Toxicology Flashcards

(177 cards)

1
Q

<div><b>Indications For Dialysis in Lithium Poisoned Patients</b></div>

A

<div>Severely symptomatic patients </div>

<div>Unable to tolerate fluid hydration </div>

<div>Renal impairment </div>

<div>Acute toxicity: Levels above 4 mEq/L </div>

<div>Chronic toxicity: Levels above 2.5 mEq/L</div>

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2
Q

<div><b>List the ECG changes potentially seen in lithium toxicity</b></div>

A

<div><b>Think about it as looking at an ECG from P to T waves</b></div>

<div><br></br></div>

<div>Bradycardia </div>

<div>AV blockade </div>

<div>QT prolongation<br></br></div>

<div>ST changes </div>

<div>Ischemic changes<br></br></div>

<div>Flattened or inverted T-waves </div>

<div>+</div>

<div>Brugada pattern</div>

<div></div>

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3
Q

“<div><span>List risk factors for toxicity in the setting of chronic lithium use</span></div>”

A

<div><i>Renal causes:</i><br></br> Nephrogenic DI </div>

<div> Renal impairment </div>

<div><i>Hypo</i>:<br></br> volemia</div>

<div> Na</div>

<div><i>Acute illness </i></div>

<div><i>Drugs:</i><br></br> Diuretic<br></br> NSAIDS<br></br> ACE/ARB </div>

<div><i>Dementia /Increased age</i></div>

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4
Q

<div><b>List disease states caused by Lithium</b></div>

A

Nephrogenic DI<div>Hypothyroidism</div><div>Hyperthyroidism</div><div>SILENT</div>

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5
Q

What is SILENT

A

“<div><span>syndrome of irreversible lithium-effectuated neurotoxicity</span></div><div><div><span>Persistent cerebellar and brainstem dysfunction, dementia, and extrapyramidal signs even after lithium use has been discontinued for more than 2 months</span></div></div>”

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6
Q

List three deadly clinical manifestations of clonidine toxicity

A

<div>Apnea/hypoventilation</div>

<div>Hypotension</div>

<div>Bradycardia</div>

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7
Q

Substances Causing Wide Anion-Gap Acidoses

A

“<b>A CAT PILES MUD</b><br></br><b><br></br></b><div><b>A: A</b>lcoholic ketoacidosis<br></br><b>C: C</b>yanide,<b>c</b>arbon monoxide (CO),<b>c</b>olchicine<div><b>A: A</b>cetaminophen (large ingestions)<br></br><b>T: T</b>oluene<br></br><b>P: P</b>araldehyde,<b>P</b>henformin</div><div><b>I: I</b>soniazid,<b>i</b>ron,<b>i</b>buprofen</div><div><b>L: L</b>actic acidosis<br></br><b>E: E</b>thylene glycol<br></br><b>S: S</b>alicylates<br></br><b>M: M</b>ethanol,<b>m</b>etformin</div><div><b>U: U</b>remia<br></br><b>D: D</b>iabetic ketoacidosis</div></div>”

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8
Q

Potentially Lethal Toxins Where Early Activated <br></br>Charcoal Administration May Be Indicated

A

<b>THE KILLER CS</b><br></br>Cyanide<br></br>Colchicine<br></br>Calcium channel blockers<br></br>Cyclic antidepressants<br></br>Cardio glycosides<br></br>Cyclopeptide mushrooms <br></br>(Amanita phalloides)<br></br>Cocaine<br></br>Cicutoxin (water hemlock)<br></br>Salicylates

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9
Q

Substances That Do NotBind to Activated Charcoal

A

<b>SAPHIL</b><div><b>S</b>olvents</div><div><b>A</b>lcohols, Acids, Alkalis</div><div><b>P</b>esticides</div><div><b>H</b>ydrocarbons, Heavy metals</div><div><b>I</b>ron</div><div><b>L</b>ithium</div>

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10
Q

Dialyzable Toxins

A

<b>STUMBLED</b><br></br>Salicylates<br></br>Theophylline<br></br>Uremia<br></br>Metformin/methanol<br></br>Barbiturates<br></br>Lithium<br></br>Ethylene glycol<br></br>Depakote (valproic acid—in massive overdose)

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11
Q

Substances Amenable to Multiple-Dose <br></br>Activated Charcoal

A

ABCDQ<br></br>Aminophylline/theophylline<br></br>Barbiturates<br></br>Carbamazepine/concretion forming drugs (eg, salicylates)<br></br>Dapsone<br></br>Quinine

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12
Q

Nalaxone dose in Clonidine Toxicity

A

<div>Escalating doses of naloxone of 0.1 mg, 0.4 mg, 2 mg, and 10 mg</div>

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13
Q

What is indicated in refractory Bradycardia in Clonidine Toxicity

A

Atropine

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14
Q

Clonidine withdrawal S/S

A

Htn<div>Anxiety</div><div>Tachycardia</div><div>Sweating</div>

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15
Q

GCS

A

“<img></img>”

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16
Q

Usual Bedside Tests

A

Blood Sugar (Accucheck)<div>ECG</div><div>Urine Preg test</div>

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17
Q

””“<u>Must have lab tests</u>”” in acute toxicity”

A

<div>Venous gas</div>

<div>Electrolytes</div>

<div>Bun</div>

<div>Cr</div>

<div>Tylenol level</div>

<div>Salicylate level</div>

<div>ETOH</div>

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18
Q

Universal Antidote

A

“Glucose<div>Oxygen</div><div>Thiamine</div><div>Nalaxone</div><div>"”Flumazenil”” in certain conditions esp children</div>”

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19
Q

Goal of Nalaxone

A

“<span>Reversal of </span><u><span>respiratory</span></u><span> depression</span>”

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20
Q

Factors of persistent neurological sequelae after CO poisoning

A

<div>significant loss of consciousness or coma</div>

<div>persistent neurological dysfunction (e.g. confusion or seizures)</div>

<div>abnormal cerebellar examination</div>

<div>metabolic acidosis</div>

<div>myocardial ischaemia</div>

<div>age >55 years</div>

<div>pregnancy</div>

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21
Q

Antidotes

A

“<img></img>”

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22
Q

“<img></img>”

A

TCA overdose<div>S in I</div><div>R in aVR</div>

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23
Q

ECG Findings in TCA overdose

A

S in lead I and aVL<div>R in aVR</div><div>Wide QRS</div><div>Rt axis deviation</div><div>Sinus tachycardia</div><div><br></br></div><div><br></br></div>

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24
Q

Mechanisms of TCA toxidromes

A

Na channels blockade (QRS prolongation)<div>K channels blockade (QT prolongation)</div><div>Antihistamine (hypotension, sedation)</div><div>Anticholinergic toxidrome</div><div>Serotonin syndrome</div><div>GABA blockade (seizure)</div><div>Alpha-1 blockade (hypotension)</div>

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25
What is the leading cause of in-hospital death from TCA overdose
"Refractory Hypotension due to:
Profound alpha antagonism
Decrease myocardial contractility leading to decrease cardiac output
"
26
How do you ‘set up a sodium bicarb infusion
Add 2 amps to 1 L of D5W and infuse at ~150-250 cc/hr
27
Target Serum ph in alkalinization 
Ph 7.45 - 7.55
28
Indications of Na bicarb in TCA overdose
QRS widening
Refractory hypotension
Ventricular Dysrrhthmia
29
Antiarrhythmic medication of choice in TCA 
Lidocaine
30
Hunter Criteria
""
31
Agents causing serotonin syndrome
"

Saints Sell Drugs That Make Me Trip On the Tram Line
St. John's Wart
SSRI/SNRI
Dextromethorphan
TCA
Meperidine
MAOI
Triptans
Ondensterone
Tramadol
Linzolid

"
32
Pathognominic dysrhythmia associated with digoxin toxicity
"Paroxysmal Atrial tachycardia (PAT) with block
Bidirectional VT
"
33
ECG findings in Digoxin Toxicity
PAT with AV block (most common)
Frequent PVCs (Bigeminy & trigeminy)
Slow AF
Any type of AV Block
VTs including plymorphic and bidirectional VT
34
Indications  of DigiFab in Acute digoxin overdose
  • Cardiac arrest
  • life threatening cardia dysrhythmia
  • ingested dose >10mg (adult) or >4mg (child)
  • serum digoxin level >15 mmol/L at any time
  • serum potassium >5.5 mmol/L
35
""
Paroxysmal atrial tachycardia with AV block
Digitoxicity
36
Is it indicated to replace Ca in cases of Digitoxicity
"No, will result in ""stone heart"""
37
How much DigiBind to use
Acute: Start with 5-10 vials
Chronic: Start with 3-5 vials
Cardiac arrest: Start with 10 vials
38
[K] in digitoxicity
Hyper K in acute
Hupo K in chronic
39
List three plants that have the potential to cause digitalis toxicity
"
Common oleander
yellow oleander
Lily of the valley
Red squill
Foxglove
dog's bane
Milkweed 
"
40
What is the main route of Digoxin elimination
Kidneys
41
What is The definition of hepatotoxicity after paracetamol overdose 
serum AST concentration ≥1000 IU/L.
42
Tylenol toxic doses
In adults and adolescents, hepatic toxicity may occur following ingestion of >7.5.  
In children the toxic dose is 140 mg/kg
43
NAC should also be started immediately or empirically when
Patients present 8 hours or more after ingestion
Serum Acetaminophen level is not available within an 8-hour time window
There is uncertainty as to the timing of the overdose
44
When do you start NAC in chronic ingestion?
"
Chronic ingestion = any ingestion(intentional, unintentional supratherapeutic) > 8hr period

Toxic level > 7.5 grams (adult)
Symptomatic regardless of APAP level
Elevated AST (> 2x upper limit normal or above 120 IU/L)
Elevated APAP > 30 mcg / ml
***Controversial:  all high risk pts (etoh and liver dx) w/ elevated AST *** 
"
45
What individuals are at increased risk for hepatocellular toxicity from chronic ingestion of APAP: 
ETOH use
Isoniazid use
Malnutrition
Dehydration 
46
List three differences between oral and IV NAC
"oral:
more n/v, 
takes longer, 
less anaphylactoid rxns

OR 

IV regimen is quicker than oral (20 hrs vs 72 hrs)
IV produces more anaphylactoid reactions compared to oral

Also acceptable:
(1) dosing errors are more likely with IV NAC
(2) possibly too much IV fluid for kids: potentially leading to hyponatremia and seizures
(2) The oral route frequently causes nausea and vomiting whereas the IV route does not
"
47
 Rumack-Matthew Nomogram is not useful in:
Chronic Overdose > 8 hrs
Delayed release tabs
Unknown time of ingestion
Co-ingestion (anticholinergics, ETOH)
glutathione deficiency 
Chronic liver diseases
Malnutrition
HIV infection
Cystic fibrosis
48
When can you stop NAC?
  1. INR <1.3
  2. AST or ALT WNL
  3. Non-Detectable acetaminophen level in the blood
49
Describe criteria for transfer to a transplant centre  
Kings College criteria, as per MDCalc, 
  1. Arterial pH < 7.30
  2. INR > 6.5 (PT > 100 sec)
  3. Creatinine 300 µmol/L
  4. Grade III or IV hepatic encephalopathy 
50
Dosing of NAC:
Oral:
Loading dose: 140 mg/kg, then
70 mg/kg q4hrs for 17 additional doses.
 
IV:
Loading dose: 150 mg/kg iv, then
Continuous infusion og 50mg/kg over 4 hrs, then
Continuous infusion of 100 mg/kg over the next 16 hrs
51
List 6 classes of medications that can cause an anticholinergic toxidrome
Antihistamines,
Antiparkinson agents,
antipsychotics
Antidepressants
mydriatics
antispasmodics
muscle relaxants
52
Causes of acidosis in toxic alcohols
Methanol: formic acid
Ethylene glycole: glycolic acid
Isopropanol: acetone (not an acid) result in ketonuria wout metabolic acidosis
53
End-organ effect of txic etoh
"
Alcohol
End Organ
Methanol:
Eyes: Blindness,     GIT: Pancreatitis
Ethylene glycol: 
Kidney: oxalic acid crystals: ARF
Isopropanol:
Hemorrhagic gastritis
"
54
Causes of Double Gap
  1. Ketoacidosis (diabetic, alcoholic).
  2. Alcohols (Ethylene glycol, methanol)
  3. Failures (renal, multiorgan)
55
Which vitamins are important in the treatment of ethylene glycol poisoning?
"
Pyridoxine 100 mg and thiamine 100 mg IV/IM drive the conversion of ethylene glycol to nontoxic metabolic’s.  

Calcium replacement may also be necessary

For methanol, folate 50 mg IVq4h to drive conversion of formic acid to Co2 and H2O
"
56
Ketosis is present in
  1. diabetic ketoacidosis,
  2. alcoholic ketoacidosis,
  3. starvation ketosis,
  4. salicylism, and
  5. cyanide and acetone ingestion
57
Advantages of Fomepizole over Ethanol:
More accurate dosing
Higher affinity to dehydrogenase

Less risk for:
Hypoglycemia
Electrolyte disturbances
CNS depression
58
List 6 indications for hemodialysis in salicylate poisoning
Clinical deterioration despite supportive care and urinary alkalinization
Salicylate level rising despite adequate therapy
Renal insufficiency or failure
Severe A/B disturbance
Altered mental status, or seizures
ARDS

59
How is ASA toxicity managed? 
1.  Start urinary alkalinization
2.  Correct hypovolemia: Urine output 2-3 mL/kg/hr
3.  Keep [K] >4.5, correct any hypomagnesemia 
4.  Give glucose for any CNS changes 
60
What is the primary cause of mortality in ASA toxicity? 
"
cerebral toxicity and metabolic acidosis
"
61
Which β blockers have intrinsic sympathomimetic activity? 
Why is this important?
"Pindolol
Acebutolol
Carteolol
Sotalol

can lead to some unusual manifestations such as ventricular dysrhythmias and sinus tachycardia instead of bradycardia

Sotalol causes Torsades
Acebutolol causes prolonged QT and VT
"
62
Why is propranolol the most lethal βB?
"
Lipophilic nature which allows it to penetrate the CNS, causing obtundation, respiratory depression and seizures.
"
63
HIET
"
  • Insulin and glucose
  •  Bolus 1 g/kg dextrose and run infusion at 0.5 g/kg/h. 
  • Insulin starts at 1 U/kg and infuse at 0.5U/kg/h. 
  • Increase in 1 hour if no hemodynamic response. 
"
64
Which β blockers can be dialysed?
"
SANTA can’t pee…..
  • Sotalol
  • Atenolol
  • Nadolol
  • Timolol
  • Acebutolol 
"
65
Indications of Deferoxamine
Fe level > 500 mcg/dL
Repeated vomiting,
toxic appearance,
lethargy,
hypotension,
shock
Metabolic acidosis
Hemochromatosis
66
What lab abnormalities are associated with HF burns?
"HypoCa 
HypoMg
HeperK
Metabolic acidosis

ECG findings:
prolonged QT
peaked T wave
"
67
Lab findings of NMS
Increased:
CK
WBC
BUN/Cr
LFT
Metabolic acidosis
68
Toxins That Cause Hypoglycemia
"

Acetaminophen
ASA Alcohol
Sulfonylureas (Gliburide)
Insulin
BB
"
69
Medications causing NMS other than antipsychotics
Metoclopromide
Li
Antidepressants
Withdrawal of Antiparkinson medication
70
Common drugs causing nystagmus
Barbiturates
Carbamazepine, 
PCP 
Phenytoin
Lithium
71
Toxins which are radiopaque on X-Ray
"CHIPES

"
72
Indications for Whole Bowel Irrigation:
  1. Ingestion of certain drugs: (Li, CCB)
  2. Extended release preparations 
  3. Illicit drug packets
  4. Metals (iron / lead)  
73
List 5 Dialyzable Drug
Properties
Low
molecular weight

Low protein
binding 

Low volume
of distribution 

Low plasma clearance   

Low
dialysate drug concentrations

High water
solubility 
74
List the “One Pill Can Kill” Drugs
"
MISCAST:
 
Methadone (and opiates)
Iron / Insulin 
Sulfonylureas 
CCBs clonidine
ASA 
Suboxone 
TCA’s  
"
75
Indications of intralipid
LA (Bupivacaine)
CCB (Verapamil)
BB (Propranolol)
Antidepressants (TCA, bupropion)
Organophosphate
76
Brady + HTN
Clonidine
77
Brady + Hypotension + Narrow QRS
Centrally acting alpha agonist (Clonidine)
BB
CCB
Cardiac Glycosides (Digoxin)
Sedative/hypnotics (benzo, barbiturates)
Opioids
Organophosphates

78
Brady + Hypotension + Wide QRS
Class 1a drugs (procainamide)
Class 1b drugs (lidocaine)
Class 1c drugs (flecainide)
BB (propranolol, acebutolol, metoprolol)
CCB
Digoxin
Hyper K

79
Tachy + HTN
Sympathomimetics (amphet, cocaine)
Anticholinergics (diphenhydramine, atropine)
80
Tachy + Hypotension
MAO
Alpha 1 aNTAgonists (prazosin, terazosin)
Phenothiazines (promethazine)
Diuretics
Nitrates
Theophylline
Caffein
81
Tachy + Hypotension + Wide QRS
TCA (amitriptyline)
M. Relaxants (cyclobenzaprine)
Anticholinergics (diphenhydramine)
Cocaine
82
Special note on decontamination: 
PPE
Remove Clothing and place in plastic bags
BRUSH OFF DRY CHEMICALS before hydrotherapy
Use gentle irrigation with low pressure water 
83
Most predictive test for cyanide toxicity
Profound lactic acidosis
(lactate > 10 mmol/L)
84
Indications for HBO
CNS: AMS, focal deficit, Coma
CVS: Syncope, Myocardial ischemia, dysrrhythmia
COHb > 25%
Pregnant 
85
Goal for CO poisoning treatment
To prevent delayed neuropsychiatric sequelae
86
Rapidly Lethal Toxins
  • Cyanide
  • Paraquat (herbicidal causing oxygen free radical concentrated in the lungs causing ARDS and resp failure)
  • Carbon monoxide
  • Hydrogen Sulfide
  • Sarin
  • VX gas
  • Fentanyl
  • Arsenic
  • Strychnine
  • Botulinum toxins 
87
Most comon digitoxicity dysrrhythmia is?
PVCs
88
Most common ECG finding in Digoxin use (toxicity or not)
ST depression with Dali Mustache
89
Criteria for increased toxicity of a hydrocarbon
High volatility
Low viscosity
Low surface tension
Halogenated
90
Effect of Hydrocarbons on the heart
Increase sensitivity of myocardium to catecholamines
Hypoxia secondary to lung injury
91
Indications of gastric lavage in Hydrocarbon toxicity
CHAMP
Camphor
Halogenated HC (Carb tetrachloride, PVC)
Aromatic HC (Benzen, toluene)
Metals HC (leaded gas)
Pesticides
92
What to avoid when treating HC toxicity dysrrhythmia
Epinephrine
Defebrillation
93
Toxicity of H2S is due to
Blockade of cytochrome oxidase leading to anaerobic metabolism and lactic acidosis
94
H2S antidote
Amyl nitrate
Na nitrate

(no Na thiosulfate)
95
INH toxicity
Decrease B6 (required for GABA synthesis)
Decrease seizure threshold
Metabolic acidosis
96
INH toxicity antidote
Pyridoxine (B6):
Known amount, dose is gram for gram
If unknown amount, dose is 5 grams
97
How INH toxicity present?
Status epilepticus
98
Toxic dose of Iron
30-40 mg/kg
99
Indications of deferoxamine
Fe level > 500 mcg/dl
Unstable vital signs
Repetitive vomiting
AMS/Coma
Seizures
100
SE of deferoxamine
Hypotension
ARDS
Increase yersinia sepsis
101
What confirms Iron overdose after giving deferoxamine
Vin Urine 
102
Blood film of lead posoining
Hypochromic microcytic anemia
basophilic stippling of the RBC
103
How is lead toxicity diagnosed?
  • Blood lead level
  • Anemia w/ basophilic stippling on smear
  • Radio-opaque lead in stomach
  • Radiographs of wrists and knees may show “lead lines”
104
Precipitating substances of hypertensive crisis in MAOI tox
Tyramine containing substances:
Amphetamines
Cheese
Wine
Fava beans
105
Causes of methemoglobinemia
Nitrites
Nitrates
Benzocaine
Dapsone
Pyridium
106
Methemoglobinemia antidote
Methylene blue (reduces Fe+3 to Fe+2)
Contraindicated in GSPD def
107
Bad prognostic sign of Mushroom poisoning
Delayed onset of symptoms of N/V/D (>6hrs) 
Ends with liver failure and renal failure
108
Antidote for sulfonylurea OD
Dextrose
Octreotide
109
What are the nicotinic effect of organophosphate poisoning
Muscle weakness
Fasciculation
Respiratory failure
110
Hyperthermia + Rhubdomyolysis
NMS
PCP 
Sympathomimetics
Opiate wirhdrawal
ETOH withdrawal
Seizures
111
Classical eye sign of PCP
Rotatory nystagmus
112
Miosis by toxins
COPS

Cholinergics, clonidine
Opioids, organophosphates
Phenothiazines, pilocarpine, pontine bleed
Sedative/hyonotics
113
Skin findings by toxins
Red: Anticholinergics, CO
Blue skin: MetHbemia
Blistering: Barbiturates, CO, spider bites, snake envenomations
114
Common toxins by odour
Bitter almonds: Cyanide
Rotten eggs: Hydrogen sulfide
Garlic: Arsenic, organoph
Fruity: DKA, isopropanol
115
Radiopaque Drugs
COINS

Chloral hydrate, cocaine packets
Opiate packets
Iron & heavy metals (Pb, As, Hg)
Neuroleptic agents
Sustained release products
116
List 10 Toxins That Cause Delirium
1.  Prescription medications (e.g., opioids, sedative-hypnotics, antipsychotics, etc…)
2.  Non-prescription medications (e.g., OTC antihistamines)
3.  Drugs of abuse (e.g., ethanol, heroin, hallucinogens, etc…)
4.  Withdrawal states (e.g., ethanol, benzodiazepines)
5.  Medication side effects (e.g.,serotonin syndrome, etc…)
6.  Poisons
                 a.  Toxic alcohols
                 b.  Inhaled toxins (e.g., carbon monoxide)
                 c.  Plant-derived toxins (e.g.,Salvia)
117
Indications for gastric lavage
❏  Lethal ingestion
❏  Early ingestion (drugs not in GI transit)
❏  No known antidote
❏  Not amenable to other decontamination strategies
❏  FACT (Fe, ASA, Colchicine, TCA) 
118
Hypoglycemia induced Toxins
❏  Beta blockers (especially in peds)
❏  Isoniazid (INH)
❏  Salicylates
❏  Sulfonylureas 
❏  Insulin 
❏  Ethanol  
119
How does co-ingestion of diphenhydramine (Benadryl) impact Tylenol OD
Co-ingestion with anticholinergics will impact gut motility, and can impact both your absorption times (i.e. interfering with nomogram interpretation) and may be associated with ongoing hepatocellular toxicity despite NAC 20hr IV protocol
120
What are the indications for dialysis in acetaminophen overdose?
  1. Highly elevated serum acetaminophen concentration (>1000 mg/L) at 4 hours post-ingestion
  2. Hepatorenal syndrome (Cr > 300)
  3. Metabolic acidosis with pH < 7.30
  4. Encephalopathy
  5. Elevated lactate (>3.5 mmol/L) 
121
Indications for Emergent Hemodialysis 
Following Acute Acetaminophen Ingestion
Highly elevated serum acetaminophen concentration (>1000 mg/L) at 4 hours post-ingestion
Hepatorenal syndrome 
Metabolic acidosis with pH <7.30
Encephalopathy
Elevated lactate (>3.5 mmol/L)
122
Indications of Physostigmine in Anticholinergic Toxicity
Delirium / Coma / Seizure
Risk of harming themselves or staff
Requiring ongoing physical restraint, or 
Interfering with effective treatment (eg, pulling out IV lines)
123
"
Contraindications of Physostigmine
"
TCA overdose
Widened QRS >100
AV blocks
Bradycardia
Narrow angle Glaucoma
Unknown co-ingestions 
124
Other than Na bicarb, what can be used in TCA toxicity related wide QRS
Hypertonic Saline
125
What are the indications of Hypertonic Saline in TCA toxicity?
Ph > 7.55 with failure of Na bicarb to shorten the QRS
126
List 3 meds to avoid in TCA overdoses
Physostigmine
Class 1a anti arrhythmic meds (procainamide)
Class 1c anti arrhythmic meds (flecainide)
Phenytoin
127
What rhythm is NOT associated with Dig toxicity
Afib with rapid ventricular response due to AV block
128
What medications/procedures to be avoided in treating Digitoxicity?
Ca
Salbutamol
Epinephrine
Defibrillation
Pacing
129
Temporizing measures while awaiting for DigiBind
Atropin for shock and bradycardia then pacing (avoid if possible)
Lidocaine & Phenytoin for tachydysrrhythmia
Maintain K (3.5-4)
130
Dose of MDAC
1g/kg every 2-4 hrs for 4 doses
131
Rx of metHbemia
O2 therapy/HBO
Methylene blue (if MetHb >25%)
Vit. C
Exchange transfusion
132
Leading cause of mortality in cocaine/sympathomimetic OD
Severe hyperthermia
Dysrrhythmia
Intractable seizures
HTN leading to ICH, aortic dissection, MI
133
DDX of aggitation + hyperthermia
SS
NMS
Sympathomimetic OD
Anticholinergic OD
Malignant hyperthermia
ASA
T4 OD
ETOH withdrawal
134
Principles of Mx of Stim-induced hyperthermia
Rapid cooling
Iv fluids
Sedation
Paralysis + intubation
135
What is a consequence of a long-term toluene abuse?
Cortical atrophy and dementia
136
"What signs/characteristics could you look for to help determine if the patient is truly in alcohol withdrawal instead of drug-seeking?"
"tongue tremor is a possible finding in alcohol withdrawal that is impossible to feign and could help confirm the patient truly has withdrawal (see link below for video). 
The general tremor of alcohol withdrawal has a few key characteristics: 
it is an intention tremor (thus there is no tremor at rest), 
it is constant, and 
it does not fatigue
"
137
Pupils in Toxicology
""
138
"TCA OD, What are your next five management steps? "
1. Obtain IV access
2. Administer sodium bicarbonate 1 amp immediately (or 1-2 mEq/kg/IV bolus). Continue bolus q3-5 mins until QRS narrows.
3. Set up a sodium bicarbonate infusion (FYI: Setting up a sodium bicarb infusion: Add 2 amps to 1 L of D5W and infuse at ~150\200 cc/hr)
4. ICU Consult
5. Consider calling poison center
6. Consider decontamination
139
"List 6 lab tests you must order in toxicology"
Best answers:
1. electrolytes
2. venous gas
3. Tylenol/acetaminophen level
4. salicylate level
5. Creatinine

Also acceptable: CBC, BUN, Cr, alcohol level, blood glucose, lactate, serum osmolality, magnesium

NOT ACCEPTABLE: random urine drug screen
140
"In TCA, What key ECG and laboratory parameters must you monitor and what are your endpoints?"
"
ECG: QRS narrowing to <120 ms

Serum pH: The patient's pH should be maintained between 7.45 and 7.55.

"
141
"Generally speaking, list 2 circumstances in which you would start NAC even before receiving any lab values. "
1. Patient presents 8 hours or more after ingestion
2. Serum acetaminophen level is not available within an 8 hour window
3. There is uncertainty re: the timing of the overdose
4. Massive overdose
142
General non-toxicological DDX of toxidromes:
1. DKA
2. Meningitis
3. Encephalopathy
4. Sepsis - any source (Pneumonia, UTI, intra-abdominal infection)
5. Peripheral vertigo/ vestibular neuritis/ meniere’s disease
6. Intracranial mass
7. Intracranial hemorrhage
8. Posterior circulation CVA
9. Gastroenteritis
10. Hyponatremia
11. Thyroid storm
143
"In ASA posoning, what history and physical findings support the diagnosis of salicylate poisoning?"
1. Tinnitus
2. Confusion
3. Tachypnea
4. Hyperthermia
5. Increased ASA use on Hx
6. Tachycardia
7. GI upset
144
"ASA, List your next 4 management priorities, including two treatments that you will need to consider."
1. High acuity monitored bed
2. IV access
3. IV fluid bolus
4. Start sodium bicarbonate infusion
5. Consider dialysis
6. Consider decontamination/Whole bowel irrigation
7. Consider starting potassium supplementation
145
"Assuming the patient has taken a massive dose of Verapamil, name 5 different treatments/medications you could treat him with?"
-High dose insulin euglycemic therapy
-Glucagon
-Calcium gluconate/chloride
-Vasopressor infusion
-Lipid emulsion therapy
-IV Fluid bolus
-Consider decontamination/Whole bowel irrigation
- Consider Atropine (low evidence)
146
Fever+ALOC DDX:
  • Sepsis,
  • Meningitis,
  • Encephalitis,
  • Serotonin syondrome,
  • NMS,
  • anticholinergic,
  • Salicylates,
  • Thyroid Storm,
  • Heat Stroke
147

List three classes of drugs that can impair lithium clearance

1.NSAIDs

2.ACE INHIBITORS

3.SSRIs

4.THIAZIDE DIURETICS

5.Nb also, topirimate

148

Besides drugs, list 3 contributors to impaired lithium clearance

1.Dehydration

2.Hyponatremia

3.Renal impairment

4.Hyperthyroid

149

List 3 likely clinical manifestations of acute lithium toxicity in the absence of impaired lithium clearance.

"

Acute lithium toxicity mainly affects the GI tract as lithium (like other metal salts) is a direct irritant. It causes nausea, vomiting, abdominal pain and diarrhoea.

If Li clearance is impaired, can see:

Neurotox (sluggishness, ataxia, confusion, tremosrs, myoclonus, seizures). 
Cardiac (arrythmias, bradycardia, prolonged QT)

"
150
  • List three ECG changes that are associated with Lithium toxicity
  1. Transient ST depression (also accept ST segment changes)
  2. Inverted T waves
  3. Occasional patients develop sinus node dysfunction and syncope (also accept heart blocks)
151
Key factors for acute Li toxicity
Volume depletion
NSAIDs
152
Universal DDx of Severe HA,N,V:
Infections:
     Meningitis
     Encephalitis
     Sinusitis
Hge:
     SAH
     SDH
Tox:
     CO poisoning
     OD: sedative, hypnotics
     W/D: ETOH
Acute angle glosire glaucoma
Metabolic:
     HypoNa
     DKA/HHS
Preeclampsia
153
What specific lab tests for CO poisoning?
CoHb conc
CK
Trop
VBG
Lactete (more reliable index of severity than COHb)
154
Causes of death in CO poisoning
MI
Dysrrhythmia
Non cardiogenic pulm edema
Rhubdomyolysis leading to renal failure
155
ECG finding of TCA
R in aVR
S in I and aVL
RAD in terminal QRS
Wide QRS > 100
RBBB
Tachycardia
Bradycardia (pre-terminal)
156
Indications for DigiBind
  • Symptomatic bradydysrhythmias
  • Ventricular dysrhythmias
  • Any patient with acute digoxin overdose and potassium concentrations >5.0 mEq/L
  • Acute ingestion of >4 mg in a healthy child (or 0.1 mg/kg)
  • Acute ingestion of >10 mg in a healthy adult
  • Serum concentration of ≥10 ng/mL 4 to 6 hours after ingestion
  • Serum concentration of ≥15 ng/mL at any time.
  • Chronic poisoning w/ significant GI sxs, altered LOC, or renal insufficiency
157

If this woman’s granddaughter had taken her digoxin acutely in a suicide attempt, how might her granddaughter’s presentation and management differ from her own?

"

1.The granddaughter’s course is less indolent – she would likely be asymptomatic for minutes to hours after exposure and then rapidly deteriorate. 

2.Grandma would be more likely have HYPOkalemia and granddaughter would more likely have HYPERkalemia.  The hypokalemia is often from concommitent diuretic use or losses from n/v/d. 

  • In fact, hyperkalemia is a marker of morbidity and mortality, although correcting it does not change the m or m

3.Granddaughter will be less likely to die than grandmother.

  1. Gastrointestinal symptoms, such as nausea and vomiting, are usually less pronounced in chronic toxicity as compared with acute toxicity.
  2. Neurologic manifestations, such as lethargy, confusion, delirium, disorientation, and weakness, may be more prominent with chronic toxicity.
  3. Visual changes are more common with chronic toxicity and may include alterations in color vision, development of scotomata, or blindness.

**In both cases, call your local poison center!!

"
158
CI of Mg Rx
Bradycardia
AV block
Renal failure
HyperMg
159
Causes of Osmolar gap and anion gap
""
160
ECG Abnormalities in Bupropiom toxicity
QRS prolongation
QT prolongation
161
"List two potentially deadly consequences of Bupropion toxicity?"
  1. Refractory status epilepticus
  2. Cardiogenic shock/hypotension/tachydysrhythmias
162
"Clonazepam + Bupropion co-ingestion. Which complication is potentially less likely in this case and why? "
A benzodiazepine co-ingestion reduces the change of seizures 
163
Urin alkalinization is useful in what Toxins?
CLAMP
Chlorpropamide
Lead
ASA
Methotrexate
Phenobab
164

Indications and Contraindications for Hemodialyis

Indications: I STUMBLE NASA

Isopropanyl, salicylates, theophylline, uremia, methanol, barbituates, lithium, ethylene glycol, nadolol, atenolol, sotalol, acebutolol

Small Vd,

Low protein binding,

Small size,

low endogenous clearance,

water soluble

165

Indications for Liver Transplant after APAP OD

  • pH < 7.3,   2 days post resus (i.e. refractory metabolic acidosis)
  • INR > 6.5 - coagulopathy
  • Hepatic encephalopathy
166

Disturbances caused by salicylate toxicity & their effect

1.Stimulates the resp center (medula)- increase RR – Resp alkalosis

2.Inhibits Kreb Cycle - increase lactate – metabolic acidosis

3.Uncoupling of oxidative-phosphorylation - increase metabolic rate - increase temp, increase O2 consumption, increase tissue glycolysis – decrease Glu

4.increase  Hepatic gluconeogenesis increase Glu

5.Direct corrosive toxicity to gut

6.increase Lipid metabolism - increase Ketones – thus Ketosis

167

Indications for serum alkalinization in TCA OD and Mechanism of Action

  • QRS > 120msec
  • VT (2nd line = lidocaine)
  • Cardiac Arrest
  • Seizures
  • Hypotension

MOA:

Uncouples tricyclic from Na channel for 10 – 15 min

decrease protein binding

Increase Na gradient

Increase pH

168

Management of Toxic Alcohols

"

1.Correct Acidosis with Bicarb ± hyperventilation – prevents diffusion of toxic metabolites into target tissues

– target pH 7.45 – 7.55

2.Fomepizole –

  Indications: OsM Gap > 10, pH < 7.3, Bicarb <20, Urine: Oxalate Crystals

3.Dialysis:

Indications: Ethylene Glycol > 8mmol, Methanol > 5mmol, Metabolic acidosis, end organ symptoms (eg. Visual/ decrease LOC) renal impairment, lyte abnormalities, unstable VS

4.Adjunctive treatment:

  • Thiamine 100mg IV
  • Folic Acid 50mg IV
  • Pyridoxine 100 mg iv
"
169

What is the antidote to iron and what are its main side-effects?

  • Deferoxamine 15mg/kg/hr IV x 24 hours
  • Side Effects:
    • decrease  BP – just slow down the infusion
    • Respiratory toxicity if prolonged infusion
170
What is the most frequent cause of treatment failure in organophosphate poisoning
Inadequate atropine.
Large doses are needed nearly 20-40 mg/day
171
Why is glucagon useful in rx of BB OD
Glucagon enhances myocardial contractility, heart rate and AV conduction by stimulation the production of cyclic AMP
It works on receptors other than BB receptors
172
What medications can cause hyperthermia
Neuroleptics
Anticholinergic
ASA
Succinylcholine
Sympathomimetics
PCP
Lithium
173
Organophosphate poisoning
""
174
Phencyclidine (PCP) Intoxication
"
·         HTN, tachycardia, hyperthermia
·         Vertical, horizontal, or rotatory nystagmus
·         Variable pupil size
·         Combative behavior
·         Complications: rhabdomyolysis, seizures
·         BZDs, cooling, IVF, charcoal

"
175
LA toxicity
Neuro:
- Tinnitus.
- Numbness of mouth.
- Confusion, anxiety, sense impending doom, HA, drowsiness, dizziness, tremors.
-Seizures.
Cardiac:
- widening PR interval, QRS, bradycardia, VT, VF, hypoTN, asystole
- Methemoglobinemia with exposure to benzocaine, prilocaine
- Hemodynamic collapse.
176
Rx of LA toxicity
Intralipid (IV fat emulsion): acts as lipid sink, pulling local anesthetics from site of toxicity
- Give 20% solution 1.5cc/kg bolus then 0.25cc/kg/min over 30-60min.

Supportive:
- Benzos for seizures
- Methylene blue for methemoglobinemia
177
Which group of local anesthetics cause most allergic reactions?
Esters, due to production of metabolite, paraaminobenzoic acid (PABA).
Note that multi-dose bottles of amide contain preservative methylparaben which is chemically related to PABA.