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Dr. Sakarn Bunnag Osmol receptor (hypothalamus) Thirst center (hypothalamus AVP secretion (Post.pituitary) Baro receptor •Aortic arch •Carotid body •Afferent arteriole (kidney) •Lt atrium Renin (juxta apparatus of kidney) AngiotensinII Aldosterone Water intake Water reabsorption Na and water reabsorption Na reabsorption Na, water reabsorption =isotonic Na reabsorption isotonic 50-100 mosmol/kg (free water) Water Reabsorption If AVP + ~1200 Mosmol/kg V2-R AVP Aquarporin II urea Aquarporin III or IV 50-100 mosmol/Kg lumen water 1200 mosmol/Kg Hypotonic Hyponatremia • Na+ < 135, • effective serum osmol <275) Intact diluting ability Impair diluting ability Urine osmol 50-100 mosmol/Kg Urine osmol >50-100 mosmol/Kg (May be + too much water intake) Low GFR? •Psychogenic polydipsia •Beer protomania AD effect + (10-20 ml/min) No Yes •renal failure (may be + others) AD effect + Low ECV Yes No Appropriate ADH •Volume deplesion •U Na+ > 20 meq/l: Renal •U Na+ < 10 meq/l: extrarenal, 3rd space loss) •Edematous stage (cirrhosis, CHF, hypo albuminemia) •Others (hypothyroid, adrenal insuff.) Inappropriate AD •N/V •Severe stress •Drug induced •SIADH •Mutation of V2R •Free water formation defect Hypernatremia High ECF volume administration of hypertonic sodium solutions • salt water drowning • NaHCO3 replacement Diuretic with water replacement Low or normal ECF volume loss of free water • central DI • nephrogenic DI • reset osmostat upward (essential hypernatremia) • osmotic diuresis • osmotic diarrhea • excessive insensible or sweat loss Inappropriate Replacement of free water • disorder of thirst center • unable to access water Water replacement with correction of specific cause. K+ < 3.5 meq/l R/O pseudo hypo K+ WC > 100,000 R/O redistribution • TTKG < 2 or • 24 hour urine K+ < 10 meq No • diarrhea • sweating • remote diuretic use • • • • • • Periodic paralysis Insulin, B2 agonist refeeding Rx neutropenia with G-CSF Rx anemia with B12, folate Ba poisoning, acute chloroquine toxic • TTKG > 4 or • 24 hour urine K+ > 20 meq = renal loss Renal K+ loss normal Metabolic acidosis High gap • DKA • ketoacidosis • methanal • ethylene glycol • • • • • Non-oligulic ATN Diuretic phase ATN low serum Mg high dose PGs TI disease Metabolic alkalosis Urine Cl- Normal gap • RTA • CA inhibitor • glue sniff < 10 meq/l (hypo-volumemia) • vomiting • NG suction >20 meq/l (hyper-volumemia or Cl- losing) Normal BP • resent diuretic use • Barter • Gitelman High renin High aldosterone • • • • RAS malignant HT scleroderma renin producing tumor High BP R/O HT with diuretic use low renin High aldosterone low renin low aldosterone • 1o hyper aldosteronism • Liddle (mutation of Na channel increase Na reabsorption) •Increase mineralocorticoid • Very high cortisol • 11 B-OH def • Licorice • fludocortisone • 17 a-OH def K+ > 5.5 meq/l R/O pseudo hyper K+ • TTKG > 7 or • 24 hour urine K+ > 200 meq • Hemolysis • WC > 70,000 • Plt > 1,000,000 If > 6.0 EKG should be done yes K+ load External source • diet • IV fluid • old blood > 5 day Internal source • intravascular hemolysis • • • • • • rhabdomyolysis tumor lysis syndrome UGIB absorb hematoma major trauma or Sx severe sepsis no Redistribution • beta-block (esp. nonselective beta 1) • metabolic acidosis • periodic paralysis • severe exercise • Digitalis toxic • fluoride toxic Defect of renal excretion Principal cell Collecting tubule ClNa+ Aldosterone + 3Na+ ATP 2K+ Aldosterone negative lumen + K+ + Aldosterone basolateral Defect of renal excretion site cause Low distal Na delivery low ECV, low GFR(<15), Gordon syndrome (psudohypoaldosterone type II) Defect of Na channel (ENAC) triamterene, amiloride Defect of Clchannel heparin, cyclosporine Defect of K+ channel (ROMK) cyclosporine Defect of aldosterone ACE-I, ARB, spironolactone, NSAIDs, heparin, cyclosporine DM,1o hypoaldosterone,1o adrenal insuff Frequent Urine Polyuria Water diuresis • primary polydipsia • DI •CDI •NDI Non-polyuria Solute diuresis • organic • glucose • Urea • osmotic agent • radiocontrast • salt • increase salt intake • renal salt loss • diuretic • UTI • hyperactive bladder • anxiety Primary polydipsia CDI NDI cause Psychiatric problem Psychiatric drug Female puberty Trauma, Sx, Tumor, Infarction, infiltrative (hypothal, pituitary) Hyper Ca, Hypo K Litium toxic, AmphoB, renal D onset gradual abrupt gradual Volume Day vs. night vary constant constant severity Vary on sign of volumedepletion Suggestive if severe ± sign of volumedepletion Rare to be severe ± sign of volumedepletion P Na Low normal To normal High normal To high High normal To high Polyuria SpGr > 1.010 or Urine osmol > 300 or U osmol/P osmol > 0.9 SpGr < 1.005 or Urine osmol < 150 or U osmol/P osmol < 0.9 Solute diuresis Water diuresis 2(U Na + U K)/U osmol < 0.4 Water deprivation test > 0.6 Organic diuresis Salt diuresis Urine glucose 4+ glucose <4 Urine osmolal gap > 200 • osmotic agent • radiocontrast < 200 • urea U osmol DDAVP 1200 1000 800 600 400 200 normal partial CDI partial NDI complete CDI complete NDI End point (Posmol>295) Water deprivation test ตรวจ serum osmol และ PNa+ • BW ลดลง> 3% • urine osmolality มีกำรเปลี่ยนแปลง <10% ติดต่อกัน 2-3 ครัง้ end point start • งดน ้ำและของเหลวต่ำงๆ • ตรวจ plasma และ urine osmolality, serum electrolytes และ ระดับ plasma AVP serum osmolality > 295-300 mOsm/kg H2O หรื อ PNa+ > 145 mEq/L DDAVP 1-2 mcg SC or IV • วัด BP, HR ผู้ป่วยเป็ นระยะ เพื่อป้องกันกำรเกิดภำวกำรณ์ขำดสำรน ้ำรุนแรง • urine osmolality ทุกครัง้ ที่ปัสสำวะ • ชัง่ น ้ำหนักตัวและวัดปริมำณปั สสำวะต่อ 1 ชัว่ โมงทุกชัว่ โมง 2 hr urine osmolality ทุกครัง้ ที่ปัสสำวะ Fixed Acid A- + H+ Volatile acid (from CO metabo) Lung Gluconeogenesis Anionic Amino acid H+ + HCO3- Renal H2CO3 NH4+ excretion(HCO3- regeneration) Tritratable acid excretion HCO3-reclamation H2O + CO2 Intracellular (Hb, protein) and Bone Buffering (carbonate) Unmeasured cation K+, Ca2+ , Mg2+ Unmeasured anion alb , phosphate , sulphate, organic cation ( M protein ) Anion gap + Na - ( Cl + HCO3 ) Measured cation Na+ Measured anion Cl-, HCO3- Delta gap in met.acidosis ; due to A( HA H+ + A- ) Delta HCO3◦ 60% H+ buffer in intracellular and bone pure met.acidosis delta gag/delta HCO3- may be 1:1 to 2:1 ◦ Resp.acidosis decrease delta HCO3◦ Resp.alk increase delta HCO3- 1-2 pure wide gap acidosis <1 wide gap + normal gap met.acidosis wide gap met.acidosis + resp.alk. >2 wide gap met.acidosis + met.alk. wide gap met.acidosis + resp.acido. =Measured osmol – calculated osmol Calculated osmol = 2(Na+K) + BUN/2.8 + Glu/18 In wide gap met.acidosis if > 25 suggest methanol or ethylene glycol ingestion Wide P osmolol gap can be found in lactic or keto acidosis Rarely elevated in salicylic acidosis because toxic level is very low. Urine anion gap (urine net charge) Unmeasured cation NH4+ Unmeasured anion Anion gap (Na+ + K+) - Cl- Measured cation Na+ + K+ Measured anion Cl- NH4+ is U unmeasured cation Urine is neutral. When acidemia high urine NH4+ high U unmeasured cation neg urine net charge =Measured osmol – calculated osmol Calculated osmol = 2(Na+K) + UUN/2.8 + Glu/18 More than half of urine osmolol gap is ammonium. Unmeasured anion are already included in 2(Na+K) Low serum HCO3Met acidosis ? R/O resp. alkalosis Or Mixed acid-base ABG Serum anion gap (collected with alb) Wide gap Delta gap/Delta HCO3- Normal gap Wide gap met.acidosis With ? Wide gap met. Acidosis Lactic acidosis Ketoacidosis (dibetes/starvation/alcoholic) Toxic (methyl or ethyl alcohol/ethylene glycol/salicylate Normal gap hyperchloremic met. acidosis Fe HCO3->15 CA-I Fe HCO3-<15 Proximal RTA (type 2) Isolated type Fanconi synd. Fe HCO3- <15 Negative urine net charge Or Urine osmolar gap > 100 mmol/l Or Urine ammonium >50 mmol/day yes High ammonium excretion (diarrhea, acid load) no Low ammonium excretion RTA type 1 (low serum K+) or RTA type 4 (high serum K+) Generation • • • • H+ loss (renal, extrarenal) H+ shift in to cells Retention of HCO3Contraction Alkalosis Correction • Increase HCO3- filtration • Decrease HCO3- reabsorption • Decrease HCO3- regeneration (=decrease NH4+ secretion) • Increase HCO3- secretion ◦ H+loss GI; vomiting, NG tube suction, antacid Renal; thiazide or loop diuretic, 1o mineralocorticoid excess, Bartter or Gitelman synd., post hypercapnia ◦ H+shift in to cell Hypo K+ ◦ HCO3- Gain; administration of NaHCO3, organic anion(citrate, acetate) ◦ Contraction alkalosis; loss CL- > HCO3 Cl- losing diarrhea Generation Maintenance Correction • • • • H+ loss (renal, extrarenal) H+ shift in to cells Retention of HCO3Contraction Alkalosis • • • • decrease ECF volume Cl- depletion K+ depletion renal failure Case 1 55 y/o female presented with UGIB Blood transfusion : WB 10 U, PRC 6 U BP 100/80 mmHg BUN/Cr 50/2 Serum Na 140 K 3.0 Cl 88 HCO3 40 mEq/L ABG: pH 7.53 PCO2 50 PaO2 80 mmHg Q? Why does the patient have metabolic alkalosis? Q? What is the expected value of urine pH and urine Na? Q? What is the appropriate treatment? Case 2 45 y/o female presented with PU and persistent vomiting 2 days BP 100/60 mmHg, poor skin turgor Serum Na 140 K 2.2 Cl 80 HCO3 42 mEq/L BUN 80/1.9 ABG: pH 7.53 PCO2 53 PaO2 80 mmHg Urine pH 5 Una 2 Uk 21 Ucl 3 mEq/L Q? Why does the patient have metabolic alkalosis and hypokalemia? Q? Why does the patient have aciduria ? Q? What is the appropriate treatment? Case 3 65y/o, COPD with pneumonia ABG: pH 7.32 pCO2 70 mmHg HCO3 35 post ET Intubation ABG pH 7.52 pCO2 40 mmHg HCO3 32 Q? Why does the patient have metabolic alkalosis? Q? What is the appropriate treatment?