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MBChB Finals > Rheumatology/Orthopaedics > Flashcards

Rheumatology/Orthopaedics Flashcards

1
Q

Autoantibodies

A

See attached

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2
Q

Which antibody can cross the placenta and cause heart conduction defects in the newborn?

A

Anti-RO

Found in SLE and Sjogrens

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3
Q

Systemic Sclerosis

A

Chronic autoimmune disease

Widespread microvascular damage
Excessive interstitial and perivascular collagen deposition (fibrosis/sclerosis)

Skin becomes hard:

  • Hard, swollen, and tight-appearing skin with fewer wrinkles
  • Mask-like facies
  • Claw-like hands

Raynaud’s phenomenonsecondary to digital vasculitis

Most common visceral complication of systemic sclerosis is esophageal dysmotilityand dysfunction. Esophageal dysfunction is seen in 90% of systemic sclerosis patients.

2 types:

  1. Diffused
    1. Mainly affects lungs, kidneys and GI tract (oesophagus, small bowel)
  2. Limited
    1. Some of these develop CREST

Diffuse systemic sclerosis presents with diffuse sclerosis of the skin at onset and early visceral involvement. Prognosis is poor due to a rapid malignant disease course withdeath secondary to respiratory failure (most common cause of death), kidney failure, heart failure, and/or intestinal malabsorption.

Limited systemic sclerosis presents with sclerosis of the skin limited to the fingers, forearms, and face at onset and late or no visceral involvement. Prognosis is fair to gooddue to a relatively benign disease course.

Anti-centromere in CREST syndrome

Anti-RNA polymerase DNA topoisomerase I (anti-Scl-70) in diffuse

ANA positive in both limited and diffuse

Treatment - immunosuppression and treat specific problems.

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4
Q

SLE

A

Systemic Lupus Erythematosus (SLE) is a chronic systemic inflammatory autoimmune disease that usually damages skin, joints, kidneys, and serosa.

less

SLE is most commonly seen in females of reproductive age and of African descent

A mnemonic to remember the features of SLE is RASH ORR PPAIN:

  • *R**ash (malar or discoid)
  • *A**rthritis
  • *S**oft tissues/serositis
  • *H**ematologic disorders
  • *O**ral/nasopharyngeal ulcers
  • *R**enal disease
  • *R**aynaud phenomenon
  • *P**hotosensitivity
  • *P**ositive VDRL/RPR
  • *A**ntinuclear antibodies
  • *I**mmunosuppressants
  • *N**eurologic disorders (e.g. seizures, psychosis)

Commonly associated with anti-phospholipid antibody syndrome which makes the patient hypercoagulable - recurrent arterial/venous thromboses:

  • Deep venous thrombosis
  • Hepatic vein thrombosis (which can lead to Budd-Chiari syndrome)
  • Placental thrombosis (which can lead to recurrent miscarriages)

Thrombocytopenia can occur regardless of the hypercoagulable state

life-long anticoagulation needed for antiphospholipid syndrome.

Antibodies:

  • ​Anti-histones will be + in drug induced lupus
  • Antinuclear antibodies (ANA) are sensitive but not specific
  • Anti-dsDNA antibodies are specific and predict a poor prognosis with renal disease
  • 98% of SLE patients have antinuclear antibodies (ANA) but are non-specific

Treatment

Avoid sun exposure
NSAIDs for mild disease
Hydroxychloroquine
Steroids
Steroid sparing agents such as azathioprine and methotrexate (esp for inflamm.arthritis)

low-dose aspirin and low-molecular weight heparin are now the treatment of choice for women with antiphospholipid syndrome and a history of miscarriage

For major organ involvement:

high-dose intravenous (IV) methylprednisolone
immunosuppressant therapies - cyclophosphamide (CYC), mycophenolate mofetil (MMF)
biological therapies - rituximab, belimumab

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5
Q

Classification of bone mineral density (T score)

A

Osteoporosis

Osteopenia -1 to -2.5

Normal -1 to +2.5

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6
Q

What is the main symptom of osteoporosis?

A

Asymptomatic but key point is that causes low energy injuries such as falling off a chair

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7
Q

Commonest fractures in osteoporosis?

A

Hip wrist and vertebral.

The vertebral fractures are stable and you should just treat the pain and symptoms

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8
Q

What bones are measured in a DEXA scan?

A

Lumbar spine and hip

Osteoporosis in males and young people should promot investigation for secondary causes

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9
Q

What does alcohol and corticosteroids do to osteoblasts

A

Suppresses the osteoblasts. Because these build bone, it can result in osteoporosis.

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10
Q

Causes of seondary osteoporosis

A
  • Hyperthyroidism (increased turnover)
  • Hyperparathyroidism (increased bone resorption)
  • Hypogonadism (Lack of steroid hormones)
  • Cushing syndrome (Steroids suppress osteoblasts)
  • Rheumatoid Arthritis (due to steroid meds and less activity)
  • Inflammatory Bowel Disease (Malabsorption, Steroids)
  • Coeliac and malabsorption states
  • Renal failure (Vitamin D deficiency)
  • Multiple myeloma (bone loss, erosions)
  • Anorexia nervosa (Malnutrition)
  • Corticosteroids (suppresses osteoblasts)
  • Anticonvulsants
  • Heparin
  • *
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11
Q

Treatment for osteoporosis

A

1st line is bisphosphonates (inhibit osteoclasts) and calcium and vitamin D supplements.

2nd line: Used when bisphosphonates not tolerated due to GI upset. Calcitonin and PTH can also be added for osteoporosis.

Weight bearing exercise

Others:

Raloxifene: not very effective. SERM. Useful in postmenopausal but increased CV and malignancy risks

Denosumab: New humanised monoclonal antibody against RANK ligand (RANK stimulates osteoclasts to eat more bone).

Prevent falls

  • Walking aids
  • Avoid hypotensive and sedative drugs
  • Improve eyesight
  • OT involvement to minimise fall risk
    *
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12
Q

What is Sjogrens?

A

Chronic autoimmune exocrinopathy. Predominantly affects salivary and lacrimal glands. - DRY MOUTH AND DRY EYES

Clinical picture is dominated by keratoconjunctivitis sicca (fancy name for dry eyes) and xerostomia

Sjogrens can occur primarily or secondary to a connective tissue disease or RA.

ANTI RO AND LO

ROLA - Rola mere beti - I can’t :( I have sjogrens and anti RO and LA :( :(

10X more females affected than males. - UNLUCKY

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13
Q

What are the extraarticular features of Sjogrens?

A

S=skin manifestations like vasculitis
P=parotid enlargement
E=exocrine glandular immune disease
N=neuropathy
D=dryness of upper airways

O=opthalmic complications
N=non specific symptoms

L=lung disease
A=arthritis
M=myalgia
B=biopsy of labial gland

Anti-ro antibodies cross placenta in preggers and cause heart block in baby

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14
Q

Sjogrens investigations?

A
  1. Schirmers test
  2. Rose bengal test for dry eyes
    • Anaesthatise eye
    • Add rose bengal solution to eye
    • Rose bengal staom will be taken up by the dead and degenerating cells that have been damaged by reduces tears (dryness), as the healthy white of the eye should not take up any of this dye
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15
Q

Sjogrens treatment?

A

No cure

Symptomatic - artificial tears, chewing gu, for salivary stimulation,

Highlight importance of dental hygiene as salivary protection is lost

Avoid anticholinergics and diuretics which will just make patient even more ‘dry’

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16
Q

What is THE BIG complication that Sjogren sufferers can go on to develop?

A

Lmyphoma!!

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17
Q

What are the causes of an acute swollen joint?

A
  • Septic arthritis
  • Crystal arthropathy
    • gout
    • pseudogout
  • Inflammatory arthritis
    • RA
    • Seronegative spondyloarthropathy
  • Transient synovitis
  • Haemarthrosis
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18
Q

Which joints do gout and pseudogout typically affect?

A

Gout - 1st MTP

Pseudogout - knee and wrist

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19
Q

Which haemataological conditions is gout particularly common in?

A

Myeloproliferative disorders

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20
Q

Which drugs predispose to gout?

A

Thiazides and low dose aspirin

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21
Q

What is the most important investigation that must be done in an acute swollen joint?

A

Joint aspiration! Septic arthritis is rapidly destructive. Timely treatment is critical. Aspirate before antibiotic adminisation. Gram stain and microscopy on aspirate. Microscopy is for crystals.

Be aware than immunosuppressed patients may present atypically with septic arthritis with low/normal inflammatory makers.

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22
Q

What is dupuytren contracture?

A

Fibromatosis of the palmar fascia, resulting in flexion contractures of the MCP and IP joints.

Fibromatosis can affect other areas:

  • Plantar fascia - Ledderhose disease
  • Penis - Peyronie disease
  • Knuckle pads - Garrod disease

In a patient presenting with dupuytren always ask aboyt similar symptoms elsewhere

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23
Q

Predisposing factors for Dupuytren contracture?

A
  • FH
  • Hepatic cirrhosis
  • DM
  • Anticonvulsants
24
Q

Clinical features of dupuytren contracture and treatment?

A

Ulnar side usually affected with fingers flexed and unable to extend. Uusally little and ring fingers. Painles. Starts off as nodule which [progresses to flexion of fingers.

Palmar fasciectomy

25
Q

What is osteoarthritis (OA)?

A

Disease of synovial joints whereby the articular surface degenerates, and new bone forms as the body attempt repair. Secondary inflammatory occurs. Please note that OA is NOT an inflammatory arthritis even though arthritis occurs.

Prevalence increases with age and it is often aymptomatic even though one would think otherwise.

26
Q

Aetiology and pathology of OA?

A

Microtrauma or abnormal loading to joints wears the cartilage surface away exposing the bone beneath it (subchondral bone).

Chondrocytes come along to try and repair it by releaseing degradative enzymes. Cysts occur because of microfracture of the articular surface.
New bone is also laid down - sclerosis.

Disorganised new bone also forms - osteophytes and effusion occurs as the inflamed synovial lining makes more fluid.

  1. JOINT SPACE NARROWING
  2. SCLEROSIS
  3. CYSTS
  4. OSTEOPHYTES
27
Q

Is OA better or worse with rest?

A

OA is worse OA (on activity)

28
Q

What kind of relationship do OA and osteoporosis have?

A

INVERSE

I don’t know why…don’t know if anyone does?

29
Q

Which joints in the hand does OA affect?

A

PIP, DIP and CMC

30
Q

How is OA treated and managed?

A
  • Encourage exercise - aerobic and weight bearing
  • Paracetamol/NSAIDs (+/- TENS) for pain relief. Opiods if needed
  • Intra articular corticosteroids for moderate-severe pain
  • Articular debridement of locked knee
  • Consider referral for joint surgery for people with osteoarthritis who experience joint symptoms (pain, stiffness and reduced function) that have a substantial impact on their quality of life and are refractory to non-surgical treatment

Taken from NICE guidelines

31
Q

What are the 4 things a surgeon can do to a joint?

A
  1. Arthroplasty - This is a joint replacement. Most commonly hip or klnee. Excellent result as usually done for pain relief and it works!
  2. Joint fusion (arthrodesis) - The two sides of the joint are removed and fused together. Most often in the foot/ankle. Provides good pain relief but sacrifices mobility
  3. Joint excision - Less common today. Occassionally used for first MTP
  4. Realignment surgery - Increased load passing through a joint because of a deformity causes OA. Realigning the limb by chopping some off helps. Usually done for knee.
32
Q

What is the immunological process underlying RA?

A

This is an inflammatory condition (SYNOVITIS). Polyarticular usually symmetrical arthritis. Hands almost always affected. Can cause significant diability - do not underestimate the importance of effective prevention of disease progression. Life expectance decreased by 3-18 years.

Immunology

T lymphocytes, B cells and macrophages are the main culprits, releasing TNF-alpha and IL-1 which stimulate inflammation and attract even more cells to destroy the synovial joint. This causes excess synovial fluid production. Cartilage is also destroyen, bone resorption occurs and Rh factor is present in 80%

Some of the population have Rh factor without RA!

A pannus is created which invades and erodes contiguous cartilage and bone. A pannus is just hypertrophies synovium.

33
Q

What happens to the hand and wrist in RA?

A
  1. Ulnar deviation of MCPs
  2. Boutonniere deformity (PIP flexion and DIP hyperextension)
  3. Swan neck deformity (PIP hyperextension and DIP flexion)
  4. Radial deviation of wrist often occurs to compensate for the ulnar deviation of fingers
34
Q

What happens to the foot in RA?

A
  1. Forefoot synovitis and damage
  2. Proximal phalanges sublux dorsally
  3. Metatarsal heads erode and displace towards floow (feels like I am walking on marbles doctor)
  4. Subtalar arthritis
35
Q

What happens to the spine in RA?

A
  1. Atlantoaxial subluxation - Inflammation and erosion affects C1, as well as C1/2 stabilising ligaments.

The atlas slips forward on the axis reducing space around the spinal cord. This causes neck pain raidating to the occiput. Any UMN damage may result in spastic quadraparesis.

Because the dens is unstable, it can move upwards through the foramen magnum abd threated the cervical cord and brainstem, sometimes resulting in sudden death from minor jolts to the head and neck.

TAKE LATERAL FLEXION XRAYS OF C-SPINE IN RA PATIENTS WHO WILL NEED GA SO THE ANAESTHATHIST CAN BE CAREFUL DURING INTUBATION

36
Q

What are the extra articular features of RA?

A
  1. Rheumatoid nodules - in friction and pressure areas such as elbows, fingers and achilles tendon. Can become infected
  2. Tenosynovitis and bursitis - because these structures are lined with synovium they are also inflamed. Bursitis at olecranon, subacromial and greater trochanter
  3. CTS - median nerve affected.
37
Q

What are the systemic features of RA?

A

People just generally feel crap. Fever, Weight loss. Lethargy.

38
Q

RA effects on distant organs?

A
  1. Anaemia
    • ​​anaemia of chronic disease
    • autoimmune haemolysis
    • Felty syndrome (triad of RA, splenomegaly and neutropenia)
    • NSAIDs can cause gastric ulcer –> chronic blood loss –> iron deficiency
    • DMARDs suppress BM
  2. Lung disease
    • ​​M>F
    • Pleural effusion
    • Lung nodules in those with Rh+ and subcutaneous nodules
    • Pulmonary fibrosis
  3. Others
    • ​​Keratoconjunctivitis sicca
    • Episcleritis
    • Slceritis
    • Amyloidosis
    • Vasculitis
    • Pericarditis
    • Myocarditis
    • Coronary arteritis
39
Q

What are the 4 main radiological findings for RA?

A
  1. Soft tissue swelling
  2. Periarticular osteoporosis
  3. Juxta-articular erosions
  4. Joint space narrowing
40
Q

How is RA treated and managed?

A
  • Pain management - NSAIDs . These DO NOT slow disease progression
  • DMARDs to slow disease progression. Mainstay of RA therapy. Take several weeks to kick in.
    • Methotrexate - GI upset, oral ulcers, BM suppression, abnormal LFTs. Give folate with it.
    • Sulfasalazine (a salicylate) - BM suppression. GI upset. Abnormal LFTs
    • Leflunomide - HTN, GI upset, BM suppression
    • Hydroxychloroquine - Retinal damage - they need regular screening
    • Gold - Rash. Proteinuria due to renal damage. BM suppression.
  • Intra articular corticosteroids for severe flare ups or pain.
  • Biological therapies
    • Infliximab, adalinumab, etanercept which are all TNH-alpha inhibitors. All are expensive and increase infection risk..
41
Q

What are the two antibodies often detected in RA patients?

A

Rheumatoid factor (IgG) and anti-CCP

42
Q

What is the commonest site of an osteoclastoma?

What is an osteoclastoma?

A

Approximately 50% of giant cell tumours (osteoclastomas) are located about the knee at the distal femur then proximal tibia (REMEMBER AROUND THE KNEE)

A giant cell tumor of bone (also known as an osteoclastoma) is a benign, aggressive, bone tumor.Radiologic imaging of giant cell tumors of bone show destructive lytic lesions near joints, with a characteristic “double bubble” or “soap bubble” appearance.

It is called an osteoclastoma/giant cell tumour due to the presence of giant cells that looks like osteoclastomas.

Most are solitary lesions so it is unlikely the patient will have another one.

43
Q

What is the commonest complication of a clavicle fracture?

A

Malunion, which results in angulation, shortening, and poor appearance.

44
Q

What is nonunion and describe the risk factors.

A

Nonunion is typically defined as failure to show clinical or radiographic progression of healing after four to six months. Several risk factors for nonunion have been identified, including:

  1. The extent of initial trauma
  2. Fracture combinations
  3. Fracture displacement
  4. Inadequate immobilisation
  5. Distal-third fractures
  6. Primary open reduction, and
  7. Refracture.
45
Q

What is the commonest bone tumour in under 21s?

A

Osteochondromas , which occur most frequently in the first two decades of life. Mostly around the knee

Osteochondromas usually present as a hard, painless mass that has been present and unchanging for years.
An osteochondroma is formed from an exostosis (a bony outgrowth) of the medullary and cortical bone capped by cartilage that initially grows at a right angle from the epiphyseal growth plate. The cartilaginous cap functions as an ectopic growth plate, allowing the osteochondroma to grow by endochondral ossification until the patient reaches skeletal maturity.

Although osteochondromas originate from the epiphyseal growth plate, they are found in the metaphysis because as young patients continue to grow, bone formerly at the epiphyseal plate moves into the metaphysis.

46
Q

What are some causes of osteomalacia?

A
  1. Malabsorption
  2. Renal disease
  3. Chronic renal failure, and
  4. Anticonvulsant therapy.
47
Q

Which organ function tests need to be monitored in those on sulfasalazine (DMARD)?

A

LFTs

48
Q

What are the features to diagnose GCA?

A
  1. Age over 50
  2. New onset of new type of localised headache
  3. ESR >50 mm/hr by the Westergreen method
  4. Temporal artery tenderness to palpation or decreased pulsation
  5. Arterial biopsy showing granulomatous inflammation or mononuclear cell infiltration usually with multinucleated giant cells.

3 OF THE 5 SHOULD BE PRESENT

49
Q

What are the contents of the carpal tunnel?

A
  1. The median nerve
  2. The four flexor digitorum profundus tendons
  3. The four flexor digitorum superficialis tendons
  4. Flexor pollicis longus
50
Q

How often does a patient need to take aldendronate?

A

One pill a week

————————————————————————————–

Supplemental info:

How to take an oral bisphosphonate for osteoporosis:

Take the tablet first thing in the morning, at least 30 minutes before other medications or food
Take with a glass of water - not juice, tea or coffee
After taking the tablet, remain upright for at least 30 minutes to allow the tablet to pass safely into the stomach.

Side effects of bisphosphonates include:

Gastrointestinal disturbance is common but usually mild
Alendronate can cause oesophagitis which can be severe
Risedronate is better tolerated when compared to alendronate
Some can cause bone pain.

Patients who have oesophagitis must stop their treatment and should be considered either for an intravenous or intramuscular bisphosphonate, or for another agent.

51
Q
A
52
Q

What is keratoderma blennorrhagica?

A

Brown plaques on skin which often occur with mouth ulcers in reactive arthritis.

53
Q

What features will you see in a patient with common peroneal nerve palsy?

A

L5-S1 dermatome loss of sensation and foot drop

54
Q

What disease should morning shoulder and neck pain make you think of?

A

Polymyalgia rheumatica!

It tends to affect shoulders and pelvis

The British Society of Rheumatology has stipulated the following criteria:

  • Age >50 years, duration >2 weeks
  • Bilateral aching of neck, shoulders and/or pelvic girdle
  • Morning stiffness >45 minutes
  • Evidence of acute phase response
55
Q
A

MBChB Finals (7 decks)

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