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Clinical Pharmacology II > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What approach must we take with every patient suspected of overdosing?

A

Assess the ABCs:
Airway
Breathing Circulation

Vital signs

Supportive care/treatment

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2
Q

What important questions must be asked when a patient is suspected of overdosing?

A

Product:
What did the patient take?
What formulation of the medication did they take (immediate release vs. extended release?)

Amount:
How much did they take?

Coingestion:
Does the patient have anything else on board?

Time:
How long ago did they take it?

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3
Q

What must you look at on a physical exam of the patient?

A 
Skin exam
Vital signs
Eye exam
Abdominal exam
Neuro exam
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4
Q

What findings are you looking for on eye exam?

A 
Pupil size
Nystagmus
Reactivity 
Scleral discoloration
Ptosis/ophthalmoplegia
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5
Q

What findings are you looking for on skin exam?

A 
Temperature
Moisture
Flushed
Cyanotic
Pale
Track marks/abscesses
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6
Q

What findings are you looking for on abdominal exam?

A

Bowel sounds
Ileus
Abdominal cramping
Diarrhea

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7
Q

What findings are you looking for on neurological exam?

A

Mental status
Gait
Reflexes
Clonus

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8
Q

What symptoms are associated with anticholinergic toxidrome?

A

BRUCE!! Dry, fast, hot

Hot as a hare = hyperthermia
Dry as a bone = Dru mucous membranes, anhidrosis
Red as a beet = Skin flushed
Mad as a hatter = Confusion, delirium 
Blind as a bat = Mydriasis, blurred vision
Seizing like a squirrel = Seizures
Full as a flask = Urinary retention
Tachy as a leisure suit = Tachycardia
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9
Q

What symptoms are associated with cholinergic toxidrome?

A

SLUDGE and Killer B’s; Wet, cold, slow

Salivation
Lacrimation
Urination
Diaphoresis
GI upset = diarrhea
Emesis

Bronchorrhea
Bronchospasm
Bradycardia

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10
Q

What are the symptoms of sympathomimetic (adrenaline) toxidrome?

A 
Agitation
Anxiety
Mydraisis
Tachycardia 
Hypertension
Hyperthermia
Diaphoresis
Seizures
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11
Q

What are the symptoms of Sedative/Hypnotic (suppression) toxidrome?

A 
Stupor/coma
Confusion
Slurred speech
Respiratory depression = most concerning
CNS depression
Atoxia
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12
Q

What are the classic triad of symptoms with opioids?

A

Miosis
Depressed mental status
Bradypnea

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13
Q

What other symptoms are associated with opioid overdose?

A

Bradycardia
Hypotension
Hypothermia

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14
Q

What are the symptoms of Serotonergic syndrome?

A

Abnormal movements

Akathisia
Tremor
Myoclonus
Hyperreflexia
Muscle Hypertonicity
Flushing
Diarrhea
Hyperthermia
Altered mental status
Diaphoresis
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15
Q

What are the symptoms of Neuroleptic Malignant Syndrome (NMS)?

A 
Hyperthermia
Altered mental status
Autonomic instability
Lead-pipe rigidity 
Similarities exist with serotonin syndrome
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16
Q

How would you differentiate between serotonin syndrome vs. NMS?

A

Serotonin syndrome occurs < 12 hours

NMS occurs 1-3 days

Medication history

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17
Q

What diagnostic testing would you obtain for overdoses?

A

1) urine/serum tox screen
2) Pregnanct test
3) Aspirin/Acetominophen
4) ABG/VBG –> pH
5) CMP –> Anion gap
6) Glucose –> AMS
7) 12 lead EKG –> Cardiac

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18
Q

What are EKG changes that can be seen in overdoses?

A

QRS interval prolongation

QT interval prolongation

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19
Q

When would QRS intervals be prolonged?

A

When patient overdoses on agents blocking cardiac fast Na+ channels

QRS > 100ms

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20
Q

When would QT intervals be prolonged?

A

When patient overdoses on agents that block K+ efflex channels

QTc > 440 ms in men
QTc > 460 ms in women

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21
Q

What should be treated first in overdoses?

A

Whatever symptoms are going to kill the patient and then handle other diagnoses

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22
Q

What are some additional diagnostic tests that can be done for overdose patients?

A

Imaging = chest xray, CT
CBC
Ammonia
Toxic Alcohols + Ethylene glycol

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23
Q

What are the three treatment strategies for treating overdoses?

A

1st line of defense = Prevent absorption

2nd/3rd lines of defense = Enhance elimination and block effects of the drug

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24
Q

How do we prevent absorption of the drug?

A

Activated Charcoal ***
Emesis = not clinically used
Gastric lavage = use within 30-60 min. of ingestion
Cathartics = Questionable benefit, used with charcoal
Whole bowel irrigation = used when all other mechanisms cannot be used

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25
Q

What are the indications for using activated charcoal?

A

Use within 1 hour of ingestion

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26
Q

What are the contraindications for using activated charcoal?

A

Patient not able to protect airway

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27
Q

What are the side effects of using activated charcoal?

A

Bloating
Vomiting
Constipation
Diarrhea

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28
Q

What drugs/toxins are poorly absorbed by activated charcoal?

A 
Alkali
Cyanide
Iron
Hydrocarbons
Alcohols
Ethylene glycol
Potassium
Lithium
Inorganic salts
Heavy metals
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29
Q

How do we enhance elimination of the drug?

A

Urine alkalinzation = urine > 7.5

Hemodialysis

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30
Q

What are the pharmacokinetics of APAP?

A

90% undergoes hepatic conjugation:
Glucuronide (40-67%)
Sulfate (20-46%)

Oxidized by CYP2E1 (5-15%) = NAPQI created and metabolized quickly by glutathione (GSH)

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31
Q

What occurs in tylenol overdose?

A

Sulfation and Glucoronidation becomes saturated and reactive CYP 2E1 metabolism becomes primary pathway for metabolism

The build up of NAPQI causes liver cell death

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32
Q

What are the toxicokinetics of APAP?

A

Peak plasma concentrations within 4 hours

NAPQI production largely results of CYP2E1

Nontoxic sulfation metabolism becomes saturated

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33
Q

What is the mechanism of APAP toxicity?

A

NAPQI formation depletes GSH supply

NAPQI accumulates causing hepatotoxicity

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34
Q

What occurs in stage 1 of APAP toxicity?

A 
Nausea
Vomiting
Malaise
Pallor
Diaphoresis
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35
Q

What occurs in stage 2 of APAP toxicity?

A

Onset of liver injury <5%
AST elevation within 24 hours
Hepatotoxicity AST >1000IU/L

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36
Q

What occurs in stage 3 of APAP toxicity?

A

Maximal hepatotoxicity at 72-96 hours
Fulminant hepatic failure - encephalopathy, coma, exsanguinating hemorrhage
AST and ALT > 10,000 IU/L

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37
Q

What is the antidote to treat APAP toxicity?

A

N-Acetylcysteine (NAC)

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38
Q

What is the MOA of NAC?

A

Prevents toxicity as a GSH precursor and substitute

Increases substrate for nontoxic situation

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39
Q

What are the dosing regimens for NAC?

A

72 hours orally

21 hours IV

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40
Q

What are the ADRs of NAC?

A 
Rash
Nausea
Vomiting
Diarrhea
Rare Anaphylactic reactions
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41
Q

What are the pharmacokinetics of Salicylates?

A

Major route of biotransformation is conjugation with glycine in the liver

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42
Q

What are the toxicokinetics of Salicylates?

A

Pathways become saturated and exhibit zero-order kinetics

Longer half-life = 2-4 hours vs. 20 hours

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43
Q

What are the classic symptoms of Salicylate toxicity?

A

pH:
Acidosis = acidic drug/metabolites; lactic acidosis
Hyperventilation = respiratory alkalosis

Tinnitus
GI irritation

CNS effects:
Vertigo
Hyperactivity
Agitation
Delirium
Hallucinations
Convulsions
Lethargy 
Stupor
44
Q

What is the treatment for Salicylate toxicity?

A

Administer IV sodium bicarbonate in order to increase pH in the blood

This will create a concentration gradient and the extra salicylate (acid) in tissues will move towards blood and then be excreted

45
Q

What is the MOA of Benzo and Barbituate toxicity?

A

Increased activity of the inhibitory neurotransmitter GABA

46
Q

What are the signs and symptoms of Benzo and Barbituate toxicity/

A 
Slurred speech
Ataxia
Incoordination
Sedation
Hypothermia
Stupor
Respiratory depression
47
Q

How do we treat Benzo and Barbituate toxicity/

A

Watch and wait

Supportive measures = fluid or pressors for hypotension; intubation if necessary

Antidote = Flumazenil

48
Q

What is the MOA of Flumazenil?

A

Specific competitive BXD receptor antagonist

49
Q

When would use of Flumazenil be indicated?

A

Rapid reversal of BZD overdose

Operative or post-op reversal of BZD sedation

50
Q

What are the precautions for using Flumazenil?

A

Routine use of flumazenil is NOT recommended

Seizures or other withdrawal symptoms may be preciptiated

51
Q

Why is it recommended to not use Flumazenil for BZD overdose?

A

Patients who overdose on BZD most likely also took a stimulant

We use BZD to treat stimulant overdose so if we reverse the BZD overdose effects, the patient would start having sitmulant overdose symptoms which are much worse

52
Q

What is the MOA of toxicity of amphetamines?

A

Increased release of DA, NE, and 5HT

53
Q

What are the signs and symptoms of amphetamine overdose?

A 
Hypertension
Tachycardia
Euphoria
Abnormal movements
Psychotic episodes (agitation, hallucinogenic, paranoid)
Hypethermia/diaphoretic
Vasoconstriction
Rhabdomyolysis
54
Q

What is the mechanism of toxicity of Cocaine?

A

Increased activation of various excitatory neurotransmitters (Epi, NE, DA, 5HT)

55
Q

What are the signs and symptoms of Cocaine toxicity?

A 
Seizures
MI/cardiac ischemia
Coma
Headache
Intracranial hemorrhage
Mydriasis
Dysrhythmia
Hyperthermia
Rhabdomyolysis
Agitation/aggression
Delirium
Confusion
Hallucinations
56
Q

What is the mechanism of toxicity of Ecstasy?

A

Increased 5HT, DA, and NE

57
Q

What are the signs and symptoms of Ecstasy overdose?

A 
Dehydration
Hyperthermia
Serotonin syndrome
Seizures
Hyperpyrexia
Rhabdomyolysis
Organ failure
Hyponatremia
Anxiety
58
Q

What is the mechanism of toxicity of Synthetic cathinones?

A

Similar to amphetamines and MDMA

59
Q

What are the signs and symptoms of Synthetic Cathinone overdose?

A

Cardiac and psychiatric episodes

Hallucinations and aggression most common

60
Q

How do we treat stimulant toxicity?

A

No specific antidote, treat what you see!

Agitation = IV/IM BZD

Seizures = IV/IM BZD

Hyperthermia = External cooling, control agitation; remove clothing, cooling fan/blanket

Hypertension = BZDs; maybe vasodilators like nitroglycerin or nitropresside or nicardipine

61
Q

What is the mechanism of toxicity of Opioids?

A

Increased stimulation of opioid receptors

62
Q

What are the signs and symptoms of opioid overdose/

A 
RESPIRATORY  DEPRESSION
MIOSIS
Bradycardia/hypotension
Hypothermia
Stupor/coma
Itching
Reduced GI mobility
Euphoria
Sedation
Seizures
63
Q

What do we use to treat Opioid overdose?

A

Naloxone

64
Q

What is Naloxone?

A

Opioid receptor antagonist

65
Q

What are the kinetics of Naloxone?

A

Duration: 1-2 hours = may need to re-administer if the opioids effect has a duration longer than this

Onset: SQ/IM = 2-5 min.; nebulizer = 5 min.; Intranasal = 8-12 min.; IV = 2 min.

66
Q

What is are the ADRs of Naloxone?

A

withdrawal symptoms = want to administer enough to create spontaneous ventilation and make sure they are breathing but not enough to cause withdrawal symptoms

67
Q

What is the mechanism of toxicity of Organophosphates?

A

Rise in ACh at muscarinic and nicotonic cholinergic receptors by irreversibly binding to acterylcholinterase

68
Q

What are muscarinic effects of organophosphates?

A

SLUDGE
Vision = miosis, blurred
Bradycardia
Wheezing

69
Q

What are nicotinic effects of organophosphates?

A

Fasiculations
Paresis/Paralysis
Hypertension
Tachycardia

70
Q

What are central effects of organophosphates?

A 
Anxiety
Confusion
Seizures
Psychosis
Ataxia
71
Q

What doe we use to treat organophosphate toxicity?

A 
Atropine
Pralidoxime (2-PAM)
72
Q

What does Atropine do to treat organophosphate toxicity?

A

Competitively blocks ACh at muscarinic receptors

Atropinization = mydriasis, dry mouth, and tachycardia

Doses of up to 40 mg/day and gradually increase this over time until toxicity effects are gone

73
Q

What does 2-PAM do to treat organophosphate toxicity?

A

Reverses nicotinic and muscarinic effects by reactivating AChE and protecting the enzyme from further inhibition

Breaks apart the complex between the organophosphate and AChE

74
Q

What is the mechanism of toxicity of Tricyclic antidepressants (TCAs)?

A

Inhibits reuptake of NE and 5HT while also blocking H1, a1, Na channels, and muscarinic receptors

75
Q

What are the signs and symptoms of TCA toxicity?

A

Cardiovascular = sinus tachy with prolongation of the QRS, QTc, and PR intervals; torsades; AV block/Right BBB; Hypotension/myocardial depression

Hypoxia
Acidosis
Seizures
Hyperthermia
AMS
Anticholinergic
76
Q

What is the treatment for TCA toxicity?

A

GET AN EKG!!

QRS interval prolongation or hypotension = sodium bicarb

Persistent cardiotoxicity = lidocaine

Torsades = Magnesium sulfate

Seizures = BZD, propofol or neuromuscular blockade if refractory

Severe TCA overdose = case reports of IV lipid emulsion therapy

77
Q

How does sodium bicarb treat the cardiac effects of TCA toxicity?

A

Increases extracellular sodium concentrations overwhelming the effective blockade of sodium channels

78
Q

What is the mechanism of toxicity of Antipsychotics?

A

Variety of effects based on potency of each agent

79
Q

What are the symptoms of Antipsychotic toxicity?

A

Cardiac = tachycardia, hypotension, QT prolongation

Neuro = Seizures, hyperthermia, sedation

Extrapyramidal side effects (EPS) = dystonic reactions (clenched jaw, neck twisting, arching back), pseudoparkinsonism (rigidity, tremor), akathisia (anxiety plus motor restlessness)

Neuroleptic Malignant syndrome

80
Q

What are the treatments for Antipsychotic toxicity?

A

Treat the symptoms

Dystonic reactions/psuedoparkinsonism = Diphenhydramine and Benztropine

NMS = Bromocriptine and Dantrolene

QRS interval prolongation = sodium bicarb

QT prolongation and torsades = Magnesium infusion or overdrive pacing

81
Q

What is the mechanism of toxicity of SSRIs?

A

Increased levels of serotonin

82
Q

What are signs and symptoms of SSRI toxicity?

A

Serotonin syndrome

83
Q

What are the treatment strategies for SSRI toxicity?

A

Supportive measures
BZD for comfort
Cyproheptadine
Chlorpromazine

84
Q

What is Cyproheptadine?

A

An effective H1 receptor antagonist also has prominent 5HT blocking activity and has weak anticholinergic activity

85
Q

What is Chlorpromazine?

A

5HT2A antagonist

86
Q

What occurs in Calcium Channel Blocker toxicity?

A 
Decreased BP
Non DHPs = Decreased HR
DHPs = Increased HR
Non DHPs = AV conduction delay
Decreased Indirect Mental Status
Hyperglycemia
87
Q

What occurs in Beta blocker toxicity?

A 
Decreased BP
Decreased HR
AV conduction delay
QRS widening (Propranolo)
QT Prolongation (Sotalol)
Decreased Direct Mental Status
Dysglycemia
88
Q

How do we treat cardiac medication toxicities?

A 
Bradycardia = atropine
Hypotension = Fluids
Refractory hypotension/bradycardia:
Calcium 
Glucagon
High Dose Insulin Therapy 
Intralipid Emulsion Therapy
89
Q

How does Glucagon treat Beta blocker toxicity?

A

Binds to G-protein and activates cascade

3-5 mg IV up to a cumulative dose of 10mg

90
Q

How does High dose insulin therapy treat beta blocker toxicity?

A

Increased intracellular glucose transport, increased inotropy, vascular dilatation, anti-inflammatory

Bolus = 1 unit/kg regular insulin

Infusion = 0.5 - 1 unit/kg/hr with dextrose 10% infusion

91
Q

How does intralipid emulsion therapy treat beta blocker toxicity?

A

Lipid sink

Offending toxin binds to the ILE and causes reversal of toxicity

92
Q

How does calcium treat CCB toxicity?

A

Give calcium to increase concentration gradient and increase heart rate

93
Q

What is Digoxin?

A

Main stay of treatment for CHF and used to control ventricular response rate in atrial tachydysrhythmias

94
Q

What is the MOA of Digoxin?

A

Inhibits Na+/K+ ATPase and promotes Ca+ influx via the Na+/Ca+ exchange pump which in turn increases force of myocardial contraction

95
Q

What are the signs and symptoms of Digoxin toxicity?

A

Sinus bradycardia
High-degree AV block
AV dissociation
Digitalis effect

96
Q

What do we use to treat Digoxin toxicity?

A

DigiFab

97
Q

What is the MOA of DigiFab?

A

Binds all free digoxin in the intravascular

Diffuses into interstitial space, binds free digoxin

Creates concentration gradient

Binding of DigiFab to digoxin is greater than digoxin to Na+/K+ ATPase

98
Q

What are toxic alcohols?

A

Common ingredients in coolant/antifreeze, windshield wiper fluid, solvents, cleaners, and fuels

99
Q

What are the symptoms of Ethylene glycol poisoning?

A 
Altered mental status
Profound metabolic acidosis
Oxalate crystalluria
Acute renal failure
Hypocalcemia
100
Q

What are the symptoms of methanol poisoning?

A

Profound metabolic acidosis

Visual changes

101
Q

What is the common symptom seen in toxic alcohol poisoning?

A

Multi-system organ failure and death

102
Q

How do we treat toxic alcohol poisoning?

A

Fomepizole

103
Q

What is the MOA of Fomepizole?

A

Competitively inhibits alcohol dehydrogenase, an enyme which catalyzes the metabolism of ethanol, ethylene glycol, and methanol to their toxic metabolites

104
Q

What is formic acid responsible for?

A

metabolic acidosi and visual disturbances of methanol poisoning

105
Q

What is Glycolate and Oxalate responsible for?

A

Metabolic acidosis and renal damage of Ethylene glycol poisoning

Clinical Pharmacology II (25 decks)

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