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Physiology Part 2 > Lec 45 Distal Tubule, Collecting Duct, ADH, RAAS, Erythropoietin, ANP > Flashcards

Lec 45 Distal Tubule, Collecting Duct, ADH, RAAS, Erythropoietin, ANP Flashcards

1
Q

What is the physiologic role of distal tubule and collecting duct?

A
  • fine tune what we excrete and what we keep

- acidify urine

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2
Q

What are mechs of Na and Cl transport in early distal tubule?

A

apical:
- Na/Cl cotransporter [1 Na in, 1 Cl in]
basolateral:
- Na/K ATPase [3 Na out, 2 K in]
- Cl channel out

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3
Q

Is early distal tubule diluting or concentrating?

A

diluting – continues to create free water

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4
Q

Is early distal tubule permeable to water?

A

no – impermeable

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5
Q

What are the two cell types of late distal tubule and collecting duct?

A

principal cells

intercalated cells

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6
Q

What do principal cells do?

A
  • reabsorb Na
  • secrete K
  • respond to ADH/aldosterone
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7
Q

What do alpha intercalated cells do?

A
  • secrete H

- reabsorb K

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8
Q

What do beta intercalated cells do?

A
  • secrete HCO3
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9
Q

What is mech of principal cells?

A 
apical:
- Na in via Na channel [driven by gradient]
- K secreted to lumen via K channel
basolateral:
- Na/K ATPase [3 Na out, 2 K into cell]
- negative
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10
Q

Is lumen positive or negative voltage in late distal tubule and collecting duct? What does this mean?

A
  • negative voltage

- means you get paracellular Cl diffusion out of lumen

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11
Q

How is Cl transported in late distal tubule and collecting duct?

A
  • via paracellular diffusion it is reabsorbed

- negative potential of lumen is driving force

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12
Q

How is K transported in late distal tubule and collecting duct?

A
  • via K channel secreted in principal

- via H-K ATPase reabsorbed in alpha intercalated

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13
Q

What is mech of alpha intercalated cell?

A

apical:

  • H-ATPase transfers H out of cell into lumen
  • H-K ATPase: [1 H into lumen, 1 K into cell]

basolateral:

  • Na-K ATPase [3 Na out of cell into capillary, 2 K into cell]
  • K channel out to capillary
  • HCO3-Cl antiporter [HCO3 out of cell into capillary, Cl into cell]
  • Cl channel out
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14
Q

What primarily drives K transport?

A

H-K ATPase

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15
Q

What happens to principal cell action when you have lots of K?

A
  • more principal cell action since principal cells are excreting K
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16
Q

Do principal cells or intercalated cells play bigger role in K regulation?

A

principal cells

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17
Q

What is the mech of HCO3 transport in alpha intercalated

A
  • HCO3 generated with H from CO2 and H2O in alpha intercalated
  • H used for the H-K ATPase that drives K transport
  • HCO3 reabsorbed using HCO3/Cl antiporter
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18
Q

What are the 3 paradigms of acid-base regulation by alpha intercalated cells?

A
  • reabsorbing HCO3
  • excreting H as titratable acid
  • excreting H as NH4
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19
Q

What is mech of H+ secretion by alpha intercalated cell? Is there a difference between this mech for secretion via titratable acid or NH4?

A
  • in cell: CO2 and H2O –> H2CO3 –> H + HCO3 via carbonic anhydrase
  • on apical side of cell: H-ATPase and H-K exchanger get rid of H into lumen
  • on basolateral side HCO3 reabsorbed via HCO3-Cl exchanger
  • no difference in mech for titratable acid vs NH4
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20
Q

What is mech of H excretion as a titratable acid in alpha intercalated? What is feedback?

A
  • some acid HA dissociated into H and A in lumen
  • extra H associates with HPO4 and SO4 –> H2PO4, HSO4
  • excreted as acid
  • extra H feeds back and inhibits H-ATPase and H-K ATPase so you don’t get too acidic
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21
Q

What is mech of H excretion via NH4+ in alpha intercalated? Why is this a preferable method of excretion?

A
  • NH3 in lumen + H –> NH4+
  • NH3 comes from proximal tubule glutaminase rxn
  • good method of excretion because it doesn’t dissociate in urine so can excrete acid without lowering pH more
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22
Q

What is mech of bicarbonate reabsorption in alpha intercalated?

A
  • H ion secreted and binds filtered HCO3 –> H2CO3 –> H2O + CO2 allows HCO3 reabsorption and H recycled
  • if not sufficient HCO3 in lumen, H excreted because there is no other way to reabsorb it
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23
Q

What are 3 ways of getting more HCO3 from alpha intercalated?

A
  • NH4 and titratable acid mech form new HCO3 that is reabsorbed
  • HCO3 recycling mech causes reabsorption of another HCO3
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24
Q

What happens to principal cell mech if you are alkylotic?

A
  • you have lots of HCO3 filtered and little H secreted

- you can’t reabsorb all the HCO3

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25
Q

What happens to principal cell mech if you are acidotic?

A
  • you secrete more H than HCO3 is filtered
  • first you will reabsorb all the HCO3 you can
  • then you will still have leftover H and you will need to secrete it
26
Q

What is long term change in kidney when you are acidotic?

A
  • upregulate glutaminase so get more NH3 creation in prox tubule
27
Q

What is ADH?

A

hormone that regulates blood volume and BP by regulating tubular transport, free water creation, and reabsorption of free water

also vasoconstricts periphery

28
Q

Where is ADH generated?

A
  • in hypothalamus precursor synthesized and then converted to ADH and secreted by posterior pituitary
29
Q

what do osmoreceptors do?

A
  • sense change in osmolarity of plasma

- at increased osmolarity –> induce ADH release

30
Q

What do baroreceptors do?

A
  • sense change in BP
  • if BP decreases by 10-20% get massive change in ADH
  • causes tubular effects and vasoconstriction
31
Q

What 4 things induce ADH receptors?

A
  • increased osmolarity via osmoreceptors
  • decreased BP via baroreceptors
  • angiotensin II
  • pain
  • nicotine
32
Q

What are three non-receptor things that increase ADH release?

A
  • angiotensin II
  • pain
  • nicotine
33
Q

What are two non-receptor things that decrease ADH release?

A
  • ANP

- ethanol

34
Q

What does angiotensin II do to ADH release?

A

increase ADH

35
Q

What does pain do to ADH release?

A

increase ADH

36
Q

What does nicotine do to ADH release?

A

increase ADH

37
Q

What does ANP do to ADH release?

A

decrease ADH

38
Q

What does ethanol do to ADH release?

A

decrease ADH

39
Q

What two ADH receptors and what types of receptors are they?

A

Vascular V1 receptor
- Gq couple –> phospholipase C –> DAG/IP3 –> increase Ca

Tubular V2 receptor - on principal cells in distal tubule and collecting duct
- Gs couple –> adenylyl cyclase –> cAMP

40
Q

What happens to urine conc with no ADH?

A
  • low activity of Na/Cl/K transport
  • no urea coming out of collecting duct
  • low/moderate longitudinal gradient
  • no permeability of late distal tubule and collecting duct to H2O
  • excrete hypotonic urine
41
Q

What happens to urine conc with ADH?

A
  • more hypertonic urine
42
Q

What is mech of ADH increasing H2O permeability in collecting duct?

A
  • bind V2 receptor
  • phosphorylate storage vesicle containing aquaporins
  • causes aquaporin-2 to insert in apical membrane
43
Q

Overview of RAAS system?

A
  • liver makes angiotensinogen
  • renin from kidney converts angiotenisnogen to angiotensin I
  • ACE from lung converts angiotensin I to angiotensin II
44
Q

What is rate limiting step of RAAS system?

A

renin converting angiotensinogen to angiotensin I

45
Q

Where is renin produced

A

juxtaglomerular cell in kidney afferent arteriole

46
Q

What are the 4 main things that control renin release?

A
  1. renal vascular baroreceptor
  2. macula densa mechanism
  3. renal sympathetic nerves
  4. Angiotensin II
47
Q

What is the macula densa mech of renin release?

A

decreased arterial pressure

  • -> decreased Pgc
  • -> decreased GFR
  • -> decreased delivery of NaCl to macula densa cells in distal convoluted tubule
  • -> macula densa signal to increase renin secretion and decrease afferent resistance [via TG-feedback]
  • -> increased renin causes increase angiotensin II
  • -> increased angiotensin II causes increased BP
48
Q

How does angiotensin II control renin release?

A

angiotensin II does feedback inhibition of renin

49
Q

How do renal sympathetic nerves control renin release?

A
  • sympathetic nerve fibers innervate juxtaglomerular cells and cause them to release renin
50
Q

How do renal vascular baroreceptors control renin release?

A
  • afferent arteriole senses low pressure

- causes juxtaglomerular cells to release renin

51
Q

How do prostaglandins control renin release?

A

stimulate renin release

52
Q

How does K control renin release?

A

stimulates renin release

53
Q

How does ADH control renin release?

A

stimulates renin release

54
Q

How does ANP control renin release?

A

inhibits renin release

55
Q

What are mech of angiotensin II?

A
  • increase sympathetic activity
  • increase proximal Na/Cl reabsorption, H2O retention
  • increase K excretion
  • stimulate adrenal cortex release of aldosterone which has direct effect on principal cells [more K excretion]
  • vasoconstrict to increase BP
  • stimulate posterior pituitary to secrete ADH [which then increases collecting duct H2O absorption]
56
Q

What does erythropoietin do?

A

kidney releases erythropoietin and causes production of RBCs

57
Q

What happens to erythropoietin in people on dialysis?

A
  • people on dialysis can’t make their own erythropoietin
58
Q

What stimulates erythropoietin?

A
  • hypoxia due to decreased RBC count
  • decreased Hb
  • decreased availability of O2
59
Q

Where is ANP released? what stimulates release?

A
  • synthesized in atrial myocytes

- release stimulated by pressure changes in heart [high P, big volume]

60
Q

What does ANP inhibit?

A

ADH

angiotensin II

61
Q

What are 4 main actions of ANP?

A
  • stimulate Na and H2O loss at kidney
  • inhibit antagonist hormones [ADH/angiotensin]
  • suppress thirst
  • dilate blood vessels
62
Q

What does ANP do to renal vasculature tone? RBF? GFR? Kf? medullary blood flow?

A
  • causes vasodilation afferent arteriole
  • increases RBF
  • increases GFR
  • increases Kf [by relaxing mesangial cells]
  • increases bloodflow through vasa rect so washes out some of longitudinal gradient so you excrete more Na/H2O

Physiology Part 2 (19 decks)

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