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Phase 2a - Jemima > MSK and Rheumatology > Flashcards

MSK and Rheumatology Flashcards

1
Q

what is the structure of bone

A

cortical bone on the outside - osteon functional units
trabecular bone on the inside - BM structural mesh

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2
Q

what is the structure of osteon

A

it is concentric lamellae and a central haversian canal which supplies a single longitudinal osteon

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3
Q

what are volkmann canals

A

these are canals that allow communication between osteons

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4
Q

what is the inorganic component of osteon made from

A

hydroxyapatite (ca2(Po4)3) = stiff

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5
Q

what is the function of hydroxyapatite in the bone

A

to provide stiffness

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6
Q

what is the organic component of the osteon

A

collagen T1

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7
Q

what is the function of collagen T1 in the bone

A

to provide elasticity

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8
Q

what are the different types of joints

A

fibrous
cartilaginous
synovial

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9
Q

where do you find fibrous joints

A

in the skull sutures - immovable

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10
Q

where do you find cartilaginous joints

A

IV disc, pubis symphysis - partially movable

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11
Q

where do you find synovial joints

A

most joints of the body - freely movable

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12
Q

what are the different kinds of synovial joint

A

articular cartilage
joint capsule (inner lining of synovial membrane)
synovial cavity filles with synovial fluid

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13
Q

what connects bone to bone

A

ligaments

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14
Q

what connects bone to muscle

A

tendons

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15
Q

what is osteoarthritis

A

it is the most common form of arthritis, characterised by non inflammatory degenerative mechanical shearing

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16
Q

what are the risk factors of osteoarthritis

A

age - over 50
obesity
occupation/sports
genetic

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17
Q

what genetic factor predisposes you to osteoarthritis

A

COL2A1

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18
Q

what is the pathophysiology of osteoarthritis

A

there is imbalanced cartilage breakdown compared to repair due to increased chondrocyte metalloproteinase secretion. this causes degradation of collagen and cyst formation. The bone attempts to overcome this with type 1 collagen leading to abnormal bony growths (osteophytes) and remodeling

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19
Q

what are the symptoms of osteoarthritis

A

transient morning pain - worse as day goes on
Bouchard + Heberden nodes on fingers
inflamed joints

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20
Q

what are features of Bouchard and Heberden nodes

A

asymmetrical hard inflamed joints
typically found on the most stressed joints of the body

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21
Q

how do you diagnose osteoarthritis from an X ray

A

LOSS
loss of joint space
osteophytes
subchondral sclerosis
subchondral cysts
Normal bloods

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22
Q

how do you treat osteoarthritis

A

lifestyle changes - weight bearing and physio
NSAID and cortisol injections
last resort = arthroplasty - replacements

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23
Q

what is rheumatoid arthritis

A

an inflammatory autoimmune polyarthritis

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24
Q

is rheumatoid arthritis symmetrical or asymmetrical

A

symmetrical

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25
Q

what are risk factors for developing rheumatoid arthritis

A

women - 30-50 (3X more likely than men post menopause)
smoking
HLA DR4/ DRB1 gene

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26
Q

what is the pathophysiology of rheumatoid arthritis

A

there is an arginine to citrulline mutation in T2 collagen causing anti cyclic-citrullinated peptide formation. INF-a causes further proinflammatory recruitment to the synovium.
synovial lining expands and tumour like mass grows past the joint margins
there is destruction of subchondral bone and articular cartilage

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27
Q

what are symptoms of rheumatoid arthritis

A

often worse in the morning - eases as day goes on
Hand: boutonniere, swan neck and Z thumb ulnar finger deviation
Baker’s cysts and popliteal synovial sac bulge
symmetrical
hot
inflamed

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28
Q

what non bone symptoms do you get in rheumatoid arthritis

A

lungs - PE and pulmonary fibrosis
Heart - increased IHD risk
eyes - Episcleritis and dry eyes
spinal cord compression
kidney - CKD
rheumatoid skin nodules

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29
Q

how do you diagnose rheumatoid arthritis

A

Bloods: increased ESR/CRP, normocytic normochromic anemia
Serology: positive anti CCP and positive RF
X ray

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30
Q

what is seen on X ray in rheumatoid arthritis

A

loss of joint space
eroded bone
soft tissue swelling
soft bones

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31
Q

what other types of anaemias can be seen in rheumatoid arthritis

A

microcytic - NSAID use
Macrocytic - methotrexate use (inhibits folate)

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32
Q

what is seen in Felty syndrome

A

triad of rheumatoid arthritis, granulocytopenia, splenomegaly

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33
Q

what is the treatment for rheumatoid arthritis

A

methotrexate
NSAID analgesia
intra articular steroid injection
Biologics - INFLIXIMAB or rituximab

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34
Q

what is gout

A

it is hyperuricemia (sodium urate) causing crystal deposition along joints and intraarticularly

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35
Q

what is the most common inflammatory arthritis in the UK

A

Gout

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36
Q

what are risk factors for gout

A

high purine rich diet - meat, seafood, beer
CKD and diuretics

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37
Q

what is the pathophysiology of gout

A

purines (via xanthine oxidase) become uric acid which is normally excreted. However if there is a build up of uric acid its converted into monosodium urate which then deposits and crystals

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38
Q

what are the symptoms of gout

A

monoarticular - typically big toe
sudden onset
severe swollen

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39
Q

how do you diagnose gout

A

joint aspirate and polarised light microscopy
- see negatively bifringent needle shaped crystals

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40
Q

how do you treat gout

A

diet : reduce purines and increase dairy
NSAIDS
potentially steroid injection
Allopurinol for prevention

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41
Q

what can be given to prevent gout formation

A

Allopurinol - Xanthine oxidase inhibitor

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42
Q

what is pseudogout

A

calcium pyrophosphate crystals deposit along the joint capsule

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43
Q

what are risk factors for pseudogout

A

elderly
female
diabetes
metabolic diseases
osteoarthritis

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44
Q

what are symptoms of pseudogout

A

often polyarticular with knee commonly involved
swollen, hot, red joint

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45
Q

what is a differential diagnosis for pseudogout

A

septic arthritis

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46
Q

how do you diagnose pseudogout

A

joint aspiration and polarised light microscopy
- see positively birefringent rhomboid shaped crystals

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47
Q

how do you treat pseudogout

A

only acute management
NSAIDS
Colchicine
steroid injections

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48
Q

what is osteoporosis

A

it is a decrease in bone density by 2.5 + standard deviations below young adult mean volume

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49
Q

what are risk factors for osteoporosis

A

SHATTERED
steroids
hyperhyroid/hyperparathyroidism
alcohol and spoking
thin
testosterone low
early menopause
renal or liver failure
erosive and inflammatory disease
DMT1 or malabsorption

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50
Q

what is the T score

A

it is the young adult bone density score
0 = normal within 1 SD
1-2.5 = decreased bone marrow density - osteopenia
over 2.5 = osteoporosis

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51
Q

what are symptoms of osteoporosis

A

FRACTURES
- proximal femur
- Forked wrist - fall onto hands
- compression vertebral crush

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52
Q

how do you diagnose osteoporosis

A

DEXA scan - duel energy X ray absorptiometry
also FRAX score - fracture risk assessment tool

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53
Q

what is the treatment for osteoporosis

A
  1. Bisphosphonates - alendronate, risedronate
  2. mAB denosumab
    HRT - oestogen and testosterone
    oestrogen receptor modulator = raloxifene
    recombinant PTH - teriparatide
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54
Q

what is the mechanism of action of bisphosphonates

A

they inhibit RANK-L signaling and therefore osteoclastic activity

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55
Q

how does Denosumab work

A

inhibits RANK-L

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56
Q

what is systemic lupus erythematosus

A

it is a hypersensitivity T3 reaction causing autoimmune systemic inflammation

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57
Q

Who is SLE most common in

A

females
afro-caribbean
20-40 (pre - menopausal)

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58
Q

what are the risk factors for developing SLE

A

female
HLA B8 / DR2 / DR3
Drugs - isoniazid

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59
Q

what is the pathophysiology of SLE

A

there is impaired apoptotic debris presented to TH2 causing B cell activation. this leads to antigen, antibody complex formation against self

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60
Q

what are symptoms of SLE

A

Butterfly rash
photosensitivity
glomerulonephritis
Seizures and psychosis
mouth ulcers
(+ Serositis, anaemia, joint pain, Raynaud’s and pyrexia)

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61
Q

how do you diagnose SLE

A

Bloods = anaemia w. raised ESR and normal CRP
Urine dip stick = haematuria, proteinuria
Serology = ANA Abs and Anti ds DNA Abs
low C3 and C4

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62
Q

how do you treat SLE

A

Lifestyle - low sunlight and stop triggering drugs
corticosteroids
hydroxychloroquine
NSAIDS
and azathioprine if severe

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63
Q

what is antiphospholipid syndrome

A

an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APS provokes blood clots (thrombosis) in both arteries and veins
- have aPL Abs

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64
Q

what can antiphospholipid syndrome cause in pregnancy

A

multiple miscarriages

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65
Q

what are symptoms of antiphospholipid syndrome

A

CLOTS
coagulopathy
Livedo reticularis - purple discoloration of skin
obstetric issues - miscarriages
thrombocytopenia
+ increased risk of arterial and venous thrombosis

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66
Q

what are the different types of antiphospholipid syndrome

A

primary - idiopathic
secondary - develop from other diseases such as SLE

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67
Q

how do you diagnose antiphospholipid syndrome

A

symptoms and
- lupus anticoagulant
- anticardiolipin antibodies (IgG/M)
- anti b2 glycoprotein -1 antibodies

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68
Q

how do you treat antiphospholipid syndrome

A

1st line = warfarin long term if patient has had a thrombosis
prophylaxis = give aspirin

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69
Q

what treatment is given in antiphospholipid syndrome if the patient is pregnant

A

Aspirin and heparin

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70
Q

what is Sjogren syndrome

A

it is an autoimmune exocrine dysfunction - DRY

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71
Q

what are the risk factors for developing Sjogren syndrome

A

Females
40-50
family history
HLAB8/DR3

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72
Q

what are symptoms of sjogren syndrome

A

dry eyes - Keratoconjunctivitis sicca
dry mouth - Xerostomia
Dry vagina
Raynauds

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73
Q

how do you diagnose Sjogren syndrome

A

Anti-RO and anti LA antibodies
ANA is often positive
Schirmer test - induce tears and place filter paper under the eyes to see how far the tears travel

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74
Q

how do you treat Sjogren syndrome

A

artificial tears, saliva and lubricant for sexual dysfunction
sometimes hydroxychloroquine is given

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75
Q

what is scleroderma (crest)

A

it is a systemic condition of which the most common type is limited cutaneous scleroderma (aka crest)

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76
Q

what does scleroderma cause

A

Calcinosis
Raynaud’s
Esophageal dysmotility
Sclerodactyly
Telangiectasia

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77
Q

what is calcinosis

A

it is when there are calcium deposits in the subcutaneous tissue
can lead to renal failure

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78
Q

what is raynaud’s

A

it is digit ischemia due to sudden vasospasm often precipitated by cold and is relieved with heat

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79
Q

what is sclerodactyly

A

local skin thickening or tightening on the fingers and toes and can lead to movement restriction

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80
Q

what is telangiectasia

A

it is spider veins - increases the risk of pulmonary hypertension

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81
Q

how do you diagnose scleroderma

A

anti centromere antibodies (ACAs) - 70%
ANA is often positive

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82
Q

how do you treat scleroderma

A

there is no cure
treat the symptoms the patient is experiencing

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83
Q

what is polymyositis or dermatomyositis

A

it is inflammation and necrosis of skeletal muscle, it is called dermatomyositis when skin is also involved.

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84
Q

what are risk factors for developing polymyositis

A

female
HLA B8 / DR3

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85
Q

what are symptoms of polymyositis/dermatomyositis

A

symmetrical wasting of the muscles of the shoulder and the pelvic girdle
hard to stand from sitting
hard to squat
hard to put hands on top of head
in dermatomyositis have Gottron Papules (scales) and Heliotrope (purple eyelid)

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86
Q

how do you diagnose polymyositis

A

muscle fibre biopsy necrosis is diagnostic
LDH and CK is raised
Anti - Jo1 and Mi2 ABs (2nd in dermatomyositis)
Bloods - serum creatinine kinase, aminotransferases, lactate dehydrogenase and aldolase are all increased

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87
Q

how do you treat polymyositis or dermatomyositis

A

bed rest and prednisolone for 1 month then taper down the dose

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88
Q

what is fibromyalgia

A

it is MSK equivalent of IBS: chronic widespread pain for over three months with all other causes ruled out

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89
Q

what pain pathway is affected in fibromyalgia

A

the non - nociceptive pathway is affected

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90
Q

what is non nociceptive pain

A

it is neuropathic pain and CNS processing of pain

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91
Q

what are risk factors for fibromyalgia

A

females
depression
stress
over 60

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92
Q

what are symptoms of fibromyalgia

A

stressed, depressed female of over 60
fatigue
sleep disturbance
morning stiffness
back and neck stiffness
pain

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93
Q

how do you diagnose fibromyalgia

A

there are no serological markers
there is no rise in ESR or CRP
there is pain in 11+ our of 18 regions palpated
clinically diagnosed

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94
Q

how do you treat fibromyalgia

A

educate the patients and physiotherapy
antidepressants for severe neuropathic pain - TCA, Gabapentin, Pregabalin, (opiates)
CBT

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95
Q

what antidepressants can be used in fibromyalgia

A

TCAs sch as amitriptyline

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96
Q

what is a differential diagnosis for fibromyalgia

A

polymyalgia rheumatica

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97
Q

what is polymyalgia rheumatica

A

large cell vasculitis presenting as chronic pain syndrome (affects muscles and joints)

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98
Q

what are risk factors for polymyalgia rheumatica

A

females
over 50

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99
Q

how do you diagnose polymyalgia rheumatica

A

increased ESR and CRP - diagnostic
temporal artery biopsy may show GCA
may have anaemia of chronic disease

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100
Q

how do you treat polymyalgia rheumatica

A

oral prednisolone

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101
Q

what is large vessel vasculitis

A

the spectrum of primary vasculitis that causes chronic granulomatous inflammation predominantly of the aorta and its major branches

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102
Q

what are the types of large vessel vasculitis

A

GCA
takayasu

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103
Q

what is medium vessel vasculitis

A

Medium vessel vasculitis (MVV) predominantly affects medium-sized and small arteries, defined as the main visceral arteries and their branches.

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104
Q

what are different types of medium vessel vasculitis

A

Polyarteritis nodosa
Buerger’s disease
Kawasaki disease

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105
Q

who does Buerger’s syndrome affect

A

male
smokers
20-40

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106
Q

what does Buerger’s disease cause

A

peripheral skin necrosis
thromboangiitis obliterans

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107
Q

who does kawasaki disease affect

A

children
causes coronary artery aneurysms

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108
Q

what is small vessel vasculitis

A

among a family of rare diseases characterized by inflammation of the blood vessels, which can restrict blood flow and damage vital organs and tissues

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109
Q

what are types of small vessel vasculitis

A

eosinophilic granulomatosis with polyangiitis
granulomatosis with polyangiitis
Henoch-Schönlein purpura

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110
Q

what is eosinophilic granulomatosis with polyangitis

A

rare autoimmune condition that causes inflammation of small and medium-sized blood vessels (vasculitis) in persons with a history of airway allergic hypersensitivity
- pANCA positive

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111
Q

what is granulomatosis with polyangiitis

A

rare condition where the blood vessels become inflamed. It mainly affects the ears, nose, sinuses, kidneys and lungs. Anyone can get it, including children, but it’s most common in adults and older people.
- cause of glomerulonerphitis
- cANCA positive

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112
Q

what is Henloch Schorilein purpura

A

it is IgA vasculitis leading to IgA deposition in the glomerular basement membrane as well as purpuric rash on the shins

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113
Q

what is the treatment for vasculitis

A

corticosteroids
- consider GI and bone protection such as PPIs and bisphosphates

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114
Q

what is Giant cell arteritis

A

it is an inflammation of the lining of your arteries

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115
Q

what are risk factors for giant cell arteritis

A

over 50
Caucasian
female

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116
Q

how does giant cell arteritis present

A

it presents with
unilateral temple headache
jaw claudication
temporal scalp tenderness
change in vision

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117
Q

what is the pathophysiology of giant cell arteritis

A

it affects the branches of the external carotid leading to inflammation affecting the temporal, ophthalmic and facial branches

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118
Q

how do you diagnose giant cell arteritis

A

there is an increase in EST +/- CRP
temporal artery biopsy is diagnostic
- see granulomatous inflammation of media and intima

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119
Q

how do you treat giant cell arteritis

A

with corticosteroids (prednisolone)

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120
Q

in giant cell arteritis biopsy why is it important to take a large chunk

A

as it has skip lesions so if you dont take enough it may look normal

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121
Q

what is a complication of giant cell arteritis

A

sudden painless vision loss in one eye
temporary = amaurosis fugax
may be permanent if nor delt with fast

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122
Q

what do you give for painless vision loss in giant cell arteritis

A

high dose IV methylprednisolone

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123
Q

what is polyarteritis nodosa

A

rare form of vasculitis in which the medium and/or smaller sized arteries become damaged and inflamed. It can sometimes be triggered by an infection

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124
Q

who is at risk of developing polyarteritis nodosa

A

males
associated with Hep B

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125
Q

what are the symptoms of polyarteritis nodosa

A

there are severe systemic symptoms
- mononeuritis multiples - ischemia or casa vasorum
- GI bleeds
- CKI/AKI
- skin SC nodules and haemorrhage

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126
Q

how do you diagnose polyarteritis nodosa

A

CT angiogram - beads on a string appearance due to microaneurysms
Biopsy - necrotising vasculitis

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127
Q

how do you treat polyartertitis nodosa

A

corticosteroids
control hypertension with ACE i
Hep B treatment AFTER corticosteroids

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128
Q

what is spondyloarthropathies

A

there are asymmetrical seronegative arthritis associated with HLAB27
- inflammatory

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129
Q

what are different types of spondyloarthropathies

A

Ankylosing spondylitis
psoariatic arthritis
reactive arthritis
+ IBD related arthritis

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130
Q

what are general features of spondyloarthropathies

A

SPINEACHE
sausage fingers
Psoriasis
inflammation - back pain
NSAIDs
enthesitis - plantar fasciitis
arthritis
crohns or collitis
HLAB27
Eyes - uveitis

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131
Q

what is Ankylosing spondylitis

A

abnormal stiffening of the joints (sacroiliac and vertebral) due to new bony formation

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132
Q

who is at risk for ankylosing spondylitis

A

young males
HLAB27 positive

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133
Q

what is the pathophysiology for ankylosing spondylitis

A

syndesmophytes (vertical abnormal bony growths) replace spinal bone damaged by inflammation and therefore makes the spine less mobile
- also causes inflamed tendons, eyes and fingers

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134
Q

at are symptoms of ankylosing spondylitis

A

young males with progressively worsening back stiffness
worse in the morning and at night
better with exercise
anterior uveitis
enthesitis
dactylitis
low natural lumbar lordosis
reduced lumbar flexion

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135
Q

what test shows reduced lumbar flexion

A

the Schober test

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136
Q

how do you diagnose ankylosing spondylitis

A

X ray - bamboo spine and sacroiliitis. Squared vertebral bodies and syndesmophytes
MRI - better screening tool
Bloods - ESR and EPR raised

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137
Q

how do you treat ankylosing spondylitis

A

Symptoms - exercise and NSAIDs
DMARD (improve disease) - TNA a blockers

138
Q

what TNF a blocker is used in ankylosing spondylitis treatment

A

infliximab

139
Q

what is psoriatic arthritis

A

a type of arthritis that affects some people with the skin condition psoriasis. It typically causes affected joints to become swollen, stiff and painful. Like psoriasis, psoriatic arthritis is a long-term condition that can get progressively worse.

140
Q

what are moderate symptoms of psoriatic arthritis

A

moderate - inflamed DIPJ joints, nail dystrophy, dactylitis, enthesitis, rash on skin

141
Q

what are severe symptoms of psoriatic arthritis

A

arthritis mutilaris - pencil in cup deformation where the osteolysis of the bone causes progressive shortening with the fingers telescoping in on themselves

142
Q

how do you treat psoriatic arthritis

A

Symptoms - NSAIDs
DMARD - methotrexate. If this fails use anti-TNF and then if that fails use IL-12+23 inhibitor

143
Q

what is reactive arthritis

A

it is sterile inflammation of the synovial membranes and tendons - reacting to distant infection usually GI or STI

144
Q

what is the aetiology of reactive arthritis

A

Gastroenteritis = C. Jejuni, salmonella or shigella
STI = C. Trachomatis or N. Gonorrhoea

145
Q

what are symptoms of reactive arthritis

A

Reiter’s triad
- Uveitis (cant see)
- Urethritis/Balanitis (cant pee)
- Arthritis + enthesitis (cant climb tree)
May have rash on sides of feet

146
Q

what is the main differential diagnosis of reactive arthritis

A

septic arthritis

147
Q

how do you diagnose reactive arthritis

A

joint aspirate
ESR and CRP raised
sexual health review
stool culture

148
Q

how do you treat reactive arthritis

A

symptoms - NSAIDs (+ steroid injection)
Mostly single attack - if another attach = chronic
then give methotrexate and then anti TNF a

149
Q

what is septic arthritis

A

it is a direct bacterial infection of the joint either due to direct access or haematogenous spread

150
Q

how do you manage septic arthritis

A

as a medical emergency - acutely inflamed joint with fever can destroy joint in 24 hours

151
Q

what organisms can cause septic arthritis

A

Most common = S. Aureus
H. influenza
N. gonarhoea
E.coli / pseudomonas

152
Q

what are risk factors of septic arthritis

A

IV drug users
immunosuppression
recent surgery
trauma
prosthetic joints
inflammatory joint disease

153
Q

how do you diagnose septic arthritis

A

urgent joint aspirate with MC+S and polarised light microscopy
increased ESR and CRP
consider blood culture
consider sexual health review

154
Q

how do you treat septic arthritis

A

joint aspirate for drainage and then empirical antibiotics (flucloxacillin, vancomycin, IM ceftriaxone and azithromycin)
stop any methotrexate and anti TNF a treatment
if on steroids, double prednisolone dose
NSAIDs for analgesia

155
Q

what is osteomyelitis

A

acutely inflamed infected BM, either haematogenous or local spread from infected joint or trauma.

156
Q

what organisms can cause osteomyelitis

A

S. aureus
Salmonella in sickle cell patients

157
Q

what are risk factors for osteomyelitis

A

IV drug users
Immunosuppression
PVD
DM
sickle cell anaemia
Inflammatory arthritis
trauma

158
Q

what is the pathophysiology of osteomyelitis

A

there is direct infection, local spread or haematogenous spread leads to acute bone change leading to bone inflammation and bone ache. Overtime this could lead to chronic bone changes

159
Q

what chronic bone changes are seen in osteomyelitis

A

Sequestra = necrotic bone embedded in pus
Involucrum = thick sclerotic bone placed around squestra to compensate: for support

160
Q

what are the symptoms of osteomyelitis

A

Acutely = dull bony pain, hot and swollen area. worse with movement
Chronically = acute + deep ulcers

161
Q

what are differential diagnosis for osteomyelitis

A

charcot joint - damage to sensory nerves due to diabetic neuropathy

162
Q

how do you diagnose osteomyelitis

A

bone marrow culture and biopsy to ID the causative organism
Blood MC and S
X-ray = osteopenia
MRI = bone marrow oedema
increased ESR and CRP

163
Q

what would be seen on a MRI in osteomyelitis

A

bone marrow oedema

164
Q

What what would be seen on X ray with osteomyelitis

A

Osteopenia

165
Q

how do you treat osteomyelitis

A

Immobilise plus antibiotics
- Vancomycin for MRSA and S.aureus
- Fusidic acid for s. aureus
- Flucloxacillin for salmonella

166
Q

what do you have to rule out when diagnosing osteomyelitis

A

tuberculosis osteomyelitis with bone marrow biopsy (granuloma positive)

167
Q

what are prosthetic joints commonly infected with

A

Coagulase negative staphs = S . Epidermis

168
Q

what are primary bone tumours

A

Osteosarcoma
Ewing sarcoma
Fibrosarcoma
Chondrosarcoma

169
Q

what are secondary bone cancers

A

due to metastasis
- breast
- lung
- prostate
- thyroid
- RCC

170
Q

what types of metastasis causes osteolytic bone cancer

A

breast and lung

171
Q

what types of metastasis causes osteoscerotic bone cancer

A

prostate cancer

172
Q

what is the most common primary bone malignancy

A

osteosarcoma

173
Q

what is osteosarcoma

A

a malignant tumour of bone in which there is a proliferation of osteoblasts.

174
Q

where does osteosarcoma metastasize to

A

the lungs

175
Q

how does osteosarcoma appear on X ray

A

sunburst appearing bone

176
Q

what does Ewing sarcoma arise from

A

Mesenchymal stem cells

177
Q

what age does ewing sarcoma often occur

A

15 years

178
Q

what is chondrosarcoma

A

it is a cartilage cancer

179
Q

what are the general symptoms of bone cancer

A

Local (dependent on tumour)
severe pain - worse at night
pathological fractures
low range of movement of long bone or vertebrae
weight loss
fatigue
fever
malaise

180
Q

how do you diagnose bone cancer

A

skeletal isotope scan - shows changes before an X ray can
X ray = osteolysis
increased ALP, ESR and CRP
hypercalcaemia of malignancy

181
Q

what is the treatment for bone cancer

A

chemotherapy
radiotherapy
bisphosphonates

182
Q

what is osteomalacia

A

it is defective bone mineralisation
- after epiphysial fusion

183
Q

what is osteomalacia due to

A

due to vitamin D deficiency and therefore reduced calcium and phosphate

184
Q

what are causes of osteomalacia

A

hyperPTH - increased calcium release from bone
Vitamin D deficiency
CKD or renal failure
Liver failure - less reaction in Vit D pathway
Anticonvulsant drugs - increases Vit D metabolism

185
Q

what is the vitamin D activation pathway

A

7 dehydrocholesterol - Cholecalciferol - 25-hydroxyvitamin D - 1,25 dihydroxy vitamin D

186
Q

what are symptoms of osteomalacia

A

fractures
proximal weakness
difficulty in weight bearing
widespread bone pain and tenderness

187
Q

what presentation do you have with defective bone mineralisation before epiphysial fusion

A

rickets

188
Q

what are the symptoms of rickets

A

skeletal deformations
- knocked knees and bowed legs
- wide epiphyses

189
Q

how do you diagnose osteomalacia

A

BM biopsy to see incomplete mineralisation
Bloods - Hypocalcaemia, increased PTH, low active vitamin D
X Ray - looser’s zones (defective mineralisation)

190
Q

how do you treat osteomalacia

A

Vitamin D replacement - calcitriol
Increased dietary intake - D3 tablets, eggs

191
Q

what is Paget’s disease

A

Focal disorder of bone remodelling where there are areas of patchy bone due to improper osteoblast/clast function
- areas of sclerosis and lysis

192
Q

what are symptoms of Paget’s disease

A

Bone pain
Bowed tibia and skull
Neurological symptoms
- nerve compression of CN8
- hydrocephalus

193
Q

how do you diagnose Paget’s disease

A

X ray - osteoporosis circus cipta and cotton wool skull (areas of lysis and sclerosis)
Urinary hydroxyproline - protein component of collagen
increased ALP

194
Q

what is used as a marker of disease progression in Paget’s disease

A

urinary hydroxyproline

195
Q

how do you treat pagets disease

A

Bisphosphonates
NSAIDs for pain relief

196
Q

what is marfans syndrome

A

it is an auto dominant FB1 mutation which reduces connective tissue tensile strength

197
Q

what are the symptoms of marfans syndrome

A

tall and thin
long fingers
pectus excavatum/carinatum
Aortic regurgitation murmur
abdominal aortic aneurysm
aortic dissection

198
Q

how do you diagnose marfans syndrome

A

clinical features
FBN -1 mutation - genetic testing

199
Q

what is Ehlers danlos

A

it is an auto dominant mutation affecting collagen proteins (about 13 subtypes)

200
Q

what are symptoms of ehlers danlos

A

joint hypermobility
cardiovascular complications - mitral regurgitation, abdominal aortic aneurysm and aortic dissection

201
Q

how do you diagnose Ehlers Danlos

A

clinical presentation
collagen mutations
Beighton score

202
Q

what is the Beighton score

A

The Beighton score is a test that measures joint hypermobility (flexibility). It involves simple maneuvers, such as bending your pinky (little) finger backward to check the joint angle. The Beighton score uses a nine-point scoring system. The higher your score, the more flexible your joints are.

203
Q

what is the presentation of lower back pain

A

its very common and often self limiting
- may be normal especially in those between 22-55
- can be trauma or work related

204
Q

what are signs for serious lower back pain pathology

A

older age - myeloma
Neuropathic pain - spinal cord compression

205
Q

what is lumbar spondylosis

A

it is the degeneration of IV disc. There is loss of compliance and it thins over time, progressively worsening

206
Q

what age group is lumbar spondylosis common in

A

older patients

207
Q

what are the most common lumbar involved in lumbar spondylosis

A

L4/5
L5/S1

208
Q

when would you X ray in lumbar spondylosis

A

If serious pathology is suspected

209
Q

how do you treat lumbar spondylosis

A

analgesia
physiotherapy

210
Q

what is the cause of osteoarthritis

A

loss of cartilage and disordered bone repair

211
Q

who does osteoarthritis affect the most

A

Females over males
Obese individuals

212
Q

what joints does osteoarthritis affect the most

A

Large weight bearing joints
- knees
- hips

213
Q

what is a herberdens node

A

Heberden’s nodes are small, pea-sized bony growths that occur on the joint closest to the tip of the finger, also called the distal interphalangeal joint.

214
Q

what is a bouchards node

A

Bouchard’s nodes are one of the characteristic signs of osteoarthritis of the finger joints. They appear as bony bumps along the middle joint of a finger

215
Q

what is the diagnostic criteria for rheumatoid arthritis

A
  • rheumatoid factor positive
  • finger/hand/wrist involvement
  • rheumatoid nodules
  • involvement of 3 or more joints
  • stiffness in the morning
  • erosions seen on X-ray
  • symmetrical involvement
216
Q

what biologics can be given in rheumatoid arthritis treatment

A

TNFa blockers: infliximab
B cell inhibitors: rituximab

217
Q

what are causes of osteoporosis

A

Endocrine - cushings, parathyroid
Haematology - myeloma
GI - malabsorption
Latrogenic - use of steroids

218
Q

what social treatments are used for osteoporosis

A

Lifestyle advice - quit smoking and alcohol
Calcium and vitamin D supplements

219
Q

what type of hypersensitivity is SLE

A

type 3 hypersensitivity

220
Q

what is antiphospholipid syndrome

A

an antibody mediated acquired thrombophilia characterised by thrombosis and recurrent miscarriages

221
Q

what other disease is antiphospholipid associated with

A

Associated with SLE in 20-30% of cases

222
Q

what is the diagnostic criteria for antiphospholipid disease

A

One or more clinical and one or more lab
clinical: vascular thrombosis, pregnancy morbidity
Lab: anticardiolipin antibody, lupus anticoagulant, anti-beta 2 glycoprotein 1 antibody

223
Q

what lifestyle changes can be made in antiphospholipid disease

A

About smoking, exercise more and healthy diet
- prevent CVS issues

224
Q

what other disorders is sjorgrens syndrome associated with

A

rheumatoid arthritis
SLE
Primary biliary cholangitis
Scleroderma

225
Q

what is the pathophysiology behind Sjorens syndrome

A

there is immunologically mediated destruction of epithelial exocrine glands - especially lacrimal and salivary glands

226
Q

what M3 agonist can be used in Sjorens syndrome

A

pilocarpine

227
Q

what other diseases is raynauds phenomenon associated with

A

SLE
Systemic sclerosis
rheumatoid arthritis
dermatomyositis

228
Q

what can raynauds phenomenon be caused by

A

Vibrational tools
smoking
beta blockers

229
Q

what is the treatment for raynauds phenomenon

A

Lifestyle - protect the hands, stop smoking
Calcium channel blockers

230
Q

what is systemic sclerosis

A

it is a multisystem autoimmune disease in which there is increased fibroblast activity, increasing collagen deposition and resulting in abnormal growth of connective tissue

231
Q

what has the highest case specific mortality out of any autoimmune rheumatic disease

A

systemic sclerosis

232
Q

what are the signs and symptoms of systemic sclerosis

A

skin involvement limited to the hands, face, feet and forearms
characteristic beak like nose and small mouth
microstomia
calcium deposits in the subcut tissue
eosophageal dysmotility or strictures
spider veins
Raynauds
GI, Renal and lung involvement

233
Q

how do you diagnose systemic sclerosis

A

Limited - anti centromere antibodies
Diffuse - Anti-topoisomerase, anti scl-70 ANAs
ASR is normal
there may be anemia

234
Q

what are the two types of systemic sclerosis

A

limited
diffuse

235
Q

how do you treat systemic sclerosis

A

Lifestyle - avoid smoking, handwarmers
Medications - PPIs, antibiotics, ACEi, cyclophosphamide

236
Q

what are symptoms of polymyositis

A

symmetrical progressive muscle weakness and wasting affecting the proximal muscles of the shoulder and pelvic girdle
- pain and tenderness are uncommon
- can lead to resp failure

237
Q

what are symptoms of dermatomyositis

A

heliotrope (purple) discolouration of the eyelids
scaly erythematous plaques over the knuckles
arthralgia, dysphagia resulting from oesophageal muscle involvement and raynauds

238
Q

what is Pagets disease

A

it is a localised disorder of bone remodelling

239
Q

what is the pathophysiology behind pagets disease

A

Increased osteoclastic bone resorption followed by increased formation of weaker bone
it leads to structurally disorganised mosaic of bone

240
Q

what is the demographic of people who get pagets disease

A

there is an increased incidence with age - rare under 40
it affects up to 10% of individuals by 90

241
Q

what are the signs and symptoms of pagets disease

A

60-80% are asymptomatic
Bone pain
joint pain
deformities - bowed tibia and skull changes
neurological complications
nerve compression of 8th cranial nerve
Blockage of aqueduct of sylvius causing hydrocephalus

242
Q

how do you diagnose Pagets disease

A

bloods - increased ALP, normal calcium and phosphate
Urinary hydroxyproline increase
X-ray - osteoarthritis

243
Q

how do you treat Pagets disease

A

Bisphosphonates
NSAIDs

244
Q

what is Rickets

A

When there is defective mineralisation at the epiphyseal growth plate

245
Q

what are symptoms of rickets

A

Leg bowing and knock knees
- tender swollen joints
- growth retardation
- bone and joint pain
- dental deformities
- enlargement of end of ribs

246
Q

who is at risk of septic arthritis

A

IV drug users
Immunocompromised
intra-articular injections

247
Q

what is pseudogout caused by

A

deposition of calcium pyrophosphate crystals

248
Q

what is gout caused by

A

deposition of monosodium urate crystals

249
Q

what is the pathway of uric acid formation

A
  1. cell breakdown and diet causes purine bases to be produced
  2. this becomes hypoxanthine
  3. xanthine oxidase converts this to xanthine
  4. xanthine oxidase converts this into uric acid
250
Q

what are the stages of gout progression

A

Stage 1: high uric acid levels building up round joints
stage 2: Acute gout were symptoms occur
stage 3: intercritital gout where there are periods of remission between attacks
stage 4: chronic gout, where pain is frequent and tophi form in the joints

251
Q

what is the definition of hyperuricaemia

A

when there is over 420umol/L in males
when there is over 360umol/L in females

252
Q

what are causes of gout

A

Diuretics - thiazides
High insulin levels
High fructose intake
Dysfunction of the URAT-1 transporter
Red meat
High saturated fat
High cell turnover rate
ALCOHOL
low dose aspirin

253
Q

what are symptoms of gout

A

red, hot, swollen joint
Acute onset

254
Q

what is the most common joint affected in gout

A

the big toe

255
Q

what are the investigations done for gout

A

Bloods
U+Es and eGFR
Uric acid levels and 4-6 weeks later again
Gold standard is joint aspiration

256
Q

what is the management plan for acute gout

A

1st line - NSAIDs or colchicine
2nd line - intra-articular steroid injection
lifestyle advice

257
Q

what is the management plan for chronic gout

A

allopurinol - inhibits xanthine oxidase
2nst line - febuxostat

258
Q

what are the three ways of infection entry into bone

A

Haematogenously
open wound
contiguously: skin into blood

259
Q

what needs to be done when someone is admitted with suspected sepsis

A
  1. Administer oxygen
  2. Take blood cultures
  3. Give IV antibiotics
  4. Give IV fluids
  5. Check serial lactates
  6. Measure urine output
260
Q

what are the stages in developing osteomyelitis

A

acute inflammation
subperiosteal abscess
sequestrum - necrotic bone attacked to healthy tissue
involucrum - layer of new bone growth outside of existing bone
Cloacae

261
Q

what diseases are classed as seronegative spondyloarthropathies

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Inflammatory bowel disease arthritis

262
Q

how does seronegative spondyloarthropathies present

A

sausage digits
psoriasis
inflammatory back pain
NSAIDs - good response
Arthritis
Crohns disease
HLA B27 positive
Uveitis - eye
Enthesitis

263
Q

what is the most common form of back pain

A

mechanical

264
Q

what are differentials for back pain

A

Congenital
trauma - fracture
infection - osteomyelitis
inflammation HLA B27
iatrogenic
miscellaneous
malignant - myeloma

265
Q

what are red flags for lower back pain

A

cauda equina syndrome
cancer of the spine
spinal fracture due to trauma or osteoporotic collapse
spinal infection

266
Q

what would you do if someone had red flag back pain

A

Bloods - look at inflammatory markers, FBS and ALP levels
DEXA scan and MRI

267
Q

what is treatment for mechanical back pain

A

Paracetamol
NSAIDS
if severe then weak or strong opiates
Lifestyle advice
physiotherapy

268
Q

in what age group is osteosarcoma common in

A

Children - metaphysis of long bones

269
Q

What is osteochondroma

A

It is a benign cancer of the bone - overproduction of the bone which deposits on the metaphysis

270
Q

what demographic is most likely to get osteochondroma

A

Men under 25

271
Q

What cancers are most likely to cause secondary bone tumours

A

Prostate
Breast
Kidneys
Thyroid
Lungs

272
Q

what investigations should be done if bone cancer is suspected

A

Bloods - FBC, U+E, ALP. PSA
Imaging - X ray and CT

273
Q

how do you manage bone cancer

A

pain management
bisphosphonates
radiotherapy
chemotherapy

274
Q

What is CRP

A

It is produced by the liver in response to infection

275
Q

What condition normally presents with pain at the base of the thumb

A

Osteoarthritis

276
Q

What are the four pillars of inflammation

A

Rubor
Dolor
Calor
Tumour

277
Q

What are differential diagnosis for osteomyelitis

A

Soft tissue infection
Damaged joint
Avascular necrosis
Gout

278
Q

How long is the treatment regime for osteomyelitis

A

6 weeks of Iv antibiotics are considered minimum

279
Q

What are features of TB osteomyelitis

A

Slower onset
Patient has systemic non specific symptoms
Biopsy is essential for diagnosis
Treatment is longer - 6 months

280
Q

What is ESR

A

Erythrocyte sedimentation rate - faster the sedimentation the more inflammation

281
Q

How do you diagnose an infected joint

A

Aspirate the joint, fluid will look cloudy/turgid/gloopy in infection

282
Q

What is the commonest cause of an infected joint

A

Staphylococcus aureus

283
Q

If someone is on prednisone (steroids) what do you do to the dose if they get an infection

A

Double the dose

284
Q

How many people with septic arthritis are over 65

A

45% of patients

285
Q

What are common organisms causing septic arthritis

A

Neisseria. G
Gram negative bacilli
Anaerobes
Mycobacteria
Fungi
S. Aureus

286
Q

What are signs of gonococcal arthritis

A

Inflammation around the tendon sheaths present in multiple joints

287
Q

How do uou diagnose prothestic joint infections

A

Wound can leak pus
Red
Swollen
Painful joint
X Ray to show changes
FBC, ESR, CRP
Micro

288
Q

What is a key diagnostic tool for prosthetic joint infection

A

Aspiration

289
Q

How do you treat prosthetic joint infection

A

Antibiotics
Detriment and implant replacement
Excision arthroplasty
Exchange arthroplasty - one stage and two stage exchange

290
Q

Who is pseudogout more common in men or women

A

Women

291
Q

In gout will uric acid be high, low or normal in the bloods

A

In a flair up it will be normal/lower as it will be crystallised in joints

292
Q

What foods can increase uric acid

A

Red meat
Shellfish
Offal

293
Q

Why do sweetened soft drinks increase gout

A

As fructose shares the renal uric acid transporters

294
Q

What are complications of gout

A

Tophi
Kidney disease - calculi, chronic urate nephropathy, acute urate nephropathy

295
Q

What measured in rheumatoid arthritis can suggest aggressive disease

A

Anti CCP
- cyclic citrullinated peptide

296
Q

What dose of methotrexate is given in rheumatoid arthritis

A

10-25mg/week

297
Q

What are the theories as to why HLA B27 increases your chance of sponyloarthritis

A
  1. Molecular mimicking
  2. B27 mis folding theory
  3. HLA B27 heavy chain homodimer hypothesis
298
Q

Why do you get a bamboo spine in analysing spondylitis

A

Because you have calcium depositing along the ligaments of the spine which eventually fuses them

299
Q

What joints can be affected in anakylising spondylitis

A

Ribs
Spine
Hips
Pelvis - sacro-iliac joints

300
Q

What are two subsets of ankylosing spondylitis

A

Non radiographic- only seen on MRI
Radiographic - seen on X Ray and MRI

301
Q

What are two subsets of ankylosing spondylitis

A

Non radiographic- only seen on MRI
Radiographic - seen on X Ray and MRI

302
Q

What are nail changes seen in spondyloarthritis

A

Pitting
Omucolysis - nail lifts from bed and thick white nail

303
Q

What infections can cause reactive arthritis

A

Salmonella
Shigella
Yersinia
Chlamydia
Ureaplasma urealytioum

304
Q

what are differential diagnosis for osteoarthritis

A

bursitis
gout
pseudogout
rheumatoid arthritis
psoriatic arthritis
avascular necrosis
internal derangements

305
Q

what are the lung manifestations of rheumatoid arthritis

A

Pleural effusion
Fibrosing alveolitis
Pneumoconiosis
Interstitial lung disease
Bronchiectasis

306
Q

what are heart manifestations of rheumatoid arthritis

A

pericarditis
pericardial rub
raynauds
pericardia effusion

307
Q

what are eye manifestations of rheumatoid arthritis

A

dry eyes
episcleritis
scleritis

308
Q

what are neuro manifestations of rheumatoid arthritis

A

peripheral sensory neuropathies
compression/entrapment neuropathies
cord compression

309
Q

what are kidney manifestations of rheumatoid arthritis

A

amyloidosis
nephrotic syndrome
CKD

310
Q

what are complications of gout

A

acute uric acid nephropathy
nephrolithiasis

311
Q

what can be affected in pseudogout

A

knees
wrists
shoulders
ankles
elbows
hands

312
Q

what are symptoms of pseudogout

A

Painful and tender joints
Osteoarthritis-like involvement of joints (wrists, shoulders)
Sudden worsening of osteoarthritis
Red and swollen joints
Joint effusion and fluctuance
Fever and malaise

313
Q

what is the pathophysiology of osteoperosis

A

mismatch between osteoclastic bone resorption and osteoblastic bone formation

314
Q

what are signs of osteoperosis

A

back pain
Kyphosis
Impaired vision
impaired gait
imbalance
low extremity weakness
vertebral tenderness

315
Q

what are risk factors for ankylosing spondylitis

A

genetics
family history
male sex

316
Q

what are the extra-articular manifestations of ankylosing spondylitis

A

osteoporosis
acute iritis/anterior uvitis
aortic valve incompetence
apical pulmonary fibrosis

317
Q

what are the complications of ankylosing spondylitis

A

Osteoporosis
Cardiac involvement
Hip involvement
Iritis
Pulmonary involvement
Neurological involvement

318
Q

what T cells play a primary role in psoriatic arthritis

A

CD8+ T cells

319
Q

what are complications of psoriatic arthritis

A

cardiovascular disease

320
Q

what percentage of reactive arthritis cases are HLA B27 positive

A

30-50%

321
Q

what are the symptoms of septic arthritis

A

Hot, swollen, painful, restricted joint
Acute presentation
Fever
Large joint
Single joint
Prosthetic joint
Proportionality of symptoms (i.e. if already got RA the symptoms would be much greater)
Sexual activity
Erythema migrans

322
Q

what are the possible complications of septic arthritis

A

Osteomyelitis
joint dystruction

323
Q

what are the causes of osteomyelitis

A

S aureus (most common)
Streptococci
Enterobacter spp
H influenzae
P aeruginosa (IVDU especially)
Salmonella spp (sickle cell especially)
Haematogenous spread, direct inoculation or direct spread from nearby infection

324
Q

what are clinical presentations of osteomyelitis

A

Limp/reluctance to weight bear
Non-specific pain at site
Malaise/fatigue
Local back pain associated with systemic symptoms
Paravertebral muscle tenderness/spasm
Local inflammation, tenderness, erythema or swelling
Fever
Spinal cord nerve root compression

325
Q

what are complications of systemic lupus erythematous

A

Anaemia
Leukopenia
Thrombocytopenia
Raynaud’s phenomenon

326
Q

What is the presentation of Ewing’s sarcoma?

A

Mass/swelling (normally in long bones)
Painful swelling
Redness in area surrounding tumour
Malaise
Anorexia
Weight loss
Fever
Paralysis +- incontinence (if affecting limb)
Numbness in limb

327
Q

what is the presentation of chrondrosarcoma

A

dull deep pain
affected area is tender and swollen
normally in the pelvis, femur, humerus, scapula and ribs

328
Q

how does osteosarcoma appear under X-ray

A

bone destruction and formation
soft tissue calcification produces a starburst appearance

329
Q

how do you treat bone tumours

A

Analgesia and anti-inflammatory drugs
Local radiotherapy to bone metastases relieve pain and reduces risk of pathological fracture
Chemo
Hormonal therapy
Bisphosphonates (alendronate) symptomatic relief

330
Q

what are risk factors of fibromyalgia

A

family history of fibromyalgia
rheumatological conditions
20-60 yrs
female sex

331
Q

what are risk factors for recurrent lower back pain

A

female
age
pre-existing chronic widespread pain
psychosocial factors

332
Q

what are main causes for mechanical lower back pain

A

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

333
Q

what is the management of mechanical lower back pain

A

Analgesia
Physio
Acupuncture
Avoid excessive rest
Re-education in manual handling
Comfortable sleeping position in medium hard mattres

334
Q

what is vertebral disc degeneration

A

Prolapse of intervertebral disc leading to acute back pain

335
Q

what are signs and symptoms of vertebral disc degeneration

A

sudden onset severe back pain
pain related to position and aggravated by movement
muscle spasm
radiation of pain depends on disc affected

336
Q

how do you manage vertebral disc degeneration

A

Acute stage - bed rest, analgesia, epidural corticosteroid injection
Surgery in severe cases
physio at recovery stage

337
Q

what is the aetiology of vasculitis

A

May be primary (this may be due to direct or indirect damage of endothelial cells of the vessel) or secondary to other conditions such as RA, SLE, hepatitis B & C, HIV, polymyositis and some allergic drug reactions.

338
Q

what is vasculitis

A

Vasculitis means inflammation of the blood vessels through either WBC attacking the endothelial lining, or attacking healthy cells near the endothelium and indirectly damaging them

339
Q

what is the pathophysiology of vasculitis

A

damaged endothelium exposes underlying collagen
this increases blood clotting restricting blood flow
the vessel becomes weaker making aneurysms more likely
as the vessels heal it becomes hard and stiff due to fibrin

340
Q

what is the pathophysiology of pagets disease

A

increased osteoclastic bone resorption
formation of new weaker bone
increased local bone blood flow and fibrous tissue
non spreading but can become symptomatic in sites which were silent

Phase 2a - Jemima (11 decks)

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