Scribd Logo
Upload

Welcome to Scribd!

  • 27 views

    Kuliah Path Clin MSK 2017

    Uploaded by

    Liora
    1. Laboratory tests are not diagnostic for osteoarthritis (OA) but can help differentiate it from other forms of arthritis. While OA shows no signs of inflammation on tests, rheumatoid factor (RF) and C-reactive protein (CRP) may be elevated in rheumatoid arthritis. 2. Synovial fluid analysis in OA shows yellow, clear fluid with a normal viscosity and less than 2,000 white blood cells per microliter, indicating no inflammation. Elevated erythrocyte sedimentation rate and CRP would suggest rheumatoid arthritis over OA. 3. The most common joints affected by OA are the hips, knees, hands, fingers, big toe,

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd

    Kuliah Path Clin MSK 2017

    Uploaded by

    Liora
    27 views26 pages
    1. Laboratory tests are not diagnostic for osteoarthritis (OA) but can help differentiate it from other forms of arthritis. While OA shows no signs of inflammation on tests, rheumatoid factor (RF) and C-reactive protein (CRP) may be elevated in rheumatoid arthritis. 2. Synovial fluid analysis in OA shows yellow, clear fluid with a normal viscosity and less than 2,000 white blood cells per microliter, indicating no inflammation. Elevated erythrocyte sedimentation rate and CRP would suggest rheumatoid arthritis over OA. 3. The most common joints affected by OA are the hips, knees, hands, fingers, big toe,

    Original Description:

    jkhgfjhg

    Original Title

    Kuliah Path Clin Msk 2017

    Copyright

    © © All Rights Reserved

    Available Formats

    PPTX, PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    1. Laboratory tests are not diagnostic for osteoarthritis (OA) but can help differentiate it from other forms of arthritis. While OA shows no signs of inflammation on tests, rheumatoid factor (RF) and C-reactive protein (CRP) may be elevated in rheumatoid arthritis. 2. Synovial fluid analysis in OA shows yellow, clear fluid with a normal viscosity and less than 2,000 white blood cells per microliter, indicating no inflammation. Elevated erythrocyte sedimentation rate and CRP would suggest rheumatoid arthritis over OA. 3. The most common joints affected by OA are the hips, knees, hands, fingers, big toe,

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    27 views26 pages

    Kuliah Path Clin MSK 2017

    Uploaded by

    Liora
    1. Laboratory tests are not diagnostic for osteoarthritis (OA) but can help differentiate it from other forms of arthritis. While OA shows no signs of inflammation on tests, rheumatoid factor (RF) and C-reactive protein (CRP) may be elevated in rheumatoid arthritis. 2. Synovial fluid analysis in OA shows yellow, clear fluid with a normal viscosity and less than 2,000 white blood cells per microliter, indicating no inflammation. Elevated erythrocyte sedimentation rate and CRP would suggest rheumatoid arthritis over OA. 3. The most common joints affected by OA are the hips, knees, hands, fingers, big toe,

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 26

    LABORATORY IN MUSCULO SCELETAL DISORDERS

    INTERPRETING LABORATORY RESULT


    The major purpose of performing analyte determinations in the clinical
    laboratory is to aid in the diagnosis an management of patients with
    disease and individuals in health assessment.

    Diagnosis of Degenerative Joint Disease


    Diagnosis is based on the medical history, physical examination, and x-ray
    findings. Lab tests do not reveal signs of inflammation, but may be
    performed to rule out other arthritic disorders.
    OSTEOARTHRITIS (OA)/ DEGENERATIVE JOINT DISEASE (DJD),
    The most common form of arthritis,
    Affecting about 20 million people in the United States.
    OA is associated with joint injury and with the aging process.
    A chronic disease that causes deterioration of the joint cartilage
    and the formation of new bone (bone spurs) at the edges of the
    joints
    Cartilage and synovial fluid
    NORMAL : Provide a smooth, low friction transition
    between the ends of bones.
    ABNORMAL :
    When cartilage loses its elasticity ---- joint movement
    becomes less smooth.
    Eventually cartilage can completely erode and the
    opposing bone ends can rub together.
    This leads to pain that may be intermittent or chronic, to
    stiffness in the morning and after rest, to small pieces of
    bone and fragments of cartilage in the remaining
    synovial fluid, and to a loss of mobility.
    OA occurs equally in men and women before age 55 but more often
    in women after that age.
    Also common in athletes who sustain multiple joint injuries over
    time.
    Causes
    The primary cause is mechanical (for example, joint damage caused
    by running or excess weight-bearing)
    Another causes : metabolic, genetic, or chemical .
    Obesity, muscle weakness, and other diseases (rheumatoid arthritis
    and hemo chromatosis) can increase the risk of developing OA.

    The joints most commonly affected by OA :


    hips, knees, hands and fingers, big toe, neck, and lower back.
    The goal of testing
    1.Diagnose OA, to distinguish it from other forms of arthritis and causes
    of joint pain and stiffness
    2.Monitor the side effects of various treatments.

    Diagnosed OA based on :
    1.Patients medical history,
    2.Physical exam
    3. X-rays,
    4.In some cases with an examination of synovial fluid from an affected
    joint.

    Laboratory test :
    There is no specific laboratory test to diagnose OA.
    1.Rheumatoid factor (RF) and Cyclic Citrullinated Peptide Antibody (CCP)
    CCP and RF ( + ) in Rheumatoid arthritis ----- used to help diagnose
    rheumatoid arthritis and differentiate it from osteoarthritis.
    2.Synovial fluid analysis
    To detect crystals that may be present in the joint and to look for
    signs of joint infection.
    3.Erythrocyte sedimentation rate ( ESR)
    Test shows the presence of inflammation in the body.
    ESR will be increased in RA but not in OA/osteoarthritis.
    4.C-reactive protein test (CRP) this test also indicates
    inflammation and tests for the activity of the disease.
    An increased level of CRP occurs in RA but not in OA.
    5.Complete Blood Count (CBC)
    It may be ordered to monitor the side effects of some OA
    treatments.
    6.Comprehensive Metabolic Panel (CMP) this is a group of tests
    that may be used to help evaluate and monitor the patients kidney
    and liver function.
    Laboratory test for Joint diseases
    1.OSTEOARTHRITIS
    Laboratory tests are normal and not helpful.
    Synovial fluid Color : Yellow clear, non inflamatory ( < 2000 WBC/uL)
    Viscosity : Normal.
    2.ARTHRITIS ASSOCIATED WITH SYSTEMIC DISEASE
    1) Arthritis associated with Hemochromatosis
    Degenerative arthropathy occurs in > 20 % of these patients
    Laboratory : Finding of hemochromatosis : Serum Iron increase
    Rheumatoid Factors : negative
    Synovial fluid : Color : pale yellow, non inflammatory
    Viscosity : adequate,

    2)Arthritis associated with Inflammatory Bowel Disease( Ulcerative


    colitis/Regional enteritis
    Joint fluid is sterile ( both microscopical & bacteriological )
    Absent RF and ANAs
    Another Lab finding due to Bowel disease : Increase CRP, ESR, WBC,
    Platelets

    3.POLYMIALGIA RHEMATICA
    Lab : ESR increase ( usually > 60 mm/hr) for 1 month
    Anemia of chr disease is commonly present
    WBC increase in some patients
    Proteins : Albumin commonly decrease
    Alf 1 & Alf 2 glob & Fibrinogen : commonly increase
    RF : neg (only 10 % positive of patient over 60 without arthritis)
    AST & ALT increase in one third of patient
    4.RHEMATOID ARTHRITIS (RA)
    Diff : Progressive systemic autoimmune disease with chronic inflammation of
    synovial tissues of unknown etiology
    Laboratory :
    a) Anti Cyclic Citrillinated Peptide ( anti CCP ; citrulline
    antibody)
    - Newly discovered immune protein.
    - Sensitivity/ Specificity : 41 80 %.
    - anti CCP detected by ELISA constitute
    early specific markers for RA .
    - The new generation of ELISA is claimed to reach 98 % specificity for
    diagnosis of RA, with 70 % sensitivity (except in child sensitivity 0,2 3%),
    which is mayor improvement over RF test.
    - Anti CCP antibodies can be detected in 50 % of patients with early RA , at
    the time when RF is negative ----improve early diagnosis --- improve early
    treatment.
    b) IgM RF :
    - Positive ( + ) in 50 -90 % RA patients ( Sensitivity/Specivisity : 71 % /
    89%) but in 6 months of illness only positive in 40 % of patients.
    - RF not specific for RA. Often positive in : other immune disorders,
    Hepatitis , TB , and 5 % healthy person.
    - For screening : use slide test, to confirm positive result with tube
    dilution. Significant titer is > 1/80. (method : ELISA,nephelometry)
    - Give useful objective evidence of RA , but negative result
    does not rule out RA ( 1/3 cases are negative.)
    c) ANA Profile :
    RA nuclear antigen is founds around 80 % of patients, ( frequently
    present in Sjogren syndrome, less often in other connective tissue
    disease)
    d) Others :
    - ESR , CRP : Increase in Rheumatoid Arthritis (95% patient)
    Used as guide to activity and to therapy , but may be normal in 5 %
    patients
    - Serum Protein Electrophoresis
    Increase in Globulins, especially in Gamma and Alfa 2, decrease in
    Albumin.
    - Erythrocyte
    Anemia normocytic hipochromic of chronic disease with decrease
    Serum Iron , normal TIBC and normal Iron Stores. Anemia diminishes
    as patient goes into remission or respond to therapy.
    - Serum CK decrease in 60 % of patients
    5.GOUT
    Laboratory:
    Serum uric acid : elevated ( >7,5 mg/dL) in 95 % of patients who have
    serial measurement during the course of an attack. How ever , single
    uric acid determination is normal in up 25 % of case, so it does not
    exclude gout, especially in patient taking uricopenic drug.

    During the acute attack, the ESR and WBC frequently elevated. Material
    aspirated from topus shows the typical crystals of sodium urate and
    confirm diagnosis .
    Laboratory tests for bone diseases:
    Use :
    - To identify patients suitable for therapy
    - To estimate response to therapy for osteoporesis over period of months to years in
    conjunction with bone mineral density.
    - Bone formation markers of osteoblast activity : Bone specific alkaline phosphates,
    osteocalcin, procollagen type I.
    - Bone resorption markers of osteoclast activity : TRAP Tartrate resistant acid
    phosphatse, hydroxyproline , pyridoline, deoxy pyridoline, N telopeptide, C
    telopeptide, urine calcium.

    Acid Phosphatase , Tartrate- Resistant ( TRAP), Serum


    Synthesized by osteoclasts in contrast to prostatic acid phosphatase that ia tartrate
    sensitive; also found in Kupfer cells and macrophages.
    Use : Marker of bone resorption
    Alkaline Phosphatase ( ALP) ,
    Synthesized by osteoblasts; is involved in calcification of bone
    matrix . Only 80% of total ALP is destroyed by heating along with
    non bone specific ALP
    Use :
    Marker of bone formation
    Increased in :
    Paget disease
    Primary hiperparathyroidism
    Osteomalacia
    Osteoporosis
    Pregnancy
    Hydroxyproline Urine
    Hydrolysis product of collagen Use
    Marker of collagen turnover
    Assess patients at risk for osteoporosis
    Classify patients with established osteoporosis
    Determine efficacy of therapy in osteo porosis or bone metastases
    Increased In :
    Increased collage catabolism ( especially Paget disease, hyperparathyroidism,
    acromegaly, psoriasis, burns)
    Certain inborn errors of metabolism ( eg, hidroxyprolinemia , familial
    aminoglycinuria)
    Osteocalcin ( Serum, Urine)
    Cytosolic calcium binding protein synthesized by osteoblasts during bone formation .
    Mayor noncollagen in bone .Excreted in urine by glomemerural filtration.
    Use
    Marker of bone turn over rather than just of resorbtion or formation
    Assess patients at risk for osteoporosis
    Classify patients established osteoporosis
    Determine efficacy of therapy in osteoporosis or bone metastases
    Increased in :
    Increase bone formation ( eg Paget disease, primary hyperparathyroidism, healing
    fractures, osteogenic sarcoma, hyperthyroidism, effective therapy for osteoporosis
    Decreased in :
    Hypoparathyroidism
    Cusshing syndrome
    Laboratory test for Skeletal Muscle Disease :
    CREATINE KINASE TOTAL ( CK TOTAL)
    CK total : CK MB + CK BB + CK MM
    CK isoenzymes
    Iso enzymes of CK : CK MB, CK BB, CK MM
    % Activity distribution of CK Isoenzymes in tissue.

    CK - MM CK - MB CK - BB
    Skeletal 99 1 0
    muscle
    Myocardium 22 77 1

    Brain 4 0 96
    Serum enzyme in Disease of Muscle :
    CK MM is the test of choice . It is more specific and sensitive than
    AST and LD
    Increases in :
    Polymyositis
    Muscular dystrophy
    Myotonic dystrophy
    Some metabolic disorders
    Malignant hyperthermia
    Prolonged exercise; peak 24 hours after extreme exercise ( eq
    marathon) ; smaller increase in well conditioned athletes.
    Wilms tumors with rhabdomyomatous features ( Ck MB also
    increased)
    Normal in :
    Sleroderma
    Acrossclerosis
    Discoid LE
    Muscle atrophy of neurologic origin ( eq , old poliomyelitis,
    polyneuritis)
    Hyperthropy myophaty

    Decreased in :
    2/3 of patients R A
    MYOGLOBINURIA
    Myoglobin urine: Normal negative or < 20 ng/mL.
    Myoglobin is the red pigment in the muscle that is responsible for its color.
    Myoglobin is exclusive to striated and non striated skeletal or cardiac muscle .
    It functions in short term oxygen storage , carrying the muscle from one
    contraction to the next.
    It is released into the interstitial fluid with elevated
    serum levels directed as early as 30 60 minutes after a
    myocardial infark or damage to any muscle tissue ,
    remains detected in urine up to 7 days later.
    When the muscle cells are damaged, from any cause, some of the myoglobin is
    liberated from the cells into the blood stream. They are collected in the kidneys,
    where they lead to discoloration of the urine.
    The myoglobin may damage the kidney leading to renal failure when it is severe.
    Causes of Myoglobinuria
    - Paroxysmal myoglobinuria may produce this and is unknown cause.
    - Crush injury to the muscles or
    - Surgical damage to the muscles can lead to myoglobinuria.
    - Stupor or coma which produces pressure injury to a muscle .
    - Prolonged seizures can lead to disruption of the muscle.
    - Acute alkohol intoxication with acute or chronic muscular disease
    - Severe burn
    - Barbiturate toxicity
    - Diabetic acydosis
    - Glycogen and lipid storage diseases
    - Severe hyper/hypotermia
    - Severe hypo kalemia and hipophosphatemia
    - Myocarditis / MCI
    - Myositis / rhapdomyolisis/ trauma/muscular dystrophia
    - Renal failure
    - Herbs or natural intoxication include licorice (Glycyrrhiza glabra)
    Signs and Symptoms of Myoglobinuria

    Urine appears dark or Coca-Cola dark /coffee colored or red urine.


    Pain and tenderness in the affected muscles.
    May be weakness of the damaged muscles or low back pain.
    In severe case : Renal failure may lead to decreased urine output
    and weight gain.

    Dep Stick Urinalysis : Blood (+) ----- hemoglobin or myoglobin ----


    need sediment urine examination
    BIBLIOGRAPHY:
    1. Jacques Wallach : Interpertation Diagnostic Test (338-367) .
    Lippincott Williams & Wilins 2007.
    2. Henry S : Clinical Diagnosis and Management by Laboratory
    Methods. 23 th ed . Saunders Elsevier 2017.
    3.Cynthia C Chernecky , Barbara J Berger: Laboratory Tests and
    Diagnostic Procedures (983 -984). Saunders Elsevier 2008.
    4. John MS. Pearce, R. J. Pennington and John Walton. Serum
    enzyme studies in muscle disease Part II Serum creatine kinase
    activity in muscular dystrophy and in other myopathic and
    neuropathic disorders . J Neurol, Neuro surgery, Psychiat. 1964
    (27,96)
    5. Anne C. Poinier, Nancy Ann Shadick, : Rheumatology
    September 9, 2014

    You might also like