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204-theme 2 -anatomy > l13:Intro to msk diseases > Flashcards

l13:Intro to msk diseases Flashcards

1
Q

what are the bursae

A

-they are synovial membrane lined pockets that serve to allow free movement of adjacent structures where otherwise there could be friction

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2
Q

describe what occurs in enthesitis

A

Inflammation of an enthesis. Entheses are the points where tendons, ligaments or joint capsules insert into bone. The largest site is the Achilles insertion.

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3
Q

define the conditions:

1-osteoporosis
2-osteomalacia
3-osteomyelitis
4-osteosarcoma

A

Osteoporosis – Reduced bone density

Osteomalacia – Poor bone mineralisation

Osteomyelitis – Bone infection

Osteosarcoma – An example of malignant bone tumour

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4
Q

what is myalgia commonly associated with

A
  • Commonly associated with viral infections.

- Can be drug induced (eg by statins).

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5
Q

define a joint

A

A joint is formed where two or more bones meet each other

This is an example of a normal joint

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6
Q

how can rheumatic disease be classified

A

Articular

       Non articular/ Periarticular

Inflammatory

       Non inflammatory/ degenerative / mechanical

Number of joints affected - Suspect infection in all acute monoarthritis

Duration of onset

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7
Q

how is joint pain classified

A

Periarticular: (point tenderness over the involved structure, pain reproduced by movement involving that structure )

Articular: Joint line tenderness, pain at the end range of movement of any direction

which structure: Bursa, tendon, tendon sheath, ligament sheath, others

inflammatory or mechanical

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8
Q

define the terms monoarthritis, oligoarthritis, polyarthritis

A

MonoARHRITIS – arthritis affecting 1 joint

OligoARTHRITIS – arthritis affecting 4 or fewer joints (2-4)

PolyARTHRITIS – arthritis affecting 5 or more joints (>=5)

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9
Q

You are asked to review a patient presenting with thenar eminence atrophy. Which nerve do you think is affected?
Ulnar nerve

A

median

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10
Q

which epicondyle is tennis elbow

A

Lateral epicondyle

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11
Q

give aeitiology of soft tissue conditions

A

Problems with radiolucent moving tissues

Very common, part of everyday life

Some examples:

- tennis elbow (lateral epicondylitis)
 	- golfers elbow (medial epicondylitis)
 	- carpal tunnel (median nerve compression as it passes through the carpal tunnel in the wrist)
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12
Q

background of rheumatic disease

A
  • very common and getting more common
  • expensive

leading cause of disability

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13
Q

background on MSK disorders

A

• MSK disorders are the second most common cause of disability worldwide, measured by years lived with disability (YLDs)

Low back pain is the single leading cause for disability globally

Disability due to MSK disorders is estimated to have increased by 45% from 1990 to 2010, in particular OA, and is expected to continue to rise with an increasingly obese, sedentary and ageing population.

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14
Q

what are the secondary effects of MSK on work

A

22.4%?30.8 million days of work lost in a year

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15
Q

look at slide 24 for statistics on MSK

A

how was it

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16
Q

what is a MSK differential for a 2 day history of a painful swollen right knee

A

1) Posttraumatic hemarthrosis
2) Gout
3) Septic arthritis

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17
Q

what tests can be done for septic arthritis

A

consider joint aspiration and gram stain

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18
Q

what are the organisms responsible for septic arthritis

A

-The commonest organisms are staph and strep

-

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19
Q

what is the pathophysiology of gout

A

Most common inflammatory arthropathy worldwide

Serum urate levels > physiological saturation point (around 408 μmol/L)
Monosodium urate. form and
crystals deposit

cartilage, bone, and periarticular tissues of peripheral joints

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20
Q

what is the common joint for gout to occur

A

first metatarsophalangeal joint

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21
Q

give a background of gout disease

A
  • Crystal deposition is often clinically silent
  • About 10% of people with hyperuricaemia develop clinical gout
  • • UK GP Studies show the prevalence of gout per 1,000 has been steadily increasing from 2.6 in 1975, to 3.4 in 1987, and 9.5 in 1993
  • 1 in 40 adults in the UK is affected by gout= 2.5% - 15 years analysis (2014)
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22
Q

who gets gout

A

• Men aged 40 years and over
∙ Women over 65 years.

It increases with age, affecting 15% of men aged over 75 in the United Kingdom

Epidemiological studies show that the metabolic syndrome and its components (insulin resistance, obesity, hyperlipidaemia, and hypertension) are strongly associated with gout

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23
Q

what are the risk factors for gout

A

Male sex
• Older age

Genetic factors (mainly reduced excretion of urate)

Chronic kidney disease (reduced excretion of urate)

• Metabolic syndrome
 • Obesity
• Hypertension
     • Hyperlipidaemia 
             • Loop and thiazide diuretics 
(reduce excretion of urate)

Osteoarthritis (enhanced crystal formation)

Dietary factors (increased production of uric acid)

24
Q

What crystals are you expecting to find in the knee fluid aspirated from our previous patient if you suspect clinically that he has gout?

A

monosodium urate

25
Q

describe the gout crystal formation

A

Gout is caused by negatively birefringent rods – monosodium urate

26
Q

what is psuedogout

A

Pseudogout (CPPD) by positively birefringent rhomboids – calcium pyrophosphate

27
Q

how do you manage acute gout attacks

A

– NSAIDs e.g. naproxen
– Colchicine
– Steroids

28
Q

how do you manage gout long term

A

Urate-lowering therapy e.g. allopurinol or febuxostat

29
Q

describe rheumatoid arthritis

A

-Common, chronic, multisystem inflammatory condition affecting up to 0.5-1% of the world population

-More common in women (3:1)
• Peak onset is 45-65 years

-Unknown cause with around 30% genetic susceptibility and the rest environmental

30
Q

what is the first component affected in rheumatoid arthritis

A

the synovium

31
Q

what is affected in osteoarthritis

A

cartilage

32
Q

what is the most important environmental factor for rheumatoid arthritis

A

Smoking

33
Q

what is the process smoking causes in rheumatoid

A

Citrilidation happens to porteins in the lung, they aren’t recognised by innate immune system, apc presents to T cells taken to B cells which produced antibodies- APA

Triggers disease

34
Q

describe the phases and classification of rheumatoid disease

A

(induction of autoimmunity )
Phase A/B- genetic and environmental

Phase C- systemic autoimmunity

( Maturation of the antibody response)

Phase D- Symptoms

Phase R- Unclassified arthritis

Phase F- no additional changes- rheumatoid

35
Q

describe the pathology behind rheumatoid arthritis

A
  • Early lymphocyte invasion of the synovium
  • Acute inflammatory reaction - swelling and increased vascular permeability
  • Synovial proliferation
  • pannus formation
  • cartilage destruction and bone erosion
36
Q

what ..articular and joints are involved in rheumatoid

A

Polyarticular symmetrical disease

In particular metacarpal phalangeal joints

37
Q

what are the symptoms and signs

A

-Onset varies, can be acute or chronic

  • Symmetrical pain and boggy swelling of the small joints of the hands and feet (MCP, PIP, wrist, MTP, subtalar.
    NOT the DIPs)
  • Early morning stiffness > 1 Hour
  • Malaise and fatigue are common
  • Systemically unwell
  • Examination - look for pain, swelling and restriction of movement
38
Q

what are the extra-articular manifestations of RA

A
  • Nodules (20%)
  • Bursitis / Tenosynovitis
  • Eyes: dry eyes (secondary Sjogren’s syndrome) / Scleritis / Scleromalacia
  • Splenomegaly (Felty’s)
  • • Anaemia of chronic disease
  • Lung fibrosis /effusion /Nodules (Caplan’s)
  • Pericarditis
  • Neurological: Atlanto-axial subluxation / Carpal tunnel syndrome / Mononeuritis multiplex
  • Renal amyloidosis (AA)
  • Leg ulcers / Pyoderma gangenosum
  • Vasculitis
  • Increased risk of cardiovascular disease
39
Q

what RA investigations can be done

A
  • • ESR and CRP
  • FBC: Anaemia of chronic disease (normochromic normocytic)

• Rheumatoid factor positive
– IgM antibody against the FC portion of human IgG antibodies :
1-can be falsely elevated by illness
2– normal raised levels in 1 in 20 of population

Anti CCP antibodies - cyclic citrullinated peptide antibodies:– Antigen present on inflamed synovium
– 98% specific for diagnosis of RA

X-Rays : normal in early disease.. erosions / peri-articular osteoporosis and reduced joint space / cysts

40
Q

look at slide 48

A

how was it

41
Q

describe the management of RA (1)

A

Early and aggressive treatment to reduce inflammation and joint damage

-Non-steroidal anti-inflammatory drugs for short periods

-Corticosteroids
• Intra-articular joint injections if only 1 or 2 troublesome
Systemic if many joints are a problem. The main routes are IM or PO though in severe disease we may give IV steroid.

42
Q

what medication do u use to manage RA

A

DMARDs – Disease Modifying Anti-Rheumatic Drugs

  • Synthetic DMARDs
    • Methotrexate
    • Sulfasalazine • Hydroxychloroquine
    • Leflunomide
  • Biologic Agents • Anti TNF agents ( Etanercept, Adalimumab, Infliximab)
    • Anti B-cell (Rituximab)
  • Anti Interleukin-6 receptor blocker (Tociluzumab)
  • Anti T-cell – selective co-stimulation modulator- CTLA4-Ig (Abatacept)
  • Janus kinase inhibitor (JAK 2) (Tofacinitib, Baricitinib)
43
Q

what is the multidisciplinary team that works on RA

A

– Nurse specialist (education and disease monitoring)
– Physiotherapy (improve strength and stamina)

– Occupational Therapy (work, home environments)

– Podiatry

44
Q

study slide 52

A

how was it

45
Q

describe osteoarthritis

A
  • Common, degenerative disease of which the prevalence increases with age
  • Affects 70% of over 65 years olds
  • • Most commonly clinically affects the knees, hips and small joints of the hands (DIP, PIP, 1st CMCJ)
  • • Characterised by joint pain and very variable degrees of functional limitation

(Distal and proximal interphalangeal joint and the 1st metacarpal joint)

46
Q

what is the pathophysiology of osteoarthritis

A
  • • Metabolically active, dynamic process involving all joint tissues (cartilage, bone, synovium, capsule, ligaments/muscles)
  • • Focal destruction of articular cartilage
  • • Remodelling of adjacent bone = hypertrophic reaction at joint margins (osteophytes)
  • • Remodelling and repair process (efficient but SLOW)
  • • Secondary synovial inflammation and crystal deposition
47
Q

what are the clinical features of osteoarthritis

A
  • Age > 50 years• Morning stiffness < 30 minutes• Persistent joint pain aggravated on use
  • Crepitus• NO INFLAMMATION• Bony enlargement and/or tenderness
48
Q

Is there a clinical correlation between the radiological changes and the symptoms in osteoarthritis?

A

no

49
Q

OA investigations

A
  • Blood tests not helpful
  • A clinical diagnosis
  • X-rays do not correlate well with symptoms
50
Q

study slide 60

A

how was it

51
Q

describe SLE

A
  • Chronic, relapsing, remitting disease
  • Broad spectrum of clinical features involving almost all organs and tissues
  • Prevalence in the UK: 97 per 100,000
  • F:M= 10-20:1
  • Peak onset between 15- 40 years
  • More common and severe in those of Afro-Caribbean, India, Hispanic and Chinese origin living in USA and Europe> Caucasians
52
Q

study slide 64

A

how was it

53
Q

what are the systemic effects of SLE

A

splenomegaly

glomerulonephritis

malar rash and discoid rash

lung inflammation

renal failure

atherosclerosis

pulm fibrosis

stroke

neurological damage affective disorder

Pain cycanosis warm up-red and painful

54
Q

SLE investigations

A
  • Urinalysis – urinary protein: creatinine ratio
  • Full blood count
  • Urea and electrolytes
  • ESR
  • CRP
  • Liver function test
  • Antibodies: ANA; ENA; Anti –dsDNA; Lupus anticoagulant; ANTI C1q;
55
Q

SLE treatment

A

MTX

CS

IV MP and CYC

204-theme 2 -anatomy (15 decks)

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