Week 5.2 Flashcards
Potassium homeostasis (2 main regulations)
- Intake of K+
- Renal secretion & urine excretion of K+
What mainly controls K+ homeostasis
Aldosterone will respond and change K+ concentration
What are the effects of abnormal potassium levels
Plasma potassium normally controls neuron excitability:
Excessive potassium -> decreases excitability, cardiac arrythmia, muscle pain.
Low potassium -> muscle cramp (hyperaldosteronism)
What could cause hyperkalaemia (3 causes)
- Kidney’s inability to excrete K+
- ICF/ECF shifts: cell lysis
- Hormone deficiency: aldosterone insufficiency (low cell intake)
maybe intake + renal.
Hypokalemia causes
- hormone: high aldosterone levels (cell uptake)
- diarrhoea
- diuretics
- alcoholism (insufficient intake)
What could severe diarrhoea lead to (3 losses):
Loss of:
Water, Potassium, Bicarbonate
Lead to:
Loss of blood volume: sodium reabsorption, reduced GFR
Loss of potassium: potassium reabsorption from urine
Loss of bicarbonate: acidosis
Significance of ECF volume
Regulate blood pressure
Significance of ECF osmolarity
prevent cell shrinkage and swelling
what system regulates ECF volume
Renin-Angiotensin System-> Aldosterone
Sodium reabsorption/Excretion
what regulates ECF osmolarity
Water balance -> regulated by ADH
antidiuretic hormone (ADH) -> increase urine concentration (retain water)
no ADH -> dilute urine
SYNDROME OF INAPPROPRIATE ADH (what is an example)
1 example: Smoker -> lung tumour
The tumour produces ADH which leads to water retention + sodium dilution.
Other examples: Malignancies, cerebral pathologies, drugs
what is hypotonicity (concentration of sodium)
low osmolarity (low plasma sodium conc) -> water enter cells swell
what could hypotonicity cause
cerebral oedema
What is osmotic demyelination syndrome
Neurological disorder: too rapid compensatory response to hyponatraemia (low sodium in blood) - hypotonicity:
When ECF concentration gets lower than brain cell ICF during correction, cells shrink.
hypovolaemia (low BP) sensed by kidney
RAAS is activated, salt reclaimed -> increase ECF.
high BP sensed by kidney
RAAS is suppressed, salt wasted -> decrease ECF.
oedema and effective circulating volume
example 1: cardiac failure, high hydrostatic pressure
example 2: nephrotic syndrome, protein loss, low oncotic pressure
ECF expand leads to oedema.
But the body is still increasing sodium reabsorption due to the low effective circulating volume.
what causes low sodium levels (hyponatraemia)
- SIADH: water retention.
- renal failure
- Oedema