WordNet

of or relating to metabolism; "metabolic rate"
undergoing metamorphosis (同)metabolous
abnormally high alkalinity (low hydrogen-ion concentration) of the blood and other body tissues

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/12/07 18:37:26」(JST)

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Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range (7.35-7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.

Terminology

Alkalosis refers to a process by which the pH is increased.
Alkalemia refers to a pH which is higher than normal, specifically in the blood.

Causes

The causes of metabolic alkalosis can be divided into two categories, depending upon urine chloride levels.^[1]

Chloride-responsive (Urine chloride < 20 mEq/L)

Loss of hydrogen ions - Most often occurs via two mechanisms, either vomiting or via the kidney.
- Vomiting results in the loss of hydrochloric acid (hydrogen and chloride ions) with the stomach contents. In the hospital setting this can commonly occur from nasogastric suction tubes.
- Severe vomiting also causes loss of potassium (hypokalaemia) and sodium (hyponatremia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis.^[2]
Congenital chloride diarrhea - rare for being a diarrhea that causes alkalosis instead of acidosis.
Contraction alkalosis - This results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use. Since water is lost while bicarbonate is retained, the increased concentration of bicarbonate "mops up" more of the hydrogen ions and raises the blood pH.
- Diuretic therapy - loop diuretics and thiazides can both initially cause increase in chloride, but once stores are depleted, urine excretion will be below < 25 mEq/L. The loss of fluid from sodium excretion causes a contraction alkalosis.
Posthypercapnia - Hypoventilation (decreased respiratory rate) causes hypercapnia (increased levels of CO2), which results in respiratory acidosis. Renal compensation with excess bicarbonate occurs to lessen the effect of the acidosis. Once carbon dioxide levels return to base line, the higher bicarbonate levels reveal themselves putting the patient into metabolic alkalosis.
Cystic Fibrosis

Chloride-resistant (Urine chloride > 20 mEq/L)

Retention of bicarbonate - retention of bicarbonate would lead to alkalosis

Shift of hydrogen ions into intracellular space - Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells. In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH.

Alkalotic agents - Alkalotic agents, such as bicarbonate (administrated in cases of peptic ulcer or hyperacidity) or antacids, administered in excess can lead to an alkalosis.
Hyperaldosteronism - Renal loss of hydrogen ions occurs when excess aldosterone (Conn's syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney. This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule. Excess sodium increases extracellular volume and the loss of hydrogen ions creates a metabolic alkalosis. Later, the kidney responds through the aldosterone escape to excrete sodium and chloride in urine.^[3]
Excess Glycyrrhizin consumption
Bartter syndrome and Gitelman syndrome - syndromes with presentations analogous to taking diuretics characterized with normotensive patients
Liddle syndrome - a syndrome from defect sodium channel deletion characterized by hypertension and hypoaldosteronism.
11β-hydroxylase deficiency and 17α-hydroxylase deficiency - both characterized by hypertension
Aminoglycoside toxicity can induce a hypokalemic metabolic alkalosis via activating the calcium sensing receptor in the thick ascending limb of the nephron, inactivating the NKCC2 cotransporter, creating a Bartter's syndrome like effect.

Compensation

Compensation for metabolic alkalosis occurs mainly in the lungs, which retain carbon dioxide (CO₂) through slower breathing, or hypoventilation (respiratory compensation). CO₂ is then consumed toward the formation of the carbonic acid intermediate, thus decreasing pH. Respiratory compensation, though, is incomplete. The decrease in [H+] suppresses the peripheral chemoreceptors, which are sensitive to pH. But, because respiration slows, there's an increase in PCO₂ which would cause an offset of the depression because of the action of the central chemoreceptors which are sensitive to the partial pressure of CO₂^{[citation needed]} in the cerebral spinal fluid. So, because of the central chemoreceptors, respiration rate would be increased.

Renal compensation for metabolic alkalosis, less effective than respiratory compensation, consists of increased excretion of HCO₃^- (bicarbonate), as the filtered load of HCO₃^- exceeds the ability of the renal tubule to reabsorb it.

References

^ "Alkalosis, Metabolic: eMedicine Pediatrics: Cardiac Disease and Critical Care Medicine". Retrieved 2009-05-10.
^ Hennessey, Iain. Japp, Alan.Arterial Blood Gases Made Easy. Churchill Livingstone 1 edition (18 Sep 2007).
^ Cho Kerry C, "Chapter 21. Electrolyte & Acid-Base Disorders" (Chapter). McPhee SJ, Papadakis MA: CURRENT Medical Diagnosis & Treatment 2011: http://www.accessmedicine.com/content.aspx?aID=10909.

UpToDate Contents

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1. 代謝性アルカローシスの原因 causes of metabolic alkalosis
2. 代謝性アルカローシスの治療 treatment of metabolic alkalosis
3. 代謝性アルカローシスの臨床症状および評価 clinical manifestations and evaluation of metabolic alkalosis
4. 代謝性アルカローシスの病因 pathogenesis of metabolic alkalosis
5. 症例のミニセッション＃3：代謝性アルカローシス mini case session 3 metabolic alkalosis

English Journal

Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: Case report and appraisal of the pathophysiology.

Bisogni V1, Rossi GP, Calò LA.
Blood pressure.Blood Press.2014 Jun;23(3):189-92. doi: 10.3109/08037051.2013.832967. Epub 2013 Sep 23.
Abstract The glicyrrhizic acid, contained in licorice, has a mineralcorticoid-like effect. Chronic excess intake of licorice induces the rare syndrome of "apparent mineralcorticoid excess", due to the inhibitory effect of glicyrrhizic acid on 11 β-hydroxysteroid dehydrogenase type 2 determining cli
PMID 24053336

Electrolyte abnormalities in cystic fibrosis: systematic review of the literature.

Scurati-Manzoni E1, Fossali EF, Agostoni C, Riva E, Simonetti GD, Zanolari-Calderari M, Bianchetti MG, Lava SA.
Pediatric nephrology (Berlin, Germany).Pediatr Nephrol.2014 Jun;29(6):1015-23. doi: 10.1007/s00467-013-2712-4. Epub 2013 Dec 11.
BACKGROUND: Cystic fibrosis per se can sometimes lead to hyponatremia, hypokalemia, hypochloremia or hyperbicarbonatemia. This tendency was first documented 60 years ago and has subsequently been confirmed in single case reports or small case series, most of which were retrospective. However, this
PMID 24326787

Type III Bartter-like syndrome in an infant boy with Gitelman syndrome and autosomal dominant familial neurohypophyseal diabetes insipidus.

Brugnara M, Gaudino R, Tedeschi S, Syrèn ML, Perrotta S, Maines E, Zaffanello M.
Journal of pediatric endocrinology & metabolism : JPEM.J Pediatr Endocrinol Metab.2014 May 13. pii: /j/jpem.ahead-of-print/jpem-2014-0052/jpem-2014-0052.xml. doi: 10.1515/jpem-2014-0052. [Epub ahead of print]
Abstract We report the case of an infant boy with polyuria and a familial history of central diabetes insipidus. Laboratory blood tests disclosed hypokalemia, metabolic alkalosis, hyperreninemia, and hyperaldosteronism. Plasma magnesium concentration was slightly low. Urine analysis showed hypercalc
PMID 24825090

Japanese Journal

臨床研究・症例報告離乳期の食事導入不良により低K低Cl性アルカローシスを来しBartter症候群との鑑別を要した1歳男児例

重田みどり,大嶋寛子,渡辺周之他
小児科臨床 65(8), 1865-1870, 2012-08-00
NAID 40019342808

A Novel Compound Heterozygous Mutation of Gitelman's Syndrome in Japan, as Diagnosed by an Extraordinary Response of the Fractional Excretion Rate of Chloride in the Trichlormethiazide Loading Test

Ueda Kohei,Makita Noriko,Kawarazaki Hiroo,Fujiwara Takayuki,Unuma Satoshi,Monkawa Toshiaki,Hayashi Matsuhiko,Fujita Toshiro
Internal Medicine 51(12), 1549-1553, 2012
… Gitelman's syndrome (GS), an inherited disorder due to loss of function of ion channels and transporters such as Na-Cl co-transporter (NCCT) in distal convoluted tubules, is characterized by hypokalemia, hypomagnesemia, hypocalciuria, metabolic alkalosis and hyperreninemic-hyperaldosteronism. …
NAID 130002062153

Related Pictures

★リンクテーブル★

リンク元	「代謝性アルカローシス」
関連記事	「metabolic」

「代謝性アルカローシス」

Metabolic alkalosis
	Classification and external resources
	Davenport diagram
ICD-10	E87.3
ICD-9	276.3
DiseasesDB	402
eMedicine	med/1459

　　[★]

英: metabolic alkalosis
関: アルカローシス、酸塩基平衡異常

酸塩基平衡異常とその代償 SP.660

	HCO3-	pCO2
呼吸性アシドーシス	↑	↑
呼吸性アルカローシス	↓	↓
代謝性アシドーシス	↓	↑
代謝性アルカローシス	↑	↓

原因

低カリウム性代謝性アルカローシス：H+とCl-の喪失：嘔吐、利尿薬など

嘔吐

細胞内からH+が供給され、K+が細胞内に移動しカリウムが低下する。H+の減少は遠位尿細管におけるHCO3-の排泄を抑制し代謝性アシドーシスが完成する。
塩素欠乏は腎臓におけるHCO3-再吸収を刺激(ICU.489)

アニオンギャップ(AG=[Na+] - [HCO3-] - [Cl-])を保つようにHCO3-が増加したと考えればよいのか。

原因による分類

ICU.493

塩素反応性：尿中塩素＜15mEq/L

1. 胃酸の喪失　→　H+, Cl-の喪失
2. 利尿薬　→　多くの利尿剤でCl-を喪失(see. 利尿薬)
3. 循環血液量不足
4. 高二酸化炭素症に対する腎性の代償：CO2↑　→　腎で代償的にHCO3-排泄↓　→　(おそらく)HCO3-の代替としてCl-が排泄

塩素抵抗性：尿中塩素＞25mEq/L

1. ミネラルコルチコイド過剰：尿細管でNa+再吸収、K+排泄亢進。体内では代償的に細胞外へのK+放出、細胞内へのH+取り込みが起こる　→　代謝性アルカローシス
2. カリウム欠乏

YN.D-155

腎からのH+喪失、重炭酸再吸収の亢進：糖質コルチコイド・鉱質コルチコイド投与、アルドステロン症、クッシング症候群、腎血管性高血圧、バーター症候群、ギテルマン症候群
細胞内へのH+移動：
消化管からのH+喪失：嘔吐、胃管による消化液吸引、慢性下痢、先天性塩類漏出症
NaCl喪失に伴う細胞外液の喪失
その他

炭酸水素ナトリウム過剰投与
ミルクアルカリ症候群
高カルシウム血症
大量輸液　　→　　抗凝固薬として加えられているクエン酸が代謝されて重炭酸イオンが形成される　　←　　どう考えてもこの代謝pathが分からない。
refeeding syndrome

水・電解質と酸塩基平衡改訂第2版 p.163

I. H+の喪失

1. 消化管からの喪失

胃液への排出(嘔吐、胃液吸引)

2. 尿中への喪失

鉱質コルチコイド過剰

利尿薬

多量のカルベニシリンなどのペニシリン誘導体等よ

高カルシウム血症

3. H+の細胞内への移行

低カリウム血症

II. HCO3-の投与

大量の輸液(大量のクエン酸摂取による)

NaHCO3の投与

ミルク・アルカリ症候群

III. contraction alkalosis

出典不明

腎でのH+再吸収低下(硫酸イオン、高カルシウム血症、副甲状腺機能低下症、ペニシリン)

症例

16歳女性、神経過食症であり、自己誘発性嘔吐を制御できなかった。この女性で予想されるK, HCO3-の状態は？

国試

103A016

「metabolic」

　　[★]

adj.

代謝性の、代謝的な、メタボリックな

関: metabolically

[urlAlkalosis.2C_Metabolic:_eMedicine_Pediatrics:_Cardiac_Disease_and_Critical_Care_Medicine-1] "Alkalosis, Metabolic: eMedicine Pediatrics: Cardiac Disease and Critical Care Medicine". Retrieved 2009-05-10.

[2] Hennessey, Iain. Japp, Alan.Arterial Blood Gases Made Easy. Churchill Livingstone 1 edition (18 Sep 2007).

[3] Cho Kerry C, "Chapter 21. Electrolyte & Acid-Base Disorders" (Chapter). McPhee SJ, Papadakis MA: CURRENT Medical Diagnosis & Treatment 2011: http://www.accessmedicine.com/content.aspx?aID=10909.

匿名

検索

案内

案内

metabolic alkalosis