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MSK Flashcards

1
Q

What is the pathophysiology of rheumatoid arthritis?

A

Infiltration of synovium by inflammatory cells. Angiogenesis, means that synovium then grows over the cartilage, forming a pannus. This destroys the bone and cartilage, leading to bony erosions. Autoimmune condition

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2
Q

What condition are pannus and bony erosions seen?

A

RA

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3
Q

What are key features of RA? (clinical presentation)

A
  • stiffness worse in the morning, lasts more than an hour
  • decreased grip strength
  • Symmetrical
  • Subcutaneous nodules
  • Ocular involvement
  • no DIP involvement (end of finger)
  • more acute development
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4
Q

What is the typical patient affected by rheumatoid arthritis?

A

Female, middle age, FHx, other AI conditions

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5
Q

What auto antibody is seen in rheumatoid arthritis?

A

Anti CCP (very specific). Also RF: less specific

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6
Q

what is seen on a xray for RA?

A

loss of joint spacy, erosions, soft tissue swelling, soft bones (osteopenia)

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7
Q

What is the treatment for RA?

A
  • DMARDs: inhibit the action of cytokines and lymphocytes. Eg, methotrexate, sulfasalazine
  • NSAIDs
  • biological agents: eg, anti-TNF
  • steroid injections
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8
Q

What is the pathphysiology of osteoarthritis?

A

loss of cartilage with bone remodelling and inflammation. Progressive destruction.

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9
Q

What condition are osteophytes seen?

A

osteoarthritis. Due to bony regrowths calcifing

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10
Q

What is the clinical presentation of OA?

A
  • slow development
  • stiffness decreases after an hour in the morning
  • worse at night
  • exacerbated by exercise
  • reduced functioning
  • bony swelling: bouchards (PIP) nodes and heberdens nodes (DIP)
  • asymmetric
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11
Q

What condition are Heberdens and Bouchards nodes seen in?

A

OA

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12
Q

What is the dx of OA?

A
  • normal CRP, no RF, no CCP

- xray: LOSS. Osteophytes

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13
Q

What is the tx for OA?

A

pain relief, exercise, weight loss. Eventually joint replacement

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14
Q

What 5 things are seen in sero-negative arthritis?

A

Seronegative spondyloarthopathies share five main traits: Predilection for axial inflammation, Asymmetrical peripheral arthritis, Absence of rheumatoid factor, Inflammation of the enthesis and a Strong association with HLA-B27

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15
Q

What are the sero-neg conditions

A

ankolysing spondylitis, reactive arthritis, psoriatic arthritis

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16
Q

what is the enthesis?

A

connective tissue between tendon/ligament and bone

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17
Q

What are severe forms of psoriatic arthritis?

A

dactylitis (pencil in a cup deformity) and mutilans (destructive form)

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18
Q

What is the clinical picture of psoriatic arthritis?

A

Large range from mild synovitis to severe progressive arthroplasty.
Usually preceded with a rash.
Nail changes
Can present similarly RA. Assymetrical large joints and spine

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19
Q

What % of patients with psoriasis develop psoriatic arthritis?

A

20%

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20
Q

What is seen in diagnosis of all sero neg arthritis?

A
  • negative for anti-CCP and RF

- raised CRP and ESR

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21
Q

What is the tx for psoriatic arthritis?

A
  • DMARDs, NSAIDs, TNF-alpha inhibitors (inflixamib)

- surgery to connect destroyed/deformed joints

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22
Q

What is spondyloarthritis?

A

inflammatory disorder of the spine. Ankolysing occurs by forming syndesmophytes (bony growth in ligaments). This fuses the spine

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23
Q

What lymphocytes are involved in spondyloarthritis?

A

CDT8

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24
Q

What is the presentation of spondyloarthritis?

A

Progressive loss of spine movement. Increasing pain and morning stiffness, which improves with exercise. Often, lower back and buttocks. Swollen knee due to inflammatory effusion. Asymmetrical.
Loss of lumbar lordosis

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25
Q

What group of people is ankylosing spondyloarthritis typically seen in?

A

Young males

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26
Q

What is the gold standard dx for ankylosing spondylitis, and what is seen?

A
  • MRI picks up more
  • detects inflammation and oedema
  • shows erosion and sclerosis
  • bamboo spine
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27
Q

What is reactive arthritis?

A
  • persistent bacterial antigen in the synovium joints. Drives inflammation
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28
Q

When does reactive arthritis occur after infection?

A

2-4 weeks

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29
Q

What is Reiter’s triad and what condition does it relate to?

A

Reactive arthritis: can’t see, can’t pee, can’t climb a tree (conjunctivitis, urethritis, arthritis)

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30
Q

What organisms commonly cause Reactive arthritis?

A
  • STD: chlamydia

- GI: campylobacter, salmonella, shigella

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31
Q

What is the dx for reactive arthritis?

A
  • stool culture
  • sexual hx
  • aspirate: exclude septic arthritis/gout
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32
Q

What is septic arthritis?

A

active infection response. Direct injury/blood borne infection can cause inflammation and loss of joint function

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33
Q

What is the presentation of septic arthritis?

A

Single, swollen joint on movement. Swollen and tender, generally monoarthritis

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34
Q

What is the most common cause of septic arthritis?

A

S.aureus infection.

Gram negative more common in older people

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35
Q

What is dx for septic arthritis?

A
  • raised CRP
  • raised neutrophils
  • joint aspirate: turbid, yellow
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36
Q

What is the tx for septic arthritis;

A

drain the joint. Empirical antibiotics: flucoxacillin.

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37
Q

What is systemic lupus erythematous?

A

inflammatory, multisystem autoimmune disease with ANA

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38
Q

What is the most specific antibody for SLE, and what is used to track development?

A
  • anti double stranded DNA antibody: most specific
  • ESR: used to track development
  • ANA also present but non specific
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39
Q

What are some key clinical presentations of SLE?

A
  • general: fatigue, malaise, raynauds
  • arthralgia: symmetrical joint and muscle pain
  • photosensitive, butterful rash (triggered by UV light)
  • pulmonary involvement
  • cardiovascular involvement
  • renal involvement: haematuria, HTN
  • neuro: various psychiatric manifestations
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40
Q

What level of hypersensitivity reaction is SLE?

A

Type III

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41
Q

What is the pathophysiology of SLE?

A

apoptotic cells and fragments inefficiently cleared by phagocytes. Transferred to lymphoid tissue, and auto antibodies produced against self cells. Clinical manifestations due to antibody formation, development and deposition of immune complexes, complement activation

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42
Q

What is the tx for lupus?

A
  • NSAIDs and corticosteroids for arthralgia

- immunosuppression for severe symptoms (rutiximab)

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43
Q

What is dermamyositosis?

A

polymyositis with skin involvement

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44
Q

What is Sjogren’s syndrome?

A

lymphocytic infiltration of exocrine glands. Chronic inflammatory disease.

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45
Q

What is the clinical presentation of Sjorgren’s syndrome?

A

dry eyes, dry mouth, enlargement of the parotid gland. Vaginal dryness, dry cough, dysphagia

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46
Q

What is Schirmer’s test diagnostic for?

A

Sjogren’s. this is when you see if the eye rehydrates. If tears roll less than 10mm = significant

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47
Q

What auto antibodies are present in Sjogren’s?

A

The antibodies associated with Sjogren’s include anti-Ro and anti-La antibodies, rheumatoid factor, and antinuclear antibodies.

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48
Q

What is antiphospholipid syndrome, and its pathophysiology?

A

Hypercoaguable state due to ALP-antibodies. These activate complement and produce antibodies against coagulation factors, activate platelets and vascular endothelium

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49
Q

What is the clinical presentation of anti phospholipid syndrome?

A
  1. coagulation problems
  2. livedo reticularis (mottled discolouration of the skin)
  3. Obstetric problems (eg, recurrent miscarriages)
  4. thrombocytopenia (affects renal, cerebral and other vessels)
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50
Q

What is the treatment for APL syndrome?

A

acute thrombolysis management

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51
Q

what is polymyositis? What is the pathophysiology?

A

Autoimmune inflammation and necrosis of skeletal muscle fibres. Mediated by cyto-toxic T cells and autoimmune factors.

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52
Q

What is the clinical presentation of polymyositis?

A

Symmetrical progressive muscle weakness and wasting; affects proximal shoulder muscle and pelvis girdle (difficulty raising arms and going up stairs). Raynauds. Can involve dysphagia and dysphonia

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53
Q

What is the dx and tx of polymyositis?

A
  • dx: muscle biopsy: increased ALT and ALP

- Tx: oral prednisolone

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54
Q

What is Raynaud’s? How is it treated?

A

Abnormalities of blood vessel wall that common occurs with autoimmune conditions. Treatment via calcium channel blockers

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55
Q

How does gout present on microscopy?

A
  • needle shaped

- negative birefringent on polarised light

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56
Q

How does pseudogout present on microscopy?

A
  • rhomboid shaped

- positive birefringence on polarised light

57
Q

What is the typical composition of gout? where is this derived from?

A

monosodium urate monohdrate crystals. Derived from purine breakdown

58
Q

Where does gout typically affect?

A

big toe base

59
Q

What are tophi, and what condition are they associated with?

A

firm nodules that can form in gout

60
Q

What is the causes of gout?

A
  • hyperuricaemia (often idiopathic). Impaired excretions (CKD, diuretics, HTN). Increased uric acid production
61
Q

What is the tx (long term and short term) for gout?

A
  • colchicine (short term)

- allopurinol (long term)

62
Q

What drug class is allopurinol, and what is its mechanism of action?

A

xanthine oxidase inhibitors. Works to decrease production of uric acid in the body

63
Q

what is the composition of pseudogout?

A

calcium pyrophosphate crystals

64
Q

What is the presentation of pseudogout?

A

Often asymptomatic. Usually affects knee or wrist: swollen, tender and erythamatous.

65
Q

What is the aetiology for pseudogout?

A

precipitated by dehydration, steroids, hyperparathyroidism (increased calcium). Can be associated with metabolic conditions such as Wilson’s and hemochromatosis in young patients.

66
Q

What is polyarteritis nodosa?

A

inflammation and subsequent necrotising arteritis of medium/small arteries. Form of vasculitits

67
Q

What are the symptoms of polyarteritis nodosa?

A

vague symptoms. weight loss, headaches, Skin can have lesions, nodules purpura

68
Q

What is an associated compx with polyarteritis nodosa?

A

microaneurysm formation, thrombosis and infarction. Can affect various organs, often the kidney, leading to hypertension induced AKI

69
Q

What is the aetiology of polyarteritis nodosa? what condition is it associated with?

A

Hep B.

70
Q

What is the dx of polyarteritis nodosa?

A

angiography or biopsy; will see microaneurysms.

71
Q

What is polymyalgia rheumatica?

A

large vessel vasculitis that causes muscle pain and stiffness.

72
Q

What is vasculitis?

A

inflammation of blood vessels. Classified by vessel side affected. Large, medium and small arteries affected (can be ANCA neg or positive)

73
Q

What is the presentation of polymyalgia rheumatica?

A

Commonly symmetrical shoulder/pelvic girdle aching pain (similar distribution to polymyositis). Worse in the morning. Malaise, weight loss, anorexia. Commonly affects temporal arteries. Pain and stiffness due to inflammatory cells concentrating in tissues surrounding joints

74
Q

What is the dx of polymyalgia rheumatica?

A

increased ESR and CRP. USS of hip and shoulder will show characteristic pathological findings

75
Q

Tx of polymyalgia rheumatica?

A

Prednisolone. NSAIDs: little effect

76
Q

What is osteoporosis?

A

progressive skeletal disease with decreased bone mass and micro deterioration.

77
Q

What is the pathophysiology of osteoporosis?

A

Inadequate peak bone mass, excess bone resorption. Inadequate new bone in remodelling. Decreased oestrogen leads to increased bone resorption and decreased bone deposition. Decreased calcium leads to more bone resorption via PTH. RANKL binds to RANK, activating osteoclasts

78
Q

What is the presentation of osteoporosis?

A

develops assymetrically. Bone fragility. Fracture often the first sign (often the neck of the femur). Fractures in thoracic vertebrae can lead to Widow’s stoop

79
Q

What is the aetiology of osteoporosis?

A

Menopause, nutritional deficiency. Steroids can activate osteoclasts

80
Q

What is the dx of osteoporosis?

A

DEXA scan

81
Q

What is the treatment for osteoporosis?

A
  • bisphosphonates: aldrenoic acid (inhibit osteoclasts)
  • ensure adequate vitamin d and calcium intake
  • oestrogen supplement
82
Q

When should bisphosphonates be taken and why?

A

In the morning, and remain upright for 30 minutes afterwards, as can lead to oesophagitis
- once a week

83
Q

What is osteomalacia?

A

inadequate mineralisation of osteoid framwork, but normal bone amount (opposite to osteoporosis)

84
Q

What is the presentation of osteomalacia?

A

proximal muscle weakness. Decreased bone density. Can lead to fracture. Children: bow legs, knock knees. Rickets if whilst growing

85
Q

What is the aetiology of Osteomalacia?

A

vitamind D deficiency (due to malabsorption, poor diet, decreased sun). Liver disease, tumour induced, renal failure.

86
Q

What is the diagnosis of osteomalacia?

A
  • plasma serum test shows decreased calcium, decreased phosphate, increased PTH, decreased calcitriol.
  • biopsy: incomplete bone mineralisation
  • xray: loss of cortical bone
87
Q

What is Paget’s disease, and the pathophysiology

A

increased bone turnover, thus large, deformed bones. Associated with increased osteoblasts and osteoclasts. Thus, rapid bone remodelling, enlargement and deformity. New bone formed is mechanically weak.

88
Q

What is the presentation of Paget’s disease?

A

xray: pathological fractures. Deep pain and bone deformity. Commonly affects the spine, skull, femur, tibia. Osteoporosis circumscripta (well defined lesions). Cotton wool skull (areas of lysis and sclerosis). V shaped defects in long bones.

89
Q

What is the possible complications of Paget’s?

A

osteoarthritis, nerve compression, osteosarcoma (due to increased bone turnover)

90
Q

What is the dx and tx of Paget’s?

A
  • Dx: xrays. Increased ALP reflects increased bone metabolism.
  • Tx: bisphosphonates
91
Q

What is mechanical back pain, and what conditions can it be associated with?

A
  • back pain in the lumbosacral region
  • hx of bowel and urinary incontinence and paraesthesia: cauda equina
  • nerve root issue: sharp, well localised pain
  • can be caused by malignancy
92
Q

What is the dx and tx for mechanical back pain?

A
  • Dx: CT/MRI to check nothing insidious

- Tx: NSAIDs, analgesics

93
Q

What is fibromyalgia?

A

chronic widespread pain and sensitivity to pressure. Associated with unrefreshing sleep and tiredness

94
Q

what is osteomyelitis?

A

infection of the bone marrow

95
Q

What can cause osteomyelitis (not the organisms, method of infection!)

A

occurs as a result of hematogenous seeding, contiguous spread from
nearby tissue or traumatic or surgical introduction of organism

96
Q

What organisms cause osteomyelitis?

A

Most commonly caused by Staphylococcus aureus (gram positive).

  • IVD users: Pseudomonas (Gram-negative, Gammaproteobacteria), E.coli (gram negative)
  • Sickle Cell patients: Salmonella (gram neg)
  • Hip or Knee prosthesis: Staphylococcus epidermidis (gram positive)
97
Q

What is a sequestrum, and what condition is it associated with?

A
  • osteomyelitits
  • forms due to chronic inflammatory destruction of bone
  • when dead bone detaches from healthy, forms sequestrum. this remains in situ, acting as a source/focus of infection
  • new bone can form around it, creating deformity
98
Q

What are the symptoms of osteomyelitits?

A
  • Pain around affected region
  • Swelling, tenderness, warmth, erythema
  • Can be associated with systemic signs: fever, tiredness
99
Q

What is the diagnosis of osteomyelitis?

A

-Blood tests: raised WCC, raised inflammatory markers (ESR, CRP)
-CT/MRI are highly sensitive but expensive; x-ray can show changes after 2
weeks
-Bone/percutaneous biopsy should be taken

100
Q

What is the treatment for osteomyelitits?

A

flocaxicillin with fusidic acid (topical skin infection)

101
Q

What is degenerative disc disease, and its pathophysiology?

A

pathological process of degeneration of invertebral discs

- fibrocartilage replaces gelatinuos mucoid nucleus pulpulos. possible herniation of the the nucleus pulpulos

102
Q

What is the Dx and Tx of degenerative disc disease?

A
  • Dx: CT/MRI

- Tx: physio, NSAIDs, epidural steroids

103
Q

What cancers commonly metastasise to bone?

A

BLT w/ Kosher Pickle

  • breast
  • lung
  • thyroid
  • kidney
  • prostate
104
Q

What is ANCA?

A

antineutrophil cytoplasmic antibodies

105
Q

What are all vasculitis associated with?

A

raised ESR and anaemia

106
Q

What is Schober’s test?

A

assess mobility of the spine. Less than 20cm range of movement

107
Q

What is Buerger’s test?

A

peripheral vascular examination, that assesses the adequacy of arterial blood supply to the legs

108
Q

what is the commonest soft tissue sarcoma in children?

A

rhabdomyosarcoma

109
Q

What is Ewing’s sarcoma? Classic presentation?

A
  • bone sarcoma

- onion skin apperance of periosteum

110
Q

What is osteosarcoma? classic presentation?

A

malignant neoplasm of immature bone. common in teens

- presen: bone pain at night. Sunburt apperance on xray and Codman’s triangle

111
Q

What are the factors for osteoporosis development?

A

SHATTERED

  • S; steroid use
  • H: hyperthyroidism/hyperparathyroidism
  • A: alcohol/tobacco
  • T: thing
  • T: testosterone decrease
  • E: early menopause
  • R: renal or liver failure
  • E: erosive/ inflammatory bone disease
  • D: dietary calcium decrease
112
Q

What are systemic RA symptoms?

A

decreased weight, appetite, more sweating, increased temperature, tiredness

113
Q

What is a FRAX score?

A

Risk of major fracture in 10 years

114
Q

What is denosumab?

A

2nd line treatment for osteoporosis. Binds to RANKL and blocks osteoclast activity

115
Q

Why does MRI provide a early diagnosis for S.A?

A

Can see the early bone marrow oedema

116
Q

What areas of the body do DMARDs work?

A

peripheral joint pain, not axial

117
Q

What are the nail changes seen in psoriatic arthritis?

A
  • onycholysis (separation of nail from nail bed)

- dactylitis (inflammation of full finger)

118
Q

What are the risk factors for septic arthritis and osteomyelitis (they’re the same)

A
  • pre existing joint disease
  • prosthetic joint/recent surgery
  • IVDU
  • penetrating injury
  • immunosuppression
  • alcohol misuse
  • diabetes
  • intra articular corticosteroid injection
119
Q

What are risk factors for primary bone tumours?

A

previous radiotherapy, previous cancer, paget’s benign bone lesions

120
Q

What are red flag symptoms for bone cancer?

A

pain worse at night, atypical bony/soft tissue swelling, pathological fractures

121
Q

What is first line and gold standard dx for bone cancer?

A
  • 1st line: xray

- gold standard: biopsy

122
Q

In which condition are these Ab seen?anti-cardiolipin antibodies and anti-beta-2 glycoprotein I antibodies)

A

anti phospholipid syndrome

123
Q

What other organ may see complications of RA?

A

Lung; interstitial lung disease, fibrosis

124
Q

What are common signs of rheumatoid arthritis?

A

Swan neck thumb, ulnar deviation, boutonniere deformity, nodules

125
Q

What causes pseudogout?

A

history of recurrent damage to joint

126
Q

What condition has the sign of correctable ulnar deviation?

A

SLE

127
Q

What halts the progression of Sjogrens?

A

hydroxychloroquine

128
Q

What is the inheritance pattern of Marfans? and what does the faulty gene effect?

A

AD. Affects the gene creating fibrillin

129
Q

What is the faulty in Ehlers Danlos syndrome?

A

faulty collagen

130
Q

What ANCA is seen in granulomatous w/ polyangiitis

A

c-ANCA

131
Q

What ANCA is seen in eosinophilic granulomatous polyangiitis?

A

p-ANCA

132
Q

What symptoms are seen in granulomatous with polyangitiis?

A

saddle shaped nose, epistaxis, sinusitis, cough, wheeze, haemoptysis

133
Q

what is the most common cause of osteomyelitis in sickle cell anaemia patients?

A

salmonella

134
Q

What is the physical test done in ankylosing spondylitis?

A

Schober’s

135
Q

What is the initial test for SLE and why?

A

ANA (more SLE patients positive for it, even if less specific)

136
Q

what medications can increase the risk of gout?

A

Thiazide diuretics, low-dose aspirin block uric acid secretion, hence increases its blood level. Hyperuricemia is a relatively common finding in people treated with a loop or thiazide diuretic and may, over some time, contribute to new-onset gout

137
Q

What is felty’s syndrome?

A

Felty’s Syndrome is a rare complication of long-standing rheumatoid arthritis. Felty’s Syndrome is characterized by a classic triad of rheumatoid arthritis, splenomegaly, and neutropenia

138
Q

What AI disease is anti phospholipid syndrome closely associated with?

A

SLE

GI P2a (12 decks)

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