Renal physiology Flashcards

1
Q

______ stimulates uric acid reabsorption in PCT

A

Hypovolemia

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2
Q

PAH concentration in a nephron

A

Minimum in bowman capsule
PCT: ↑ (excreted)
Descending limb: ↑ (water reabsorbed)
Ascending limb and DCT: Remains constant (impermeable to water)

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3
Q

Urine pH is chiefly regulated by ______

A

H+ secretion by late distal and collecting tubules

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4
Q

In vomiting and DKA ► Blood Na+ will be?

A

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

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5
Q

In severe vomiting, total body and serum potassium?

A

Both ↓ due to GI (vomiting) and renal loss (aldosterone)

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6
Q

PAH filtration, secretion, excretion:

A

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.

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7
Q

Patient should be tested for ____ before treatment with EPO

A

Iron deficiency

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8
Q

Dopamine Secreted by

At low doses:

A

PCT cells, promotes natriuresis.
At low doses; dilates interlobular arteries, afferent arterioles, efferent arterioles →↑RBF, little or no change in GFR.

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9
Q

In volume depleted states (vomiting, diarrhea), it is easy to get Na+ abnormalities because

A

ADH now responds to volume loss, not to high osmolality

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10
Q

Why sodium levels are determined by intake and loss of salt in HF patients

A

Because ADH is triggered by volume censors (non-osmotic) in these patients

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11
Q

Hyponatremia with ↑osmolality is seen in

A

hyperglycemia and mannitol → draws water out of cell → hyponatremia

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12
Q

ANP and ATII have same effect on GFR and efferent arterioles, how are they different

A

ANP: no compensatory Na reabsorption in distal tubule
ATII: compensatory Na reabsorption in PCT and distal tubule

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13
Q

Most concentrated part of nephron in the presence and absence of ADH

A

In ADH absence: lowermost part of loop of henle

In ADH presence: Medullary part of collecting duct

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14
Q

ADH binds to V2 receptors on _____ cells

A

principal

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15
Q

_______ are primary mediators of K+ regulation in hyper or hypokalemia

A

principal and α-intercalated cells of distal and cortical collecting tubules

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16
Q

Hypokalemia stimulates reabsorption of K+ via __________

A

Apically locatedH+/K+ ATPase on α-intecalated cells

17
Q

Water reabsorption in a nephron dependent/independent of hydration status

A

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)

18
Q

Most amount of water reabsorbed in a water deprivation state

A

PCT >60

19
Q

Refractory hypokalemia us seen in ____

A

Mg deficiency

Normally Mg inhibits K+ excretion by acting on ROMK

20
Q

Hypomagnesimia caused by?

A
  1. GI loss
  2. Omeprazole, Foscarnet
  3. Renal loss (loop and thiazides)
  4. Alcohol abuse
  5. Acute Pancreatitis (sponification of Ca/Mg)
21
Q

If alcoholic comes to you in ER, he is most probably deficient in ___ electrolyte

A

Mg

22
Q

A decrease in both intra and extracellular K+ conc. is seen in

A
  1. Mineralocorticoid excess
  2. Chronic GI loss
  3. Diuretics
23
Q

A increase in both intra and extracellular K+ conc. is seen in

A

Chronic renal failure

24
Q

In acute hypercalcemia, nephrogenic diabetes insipidus is due to____

A

downregulation of aquaporin channels

25
Q

Humoral hypercalcemia of malignancy : PTHrP performs all functions of PTH except

A

1,25 dihydroxy Vit D production

26
Q

Hypokalmeia symptoms

A

U waves and flattened T waves on ECG, arrhythmias, muscle cramps, spasm, weakness

27
Q

Hypermagnesimia symptoms

A

DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia