水与电解质平衡紊乱 (Disturbances of water and electrolyte
水电解质代谢紊乱 (6)可编辑全文
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经肾丢失
肾外丢失
长期连续用高效利尿剂--抑制钠离子重吸收
肾上腺皮质功能不全--醛固酮分泌不足
肾实质疾病--慢性间质性肾疾患使髓质和髓袢 ห้องสมุดไป่ตู้ 升支功能受损
肾小管酸中毒
Renal tubular acidosis,RTA
是一种以肾小管排酸障碍为主的疾病
发病环节
集合管泌氢功能降低
醛固酮分泌不足
肾上腺
肾小管对钠(及水)的重吸收
血容量↑
肾动脉压↑
转换酶
氨激肽酶
各种肽酶
细胞外液 [K+]↑[Na+]↓
血管收缩
醛固酮分泌的调节及其作用示意图
+
+
+
→
+
+
醛固酮
4.心房钠尿肽 (atrial natriuretic peptide,ANP)的调节作用
分泌部位:
心房肌细胞
作 用:
排钠,利尿,扩血管
水肿
脱水
低渗
高渗
等渗
正常钾代谢
高钾血症
低钾血症
水中毒
水,钠代谢紊乱 的具体类型特点
水钠代谢紊乱
依体液容量和血钠浓度分类
体液容量
脱水
血钠升高:高渗性脱水
血钠降低:低渗性脱水
血钠正常:等渗性脱水
血钠正常:水肿
【水钠代谢紊乱的具体类型特点】
dehydration
体液容量的明显减少在临床上称为~。
4
4
Cl-
2
115
103
HCO3-
8
30
27
HPO42-
70
1
1
水电解质紊乱完整版本
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(Water and Electrolyte
Disorders)
中南大学病理生理学教研室
精品课件
主要内容
第一节 水、钠代谢的生理学基础 第二节 水、钠代谢紊乱 第三节 钾代谢紊乱
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第一节 水、钠代谢的生理学基础 (physiologic basis of
water and sodium balance)
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细调节:
抗利尿激素 (antidiuretic hormone ,ADH)
醛固酮 (aldosterone,ADS)
心房利钠肽 ( atrial natriuretic peptide ,ANP)
水通道蛋白 ( aquaporins,AQP)
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抗 利 尿 激 素 的 调 节 作 用
2. 在维持细胞内外体液交换方面起重要 作用。
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渗透压平衡的自身调节:
正常时:血管内外、细胞内外的渗透压是相等的。
失衡时→再平衡:低渗溶液中的水向高渗溶液流动。
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2. 电解质的功能
维持体液的渗透压和酸碱平衡。 维持细胞的静息电位、参与动作电位形成。 参与新陈代谢和生理功能活动 。
精品课件
和电解质自由 交换
水自由通过, 蛋白质、Na+ 、 K+、Ca 2+等不 能自由通过
细胞内外、血管内外水的交换
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三、电解质的分布、功能及钠的平衡 电解质(Electrolyte ):以离子状态溶于 体液中的各种无机盐或有机物。
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1. 电解质在体内的分布
特点:1)细胞内外阴、阳离子构成不同 ; 3) 电中性法则; 2)各体液中阴、精品课阳件 离子数不一致; 4) 渗透
病理生理学--水、电解质代谢紊乱课件
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呼吸困难 端坐呼吸
右心衰→心性水肿
下垂性水肿 静脉压升高 肝肿大 腹水 双下肢明显水肿
❖ 肾性水肿(renal edema) 肾炎性水肿:早期眼睑和面部水肿 肾病性水肿:三高一低
❖ 肝性水肿 特点:腹水
4、水肿对机体的影响
❖炎性水肿稀释毒素 ❖细胞营养障碍 ❖水肿对器官组织功能活动的影响
碱中毒(alkalosis)
H+
肾小管
H+
K+
[H+]
Na+
K+
Na+
血[K+]
与膜电位异常相关的障碍
对膜电位的影响 对细胞膜离子通透性的影响
对骨骼肌和平滑肌细胞膜的K+通透性影 响不大。
对心肌细胞膜 对K+ 通透性降低 对Ca+ 通透性增加 可致Na+ 通道失活
(二)对机体的影响
1. 对肌肉组织的影响
Blood hydrostatic pressure(BHP) 60 mmHg out Colloid osmotic pressure(COP) -32 mmHg in Capsular pressure(CP) -18 mmHg in
Net filtration pressure(NFP) 10 mmHg out
缺钾(potassium deficit):细胞内钾缺失
(-)原因和机制
食物
ECF
K+ 血钾
3.5-5.5 mmol/L
ICF 钾 150mmol/L 体钾98%
消
多摄多排
化 道
肾 少摄少排
不摄也排
体钾
食物
①
1 水、电解质代谢紊乱(1 disorders of water and electrolyte metabolism)
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---------------------------------------------------------------最新资料推荐------------------------------------------------------1 水、电解质代谢紊乱(1 disorders of water andelectrolyte metabolism)1 水、电解质代谢紊乱(1 disorders of water and electrolyte metabolism) 1 水、电解质代谢紊乱(1 disorders of water and electrolyte metabolism) Dehydration (dehydration) \ hypotonic dehydration (Hypotonic dehydration) \ dehydration symptoms (Dehydrate, symptom) \ [hypertonic dehydration (Hypertonic, dehydration) / isotonic dehydration (Isotonic, dehydration) / water intoxication (Water, intoxication) \ hyponatremia (hyponatremia) \ hypernatremia (hypernatremia) A disorder of water and sodium metabolism Dehydration (dehydration): a decrease in body fluid volume (more than 2% of body weight) and a series of pathological disorders of function and metabolism. The water of the body is mainly the loss of extracellular fluid, while sodium ions are the most important cations in the extracellular fluid, so dehydration is often associated with the loss of sodium (I) hypotonic dehydration (Hypotonic, dehydration); Hypotonic dehydration: loss of sodium, more than water loss, serum sodium concentration 135mmol/L, plasma osmotic pressure 280mmol/L, and accompanied by decreased extracellular fluid volume, known as hypotonic dehydration.1 / 20Also called hyponatremia of low volume The etiology and pathogenesis of * * * * Mainly the loss of isotonic or hypotonic fluid. 1) extra renal causes A. digestive juices are lost in large amounts, B. fluids accumulate in large amounts in the body cavity, and C. accumulates large amounts of sweat or burns in large areas 2) renal causes A large number of long-term use of sodium intake or natriuretic drug limit A. (hydrochlorothiazide and furosemide and ethacrynic acid etc.)B. chronic renal interstitial disease, ascending limb of Henle and Na with renal dysfunction increased lostC. acute renal failure polyuria period, GFR increase, tubular function did not recover, sodium and water excretion increasedD. salt losing nephritis, tubular epithelial cell lesions of Ald (aldosterone) response to the decrease in sodium reabsorption in renal sodium excretion, reduce excessive The adrenal cortex and e., such as Addison disease, Ald secretion of Na, the decrease in tubular reabsorption and decrease renal sodium excretion and drainage increased F. excessive osmotic diuresis and renal excretion of Na and H2O increase 2. of the impact of the body The basic changes were obvious decrease of extracellular fluid and decrease of osmotic pressure Loss of sodium and water loss, the osmotic pressure of extracellular fluid, the decrease in---------------------------------------------------------------最新资料推荐------------------------------------------------------ extracellular to intracellular water transfer to intracellular water up to cell edema, extracellular fluid decreased more obviously Clinical manifestation 1) circulatory failure (Symptom of, circulatory, failure) The water from the cell to cell outward transfer of extracellular fluid and blood volume down down down down down down, blood pressure, shock 2) dehydration symptoms (Dehydrate, symptom) Lower skin elasticity, sunken socket, and three concave signs in infants.(3) other clinical manifestations (Other, manifestation); - thirsty: early without thirst; in late, there will be thirsty. CNS - symptoms: severe hypotonic dehydration with haziness, drowsiness, coma. - urinary sodium:: urinary sodium or no 10mmol/L. According to the clinical symptoms of the severity of clinical hypotonic dehydration of three degrees (two) hypertonic dehydration (Hypertonic, dehydration); Hypertonic dehydration: dehydration more than sodium loss, serum sodium concentration 145mmol/L, plasma osmotic pressure 310mmol/L, and accompanied by decreased extracellular fluid volume, Hypertonic dehydration. Also called low volume hypernatremia. 1. etiology and pathogenesis Dehydration or loss of low osmotic fluid is the main cause of3 / 20hypertonic dehydration 1) simple dehydration A. is C. through the lung, B. by the skin, and by the kidneys (2) loss of hypotonic fluid C. loss of hypotonic fluid through the gastrointestinal tract, B. profuse sweating, and repeated osmotic diuresis caused by repeated use of mannitol or hypertonic glucose in the a. 2., the impact on the body 1) compensatory response of organism - drink (except for thirst thirst disorder) Plasma osmotic pressure increases, osmoreceptor (+) - (+) - thirsty thirst Here, AGTII relax, thirsty central blood volume (+) - thirsty Hypertonic dehydration, saliva, throat dry down While the proportion of high - oliguria (excluding diabetes insipidus patients) In the water from the cell within the extracellular transfer to the osmotic pressure of extracellular fluid decreased somewhat These three aspects make the extracellular fluid osmotic pressure fall back, so that the early blood volume of dehydration is not easy to drop to the degree of shock 2) the clinical manifestation varies with the degree - urinary sodium Mild hypertonic dehydration (early stage) The osmotic pressure of extracellular fluid, increase blood volume decrease is not obvious, the reabsorption of water and sodium, high urine sodium. Medium and severe hypertonic dehydration---------------------------------------------------------------最新资料推荐------------------------------------------------------ (late) Blood volume and renal blood flow was significantly lower, Ald (aldosterone) secretion, increase urinary sodium down - CNS symptoms Severe hyperosmolar dehydration, intracellular fluid, brain cell dehydration and significantly decrease brain pressure decreases, the severity of the symptoms of CNS - thermal dehydration Here, the body temperature down to increase heat dissipation function, sweat gland secretory cells: liquid - shock, renal failure According to the severity of clinical symptoms, the hypertonic dehydration was three degrees (three) isotonic dehydration (Isotonic, dehydration); Isotonic dehydration: when water and sodium are lost in proportion or after losing fluid, the plasma osmotic pressure is still within normal range, the serum sodium concentration is 135~145mmol/L, and the plasma osmotic pressure is 280~ 310 mmol/L. 1. etiology and pathogenesis Vomiting and diarrhea, a large number of pleural and ascites formation, extensive burns and severe trauma, such as plasma loss. 2., the impact on the body Isotonic dehydration often has clinical manifestations of hypotonic and hypertonic dehydration. A massive loss of isotonic fluid, extracellular fluid, blood volume, blood pressure down, down to the decrease5 / 20in urine volume, body temperature, dehydration obvious appearance Isotonic dehydration can only be converted into hypotonic dehydration if only water is added to the treatment without attention to sodium supplementation. Water intoxication Water intoxication (Water intoxication): when the water intake, over regulating nerve endocrine system and kidney drainage ability, make a lot of water retention in the body, resulting in volume of intracellular fluid and extracellular fluid expansion, and the emergence of a series of diseases including hyponatremia, physical and physiological changes. 1. etiology and pathogenesis 1) take in or enter too much electrolyte free liquid 2) acute or chronic renal insufficiency 3) excessive secretion of ADH Excessive secretion of ADH is defined as abnormal secretion of ADH under certain pathological conditions. (a) ADH abnormal growth syndrome (SIADH): Hypothalamic diseases (encephalitis, brain tumors) and ectopic ADH secretion (lung, oat cell carcinoma) B) other reasons In pain, nausea and emotional stress: relax, ADH secretion of water intoxication In the case of adrenocortical function: GC (glucocorticoid), inhibition of hypothalamic ADH secretion function down down - exogenous ADH input (vasopressin and oxytocin) 4) certain special---------------------------------------------------------------最新资料推荐------------------------------------------------------ pathological states A) heart failure, hepatic ascites, effective circulating blood volume down, down to the water load increase renal drainage and water poisoning (b) hypotonic dehydration - a large amount of electrolyte free water intoxication 2., the impact on the body Prominent manifestation: increased intracellular fluid volume or cell edema When water poisoning occurs, the extracellular fluid increases obviously, and the low permeability of extracellular fluid causes a large amount of water to enter the cell Mild water intoxication, the increase of intracellular and external fluid is not obvious, the symptoms are not obvious, may be weak, dizziness and so on Acute poisoning with water intoxication can cause brain cell edema and increased intracranial pressure, which can be life-threatening test questions 1. the balance of osmotic pressure inside and outside cells mainly depends on the movement of the following substances A., Na+, B., K+, C., Cl-, D., H2O, Ca++, E. 2., a large amount of water is added to the patients with severe hypotonic dehydration, while no sodium salt is added A. hypertonic dehydration, B. isotonic dehydration, C. poisoning, D. hypokalemia, E. edema 3. what are the major characteristics of hypotonic dehydration? 4.7 / 20why is hypertonic dehydration less prone to circulatory failure in the early stage? 5., we compared the similarities and differences between hypotonic dehydration and hypertonic dehydration. Case analysis Male patients, 2 years old, diarrhea 2 days, 6-7 times a day, watery stools; vomiting 3 times, vomiting is the milk consumed, can not eat. Accompanied by thirst, oliguria and bloating. Physical examination: the spirit of malaise, T37oC, BP11.5/6.67KPa (86/50mmHg), skin elasticity, eyes sag, bregmatic subsidence, fast heartbeat and weak, no abnormal lung, abdominal distension, abdominal reflex, decreased bowel sounds, knee reflex, cold extremities. Laboratory tests: serum K+3.3mmol/L, Na+140mmol/L. What kind of water and electrolyte disorder occur in the child? On the basis of what? Comparison of three kinds of dehydration Disturbance of sodium metabolism 1. hyponatremia Hyponatremia (hyponatremia) refers to serum sodium concentrations below 135mol/l. Plasma osmolality mainly depends on the concentration of serum sodium ions, so hyponatremia is usually associated with low osmolarity. (I) hypotonic hyponatremia (hypotonic, hyponatremia): The vast majority of hyponatremia is associated with a decrease in plasma osmolality 1) low capacity hyponatremia (hypovolemic,---------------------------------------------------------------最新资料推荐------------------------------------------------------ hyponatremia) The loss of sodium is more than the loss of water, and the volume of extracellular fluid is decreased, that is, hypotonic dehydration 2) hyponatremia (isovolemic) It is seen in ADH secreting abnormal growth syndrome and osmotic reset 3) high capacity hyponatremia (hypervolemic, hyponatremia) The main causes are congestive heart failure, liver cirrhosis, ascites, nephrotic syndrome and so on, which lead to the pathological changes of the effective circulation and blood loss. Water intoxication (two) isotonic hyponatremia (chronic hyponatremia) (isotonic, hyponatremia); Hyperlipidemia or hyperlipoproteinemia patients, due to the increase of plasma lipid or protein content, serum water proportion decreased, so the serum sodium concentration under normal water, plasma sodium concentration in the clinically measured reduced, then called isotonic hyponatremia. (three) hypertonic hyponatremia (hypertonic, hyponatremia); Hyperosmolar hyponatremia: Sodium by outside impermeable solute permeability caused by increased extracellular fluid pressure increased, the water inside the cells to transfer, extracellular fluid sodium concentration decreases, which leads to the occurrence of hyponatremia in. 2. hypernatremia9 / 20Hypernatremia (hypernatremia): serum sodium concentration is higher than 145mmol/l. With the increase of plasma osmotic pressure, the basic changes of hypernatremia are common when the cells are dehydrated. (I) hyponatremia of low volume Mainly because of the large loss of water or hypotonic fluid, the loss of water exceeds the loss of sodium, which leads to the decrease of extracellular fluid and the increase of serum sodium concentration, which is called hypertonic dehydration (two) hypernatremia with equal capacity It is found in primary hypernatremia, impaired central nervous system and so on (three) hypernatremia with high volume The main reason is the excessive input of sodium solution. In patients who have been rescued from cardiac arrest and respiratory arrest, a large amount of NaHCO3 is added to fight lactic acidosis, resulting in an increase in extracellular fluid volume and sodium concentration. Two 、potassium metabolism disorder Disturbance of potassium metabolism: abnormal changes in K+ concentration in extracellular fluid (especially serum), and the patient’s clinical symptoms and signs depend mainly on the speed and extent of abnormal changes in blood potassium concentration (I) hypokalemia (hypokalemia); When serum potassium concentration is below 3.5mmol/L, it is called---------------------------------------------------------------最新资料推荐------------------------------------------------------ hypokalemia. Potassium depletion: intracellular potassium and loss of total potassium in the body. 1. causes and mechanisms 1) lack of potassium intake 2) excessive potassium loss The loss of potassium through the stomach and intestines (hypokalemia) Loss of kidney by potassium (a) loss of kidney due to increased renal flow at the distal end of the renal tubule A large number of diuretics use: increasing the distal flow velocity of the renal tubule and increasing the exchange of Na with K Renal insufficiency, renal failure (b) aldosterone: aldosterone is the major mineralocorticoid that promotes reabsorption of sodium and the secretion of potassium and hydrogen, causing potassium loss (c) renal tubule transmembrane potential increases negatively, resulting in potassium loss D) loss of potassium caused by low Mg blood Magnesium deficiency in the body, caused by the thick ascending limb of Henle epithelial cell Na, inactivation of the K-ATP enzyme, caused by potassium reabsorption and potassium loss.E) other Type I renal tubular acidosis: obstruction of the distal convoluted tubule to H+ Type II renal tubular acidosis: reabsorption of proximal convoluted tubules in HCO3- Type IV renal tubular acidosis: simultaneous presence of malabsorption11 / 20of Na+ and obstruction of the distal convoluted tubule with H+ Loss of skin by potassium 3) potassium to intracellular transfer (a) alkalosis (b) the use of insulin (c) hypokalemic familial familial periodic paralysis (d) barium poisoning, crude cottonseed oil poisoning 2. effects of hypokalemia on the body Related to the speed, amplitude and duration of blood potassium lowering, the faster the rate of blood potassium lowering, the lower the serum potassium concentration, the greater the impact on the body. 1) the effect on neuromuscular excitability The excitability and conductivity of nerve and muscle tissue are significantly affected Acute hypokalemia, extracellular fluid with constant liquid concentration decreased, intracellular potassium concentration, the results make the intracellular potassium concentration, the ratio of increase of intracellular potassium efflux increased, the absolute value of the resting membrane potential increases, and increase the threshold potential gap, the stimulation threshold excited should also be increased, it caused the excitability of nerve muscle cells decreased. When chronic hypokalemia occurs, the extracellular potassium can be replenished by intracellular potassium, because the potassium concentration in the---------------------------------------------------------------最新资料推荐------------------------------------------------------ extracellular fluid is slowed down, so the symptoms are not obvious. Clinical manifestations: symmetrical limbs, flaccid paralysis, even soft paralysis, paralytic ileus, abdominal distension and so on. Physical examination: reduction of muscle tone in the limbs and decrease or disappearance of tendon reflex. Reason: the excitability of skeletal muscle cells decreases, and the gastrointestinal smooth muscle can also be involved 2) the effect on the heart Mainly cause arrhythmia, severe ventricular fibrillation, leading to heart failure A) physiological changes of myocardium [K +]e decreased, membrane permeability decreased, phase 4 K + efflux decreased, Na + or Ca2 + increased, and autonomic cells automatically increased rapidly and increased automaticity; The reduced membrane permeability decreased [K]e?? Em cell move, Em-Et spacing increased excitability?; The Em shift and Em-Et spacing decrease, the slope of the 0 phase curve increases, the front potential decreases, and the conductivity decreases; The [K +]e decreased 2? Ca2 + influx of [Ca2 +]i increased rapidly accelerated?? myocardial contractility increased (severe and chronic hypokalemia due to intracellular potassium deficiency, affecting cell metabolism, myocardial damage,13 / 20decrease of myocardial contractility). (b) electrocardiographic changes The obvious U wave after S-T segment depression and T wave is characteristic of hypokalemia Conduction prolongation, P-R interval prolongation, ORS wave presentation and broadening The calcium influx in the 2 stage accelerates the potassium efflux, the 2 stage repolarization accelerates and the S-T depression decreases The 3 phase of potassium efflux slowed down to repolarization, and the 3 phase extended to U wave obviously C) arrhythmia In hypokalemia, the myocardial excitability increased, the supernormal period prolonged and the ectopic pacemaker increased automaticity. At the same time, the conductivity decreased, the conduction slow and the effective refractory period shortened, and it was easy to cause excited reentry. Therefore, hypokalemia is prone to premature beats, atrioventricular block, ventricular fibrillation, and other arrhythmias. 3) the influence on acid-base equilibrium Hypokalemia may cause alkalosis (paradoxical uric acid) 4) the effect on the kidney The accumulation of renal dysfunction occurs in the so-called depletion of postassiun (nephropathy) 5) the effect on blood vessels Reducing peripheral vascular resistance to hypokalemia is associated with vertigo, hypotension and other---------------------------------------------------------------最新资料推荐------------------------------------------------------ symptoms 3. prevention and treatment principle of hypokalemia 1) prevention and treatment of primary diseases 2) proper potassium supplementation during treatment. The principle of potassium supplementation: feeding can be taken orally as possible potassium supplement; intravenous potassium supplementation should pay attention to low concentration (20~40 mmol/L) and low flow rate (10 mmol/h); daily potassium supplementation can be controlled at 40~120 mmol. Special attention should be paid to intravenous potassium supplementation only when the renal function is good. When the amount of urine is greater than 500 ml, the potassium supplementation is safe. Potassium deficiency is caused by magnesium deficiency, Magnesium should be supplied before potassium can be effectively supplied. Attention should be paid to the acid-base balance of the patient. (two) hyperkalemia (hyperkalemia); Serum K + concentration greater than 5.5 mmol/L is called hyperkalemia. 1. causes and mechanisms 1) excessive penetration 2) renal excretion of potassium decreased Acute renal failure, oliguria stage, end-stage renal failure. High potassium type distal tubular acidosis Decreased aldosterone secretion or decreased renal15 / 20tubular aldosterone response to aldosterone Long term use of diuretics that can cause potassium retention 3) extracellular release of stromal cells Acidosis A great deal of hemolysis or tissue damage and necrosis When diabetic ketoacidosis occurs Membrane dysfunction of sodium pump Familial familial periodic paralysis of hyperkalemia 2. effects of hyperkalemia on the body 1) the effect on neuromuscular excitability Mild hyperkalemia (5.5 ~ 7.0mmol/L) often results in increased excitability. There are hand foot and foot abnormalities, tremors, myalgia, or colic, and diarrhea; Severe hyperkalemia (7 ~ 9.0mmol/L) often makes the muscle cells appear to be depolarized and blocked, causing muscle paralysis, and clinical weakness of muscle, flaccid paralysis and other symptoms. 2) the effect on the heart The effect on the heart, like hypokalemia, can also cause arrhythmias or ventricular fibrillation, but unlike hyperkalemia, severe hyperkalemia can cause cardiac arrest. (a) characteristics of myocardial physiological changes [K +]e increased, and the permeability of the membrane to K + increased after the repolarization of the self regulatory cells. The 4 phase of K + flow increased, the automatic depolarization slowed down, and the automaticity decreased. Increase of [K +]e, decrease of---------------------------------------------------------------最新资料推荐------------------------------------------------------ Em negative value in cardiac working cells, decrease of Em-Et distance, increase of excitability in mild disease and decrease in severe condition. The Em-Et interval is reduced. In the 0 stage, the depolarization is decreased and the potential is decreased, and the conductivity is decreased. Increase of [K +]e, decrease of calcium influx in 2 stage and decrease in contractility. B) changes in the electrocardiogram The action potential of cardiac myocytes decreased and P wave decreased, widened or disappeared The conductivity decreased, prolonged P-R interval, QRS composite is wide The T wave is high, the Q-T interval shortens and the S-T elevation (c) the manifestation of arrhythmia Acute hyperkalemia is reduced and slow conduction conductivity caused by unidirectional conduction block, and effective refractory period shortened, and also easy to cause the reentry arrhythmia, including ventricular fibrillation. Severe hyperkalemia can result in cardiac arrest due to reduced automaticity, block of conduction, and loss of excitability 3) the influence on acid-base equilibrium Hyperkalemia results in the metastasis of H + to the extracellular region and the decrease of H + in kidney, so metabolic acidosis can occur. (paradoxical alkaline urine) 3.17 / 20prevention and treatment principle of hyperkalemia 1) prevention and treatment of primary diseases 2) reduce blood potassium: myocardial toxicity against high potassium; promote K+ into cells; accelerate K+ excretion Hypokalemia * reasons Insufficient intake of potassium: can not eat or fasting, stomach, parenteral K solution too much: often iatrogenic, such as kidney dysfunction, more rapid, potassium supplementation Potassium loss or discharge excessive vomiting, diarrhea, intestinal fistula; using Paul sodium and osmotic diuresis; renal dysfunction and interstitial renal disease; aldosterone; magnesium deficiency; sweat reduction; renal failure and some kidney diseases; Adrenal cortical insufficiency; potassium sparing diuretic use * k the abnormal distribution of extracellular potassium into the cell: alkalosis; insulin; periodic paralysis; intracellular potassium escape cell barium poisoning: acid poisoning; severe hypoxia; periodic paralysis; hemolysis or serious tissue damage excessive muscle movement; the use of digitalis or propranolol. Effects on the organism * nerve muscle excitability is chronic; varies little Acute: lower chronic: little change Acute: mild increase, severe decrease * cardiac automaticity increases and decreases Excitability increased, slightly increased, decreased when---------------------------------------------------------------最新资料推荐------------------------------------------------------ severe Decreased conductivity Decreased contractility Extend the ECG characteristics of the P-R interval, QRS wave width; S-T segment depression, T wave flat, U wave, Q-T wave, P wave interval prolonged low width, prolonged P-R interval, QRS wave width; S-T elevation, T wave tip The Q-T interval is shortened or normal * clinical presentation, tachycardia, arrhythmia, or ventricular fibrillation, arrhythmia, or cardiac arrest * acid base balance secondary metabolic alkalosis secondary metabolic acidosis * gastrointestinal peristalsis, abdominal distension, paralytic ileus, colic, diarrhea Three, acid-base balance and acid-base balance disorders Under physiological conditions, the pH of the extracellular fluid is between pH37.35-7.45 and the average value is 7.40. Extracellular fluid pH is in this relatively stable state, that is called acid-based (balance), that is, the relative concentration of hydrogen ion concentration ([H+]) in the blood. The maintenance of acid-base balance depends on the humoral buffer system and the mediation of the lungs and kidneys. The acid-base equilibrium disorder refers to various causes accumulation or lack of body acidic or alkaline substances, leading to environmental damage in body fluid acid-base19 / 20homeostasis, which is caused by various reasons of arterial blood [H+] exceeded the normal range (increase or decrease) of the pathological changes.。
小儿液体疗法
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脱水性质
脱水程度
小儿液体疗法
轻度 中度 重度
等渗 低渗
高渗
第13页
脱水 分度
轻度 中度
重度
精 神 稍差 萎靡、烦躁 很差、昏迷
眼 泪 少 显著降低
无
尿 量 稍少 显著降低 极少或无Leabharlann 皮肤弹性 尚可 差极差
前囟眼窝 稍凹陷 显著凹陷 深陷
末梢循环 正常 四肢稍凉 四肢厥冷
小儿液体疗法
5
80
5
70
5
65
5 55~60
第10页
胃
肠
肺
血浆
(占体重5%)
肾
间质液
(占体重25%)
细胞内液
(占体重40%)
小儿液体疗法
第11页
正常小儿每日失水
肺 不显性失水
皮肤 皮肤显性出汗
大便
尿
小儿每日需水量: 120~150ml/100cal
小儿液体疗法
第12页
水、电解质和酸碱平衡紊乱 一、脱水
液体疗法时惯用溶液 Common Solution of Liquid Therapy
小儿腹泻液体疗法 Infantile Diarrhea Liquid Therapy
小儿液体疗法
第2页
目标要求 Objective
• 了解小儿体液平衡特点
Realized: Characteristic of Infantile Body Fluid Balance
小儿液体疗法
第21页
代谢性酸中毒
主要因为 H 或[ HCO 3]丢失所致。
1.体内碱性物质经消化道或肾大量丢失:如 腹泻、肾小管酸中毒。。
水、电解质代谢紊乱概述与障碍特点
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无机电解质的主要功能:
维持体液的渗透平衡和酸碱平衡。
维持细胞的静息电位, 并参与动作电位形成
参与新陈代谢和生理功能。
水、电解质代谢紊乱概述和障碍特点
钠平衡
体内 含钠 量 40~50
mmol/kgW
40%不可交换
60%可交换
ICF 10%
ECF 50%
结合于骨骼的基质
细胞内液中的Na+浓度 仅为 10 mmol/L左右
水、电解质代谢紊乱概述和障碍特点
(四) 水的生理功能和水平衡 1. 水的生理功能
促进物质代谢 调节体温 润滑作用 结合水:与蛋白质、粘多糖、磷脂结合。
水、电解质代谢紊乱概述和障碍特点
(四) 水的生理功能和水平衡
2. 水平衡 正常人每日水的摄入和排出
摄入(ml) 饮水 1000~1300 食物水 700~900 代谢水 300
合计 2000~2500
排出(ml)
尿量 1000~1500
皮肤蒸发 500
呼吸蒸发 350
粪便水
150
2000~2500
水、电解质代谢紊乱概述和障碍特点
(五)电解质的生理功能和钠平衡
电解质
有机电解质 (如蛋白质)
无机电解质
阳离子: K+ Na+ Ca2+ Mg2+ 阴离子: Cl- HCO3- HPO4-
程中有着不同的作用和调节机制。
水、电解质代谢紊乱概述和障碍特点
水、电解质代谢紊乱概述和障碍特点
二、水、钠代谢障碍的分类
Classification of disturbance of water and sodium balance
根据体液的渗透压分类
《基础医学各论2》资料:6水、电解质代谢
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②血清钠测定:血清钠浓度低于135mmol/L, 有低钠血症。血清钠浓度越低,病情越重
③红细胞计数、血红蛋白量、血细胞比容及血 尿素氮值均有增高。
低渗性脱水 (低血钠性)
• 5 治疗原则
• 去掉病因; • 补等渗液(0.9% NaCl)
70
Obese
50
50
70
60
80
42
60
年 龄
性 别
小儿年龄越小,体 液代谢越快,病理 情况下越容易脱水!
胖 瘦
脂肪组织含水量:10%-30% 肌肉组织含水量:75%-80%
(二)体液呈电中性,Na+是细胞外主要阳离
子,K+是细胞内主要阳离子
细胞内液 组织间液
血浆
Na+
10
145
141
K+
160
④等渗性脱水治疗时补充水分过多。
此外:大量体液丢失 细胞外液容量减少 容量感受器 ADH分泌 肾脏重吸水增加 细胞外液低渗
3 对机体的影响
• 失钠>失水
• ECF低渗 不口渴
•
ADH↓ 早期尿量不减少
• 细胞外水向胞内移动
•
ADS ↑ 尿 Na+↓
• ECF进一步↓↓ 血容量↓
•
血浓缩
组织间液↓↓ 皮肤弹性↓
水通道蛋白(aquaporin):
二、机体水、钠平衡
(一) 水的平衡
机体中水的生理作用:
• 1.良好的溶剂 • 2.生化反应的场所 • 3.调节体温 • 4.润滑作用 • 5. 维持组织坚韧性
正常人每日水的摄入和排出量
水电解质紊乱-PPT可编辑全文
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⑴水源断绝 ⑵进水困难 ⑶失去主动摄水能力 ⑷失去渴感
34
2)水丢失过多
⑴经胃肠道丢失:
⑵经肾脏丢失: 尿崩症(中枢性、肾性)
尿崩症:ADH合成和释放不足; 尿崩症:肾远曲小管和集合管对ADH的反应降低 溶质性利尿:甘露醇、高渗葡萄糖、鼻饲高蛋白饮食
⑶经呼吸道丢失
发热、癔病、代酸引起过度通气,水分大量蒸发
❖体液的容量(volume) ❖化学成分(composition) ❖渗透压(osmotic pressure) ❖分布(distribution)
影响体液量及分布的因素
成 人 儿童 婴儿 新生 老
(男)(女) (2~14岁) (1岁) 儿 人
体液总量 60 55
65
70 80 52
细胞内液 40 35
23
水通道蛋白 aquaporins, AQP
Agre mid-1980 2003Nobel-pride
(1)分布:广泛分布于动、植物和微生物界。
(2)特性: 细胞膜转运蛋白、水通透性有关,有 其特异性组织分布。
(3)种类: 有13种,AQP 0~12。
水、钠代谢紊乱的分类
Classification of disturbances of water and sodium balance
水钠代谢障碍的分类
体液量减少
体液量增多 体液量不变
低钠血症
低容量性 低钠血症 (低渗性脱水)
高钠血症
低容量性 高钠血症 (高渗性脱水)
高容量性 低钠血症 (水中毒)
高容量性 高钠血症 (盐摄入过多)
等容量性 低钠血症 (ADH分泌异常)
等容量性 高钠血症 (下丘脑损害)
水与电解质平衡紊乱(Disturbancesofwaterandelectrolytebalance)
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量 ADH分泌增多)
对机体的影响
3.对机体的影响
失液+补水
失钠>失水 (ECF低渗)
早期不口渴 血容量降低 晚期轻度口渴
ADH↓ 水吸收↓
尿不少
细胞外液进入细胞内,血容 量进一步减少易发生休克
影响
失Na+>失水
无口 渴感
ECF渗 水移入 ECF量 组织液 脱水征
2.原因
丢失等渗液(lost isotonic fluid)
胃肠道丢失(gastrointestinal losses) 液体积聚在第三间隙(accumulate in
third space)
3.影响(effects)
(1)血浆渗透压和血钠的变化?
ECF渗透压正常,血[Na+]正常
(2)容量的变化?脱水的主要部位?
ECF减少 血容量↓组织液量↓ ICF变化不明显
(3)激素水平的变化?
醛固酮、ADH分泌
尿量
腹泻
高渗性脱水
大汗
等渗性脱水
低渗性脱水
脱水间的相互关系
三种类型脱水的比较
高渗性脱水
低渗性脱水 等渗性脱水
原因 饮水不足或失 水过多
细胞外液 升高 渗透压
体液丧失仅补水 钠水等比例丧失
降低
正常
失水部位 细胞内液为主 主要表现 口渴、尿少、
(Physiologic function of water and sodium)
(一)水的生理功能
(Function of body water)
促进物质代谢 调节体温 润滑 结合水
(二)钠的生理功能 (Physiologic function of sodium)
儿科液体疗法
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极差
极凹陷
极干燥
无
极少 或无
水电解质和酸碱平衡紊 乱
脱水性质:
是指体液渗透压的改变,根据水和电解质损失比例的 不同,可分为等渗性(最常见)、低渗性(其次)和高渗 性脱水(少见)。
水电解质和酸碱平衡紊乱
二 脱水性质 病因
多见急性胃 肠液丢失
临床表现 脱水性质 等渗脱水 低渗脱水
血清纳
130~150 mmol / L
口服补液:(oral rehydration salt,ORS)
适应症:
1.轻度或中度脱水、呕吐不严重的患儿 2.用于补充累积损失量,用于补继续丢失量和生理需要量 时要适当稀释
相对禁忌症:
1. 2. 3. 4. 重度脱水 休克、心肾功能不全或存在其他严重并发症者 新生儿 严重呕吐者
口服补液盐(ORS)
正常水平
正常水平
血 浆
组 织 间 隙
细 胞 内 液
血 浆
组 织 间 隙 脱水征相对重
细 胞 内 液
血 浆
组 织 间 隙 脱水征相对轻
细 胞 内 液
等渗性脱水 电解质损失 与水成比例
低渗性脱水 电解质损失>水
高渗性脱水 电解质损失<水
小儿不同性质脱水的鉴别诊断要点
等渗性脱水 低渗性脱水 高渗性脱水
六版教材:
NaCl 3.5g 碳酸氢钠 2.9g
七版教材:
NaCl 2.6g 枸橼酸钠 2.9g
枸橼酸钾 1.5g
葡萄糖 20.0g
KCl
1.5g
葡萄糖 13.5g
其电解质的渗透压为245mOsm/L(1/3张) 总渗透压是
加水到1000ml
其电解质的渗透压为220mOsm/L(3/2张) 总渗透压是310mOsm/L
水、电解质紊乱二组
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第三间隙积液
经皮肤失液
含大量 H2 O、Na + 的液体 丧失
(1)病因:
对机体的影响 体液量 渗透压 血 浆 ADH分泌减少
多尿 低比重尿
伍
无口渴感
肆
明显失水体征
叁
易发生休克
贰
细胞外液减少
壹
组织间液
脱水征
血容量
休克
少尿
抑制渗透压感受器
ADH
肾小管重吸收水
无口渴
多尿,低比重尿
(三)低钠血症(hyponatremia)
1. 低容量性低钠血症——低渗性脱水
特点:失Na+大于失水,血清Na +浓度小于130mmol/L ,血浆渗透压小于280mmol/L,伴有细胞外液量的减少。
经肾丢失
肾外丢失
利尿剂
肾上腺皮质功能不全
肾脏疾病
肾小管酸中毒
肾脏 重吸收 H2O 、 Na+ 减少
钾的生理功能
维持新陈代谢 保持细胞静息膜电位 与神经系统的传导关系密切 调节细胞内外渗透压 调节酸碱平衡
1
2
(二)低钾血症(hypokalemia)
1.概念:血清钾浓度<3.5mmol/L
2. 原因和机制:
摄入不足
丢失过多
跨细胞转移
肾脏丢失
胃肠道丢失
皮肤出汗
利尿剂
盐皮质激素
肾小管性酸中毒
缺镁
血液浓缩
口渴
细胞外液减少,早期无休克
01
防治原发病;
02
补液以5%~10%葡萄糖为主,适量补Na+ (先糖后盐)。
(4)防治原则
(五)细胞外液容量不足—等渗性脱水
2011-水电解质代谢紊乱、水肿
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第一节
水与电解质的正常代谢 (Normal metabolism of water and electrolyte)
一 、体液及电解质的概念 • 机体内含量最多的物质是水。但无论在 机体内含量最多的物质是水。 细胞内、 细胞内、外,各种无机物和有机物大多 以水为溶剂而形成水溶液, 以水为溶剂而形成水溶液,这种水溶液 就称为体液。 就称为体液。 体液 • 体液中的各种无机盐,一些低分子有机 体液中的各种无机盐, 物和蛋白质等都是以离子状态存在的, 物和蛋白质等都是以离子状态存在的, 故称为电解质。 故称为电解质。 电解质
多吃多排,少吃少排, 多吃多排,少吃少排,不吃不排
六、水和钠平衡的调节
• 水和钠的平衡受神经和体液的调节 水平衡:渴感的作用 水平衡: 抗利尿激素(ADH) 抗利尿激素(ADH)的作用 钠平衡:醛固酮(ADS)的作用 钠平衡:醛固酮(ADS)的作用 心房利钠因子(ANP) 心房利钠因子(ANP)的作用
水、Cl-、HCO3-等可自由 通过,但蛋白质、 通过,但蛋白质、Na+、 K + 、Ca2+、 Mg2+等阳离子不 、 能自由通过; 能自由通过; Na+ - K+ -ATP酶的作用 酶的作用
由于Na+、 K+ 分别是细胞内 外液中的主要电解质,所以晶体 渗透压在维持细胞内外水的平衡 中起决定性作用
Na+ K+ Ca2+ Mg2+ 总计
表2 血浆 细胞间液 细胞内液 (mEq/L) (mEq/L) (mEq/L) Cl104 112 3 HCO324 24 10 HPO422 2 100 SO421 1 20 有机酸 5 5 -蛋白质 15 1 65 总计 151 145 198
体液中电解质的含量,有如下特点: 体液中电解质的含量,有如下特点: • 无论在细胞内液或细胞外液,阳离子所 无论在细胞内液或细胞外液, 带正电荷的总数,与阴离子所带负电荷 带正电荷的总数, 的总数正好相等,因而体液呈电中性; 的总数正好相等,因而体液呈电中性; 体液呈电中性
水钠平衡PPT课件
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1氧0化0 (10%)
300-400
600-800
(70kg man)
日排出量 (ml)
尿液
1400-1800
粪便
皮肤 (10%) 300-500
肺部(28%)
Function of body water promoting material metabolism regulation body temperature lubrication
23
分类依据 ﺸ渗透压(280ﺸ31血0钠m浓m度ol及/L体) 液容量 (130-150mmol/L)
24
表. 水、钠平衡紊乱的基本分类
渗透压
细胞外
体液容量 容量不足
(低容量性)
正常 (280~310)
低容量血症 等渗性脱水
降低(<280) 增高(>310) 低钠血症 高钠血症
低容量性低钠血症 低容量性高钠血症
低渗性脱水 高渗性脱水
容量过多
(高容量性)
பைடு நூலகம்
等渗性容量过多
全身性水肿
高容量性低钠血症 高容量性高钠血症
水中毒 盐中毒(少见)
容量正常
(等容量性)
正常人
等容量性低钠血症 等容量性高钠血症
SIADH
(少见)
﹝注﹞渗透压单位为: mOsm/kg H2O
25
第一节 水、钠代谢障碍
正常水钠代谢 水钠代谢障碍分类 低钠血症 高钠血症 等渗性脱水 水肿
26
等渗性脱水
(isotonic dehydration)
1.概念
机体水和钠的丢失呈等比例 失液后经机体调节血清钠浓度和血浆渗透压与正常值相一致。
水盐失衡
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②ECG改变: T波低平,ST段下移,出现U 波,QRS波增宽, 心律失常等. ③心肌功能损害 A.心律失常 B.对洋地黄类药物敏感性↑,易中毒. (3)对神经肌肉的影响 ①骨骼肌:超极化阻滞,产生肌无力,甚至麻痹. ②胃肠平滑肌:胃肠运动↓,肠麻痹. 2)与细胞代谢障碍有关的损害 (1)骨骼肌损害 (2)肾损害 3)对酸碱平衡的影响:易诱发代谢性碱中毒. 3.防治原则
中毒时正好相反 5)渗透压:细胞外液急性高渗促进钾移出细胞. 6)运动:运动引起血钾升高. 7)体钾总量:体钾总量↓时,细胞外液钾浓度下降更明 显;反之则反 2.肾排钾能力:主要依靠远曲小管和集合管对钾的分泌 和重吸收来调节.其影响因素有: 1)醛固酮 2)细胞外液的钾浓度 3)远曲小管的原尿流速 4)酸碱平衡状态 3.结肠的排钾功能 (二)钾的生理功能 1.参与细胞代谢 2.维持细胞静息电位 3.调节细胞内外渗透压和酸碱平衡
�
2)对机体的影响
ADH↓(早期) 醛固酮,ADH↑
失钠>失水→血浆低渗→ 水移入细胞内→血容量↓ → 循环衰竭 COP↑ 脱水症
3)防治原则: (1)防治原发病 (2)纠正失当 的补液 (3)原则上以补等渗NaCl为主
2,高容量性低钠血症(hypervolemic hyponatremia) 又称水中毒(water intoxication),体Na+总量正常或 增多. 1)原因和机制 (1)摄水过多>肾排水能力 (2)肾排水↓:ARF,ADH分泌过多 2)对机体的影响 (1)细胞外液量↑,血液稀释 (3)CNS:颅内压↑→脑疝 (2)细胞水肿 (4)实验室检查
(2)体内外液体交换失平衡——钠水储留 ①GFR↓ ②近曲小管重吸收↑ A.ANP↓ B.F.F(filtration fraction)↑ ③远曲小管,集合管重吸收↑ A.醛固酮↑ A. ↑ B.ADH↑ 2)水肿特点及对机体的影响 (1)特点:水肿液的性状(渗出液,漏出液),水肿皮肤特 点(隐形,显性水肿),全身性水肿分布特点(重力效 应,组织结构特点,局部血流动力学因素) (2)影响:细胞营养障碍,组织器官功能活动↓
水电解质平衡--英文版--病理生理--复旦精品
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Baroreceptor Volume receptor
Angiotension II Emotional stress Pain
ADH promotes the reabsorption of water in the late distal tubule and collecting duct
Efferent arteriole
FLUID AND ELECTROLYTE BALANCE AND IMBALANCE
NING SUN
Office:Room 256, Building 7, West campus Phone: 54237781 E-mail: sunning@
Body Fluid and Electrolyte Balance
Water within the body and the substances dissolved in it.
Function of body water
Body Fluid Homeostasis
Total Fluid Volume Body Fluid Distribution Body Fluid Composition Osmolality of the Body Fluid
diuresis、natriuresis、vascular dilation
Summary
Body organs and tissues cooperate to maintain the body fluid and electrolyte homeostasis by intricate mechanisms, such as Thirst 、 ADH 、 RAAS、and ANP.
40% ISF 15%