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TRANSITION BLOCK > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

Where is ADH released from?

A

POSTERIOR pituitary

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2
Q

What is the function of ADH?

A

Water reabsorption from the renal tubules

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3
Q

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

A

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

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4
Q

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

A

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

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5
Q

How do mineralocorticoid levels affect sodium levels?

A

Sodium balance is controlled by steroids

Too much mineralocorticoid means there will be sodium gain

Too little mineralocorticoid means there will be sodium loss

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6
Q

Which is the main steroid which controls sodium balance?

A

Aldosterone

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7
Q

Sodium is confined to which compartment?

A

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

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8
Q

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

A

Increased sodium loss

Decreased sodium intake

Decreased water excretion e.g SIADH

Increased water intake e.g compulsive drinking

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9
Q

What is Addison’s?

A

Autoimmune destruction of the adrenal cortex (primary adrenal insufficiency)

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10
Q

Why is addison’s associated with hyponatraemia?

A

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

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11
Q

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

A

Anorexia and weight loss

Fatigue

Dizziness

Hypotension

Abdo pain and N&V

Hyperpigmentation of the skin

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12
Q

What biochemistry results is Addison’s associated with?

A

HYPERkalaemia

HYPOnatraemia

HYPOglycaemia

Increased renin to aldosterone ratio

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13
Q

What autoantibodies is Addison’s associated with?

A

Anti-adrenal autoantibodies

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14
Q

What is the management for Addison’s?

A

Hydrocortisone

Fludrocortisone

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15
Q

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

A

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

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16
Q

Why does Central Diabetes Insipidus result in hypernatraemia?

A

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.

17
Q

What are some of the causes of central diabetes insipidus?

A

Familial (DIDMOAD)

Trauma

Tumours

Infiltrative disease e.g sarcoidosis

18
Q

What is the difference between central and nephrogenic diabetes insipidus?

A

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

19
Q

What is the investigation for diabetes inspidus?

A

Water deprivation test

urine will remain dilute due to lack of ADH

20
Q

What is the management of diabetes insipidus?

A

Desmospray/

Desmopressin

21
Q

What is SIADH?

A

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

22
Q

How does SIADH present clinically?

A

Hypotension

Pain

N&V

23
Q

What ECG changes are associated with hyperkalaemia?

A

Peaked T waves

Flattened P waves

Prolonged QRS duration

24
Q

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

A

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)

25
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

26
Q

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

A

HYPOkalaemia

Alkalosis

Aldosterone excess

27
Q

What investigations are done for primary hyperaldosteronism

A

Adrenal CT

Adrenal vein sampling

28
Q

What are the causes of primary hyperaldosteronism?

A

Conn’s syndrome

Adrenal adenomas

Bilateral idiopathic adrenal hyperplasia

29
Q

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

A

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

30
Q

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

A

Measurement of ACTH

31
Q

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

A

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

32
Q

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

A

Antihypertensive drugs such as spironolactone

33
Q

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

A

Potassium salts in intravenous drugs (e.g antibiotics)

34
Q

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

A

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

35
Q

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

A

Pseudohyponatraemia

36
Q

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

A

Primary adrenal insufficiency

due to ACTH

37
Q

When should potassium give to patients with DKA?

A

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.

TRANSITION BLOCK (10 decks)

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