2. 91 y.o. Chinese female
Premorbidly
ADL assisted
Ambulant with WF
Independent in grooming and feeding
BARTHEL 12/20
AMT 6/10
Social
Widowed
1 adopted daughter :Main carer
3. DM
HBAIC : 6.1 13/5/13
HYPERTENSION
HYPERLIPIDEMIA
TB OF KIDNEYS 1980
Bleeding GIT 2009
-extensive diverticular
disease
- Antral erosions
Fracture Right IT 4 S/P
DHS 2006
Fracture left IT s/P PFNA
in 2010
Fall 5/2013 with Left
Olecranon fracture
S/P ORIF left Olecranon
Left Humerus Fracture
▪ Conservative management
▪ Discharged to AMKCH for rehab
▪ BMD: T score -2.2 2010
4. 6/5 /2013
Spiked fever (+) cough
Bibasal creps (+) SOB , SP02 89%-95%
CXR: no consolidation/ effusion
CPR 1 TW 6.8 PLT: 203 crea 98
UFEME: suggestive of UTI
Urine CS: Proteus
Given IV Rocephine, Flagyl
10/5/2013 Repeat bloods
HB 8.8 TW 5.9 crea 187, Na 140 K 3.7
5. Oriented TPP
Non toxic looking
Neck : supple
H : S1 S2
C : bibasal creps
A : soft , no palpable bladder
C: supple bilaterally
DRE: Brown stools, No blood
Motor 5/5 uLE
6.
7.
8. Hb 9.3
MCV 98.2 H
MCH 32.4 H
MCHC 33
TW 5.9
Plt 258
Crea 179 H
Urea: 6.7
TCalcium 2.09L
Cor Ca 2.35
iPhosphate 1.36
Vit B12 209
Folate : 5.20
Transferrin 1.29
Ferritin 270.7
Iron serum 12.1
Iron sat 42%
Haptoglobin 157
Vit d 5ug/L
CRP 8.0
Procalcitonin 0.27
PTH 19.68
9. TSH 12.9
T4 0.719
Hbaic 6.1
Albumin 25
CK Normal
LFT: Normal
APTT /PT Normal
UFEME 23/48/0
(-) protein
(+) esterase
Urine CS: NBG
Sputum CS: normal
flora
AFB Smear: negative
x3 takings
10. Fracture Distal shaft of fifth Metatarsal bone L
Xray toes:
diffuse bony osteopenia, healing fracture of distal
shaft of the fifth metatarsal bone noted
Seen By ORTHO
Casting done
11.
12.
13. 23/5
Urine PCR 2.07
UFEME 20/270/0 (+) protein (+) esterase
ANA screen negative
ENA screen negative
DsDNA <25
ANCA
Anti MPO negative
Anti PR3 negative
14.
15.
16. Patient doesn’t qualify for DDX of MM
Crea -->Prob post TB Kidneys and CRPD
M band is just 3G/L
Calcium is normal
Anemia not completely worked up
▪ for skeletal survey
▪ B2 Macroglobulin
17. There is no evidence of lytic lesions in skull
or the bones to suggest presence of MM
deposits
Unlikely MM, (?) likely MGUS
Needs Further anemia WU
Not for BMA
BETA 2 MACROGLOBULIN 14,392
18.
19. Patient Multiple Myeloma Tuberculosis
kidney/chest
MGUS
Age 91 older adult
MA >60
* mean age >70
Anemia * * Not seen
Deranged Creatinine * * Not seen
Chronic renal
parenchymal disease
* Not seen
Calcium normal * *
Low VIT D
Osteopenia
*
Absent skeletal lytic
lesions
* * *
Infection * *
AFB Negative
B2 microglobulin Poor prognosis
20. Diagnosed only if
Serum Monoclonal Protein( IgA, IGg, IgM) < 3
g/dl)
Clonal BM plasma cells < 10%
Absent of lytic lesions. Anemia, hypercalcemia,
renal insufficiency ( end organ damage) that can
be attributed to plasma cell proliferative disorder
21. Past TB of kidney
Discordant kidney size
Recurrent or resistant urinary tract infection, sterile pyuria
with or without hematuria .
Renal (hydronephrosis/pyonephrosis)
Renal failure (Chronic kidney disease due to parenchymal
infection and obstructive uropathy
Infertility and pelvic inflammatory disease.
Urine AFB smear ( 55% sensitivity)
Urine AFB culture ( 41% sensitivity)
Indian J Urol. 2008 Jul-Sep; 24(3): 401–405.
22. Older age
Anemia , leukopenia, low albumin
Unexplained renal dysfunction
Multiple fractures
Elevated b2 macroglobulin
M proteins
Raised IgA, ( 20% of MM)
Protein electrophoresis
Raised K/L freeLight chains ( 20% of MM)
Immunofixation : (+) monoclonal bands
23. 1% of all cancers
10% of all hematologic cancer
F>M (1.4.:1)
Incurable
Disease of older adults ( mean age: 66y.o)
Small but unknown fraction of cases are
familial
Evolve from MGUS
24. Complex , poorly understood
Establishment of a limited clonal
proliferation
Progression of MGUS to MM
27. Presence of M –protein in serum
No specific level of m-protein is used as a cut off
value
40% percent of patients with symptomatic MM
will have an M protein of < 3 g/dl
Presence of 10% clonal bone marrow plasma
cells
Related organ or tissue impairment
CRAB
28. 1. Hypercalcemia: serum calcium>2.75 mmol/L
2. Renal dysfunction: serum creatinine>173 mmol/L
3. Anemia: hemoglobin 2 g/dL below lower limit of
normal
4. Lytic bone lesions (CT and MRI may be used to
identify suspicious findings on plain films)
5. Symptomatic hyperviscosity
6. Amyloidosis
7. Recurrent bacterial infections (more than two
episodes in 1 year)
31. Stage I
B2 M < 3.5g/dl, albumin >/ 3.5g/dl
Stage II
B2M < 3.5mg/dl, alb <3.5g/dl or
B2M 3.5—5.5 mg/L irrespective of serum albumin
Stage III
B2M >/ 5.5 mg/dl
32. Stage 1 Stage 1 Stage 2 Stage 3
HB > 10g/dl < 8.5mg/dl
calcium Normal > 12 mg/dl
Skeletal survey: Normal
Single plasmacytoma or
osteoporosis
3 or more lseions
Serum paraprotein
level
< 5 g/dl If IgG
<3 g/dl id IgA
7 g/dl
5 g/dl 9.31
Urinary light
chains excretion
< 4 g/24h > 12 g/24
Survival rate 62 mos 45 mos 29 mos
35. Urine electrophoresis
Protein electrophoresis
Monoclonal band detected and bands in alpha 1,
alpha 2, beta and gamma globulin regions seen
Immunofixation electrophoresis
Monoclonal band detected with anti lambda
Total protein urine
1.94g/L
Editor's Notes
Patient was admitted in ht=this isntitutio last march -- fro fracture, was dischrage to AMKCH for rehab. On 6the pf may, patient dtated to
The heart size cannot be assessed on this projection...... Calcified old granulomas... CXR: calcified old granulomas on both upper lung fields and left mid lung zone
Since patient h was difficulty weaning from 02, rpt xray done 5 Days later. The hear size is enlarge, prominent hilum is likely due to vascular shadows, fribrocalcific foci in bilateral upper znes and left mid zone are in keeping with previous granulomatous infection, ther is blunting of costophrenic angle, suggestive of bilateral pluerl effusin. Referral to pulmologistr was done.. Bedside ultrasound was done which showed no tapable pleural effsuin
In view of elevated creatinine, it was trended. It was initially thought as AKI, hence hydration was done, then... But it reached up to 300 (+0 mg /dl Renal consult was done.
Renal AKI w/ leucocytomia and past hx of TB kidney T?RO vasculitis Ddx: chronic interstitial nephritis or acute interstitial nephritis Small left kidney may be sec to tb 2. Pnemnia 5 th metatarsal fracture Myeloperoxidase deficiency is a hereditary deficiency of the enzyme, which predisposes to immune deficiency . [7] Antibodies against MPO have been implicated in various types of vasculitis, most prominently crescentic glomerulonephritis and Churg-Strauss syndrome. They are detected as perinuclear ANCAs (p-ANCAs), as opposed to the cytoplasmic ANCAs (c-ANCAs) against proteinase-3 (PR3), which are strongly associated with Wegener's granulomatosis. P; IV HYDRATION DAILY RENAL PANEL MYELOMA TESAT TB AFB ABD CULTURE
Unexplained renal insuffiency suggests possible invlvement by the light chains due to MGUS, MM or related malignacy Diagnosis of DGUS is olny considered of the following 3 criteria is considered... SO ANY PATIENT WITH A NON Igm MONOCLONAL protein> 3 or with >10 % CLONAL PLASMA CELLS IN BONE MARROW DOES NOT HAVE mgus. However, could this patient ..........
ANOTHER DDS IS ---TB of the kidneys. Genitourinary tuberculosis (GUTB) is the second most common form of extrapulmonary tuberculosis after lymph node involvement . Kidney is usually the primary organ infected in urinary disease, and other parts of the urinary tract become involved by direct extension. The GUTB has varied presentation and some of the common ways are: Recurrent or resistant urinary tract infection, sterile pyuria with or without hematuria . Irritative voiding symptoms, i.e., frequency, urgency, and dysuria.An incidental diagnosis in a known case of tuberculosis. Renal (hydronephrosis/pyonephrosis) or epididymal mass. Infertility and pelvic inflammatory disease. Renal failure (Chronic kidney disease due to parenchymal infection and obstructive uropathy. The various other ways of presentation described are: flank pain with acute pyelonephritis, non-healing wounds, sinuses, or fistulae (nephrocutaneous fistula or vesicovaginal fistula), and hemospermia. The most common symptoms with which the patients have presented are in the form of irritative voiding, which are found in more than 50% of the patients. The other symptoms in GUTB can be fever, weight loss, anorexia, backache, and abdominal pain.[
unexplained renal dysfunction, anemia, or pathologic fracture should prompt evaluation for this diagnosis. . a clearly elevated B2 macroglobulin in the absence of renal faliure or an inflammatory process would suggest a diagnosis of MM and the patient should be carefully examined.
pATHOBIOOLOgy of MM is a complex prc3ess of malignant clone of plasma cell origin. Virtually all MM myeloma cases are preceded by a premalignant plasma cell prolifereation disorder of the Monoglonal gammopathy of undetermined significance. MGUS is present in over 3 percent of thhe population above 50 and prgresses to Myeloma or arelated malignancy at a rate of 1 % per year
Epidemiologic data suggest a genetic predisposition as well as other potential risk factors including… Radiologists exposed to large doses of long term radiation have an increased risk of MM Workes in nuclear plants and farmers who use herbicieds, insecticides and those who employ benzene and petroleum products have increased risk of MM but the evidence is not compelling.
A restospective analysis of 1027 sequential patients diagnoised with MM at a single instituion found the following symproms and signs at presentaiton.
Symptomatic hyperviscosity……..
Bisphosphonates are given to prevent fracture , routine administered to prevent fractures, they also have been observed to have direct anti tumor effect in patients without known skeletal disease. Chemotherapy Autologous SCT: - not curative but prolong overall survival and complete remission Allogenic SCT- has potential cure but is ony avialable to asmall percentage
This staging is only in patients who meet diagnostic criteria of myeloma. Patients with MGUS and aymptomatic myeloma who have renal dysfuntion from unrelated causes such as diabetes or hypertension may have elevated b2M levels just from the renal dysfunction and cannot be considered as stage III myeloma.This is one of the drawbacks of the Iss. It daoes not really quantify quantity tumor burden or extent unlike staging used in other cancers. It is recommended to use along durie salmon staging system.
Staging and classification of multiple myeloma A staging system is used by the medical profession to describe how advanced the myeloma is, and how it is affecting the body. A common staging system is called the Durie-Salmon system. The four factors of the Durie-Salmon system: What is the red blood cell count? How much calcium is in the blood? How much paraproteins (monoclonal proteins, or M proteins) is in the blood? The general state of the patient's bones. Stage one (Durie-Salmon system) Blood calcium levels are normal Red blood cell levels are either normal or slightly below normal Low levels of paraproteins (monoclonal proteins, or M proteins) in the blood Bones are either undamaged or slightly damaged Most patients have no symptoms Stage two (Durie-Salmon system) Red blood cell levels still relatively normal Calcium blood levels still relatively normal Levels of paraproteins (monoclonal proteins, or M proteins) still low Damage is present in one or two bones Stage three (Durie-Salmon system) Red blood cell levels have fallen. Symptoms of anemia are probably present. Blood calcium levels have risen. Symptoms of hypercalcemia are likely. High levels of paraproteins (monoclonal proteins, or M proteins) in the blood. Damage to three or more bones. The Durie-Salmon system also has a system to indicate the health or deterioration of the kidneys: A - kidneys are either undamaged or only slightly damaged. B - kidneys are damaged, kidney function is abnormal. Kidney damage is more likely during stages two or three, but can also occur in stage one.
PLAN REFER TO HEMATOLOGY SINGLE KIDNEY: CONTRAINDICATION FOR RENAL BIPSY