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Phase 2A > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What are the characteristic features of osteoarthritis?

A

loss of cartilage, disordered remodelling of adjacent bone and associated inflammation.

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2
Q

What type of joint does osteoarthritis most commonly affect?

A

Synovial joints

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3
Q

What is the pathology of osteoarthritis?

A

It is the degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage and the inflammatory cells surrounding tissues.

The process is mediated by cytokines.

The release of enzymes from these cells break down collagen and proteoglycans destroying the articular cartilage.

The exposure of the underlying subchondral bone results in sclerosis.

This is followed by reactive remodelling changes that lead to the formation of osteophytes and subchondral bone cysts.

Secondary inflammation.

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4
Q

What cell has an active response in the osteoarthritis pathology?

A

Chondrocytes in the articular cartilage

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5
Q

What type of aetiology does osteoarthritis have?

A

multifactorial aetiology

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6
Q

What are the two types of osteoarthritis?

A

Can be primary (no obvious cause and generalised)

Can be secondary (to joint diseases or other conditions e.g obesity or occupational)

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7
Q

Name 4 risk factors for developing osteoarthritis?

A

Ageing
Cumulative effect of traumatic insult

Female

Obesity
Being obese is a low grade proinflammatory state producing cytokines

Occupation
Manual labour is associated with OA of the hands
Farming associated with OA of the hips
Football associated with OA of the knees

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8
Q

What are the most common joints affected by osteoarthritis?

A

Small joints of the hands
Small joints of the feet
Hip joint
Knee joint

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9
Q

What are the symptoms of osteoarthritis?

A

Usually gradual on onset and progressively worse
Joint pain that is exacerbated by exercise and relieved by rest
Rest and night pain in advanced disease
Joint stiffness in the morning
Reduced function and participation restriction (walking and AODL)

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10
Q

What exacerbates the pain in patients with osteoarthritis?

A

exercise

pain is relieved with rest

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11
Q

What are the signs of osteoarthritis?

A
  • Reduced range of movement
  • Alteration in gait
  • Pain on movement of the joint or at extremes of joint movement
  • Joint swelling
  • Bony enlargement
  • Effusion
  • Synovitis
  • Periarticular tenderness
  • Crepitus
  • No systemic features (fever or rash)
  • Muscle weakness or wasting around the affected joint
  • Bony swelling and deformity due to osteophytes
  • Distal interphalangeal joint : Heberden’s nodes
  • Proximal interphalangeal joints: Bouchard’s nodes
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12
Q

What is a bony swelling and deformity at the distal interphalangeal joint known as ?

A

Heberden’s nodes

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13
Q

What is the bony swelling and deformity at the proximal interphalangeal joint known as?

A

Bouchard’s nodes

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14
Q

What investigations do you do in osteoarthritis?

A

Bloods
- may be a raised CRP

Plain X-ray

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15
Q

What are the diagnostic features you can see on an X-ray in a patient with osteoarthritis?

A 
Joint space narrowing 
Osteophyte formation 
Subchondral sclerosis
Subchondral cysts 
Abnormalities of bone contour
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16
Q

What are the 3 core treatments for osteoarthritis?

A

Patient education
Activity and exercise (improves prognosis and muscle strength and general aerobic fitness)
Weight loss

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17
Q

What are the non-pharmacological treatments for osteoarthritis?

A 
Core treatments plus..
Physiotherapy 
Occupational therapy 
Footwear 
Orthoses 
Walking aids (stick, frame)
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18
Q

What are the pharmacological treatment options for osteoarthritis?

A

Topical

  • NSAIDs (voltarol gel)
  • Capsaicin

Oral

  • Paracetamol
  • NSAIDs
  • Opioids

Transdermal patches

  • Buprenorphine
  • Lignocaine

Intra-articular steroid injections
Only in patients that have no other options

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19
Q

What are the surgical treatment options for osteoarthritis?

A

Arthroscopy to wash away loose debris
Osteotomy - bone is cut to shorten it to change its alignment
Arthroplasty
Fusion - used in complicated joints to stop pain

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20
Q

When would a patient with osteoarthritis need an arthroplasty?

A

If the patient has uncontrolled pain, particularly at night or patient has a significant limitation of function

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21
Q

How long does a joint replacement usually last for?

A

20-22 years

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22
Q

When would you fuse joints together in a patient with osteoarthritis?

A

If it is a complicated joint and the pain is really unbearable

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23
Q

Define rheumatoid arthritis?

A

A chronic systemic inflammatory autoimmune disease characterized by a symmetrical deforming peripheral polyarthritis affecting the synovial joints

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24
Q

What is the pathology of rheumatoid arthritis?

A
  1. Chemoattractants produced in the joint recruit circulating inflammatory cells
  2. The inflammatory cells (macrophages, B lymphocytes and T lymphocytes and plasma cells) interact leading to the over production of TNF-alpha
  3. Generation of new synovial blood vessels force leukocytes into the synovium where they can trigger inflammation
  4. Synovium proliferates, thickens and grows out over the surface of the cartilage producing a tumour like mass (pannus)
  5. The pannus of inflamed synovium damages the underlying cartilage by blocking its route for nutrition and by direct effects of cytokines on the chondrocytes
  6. The cartilage becomes thin and the underlying bone is exposed
  7. The pannus destroys the articular cartilage and subchondral bone resulting in focal bony erosions
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25
Q

Aetiology of rheumatoid arthritis?

A

Autoimmune disease
Autoantibodies Rheumatoid Factor and anti-cyclic citrullinated peptide
RF is an antibody against the Fc portion of IgG that has a role in modulating the immune response
Cyclic citrullinated peptide is a marker of disease and is not pathogenic

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26
Q

What is the antigen that triggers the inflammatory response that causes rheumatoid arthritis?

A

Unknown!

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27
Q

Name 3 risk factors that can increase your likelihood of developing Rheumatoid Arthritis?

A
  • Female (3x more likely to develop than males before menopause)
  • Family history
  • Genetics (HLA-DR4 and HLA-DRB1 are associated with development of a more severe erosive disease
  • Smoking
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28
Q

What genes are associated with the development of a more severe rheumatoid arthritis disease?

A

HLA-DR4 and HLA-DRB1

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29
Q

What is the main symptom that suggests rheumatoid arthritis?

A

Symmetrical swollen, painful and stiff small joints of the hands and feet

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30
Q

What are the symptoms of rheumatoid arthritis?

A
  • Symmetrical swollen, painful and stiff small joints of the hands and feet
  • Pain is worse in the morning and in the cold
  • Morning stiffness can last several hours
  • Pain may improve with activity
  • Loss of function
  • General fatigue or malaise
  • Shoulder and elbows may become swollen or stiff
  • May be systemic illness (fever, weight loss, fatigue)
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31
Q

In a patient with rheumatoid arthritis when is their pain most likely to be worse?

A

In the morning and in the cold

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32
Q

What can relieve the pain experiences in rheumatoid arthritis?

A

activity

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33
Q

What are the early signs of rheumatoid arthritis?

A

Inflammation, no joint damage
Red, swollen, tender, warm joints
Swollen MCP, PIP or wrist or MTP joints (symmetrical) - usually the DIP is spared!
Tenosynovitis

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34
Q

What joint tends to be spared in the rheumatoid arthritis?

A

Distal interphalangeal joint

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35
Q

What are the later signs of rheumatoid arthritis?

A

Ulnar deviation
Boutonniere and swan-neck deformities of the fingers
Z-deformity of the thumb

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36
Q

What is the difference between boutonniere and swan neck deformities of the finger in rheumatoid arthritis?

A

Boutonniere: PIP in flexion, DIP in hyperextension

Swan neck: PIP in hyperextension, DIP in flexion

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37
Q

Name 5 extra-articular manifestations of rheumatoid arthritis?

A

Eyes

  • Dry eyes
  • Episcleritis (non-severe mild redness of the eye)
  • Scleritis (corneal ulceration - severe pain)

Neurological

  • Mild primary sensory peripheral neuropathy
  • Entrapment neuropathies (soft tissue swelling due to inflammation at the site where rigid structures contain nerves)
  • Cervical instability (usually seen in advanced disease. Erosive process that effects C1-C2 region. Can compress nerve roots)

Haematological

  • Lymph nodes may be palable
  • Spleen may be enlarged
  • Anaemia (normochromic normocytic)

Lungs

  • Pleural effusion
  • Rheumatoid nodules

Kidneys
- Amyloidosis in advanced RA. Deposits of amyloid protein cause proteinuria and renal impairment

Skin

  • Vasculitis
  • Small digital infarcts along the nail bed
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38
Q

What is needed to diagnose Rheumatoid Arthritis?

A

Clinical history
- number of joints involved - small vs large

Serology

  • Positive Rheumatoid Factor in 80%
  • Positive anti-ccp

Bloods
- Raised CRP or ESR

Duration of symptoms
- more than 6 weeks = more likely

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39
Q

What does late diagnosis of rheumatoid arthritis increase the risk of?

A

erosive joint damage

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40
Q

What are the non-pharmacological treatment options for rheumatoid arthritis?

A

Physiotherapy (improve general fitness and encourage regular exercise. Learn exercises for enhancing joint flexibility, muscle strength and managing other functional impairments)

Occupational therapy (it patients have difficulty with any of their everyday activities)

Hand exercise programmes
Consider a tailored strengthening and stretching hand exercise programme for adults with RA with pain and dysfunction of the hands

Podiatry
- May need functional insoles

Psychological interventions

  • Relaxation
  • Stress Management
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41
Q

What are the pharmacological monotherapy treatments used in Rheumatoid Arthritis?

A

Disease modifying antirheumatic drugs
ORAL METHOTREXATE or leflunomide or sulfasalazine

Alternative: hydroxychloroquine as an alternative for mild disease

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42
Q

When should you start a patient who has rheumatoid arthritis on DMARDs ?

A

Within 3 months of onset of persistent symptoms

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43
Q

What is the dual therapy used in a patient with Rheumatoid arthritis?

A

DMARD + hydroxychloroquine

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44
Q

What biological agents are there that you can use in the treatment of rheumatoid arthritis?

A

TNF-alpha inhibitors

  • Infliximab
  • Used if methotrexate is contraindicated it can be used as a monotherapy

B-cell depletion

  • Rituximab
  • Used in combination with methotrexate
  • severe RA where TNF-alpha inhibitor has failed

IL-1 and IL-6 inhibition

  • Tocilizumab
  • In combination methotrexate where TNF-alpha blocker has failed

Inhibition of T cell co-stimulation

  • Abatacept
  • Patients have not responded to DMARDs or TNF-alpha blocker
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45
Q

What are the side effects of DMARDs?

A

Immunosuppression
- increased susceptibility to infection and neutropenic sepsis
Oral ulcers
Pneumonitis

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46
Q

What is the difference in pain between rheumatoid and osteoarthritis?

A

RA : pain eases with use

OA: Pain increases with use

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47
Q

What is the difference in stiffness between OA and RA?

A

RA: significant (Over 60 mins), early morning/rest
OA: not prolonged

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48
Q

What is the difference in speed of onset of RA and OA?

A

RA: relatively rapid, over weeks-months
OA: slow progression

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49
Q

What is the difference in pattern of joints affected between RA and OA?

A

RA: small and large joints on BOTH sides of the body
OA: Symptoms often begin on one side of the body and may spread to the other side. Often limited to one set of joints

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50
Q

What form of arthritis responds to NSAIDs and what does that suggest?

A

RA - it is inflammatory

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51
Q

what is a crystal?

A

homogeneous solid in an organised pattern. They consist of ions bonded closely in an ordered, repeating, symmetric arrangement

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52
Q

what are the two crystal arthropathies in joints?

A

Urate (gotut)

Calcium pyrophosphate (pseudogout)

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53
Q

What is the pathology of gout?

A

Uric acid is produced from nucleic acid/purine metabolism

If there is excess uric acid in the blood it combines with sodium to form monosodium urate

These crystals can get deposited in joints and cause inflammation and pain

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54
Q

What serum levels can suggest that crystal deposition is likely?

A

If serum levels rise above 0.36mmol/L there is a risk of crystal deposition
If plasma concentration rises above 0.42mmol/L this is supersaturation and crystal deposition is very likely.

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55
Q

What is the key enzyme in the purine metabolism pathway?

A

xanthine oxidase

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56
Q

What are the two different presentations of gout?

A

Acute attack/ inflammation

Chronic, long term deposition

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57
Q

What are the causes of gout (under excretion of uric acid)

A 
Alcohol
Renal impairment 
Hypertension 
Hypothyroid, hyperparathyroidism 
Obesity
Diabetes (insulin resistance) 
Drugs
- Low dose aspirin decreases renal excretion 
- Diuretics (esp thiazides) 
- Cyclosporin 
- Ethambutol
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58
Q

What are the causes of gout (overproduction of uric acid)

A 
Hyperlipidemia (metabolic) 
Myeloproliferative disease 
Psoriasis
Diet 
- Alcohol
- Excess meat, shellfish, offal
- Gravy, meat extract 
- Yeast extract 
- Fructose sweetened drink
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59
Q

What are the risk factors for developing gout? Including diet.

A 
High purine diet 
- Shellfish
- Beer
- Red meat 
- Liver 
- Sugary/fizzy drinks
Kidney disease
Hyperuricaemia 
- Affects up to 10% of the population
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60
Q

Name 3 scenarios that can precipitate an acute attack of gout?

A

Aggressive introduction of hypouricemic therapy
Alcohol or shellfish binge
Sepsis
MI
Acute severe illness
Sudden cessation of hypouricemic therapy
Trauma

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61
Q

What is the clinical presentation of acute gout?

A

Development of acute pain in a joint which becomes swollen, tender and erythematous and which reaches its crescendo over a 6-12 hour period is highly suggestive of crystal arthropathy

Florid synovitis and swelling and extreme tenderness with overlying erythema. Untreated the attack resolves spontaneously over 5-15 days usually with itching over the skin.

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62
Q

What joint is most commonly affected by gout? Name 2 other joints where gout can be?

A

BIG TOE

ankle/foot
knee/finger
Elbow
Wrist

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63
Q

What investigations do you do in gout?

A

Polarized light microscopy of the crystals in the joint

Bloods: serum urate is normally raised

X-ray

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64
Q

What type of crystals are gout crystals?

A

negatively birefringent urate crystals

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65
Q

What do radiographs show in a patient with gout?

A

Early : soft tissue swelling

Late : rat bite erosions in the juxta-articular bone (these are irreversible!)

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66
Q

Name 3 preventative measures to reduce the likelihood of developing gout?

A

Lose weight
Avoid prolonged fasts
Avoid drinking excess alcohol
Avoid purine rich meats

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67
Q

What is the acute treatment for gout?

A 
High dose NSAIDs
Colchicine if NSAIDs are contraindicated
Steroids
Rest and elevate the joint 
Ice packs
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68
Q

What is the long term treatment for gout? Name two examples of these drugs?

A

Xanthine oxidase inhibitors
Allopurinol
Febuxostat

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69
Q

When would a patient need long term treatment for chronic gout?

A

Used if have had more than 1 attack in the past year, have tophi or have renal stones

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70
Q

What is the pathology of pseudogout?

A

Deposition of calcium pyrophosphate crystals on joint surface causing an acute inflammatory response

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71
Q

What may precipitate a pseudogout attack?

A 
May be precipitated by 
Dehydration 
Intercurrent illness
Hyperparathyroidism 
Surgery 
Direct trauma to the joint 
Joint lavage 
Blood transfusion

However most acute attacks are spontaneous

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72
Q

What joints are typically involved in pseudogout?

A

Typical distribution : Knee > wrist > shoulder > ankle > elbow

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73
Q

What is the usual symptom of pseudogout?

A

Often asymptomatic and is found incidentally on radiology

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74
Q

What are the symptoms of acute pseudogout?

A

Acute monoarticular arthritis - affecting the above joints
Acute joint pain and swelling (milder than gout)
Affected joints are acutely inflamed with swelling, effusion, warmth, tenderness and pain on movement (stiffness)
Resolution in 1-3 weeks

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75
Q

What are the symptoms of chronic psuedogout?

A

Can show destructive changes that resemble osteoarthritis

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76
Q

What are the differing features that distinguish pseudogout from osteoarthritis?

A

The pattern of involvement
Marked inflammatory component
Superimposition of acute attacks

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77
Q

What investigations do you do in pseudogout?

A

Joint X-ray

Aspiration of the joint fluid

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78
Q

What would a joint X-ray show in a joint that had pseudogout?

A

Shows chondrocalcinosis (deposition of CPPD crystals into fibrous or hyaline cartilage)

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79
Q

What would the joint fluid show in a patient with pseudogout

A 
Raised WCC (mainly neutrophils) 
Intracellular and extracellular weakly positive birefringent rhomboids
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80
Q

What type of crystals are pseudogout

A

weakly positive birefringent rhomboids

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81
Q

What is the type of treatment for pseudogout?

A

Symptomatic treatment

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82
Q

What is the acute treatment for pseudogout?

A

Ice packs and temporary rest
Aspiration of the joint
NSAIDs (maybe not in elderly patients)
Physiotherapy

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83
Q

What is a potential long term treatment for patients with chronic pseudogout?

A

Trial of anti-rheumatic treatment e.g methotrexate if continued inflammatory changes

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84
Q

What is osteoporosis?

A

Systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue with consequent increase in bone fragility.

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85
Q

What is bone strength determined by?

A

Bone density
Bone size
Bone quality

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86
Q

What is happens to the bone density in osteoporosis?

A

Bone density declines as we age (faster in post-menopausal women). As ageing continues the bone mass density gets low enough so that bone strength is impaired.

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87
Q

What do we measure and use to clinically diagnose osteoporosis?

A

Bone mineral density

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88
Q

What is bone mineral density?

A

Combination of how much bone you have built while the skeleton is growing and developing and how much bone you have lost over time or due to injury

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89
Q

What is the age of peak bone mass?

A

25-30

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90
Q

Why at age 50 to women have a more rapid bone loss than compared to men?

A

Oestrogen declines during the menopause

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91
Q

What happens to bone quality in osteoporosis?

A

Bone quality decreases. In post-menopausal osteoporosis, the restraining effects of bone turnover by oestrogen are lost so bone turnover increases resulting in a net less of bone.
Additionally in the microarchitecture the horizontal trabeculae connections decrease in number which decreases the strength of the structure the bone is supporting. This leads to less stable bone architecture

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92
Q

What happens to the bone size in osteoporosis?

A

Decreases

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93
Q

What are the causes of osteoporosis?

A

Increasing age + pneumonic :

SHATTERED

Steroid use
Hyperthyroidism
Alcohol 
Thin (low BMI) 
Testosterone decreased
Early menopause
Renal or liver failure
Erosive or inflammatory bone disease (RA) 
Dietary (decreased calcium, malabsorption)
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94
Q

What is the clinical presentation of osteoporosis?

A

The process that leads to established osteoporosis is asymptomatic and the condition usually presents only after a bone fracture

Be suspicious to low trauma fragility fractures

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95
Q

What investigations do you do in osteoporosis?

A

X-ray
Bone densitometry
DEXA scan
FRAX assessment to assess a fracture risk

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96
Q

What does DEXA stand for?

A

Dual energy X-ray absorptiometry

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97
Q

How do we use DEXA scanning to diagnose osteoporosis?

A

Bone mineral density is compared with that of a young healthy adult
T score is the number of standard deviations the bone mineral density is from the youthful average

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98
Q

What is the normal T score on a DEXA Scan

A

Greater than -1

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99
Q

What does a DEXA scan T score of -1 to -2.5 show?
What is the risk?
What advice do you give?

A

Osteopenia
Risk of later osteoporotic fracture
Offer lifestyle advice

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100
Q

What does a DEXA scan T score of -2.5 or worse show?

What is the management?

A

Osteoporosis
Offer lifestyle advice and treatment
Repeat DEXA in 2 years

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101
Q

What does a T score of -2.5 + a fracture show?

A

Severe osteoporosis

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102
Q

What is the non-pharmacological treatment of osteoporosis?

A 
Quit smoking 
Reduce alcohol intake 
Weight bearing exercise (may increase bone mineral density) 
Balance exercises 
Calcium and vitamin D rich diet
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103
Q

What are the pharmacological treatment options for osteoporosis?
Which is first line?
Are they anti-resorptive or anabolic?

A

FIRST LINE: Bisphosphonates
Hormone replacement therapy
Denosumab

Teriparatide (only one that is anabolic)

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104
Q

Name three examples of bisphosphonates?

A

alendronate, risedronate, ibandronate

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105
Q

What is the mechanism of action of bisphosphonates?

A

Inhibit the enzyme Farnesyl Pyrophosphate Synthase in the HMG-CoA pathway.

Stick to the hydroxyapatite on the bone surface and osteoclast resorbs the bone with the bisphosphonates on it, internalizes and disables itself slowing down bone resorption

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106
Q

Pros and cons of using HRT in treatment of osteoporosis?

A

Pros

  • reduces risk of fractures
  • stops bone loss
  • prevents hot flushes and other menopausal symptoms

Cons

  • Increase risk of breast cancer
  • stroke
  • CVD
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107
Q

What is the mechanism of action of Denosumab?

A

Monoclonal antibody to RANK ligand - slowing down osteoclast activity

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108
Q

What is the mechanism of action of teriparatide? What patients would you use this as a treatment?

A

Anabolic. Works as a PTH analogue and increases bone formation, restoring mechanical strength to the bone

It is expensive and so is reserved for patients with severe disease

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109
Q

Name three diseases that fall into the category ‘Spondyloarthritises’

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis

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110
Q

What tissue type is associated with spondyloarthritis?

A

HLA-B27

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111
Q

What is HLA-B27 and where is it expressed in the body?

Does everyone have it?

A

It is a tissue type with a role in antigen presentation within the immune system.

It is a class I surface antigen on all cells (except RBC)

You are either HLA-B27 positive or negative

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112
Q

Does everyone who is HLA-B27 positive develop spondyloarthropathies?

A

No, the vast majority of people who are B27 positive do not develop these diseases

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113
Q

What are the three theories as to why B27 is linked with spondyloarthropathies?

A
  1. Molecular mimicry
    - infection induces an immune response. Infectious agent looks like HLA-B27 peptides - generates an autoimmune response against HLA-B27.
  2. Mis-folding theory
    - unfolded HLA-B27 proteins accumulate in the ER. Proinflammatory stress response chain happens. IL-23 and IL-12 are released activating the pro inflammatory response
  3. HLA-B27 heavy chains homodimer hypothesis
    - B27 heavy chains dimerize and accumulate in the ER. Initiates a proinflammatory stress response chain
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114
Q

What are important therapeutic targets for spondyloarthropathies?

A

IL-23 and IL-12

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115
Q

Are spondyloarthropathies positive or negative for Rheumatoid Factor?

A

Negative

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116
Q

What are the features of spondyloarthritis?

A 
SPINEACHE
Sausage digit
Psoriasis
Inflammatory back pain
NSAID (good response) 
Enthesitis (inflammation of the site of insertion of tendon or ligament into bone) 
Arthritis (spinal or peripheral) 
Crohn's or colitis (may be subclinical) 
HLA-B27
Eye (iritis)
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117
Q

What is enthesitis?

A

inflammation of site of insertion of tendon or ligament into bone

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118
Q

Define ankylosis?

A

abnormal stiffening and immobility of joint due to new bone formation

119
Q

What is the pathology of ankylosing spondylitis?

A

There is chronic inflammation of the spine, ribs and sacroiliac joints.

Then there is erosive damage repair where fat is lay down in the corners of bone (irreversible)

Then there is new bone formation and bony proliferations due to enthesitis- which can fuse with the above vertebrae in the spine.

In later stages of the disease these can calcify causing bamboo spine

120
Q

Aetiology of ankylosing spondylitis?

A

Unknown

121
Q

Risk factor for ankylosing spondylitis?

A

HLA-B27

122
Q

What is the clinical presentation of Ankylosing Spondylitis?

A

Inflammatory back pain

Progressive loss of spinal movement in all directions and thoracic expansion is decreased

Peripheral enthesitis

Peripheral arthritis

Characteristic spinal abnormalities

123
Q

What are the features of the inflammatory back pain experienced in ankylosing spondylitis?

A

Gradual onset of lower back pain
Worse at night
Spinal morning stiffness that may be relieved by exercise
Pain may radiate to the hips/buttocks

124
Q

What is usually the first manifestation of ankylosing spondylitis?

A

Episodic inflammation of the sacroiliac joints (where it starts) in the late teens / early twenties is usually the first manifestation of the disease.

125
Q

What are the common peripheral enthesitis that can present as ankylosing spondylitis?

A

Achilles tendonitis
Plantar fasciitis
Tibial tuberosity

126
Q

What is the joint involvement in peripheral arthritis that present in 1/3 of patients with ankylosing spondylitis?

A

Joint involvement is usually asymmetrical

Involves hips, shoulder girdle, joints of the chest wall and symphysis pubis

127
Q

What are the characteristic spinal abnormalities in patients with ankylosing spondylitis?

A 
Loss of lumbar lordosis (normal inward curving of the spine) 
Increased kyphosis (rounded back) 
Reduced spinal flexion 
Vertebral syndesmophytes are characteristic
128
Q

Vertebral syndesmophytes are often characteristic of ankylosing spondylitis. What are they?

A

Bony proliferation due to enthesitis between ligaments and vertebrae. They fuse with the vertebrae above causing ankylosis
Later, in more advanced disease, calcification of ligaments with ankylosis lead to a bamboo spine appearance

129
Q

What investigations do you do in ankylosing spondylitis?

What do they show?

A

MRI

  • Detection of active inflammation (bone marrow oedema)
  • Shows destructive changes
    • Sacroiliitis (one or both sacroiliac joints becomes inflamed)
      - Erosions
      - Sclerosis
      - Ankylosis

X-ray
- Can show sacroiliac joint space narrowing or widening, sclerosis, erosions and fusion

130
Q

What is the diagnostic criteria for ankylosing spondylitis in a patient who has had 3 or more months of back pain and age of onset is less than 45?

A

Sacroiliitis on imaging + 1 or more SpA feature

HLA-B27 + 2 or more SpA features

131
Q

What is the treatment for ankylosing spondylitis?

A

Exercise for backache
Intense exercise regimes
Specialist physiotherapist
Maintain posture and mobility

NSAIDs
Usually relieve symptoms within 48 hours and may slow radiographic progress

TNF-alpha blockers
Etanercept, adalimumab
Severe disease

Local steroid injections

Surgery
Hip replacement
Rarely : spinal osteotomy

132
Q

Name 2 TNF-alpha blockers that can be used in the treatment of ankylosing spondylitis?

A

Etanercept, adalimumab

133
Q

Ankylosing spondylitis is associated with an increased risk of what other disease? What could you give to minimise this risk

A

There is an increased risk of osteoporitic fractures so consider bisphosphonates

134
Q

What is psoriatic arthritis? What patients can develop this condition?

A

Chronic inflammatory disease of the joints and the places where tendons and ligaments connect to bone. The immune system creates inflammation that can lead to swelling, pain, fatigue and stiffness in the joints.

Occurs in 10-40% of people with psoriasis but it can develop without having psoriasis!

135
Q

Name 2 risk factors of psoriatic arthritis?

A

Associated with HLA-B27

Risk factors: history of psoriasis, have psoriasis

136
Q

What are the symptoms of psoriatic arthritis?

A

Joint stiffness
Pain and swelling
Tenderness of the joints and surrounding ligaments and tendons

137
Q

What are the 5 patterns of disease of psoriatic arthritis

A

Symmetrical polyarthritis of small joints

Distal interphalangeal joints only
Most typical. Often with adjacent nail dystrophy

Asymmetrical large joint oligoarthritis (2-4 joints)

Axial (spinal)

Psoriatic arthritis mutilans

138
Q

What is the characteristic appearance does psoriatic arthritis mutilans?

A

Resorption of the terminal phalanx, giving a telescopic, shortened digit appearance

139
Q

What is the most common pattern of psoriatic arthritis disease?

A

DIP joints involvement only

140
Q

Where are hidden sites for psoriasis?

A

behind/inside the ear, scalp, pitting in nails or onycholysis (nail lifts off the nail bed and looks brittle and flaky), umbilicus, penile psoriasis

141
Q

What sign may you see on radiology in a patient with psoriatic arthritis?

A

Erosive changes with pencil in a cup deformity in severe cases

142
Q

What is the treatment options for psoriatic arthritis?

A

NSAIDs to relieve MSK symptoms

Early intervention with DMARDs

  • Methotrexate
  • Leflunomide

Anti-TNF drugs

  • Etanercept
  • Adalimumab

IL-12 and IL-23 blockers
- Ustekinumab

143
Q

What is reactive arthritis?

A

Sterile inflammation of the synovial membrane, tendons, fascia triggered by an infection at a distant site

144
Q

Aetiology of reactive arthritis?

A

Autoimmune response to infection elsewhere in the body

Gut associated infections
Salmonella
Shigella
Yersinia

STIs
Chlamydia

145
Q

What is the characteristic triad of symptoms associated with reactive arthritis?

A 
Arthritis 
- Typically 2 - 14 days post infection
- Pain and inflammation in the joint 
 Conjunctivitis 
Sterile urethritis
146
Q

Aside from the triad, what other symptoms are present in reactive arthritis?

A

Iritis
Keratoderma blennorrhagica (brown, raised plaques on the soles and palms)
Circinate balanitis (painless penile secretion due to chlamydia)
Mouth ulcers
Enthesitis

147
Q

What investigations do you do in reactive arthritis?

A 
Inflammatory markers
- Increased ESR and CRP 
Stool culture if there is diarrhoea
Infectious serology
Aspirate joint to exclude infection or crystals 
Contact tracing if necessary (chlamydia)
148
Q

What is the treatment for reactive arthritis?

A

Splint the affected joints acutely

NSAIDs or local steroid injections

149
Q

What is septic arthritis ?

A

The invasion of a joint by an infectious agent resulting in joint inflammation.

150
Q

What is the most frequent pathogen responsible for septic arthritis?

A

Staph aureus

151
Q

Name 3 organisms that can cause septic arthritis?

A 
Staph aureus
Streptococci - Gp A (beta haemolytic) 
Neisseria gonorrhoea 
Gram negative bacilli 
- E.coli 
- pseudomonas aeruginosa
152
Q

What are 3 risk factors that increase your likelihood for developing septic arthritis?

A 
Increasing age 
IVDU
Diabetes
Prior joint damage 
- Rheumatoid arthritis 
-Gout
-Systemic connective tissue disorder 
Joint surgery 
Hip or knee prosthesis
Immunodeficiency 
Immunosuppression
Chronic renal failure
153
Q

Clinical presentation of septic arthritis?

What are the majority of cases?

A

Painful, red, hot swollen joint
Pain on active or passive movement

Fever

90% of cases are monoarthritis

154
Q

What joints does septic arthritis tend to affect?

A

Affects mainly Knee > hip > shoulder

155
Q

What is the investigation in septic arthritis?

A

Urgent joint aspiration for synovial fluid microscopy and culture
Must be done with patient off antibiotics for 2 weeks at least

Blood cultures

156
Q

What is the treatment for septic arthritis?

A

Antibiotics guided by the results of the aspiration
Can start empirical IV antibiotics until sensitivities are known

Long course antibiotics
At least 6 weeks
Flucloxicillin

Joint wash out / repeat aspiration until there is no recurrent effusion

Rest/splint/physiotherapy

Analgesia

Stop any immunosuppression temporarily if you can

157
Q

Name three techniques used to prevent infection in joint prosthesis surgery?

A
  • Barrier between surgical and anaesthetic team
  • Aseptic techniques
  • Cement used has antibiotics in
  • Give patients systemic antibiotics as prophylaxis (usually gentamicin)
158
Q

What is the presentation of an infected joint prosthesis?

A
  • Scar can be red and hot and swollen
  • Pus
  • Most of time presentation is subtle and can be difficult to make a diagnosis
159
Q

What features on an X-ray may suggest that the joint prosthesis is infected?

A

features suggestive of infection

  • periosteum is fluffy around the joint replacement
  • lytic areas

Irritable joint

160
Q

What may the inflammatory markers be like in an infected prosthetic joint?

A

Increased ESR and CRP

161
Q

What are the treatment options for an infected prosthetic joint?

A
  1. Antibiotic suppression (patients that are unfit for surgery)
  2. Debridement and retention of prosthesis (do when infection is acute)
  3. Excision arthroplasty (take out the infected joint with no plan to put in a replacement)
  4. One stage exchange arthroplasty (take out the old joint and replace with new one straight away)
  5. Two stage exchange arthroplasy (take the joint out and leave it for a while and then put it back)
  6. Amputation
162
Q

What is osteomyelitis?

A

Infection localized to the bone

163
Q

What is the difference between acute and chronic osteomyelitis?

A

Acute: associated with inflammatory bone changes caused by pathogenic bacteria

Chronic: involves bone necrosis

164
Q

What is the routes of transmission that cause osteomyelitis. Who is most likely to develop which OM?

A

Children mainly have acute haematogenous osteomyelitis

Adults mainly have contiguous osteomyelitis

165
Q

What is the pathology of haematogenous osteomyelitis in children?

A

In long bone (children) the metaphysis is very metabolically active so has a large flow of blood.
Vasculature penetrates the midshaft and then goes to either end of the long bone to form vascular loops in the metaphysis.
In the metaphysis the blood flow is slower and there are no endothelial basement membranes. Capillaries also lack phagocytic lining cells. These factors allow transmission of bacteria from the blood to this site allowing the growth of microorganisms.

166
Q

Adults can get haematogenous osteomyelitis as well, where are they most likely to get this and why?

A

Can get this type of transmission in adults but it is in the vertebrae as they become more vascular with age

167
Q

What is contiguous spread that causes osteomyelitis mainly in adults?

A

Spread of infection from adjacent soft tissues and joints to bone.

168
Q

What are 3 risk factors that increase a persons risk for developing osteomyelitis?

A 
Vascular supply 
- Arterial disease
- Diabetes
- Sickle Cell
Pre-existing bone/joint problems 
Immune deficiency / immunosuppression 
Behavioural 
Increasing the risk of trauma
169
Q

What are the causative organisms of osteomyelitis?

A 
Staphylococcus aureus 
MRSA
Coagulase negative staphylococci 
Aerobic Gram-negative bacilli 
In the immunocompromised
- Fungi 
- Mycobacterium tuberculosis 
Sickle cell
- Salmonella
170
Q

What are the symptoms of osteomyelitis?

A

Onset over several days
Dull pain at the site of infection
May be aggravated by movement

171
Q

What are the signs of osteomyelitis?

A

Systemic

  • Fever
  • Rigors
  • Sweats
  • Malaise

Local
Acute : tenderness, warmth, erythema, swelling
Chronic : swelling, tenderness, deep/large ulcers that fail to heal despite several weeks treatment, non-healing fractures

172
Q

What investigations do you do in osteomyelitis?

A

Labs
Acute : Increased WCC, Increased ESR and CRP

Chronic : Can all be normal

X-rays

MRI

Bone biopsy

Blood cultures

173
Q

What is the benefit of using MRI compared to X-rays in diagnosing osteomyelitis?

A

X-rays have poor sensitivity and specificity in early osteomyelitis whereas MRI can show marrow oedema after 3-5 days

174
Q

What may X-rays show in chronic osteomyelitis (name 2 things) ?

A 
Cortical erosions
Periosteal reaction 
Mixed lucency
Sclerosis
Sequestra (dead bone tissue formed within a diseases or injured bone) 
Soft tissue swelling
175
Q

What does a bone biopsy of a patient with osteomyelitis show?

A

Histology shows inflammatory exudate in the marrow

Shows osteonecrosis

176
Q

What is the treatment options for osteomyelitis?

A

Surgical
Debridement
Replacement or removal of bone

Antimicrobial
Start broad spectrum empirical therapy : FLUCLOXACILLIN
Then later tailor the antibiotics to the culture and sensitivities
Prolonged duration of antimicrobials
Need to consider the bone penetration of the drugs

177
Q

What antibiotic do you start patients with osteomyelitis on?

A

Flucloxacillin

178
Q

What is Systemic Lupus Erythematosus ?

A

Multisystemic autoimmune disease.

179
Q

What is the pathology of SLE?

A
  1. Cells die by apoptosis and cellular remnants (e.g DNA, histones that are normally hidden from the immune system) appear on the cell surface as small blebs.
  2. In SLE the removal of blebs is inefficient
  3. Blebs are transferred to the lymphoid tissue where are taken up to become an antigen presenting cell
  4. Self-antigens from blebs are presented to T cells which stimulate B cells to produce autoantibodies directed against the antigens
  5. These autoantibodies either form circulating complexes or deposit by binding directly to tissues
  6. Activation of complement and influx of neutrophils → inflammation
  7. Abnormal cytokine production → increased IL-10 and interferon alpha
  8. High activity of inflammation
180
Q

What is the cause of SLE?

A

unknown

181
Q

What are the genetic associations in SLE?

A

HLA-DR2

HLA-DR3

182
Q

What are the symptoms of SLE? What organs are involved?

A 
Fatigue 
Malaise
Arthritis 
- Symmetrical 
- Less proliferative than rheumatoid arthritis 
- Can be deforming 
- Non-erosive 
- 90% of cases 
Mouth ulcers (v common) 
SKIN
Butterfly rash - acute 
Discoid rash - chronic
Can have photosensitive rashes
Alopecia 
Raynaud’s phenomenon

LUNG
Recurrent pleural effusions

KIDNEY
Glomerulonephritis with persistent proteinuria

CNS
Depression
Epilepsy
Seizures (with no causative agent)

EYES
Retinal vasculitis 
Episcleritis 
Conjunctivitis 
Sjogren’s 
Other
Weight loss
Arterial thrombosis 
Anaemia 
Thrombocytopenia
Neutropenia
Lymphopenia
183
Q

What tests do you do in SLE?

A

Immunology
Inflammatory markers
Screening for major organ involvement
Complement

184
Q

What immunological markers are you looking for in a patient with SLE?

A

Positive antinuclear antibody
High anti-dsDNA is highly specific
Extractable nuclear antigen may be positive
Antiphospholipid antibodies may be positive

185
Q

What is the treatment for SLE?

A

Patient education and support
UV protection
Hydroxychloroquine
Topical steroids for skin flares (rashes)

186
Q

What is the treatment for severe SLE?

A 
High dose prednisolone 
Cytotoxic drugs 
- Azathioprine 
- Cyclophosphamide
- Ciclosporin 
- Mycophenolate

Anticoagulants for antiphospholipid syndrome

Biological therapies

  • Rituximab
  • Belimumab
187
Q

What is antiphospholipid syndrome?

A

Body’s immune system produces abnormal antiphospholipid antibodies.

Immune system produces these that mistakenly bind to the phospholipid surface on blood cells and endothelium.

Causes the blood to clot more easily.

188
Q

Clinical presentation of antiphospholipid syndrome?

A 
Thrombosis 
Livedo reticularis - lace like purplish discolouration of the skin
Miscarriage (recurrent) 
Ischaemic stroke 
Thrombocytopenia
189
Q

Treatment of antiphospholipid syndrome?

A 
Anticoagulant (warfarin, low dose aspirin, heparin)
Don't smoke
Eat a healthy and balanced diet 
Regular exercise
Maintain a healthy body weight
190
Q

What can cause bone pain?

A

Myeloma
Lymphoma
Primary bone tumours
Secondary bony metastases

191
Q

Name 4 malignant primary bone tumours?

A

Osteosarcoma
Ewing’s sarcoma
Fibrosarcomas
Chondrosarcoma

192
Q

What are the 5 most common tumours that form bony mets?

A 
Breast 
Lung 
Prostate
Kidney
Thyroid
193
Q

What are the red flag signs in bone tumours?

A 
Rest pain
Night pain
Lump present 
- Tender
- Enlarging 
- Deep to fascia
- Above 5cm in diameter
Loss of function 
Neurological symptoms 
Unwell/weight loss
194
Q

What are three special signs that you may be able to see on an X-ray in a patient with bone tumour?

A

Codman’s triangle
Sunburst appearance
Onion skin appearance

195
Q

What investigations can you do in a patient who presents with a bony mass?

A 
Blood tests (FBC, U&Es, Ca2+, ALP (usually raised))
Plain X-rays
- looks for definition, bone density, periosteal reaction 
Ultrasound
- Assessing soft tissue masses 
CT Scan
- does 3D construction which can help plan plan resection 
- also used for staging 
MRI
- Soft tissue involvement of bony mass
- Skip lesions 
Bone scan
Biopsy
196
Q

What is Codman’s triangle?

A

triangular area of new subperiosteal bone that is created when a lesion, often a tumour, raises the periosteum away from bone

197
Q

What is a sunburst appearance on X-ray?

A

Occurs when the lesion grows too fast and the periosteum does not have enough time to lay down a new layer

198
Q

What is an onion skin appearance on X-ray?

A

multiple concentric parallel layers of new bone adjacent to the cortex. Thought to be due to periods of variable growth

199
Q

These are the prefixes, who would each tumour relate to?

  1. Osteo
  2. Chondro
  3. Rhabdomyo
  4. Lipo
A
  1. bone
  2. cartilage
  3. skeletal muscle
  4. fat
200
Q

These are suffixes, what does each one mean?

  1. ..oma
  2. …sarcoma
  3. ..carcinoma
  4. ..blastoma
A
  1. benign
  2. malignant connective tissue
  3. malignant epithelial/endothelial tumour
  4. malignant tumour of embryonic cells
201
Q

What is the pathology of osteosarcoma?

A

Spindle cell neoplasms that produce osteoid (the unmineralized organic compound of bone)

202
Q

What are osteosarcomas associated with?

A

Associated with p53 mutation

203
Q

Name the three places most likely for osteosarcoma to present?

A

Knee
Proximal humerus
Distal femur

204
Q

How may an osteosarcoma present?

A

Pulmonary metastases in 10-20%

High-grade is a relatively painless tumour.

Lump present

205
Q

What would the X-ray show of an osteosarcoma?

A

Codman’s triangle

Sunburst appearance

206
Q

Treatment for osteosarcoma?

A

Multi-agent chemotherapy pre-operative 8-12 weeks

Limb salvage surgery

207
Q

What cells does Ewing’s sarcoma arise from?

A

Arises from neural crest cells

208
Q

Where does Ewing’s sarcoma commonly present?

A

Femur

(pelvis, distal tibia, proximal humerus_

209
Q

What is Ewing’s sarcoma associated with?

A

Banded translocation t(11;22)

210
Q

What is the average age of onset for Ewing’s sarcoma>

A

15

211
Q

What are the symptoms of Ewing’s sarcoma?

A 
Painful swelling 
Redness in the area surrounding the tumour
Malaise
Anorexia
Weight loss
Fever
Paralysis 
Numbness in the affected limb
212
Q

What type of lesion is Ewing’s sarcoma usually?

A

diaphyseal lesion and presents with a mass/swelling in the long bones

213
Q

What would the X-ray show in a patient with Ewing’s sarcoma?

A

Onion skin appearance

Codman’s triangle, sunburst appearance

214
Q

What would the bone biopsy of a Ewing’s sarcoma tumour show?

A

Monotonous blue cell tumour
Indistinct cell borders
No matrix production by the tumour cells

215
Q

What is the treatment for Ewing’s sarcoma?

A

Chemotherapy
Radiotherapy
Surgical excision / reconstruction

216
Q

What is a chondrosarcoma?

A

Cancer of the cartilage

Most common adult sarcoma

217
Q

What is the presentation of a chondrosarcoma?

A

Dull deep pain

Affected area is swollen and tender

218
Q

Where do chondrosarcomas typically present?

A

Pelvis

219
Q

What is the treatment for chondrosarcoma?

A

Surgery and adjuvant chemotherapy

220
Q

What are the symptoms of bony metastases?

A

Bone pain

Systemic symptoms such as malaise, pyrexia, anorexia, weight loss

221
Q

What investigations do you do in bony metastases? What do they show?

A

Skeletal isotope scan
- Show bony mets before radiological changes occur
X-rays
- May show mets as osteolytic areas with bony destruction
- Osteosclerotic mets (increased bone density) are characteristic of prostate carcinoma

222
Q

What are the treatment options for bony metastases?

A

Analgesics and anti-inflammatory drugs

Local radiotherapy to bone mets relieves pain and reduces risk of fracture

Some may respond to chemotherapy

Some tumours are hormone dependent and may respond to hormonal therapy

Bisphosphonates help symptomatically

223
Q

What are 5 risk factors that may increase likelihood of developing fibromyalgia?

A 
Depression
Anxiety
Stress
Dissatisfaction at work
Middle aged
Low income
Divorced
Low educational status
224
Q

What are the symptoms of fibromyalgia?

A

Chronic widespread pain associated with unrefreshing sleep and tiredness

Chronic pain at multiple sites and widespread
- Lower back pain with/without radiation to the buttocks and legs and pain in the neck and across shoulders

Fatigue
Sleep disturbance
Morning stiffness
Problems with cognition 
- Poor concentration 
Fluctuations in weight 
Anxiety and depression
225
Q

What makes the symptoms of fibromyalgia worse?

A

cold weather
humid weather
stress

226
Q

What investigations do you in fibromyalgia?

A 
Bloods will all be normal
FBC
ESR
CRP
CK
TFTs
Ca2+

Pain at 11 out of 18 tender points on digital palpation (neck, back, elbows, hips, lower back, knees)

Full social, personal, family and psychological history should be taken.

227
Q

how is fibromyalgia diagnose?

A

diagnosed after other diseases have been excluded

228
Q

What is the non-pharmacological treatment for fibromyalgia?

A

Educate the patient and family

Exercise programmes
Aerobic exercise
Strength training 
Tailored programmes to the individual 
Cognitive behavioural therapy

Relaxation, rehabilitation, physio and psychological support

229
Q

What is the pharmacological treatment for fibromyalgia?

A

Paracetamol, weak opioids, tramadol
Venlafaxine - antidepressants
Pregabalin - small benefit in reducing pain and sleep problems

230
Q

What can is the pathology of mechanical back pain?

A

Spinal movement occurs at the disc and the posterior facet joints - stability is normally achieved by a complex mechanism of spinal ligaments and muscles.

Any of these structures may be a source of pain

231
Q

Name 3 causes of mechanical lower back pain?

A 
Lumbar disc prolapse
Osteoarthritis 
Fractures
Spondylolisthesis 
Heavy manual handling 
Stooping and twisting whilst lifting 
Exposure to whole body vibration
232
Q

Name 3 risk factors for mechanical back pain?

A

Risk Factors
Psychosocial distress
Smoking and dissatisfaction with work

Risk factors for recurrent back pain
Female
Increasing age 
Pre-existing widespread chronic pain
Psychosocial factors (high levels of distress, poor self-rated health)
233
Q

What are the symptoms of mechanical back pain?

A

Back is stiff and scoliosis may be present when the patient is standing
Muscular spasm is visible and palpable and causes local pain and tenderness
Pain is often unilateral and helped by rest
Episodes are generally short lived and self-limiting
Sudden onset
Pain is worse in the evening
Morning stiffness is absent
Exercise aggravates pain

234
Q

What are the red flag signs for serious spinal pathology?

A 
Age of onset is less than 20 or over 55
Violent trauma (fall, RTC) 
Constant-progressive, non-mechanical back pain
Thoracic pain
Systemic steroids, drug abuse, HIV
Systemically unwell, weight loss
Widespread neurology
Persisting severe restriction of lumbar flexion 
Structural deformity
235
Q

What investigations do you do in mechanical back pain?

A

Spinal X-rays are only used if a red flag sign occurs

MRI

Bone scans

236
Q

What is the treatment for mechanical back pain?

A

Analgesic - paracetamol, NSAIDs

Physiotherapy, back muscle training regimens and manipulation

Acupuncture

AVOID excessive rest

Re-education in lifting and exercises to prevent further attacks of pain

Comfortable sleeping position

237
Q

What is osteomalacia?

A

Poor bone mineralisation after the fusion of the epiphyses in an adult leading to soft bone due to the lack of Ca2+.

238
Q

What is the aetiology of osteomalacia?

A 
Hypophosphatemia
Vitamin D deficiency
Renal disease
Drug induced
Liver disease
Tumour induced
239
Q

How can Hypophosphatemia lead to osteomalacia?

A

Due to hyperparathyroidism
Excess release of PTH results in decreased absorption of phosphate in the kidneys resulting in more excretion in the urine in response to a decreased Ca2+ absorption

240
Q

How may someone be vitamin D deficient?

A

Malabsorption
Since vitamin D is fat soluble, may be due to GI disease
Poor diet
Lack of sunlight

241
Q

How can renal disease cause osteomalacia?

A

Renal failure means that there is inadequate conversion of 25-hydroxyvitamin D to 1,24-hydroxyvitamin D

242
Q

What are the symptoms of osteomalacia?

A

Muscle weakness
Waddling gait
Difficulting climbing stairs
Difficulting getting out of a chair

Bone pain and tenderness

Fractures
Particularly of the femoral neck

243
Q

What tests do you do in osteomalacia?

A

Bloods
Biopsy
X-rays

244
Q

What do the blood tests show in a patient with osteomalacia?

A 
Low Ca2+ 
Low phosphate 
Raised ALP 
Elevated PTH
Low 25-hydroxyvitamin D
245
Q

What does the bone biopsy show in a patient with osteomalacia?

A

incomplete mineralisation

246
Q

What does the X-ray show in a patient with osteomalacia?

A

Shows defective mineralisation
Looser’s pseudofractures/zones
- Low density bands extending from the cortex inwards in the shafts of the long bones

247
Q

What is the treatment for osteomalacia where the cause is…

  1. lack of dietary vitamin D?
  2. lack of vitamin D caused by malapsorption?
  3. Renal disease
A
  1. Calcium D3 forte
  2. Oral ergocalciferol
  3. Alfacidol
248
Q

What are the vasculitides?

A

inflammatory disorders of the blood vessel.

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

  • vessel wall destruction
  • endothelial injury
249
Q

How are vasculitide diseases classified?

A

Size of the blood vessel

Presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA)

250
Q

What vessels are classified as large vessels in vasculitis?

A

Branches of the aorta

  • common carotid
  • subclavian
  • pulmonary
  • axillary
  • brachial
  • renal
  • iliac
  • femoral
251
Q

What vessels are medium size in vasculitis?

A

Medium and small sized arteries and arterioles

252
Q

What vessels are small in vasculitis?

A 
small arteries
small arterioles
venules
capillaries
tend to be ANCA positive
253
Q

What conditions are associated with secondary vasculitus?

A 
Subacute infective endocarditis
Vasculitis with rheumatoid arthritis
SLE
Scleroderma
Polymyositis 
Good pasture syndrome and IBC (crohn's and UC)
254
Q

What is the pathology of giant cell arteritis?

A

Inflammatory granulomatous arteries of large cerebral arteries as well as other large vessels (e.g aorta) which occurs in association with polymyalgia rheumatica in 50% of cases

Arteries become inflamed, thickened and can obstruct blood flow.
Activation of dendritic cells in the adventitia
Recruitment and activation of T cells
Recruitment of CD8+ cells and monocytes
Vascular damage and remodelling

255
Q

What arteries are affected in giant cell arteritis?

A

Cerebral

Commonly temporal arteries

256
Q

What are the symptoms of giant cell arteritis?

A

Symptoms
Headache that is : new, abrupt, unilateral and temporal pulsating
Temporal artery and scalp tenderness
Tongue/jaw claudication
Indicates a high risk of ischaemic complications

Visual disturbances
Amaurosis fugax
Diplopia
SUDDEN UNILATERAL BLINDNESS: medical emergency that needs to be treated ASAP. Optic disc is pale/swollen

Extracranial symptoms 
Malaise
Myalgia
Dyspnea
Weight loss
Morning stiffness
Unequal or weak pulses
257
Q

What are the signs of giant cell arteritis?

A

Temporal arteries may be prominent, beaded, tender and pulseless
Fever

258
Q

What are the complications of giant cell arteritis?

A

Stroke

Visual loss

259
Q

What tests do you do in giant cell arteritis?

A

Blood tests
Temporal artery biopsy (take a large sample as skip lesions occur)
Ultrasound
PET-CT scan

260
Q

What are the blood results in a patient with GCA?

A 
ESR and CRP are high 
High platelets 
High ALP
Low Hb
ANCA negative
261
Q

What are the histological features of the temporal artery biopsy ?

A

Cellular infiltrates of CD4+ T lymphocytes, macrophages and giant cells in the vessel wall
Granulomatous inflammation of the intima and media
Breaking up of the elastic lamina

262
Q

What is the treatment for GCA?

A

Start prednisolone immediately

  • Stops vision loss
  • High dose
  • Gradual reduction of steroids over 12-18 months. Reduce once symptoms have resolved and ESR has decreased.

Give GI and bone protection

  • Lansoprazole
  • Alendronate
  • Calcium
  • Vitamin D
263
Q

If you cannot wean a patient with GCA off glucocorticoids what is the next treatment option?

A

If failure to wean of glucocorticoids
DMARDs
Tocilizumab

264
Q

What are three key conditions of ANCA associated vasculitis?

A

Granulomatosis with polyangiitis (PR3 ANCA pattern)
Eosinophilic granulomatosis with polyangiitis
Microscopic polyangiitis (MPO-ANCA pattern)

265
Q

What vessels do ANCA associated vasculitis affect?

A

Small

266
Q

Pathology of ANCA associated vasculitis

A

Anti-neutrophil cytoplasmic antibodies can activate primed circulating neutrophils causing them to enter the vessel wall and cause fibrin deposition

267
Q

Symptoms of ANCA associated vasculitis?

A 
ENT symptoms 
Epistaxis
Crusts
Stuffiness
Hearing loss
Hoarseness
Stridor
Iritis 
Cough
Rash (red dots on fingers) 
Numbness, tingling, foot/wrist drop 
Joint pain, swelling 
- Asymmetric polyarthritis
268
Q

What investigations do you do in ANCA associated vasculitis?

A 
ANCA testing 
Tissue biopsy 
Assessment of organ involved
CT thorax (abdo/pelvis - exclude malignancy, look for lung nodules) 
Urine protein/creatinine ratio
CT head/sinuses/neurophysiology 
Bony erosions
Mononeuritis multiplex
269
Q

What is the treatment for ANCA associated vasculitis?

A

Induction into remission
Glucocorticoids
Cyclophosphamide OR Rituximab
Plasma exchange if the patient has pulmonary haemorrhage or severe renal disease

Maintenance of remission
DMARDs
Taper glucocorticoid

270
Q

what is acute vertebral disc prolapse often caused by?

A

strenuous activity

271
Q

Symptoms of acute vertebral disc prolapse

A

Sudden onset of back pain (usually lumbar region)
Pain is aggravated by movement
Muscle spasm leads to a sideways tilt when standing
Radiation of pain and clinical findings depend on the disc

272
Q

What are the features of a root lesion at S1?

A

(buttock pain down back of thigh to ankle/foot. Loss of ankle jerk reflex)

273
Q

What are the features of a root lesion at L4?

A

(pain across knee to medial malleolus. Lost knee jerk reflex)

274
Q

What are the features of a root lesion at L5?

A

L5 (pain from buttock to lateral aspect of leg and top of foot)

275
Q

Investigations in acute vertebral disc degeneration?

A

X-ray

MRI in surgery is being considered

276
Q

Treatment of acute vertebral disc degeneration?

A

Bed rest on a firm mattress
Analgesia
In severe cases - epidural corticosteroid injection

Surgery only if severe or increasing neurological symptoms

Physiotherapy in the recovery phase

277
Q

What is chronic vertebral disc degeneration associated with?
Symptoms?
Treatment?

A

degenerative changes in the lower lumbar discs and facet joints
Mechanical pain
Sciatic radiation may occur
Pain is long-standing
NSAIDs, physiotherapy and weight loss can be helpful

278
Q

What is the pathology of Paget’s disease?

A

Increased bone turnover associated with increased numbers of osteoblasts and osteoclasts

Bone remodelling, bone enlargement, deformity and weakness

Increased bone mass but the bone is disordered and weak

279
Q

Symptoms of Paget’s disease?

Where does it typically present?

A

Asymptomatic in 70%
Dull, boring pain
Bony enlargement and deformity

Typically of
Pelvis
Lumbar spin
Skull 
Femur
Tibia
280
Q

Complications of Paget’s disease?

A 
Pathological fracture
Osteoarthritis 
Increased Ca2+ 
Nerve compression due to bone overgrowth (deafness) 
Osteosarcoma
281
Q

investigations in Paget’s disease?

A

X-ray

Bloods

282
Q

what does the X-ray of a patient with Paget’s disease show?

A

Localized enlargement of bone
Patchy cortical thickness with sclerosis
Osteolysis
Deformity

283
Q

Treatment for Paget’s disease?

A

Analgesia

Alendronic acid may be tried to reduce pain and / or deformity

284
Q

What complications can occur with a fracture?

A 
Nerve injury 
Damage to blood supply
Contamination 
Compartment syndrome 
Fat embolism
Shock 
Crush syndrome 
PE
Pneumonia
285
Q

Why does crush syndrome cause kidney failure?

A

Myoglobin is released that blocks the kidneys

286
Q

What are late complications of a fracture?

A 
Delayed union 
Non-union
Mal-union
Avascular necrosis 
Arthritis 
Osteomyelitis
287
Q

What can increase a person’s risk of delayed union/non-union of a fracture

A

Smoker
Diabetic
Steroids

288
Q

What is the blood supply to the femur

A

comes from the medial femoral circumflex artery

Supply comes distal and goes proximal

289
Q

What 2 fractures are usually associated with avascular necrosis?

A

hip and scaphoid

290
Q

what is the presentation of a femoral fracture?

A

Externally rotated and short leg
groin pain
inability to weight bare
pain on axial loading

291
Q

Management of a femoral fracture

A

Morphine
Regional nerve block
If intracapsular - surgical may need a hemi or total hip replacement

292
Q

What is compartment syndrome?

A

There is damage to the blood supply which causes veins to collapse to blood enters the compartment. The fascia means that blood continues to build up in the compartment and compresses the nerves

293
Q

What are the features of compartment syndrome?

A

Pain that is disproportionate to injury - passive stretching of the muscle in the calf makes symptoms worse

Pain
Pallor
Perishingly cold
Paralysis
Pulselessness
294
Q

Treatment of compartment syndrome?

A

Fasciotomy

Phase 2A (11 decks)

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