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Clinical Pharmacology II > Toxicology > Flashcards

Toxicology Flashcards

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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
What are the indications for using activated charcoal?
Use within 1 hour of ingestion
26
What are the contraindications for using activated charcoal?
Patient not able to protect airway
27
What are the side effects of using activated charcoal?
Bloating Vomiting Constipation Diarrhea
28
What drugs/toxins are poorly absorbed by activated charcoal?
``` Alkali Cyanide Iron Hydrocarbons Alcohols Ethylene glycol Potassium Lithium Inorganic salts Heavy metals ```
29
How do we enhance elimination of the drug?
Urine alkalinzation = urine > 7.5 | Hemodialysis
30
What are the pharmacokinetics of APAP?
90% undergoes hepatic conjugation: Glucuronide (40-67%) Sulfate (20-46%) Oxidized by CYP2E1 (5-15%) = NAPQI created and metabolized quickly by glutathione (GSH)
31
What occurs in tylenol overdose?
Sulfation and Glucoronidation becomes saturated and reactive CYP 2E1 metabolism becomes primary pathway for metabolism The build up of NAPQI causes liver cell death
32
What are the toxicokinetics of APAP?
Peak plasma concentrations within 4 hours NAPQI production largely results of CYP2E1 Nontoxic sulfation metabolism becomes saturated
33
What is the mechanism of APAP toxicity?
NAPQI formation depletes GSH supply NAPQI accumulates causing hepatotoxicity
34
What occurs in stage 1 of APAP toxicity?
``` Nausea Vomiting Malaise Pallor Diaphoresis ```
35
What occurs in stage 2 of APAP toxicity?
Onset of liver injury <5% AST elevation within 24 hours Hepatotoxicity AST >1000IU/L
36
What occurs in stage 3 of APAP toxicity?
Maximal hepatotoxicity at 72-96 hours Fulminant hepatic failure - encephalopathy, coma, exsanguinating hemorrhage AST and ALT > 10,000 IU/L
37
What is the antidote to treat APAP toxicity?
N-Acetylcysteine (NAC)
38
What is the MOA of NAC?
Prevents toxicity as a GSH precursor and substitute Increases substrate for nontoxic situation
39
What are the dosing regimens for NAC?
72 hours orally | 21 hours IV
40
What are the ADRs of NAC?
``` Rash Nausea Vomiting Diarrhea Rare Anaphylactic reactions ```
41
What are the pharmacokinetics of Salicylates?
Major route of biotransformation is conjugation with glycine in the liver
42
What are the toxicokinetics of Salicylates?
Pathways become saturated and exhibit zero-order kinetics Longer half-life = 2-4 hours vs. 20 hours
43
What are the classic symptoms of Salicylate toxicity?
pH: Acidosis = acidic drug/metabolites; lactic acidosis Hyperventilation = respiratory alkalosis Tinnitus GI irritation ``` CNS effects: Vertigo Hyperactivity Agitation Delirium Hallucinations Convulsions Lethargy Stupor ```
44
What is the treatment for Salicylate toxicity?
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
What is the MOA of Benzo and Barbituate toxicity?
Increased activity of the inhibitory neurotransmitter GABA
46
What are the signs and symptoms of Benzo and Barbituate toxicity/
``` Slurred speech Ataxia Incoordination Sedation Hypothermia Stupor Respiratory depression ```
47
How do we treat Benzo and Barbituate toxicity/
Watch and wait Supportive measures = fluid or pressors for hypotension; intubation if necessary Antidote = Flumazenil
48
What is the MOA of Flumazenil?
Specific competitive BXD receptor antagonist
49
When would use of Flumazenil be indicated?
Rapid reversal of BZD overdose | Operative or post-op reversal of BZD sedation
50
What are the precautions for using Flumazenil?
Routine use of flumazenil is NOT recommended Seizures or other withdrawal symptoms may be preciptiated
51
Why is it recommended to not use Flumazenil for BZD overdose?
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
What is the MOA of toxicity of amphetamines?
Increased release of DA, NE, and 5HT
53
What are the signs and symptoms of amphetamine overdose?
``` Hypertension Tachycardia Euphoria Abnormal movements Psychotic episodes (agitation, hallucinogenic, paranoid) Hypethermia/diaphoretic Vasoconstriction Rhabdomyolysis ```
54
What is the mechanism of toxicity of Cocaine?
Increased activation of various excitatory neurotransmitters (Epi, NE, DA, 5HT)
55
What are the signs and symptoms of Cocaine toxicity?
``` Seizures MI/cardiac ischemia Coma Headache Intracranial hemorrhage Mydriasis Dysrhythmia Hyperthermia Rhabdomyolysis Agitation/aggression Delirium Confusion Hallucinations ```
56
What is the mechanism of toxicity of Ecstasy?
Increased 5HT, DA, and NE
57
What are the signs and symptoms of Ecstasy overdose?
``` Dehydration Hyperthermia Serotonin syndrome Seizures Hyperpyrexia Rhabdomyolysis Organ failure Hyponatremia Anxiety ```
58
What is the mechanism of toxicity of Synthetic cathinones?
Similar to amphetamines and MDMA
59
What are the signs and symptoms of Synthetic Cathinone overdose?
Cardiac and psychiatric episodes Hallucinations and aggression most common
60
How do we treat stimulant toxicity?
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
What is the mechanism of toxicity of Opioids?
Increased stimulation of opioid receptors
62
What are the signs and symptoms of opioid overdose/
``` RESPIRATORY DEPRESSION MIOSIS Bradycardia/hypotension Hypothermia Stupor/coma Itching Reduced GI mobility Euphoria Sedation Seizures ```
63
What do we use to treat Opioid overdose?
Naloxone
64
What is Naloxone?
Opioid receptor antagonist
65
What are the kinetics of Naloxone?
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
What is are the ADRs of Naloxone?
withdrawal symptoms = want to administer enough to create spontaneous ventilation and make sure they are breathing but not enough to cause withdrawal symptoms
67
What is the mechanism of toxicity of Organophosphates?
Rise in ACh at muscarinic and nicotonic cholinergic receptors by irreversibly binding to acterylcholinterase
68
What are muscarinic effects of organophosphates?
SLUDGE Vision = miosis, blurred Bradycardia Wheezing
69
What are nicotinic effects of organophosphates?
Fasiculations Paresis/Paralysis Hypertension Tachycardia
70
What are central effects of organophosphates?
``` Anxiety Confusion Seizures Psychosis Ataxia ```
71
What doe we use to treat organophosphate toxicity?
``` Atropine Pralidoxime (2-PAM) ```
72
What does Atropine do to treat organophosphate toxicity?
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
What does 2-PAM do to treat organophosphate toxicity?
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
What is the mechanism of toxicity of Tricyclic antidepressants (TCAs)?
Inhibits reuptake of NE and 5HT while also blocking H1, a1, Na channels, and muscarinic receptors
75
What are the signs and symptoms of TCA toxicity?
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
What is the treatment for TCA toxicity?
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
How does sodium bicarb treat the cardiac effects of TCA toxicity?
Increases extracellular sodium concentrations overwhelming the effective blockade of sodium channels
78
What is the mechanism of toxicity of Antipsychotics?
Variety of effects based on potency of each agent
79
What are the symptoms of Antipsychotic toxicity?
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
What are the treatments for Antipsychotic toxicity?
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
What is the mechanism of toxicity of SSRIs?
Increased levels of serotonin
82
What are signs and symptoms of SSRI toxicity?
Serotonin syndrome
83
What are the treatment strategies for SSRI toxicity?
Supportive measures BZD for comfort Cyproheptadine Chlorpromazine
84
What is Cyproheptadine?
An effective H1 receptor antagonist also has prominent 5HT blocking activity and has weak anticholinergic activity
85
What is Chlorpromazine?
5HT2A antagonist
86
What occurs in Calcium Channel Blocker toxicity?
``` Decreased BP Non DHPs = Decreased HR DHPs = Increased HR Non DHPs = AV conduction delay Decreased Indirect Mental Status Hyperglycemia ```
87
What occurs in Beta blocker toxicity?
``` Decreased BP Decreased HR AV conduction delay QRS widening (Propranolo) QT Prolongation (Sotalol) Decreased Direct Mental Status Dysglycemia ```
88
How do we treat cardiac medication toxicities?
``` Bradycardia = atropine Hypotension = Fluids Refractory hypotension/bradycardia: Calcium Glucagon High Dose Insulin Therapy Intralipid Emulsion Therapy ```
89
How does Glucagon treat Beta blocker toxicity?
Binds to G-protein and activates cascade 3-5 mg IV up to a cumulative dose of 10mg
90
How does High dose insulin therapy treat beta blocker toxicity?
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
How does intralipid emulsion therapy treat beta blocker toxicity?
Lipid sink Offending toxin binds to the ILE and causes reversal of toxicity
92
How does calcium treat CCB toxicity?
Give calcium to increase concentration gradient and increase heart rate
93
What is Digoxin?
Main stay of treatment for CHF and used to control ventricular response rate in atrial tachydysrhythmias
94
What is the MOA of Digoxin?
Inhibits Na+/K+ ATPase and promotes Ca+ influx via the Na+/Ca+ exchange pump which in turn increases force of myocardial contraction
95
What are the signs and symptoms of Digoxin toxicity?
Sinus bradycardia High-degree AV block AV dissociation Digitalis effect
96
What do we use to treat Digoxin toxicity?
DigiFab
97
What is the MOA of DigiFab?
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
What are toxic alcohols?
Common ingredients in coolant/antifreeze, windshield wiper fluid, solvents, cleaners, and fuels
99
What are the symptoms of Ethylene glycol poisoning?
``` Altered mental status Profound metabolic acidosis Oxalate crystalluria Acute renal failure Hypocalcemia ```
100
What are the symptoms of methanol poisoning?
Profound metabolic acidosis Visual changes
101
What is the common symptom seen in toxic alcohol poisoning?
Multi-system organ failure and death
102
How do we treat toxic alcohol poisoning?
Fomepizole
103
What is the MOA of Fomepizole?
Competitively inhibits alcohol dehydrogenase, an enyme which catalyzes the metabolism of ethanol, ethylene glycol, and methanol to their toxic metabolites
104
What is formic acid responsible for?
metabolic acidosi and visual disturbances of methanol poisoning
105
What is Glycolate and Oxalate responsible for?
Metabolic acidosis and renal damage of Ethylene glycol poisoning

Clinical Pharmacology II (25 decks)

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