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Pharmacology > Management Of Poisoned Patient > Flashcards

Management Of Poisoned Patient Flashcards

1
Q

What is the golden rule for poison management

A

Treat the patient not the poison

First stabilize the patient and treat the symptoms

Secondly worry about the poison

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2
Q

Many poisons acts as ?

A

CNS depressants

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3
Q

Common sx of poison that needs to be treated as CNS depressant

A

Coma

Loss of airway protective reflexes and respiratory drive

Flaccid tongue

Aspiration of gastric content

Respiratory arrest

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4
Q

Other poison sx that can lead to death

A

Cardiovascular toxicity

Cellular hypoxia

Seizures

Delayed symptoms

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5
Q

Sx of cardiovascular toxicity

A

Hypotension from depressed cardiac contractility

Hypovolemia from vomiting, diarrhea or fluid sequestration

Peripheral vascular collapse caused by blockage of alpha adrenergics

Cardiac arrhythmia

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6
Q

Signs of lethal arrhythmia

A

Ventricular tachycardia

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7
Q

What drugs can cause lethal arrhythmia

A

Ephedrine

Amphetamines

Cocaine

Digitalis

Theophylline

TCA

Antihistamine

Some opioids

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8
Q

What agents can induce hypoxia

A

Cyanide

H2S

CO

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9
Q

Signs of cellular hypoxia

A

Cyanosis

Tachycardia

Hypotension

Severe lactic acidosis

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10
Q

What is the initial management of poisoned patients

A

Treat and stabilize patient

Address coma or seizures

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11
Q

What are the ABCD of supportive measures

A

Airway

Breathing

Circulation

Dextrose for decreased mental status

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12
Q

How is airway addressed

A

Cleared of vomit or obstacles

  • Insert endotracheal tube if needed
  • May need to lay patient on side
  • Move flaccid tongue out of airway
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13
Q

How is breathing addressed

A

Observe and assess oximetry (pulse)

  • When in doubt measure arterial blood gas if you have time
  • Patients with respiratory insufficiency should be intubated and mechanically ventilated
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14
Q

How is circulation addressed

A

Continuous monitoring of pulse rate and blood pressure

  • Urinary output
  • Evaluation of peripheral perfusion
  • Use of IV if needed
  • Blood drawn for serum glucose and other factors
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15
Q

How is dextrose used as initial management

A

Use with patients with altered mental status

  • Don’t use if you know patient is not hypoglycemic
  • Rapid bedside test (treat patient first)
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16
Q

What is the dose of dextrose for adult and children

A

Adult = 25 g (50 ml 50% dextrose) with IV for adults

Children = 0.5 g/kg (2 mL/kg 25% dextrose)

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17
Q

What is the ER Assessment: Oral Statement

A
  • Amount of drug
  • Type of drug
  • “House” everybody lies
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18
Q

What is ER assessment: Environment

A
  • Talk to family members
  • 1st responders (fire department, paramedics)
  • What was the house like?
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19
Q

In ER assessment what should you bring to ER

A
  • Syringes
  • Empty bottles
  • Household products
  • OTCs
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20
Q

What is the standard ER assessment to check for vitals

A
  • Pulse
  • Heart rate
  • Blood pressure
  • Temperature
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21
Q

What other part of the body can be assessed for vital signs during ER assessment

A
  • Eyes
    • Reactive
    • Dual reaction
  • Mouth
  • Skin
  • Abdomen
  • CNS
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22
Q

What medication can induce hypertension or tachycardia

A

Amphetamines

Cocaine

Anti-muscarinic

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23
Q

What medication can induce hypotension or bradycardia

A

Calcium channel blockers

Beta-blockers

Clonidine

Sedative hypnotics

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24
Q

What medication can induce hypotension or tachycardia

A

TCAs

Trazadone

Quetiapine

Vasodilator

Beta agonist

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25
Q

During eye assessment what drugs can induce mitosis- constriction

A
  • Opioids
  • Clonidine
  • Cholinesterase inhibitors
  • Sedatives (coma)
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26
Q

During eye assessment what can drugs can cause mydriasis-dilation

A
  • Amphetamines
  • Cocaine
  • LSD
  • Atropine
  • Anticholinergic drugs
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27
Q

During eye assessment what drugs can cause horizontal nystagmus

A
  • Phenytoin
  • Alcohol
  • Barbiturates
  • Sedatives
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28
Q

During eye assessment what drugs can cause both vertical and horizontal nystagmus

A

Phenycyclidine (PCP)

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29
Q

During ER assessment what signs of nervous system should be assessed

A
  • Focal seizures/motor deficits
  • Nystagmus, dysarthria (motor speech problem), ataxia
  • Twitching/muscular hyperactivity
  • Muscular rigidity
  • Seizures
  • Flaccid coma with no reflexes
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30
Q

How can electrolytes be used during ER assessment

A

Calculate ion gap

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31
Q

What is the anion gap

A

Cations - anions

Cations are usually greater by 12-16 mEq

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32
Q

What drugs can induce anion gap

A

Aspirin

Methanol

Ethylene glycol

Isoniazid

Iron

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33
Q

How does TCA overdose impact EKG

A

Widening QRS complex by > 100 msec

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34
Q

What drugs impact EKG by prolonging QTc interval by > 400 msec

A

Quinidine

New antidepressant

New antipsychotic

Lithium

Arsenic

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35
Q

Which drugs impact EKG through variable AV block

A

Digoxin

Cardiac glycosides

CO

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36
Q

What is the reality of toxicology screening

A

Time consuming

Expensive

Unreliable

Not all drugs can be included in screen

Results may take days

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37
Q

Which drugs might not be included in screenings

A

Beta blocker

Calcium channel blockers

Isoniazid

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38
Q

True or False: Every existing poison has an antidote

A

False

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39
Q

How is skin decontamination done as an antidote

A

Remove contaminated clothing and double bag to prevent exposure

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40
Q

What GI approaches are performed as antidote decontamination for GI

A

Emesis

Gastric lavage

Activated Charcoal

Cathartics

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41
Q

When is GI emptying as an antidote method more effective

A

Within 1 hour of ingestion

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42
Q

How does activated charcoal work as an antidote

A

Absorbs poison

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43
Q

What can be used for emesis

A

Ipecac syrup not extract

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44
Q

When should ipecac Symptoms not used

A

If toxicants is corrosive, petroleum based or rapid acting convulsant

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45
Q

Should salt water or finger used to induce emesis

A

No

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46
Q

How can gastric aspiration induced mechanically

A

Use nasogastric or orogastric tube to remove stomach content

Requires anesthesia and stomach pumping

Use 0.9% saline at body temperature

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47
Q

What is the MOA of activated charcoal

A

Adsorb many drugs and poison due to large surface area

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48
Q

How is activated charcoal dosed compared to the weight of toxicant

A

Charcoal: toxicant weight (10:1)

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49
Q

What is the dosage form of activated charcoal

A

Tablets or powders

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50
Q

Which toxins does charcoal not bind to

A

Iron

Lithium

Potassium

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51
Q

Which toxins does charcoal bind poorly to

A

Alcohol

Cyanide

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52
Q

What can repeated doses of activated charcoal do

A

Enhance systemic elimination of drugs (i.e gut dialysis)

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53
Q

What is another name of Cathartics

A

Laxatives

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54
Q

What is the mechanism of action Cathartics

A

May hasten removal of toxins from GI and alter absorption

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55
Q

What are the products are used as Cathartics

A

Rushpills

Polyethylene glycol electrolyte solution

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56
Q

What procedure can Cathartics be used prior

A

Colonoscopy

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57
Q

Which toxin does cathartics increase its guts elimination

A

Iron

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58
Q

What is the two prone approach to designing specific antidotes

A

Pharmacokinetic

Pharmacodynamic

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59
Q

How does the pharmacokinetic work

A

Prevent absorption and distribution

Enhance elimination

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60
Q

How does pharmacodynamic work

A

Pharmacological

Interfere with the binding to target

Antagonistic

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61
Q

What are the non-specific antidotes

A

Dialysis

Hemodialysis

Forced diuresis and urinary pH manipulation

Renal elimination

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62
Q

Dialysis: peritoneal dialysis

A

Simple but ineffective and works into the abdominal cavity

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63
Q

What are the benefits of hemodialysis

A

Assist in fluid correction and electrolyte balances

Enhance removal of toxic metabolite

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64
Q

Efficiency of hemodialysis is dependent on what factor

A

Molecular weight

Water solubility

Protein binding endogenous clearance

Tissue distribution

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65
Q

Can toxin be eliminated by hemodialysis if it is not in the blood

A

No

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66
Q

Why has forced diuresis and urinary pH manipulation lost favor

A

It can cause volume overload and electrolyte imbalance

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67
Q

How does renal elimination work

A

Can increase by adjusting urinary ph

Salicylate are eliminate by urinary alkalization

Can increase rhabdomylosis

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68
Q

What is rhabdomylosis

A

Damaged skeletal muscle break down quickly and enters the bloodstream and proteins cause damage to the kidney and cause renal failure

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69
Q

What can cause rhabdomylosis

A

Seizure

Muscle rigidity

Crush injury

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70
Q

What are the symptoms of rhabdomylosis

A

Muscle pain

Vomiting

Confusion

Brown-urine house

71
Q

When is acetaminophen over dose usually seen

A

Suicide attempts

Accidental poisonings

72
Q

What are the symptoms of acetaminophen overdose

A

Initial mild GI

Nausea

Vomiting

73
Q

When does lever toxicity occurs and what are the signs and symptoms

A

24-36 hours

Increased aminotransferases

Hypoprothrombinemia

74
Q

Severe acetaminophen poisoning is characterized by

A

Liver failure

Hepatic encephalopathy

Renal failure

75
Q

Come back to the flow chart on slide 25

A

Sure will

76
Q

What is acetaminophine overdose concentration after the

A

> 150-200 mg/L

77
Q

Who are at greater risk of acetaminophen toxicity

A

Alcoholics or those taking drugs metabolized by CYP450

78
Q

What is the antidote of acetaminophen overdose

A

Acetylcysteine - acetate or mucomyst

79
Q

MOA of acetadote

A

Acts like GSH and binds to toxic metabolite of acetaminophen

80
Q

When is acetadote most effective

A

When given early (8-10 hours)

81
Q

What is the antidote in severe cases of acetaminophen toxicity

A

Liver transplantation

82
Q

What drugs contribute to amphetamine overdose

A

Cocaine

Methamphetamine

Methyldioxymethamphetamine (MDMA, ecstasy)

Pseudoephedrine

Ephedrine (Ma-Huang)

Caffeine

83
Q

When used recreationally, what can a person experience with amphetamine

A

Sense of power

Euphoria

Well being

84
Q

What results from amphetamine taking higher doses at

A

Restlessness

Agitation

Acute psychosis

HTN and tachycardia

Increased muscle activity (dehydration and hypotension)

Seizures ( hyperthermia or rhabdomylosis)

Extreme increase in body temperature 42°C or 107.6°F (brain damage, hypotension, coagulopathy, renal failure )

85
Q

How is amphetamine overdose treated

A

Supportive care

No specific antidote

Manage seizures and hyperthermia aggressively

86
Q

What medication is used to battle amphetamine seizure overdose

A

IV benzodiazepines

87
Q

What does anticholinergics do

A

Inhibit acetylcholine effect on muscarnic receptors

88
Q

Which anticholinergics do not target cholinergic receptors

A

Antihistamine

TCAs

89
Q

What is the muscarnic symptoms of anticholinergic toxicity

A

Skin flushing

Hyperthermia

Dry mucosal membrane w/o sweating

Blurred vision, cychoplegia

Confusion

Delirium

90
Q

What are other anticholinergie toxicity

A

Sinus tachycardia

Dilated pupil

Coma

Seizures (if patient took TCA or anti histamine)

91
Q

What is the treatment for anticholinergic toxicity

A

Largely supportive

Agitation is controlled with sedation, benzodiazepine or antipsychotics

Physostigmine

92
Q

What is the MOA of physostigmine

A

Inhibits acetycholine esterase activity to increase acetylcholine levels

93
Q

What receptors does physostigmine work on

A

Nicotinic and muscarinic

94
Q

How is physostigmine dosed

A

0.5-1 mg IV

95
Q

What is physostigmine ADR

A

Bradycardia

Seizure

96
Q

Who should avoid physostigmine use

A

Patient with TCA overdose due to increased risk of cardiotoxicity and asystole

97
Q

What dose of antidepressant can be lethal or classified as an overdose

A

1 g or 15-20 mg/kg

98
Q

What’s antidepressant such as TCA MOA

A

Competitive antagonist at muscarinic receptors

99
Q

What are the ADR of TCA antidepressants

A

Tachycardia

Dry mouth

Dilated pupils

Strong alpha blockers can lead to vasodilation

100
Q

What are the symptoms of antidepressant toxicity

A
  • Tachycardia
  • Dilated pupils
  • Vasodilation
  • Seizures
  • Depression
  • Hypotension
101
Q

What are quinidine like depressants effect that can be symptoms of antidepressants toxicity

A
  • Slowed conduction
  • Wide QRS interval
  • Depressed cardiac contractility
  • Lead to arrhythmias with ventricular conduction block
  • Ventricular tachycardia
102
Q

What is the antidepressant overdose treatment

A
  • General supportive care
  • Endotracheal intubation with assisted ventilation
  • IV fluids for electrolyte loss
  • Dopamine or norepinephrine if needed
103
Q

In antidepressants overdose when is norepinephrine used as the initial drug

A

If hypotension is present

104
Q

How is quinidine like cardiac toxicity with wide QRS managed

A

Sodium bicarbonate

105
Q

Why should physostigmine not used in quinidine like cardiac toxicity

A

Can aggravate depression of cardiac conduction and cause seizure

106
Q

What other form can patients overdose with antidepressants

A

With MAOIs

107
Q

MAOIs

A

Tranylcypromine

Phenelzine

Older antidepressants

108
Q

What are MAOIs Symptoms

A

Anticholinergic

Severe hypertension

Interact with SSRIs

109
Q

What new anti depressants can cause toxicity

A

Fluoxetine

Paroxetine

Citalopram

Venlafaxine

Bupropion

110
Q

Mostly SSRIs

Generally safer than TCA and MOI

Can cause seizures

A

Venlafaxine

111
Q

Not an SSRI but can cause seizures

A

Bupropion

112
Q

Old antipsychotics

A

Phenothiazine

Butyrophenones

113
Q

New atypical

A

Clozapine

Quetiapine

Risperidone

114
Q

What are the symptoms of antipsychotic overdose

A

Drowsiness - proceeds to coma with brief agitation

QT prolongation

CNS depression

Seizures

Hypotension

115
Q

What class of antipsychotics can cause parkisonian like disorder

A

D2 blocker

116
Q

How is antipsychotic overdose treated

A

Supportive care

  • Gastric lavage
  • Activated charcoal
  • Saline cathartic
117
Q

Antidote for antipsychotic induced hypotension

A

Norepinephrine

118
Q

Antidote for antipsychotic induced seizures

A

Diazepam

119
Q

Antidote for antipsychotic lithium overdose

A

Dialysis

120
Q

What accounts for numerous suicide and accidental poisonings

A

Aspirin

121
Q

Chronic overdose of aspirin in elderly is usually due to

A

Forgetting if they took it or not

122
Q

Aspirin MOA

A
  • Ion gap
  • Metabolic acidosis
  • Respiratory alkalosis
  • Platelet dysfunction and bleeding
123
Q

Acute aspirin overdose symptoms

A
  • Hyperventilation
  • Respiratory alkalosis with medulla stimulation
  • Metabolic acidosis
  • Increased ion gap from lactate excretion of bicarbonate in urine
  • Increase in body temperature from uncoupled oxidative phosphorylation
  • Vomiting
  • Hyperpnea
124
Q

Aspirin severe overdose symptoms

A

Profound metabolic acidosis

  • Seizures
  • Coma
  • Pulmonary edema
  • Cardiovascular collapse
125
Q

Aspirin overdose treatment

A

Supportive care

Treat ion gap

Treat seizures

Treat fever

Aggressive gut decontamination

Gastric Savage

Repeated activated charcoal

126
Q

Why is I.V fluid given in aspirin overdose treatment

A

To replace fluid loss from tachycardia, vomiting and fever

127
Q

How is moderate intoxication of aspirin treated

A

• IV with sodium bicarbonate to Alkalizes urine, which increases salicylate excretion by trapping ion

128
Q

What is considered severe aspirin intoxication

A

> 100 tablets

129
Q

How is severe cases of aspirin intoxication managed

A

Hemodialysis

Restore acid/ base balance

Restore salts

130
Q

Why are beta blockers administered

A

Raise BP and HR

131
Q

Glucagon function of cardiac cells

A

Increase cAMP independent of b-adrenoreceptor

132
Q

Treatment of beta blocker overdose

A

B-agonist

Atropine: won’t work for Na block

Glucagon

133
Q

Why is the aim to increase cAMP for better blocker over close

A

Because cAMP inhibits MLCK phosphorylation preventing contraction

134
Q

Why should one be careful with calcium channel blockers

A

Toxicity and death can occur at relatively low doses

135
Q

How can calcium charnel blockers induce toxicity and death

A

Depress sinus node automaticity

  • Slow AV node conduction
  • Decrease cardiac output
  • Decrease blood pressure
  • Serious hypotension
136
Q

Example of calcium channel blockers

A

Nifedipine

Dihydropyridines

137
Q

For calcium channel blocker in sustained released form how can toxicity be addressed

A

Whole bowel irrigation

Oral activated charcoal

138
Q

Calcium intravenous at 2-10 g are good to treat what type of calcium channel blocker toxicity

A

Depressed Cardiac contractility but not for peripheral collapse

139
Q

What drugs can be given for Cardiac channel blocker toxicity

A

Glucagon

Vasopressin

Epinepherine

High dose insulin and glucose

140
Q

What are the types of cholinesterase inhibitor

A

Organophosphate

Carbamate cholinesterase inhibitors

Insecticides

141
Q

How can one be exposed to cholinesterase inhibitors

A

Insecticides/pesticides

Suicides

Rarely food

142
Q

What tragic event has Cholinesterase inhibitors be used for

A

Warfare

Tokyo subway 95

143
Q

What are the muscarinic stimulation Symptoms of cholinesterase inhibitor overdose

A
  • Abdominal cramps
  • Excessive salivation
  • Sweating
  • Increased urinary frequency
  • Increased bronchial secretion
144
Q

What are the CNS effect Symptoms of cholinesterase inhibitor overdose

A
  • Agitation
  • Confusion
  • Seizures
145
Q

What are the Nicotinic stimulation Symptoms of cholinesterase inhibitor overdose

A
  • Generalized ganglionic activation
  • Hypertension
  • Tachycardia or bradycardia
  • Muscle twitching and fasciculations
146
Q

What other Symptoms are shown in cholinesterase inhibitor over dose

A
  • Diarrhea
  • Urination
  • Miosis and muscle weakness
  • Bronchospasm
  • Excitation
  • Lacrimation
  • Seizures, sweating and salivation
147
Q

Cholinesterase inhibitor treatment

A

Generalized supportive care

Atropine: muscarnic Only

Pralidoxine; nicotinic and muscarinic receptors

The Rock

148
Q

What are cyanide forms

A

CN salts

HCN

149
Q

Uses of cyanide

A
  • Chemical synthesis
  • Rodenticides
  • Executions at one time
  • Suicide/homicide
150
Q

Sources of cyanide

A
  • Burning of plastics
  • Burning of wool
  • Synthetic and natural products
  • Plant and seeds
  • Apple seeds
  • Peach
151
Q

Cyanide MOA

A

Bind cytochrome oxidase in mitochondria to induce cellular hypoxia and lactic acidosis

152
Q

Symptoms of cyanide poisonings

A
  • Shortness of breath
  • Agitation
  • Tachycardia
  • Seizures
  • Hypotension
  • Death
  • Characterized by severe metabolic acidosis
153
Q

Cyanide treatment

A

Rapid Administration of activated charcoal

General supportive care

Antidote Kit

Cyanokit (EMD pharmaceuticals)

154
Q

Cyanide antidote kit

A
  • Forms of nitrite
  • Amyl nitrite
  • Sodium nitrite
  • Sodium thiosulfate
  • Induce methemoglobinemia that binds free CN-
    * Creates a less toxic cyanomethemoglobin
  • Thiosulfate
    * Enzyme cofactors
    * Facilitates conversion to CN to less toxic hydroxocobalamin
155
Q

Cyanokit

A
  • Concentrated Hydroxocobalamin

* Combines with CN- to form cyanocobalamin (B12)

156
Q

Symptoms of acute digoxin overdose

A
  • Renal insufficiency
  • Diuretics with digoxin
  • Vomiting
  • Hyperkalemia
  • Hypokalemia with long term use
  • Cardiac rhythmic distrubances
            * Sinus bradycardia 
        * AV block 
        * Atrial tachycardia 
        * Accelerated junctional rhythm
157
Q

When is atropine used in digoxin overdose treatment

A

Bradycardia or sinus block occur

158
Q

What type of antibiotics can be used with digoxin overdose treatment

A

Digoxin antibodies

  • IV administration at indicated dosages
  • Symptoms usually improve 30-60 min
  • Can be used for other cardiac glycosides
  • Oleander
159
Q

Ethanol and sedative hypnotic drugs

A
  • Ethanol
  • Benzodiazepines
  • Barbiturates
  • G-hydroxbutyrate (GHB)- date rape
  • Carisoprodol (Soma)
160
Q

Symptoms of ethanol and sedative hypnotic drugs

A
  • Drunk
    * Euphoria • Rowdy
  • Dead drunk
    * Stupor • Coma

• Decreased respiratory drive

  • Decreased protective respiratory reflexes
    * Can result in aspiration of gastric contents
    * Tracheal aspiration
  • Hypothermia
    * Exposure
    * Decreased shivering
161
Q

Ethanol and sedative hypnotic drugs treatment

A
  • Supportive care
    * Protect the airway
    * Intubation if needed
  • IV fluids for hypotension
  • Dopamine if needed
162
Q

Benzodiazepine antidotes

A
  • IV flumazenil
  • Benzodiazepine antagonist (Can cause seizures in patients addicted to benzodiazepines)
  • Don’t give with patients with TCA overdose
163
Q

True/False: There is no antidote for ethanol, barbiturates or other sedative drugs

A

True

164
Q

Ethylene glycol and methanol description

A

Metabolized into organic
acids

  • Cause CNS depression
  • Drunken state similar to Ethanol
165
Q

Product of methanol metabolism and effect

A

Metabolized to formic acid and Causes metabolic acidosis

166
Q

Product of ethylene glycol metabolism and effect

A

Metabolized to hippuric acid and oxalic acid and causes renal failure

167
Q

Symptoms of ethylene glycol and methanol overdose

A
  • Drunkenness and altered mental status
  • Anion gap
  • Severe metabolic acidosis
  • Hyperventilation
  • Blurred vision and blindness
168
Q

Treatment of ethylene glycol and methanol

A
  • Fomepizole (4-methypyrazole)
  • Inhibits alcohol dehydrogenase
  • Don’t use with alcohol
  • Hemodialysis
  • Ethanol, but hard to get to high enough dose
169
Q

What was thophylline once used to treat

A
  • Bronchospasm
  • Asthma
  • Bronchitis
  • 20-30 tablets is toxic
170
Q

What are Symptoms of theophylline toxicity

A
  • Sinus tachycardia
  • Tremor
  • Vomiting
  • Hypotension
  • Hypokalemia
  • Hyperglcemia
171
Q

Antidote for opioid overdose

A

Naloxone: short window of action

Patient can slip in and out of coma

172
Q

Naloxone dose

A

0.1-0.4 mg

173
Q

How is naloxone used to block all effects of heroin

A

Give on alternate days

174
Q

Used to maintain addicts

A

Naloxone

Pharmacology (4 decks)

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