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Pathophysiology Disorders of water and sodium metabolism
Mind map of pathophysiology of water and sodium metabolism disorders, body fluid capacity: children > adults, men > women (more fat); body fluid accounts for 60% of body weight in men and 50% in women.
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Pathophysiology Disorders of water and sodium metabolism
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Pathophysiology Disorders of water and sodium metabolism
Water and sodium metabolism disorders
normal water and sodium balance
Volume and distribution of body fluids
Children>adults, men>women (more fat); male body fluids account for 60% of body weight, women 50%.
body fluid
Intracellular fluid 40%
Extracellular fluid 20%
Plasma 5%
Interstitial fluid 15%
electrolyte composition of body fluids
The cations are mainly Na, followed by K, Ca, and Mg (extracellular fluid)
The anions are mainly Cl-, followed by hco3, hpo4, so4 and organic acids and proteins (extracellular fluid)
intracellular fluid
K is an important cation, HPO4 and protein are the main anions
Osmotic pressure of body fluids
90%-95% of the extracellular fluid osmotic pressure comes from Na, Cl-, HCO3-
Plasma osmotic pressure is between 290-310mmol/L
The intracellular fluid osmotic pressure is mainly K and HPO4-especially potassium ions
Physiological functions of water and water balance
Physiological functions of water
Promote substance metabolism
regulate body temperature
lubrication
Most of the water in the body exists in the form of bound water
water balance
Excretion of water: 150ml of feces, skin (500ml of explicit sweat and non-explicit evaporation), lungs (350ml of respiratory evaporation), kidneys (1000-1500ml of urine). Normal adults excrete at least 500ml of urine and need 1500-2000ml of water every day.
Physiological functions of electrolytes and sodium balance
The normal range of sodium ions is 135-150mmol/L
Regulation of body fluid volume and osmotic pressure
The relative stability of extracellular fluid volume and osmotic pressure is achieved through the regulation of the neuro-endocrine system
OsmoreceptorsHypothalamic supraoptic nucleus and paraventricular nucleus
Increased extracellular fluid osmotic pressure → hypothalamic supraoptic nucleus receptors → thirst center excitement → drinking water
Increased ADH secretion → Binds to V2 receptors in the distal convoluted tubule and collecting duct → Enhances water reabsorption in the distal convoluted tubule and collecting duct
Inhibit the secretion of aldosterone → weaken the reabsorption of sodium ions → increase the excretion of sodium ions → reduce the concentration of sodium ions in the extracellular fluid → return the osmotic pressure of the extracellular fluid to normal
Renal urination can regulate water balance. Only when renal function is severely impaired will it have a greater impact on the total water balance.
Atrial natriuretic peptide ANP affects water and sodium metabolism: reduces renin secretion; inhibits aldosterone secretion; antagonizes the vasoconstrictor effect of angiotensin; antagonizes the sodium ion retention effect of aldosterone
Aquaporin AQP
ADH receptor V2R and AQP2 are closely related
Classification of water and sodium metabolism disorders
dehydration
hypotonic dehydration
hypertonic dehydration
isotonic dehydration
water intoxication
Edema
dehydration
Hypotonic dehydration: sodium loss is more than water loss, serum sodium ions are less than 135mmol/L, and plasma osmotic pressure is <290mmol/L
Causes and Mechanisms
lost through kidneys
Long-term continuous use of diuretics inhibits the reabsorption of sodium ions by the ascending branch of the medullary loop.
Adrenocortical insufficiency, insufficient aldosterone secretion, and reduced renal tubular sodium reabsorption
Renal parenchymal disease, chronic interstitial renal disease destroys the medullary interstitial structure and damages the ascending branch of the medullary loop.
Renal tubular acidosis, reduced H secretion function of collecting ducts, reduced hydrogen and sodium exchange
Extrarenal loss
fluid loss through gastrointestinal tract
Liquid accumulates in the third gap
lost through skin
Effect on the body
Decreased extracellular fluid, prone to shock
Decreased plasma osmolality
There is an obvious pattern of water loss
Patients with hyponatremia who lose sodium through the kidneys have increased urinary sodium content
Prevention and control
Prevent and treat primary disease and remove the cause
Proper rehydration
Give isotonic fluids to restore extracellular fluid volume
Hypertonic dehydration: water loss exceeds sodium loss, serum sodium ion concentration >150mmol/L, plasma osmotic pressure >310mmol/L
Causes and Mechanisms
reduced water intake
Too much water loss
Transrespiratory water loss: hyperventilation
Transcutaneous water loss: excessive sweating, hyperthyroidism
Transrenal water loss: insufficient ADH release in diabetes insipidus
Gastrointestinal losses: vomiting and diarrhea
Effects on the body
Thirsty
Decreased extracellular fluid content
Transfer of intracellular fluid to extracellular fluid
Hemoconcentration
Central nervous system dysfunction: extracellular fluid loss and hypertonicity cause severe dehydration of brain cells
Dehydration fever: less water evaporates from the skin, heat dissipation is affected, and body temperature rises
Prevention and control
Prevent and treat primary disease and remove the cause
Replenish lack of water in the body
Properly replenish sodium ions. Although the patient’s blood sodium concentration is high, the content is small.
Proper supply of potassium ions
isotonic dehydration
Water and sodium are lost in proportion but the concentration remains normal
It can be seen in vomiting and diarrhea, large area burns, and large amounts of pleural effusion and ascites.
water intoxication
Excessive water retention, decreased blood sodium, sodium ion concentration <135mmol/L, plasma osmotic pressure <290mmol/L
Causes and Mechanisms
Too much water intake
Reduced water excretion: more common in acute renal failure and excessive secretion of ADH
Effects on the body
Increased extracellular fluid volume, blood dilution
Intracellular edema, transfer of external fluid into cells
Central nervous system symptoms, cell swelling, and central nervous system compression symptoms caused by increased intracranial pressure
Prevention and control
Prevention and treatment of primary diseases: acute renal failure, postoperative heart failure patients, limiting water intake
Mild patients, limit fluid intake
Severely ill patients should be given strict fluid intake and hypertonic saline or diuretics
Edema
Classification of edema
systemic, local
Causes
Cardiac edema (congestive heart failure)
Renal edema (nephrotic syndrome and nephritis)
Hepatic edema (liver disease)
dystrophic edema
inflammatory edema
Lymphedema
The pathogenesis of edema
Imbalance of fluid exchange inside and outside blood vessels (effective hydrostatic pressure, effective colloid osmotic pressure and lymphatic reflux)
factor
Effective hydrostatic pressure: mean capillary blood pressure - tissue hydrostatic pressure
Effective colloid osmotic pressure: interstitial fluid colloid osmotic pressure - plasma colloid osmotic pressure
Under normal circumstances, effective filtration pressure = effective hydrostatic pressure - effective colloid osmotic pressure, tissue fluid production > reflux
reason
Increased capillary hydrostatic pressure
Decreased plasma colloid osmotic pressure
Depends on plasma albumin content
Reasons for decreased albumin content
Protein synthesis disorder, cirrhosis and malnutrition
Excessive protein loss, nephrotic syndrome
Enhanced protein catabolism, chronic infection, malignancy
Increased microvascular wall permeability
Infection, burns, frostbite - inflammatory mediators increase microvascular permeability
Imbalance of fluid exchange inside and outside the body - sodium and water retention, bulbar balance
Decreased glomerular filtration rate
Extensive glomerular disease
Effective circulating blood volume is significantly reduced
Increased reabsorption of sodium and water by the proximal convoluted tubule
Decreased atrial natriuretic peptide secretion
Increased glomerular filtration fraction
Increased reabsorption in the distal tubule and collecting duct
Increased aldosterone levels
Increased secretion
Decreased inactivation
Increased secretion of antidiuretic hormone
Characteristics of edema and its impact on the body
Characteristics of edema
Characteristics of edema fluid
Leakage
exudate
More albumin, seen in inflammatory edema
Edema skin characteristics
Pitting edema (overt edema)
Hidden edema: increased tissue fluid, up to 10% of original body weight
Characteristics of generalized edema
Gravity effect: Capillary hydrostatic pressure is directly proportional to the influence of gravity
Organizational structure characteristics
Local blood flow is blocked, hepatic venous return is blocked, and ascites occurs.
The impact of edema on the body
cell dystrophy
Effects of edema on functional activities of organs and tissues
Increased intracranial pressure, brain herniation
Laryngeal edema, airway obstruction
Potassium metabolism disorders
Normal potassium metabolism: serum potassium concentration 3.5-5.5mmol/L
potassium balance
cell membrane sodium potassium pump
Extracellular hydrogen and potassium exchange
Changes in the transmembrane potential inside and outside the renal tubular epithelial cells affect their potassium excretion
Aldosterone and distal tubule fluid flow rate
Colon excretion of potassium and sweating
Potassium metabolism disorders
Hypokalemia
Causes and Mechanisms
Insufficient sodium intake
Too much potassium loss
Loss of digestive tract: loss of digestive juices
Transcutaneous potassium loss: profuse sweating
lost through kidneys
Long-term use of diuretics (potassium depleting)
Mineralocorticoid excess (sodium retention and potassium excretion)
renal tubular acidosis
Type I (distal convoluted tubule), increased sodium and potassium exchange, excessive potassium excretion
Type II (proximal tubular), multiple substance reabsorption disorder
magnesium deficiency
Renal tubular epithelial sodium-potassium-ATPase inactivation, potassium reabsorption disorder, potassium loss
transfer of potassium into cells
Alkalosis
When the pH is high, hydrogen ions leave the cell and potassium ions enter the cell.
The exchange of hydrogen and sodium in the renal tubular epithelium is weakened and the exchange of sodium and potassium is enhanced, resulting in excessive urinary potassium excretion.
excess insulin
Activates sodium-potassium ATPase, allowing extracellular potassium to enter the cell
Promote glycogen synthesis, transfer extracellular potassium into cells along with glucose
Poisoned
Potassium channel blockage, decreased potassium ion outflow
hypokalemic periodic paralysis
Increased beta-adrenergic receptor activity
Enhanced sodium-potassium pump activity
Effects on the body
Disorders associated with abnormal membrane potential
Neuromuscular effects of hypokalemia
Effects of hypokalemia on myocardium
Changes in physiological properties of myocardium
Increased excitability
Increased self-discipline
reduced conductivity
Damage associated with cellular metabolic disorders
Effect on acid-base balance
hyperkalemia
Magnesium metabolism disorders
Calcium and phosphorus metabolism disorders