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APPROACH TO ARTICULAR AND MUSCULOSKELETAL DISORDERS

Emmanuel C. Perez, MD, MPH March 6, 2014; 1:00-3:00 PM Internal Medicine


I only see grown men cry when: they see their first born, when their favourite basketball or sports team wins the series, an d when they have gout. Dr. Perez OUTLINE Pain in or around a joint Evaluation of patients with musculoskeletal complaints Approach to patient with articular and musculoskeletal complaints Drug-induced musculoskeletal conditions Arthritis Specific types of arthritis OBJECTIVES To localize musculoskeletal complaints by differentiating between clinical features of articular and non-articular conditions To determine the nature of the pathology by distinguishing between inflammatory and noninflammatory articular conditions To discuss specific physical examination maneuvers employed in articular and musculoskeletal disorders To discuss appropriate laboratory, serological examinations and ancillary procedures used in the diagnosis of articular disorders To differentiate between normal and pathologic synovial fluid characteristics

Laboratory examinations Arthrocentesis Imaging procedures Algorithm for the diagnosis of musculoskeletal complaints Case

To present an algorithm for the evaluation of


articular and musculoskeletal disorders

PAIN IN OR AROUND A JOINT


Musculoskeletal complaints are usually due to pain, and you must differentiate whether the pain was emanating from certain structures or from a certain pathologic condition The history helps define the pathology Mechanical vs. inflammatory The physical examination helps define which anatomical part in involved Articular vs. periarticular or somewhere around the joint vs. referred

EVALUATION OF PATIENTS WITH MUSCULOSKELETAL COMPLAINTS


Anatomic localization of complaints Articular vs. non-articular Determination of the nature of the pathologic process (take note of the hallmarks of inflammation: Calor, rubor, tumor, dolor, and function laesa) Inflammatory vs. non-inflammatory Determination of the extent of involvement Monoarticular vs. polyarticular Focal vs. widespread Determination of chronology Acute vs. chronic JOINT ANATOMY It is important to differentiate which structures are closely associated to joints and which are non-joint structures. When were talking about the joint, these particular parts are involved: Hyaline articular cartilage Joint space Fibrocartilaginous pads Synovium Joint capsule Anything other than the items mentioned like the bones, skin and subcutaneous tissue, soft tissue structures like bursa, enthesis, tendons and tendon sheaths, and muscles are all periarticular or non-articular. For example, if there is inflammation of the synovium, you have synovitis and it is a hallmark of arthritis. If you have destruction of the hyaline articular cartilage, then that may be a form of pathology involving a specific part of arthritis.

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ANATOMIC LOCALIZATION OF COMPLAINTS ARTICULAR Deep or diffuse pain Limited range of motion on BOTH active and passive movement Swelling, bone crepitation, joint instability, locking or gross deformity on physical examination

NON-ARTICULAR Point or focal tenderness Limited range of motion ONLY on active movement Physical findings remote from the joint capsule

For example, if you have inflammation of the bursa, or inflammation of the tendons or ligaments, then you would definitely have point or focal tenderness. DETERMINATION OF THE NATURE OF THE PATHOLOGIC PROCESS INFLAMMATORY NON-INFLAMMATORY Infections, crystal induced, immune- related, Trauma, repetitive use through recreational or reactive or idiopathic occupational activities, ineffective repair/ degeneration, neoplasm, pain amplification Cardinal signs of inflammation Pain but without the cardinal signs of inflammation If not all are present, at least majority of Theres usually an absence of warmth, sometimes them. So there has to be a form of swelling, with minimal swelling, but usually no rubor or calor redness, warmth, etc. (+)Systemic symptoms No systemic symptoms (minimal morning stiffness) Arthritis in association with skin manifestations or eye conditions, or pathologies in the GIT or in the kidneys Laboratory evidence of inflammation Normal lab exams CAUSES OF MORNING STIFFNESS INFLAMMATORY Precipitated by prolonged rest Several hours in duration IMPROVES with activity and NSAIDs (usually improves before lunch, or it could take 2-3 hours for severe inflammatory arthritis. It basically improves within the day when the patient starts moving the joints and taking NSAIDs)

NON-INFLAMMATORY Precipitated by brief periods of rest Lasts <1 hour, sometimes 10-15 minutes Exacerbated by activity

Dr. Perezs example: For non-inflammatory, think of osteoarthritis. Old individuals who sit for long periods of time, watching TV, then they start to rise up from their seats, they will have stiffness of the joints. And it is usually precipitated by brief periods of rest whether youre lying down or sitting. In contrast to that, when you have Rheumatoid Arthritis which is a highly inflammatory arthritis, morning stiffness is most prominent upon waking up.

APPROACH TO PATIENT WITH ARTICULAR AND MUSCULOSKELETAL COMPLAINTS


PATIENTS PROFILE Age: Young vs. elderly Degenerative osteoarthritis is usually seen in the advanced age group but you may develop osteoarthritis earlier on as a function of your recreational activities or your job. For example, athletes are very prone to develop osteoarthritis on weight-bearing joints. (Here he used the recent winter Olympics competitor Michael Martinez (18 years old) as an example) Gender: Male vs. female Gouty Arthritis, as seen in Harrisons, is more common in middle-aged MEN but sometimes its not appropriate anymore because we can now see people younger than 40 with this complaint. On the other hand, Rheumatoid Arthritis is common among middle-aged FEMALES and is usually polyarticular. Race: Americans vs. Africans vs. Asians Familial aggregation or family history CHRONOLOGY OF THE COMPLAINT Onset: Abrupt vs. indolent Evolution: Chronic, intermittent, migratory, additive Duration: Acute vs. chronic EXTENT OF JOINT INVOLVEMENT Number and distribution of involved joints: Mono- vs. Oligo- vs. Polyarticular Focal vs. Widespread Symmetric (both knees, both wrists, etc ) vs. Asymmetric (one knee only) Upper vs. Lower extremities vs. Spine

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PRECIPITATING FACTORS Trauma (He emphasized this over and over again. It is very important to elicit this in the history.) Drug exposure Antecedent or intercurrent illness Diabetes mellitus Renal insufficiency Myeloma/ cancer RHEUMATOLOGIC HISTORY (IN SUMMARY) Is the problem: Regionalized (localized) vs. Generalized Symmetric vs. Asymmetric Peripheral vs. Central Acute vs. Subacute vs. Chronic Self-limiting vs. Progressive

Do symptoms suggest inflammation or damage to musculoskeletal structures? Any evidence of a systemic process? Any extraarticular features? Other organ involvement? Any functional loss and disability caused by deformities? (especially in chronic arthritis) Any family history of arthritis? Past medical history Medications (NSAID use) especially in chronic arthritis where patients abuse pain medications Previous surgical procedures Family history Personal/ social history Functional limitation and disability Psychosocial consequence of disease Review of systems

DRUG-INDUCED MUSCULOSKELETAL CONDITIONS


CONDITION ARTHRALGIAS DRUGS ASSOCIATED Quinidine, cimetidine, quinolones, IL-2, interferon, nicardipine, rifambutin, chronic acyclovir, vaccines, aromatase and HIV protease inhibitors Dr. Perezs example: His patient was a 23 year old call center agent presenting with severe arthralgia. Upon examination, there was no inflammation of the joint but there is severe joint tenderness on range of motion. And then by further probing into the history, the patient disclosed that he was HIV positive and he was already on certain medications for it. MYALGIAS/ Steroids, penicillamine, HCQ, AZT, statins, clofibrate, interferon, IL-2, alcohol, cocaine, MYOPATHY colchicine, taxol, docetaxel, quinolones, cyclosporine Myalgias are common in dyslipidemic patients using statins and other enzyme inhibitors. TENDON RUPTURE Quinolones, steroids GOUT Diuretics, aspirin, ethambutol, alcohol, cytotoxic agents, cyclosporine, moonshine Referrals from patients of cardiologists given diuretics which triggered acute attacks of gouty arhthritis. OSTEOPENIA Steroids, chronic heparin, phenytoin, methotrexate DRUG-INDUCED Hydralazine, procainamide, quinidine, phenytoin, INH, carbamazepine, methyldopa, LUPUS chlorpromazine, lithuim, ACE-inhibitors, penicillamine, TNF-inhibitors tetracycline, ticlodipine OSTEONECROSIS Steroids, alcohol, radiation, bisphosphopnates SCLERODERMA Vinyl chloride, bleomycin, organic solvents, carbidopa, pentazocine, tryptophan, grapeseed oil VASCULITIS Allopurinol, amphetamines, TNF-inhibitors, cocaine, thiazides, penicillamine, propylthiouracil, montelukast, hepatitis B vaccine, trimethoprim/sulfamethoxazole I know, toxic table. Good thing Dr. Perez said to only familiar with Gout, Myalgia and Arthalgias conditions. RHEUMATIC ROS Fever Rash Nail abnormalities Myalgia Weakness Organ involvement: Eyes GIT Genitourinary Nervous system

ARTHRITIS
PRINCIPLES OF RHEUMATOLOGIC EXAMINATION Screening musculoskeletal exam: GALS Cardinal signs of articular inflammation Joint motion (passive and active ROM) recall articular versus non-articular Deformities (loss of alignment & loosening of soft tissue structures) Muscle weakness (manual muscle testing) & atrophy Gait disturbance involving the knee or hips, if the patient has poliomyelitis or had a history of stroke Other organ systems: integument, eyes, etc.

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HISTORY History of previous trauma to specific joint Past or family history of arthritis/ connective tissue disease History of past sexual contacts or genitourinary infections or high-risk behavior Gastrointestinal symptoms: Bowel irregularity/ diarrhea or bloody stool Recent food poisoning Symptoms of inflammation of the eyes/ skin/ spine or sacroiliac joints

PE OF THE JOINTS Stability Deformities Ligamentous destruction, contractures, bony enlargement, ankylosis involving the spine, erosive disease (commonly seen in radiographs) or subluxation, valgus/ varum involving the knees Presence of effusion Dislocation Range of motion or inflexibility Crepitus

68 year old woman with Rheumatoid Arthritis This patient could probably have Boutonnieres deformity or hyperextension of the distal interphalangeal joints, flexion of the proximal interphalangeal joints, and remarkable ulnar deviation of the phalanges in relation to the metacarpophalangeal joints. In medicine, when in doubt, refer to yourself as being normal.

21 year old electrician with Chronic Tophaceous Gouty Arthritis This patient has a history of chronic arthritis since he was 105 years old. He has soft tissue swelling or tumor on top rd th of the 3 metacarpophalangeal joint as well as in the 4 metacarphophalangeal joints. If elevated uric acid is left untreated, they can deposit in the soft tissue structures near the joints or worse, be deposited in the kidneys.

Patient with Psoriatic arthritis There is swelling at the second and third th th metacarpophalangeal joints, between the 4 and the 5 ones, also in the distal interphalangeal joints. The most striking feature is the rashes.

69 year old retired teacher with Osteoarthritis Patient presents with deformities in the hands involving the bony prominences, the distal and proximal interphalangeal joints, and even the thumb has a zdeformity. Also, bow-legged deformity in the legs aside from the varicose veins (genu varum) is also present.

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EXAMINATION AND CLINICAL CORRELATION Genital examination (i.e. balanitis) and microbiologic examination of the urethra or cervix, even among asymptomatic sexually active patients Psoriasis (including nails and scalp); alopecia (associated with SLE, other connective tissue disease, genetic predisposition, dermatophytoses, fungal infections, hyperthyroidism, or hypothyroidism) or other skin rashes Tophi (ears, hands or feet) Tendinitis: seen typically with Gonococcal arthritis

Rheumatoid nodules over pressure points Spine and sacroiliac joints for evidence of spondylitis Ophthalmologic evaluation: conjunctivitis, scleritis or uveitis Metabolic conditions such as ochronosis or Wilsons disease may rarely present as monoarthritis Microscopy and culture of stool, even when patients are asymptomatic

SPECIFIC TYPES OF ARTHRITIS


I. ACUTE MONOARTHRITIS Bacterial arthritis Septic arthritis Diabetes Immunosuppressed individuals and chemotherapy patients Constant use of steroids Gout (inflammatory type or crystal-induced) Spondyloarthropathy Juvenile Rheumatoid Arthritis Hemarthrosis Trauma Anticoagulant therapy Leukemia (common in younger patients) Rheumatoid arthritis Sarcoid arthritis Hemarthrosis Coagulopathy Dialysis arthropathy Osteochondromatosis Pigmented villonodular synovitis (PVNS) II. CHRONIC MONOARTHRITIS Must rule out whether infection is present for 6 weeks already or 2-3 months. Non-Infectious Osteoarthritis (usually involves 1 or 2 joints and affects weight bearing joint) Spondyloarthropathy Monoarticular RA Osteonecrosis CPPD Sarcoid arthropathy Neoplasms Infectious Tuberculous Pyogenic bacterial (if left untreated) Fungal Lyme disease (common in patients with history of international travel; a tick-borne infection acquired through travel to rocky mountain areas) III. ACUTE POLYARTHRITIS Migratory Rheumatic fever (common in the Philippines and with predilection for the PEDIATRIC age group) Post-Streptococcal Rheumatic Fever (a variant of Rheumatic Fever but without the cardiac manifestation) Disseminated Gonococcal Infection (acute joint inflammation, usually involving the bigger joints like in the knees, hands, with tendinitis and unusual rashes) Viral arthritis (i.e. Chikungunya - common in patients with history of international travel) Lymes disease Non-Migratory Rheumatoid arthritis SLE Polyarticular gout Polyarticular JRA Serum sickness Hematologic disorders IV. CHRONIC POLYARTHRITIS RA SLE Polyarticular gout (must be differentiated from Rheumatoid Arthritis) Polyarticular JRA Connective tissue disease Scleroderma PM/ DM MCTD Spondyloarthropathy Sarcoid arthritis V. ARTHRITIS-RASH SYNDROMES Viral arthritis Rheumatic fever (rash: Erythema marginatum) Gonococcal arthritis Reiters syndrome Psoriatic arthritis Systemic lupus erythematosus Dermatomyositis Scleroderma Vasculitis (Henoch-Schonlein purpura) Erythema nodosum

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LABORATORY EXAMINATIONS
Acute phase reactants Rheumatoid factor Antinuclear antibody (ANA) Specific autoantibodies associated with connective tissue diseases Antineutrophil cytoplasmic antibodies (ANCA) Complements Cryoglobulin Others: CBC, Urinalysis, BUA, ASO titer, etc.

DIAGNOSTIC CLUES FROM BASIC LABORATORY EXAMS Complete blood count Anemia and thrombocytopenia which denotes systemic involvement: SLE, vasculitis Leukopenia: SLE Erythrocyte sedimentation rate Usually elevated in ALL inflammatory arthritis Urinalysis Pyuria: Reiters (if you are looking at a reactive type arthritis) Proteinuria, hematuria, cylinduria, and casts: SLE, HSP (Henoch-Schonlein Purpura) OTHER LABORATORY TESTS Azotemia: Poor prognosis in SLE, vasculitis AST, ALT elevation: Hepatitis or myositis (In cases of hepatic or muscle involvement, creatinine will be elevated, as well as the transaminases) Hypocomplementemia: SLE Arthrocentesis Differentiate from non- inflammatory vs. inflammatory vs. septic Crystal identification ANTINUCLEAR-ANTIBODY (ANA) PATTERNS AND CLINICAL ASSOCIATIONS ANA PATTERN DIFFUSE PERIPHERAL NUCLEOLAR CENTROMERE SPECKLED ANTIGEN IDENTIFIED Deoxyribonucleoprotein Histones Ds-DNA RNA polymerase I Kinetochore U1-RNP Sm Ro (SS-A) La (SS-B) Scl-70 PM-1 Jo-1 CLINICAL CORRELATION Non-specific Drug-induced lupus 50% of SLE (specific) 40% of PSS 75% CREST (limited scleroderma) >90% of MCTD 30% of SLE (specific) 60% of Sjogrens, SCLE, neonatal lupus, ANA (-) lupus 50% of Sjogrens, 15% lupus 40% of diffuse scleroderma Polymyositis (PM), dermatomyositis PM with pneumonitis + arthritis

ARTHROCENTESIS
Withdrawal of synovial fluid from an effused joint which has diagnostic as well as therapeutic role This is also used to rule out gouty arthritis regardless of an increase or decrease in uric acid Contraindications Infection in overlying skin or soft tissue Severe coagulation disorder Diagnostic SF exam including crystal identification Therapeutic Relieve pain by decreasing joint pressure Instillation of steroids and other antiinflammatory medications to prevent reaccumulation of fluid

Man with gout due to alcohol bingeing undergoing anthrocentesis

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GROSS EXAMINATION OF SYNOVIAL FLUID

Viscosity

Mucin Clot

Color

Clarity

MICROSCOPIC EXAMINATION OF SYNOVIAL FLUID 3 WBC and differential count 200 to 2000 cells/mm Special stains Wrights stain, Gram stain, Congo red stain, PAS stain, Prussian blue stain, Alizerin Red-S stain

COMPENSATED POLARIZED MICROSCOPIC EXAMINATION (under the light microscope)

MSU Crystals -crystals outside the cell

Crystal Pyrophosphate Dihydrate (CPPD) Crystals -crystals engulfed by the cell

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MICROBIOLOGIC STUDIES Gram stain and Acid-fast stain methods Preferred since results are quickly obtained and it could be established whether the arthritis is due to microbial organisms Culture studies to isolate microorganisms using appropriate culture media

SYNOVIAL FLUID CHARACTERISTICS Usually, we have <8-10 mL; if underweight, <5mL. If exceeding 15mL, high index of suspicion GROUP I NONINFLAMMATORY >3.5 ml High Straw Transparent Firm 200-2,000 <25 (-) GROUP II INFLAMMATORY >3.5 ml Variable Variable Transluscent/ opaque Friable 2,000-50,000 Often >50 (-) GROUP III SEPTIC >3.5 ml Low Purulent Opaque/ pus-like Friable > 100,000 >75 (+)

NORMAL VOLUME VISCOSITY COLOR CLARITY MUCIN CLOT 3 WBC/MM PMNS (%) CULTURE <3.5 ml Very high Yellow Clear/ transparent Firm <200 <25 (-)

In terms of viscosity, the synovial fluid becomes less viscous when inflammatory cells are present as seen in inflammatory and infectious arthritis. Highest WBC count is observed in Septic Arthritis. DIFFERENTIAL DIAGNOSIS BY JOINT FLUID GROUPS GROUP I NON-INFLAMMATORY Osteoarthritis Avascular necrosis Osteochondritis dessicans Villonodular Synovitis GROUP II INFLAMMATORY Rheumatoid arthritis Crystal-induced arthritis Psoriatic arthritis Reactive arthritis SLE Rheumatic fever Scleroderma Amyloidosis Myxedema Ochronosis GROUP III SEPTIC Bacterial arthritis TB arthritis GROUP IV HEMARTHROSIS Trauma Charcots joint Hemorrhagic diasthesis Hemophilia joint Hemangioma PVNS High levels of anticoagulants

INTERPRETATION OF SYNOVIAL FLUID ASPIRATION

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IMAGING PROCEDURES
X-rays CT scan MRI Ultrasound Bone scan (scintigraphy) Bone mineral densitomety (DXA)

Radioimaging modalities are not usually requested when dealing with Acute Monoarthritis but when you are highly suspecting that there are soft-tissue tears, for example a basketball player or a football player comes to you limping, complaining of pain in the knees and theres some sort of effusion then X-rays will not be appropriate to obtain in this patient because soft tissue structures would not show clearly on x-rays. You might have to use CT scan or MRI. Sometimes patients would complain of swelling in the popliteal area, which means there is some form of cystic lesions which is diagnosed through ultrasound.

Advanced Osteoarthritis on x-ray: diminution or joint spaces or joint space narrowing in the medial portion. As Dr. Perez said, may matatalas na buto.. nagkakanto na siya. Kasi usually ang bones natin very smooth ang bone surface area niya no, pag medyo nagka-kanto na tumutulis na siya, that is a hallmark of osteoarthritis.

Osteoarthritis of the hips. Delineation of the joint space is not seen

DIAGNOSTIC IMAGING TECHNIQUES FOR MUSCULOSKELETAL DISORDERS You might want to study this cause theres probably an exam question from this table, okay? Dr. Perez METHOD ULTRASOUND RADIONUCLIDE SCINTIGRAPHY
99M

IMAGING TIME (HOUR) <1 1-4

COST + ++

CURRENT INDICATIONS Synovial cysts, rotator cuff tears, tendon injury Metastatic bone survey, evaluation of Pagets disease, acute and chronic osteomyelitis Acute infection, prosthetic infection, acute osteomyelitis Acute and chronic infection, acute osteomyelitis Herniated intervertebral disc, sacroiliitis, spinal stenosis, spinal trauma, osteoid osteoma, stress fracture AVN, osteomyelitis, intraarticular derangement and soft tissue injury, derangements of axial skeleton and spinal cord, PVNS, herniated intervertebral disc, inflammatory and metabolic muscle pathology

TC
111

IN-WBC
67

24 24- 48 <1 -2

+++ ++++ +++ +++++

GA COMPUTED TOMOGRAPHY MAGNETIC RESONANCE IMAGING

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EVALUATION OF PATIENTS WITH MUSCULOSKELETAL COMPLAINTS


GOALS Accurate diagnosis early on Timely provision of therapy/ treatment Avoidance of unnecessary diagnostic testing APPROACH Anatomic localization of complaint Determination of the nature of the pathologic process, extent of involvement & chronology Consider the most common disorders first Formulation of differential diagnosis

ALGORITHM FOR THE DIAGNOSIS OF MUSCULOSKELETAL COMPLAINTS Initial rheumatic history and physical exam to determine whether pain: Is it articular or periarticular? Is it acute or chronic? Is inflammation present? How many / which joints are involved?

CASE
SALIENT FEATURES 35 M 3 days Right Knee Joint pain and swelling with no associated fever and history of trauma = ACUTE Slight relief of pain with intake of Paracetamol Doc ano pong trabaho niya? Male executive Physical activity? Hes so busy in office he doesnt really have any recreational activities Diet preference? Mahilig uminom kasi diba sila ay madalas may ineentertain na clients, syempre pag may iniinom, may kasamang pulutan Family history? Nothing significant Progression of the pain throughout the day? He initially said that it started middle of the night o madaling araw, and for the past 3 days nagiincrease yung intensity ng pain. So, within the first 24 hours, di na siya makapag-sapatos, at hirap na siyang maglakad Any maintenance medication? He is taking maintenance medication for his heart condition. I think he has Diuretics, and he has Aspirin.

HISTORY AND PE History of hypertension for the past 3 years with current medications of furosemide, captopril, and low dose aspirin PE: overweight with stable vital signs, knee joint was warm, effused and tender with pain, limited range of motion Any rashes? None Tophi? None found. No subcutaneous nodules noted on PE Myalgias? None. Masakit lang yung tuhod niya. Masakit both on active and passive range of movement. Hindi mo nga mahawakan nang hindi umaaray Mainit po ba? Yes. INITIAL MANAGEMENT (refer to the algorithm) Doc: What do you request for? Batch: Complete Blood counts for WBC levels to rule out infection; increased WBC, shift to the right on differential count, predominance of segmenters; Doc: Why do you want to request for Uric Acid? To document whether there is hyperuricemia because usually gout is associated with a history of hyperuricemia. Assuming that this is Gouty arthritis: Management 1: Colchicines and Diclofenac (antiinflammatory medications, COX2 inhibitors, celecoxib, indomethacin, ibuprofen, mefenamic acid, ketorolac, ketoprofen, naproxen)

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Basically, any anti-inflammatory medication can be given in combination with colchicines which is your anti-gout medication There was only relief of pain but persistence of the knee swelling over the next 6 weeks with additional sites of joint tenderness and swelling developing on the left elbow and small joints of the hands (MCP/PIP) as well as morning stiffness probably progressed to Chronic Polyarthritis Subsequently given Allopurinol to lower down the uric acid levels DIAGNOSTICS Additional laboratory exams done revealed ESR >100mm/hour, (+) CRP, (-) RF inflammatory markers not quite in the range of septic arthritis so it might be inflammatory arthritis Arthrocentesis of the knee joint revealed yellowish, slightly turbid synovial fluid with WBC 3 count 5,000/mm (mostly PMNs); no crystals were seen with both gram stain and cultures, (-) for microbes Radiographs of the knee were normal

CONTINUING MANAGEMENT Management 2: Steroids (i.e. prednisone, hydrocortisone, dexamethasone, methylprednisolone) with Proton Pump Inhibitors (i.e. omeprazole) Just be cautious that the patient does not develop side effects of steroids which is usually gastrointestinal; for acute conditions, just give the short-acting ones The patient claimed better pain relief with diminution of joint swelling within the next 2 weeks; subsequently, he noted appearance of dandruff and pruritic scaly plaques on his torso and upper extremities REFERRALS AND DEFINITIVE MANAGEMENT Dermatology consult revealed family history of psoriasis with subsequent confirmation via skin biopsy; he was prescribed topical steroids and other emollients Further management: maintain steroids with additional DMARDs (i.e. MTX); option of adding biologic therapy (TNF- blocker) for control of both skin and joint manifestations of psoriasis

-ENDTRANSCRIPTION DETAILS
BASIS REMARKS To the transcriber of this particular topic who wishes to remain anonymous. 1 out of 3 for Evals 6. Dr. Perez highly recommends the students to read and study the book because all questions in the examination will be based there. Past PPT RECORDINGS + NOTES + DEVIATIONS 5-10% CREDITS

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