Fluid pathophysiology Flashcards

1
Q

what % of total body water is in the intracellular and extracellular fluid compartments

A
  • 66% intracellular
  • 33% extracellular
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2
Q

How is the extracellular fluid further subdivided

A
  • Interstitial is 75% of ECF (25% total water)
  • intracellular is 25% of ECF (8% tota water)
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3
Q

how are the intracellular and extracellular fluid compartments separated

A

Semi-permeable membrane.
- freely permeable to water but solutes (electrolytes) only by pumps.
- allows generation of electrochemical gradient across the membrane.

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4
Q

How does the semi permeable membrane differ from the vascular endothelium?

A
  • Vascular endothelium permeable to most ions and solutes as well as water.
  • not permeable to larger colloid molecules (albumin. globulin and fibrinogen).
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5
Q

What is the difference in osmolality and osmotic pressure (tonicity)?

A

osmolality is a measure of ALL solutes and particules dissolved in a compartment, wether or not they can cross the membrane.

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6
Q

What is the equation for a rough calculation of plasma osmolaity

A

2(Na + K) + glucose + BUN

normal arund 300mosm/ug dogs (310 cats)

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7
Q

What is Colloid Osmotic pressure (oncotic pressure)?

A

Contribution of colloid molecules and their associated electrolytes to plasma osmotic pressure.
- Albumin most important, highly negatively charged, so carriers multiple cations which also contribute.
- only about 0.5% of overall osmotic pressure

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8
Q

What is the glycocalyx

A

a gel like matrix of glycoproteins and proteoglycans on the luminal surface of endothelial cells.

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9
Q

what are the proposed functions of the glycocalyx

A
  • Control vascular permeability
  • mechanotransduction of shear stress to vessel walls.
  • blood cell/vessel wall interactions
  • binding of mediators of inflammation and coagulation.
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10
Q

What is the theory of the revised starling principle

A
  • beneath glycocalyx = subglycocalyx space, small, low protein.
  • oncotic pressure gradient between plasma and the subglycocalyx space is key to fluid flux (not interstitium)
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11
Q

What is the significance of glycocalyx shedding?

A
  • associated with poor outcomes in people.
  • numerous conditions eg trauma and sepsis can cause.
  • exacerbated by hypervolaemia, be cautious.
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12
Q

What are the key difference in solutes between intravascular, interstitial and intercellular fluid?

A
  • Intravascular and interstitial are the same except proteins (both extracellular).
  • intracellular fluid has high K+ and low Na+, extracellular the opposite.
  • intracellular also has lower chloride and higher protein.
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13
Q

Define hypovolaemia

A

A deficit of fluid from the intravascular space = decreased effective circulating volume.

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14
Q

What is relative hypovolaemia?

A

Abnormal vasodilation causes blood pooling in kidneys, depleting the central circulation giving shock signs even when total vascular volume remains unchanged.

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15
Q

What is dehydration

A

Fluid deficit from the interstitial and intracellular spaces. (intravascular not effected until dehydration is severe).

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16
Q

What are the immediate homeostatic responses to fluid loss

A
  • Baroreceptors detect decreased stretch - simulate SNS. (increase HR, contractility, vasconstrict and stim RAAS)
  • transcapillary refill, reduced capillary hydrostatic pressure causes fluid flux into the vessel (starling).

Transcapillary refill a reason for TS drop in HAem

17
Q

How does the RAAS compenstae for hypovolaemia?

in summary

A

It causes sodium and water retention and stimulates thirst

18
Q

What are the steps in the RAAS

A
  • Sympathetic stimularion from baroreceptors = renin release.
  • Renin converts angiotensinogen to angiotensin 1.
  • ACE produced in lung converts angiotensin 1 to angiotensin 2.
  • angiotensin 2 = vasoconstriction, sodium and water absorption at proximal tubule and release of ADH and aldosterone.
19
Q

What is the role of aldosterone

A
  • release from adrenals stimulated by angiotensin 2
  • causes sodium resorption at the distal tubule.
20
Q

What is the role od ADH (vasopressin)

A
  • increased osmolality and angiotensin 2 sitimulate ADH release from the pituitarty.
  • increases renal resorption of water at the collecting duct