Endocrine 2.28-36 Flashcards
Which hormones are released by the hypothalamus to inhibit TSH production? i.e. opposite of TRH?
Somatostatin, dopamine.
What is congenital adrenal hyperplasia?
Umbrella term but vast majority is 21-hydroxylase deficiency. Most frequent cause of virilisation in 46XX females; get clitoromegaly and labial fusion; males appear normal because most sex hormones come from testes. Occurs because enzyme is needed for aldosterone/cortisol pathways; instead drive androgen production. If have complete (salt-wasting) form then have life threatening minerol/gluco deficiency
Cretinism?
Mental developmental delay and growth restriction in children for iodine deficient regions who are not treated in early childhood; thyroid very efficiently extracts iodide from blood. Oversupply of iodine associated with AI thyroid disease.
Things that affect T4 to T3 conversion?
Systemic illness, acute trauma, fasting, drugs e.g. amiodarone, proplthiouracil, propranolol, glucocorticoids.
Testosterone production in males?
95% from testicular secretion; rest is from direct adrenal secretion or peripheral conversion of androstenedione to testosterone.
Marijuana and testosterone?
Causes reduced GnRH secretion, leading to decreased testosterone. Anabolic steroids can have the same effect as endogenous production is suppressed
Biochemical features of ectopic ACTH production e.g. SCLC?
Hypernatraemia, hypokalaemia, metabolic alkalosis, hyperglycaemia, lung malignancy. May not see typical features of Cushing’s.
Confirming Cushing’s syndrome?
Take history inc. exogenous steroids!
- Overnight dex. suppression test shows no suppression can also do 48 hour low dose dex suppression. Measure at 9am after 1mg at midnight. <50 = Cushing’s unlikely
- Urinary free cortisol (24 hours); can have false negatives.
Localising Cushing’s syndrome?
- Do overnight dex suppression and 24 hr UFC to confirm diagnosis.
- Plasma ACTH; if very high (>300) likely to be ectopic; undetectable may be adrenal tumour/hyperplasia
- If undetectable, CT adrenals; if no mass do adrenal vein sampling.
- If detectable, do high dose dex suppression; if cortisol suppressed (>50%) may be pituitary. Alternatively, do CRH test; will cause rise in pituitary disease, not in ectopic.
- Then either do high contrast CT C/A/P to find tumour, or MRI if suspect pituitary.
- K+ likely to be low in ectopic.
Criteria for SIADH?
Need hyponatraemia, urine osmolarity >100 and urine Na >20. When plasma is dilute, urine should be maximally dilute therefore low osm. Need absence of cofounders!
Potential cofounders in SIADH diagnosis?
Non-osmotic AVP release (pain, surgery, nausea),
Why is hyponatraemia with surgery a real concern?
Release ADH with any surgery; usually given fluids; if given to excess can die. Get dilutional hyponatraemia and cerebral oedema. If going to fluid restrict, must stop oral and IV!
Over-rapid correction of hyponatraemia?
May have patient with chronically low Na+; falls further and present, given hypertonic saline as acutely unwell (correctly). Then fluid restricted to prevent ascites as had ALD. Given further hypertonic saline inappropriately. Get osmotic demyelination syndrome! Key is only give enough to resolve acute problem and no more than 10mmol/L in 24 hrs.
What is osmotic demyelination syndrome?
Correct hyponatraemia too quickly; get demyelination and necrosis. Can get quadriplegia, opthalmoplegia, pseudubulbar palsy, coma. Also called central pontine myelinolysis.
Management algorithm in hyponatraemia?
Rule out hyperglycaemia/lipids/protein first (pseudohyponatraemia). Then, are they acutely unwell (coma, seizures); if yes treat with hypertonic saline (slowly); if not check urine osmolality! Begins on diagnostic pathway as treatment is cause-specific.
Diagnostic algorithm in hyponatraemia?
Exclude pseudo, check urine osmolality, if low then primary polydipsia, inappropriate VT, low solute intake. If high (>100), check urine Na. If <30 then are retaining it appropriately (HF/LF/RF/GI loss); if >30 then on diuretics/ACE? If not then may be SIADH, hypoadrenalism, AVP like drugs.
Causes of hypernatraemia?
Too little water or too much salt. Dehydration (elderly, terminal illness, water loss > intake), or excess Na+ in IV therapy (i.e. too much normal saline). Think are you “filling a hole” or “keeping a hole full” [maintenance]. Replacement must match requirements!
Cardiac effects of hyperkalaemia and hypokalaemia?
Tenting of T waves, broad QRS, sine wave appearance pre-arrest. Hypokalaemia; gives flattened T waves and broad QRS.
K+ distribution?
96% IC so measuring not representative. Higher in renal failure. Comes in via Na/K exchanger, leaves via K+ channel. Flux affected by pH, hormones etc. If pH falls, too many hydrogen ions, try to get rid of them IC so K+ comes out to replace charge and get hyperkalaemia in ECF. Can get it in rhabdomyolysis (trauma, extreme exercise).
Where is K+ actually stored?
IC - mostly in muscles, liver and red cells.
Things causing K+ efflux into ECF and therefore hyperkalaemia?
Acidosis, A-adrenergic agonists, strenuous exercise/trauma.
Things causing K+ influx into cells and therefore hypokalaemia?
Alkalosis, B-adrenergic agonists (hence salbutamol used in acute hyperkalaemia), insulin (same reason). These methods are a “sticking plaster” as total body potassium remains the same.
Problem with continuous K+ efflux?
Measuring K+ seems high, but actual body stores low.
Renal K+ handling?
Most reabsorbed in PCT and thick ascending limb; actual control is in DCT.