Meeran Chempath Flashcards
When does pseudohyponatraemia occur and why?
Occurs in hyperlipidaemia or hyperproteinaemia as they occupy a high proportion of the total serum volume. This dilution then causes an apparent hyponatraemia.
What electrolyte imbalance does Addison’s disease show?
Hyponatramemia and hyperkalaemia due to impaired aldosterone synthesis (though ACTH will be high)
You can also get hypoglycaemia due to reduced cortisol production
How do you differentiate CKD vs heart failure in hypervolaemic hyponatraemia
urine osmolality > 20mmol/l = suggestive of renal cause
What can cause a redistributive hypokalaemia (i.e. potassium shifts from extracellular space into intracellular space)?
Insulin overdose
Metabolic acidosis
Adrenaline
Re-feeding syndrome
How does renal failure cause hyperkalaemia?
It is secondary to reduced distal renal delivery of sodium ions - this means there is reduced potassium exchange at Na/K ATPase pump in the collecting duct. This causes an accumulation of K in the blood.
*Renal failure will also present with deranged urea and creatinine levels
What is Bartter syndrome?
autosomal recessive condition causing a defect in the ascending limb of the loop of Henle –> hypokalaemia, alkalosis and hypotension. It is associated with NKCC2 or ROMK genes
It can calso cause increased calcioum loss via the urine (hypercalcuria) and the kidneys (nephrocalcinosis)
What is renal tubular acidosis?
There is a defect in the H+ secretion into the renal tubules. This then means there is increase potassium secretion into the renal tubules to balance the sodium reabsorped, producing a picture of hypokalaemia with acidosis.
4 different types according to location of defect
Type 1 = distal tubule
Type 2 = proximal tubule
Type 3 = distal and proximal
Type 4 (hyperkalaemia with acidosis) = reduced aldosterone production secondary to defect in adrenal glands
LFTs of gallstones
raised GGT and ALP (obstructive picture), that are greater than raises in AST and ALT
LFT for Gilbert’s syndrome
normal LFTs apart from raised unconjugated bilirubin.
Conjugated bilirubin is normal
LFTs for non-alcohol fatty liver disease (NAFLD)
raised AST and ALT (AST:ALT ratio <1), and increased GGT
Bilirubin and albumin normal
LFTs for alcohol abuse
in absence of underlying liver disease, they can present with only an isolated rise in GGT.
Sometimes mild elevations in AST and ALT to suggest mild hepatic damage
*Isolated rises in GGT can also be due to consumption of enzyme-inducing drugs like phenytoin, carbamazepine and phenobarbitone
LFTs for alcohol liver disease
raised GGT, AST and ALT (with AST:ALT ratio >2)
LFTs of hepatocellular carcinoma
raised AFP
There may be deranged LFTs but that would be of underlying pathology
What does a short synACTHen test do?
Measure plasma cortisol at 0 minutes
Give 250ug of synthetic ACTH at 30 minutes
Measure plasma cortisol at 60 minutes (if <550nmol/L, then there is a defect in cortisol production
What does a long synACTHen test do?
It distinguishes between a primary and secondary adrenal insufficiency issue.
A 1mg dose of synthetic ACTH is administered - after 24hrs if the cortisol level is <900nmol/L then this means there is a primary defect
How are prolactinomas classified?
Microprolactinoma: <10mm
Macroprolactinoma: >10mm
What clinical consequences of prolactinomas are there?
- Hormonal effect from increase in prolactin production (e.g amenorrhoea, galactorrhoea and gynaecomastia in males)
- Mass effect of tumour (compression of pituitary cells which affects other hormone production like TSH, GH and ACTH)
What is the diagnostic test for acromegaly?
Oral glucose tolerance test (OGTT) of 75mg glucose - if growth hormone is not suppressed to below 2mU/L, then acromegaly is diagnosed
What is Kallman’s syndrome?
Hypogonadotropic hypogonadism –> leads to reduced LH and FSH production.
Anosmia is also an associated feature
What is De Quervain’s thyroiditis?
Post-virus induced thyroiditis which initially presents as hyperthyroidism because thyroxine from colloid cells enters the circulation. Then hypothyroidism ensures for a period as thyroxine stores are depleted
Clinical blood test for Paget’s?
All calcium blood studies will be normal apart from a raised ALP
*Thought to be due to paramyxovirus which causes impaired bone remodelling - new bone is larger but weaker and prone to fracture
What differentiates secondary hyperparathyroidism from osteolamacia?
Secondary hyperparathyroidism is the release of PTH as a consequence of hypocalcaemia that arises from non-parathyroid pathology (i.e. chronic renal failure).
Osteomalacia is due to insufficient bone mineralisation 2º to vitamin D or phosphate deficiency. Low vitamin D causes hypocalcaemia due to reduced 1,25-dihydroxyvitamin D production so there is reduced calcium resorption from the gut - this then causes an increase in PTH production - this causes increased bone resorption so ALP rises
What is familial benign hypercalcaemia?
Genetic condition that results in a mutation in the calcium receptor on parathyroid glands and kidneys. This causes an underestimation of calcium which leads to increased PTH production, and therefore a hypercalcaemic picture. The receptor failure in kidneys reduces calcium excretion, so there is also a hypocalcuric state.
What is pseudohypoparathyroidism?
Genetic condition where there is resistance to PTH. Therefore, patients have high PTH and phosphate, but low calcium.
Where is amylase produced?
Parotid glands and pancreas
*In inflammation of the parotid glands (i.e. mumps), high levels of amylase get released into the blood stream. It can also be used to diagnose pancreatitis
How does ferritin distinguish between different causes of microcytic anaemia?
*Ferritin is responsable for the storage of iron. It is also an acute phase protein so will raise secondary to inflammation
Iron deficiency anaemia (i.e. GI bleed) - reduced ferritin, reduced serum iron, raised TIBC
Anaemia of chronic disease - raised ferritin
Thalassaemia - normal ferritin
