Vascular and Fluid Balance

Question 0

What is the function of electrolytes and what are their functions?

Answer 0

Stability of the cellular environment.
K, Mg, Ca- normal cell function
Na, Cl- maintenance of extracellular osmotic pressure
HCO3- control of extracellular pH

Question 1

How is water distributed?

Answer 1

Total body water is the sum of all the water contained in different body compartments- transport of metabolites and waste.
2/3 in the ICF and 1/3 in the ECF: made of ISF, intravascular fluid (plasma), transcellular fluid (CSF). TBW is 60-70% lean weight.

Question 2

What are the 5 main ways that body fluids and electrolytes are regulated?

Answer 2

1) GFR 2) RAAS 3) ADH 4) ANP 5) Thirst

Question 3

How is GFR maintained?

Answer 3

By maintaining ECV by varying vascular resistance, CO, renal Na and water excretion

Question 4

What does a lowered ECV result in and what does it lead to?

Answer 4

decreased venous return, decreased CO and decreased BP which leads to decreased GFR so less Na is excreted= increased water reabsorption and increased ECV.

Question 5

How are volume and pressure detected and what happens if there is a drop in either?

Answer 5

By receptors in the cardiopulmonary system and kidneys: increased sympathetic tone and increased vasoconstriction, increased cardiac contractility and HR= inc CO and BP.
Activation of the RAAS system= aldosterone = enhanced renal absorption.

Question 6

What is the function of the RAAS systems and how does it work?

Answer 6

It maintains ECV. Renin is produced in juxtaglomerular cells in the afferent arteriole. It is released in response to decreased perfusion and it converts angiotensinogen to angiotensin I which converts to angiotensin II. Angiotensin II increases aldosterone production by the adrenal cortex which enhances Na reabsorption.

Question 7

What is the role of ADH and when is it secreted?

Answer 7

It controls the permeability of distal tubules and collecting ducts. It can be released from the hypothalamus when the osmoreceptors are stimulated by increased osmolarity or when decreased blood volume= decreased blood pressure which is picked up by baroreceptors in the atrium of the heart.

Question 8

What happens if ADH is present or absent?

Answer 8

1) water permeability will be high which allows water to follow Na into the bloodstream so that urine vol is low.
2) water permeability is low, preventing water from following Na into the bloodstream so that urine vol is high.

Question 9

How can ADH release be stimulated by pressure?

Answer 9

Baroreceptors in the left atrium are stimulated by increased blood volume, impulses pass to the neurones in the hypothalamus where they inhibit ADH release so that urine vol is high and pressure will drop.
Low BP leads to decreased firing of baroreceptors and increased ADH secretion so urine volume is low and pressure will increase.

Question 10

How does ANP release regulate water balance?

Answer 10

ANP is released on response to stretching of the heart, they reduce CO and blood pressure by promoting the loss of Na and water from the kidneys and through vasodilation.

Question 11

What is the ultimate compensation for water loss?

Answer 11

Thirst which is driven by low ECV, high plasma osmolarity and the osmoreceptors and baroreceptors seen before.

Question 12

How is ISF composition controlled?

Answer 12

It requires control of fluid movement across capillaries which depends on:

1) hydrostatic pressure at the arteriolar end of the vascular network
2) osmotic pressure exerted by plasma proteins relative to interstitial proteins at the venous end.

Question 13

Give four examples of how abnormal plasma concentrations can occur.

Answer 13

1) decreased or increased intake
2) shifts to and from the ICF
3) increased renal retention
4) increased loss via usual routes

Question 14

What are the two ways that hypernatraemia can occur and what does it do to the cell?

Answer 14

Water deficiency due to decreased intake (throat abscess) or uncontrolled loss (renal disease) or water loss > Na loss (osmotic diuresis/ diarrhoea
Sodium excess- excess dietary (salt poisoning) or decreased renal excretion of Na (hyperaldosteronism-rare)
Cell dehydrates and dies when water moves to the ECF because Na is high there.

Question 15

What are the two ways that hyponatraemia can occur and what are its effects?

Answer 15

Sodium deficit- Alimentary loss (excess salivation), renal loss, prolonged diuresis (furusomide), sweating.
Loss of Na and Cl= depletion of ECF osmolarity and water loss= moves into cells= over hydration and rupture. Also= ECF vol drop=haemoconcentration and circulatory failure.

Water excess- oedema (CHF), too much fluid therapy= water into cells (ECF osmol red)=intracellular oedema=CNS convulsions

Question 16

Give a cause of hyperkalaemia and hypokalaemia internally and externally?

Answer 16

1) Addition of K from the environment- high fluid therapy or internal add of K shift from ICF to ECF due to diabetes mellitus.
2) decrease in total body K=profuse sweating in horses or shift from ECF to ICF due to high insulin levels.

Question 17

Give two causes of hypomagnesaemia and hypermagnesaemia?

Answer 17

1) decreased absorption (staggers) or excess urinary excretion
2) decreased renal excretion or Increased PTH (milk fever)

Question 18

Give two causes of Hypocalcaemia and hypercalcaemia?

Answer 18

1) milk fever in cows/eclampsia in bitches (dec PTH so dec Ca released) or hypoproteinaemia
2) malignant neoplasia or renal failure in horses.

Question 19

What is the definition of oedema and what does it indicate?

Answer 19

An increased accumulation of fluid. It is not a disease itself but it acts as an indicator of diseased state when the fluid balance has gone awry.

Question 20

Where does extra fluid accumulate?

Answer 20

In the interstitial space mainly but it can accumulate in other body cavities.

Question 21

What is dependant oedema?

Answer 21

The fluid tends to sink with gravity so that the ventral abdomen and limbs are mainly affected.

Question 22

What is pitting oedema?

Answer 22

With severe subcutaneous oedema a finger pressed into the expanded interstitium will leave an indentation.

Question 23

What is hydrothorax?

Answer 23

Accumulation of fluid in the pleural cavity

Question 24

What is Hydropericardium?

Answer 24

accumulation of fluid in the pericardial sac

Question 25

What is ascites?

Answer 25

Accumulation of fluid in the peritoneal cavity

Question 26

What is anasarca?

Answer 26

severe, generalised oedema involving the cavities and subcutis.

Question 27

What does Starling equilibrium state?

Answer 27

That at rest, hydrostatic pressure forces fluid out of the arteriolar end of the capillary network and into the tissue spaces. At the venous end, the hydrostatic pressure has decreased and the osmotic pressure of plasma proteins exceeds venous hydrostatic pressure do fluid is reabsorbed.

Question 28

What are the three major factors that control reabsorption of fluid?

Answer 28

1) a functioning circulatory system, including an intact endothelial barrier.
2) A functioning lymphatic system
3) serum albumin levels

Question 29

What are the four main mechanisms that underpin oedema?

Answer 29

1) increased blood hydrostatic pressure
2) increased vascular permeability
3) decreased plasma colloidal-osmotic pressure
4) lymphatic obstruction

Question 30

What are the two types of oedema that can occur as a result of increased blood hydrostatic pressure?

Answer 30

(oncotic pressure> hydrostatic pressure)
Generalised oedema- cardiac failure=inc venous pressure. RS=systemic congestion= systemic oedema, LS=pulmonary congestion=pulmonary oedema.
Localised e.g. thrombus, vascular torsion

Question 31

What type of pathology is associated with increased vascular permability?

Answer 31

Oedema of inflammation- opening of interendothelial gaps allows leakage of plasma proteins and inflammatory cells. This oedema has a higher protein content.

Question 32

What is oncotic pressure?

Answer 32

The measure of the ability of osmotic solutes to draw water towards them. The most important group of proteins are the plasma proteins and in particular albumin.

Question 33

How are oedema and oncotic pressure connected?

Answer 33

A decrease in plasma oncotic pressure will cause an oedema. This is usually due to a hypoalbuminaemia.

Question 34

What are the two causes of hypoalbuminaemia?

Answer 34

1) inadequate albumin production e.g. starvation, chronic liver disease.
2) net loss of albumin from either then kidney (glomerulonephritis) or the GIT (haemoncus parasitism- whole blood lost)
These are examples of generalised oedema.

Question 35

How can lymphatic obstruction cause an oedema?

Answer 35

The drainage mechanism is blocked by trauma, surgery, inflammation or neoplasia. It is a localised oedema because the underlying lesion is localised- torsion of the testes.

Question 36

What are the two causes of pulmonary oedema?

Answer 36

Haemodynamic and Microvascular injury.
due to damage of:
alveolar BM, lymphatic drainage and fluid dynamics

Question 37

How does haemodynamic pulmonary oedema occur?

Answer 37

Due to increased hydrostatic pressure, secondary to Left heart failure and backing up of blood into the pulmonary system.
Or pulm v obstruction, lymphatic obstruction and causes of lowered oncotic pressure.

Question 38

How does microvascular injury occur?

Answer 38

Capillaries in the pulmonary vascular bed are damaged- endothelial cells are damaged and hydrostatic pressure is normal.

Question 39

What is the pathogenesis of pulmonary oedema?

Answer 39

1) fluid exceeds capacity of lymphatic drainage
2) fluid accumulates in the interlobar septa, perivascular and peri-airway CT
3) alveolar walls fill with fluid
4) alveolar spaces fill with fluid
5) grossly the lungs become heavy and wet, exuding red-tinged fluid on cut section

Question 40

What are the clinical consequences of oedema?

Answer 40

Outcome depends on extent, location and duration of oedema. In the brain and lungs it can be fatal. Cerebral oedema which results in cerebellar herniation= suppression of respiratory centres.
Pulmonary oedema impedes gas exchange potentially leading to hypoxia.

Question 41

What is the difference between transudate and exudate?

Answer 41

1) due to inc hydrostatic pressure or decreased oncotic pressure
2) an acute inflammatory response and show the presence of cells

Question 42

What are the characteristics of transudate?

Answer 42

Colour- pale, clear, straw
Consistency- thin and serous
protein- 0.5% albumin
coagulability- none
Specific gravity- low
Cells- low
underlying cause- all but inflammation

Question 43

What are the characteristics of exudate?

Answer 43

Colour- dark yellow, red, brown, cloudy
Consistency- viscous
Protein- >2-4%
Coagulability- will due to fibrin content
Specific gravity- High >1.012
Cell content- High
Underlying cause- inflammation