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Human Physiology - Hormones and Health > Regulation of ECF Volume and Osmolality > Flashcards

Regulation of ECF Volume and Osmolality Flashcards

1
Q

What is the distribution of body water?

A
  • 2/3 in ECF
  • 1/3 in ICF (20% plasma, 80% interstitial)
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2
Q

What is osmolarity?

A

a measure of the concentration of substances

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3
Q

What does increased osmolarity (hypertonicity) lead to?

A

water leaving the cells → shrinkage

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4
Q

What does decreased osmolarity (hypotonicity) lead to?

A

water entering cells → swelling

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5
Q

What can disturbances in osmolality lead to?

A
  • pure water loss without losing electrolytes
  • increase in osmotically active external substances
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6
Q

What can disturbances in fluid volume lead to?

A

vomiting and diarrhoea i.e. both fluid and electrolytes are lost

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7
Q

What are the compensatory mechanisms for disturbances in osmolality and fluid volume respectively?

A
  • osmolality = increase total body water
  • volume = increase body water and electrolytes
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8
Q

What does thirst do?

A

increase the water intake and dilute the ECF

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9
Q

What are the 2 responses to increased ECF osmolality?

A
  • thirst
  • increased ADH secretion
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10
Q

Where is ADH synthesised and stored?

A
  • synthesised in hypothalamus
  • stored in posterior pituitary
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11
Q

When is ADH secretion increased?

A
  • increased plasma osmolality
  • decreased ECF volume
  • low BP
  • pain, emotion, stress, nausea and vomiting
  • angiotensin II
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12
Q

When is ADH secretion decreased?

A
  • reduced plasma osmolality
  • increased ECF volume
  • increased BP
  • alcohol
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13
Q

What are the actions of ADH?

A
  • vasoconstriction mediated by V1 receptors in vascular smooth muscle
  • water reabsorption and concentration of urine mediated by V2 receptor
  • increased reabsorption of urea at the medullary collecting duct
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14
Q

What does increased reabsorption of urea at the medullary collecting duct lead to?

A

increased solute concentration in the medulla, increasing the efficiency of the countercurrent mechanism

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15
Q

What does the countercurrent mechanism lead to?

A

an increase in the concentration of urine because ADH is able to reabsorb water more efficiently in the presence of the gradient

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16
Q

Where does ADH act?

A

only on the distal part of the nephron, mainly on the collecting ducts

17
Q

What are the 7 steps of the ADH mechanism of action?

A
  1. water deficit
  2. ↑ extracellular osmolarity
  3. ↑ ADH secretion
  4. ↑ plasma ADH
  5. ↑ water permeability in distal tubules and collecting ducts
  6. ↑ water reabsorption
  7. ↓ water excretion
18
Q

What can excess ADH production lead to?

A

SIADH (syndrome of inappropriate ADH secretion)

19
Q

What causes nephrogenic diabetes insipidus?

A

inability of the kidneys to respond to ADH (desensitivity)

20
Q

What is the mechanism of action in individuals with diabetes insipidus?

A
  1. ADH deficiency (central DI)/inability to respond to ADH (nephrogenic DI)
  2. inability to concentrate urine
  3. production of large amount of dilute urine causing polyuria
  4. increased thirst (polydipsia)
21
Q

When is thirst increased?

A
  • ↑ plasma osmolarity
  • ↓ blood volume
  • ↓ BP
  • ↑ angiotensin II
  • dry mouth
22
Q

When is thirst decreased?

A
  • ↓ plasma osmolarity
  • ↑ blood volume
  • ↑ BP
  • ↓ angiotensin II
  • gastric distention
23
Q

How can nephrogenic DI be distinguished from central DI?

A

by administration of desmopressin, the synthetic analogue of ADH; urine output will reduce upon desmopressin administration in central DI

24
Q

What is renin?

A

an acid protease secreted by granular cells in the juxtaglomerular apparatus into the bloodstream

25
Q

What is renin secretion caused by?

A
  • hypotension
  • increased renal SNS activity
  • decreased NaCl concentration
  • increased circulating catecholamines
26
Q

When is renin secretion inhibited?

A
  • increased NaCl absorption from macula densa
  • increased afferent arteriolar pressure
  • angiotensin II
  • ADH
27
Q

What is angiotensin II?

A

one of the most potent known vasoconstrictors

28
Q

What are the 4 steps of angiotensin II production?

A
  1. in response to low plasma volume, the juxtaglomerular cells secrete renin
  2. renin cleaves angiotensinogen to angiotensin I
  3. angiotensin I make its way through the circulation to come into contact with ACE
  4. ACE converts angiotensin I to angiotensin II
29
Q

What does angiotensin II in the kidney do?

A
  • stimulate aldosterone secretion which increases sodium reabsorption
  • constrict efferent arterioles more than afferent arterioles
30
Q

What happens when efferent arterioles are more constricted than afferent arterioles?

A
  • ↓ peritubular capillary hydrostatic pressure
  • ↑ tubular reabsorption
  • ↑ filtration pressure and GFR
31
Q

What does more sodium reabsorption lead to?

A

more water reabsorption

32
Q

What does increased arteriolar constriction by angiotensin II lead to?

A

a rise in both systolic and diastolic BP

33
Q

How is aldosterone secreted?

A

by angiotensin II from the adrenal cortex

34
Q

Where does aldosterone act?

A

distal convoluted tubules

35
Q

What does aldosterone do?

A
  • increase the insertion of the sodium potassium pump in the basal lateral membrane of the distal convoluted tube
  • increase the expression of the sodium channels on the apical membrane of the same cells
36
Q

What are the effects of aldosterone?

A

increased sodium reabsorption from the filtrate which stimulates osmosis, increases plasma volume and therefore blood pressure

37
Q

How can the renin-angiotensin-aldosterone axis be manipulated?

A
  • ACE inhibitors
  • angiotensin receptor blockers
  • aldosterone antagonists
38
Q

When are ANPs released?

A

in response to increased ECF volume which stretches the atria

39
Q

What do ANPs do?

A
  • dilate afferent arterioles and relax mesangial cells
  • this reduces the renin secretion and angiotensin II formation
  • increase salt and water excretion

Human Physiology - Hormones and Health (14 decks)

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