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MindMap Gallery Water, electrolyte and acid-base balance disorders

Water, electrolyte and acid-base balance disorders

This is a mind map about water, electrolyte and acid-base balance disorders. Water, electrolyte and acid-base balance disorders refer to the imbalance in the quantity or proportion of water and electrolytes in the body, leading to physiological dysfunction.

Edited at 2023-11-13 08:15:03

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Water, electrolyte and acid-base balance disorders

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Outline

Pathophysiology-Acid-base balance disorders mind map
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Pathophysiology - Acid-base balance disorder
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Mason·Carter

Water and electrolyte metabolism disorders

Water and sodium metabolism disorders

Normal water and sodium balance

Body fluids: ICF 40%; ECF 20%

Electrolyte: Na, K, Ca2, Mg2; CI-, HCO3-, HPO42-, SO42-

Osmotic pressure of body fluids

Extracellular fluid: Na, CI-, HCO3- (90% ~95%)

Intracellular fluid: mainly K, HPO42-

Physiological functions of water

Promote substance metabolism

regulate body temperature

lubrication

bound water

water balance

Physiological functions of electrolytes

Inorganic electrolyte

Maintain osmotic pressure and acid-base balance of body fluids

maintain resting potential

Participate in action potential

Participate in metabolism and physiological functions

sodium balance

If you take in more, you will excrete more; if you take in less, you will excrete less.

Osmoreceptors

Hypothalamus (supraoptic nucleus and paraventricular nucleus)

Affects antidiuretic hormone (ADH) release

Enhance water reabsorption by renal distal convoluted tubules and collecting ducts

nephron

renal corpuscle

glomerulus

form original urine

renal capsule

renal tubules

proximal tubule

Recycles 99% of water, all Glc

distal tubule

Reabsorb part of sodium and water and excrete potassium

Water and sodium metabolism disorders

dehydration

hypotonic dehydration

The sodium loss is more than the water loss, the serum Na concentration is <135mmol/L, and the plasma osmotic pressure is <290mmol/L.

Mostly due to hormonal problems, such as insufficient secretion of aldosterone;

After a large amount of water loss, only replenishing water can also cause hypotonic dehydration.

hypovolemic hyponatremia

isotonic dehydration

Vomiting, diarrhea, extensive burns, pleural effusion, and ascites

hypertonic dehydration

reduced intake

water source cut off

Difficulty drinking water

Lost too much

Profuse sweating (hypotonic fluid)

diabetes insipidus

hypovolemic hypernatremia

water intoxication

Water retention significantly increases body fluid volume and decreases blood sodium

hypervolemic hyponatremia

Causes and Mechanisms

Too much intake

exclude reduction

Acute renal insufficiency and inappropriate infusion (excessive secretion of ADH)

Edema

Imbalance of fluid exchange inside and outside blood vessels

Increased capillary flow static pressure

heart failure; tumor compression

Decreased plasma colloid osmotic pressure

Cirrhosis; protein loss; chronic wasting disease

Increased microvascular wall permeability

Infections, burns, frostbite

Lymphatic drainage is blocked

Malignant tumors; radical mastectomy for breast cancer

Imbalance of fluid exchange inside and outside the body - sodium and water retention

Decreased glomerular filtration rate

glomerular disease

Increased reabsorption of sodium and water by the proximal convoluted tubule

Decreased atrial natriuretic secretion

Increased glomerular filtration fraction

Increased water reabsorption by the distal convoluted tubule and collecting duct

Increased aldosterone levels

Increased secretion

Decreased inactivation

Increased secretion of antidiuretic hormone

congestive heart failure

Activation of the renin-angiotensin-steroid system

Potassium metabolism disorders

Normal potassium content is about 50~55mmol/kg

Eat more and row more, eat less and row less, and skip even if you don’t eat.

Plasma potassium balance

cell membrane sodium potassium pump

Sodium and potassium exchange inside and outside the cell

Changes in transmembrane potential

Aldosterone and distal tubule fluid flow rate

Colonic potassium excretion and sweating

mechanism

Hypokalemia

Serum potassium concentration is less than 3.5mmol/L

Inadequate intake of potassium

Digestive tract obstruction, coma, anorexia, postoperative fasting

Too much potassium loss

Potassium loss through gastrointestinal tract

Vomiting, diarrhea, gastrointestinal decompression and intestinal flaccidity

Potassium loss through kidney

Myeloid or thiamine diuretics

Primary and secondary hyperaldosteronism

Kidney disease (kidney nephritis, acute renal failure)

Type I and II acidosis

magnesium deficiency

Transcutaneous potassium loss

manual labor

Transfer of extracellular potassium into cells

Alkalosis

excessive insulin use

Increased B-adrenergic receptor activity

hyperkalemia

Serum potassium concentration higher than 5.5mmol/L

Too much potassium

Commonly seen in improper handling

Decreased potassium excretion

renal failure, acute renal failure, chronic renal failure

Mineralocorticoid deficiency

Absolute: Adrenocortical insufficiency

Relative: for renal tubular diseases

Long-term use of potassium-sparing diuretics

Transfer of potassium from intracellular to extracellular

acidosis

Hemolysis

hypoxia

Effects on the body

Hypokalemia

Metabolic alkalosis (paradoxical aciduria)

Low potassium (in collecting ducts)

Sodium-potassium pump is inhibited

Increased sodium-potassium pump transport

More hydrogen ions are emitted

hyperkalemia

Metabolic acidosis (paradoxical alkaline urine)

Neuro-muscular effects

Hypokalemia

acute

Potassium concentration drops sharply

The ratio of [K ]i and [K ]e becomes larger

Resting potential (Em) negative value increases

Cell hyperpolarization block state

Chronic

The ratio of [K ]i and [K ]e is not large

The course of the disease is slow and no obvious changes

hyperkalemia

Acute (mild)

Em absolute value decreases

Increased excitability

Acute (severe)

The Em value drops or is almost close to the Et level

fast sodium channel inactivation

Cell depolarization block

Chronic

The ratio of [K ]i and [K ]e is not large

The course of the disease is slow and no obvious changes

Effect on myocardium

Hypokalemia

Myocardial physiological properties

Increased excitability

Increased self-discipline

reduced conductivity

Contractile changes

changes in electrocardiogram

Impairment of myocardial function

Arrhythmia

Increased sensitivity to cardiotonic drugs

hyperkalemia

Myocardial physiological properties

excitability changes

reduced self-discipline

reduced conductivity

reduced contractility

changes in electrocardiogram

Impairment of myocardial function

Conduction delay and unidirectional block

The effective refractory period is shortened again

severe cardiac arrhythmia

Acid-base balance disorder

Normal values of the body and sources of acid and alkali substances

Arterial blood pH is 7.35 to 7.45, with an average of 7.40

Acidic substances: 1. Volatile acid ➡️H2CO3 2. Fixed acid: excreted in urine through kidneys

Alkaline substances mainly come from food

Regulation of acid-base balance

buffering effect of blood

bicarbonate buffer system

Phosphate buffer system

protein buffer system

regulation of lungs

Central regulation of respiratory movement: The chemoreceptors of the respiratory center are sensitive to changes in H⁺ in the cerebrospinal fluid and local extracellular fluid. Once the H⁺ concentration increases, the respiratory center is excited, making the respiratory movement deepen and accelerate. However, H⁺ in the blood cannot easily pass through the blood-brain barrier, so changes in blood pH have less effect on the central chemoreceptors. However, CO2 in the blood can quickly pass through the blood-brain barrier, increasing the H⁺ concentration around the chemoreceptors, thereby increasing the concentration of H⁺ around the chemoreceptors. The respiratory center is excited.

Peripheral regulation of respiratory movements: sensing hypoxia and causing excitement of the respiratory center.

regulation of tissue cells

Ion exchange

Regulatory function of the kidney (excretion of H⁺, excretion of NH₄⁺, reabsorption of Na⁺, HCO3-)

Proximal tubule secretes H⁺ and reabsorbs NaHCO3

The distal convoluted tubule and collecting duct secrete H⁺ and reabsorb NaHCO3 (urine acidification)

Emission of NH₄⁺

simple acid-base balance disorder

Metabolic acidosis ➡️Plasma HCO3-primary decrease

reason

Kidneys excrete acid and maintain alkali⬇️

kidney failure

Type I and II renal tubular acidosis

Use carbonic anhydrase inhibitors

HCO3-too much direct loss

metabolic dysfunction

lactic acidosis

ketoacidosis

other reasons

Too much exogenous acid intake

hyperkalemia

Hemodilution (large amounts of saline)

Classification

AG-increased metabolic acidosis

AG normal metabolic acidosis

compensatory adjustment

Blood compensation, causing hyperkalemia

Pulmonary compensation, causing respiratory center ⬆️

Renal compensation (not caused by renal factors), secreting H⁺, protecting HCO3-

Metabolic alkalosis➡️Plasma HCO3-primary increase

reason

Too much acid loss (via stomach, kidneys)

HCO3-excess load

Hypokalemia

liver failure

Classification

saline reactive acidosis

saline resistant acidosis

compensatory adjustment

OH- is buffered by weak acid, and the HCO3- concentration increases. In addition, intracellular H⁺ escapes, and extracellular K⁺ enters the cell, resulting in hypokalemia.

Lung compensation, reduced ventilation

Renal compensation: secretion of H⁺, decrease in NH₄⁺, and decrease in HCO3- reabsorption

Respiratory acidosis ➡️ Primary increase in plasma H2CO3

reason

Respiratory center depression

airway obstruction

Respiratory muscle paralysis

Thoracic lesions

lung disease

Improper management of artificial respirators

Too much CO2 intake

Classification

acute respiratory acidosis

chronic respiratory acidosis

compensatory adjustment

Compensation of acute respiratory acidosis: H⁺ is buffered by hemoglobin and oxyhemoglobin, HCO3- is exchanged with Cl-

Compensation of chronic respiratory acidosis: secretion of H⁺ and NH₄⁺ by renal tubular epithelial cells and increased reabsorption of HCO3-

Respiratory alkalosis ➡️ Primary decrease in plasma H2CO3 concentration

reason

Hypoxemia and lung disease

Respiratory center stimulation or psychogenic hyperventilation

Strong body metabolism

Improper use of artificial respirator

Classification

acute respiratory alkalosis

chronic respiratory alkalosis

compensatory adjustment

Ion exchange inside and outside the cell and intracellular buffering: H⁺ combines with HCO3- from intracellular to extracellular, reducing HCO3- and increasing H2CO3

Renal compensation: renal tubular epithelial cells compensatory secretion of H⁺, NH3 decreases, HCO3- is excreted in urine, and plasma HCO3- decreases

Aldosterone (ALD) preserves sodium and potassium

Atrial natriuretic peptide (ANP) inhibits proximal tubule reabsorption