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ACEM Part 1 > Pharmacology - Endocrine & Toxicology > Flashcards

Pharmacology - Endocrine & Toxicology Flashcards

1
Q

What is the mechanism of action and side effects of Carbimazole

A

mechanism:
prevents synthesis of T3/T4 by inhibiting thyroid peroxidase = limits organification of iodine

side effects:
GIT disturbance
maculopapular rash
pruritus
transaminitis
bone marrow suppression

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2
Q

How does Carbimazole differ from Propylthiouracil

A

Carbimazole is a prodrug and is converted to the more potent Methimazole

Propylthiouracil also inhibits peripheral conversion of T4 to T3 and crosses the placenta less (better in pregnancy)

Both inhibit TPO

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3
Q

What is the mechanism of action and side effects of steroids

A

mechanism:
works via widely distributed glucocorticoid receptors
enters cell to have its effect by binding to intracellular receptor, causing increased transcription of target genes

side effects: 
short term (\<2 weeks) = insomnia, behaviour changes, peptic ulcer, pancreatitis, hyperglycaemia 
long term (\>2 weeks) = cushing syndrome, diabetes, osteoporosis, adrenal suppression, poor wound healing
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4
Q

How are corticosteroid classified

A
  • length of action: long acting (dexamethasone and bethamethasone), short acting (hydrocortisone, prednisolone)
  • anti-inflammatory activity: dexamethasone > fludrocortisone > prednisolone > hydrocortisone
  • mineralocorticoid activity: fludrocortisone > hydrocortisone > prednisolone
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5
Q

What are the effects of hydrocortisone

A
  • breakdown proteins
  • increase arterial contractile sensitivity to NA
  • increase blood glucose levels (increased gluconeogenesis and anti-insulin action)
  • suppress immune system
  • vasoconstriction when applied directly to skin
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6
Q

What is the usual dose of Dexamethasone in the treatment of croup

A

-PO 0.15-0.6mg/kg single does

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7
Q

What are routes of Dexamethasone and how does its anti-inflammatory property compare to Hydrocortisone

A
  • route: PO, IV, IM, topical
  • Dexamethasone is 30 times more potent and is longer lasting than Hydrocortisone and contains no salt retention
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8
Q

What are the uses of Dexamethasone

A

diagnosis (dexamethasone suppression test to diagnose cushing syndrome)
anti-inflammatory
croup

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9
Q

Describe the anti-inflammatory and immunosuppressive effects of glucocorticoids

A

Reduces concentration, distribution and function of peripheral leucocytes
Suppression of inflammatory mediators (cytokines, chemokines)
Inhibits function of macrophages and APC
Decreases histamine release by mast cells

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10
Q

Outline the drugs used to treat hyperglycaemia in diabetes

A
  • insulin (novorapid): mimics endogenous insulin
  • sulphonylurea (gliclazide): binds to sulphonylurea receptor and causes release of pre-formed insulin
  • biguanides (metformin): mechanism unclear but causes decreased hepatic glucose production
  • thiazolidinediones (pioglitgazone): decreases insulin resistance
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11
Q

What is the mechanism of action and different formulations of insulin

A

-mechanism: activates insulin receptor (transmembrane receptor tyrosine kinase)
promotes uptake of glucose from blood into tissues (fat, liver, skeletal muscle) by translocating GLUT
promotes glycogen synthesis
increases protein synthesis
-formulations: rapid/short acting (novorapid) = clear solution, neutral pH, rapid onset, short DOA
intermediate acting (isophane) = turbid solution, neutral pH
long acting (lantus) = clear solution, soluble, slow onset, prolonged action

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12
Q

What are the actions of insulin on the liver

A
  • anabolic = increased glycogen synthesis, increased lipogenesis
  • anti-catabolic = reduced glycogenolysis and gluconeogenesis
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13
Q

What methods are used to optimise blood sugar control when giving insulin

A
  • titration of dose to BSL
  • combinations of insulins with different durations of action aimed to replace basal and meal insulin requirement
  • continuous SC insulin infusion devices
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14
Q

What type of insulin is used for IV infusions and why

A

short acting insulin because it immediately dissociates on dilution and is more precisely delivered

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15
Q

Describe the principles of an insulin pump

A
  • delivers individual basal and bolus insulin replacement doses based on blood glucose monitoring
  • consists of insulin reservoir, program chip, keypad and display screen attached to subcutaneous infusion set
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16
Q

What are complications of insulin therapy

A

hypoglycaemia
insulin allergy
lipodystrophy at injection site
immune insulin resistance

17
Q

What is a use of insulin in the emergency department other than glycaemic control

A

hyperkalaemia
calcium channel blocker overdose

18
Q

What is the pharmacologic effect of glucagon and what are its clinical uses and adverse reactions

A

-metabolic: catabolism of glycogen and increased gluconeogenesis to increase glucose, increases insulin release
use = severe hypoglycaemia

-cardiac: positive inotropic and chronotropic effects (does not require functioning beta adrenoreceptors)
use = beta-blocker overdose

-other: relaxation of intestinal smooth muscle
use = relax intestine in food bolus

-adverse reactions: nausea, vomiting, hyperglycaemia

19
Q

Describe the mechanism of action, pharmacokinetics and adverse effects of Metformin

A

mechanism:
unclear, decreases hepatic glucose production, may stimulate glycolysis
does not depend on functioning beta cells

pharmacokinetics:
well absorbed, t1/2 1.5-3 hours, not bound to proteins, not metabolised
excreted by kidneys as active compound

side effects:
lactic acidosis, GIT disturbance, vitamin B12 deficiency

20
Q

What is the mechanism of action, pharmacokinetics and side effects of Glicizide (sulphonylurea)

A

-mechanism: binds to sulphonylurea receptor and causes the release of pre-formed insulin
work by blocking the K+ channel, leading to depolarisation and opening of Ca+2 channels, causing insulin release
requires functioning beta cells to work
-pharmacokinetics: hepatically metabolised, renally excreted, t1/2 12 hours
-side effects: hypoglycaemia (more common than with metformin), alcohol intolerance, jaundice, GIT symptoms

21
Q

What is the mechanism of action, pharmacokinetics and side effects of Octreotide

A

-mechanism:
somatostatin analog, reduces splanchnic and portal blood flow by poorly understood mechanism
inhibits secretion of: insulin, glucagon, gastrin, GH, TSH
-pharmacokinetics: t1/2 80 minutes, metabolised by liver, 20% excreted unchanged by kidney
-routes: IV, IM, SC
-adverse effects: anaphylaxis, local irritation, GIT symptoms, bradycardia, flatulence, steatorrhoea
-uses: control GI bleed from esophageal varices, sulphonylurea overdose
-administration in acute bleed: IV bolus (50mcg) and infusion due to short half life (25-50mcg/hour)
-other drugs used in esophageal bleed = terlipressin

22
Q

What is the difference between Octreotide and Somatostatin

A

Octreotide is a somatostatin analogue that has a longer half life

23
Q

Describe the metabolism of methanol

A
  • methanol is converted by alcohol dehydrogenase to formaldehyde
  • formaldehyde is then converted by aldehyde dehydrogenase to formic acid, which is highly toxic
  • may cause snow storm vision and metabolic acidosis
  • treatment: alcohol competes with methanol for alcohol dehydrogenase

fomepizole acts as an alcohol dehydrogenase antagonist

dialysis

24
Q

What are decontamination methods

A
  • skin: remove clothes, wash contaminated skin
  • GIT: emesis, gastric lavage, activated charcoal, whole bowel irrigation
25
Q

How does activated charcoal work

A
  • has a large surface area and absorbs many drugs and poisons
  • does not bind to lithium or potassium and binds alcohol and cyanide poorly
  • not useful in corrosive mineral acids or alkali
  • repeated doses help elimination of certain drugs = carbamazepine, dapsone, theophylline
26
Q

What is the mechanism of NAC in paracetamol overdose

A

-paracetamol may undergo 3 methods of metabolism

glucuronidation to non-toxic compound

sulphation to non-toxic compound

hydroxylation to toxic napqi, which is then converted to non-toxic compound by glutathione

  • nac has several effects: increases glutathione activity direct binding to napqi, reduction of napqi back to paracetamol
  • adverse effects of nac: nausea, vomiting, flushing, rash, angio-edema, anaphylaxis
27
Q

What is the mechanism of action of naloxone

A
  • naloxone is a pure opioid antagonist with a high affinity for the mu receptor and low affinity for kappa and delta receptor
  • onset of action 1-3 minutes, duration of action 1-2 hours
  • complications: opioid withdrawal, re-sedation avoid with smaller/titrated doses and infusions
28
Q

What is the mechanism of action of flumazenil

A
  • high affinity competitive antagonist for the benzodiazepine binding site on the GABAa receptor
  • blocks GABA induced increase in Cl- permeability
  • reverse sedative effects of benzodiazepines, but respiratory depression is less predictable
  • indications: avoid intubation in benzodiazepine overdose and reverse effect post procedure and diagnostic role
  • complications: precipitate seizures (especially if patient taking bzd to control epilepsy), precipitate withdrawal symptoms
29
Q

What is antivenom

A
  • immunoglobulin or antibody produced by another animal in response to venom
  • used iv or im to neutralise venom
  • examples used in australia: snake (polyvalent or monovalent), stonefish, redback, box jellyfish, funnelweb spider
  • side effect: allergy, anaphylaxis, serum sickness
  • what animals are used: horse for snake, rabbit for funnel web, sheep for box jellyfish
30
Q

What are the therapeutic uses of penicillamine

A
  • penicillamine is a metal binding agent
  • wilsons disease, copper poisoning, severe rheumatoid arthritis
  • side effects: nausea, vomiting, hypersensitivity, pancytopenia, pemphigus

ACEM Part 1 (38 decks)

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