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Urinary Block > Tubular Transport > Flashcards

Tubular Transport Flashcards

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?

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?

A

Quick absorption of solutes and disruption of the countercurrent multiplier

21
Q

Describe the mechanism of calcium and magnesium reabsorption.

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?

A

NKCC inhibitor

23
Q

What are the side effects of loop diuretics?

A

hypokalemia, hypocalcemia, polyuria

24
Q

Why do loop diuretics cause hypocalcemia?

A

no electrical gradient is formed, so nothing drives reabsorption

25
Q

Why do loop diuretics cause hypokalemia?

A

NKCC stops absorbing K+, but ROMK is still open to secrete K+

26
Q

What is Bartter’s Syndrome? Inheritance?

A

Defect in NKCC; auto recessive

27
Q

What are the symptoms of Bartter’s syndrome?

A

same as loop diuretics; hypokalemia, alkalosis, polyuria, polydipsia, dehydration

28
Q

What ion channels are present in the early distal tubule?

A

Na/Cl cotrans (NCC), Na/K-ATPase

29
Q

What basolateral and luminal ion channels are present in the principal cells of the LDT/CCD?

A

baso: Na/K-ATPase, K+ channels
luminal: ENaC, K+ channels

30
Q

What is the function of the alpha cells of the LDT/CCD?

A

H+ secretion and HCO3 reabsorption

31
Q

What is the MoA of thiazide diuretics?

A

inhibit NCC (EDT)

32
Q

What are the K+ sparing diuretics?

A

amiloride and triamterene

33
Q

What is the MoA of K+ sparing diuretics?

A

inhibit ENaC (LDT/CCD)

34
Q

What is Gitelman’s Syndrome? Symptoms?

A

loss of funciton of NCC (thiazides); hypokalemia, alkalosis, salt craving

35
Q

What is Gordon’s Syndrome? Symptoms?

A

Gain of function of NCC; htn, hyperkalemia, acidosis, low renin, low aldosterone

36
Q

What is Liddle’s Syndrome? Symptoms?

A

Gain of function of ENaC; htn, hypokalemia, alkalosis

37
Q

What is pseudohypoaldosteronism type I? Symptoms?

A

loss of function of ENaC (K+ sparing); hypovolemia, hyponatremia, hyperkalemia, high aldosterone

38
Q

What is Distal RTA?

A

impaired H+ secretion in the distal tubule, usually due to H+ATPase inactivity

39
Q

What is hyperkalemic RTA?

A

absence of aldosterone; no ENaC, no K+ secretion

40
Q

What is the Syndrome of Apparent Mineralocorticoid Excess (SAME)? Symptoms?

A

deficiency in an enzyme that converts cortisol to cortisone, more cortisol to stimulate aldosterone receptor; htn, hypokalemia, alkalosis, low renin, low aldo

41
Q

What hormones act on principal cells? Effects?

A

aldosterone: stimulate ENaC and K+ channel insertion
ADH: stimulate aquaporin insertion
ANP: inhibits aldo

42
Q

What hormones act on intercalated cells (alpha cells)? Effects?

A

aldosterone: stimulate H+ATPase to secrete acid

43
Q

What is reabsorbed in the medullary collecting duct?

A

water and urea (both +ADH)

44
Q

What is ADH MoA (for water)?

A

binds to V2 receptor, activates adenylate cyclase, cAMP-PKA phosphorylates aquaporin 2, stimulating insertion into luminal membrne

45
Q

What are the physiologic stimuli for ADH release?

A

high osmolality, low ECF volume, low BP

46
Q

What is the most sensitive ADH stimulus? Most powerful?

A

high osmolality; low blood pressure

47
Q

Why do CHF patients have high ADH?

A

Low effective blood pressure to the kidneys due to cardiogenic shock

Urinary Block (8 decks)

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