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排尿促進の,利尿の / 利尿剤

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/07/26 16:00:50」(JST)

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A diuretic is any substance that promotes the production of urine. This includes forced diuresis. There are several categories of diuretics. All diuretics increase the excretion of water from bodies, although each class does so in a distinct way. Alternatively, an antidiuretic such as vasopressin, or antidiuretic hormone, is an agent or drug which reduces the excretion of water in urine.

1 Medical uses
2 Types
- 2.1 High ceiling/loop diuretic
- 2.2 Thiazides
- 2.3 Carbonic anhydrase inhibitors
- 2.4 Potassium-sparing diuretics
- 2.5 Calcium-sparing diuretics
- 2.6 Osmotic diuretics
- 2.7 Low ceiling diuretics
3 Mechanism of action
4 Adverse effects
5 Banned use in sports
6 See also
7 References
8 External links

Medical uses

In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension, water poisoning, and certain kidney diseases. Some diuretics, such as acetazolamide, help to make the urine more alkaline and are helpful in increasing excretion of substances such as aspirin in cases of overdose or poisoning. Diuretics are often abused by sufferers of eating disorders, especially bulimics, in attempts at weight loss.

The antihypertensive actions of some diuretics (thiazides and loop diuretics in particular) are independent of their diuretic effect.^{[citation needed]} That is, the reduction in blood pressure is not due to decreased blood volume resulting from increased urine production, but occurs through other mechanisms and at lower doses than that required to produce diuresis. Indapamide was specifically designed with this in mind, and has a larger therapeutic window for hypertension (without pronounced diuresis) than most other diuretics.

Types

High ceiling/loop diuretic

High ceiling diuretics may cause a substantial diuresis – up to 20%^[1] of the filtered load of NaCl (salt) and water. This is large in comparison to normal renal sodium reabsorption which leaves only about 0.4% of filtered sodium in the urine. Loop diuretics have this ability, and are therefore often synonymous with high ceiling diuretics. Loop diuretics, such as furosemide, inhibit the body's ability to reabsorb sodium at the ascending loop in the nephron, which leads to an excretion of water in the urine, whereas water normally follows sodium back into the extracellular fluid. Other examples of high ceiling loop diuretics include ethacrynic acid and torsemide.

Thiazides

Thiazide-type diuretics such as hydrochlorothiazide act on the distal convoluted tubule and inhibit the sodium-chloride symporter leading to a retention of water in the urine, as water normally follows penetrating solutes. Frequent urination is due to the increased loss of water that has not been retained from the body as a result of a concomitant relationship with sodium loss from the convoluted tubule. The long-term anti-hypertensive action is based on the fact that thiazides decrease preload, decreasing blood pressure. On the other hand the short-term effect is due to an unknown vasodilator effect that decreases blood pressure by decreasing resistance.

Carbonic anhydrase inhibitors

Carbonic anhydrase inhibitors inhibit the enzyme carbonic anhydrase which is found in the proximal convoluted tubule. This results in several effects including bicarbonate accumulation in the urine and decreased sodium absorption. Drugs in this class include acetazolamide and methazolamide.

Potassium-sparing diuretics

These are diuretics which do not promote the secretion of potassium into the urine; thus, potassium is retained and not lost as much as with other diuretics. The term "potassium-sparing" refers to an effect rather than a mechanism or location; nonetheless, the term almost always refers to two specific classes that have their effect at similar locations:

Aldosterone antagonists: spironolactone, which is a competitive antagonist of aldosterone. Aldosterone normally adds sodium channels in the principal cells of the collecting duct and late distal tubule of the nephron. Spironolactone prevents aldosterone from entering the principal cells, preventing sodium reabsorption. Similar agents are eplerenone and potassium canreonate.

Epithelial sodium channel blockers: amiloride and triamterene.

Calcium-sparing diuretics

The term "calcium-sparing diuretic" is sometimes used to identify agents that result in a relatively low rate of excretion of calcium.^[2]

The reduced concentration of calcium in the urine can lead to an increased rate of calcium in serum. The sparing effect on calcium can be beneficial in hypocalcemia, or unwanted in hypercalcemia.

The thiazides and potassium-sparing diuretics are considered to be calcium-sparing diuretics.^[3]

The thiazides cause a net decrease in calcium lost in urine.^[4]
The potassium-sparing diuretics cause a net increase in calcium lost in urine, but the increase is much smaller than the increase associated with other diuretic classes.^[4]

By contrast, loop diuretics promote a significant increase in calcium excretion.^[5] This can increase risk of reduced bone density.^[6]

Osmotic diuretics

Osmotic diuretics (e.g. mannitol) are substances that increase osmolality but have limited tubular epithelial cell permeability. They work primarily by expanding extracellular fluid and plasma volume, therefore increasing blood flow to the kidney, particularly the peritubular capillaries. This reduces medullary osmolality and thus impairs the concentration of urine in the loop of Henle (which usually uses the high osmotic and solute gradient to transport solutes and water). Furthermore, the limited tubular epithelial cell permeability increases osmolality and thus water retention in the filtrate.^[7]

It was previously believed that the primary mechanism of osmotic diuretics such as mannitol is that they are filtered in the glomerulus, but cannot be reabsorbed. Thus their presence leads to an increase in the osmolarity of the filtrate and to maintain osmotic balance, water is retained in the urine.

Glucose, like mannitol, is a sugar that can behave as an osmotic diuretic. Unlike mannitol, glucose is commonly found in the blood. However, in certain conditions, such as diabetes mellitus, the concentration of glucose in the blood (hyperglycemia) exceeds the maximum reabsorption capacity of the kidney. When this happens, glucose remains in the filtrate, leading to the osmotic retention of water in the urine. Glucosuria causes a loss of hypotonic water and Na⁺, leading to a hypertonic state with signs of volume depletion, such as dry mucosa, hypotension, tachycardia, and decreased turgor of the skin. Use of some drugs, especially stimulants, may also increase blood glucose and thus increase urination.

Low ceiling diuretics

The term "low ceiling diuretic" is used to indicate a diuretic has a rapidly flattening dose effect curve (in contrast to "high ceiling", where the relationship is close to linear). It refers to a pharmacological profile, not a chemical structure. However, certain classes of diuretic tae usually fall into this category, such as the thiazides.^[8]

Mechanism of action

Diuretics are tools of considerable therapeutic importance. First, they effectively reduce blood pressure. Loop and thiazide diuretics are secreted from the proximal tubule via the organic anion transporter-1 and exert their diuretic action by binding to the Na(+)-K(+)-2Cl(-) co-transporter type 2 in the thick ascending limb and the Na(+)-Cl(-) co-transporter in the distal convoluted tubule, respectively.^[9] Classification of common diuretics and their mechanisms of action.

	Examples	Mechanism	Location (numbered in distance along nephron)
–	ethanol, water	Inhibits vasopressin secretion		Acidifying salts	CaCl₂, NH₄Cl	1.
Arginine vasopressin receptor 2 antagonists	amphotericin B, lithium citrate	Inhibits vasopressin's action	5. collecting duct
Aquaretics	Goldenrod^{[citation needed]}, Juniper^{[citation needed]}	Increases blood flow in kidneys^{[citation needed]}	1.^{[citation needed]}
Na-H exchanger antagonists	dopamine^[10]	Promotes Na⁺ excretion	2. proximal tubule^[10]
Carbonic anhydrase inhibitors	acetazolamide,^[10] dorzolamide	Inhibits H⁺ secretion, resultant promotion of Na⁺ and K⁺ excretion	2: proximal tubule
Loop diuretics	bumetanide,^[10] ethacrynic acid,^[10] furosemide,^[10] torsemide	Inhibits the Na-K-2Cl symporter	3. medullary thick ascending limb
Osmotic diuretics	glucose (especially in uncontrolled diabetes), mannitol	Promotes osmotic diuresis	2. proximal tubule, descending limb
Potassium-sparing diuretics	amiloride, spironolactone, eplerenone, triamterene, potassium canrenoate.	Inhibition of Na+/K+ exchanger: Spironolactone inhibits aldosterone action, Amiloride inhibits epithelial sodium channels^[10]	5. cortical collecting ducts
Thiazides	bendroflumethiazide, hydrochlorothiazide	Inhibits reabsorption by Na⁺/Cl⁻ symporter	4. distal convoluted tubules
Xanthines	caffeine, theophylline, theobromine	Inhibits reabsorption of Na⁺, increase glomerular filtration rate	1. tubules

Chemically, diuretics are a diverse group of compounds that either stimulate or inhibit various hormones that naturally occur in the body to regulate urine production by the kidneys.

As a diuretic is any substance that promotes the production of urine, aquaretics that cause the excretion of free water are a sub-class. This includes all the hypotonic aqueous preparations, including pure water, black and green teas, and teas prepared from Herbal medications. Any given herbal medication will include a vast range of plant-derived compounds, some of which will be active drugs that may also have independent diuretic action.

Adverse effects

The main adverse effects of diuretics are hypovolemia, hypokalemia, hyperkalemia, hyponatremia, metabolic alkalosis, metabolic acidosis, and hyperuricemia.^[10]

Adverse effect	Diuretics	Symptoms
Hypovolemia	loop diuretics^[10] thiazides^[10]	lassitude^[10] thirst^[10] muscle cramps^[10] hypotension^[10]
hypokalemia	acetazolamides^[10] loop diuretics^[10] thiazides^[10]	muscle weakness^[10] paralysis^[10] arrhythmia^[10]
Hyperkalemia	amilorides^[10] triamterenes^[10] spironolactone^[10]	arrhythmia^[10] muscle cramps^[10] paralysis^[10]
hyponatremia	thiazides^[10] furosemides^[10]	CNS symptoms^[10] coma^[10]
metabolic alkalosis	loop diuretics^[10] thiazides^[10]	arrhythmia^[10] CNS symptoms^[10]
metabolic acidosis	acetazolamides^[10] amilorides^[10] triamterene^[10]	Kussmaul respirations^[10] muscle weakness neurological symptoms^[10] lethargy coma seizures stupor
hypercalcemia	thiazides^[10]	gout tissue calcification^[10] fatigue depression confusion anorexia nausea vomiting constipation pancreatitis increased urination
hyperuricemia	thiazides^[10] loop diuretics^[10]	gout^[10]

Banned use in sports

A common application of diuretics is for the purposes of invalidating drug test.^[11] Diuretics increase the urine volume and dilute doping agents and their metabolites. The other use would be to rapidly lose weight to meet a weight category in sports like boxing, wrestling and others.^[12]^[13]

References

^ Drug Monitor – Diuretics
^ Shankaran S, Liang KC, Ilagan N, Fleischmann L (April 1995). "Mineral excretion following furosemide compared with bumetanide therapy in premature infants". Pediatr. Nephrol. 9 (2): 159–62. doi:10.1007/BF00860731. PMID 7794709.
^ Bakhireva LN, Barrett-Connor E, Kritz-Silverstein D, Morton DJ (June 2004). "Modifiable predictors of bone loss in older men: a prospective study". Am J Prev Med 26 (5): 436–42. doi:10.1016/j.amepre.2004.02.013. PMID 15165661.
^ ^a ^b Champe, Pamela C.; Richard Hubbard Howland; Mary Julia Mycek; Harvey, Richard P. (2006). Pharmacology. Philadelphia: Lippincott William & Wilkins. p. 269. ISBN 0-7817-4118-1.
^ Rejnmark L, Vestergaard P, Pedersen AR, Heickendorff L, Andreasen F, Mosekilde L (January 2003). "Dose-effect relations of loop- and thiazide-diuretics on calcium homeostasis: a randomized, double-blinded Latin-square multiple cross-over study in postmenopausal osteopenic women". Eur. J. Clin. Invest. 33 (1): 41–50. doi:10.1046/j.1365-2362.2003.01103.x. PMID 12492451.
^ Rejnmark L, Vestergaard P, Heickendorff L, Andreasen F, Mosekilde L (January 2006). "Loop diuretics increase bone turnover and decrease BMD in osteopenic postmenopausal women: results from a randomized controlled study with bumetanide". J. Bone Miner. Res. 21 (1): 163–70. doi:10.1359/JBMR.051003. PMID 16355285.
^ https://www.uic.edu/classes/pcol/pcol425/restricted/Du/diuretics.PDF
^ Mutschler, Ernst (1995). Drug actions: basic principles and therapeutic aspects. Stuttgart, German: Medpharm Scientific Pub. p. 460. ISBN 0-8493-7774-9.
^ Ali SS, Sharma PK, Garg VK, Singh AK, Mondal SC (Apr 2012). "The target-specific transporter and current status of diuretics as antihypertensive". Fundam Clin Pharmacol 26 (2): 175–9. doi:10.1111/j.1472-8206.2011.01012.x. PMID 22145583.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l ^m ⁿ ^o ^p ^q ^r ^s ^t ^u ^v ^w ^x ^y ^z ^aa ^ab ^ac ^ad ^ae ^af ^ag ^ah ^ai ^aj ^ak ^al ^am ^an ^ao ^ap ^aq ^ar Boron, Walter F. (2004). Medical Physiology: A Cellular And Molecular Approach. Elsevier/Saunders. p. 875. ISBN 1-4160-2328-3.
^ Bahrke, Michael (2002). Performance-Enhancing Substances in Sport and Exercise.
^ Agence France Presse (2012-07-17). "UCI announces adverse analytical finding for Frank Schleck". VeloNews. Retrieved 2012-07-18.
^ The abuse of diuretics as performance-enhancing drugs and masking agents in sport doping: pharmacology, toxicology and analysis, British Journal of Pharmacology, 2010-09.

External links

Diagram at cvpharmacology.com
"Caffeine and Electrolyte Imbalance" by Dana George August 23, 2011

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 利尿剤の作用機序 mechanism of action of diuretics
2. 心不全患者における利尿剤の使用 use of diuretics in patients with heart failure
3. ループ利尿剤：最大有効量および主な副作用 loop diuretics maximum effective dose and major side effects
4. 高血圧治療におけるサイアザイド系利尿剤とループ利尿剤の比較 thiazides versus loop diuretics in treatment of hypertension
5. 成人における浮腫に対する治療の一般原則 general principles of the treatment of edema in adults

English Journal

β1 selectivity of β-blockers and reduced risk of fractures in elderly hypertension patients.

Song HJ, Lee J, Kim YJ, Jung SY, Kim HJ, Choi NK, Park BJ.SourceDepartment of Family Medicine, Health Promotion Center, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, 896 Pyeongchon-Dong, Anyang-Si, Gyeonggi-do, Republic of Korea. Electronic address: hongjisong5@gmail.com.
Bone.Bone.2012 Dec;51(6):1008-15. doi: 10.1016/j.bone.2012.08.126. Epub 2012 Aug 30.
INTRODUCTION: Hypertension and osteoporosis are prevalent in the elderly population. Treatments beneficial to both conditions would be helpful. We examined the protective effect of β-blockers (BBs) and their receptor selectivity against fractures compared to other antihypertensives.MATERIALS AND ME
PMID 22960238

A phase 1 study of efatutazone, an oral peroxisome proliferator-activated receptor gamma agonist, administered to patients with advanced malignancies.

Pishvaian MJ, Marshall JL, Wagner AJ, Hwang JJ, Malik S, Cotarla I, Deeken JF, He AR, Daniel H, Halim AB, Zahir H, Copigneaux C, Liu K, Beckman RA, Demetri GD.SourceLombardi Comprehensive Cancer Center, Developmental Therapeutics Program, Georgetown University Medical Center, Washington, District of Columbia. pishvaim@georgetown.edu.
Cancer.Cancer.2012 Nov 1;118(21):5403-13. doi: 10.1002/cncr.27526. Epub 2012 May 8.
BACKGROUND: Efatutazone (CS-7017), a novel peroxisome proliferator-activated receptor gamma (PPARγ) agonist, exerts anticancer activity in preclinical models. The authors conducted a phase 1 study to determine the recommended phase 2 dose, safety, tolerability, and pharmacokinetics of efatutazone.M
PMID 22570147

Japanese Journal

利尿薬とβ遮断薬の使い方 (第5土曜特集高血圧のすべて2012 : 研究と診療の最前線) -- (最新のエビデンスに基づく高血圧診療2012)

冨山博史,山科章
医学のあゆみ 241(13), 1163-1168, 2012-06-30
NAID 40019316045

利尿薬とβ遮断薬の評価 (第5土曜特集高血圧のすべて2012 : 研究と診療の最前線) -- (高血圧治療のあらたなエビデンス)

植田真一郎
医学のあゆみ 241(13), 1078-1081, 2012-06-30
NAID 40019315878

Related Pictures

★リンクテーブル★

リンク元	「100Cases 27」「利尿薬」「100Cases 16」「diuretic drug」「diuretic agent」
関連記事	「diuretic」

「100Cases 27」

Diuretic
	Drug class
Use	Forced diuresis, hypertension
ATC code	C03

　　[★]

☆case27　関節痛

■症例

37歳　女性

主訴：関節痛

現病歴：数ヶ月、膝の痛みがだんだん強くなっていると感じていた。痛みは手や足の小関節に多く、朝歩くときに最もこわばる。痛みはジクロフェナクを飲むと和らぐ。そのほかの症状として疲労感を感じ、最近、体重が３ヶ月で４ｋｇ減っている。

喫煙歴：なし。

飲酒歴：機会飲酒

既往歴：なし

家族歴：既婚、子供は２人

服薬歴：ジクロフェナク

職業歴：legal sevretary

身体所見 examination

　顔貌　青白、臨床的な貧血を認める。近位指節間関節・中手指節関節　腫脹・effusionを伴う疼痛。中足趾節関節　圧痛。それ以外は正常。

検査　 investigation

　血液検査

　　Hb低下

　　ESR 上昇

　　尿素軽度上昇

　　クレアチニン軽度上昇

　　正常：白血球、MCV、血小板、ナトリウム、カリウム、グルコース、アルブミン

　尿検査

　　蛋白(-)、尿糖(-)、潜血(-)、

■問題

　本症例では診断とその根拠を考えるのは簡単なので、鑑別疾患をあげてその疾患に特徴的な症候を列挙しましょう。

■関節痛 DIF.283

　V Vascular

　　血友病 hemophilia　血友病性関節症(急性：疼痛、腫脹、熱感(SOR.241)

慢性：可動域の低下、変形、関節周囲筋萎縮(SOR.241))。家族歴

　　壊血病 scurvy　。生活環境。食事歴

　　無菌性骨壊死 aseptic bone necrosis (Osgood-Schlatter diseaseとか)

　I Inflammatory

　　感染性関節炎(細菌性関節炎(化膿性関節炎・淋菌性関節炎・結核性関節炎・嫌気性菌関節炎 )、真菌性関節炎、スピロヘータ関節炎(梅毒性関節炎・ライム関節炎)、マイコプラズマ関節炎、ウイルス性関節炎)

　N Neoplastic disorders

　　骨原性肉腫 osteogenic sarcoma

　　巨細胞腫 giant cell tumors

　D Degenerative disorders

　　degenerative joint disease

　　変形性関節症 osteoarthritis

　I Intoxication

　　痛風 gout (uric acid)

　　偽痛風 pseudogout (calcium pyrophosphate)

　　ループス症候群 lupus syndrome of hydralazine (Apresoline) and procainamide

　　gout syndrome of diuretics

　C Congenital and acquired malformations bring to mind the joint deformities of tabes dorsalis and syringomyelia and congenital dislocation of the hip. Alkaptonuria is also considered here.

　A Autoimmune indicates

　　関節リウマチ RA

　　血清病 serum sickness

　　全身性エリテマトーデス lupus erythematosus

　　リウマチ熱 rheumatic fever

　　ライター症候群 Reiter syndrome

　　潰瘍性大腸炎 ulcerative colitis

　　クローン病=限局性回腸炎 regional ileitis

　　乾癬性関節炎 psoriatic arthritis

　　リウマチ性多発筋痛症 polymyalgia rheumatica

　T Trauma

　E Endcrine

　　先端肥大症 acromegaly

　　閉経 menopause

　　糖尿病 diabetes mellitus

■関節炎の分類

・炎症部位の数

　単関節炎：痛風、偽痛風、離断性骨軟骨炎、血行性の化膿性関節炎のほとんど

　多関節炎：リウマチ性疾患、ウイルス性疾患、白血病での関節症状、易感染性宿主における血行性の化膿性関節炎

■関節リウマチ

　診断基準

　関節症状

　　朝のこわばり、疼痛、腫脹、関節の動揺、関節可動域制限、変形(手指、足趾、膝関節)。(SOR.211)

　　手指の近位指節間関節(PIP 関節)、中手指節関節(MP 関節)。遠位指節間関節(DIP 関節)に初発することは稀。(SOR.211)

　　左右対称性に生じることが多い。手関節、足趾、膝関節に初発する。(SOR.211)

　関節外症状

　　全身症状：発熱

　　皮膚症状：リウマトイド結節(肘の伸側、後頭部、手指)

　　眼症状：上胸膜炎(10日の経過で治癒)、強膜炎(予後不良)。稀に角膜穿孔

　　血液障害：(高頻度)貧血、白血球減少(Felty病。DMARDs投与中の場合は薬剤性の骨髄抑制を考慮)

　　アミロイドーシス：ネフローゼや下痢を来した症例で疑う。アミロイド蛋白はAA

　　腎障害：稀。アミロイドーシスの続発症か薬剤性を考慮。

　　呼吸器症状：間質性肺炎の合併多い。下肺野に好発。通常無症状。メトトレキセートなどの使用により薬剤性の急性間質性肺炎を生じることがある。

　　心・血管障害：リンパ管炎による難治性の浮腫。

　　神経症状：環軸関節亜脱臼により項部痛や脊髄症上が出現しうる。

　　骨粗鬆症

　　腱鞘滑膜炎：手指、手関節、足関節

■両側性多関節炎の鑑別疾患

　OA：遠位指節間関節を冒すのが特徴的で、近位指節間関節、中手指節関節を冒しうる。

　RA：

　SLE：軽度、症状の程度が変動する非びらん性の関節炎

　gout：単関節炎からはじまる。

　血清陰性関節炎：強直性脊椎炎、感染、ライター病：中～大関節に非対称性の関節炎。仙腸関節と遠位指節間関節にも関節炎

　急性ウイルス性関節炎：風疹。

■KEY POINTS

・RAでは遠位指節間関節は冒されない傾向がある。

・RAの全身症状は関節症状に先行することがある。

・RAの活動性と貧血及びESRは相関している。

・NSAIDsは腎機能に悪影響を与えることがある。

■initial plan

　Dx 1. 単純X線写真

　　　　・亜脱臼、関節周囲の骨萎縮(傍関節性骨骨粗鬆症,juxta-articular osteoporosis)、関節裂隙の狭小化、関節辺縁のびらん(bony erosion)

　　　　　・初期のRAで第5趾に骨びらんが一般的に見られる。

　　　　・血液検査

　　　　　・RF、抗DNA 抗体

　Tx 1. 鎮痛薬

　　　　・NSAIDs：鎮痛とこわばりの軽減

　　 2. DMARDs(メトトレキセート、レフルノミド、金製剤、ペニシラミン)

　　　　・NSAIDsで症状が治まらない場合に考慮

　　 3. 抗TNF 抗体

　　　　・重症のRAで効果がある場合がある。

■参考文献

SOR　標準整形外科学第10版医学書院

DIF　Differential Diagnosis in Primary Care Fourth Edition版 Lippincott Williams & Wilkins

「利尿薬」

　　[★]

英: diuretic, diuretics
関: 尿細管

適応

心不全、腎不全、高血圧症、肝硬変による腹水貯留、妊娠中毒症

利尿薬の種類 (GOO.744)

CATIONS

ANIONS

尿酸

腎血液動態

Na⁺

K⁺

H⁺

Ca²⁺

Mg²⁺

Cl^-

HCO₃^-

H₂PO₄^-

急性

慢性

RBF

GFR

FF

TGF

炭酸脱水酵素阻害薬

炭酸脱水酵素阻害

近位尿細管
　

＋

＋＋

－

NC

V

(＋)

＋＋

I

－

NC

＋

浸透圧利尿薬

浸透圧

ヘンレループ
　

＋＋

＋

I

＋

＋＋

＋

I

＋

NC

－

I

ループ利尿薬

Na⁺-K⁺-2Cl^- symport阻害

太い上行脚
　

＋＋

＋

＋＋

＋⁽¹⁾

＋

－

V(＋)

NC

V(－)

－

チアジド系利尿薬

Na⁺-Cl^-symport阻害

遠位尿細管
　

＋

＋＋

＋

V(－)

V(＋)

＋

＋⁽¹⁾

＋

－

NC

V(－)

NC

カリウム保持性利尿薬

上皮性ナトリウムチャネル阻害

遠位尿細管後部と集合管
　

＋

－

＋

(＋)

NC

I

－

NC

アルドステロン受容体拮抗

遠位尿細管後部と集合管
　

＋

－

I

－

＋

(＋)

I

－

NC

利尿薬の例

浸透圧利尿薬

炭酸脱水酵素阻害薬

ループ利尿薬

チアジド系利尿薬

ヒドロクロロチアジド hydrochlorothiazide

カリウム保持性利尿薬

上皮性ナトリウムチャネル阻害薬

アルドステロン受容体阻害薬

スピロノラクトン spironolactone

利尿薬の作用部位

ホルモンと利尿薬の作用部位についての簡単なまとめは→尿細管

参照

http://hobab.fc2web.com/sub4-Diuretics.htm

「100Cases 16」

　　[★]

☆case16　膝の痛み

■glossary

indigestion 消化障害、消化不良

■症例

80歳　男性

主訴：左膝の痛みと腫脹

現病歴：左膝の痛みを2日前から認めた。膝は発熱・腫脹しており、動かすと疼痛を生じる。時々胸焼けと消化不良が見られる。6ヶ月前のhealth checkで、高血圧(172/102mmHg)と血中クレアチニンが高い(正常高値)こと以外は正常といわれた。その4週間数回血圧を測定したが、高値が継続したため、2.5mg bendrofluamethizide(UK)/ベンドロフルメチアジド bendroflumethiazide(US)で治療を開始した。最近の血圧は138/84 mmHgであった。

喫煙歴：なし。

飲酒歴：一週間に平均4unit。

既往歴：股関節に中程度(mild)の変形性関節症

家族歴：特記なし

服薬歴：アセトアミノフェン(股関節の疼痛に対して)

身体所見 examination

　血圧 142/86mmHg。体温37.5℃。脈拍88/分。grade 2 hypertensive retinopathy(高血圧症性網膜症)。心血管系、呼吸器系に検査場異常なし。手にDIPにヘバーデン結節なし。

　左膝が発熱し腫脹している。関節内に液、patellar tap陽性。90℃以上膝関節を屈曲させると痛みを生じる。右の膝関節は正常に見える。

検査　 investigation

　生化学：白血球増多、ESR 上昇、尿素高値、グルコース高値

　単純X線：関節間隙やや狭小。それ以外に異常は認めない。

■problem list

　#1 左膝の痛み

　#2 胸焼け

　#3 消化不良

　#4 高血圧

　#5 クレアチニン正常高値

　#6 股関節の変形性リウマチ

　#7 高血圧性網膜症

■考え方

　・関節痛の鑑別診断を考える。

　・VINDICATEで考えてみてもよいでしょう。

　・関節痛の頻度としては　外傷＞慢性疾患(OAなど)＞膠原病＞脊椎疾患＞悪性腫瘍

■関節痛の鑑別疾患

DIF 282

V Vascular 血友病 hemophilia, 壊血病 scurvy, 無菌性骨壊死 aseptic bone necrosis (Osgood-Schlatter diseaseとか)

I Inflammatory 淋疾 gonorrhea, ライム病 lyme disease, 黄色ブドウ球菌 Staphylococcus, 連鎖球菌 Streptococcus, 結核 tuberculosis, 梅毒 syphilis, 風疹 rubella, 単純ヘルペス herpes simplex, HIV human immunodeficiency virus, サイトメガロウイルス cytomegalovirus

N Neoplastic disorders 骨原性肉腫 osteogenic sarcoma, 巨細胞腫 giant cell tumors

D Degenerative disorders degenerative joint disease or 変形性関節症 osteoarthritis

I Intoxication 痛風 gout (uric acid), 偽痛風 pseudogout (calcium pyrophosphate), ループス症候群 lupus syndrome of hydralazine (Apresoline) and procainamide, gout syndrome of diuretics

C Congenital and acquired malformations bring to mind the joint deformities of tabes dorsalis and syringomyelia and congenital dislocation of the hip. Alkaptonuria is also considered here.