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Phase 2a Annabel > Msk + Rheumatology > Flashcards

Msk + Rheumatology Flashcards

1
Q

What is the MC arthritis?

A

Osteoarthritis

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2
Q

Define oseoarthritis (OA)

A

Progressive synovial joint damage ‘wear and tear’
Effectively non inflammatory degeneration

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3
Q

Who is commonly affected by OA?

A

> 55
Women

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4
Q

What are the risk factors of OA?

A

Increased age
Female
Obesity
Manual labour
Genetics

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5
Q

What gene can predispose OA?

A

COL2A1 (type 2 collagen)

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6
Q

What cartilage is most commonly affected by OA?

A

articular cartilage

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7
Q

Outline the pathophysiology of OA

A

Destruction and breakdown of cartilage -> imbalanced collagen breakdown and repair -> chondrocytes secreted -> degrade collagen -> bone attempts to replace -> abnormal bony growths

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8
Q

What are the symptoms of OA?

A

Transient morning pain worsening throughout the day
Bouchard and hebderen nodes on fingers
Asymmetrical hard joints

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9
Q

Where are Bouchard nodes located?

A

proximal interphalangeal joints (PIPJs)

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10
Q

Where are Hebderen nodes located

A

Distal interphalangeal joints (DIPJs)

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11
Q

What is the way to remember the location of Hebderen and Bouchard nodes?

A

B is before H so Bouchard’s are more proximal than Heberden’s

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12
Q

How is OA diagnosed?

A

X-ray: (LOSS) Loss of joint space, Osteophytes, subchondral sclerosis and cysts

Rheumatoid factor and Antinuclear antibodies are NEGATIVE

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13
Q

How is OA treated?

A

Weight loss and physio
NSAIDs
Steroid injections
Surgery (arthroplasty- hip or knee replacement)

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14
Q

Define rheumatoid arthritis

A

autoimmune disorder causing symmetrical polyarthritis and destruction of the synovial joints

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15
Q

What are the risk factors of RA?

A

Smoking
Women 30-50
FHx
Autoimmune disease

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16
Q

Outline the pathophysiology of RA

A

Overproduction of TNF-alpha -> synovitis and joint destruction -> leukocytes forced into synovial -> inflammation -> damages cartilage -> bone exposed

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17
Q

What are the symptoms of RA?

A

Pain worse in morning but easier as day goes on
Symmetrical joints
Extraarticular symptoms
Swollen,tender and warm
Hand deformities

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18
Q

What are 3 hand deformities in RA?

A

Ulnar deviation
Swan neck/Z thumb
Boutonniere deformity

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19
Q

What genes predispose RA?

A

HLA DR4
HLA DR1

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20
Q

How is RA differentiated from PA?

A

DIP spared in RA

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21
Q

How is RA differentiated from Spondylarthropathies?

A

RA spares lumbar spine

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22
Q

What is ulnar deviation?

A

Fingers deviate medially towards the ulna at MCP

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23
Q

What is Bouttonieres deformity?

A

PIP flexion + DIP hyperextesnion

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24
Q

What is swan neck deformity?

A

PIP hyperextension + DIP flexion

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25
Q

What 6 other organs can be affected by RA?

A

Lungs
Heart
Eyes
Brain and CNS
Kidneys
Skin

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26
Q

What does splenomegaly indicate in RA?

A

Feltys syndrome

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27
Q

What is Feltys syndrome?

A

Triad of
RA
Splenomegaly
Neutropenia

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28
Q

How is RA diagnosed?

A

ESR and CRP raised
Positive rheumatoid factor (RF)
Positive anti-CCP
X-ray

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29
Q

What are the signs of RA on X-ray?

A

LESS

Lost joint space
Bony Erosion
Soft tissue swelling
Periarticular osteopenia

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30
Q

How is RA treated?

A

Urgent referral to prevent deformity

DMARDs (GS)
NSAID analgesia
Intraarticular steroid injections
Biologicals

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31
Q

What is an example of a DMARD?

A

methotrexate

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32
Q

What are 2 biological treatments of RA?

A

Infliximab
Rituximab

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33
Q

What type of drug is infliximab?

A

TNF-a inhibitor

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34
Q

What type of drug is rituximab?

A

CD40 B cell inhibitor

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35
Q

What are 3 differences between RA and OA?

A

RA pain eases with use, OA gets worse
RA is hot and red
RA usually presents younger and is more genetic
OA affects knees
RA responds to NSAIDs, OA not as much
RA has faster onset

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36
Q

What are 2 crystal arthropathies?

A

Gout
Pseudogout

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37
Q

What is the MC inflammatory arthritis in the UK?

A

Gout

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38
Q

Define gout

A

Inflammatory arthritis caused by hyperuricaemia and intraarticular monosodium urate crystals

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39
Q

Define hyperuricaemia

A

High levels of uric acid

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40
Q

Define gouty tophi

A

nodular masses of monosodium urate crystals deposited in the soft tissues of the body

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41
Q

Who is most affected by gout?

A

Overweight middle aged men

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42
Q

Why are women less likely to develop gout?

A

Oestrogen promotes uric acid excretion in kidneys

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43
Q

What are the risk factors of gout?

A

High alcohol intake (especially beer)
Purine rich foods (red meat)
diuretics
High fructose intake
FHx
Obesity

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44
Q

Outline the pathophysiology of gout

A

Purines ->uric acid via xanthine oxidase -> monosodium urate crystals -> symptomatic gout and pain

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45
Q

Will everyone with hyperuricaemia develop gout?

A

No- only round 1/5

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46
Q

What are the symptoms of gout?

A

Sudden very painful onset and swelling and redness in big toe (MTP)
Can also affect ankle, base of thumb
Gouty tophi (chronic)

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47
Q

How is gout diagnosed?

A

Joint fluid aspiration and light microscopy
-negatively bifringent needle shaped urate crystals
- no bacterial growth
Increased urate on blood test
Joint X-ray: punched out erosions and lytic lesions

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48
Q

How are acute gout flare ups treated?

A

NSAIDs
Colchicine (targets acid crystalisation)
IM injections (eg Prednisolone)

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49
Q

When should gout prophylaxis be initiated?

A

1-2 weeks post flare up

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50
Q

What is used in gout prophylaxis?

A

1.Allopurinol
2. Febuxostat

Reduce red meat and eat more dairy!

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51
Q

How does allopurinol work?

A

Inhibits xanthine oxidase = less uric acid production

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52
Q

How does febuxostat work?

A

Non-purine xanthine oxidase inhibitor- basically same as allopurinol but used if contraindicated?

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53
Q

What are negatively bifringent needle shaped urate crystals indicative of?

A

Gout

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54
Q

Define pseudogout

A

Deposition of calcium pyrophosphate crystals on joint surface

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55
Q

Who is mostly affected by pseudogout?

A

Elderly women

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56
Q

What are 3 risk factors of pseudogout?

A

Old age
DM
Osteoarthritis
Hyperparathydroidism

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57
Q

What are the symptoms of pseudogout?

A

Hot swollen tender joint
Usually knee or wrist
Fever

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58
Q

What is the differential diagnosis of pseudogout?

A

Septic arthritis

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59
Q

How is pseudogout diagnosed?

A

Joint aspiration:
- positively bifringent rhomboid shaped crystals (Positive = Pseudo)
X-ray: chondrocalcinosis
Rule out septic arthritis

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60
Q

How is pseudogout treated?

A
  1. NSAIDs
  2. Colchicine
  3. Corticosteroid eg. Prednisolone

Joint aspiration can be very helpful

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61
Q

What are 3 differences between gout and pseudogout?

A

Pseudogout patients tend to be older
Pseudogout affects larger joints
Swelling worse in gout
Gout = uric acid deposition, pseudo = calcium pyrophosphate
Gout= negatively bifringest, pseudo= positively

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62
Q

What do positively bifringent rhomboid shaped crystals indicate?

A

Pseudogout

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63
Q

What is deposited in gout?

A

Uric acid/ urate crystals

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64
Q

What is deposited in pseudogout?

A

Calcium pyrophosphate

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65
Q

Define osteoporosis

A

Bone mineral density (BMD) >2.5 standard deviations below the young adult mean value

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66
Q

Define osteopenia

A

Precursor to oesteoporosis

BMD between 1-2.5 standard deviations below the young adult mean value

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67
Q

Define osteomalacia

A

Poor bone mineralisation causing soft bone due to lack of Ca2+, vitamin D and phosphate

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68
Q

What is a DEXA scan?

A

Dual energy X-ray absorptiometry

Used to calculate T score

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69
Q

What does a T score of >-1 indicate?

A

Normal

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70
Q

What does a T score of -1 to -2.5 indicate?

A

Osteopenia

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71
Q

What does a T score of >-2.5 indicate?

A

Osteoporosis

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72
Q

Who is most commonly affected by osteoporosis?

A

Post menopausal women >50

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73
Q

What are the risk factors of osteoporosis?

A

SHATTERED

Steroid use
Hyper(para)thyroidism
Alcohol and tobacco
Thin
Testosterone decreased
Early menopause
Renal or liver failure
Erosive/inflammatory bone disease
Dietary calcium low

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74
Q

What are the symptoms of osteoporosis?

A

Only fracture!

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75
Q

What are 3 mc fractures in oesteoporosis?

A

Proximal femur
Vertebral crush fracture
Colles fracture of the wrist

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76
Q

How is osteoporosis diagnosed?

A

DEXA scan (GS)
FRAX score

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77
Q

What is FRAX score used for?

A

Uses data to calculate risk of fracture over 10 years

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78
Q

How is osteoporosis treated?

A
  1. Bisphosphonates (sit for 30 mins after)
  2. Vitamin D and calcium supplements
    -HRT in women
    -Denosumab
    - Recombinant PTH
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79
Q

What are 2 biphosophate drugs?

A

MC: Alendronate (once weekly)
Risedronate (once weekly)
Zolendronic acid (once yearly) IV

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80
Q

How do bisphosophates work?

A

Inhibit bone breakdown by decreasing osteoclast activity

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81
Q

How does denosumab work?

A

Inhibits RANK so osteoclasts can not be activated

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82
Q

What is an example of a recombinant PTH drug?

A

Teriparatide

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83
Q

How do recombinant PTHs work?

A

Increases osteoblast activity and bone formation

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84
Q

Define fibromyalgia

A

Widespread MSK pain for 3+ months after all other diseases have been excluded

  • Basically MSK version of IBS
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85
Q

Who is most commonly affected by fibromyalgia?

A

Usually women
Any age (usually 20-50)
Depression and stress

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86
Q

What are the symptoms of fibromyalgia?

A

Chronic widespread pain
Aggravated by stress, cold and activity
Fatigue and irritability
Waking up in the night

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87
Q

What are 2 differential diagnoses of fibromyalgia?

A

PMR
SLE
Hypothyroidism
Low vitamin D
RA

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88
Q

What pain pathway is affected by fibromyalgia?

A

Non-nocioceptive

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89
Q

How is fibromyalgia diagnosed?

A

Exclude everything else (TFT, ESR+CRP, low vit D)
Pain in 11/18 tender points on body on palpation

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90
Q

How is fibromyalgia treated?

A

Educate patient and family
Physio
Low dose antidepressants and anticonvulsant

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91
Q

What are the complications of fibromyalgia?

A

Really bad quality of life :(
Opiate addiction
Anxiety and depression

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92
Q

Define polymyalgia rheumatica (PMR)

A

Large vessel vasculitis presenting as chronic pain syndrome

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93
Q

Who is mc affected by PMR?

A

Women ALWAYS >50

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94
Q

What are the symptoms of PMR?

A

Similar to fibromyalgia

Sudden onset of severe pain and stiffness of joints, hips, and lumber spine
Worse in morning
Fatigue, weight loss, depression

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95
Q

How is PMR diagnosed?

A

ESR and CRP raised
Clinical history
May have anaemia of chronic disease
Temporal artery biopsy may show GCA

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96
Q

How is PMR treated?

A

Oral Prednisolone or corticosteroids help a lot
-Prevent osteoporosis

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97
Q

Define Sjögren’s syndrome

A

Chronic t4 inflammatory autoimmune mediated destruction of epithelial exocrine glands

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98
Q

What are the 2 categories of Sjögren’s syndrome?

A

Primary: MC in females
Secondary: secondary to connective tissue disease eg. RA, SLE

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99
Q

What are the risk factors of sjogrens?

A

Female
7x more likely with first degree relative
>50

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100
Q

What gene is associated with primary Sjögren’s?

A

HLA-B8/ DR3

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101
Q

What are the symptoms of Sjögren’s?

A

Keratoconjunctivitis sicca (dry eyes)
Xerostomia (dry mouth)
Dryness of skin and vagina
Some have systemic symptoms

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102
Q

What is xerostomia?

A

Dry mouth due to decreased saliva production

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103
Q

What is keratoconjunctivitus sicca?

A

Dry eyes

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104
Q

How is Sjögren’s diagnosed?

A

Anti-Ro and anti LA
Schirmer tear test
Rose bengal staining

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105
Q

What is a schirmer tear test?

A

Strip of test paper put in lower eyelid
- wetting of <10mm in 5 mins indicates Sjögren’s

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106
Q

What is rose bengal staining?

A

Staining of eyes shows keratitis in sjogrens

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107
Q

What are anti-Ro and anti-La antibodies specific to?

A

Sjögren’s

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108
Q

How is sjogrens treated/managed?

A

Artificial tears and saliva replacement
NSAIDs and hydrxychloroquine
Vaginal lube

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109
Q

What are the complications of Sjögren’s?

A

Eye infections
Vaginal problems
Oral problems
Vasculitis
Neuropathy

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110
Q

What are 3 categories of vasculitis?

A

Large vessel
Medium vessel
Small vessel

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111
Q

Define vasculitis

A

Inflammation of vessel wall

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112
Q

What is the main treatment of vasculitis?

A

Corticosteroids

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113
Q

What are 2 types of large vessel vasculitis?

A

Giant cell arteritis/ polymyalgia rheumatica (MC)
Takayasu’s arteritis

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114
Q

What are 2 types of medium vessel vasculitis?

A

Polyarteritis nodosa / PAN (MC)
Kawasaki’s disease

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115
Q

What are 2 types of small vessel vasculitis?

A

Granulomatosis with polyangitis/ Wegners/GPA (MC)
Eosinophilia granulomatosis with polyangitis/ churg Strauss(EGPA)

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116
Q

What do ANCAs indicate in vasculitis?

A

Small cell vasculitis

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117
Q

Define giant cell arteritis (GCA)

A

Inflammatory granulomatous arteritis of large cerebral arteries and other large vessels such as the aorta

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118
Q

Who is commonly affected by GCA?

A

> 50
Women
Northern European

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119
Q

What are the symptoms of GCA?

A

Unilateral temple headache
Tenderness of scalp
Claudication of jaw when eating
Visual disturbances

120
Q

How is GCA diagnosed?

A

Raised ESR
Temporal artery biopsy (GS)
- patchy so take a big chunk

121
Q

What artery is mc affected by GCA?

A

External carotid

122
Q

How is GCA treated?

A

Rapid corticosteroids (eg Prednisolone)
- give GI (PPI) and bone (Ca2+) protection

123
Q

What is the complication of GCA?

A

Sudden painless vision loss in one eye
- can be permanent
EMERGENCY

124
Q

How is the sudden painless vision seen sometimes in GCA treated?

A

Methycprednisolone

125
Q

Who is affected by Takayatsu’s arteritis?

A

Asian/Japanese women

126
Q

Who is affected by Kawasaki disease?

A

Children

127
Q

What does Kawasaki disease cause?

A

Coronary artery aneurysm

128
Q

What are the risk factors of polyarteritis nodosa (PAN)?

A

Hep B
Middle age
Male

129
Q

What are the symptoms of PAN?

A

Subcutaneous nodules
Numbness and tingling, loss of function (mononeuritis vasculitis)
GI bleeds
Prerenal AKI and HTN
Livedo reticularis
Gangrene

130
Q

How is PAN diagnosed?

A

CT contrast angiogram “BEADS ON A STRING”
Raised ECR and CRP
Biopsy

131
Q

How is PAN treated?

A

Control BP
Corticosteroids
Treat Hep B after steroids

132
Q

What are the symptoms of Kawasaki disease?

A

Strawberry tongue
Bilateral conjunctivitis
Erythema and desquamation

133
Q

How are EGPA and GPA/Wegners differentiated?

A

EGPA = p-ANCA positive and eosinophilia
GPA = c-ANCA positive

134
Q

What 2 organs are affected by GPA/Wegners?

A

Respiratory tract
Kidneys

135
Q

Who is most affected by GPA/Wegners?

A

Late teens
Early adulthood

136
Q

What are the symptoms of GPA/Wegners?

A

Saddle shaped nose
Epistaxis (nosebleed)
Cough, wheeze and haemoptysis
GLOMERULONEPHRITIS

137
Q

How is GPA/Wegners diagnosed?

A

c-ANCA positive
Granulomas on histology
Biopsy

138
Q

How is GPA/Wegners treated?

A

Nasal corticosteroids
Cyclophosphamide

139
Q

What is the main complication of GPA/Wegners?

A

Glomerulonephritis

140
Q

What are 2 inflammatory markers?

A

ESR
CRP

141
Q

What does ESR stand for?

A

Erythrocyte sedimentation rate

142
Q

What produces CRP?

A

Liver

143
Q

What does CRP stand for?

A

C-reactive protein

144
Q

Why is CRP produced?

A

In response to IL-6

145
Q

Define Paget’s disease

A

Focal disorder of bone remodelling causing patchy bone

146
Q

Outline the pathophysiology of Pagets

A

Excessive osteoblast and osteoclast activity -> excessive bone turnover -> formation of weaker new bone -> enlarged and deformed bones -> increased risk of fracture

147
Q

Who is most affected by Pagets?

A

Increases with age
Europeans and northern English people
MC in UK!
Females

148
Q

What causes Pagets?

A

Idiopathic!
May be linked to latent viral infection
FHx

149
Q

What are the symptoms of Pagets?

A

Bone pain
Bone deformity
Neurological complications (deafness, paraparesis)
Osteosarcoma
Fracture

150
Q

How is Pagets diagnosed?

A

X-ray: cotton wool skull, osteolysis
Urinary hydroxyproline

151
Q

How is Pagets treated?

A

Biphosphonates
NSAIDs
Surgery

152
Q

What gene is associated with spondyloarthropathies (SpA)?

A

HLA-B27 - MHC 1 serotype

153
Q

What are the general features of SpA?

A

SPINEACHE

Sausage digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAIDs good response
Enthesitis (plantar fasciitis)
Arthritis
Crohn’s, colitis, elevates CRP
HLA-B27
Eye (uveitis)

154
Q

What are 4 SpAs?

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Enteric arthritis

155
Q

Define ankylosing spondylitis

A

Chronic inflammatory disorder of the spine, ribs, and sacroiliac joints

156
Q

Define ankylosis

A

Abnormal stiffening and immobility of joint due to new bone formation

157
Q

Who is affected by ankylosing spondylitis?

A

Mc in males and also more severe (women under diagnosed)
Presents at 16 or <30
HLA-b27 positive
Native Americans suffer a lot

158
Q

Outline the pathophysiology of ankylosing spondylitis

A

Sydesmophyte replaces spinal bone damaged by inflammation -> heals in weird places -> reduced mobility

159
Q

What are the symptoms of ankylosing spondylitis?

A

Young male with progressively worsening back stiffness made better by exercise
Question mark back
Loss of lumbar lordosis
Wakes up second half of night but goes back to sleep fine
Anterior uveitis (inflammation of middle layer of eye)

160
Q

How is Ankylosing spondylitis diagnosed?

A

ESR! And CRP raised
X-ray: bamboo spine, sydesmophytes, fusion of sacroiliac spine
MRI: shows sacrolitis before seen on X-ray
Schober’s test: <20cm
Genetic test

161
Q

How is ankylosing spondylitis treated?

A

Lots of exercise and physiotherapy

  1. NSAIDs
  2. DMARDs
  3. TNF-a (infliximab)
162
Q

What are 2 TNF-alpha blockers?

A

Infliximab
Adalimumab

163
Q

Does psoriasis have to be present for the patient to develop psoriatic arthritis?

A

No

164
Q

How many people with psoriasis develop psoriatic arthritis?

A

10-40% within 10 years
Can present before skin changes

165
Q

Define psoriatic arthritis

A

Inflammatory arthritis associated with psoriasis

166
Q

What are the symptoms of psoriatic arthritis?

A

DIPJs involved
Dactylitis (sausage fingers)
Oncholysis (separation of nail from nail bed) + pitting
Arthritis mutilans
Psoriasis

167
Q

What is arthritis mutilans?

A

Affects around 5% of psoriatic arthritis patients
Causes bone shortening and destruction of small bones in the hands and feet
Pencil in cup deformity

168
Q

How is psoriatic arthritis diagnosed?

A

Exclude RA (negative anti CCP and RF)
PEST screening in people with psoriasis
X-ray: pencil in cup deformity in IPJ, erosion in DIPJ, periostitis

169
Q

How is psoriatic arthritis treated?

A

DMARDs
Anti TNFs
Ustekinumab

170
Q

Define reactive arthritis

A

Sterile inflammation in the synovium/joint triggered by a distant infection (usually GI or STI)

171
Q

Are men or women MC affected by reactive arthritis?

A

Men

172
Q

What are 3 causes of reactive arthritis?

A

GI: salmonella, shingella, c.jejuna
STI: chlamydia trachomatis (MC) , gonorrhoea

173
Q

Outline the pathophysiology of reactive arthritis

A

Bacterial antigens found in inflamed synovium suggesting the antigenic material drives the inflammatory response

174
Q

What are the symptoms of reactive arthritis?

A

Days-weeks post infection
Can’t see, cant wee, cant climb a tree
- acute anterior uveitis, circinate balanitis (ulceration of penis), arthritis and enthesitis
Asymmetrical lower limb arthritis

175
Q

How is reactive arthritis diagnosed?

A

ESR and CRP raised
Find cause
Aspirated fluid is sterile and no crystallography

176
Q

How is reactive arthritis treated?

A

NSAIDs and corticosteroids
Treat infection with Abx
Relapse = methotrexate
Last line = TNF alpha blockers

177
Q

What is the differential diagnosis of reactive arthritis?

A

Septic arthritis

178
Q

What is enteric arthropathy associated with?

A

Crohn’s
IBD
Coeliac

Basically any IBD before after or during

179
Q

Define enteric arthropathy

A

Arthritis secondary to IBD

180
Q

Who is affected by enteric arthropathy?

A

Males more
10-20% IBD patients

181
Q

What are the symptoms of enteric arthropathy?

A

Asymmetric joint involvement
Synovitis in peripheral joints
Sacroilitis
Mouth ulcers
Signs of IBD

182
Q

How is enteric arthropathy treated?

A

No NSAIDs!
DMARDs

183
Q

What are 2 types of infective arthritis?

A

Septic arthritis
Osteomyelitis

184
Q

Define septic arthritis

A

Infection of the joints by direct action or hematogenous spread

185
Q

What joint is most commonly affected by septic arthritis?

A

Knee

186
Q

What are the symptoms of septic arthritis?

A

Medical emergency!

Extremely painful tender hot and swollen
Fever
Children may avoid using joint
Usually only affects one joint

187
Q

What is the complication of septic arthritis?

A

Joint can be destroyed in <24 hours

188
Q

What is the MC cause of septic arthritis?

A

Staph aureus

189
Q

What is the MC cause of septic arthritis in children?

A

Haemophilius influenzae

Now rare due to vaccines :)

190
Q

What are 3 other causes of septic arthritis?

A

Strep
N. Gonorrhoea
E. Coli

191
Q

What are the risk factors of septic arthritis?

A

Pre existing joint disease
Recent joint surgery
Prosthetic joints
IVDU
>80 and infants
DM
Immunosuppression

192
Q

How is septic arthritis diagnosed?

A

Urgent joint aspiration, microscopy, culture and sensitivity
- thick fluid due to WCC
High CRP, ESR, WCC

193
Q

How is septic arthritis treated?

A

Aspirate to drain
IV Abx
NSAID analgesia
STOP methotrexate and anti-TNF
Double Prednisolone if on it long term

194
Q

What is the prognosis of septic arthritis?

A

10% mortality

195
Q

Define osteomyelitis

A

Inflammation/ infection in bone and bone marrow due to haematogenous spread or local infection

196
Q

Who is usually affected by haematogenous spread osteomyelitis?

A

Children (long bones)

197
Q

Who is most commonly affected by contiguous/ direct osteomyelitis?

A

Adults (adjacent soft tissue)

198
Q

Why are different bones affected by osteomyelitis in adults and children?

A

Long bones have faster blood flow in children
Vertebrae affected in adults (haematogenous) due to increased vascularisation

199
Q

What is the MC cause of osteomyelitis?

A

Staphylococcus aureus

200
Q

What are 3 ways osteomyelitis is spread haematogenously?

A

Catheter
IV
Sickle cell

201
Q

What are 2 ways osteomyelitis is spread non-haematogenously?

A

Direct innoculation from trauma/ medial procedures
Continuous spread from directly infected tissue

202
Q

What are 3 risk factors of osteomyelitis?

A

DM
PVD
Decreased immunity
Sickle cell
Trauma

203
Q

What are the symptoms of osteomyelitis?

A

Children refuse to use limb
Fever, sweats
Tenderness, warmth, erythema, swelling

204
Q

How is osteomyelitis diagnosed?

A

BM biopsy and culture to find cause
Raised ESR, CRP, WCC (acute)
X-ray for chronic

205
Q

What is the main differential diagnosis of osteomyelitis?

A

Charcot joint (damage due to sensory nerves affected by DM)

206
Q

How is osteomyelitis treated?

A

Flucloxacillin and rifampicin >6 weeks
Debridement or affected implant
Immobilise

207
Q

What should be ruled out in osteomyelitis?

A

Tuberculosis osteomyelitis (biopsy)

208
Q

Define systemic lupus erythematosus (SLE)

A

Inflammatory autoimmune connective tissue disease

209
Q

What type of hypersensitivity reaction is SLE?

A

Type 3

210
Q

Who is commonly affected by SLE?

A

Females&raquo_space;»> males
20-40
Afro-carribeans and Asians

211
Q

What are the risk factors of SLE?

A

Female
Polymygia Rheumatica
FHx
HLA genes and DR2/3
Drugs
EBV

212
Q

What are 3 drugs that can cause SLE?

A

Isoniazid
Penicillamine
Hydralazine

213
Q

Outline the pathophysiology of SLE

A

Impaired apoptotic debris presented to TH2 -> B cell activation -> antigen antibody complexes form -> ANA and aDsDNA autoantibodies attack

214
Q

What are the symptoms of SLE?

A

Photosensitive malar butterfly rash on cheeks and bridge of nose
Alopecia
Ulcers
Seizures and psychosis
Glomerulonephritis with proteinuria
Raynaud’s

215
Q

How is SLE diagnosed?

A
  1. ANA positive
    Anti-dsDNA positive (GS)

Anti Smith positive
ESR raised but CRP normal
Prolonged PTT

216
Q

How is SLE treated?

A

Suncream and avoid sun
1. NSAIDS + hydroxychloroquine (helps skin) + steroids (prednisolone)
2. Azathioprine

217
Q

What is used for SLE patients in remission?

A

Hydroxychloroquine

218
Q

Define anti phospholipid syndrome (APS)

A

blood more prone to clotting ‘hyper-coagulable state’ due to APL antibodies activating platelets

219
Q

What are the 2 categories of APS?

A

Primary: on its own
Secondary: SLE! ESP ect

220
Q

Is APS more common in males or females?

A

Females

221
Q

Outline the pathophysiology of APS

A

Antiphospholipid antibodies (aPL) bind to phospholipid normally and cause thrombosis

222
Q

What are symptoms of APS?

A

CLOTs

Coagulation defect
Livedo reticularis (lace like purple discolouration on skin)
Obstetric issues- ie miscarriage
Thrombocytopenia (low platelets)

223
Q

How is APS diagnosed?

A

Hx of thrombo events and miscarriage

  1. Lupus anticoagulant (LA) +
  2. Anticardiolipin test (aCL) +
  3. Anti-B2-glycoprotein I +

Made after 2 abnormal tests more than 12 weeks apart

224
Q

How is APS treated?

A

Long term warfarin if had a thrombosis
Pregnant: aspirin and SC heparin
Prophylactic: aspirin

225
Q

What is the difference between polymyositis (PM) and dermatomyositis (DM)?

A

PM = skeletal muscle fibres
DM = skin involved

226
Q

Define DM/PM

A

Rare muscle disorder of unknown aetiology where there is inflammation and necrosis of skeletal muscle/skin

227
Q

Define myositis

A

Proximal muscle weakness + myalgia (muscle pain)

228
Q

What happens when PM/DM affects the lungs?

A

Interstitial lung disease

229
Q

What are the symptoms of PM?

A

Symmetrical progressive muscle weakness and wasting affecting the proximal muscles of the shoulder and pelvis
Can’t raise arms above head
Can’t rise from chair
Dysphagia, dysphonia, respiratory failure

230
Q

What are the symptoms of DM?

A

Heliotrope (purple) discolouration of eyelids
Gottrons papules
Raynauds
Dysphagia
SC calcitonis
Shawl sign

231
Q

What are gottrons papules?

A

Scaly erythematous plaques over knuckles

232
Q

What are 3 risk factors of PM/DM?

A

Coxsackie virus
Rubella
Influenza
HLA-B8/DR3

233
Q

How is DM/PM diagnosed?

A

Rise in creatine kinase
EMG
Muscle biopsy shows necrosis (GS)

234
Q

What autoantibodies are specific to PM?

A

Anti-Jo-2 antibodies

235
Q

What 2 autoantibodies are specific to DM?

A

anti-nuclear antibodies
Anti-Mi-2 antibodies

236
Q

How is PM/DM treated?

A
  1. Oral Prednisolone
    Bed rest with exercise programme
    Screen for malignancy
    Early intervention with immunosuppressant (azathioprine)
237
Q

Define scleroderma / systemic sclerosis

A

Fibrosis of small vessels, and thickening and tightening of skin due to excess collagen production

238
Q

Who is scleroderma most common in?

A

Females
30-50
Rare in children

239
Q

What are 2 types of scleroderma?

A

Limited: only CREST
Diffuse: CREST and affects internal organs

240
Q

What are 3 causes of scleroderma?

A

Vinyl chloride
Silica dust
Bleomycin
Genes

241
Q

What are the symptoms of scleroderma/systemic sclerosis?

A

CREST

Calcinosis (calcium deposition in SC)
Raynauds
Eosophageal strictures or dysmotility
Sclerodactyly (thickening of skin on fingers and toes)
Telenagiectasia (spider veins)

+ scleroderma

242
Q

What are some diffuse symptoms of scleroderma?

A

CKD
Atony of oesophagus, SI, colon (obstructed)
Lung fibrosis
Myocardial fibrosis

243
Q

How is scleroderma diagnosed?

A

Limited: Anti centromere bodies (ACA)
Diffuse: anti-sci-70, anti-RNA polymerase
ANA positive in almost all
Nailfold capilaroscopy

244
Q

How is scleroderma treated?

A

Physio and gentle stretching
Symptomatic management: PPI, ACE-inhibitor, CCB, hand warmers for Raynauds

245
Q

What are red flags for back pain?

A

TUNA FISH

Trauma- osteoporosis
Unexplained weight loss- cancer
Neurological symptoms- cauda equina
Age >50 or <20- Ankylosing spondylitis, herniated disc

Fever- infection
IVDU- infection
Steroid use- infection
History of cancer- metastasis to spine

246
Q

Define lumbar spondylitis

A

Degradation of IV disc over time

247
Q

Where does lumbar spondylitis most commonly affect?

A

L4-L5
L5/S

248
Q

What is Ricket’s?

A

Defective mineralisation before fusion of the epiphyses

249
Q

What is dietary vitamin D found in?

A

Oily fish
Egg yolks
Margarine

250
Q

What are the causes of osteomalacia?

A

Hyperparathydroidism (hypophosphatemia)
Vitamin D deficiency
Renal disease
Drugs
Liver disease

251
Q

What are the symptoms of oestomalacia?

A

Fatigue and bone pain
Fractures
Muscle weakness (waddling gait)

252
Q

What are the symptoms of Rickets?

A

In kids only!

Growth retardation and hypotonia
Knock knees and bowed legs
Widened epiphyses at wrist
Hypocalcaemic tetany (muscle spasms) if severe

253
Q

How is osteomalacia diagnosed?

A

GS: biopsy shows incomplete mineralisation
X-ray shows loss of cortical bone and incomplete mineralisation and Loosers zone
Low Ca2+ and phosphate
Low 25-hydroxy vitamin D*

254
Q

How is osteomalacia treated?

A

Calcitriol (vit D replacement)
Increase dietary intake

255
Q

What are 4 primary bone tumours?

A

Osteosarcoma
Firbosarcoma
Chondrosarcoma
Ewings tumour

256
Q

What are 5 locations of cancers that metastasise to bone?

A

KP BLT

Kidney
Prostate
Breast
Lungs (bronchus)
Thyroid

257
Q

Who do primary bone tumours commonly affect?

A

Young people- rare

258
Q

What are the symptoms of primary bone tumours?

A

Pain worst at night
Bony masses
Inflammatory symptoms
Motility issues

259
Q

How are primary bone tumours diagnosed?

A
  1. X-ray
    GS: bone biopsy
    Skeletal isotope scan
    CT
    Hypercalcaemia
260
Q

How are primary bone tumours treated?

A

Chemo and radiotherapy
Biphosphonates
Analgesia

261
Q

How are bone tumours staged?

A

Enneking staging

G0= benign
G1= low grade malignant
G2= high grade malignant

262
Q

Where does Ewing’s sarcoma arise from?

A

Neuroectoderm blue cells

263
Q

Who is most commonly affected by Ewing’s sarcoma?

A

Usually 15
<30

264
Q

Where does Ewing’s sarcoma most commonly affect?

A

Femur (MC)
Pelvis
Distal tibia

265
Q

What are the findings of Ewing’s sarcoma on X-ray?

A

Onion skin appearance

266
Q

What is the MC primary bone tumour?

A

Osteosarcoma

267
Q

What disease is osteosarcoma associated with?

A

Pagets

268
Q

What is the peak onset age of osteosarcoma?

A

15-19

269
Q

Where do osteosarcomas most commonly occur?

A

Knee (MC)
Proximal humerus

270
Q

Where does osteosarcoma usually metastase to?

A

Lungs

271
Q

What are the signs of osteosarcoma on X-ray?

A

Sunburst appearance
Codmans triangle

272
Q

Define chondrosarcoma

A

Cancer of the cartilage

273
Q

What age group is mc affected by chondrosarcoma?

A

Middle aged

274
Q

What are the appearances of chondrosarcoma on X-ray?

A

Popcorn calcification
Moth eaten in high grade

275
Q

What are 2 connective tissue disorders?

A

Marfans syndrome
Ehlers-danlos

276
Q

What gene is mutated in Marfans syndrome?

A

Autodom fibrillin 1 mutation

277
Q

Outline the pathophysiology of Marfans syndrome

A

Gene involved in fibrilin (in connective tissue) -> abnormal connective tissue -> decreased tensile strength

278
Q

What are the symptoms of Marfans syndrome?

A

Tall
Long neck, limbs, and fingers
Hyper mobility
Pectus carinatum/excavatum (protruding/indented chest)
Aortic complications (AAA, regurgitation, dissection)
High arch palate
Eye issues

279
Q

How is Marfans diagnosed?

A

Physical exam
Ghent criteria
Genetic test

280
Q

What are the complications of Marfans?

A

AAA
Lens dislocation
Pneumothorax
GORD
Scoliosis

281
Q

How is Marfans managed?

A

BBs
Physio to strengthen joints
Yearly echo

282
Q

What is the MC cause of death in Marfans?

A

CVD complications (aortic rupture)

283
Q

What causes Ehlers-Danlos syndrome (EDS)?

A

Autodom mutations affecting type III collagen

284
Q

How many types of EDS are there?

A

Around 13
MC = hyper mobile

285
Q

What are the symptoms of EDS?

A

Joint hyper mobility
Easily stretched skin (hyper extensibility)
Chronic joint pain
Reoccurring dislocation
CVD complications

286
Q

How is EDS diagnosed?

A

Beighton score to assess hypermobility (max 9)
Exclude Marfans

287
Q

How is EDS managed?

A

Fitness
Physio
Occupational therapy
Psychological support

288
Q

What is Raynaud’s phenomenon associated with?

A

Systemic sclerosis!
SLE
RA
DM/PM

289
Q

Define Raynaud’s

A

Intermittent spasm of arteries in the fingers and toes caused by cold and relieved by heat

290
Q

What is the difference between Raynaud’s disease and Raynaud’s phenomenon?

A

No underlying cause = disease
Underlying cause = phenomenon

291
Q

What are the symptoms of Raynauds?

A

Skin pallor -> cyanosis -> redness
Numbness and burning as fingers warm up

292
Q

How is Raynauds treated conservatively?

A

Avoid cold
Hand warmers
Wear gloves and warm clothes
Stop smoking
Stop beta blockers

293
Q

How is Raynaud’s treated pharmacologically?

A

CCB- nifedipine
Vasodilators

294
Q

What can cause a false positive for APS?

A

Syphilis

295
Q

What are 2 pieces of advice given to people taking bisphosphonates?

A

Doses should be taken while sitting or standing.
On an empty stomach / at least 30 minutes before breakfast
Patient should stand or sit upright for at least 30 minutes after
administration.

296
Q

What chromosome is HLA B27 found on?

A

6

Phase 2a Annabel (12 decks)

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