Toxicology Flashcards
What are the 4 stages and pathophysiology of ASA poisoning
1- Respiratory alkalosis
Stimulation of the medulla
2- Metabolic Acidosis
Uncoupling of oxidative phosphorylation
3- Primary mixed resp alkalosis and resp acidosis
Patient not decompensating.
4- Acidosis
Mainly due to respiratory decompensation. Patient develops respiratory acidosis
Describe the symptoms associated with the stages of ASA poisoning
1- Early stage 0-4 hours GI,Hyperpnea, Tinnitus 2-Moderate stage 2- 12 hrs Severe hyperpnea,lethargy or agitation 3- Severe stage Fxts - Respiratory alkalosis/acidosis + metabolic acidosis with acidemia Severe hyperpnea Coma Seizures Delirium Hyperthermia Pulmonary oedema
Indications for urine alkalinization in ASA poisoning
1- Signs and symptoms of salicylate toxicity
Hyperpnea,tinnitus,agitation
2- Serum level >2.0-2.5mmol/L or expected to reach this range (Note levels should be taken 2 hrly)
3- Significant acid base disturbance
Indications to stop urine alkalinization in ASA poisoning
1- Clinical improvement of patient
2- Normalised metabolic parameters
3- ASA levels <2.8 and consistently trending downwards on 2 hrly checks.
List seven indications for hemodialysis in ASA poisoning.
1- Worsening clinical status despite urine alkalinization
2- Severe acid base disturbance
3-End organ toxicity (ie pulm oedema, AKI,CNS)
4- Volume overload
5- Inability to alkalinize the urine
6- Salicylate levels >7mmol/L acute
> 3mmol/L chronic
7- Rapidly rising salicylate levelList 5 causes of CO poisoning
Fires
Engine exhaust
Propane powered boats or vehicles
Home sources (ie furnaces,wood stoves,water heaters/boilers)
Inhalational anesthetics
Methylene chlorine (paint thinners)
Patients presenting in a group with N/V,HA
List 5 pathophysiologic mechanisms of CO poisoning
COHb does not carry O2
Shifts O2-Hb dissociation curve to the left
CO binds to myoglobin
Binds to cytochrome oxidase
Induces CNS Lipid peroxidation -responsible for delayed neurological sequelae.
How do you screen for CO poisoning/
How do you interprete CO levels
Mild - 5 -10% mild HA,mild dypnea
Moderate 10 -30% HA,weakness,dyspnea,irritability
dizziness,N/V ,Impaired judgement
Severe 30 -50% coma,seizures,death
What is the 1/2 life of CO
1 -RA = 4-6 hours
2- 100& O2 = 90 mins
3- HBO (3 atm) = 30 mins
Whats the antidote for CO poisoning what is the mechanism of action.
HBO 1- Decreases half life of CoHb 2-Displaces CO from Mb and cytochrome oxidase in tissues 3-Increases O2 content of blood 4-Decreases lipid peroxidation
Indications for HBO in CO poisoning mgt
A - Evidence of end organ toxicity CNS LOC,Coma,Seizure Focal neurological deficit,visual symptoms,cognitive defects CVS MI,Arrhythmias Metabolic acidosis
B -COHb Levels
>25%
>15% in pregnant patients (fetal Hb has a greater affinity for CO,so treatment strarted earlier to preserve foetus)
Abnormal neuropysch examination with CO exposure
Pulmonary injury -Inablity to oxygenate
List conditions 5 that could lead to CN toxicity
1- Occupational ie jewelers,photographers,lab techs,fumigation
2- Smoke inhalation from fires
3-Intentional
4- Medicinal source - Na nitroprusside
5-Food sources -Amygdalin from apricot pits,bitter almond,cherry,peach
List 10 clinical presentations of CN toxicity
1-HA 2-Anxiety 3-Agitation 4-Confusion 5-Seizures 6-Coma 7-Hypotension 8-Severe bradycardia 9-Metabolic acidosis (lactate >10) 10-Abdominal pain 11- Vomiting
Chronic
1- Parkinsonian symptoms
2- Ataxic neuropathy
3- Visual loss
What is the antidote and mechanism of action
What are the complications
Hydroxocobalamin (HCB) (5g first)
Binds with CN to form Cyanocobalamin -Vit B12
Side effects
1- Htn
2-Red discolouration of urine
3-Interferes with further lab tests (Inform lab when samples are drawn)
What are the major causes of death from toxicologic agitated delirium
1 Psychomotor agitation
2 Hyperthermia
What are the 5 clinical stages of Fe toxicity
1 Local GI irritation vomitting, GI bleed, black tarry stools 2 Latent stage GI symptoms disappear 3 Metabolic and CVS stage Acidosis, hypotension 4 Hepatic stage 5 Delayed GI effects -weeks,months Pyloric stenosis
What are the 3 ways to determine/ evaluate Fe toxicity
1 Clinical presentation
Persistently vomiting,black tarry stools,UGIB
2 Serum Fe levels
3 Amount ingested
Fe Levels and Iron load (Ingested) Gluconate preps 10% Sulphate 20% Fumarate 30% of elemental Fe <20mg/kg Non toxic 20 60 -Mild moderate toxicity >60 Severe toxicity
Serum levels correlate well 4-6 hours after ingestion
Represents Fe bound to transferrin and free Fe in blood.
<50 umol/L Non toxic
50 -90 Moderate -support with other parts of history and clinical presentation
> 90 severe toxic
What are the indications for treatment
and the treatment options
1- Moderate serum /ingested levels with clinical features suggestive of Fe toxicity
2 Severe toxicity
Antidote - Deferoxamine (DFO) 15mg/kg/hr IV
List 5 complications of Deferoxamine in treating Fe poisoning
1 Infusion rate related hypotension 2 Anaphylactoid reaction 3 Yersinia enterocolitis 4 Oto and visual toxicity 5 ARDS with high dosing for days 6 Painful IM injection No evidence of toxicity to fetus
List 3 differences btw Nicotinic and Muscarinic Ach receptors
Nicotinic
Parasymp + Symp
Inotropic
Excitatory
Muscarinic
Parasymp
G-proteins
Excitatory + Inhibitory
List 4 drug agents that can cause miosis
COPS C= cholinergics,clonidine O =opioids,organophosphates P = Phenothiazines(anti-psychs),pilocarpine S= sedative-hypnotics
List 3 drug agents that can cause mydriasis
SAWS
S= sympathomimetics
A= anticholinergics
W= withdrawal syndromes
List 7 drug agents that can cause coma
LETHARGIC
L= lead, lithium E= Ethanol, ethylene glycol T= Toluene,TCA,thallium H= hemlock, heroin,hypoglycemics A = Arsenic,antihistamines,antipsychotics R= rophynol,risperidone G= gamma hydroxybutyrate GHB I = isoniazid,insulin C= clonidine,CO,CN
List 7 drug agents that can cause seizures
OTIS CAMPBELL
O= organophosphates, oral hypoglycemics T= TCAs I = Isoniazid,insulin S= salicylates,sympathomimetics,strychnine C= cocaine,CO,CN A = amphetamines,anti-cholinergic M= methanol,methylxanthines P = phencyclidine,propanolol B= water hemlock,nicotine E= EtOH withdrawal,ethylene glycol L = Lead,lithium L = Lindane,lidocaine
List 4 agents that can cause diaphoretic skin findings
SOAP
S= sympathomimetics O= organophosphates A= Acetylsalicylic acid P= Phencyclidine (PCP)
List 7 drug agents that can cause cyanosis
ANNE-PADS
A =Aniline dye N =Nitrate N= Nitrites E=ergotamine P=phenazopyridine A=agents causing hypoxemia,hypotension,methHb D= dapsone
List 5 features of the sympathomimetic toxidrome
( Remember features of the fight/flight rxn)
1- Altered mental status
2- Elevated vital signs (HR,BP,RR,hyperthermia)
3- Mydriasis
4-Diaphoresis
5- Treatment refractory shock (high doses)
6 -Arrhytmias
7-Seizures
8-Flushed skin
List 5 features of the anticholinergic toxidrome
Remember- This is due to the alteration of the homeostatic balance btw the sympathetic and parasympathetic system. The sympathetic side fxns unopposed
1 Delirium (mad as a hatter) 2 Hyperthermia ( Hot as a hare) 3 Mydriasis (blind as a bat) 4 Cutaneous flushing (red as a beet) 5 Dry skin,urinary retention (dry as a bone ) 6 Tachycardia
Describe the pathophysiology of the cholinergic toxidrome and list 5 features
This is due to overstimulation of the parasympathetic part of the ANS,which conrols the rest and digest fxn. Agents of concern are primarily organophosphates and carbamate insecticides
The features are due to excessive accumulation of acethylcholine at the NMJ and synapses,causing symptoms of nicotinic and muscarinic toxicity. These include
Muscarinic = DUMBBELLS Diaphoresis, diarrhoea Urination Miosis Bradycardia Bronchorrhea Emesis Lacrimation Lethargic Salivation
Nicotinic - Days of the week Mydriasis Tachycardia Weakness Tremors Fasciculations Seizures Somnolent (Nicotine poisoning can resemble both sympathomimetic and cholinergic toxidromes -due to its role in the CNS and ANS)
List 7 fxts of the opioid toxidrome
Miosis/Mydriasis Hypoventilation Diarrhoea Lacrimation Hypertension Hallucinations Seizures
List 5 features of the SS toxidrome
Altered mental status Agitation Clonus Hyperreflexia Hyperthermia Diaphoresis
List the pathophysiology of Neuroleptic malignant syndrome and 5 fxts
Due to depletion of dopamine secondary to use of dopamine antagonists eg antipsychotics
Rigidity Agitation Altered mental status Hyperthermia Decreased reflexes
List 5 causes of altered mental status
AEIOU
Alcohol/Acidosis Encephalopathy Infection Overdose/opioids Uremia
TIPS
Trauma
Insulin (hypo/hyperglycemia)
Psychosis
Seizure
List 5 clinically relevant false positives for urinary amphetamine testing
Labetalol Amantadine Ranitidine Bupropion Trazodone Promethazine
List 2 clinically relevant false positive tests for benzodiazepines
Sertraline
Oxaprozin
List 2 clinically relevant false positive tests for cannabinoid
PPI
Efavirenz
Dronabinol
List 2 clinically relevant false positive tests for opioids
Dextromethorphan
Quinolones
Diphenhydramine
List 2 clinically relevant false positive tests for PCP
Dextromethorphan
Diphenhydramine
Ibuprofen
Tramadol
List 4 indications for use of single dose activated charcoal
Patient is alert and cooperative. Anticipated to remain alert.
Within 1 hour of ingestion (within 2 hr for SR,or massive ingestions)
Ingestion of highly toxic agent eg killer Cs
colchicine
CN
cocaine
cyclic antidepressants
CCB
cicutoxin
ASA
Evidence of massive ingestion of toxic agent
Effective antidote not available
Ingested agent must be amenable to adsorption by AC
List 3 contra-indications for use of single dose activated charcoal
Sedated patient
Unprotected airway
Refusal
List 5 substances that do not bind to activated charcoal
PHAILS Pesticides Heavy metals Acids/Alkalis Iron Lithium Solvents
List 3 characteristics of toxic agents amenable to dialysis
Low molecular weight Low protein binding High water solubility Examples STUMBLED Salicylates Theophylline Uremia Methanol/metformin Barbiturates Lead Etylene glycol Depakote (valproic acid)
Describe the mode of action of multiple dose AC
1 Decreases xenobiotic absorption and elimination half live,when large doses are ingested and dissolution delayed.
2 Creates a hemoperfusion substrate for the gut wall microcirculation,creating a concentration gradient into the stool of certain poisons (gastrointestinal dialysis)
3 Interferes with entero-hepatic circulation,reducing absorption.
List 4 drugs amenable to multiple dose AC
ABCDQ Aminophylline/theophylline Barbiturates Dapsone Quinine
List 3 complications from the use of intralipids
Extreme lipemia -interfering with blood results
ARDS
Pancreatitis
List 4 DDs for ASA poisoning
Sepsis
CNS infection
Withdrawal symptoms
EtOH/DM ketoacidosis
Itemise the precautions to be taken if a patient with ASA poisoning requires intubation
Administer 50 -100mEq of NaHCO3 prior to procedure,irrespective of the pH
Adjust post intubation tidal volume to match pre-intubation PCO2
Establish an elevated minute volume
Difficulties in alkalinizing urine during ASA poisoning mgt
Salicylic acid
H ion replaced in urine for Potassium
Clinical features of simple asphyxiation
Due to manifestations of ischemia Ataxia Dizziness Confusion Incoordination Tachycardia Tachypnea Dyspnea
Indications for treatment with NAC after IV overdose with Acetaminophen
1- > 60mg/kg
2- >50ug/ml of Acetaminophen ,4 hours after infusion stopped.
List 4 at risk patients for chronic acetaminophen toxicity
1- Regular ingestion of INH
2- Malnourished
3- Chronic EtOH abuse
4 Severe dehydration
List 4 indications for hemodialysis in Acetaminophen toxicity
1- Levels > 1000 ug/ml at 4 hours post ingestion 2- Hepatorenal syndrome 3- Metabolic acidosis < 7.30 4- Lactate levels >3.5 mmol/L 5 Encephalopathy
List 4 criteria for immediate Liver transplant in Acetaminophen toxicity
pH <7.3 /Lactate >3.5 after resuscitation
PTT >100 / INR >5
Grade 3/4 hepatic encephalopathy
Cr >3.3
List 4 mechanisms of toxicity of formic acid
1- Inhibition of mitochondrial cytochrome oxidase Inhibiting intracellular respiration 2- Free radical formation 3 - Antioxidant impairment 4- Lipid peroxidation
What the the stages of ethylene glycol toxicity and list 3 clinical features for each stage
Acute neurologic stage (30 mins -12 hours post ingestion) 1- Inebriation 2- Euphoria 3- Seizures 4- Coma 5- Hypotonia 6- Ataxia 7- Nystagmus 8- Myoclonic jerks
Cardiopulmonary stage (12 -24 hours) 1- Tachycardia (metab acidosis) 2-Tachypnea 3- Hypoxia 4- ARDS 5- Circulatory collapse
Renal Stage (24 to 72 hours) 1- Flank pain 2- Hematuria 3- ARF ( Anuric,oliguric ,non-oliguric Reversible renal failure with tx
Delayed neurologic stage (5 - 20 days) Bulbar palsy with CN VII and VIII dysfunction 1- Vertigo 2- Facial droop 3- opthalmoplegia 4- Nystagmus 5-Facial sensory loss 6- Hearing loss Autonomic nerve dysfunction 1- Postural hypotension 2-Gastroparesis
