Rheumatology Flashcards

1
Q

define OA

A

A progressive disorder of the joints caused by gradual loss of cartilage and resulting in the development of bony spurs and cysts at the margins of the joints.

Commonest form of arthritis
‘Wear & Tear’ or ‘Degenerative Joint Disease’

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2
Q

pathophysiology of OA

A

Pathophysiology
Loss of cartilage & narrowing of the joint space
Low grade synovial inflammation
Thickening of subchondral bone
Development of bony outgrowths - osteophytes

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3
Q

secondary causes of OA

A

Primary causes of Osteoarthritis

  1. Metabolic
    - Ochronosis, hemochromatosis, acromegaly, COPD
  2. TRAUMA
    - major trauma , fracture, meniscectomy, chronic occupation, repetitive injury / stress
  3. ANATOMICAL
    - congenital, slipped epiphysis, AV necrosis, congenital hip
  4. POST ARTHRITIS
    - inflam arthritis, RA
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4
Q

Primary causes of OA

A
Age (4) 
Obesity
Heredity (TWIN STUDY - mutation in type 2 college fibre)
Sex (WOMEN) 
Occupation
Predisposing secondary causes
Trauma/injury
Joint shape
Repetitive Use
Muscle weakness
Joint Laxity
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5
Q

how does increase age put you at risk of OA

A
  1. Old cartilage heals less well
  2. Decrease muscle strength and muscle bulk
  3. decrease joint propiception
  4. increase incidence to old age
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6
Q

ddx for OA

A
  1. Crystalloid arthritis (gout, pseudo gout)
  2. inflam arthritis
  3. SN arthropathies
  4. Septic arthritis
  5. Pos-infectious arthropathy
  6. Fibromyalgia
  7. tendonitis
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7
Q

important mediators involved in cartilage damage

A

Cytokines: TNF-a, IL-1, Il-6

collagenases, metalloprotineases, aggrecanases

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8
Q

important mediators in protecting cartilage

A

IL-4 and TIMP , TGF-b, & IGF-1 protective

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9
Q

Complications of OA

A
Chondrolysis – Rapid, complete breakdown ofcartilageresulting in loose tissue material in thejoint(Bone death (osteonecrosis).
Stressfractures(hairline crack in the bone that develops gradually in response to repeated injury or stress).
Heamarthroses – Bleedinginside the joint.
Septic arthritis – Infection in the joint.
Gout/Pseudogout
Joint instability – Deterioration or rupture of the tendons and ligaments around the joint, leading to loss of stability.
Pinched nerve (in osteoarthritis of the spine)
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10
Q

strong risk factors for gout

A
Increasing age
Male gender
Menopausal state
Use of diuretics
Iatrogenic 
Tacrolimus, aspirin
High cell turnover
Lymphoma’s, chemo
Genetic susceptibility
Triggers:
Alcohol, dehydration
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11
Q

Ddx gout

A

Pseudogout (calcium pyrophosphate deposition)

Septic arthritis
Trauma
Rheumatoid arthritis
Psoriatic arthritis
Reactive arthritis
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12
Q

when do you do uric acid level

A

Wait > 2 weeks

DO NOT PERFORM in acute attack

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13
Q

x- ray findings in gout

A

X-Ray of affected joint:
Peri-articular erosions
Punched out appearance
Over hanging edge

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14
Q

3 complication of gout

A

Nephrolithiasis
Acute uric acid nephropathy
Increased CAD/CVD risk

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15
Q

A 46 year old female patient of Maori heritage presents to her General Practitioner with an acute mono-articular pain, very sudden on onset and 10 out of 10 in severity. She has a history of diabetes mellitus and peptic ulcer disease. The presumptive diagnosis is acute gout. What is the most likely risk factor contributing to her illness?

A

Maori heritage (family history)

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16
Q

Red flags for back pain

A

Major trauma
Relative minor trauma if known or suspected osteoporosis
Fever, weight loss, systemic symptoms
Intractable pain
No improvement in 4-6/52, or increasing pain severity
Nocturnal pain
Neurologic symptoms or signs especially if bilateral
Morning pain and stiffness in younger patients
Inflammatory back pain
History of cancer or symptoms suggestive of cancer or referred pain
Check PSA in men

17
Q

Renal disease in Multiple Myeloma

A

Hypercalcaemia
Light chain nephropathy
Amyloidosis
Analgesic nephropathy

18
Q

what gene is ass. w/ RA

A

HLADR4

Associated with part of HLA-DR4 and the DR– associated alleles
(DRB10401 and DRB10404
Sometimes called the “Shared Epitope

19
Q

eye finds in RA (10)

A
Anterior uveitis (iritis)
Conjunctivitis
Keratoconjunctivitis
Keratoconjunctivitis sicca
Scleritis
Episcleritis
Retinal detachment
Sicca complex (xerophthalmia and xerostomia)
Scleromalacia
Scleromalacia perforans
20
Q

lung findings in RA (6)

A
Pulmonary nodules
Pleural effusions
Pulmonary fibrosis
Caplan syndrome
Bronchiolitis obliterans
Organising pneumonia
21
Q

heart (8) and vascular RA(3) symptoms

A
Pericarditis
Myocarditis
Cardiac nodules
Coronary artery disease
Pericardial effusions 
Heart failure
Atrial fibrillation
Aseptic endocarditis 

Valvular: PVD, stroke , Vasculitis

22
Q

neuro symptoms RA (5)

A
Peripheral neuropathy
Mononeuritis multiplex
Compression neuropathy/radiculopathy
Atlanto-axial subluxation- cervical subluxation
Muscle weakness/myositis
23
Q

team RA smp (4)

A

Anaemia
NN– chronic disease
Meg and mac – B12/Folate deficiency, methotrexate/azathioprine therapy
HC, microcytic – Fe decrease - chronic GI bleeding (NSAIDs)

Haemolytic anaemia – rare
Pancytopaenia - aplastic anaemia (gold, penicillamine, azathioprine, cyclophosphamide)
Felty’s syndrome (anaemia, neutropaenia, splenomegaly)

24
Q

Kidney RA ( 4)

A

Drug-induced injury – penicillamine, gold, ciclosporin
Glomerulonephritis
Amyloidosis
Increased UTIs due to immunosuppression

25
Q

Skin RA 7

A
Rheumatoid nodules
Ulcers
Pyoderma gangrenosum
Vasculitic rash
Drug-induced urticaria
Neutrophilic dermatoses
Steroid induced skin tinning and ecchymoses
26
Q

2010 ACR/EULAR criteria

A
Number and site of involved joints
2 - 10 large joints = 1 point
1 - 3 small joints  = 2 points
4 to 10 small joints = 3 points
>10 joints (including at least 1 small joint) = 5 points 
Serological abnormality (rheumatoid factor or anti-citrullinated peptide/protein antibody)
Low positive (> ULN) = 2 points
High positive (3X >ULN) = 3 points

Elevated acute phase response (erythrocyte sedimentation rate or C-reactive protein) above the ULN = 1 point

Symptom duration at least six weeks = 1 point

NEW PRESENTATION OF RA

27
Q

ongoing follow up if patient is on MTX

A

3 monthly bloods for FBC, UE, LFT

28
Q

if starting immunosuppressant medications what should be done first

A

CXR and Tb skin test

29
Q

complications of septic arthritis

A

Septic shock
Osteomyelitis
Persistent, recurrent infections
Marked decrease in joint mobility, ankylosis, persistent pain
Irreversible joint destruction and an increase in mortality

30
Q

DDX septic arthritis

A
  1. Primary Rheum Disorders (Rheumatoid and osteoarthritis , Psoriatic arthritis, SLE, Crystal arthropathies e.g. gout and pseudo gout)
    2.Lyme Disease
  2. Reactive arthritis
    Post-infectious diarrhoea (salmonella, campylobacter, cryptosporidium), Reiter’s Syndrome (chlamydia), Post-meningococcal , Post-gonococcal )
  3. Trauma/joint injury (Haemarthrosis (warfarin), Meniscal tear
    Effusion)
  4. Systemic conditions (Sarcoidosis, haemochromotosis, malignancy, IBD,Sickle cell anaemia
31
Q

risk factor for scleroderma

A
  1. Genetic
  2. Enciromental (silica and vinyl exposure)
  3. Viral triggers
  4. Drugs - Bleomycin
32
Q

MSK findings in Systemic scleroderma

A

Non-erosive arthritis
Fibrosis of fascia and muscle
Tendon friction rubs

33
Q

treatment of pulm hTN seen in diffuse scleroderma

A

Endothelin 1 antagonists (Bostentan)
Prostaglandins
Phosphodiesterase inhibitors