Endocrinology and Diabetes Flashcards
Give one drug which can cause hyperthyroidism other than levothyroxine
Amiodarone
A patient with graves has a thyroidectomy, why may they still develop thyroid eye disease?
Autoantibodies still present, thyroid eye disease is due to autoantibodies rather than thyroid hormone
How is thyroid eye disease treated? (vaguely)
Steroids
Suggest 2 investigations to find the cause of hyperthyroidism?
- thyroid auto- antibodies
- technetium uptake scan
- USS
Describe how the appearance of a technetium uptake scan would differ between graves, a single toxic nodule and a multi nodular goitre
Graves= Same absorbtion distribution as normal thyroid but darker as more uptake
Single toxic nodule= one dense area, not thyroid shaped
Multi-nodular goitre= many dense areas, with outline of thyroid seen
When should a patient on carbimazole stop taking their medication and why?
If they get an infection, because it can cause bone marrow surpression and decrease WBCC
Describe Na+ and osmolality changes to blood and urine in SIADH?
High Na+ conc in urine (as retaining water) and high urine osmolality (>100)
Low Na+ conc in blood (<135 mmol/l) with low serum osmolality (<280)
Other than SIADH, what else could cause hyponatuaemia with high urine Na+?
Adrenal insufficiency- less mineralcoritcoid production= less reuptake of Na+ in collecting duct
What is pituitary apoplexy?
Bleeding into or impaired blood supply to the pituitary gland
How does pituitary apoplexy present?
Headache with cavernous sinus signs (4th, 6th, 3rd nerve palsys), also hypopituitaryism
How is pituitary apoplexy treated? (Vaguely)
If optic chiasm involvement (bitemporal hemianopia) then usually needs surgery.
If not just need to medically replace hormones and wait for recovery.
Which causes a higher prolactin, prolactinoma or tumour stopping dopamine effect by compression stalk?
Prolactinoma (v high prolactin, treat with dopamine agonists)
Pituitary stalk tumour (lower prolactin, treat with surgical removal)
How can diabetes be diagnosed? (3 ways)
- random blood glucose test over 11.1 with symptoms
- fasting glucose >7, if theyre asymptomatic you need two >7
- Hba1c> 6.5%
Give 5 symptoms of diabetes mellitus?
- tiredness
- frequent UTIs
- Weightloss (T1 only)
- Polyurea
- Polydipsia
Describe the presentation of decompensated ketoacidosis?
- onset over 24 hrs
- PMH T1 diabetes, recent precipitating factor
- polyurea and poly dipsia
- N+ V
- Altered mental state
- weakness
- lethargy
- hyperventilation
- pear drop smell on breath
- dehydrated and volume deplete on examination
What may precipitate DKA? (4)
- Infection.
- Discontinuation of insulin (unintentional or deliberate).
- Inadequate insulin.
- Cardiovascular disease - eg, stroke or myocardial infarction.
- Drug treatments - eg, steroids, thiazides or sodium-glucose co-transporter 2 (SGLT2) inhibitors.
How should DKA be investigated? (group into diagnosis, finding cause and assessment of severity/ complications)
- To diagnose: Blood glucose, blood ketones, urine dip for ketones, ABG showing low bicarbonate (metabolic acidosis)
- To asses severity: U&E- for dehydration and hyperkalaemia, also urea and creatine raised if AKI, 12 lead ECG, CT/ MRI of head, anion gap raised
- to find cause: blood cultures, urine dip, CXR to look for infection
Describe and explain serum osmolality, K+ and Na+ changes in DKA?
- K+ usually high due to acidosis meaning H+ going into cells and K+ coming out, however may be low due to osmotic diuresis
- Osmolality is low due to glucose and ketones causing osmotic diuresis, which is also why Na+ conc seems high or normal. Can be low as body compensates by letting sodium go