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Renal Exam 2 > Reg of Body Fluid Osmolality-Regulation of Water Balance > Flashcards

Reg of Body Fluid Osmolality-Regulation of Water Balance Flashcards

1
Q

Any mechanism that will concentrate urine must be able to reabsorb _ from the tubular fluid as it passes through the collecting ducts

A

Water

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2
Q

_ acts as a countercurrent multiplyer and produces a _ medulla by pooling _ in the interstitium

A

Loop of Henle

hypertonic

NaCl

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3
Q

Maximum osmolarity at the tip of the LOH

The fluid leaving the LOH is _

A

1200-1400 mOsm

Hypotonic

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4
Q

The tubular fluid entering the LOH from the proximal tubule is _

A

Isotonic

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5
Q

The descending LOH is permeable to _ but impermeable to _

This creates a _ solution at the tip of the LOH

The ascending LOH is permeable to _ but impermeable to _

This creates a _ solution

A

Water

Solutes

Hypertonic

Solutes

Water

Hypotonic

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6
Q

Steps of fluid flow through the LOH

A
  1. Tubular fluid entering the descending limb is isotonic
  2. As fluid flows thru descending LOH, tubular fluid becomes more concentrated (losing water, retaining salt)
  3. As fluid flows thru ascending LOH, tubular fluid becomes less concentrated and interstitial fluid becomes MORE concentrated
  4. The more concentrated interstitial fluid created from salt reabsorption in the ascending LOH creates an osmotic gradient for water to be reabsorbed into the interstitial fluid
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7
Q
  • Functions of the vasa recta
A
  • Supply blood to medulla
  • Remove water and solute that is continuously added to the medullary interstitium
  • Ability to maintain interstitial gradient is flow dependent
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8
Q

An increase in vasa recta blood flow _ the medullary gradient

A

Decreases

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9
Q
  • Decreased blood flow to the vasa recta _ salt and solute transport
A

Decreases

Reduces ability to concentrate the urine

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10
Q
  • Where are UT-A1 and UTA-3 transporters found?
  • What is their function?
A
  • Apical membrane of medullary collecting duct
  • Urea recycling
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11
Q
  • Where are UT-A2 transporters located?
  • What is their function?
A
  • Apical membrane of Descending LOH
  • Reabsorb Urea into tubular fluid and Urea recycling
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12
Q
  • How much urea is reabsorbed in the PCT?
A
  • 50%
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13
Q
  • Steps for Urea Recycling
A
  • Urea flows into inner medullary collecting duct
  • Via UT-A1 and UT-A3, urea diffuses into medullary interstitium
  • Urea can go three different directions
    • Can go thru UT-A2 back into descending LOH
    • Can diffuse thru ascending LOH
    • Can be excreted in urine (~20%) [If it doesn’t go thru UR-A1 and UR-A3]
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14
Q
  • What created the medullary interstitial osmotic gradient?
A
  • AQP channels and absence of tight junctions in the thin descending LOH creates path for h20 movement
  • Anatomic arrangement of LOH and collecting ducts (countercurrent multiplication)
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15
Q
  • What area of the brain secretes ADH?
A
  • Posterior pituitary
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16
Q
  • Where is ADH synthesized?
A
  • Supraoptic and paraventricular nuclei of hypothalamus
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17
Q
  • Supraoptic and paraventricular nuclei are stimulated by _
  • This causes nerve impulses to pass down nerve endings and altering membrane permeability to _
  • _ from the secretory vesicles of nerve endings is released
A
  • Increases in plasma osmolarity
  • Ca2+
  • ADH
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18
Q
  • Osmoreceptors are sensitive to what percentage of changes in plasma osmolarity?
  • What two pathways are stimulated as a result?
  • Which pathway is activated first?
A
  • 1-2% increase
  • ADH pathway and thirst pathway
  • ADH pathway
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19
Q
  • What two cell types are found in the late distal tubule and collecting duct?
  • What is their primary function
A
  • Principal cells
    • Reabsorb Na+, Cl- and H2O and secrete K+
  • Intercalated cells
    • Reabsorb K+
    • Secrete H+
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20
Q
  • How do principal cells reabsorb Na+?
  • How do principal cells help with water reabsorption?
  • How do principal cells secrete K+?
A
  • Reabsorb Na+ thru Na+/K+ ATpase across basolateral membrane of distal tubule and collecting duct
  • Principal cells respond to ADH by inserting AQP2s on the apical membrane of the distal tubule and collecting duct
  • K+ is brought into the cells of the distal tubule and collecting duct via the Na+/K+ ATPase, and then K+ diffuses down electrochemical gradient into tubular fluid
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21
Q
  • How do intercalated cells secrete H+?
A
  • Aldosterone
  • Stimulation of the H+ ATPase on Apical surface of intercalated cells
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22
Q
  • What causes a release of aldosterone from the adrenal cortex?
  • What is the overall effect of aldosterone?
A
  • Directly released in response to increases in plasma K+
  • Angiotensin II
  • Decrease in plasma Na+ concentration stimulates aldosterone secretion by means of RAAS pathway
  • Overall effect is to increase Na+ reabsorption and K+ secretion
23
Q
  • Aldosterone increases which type of channels
  • What does this cause
A
  • eNACs on the APICAl surface of the distal tubule and collecting duct
  • Increased Na+ reabsorption
  • K+ secretion
24
Q
  • How many Na+ ions does the eNaC transport into the cell?
25
Q

_ collecting ducts are IMpermeable to water at all times

26
Q
  • Permeability of the medullary collecting ducts to water is controlled by secretion of which hormone?
27
Q
  • When there is a _ in plasma osmolarity, ADH secretion is decreased
  • This leads to the production of _ urine and excretion of _
  • This _ the plasma osmolarity back to normal
A
  • decrease
  • dilute, water
  • increases
28
Q
  • When there is an _ in plasma osmolarity, ADH secretion is increased
  • This leads to the production of _ urine and excretion of more _
  • Plasma osmolarity _ back to normal (via reabsorption of more water)
A
  • Increase
  • Concentrated, Solutes
  • Decreases
29
Q
  • Besides an increase in ADH secretion, an increase in plasma osmolarity also results stimulation of _
  • This leads to an _ in water intake
A

Thirst

Increase

30
Q
  • People who are dehydrated have more or less ADH release?
  • People who are overhydrated have more or less ADH release?
A

MORE

LESS

ADH is produced when you are DEHYDRATED

31
Q
  • What are the two types of diabetes insipidus?
A
  • Central “Neurogenic”
    • Failure to produce or release ADH
  • Nephrogenic
    • Kidneys cannot respond to ADH
32
Q
  • Clinical presentation of patient with central “neurogenic” diabetes insipidus
  • Tx
A
  • Head injury/congenital defect
  • Forming large volumes of dilute urine (can exceed 15 L/day)
  • When water intake is restricted, severe dehydration can rapidly occur
  • Desmopressin-synthetic analog of ADH
    • ​Acts on V2 receptors to increase water permeability in late distal and collecting tubules
33
Q
  • Clinical presentation of patient with neprhogenic diabetes insipidus
  • What medications can make sx worse?
A
  • Normal or elevated ADH levels
  • Failure of countercurrent mechanism to form hyperosmotic renal medullary interstitium or failure of distal and collecting tubules to respomd to ADH
  • LARGE volumes of dilute urine are formed, causing dehydration unless fluid intake is increased by SAME amount that urine volume is increased
  • Lithium Tetracyclines Loop Diuretics
34
Q
  • ****How can you distinguish between central and neprhogenic diabetes insipidus?****
A
  • Administration of desmopressin
  • If patient responds, they have central diabetes insipidus
  • Have nephrogenic diabetes insipidus if they do not respond
35
Q
  • What is SIADH?
A
  • Inappropriate secretion of ADH
  • Inappropriate excess water retention
  • Disturbances in fluid and electrolyte balance
  • Fluid shifts into swells (can cause water intoxication)
  • LOW NA+ LEVELS (more Na+ is being excreted)
36
Q

Dilution is dependent on the _ of the LOH

A

Thick ascending Limb

(Because solutes are reabsorbed here without water)

37
Q
  • What happens to ADH secretion if a person consumes large quantities of water?
A
  • Decreased
  • Increased volume of dilute urine produced
  • Filtrate entering the distal tubule has osmolarity of 100 mOsm
38
Q
  • What happens to ADH secretion if a person is dehydrated?
  • What is the net result?
A
  • Increase
  • Increase H2O reabsorption through AQP2s on the Basolateral surface? of the distal tubule and collecting ducts
  • Also increase in solute excretion
  • Small volume of concentrated urine produced
39
Q
  • What is hyponatremia?
  • How does it develop?
A
  • Low Sodium relative to water in body
  • ADH diminishing excretion of free water
  • Also can develop from drugs, pain, nausea, decreased afferent arteriole volume, strenuous exercise
40
Q
  • What is hypernatremia?
  • How does it develop?
A
  • Deficit in free water relative to solute (basically saying you have excess Na+)
  • Inadequate free water intake
  • Usually associated with concurrent volume depletion
41
Q
  • What is a normal urine volume?
42
Q
  • What is polyuria?
  • What are some causes?
A
  • Excess urine production (>2.5 L/day)
  • Diabetes mellitus
  • Diabetes insipidus
  • Excess caffeine or alcohol
  • Diuretics
  • Sickle Cell Anemia
  • Excessive Water Intake
43
Q
  • What is oliguria?
  • What are some causes?
A
  • Output below mimimum volume (300-500 mL/day)
  • Dehydration
  • Blood Loss
  • Diarrhea
  • Cardiogenic Shock
  • Kidney Disease
  • Enlarged Prostate
44
Q
  • What is anuria?
  • What are some causes?
A
  • Virtual absence of urine production (<50 mL/day)
  • Kidney failure
  • Obstruction (kidney stone or tumor)
  • Enlarged prostate
45
Q
  • What are the four mechanisms that can cause polyuria?**
A
  1. Increased intake of fluids
  2. Increased GFR
    1. Hypothyroidism
      Fever
    2. Hyopermetabolic states
  3. Increased output of solutes
    1. DM
    2. Hyperthyroidism
    3. Hyperparathyroidism
    4. Diuretics
  4. Inability of the kidney to reabsorb water in the DCT
    1. CDI
    2. NDI
    3. Drugs
    4. CRF
46
Q
  • What is water diuresis?***
  • What can cause it?
A
  • Increased water excretion without increase in salt excretion
  • Primary cause-increased intake of water
    • Polydipsia
    • Diabetes Insipidus
47
Q
  • What is solute (osmotic) diuresis?***
  • What causes it?
A
  • Increased water excretion with increased salt excretion
  • Primary cause=increase in salt present in the tubular fluid
    • IV NaC;
    • Hyperglycemia
    • High Protein Intake
    • Recovery from AKI
48
Q
  • How do you calculate FREE WATER CLEARANCE?
A

Ch2o= V-Cosm

CH2O=V-(Uosm x V/Posm)

V should be in mL/min

If free water clearance is +, excess water is being excreted by the kidneys

If free water clearance is -, excess solutes are being removes and water is being conserved

Whenever urine osmolarity is > plasma osmolarity, free water clearance will be negative, indicating water conservation

49
Q
  • Ratio of urine osmolarity
  • Uosm:Posm >1
  • Uosm:Posm =1
  • Uosm:Posm < 1
A
  • >1 indicates that the kidneys are able to concentrate the urine
  • =1 indicates that water and solute are being excreted in a state that is iso-osmotic with plasma
  • <1 indicates that kidneys are able to dilute urine
50
Q
  • What can cause an increase in serum osmolarity?
A
  • Dehydration/sepsis/fever/sweating/burns
  • Diabetes mellitus (hyperglycemia)
  • Diabetes insipidus
  • Uremia
  • Hypernatremia
  • Ethanol, methanol, ethylene glycol ingestion
  • Mannitol therapy
51
Q
  • What can cause an increase in urine osmolarity?
A
  • Dehydration
  • SIADH
  • Adrenal insufficiency
  • Glycosuria
  • Hypernatremia
  • High Protein Diet
52
Q
  • What can cause a decrease in serum osmolarity?
A
  • Excess hydration
  • Hyponatremia
  • SIADH
53
Q
  • What can cause a decrease in urine osmolarity?
A
  • Diabetes insipidus
  • Excess fluid intake
  • Acute renal insufficiency
  • Glomerulonephritis
54
Q
  • Diabetes insipidus v/ SIADH

Renal Exam 2 (8 decks)

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