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Phase 2a > Musculoskeletal and Rheumatology > Flashcards

Musculoskeletal and Rheumatology Flashcards

1
Q

What are the 2 types of bone at a macro level?

A

Cortical:
* Compact
* Dense, solid
* Only spaces are for cells and blood vessels

Trabecular:
* Cancellous (spongy)
* Network of bony struts (TRABECULAE)
* Looks like sponge, many holes filled with bone marrow
* Cells reside in trabeculae and blood vessels in holes

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2
Q

What are the different types of bone at a micro level?

A

Woven bone:
* Made quickly
* Disorganised
* No clear structure

Lamellar bone:
* Made slowly
* Organised
* Layered structure

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3
Q

What is the function of hollow long bones?

A

Keeps mass AWAY from the neutral axis and minimised deformation

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4
Q

What is the function of Trabecular bone?

A

Give structural support while minimising mass

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5
Q

What is the function of bone that has wide ends?

A

Spreads load over weak, low friction surface

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6
Q

What is the composition of bone in adults?

A
  • 50-70% mineral:
  • Hydroxyapatite - crystalline form of calcium phosphate
  • 20-40% organic matrix:
  • Type 1 Collagen - 90% of all protein
  • Non-collagenous proteins - 10% of all protein
  • 5-10% water
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7
Q

What do the minerals and collagen provide to bone respectively?

A

Minerals - Stiffness

Collagen - Elasticity

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8
Q

What is the function of a joint?

A
  • Allow movement in 3 dimensions
  • To bear weight
  • To transfer the load evenly to the musculoskeletal system
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9
Q

Give some key joints and examples

A
  • Fibrous - teeth sockets
  • Cartilaginous - intervertebral discs
  • Synovial - metacarpophalangeal and knee joint:
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10
Q

What are the main features of a synovial joint?

A
  • Articular cartilage
  • Joint capsule - the inner layer is the
    synovial membrane
  • Joint (synovial) cavity - space filled with synovial fluid
  • Synovial fluid
  • Reinforcing ligaments

+Bursae and Menisci

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11
Q

What is the function of Synovial Fluid?

A

Lubrication
Shock absorption
Nutrient Distribution

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12
Q

What is ESR?

A

Erythrocyte Sedimentation
An Inflammatory marker That rises with inflammation and infection.
ESR rises and falls slowly

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13
Q

What is CRP?

A

C-Reactive Protein
Acute phase marker of inflammation and infection.
Produced by the liver in response to IL-6
Rises and falls rapidly (acute inflammation CRP rises but ESR takes longer)

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14
Q

Define Osteoarthritis

A

A non-inflammatory degenerative joint disorder characterised by joint pain and functional limitation.
Osteoarthritis is an age-related, dynamic reaction pattern of a joint in response to insult or injury (Wear and Tear)
All tissues of the joint are involved
Articular cartilage is the most affected – produced by chondrocytes

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15
Q

What is the pathophysiology of OA?

A

Imbalance in process of cartilage breakdown by wear and tear and by chondrocytes releasing cartilage breakdown Factors leading to erosion of the articular cartilage in synovial joints.

  • Faulty cartilage undergoes erosion
  • disordered repair
  • fibrillations occur
  • cartilage ulceration which exposes underlying bone to increased stress
  • microfractures and cysts
    exposed bone attempts repair
  • abnormal sclerotic subchondral bone and overgrowth at joint margins (osteophytes)
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16
Q

What are the main features in the pathology of OA?

A

Loss of cartilage through wear and tear
Disordered bone repair

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17
Q

What controls the development of OA?

A

Mediated by cytokines:
IL-1, TNFa, NO

Driven By mechanical Forces

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18
Q

What is the epidemiology of OA?

A

Most common type of arthritis
Especially in elderly and females
Most common condition affecting synovial joints
Most important condition relating to disability as a result of locomotor symptoms
8.75 million people in the UK seek treatment for OA

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19
Q

What are the non-modifiable risk factors for OA?

A

Genetics -COL2A1 has a role

Increasing Age - strongest RF

Female - Hip OA 2x more common

High bone density - protective against osteoporosis but RF for OA

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20
Q

What are the modifiable Risk factors for OA?

A

Obesity

Joint injury/damage

Exercise stress

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21
Q

What are the symptoms of OA?

A

Joint pain - exacerbated by movement and relieved by rest
Worse as the day goes on

Joint Stiffness
Crepitus

Swelling

Joint Locking - inability to straighten joints

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22
Q

What is the typical Presentation of OA?

A

Elderly Px with knee/hip pain.
Morning stiffness lasting less that 30 mins
Pain increases with use (crepitus) and during the day
Asymmetrical joint involvement.
Bony swellings DIP/PIP

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23
Q

What are the clinical signs of OA?

A

Hands:
Bouchard’s Nodes (PIPJ)
Heberden’s Nodes (DIPJ)
Thenar Muscle wasting
First CMC Joint affected most

Knees:
Crepitus

Hips:
Antalgic gait
Restricted internal rotation

All affected Joints:
Joint tenderness

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24
Q

What is Heberden’s and Bouchard’s Nodes?
What condition are they seen in?

A

Seen in OA.

Bouchard’s - Bony swelling at PIP
Heberden’s - Bony swelling at the DIP

Remember B before H and proximal before distal

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25
Q

What is the most commonly affected joint in OA?

A

First Carpometacarpal joint of the thumb

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26
Q

What joints are the most commonly affected in OA?

A

Hips
Knees
Sacro-iliac joints
Distal-interphalangeal joints in the hands (DIPs)
The carpometacarpal joint at the base of the thumb (CMC)
Wrist
Cervical spine

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27
Q

What is Crepitus?

A

Crackling or grating sensation when moving a joint

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28
Q

What is a common differential diagnosis to OA?

A

Rheumatoid arthritis
Gout/Pseudogout

This differs from RA due to the absence of systemic features and the pattern of joint involvement.

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29
Q

What are the primary investigations to diagnose OA?

A

Joint X rays show OA hallmarks: LOSS:

Loss of Joint space (Joint space narrowing)
Osteophyte formation
Subarticular Sclerosis
Subchondral Cysts

(+ Abnormalities of Bone Contours)

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30
Q

What other investigations may be done in OA?

A

Diagnosis can be made if Px is over 45, has typical OA pain and this is not associated with early morning stiffness (like in RA)

Bloods - normal in OA

ESR/CRP - inflammatory markers to distinguish between RA or Gout

Negative anti-nuclear and RF antibodies

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31
Q

What is the conservative management of OA?

A

Weight loss if overweight to reduce the load on the joint

Physiotherapy to improve strength and function

Occupational therapy to support activities and function

Orthotics to support activities and function (e.g., knee braces)

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32
Q

What medical treatments can be used in OA?

A

Analgesics to control pain and Sx:
1st. Oral paracetamol / topical NSAIDs
2nd. Add oral NSAIDs
3rd . Consider Opiates - Codeine

If these fail:
Inter-articular steroid injections
Surgical - Joint replacement/osteotomy/arthroplasty

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33
Q

When should oral NSAIDs be used with caution for OA?

A

In an older patient who may be on anticoagulants such as aspirin/DOACs

There may be some drug interactions/side effects using both Tx

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34
Q

Define Rheumatoid Arthritis (RA)

A

A chronic systemic autoimmune arthritis that progresses from a symmetrical deforming poly-arthropathy affecting the synovial joints to a multi-system disorder

Characterised by deposition of immune complexes in synovial joints

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35
Q

What is the pathophysiology of RA?

A

RA is primarily a synovial disease that spreads to extra articular areas.

Genetic predisposition allows a triggering factor to cause Arginine - citrulline mutation in T2 collagen - anti-CCP Abs form.

When chemoattractant (IFN and TNF-alpha) produced in the joint, this recruit circulating inflammatory cells

The Synovium is thickened by inflammatory cells and it proliferates to produce a “pannus”

The pannus DESTROYS the articular cartilage and subchondral bone resulting in bony erosions

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36
Q

What is the key chemoattractant involved in the progression of RA?

A

IFN and TNF-alpha

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37
Q

What is the epidemiology of RA?

A

Affects 1% of global population
More common in females than males
Linked to autoimmune conditions
Prevalence peaks at 30-50yrs

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38
Q

What are the genetic factors for RA?

A

HLA-DR1 and HLA-DR4 (crucial in activating T-cells)

PTPN22

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39
Q

What are the risk factors for RA?

A

Increasing age
Genetics (HLA-DRB1, HLA-DR4)
Female - (pre-menopause)
FHx
Smoking

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40
Q

What is the role of the immune system in RA?

A

Triggering antigen is unknown but immune system has a role in synovial inflammation:
- T cells - interferon, IL-2 & -4
- Macrophages - IL-1 & -8 & TNF-alpha
- Mast cells - histamine & TNF-alpha
- Fibroblasts - IL-6

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41
Q

What are the symptoms of RA?

A

Morning stiffness/pain - >30 mins and improves throughout the day
Joint pain worse in cold environments but eases with use.
Loss of function of joints

Constitutional Sx - malaise, myalgia, fever
Extra Articular involvement
sleep disturbances

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42
Q

What are the clinical signs of RA?

A

Hand:
Symmetrical polyarthritis
Boutonniere Deformity
Swan neck deformity
Z thumb deformity
Ulnar deviation

Symmetrical
Hot/warm inflamed joints
Extra articular complications

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43
Q

What joints does RA most commonly affect?

A

Early disease:
Symmetrically affects Joints of the hands and feet (MCP, PIP, MTP)

Progressed Disease:
Wrists
Elbows
Shoulders
Knees
Ankles

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44
Q

What is Boutonniere deformity?

A

PIP flexion and DIP hyperextension seen in RA

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45
Q

What is Swan neck deformity?

A

PIP hyperextension and DIP flexion seen in RA

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46
Q

What are some extra articular complications seen in RA?

A

Lungs - Plural Effusions/ pulmonary fibrosis
Heart - increased IHD risk, Pericardial effusion
Eyes -Episcleritis
Spinal Cord - compression
Kidney - CKD/amyloidosis
Skin - Rheumatoid skin nodules

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47
Q

What is the Diagnostic Criteria for RA?

A

Need 4/7
1. Morning stiffness
2. Arthritis of 3 or more joints
3. Arthritis of hand joints
4. Symmetrical
5. Rheumatoid nodules
6. Rheumatoid factor positive
7. Radiographic changes – LESS

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48
Q

What are the primary investigations in RA?

A

Bloods:
ESR/CRP raised - inflammation
NORMOCYTIC, NORMOCHROMATIC anaemia

Serology:
Positive rheumatoid factor - 80% (not specific)
Positive anti-CCP Abs - 30% (very specific for RA)

XR = LESS

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49
Q

What is the X-ray like in RA?

A

LESS:
Loss of joint space
Eroded Bone
Soft tissue Swelling
Soft Bones (osteopenia)

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50
Q

What Antibodies are present in RA?

A

Positive Rheumatoid Factor Abs - Not specific
Positive Anti-CCP Abs (Anti - Cyclic Citrullinated Peptide) - Very specific

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51
Q

What is the treatment of RA?

A

No cure - Sx management:

Initially NSAIDs analgesia - Often co prescribed with PPI (gastric protection)

Induce remission
DMARDs:
eg. methotrexate - GS treatment (others such as sulfasalazine)

If unsuccessful then combination of Biologics (often in combination with DMARDs)

If severe pain/flare ups - Intraarticular steroid injection (prednisolone)

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52
Q

What are DMARDS?

A

Disease Modifying anti Rheumatic Drugs:
Methotrexate is given as monotherapy or alongside biologics (but these are very expensive)

Also Hydroxychloroquine and Sulfasalazine

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53
Q

When is methotrexate Contraindicated?

A

Pregnancy as it is a folate inhibitor and therefore DNA synthesis is affected

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54
Q

What is the mechanism of action of methotrexate?
What must always be co-prescribed with methotrexate?

A

Folate acid synthesis inhibitor (inhibits dihydrofolate reductase)
Therefore must co-prescribe Folic Acid

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55
Q

What biologics are used in combination with DMARDs in RA?

A

1st - TNF-a inhibitor - INFLIXIMAB

2nd- B cell inhibitor (CD20 target) - RITUXIMAB

ADALIMUMAB - Monoclonal Ab

TOCOLIZUMAB - Il-6 antagonist

ABATERCEPT - Blocks T cell activation

BARACITINIB

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56
Q

What are the types of crystal arthritis?

A

Gout

PseudoGout

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57
Q

What type of crystals are formed in crystal arthritis?

A

Gout:
Needle Shaped Urate Crystals
Negatively Birefringent in polarised light

Pseudogout:
Rhomboid Brick shaped Pyrophosphate crystals
Positively Birefringent in Polarised Light

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58
Q

Define Gout?

A

Gout is an inflammatory arthritis caused by deposition of monosodium urate crystals within joints due to hyperuric acid levels

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59
Q

What is the most common inflammatory arthritis in the UK?

A

Gout

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60
Q

Who does Gout affect?

A

More common in males than females (2-7:1)
Typically in adulthood >40 years
Rises in postmenopausal women - due to oestrogen protection prior to menopause

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61
Q

What are the risk factors for gout?

A

Male
Obesity - high fructose intake
High purine diet (e.g. meat and seafood)
Alcohol (beer/larger)
Diuretics
Existing cardiovascular or kidney disease
Family history

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62
Q

What factors can increase uric acid production?

A

Malignancy - increased cell turnover
Cytotoxic drugs
Purine rich diet
Obesity
Surgery
Psoriasis

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63
Q

What factors can impair the excretion/removal of uric acid?

A

CKD
Diuretics
Pyrazinamide
Lead Toxicity

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64
Q

What are the causes of Gout?

A

Under excretion of uric acid:
Hyperuricaemia
Drugs
Alcohol/obesity
CDK

Overproduction of purines:
High purine Diet (meat, beer, seafood)
Psoriasis
Malignancy

Renal Causes

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65
Q

What is the pathogenesis of Gout?

A

High purine intake (food/alcohol)
Is oxidised to Uric acid by Xanthine oxidase.

Normally uric acid is then excreted by the kidneys

But in hyperuricaemia this cannot occur fast enough and this can lead to kidney damage

The Uric acid is converted to monosodium urate crystals that trigger intracellular inflammation.

These deposit in joints and cause an inflammatory arthritis

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66
Q

What are common causes of a gout attack?

A

Anything that causes sudden alteration in uric acid concentration
Alcohol
Diet
MI
Trauma

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67
Q

What food substances can be anti-gout?

A

Dairy

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68
Q

What are the symptoms of gout?

A

Often ASx hyperuricaemia but attacks come on in episodes.

Rapid onset severe joint pain
Joint stiffness
Commonly swollen red big toe which is painful you cannot put weight on it (TOE ON FIRE)

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69
Q

What are the clinical signs of gout?

A

Monoarticular/oligoarticular - 1-4 joints affected

1st joint = MTP of big toe

Ankle and wrist also affected

Gouty Tophi - nodular masses of urate acid crystals

Precipitated by purine triggers. Often have recurrent episodes.

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70
Q

What are the primary investigations for Gout?

A

Joint aspirate and POLARISED:
Negatively BIREFRINGENT needle shaped crystals

Serum Urate - may give an indication if hyperuricaemia (but may be normal)

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71
Q

Why may there be low serum uric acid levels in a Px who is having a gout attack?

A

Due to all the uric acid forming crystals that has collected in the joints and therefore is not present in the blood.

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72
Q

What result do gout crystals give when undergoing polarised microscopy?

A

Negatively Birefringent needle shaped crystals

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73
Q

Why must you always aspirate a red hot joint?

A

To rule out septic arthritis

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74
Q

What is the management of Gout?

A

Low uric acid level:
Lifestyle Mx
Diety - decrease purines and increase dairy
Weight loss
Reduce alcohol.
Prophylaxis - Allopurinol

Pain Mx:
1st - High dose NSAIDs
2nd Colchicine (if NSAIDs CI)
3rd - Steroid injection -

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75
Q

What is the management of Gout?

A

Low uric acid level:
Diety - decrease purines and increase dairy

Pain Mx:
1st - High dose NSAIDs - Naproxen/ibuprofen
2nd Colchicine (if NSAIDs CI)
3rd - Steroid injection - IM Prednisolone

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76
Q

What is given to prevent gout (prophylaxis)?

A

Allopurinol -Xanthine oxidase inhibitor to reduce uric acid production.

Given after resolution of the first attack of gout.

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77
Q

Why must you be careful when prescribing Allopurinol?

A

Shouldn’t be used during a gout attack.
Cover with Colchicine or NSAIDs to prevent a Gout Flare

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78
Q

What is Pseudogout?

A

Pseudogout is a form of inflammatory arthritis caused by deposition of calcium pyrophosphate crystals in the synovium and joint capsule

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79
Q

Who is affected by pseudogout?

A

Typically elderly women >70 yrs

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80
Q

What are the risk factors for pseudogout?

A

Elderly Female
Diabetes
Metabolic diseases - Hyperparathyroidism, HH
Hypophosphataemia
OA - High overlap with OA and pseudogout

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81
Q

What can cause an acute pseudogout attack?

A

Direct trauma to the joint
Intercurrent illness
Surgery – especially parathyroidectomy
Blood transfusion, IV fluid
T4 replacement
Joint lavage

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82
Q

What is the pathophysiology of Pseudogout?

A

Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue producing the radiological appearance of chondrocalcinosis

Typical distribution – usually affects larger joints
Knee > wrist > shoulder > ankle > elbow

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83
Q

What is the clinical presentation of pseudogout?

A

Resembles gout however the most commonly affected joints are Knee, shoulder and wrist

(MTP joint is primary affected joint in gout)

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84
Q

What are the common clinical features of Pseudogout?

A

Asymptomatic
Severe joint pain
Acute synovitis – due to shedding of crystals into joint
Acute hot and swollen joint or OA joint
Fever
Stiffness

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85
Q

What is the primary investigation for pseudogout?

A

Joint aspiration + polarised microscopy:
Weakly - Positively BIREFRINGENT rhomboid shaped crystals

XR - Evidence of chondrocalcinosis

FBC - Raised WCC

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86
Q

What is the management of Pseudogout?

A

Only acute management:
1st - NSAIDs
2nd - Colchicine
3rd Steroid injection - IM Prednisolone

+ physiotherapy and rest/icepacks

Long term Tx with DMARDs may be considered if poor inflammatory change

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87
Q

How can you distinguish Osteoarthritis from Pyrophosphate arthropathy?

A
  1. Pattern of involvement – knee, wrists, shoulders, ankles, elbows
  2. Marked inflammatory component
  3. Superimposition of acute attacks
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88
Q

What is Osteoporosis?

A

Osteoporosis is the reduction in trabecular bone mass/density and disruption of bone microarchitecture, resulting in porous bone with increased fragility and fracture risk

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89
Q

Define Osteoporosis?

A

Defined as bone mineral density (BMD) MORE than 2.5 standard deviations
BELOW the young adult mean value (T score < -2.5)

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90
Q

What is Osteopenia?

A

Pre-cursor to osteoporosis characterised by low bone density

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91
Q

Define Osteopenia?

A

Defined as BMD between 1-2.5 standard deviations BELOW the young adult
mean value (-1< T score > -2.5)

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92
Q

What is Osteomalacia?

A

Poor bone mineralisation leading to soft bone due to lack of Ca2+ (adults
form of Ricket’s)
Rickets is poor bone mineralisation in children

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93
Q

What is the key difference between osteoporosis and osteomalacia?

A

Osteoporosis is poor bone density
Osteomalacia is poor bone mineralisation

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94
Q

Who does osteoporosis typically affect?

A

Typically 50yrs + post menopausal Caucasian women
1/2 of Women and 1/5th of men over 50
230, 000 osteoporotic fractures each year

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95
Q

What are the risk factors for osteoporosis?

A

SHATTERED

Steroids
Hyperthyroidism
Alcohol + Smoking
Thin (Low BMI)
Testosterone (Low)
Early Menopause
Renal / Liver Failure
Erosive Disease
Diabetes Type 1 / Diet

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96
Q

What are the causes of Osteoporosis?

A

Primary: Post Menopausal

Secondary (SHATTERED):
Steroids
Hyperthyroid/Hyperparathyroid
Alcohol/Smoking
Thin (low BMI)
Testosterone (low)
Early menopause (low estrogen)
Renal/liver failure
Erosive + inflammatory disease
Diabetes Mellitus - Type 1

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97
Q

What is the T score?

A

Young adult bone Density

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98
Q

What is the pathogenesis of Osteoporosis?

A

Increased resorption by osteoclasts
Decreased bone formation by osteoblasts
Inadequate peak bone mass
Changes in trabecular architecture with ageing

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99
Q

How does oestrogen affect bone remodelling in osteoporosis?

A

Post menopausal women
Oestrogen deficiency
Remodelling imbalance - net loss of bone
(preventable by oestrogen replacement)

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100
Q

What are the symptoms of Osteoporosis

A

ASx until fracture.

HIP - Neck of Femur if elderly falls on side or back
Wrist - Distal radius if fall on outstretched arm

May have evidence of acute fractures (vertebrae, fragility fractures)

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101
Q

What are the clinical signs of Osteoporosis?

A

Fractures of:
Proximal femur

Colles’ Fracture (forked wrist)

Compression of vertebral column - Kyphosis

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102
Q

What are the primary investigations of Osteoporosis?

A

DEXA Scan (Dual Energy X-ray Absorptiometry)

Yields T score - compares Px BMD to reference

FRAX Score - Fracture risk assessment

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103
Q

What result on the DEXA score indicates osteopenia/ osteoporosis?

A

DEXA score is normal distribution of BMD
-1 to -2.5 SD below mean is osteopenia

> -2.5 SD below mean is osteoporosis

> 3 SD below mean is severe osteoporosis

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104
Q

What is the FRAX score?

A

Fracture risk assessment tool:
Age
Sex
BMI
Previous Fractures
Steroids

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105
Q

What is the management of Osteoporosis?

A

Conservative:
Lifestyle changes - reduce RFs
Vit D and Calcium supplements

Medical:
1st Line - Bisphosphonates - Alendronate, Risedronate

2ndLine - Different Bisphosphonate (risedronate)

3rd Line - mAB Denosumab or HRT

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106
Q

What is the first line treatment of osteoporosis and what is the mechanism of action?

A

Bisphosphonates:
Interfere with osteoclasts by inhibiting RANK-L signalling to reduce the amount of bone resorption

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107
Q

Give some examples of bisphosphonates?

A

Alendronate
Risedronate
Zoledronic Acid

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108
Q

What are some key side effects of Bisphosphonates?

A

Reflux and Oesophageal Erosions
Atypical Fractures
Osteonecrosis of the jaw
Osteonecrosis of external auditory canal

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109
Q

What are some third line treatments for osteoporosis?

A

Denosumab - monoclonal Ab against RANK-L

Raloxifene - used as secondary prevention as an oestrogen receptor modulator

HRT - Oestrogen inhibits bone resorption of osteoclasts by promoting osteoclast apoptosis

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110
Q

What is the Primary Prevention of Osteoporosis?

A

o Adcal D3 – Vitamin D + calcium
o Calcium-rich diet e.g. dairy or sardines, white beans
o HRT – menopausal women
o Corticosteroids – consider prophylactic bisphosphonates
o Regular weight bearing exercise
o Smoking and alcohol cessation
o DEXA scans

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111
Q

What is Fibromyalgia?

A

A syndrome characterised by widespread pain and tender points at specific anatomical sites.
No signs of inflammation - Non-specific muscular disorder
It is often accompanied by depression, fatigue and sleep disturbance

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112
Q

Define Fibromyalgia?

A

Fibro - Soft tissue
Myalgia - Muscle Pain

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113
Q

What is Fibromyalgia equivalent to?

A

Equivalent to IBS:

Chronic widespread MSK pain for 3+ months when all other causes have been ruled out

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114
Q

What is the definition of Fibromyalgia?

A
  • Widespread musculoskeletal pain for at least 3 months AFTER other diseases have been excluded
  • Pain at 11 of 18 tender point sites on digital palpation (with enough pressure so that the thumb blanches)
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115
Q

What are the risk factors for fibromyalgia?

A

Females: Middle aged -60+
Depression
Stress
Poverty
IBS

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116
Q

What are the symptoms of fibromyalgia?

A

Chronic Muscle pain > 3 months
Pain worse with stress and cold weather
Morning stiffness <1hr
non-restorative sleep

Fatigue
Mood disorder
Sleep Disturbances
Headaches and difficulty concentrating

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117
Q

What are the clinical signs of fibromyalgia?

A

Specific tender points throughout body:

Occiput
Low cervical region
Trapezius
Supraspinatus
Second rib
Lateral epicondyle
Gluteal region
Greater trochanter
Knees

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118
Q

What pain pathway is affected in fibromyalgia

A

Non-nociceptive (neuropathic) pain pathway
Low serotonin - lack of pain signal inhibition
Raised Substance P - Increased pain signals

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119
Q

What is the diagnosis of fibromyalgia?

A

Diagnosis of exclusion:
No serological markers - rule out SLE
No ESR/CRP raised - rule out inflammatory arthritis
TFTs - rule out hypothyroidism

Pain in 11+ of 18 tender regions palpated

Clinically made diagnoses

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120
Q

What primary investigations are made to rule out other conditions in fibromyalgia?

A

TFTs - exclude hypothyroidism

ESR/CRP - exclude inflammatory arthropathy

Creatine kinase

Bone profile and LFTs - Exclude hyperparathyroidism and osteomalacia

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121
Q

What is the management of fibromyalgia?

A

1st line: HOLLISTIC APPROACH
Patient education of condition
Physical Therapy
Exercise
Analgesia

2nd Line:
Antidepressants and CBT for severe neuropathic pain.
Amitriptyline for sleep

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122
Q

What is an important differential diagnosis of fibromyalgia?

A

Polymyalgia Rheumatica (PMR)
Hypothyroidism
SLE
Inflammatory Arthritis

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123
Q

What is Polymyalgia Rheumatica?

A

Chronic inflammatory rheumatic condition causing chronic pain in the shoulders, pelvic girdle and neck.

This condition affects both muscles and joints

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124
Q

What is polymyalgia rheumatica associated with?

A

Giant cell Arteritis (a form of large cell vasculitis).
These conditions often occur together

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125
Q

What is the epidemiology for polymyalgia rheumatica

A

ALWAYS over 50 +yrs
Females
Caucasian
Giant Cell Arteritis

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126
Q

What are the risk factors for Polymyalgia Rheumatica?

A

Over 50
Females
SLE
Polymyositis/Dermatomyositis

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127
Q

What is the pathology of PMR?

A

Inflammatory disorder causing pain or stiffness in shoulders and hips
Muscles are actually spared
Pain comes from bursae and tendons 🡪 referred pain

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128
Q

What is the presentation of polymyalgia rheumatica?

A

Bilateral shoulder/pelvic girdle pain that presents for more than 2 weeks

Morning stiffness (>30 mins) typically in shoulders and proximal limb muscles
Pain more severe in morning and evening
Improves with activity
Symmetrical aching

50% of Px have Systemic Sx:
Fever
Weight loss
Fatigue

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129
Q

What are the primary investigations for polymyalgia rheumatica?

A

Clinical Hx can be diagnostic - Px is ALWAYS OVER 50
ESR/CRP raised

Other Ix are typically normal

Temporal artery biopsy - may show GCA

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130
Q

What is the treatment for polymyalgia rheumatica?

A

Oral 15mg Prednisolone

if used long term give GI and bone protection:
Lanzoprazole + alendronate

Exercise and healthy diet

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131
Q

What are some important differential Diagnoses that should be ruled out in Polymyalgia Rheumatica?

A

Osteoarthritis
Rheumatoid arhtirits
Systemic lupus erythematosus
Myositis (from conditions like polymyositis or medications like statins)
Cervical spondylosis
Adhesive capsulitis of both shoulders
Hyper or hypothyroidism
Osteomalacia
Fibromyalgia

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132
Q

What is Sjogren’s Syndrome?

A

Chronic inflammatory autoimmune disorder that is characterised by the destruction of epithelial exocrine glands:
Specifically the lacrimal and salivary glands.

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133
Q

What is the difference between primary and secondary Sjogren’s Syndrome?

A

1’: (Sicca Syndrome ONLY)
Syndrome of dry eyes in the absence of RA due to genetic factors

2’:
Sjogren’s Syndrome associated with other Connective tissue disease; RA, SLE

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134
Q

What are the risk factors for Sjogren’s Syndrome?

A

Females
FHx
Age 40-50
Genetics
Other Autoimmune disorders (SLE, RA, PBC)

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135
Q

What are the genetic associations of Sjogren’s Syndrome?

A

HLA-D8 and HLA-DR3

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136
Q

What is the pathophysiology of Sjogren’s Syndrome?

A

Autoimmune, Lymphocytic infiltration and fibrosis of exocrine glands, especially the lacrimal and salivary glands leading to dry mucous membranes

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137
Q

What are the symptoms of Sjogren’s Syndrome?

A

Dry Eyes (keratoconjuctivitis Sicca)
Dry Mouth (xerostomia)
Dry Vagina

Fatigue and Joint pain

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138
Q

What are the Primary investigations of Sjogren’s Syndrome?

A

Saliometry - Low Saliva Flow

Serology:
Anti-Ro
Anti-LA antibodies
ANA often positive
Presence of Anti-SS-A and Anti-SS-B Abs

Schirmer Test - Conjunctival Dryness

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139
Q

What is the Schirmer test and what condition is it used to diagnose?

A

Diagnose - Sjogren’s Syndrome

Filter paper on inside of lower eyelid - tears travel along strip - a result of <10mm travel is significant

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140
Q

What is the treatment for Sjogren’s Syndrome?

A

Artificial Tears and Saliva replacement
Vaginal Lubricants

NSAIDs and Sometimes Hydroxychloroquine - halts progression

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141
Q

What are some complications of Sjogren’s Syndrome?

A

Eye infections
Oral problems
Vaginal problems

Can increase risk of lymphomas

142
Q

What is a big risk of Sjogren’s Syndrome?

A

Risk of B-Cell Lymphoma with Sjögren’s as the lymph nodes are often hyperplastic 🡪 emergence of dominant B-cell clone responsible for a marginal zone lymphoma

143
Q

What is Vasculitis?

A

Inflammatory Disorder or Blood vessel walls
Leads to aneurysm/rupture or stenosis of vessel

144
Q

What are the different type of vasculitis conditions?

A

Characterised by size of vessel:

Large:
Giant Cell Arteritis
(Polymyalgia Rheumatica (PMR) can be considered)

Medium:
Polyarteritis Nodosa

Small:
Granulomatosis w/ Polyangiitis
Wegener’s Granulomatosis

145
Q

What Vasculitis conditions affect the large vessels?

A

Giant cell Arteritis
Takayatsu Arteritis

146
Q

What Vasculitis conditions affect the Medium sized Vessels?

A

Polyarteritis Nodosa

Buerger’s Disease
Kawasaki Disease

147
Q

What Vasculitis Conditions affect the small sized vessels?

A

Granulomatosis w/ Polyangiitis (GPA)

Henoch-Schonlein Purpura
Churg-Strauss Syndrome

148
Q

What is the general treatment for Vasculitis?

A

Corticosteroids

149
Q

What should you consider when prescribing steroids long term?

A

GI and Bone protection:
Give PPI - Lansoprazole
Give Bisphosphonates - Alendronate

150
Q

What are some conditions associated with Systemic Vasculitis?

A

Infective:
Subacute infective endocarditis

Non-infective:
Vasculitis with RA
SLE
Scleroderma
IBD and good pastures syndrome

151
Q

What is Systemic Vasculitis?

A

Is a histological term describing inflammation of the vessel wall

152
Q

How are systemic Vasculitis conditions categorised?

A

By size of blood vessel involved and the presence or absence of anti- neutrophil cytoplasmic antibodies (ANCA)

153
Q

What is Giant Cell Arteritis (GCA)?

A

Inflammatory granulomatous arteritis of large vessels that affects adults, and usually affects branches of the carotid artery, cerebral arteries or Aorta.

154
Q

What arteries are commonly affected in GCA and what signs might these present with?

A

Aorta
Cerebral Arteries:

  • Superficial Temporal Artery - Headache and scalp tenderness
  • Mandibular Artery - Jaw claudication
  • Ophthalmic Artery - Visual loss
155
Q

What is the main association of GCA?

A

Polymyalgia Rheumatica (PMR)

156
Q

What is the epidemiology of GCA?

A
  • Primarily in those OVER 50
  • Incidence increases with age
  • More common in FEMALES than males
157
Q

What are the risk factors of GCA?

A
  • Over 50
  • Female
  • RA, SLE, scleroderma
158
Q

What is the pathophysiology of GCA?

A

Granulomatous inflammation along the vessel wall occurs segmentally.

The result is intimal thickening and a narrowed vascular lumen.

This can lead to obstruction and downstream ischaemia

159
Q

What are the symptoms of GCA?

A

Unilateral temporal headaches
Scalp Pain
Jaw claudication
Vision loss
Sx of PMR

160
Q

What are the primary investigations of GCA?

A

1st line:
Increased ESR
ANCA Negative

Temporal Artery biopsy - diagnostic

Fundoscopy

161
Q

What would be seen on a temporal artery biopsy in GCA?

A

Granulomatous inflammation of media and intima

Patchy skip lesions and therefore a large chunk must be taken

162
Q

What is the treatment for GCA?

A

1st Line:
Corticosteroids - Prednisolone

163
Q

What are some complications of GCA?

A

Amaurosis Fugax: Sudden painless vision loss of one eye (optic neuropathy)

Must be dealt with ASAP via high dose IV METHYL PREDNISOLONE

164
Q

What are some differential diagnoses of GCA?

A

Migraine
Tension headache
Trigeminal neuralgia
Polyarteritis nodosa

165
Q

What is the treatment of GCA?

A

Corticosteroids - Prednisolone
Prophylaxis of Osteoporosis
Visual Changes - IV Methylprednisolone

166
Q

What is Polyarteritis Nodosa?

A

A medium vessel arteritis that is associated with Hepatitis B infection

167
Q

What is Polyarteritis nodosa associated with?

A

Males
Middle aged
Hepatitis B

168
Q

What is the pathology of Polyarteritis Nodosa?

A

Necrotising vasculitis that causes aneurysms and thrombosis in medium sized vessels, leading to infarction in affected organs

169
Q

What are the symptoms of polyarteritis nodosa?

A

Severe systemic Sx:
Fever, malaise, myalgia, weight loss.

Followed by severe organ infarction:
Mononeuritis Multiplex
Coronary arteritis - MI/AF
GI bleeds - Abdominal Pain
CDK/AKI - Haematuria/proteinuria
Skin nodules + haemorrhage

170
Q

What is the diagnostic investigation for polyarteritis nodosa?

A

Bloods:
Anaemia
WBC raised
Raised ESR
ANCA Negative

CT angiogram:
Beads on a string - micro aneurysms

Biopsy - of kidney - Shows necrotising vasculitis due to HTN

171
Q

What is the treatment for polyarteritis nodosa?

A

Corticosteroids - prednisolone w/ immunosuppressive drugs (azathioprine/Cyclophosphamide)

Control HTN - ACEi

HepB Tx after corticosteroids

172
Q

What is Granulomatosis w/polyangiitis?

A

Wegener’s Disease
A small vessel vasculitis that is ANCA positive and tends to affect the lungs and the kidneys arterioles, capillaries and venules

173
Q

What is the Epidemiology of Granulomatosis W/ polyangiitis?

A

Typically presents at 25-60
Associated with ANCA

174
Q

What can Granulomatosis w/polyangiitis cause?

A

glomerulonephritis + pulmonary syndromes therefore you get Sx of these.

175
Q

What are the clinical signs and symptoms of granulomatosis w/polyangiitis?

A

Nose bleeds - Epistaxis
Sinusitis
SADDLE SHAPED NOSE
Cough/wheeze/Haemoptysis
Glomerulonephritis

176
Q

What are the investigations of Granulomatosis w/ polyangiitis?

A

Bloods:
Raised ESR
C-ANCA Positive (90%)

Biopsy of Kidneys, Lungs, Upper Resp Tract = Granulomas
CXR - nodules

177
Q

What is the treatment for Granulomatosis w/ polyangiitis?

A

High dose corticosteroids e.g. prednisolone
Cyclophosphamide
Biologics

Remember it as the rule of C’s – C in body (nose, upper resp. tract, kidneys), C-ANCA +, biopsy (Cross-section), Corticosteroids and Cyclophosphamide

178
Q

What is Churg Strauss disease?

A

A small vessel vasculitis
P-ANCA
No nasopharyngeal involvement
No granuloma

179
Q

What is Pagets Disease of Bone?

A

A disease characterised by a Focal disorder of bone remodelling/turnover due to the excessive activity of osteoblasts and osteoclasts.

This leads to increased bone resorption.

180
Q

What are the stages of Pagets disease pathophysiology?

A

Initial osteoclastic activity leading to bone resorption

Mixed osteoclastic and osteoblastic activity resulting in deposition of structurally abnormal bone

Chronic, sclerotic phase in which bone formation supersedes bone resorption

181
Q

What is the epidemiology of Pagets disease?

A

Age >55yrs
More common in females
FHx is high RF
UK has highest prevalence in the world

182
Q

What are the risk factors for Paget’s Disease?

A

FHx
Increasing age
Female sex

183
Q

What are the symptoms of Paget’s Disease?

A

Bone pain
Bone deformities - Bowed Tibia

Neurological Sx:
Compression of CN VIII - deafness
Hydrocephalus - Sylvian Duct blockage

184
Q

What are the primary investigations of Paget’s Disease?

A

XR:
Bone enlargement/deformities
Osteoporosis circumscripta
Cotton wool appearance of skull

Biochemistry:
Raised Alkaline Phosphatase
Normal Calcium, Normal phosphate

Urinary Hydroxyproline excretion - marker of disease activity

185
Q

What is the management of Paget’s Disease?

A

Bisphosphonates - alendronate

NSAIDs for bone pain

186
Q

What are the key complications of Paget’s Diseaes?

A

Osteosarcoma
Spinal stenosis /cord compression

187
Q

What are the different types of Spondyloarthropathies?

A

Ankylosing Spondylitis
Psoriatic arthritis
Reactive arthritis
Enteric arthritis

188
Q

What are the general features of Spondylarthropathies?

A

SPINEACHE:
Sausage fingers (dactylitis)
Psoriasis
Inflammatory back pain
NSAIDs = good response
Enthesitis - inflammation of entheses
Arthritis
Crohn’s/Colitis
HLAB27
Eyes - Uveitis

189
Q

What are Spondylarthropathies?

A

Group of Asymmetrical SERONEGATIVE (absence of rheumatoid factor) arthritic conditions

associated with HLAB27.

Share certain clinical features

190
Q

What is HLAB27?

A

An MHC Class I surface antigen that interacts with T cells

Present in Spondylarthropathies

191
Q

When should you think Spondyloarthropathies?

A

If you see:
Inflammatory back pain
Asymmetrical (large joint) arthritis
Skin Psoriasis
Inflammatory bowel disease
Inflammatory eye disease

192
Q

What is Ankylosing Spondylitis?

A

An autoimmune Inflammatory arthritis of the intervertebral and facet joints in spine and rib cage – eventually leading to new bone formation and fusion of the joints (bamboo spine)

193
Q

What joints/areas are most commonly affected in Ankylosing Spondylitis?

A

Spine/vertebral column
Sacroiliac joints

194
Q

Define ankylosis?

A

Abnormal stiffening and immobility of joints due to new bone formation

195
Q

What is the pathophysiology of Ankylosing Spondylitis?

A

The autoimmune process attacks the entheses, where ligaments and tendons attach to bone,

leading to inflammation, bone erosion and syndesmophyte (new bone) formation

196
Q

Who is typically affected by ankylosing spondylitis?

A

More common and severe in males
Usually presents at16 to <30 yrs
88% HLA-B27 Positive
Native North Americans have high incidence

197
Q

What are the risk factors for ankylosing spondylitis?

A

FHx
Genetics - HLAB27
Smoking
Age - young adults

198
Q

What is the typical presentation of ankylosing spondylitis?

A

Typical patient is a man < 30 yrs with gradual onset of low back pain, worse at night, with spinal morning stiffness that is relieved by exercise

199
Q

What are the symptoms of Ankylosing Spondylitis?

A

Weight loss
Fever
Fatigue
Buttock/thigh pain – sacroiliac joints
Neck or back pain/stiffness – cervical/thoracic region
Can lead to SOB

200
Q

What is the pain like in ankylosing spondylitis?

A

Progressively worse back pain that is worst in the morning and at night

it gets better with exercise

201
Q

What are the clinical signs of Ankylosing Spondylitis?

A

SPINEACHE Signs

Pain in buttock/axial spine

Reduced natural lumbar lordosis (more kyphosis of thoracic and cervical spine)

Schober test - Reduced lumbar flexion

202
Q

Define Spondylitis?

A

Inflammation of the joints of the backbone

203
Q

What are the diagnostic investigations for Ankylosing Spondylitis?

A

XR:
Bamboo spine
Sacroilitis (inflammation of sacroiliac joint)
Squared vertebral bodies
Syndesmophytes - fusion of vertebral bodies

MRI - More sensitive

Bloods:
ESR/CRP raised
HLAB27 positive (not required for diagnosis)
Raised ALP
Normocytic Anaemia

204
Q

What provides a Definitive Diagnosis of Ankylosing Spondylitis?

A

Diagnosis – In patients with > 3 months back pain and age at onset <45
Sacroiliitis (XR/MRI) + > 1 SPINEACHE feature

205
Q

What are the treatments of ankylosing spondylitis?

A

Physio and hydrotherapy

Long term high dose NSAIDs e.g. ibuprofen or naproxen
Risk of peptic ulcer, vascular disease, renal damage etc.

DMARDs e.g. methotrexate – treat peripheral arthritis but not the disease

Biologics– specifically anti-TNFs e.g. etanercept, adalimumab
Stop syndesmophytes forming – once formed, nothing can reverse/stop progress

206
Q

What conservative management may be used in ankylosing spondylitits?

A

Physiotherapy
Exercise and mobilisation
Avoid smoking

207
Q

What is a differential Diagnosis of Ankylosing Spondylitis?

A

Mechanical Back Pain

208
Q

What is Psoriatic Arthritis

A

An inflammatory arthritis associated with psoriasis (can occur without psoriasis)
Psoriasis - Red scaly patches

Within the group of SERONEGATIVE spondyloarthropathies and has a link to HLAB27

209
Q

What is the epidemiology of psoriatic arthritis and what are the risk factors?

A

Psoriasis in 2-3% of population
10-40% of Px with psoriasis develop it within 10yrs

RFs - FHx of Psoriasis

210
Q

What are the symptoms of Psoriatic Arthritis?

A

Typically painful and inflamed DIP joints

Swollen fingers/toes

Back pain

211
Q

What are the clinical signs of Psoriatic Arthritis?

A

DIP joint tenderness

Nail Dystrophy - Onycholysis
Dactylitis
Enthesitis

Psoriasis

212
Q

What is Arthritis Multilans?

A

Affects 5% of Px with psoriasis and causes periarticular osteolysis.

Telescoping and shorting of fingers

Show Pencil in CUP deformity on XR

213
Q

What are the hidden sites for psoriasis?

A

Behind ear
Scalp
Under nails
Penile

214
Q

What are the primary investigations for psoriatic arthritis?

A

No definitive diagnostic Ix

Bloods:
Raised ESR
HLA-B27 positivieRF and Anti-CCP negative

XR - Erosive changes (pencil in CUP)

Testing for Rheumatoid factor and plain XR to fill out CASPAR criteria

215
Q

What is the treatment for Psoriatic arthritis?

A

Sx:
NSAIDs - pain
Physiotherapy

DMARDs - delay progression
methotrexate

If fails - anti-TNF (biologics eg. adalimumab/etanercept)

216
Q

What is Reactive Arthritis?

A

A form of sterile inflammatory arthritis affective the synovial membranes (synovitis) that occurs in response to an infection in a distant site.

It is part of the spondyloarthropathies and has a link to HLAB27

217
Q

What type of arthritis is caused by reactive arthritis?

A

It causes an acute monoarthritis

218
Q

What are the main causes of reactive arthritis?

A

GI infection:
Campylobacter
Salmonella
Shigella

STI:
C. trachomatis
N. gonorrhoea

219
Q

What are the risk factors for reactive arthritis?

A

Sexual intercourse
Distal Infection - usually GI/STI
Male
Young adults - 20-40yrs

220
Q

What are the symptoms of Reactive arthritis?

A

Reiter’s Traid:
Conjunctivitis
Urethritis
Arthritis
CANT SEE, CANT PEE, CANT CLIMB A TREE

Pain and swelling of:
Single large joint
Ankles, hips, small joints in feet
Multiple joints

221
Q

What is the main differential diagnosis of reactive arthritis?

A

Septic arthritis :
Painful hot swollen joints,
Signs or Hx of infection

Gout

222
Q

What are the primary investigations of reactive arthritis?

A

Joint aspirate:
shows no organism (excludes septic arthritis)
High Neutrophil count - should be sterile

Plane polarised light microscopy - negative for crystal-arthropathy

Raised ESR/CRP
HLAB27 positive

Stool culture if diarrhoea
Urethral swab and STI screen for infection cause

223
Q

What is the treatment for reactive arthritis?

A

Treat cause of infection - Abx

Sx management:
NSAIDs
Steroid injection (intra-articular)

In chronic Px/unresponsive
Use DMARDs

224
Q

What is Enteric/Enteropathic arthritis?

A

Joint inflammation that occurs in Px who have IBD

Part of the seronegative spondyloarthropathies and linked with HLAB27

225
Q

What are the types of infective arthritis?

A

Septic arthritis
Osteomyelitis

226
Q

What is Septic arthritis?

A

Direct bacterial infection in a joint leading to severe inflammation and potential joint destruction w/ fever

MEDICAL EMERGENCY

227
Q

What is the most commonly affected joint in Septic arthritis?

A

The knee joint

Can destroy the knee in <24hrs

228
Q

What are the common organisms that can cause septic arthritis?

A

Staphylococcus aureus - most common

Group A strep - children

Staph Epidermidis - prothesis

N. gonorrhoea - young sexually active

P.aeruginosa - IVDU/ immunocompromised

229
Q

What are the risk factors for septic arthritis?

A

Elderly >80
Pre-existing joint disease

Diabetes mellitus:

  • Skin breaks/ulcers

Prosthetic joints
Immunosuppression
Penetrating trauma

230
Q

What is a typical presentation of septic arthritis?

A

Affects a Px who was previously fit and well
Typically affects a single joint:

Rapid onset
Hot, red, swollen
EXTREMELY PAINFUL

Systemic Sx - lethargy, fever and sepsis

231
Q

What is the pathophysiology of Septic Arthritis?

A

Bacterial Infection - via various causes/routes
Spreads contiguously/haematogenously into the joint space
Infection causes inflammation and arthritis

232
Q

What are the investigations for septic arthritis?

A

Joint aspiration with culture and Gram stain - fluid will be cloudy/opaque

Increased ESR/CRP and WCC raised

Blood Cultures - Joint seeded by bacteraemia

Polarised light microscopy - exclude gout/pseudogout

233
Q

What are the important differential diagnoses of septic arthritis?

A

Gout - Uric acid crystals and -tve birefringent

Pseudogout - +tve birefringent and Ca pyrophosphate crystals

Reactive arthritis - sterile

Haemarthrosis - bleeding into joint

234
Q

What is the treatment for Septic arthritis?

A

EMERGENCY:
Joint aspiration (drainage) + EMPRICAL Abx:

Staph Aureus Sensitive Abx:
Flucloxacillin
Vancomycin/Teicoplanin
Ceftriaxone + Azithromycin

Stop Immunosuppressives
Prednisolone DOUBLED if on long term prednisolone

235
Q

What additional considerations should be made in Septic arthritis?

A

If on Methotrexate/anti-TNF - STOP

If on Steroids (long term) - DOUBLE PREDNISOLONE

NSAIDs for analgesia

236
Q

Which of the following is now a rare cause for joint infection in INFANTS, due to the standard childhood immunisation schedule in the UK?

  • Staphylococcus Aureus
  • Gp A (Beta-haemolytic)
  • Varicella Zoster
  • Rubella
  • Haemophilus Influenzae
A

Haemophilus Influenzae

237
Q

What is Osteomyelitis?

A

Osteomyelitis (OM) is an inflammatory condition affecting any bone and bone marrow in the skeleton, usually as a result of bacterial infection

238
Q

How can Osteomyelitis occur?

A

Infection is spread via haematogenous or direct Local infection by causative organism

239
Q

What are the most common organisms causing OM?

A

S. aureus (90%)

S. pneumoniae - children
P. aeruginosa - IVDU
Salmonella in SICKLE CELL Px

240
Q

What are the risk factors for OM?

A

IVDU
Immunosuppressed
PVD
DM
Sickle cell anaemia
Trauma

241
Q

Who is typically affected by OM?

A

Often affects children

Can be acute OM
Can be Chronic OM

242
Q

What is the pathophysiology of OM?

A

Exposed bone from trauma allows for Direct inoculation, local infection or haematogenous spread of causative organism.

Will cause acute bone inflammation and bone oedema

If chronic - can lead to:
sequestra (necrotic bone embedded in pus)
Involucrum - Thick sclerotic bone placed around sequestra

243
Q

Explain how Diabetes can lead to Osteomyelitis?

A

Diabetes can lead to severe Vascular Compromise
Can lead to foot ulcers which become infected.
This infection can spread to nearby bone via contiguous spread.

244
Q

What are the symptoms of OM?

A

Dull bony pain/tenderness at site of infection

fatigue - chronic Sx
Fever
Reduced range of motion

Chronically may have sequestra (deep ulcers)

245
Q

What is an important differential diagnosis of OM?

A

Charcot Joint:
damage to sensory nerves due to diabetic neuropathy.
Causes progressive degeneration of weight bearing joint and bony destruction.

Soft Tissue Infection - Cellulitis

246
Q

What is the primary investigation for OM?

A

BM biopsy and culture to ID organism

XR - osteopenia

Increased ESR/CRP - inflammation
Raised WBC

247
Q

What histopathological signs would be seen in Osteomyelitis?

A

Acute changes

  • Inflammatory cells
  • Oedema
  • Vascular congestion
  • Small vessel thrombosis

Chronic changes:

  • Necrotic bone “sequestrum”
  • New bone formation – involucrum
  • Neutrophil exudates
  • Lymphocytes and histiocytes (tissue macrophages)
248
Q

What is the treatment of OM?

A

Immobilise + Abx therapy

6 weeks for acute OM
3 months for chronic OM

Abx:
IV Flucloxacillin
IV Teicoplanin - Empirical

Surgical - Debridement/Removal of dead bone

249
Q

How do you rule out Tuberculous Osteomyelitis?

A

BM Biopsy:

TB-OM shows caseating granulomas

250
Q

What are the Autoimmune Rheumatological Disorders?

A

SLE
Anti-Phospholipid Syndrome
Sjogren’s Syndrome
Systemic Sclerosis
CREST Syndrome
Polymyositis/Dermatomyositis

251
Q

What is Systemic Lupus Erythematosus (SLE)?

A

A chronic inflammatory autoimmune disease that affects multiple organs and systems.

Characterised by a T3 hypersensitivity reaction

252
Q

What hypersensitivity reaction is SLE?

A

Type 3 - Antigen-antibody immune complex deposition

253
Q

Who is typically affected by SLE?

A

Females - 12x more than male
Afro-Caribbean
20-40 yrs (pre-menopause)

254
Q

What are the risk factors for SLE?

A

FHx
Genetics - HLAB8, HLA-DR2, HLA-DR3
Drugs - Isoniazid, Procainamide
EBV - potential trigger

255
Q

What is the pathophysiology of SLE?

A

Apoptotic debris is poorly cleared

These bodies are presented to Th2 which activate B cells and produce autoantibodies

activates an immune response generating antibody-antigen complexes.

Which then deposit in tissues and activate complement, causing tissue inflammation and damage

256
Q

What antibodies are significant in SLE?

A

Anti-nuclear antibodies (ANA): (99% of cases) - very sensitive

Anti-dsDNA Abs: - very specific
Abs against DNA from apoptotic bodies

257
Q

What are the key clinical signs and symptoms of SLE?

A

Malar “butterfly” rash - photosensitive (worse in sunlight)

Fatigue

Raynaud’s Phenomenon

Sx Similar to RA

Glomerulonephritis

Seizures + psychosis

Mouth Ulcers

258
Q

What are some other possible signs/symptoms of SLE?

A

Non-specific Sx:

Weight loss
myalgia
fever
Anaemia
Joint pain

259
Q

What are the Primary investigations for SLE?

A

Autoantibodies
- ANA (90%) sensitive but not specific
- Anti-dsDNA (70%) specific but not sensitive

Bloods:
anaemia
Increased ESR - NORMAL CRP

Urine dipstick - Haematuria + proteinuria - Nephrotic Syndrome

C3/C4 decreased

MRI/CT Brain

260
Q

What is Required for a Diagnosis of SLE?

A

Must have 4 or more /11

  • MD SOAP BRAIN:
  • Malar rash – butterfly rash on face
  • Discoid rash
  • Serositis – pleuritis, pericarditis
  • Oral ulcers in mouth
  • Arthritis – similar to RA
  • Photosensitivity – rashes on sun exposed area
  • Blood (haematological) disorder – all low (anaemia, leukopenia, - thrombocytopenia)
  • Renal disease – proteinuria (glomerulonephritis)
  • Anti-nuclear antibody positive
  • Immunological disorder – anti-dsDNA
  • Neurological disorder – seizures, cerebrovascular disease, myasthenia gravis
261
Q

What antibodies may rise secondary to SLE?

A

anti-phospholipid Abs in antiphospholipid syndrome that can arise secondary to SLE in up to 40% of cases

262
Q

What is the treatment of SLE?

A

Lifestyle changes - avoid sunlight, smoking, weight loss.

Medical Mx:
Corticosteroids + Hydroxychloroquine (anti-malarial) + NSAIDs

Overtime taper off other drugs till Hydroxychloroquine monotherapy

In severe cases use immunosuppressants (azathioprine, Methotrexate)

263
Q

What is the most specific auto-antibody in SLE?

A

Anti-Smith Ab

most specific but has low sensitivity (30%)

264
Q

What are some key complications of SLE?

A

CVD
Infection
Pericarditis
Neuropsychiatric
Lupus Nephritis
+ others
(Many affected organs and systems)

265
Q

What is antiphospholipid Syndrome?

A

disorder associated with antiphospholipid antibodies where the blood becomes prone to clotting. The patient is in a hyper-coagulable state.

266
Q

What are the main associations of Antiphospholipid syndrome?

A

The main associations are with thrombosis and complications in pregnancy, particularly recurrent miscarriage.

267
Q

What is Primary and Secondary antiphospholipid Syndrome?

A

Primary - occurs idiopathically (more common)

Secondary - occurs as a result of other autoimmune conditions, particularly SLE

268
Q

Who is typically affected by antiphospholipid syndrome?

A

More common in females
20-30% of SLE

269
Q

What are the causes of Anti-phospholipid Syndrome?

A

HLA-DR7 mutation and environmental trigger
Infection (HIV, Malaria)
Drugs – CV drugs (propranolol, hydralazine) and anti-psychotics (phenytoin)

270
Q

What is the pathophysiology of antiphospholipid syndrome?

A
  • Antiphospholipid antibodies (aPL) play a role in thrombosis by binding to phospholipid on the surface of endothelial cells, platelets and
    monocytes
  • Once bound, this change alters the functioning of those cells leading to
    thrombosis and/or miscarriage
  • Causes CLOTS:
    Coagulation defect
    Livedo reticularis – lace-like purplish discolouration of skin
    Obstetric issues i.e. miscarriage
    Thrombocytopenia – low platelets
271
Q

What antibodies are associated with antiphospholipid syndrome?

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

272
Q

What are the symptoms/associations of antiphospholipid syndrome?

A

CLOTS:
Coagulopathy - DVT, PE, Budd Chiari
Livedo Reticularis - Purple discolouration of skin
Obstetric issues - Miscarriages
Thrombocytopenia
Stroke - increased risk

273
Q

What does antiphospholipid syndrome increase a Px risk of?

A

Px is in a hypercoagulable state and therefore can clot easily leading to:
Stroke
MI
Venous Thrombosis (DVT)

274
Q

What is the diagnosis of antiphospholipid syndrome?

A

Diagnosis is made with a Hx of thrombosis and pregnancy complications PLUS: (persistent Abs)
Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

275
Q

What is the Treatment of Antiphospholipid syndrome?

A

Mx Thrombosis RFs - Smoking, Weight loss, Diet, DM, HTN

1st Line :
Warfarin - long term with an INR of 2-3
(If pregnant give LMWH + Aspirin)

276
Q

What prophylactic treatment can be provided for a Px with antiphospholipid syndrome?

A

Aspirin / Clopidogrel

277
Q

What is Scleroderma (CREST)?

A

Multi-Systemic Sclerotic condition of which the most common type is:
Limited Cutaneous Scleroderma.

Involvement of Skin and Reynaud’s Phenomenon

278
Q

What is CREST acronym in Scleroderma for?

A

The main clinical features of Limited cutaneous scleroderma

279
Q

Who is typically affected by Scleroderma?

A

Women
Age 30-50

Positive ANA Abs

280
Q

What are the Risk Factors of Scleroderma?

A

Exposure to vinyl chloride, silica dust, adulterated rapeseed oil and trichloroethylene
Drugs e.g. bleomycin
Genetic

281
Q

What is the Pathophysiology of Scleroderma?

A
  • Genetic predisposition, immune activation, infection and an environmental toxin initiate an endothelial cell lesion and widespread vascular damage
  • Increased Vascular Permeability
  • Upregulation of cell-cell and cell-matrix adhesions. These stimulate cytokine and GFs that proliferate
  • Uncontrolled proliferation of connective tissue and thickening of vascular walls - narrowing lumen
  • Damage to small blood vessels and subsequent ischaemia
282
Q

What are the presentations of Scleroderma?

A

Limited - CREST Sx

Diffuse - Widespread organ fibrosis (GI, Renal, Lung, Myocardial)

283
Q

What are the symptoms of Scleroderma?

A

CREST:
- Calcinosis - calcium deposition in subcutaneous tissue

  • Raynauds
  • Eosophageal dysmotility or strictures
  • Sclerodactyly - local thickening/tightness of skin on fingers/toes
  • Telenagiectasia - spider veins
284
Q

What are the diagnostic investigations for scleroderma?

A

Anti-centromere antibodies (ACAs) in 70% of cases (LIMITED)

Anti Topoisomerase 1 Abs (DIFFUSE)

285
Q

What is the management of Scleroderma?

A

No cure - progressive condition

Treat Sx:
Analgesia
Calcium channel blockers for Raynauds (i.e. nifedipine)
Topic skin emollients
PPI and antacids for oesophageal reflux
Treating PAH (bosentan, sildenafil, iloprost)

286
Q

What is Polymyositis/Dermatomyositis?

A

Rare autoimmune disorders where there is inflammation within the muscles:

Polymyositis is a condition of chronic inflammation and necrosis of muscles.

Dermatomyositis is a connective tissue disorder where there is chronic inflammation of the skin AS WELL AS the muscles.

287
Q

Who is typically affected by Polymyositis/Dermatomyositis?

A

More common in women
Adults and children affected

288
Q

What are the risk factors of polymyositis/dermatomyositis?

A

Genetic predisposition:
HLA-D8, HLA-DR3 (Sjogren’s) at increased risk

289
Q

What is the Pathology of Polymyositis/Dermatomyositis?

A

Polymyositis – immune system attacks the muscles due to molecular mimicry (immune cells confuse normal muscle proteins with foreign antigens)

Dermatomyositis – immune system attacks muscle and skin

290
Q

What is the clinical presentation of Polymyositis?

A

Progressive symmetrical muscle wasting of muscles of the shoulders and pelvic girdle.

Difficulty walking up stairs, standing from sitting, putting hands on head

Muscle pain, Fatigue and weakness

May have involvement of respiratory and pharyngeal muscles

291
Q

What is the clinical presentation of Dermatomyositis?

A

Sx of Polymyositis + Skin involvement:

Gottron lesions (scaly erythematous rash on knuckles)

Photosensitive Erythematous rash on shoulders/back

Heliotrope - purple rash on eyelids

292
Q

What are the primary investigations for polymyositis/dermatomyositis?

A

Clinical presentation

Elevated creatine kinase

Autoantibodies

Muscle Biopsy can be used to establish diagnosis = necrosis

293
Q

What autoantibodies are found in polymyositis and dermatomyositis respectively that are used for diagnosis?

A

Anti-Jo-1 antibodies: polymyositis (but often present in dermatomyositis)

Anti-Mi-2 antibodies: dermatomyositis.

Anti-nuclear antibodies: dermatomyositis.

294
Q

What is the management of polymyositis/dermatomyositis?

A

1st Line:
Corticosteroids (prednisolone)
Exercise + physiotherapy

2nd Line:
Immunosuppressive agents if steroids are inadequate
(Hydroxychloroquine and Tacrolimus)

295
Q

What are the key primary bone tumours?

A

Osteosarcoma
Ewing sarcoma
Fibrosarcoma
Chondrosarcoma

296
Q

Who is affected by Primary Bone tumours?

A

Rare tumours
Usually only seen in children and young adults

297
Q

What are the key malignancies that can spread to bone to cause a secondary bone tumour?

A

BLT KP:
Breast
Lung
Thyroid
Kidney
Prostate

298
Q

Which secondary causes of bone cancer are osteolytic?

A

Breast and lung

299
Q

Which Secondary causes of bone cancer are osteoslcerotic?

A

Prostate
Thyroid
RCC

300
Q

Which are more common causes of bone cancer, primary or secondary?

A

Secondary bone cancers are more common than primary

301
Q

What is Osteosarcoma?

A

Most common primary bone cancer.
Associated with Paget’s Disease
Affects 15-19 yr olds
Will metastasis to the lung
XR shows “Sunburst” appearing bone

302
Q

What is Ewing’s Sarcoma?

A

Arises from mesenchymal stem cells
affects 15 yr olds
Very rare

303
Q

What is Chondrosarcoma?

A

Malignant neoplasm of cartilage

304
Q

Who is affected by primary bone cancers?

A

Only seen in young

305
Q

What are the symptoms of bone cancer?

A

Local persistent severe Bone pain often worse at night

Systemic:
Weight loss, fatigue, fever, malaise

306
Q

What are the diagnostic investigations of bone tumours?

A

Skeletal isotope scan - shows change before XR

XR - osteolysis/osteosclerosis

Bone Biopsy

Increased ALP, ESR, CRO

Hypercalcaemia due to malignancy

307
Q

What are the XR features of the Main primary Bone Cancers?
Osteochondroma
Giant cell tumour
Osteosarcoma
Ewing’s sarcoma

A

Osteochondroma - exostosis
Giant cell tumour – soap bubble appearance
Osteosarcoma – sunburst appearance and Codman’s triangle
Ewing’s sarcoma – Onion skin appearance

308
Q

What is the treatment of bone cancer?

A

Benign - Surgical resection - often limb amputation
Malignant - Adjuvant Chemo/radiotherapy

Bisphosphonates

309
Q

What would be used to stage a bone tumour?

A

CT
MRI
PET

310
Q

Define Osteomalacia?

A

Defective bone mineralisation that has occurred after fusion of the epiphyseal growth plates therefore only occurs in adults.

311
Q

What is Rickets?

A

Disorder of defective bone mineralisation that has occurred prior to fusion of the epiphyseal growth plates and therefore occurs in children

312
Q

What is the pathophysiology of osteomalacia?

A

Commonly Vitamin D deficiency leading to reduced calcium and phosphate absorption from the GI tract.

Therefore there is inadequate production of Calcium Hydroxyapatite to mineralise bone

313
Q

What are the causes of Osteomalacia?

A

Vitamin D deficiency:
Malabsorption, Low intake, poor sunlight

CKD - low vitamin D activation cannot produce 1,25-hydroxyvit D)

Liver failure - Low reaction of Vit D pathway

Hyperparathyroidism - secondary to Vit D deficiency

314
Q

What is the process of vitamin D activation?

A

7-Dehydrocholesterol - Cholecalciferol (via UVB light)

Cholecalciferol - 25 hydroxyvit D (by liver)

25-Hydroxyvit D to 1,25-Hydroxyvit D in the kidneys

315
Q

What is the function of Vitamin D?

A

Increased absorption of Ca and Phosphate in the GI Tract

Increased resorption of bone to release Ca

Increase renal reabsorption of Ca and Excretion of phosphate

316
Q

What is the active and inactive form of vitaminD?

A

Inactive - Cholecalciferol

Active - 1,25-Hydroxyvitamin D

317
Q

How can anti-convulsant drugs cause osteomalacia?

A

Increase CYP450 metabolism of vitamin D leading to deficiency and hence subsequent osteomalacia

318
Q

What are the symptoms of osteomalacia?

A

Generalised Bone Pain
Fractures of bone
Proximal weakness
Difficulty bearing weight

319
Q

Where are fractures most common in Osteomalacia?

A

Fractures of the femoral neck

320
Q

What are the symptoms of Rickets?

A

Skeletal deformities

Knocked knees and Bowed Legs
Wide Epiphyses

321
Q

What are the investigations for osteomalacia?

A

LOW Serum 25-OH-Vit D (<25nmol/l)

Serum Calcium/Phosphate

Serum PTH (possibly high due to 2’ hyperparathyroidism)

Serum ALP - raised in 80% of cases

XR - Looser Zones - defective mineralisation

BM biopsy - incomplete mineralisation

322
Q

What is the Treatment for osteomalacia?

A

Correct initial Vit D and then maintenance:

Vitamin D replacement - Calcitriol

Increase dietary intake of Vit D (D3 tablets/eggs)

323
Q

What is a common cause of mechanical lower back pain?

A

Prolapse of the vertebral disc causing acute pain.
Vertebral disc degeneration

324
Q

What is the epidemiology of lower back pain?

A

Very common presenting complaint in community
Associated with heavy Manual Handling, Stooping, Twisting whilst lifting.

Disease of younger people (20-40)
In older Px its more likely to be Sciatica

325
Q

What are the Risk Factors of Lower Back Pain?

A

Manual labour work
Smoking
Low socioeconomic status
Poor working conditions
Females – pregnancy, kids
Age
Psychological disorders – high levels of psychological distress, self-rated health and dissatisfaction with work
Pre-existing chronic widespread pain - fibromyalgia

326
Q

What can cause lower backpain?

A

Trauma
Work related
Exercise related
Heavy Lifting
Lumbar Disc Prolapse

327
Q

When is there sign of serious pathology in lower back pain?

A

Neuropathic pain - spinal cord compression

Elderly - due to myeloma?

328
Q

What is the clinical presentation of a vertebral disc degeneration?

A

Sudden onset of severe back pain

  • often following a strenuous activity
  • Pain is often clearly related to position and is aggravated by movement
  • Muscle spasm leads to a sideways tilt when standing
329
Q

What are the RED FLAG signs of Lower Back Pain?

A

Red flags – TUNAFISH
T – trauma, TB
U – unexplained weight loss and night sweats
N – neurological deficits, bowel and bladder incontinence
A – age <20 and > 55
F - fever
I – IV drug user
S - steroid use or immunosuppressed
H – history of cancer, early morning stiffness

330
Q

What are the most commonly affected discs resulting in lower back pain and what are the associated pain regions?

A

Lower 3 discs

L4 - lateral thigh to medial calf

L5 - Buttock to lateral leg and top foot

S1 - Buttock down back of thigh to ankle/foot

331
Q

What is Lumbar Spondylosis?

A

Degeneration of the intervertebral disc where it loses its compliance and thins over time.

These are initially ASx but will progress and worsen over time.

332
Q

What are the Investigations for Lower Back Pain?

A

Unnecessary unless chronic (>12 weeks)
If young:
- CRP/ESR – to rule out myeloma, infection, tumour
- X-Ray only if there are red flags

MRI more preferable than CT
Bone scans

333
Q

When should you XR for lower back pain?

A

if serious condition is suspected
Neurological pain etc

334
Q

What are the treatments for Lower Back Pain?

A

Majority (90%) resolve after 6 weeks
Continue normal activities – DON’T REST
Lifestyle
Avoid slouching
Proper lifting technique
Heat pads
Swimming
Analgesic ladder
Diazepam if insufficient
Physio, acupuncture, CBT
Urgent neurosurgical referral if there is neurological deficit

335
Q

What is the treatment for Acute disc injurys?

A

Often self limiting

Bed rest, analgesia and physiotherapy if acute mechanical pain

336
Q

What are the key connective tissue disorders?

A

Marfan’s Syndrome

Ehlers Danlos Syndrome

337
Q

What is Marfan Syndrome?

A

Autosomal dominant condition affecting the FB1 gene which results in abnormal fibrillin production and therefore a reduced connective tissue strength

338
Q

What are features of Marfan Syndrome?

A

Marfans Body Habitus:
Tall stature
Long neck, Limbs, Fingers (arachnodactyly)
Thin
Hypermobility
Pectus carinatum/excavatum

Aortic Complications:
Aortic/Mitral regurgitation murmur
AAA
Aortic Dissection

339
Q

What is the diagnosis of Marfan Syndrome?

A

Clinical patient + FBN-1 mutation

340
Q

What is the management of Marfan Syndrome?

A

Minimise HR and BP to reduce risk of cardiovascular complications:

beta blockers / Angiotensin II antagonists

Physiotherapy - strengthen joints

341
Q

What are the complications of Marfan Syndrome?

A

Joint Dislocations due to hypermobility

Aortic Aneurysm
Aortic Dissection
Aortic valve prolapse
Mitral Valve prolapse

342
Q

What is Ehlers Danlos Syndrome (EDS)?

A

A group of genetic conditions that lead to defects in collagen resulting in hypermobility and other connective tissue abnormalities

343
Q

How many subtypes of Ehlers Danlos Syndrome are there and what is the most common type?

A

13 different subtypes

Hypermobile Ehlers Danlos Syndrome is most common and least severe

344
Q

What is the cause of Ehlers Danlos Syndrome?

A

Autosomal Dominant mutations affecting collagen proteins.

345
Q

What are the main symptoms/clinical features of Ehlers Danlos Syndrome?

A

Joint Hypermobility

CV complications:
Mitral Regurgitation
AAA
Aortic Dissection

346
Q

What is the diagnosis for Ehlers Danlos Syndrome?

A

Clinical Patient
Beighton Score

Examine Px to exclude Marfan features (long arm span etc)

347
Q

What is the Beighton Score?

A

Used to assess the extent of Hypermobility to diagnose Ehlers Danlos Syndrome

348
Q

What is the management of Ehlers Danlos Syndrome?

A

No cure

Physiotherapy
Occupational Therapy

349
Q

What conditions should you think of if you see these Antibodies?
Rheumatoid Factors
Anti-CCP
ANA/Anti-dsDNA
Anti-Ro/Anti-La
c-ANCA
p-ANCA
Anti-Jo1
Anti-centromere/Anti-topoisomerase –
Anti-GBM
Anti-tTG and Anti-EMA

A

Rheumatoid Factors – RA (poor specificity)
Anti-CCP – RA (high specificity)
ANA/Anti-dsDNA – SLE
Anti-Ro/Anti-La – Sjogren’s
c-ANCA – Wegener’s
p-ANCA – Churg-Strauss
Anti-Jo1 – poly/dermatomyositis
Anti-centromere/Anti-topoisomerase – CREST/systemic sclerosis
Anti-GBM – Goodpasture’s
Anti-tTG and Anti-EMA - Coeliac

350
Q

What classical features should you think of for these conditions?
OA
RA
GCA
SLE
Psoriatic arthritis
Ankylosing spondylitis
Myeloma

A

OA – Bouchard’s/Heberden’s nodes, LOSS
RA – Swan neck, Boutonniere’s, ulnar deviation, Z-deformity, LESS
GCA – pain on combing hair
SLE – butterfly rash
Psoriatic arthritis – Dactylitis (sausage digits), pencil in cup deformity
Ankylosing spondylitis – bamboo spine, Syndesmophytes, dagger sign, sacroiliitis
Myeloma – Bence Jones protein, pepper pot skull

Phase 2a (24 decks)

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