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GIR Test 2 > B5.040 Renal Physiology III: Regulation of Extracellular Fluid Volume and Osmolarity > Flashcards

B5.040 Renal Physiology III: Regulation of Extracellular Fluid Volume and Osmolarity Flashcards

1
Q

what is regulated to maintain ECF volume

A

Na+ intake and excretion

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2
Q

what is regulated to maintain ECF osmolarity

A

water intake and excretion

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3
Q

water balance in the body

A

2.4 L/day intake (2 L ingested, 0.4 L from metabolism)

loss of 2.4 L/day (1.5 L from kidney, 0.4 L from skin and lungs, and 0.1 L from intestine)

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4
Q

what controls water uptake

A

mechanism of thirst

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5
Q

what controls water elimination

A

reabsorption in the kidney

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6
Q

discuss the mechanisms involved when there is an increase in extracellular fluid osmolarity

A

rise in osmolarity > stimulated thirst center and osmoreceptors > water ingestion stimulated by thirst center > ADH production stimulated by osmoreceptors > ADH stimulates reabsorption of water from collecting duct > urine osmolarity increases and volume decreases

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7
Q

what portions of the nephron are the key players in water reabsorption

A

proximal tubule- automatic fashion

distal/collecting tubule- regulated by ADH

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8
Q

other name for ADH

A

AVP

arginine vasopressin

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9
Q

where is ADH synthesized

A

hypothalamus

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10
Q

discuss the relationship between plasma oncotic concentration and ADH release

A

linear relationship, a small variation in osmolality can cause immediate changes in ADH
basal ADH = 2ish
max effective concentration of ADH on kidneys = 4ish

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11
Q

pressure/volume changes effects on ADH release

A

decreases in pressure and volume both cause release of ADH

ADH is more sensitive to osmotic changes than to pressure/volume changes, however

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12
Q

general function of ADH

A

establishes a high water permeability at the distal and predominantly collecting tubules
causes water to be rapidly reabsorbed
urine volume diminishes and osmolarity increases

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13
Q

relationship between plasma ADH levels, urine osmolality and flow rate

A

low ADH = max flow, min osmolality

high ADH = min flow, max osmolality

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14
Q

mechanism of ADH in renal tubule

A

binds to V2 receptor on BM
activates cAMP and thus PKA
phosphorylation of aquaporin 2 molecules cause them to move to the membrane
once in membrane, aquaporins facilitate reabsorption of water from lumen

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15
Q

mechanism of ADH in vasculature

A

binds to V1 receptor on smooth muscle cell
stimulates Ca2+ entry into cell and release from sarcoplasmic reticulum in cell
increased Ca2+ conc increased actin-myosin coupling
vasoconstriction is triggered

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16
Q

discuss the countercurrent exchange mechanism of the loop of henle

A

descending loop: permeable to salt and water, water flows out and salt flows in to equilibrate with the medulla, generating an extremely hypertonic solution at the bottom of the loop
ascending loop: permeable to salt but NOT water, salt pumped out against gradient by NKCC yielding an extremely hypotonic solution at the top of the loop

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17
Q

discuss the effect of the countercurrent mechanism on the distal and collecting tubules

A

receive hypotonic solution from loop of henle

in presence of ADH, transport excess fluid out of tubule into ISF down the conc gradient into the salty medulla

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18
Q

descending loop of henle

A

concentrating segment

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19
Q

ascending loop of henle

A

diluting segment

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20
Q

discuss the vasa recta as a part of the countercurrent exchange mechanism

A

very slow rate of blood flow in a hairpin formation
allows blood to flow through cortex without disturbing osmotic gradient
both limbs of vasa recta permeable to salt and waterr

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21
Q

recycling of urea as a part of the countercurrent exchanger

A

urea concentrated in medullary ISF and in the tubular fluid
inner medullary collecting duct is permeable to urea and there is a gradient for passive diffusion of urea into medullary ISF
urea then diffuses from ISF into vasa recta
as vasa recta ascends, urea diffuses back into the ISF and then back into the descending capillary

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22
Q

primary engine of the countercurrent mechanism

A

reabsorption of salt without water by the thick ascending limb of the loop of henle

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23
Q

where are salt and urea trapped and why

A

medulla
countercurrent flow arrangement traps them while minimizing the water that enters
establishes a gradient to be capitalized on by the collecting tubule when ADH is present

24
Q

factors affecting the kidney’s ability to concentrate the urine

A
  1. length of loops of henle (modifies vertical osmotic gradient)
  2. ADH levels that control water permeability in the collecting tubule
  3. blood flow rate through the medullary capillaries (when increased, more salt is reabsorbed from the interstitium and countercurrent effect decreases)
  4. factors that influence concentration of urea, higher urea in medulla favors countercurrent mechanism
  5. drugs and diuretics that affect salt reabsorption in the loop of henle inhibit countercurrent effect
25
Q

describe the process of water diuresis

A

excess water ingested (polydipsia) > decreased extracellular fluid osmolarity > decreased ADH secretion > decreased permeability of distal nephron to water reabsorption > solute reabsorption continues > increased urine dilution

26
Q

diabetes insipidus

A

defect in ADH-dependent water reabsorption

27
Q

max water excretion

A

20 L/day

11% of GFR

28
Q

polyuria

A

> 3 L of water per day

29
Q

describe the process of solute diuresis

A

excess solutes in the filtrate > decreased water reabsorption in the proximal tubule > partial, but insufficient compensation by distal tubule reabsorption > urine osmolarity isotonic or close to plasma > increased urine volume

30
Q

why might there be excess solutes in the filtrate

A

due to presence of osmolites

inhibition of salt reabsorption by diuretics

31
Q

response to: loss of water > solutes

A

water reabsorption
urine volume decreases
urine concentration increases

32
Q

response to: excess water over solutes

A

water excretion
urine volume increases
urine concentration decreases

33
Q

response to: excess of isotonic fluid

A

water and solute excretion
urine volume increases
urine concentration isotonic

34
Q

range of urine osmolarity

A

50-1200 mOsmole/kg H2O

35
Q

range of urine volume

A

0.5 to 20 L

36
Q

which 4 parallel effector pathways are stimulated by changes in effective circulating volume

A
  1. renin-angiotensin system
  2. sympathetic nervous system
  3. ADH
  4. ANP
    these all act on the kidney to change reabsorption of salt or modify renal hemodynamics
37
Q

ADH actions at low vs high levels

A

levels under 5 = major effect on tubular water absorption
levels above 5 = have reached maximum effect on kidneys, exert additional effect by causing vasoconstriction of arterioles

38
Q

4 primary natriuretic peptides, their location, and their stimulus for release

A

ANP - atria - increased heart volume
BNP - ventricle - increased heart volume
CNP - brain - increased intravascular volume
urodilatin - kidney- increased volume and Na+ load

39
Q

mechanism of action of NPs on vascular cells

A

opposite of ADH

caused vasodilation

40
Q

mechanism of action of NPs on collecting duct cells

A

inhibit Na+ reabsorption by down regulating ENac channel

41
Q

how do NPs differ from the other 4 mechanisms involved in volume regulation

A

only mechanism that products from TOO MUCH volume, all others worried about too little volume

42
Q

effect of NPs on juxtaglomerular apparatus

A

increased blood volume > increased ANP released from atria > afferent arteriole vasodilation > increased GFR > increased Na+ load to macula densa > decreased renin release > increased salt and water excretion, decreased BP

43
Q

effects of NPs on adrenal corext

A

decrease aldosterone to increase salt and water excretion and decrease BP

44
Q

if u don’t know the renin-angiotensin-aldosterone system yet r u even TRYING

A

ugh idk i just really don’t want to type it out again

45
Q

what is the ~new~ function of angiotensin II tho

A

stimulates ADH release to stimulate water reabsorption in collecting duct

46
Q

stimuli of increased renin release

A

decreased BP
decreased Na+ delivery to macula dense
increased sympathetic activity

47
Q

how does sympathetic nerve activity influence blood volume

A

decreased atrial volume > stimulates sympathetic nerve activity > acts on renin angiotensin system BUT also directly stimulates tubular reabsorption via a receptors

48
Q

effects of all pathways to an increased filling volume in the atria

A
  1. decreased ADH
  2. increased ANP
  3. decreased renin secretion
  4. decreased sympathetic discharge
    INCREASE SALT AND WATER EXCRETION
49
Q

sensors of ECF volume

A

baroreceptors

volume receptors

50
Q

sensors of ECF osmolarity

A

hypothalamic osmoreceptors

51
Q

effector pathways of ECF volume regulation

A

ADH
ANP
renin-angiotensin-aldosterone
sympathetic nerves

52
Q

effector pathways of ECF osmolarity

A

ADH

thirst

53
Q

effects of regulatory pathways on ECF volume

A

short term: heart, vessels

long term: kidneys

54
Q

effects of regulatory pathways on ECF osmolarity

A 
kidney
brain (water intake)
55
Q

what is regulated for ECF volume

A

short term: BP

long term: Na+ excretion

56
Q

what is regulated for ECF osmolarity

A

renal water excretion

water intake

GIR Test 2 (20 decks)

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