Table of Contents
Page created on May 10, 2020. Last updated on April 2, 2022 at 15:07
According to the topic list, these are not exam question topics but rather the “mandatory requirements for a successful exam”, so basically MRTs. I think they’re a good place to start for learning rheuma. There’s considerable overlap between these “MRTs” and the real “topics”, so hopefully these are the most important things to know for the subject.
1. When do you suspect a systemic autoimmune disease?
- Typical symptoms in rheumatological diseases
- Recurrent fever of unknown origin
- Myalgia, arthralgia
- Pain or stiffness in muscles, joints, neck, back
- Muscle pain is often symmetrical and proximal
- Skin symptoms
- Rash
- Urticaria
- Skin lesions
- Discoloration
- Vespertilio = butterfly rash
- Livedo reticularis
- Net-like reddish-blue skin discoloration
- Lilac discoloration of hands or feet
- Raynaud syndrome
- Headache, dizziness
- Sicca symptoms
- Feelings of dryness in eyes or mouth
- Weakness of extremities (muscle weakness)
- Thrombosis, embolization
- Spontaneous abortion
- Typical signs of rheumatological diseases
- Leukopaenia or pancytopaenia
- Leukocytosis
- Hepatosplenomegaly
- Lymphadenomegaly
- Urine test
- Proteinuria
- Haematuria
- Cylindruria
- Polyneuritis, neuropathy
- Lung fibrosis
- Pulmonary arterial hypertension
- Elevated ESR, CRP, CK
- Abnormal liver or kidney function
- Family with autoimmune disease
2. Autoantibody screening tests, most important specific autoantibody tests.
- Autoantibodies are classified depending on the location of the antigen
- Anti-nuclear antibodies (ANAs)
- Antigens are located in the nucleus
- Anti-neutrophil cytoplasmic antibodies (ANCAs)
- Antigens are located in the cytoplasm
- Miscellaneous antibodies
- Anti-nuclear antibodies (ANAs)
- When testing for autoantibodies we can test for the specific autoantibodies (more expensive) or for a larger group of autoantibodies (like ANAs and ANCAs)
- For example, when screening for SLE we check the ANA titre (levels) of the patient, i.e. if the patient has elevated levels of any anti-nuclear antibody
- ANA titre is very sensitive for SLE, but is not specific
- Someone with negative ANA titre probably doesn’t have SLE, but someone with a positive titre can have SLE or any other rheumatological disease
- Anti-dsDNA and Anti-Sm, however, are specific for SLE
- ANAs
- ANA titre is typically elevated in connective tissue diseases
- Anti-dsDNA
- Antibody against double-stranded DNA
- Specific for SLE
- Elevated in 70% of SLE patients
- Correlates with disease activity and lupus nephritis
- Anti-Sm
- Antibody against Smith antigens (nonhistone nuclear proteins)
- Specific for SLE
- Elevated in 30% of SLE patients
- Anti-histone
- Elevated in SLE and drug-induced lupus erythematosus
- Elevated in 95% of drug-induced LE patients
- Meaning it’s very sensitive for it
- Anti-Ro/SSA and anti-La/SSB
- Elevated in Sjögren and SLE
- 70% of Sjögren patients are positive for one or both antibodies
- Anti-Scl-70
- Antibody against topoisomerase I
- Elevated in 50% diffuse systemic sclerosis, and is associated with poorer prognosis
- Can be elevated in other diseases, too
- Myositis-specific antibodies
- They are specific but not sensitive for inflammatory myopathies
- Dermatomyositis, polymyositis, etc.
- Anti-Jo1
- Elevated anti-Jo1 means worse prognosis
- Anti-Mi2
- Elevated anti-Mi2 means better prognosis
- They are specific but not sensitive for inflammatory myopathies
- ANCAs
- ANCA titre is typically elevated in vasculitides
- c-ANCA (cytoplasmic ANCA)
- Antibody against proteinase 3
- Elevated in granulomatosis with polyangiitis
- Both specific and sensitive
- p-ANCA (perinuclear ANCA)
- Antibody against myeloperoxidase
- Elevated in microscopic polyangiitis, Churg-Strauss syndrome and primary sclerosing cholangitis
- Miscellaneous antibodies
- Antiphospholipid antibodies
- These autoantibodies are pro-coagulant and are the hallmark of antiphospholipid syndrome
- The autoantibodies deactivate anticoagulant proteins or activate platelets
- Most common:
- Anti-cardiolipin
- Lupus anticoagulants
- Anti-C1q antibodies
- Elevated in SLE
- Correlates with disease activity and lupus nephritis
- Anti-centromere
- Elevated in CREST syndrome (limited cutaneous systemic sclerosis)
- Rheumatoid factor (RF)
- Antibody against the Fc-region of IgG
- Can be elevated in many conditions, but was classically associated with RA
- Can even be elevated physiologically
- Anti-CCP
- Antibody against cyclic citrullinated peptide
- Elevated in RA, more specific than RF
- Antiphospholipid antibodies
- Autoantibody screening test
- Many autoimmune diseases cause elevation of ANAs, so screening for elevated ANA titre is an appropriate first step when these diseases
- SLE
- Systemic sclerosis
- Inflammatory myositis
- Sjögren syndrome
- Many autoimmune diseases cause elevation of ANAs, so screening for elevated ANA titre is an appropriate first step when these diseases
3. In case of unknown inflammation, what conditions can be considered?
- Definition of inflammation of unknown origin (IUO)
- Signs of inflammation (elevated CRP, ESR)
- No established etiology despite initial evaluation and diagnostic testing
- These patients often don’t have symptoms which are specific for the disease they suffer from
- Fever of unknown origin
- There is significant overlap between fever of unknown origin (FUO) and inflammation of unknown origin
- However, some patients have signs of inflammation without fever
- Regardless, the same etiologies and diagnostic approaches can be applied to FUO as IUO
- IUO and FUO are temporary diagnoses, both of which prompt more rigorous diagnostics to determine the underlying cause
- However, up to 50% of FUO patients remain undiagnosed despite efforts. These patients often have good outcome, despite remaining undiagnosed
- Many cases of IUO and FUO are serious conditions which have coincidentally been caught before they produce symptoms
- Early diagnosis of these conditions will improve the prognosis
- Diagnostic approach to IUO and FUO
- Repeated and thorough medical history and physical examination
- Laboratory testing
- Autoantibody screening
- Blood cultures
- LDH
- Viral serology
- Tuberculin skin test
- Serum protein electrophoresis
- Imaging
- FDG-PET/CT
- Can detect foci of inflammation and malignancy
- CT abdomen and chest
- FDG-PET/CT
- Common causes of inflammation and fever of unknown origin
- These are conditions that can remain symptomless for a long time
- Inflammatory diseases
- SLE
- RA
- Juvenile idiopathic arthritis
- Systemic vasculitides
- Especially giant cell arteritis
- Inclusion body myositis
- Spondyloarthropathies
- Psoriatic arthritis
- Ankylosing spondylitis
- Inflammatory bowel disease
- Polymyalgia rheumatica
- Adult Still’s disease
- Infections
- Tuberculosis
- Abscesses
- Malignancies
- Lymphomas
- Leukaemia
- Other solid cancers
4. Differentiation between pain in degenerative disorders (osteoarthritis) and inflammatory conditions (arthritis)
- Degenerative pain
- Often develops more suddenly
- Pain often worsens with movement
- Pain often improves with rest
- Often affects weight-bearing joints
- Often asymmetrical
- Inflammatory pain
- Often responds better to NSAIDs
- Often improves with movement and exercise
- Often described as throbbing or deep
- Often does not improve with rest
- Is often present during the night
- Is often associated with morning stiffness for > 30 minutes
5. Main causes of monoarthritis.
- Almost all causes of polyarthritis can initially cause monoarthritis
- Crystal arthropathies
- (Gout, pseudogout, …)
- The most common
- Septic arthritis (= infectious arthritis)
- The second most common
- Gonococcus, staph. aureus, pneumococcus or gram-negatives
- Mycobacterial and fungal are rare
- Lyme arthritis
- Trauma with or without haemarthrosis
- The third most common
- Tumour in or around joint
- Juvenile idiopathic arthritis
6. Main causes of polyarthritis.
- Symmetric
- Rheumatic diseases
- SLE
- Systemic vasculitis
- Systemic sclerosis
- Inflammatory myopathies
- Rheumatoid arthritis
- Osteoarthritis
- Viral arthritis
- Viral arthritis more often causes polyarthritis
- Often parvovirus B19 or hepatitis B, C
- Rheumatic diseases
- Asymmetric
- Bacterial arthritis
- Often cause monoarthritis, but can cause polyarthritis
- Lyme arthritis
- Crystal arthropathies
- Gout, pseudogout
- Spondylarthritides
- Rheumatic fever
- Reactive arthritis
- Ankylosing spondylitis
- Psoriatic arthritis
- IBD-associated arthritis
- Bacterial arthritis
7. Main causes of Raynaud´s syndrome.
- Rheumatological diseases
- Systemic sclerosis
- Mixed connective tissue disease
- Sjögren syndrome
- SLE
- Inflammatory myopathies
- Drugs
- Non-selective beta blockers
- Ergotamine
- Bleomycin, cisplatin and other chemotherapeutical agents
- Hyperviscosity
- Polycythaemia
- Multiple myeloma
- Waldenström disease
- Croglobulinaemia
- Other
- Hand-arm vibration syndrome (vibrational injury)
- Smoking
8. Main causes of proximal muscle weakness.
- Proximal muscle weakness suggests myopathy or myositis
- Inflammatory myopathies
- Polymyositis
- Dermatomyositis
- Muscular dystrophies
- Duchenne muscular dystrophy
- Becker muscular dystrophy
- Diseases affecting NMJ
- Myasthenia gravis
- Drug-induced myopathy
- Glucocorticoids (Cushing syndrome)
- Statins
- Alcohol
- Endocrinopathies
- Hyperthyroidism
- Hypothyroidism
- Addison disease
- Conn syndrome
- Acromegaly
- Diabetic amyotrophy/proximal diabetic neuropathy
9. Main causes of dryness of the eyes.
- Sjögren syndrome
- Primary
- Secondary
- SLE
- RA
- Scleroderma
- Drugs
- Antihistamines
- Anticholinergics
- Tricyclic antidepressants
- Isotretinoin
- Vitamin A deficiency
- Contact lens use
- Sarcoidosis
- Aging
- Graves ophthalmopathy
- Viral
10. What diagnostic steps should be made in upper limb complaints?
- Differential diagnosis
- Carpal tunnel syndrome
- Tenosynovitis
- Lateral epicondylitis (tennis elbow)
- Medial epicondylitis (golfer’s elbow)
- Thoracic outlet syndrome (TOS)
- Clinical features of upper limb complaints
- Pain
- Tension
- Weakness
- Tingling
- Numbness
- Cramp
- Diagnostic steps
- History
- When did symptoms start?
- Were there any injuries?
- What exacerbates or relieves the pain?
- Inspection
- Asymmetry, swelling, deformities, atrophy
- Range of motion
- First active, then passive
- Look for decreased ROM, pain, crepitation
- Palpation
- Look for pain, swelling, warmth
- Muscular and neurological exams
- Compare muscle strength and sensitivity to other side
- Nerve conduction studies
- Abnormal in carpal tunnel
- X-ray
- Can show cervical rib, the most common cause of TOS
- Can show abnormalities of the joints, bones
- Labs
- Autoantibodies, inflammatory markers
- History
11. Most common rheumatological reasons of back pain.
- Seronegative spondyloarthropathies
- Ankylosing spondylitis
- Reactive arthritis
- Psoriatic arthritis
- IBD-associated spondyloarthropathy
12. Most common non-rheumatological reasons of back pain.
- Idiopathic
- 85% of cases are idiopathic
- Osteoarthritis (of facet joints)
- Vertebral compression fracture
- Trauma
- Radiculopathy
- = symptoms due to nerve root damage
- Degenerative changes in vertebrae
- Spinal disc herniation
- Sciatica is often due to radiculopathy
- Spinal stenosis
- Spinal deformities
- Osteomyelitis of vertebrae
- Bone metastases
- Cauda equina syndrome
13. Lumboischialgia (sciatica), clinical features.
- Lumboischialgia = sciatica = back pain that radiates down one leg below the knee
- It’s usually due to nerve root damage
- Usually sharp or burning pain
- Valsalva or movement of lumbosacral spine exacerbates symptoms
14. Clinical signs of L4 root damage.
- Altered gait
- Difficulty walking down stairs
- Pain
- Back
- Radiating into anterior thigh -> medial lower leg
- Sensory loss
- From distal lateral thigh area up to the inner side of the lower leg
- Muscle weakness
- Hip flexion and adduction
- Knee extension
- Reflex deficits
- Patellar reflex
15. Clinical signs of L5 root damage.
- Altered gait
- Difficulty walking on the heels
- Pain
- Back
- Radiating into buttock -> lateral thigh -> lateral calf -> dorsum foot -> big toe
- Sensory loss
- Lateral calf
- Dorsal surface of foot
- Muscle weakness
- Hip abduction
- Knee flexion
- Foot dorsiflexion
- Toe extension and flexion
- Reflex deficits
- Posterior tibial reflex
16. Clinical signs of S1 root damage.
- Altered gait
- Causes difficulty walking on toes
- Pain
- Back
- Radiating into buttock -> lateral or posterior thigh -> posterior calf -> lateral or plantar foot
- Sensory loss
- Posterior calf
- Lateral or plantar foot
- Muscle weakness
- Hip extension
- Knee flexion
- Plantar flexion of foot
- Reflex deficits
- Achilles tendon reflex
17. Side effects of NSAIDs.
- Gastric and duodenal ulcers
- Increased risk of heart attack and stroke
- Decreased renal function
- Analgesic nephropathy (tubulointerstitial nephritis)
- “Aspirin asthma”
18. Contraindications of NSAID therapy. Necessary precautions.
- Contraindications
- Gastroduodenal ulcers
- IBD
- Renal failure
- Recent ACS or heart failure
- High risk for CVD
- Before surgery
- Pregnancy
- Precautions
- To prevent side effects in those who take NSAIDs for chronic conditions, intermittent dosing and the lowest effective dose should be utilized
- To prevent ulcers, PPIs or other mucosal protectants like misoprostol can be used
19. Side effects of glucocorticoids.
- Skin atrophy
- Stretch marks
- Acne
- Hypertrichosis
- Hypertension
- Cushingoid appearance
- Hyperglycaemia / secondary diabetes
- Secondary osteoporosis
- Mood disorders
- Cataract, glaucoma
- Avascular necrosis of bone
- Glucocorticoid-induced myopathy and atrophy
- Peptic ulcers
- Adrenocortical atrophy
20. What kind of supportive treatment is necessary in case of systemic corticosteroid therapy?
- Calcium and vitamin D supplementation
- Prevents osteoporosis
- Calcium and vitamin D supplementation are recommended
- For patients at high risk for osteoporosis, bisphosphonates may be used
- Exercise, especially weightbearing exercise
- Prevents osteoporosis, weight gain and muscle atrophy
- Exercise is recommended
- If hypokalaemia develops -> potassium supplementation
- If ulcers develop -> antacids
- Glaucoma -> eye drops
21. What is necessary during emergencies in patients on long term corticosteroid therapy? (infections, injuries)
- Due to glucocorticoid-induced adrenocortical atrophy, stress situations such as infections or injuries cause a relative adrenal insufficiency
- To prevent this, patients on long-term glucocorticoid therapy should receive increased dose of glucocorticoid during infections, injuries, and surgeries
22. Side effects of cytostatic therapies.
- Side effects of methotrexate
- Anorexia
- Gastrointestinal symptoms
- Nausea, vomiting, diarrhoea
- Bone marrow toxicity
- Pancytopaenia/anaemia
- Mucositis
- Especially stomatitis, enteritis
- Hepatotoxicity
- Nephrotoxicity
- Interstitial pneumonitis
- Side effects of azathioprine
- Gastrointestinal symptoms
- Hepatotoxicity
- Bone marrow toxicity
- Increased risk for malignancies
- Side effects of cyclophosphamide
- Increased risk for malignancies
- Especially bladder cancer
- Bone marrow toxicity
- Infertility
- Haemorrhagic cystitis
- SIADH
- Increased risk for malignancies
- Side effects of mycophenolate mofetil
- Gastrointestinal symptoms
- Bone marrow toxicity
- Side effects of calcineurin-inhibitors (cyclosporin, tacrolimus)
- Nephrotoxicity
- Hypertension
- Neurotoxicity
23. Meaning of DMARD
- Disease-modifying antirheumatic drugs (DMARDs)
- Drugs which are primarily used to treat RA, but can be used in other rheumatic diseases as well, like SLE, spondyloarthropathies
- Classic DMARDs
- Methotrexate
- Hydroxychloroquine
- Sulfasalazine
- Cyclophosphamide
- Cyclosporine
- Mycophenolate mofetil
- Leflunomide
- Biological DMARDs
- TNF-alpha or receptor antagonists
- Etanercept
- Infliximab
- Adalimumab
- Golimumab
- Certolizumab
- IL-1 or receptor antagonists
- Anakinra
- Canakinumab
- IL-6 or receptor antagonists
- Tocilizumab
- Sarilumab
- IL-12/IL-23 antagonists
- Ustekinumab
- IL-17 antagonists
- Secukinumab
- CD20 antagonists
- Rituximab
- CD80/86 antagonists
- Abatacept
- Belatacept
- Kinase inhibitor
- Tofacitinib
- TNF-alpha or receptor antagonists
24. Contraindications and side effects of biological therapy.
- Contraindications
- Severe heart failure (NYHA III or IV)
- Known allergy
- Severe infection
- Active or latent TB
- All patients who initiate biological therapy must first be checked for latent TB
- Latent TB must be treated before initiation of biological therapy
- Current fungal infection
- Current or recent cancer
- Demyelinating diseases
- Live vaccines
- Side effects of TNF-alpha antagonists
- Reactions during injection/infusion
- Neutropaenia
- Increased risk for infection
- Bacterial infections, especially intracellular bacteria
- Herpes zoster
- TB
- Opportunistic infections
- Heart failure
- Side effects of CD20 antagonists
- Reactions during injection/infusion
- Increased risk for infection
- Hypogammaglobulinaemia
25. What are the necessary steps in sterile leukocyturia?
- Sterile leukocyturia/pyuria refers to WBCs in the urine without bacteria
- Differential diagnosis of sterile leukocyturia
- Renal tuberculosis or other atypical bacteria
- Nephrolithiasis
- Tubulointerstitial disease (= interstitial nephritis)
- Allergic nephritis
- Nephritis associated with Sjögren or SLE
- Urothelial cancer
- Urinary tract infection treated with antibiotics
- Indwelling catheters or stents, or recent procedures in the urinary tract
- Steps in diagnosis
- Repeat urine analysis
- Contamination or wrong sampling may cause apparent sterile leukocyturia
- Clinical history
- Recent drug or antibiotic use
- Recent travel to places endemic for TB
- Family history of rheumatic disease
- Recent weight loss
- Look for other symptoms of possible diagnoses
- Skin symptoms
- Lymphadenomegaly
- Haematuria
- Labs
- CBC
- Renal function
- Liver function
- Culture of mycobacteria
- Repeat urine analysis
Main rheumatological illnesses.
26. Most common early clinical signs in SLE.
- Discoid rash
- Arthritis
- Photosensitivity
- Malar rash
- Raynaud phenomenon
- Low-grade fever of unknown origin
27. Most common laboratory changes in SLE. What is to be done in SLE?
- Labs
- Increased ESR
- CRP is often normal
- Cytopaenias
- Autoimmune haemolytic anaemia
- Thrombocytopaenia
- Leukopaenia
- Lymphopaenia
- Autoantibodies
- Anti-dsDNA
- Anti-Sm antibodies
- Antiphospholipid antibodies
- Decreased level of complement factors
- Urine analysis
- Proteinuria
- Cylindruria
- Haematuria
- Increased ESR
- Aim of treatment of SLE
- Suppression of autoimmune phenomena (disease activity)
- Prevention and treatment of organ damage
- Preventing relapses
- Treatment of symptoms
- Improve quality of life
- Treatment
- NSAIDs
- If arthritis
- Hydroxychloroquine or chloroquine
- In all SLE patients without contraindications
- Prolongs disease-free periods, prevents relapses
- Induction therapy
- Short period of glucocorticoids ± other immunosuppressants
- Lasts until remission is achieved
- Mycophenolate mofetil or cyclophosphamide
- If lupus nephritis
- Blood pressure control
- To protect kidneys
- NSAIDs
28. Most common clinical signs in antiphospholipid syndrome.
- Recurring thrombosis of any organ is typical for APS
- Venous
- DVT/PE
- Livedo reticularis
- Arterial
- Stroke, TIA
- Occlusion of arteries anywhere
- Miscarriages
- Splinter haemorrhages
- Small haemorrhages under the nails
29. Possible reasons of thrombosis in a young patient.
- Acquired
- Oral contraceptives
- Smoking
- Pregnancy
- Surgery/hospital admission
- Antiphospholipid syndrome
- Cancer
- Hyperhomocysteinaemia
- Hypertension
- Dyslipidaemia
- Inherited thrombophilia
- Protein S or C deficiency
- Factor V Leiden mutation
30. Most common early clinical signs in rheumatoid arthritis.
- Affected joints
- Wrist
- Knee
- Proximal interphalangeal joints (PIP)
- Metacarpophalangeal joints (MCP)
- DIP joints are rarely affected in RA
- Morning stiffness of joints
- Swelling of joints
31. Most common laboratory and radiological changes in RA.
- Labs
- Anti-citrullinated peptide autoantibody (ACPA)
- Anti-CCP (cyclic citrullinated peptide) is the most common form
- Elevates earlier than RF
- More specific for RA than RF
- Rheumatoid factor (RF)
- No specific for RA
- Elevated CRP and/or ESR
- Anti-citrullinated peptide autoantibody (ACPA)
- Radiological changes
- Symmetric joint space narrowing
- Local, juxtaarticular osteoporosis
- Marginal erosions of cartilage and bone
32. Most common early clinical signs in ankylosing spondylitis
- Lower back pain of inflammatory character
- Lasts more than 3 months
- Onset before 40 years
- Waking up during the night because of pain
- Alternating buttock pain
33. Most common early clinical signs in psoriatic arthritis.
- Peripheral arthritis
- Joints of hand, feet
- Axial arthritis
- Joints of spine
- Enthesitis
- Dactylitis
34. Clinical signs and management in acute gout.
- Clinical signs of acute gout
- Monoarthritis
- Most typical
- Often involving the big toe, in which case it’s called podagra
- Polyarthritis
- Less typical (< 15% of cases)
- Mostly the small joints of the hands or feet
- Sudden unbearable pain
- Oedematous and erythematous joint
- Monoarthritis
- Management of acute gout
- Ice and rest
- NSAIDs or colchicine, depending on contraindications and previous experience of what works best
- If contraindications to both and only one joint is affected -> intraarticular glucocorticoids
- If contraindications to both and multiple joints are affected -> oral glucocorticoids
- Reasons to not prefer NSAIDs:
- Renal failure
- Hyperkalaemia
- GI ulcer
- Known allergy
- Reasons to not prefer colchicine
- Known allergy
- Renal or hepatic failure
- Drug interactions
- The time between episodes of acute gout is called intercritical gout
- During this stage patients are asymptomatic
- Most patients experience another attack within 1 year
- The intercritical period may last for years
35. Clinical signs and management in chronic gout.
- Chronic gout
- Chronic gout is the stage where, after many episodes of acute gout over many years, the joints have been progressively destroyed, causing constant symptoms
- Formation of tophi also occurs during this stage
- Thanks to modern treatment and prevention of acute gout episodes, chronic gout has become rare
- Prevention of acute gout episodes
- Weight loss
- Diet low in purines
- Decrease alcohol consumption
- Ensure sufficient fluid intake
- Medical therapy
- Initiation of medical therapy may trigger an acute gout attack
- Colchicine should be given for a while to prevent this
- Xanthine oxidase inhibitors
- First-line treatment
- Allopurinol
- Febuxostat
- Uricosuric medications
- Second-line treatment
- Probenecid
- Benzbromarone
- Recombinant uricase
- Third-line treatment
- Usually only used in case of tophi
- Pegloticase
- Biological therapy
- For severe gout
- Anakinra
- Rilonacept
- Canakinumab
- Fenofibrate and losartan have slight uricosuric effects, and may be useful in treating patients with gout and hypertriglyceridaemia or hypertension, respectively
36. Infectious arthritis, complaints, clinical features, investigations.
- Septic or infectious arthritis refers to infection of a joint
- It is a medical emergency
- May cause serious disability or death
- May enter the joint directly or by haematogenous spread
- Etiology
- Old age
- Pre-existing joint disease
- Recent joint procedures
- IV drug use
- Immunosuppression
- Microbiology
- Bacteria (most common)
- Staphylococcus aureus (most common)
- Streptococci
- Gram negative bacilli
- Viruses
- Parvovirus B19
- HBV, HCV
- Bacteria (most common)
- Clinical features
- Monoarthritis
- Knee most commonly affected
- Also wrists, ankles, hips
- Polyarthritis
- Rare
- Less rare in patients with pre-existing joint disease and viral cause
- Swollen and painful joint
- Warm joint
- Decreased range of motion
- Fever
- Monoarthritis
- Diagnosis
- Synovial fluid analysis
- All suspected cases must undergo synovial fluid analysis
- Fluid is retrieved by arthrocentesis
- Elevated WBCs (> 50 000 cells/µL)
- Mostly neutrophils
- Yellowish-green, turbid synovial fluid
- Gram stains
- Bacterial culture
- Crystal analysis by polarizing microscopy
- To rule out gout, pseudogout
- Blood culture
- To rule out bacteraemia
- Imaging of the joint
- To identify extent of damage, rule out concurrent bone and joint disease, etc.
- X-ray, ultrasound, etc.
- Synovial fluid analysis
- Treatment
- Antibiotics based on culture results
- Joint drainage
Non inflammatory rheumatological conditions.
37. Clinical signs of knee osteoarthritis
- Usually bilateral
- Mechanical/degenerative type pain
- Pain worsens when weight bearing and walking downhill
- Swelling of knee
- Crepitus
38. Clinical signs of hip osteoarthritis
- Usually unilateral
- Pain in inguinal area and above greater trochanter
- Contractures
- Decreased extension, internal rotation, abduction
- Internal rotation is usually the earliest affected movement
- Pain worsens when walking uphill and rising from seated position
39. Investigations in osteoporosis
- Dual-energy X-ray absorptiometry (DEXA scan)
- Gold standard
- Calculates bone mineral density
- If T-score < – 2,5 -> osteoporosis
- Clinical diagnosis of osteoporosis
- If a fragility fracture is present, the diagnosis of osteoporosis can be made without DEXA
- Fragility fractures are most common in the vertebra (vertebral compression fracture), hip, and wrist
- Fragility fractures are fractures which occur spontaneously or from very minor trauma
- Excluding causes of secondary osteoporosis
- Patient history
- Glucocorticoid use
- Smoking
- Alcohol abuse
- Physical inactivity
- Physical examination
- Features of Cushing syndrome
- Laboratory tests
- Biochemistry profile
- CBC
- TSH
- Vitamin D level
- Alkaline phosphatase
- Patient history
40. Calculation of FRAX index
- Fracture risk assessment tool (FRAX)
- Estimates 10-year probability of hip fracture or other osteoporotic fractures for untreated patients
- This probability, combined with DEXA score and clinical judgement, are used to guide treatment
- Based on
- Age
- Gender
- Weight
- Height
- Previous fracture
- Parent with fractured hip
- Currently smoking
- Currently taking glucocorticoids
- Currently has RA
- Currently has secondary osteoporosis
- Drinks 3 or more units per day
- Bone mass density of femoral neck (measured with DEXA)
41. Main reasons of secondary osteoporosis
- Cushing syndrome
- Vitamin D deficiency
- Chronic renal disease
- Malabsorption
- Liver disease
- Alcohol abuse
- Drugs
42. Medications that cause osteoporosis. Prevention.
- Medications that cause secondary osteoporosis
- Glucocorticoids
- PPIs
- Anticonvulsants
- Anticoagulants
- Prevention of osteoporosis
- Avoid risk factors
- Ensure sufficient intake of calcium and vitamin D
- Physical exercise, especially weight and balance training
43. Compression fracture of the spine.
- Most common type of vertebral fracture
- Etiology
- Trauma (usually axial force)
- Osteoporosis (fragility/pathological fracture)
- Ankylosing spondylitis
- Clinical features
- Progressive thoracic kyphosis
- Loss of height
- If due to osteoporosis -> asymptomatic
- Treatment
- Physical therapy
- Orthotics
- Surgery
- Vertebroplasty – injection of bone cement into compressed vertebrae
- Kyphoplasty – inflating of balloon in compressed vertebrae + injection of bone cement
44. Most common signs of gout.
- See 34, 35
45. What should be excluded in case of carpal tunnel syndrome?
- Rheumatoid arthritis
- Diabetes mellitus
- Hypothyroidism
- Connective tissue diseases
- Systemic sclerosis
- Polymyositis
- Polymyalgia rheumatica
46. Management of anaphylactic shock.
- First-line treatments
- Withdrawal of offending agent
- Supine position with feet elevated
- Ensure airways
- O2 by mask
- Epinephrine IM
- 0,3 – 0,5 mg IM
- Repeat every 5 – 15 minutes if needed
- Adjunctive treatments
- Methylprednisolone
- Albuterol/salbutamol
- If bronchospasm doesn’t improve after epinephrine
- Inhaled
- Antihistamines IV
- Only relieves cutaneous symptoms
- IV saline
- If hypotension
Practical skills during patient examination
These are not technically a part of the MRTs (I think) but they’re important to know anyway.
1. GALS examination.
- GALS is an objective and quick screening for locomotor abnormality and functional disability
- High sensitivity, low specificity
- Questions
- Do you have any pain or stiffness in muscles or joints?
- Can you dress yourself completely without difficulty?
- Can you walk up and down stairs without difficulty?
- Aims
- Are any of the joints abnormal?
- What is the nature of the joint abnormality?
- What is the extent (distribution) of the joint involvement?
- Are any other features of diagnostic importance present?
- Gait
- Observe patient walking, turning and walking back
- Look for:
- Smoothness and symmetry of leg, pelvis, arms movement
- Normal stride length
- Ability to turn quickly
- Examples of abnormalities
- Limping
- Parkinson patients have poor arm swing and turn slowly
- Arms
- Examine muscle bulk and joint deformities in the anatomical position
- Check that elbows are straight and in full extension
- Ask patient to place both hands behind the head, then push elbows back
- Observe shoulder joints, clavicular joints, rotator cuff function, elbow flexion
- Inspect palm and back of the hands
- Observe muscle bulk, joint swelling, deformities
- Ask patient to perform supination and pronation of the hand
- Ask patient to make a fist
- Ask patient to squeeze 2 of your fingers as hard as they can
- Observe grip strength
- Ask patient to touch each finger of each hand to the thumb
- Squeeze joints of the hand and look for pain
- Examine muscle bulk and joint deformities in the anatomical position
- Legs
- Examine lower extremities for deformities, rashes or calluses
- Passively flex and extend the hip and knee
- Observe range of motion, feel for crepitus
- Passively internally and externally rotate the hip, with the knee bent
- Examine each knee for the presence of fluid
- Press the patella down
- Squeeze joints of the foot and look for pain
- Spine
- From behind
- Examine back and gluteal muscle bulk and symmetry
- Examine straightness of spine
- Check levels of iliac crest
- Check for popliteal swellings
- Check Achilles tendons
- Press over the mid-point of each supraspinatus muscle
- Tenderness suggests fibromyalgia
- Squeeze the skin over each trapezius muscle
- Tenderness suggests fibromyalgia
- From the side
- Examine curvatures of the spine
- Examine deformities of the hip or knees
- Ask patient to bend forward
- Assess lumbar spinal and hip flexion
- From the front
- Ask the patient to raise the shoulder on each side
- Assesses lateral cervical flexion
- Ask the patient to open mouth wide and move the jaw from side to side
- Assesses TMJ function
- Ask the patient to raise the shoulder on each side
- From behind
2. Characteristic cutaneous signs in rheumatology. (Infectious arthritis, gout, livedo, scleroderma, erythema, vasculitis, psoriasis).
- See derma
3. Physical examination of the hand. (synovitis, arterial pulse, skin signs, characteristic deformities, carpal tunnel syndrome, Heberden-Bouhard nodes etc.).
- Synovitis of hand
- Pain upon passive extension of affected tendon
- Swelling
- Crepitation
- Deformities of the hand in RA
- Swan neck deformity
- PIP hyperextension + DIP flexion
- Boutonniere deformity
- PIP flexion + DIP hyperextension
- Ulnar deviation of hand
- Hitchhiker thumb deformity
- Hyperextension of interphalangeal joint + flexion of MCP joint
- Swan neck deformity
- Carpal tunnel syndrome
- Clinical features
- Paraesthesia of area innervated by median nerve
- Weakened grip
- Thenar atrophy
- Physical examination
- Tinel sign
- The are over the carpal tunnel is percussed
- If this leads to pain or paraesthesia of the affected area, the test is positive
- Phalen manoeuvre
- Wrist is held in full flexion for a minute
- If pain or paraesthesia of affected area occurs, the test is positive
- Tinel sign
- Clinical features
- Heberden nodules
- Seen in osteoarthritis
- Pain and nodular thickening on dorsal side of DIP
- Bouchard nodules
- Seen in osteoarthritis
- Pain and nodular thickening on dorsal side of PIP
4. Differentiation between inflammatory and degenerative back pain.
- See 4
5. Other physical examination tests
- Schober test
- With patient standing, find the patients L5. Mark two points, one point 10 cm above the L5 and one point 5 cm below it
- Ask patient to touch their toes while keeping knees straight
- The distance between the two points should increase by at least 5 cm
- If not = restriction in lumbar flexion. Typical in ankylosing spondylitis
- Domján test (lateral spinal flexion test)
- Patient stands with arms next to their body
- A mark is made on the leg at the level of the tip of the middle finger
- The patient is asked to laterally flex their spine towards the side where the mark was made. This causes the arm on that side to move further down the body
- Another mark is made on the leg at the level of the tip of the middle finger
- The distance between the two marks reflects the degree of lateral spinal flexion
- > 10 cm is normal
- Mennel sign
- Patient lies on their belly
- Examiner lifts one of the patient’s legs up while pressing on the lumbar spine with the other hand
- Pain implies sacroiliitis
- Lasegue test (straight leg raise test)
- Patient lies on their back
- Examiner lifts one of the patient’s legs up while keeping the knee straight
- Pain implies herniated disc
- Detailed examination of the knee
- See ortho
Hi! Thank you for the great notes.
I’m asking this question on behalf of a friend:
Imagine my friend did something very stupid and signed up for rheuma exam with only three days to study.
Do you think my friend would pass this exam just by studying these MRT notes?
I don’t know whether you have oral or written this semester, but I don’t think they’ll be enough in either case. They’re definitely not enough for written. They might approach “enough” for an oral exam, but I think you need a bit more than this.