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TOP 10 NEPHRO SLIDES TOP 10 NEPHRO SLIDES IN BOARD EXAMS IN BOARD EXAMS
BOARD EXAM SLIDESBOARD EXAM SLIDES
WHAT IS THIS ?WHAT IS THIS ?
WHAT IS THIS ?WHAT IS THIS ?
WHAT IS THIS ?WHAT IS THIS ?
WHAT IS THIS ?WHAT IS THIS ?
WHAT IS THIS ?WHAT IS THIS ?
WHAT IS THIS ?WHAT IS THIS ?
WHAT IS THIS ?WHAT IS THIS ?
COMMONEST NEPHRO CASES IN COMMONEST NEPHRO CASES IN BOARD EXAM – TRICKS AND CLUESBOARD EXAM – TRICKS AND CLUES MOST OF THE CASES CONTAIN ONE SINGLE MOST OF THE CASES CONTAIN ONE SINGLE
OUTSTANDING CLUE THAT CAN GIVE YOU OUTSTANDING CLUE THAT CAN GIVE YOU THE DIAGNOSIS --- THE DIAGNOSIS ---
LOOK FOR THAT CLUELOOK FOR THAT CLUE
THIS IS THE M-KASAP TYPE OF QUESTIONSTHIS IS THE M-KASAP TYPE OF QUESTIONS
GLOMERULONEPHRITIS EXAM GLOMERULONEPHRITIS EXAM TRICKS AND CLUESTRICKS AND CLUES
A.RBC CASTS:A.RBC CASTS: 1. MPGN1. MPGN 2.IGA2.IGA 3.POST STREP GN3.POST STREP GN 4.SLE NEPRITIS4.SLE NEPRITIS 5.RPGN AS ANCE NEPHRITIDES5.RPGN AS ANCE NEPHRITIDES
CONTINUES CLUESCONTINUES CLUES
A PATIENT WITH GLOMERULAR A PATIENT WITH GLOMERULAR PROTIENUREA AND INCREASED LIVER PROTIENUREA AND INCREASED LIVER ENZYMES IS MPGN DUE TO HEP CENZYMES IS MPGN DUE TO HEP C
A PATIENT OBESE WITH PROTIENUREA IS A PATIENT OBESE WITH PROTIENUREA IS FSGSFSGS
CONTINUECONTINUE
A PATIENT WITH HEROIN ABUSE AND A PATIENT WITH HEROIN ABUSE AND PROTIENUREA IS FSGSPROTIENUREA IS FSGS
A PATIENT WITH PROTIENUREA AND RENAL A PATIENT WITH PROTIENUREA AND RENAL IMPAIRMENT AND FEW + DIPSTICK WITH IMPAIRMENT AND FEW + DIPSTICK WITH LARGR TOTAL 24 HRS PROTIENUREA ID M LARGR TOTAL 24 HRS PROTIENUREA ID M MYELOMAMYELOMA
CONTINUESCONTINUES
A PATIENT ON NSAID AND PROTIENUREA IS A PATIENT ON NSAID AND PROTIENUREA IS MMDMMD
A PATIENT WITH CANCER AND NEPHROTIC A PATIENT WITH CANCER AND NEPHROTIC PROTIENUREA IS MGN EXCEPT IF HE HAS PROTIENUREA IS MGN EXCEPT IF HE HAS HODJKINS LYPHOMA IT IS MIN CHANGE HODJKINS LYPHOMA IT IS MIN CHANGE DISEASEDISEASE
CORRECT ANSWER IS ACORRECT ANSWER IS A
CHOLESTEROL EMBOLISATATIONCHOLESTEROL EMBOLISATATION ONE OF THE MOST AND TOP QUESTIONS IN ONE OF THE MOST AND TOP QUESTIONS IN
ARAB-SAUDI-AMERICAN BOARD EXAMSARAB-SAUDI-AMERICAN BOARD EXAMS
SIMPLY EXAMINERS THEY LOVE IT !!!SIMPLY EXAMINERS THEY LOVE IT !!!
I TOLD U LOOK FOR THE CLUE!!I TOLD U LOOK FOR THE CLUE!!WHERE IS THE CLUE HERE ?WHERE IS THE CLUE HERE ?
THE CLUE IS THE TIME OF INCREASE IN CR THE CLUE IS THE TIME OF INCREASE IN CR WHICH IS AFTER 48 HRSWHICH IS AFTER 48 HRS
CONTRAST GIVE U INCREASE CR WITHIN CONTRAST GIVE U INCREASE CR WITHIN FIRST 24 HRS OF THE ANGIO BUT CE THE FIRST 24 HRS OF THE ANGIO BUT CE THE RISE IS AFTER 48 HRSRISE IS AFTER 48 HRS
OTHER CLUES LOW COMPLEMENTS,AND OTHER CLUES LOW COMPLEMENTS,AND HIGH ESRHIGH ESR
CE-CASECE-CASE
ESINOPHILLIAESINOPHILLIA DIGITAL INFARCTSDIGITAL INFARCTS LIVEDO RETICULARISLIVEDO RETICULARIS RETINAL EMBOLI AND HEMORRHAGESRETINAL EMBOLI AND HEMORRHAGES RISK INCREASED BY HEPARINERISK INCREASED BY HEPARINE AS CTDAS CTD PROGNOSIS GRAVE ( NO SINGLE CASE HAS BEEN PROGNOSIS GRAVE ( NO SINGLE CASE HAS BEEN
RECOVEREDRECOVERED
Cr timingCr timing
Cr increase in contrast within first 24 hrsCr increase in contrast within first 24 hrs
Cr increase in embolisation after 24-72 hrsCr increase in embolisation after 24-72 hrs
Cr increase in gentamycine after 7-10 daysCr increase in gentamycine after 7-10 days
All the follwing are true of All the follwing are true of preclampcia EXCEPT :preclampcia EXCEPT :
A. high uric acidA. high uric acid B. high CrB. high Cr C. no urine RBC castsC. no urine RBC casts D. high urine calciumD. high urine calcium E. high urine protienE. high urine protien
36 yrs female known case of SLE 36 yrs female known case of SLE want to become pregnant, what want to become pregnant, what
would u advice her ?would u advice her ? A. the single most important is Cr level at the A. the single most important is Cr level at the
time of conceptiontime of conception B.the single most important is disease activity B.the single most important is disease activity
level at conceptionlevel at conception C.the single most imprtant is protienureaC.the single most imprtant is protienurea D.A AND BD.A AND B E.B AND CE.B AND C
25 OLD MALE COCCAINE ABUSER 25 OLD MALE COCCAINE ABUSER PRESENTED TO ER WITH :PRESENTED TO ER WITH :
VOMITING,HYPERTENTION,AND FEVER WITH VOMITING,HYPERTENTION,AND FEVER WITH DECREASE URINE OUTPUTDECREASE URINE OUTPUT
O/E BP 170 / 98 T 38 O/E BP 170 / 98 T 38 CVS S1,S2 NORMAL WITH ESMCVS S1,S2 NORMAL WITH ESM LUNGS CLEAR,ABD NO ORGANOMEGALYLUNGS CLEAR,ABD NO ORGANOMEGALY HX OF CHANGE OF URINE COLOURHX OF CHANGE OF URINE COLOUR
LABSLABS
CBC WBC 7,PLAT 230,Hb 10.6CBC WBC 7,PLAT 230,Hb 10.6 LFT NORMALLFT NORMAL Cr 600 AND ONE MONTH AGO WAS 78Cr 600 AND ONE MONTH AGO WAS 78 Na 137, K 6.8,Ca 1.2,Ph 1.9Na 137, K 6.8,Ca 1.2,Ph 1.9 Uric Acid 600Uric Acid 600 UA POSITIVE FOR BLOOD +++ ON UA POSITIVE FOR BLOOD +++ ON
DIPSTICK,PROT +,RBC 1-5DIPSTICK,PROT +,RBC 1-5
THE MOST LIKELY DX:THE MOST LIKELY DX:
A. RHABDOMYOLYSISA. RHABDOMYOLYSIS B. SBEB. SBE C.TUMOR LYSIS SYNDROMEC.TUMOR LYSIS SYNDROME D.POST INF GND.POST INF GN E.POLYARTERITIS NODOSAE.POLYARTERITIS NODOSA
RHABDOMYOLYSIS-THINGS IN RHABDOMYOLYSIS-THINGS IN EXAM TO REMEMBEREXAM TO REMEMBER
THE COMMONEST CAUSE IS TRUMA-SOLDIER THE COMMONEST CAUSE IS TRUMA-SOLDIER SYNDROMESYNDROME
THE COMMONEST DRUG IS COCCAINETHE COMMONEST DRUG IS COCCAINE OTHER DRUGS HMG-COENZ-RED-INHIBITORS OTHER DRUGS HMG-COENZ-RED-INHIBITORS
AS STATINSAS STATINS THE SINGLE MOST IMPORTANT STEP IN THE SINGLE MOST IMPORTANT STEP IN
MANAG IS IVF AND IVF AND IVFMANAG IS IVF AND IVF AND IVF
COMMON MCQ IN EXAMS-GNCOMMON MCQ IN EXAMS-GN
54 YRS MALE PRESENTED WITH 54 YRS MALE PRESENTED WITH WEAKNESS,DIAZINESS, FOR 4 MONTHSWEAKNESS,DIAZINESS, FOR 4 MONTHS
CBS HB 8GM,WBC 5,PLAT 230CBS HB 8GM,WBC 5,PLAT 230 LFT Na 137,K 6,Ca 2.6,LFT Na 137,K 6,Ca 2.6, U/A DIPSTICK PROTIEN +,BLOOD –U/A DIPSTICK PROTIEN +,BLOOD – MICROSCOPY NO RBC CASTSMICROSCOPY NO RBC CASTS TOTAL 24 HRS PROTIEN 8 GMTOTAL 24 HRS PROTIEN 8 GM
RENAL BX;RENAL BX;
THE MOST LIKELY DX IS ;THE MOST LIKELY DX IS ;
A.AMYLOIDOSISA.AMYLOIDOSIS B.MYELOMA KIDNEYB.MYELOMA KIDNEY C.MEMRANOUS GNC.MEMRANOUS GN D.FSGSD.FSGS E.MINIMAL CHANGE DISEASEE.MINIMAL CHANGE DISEASE
MYELOMA KIDNEY-EXAM MYELOMA KIDNEY-EXAM FAVOURITE FAVOURITE
THE MOST IMPORTANT CLUE IN EXAM IS THE MOST IMPORTANT CLUE IN EXAM IS DIPSTICK URINE NEGATIVE FOR PROTIEN OR DIPSTICK URINE NEGATIVE FOR PROTIEN OR MILD + POSITIVE BUT THE 24 HRS URINE MILD + POSITIVE BUT THE 24 HRS URINE COLLECTION FOR PROTIEN IS MORE THAN 3 COLLECTION FOR PROTIEN IS MORE THAN 3 GM. WHY ?GM. WHY ?
LARGE KIDNEY. WHAT OTHER CAUSES OF LARGE KIDNEY. WHAT OTHER CAUSES OF LARGE KIDNEY ????LARGE KIDNEY ????
TWO TYPES OF MYELOMA KIDNEYTWO TYPES OF MYELOMA KIDNEY
A. TUBULAR WITH LIGHT CHAIN DEPOSITION A. TUBULAR WITH LIGHT CHAIN DEPOSITION AND GIVE U FRACTURED CAST DIAGNOSTIC AND GIVE U FRACTURED CAST DIAGNOSTIC OF MM.THIS TYPE HAS GOOD PROGNOSISOF MM.THIS TYPE HAS GOOD PROGNOSIS
B.LDD-CHARACTERISED BY NODULAR B.LDD-CHARACTERISED BY NODULAR SCELEROSIS AND POOR PROGNOSISSCELEROSIS AND POOR PROGNOSIS
MEMBRANOUS GN-EXAM POINTSMEMBRANOUS GN-EXAM POINTS
THE COMMONEST CAUSE OF RENAL VIEN THE COMMONEST CAUSE OF RENAL VIEN THROMBOSISTHROMBOSIS
THE COMMONEST CAUSE OF NEPHROTIC THE COMMONEST CAUSE OF NEPHROTIC SYNDROME IN ADULTSSYNDROME IN ADULTS
COMPLEMENTS NORMAL,NO RBC CASTSCOMPLEMENTS NORMAL,NO RBC CASTS ASSOCCIATED WITH MALIGNANCY COLONASSOCCIATED WITH MALIGNANCY COLON
MGNMGN
IDIOPATHICIDIOPATHIC SECONDARY TO DRUGS ( ACE,GOLD,PENCILLAMINE )SECONDARY TO DRUGS ( ACE,GOLD,PENCILLAMINE ) INFECTIONS(MALARIA,HEP B)INFECTIONS(MALARIA,HEP B) TREATMENT( ACE,PONTICELLI TREATMENT( ACE,PONTICELLI
PROTOCOL=CHLORAMPUCIL ALTERNATING WITH PROTOCOL=CHLORAMPUCIL ALTERNATING WITH STEROIDS OR IMMURAN STEROIDS OR IMMURAN
RESISTANT USE CYCLOSPORINERESISTANT USE CYCLOSPORINE
PROGNOSIS-THE 25 % DISEASEPROGNOSIS-THE 25 % DISEASE
25 % COMPLETE RECOVERY25 % COMPLETE RECOVERY 25 % PARTIAL RECOVERY25 % PARTIAL RECOVERY 25 % ESRD25 % ESRD 25 % RELAPSE ON AND OFF25 % RELAPSE ON AND OFF
FSGS-EXAM QUESTIONSFSGS-EXAM QUESTIONS
THE COMMONEST QUESTIONS IS CAUSES THE COMMONEST QUESTIONS IS CAUSES OR A CASE WHICH TELL U THE CAUSEOR A CASE WHICH TELL U THE CAUSE OBESE PATIENT WITH PROTIENUREA IS FSGSOBESE PATIENT WITH PROTIENUREA IS FSGS A PATIENT WITH HIV THE COOMNEST RENAL A PATIENT WITH HIV THE COOMNEST RENAL
BX FINDING IS COOLAPSING FSGSBX FINDING IS COOLAPSING FSGS A PATIENT ON HEROINE OR DRUG ABUSER IS A PATIENT ON HEROINE OR DRUG ABUSER IS
FSGS OR INF-@FSGS OR INF-@
FSGSFSGS
A PATIENT WITH SINGLE KIDNEY AND A PATIENT WITH SINGLE KIDNEY AND PROTIENUREA IS FSGSPROTIENUREA IS FSGS
A PATIENT WITH REFLUX HAS FSGSA PATIENT WITH REFLUX HAS FSGS STEROIDS CAN INDUSE REMISSION IN 40 % STEROIDS CAN INDUSE REMISSION IN 40 %
OF CASESOF CASES IT IS THE HIGHEST AND FASTEST IT IS THE HIGHEST AND FASTEST
RECURRENCE OF RENAL TX WITH MPGNRECURRENCE OF RENAL TX WITH MPGN
HIV NEPHROPATHYHIV NEPHROPATHY
POINTS TO REMEMBER IN EXAMS:POINTS TO REMEMBER IN EXAMS: 1.LARGE KIDNEY1.LARGE KIDNEY 2.CYSTIC TUBULAR DILATATION2.CYSTIC TUBULAR DILATATION 3.ENDTHELIAL CYTOPLASMIC 3.ENDTHELIAL CYTOPLASMIC
RETICLOTUBULAR STRUCTURES ON EMRETICLOTUBULAR STRUCTURES ON EM 4.COLLAPSING FSGS IS THE COMMONEST 4.COLLAPSING FSGS IS THE COMMONEST
VARIETYVARIETY
MCD-EXAM QUESTIOSMCD-EXAM QUESTIOS
NSAID IS THE ONLY DRUG KNOWN TO CAUSE NSAID IS THE ONLY DRUG KNOWN TO CAUSE MCD WITH INF-@MCD WITH INF-@
ALL MALIGNANCY ASSOCIATED WITH ALL MALIGNANCY ASSOCIATED WITH MEMBRANOUS GN EXCEPT ONE MLIGNANCY MEMBRANOUS GN EXCEPT ONE MLIGNANCY ASSOCIATED WITH MCD DO U KNOW WHAT IT ASSOCIATED WITH MCD DO U KNOW WHAT IT IS ????????????IS ????????????
Hodgkin’s lymphoma.Hodgkin’s lymphoma.
MCD-EXAM POINTSMCD-EXAM POINTS
• IN A PATIENT WITH MCD WHO IS NOT RESPONDING TO IN A PATIENT WITH MCD WHO IS NOT RESPONDING TO ADEQUATE COURSE OF STEROIDS THE MOST LIKELY ADEQUATE COURSE OF STEROIDS THE MOST LIKELY CAUSE IS FSGS SO DO RENAL BXCAUSE IS FSGS SO DO RENAL BX
• THE MOST IMPORTANT POINTS ABOUT MCD IS THISTHE MOST IMPORTANT POINTS ABOUT MCD IS THIS
• IN CHILDREN A COURSE OF 8 WEEKS STEROIDS IS IN CHILDREN A COURSE OF 8 WEEKS STEROIDS IS ADEQUATE TO INDUSE REMISSIONADEQUATE TO INDUSE REMISSION
BUT IN ADULTS THE STORY IS BUT IN ADULTS THE STORY IS DIFFERENTDIFFERENT
IN ADULTS DO NOT LABEL THE PATIENT AS IN ADULTS DO NOT LABEL THE PATIENT AS STEROIDS RESISTANT UNLESS U GIVE 12 STEROIDS RESISTANT UNLESS U GIVE 12 WEEKS OF STEROIDS WEEKS OF STEROIDS
REMEMBER AT LEAST 12 WEEKSREMEMBER AT LEAST 12 WEEKS DO U KNOW THE DIFFERENCE BETWEEN DO U KNOW THE DIFFERENCE BETWEEN
STEROIDS DEPENDENT AND STEROIDS STEROIDS DEPENDENT AND STEROIDS RESISTANT AND STEROIDS RELAPSERRESISTANT AND STEROIDS RELAPSER
MPGN-EXAM POINTSMPGN-EXAM POINTS
THE HIGHEST RECURRENCE OF DISEASE IN THE HIGHEST RECURRENCE OF DISEASE IN TX ( 80 % )TX ( 80 % )
THE COMMONEST CAUSE OF MPGN IN THE THE COMMONEST CAUSE OF MPGN IN THE WORLD NOW IS …………… Hepatitis C ……………WORLD NOW IS …………… Hepatitis C ……………
CRYOGLOBULINEMIA IS IMPORTANT CAUSECRYOGLOBULINEMIA IS IMPORTANT CAUSE
FREQUENT AND COMMON BOARD FREQUENT AND COMMON BOARD EXAM QUESTION IS THIS ONEEXAM QUESTION IS THIS ONE
54 YRS MALE PRESENTED WITH HEAVY 54 YRS MALE PRESENTED WITH HEAVY PROTIENUREA OF 7GMPROTIENUREA OF 7GM
HIS LFT IS ABNORMALAHIS LFT IS ABNORMALA THE RENAL BIOBSY WILL THE RENAL BIOBSY WILL
SHOW…………………………….SHOW…………………………….
RPGN-THE MOST FREQUNT RPGN-THE MOST FREQUNT QUESTION COMES IN EXAMSQUESTION COMES IN EXAMS
IT IS A MEDICAL EMERGENCYIT IS A MEDICAL EMERGENCY IN FACT IT IS THE ONLY GN THAT IS IN FACT IT IS THE ONLY GN THAT IS
EMERGENCYEMERGENCY IT CAN KILL THE KIDNEY IN 72 HRS IF U DID IT CAN KILL THE KIDNEY IN 72 HRS IF U DID
NOT ACTNOT ACT U START RX EVEN BEFORE THE BX RESULTU START RX EVEN BEFORE THE BX RESULT
CAUSES;CAUSES;
WEGNERSWEGNERS PANPAN CHURG-STRAUSSCHURG-STRAUSS ANTI-GBMANTI-GBM
Case presentation
58 yrs male working as a business man Started to have muscle weakness,fever,wight
loss,and bloody urine ,hemoptysis,and new hypertention for the last 3 months .
BP 210/ 12O His Cr 6 months ago was 120 ,now 440 ESR 89
P-ANCAP-ANCA
WEGNERSWEGNERS MICROSCOPIC POLYANGIOPATHYMICROSCOPIC POLYANGIOPATHY CHURG-STRAUSSCHURG-STRAUSS IDIOPATHIC RPGN IN THE ELDERLYIDIOPATHIC RPGN IN THE ELDERLY
REVERSAL OF RENAL FUNCTION IN REVERSAL OF RENAL FUNCTION IN ANTI-GBM DISEASE(GODPASTUER)ANTI-GBM DISEASE(GODPASTUER)
IF Cr LESS THAN 550IF Cr LESS THAN 550 IF PATIENT NOT YET STARTED ON DIALYSISIF PATIENT NOT YET STARTED ON DIALYSIS IF PLASMAPHRESIS STARTED EARLYIF PLASMAPHRESIS STARTED EARLY
BEST RX FOR GODPASTUREBEST RX FOR GODPASTURE
PLASMAPHRESISPLASMAPHRESIS
PULSE IV STEROIDSPULSE IV STEROIDS
BEST RX FOR WEGNERSBEST RX FOR WEGNERS
PULSE IV STEROIDSPULSE IV STEROIDS
CYCLOPHOSCYCLOPHOS
PLASMAPHRESISPLASMAPHRESIS
C-ANCA-ONLY WEGNERSC-ANCA-ONLY WEGNERS
THE MOST IMPORTANT SLIDE IN THE MOST IMPORTANT SLIDE IN GLOMERULONEPHRITISGLOMERULONEPHRITIS
ANY CASE IN THE EXAM MENTION UA ANY CASE IN THE EXAM MENTION UA CONTAIN RBC-CASTCONTAIN RBC-CAST
THERE ARE ONLY 5 DDX IN MEDICINETHERE ARE ONLY 5 DDX IN MEDICINE
DO U KNOW WHAT ARE THEY ??????? ??DO U KNOW WHAT ARE THEY ??????? ??
CAUSES OF RBC-CAST THIS IS CAUSES OF RBC-CAST THIS IS CALLED ACTIVE URINE SEDIMENTCALLED ACTIVE URINE SEDIMENT
1. MPGN1. MPGN 2.IGA NEPHROPATHY2.IGA NEPHROPATHY 3.POST-INFECTIOUS GN AS POST-3.POST-INFECTIOUS GN AS POST-
STREPTOCOCCAL GNSTREPTOCOCCAL GN 4.SLE4.SLE 5.RPGN5.RPGN
WHAT IS THE SINGLE WHAT IS THE SINGLE MOST IMPORTANT TEST MOST IMPORTANT TEST
TO DIFFRENTIATE TO DIFFRENTIATE BETWEENBETWEENPRERENAL AND POSTRENAL PRERENAL AND POSTRENAL
AZOTEMIA ( ATN ) ??AZOTEMIA ( ATN ) ??
IT IS FENAIT IS FENA
PROXIMAL RTA
MA WITH NORM AGURINE PH < 6 ACIDIFY THE URINEDISTAL RTA ALWAYS URINE PH >6DISTAL RTA GIVE LOW HCO3
CONTINUE
DISTAL RTA SEVERE MUSCLE WEAKNESS AND VERY LOW HCO3
PROX RTA GLYCOSURIA AMINOCIDUREA
RTA TYPE 4
HYPORENEMIC HYPOALDO HYPERKALEMIC HYPERCHLREMIC MA DM
CEREBRAL SALT WATING CSW
HYPONATREMIAHIGH URINE OSMOL >600 AND HIGH U NA >100
HYPOVOLEMIA WITH ORTHOSTATIC DROP BP
SIADH NO VOLUME DEPL AND URIC ACID IS VERY LOW
Isopropyl alchol
NO MA
SERUM AND URINE KETONES++
HIGH OSMOLAL GAP
Q 8 MKSAP 15
TOLUENE
MA SEVERE HYPOKALEMIA HYPOPHOSPHATEMIA CPK ENZYME HIGH RHABDOMYOLYSIS
22 yrs male found comatose and his 22 yrs male found comatose and his friends mention that he had friends mention that he had problems with his wife and problems with his wife and
attempted suicide and his labs;attempted suicide and his labs;Na 140,k 5,cl 95,CO2 10,GLUCOSE Na 140,k 5,cl 95,CO2 10,GLUCOSE
7,PLASMA OSMOL 325,BUN 137,PLASMA OSMOL 325,BUN 13
PH 7.1,PCO2 24,PO2 85PH 7.1,PCO2 24,PO2 85
WHAT ACID BASE DISTURBANCE ?WHAT ACID BASE DISTURBANCE ? IS IT SIMPLE OR MIXED ?IS IT SIMPLE OR MIXED ? WHAT IS THE DX ?WHAT IS THE DX ?
Expected PCO2 = 1.5 X HCO3 + 8 ( + Expected PCO2 = 1.5 X HCO3 + 8 ( + OR – 2 )OR – 2 )
MA WITH HIGH AGMA WITH HIGH AG EXP PCO2 IS 21 – 25EXP PCO2 IS 21 – 25 MA POISONINGMA POISONING
5-DAYS LATER HIS ABG :5-DAYS LATER HIS ABG :
PH 7.2PH 7.2 HCO3 16HCO3 16 PCO2 45PCO2 45
WHAT ACID BASE IS THIS ?WHAT ACID BASE IS THIS ?
EXP PCO2=1.5 X 16 + 8=32EXP PCO2=1.5 X 16 + 8=32
BUT PCO2 IS 45 SO THIS IS MIXED MA + RESP BUT PCO2 IS 45 SO THIS IS MIXED MA + RESP ACIDOSISACIDOSIS
Where do u see it???
ASA LATE STAGE
SEPSIS
COPD + SEPSIS
NORMAL AG
IF AG NORMAL THINK OF RTA AND
DIARRHEA THEN LOOK AT THE UA GAP
UA AG= (NA + K )- CL IF THE CHARGE IS NEGATIVE IT IS DIARRHEA AND IF + IT IS RTA
If urinary K more than 10 there are only 8 causes in medicine
Vomiting ( the commonest ) Diuretics Mineral corticoid Excess( conn syndrome ) Licorice Cushing RTA Barters / Gitelman Mg low ( the forgotton one )
Case presentation
34 yrs old female presents with severe hypertensions BP 200 / 120 .EXAM NEGATIVE Apart from LL OEDEMA
Serum K 2.5 AND URINE K 60 Resting PRA 60,Aldosterone 100 ng/dl Renal Angiogram shows normal renal arteries
and vascular blush
Case presentation
25 yrs old male with new onset High BP BP 180 / 11O,P90,Hypertensive retinopathy,S4
gallop UA + protein Labs Na 140,K2.4,Cl 97,HCO3 30,PH 7.44 Cr 80,PRA 0.1 ng/ml/hr ( low ),plasma
Aldosterone 4 ng/dl (low) 24 hrs urine Na 200 mEq,K 40mEq
28 yrs male DX as HIV developed PCP and was started on iv septra?
Serum Na 135,CL 90,K 6 PH 7.36,Cr 70, What is the most likely cause of hyperkalemia ?
35 yrs male post renal TX on CS A,Pred and cellcept?
Serum K 6,Na 138,CL 114,HCO3 15 Cr 80 What is the most likely DX and cause of
hyperkaemia ?
30 yrs male admitted with pulmonary embolism and started on
anticoagulant?
Serum Na 128,K 6,Cr 67 HCO 24,Mg 1,Ca 2.8 What is the most likely cause of hyperkalemia?
TTKG
TTKG= (KU) X BLOOD OSMOL ------------------------------
(K BLOOD) X U OSMOL
TTKG
UK XPLASMA OSMOL=14 X 285 = 3990
PLASMA K X URINE OSMOL= 6.4X 351=2246
TTKG= 3990 / 2246 = 1.7 THIS IS MINERALOCORTICOID INSUFF
25 yrs female presented with muscular weakness?
K 2.5, HCO3 32,PH 7.48,Mg normal Urinary K 40, urine CL 150 Bp is normal What is ur DDX and most likely DX ?
If urinary K more than 10 there are only 8 causes in medicine
Vomiting ( the commonest ) Diuretics Mineral corticoid Excess( conn syndrome ) Licorice Cushing RTA Barters / Gitelman Mg low ( the forgotton one )
DDX OF HIGH URINE K WITH HYPOKALEMIA
Vomiting? NO Because urine CL is high .in vomiting and any volume depletion the first electrolyte to be down in urine is CL BECAUSE Na will be normal initially and later will be low ,but CL WILL BE LOW FROM THE START
IS IT RTA?
RTA ? No ? Because there is no metabolic acidosis HER PH IS ALKALOTIC
IS IT CONN OR CUSHING?
NO BECAUSE BP IS NORMAL AND NO SIGN OF CUSHING CLINICALLY
SO HER DDX SHOULD BE ONE OF THESE TWO:
DIURETIC ABUSE BARTTAR / GITELMAN
GITELMANS AND BARTTARS
Gitelman syndrome is a rare inherited defect in the distal convoluted
Bartter syndrome, which is a rare inherited defect in the thick ascending limb of the loop of Henle.
identical to those of patients who are on thiazide diuretics
Gitelman's syndrome
Clinical symptoms for this disease are hypochloremic metabolic alkalosis, hypokalemia, and hypocalciuria. Hypomagnesemia is present in many but not all cases.
BARTTERS
Evidence for a tubular defect in the loop of Henle
an inherited defect in the renal tubules that causes low potassium levels, low chloride levels, which in turn causes metabolic alkalosis. Bartter Syndrome, is not a single disorder but rather a set of closely related disorders.
Bartter and Related Syndromes, the Puzzle is Almost Solved
can be divided into three different genetic and clinical entities
Bartter syndromes are defined as a family of inherited recessive autosomal tubulopathies. They are characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with potassium renal leakage and normal blood pressure despite increased plasma renin activity.
hypercalciuria and nephrocalcinosis
This lady should have one of the following:
Diuretics abuseBarttar/gitelman syndromeWhy ???
The Four golden keys to make DX of Hypokalemia :
URINE K
BP
ACID-BASE STATUS
Mg level
ABDOMINAL CT WITH IODINATED CONTRAST
IT IS THE PROCEDURE OF CHOICE IN CKD PATIENTS ON DIALYSIS FOR DIAGNOSING MALIGNANCY CHANGE IN CYSTS OF KIDNEY
REMEMBER MRI WITH GADOLINIUM CONTRAST
CONTINUE CAN CAUSE NSF CHARACTERIZED BY
EDEMA AND THICKENED SKINS OF HAND AND FEET
HIGHEST RISK IS WITH GFR <40ML/MIN
MKSAP Q 12 NEPH EDIT 15
A DYNAMIC BONE DISEASE-MKSAP Q19ED15
COMMONEST BONE DISEASE IN PAT ON PERITON DIALYSIS
COMMONEST IN DM BONY PAIN ,OSTEOPENIA,PTH <100 AND
NORMAL ALK PHOSPH
B2-MICROGLOBULIN
AMYLOID X-RAY LARGE CYSTS DILATED AT LONG
BONES ENDS OSTITIS FIBROSA CYSTICA
In patients with recurrent calcium oxalate stones and hyperoxaluria,
increased dietary calcium intake and avoidance of oxalate-rich foods such as rhubarb, peanuts, spinach, beets, and chocolate are recommended to decrease the risk of stone formation.
Key PointIn patients with chronic kidney disease,
iron deficiency anemia should be corrected before initiation of an erythropoiesis-stimulating agent .
Key PointIn patients with symptomatic, acute
hyponatremia, rapid normalization of the extracellular fluid osmolality with
hypertonic saline is indicated .
Key PointAdherence to a high-calcium diet (generally defined as 1 to 4 g/d of
calcium) has been shown to decrease the risk of incident and recurrent calcium
oxalate stone formation .
The cathartic agent sodium phosphate may cause acute phosphate nephropathy resulting in acute kidney injury and hyperphosphatemia out of proportion to the degree of kidney failure
Key PointObstructive nephropathy must always be included in the differential diagnosis of a patient with acute kidney injury to ensure prompt diagnosis and reversal of kidney
injury .
Key PointThe target blood pressure in patients with type 2 diabetes mellitus and nondiabetic chronic kidney disease in the absence of
proteinuria is less than 130/80 mm Hg.
Ethylene glycol poisoning is associated with an anion gap
metabolic acidosis, an increased osmolal gap, kidney injury, and calcium oxalate crystals in the
urine.
Key PointAngiotensin receptor antagonists and
angiotensin-converting enzyme inhibitors are contraindicated during
pregnancy.
Key PointIn the hospital setting, patients with chronic alcoholism may have normal serum phosphorus levels on admission
to the hospital but often develop severe hypophosphatemia over the first 12 to 24 hours
Severe hypophosphatemia often develops over the first 12 to 24 hours after admission, usually because of intravenous glucose administration. This agent helps to release insulin and rapidly reverses alcoholic ketoacidosis, which causes phosphate to shift into cells.
The sudden development of hypophosphatemia may cause confusion, rhabdomyolysis, hemolytic anemia, and severe muscle weakness that can lead to respiratory failure.
Key PointIn patients with chronic kidney
disease who have persistent hypertension and proteinuria, a diuretic should be added if an
angiotensin-converting enzyme inhibitor or angiotensin receptor blocker and restriction of dietary
sodium are not helpful.
Key PointThe most common cause of HIV-
associated nephropathy is collapsing focal segmental glomerulosclerosis, which is characterized by massive
proteinuria .
Key PointCorticosteroid therapy is the initial treatment of choice in patients with minimal change disease, which is
characterized by the sudden development of an elevated urine protein-creatinine
ratio that may exceed 9 mg/mg .
Key PointLithium-induced nephrotoxicity may
manifest as nephrogenic diabetes insipidus and typically progresses slowly .
Key PointIsopropyl alcohol poisoning is
characterized by an increased osmolal gap in the setting of positive serum and
urine ketones and does not cause metabolic acidosis.
Key PointAmbulatory blood pressure monitoring
is the gold standard for diagnosing white coat hypertension .
Key PointProximal (type 2) renal tubular acidosis
secondary to multiple myeloma is characterized by a normal anion gap
metabolic acidosis, hypokalemia, and an intact ability to lower the urine pH .
Key PointThe diagnosis of polycystic kidney
disease can be confirmed by the presence of at least two cysts in each kidney on
kidney ultrasonography in a patient with a family history of this condition
Key PointThe most important risk factor for
intracranial aneurysm in patients with autosomal-dominant polycystic kidney
disease is a family member with an intracranial aneurysm
Key PointChronic kidney disease is the most
likely diagnosis in patients with elevated serum creatinine levels and
proteinuria early in pregnancy .
Key PointImmune complex–mediated glomerular
nephritis is characterized by hypocomplementemia and dysmorphic
erythrocytes and erythrocyte casts seen on urinalysis .
Key PointDietary protein restriction and an
angiotensin-converting enzyme inhibitor or angiotensin receptor blocker can be tried for 6 months in patients with membranous
nephropathy who have a urine protein-creatinine ratio of 4 to 8 mg/mg and normal
kidney function .
Key PointKidney biopsy is the study of choice in adults when the nephrotic syndrome is
suspected and helps to differentiate among the causes of this conditio
Key PointAlkalinization of the urine with potassium citrate therapy to obtain a urine pH above
6.0 decreases the risk of recurrent uric acid stones .
Key PointCerebral salt wasting may affect patients
undergoing neurosurgery, particularly those with subarachnoid hemorrhage,
and manifests as hyponatremia, increased urine sodium excretion, concentrated urine, and evidence of hypovolemia
Key PointManifestations of primary aldosteronism
include hypernatremia, hypokalemia, mild metabolic alkalosis, suppressed
plasma renin activity, and stage 2 hypertension .
In addition to therapy to inhibit the renin-angiotensin system,
immunosuppressive therapy is indicated in patients with IgA
nephropathy at risk for progression to kidney failure who do not yet have significant loss of kidney function .
type 1 diabetes mellitus who have abnormal findings on annual measurement of the urine albumin excretion should undergo repeat urinalyses twice within the next 6 months; positive findings on two of the three urine samples would confirm a diagnosis of microalbuminuria (defined as a urine albumin-creatinine ratio between 30 and 300 mg/g).
Key PointSalicylate toxicity is a common cause
of mixed anion gap metabolic acidosis and respiratory alkalosis .
Key PointThe accuracy of timed urine collection can be
assessed by comparing the total urine creatinine excretion with the expected value
of creatinine excretion
the expected value of creatinine excretion (20 to 25 mg/kg/24 h (20 to 25 mg/kg/d) in men, 15 to 20 mg/kg/24 h in women
Key PointThe gold standard for diagnosing
renovascular hypertension is intra-arterial digital subtraction
angiography .
Key PointIn patients with nonglomerular
hematuria, kidney ultrasonography and cystoscopy are indicated to exclude a
genitourinary tract malignancy in individuals with risk factors for this
condition .
Key PointDiagnosis of AL amyloidosis is
established by
Abdominal fat pad biopsy
Clinical trials suggest that medical therapy rather than angioplasty or revascularization can effectively manage renovascular hypertension secondary to atherosclerosis and may be the best option for patients with well-controlled blood pressure on medical therapy alone.
Referral to a nephrologist
Manage a patient with myeloma cast nephropathy
Hemodialysis, plasmapheresis, and chemotherapy
Methyldopa and labetalol are safe for treatment of hypertension during
pregnancy .
Multiple myeloma may manifest as hypercalcemia, anemia, kidney insufficiency, and proximal (type
2) renal tubular acidosis
Key PointKidney manifestations of sarcoidosis
include interstitial nephritis with granuloma formation,
hypercalciuria, nephrocalcinosis, and various glomerular diseases .
Key PointThe treatment of choice for
pheochromocytoma is surgical resection .
Key PointPrerenal disease is usually associated with
a fractional excretion of sodium of less than 1%, but this value is usually higher in patients with chronic kidney disease.
Key PointNephrostomy tube placement is indicated to manage urinary tract obstruction associated
with acute kidney injury when the obstruction is not relieved with bladder catheter
placement .
Manage hypertension in a patient more than 80 years of age.
Hydrochlorothiazide
Diagnose bone disease due to secondary hyperparathyroidism in a patient with end-stage kidney disease.
associated with elevated serum parathyroid hormone and alkaline phosphatase levels, hyperphosphatemia, and hypocalcemia.
Key PointAcute tubular necrosis usually develops after a sustained period of ischemia or exposure to
nephrotoxic agents such as cisplatin, intravenous aminoglycosides, or radiocontrast and is associated with muddy brown casts on
urinalysis
Key PointUse of tacrolimus and another
cytochrome P450 3A4 inhibitor can cause tacrolimus toxicity, which may
lead to acute kidney dysfunction .
Erythromycin
Key PointSurgical resection is indicated for patients
with Bosniak category III and IV kidney cysts .
Complex cystic structures or mass lesions, especially those greater than 4 cm, should raise suspicion for malignancy
Bosniak category III cysts are characterized by irregularly shaped walls with septal calcification. These cysts enhance after the administration of iodinated contrast agents. Approximately 50% of Bosniak category III cysts are malignant; therefore, surgical resection is indicated for patients with these cysts.
Mineralocorticoid receptor antagonists are particularly effective in treating
resistant hypertension .
Spironolactone
Diagnose polyarteritis nodosa as a cause of kidney failure.
Angiography of the renal arteries
Key PointPercutaneous nephrolithotomy is the treatment of choice in patients with
staghorn calculi .
This intervention allows for direct visualization of the kidney and verification of stone removal via nephroscopy and is associated with an estimated initial cure rate of 80%.
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