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x 2nd Year Medicine > MSK > Flashcards

MSK Flashcards

1
Q

What does arthropathy mean?

A

Something wrong with a joint

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2
Q

What does arthralgia mean?

A

Joint pain

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3
Q

What is arthritis?

A

Joint inflammation

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4
Q

What are the common features of inflammatory conditions?

A

Joint pain with diurnal variation
Morning stiffness
Synovitis (soft tissue swelling)

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5
Q

What are the common features of mechanical conditions?

A

Worse with activity
Generally localised
Normal blood tests

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6
Q

Give an example of an inflammatory joint condition

A

RA

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7
Q

Give an example of a non-inflammatory joint condition

A

OA

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8
Q

Give an example of an inflammatory condition not related to the joint

A

Giant cell arteritis

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9
Q

Give an example of an non-inflammatory condition not related to the joint

A

Fibromyalgia

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10
Q

What are the 3 types of inflammatory joint conditions?

A

Connective tissue diseases and vasculitides (group of diseases that destroy blood vessels by inflammation)
Sero-negative arthritides
Crystal arthropathies

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11
Q

Give examples of the Connective tissue diseases and vasculitides.

A

RA
SLE
Scleroderma
Wegener’s granulomatosis

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12
Q

Give examples of Sero-negative arthritides

A

Ankylosing spondylitis
Psoriatic arthritis
Reiters syndrome
Gut associated arthropathy

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13
Q

Give examples of crystal arthropathies

A

Gout

Pseudogout

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14
Q

What is enthesitis?

A

Inflammation of the area where tendons and ligaments insert into bone

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15
Q

What are some of the extra-articular symptoms of RA?

A 
Raynauds
Sicca (mucosal dryness)
ILD
Neuropathy
Vasculitis
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16
Q

What are some of the extra-articular symptoms of sero-negative arthritides?

A

Psoriasis
Uveitis/iritis
Tendonitis
IBD

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17
Q

What does LOSS describe with relation to OA?

A

Loss of cartilage
Osteophyte formation
Subchondral cysts
Subchondral sclerosis (hardening of tissue)

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18
Q

How can connective tissue diseases as a group be defined as?

A

They have spontaneous over-activity of the immune system and are often associated with specific auto-antibodies

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19
Q

What is SLE?

A

A systemic AI disease that can affect any part of the body resulting in inflammation and tissue damage.

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20
Q

Is SLE commoner in males or females?

A

Females

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21
Q

Per 100,000 people, how many will have SLE?

A

20-150 depending on the ethnic group

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22
Q

There are 4 factors which can influence SLE development, what are these?

A

Genetic
Environmental
Hormonal (higher oestrogen exposure)
Immunological

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23
Q

What environmental factors can influence SLE development?

A

Viruses e.g. EBV
UV light
Silica dust is cigarette smoke and cleaning powders

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24
Q

Name some of the general symptoms of SLE

A 
Fever
Malaise
Poor apetite
Weight loss
Fatigue
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25
Q

What are the mucocutaneous features of SLE?

A

Photosensitivity
Malar rash
Discoid lupus erythematosus
Subacute cutaneous lupus

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26
Q

What are the MSK features of SLE?

A

Non-deforming polyarhritis
Jaccoud’s arthritis = deforming arthropathy
Myopathy - weakness, myalgia (muscle pain) and myositis (muscle inflammation)

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27
Q

What are the pulmonary features of SLE?

A 
Pleuricy
Infection
Diffuse lung infiltration and fibrosis
Pulmonary hypertension
Pulmonary infarct
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28
Q

What are the cardiac features of SLE?

A

Pericarditis
Cardiomyopathy
Pulmonary hypertension
Libmen Sacks endocarditis (sterile)

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29
Q

Golemulonephritis can occur in SLE, what does this present with?

A

Proteinuria
Hypertension
Acute or chronic renal failure

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30
Q

What are the neurological features of SLE?

A 
Depression
Migranous headache
TIA/stroke
Cranial/peripheral neuropathy
Cerebellar ataxia (condition affecting balance)
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31
Q

What are the haematological features of SLE?

A

Lymphadenopathy (v.common)
Leucopenia (low WBC)
Anaemia
Thrombocytopenia (low platelets)

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32
Q

SLE can also increase an individuals susceptibility to infection. Why is this?

A

Individual has a compromised immune system and drugs used to treat lupus can compromise immune system more.

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33
Q

What screening tests would be done for an individual with suspected SLE?

A 
FBC
Renal function tests
Anti-nuclear antibody
Anti-double stranded DNA antibodies
ENA
Complement levels
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34
Q

ANA is present in what % of SLE patients?

What is the downside of ANA?

A

95%

20% of the healthy population have positive ANA. Also found in a variety of other conditions

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35
Q

A positive ANA test should be taken seriously if they have CTD symptoms or if other antinuclear antibodies are positive; what are these other autoantibodies?

A

Anti-dsDNA
Anti-Sm
Anti-Ro
Anti-RNP

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36
Q

How often does anti-dsDNA occur in SLE patients?

A

60% of patients

Highly specific for SLE

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37
Q

What is Anti-Ro associated with?

A

Anti-La and cutaneous manifestations

Also neonatal LE

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38
Q

How do you monitor SLE activity?

A 
BP
Anti-dsDNA levels - +ve correlation
C3/C4 levels - -ve correlation
Urine
FBC and blood biochem
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39
Q

What is the 1st thing tried to treat mild SLE?

A

NSAIDs and simple analgesia

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40
Q

What other drug treatment can be used in SLE?

A

Anti-malarials: Chloroquine and hydroxychloroquine
Steroids: dose and type depends on symptoms
Immunosuppressives:
azathioprine, cyclophosphamide, methotrexate, mycophenolate mofetil
Biologics:
Rituximab and Belimumab

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41
Q

What is sjogrens syndrome?

A

AI condition - lymphocyte infiltration of exocrine glands causing xerostomia and keratoconjunctivitis sicca (dry mouth and dry eyes)

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42
Q

What are the classification criteria for Sjogrens?

A 
Ocular symptoms (daily for >3 months)
Oral symptoms (daily for >3 months)
Evidence of ocular dryness
Evidence of salivary gland involvement
Immunology - Ro, La, or both
Biopsy evidence of lymphocytic infiltrate

Must have 4 of 6 inc. Immunology or biopsy

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43
Q

What test can be done to prove Sjogrens clinically?

A

Schirmers test

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44
Q

What classifies secondary Sjogrens syndrome?

A

Caused by or alongside other AI conditions

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45
Q

What other manifestations of Sjogren’s disease are there?

A

Fatigue, arthralgia, raynauds, ILD, neuropathy, skin and vaginal dryness, Lymphoma (x40 risk), Neonate complete heart block (anti-Ro)

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46
Q

What is the prevalence of Sjogrens?

A

1-3%

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47
Q

Who is most likely to be affected by Sjogrens syndrome?

A

40-60 year old Females

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48
Q

How do you treat Sjogrens syndrome?

A

Eye drops, saliva replacement
Pilocarpine - for dry mouth (stimulates saliva production)
Hydroxychloroquine - anti-malarial and antinflammatory
Steroids and immunosupression

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49
Q

What are the 2 types of Systemic sclerosis?

A

Limited and Diffuse

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50
Q

What are the common symptoms of limited systemic sclerosis?

A

Calconosis - calcium deposits in the tissue
Raynaud’s
Eosophageal dysmotility
Sclerodactyly -localized tightening and thickening of skin on fingers and toes
Telangiectasia - small widened blood vessels of the skin
Pulmonary hypertension (in 30%)

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51
Q

What autoantibodies are associated with limited systemic sclerosis?

A

anti-centromere

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52
Q

What are the common symptoms of diffuse systemic sclerosis?

A

Truncal and acral skin involvement
Early organ involvement
Quicker and more severe than the limited disease in general

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53
Q

What is systemic sclerosis?

A

A multisystem autoimmune disease in which there is increased fibroblast activity resulting in abnormal growth of connective tissue, causing vascular damage and fibrosis.

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54
Q

What autoantibody is associated with Diffuse systemic sclerosis?

A

Anti-Scl-70

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55
Q

What are the GI manifestations of Systemic sclerosis?

A

Small bowel, oesophageal and rectal hypomobility

Pancreatic insufficiency

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56
Q

What are the Respiratory manifestations of Systemic sclerosis?

A

ILD
Pulmonary hypertension
Chest wall restriction

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57
Q

What are the Renal manifestations of Systemic sclerosis?

A

Hypertensive renal crisis

Ischaemic

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58
Q

What are the Cardio manifestations of Systemic sclerosis?

A

Raynaud’s with digital ulceration
Atherosclerotic disease
Hypertensive cardiomyopathy

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59
Q

Who is most likely to develop systemic sclerosis?

A

25-55 year old females

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60
Q

What can be used to treat systemic sclerosis?

A 
CCbs
Prostacyclin (Iloprost)
ACEIs
Prednisolone
Immunosuppression
Bosentan, Sildenafil
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61
Q

What are some of the major criteria for Mixed Connective tissue Disease (MCTD)?

A 
Severe myositis
Pulmonary involvement
Raynauds
Swollen hands
Sclerodactyly
Anti-U1-RNP
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62
Q

What are some of the minor criteria for MCTD?

A 
Alopecia
Leukopenia - low WBCs
Anaemia
Pleuritis
Pericarditis
Arthritis
Malar rash
Thrombocytopenia
Mild myositis
Histroy of swollen hands
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63
Q

What is Anti-phospholipid syndrome?

A

An AI disorder characterised by arterial and venous thrombosis, adverse pregnancy outcomes (for mother and fetus), and raised levels of antiphospholipid (aPL) antibodies

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64
Q

What are the Diagnostic criteria for Anti-phospholipid syndrome?

A

+ anti-cardiolipin antibodies/
lupus anticoagulant activity/
Anti-beta2-glycoprotein; on 2 occasions 12 weeks apart

Arterial/Venous thrombosis

Pregnancy loss with no other explanation (10-34/40)/
3 pregnancy losses with no other explanation (<34/40) due to eclampsia, severe pre-eclampsia or placental insufficiency

1 lab and 1 clinical to make diagnosis

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65
Q

What are the features of anti-phospholipid syndrome?

A

Superficial thrombophlebitis and livedo reticularis ( mottled reticulated vascular pattern)
Mild/Mod thrombocytopenia
Migraine
Libman-Sacks endocarditis

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66
Q

How is anti-phospholipid syndrome treated?

A

Thrombosis - lifelong anticoagulation

Pregnancy loss - aspirin + heparin during pregnancy

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67
Q

What are the 3 types of joint?

A

Synovial
Fibrous
Cartilaginous

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68
Q

Give an example of a fibrous joint

A

Bones in the skull

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69
Q

Give an example of a cartilaginous joint

A

Intervertebral discs

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70
Q

Give an example of a synovial joint

A

Knee

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71
Q

What is a simple synovial joint?

A

One pair of articular surfaces e.g. phalanges

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72
Q

What is a compound synovial joint?

A

More than one pair of articular surfaces e.g. elbow

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73
Q

What helps stabilise the joints during purposeful motion?

A

Shape of the bone
Ligaments
Synovial fluid

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74
Q

What helps lubricates the joints?

A

Cartilage interstitial fluid

Synovium-derived hyaluronic acid and lubrcin

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75
Q

What is synovial fluid absorbed and replenished by?

A

Synovial membrane

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76
Q

The synovial fluid has few cells, but what cells usually do exist in it?

A

Mononuclear leucocytes

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77
Q

What is needed for rapid movement of a joint to occur?

A

Decreased viscosity and increased elasticity of the synovial fluid

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78
Q

What are the main roles of articular cartilage?

A

Helps prevent joint wear and tear by allowing a low-friction surface
Distributes contact pressure to sunchondral bone

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79
Q

What is the ECM of articular cartilage made of?

A

Water (70%) - lubrication
Collagen (mainly type II) (20%) - strength
Proteoglycans (10%) - compression

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80
Q

What are the proteoglycans in cartilage made mainly of?

A

Glycosaminoglycan

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81
Q

Cartilage is 98% ECM, what is the other 2%, and what is its role?

A

Chondrocytes - synthesise, organise, degrade and maintain the ECM

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82
Q

Articular cartilage is avascular, so how does it receive its nutrients and oxygen?

A

Via the synovial fluid

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83
Q

With regards to the structure of cartilage, what can cause joint disease?

A

Changes in relative amounts of water, collagen and proteoglycans
ECM degredation exceeding rate of synthesis

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84
Q

What do catabolic factors do to cartilage matrix turnover?

A

Stimulate proteolytic enzymes and inhibit proteoglycan synthesis (TNF + IL-1)

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85
Q

What do anabolic factors do to cartilage matrix turnover?

A

Stimulate proteoglycan synthesis and counteracts the effects of IL-1 (TGF + IGF-1)

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86
Q

How can you tell if cartilage degradation is occuring?

A

Increased serum and synovial keratin sulphate levels

Type II collagen in the synovial fluid

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87
Q

What structural changes occur in an osteoarthritic knee?

A 
Thickened joint capsule
Cyst formation
Subchondral sclerosis
Fibrillated cartilage (softer with gaps)
Synovial hypertrophy
Osteophyte formation
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88
Q

What is seen microscopically in gout?

A

Deposition of needle shaped uric acid crystals

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89
Q

What is seen microscopically in psuedo-gout?

A

Deposition of rhomboid shaped calcium pyrophosphate crystals

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90
Q

What is the prevalence of RA?

A

1%

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91
Q

What genes are thought to be associated with RA?

A

HLA DR4 and DR1

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92
Q

What happens to the synovium in RA?

A

Macrophage, fibroblast and multi-nucleated giant cell infiltration
Membrane expands and erodes bone and cartilage

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93
Q

What are some symptoms of RA?

A

Morning stiffness
Malaise
Fatigue
Joint pain and swelling

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94
Q

How is RA classified?

A

Number and site of involved joints
Serological abnormality
Elevated acute phase response
Symptom duration

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95
Q

How can RA be investigated for?

A

Anti-CCP
RF
Inflammatory markers

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96
Q

What are the principles of RA treatment?

A

Early initiation of DMARDs with steroids to cover the lag phase

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97
Q

What biologic approaches have proved important in RA treatment?

A

Anti-TNF
B cell depletion
Disruption of T cell costimulation
IL-1 inhibition

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98
Q

What drugs target TNF inhibition in RA?

A

Inflximab
Adalimumab
Etanercept

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99
Q

What drugs target B cell depletion in RA?

A

Rituximab

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100
Q

What drugs target disruption of T cell costimulation if RA?

A

Abatacept

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101
Q

What drugs target IL-1 inhibition in RA?

A

Anankira

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102
Q

What is a motor unit?

A

A single alpha motor neuron and all the skeletal muscle fibres it innervates

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103
Q

When is calcium released from skeletal muscle fibres?

A

Surface AP spreads down transverse T tubules

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104
Q

What does the A band in a sarcomere contain?

A

Thick filaments, with the overlapping parts of the thin filaments

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105
Q

What does the H-zone in the sarcomere contain?

A

Middle of A bands where thin filaments dont reach

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106
Q

What is the M-line of a sarcomere?

A

It extends vertically down the middles of the A-band and the H-zone

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107
Q

What does the I-band of a sarocomere consist of?

A

Remaining portion of thin filaments that the A-band does not cover.

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108
Q

What are Z-lines?

A

Connect 2 sarcomeres

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109
Q

When is ATP required in the muscles?

A

Contraction and relaxation

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110
Q

When is caqlcium required in muscle movement?

A

Calcium binds the thin to thick filaments, allowing the process of contraction to begin

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111
Q

How does calcium switch on cross bridge formation?

A

It binds to troponin on actin, and the troponin-tropomyocin complex moves to uncover the cross bridge binding sites

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112
Q

Where is calcium released from in skeletal muscle movement?

A

Sarcoplasmic Reticulum

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113
Q

If AP duration is shorter than the muscle “twitch” associated with it, what does this mean in terms of muscle work?

A

Possible to summate twitches to bring about stronger contraction

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114
Q

How does tetanus in skeletal muscle occur?

A

If the fibres are stimulated so rapidly, that they do not have a chance to relax between stimuli.

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115
Q

Can cardiac muscle be tetanised?

A

No, the long refractory period prevents this occurring.

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116
Q

What is isotonic muscle contraction?

A

Body movements and moving objects.

Muscle tension is constant as length increases.

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117
Q

What is isometric muscle contraction?

A

Supporting objects in fixed positions and maintaining body posture.
Muscle tension changes whilst muscle remains the same length

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118
Q

What is the stretch reflex?

A

Negative feedback system that resists passive change in muscle length to maintain optimal resting length of muscle

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119
Q

What are muscle spindles?

A

A collection of specialised muscle fibres.

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120
Q

Where are muscle spindles found?

A

Within the belly of muscles, running parallel to the ordinary muscle fibres.

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121
Q

What are muscle spindles also known as?

A

Intrafusal fibres

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122
Q

What are ordinary muscle fibres also known as?

A

Extrafusal fibres

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123
Q

What are the sensory nerve endings of muscle spindles called?

A

Annulospiral fibres

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124
Q

What neurons will increase firing rate when a muscle is stretched?

A

Afferent neurons

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125
Q

What are the efferent neurons called that supply the muscle spindles?

A

Gamma motor neurons

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126
Q

What do gamma motor neurons do?

A

Adjust the level of tension in muscle spindles to maintain their sensitivity when the muscle shortens in contraction

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127
Q

What are the main differences between types of muscle fibre?

A

Enzymatic pathways for ATP-synthesis
The resistance to fatigue
Activity of myosin ATP-ase

128
Q

What is the immediate source of ATP for muscle fibres?

A

Transfer of high energy phosphate from creatine phosphate to ADP

129
Q

What is the main source of ATP for muscle fibres in aerobic conditions?

A

Oxydative phosphorylation

130
Q

What is the main source of ATp for muscle fibres in anaerobic conditions?

A

Glycolysis

131
Q

What are slow oxidative type I muscle fibres?

A

Slow-twitch fibres

Used mainly for prolonged, low-work, aerobic activities

132
Q

What are fast oxidative Type IIa fibres?

A

Intermediate-twitch fibres

Used in aerobic and anaerobic conditions when doing prolonged, relatively moderate work.

133
Q

What are fast glycotic Type IIx fibres?

A

Fast-twitch fibres

Used in anaerobic conditions for short-term, high intensity activities

134
Q

What are the 4 main features of OA?

A

Loss of joint space
Osteophyte formation (articular cartilage failure)
Subchondral sclerosis
Subchondral cysts

135
Q

What does cartilage mainly consist of?

A

Collagen type II

136
Q

What is the matrix of the cartilage formed by?

A

Chondrocytes embedded within it

137
Q

In disease the matrix is lost, but what else occurs?

A

Release of cytokines (TNF, IL1)
Release of mixed metalloproteinases
Prostaglandin release by chondrocytes

138
Q

How does cartilage attempt to repair itself?

A

Osteophyte formation

139
Q

Which joints are most commonly affected in OA?

A 
Hands
Feet
Knee
Hip
Spine
140
Q

What can cause secondary OA?

A 
Previous injuries
RA
Genetic elements
Acromegaly
Calcium crystal deposition disease
141
Q

What are the main risk factors for OA?

A 
Increasing age
Female
Obesity
Occupation (physical)
Sports
Previous injury
Muscle weakness (body more reliant on bone
142
Q

How would a person with OA present to a clinic?

A

Pain which worsens on activity and is relieved by rest

Morning stiffness usually lasting <30mins

143
Q

What would be seen/felt on examination of this patient?

A 
Joint tenderness
Joint effusion
Crepitus
Bony enlargements (osteophytes)
144
Q

Which joints in the hands are most commonly affected in OA?

A

DIP
PIP
1st CMC

145
Q

What are the hand features of OA?

A

Bony enlargements at:
DIPs = Heberdens nodes
PIPs = Bouchards nodes
Squaring of the thumb

146
Q

What are the knee features of OA?

A

Genu varus (wide knees) and valgus (knock-knees) deformities
Baker’s cyst - swelling in the popliteal fossa
Restricted movements

147
Q

What are the Hip features of OA?

A

Pain may be in groin or radiate to knee, or felt in lower back
Movements are restricted

148
Q

What are the Spinal features of OA?

A

Cervical - pain and movement restriction. Osteophytes may impinge on nerve roots

Lumbar - osteophytes may cause spinal stenosis if they encroach on the spinal canal

149
Q

What is the non-pharmalogical management of RA?

A 
Physio - muscle strengthening
Walking aids (if necessary)
150
Q

What is the pharmalogical management of OA?

A

Analgesia - paracetamol, topical treatments
NSAIDs
Pain modulators e.g. amitriptyline/gabapentin etc.

151
Q

What can be done intra-articularly for OA?

A

Steroid injections

Hyaluronic acid

152
Q

What can be done surgically for OA?

A

Arthroscopic washout
Loose body/soft tissue trimming
Joint replacement

153
Q

What is gout?

A

An acute inflammatory response to the deposition of urate crystals (needle shaped) as well as the phagocytosis of the crystals

154
Q

Gout is caused by hyperuricaemia, but what can cause this? (generally)

A

Increased urate production OR Reduced urate excretion

155
Q

What causes increased urate production?

A

Inherited enzyme defects
Psoriasis
Alcohol
High dietary purine intake

156
Q

What causes reduced urate excretion?

A 
CKD
Hypothyroidism
Diuretics
HF
Cytotoxins
157
Q

Gout usually only affects 1 joint; which are the most commonly affected joint?

A

1st MTP > ankle > knee

158
Q

Gout will settle within 10 days without any treatment, but how long does it take to settle with treatment?

159
Q

Does gout gradually or acutely present?

A

Acutely (often overnight)

160
Q

A patient presenting with a red swollen 1st MTP with a 12 hour history has a normal uric acid measurement. Does this exclude gout?

A

No, uric acid is sometimes normal during an acute attack

161
Q

What is chronic tophaceous gout?

A

A recurrent form of arthritis that is caused by a build up of uric acid crystals in the fluid around the joints

162
Q

What drug type can be associated with tophaceous gout?

163
Q

What investigations can be done to confirm a diagnosis of gout?

A

Serum uric acid - may be raised or normal
Inflammatory markers - raised
Polarised microscopy of synovial fluid
X-ray
Renal impairment - can be both a cause and an effect

164
Q

What treatments are used in the acute gout attack?

A

NSAIDs
Colchicine
Steroids

165
Q

What treatments are used for prophylaxis after a gout attack?

A

Allopurinol
Febuxostat
Started 2-4 weeks after the acute attack

166
Q

What is Calcium Pyrophosphate Deposition Disease? (CPPD)

A

A metabolic arthropathy caused by the deposition of calcium pyrophosphate dihydrate in and around joints, esp. in articular cartilage and fibrocartilage

167
Q

Is CPPd more common in older or younger patients?

168
Q

Where does CPPD affect the fibrocartilage?

A

Knees
Wrists
Ankles

169
Q

An acute attack of CPPD is also known as what? What happens?

A

Pseudogout

Shedding of envelope-shaped calcium pyrophosphate crystals into the joint

170
Q

How is CPPD treated?

A

NSAIDs
Colchicine
Steroids
Rehydration

171
Q

What is “Milwaukee shoulder”?

A

Hydroxyapatite crystal deposition in or around the joint - release of collagenases, serine proteinases + IL-1

172
Q

What is the treatment for Milwaukee shoulder?

A

NSAIDs
Intra-articular steroid injection
Physio
Partial/total arthroplasty

173
Q

What is soft tissue rheumatism?

A

Pain caused by inflammation/damage to ligaments, tendons, muscles or a nerve near a joint

174
Q

Soft tissue rheumatism is usually well localised, if there is more generalised soft tissue pain, what diagnosis should be considered?

A

Fibromyalgia

175
Q

Where is the commonest area for soft tissue injury?

176
Q

Soft tissue rheumatism does not normally require investigation, but what ones can be done in some cases?

A

X-ray
MRI
Identification of precipitating factors

177
Q

What can be used to treat soft tissue rheumatism?

A 
Pain control
Rest + ice compressions
PT
Steroid injections
Surgery
178
Q

Joint hypermobility syndrome is diagnosed using the modified Beighton score - what are the criteria in this list? How many must a patient have to be diagnosed?

A

> 10 degree hyperextension of the elbows (R+L)
Passively touching forearm with the thumb whilst flexing the wrist (R+L)
Passive extension of the fingers or a 90 degree or more extension of the 5th finger (R+L)
Knees hyperextension >10 degrees (R+L)
Touching the floor with the palms of the hands, without bending the knees

Hypermobility = >= 4/9

179
Q

What can be used to treat someone presenting with arthralgia due to joint hypermobility syndrome?

A

Physio
Explanation
Analgesia

180
Q

What are sero-negative arthropathies?

A

Family of inflammatory arthritides characterised by involvement of both the spine and joints

181
Q

There are a number of sero-negative arthropathies, but they all share some common features, what are these?

A

Sacroilliac and spinal involvement
Enthesitis
Inflammatory arthritis
Dactylitis (“sausage” digits)

182
Q

What other extra-articular features can sero-negative arthropathies have in common?

A

Occular inflammation
Muco-cutaneous lesions
(Rare) Aortic incompetence or heart block

183
Q

When does ankylosing spondylitis most commonly present?

A

Late adolescent/ early adult men

184
Q

What HLA type is ankylosing spondylitis associated with?

185
Q

What are the clinical features of ankylosing spondylitis?

A

Inflammatory low back pain
Enthesitis
Peripheral arthritis
Amylodosis

186
Q

What are the extra-articular features of ankylosing spondylitis? (The “A” disease(

A 
Anterior uveitis
Cardio involvement - aortic regurg
Pulmonary invovement - atypical fibrosis
Asymptommatic enteric mucosal inflammation
Neurological involvement
187
Q

What investigations should be done to help diagnose ankylosing spondylitis?

A 
FBC
U&E
Inflammatory markers
HLA-B27
X-ray
MRI
188
Q

What are the New York criteria used in diagnosing Ankylosing spondylitis (AS)?

A
  1. Lower back pain for 3 months (improved by exercise but not relieved by rest )
  2. Limited lumbar motion - Schober’s test (tape measure)
  3. Reduced chest expansion
  4. Bilateral, Grade 2-4, sacroiliitis on xray
  5. Unilateral, grade 3-4, sacroiliitis on xray
189
Q

What is sacroiliitis?

A

An inflammation of one or both of your sacroiliac joints

190
Q

When can definite AS be diagnosed based on the New York criteria?

A

If criteria 4 or 5 present
PLUS
1, 2, or 3

191
Q

How is AS treated?

A 
Home exercise
Physio
OT
NSAID
Corticosteroids
Anti-TNF - Infliximab/Adalimumab
192
Q

What is psoriatic arthritis?

A

Inflammatory arthritis found in those with psoriasis. RF-ve and equally affects both men and women

193
Q

What are the clinical features of psoriatic arthritis?

A 
Inflammatory arthritis (5 subgroups)
Sacroiliitis
Nail invovement (pitting, onycholysis)
Dactylitis
Enthesitis
194
Q

What are the clinical subgroups of psoriatic arthritis?

A
  1. Confined to DIPs (hands/feet)
  2. Symmetric polyarthritis
  3. Spondylitis with or without peripheral joint involvement
  4. Asymmetric oligoarthritis with dactylitis
  5. Arthritis mutilans (severe derangement of any joint)
195
Q

What is AS?

A

Inflammation of multiple articular and para-articular structures, frequently resulting in bony ankylosis. “stiffening of the vertebrae”

196
Q

How is psoriatic arthritis diagnosed?

A 
Inflammatory markers are raised
RF -ve
Marginal erosions on x-ray
"pencil in cup" deformity on xray
osteolysis
197
Q

How is psoriatic arthritis treated medically?

A

NSAIDs
Corticosteroids/joint injections
Disease modifying drugs - methotrexate
Anti-TNF - etanercept

198
Q

How is psoriatic arthritis treated non-pharmacologically?

A

Physio
OT
Orthotics
Chiropodist

199
Q

What is reactive arthritis?

A

Infection-induced systemic illness characterised primarily by an inflammatory synovitis from which viable microorganisms cannot be cultured.

200
Q

How long is it before reactive arthritis occurs after an infection?

201
Q

What are the most common infections causing reactive arthritis?

A

Chlamydia
Salmonella
Shigella
Yersinia

202
Q

What are the clinical features of reactive arthritis?

A 
Fever, fatigue, malaise
Asymmetric mono- or oligo-arthritis
Enthesitis
Mucocutaneous lesions
Occular lesions (conjuctivitis, iritis)
Visceral manifestations (mild renal disease and carditis)
203
Q

What is Reiter’s syndrome?

A

A form of reactive arthritis

204
Q

What is the classical traid of symptoms in Reiter’s syndrome?

A

Arthritis
Urethritis
Conjunctivitis

205
Q

How do you diagnose reactive arthritis?

A 
History
Examination
Bloods (Inflammatory markers, FBC, U&Es)
Cultures (blood, urine stool)
Joint fluid analysis
xray
206
Q

How is reactive arthritis treated?

A 
NSAIDs
Corticosteroids
Antibiotics
DMARDS - if resistant/chronic
Physio
OT
207
Q

What is the prognosis of reactive arthritis?

A

Generally good
Recurrences not uncommon
Some develop a chronic form

208
Q

What is vasculitis?

A

Inflammation of the blood vessel walls

209
Q

What are the general types of vasculitis?

A

Large vessel
Medium vessel
Small vessel

210
Q

Give 2 examples of a large vessel vasculitis.

A 
Polymyalgia rheumatica (PMR)
Giant cell (temporal) arteritis
211
Q

How does PMR present?

A

Sudden onset of severe pain and stiffness of the shoulders, neck, hips and lumbar spine
Symptoms are worse in the morning - lasting from 30 minutes to several hours

212
Q

What age group is PMR most likely to affect

213
Q

1/3 of patients with PMR develop systemic features, what are some of these?

A 
Tiredness
Fever
Weigh loss
Depression
Occasionally night sweats
214
Q

How is PMR investigated?

A

Raised ESR and/or CRP is almost always present
Serum ALP may also be raised
Anaemia is often present
Temporal artery biopsy - shows GCA in some cases but rarely done unless GCA is also suspected.

215
Q

What is Giant cell arteritis (GCA)?

A

An inflammatory granulomatous arteritis of large cerebral arteries, occuring alongside PMR.

216
Q

How does GCA present?

A

Severe headaches
Scalp tenderness
Jaw claudication
Tenderness and swelling of 1 or more temporal or occipital artery
Sudden painless temporary or permanent loss of vision in 1 eye

217
Q

What are the systemic manifestations of GCA?

A

Severe malaise
Tiredness
Fever

218
Q

What investigations are done for GCA?

A

Normochromic, normocytic anaemia
ESR (raised)
ALP (raised)
Temporal artery biopsy is the definitive test

219
Q

What are the histological features seen on a temporal artery biopsy showing GCA?

A

Cellular infiltrates id CD4+ T lymphocytes, macrophages and giant cells in the vessel wall
Granulomatous infiltration of the intima and media
Breaking up of elastic lamina
Giant cells, lymphocytes and plasma cells in the interal elastic lamina

220
Q

What is the main treatment used in PMR and GCA and why?

A

Corticosteroids - significantly reduces risks of irreversible visual loss and produces a dramatic reduction of symptoms

221
Q

Give 2 examples of medium vessel vasculitis

A 
Polyarteritis nodosa (PAN)
Kawasaki's disease
222
Q

What is PAN?

A

A rare condition accompanied by severe systemic manifestations.

223
Q

What is found pathologically in PAN?

A

Fibrinoid necrosis of vessel walls with microaneurysm formation, thrombosis and infarction.

224
Q

What are the clinical features of PAN?

A

Fever, weight loss, malaise and myalgia

This is followed by dramatic acute features due to organ infarction

225
Q

What investigations should be done for PAN?

A

FBC - anaemia, leucocytosis and a raised ESR
Biopsy - of affected organs
Angiography - demonstration of microaneurysms
Others - depending on organs affected

226
Q

What is the treatment of PAN?

A

Corticosteroids usually in combination with immunosupressives (azothioprine)

227
Q

What is Kawasaki’s disease?

A

An acute systemic vasculitis mainly affecting children <5.

228
Q

What are the clinical features of Kawasaki’s disease?

A 
(think avatar)
Fever lasting >5 days
Bilateral conjunctival congestion
Dry and red lips
Cervical lymphadenopathy
Polymorphic rash
Redness and oedema of palms and soles
229
Q

What investigation findings can help diagnose Kawasaki’s disease?

A

Leucocytosis, thrombocytosis and a raised CRP

230
Q

What is the treatment of Kawasaki’s disease?

A

Single dose IV immunoglobulin to prevent coronary artery disease
Aspirin after the acute phase

231
Q

Small vessel vasculitis diseases are based on whether they are ANCA positive or ANCA negative. What is ANCA?

A

Anti-neutrophil cytoplasmic antibodies - IgG autoantibodies directed against the primary granules of neutrophil and macrophage lysosomes

232
Q

What are some of the ANCA positive small cell vasculitis diseases?

A

Wegener’s granulomatosis
Churg-Strauss granulomatosis
Microscopic polyangitis

233
Q

What is Wegener’s granulomatosis characterised by?

A

Lesions in the URT, lungs and kidneys

234
Q

What are the symptoms of Wegener’s granulomatosis?

A 
Rhinorrhoea
Nasal mucosal ulceration
Cough
Haemoptysis
Pleuritic pain
235
Q

What can be seen on x-ray in Wegener’s granulomatosis?

A

Single or multiple nodular masses which clear and appear spintaneously.

236
Q

What treatment is used for Wegener’s granulomatosis?

A

Cyclophosphamide

Rituximab

237
Q

How does Churg-Strauss syndrome present?

A

rhinitis
asthma
eosinophillia
systemic vascultis

238
Q

Where does Churg-Strauss syndrome typically affect?

A

lungs
peripheral nerves
skin

239
Q

What changes may be seen on x-ray in Churg-Strauss syndrome?

A

Pneumonia-like shadows

240
Q

What skin changes may be associated with Churg-Strauss syndrome?

A

subcutaneous nodules and petechial or purpuric lesions

241
Q

What is the recommended treatments for Churg-Strauss syndrome?

A

Corticosteroids

242
Q

What organs are involved in microscopic vasculitis?

A

Kidneys

Lungs (recurrent haemoptysis)

243
Q

Give examples of ANCA negative small vessel vascultis diseases

A

Henoch-Schonlein purpura
Cryoglobulinaemic vasculitis
Cutaneous leucocytoclastic vasculitis

244
Q

What is the treatment of small cell vascultis?

A

Depends on organ involvement

May range from topical skin treatment to high dose corticosteroids

245
Q

What name is given to the structure that completely surrounds a muscle?

246
Q

What name is given to the structure that completely surrounds bundles of muscle fibres?

A

Perimysium

247
Q

What name is given to the structure that completely surrounds each individual muscle fibre?

A

Endomysium

248
Q

What are the distinguishing features of a red muscle fibre (Type 1)

A

Slow twitch fibre
Large mitochondria
Increased myoglobulin

249
Q

What are the distinguishing features of a white muscle fibre? (Type 2)

A

Fast twitch fibre
Small mitochondria
Large motor end-plates

250
Q

What are the indications for a muscle biopsy?

A

Evidence of muscle disease
Presence of neuropathy
Presence of vascular disorder

251
Q

What level of CK would be considered high, and what muscular disease(s) could this indicate?

A

200-300x normal

Muscle dystrophies

252
Q

What level of CK would be considered intermediate, and what muscular disease(s) could this indicate?

A

20-30x normal

Inflammatory myopathy

253
Q

What level of CK would be considered low, and what muscular disease(s) could this indicate?

A

2-5x normal

Neurogenic disorder

254
Q

What is the age of onset for DMD?

255
Q

What is the life expectancy of an individual with DMD?

256
Q

What are the symptoms of DMD?

A

Proximal weakness
Pseudohypertrophy of calves
Raised CK

257
Q

What causes DMD?

A

Mutations in the dystrophin gene on the long arm of the X-chromosome

258
Q

What is the histopathological process behind DMD?

A

Mutation causes alterations in how the actin cytoskeleton anchors to the basement membrane
This means that muscle fibres are liable to tearing
And there is uncontrolled calcium influx into the muscle cells

259
Q

What histological changes are seen in DMD?

A

Muscle fibre necrosis and phagocytosis
Regeneration
Chronic inflammation and fibrosis
Hypertrophy

260
Q

What is Becker’s muscular dystrophy? (BMD)

A

A varient of DMD with a later onset and a slower progress

261
Q

What are the symptoms of myotonic dystrophy?

A

Muscle weakness

Myotonia

262
Q

What are the genes affected by myotonic dystrophy?

A

Ch19 and Ch3

263
Q

What muscles are most commonly affected by myotonic dystrophy?

A

Face
Distal limbs
Late stage - respiratory muscles

264
Q

What are the histological features of myotonic dystrophy?

A 
atrophy of type 1 nerve fibres
central nuclei
ring fibres
fibre necrosis
fibrofatty replacement
265
Q

What are the symptoms of polymyositis?

A

progressive muscular weakness, pain and tenderness

266
Q

What is the mortality rate of polymyositis?

267
Q

What is the pathophysiology of polymyositis?

A

Cell-mediated immune response to muscle antigens

Endomysial lymphocytic infiltrate of muscle by CD8+ T lymphocytes

Segmental fibre necrosis

268
Q

How does dermatomyositis differ from polymyositis?

A

Skin changes are present

269
Q

How does dermatomyositis present?

A

Upper body erythema

Eyelid swelling with purple discolouration

270
Q

How likely is it that dermatomyositis is associated with malignancy?

A

10% chance

271
Q

What is the histopathology of dermatomyositis?

A

Immune complex and complement deposition around capillaries within muscle

Perifascicular muscle fibre injury

272
Q

What immune cells are involved in dermatomyositis?

A

B lymphocytes

CD4+ T cells

273
Q

Define a neurogenic disorder of muscle.

A

Stereotyped changes after nerve damage with subsequent re-innervation

274
Q

What would be seen on biopsy in an individual with a neurogenic muscle disorder?

A

Small angulated nerve fibres
Target fibres
Fibre type grouping
Grouped atrophy

275
Q

What is motor neuron disease?

A

Progressive degeneration of anterior horn cells

276
Q

What symptoms would a person with motor neuron disease present with?

A

Denervation atrophy
Weakness
Fasciculation (muscle fibres twitch visibly under skin)

277
Q

What is spinal muscular atrophy?

A

An inherited AR trait affecting Ch5 where degeneration of the anterior horn cells in the spinal cord occurs

278
Q

What is myasthenia gravis?

A

An AI condition causing weakness, proptosis, fatigue and dysphagia

279
Q

Who is most likely to get myasthenia gravis?

A

Women 20-40

280
Q

What do 25% of those with myaethenia gravis have?

A

Thymoma (tumour of the thymus)

281
Q

What is rhabdomyolysis?

A

A breakdown of skeletal muscle causing myoglobulinuria, hyperkalaemia, necrolysis and shock

282
Q

What is the result of rhabdomyolysis?

A

AKI
Hypovolaemia and hyperkalaemia
Metabolic acidosis
Disseminated intravascular coagulation

283
Q

What common features do CTD’s share?

A

Multi-system features
Affect women more commonly than men
Immunological abnormalities are common
Usually respond to anti-inflammatories

284
Q

What is SLE?

A

An AI multi-system disorder

285
Q

What antibodies are usually present in individuals with SLE?

A

ANAs (antinuclear)

286
Q

What drugs may induce SLE?

A

Hydralazine

Pracainamide

287
Q

How may SLE affect the skin?

A

“butterfly” rash, discoid lupus erythematosus

288
Q

How may SLE affect the joints?

A

arthralgia

289
Q

How may SLE affect the kidneys?

290
Q

How may SLE affect the CNS?

A

psychiatric symptoms

Focal neurological symptoms

291
Q

How may SLE affect the CVS?

A

Pericarditis
Myocarditis
Necrotising vasculitis

292
Q

How may SLE affect the lymphatic system?

A

Lymphadenopathy and splenomegaly

293
Q

How may SLE affect the lungs?

A

Pleuritis

Pleural effusions

294
Q

How may SLE affect the blood?

A

Anaemia
Leucopenia
Thrombophilia

295
Q

What type of hypersensitivity are the visceral lesions in SLE mediated by?

296
Q

What type of hypersensitivity are the haematological effects in SLE mediated by?

297
Q

What is polyarteritis nodosa (PAN)?

A

Inflammation and fibrinoid necrosis of small/medium arteries

298
Q

What are the main organs which PAN affects?

A

Kidneys, heart, liver, GI tract

299
Q

What other organs does PAN affect other than the major ones?

A 
Skin
Joints
Muscles
Nerves
Lungs
300
Q

How does PAN present clinically?

A

Depends on organ(s) affected.

301
Q

How is PAN diagnosed?

A

Biopsy for fibrinoid necrosis of vessels

Serum samples for pANCA

302
Q

What is pANCA?

A

Perinuclear antineutophil cytoplasmic autoantibody

303
Q

How does PMR present?

A

Pain and stiffness in the shoulder and pelvic girdles esp in the elderly

304
Q

What is used to treat PMR?

A

Corticosteroids

305
Q

What is temporal arteritis?

A

Inflammation affecting the cranial vessels

306
Q

What are the risks of temporal arteritis?

A

Blindness if the terminal branches of the opthalmic artery are affected

307
Q

How does temporal arteritis present?

A

Headaches and scalp tederness

308
Q

How is temporal arteritis diagnosed?

A

By raised ESR

Temporal artery biopsy

309
Q

What is scleroderma?

A

Excessive fibrosis of organs and tissues (excessive collagen production)

310
Q

How can scleroderma affect the skin?

A

Tight, tethered skin causing decreased joint movement

311
Q

How can scleroderma affect the GI tract?

A

Fibrous replacement of the muscularis

312
Q

How can scleroderma affect the heart?

A

Pericarditis and myocardial fibrosis

313
Q

How can scleroderma affect the lungs?

A

Interstitial fibrosis

314
Q

How can scleroderma affect the kidneys?

A

Renal artery hypertension

315
Q

How can scleroderma affect the MSK system?

A

Polyarteritis and myositis

316
Q

What syndrome is scleroderma associated with?

A 
CREST
C = calcinosis
R = Raynaud's
E = (O)esophageal dysfunction
S = Slerodactyly
T = Telangectasia (dilation of blood vessels close to the skin surface)
317
Q

How can scleroderma eventually cause death?

A

Renal failure secondary to malignant hypertension
Severe respiratory compromise
Cor pulmonale
HF or arrhythmias secondary to myocardial fibrosis

x 2nd Year Medicine (10 decks)

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