Control Of Body Fluid Volume + Osmolality Flashcards

1
Q

Action of angiotensin II

A
  • vasoconstriction of EA
  • releases ADH
  • stimulates thirst
  • causes aldosterone to be released from adrenal cortex > increases Na+ reabsorption from DCT (ENaC)
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2
Q

How do prostaglandins affect Na+ reabsorption?

A

Decrease in circulating volume stimulates PG synthesis which results in:

  • vasodilators > preventing excessive vasoconstriction
  • renin release > Na+ reabsorption due to increased aldosterone
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3
Q

How does atrial natriuretic peptide affect Na+ reabsorption

A

Produced by cardiac atrial cells in response to increased circulating volume > results in:

  • inhibit NaK ATPase + closes ENaC channels > reduced Na+ reabsorption
  • vasodilation of AE > increases GFR
  • inhibit aldosterone secretion
  • inhibit ADH release
  • decrease renin release
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4
Q

Renal responses to a increase in BP

A
  • Release of ANP: inhibit NaK ATPase + reduced ENaC expression > decreases Na+ reabsorption > increased Na+ + H2O excretion
  • increase in hydrostatic pressure of peritubular capillaries: pressure natriuresis + diuresis
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5
Q

Renal responses to decrease in BP

A
  • prostaglandin release
  • RAAS activated: AngII > constriction of EA + release of aldosterone > stimulates ADH + thirst | increased expression of ENaC
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6
Q

Renal response in congestive cardiac failure -

A
  • cardiac output falls
  • hypotension > Na+ and H2O retention > oedema
  • renal hypotension after a fall in CO is sensed by kidneys as hypovolaemia > compensation by retaining NaCl + H2O to increase fluid volume
  • increased pulmonary venous pressure > pulmonary oedema
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7
Q

Management of pulmonary oedema due to congestive cardiac failure

A

Loop diuretics
ACE inhibitors
Vasodilators
Nitrates

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8
Q

Presentation of hypervolemia

A
  • ascites > swelling in abdomen
  • pleural effusion
  • pulmonary oedema
  • peripheral oedema in legs
  • coughing
  • shortness of breath
  • pumping action of heart grows weaker
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9
Q

Causes of hypervolemia

A
  • kidney rotation of sodium + water
  • reduced effective arterial volume e.g. congestive cardiac failure
  • excessive sodium or fluid intake
  • cirrhosis
  • hyperaldosteronism
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10
Q

Treatment of hypovolemic shock

A

Isotonic fluid replacement - saline solution

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11
Q

What is hypertensive renal disease?

A

High BP caused by narrowing of arteries to kidney

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12
Q

What are hypertensive changes in the kidney

A
  • arteriosclerosis of major renal arteries
  • hyalinisation of small vessels with intimal thickening
    .
  • causes chronic ENaC damage + reduced kidney size
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13
Q

Outline the regulation of osmolality

A
  • changes in plasma osmolarity sensed by hypothalamic osmoreceptors
    Two pathways initiated:
    -ADH in kidneys > affects renal water excretion
    -thirst > affects water intake
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14
Q

Where are osmoreceptors located?

A

Hypothalamus

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15
Q

Actions of ADH when plasma osmolality increases

A
  • blood vessel vasoconstriction: V1 receptor mediated response
  • increased water reabsorption: V2 receptor mediated response
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16
Q

What stimulates the thirst response?

A

Increase in plasma osmolarity

17
Q

If plasma osmolality decreases, what type of urine is made?
How is this done?

A

hypoosmotic urine
- decrease ADH conc > decreased aquaporins > decreases H2O reabsorption
- loss of large amounts of dilute urine

18
Q

If plasma osmolality increases, what type of urine is made?
How is this done?

A

Hyperosmotic urine
- increase in ADH > increased aquaporins > increased H2O reabsorption in collecting duct
- concentrated urine

19
Q

What causes a release of renin?

A
  • increased sympathetic innervation
  • decrease in BP
  • decreased Na+ to macula densa cells
20
Q

How does a decrease in Na+ activate renin release?

A
  • less Na+ to macula dense
  • MD stimulated > secrete prostaglandins
  • prostaglandins act on granular cells
  • renin released
21
Q

How do prostaglandins affect Na+ reabsorption?

A
  • vasodilator effect (prevents excessive Vasoconsition)
  • act on granular cells to release renin > activates RAAS > increases Na+ reabsorption from DCT
22
Q

Where does prostaglandin synthesis occur in the kidney?

A

Cortex
Medullary interstitial cells
Collecting duct epithelial cells

23
Q

Where are atrial natriuretic peptides produced by?
In response to what?

A

Caridac atrial cells
In response to increase in ECF volume

24
Q

How does angiotensin II maintain GFR?

A

Constricts efferent article > increases pressure in glomerulus

25
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion

26
Q

Presentation of SIADH

A
  • fluid overload
  • weight gain
  • low urinary output
  • conc. urine
  • hyponatremia
27
Q

What is antidiuresis?

A

Reduction in renal water excretion