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EM > WK 2-Toxicology and Endocrine Emergencies > Flashcards

WK 2-Toxicology and Endocrine Emergencies Flashcards

1
Q

What is a toxidrome

A

syndrome caused by a dangerous level of toxins in the body–> each drug can present with different symptoms so useful to know the toxidrome to determine the drug taken

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2
Q

What important points are involved in a risk assessment after drug/poison ingestion

A
  • how bad is it and what to do to make it less dangerous
  • Agent (s)
  • Dose
  • Time since ingestion (charcoal can be effective if given early enough)
  • Clinical features + expected course
  • Patient factors (was it a suicide attempt)
  • Safety of staff + other patients (especially for organophosphate toxins→ first thing to do is shower them
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3
Q

What is symptomatic supportive care

A

treating the symptoms

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4
Q

What aspects of ABC need to be controlled

A

Airway: intubatation

  • Breathing: Supplemental 02, ventilation
  • Circulation: correct low or high BP and hypovolemia
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5
Q

Apart from ABC, what else needs to be monitored

A

-Control seizures: most seizures last 45 seconds because muscles become hypoxic and stop contracting→ if prolonged can give benzo→ 1st line - titrated IV benzodiazepines (midazolam/diazepam), 2nd line - IV barbiturates (phenobarbitone))→ also always check glucose (hypoglycaemia causes seizures)
-Correct hypoglycaemia
-Correct hyperthermia: when left uncontrolled can cause rhabdomyolysis and renal failure→Temp greater than 38.5→ continuous core temp monitoring
T greater than 39.5→ active cooling, neuromuscular paralysis, intubation + ventilation

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6
Q

What is decontamination

A

Removal of the substance from the body

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7
Q

What is an example of decontamination

A
  • Use of activated charcoal
  • charcoal is fine charcoal with a large surface area that works by binding drug in the GIT lumen→ decreasing absorption in the GIT and drawing the drug into the GIT from the blood (down the conc gradient)
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8
Q

When is activated charcoal used and not used

A 
Used: rarely, only when highly toxic drug is ingested and there is no chance of aspiration- use when pt is unconscious and intubated
Not used:-Initial resuscitation incomplete
-Risk of aspiration
-Altered level of consciousness
-Expected clinical course –
imminent seizures or coma
-Agent not bound
-Metals, Alcohols, Corrosives
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9
Q

What is enhanced elimination

A

Whole bowel irrigation→ large volume of polyethylene glycol (golytely- prep c)→ for sustained release tablets, used with charcoal→ start when pt is moving to ward

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10
Q

What is the antidote for paracetamol and how does it work

A

N-acetylcysteine
-paracetamol can be excreted as a harmless metabolite bound to a cysteine conjugate, but if you change the metabolic pathway it can become a toxic metabolite (NAPQ)→will immediately cause hepatocellular necrosis (irreversible) → if you give N-acetylcysteine (NAC) it will get metabolised to glutathione and increase supplies of glutathione in the liver→ glutathione binds to the toxic metabolite to make it harmless/makes it take the non-toxic metabolic pathway→ when given glutathione within 15 hours can reverse/inhibit activity of toxic metabolite

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11
Q

What is the antidote for opioid and how does it work

A

Naloxone

  • will bind irreversibly to the mu opioid receptors and boot the opioid off
  • given IV bolus 100microg
  • Repeat every 30s until adequate airway, breathing and GCS 13-14
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12
Q

What is the antidote for tricyclics and how does it work

A

Tricyclics cause acidosis-> give bicarb to reverse the metabolic acidosis and ptortect the heart, then intubate and ventilate

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13
Q

What is the antidote for organophosphates and how does it work

A

atropine as an antidote (IV 1.2mg, doubling dose every 2-3mins until drying of respiratory secretions (listen for crackles)- give amost 50/100 doses of atropine till lungs sound clear), also give Pralidoxime

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14
Q

What is the antidote for benzos and how does it work

A

Flumazenil
IV bolus 20microg/kg
-Limited role – paeds ingestion or iatrogenic→ rarely used due to inefficacy and half life being so short
-can cause precipitate seizures

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15
Q

Why is there caution with naloxone and how do you overcome it

A

-can cause precipitate withdrawls–> Re-sedation due to short half-life of naloxone (potential of pt become unconscious again due to short action of naloxone→ give IM dose and IV dose)

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16
Q

T or F- all patients with deliberate self-poisoning should undergo psychosocial assessment before discharge

A

TRUE

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17
Q

What is the toxidrome for opioid overdose

A

Classic triad

  • CNS depression
  • Respiratory depression
  • Miosis (pinpoint pupils
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18
Q

What is the toxidrome for benzo overdose

A

-CNS depression -> loss of
airway + respiratory
depression (require high dosage)→ one of the most harmless overdose

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19
Q

What is the toxidrome for organophosphate poisoning

A

-organophosphates inhibit ACE–> cause increase in acetylcholine which acts on nicotinic and muscarinic receptors
-Muscarinic – DUMBBELS
→Diarrhoea, urination, miosis, bronchorrhoea, bronchospasm, emesis,
lacrimation, salivation
Nicotinic→ Weakness, fasciculation, respiratory muscle paralysis, bradycardia, hypotension
CNS→ Agitation, confusion, coma, seizures

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20
Q

What is the tx for organophosphate poisoning

A

resuscitation and decontamination to occur in parallel→ use atropine and pralidoxime

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21
Q

What is paraquat

A

non selective herbicide that is fatal and rapidly absorbed→ causes production of oxygen free radicals and multi-organ failure→ only hope of survival is immediate decontamination before absorption (clay or charcoal

22
Q

What is a nomogram

A

allows you to see the level of drug in the system an determine whether the levels are toxic

23
Q

What is the toxidrome for paracetamol overdose

A

there is not one

24
Q

What is the toxidrome for TCA overdose

A

-Cardiac, coma/convulsions, cholingeric

25
Q

What is the pathogenesis of DKA

A

DKA is not enough insulin and too much glucose in the blood stream (Not being utilised by cells) so the body will turn to burning fat and muscle for energy→ will cause the release and metabolism of free fatty acids from cells→ cause release of ketones (acid)→ lead to metabolic acidosis

26
Q

What symptoms do patients in DKA present with

A

Hyperglycemia (BSL > 14mmol/L), Metabolic acidosis (pH <7.35, HCO3 <15),polyuria (polyuria (due to large excretion of glucose (and glucose having a strong osmotic effect and drawing water into the nephrons), polydipsia, nausea, vomiting, abdo pain, polyphagia, hypovolemia, tissue hypoperfusion and lactic acidosis

27
Q

What are the complicated of DKA

A

potential shock due to hypovolemia and altered level of consciousness due to cerebral oedema-> can lead to coma and death

28
Q

What is the management for DKA

A
  • volume replacement (to prevent shock and increase BP)→ use isotonic fluids (hypotonic can cause cerebral oedema), if shocked use IV fluid bolus 10ml/kg
  • insulin (to correct the acidosis by moving glucose into the cell→ give IV actrapid 0.1 units/kg/hr)→ sllow decrease in BSL to 6-10mmol/L, once BSL is below 14 add IV dextrose 100ml/hr and check BSL hourly→ when the acidosis is corrected change to sub-cut insulin
  • potassium replacement (potassium is lost in the urine and also by being pushed into cells)→ give K infusion prior to starting insulin
  • treat precipitants → infection (early antibiotics and control source), GIT, MI
29
Q

Who is at risk for DKA

A

-Infection, Undiagnosed diabetes, Treatment error, GIT cause – pancreatitis, GIT bleed, Other – alcohol, myocardial infarction

30
Q

What is the definition of hypoglycaemia

A

normal BSL is below 4mmol/L in hypoglycaemics

31
Q

What are the symptoms of hypoglycaemia

A

CNS (altered level of consciousness→ agitated, drowsy, coma, seizures, confused) and Autonomic (anxiety, sweating, palpitations, hunger, nausea)
–> if prolonged and severe can cause brain damage or death

32
Q

What are the causes of hypoglycaemia

A

diabetes (tx error, unusual exercise, missed /delayed/ inadequate meal), alcohol, drugs (insulin or oral hypoglycemics, B blockers), infection, endocrine (adrenal crisis, hypothyroidism)

33
Q

What is the management of hypoglycaemia

A

supportive care, correct glucose (IV or oral if alert) and give glucagon (IM if glucose PO or IV unavailable)

34
Q

What is a thyroid storm

A

extreme levels of thyroid hormone in blood

35
Q

What are the causes of a thyroid storm

A
  • Hyperthyroidism→ either undiagnosed or undertreated
  • Drugs→ Withdrawal of anti-thyroid drugs, Thyroxine toxicity or overdose, Iodine
  • Infection
  • Surgery
  • Trauma
36
Q

What are the symptoms of a thyroid storm

A

fever, altered mental state, cardiac failure, symptoms and signs of hyperthyroidism

37
Q

What is the management required for a thyroid storm

A

-supportive
-specific
→Block peripheral effects of thyroid hormone: IV beta-blocker – titrated IV metoprolol 1mg/min to 10mg
→Inhibit thyroid hormone synthesis: PO/NG propylthiouracil 1200mg
→Inhibit thyroid hormone release: PO Lugol’s iodide 10 drops > 1hr after propylthiouracil
-Decrease peripheral conversion of T4 to T3: IV hydrocortisone 200mg
-Treat precipitant

38
Q

What is an adrenal crisis

A

adrenal insufficiency

39
Q

What are the primary and secondary causes of an adrenal crisis

A 
Primary – adrenal disease
-Addison’s disease
-Autoimmune
-Haemorrhage
-Infection
-Malignancy
Secondary
-Pituitary
-Hypothalamic
-Abrupt steroid withdrawal
-Sepsis 
-Trauma
-Severe illness
40
Q

What are the symptoms of an adrenal crisis

A 
-Hypotension – unresponsive to
fluids
-Hyponatremia
-Hyperkalemia
-Hypoglycemia
-Normal anion gap metabolic
acidosis
41
Q

What is the management required for an adrenal crisis

A
  • Supportive
  • Replace steroids
  • IV dexamethasone or IV hydrocortisone
  • Treat precipitant
42
Q

What is the MOA of actrapid insulin

A

Acts on insulin receptor. A transmembrane tyrosine kinase, producing a variety of effects:

  • Liver- Increased- GLC uptake into cells, decreased protein catabolism, decreased gluconeogenesis, increased glycogen production
  • Skeletal muscle -Stimulates glycogen sythesis, Glucose uptake into cells
  • Adipose tissue – Facilitates triglyceroide storage, increased glucose uptake, decreased lipolysis
  • -> causes decrease in plasma glucose level and decreased ketone production but can cause HYPOGLYCAEMIA
43
Q

Paracetamol toxicity is caused by inadequate supplies of which substrate?

A

glutathione

44
Q

How does NAC work?

A

NAC replaces stores of glutathione

45
Q 
A young man is brought in by ambulance, GCS 6, respiratory rate 8, pinpoint pupils.What class of drug is likely to be the cause?
-what is the antidote
A

Opiates

-naloxone

46
Q

What is the main potential problem in using naloxone to treat recreational opiate overdose?

A

It has a very short half life compared to the opiates that it is used to treat
-give IM initially and then IV

47
Q

A 65 year old farmer presents with bradycardia, salivation, meiosis and respiratory depression. What is the likely agent in this overdose? What treatment is required

A

Organophosphates

-atropine

48
Q

A young woman has been found unconscious with an empty bottle of tricyclic antidepressant tablets. What is an antidote for the cardiac effects of TCA’s?

A

Bicarbonate

49
Q

A patient has taken an overdose. In which circumstances would you consider using gastric lavage?

A

Life threatening drug with no antidote

50
Q

In which overdose would you give activated charcoal routinely?

A

paraquat

51
Q

A 12 year old child presents with vomiting and dehydration. His breath smells ketotic and he has a blood glucose of 24 mmol/l. What is the likely diagnosis?
-what tx is required

A

DKA

-insulin infusion

52
Q

During this DKA how long should the insulin infusion be continued for?

A

Until the acidosis has resolved->

EM (11 decks)

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