RHEUM1 Flashcards

(50 cards)

1
Q

Clinical features of PMR?

A

USUALLY:

Bilateral ache and stiffness in the shoulders

Elevated ESR

AGE over 50

Supportive:

MORNING STIFFNESS over 45minutes

hip girdle discomfort or limited ROM

Absence of other joint involvement

Absence of RF and CCP antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the treatment for polymyalgia rheumatica

A
  1. Oral Corticosteroid therapy.
  2. Keep active - gentle exercise
  3. Monitor progress - safety netting re: relapse during treatment or signs or symptoms of GCA (to re-present immediately)

Prednisolone 15mg for 4 weeks

Then reduce dose by 2.5 mg every 4 weeks until 10mg

Then Reduce dose by 1mg every 4 to 8 weeks

then stop.

IF active symptoms do not reduce dose.

Warn patients that with reductions in dose they may feel transient symptoms - flu like symptoms and mild ache - continue with planned reductions unless significant relapse in symptoms occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What percentage of people with PMR also have GCA?

A

About 15 percent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the clinical features of GCA

A

Age over 50

Female > M

New onset localised headache

ESR over 50

Tenderness over temporal artery (pos temp art biopsy)

JAW CLAUDICATION

Visual symptoms

Malaise

Require urgent referral to Opthalmologist

Commence oral predinisolone 40mg daily for MINIMUM 4 weeks

Reduce by 10 mg every 2 weeks to 20mg

then reduce by 2.5 mg every 2 weeks to 10mg

then 1mg every 4 weeks to stop

(PROVIDED THERE IS NO RELAPSE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What considerations will you take into account when commencing long term corticosteroid therapy

A
  1. Adequate supplementation of Calcium 1200mg/day
  2. Adequate supplementation of Vitamin D 800 IU/day
  3. Measure BMD (Lumbar spine and hip)
  4. If BMD less than 1.5 consider commencement of bisphosphonate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How would you describe the pathophysiology of osteoarthritis? HOw would you explain the condition to a patient?

A

OA is an ACTIVE process where the join is responding to a) underlying structural damage within the joint or b) to obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the risk factors for osteoarthritis

A

Modifiable

Obesity

Injury

Mal-alignment

Non Modifiable

Female sex

Older Age

Family History of OA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which joints are affected in Osteoarthritis

A

Any joint

Commonly

Hands - DIPs (with heberdens), PIP (bouchards), and 1st CMC (carpal-metacarpal) (thumb)

Cervical spine

Lumbar spine

Knees

Hips

Feet

CAN be: Monoarticular, oligoarticular, polyarticular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What questions would you ask on history for a patient with Osteoarthritis/joint pain?

A

How long have you had the symptoms and how have they changed? Has anything made it worse?

Which joints are most painful?

Do you find symptoms are worse in the morning? Do you feel stiff firts thing in the morning? if So for how long?

Do you find your pain is exacerbated by activities? If so which activities?

Do you have any swelling? Is it constant or does it fluctuate?

Do you have a family history of joint problems?

Do you have pain at night?

Associated conditions: Psoriasis, Inflammatory bowel disease, other autoimmune diseases

Exercise levels, Diet, Weight

Menopause? Hormonal changes?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examination features of OA?

A

Weight and BMI

Joint examination to confirm changes associated with OA such as bony deformity and enlargement

Signs of inflammatory joint disease such as boggy swelling of joints, fluid in joints, heat and erythema

Muscle condition (wasting or weakness)

Extra-articular signs of rheumatic disease - eg psoriasis?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What Xray features are consistent with OA

A

Characteristic joints affected

  • in hands - DIPs, PIPs, 1st CMC joint

relative sparing of the MCPs

  • peri-articular bone sclerosis

marginal osteophyte formation

loss of cartilage

–> Loss of joint space

Cyst formation

Can get joint subluxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Xray of hands with Rheumatoid?

A

No osteophyte formation or sclerosis

Relative sparing of DIPs and PIPs

MCPs are affected

EROSIONS, JOINT SPACE NARROWING, SUBLUXATION

bone becomes osteoporotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Xray of Gout

A

No erosion, No sclerosis

Punched out lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you diagnose OA?

A

Clinical diagnosis

no Xray needed or blood test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When would you use MRI in a patient with OA

A

To investigate Red flag conditions:

Avascular necrosis

Pigmented vilonodular synovitis

Osteochondritis dissecans

  • REFER TO SPECIALIST
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mangement approach for Osteoarthritis?

A

NON PHARM (Ewe self psycapo)

  1. Education in OA and self management
  2. Weight loss program
  3. Land based Exercise program
  4. Self management programs
  5. Psychological interventions (CBT) if required.
  6. Aquatic Based Exercise/ TENS/Tai Chi

CONSIDER referral to Physio or OT - if weak stiff or limited ADLs

  • Assisted devices
  • Individualised exercise program
  • Neuromuscular training

Pharmacological Interventions (nodi)

-Topical NSAID - short term

  • Oral NSAID - short term only - monitor Blood pressure and Renal function
  • Intermittent Paracetamol
  • Duloxetine -
  • Intra articular corticosteroid (short term)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How long should you use Oral NSAIDs in chronic osteoarthritis?

A

Oral NSAIDs are not a long term solution

Can be used in the short term - montior renal function and blood pressure. Evaluate for any drug interactions - eg ACEI, Diuretics. or side effects.

Long term/Chronic -

Land based exercise

Weight lose 5-10%

Possibly - Opioid therapy for severe pain, With Intra-articular corticosteroid injection for short term flares.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Red flags in hip and knee OA assessment?

A

Signs and symptoms of infection

History of cancer

Unexpected weight loss

Fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Knee exam in ?OA

A
  • Malalignment or deformitiies
  • Bony enlargement
  • effusion
  • Joint line tenderness
  • Restricted movement?
  • Crepitus
  • Gait abnormalities
  • Limited ROM - hip internal rotation/hip flexion

knee - flexion/extension

pain on hip internal rotation/flexion

22
Q

When would you refer knee or hip OA to an orthopaedic surgeon?

A

If TRUE MECHANICAL LOCKING - refer for arthroscopy

If there is severe OA - despite all conservative options

  • Xray and refer for consideration of joint replacement
23
Q

What is JIA?

A

Juvenile Idiopathic arthritis - it is an inflammatory arthritis beginning before the age of 16 and present for at least 6 weeks for which no underlying cause can be found.

Present with Fever, arthritis, rash (often macular salmon pink - can be itchy) can also get hepatosplenomegaly

REMEMBER MIMICS must be excluded

Ix - FBE, ESR, CRP

then refer to paediatric rheumatologist for further advice

Patients with a diagnosis of JIA must be screened for asymptomatic anterior uveitis regularly with slit lamp by ophthalmologist- timing depnedns on whether they are ANA positive , form of JIA and the age of onset.

24
Q

What is the long term management of JIA?

A
  1. Psychosocial support for family, carers, patients
  2. Ongoing education on disease management and medications
  3. Assess arthritis activity at least 3 times a year and adjust therapy to maintain swollen and tender joint count as low as possible
  4. Monitor toxicity and medication side effects
  5. Paed Rheum review regularly
  6. Opthalmology review regularly (uveitis)
  7. Immunisations UTD
  8. Monitor weight/ growth/nutrition

(ewi 3 amp psychapop)

Mx of acute flares

  1. Short term NSAID - 10mg/kg Ibuprofen 3 times daily (max 2400mg/day), Ice and relative rest
  2. Beware of co infections in the context of immunosuppresive therapies
  3. Refer to Rheum for advice if persisting flare or atypical features
25
What are the characteristics of Rheumatoid A?
persistent synovitis Systemic inflammation Presence of antibodies Presents as a symetrical polyarthritis Usually: 1. MCP's 2. PIPs 3. Interphalangeal joints of thumbs and wrists 4. Toe MTPs
26
Features consistent with inflammatory pain?
Joint swelling and warmth Stiffness after inactivity Early morning stiffness lasting longer than one hour Pain worse at either end of the day Improvement with NSAIDs
27
What hand deformities do you see with Rheumatoid?
**Boutonnieres** - Flexion of PIP/hyperextension of DIP **Swan neck** - Hyperextension of PIP/Flexion of DIP **Z** deformity of thumb **Ulnar deviation**
28
What are features suggestive of Rheumatoid arthritis?
1. Symmetrical arthritis 2. Swelling in multiple joints (3 or more) 3. Early morning stiffness lasting more than one hour 4. RF positivity 5. CCP antibody positivity 6. Sx for longer than 6 weeks 7. Elevated ESR, CRP 8. Bony erosions on Xrays - uncommon early
29
What is the Differential diagnosis for RA
**Post viral** arthritis - Parvovirus B19, Hep B and C, Mosquito borne - ross river, Barmah forest virus - can cause self limiting sym polyarthritis **Connective tissues disease** - SLE, Sjogrens, Dermatomyositis - rash? dry mouth and eyes? Alopecia? **Reactive arthritis and IBD associated** - usually mono or oligo - ask about urethritis, conjunctivitis **Crystal arthropathy** - prior history of gout, tophi? Urate? **Psoriatic arthritis** (Ask about nail and skin changes) **Sarcoid arthropathy** - Usually chest symptoms , bilateral hilar LN, skin? eyes?
30
Dx in RA is based on?
Clinical features AutoAntibodies Systemic inflammation - ESR, CRP
31
Investigations in RA?
1. **FBE, ESR, CRP** 2. **CCP antibodies, RF** 3. LFT, UEC 4. ACE/ CXR 5. Uric acid 6. **Xray of affected joints** 7. Serology for Hep B, C 8. ANA - if rash or sicca symptoms
32
When should referral to Rheum occur in RA
**Joint swelling for six weeks**. Refer urgently as early treatment with DMARDS can attenuate disease progression and alter long term outcomes.
33
How do you assess disease activity in RA?
Measures include: 1. number of swollen joints 2. duration of early morning stiffness 3. ESR and CRP 4. Functional assessment
34
Initial management of RA
Referal to Rheumatologist for commencement on DMARD therapy Simple analgesics - intermittent paracetamol Patient Education - eg Arthritis Australia Land based exercise Ice and/or heat Short term NSAID for pain Allied health referrals (physio, podiatry, OT) Assessment of weight, BMI, fatigue, sleep, Impact on ADLs
35
What are ADR of Methotrexate and interventions
**Nausea and vomiting** - increase dose of folate. - Split the once a week dose into 2 or 3 divided doses given in 24 hours. **Alopecia** - Hair normally grows back on cessation of methotrexate **Hepatotoxicity and Cirrhosis** Check LFTs ever 2 to 4 weeks for first three months then every 3 months (or more frequently if clincally indicated) If LFTs are three times the upper limit of normal - consider cessation of Methotrexate **Pulmonary toxicity - Pneumonitis** Base line CXR is important **Mouth ulcers -** **Macrocytosis, leukopenia, anaemia, thrombocytopenia** FBE every 2 - 4 weeks for first three months then 3 monthly or more frequently if indicated **Headaches** **Photosensitivity** sun protection **Increased susceptibility to infection** w/hold in patients with severe infection
36
What are extraarticular manifestations of RA?
37
What is AntiPhospholipid Syndrome? What are the clinical manifestations?
This is a multisystem disorder characterised by **thromboembolic events in Venous, arterial and small vessel** systems **+/- pregnancy morbidity** in the presence of **persistently elevated Anti Phosphlipid antibodies** _Presents with_**:** 1) Recurrent venous or arterial thrombosis 2) Recurrent 1st trimester miscarriage 3) Decreased platelets with Elevated APL antibodies Ix - **Lupus anticoagulant, Anti B2 Glycoprotein I antibodies - Anti B2 GPIAbs, AntiCardiolipin antibodies** Mx - REFER TO HAEMATOLOGY/RHEUM - Needs mx of acute thromboembolism and consideration of long term anticoagulation (asprin/warf)
38
What is scleroderma - when should you consider it?
The scleroderma disorders represent a spectrum of disease which begins with **a) limited skin involvement** **b) CREST calcinosis/raynauds/Esophageal dysmotility/sclerodactyly/telangiectasia and** **c) systemic sclerosis (thickening of skins, with digital ulcers and ischaemia, and constitutional symptoms and gord)** IX - FBE, UEC(renal imp), CPK (muscle involvement) Urinalysis and Antibodies - **ANA and then Anti-Scl-70 and ACA** If **systemic sclerosis** is considered - **Interstitial lung disease and pulmonary HT** is possible Ix - HRCT, TTE, Lung function testing MX - Rheumatologist **NSAID and D-Pencillamine are treatments**
39
What are the clinical manifestations of Sjogrens syndrome?
1. **Dry eyes** 2. **Dry mouth** 3. **Dry Vagina** 4. **Fatigue** 5. **Arthralgia - NON erosive arthritis** 6. **Raynauds** Sjogrens may be PRIMARY or SECONDARY - **Rheuamatoid, SLE, or Systemic Sclerosis (Ask about autoimmue conditions/fhx)** This is considered benign but has been associated with NON HODGKINS lymphoma
40
How is the diagnosis of Sjogrens made?
**Sicca symptoms** PLUS **Polyclonal hypergammaglobulinaemia** **Positive ANA Antibodies to RO and LA (ENA)** Mx - RHEUM REFERRAL NSAIDS, oral steroids, Hydroxychloroquine Patient education
41
What are the diagnostic criteria for SLE?
**3 skin and HIA ROSAN** **3 skin** - malar rash, discoid rash, photosensitivity **Haematological** - haemolytic anaemia, leucopenia, lymphopenia, thrombocytopenia, **Immunological** - Presence of DS DNA antibodies, Anti Phospholipid Antibodies, Anti Smith antibody **ANA (presence of)** **R**enal - lupus nephritis, proteinuria, cellular casts **O**ral - mouth ulcers **S**- serositis - Pleuracy, pericarditis **ARTHRITIS - _NON EROSIVE ARTHRITIS_ INVOLVING 2 OR MORE PERIPHERAL JOINTS WITH SWELLING, TENDERNESS OR EFFUSION** **N**europsychiatric - Seizures, Psychosis
42
Management of SLE?
1. Monitor inflammation (ESR, CRP, DsDNA and complement levels) 2. Rheum review 3. Monitor for complications - endorgan damage -refer urg 4. Hydroxychloroquine is often used 5. CV risk factor management
43
What are the spondyloarthropathies?
Related inflammatory arthropathies including: Axial - **Ankylosing spondylitis** **Reactive arthritis** **Enteropathic arthritis** **Psoriatic Arthritis** **Juvenile spondyloarthritis (50% become AS in adults)** * *ARTICULAR AND PERIARTICULAR FEATURES (ESPD) - Enthesitis (inflammation at sites of tendon/ligament attachment)** **-Spondylitis (inflammation of the spine - characterised by sacroillitis)** **- Peripheral arthritis (Thats often: oligoarticular, asymetrical, lower limbs, large joints)** -**Dactylitis (whole finger or toe, sausage digits)** **POSSIBLE EXTRA-ARTICULAR FEATURES** **rash -psoriatic** **conjunctivitis or anterior uveitis** **chronic gastro-intestinal inflammation** **chronic genito-urinary inflammation**
44
Who does Ank Spond affect?
Predom men 90% will be HLA B27 positive however 10% of normal population are also HLA b27 positive so its not useful on its own.
45
How would you diagnose Ank Spond?
46
What does this Xray demonstrate?
Bamboo spine - feature of late ank spond. Note undulating contour and evidence of vertebral fusion
47
Clinical features of Ank spond?
1. **Spondylitis** - initially sacroillitis then involves lumbar spine- progressive inflammation. - Pain and infllamtion leads to stiffness - **Prolonged morning stiffness** (over 45mins) and night pain, **responds well to NSAIDS** **- Sacroillitis** - Pain and stiffness in buttocks - **alternating buttock pain** **ENTHESITIS - central and peripheral (affecting achilles tendon and plantar fascia - tendonitis and fasciitis)** **Extra-articular - _Anterior uveitis, apical fibrosis, Aortic Regurgitation, psoriasis, IBD_** **Dactylitis and Peripheral arthritis (lower limbs/oligoarticular)**
48
49
What specific examination findings would you look for in Ank Spondylitis?
_1.REDUCED lumbar flexion_ on **Modified SCHOBER TEST** (normal is greater than/equal to 15cm) - document serial values 2. INCREASED **occiput to wall distance** (zero in normal) - sign of loss of cervical lordosis and increasing thoracic kyphosis) 3. DECREASED **lateral lumbar flexion** (greater than 10cm is normal) - BEST indicator of active disease 4. REDUCED **chest expansion** (less than 2.5cm is abnormal) Then examine for **extra-axial** - eg achilles tendonitis, plantar fascitis and **extra-articular** - apical fibrosis, ibd, psoriasis. uveitis, aortic insufficiency
50
Keratoderma Blenorrhagica - extra-articular for reactive arthritis