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Renal Exam 1 > Transport Mechanisms 2 > Flashcards

Transport Mechanisms 2 Flashcards

1
Q

effect of loops diuretics (furosemide) on ascending limb of LOH

A
  • inhibits Na/K/2Cl transporter

- increases urination

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2
Q

result of inhibition of Na/K/2Cl transporter in LOH

A
  • decreased K+ and Ca2+ reabsorption

aka hypokalemia (and alkalosis) and hypocalcemia

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3
Q

how do we have decreased Ca2+ with decreased K+

A
  • electrochemical gradient that is usually formed by the back leak of K+ will lead to paracellular Ca2+ transport
  • that has now been lost
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4
Q

Bartter’s syndrome affects what part of the kindey

A
  • ascending limb of LOH
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5
Q

cause of Bartter’s syndrome

A
  • defect in Na/K/2Cl transporter
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6
Q

genetics of Bartter’s syndrome

A
  • autosomal recessive
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7
Q

symptoms of Bartter’s syndrome

A
  • hypokalemia
  • metabolic alkalosis
  • polyuria
  • polydipsia
  • dehydration
  • high urine calcium
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8
Q

what transporter does the early distal tubule have

result

A
  • Na/Cl cotransporter (NCC)

- dilutes tubular fluid

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9
Q

epithelium in early distal tubule

result

A
  • tight epithelial
  • transcellular Na+ movement via the Na/Cl cotransporter
  • impermeable to H20
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10
Q

how much Na is reabsorbed in the early distal tubule

A
  • 5-10%
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11
Q

what transporter is located in the late distal tubule/cortical collecting duct

A
  • epithelial Na Channel (ENaC)

- alpha intercalated cells

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12
Q

what is the epithelial Na Channel dependent on

A
  • aldosterone
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13
Q

result of epithelial Na channel

A
  • Na enters cell down chemical gradient through ENaC
  • creates negative electrical potential
  • results in K+ secretion into tubular lumen
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14
Q

result of alpha intercalated cells

result of beta intercalated cell

A
  • H+ secretion into tubular lumen
  • HCO3/Cl- ATPase
  • HCO3 extruded into the lumen
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15
Q

H+ secretion into tubular lumen through what mechanisms

A
  • H+ ATPase

- H/K ATPase

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16
Q

what happens with the secreted H+ in late distal tubule

what happens with HCO3- in the late distal tubule

A
  • binds to NH3 and other buffers

- results in HCO3 reabsorption into blood through HCO3/Cl- exchanger

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17
Q

result of the thiazide diuretics such as hydrochlorothiazide and chlorthalidone

A
  • inhibit the Na/Cl cotransporter in the early distal tubule
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18
Q

result of amiloride/triamterene

what are they also referred to as

A
  • inhibit epithelial sodium channel

- K+ sparing diuretics

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19
Q

why are amiloride/triamterene referred to as K+ sparing diuretics

A
  • they do not promote K+ secretion
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20
Q

we generally use amiloride/triamterene in combination with

A
  • thiazide or loop diuretic
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21
Q

cause of Gitelman’s

result

A
  • loss of function of Na/Cl cotransporter
  • increased surface expression of K in collecting duct
  • Na+ loss into urine
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22
Q

Gitelman’s acts like what

A
  • a thiazide diuretic
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23
Q

symptoms of Gitelman’s

A
  • hypokalemia - loss of K+ in the urine
  • metabolic alkalosis
  • salt craving
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24
Q

cause of pseudohypoaldosteronism II

result

A
  • gain of function of Na/Cl cotransporter
  • increases Na and Cl reabsorption
  • decreases surface expression of K channels in collecting duct.
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25
Q

symptoms of pseudohypoaldosteronism II

A
  • hypertension - increase Na reabsorption
  • hyperkalemia - potassium cannot be secreted into the urine
  • Metabolic Acidosis
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26
Q

renin and aldosterone levels in pseudohypoaldosteronism II

A
  • low

- you’re having high BP so you have increased perfusion and don’t need the RAAS system

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27
Q

cause of Liddle’s

result

A
  • gain of function in epithelial Na channel

- uncontrolled Na retention in blood

28
Q

symptoms of Liddle’s

A
  • hypertension - increase Na+ reabsorption
  • hypokalemia - you have reabsorbed all this sodium which creates an even greater gradient for K+ secretion so your K+ in blood is less.
  • metabolic alkalosis
29
Q

cause of pseudohypoaldosteronism type I

A
  • loss of function of epithelial Na channel
30
Q

symptoms of pseudohypoaldosteronism type I

A
  • hypovolemia
  • metabolic acidosis
  • sodium wasting
  • hyperkalemia
  • hyponatremia
31
Q

aldosterone levels in pseudohypoaldosteronism type I

A
  • elevated due to hypovolemia
32
Q

cause of distal RTA type I

A
  • impaired H+ secretion
33
Q

distal RTA type I impaired H+ secretion leads to

A
  • non-anion gap acidosis
  • low bicarb
  • hypokalemia
  • cannot acidify urine
34
Q

most common cause of distal RTA type I

A
  • diminished H+ ATPase activity
35
Q

less common causes of distal RTA type I

A
  • increased lumenal membrane permeability leading to backleak of H+
  • diminished activity of H+/K+/ATPase
36
Q

signs of hyperkalemic RTA type 4

A
  • hyperkalemia

- mild non-anion gap metabolic acidosis

37
Q

cause of hyperkalemic RTA type 4

result

A
  • hypoaldosteronism due to a true deficiency or resistance

- decreased Na+ reabsorption and less K+ secretion

38
Q

syndrome of apparent mineralocorticoid excess (SAME) cause

A

-deficiency in enzyme that converts cortisol to cortisone

39
Q

what binds the mineralcorticoid receptor

A
  • cortisol
40
Q

plasma cortisol concentration compared to aldosterone in syndrome of apparent mineralocorticoid excess (SAME) cause

A
  • 100x higher

- basically still acts like aldosterone

41
Q

blood pressure in syndrome of apparent mineralocorticoid excess (SAME)

A
  • hypertension
42
Q

potassium levels in syndrome of apparent mineralocorticoid excess (SAME)

A
  • hypokalemia due to K+ secretion
43
Q

acidosis/alkalosis in syndrome of apparent mineralocorticoid excess (SAME)

A
  • metabolic alkalosis - hydrogen ion secretion

- ACTS LIKE ALDOSTERONE WHICH CAUSES H+ SECRETION

44
Q

plasma renin activity in syndrome of apparent mineralocorticoid excess (SAME)

A
  • low
45
Q

plasma aldosterone concentration in syndrome of apparent mineralocorticoid excess (SAME)

A
  • low
46
Q

what hormones regulate in the early distal tubule

A
  • none
47
Q

what hormones regulate in the late distal tubule and cortical collecting duct - principal cells

A
  • aldosterone
  • ADH
  • ANP
48
Q

what hormones regulate in the late distal tubule and cortical collecting duct - intercalated cells

A
  • aldosterone
49
Q

role of aldosterone in the late distal tubule and cortical collecting duct - principal cells

A
  • binds to intracellular receptor

- stimulates insertion of epithelial Na channel and K channels in luminal membrane

50
Q

role of ADH in the late distal tubule and cortical collecting duct - principal cells

A
  • binds to V2 receptor in basolateral membrane
  • V2 receptor activates adenylate cyclase to convert ATP -> cAMP to activate PKA
  • phosphorylation of aquaporin 2 causes shuttling and stimulates insertion of aquaporin 2 in luminal membrane
51
Q

role of ANP in the late distal tubule and cortical collecting duct - principal cells

A
  • inhibits aldosterone effects
52
Q

role of aldosterone late distal tubule and cortical collecting duct - intercalated cells

A
  • stimulates H+ ATPase activity
53
Q

hormonal regulation in the medullary collecting duct

A
  • ADH dependent water reabsorption
  • ADH dependent urea reabsoprtion
  • aldosterone dependent Na+ reabsorption and K+ secretion
54
Q

RAAS during hypovolemia

A
  • decreased distal delivery of NaCl to macula densa
  • increased renin release by JG cells
  • increase in angiotensin II to maintain GFR
55
Q

H2O enter lumen via which aquaporin and enters how

A
  • 2

- enters along osmotic gradient

56
Q

H2O leaves via which aquaporin

A
  • 3
57
Q

importance of aquaporin 3

A
  • constitutively expressed

- not ADH regulated

58
Q

what does high urine osmolarity reflect about ADH and urine volume

A
  • ADH present
  • water reabsorbed
  • low urine volume
59
Q

what does low urine osmolarity reflect about ADH and urine volume

A
  • ADH not present
  • water not reabsorbed
  • high urine volume
60
Q

the V2 receptor also activates which other transporter

where is this transporter expressed

A
  • urea transporter

- expressed in medullary collecting duct

61
Q

urea is reabsorbed where and how

A
  • across luminal membrane through UT1

- along a concentration gradient

62
Q

urea exits where and how

A
  • exits basolateral membrane through UT3
63
Q

what is the location of AQP2 and AQP3

A
  • distal tubule

- cortical and medullary collecting duct

64
Q

which AQP is located on the apical membrane

A
  • 2
65
Q

which AQP is located on the basolateral membrane

A
  • 3
66
Q

ANP is released in response to

A
  • atrial volume
67
Q

result of ANP

A
  • enhances Na+ excretion
  • counters effects of RAAS
  • relax vascular smooth muscle
  • vasodilator
  • increase diuresis

Renal Exam 1 (24 decks)

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