Control & Abnormalities of Body Water Flashcards
1
Q
Describe how osmotic forces determine water distribution between ECF and ICF when pure water is added/removed and when water + salt is added
A
- The water and solutes in the ECF and ICF are balanced to stop movement via osmosis
- In the ICF the main solutes are K+ and associated anions and in the ECF it is Na+ and associated anions
- Pure water is added to the ECF which dilutes the solute concentration which changes osmolarity
- The water distributes in the ECF and ICF by going down the water potential gradient into the ICF as the ICF is more concentrated
- Hence both the ECF and ICF are expanded
- The opposite happens during dehydration as the ECF becomes more concentrated as water is lesser so water moves from the ICF into the ECF and both are reduced
- If both salt and water are added the solution expands the ECf but there is no change in concentration so there is no osmotic gradient and so ICF volume doesn’t change
- Adding or removing pure water is osmoregulation by the kidney
2
Q
What does water excess and deficit lead to (briefly)?
A
Water excess leads to a decrease in body fluid osmolality
Water deficit leads to an increase in body fluid osmolality
3
Q
What are 2 ways concentration of a solution can be changed and which applies to the ECF?
A
Add/remove solute
Add/remove water
The osmolarity of the ECF an only be adjusted by adding or removing water not solute
4
Q
The renal tubule is the only site of regulated water loss- what happens in water excess and deficit?
A
- The amount of solute free water excreted by the kidney can be varied
- Water excess leads to a large volume of dilute urine
- Water deficit leads to a small volume of concentrated urine
5
Q
Describe the 2 key components that contribute to osmoregulation including what causes these components, and what conservation/excretion of water depends on
A
- Concentration of interstitial fluid in medulla - depends on countercurrent mechanisms in the loop of Henle and vasa recta, the permeability of the descending limb to water and the ion transporters in the ascending limb - urine is most concentrated at the end of the descending limb and most dilute at the end of the ascending limb
- Dilution of urine in ascending limb and distal tubule
- (Urine concentration can be varied between these limits)- need to be able to concentrate the urine by reabsorbing water and dilute the urine by excreting it
- Conserving water depends on generating high osmolarity
- Excreting water depends on dilution of urine (low osmolarity)
6
Q
Describe what ADH does (not mechanism just brief)
A
- Urine entering the collecting duct is maximally dilute
- Osmotic gradient for water reabsorption is large but in the absence of ADH the collecting duct is impermeable to water
- Maximally dilute urine is excreted
- ADH is required to unlock water permeability of the collecting duct - with low levels of ADH some water will be reabsorbed so urine osmolality larger than 100 mOsmol/Kg is considered to show presence of ADH at low levels
- ADH at maximum levels can concentrate urine to 1200 mOsmol/Kg - this is the maximum urine concentration that can be achieved
7
Q
Show the mechanism of ADH action
A
- Vasopressin binds to V2 receptors on principal cells on the CD
- The receptor activated cAMP secondary messenger system
- The signals activate storage vesicles that contain aquaporin 2 water pores
- Insertion of the aquaporin 2 water channels into the membrane via exocytosis of vesicles
- This then allows the movement of water through the collecting duct cells and into the vasa recta
- V1 receptors on vascular smooth muscle - vasoconstriction but only significant with very high ADH levels
8
Q
Describe how ADH acts as a defence against dehydration - include normal range of osmolarity and what happens when it changes
A
- Net water loss increases ECF osmolarity
- Normal range is between 285 to 295 mOsm/Kg
- Changes detected by osmoreceptors in anterior hypothalamus
- Project to magnocellular neurons of paraventricular and supraoptic nuclei of hypothalamus
- PVN and SON neurons release ADH from their axon terminals in posterior pituitary
- Threshold for ADH release is 280-285 mOsm/Kg
- Above this range small changes in osmolality produce large changes in ADH secretion
- ADH also stimulated by large decreases in blood volume/pressure
9
Q
Describe how thirst acts as a defence against dehydration including what happens when osmolarity changes
A
- Changes detected by osmoreceptors in anterior hypothalamus
- Project to centres mediating thirst - drinking
- There is a strong desire to drink when plasma osmolality is over 295 mOsm/Kg
- Oropharyngeal and upper gastrointestinal receptors reduce thirst on drinking
- Thirst is also stimulated by large drops in blood volume/pressure and angiotensin II acting on the hypothalamus
10
Q
Describe how much plasma [Na+] contributes to ECF osmolarity and how it can be estimated based on this
A
- Na+ is the main cation in ECF
- Principle of electroneutrality dictates that a molar equivalent number of anions must be present
- Mainly Cl-, significant amount HCO3-, small contribution from other inorganic and organic anions
- Contribution of Na+ to ECF osmolality is 2 x plasma [Na+] to account for the anions
Plasma osmolarity is mOsm L-1 can be estimated from 2[Na+] + 2[K+] + [glucose] + [urea]
11
Q
Describe what happens to ECF during water excess and deficit and what happens to Na+
A
- Water deficit -
- ECF osmolality increases
- Hypernatremia (Na is above 145)
- Water excess -
- ECF osmolality decreases
- Hyponatremia (Na is less than 135)
12
Q
Describe what hypernatremia is
A
- Remember hypernatremia does not mean too much Na but means too little water
- The total amount of Na may be the same or may be decreased or increased - change in Na concentration means there is a relative water deficit
- Hypernatremia (Na above 145) always means hyperosmolality of ECF
13
Q
What are the potential causes of hypernatremia and include why one is much rarer than the other and what can cause each
A
- Causes -
- Gain of sodium
- Loss of water
- Gain of sodium -
- Rare because the gain of sodium must be greater than the relative intake of water
- Iatrogenic - consequence of medical treatment
- Excess ingestion
- Excess mineralocorticoid activity e.g. primary hyperaldosteronism - hypernatremia is mild if present
- Loss of water -
- Can occur in various conditions associated with fluid loss - loss of water must be greater than loss of Na
- Extrarenal loss - dehydration, infection (as it causes increased loss from lungs and skin)
- Renal losses- osmotic diuresis (presence of an osmotically active solute that prevents dilution and decreases osmotic gradient) and diabetes insipidus (caused by lack of ADH secretion or activity)
- Diabetes mellitus- when glucose exceeds the amount that can be reabsorbed it can then be found in the urine and increases osmolarity which impacts gradient for water reabsorption - example of osmotic diuresis
- Diabetes insipidus -
- Renal water loss so inability to concentrate the urine
- Lack of effective ADH either central (failure of secretion) or nephrogenic (lack of renal response)
- Presents with polydipsia and polyuria- thirst mechanism alone is normally enough to prevent significant hypernatremia but will develop if access to water is restricted
14
Q
Describe why hyponatremia is more complicated to define
A
- Hypernatremia always causes hyperosmolarity
- Hyponatremia is more complicated - you cannot assume that if sodium levels are below the normal level (300) that the person is hypoosmolar as there may be another osmotically active solute present having an impact of osmolarity
- E.g. if the patient has ingested a poisonous substance, or has diabetes mellitus and has high [plasma glucose]
15
Q
State what true and pseudo hyponatremia are
A
- Hypoosmotic hyponatremia - sometimes called true hyponatremia
- Pseudo hyponatremia occurs when another solute present in sufficient quantity that the proportional contribution of sodium to plasma osmolality is reduced
- True hyponatremia is associated with hyperosmolarity - it signifies water excess
