Brainscape's Knowledge GenomeTM

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


See full index

FRCPC-EM > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What are the 4 stages and pathophysiology of ASA poisoning

A

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

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

Describe the symptoms associated with the stages of ASA poisoning

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

Indications for urine alkalinization in ASA poisoning

A

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

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

Indications to stop urine alkalinization in ASA poisoning

A

1- Clinical improvement of patient
2- Normalised metabolic parameters
3- ASA levels <2.8 and consistently trending downwards on 2 hrly checks.

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

List seven indications for hemodialysis in ASA poisoning.

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

List 5 causes of CO poisoning

A

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

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

List 5 pathophysiologic mechanisms of CO poisoning

A

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

How do you screen for CO poisoning/

How do you interprete CO levels

A

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

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

What is the 1/2 life of CO

A

1 -RA = 4-6 hours
2- 100& O2 = 90 mins
3- HBO (3 atm) = 30 mins

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

Whats the antidote for CO poisoning what is the mechanism of action.

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

Indications for HBO in CO poisoning mgt

A 
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

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

List conditions 5 that could lead to CN toxicity

A

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

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

List 10 clinical presentations of CN toxicity

A 
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

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

What is the antidote and mechanism of action

What are the complications

A

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)

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

What are the major causes of death from toxicologic agitated delirium

A

1 Psychomotor agitation

2 Hyperthermia

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

What are the 5 clinical stages of Fe toxicity

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 ways to determine/ evaluate Fe toxicity

A

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

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

What are the indications for treatment

and the treatment options

A

1- Moderate serum /ingested levels with clinical features suggestive of Fe toxicity
2 Severe toxicity

Antidote - Deferoxamine (DFO) 15mg/kg/hr IV

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

List 5 complications of Deferoxamine in treating Fe poisoning

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

List 3 differences btw Nicotinic and Muscarinic Ach receptors

A

Nicotinic
Parasymp + Symp
Inotropic
Excitatory

Muscarinic
Parasymp
G-proteins
Excitatory + Inhibitory

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

List 4 drug agents that can cause miosis

A 
COPS
C= cholinergics,clonidine
O =opioids,organophosphates
P = Phenothiazines(anti-psychs),pilocarpine
S= sedative-hypnotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

List 3 drug agents that can cause mydriasis

A

SAWS
S= sympathomimetics
A= anticholinergics
W= withdrawal syndromes

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

List 7 drug agents that can cause coma

A

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
24
Q

List 7 drug agents that can cause seizures

A

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
25
Q

List 4 agents that can cause diaphoretic skin findings

A

SOAP

S= sympathomimetics
O= organophosphates
A= Acetylsalicylic acid
P= Phencyclidine (PCP)
26
Q

List 7 drug agents that can cause cyanosis

A

ANNE-PADS

A =Aniline dye
N =Nitrate
N= Nitrites
E=ergotamine
P=phenazopyridine
A=agents causing hypoxemia,hypotension,methHb
D= dapsone
27
Q

List 5 features of the sympathomimetic toxidrome

A

( 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

28
Q

List 5 features of the anticholinergic toxidrome

A

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
29
Q

Describe the pathophysiology of the cholinergic toxidrome and list 5 features

A

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)
30
Q

List 7 fxts of the opioid toxidrome

A 
Miosis/Mydriasis
Hypoventilation
Diarrhoea
Lacrimation
Hypertension
Hallucinations
Seizures
31
Q

List 5 features of the SS toxidrome

A 
Altered mental status
Agitation
Clonus
Hyperreflexia
Hyperthermia
Diaphoresis
32
Q

List the pathophysiology of Neuroleptic malignant syndrome and 5 fxts

A

Due to depletion of dopamine secondary to use of dopamine antagonists eg antipsychotics

Rigidity
Agitation
Altered mental status
Hyperthermia
Decreased reflexes
33
Q

List 5 causes of altered mental status

A

AEIOU

Alcohol/Acidosis
Encephalopathy
Infection
Overdose/opioids
Uremia

TIPS

Trauma
Insulin (hypo/hyperglycemia)
Psychosis
Seizure

34
Q

List 5 clinically relevant false positives for urinary amphetamine testing

A 
Labetalol
Amantadine
Ranitidine
Bupropion
Trazodone
Promethazine
35
Q

List 2 clinically relevant false positive tests for benzodiazepines

A

Sertraline

Oxaprozin

36
Q

List 2 clinically relevant false positive tests for cannabinoid

A

PPI
Efavirenz
Dronabinol

37
Q

List 2 clinically relevant false positive tests for opioids

A

Dextromethorphan
Quinolones
Diphenhydramine

38
Q

List 2 clinically relevant false positive tests for PCP

A

Dextromethorphan
Diphenhydramine
Ibuprofen
Tramadol

39
Q

List 4 indications for use of single dose activated charcoal

A

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

40
Q

List 3 contra-indications for use of single dose activated charcoal

A

Sedated patient
Unprotected airway
Refusal

41
Q

List 5 substances that do not bind to activated charcoal

A 
PHAILS
Pesticides
Heavy metals
Acids/Alkalis
Iron
Lithium
Solvents
42
Q

List 3 characteristics of toxic agents amenable to dialysis

A 
Low molecular weight
Low protein binding
High water solubility 
Examples STUMBLED
Salicylates
Theophylline
Uremia
Methanol/metformin
Barbiturates
Lead
Etylene glycol
Depakote (valproic acid)
43
Q

Describe the mode of action of multiple dose AC

A

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.

44
Q

List 4 drugs amenable to multiple dose AC

A 
ABCDQ
Aminophylline/theophylline
Barbiturates
Dapsone
Quinine
45
Q

List 3 complications from the use of intralipids

A

Extreme lipemia -interfering with blood results
ARDS
Pancreatitis

46
Q

List 4 DDs for ASA poisoning

A

Sepsis
CNS infection
Withdrawal symptoms
EtOH/DM ketoacidosis

47
Q

Itemise the precautions to be taken if a patient with ASA poisoning requires intubation

A

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

48
Q

Difficulties in alkalinizing urine during ASA poisoning mgt

A

Salicylic acid

H ion replaced in urine for Potassium

49
Q

Clinical features of simple asphyxiation

A 
Due to manifestations of ischemia
Ataxia
Dizziness
Confusion
Incoordination
Tachycardia
Tachypnea
Dyspnea
50
Q

Indications for treatment with NAC after IV overdose with Acetaminophen

A

1- > 60mg/kg

2- >50ug/ml of Acetaminophen ,4 hours after infusion stopped.

51
Q

List 4 at risk patients for chronic acetaminophen toxicity

A

1- Regular ingestion of INH
2- Malnourished
3- Chronic EtOH abuse
4 Severe dehydration

52
Q

List 4 indications for hemodialysis in Acetaminophen toxicity

A 
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
53
Q

List 4 criteria for immediate Liver transplant in Acetaminophen toxicity

A

pH <7.3 /Lactate >3.5 after resuscitation
PTT >100 / INR >5
Grade 3/4 hepatic encephalopathy
Cr >3.3

54
Q

List 4 mechanisms of toxicity of formic acid

A 
1- Inhibition of mitochondrial cytochrome oxidase
   Inhibiting intracellular respiration
2- Free radical formation
3 - Antioxidant impairment
4- Lipid peroxidation
55
Q

What the the stages of ethylene glycol toxicity and list 3 clinical features for each stage

A 
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

FRCPC-EM (3 decks)

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