Regulation of Extracellular Fluid Osmolarity and Sodium Concentration Flashcards

1
Q

Which hormone is a major determining factor in urine concentration?

A

ADH

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2
Q

Increase in OSMOLARITY in the body

A
  • INCREASE ADH
  • INCREASE water permeability
  • large REABSORPTION of water
  • INCREASED concentration of urine
  • no marked change in excretion of solutes
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3
Q

Osmolarity in proximal tubule

A

Stays ISOTONIC

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4
Q

Osmolarity in loop of Henle

A

-enters loops being ISOTONIC

**water is reabsorped by OSMOSIS in the DESCENDING segment of the loop of Henle

  • thin and think ascending segments are NOT permeable to water!!!
    • solutes are ACTIVELY transported out (THICK)
  • tubular fluid becomes more DILUTE as it travels up ascending segments

-leaves loop of Henle as a HYPOTONIC solution

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5
Q

T/F: renal medulla interstitial fluid is very HYPERTONIC

A

True

-tubular fluid becomes more concentrated as it travels into the medulla

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6
Q

Osmolarity in the distal tubule and collecting ducts

A
  • enters being DILUTE
  • later parts:
    • additional reabsorption of sodium
  • absence of ADH = dilute urine excreted
  • presence of ADH = concentrated urine excreted
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7
Q

Urine Specific Gravity

A
  • used as a measurement in clinical settings to assess the concentration of urine
    1) high concentration = high specific gravity
    2) low concentration = low specific gravity
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8
Q

Basic requirements for forming a concentrated urine

A

1) HIGH level of ADH

2) HIGH osmolarity in the medulla tissue

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9
Q

How do we create a hyperosmotic renal medullary interstitial fluid?

A
  • COUNTERCURRENT MECHANISM
  • juxtamedullary nephrons
  • vasa recta
  • collecting ducts
  • molarity of the renal medullary interstitial fluid
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10
Q

What is the osmolarity around the papilla of the renal pyramids?

A

~1200mOsm/L

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11
Q

Countercurrent multiplier

A

the repetitive reabsorption of NaCl by the THICK ASCENDING loop of Henle and continued inflow of new Na+ from the PROXIMAL TUBULE into the loop of Henle

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12
Q

Vasa Recta and urine concentration

A
  • Countercurrent exchangers
  • minimizes washout of solutes from the interstitium
  • preserve the high solute concentration in the renal medulla
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13
Q

A high concentration of UREA is found in the…

A

inner medullary collecting ducts

-diffusion of urea into the renal medulla (facilitated by urea transporters)

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14
Q

Thirst

A

when sodium content increases 2mEq/L above normal there is a desire to ingest fluid

**the THRESHOLD FOR DRINKING

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15
Q

Thirst center

A
  • an area along the anteroventral wall of the THIRD ventricle that promotes ADH release also stimulates thirst
  • anterolateral in the PREOPTIC NEURONS
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16
Q

Factors that increase thirst

A
  • INC plasma osmolarity
  • DEC blood volume
  • DEC blood pressure
  • INC angiotensin II
  • a dry mouth
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17
Q

Factors that decrease thirst

A
  • DEC plasma osmolarity
  • INC blood volume
  • INC blood pressure
  • DEC angiotensin II
  • gastric distension
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18
Q

Extracellular fluid volume (ECV)

A
  • determined by intake and output of fluid and sodium

- usually dependent on person’s HABITS

19
Q

Homeostatic state of ECV

A
  • must excrete almost the same amount of sodium that you take in (w/in a few days)
  • not much change in extracellular fluid
  • ADH
  • osmolality and sodium concentration are maintained
20
Q

What happens if ECV can not maintain a steady balance?

A
  • change in BP
  • change in circulating hormones
  • change in SNS
21
Q

Pressure diauresis

A

increased blood pressure raising urinary volume excretion

22
Q

Pressure natriuresis

A

the raise in sodium excretion that occurs with elevated blood pressure

23
Q

T/F: pressure diauresis and pressure natriuresis occur concurrently

A

True

24
Q

As long as the pressure diauresis mechanism is working the body will be able to handle an increase in fluid and salt intake with LITTLE change to:

A
  • blood volume
  • ECF volume
  • cardiac output
  • arterial pressure
25
Q

What circumstances would change the fact that ECF volume and blood volume are controlled together?

A
  • INC capillary hydrostatic pressure
  • DEC plasma colloid osmotic pressure
  • INC permeability of the capillaries
  • obstruction of lymphatic vessels
26
Q

T/F: an inhibition of sympathetic activity may help to rapidly eliminate excess fluid and sodium when large amounts are consumed

A

True

27
Q

What stimulates SNS activity on the kidneys?

A

an extensive decrease in blood volume (i.e., hemorrhage)

  • signals kidneys to HOLD ON TO salt and fluid
  • constriction of renal arterioles -> DEC GFR
  • increase tubular reabsorption
  • stim of renin release -> INC angiotensin II and aldosterone -> INC tubular reabsorption
28
Q

T/F: Angiotensin II level generally have a big impact on extracellular fluid or blood volume

A

FALSE; little impact

-Angiotensin II is a powerful controller of SODIUM EXCRETION

29
Q

T/F: a small increase in blood pressure causes an increase in sodium excretion when sodium levels rise

A

TRUE - due to angiotensin II

30
Q

Salt sensitivity

A

a little bit of salt will cause a large increase in blood pressure
-in these patients, renin secretion can NOT be decreased; NEED higher BP to excrete excess sodium

31
Q

Increased Aldosterone will cause

A
  • INC sodium and water REABSORPTION in the cortical collecting tubules
  • INC potassium excretion
32
Q

Increased ADH will cause

A
  • INC reabsorption of fluid

- concentrated urine

33
Q

Decreased ADH will cause

A
  • REDUCED reabsorption of fluid

- decreases fluid volume in the body

34
Q

Omsoreceptor-ADH Feedback System

A
  • water defecit
  • osmoreceptor cells in the Anterior Hypothalamus SHRINK
  • osmoreceptors cells fire and stimulate the Posterior Pituitary to RELEASE ADH
  • ADH transported in blood to kidneys
  • LATE DISTAL TUBULE, CORTICAL COLLECTING TUBULES, and MEDULLARY COLLECTING DUCTS increase water permeability
  • water reabsorption, and excretion of concentrated urine
35
Q

AV3V region

A
  • anteroventral region of the third ventricle

- signals posterior pituitary to release ADH

36
Q

Arterial baroreceptor reflexes

A

decreased arterial pressure causes an increase in ADH

37
Q

Cardiopulmonary reflexes

A

Decreased blood volume causes an increase in ADH

38
Q

Other things that increase ADH secretion

A
  • nausea
  • hypoxia
  • drugs (morphine, nicotine, cyclophosphophamide)
39
Q

Inhibitors of ADH

A
  • alcohol
  • clonidine
  • haloperidol
40
Q

Mechanisms that increase sodium excretion

A

1) activation of low pressure receptor reflexes in the right atrium and pulmonary vessels
2) suppression of Angiotensin II
3) Stimulation of natiruretic system
4) Small increase in arterial pressure

41
Q

What happens to ECF and blood volume when there’s a leakage of fluid into the interstitium?

A

INCREASE in ECF
blood volume remains same or decreases

  • kidneys sense a decrease in blood volume
  • respond by retaining salt and fluid
  • retained fluid leaks into interstinum (increased edema)
42
Q

What happens to ECF and blood volume during congestive heart failure? (or anything that increases vascular capacity, i.e. pregnancy, vericose veins)

A
INCREASE ECF (200%)
INCREASE blood volume (15-20%)
  • heart reduces ability to pump = decreased output
  • kidneys retain salt and fluid to normalize pressure
  • work well; however, extra fluid
43
Q

What happens to ECF and blood volume during Nephrotic Symdrome?

A

INCREASE ECF
blood volume remains the SAME

  • loss of large amounts of PROTEIN in urine
  • osmotic pressure in capillaries falls
  • fluid moves from capillaries to tissues
  • causes BP to fall
  • kidneys activate measures to retain water/sodium
44
Q

What happens to ECF and blood volume during Liver Cirrhosis?

A

INCREASE ECF
blood volume remains the SAME

  • liver cannot synthesize enough plasma proteins
  • osmotic pressure in capillaries falls
  • fluid moves from capillaries to tissues
  • causes BP to fall
  • kindeys activate measures to retain water/sodium
  • liver develops fibrous tissue = impedes portal blood flow
  • raises capillary pressure in the portal vascular bed
  • leakage of fluid and proteins into the peritoneal cavity