WK 2-Toxicology and Endocrine Emergencies Flashcards Preview

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Flashcards in WK 2-Toxicology and Endocrine Emergencies Deck (52):
1

What is a toxidrome

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

2

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

-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

3

What is symptomatic supportive care

treating the symptoms

4

What aspects of ABC need to be controlled

Airway: intubatation
-Breathing: Supplemental 02, ventilation
-Circulation: correct low or high BP and hypovolemia

5

Apart from ABC, what else needs to be monitored

-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

6

What is decontamination

Removal of the substance from the body

7

What is an example of decontamination

-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)

8

When is activated charcoal used and not used

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

9

What is enhanced elimination

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

10

What is the antidote for paracetamol and how does it work

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

11

What is the antidote for opioid and how does it work

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

12

What is the antidote for tricyclics and how does it work

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

13

What is the antidote for organophosphates and how does it work

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

14

What is the antidote for benzos and how does it work

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

15

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

-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)

16

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

TRUE

17

What is the toxidrome for opioid overdose

Classic triad
-CNS depression
-Respiratory depression
-Miosis (pinpoint pupils

18

What is the toxidrome for benzo overdose

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

19

What is the toxidrome for organophosphate poisoning

-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

20

What is the tx for organophosphate poisoning

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

21

What is paraquat

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

What is a nomogram

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

23

What is the toxidrome for paracetamol overdose

there is not one

24

What is the toxidrome for TCA overdose

-Cardiac, coma/convulsions, cholingeric

25

What is the pathogenesis of DKA

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

What symptoms do patients in DKA present with

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

What are the complicated of DKA

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

28

What is the management for DKA

-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

Who is at risk for DKA

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

30

What is the definition of hypoglycaemia

normal BSL is below 4mmol/L in hypoglycaemics

31

What are the symptoms of hypoglycaemia

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

What are the causes of hypoglycaemia

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

33

What is the management of hypoglycaemia

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

34

What is a thyroid storm

extreme levels of thyroid hormone in blood

35

What are the causes of a thyroid storm

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

36

What are the symptoms of a thyroid storm

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

37

What is the management required for a thyroid storm

-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

What is an adrenal crisis

adrenal insufficiency

39

What are the primary and secondary causes of an adrenal crisis

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

40

What are the symptoms of an adrenal crisis

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

41

What is the management required for an adrenal crisis

-Supportive
-Replace steroids
-IV dexamethasone or IV hydrocortisone
-Treat precipitant

42

What is the MOA of actrapid insulin

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

Paracetamol toxicity is caused by inadequate supplies of which substrate?

glutathione

44

How does NAC work?

NAC replaces stores of glutathione

45

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

Opiates
-naloxone

46

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

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

47

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

Organophosphates
-atropine

48

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?

Bicarbonate

49

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

Life threatening drug with no antidote

50

In which overdose would you give activated charcoal routinely?

paraquat

51

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

DKA
-insulin infusion

52

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

Until the acidosis has resolved->