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Pathophysiology Water and electrolyte disorders
This is a mind map about the pathophysiology of water and electrolyte disorders, including normal water and sodium metabolism, water and sodium metabolism disorders, potassium metabolism disorders, etc. The content is comprehensive, if you hope, you can like and collect it~~
Edited at 2023-12-10 16:40:40
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Pathophysiology Water and electrolyte disorders
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This Valentine's Day brand marketing handbook provides businesses with five practical models, covering everything from creating offline experiences to driving online engagement. Whether you're a shopping mall, restaurant, or online brand, you'll find a suitable strategy: each model includes clear objectives and industry-specific guidelines, helping brands transform traffic into real sales and lasting emotional connections during this romantic season.
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- Outline
Water and electrolyte imbalance
Normal water and sodium metabolism
Volume distribution of body fluids
capacity
Adult body fluids account for approximately 60% of body weight
Intracellular fluid 40%
subtopic
Extracellular fluid 20%
The proportion of body fluid in children is higher than that in adults, which mainly increases extracellular fluid. Children are more susceptible to dehydration.
distributed
Major extracellular ions Na, Cl, HCO3
The main intracellular ions K, HPO4
body fluid osmotic pressure
Plasma osmotic pressure = anion concentration + cation concentration + non-electrolyte concentration, normal range 280 ~ 310mOsm/L
The osmotic pressure generated by plasma proteins is colloid osmotic pressure, which plays an important role in maintaining body fluid exchange and blood volume inside and outside blood vessels.
Crystal osmotic pressure plays a decisive role in maintaining the balance of water inside and outside the cell
Water and sodium balance and regulation
water and sodium balance
The daily requirement of water is 1500~2000ml.
The normal range of serum Na concentration is 130~150mmol/L
Water and sodium balance regulation
water balance
thirsty
The increase in plasma crystalloid osmotic pressure is the main stimulus for excitement of the thirst center
Decreased effective blood volume and increased angiotensin II can also cause thirst
Regulation of antidiuretic hormone (ADH)
Neurons in the supraoptic nucleus and paraventricular nucleus of the hypothalamus secrete to increase the permeability of the renal distal tubule and collecting tubule to water and increase water reabsorption.
The main stimuli that promote the release of ADH are the increase in plasma crystalloid osmotic pressure and the decrease in circulating blood volume.
Severe pain, emotional stress, nausea, and increased angiotensin II can also increase ADH release.
sodium balance
aldosterone
Promote the active reabsorption of Na, Cl water reabsorption, and excretion of K and H by the renal distal tubules and collecting tubules
Regulated by RAS system and Na, K concentration
Renal sympathetic nerve excitement, epinephrine and norepinephrine stimulate renin secretion
Atrial natriuretic peptide ANP
Acute blood volume increase releases ANP, causing strong transient diuresis and natriuretic relaxation of vascular smooth muscle.
Inhibits the secretion of renin and aldosterone, antagonizes the release of angiotensin II and sympathetic nerve terminals
Physiological functions of water and sodium
Sodium is the basis for maintaining extracellular fluid osmotic pressure and blood volume, and participates in the formation of action potentials
Water and sodium metabolism disorders
Decreased body fluid volume—dehydration
isotonic dehydration
Water and sodium are lost according to the concentration ratio in normal plasma concentration, Na concentration is 130~150mmol/L, and plasma osmotic pressure is 280~310mmol/L.
reason
Paralytic intestinal obstruction, large amounts of fluid retention in the intestinal lumen
Drain large amounts of pleural effusion, ascites, large area burns, massive vomiting, and diarrhea
Loss of digestive juices in newborns
Effect on the body
Extracellular fluid is lost, plasma volume and interstitial fluid are reduced, and intracellular fluid changes little.
Enhanced secretion of ADH and aldosterone
Decreased urine output, decreased Na and Cl
Drops in blood pressure, shock and even kidney failure may occur
Prevention and control principles
Prevent and treat primary disease
Intravenous infusion of balanced salt solution or isotonic saline to replenish blood volume as soon as possible
hypertonic dehydration
Body fluid volume is reduced, water loss is more than sodium loss, serum Na>150mmol/L, plasma osmotic pressure>310mOsm/L
Causes and mechanisms
Not enough drinking water
water source cut off
Can't drink water
thirst disorder
Too much water loss
simple water loss
Transpulmonary water loss: Hyperventilation makes the respiratory tract insensitive to evaporation and increases
Transcutaneous water loss: fever or hyperthyroidism, no sense of evaporation
Transrenal water loss: insufficient production and release of ADH, or decreased sensitivity to ADH, diabetes insipidus
Water loss is greater than sodium loss
Gastrointestinal fluid loss (diarrhea in infants and young children)
sweating profusely
transrenal loss of hypotonic fluid
Repeated intravenous injection of hypertonic solutions such as mannitol, osmotic diuresis
Influence
feeling of thirst
Oligouria, except for diabetes insipidus, increased ADH, increased water reabsorption by the kidneys, and decreased urine output
The intracellular fluid shifts to the outside of the cells, and the reduction in extracellular fluid and blood volume is not as obvious as in hypotonic dehydration.
Central nervous system dysfunction, dehydration of brain cells, local intracerebral hemorrhage and subarachnoid hemorrhage
In the early stage, there is no obvious change in urinary sodium. In the later stage, blood volume decreases, aldosterone secretion increases, and urinary sodium content decreases.
Dehydration fever: The skin evaporates less water, the body's heat dissipation is affected, and the body temperature rises (infants and young children are more susceptible)
Prevention and control principles
Prevent and treat primary disease
Mainly supplement sugar, first sugar and then salt
In hypertonic dehydration, the blood sodium concentration is high, but the patient still loses sodium, and a certain amount of sodium-containing solution should be added to prevent the extracellular fluid from becoming hypotonic.
hypotonic dehydration
Sodium loss is greater than water loss; blood sodium concentration <130mmol/L; plasma osmotic pressure <280mOsm/L
Causes and mechanisms
Loss of digestive juices and only replenishing water
Just replenish water after sweating profusely
For large area burns, only add water
renal sodium loss
Continuous long-term use of natriuretic diuretics in patients with edema
Acute renal failure, polyuria stage, water and sodium reabsorption disorder
Salt-wasting nephritis, decreased responsiveness of renal tubular epithelial cells to aldosterone, and reabsorption disorder
In Addison's disease (adrenocortical insufficiency), only replenish water and ignore sodium supplementation.
Cerebral Salt Wasting Syndrome CSWS
Hyponatremia＜130mmol/L＞
High urinary sodium >20mmol/L
Decreased extracellular fluid volume
body effects
Shock is prone to occur, the extracellular fluid is reduced, water moves from the extracellular fluid to the intracellular fluid, and hypovolemia is further aggravated.
Signs of dehydration are obvious, skin elasticity is lost, and eye sockets are sunken.
In the early stage, urine output generally does not decrease, extracellular osmotic pressure increases, ADH secretion decreases, and water reabsorption decreases. Urinary output generally does not decrease in the early stage, and severe dehydration and oliguria occur.
Extrarenal causes, low osmotic pressure, reduced ADH, no reduction in urine output, increased secretion of low sodium aldosterone, reduced urinary sodium, late stage hypovolemia activates the RAS system, increased renal tubular sodium reabsorption, decreased urine output, and reduced urinary sodium content picked up again Loss of sodium from the kidney results in an increase in urinary sodium
Prevention and control principles
Actively treat the underlying disease
Supplement isotonic saline, or hypertonic saline if the condition is severe
Increased body fluid volume
Edema (isotonic fluid)
The pathological process in which excess fluid accumulates in tissue spaces or body cavities
Classification
generalized edema
localized edema
The mechanism
Imbalance in fluid exchange inside and outside blood vessels leads to more tissue fluid production than backflow'
Increased capillary hydrostatic pressure (increased venous pressure)
Decreased plasma colloid osmotic pressure (decreased plasma protein concentration)
Increased permeability of microvascular walls, filtration of plasma proteins and albumin
Lymphatic drainage is blocked
Disturbances in the balance of water in and out throughout the body lead to an increase in the total amount of extracellular fluid
Decreased glomerular filtration rate
Primary (glomerular disease)
Secondary (reduced effective circulating blood volume such as heart failure and nephrotic syndrome)
Increased absorption of water and sodium by renal tubules ()
Increased secretion of aldosterone
Increased secretion of antidiuretic hormone
Decreased secretion of ANP
Renal blood flow redistribution
cortical ischemia
medullary congestion
Performance characteristics and effects on the body
Edema fluid properties
Leakage
Non-inflammatory, no increase in capillary permeability, low protein content, low cell number, and low fluid specific gravity
exudate
Inflammation, increased capillary permeability, high protein content, large number of cells, a large number of white blood cells, and a large proportion of fluid
Effects of edema on the body
Weight gain, BP increase, jugular vein filling, CVP increase
Common characteristics of edema
cardiac edema
Cardiogenic pulmonary edema caused by left heart failure
Edema of the right heart causing generalized edema (cardiac edema)
Renal edema (eyelid and facial edema)
Hypoalbuminemia due to massive proteinuria (nephrotic edema)
Decreased plasma colloid osmotic pressure due to hypoalbuminemia
Increased glomerular basement membrane permeability
Nephritis edema caused by significant decrease in glomerular filtration rate
acute glomerulonephritis
hepatic edema
Ascites is the main manifestation, intrahepatic blood vessel obstruction, extrahepatic portal vein capillary fluid static pressure increases, and secondary water and sodium retention
Pulmonary Edema
pressure pulmonary edema
Increased pulmonary capillary hydrostatic pressure due to left heart failure
Hyperpermeability pulmonary edema with diffuse alveolar damage
Common in acute respiratory distress syndrome, with extensive alveolar damage, lung consolidation, and hypoxemia
Do not treat hyperpermeability pulmonary edema with alveolar damage
Increased permeability of vascular endothelial cells without alveolar epithelial damage, mainly pulmonary interstitial edema
mixed pulmonary edema
Both hydrostatic pressure and increased permeability
Brain edema
Classification
Vasogenic cerebral edema
Increased capillary permeability in the brain, increased protein-containing fluid entering the intercellular space, and accumulation of large amounts of fluid in the white matter intercellular space
Cytotoxic cerebral edema
Edema fluid is mainly distributed in cells. Nerve cells, glial cells and vascular endothelial cells swell, and intercellular spaces shrink. Both gray and white matter are present, mainly white matter.
interstitial cerebral edema
Tumor inflammation or gliosis blocks aqueducts or ventricular orifices, hydrocephalus and corresponding periventricular white matter interstitial edema
treat
Use dehydrating agents as soon as possible to eliminate edema and reduce intracranial pressure.
cell membrane stabilizer
surgical decompression therapy
water intoxication
Water excretion and retention in the body, accompanied by hypokalemia and brain cell neuroedema
Cause mechanism
Insufficient renal drainage function
Acute and chronic renal insufficiency, oliguric phase, severe heart failure or liver cirrhosis, reduced effective circulating blood volume and reduced renal blood flow
Late stage hypotonic dehydration
Extracellular fluid is transferred into the cell and a large amount of water is input
Patients with increased ADH secretion receive too much water
ADH dyssecretion syndrome
Malignant tumors, central nervous system diseases, lung diseases
drug
stress
Surgical trauma, severe mental disorder
Decreased effective circulating blood volume or adrenal insufficiency
Influence
The blood sodium concentration decreases and the osmotic pressure decreases, causing cell edema (pitting edema).
Acute water intoxication causes edema of brain nerve cells and increased intracranial pressure, and brain symptoms appear earliest
Mild chronic water intoxication may cause hyposalinism syndrome, drowsiness, headache, nausea, vomiting, weakness, and muscle spasms.
Prevention and control
Prevent and treat primary diseases
Strictly control water intake
Promote the discharge of water in the body, reduce edema of brain cells, and pay close attention to heart function
Potassium metabolism disorders
Normal metabolism of potassium
potassium balance
Serum potassium concentration is normal 3.5~5.5mmol/L
Intracellular potassium concentration is as high as 160mol/L
Total potassium content 50～55mmol/Kg
Potassium excretion by the kidneys is related to the intake of potassium. Eat more and you will excrete less. Eat less and you will excrete less. But you can excrete it even if you don’t eat.
Regulation of potassium balance
Transcellular transfer of potassium
The pump-leak mechanism is a fundamental mechanism regulating transcellular transfer of potassium
The pump is a sodium-potassium pump, that is, sodium-potassium ATPase, which leaks potassium ions into the extracellular fluid along the concentration difference.
The main factor that promotes the transfer of extracellular potassium into cells
Insulin is the main hormone that affects the transcellular transfer of potassium (rescuing hyperkalemia). β-adrenergic receptor activation and the increase in extracellular potassium ion concentration directly stimulate the sodium-potassium ATPase activity and promote cellular potassium uptake.
Alkalosis can also promote the entry of potassium ions into cells
The main factor that promotes the transfer of potassium ions from intracellular to extracellular
Alpha adrenoceptor activation, acidosis, acute increase in extracellular fluid osmotic pressure and muscle contraction during strenuous exercise, etc.
Kidney's potassium excretion function
Mainly relies on the regulation of potassium secretion and reabsorption by the distal tubule and collecting tubule
Distal tubule, collecting tubule regulate potassium balance
Balance between urinary potassium intake and excretion
Potassium secretion from the distal collecting tubule
About one-third of urinary potassium is secreted from this, which is completed by the chief cells of the tubule epithelium in this segment.
Sodium is pumped into the intertubular fluid, and potassium in the intertubular fluid is pumped into the main cells, increasing the intracellular potassium concentration, increasing the potassium concentration gradient between the intracellular and tubular fluid, and promoting potassium ion secretion.
Potassium reabsorption by collecting ducts
Only when the amount of potassium uptake is obviously insufficient, the distal tubule and collecting tubule show net absorption of potassium. The lumen surface of intercalated cells is distributed with a hydrogen-potassium ATPase, also known as a proton pump, which secretes hydrogen into the lumen and reabsorbs potassium.
Regulatory factors affecting potassium excretion from distal tubules and collecting tubules
Aldosterone increases the activity of the sodium-potassium pump and increases the permeability of main cells to potassium.
Extracellular fluid potassium concentration increases the rate of potassium secretion in the distal tubule and collecting tubule
Increasing the original urine flow rate in the distal tubule can promote potassium excretion
acid-base balance state
During acidosis, renal potassium excretion is reduced, and the increase in hydrogen ion concentration can inhibit the sodium-potassium pump of the main cell, impeding potassium secretion function.
Increased renal potassium excretion in alkalosis
Colon potassium excretion function
Normally 90% of potassium is excreted by the kidneys and 10% by the colon. Colonic potassium secretion is regulated by aldosterone. In kidney failure, the filtration rate drops by up to one-third
Main physiological functions
Maintain cell metabolism
Related to glycogen synthesis and protein synthesis
maintain cell resting potential
Regulate intracellular and intracellular fluid osmotic pressure and acid-base balance
Hypokalemia
Hypokalemia with blood potassium concentration <3.5 mmol, abnormal potassium distribution in the body, and reduced serum potassium concentration
Etiology and pathogenesis
Insufficient potassium intake
Common in long-term inability to eat
Too much potassium loss
Potassium loss through gastrointestinal tract
The potassium content of digestive juice is higher than that of plasma, and a large amount of potassium is lost in digestive juice.
The loss of a large amount of digestive juice leads to a decrease in blood volume and an increase in aldosterone secretion, which promotes an increase in potassium excretion by the kidneys.
Potassium loss through kidney
Use certain diuretics to increase the exchange of potassium ions and sodium ions in the distal tubule and promote potassium excretion
Hypersecretion of aldosterone
Increased distal tubular primary urinary flow velocity
Magnesium deficiency, sodium-potassium ATPase requires Mg activation, potassium reabsorption disorder
Distal tubular acidosis, decreased renal tubular hydrogen secretion, increased potassium and sodium exchange, and increased urinary sodium excretion
The anions that are difficult to absorb in the distal tubule increase in the distal tubule, which can increase the negative charge of the renal tubular fluid and increase potassium secretion.
Transcutaneous potassium loss
Hypokalemia caused by excessive sweating
Too much potassium enters cells
Glycogen synthesis is enhanced. Large-dose insulin treats diabetic ketoacidosis. Serum potassium enters the cells with glucose to synthesize glycogen.
Acute alkalosis, pH increases by 0.1, serum potassium decreases by 10 to 15%
Enhanced beta-adrenergic receptor activity promotes potassium entry into cells
Barium poisoning specifically blocks the outflow of potassium from cells, causing potassium to be retained in cells.
hypokalemic periodic paralysis
Effects on the body
Severe symptoms occur only when serum potassium ion is lower than 3.0
muscle tissue
Muscle flaccidity or flaccid paralysis (even respiratory muscle paralysis is the main cause of death in patients with hypokalemia)
Acute hypokalemia, a sharp decrease in the extracellular potassium ion concentration, an increase in the ratio of intracellular and extracellular potassium ion concentrations, an increase in the resting potential, neuromuscular hyperpolarization block state, depolarization disorder, and reduced excitability.
In chronic hypokalemia, the ratio of intracellular and intracellular potassium ion concentrations can be close to normal, the resting potential can be normal, and the clinical symptoms are not obvious.
During hypokalemia, muscle weakness is affected by plasma calcium ion concentration and pH. Calcium ion concentration increases, competitive sodium ion influx is inhibited, phase 0 depolarization is affected, threshold potential shifts upward, and cell excitability decreases.
rhabdomyolysis
Potassium regulates skeletal muscle blood flow. Increased local potassium ion concentration can cause vasodilation and increase blood flow.
Severe potassium deficiency means that muscles cannot release enough potassium during exercise, resulting in ischemia and hypoxia, causing muscle spasm, ischemic necrosis, rhabdomyolysis, and possible renal failure.
heart
Hypokalemia can cause various cardiac arrhythmias
myocardial excitability
The inward rectifier potassium channel on the myocardial cell membrane is the main ion channel that determines the resting potential of myocardial cells. The extracellular potassium ion concentration decreases, the activity of the inward rectifier potassium channel decreases, and the permeability of myocardial cells to potassium ions decreases.
In acute hypokalemia, the activity of inward rectifying potassium channels in the myocardial cell membrane decreases, the absolute value of the resting potential decreases, approaches the threshold potential, and the cell excitability increases.
myocardial conductivity
In hypokalemia, the resting potential of Purkinje fibers is small, the expansion rate of excitement is slowed down, and myocardial conductivity is reduced.
Atrial myocardial ventricular myocardial conductance almost no longer increases
myocardial self-discipline
Fast-responsive cells in tissues such as the Purkinje fiber system accelerate automatic depolarization in the fourth phase and improve their self-discipline.
myocardial contractility
Acute hypokalemia increases membrane permeability to calcium ions, accelerates calcium ion influx, increases intracellular calcium ions, enhances excitation-contraction coupling, and enhances myocardial contractility.
Urinary concentrating dysfunction. When potassium is lacking, epithelial cells of collecting tubules and distal tubules are damaged, cAmp is insufficient, water reabsorption is impaired, and sodium chloride reabsorption is impaired in the thick ascending branch of the medullary loop, which hinders the formation of the medullary osmotic gradient and affects Reabsorption of water, resulting in polyuria and low relative density urine (lowered urine specific gravity)
In severe cases, myocardial contractility is reduced
kidney
Functional changes
Hypokalemia, increased NH3 production by renal tubular epithelial cells, and enhanced HCO3 reabsorption by the proximal tubules, one of the causes of alkalosis caused by hypokalemia
Morphological and structural changes
Vacuolar degeneration of proximal tubule epithelial cells
digestive system
Hypokalemia causes weakened gastrointestinal motility, and patients often suffer from nausea, vomiting, anorexia, severe lack of abdominal distension, and even paralytic ileus.
Glucose metabolism
Hypokalemia can cause mild elevation of blood sugar and decreased insulin secretion or weakened action
metabolic alkalosis
causing paradoxical aciduria
Prevention and control principles
Treat primary disease
Potassium supplementation is best taken orally, intravenous injection of potassium is prohibited
Treatment complications
hyperkalemia
Serum potassium higher than 5.5
Etiology and pathogenesis
Decreased renal potassium excretion (main cause)
Decreased glomerular filtration rate, oliguria or anuria in acute renal failure
Mineralocorticoid deficiency, adrenocortical insufficiency, bilateral adrenalectomy, hypoaldosteronism, type IV renal tubular acidosis
Long-term use of potassium-sparing diuretics
Transfer of intracellular potassium to the outside of the cell
Acute acidosis, hydrogen ions from extracellular fluid enter the cells, and intracellular potassium ions enter the outside of the cells
Hypoxia causes cell membrane sodium pump transport disorders, sodium ions are retained in the cells, and potassium ions in the extracellular fluid do not enter the cells. Hypoxia causes acid damage in the cells. Intracellular potassium ions are released and aggravate hyperkalemia.
Tissue decomposition causes large amounts of potassium ions to be released from cells
Hyperkalemic periodic paralysis
Excessive potassium intake, excessive intravenous potassium salt infusion too quickly, and low renal function are more likely to occur.
Effect on the body
muscle
Serum potassium ions higher than 8 can also lead to muscle weakness and even paralysis.
In acute hyperkalemia, the ratio of intracellular and intracellular potassium ion concentrations is significantly reduced, and changes in muscle function depend on the degree of increase in serum potassium.
Mild hyperkalemia, reduced potassium concentration difference inside and outside the cell membrane, reduced resting potential, increased muscle excitability, abnormal hands and feet, pain and mild muscle tremor
Severe hyperkalemia, the resting potential is close to the threshold potential level, the cell membrane is in a state of depolarization block, the resting potential is too small, the formation and transmission of action potentials are impaired, the excitability is reduced, the limbs are weak and tendon reflexes disappear, and even flaccid paralysis
chronic hyperkalemia
Slow retention, there is also an increase in cells to a certain extent, the ratio of intracellular and intracellular potassium ion concentration becomes less obvious, and the changes in neuromuscular function are not as obvious as acute ones.
heart
myocardial excitability
Similar effects on neuromuscular excitability
myocardial conductivity
The resting potential decreases, the action potential phase 0 amplitude becomes smaller, the speed slows down, the myocardial expansion slows down, the conductivity decreases, sinus node may occur, in the new chamber, atrioventricular conduction block and ventricular arrest may occur
myocardial self-discipline
Less likely to produce ectopic heart rhythms
electrocardiogram
conduction delay or block
myocardial contractility
Decreased myocardial contractility
metabolic acidosis
Paradoxical alkaline urine
Prevention and control principles
Treat primary disease
Reduce serum potassium
Potassium is transferred into cells, and glucose and insulin are injected intravenously at the same time
Use sodium bicarbonate to increase pH
peritoneal dialysis or hemodialysis
Potassium is excreted from the body
Inject calcium and sodium salts to improve myocardial electrophysiological properties