Nephrology e tutoring2

ARCHER NOTES

1. Nephrology & UrologyNephrology & Urology
Archer Online USMLE ReviewsArcher Online USMLE Reviews
www.ccsworkshop.comwww.ccsworkshop.com
All rights reservedAll rights reserved

2. Renal FailureRenal Failure
Acute Vs. ChronicAcute Vs. Chronic
Acute : Pre-Renal, Renal, Post –renal, Glomerular, Acute : Pre-Renal, Renal, Post –renal, Glomerular,
tubular, intersititialtubular, intersititial
Indicators : BUN/CREA, FeNA, Urine Spgravity, Indicators : BUN/CREA, FeNA, Urine Spgravity,
serum Sodium, serum osmolality, urine output.serum Sodium, serum osmolality, urine output.
Chronic – stages Chronic – stages  elective hemodialysis Stage V, elective hemodialysis Stage V,
Emergent hemodialysis indications Emergent hemodialysis indications
Acute tubular necrosis : toxic, pigment induced, Acute tubular necrosis : toxic, pigment induced,
IschemicIschemic
Evaluating renal function : urinalysis - ? Protein, ?rbc , ? Evaluating renal function : urinalysis - ? Protein, ?rbc , ?
Wbc, ? Casts , ? Crystals, ? Bacteria, ? Nitrite, ? Wbc, ? Casts , ? Crystals, ? Bacteria, ? Nitrite, ?
Cytology , ? Leucoesterase, Cytology , ? Leucoesterase,
- Creatinine clearance, Renal ultrasound, Renal biopsy- Creatinine clearance, Renal ultrasound, Renal biopsy

3. RENAL BIOPSYRENAL BIOPSY
Indications: Indications:
Nephrotic syndromeNephrotic syndrome
Glomerular diseaseGlomerular disease
Unexplained renal failureUnexplained renal failure
Contraindications: single kidney, bleeding, Contraindications: single kidney, bleeding,
severe hypertension. obesity and uncooperative severe hypertension. obesity and uncooperative
patientpatient

4. DEFINITION OF ARFDEFINITION OF ARF
PP
CrCr > 0.5mg/dL if baseline < 3.0mg/dL > 0.5mg/dL if baseline < 3.0mg/dL
 PP
CrCr > 1.0 mg/dL if baseline > 3.0 mg/dL > 1.0 mg/dL if baseline > 3.0 mg/dL
Urine Output : Urine Output :
TOTAL ANURIA 0 ccTOTAL ANURIA 0 cc
ANURIA < 100 ccANURIA < 100 cc
OLIGURIA 100-400 ccOLIGURIA 100-400 cc
NON OLIGURIA 400-1000ccNON OLIGURIA 400-1000cc
POLYURIA > 1000ccPOLYURIA > 1000cc

5. CAUSES OF NONOLIGURIC PRE CAUSES OF NONOLIGURIC PRE
RENAL ARFRENAL ARF
DiureticsDiuretics
Osmotic diuresisOsmotic diuresis
HypercalcemiaHypercalcemia
Protein malnourishedProtein malnourished
Post obstructive diuresisPost obstructive diuresis
Diabetes InsipidusDiabetes Insipidus

6. NSAID ARFNSAID ARF
Form of pre renalForm of pre renal
Occurs in states where RBF decreased and thus Occurs in states where RBF decreased and thus
prostaglandin dependentprostaglandin dependent
Nonselective and selective NSAID’s inhibit Nonselective and selective NSAID’s inhibit
compensatory afferent arteriolar vasodilationcompensatory afferent arteriolar vasodilation
Volume contraction, CHF, cirrhosis, CKD, Volume contraction, CHF, cirrhosis, CKD,
vascular disease and elderly – increases risk.vascular disease and elderly – increases risk.
COX-2 inhibitors have similar effectCOX-2 inhibitors have similar effect
Allergic interstitial nephritis can also occurAllergic interstitial nephritis can also occur

7. ACE INHIBITOR ARFACE INHIBITOR ARF
Rapidly reversible ARFRapidly reversible ARF
Increase SIncrease S
Cr > Cr > 0.5Mg/dL if < 2.0 mg/dL or increase S0.5Mg/dL if < 2.0 mg/dL or increase S
Cr > Cr >
1.0 mg/dL if > 2.0 mg/dL1.0 mg/dL if > 2.0 mg/dL
Bilateral renal artery stenosis, unilateral stenosis in Bilateral renal artery stenosis, unilateral stenosis in
solitary kidney, small vessel disease and decreased RBF: solitary kidney, small vessel disease and decreased RBF:
CHF, cirrhosis, decreased ECFCHF, cirrhosis, decreased ECF
Inhibition of A-II efferent arteriole vasoconstriction Inhibition of A-II efferent arteriole vasoconstriction
leads to decrease Pleads to decrease P
GC GC and GFR and GFR

Age, diuretics, diabetes, NSAID’s, cyclosporine and Age, diuretics, diabetes, NSAID’s, cyclosporine and
CKD are risk factorsCKD are risk factors
ARB’s pose similar riskARB’s pose similar risk

8. POST RENAL ARFPOST RENAL ARF
Caused by anatomic obstruction of urine flowCaused by anatomic obstruction of urine flow
Accounts for 5-10% of ARFAccounts for 5-10% of ARF
Patients are often asymptomatic and thus should always Patients are often asymptomatic and thus should always
be consideredbe considered
Ultrasound useful, but can have 10-20% false negativesUltrasound useful, but can have 10-20% false negatives
Patients are often oligo-anuric, but any pattern of urine Patients are often oligo-anuric, but any pattern of urine
output may occuroutput may occur
Intraureteric obstruction, Extraureteric obstruction, Intraureteric obstruction, Extraureteric obstruction,
Urethral obstructionUrethral obstruction

9. INTRARENAL ARFINTRARENAL ARF
Renal parenchymal diseasesRenal parenchymal diseases
GlomerularGlomerular
VascularVascular
TubularTubular
InterstitialInterstitial
Acute tubular necrosis – most commonAcute tubular necrosis – most common

10. Glomerular syndromes –Glomerular syndromes –
Nephrotic Vs Nephritic SyndromesNephrotic Vs Nephritic Syndromes

NEPHROTIC SYNDROMENEPHROTIC SYNDROME
Urinary albumin > 3.0 – 3.5 Urinary albumin > 3.0 – 3.5
gm/24 hoursgm/24 hours
HypoalbimunemiaHypoalbimunemia
EdemaEdema
HyperlipidemiaHyperlipidemia
LipiduriaLipiduria
FSGN ( HIV), MGN( SLE, hepb, FSGN ( HIV), MGN( SLE, hepb,
Cancer – solid tumors ), Minimal Cancer – solid tumors ), Minimal
( children), MPGN ( HepC)( children), MPGN ( HepC)
FSGN – Rx High dose steroids, FSGN – Rx High dose steroids,
cyclosporinecyclosporine
MGN – Methylprednisolone pulse, MGN – Methylprednisolone pulse,
cyclosporincyclosporin
Others : DM, Malignancy, Others : DM, Malignancy,
vasulitis, amyloidosisvasulitis, amyloidosis
Nephritic SyndromeNephritic Syndrome
Hematuria/ RBC CastsHematuria/ RBC Casts
OliguriaOliguria
HypertensionHypertension
Decreased GFRDecreased GFR
Proteinuria +/-Proteinuria +/-
 Focal glomerulonephritisFocal glomerulonephritis
IgA nephropathyIgA nephropathy
Focal SLE ( Type III )Focal SLE ( Type III )
 Diffuse glomerulonephritisDiffuse glomerulonephritis
Post infectiousPost infectious
Diffuse SLE ( Type IV )Diffuse SLE ( Type IV )
 IgA nephropathy : most common IgA nephropathy : most common
presentation asymptomatic presentation asymptomatic
microhematuria with mild microhematuria with mild
proteinuria proteinuria

11. RAPIDLY PROGRESSIVE RAPIDLY PROGRESSIVE
GLOMERULONEPHRITISGLOMERULONEPHRITIS
Characterized by > 50% decrease in GFR over days to weeksCharacterized by > 50% decrease in GFR over days to weeks
Characterized pathologically by crescent formation and clinically Characterized pathologically by crescent formation and clinically
by progression to ESRD in untreated patients within weeks by progression to ESRD in untreated patients within weeks
Related to the degree of crescent formationRelated to the degree of crescent formation
Present with active urine sediment, hypertension and oliguric Present with active urine sediment, hypertension and oliguric
ARFARF
Nephrologic emergencyNephrologic emergency
Classification of RPGN:Classification of RPGN:
Type 1: Anti GBMType 1: Anti GBM
Type 2: Immune complexType 2: Immune complex
Type 3: Pauci-immune ( p-ANCA )Type 3: Pauci-immune ( p-ANCA )
 Early evaluation and biopsyEarly evaluation and biopsy

12. Proteinuria - MicroalbuminuriaProteinuria - Microalbuminuria
Normal: 150 mg/dayNormal: 150 mg/day
Albumin 30 mgAlbumin 30 mg
Plasma proteins 60 mgPlasma proteins 60 mg
Tubular protein 60 mgTubular protein 60 mg
Dipstick test detects (-) Dipstick test detects (-)
charge charge
Does not detect light chainsDoes not detect light chains
Function of urine Function of urine
concentrationconcentration
Total Protein : creatinine Total Protein : creatinine
ratio estimates 24 hour urine ratio estimates 24 hour urine
collectioncollection
Microalbuminuria Microalbuminuria 
Albumin excretion rate > 15 Albumin excretion rate > 15
ugm/min = 30 mg/dayugm/min = 30 mg/day
Predictor of early diabetic Predictor of early diabetic
nephropathy and CVDnephropathy and CVD
Urine albumin: urine Urine albumin: urine
creatinine < 0.03creatinine < 0.03
Positive in exercise, fever, Positive in exercise, fever,
stress, CHFstress, CHF
Repeat urinalysis in 3-6 Repeat urinalysis in 3-6
months if u think its months if u think its
transient proteinuriatransient proteinuria
ACE Inhibitor *****ACE Inhibitor *****

13. ATNATN
Ischemic (50%)Ischemic (50%)
Toxic: Toxic:
EXOGENOUS TOXIN ATN :EXOGENOUS TOXIN ATN :
-Antibiotics, Radiocontrast, Non steroidals, -Antibiotics, Radiocontrast, Non steroidals,
Anesthetics, Chemotherapeutics, Heavy metals/ Anesthetics, Chemotherapeutics, Heavy metals/
solventssolvents
ENDOGENOUS TOXIN ATN :ENDOGENOUS TOXIN ATN :
Pigment Nephropathy Pigment Nephropathy  Myoglobin, Hemoglobin Myoglobin, Hemoglobin
Crystal Nephropathy Crystal Nephropathy  Uric acid , Calcium, Uric acid , Calcium,
Oxalate Oxalate

14. RADIOCONTRAST ATNRADIOCONTRAST ATN
Risk factors: CRF especially diabetic, CHF, elderly and multiple Risk factors: CRF especially diabetic, CHF, elderly and multiple
myelomamyeloma
ATN begins abruptly and SATN begins abruptly and S
Cr Cr peaks in 3-5 dayspeaks in 3-5 days
Usually reversible, but some have prolonged renal damageUsually reversible, but some have prolonged renal damage
Usually nonoliguric, but oliguria can be seen and FE Usually nonoliguric, but oliguria can be seen and FE
NaNa decreased decreased
Prevention : Consider non contrast study if high riskPrevention : Consider non contrast study if high risk
D/C NSAID’s, ACE inhibitors. ARB’s etcD/C NSAID’s, ACE inhibitors. ARB’s etc
Ensure optimal volume status and RBFEnsure optimal volume status and RBF
0.9% saline @ 1cc/kg/hr for 6 hours prior0.9% saline @ 1cc/kg/hr for 6 hours prior
DD
55W + 3 amps NaHCO3 @ 3.5 cc/kg/hr for 1 hour and W + 3 amps NaHCO3 @ 3.5 cc/kg/hr for 1 hour and
then 1 cc/kg/hour for 6 hours afterthen 1 cc/kg/hour for 6 hours after
N-acetylcysteine 600mg bid pre and day of studyN-acetylcysteine 600mg bid pre and day of study

Minimize amount of contrast and consider iso-osmolar agentMinimize amount of contrast and consider iso-osmolar agent - -
nonionic and/or isosmolar contrast are less nonionic and/or isosmolar contrast are less
nephrotoxicnephrotoxic

15. ATHEROEMBOLIC ARFATHEROEMBOLIC ARF
Results from cholesterol emboli to small renal Results from cholesterol emboli to small renal
arteries and arteriolesarteries and arterioles
Livedo reticularis – A clue!!!Livedo reticularis – A clue!!!
Aortic surgery, trauma, angiography, fibrinolytic Aortic surgery, trauma, angiography, fibrinolytic
therapy or spontaneouslytherapy or spontaneously
Eosinophilia, eosinophiluria, leukocytosis and Eosinophilia, eosinophiluria, leukocytosis and
complement activationcomplement activation
Retinal, peripheral and abdominal vesselsRetinal, peripheral and abdominal vessels

16. MYOGLOBINURIC ARFMYOGLOBINURIC ARF
Rhabdomyolysis: trauma,alcohol, cocaine, seizures, Rhabdomyolysis: trauma,alcohol, cocaine, seizures,
hypokalemia, hypophosphatemiahypokalemia, hypophosphatemia
ECF volume depletionECF volume depletion
Heme (+) urine without RBC’s, hyperkalemia, Heme (+) urine without RBC’s, hyperkalemia,
hyperuricemia, hyperphosphatemia and hypocalcemiahyperuricemia, hyperphosphatemia and hypocalcemia
Decreased FE Decreased FE
NaNa
ECF volume repletion, ?mannitol, and ?alkaline diuresisECF volume repletion, ?mannitol, and ?alkaline diuresis
Hypercalcemia during recoveryHypercalcemia during recovery

17. ACUTE INTERSTITIAL ACUTE INTERSTITIAL
NEPHRITISNEPHRITIS
Fever, rash, eosinophila, eosinophiluria and Fever, rash, eosinophila, eosinophiluria and
active urine sedimentactive urine sediment
Occurs 10-15 days after exposure to usually new Occurs 10-15 days after exposure to usually new
medicationmedication
NSAID induced associated with NSAID induced associated with nephrotic nephrotic
syndromesyndrome
? Renal biopsy? Renal biopsy
Rx: Stop the agent and ?steroidsRx: Stop the agent and ?steroids

18. CRYSTAL INDUCED ARFCRYSTAL INDUCED ARF
Uric acidUric acid
Calcium oxalateCalcium oxalate
MethotrexateMethotrexate
SulfonamidesSulfonamides
AcyclovirAcyclovir
IndinavirIndinavir

19. DIAGNOSTIC MANAGEMENT DIAGNOSTIC MANAGEMENT
ARFARF
History / Chart reviewHistory / Chart review
Physical examPhysical exam
UrinalysisUrinalysis
Urine indicesUrine indices
Radiologic studiesRadiologic studies
Miscellaneous studiesMiscellaneous studies

20. NON DIALYTIC MANAGEMENT NON DIALYTIC MANAGEMENT
ARFARF
Preventive measuresPreventive measures
Fluid balanceFluid balance
Acid base balanceAcid base balance
Electrolyte balanceElectrolyte balance
Nutritional balanceNutritional balance
Drug managementDrug management
Management of uremiaManagement of uremia

21. INDICATIONS FOR Emergency INDICATIONS FOR Emergency
DIALYSISDIALYSIS
REFRACTORYREFRACTORY
HyperkalemiaHyperkalemia
AcidemiaAcidemia
Hypoxemia/ volume overloadHypoxemia/ volume overload
Uremia - manifestationsUremia - manifestations
? Prophylactic when BUN > 60-100 mg/dL? Prophylactic when BUN > 60-100 mg/dL

22. Chronic Tubulo-Interstitial DiseasesChronic Tubulo-Interstitial Diseases
Chronic issues :Chronic issues :
Toxins: Analgesics, Heavy metals, Chinese herbs, Lithium, Toxins: Analgesics, Heavy metals, Chinese herbs, Lithium,
Cyclosporine, Radiation, CisplatinCyclosporine, Radiation, Cisplatin
Hematologic diseases: MyelomaHematologic diseases: Myeloma
Immunologic: Sjogren’s syndrome, Transplant rejectionImmunologic: Sjogren’s syndrome, Transplant rejection
Infection: Bacterial pyelonephritis, Tuberculosis, SarcoidInfection: Bacterial pyelonephritis, Tuberculosis, Sarcoid
Anatomic: Obstruction, RefluxAnatomic: Obstruction, Reflux
Metabolic disorders: Gout, Oxalosis, Hypercalcemia, Metabolic disorders: Gout, Oxalosis, Hypercalcemia,
Hypokalemia, CystinosisHypokalemia, Cystinosis
Hereditary: ADPKD, MCDHereditary: ADPKD, MCD
Vascular : Nephrosclerosis, Ischemic nephropathy, Vascular : Nephrosclerosis, Ischemic nephropathy,
Atheroembolic diseaseAtheroembolic disease
Acute cases : check urine eosinophil count, peripheral eosinophiliaAcute cases : check urine eosinophil count, peripheral eosinophilia

23. Oxalate NephropathyOxalate Nephropathy
Precipitation of calcium oxalate can cause Precipitation of calcium oxalate can cause
interstitial and intratubular crystals leading to interstitial and intratubular crystals leading to
inflammation and fibrosisinflammation and fibrosis
Primary hyperoxaluria leads to ESRDPrimary hyperoxaluria leads to ESRD
Ethylene glycol, methoxyflurane, excessive Ethylene glycol, methoxyflurane, excessive
intake ascorbic acidintake ascorbic acid
Increase intestinal absorption: Ileal bypass, short Increase intestinal absorption: Ileal bypass, short
bowel syndrome and Crohn’s diseasebowel syndrome and Crohn’s disease

24. Chronic Urate NephropathyChronic Urate Nephropathy
Related to deposition of sodium urate in the Related to deposition of sodium urate in the
medullary interstitiummedullary interstitium
Secondary inflammation and interstitial fibrosis Secondary inflammation and interstitial fibrosis
and CRFand CRF
Hypertension, bland urinalysis and hyperuriceniaHypertension, bland urinalysis and hyperuricenia
Associated with tophaceous gout or an increase Associated with tophaceous gout or an increase
in uric acid out of proportion to degree of CRF in uric acid out of proportion to degree of CRF

25. Analgesic NephropathyAnalgesic Nephropathy
NSAID induced interstitial nephritis ( associated NSAID induced interstitial nephritis ( associated
with nephrotic syndrome with nephrotic syndrome  proteinuria) proteinuria)
NSAID induced vasomotor renal insufficiencyNSAID induced vasomotor renal insufficiency

26. Hepatorenal SyndromeHepatorenal Syndrome
The diagnosis of HRS iS The diagnosis of HRS iS of exclusionof exclusion and depends mainly on serum creatinine level, as no specific tests establish the and depends mainly on serum creatinine level, as no specific tests establish the
diagnosis of HRS. diagnosis of HRS.
Serum creatinine level is a poor marker of renal function in patients with cirrhosis. But no other reliable noninvasive Serum creatinine level is a poor marker of renal function in patients with cirrhosis. But no other reliable noninvasive
markers exist for monitoring renal function in these patients. markers exist for monitoring renal function in these patients.
Diagnosis of HRS depends on the presence of a reduced GFR in the absence of other causes of renal failure in patients Diagnosis of HRS depends on the presence of a reduced GFR in the absence of other causes of renal failure in patients
with chronic liver disease. with chronic liver disease.
Major criteria (Major criteria (All All major criteria are required to diagnose HRSmajor criteria are required to diagnose HRS.) .)
Low GFR, indicated by a serum creatinine level higher than 1.5 mg/dL or 24-hour creatinine clearance Low GFR, indicated by a serum creatinine level higher than 1.5 mg/dL or 24-hour creatinine clearance
lower than 40 mL/min lower than 40 mL/min
Absence of shock, ongoing bacterial infection and fluid losses, and current treatment with nephrotoxic Absence of shock, ongoing bacterial infection and fluid losses, and current treatment with nephrotoxic
medications medications
No sustained improvement in renal function (decrease in serum creatinine to <1.5 mg/dL or increase in No sustained improvement in renal function (decrease in serum creatinine to <1.5 mg/dL or increase in
creatinine clearance to >40 mL/min) after diuretic withdrawal and expansion of plasma volume with 1.5 L creatinine clearance to >40 mL/min) after diuretic withdrawal and expansion of plasma volume with 1.5 L
of plasma expander of plasma expander
Proteinuria less than 500 mg/d and Proteinuria less than 500 mg/d and nono ultrasonographic evidence of obstructive uropathy or intrinsic ultrasonographic evidence of obstructive uropathy or intrinsic
parenchymal diseaseparenchymal disease
Additional criteria (Additional criteria are not necessary for the diagnosis but provide supportive evidence.) Additional criteria (Additional criteria are not necessary for the diagnosis but provide supportive evidence.)
Urine volume less than 500 mL/d Urine volume less than 500 mL/d
Urine sodium level Urine sodium level less than 10 mEq/Lless than 10 mEq/L
Urine osmolality greater than plasma osmolality , Urine red blood cell count of less than 50 per high-power Urine osmolality greater than plasma osmolality , Urine red blood cell count of less than 50 per high-power
field & Serum sodium concentration greater than 130 mEq/Lfield & Serum sodium concentration greater than 130 mEq/L
Urinary indices are not considered major criteria because Urinary indices are not considered major criteria because a subset of patients with HRS may have high urine a subset of patients with HRS may have high urine
sodium levels and low urine osmolalitysodium levels and low urine osmolality (similar to acute tubular necrosis [ATN]), while other patients with (similar to acute tubular necrosis [ATN]), while other patients with
cirrhosis and ATN may have low urine sodium levelscirrhosis and ATN may have low urine sodium levels and high urine osmolality. and high urine osmolality.

27. Case StudiesCase Studies
) A 25 y/o male comes to your office with complaints of dark red colored urine and ) A 25 y/o male comes to your office with complaints of dark red colored urine and
pain in the legs that started this morning. He has been working out at the local gym pain in the legs that started this morning. He has been working out at the local gym
excessively for the past three days. He does consume alcohol on weekends but reports excessively for the past three days. He does consume alcohol on weekends but reports
having involved in a binge drinking episode that included 10 beers yesterday. On having involved in a binge drinking episode that included 10 beers yesterday. On
physical examination, he weighs 70kg and he has some tenderness in his calf muscles physical examination, he weighs 70kg and he has some tenderness in his calf muscles
which he attributes to the excessive squats he performed yesterday. Urine dipstick which he attributes to the excessive squats he performed yesterday. Urine dipstick
reveals large blood. If this patient develops acute renal failure , the most likely reveals large blood. If this patient develops acute renal failure , the most likely
mechanism would be: mechanism would be:
A) Interstitial nephritis due to pigment A) Interstitial nephritis due to pigment
B) Glomerulonephritis B) Glomerulonephritis
C) Acute Tubular necrosis due to pigment deposition C) Acute Tubular necrosis due to pigment deposition
D) Acute Tubular Necrosis due to Ischemia D) Acute Tubular Necrosis due to Ischemia
E) Alcohol related direct toxic injury E) Alcohol related direct toxic injury
1b) Lab studies revealed normal electrolytes and normal creatinine but a CPK of 1b) Lab studies revealed normal electrolytes and normal creatinine but a CPK of
50,000. His Urine output has been at 70 ml/hr for the past 6 hours. Your first step in 50,000. His Urine output has been at 70 ml/hr for the past 6 hours. Your first step in
the management to prevent development of patient's Acute Renal Faliure : the management to prevent development of patient's Acute Renal Faliure :
A) Intravenos Fluids A) Intravenos Fluids
B) Furosemide B) Furosemide
C) Calcium Gluconate C) Calcium Gluconate
D) No treatment because serum creatinine is normal D) No treatment because serum creatinine is normal
D) Sodium Bicarbonate D) Sodium Bicarbonate

28. Case StudyCase Study
A 7-year-old boy is brought to the emergency department by his mother A 7-year-old boy is brought to the emergency department by his mother
because of "tea-colored urine" for the last several days. He has also had some because of "tea-colored urine" for the last several days. He has also had some
nausea and vomiting, and his eyes appear swollen when he wakes up in the nausea and vomiting, and his eyes appear swollen when he wakes up in the
morning. The eye swelling tends to resolve over the course of the day. He is morning. The eye swelling tends to resolve over the course of the day. He is
generally very healthy and there is no family history of any chronic diseases. generally very healthy and there is no family history of any chronic diseases.
His temperature is 36.7 C (98.0 F), blood pressure is 130/90 mm Hg, pulse is His temperature is 36.7 C (98.0 F), blood pressure is 130/90 mm Hg, pulse is
96/min, and respiratory rate is 16/min. Physical examination is unremarkable. 96/min, and respiratory rate is 16/min. Physical examination is unremarkable.
A urinalysis shows red cell casts. At this time the most appropriate study to A urinalysis shows red cell casts. At this time the most appropriate study to
confirm your diagnosis is confirm your diagnosis is
A. antinuclear antibodyA. antinuclear antibody
B. antistreptolysin O antibodyB. antistreptolysin O antibody
C. renal biopsyC. renal biopsy
D. renal ultrasoundD. renal ultrasound
E. urine culture E. urine culture

29. Case studies contd…Case studies contd…
1c) The above patient has been adequately treated but his repeat CPK after 2 1c) The above patient has been adequately treated but his repeat CPK after 2
days is still elevated at 48,000. He complains of increasing pain in his left leg days is still elevated at 48,000. He complains of increasing pain in his left leg
and some tingling and pricking sensations. On examination his left leg was and some tingling and pricking sensations. On examination his left leg was
mildly swollen and there was pain on passive stretching of the leg muscles. mildly swollen and there was pain on passive stretching of the leg muscles.
Dorsalis pedis and posterior tibial pulses are intact. The most likely diagnosis Dorsalis pedis and posterior tibial pulses are intact. The most likely diagnosis
at this time: at this time:
A) Deep Vein Thrombosis A) Deep Vein Thrombosis
B) Cellulitis B) Cellulitis
C) Compartment Syndrome C) Compartment Syndrome
D) Edema due to renal failure D) Edema due to renal failure
E) Congestive Heart Failure E) Congestive Heart Failure
1d) The immediate course of treatment in this condition would be : 1d) The immediate course of treatment in this condition would be :
A) Anticoagulation with Heparin A) Anticoagulation with Heparin
B) Antibiotics B) Antibiotics
C) Emergency Fasciotomy C) Emergency Fasciotomy
D) Loop diuretics D) Loop diuretics
E) Elevation of the leg E) Elevation of the leg

30. Case Study 2Case Study 2
Q1) A 12 y/o boy is brought to you by his mother for skin rash and complaints of intermittent Q1) A 12 y/o boy is brought to you by his mother for skin rash and complaints of intermittent
abdominal pain, joint pains for past 2 days. He did have an upper respiratory infection about 2 days abdominal pain, joint pains for past 2 days. He did have an upper respiratory infection about 2 days
ago. On physical exam, his vitals are normal. Abdomen is benign with out any tenderness or rigidity. ago. On physical exam, his vitals are normal. Abdomen is benign with out any tenderness or rigidity.
However, you notice patchy purple discolorations on his extremities and the back. Lab studies are However, you notice patchy purple discolorations on his extremities and the back. Lab studies are
obtained that revealed obtained that revealed
WBC: 6.6 , HGB: 15.3 , MCV: 88 , Platelets: 290,000 ( normal 180k to 400k) WBC: 6.6 , HGB: 15.3 , MCV: 88 , Platelets: 290,000 ( normal 180k to 400k)
BUN: 11 , Creatinine : 0.6 ( normal) , Anti streptolysin O titer : negative BUN: 11 , Creatinine : 0.6 ( normal) , Anti streptolysin O titer : negative
Streptozyme : negative ,Urine dipstick : normal without any blood Streptozyme : negative ,Urine dipstick : normal without any blood
Urinalysis : normal/ no rbcs/ no protein Urinalysis : normal/ no rbcs/ no protein
The mother is very anxious and asks about the long term prognosis of her son. Your response : The mother is very anxious and asks about the long term prognosis of her son. Your response :
A) Reassure the mother that boys disorder is self limiting and does not require any follow up A) Reassure the mother that boys disorder is self limiting and does not require any follow up
B) Tell her the boy needs to be admitted and treated vigorously to prevent renal failure B) Tell her the boy needs to be admitted and treated vigorously to prevent renal failure
C) Tell her that renal failure develops 100% of such cases and hence needs very cautious follow up C) Tell her that renal failure develops 100% of such cases and hence needs very cautious follow up
D) Tell her that 50% of such cases progress to end stage renal disease. D) Tell her that 50% of such cases progress to end stage renal disease.
E) Tell her that the boy requires follow up monthly urinalysis for at least 3 months in order to make E) Tell her that the boy requires follow up monthly urinalysis for at least 3 months in order to make
sure there is no heamaturia/ renal dysfunction. sure there is no heamaturia/ renal dysfunction.
If the boy presented with Renal failure in the above case, the most likely underlying pathology If the boy presented with Renal failure in the above case, the most likely underlying pathology
would be : would be :
A) IgA mediated vasculitis A) IgA mediated vasculitis
B) Post streptococcal glomerulonephritis B) Post streptococcal glomerulonephritis
C) Anti GBM disease C) Anti GBM disease
D) Acute tubular necrosis D) Acute tubular necrosis
E) Interstitial Nephritis. E) Interstitial Nephritis.

31. UTIsUTIs

32. CASE STUDYCASE STUDY
A 76 YO DEBILITATED MALE, In extended care facility , A 76 YO DEBILITATED MALE, In extended care facility ,
develops every 6 months mild fever, frequency of micturation develops every 6 months mild fever, frequency of micturation
with urinary incontinence. USUALLY E.COLI count is with urinary incontinence. USUALLY E.COLI count is
>100,000.>100,000.
What is the appropriate treatment?What is the appropriate treatment?
A. CYSTOSCOPY and IVPA. CYSTOSCOPY and IVP
B. Continuous low dose antibioticsB. Continuous low dose antibiotics
C. Catheterize and irrigate the Bladder dailyC. Catheterize and irrigate the Bladder daily
D. Treat only the acute episode of infection D. Treat only the acute episode of infection
E. No need of treatment as this is colonizationE. No need of treatment as this is colonization

33. Symptomatic complicated UTI should be Symptomatic complicated UTI should be
treated. Number of UTI are less than 2 in 6 treated. Number of UTI are less than 2 in 6
mos- no need for continuous Abx. mos- no need for continuous Abx.
His Symptoms are associated with UTI and are His Symptoms are associated with UTI and are
not persistent. So just treat the acute episodenot persistent. So just treat the acute episode
REMEMBER THE INDICATIONS FOR REMEMBER THE INDICATIONS FOR
TREATING “ASYMPTOMATIC “ TREATING “ASYMPTOMATIC “
BACTERIURIA.BACTERIURIA.

34. Recurrent UTIsRecurrent UTIs
DEFINED AS 2 OR MORE EPISODES IN DEFINED AS 2 OR MORE EPISODES IN
PAST 6 MONTHS OR 3 OR MORE PAST 6 MONTHS OR 3 OR MORE
EPISODES IN PAST ONE YEAR. EPISODES IN PAST ONE YEAR.
Use Bactrim DS post sexual activity for women Use Bactrim DS post sexual activity for women
with hx of recurrent UTIs related to sexual with hx of recurrent UTIs related to sexual
activity. activity.
Use daily bactrim for people withj no relation to Use daily bactrim for people withj no relation to
sex activity. sex activity.

35. OTHER ISSUESOTHER ISSUES
Evaluating painless hematuria elderlyEvaluating painless hematuria elderly
Painful hematuriaPainful hematuria
Treating asymptomatic bacteriuriaTreating asymptomatic bacteriuria
Pyelonephritis – pyonephric abscessPyelonephritis – pyonephric abscess
When to admit and when to order imaging When to admit and when to order imaging
studies in pyelonephritis?studies in pyelonephritis?

36. Painless HematuriaPainless Hematuria
The recommended definition of microscopic hematuria is The recommended definition of microscopic hematuria is three orthree or
more red blood cells per high-power field on microscopic evaluation more red blood cells per high-power field on microscopic evaluation
of urinary sediment from of urinary sediment from two of threetwo of three properly collected urinalysis properly collected urinalysis
specimens. specimens.
Always confirm on repeat testingAlways confirm on repeat testing
If Red cell casts/ dysmorphic RBCs or Renal function is If Red cell casts/ dysmorphic RBCs or Renal function is
compromised/ new onset HTN, combined with mild proteinuria compromised/ new onset HTN, combined with mild proteinuria 
consider glomerulonephritis.consider glomerulonephritis.
Recurrent painless Hematuria Recurrent painless Hematuria  consider IgA nephropathy consider IgA nephropathy
Other causes : 1. Consider strongly CA.Bladder in the elderly and in Other causes : 1. Consider strongly CA.Bladder in the elderly and in
smokerssmokers
2. R/O benign causes like BPH ( Ask for symptoms of 2. R/O benign causes like BPH ( Ask for symptoms of
BPH)BPH)
3. R/O Prostate Ca in the elderly and in those with 3. R/O Prostate Ca in the elderly and in those with
family historyfamily history
DO NOT NEGLECT POSSIBILITY OF BLADDER CA IN PTS DO NOT NEGLECT POSSIBILITY OF BLADDER CA IN PTS
WITH HEMATURIAWITH HEMATURIA

37. Painless HematuriaPainless Hematuria
Risk Factors for Significant Disease in Patients with Microscopic Hematuria : Risk Factors for Significant Disease in Patients with Microscopic Hematuria :
Smoking history Smoking history
Occupational exposure to chemicals or dyes (benzenes or aromatic Occupational exposure to chemicals or dyes (benzenes or aromatic
amines) amines)
History of gross hematuria History of gross hematuria
Age >40 years Age >40 years
History of urologic disorder or disease History of urologic disorder or disease
History of irritative voiding symptoms History of irritative voiding symptoms
History of urinary tract infection History of urinary tract infection
Analgesic abuse Analgesic abuse
History of pelvic irradiationHistory of pelvic irradiation
The presence of significant proteinuria, red cell casts or renal The presence of significant proteinuria, red cell casts or renal
insufficiency, or a predominance of dysmorphic red blood cells in the insufficiency, or a predominance of dysmorphic red blood cells in the
urine should prompt an evaluation for renal parenchymal disease or urine should prompt an evaluation for renal parenchymal disease or
referral to a nephrologist.referral to a nephrologist.

40. Bladder CaBladder Ca
Most common histology is Transitional Cell caMost common histology is Transitional Cell ca
Routine screening in all patients for bladder ca with Routine screening in all patients for bladder ca with
either urinalysis or cytology is either urinalysis or cytology is notnot recommended recommended
Screening for bladder cancer in high risk individuals Screening for bladder cancer in high risk individuals
( those exposed to dyes/ leather, smokers) is ( those exposed to dyes/ leather, smokers) is
controversial controversial  no clear recommendations. no clear recommendations.
High risk History : Smoking history, Occupational High risk History : Smoking history, Occupational
exposure to dyes, rubber, or leather, exposure to dyes, rubber, or leather, previous previous
exposure to Cyclophosphamideexposure to Cyclophosphamide

41. Bladder CaBladder Ca
Do not routinely screen but however, if you find Do not routinely screen but however, if you find
Hematuria ( even microscopic) on routine Hematuria ( even microscopic) on routine
urinalysis that was done for another purpose urinalysis that was done for another purpose 
do not neglect this finding. ABNORMAL LAB do not neglect this finding. ABNORMAL LAB
always need to be addressed always need to be addressed  pursue further pursue further
w/u for this hematuria ( BPH, Ca.Bladder, w/u for this hematuria ( BPH, Ca.Bladder,
ca.prostate, cystitis, r/o glomerulonephritis)ca.prostate, cystitis, r/o glomerulonephritis)
Remember Micro-HEMATURIA is the Remember Micro-HEMATURIA is the most most
commoncommon manifestation of bladder cancer. manifestation of bladder cancer.

42. Clinical Symps/ SignsClinical Symps/ Signs
Hematuria Hematuria
Urinary frequency or dysuria Urinary frequency or dysuria
Flank or suprapubic pain Flank or suprapubic pain
Constitutional symptoms, such as weight lossConstitutional symptoms, such as weight loss
Weight loss Weight loss
Adenopathy Adenopathy
Palpable suprapubic mass Palpable suprapubic mass
Organomegaly Organomegaly
BLADDER CA CAN BE TOTALLY BLADDER CA CAN BE TOTALLY
ASYMPTOMATICASYMPTOMATIC

43. IMPORTANTIMPORTANT
Refer all patients ( especially those at Refer all patients ( especially those at
high risk) presenting with unexplained high risk) presenting with unexplained
hematuria for cystoscopy, even if their hematuria for cystoscopy, even if their
hematuria is hematuria is intermittentintermittent, and regardless , and regardless
of the findings on history and physical of the findings on history and physical
exam. exam.

44. Bladder Ca - DiagnosisBladder Ca - Diagnosis
Freshly voided urine sample for cytology Freshly voided urine sample for cytology
Imaging of the urinary tract Imaging of the urinary tract
Cystoscopy and exam under anesthesia with Cystoscopy and exam under anesthesia with
biopsies biopsies
Additional diagnostic evaluations, based on Additional diagnostic evaluations, based on
findings from the cystoscopy and pathologic findings from the cystoscopy and pathologic
evaluation of the tumor, to assess the upper evaluation of the tumor, to assess the upper
urinary tract or to look for metastatic disease urinary tract or to look for metastatic disease 
lfts, ivp, cxr, ct scan of abd/pelvis, bone scan.lfts, ivp, cxr, ct scan of abd/pelvis, bone scan.

45. Bladder Ca - RxBladder Ca - Rx
Surgical resection for non invasive bladder ca. Surgical resection for non invasive bladder ca.
Radical Cystectomy – Rx of choice for muscle-invasive Radical Cystectomy – Rx of choice for muscle-invasive
bladder ca. bladder ca.
Adjuvant Intravesical therapy with BCG/ mitomycin-c Adjuvant Intravesical therapy with BCG/ mitomycin-c
for for  Cis, T1 tumors, tumor > 5cm size. Cis, T1 tumors, tumor > 5cm size.
Adjuvant chemotherapy on case-by case basis Adjuvant chemotherapy on case-by case basis 
gemcitabine+cisplatin or methotrexategemcitabine+cisplatin or methotrexate
Local side effects of BCG include: Cystitis (90% of Local side effects of BCG include: Cystitis (90% of
patients) , Hematuria (30%) , Contracted bladder , patients) , Hematuria (30%) , Contracted bladder ,
Ureteral obstruction, Inflammation (prostatitis, Ureteral obstruction, Inflammation (prostatitis,
epididymitis, epididymoorchitis) epididymitis, epididymoorchitis)
Systemic side effects of BCG, which should resolve in Systemic side effects of BCG, which should resolve in
48 hours, include: Flu-like symptoms , Arthralgias , 48 hours, include: Flu-like symptoms , Arthralgias ,
Rash Rash

46. Bladder Ca Bladder Ca
Post – radical cystectomy requires urinary Post – radical cystectomy requires urinary
diversion diversion
External diversions include conduits, usually External diversions include conduits, usually
composed of a section of bowel (ileum or composed of a section of bowel (ileum or
colon). colon).
 Internal conduits include those that require a Internal conduits include those that require a
stoma to empty the reservoir (Kock pouch and stoma to empty the reservoir (Kock pouch and
Indiana pouch) and orthotopic replacements Indiana pouch) and orthotopic replacements
(e.g., Le Bag, Mainz pouch, (e.g., Le Bag, Mainz pouch,

47. Complications – Urinary diversionComplications – Urinary diversion
Watch for the following after urinary diversion: Watch for the following after urinary diversion:
Bleeding , Infection , Hernias , Necrosis , Reflux, Bleeding , Infection , Hernias , Necrosis , Reflux,
Incontinence , Obstruction of conduit, upper tract, or Incontinence , Obstruction of conduit, upper tract, or
intestines and Recurrent cancer intestines and Recurrent cancer
Monitor for bacteremia, treat patients with Monitor for bacteremia, treat patients with ProteusProteus or or
PseudomonasPseudomonas sp., and observe patients with other sp., and observe patients with other
organisms if they are asymptomatic. organisms if they are asymptomatic.
Monitor closely: Monitor closely:
Vitamin B12 levels , Acid/base status , Electrolyte levels and Vitamin B12 levels , Acid/base status , Electrolyte levels and
Bone mineralizationBone mineralization

48. Painful HematuriaPainful Hematuria
UTI/ Cystitis/ PyelonephritisUTI/ Cystitis/ Pyelonephritis
Renal CalculiRenal Calculi
IMAGING CHOICES: IMAGING CHOICES:
Computed tomography ( NON CONTRAST) is the Computed tomography ( NON CONTRAST) is the
best imaging modality for the evaluation of urinary best imaging modality for the evaluation of urinary
stones, renal and perirenal infections, and associated stones, renal and perirenal infections, and associated
complications complications
Ultrasound : Excellent for detection and Ultrasound : Excellent for detection and
characterization of renal cysts (Limitations in detection characterization of renal cysts (Limitations in detection
of small solid lesions (<3 cm)) of small solid lesions (<3 cm))  Also, used for stones Also, used for stones
eval in pregnancy. eval in pregnancy.

49. ElectrolytesElectrolytes

50. HypernatremiaHypernatremia

51. HypernatremiaHypernatremia
Defined as serum sodium > 145 meq/LDefined as serum sodium > 145 meq/L
Hospital acquired in >80% of patientsHospital acquired in >80% of patients
Requires defect in renal concentrating ability and Requires defect in renal concentrating ability and
defect in thirst mechanismdefect in thirst mechanism
Normal patients do not become hypernatremicNormal patients do not become hypernatremic
Hypernatremia occurs in very young and very Hypernatremia occurs in very young and very
old with a defect in thirstold with a defect in thirst
Isovolemic, Hypovolemic & HypervolemicIsovolemic, Hypovolemic & Hypervolemic

52. Isovolemic Hypernatremia : Usually hemodynaically Isovolemic Hypernatremia : Usually hemodynaically
stable unless serum sodium > 170 meq/Lstable unless serum sodium > 170 meq/L
Causes:Causes:
HypodipsiaHypodipsia
Increases insensible lossesIncreases insensible losses
Nephrogenic diabetes insipidus – congenital, Nephrogenic diabetes insipidus – congenital,
acquired acquired  CRF, Hypokalemia, Hypercalcemia, Sickle cell CRF, Hypokalemia, Hypercalcemia, Sickle cell
disease Amyloidosis, Obstruction, Alcohol, Lithium, disease Amyloidosis, Obstruction, Alcohol, Lithium,
Demeclocycline, Glyburide, AmphotericinDemeclocycline, Glyburide, Amphotericin
 Essential hypernatremiaEssential hypernatremia
Central Diabetes Insipidus : Granulomas, Histiocytosis, Central Diabetes Insipidus : Granulomas, Histiocytosis,
Infections, CVA, Postpartum necrosis, Pregnancy, Head Infections, CVA, Postpartum necrosis, Pregnancy, Head
traumaPost hypophysectomy, Suprasellar masses, Intrasellar traumaPost hypophysectomy, Suprasellar masses, Intrasellar
massesmasses

53. PolyuriaPolyuria
? Water or solute diuresis? Water or solute diuresis
Water diuresis i.e. diabetes insipidus vs Water diuresis i.e. diabetes insipidus vs
polydipsia ( Upolydipsia ( U
osmosm < 150 mOsm ) < 150 mOsm )
Solute diuresis i.e. electrolyte vs non electrolyte ( Solute diuresis i.e. electrolyte vs non electrolyte (
UU
osm osm 300 - 400 mOsm )300 - 400 mOsm )
Diagnostics: Urinalysis, urine osmolality, and Diagnostics: Urinalysis, urine osmolality, and
urine electrolytesurine electrolytes

55. Hypovolemic Hypernatremia Causes Hypovolemic Hypernatremia Causes
Renal causesRenal causes
Loop diureticsLoop diuretics
Osmotic diuresisOsmotic diuresis
Gastrointestinal causesGastrointestinal causes
Vomiting / nasogastric drainageVomiting / nasogastric drainage
Diarrhea / catharticsDiarrhea / cathartics
Water loss into cellsWater loss into cells
Exercise / seizuresExercise / seizures
Cuteaneous causesCuteaneous causes
Burns / excessive sweatingBurns / excessive sweating

56. Hypervolemic HypernatremiaHypervolemic Hypernatremia
Causes :Causes :
Hypertonic sodium solutionsHypertonic sodium solutions
Hypertonic feedingsHypertonic feedings
Ingestion of sea waterIngestion of sea water
Hypertonic dialysisHypertonic dialysis
Primary aldosteronismPrimary aldosteronism
Cushing’s syndromeCushing’s syndrome

57. Signs and Symptoms HypernatremiaSigns and Symptoms Hypernatremia
Depend on rate, degree and duration Depend on rate, degree and duration
Depressed sensoriumDepressed sensorium
IrritabilityIrritability
Focal neurologic deficits / seizuresFocal neurologic deficits / seizures
Muscle spasmsMuscle spasms
Nausea/vomitingNausea/vomiting
Thirst / feverThirst / fever
Volume depletion / hyperglycemiaVolume depletion / hyperglycemia

58. Therapy of HypernatremiaTherapy of Hypernatremia
Hemodynamic or osmolal problem?Hemodynamic or osmolal problem?
Acute or chronic problem?Acute or chronic problem?
Prior losses and present losses?Prior losses and present losses?
Rate of correction?Rate of correction?
Acute: 1-1.5 meq/L/hour reductionAcute: 1-1.5 meq/L/hour reduction
Chronic: 0.5 meq/L/hour reduction or 50% within first 24hoursChronic: 0.5 meq/L/hour reduction or 50% within first 24hours
-- WHICH FLUID ? WHICH FLUID ?
IsovolemicIsovolemic
 water: PO or intravenouswater: PO or intravenous
 Water deficit = 0.6 (BWWater deficit = 0.6 (BW
KgKg) x (P) x (P
nana/140 -1)/140 -1)
Hypovolemic – unstable pt????Hypovolemic – unstable pt????
Correct volume problem i.e. normal salineCorrect volume problem i.e. normal saline
Correct osmolal problemCorrect osmolal problem
HypervolemicHypervolemic
Salt removal with loop diuretics and free waterSalt removal with loop diuretics and free water

59. CASE STUDYCASE STUDY

60. HypercalcemiaHypercalcemia
EtiologyEtiology
Clinical features : bones, moans, stones, groansClinical features : bones, moans, stones, groans
Investigations: Ca, Phos, EKG, PTH, Urinary calcium excretion ( R/o familial Investigations: Ca, Phos, EKG, PTH, Urinary calcium excretion ( R/o familial
hypocalciuric hypercalcemia)hypocalciuric hypercalcemia)
Management:Management:
Criteria for surgery in primary hyperparathyroidismCriteria for surgery in primary hyperparathyroidism
Sestamibi scan only if surgery is planned/indicatedSestamibi scan only if surgery is planned/indicated
Hypercalcemic crisis management – ivf + lasix after volume repletion onlyHypercalcemic crisis management – ivf + lasix after volume repletion only
Indications for corticosteroids : are useful for treating Indications for corticosteroids : are useful for treating hypercalcemiahypercalcemia caused caused
by vitamin D toxicity, certain malignancies (eg, multiple myeloma, lymphoma), by vitamin D toxicity, certain malignancies (eg, multiple myeloma, lymphoma),
sarcoidosis, and other granulomatous diseases sarcoidosis, and other granulomatous diseases
Cinacalcet (Sensipar) -- Directly lowers parathyroid hormone (PTH) levels by Cinacalcet (Sensipar) -- Directly lowers parathyroid hormone (PTH) levels by
increasing sensitivity of calcium sensing receptor on chief cell of parathyroid increasing sensitivity of calcium sensing receptor on chief cell of parathyroid
gland to extracellular calcium. Also results in concomitant serum calcium gland to extracellular calcium. Also results in concomitant serum calcium
decrease decrease  Indicated for Indicated for hypercalcemiahypercalcemia with parathyroid carcinoma. with parathyroid carcinoma.
Do not lower Calcium too much Do not lower Calcium too much  Serum calcium reduction may cause lowered Serum calcium reduction may cause lowered
seizure threshold, paresthesia, myalgia, cramping, and tetany; seizure threshold, paresthesia, myalgia, cramping, and tetany;

61. Criteria for Surgery – Primary Criteria for Surgery – Primary
hyperparathyroidismhyperparathyroidism
Serum total calcium level >12 mg per dL (3 mmol per L) at any time Serum total calcium level >12 mg per dL (3 mmol per L) at any time
Hyperparathyroid crisis (discrete episode of life-threatening Hyperparathyroid crisis (discrete episode of life-threatening
hypercalcemiahypercalcemia) )
Marked hypercalciuria (urinary calcium excretion more than 400 mg Marked hypercalciuria (urinary calcium excretion more than 400 mg
per day) per day)
Nephrolithiasis Nephrolithiasis
Impaired renal function Impaired renal function
Osteitis fibrosa cystica Osteitis fibrosa cystica
Reduced cortical bone density (measure with dual x-ray Reduced cortical bone density (measure with dual x-ray
absorptiometry or similar technique) absorptiometry or similar technique)
Bone mass more than two standard deviations below age-matched controls (Z Bone mass more than two standard deviations below age-matched controls (Z
score less than 2) score less than 2)
Classic neuromuscular symptoms Classic neuromuscular symptoms
Proximal muscle weakness and atrophy, Proximal muscle weakness and atrophy, hyperreflexiahyperreflexia, and gait , and gait
disturbance disturbance
Age younger than 50Age younger than 50

62. Hypercalcemia – Breast CancerHypercalcemia – Breast Cancer
Management: Management:
Principal Rx : Bisphosphonates for moderate to severe Principal Rx : Bisphosphonates for moderate to severe
hypercalcemia ( Aridia, Zolendronic acid) ( and also hypercalcemia ( Aridia, Zolendronic acid) ( and also
prevent osteoporosis) ( esply pts on Aromatase prevent osteoporosis) ( esply pts on Aromatase
inhibitors are even prone to osteoporosis)inhibitors are even prone to osteoporosis)
 Manage hypercalcemic crises as in all other cases ( IV Manage hypercalcemic crises as in all other cases ( IV
Fluids and only after complete hydration, then Fluids and only after complete hydration, then
furosemide)furosemide)

63. HyponatremiaHyponatremia
Classify – Hypotonic, Isotonic and HypertonicClassify – Hypotonic, Isotonic and Hypertonic
Classify – hypovolemic or euvolemicClassify – hypovolemic or euvolemic
Hypovolemic Hyponatremia – Diarrhea, Vomiting, Hypovolemic Hyponatremia – Diarrhea, Vomiting,
early excess diuresisearly excess diuresis
Euvolemic Hyponatremia Euvolemic Hyponatremia  SIADH SIADH
Isotonic Hyponatremia Isotonic Hyponatremia  Pseudohyponatremia Pseudohyponatremia
( Hyperglycemia, Hypertriglyceridemia, does not occur ( Hyperglycemia, Hypertriglyceridemia, does not occur
with uremia)with uremia)
Rx Rx  Correct volume and then osmolal problem Correct volume and then osmolal problem
Volume problem Volume problem  Isotonic saline always !!!!!!!!!! Isotonic saline always !!!!!!!!!!
Asymptomatic Asymptomatic  fluid restriction fluid restriction
CNS symptoms CNS symptoms  3% Saline 3% Saline

64. HyperkalemiaHyperkalemia
Several causes : Medication interaction is a Several causes : Medication interaction is a
common one ( ACEI+Spironolactone+beta common one ( ACEI+Spironolactone+beta
blocker, HEPARIN), renal failure, Addisons blocker, HEPARIN), renal failure, Addisons
disease, Rhabdomyolysis, Metabolic acidosis, disease, Rhabdomyolysis, Metabolic acidosis,
Hyperglycemic states. Hyperglycemic states.
Effects : arrhythmias, Can lead to tall tented t-Effects : arrhythmias, Can lead to tall tented t-
waves on EKG waves on EKG

65. Ekg- HyperkalemiaEkg- Hyperkalemia
The following changes may be seen in hyperkalaemiaThe following changes may be seen in hyperkalaemia
small or absent P waves small or absent P waves
atrial fibrillation atrial fibrillation
wide QRS wide QRS
shortened or absent ST segment shortened or absent ST segment
wide, tall and tented T waves wide, tall and tented T waves
ventricular fibrillation ventricular fibrillation

66. 58 year old man on
haemodialysis presents with
profound weakness after a
weekend fishing trip.

67. The man’s K was 9.6The man’s K was 9.6
Next Step Next Step  IV CALCIUM CHLORIDE IV CALCIUM CHLORIDE
( CALCIUM GLUCONATE AN ( CALCIUM GLUCONATE AN
ALTERNATIVE)ALTERNATIVE)

68. 30 y/o woman evaluated in the emergency department for a 2-
day history of muscle weakness. An electrocardiogram taken in
the emergency department is shown.
Which of the following is the best immediate treatment
option?
( A ) Hemodialysis
( B ) 50% glucose, 50 mL, intravenously
( C ) Calcium gluconate, 10 mL
( D ) Sodium polystyrene sulfonate (Kayexalate), 50 g, in
sorbitol, rectally
( E ) Peritoneal dialysis

69. Hyperkalemia - TreatmentHyperkalemia - Treatment
MNEMONIC – CBIGKDropMNEMONIC – CBIGKDrop
Check the EKG Check the EKG  If EKG changes, calcium If EKG changes, calcium
gluconate IVgluconate IV
B – BICARBONATE/ Beta agonistsB – BICARBONATE/ Beta agonists
I – INSULINI – INSULIN
G – DEXTROSEG – DEXTROSE
K – KAYEXALATE If total body potassium is K – KAYEXALATE If total body potassium is
an issuean issue
D – Hemodialysis for refractory HyperkalemiaD – Hemodialysis for refractory Hyperkalemia

70. HYPOKALEMIA - EKGHYPOKALEMIA - EKG
The following changes may be seen in The following changes may be seen in
hypokalaemia.hypokalaemia.
small or absent T waves small or absent T waves
prominent U waves prominent U waves
first or second degree AV block first or second degree AV block
slight depression of the ST segment slight depression of the ST segment

71. Acid Base DisordersAcid Base Disorders
Formulas, Case studies and Formulas, Case studies and
ManagementManagement

72. Acid Base DisordersAcid Base Disorders
Metabolic AlkalosisMetabolic Alkalosis
Respiratory AlkalosisRespiratory Alkalosis
Metabolic AcidosisMetabolic Acidosis
Respiratory AcidosisRespiratory Acidosis
Mixed DisordersMixed Disorders

73. Acid Base DisordersAcid Base Disorders
Common clinical problemsCommon clinical problems
Associated with life threatening conditionsAssociated with life threatening conditions
Often misdiagnosedOften misdiagnosed
Demands an understanding of physiology and Demands an understanding of physiology and
pathophysiologypathophysiology
pH is a major determinant of enzymatic reactions pH is a major determinant of enzymatic reactions
– Acedemia denatures the enzymes, decreases – Acedemia denatures the enzymes, decreases
threshold for ventricular fibrillation and increases threshold for ventricular fibrillation and increases
respiratory drive. Alkalemia suppresses respiratory respiratory drive. Alkalemia suppresses respiratory
drive, can cause myocardial ischemia, coronary drive, can cause myocardial ischemia, coronary
vasospasm etcvasospasm etc

74. Acid Base DisordersAcid Base Disorders
- CARBONIC ACID - BICARBONATE - CARBONIC ACID - BICARBONATE
SYSTEM : H + HCOSYSTEM : H + HCO
33 ↔↔ H H
22COCO
33 ↔ ↔ H H
22O + O +
COCO
22
-HENDERSON-HASSELBACHHENDERSON-HASSELBACH
EQUATION : pH = pKEQUATION : pH = pK
a a + log HCO+ log HCO
33 / H2CO / H2CO
33
-PLASMA ACIDITYPLASMA ACIDITY : determined by : : determined by :
Balance between concentration of plasma Balance between concentration of plasma
bicarbonate and pCO2bicarbonate and pCO2
Measured as pH or H ion concentrationMeasured as pH or H ion concentration

75. Acid Base DisordersAcid Base Disorders
1. Factors affecting plasma Bicarbonate :1. Factors affecting plasma Bicarbonate :
Rate of H ion inputRate of H ion input
Rate of H ion excretion via kidneysRate of H ion excretion via kidneys
Rate of H ion or bicarbonate loss via GI tractRate of H ion or bicarbonate loss via GI tract
Availability of non bicarbonate buffersAvailability of non bicarbonate buffers
Volume of distribution of bicarbonateVolume of distribution of bicarbonate
2. Factors affecting pCO2 2. Factors affecting pCO2
Rate of CO2 excretion via alveolar ventilationRate of CO2 excretion via alveolar ventilation
Rate of CO2 productionRate of CO2 production

76. ACIDEMIA-ALKALEMIAACIDEMIA-ALKALEMIA
Refers to plasma acidityRefers to plasma acidity
Acidemia: pH < 7.36Acidemia: pH < 7.36
Alkalemia: pH > 7.44Alkalemia: pH > 7.44
Metabolic Disorder: Metabolic Disorder:
- Acid-base disorder caused by primary - Acid-base disorder caused by primary
change in plasma bicarbonatechange in plasma bicarbonate
- Plasma bicarbonate = 24-28 meq/L- Plasma bicarbonate = 24-28 meq/L
Respiratory DisorderRespiratory Disorder
- Acid-base disorder caused by primary - Acid-base disorder caused by primary
change in pCO2change in pCO2
-pCO2 = 36 - 44 mmHgpCO2 = 36 - 44 mmHg
Compensatory Mechanisms : Compensatory Mechanisms :
Appropriate proportional physiologic Appropriate proportional physiologic
responses responses which tend to restore pH which tend to restore pH
toward, but not to normaltoward, but not to normal
Terms “over” and “under” Terms “over” and “under”
compensation should be avoidedcompensation should be avoided – –
INSTEAD USE “ MIXED “ INSTEAD USE “ MIXED “
DISORDER!!!DISORDER!!!

77. Metabolic AcidosisMetabolic Acidosis
Calculate Anion Gap : Na - (Cl + HCOCalculate Anion Gap : Na - (Cl + HCO
33) - Normal 3 - 10 ) - Normal 3 - 10
meq/Lmeq/L
Given entirely by Unmeasured anions are related to (-) charge Given entirely by Unmeasured anions are related to (-) charge
on albumin on albumin  One gram albumin = 2.5 meq/L anion One gram albumin = 2.5 meq/L anion
i.e.i.e.Albumin of 4 gm/L, baseline anion gap would be 10 Albumin of 4 gm/L, baseline anion gap would be 10
meq/L which is Normal. Correct Gap for Albumin!!! meq/L which is Normal. Correct Gap for Albumin!!!  If If
albumin is 2gm%, the baseline anion gap should be 5 in albumin is 2gm%, the baseline anion gap should be 5 in
which case 10 should be assumed as increased Anion gap.which case 10 should be assumed as increased Anion gap.
Delta Gap : Delta AG / Delta HCO3:Delta Gap : Delta AG / Delta HCO3:
1:1 = Anion gap acidosis1:1 = Anion gap acidosis
>1 = Anion gap acidosis plus metabolic alkalosis >1 = Anion gap acidosis plus metabolic alkalosis
< 1 = Increased Anion gap acidosis plus normal < 1 = Increased Anion gap acidosis plus normal
anion gap acidosisanion gap acidosis
Classify Metabolic Acidosis Classify Metabolic Acidosis
– – Increased GapIncreased Gap
- Normal Anion gap- Normal Anion gap
- Mixed : Gap + non gap- Mixed : Gap + non gap

78. Calculate CompensationCalculate Compensation
Compensation Metabolic AcidosisCompensation Metabolic Acidosis
Occurs in 12-24 hours and limit PCO2 10 Occurs in 12-24 hours and limit PCO2 10
mmHg :mmHg :
Expected Expected pCO2 = 1.5x HCO3 + 8 +/- 2pCO2 = 1.5x HCO3 + 8 +/- 2
pCO2 = last 2 digits pHpCO2 = last 2 digits pH
pCO2 = HCO3 + 15pCO2 = HCO3 + 15
If measured Pco2 is less than expected pco2 as If measured Pco2 is less than expected pco2 as
calculated by this equation – suspect a primary calculated by this equation – suspect a primary
respiratory alkalosis. If it is more than expected respiratory alkalosis. If it is more than expected
suspect primary respiratory acidosis. This is how suspect primary respiratory acidosis. This is how
you diagnose mixed disorders!!!you diagnose mixed disorders!!!

79. ExampleExample
65 y/o man with CAD 65 y/o man with CAD  and then and then
cardiogenic shock. Ph 7.26. PCo2 40 HCO3- cardiogenic shock. Ph 7.26. PCo2 40 HCO3-
10 Na+ 136 Cl- 110 Albumin 2.010 Na+ 136 Cl- 110 Albumin 2.0
1.1.What's the Anion Gap?What's the Anion Gap?
2.2.Corrected Anion Gap ? {gap + 2.5(measured Corrected Anion Gap ? {gap + 2.5(measured
albumin)}albumin)}
3.3.Delta Anion Gap?Delta Anion Gap?
4.4.Delta Hco3-? ( 24 – bicarb)Delta Hco3-? ( 24 – bicarb)
5.5.Delta Gap?Delta Gap?
6.6.Adequately Compensated or mixed ?Adequately Compensated or mixed ?
7.7.Name the disorder ? Name the disorder ?

80. Normal Anion-Gap Metabolic AcidosisNormal Anion-Gap Metabolic Acidosis
Gastrointestinal Loss of BicarbonateGastrointestinal Loss of Bicarbonate
 DiarrheaDiarrhea
 Urinary diversionUrinary diversion
 Small bowel, pancreatic, or bile drainage ( fistulas, surgical Small bowel, pancreatic, or bile drainage ( fistulas, surgical
drains )drains )
 CholestiramineCholestiramine
Renal Loss of Bicarbonate ( or Bicarbonate equivalent )Renal Loss of Bicarbonate ( or Bicarbonate equivalent )
 Renal tubular acidosisRenal tubular acidosis
 Recovery phase of KetoacidosisRecovery phase of Ketoacidosis
 Renal InsufficiencyRenal Insufficiency
 Acidifying Substances- HCl, NH4Cl, Arginine HCl, Lysine HCl, Acidifying Substances- HCl, NH4Cl, Arginine HCl, Lysine HCl,
Sulfur Sulfur
To differentiate calculate Urinary Anion Gap = Urine (Na + k) – To differentiate calculate Urinary Anion Gap = Urine (Na + k) –
(cl-). Normal is from +10 to -10. If UAG > +10 (cl-). Normal is from +10 to -10. If UAG > +10  Renal loss. Renal loss.
If UAG < -10 or more negative If UAG < -10 or more negative  GI Causes GI Causes

81. Increased Anion Gap AcidosisIncreased Anion Gap Acidosis
Ketoacidosis - diabetic, alcoholic, starvationKetoacidosis - diabetic, alcoholic, starvation
Lactic acidosisLactic acidosis
UremiaUremia
Toxins - Ethylene glycol, methanol, salicylate, Toxins - Ethylene glycol, methanol, salicylate,
paraldehyde paraldehyde
Osmolar Gap = Measured Osmolarity – Osmolar Gap = Measured Osmolarity –
Calculated OsmolarityCalculated Osmolarity
Calculated SerumCalculated Serum
osmosm = 2(Na) + Glucose/18 = 2(Na) + Glucose/18
+BUN/2.8 ( + ethylalcohol/4.5)+BUN/2.8 ( + ethylalcohol/4.5)

82. Plasma Level v. OsmolalityPlasma Level v. Osmolality
Ethanol ÷ 4.6Ethanol ÷ 4.6
Methanol ÷ 3.2Methanol ÷ 3.2
Ethylene glycol ÷ 6.2 Ethylene glycol ÷ 6.2
Isopropanol ÷ 6.1Isopropanol ÷ 6.1
For example, a blood ethanol level of 100mg/dL For example, a blood ethanol level of 100mg/dL
would increase plasma osmolality 100/4.6 or 22 would increase plasma osmolality 100/4.6 or 22
mOsm/LmOsm/L

83. Case StudyCase Study
Sam is a 35 y/o alcoholic who is brought to the ER in a comatose state. Sam’s Sam is a 35 y/o alcoholic who is brought to the ER in a comatose state. Sam’s
wife tells you that she had an argument in the evening about 5 hrs ago over wife tells you that she had an argument in the evening about 5 hrs ago over
Sam’s alcohol habits. Sam apparently got mad over the discussion, drove his Sam’s alcohol habits. Sam apparently got mad over the discussion, drove his
car and returned an hour ago in a very intoxicated state. Wife called the EMS car and returned an hour ago in a very intoxicated state. Wife called the EMS
and rushed him to the ER. On examination Sam is disoriented and and rushed him to the ER. On examination Sam is disoriented and
hallucinating , Pulse 120 Tm 99, RR 26 BP 126/76. The rest of the physical hallucinating , Pulse 120 Tm 99, RR 26 BP 126/76. The rest of the physical
exam is normal except for stuporos state and alcohol smell. Lab studies exam is normal except for stuporos state and alcohol smell. Lab studies
revealed Na 130 k 3.4 cl- 95 Hco3 16, Glucose 90 Creatinine 1.6 BUN 45. revealed Na 130 k 3.4 cl- 95 Hco3 16, Glucose 90 Creatinine 1.6 BUN 45.
Blood Ethylalcohol level was 180. Serum osmolarity was 360mg%. ABGs Blood Ethylalcohol level was 180. Serum osmolarity was 360mg%. ABGs
revealed 7.28, Pco2 28, Po2 76 Sao2 93. The next best step in management ?revealed 7.28, Pco2 28, Po2 76 Sao2 93. The next best step in management ?
A) Endotracheal intubation in view of severe acidosisA) Endotracheal intubation in view of severe acidosis
B) Hemodialysis because this is an acute renal failure causing acidosisB) Hemodialysis because this is an acute renal failure causing acidosis
C) Fomepizole because of suspicion of ethylene glycol intoxicationC) Fomepizole because of suspicion of ethylene glycol intoxication
D) Supportive treatment for now because this is an ethylalcohol induced D) Supportive treatment for now because this is an ethylalcohol induced
lactic acidosislactic acidosis
E) Bicarbonate drip to reverse the acidosis because this is renal tubular E) Bicarbonate drip to reverse the acidosis because this is renal tubular
acidosisacidosis

84. Ethylene Glycol PoisoningEthylene Glycol Poisoning
Envelope shaped crystals Envelope shaped crystals
Treatment : Consider Antidote Treatment : Consider Antidote
( Fomepizole or Ethanol ) if Level > ( Fomepizole or Ethanol ) if Level >
20mg% or if you suspect ethylene 20mg% or if you suspect ethylene
glycol intake with 2 or more – a) glycol intake with 2 or more – a)
arterial ph < 7.3, Hco3 <20, osmolar arterial ph < 7.3, Hco3 <20, osmolar
gap>10, calcium oxalate crystals in gap>10, calcium oxalate crystals in
urine.urine.
Antidote blocks Alcohol Antidote blocks Alcohol
dehydrogenase and prevents the dehydrogenase and prevents the
Glycolic acid formation. In case of Glycolic acid formation. In case of
methanol, toxic meatbolite is formic methanol, toxic meatbolite is formic
acidacid
Ethylene glycol found in Ethylene glycol found in
antifreeze and de-icerantifreeze and de-icer
Toxicity results at doses >1.0 Toxicity results at doses >1.0
ml/kg ml/kg
Ethylene glycol causes CNS Ethylene glycol causes CNS
depression , converts to depression , converts to
Glycolic AcidGlycolic Acid (metabolite) (metabolite)
effects effects 
M t ol M os s
e ab ic cid i
M t ol M os s
e ab ic cid i
& &Renal FailureRenal Failure
Oxalic acid (metabolite) Oxalic acid (metabolite)
effects effects  Calcium oxalate Calcium oxalate
crystal depositioncrystal deposition

C/F: C/F: Confusion, Ataxia, Confusion, Ataxia,
Slurred speech Slurred speech
,Hallucination, ,Hallucination, TetanyTetany
SeizureSeizures (s (HypocalcemiaHypocalcemia) )
HypertensionHypertension
Tachycardia Tachycardia

85. Increased Osmolal GapIncreased Osmolal Gap
EthanolEthanol
MethanolMethanol
Ethylene GlycolEthylene Glycol
FormaldehydeFormaldehyde
Paraldehyde Paraldehyde
Lactic AcidosisLactic Acidosis
ESRDESRD
KetoacidosisKetoacidosis
MannitolMannitol
Isopropyl alcoholIsopropyl alcohol
HyperlipidemiaHyperlipidemia
HyperproteinemiaHyperproteinemia
Diethyl etherDiethyl ether

86. Isopropanol IngestionIsopropanol Ingestion
Present with CNS depression, hypotension, Present with CNS depression, hypotension,
arrhytmias and gastritisarrhytmias and gastritis
Acetest reaction positiveAcetest reaction positive
Increased osmolal gapIncreased osmolal gap
No metabolic acidosisNo metabolic acidosis
Anion gap normalAnion gap normal

87. Renal Tubular AcidosisRenal Tubular Acidosis
Type 1 ( distal)Type 1 ( distal)
Type 2 (proximal)Type 2 (proximal)
Type 4 (hyporeninemic hypoaldosteronism)Type 4 (hyporeninemic hypoaldosteronism)

88. Type I RTA (Distal)Type I RTA (Distal)
Causes: autoimmune diseases, hyperglobinemia Causes: autoimmune diseases, hyperglobinemia
states and hereditarystates and hereditary
Present with normal anion gap acidosis, urine pH Present with normal anion gap acidosis, urine pH
>5.5, hypokalemia, hypercalciuria, >5.5, hypokalemia, hypercalciuria,
nephrocalcinosis and stonesnephrocalcinosis and stones
Treatment: alkali i.e. K citrateTreatment: alkali i.e. K citrate

89. Type II RTA (Proximal)Type II RTA (Proximal)
Isolated defect or associated with generalized proximal Isolated defect or associated with generalized proximal
dysfunction i.e. Fanconi syndromedysfunction i.e. Fanconi syndrome
Failure to reclaim filtered bicarbonateFailure to reclaim filtered bicarbonate
Increase FEIncrease FE
HCO3HCO3
Urine pH > 5.5, but may be < 5.5 once HCOUrine pH > 5.5, but may be < 5.5 once HCO
33 < 16 < 16
meq/Lmeq/L
Causes: Causes:
Multiple myelomaMultiple myeloma
AcetozolamideAcetozolamide
Ifosfamide Ifosfamide
Lead, cadmium, copperLead, cadmium, copper

90. Type 4 RTAType 4 RTA
Hypoaldosteronism or aldosterone resistanceHypoaldosteronism or aldosterone resistance
Causes: diabetes mellitus, HIV and tubulo-Causes: diabetes mellitus, HIV and tubulo-
interstitial diseaseinterstitial disease
Present with hyperkalemia, normal anion gap Present with hyperkalemia, normal anion gap
acidosis and normal urine pH acidosis and normal urine pH

91. Metabolic AlkalosisMetabolic Alkalosis
Calculate compensation Calculate compensation
PCO2= ( 0.7 x HCO3 ) + 21 . If measured Pco2 PCO2= ( 0.7 x HCO3 ) + 21 . If measured Pco2
is more than this then there is concomitant is more than this then there is concomitant
respiratory acidosis. If less than this then respiratory acidosis. If less than this then
concomitant respiratory akalosis.concomitant respiratory akalosis.
Delta Gap to r/o mixed disorder – metabolic Delta Gap to r/o mixed disorder – metabolic
acidosis + metabolic alkalosis if delta gap >1acidosis + metabolic alkalosis if delta gap >1

92. Causes of Metabolic AlkalosisCauses of Metabolic Alkalosis
Saline responsive : ECF depleted ( contraction alkalosis ), Urine Saline responsive : ECF depleted ( contraction alkalosis ), Urine
chloride < 10 meq/L, do not go by urine sodium in assessing chloride < 10 meq/L, do not go by urine sodium in assessing
volume statusvolume status
Gastrointestinal Loss eg : Surreptious vomiting, NG tube Gastrointestinal Loss eg : Surreptious vomiting, NG tube
suctions,Villous adenoma, Chloride diarrhea, Diuretics (late),Post suctions,Villous adenoma, Chloride diarrhea, Diuretics (late),Post
hypercapneahypercapnea
Saline resistant : Saline Resistant Metabolic AlkalosisSaline resistant : Saline Resistant Metabolic Alkalosis , , Increased Increased
mineralocorticoid effect,Urine Cl > 20 meq/Lmineralocorticoid effect,Urine Cl > 20 meq/L
 Hypertensive causes:Primary aldosteronismCushing’s syndrome, Hypertensive causes:Primary aldosteronismCushing’s syndrome,
11 or 17 hydroxylase deficiency, Licorice / carbenoxolone, 11 or 17 hydroxylase deficiency, Licorice / carbenoxolone,
Liddle’s syndrome, SteroidsLiddle’s syndrome, Steroids
 Normotensive causes: Bartter’s syndrome ( thiazide), Gitelman’s Normotensive causes: Bartter’s syndrome ( thiazide), Gitelman’s
syndrome ( like loop diuretic), Diuretics (present), Severe syndrome ( like loop diuretic), Diuretics (present), Severe
potassium depletion, Severe magnesium depletionpotassium depletion, Severe magnesium depletion

93. Metabolic Alkalosis - TreatmentMetabolic Alkalosis - Treatment
Saline responsiveSaline responsive
Normal saline to volume repleteNormal saline to volume replete
KClKCl
Saline resistantSaline resistant
Inhibit or remove excess mineralocorticoid effectInhibit or remove excess mineralocorticoid effect
MiscellaneousMiscellaneous
Acetazolamide, HCl, NH4ClAcetazolamide, HCl, NH4Cl
Hemodialysis Hemodialysis

94. Case StudyCase Study
 A 26 year old woman presents to the ER with generalized weakness associated with
perioral numbness. She is moderately built and looks slightly depressed. On
physical exam, she has mild pallor. She denies use of any medications. BP 120/88
mmHg and physical exam is normal. Lab data: Cr 1.2mg/dL, BUN 15mg/dLNa
136 , K 2.8 , Cl 88 , HCO3 38. Urine Na 45 meq/L, Urine K 35 meq/L, Urine Cl
8 meq/L, Urine specific gravity 1.010, Urine pH 7
The most likely diagnosis is :
A)Laxative Abuse
B)Surreptious vomiting
C)Licorice abuse
D)Malabsorption Syndrome
E)Hyporeninemic Hypoaldosteronism
Treatment :
A)IV normal saline
B)Spronolactone
C)Amiloride
D)Psychiatry consult
E)Reassurance because this is self limiting