Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ID final > toxicology > Flashcards

toxicology Flashcards

1
Q

top medication overdoses

A

adults - analgesics, sedatives/hypnotics/anti-psychotics, antidepressants, CV drugs, cleaning substances, alcohol
pediatric - cosmetics, cleaning substances, analgesics, foreign bodies, topicals, vitamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

first things first

A

Stabilization: ABC management***, Vital signs, IV access, Oxygenation
Exposure history: Medications/substances, Dose(s), Time of ingestion, Family/EMS report, Pill count
Assessment: Physical exam, Labs, APAP/ASA concentrations, EtOH/toxic alcohol panel
Decontamination: Activated charcoal, Cathartics, Gastric lavage, Whole bowel irrigation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

anticholinergic toxidromes

A 
blind as a bat
hotter than hell
red as a beet
dry as a desert
mad as a hatter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

urine drug screens detect…

A

Amphetamines, Barbiturates, Benzodiazepines, Cannabinoids, Cocaine, Opioids, Phencyclidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

anion gap

A

Difference between primary measured cations and primary measured anions
(Na+ + K+) – (Cl- + HCO3-) *
Gap is present if greater than 14
MULEPAK (methanol, uremia, lactic acidosis, ethanol, paraldehyde, aspirin, ketoacidosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

osmolar gap

A

Presence of additional unmeasured low molecular weight molecules that are osmotically active (reference range: 285-300 mOSm/kg)
Gap = Measured - Calculated
Calculated = (2 x Na+) + (BUN/2.8) + (Glu/18) + (EtOH/4.6) ***
Gap is present if greater than 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

activated charcol

A

44-95% prevention of absorption
Pros: Decreases time related problems, Absorbs most toxins
Cons: Difficult administration, must be given within 4 hours
1-2 gm/kg ABW or 50-100 gm in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cathartics

A

Decreases GI transit
-Magnesium citrate 2-4 mL/kg/dose (up to 300 mL)
-Sorbitol 70% solution 1-2 mL/kg (up to 1 gm/kg)
rarely used due to OTC abuse - weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

gastric lavage

A

“stomach pump”
Efficacy: 8-59%
Complications: Vomiting, Aspiration, Mechanical injury
Advantages: Difficult to refuse, Comatose patients, Use with other agents
Disadvantages: Proper technique, Delay in implementation, Tablet size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

whole bowel irrigation

A

Polyethylene glycol
Sustained-release products, “body packers/stuffers”, iron, lithium
Dosing: 500 mL/hr in children 9 months to 6 years; 1,000 mL/hr in children 6 years to 12 years; 1,000-2,000 mL/hr in adolescents and adults
Patient should remain seated on a bedside toilet
Continue until presence of clear rectal effluent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

hemodialysis

A

Effective for the following medications: Alcohols, Lithium, Salicylates, Theophylline
must have low molecular weight and small V(d)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

s/sxs of opioid toxicity

A

Nausea/vomiting, Drowsiness, Constipation, Pinpoint pupils, Hypotension, Bradycardia, Respiratory depression, Seizure activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

general management of opioid toxicity

A

ABC management
Monitor vital signs, pulse oximetry, and ECG changes
Monitor signs/symptoms of CNS and respiratory depression
Oxygen supplementation (if needed)
UDS and acetaminophen (APAP)/salicylate concentrations
Administer activated charcoal (if presentation within two hours of ingestion)
Administer naloxone (Narcan®)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

opioid antidote

A

naloxone
Mechanism of action - Antagonizes opioid effects by binding to same receptor sites
Dosing - 0.4 to 2 mg IV push, IM, SQ, ET, or intranasally
-Utilize lower doses initially in patients with chronic opioid dependence due to withdrawal symptoms - GI upset, restlessness, piloerection, hypertension, tachycardia
-May consider continuous infusion with longer acting opioids - Prolonged signs/symptoms; RR under 8 breaths/min to prevent intubation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

opioid toxicology tidbits

A

Severity dependent on medication, dose, duration of action, and patient
Comprises both prescription and illicit drug use - Methadone, Heroin
Aaron’s Law

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

risk for APAP OD

A 
Induced p450s (CYP2E1 mainly): Isoniazid, Acetone, Chronic EtOH
Patients with depleted glutathione: Malnourished, Anorexic, Alcoholics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

protected for APAP OD

A

Children - Increased sulfation pathway, Large liver-to-body ratio
Acute EtOH
Cimetidine and disulfiram - Inhibit CYP2E1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

APAP phases of tocivity

A

1) 0.5 to 24 hours post ingestion - Nausea, vomiting, diaphoresis, malaise, pallor
2) 24-72 hours post ingestion - Hepatic injury (abdominal pain/tenderness, oliguria)
3) 72-96 hours post ingestion - Hepatic failure (jaundice, coagulopathy, encephalopathy, coma)
4) Greater than 96 hours post ingestion - Full recovery or death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

APAP tox general management

A

ABC management
Acetaminophen (APAP) concentration at least 4 hours post ingestion
Toxic doses in acute ingestions
-Adults: 150 mg/kg or 7.5-10 gm (OR 4 grams)
-Children: 200 mg/kg
Administer activated charcoal (if presentation within two to four hours of ingestion)
Evaluate for potential N-acetylcysteine (NAC) therapy using Rumack-Matthew nomogram (can only be used after 4+ hours of ingestion - plots time v conc - 2 lines to represent if tox is unlikely or if probable hepatic tox)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

APAP antidote

A

N-acetylcysteine (Acetadote®)
Glutathione precursor
Mechanism of action: Increases glutathione stores, Acts as a glutathione substitute, Enhances sulfate conjugation
May also have anti-inflammatory, anti-oxidant, inotropic, and vasodilating effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

acetylcystine dosing

A

IV:
-LD: 150 mg/kg IV over 1 hour
-Second infusion: 50 mg/kg IV over 4 hours
-Third infusion: 100 mg/kg IV over 16 hours
PO:
-LD: 140 mg/kg
-Scheduled regimen: 70 mg/kg PO every 4 hours x 17 doses
capped at 100 kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

salicylate toxicity

A

Mixed acid base disorders: ↑ anion gap - metabolic acidosis; Respiratory alkalosis (early) - hyperventilation
Electrolyte disturbances: Hypokalemia, Hypo/hypernatremia
Salicylate concentrations:
-Analgesic properties: 10-15 mg/dl
-Anti-inflammatory properties: 15-20 mg/dl
-Mild toxicity: > 30 mg/dL (tinnitus, dizziness)
-Severe toxicity: > 80 mg/dL (CNS effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

salicylate toxicity s/sxs

A

CNS: tinnitus, vertigo, delirium, hallucinations, agitation, hyperactivity, seizures, stupor, lethargy
GI: NV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

salicylate toxicity general management

A 
ABC management
Monitor vital signs and pulse oximetry
Salicylate (ASA) concentration
Ventilation, ABG
BMP to measure anion gap
Administer activated charcoal (if presentation within two hours of ingestion)
Fluid/electrolyte management
Hemodialysis
Urine alkalization - Sodium bicarbonate: 1 to 2 mEq/kg (50 to 100 mEq) IV push over 1 to 2 minutes; Continuous infusion may be initiated afterwards and titrated to effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

sedative/hypnotics toxicity s/sxs

A 
CNS depression
Respiratory depression
Hypotension
Bradycardia
Hypothermia
Rhabdomyolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

sedative/hypnotics toxicity antidote

A

Flumazenil (Romazicon®)
Mechanism of action - Competes with BZDs at BZD binding site of GABA complex
Dosing: 0.2 mg IV push
-Use with caution in patients
with seizures - Can induce seizure activity** even in seizure naive patients
-Can induce withdrawal
symptoms - Nausea/vomiting, agitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

TCAs toxicology tidbits

A

Linked to more drug related deaths than any other prescription medication
-Starting to see less in clinical practice due to new antidepressant medications (e.g., SSRIs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

TCAs in clinical practice

A

Indications: depression, neuropathy, insomnia, migraines, bed wetting
examples: amitriptyline, doxepin, nortriptyline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

TCA PKs

A

Initially, rapidly absorbed from the GI tract - Anticholinergic effects may slow GI motility, Decrease rate of absorption
Large Vd (10-50 L/kg)
Acidemia increases the percentage of unbound TCA
Highly lipophilic
t1/2 = 4-93 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

TCA pharmacology

A 
Anticholinergic activity
Alpha receptor blockade
Serotonin, norepinephrine, and dopamine reuptake inhibition
Sodium and potassium channel blockade
CNS and respiratory depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

TCA toxicity s/sxs

A

Altered mental status, Hypotension, Tachycardia, ECG changes (QRS prolongation), Seizure activity, CNS depression, Anticholinergic
symptoms, Drowsiness, Respiratory depression, Decreased GI motility, Metabolic acidosis, Rhabdomyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

TCA toxicity effects of QRS prolongation

A

QRS interval > 100 msec - Increased risk of seizure activity
QRS interval > 150 msec - Increased risk of cardiac arrhythmias
May also result in metabolic acidosis - Promotes unbinding of drug from proteins

33
Q

TCAs toxicity general management

A

ABC management
Monitor vital signs and ECG changes
UDS, urinalysis, serum electrolytes, and ABG/VBGs
Serum TCA concentrations?
Fluid hydration +/- vasopressors for hypotension
Seizure activity management (if applicable)
Consider activated charcoal (if presentation within two hours of ingestion and no signs/symptoms of ileus)
Consider sodium bicarbonate based on ECG results (QRS prolongation)

34
Q

TCA tox antidote

A

Sodium bicarbonate
Mechanism of action: Increases sodium gradient of poisoned sodium channels
Indications: QRS interval > 100 msec, TCA induced arrhythmias or hypotension, Metabolic acidosis
Dosing: 1 to 2 mEq/kg (50 to 100 mEq) IV push over 1 to 2 minutes
-Continuous infusion may be
initiated afterwards and titrated
to effect
Monitoring
-Serum pH 7.45-7.55
-D/C when: QRS interval under 100 msec, Resolution of ECG abnormalities, Hemodyamically stable

35
Q

Seizure management of TCA toxicity

A 
**Benzodiazepines - Lorazepam (Ativan®), diazepam (Valium®), midazolam (Versed®)
Phenobarbital (Luminal®)
Phenytoin (Dilantin®)?
Fosphenytoin (Cerebyx®)?
Levetiracetam (Keppra®)?
36
Q

antipsychotics: pharmacology

A

First Generation - D2 antagonism

Second Generation - 5HT2A/D2 antagonism

37
Q

antipsychotic examples

A

typical: haloperidol, fluphenazine, chlorpromazine, thioridazine, perphanazine, trifluoperazine, pimozide
atypical: aripiprazole, clozapine, olanzapine, risperidone, quetiapine, ziprasidone, paliperidone

38
Q

antipsychotic toxicity S/sxs

A

CV: Hypotension, Tachycardia, QT and QRS prolongation
neuro: Extrapyramidal symptoms (EPS), Neuroleptic malignant syndrome (NMS), Sedation, Seizure activity

39
Q

atypical antipsychotics toxicity

A 
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
40
Q

extrapyramidal sxs

A

Benztropine 2 mg IM
-Onset ~ 15 - 20 minutes
-Longer half life
Diphenhydramine 1- 2 mg/kg IV/IM (up to 50 mg) over several minutes
-Onset ~ 5 minutes
-Continue with oral therapy for 3 - 4 days - Diphenhydramine 50 mg PO TID

41
Q

neuroleptic malignant syndrome

A

Hyperpyrexia up to 42.2C (108F) with altered mental status (delirium or coma) and “lead pipe” muscular rigidity
Occurs 3-9 days after initiating therapy or after adding a second agent
Often these patients are under 40 years of age and more often males

42
Q

NMS complications

A

Continues for 5-10 days
84% of cases - Haloperidol, depot fluphenazine, or chlorpromazine use
Death is secondary to rhabdomyolysis, renal failure, cardiovascular collapse, respiratory failure, arrhythmias, or thromboembolism

43
Q

NMS treatment

A

D/C offending agent
Rapid external cooling
Benzodiazepines
Dantrolene - Initial dose of 2.5 mg/kg to a maximum of 10 mg/kg IVP; Maintenance dose is 2.5 mg/kg Q6H until resolved
Bromocriptine has also been utilized - 2.5 mg BID initially, increasing to 5 mg TID; Doses as high as 60 mg/day have been used

44
Q

serotonin syndrome

A

Toxic hyperserotonergic state - Excessive stimulation of the post-synaptic receptors in the CNS
Triad of symptoms: Altered mental status, Autonomic instability, Neuromuscular abnormalities
Development of serotonin syndrome is rapid - Within six hours of an increase in the precipitating medication

45
Q

serotonin syndrome: pharmacology

A

Direct agonists: Buspirone, Lithium, Lysergic acid diethylamide (LSD), Sumatriptan
Increased release of serotonin: Amphetamines, Cocaine, Mirtazapine, MDMA (“ecstasy”)
Inhibitors of serotonin metabolism: Monoamine oxidase inhibitors, Linezolid
Reduced uptake of serotonin:
-Selective serotonin reuptake inhibitors (SSRIs) - Citalopram, fluoxetine, sertraline,
paroxetine
-Tricyclic antidepressants (TCAs) - Amitriptyline, imipramine, nortriptyline
-Serotonin norepinephrine reuptake inhibitors (SNRIs) - Duloxetine, Venlafaxine
-Trazodone
-Dextromethorphan

46
Q

treating serotonin syndrome

A

D/C offending agent
Benzodiazepines
Aggressive cooling
Cyproheptadine (Periactin®)
-1st generation histamine receptor blocking agent
-Non-specific 5-HT1A and 5-HT2A receptor blocking effects - 4 mg PO Q1H; Maximum dose: 16 mg

47
Q

serotonin syndrome vs NMS

A

SS: lasts under 24 hours, lower limbs more affected
NMS: higher fever, lasts over 24 hours, diffuse lead pipe rigidity

48
Q

digoxin in clinical practice

A

Indicated for the treatment of atrial fibrillation (AF) and heart failure (HF)
Monitored with serum concentrations due to narrow therapeutic index
-Goal range usually 0.8 to 2 ng/mL - May be 0.5 to 1 ng/mL in HF
-Must be drawn at least 6 hours after previous dose

49
Q

digoxin tox s/sxs

A

Non Cardiac: Nausea/vomiting, Abdominal pain, Anorexia, Confusion, Vision changes
Cardiac: Bradycardia, 2nd or 3rd degree heart block, Arrhythmias, Hyperkalemia( 5 to 6.4 mEq/L ~ 35% mortality, > 6.4 mEq/L ~ 90% mortality)

50
Q

digoxin toxicity general management

A

Discontinue digoxin
ABC management
Obtain serum digoxin concentration, BMP
Monitor vital signs and ECG changes (arrhythmias, bradycardia)
Administer activated charcoal (if presentation within two hours of ingestion)
Consider administration of Digibind®
Hemodialysis is not* effective

51
Q

digoxin antidote

A

Mechanism of action: 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
dosing: Each vial binds approximately 0.5 mg* of digoxin
-Based on acute ingestion of known amount - Total body load (TBL) = mg digoxin ingested x 0.8; TBL/0.5 mg = # Digibind ® vials to administer
-Based on serum digoxin concentrations in adults
— # Digibind ® vials = digoxin concentration (ng/mL) x patient’s weight (kg) / 100

52
Q

digoxin toxicology tidbits

A

Toxicity can occur with acute ingestion and chronic therapy
Must correlate signs/symptoms with serum concentration - Time of ingestion? Time of concentration?
Serum digoxin concentrations are clinically useless after Digibind® administration

53
Q

CCBs and BBs in clinical practice

A

CCBs: Angina, Hypertension, Arrhythmias (e.g., AF), HF
BBs: Angina, Hypertension, Arrhythmias, HF, Myocardial infarction, Migraine headaches, Tremor, Portal hypertension

54
Q

CCB and BB toxicity s/sxs

A

CCBs: Hyperglycemia, Metabolic acidosis, Pulmonary edema, Ileus (SR)
BBs: Hypoglycemia, Bronchospasm
both: Hypotension, Bradycardia, Arrhythmias, Cardiogenic shock, CNS depression

55
Q

CCB and BB general management

A

ABC management
Monitor vital signs and ECG changes (arrhythmias, bradycardia)
Administer activated charcoal (if presentation within two hours of ingestion)
Potential antidotes: Atropine, Calcium, Vasopressor therapy, Glucagon, High dose insulin therapy

56
Q

CCBs and BBs : atropine

A

Mechanism of action: Blocks parasympathetic activity to increase heart rate
Dosing: 0.5 to 1 mg IV push - Maximum dose: 3 mg

57
Q

CCBs and BBs : calcium

A

Mechanism of action: Enters open voltage sensitive calcium channels to promote calcium release from sarcoplasmic reticulum resulting in myocardial contractility, More effective in CCB overdoses vs BB overdoses
Dosing: Calcium chloride: 5 to 10 mL of 10% solution; Calcium gluconate: 10 to 20 mL of 10% solution
-Note: Calcium chloride has three times more elemental calcium than calcium gluconate

58
Q

CCBs and BBs : vasopressor therapy

A

May require higher doses to overcome receptor blockade
Medication selection depends on clinical presentation
-α stimulates effects on blood pressure
-β stimulates effects on heart rate
Review patient’s ingestion history and monitor vital signs to select appropriate agent

59
Q

CCBs and BBs : glucagon

A

Mechanism of action: Bypasses beta receptors and acts directly on Gs to stimulate conversion of ATP to cAMP
Dosing: 3 to 10 mg IV bolus (adults); 50 to 150 mcg/kg IV bolus (children)
-Initiate infusion at same dose as effective bolus dose (in mg/hr) - Patient responds to 5 mg IV bolus, start infusion at 5 mg/hr

60
Q

CCBs and BBs : high dose insulin therapy

A

Mechanism of action: Facilitates myocardial utilization of carbohydrates
Dosing: Insulin drip at 0.5 to 1 unit/kg/hr IV; Dextrose at 0.5 gm/kg/hr IV
-Titrate to systolic blood pressure > 90 to 100 mm Hg or effect every 30 to 60 minutes (improved contractility, decreased symptoms)
Monitoring: Improved contractility within 15 to 60 minutes; Goal glucose: 100 to 250 mg/dL; Serum electrolytes every 1 to 2 hours (glucose, potassium)

61
Q

CCBs and BBS: toxicology tidbits

A

Atropine - Not likely to be effective in either CCB or BB overdoses
Calcium - More likely to be effective with CCB overdoses vs BB overdoses; Chloride has three times more elemental calcium vs. gluconate, but extravasation more likely with chloride formulation
Vasopressor therapy - Should utilize higher doses to overcome beta receptor blockade
Glucagon - May need to pre-medicate with ondansetron (Zofran®) and add PRN regimen due to nausea/vomiting with glucagon
High dose insulin therapy - Communicate with health care providers to address patient safety

62
Q

Iron toxicology tidbits

A

Toxicity can occur at 10 to 60 mg/kg of elemental iron
Prenatal vitamins contain approximately 65 mg of elemental iron
Children’s vitamins contain approximately 10 to 18 mg of elemental iron
Concern is absorption of iron into tissue - Can still experience toxicity with normal serum iron concentrations
Human body has no natural mechanism to handle iron overload
-Excretion: Male = 1 mg daily; Female = 2 mg daily

63
Q

Iron phases of toxicity

A

1) 0.5 to 2 hours post ingestion - GI upset, abdominal pain, hematemesis, hematochezia
2) 6 to 24 hours post ingestion - Latent phase resembling recovery; continue to monitor
3) 2 to 24 hours post phase 1 - Shock stage (acidosis, hypotension, hypovolemia, poor cardiac output)
4) 48 to 96 hours post ingestion - Hepatoxicity
5) Days to weeks post ingestion - GI scarring, obstructions, strictures

64
Q

iron tox - general management

A 
ABC management
Monitor vital signs
Fluid hydration
Serum iron concentration 4 hours post ingestion
Activated charcoal is not effective
KUB (kidneys, ureter, and bladder) scan
Whole bowel irrigation 
Consider administration of deferoxamine for chelation
65
Q

iron antidote

A

Deferoxamine (Desferal®)
Mechanism of action: Chelates iron and enhances renal elimination
Indications: Metabolic acidosis or other signs of shock, Clinical deterioration despite IV fluid administration, Presence of iron tablets on KUB Serum iron concentration > 500 mcg/mL
dosing: Start at 15 mg/kg/hour - May increase to 45 mg/kg/hour for patients with severe poisoning; Decrease rate if patient experiences hypotension - Usually continued for 12 to 24 hours; May titrate down based on resolution of symptoms and/or absence of vin rose urine

66
Q

toxic alcohol examples

A

Ethylene glycol - Antifreeze, brake fluid, and industry solvents
Methanol - Windshield washer fluid, paint remover, copier fluid, some antifreeze, and some engine fuels
Isopropyl alcohol - Rubbing alcohol, paint remover, cements, cleaners

67
Q

toxic alcohols - clinical presentation

A

anion gap and osmolar gap (know equations!!!)

68
Q

interpretation of results for alcohol tox

A 
Anion gap PLUS osmolar gap
-Methanol toxicity
-Ethylene glycol toxicity
-Alcoholic ketoacidosis
Osmolar gap WITHOUT anion gap
-Isopropyl alcohol (acetone) toxicity
69
Q

ethylene glycol PKs

A

Rapidly absorbed from the GI tract
Rapidly distributed throughout the body
t ½ = 2.5-4.5 hrs In the presence of normal renal function; 20% excreted unchanged in the urine
Alcohol dehydrogenase in the liver is the first rate-limiting step in the breakdown

70
Q

ethylene glycol phases of toxicity

A

1) 30 minutes to 12 hours post ingestion - CNS effects, nausea/vomiting, inebriation, lethargy/coma (within 4-8 hours), seizures
2) 12-24 hours post ingestion - Metabolic effects, cardiac compromise, anion gap acidosis***
3) 2 to 3 days post ingestion - Renal effects (calcium oxalate crystals), ATN within 12-48 hours

71
Q

ethylene glycol toxicology tidbits

A

Presence of osmolar gap?
Ethylene glycol, methanol and ethanol serum concentrations
Wood’s lamp evaluation of urine

72
Q

methanol: PKs

A

t1/2 = 14-30 hrs, peak levels in 20-90 min
Oral ingestion, inhalation, or dermal absorption
Metabolized by alcohol dehydrogenase to formaldehyde then to formic acid - Reaction is slow, so delay in toxic metabolite formation

73
Q

methanol phases of toxicity

A

1) Headache, dizziness, ataxia, confusion

2) During formic acid accumulation, Pronounced visual symptoms, Anion gap

74
Q

ethylene glycol and methanol: general management

A

Non-Pharmacologic - Gastric lavage and aspiration if presents in less than one hour; Charcoal is NOT effective; Hemodialysis if: EG concentration greater than 100 mg/dL, Methanol concentration greater than 45 mg/dL, Refractory acidosis, Renal Failure, Symptomatic
Pharmacologic:
-Ethanol and fomepizole - Inhibition of alcohol dehydrogenase limits metabolism of ethylene glycol)
-Adjunctive therapy - Shunt metabolism toward nontoxic metabolites (Thiamine (EG), Pyridoxine (EG), Magnesium (EG), Folate (Methanol) )
-sodium bicarb: Large amounts may be necessary to maintain normal pH; Helps in conversion of formic acid to carbon dioxide and water
Correct hypocalcemia and hypoglycemia

75
Q

ethanol therapy

A

Greater affinity for alcohol dehydrogenase
0.6 gm/kg IV bolus then 110 mg/kg/hr - If HD started, increase dose to 250-350 mg/kg/hr
Optimal blood ethanol concentration of 100-150 mg/dL
Side effects: phlebitis, altered mental status, hypoglycemia

76
Q

fomepizole

A

to treat ethanol glycol and methanol tox
Dose
-15 mg/kg IV load followed by 10 mg/kg Q12H x 4 doses
-Need to increase to 15 mg/kg IV Q12H if continued
-Administer Q4H during
hemodialysis
Advantages: No CNS depression, ICU stay not required
Disadvantage - Cost?

77
Q

isopropyl alcohol PKs

A

50-80% metabolized by alcohol dehydrogenase to acetone
t1/2 of isopropyl = 3 hrs; acetone = 10-20 hrs
Acetone eliminated via kidneys and lungs
Lethal dose greater than 400 mg/dL
Potency is double-strength ethanol
Peak levels 30 min after ingestion

78
Q

isopropyl alcohol toxic effects

A

Prolonged CNS depression
Nystagmus or miosis
Ketonemia
Hemorrhagic gastritis
Elevated osmolar gap
Increased serum isopropanol concentrations
Bradycardia/hypotension at high concentrations

79
Q

isopropyl alcohol treatment

A

Gastric lavage
Hydration
Correct electrolyte abnormalities
Hemodialysis - Lethal doses, Coma, Refractory shock

ID final (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions