Plasma and interstitial fluid are identical in ionic composition. the difference between plasma and interstitial fluid is protein content. Plasma contains a large amount of protein, while the interstitial fluid contains less.
? ? Na + Cl - HCO 3 - Extracellular fluid K + Mg 2+ PO 4 3- Intracellular fluid Cation Anion
movement of water or solvent across a membrane from a less concentrated solution to a more concentrated solution
Pull that draws solvent through the membrane to the more concentrated side (or side with solute ).
Determined by the number of particles instead of the mass of the solute in the solution.
Can be divided in two types:
Crystal osmotic pressure : formed by a lot of small molecular weight materials, such as electrolyte, Glucose, BUN and so on.
Colloid osmotic pressure : formed by large molecular weight materials such as proteins
Osmosis When a bottle bottomed with a semi-permeable membrane is filled with 3% salt solution and put into a glass of water, the water in the glass will move into the bottle, this phenomenon is call osmosis. Osmosis make the salt solution rising and solution stops rising when weight of column equals osmotic pressure.
Initiated by the osmoreceptors in hypothalamus that are stimulated by increase in osmotic pressure of body fluids
Also stimulated by a decrease in the blood pressue through the receptor of baroreceptor.
THIRST 1. The sensation of thirst
The vascular organ of the lamina terminalis (OVLT) contains osmoreceptive neurons – also the subfornical organ (SFO) and the median preoptic n. (MnPO) Osmoreceptors stimulate AVP secretion and thirst These cells project to the paraventricular nuclei ( PVN) and supraoptic nuclei ( SON) to produce AVP secretion
Not a change in the extracellular fluid osmolality per se
But a change in osmoreceptor neuron size or in the some intracellular substance.
Thirst is inhibited by decreased plasma osmolality (OVLT receptors) and by increased blood pressure (hypervolemia) Thirst is triggered by increased plasma osmolality (OVLT receptors) , decreased plasma volume, and increased plasma Ang Ⅱ which is caused by decreased plasam volume. (angiotensin II in SFO). Thirst precisely regulate the volume and osmolality of ECF
ADH is more sensitive to the change of osmotic pressure. 1-2% change of osmotic pressure will change the production of ADH. At first, when blood volume is not markedly decrease, ADH will not be increased. When blood volume is decreased >10%, ADH will be increased At this time, the decrease of blood volume may be life-threatening. ADH released BP/Blood volume + Stretch receptor + Plasma osmotic pressure + Osmoreceptor + Plasma osmotic pressure - Osmoreceptor - ? maintenance of body fluid volume has priority over maintenance of body fluid osmolality.
Guanylin binding to the extracellular side of the receptor causes activation of guanylyl cyclase at the intracellular side of the receptor and further synthesis of cGMP in intestinal epithelial cells, which further leads to biological effect.
Sodium is the primary cation in the extracellular fluid-> sodium content determine the osmolality in ECF -> while osmolality gradient across cell membrane is the driving force of water movement -> so disturbance of sodium is always accompanied with water disturbance.
The dehydration in which the water loss is in excess of salt loss and the remaining ECF of the body is hypertonic (serum Na+ >150mmol/L, plasma osmotic pressure> 310mmol/L) is termed of hypertonic dehydration.
Difficulty in drinking, i.e. esophageal tumor, coma
Impaired thirst, i.e. CNS disease
Via gastrointestinal tract
i.e. diarrhea and vomitting i.e. ↑environmental and body temperature i.e. diabetes insipidus, Osmotic diuresis ↓ ↑
Diabetes Insipidus Central diabetes insipidus is characterized by decreased secretion of antidiuretic hormone (ADH) that results in polyuria and polydipsia by diminishing the patient's ability to concentrate urine. Nephrogenic diabetes insipidus is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney.
Osmotic diuresis Increased blood glucose ↑ Glomerular filtration of glucose ↑ Osmotic pressure of renal tubular fluid ↓ Water reabsorption Osmotic diuresis H 2 O reabsorption ↑ glucose filtration Osmotic diuresis ↑ Osmolality -
4. Early stage, change of blood volume not obvious->ADS not increase->Na + reabsorption not increase
Alterations of metabolism and function (continued) ↑ ADH ->H 2 O reabsorption increase ↑ Urinary sodium Late state, decrease of blood volume ->increase of ADS -> Na + reabsorption increase ->↓urinary sodium 5. Brain cell dehydration-> CNS dyfunction, such as twitching, somnolence, coma 6. hypovolemia-> reduced blood pressure, elevation in body temperature
Principles of Therapy: Treating the primary disease Supplying 5%-10% Glucose Adding a small amount of NaCl solution Adding K + properly
The dehydration in which the salt loss is in excess of water loss and the remaining ECF of the body is hypotonic (Serum Na+ <130mmol/L, Plasma osmotic pressure< 280mmol/L) is termed of hypertonic dehydration.
Hypotonic dehydration almost all appear after inappropriate therapy, that is after excessive loss of water and salt, only water but not salt is given.
Via gastrointestinal tract
Body fluid accumulation in the third space
1. Loss of sodium via kidney
inappropriate long-term use of diuretics
Renal tubular acidosis
2. Loss of sodium via extra-kidney furosemide->inhibit Na+ reabsorption by Henle’s loop ascending branch -> ↓ ADS -> ↓renal Na + reabsorption Chronic interstitial nephritis -> impairment of medullary interstitium and dysfunction of Henle’s loop ->↑urinary Na + excretion A decrease in H + excretion in the collecting duct causes the dysfunction of H + -Na + exchange -> ↑urinary sodium excretion Vomitting, diarrhea Serious perspiration, burn peritonitis->ascites
1. hypoospmolality of ECF ->inhibit thirst mechanism ->no thirst
2. Early stage, hypoosmolality of ECF -> inhibit secretion of ADH -> ↓ renal tubular reabsorption of water -> polyuria and & urinary dilution late stage, blood volume seriouly decreased ->↑ADH -> oliguria 3. Hypoosmolality of ECF ->water shift from extracellular to intracellular compartment -> ECF volume further decrease The relative volume change of ICF, interstitial fluid and plasma. ICF Interstitial fluid plasma Decrease skin turgor, postural hypotension, tachycardia, shock
Alterations of metabolism and function (continued) If sodium loss via extra-kidney, decrease of blood volume ->increase of ADS -> Na + reabsorption increase ->↓urinary sodium 4. Water movement into cells -> Brain cell swelling-> CNS dyfunction , such as nausea, vomiting, twitching, confusion, lethargy, stupor and coma.
Principles of Therapy: Treating the primary disease Supplying 5%Glocose normal saline or 0.9% NaCl solution
A hyponatremia with increased extracellular fluid volume, always associated with increased total body sodium and total body water, but the increase of water is greater than that of sodium.
When hypotonic ECF is excessively increased, this disorder is also termed water intoxication .
Serum Na + < 130mmol/L
Plasma osmotic pressure < 280mmol/L
Etiology and pathogenesis (1). Excessive water intake (2). Decreased Water loss
Tap water enema
Excessive intravenous infusion of hypotonic solution
Acute renal failure
Over secretion of ADH caused by phobia, pain, hemorrhage, shock and trauma
Over retention of hypotonic fluid in the body In general, water intoxication mostly occurred in patient with acute renal failure and infused inappropriately at the same time. which exceed the ability of renal excretion of water
serum sodium concentration is increased, while extracellular fluid volume is normal.
Characteristics: Etiology and pathogenesis: Osmoreceptor insensitive to osmotic stimulus Only osmotic pressure is obviously higher than normal level Baroreceptor, stretchreceptor Change of blood volume or pressure Hypothalamus disease abnormal normal Normal: >150mmol/L Abnormal: >160mmol/L 150-160mmol/L [Na + ] upward resetting of osmolar set-point Thirst, ADH secretion hypernatremia normovolemia
Effects of hypernatremia on the brain. Brain shrinkage within minutes of development of hypertonicity.Rapid adaptation in few hrs. Rapid correction results in cerebral edema
Effects of hyponatremia on the brain and adaptive responses. Brain swelling occurs in minutes of developing hypotonicity, Partial restoration in hrs, normalization of brain vol in days. Overly aggressive correction of Na can lead to irreversible brain damage
Michael has recently started working outdoors in the hot weather to earn money for his tuition. After a few days he experienced headaches, low blood pressure and a rapid heart rate. His blood sodium was down to 125 meq/L. The normal is 144 meq/L. How do you explain this?
Michael lost sodium by perspiration. The low sodium in his blood allowed fluid to move into cells by osmosis. Lack of fluid lowered his blood pressure to give him a headache. The increased heart rate was his bodies way of trying to increase blood pressure.
Proportional to the number of osmotic particles formed: Osm/L = moles x n (n, # of particles in solution)
Assuming complete dissociation:
1mole of NaCl forms a 2 osmolar solution in 1L
1mole of CaCl 2 forms a 3 osmolar solution in 1L
milliOsmolar units most appropriate
1 mOSM = 10 -3 osmoles/L
e.g. 1 M NaCl = 2 M Glu in Osm/L
Classification of disorders of water and sodium metabolism ECF volume Hypervolemia Normovolemia Hypovolemia Disorders of water & sodium metabolism with normal serum sodium concentration Hypotonic dehydration Isotonic dehydration Hypertonic dehydration Normal Water intoxication Edema Hyponatremia Hypernatremia Dehydration : an excessive loss of body fluid. Serum sodium concentration SIADH Rest osmostat Upward resetting of hypothalamus osmolar set-point Sodium intoxication (<130mmol/L) (130-150mmol/L) (>150mmol/L)