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Rheumatology > Rheum I > Flashcards

Rheum I Flashcards

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1
Q

Outline the pathology of OA

A 
Joint pain and functional limitations with reduced QoL
Caused by a detonation in the articular cartilage and formation of new bone 
Osteophytes at the joint margins 
Affected 
- Knees
- Hips 
- Small joints 
- Hands 
- Spine
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2
Q

List the clinical features associated with OA

A 
Reduced ROM 
Crepitus 
Pain on movement 
Bony swelling and deformity 
(DIP = Heberden's) 
(PIP = Bourchard's)
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3
Q

Discuss the findings seen on xr in patients with OA

A

Loss of joint space
Osteophytes
Subchondral/subarticular sclerosis
Subchondral cyst

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4
Q

Management of patients with OA

A
  1. Patient education, weight loss, exercises for muscle strength
  2. Local analgesic
    - Topical NSAIDs
  3. Oral analgesic
    - Parcetamol
    - NSAIDs with PPI
  4. Intra-articular steriod injections for acute exacerbation
  5. Arthroplasty or arthrodesis
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5
Q

Outline the pathology of RA

A

Inflammation of the synovium

  • increased angiogeneis
  • influx of inflammatory cells
  • cellular hyperplasia

Proliferation
- angiogenesis and hypertrophic synovium

Locally invasive synovial tissue

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6
Q

Clinical features of rheumatoid arthritis

A 
Arthritis 
- Symmetrical 
- Polyarthritis of the MCP's and the PIP's 
- Deformaties 
Swan neck
Boutonniere
Z-thumb
Ulnar deviation of the fingers 
Dorsal sublaxation 
- Morning stiffness > 1h lasting > 6/52 
- Nodules
- Tenosynovitis 
- Immune features ( AIHA, Vasculitis, Amyloid)

NOTE

  • Pericarditis
  • Fibrosis and pleural effusions of the lungs
  • Scleritis
  • Raynauds
  • Felty’s syndrome
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7
Q

What is the triad seen in fealty’s syndrome?

A

Rheumatoid arthritis
Splenomegaly
Neutropenia

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8
Q

List the diagnostic criteria that must be met to dx RA

A

4/7 of:

  1. Morning stiffness > 1hr (lasting for >6/52)
  2. Arthritis of >3 joints
  3. Arthritis of hand joints
  4. Symmetrical
  5. Rheumatoid nodules
  6. +ve RF
  7. Radiographic changes
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9
Q

Discuss the features of RA lung disease

A

Interstitial lung disease- corticosteroid
Rheumatoid nodules: pleural effusion
Caplan’s: link with coal workers lung
Methotrexate pneumonitis: cogu and fever

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10
Q

A patient presents to your GP surgery complain of increasing morning stiffness in his hand, especially over his PIP.
O/E his hands look swollen and inflammed bilateral.
You suspect he has RA. What investigations would you request?

A

Bloods

  • RF ( antibody against the Rc portion of IgG )
  • Anti CCP
  • FBC ( likely to have normochromic, normocytic chronic disease)
  • ANA +ve
  • Rasied ESR and CRP
  • High platelets
  • Raised ferritin
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11
Q

What scoring system is used to monitor disease

A

DAS28
<3.2 = well controlled
>5.1 = active disease

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12
Q

Management of patients with RA

A

1) Regular exercise and PT. Referral to RA clinic
2) Medical
- DAS28
- DMARDS & biologics, use early
- IM steroids for execrations
- NSAIDs for symptom relief

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13
Q

Discuss the DMARDS used in the treatment of RA

A

DMARDS

  • 1st line
  • Start early to reduce joint deformity
  • Beware of MYELOSUPRESSION

Agents used

  • Methotrexate (pulmonary fibrosis) prevents cellular replication by inhibiting DNA synthesis
  • Sulfasalazine (hepatotoxic)
  • Hydroxychloroquine (retinopathy)
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14
Q

Discuss the biologics used in the treatment of RA

A

Anti-TNF

  • Severe RA not responding to DMARDS
  • Screen and rx TB first
  • AGENTS
  • Infliximab (anti-tnf ab)
  • Etanercept ( TNF receptor)
  • Adalimumab (anti TNF ab)
  • SE
  • Infection, sepsis
  • increased AI disease
  • Increased Ca

Rituximab

  • anti-CD20 mAb
  • severe RA not responding to anti-TNF

Tocilizumab
- anti IL6 receptor therapy

Abatacept
- anti t-cell

Failure to respond to 2 DMARDs after 2 trials of 6 months

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15
Q

Causes of osteoporosis

A

Decreased bone mass
Can be
- Age related
- Drugs or other condition

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16
Q

List the risk factors for developing osteoporosis

A 
SHATTERED 
Steriods 
Hyperthyroidism, HPT, HIV 
Alcohol and cigs 
Thin (BMI<22)
Testosterone low 
Early menopause 
Renal/Liver failure
Eroxive/ inflame bone disease 
Dietary calcium low/malaborption
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17
Q

An young girl with a low BMI is being investigations for low bone density following a NOF#.
What investigations would you do

A 
BLOODS
-Bone profile 
(* Ca, PO4, ALP, PTH)
- FBC
- U+E

DEXA scan
- T score of >2.5

Indications for requesting a DEXA

  • Low trauma #
  • Women >65yrs
  • Prior to giving long term steroids
  • PTH disorders , myeloma, HIV

FRAX
- estimate ten year risk of having a NOF#

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18
Q

Management plan of patients with osteoporosis

A

1) Conservative
- Stop smoking, decrease EtOH
- Wt bearing or balancing exercises ( tai chi)
- Ca and Vit D rich diet
- Home based falls prevention team assessment

2) Bisphosphonates
- alendronate
- can also give Ca and VitD supplements

3) Alternatives
- Raloxifene (SERM)
- Teriparetide: PTH analogue for new bone formation
- Denosumab: anti RANK, decrease osteoclast formation

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19
Q

Side effects of bisphosphonates

A 
GI upset 
Oesophageal ulceration/ erosion (take with plenty of water on an empty stomach, do not lie down, do not eat for 30 minutes) 
Diffuse musculoskeletal pain 
Atypical NOF#
Osteonecrosis of the jaw
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20
Q

Discuss the pathology of AI connective tissue disease

A 
IgG antibody and antigen 
Forms complex 
Deposition in the tissue 
Attracts complement 
Reaction with complement attracts neutrophils 
Inflammation 
Enzymes and cytokines
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21
Q

SLE is a mutlisystem disease affect many organ systems. List some of the features of SLE

A

ARTHRITIS
- peripheral joints

RENAL

  • proteinuria
  • HTN

ANA +ve

SEROSITIS

  • pleuritis (effusions)
  • pericaridits

HAEM

  • AIHA
  • low wcc
  • low plats

PHOTOSENSITVITY

ORAL ULCERS

IMMUNE phenomenon

  • anti-dsDNA
  • anti-Sm
  • anti-phospholipid

NEURO

  • seizures
  • psychosis

MALAR rash

DISCOID RASH

  • facial erythema
  • pigemented hyperkeratotic papules
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22
Q

Discuss the specific immunology associated with SLE

A 
ANA+ve 
sDNA very specific
Also present 
- anti-ro
- anti-la
- anti- sm
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23
Q

What other investigations are relavant in a patient with suspect SLE

A

Bloods

  • FBC
  • U&E
  • CRP
  • Clotting

Urine
- PRC

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24
Q

What markers are used to monitor disease activity in SLE?

A 
Anti-sDNA titres 
Complement 
- low C3 
- low C4 
High ESR
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25
List the causes of drug induced lupus
``` Procainamide Phenytoin Hydralazine Isoniazid Anti-histone Abs Disease will remit if drug is stopped ```
26
Name the two types of anti-phospholipid syndrome
Primary | Secondary to SLE
27
List the antibodies present in anti-phospholipid syndrome
Anti-cardiolipin | Anti-b2glycoprotein
28
Outline the features that would be seen in patients with anti-phospholipid syndrome
Clots: venous (DVT) and arterial (stroke, TIA) Coagulation defect Increase APTT Livido reticularis Obstetric complications: reccurrent 1st trimester abortions Thrombocytopenia
29
Treatment of anti-phospholipid syndrome
1. Warfarin, aim for an INR of 2-3 2. Hoping to concieve: Heparin 3. Pregnant: aspirin and low molecular weight heparin If uncontrolled - High dose steriod - plasmapheresis
30
Outline the management of SLE both for acute flares and maintenance
ACUTE - in cases of AIHA, nephritis, pericarditis or CNS disease - High dose prednisolone - IV cyclophosphamide Maintenance - NSAIDs - Hydroxychloroquine - -/+ low dose steriods Treat proteinuria with ACEi
31
Discuss the features of Sjorgen's syndrome including a description of Sicca
Sicca 1. Dry eyes (xerophthalmia, keratoconjuctivitis) 2. Dry mouth (Xerostomia) 3. Enlarged parotid gland May present alone or with SLE, RA, systemic sclerosis and CREST
32
List the diagnostic tests to confirm Sjorgens
Schirmer tear test: less than 5mm in 5minutes Antibodies: ANA, anti Ro, anti La Parotid biopsy
33
Treatment of patients with Sjorgens
1. Artificial tears 2. Saliva replacements 3. NSAIDs + hydroxychloroquine (for arthralgia) 4. Immunosuppression
34
Name the two types of systemic sclerosis
``` 1. Limited Systemic Sclerosis (CREST) - Calcinosis - Raynaud's - OEsophageal and gut dysmotolity ( - Sclerodactyly - Telangiectsia ``` Skin involvement is limited to the face and hands - Beak nose - Microstomia Some develop PHTN 2. Diffuse Systemic Sclerosis - Diffuse skin involvement - Organ fibrosis GI: GOR, aspiration and incontinence Lung: Fibrosis and PHTN Cardiac: arrhythmias and conduction defects Renal: acute hypertensive crisis
35
A patient present to rheum outpatients clinic with symptoms in keeping with a dx of systemic sclerosis. What ix would you do to confirm your suspicions?
Bloods - FBC (anaemia) - U&E (renal impairment) Antibodies - Centromere: limited - Scl70/topoisomerase: diffuse - RNA pol 1,2,3: diffuse * Anti-Scl70: poor prognosis, die earlier * RNA pol 1,2,3: Renal problems Urine - PCR for protein Imaging - CXR: cardiomegaly, bibasal fibrosis - Hands: calcinosis - Ba swallow: impaired oseophageal motility - HiRes CT - Echo to look for pulmonary HTN
36
Management of patients with systemic sclerosis
1. Exercise and skin lubricants 2. Hand warmers for Raynaud's 3. Medical - Nifedipine for Raynauds - PPI ( GI) - Cyclophosphamide (pulmonary) - Prednislone ( arthrititis) - ACEi (renal crisis)
37
Indicate the pathology behind Polymyositis and dermatomyositis
Poly does not have skin involvement Progressive symmetrical proximal muscle weakness no pain. Different from PMR - Wasting of the shoulder and pelvic girdle - Dysphagia, dysphonia and respiratory weakness Myalgia Arthralgia Linked with paraneoplastic syndrome - lung - pancreas - ovarian - bowel
38
Outline the key skin signs seen in dermatomyositis
Heliotrope rash: eyelid rash with oedema Macular rash: shawl sign, over the back and the shoulders) Nailfold erythema: Gottron's papules: knuckles, elbows, knees Mechanics hands: painful rough skin cracking of finger tips Retinopathy: haemorrhages and cotton wool spots Subcuntaneous calcifications
39
Polymyosistis and dermatomyositis involve proximal muscle weakness +/- skin changes. What are the extra muscular features that are seen?
``` Fever Arthritis Bibasal pulmonary fibrosis Raynaud's phenomenon Myocardial invovlement ```
40
Outline the investigations you would do in a patients who present with features suggestive of polymyosisits
Muscle enzymes - high CK - high AST - high ALT - high LDH (link with a worse prognosis) Antibodies - Anti-Jo1 EMG Muscle biopsy Screen for malignancies - Tumour markers - CXR - Mammogram - Pelvic/abdo US
41
Treatment of polymyositis/dermatomyositis
1. Steriods (if anti-Jo1 = long term) 2. Immunosuppressive (azathioprine) 3. Lung disease (cyclophosphamide)
42
Classify Raynaud's and outline how it presents
``` Idiopathic Secondary - Systemic sclerosis - SLE - RA - Thrombocytosis - B-blockers ``` Digit pain and triphasic colour change WBC Digit ulceration and gangrene
43
Treatment of Raynaud's
Wear gloves CCBs: nifedpine ACEi IV iloprost
44
List the features that are suggestive of seronegative spondyloarthropathies
``` SPINEACHE Sausage digit Psoriasis Inflammatory back pain NSAID response Enthesitis ``` Arthritis Crohn's, Raised CRP HLAB27 Eyes
45
Outline the features of anky spond
Gradual onset back pain - worse @ night - relieved by exercise Progressive loss of all spinal movements - Schober's test <5cm Costochondritis * Also present with - Actue iritis/ anterior uveitis - Aortic valve incompetence - Apical pulmonary fibrosis
46
Invesitgations for ankylosing spondylitis
``` Pelvic XR: sacrolitis (blurring, loss of definition) HLA B27 Spinal XR: (BESS) - Bamboo spine - Erosions - Squaring - Syndesmophytes ```
47
Management of ankylosing spondylitis
1. Physiotherapy + rehabilitation 2. NSAIDs 3. TNF alpha inhibitor (infliximab) 4. Can give interarticular steroids to help with symptomatic relief
48
List the 6 A's associated with Ankylosing spondylitis
``` Apical fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis AV node block Amyloidosis ```
49
List the features seen in psoriatic arthritis
``` DIP arthritis Sometimes arthritis mutilans Psoriatic plaques Nail changes - pitting - hyperkeratosis - onchyolysis Dactylitis ``` Pencil in cup erosion as seen on X-ray
50
Treatment of psoriatic arthritis
NSAIDs Sulfasalazine, methtrexate, ciclosporin Anti-TNF
51
Pathology of reactive arthritis
``` Occurs 1-4 weeks post GI / GU infections Organsism - Campylobacter - Salmonella - Shigella - Chlamydia ``` Usually lower limb large joints
52
What is Reiters
Can't see Can't wee Can't climb a tree
53
Management of reactive arthritis
NSAIDs Rest Intra-articular joint steriods ABx for chlamydia (azothromycin)
54
Treatment of enteropathic arthritis
Arthritis associated with IBD Rx Sulfasalazine to treat both Can get circinate banalities
55
What is included in a vasculitis screen
Haem - FBC - ESR - Clotting screen Biochemistry - U&E - LFTs - CRP Immunology - ANCA - RF - C3/C4 - Anti-cardiolipin - Anti-b2glycoprotein Serology - HBV - HCV Radiology - CXR
56
Pathology of gout
Deposition of monosodium urate crystals in and around joints Erosive arthritis
57
Causes of gout
``` Hereditary Drugs - diureticcs - NSAIDs - cytotoxic ``` Decreased excretion - 1 gout, renal impairment Increased cell turnover - Lymphoma, leukaemia, psoriasis EtOH excess Purine rich food - beef - pork - seafood
58
Investigations in cases of suspected gout
``` Polarised light microscopy - negatively birefringent needle-shaped crystals Normal or low serum rate Xray changes - Punched out erosions - Decreased joint space ```
59
Treatment of gout 1. Acute rx 2. Prevention
ACUTE - NSAID: diclofenac - Colchicine: if NSAIDs contraindicated, can cause diarrhoea - renal impairment must use steroids Preventions - Conservative: weight loss, avoid prolonged fast, EtOH excess - Xanthine Oxidase Inhibitors: Allopurinol, for recurrent attacks Introduce with NSAIDs or coclchine - Febuxostat if hypersensitivity
60
Pathology of pseudogout
Calcium pyrophospahte deposition in articular and periarticular tissues Usually spontaneous and self limiting
61
Risk factors for developing pseudo gout
``` Age OA DM Hypothyroid Hyperparathyroidism Hereditary haemochromatosis Wilson's disease ```
62
Investigations of pseudogout
``` Polarised light microscopy - positively birefringent rhomboid shaped crystals Xray - chondrocalcinosis - Ca depsotion ```
63
Treatment of pseudo gout
Analgesia NSAIDs Steriods
64
Pathology of Paget's disease of the bone
Increased bone turnover Lytic phase: Increased bone resorption by osteoclast Sclerotic phase: Rapid bone formation by osteoclasts - disorgansied and mechanically weaker - Deformity
65
Presentation of paget's disease of the bone
Axial skeleton - pelvis - lumbar spine - skull - femur - tibia Bone pain Pathological # Deformity Nerve compression (Deafness) Osteosarcoma
66
Investigations for paget's disease of the bone
Bone profile - High ALP - Normal Ca and PO4 Bone scan - hot spots XRAY - bone enlargement - sclerosis - patchy cortical thickening - wedged shaped lytic lesions
67
Treatment of page's disease of the bone
``` Analgesia Alendronate (redue pain and deformity) ```
68
Causes of osteomalacia
``` Vit D deficiency Renal osteodystrophy Drugs: AEDs, increased hepatic metabolism of it D Vit D resistance Hepatic disease: malabsorption Malignancy ```
69
What would be seen on the bony profile in a patient with osteomalaica
``` Low Ca Low PO4 High ALP Increase PTH Low VIt D ``` XRAY - Loss of cortical bone - Pseudofractures
70
Treatment of osteomalacia
Dietary calcium Malabsorption or hepatic disease Renal disease/ Vit D resistance Plasma Ca
71
Features and management of lupus nephritis
``` Haematuria (>0.5g/d) Intensive immunosuppression - Steroids + - Cyclophosphamide/ Mycophenolate - BP control is vital (ACEi) ```

Rheumatology (2 decks)

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