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Semester 3 - Urinary > Session 5 - Blood Osmolarity > Flashcards

Session 5 - Blood Osmolarity Flashcards

1
Q

What happens in terms of plasma osmolality when water intake is less than water excretion?

A

• Plasma osmolarity increases

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2
Q

In what situation does plasma osmolarity decrease?

A

• When water intake is greater than water excretion

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3
Q

What is the typical osmolarity of urine?

A

• 50-1200 Osm/l

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4
Q

Do changes in water balance affect volume?

A
  • No, they effect osmolarity

* Problems with Na+ balance affect

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5
Q

What is the osmolarity of body fluids?

A

275 - 295 mOsm/kg

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6
Q

What do problems with Na+ balance cause?

A

• Changes in ECF volume

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7
Q

Where is plasma osmolality sensed?

A

• By hypothalamic osmoreceptors in the organum vasculoum of the laminae terminals (OVLT) of the hypothalamus

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8
Q

Where is the OVLT found?

A

• Anterior and ventral to the third ventricle

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9
Q

What is special about the OVLT?

A

• Fenestrated leaky endothelium which exposes it directly to systemic circulation

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10
Q

What are the two efferent pathways which regulate osmolarity?

A
  • Thirst

* ADH

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11
Q

Which method of regulation is the first line of defence in modulating osmolarity?

A

ADH

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12
Q

What two changes trigger release of ADH?

A
  • Increase in osmolarity of the blood

* Baroceptors detecting decreased stretch (low blood volume)

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13
Q

What are the effectors of thirst, and what is affected?

A

• Brain - Drinking behaviour

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14
Q

What is the effector of ADH, and what is the consequence?

A
  • Kidney

* Renal water excretion

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15
Q

When is ADH released?

A

• When water is lost and osmolarity increases by 1%, osmoreceptors in the hypothalamus initiates release of ADH from posterior pituitary

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16
Q

How is ADH secretion inhibited?

A

Decreased osmolarity

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17
Q

What is thirst stimulated by?

A
  • Large increase in fluid osmolarity

* <10% changes in osmolarity or decrease in volume

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18
Q

What is drinking induced by?

A
  • Increase in plasma osmolarity

* Decrease in ECF volume

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19
Q

When is ADH released stimulated?

A

• When there is a 1% increase in plasma osmolarity due to loss of water

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20
Q

Describe ADH

A
  • Small peptide hormone

* 9 AA long

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21
Q

What initiates the release of ADH?

A

• Osmoreceptors in the OVLT of the hypothalamus initiate the release of ADH from the posterior pituitaruy

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22
Q

What does ADH act on to regulate volume and osmolarity of urine?

A

• The kidney

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23
Q

What happens if ADH is low?

A

• Water diuresis will occur due to decreases reabsorption

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24
Q

What happens if ADH is high?

A

• Small volume of urine excreted

25
Q

What are the three main effects of ADH?

A
  • Increases the permeability of the collecting duct to water via the addition of aquaporin
    • Increases permeability of collecting duct to urea
    • Increases activity of Na/K/Cl- co-transporter in the TAL of the loop of henle (Assists in generation of hypertonic medullary intersticium)
26
Q

Where is ADH secreted from?

A

• The posterior pituitary

27
Q

Where is ADH synthesised?

A
  • As a preprohormone in the
    • Supraoptic nuclei of hypothalamus
    • Paraoptic nuclei of hypothalamus
    • Is then sent to posterior pituitary and stored
28
Q

Outline the effects of ADH on the nephron

A
  • Vasoconstriction at glomerulus
    • Increased Na/K+/2Cl- cotransport absorption at ascending limb of loop of henle
    • Increased water reabsorption in late DT and Cortical collecting duct via addition of aquaporin 2 to the apical membrane
    • Increased K+ secretion of and Urea reabsorption in cortical collecting duct
    • Insert aquaporin 2 in the apical membrane of cells in collecting duct
29
Q

What exactly does ADH in relation to Urea?

A
  • Increases permeability of medullary region of collecting duct, causing its reabsorption
    • Rise in urea concentration in the tissues allows it to passively move down its conc gradient into the ascending limb
30
Q

What is the apical membrane of the collecting duct like the absence of ADH?

A

Does not contain aquaporin 2, so no water reabsorption

31
Q

What is Urea recycling?

A
  • ADH increases permeability of medullary part of collecting duct to urea, causing its reabsorption
    • This causes water to follow (THE POINT OF ADH! :D)
    • Rise in urea conc in the tissues causes Urea to passively move down its conc gradient into TAL, which is permeable to Urea but not to H20 (NO WATER REABSORPTION!)
    • Urea then passes into collecting duct, where it is reabsorbed
32
Q

What does the basolateral membrane of a cell always contain?

A
  • Aquaporin 3 and 4
    • Constantly permeable to water
    • Allows water that enters across the apical membrane to pass into peritubular blood
33
Q

How is hypo-osmotic urine generated?

A
  • Reabsorb solute from nephron
    • No ADH stimulation means no aquaporin in the DCT and collecting ducts
    • Limited water reuptake in latter DCT and limited in collecting duct
    • Tubular fluid rich in water passes through the hyperosmotic ranal pyramid with no change in water
34
Q

What is required if body needs hyperosmotic urine?

A
  • Kidney must reabsorb as much water as possible
    • Requires a hypertonic interstitium
    • ADH secreted and assists
35
Q

What is the corticopapillary osmotic gradient?

A
  • Osmotic potential of medulla increases as you go down
    • Isosmotic at cortico-medullary border

Medullary intersticium hyperosmotic at papilla

36
Q

What is the max osmolarity of the medullary interstitcium?

A

100 mOsmol/kg

37
Q

What are the three key mechanisms involved in establishing the cortiocopapillary osmotic gradient?

A
  • Active NaCl transport out of TAL
    • Recycling of urea
    • Unusual arrangement of blood vessels in medulla descending components act in close opposition to ascending components
38
Q

How does the action of the thick ascending limb of the loop of henle generate the medullary gradient?

A
  • Diluting action on filtrate

* Removes solute without water , increasing osmolarity of the intersticium

39
Q

What do loop diuretics do?

A
  • Block NaK2Cl transporters

* Medullary intersticium becomes isosmotic and copious dilute urine is produced

40
Q

How is movement of urea significant?

A
  • Permeable to most membranes
    • Moves out of collecting duct, water follows
    • Water is taken into peritubular capillaries
41
Q

Outline the process of countercurrent multiplication

A
  • Tubule filled with isotonic fluid
    • Na+ ions pumped out at ascending loop into intersticium, raising osmotic pressure outside tubule and lowering it inside
    • Fresh fluid enters descending limb which is permeable to water. Water leaves and enters medullary intersticium
    • More fluid enters from glomerulus, pushing concentrated fluid into TAL
    • Na+ pump in ascending limb pumps out more into intersticium
42
Q

What is the final gradient of countercurrent multiplication limited by?

A

• The diffusional process

43
Q

What is the max conc difference between inside and outside of the tubule?

A

• 200 mOsmol

44
Q

What is counter current multiplication maintained by?

A

• Counter current exchange at the vasa recta

45
Q

What is counter current exchange?

A

• Flow of blood in organised vasa recta opposite to flow of fluid in tubules maintains concentration gradient

46
Q

What is the dilemma surrounding blood flow to the medulla?

A
  • Must maintain concentration gradient (medullary hyper-tonicity)
    • Need to deliver nutrients
47
Q

What are the two ways in which vasa recta preserve the hypertonicity of the medullary intersticium?

A
  • Low blood flow to prevent wash out

* Travel in counter current direction

48
Q

What is the configuration for the vasa recta known as?

A

• Hair pin configuration

49
Q

What is the exchange which occurs in vasa recta as it moves along the loop of henle?

A
  • Isosmotic blood in descending limb of vasa recta enter hyperosmotic milieu of medulle
    • Ions diffuse into vasa recta and water diffuses out
    • Osmolarity of vasarecta increases until in reaches tip of hairpin loop, where it is isosmotic with medullary intersticium
    • Blood ascending has higher solute concentration than medulla, so solute moves out and water moves in

Little net dilution

50
Q

Where is the vasa recta most concentrated?

A

• At the bottom of the hair pin bend

51
Q

What happens as the vasa recta moves up the ascending portion of the loop of henle?

A
  • Solutes conc outside becomes less concentrated

* Water moves into vasa recta and solutes move out

52
Q

What is SIADH?

A

• Syndrome of inappropriate Anti-Diuretic Hormone secretion

53
Q

Give a mechanism by which SIADH can come about

A

• Secretion of ADH is not inhibited by the lowering of blood osmolarity

54
Q

What are the consequences of SIADH?

A

• Excessive amounts of water retained, causing blood osmolarity to drop and causing hyponatraemia

55
Q

Give four causes of SIADH

A
  • Malignant tumours secreting ADH analogues
    • Head trauma causing ADH release
    • Non-malignant pulmonary disorders

Drugs

56
Q

Give five symptoms of hyponatremia

A
  • Nausea
    • Vomiting
    • Headache
    • Confusion

Lethargy

57
Q

What can NIADH be treated with?

A
  • ADH receptor antagonists
    • Treating underlying cause

Hypertonic saline infusion

58
Q

Other than NIADH, give another condition which comes about as a result of abnormal ADH secretion

A

Diabetes insipidus

59
Q

What are two causes of Diabetes insipidus?

A
  • Failure of ADH secretion - Causes Central Diabetes Insipidus
    • Inadequate response of kidneys to ADH - Causes Nephrogenic Diabetes Insipidus

Semester 3 - Urinary (33 decks)

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