2012-2013

Basics of

Rheumatology and Rehabilitation

STAFF OF
Rheumatology and
Rehabilitation
Department
 Preface
This book is written by the staff members of Rheumatology, Physical
Medicine and Rehabilitation Department, Faculty of Medicine, Mansoura
University. It has been made to provide, in brief, the basic knowledge of this
specialty in a systemic, concisely written, well-illustrated and comprehensive
manner to be easily memorized by the undergraduate students.
We hope that this book provides our students with adequate basic
rheumatological knowledge to make accurate clinical observations, arrive at
a diagnosis and be aware of relevant differential diagnosis. We hope that
this book can also provide our students with different modalities of physical
medicine and role of interdisciplinary rehabilitation program in different
medical conditions.
Also we hope that this book will be beneficial to general practitioner
helping them to diagnose and manage some medical disease with
rheumatological manifestation (how to deal with! And when to consult!).

Editor in chief Head of the department

Dr. Mohammed Kamal Prof. Ibraheem El.Boghdady
 STAFF MEMBERS
of Rheumatology, Physical Medicine and Rehabilitation Department
Faculty of Medicine
Mansoura University

Prof. Ibraheem El.Boghdady Dr. Hisham Habib

Prof. M. Fathy El.Batouty Dr. Sherein Mashaly
Prof. Wahid Soltan Dr. Shereif Refaat
Prof. Atif El.Ghaweet Dr. Sherein Olama
Prof. Seif El.Dein Farag Dr. Hamada Sayed
Prof. Amir Abd-Elrahman Dr. Inas Hammad
Prof. Salah Hawas Dr. Tamer El.Saeed
Prof. Basma El.Kady Dr. Abeer Fekry
Prof. Wafaa El.Tarshoby Dr. Reham Magdy
Prof. Abd-Elmoety Afify Dr. Rehab Abd-Elraof
Prof. Manal Awad Dr. Amr Okasha
Prof. Elwaleed Elshal Dr. Shereif Farrag
Prof. Adel Abd-Elsalam Dr. Amany El.Bahnasawy
Prof. Mona Mohsen Dr. Iman Abd-Elrazik
Dr. Mohammed Kamal Dr. Sherein Abd-Elrahaman
Dr. Hazem Youssef
Dr. Nanis Onsy
 CLINICAL EVALUATION OF A PATIENT WITH RHEUMATIC DISEASE

 Joint stiffness after rest may indicate

Rheumatism: is any painful disorder affecting the
musculoskeletal system including: joints, muscles, osteoarthritis (gelling).
connective tissues, soft tissues around the joints  Fibromyalgia.
and bones. Weakness
Rheumatology: science dealing with the diagnosis Caused by: muscle weakness, pain, mechanical
and management of painful conditions in
factors (e.g. tendon and joint impairment) and
musculoskeletal system from conservative aspect.
nerve damage.
The diagnosis of many rheumatic diseases is
mainly clinical. Limitation of movement
Caused by pain, contracture, arthritis, capsular
3 SIMPLE SCREENING QUESTIONS fibrosis (e.g. frozen shoulder).
1. Have you any pain or stiffness in your muscle, Deformities
joints or back? e.g. genu varus, genu valgum, Boutonnière
2. Can you dress yourself without any difficulty?
deformity, Swan-neck deformity, Dupuytren's
3. Can you walk up and down stairs easily?
contracture.
If any answer is positive to any question, then
detailed history must be obtained. ANALYZE SYMPTOMS

Precipitating Factor
ARTICULAR SYMPTOMS
e.g. recent trauma, administration of a new drug,
Pain recent infection … etc.
 Articular pain: localized to joint.
Acute or Chronic
 Non-articular pain: originates from peri-  Acute (<6 weeks duration): infectious arthritis,
articular structures e.g. tendon or bursae. gout.
 Referred pain: e.g. cervical spondylosis  Chronic: OA, RA.
presenting as shoulder pain.
Onset and Course of the Disease
 Inflammatory disease: joint pain tends to be
worse at night.  Slow insidious pattern: degenerative arthritis.
 Mechanical disorder: pain is worse at the end  Rapid onset, severe, self-limiting: Crystal-
of the day and after activity; relieved by rest. related inflammation.
 Remission and exacerbation: Inflammatory
Swelling
arthritis.
 Diffuse: synovial effusion; synovial
Inflammatory or mechanical in nature
hyperplasia.
 Localized: swelling of the structures Feature Inflammatory Mechanical
surrounding the joint (e.g. bursa); Heberden's Morning stiffness >1 hour <30
minutes
nodes; Bouchard's nodes. Fatigue Significant Minimal
Fatigue Activity Improve Worsen
symptoms symptoms
 Important feature of many rheumatic Rest Worsen Improve
disorders (e.g. rheumatoid arthritis and SLE). symptoms symptoms
 Prominent feature in fibromyalgia. Systemic involvement Yes No
Corticosteroid Yes No
Stiffness requirements

 Early morning stiffness: inflammatory arthritis Which Joints are Involved

(may last for several hours).  Peripheral: RA, OA, psoriatic.
 Axial: sero-ve arthropathy, OA.
3
Number of Joints Affected fibrosis or cardiac affection e.g. aortic
 Mono: Septic arthritis, trauma, crystal regurgitation (spondyloarthropathies).
arthritis  Neurological:
 Oligo (< 4 joints): Lower limb oligo-arthritis  Peripheral neuropathies, e.g. entrapment
in reactive arthritis. neuropathy e.g carpal tunnel syndrome.
 Poly (> 5joints): RA, SLE.  Migraine; depression; stroke (e.g. SLE,
vasculitis; antiphospholipid syndrome).
Symmetry
 Symmetric: RA, SLE, SSc, PM/DM. OTHER RELEVANT HISTORY
 Asymmetric: sero-ve arthropathy.
 Prodromal symptoms and events: Acute
Sequence of joint involvement rheumatic disease may follow events
 Additive: e.g. OA, RA. e.g. upper respiratory tract infections,
 Migratory: e.g. Rheumatic fever, viral diarrhoea, genitourinary infection, insect
arthritis. bites (e.g. Lyme disease) and vaccinations.
 Intermittent: e.g. gout.  Medication: e.g. hydralazine induces drug
induced lupus.
EXTRA-ARTICULAR SYMPTOMS  Past history: previous attacks of the
 Constitutional symptoms (fever, weight symptoms; psoriasis; diarrhea; risk
loss, fatigue): connective tissue disease of sexually transmitted infection.
(CTD), vasculitis.  Family history: inflammatory arthritis,
psoriasis.
 Nodules: RA; rheumatic fever; connective
tissue diseases; sarcoidosis; gout. EXAMINATION
 Mucocutaneous: SLE (malar rash; discoid
General
lesion; alopecia; oral ulcers), psoriasis,
Behcet's disease (oral ulcer), Reiter's  Patient appears ill: septic arthritis.
disease (circinate balanitis), Sjogren (dry  Check for associated features: skin or eye
eye: sicca syndrome; dry mouth: involvement; disorders of the respiratory,
xerostomia). cardiovascular, abdominal or neurological
systems.
 Raynaud's syndrome: Systemic sclerosis,
SLE, mixed CTD. Joint examination
 Check joints for tenderness and swelling;
 Diarrhea: enteropathic arthritis (ulcerative
asymmetry of colour; deformity;
colitis; Crohn’s disease); coeliac disease;
limitation of movement; muscle wasting.
Whipple’s disease; proceed reactive
arthritis.
 Check both passive and active range of
joint movements.
 Urethritis: Reiter's disease.
 Eyes: conjunctivitis; iritis (Reiter’s A) Upper limbs
syndrome), uveitis (seronegative spondylo-  Shoulder examination: test
arthropathies), episcleritis (RA), scleritis glenohumeral, acromioclavicular and
(RA), kerato-conjuctivitis sicca (RA and sternoclavicular joints.
Sjogren's syndrome).  Check for swelling or deformity of the
 Cardio-respiratory: Episodes of pericardial elbow and hand.
or pleuritic chest (connective tissue  Assess pronation, supination and grip,
disease). Dyspnea due to pulmonary and dexterity by placing tip of each finger
on tip of thumb.

4
  Pain when 2nd to 5th metacarpals are arthritis), eosinophilia (polyarteritis nodosa),
squeezed suggests synovitis.  Platelets: may be  in RA and may be  in SLE.
B) Lower limbs Acute phase proteins:
 Observe patient standing to check for  ESR and CRP in inflammatory activity.
deformity of upper leg, lower leg or foot.
Serologic
 Gait: observe the patient walking, turning,
 Rheumatoid factor support diagnosis of RA.
and walking back.
 Anti-CCP: more specific than rheumatoid
 Knee and hip examination:
factor in RA.
 with patient on couch: check hip and
 ANA (Table 1).
knee ROM; knee crepitus.
 Examine each knee for joint effusion: Genetic
patellar tap, cross fluctuation tests.  HLA B27: increased positivity in ankylosing
 Check for quadriceps bulk. spondylitis and other spondyloarthropathies.
 Check feet for synovitis, for callosities, Synovial fluid
deformities and high or low arch.
 Raised White cell count (infection)
C) Spine  Gram stain (tuberculosis)
 With the patient standing, check from  Culture and sensitivities.
behind to detect lateral spinal curvature,  Crystal identification: urate, calcium
difference in level of the iliac crests and pyrophosphate.
asymmetry of the paraspinal muscles.
Others
 From the side, check for anteroposterior
curvature.  Urine: proteinuria (SLE).
 Assess all movements of neck and lower  Serum uric acid: may be raised in gout.
back. Imaging:
 Check lumbar spine and hip flexion  X-rays: RA (juxta-articular osteoporosis;
(modified Schober's test). erosions); OA (osteophytes; asymmetric
narrowing).
INVESTIGATIONS  Ultrasound.
 CT scan
Full blood count:
 MRI: much greater information of bone, joint
 Anaemia: of chronic disease or blood loss
and soft tissue.
from gastric irritation secondary to NSAIDs.
 White cells: leucopenia (SLE); neutropenia Arthroscopy:
(Felty's syndrome); neutrophilia (septic Direct view of joint and intra-articular structures.

Table 1: Selected ANA with High Sensitivity or Specificity for Rheumatic Diseases
Anti- SLE Other conditions
dsDNA 60–80%, Highly Specific to SLE (>97%)
Serum Level correlate with lupus nephritis and SLE flare
Sm 10–40%, Highly Specific to SLE
U1 RNP 30–40% MCTD: 100%
Ro (SS-A) 50%, associated with photosensitivity, subacute cutaneous Sjögren syndrome: 75%
lupus, interstitial lung disease. RA: 10–15%
Can cross the placenta causing neonatal cutaneous lupus and
congenital complete heart block.
La (SS-B) 10–15% Primary Sjögren syndrome: 40–50%
congenital complete heart block: 90%
neonatal cutaneous lupus: 70%
centromere CREST: 60% (Highly specific: >98%)
Scleroderma: 15%
Scl-70 Scleroderma: 40% (Specificity, 100%).
Histones SLE: 50–70% Drug induced lupus: >95%
5
 Connective Tissue Diseases • The thin synovium becomes inflamed and
proliferates (thickened) forming pannus.
A group of chronic inflammatory disorders • As the disease progresses, the pannus invades
predominantly affecting females. and damages the cartilage and bone 
They involve many different organs  therefore erosion and deformity (Figure 1).
exhibit a wide spectrum of clinical manifestations. Triggering factor
Their etiology is unknown but generally thought to (?? Infection, trauma, environmental)
be multifactorial involving immunological, genetic, 
Hitting genetically predisposed patient
environmental and possibly viral factors.
(HLA-DR4)
Common features of CTD 
Formation of immune complex
• Constitutional features. (Antigen+Anti-body+complement)
• Overlapping clinical features. 
• Overlapping pathologic features. Immune complex precipitate in synovium
• Prominent immunologic abnormalities. 
Pannus formation
CTD include (inflamed, proliferated synonium)
• RA. 
• SLE. Invade cartilage, bone and surrounding tissues

• Systemic sclerosis.
Damage and deformity
• Poly- and dermato-myositis.
• Mixed connective tissue disease. Figure 1. Summary of Etio-Pathogenesis of RA
• vasculitis
Clinical picture
Rheumatoid Arthritis Onset and Course
A chronic systemic inflammatory disease involving • Insidious onset (70% of cases).
synovial joints and occasionally extra-articular • Less common onset
manifestations are present.  Acute mono- or poly-arthritis (15%)
 Palindromic onset: recurrent episodic self-
Epidemiology
limited arthritis (5%)
• Incidence: 1-3% of the population (most  Extra-articular onset
common inflammatory arthritis). • Course: remission and exacerbation.
• Age: most often starts at age of 40-60 years Musculoskeletal Manifestations
(any age can be affected). • Chronic polyarthritis (bilateral, symmetric):
• Female : male ratio = 3:1. usually affect peripheral small joints of the
Etiology hands: MCP, PIP, and wrist joints (sparing DIP)
and feet: ankle, MTP joints (figure 2). Also
Unknown, but many theories are suggested other joints of the body may be affected.
• Autoimmunity: antibodies against self antigen.
• Genetic: being in more than one member in
the family, associated with HLA-DR4.
• Endocrinal: more in females, remission with
contraceptive pills and during pregnancy,
exacerbate after labour.
• Infection: some organisms isolated from the
synovial fluid mostly viruses.
• Trauma: physical or psychological.
Pathogenesis
• The primary site of inflammation is the
synovium of the joint.

Figure 2: distribution of joint affection in RA.

6
 Extra-articular Manifestations
• The affected joint is warm, tender, swollen
• Constitutional: low grade fever, anorexia, easy
and painful on movement.
fatigability, weight loss.
• Morning stiffness: lasting for > 1 hour.
• Rheumatoid subcutaneous nodules.
• Tenosynovitis, particularly affecting the flexor
 20-30% of sero+ve RA patients.
tendons in the palm of the hand, can cause
 Painless.
trigger finger.
 Any site, most commonly over joints,
• Bursitis e.g. Baker’s cyst.
extensor surface of forearm and pressure
• Muscle wasting, particularly in the hand.
points (Figure 4).
• Osteoporosis, early juxta-articular. Later,
 Associated with more severe disease,
generalized.
enlarge when RA is active.
• Deformities may occur in long-standing RA:
Common in sero +ve disease, neglected cases,
badly managed cases or late diagnosis cases.
Examples (Figure 3):
 ulnar deviation of fingers at level of MCPj
 Swan neck deformity (hyperextension of
PIPj + flexion of DIPj)
 Boutonniere deformity (flexion of PIPj +
hyperextension of DIPj)
 Z-shaped thumb (flexion of MCP +
hyperextension of IPj). Figure 4. Common site for rheumatoid nodules
 Hammer toe (hyperextension of MTPj +
flexion of IPj). • Skin: palmar erythema, purpuric eruption,
vasculitis, Raynaud's phenomenon.
• Chest: pleural effusion, pleurisy, pulmonary
fibrosis, rheumatoid nodules.
• Eye: keratoconjunctivitis sicca (Sjogren
syndrome in 10%), episcleritis, scleritis,
scleromalacia, scleromalacia perforans.
• Heart: Pericarditis and pericardial effusion
(usually asymptomatic).
• Vasculitis:
 May occur in severe and long-standing RA.
 Small vessel vasculitis: nailfold infarct, leg
ulcers, purpura.
 Medium vessel vasculitis: large areas of
skin necrosis, digital gangrene.
• Nervous system:
 Compression neuropathy e.g. carpal
tunnel syndrome.
 Peripheral neuropathy: mild glove and
stock sensory impairment.
 Mononeuritis multiplex: occurs as a result
of vascultitis.
 Atlanto-axial subluxation, a common
finding in x-ray (25%), usually
asymptomatic (cervical cord compression
is rare).
• Renal: secondary amyloidosis with proteinuria
and nephrotic syndrome.
• Felty syndrome: triad of RA + splenomegaly +
neutropenia.
Figure 3. common hand deformities in RA.
7
Laboratory Investigations Radiologic Features
Blood count • Early plain x-ray may be normal.
• Juxtra-articular osteoporosis.
• Anemia of chronic disease, iron deficiency
• Soft tissue swelling.
anemia.
• Erosions and joint space narrowing.
• Leukocytosis.
• Deformities.
• Neutropenia (Felty syndrome).
(Figure 5)
RF:
+ve in 85% of RA patients (70% in early RA).
• Value of RF:
 Help in diagnosis (one of the criteria for
diagnosis). Sites susceptible to
 +ve RF does not make diagnosis: as RF can direct attack by
pannus
be found in other conditions (Table 2).
 -ve RF does not exclude possible RA.
 +ve FR factor indicate bad prognosis.
 Help in follow up of treatment (titer
decreases with good control).
Table 2. conditions other than RA with positive
RF.
Normal Overall 4%
population Elderly 25% Erosion in carpal
Other Sjogren syndrome 90% bones, distal radius
Rheumatic SLE 35% and ulnar styloid
diseases Scleroderma 30% process.
Dermatomyositis 5%
Other Sarcoidosis
immunologic Cryoglobulinaemia
diseases Transplant recipients
Chronic HCV 60%
infections TB 15%
(usually low Bacterial endocarditis 25%
titer) Syphilis 10%
Leprosy 10%
Parasitic: bilharziasis,
malaria
Miscellaneous Neoplasms especially after
radiation and Hands damage in
chemotherapy. advanced RA
• Anti CCP:
 Highly specific for RA (98%).
 Found in 33% of RF –ve RA patients.
 Can be detected in early RA.
 Useful in differentiating RA from disorders
with articular symptoms and are RF +ve
e.g. HCV. Figure 5. Common radiologic features in RA.

• ESR and CRP Rheumatoid Arthritis Classification Criteria

 Increased especially in active disease The ACR Criteria
• Synovial fluid To be diagnosed as having RA, a patient must
 Yellow, cloudy, low viscosity, cell count meet 4 or more of the following 7 criteria (Criteria
2000-40000/mm3. 1,2,3,4 should present for at least 6 weeks):

8
 • Radiographic erosions within the first 2 years
1. Morning stiffness in or around joints for
from onset.
at least l hour before maximal
• HLA-DR4 genetic marker.
improvement.
2. Soft-tissues swelling (arthritis) of 3 or Treatment
more joint areas.
A) Patient education: explain the chronic nature
3. Swelling (arthritis) of PIP, MCP, or wrist
of the disease and the value of follow-up and the
joints.
drug side effects.
4. Symmetric arthritis
5. Subcutaneous nodules B) Measures to decrease pain and stiffness:
6. Positive test for RF • Physical: heat therapy, paraffin wax bath,
7. Radiographic erosions or peri-articular ultra-sound therapy, interferential current and
osteopenia in hand or wrist joints. TENS for muscles and tender points.
• Medical:
The 2010 ACR / EULAR Criteria
 NSAIDs: relief pain and stiffness but have
Every patient with a point total of 6 or higher is no disease modifying effect.
classified as an RA patient, provided he has  Systemic steroids: 5-10 mg daily to
synovitis in at least one joint and given that there achieve symptomatic control as a "bridge
is no other diagnosis better explaining the therapy" before the onset of action of
synovitis (Table 3). DMARDs.
Table 3. 2010 ACR/EULAR rheumatoid arthritis  Local steroid injections: of inflamed
classification criteria tendons, bursae or intra-articular.
Finding Points C) Measures to prevent disease progression:
Joint involvement • Conventional (synthetic) DMARDs:
nd
(designing MCPj, PIPj, IPj of the thumb, 2  Early treatment with DMARDs significantly
th
through 5 MTPj and wrist as small joints,
results in better outcome (as articular
and shoulders, elbows, hip, knee and
ankles as large joints):
damage in RA occurs in the early stages of
the disease).
 1 large joint --------------------------------------- 0  They decrease the levels of inflammatory
 2-10 large joints --------------------------------- 1 indices and retard radiographic
 1-3 small joints (with or without
progression of articular affection.
involvement of large joints) ------------------ 2
 4-10 small joints (with or without
 Used either single or in combination of
involvement of large joints) ------------------ 3 more than one drug.
 Involvement of more than 10 joints (with  Methotrexate: Based on efficacy, rapidity
involvement of at least 1 small joint) ------ 5 of action and safety MTX is considered the
1st drug of choice (the gold standard
Serological parameters
 -ve RF and -ve ACPA ---------------------------- 0
therapy for RA).
 Low +ve RF or low +ve ACPA ----------------- 2  Leflunamide: a valuable alternative for
 High +ve RF or +ve ACPA ---------------------- 3 patients intolerant to MTX.
 Hydroxychloroquine and sulfasalazine:
Acute phase reactants
used in milder diseases or if the previous
 Elevated ESR or CRP ---------------------------- 1
two drugs are contraindicated.
Duration of arthritis
 Symptoms lasting six weeks or longer ----- 1 • Biologic agents
 Newly developed targeted therapies with
Factors indicating bad prognosis rapid onset of action and highly effective
• Generalized poly-arthritis (>20 total joints). for control of disease activity and
• Male patient. prevention of structural joint damage.
• Extra-articular affection.  Highly indicated in patients with active
• Persistent elevation of ESR and CRP. disease who did not respond to DMARDs.
• Positive RF.  Can be used in combination with MTX as a
• Functional disability at 1 year after start of 1st line therapy in patients with severe RA.
disease  Limitations: very high cost and unknown
long term consequences.
9
  Examples: anti TNF-α (e.g. etanercept, Renal manifestations
infliximab, adalimumab). • Common in SLE (> 50%).
• Patients with active lupus nephritis have
D) Measures to prevent or correct deformity:
proteinuria >0.5 gm/day (commonest, may be
• Splints
asymptomatic), hematuria (microscopic).
• Static exercise during pain and inflammation.
•  serum creatinine and BUN.
• Active graduated exercises when pain
• Renal biopsy in patients with active urinary
subsides.
sediment to determine type and activity of
• Passive stretching
renal pathology (Table 4).
• Hydrotherapy
• Ultrasound
Table 4. WHO classification of glomerulonephritis in
• Electric muscle stimulation: faradic SLE
stimulation help strengthening weak muscles.
WHO classification Clinical features
E) Surgical for fixed uncorrectable deformities.
I. Normal glomeruli Asymptomatic
Systemic Lupus Erythematosus II. Mesangial disease Low grade hematuria or
proteinuria
A chronic inflammatory multisystem connective
tissue disease predominantly affect females, III. Focal proliferative GN Nephritic urinary
characterized by a wide range of clinical sediment (hematuria,
casts), proteinuria
manifestations accompanied by striking
immunologic abnormalities. IV. Diffuse proliferative GN Hypertension, variable
renal insufficiency.
Epidemiology
• Female:male ratio is 9:1 V. Membranous Nephrotic syndrome
nephropathy
• Age: mainly in age of 18-45 years (females in
the child bearing period). VI. Sclerosing nephropathy Inactive urinary
sediment, azotemia
Clinical features
Cardiac
Constitutional manifestations • Pericarditis with small pericardial effusion
• Low grade fever. (common).
• Anorexia. • Myocarditis.
• Malaise. • Coronary artery vasculitis (in severe cases).
• Chronic fatigue. • Premature atherosclerosis (especially in
Musculoskeletal manifestations patients treated with steroids).
• Arthralgia (commonest > 90%). • Non bacterial endocarditis (Libman sack’s
• Arthritis (non erosive). endocartitis).
• Joint deformities due to tendon or ligament Pulmonary manifestations
laxity (joint erosion is uncommon). • Recurrent pleurisy and pleural effusion
• Inflammatory myopathy may cause muscle (common),
wasting. • Pulmonary hypertension (secondary to
Dermatologic and mucosal manifestations pulmonary vasculitis).
• Butterfly rash: erythema over cheeks and Nervous system manifestations
nose (malar rash) sparing nasolabial fold. • Central: depression, psychosis, cognitive
• Discoid lesions: coin shapes. abnormalities, seizures.
• Non-specific rash in exposed areas. • Peripheral: sensory or sensorimotor
• Mucous membrane ulcerations (painless). neuropathies, vasculitis may cause
• Alopecia: focal or generalized. mononeuritis multiplex.
• Vasculitis: lesions at finger tips and around
nail fold. Gastrointestinal manifestations
• Photosensitivity: skin rash as a result of • Non-specific symptoms: nausea, vomiting,
unusual reaction to sun light. abdominal pain are frequent.
• Raynaud’s phenomenon. • Vasculitis of mesenteric vessels  bowel
ischemia, infarction, perforation.
10
• Pancreatitis secondary to disease or steroid • Hematologic disorder (hemolytic anemia,
use. leucopenia <4000/mm3, lymphopenia,
• Gastritis secondary to NSAIDs or steroids. thrombocytopenia <100 000/mm3).
• Immunologic disorder (+ve LE cell, anti DNA,
Hematological manifestations
anti SM or false +ve VDRL).
• Anemia (of chronic disease, hemolytic)
• Antinuclear antibody.
• Lymphopenia.
• Thrombocytopenia. Treatment
• Elevated ESR, normal CRP but raised if Treatment should be tailored to the patients
secondary infection occurs. findings.
• Coagulation abnormalities:
Preventive measures
 Phospholipid antibody (lupus anti co-
• Patient education.
agulant). Interference with coagulation
• Regular evaluation.
profile causing prolongation of the PTT.
• Photoprotection
 However, patients are not prone to
 Avoid exposure to sun.
bleeding but rather have higher incidence
 Sun screens
of thrombosis.
• Pregnancy
 Recurrent 2nd trimester abortion.
 Birth control with active lupus (especially
Immunological abnormalities nephritis) and with cytotoxic drugs.
• Low C3 and C4 level reflect activation of • Infection control.
immune complex cascade.  Suspect infection whenever there is fever.
• Hyper gammaglobulinaemia due to  Antibiotic prophylaxis for dental,
hyperactivity of B cells. gynecologic procedures.
• Autoantibodies are common:
Mild disease
o ANA are present almost in all SLE patients
• NSIADs: for joint pain, fever and mild systemic
(patients with –ve ANA are unlikely to
features e.g. serositis.
have SLE).
• Anti-malarials (chloroquine and hydroxyl-
o +ve ANA are found in many other
chloroquine): for arthritis and skin lesions and
conditions (high sensitivity but low
fatigue.
specificity).
• Steroids:
 Anti-dsDNA: specific to SLE but present in
 Topical preparations: for skin lesions.
60% of patients, levels of these antibodies
 Low dose steroids (5-10 mg/day).
rise with active disease.
 Anti-Sm: specific for SLE. Moderate and severe disease
 Anti-histone antibodies specific for drug • Systemic steroids
induced lupus.  The mainstay for treatment.
 Anti-Ro and anti-La antibodies: seen in SLE  For arthritis, serositis, severe hemolysis,
and Sogren’s Syndrome. thrombocytopenia, pneuminitis, vasculitis,
 Antiphospholipid antibodies (40%), but cardiac involvement, central or peripheral
only minority has thrombotic events. nervous involvement, renal disease.
 In acute and life-threatening
Diagnostic criteria
manifestations, starting doses of 40-80 mg
Patient must have at least 4 of the following
prednisolone orally daily are used.
criteria:
 With remission reduce dose gradually to
• Malar rash.
maintain at 5-10 mg/day.
• Discoid rash.
• Pulse steroid: 1 gm IV for 3 successive days for
• Photosensitivity.
severe lupus (renal, CNS, cardio pulmonary or
• Oral ulcers.
hemolytic abnormalities).
• Arthritis (non erosive).
• Cytotoxic therapy:
• Serositis (pleuritis or pericarditis).
 Azathioprine, methotrexate,
• Renal disorders (persistent proteinuria
cyclophosphamide.
>0.5gm/day or presence of cellular casts).
 For severe cases: particularly renal disease
• Neurologic disorder (seizures or psychosis).
refractory to systemic steroids.

11
• Others in severe refractory cases: Distribution
 Biologics (Rituximab).
Commonest joints (Figure 7)
 IVIg.
Knee joint, lumbar and cervical vertebrae, hand
 Plasmapharesis. (PIPj with Bouchard’s nodes, DIPj with Heberden’s
nodes, 1st MCj) and feet (1st MTPj).
Osteoarthritis
Rarely affected joints
Joint symptoms and signs of articular cartilage Ankle, shoulders, lateral MTPj of the feet.
degeneration, in addition to the related changes
in the underlying bone and at the joint margin.
Classification of OA
• Primary: unknown cause, affect certain joints
in old age.
• Secondary (can affect any joint at any age): to
- Local mechanical factors (trauma,
menisectomy).
- Joint diseases (RA, septic arthritis).
- Systemic diseases (hyperparathyroidism).
Primary OA
Risk factors
• Age: advancing age  loss of glycosamino-
glycan  leaving unsupported cartilage
collagen fibers. Figure 7: joints commonly affected by OA.
• Genetic: may be present especially in
Symptoms
generalized OA.
• Sex: both sexes are affected but generalized • Pain: arising from several structures (bone,
OA is commoner in females especially after synovium, ligaments, capsules and muscle).
menopause. Pain worsened by exercise and weight
• Obesity: predisposes to knee OA. bearing. Pain is aching and poorly localized. As
• Repeated overload disease progresses, pain during rest.
• Inactivity stiffness: present for few minutes.
Pathology
• Stiffness: morning stiffness is usually not a
• Manifested first by fibrillation of the cartilage prominent feature in OA, and when present
articular surface. lasting no more than ¼ hour.
• Clefts in the cartilage surface then develop • Limitation of movement and activity.
and eventually loss of the cartilage can be
seen. Signs
• Synovial membrane hypertrophy, fibrosis and • Swelling due to synovial thickening, effusion
contracture of the capsule. or bony swelling.
• Bone changes include: subchondral sclerosis, • Wasting of muscles acting on the affected
marginal osteophytes (Figure 6) joints.
• Joint tenderness.
• Joint crepitus (coarse).
• Deformity e.g. flexion deformity of the knee,
genu varum, genu valgum.
Investigations
• Laboratory features are normal.
• Synovial fluid: good viscosity, normal mucin
clot, slight increase in cell count.
• Plain x-ray: the most useful form of imaging to
evaluate OA (Figure 8):
Figure 6. Pathologic changes in OA. - Joint space narrowing.

12
 - Subchondral bone sclerosis.  Improve joint range of motion.
- Subchondral bone cysts  Strengthen peri-articular structures 
- Osteophytes (bone spurs) improve joint support.
- Central bone erosions in erosive OA.  Improve blood supply and metabolism.

• Use simple analgesic for pain.

• Short courses of NSAIDS to control symptoms.
• Assistive devices (knee brace; stick)
Major
radiographic partially unload the joint.
features of OA • Chondroprotective and viscosupplements
(debatable).
• Surgical treatment in advanced cases:
 Osteotomy to correct deformity.
 Arthroplasty (partial or total joint
Severe joint space replacement).
narrowing in the
medial knee Gout
compartment.
Note the lateral Disorders of purine metabolism, which are
marginal characterized by serum uric acid elevation
osteophytes
(hyperuricaemia) and urate deposition in the
articular or extra-articluar tissue (Figure 9).

Black arrows
point to
subchondral
sclerosis. White
arrow points to
osteophytes.
Black
arrowheads point
to joint
narrowing in
medial
compartment

Figure 8: common radiologic features in OA

Treatment
• Assurance. Figure 9: Gouty arthritis.
• Instructions for joint protection (to avoid Classification
overstress the affected joints.): 1. Primary gout (90%): hyperuricemia result from
 Don’t lie or sit too long in one position. disorders of purine metabolism or abnormal
 Don’t use low chairs. excretion of uric acid.
 Don’t stand in same position or walk for 2. Secondary gout (10%): due to either:
long periods. a) Impaired excretion: caused by:
 Don’t over exercise the affected joints.  Chronic renal diseases.
 Don’t use faulty postures that place stress  Drugs (thiazide diuretics, low dose
on affected joints. aspirin).
 Don’t load the joint when it is very painful.  Hypertension.
 Reduction of body weight in obese  Lead toxicity.
patients.  Hyperparathyoidism.
• Physiotherapy (heat, Cold, electric  Hypothyroidism.
stimulation, laser, massage and exercise).  Increased lactic acid production (e.g.
Benefits of physiotherapy include alcohol, starvation).
 Decrease pain, stiffness, muscle spasm.  Glucose 6 phosphatase deficiency.

13
 b) Increased uric acid production
 Myeloproliferative disorders (e.g.
polycythemia vera). Gout involving the
 lymphoproliferative disorders (e.g. 1st MTPj. Peri-
articular swelling
leukemia)
with ‘punched out’
 Others e.g. severe psoriasis. erosion located
Clinical picture away from the
articular surface
Acute gouty arthritis with an over-
hanging lip
Typical attack (95%): Acute gouty arthritis with: appearance.
• severe pain develops overnight, reaches a
peak within hours
• The patient can’t bear weight or even touch of
the bed clothes
• The skin is red and may peel.
• Slight fever and chills may present.
• The most commonly affected joints are 1st
MTPj, dorsum of the foot, knee (joints of Large tophaceous
upper limb are rarely affected). deposits

Intercritical gout
• Asymptomatic intervals between acute attacks
of gout.
nd
• Some patients never experience 2 attack.
• With repeated attacks of acute arthritis, the
Figure 10: common radiologic features of gout.
interval between attacks progressively
shortens, and finally, joints become Treatment
permanently mildly swollen and deformed with
Treatment of acute attack:
mild to moderate persistent pain.
• NSAIDs in maximum doses.
Chronic gout • Colchicine: 0.5 mg/3 hours for 12 hours.
• Recurrent acute attacks may lead to • In resistant cases: systemic steroids.
progressive joint damage, deformity and pain. • Effusion in large joints should be aspirated
• Chronic tophaceous gout: large MSU crystals and corticosteroid injected to reduce
deposits produce firm nodules (tophi), usual inflammation.
sites around extensor surfaces of fingers,
Long term Treatment:
hands, elbows, Achilles tendon and the ear.
Considered when acute attack subsides.
Investigations • Patient education: maintain ideal body
• Fresh synovial fluid examination under weight, ingestion of at least 2 liters of fluids
polarized light microscope for presence of per day to prevent renal stones, avoid low
urate crystals (diagnostic). Synovial fluid is dose aspirin.
inflammatory in nature with predominance of • Diet: avoidance of high-purine foods e.g. meat
neutrophils. and sea-food. Encourage intake of low fat
• Elevated serum uric acid (not diagnostic): may dairy products and vegetable proteins.
be normal in 30% of patients at time of acute • Colchicine (prophylaxis): 0.5-1 mg/day to
attack. A high level alone is not diagnostic as prevent gout flares.
asymptomatic hyperuricaemia is common • Allopurinol:
• Blood tests: leucocytosis, raised ESR and CRP  Action: inhibits xanthine oxidase enzyme,
(varies with gout severity). diverting purine breakdown to xanthines,
• Radiologic features (Figure 10): which are more soluble in water.
- Soft tissue swelling around the affected joint.  Dose: 100-300 mg/day.
- In chronic gout: tophi, punched out erosions  Side effects: rash, vasculitis,
with sclerotic margin and overhanging edge. agranulocytosis.

14
  Contraindications: acute gout. Alarming (Red flag) Suggested
 Concurrent treatment: low dose NSIADs symptom/sign serious
or colchicin for at least 4 months. diagnosis
• Uricosuric drugs: (probencid,
sulphinpyrazone): Severe persistent pain not Infection,
 Side effects: occasionally rash or hepatitis. changes by position, not malignancy
improved by rest
 Contraindications: acute gout.
 Concurrent treatment: low dose NSIADs Fever, chills, weight loss Infection,
or colchicin for at least 4 months. malignancy
• Joint aspiration for joint effusion and intra-
articular corticosteroid injection for patients Pain worse in walking, radiating spinal stenosis
with persistent synovitis. to lower limbs, exacerbated by
• Prevention of renal stones: spinal extension and relieved by
 Alkalinization of urine (to maintain pH at sitting in flexion
6): use sodium or potassium citrate or
acetazolamide 500 mg at bedtime. Pain and stiffness > 30 minutes, Spondylo-
worse in the morning in young arthropathy
 Intake of adequate fluid to produce at
adult male
least 2 liters of urine daily.
Low Back Pain Bilateral radiation of pain, Cauda equina
Abnormal neurologic findings, compression (e.g.
A very common condition affecting 80% of the
sensory deficit, bowel/ bladder Central disc
individuals at some point in their life time. dysfunction, saddle anesthesia, prolapse, rarely
Causes of LBP +ve Babiniski, ankle clonus cancer)
• Congenital: e.g. spina bifida, scoliosis.
Acute severe pain with point Fracture
• Traumatic: e.g. lumbar disc prolapse, fracture
tenderness, history of Severe
of the spine, tears or sprain of spinal ligament
trauma (or even minor trauma in
and/ or muscle. osteoporosis).
• Degenerative: e.g. intervertebral disc (lumbar
spondylosis), facet joint (osteoarthritis), spinal Mechanical LBP
canal stenosis.
• Postural: e.g. bad posture (sitting, standing), • Over 95% of LBP.
inequality of limb length, high heels, • Due to anatomic or functional abnormality,
pendulous abdomen. without underlying inflammatory or
• Inflammatory: e.g. ankylosing spondylitis, neoplastic diseases.
Reiter's disease, psoriatic arthritis, • Pain increases with physical activity and is
enteropathic arthritis. released by rest and recumbency.
• Infection: e.g. non-specific (osteomyelitis), • Causes:
specific (Pott's disease in TB).  Postural (sprain or strain, lumbago, non
• Metabolic: e.g. osteoporosis, osteomalacia, specific): 70%.
Paget's diseases.  Lumbar spondylosis: 10%.
• Neoplasm: benign, malignant (secondaries are  Disc herniation: 6%.
more common than primaries).  Spinal stenosis.
• Referred (visceral): e.g. peptic ulcer,  Spondylolisthesis.
pancreatitis, pancreatic tumor, pyelonephritis,  Diffuse idiopathic skeletal hyperostosis.
aortic aneurysm, peritoneal tumor, pelvic  Factures.
disease.
• Psychogenic LBP. 1. Postural back pain (strain and
sprain, lumbago).
N.B.
• Bad posture is probably the most common
Although the most of LBP is mechanical in nature
cause of persistent back pain.
(e.g. disc prolapse, spondylosis, postural),
however, the most serious rare causes must be • Common predisposing factors:
excluded.
15
  Prolonged sitting or standing with leaning  Muscle relaxants.
forward  flat lordosis.  Anticonvulsants.
 Anti-depressants.
 High heeled shoes, pendulous abdomen
 exaggerated lordosis. Physical Therapy
 Unequal leg length, asymmetric lifting • Physical agents: (e.g. SWD, US, TENS).
heavy weight  scoliosis Advantages:
• Correcting bad postural habits may be difficult  Local anti-inflammatory effect.
for a patient to accept and may need re-  Decrease pain and muscle spasm.
inforcement through programs as back school.  Decrease fibrosis and adhesions.
• Exercise program
2. Lumbar Spondylosis  Cornerstone of conservative treatment
Degenerative joint disease affecting lumbar and prevention.
vertebrae and intervertebral disc causing pain and  Benefits:
stiffness, sometimes with sciatic radiation (L4-5,  Support vertebral column.
S1,2,3) due to nerve root pressure by associated  Restore normal curves of the spine.
osteophytes.  Decrease intradiscal pressure.
 Decrease load on facet joints and
Clinical Features open intervertebral foramina.
• Pain: midline, radiating to the region of  Restore strength, flexibility, function.
buttock, occasionally sciatica. Pain worse  Reduce pain.
towards end of the day and often not
aggravated by coughing and sneezing. • Traction:
• Lumbar morning stiffness, inactivity stiffness.  Help suction of prolapsed disc.
• Diminished spinal mobility.  Stretch vertebral ligaments, support the
• Midline tenderness. disc.
• Sensory and motor neurological signs (if there • Others e.g. local injection, manipulation,
is root compression by osteophytes). acupuncture
Radiology • Surgical treatment: indications
• Narrow disc space.  Progressive muscle weakness.
• Osteophytes.  Sphincteric disturbance.
• Evidence of apophyseal osteoarthritis.  Failure of conservative treatment after 12
Treatment of Mechanical LBP weeks with severe persistent pain.

Conservative treatment is the main line. Tailored 3. Lumbar Disc Prolapse

to the specific needs of the individual patient. One of the causes of mechanical LBP.
Rest Etiology
• Days to few weeks. Trauma, is usually not a direct one, typically lifting
• Kept to minimum and early mobilization a heavy weight while back unsupported (bending).
should be encouraged.
• Early referral to physical therapy is essential. Pathology

Instructions  Direction of prolapse mainly posterior or

• Positioning: postero-lateral.
 Sleep on firm matrix  avoiding back sagging.  Commonest site between L4-5 and L5-S1.
 Setting: increase disc pressure  minimize in Symptoms (of 1st attack)
disc prolapse. • Sudden onset of LBP while patient lifting a
 Standing: avoid prolonged standing. heavy object.
• Weight reduction. • Pain worse by straining (sneezing, coughing).
Medication • Pain increase by movement, relieved by rest.
 Analgesics and NSAIDs: during acute attack, • Sciatic pain: pain along the course of the
infrequent courses. affected nerve.
16
Signs • Plain x-ray: Narrow disc space, sometimes
normal if small disc prolapse.
Back signs
• CT scan: Localize exactly site of prolapsed disc.
• Diminished or obliterated lumbar lordosis.
• MRI: better imaging of soft tissues (Figure 13).
• Sciatic scoliosis (lateral bending to one side).
• Myelography: detect prolapse as filling defect.
• Midline tenderness opposite prolapsed disc.
• Dsciography.
• Restriction of back movement.
• Radiculography.
Stretch signs
• +ve straight leg raising test (sciatic stretch):
indicate sciatic compression i.e. lower lumbar
disc prolapse (Figure 11).
• +ve femoral stretch test: indicate femoral
nerve compression i.e. high lumbar disc
prolapse (Figure 12).
Figure 13: MRI of herniated disc between L5-S1.
The leg is lifted
with knee Psychogenic LBP
extended. • Psychogenic illness may be manifested as LBP.
Sciatic roots are
• Diagnosis is usually based on:
tightened over
a herniated disc
 Detection of inadequate personality and
between 30
o psychological illness.
and 70 .
o  An organic disease is excluded.
• Symptoms usually very diffuse and not follow
Figure 11: Straight leg raising test. anatomic distribution.
The knee is • The description of pain is exaggerated.
flexed and lifted • Patient is usually highly demonstrative, hands
superiorly. used to point out various painful areas.
Sharp pain that • No root signs could be detected and patient is
is generated in hesitating about areas of paraesthesia.
the anterior
thigh is Inflammatory LBP
considered a
positive test. Inflammatory diseases can cause LBP (e.g.
Figure 12: Femoral stretch tests. ankylosing spondylitis, enteropathic arthritis,
psoriatic arthritis and reactive arthritis).
Neurologic signs
Lumbar spine involvement in RA is rare.
Are usually localizing signs and depend on which
root is compressed by the prolapsed material. Inflammatory LBP must be differentiated from
mechanical LBP (Table 5).
Investigations

Table 5. Mechanical versus inflammatory back pain.

Mechanical Inflammatory
Example Disc prolapse Ankylosing spondylitis
Onset Acute Insidious
Age Any age Usually < 35 years
Effect of exercise Worsen pain Improve pain
Morning/inactivity stiffness + +++
Pain radiation Anatomical (L4, L5, S1) Diffuse
Sensory/motor deficit + -
Other system is involved - +
Sleep disturbance + +++
Scoliosis + -
Decrease ROM Asymmetric Symmetric
Spinal tenderness Localized Diffuse
Sacroiliac/hip involvement - ±

17
 Table 6. Differential Diagnosis of Common Arthropathies
Arthropathy Characteristic features Coexisting disorders Investigations
Rheumatoid  F:M ratio = 3:1.  X-rays: rheumatoid
arthritis  Most often starts at age of 40-60 changes.
years (any age can be affected).  RF +ve in 80% of cases.
 Symmetrical Polyarthritis often 
ESR usually raised
starting at MCPj, PIPj and wrists (during activity)
(usually sparing DIPj).
 Joints are swollen, painful, stiff
and tender.
 Morning stiffness > 1hour.
Osteoarthritis  Middle-aged or elderly.  Old injury to joints  ESR not elevated.
 1ry or 2ry affects weight bearing may have been  X-rays: characteristic OA
joints: knee, hip. present changes.
 Pain and inactivity stiffness.

Gout  Acute pain, swelling, redness in Possibly  Raised serum uric acid.
MTPj or ankle (less common in  Renal disease (in 2ry  Urate crystals in synovial
knee). gout) fluid.
 90% males.  Hypertension
 Onset at night  Obesity
Rheumatic  Age: 5-15 years.  Sore throat 1-3 weeks  ESR and CRP elevated in
arthritis  Migratory polyarthritis affecting prior to the attack all active cases
(Rheumatic fever) large joints, fleeting in character  Carditis, fever, S.C.  ASO titer: raised
 Effusions are common. nodules, erythema  Blood picture: anemia,
 No residual joint damage marginatum, chorea. leucocytosis
Calcium  Males = females.  Pyrophosphate crystals
Pyrophosphate  Knee commonest site. in joint fluid.
arthropathy  Acute pain and swelling.  X- rays helpful in
(pseudogout) diagnosis.

Systemic lupus  90% females.  Sometimes  ANA + ve.

erythematosus  Marked variation in symptoms Antiphospholipid  ESR raised.
referred to any system. syndrome.  Anti ds-DNA + ve.
 Patients often more ill than  Often anaemic.
arthritic and often febrile.
Polymyositis  Proximal muscle pains, weakness  Muscle biopsy:
and tenderness. inflammatory muscle
 May complain of joints pain with infiltration.
morning stiffness.  EMG: abnormal.
  Serum creatin kinas,
and other enzymes.
Dermato-myositis  Heliotrope rash around eye.  Malignant disease  Biopsy.
 Proximal muscle weakness and may be present.  Muscle enzymes.
tenderness.  EMG.
Progressive  Tight fingers, blanched fingers  Dysphagia  Skin Biopsy
systemic sclerosis and face.  Raynaud’s
(Scleroderma)  Raynaud’s phenomenon phenomenon
 Often dysphagia.  Pulmonary
 More common in females. hypertension
Psoriatic  Patchy polyarthritis with DIP  Psoriasis sometimes  RF -ve.
arthropathy joints often involved. slight.
 Sometimes spondylitis with  Nail changes of
sacro-iliac joint affection. psoriasis.

18
Ankylosing  Mostly young males.  RF- ve
spondylitis  Axial arthritis  HLA B27 +ve in 95% of
 Stiffness and pain in spine and cases.
girdle joints (hips and shoulders).  Sacroiliac joint
 Iritis in 30% involvement evident in x-
ray.
Enteropathic  Asymmetrical polyarthritis often  Ulcerative colitis or  RF – ve.
arthropathy associated with relapse of colitis.  Crohn’s disease.
st
Polymyalgia  Pains and morning stiffness in  Low grade fever.  ESR > 50 in 1 hour.
rheumatica girdle muscles (shoulders and  Fatigue  RF –ve.
hips).  Weight loss
 Patient usually >60 years of age.  Arteritis with risk of
blindness.

Table 7. Causes of polyarthritis

Cause Characteristics
1. Inflammatory
Very acute, self-limiting
Viral arthritis
Rheumatoid arthritis Symmetrical, small and large joints, upper and
lower limbs.
Seronegative spondarthritis (psoriasis, reactive, Asymmetrical, large > small joints, lower > upper
ankylosing spondylitis, enteropathic arthropathy) limbs, spondylitis, sacroiliitis.
Lupus Symmetrical, small > large joints, joint damage
uncommon
Chronic gout Distal > proximal joints, preceded by acute attack
Juvenile idiopathic arthritis Symmetrical, small and large joints, upper and
lower limbs
Chronic sarcoidosis Symmetrical, small and large joints
Scleroderma and polymyositis Rare, small and large joints
Hypertrophic osteoarthropathy Rare, large > small joints, clubbing
2. Non-inflammatory
Generalized osteoarthritis Very common, Symmetrical, small and large joints,
Heberden's nodes, only a few joints symptomatic
at any one time
hemochromatosis Rare, small and large joints
Acromagally arthropathy Rare, mainly large joints, spine

Causes of monoarthritis
1. Septic arthritis
2. Crystal arthritis (gout, pseudogout)
3. Traumatic
4. Monoarticular presentation of oligo or polyarthritis.
Any patient with acute inflammatory monoarticular arthritis needs a joint aspiration to rule out septic
arthritis and crystalline arthropathy.

19
 Anti-Rheumatic Drugs Mechanism of action

Analgesics • Mainly via anti-prostaglandin effect.

• Prostaglandins are important mediators of
• Drugs used to relieve pain only and have no inflammation and pain but they also have
anti-inflammatory effects. many other physiological effects e.g.
• e.g. salicylates in small doses, paracetamol, protective for the stomach,  gastric HCl
nefopam (acupan), glafinene. secretion,  renal blood flow,
Non-steroidal anti-inflammatory bronchodilatation.
Drugs (NSAIDs) Side effects
• Group of drugs have an analgesics and anti- Most of them are due to inhibition of
inflammatory effects. prostaglandins
• They are similar to corticosteroids in some
• Hypersensitivity reaction.
characters but have no steroid ring in their
• GIT: dyspepsia, heart burn, gastritis, peptic
chemical structure.
ulcer, even perforation and GIT bleeding (may
• They are less potent and have less side effects
occur even if given by injection or supp).
than corticosteroids.
• Liver: transient elevation of liver enzymes.
Classification • Respiratory: bronchospasm and aggravation
• There are more than 100 types of NSAIDs in of bronchial asthma in susceptible patients.
the market. • Renal:  renal blood flow in renal impaired
• The classification is based on the acid patients.
component (Figure 14). • CVS: salt and water retention.
• The drugs in each class tend to have similar • CNS: headache (especially indomethacin).
side effects. • Blood: salicylates inhibit platelet function 
• If a drug in one classification is ineffective, try bleeding tendency and potentiate the effect
a different structural compound instead of of anticoagulant.
repeatedly using drugs from same structural • Joints: long term use  enhances
group. degeneration process.

Figure 14. Structural classification of NSAIDs

Carboxylic Enolic acids Non acidic
acids compounds

Salicylic Acetic Propionic Fenamic Pyrazolones Oxicams

acids acids acids acids

Phenyacteic Carbo- and

acids heterocyclic
acids

Aspirin Diclofenac Etodolac Flurbiprofen Mefanamic Phenyl- Piroxicam Nabumetone

Difunisal Indomethacin Ketoprofen butazone Meloxicam
Trisalicylate Sulindac Oxaprozin
Salicylate Tolmetic Ibuprofen
Ketorolac Naproxen
Fenoprofen
COX-2 selective inhibitors

Celecoxib Etodolac
Rofecoxib Lumiracoxib
Meloxicam Valdecoxib
Nimesulide Deracoxib
Paracoxib Etoricoxib

20
Contraindications  Consider the use of other modalities (e.g.
Physical therapy) which are effective in
• Absolute: Hypersensitivity to drug.
treating local pain and inflammation without
• Relative contraindications
causing side effects of NSAIDs and decreases
 Peptic ulcer.
the need for them.
 Bleeding tendency.
 Bronchial asthma. Disease Modifying anti-rheumatic
 Hepatic impairment. Drugs (DMARDs)
 Renal impairment. Group of drugs used in systemic rheumatic
 Pregnancy and lactation. diseases to minimize disease activity and
Precautions for the use of NSAIDs progression (Table 8).

 Do not prescribe NSAIDs when they are not Synonyms

necessary: in degenerative joint diseases, (no • Specific anti-rheumatic drugs
evidence of inflammation) simple analgesics • Slow Acting Anti-Rheumatic Drugs (SAARDs):
may do the same function with much less side their effect takes 4-8 weeks to appear
effects. • 2nd line anti-inflammatory drugs.
 Prescribe one NSAIDs: combination of two or
Mechanism of action
more NSAIDs increase side effects with no
better efficacy. One or more of the following
 Use NSAIDs at the lowest possible effective • Inhibition of lysosomal enzymes.
dose, never exceed therapeutic dose. • Inhibition of phagocytosis.
 Use NSAIDs for shortest time needed. • Inhibition of prostaglandins.
 Select proper group for the patient: response • Inhibitory effect on immune system
to NSAIDs varies from patient to patient • Reduction of immune complex formation.
(individual variation). • Sulphasalazine has antimicrobial activity.
 Beware of high risk patients. • Immunosuppressive drugs has anti RNA and
 Maintain close supervision. anti DNA properties.

Table 8. Examples of DMRADs

Drug Dose Main side effects Monitoring
Methotrexate 7.5 -30 mg/week orally, IM or SC injection. Oral ulcers, hepatic toxicity, CBC and liver enz at
(MTX) bone-marrow suppression, baseline and
After 20mg is reached, no further MTX is
pneumonitis, teratogenicity monthly for 3
absorbed orally: shift to injection
months, then every
Folic acid 5gm once /week should be 3 months
administrated
Leflunomide 100mg orally/day for 3 days, then 10-20 GIT upset, hepatic enz As MTX
mg daily elevation, neutropenia,
teratogenicity, hypertension
Sulphasalazine Maximum dose allowed is 2gm/day in two GIT upsets, hepatic enz As MTX
divided doses. Start at 500mg and elevation, reversible
increase by 500mg each week. azospermia. Neutropenia
Antimalarials Hydroxy-chloroquine: 200 – 400 mg/day. Retinopathy, Skin rash, Fundus ex. Before
Chloroquine 250mg/day Myopathy use and then every 6
months
Azathioprine 50-100mg /day orally. Bone marrow suppression, As MTX
Allergic hepatitis.
Cyclo- 50-100mg /day orally Bone marrow suppression, Regular CBC
phosphamide
↑ incidence of infection,
teratogenicity, infertility

21
 Biological agents Miscellaneous Anti-rheumatic Drugs
(Anticytokine therapy) Muscle Relaxants
Anti-TNF-α  Indicated in conditions associated with muscle
spasm.
• TNF is a major inflammatory mediator in RA
and a potent inducer of IL-1. Colchicine
• TNF-α and IL-1 are considered to be master  In gouty arthritis, sarcoidosis, and familial
cytokines in RA. Mediterranean fever.
• Anti-TNF therapy shows great efficacy in RA
patients. However, it is not effective in all Nerve tonics
patients, nor does it fully control the arthritic  e.g. drugs containing vit B1, B6 and B12 used
process in affected joints of good responders. in diseases associated with neuralgias e.g.
• Indications: RA, spondyloarthropathy, sciatica, brachialgia.
polyarticular JIA.
• Precautions: chest x-ray and tuberculin test Hypouricaemic drugs
(to avoid activation of TB), hepatitis b  Decrease serum uric acid level in chronic gout.
scereening.
• Examples: etanercept, infliximab, adalimumab Tricyclic antidepressants, gabapentin,
pregabalin
(Table 9).
 Used in fibromyalgia, neuropathic pain.
Anti-IL-1
• E.g. Anakinra: IL-1 receptor antagonist, given
subcutaneously in a dose of 100 mg daily.
• Toxicities include injection-site reactions and
pneumonia.

Anti-IL-6
• Indications: systemic JIA.
• E.g. tocilizumab.

B cell depletion
• Indications: SLE, vasculitis.
• E.g. rituximab.

Table 9. Examples of Biologic agents

Drug Dose Mechanism Common adverse effects

Etanercept Subcutaneously TNF-α soluble receptor Injection site reaction, upper respiratory
(Enbrel) (TNF-α blocker) infection (URI), development of
25 mg twice weekly antibodies to drug

Infliximab Intravenously at 0, 2, 6 TNF-α blocker Injection site reaction, hypotension,

(Remicade) weeks, then every 2 months rash, URIs, reactivation of TB,
3-5 mg/kg development of autoantibodies.

Adalimumab Subcutaneously TNF-α blocker URIs, injection site pain, headache, rash,
(Humira) sinusitis, autoantibodies
40 mg every 2 weeks

Anakinra Subcutaneously IL-1 receptor injection-site reactions and pneumonia

antagonist
100 mg daily

22
Physical Therapy and Rehabilitation • LMNL e.g. Bell's palsy, neuropathy.
• UMNL e.g. hemiplegia, paraplegia,
Rehabilitation monoplegia.
Rehabilitation means the restoration of the • Post-operative e.g. laminectomy, repair of
maximum possible function of an organ or part of nerve lesions.
the body. 3. Pediatric conditions
The rehabilitation program is individualized • Erb's palsy
according to patient needs. This requires proper • Torticollis
evaluation. • Cerebral palsy
• Spina bifida
Rehabilitation program include:
4. Orthopedic conditions
• Rest: during active stages and acute • Post-plaster stiffness of joints.
exacerbations. The amount and type of rest • Correction of deformities.
vary with joint involvement and severity of
the disease. 5. Sports injuries
• Medical treatment: according to the cause of • Sprains, tears etc.
the disease. 6. Gynecologic conditions
• Physical therapy. • Short wave diathermy in pelvic tubal
• Splints and walking aids. adhesions (in infertility).
• Surgical treatment when indicated. • Post-partum abdominal muscle weakness.
7. Others
Physical Therapy
• Cardiac rehabilitation.
It is the use of physical agents in treatment of the • Respiratory rehabilitation.
musculoskeletal disorders. • Rehabilitation of peripheral vascular diseases.
• Geriatric rehabilitation.
Various forms of physical agents play an
important role in the treatment of Forms of physical therapy
musculoskeletal disorders • Heat therapy.
Physiotherapy may be prescribed alone or in • Cold therapy.
conjunction with medical and other measures to • Electrotherapy.
get therapeutic benefits without the hazardous • Exercise therapy.
effect of the anti-inflammatory drugs. • Massage.
• Others e.g. traction, suspension, laser etc.
Therapeutic benefits
• Relief of pain and stiffness. Cold Therapy
• Relief of muscle spasm The external use of cooling for therapeutic
• Restoration of movement. purposes.
• Increase muscle strength.
• Prevent deformity. Forms
• Restoration of maximal functional capacity. • Various forms of ice
Indications • Frozen gel packs
Therapeutic effects
1. Rheumatic conditions
• Osteoarthritis. • Sedative effects on sensory nerves  pain
• Rheumatoid arthritis. relief.
• Cervical spondylosis and disc prolapse. • Reduction of spasticity and spasm.
• Lumbar spondylosis and disc prolapse. • Vasoconstriction of blood vessels which
• Joint pain or stiffness e.g. frozen shoulder reduce swelling and bleeding (used in
syndrome. mechanical trauma).
• Soft tissue rheumatism e.g. tendinitis, bursitis. • Cryotherapy improves inflammation, more
• Sciatica. effectively in the acute phase than in the
chronic phase.
2. Neurologic and neurosurgical conditions
23
 Heat Therapy patients with RA or after knee surgery or knee
effusion and lower motor neuron lesions.
Forms of heat therapy • Training of new muscle action after tendon
Superficial heat transplantation.
• For heating of superficial tissues (at a depth of • Analgesic effect: low frequency current for
about 0.5 cm beneath the skin) e.g. superficial stimulating afferent sensory component of
ligaments, small joints, tendons, muscles. peripheral nerves for relief of pain (acute or
• e.g. infra-red rays chronic) e.g. back pain, neck pain, OA, RA,
neuralgia.
Deep heat
• For heating superficial and deep structures at Exercise therapy
a depth may reach 5 cm under the skin e.g.
Passive exercise
large joints, bulky muscles.
• e.g. short wave diathermy, ultrasonic waves, • Accomplished only by therapist or apparatus
microwave. • Used to maintain body mobility and prevent
contracture when muscles are weak.
Therapeutic effects
Active exercise
1. Anti-inflammatory effects
Active assistive:
Dilatation of arterioles and capillaries 
increase blood flow  increase O2 supply, • Accomplished by active contraction by the
food stuffs, antibiotics, WBCs  removal of patient with the assistance of the therapist or
waste products resolution of inflammation mechanical devices
and healing. • Used as first step in the muscle re-education
for weak muscles.
2. Analgesic effect
Active exercise
Application of heat to peripheral nerves 
increase pain threshold in the area supplied • Accomplished by patient without assistance
by the nerve without affecting the motor • Used to improve function and strength.
function.
Active resisted
3. Effect on muscles
• Accomplished by the patient with various
Muscle relaxation, decrease muscle spasm. additional resistance either manual or
mechanical depending on the muscle power.
4. Mechanical effect
• Used to develop muscle power
The to-and-fro movements of the ultrasound
Stretching
waves through the tissue particles causing
micro-massage which soften adhesions • Accomplished by forced motion to restore
5. Biologic effect of US and laser normal range of motion which is limited due
to loss of elasticity of soft tissues.
Stimulate growth of tissue  tissue repair and
healing (e.g. ulcers and bed sores). Massage

Electrotherapy Therapeutic effects

Forms • Assists blood and lymph drainage  

swelling.
• Faradic current • Decrease adhesions between muscle fibers.
• Galvanic current • Decrease pain sensation.
• TENS • Muscle relaxation.
Therapeutic uses Spinal Traction
• Facilitate muscle contraction when it is A technique that utilizes a traction force of
hindered by pain, weakness or denervation sufficient magnitude and duration applied to the
e.g. isometric contraction of the quadriceps in spine to produce separation of the vertebrae,
facets and increase size of foramina.
24
Used mainly for cervical and lumbar spine.  Tighten the posterior longitudinal ligament to
exert a centripetal force on the annulus
Techniques
 Manual: force applied by therapist hands. fibrosis.
Used in cervical traction only (Figure 15).  Widen the intervertebral foramina  relief
 Mechanical: administered using pulley and root compression
free weight system (Figure 15).  Separate apophyseal joints  relief of pain
 Motorized: mechanical traction applied by following degenerative joint space narrowing.
motorized system, administered in continuous
Splints
or intermittent periods.
Aim and types
 Gravity: hanging upside down.
• Rest splints
 Auto-traction: uses specially designed device Rest and relief from pain for active joints
that self-administers. • Corrective splint.
Prevention and correction of deformities.
• Functional splint
Fixation of damaged joint in good functional
position.
Walking aids
• Crutches (Figure 16).
• Canes (Figure 16).
• Walker (Figure 16).
• Wheel chair.
a

cane Quad cane crutches walker

b Figure 16: walking aids.
Figure 15: Motorized Traction (a) cervical
motorized traction and (b) lumbar motorized
traction.

Therapeutic effects
 Prolonged pull on the muscle may lead to
paraspinal muscle fatigue which alleviates
muscle spasm.
 Enlarge the intervertebral space leading to
retraction of herniated disc material.

25
 Clinical signs
Testing for swelling.
The bulge sign in the knee: The
back of the hand gently pushes
the fluid from one side of the
knee to the other, filling out the
“dimples” on either side of the
patella. This is most helpful in
detecting small knee effusions.

Testing for swelling.

The patellar tap. One hand is
used to cup the patella and
compress the suprapatellar
pouch, and the fingers of the
other hand press down on the
patella to feel for cross-
fluctuation.

Rheumatoid nodules in a
patient with rheumatoid
arthritis

The hand in early RA.

Showing swelling of the MCP
and PIP joints.

26
Boutonniere deformity.
PIP flexion and DIP
hyperextension.

The swan-neck deformity.

PIP hyperextension, and DIP
flexion.

Ulnar deviation of the fingers at

level of MCPjs In right hand.

Tenosynovial swelling overlies

the metacarpals of the hand.
Bulging becomes accentuated
with full extension of all the
fingers of the hand.

Subluxation of the wrist in

severe disease, associated with
extensor tenosynovitis and
extensor tendon rupture.

27
Nailfold infarcts due to
vasculitis in a patient with
rheumatoid arthritis

Malar (butterfly) rash in young

woman with systemic lupus
erythematosus 0ver bridge of
nose and cheeks, sparing
nasolabial folds.

Alopecia affecting the frontal

scalp with lupus hairs (receding
hair line).

Oral aphthoid lesions and

ulcerations of the palatal
mucosa in a patient with
systemic lupus erythematosus.

28
Classic discoid lupus
erythematosus of the face.
Note central scarring and
erythematous hyperkeratotic
borders.

Podagra or acute gout of the

first sMTP joint is shown. The
hyperintense erythema with a
dusky hue is characteristic. The
area of inflammation usually
extends beyond the area of the
involved joint

Advanced gout of the hands

and wrists demonstrates an
asymmetric arthritis with
articular and interarticular
tophi. The large tophus
involving the distal left fourth
digit shows very superficial
crystalline deposits

Subcutaneous tophi in the

palmar creases of the distal
inter-phalangeal joints are an
uncommon finding but an easy
source of crystals for the
diagnostic confirmation of gout.

29
Large tophi involving the distal
interphalangeal joints are
commonly seen in gouty
patients. This is particularly
characteristic of late-onset
gout.

Osteoarthritis is the most

common disorder affecting this
segment (Heberden’s nodes).

Heberden’s node (black arrow)

and Bouchard’s node (white
arrow) in hand osteoarthritis

30
Hand orthoses may decrease
pain and correct deformities.
From top to bottom: a resting
splint that restricts motion and
maintains a functional position,
a functional wrist splint that
supports the wrist during hand
activities, and a silver ring splint
that corrects and/or prevents
deformities.

31
MCQ Which has the most specificity for the disease
matched?
Which of the following is most specific for SLE?
a) Anti-Ro (SS-A) – Sjögren’s
a) Anti-Sm
b) ANA – SLE
b) anti Jo 1
c) Anti-Sm – SLE
c) ANA
d) Rheumatoid factor – Rheumatoid arthritis
d) Anti-La
e) Anticentromere
Which of the following is the most sensitive to
differentiate RA from SLE?
Q2:A 25 year old woman in her first pregnancy is
concerned about her sister’s history of a child that
a) Rheumatoid factor
died in the neonatal period with complete heart
b) Keratoconjunctivis sicca
block. Best choice of investigations for this
c) Bilateral knee effusions
woman?
d) Nodules over the MCP joint
a) ANA
e) Erosion of the ulnar styloid
b) Anti La (SSB) antibodies
c) Anti-phospholipid antibodies
Female patient with rheumatoid arthritis and
d) Anti-cardiolipin antibodies
occipital headaches. Next Investigation should be
e) Anti DNA
a) CT of neck
b) Lateral flexion X-ray of cervical spine
Which of the following is not included in the
c) ESR
American College of Rheumatology (ACR)
d) Myelogram
diagnostic criteria for SLE?
e) Anti-CCP
a) Thrombocytopenia
b) Elevated ANA antibody titre
Uric acid excretion is
c) Psychosis
a) increased by low dose aspirin
d) Alopecia
b) decreased in leukemia
e) Photosensitivity
c) Increased in hypertension
d) increased by alcohol consumption
A disproportionate rise in CRP compared to the
e) largely unaffected by Indomethacin
ESR is typically found in which of the following
clinical situations?
A 26-year-old woman attended the early arthritis
a) RA
clinic with a 3-month history of an inflammatory
b) Sepsis in a patient with SLE
polyarthritis affecting her hands and feet.
c) Gout
Investigations: haemoglobin 125 g/L (115–165),
d) Cerebral lupus
white cell count 7.3 x 109/L (4.0–11.0), platelet
e) Felty's syndrome
count 350 x 109/L (150–400), ESR 40 mm/1st h
(<20), X-rays of hands and wrists periarticular
A patient has mild SLE with butterfly rash &
osteopenia. What investigation is most likely to
Arthralgia. ESR ↑, ANA +ve, renal function
distinguish between persistent and self-limiting
normal, platelets mildly ↓. What is the best
arthritis?
treatment?
a) Anti-citrullinated peptide antigen antibodies
a) Prednisone
b) Antinuclear antibodies
b) Hydroxychloroquine
c) IgA rheumatoid factor
c) NSAID
d) IgG rheumatoid factor
d) Cyclophosphamide
e) IgM rheumatoid factor
e) Observe
Which of the following is not a feature in
Which of the following has the least prognostic
rheumatoid hand
value in early RA?
a) Wasting of small muscles of the hand
a) C-reactive protein
b) Tenosynovitis
b) Extra-articular affection
c) Heberden's nodules.
c) Radiographic evidence of erosions
d) Swan neck deformity
d) Decreased peripheral lymphocyte count
e) Z shaped thumb
32
Which of the following articular regions are Regarding rheumatoid factor, which of the
unlikely to be involved in rheumatoid arthritis following is not true?
a) Distal interphalangeal joints a) May be present in the absence of rheumatoid
b) Proximal interphalangeal joints arthritis.
c) Metaocarpophalangeal joints b) High titer early in rheumatoid arthritis
d) Knee joints indicate bad prognosis.
e) Wrist joints c) Usually present in rheumatoid patients with
subcutaneous nodules
Which of the following radiologic appearance is d) Absent in normal population
not associated with in rheumatoid arthritis e) One of the criteria of diagnosis of rheumatoid
a) Marginal erosions. arthritis.
b) Juxtaarticular osteoporosis.
c) Increased joint space Which of the following is most specific for
d) Subluxation rheumatoid arthritis
e) Soft tissue swelling a) Rheumatoid factor
b) Anti CCP
Regarding systemic lupus erythematosus, which of c) Anti ds DNA
the following is true? d) Anti Sm
a) It is commoner in males. e) Anti Ro
b) Phtotsensitivity may occur
c) Complement level C3 and C4 are increased The following is associated with poor prognosis in
d) Erosion is common in plain x-ray rheumatoid arthritis except
e) Antinuclear antibodies are usually negative a) Acute onset
b) Bone erosion on x-ray
The following is not a clinical feature of SLE c) Subcutaneous nodules
a) Depression d) Low ESR
b) Alopecia e) Extraarticular manifestations
c) Pleural effusions
d) Extraarticular nodules. Chloroquine
e) Arthralgia a) Used in treatment of osteoarthriris
b) May cause retinopathy
Hyperuricaemia may result from low dose of c) May cause hyperuricaemia
a) Methotrexate d) Contraindicated in rheumatoid arthritis
b) Aspirin e) 2nd line treatment of osteoarthritis
c) Corticosteroids
d) Anti-TNF α agents The following is not a feature of Felty's syndrome
e) Indomethacin a) Associated with rheumatoid arthritis
b) Splenomegaly
The following drug is used in acute gout c) Dry eye and mouth
a) Aspirin d) Neutropenia
b) Probenecid e) Rheumatoid factor is usually positive
c) Allopurinol
d) Colchicine Which of the following is not a feature of
e) Methotrexate osteoarthritis
a) Heberden's nodes
Gout b) Osteophyte formation
a) Is associated with calcium pyrophosphate c) Bouchard's nodes
crystals deposited in the cartilage. d) Raised ESR.
b) May cause subcutaneous nodules. e) Morning stiffness < 1 hour.
c) Commonly affect 1st metacarpophalangeal
joint. Regarding rheumatoid arthritis, which of the
d) Typically has symmetric polyarthritis pattern following is not true?
e) Associated with HLA-DR a) Commoner in females
b) Associated with HLA-DR
33
c) Insidious onset indicate bad prognosis Regarding therapeutic cold, which of the following
d) Corticosteroids in high doses is a mainstay of is not true?
the treatment a) Has sedative effect on sensory nerves
e) Pregnancy usually associated with disease b) increase spasticity
remission c) Reduce swelling
d) Reduce bleeding
Which of the following is not a side effect of e) Used in mechanical trauma
NSAIDs
a) Long term use may enhance joint Forced motion used to restore normal range of
degeneration process. motion which is limited due to loss of elasticity of
b) Headache soft tissues
c) Peptic ulcer a) Passive exercise
d) Retinal damage b) Active assistive exercise
e) Transient elevation of liver enzymes c) Active resisted exercise
d) Stretch exercise
The following may exacerbate systemic lupus e) Traction
erythematosus
a) Low dose aspirin Patient with osteoarthritis is advised to
b) Exposure to the sun a) Sit too long in one position.
c) High purine diet b) Use low chairs.
d) Prednisolone c) Walk for long periods.
e) Alcohol d) Over exercise the affected joints.
e) Reduce his body weight.
Regarding sjogren's syndrome:
a) Associated with systemic lupus As regards physical therapy, which of the
erythematosus. following is not true?
b) Associated with dry eye and mouth a) It is the use of physical agents in treatment of
c) Associated with Anti-Sm in most patients the musculoskeletal disorders.
d) Associated with high serum uric acid b) Heat and cold are forms of physical therapy
e) Osteophyte is a common finding in x-ray agents
c) Has no rule in female infertility
Sulphasalazine d) Good alternative that reduce hazards of
a) Is ineffective in RA. NSAIDs
b) Is effective in osteoarthritis e) Have a role in sports injuries
c) May cause infertility in male
d) May cause neutrophilia Splints are not used to
e) Is the first drug of choice in chronic gout a) Relief pain for active joints
b) Prevent deformities
Regarding osteoarthritis c) Correct deformities.
a) Knee joint affection is rare d) Place of damaged joint in good functional
b) Tophi are common findings position.
c) There is articular cartilage destruction e) Produce separation of the vertebrae
d) Obesity is a risk factor
e) Methotrexate is effective Red flags for low back pain include the following
except
Therapeutic heat a) Bilateral radiation of pain
a) Produce capillary and arteriolar b) Bowel or bladder dysfunction
vasoconstriction c) Saddle anesthesia
b) Decrease pain threshold d) Positive stretch test
c) Increase muscle spasm e) Pain and stiffness > 30 minutes,
d) Used in muscle re education
e) Has analgesic effect
f) Stretch adhesions in among muscle fibers

34