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Case
• 77 y.o WF who presented with a chief complain of Diarrhea.
• Also found to have Hypokalemia and Hypomagnesaemia.
• HPI:- 7 days hx of diarrhea with decreased oral intake.- No F/C/S
Case
• Home Medications:- ASA 81 mg daily- Lasix 20 mg daily- Robitussin 20 mEq p.o BID- Tylenol 650 mg PO q4h prn- Folic Acid 1 mg po bid- Loratadine 10 mg po daily
Physical Exam
• VS: Tmp 99 HR 94 BP 101/51 RR 16 SaO2 92%Gen: A&O x 3, in mild distressHEENT: AT/NC, EOMI, PERRLANeck: Supple, No JVD, No thyromegalyChest: CTABCVS: S1, S2 normal, No M/R/G, NSRABD: Soft, NT, BS present, No organomegalyEXT: No C/C/E
Labs @ presentation
• WBC 6.2 Hgb 11.3 Plt 60• Na 137 K 2.1 Cl 95 CO2 28
AG 16 Glu 101 BUN 18 Cr 1.1Ca 7.8 Alb 3.2 Mg 1.4
• UA pH 6.5 Trace Protein Positive NitriteModerated Leuk. Esterase Spec Gravity 1.009
Cloudy RBC 0-3 WBC 15-2• C-Diff neg. Urine culture was positive for E.coli
Causes of Hypokalemia
• Decreased K Intake• Increased entry into cells
- Elevation in pH- Increased Insulin- Elevated B-agonist activity- Hypokalemic periodic paralysis- Marked increase in blood cell production- Hypothermia- Chlorquine intoxication
Causes of Hypokalemia• Increased urinary losses
- Diuretics- Primary mineralocorticoid excess- Loss of gastric secretions- Nonreabsorable anions- Metabolic acidosis- Hypomagnesaemia- Amphotericin B- Salt-wasting nephropathies – including Batter’s or Gitelman’s syndrome- Polyuria
Diagnosis of Hypokalemia
• Can usually be determined from the history• In other case, the diagnosis is not readily
apparent• Measurement of BP, urinary K exertion and
assessment of AB balance are often helpful
Urinary response
• The minimum urine K concentration in response to Hypokalemia is 5 to 15 meq/L
• A normal subject can lower urinary potassium exertion below 25 to 30 meq per day in the presence of potassium depletion.
• < 15 meq per day is likely representative of extrarenal losses
Acid Base Assessment
• Metabolic Acidosis- with Low urine K exertion in asymptomatic patient is suggestive of Lower GI losses due to Laxative abuse or villous adenoma- with K wasting is most often due to DKA, Type 1 or Type 2 RTA
Acid Base Assessment
• Metabolic Alkalosis:- With low Urine K exertion is due to surreptitious
vomiting or diuretic use- With K wasting and normal BP is most often due to
surreptitious vomiting or diuretic use or to Batter’s syndrome. Urine pH and Urine Cl concentration are helpful
- With K wasting and HTN is suggestive of surreptitious diuretic Rx in Pts with underlying HTN, renovascular disease or primary mineralocorticoid excess
Bartter’s & Gitelman’s Syndrome
• Autosomal recessive disorders• Hypokalemia• Metabolic Alkalosis• Hyperreninemia• Hyperplasia of juxtaglomular apparatus• Hyperaldosteronism• Occasionally hypomagnesaemia
Bartter’s Syndrome
• Named after Dr. Frederic Bartter• Prevalence 1 per million• Often, but not always associated with MR• Pt with a variant of classic Bartter’s syndrome
suffer from the same electrolytes disorders, but also has sensorineural deafness and renal failure
Gitelman’s Syndrome
• After Dr. Hillel Gitelman• Prevalence is 1 per 40000• More benign than Bartter’s
Distinctions between Batter’s & Gitelman’s Syndrome
Bartter’s Syndrome Gitelman’s Syndrome
Localization of defect Ascending limb of Hanle Distal Tubule
Age of Presentation Prenatal, during infancy, early childhood
Mostly late childhood or at adult age
Biochemical difference Serum Mg may be decreased
Serum Mg is decreased
Urinary exertion of Ca is increased
Urinary exertion of Ca reduced
Functional Studies Concentrating capacity severely impaired
Concentrating capacity normal or slightly impaired
GFR may be normal or declining
GFR is normal
Back to our Pt
• Day 4 of hospitalizationMg 1.6K in 24 hour urine was 57 and Ca was 32
• Day 9 of hospitalizationMg 1.8K in 24 hour urine was 81 and Ca was 52