water balance and regulation of osmolality department of pathophysiology, the school of medicine,...

Water balance and regulation of osmolality

Department of Pathophysiology, the School of Medicine, Shandong University

薛冰 xuebing@sdu.edu.cn,

How will we learn in this chapter?

Causes and assessment of polyuria Renal mechanism for urine concentration and dilution Feedback control of plasma osmolality Faliure to concentrate /dilute urine Disorder of water and sodium balance

Part I :Causes and assessment of polyuria

polyuria （ >2000ml/d ）

Solute excretion increase (Osmotic diuresis)

Water excretion increase

I Solute excretion increase (Osmotic diuresis)

• = Solute Diuresis

• large amounts of a poorly reabsorbed solute such as glucose or urea

I Solute excretion increase (Osmotic diuresis)

Filtration of poorly reabsorbed solute

Reabsorption of solute

Osmotic DiuresisOsmotic Diuresis

Poorly reabsorbed Osmolyte

H20 H20 H20

Na Na Na

H20H20H20

Na Na Na

HypotonicSaline

Osmolyte = glucose, ,urea

Causes of Osmotic diuresis

Infusion of manitol Diabetes mellitus Plasma glucose filtration ＞ reabsorption Chronic kidney disease (azotemia ) Diuretic drugs

II Dilute polyuria(water excretion )

Overdrinking （ psychiatric disturbance) + kidney dysfunction

Psychogenic polydipsia

Central or nephrogenic DI

Summary:Diagnostic approach of polyuria

Part II:Renal mechanism for urine concentration or dilution

Importance: keep the normal osmolatily of plasma(290mosm/liter)

When there is excess water in the body and body fluid osmolarity is reduced, the kidney can excrete urine with an osmolarity as low as 50 mosm/liter, a concentration that is only about one sixth the osmolarity of normal extracellular fluid.

Conversely, when there is a deficient of water and extracellular fluids osmolarity is high, the kidney can excrete urine with a concentration of about 1200 to 1400 mOsm/liter

The basic requirements for forming a concentrated or diluted urine

(1)a high osmolarity of the renal medullary interstitial fluid,

which provides the osmotic gradient necessary for water reabsorption-(loop of Henle)

(2) the controlled secretion of antidiuretic hormone (ADH), which regulates the permeability of the distal tubules and collecting ducts to water;

  I The Counter-Current Mechanism Produces a Hyperosmotic Renal Medullary Interstitium

Key substance I:sodium chloride

Figure 26.13c

Key substance II:urea

The vasa recta trap salt and urea within the interstitial fluid but transport water out of the renal medulla

Vasa recta remove more solute than water

Increased osmolarity

ADH

Post. Pituitary

Urge to drinkSTIMULUS

cAMP+

II Action of ADH in collecting ducts

The Role of ADH

• There is a high osmolarity of the renal medullary interstitial fluid, which provides the osmotic gradient necessary for water reabsorption to occur.

• Whether the water actually leaves the collecting duct (by osmosis) is determined by the hormone ADH (anti-diuretic hormone)

• Osmoreceptors in the hypothalamus detect the low levels of water (high osmolarity), so the hypothalamus sends an impulse to the pituitary gland which releases ADH into the blood stream.

• ADH makes the wall of the collecting duct more permeable to water.

• Therefore, when ADH is present more water is reabsorbed and less is excreted.

Figure 26.15a, b

The Effects of ADH on the distal collecting duct and Collecting Ducts

Summary: Conditions required for urinary concentration and dilution

To concentrate the urine

Adequate soulte delivery to the loop of Henle

Normal function of the loop of Henle

ADH

To dilute the urine

Adequate soulte delivery to the loop of Henle and early distal tubule

Normal function of the loop of Henle and early distal tubule

No ADH

Hyperosmotic Renal Medullary Inters

titium

Part III:Feedback control of plasma osmolity

ADH has half-life of 10-15 minutes. It is metabolized in liver and kidney. Effects of ADH on collecting tubule are rapid on and rapid off.

Releationship between the plasma osmolality and the concentration of ADH

• Decrease in Blood Volume• Decrease in Blood Pressure• Stress ,pain, nausea

Other factors that controll ADH secretion

Mechanism of ADH action in the kidney

Receptor of A

DH

: V1A

, V1b,V

2(kidney)

AQP-2

Other actions of ADH Intensification of the medullary interstitial concentratio

n:①increase the activity of the sodium chloride reabsorption in thick ascending limb of the loop of the Henle

②increase the permeability of the inner medullary duct to urea

Vasoconstriction(V1 receptor):

Part IV:Failure to concentrate the urine

Failure to generate the medullary concentration gradient:

poor solute delivery to the loop of Henle impaired action of thick ascending limp of loop Failure to ADH effect No ADH release No ADH action in kidney

Part V:Failure to dilute the urine

Renal failure

ADH secretion increase

Part VI:Disorders of Water and Sodium balance

I Classification

According to the changes of [Na+]e:

(1)Hypernatremia

(2)Hyponatremia

According to the changes of volume:

(1)Dehydration (Hypovolemia)

(2)Overhydration (Hypervolemia)

According to the changes of both [Na+]e and volume at the same time:

(1)Hypernatremia

1) Hypovolemic hypernatremia

Hypertonic dehydration(water deficit more than sodium deficit;water deficit)

2) Hypervolemic hypernatremia

3) Normovolemic hyperhatremia

(2)Hyponatremia

1) Hypovolemic hyponatremia

Hypotonic dehydration

2)Hypervolemia hyponatremia

Hypotonic overhydration (water intoxication)

3) Normovolemic hyponatremia

(3) Normal serum [Na+]

1)Isotonic dehydration

2) Isotonic overhydration (edema)

According to the clinic importance:Dehydration1. Hypertonic dehydration (hypovelemic hypernatremia)

2. Hypotonic dehydration (hypovelemic hyponatremia)

3. Isotonic dehydration

Overhydration4. Hypotonic overhydration

Water intoxication(hypervolemic hyponatremia)

5. Isotonic overhydration

Edema

I Dehydration

---------------------------------------------------------------

Dehydration [Na+] Osmotic pressure (mmol/L) (mOsm/L)

---------------------------------------------------------------

Hypertonic >150 > 310

Hypotonic <130 < 280

Isotonic 130~150 280~ 310

----------------------------------------------------------------

1. Hypertonic Dehydration(hypovolemia hypernatremia )

(1) Concept

Both water and sodium are lost (hypovolemia), but the water loss is in excess of salt loss (hypernatremia).

(basic reason)

Then the volume of ECF is reduced.

The [Na+] is over 150 mmol/L,

The plasma osmotic pressure is >310 mOsm/L.

(2) Etiology(water decrease)1) Decreased water intake: ①no water during navigation or

in desert ②difficulty in swallowing becau

se of esophageal diseases ③ no sense of thirst due to brai

n injury or coma ④ severe vomiting,. underdose of infusion in treat⑤

ment of patients

gains (ml/day) loss (ml/day)----------------------------------------------drink 1200 lung 300food 1000 skin 500metabolic feces 200water 300 urine 1500----------------------------------------------total 2500 2500

At the same time, pure water loss from At the same time, pure water loss from lung (300ml/d) and skin (500ml/d) is not lung (300ml/d) and skin (500ml/d) is not avoidable, even increased. avoidable, even increased.

2) Increased loss of water①via skin ② via respiration ③ via gastrointestinal tract ④ via kidney, if water replenish is not

enough.

gains (ml/day) loss (ml/day)----------------------------------------------drink 1200 lung 300food 1000 skin 500metabolic feces 200water 300 urine 1500----------------------------------------------total 2500 2500

①via skin: Normally 500 ml of pure water

will be lost by insensible evaporation from skin each day.

When the environmental or body temperature is increased, the evaporation (insensible loss) will increase from skin.

Since sweat is hypotonic (0.2%NaCI), there will be more water loss than salt loss during sweating.

Elevation of 1 (celsius) will incr℃ease loss of 500 ml pure water by evaporation each day.

gains (ml/day) loss (ml/day)----------------------------------------------drink 1200 lung 300food 1000 skin 500metabolic feces 200water 300 urine 1500----------------------------------------------total 2500 2500

② via respiration:

Since the expired air contains water vapour, the water loss from lung is 300 ml of pure water each day.

The pure water loss is increased to 1300ml/day. during hyperventilation.

(metabolic acidosis, bronchitis, fever)

gains (ml/day) loss (ml/day)----------------------------------------------drink 1200 lung 300food 1000 skin 500metabolic feces 200water 300 urine 1500----------------------------------------------total 2500 2500

③ via gastrointestinal tract Vomiting and diarrhe

a will lose a lot of body fluid.

Gastric juice is isotonic, loss of gastric juice with the loss of pure water from skin and lung may lead to hypertonic dehydration.

The [Na+] of watery stool is about 60 mmol/L (hypotonic fluid).

gains (ml/day) loss (ml/day)----------------------------------------------drink 1200 lung 300food 1000 skin 500metabolic feces 200water 300 urine 1500----------------------------------------------total 2500 2500

④ via kidney: When the ADH secretion is red

uced, such as diabetes insipidus. Increased water loss occurs.

Patients with diabetes also have increased urinary water loss due to the osmotic diuresis.

Tube feeding with a high concentration of protein is used to unconscious (coma) patients.

The urea will increase in the urine, which causes osmotic diuresis.

gains (ml/day) loss (ml/day)----------------------------------------------drink 1200 lung 300food 1000 skin 500metabolic feces 200water 300 urine 1500----------------------------------------------total 2500 2500

(3)Alterations of metabolism and function

1) Adaptive (compensatory) responses of the body

2) Characteristic effects of hypertonic dehydration on the body

1) Adaptive (compensatory) responses of the body

① Drink more water because of severe thirst Hyperosmolarity and hypovolemia stimula

te the sense of thirst via central osmoreceptors.

Diminished saliva and the dry mucous membranes lead to the sense of thirst.

no thirst

increase of ECF osmolality (1~2%)

hypovolemia elevated angiotensin II vasoconcentration

dryness ofmouth

osmoreceptor (anterior hypo

thalamus)

volume receptorin venae cavae and atrium

thirst center (anterior hypothalamus)

sense of thirst and drink of water

decrease of ECF

osmolality increase of ECF volume

decrease of angiotensin concentration II

disappear of dryness of mouth

Obvious thirst occurs at early stage of hypertonic dehydration. If possible, the patient may drink water until the patient has again normal osmolarity and normal volume of ECF.

NormalNormal

Plasm

aP

lasma Interstitial Interstitial

fluidfluidIntracellular fluidIntracellular fluid

②Increased water reabsorption by increased ADH

ADH release is stimulated by the hyperosmolarity of the ECF and the hypovolemia.

increase of ECF osmolality (1~2%) via osmoreceptor

hypovolemia via volume receptor

synthesis and release of ADH

decrease osmolality of ECF

increase volume of ECF

increases the reabsorption of water in increases the reabsorption of water in kidneyskidneys

ADH increases the reabsorption of water in kidneys. The volume of ECF will increase. The high osmolarity will decrease to normal.

2) Characteristic effects of hypovolemic hypernatremia (hypertonic dehydration) on the body

①Thirst occurs at the early stage of hypertonic dehydration.

②Oliguria(except for diabetes insipidus )

at the early stage of hypertonic dehydration. (<400~500 ml/day).

Urine specific gravity

Metabolic wastes(urea, uric acid) are retained in the body (azotemia,uremia)

③Fever

infantile dehydration fever.

④Intracellular dehydration

In which organ is the cell shrinkage

most dangerous to the patient?

Brain cell dehydration produces brain dysfunction like lethargy (weakness, apathy, absence of interest), which may progresses to coma (unconsiousness) when the water deficient is severe.

Increased irritability (muscular twitch, delirium) may occur, especially in children.

Twitch: uncontrollable sudden, quick movement of muscle

Delirium: violent mental disturbance accompanied by wild talk (wild excitement)

cerebral hemorrhage

⑤loss of body weight

⑥urine sodium content ： early or mild: urine sodium content normal ,the con

centration even increase

Later phase or serious: sodium content decrease(aldosterone )

1) Treat the primary disease, such as diarrhea or diabetes insipidus.

2) Replace first with 5% glucose solution to reduce the hyperosmolarity and to increase the volume of ECF.

3) Add small amount of 0.9% NaCl after infusion of 5% glucose solution.

(4) Principle of treatment(4) Principle of treatment

4)How to decide the volume of fluid replacement?

Degree Volume of water loss (of % body weight)

clinic manifestation

Mild 2~4% thirst, skin elasticity decrease,oliguria,urine osmotic pressure>600mOsm/L ,urine specific gravity>1.020

Moderate 4~6%

severe thirst ， Postural hypotension, urine osmotic pressure>800mOsm/L, urine specific gravity>1.025 apathy,fever, acidosis

Severe >6% Shock, oliguria or anuria, BP decrease,hyperkalemia,serious acidosis, death

2. Hypotonic Dehydration(hypovolemic hyponatr

emia)

(1) Concept

There is loss of both water and sodium (hypovolemia), the salt loss is in excess of water loss (hyponatremia).

The ECF is hypotonic ([Na+]<130 mmol/L), the osmolarity is lower than 280mOsm/L.

(2) Causes1)Inappropriate treatment:

Replace of water only to the patients with dehydration caused by vomiting, diarrhea, gastric suction(digestive juice) ， excessive sweating (hypotonic solution with sodium)

2)Renal loss of Na+:

Adrenocortical insufficiency (Addison’s disease)

Inappropriate long-term use of diuretics: Some diuretics (e.g. Frusemide) inhibit the Na+ reabsorption in renal tubules.

Acute kidney faliure(diuretic phase)

Renal tubular acidosis: Dysfunction of H+-Na+ exchange leads to a d

ecrease of H+ secretion, the urinary Na+ excretion is increased.

3)other way that increase the extrarenal sodium loss:

Serious burn, body fluid accumulation in the “third space”(peritonitis)

(3)Alterations of metabolism and function 1)Adaptive responses

Aldosterone secretion is stimulated by the low sodium concentration, except in the case of adrenocortical insufficiency.

NormalNormal

Interstitial fluidInterstitial fluid

Intracellular fluidIntracellular fluidP

lasma

Plasm

a

2) Characteristic effect of hypotonic dehydration on the body  

urine specific urine volume gravity [Na+] ---------------------------------------------------------- early ADH ± or

stage ALD  

late ADH stage ALD -----------------------------------------------------------(注：经肾失钠的低渗性脱水，尿钠不减少 ) sodiun loss through kidneys: urine sodium concentration increrase

① Urine

②Hypotension even shockExtracellular fluid sodium concentra

tion decrease. Then water transport from interstitial fluid to intracellular fluid.ECF decrease.

The blood pressure may decrease. Postural hypotension and shock will occur because the decreased blood volume. (urine doesn’t decrease at the early stage and water shifts into the cells)

③Severely reduced interstitial fluid(dehydration sign)

Decreased fluid in the skin tissue results in the reduce of skin elasticity. When the skin is pinched, it tends to remain in fold.

Eyeball tension is decreased, the eyeballs are soft and sunken. (low protein concentration and colloid osmotic pressure)

Interstitial Interstitial fluidfluid

Intracellular Intracellular fluidfluid

Plasm

Plasmaa

④Intracellular overhydration

Water will shift from ECF to ICF because the ICF is relatively hypertonic. The cell will swell.

Brain cell overhydration produces brain dysfunction. (Cranial cavity is fixed)

(severe headache, high brain pressure, nausea, vomitting, confusion and coma)

Note: If the hyponatremia lasts over a long time, there will be an adaptive loss of solutes from ICF.This response mitigates the brian cell swelling.

⑤There is no obvious thirst at early stage because of the low crystal osmotic pressure.

(4) Principles of treatment

Cure the primay disease(correct the sidium loss)

Replacement of isotonic saline (0.9% NaCl) first.

Replacement of hypertonic fluid may lead to hypertonic state.

Pure water is easy to loss via skin and lung.

Hyperosmotic fluid are seldom used, except in urgent state of brain edema. 

3. Isotonic Dehydration

(1) Concept

There is loss of fluid (dehydration), the water loss is equal to salt loss. The ECF in the body is isotonic.

The [Na+] is 130~145 mmol/L.

The osmolarity is 280~310 mOsm/L.

2) Causes

(a) Loss of fluid is caused by vomiting,diarrhea, hemorrhage and from the burned area.

(b) The isotonic dehydration can be induced from hypertonic and hypotonic dehydration by the renal regulation.

3) Adaptive responses The main change in isotonic dehydration is the re

duced volume of ECF. (a) It stimulates the thirst, so that the patient

will ask to drink water to replace the volume of ECF. (not as strong as hypertonic dehydration)

(b) ADH release is stimulated, so that the water reabsorption will increase to replace the volume of ECF.(not as much as hypertonic dehydration)

(c) Secretion of aldosterone is increased due to hypovolemia.(not as much as hypotonic dehydration)

4) Effect on the body (a) Urine volume is diminis

hed because of the decreased GFR, increased ADH and aldosterone secretion.

(b) No water shift and related symptoms and signs.

(c) Poor skin elasticity and sunken eyeball, because of the reduction of interstitial fluid.

5) Principle of treatment Hypotonic saline is needed

to replace the fluid deficiency.

III. Overhydration

According to the sodium concentration:

(1)Hypertonic overhydration

(2) Hypotonic overhydration (water intoxication)water intoxication)

(3) Isotonic overhydration (edema)

(I) water intoxication (Hypotonic overhydration) 1 Concept Excessive fluid in the body is called overhydr

ation. Excessive hypotonic fluid in the body is called

hypotonic overhydration (water excess ). Severe water excess causes a serial of symp

toms and signs, and is called water intoxication.

2 Causes The main causes are excessive water intake

and less loss of water. (a) Excessive water intake ①Excessive venous infusion of 5% glucose

solution. ②Excessive water intake of psychotic

disturbances (e.g. schizophrenia) may cause water intoxication.

At the same time, the kidneys cannot eliminate the excessive water.

Chicago Daily News Aug. 9, 1958 reported that the world’s water drinking champion (1935) drank 20 L of water within 30 min, and was awarded a “hose”.

  It is obvious that this champion is healthy (without water intoxication).

Excessive water intake only can not lead to the water intoxication .

(b) Decreased water loss

①Oliguria due to low renal blood flow( in congestive heart failure,renal failure).

② Oliguria due to excessive secretion of ADH Several factors can stimulate the ADH secretion,

like fear, stress, anesthesia, pain and some drugs (e.g. morphine and meperidine),

At the same time, fluid intake (intravenous or oral) is not carefully controlled.

③ Syndrome of inappropriate secretion of ADH (SIADH)

Causes of SIADH are:

Pulmonary diseases (viral and bacterial pneumonias, tuberculosis, fungal infection, lung abscess)

diseases of central nervous system ( brain tumor, brain abscess, encephalitis and meningitis)

Tumors of lung, pancreas, thymus and duodenum lead to ectopic ADH synthesis.

3 Effects on the body (a) Dilutional hyponatremia Low serum protein concentration. Low serum osmosity Increased blood volume. (b) A rapid weight gain in acute water intoxication (c) Cellular overhydration of central nervous syst

em. appetite disorder , nausea, vomiting Muscular weakness and twitching Mental disturbances, convulsive seizures, stup

or, and coma. (d) Peripheral and pulmonary edema

4 Principle of treatment

(a) Restriction of water intake (b) Diuretics to excrete the excessive water ；

Mannitol infusion (c) Hypertonic saline (3%NaCl) for severe cas

e, to raise the osmolarity of ECF quickly, to start the movement of water from the cell

s into extracellular space, then excretion from kidneys.

Case discussion

  A 25-year-old male has a head injury and unable to eat. He received 4~5 L of 5%glucose per day to replace his fluid losses and for nutritional purposes. On the 5th day he experienced convulsions and coma. The followings are his laboratory findings.

---------------------------------------------------------------------------Day Body weight Plasma[Na+] Plasma osmolarity (Kg) (mmol/L) (mOsm/L)---------------------------------------------------------------------------O 75 140 3001 76 137 2952 78 130 2803 79 125 2704 80 120 2605 82 115 250--------------------------------------------------------------------------Questions: (1)What is the problem (pathological process) he

had? (2) Is this the normal response to intravenous inf

usion of 5%GS? (3)What is the reason of convulsion and coma?

(II) Isotonic overhydration (Edema)

1. Concept and classification

(1)Concept:excessive fluid accumulated

within the interstitial space

and cavity (hydrops).

Hydrops Ascites (peritoneal cavity)

hydrothorax (pleural cavity)

articular cavity (hydrarthrus)

(2) Classification

1) According to the distribution of edematous fluid:

(a) Local edema: Local edema occurs in one organ or

a part of the body. (brain edema, pulmonary edema, etc).

(b) Generalized edema(anasarca): Generalized edema occurs in whole b

ody (cardiac edema, renal edema, etc).

Lower extremity edema

2) According to the causes of edema:

cardiac edema

renal edema

hepatic edema

idiopathic edema

3) According to the gravity of edema:

recessive (non-pitting) edema;

frank (pitting) edema.

2. pathogenesis of edema

Basic pathogenesis:

(1) Retention of water and sodium in the interstitial space

( Imbalance of exchange between intra-vascular and extra-vascular fluid. )

  (2) Retention of fluid in the body.

( Imbalance of exchange between intra- and extra-body fluid)

(1) Imbalance of exchange between intra-vascular and extra-vascular fluid

1) Increased capillary hydrostatic pressure (CHP)

2) Decreased plasma colloidal osmotic pressure COP

3) Increased permeability of the capillary wall

4) Obstruction of lymphatic return

capillary hydrostatic pressure (CHP):A(30mmHg);V(12mmHg)capillary hydrostatic pressure (CHP):A(30mmHg);V(12mmHg)

interstitial hydrostatic pressure(IHP):10mmHginterstitial hydrostatic pressure(IHP):10mmHg

effective HPeffective HPCHP

IHP

colloid osmotic pressure(COP):sercum COP 25mmHg;colloid osmotic pressure(COP):sercum COP 25mmHg;

Interstitial COP 15mmHgInterstitial COP 15mmHg

S-COP

I-SOPEffective COP

Effective filtration pressure: A(10mmHg) V(-8mmHg)

1) Increased capillary hydrostatic pressure (CHP)

Venous obstruction:thrombophlebitis, oppress

Heart failure, pregnancy

The increase of effective filtration pressure should overtakes the compensation of increased lymphatic return before edema occur.

2) Decreased plasma colloidal osmatic pressure

Causes: ① Increased loss of plasma albumin, such as in exten

sive burn, nephrotic syndrome(10g protein/day), etc. ② Decreased synthesis of plasma albumin, such as in

hepatic dysfunction and starvation. ③ Increased protein consumption in malignant tumor

s, chronic inflammation(tuberculosis). ④ Dilution of serum protein due to over-infusion of

water and sodium.

Albumin is the main factor for the serum COP. The albumin has the highest concentration and the lowest molecular weight, so albumin has the most particles in serum.

--------------------------------------------------------------------------------

1 g osmotic P. Content MW

(mmHg) (g/100 ml serum) (KD)

-------------------------------------------------------------------------------

albumin 5.5 3.5~4.5 <70

globulin 1.4 2.5~3.8 160KD(IgG)

fibrinogen 1.0 0.2~0.4 >300

------------------------------------------------------------------------------

3) Increased permeability of the capillary wall  Causes: ① infection, the hyaluronidase 透明质酸 released by bacteria

can damage (hydrolyze the connective tissue) the capillary wall.

② Hypoxia, acidosis, radiation damage, trauma and bur

n may lead to the degeneration of basement membrane of capillary.

③ Inflammatory media such as histamine(HA) ， kinins

and 5-hydroxy`tryptamine(5-TH) may cause the contraction of microfilament in endothelial cells and the formation of “gap” between endothelial cells.

4) Obstruction of lymphatic return

Causes  ① tumor:

② The parasites enter into the lymphatic vessels.

The edema caused by lymph obstruction is called lymph edema.

elephantiasis infestation

(2)Imbalance of exchange between intra- and extra-body fluid

1) Decreased glomerular filtration rate(GFR)

① primary decrease of GFR: acute or chronic glomeronephritis

② secondary decrease of GFR:

effective blood volume (heart failure)

2) Increased reabsorption of water and sodium in renal tubules

①blood redistribution in kidney:

increased sympathetic excitability: the cortical artery contracts , large amount of blood flow shifts from cortical nephrons to juxtameddulary nephrons, so the reabsorption of water and sodium is increased.

②②Decreased secretion of Decreased secretion of atrial natriatrial natriuretic peptideuretic peptide (ANP):inhibit sodium (ANP):inhibit sodium reabsorption in proximal tubulereabsorption in proximal tubule

③Increased secretion of aldosterone decreased effective increased [K+] circulating volume decreased [Na+] in ECF   activation of renin- angiotensin system,   secretion of aldosterone.   increased Na+

reabsorption increased ADH release   retention of water and sodium

④④Increased secretion of antidiuretic hormone (ADH)Increased secretion of antidiuretic hormone (ADH)

(3) Alterations of metabolism and function

 1) Properties of edematous fluid-----------------------------------------------------------------------------------------------Edematous causes protein appearance specific fluid concentration gravity------------------------------------------------------------------------------------------transudate effective filtration↑ <25g /L clear <1.015 pressure

exudates permeability of↑ 30-50g/L muddy >1.018 vascular wall

--------------------------------------------------------------------------------------------

2)Distribution of anasarca2)Distribution of anasarca

(3) Effects of edema on the body

1) Beneficial effects 2) Harmful effects

1) Beneficial effect①Protective effects in inflammatory edema

(a) Dilute and neutralize the toxin by the edematous fluid.

(b) Promote transportation of antibody and drugs to the inflammatory area due to the increased permeability of vascular wall.

(c) Form the fibrin net to prevent bacteria from spreading to the peripheral area.

.

② ‘Safety valve’ of circulatory system When the volume of plasma is rapidly expanded

(venous infusion), large amount of fluid may transfer to the interstitial space.

It is an important way to regulate the blood volume.

2) Harmful effects

①Increase the distance between capillary and cells. The supplies of nutrients and oxygen will be reduced. The edematous tissue will be dystrophic( 营养障碍 ). The potential of anti-infection is reduced. The wound will be not easy to heal.

②Dysfunction of edematous organs and tissue

Dysfunction of edematous organs and tissue depends on the rate and extent of development of edema.

Edema of vital organs (lungs, brain, ·larynx 喉) will be dangerous for the life.

Laryngeal edema (asphyxia)

(5) Priciples of treatment

1) Eliminate the primary causes of edema (hepatic cirrhosis, heart failure)

 2) Therapeutic methods for the pathogenesis of ede

ma ①restriction of salt intake ②promote the excretion of water and sodium. ③Increase of protein intake. ④Glucocorticoids for decrease of the vascular permeability.