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Urinary Block > Tubular Transport > Flashcards

Tubular Transport Flashcards

(47 cards)

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1
Q

What are the two paths of secretion/reabsorption?

A

transcellular and paracellular

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2
Q

What regions of the nephron are “leaky” to allow paracellular transport?

A

proximal tubule, descending loop

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3
Q

What is the mechanism of Na reabsorption in the proximal tubule?

A

Na/K-ATPase pumps Na out of the epithelium into the interstitium which draws Na from the lumen into the cell.

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4
Q

What are the luminal transporters in the proximal tubule?

A

Na/Cl cotrans, Na/glc cotrans, Na/AA cotrans, Na/H exchange, aquaporin 1

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5
Q

What are the basolateral transporters in the proximal tubule?

A

Na/K-ATPase, GLUT, AA trans, Na/HCO3 cotrans, aquaporin 1

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6
Q

The sodium gradient is used in what transport mechanisms in the proximal tubule?

A

reabsorb glc and AA, secrete H+

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7
Q

What is the max concentration of glucose that can be completely reabsorbed?

A

180mg/dL

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8
Q

How is bicarb reabsorbed?

A

brush border carbonic anhydrase creates CO2/H2O that is reabsorbed. Intracellular CA reforms bicarb which is transported with Na out of the cell

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9
Q

How is new bicarb formed in the proximal tubule?

A

glutamine is reabsorbed and broken down into NH4 and bicarb inside the cell. NH4 is secreted via Na/H exchanger

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10
Q

How is K+ reabsorbed in the proximal tubule?

A

H2O follows sodium. K+ follows water via pericellular pathway (solvent drag)

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11
Q

How is urea reabsorbed in the proximal tubule?

A

urea is concentrated by H2O reabsorption. Urea diffuses out slowly

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12
Q

What happens to urea when GFR decreases?

A

more urea is reabsorbed, so BUN increases

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13
Q

What is countercurrent multiplication?

A

shape and permeability of the loop creates a concentration gradient that can be used to reabsorb water form the collecting duct

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14
Q

What is the descending loop permeable to?

A

H2O

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15
Q

What is the ascending loop permeable to?

A

NaCl

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16
Q

What is the concentration gradient between the ascending and descending loop

A

ascending is 200 mOsm/L higher

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17
Q

What protein transports ions in the ascending loop?

A

NKCC (Na/K/2Cl)

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18
Q

What determines whether H2O is reabsorbed from the collecting duct?

A

ADH

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19
Q

What effect does ADH have on urea?

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A

ADH upregulates UT1 transporters in the collecting duct which reabsorb 55% of urea, adding to the osmotic gradient

20
Q

What is the effect of higher blood flow through the vasa recta?

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A

Quick absorption of solutes and disruption of the countercurrent multiplier

21
Q

Describe the mechanism of calcium and magnesium reabsorption.

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A

The NKCC channel and ROMK backleak creates a net positive charge in the lumen of the ascending loop which drives the paracellular transport of Ca, Mg

22
Q

What is the MoA of loop diuretics?

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A

NKCC inhibitor

23
Q

What are the side effects of loop diuretics?

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A

hypokalemia, hypocalcemia, polyuria

24
Q

Why do loop diuretics cause hypocalcemia?

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A

no electrical gradient is formed, so nothing drives reabsorption

25
Why do loop diuretics cause hypokalemia?
NKCC stops absorbing K+, but ROMK is still open to secrete K+
26
What is Bartter's Syndrome? Inheritance?
Defect in NKCC; auto recessive
27
What are the symptoms of Bartter's syndrome?
same as loop diuretics; hypokalemia, alkalosis, polyuria, polydipsia, dehydration
28
What ion channels are present in the early distal tubule?
Na/Cl cotrans (NCC), Na/K-ATPase
29
What basolateral and luminal ion channels are present in the principal cells of the LDT/CCD?
baso: Na/K-ATPase, K+ channels luminal: ENaC, K+ channels
30
What is the function of the alpha cells of the LDT/CCD?
H+ secretion and HCO3 reabsorption
31
What is the MoA of thiazide diuretics?
inhibit NCC (EDT)
32
What are the K+ sparing diuretics?
amiloride and triamterene
33
What is the MoA of K+ sparing diuretics?
inhibit ENaC (LDT/CCD)
34
What is Gitelman's Syndrome? Symptoms?
loss of funciton of NCC (thiazides); hypokalemia, alkalosis, salt craving
35
What is Gordon's Syndrome? Symptoms?
Gain of function of NCC; htn, hyperkalemia, acidosis, low renin, low aldosterone
36
What is Liddle's Syndrome? Symptoms?
Gain of function of ENaC; htn, hypokalemia, alkalosis
37
What is pseudohypoaldosteronism type I? Symptoms?
loss of function of ENaC (K+ sparing); hypovolemia, hyponatremia, hyperkalemia, high aldosterone
38
What is Distal RTA?
impaired H+ secretion in the distal tubule, usually due to H+ATPase inactivity
39
What is hyperkalemic RTA?
absence of aldosterone; no ENaC, no K+ secretion
40
What is the Syndrome of Apparent Mineralocorticoid Excess (SAME)? Symptoms?
deficiency in an enzyme that converts cortisol to cortisone, more cortisol to stimulate aldosterone receptor; htn, hypokalemia, alkalosis, low renin, low aldo
41
What hormones act on principal cells? Effects?
aldosterone: stimulate ENaC and K+ channel insertion ADH: stimulate aquaporin insertion ANP: inhibits aldo
42
What hormones act on intercalated cells (alpha cells)? Effects?
aldosterone: stimulate H+ATPase to secrete acid
43
What is reabsorbed in the medullary collecting duct?
water and urea (both +ADH)
44
What is ADH MoA (for water)?
binds to V2 receptor, activates adenylate cyclase, cAMP-PKA phosphorylates aquaporin 2, stimulating insertion into luminal membrne
45
What are the physiologic stimuli for ADH release?
high osmolality, low ECF volume, low BP
46
What is the most sensitive ADH stimulus? Most powerful?
high osmolality; low blood pressure
47
Why do CHF patients have high ADH?
Low effective blood pressure to the kidneys due to cardiogenic shock

Urinary Block (8 decks)

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