Biochemistry

Question 1

Where is ADH released from?

Answer 1

POSTERIOR pituitary

Question 2

What is the function of ADH?

Answer 2

Water reabsorption from the renal tubules

Question 3

What effect does high ADH have on volume and osmolality of urine?

Answer 3

High ADH causes a small volume of concentrated urine (high osmolality)

Question 4

What effect does low ADH have on volume and osmolality of urine?

Answer 4

Low ADH causes a large volume of dilute urine (low osmolality)

Question 5

How do mineralocorticoid levels affect sodium levels?

Answer 5

Sodium balance is controlled by steroids

Too much mineralocorticoid means there will be sodium gain

Too little mineralocorticoid means there will be sodium loss

Question 6

Which is the main steroid which controls sodium balance?

Answer 6

Aldosterone

Question 7

Sodium is confined to which compartment?

Answer 7

Sodium is confined to the ECF. Sodium loss or gain is solely from and to the ECF

Question 8

What are some of the possible causes/ mechanisms of low sodium?

Answer 8

Increased sodium loss

Decreased sodium intake

Decreased water excretion e.g SIADH

Increased water intake e.g compulsive drinking

Question 9

What is Addison’s?

Answer 9

Autoimmune destruction of the adrenal cortex (primary adrenal insufficiency)

Question 10

Why is addison’s associated with hyponatraemia?

Answer 10

Patients with addison’s have primary adrenal insufficiency which means they can’t make enough steroids so they can’t retain sodium

Question 11

What are some of the signs and symptoms of Addison’s?

Answer 11

Anorexia and weight loss

Fatigue

Dizziness

Hypotension

Abdo pain and N&V

Hyperpigmentation of the skin

Question 12

What biochemistry results is Addison’s associated with?

Answer 12

HYPERkalaemia

HYPOnatraemia

HYPOglycaemia

Increased renin to aldosterone ratio

Question 13

What autoantibodies is Addison’s associated with?

Answer 13

Anti-adrenal autoantibodies

Question 14

What is the management for Addison’s?

Answer 14

Hydrocortisone

Fludrocortisone

Question 15

What are some of the possible causes/ mechanisms of high sodium?

Answer 15

Increased sodium intake (e.g IV meds and malicious causes - very rare)

Decreased sodium loss

Increased water loss (e.g diabetes insidious)

Decreased water intake

Question 16

Why does Central Diabetes Insipidus result in hypernatraemia?

Answer 16

Central DI is a posterior pituitary problem

ADH Is not secreted from the posterior pituitary so there is no ADH to act on the kidneys to cause water to be reabsorbed. Water is therefore lost in the urine so sodium concentration is high reflecting the water deficit.

Question 17

What are some of the causes of central diabetes insipidus?

Answer 17

Familial (DIDMOAD)

Trauma

Tumours

Infiltrative disease e.g sarcoidosis

Question 18

What is the difference between central and nephrogenic diabetes insipidus?

Answer 18

Central DI is a posterior pituitary problem - ADH is not secreted

Nephrogenic DI is an issue with the kidneys being resistant to the action of ADH

Question 19

What is the investigation for diabetes inspidus?

Answer 19

Water deprivation test

urine will remain dilute due to lack of ADH

Question 20

What is the management of diabetes insipidus?

Answer 20

Desmospray/

Desmopressin

Question 21

What is SIADH?

Answer 21

Syndrome of inappropriate ADH secretion. There is water retention which causes hyponatraemia due to the effects of dilution.

Question 22

How does SIADH present clinically?

Answer 22

Hypotension

Pain

N&V

Question 23

What ECG changes are associated with hyperkalaemia?

Answer 23

Peaked T waves

Flattened P waves

Prolonged QRS duration

Question 24

What are the treatment options for hyperkalaemia? How do these work?

Answer 24

Calcium gluconate
(protects the myocardium)

Insulin (act rapid) and dextrose
Salbutamol
(move K+ back into cells)

Calcium resonium - NOT in the acute setting
(Prevents potassium absorption fro the GI tract)

Question 25

What is Conn's syndrome?

Answer 25

Primary hyperaldosteronism

Question 26

What biochemistry results is primary hyperaldosteronism (Conn's) associated with?

Answer 26

HYPOkalaemia Alkalosis Aldosterone excess

Question 27

What investigations are done for primary hyperaldosteronism

Answer 27

Adrenal CT Adrenal vein sampling

Question 28

What are the causes of primary hyperaldosteronism?

Answer 28

Conn's syndrome Adrenal adenomas Bilateral idiopathic adrenal hyperplasia

Question 29

What is used to distinguish between central and nephrogenic diabetes insipidus?

Answer 29

DDAVP (synthetic analogue of AVP(ADH)) is used to distinguish between central and nephrogenic diabetes insipidus

Question 30

What is used to distinguish between primary and secondary adrenal insufficiency?

Answer 30

Measurement of ACTH

Question 31

Rehydration is always instituted early in the management of severe hypercalcaemia. Why is this?

Answer 31

Hypercalcaemia interferes with proximal tubular reabsorption of sodium and so causes loss of sodium and water, leaving patients dehydrated.

Question 32

Once haemolysis and renal failure have been excluded, what is the next most likely cause of hyperkalaemia?

Answer 32

Antihypertensive drugs such as spironolactone

Question 33

What is the most common cause of hyperkalaemia in hospital patients?

Answer 33

Potassium salts in intravenous drugs (e.g antibiotics)

Question 34

Is SIADH usually associated with clinical evidence of water overload, e.g oedema?!

Answer 34

It is often not as the water is distributed across the whole body

Question 35

What should you suspect when sodium appears really really low but the patient seems fine?

Answer 35

Pseudohyponatraemia

Question 36

Is palmar pigmentation a feature of primary or secondary adrenal insufficiency?

Answer 36

Primary adrenal insufficiency | due to ACTH

Question 37

When should potassium give to patients with DKA?

Answer 37

Potassium is usually required for patients with DKA. There is usually potassium depletion and even if levels look normal it is usually given anyway. It would only be if potassium levels were abnormally high that potassium replacement wouldn't be given in DKA.