ENDOCRINE DRUGS

Question 1

METFORMIN

Answer 1

I: TD2M
MOA: Reduces hepatic glucose output (preventing glugogenesis and glycogenolysis) and involves the activation of adenosine monophosphate activated protein kinase (AMP kinase). DOES NOT CAUSE HYPOGLYCEAMIA
SE: GI upset (nausea, vomiting, taste disturbance, anorexia, diarrhoea), increased lactic acid production -> lactic acidosis (muscle cramps).
CI: AKI, severe tissue hypoxia (resp failure, sepsis), acute alchol intoxication (risk of hypoglycaemia due to )
C: renal impairment, hepatic impairment (low dose of metformin as it can accumulate), chronic alcohol abuse
KI: withold before and after 48 after injections of IV contrast media (CT scans, coronary angiography)- increased risk of renal impairment. Prednisolone, thiazide, loop reduce efficacy of metformin by increasing blood glucose. ACEi, NSAIDS, duiretics use in caution in renal impairments
M:
PC: Lifestyle measures, urgent medical advice if they develop chest pain, fever, SOB. investigate for lactic acid - stop metformin if they have lactic acidosis. Inform doctor they take metformin before having x-ray operation.
M: HbA1c every 3 months. <48 mmol normal, add treatment above >58mmol, new target <53
- Annual renal function
- 2x renal function tests for increased renal impairment

Question 2

INSULIN

Answer 2

I: T1DM, uncontrolled T2DM, IV for diabetic emergencies (DKA, HSS Hyperosmolar syndrome), perioperative glycaemic control, alongside glucose to treat hyperkalaemia
MOA: Diabetes - functions similarly to endogenous insulin (increases glucose uptake from the circulation into the tissues including skeletal muscle and fat and increases use of glucose as an energy source)
Hyperkalaemia- drives K+ into cells, reducing serum K+ concertrations
Types of insulin: rapid acting (immediate onset, short duration), Intermediate acting (intermediate onset and duration), long acting.
SE: Hypoglyceamia - lead to coma and death, fat overgrowth over injection site (lipohypertrophy), weight gain
C: renal impairment (incident clearance reduced - risk of hypoglyceamia) low dose
KI: other hypoglycaemic drugs (sulfonyurea) , need more insulin if pt on systemic corticosteroids
PC: lifestyle measures, risk of hypoglyceamia (take something surgary - glucose tablets, lucozade)
M: Finger prick glucose, annual Hb1ac, insulin IV , hyperkalaemia: measure K+ every 4 hours

Question 3

THYROXINE- levothyroxine (LT4), liothyronine

Answer 3

I: primary hypothyroidism, hypothyroidism secondary to hypopituitarism
MOA: Converts T4–> T3- regulates metabolism and growth- deficiency leads to sx. Levothyroxine is a synthetic T4. Liothyronine (T3)-short half life and quicker onset then LT4.
SE: sx of hyperthyroidism;
cardiac (arryhtmias, palpitation, angina)
neuro (tremor, restless, insomnia)
GI (diarrhoea, vomiting and weightloss)
C: caution; CAD- lower dose - risk of cardiac ischaemia
hypopituitarism- initiate corticosteroid before LT4 tx to avoid Addisonian crisis.
I: ↓ GI absorption with antacids, Ca and Fe salts- 4hr gap. High doses when taking with CYP inducers (phenytoin, carbamezine). Increase Insulin and other hypoglycaemic requirement due to metabolism. Enhances warfarin effects.
PC: Symptoms safetynetting - too high a dose. if they take Ca or Fe supplements, leave a 4 hr gap
M: TFTs (TSH, T4,T3) every 3 months after starting treatment/ dose change. Once stable, Annual review of TFTs