Topic 4 – Body salt and water – tissue fluid – controls

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					Topic 4 – Body salt and water – tissue fluid – controls BODY FLUID COMPARTMENTS  Total body water is 60% of body weight  Composed of 2/3rds intracellular fluid and 1/3rd extracellular fluid.  Extracellular fluid is composed of plasma i.e. fluid in blood vessels, and interstitial fluid – fluid outside both cells and vessels. INTRACELLULAR FLUID  The major cations are potassium and magnesium.  The major anions are proteins and inorganic phosphate – this is due to the relative impermeability of the membrane to these ions. EXTRACELLULAR FLUID  The major cation is sodium – this is due to sodium-potassium ATPase extruding sodium and bringing potassium into the cell.  The major anions are chloride and bicarbonate.  Plasma has a larger protein concentration (mainly albumin and globulins) because of the capillary endothelium being impermeable to proteins.  Interstitial fluid is an ultrafiltrate of plasma. OSMOLARITY  All these three compartments have identical osmolarity because water can travel freely between the compartments. EXCHANGE BETWEEN COMPARTMENTS  This is explained by the attached diagram, and by understanding Starling’s Law of Ultrafiltration – if you know the equation by heart and can appreciate the effect that each variable has on the solution, then you will be able to answer any question thrown at you.  Net filtration pressure is the amount of fluid moving between the plasma and the interstitial fluid.  If NFP is positive, fluid is moving into the interstitium from the plasma (filtration). The reverse is true if NFP is negative (reabsorption).  Under normal conditions, there is slight net filtration. The excess fluid is drained by the lymphatics.  Blood hydrostatic pressure (BHP) is the blood pressure in the capillaries forcing the fluid out. When BP increases, the BHP also increases, promoting net filtration.  Interstitial fluid osmotic pressure (IFOP) is the pressure generated by osmotically active particles in the interstitium. Usually very low because protein has no business here! Rupture of capillaries causing leakage of plasma will increase this, promoting filtration.  Blood colloid osmotic pressure (BCOP) – this is the osmotic force generated by the osmotic particles, mainly proteins, in the plasma. It promotes reabsorption of fluid.  Hypoalbuminaemia  decreased BCOP  increased NFP  more fluid escaping into interstitium  oedema.  Interstitial fluid hydrostatic pressure (IFHP) – the pressure exerted by the volume of fluid in the interstitium, pushing fluid back into the capillaries.  Lymphatics blocked  fluid building up as oedema  IFHP increases  decreased NFP  more reabsorption  less oedema.

LYMPHATICS  Important in draining excess tissue fluid and proteins back into the blood  Lower protein concentration than plasma.  Contains coagulation factors and an electrolyte concentration similar to plasma.  Lymph flow is increased by an condition that increased net filtration out of capillaries:  Increased surface area (distension)  Increased capillary permeability (temperature)  Movement – muscles squeeze tissues and force fluid through the lymphatic system  Chemical mediators causing vasodilation CONTROL OF BODY SALT AND WATER WATER BALANCE  Increased plasma osmolarity  osmoreceptors in hypothalamus are stimulated.  These osmoreceptors are turned on when they shrink – either by a deficit in total body water or by sodium and chlorine ions accumulating in the extracellular fluid (they are excluded from the intracellular fluid).  Either of these will cause fluid to move out of the osmoreceptors  they shrink  this causes their activation.  Osmoreceptor activation  increased secretion of ADH from posterior pituitary into the bloodstream  ADH inserts aquaporins into the collecting duct and late distal tubule  causes water reabsorption  increased blood volume  plasma osmolarity decreased  osmoreceptors stop firing.

 Osmoreceptors are very sensitive to changes of osmolarity: a small change in osmolarity causes a big change in ADH  Decreased plasma volume sensed by baroreceptors  inhibits the firing of these receptors  reflex stimulation of thirst and ADH secretion.  Baroreceptors also covered in Topic 8.  Baroreceptors are less sensitive than osmoreceptors, but provide a stronger response.  A very low plasma volume will cause thirst and ADH secretion even in the presence of low plasma osmolarity.  A very high plasma volume will suppress thirst and ADH secretion even if plasma osmolarity is very high. SALT BALANCE  Input is entirely based on diet – there is no direct physiological control.  Urine is the most important way we lose sodium.  Sodium balance is achieved by matching intake to output via three mechanisms.  1. Changes in GFR: increase in sodium intake which is primarily an extracellular solute  increase in plasma osmolarity  stimulation of thirst and ADH secretion  expansion of plasma volume  increase of GFR  increased filtered sodium load  increased sodium excretion.  2. Aldosterone is most important – decreases in plasma sodium causes aldosterone release  Aldosterone secretion mainly controlled by RAAS: decreased plasma sodium  decreased plasma osmolarity  decreased plasma volume  sensed by kidney as decreased perfusion pressure  increased renin secretion  renin-angiotensin pathway  increased aldosterone  increased sodium reabsorption.  Decreased plasma sodium has a weak direct effect on the adrenal cortex  stimulates aldosterone release  reabsorption of sodium.  3. Third factor effect. When the first two factors are controlled, the kidney can still regulate sodium excretion to match input.  This is not well understood. The mechanisms behind this are not essential; be aware this exists and if you REALLY, REALLY need more, see pages 483-4 of Best and Taylor’s. BLOOD VOLUME CONTROLS – TISSUE O2 DEMANDS This material has been covered in other parts of our notes – autoregulation, baroreceptor reflexes and RAAS, again. Seek ye therefore elsewhere to find satisfaction. PAST EXAM QUESTIONS 2000 Question 12 A 37 year old man presented to hospital with a two month history of increasing thirst and increasing urine output (4L/24hrs). Just prior to admission, he had been involved in a minor car accident and at the time of examination he had been without any fluid intake for six hours. No glucose was found in his urine. Subsequent investigation revealed a tumour involving the pituitary gland.

Explain the following: a) The patient’s blood osmolality was 325mosmol/kg H20 [normal 280 – 300 mosmol/kg H20] while urinary osmolality was 200 mosmol/kg H20.  fluid intake   extracellular fluid   plasma osmolality. Normally  osmolality would stimulate the osmoreceptors in the hypothalamus to release ADH   synthesis of aquaporins and insertion of aquaporins into the principal cells of the collecting duct of nephron   water reabsorption through the aquaporins from tubular lumen into the peritubular fluid  concentrates the urine +  plasma osmolality back towards normal. The tumour in the pituitary gland is stopping normal release of ADH from the posterior pituitary  thus the kidneys are unable to concentrate the urine (urine remains with low osmolality), and blood osmolality stays high. b) He was thirsty This mechanism is also covered in Topic 9. The accident +  fluid intake   plasma fluid volume  stimulates AV3V region of CNS  thirst is stimulated. Also:  plasma fluid volume   blood pressure   renal arteriole perfusion pressure  stimulates activation of Renin-Angiotensin System   Angiotensin II levels  stimulates AV3V region of CNS  thirst is stimulated. c) The patient was 2kg lighter than he had been earlier that day. The patient is unable to concentrate his urine (see above) and is losing too much fluid in the urine – with no fluid intake for 6 hours, he has lost fluid without gaining any   weight. d) One week before admission, his general practitioner had found his serum sodium concentration was normal (142 mmol/L) and his 24 hour urinary sodium excretion was normal. I assume this question is hinting that his serum sodium is now NOT normal… A week ago, though he was losing a lot of fluid through dilute urine, he could prevent his plasma osmolality from getting too high by drinking water. When serum osmolality began to rise, feedback mechanisms would have stimulated his thirst, and he would have drunk water to  plasma osmolality back to normal. With the accident today, he wasn’t able to drink, thus no return of plasma osmolality to normal. 1997 Question 9 An 18 year old man was admitted to hospital with gross oedema of both legs that had developed over the past 3 weeks. Investigation revealed a low serum albumin of 21g/L (due to protein loss from his gut). His creatinine was normal. Explain the following: a) The oedema of his legs.

Low serum albumin   blood oncotic pressure in the capillaries   pressures promoting reabsorption (Starling’s Law of the capillary)   net filtration of fluid from the plasma into the interstitial space  oedema. The fact that this developed over 3 weeks has to do with albumin having a half-life of 16 – 24 days, thus a  synthesis in albumin would not  serum albumin immediately, but over a course of 3 weeks. b) He complained of being thirsty and drank 2.5 L of fluid daily.  albumin   filtration of fluid from the capillaries into the interstitial space   plasma volume   plasma osmolarity  stimulates AV3V region of CNS  thirst is stimulated. Also:  plasma fluid volume   blood pressure   renal arteriole perfusion pressure  stimulates activation of Renin-Angiotensin System   Angiotensin II levels  stimulates AV3V region of CNS  thirst is stimulated. c) He had a 24 hour urine volume of 600mL Again, this is properly covered in Topic 9.  plasma volume  activates baroreceptor reflex  stimulates SNS activity to kidney  activates rennin-angiotensin system  angiotensin II constricts afferent and efferent arterioles of the kidney and sympathetic stimulation also does this directly   GFR   urine volume. Also  blood volume   osmolarity of plasma  stimulates osmoreceptors in the hypothalamus  ADH secretion stimulated  aquaporins inserted into the distal tubule and collecting duct  water reabsorbed from filtrate  urine concentrated   urine volume. d) his 24hr urinary sodium 10 mmol, and his 24 hr urinary potassium was 95 mmol.  blood volume  rennin-angiotensin system activated  angiotensin II levels   angiotensin II causes release of aldosterone  aldosterone acts in the kidney to  tubular reabsorption of sodium and  tubular secretion of potassium  urinary sodium  and urinary potassium .