspnea 2. Cardiovascular: Arrythmia, hypotension 3. GI signs: comiting, diarrhoea, burning sensation 4. Fever (lasting \<48h, if \>48 suspect bacteria) 5. Dermal signs: blistering, pain or redness after HC contact 6. CNS: visual symptoms, metal status change, ataxia, dizziness 7. Smell: certain hydrocarbon-rich substances have a special smell (ie. petroleum odor, sweed solvent odor, pine etc...)

Answer 130

1. Urinalysis: certain HCs have metabolites excreted in urine 2. Blood lvls: Toluene lvls, Creatinine Kinase lvls 3. CBC for leukocytosis, leukemia or enmia 4. Metabolic panel: BUN, vreatinine, glucose, electrolytes (anion gap) 5. AST and ALT when suspecting hepatotoxicity 6. Pulse oximetry (especially for inhaled HCs) 7. ABG (especially for inhaled HCs, and monitors pH changes) 8. Chest X-ray (if patient has respiratory symptoms) 9. ECG (in case of arrythmia)

Answer 131

1. Airway management, give O₂ or bronchodilators if needed, intubate if necessary, or ECMO if intubatiion doesn't help 2. If patient has brionchospasms give B₂-agonists 3. If patient has seizures give benzodiazepines 4. Give IV fluids if hypotensive 5. Dermal and eye decontamination if necessary 6. If HCs are ingested, start GI decontamination

Answer 132

1. Nasogastric lavage: only if CHAMP is high, the amounts ingested are high and symptoms appear within 1h 2. Activated Charcoal: best for HCs that have toxic additives

Answer 133

Observe for 6 hours, if you see any of the following during the observation period, admit the patient: 1. Patient experiences symptoms even though X-ray is normal 2. Patient experiences symptoms due the toxic additives 3. Patient has mild symptoms, normal X-ray, but fails to improve 4. Asymtpomatic patient, normal X-ray, but cannot come back for follow-up \* if the hydrocarbon exposure was intentional, always admit the patient as this is a sign of suicide tendencies

Answer 134

Observe the patient for 6 hours and if the following is seen, you can discharge them: 1. Asymptomatic patient with normal \>4h old chest X-ray 2. Asymptomatic patient with mildly abnormal chest X-ray, can come back the next day for outpatient follow-up

Answer 135

Trade products (ie. pesticides in cans and other containers) often are a combination of the pesticide itself and a solvent that often is a hydrocarbon. Therefore pestecide exposure = treat for not only pesticide but also the solvent (HC treatment)

Answer 136

They are made of organophosphates and are divided into two groups: 1. Diethyl organophosphates 2. Dimethyl organophosphates

Answer 137

1. Acute cholinergic crisis 2. Intermediate syndrome 3. Delayed polyneuropathy

Answer 138

They strongly bind to the enzyme Acethylcholinesterase (AChE) --\> decreased acethylcholine breakdown --\> strong cholinergic effects on peripheral and central nerves

Answer 139

Diethyl organophosphates have a much longer half-life than dimethyl, a wider therapeutic window and a stronger binding affinity to AChE

Answer 140

SLUDGE: * S: Salivation/Sweating/Seizures * L: Lacrimation * U: Urination * D: Defaecation * G: Gastrointestinal cramps * E: Emesis + Miosis and BBB (Bradycardia, Bronchospasm, Bronchorroea)

Answer 141

1. Fasciculations 2. Muscle cramps 3. Fatigue 4. Paralysis 5. Tachycardia 6. Hypertension

Answer 142

1. headache 2. tremors 3. restlessness 4. ataxia 5. weakness 6. confusion 7. slurred speech 8. coma 9. seizures

Answer 143

* Condition that develops in 20-50% of organophosphate intoxications * Occurs after cholinergic crisis have subsided, but before polyneuropathy starts (usually within 1-4 days) * Symptoms: 1. Weakness of neck flexion 2. Respiratory muscle weakness 3. Cranial nerve palsies (typically III, IV, VI, VII and X) 4. Proximal muscle weakness of extremities

Answer 144

1. Organophosphate-induced delayed neuropathy (OPIDN) 2. Psychiatric disorders (schitzo, depression, confusion) 3. Myonecrosis 4. Pancreatitis

Answer 145

* Distal ascending neuropathy that occurs 10-21 days after exposure * Paraesthesiae and motor weakness are common

Answer 146

1. AChE lvl \<50% (although symptoms occur at \<20%) 2. Decreased BChE (butyrylcholinesterase) lvl \*Certain organophosphates decrease BChE more than AChE

Answer 147

1. Sickle cell disease 2. Thalassaemia 3. Severe anaemia

Answer 148

Atropine IV 1.8-3.0mg (repeat every 3-5min, doubling the dose each time), then continous infusion of 10-20% of the initial dose that was needed to reach atropinization * Often given with Glycopyrrolate IV so the atropine amount given can be less

Answer 149

1. bradycardia (\<80/minute) 2. hypotension (systolic \<80 mmHg) 3. typical cholinergic symptoms

Answer 150

Atropinization is reached when we see the following indicators 1. dry skin and mucous membranes 2. heart rate \>80 per minute 3. systolic pressure \>80 mmHg 4. pupil dilation If you see more severe anticholinergic symptoms, it means you have over-atropinized

Answer 151

AChE reactivators (help against organophosphate poisoning) 1. Mostly benefitial at nicotinic synapses 2. Mostly beneficial for diethyl poisonings 3. Example: Pralidoxime, Obidoxime

Answer 152

1. Glycopyrrolate: often given with the atropine, so we can use less atropine during treatment

Answer 153

1. Insecticides with effect similar to organophosphates 2. Reversibly inhibit AChE and BChE 3. Doesn't effect CNS as much as organophosphates due to poor permeability through blood-brain barrier 4. Also treated with atropine, but not oximes

Answer 154

Can enter transdermally, by ingestion or by inhalation (depending on the solvent)

Answer 155

1. Impair the nervous system by depolirizing nerve membranes 2. Inhibit the GABA-chloride channel complex --\> less inhibition through GABA --\> more nerve excitation Additional cardiological effects: * Sensitizes myocardiom to cathecholamines --\> arrythmias * Cardiovascular dystrophy (mainly due to lindane)

Answer 156

Onset in 30 min after ingestion, mainly epileptic symptoms 1. Nausea and vomiting 2. **Seizures: myoclonus, opsoclonus, status epilepticus** 3. Dizziness 4. Tremors 5. Confusion 6. Coma

Answer 157

Cholestyramine Resin 1. Accelerates biliary-faecal excretion of organochlorines 2. Dosing 4g four times a day 3. Treatment may take weeks to fully resolve toxicity

Answer 158

1. Monitor for seizures 2. Maintain open airways 3. Skin and gastric decontamination if necessary 4. Dopamine for hypotension if severe 5. Cholestyramine resin (main treatment)

Answer 159

1. Insecticides 2. Can enter transdermally, by ingestion, or by inhalation 3. Low dose --\> delay of sodium channel closing in nerve fibers --\> paraesthesiae 4. High dose --\> conduction block

Answer 160

1. Insecticides of pyretheroid kind 2. Inhibit GABA signaling --\> seizures and other organochlorine-like symptoms

Answer 161

Within minutes (local symptoms): 1. Nausea, vomiting and abdominal pain 2. Sore throat, salivation and dysphagia Within hours (neurological): 1. Headache, dizziness and coma 2. Blurred vision 3. Convulsions

Answer 162

Transdermal: 1. Paraesthesiae and stinging sensation 2. Various forms of dermatitis Inhalation: Breathlessness and asthma

Answer 163

Mainly supportive 1. O₂ and bronchodilators if necessary 2. Skin decontamination if necessary 3. If seizures, give benzodiazepines 4. The paraesthesiae usually resolves by itslef within 12-24h

Answer 164

1. Herbecides 2. Exposure trough inhalation, ingestion or transdermal 3. Paraquat and diquat: two special types of bipyridil

Answer 165

1. Oral ingestion: free radical formation --\> lipid peroxydation --\> hepato-, nephro, and pneumotoxicity 2. Paraquat: type of bipyridil that builds up in the lungs --\> alveolitis --\> pulmonary edema and ARDS --\> pulmonary fibrosis

Answer 166

1. Gastrointestinal corrosive injury 2. Hepatic failure 3. Renal failure 4. Arrythmias and hypotension 5. CNS depression and seizures 6. Pulmonary edema --\> fibrosis 7. Rhabdomyolysis Symptoms and severity depend on amount of dose ingested

Answer 167

1. Corrosive effect on the GI tract 2. CNS symptoms: mental status changes and seizures 3. Pulmonary symptoms (though not as severe as paraquat) 4. Mild liver injury 5. Severe renal injury (tubular necrosis etc...) 6. Cardiac symptoms: VF and hemmorhage

Answer 168

1. Colorimetric urine test (special type of urine chemichal test, where urin turns a certain color, when it contains biperidyls) 2. Urinary excretion of the biperidyls 3. Plasma biperidyl concentration

Answer 169

Bipitydil has no antidote, treatment is mainly supportive 1. Nasogastric decontamination 2. Extracorporeal filtration might help 3. Imunosuppressive therapy, mainly for paraquat (corticosteroids) 4. Fluid resuscitation for renal failure 5. Oxygen therapy: only if patint is very hypoxic, it might increase lung free radicals from paraquat poisoning 6. Lung transplantation if necessary

Answer 170

1. Dose-dependent cell membrane damage 2. Disturbing aerobic metabolism 3. Disturbing acetly-CoA metabolism

Answer 171

1. GI symptoms: nausea, vomit, abdominal pain, diarrhoea 2. Hypotension 3. Hypoventilation 4. Neuromuscular symptoms: ataxia, hypertonia, hyperreflexia, fasciculations and paralysis 5. Motoric: limb muscle weakness and rhabdomyolysis 6. Metabolic acidosis and renal failure

Answer 172

Chromatographic identification test

Answer 173

1. _Alkaline diuresis_ (enhances excretion) 2. Skin or GI decontamination if necessary 3. Haemodialysis

Answer 174

1. Highly toxic hermecides 2. Can be ingested, inhaled or transported transdermally 3. Mechanism of toxicity: disrupts mitochondrial metabolism

Answer 175

1. Symptoms of increased metabolism: hyperpyrexia, tachycardia, tachypnea, hypertension, diaphoresis 2. Yellow urine and yellow stool 3. Yellow skin after dermal contact 4. When severe: hepatic-, renal- and respiratory failure, seizures, bone marrow disruption,

Answer 176

1. Skin and GI decontamintion if necessary 2. Fever reduction - external cooling, no salicylates! 3. Fluids to prevent dehydration due to hyperthermia 4. O₂ and ventilation if necessary 5. Benzodiazepines if patient has seizures or is agitated

Answer 177

1. An herbecide 2. Is not by itself toxic, but the mixtures it comes commercially in are toxic

Answer 178

1. GI symptoms: nausea, vomiting, diarrhoea 2. Oral and throat irritation when inhaled 3. Conjunctivitis and corneal injury when exposed to eyes 4. Erythema and skin irritation when exposed to skin 5. In its most potent mixture it can cause GI burns, renal-, hepatic- and respiratory failure, arrythmia and bradycardia, and CNS symptoms like seizures

Answer 179

Mild toxicity: * Oral dilution or irrigation, antiemetics, pain medications Severe toxicity: 1. Nasogastric aspiration 2. Gastroscopi to evaluate GI burns 3. Airway management if necessary 4. Fluids or vasopressors for hypotension 5. Correcting electrolyte lvls and metabolic acidosis 6. Haemodialysis

Answer 180

1. They are fungicides 2. Symptoms based on the 3 types: * Chlorothalonil: dermatitis * Pentachlorophenol: local irritation, hyperthermia, hepatotoxicity and seizures * Hexachlorobenzene: porphyria cutanea tarda \*Treatment is only supportive and based on symptoms

Answer 181

* Fungicides * Symptoms include: 1. Headache, delirium and encephalopathy 2. Disulfiram-like reaction (red face and neck) 3. Local irritation of contaminated area * Treatment: decontamination if neccesary, O₂ or B-agonists if intake is due to inhalation

Answer 182

1. Mercury-containing fungicides 2. Intake through all three routes 3. The murcery often builds up in RBCs and CNS

Answer 183

Early: 1. Numbness and tingling of digits and face 2. Tremors and mental status change Severe: 1. Loff senses (vision, hearing, balnce etc...) 2. Spasticity and rigidity of muscles 3. Further mental status change

Answer 184

Chelation, using Succimer (DMSA) \*Extracorporeal treatment might also help

Answer 185

* Fungicides * Interfere with mitochondrial metabolism * Symptoms: 1. Nausea and vomiting 2. Hepatotoxicity 3. Dermal irritation 4. Headache, dizziness, blurred vision 5. Tremors and weakness \*Treatment is supportive, only treat symptoms

Answer 186

Early: 1. Abdominal pain, nausea, vomiting 2. Hematochezia 3. Stomatitis and ileus 4. Hypotension and arrythmia CNS (days to \>1 week): 1. Headache, lethargy, weakness 2. Paraesthesiae, tremor and ataxia 3. Seizures, delirium, coma \>2 weeks later - alopecia

Answer 187

1. _Prussian blue (increases excretion)_ 2. Haemodialysis (also helpful) 3. Electrolyte and fluid correction (decrease seizures)

Answer 188

1. Prolonged PT and INR (earliest symptom) 2. Bleeding from nose, gums and lips 3. Bloody urine, feces and vomit 4. Hematomis in joints 5. Cerebral hemorrhage --\> paralysis \*all symptoms are bleeding-related

Answer 189

**Main treatment:** 1. _Vit K₁ IV solution_ 2. Fresh Frozen Plasma (the next best) Management: 1. Activated Charcoal 2. Gastric lavage 3. PT and INR monitoring

Answer 190

1. Inhibit the same as normal warfarin, but has a longer duration of action 2. Prolongation of PT and INR appears later than in normal warfarin, but lasts can last for months 3. Same treatment as warfarin (Vit K₁ and FFP)

Answer 191

1. Inhalation rodenticide (becomes phosphine in air) 2. Toxicity: lipid peroxidation --\> various organ damage 3. When ingested, the liver also metabolises it to phosphine --\> delayed/slow toxic effects

Answer 192

1. Mild: local irritation, dizziness, respiratory distress 2. Moderate: diplopia, ataxia, tremors 3. Severe: ARDS, arrythmias, liver- and renal failure, seizure

Answer 193

1. GI: epigastric pain, repeated vomiting, diarrhoea 2. Circulation: hyptension, tachycardia, myocarditis, arrythmia 3. Respiratory: cough, dyspnoea, cyanosis, ARDS 4. Metabolic acidosis and hemolysis + Benign oesophageal strictures due to local corrosion

Answer 194

Mainly supportive 1. Gastric lavage with potassium permanganate if ingested 2. Saline in case of shock 3. Sodium bicarbonate in case of metabolic acidosis

Answer 195

1. Rodenticide powder that releases phosphine gas when in contact with water 2. Symptoms similar to Aluminium Phosphide, but slower 3. Treatment: symptom management similar to AP poisoning

Answer 196

* Rodenticides * Mechanism: interfere with Na-K pump --\> change of cell-membrane permeability --\> muscle paralysis * Symptoms: 1. Vomiting and abdominal pain 2. Muscle ightness and tremors 3. Convulsions, paresthesiae, ascending quadriparesis --\> breathing difficulty 4. Hypokalemia and arrythmias

Answer 197

1. Gastric lavage 2. Eating Magnesium sulphate (precipitates the barium) 3. Correcting hypokalemia and monitoring arrythmias

Answer 198

1. Molluscicide similar to acetaldehyde 2. Intak trough inhalation, GI and skin 3. Mechanism: decrease effect of GABA --\> seizures 4.

Answer 199

1. Fever and facial flushing 2. Nausea, vomiting and abdominal cramps 3. Drowsiness, spasms and tachycardia 4. Ataxia and increased muscle tone 5. Seizures, tremor, hyperreflexia 6. Muscle twiching, coma and death

Answer 200

1. GI decontamination if necessary 2. N-acetylcysteine might help a little 3. O₂ and ventilation in case of hypoxia 4. Correction of dehydration and acidosis 5. Benzodiazepines for seizures

Answer 201

* Insect repellent * Intake trough inhalation, ingestion and transdermally * Symptoms: 1. Systemic: hypotension and respiratory depression 2. Dermal: local irritation and bullous eruptions 3. CNS: mental change, ataxia, seizures, paralysis and areflexia * Management: skin decontamination and supportive care

Answer 202

A highly toxic fumigant pestecide (absorbed by all routes)

Answer 203

1. Ulcerations 2. Conjunctivitis 3. Gastrointestinal and mucosal irritation 4. CNS depression

Answer 204

1. Vomiting, diarrhoea and burning sensation 2. Tremors and CNS depression 3. Hypotension 4. Oliguria 5. Jaundice 6. Pulmonary edema \*If death ocurrs within first 24h it's usually due to respiratory- or circulatory failure, while if it ocurrs after it's usually due to liver- or renal failure

Answer 205

1. Serum bromide 2. Urea and creatinine lvl 3. Level of bilirubin and liver enzymes 4. Level of protein/blood in urine

Answer 206

1. Gastric lavage or activated charcoal (within 2h of ingestion) 2. Haemodialysis (helpful) 3. Supportive care of symptoms (ventilation, fluids etc...) 4. Endoscopy (look for esophageal burns)

Answer 207

Methylene Chlroide, when ingested 1/3 of it is metabolised in the liver into CO (slow toxicity, longer duration)

Answer 208

It reversibly binds to one of the 4 seats of hemoglobin with high affinity and causes the rest 3 seats to bind oxygen very strongly --\> oxygen not released when blood reach the tissues --\> hypoxia and necrosis of organs and tissues \*the brain and the heart are especially at risk

Answer 209

By monitoring the lvl of HbCO * Already at 10% headache start to appear * HbCO of 50-70% result inseizure, coma and death

Answer 210

1. COPD patients 2. Neonates (they have already high O₂ affinity)

Answer 211

Although there are MANY symptoms, these are the most important: 1. Hyperthermia and **cherry red skin** 2. Pale sclera (pallor) and bright red retinal veins 3. Noncardiac pulmonary edema 4. Flu-like symptoms 5. Tachycardia and tachypnea 6. Hypertension or hypotension

Answer 212

1. Memory disturbance 2. Emotional disturbance 3. Gait disturbance 4. Sensory disturbance 5. Apraxia and ataxia 6. Stupor 7. Long-time exposure = longer time to recover

Answer 213

1. ABG - acidosis monitoring 2. ECG: in case of sinus tach or arrythmias 3. Cardiac ischemia markers: troponin C, CK-MB, myoglobin 4. CBC: in case of leukocytosis DIC and TTP 5. Electrolyte lvl 6. Liver screening panel 7. Renal screening panel

Answer 214

1. Chest X-ray: if severe CO poisoning or if considering using hyperbaric chamber 2. Head CT: look for edema or focal lesions 3. MRI: more accurate for focal lesions and white matter demyelination - helsp monitor recovery 4.

Answer 215

1. Cardiac monitor 2. Venous HbCO lvl (pulsoxymetry is useless here!) 3. Give 100% O₂ (CO half-life goes from 3-4h to 30-90min) 4. Hyperbaric chamber if HbCO \>40% (CO half-life 15-20min)

Answer 216

1. Do not agressivly treat acidosis as it may increase effect of CO, oxygen is usually enough 2. If you consider Cyanide poisoning and wnt to start cyanide treatment aswell, first give sodium thiopental as it prevents the enhancing effect cyanide antidotes have on CO 3.

Answer 217

Although hyperbaric chamber isn't considered to be in protocol, it is often used when the following is seen: 1. Loss of conciousness or coma 2. Ischemic ECG changes 3. Focal neurological deficits 4. HbCO lvl \>40%

Answer 218

100% O₂ at 2.4-3atm for 90-120 minutes, repeat if necessary

Answer 219

1. Natural substances found in plants 2. Have anticholinergic effects 3. Example: atropine, scopolamine, hyoscyamine

Answer 220

1. Contain tropane alkaloids --\> anticholinergic symptoms 2. Found in all parts of these plants, mainly in roots and seeds 3. Scopolamine is the main tropane alkaloid in these plants, affecting both central and peripheral nerves 4. Atropine amount varies between species, highly concentrated in the seeds

Answer 221

1. Physostigmine IV 2mg (antidote) 2. Activated charcoal - helpful 3.

Answer 222

Cardiac monitoring to be on a lookout for cholinergic crisis (seizures, respiratory distress, asystole), in that case give atropine IV 1/2 dose of physostigmine given

Answer 223

1. unresponsive to supportive treatment 2. tachydysrhythmias and hemodynamic changes 3. seizures unresponsive to benzodiazepines 4. extremely severe agitation or psychosis

Answer 224

Absolute: * If the patient takes any medication causing cardiac-rythm abnormalities (e.g TCA's, quinidine, procainamide etc...) Relative: * Reactive airways * Intestinal obstruction * Intake of depolarizing paralytic agents

Answer 225

1. Muscimol - GABA agonist (Muscimol-induced GABAergic syndrome) 2. Ubotenic acid - glutamate agonist (Glutaminergic syndrome) 3. Becaus these mushrooms contain these two opposite substances, symptoms are both inhibitory and exitatory 4. CNS symptoms range from agitation to coma 5. Effects within 30min-1h of ingastion, last up to 8h

Answer 226

1. lethargy 2. ataxia 3. dysarthria 4. sleep 5. coma

Answer 227

1. hallucinations 2. hyperactivity 3. ataxia 4. myoclonic jerks 5. convulsions

Answer 228

1. Contain **mainly** muscimol and ibotenic acid, but also a small amount of muscarinic agonists 2. Does not contain the deadly amatoxin that is found in certain Amanita species 3. Symptoms are a mix of excitation, sedation and hallucination

Answer 229

1. Contain Muscarine (M1, and M2 agonist) 2. Don't cross blood-brain barrier, only peripheral symptom 3. Symptoms: typical cholinergic symptoms (salivation, diaphoresis, bradycardia, bronchoconstriction, increased GI motility etc...) 4. Mainly supportive treatment, but give atropine or ipratropium if respiratory secretions become severe

Answer 230

* Contain psilocybin and psilocin (LSD and seretonin analogs) * Cause hallucinations and psychosis similar to LSD + some anticholinergic symptoms * Treatment: 1. Mainly supportive of symptoms 2. Gastric lavage or activated charcoal if necessary 3. Benzodiazepines if the get too agitated/psychotic or experience seizures

Answer 231

1. A toxin found in several Amanita mushrooms 2. Causes gastroenteritis-like effects after ingestion 3. Often ingested alongside amatoxin

Answer 232

1. A toxin found in several Amanita mushrooms 2. Interferes with DNA and RNA transcription (affects tissues of high protein synthesis) 3. 60% is excreted into the bile abd then eliminated with urine and GI after 70-90h 4. Hepatotoxic symptoms are the earliest, then renal

Answer 233

Stage 1: Nausea, vomiting, watery diarrhea, and cramping abdominal pain, 6-12 hours after ingestion Stage 2: Resolution of symptoms, but hepatic and renal damage is ongoing Stage 3: if discharged, patients may return to the hospital 2-6 days later with severe coagulopathy, renal failure, and encephalopathy

Answer 234

1. Liver function test 2. Electrolyte, glucose, BUN and creatinine levels (renal) 3. Spore analysis in stomach contents and feces' 4. ELISA test of urine sample for amatoxin 5. Liver biopsy - histological examination

Answer 235

1. Silymarin (Silibinin) IV (main antidote used in EU) 2. Gastric lavage and activated charcoal might help 3. Alkaline diuresis (helpfun within 2-4h of ingestion) 4. Haemodialysis in case of renal failure 5. Hepatic dialysis system (e.g MARS) until liver transplant is available

Answer 236

1. A toxin found in Coprinus atramentarius mushrooms 2. Blocks the enzyme aldehyde dehydrogenase (ALDH) --\> acetaldehyde buildup --\> disulfiram-like symptoms 3. Treatment: Fomepizole (blocks alcohol dehydrogenase, decrasing amount of acetaldehyde made after drinking ethanol)

Answer 237

* It's made after gyromitrin and hydrazone react in the stomach after ingestion of Gyromitra mushrooms, this results in the making of MMH * MMH is a water-soluble toxin that causes: 1. Gastroenteritis 2. Hemolysis Methemoglobinemia 3. Hepatorenal failure 4. Seizures and coma

Answer 238

_Neurotoxicity:_ Like isoniazid, inhibits pyridoxine kinase --\> decreased glutamate synthesis and inhibit GABA production (due to inhibiting GAD enzyme aswell) Gastrointestinal toxicity: Inhibition of diamine oxidase in intestinal mucosa ..\> several GI symptoms + hepatotoxicity Hematopoietic toxicity: Hemolysis and methemoglobinemia --\> hematuria --\> renal failure

Answer 239

1. Treat seizures with pyridoxine and benzodiazepines 2. Treat methemoglobinemia with methylene blue 3. Blood transfusions for anemia

Answer 240

1. Nephrotoxic compund found in cortinarius mushrooms 2. Affects ATP production in proximal tubule cells --\> tubulointerstitial nephritis 3. Renal failure within the first days of ingestion 4. Treatment: early hemodialysis and hemoperfusion to prevent renal failure + fluid and electrolyte correction

Answer 241

1. AChE inhibitors --\> overexcitation or paralysis 2. Main cause of death: respiratory paralysis 3. Cause muscarinic, nicotinic and CNS effects 4. Include the following agents: * **Sarin**: EEG changes, arrhythmias, hypoxia, low-grade fever * **Tabun**: peripheral neurotoxicity, CNS and other organ system hypoxic sequelae

Answer 242

1. Atropine 2. Oximes (e.g pralidoxime) 3. HI-6 (oxime alternative, good for sarin poisoning) 4. Pyridostigmine bromide (prophylactic antidote) - reversibly binds AChE to protect it from strong inhibition

Answer 243

* Gas agents producing skin blistering, upper respiratory damage, and severe eye injuries * Include: 1. Sulfur Mustard 2. Nitrogen Mustard 3. Lewisite

Answer 244

Sulfur Mustard: Yellow, mustard-smelling compund that passes into cells --\>irreversible alkylation of DNA, RNA and proteins --\> cell death Nitrogen Mustard: Colorless, garlic-smelling polyfunctional alkylating agent of DNA --\> cell death

Answer 245

Skin: spreading erythaema and blister formation Inhalation: 1. Burning respiratory passages and bronchitis 2. Dyspnoea and hypoxia --\> respiratory acidosis 3. Erythaema, oedema, and ulceration of affected mucosa Ocular: lacrimation, photphobia, eyelid blisters, corneal ulceration Systemic: Fever, bone marrow disturbance, seizure, shock

Answer 246

1. No spesific antidote once mustard reach the cells 2. Decontaminate eyes and skin 3. 100% humidified supplemental O₂ and ventilation 4. Tracheotomy in case of airway obstruction due to irritation 5. Atropine into eyes for relief of pain (decrease ciliary spasms) 6. Surgical debridement ans skin grafts if necessary 7. Colony stimulating factor (CSF) in granulocytopenic patients

Answer 247

1. Arsenic compund that prevent acetyl-CoA formation --\> blistering 2. Also increase capillary permeability --\> haemoconcentration and hypotension (lewisite shock)

Answer 248

* Skin: Blisters * Eyes: burning, spasms and loss of vision within 1 min * Systemic: 1. Pylmonary edema 2. Hypothermia and hypotension (lewisite shock) 3. Haemolytic anaemia 4. Liver and gallbladder necrosis 5. Kidney damage Sequela: Bowen's Disease (cause lewisite is teratogenic)

Answer 249

1. BAL (dimercaprol) injected IM + skin ointment version (antidote) 2. Decontaminate with an alkaline agent (soap) 3. Supportive treatment of symptoms

Answer 250

* Cyanide-containing gases or liquids used in chemichal warfare to cause asphyxia * Mechanism of action: CN binds to cyt C oxidase i mitochondria --\> inhibition of respiratory chain --\> depression of CNS, respiration and myocardial activity --\> hypoxemic-cytotoxic hypoxia

Answer 251

1. Almond odour in breath 2. CNS: Headache, lighdheadedness, vertigo, agitation, seizures and coma 3. Respiratory: tachypnea and hyperpnea followed by dyspnea and then apnea 4. Cardiac: Hypertension and tachycardia followed by hypotension and bradycardia, arrythmia Cyanosis is not common due to detah occuring within minutes

Answer 252

1. Hydroxocobalamine/sodium thiosulfate 2. Cyanide antidote kit 3. Sodium nitrite 4. Dicobalt-EDTA 5. Symptomatic support

Answer 253

* Greenish-yellow gas with strong, pungent odour * React with moist tissue and causes oxidization --\> damage * Reaction also causes production of certain acids like HCL --\> more damage * Symptoms: 1. Airway burning and irritation --\> feeling of suffocation 2. Pulmonary edema and respiratory arrest * Treatment: symptomatic treatment + humidified NaHCO₃ might help

Answer 254

* Alkylating choking agent that causes inhibition of several enzymes and interferes with oxygen transportation by Hb * No antidote, only supportive care

Answer 255

1. Irritation of all body surfaces in contact 2. Lacrimation and eye pain 3. Pharyngeal or pulmonary edema 4. Rhinorrhea 5. Erythema

Answer 256

1. Choking agent that produce HCL when in contact with moist tissue 2. AlsoI increases pulmonary vascular permeability --\> pulmonary edema 3. Also causes bronchial epithelial damage --\> local emphysema and partial atelectasis

Answer 257

1. Lacrimation 2. Nausea and vomiting 3. Dyspnea and pulmonary edema 4. Bloody or foaming white sputum 5. Cyanosis 6. Nephrotoxicity 7. Polycythemia \* Mainly supportive/symptomatic treatment, maybe aminophylline for the pulmonary edema

Answer 258

1. Mainly supportive/symptomatic treatment

Answer 259

Inactivate SH-containing enzymes and activate **TRPA1** receptors (noxious/irritation receptors)

Answer 260

\*Treatment is mainly symptomatic/supportive

Answer 261

1. Non-selective anticholinergic gas used as psychomimetic/incapacitating agent 2. Much stronger than atropine 3. Anticholinergic symptoms 4. Treated with physostigmine

Answer 262

Mechanism: Prevents presynaptic release of ACh Ocular: ptosis, blurred or double vision, strabismus, nystagmus GI: constipation, dysphagia Respiration: respiratory failure Nurological: descending paralysis, weakness

Answer 263

Spesific antitoxin therapy: antitoxin binds circulating toxin and prevents progression

Answer 264

1. Mycotoxic compund that is cytotoxic to rapid-dividing tissue (e.g spleen, bone marrow, GI, thymus etc...) 2. Its toxic effects resemble damage done by radiation

Answer 265

Four ways of effecting the body: 1. Binding to ribosomal subunit --\> inhibition of protein synthesis 2. Aactivation of apoptic pathways 3. Direct cell membrane damage 4. Stimulate release of inflammatory cytokines

Answer 266

1. Early fever 2. Nausea, vomiting and diarrhoea 3. Irritation of GI mucosae --\> GI hemorrhage 4. Hepatic and renal damage 5. Adrenal insufficiency 6. CNS depression If it is injected instead of ingested, the above symptoms occurr very fast and patient dies within 3 days!

Answer 267

1. No antidote yet 2. Gastric lavage and activated charcoal 3. Whole-bowel irrigation with polyethylene glycol 4. Supportive treatment of symptoms

Answer 268

* Taken for Asthma and COPD * Therapeutic lvls 10-20 mcg/mL * Toxic lvl \>20 mcg/mL * Mainly metabolised in the liver * Half-life varies (somwehere around 5-8h)

Answer 269

1. Phosphodiesterase inhibition --\> increased cAMP --\> adrenergic simulation --\> B1 and B₂ stimuli --\>vasodilation and vasoconstriction 2. A₂ receptor antagonist --\> increased HR and contraction

Answer 270

1. Metabolic: Hyperglycemia, Hypercalcemia, Hypophosphatemia and Hypokalemia 2. CNS: Tremors, agitation, hallucination, seizures 3. Cardiac: Dysrythmias, Supraventricular tachycardia --\> ventricular tachycardia --\> VF --\> PEA 4. Pulmonary: Acute lung injury and respiratory alkalosis --\> respiratory failure

Answer 271

1. Serum Theophylline lvl 2. Serum lvl of other medications to check for cross-reaction (common cause of chronic theophylline injury) 3. Electrolyte lvl (monitor metabolic symptoms) 4. ABG - monitor metabolic acidosis 5. ECG - monitor cardiac symptoms

Answer 272

1. Multidose Activated Charcoal (main treatment) 2. Cathartics (with first dose of MDAC) 3. Gastric lavage - often helpful 4. Whole Bowel Irrigation - for Theophylline SR 5. Benzodiazepines in case of seizures 6. Fluids for hypotension, a₁ agonists or B-antagonists (Esmolol) also helpful 7. Antiemetics in case of vomiting 8. Extracorporeal treatment

Answer 273

1. Symptomatic patients \> 90 mcg/mL 2. Long-time theophylline concentrations \> 40 mcg/mL 3. Life-threatening toxicity 4. Persistent seizures 5. Hypotension that is not responding to IV fluids 6. Ventricular dysrhythmia

Answer 274

80%: Ethanol --\> Acetaldehyde --\> H₂O and CO₂

Answer 275

1. Downregultes GABA in CNS --\> sedation 2. Disrupt motor cortex in cerebellum --\> ataxia 3. Inhibits NDMA receptors --\> memory disturbances, slurred speech and black out 4. Increase endogenous opioid release --\> Euphoria and analgesics 5. Seretonin analog --\> antidepressive 6. Dopamine analog --\> Dependance 7. Inhibit ADH release --\> dehydration 8. Loss of thermoregulation --\> Hypothermia

Answer 276

Common: 1. Many metabolic dearrangement (Everything is hypo) 2. Behavioural effects 3. Children suffer more from hypoglycemia (less glycogen stores) Severe: 1. CNS- and respiratory depression 2. Arrhythmias hypogylcemia 3. Hypotension 4. Hypothermia 5. Lactic acidosis

Answer 277

1. Clinical features and Breathalyzer (main way of diagnosis) 2. ABG and blood sample 3. Exclude all ATOMIC criteria 4. Osmolar gap \>10 (osmolar gap: 2xNa + glucose + urea) 5. Anion gap \> 20 (anion gap: Na + K - (Cl + HCO₃)) 6.

Answer 278

1. Mild: Autonomic hyperactivity, tremor, weakness, anxiety, headache sweating 2. Hyperreflexia and GI sympotoms. \< 6h 3. Tonic-Clonic seizures \<48 h 4. Alcoholic hallucinations: Conciousness remains 5. Delirium tremens: 48-72h: Anxiety attacks, increasing confusion, poor sleep (scared), profuse sweating, tachycardia, hyperpyrexia and severe depression

Answer 279

1. Rubbing alcohol 2. Metabolised to Acetone and excreted through the kidneys 3. Intoxication produces KETOSIS (not acidosis) 4. Diagnosis similar to ethanol, but look for ketosis 5. Treatment: supportive

Answer 280

1. Found in antifreeze (ask about fluid color) 2. Mechanism: Ethylene glycol → Glycoaldehyde (nephrotoxic) → Glycolic acid (Acidosis)→glyoxylic acid→ Glycine, **OXALATE** **(nephrotoxic)** and a-hydroxy-b-ketodiapate \*Thiamine and pyridoxime deficiencies will further increase oxalate metabolite, because they are needed as co-factors when glycine and a-hydroxy-b-ketoadipate are made

Answer 281

* Phase 1: Neurological/drunk \<12h * Phase 2: Cardiopulmonary phase 12-24h * Hypocalcaemia with QT elongation → arrhythmias * High metabolic acidosis with kussmaul breathing * Phase 3: Renal toxicity

Answer 282

* Diagnosis: calcium oxalate crystals in urine * Treatment: Fomepizol (antidote) + kidney transplant if necessary

Answer 283

Methanol → formaldehyde → Formate (Accumulates, can cross BBB) → C02 and H20 * Metabolism is VERY slow, which means formic acid has time to accumulate and cause systemic acidosis * It also inhibits mitochondrial activity, causing tissue hypoxia and lactic acidosis

Answer 284

1. CNS: Coma and convulsions + basal ganglia necrosis = parkinsonism 2. Retinal: Mydriasis, Optic nerve hyperaemia, photophobia (toxicity due to formic acid buildup in optic disc and nerve) 3. Cardiac: Tachycardia, hypertension --\> hypotension 4. Respiratory: Tachypnea

Answer 285

1. Fomepizole 2. Ethanol 3. Hemodialisys (if acidosis is severe or there's renal failure)

Answer 286

ABG (acidosis **does not occur** in ethylene glycol toxication)

Answer 287

* Psychoactive stimulant * Can be snorted or injected * Dopamine reuptake inhibitor * Effect: 1. Spontanous motor activity 2. Appetite and drink suppression 3. Euphoria

Answer 288

* An aphrodisiac stimulant * Norepinephrine-reuptake inhibitor

Answer 289

Short-term: 1. Tachycardia and hypertension 2. Increased alertness, anxiety and arousal Severe: Panic attacks and psychosis from sleep withdrawl Long-term: Comedown syndrome (lethargy, headache, depression)

Answer 290

Same psychoactive effect as natural but: 1. THC lvl cannot be measured in patients using them 2. Much more addictive 3. Effect last much longer \*Symptomatic treatment + benzo or SSRI's in case of psychotic agitation

Answer 291

* Group of drugs causing CNS depression * Include Barbiturates and non-barbiturates (Benzo,carbamates, GHB etc...)

Answer 292

* Non-barbiturate that increase GABA B receptor activity and dopamine levels in the CNS * Date-rape drugs (cause loss of conciousness) * Symptoms: 1. Slurred speech 2. CNS- and mild respiratory depression 3. Seizures 4. Coma

Answer 293

* Non-barbiturates used for many medical conditions * Bind to allosteric site of GABA receptors --\> increased receptor stimulation --\> depression of spinal reflexes and RAS * Addictive and cause withdrawl syptoms similar to ethanol withdrawl

Answer 294

Mild: 1. Sedation 2. Slurred speech 3. Ataxia Severe: 1. Hypotension and hypothermia 2. Respiratory depression 3. Coma 4. Rhabdomiolysis

Answer 295

1. Flumazenil (main antidote) 2. Gastric lavage and activated charcoal 3. Supportive treatment of symptoms (e.g ventilation)

Answer 296

1. TCA's 2. Cocaine

Answer 297

* Sedative hypnotics used for sedation and treatment of epilepsy, including status epilepticus * Increase stimulation of GABA receptors * Symptoms: 1. CNS depression: somnolescense, ataxia, coma 2. Myocardial depression --\> hypotension, collapse 3. Respiratory depression (cause of death) 4. Blisters

Answer 298

1. No antidote! 2. Activated Charcoal - might help 3. Monitor heart and kidneys 4. Intubate in case of hypoxia 5. Correct hypothermia and hypotension 6. Hemodialisys - if nothing else helps

Answer 299

1. Includes phenobarbital 2. They have longer effect and severe symptoms come early 3. Can be monitored (at least serum phenobarbital lvl) 4. Urine alkalinization works for long-acting, but not short-acting!

Answer 300

1. An antiepileptic drug with large destribution 2. Lipid soluable, easily enters the brain 3. Selectivily inhibit overactive epileptic foci by blocking Na-K pump, while normal-firing neurons are not affected 4. Has an active metabolite (carbamezipine epoxide) that can buildup

Answer 301

1. Nystagmus 2. Tachycardia and hypotension 3. Ataxia 4. Variation between CNS agitation and depression --\> coma 5. Respiratory depression and apnea 6. Urinary retention 7. Toxic Epidermal Necrolysis (TEN), blisters 8. DRESS syndrome 9. Stevens-Johnson syndrome

Answer 302

1. Serum Carbamezipine lvl 2. Glucose and electrolytes for differentials 3. Abdominal radiograph (might see pill buildup) 4. ECG: Sinus tach, AV-block, long WRS and QTc

Answer 303

1. Multiple Doses of Activated Charcoal 2. Gastric lavage 3. WBI 4. Symptomatic treatment

Answer 304

1. Prolongs recovery period of inactiva Na channels --\> less nerve firing (similar effect as carbamezipine) 2. Increase amount of GABA release at synapses 3. Interfere with urea cycle --\> hyperammonemia 4. Interfere with fatty acid metabolism and deplete carnitine lvls --\> fatty liver 5. Metabolised to active metabolites --\> prolonged action \*Used for seizures, as mood stabilizers and bipolar disease

Answer 305

1. Nusea and vomiting (most common) 2. Lethargy, cerebral edema and coma 3. Fever 4. Hypotension

Answer 306

1. Serum Valproic Acid lvl 2. Liver panel 3. Anion gap 4. CT head: cerebral edema

Answer 307

1. Hemodialisys (main treatment) 2. L-carnitine supplementation (may resolve some symptoms) 3. GI decontamination 4. Supportive treatment

Answer 308

1. Reduse delisions, confusion and agitation in psych-patients 2. Used as sedatives and tranquilizers 3. Used as anitemetics

Answer 309

Antagonise the following: 1. Central D₂ receptor) 2. Muscarinic receptors 3. Serotonin receptors 4. a₁-receptors 5. H₁-receptors Pathophysiology include anticholinergic and extrapyramidal symptoms

Answer 310

1. A special reaction to neuroleptic drugs 2. Often linked with haloperidol use 3. Linked to D₂-receptor inhibitory effect of neuroleptics

Answer 311

1. **Hyperthermia** 2. **Autonomic dysfunction: tachycardia, BP instability, arrythmia** 3. **Lead-pipe rigidity** 4. **Altered mental status** 5. Hypotension and seizures might also occur The first 4 clinical findings are enough for diagnosis +also look for high CK lvls in urine

Answer 312

1. The 4 main symptoms are enough for diagnosis 2.

Answer 313

1. Dantrolene (main antidote) 2. Dopamine agonists - Bromocriptine and Amantadine 3. Supportive treatment

Answer 314

For treating the dystonia caused by Neuroleptics and other antipsychotic drugs

Answer 315

1. Sertraline 2. Fluoxetine 3. Paroxetine 4. Fluvoxamine

Answer 316

CNS: 1. Mood and personality 2. Temperature 3. Wakefulness Systemic: 1. Vascular tone 2. Platelet activation 3. Peristalisis

Answer 317

* A series of severe side effects of SSRI's * Charcterized by: 1. Mental status changes 2. Neuromuscular dysfunction 3. Autonomic instability

Answer 318

1. Symptoms increase with increased SRRI intake 2. Three of the following is seen: altered mental status, agitation, tremor, shivering, diarrhea, hyperreflexia, myoclonus, ataxia, or hyperthermia 3. Other causes are excluded 4. Patient has not taken neuroleptics before symptoms occur

Answer 319

1. No antidote! 2. WBI 3. Activated Charcoal 4. Airway management and benzo for seizures 5. Supportive treatment

Answer 320

1. A drug-induced or stress-induced hypermetabolic syndrome 2. Characterized by hyperthermia, muscle contractions, and cardiovascular instability 3. Linked to genetic Ca-transport defect of skeletal muscles 4. Several drugs like Halothane and Succinylcholine are triggers of this syndrome

Answer 321

1. May occur within 30 min of anesthesia 2. Begins with muscle rigidity of the chest, then spreads 3. Following tachycardia 4. And finally hypertension

Answer 322

**Dantrolene** (main treatment) - stops muscular overactivity by stopping release of Ca from the sarcoplasmatic reticulum in muscles \*CC-blockers are useless for malignant hyperthermia

Answer 323

1. Inhibit reuptake of seretonin and norepinephrine 2. In chronic use may inhibit alpha-, Beta, and seretonin receptors

Answer 324

1. Cholinolityk properties --\> anticholinergic symptoms 2. Cardiotoxic: Long QRS and QT, Torsades, myocardial depression and a-antagonism --\> hypotension 3. Cross BBB --\> delirium and seizures 4. Discontinuation --\> withdrawl symptoms \* Diagnose by tox analysis and ECG

Answer 325

1. Exercise induced 2. Traumatic (blunt force trauma etc...) 3. Toxicologic 4. Metabolic disorders 5. Genetic disorders 6. Infections

Answer 326

1. Hypovolemia (water goes into injured myocites) 2. Hyperkalemia (release of cellular K into blood) 3. Metabolic acidosis (release of cellular phosphate and sulfate) 4. Acute renal failure (nephrotoxic effects of myocyte components) 5. Disseminated intravascular coagulation (DIC) 6.

Answer 327

1. Increased serum CK (most useful) 2. Positive urine dipstic for hemoglobin/myoglobin 3. High serum creatinine 4. Increased LDH 5. Hyperkalemia 6. Hypocalcemia 7. Hyperuricemia + ECG abnormalities might also be seen

Answer 328

Mainly supportive treatment to prevent end-organ damage, especially kidneys, monitor CK while you do this: 1. Crystalloid fluid to keep urinary output 2. Urinary alkanization + consider osmotic- or loop diuretics 3. Treat electrolyte abnormalities and DIC

Toxicology Flashcards

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