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PHRM 865 Final > Toxicology > Flashcards

Toxicology Flashcards

(46 cards)

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1
Q

Stabilization

A

ABC management
Oxygenation
Vital signs
IV access

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2
Q

Exposure

A

Medications/illicit substances
Doses
Time of ingestion
Family/EMS report
Pill count

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3
Q

Assessment

A

PE
Labs
APAP/Salicylate concentrations
EtoH/toxic alcohol panel
Decontamination?

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4
Q

Anion gap

A

(Na+ + K+) - (Cl- + HCO3-)

Gap is present if > 14

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5
Q

Activated Charcoal

A

If they present after 1-2 hours of ingestion it is not recommended

Positives: decreases time related problems, absorbs most toxins

Negatives: difficult administration, should not be administered if airway is unprotected

1-2 gm/kg ABW or 50-100 gm in adults

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6
Q

Polyethylene glycol

A

1,000-2,000 mL/hr in adolescents or adults

Pt should remain seated on bedside toilet

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7
Q

Hemodialysis

A

Effective for:
Alcohols
Lithium
Salicylates
Theophylline

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8
Q

Salicylate toxicity risk factors

A

Mixed acid/base disorders:
- increase anion gap–>metabolic acidosis
- early respiratory alkalosis–>hyperventilation

Electrolyte disturbances:
- hypokalemia
- hypo/hypernatremia

Salicylate concentrations:
- mild toxicity: > 30 mg/mL (tinnitus, dizziness)
- severe toxicity: > 80 mg/mL (CNS effects)

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9
Q

Salicylate toxicity signs and symptoms

A

N/V
Tinnitus and diaphoresis
Decreased GI motility
Altered mental status
Seizures
Hyperventilation

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10
Q

Salicylate general management

A

Stabilization: ABC management, oxygenation, vital signs, IV access, CNS/respiratory depression

Exposure: medications/illicit substances, doses, time of ingestion, family/EMS report, pill count

Assessment: PE, labs, salicylate/APAP concentrations, activated charcoal?, fluids with KCl, sodium bicarb

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11
Q

Salicylates: Antidote

A

Sodium bicarbonate: urine alkalization

Indications:
- serum level > 30 mg/mL
- anion gap metabolic acidosis
- altered mental status

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12
Q

Sodium bicarbonate dosing

A

1-2 mEq/kg (50-100 mEq) IV push over 1-2 minutes

May consider continuous infusion and titrate to effect

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13
Q

Sodium bicarbonate monitoring

A

Serum pH 7.5-8
Electrolytes (potassium, calcium)

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14
Q

Sedative toxicity signs and symptoms

A

CNS depression
Respiratory depression
Hypotension
Bradycardia

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15
Q

Sedatives: Flumazenil

A

Competes with BZDs at BZD binding site of GABA complex

0.2 mg IV push
Use with caution in patients with seizures: can induce seizure activities

Can induce withdrawal symptoms: N/V, agitation

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16
Q

TCAs indications

A

Bed wetting
Depression
Insomnia
Migraines
Neuropathy

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17
Q

TCAs pharmacology

A

Anticholinergic activity
Alpha receptor blockade
Serotonin, norepi, dopamine inhibition
Na and K channel blockade
CNS and respiratory depression

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18
Q

TCAs toxicity signs and symptoms

A

Altered mental status
Hypotension
Tachycardia
Prolonged QRS
Seizures
Anticholinergic symptoms

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19
Q

TCAs: Effects of QRS prolongation

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A

QRS interval > 100 msec
- increased risk of seizure activity

QRS interval > 150 msec
- increased risk of arrhythmias

Metabolic acidosis
- promotes unbinding of drug from proteins

20
Q

TCAs general assessment

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A

With the alpha receptor blockade you have hypotension patients not respond well to fluids so vasopressors will be used

Seizure management

21
Q

TCAs: Antidote

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A

Sodium bicarbonate: increases sodium gradient of poisoned sodium channels

Indications:
- QRS > 100 msec
- TCA induced arrhythmias or hypotension
- Metabolic acidosis

22
Q

TCA antidote when to stop

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A

QRS < 100
Resolution of ECG abnormalities
Hemodynamically stable

23
Q

TCAs: seizure management

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A

Benzodiazepines
Phenobarbital

24
Q

Antipsychotics: Pharmacology

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A

1st generation: D2 antagonism

2nd generation: 5HT2A/D2 antagonism

25
Antipsychotics: Toxicity signs and symptoms
Hypotension Tachycardia QT/QRS prolongation EPS Neurologic malignant syndrome (NMS) Sedation
26
Atypical antipsychotic's: Toxicity
Toxic doses are not well defined Often co-ingested with other agents Symptoms are typically seen within 1-2 hours of ingestion Peak symptoms in 4-6 hours Duration is roughly 12-48 hours
27
EPS
Benztropine 2 mg IM Diphenhydramine 1-2 mg/kg IV/IM (up to 50 mg) over several minutes - continue with oral therapy for 3-4 days
28
Neuroleptic Malignant Syndrome (NMS)
Hyperpyrexia with altered mental status and "lead pipe" muscular rigidity Occurs 3-9 days after initiating therapy or after adding a second agent < 40 years of age and male
29
NMS: Treatment
D/C offending agent Rapid external cooling Benzodiazepines Dantrolene Bromocriptine
30
Serotonin Syndrome
Toxic hyperserotonergic state Triad of symptoms: altered mental status, autonomic instability, neuromuscular abnormalities Develops within 6 hours of an increase in precipitating medication
31
Serotonin syndrome: Treatment
D/C offending agent BZDs Aggressive cooling Cyproheptadine - 1st gen histamine receptor blocking agent
32
Serotonin syndrome VS NMS
Serotonin syndrome: - lower fever - myoclonus hyperreflexia - lasting < or equal to 24 hrs - responds to cyproheptadine - lower limbs are affected more than upper limbs NMS: - higher fever - lasting > or equal to 24 hrs - responds to bromocriptine - diffuse lead pipe rigidity
33
Digoxin: Toxicity signs and symptoms
Non-Cardiac: - N/V - abdominal pain - anorexia - confusion - vision changes Cardiac: - bradycardia - 2nd or 3rd degree heart block - arrhythmias - hyperkalemia
34
Digoxin: General Management
D/C Digoxin ABC management Obtain serum digoxin concentration, BMP Monitor vital signs and ECG changes Administer activated charcoal (if presented within 2 hours of ingestion) Consider Digibind Hemodialysis is not effective
35
Digibind: Antidote
Digibind: binds free digoxin and tissue bound digoxin released during equilibrium state Indications: Ventricular arrhythmias, bradycardia/2nd or 3rd degree heart block not responsive to atropine * Hyperkalemia (K > 5.5 mEq/L) with signs/symptoms of toxicity * Serum digoxin concentrations > 10-15 ng/mL drawn at least 6 hours after time of ingestion * Ingestion > 10 mg in adults, > 4 mg in children
36
Digoxin: Toxicology Tidbits
Toxicity can occur with acute ingestion and chronic therapy Must correlate signs and symptoms with serum concentration
37
CCBs Toxicity signs and symptoms
Hyperglycemia Metabolic acidosis Pulmonary edema Ileus
38
BBs Toxicity signs and symptoms
Hypoglycemia Bronchospasm's
39
CCBs and BBs toxicity signs and symptoms
Hypotension Bradycardia Arrhythmias Cardiogenic shock CNS depression
40
CCBs and BBs general management
ABC management Monitor vital signs and ECG changes Administer activated charcoal (based on time) Potential antidotes: - atropine - calcium - vasopressor - glucagon - high dose insulin therapy - lipid emulsion therapy
41
Atropine
Blocks parasympathetic activity to increase HR not likely to be effective in either CCB or BB overdose
42
Calcium
More effective in CCB overdose than BB Enters open voltage sensitive calcium channels to promote calcium release from sarcoplasmic reticulum resulting in myocardial contractility Calcium chloride has 3x more elemental calcium than calcium gluconate
43
Vasopressor therapy
Vasodilatory shock-->norepinephrine Cardiogenic shock-->epinephrine Should utilize higher doses to overcome beta receptor blockade
44
Glucagon
bypasses beta receptor and acts directly on Gs to stimulate conversion of ATP to cAMP May need to pre-medicate with ondansetron and add PRN regiment due to N/V with glucagon
45
High dose insulin therapy
Increased inotropy and increased intracellular glucose transport Insulin drip at 0.5 to 1 unit/kg/hr IV Dextrose at 0.5 gm/kg/hr Communicate with HC providers to address patient safety
46
Lipid emulsion therapy
limits bioavailability of lipophilic medication by creating a "lipid sink" Indiana poison center - 1.5 mL/kg bolus - 0.025 mL/kg/min OR - 2.25 mL/kg bolus - 0.025 mL/kg/min Total max dose: 10 mL/kg

PHRM 865 Final (3 decks)

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