Biochemistry Flashcards
Normal concentration of sodium in a) the ICF b) the ECF
a) 4mmol/l
b) 140mmlol.l
Which steroids have mineralocorticoid activity?
aldosterone and cortisol
What does the term “mineralocorticoid activity” refer to?
Retain sodium in the kidney in exchange for potassium and/or hydrogen ions
How does the RAAS system work to retain sodium?
Falling blood pressure
Release of renin, which converts angiotensinogen to angiotenin I
AT1 converted to AT2
AT2 exerts effects on the adrenal cortex causing release of aldosterone, and retention of sodium (and hence water) at the kidneys
What is another name for ADH?
Arginine vasopressin
How does ADH release cause urine to be concentrated?
Causes reabsorption of water from the renal collecting tubules
Where is ADH released from?
Posterior pituitary
Main causes of hyponatraemia (2)
Too much water (mainly reduced excretion- SIAD)
Too little sodium (mainly increased gut/skin/kidney loss)
Why is clinical assessment of volume status important in assessing the cause of hyponatraemia?
Clinically dehydrated suggests a deficit of sodium and water as a consequence; unremarkable clinical volume status suggests too much water as a cause for the hyponatraemia
What does oedema in the presence of hyponatraemia suggest?
Suggests hyponatraemia as a consequence of fluid overload; heart failure and hypoalbuminaemia cause fluid retention
Patient presentation: tired dizzy pigmented skin weight loss low sodium
Addisons disease- adrenal insufficiency, hence loss of sodium + water
Reason for skin pigmentation in addisons disease
Increased ACTH from pituitary; ACTH bears the sequence for melanocyte-stimulating hormone (MSH) within it, so when ACTH increased there can be cross-stimulation of MSH receptors
What will the potassium be like in a patient with “acute” addisons disease?
High
Patient presentation:
in hospital with other illness
low sodium
clinical volume status unremarkable
Syndrome of inappropriate anti-diuresis- release of ADH in response to non-osmotic stimuli e.g. pain, nausea/vomiting, hypoglycaemia
Main causes of hypernatraemia (2)
Too little water (diabetes insipidus or reduced intake)
Too much sodium (rare)
Patient presentation:
head injury
high sodium
high urine output/IV fluid requirements
Diabetes insipidus (failure to produce ADH due to pituitary damage, hence excessive water loss)
How is diabetes insipidus managed?
Fluid replacement
Desmopressin (exogenous ADH)
What symptoms can be seen with either very high or very low sodium?
Altered consciousness
Confusion
Nausea
If adrenal insufficiency is suspected what should be measured?
serum cortisol (low) and ACTH (high)
Normal range of serum potassium
3.5-5.3mmol/l
ECG changes in hyperkalaemia (2)
Tall “tented” T-waves
Widening of the QRS complex
What is the main cause of hyperkalaemia?
Reduced GFR and hence reduced excretion of potassium
What are the main causes of reduced GFR leading to hyperkalaemia? (2)
Renal failure
Hypoaldosteronism (usually due to use of ACE inhibitors/ARBs. These cause increased secretion of sodium with retention of potassium)
In what situations can there be increased potassium release from cells?
Massive cellular damage e.g. rhabdomyolysis
Metabolic acidosis
Insulin deficiency
