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Phase 2a flashcards (Alec's) > MSK + Rheum > Flashcards

MSK + Rheum Flashcards

1
Q

What is the functional unit of bone?

A

Osteon

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2
Q

What bone is found on the inside and which on the outside?

A
  • Outside = hard cortical bone
  • Inside = soft spongy trabecular/cancellous bone
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3
Q

What is found within trabecular bone?

A

Bone marrow

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4
Q

What canals travel vertically within bone?

A

Haversion canal

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5
Q

What canals travel horizontally within bone and connect osteons?

A

Volkmann canal

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6
Q

What is the main inorganic component of bone?

A

Hydroxyapetite

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7
Q

What is the main organic component within bone?

A

Type 1 collagen

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8
Q

What are the three types of joint?

A
  • Fibrous - skull sutures
  • Cartilaginous - IV discs
  • Synovial
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9
Q

What are the 3 components of synovial joint?

A
  • Articular cartilage
  • Joint capsule
  • Synovial cavity (filled with fluid)
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10
Q

What is the most common type of arthritis?

A

Osteoarthritis

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11
Q

What causes joints to become osteoarthritic?

A

Mechanical shearing forces

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12
Q

What are some risk factors for osteoarthritis (5)?

A
  • Age (50+)
  • Female
  • Obesity
  • Occupation/ lifestyle
  • Genetics
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13
Q

What gene has been linked to osteoarthritis?

A

COL2A1

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14
Q

How do arthritic joints form in osteoarthritis?

A

Chondrocyte metalloproteinase production (degrades T2 collagen) –> imbalanced cartilage breakdown > repair

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15
Q

Where is T2 collagen found?

A

Cartilage

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16
Q

How does bone try and compensate for its degradation in OA?

A

T1 collagen grows to replace T2 breakdown; abnormal bony growths form

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17
Q

What are the abnormal bony lumps seen in osteoarthritis called?

A

Osteophytes

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18
Q

When is joint pain worse in osteoarthritis?

A

Worse with movement, as day goes on

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19
Q

Which joints are affected the most by osteoarthritis (5)?

A
  • Hips
  • Knees
  • DIP
  • Base of thumb (1st CMC)
  • Wrist
    Mostly weight bearing joints
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20
Q

What are bony growths/ nodes called on the DIP and PIP?

A
  • DIP = Hebdern nodes
  • PIP = Bouchard nodes
    H after B, therefore further away (DIP)
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21
Q

How is OA investigated?

A
  • X-ray of affected joints
    Not essential if patient over 45
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22
Q

What signs are seen in an OA X-ray (4)?

A
  • Loss of joint space
  • Osteophytes
  • Subchondral sclerosis (increased density along joint line)
  • Subchondral cysts
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23
Q

How is OA managed (3)?

A
  • Lifestyle changed (reduce weight, physio)
  • NSAIDs (pain relief, inflammation)
  • Surgical joint replacement
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24
Q

What is the restoration of a joint called?

A

Arthroplasty

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25
Q

What is rheumatoid arthritis?

A

Inflammatory, autoimmune polyarthritis

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26
Q

What pattern does RA affect the joins?

A

Symmetrically

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27
Q

What are some risk factors for RA?

A
  • Female
  • 30-50 years
  • Smoking
  • Genetics
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28
Q

What genes are associated with RA (2)?

A
  • HLA-DR4
  • HLA-DRB1
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29
Q

What protein mutation is seen in RA?

A

Arginine –> citruline; mutation in T2 collagen

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30
Q

What antibodies form as a result of this mutation in T2 collagen in RA?

A
  • RF antibody (against IgG)
  • Anti-CCP (against citruline)
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31
Q

What is released in RA joints that causes the synovial lining to proliferate?

A

Cytokines (e.g. interferons, TNF)

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32
Q

What is the growth + expansion of the synovial lining called?

A

Pannus

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33
Q

What effects does the growth of the pannus have within the joint?

A

Damages bone + cartilage –> more inflammation

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34
Q

When is joint pain worse with RA?

A

Worst in the morning, improves with movement

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35
Q

What signs are seen in the hands of people with rheumatoid arthritis (4)?

A
  • Boutonnières deformity (hyperextended DIP, flexed PIP)
  • Swan neck deformity (flexed DIP, hyperextended PIP)
  • Z thumb shape
  • Ulna deviation of fingers
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36
Q

Which joints are commonly affected in RA (4)?

A
  • PIP
  • MCP
  • Wrist + ankle
  • Cervical spine
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37
Q

What temperatures are RA joints?

A

Often hot

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38
Q

What are some extra-articular manifestations of RA (4)?

A
  • Pulmonary fibrosis
  • Atherosclerosis
  • Skin nodules (often on elbows)
  • Spinal cord compression
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39
Q

How is RA investigated (3)?

A
  • ESR/CRP high
  • RF +ve, anti-CCP (more specific 80%)
  • X-ray
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40
Q

What is seen in an X-ray of those with RA (4)?

A
  • Loss of joint space
  • Boney erosions
  • Soft tissue swelling
  • Periarticular osteopenia
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41
Q

How is RA managed order medications are used?

A
  • NSAIDs/ steroids for flares
  • DMARD
  • 2 DMARDs
  • DMARD + biologic
  • DMARD + rituximab
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42
Q

What is the first line DMARD for RA?

A

Methotrexate

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43
Q

What DMARDs can be used in combination?

A
  • Sulfasalazine
  • Hydroxychloroquine (more mild, anti-malarial)
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44
Q

How does methotrexate work?

A

Interferes with folate metabolism

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45
Q

What is sometimes taken with methotrexate?

A

Folic acid

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46
Q

What is the first line biologic class for RA?

A

TNF inhibitor

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47
Q

Give an example of a TNF inhibitor?

A

Infliximab

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48
Q

What is infliximab?

A

Monoclonal antibody against TNF

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49
Q

What is a second line biologic drug?

A

Rituximab

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50
Q

How does rituximab work?

A

Monoclonal antibody, targets CD20 on B-cells

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51
Q

What is gout?

A

Deposition of uric acid crystals along a joint

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52
Q

Is gout inflammatory or non inflammatory?

A

Inflammatory (most common inflammatory arthritis in uk)

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53
Q

What are some risk factors for gout (5)?

A
  • Male
  • Obesity
  • High purine diet
  • Kidney disease
  • Middle aged (50-70)
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54
Q

Give some examples of purine rich foods (3)?

A
  • Red meat
  • Seafood
  • Alcohol (especially beer)
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55
Q

What food type is protective against gout?

A

Dairy

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56
Q

What is the most common type of uric acid crystal?

A

Monosodium urate crystals

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57
Q

Explain how monosodium urate crystals form?

A

Purine –> uric acid –> monosodium urate

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58
Q

What is the pattern of joints affected by gout?

A

Often only 1 joint is affected

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59
Q

Which joints are commonly affected by gout (3)?

A
  • Big toe (MTP)
  • Wrist
  • Base of thumb (CMC)
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60
Q

What are the sign/ symptoms of gout at the joint?

A

Sudden onset (pain, red, swollen, hot, can’t put weight on it)

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61
Q

How is gout diagnosed?

A

Joint needle aspiration

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62
Q

What features are present in fluid aspirated by a needle of those with gout (3)?

A
  • Needle shaped crystals, yellow
  • No bacterial growth
    Known as -ve birefringent
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63
Q

How is gout treated (3)?

A
  • NSAIDs
  • Colchicine
  • Steroid injection
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64
Q

What medication can be given as a gout prophylaxis?

A

Allopurinol

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65
Q

How does allopurinol work?

A

Xanthine oxidase inhibitor

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66
Q

What does xanthine oxidase do?

A

Converts purines to uric acid

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67
Q

What is pseudogout?

A

Calcium pyrophosphate crystal deposition along joints

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68
Q

What are some risk factors for pseudo gout (5)?

A
  • Female
  • Old (70+)
  • Diabetes
  • Metabolic diseases
  • OA
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69
Q

What is the pattern of joint involvement in pseudogout?

A

Often polyarticular with knee involvement

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70
Q

What features are present in pseudo gout joint aspiration (3)?

A
  • Rhomboid shaped crystals
  • No bacterial growth
    +ve birefringent
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71
Q

How is gout managed (3)?

A
  • NSAIDs
  • Colchicine
  • Steroid injection
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72
Q

What is osteoporosis?

A

Low bone density

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73
Q

What is osteomalacia?

A

Low mineralisation of bone

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74
Q

What are some risk factors for osteoporosis (9)?

A
  • Steroids
  • Hyper(para)thyroidism
  • Alcohol + smoking
  • Thin (low BMI)
  • Testosterone low
  • Early menopause (low oestrogen)
  • Renal/ liver failure
  • Erosive + inflammatory disease
  • DMT1 (malabsorption)
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75
Q

What score measures the extent of osteoporosis?

A

T score

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76
Q

What is the T score?

A

Number of standard deviations below a healthy adults bone density

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77
Q

What are the ranges of normal/ abnormal T scores (3)?

A
  • 0 to -1 = normal
  • -1 to -2.5 = osteopenia
  • <-2.5 = osteoporosis
    Fracture = severe osteoporosis
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78
Q

What is the main symptom of osteoporosis?

A

f R a C T Ur E s

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79
Q

How is osteoporosis investigated?

A

DEXA scan

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80
Q

How does a DEXA scan work?

A

Two X ray beams, absorption by bone measured, compared to reference value

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81
Q

What is the first line drug for osteoporosis prevention?

A

Bisphosphinates

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82
Q

Give an example of a bisphosphinate?

A

Alendronate

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83
Q

How do bisphosphinates work?

A

Inhibit RANK-L singling (inhibit osteoclasts)

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84
Q

What other medications can be used to treat osteoporosis?

A
  • Denosomab (monoclonal antibody)
  • HRT (oestrogen)
  • Raloxifene (stimulates oestrogen receptors on bone)
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85
Q

What supplement can be given to people with osteoporosis?

A

Calcium + vitamin D3 (e.g. adcal-D3)

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86
Q

What is systemic lupus erythematosis?

A

Type 3 hypersensitivity reaction involving anti-nuclear antibodies

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87
Q

How does SLE cause inflammation?

A

Apoptosis occurs –> inside debris exposed to immune cells (particularly nuclear antigens) –> anti-nuclear antibodies form –> immune complex deposition = inflammation

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88
Q

What are some risk factors/ causes of SLE (5)?

A
  • Female
  • Afro-carribean
  • Genetics
  • Younger adult (20-40)
  • Sunlight exposure (more apoptosis)
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89
Q

What genes are associated with SLE (3)?

A
  • HLA B8
  • HLA DR2 or 3
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90
Q

What are the signs/ symptoms of SLE (6)?

A
  • Butterfly rash (malar rash - photosensitive)
  • Glomerulonephritis
  • Joint pain
  • Raynauds
  • Vasculitis
  • Serositis (mesothelium inflammation - e.g. pleurisy)
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91
Q

How is SLE diagnosed (3)?

A
  • Bloods = high ESR (CRP often normal, anaemia
  • Urine = haematuria, proteinurea (nephritic)
  • Serology = ANA Abs, anti ds DNA Abs
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92
Q

How is SLE treated (3)?

A
  • Lifestyle - avoid sun
  • NSAIDs/ steroids
  • DMARDs - hydroxychloroquine
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93
Q

What is anti-phospholipid syndrome?

A

Antiphospholipid antibodies are present in the blood leading to a hyper coagulable state

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94
Q

What are the two types of antiphospholipid syndrome?

A
  • Primary - idiopathic
  • Secondary - to another disease e.g. SLE
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95
Q

What are the symptoms/ signs of antiphospholipid syndrome (4)?

A
  • Arterial/ venous clots
  • Recurrent miscarriages
  • Thrombocytopenia
  • Livedo reticularis
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96
Q

What is livedo reticularis?

A

Purple lace like rash on skin

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97
Q

What 3 antibodies would suggest a diagnosis of aPL syndrome?

A
  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein 1 antibodies
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98
Q

How is aPL syndrome treated?

A

Warfarin (INR=2-3)

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99
Q

How is aPL syndrome treated in a pregnant woman?

A

Aspirin + heparin

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100
Q

What is scleroderma?

A

Autoimmune condition characterised by excessive production of collagen (fibrosis)

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101
Q

What is systemic scleroderma?

A

Scleroderma that affects the whole body not just localised to the skin

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102
Q

What is the most common type of systemic scleroderma?

A

Limited cutaneous systemic scleroderma (CREST syndrome)

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103
Q

What are the symptoms of scleroderma (5)?

A
  • Calcinosis
  • Raynauds - digit ischemia due to vasospasm, (often brought on by cold)
  • OEsophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
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104
Q

What is calcinosis in scleroderma?

A

Calcium deposits under skin (subcutaneous tissue)

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105
Q

What is sclerodactyly?

A

Thickening and hardening of the skin on the hands

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106
Q

What is telangiectasia?

A

Dilated small BVs in skin

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107
Q

What are some other signs/ symptoms of scleroderma ((other than CREST), (2)?

A
  • Pulmonary fibrosis
  • Hypertension
108
Q

How is scleroderma diagnosed (2)?

A
  • ANA antibodies
  • Anti-centromere antibodies
    These suggest scleroderma along with symptoms
109
Q

How is scleroderma treated?

A

No proper treatment - steroids help along with supportive treatment

110
Q

What is Sjogren’s syndrome?

A

Autoimmune condition affecting exocrine glands –> dry eyes + mouth

111
Q

What are some causes/ risk factors of Sjogren’s (3)?

A
  • Secondary Sjogren’s (e.g. SLE)
  • Female
  • Family history/ genetics
112
Q

Which genes have been linked to Sjogren’s (2)?

A
  • HLA-B8
  • HLA-DR3
113
Q

What are the symptoms of Sjogren’s (3)?

A
  • Dry eyes, mouth, vagina
  • Conjunctivitis
  • Dental cavities
114
Q

How is Sjogren’s syndrome diagnosed?

A
  • Serology
  • Schirmer test
115
Q

What antibodies are present in Sjogren’s syndrome (2)?

A
  • Anti-RO
  • Anti-LA (more specific to SLE)
116
Q

What is schirmer test?

A

Filter paper inserted into eye, length tears travel along paper determines “wetness” of eye

117
Q

How is Sjogren’s syndrome treated?

A
  • Artificial tears/ saliva
  • Hydroxychloroquine (may be given)
118
Q

What does Sjogren’s syndrome increase the risk of?

119
Q

What is polymyositis?

A

Autoimmune inflammation + necrosis of the muscle

120
Q

What is polymyositis called when there is skin/ connective tissue involvement?

A

Dermatomyositis

121
Q

What are some risk factors/ causes of polymyositis?

A
  • Female
  • Genetics
122
Q

Which genes have been linked to polymyositis?

A
  • HLA-B8
  • HLA-DR3
123
Q

What is the presentation of polymyositis?

A

Symmetrical muscle waisting around shoulders and pelvic girdle (hard to stand up + put hands on head)

124
Q

What dermatological changes are seen in those with dermatomyositis (3)?

A
  • Grotten lesions
  • Photosensitive erythematous rash on back + shoulders
  • Heliotrope
125
Q

What are Grotten lesions seen in dermatomyositis?

A

Scales on knuckles, elbows and knees

126
Q

What is a heliotrope seen in dermatomyositis?

A

Purple eyelids

127
Q

What Abs are present in poly/dermatomyositis (2)?

A
  • Anti-Jo-1
  • Anti-Mi-2 (dermatomyositis only)
128
Q

How can polymyositis be diagnosed?

A

Muscle biopsy = necrosis

129
Q

What may be elevated in the blood in those with polymyositis?

A

Creatine kinase - enzyme found in muscle, released when inflamed

130
Q

How is polymyositis treated?

A

Corticosteroid (prednisolone)

131
Q

What is fibromyalgia?

A

Functional pain disorder, chronic + widespread pain in muscles and skin

132
Q

What are some risk factors/ causes of fibromyalgia (2)?

A
  • Female
  • Depression/ stress/ trauma
133
Q

What chemical is the main modulator/ neurotransmitter of pain?

A

Substance P

134
Q

What chemicals dampen pain reception (2)?

A
  • Serotonin
  • Noradrenaline
135
Q

What is thought may cause fibromyalgia?

A

Imbalances between substance P and serotonin/ NAd

136
Q

What are the signs/ symptoms of fibromyalgia (3)?

A
  • Stressed/ depressed
  • Pain + stiffness over all body
  • Sleep disturbances
137
Q

How is fibromyalgia diagnosed?

A
  • Exclusion of other conditions (no ANA, high ESR/ CRP)
  • Pain in multiple places/ when palpated
138
Q

How is fibromyalgia treated?

A
  • Antidepressants (TCAs e.g. amitriptyline)
  • CBT
139
Q

What is a differential diagnosis for fibromyalgia?

A

Polymyalgia rheumatica

140
Q

What is polymyalgia rheumatica?

A

Unknown cause inflammatory disorder related to vasculitis

141
Q

What are the symptoms of polymyalgia rheumatica?

A

Muscle/ joint pain in shoulder and hip - worse with movement

142
Q

How is polymyalgia rheumatica diagnosed (2)?

A
  • High ESR/CRP
  • Exclusion of other conditions
143
Q

How is polymyalgia rheumatica treated?

A

Steroids (prednisolone)

144
Q

What is vasculitis?

A

Inflammation of blood vessels

145
Q

What can cause vasculitis/ how can it occur (2)?

A
  • Direct attack on BV wall by immune cells (due to molecular mimicry)
  • Indirect damage to endothelium/ BV wall due to nearby cells being attacked
146
Q

What are the three types of vasculitis?

A
  • Large vessel
  • Medium vessel
  • Small vessel
147
Q

What are 3 general symptoms of vasculitis due to the inflammatory response?

A
  • Fever
  • Weight loss
  • Fatigue
148
Q

What are two types of large vessel vasculitis?

A
  • Giant cell arteritis
  • Takayatsu arteritis
149
Q

What is giant cell arteritis?

A

Inflammation of large arteries (thought to be autoimmune)

150
Q

Which arteries are commonly affected by GCA (3)?

A

Branches of external carotid:
* Temporal artery
* Ophthalmic artery
* Facial artery (supplies jaw)

151
Q

What are the symptoms of GCA (3)?

A
  • Unilateral temporal headache/ scalp tenderness
  • Jaw pain while chewing (claudication)
  • Change in vision
152
Q

What is a complication of GCA?

153
Q

How is GCA investigated (2)?

A
  • High ESR/ CRP
  • Temporal artery biopsy
154
Q

What would be present in temporal artery biopsy?

A

Granulomatous inflammation of intima + media (skip lesions - therefore take long biopsy)

155
Q

How is GCA treated?

A

Steroids - Prednisolone

156
Q

What is GCA strongly associated with?

A

Polymyalgia rheumatica

157
Q

What are three types of medium vessel vasculitis?

A
  • Polyarteritis nodosa
  • Buergers disease
  • Kawasaki disease
158
Q

What is polyarteritis nodosa associated with?

A

Hep B/ HIV infection

159
Q

What are some symptoms/ signs of polyarteritis nodosa (4)?

A
  • Mononeuritis multiplex (type of peripheral neuropathy that affects 2+ nerves)
  • CKD/AKI (pre renal) due to narrowing of arteries
  • GI bleeds
  • Skin nodules/ haemorrhages
160
Q

How is polyarteritis nodosa diagnosed?

A
  • CT angiogram = beads on string (micro aneurisms)
161
Q

How is polyarteritis nodosa treated (2)?

A
  • Steroids
  • Treat htn
162
Q

What does Buerger’s disease commonly cause/ affect?

A

Peripheral skin necrosis

163
Q

Who is typically affected by Buerger’s disease?

A

Male smoker 20-40

164
Q

Who is typically affected by Kawasaki disease?

A

Young children <5

165
Q

What does Kawasaki disease cause?

A

Coronary artery aneurism

166
Q

What are 3 small vessel vasculitis?

A
  • Granulomatosis with polyangitis
  • Eosinophilic granulomatosis with polyangitis
  • Henoch Schonlein purpura
167
Q

What is Henoch Schonlein purpura?

A

An IgA vasculitis (basically systemic IgA nephropathy)

168
Q

Where does granulomatosis with polyangitis commonly affect (2)?

A
  • Repiratory tract
  • Kidneys
169
Q

What are 4 seronegative spondyloarthropathies?

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Enteric arthritis
170
Q

What do seronegative arthropathies have in common (2)?

A
  • Affect the axial skeleton
  • Seronegative for RF and ANA
171
Q

What are the general features of spondyloarthropathies (9)?

A
  • Sausage digit (dactylics)
  • Psoriasis
  • Inflammatory back pain
  • NSAIDs good reponse
  • Enthesitis
  • Arthritis
  • Crohns/UC
  • HLA-B27
  • Eye (uveitis)
172
Q

What is enthesitis?

A

Inflammation of entheses (sites where tendons/ ligaments insert onto bone)

173
Q

What happens in ankylosing spondylitis?

A

New bone growth between vertebrae stiffens the spine

174
Q

What is the name of the vertical new abnormal bony growth?

A

Syndesmophytes

175
Q

What are the signs/ symptoms of ankylosing spondylitis (5)?

A
  • Anterior uveitis
  • Enthesitis (plantar fasciitis/ achilles tendonitis)
  • Dactylitis
  • Kyphosis + decreased lordosis (inward curving above bum)
  • Progressive back stiffness, worse in morning
176
Q

What is Schober test?

A

Measures amount of spine flexion; two points on back marked, then measured when spine flexed

177
Q

How is ankylosing spondylitis investigated (3)?

A
  • Xray/ MRI
  • ESR/CRP high
  • HLA-B27 +ve
178
Q

What changes are seen in xray of those with ankylosing spondylitis (3)?

A

“Bamboo spine”:
* Squared vertebral bodies
* Syndesmophytes
* Sacroilitis (inflammation of sacroiliac joint)

179
Q

How is ankylosing spondylitis treated?

A
  • NSAIDs (+ steroid injections)
  • TNF alpha blockers
180
Q

Give 2 examples of TNF alpha blockers?

A
  • Infliximab
  • Etanercept
181
Q

How does etanercept work?

A

Soluble TNF alpha receptor –> binds TNF alpha preventing it having effects

182
Q

Which joints does psoriatic arthritis usually affect?

A

Hands wrists and feet

183
Q

Which joints does psoriatic spondylitis (specific type / pattern of psoriatic arthritis) affect?

A

Lumbar spine region

184
Q

What are some symptoms/ signs of psoriatic arthritis (5)?

A
  • Dactylitis
  • Enthesitis
  • Onycholysis (separation of nail from bed)
  • Psoriatic rash (often under nails)
  • Joint pain
185
Q

What is a severe form of psoriatic arthritis known as?

A

Arthritis mutilans

186
Q

What percentage of psoriatic arthritis is mutilans?

187
Q

What happens in arthritis mutilans?

A

Osteolysis of phalanxes –> telescoping of digits

188
Q

What features are seen on an x-ray of psoriatic arthritis (5)?

A
  • Periostitis
  • Ankylosis (joining of bones)
  • Dactylitis
  • Osteolysis
  • Pencil in a cup appearance
189
Q

How is psoriatic arthritis treated?

A
  • NSAIDs (+ steroid injections)
  • 1st = methotrixate
  • Anti TNF
  • IL 12/ 23 inhibitor
190
Q

Give an example of an IL12/23 inhibitor?

A

Ustekinumab

191
Q

What is reactive arthritis?

A

Sterile inflammation of joints + tendons reacting to distant infection

192
Q

What infections commonly cause reactive arthritis (2)?

A
  • Gastroenteritis
  • STIs (e.g. chlamydia, gonorrhoea)
193
Q

What are the main 3 symptoms of reactive arthritis?

A
  • Cant See (anterior uveitis = iritis)
  • Cant Pee (urethritis)
  • Cant climb a tree (arthritis of knee joint - commonly)
194
Q

How is reactive arthritis investigated (2)?

A
  • Joint aspirate
  • identification of infection (sexual health review, stool culture)
195
Q

What would a joint aspirate show in reactive arthritis (2)?

A
  • Sterile
  • -ve for crystal arthropathy
196
Q

How is reactive arthritis treated?

A
  • NSAIDs + steroids
  • If chronic = DMARD/ anti-TNF
197
Q

What is enteric arthritis?

A

Arthritis that occurs with IBD

198
Q

Which joints are commonly affected in enteric arthritis?

A

Asymetric lower limb arthritis

199
Q

How many people with IBD get enteric arthritis?

200
Q

What is septic arthritis?

A

Direct infection of a joint

201
Q

Is a septic joint serious?

A

Yes its a medical emergency

202
Q

What are the signs/ symptoms of septic arthritis (3)?

A
  • Red, hot swollen joint
  • Extremely painful
  • Pyrexia
203
Q

Which organism most commonly causes a septic joint?

A

Staph aureus

204
Q

Which other bacteria commonly infect joints (4)?

A
  • Strep A (strep pyogenes)
  • H. influenzae
  • E. coli
  • N. gonorrhoea
205
Q

What are some risk factors for septic arthritis (4)?

A
  • IVDU
  • Prosthetic joint
  • Inflammatory joint disease (e.g. RA)
  • Immunosuppression
206
Q

How is septic arthritis investigated?

A

Joint aspirate (microscopy and sensitivity)

207
Q

Which antibiotics are commonly used for septic joints (2)?

A
  • Flucloxocillin/ vancomycin
    plus …
  • Rifampicin
208
Q

What adjustments to medication should be done if someone is found to have a septic joint (2)?

A
  • Double steroid dose (sick day rules)
  • Stop DMARDs
209
Q

What is osteomyelitis?

A

Inflammation of bone/ bone marrow

210
Q

What are the three ways an infection can spread to bone?

A
  • Haematogenous (through blood, most common in children)
  • Local spread (most common in adults)
  • Direct inoculation
211
Q

What is the most common organism to cause osteomyelitis?

A

Staph aureus (90%)

212
Q

Which organism are sickle cell diseased patients most at risk of infecting their bone?

A

Salmonella

213
Q

What are some risk factors for developing osteomyelitis (5)?

A
  • IVDU
  • Immunosuppression
  • Inflammatory arthritis
  • PVD/ diabetes
  • Trauma/ surgery
214
Q

What is a bone change seen acutely with osteomyelitis?

A

Inflammation + oedema

215
Q

What are 2 chronic bone changes seen in chronic osteomyelitis?

A
  • Sequestra
  • Involucrum
216
Q

What is sequestra?

A

A piece of bone separated from healthy bone

217
Q

What is involucrum?

A

Bone growth around sequestra for support

218
Q

What are the signs/ symptoms of osteomyelitis (3)?

A
  • Red, hot, swollen bone
  • Dull pain in bone
  • Fever
219
Q

What is a differential diagnosis for osteomyelitis?

A

Charcot joint = neuropathy (damage to sensory nerves) –> lack of sensation in foot –> fractures + damage goes unnoticed

220
Q

How is osteomyelitis investigated?

A
  • X-ray
  • MRI
  • Bone marrow biopsy
221
Q

What change may be seen on x-ray?

A

Localised osteopenia (thinning of bone)

222
Q

How is osteomyelitis treated?

A
  • Surgical debridement
  • Antibiotics
223
Q

Which antibiotics are commonly used for osteomyelitis (2)?

A

Flucloxacillin + rifampicin

224
Q

What are 5 tumours that can spread to bone?

A
  • Breast
  • Lung
  • Thyroid
  • Kidney
  • Prostate
    BLT KP
225
Q

What sort of bone lesions do breast and lung cancer cause?

A

Osteolytic (bone breakdown)

226
Q

What sort of bone lesions does prostate cancer cause?

A

Osteosclerotic (bone building)

227
Q

What are 4 types of primary bone cancer?

A
  • Osteosarcoma
  • Ewing sarcoma
  • Chondrosarcoma
  • Fibrosarcoma
228
Q

What is the most common primary bone cancer?

A

Osteosarcoma

229
Q

What cell do osteosarcoma originate from?

A

Mesenchymal stem cells or osteoblasts

230
Q

What cell does a Ewing sarcoma originate from?

A

Mesenchymal stem cell

231
Q

What do chondrosarcoma affect?

A

Cartilage cancer (chondroblasts)

232
Q

What age do these bone cancers usually affect?

A

Children (15 years)

233
Q

What are some symptoms/ signs of bone cancer (4)?

A
  • Bone pain worse at night
  • Fractures
  • Fever
  • Weight loss
234
Q

How is bone cancer investigated (3)?

A
  • X-ray/ bone scan
  • Bloods = high ALP, hypercalcaemia
  • Bone biopsy
235
Q

What does high alkaline phosphatase suggest generally?

A

Bone or liver disease

236
Q

How is bone cancer treated?

A

Chemo/radio therapy

237
Q

What drug can be given to protect bone?

A

Bisphosphanates

238
Q

What is osteomalacia?

A

Defective bone mineralisation –> soft bones

239
Q

What is osteomalacia in childhood before growth plate (epiphyseal) fusion known as?

240
Q

What are the effects of activated vitamin D3 in the body (3)?

A
  • Increase bone resorption
  • Increase absorption from intestines
  • Increase reabsorption in kidneys (PCT)
241
Q

Describe the pathway of vit D3 activation?

A

7-dehydrocholestrol + UV light –> Cholecalciferol (Vit D3) in liver –> 25-hydroxy vit D3 in kidney –> 1,25-dihydroxy vit D3

242
Q

What can cause osteomalacia (4)?

A
  • Vit D deficiency
  • Renal disease (can’t activate D3)
  • Liver failure (can’t activate vit D)
  • Drugs (interfere with CYP450)
243
Q

What type of parathyroidism can vit D deficiency cause?

A

Secondary hyperparathyroidism

244
Q

What are some symptoms/ signs of osteomalacia (3)?

A
  • Fractures
  • Bone pain
  • Muscle weakness/aches
245
Q

What is an extra sign/ symptom of rickets?

A

Skeletal deformities

246
Q

How is osteomalacia investigated?

A
  • Bloods
  • X-ray
  • BM biopsy (diagnostic)
247
Q

What would bloods show in osteomalacia?

A
  • Hypocalcaemia
  • High PTH
  • Low 25-hydroxy vitamin D3 (best marker)
248
Q

How is osteomalacia treated?

A

Calcitriol + increase dietary intake

249
Q

What is Paget’s disease?

A

Disorder of remodelling of bone - imbalanced osteoclasts/ blast activity

250
Q

What are the symptoms/ signs of Paget’s disease (3)?

A
  • Bone pain
  • Bone changes (skull + bowed tibia)
  • Neurological (CN compression by skull)
251
Q

How is Paget’s disease diagnosed (2)?

A
  • High ALP
  • X-ray changes = cotton wool skull
252
Q

How is Paget’s disease treated (2)?

A
  • Bisphosphinates
  • NSAIDs
253
Q

How is Marfan’s syndrome inherited?

A

Autosomal dominant

254
Q

What gene mutation is linked to Marfan’s syndrome?

A

FBN-1 mutation

255
Q

What does an FBN-1 mutation in Marfan’s disease cause to be produced abnormally?

A

Decrease in connective tissue (fibrillin) strength

256
Q

What are the symptoms of Marfan’s syndrome (3)?

A
  • Tall + thin, long fingers, sternum caved in or out (pectus excavatum/ carinatum)
  • Aortic regurgitation, dilated base
  • Lense dislocation
257
Q

How is Marfan’s syndrome diagnosed (2)?

A
  • Ghent criteria
  • FBN-1 mutation
258
Q

How is EDS inherited?

A

Autosomal dominant

259
Q

What do mutations affect the production of in EDS?

A

Various types of collagen

260
Q

What are the symptoms of EDS (3)?

A

Depends on type
* Joint hyper mobility
* Vascular involvement (e.g. mitral regurg)
* Stretchy skin

261
Q

How is EDS diagnosed (2)?

A
  • Clinical observations
  • Genetic mutations
262
Q

What is lumbar spondylosis?

A

Age related degeneration - thinning of vertebral discs

263
Q

Where does vertebral disc thinning most commonly occur (2)?

A
  • L4/5
  • L5/S1
264
Q

How is lumbar spondylosis investigated?

A

X-ray/ MRI

265
Q

How is lumbar spondylosis treated (3)?

A
  • Analgesia
  • Physiotherapy
  • Surgery (if severe or complications)

Phase 2a flashcards (Alec's) (13 decks)

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