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2a Bateman - Phase 2a MASTER DECK > Musculoskeletal System > Flashcards

Musculoskeletal System Flashcards

1
Q

What is HLA B27 associated with?

A

Spondyloarthritis (SpA) such as:

Ankylosing spondylitis

Psoriatic arthritis

Reactive arthritis

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2
Q

What is HLA B27?

A

Human Leucocyte Antigen (HLA) B27

Class I surface antigen (all cells, except red blood cells)

Encoded by Major Histocompatibility Complex (MHC) on chromosome 6

Antigen presenting cell

Essentially a tissue type

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3
Q

Why is HLA B27 linked with disease?

A

“Molecular mimicry”

Infection → immune response → infectious agent has peptides very similar to HLA B27 molecule → auto-immune response triggered against HLA B27

Mis-folding theory

HLA B27 heavy chain homodimer hypothesis.

Remember not all patients are B27 positive!

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4
Q

How does the mis-folding theory work?

A

These unfolded HLA-B27 proteins accumulate in the endoplasmic reticulum (ER).

A proinflammatory stress response called the endoplasmic reticulum unfolded protein response (ERUPR) ensues.

As a result, interleukin 23 (IL-23) is released, activating a proinflammatory response via interleukin-17+ T lymphocytes.

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5
Q

How does the heavy chain homodimer hypothesis work?

A

It is suggested that B27 heavy chains can form stable dimers, which tend to dimerize and accumulate in the endoplasmic reticulum.

In turn, this initiates the proinflammatory ERUPR.

In addition, these heavy chains and dimers can bind to other regulatory immune receptors such as the natural killer receptors (NKRs).

This causes the expression and survival of more proinflammatory leukocytes and subsequent production of proinflammatory mediators.

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6
Q

WHAT IS ANKYLOSING SPONDYLITIS OR “AXIAL SPONDYLOARTHRITIS”?

A

Inflammatory arthritis of the spine, rib cage and sacroiliac joints
– eventually leading to new bone formation and fusion of the joints.

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7
Q

When does ankylosing spondylitis start?

A

Typically starts in late teenage years/ 20s.

More common in Men.

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8
Q

What are the clinical features of SpA?

A

_Low back pain – improves with activity not improved with rest
Morning stiffness_

Inflammatory arthritis of the “axial skeleton”, which results in new bone formation and “fusion” of the vertebrae/costovertebral / SIJ,

Enthesitis (inflammation of junction between ligament/ tendon and bone),

Acute anterior uveitis (irits) ie inflammation of the anterior chamber of the eye

Peripheral arthritis (often large joint oligoarthritis but in PsA can be small joint just like RA)

Skin psoriasis

May also have (sub-clinical) inflammatory bowel disease

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9
Q

What does SPINEACHE help with and what does it represent?

A

Sausage digit (dactylitis)

Psoriasis

Inflammatory back pain

NSAID good reponse

Enthesitis (heel)

Arthritis

Crohn’s/ Colitis/ elevated CRP*

HLA B27

Eye (uveitis)

Symptoms of SpA.

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10
Q

What is Syndesmophytes?

A

Bone growth originating inside ligaments.

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11
Q

What is Sacroiliitis?

A

Inflammation of one or both of your sacroiliac joints

Sclerosis, erosions, loss of joint space,fusion.

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12
Q

What is Kyphosis?

A

Curvature of the spine at the top.

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13
Q

What is the proposed method for Ankylosing spondylitis?

A

Delayed damage theory”

ie once inflammation has occurred – new bone formation is inevitable, therefore once treatment started, new bone continues to form for some time after

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14
Q

What are the tests for ankylosing spondylitis?

A

Diagnosis is clinical, supported by imaging

MRI is most sensitive and better at detecting early disease.

Sacroiliitis is the earliest X-ray feature, but may appear late: look for irregularities, erosions, or sclerosis affecting the lower half of the sacroiliac joints, especially the iliac side.

Syndesmophytes common later stages on radiography.

‘Bamboo spine’ In later stages, calcification of ligaments with ankylosis lead to this

FBC (normocytic anaemia), increased ESR, increased CRP, HLA B27+ve (not diagnostic).

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15
Q

What is the ASAS criteria used for? What does the criteria require?

A

Ankylosing spondylitis.

Confirmation of sacroiliitis on imaging plus more than or equal to 1 SpA feature

or HLA-B27 plus more than or equal to 2 SpA features.

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16
Q

What is the treatment for ankylosing spondylitis?

A

Exercise

NSAIDS
Ibuprofen or Naproxen.

TNF alpha blockers
Golimumab

Local steroid injections

Surgery includes hip replacement/spinal osteomy

Bisphosphonates (consider)
Alendronate
There is increased risk of osteoporotic spinal fractures

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17
Q

WHAT IS PSORIATIC ARTHRITIS?

A

Psoriatic arthritis is a form of arthritis affecting the joints in people with the skin condition psoriasis

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18
Q

What is the epidemology of psoriatic arthritis?

A

1 in 5 people with psoriasis and can present before skin changes.

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19
Q

What are the clinical manifestations of disease for Psoriatic Arthritis?

A

Spinal/Axial, (Similar to AS)

Arthritis mutilans

DIPJ only, (Distal interphalangeal joint)

Oligoarthritis (2-4 joints in first 6 months) (Like RA) Large joint
Asymmetrical

Polyarthritis = >5 joints RA like (symmetrical small joint).

Also
Dactylitis
Nail changes

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20
Q

What is arthritis mutilans?

A

An extremely severe form of chronic rheumatoid or psoriatic arthritis characterized by resorption of bones and the consequent collapse of soft tissue.

When this affects the hands, it can cause a phenomenon sometimes referred to as ‘telescoping fingers.’

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21
Q

What are the investigations for psoriatic arthritis?

A

‘Pencil-in-cup’, erosive changes, with deformity in severe cases.

Nail changes in 80%

Synovitis (dactylitis)

Rashes
Acneiform rashes and palmo-plantar pustulosis.

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22
Q

What is the treatment for Psoriatic Arthritis?

A

Similar to RA

NSAIDs

DMARDs
MTX, ciclosporin
DMARDs often help skin disease

Anti TNF drugs
Golimumab, infliximab

IL12/23 blockers
Ustekinumab

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23
Q

WHAT IS REACTIVE ARTHRITIS?

https://www.youtube.com/watch?v=dzQwIqc6dQE

A

Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually gastro-intestinal or genital.

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24
Q

What is the epidemology of reactive arthritis?

A

Mostly Male

20-40

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25
Q

What are some causes of reactive arthritis?

A

Gut associated infections
Salmonella
Shigella

Sexually acquired infection (NSU)
Chlamydia
Ureaplasma urealyticum.

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26
Q

What is Reiter’s syndrome?

A

Classical triad of

Arthritis (large joints)

Urethritis.

Conjunctivitis

CANT PEE, CANT SEE, CANT CLIMB A TREE

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27
Q

What are some symptoms of reactive arthritis?

A

Iritis

Keratoderma blenorrhagica
Brown, raised plaques on soles and palms

Circinate Balanitis
Painless penile ulceration secondary to Chlamydia

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28
Q

What are some differential diagnosis of reactive arthritis?

A

Hot swollen joint

Think
Septic arthritis.
Gout.

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29
Q

What are some tests for reactive arthritis?

A

Blood test
Raised ESR/CRP

Aspirate joint
To exclude infection/crystals.

Urethral swab, stool culture
Show infection.

Contact tracing if necessary.

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30
Q

What is the management for reactive arthritis?

A

No specific cure

Antibiotics

Splint joints

NSAIDS or local steroid injections

Sulfasalazine or methotrexate
If symptoms >6 months. (Consider)

Treating the original infection may make little difference to the arthritis.

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31
Q

WHAT IS ENTEROPATHIC ARTHRITIS?

A

Inflammatory arthritis associated with the occurrence of an inflammatory bowel disease (IBD), the two best-known types of which are ulcerative colitis and Crohn’s disease.

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32
Q

Where does enteropathic arthritis occur in men and women?

A

Men – axial/spinal (esp.HLA-B27+)

Women – peripheral/limb

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33
Q

What are the symptoms of enteropathic arthritis?

A

Peripheral synovitis

Asymmetric lower limb arthritis

AS occurs in 7% of patients with IBD.
50% of patients with IBD and HLA-B27 +ve develop sacroiliitis

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34
Q

What are the treatments for enteropathic arthritis?

A

No specific cure

Antibiotics

Splint joints

NSAIDS or local steroid injections

Sulfasalazine or methotrexate
If symptoms >6 months. (Consider)

Treating the original infection may make little difference to the arthritis.

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35
Q

What are some examples of inflammatory joints?

A

Auto-immune.

Crystal arthritis.

Infection.

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36
Q

WHAT IS RHEUMATOID ARTHRITIS?

https://www.youtube.com/watch?v=6ylzE5usu7o

A

Auto-immune inflammatory disease affecting joints and other systems

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37
Q

What is the epidemology rheumatoid arthritis?

A

Common inflammatory arthritis~1% population

Women more common

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38
Q

What are the classical signs of inflammation?

A

Rubour (red)

Calor (heat)

Tumour (swelling)

Dolor (pain)

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39
Q

What are the properties of an inflammatory disorder?

A

Pain eases with use

Stiffness
Significant (>60 mins)
Early morning/ at rest (evening)

Swelling Synovial +/- bony

Hot & red?

Pt demographics
Eg young, psoriasis, family history

Joint distribution
Eg hands & feet

Responds to NSAIDs

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40
Q

What are the properties of a degenerative disorder?

A

Pain increases with use
clicks/ clunks

Stiffness
Not prolonged (<30 mins)
Morning/ evening

Swelling
None, bony

Not clinically inflamed

Pt demographics
Eg older, prior occupation/ sport

Joint distribution
Eg 1st CMCJ, DIPJ, knees

Less convincing response to NSAIDs

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41
Q

What does a normal synovial joint look like?

A

2 articulating bone surfaces
covered with hyaline cartilage

Fibrous capsule lined with synovium

Joint space filled with synovial fluid.

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42
Q

What does inflammation of a synovial joint cause?

A

Arthritis.

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43
Q

What is the cause of rheumatoid arthritis?

A

Genetic and environment

HLA DR1 and 4

Ciagrette smoke or infection

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44
Q

What happens when citruillination happens?

A

Arginine converted into citruline in collagen type 2 and vermentin

Host no longer recognises these as self

Antigens get picked up by antigen presenting cells

Carried to lymph nodes which activate CD4 cells

CD4 cells activate B cells

Generate antibodies against these cells

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45
Q

What happens when the antibodies travel in the blood to the joint?

A

CD4 cells secrete cytokines

Recruit macrophages into joint space

Macrophages also produce cytokines

Stimulate synovial cells to proliferate

This causes a pannus

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46
Q

What is a pannus made up of?

A

Fribroblasts

Myofibroblasts

Inflammatory cells

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47
Q

What happens once the pannus is formed in rheumatoid arthritis?

A

Causes damage to

Cartilage

Other soft tissue

Errode bone

Activates synovial cells also release proteases which break down cartilage

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48
Q

What do T cells express on there surface and what does this do?

A

RANK-L

Activates osteoclasts

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49
Q

What antibodies appear in the synovial fluid?

A

Rheumatoid factor

Anti-CCP

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50
Q

What is rheumatoid factor?

A

Antibody against the Fc portion of IgG

Fc: region within heavy chain, role in modulating immune response

Occurs in many other diseases

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51
Q

What is Cyclic citrullinated Peptide?

A

Marker of disease; not pathogenic itself
Reacts with Filaggrin protein in keratin

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52
Q

What do the immune complexes activate?

A

Activate the complement system

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53
Q

What are the symptoms of rheumatoid arthritis?

A

Joint pain often worse in morning

Morning stiffness-several hours

Loss of function

General-fatigue, malaise

Extra-articular involvement.

(may improve with activity)

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54
Q

What is some signs of rheumatoid arthritis?

A

Symmetrical small joints
MCP
PIP

More than 5 usually

Ulnar deviation of the fingers.

Boutonnière and swan-neck deformities of fingers or Z-deformity of thumbs occur.

Baker (poploteal cyst)

Larger joints can be involved.
Atlanto-axial joint subluxation may threaten the spinal cord (rare).

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55
Q

What other organs can be involved?

A

Lungs

Heart

Gastrointestinal tract

Skin

Eyes

Kidneys.

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56
Q

What soft tissue involvement can there be in rheumatoid arthritis?

A

Nodules

Bursitis

Tenosynovitis

Muscle wasting

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57
Q

What are some eye involvements of rheumatoid arthritis?

A

Sicca (dry eyes)

Secondary Sjorgren’s syndrome

Episcleritis

Scleritis (corneal ulceration).

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58
Q

What are some haematological involvements of rheumatoid arthritis?

A

Lymph nodes can be palpable

Spleen may be enlarged

Anaemia

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59
Q

What are some lung involvements of rheumatoid arthritis?

A

Fibroblasts causing scar tissue

Decrease gas exchange

Pleural cavities fill with fluid

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60
Q

What is vasculitis?

A

Most common manifestation is small digital infarcts along nailbeds

Abrupt onset of ischaemic mononeuropathy (MMx) or progressive scleritis typical of rheumatoid vasculitis

Seropositive usually, persistently active disease

Can occur when joints inactive

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61
Q

What are some investigations for rheumatoid arthritis?

A

Blood tests
Rheumatoid Factor 80%
Anti-Cyclic Citrullinated Peptide (Anti-CCP) antibody c.80%
Anaemia
High ESR/CRP
Anti-nuclear antibody (ANA) < 50%
Negative for all c.20%

X-Ray
Soft tissue swelling, juxta-articular osteopenia and loss joint space.

_Ultrasound
MRI_
Identify synovitis more accurately, greater sensitivity.

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62
Q

What are the managements for rheumatoid arthritis?

A

DMARDS

  • *Rituximab** - B cells
  • *Abatacept** - T cells

Steroids
Rapidly reduce symptoms and inflammation. Methylprednisolone

NSAIDS
Symptom relief, no efect on disease progression.
Paracetamol and weak opiates are rarely effective.
Physio- and occupational therapy, eg for aids and splints.

Surgery
May relieve pain, improve function and prevent deformity.
There is increased risk of cardiovascular and cerebrovascular disease, as atherosclerosis is accelerated in RA.

Manage risk factors
Smoking also increases symptoms of RA.

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63
Q

WHAT IS VASCULITIS?

https://www.youtube.com/watch?v=ise3cEqmEqU

A

Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow

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64
Q

What is the cause of vasculitis?

A

Autoimmune disease, confusing part of the blood vessel as foregin

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65
Q

What are the different damage pathways of vasculitis?

A

Molecular mimicry and directly attack it
Medium and large vessel vasculitis

Indirect damage from damage of an overlying pathogen
Small vessel vasculitis

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66
Q

What happen in vasculitis after endothelial damage?

A

Collagen exposed

Platelets adhere to the vessel wall

Blood vessel wall becomes weakend

Anneurysms become more likely

As the vessel heals and fibrin is deposited the wall becomes stiffer

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67
Q

What happens in the cells for vasculitis?

A

Vessel wall infiltration

Neutrophils, mononuclear cells +/or giant cells

Fibrinoid necrosis

Leukocytoclasis (dissolution of leucocytes)

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68
Q

How do you classify vasculitis?

A

Size of vessel
Small – medium - large vessel disease

Target organ(s)

Anti-neutrophil cytoplasmic antibodies (ANCA)
Present or not

Primary vs secondary

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69
Q

What are the different classifications of vasculitis?

A

Large

Medium

Small

ANCA +ve vasculitis

ANCA –ve vasculitis

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70
Q

What are the different large vasculitis’?

A

Giant cell arteritis, Takayasu’s arteritis

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71
Q

What are the different medium vasculitis’?

A

Polyarteritis nodosa, Kawasaki disease

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72
Q

What are the different small vasculitis’?

A

Microscopic polyangitis, Wegener’s granulomatosis

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73
Q

How does vasculitis present?

A

No single typical presentation

Systemically unwell
Fever
Arthralgia/arthritis
Rash
Weight loss
Headache
Footdrop
Major event eg stroke, bowel infarction.

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74
Q

What must be excluded to ensure correct diagnosis of vasculitius?

A

–Sepsis-SBE, hepatitis

–Malignancy

–Other-eg cholesterol emboli

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75
Q

What are some common tests for vasculitis?

A

ESR/CRP increase. ANCA may be +ve.

Increase in Creatinine if renal failure.

Urine: proteinuria, haematuria, casts on microscopy.

Angiography ± biopsy may be diagnostic.

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76
Q

What is the usual treatment for vasculitis?

A

Cyclophosphamide.

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77
Q

What is ANCA-associated vasculitis?

A

Antineutrophil cytoplasmic antibodies

Small/medium vessel vasculitis

Specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes.

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78
Q

What are the investigations for ANCA-associated vasculitis? What are the two major patterns?

A

Detected with indirect immunofluorescence microscopy

Two major patterns

Cytoplasmic ANCA (c-ANCA) Major antigen Proteinase 3

Peri-nuclear ANCA (p-ANCA) Major antigen Myeloperoxidase (MPO)

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79
Q

WHAT IS GIANT CELL (TEMPORAL) ARTERITIS?

https://www.youtube.com/watch?v=ise3cEqmEqU

A

Granulomatous arteritis of aorta + larger vessels-extracranial branches of carotid arteries

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80
Q

What is the epidemology of Giant cell arteritis?

A

Primarily>50yrs old

Incidence increases with age

Twice as common in women

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81
Q

How does giant cell (temporal) arteritis present?

A

Headache

Scalp tenderness

Jaw claudication

Acute blindness

Non specific malaise

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82
Q

What does the American College of Rheumatology Diagnostic criteria require?

A

3 or more of:
Age>50
New headache
Temporal artery tenderness or decreased pulsation
ESR > 50 mm/h
Abnormal artery biopsies showing necrotizing arteritis with mononuclear infiltrate or granulomatous inflammation

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83
Q

What do giant cell arteritis temporal arteries look like?

A

Palpable
Tender
Reduced pulsation.

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84
Q

What is AION(Arteritic) anterior ischemic optic neuropathy ?

A

Sudden, painless, monocular and severe visual loss.

May be preceded by transient visual loss

The optic disc becomes pale and swollen, often with flame-shaped haemorrhages at the margin.

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85
Q

What are the tests for giant cell arteritis?

A

ESR & CRP increase

Platelets increase

Alk phos increase

Hb lower

Get a temporal artery biopsy within 7 days of starting steroids.

Skip lesions occur, so don’t be put off by a negative biopsy (up to 10%).

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86
Q

What is the treatment for GCA?

A

Corticosteroids
Prednisolone

Steroid sparing agents
Eg Azathioprine/Methotrexate/biologics

Prophylaxis of osteoporosis
Lifestyle advice
Calcium/Vitamin D + Bisphosphonate
DEXA scan

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87
Q

WHAT IS POLYARTERITIS NODOSA (PAN)?

https://www.youtube.com/watch?v=ise3cEqmEqU

A

PAN is a necrotizing vasculitis that causes aneurysms and thrombosis in medium-sized arteries

Leading to infarction in affected organs, with severe systemic symptoms.

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88
Q

What is the cause of polyarteritis nodosa?

A

Some associated with Hep B

Others unknown

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89
Q

What is the epidemology of polyarteritis nodosa?

A

Women more than men.

Rare in UK

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90
Q

What is the pathology of polyarteritis nodosa?

A

Immune cells confuse the vessel wall with hep B virus

Causes transmural inflammation
All layers die

Fibosis as vascular wall heals

This process is fibrinoid necrosis

Anneurysms occur through weakness of artery

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91
Q

What are the symptoms of polyarteritis nodosa?

A

Typically systemic features

Skin
Rash and ‘punched out’ ulcers

Renal
Hypertension

Cardiac
Angina or MI

GI

GU

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92
Q

What are the tests for polyarteritis nodosa?

A

Often WCC increase
Mild eosinophilia (in 30%)
Anaemia
ESR increase
CRP increase
ANCA –ve.

Angiography
String of beads

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93
Q

What is the treatment of polyarteritis nodosa?

A

Control BP

Corticosteroids
Prednisolone

Cyclophosphamide

Hepatitis B should be treated with an antiviral after initial treatment with steroids.

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94
Q

WHAT IS POLYMYALGIA RHEUMATICA (PMR)?

A

Polymyalgia rheumatica is a disease of the muscles and joints characterized by muscle pain and stiffness, affecting both sides of the body, and involving the shoulders, arms, neck, and buttock areas.

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95
Q

What disease is common with polymyalgia rheumaticia?

A

PMR and GCA share the same demographic characteristics and, although separate conditions, the two frequently occur together

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96
Q

What is the epidemology of polymyalgia rheumatica (PMR)?

A

Over 50 years olds

Women more than men

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97
Q

What is the pathogenesis of Polymyalgia rheumatica (PMR)?

A

Unknown

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98
Q

What are the symptoms of polymyalgia rheumatica?

A

Tenderness and morning stiffness

Bilateral aching

Tenosynovitis

Carpal tunnel syndrome

B symptoms

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99
Q

What are the investigations for polymyalgia rheumatica?

A

CRP increased,

ESR increased

ALP is increased

Note creatinine kinase levels are normal (helping to distinguish from myositis/myopathies)

MRI

Ultrasound

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100
Q

What are the differential diagnosis for polymyalgia rheumatica?

A

Recent onset RA

Polymyositis

Primary muscle disease

Malignancy or infection

Osteoarthritis

Spinal stenosis

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101
Q

What are the treatment options for polymyalgia rheumatica?

A

Corticosteroids
Prednisolone

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102
Q

What is osteoarthritis?

https://www.youtube.com/watch?v=sUOlmI-naFs&t=63s

A

A non inflammatory disorder

Deterioration of articular cartilage

Formation of new bone of the joint surfaces and margins

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103
Q

What is the cause of osteoarthritis?

A

Unknown but risk factors have a big impact

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104
Q

What is the prevalence of osteoarthritis?

A

Commonest joint disorder

M=F

<45yrs prevalence greater in males

>55yrs prevalence greater in females

Common in Caucasians

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105
Q

What are the different classifications of osteoarthritis?

A

Primary or idiopathic
No identifiable predisposing cause

Secondary
When an underlying cause is implicated

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106
Q

What are the predisposing factors for oesteoarthritis?

A

Genetic.

Trauma.

Deformities.

Occupation.

Obesity

Bone density.

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107
Q

What is the basic pathogenesis for osteoarthritis?

A

Articular cartilage failure

Friction

Inflammation

Pain

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108
Q

What do chondrocytes produce?

A

Type 2 collagen

Proteoglycans
Hyularonic acid
Keratin Sulphate

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109
Q

What is the pathogenesis for osteoarthritis?

A

Chondrophytes release degredation enzymes and synthetic enzymes

Something tips balance in favour of degredation enzymes

Articular cartilage failure trigger chondrcytes

Less proteoglycans made and more type 1 collagens made

Chondrocytes then die

Synovium cells take in dead cells, macrophages release inflammatory mediators

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110
Q

What cells are involved with the pathogenesis of osteoarthritis?

A

Proteases
Metalloproteases

Catabolic cytokines
IL-1, TNF- alpha

Anabolic cytokines
Insulin like growth factor, TGF – beta

Inflammation

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111
Q

What in a history would indicate osteoarthritis?

A

Pain

Insidious and increases over months or years

Aggravated by activity

Relieved by rest

May be referred pain

Swelling

Stiffness

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112
Q

What does osteoarthritis look like on examiantion?

A

Swelling

Muscle wasting

Deformity

Decreased ROM

Crepitus (cracking or clicking of joint movement)

Osteophytes palpable

Joint instability (later on)

Heberdens

Bouchards

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113
Q

What are Heberdens and Bouchards?

A

Heberden’s nodes are hard or bony swellings that can develop in the distal interphalangeal joints (DIP)

Bouchard’s nodes are hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints

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114
Q

What are the differential diagnosis to osteoarthritis?

A

Rheumatoid Arthritis

Gout

Osteonecrosis

Neuropathic Joint

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115
Q

What investigations can you do for osteoarthritis?

A

Imaging
X-RAY DIAGNOSTIC

Laboratory Tests
Blood & Synovial Fluid

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116
Q

What are you looking for in a X-ray of osteoarthritis?

A

Loss of joint space

Osteophytes (bony projection associated with the degeneration of cartilage at joints.)

Subarticular sclerosis (denser area of bone just under the cartilage in your joint, appearing as abnormally white bone along the joint line)

Subchondral cysts (The cartilage tries to repair itself, the bone remodels, the underlying (subchondral) bone hardens, and bone cysts form.)

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117
Q

What labratory tests could you do for osteoarthritis?

A

Blood
ESR, FBC, Rh Factor, Calcium, ALP, Electrophoresis
All Normal

Synovial Fluid Analysis
Non specific in OA

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118
Q

What are the different types of management of osteoarthritis?

A

Conservative / Non surgical

Injection

Surgical

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119
Q

What is the conservative / non surgical management of osteoarthritis?

A

Exercise

Topical Products
Capsaicin decreases pain by depleting stores of substance P

Tablets
Analgesics and Glucosamine
Paracetamol and NSAIDs
Cox-2 inhibitors

Lifestyle Modification

Splints and Orthotics

Physiotherapy

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120
Q

What do Glucosamine & Chondroitin sulfate do in osteoarthritis?

A

Important constituents of proteoglycans (matrix) which resists compression forces in the joint.

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121
Q

What injections can be given for osteoarthritis?

A

Steroid - short term
Methylprenisolone

Viscosupplementation agent
Hyaluronic Acid

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122
Q

What surgical managements can you do of osteoarthritis?

A

Debridement of Joint

Realignment Osteotomies

Joint Excision

Joint Fusion (arthrodesis)

Joint Replacement (arthroplasty)

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123
Q

WHAT IS SYSTEMIC LUPUS ERYTHEMATOSUS?

https://www.youtube.com/watch?v=0junqD4BLH4

A

SLE is a multisystemic autoimmune disease in which autoantibodies are made against a variety of autoantigens (eg ANA).

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124
Q

What is the epidemology of systemic lupus erythematosus?

A

Women of child bearing age

Genetic Association:

HLA: DR2, DR3
C4 A Null Allele

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125
Q

What happen in systemic lupus erythematosus?

A

UV light or other trigger causes death of cell

Nucleic contents spill out

Antibodies made against these

Complex sticks to vessel wall and cuases damage

Type 3 hypersensitivity

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126
Q

What are the clinical features of SLE?

A

Malaise, fatigue, myalgia and fever.

Arthritis

Skin rashes
Butterfly, Discoid, photosensitive rash.

Mucosal ulceration

Pleurisy

Pericarditis

Raynaud’s phenomenon

Glomerulonephritis

127
Q

What are some classic distuingishers of SLE?

A

Butterfly rash

Dicoid rash

Photosensitive rash

Alopecia

Mouth ulcers

Lupus nephritis

128
Q

What does SLE arthritis look like?

A

Symmetrical

Less proliferative than RA

Can be deforming

Non-erosive

129
Q

What immunology/testing can be done for SLE?

A

Anti-nuclear antibody: Not specific for lupus (screening test)

Double stranded DNA antibody: Specific

Other antibodies:
Rheumatoid factor
Cardiolipin antibodies, Anti Ro, La, Sm, RNP

ESR increase but normal CRP

130
Q

What does the SLE : ACR 1982 Classification Criteria
require for diagnosis of SLE?

A

Four or more of the following.

Malar rash

Discoid rash

Photosensitivity

Oral ulcers

Arthritis

Serositis

Renal disorder

Neurological disorder

Haematological disorder

Immunological disorder

Anti-nuclear antibody

131
Q

What is the management for SLE?

A

Topical steroids and sunblock
Rashes

NSAIDS and hydroxychloroquine
Joint and skin symptoms.

Steroids
Suppress immune system

Immunosupressants
Azathiprine, methotrexate and mycophenolate are used as steroid-sparing agents.

Rituximab.
Belimumab

132
Q

What is antiphospholipid syndrome?

A

Antibodies against protein in the phospholipid membrane

Associated with Lupus

133
Q

What does antiphoshpholipid syndrome cause?

A

Antiphospholipid antibodies (anticardiolipin & lupus anticoagulant) cause CLOTS:

Coagulation defect

Livedo reticularis (mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin)

Obstetric (recurrent miscarriage)

Thrombocytopenia (reduced platelets)

134
Q

How do you diagnose antiphospholipid syndrome?

A

Lupus anticoagulant

And/or

Cardiolipin Antibodies

Positive on 2 occasions 12 weeks apart

135
Q

How can you treat antiphospholipid syondrome?

A

Aspirin

Warfarin

136
Q

WHAT IS RAYNAUD’S PHENOMENON?

https://www.youtube.com/watch?v=n809IRTYYeU

A

Discoloration of the fingers and/or the toes

After exposure to changes in temperature or emotional events.

137
Q

What are the colour changes of Raynaud’s?

A

Fingers or toes ache and change colour:

pale (ischaemia) to

blue (deoxygenation) to

red (reactive hyperaemia)

138
Q

How is Raynaud’s phenomenon caused?

A

Primary
Raynaud’s disease

Secondary
Connective tissue diseases
Drugs
Vascular damage
Raynaud’s syndrome

139
Q

How is Raynaud’s phenomenon caused connective tissue diseases?

A

Secondary
Connective tissue diseases
Systemic sclerosis
Mixed connective tissue disease
SLE

140
Q

How is Raynaud’s phenomenon caused drugs?

A

Drugs
Beta-blockers

141
Q

How is Raynaud’s phenomenon caused vascular damage?

A

Vascular damage
Atherosclerosis
Frost bite
Vibrating tools

142
Q

What happens in raynaud’s when there is a change in temperature?

A

Nerves oversitimulated

Leading to vascontrction of blood vessels

143
Q

What are the symptoms of raynaud’s?

A

Colour changes

Numbness, tingling and pain

Could cause tissue death

144
Q

What is the diagnosis of raynaud’s phenomenom?

A

Description of episodes

Explore underlying condition

Nailfold capillary microscopy

145
Q

What is the treatment for Raynaud’s phenomenon?

A

Avoid triggers

Stop smoking

Vasodilators
Nifedipine or sildenafil

Surgery

146
Q

WHAT IS SYSTEMIC SCLEROSIS?

https://www.youtube.com/watch?v=ErchMUH0oXY

A

Autoimmune disease of the connective tissue

Thickening of the skin caused by accumulation of collagen

And by injuries to small arteries

147
Q

What are the different types of systemic sclerosis?

A

Limited and diffuse

148
Q

What does limited systemic sclerosis show?

A

Calcinosis (calcium deposits form in the skin)

Raynaud’s phenomenon

Oesophageal reflux, strictures

Sclerodactyly (localized thickening and tightness of the skin of the fingers or toes)

Telangectasia (widened venules (tiny blood vessels) cause threadlike red lines or patterns on the skin.)

Pulmonary arterial hypertension

149
Q

What is the antibody for limited systemic sclerosis?

A

Anticentromere

150
Q

What does diffuse (skin) systemic sclerosis show?

A

Additional features:

Proximal scleroderma

Pulmonary fibrosis

Bowel involvement

Myositis

Renal crisis: hypertension

151
Q

What is the antibody for diffuse systemic sclerosis?

A

Antibodies: Scl-70, nucleolar, RNA polymerase

152
Q

What is the pathogenesis of systemic sclerosis?

A

Vasculopathy

Excessive collagen deposition

Inflammation

Auto-antibody production

153
Q

What is the management of systemic sclerosis?

A

NO CURE

Treat symptoms

Cyclophosphamide
Supression of immune system

154
Q

WHAT IS SJÖGREN’S SYDROME?

https://www.youtube.com/watch?v=d3qPMecBrY0

A

Exocrine glands destoryed

155
Q

Which glands are mainly affected in sjorens?

A

Lacrimal and salivary glands

156
Q

What are some systemic involvements of sjorens?

A

Polyarthritis/arthralgia

Raynaud’s

157
Q

What are the features of Sjögren’s Syndrome?

A

Sicca complex:
Dry eyes
Dry mouth
Enlarged salivary glands

Systemic features
InflammatoryArthritis
Rash (sub-acute lupus)
Neuropathies
Vasculitis
Neonatal lupus

158
Q

What would the tests show to diagnose Sjögren’s Syndrome?

A

Schirmer’s test
Conjunctival dryness

Auto-antibodies
ANA (in most)
Rheumatoid factor
Ro
La

Raised immunoglobulins,
ESR up

Biopsy
Lymphocyte infiltration in glands

159
Q

What is the Management of Primary Sjogren’s?

A

Tear and saliva replacement
Hypromellose

Immuno-suppression for systemic complications

Treat arthralgia

160
Q

WHAT IS DERMATOMYOSITIS/POLYMYOSITIS?

A

Progressive symmetrical proximal muscle weakness

Autoimmune-mediated striated muscle inflammation (myositis)

Myalgia ± arthralgia.

161
Q

What is affected most in Dermatomyositis/Polymyositis?

A

Muscle and skin mainly affected: rash and muscle weakness

Lungs can be affected (Interstitial lung disease)

162
Q

What are the autoantibody associations with polymyosits/dermatomyositis?

A

Jo-1
PM-Scl
Mi-2

163
Q

What are the symptoms for dermatomyositis?

A

Macular rash

Rash on eyelids

Dysphagia

Dysphonia

164
Q

What investigations can you do for Dermatomyositis/Polymyositis?

A

Muscle enzymes

EMG

Muscle/skin biopsy

Screen for malignancy

Chest X ray, PFTs, High resolution CT lungs

165
Q

What is the management for Dermatomyositis/Polymyositis?

A

Steroids

Immunosuppressive drugs

Hydroxychloroquine (skin rash)

166
Q

WHAT IS LOWER BACK PAIN?

A

Pain of the lower back

167
Q

When does mechanical lower back pain present?

A

Ages of 20-55.

168
Q

Where is lower back pain?

A

Located in lumbrosacral region, buttocks and tighs.

169
Q

What does mechanical lower back pain vary with?

A

Activity and time.

170
Q

What are the red flags for possible serious spinal pathology?

A

Age on onset less than 20 or greater than 55.

Violent trauma e.g. fall from a heigh

Constant progressive, non-mechanical back pain

Thoracic pain

PMH carcinoma, systemic steroids, drug abuse, HIV

Systemically unwell, weight loss

Persisting servere resistriction of lumbar flexion

Structural deformity

171
Q

What examination would you do for a patient with lower back pain?

A

With the patient standing, gauge the extent and smoothness of lumbar forward/ lateral flexion and extension.

Clinical tests for sacroiliitis: direct pressure, lateral compression, sacroiliac stretch test (pain on adduction of the hip, with the hip and knee flexed).

Signs of generalized disease—eg malignancy. Examine other systems (eg abdo- men) as pain may be referred.

172
Q

What are the causes of lower back pain?

A

15–30yrs:
Prolapsed disc, trauma, fractures, ankylosing spondylitis, spondylolisthesis (a forward shift of one vertebra over another, which is congenital or due to trauma), pregnancy.

30–50yrs:
Degenerative spinal disease, prolapsed disc, malignancy (primary or secondary from lung, breast, prostate, thyroid or kidney ca).

>50yrs:
Degenerative, osteoporotic vertebral collapse, Paget’s, malignancy, myeloma, spinal stenosis.

173
Q

How can a person damage their lower back?

A

SIngle excessive force

Static loading

Repetative wear and tear

A bit of reality

174
Q

What investigations can you do for back pain?

A

Arrange relevant tests if you suspect a specific cause, or if red flag symptoms:

FBC,
ESR and CRP (myeloma, infection, tumour), U&E, ALP (Paget’s), serum/urine electrophoresis (myeloma), PSA.

X-rays
Exclude bony abnormality but are generally not indicated.

MRI
Is the image of choice and can detect disc prolapse, cord compression (fig 1), cancer, infection or inflammation (eg sacroiliitis).

175
Q

What is the management for back pain?

A

For non-specific back pain, focus on education and self-management.

Continue with normal activites and be active.

Manage pain
Regular paracetamol ± NSAIDS ± codeine

Physiotherapy, acupuncture or an exercise programme if not improving.

Psychosocial issues

Surgery

176
Q

WHAT IS OSTEOMYELITIS?

https://www.youtube.com/watch?v=kta5vCz_8Lw

A

Infection localized to bone.

177
Q

What is the epidemology of osteomyelitis?

A

Children more

Males twice more than women

178
Q

What are the different types of osteomyelitis? Which bacteria are involved?

A

Pyogenic (involving or relating to the production of pus)
S. aureus

Non-pyogenic
M. tb

179
Q

How can the infection of bone take place?

A

Direct

Contiguous

Haematogenous

180
Q

What are the different microbials for each type of spread?

A

Direct
Polymicrobial or monomicrobial

Contiguous
Polymicrobial or monomicrobial

Haematogenous
Monomicrobial

181
Q

What are the host factors for osteomyelitis?

A

Behavioural factors
I.e. risk of trauma

Vascular supply
Arterial disease
Diabetes mellitus
Sickle cell disease

Pre-existing bone / joint problem
Inflammatory arthritis
Prosthetic material

Immune deficiency
Immunosuppressive drugs
Primary

182
Q

In children where is the most common site for osteomyelitis infection?

A

Long bones

In metaphysis
Blood flow is slower
Endothelial basement membranes are absent
The capillaries lack or have inactive phagocytic lining cells
High blood flow in developing bones in Children

183
Q

In adults where is the most common site for osteomyelitis infection?

A

Vertebrae

With age the vertebrae become more vascular, making bacterial seeding of the vertebral endplate more likely

184
Q

What are the acute changes occur to the bone as a result of osteomyelitis?

A

Acute changes
–Inflammatory cells
–Oedema
–Vascular congestion
–Small vessel thrombosis

185
Q

What are the chronic changes occur to the bone as a result of osteomyelitis?

A

Chronic changes
–Necrotic bone ‘sequestra’
–new bone formation ‘involucrum’
–neutrophil exudates
–lymphocytes & histiocytes

186
Q

How are sequestra and involucrum produced?

A

Interruption of periosteal blood supply causing necrosis.

Leaves pieces of separated dead bone ‘sequestra’

New bone forms here ‘involucrum’.

187
Q

What are the signs and symptoms of osteomyelitis?

A

Systemic:
Fever, rigors, sweats, malaise

Local:
Acute OM
Tenderness, warmth, erythema, and swelling

Chronic OM
Tenderness, warmth, erythema, and swelling
Draining sinus tract
Deep / large ulcers
Non-healing fractures

188
Q

What tests can you do for osteomyelitis?

A

Physical examination

Laboratory tests

Imaging

189
Q

What are the labratory tests you can do for osteomyelitis?

A

FBC/WCC
Rasied or normal

CRP/ESR
Raised

Blood culture

Bone aspiration

190
Q

What are the imaging tests you can do for osteomyelitis?

A

X-Rays
Normal
Periosteal evelvation
Osteolysis

CT Scan
Cortical destruction
Lytic lesions

Bone Scan
Visulising bone remodelling

191
Q

What are the differential diagnosis for osteomyelitis?

A

Soft tissue infection

Charcot joint

Avascular necrosis of bone

Gout

Fracture

Bursitis

Malignancy

192
Q

What is the treatment for osteomyelitis?

A

Antibiotics

Surgical

Splintage

Supportive

193
Q

WHAT IS SEPTIC ARTHRITIS?

https://www.youtube.com/watch?v=Tz07Uqx7_VY

A

Inflammation of a joint that’s caused by infection.

194
Q

What is septic arthritis caused by? What does it affect?

A

Bacteria. It can also be caused by a virus or fungus.

Typically, septic arthritis affects one large joint in the body, such as the knee or hip.

195
Q

What are the risk factors for septic arthritis?

A

Pre-existing joint disease

Vascular e.g. diabetes mellitus,

Immunosuppression

Chronic renal failure

Recent joint surgery

Prosthetic joints, IV drug abuse, age >80yrs

196
Q

What are the symptoms for septic arthritis?

A

Fever

Monoarthritis

Irritability

197
Q

What tests can you do for septic arthritis?

A

FBC/ESR/CRP

Joint aspiration for synovial fluid microscopy and culture

Blood cultures

Plain radiographs and CRP may be normal

198
Q

What are the differential diagnosis for septic arthritis?

A

Crystal arthropathies.

199
Q

What are the treatment options for septic arthritis?

A

Antibiotics IV

Joint drainage

Flucloxacillin

Vancomycin IV if MRSA

Cefotaxime IV if gonococcal or Gram –ve or- ganisms suspected.

200
Q

WHAT IS BONE CANCER?

A

Cancer of the bone

201
Q

What can you find out from the history for bone cancer?

A

Presenting Complaint
Mass
Pain
Loss of Function

History of Presenting Complaint

Duration of symptoms, including full Pain / Mass history

How issue came to patient’s attention

Past Medical History and Medication History

Family History

Social History

202
Q

What are the red flags signs for a MSK malignancy?

A

Rest pain

Night pain

Lump present – tender, enlarging, deep to fascia, above 5cm in diameter

Loss of function

Neurological symptoms

Unwell / Weight loss

203
Q

What inital investigations can you do for MSK malignancies?

A

Blood tests – FBC, U+E, Ca2+, Alk Phos

Plain Xrays

Ultrasound

CT Scan
Better for assessing bone quality, as well as solid tumours
Staging CT of Chest / Abdo / Pelvis essential if suspect metastases

MRI Scan
Better for assessing reactive changes of soft tissue / bone marrow
Recent studies assessed full-body MRI to look for metastases

Bone Scan
Technetium; Tc99. Good for assessing for skeletal metastases

204
Q

What are plain X-rays used for in bone cancer?

A

Look to see what the lesion is doing to the bone and vise-versa
Definition / Bone density / Zone of Transition / Periosteal reaction
Osteoblastoma vs Osteosarcoma

Special Signs:
Codman’s Triangle (Osteosarcoma, Ewing’s, GCT, Osteomyelitis, Metastasis)
Sunburst appearance (Osteosarcoma, Ewing’s)
Onion-skin appearance (Ewing’s)

205
Q

What is the ultrasound used for in bone cancer?

A

Quick, cheap method of assessing soft tissue masses

Real time assessment, no radiation. However operator dependant.

Excellent to differentiate Normal vs Abnormal, Solid vs Cystic

206
Q

What are CTs used for in bone cancer?

A

Used to perform 3D reconstruction of bony lesions which can help plan resection. Also used for Staging (CT Chest, Abdo and Pelvis)

207
Q

What does an MRI show you in bone cancer?

A

T1 imaging: anatomy

T2 imaging: pathology

Displays:
Soft tissue involvement of bony mass
Periosteal and Endosteal reaction
Skip Lesions
Soft tissue masses – heterogenous masses are more suspicious of malignancy

208
Q

What is shown on a bone scan for bone cancer?

A

3 Phase Scan
Arterial (1 minute)
Blood Delivery

Blood Pooling (5 minutes)
Capillary dilation

Delayed (2-4 hours)
Uptake within bone

Gamma Camera

Technetium (Tc99-MDP)

209
Q

How should staging of a bone cancer be done?

A

Stage Locally

Xray

Ensure whole bone is imaged

Limb alignment views for lower limb

MRI

Useful to assess for “skip lesions”

Stage Distally

CT Chest / Abdo / Pelvis

Bone Scan

Whole-body MRI scan

210
Q

What is the staging of malignant tumours?

A
  • Enneking system
  • G0 = Histologically Benign
  • Well Differentiated i.e. resemble cell of origin
  • Low mitotic count
  • G1 = Low Grade Malignant
  • Moderate differentiation; Few mitoses
  • Local spread only. Low risk of metastasis
  • G2 = High Grade Malignant
  • Poorly differentiated; Frequent mitoses

High risk of metastasis

211
Q

What is the staging of benign tumours?

A
  • Enneking Classification
  • Grade 1 – Latent
  • Well defined margin. Grows slowly then stops
  • May heal spontaneously and very low risk of recurrence
  • Grade 2 – Active
  • Progressive growth limited by natural barriers
  • Well defined margin but may expand and thin cortical bone (e.g. ABC)
  • Negligible recurrence after marginal resection
  • Grade 3 – Aggressive
  • Growth not limited by natural barriers (e.g. GCT)
  • Metastasis present in 5% patients
  • High recurrence following marginal resection (extended resection therefore needed)
212
Q

How do you name the different types of tumour?

A
  • Prefix will be tissue of origin, for example:
  • Osteo… = Bone
  • Chondro… = Cartilage
  • Rhabdomyo… = Skeletal Muscle
  • Lipo… = Fat
  • Suffix tells you whether it is benign or malignant
  • …oma = Benign tumour
  • …sarcoma = Malignant connective tissue tumour
  • …carcinoma = Malignant epithelial/endothelial tumour

…blastoma = (Malignant) Tumour of embryonic cells

213
Q

Where do tumours normally present?

A
214
Q

What are osteosarcomas?

A

•Spindle cell neoplasms that produce osteoid

215
Q

What are the different primary osteosarcomas?

A
  • Intramedullary osteosarcoma (high grade)
  • Parosteal osteosarcoma (low grade)
  • Periosteal sarcoma (high grade)
  • Telangiectatic osteosarcoma
216
Q

What are the different secondary osteosarcomas?

A

Paget’s, Post-Radiation, Fibrous Dysplasia

Associated with p53 mutation

Also associated with Chondrosarcoma and STS

217
Q

What is a high-grade intramedullary osteosarcoma? Where is it most common?

A
  • “Classic” osteosarcoma
  • Most common type
  • Location: knee, proximal humerus, proximal femur
  • Age: children, young adults
  • 90% are high grade and penetrate the cortex early forming a soft tissue mass (IIB lesion)
  • 10-20% have pulmonary mets
  • X-rays: bone formation with bone destruction
  • MRI useful for staging
218
Q

What is secondary osteosarcoma secondary to?

A
  • Paget’s Disease
  • Older population only. Pagets present in 0.7-0.9% population, hence this is rare
  • Median age 64yrs for onset. High risk for pulmonary metastasis
  • Irradiation (60-70% survival for extremity lesions, 27% axial lesions)
  • Children treated with high dose radiotherapy at greatest risk
  • Tend to be high-grade tumours. High risk of pulmonary metastasis
  • Treat as per primary bone tumour guidelines
  • Fibrous Dysplasia
  • Associated with McCune-Albright syndrome and Polyostic Fibrous Dysplasia
  • McCune-Albright = fibrous dysplasia + café-au-lai spots + endocrine abnormalities
219
Q

What is the treatment for an osteosarcoma?

A
  • Initial treatment with multi-agent chemotherapy pre-op 8-12 weeks
  • Aims to kill tumour cells, reduce further spread, treat micro-metastases
  • Repeat procedures to Stage the Tumour
  • Limb Salvage surgery (where possible) + adjuvant chemotherapy
220
Q

What are the treatment options for bone tumours?

A
  • Histological tests help to show sensitivity of tumour to Chemotherapy agents and Radiotherapy
  • Chemo/Radio-therapy can be given:
  • Neo-adjuvant (i.e. before surgery)
  • Adjuvant (at the time/post surgery)
  • Radiotherapy: Ewing’s, Myeloma, Lymphoma, STS, Metastasis
  • Surgery can either be Limb-Sparing or Limb-Sacrificing
  • Local recurrence vastly increases risk of future Amputation
221
Q

What are the different surgical margins that can be achieved during oncologic surgery?

A
  • Intralesional: The plane of surgery goes through the tumour.
  • Marginal: The plane of surgery goes through the reactive zone of the lesion (the reactive zone contains oedema, tumour cells, fibrous tissue, and inflammatory cells).
  • Wide: The plane of dissection goes through normal tissue.
  • Radical: The entire anatomic compartment of the lesion is removed.
222
Q

WHAT IS A CRYSTAL IN CRYSTAL ARTHRITIS?

A

Homogenous solid
ions bonded closely in ordered, repeating, symmetric arrangement

Stable, hard, high density

223
Q

Where are crystals and what do they do?

A

All animals
Strengthen endo & exo-skeleton
Remove excess ions (surface binding)

224
Q

Why are crystals common in the gall bladder and kidney?

A

They are the two routes of excretion of uric aicd.

225
Q

What is the pathway of excretion of uric acid?

A

Purines -> HypoXanthine-> Xathine -> Uric acid -> monosodium urate

226
Q

WHAT IS GOUT?

https://www.youtube.com/watch?v=bznoU5bke4U

A

Monosodium urate crystals deposited in joints

227
Q

What is the epidemology of crystal arthropothies?

A

Commonest arthritis in men >40yrs

Uncommon men<30yrs

Rises in post-menopausal women

Men more than women

Worldwide

228
Q

What is the cause of gout?

A

Hyperuricemia

Too much uric acid in the blood

229
Q

What is the pathogenesis of gout?

A

Too much uric acid

Formation of sharp crystals

In areas of slow blood flow

Joints and kidneys

Overtime results in destruction of tissue leading to arthritis

Inflammation from WBC releasing proinflammatory mediators

230
Q

Where does uric acid come from?

A

When cells are broken down

Purines in DNA are broken down

Into uric acid and excretes into urine

231
Q

How does hyperuricemia happen?

A

When uric acid exeedes its solubility.

232
Q

What changes happen to uric acid at pH 7.4?

A

Loses a proton and binds sodium to form monosodium urate crystals.

233
Q

What is the key enzyme in formation of uric acid from purines?

A

Xanthinine oxidase.

234
Q

How can monosodium urate crystals be formed?

A

Increased consumption

Increased production

Decreased clearance

Obesity and diabetes
Chemo and radiotherapy
Genetic predisposition
Chronic kidney disease

235
Q

In what food are purines rich?

A

Shellfish

Anchiovies

Red meat

Organ meat

236
Q

What causes an increased production of purines?

A

High-fructose corn syrup drinks

237
Q

Where are the most common areas for gout to form?

A

Occur at the first metatarsophalangeal joint of the big toe

This is called Podagra

Other common joints are the ankle, foot, small joints of the hand, wrist, elbow or knee.

238
Q

What are the symptoms of gout?

A

Podagra

Pain

Hot

Red

239
Q

What is the differential diagnosis of gout?

A

Exclude septic arthritis in any acute monoarthropathy.

Then consider haemarthrosis, CPPD and palindromic RA

240
Q

What are the investigations of gout?

A

Polarized light microscopy of synovial fluid
Shows negatively birefringent urate crystals

Serum urate
Raised

Radiographs
Soft-tissue swelling
‘Punched out’ erosions
There is no sclerotic reaction, and joint spaces are preserved until late

241
Q

How do you treat the acute gout attack?

A

Decrease pain and swelling
NSAIDs
Corticosteroids
Colchicine - reduces WBC migration

Underlying cause
Change in diet

Medications
Xanthinine oxidase inhibitors
Allopurinol

Uricosuric medication
Probenicid

242
Q

What are the permenant depositis of urate crystals called?

A

Tophi

243
Q

What are the triggers of the acute attack of pseudogout and gout?

A

Direct trauma to the joint

Intercurrent illness

Surgery – especially parathyroidectomy

Blood transfusion, IV fluid

T4 replacement

Joint lavage

Most are spontaneous

244
Q

WHAT IS PSEUDOGOUT?

A

Calcium pyrophosphate deposition in joints

245
Q

Where is pseudogout most common?

A

Typical distribution – (MCPs), wrists, knees, (ankles)

246
Q

What is the differential diagnosis of pseudogout?

A

Rheumatoid arthritis.

247
Q

What is the epidemology of pseudogout?

A

After 30

Peak at 60

248
Q

What are the clincial features of pseudogout?

A

Commonly incidental finding on radiology

Severe pain, stiffness, swelling

Marked synovitis, difficult to distinguish from gout

Fever

249
Q

How do you distinguish OA from pyrophosphate arthropathy?

A

Pattern of involvement
Wrists, shoulders, ankles, elbows

Marked inflammatory component

Superimposition of acute attacks

250
Q

What are the tests for pseudogout?

A

Polarized light microscopy
Positively birefringent crystal

It is associated with soft tissue calcium deposition on x-ray.

251
Q

What is the acute management of pseudogout?

A

Acute
NSAIDs, analgesia, colchicine

Injection

Physiotherapy

Immunosuppresants
Methotrexate and hydroxychloroquine for chronic pseudogout

252
Q

WHAT IS OSTEOPOROSIS?

A

Low bone mass and deterioration of bone tissue

Consequent increase in bone fragility and susceptibility to fracture.

253
Q

What are the different types of osteoporosis?

A

Primary (age)

Secondary (related to a condition)

254
Q

What is the epidemiology of osteoporosis?

A

1/2 women and 1/5 men over 50

255
Q

What are some causes and risk factors of osteoporosis?

A

Inflammatory disease

Endocrine disease.

Reduced skeletal loading

Medication.

Alcohol and smoking.

256
Q

What is the pathophysiology of fractures?

A
257
Q

What is bone density equal to?

A

Amount of bone you made and how much bone you lost.

258
Q

When does bone density increase and decrease?

A

Increase in childhood, in puberty increases more then finishes increasing at around 25 then starts to decrease around 30, and woman faster after menopause.

259
Q

What is the normal bone remodelling cycle?

A

Chemical chnages, osteoclasts break the bone down which sends signals to osteoblasts to build new bone.

260
Q

What happens in postmenopausal osteoporosis?

A

Loss of restraining effects of oestrogen on bone turnover

Preventable by oestrogen replacement

Characterized by
High bone turnover (resorption > formation)
Predominantly cancellous bone loss
Microarchitectural disruption

Trabecullar bone more because it has more cells on the surface

261
Q

What are the bones mechoceptors?

A

Osteocytes

262
Q

What is Eular buckling theory?

A

A structure without horizontal conections will be 16 times weaker than that of one with.

263
Q

What is the importance of high turnover to low turnover in bone remodelling?

A

The high turnover will be weaker that the low turnover.

264
Q

How do we diagnose osteoporosis?

A

Bone densitometry
Dual energy X-ray absorptiometry. (DEXA)

Bloods
Calcium and Phosphate

265
Q

How does a DEXA work?

A

Uses to different beams to assess how much calcium is in the bone.

Low radiation dose

Measures important fracture sites

266
Q

What is a T-score?

A

Standard deviation score, it compares your score with gender-matched young adult average (peak bone mass)

267
Q

What do you use the T-score for?

A

Diagnose osteoporsis.

< -1.0
Normal

-1.0 to -2.5
Osteopenia

> -2.5
Osteoporosis

> -2.5 plus fracture
Severe osteoporosis

268
Q

What do inflammatory diseases do to bone? What are some common associated conditions?

A

Inflammatory cytokines increase bone resorption

Rheumatoid arthritis, seronegative arthritis, connective tissue diseases

Inflammatory bowel disease

269
Q

What do endocrine disease do to bone? What are some examples of some diseases?

A

Thyroid and parathyroid hormone increase bone turnover
Hyperthyroidism
Primary hyperparathyroidism

Cortisol increases bone resorption and induces osteoblast apoptosis
Cushing’s syndrome

Oestrogen/testosterone control bone turnover
Menopause
Male hypogonadism
Anorexia/athletes

270
Q

What happens during reduced skeletal loading? How does this happen?

A

Reduced skeletal loading increases resorption
Low body weight
Immobility

271
Q

What medications cause an increase risk of osteoporosis?

A

Glucocorticoids (corticosteroids)

GnRH analogues

Androgen deprivation

272
Q

What is FRAX?

A

A genorator to see how much at risk of a fracture you are?

273
Q

What are the treatment options for osteoporosis?

A

Anti-resorptive
Decrease osteoclast activity and bone turnover
Bisphosphonates
HRT
Denosumab - antibody to RANK

Anabolic
Increase osteoblast activity and bone formation
Teriparatide

274
Q

What are benefits and risks of hormone replacement therapy?

A

Benefits
Reduce the risk of fractures
Stop bone loss
Prevents hot flushes
Reduces risk of colon cancer

Risks
Breast cancer
Stroke
Cardiovascular disease

275
Q

When are bisphosphonates used and why? What are some oral and intravenous drugs?

A

First line treatment

ORAL
Alendronate (daily or weekly)
Risedronate (daily or weekly)
Ibandronate (monthly)
Etidronate (two weeks of 13)

IV
Ibandronate (3-monthly)
Zoledronate (once yearly)

276
Q

What do bisphosphonates do?

A

Bisphosphonates inhibit an enzyme in the cholesterol synthesis pathway – Farnesyl Pyrophosphate Synthase

277
Q

What are bisphosphonantes action?

A
278
Q

What is Denosumab?

A

Monoclonal antibody to RANK ligand

Switches off bone resorption.

Rebound increase of bone turnover when stopped

279
Q

What is Teriparatide?

A

PTH analogue

First anabolic treatment

Increases bone density,

280
Q

WHAT IS OSTEOMALACIA?

A

Osteomalacia there is a normal amount of bone but its mineral content is low (there is excess uncalcified osteoid and cartilage).

281
Q

What is the cause of osteomalacia?

A

Vitamin D deficiency

Renal failure
1,25-dihydroxy-cholecalciferol deficiency

Drug-induced
Increased breakdown of 25-hydroxy-vitamin D.

Vitamin D resistance:
Osteomalacia responds to high doses of vitamin D

Liver disease
Due to reduced hydroxylation of vitamin D to 25-hydroxy-cholecalciferol and malabsorption of vitamin D, eg in cirrhosis

Tumour

282
Q

What are the signs and symptoms of osteomalacia?

A

Bone pain and tenderness

Fractures

Proximal myopathy (waddling gait)

283
Q

What are the investigations for osteomalacia?

A

Plasma
Mildly decerease Ca2+
Decrease PO43–; alk phos increase; PTH high; 25(OH)-vitamin D low, except in vitamin D resistance.
In renal failure 1,25(OH)2-vitamin D low

Biopsy
Bone biopsy shows incomplete mineralization.
Muscle biopsy (if proximal myopathy) is normal.

X-ray
Loss of cortical bone

284
Q

What are the treatments for osteomalacia?

A

Vitamin D

285
Q

WHAT IS PAGETS DISEASE OF BONE?

A

Also called osteitis deformans

Increased bone turnover associated with increased numbers of osteoblasts and osteoclasts

With resultant remodelling, bone enlargement, deformity, and weakness

286
Q

What is the epidemiology of Paget’s diease of bone?

A

Rare in the under-40s.

Incidence rises with age (3% over 55yrs old).

287
Q

What are the signs symptoms of paget’s disease of bone?

A

Asymptomatic

Deep, boring pain, and bony deformity and enlargement

Classically a bowed sabre tibia

288
Q

What are the investigations for paget’s disease of bone?

A

X-ray
Localized enlargement of bone.
Patchy cortical thickening with sclerosis, osteolysis, and deformity

Blood chemistry
Ca2+ and PO43 normal
Alk phos markedly raised.

289
Q

What is the treatment for paget’s disease of bone?

A

Analgesia

Alendronate

290
Q

WHAT IS FIBROMYALGIA?

https://www.youtube.com/watch?v=Jyl98z07ZHM

A

Fibromyalgia is a chronic condition affecting fibrous tissue and muscle causing pain

291
Q

What is the epidemology of fibromyalgia?

A

Female more than men

292
Q

What is the normal pathway of pain?

A

Pain in finger

Nocicepter converts stimulates into electrical signal

Signal transmitted to cell body in dorsal root ganglion

If strong enough, substance P released

Substance P released onto secondary neuron in dorsal horn

Inhibitory neuron release serotonin and norepinephrine to dampen pain signal

293
Q

What happens at the site of damage for fibromyalgia?

A

Cells release nerve growth factor

Mast cells release more nerve growth factor

High levels of nerve growth factor

Growth, sensitivity and more nerve growth factor.

294
Q

What is the cause of fibromyalgia?

A

Unknown

Thought to be caused by the way the brain receieves pain signals

295
Q

What is the pathology of fibromyalgia?

A

Lower levels of serotonin, this normally decreases pain

Higher levels of substance P
Higher levels of nerve growth factors
BOTH involved with increasing pain

296
Q

What are the risk factors for fibromyalgia?

A

Genetics

Environmental
Child abuse
Depression
Anxiety
Negative beliefs

297
Q

What are the symptoms of fibromyalgia?

A

Widespread pain over the body

298
Q

What are the investigations for fibromyalgia?

A

Pain location in more than 7 areas with a symptom severity score of 5/12

OR

Pain location in more than 5 areas with a symptom severity score of 9/12

SYMPTOMS must be present for more than 3 months

NOT due to another disease

299
Q

What are the treatment options for fibromyalgia?

A

Exercise

Relaxation techniques

Sleep hygiene

Medications
Amitriptyline
Serotonin and nor-adrenaline reuptake inhibitors
Anticonvulsants - Pregabalin - slow nerve impulses

300
Q

WHAT ARE SOME VERTEBRAL DISC PROBLEMS?

A

Disorders effecting intervertebral discs: herniation, degeneration, infection.

301
Q

What is disc herniation?

A

Herniation = prolapsed vertebral disc.

302
Q

What is disc degeneration?

A

Major cause of lower back pain.

Exact cause is known

Could be natural part of ageing

Can occur in young people: genetic, environmental, traumatic, inflammatory, infectious, etc.

May lead to disc herniation.

303
Q

What is the pathophysiology of disc prolapse?

A

Nucleus pulposus herniates, it can irritate or compress the adjacent nerve root - symptoms of sciatica

304
Q

What is the epidemology of disc prolapse?

A

More common in under 40s, whereas degeneration is more common in over 40s.

305
Q

What is the presentation of a disc prolapse?

A

Symptoms of sciatica

Compress cauda equine

Nerve root compression

Symptoms can correspond to the level.

306
Q

What are the investigations for disc prolapse?

A

Symptoms may settle within 6 weeks

MRI very sensitive

CT

Plain x-rays sometimes useful

307
Q

What is the management for a disc prolapse?

A

Analgesia

Encourage to keep active

Heat and massage to relieve muscle spasm

Avoid activities that aggravate pain

Physiotherapy

Surgery.

308
Q

What is discitis?

A

Pyogenic infection of the spine

Rare

Incidence ­ due to ­ life expectancy

309
Q

What is the pathopgysiology of discitis?

A

Inflammation of vertebral disc space

Can co-exist with osteomyelitis

Most commonly effects lumbar spine

Usually haematogenous spread of infection from other parts of the body

Common sources; urinary tract, lungs, soft tissues

310
Q

What is the epidemology of discitis?

A

Staphylcoccus aureus is most common pathogen

Most commonly affects males in 50s

311
Q

What are some risk factors to discitis?

A

Immunosuppressed

IV drug use.

312
Q

What is the presentation of discitis?

A

Insidious onset

Neck or back pain and localized tenderness

Pain worse on movement

Restricted mobility

Associated fever and weight loss

Neurological deficit.

313
Q

What are the investigations for discitis?

A

ESR and CRP ­

WCC may be normal

Blood cultures, sputum, urine

X-ray may show disc space narrowing, calcification

CT and MRI show changes earlier than X-ray

CT guided biopsy.

314
Q

What is the management for discitis?

A

Antibiotics (adjusted after culture results)

Immobilization (2 weeks bed rest, then immobilization with brace)

Analgesia prescribed as requird

Surgery if neurological deficit, deformity or lack of response tp antibiotics.

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