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Phase 2 Med > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

Osteoarthritis definition

A

Non-inflammatory degenerative arthritis. The result of mechanical and biological events that destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix and subchondral bone. It involved the entire joint, including the articular cartilage, subchondral bone, pericapsular muscles, capsule and synovial, The condition leads to loss of cartilage, sclerosis and eburnation (degeneration of bone) of the sunchondral bone, osteophytes, subchondral cysts. It is clinically characterised by joint pain, stiffness and functional limitation.

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2
Q

Osteoarthritis epidemiology

A

Ver common condition

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3
Q

Osteoarthritis aetiology

A

No single cause. High bone mineral density and low oestrogen, such as in post-menopausal women.

Primary (idiopathic): no preceding injury to the joint, further categorised into localised OA, mostly affecting the hands, hip or foot or generalised OA, usually affecting the hands and another joint.

Secondary: a previous insult to the joint such as a congenital abnormality, trauma, inflammatory arthropathies and ongoing strenuous physical activities.

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4
Q

Osteoarthritis risk factors

A

Age, female sex, obesity, genetic factors

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5
Q

Osteoarthritis signs and symptoms

A

Pain: usually associated, pain at rest is unusual except in advanced OA

Functional difficulties: for example a knee giving way to locking. Can reflect internal derangement such as partial meniscus tear or a loose body within the joint

Knee, hip, hand or spine involvement: commonly involved joints are the knee, hip, hands and lumbar and cervical spine.
Hand OA spares the metacarpophalangeal (CP) joints and the proximal interphalangeal (PIP) and distal interphalangeal joints, which helps distinguish it from rheumatoid arthritis.

Bones deformities: particularly in the hands and leads to enlargement of proximal interphalangeal (PIP) joints (Bouchard’s nodes) and distal interphalangeal (DIP) joints (Heberden’s nodes)

Limited range of motion

Malalignment

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6
Q

Osteoarthritis 1st line investigations

A

X-ray of affected joints: LOSS

  • loss of joint space
  • osteophytes
  • subarticular sclerosis
  • subchondral cysts

Serum CRP and ESR: normal, should be ordered if inflammatory arthritis suspected

Rheumatoid factor (RF): if RA suspected

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7
Q

Osteoarthritis management

A

‘Analgesic ladder’

Knee replacement

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8
Q

Rheumatoid arthritis definition

A

Rheumatoid arthritis is a chronic inflammatory condition affecting around 1% of the population. It primarily affects the small joints of the hands and feet and can cause major work loss, decreased quality of life, need for joint replacement surgery and mortality

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9
Q

Rheumatoid arthritis aetiology

A

Unknown. DRw4 antigen is more common in RA patients. Infection may be a triggering factor in genetically susceptible individuals.

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10
Q

Rheumatoid arthritis risk factors

A

50-55yrs, female sex

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11
Q

Rheumatoid arthritis pathophysiology

A

Inflamed synovial showing increased angiogenesis, cellular hyperplasia, influx of inflammatory cells, changes in adhesion molecules and cytokines. Cytokines such as TNF, IL-1 and IL-6 are abundant in the joints.

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12
Q

Rheumatoid arthritis signs and symptoms

A

Active symmetrical arthritis lasting > 6 weeks

Joint pain and swelling: commonly bilateral MCP, PIP and MTP joints are involved. Painful to touch and when range of motion exercises are performed.

Morning stiffness (may be present with OA but lasts longer in RA)

Less common but specific:

  • ulcer deviation
  • boutonniere deformity
  • swan neck/Z-thumb
  • extra-articular involvement - eg lung (pulmonary nodules), eyes (scleritis) and cord compression

Important to note onset can be at any time and progress quickly compared to OA. There will often by systemic symptoms unlike in OA

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13
Q

Rheumatoid arthritis 1st line investigations

A

Bloods: CRP and/or ESR raised

Rheumatoid factor: positive in about 60-70% of patients

Anti-CCP antibody: positive in about 70% of patients. Helpful in RF-negative patients because it may be positive in these patients

X-ray: LESS

  • L-loss of joint space
  • E-erosion (periarticular)
  • S-soft tissue swelling
  • S- soft bones (osteopenia)
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14
Q

Rheumatoid arthritis management

A

Joint stiffness/pain - NSAIDs and aspirin
Analgesic ladder
Suppress disease - corticosteroid
DMARDS - methotrexate

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15
Q

Rheumatoid arthritis complications

A

Extra-articular involvement - lung (pulmonary nodules), eye (scleritis) and cord compression

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16
Q

Crystal arthropathy - gout definition

A

A syndrome characterised by hyperuricemia and deposition of rate crystals causing attacks of acute inflammatory arthritis; top around the joints and possible joint destruction, renal glomerular, tubular and interstitial disease and uric acid urolithiasis

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17
Q

Crystal arthropathy - gout aetiology

A

Under excretion of uric acid

  • diabetes - nephropathy
  • chronic kidney disease
  • drugs - aspirin (decreases renal excretion) and diuretic eg thiazides
  • dehydration

Overproduction of uric acid

  • high purine diet - alcohol, purine rich food (red meat and shellfish), fructose sweetened drinks
  • increased cell turnover - leukaemia, lymphoma, psoriasis
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18
Q

Crystal arthropathy - gout risk factors

A

More common in middle aged males

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19
Q

Crystal arthropathy - gout pathophysiology

A

Purines from diet
Purines -> hypoxanthine -> xanthine
Xanthine -> uric acid (catalysed xanthine oxidase) and excreted in kidneys
Process not efficient so excess uric acid can be converted to monosodium crystals

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20
Q

Crystal arthropathy - gout key presentations

A

Rapid onset of severe pain

Obese man with a toe pain who had an alcohol and shellfish

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21
Q

Crystal arthropathy - gout investigations

A

Joint aspiration - rule out septic arthritis
Polarised light microscopy
- negatively birefringent
- needle-shaped monosodium crystals

Bloods - raised WBC, ESR and urate
X-ray

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22
Q

Crystal arthropathy - gout management

A

Weight loss, less alcohol, hydration and dairy products - protective
NSAIDs - naproxen, ibuprofen or colchicine if contraindicated
Prophylaxis - allopurinol - xanthine oxidase inhibitor

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23
Q

Crystal arthropathies - pseudogout definition

A

Calcium pyrophosphate deposition (pseudo gout) is associated with both acute and chronic arthritis. Acute CPP crystal arthritis occurs in one more joints.
Chronic CPP arthritis mimics OA or RA and is associated with variable degrees of inflammation

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24
Q

Crystal arthropathies - pseudogout aetiology

A

Possible causes:

  • direct trauma to the joint
  • intercurrent illness
  • hypothyroidism
  • hyperparathyroidism - more calcium production
  • surgery - especially parathyroidectomies
  • hypercalcaemia
  • blood transfusions - excess iron
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25
Q

Crystal arthropathies - pseudogout risk factors

A

Predominantly a disease of the elderly (70+), typically older females

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26
Q

Crystal arthropathies - pseudogout 1st line investigations

A

Joint aspiration - rule out sceptic arthritis
Polarised light microscopy
- positively birefringent
- rhomboid-shaped calcium pyrophosphate crystals

Xray: evidence of chonedrocalcinosis

Bloods: raised WBCs and calcium

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27
Q

Crystal arthropathies - pseudogout management

A

NSAIDs, colchicine

No current medical prophylaxis

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28
Q

Osteoporosis definition

A

A systemic skeletal disease characterised by low bone mass and micro architectural deterioration of bone tissue, with consequent increase in bone fragility and susceptibility to fracture

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29
Q

Osteoporosis aetiology

A

Primary - menopause and age - oestrogen protects the bone
Secondary - disease or drugs which increase bone turnover - SHATTERED
- S-steroids (prednisolone)
- H-hyperthryroidism/hyperparathyroidism
- A-alcohol/smoking
- T-thin (low BMI)
- T-testosterone low
- E-early menopause
- R-renal or liver failure
- E-erosive/inflammatory bone disease eg RA, myeloma
- D-dietary calcium low, malabsorption

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30
Q

Osteoporosis risk factors

A

Age, female sex, low oestrogen/testosterone (hypogonadism, anorexia, menopause)

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31
Q

Osteoporosis pathophysiology

A

Mismatch of bone remodelling - osteoclastic bone resorption not compensated by osteoblastic bone formation.
Bone remodelling is regulated by various cytokines.

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32
Q

Osteoporosis key presentations

A

Asymptomatic until fracture

  • hip - neck of femur after fall onto side or back
  • wrist - distal radius = Colle’s/Smith’s fractures after fall on outstretched arm
  • Vertebra - shorter and stooping posture - sudden onset of severe spine pain radiating to front
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33
Q

Osteoporosis investigations

A

Gold standard: DEXA Bone Mineral Density (BMD) scan - T score. Based off mean BMD of a 30 year old

  • more than 1.0 below T score = normal
  • between 1-2.5 SD below T score = osteopenia
  • less than -2.5 SDs = osteoporosis
  • less than -2.5SDs and fracture = severe osteoporosis

X-ray
FRAX - risk score to predict fracture risk
Raised alkaline phosphatase due to bone breakdown

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34
Q

Osteoporosis 1st line management

A

Oral bisphosphates eg alendronate (careful of oesophageal risks)
Lifestyle; smoking cessation, alcohol abstinence, regular weight-breaking exercise
Vitamin D supplements
Calcium rich diet
Give HRT - oestrogen replacement)
Anabolic

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35
Q

Osteoporosis 2nd line management

A

Denosumab - monoclonal antibody against RANKL to prevent osteoclast production

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36
Q

Osteoporosis 3rd line management

A

Daily submit Teriparatide injection (PTH receptor agonist) - chronically elevated PTH decreases bone density by stimulating osteoclast activity, however intermittent exposure to PTH (or teriparatide) activated osteoblasts more than osteoclasts, therefore increasing bone density

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37
Q

Ankylosing spondylitis definition

A

Seronegative spondyloarthropathies are a group of autoimmune conditions with similar features that includes: ankylosing spondylitis psoriatic arthritis, reactive arthritis. They are all associated with the following features:
- axial inflammation - spine and sacroiliac joints
- asymmetrical peripheral arthritis
- absence of RF
- strong association with HLA-B27
Chronic progressive inflammatory condition in which the spine and other areas of the body become inflamed.

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38
Q

Ankylosing spondylitis epidemiology

A

Men more than women

Late adolescence/early adulthood

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39
Q

Ankylosing spondylitis aetiology

A

No known specific cause, though genetic factors seem to be involved.
In particular, people who have a gene called HLA-B27

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40
Q

Ankylosing spondylitis risk factors

A
  • endoplasmic reticulum aminopeptidase (ERAP1) and interleukin 23 receptor (IL23R) genes
  • positive family hisotry of AS
  • Klebsiella pneumoniae
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41
Q

Ankylosing spondylitis clinical manifestations

A

Generic for Seronegative Spondyloarthropathies: (SPINE ACHE)

  • S-sausage digits (dactylitis) -inflammation of tendon sheaths and joints in fingers
  • P-psoriasis
  • I-inflammatory back pain
  • N-NSAIDs good response
  • E-Enthesitis (inflammation of the entheses, where tendons or ligaments inset into the bone, in these conditions it normally occurs in the heels)
  • A-arthritis
  • C-Crohn’s/UC/elevated CRP
  • H-HLA-B27
  • E-eye (uveitis)
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42
Q

Ankylosing spondylitis signs and symptoms

A

Symptoms: weight loss, fever, fatigue, buttock/thigh pain - sacroiliac joints, neck or back pai/stiffness - cervical/thoracic region can cause SOB

Signs: SPINE ACHE, slow onset of monitoring stiffness, severe kyphosis of thoracic and cervical spine

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43
Q

Ankylosing spondylitis investigations

A

Bloods: HLA-B27, raised ESR/CRP

X-ray: sacroilitis, syndesmophytes fusing (bamboo spine, seen below)

MRI: more sensitive

Diagnosis is made in patients with over 3 months of back pain and age of onset below 45 with sacroilitis as well as at least one SPINE ACHE feature

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44
Q

Ankylosing spondylitis management

A

Non-pharmacological management

  • exercised - reduce pain and stiffness
  • physiotherapy

Pharmacological management

  • NSAIDs
  • DMARDs - methotrexate
  • Anti TNFs eg etanercept
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45
Q

Ankylosing spondylitis complications

A

New bone forms (body’s attempt to heal) and bridge gap between vertebrae/eventually fuses sections of vertebrae
Eye inflammation (uveitis)
Compression fractures
Heart problems

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46
Q

Psoriatic arthritis definition

A

Immune system attacks healthy cells and tissue

Abnormal immune response causes inflammation in joints and over production of skin cells

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47
Q

Psoriatic arthritis aetiology

A

Psoriasis

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48
Q

Psoriatic arthritis risk factors

A
  • FHx if psoriasis or psoriatic arthriits
  • Hx of joint or tendon trauma
  • HIV infection
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49
Q

Psoriatic arthritis pathophysiology

A

T cell mediated attack of joints in people with psoriasis

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50
Q

Psoriatic arthritis clinical manifestations

A

Symptoms:

  • joint pain and stiffness
  • peripheral arthritis
  • pain at site of tendon attachment
  • spinal stiffness
  • reduction of cervical spine mobility

Signs:
- dactylitis

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51
Q

Psoriatic arthritis 1st line investigations

A

Plain film x-rays of the hands and feet
- erosion distal interphalangeal (DIP) joint and periarticular new-bone formation

ESR and C-reactive protein - normal/elevated

Rhematoid factor negative
Anti cyclic citrullinated peptide antibody
- negative

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52
Q

Psoriatic arthritis other investigations

A

Plain film x-ray of the spine and pelvis

MRI scan of sacroiliac joints

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53
Q

Psoriatic arthritis differential diagnosis

A

Polyarticular PA distinguished from R. arthritis by:
Presence of:
- catylitis - a fusiform swelling of an entire digit, and sacroilitis are manifestations not observed in RA

Absence of anticlyclic citrullinated peptide antibodies

  • frequent oligoarticular or monoarticular initial pattern of join involvement
  • distal interphalangeal joint (DIP) involvement
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54
Q

Psoriatic arthritis management

A

NSAIDS/physiotherapy
Crticosteroids
Early intervention with disease modifying antirheumatic drugs (DMARDs)
- methotrexate, leflunomide, sulfasalazine
Anti-TNF drugs
IL 12/23 blockers
IL 17 blockers

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55
Q

Psoriatic arthritis complications

A
  • diabetes
  • eye health issues
  • cardiovascular problems
  • depression
  • lung health problems
  • stomach and digestive issues
  • liver and kidney issues
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56
Q

Reactive arthritis definition

A

Joint pain.swelling triggered by an infection in another part of the body - most often your intestines, genitals or urinary tract

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57
Q

Reactive arthritis epidemiology

A

Young adults around 20-40 age group,
men more than women (3:1)
Risk 50 times greater in HLA B27 positive people

58
Q

Reactive arthritis aetiology

A

GI: campylobacter, salmonella, shigella
GU: chalmydia, gonorrhoea

59
Q

Reactive arthritis pathophysiology

A

Joint inflammation 2-6 weeks following a bacterial GI/GU infection

60
Q

Reactive arthritis clinical manifestations

A

Reiter’s triad: conjunctivitis/uveitis, urethritis, olioarthritis/polyarthritis

Psoriatic-like skin lesions: keratoderma blennorrgagica (rash on feet), circinate balanitis (skin inflammation around the penis)

SPINE ACHE features

61
Q

Reactive arthritis 1st order investigations

A
  • ESR/CRP: elevated
  • antinuclear antibody (ANA): negative
  • rheumatoid factor: negative
  • urogenital/stool cultures: negative (unless just after infection)
  • arthrocentesis with synovial fluid analysis (for DDx vs gout or pseudogout)
  • x-ray (looking for sacroilitis)
62
Q

Reactive arthritis management

A

Treat causative agent with ABx
NSAIDs
Corticosteroid joint injections (eg prednisolone)
If chronic: DMARDs (eg sulfasalazine)

63
Q

Reactive arthritis key presentations

A

Hot, swollen, painful, restricted joint - usually only in one joint, most common site is the knee
Fever
Unusually severe symptoms for underlying disease

64
Q

Reactive arthritis 1st line investigations

A

Aspiration of synovial fluid: microscopy with gram staining, cultures, WCC
Blood cultures
Calprotein (emerging but not widely available test): raised

65
Q

Reactive arthritis differential diagnosis

A

Calprotein forms DDx for septic vs aseptic arthritis

66
Q

Reactive arthritis management

A

Standard sepsis treatment (IV Abx, fluids, ect)
Aspiration of the joint
NSAIDS

67
Q

Systemic lupus erythematosus (SLE) definition

A

A chrnoic multisystem disorder that most commonly affects women during their reproductive years

68
Q

Systemic lupus erythematosus aetiology

A

Aetiology is not fully known (common for autoimmune disorders) SLE is common in those with complement deficiency

69
Q

Systemic lupus erythematosus risk factors

A

Strong female preponderance
Age 15-45 years
African/Asian descent in Europe and US

70
Q

Systemic lupus erythematosus pathophysiology

A

An antigen-driven immune-mediated disease characterised by high affinity IgG antibodies.
T-cell dysregulation of B cells may arise, resulting in autoimmunity. This is why monoclonal antibodies may be useful in treatment

71
Q

Systemic lupus erythematosus key presentations

A

Malar (butterfly rash
Photosensitive rash (rash occuring after sun exposure)
Discoid rash

72
Q

Systemic lupus erythematosus signs and symptoms

A

Signs: oral ulcers, alopecia, Raynaud’s phenomenon (colour changed of the digits induced by cold or emotion), HTN, signs of nephrosis such as oedema, peripheral lymphadenopathy

Symptoms: fatigue, weight loss, fibromyalgia, chest pain and SOB, abdo pain

73
Q

Systemic lupus erythematosus 1st line investigations

A

FBC: anaemia, leukopenia (normally lymphopenia), thrombocytopenia and rarely pancytopenia

U&Es: elevated urea and creatinine

ERS and CRP: may be raised

Antibodies: ANA antibodies almost always present but not specific. Anti-dsDNA and anti-Smith antbodies are highly specific for SLE

Urinalysis: (assess renal involvement) haematuria, or proteinuria

74
Q

Systemic lupus erythematosus management

A

1st line:

  • hydroxychloroquine
  • NSAIDS and corticosteroids (prednisolone)
  • methotrexate and folinic acid

Lupus nephritis
- add immunosuppression such as cyclophosphamide

75
Q

Systemic lupus erythematosus complications

A

Anaemia, leukopenia, thrombocytopenia and corticosteroid related complications

76
Q

Osteomyelitis definition

A

Inflammatory condition of bone caused by an infecting organism, either by local infection or via blood

77
Q

Osteomyelitis epidemiology

A

Acute occurs predominantly in children whereas chronic is more common in elderly

78
Q

Osteomyelitis aetiology

A

Infecting organism, most commonly Staphylococcus aureus followed by Staphylococcus Epidermis

Salmonella as a complication of sickle cell

79
Q

Osteomyelitis risk factors

A
  • previous osteomyelitis
  • penetrating injury
  • IV drug misuse
  • diabetes
  • HIV infection
  • recent surgery
  • distant or local infection
  • sickle cell disease
  • rheumatoid arthritis
  • chronic kidney injury
  • immunocompromising condition
80
Q

Osteomyelitis pathophysiology

A

Severity staged depending on aetiology of infection,

  • pathogenesis
  • extent of bone involvement
  • duration
  • host factors particular to individual patient

Broadly, bone infection is either

  • haematogenous
  • contiguous-focus

Necrotic bone sequestra may be present in chronic disease

81
Q

Osteomyelitis clinical manifestations (acute)

A

Pyrexia
Swelling and extreme tenderness over site
- erythema and warmth

Severe pain, exacerbated by movement
Effusion into neighbouring joints, can result in septic arthritis

82
Q

Osteomyelitis clinical manifestations (chronic)

A

Erythema, tenderness and swelling over site
Non-healing ulcer
Draining sinus tracts (ie tunnelling wound)
Neighbouring joints have decreased ROM

83
Q

Osteomyelitis investigations

A

Imaging

  • X-ray
  • MRI may show marrow oedema

Bloods

  • raised WCC
  • raised CRP and ESRs
  • blood cultures

Gold standard: bone biopsy and cultures

84
Q

Osteomyelitis management

A

Immobilisation of the bone to aid healing
Antimicrobial therapy
- IV flucloxacillin is common treatment
Surgical debridement and removal of sequestra (dead bone)

85
Q

Primary and secondary bone tumours definition

A

Primary bone tumours: osteosarcomas, fibromas, sarcomas

Secondary: most common places to metastasise to bone: lung, breats, prostate, thyroid, kidney

86
Q

Primary and secondary bone tumours clinica maifestations

A

Pain at tumour location associated with localised bone pain. Malaise, pyrexia, aches, pains and hypercalcemia

87
Q

Primary and secondary bone tumours 1st line investigations

A

Skeletal isotope scan

88
Q

Primary and secondary bone tumours management

A

Analagesics and antiinflammatory drugs
Radiotherapy, chemotherapy, hormonal therapy
Bisphosphates

89
Q

Fibromyalgia definition

A

A chronic pain syndrome disgnosied by the presence of widespread body pain

90
Q

Fibromyalgia aetiology

A

Aetiology and pathophysiology are unknown. Associated with abnormalities in the stress response and triggering events. More common in females.

91
Q

Fibromyalgia diagnosis

A

Clinical diagnosis: presence of >3 months of widespread pain and associated symptoms

92
Q

Fibromyalgia management

A

Non-pharmacological: exercise, relaxation therapies, CBT

Pharmacological: analgesia (paracetamol, weak opioids), antidepressants (amitriptyline or duloxetine)

93
Q

Osteomalacia definition

A

Poor bone mineralisation due to a lack of Ca++ but the amount/density is normal.
Rickets is osteomalacia but before the fusion of the epiphyseal plates (ie growth plates)

94
Q

Osteomalacia aetiology

A

Vitamin D deficiency is the main cause (poor diet, lack of sun)
Renal/liver disease
Drug-induced such as anticonvulsants
Tumour induced

95
Q

Osteomalacia presentation

A

Muscle weakness and pain: characteristic waddling gait, can’t get out of chair

Bone pain: widespread, dull ache, worse on weight bearing

Fractures
Imparied growth
Bowed legs
Hypocalcemic tetany in severe cases

96
Q

Osteomalacia diagnosis

A

Bloods:

  • U&Es: low Ca++, high phosphate
  • PTH - low
  • alkaline phosphatase (usually raised)
  • 25-hydroxyvitamin D - low

Gold standard: biopsy showing incomplete mineralisation
X ray: defective mineralisation

97
Q

Osteomalacia management

A

Vitamin D replacement

  • poor diet - calcium D3 Forte
  • malabsorption - calcitriol
  • renal - calcitriol
98
Q

Paget’s disease of bone definition

A

A disorder in which there is a focal disruption of bone remodelling. There is increased osteoclastic bone resorption followed by formation of weaker new bone. This bone is disorganised making it mechanically weaker as well as being less compact and more vascular. This process predisposes patients to deformity and fractures.

99
Q

Paget’s disease of bone aetiology

A

Unknown

100
Q

Paget’s disease of bone presentation

A

Most are asymptomatic and discovered on x-ray incidentally
Bone pain
Deformity - bowing of tibias, kyphosis
Fractures
Can affect a single bone (monostotic) or multiple bones (polyostotic)
Deafness/tinnitus due to compression of CNVIII due to deformity

101
Q

Paget’s disease of bone diagnosis

A

1st line: x-ray - localised bony distorrtion and enlargement, sclerotic changes (increased density), osteolytic areas (reduced density)

Bloods

  • high alkaline phosphatase (increase bone turnover)
  • normal Ca++, phosphate and PTH

Gold standard: isotope bone scan, unable to distinguish between Paget’s and secondary metastatic bone carcinoma so will need biopsy

102
Q

Antiphospholipid syndrome definition

A

Antiphospholipid antibodies (aPL) to phospholipid-binding proteins leads to a hyper coagulable state and an increased risk of venous and arterial thrombosis

103
Q

Antiphospholipid syndrome aetiology

A

Aetiology is unclear. More common in white female young adults. Associated with SLE (30-40% with SLE)

104
Q

Antiphospholipid syndrome presentation

A 
Recurrent thrombosis (DVT, PE, storke, MI) 
Pregnancy complications (recurrent miscarriage, stillbirth, preeclampsia) 
Arthralgia, lived reticularis
105
Q

Antiphospholipid syndrome diagnosis

A

Presence of aPL, thrombocytopenia, history of thrombosis

106
Q

Antiphospholipid syndrome management

A

LMWH and warfarin

107
Q

Sjogren syndrome definition

A

Chronic systemic auto-immune disorder characterised by diminished lacrimal and salivary gland secretion

108
Q

Sjogren syndrome aetiology

A

Lymphocytic infiltration into lacrimal and salivary glands leading to dry eyes and mouth
Secondary Sjogren’s: secondary to SLE, systemic sclerosis, RA (60% of Sjogren’s diagnosed)

109
Q

Sjogren syndrome presentation

A

Fatigue, dry eyes, dry mouth

110
Q

Sjogren syndrome diagnosis

A

Schirmer’s test: filter paper in lower conjunctival sac

Autoantibodies: anti-Ro and anti-La

111
Q

Sjogren syndrome management

A

Artificial tears, salivary substitutes

112
Q

Marfan syndrome definition

A

An inherited connective tissue disorder

113
Q

Marfan syndrome aetiology

A

75% of cases are inherited (autosomal domiant), 25% spontaneous mutation
Mutations in fibrillin-1 genes, production of abnormal fibrillin protein, connective tissue abnormalities
Affects both men and women equally

114
Q

Marfan syndrome presentation

A

Tall stature, wide arm span, arachnodactyly (long and slender fingers), high arched palate, positive thumb and wrist sign, pectus excavatum/carinatum, hypermobility
Subluxed eye lens, aortic/mitral valve murmur

115
Q

Marfan syndrome diagnosis

A

Echocardiogram
CT thorax
Slit - lamp eye exam
USS, CT, MRI abdomen

116
Q

Marfan syndrome management

A

BBs to reduce MAP and pulse rate

Surgical interventions: aortic repair, orthopaedic bracing, correction of ectus excavatum/carinatum

117
Q

Vasculitis definition

A

Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow to end organs

118
Q

Vasculitis aetiology

A

This may be tirggered by an infection or a medicine, although often cause is unknown

119
Q

Vasculitis pathophysiology

A

Combination of:

  • vessel wall destruction > perforation and haemorrhage into tissues
  • endothelial damage predisposing patient to thrombosis and subsequent ischaemia/infarction on dependent tissues

Classification done by:

  • size of vessel affected (small, medium, large)
  • target organs
  • presence/absence of anti-neutrophil cytoplasmic antibodies (ANCA)

It can also be classified into

  • primary, spontaneous development on its own
  • secondary - to another disease process (eg cancer, infection, other autoimmune conditions)
120
Q

Vasculitis clinical manifestations

A 
Constiutional symptoms: 
- fever, athralgia 
- arthritis 
- rash
- weight loss 
- headache 
- foot drop 
Major event such as: 
- stroke 
- bowel infarction

Large vessel vasculitis associated with

  • vision loss
  • upper extremity claudication
  • asymmetric brachial pulses
  • bruits

Medium vessel

  • abdo pain
  • foot drop
  • cutaneous ulcers

Small vessel

  • haematuria
  • palpable purpura
  • otorrhoea, ear pain
  • nasal symptoms
  • sinus pain
  • wheeze
121
Q

Vasculitis investigations

A

ESR = >100 mm/hour
CRP = elevated
ANCA = positive
- antibodies present in patients with small/medium (not large) vessel vasculitis
- directed against specific antigens in cytoplasmic granules of neutrophils and monocyte lysosomes

Srum urea and creatinine = norm/elevated
Urinalysis = haematuria, proteinuria, red blood cell casts
Biopsy

122
Q

Vasculitis management

A

Medication

  • corticosteroid drug eg prednisone
  • medication used depends on type of vasculitis
  • methotrexate, azathioprine, mycophenolate, cyclophosphamide, tocilizumab or rituximab

Surgery

123
Q

Avascular necrosis definition

A

Death of bone tissue due t an interruption of the blood supply

124
Q

Avascular necrosis aetiology

A

The neck of femur is the classic location as the artery supplying the femoral head obliterates by adulthood meaning if the neck is fractured the blood supply is cut off

125
Q

Avascular necrosis resentation

A

Usually there is pain and joint discomfort that progresses over time, however often it is associated with traumatic fractures to certain long bone

126
Q

Avascular necrosis diagnosis

A

Often done by x-ray but MRIs can confirm but not usually needed

127
Q

Avascular necrosis management

A

Almost always surgical and usually requires a replacement of the joint

128
Q

Myositis - polymyositis and dermatomyositis definition

A

Chronic inflammation of muscles (polymyositis) and skin (dematomyositis)

129
Q

Myositis presentation

A

Slow onset proximal muscle weakness, fatigue, weight loss

Dermatomyositis only: gottron’s papules, photosensitive erythematous rash, periorbital oedema

130
Q

Myositis diagnosis

A

Raised creatinine kinase: enzyme found in muscle cells
Muscle biopsy, electromyogram (EMG)
Antibodies: anti-Jo-1 (both), anti-Mi-2, ANA (dermatomyositis only)

131
Q

Myositis management

A

Steroids (prednisolone)
Sun protection
IV immunoglobulin in severe disease

132
Q

Systemic sclerosis (scleroderma) definition

A

Multisystem autoimmune disease characetrised by vascular damage and fibrosis.
Types:
- limited cutaneous (CREST syndrome): milder, less skin involvement, slow progression
- diffuse cutaneous: faster onset, internal organ involvement more common

133
Q

Systemic sclerosis (scleroderma) aetiology

A

Increased fibroblast activity = abnormal growth of connective tissue. Excessive collagen production and deposition
Very rare condition, more common in females, peak onset 40-50yrs

134
Q

Systemic sclerosis (scleroderma) presentation

A

Pulmonary: pulmonary hypertension, interstitial lung disease

Cardio: Raynaud’s, CAD, pericarditis, arrhythmias

GI: GORD, oesophageal scarring, reduced small bowel motility

MSK: skin thickening, sclerodactyly (hardening of skin of the hands)

135
Q

Systemic sclerosis (scleroderma) diagnosis

A

Nailfold capillaroscopy

Autoantibodies: 90% have ANA

136
Q

Systemic sclerosis (scleroderma) management

A

Avoid cold exposure, gentle stretching, smoking cessation, occupational therapy as needed
PPIs for GORD, ACEi for HTN, emollient/steroid for skin

137
Q

Ehlers-Danlos syndromes definition

A

A group of connective tissue disorders

138
Q

Ehlers-Danlos syndromes aetiology

A

Inherited. Hypermobile EDS is the most common form. More common in females

Genetic mutation leads to production of faulty connective tissue proteins (eg collagen) leading to hypermobility or fragility

139
Q

Ehlers-Danlos syndromes presentation

A

Skin elasticity/fragility, hypermobility, fatigue, easy bruising, striae

140
Q

Ehlers-Danlos syndromes diagnosis

A

Clinical diagnosis, genetic testing

141
Q

Ehlers-Danlos syndromes management

A

Physiotherapy, CBT, analgesia

Phase 2 Med (9 decks)

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