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Toxicology Flashcards

1
Q

Which toxins cause hypoglycemia?

A

ethanol, oral hypoglycemics, Bblockers, salicylates and insulin ingestion

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2
Q

What are the universal antidotes?

A

DONT= dextrose, oxygen, naloxone, thiamine (consider in adolescent patients who may be thiamine deficient (100 mg IV) ie. eating disorder, alcoholism or chronic disease (IBD))

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3
Q

Dose of naloxone?

A

Adolescent patient (without habituation): 2 mg bolus q2min up to 8-10 mg, if chronic abuse suspected: 0.2 mg or less warranted

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4
Q

Contraindications to activated charcoal?

A

unprotected airway or disrupted GI tract (severe caustic ingestion), if charcoal will increase risk/severity of aspiration (e.g. hydrocarbons)

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5
Q

List 4 other ingestions when NOT to use charcoal

A 
Pesticides, petroleum distillates
Hydrocarbons, heavy metals
Acids/Alkali, alcohol 
Iron
Lithium
Solvents
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6
Q

3 indications for WBI

A 
●	Sustained release pills
●	Ingestions of metals/lithium
●	Body packers or body stuffers
●	Ingestion of pharmaceutical patches
●	Massive overdose
●	Bezoar of pills
●	Increasing serum level despite gastric decontamination
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7
Q

4 contraindications to WBI?

A

airway not protected
peritonitis
GI obstruction
hemodynamic instability

Complications: nausea, vomiting, cramping, bloating, aspiration

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8
Q

How to calculate anion gap?

Some causes of high AG?

A

Calculation: Na- (Cl+HCO3)
normal: 8-12 (depends on lab)
Elevated AG = MUDPILES

(methanol, uremia, DKA, Paraldehyde, INH, lactic acid, ethylene glycol, salicylates)

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9
Q

Differential diagnosis of 1 pill can kill

A
  • Beta blockers (propranolol)
  • Clonidine (0.1 mg)
  • Calcium channel blockers
  • Glyburides (sulfonylurea)
  • Theophylline
  • TCA
  • Methylsalicylate (oil of wintergreen)
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10
Q

General tox management

A
  • ABC
  • Disability – drugs (universal antidotes – oxygen, glucose, naloxone + specific antidotes), decontamination (activated charcoal), draw labs
  • Exposure/ examine + enhanced elimination
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11
Q

Calculation of osmolar gap (and causes of high OG)

A

o Osmolar gap = measured osm – calculated osm (2x Na + BUN + glucose)

High osmolar gap suggests ethanol, methanol, ethylene glycol, acetone, sugars (ie. mannitol)
> 10-15 is a high osmolar gap

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12
Q

Which drugs are radio-opaque on xray?

A

chloral hydrate, heavy metals (iron, lead), iodine, phenothizines, psychotropics, slow-release/ enteric-coated meds

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13
Q

Sympathomimetic toxidrome - drug causes, features, treatment

A

Cocaine, amphetamines, MDMA

Inc HR, BP, T, Sweaty, Mydriasis, Agitation, psychosis, seizures

Tx- supportive care, benzos, cooling

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14
Q

Features of anticholinergic toxidrome

A 
Inc HR, BP, T
Blind – mydriasis
Dry 
Red – flushed skin
Mad – delirium
Dec bowel sounds
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15
Q

Tx of anticholinergic toxidrome

A
  • NaBicarb if prolonged QRS (TCA)
  • Lorazepam for agitation I(avoid Haldol)
  • Cooling
  • Physostigmine if peripheral and central toxicity (delirium) – NOT in TCA overdose
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16
Q

Features of cholinergic toxidrome

A

“SLUDGE”: salivation, lacrimation, urination, defecation, gastric cramping, emesis
+ miosis, generally bradycardic, bronchorrhea, bronchospasm (killer B’s)

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17
Q

Tx of cholinergic toxidrome

A
  • Oxygen
  • early intubation (avoid succ)
  • Remove clothing and vigorously irrigate skin
  • Atropine 0.05 mg/kg IV/IM/IO bolus Q5min until secretions and wheezing stops
  • Inhaled ipratropium – Pralidoxime (2-PAM)
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18
Q

Toxicologic causes of hyperthermia

A

Sympathomimetics, anticholinergics, salicylates, Neuroleptics (NMS), SSRI (serotonin syndrome), Succinylcholine (MH)

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19
Q

Tox causes of miosis

A

Opioids, Organophosphates (cholinergic syndrome), Ethanol, Clonidine, PCP, Barbiturates

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20
Q

When is multi-dose activated charcoal recommended?

A
  • Interrupts enterohepatic recirculation: phenobarbital, phenytoin, carbamazepine, VA, TCA, digoxin, dapsone, quinine, theophylline
  • Sustained-release medications
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21
Q

Which toxins are dialysable?

A

lithium, salicylates, toxic alcohols, phenobarbital, theophylline

Must have low molecular weight, water soluble, low volume of distribution (ie. Not digoxin – large volume), not highly protein-bound

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22
Q

How does naloxone work? What are some side effects?

A

● Pure opioid receptor antagonist, serum ½ life 1 hr, duration of action 1-4 hr
● Competitively displaces narcotic analgesic at central opioid receptor site
● can cause withdrawal sx ( GI upset, tachycardia, hyperpnea, HTN, sialorrhea, mydriasis, piloerection, yawning, rhinorrhea, hyperalgesia, restlessness, discomfort, diaphoresis, anxiety)

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23
Q

Antidotes for cyanide toxicity

A

● Sodium thiosulfate

● Hydroxocobalamin - binds cyanide to form vit B12 excreted in the urine

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24
Q

Mechanism of action of NAC

A

i. Acting as a precursor for glutathione to increase available glutathione (major).*
ii. Increasing non-toxic sulfation metabolism (major).**
iii. Directly reducing NAPQI to APAP (minor).
iv. Directly conjugating NAPQI (minor).
v. Mitigation of adverse intracellular cascades even after NAPQI covalent binding occurs.

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25
Q

Toxic dose of acetaminophen

A

Toxic Dose: 7.5-10 g or 150-200 mg/kg

Plasma APAP level (at 4hr): ONLY reliable indication of potential severity of hepatic damage

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26
Q

Pathophysiology of acetaminophen toxicity

A

● Metabolized in the liver via 1) glucuronidation 2) sulfation and 3) metabolism via CYP 450 to produce NAPQI (hepatoxic)
● NAPQI conjugates with glutathione - non-toxic metabolites
● Massive overdose: glutathione depleted - NAPQI binds to hepatocytes and leads to cellular necrosis - Elevated ALT/AST - hepatic failure/death

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27
Q

Side effects of NAC

A

anaphylactoid reaction (caution with history of asthma), hyponatremia

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28
Q

Indications for NAC tx

A

o APAP level above “treatment” line on nomogram following acute ingestion,
o single ingestion more 150 mg/kg more 8 hours ago (ie. Serum level won’t be available before 8 hours post-ingestion)
o unknown ingestion time and APAP level > 66 mgl/L
o delayed presentation and evidence hepatotoxicity

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29
Q

Stages of acetaminophen toxicity

A
  • Stage I (0-24 hours): nausea, vomiting, anorexia, may be asymptomatic
  • Stage II (24-48 hours): symptoms resolve then RUQ pain, elevated liver enzymes, elevated INR/PTT
  • Stage III (48-96 hours): peak hepatotoxicity, renal insufficiency, cerebral edema, coma, acidosis, possibly death (due to cerebral edema)
  • Stage IV (4-14 days): resolution of symptoms
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30
Q

best indication for severity of liver disease in acetaminophen toxicity

A

Mental Status, INR and pH

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31
Q

List 3 ways to prevent accidental overdose in a toddler

A

Primary Prevention (UTD)

  1. Legislation
  2. Product Engineering (regulating number of tablets per container, child-resistant packaging, unit-dose packaging, storage/locking devices, use of flow restrictors for bottles of liquid medication, bittering agents to make substances unpalatable)
  3. Educational Efforts

Environment Factors

  1. Storing all medications in locked cupboards or out of reach from children
  2. Close supervision of children at all times
  3. Ensuring all medication bottles have child safety lids/closures
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32
Q

What are some toxins that can cause an anticholinergic toxidrome?

A

Jimsen Weed, deadly night shade plant, TCA, antihistamines, atropine, benztropine, olanzapine

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33
Q

Side effects of physostigmine

A

Side effects: can precipitate seizures, bronchospasm, bradycardia, asystole (can give atropine if bradycardia occurs, treat seizures with benzos)

Do NOT give in TCA overdose - do not given if QRS > 100 msec, PR > 200 msec, RBBB

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34
Q

What is the normal QTc cut off?

How do you calculate QTc?

A

< 440 ms

QT/square root of previous R-R interval (usually in lead II)

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35
Q

Acid-base status in salicylate toxicity

A

mixed respiratory ALKalosis and metabolic ACIDosis (ie pH typically 7.41-7.55, if < 7.35 consider severe resp acidosis from CNS depression, PC02 < 30, HCO3: 15-20)

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36
Q

Toxic dose of ASA?

A

Toxic dose: 150-300 mg/kg= mild sx
300-500 mg/kg = moderate toxicity
>500 mg/kg = lethal

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37
Q

Clinical features of ASA toxicity?

A

Stimulates medullary respiratory center –> tachypnea/ resp alkalosis. Uncoupling of oxidative phosphorylation –> lactic acidosis (mixed gas). Fever, hypokalemia, N/V, lethargy, seizures, tinnitus. Hyperglycemia –> hypoglycemia (and CNS hypoglycemia with both)

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38
Q

Tx of ASA toxicity

A
  • AC up to 4 hours (delayed gastric emptying and bezoars), consider MDAC
  • Alkalinize serum (and urine) with IV sodium bicarbonate (keep blood pH 7.45-7.5) – keeps ASA out of the CNS
  • Glucose for all patients with change in mental status, treat hypokalemia
  • Hemodialysis
  • AVOID intubation/sedation
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39
Q

indications for dialysis in ASA toxicity?

A
  1. serum salicylate > 100 mg/dL after acute ingestion or 60 mg/dL after chronic
  2. Severe acidosis or electrolyte disturbance
  3. Renal failure
  4. Persistent neurological dysfunction
  5. Pulmonary edema
  6. Progressive clinical deterioration despite standard treatment
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40
Q

List 6 signs/symptoms of salicylate toxicity

A
  1. CNS: seizures, coma
  2. HEENT: Tinnitus
  3. Hyperpyrexia
  4. Resp: tachypnea, pulmonary edema
  5. CVS: tachycardia, VT/VF
  6. GI: N/V, hepatitis
  7. Rhabdomyolysis
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41
Q

Pathophysiology of Hypernatremia in ASA toxicity

A

dehydration, fluid loss (high free water loss)

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42
Q

Pathophysiology of Hyperthermia in ASA toxicity

A

uncoupling of oxidative phosphorylation

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43
Q

Features of beta-blocker overdose

A
  • Bradycardia, AV blocks, hypotension, can may QRS and QT prolongation (sotalol – blocks K channels), vasodilation, hypoglycemia, coma, seizures, resp depression, bronchospasm
  • High lipid solubility = increased CNS effects (seizures, dec LOC) – ex: propranolol, carvedilol
  • Membrane stabilizing activity (Na channel blockade) –> leads to QRS widening (ex: propranolol)
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44
Q

Treatment of beta-blocker overdose

A

IV fluids, vasopressors, calcium, glucagon (controversial), high-dose insulin euglycemic therapy. Most are not dialysable, with a few exceptions

45
Q

Features of CCB overdose

A
  • Refractory hypotension, bradycardia, mental status often maintained
  • Cardiac: decrease inotropy leading to sinus bradycardia, AV node block (verapamil and diltiazem) = calcium gluconate, atropine, pacing
  • PVS: vasodilation leading to hypotension = IV fluids and vasopressor
  • Pancreas: leads to hypoinsulinemia resulting in hyperglycemia
46
Q

Treatment of CCB overdose

A

o AC within1 hour, consider WBI especially for extended-release
o Atropine, pacing
o calcium gluconate bolus or infusion
o NE vasopressor
o high dose insulin euglycemic therapy (D10W 2.5 ml/kg IV and insulin R 1 U/kg at 1 U/kg/hr +K)
o intralipids – second line/ if arresting

47
Q

What are some of the plant cardiac glycosides

A

Foxglove, oleander, lily of the valley

48
Q

Sx of acute digoxin overdose

A

Symptoms in acute overdose: cardiac primarily, N/V, lethargy, visual disturbances, weakness, confusion. HyperK is a marker of severe toxicity

49
Q

ECG findings in digoxin overdose

A

high-degree heart block and increased automaticity (ventricular or supraventricular escape rhythms), peaked T waves
o Digitalis effect (scooped ST segments, prolonged PR) can also be seen with therapeutic levels

50
Q

Features of clonidine overdose? Antidote? Toxic dose?

A

Miosis, coma, hypothermia, resp depression. Initial hypertension (peripheral vascular activation initially)–> hypotension and bradycardia

trial of naloxone (may not be effective)
Toxic dose is 0.1 mg

51
Q

A 2 year old male presents after being found with several tablets of his grandmothers CCB. List 4 clinical features of CCB overdose and the mechanism behind each feature

A
  1. Hypotension- blockage of the L type Ca channels peripherally ( dihydropyridines)
  2. Bradycardia – blockage of the L type Ca channels in the myocardium ( non-dihydropyridines)
  3. Hyperglycemia- impaired Ca mediated insulin release/ and insulin resistance
  4. Metabolic acidosis- inhibits the Ca-stimulated mitochondrial activity and ATP hydrolysis, also tissue hypoperfusion
52
Q

Indications for digifab?

A
  1. Progressive signs and symptoms of intoxication
  2. Life threatening cardiac arrhythmias
  3. Severe hyperkalemia ( K > 5.5 mEq/L)
53
Q

Toxic dose of iron?

A

> 40 mg/kg

20 mg/kg of elemental iron = GI toxicity
40 mg/kg = moderate toxic effects
>60 mg/kg = profound toxicity

54
Q

Best decontamination method for iron?

A

WBI if tablets on xray or less 6 hours, NOT gastric lavage or AC

55
Q

5 stages of iron OD and their timing?

A
  • Stage 1 (0-6 hours): GI phase - N/V/D, GI bleed
  • Stage 2 (6-24 hours post-ingestion): quiescent stage – resolution of GI symptoms (iron accumulates in mitochondria)
  • Stage 3 (1-3 days post-ingestion): metabolic acidosis, shock, GI hemorrhage, coagulopathy, resp failure, seizures, coma = shock and lactic acidosis
  • Stage 4 (2-3 days): liver failure, ARDS
  • Stage 5 (2-8 weeks ): bowel obstruction: gastric stricture, pyloric or bowel stenosis
56
Q

Indications for deferoxamine?

A

greater 60 mg/kg ingested, systemic symptoms (other than mild GI), elevated AG metabolic acidosis, peak serum greater 90 umol/L, significant number of pills on AXR

57
Q

2 reasons to discontinue use of deferoxamine

A 
Patient improves:
●	serum iron normalizes
●	metabolic acidosis resolves
●	clinical improvement
●	urine colour normalizes
Side effect/complications:
●	Hypersensitivity reaction
●	ARDS
●	Hypotension
●	toxic retinopathy
●	Yersinia sepsis
58
Q

Triad seen in INH toxicity?

A
  1. Seizures- GTCs, have a rhythmic recurrence and are difficult to treat ( comatose between seizures)
  2. Metabolic acidosis (severe! pH of 6.4 reported) high anion gap metabolic acidosis
  3. Coma – prolonged
59
Q

Glyburide (sulfonylurea) ingestion - mechanism of action? Tx?

A

MOA : Stimulate pancreatic insulin secretion and reduce glucagon secretion and improve insulin sensitivity
Tx: Dextrose bolus then infusion, octreotide (glucagon not recommended routinely, only if not IV access)

60
Q

Side effects of metfromin overdose?

A

Does NOT cause hypoglycemia - leads to lactic acidosis. (Increases insulin sensitivity)

61
Q

Common side effect of phenothiazines (and its tx)

A

Dystonic reaction (with chlorpromazine in particular and other anti-dopaminergic agents, ie. Antiemetics, metoclopramide) – unrelated to dose ingested, can be delayed 8-40 hours post-ingestion. Treat with IM/IV diphenhydramine (Benadryl), benztropine, or diazepam

62
Q

A young child is thought to have ingested his grandmother’s cyclic antidepressants at her home. You examine him in your ED. List 4 clinical features associated with this type of poisoning

A
  1. CNS: seizures, altered LOC, hallucinations, ataxia coma
  2. CVS: arrythmias ( wide QRS), myocardial depression, Vtach/Vfib
  3. Anticholinergic: hyperpyrexia, dry skin, decreased GI motility
  4. Antihistamine: sedation
  5. Alpha blockade: hypotension
  6. Serotonin effects: myoclonus, autonomic sx
63
Q

TCA’s - 4 mechanisms of action (other than Na blockade)

A
  1. Anticholinergic
  2. a adrenergic blockade- hypotension, vasodilation
  3. Na channel blockade- prolonged QRS, can lead to complete heart block or ventricular arrythmias (VTach) , myocardial depression (decreased inotropy), also find R wave > 3 mm amplitude in aVR ( classic finding in TCA),
  4. NE/Serotonin reuptake- early hyperadrenegic symptoms, increased DTRs
  5. Antihistamine: sedation
  6. Anti-GABA: seizures
  7. K channel blockade- long QT
64
Q

Typical EKG findings in TCA overdose?

A
  • QRS > 100 in lead 2
  • Right axis deviation
  • Terminal R wave > 3mm in AVR
65
Q

Treatment of TCA overdose?

A

AC (slow GI motility so consider if >1 hour), sodium bicarbonate for QRS > 100 1-2 mEq/kg IV then infusion; NE if hypotensive; physostigmine contraindicated

Treat seizures with benzos. Avoid phenytoin/ fosphenytoin as act as Na-channel blockers

66
Q

Serotonin syndrome triad?

A

autonomic instability, clonus/tremor, altered mental status

67
Q

a. What are 5 neuromuscular findings of serotonin syndrome

b. What are 4 autonomic findings of serotonin syndrome

A
  • Autonomic findings: diaphoresis, tachycardia, hyperthermia, hypertension, vomiting, and diarrhea
  • Neuromuscular findings: tremor, muscle rigidity, myoclonus, hyperreflexia, and bilateral Babinski sign
68
Q

Features of isopropyl alcohol intoxication?

A

Hallmark is ketosis without acidosis, severe gastritis; myocardial depression at high doses

69
Q

Toxic metabolite of methanol ingestion, and its effects?

A

Formic acid: metabolic acidosis + ocular toxicity

classic “ looking through a snowstorm”

70
Q

List 3 medications that can be used to treat methanol intoxications?

A

Folic acid, fomepizole, ethanol (if fomepizole not available), NaHC03 +/- dialysis

71
Q

Toxic metabolite of ethylene glycol intoxication, and its effects?

A

glycolic acid and oxalate

Metabolic acidosis + deposition of calcium oxalate crystals in organs

72
Q

Tx of ethylene glycol intoxication

A

Nabicarb
Fomepizole (ethanol) if early
Dialysis if late
Cofactors: pyridoxine, thiamine

73
Q

3 stages of ethylene glycol toxicity

A 
Stage 1: CNS manifestations+ metabolic acidosis
Stage 2: Cardiopulmonary failure (due to acidosis)
Stage 3 (24-72 hours): Renal failure (ATN)
74
Q

What are the 2 most serious complications of ethylene glycol ingestions

A
  1. Cardiorespiratory failure

2. Renal failure

75
Q

What is the first enzyme responsible for metabolizing ethylene glycol

A

alcohol dehydrogenase

76
Q

What electrolyte abnormality is typically seen in ethylene glycol toxicity, side effect?

A

hypocalcemia - prolonged QTc, arrythmias

77
Q

Red flags in caustic ingestions?

A

stridor, drooling, vomiting = indications for scope

78
Q

Indications for scope in toxic ingestion?

A

all intentional ingestions (drink a larger amount), stridor, drooling, vomiting, pain. Ideal timing within 12-24 hours (later = risk of esophageal perforation)

Uptodate says upper scope for pretty much all caustic ingestions – unless questionable ingestion, non-dangerous product AND asymptomatic

79
Q

Concern with hydrofluoric acid ingestion?

A
  • Weak acid, systemic complications are the concern: hypocalcemia, hypoMg, hyperkalemia
  • Treat with calcium
80
Q

Features of hydrocarbons that allow for pneumonitis to occur

A

Low viscosity, low surface tension –> allow to spread over large surface area (lungs) – and high volatility

81
Q

4 causes/sources of lead poisoning

A

lead based paint ( homes through 1950s), burning of battery casings, water carried by outdated pipes, improperly home glazed ceramics, lead contamination in spices/cosmetics, dust/dirt contaminated by vehicles which one used leaded gasoline

82
Q

2 neurologic sequelae of lead poisoning

A

lead encephalopathy

seizures ( secondary to cerebral edema)

83
Q

symptoms of lead exposure

A
  1. Persistent vomiting, listlessness, or irritability, clumsiness or loss of recently acquired developmental skills
  2. Afebrile convulsions
  3. PICA
84
Q

Pathophysiology/ effects of organophosphate toxicity?

A

• Irreversibly inactivates acetylcholinesterase –> Ach builds up (effect at cholinergic junctions)
1- autonomic sites (muscarinic) = SLUDGE, miosis, bradycardia, bronchorrhea/wheezing
2- skeletal muscle (nicotinic) = sweating, muscle twitching, tremors, weakness, paralysis
3- CNS = dizziness, headache, ataxia, coma

85
Q

Management of organophosphate toxicity?

A
  • skin decontamination, remove clothing and vigorously irrigate skin (activated charcoal ineffective)
  • early intubation (avoid succ)
  • Oxygen
  • Atropine 0.05 mg/kg IV/IM/IO bolus Q5min until secretions and wheezing stops (may need to be continued over hours to days)
  • Inhaled ipratropium
    – Pralidoxime (2-PAM) – helpful for weakness/ paralysis (regenerates active acetylcholinesterase – where the organophosphates block)
86
Q

What class of antipsychotic is contraindicated in organophosphate poisoning?

A

Phenothiazines (affect the uptake of acetylcholine and its release)

87
Q

A child eats a bunch of berries and is noted to be tachycardic, hypertensive and hyperthermic. What are 5 other symptoms?

A

Child ingested Belladonna (atropine) = anticholinergic toxidrome

Symptoms: Mydriasis, hallucinations, flushing, gastroparesis, urinary retention, dry mouth, dry skin, lethargy, agitation, seizures

88
Q

Plants that contain cyanogenic glycosides?

A

seeds – pears, apple; plum, peach, apricot, bitter almond

89
Q

Which mushrooms are most dangerous? Typical timing of symptom onset?

A

Delayed onset of symptoms (> 6 hours) –> Amanita phalloides mushroom

Long latent period, then GI symptoms ~24 hours after ingestion (phallotoxin), hepatotoxicity, renal failure (amatoxin) and death (need liver transplant)

90
Q

List 4 street drugs that can cause hallucinations

A

psilocybin, LSD, mescaline, MDMA (ie. Ecstasy, Molly), synthetic cathinones

91
Q

Features of PCP intoxication (angel dust)

A
  • NMDA antagonist, structurally similar to ketamine (dissociative anesthetic)
    Hallmark = muscle rigidity + crazy
  • Clinical: Seizures and delirium with fluctuating behaviour with delirium, paranoia, agitation, violence (acute brain syndrome), respiratory depression and coma, nystagmus while awake (vertical or rotary)
  • Dystonic posturing, muscle rigidity, myoclonus
  • Sympathomimetic actions: Hypertension, tachycardia
92
Q

When is THC seen on urine tox screen for acute/ chronic daily use?

A

3 days after single use; up to 30 days with regular chronic use

93
Q

Tx of agitation for PCP overdose?

A

● Avoid physical restraints can lead to rhabdomyolysis, myoglobinuria and renal injury
● Chemical restraints: lorazepam or haloperidol

94
Q

What is the most common cause of death from ecstasy?

A

Hyperthermia

95
Q

15 yo girl given a pill in a concert. She is now agitated, sweaty, hypertensive, and has mydriatic pupils.

a) What is 1 drug to give now for her agitation? 
b) What are 4 complications of this toxidrome?
A

MDMA (ecstacy) ingestion:

a) benzodiazepenes
b) serotonin syndrome, hyperthermia, rhabdo, seizures, hyponatremia, cerebral edema, hepatotoxicity (MDMA)

96
Q

What is a body packer vs body stuffer?

A

“body packer” (enclosed in plastic bags and swallowed for smuggling) and “body stuffer” (sudden ingestion of cocaine – higher risk as more likely to leach out of bag)

o Bags can rupture leading to sudden large ingestion
o Activated charcoal and WBI indicated, rarely surgical removal
o AXR to assess extent of stuffing, CT if unclear on xray

97
Q

Features of benzo overdose?

A

Coma with relatively normal vitals, resp depression can be seen

98
Q

Indications for flumazenil?

A

Rareoy indicated, except:

  1. Reverse a witnessed, unintentional benzodiazepine overdose in a young child
  2. To prevent airway intubation after iatrogenic overdose
99
Q

A teen comes in after an ingestion and is very agitated. He is hyperthermic, has dilated pupils and dry skin. What antipsychotic do you NOT want to give him?

A

Do not give haloperidol (may lower the seizure threshold of the overdose patient, may add to the cardiovascular neurotoxicity and may limit the patient’s ability to dissipate heat)

USE benzo’s instead

100
Q

Indications for physostigmine, and side effects?

A

In anticholinergic overdose, with both peripheral and central toxicity – ie. Delirium, agitation = acetylcholinesterase inhibitor. Can be diagnostic/ therapeutic
S/E: can precipitate seizures, bronchospasm, bradycardia, asystole (can give atropine if bradycardia occurs, treat seizures with benzos)
do NOT give in TCA overdose

101
Q

Triad of opioid overdose?

A

Miosis, Resp depression, coma

102
Q

Side effects of naloxone?

A

opioid withdrawal (GI upset, tachycardia, HTN, mydriasis, rhinorrhea, diaphoresis, anxiety), rare – pulmonary edema, seizures

103
Q

Precursors of GHB?

A

GABA, gamma-butyrolactone and 1,4 butanediol (solvents) are metabolised to GHB

104
Q

4 non-opioid causes of myosis

A 
Opioids
Organophosphates
Ethanol
Barbiturates 
Phenothiazines
Phencyclidine
Clonidine
105
Q

4 complications of a fentanyl infusion in neonates

A 
nausea, vomiting, itching 
muscle rigidity
seizure like activity ( high doses) 
urinary retention
respiratory depression 
bradycardia 
hypothermia
106
Q

Contraindications for Naloxone

A

Hypersensitivity
use with caution in neonates born to opiate addicted mothers ( seizures)
known chronic user (precipiates withdrawal)
cardiac disease

107
Q

2 eye findings in GHB overdose and 3 excitatory neurological/behavioral findings

A

● Eye: disconjugate gaze, nystagmus ( horizontal and vertical), blurred vision, loss of peripheral vision, variable pupillary reaction, miosis
● 3 excitatory neurological/behavioral findings: agitation when disturbed, disinhibition, self-injurious or bizarre behaviors

108
Q

Risk factors for unintentional Ingestions?

A

Child: 1-4 years old, male, hyperactive, PICA
Environmental: acute stressor, parental illness
Agent: pallatability, attractiveness

109
Q

How much elemental iron in ferrous gluconate, sulfate, fumarate?

A 
Fumarate = 30%
Sulfate = 20%
Gluconate = 10%

“FSG 3-2-1”

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