Tox 1 Flashcards by Sara Fieger

who do you ask for hx?

EMS
Family
Pt (pt not reliable)

How well did you know this?

Not at all

Perfectly

imp. historial details

timing
drugs/substance
acute v chronic
WHY (accidental, environment, depression, etc)

How well did you know this?

Not at all

Perfectly

primary survey

ABCD(decontamination)

airway and IV access, cardiac monitor and EKG

How well did you know this?

Not at all

Perfectly

secondary survey

seek more history
repeat exam
consult toxicology and poison control

How well did you know this?

Not at all

Perfectly

COMA cocktail

DONT

D-50 (get a glucose)
Oxygen
Narcan
Thiamine (500 mg IV)

How well did you know this?

Not at all

Perfectly

decontamination strategies

Protect yourself
Eye: NS irrigation
Skin: Soap and water

How well did you know this?

Not at all

Perfectly

drugs with an increased risk to cause hypoglycemia

insulin
DM drugs (I.e. sulfonuryeas) 
Alcohol
Salicylates 
acetaminophen

How well did you know this?

Not at all

Perfectly

clinical features of sympathomimetic OD

Mydriasis (DILATED Pupils)
HTN, Hyperthermia
Diaphoresis
Agitated and excitable

How well did you know this?

Not at all

Perfectly

sympathomimetic toxicology tx

IV hydration
benzos
cooling
intubation

DO NOT RESTRAIN for long time

How well did you know this?

Not at all

Perfectly

opiates v opioids

opiATE: made from the poppy seed (heroin, opium, codeine, morphine)

opiOID: synthetic (oxygen, fentanyl, Percocet)

How well did you know this?

Not at all

Perfectly

symptoms of opioid toxicity

respiratory depression
CNS depression
mitosis (pinpoint pupil)

How well did you know this?

Not at all

Perfectly

anticholinergics toxicity sx

mydriasis 
tachycardia 
hyperthermia 
urinary retention 
ventricular dysrhythmia (Prolonged QRS, VTach)

How well did you know this?

Not at all

Perfectly

anticholinergics toxicity tx

IVF and Benzo first line

Physostigmine if severe

How well did you know this?

Not at all

Perfectly

TCA OD tx

sodium bicarb (dysrhythmia)

fluid bolus, benzos (seizure/agitation)

physostigmine = CHF risk, seizures, heard block

How well did you know this?

Not at all

Perfectly

TCA drugs names

amitriptyline (elvail)

Imipramine (Tofranil)

How well did you know this?

Not at all

Perfectly

TCA

Clinical Features:

Combative, Seizure, HoTN, Dysrhythmia

How well did you know this?

Not at all

Perfectly

TCA Patho:

direct myocardial depression, inhibition of norepinephrine uptake

How well did you know this?

Not at all

Perfectly

TCA ECG:

QRS prolongation,
tachycardia,
aVR

How well did you know this?

Not at all

Perfectly

Cholinergic OD Symptoms

Vomiting
Fasciculation

DUMBELS

Diarrhea,diaphoresis
Urination 
Miosis
Bronchorrhea,bronchospasm, bradycardia
Emesis
Lacrimation 
Salivation

Cholinergic Treatment

Skin decontamination
Atropine
2-PAM (pralidime)

clinical features of sedatives.hypnotic OD

normal vital signs + CNS depression

Sedative/hypnotic OD tx

supportive (Airway, IV hydration, cardiac monitor)

Acetaminophen metabolization

liver

depletion of gluthione = accumulation

Acetaminophen stages of toxicity

24hrs: nausea, vomiting, malaise 24-48 hrs: asymptomatic, liver enzyme elevation 48-96 hrs: hepatic failure, encephalopathy, coagulopathy 7-8 days: recovery

what scale monitors Acetaminophen toxicity?

rhumack Matthews taken at arrival and 4hrs later

Acetaminophen toxicity tx

NAC (PO) if toxic rhumack or evidence of renal failure within 8 hrs (ineffective after 24 hrs)

beta blocker toxicity present when?

MC within 1-4 hrs of ingestion

primary organ system affected by beta blocker toxicity

cardiovascular system

hallmark of severe beta blocker toxicity

bradycardia | shock

cause of bradycardia in beta blocker toxicity

sinus node suppression or conduction abnormality

beta blocker toxicity affects which systems

Cardio CNS pulmonary system

neuro manifestation of beta blocker toxicity

depressed mental status coma seizure psychosis

CV manifestations of beta blocker toxicity

``` HoTn Bradycardia conduction delay/blocks ventricular dysrhythmia asystole decreased contractility ```

electrolyte manifestation of beta blocker toxicity

hypoglycemia | hyperkalmia

beta blocker toxicity w/u

``` renal function 12-lead EKG glucose stick acid base status oxygenation ```

beta blocker toxicity tx list (8)

``` Glucagon Adrenergic receptor agonist high dose insulin therapy atropine calcium Calcium Salts Sodium Bicarbonate Cardiac Pacing ```

glucagon beta blocker toxicity

first line for bradycardia and HoTN effects occur 1-2 min ADR: n/v

adrenergic receptor agonist beta blocker toxicity

Norepinephrine, epinephrine, dopamine esp. NE and E due to chronotropic

high dose insulin tx beta blocker toxicity

inotrope facilitates myocardial glucose usage = energy supply during stress stimulated contraction

ADRs of high dose insulin tx in beta blocker toxicity

hypoglycemia and lower K dextrose infusion and supplemental K ( <2.8 mEq)

atropine beta blocker toxicity

muscarinic blocker not effective in management of BB Brady and HoTN but not harmful

calcium beta blocker toxicity

inotrope reverse myocardial depression not often used, but option for refractory cases

calcium salts beta blocker toxicity

Ca gluconate = peripheral administration Ca chloride = central line (sclerosis risk)

sodium bicarbonate beta blocker toxicity

severe acidosis wide QRS interval dysrhythmia given if QRS > 120-140