Renal physiology Flashcards
______ stimulates uric acid reabsorption in PCT
Hypovolemia
PAH concentration in a nephron
Minimum in bowman capsule
PCT: ↑ (excreted)
Descending limb: ↑ (water reabsorbed)
Ascending limb and DCT: Remains constant (impermeable to water)
Urine pH is chiefly regulated by ______
H+ secretion by late distal and collecting tubules
In vomiting and DKA ► Blood Na+ will be?
Decreased (ADH results in more water absorption)
Aldosterone absorbs Na+ but at the same time it also absorbs water with it.
so the combined effect of both these hormones will be ↓Na+ in blood
In severe vomiting, total body and serum potassium?
Both ↓ due to GI (vomiting) and renal loss (aldosterone)
PAH filtration, secretion, excretion:
Filtration: can’t be saturated as it is freely filtered
Secretion: Saturated (Carrier protein mediated)
Excretion = Filtration + Secretion - Absorption
so, Excretion can never be saturated as it includes filtration too.
Patient should be tested for ____ before treatment with EPO
Iron deficiency
Dopamine Secreted by
At low doses:
PCT cells, promotes natriuresis.
At low doses; dilates interlobular arteries, afferent arterioles, efferent arterioles →↑RBF, little or no change in GFR.
In volume depleted states (vomiting, diarrhea), it is easy to get Na+ abnormalities because
ADH now responds to volume loss, not to high osmolality
Why sodium levels are determined by intake and loss of salt in HF patients
Because ADH is triggered by volume censors (non-osmotic) in these patients
Hyponatremia with ↑osmolality is seen in
hyperglycemia and mannitol → draws water out of cell → hyponatremia
ANP and ATII have same effect on GFR and efferent arterioles, how are they different
ANP: no compensatory Na reabsorption in distal tubule
ATII: compensatory Na reabsorption in PCT and distal tubule
Most concentrated part of nephron in the presence and absence of ADH
In ADH absence: lowermost part of loop of henle
In ADH presence: Medullary part of collecting duct
ADH binds to V2 receptors on _____ cells
principal
_______ are primary mediators of K+ regulation in hyper or hypokalemia
principal and α-intercalated cells of distal and cortical collecting tubules
Hypokalemia stimulates reabsorption of K+ via __________
Apically locatedH+/K+ ATPase on α-intecalated cells
Water reabsorption in a nephron dependent/independent of hydration status
PCT: >60% (independent of hydration status)
Descending limb: 20% (independent of hydration status)
Upto 20% by late distal and collecting tubules (dependent of hydration status)
Most amount of water reabsorbed in a water deprivation state
PCT >60
Refractory hypokalemia us seen in ____
Mg deficiency
Normally Mg inhibits K+ excretion by acting on ROMK
Hypomagnesimia caused by?
- GI loss
- Omeprazole, Foscarnet
- Renal loss (loop and thiazides)
- Alcohol abuse
- Acute Pancreatitis (sponification of Ca/Mg)
If alcoholic comes to you in ER, he is most probably deficient in ___ electrolyte
Mg
A decrease in both intra and extracellular K+ conc. is seen in
- Mineralocorticoid excess
- Chronic GI loss
- Diuretics
A increase in both intra and extracellular K+ conc. is seen in
Chronic renal failure
In acute hypercalcemia, nephrogenic diabetes insipidus is due to____
downregulation of aquaporin channels
