Electrolytes Flashcards
What does the sodium potassium pump do?
3 Na+ out of cell and 2 K+ into cell
What is the ECF concentration of potassium?
s normally at 4.2mmol/L, ranges from 3.5-5
What regulates potassium under normal conditions?
- Insulin - postprandial release of insulin also shifts dietary K+ into cells until the kidney excretes the K+ load
- Catecholamines
What factors affect potassium distribution?
What is conn’s syndrome?
excess aldosterone secretion is associated with hypokalaemia due to movement of extracellular K+ into cells
What are acid-base transport pathways?
A- Na+-H+ exchange - Na+ that enters by this route must be removed by the Na+/K+-ATPase =
- K+ uptake will be greater when Na+-H+ exchange activity is stimulated
- K+ uptake will be diminished when the rate of Na+-H+ exchange is reduced
B- e.g. in Acidosis with acidemia
- decrease in extracellular
HC03 - = inhibition of the inward rate of Na+-HCO3 cotransport
- = fall in intracellular Na+ and reduced Na+/K+ATPase activity
C- e.g. Acidosis with acidemia
- CI-HCO3 exchange also may contribute to apparent K+-H+ exchange
- = decrease in extracellular HCO3 = increase the inward movement of CI- by CH- HCO3 exchange = rise in intracellular CI-= K+ efflux by K+-CI- cotransport
What is renal potassium excretion determined by?
- the rate of K+ filtration (= glomerular filtration rate x plasma K+ concentration). The normal rate of K+ filtration by the glomerular capillaries is about 756 mEq/day. E.g. 180 L/day (GFR) × 4.2 mEg/L (plasma K+ concentration)
- the rate of K+ reabsorption by the tubules
- the rate of K+ secretion by the tubules
What is the tubular handling of potassium under normal conditions?
What is the role of intercalated cells?
What are the factors the regulate potassium secretion?
- increased ECF potassium concentration
- increased tubular flow rate
- increased aldosterone
How does increased ECF potassium concentration regulate potassium secretion?
Increased dietary K+ intake and increased ECF K+ concentration stimulate K+ secretion by 4 mechanisms:
- Increased ECF K+ concentration stimulates the Na+/ K+ ATPase pump = increasing K+ uptake across the basolateral membrane. This increased K+ uptake increases intracellular K+ concentration -> K+ to diffuse across the luminal membrane into the tubule
- Increased extracellular K+ concentration increases the K+ gradient from the renal interstitial fluid to the interior of the epithelial cell. Reduces backleakage of K+ ions from inside the cells through the basolateral membrane
- Increased K+ intake stimulates synthesis of K+ channels and their translocation from the cytosol to the luminal membrane -> increases the ease of K+ diffusion through the membrane
- Increased K+ concentration stimulates aldosterone secretion by the adrenal cortex -> further stimulates K+ secretion
How does increased tubular rate regulate potassium secretion?
There are 2 effects of high-volume rate that increase K+ secretion:
- When K+ is secreted into the tubular fluid - the luminal concentration of K+ increases = reducing the driving force for K+ diffusion across the luminal membrane. With increased tubular flow rate = the secreted K+ is continuously flushed down the tubule. The rise in tubular K+ concentration becomes minimised and net K+ secretion is increased
- A high tubular flow rate also increases the number of high conductance BK channels in the luminal membrane -> increasing conductance of K+ across the luminal membrane
How does increased aldosterone regulate potassium secretion?
- increases intracellular K+ concentration by stimulating the activity of the Nat/K+-ATPase in the basolateral membrane
- stimulates Na+ reabsortion across the luminal membrane = increases the electronegativity of the lumen = increasing the electrical gradient favoring K+ secretion
- increases the number of K+ channels in the luminal membrane and therefore its permeability for K+
What are the effects of high sodium?
What are the electrolyte levels associated with purging?
What happens in hypokalemia?
- The hypokalaemia observed in purging individuals is not a direct consequence of K+ loss from vomiting but due to its effect on triggering the activation of the RAAS in response to blood volume depletion
- Increase aldosterone secretion = increases K+ excretion through increasing expression K+ channels and Na+/K+ ATPase in the principal cells of the collecting duct = increased urinary K+ losses
- QT prolongation is seen in patients with bulimia nervosa. QT prolongation is due to a slower rate of repolarisation of ventricular myocytes. Hypokalaemia is thought to inhibit the conductance of the slow delayed-rectifier voltage-gated K+ channel that is responsible for speeding up the repolarisation of the ventricular myocytes There are a number of suggested mechanisms for this including:
- faster inactivation
- enhanced Na+-dependent inhibition
- downregulation of the expression of the K+ channel in acute-maintained hypokalaemia
Glomerular filtration rate (GFR)=
Kf is the filtration coefficient (how permeable the capillary is to water). This is high in glomerular capillaries as they need to be very leaky to do their
job.
σ (sigma) is the reflection coefficient (how permeable the capillary is to protein). This can change if the patient loses the negative charge of the basement membrane (eg in nephrotic syndrome)
P= hydrostatic pressure
Pi= oncotic pressure
Afferent vs efferent arteriolar constriction effect of GFR
Puf= Pressure of urine filtration
How does the sympathetic nervous system affect renal blood flow?
How does angiotensin II affect renal blood flow?
How does atrial and brain natriuretic peptide (ANP and BNP) affect renal blood flow?
How does prostaglandins affect renal blood flow?
How does dopamine affect renal blood flow?
Shifts blood flow from skin and muscle to vital organs, can be used to treat haemorrhage
How does nitric oxide affect renal blood flow?
Vasoconstrictors vs vasodilators in regulation of renal blood flow
What is the myogenic response?
What is tubuloglomerular feedback?
Filtered load=
the amount of a substance filtered into Bowman’s space per unit time.
= GFR X P[x] (plasma concentration of substance)
Where is Na+ reabsorbed across the nephron?
Response to increased vs decreased Na+ intake?
How is phosphate renally handled?
How is calcium renally handled?
How is magnesium renally handled?
What is the timeline of the response to a haemorrhage?
