toXXX Flashcards by Caroline Mak | Brainscape

Q

Poison control #

A

1-800-222-1222

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Q

What information to collect when a patient calls or presents with substance poisoning

A

Age, weight
PMH
Time of exposure and route
Present s/s
Exact name of product, formulation, strength
- How much has been ingested
Occupation
Were there suicide notes?

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Q

General management to a patient with substance poisoning

ABCDE

A

Airway
Breathing
Cirulaation
Dextrose/Decontamination
EKG/Elimination

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Q

Non-pharm for substance poisoning

A

If the agent was inhaled: remove pt from the exposure area
If agent is topical/derm: irrigate with soap and water
If agent is ingested: can consider orgogastric (“stomach pumping”)
hemodialysis can also be considered for specific situations

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Q

When to use orgogastric methods in substance poisoning

stomach pumping

A

Ingestant has potential for serious toxicities
No antidotes exist
Time window gives reason to believe agent may still be in stomach

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Q

When to use hemodialysis in substance poisoning

A

Other elimination strategies not effective or are contraindicated
Ingestant has potential to produce serious ADR
Agent is able to be removed through filtration
EXTRIP is a good source to find out if hemodialysis would work

ex: ASA and tox alcohols

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Q

GI decontamination methods (pharm-ish) for substance poisoning

A

do NOT use Ipecac
Can consider activated charcoal: enhances gastric dialysis of certain drugs and prevents prolonged absorption or enterhepatic recirculation
Can consider PEG3350 with electrolytes (whole bowel irrigation)
- golytely, nulytely, colyte, NOT miralax

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Q

When to use activated charcoal in substance poisoning

A

Most benefit if used within an hour of ingestion (doesn’t mean you can’t use it if it’s been mmore than an hour)
- It helps prevent absorption
No benefit if the ingested substance is
- Ionized metals: lithium, iron
- Alcohols
- Gasoline

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Q

Activated charcoal dosing

A

sometimes the first dose is formualted with sorbitol to improve palatability tho no big evidence for benefit of sorbitol
- 1g/kg
pediatric dosing
- 0.5-1g/kg OR
- multiple dose: loading dose of 1g/kg followed by 0.5g/kg Q4-6H up to 24 hrs

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Q

Activated charcoal AE

A

vomitting, black tarry stools
- Do NOT want pt to vomit this up and have it in their airways

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Q

When to use whole bowel irrigation in substance poisoning and dose

A

Goal is to minimize time that ingestant is in GI tract for absormption
Beneficial for XR products, metals (Fe), and body packers (people who store packets of illicit drugs in their GI system to smuggle across borders)
1-2 L/hr or until rectal effluent is clear
peds: NG is easier to use
- 0.5L/hr in small children Q4-h H
- 1.2-2L/hr in older chilren/adolescants Q4-6 H

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Q

Toxidrome defininiotn

A

s/s that point to a class of toxin based on understanding of pharmacology

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Q

Drug(s) that have adrenergic/sympathomimetic toxidrome

A

Cocaine
Amphetamines
Bathsalts
Pseudoephedrine
Nootropics
Bupropion

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Q

Drug(s) that have cholinergic toxidrome

A

Organophosphates
Pesticides

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Q

Drug(s) that have anticholinergic toxidrome

A

TCAs
antihistamines (like benadryl)

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Q

Drug(s) that have sedative/hypnotic toxidrome

A

Benzos
EtOH

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Q

Drug(s) that have opioid toxidrome

A

opioids
heroin
morphine
loperamide (need 30-200mg → cross BBB and PGP can’t kick it out)

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Q

Adrenergic/sympathomimetic toxidrome S/S

A

Enlarged pupils
Increased BP
Increased HR
Increased RR
Increased temp
Bowel sounds
Tremor
Seizures

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Q

Cholinergic toxidrome S/S

A

Salivation
Lacrimation
Urination
Defecation
Gastric cramps
Emesis
Bradycardia
Bronchorrhea
Bronchospasm
Pinpoint pupils
Bowel sounds

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Q

Anticholinergic toxidroe S/S

A

Blind as a bag
Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter (agitated)
Enlarged pupils
Increased BP
Increased HR
Increased RR
Increased temp
Urinary retention
Tremor
Seizures

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Q

Sedative/hypnotic toxidrome S/S

A

Sleepy with normal vitals
- bp, hr, rr may be a little decreased

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Q

Opioid toxidrome S/S

A

Unresponsive to painful stimuli
Pinpoint pupils
Low RR
Low BP
Low HR
Low temp
Hyporeflexia
Decreased mental status

Loperamide can cause arrhythmias

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Q

Treatment for pts with cholinergic toxidrome

A

Atropine: inhibits muscarinc actions of ACh
- 1mg IV titrated to effect, no MDD

Pralidoxime: reactivates cholinesterase
- 30mg/kg IV load
- 8-10mg/kg/hr continuous infusion

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Q

Treatment for pts with anticholinergic toxidrome d/t antihistamine overdose

A

Physostigmine: ACh inhibitor
- 0.5 - 2 mg IV

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Q

Treatment for pts with benzo overdose

A

Benzos alone aren’t that bad, can be handled with monitoring, supportive care; intuation if needed
- NOT LETHAL

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Q

The problem with flumazenil and when to use it

A

Can send someone who is benzo overdosed (not lethal) into withdrawal (lethal)
_
So when to use flumazenil?
- procedural sedation
- in peds accidental overdose who are not benzo dependent
- Z-drug overdose (not really tho)

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Q

Flumazenil dosing

A

competitivte antag at benzo receptor site
- 0.2mg IV over 15 seconds
- peds: 0.01 mg/kg IV
- onset: 1-2 min

idk if this is just for benzo overdose or in general

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Q

Opioid overdose treatment

A

IV naloxone dose
- 0.4mg for non-opioid dependent
- 0.04mg for opioid dependent pt
- titrate to effect (ideally)
- continuous inf: 1/2 of initial effective dose as bolus then 2/3 of effective dose/hr
Protect airway or breath for them

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Q

Naloxone IV vs. nasal

A

IV: quick onset, quick wear off
IN: longer onset and duration
IM: somewhere inbetween

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Q

Naloxone AE

A

flash pulmonary edema: treat with nitroglycerin, diuretic, and positive pressure ventilation
runny nose

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Q

Loperamide overdose treatment

A

Naloxone
IF CARDIAC DISTURBANCE
- IV Mg
- Sodium bicarb
- IV isoproteronol or transcutaneous pacer

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Q

What drug levels do we like to draw in patients who present with overdose/substance poisoning?

A

Digoxin
Vanco
Phenytoin
Lithium
APAP - no toxidrome
ASA - unique toxidrome

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Q

Polysubstance overdose approach

A

Eliminate: activated charcoal
Admin antidotes: naloxone, NAC
Supportive care: benzos

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Q

Benzo withdrawal s/s

A

Severe sleep disturbance
Irritability
Increased tension and anxiety
Panic attacks
Sweating
Difficulty in concentration
Dry retching and nausea
Palpitations
Headache
Psychotic reaction
Seizures
Death

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Q

Which is deadlier? benzo overdose or benzo withdrawal

A

WITHDRAWAL

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Q

OTC that can cause asa/ salicylates overdose

A

Peptobismol
Alkaselzter
Oil of wintergreen: 98% methyl salicyalte (98g/100ml)
Icy hot
Bengay
ASA

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Q

ASA/salicylate toxic levels (adults)

A

Toxic at >150mg/kg
Life threatening at >500mg/kg

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Q

ASA/salicylate mechanism of tox

A

metabolic acidosis and uncoupled oxidative phosphorylation (can’t produce ATP and excess H+)

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Q

ASA/salicylate overdose S/S

A

Resp: tachypnea/hyperpnea
GI: disrupt nucosal barrier, N/V, hemorrhagic gastritis, bezoar formation
CNS: neuoronal energy depletion, hypoglycorrachia (hypoclycemia in brain only), AMS, tinnitus, hyperpyresxia, tachycardia, fever, coma, seizures
Non-cardiogenic pulmonary edmea
Renal and hepatic injury

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Q

ASA/salicylate overdose acid/base labs

A

Early on in overdose: resp alkalosis
Middle of overdose: mixed metabolic acidosis and resp alkalosis
Late/preterminal overdose: metabolic and resp acidosis
- Body can no longer compensate and you can’t even compensate by breathing hard

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Q

What is a bezoar formation

A

concrete ball of salicylate in stomach that can break off and release more drug into system

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Q

ASA/salicylate overdose electroytes presentation

A

Hypo or hyperglycemia
Increased fluid and electrolyte losses
Increased anion gap
Urine: ketones in urine

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Q

ASA/salicylate overdose treatment

A

Airway, breathing, circulation (do NOT ventilate)
Enhance elimination
- Multiple doses of activated charcoal (1g/kg)
- Urine alkalization (we want a pH >7.5)
- Can consider hemodialysis
Dextrose (even if normal glucose levels): 0.5-1g/kg
Fluid maintenance
- Serum pH 7.45-7.55
- 150 mEq of sodium bicarb in D5W at twice maintenance rate (alkalinize urine)
- Treat spefic AE too (seizures, edema, etc.)

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Q

ASA/salicylate overdose monitorng

A

Monitor Q2H
- Mental status
- Urine and blood pH
- Salicylate levels
- Fluid and electrolytes
- Maintain K (often low)

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Q

ASA/salycylate overdose: if pt is on hemodilaysis for the overdose, when to stop

A

Stay on hemodilaysis until clear inprovement in pt AND salicylate level <19mg/dL
- Or 4-6 hrs if you can’t get labs

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Q

ASA/salicylate overdse: who qualifies for hemodialysis

A

Serum level >100mg/dL in pts with acute
Serum level >60mg/dL in pts with chronic
Neurologic deterioration
Seizures
Intractable acidosis (pH <7.2)
Renal failure
Pulmonary edema

Q

Purpose of urine alkalinzation in asa/salicylate overdose

A

shift salicylate into un-ionized form → move across barriers → more excretion

Q

If you overdose on an antidepressant, will it present as serotonin syndrome?

A

Very unlikely, usually only see serotonin syndrome if polypharmarcy with multiple serotenergic agents or with drug specific for 5HT2A or 5HT1A

Q

Serotonin syndrome presentation

A

Spontaneous clonus
Agitation
Diaphoresis
Hyperthermia
Tremor
Hyperreflexia
Diarrhea
AMS
Incoordination

Q

SSRI overdose presentation

A

Seroternergic features
- AMS
- Tachycardia
- Myoclonus
- Tremors
- Diarrhea

Q

Serotonin syndrome antidone

A

cyproheptadine but it is very anticholinergic, so not used often
- Can use benzos and propranolol for symptom treatment

Q

Serotoin overdose treatment

A

Supportive care
Monitoring
Escitalopram and citalopram are most likely to cause seizures and QTc prolongation

Q

List the TCAs

A

amitriptyline
nortriptyline
doxepin
imipramine
desipramine

Q

TCAs MOA and related overdose S/S

A

Catechol reuptake inhibitior: hypotension
Alpha adrenergic blocker: hypotension
GABA antag: seizure
Sodium channel blocker: dysarrythmias → lethal

initial increase in BP and HR and then quick drop; anticholinergic toxidrome

Q

TCA and EKG/ECG

A

If there’s an R wave in aVR: there was some exposure to TCA (not necessarily a TCA overdose, but it is present)
Elevated QRS → increased risk of seizure
Bigger R wave amplitude → higher incidence of seizure

Q

TCA overdose treatment

don’t worry about the treatments for specific s/s for this card

A

If pt came in early enough; can consider
- orogastric lavage (GI flush) or activated charcoal
hypertonic sodium bicarb 1-2 mEq/kg bolus and then 150 mEq in 1L D5W at twice maintenance rate (150-200 ml/hr); give until
- Do this until QRS narrows
- We would also like to see blood pH go back to normal (<7.5) but fixing QRS is more important

Q

Hypertonic sodium bicarb MOA in TCA overdose

A

Sodium (hypertonic sodium like 3% NaCl) → prevents lethal sodium channel blockade
Alkalinzation (via hyperventiliation) may also be effective

Q

TCA overdose: additional treatment if pt is experiencing seizures

A

Benzos
Barbituates
do NOT give phenytoin: can increase frequency and duration of VT
do NOT give flumazenil: prevents benzo protection against seizure and can worsen seizures

Q

TCA overdose: addition treatment if dysrhythmias aren’t going away

A

Mg
Lidocaine (replace TCA with a more benign sodium channel blocker)

Q

TCA overdose: additional treatment if pt is hypotensive

A

Ne, E, vasopressin, phenylephrine
Methylene blue, lipid emulsion, high dose insulin

Q

Bupropion overdose S/S

A

May be asymptomatic until like 24 hrs later when they suddenly have a seizure -> hold pt until certain no seizures
Widening of QRS complex but does NOT respond to sodium bicarb
Sympathomimetic crisis
Cardiogenic shock
Status epilepticus
Lazarus effect (pronouced dead but then randomly wakes up later)
Death

Q

Bupropion overdsoe treatment

A

Supportive care
Maybe lipid emulsion and ECMO
Maybe orogastric lavage or activated charcoal or whole bowel irrigation
IF HTN, can try benzos

Q

Antihypertensive overdose general presentation

A

Toxidrome: bradycardia, hypotension

Cardiac: AV blocks and CHF
- Sotalol can cause torsades
CNS: depressed LOC
- Propranolol can cause seizures

Q

Differentiation dx between CCB and BB overdose

A

CCB has elevated glucose

Q

CCB specific overdose presentaiton

A

Alert initially
Elevated blood sugar
Hypotension (d/t vasodilation)
non-DHP CCBs:
- decreased ventricular contratility
- sinus node depression
- AV node depression -> various blocks

Q

CCB and BB overdose treatment

A

GI decontamination if applicable
fluids: isotonic crystalloids (0.9 NaCl, LR)
atropine: 0.5-1mg Q5min 3x
calcium
- CaCl (can cause sclerosing): 1-3g IV
- Ca gluconate: 3-9g IV
high dose insulin (HIET)
- 1 U/kg bolus then 1-10 U/kg/hhr
- give glucose to counteract insulin
- maintain glucose >100 mg/dL
- 30-60 min onset
potassium prn to maintain 2.8-3.5 mg/dL

Same as BB

Q

Other than the normal treatment steps, what other agents might you use in the setting of CCB and BB overdose?

A

vasopressors: NE and E
- can be used as monotherapy in mild overdose
- can also be used as bridge insulin
inotropes: dobutaminne (CCB), milrinone (BB)
cardiac pacing
intralipid:
- pull toxin off of site
- modulate myocardial energy
ECMO
BB ONLY: glucagon 3-5mg bolus then 3-5mg/hr + zofran (n/v)

Q

Why can glucagon be considered in BB overdose but not CCB?

A

it’s like a beta agonist that bypasses the beta receptor

Q

Glucagon AE

A

vomiting (zofran ppx)
- avoid use in pts wtih AMS

Q

Alpha agonist specific overdose s/s

A

Decreased mental status
Small pupils
No delay in onset
CLONIDINE SPECIFIC
- transient HTN and tachycardia before suddenly going to bradycardia and hypotension
- CNS depression
- Respiratory depression

Q

Alpha agonist overdose treatment

A

Suportive care
Clondine: naloxone for respiratory depression
- 5-10mg bolus
- can start an infusion if response

Q

Acute digoxin toxicity s/s

A

Predistribution
- N/V
- Hyperkalemia: guaranteed death if K >5.5
Post distribution (6 hrs)
- Hypotension
- Bradycardia
- Dysrhythmias
- Death

Q

Chronic digoxin toxicity S/S

A

less typical and K level is unhelpful

Q

Digifab indication in chronic digoxin tox

A

Post-distribution (>6 hrs after ingestion) level of >6 mcg/L
Progressing or severe signs of tox

Q

Digifab dosing in practice

A

2 vials and then titrate to effect
- Give every hr if no response is seen

Q

Acute digoxin tox treatment

A

GI decontamination: activated charcoal, repeat doses needed in renal failure
Digifab if appropriate
- K >5
- Digoxin level >20 mg/dL
- Progresing signs of tox
Temporizing measures: Ca if patient is looking bad (high K+)

But too much calcium induces “stone heart” = irreversible contraction of heart
Data says still give calcium too

Q

MUDPILES

A

M - Methanol
U – Uremia
D – DKA, SKA, AKA
P – Phenformin (metformin), Paraldehyde
I – Isoniazid, INH
L – Lactate, CO, CN, MetHb
E – Ethylene Glycol
S – Salicylates

Causes of anion gap metabolic acidosis

Q

Anion gap calculation

A

Calculating anion gap: gap = Na - (Cl + HCO3)

normal = 4-12

Q

Clinical presentation after ingestion of toxic alcohols

A

Early:
- AMS - like they’re drunk
- GI distress
Late:
- High anion gap metabolic acidosis
- Specific differences between EtOHs
  - Methanol: visual changes “blind”
  - Ethylene glycol: nephrotox, hypocalcemia

Q

Toxic alcohols

A

Methanol: high volatility - in gasline antifreeze and windshield washer fluid
Ethylene glycol: low volatility - in engine fluid

Q

What labs to look at in pts who present for ingestion of toxic alcohol

A

Electrolytes - and treat where needed
Arterial blood gas
Ethanol level
Methanol and ethylene glycol levels
- The labs won’t return until the next day, so for the first day that they present, you don’t really know which they have
Measured osmolality

Q

Management/treatment of ingestion of toxic alcohols

A

GI decontamination: useless
alcohol dehydrogenase (ADH) inhibitor: ethanol OR 4-methylpyrazole-fomepizole (4-MP, Antiol: preferred agent)
Supplementation
- ethylene glycol
  - B6 pyroxidone IV 100mg QD
  - B1 thiamine IV 100mg QD
- methanol
  - folic acid: 1mg/kg Q4-6H for 24hrs
- Mg
Sodium bicarb: to correct acidosis

supplement doses are from peds lecture, idk what adult doses are

Q

Ethanol dosing in ingestion of toxic alcohols

A

adults:1g/kg to maintain a BAC of ~100 mg/dL
peds: loading dose of 8 ml/kg over 1 hr → 0.8 ml/kg/hr IV
- Goal serum [ ]: 100-150 mg/dL
- Goal [ ] of toxic alcohols: <25 mg/dL

Q

Ethanol formulations

A

IV 10% soln
PO: shots x 4

Q

Ethanol AE

A

CNS inebriation
thrombophlebitis (IV)
GI symptoms

Q

4-MP (fomepizaole) AE

A

HA
Dizziness
Minor allergic reactions

Q

4-MP (fomepizaole) dosing in ingestion of toxic alcohols

A

15 mg/kg load, then 10mg/kg Q12h x4, then 15mg/kg Q12H
- Dilute in NS or D5W and infuse over 30 min
- Lower then re-up dose d/t autoinduction
- Dose increased during hemodialys
peds: same dosing as adults
- goal toxic alcohol [ ]: <25 mg/dL

Q

Who needs hemodilaysis in pts who have ingested toxic alcolhols

A

Methanol or ethylene glycol level 25-50 mg/dL
High osmal gap (>10) without aother cause
- A normal gap could mean pt is doing well or tthat pt is doing trash, not super specific or helpful
End organ manifestations of tox (renal, vision)
Severe metabolic acidosis

Q

CB1 receptors

A

CNS
GPCRs
Motor activity
Thinking
Pain perception

Q

CB2 receptors

A

Periphery
GPCRs
Immune modulation
Anti-inflammatory

Q

Unwanted effects form phytocannabinoids

A

Short term memory difficulties
Agitaion
Feeling intense
Anx
Dizziness
Lightheadedness
Confusion
Loss of coordination

Q

Phytocannabioids

A

natural cannabis
THC parital agonism at CB1 receptor

Q

Sythetic cannabinoids

A

Full agonist (act on CB1 AND CB2)
Higher receptor affinity
Longer half lives

Q

Synthetic cannabinoids tox clincal presentation

A

CNS depression
Disorientation
Restlessness/agitation
Hallucinations
Seizures
Comativeness
Anx
Mydriasis
Tachycardia
Vomitting

Q

Synthetic cannabinoids tox labs

A

Hypokalemia
Increased blood glucose
Increased SCr
Increased WBC
Increased Creatinine kinase

Q

synthetic cannabinoids tox treatment

A

Agitation: treat with benzos
Seizures: treat with benzos
Dehydration: treat with IV crystalloids
HTN/tachycardia: treat with benzos ad if benzos don’t work, IV antihypertensives

Q

synthetic cannabinoids n/v moa and dx

A

excessive vomitting d/t dysregulation of endocannabinoid system and alteration in TRPV2 receptor
dx
- Hx of regluar cannabis use
- Cyclic N/V
- Generalized diffuse abdominal pain
- Compulsive hot showers with symptom improvement

Q

synthetic cannabinoid n/v presentation: pre-emetic phase

A

months-years
diffuse abdominal dyscomfort
feelings of agitaiton or stress
morning nausea
fear of vomiting
Often pts will self treat with more marijuana

Q

synthetic cannabinoid n/v presentaito: hyperemetic phase

A

24-48 hrs
Cyclic episodes of N/V
Diffuse, severe abdominal pain

Q

Synthetic cannabinoid n/v presentation: recovery phsase

A

Only upon cessation of cannabis (may take a month for full resolution)
Bowel regimens
Fluids
Electrolyte replacement

Q

synthetic canabinod n/v treatment

A

Activate TRPV1
- Hot showers
- Caapsaicin topical cream
Anti-nausea
- Haloperidol - better opiton
- Ondansetron
- Benzos: inhibitory effect on medullary and vestibular nuclei associated with n/v
Supportive care
- Fluids
- Electrolytes

Q

Cocaine specific tox s/s

A

euphoria
seizures
dysrhythmias
HTN
coronary artery spasm MI

Q

cocaine speific tox treatment

A

benzos
supportive care

Q

amphetamines specfic tox s/s

A

agitation
seizures
hyperthermia
HTN
delirium

longer acting than cocaine

Q

Amphetamine specific tox treatment

A

benzos or barbituates
anti-htn
supportice care

Q

Bath salts specific tox s/s

A

agitation
tachycardia
insomnia
paranoia
seizures
violent unpredictable behavior

Q

Bath salts specific tox treatment

A

supportive care

Q

sympathomimetic (general) treatment

A

Elimination strategies (charcoal)
Clinical effects: Benzos
Airway protection: intubation
Hyperthermia: Ice baths, benzos, antipyretics
Dysrrthmias: Sodim bicarb, lidocaine
Rhabdo: Fliuds
Antihypertensives
Anti-psych
Electrolyte management

Q

Peds poisoning labs to get

A

Lab evals as is relevant to the H&P and pt presentation
- but almost always at least serum chemistries and acid-base
- strong consideration for serum APAP (also salicylates, ethanol, iron) d/t easy access/OTC status

Q

toxic APAP doses in peds

A

> 200mg/kg PO or >60mg/kg IV

Q

Peds apap overdose treatment

A

GI contamination with activated charcoal if it has been less than an hr
NAC dosing
- PO: 140mg/kg x1 → 70mg/kg Q4H x17
- IV (more often used): 150mg/kg over 1 hr → 50mg/kg over 4 hrs → 100mg/kg over 16 hrs
  - To prevent hypoNa, product should be diluted to a [ ] of 40mg/dL

Q

household cleaners/caustic exposures: possible causes and treatment

A

Cleaners: bleaches, detergents, soaps
Caustics: toilet cleanere, drain cleaner, oven cleaner
JUST SUSPPORTIVE CARE
- If GI injury can consider PPIs
- do NOT use GI decontamination

Q

Foreign body ingestion treatment

A

GI decontamination: manual removal if esophagaeal impact suspected

Q

Peds cough and cold: overdose/tox treatment

A

Products should be avoided in pts < 6 per FDA 2017
Use activated charcoal
Symptomatic management
- HTN: labeatol, nicardipine
- Arrhythmias: amiodarone
- Seizures: benzos

Fatalities due to pseudoephedrine