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Renal Final > Regulation of Body Fluid and Water Balance > Flashcards

Regulation of Body Fluid and Water Balance Flashcards

1
Q

What must occur for urine to be concentrated as it passes through the collecting duct?

A

Water reabsorption from tubular fluid

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2
Q

Where is tubule is osmolarity the highest (most concentrated/ saltiest) ?

A

Inner Medulla ( Loop of Henle and Collecting Duct)

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3
Q

Basic Concept of countercurrent multiplier in Loop of Henle

  • movement
  • regulation
A

produce HYPERtonic medulla by pooling NaCl in interstitium

  • favors subsequent movement of water out of the collecting duct
  • regulated by ADH
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4
Q

How much of difference is between tubular fluid and interstitium along thick, ascending limb?

A

200 mOsmol/ kg H2O

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5
Q

Maximum osmolarity of interstitium at tip of loop

A

1200-1400 mOsmol/ Kg H2O

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6
Q

What is the characteristic/value of fluid leaving Loop of Henle?

A
  • HYPOtonic

- 100 mOsmol/ kg H2O

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7
Q

First Step of Counter Current Multiplier

A
  • Tubular Fluid entering descending limb from proximal tubule is isotonic
  • Medullary interstitial fluid concentration AND body fluids are uniformly 300 mOsm/L
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8
Q

Second Step of Counter Current Multiplier

A
  • Active salt pump in ascending LOH transports NaCl out of lumen until surrounding interstitial fluid is 200 mOsm/L more concentrated than tubular fluid in this limb
  • When ascending LOH starts actively extruding NaCl, medullary interstiial fluid becomes HYPERtonic
  • no water flow in ascending LoH bc impermeable to H2O
  • Net diffusion of H2O occur from descending limb into interstitial fluid
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9
Q

Third Step of Counter Current Multiplier

A
  • Net diffusion of H2O out of Descending LoH (highly permeable to H2O) into more concentrated interstitial fluid
    • passive movement of H2O out of descending LoH continues until osmolarities in descending and interstitial fluid become equilibrated
  • Tubular fluid entering ascending LoH immediately becomes more concentrated as it loses H2O
  • At equilibrium, osmolarity of ascending limb fluid is 200 mOsm/L
  • osmolarities of interstitial fluid and descending limb fluid are equal at 400 mOsm/L
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10
Q

Fourth Step of Counter Current Multiplier

A
  • a mass of 200 mOsm/L fluid exits top of ascending limb into distal tubule -> a new mass of isotonic fluid at 300 mOsm/L enters the top of the descending limb from proximal tubule
  • At bottom of the loop, a comparable mass of 400 mOsm/L fluid from descending limb moves forward around tip into ascending limb, placing it opposite a 400 mOsm/L region in descending limb
  • additional ions are pumped into interstitium, with water remaining in tubular fluid, until a 200 mOsm/L osmotic gradient
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11
Q

Fifth Step of Counter Current Multiplier

A
  • additional flow of fluid into LoH from proximal tubule -> causes HYPERosmotic fluid previously formed in descending lumb to flow into ascending limb
  • ascending limb, additional ions are pumped into interstitium (water stays in tubular fluid) until 200 mOsm/L osmotic gradient is established, with interstitial fluid osmolarity rising to 500 mOsm/L
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12
Q

Seventh Step of Counter Current Multiplier

A
  • Step 4-6 repeated over

- net effect of fluid in descending LoH more hypertonic until max concentration (1200-1400 mOsm/L) at bottom of loop

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13
Q

Where does interstitial fluid achieve equilibrium?

What is final concentration gradient range in counter current multiplier?

A
  • in descending limb

- 300-1200 mOsm/L

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14
Q

After counter current multiplier is complete, what is concentration of tubular fluid? where? how?

A
  • decreases
  • in ascending limb as
  • NaCl is pumped out but H2O is unable to follow
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15
Q

After counter current multiplier is complete, what is tonicity of tubular fluid?

A
  • hypotonic before leaving the ascending limb to enter distal tubule
    (100 mOsm/L)
    • 1/3 the normal concentration of body fluids
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16
Q

Vasa Recta

  • function
  • signficance
A
  • supply blood to medulla
  • highly permeable to solute and water
  • remove water and solute that is continuously added to medullary interstitium by different nephron segments
  • maintains medullary interstitial gradient (flow DEPENDENT)
  • Increase vasa recta blood flow => dissipates the medullary gradient (medullary washout)
  • INCREASE blood flow= decrease salt and solute transport by nephron segments in medulla -> reduce ability to concentrate urine
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17
Q

Urea Recycling in thick limb of LoH

A

little urea reabsorption

impermeable to urea

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18
Q

Urea Recycling in distal tubule and cortical collecting tubule

A

little urea reabsorption

impermeable to urea

forms concentrated urine

secretes high levels of ADH

increase reabsorption of water

increase tubular fluid concentration of urea

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19
Q

Urea Recycling in inner medullary collecting tubule

A

Urea transporters:

  • UT-A1
  • UT- A3
  • cause urea to diffuse into medullary interstitium
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20
Q

Mechanism of urea recycling

A

some of urea that moves into medullary interstitium diffuses into thin LoH -> passes upward through ascending LoH, distal tubule, cortical collecting tubule-> down into medullary collecting duct again

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21
Q

Purpose of Countercurrent exchange

A

establish salt gradient in medulla of kidney

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22
Q

What created the medullary interstitial osmotic gradient? (2)

A

1) aquaporins and absence of tight junctions within thin limb provides a pathway for water without sodium from lumen of descending limb to interstitium of renal medulla

2) anatomic arrangement of LoH and collecting ducts contribute to “countercurrent multiplication”
- increases in osmolality as loop dips deeper into medulla
=> due to interstitial gradient, water flows out of descending limb (concentrate remaining tubular filtrate)
=> Na/K ATPase continue to extrude sodium ions and build concentration gradient

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23
Q

Anti-diuretic Hormone

  • location
  • mechanism of secretion
A
  • aka arginine vasopressin
  • Two types of large neurons that synthesize ADH in supraoptic and paraventricular nuclei of hypothalamus

stimulated by increase osmolarity (rapid) -> nerve impulses pass down these nerve ending -> change membrane permeability-> increase calcium entry -> secretory vesicles containing ADH released in nerve ending in posterior pituitary

=> plasma ADH levels increase fast-> rapid changes in renal excretion of water (more water reabsorption)

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24
Q

Mechanism pathway for ADH

  • what will inhibit pathway
A

plasma osmolality-> osmoreceptor activation-> AVP secretion from supraoptic and paraventricular nuclei-> plasma vasopressin-> vasopressin receptor activation -> inhibits water excretion, promotes water reabsorption

  • drinking water and water reabsorption will inhibit pathway
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25
Q

How sensitive are osmoreceptors? what do they activate?

A
  • sensitive to small changes in plasma osmolality (1-2%)

- activate ADH pathway and thirst stimulation

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26
Q

Which one is activated first? thirst pathway or ADH pathway?

A

ADH pathway before thirst pathway

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27
Q

What happens when there is an increase in plasma concentration? How is this significant in daily life?

A

concentrate urine and later thirst develops

adequate timing allows us to go about our daily activity, conserving water through concentrating urine rather than constantly being thirsty

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28
Q

Two Cell Types found in late distal tubule and collecting duct

A

Principal cells

Intercalated Cell

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29
Q

Principal Cells

  • function
  • mechanism (4)
A

reabsorbs Na+, Cl-, and H2O
secrete K

1) Na reabsorption
- Na actively transported using Na/K ATPase across basolateral membrane
2) H2O absorption occurs in response to effect of ADH on principal cells
3) ADH increase H2O permeability by directing the insertion of H2O via aquaporin-2 channels in luminal membrane
- no ADH= principal cells impermeable to water
4) K secretion
- K uptake across basolateral membrane occurs via Na/K ATPase -> diffusion down its electrochemical gradient across apical membrane into tubular fluid

30
Q

Intercalated cells

  • function
  • mechanism
  • significance
A

reabsorbs K
secretes H

Aldosterone increases H+ secretion by intercalated cells by stimulating H+ Atpase
- important for acid-base balance

31
Q

Aldosterone

  • function
  • mechanism steps (3)
  • effects with K and Na
A
  • salt retaining hormone
  • released from adrenal cortex
  • responds to angiotensin II or increase plasma K

1) Aldosterone=> increase ENaC channels => increase sodium reabsorption
2) Sodium tranported into interstitial fluid in exhange for K+
3) Potassium exits cells=> increase urinary excretion and excess K elimination

increase K= increase aldosterone
decrease K= decrease aldosterone
decrease plasma Na= increase aldosterone ( via RAAS)
* increase aldosterone= increase NA reabsorption and K secretion

32
Q

Aquaporin 2 Channel

  • location
  • function
  • what happens when less ADH
  • regulates what?
A

apical membrane of principal cells

  • water osmotically pulled from collecting duct into interstitial space=> more concentrated urine
  • Less ADH= less aquaporin channels inserterd= less water is recovered => dilute urine
  • regulates blood osmolarity, blood pressure, and osmolality of urine
33
Q

Cortical collecting duct vs medullary collecting duct in relation to water

A

Cortical CD always permeable to water

Medullary CD depends on ADH secretion (hypothalmic osmoreceptors to plasma osmolality and volume)

34
Q

What happens when ADH is secreted?
where does it travel to?
what does it stimulate?
-effects

A

travels to kidney

stimulates insertion of aquaporins into tubular membrane

allow water to move by osmosis into hypertonic interstitium

35
Q

What causes stimulation ADH secretion? cessation of ADH secretion?

A

increase plasma osmolality = stimulate ADH secretion (collecting tubule permeable to water)

  • water goes into hypertonic interstitium via osmosis
  • less water excreted=> decreased osmolality

decrease plasma osmolality= decrease ADH secretion (collecting tubule impermeable to water)
- excess water excreted into urine=> increase plasma osmolarity

36
Q

What is simple rules of ADH?

  • normal plasma osmolality value
  • value for dehydrates
A

Overhydrated=> ADH inhibited

Dehydrated=> ADH released

normal= 275-295 mOsm/kg
dehydrated > 300 mOsm/kg

37
Q

Diabetes Insipidus

2 types

A

1) Failure to produce ADH
- Central Neurogenic Diabetes Insipidus

2) Inability of Kidneys to respond to ADH
- Nephrogenic Diabetes Insipidus

38
Q

Central Neurogenic Diabetes Insipidus

  • causes
  • mechanism
  • treatment
A
  • can’t produce/release ADH in posterior pituitary
  • caused by head injury/infection, congenital, or unconsciousness ( severe dehydration can rapidly occur)
  • no ADH= distal tubular segments cannot reabsorb water
    • > diluted urine

Treatment:

  • water restriction
  • desmopressin (acts selectively on V2 receptors -> increase water permeability in late distal and collecting tubules-> restore urine output to normal
39
Q

Nephrogenic Diabetes Insipidus

  • causes
  • effects
A

ADH present but renal tubular segments cannot respond appropriately

Causes

  • failure of countercurrent mechanism that would normally lead to a hyperosmotic renal medullary interstitium
  • failure of distal and collecting tubules and CD to respond to ADH
  • drugs ( lithium/ tetracyclines) impair ability of distal nephron to respond to ADH

Effects

  • diluted urine
  • body= dehydration
  • compromised urine-concentrating ability
40
Q

Central vs. Nephrogenic diabetes

A

** distinguished by administration of desmopressin

injection of desmopressin => 2 hours later=> decrease of urine volume and increase of urine osmolarity
- if this effect doesn’t show up => will indicate nephrogenic diabetes insipidus

** low sodium diet and thiazide diuretic will help hypernatremia of nephrogenic DI

41
Q

SIADH

A

Such Immense Anti Diuretic Hormone Secretion

  • excessive release of ADH => excessive water retention ( Increase ECF)
  • > decreased plasma osmolality, hyponatremia, diminished aldosterone secretion, increased GFR
  • > increased Na excretion

ECF is hypotonic to cell
Cell is hypertonic to ECF
- fluid shift to cells => cells swell ( water intoxication)

42
Q

Diabetes Insipidus vs SIADH

A

DI

  • high urinary output
  • low ADH levels
  • hypernatremia
  • dehydrated
  • lose too much fluid
  • Excessive thirst

SIADH

  • low urinary output
  • high levels of ADH
  • hyponatremia
  • overhydrate
  • retain too much fluid
  • Excessive Thirst
43
Q

What part of the nephron depends on Dilution? Why?

A

thick ascending limb of loop of Henle

  • solutes (Na, Cl, K) are reabsorbed here without water
  • impermeable to water
44
Q

Water Excess

A
  • large volume of dilute urine
  • no ADH is secreted
  • urine flow rate is increased
45
Q

Water Deficit

A
  • small volume of concentrated urine
  • ADH secretion increased
  • H2O reabsorption
46
Q

Hyponatremia

- causes

A
  • excess of water relative to solute in body
  • develops as a result of ADH in kidney to diminish free water excretion
  • drugs, pain, nausea, decreased effective arterial volume, strenuous exercise
  • water intoxication <100 mOsm/kg (urine osmolality)
  • low solute intake
47
Q

Hypernatremia

A

deficit of free water relative to solute

due to impaire access/ thirst
- inadequate free water intake

  • volume depletion

high salt intoxication
diabetes insipidus

48
Q

Polyuria

- mechanism (4)

A
  • passage of excessive quantity of urine
  • water/solute diuresis of 2.5-3L/ day
  • urine volume of more than 40 ml/kg/day

associated with polydipsia (water intake of more than 6L/day)

1) increase intake of fluid (psychogenic causes, stress, anxiety)
2) increased GFR
(hyperthyroidism, fever, hypermetabolic states)
3) increased output of solute ( DM, hyperthyroidism, hyperparathyroidism, diuretics)
4) inability of kidney to reabsorb water in DCT (CDI, NDI, drugs, chronic renal failure)

49
Q

Water diuresis

- causes

A
  • increased water excretion without corresponding increase in salt excretion

Causes:

  • increase intake of water
  • polydipsia
  • diabetes insipidus
50
Q

Solute (osmotic) diuresis

- causes

A
  • increased water excretion concurrent with increased salt excretion

Causes:

  • significant increase in salt in tubular fluid
  • NaCl
  • hyperglycemia
  • high protein intake
  • recovery from AKI
51
Q

Minimum amount of solute human must excrete

A

700 -1000 mOsm/ day

52
Q

Maximal volume of concentrated urine

A

1200 mOSm/L

53
Q

Obligatory Urine Volume

A
  • minimal volume of urine that must be excrete
    0. 5 L/ day

if less than 0. 5 L/ day=> oliguria

54
Q

Free Water Clearance

  • if (+)? (-)?
  • equation
A

rate at which solute-free water is excreted by kidneys

(+)= excess water is being excreted by kidneys

(-) = excess solutes are being removed by blood by kidneys and water is being conserved

  • urine osmolarity > plasma osmolarity
  • water conservation

C= V (urine flow rate)- C = V- (Ux V)/P

55
Q

Ratio of Urine Osmolality to plasma osmolality

A

determine ability of kidneys to concentrate/dilute urine

if >1= concentrated urine
if 1= isoosmotic with plasma
if <1= dilute urine

56
Q

Conditions that increased osmolality

  • Serum
  • Urine
A

Serum

  • dehydration/ sepsis/ fever/ sweating/ burns
  • DM
  • DI
  • uremia
  • hypernatremia
  • ethanol, methanol, ethylene glycol ingestion
  • mannitol therapy

Urine

  • dehydration
  • SIADH
  • adrenal insufficiency
  • glycosuria
  • hypernatremia
  • high protein diet
57
Q

Conditions that decrease osmolality

  • Serum
  • Urine
A

Serum

  • excess hydration
  • hyponatremia
  • SIADH

Urine

  • DI
  • excess fluid intake
  • acute renal insufficiency
  • glomerulonephritis
58
Q

Negative C H2O

A

excess solutes are removed

water conservation

59
Q

Positive C H2O

A

water is being excreted
dilute urine
water excess

60
Q

What is the mechanism for when plasma osmolality if high?

think in relation to K+

A
  • Water is being removed from plasma by kidneys meaning plasma is becoming more concentrated
  • Plasma becomes more concentrated than more k channels are created from principals cells on apical surface
  • More K leave inside of principal cells ( high to low concentration ) and becomes excreted in urine
  • MORE potassium being excreted in urine
61
Q

Head Trauma

A

Neurogenic diabetes insipidus

  • Dysfunction of hypothalamic- pituitary axis attributed to direct mechanical impact to acceleration-deceleration effect in motor vehicle accidents
  • Changes in rotational velocity of head are the main mechanism of post- traumatic damage of hypothalamo-pituitary unit

-Damage of hypothalamic ADH producing neurons, their axons or posterior pituitary leads to post-traumatic central DI

62
Q

What happens when you have too much H2O? (think plasma osmolality)

A

Plasma osmolality decrease -> hypothalamic osmoreceptors will turn ADH off -> dilute urine -> water excreted -> plasma osmolarity increased back to normal

63
Q

What happens when you have too much solute?

A

Plasma osmolality increase -> hypothalamic osmoreceptors will turn ADH on AND increase thirst -> concentrate urine -> solute excreted -> plasma osmolarity decreased back to normal

64
Q

Adenosine receptor antagonists

A
  • Caffeine and theophylline
  • Modest non-specific inhibition of adenosine receptors
    ○ NHE3 ( na/h exchanger) in proximal convoluted tubule
    ○ Interfere with adenosine-mediated enhancement of the collecting tubule K secretion
  • Basis for new pharmacological research
    Viable selective A1 antagonist
65
Q

Polyuria

  • definition
  • Volume
  • causes
A

excessive urine production

> 2.5 L/day

Diabetes Mellitus
Diabetes insipidus
excess caffeine or alcohol
kidney disease
certain drugs (diuretics)
sickle cell anemia
excessive water intake
66
Q

Oliguria

  • definition
  • Volume
  • causes
A

Output below minimum volume

300-500 ml/day

Dehydration 
Blood loss
diarrhea
cardiogenic shock
kidney disease
enlarged prostate
67
Q

Anuria

  • definition
  • Volume
  • causes
A

Virtual Absence of urine

<50ml/day

Kidney failure
Obstruction such kidney stone or tumor
Enlarged prostate

68
Q

ADH characteristics

  • is it measurable
  • effect of high ADH? what is sodium controlled by now?
  • what does increase intake mean?
A
  • cannot measure ADH directly
  • high ADH can cause hyponatremia
    • sodium is no longer controlled by ADH, will be by free water

-increase intake mean diluted plasma equal hyponatremia

69
Q

Hyponatremia

  • definition
  • values
A

urine diluted

more free water than solutes

low urine osmolality
low urinary sodium

serum Na <135
serum osmolality <280

70
Q

How do you know if kidney is responding appropriately during hyponatremia?

A

1) if urine diluted = good
- bc ADH levels are low
- problem outside kidney

2) if urine NOT diluted
- too much ADH
- problem within kidney

71
Q

SIADH

  • definition
  • symptoms
A

too much ADH

hyponatremia - high urinary Na (>40 meq/L)

high urinary osmolality (>100 mOsm/kg)

Renal Final (7 decks)

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