Acidosis & alkalosis ´ëÀå°æ Á¤¸®
1. severe acidosis°¡ ½Åü¿¡ ¹ÌÄ¡´Â ¿µÇâ
1) cardiovascular
¼öÃà·Â °¨¼Ò, arterial vasodilation, venoconstriction, blood volume centralization
pulmonary vascular resistance¡è, BP¡é, hepatic & renal blood flow¡é
arrhythmia threshold°¨¼Ò, catecholamine¿¡ ´ëÇÑ ¹ÝÀÀ °¨¼Ò
2) respiratory
hyperventilation, dyspnea
3) metabolic
metabolic demands¡è, insulin resistance¡è, anaerobic glycolysis¾ïÁ¦
ATP synthesis¡é, hyperkalemia, protein degradation¡è
4) cerebral
metabolism & cell-volume regulation¡é
obtundation & coma
2. urine acidification Æò°¡¹æ¹ý
urine pH, urine anion gap, urine osmolar gap
3. ½ÅºÎÀü¶§ »ý±â´Â metabolic acidosis ±âÀü
½ÅºÎÀü Ãʱ⿡ nephron mass°¨¼Ò·Î NH3»ý¼ºÀÌ °¨¼ÒµÇ¾î hyperchloremic acidosis°¡
»ý±ä´Ù.
½ÅºÎÀüÀÌ ÁøÇàÇÔ¿¡ µû¶ó organic anionÃàÀûµÇ¸é¼ high AG metabolic acidosis·Î ÁøÇà
serum HCO3-°¡ °¨¼ÒÇÏÁö¸¸ 15 mEq/LÀÌÇϷδ ¶³¾îÁöÁö ¾Ê´Âµ¥ ÀÌ´Â boneÀÇ calcium
carbonateµîÀÌ buffer·Î ÀÛ¿ëÇϱ⠶§¹®ÀÌ´Ù.
½ÅºÎÀü¶§ HCO3-¸¦ 20-24 mmol/L·Î À¯ÁöÇϱâ À§ÇØ alkali tx°¡ ÇÊ¿äÇѵ¥
sodium citrate´Â À§Àå°ü¿¡¼ aluminumÈí¼ö¸¦ Áõ°¡½ÃŰ¹Ç·Î, aluminumÇÔÀ¯ Á¦»êÁ¦¿Í
°°ÀÌ Åõ¿©Çϸé aluminumÁßµ¶ÀÇ À§ÇèÀÌ ÀÖÀ¸¹Ç·Î ÁÖÀÇÇØ¾ß ÇÑ´Ù.
4. effective osmolality
= 2(Na+K) + glu/18
5. osmolar gap = measured osm - calculated osm
6. high AG metabolic acidosis¸¦ ÀÏÀ¸Å°´Â ¾à¹°
salicylate, methanol, ethylene glycol, paraldehyde
cf. hyperchloremic metabolic acidosis + hyperkalemiaÀÏÀ¸Å°´Â ¾à¹°
: K-sparing diuretics, pentamidine, ACEI, NSAIDs, cyclosporine, trimethoprim
7. high AG metabolic acidosis¿øÀÎ
lactic acidosis, ketoacidosis, drug(salicylate, ethylene glycol, methanol)
renal failure(acute and chronic)
8. ethylene glycol poisoning
s-osmolarity¡è, urine oxalate crystal, ATN(proteinuria, oliguria, anuria)
ethanol·Î Ä¡·á
9. alcoholic ketoacidosisÄ¡·á : normal saline IVÇÏ¿© volume expansion½ÃŲ´Ù.
insulinÀº ±Ý±âÀ̸ç K, P, Mg, vitµîÀ» º¸ÃæÇÑ´Ù.
10. urine anion gap = (Na + K) - Cl
hypercholremic acidosisȯÀÚ¸¦ Æò°¡Çϴµ¥ À¯¿ëÇÏ´Ù.
(+) : renal tubular disorder
(-) : extrarenal cause
11. metabolic acidosis¿¡¼ÀÇ urine net charge(UNC)
renal or nonrenal hyperchloremic acidosis¸¦ °¨º°ÇÏ´Â ¹æ¹ýÀÌ´Ù.
RTA¿¡¼´Â NH4+ ÇÕ¼º ¹× ¹è¼³ °¨¼Ò·Î UNC°¡ Áõ°¡ÇÑ´Ù.
¼³»ç·Î ÀÎÇÑ metabolic acidosis¶§´Â NH4+ÇÕ¼º ¹× ¹è¼³ Áõ°¡·Î UNC°¡ °¨¼ÒÇÑ´Ù.
12. amphoterin B -> typeI RTAÀÏÀ¸Å´
13. metabolic acidosis¸¦ Ä¡·áÇϱâ À§ÇØ sodium bicarbonate¸¦ Åõ¿©ÇÒ¶§ÀÇ ºÎÀÛ¿ë
: volume expansion(pul. edema, hypertension ¾ÇÈ), hypocalcemia, hypokalemia
metabolic & respiratory alkalosis
14. metabolic acidosis + hypokalemia
type I, II RTA, diarrhea, DKA, carbonic anhydrase inhibitor
15. distal RTA
Calcium phosphate, nephrocalcinosisµîÀÌ Àß ¹ß»ýÇÏ¸ç ±× ¿øÀÎÀ¸·Î´Â hypercalciuria,
alkaline urine, low level of citrate µîÀÌ´Ù.
urine pH°¡ ³ô¾Æ¼ ü³»¿¡¼ »ý¼ºµÈ total acidº¸´Ù net acid excretionÀÌ °¨¼ÒµÇ¾î ÀÖ´Ù.
acidosis¿Í hypercalciuria°¡ ±³Á¤µÉ¶§±îÁö 1-3 mEq/kgÀÇ alkaliÄ¡·á°¡ ¿ä±¸µÈ´Ù.
´ëºÎºÐ K supplement´Â ÇÊ¿äÄ¡ ¾Ê´Ù.
16. distal RTA¿¡¼ ½Å°á¼®ÀÌ Àß ¹ß»ýÇÏ´Â ±âÀü
hypercalciuria & hyperphosphaturia
urine pH¡è
hypocituria
17. Fanconi syndrome: type2 RTA, glycosuria + normal serum glucose,
hypophosphatemia hypouricemia, hypokalemia, aminoaciduria
18. diuretics¿¡ ÀÇÇØ metabolic alkalosis°¡ »ý±â´Â ±âÀü
ECF volume°¨¼Ò, secondary hyperaldosteornism, K deficiency, diureticsÀÇ Á÷Á¢Àû ÀÛ¿ë
19. metabolic alkalosis°¡ Áö¼ÓÇϵµ·Ï ÇÏ´Â ÀÎÀÚ
1) proximal bicarbonate reabsorption¡è
ECF volume contraction, K depletion, hypercapnia
2) net bicarbonate regeneration
distal salt delivery¡è, mineralocorticoid excess
20. Bartter's syndrome Ä¡·á
NSAIDs, aldactone, ACE inhibitor, ¥â-blocker
21. RTAÀÇ °øÅëµÈ Ư¡: hyperchloremic metabolic acidosis
1) type 1(distal) RTA: distal tubule¿¡¼ acidificationÀå¾Ö·Î alkaline urine¸¸ ³ª¿È
lumen-> blood·Î H+ back diffusionµÇ¾î lumen³» H+¡é
³ôÀº pH gradient¿¡µµ ºÒ±¸Çϰí H+ transport¡¿
=> urine pH°¡ 5.5ÀÌÇÏ·Î ¶³¾îÁöÁö ¾Ê´Â´Ù.
chronic acidosis -> 2ndary hyperparathyroidism, renal hypercalciuria
-> calcium phosphate stone, nephrocalcinosis°¡ Àß »ý±ä´Ù.
vit D»ý¼º°¨¼Ò·Î ÀÎÇÏ¿© osteomalacia°¡ »ý±âÁö¸¸ bone disease´Â type 2 RTA¿¡¼ ´õ
¹®Á¦
oral NH4Cl loading test½ÃÇà½Ã systemic acidosis°¡ ¾ÇȵǸç urine pH´Â 5.5ÀÌÇÏ·Î
³»·Á°¡Áö ¾Ê´Â´Ù.
2) type 2(proximal) RTA ; proximal tubule¿¡¼ bicarbonate reabsorptionÀå¾Ö
acidosis½Ã Á¤»ó acid urine
Á¤»ó plasma bicarbonate³óµµ½Ã renal bicarbonate wasting¡è
potassium wastingÀÌ µ¿¹ÝµÇ¸ç alkali¸¦ ÁÖ¸é wastingÀÌ ´õ Áõ°¡ÇÑ´Ù.
oral NH4Cl loading test½Ã urine pH°¡ 5.5ÀÌÇÏ·Î ¶³¾îÁø´Ù.
Ưº°ÇÑ Ä¡·á´Â ÇÊ¿ä¾øÀ¸³ª acidosis°¡ ½ÉÇÒ°æ¿ì¿£ bicarbonate¸¦ Åõ¿©ÇÑ´Ù.
±×·¯³ª À̶§ potassiumµµ °°ÀÌ ÁÖ¾î¾ß ÇÑ´Ù.
thiazide + low salt diet
Fanconi syndrome°ú ¿¬°ü
3) type 4 RTA
distal nephronÀÇ aldosterone deficiency or aldosterone antagonism
-> hyperkalemia, hyperchloremic metabolic acidosis
22. type 4 RTA°¡ Àß »ý±â´Â »óȲ
i) diabetic nephropathy
ii) nephrosclerosis from hypertension
iii) chronic tubulointerstitial nephropathy
23. type 2 RTA ¿øÀÎ
dysproteinemia, heavy metal intoxication, vit D deficiency or resistance
cancer chemotherapy(ifosfamide), acetazolamide,
genetic ds(Wilson's disease, hereditary fructose intolerance)
Renal physiology & Pathophysiology
1. glomerular microcirculation¿¡¼ vasodilator
: PGE2, PGI2, NO, ANP
2. contrast nephropathy, cyclosporine nephropathy¿¡¼ intrarenal vasoconstriction°ú
mesangial cell contractionÀ» ÀÏÀ¸Å°´Â ¹°Áú? endothelin
3. ¼Õ»óµÈ renal tubular cellÀÇ Àç»ý¿¡ °ü¿©ÇÏ´Â growth factor
: EGF, HGF(hepatocyte-GF), IGF
4. ½ÅÀå»ý¸®
1) PTH´Â proximal tubule¿¡ ÀÛ¿ëÇÏ¿© CaÀº Èí¼öÇϰí, P¹è¼³À» Áõ°¡½ÃŲ´Ù.
2) 1,25(OH)2vitD3´Â Àå¿¡¼ Ca, PÈí¼ö¸¦ Áõ°¡½Ã۰í, bone¿¡¼ CaÈí¼ö¸¦ ÃËÁøÇÑ´Ù.
3) »ç±¸Ã¼¿¡¼ ¿©°úµÈ bicarbonate, amino acids, glucose, phosphateÀÇ ´ëºÎºÐÀº
proximal tubule¿¡¼ ÀçÈí¼öµÈ´Ù.
4) proximal tubuleÀÇ pars recta´Â organic solute transport¿Í ¹«°üÇÏ°Ô active electrogenic
sodium transport¸¦ ÇÑ´Ù.
5) distal tubule°ú collecting duct¿¡¼ Na reabsorptionÀº thiazide¿¡ ÀÇÇØ ¾ïÁ¦µÈ´Ù.
6) furosemideÀÇ ÀÛ¿ëºÎÀ§´Â Henle's loopÀÇ thick ascending limbÀÇ Na:K:2Cl cotransport
mxÀÌ´Ù.
5. cortical collecting duct¿¡ ÁÖ·Î Á¸ÀçÇϸç aldosteroneÀÇ targetÀÌ µÇ´Â ¼¼Æ÷: principle cell
6. ÀÌ´¢Á¦
1) acetazolamide´Â proximal tubule¿¡ ÀÛ¿ëÇÏ´Â ÀÌ´¢Á¦·Î type 2 RTA¸¦ À¯¹ßÇÒ¼ö ÀÖ´Ù.
2) thiazide´Â distal tubule¿¡ ÀÛ¿ëÇϸç GFRÀÌ 50%´Â ³Ñ¾î¾ß È¿°ú°¡ ÀÖ´Ù.
7. Ç÷¾ÐÃøÁ¤
ÀϹÝÀûÀ¸·Î sitting position¿¡¼ ÃøÁ¤Çϳª ´©¿ö¼ Àê¶§´Â 2-3 mmHgÁ¤µµ ´õ ³ô°Ô ÃøÁ¤µÈ´Ù.
Ç÷¾Ð°èÀÇ cuff¸¦ ÀÛÀº °ÍÀ» ¾²¸é ¼öÃà±â Ç÷¾ÐÀÌ ½ÇÁ¦º¸´Ù ³ô°Ô ³ª¿Â´Ù.
ûÁø±â·Î brachial artery¸¦ ³Ê¹« ¼¼°Ô ´©¸£¸é À̿ϱâ Ç÷¾ÐÀÌ ½ÇÁ¦º¸´Ù ³·°Ô ³ª¿Ã¼ö ÀÖ´Ù.