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Phase 2a > MSK > Flashcards

MSK Flashcards

1
Q

Define osteoarthritis

A

‘wear and tear’ of the joints

Result of mechanical and biological events.

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2
Q

Describe the pathophysiology of osteoarthritis

A

Destabilise normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix and subchondral bone.

Imbalance between cartilage damage and the chondrocyte response.

Involves the entire joint

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3
Q

Name the commonly affected joints in osteoarthritis

A

Hips
Knees
DIP joints in hands
CMC joints at the base of the thumb
Lumbar spine
Cervical spine

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4
Q

Name the 4 x-ray changes that would be seen in osteoarthritis

A

LOSS

Loss of joint space
Osteophytes - bone spurs

Subarticular sclerosis - increased density of the bone along the joint line

Subchondral cysts - fluid filled holes in the bone

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5
Q

What are the causes of osteoarthritis

A

Multi-factorial disease

Genetic
Biological
Chemical

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6
Q

Risk factors of osteoarthritis

A

Age > 50 years
Female sex
Obesity
Genetic factors - family history
Physically demanding occupation/sport
Post trauma/injury

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7
Q

Describe the main symptoms of osteoarthritis

A

Joint pain and stiffness

Worse with activity and end of day

Reverse of the pattern in inflammatory arthritis

Results in - deformity, instability and reduced function of the joint

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8
Q

Name the clinical signs of osteoarthritis

A

Bulky, bone enlargement of the joint

Restricted range of motion

Crepitus on movement

Effusions (fluid) around the joint

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9
Q

By NICE guidelines what is the diagnosis of osteoarthritis

A

Diagnosis can be made with no investigations if

Patient over 45 + typical pain is associated with activity + no morning stiffness (or lasts under 30 minutes)

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10
Q

Describe the management of osteoarthritis

A

Patient education + lifestyle change

Topical NSAIDs - 1st line knee
Oral NSAIDs

Weak opiates and paracetamol

Intra-articular steroid injections

Joint replacement

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11
Q

Name 5 differential diagnosis of osteoarthritis

A

Bursitis
Gout
Pseudogout
Rheumatoid arthritis
Psoriatic arthritis

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12
Q

Define rheumatoid arthritis

A

Autoimmune condition that causes chronic inflammation in the synovial lining of the joints, tendon sheaths and the bursa

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13
Q

Describe the pathogenesis of rheumatoid arthritis

A

Inflamed synovial central pathogenesis

Synovial becomes hyperplastic, with infiltration of mononuclear

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14
Q

Describe the antibodies of rheumatoid arthritis

A

Rheumatoid factor - present in 70% of patients (IgM)

Anti-CCP - positive around 80%. Often pre-date development

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15
Q

Name the risk factors for rheumatoid arthritis

A

Genetics

Smoking (weak)

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16
Q

Describe the clinical features of rheumatoid arthritis

A

Onset - rapid or gradual

3 joint symptoms
- Pain
- Swelling
- Stiffness

Associated systemic symptoms

Extra-articular manifestations and eye manifestations

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17
Q

Describe the examination of rheumatoid arthritis

A

Joints - tenderness + synovial thickening

Hand signs of the disease

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18
Q

Describe the hand signs of rheumatoid disease

A

Z-shaped deformity of thumb

Swan neck deformity - hyperextended PIP and flexed DIP

Boutonniere deformity - hyperextended DIP and flexed PIP

Ulnar deviation of the fingers at the MCP joints

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19
Q

What are the investigations for rheumatoid arthritis

A

Joint aspiration (if suspected infection)

Rheumatoid factor

Anti-CCP antibody

Inflammatory markers - CRP,, ESR

Radiograph - x-ray, MRI

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20
Q

Describe the management of rheumatoid arthritis

A

Short term-steroids (acute)

Modifying anti-rheumatic drugs + biological DMARDs

NSAIDs

Surgery

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21
Q

What is used to monitor the success of rheumatoid arthritis treatment

A

C-reactive

DAS28

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22
Q

Name 4 differential diagnosis of rheumatoid arthritis

A

Psoriatic arthritis
Infectious arthritis
Gout
Systemic lupus erythematosus

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23
Q

Define gout

A

Crystal arthropathy associated with chronically high blood uric acid levels

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24
Q

Describe the pathophysiology of gout

A

Urate crystals are deposited in the joint, causing it to become inflamed.

Characterised by hyperuricaemia and deposition of urate crystals causing attacks of acute inflammatory arthritis.

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25
Q

Describe the cause of gout

A

Hyperuricaemia - due to under-excretion of urate or over-production.

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26
Q

What are the risk factors for hyperuricaemia

A

Dietary factors (seafood, meat, beer)

Obesity, insulin resistance and hypertension

High cell turnover

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27
Q

Name the risk factors of gout

A

Male
Family history
Obesity
High purine diet
Alcohol - BEER
Diuretics
Cardiovascular disease
Kidney disease
Fructose
Aspirin

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28
Q

What are the clinical features of gout

A

Gouty tophi

Acute onset of:
- fever joint pain with:
- swelling
- effusion
- warmth
- erythema
- OR tenderness of the involved joints

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29
Q

What are the most affected joints in gout

A

The base of the big toe - metatarsophalangeal joint

The base of the thumb - the carpometacarpal joint

Wrist

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30
Q

Describe the investigations of gout

A

Bloods

Aspirated joint fluid

X-ray - if concern sepsis or recurrent arthritis

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31
Q

Define gouty tophi

A

Subcutaneous uric acid deposits are typically seen on hands, elbows and ears

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32
Q

How do you define between gout and pseudogout

A

Gout - needle-shaped and negatively birefringent of polarised light. Monosodium urate crystals.

Pseudogout - Rhomboid-shaped and positively birefringent. Calcium pyrophosphate crystals

Both - no bacterial growth

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33
Q

Describe what is seen on an aspirated joint fluid of gout including the type of crystal

A

Monosodium urate crystals

Needle-shaped and negatively birefringent of polarised light

No bacterial growth

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34
Q

Describe the x-ray seen in gout

A

No loss of joint space

Lytic lesions in the bone

Punches out erosions

Erosion can have sclerotic borders with overhanging edges

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35
Q

What is the clinical diagnosis of gout

A

Clinical + raised serum levels of blood test

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36
Q

Describe the management of gout

A

Acute flares
- NSAIDS (1)
- Colchicine (2)
- Oral steroids (3)

Prophylaxis
- xanthine oxidase inhibitors

Lifestyle changes
- losing weight
- staying hydrated
- minimising alcohol and purine-based food

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37
Q

Describe the differential diagnosis of gout

A

Critical - septic arthritis

Pseudogout

Trauma

Rheumatoid arthritis

Reactive arthritis

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38
Q

How are infectious prosthetics avoided

A

Surgery
- Laminar flow in surgery
- 10-sides
- Double gloving

IV Peri-operative antibiotics

Cemented implant - cement contains antibiotics

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39
Q

Describe the diagnosis of prosthetic infections

A

History
Examination
X-ray
FBC, ESR, CRP
Microbiology culture

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40
Q

What is the key investigation done in prosthetic infection

A

Aspiration

  • confirms diagnosis
  • identify organism (s) and antibiotic sensitivities
  • MUST be done with patient off antibiotics for at least 2 weeks
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41
Q

Name the 3 aims of treatment in prosthetic infection

A

Eradicate sepsis
Relieve pain
Restore function

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42
Q

Name the treatment options for prosthetic infection

A

Antibiotics

Debridement & Implant retention (acute infection)

Excision Arthroplasty (poor functional outcome)

Exchange Arthroplasty

One-stage exchange (implantation of new prosthesis - cemented)
Two-stage exchange

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43
Q

Define pseudogout

A

Crystal arthropathy caused by calcium pyrophosphate crystals collecting in the joint

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44
Q

Name the risk factors for pseudogout

A

Advanced age
Injury
Hyperparathyroidism
Haemochromatosis
Family history
Hypomagnesemia
Hypophosphatasia

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45
Q

Describe the symptoms of pseudogout

A

Tender to be milder than gout or septic arthritis

Painful and tender joints

Osteoarthritis-like involvement of joints

Sudden worsening of osteoarthritis

Red and swollen joints

Joint effusion and fluctuance

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46
Q

Describe the joint aspiration results seen in pseudogout

A

Used to confirm diagnosis

Shows calcium pyrophosphate crystals

Rhomboid-shaped and positively birefringent of polarised light

No bacterial growth

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47
Q

Describe the x-ray of pseudogout

A

Chondrocalcinosis

Calcium deposits in the joint cartilage

LOSS
- loss of joint space
- osteophytes
- subarticular sclerosis
- subchondral cysts

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48
Q

Describe the management of pseudogout

A

Targeted at symptoms

Asymptomatic = no treatment

Symptoms
1. NSAIDs
Colchicine
Intra-articular steroid injection
Oral steroids

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49
Q

Name 5 differential diagnosis of pseudogout

A

Acute gouty arthritis
Acute septic arthritis
Milwaukee shoulder syndrome
Osteoarthritis
Rheumatoid arthritis

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50
Q

Define osteoporosis

A

Significant reduction in bone density

Systemic skeletal disease characterised by a low bone mass and abnormal bone architecture, which leads to compromised bone strength and a consequent increase in bone fragility and risk of fracture

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51
Q

What is T-score

A

Number of standard deviations the patient is from an average healthy young adult

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52
Q

What is the T-score of osteopenia

A

-1 to -2.5

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53
Q

What is the T score of osteoporosis

A

Less than -2.5

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53
Q

What is the T-score of severe osteoporosis

A

Less than -2.5 + fracture

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53
Q

Describe the pathophysiology of osteoporosis

A

Oversupply of osteoclasts or osteoblasts relative to the need for remodelling or cavity repair

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54
Q

Describe the cause of osteoporosis

A

Cause = low bone mass

Either
- low peak bone mass
- loss of bone mass with ageing

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55
Q

Name the risk factors of osteoporosis

A

Older age
Post-menopausal women
Reduced mobility and activity
Low BMI
Low calcium or vitamin D intake
Alcohol or smoking
Personal or family history of fractures
Chronic disease
Long-term corticosteroids
Certain medications

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56
Q

Name the clinical feature of osteoporosis

A

Asymptomatic until fracture occurs

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57
Q

What would a joint aspirate in septic arthritis show

A

Turgid fluid

Leucocytes ++

Gram stain - gram positive cocci

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58
Q

Name the causes of inflammatory arthritis

A

Rheumatoid arthritis

Seronegative spondylarthritis
- psoriatic
- ank spond
- reactive arthritis
- enteropathic - chrons & UC

Crystal arthritis

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59
Q

What are the 4 stages of gout if left untreated

A
  1. Asymptomatic hyperuricemia
  2. Acute/recurrent gout
  3. Intercritical gout
  4. Chronic tophaceous gout
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60
Q

What is the aim of chronic gout management

A

Treat to target

Reduce uric acid below < 300 umol/L

Allopurinol and increase every 2-4 weeks until target met

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61
Q

Define septic arthritis

A

Infection of a joint

May occur in a native (original) joint or a prosthetic joint replacement

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62
Q

What is the most causative organism septic arthritis

A

Staphylococcus aureus

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63
Q

Describe gonococcal arthritis

A

Occurs with disseminated gonococcal infection

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64
Q

Name 4 specific risk factors of septic arthritis

A

Any cause for bacteraemia

Direct/penetrating trauma

Local skin breaks/ulcers

Damaged joint

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65
Q

Name 4 general risk factors of septic arthritis

A

Immunosuppression

Elderly

Rheumatoid arthritis (or other immune driven disease)

Diabetes

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66
Q

Describe the clinical features of septic arthritis

A

90% monoarthritis

Knee > hip > shoulder

Presents with
- hot, red, swollen and painful joint
- fever
- stiffness and reduced range of motion
- systemic symptoms

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67
Q

Describe the investigations of septic arthritis

A

Joint examination fluid

Bloods

Imaging - plain x-ray, ultrasound

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68
Q

Describe the management of septic arthritis

A

Joint aspiration fluid - antibiotics guided by

Empirical antibiotics - 6 weeks minimum. 1st line = flucloxacillin

Other
- joint washout
- rest/splint/physio
- analgesia
- stop immune suppression temporality if possible

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69
Q

What antibiotics are given for septic arthritis caused by staphylococcus

A

Flucloxacillin
Erythromycin
Doxy/tetracycline

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70
Q

Name 4 differential diagnosis of septic arthritis

A

Gout
Pseudogout
Reactive arthritis
Hemarthrosis

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71
Q

Define reactive arthritis

A

Inflammatory arthritis that occurs after exposure to certain GI and GU infections.

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72
Q

Describe the pathophysiology of reactive arthritis

A

Involves synovitis in one or more joints in response to an infective trigger.

No infection inside the joint

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73
Q

Name the triggers of reactive arthritis

A

Gastroenteritis

Genitourinary infections - STI
- Chlamydia
- Gonorrhoea (normally causes septic)

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74
Q

Name 3 risk factors of reactive arthritis

A

Male sex
HLA-B27 genotype
Preceding chlamydia or GI infection

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75
Q

Name the clinical features of reactive arthritis

A

Fever

Peripheral and axial arthritis

Enthesitis

Dactylitis

Conjunctivitis and iritis

Skin lesions

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76
Q

Define Enthesitis

A

Inflammation where tendon is inserted into the bone

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77
Q

Define dactylitis

A

Swelling of an entire finger or toe

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78
Q

Define skin lesions

A

Circinate balanitis and keratoderma blennorrhagicum

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79
Q

Describe the investigations for reactive arthritis

A

Bloods
- ESR/CRP
- ANA
- Rheumatoid factor

Urogenital and stool cultures

Plain x-rays

Arthrocentesis with synovial fluid analysis

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80
Q

Describe the management of reactive arthritis

A

Treatment according to the hot joint policy

Joint aspiration

Pharmacology
- Treatment of triggering infection
- NSAIDs
- Steroid injection into the affected joints
- Systemic steroids (multiple joints)

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81
Q

What are the associations of reactive arthritis

A

Can’t see, pee or climb a tree

Bilateral conjunctivitis - non infective

Anterior uveitis

Urethritis - non-gonococcal

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82
Q

Define giant cell arthritis

A

Type of systemic vasculitis affecting the medium and large arteries (extracranial branches of the carotid artery - usually affected)

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83
Q

Name 2 risk factors of giant cell arthritis

A

Age > 50 years

Female sex

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84
Q

Describe the clinical features of giant cell arthritis

A

Primary presenting feature = unilateral headache (severe, around temple)

Associated
- scalp tenderness
- jaw claudication
- blurred/double vision
- loss of vision if untreated

Temporal artery - may be tender, thickened. Reduced or absent pulsation

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85
Q

Name the investigations of giant cell arthiritis

A

Inflammatory markers - ESR

Biopsy - temporal artery biopsy

Duplex ultrasound

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86
Q

What is clinical diagnosis of giant cell arthiritis based off

A

Clinical presentation

Raised inflammatory markers

Temporal artery biopsy

Duplex ultrasound

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87
Q

Describe the management for giant cell arthiritis

A

Main steroids
- prednisolone - no visual symptoms or jaw claudication
- methylprednisolone - with

Other medications
- aspirin
- proton pump inhibitor
- bisphosphonates and calcium and vitamin D

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88
Q

Name 5 differential diagnosis of giant cell arthiritis

A

Polymyalgia rheumatica

Solid organ cancers/haematological malignancies

Chronic infections

Rheumatoid arthiritis

Amyloidosis

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89
Q

Define systemic lupus erythematosus

A

Inflammatory autoimmune condition disorder.

Systemic = affects multiple organs and systems.

Erythematosus = typical red malar rash across the face

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90
Q

Describe the pathophysiology of systemic lupus erythematosus

A

Anti-nuclear antibodies generate chronic inflammatory response.

Inflammation - immune complex mediated leads to tissue damage

Thrombosis - phospholipid antibodies

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91
Q

Who is systemic lupus erythematosus most common in

A

Women

Asian, African, Caribbean, Hispanic ethnicity

Young to middle-aged adults

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92
Q

Describe the causes of systemic lupus erythematosus

A

Genetic factors

Environmental factors
- Non infectious - drugs
- Infectious

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93
Q

Name 4 risk factors for systemic lupus erythematosus

A

Female sex
Age > 30 years
African descent in Europe or US
Drugs

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94
Q

Name the clinical features of systemic lupus erythematosus

A

Relapsing-remitting cause

Many symptoms
- arthralgia
- non-erosive arthiritis
- myalgia
- photosensitive malar rash
- SOB
- Hair loss
- Raynaud’s phenomenon
- Oedema

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95
Q

Describe the haematological features of systemic lupus erythematosus

A

Anaemia
- haemolytic
- coombs positive

Neutropenia
Thrombocytopenia
Lymphopenia

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96
Q

Describe the investigations of systemic lupus erythematosus

A

Autoantibodies

FBC
CRP/ESR
C3&4

Urinalysis, urine protein: creatinine ratio

Renal biopsy

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97
Q

Describe the management of systemic lupus erythematosus

A

1st line
Can have no treatment
Hydroxychloroquine
Topical - sun avoidance
NSAIDs
Steroids

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98
Q

Name the differential diagnosis of systemic lupus erythematosus

A

Rheumatoid arthiritis
Antiphospholipid syndrome
Systemic sclerosis
Lyme disease
HIV
Infectious mononucleosis

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99
Q

Name some complications of systemic lupus erythematosus

A

Chronic inflammation
Antiphospholipid antibodies/syndrome
Anaemia
Interstitial lung disease
Neuropsychiatric SLE

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100
Q

What are the 2 main pathological features of osteoarthritis

A

Loss of cartilage

Disordered bone repair

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101
Q

Name the 3 cytokines which mediate osteoarthritis

A

ILA-1
TNF-a
NO

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102
Q

Describe erosive/inflammatory subset of osteoarthritis

A

Strong inflammatory component

DMAR therapy

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103
Q

Name the surgical options for osteoarthritis

A

Arthroscopy
Osteotomy
Arthroplasty
Fusion

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104
Q

What are the 4 Rs of orthopaedic principles

A

Resuscitate
Reduce
Retain
Rehab

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105
Q

Describe the steps of bone remodelling (direct)

A
  1. Resting
  2. Reabsorption
  3. Formation
  4. Mineralisation
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106
Q

Describe the steps of callus formation (indirect)

A
  1. Bleeding
  2. Soft callus
  3. Bony callus
  4. Remodelling
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107
Q

Define Sjogren syndrome

A

Autoimmune condition affecting exocrine glands (lacrimal and salivary glands) causing symptoms of dry mouth, eyes and vagina

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108
Q

Describe the types of Sjogren’s syndrome

A

Primary - condition occurs in isolation

Secondary - occurs due to other diseases
- SLE
- Rheumatoid arthiritis
- Scleroderma
- Primary biliary cirrhosis
- Other autoimmune disease

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109
Q

What are the antibodies present in Sjogren’s syndrome

A

Anti-SS-A antibodies (anti-Ro)

Anti-SS-B antibodies (anti-La)

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110
Q

Describe the epidemiology of Sjogren’s syndrome

A

More common in women (maybe oestrogen)

Typically presents in middle age

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111
Q

Name the risk factors for Sjogren’s syndrome

A

Female
SLE
Rheumatoid arthiritis
Systemic sclerosis
HLA class II markers
Age 40-70

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112
Q

Describe the clinical features of Sjogren’s syndrome

A

Dry eyes and dry mouth (Sicca symptoms)

Arthritis
Rash
Neurological features
Vasculitis
ILD
Renal tubular acidosis

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113
Q

Describe the Schirmer Test

A

For Sjogren’s syndrome

Folder filter paper under eye

Moisture from eye will travel down

After 5 minutes distance is measured

Less than 10mm = significant

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114
Q

Describe the investigations of Sjogren’s syndrome

A

Positive - ANA, RF, Ro and La

Negative - immunoglobins

Abnormal salivary glands on ultrasound

Sialadenitis on lip biopsy

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115
Q

Describe the management of Sjogren’s syndrome

A

Tear and saliva replacement

Pilocarpine

Vaginal lubricants

Hydroxychloroquine

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116
Q

Name the complications of Sjogren’s syndrome

A

Eye problems
- Keratoconjunctivitis sicca
- Corneal ulcers

Oral problems
- dental cavities
- candida infections

Vaginal problems
- candida infection
- sexual dysfunction

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117
Q

Describe the clinical diagnosis of Sjogren’s syndrome

A

Clinical features + presence of biopsy

May use - salivary biopsy

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118
Q

Define dermatomyositis/polymyositis

A

Autoimmune disorders causing muscle inflammation (myositis)

Poly - occurs without any skin features

Dermato - with skin features

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119
Q

Describe the causes of dermatomyositis/polymyositis

A

Paraneoplastic syndromes - underlying cancer

Viral infections e.g. Coxsackie or HIV

120
Q

Name the risk factors for dermatomyositis/polymyositis

A

Genetic predisposition

Bimodal age distribution

Female sex

Black race

UV radiation

121
Q

Name the clinical features of dermatomyositis/polymyositis

A

Muscle and skin
- rash
- muscle weakness (symmetrical)
- Interstitial lung disease
- para-neoplastic syndrome

122
Q

Describe the investigations of dermatomyositis/polymyositis

A

1st line
- muscle enzymes (creatinine kinase)

Other
- antibody screen
- EMG
- Muscle/skin biopsy
- Screen for malignancy

123
Q

What is clinical diagnosis of dermatomyositis/polymyositis based upon

A

Clinical features

Elevated creatinine kinase

Autoantibodies

Electromyography

Magnetic resonance imaging

Muscle biopsy

124
Q

Name the management of dermatomyositis/polymyositis

A

1st line - corticosteroids

Other
- immunosuppressive drugs
- IV immunoglobulins
- Biological therapy

125
Q

Define systemic sclerosis (scleroderma)

A

Autoimmune connective tissue disease involving inflammation and fibrosis of the connective tissues, skin and internal organs

126
Q

Name the 4 main components of the pathophysiology of systemic sclerosis (scleroderma)

A

Vasculopathy
Excessive collagen deposition
Inflammation
Auto-antibody production

127
Q

Name the clinical subsets of systemic sclerosis

A

Limited cutaneous - CREST

Diffuse cutaneous - CREST + internal organs

128
Q

Describe crest in systemic sclerosis

A

Calcinosis

Raynaud’s phenomenon

Oesophageal dysmotility

Sclerodactyly

Telangiectasia

129
Q

Name the risk factors of systemic sclerosis

A

Family history

Immune dysregulation

130
Q

Describe the clinical features of systemic sclerosis

A

Raynaud’s phenomenon

Scleroderma

Sclerodactyly

Telangiectasia

Calcinosis

Oesophageal dysmotility

Systemic and pulmonary hypertension

Pulmonary fibrosis

131
Q

Describe the investigations for systemic sclerosis

A

Autoantibodies

Nailfold capillaroscopy

132
Q

Describe nailfold capillaroscopy

A

Examine peripheral capillaries

Suggests systemic sclerosis:
- abnormal capillaries
- avascular areas
- micro-haemorrhages

133
Q

Describe the management of systemic sclerosis

A

Raynaud’s

PPU
ACE inhibitors
Echo and pulmonary function tests

Treatment of the complications/symptoms

134
Q

What are the options of management in systemic sclerosis in diffuse disease

A

DMARDs - methotrexate

Biological therapies

Steroids (may be considered)

135
Q

Describe the non-medical management of systemic sclerosis

A

Avoid smoking

Gentile skin strength to maintain range of motion

Regular emollients

Avoid cold triggers for Raynaud’s

Physiotherapy

Occupational therapy

136
Q

Name 4 spondyloarthropathies

A

Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis
Enteric arthiritis

137
Q

Name the clinical features of spondyloarthropathies

A

SPINEACHE

Sausage digits - dactylitis
Psoriasis
Inflammatory back pain
NSAID good response
Enthesitis - heel
Arthritis
Crohn’s/Colitis/elevated CRP
HLA B27
Eye - uveitis

138
Q

Define ankylosing spondylitis

A

Inflammatory condition affecting the axial skeleton (mainly the spine and sacroiliac joints), causing progressive stiffness and pain

139
Q

Name the cause of ankylosing spondylitis

A

HLA-B27

140
Q

Name 4 risk factors of ankylosing spondylitis

A

HLA-B27 (90%)

Endoplasmic reticulum aminopeptidase 1 and interleukin-23 receptor genes

Positive family history of AS

Male sex

141
Q

Describe the clinical features of ankylosing spondylitis

A

Joint pain adult male in 20s - gradually developed over 3 months

Stiffness and pain in lower back (> 30 minutes in the morning)

Sacroiliac pain (in buttock region)

142
Q

Name the main affected joints in ankylosing spondylitis

A

Sacroiliac joints
Vertebral column joints

143
Q

Does movement improve or make worse ankylosing spondylitis

A

Improves with movement

Improve activity

Worsen with rest

144
Q

Name the additional features which can be present with alkyalosing spondylitis

A

Chest pain
Enthesitis
Dactylitis
Vertebral fracture
Shortness of breath

145
Q

Name the 5 associations with ankylosing spondylitis

A

5 As

Anterior uveitis
Aortic regulation
Atrioventricular block - heart block
Apical lung fibrosis
Anaemia of chronic disease

146
Q

Name the key investigations of ankylosing spondylitis

A

Inflammatory markers - CRP, ESR

HLA B27 - genetic testing

X-ray of spine and sacrum

MRI of spine

Schober’s test

147
Q

Describe Schober’s test of ankylosing spondylitis

A

Assesses spinal mobility

Standing straight - L5 15cm apart

Bend forward as far as possible - distance measured

< 20cm = indicated restriction in lumbar spine

148
Q

Describe the x-ray changes in ankylosing spondylitis

A

Bamboo spine

Squaring of the vertebral bodies

Subchondral sclerosis and erosions

Syndesmophytes

Ossification

Fusion

149
Q

Describe the medical management of ankylosing spondylitis

A

1st line - NSAIDs
2nd line Anti-TNF

150
Q

Describe the additional management of ankylosing spondylitis

A

Physiotherapy
Exercise and mobilisation
Avoid smoking
Bisphosphates for osteoporosis
Surgery - occasionally required for severe joint deformity

151
Q

Name 5 differential diagnosis for ankylosing spondylitis

A

Osteoarthritis
Diffuse idiopathic skeletal hyperostosis
Psoriatic arthiritis
Reactive arthiritis
Vertebral fracture

152
Q

Define enteric arthiritis

A

Arthritis associated with inflammatory bowel disease

153
Q

Name the cause of enteric arthiritis

A

HLA-B27

Endoplasmic reticulum aminopeptidase 1 and 2

154
Q

What are the risk factors of enteric arthiritis

A

Family history
Smoking

155
Q

Describe the clinical features of enteric arthiritis

A

Asymmetric lower limb arthiritis

Insidious onset of pain before the age 45

Morning stiffness

Pain worsening with rest and improving with movement

Awaking towards later portion of night

IBS symptoms

156
Q

Describe the investigations for enteric arthiritis

A

Physical examination

Modified Schober test

Abdominal examination

Lab tests

Imaging - colonoscopy

157
Q

Describe the management of enteric arthiritis

A

Treatment for IBD + treatment of arthiritis

158
Q

Name 4 differential diagnosis of enteric arthiritis

A

Fibromyalgia
IBS
Reactive arthritis
Celiac disease

159
Q

Describe the prognosis of enteric arthiritis

A

Remission is related to suppression of bowel disease

Can cause significant mortality

160
Q

Define psoriatic arthiritis

A

Chronic inflammatory musculoskeletal disease associated with psoriasis

161
Q

What are the 5 patterns of psoriatic arthiritis

A

Asymmetrical oligoarthritis - affect 1-4 joints, same side of body

Symmetrical polyarthritis - presents like rheumatoid arthiritis

Distal interphalangeal predominant pattern - primarily affects the DIP joints

Spondylitis - presents with back stiffness and pain

Arthritis mutilans - more severe form

162
Q

Describe the pathophysiology of psoriatic arthiritis

A

May be maintained by adaptive immune system - both CD4+ and CD8+ cell play contributing role in both skin and the synovium

Angiogenesis and endothelial dysfunction

163
Q

Name the causes of psoriatic arthiritis

A

Hereditary/genetic factors

Joint or tendon trauma

Infection - HIV, streptococcal infection

Smoking

Immune system dysfunction

164
Q

Name the risk factors of psoriatic arthiritis

A

Psoriasis

Family history

165
Q

Describe the clinical features of psoriatic arthiritis

A

Plaques of psoriasis on the skin

Nail pitting

Onycholysis

Dactylitis

Enthesitis

166
Q

Describe the x-ray results in psoriatic arthiritis

A

Periostitis

Ankylosis

Osteolysis

Dactylitis

Digits

167
Q

Describe the investigations in psoriatic arthiritis

A

X-ray

ESR/CRP

Anti-CCP

Lipid profile

Fasting blood glucose

Uric acid level

168
Q

Describe the clinical diagnosis of psoriatic arthiritis

A

Screens for psoriatic arthiritis in patients with psoriasis

Involves questions about joint pain, swelling, a history of arthiritis and nail pitting

High score = referral to rheumatologist

169
Q

Name the management of psoriatic arthiritis

A

Depends on severity

NSAIDs
Steroids
DMARDs
Anti-TNF medications
Ustekinumab

170
Q

Name the differential diagnosis of psoriatic arthiritis

A

Rheumatoid arthiritis
Gout
Erosive arthiritis
Reactive arthiritis
Mycobacterial tenosynovitis
Sarcoid dactylitis

171
Q

Name a diet change which would reduce the risk of gout

A

A diet rich in dairy products

Beer, larger and stout - all the same drink (not the answer)

172
Q

Which of these is not an autoimmune connective tissue disease

Systemic Lupus Erythematosus
Ehler Danlos Syndrome
Primary Sjogren’s syndrome
Systemic sclerosis
Dermatomyositis

A

Ehler Danlos Syndrome

173
Q

Name a medication for the 1st line treatment of SLE

A

Anti-malarial
- hydroxychloroquine
- Methoprene

174
Q

Define Marfan’s

A

Autosomal dominant condition affecting the gene responsible for creating fibrillin

175
Q

Describe the pathophysiology of Marfan’s

A

Abnormal fibrillin protein leads to abnormalities in mechanical stability and elastic properties of connective tissue

176
Q

Describe the cause of Marfan’s

A

Mutation in fibrillin-1 gene

75% autosomal dominant

25% mutation occurs spontaneously

177
Q

Name 2 connective tissue disorders

A

Marfan’s

Ehlers Danlos

178
Q

Name 2 risk factors in Marfan’s

A

Family history of Marfan syndrome

Family history of aortic dissection or aneurysm

179
Q

Name the clinical features of Marfan’s

A

Tall
Long neck
Long limbs
Long fingers
High arch palate
Hypermobility
Pectus carinatum or pectus excavatum
Downward sloping palpable fissures

180
Q

Name the associated conditions of Marfan’s

A

Lens dislocation in the eye

Joint dislocation and pain

Scoliosis

Pneumothorax

GORD

Mitral/Aortic valve prolapse

Aortic aneurysms

181
Q

Describe the investigations of Marfan’s

A

Echo

Silt-lamp examination with intra-ocular pressure measurement

Imaging

182
Q

What is the aim of treatment in Marfan’s

A

Minimise blood pressure and heart rate

183
Q

Describe the management of Marfan’s

A

Lifestyle changes - avoid intense exercise and avoid caffeine and other stimulants

Preventative measures - beta blockers and angiotensin II receptor antagonists

Physiotherapy

Genetic counselling

184
Q

What is the monitoring of Marfan’s

A

Echo and ophthalmologist

185
Q

Name the differential diagnosis of Marfan’s

A

Aortic dissection

Bicuspid aortic valve

Ehlers-Danlos syndrome

XXY (Klinefelter) syndrome

186
Q

What is the greatest risk in complication in Marfan’s

A

Cardiac complications

Valve prolapse

Aortic aneurysm

187
Q

Define Ehlers-Danlos Syndrome

A

Group of genetic conditions involving defects in collagen causing hypermobility in the joints and abnormalities in the connective tissue of the skin, bones, blood vessels and organs

188
Q

Describe the 3 effects that the pathophysiology of Ehlers-Danlos syndrome causes

A

Biochemical abnormality

  1. Ligament laxity
  2. Inherent fragility of connective tissue
  3. Impaired healing
189
Q

Name the 4 types of Ehlers-Danlos syndrome

A

Hypermobile

Classical

Vascular

Kyphoscoliotic

190
Q

Describe hypermobile Ehlers-Danlos syndrome

A

Most common

Less severe

Key features - joint hypermobility and soft and stretchy skin

191
Q

Describe classical Ehlers-Danlos syndrome

A

Key features - stretchy skin that feels smooth and velvety

Severe joint hypermobility, joint, pain and abnormal wound healing

Lumps over pressure points

192
Q

Describe Vascular Ehlers-Danlos syndrome

A

Most severe and dangerous

Blood vessels and particularly fragile and prone to rupture

Characteristic thin, translucent skin

193
Q

Describe kyphoscoliotic Ehlers-Danlos syndrome

A

Poor muscle tone as neonate

Followed by kyphoscoliosis as grow

Joint dislocation common

194
Q

Describe the inheritance pattern of hypermobile Ehlers-Danlos syndrome

A

Autosomal dominant

195
Q

Describe the inheritance pattern of classical Ehlers-Danlos syndrome

A

Autosomal dominant

196
Q

Describe the inheritance pattern of vascular Ehlers-Danlos syndrome

A

Autosomal dominant

197
Q

Describe the inheritance pattern of kyphoscoliotic Ehlers-Danlos syndrome

A

Autosomal recessive

198
Q

Name the risk factors of Ehlers-Danlos syndrome

A

Family history of joint hypermobility or EDS

Genetic mutations

199
Q

Describe the clinical features of Ehlers-Danlos syndrome

A

Key = joint pain and hypermobility

Multisystem disorder (more symptoms).

200
Q

Describe postural orthostatic tachycardia syndrome as a clinical feature of hypermobile Ehlers-Danlos syndrome

A

Results = autonomic dysfunction

Symptoms
- presyncope
- syncope
- headaches
- disorientation
- nausea
- tremor

201
Q

Define presyncope

A

Light-headedness

202
Q

Describe syncope

A

Loss of consciousness

203
Q

Describe the investigations of Ehlers-Danlos syndrome

A

Clinical diagnosis

Genetic testing (except hypermobile EDS)

Beighton score

204
Q

Describe Beighton score

A

Assesses hypermobility and supports of diagnosis

1 point for each side of the body - maximum 9

Place palms flat on floor with legs straight
Hyperextended knees
Hyperextended elbows
Bend their thumbs to touch their forearms
Hyperextended their little finger past 90 degrees

205
Q

Describe the management of Ehlers-Danlos syndrome

A

No cure

Follow ups
Physiotherapy
Occupational therapy
Moderating activity
Psychology
Pain management
Joint dislocation

206
Q

Describe how Marfan’s is different to Ehlers-Danlos syndrome

A

Marfans
- High arch palate
- Arachnodactyly
- Increased arm span to body height ratio

207
Q

Describe 5 differential diagnosis of Ehlers-Danlos syndrome

A

Marfan syndrome
Fibromyalgia
Chronic fatigue syndrome
Von Willebrand’s disease
Corticosteroid excess

208
Q

Describe the prognosis of Ehlers-Danlos syndrome

A

Many patients live healthy, unaffected lives and never come to clinical attention

Vascular - associated with shortened lifespan

209
Q

Name a complication of Ehlers-Danlos syndrome

A

Premature osteoarthritis

210
Q

Define fibromyalgia

A

Syndrome characterised by widespread pain in the body present for at least 3 months

211
Q

Describe the epidemiology of fibromyalgia

A

Women 1.5 x more likely

Any age

Chance increases with age

212
Q

Name the risk factors of fibromyalgia

A

Family history

Rheumatological conditions

Age 20-60 years

Female sex

Stressful events

Sleep problems

Infections

213
Q

Describe neoplastic pain

A

In fibromyalgia underlying mechanism of pain originating from the CNS

214
Q

Describe the clinical features in fibromyalgia

A

Chronic
- waxing and waning
- widespread body pain

Comorbid symptoms
- fatigue
- memory difficulties
- sleep and mood difficulties

215
Q

Describe the investigations in fibromyalgia

A

Clinical diagnosis

> 3 months
Widespread body pain and associated symptoms

Some tests - to remove alternative causes

216
Q

Describe the management of fibromyalgia

A

Therapies

Education
Exercise
Cognitive behavioural therapies
Tricyclic behavioural antidepressants
Gabapentinoids
Serotonin-noradrenaline reuptake inhibitors.

217
Q

What is the goal of treatment in fibromyalgia

A

Decrease physical and mental symptoms

No cure

218
Q

Define antiphospholipid syndrome

A

Autoimmune disorder caused by antiphospholipid antibodies

219
Q

Describe the pathophysiology of antiphospholipid syndrome

A

Antibodies target the proteins that bind to the phospholipids on the cell surface, causing inflammation and increasing the risk of thrombosis

220
Q

Name the 3 antiphospholipid antibodies

A

Lupus anticoagulant

Anticardiolipin antibodies

Anti-beta-2 glycoprotein I antibodies

221
Q

Describe the cause of antiphospholipid syndrome

A

Primary - no evidence of autoimmune disorder

Secondary - presence of autoimmune (40%

Infections - induction of antiphospholipid antibody formation e.g. HIV

Drugs which induce APLA production

222
Q

Name the risk factors of antiphospholipid syndrome

A

History of:

Systemic lupus erythematosus

Other autoimmune rheumatological disorders

Other autoimmune disease

223
Q

Describe the clinical features of antiphospholipid syndrome

A

Hallmarks - arterial or venous thrombosis and pregnancy-related complications

Other (involvement of):
- cutaneous
- Vascular
- neurological
- pulmonary
- renal

Catastrophic anti-phospholipid syndrome

224
Q

Describe the investigations of antiphospholipid syndrome

A

Lupus anticoagulant

Anticardiolipin antibodies

Anti-beta2-glycoprotein I antibodies

Antinuclear antibody, double-stranded DNA, and extractable nuclear antigen antibodies

FBC

Creatinine and urea

225
Q

Describe the diagnosis of antiphospholipid syndrome

A

Clinical features + antiphospholipid syndrome

226
Q

Describe the management of antiphospholipid syndrome

A

Long term warfarin
- target INR 2-3
- contraindicated in pregnancy

Low molecular weight heparin and aspirin

227
Q

Name 2 differential diagnosis of antiphospholipid syndrome

A

Sneddon’s syndrome

Inherited thrombophilia

228
Q

Name the associations of antiphospholipid syndrome

A

Livedo reticularis
Libmann-Sacks Endocarditis
Thrombocytopenia

229
Q

Name the complications of antiphospholipid syndrome

A

Venous thromboembolism

Arterial thrombosis

Pregnancy-related complications

Catastrophic phospholipid syndrome

230
Q

Describe catastrophic antiphospholipid syndrome

A

Rare complication with rapid thrombosis in multiple organs within a few days

High mortality rate

231
Q

Define paget’s disease of bone

A

Involves excessive bone turnover due to increased osteoclast and osteoblast activity

232
Q

Describe the pathophysiology of Paget’s disease of bone

A

Excessive turnover is not coordinated

= patchy areas of high density (sclerosis) and low density (lysis)

= enlarged misshapen bones, structural problems and increased risk of pathological fractures

233
Q

What does Paget’s disease of bone particularly affect

A

Axial skeleton - bones of head and spine

234
Q

Name 2 risk factors of Paget’s disease of bone

A

Family history

Age > 50

235
Q

Describe the clinical features of Paget’s disease of bone

A

May be asymptomatic

Or present with:
- bone pain
- bone deformity
- fractures
- hearing loss

236
Q

Describe the investigations in Paget’s disease of bone

A

X-ray findings

Blood tests
- raised alkaline phopshatase

Bone biopsy (ultimate confirmatory test - rarely necessary)

237
Q

Describe the x-ray investigations in Paget’s disease of bone

A

Bone enlargement and deformity

Osteoporosis circumscripta

Cotton wool appearance of the skull

V-shaped osteolytic defects in the long disease

238
Q

Describe the management of Paget’s disease of bone

A

1st line - bisphosphonates

Other
- calcitonin
- analgesia
- calcium and vitamin D supplementation
- surgery

239
Q

Describe the action of bisphosphonates in Paget’s disease of bone

A

Interfere with osteoclast activity and restore normal bone metabolism

Improve symptoms and prevent further abnormal bone formation

240
Q

Describe the monitoring Paget’s disease of bone

A

Serum alkaline phosphatase (ALP)

Review symptoms

241
Q

Name 2 differential diagnosis of Paget’s disease of bone

A

Osteomalacia

Fibrous dysplasia

242
Q

Describe the complications of Paget’s disease of bone

A

Hearing loss
Heart failure
Osteosarcoma
Spinal stenosis and spinal cord compression

243
Q

Describe Spinal stenosis and spinal cord compression as a complication of Paget’s disease of bone

A

Deformity in the spine leads to spinal canal narrowing

Pressure on spinal nerves can cause neurological signs and symptoms

Treated with bisphosphonates

Surgical intervention may be necessary

244
Q

Define osteomyelitis

A

Inflammation in a bone and bone marrow, usually caused by a bacterial infection

245
Q

Define haematogenous osteomyelitis

A

When a pathogen is carried through the blood and seeded in the bone.

246
Q

Name 2 modes of infection in osteomyelitis

A

Haematogenous osteomyelitis (most common)

Direct contamination of the bone

247
Q

What is the most common cause of osteomyelitis

A

Staphylococcus aureus

248
Q

Name the risk factors of osteomyelitis

A

Open fractures

Orthopaedic operations (prosthetic joints)

Diabetes

IV drug use

Immunosuppression

249
Q

Name the clinical features of osteomyelitis

A

Can be non-specific/generalised symptoms

Fever
Pain and tenderness
Erythema
Swelling

Acute or chronic

250
Q

Describe the investigations of osteomyelitis

A

X-ray

MRI (diagnosis)

Blood tests

Blood cultures

251
Q

What x-ray changes would be seen on osteomyelitis

A

Periosteal reaction

Localised osteopenia

Destruction of areas of the bone

(Often do not show changes)

252
Q

Describe the management of osteomyelitis

A

Combination of:

Surgical debridement of infected bone and tissues

Antibiotic therapy
- prolonged cause

253
Q

Describe the pathophysiology of vasculitis

A

Narrowing of blood vessels due to filtration of media with inflammatory cells.

Myofibroblasts proliferate causes narrowing, stimulates the vascular smooth muscle cell remodelling.

Vessel wall infiltration, proliferation, and damage causes weakening and occlusion of blood vessels

254
Q

Describe the mechanism of vasculitis

A

Primary or secondary phenomena

Primary = idiopathic autoimmune process.

Secondary = drugs, infection, other autoimmune disease.

Immune complex = ANCA mediated

255
Q

Name the classifications of vasculitis

A
  1. Vessel size
  2. Consequence classification - hybrid classification of vessel size, pathophysiology and underlying cause
256
Q

Name the 2 risk factors of polyarteritis Nodosa

A

Hepatitis B virus

Age 40-60 years

257
Q

Describe the risk factors (4 weak) of granulomatosis with polyangiitis

A

Genetic predisposition

Infection

Environmental exposure

White ethnicity

258
Q

Describe the clinical features (generic) of vasculitis

A

Joint and muscle pain
Peripheral nephropathy
Renal impairment
Purpura
Necrotic skin ulcers
GI symptoms
Systemic symptoms

259
Q

Define purpura

A

Purple coloured non blanching spots caused by blood leaking from vessels under the skin.

260
Q

Describe the investigations for vasculitis

A

Serological testing - ANCA (often negative)

Biopsy

Kidney (as no symptoms)

Cross-sectional imaging

261
Q

What are the two phases of management in vasculitis

A
  1. Induction of remission
  2. Maintenance of remission
262
Q

Describe the management of induction of remission in vasculitis

A

1st line = steroids

+/- immunosupressents

263
Q

Describe management of maintanance of remission in vasculitis

A

Aiming to prevent life threatening relapses

May be lifelong

Aim to reach minimum effective dose

DMARDs

264
Q

In vasculitis when would there be a prognosis of early mortality

A

With lung and renal involvement

265
Q

Name 3 types of vasculitis

A

Giant cell arteritis

Wegener’s granulomatosis

Polyarteritis nodosa

266
Q

What vessel does polyarteritis affect

A

Medium

267
Q

Describe the aetiology of polyarteritis nodosa

A

Idiopathic

Secondary to infection (hepatitis B)

268
Q

Describe the key clinical features of polyarteritis nodosa

A

Renal impairment

Hypertension

Cardiovascular events
- MI
- Stroke
- Mesenteric arteries causing intestinal symptoms

Tender, erythematosus skin nodules

269
Q

What type of vessel does granulomatosis with polyarteritis

A

Small vessels

270
Q

What would be the lab finding in granulomatosis with polyarteritis

A

c-ANCA

271
Q

Name a clinical finding in granulomatosis with polyangiitis

A

Saddle-shaped nose due to nasal bridge collapse (nasal bridge dip downwards)

272
Q

Describe the key clinical features of granulomatosis with polyarteritis

A

Primarily affects - respiratory tract and kidneys

Nasal symptoms
- nose bleeds, crusting of nose and nasal secretions.

Respiratory symptoms
- ears, causing hearing loss.
- sinuses, causing sinusitis

Glomerulonephritis

273
Q

What type of vessel does giant cell arteritis affect

A

Large vessels

274
Q

What would be a lab finding in giant cell arteritis

A

Raised ESR

275
Q

Name 3 key clinical features in giant cell arteritis

A

Unilateral headache

Scalp tenderness

Vision loss

276
Q

Define polymyalgia rheumatica

A

Inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck

277
Q

Describe the pathophysiology of polymyalgia rheumatica

A

Remains unclear

278
Q

Describe the epidemiology of polymyalgia rheumatica

A

Often occurs with giant cell arteritis

More common in older white patients

279
Q

Describe the aetiology of polymyalgia rheumatica

A

Not understood

No relevant antibodies

280
Q

Name the risk factors (2) for polymyalgia rheumatica

A

Age > (or equal to) 50 years

Giant cell arteritis

281
Q

Describe the onset clinical features of polymyalgia rheumatica

A

Rapid onset over days/weeks (present for 2 weeks before diagnosis)

282
Q

Where would pain and stiffness be in polymyalgia rheumatica

A

Shoulders - radiating to the upper arm and elbow

Pelvic girdle (around the hips) - potentially radiating to the thighs

Neck

283
Q

Describe the features of pain and stiffness in polymyalgia rheumatica

A

Worse in the morning
Worse after rest or inactivity
Interfere with sleep
Morning stiffness > 45 minutes
Somewhat improves with activity

284
Q

Describe the investigations of polymyalgia rheumatic

A

Inflammatory markers

Additional investigations (differential diagnosis)
- ANA
- anti-CCP
- Urine Bence jones protein
- Chest x-ray

285
Q

What is NICE guidelines on initiating steroids

A

Advice full investigations

286
Q

Describe the clinical diagnosis of polymyalgia rheumatica

A

Clinical presentation + response to steroids + excluding differentials

287
Q

What is the 1st line management in polymyalgia rheumatica

A

Steroids

Rapid improvement often occurs within 24-72 hours

288
Q

What is the management of patients on long term steroids

A

Don’t STOP

Don’t - steroid dependence occurs after 3 weeks

Sick day rules

Treatment card

Osteoporosis prevention

Proton pump inhibitors

289
Q

Name 5 differential diagnosis of polymyalgia rheumatica

A

Osteoarthritis
Rheumatoid arteritis
Systemic lupus erythematosus
Osteomalacia
Fibromyalgia

290
Q

What are the two types of bone tumours

A

Primary
- arise from cells which constitute the bone
- divided into benign or malignant

Secondary
- metastasis
- most common site = spine

291
Q

What cancers spread to bone

A

Kidney
Thyroid
Lung
Prostate
Breast

292
Q

What are the risk factors of bone tumours

A

Genetic association
- PB1 and P53
- Mutations TSC1 and TSC2

Exposure to radiation or alkylating agents

Benign bone conditions (osteosarcoma)
- Paget’s disease
- Fibrous dysplasia

293
Q

What are the clinical features of primary bone tumours

A

Main symptom = pain

Not associated with movement

Worse at night

= red flag symptoms

Enlargement - may cause pathological fractures

294
Q

What are the investigations of bone tumours

A

Plain film radiographs

MRI imaging

CT imaging

Bone biopsy

295
Q

What staging system is used in bone tumours

A

Enneking staging system

296
Q

Describe the management of bone tumours if they are from metastatic spread

A

Rarely treated with surgery

Systemic therapies

Often palliative

Prophylactic nailing

297
Q

Name 4 differential diagnosis of bone tumours

A

Osteomyelitis
Multiple myeloma
Metabolic bone disease
Pathological fracture

298
Q

Name the examples of benign primary bone tumour

A

Osteoid osteoma
Osteochondroma
Chondroma
Giant cell tumour (osteoclastomas)

299
Q
A

Phase 2a (15 decks)

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