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Phase 2 mine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is osteoporosis?

A

Systemic skeletal disease with low bone mass and architecturale deterioration of bone tissue and increase in bone fragility and susceptibility

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2
Q

What is the most common presentation of osteoporosis?

A

Fractures

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3
Q

Who does osteoporosis affect?

A

1/2 women and 1/5 men over 50

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4
Q

Why are hip fractures bad?

A

kills 20% 80% lose some function

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5
Q

What affects bone strength?

A

Bone mass density, bone size, bone quality

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6
Q

What affects Bone mass density?

A

Peak bone mass, rate of bone loss

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7
Q

What can affect bone quality?

A

Bone turnover, architecture mineralisation

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8
Q

Which fractures are very common in the elderly?

A

Coles’ vertebrae and hip

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9
Q

What is the best risk factor for fractures?

A

age

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10
Q

Why are hip fractures more common in older people?

A

Cant protect with their hands

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11
Q

What happens in postmenopausal osteoporosis?

A

Loss of restriang effect of oestrogen on bone turnover, high bone turnover but too fast for osteoblasts to rebuild, disrupts the architectural integrity of the bone

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12
Q

When is peak bone mass reached?

A

In the 30s

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13
Q

Which cells sense bone stress and direction?

A

Osteocytes

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14
Q

What is Eula’s buckling theory?

A

need crosslinking of bone struts to give 16 times strength

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15
Q

What is Eula’s buckling theory?

A

need crosslinking of bone struts to give 16 times strength

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16
Q

How is osteoporosis diagnosed?

A

Bone densitometry that looks at bone mineral density

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17
Q

What is DEXA scan?

A

Dual energy X-ray absorptiometry. Looks at resorption in low dose radiation and measure lumbar spine hip and distal radius

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18
Q

What are the measures of a dexa scan?

A

Bone mineral density, T score Z score, T score is for diagnosing osteoporosis

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19
Q

What is a T score?

A

Standard deviation score, compared with gender-matched young adult average

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20
Q

How are T scores classified ?

A

> -1 is normal,

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21
Q

What can increase risk of osteoporosis?

A

Infammatory diseases (Rheumatoid artheritis, arthritis and inflammatory bowel diseases) Endocrine disease(hyperthyroid and hyperparathyroidism, crushing’s kills osteoblasts and oestrogen and testosterone lowering causes it) low skeletal loading , glucocorticoids, depo-provera aromatase inhibitors, GnRH anlogues Androgen deprivation

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22
Q

What can cause low skeletal loading?

A

Low bodyweight and immobility

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23
Q

What separate other risk factors for osteporosis exist?

A

Previous fracture, family history of osteoporosis or fracture alcohol and smoking

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24
Q

What is FRAX?

A

Uses weight height previous fractures history current smoking RA and bone density to give risk of fracture

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25
Q

What are the treatments for bone diseases?

A

antiresorptive Bisphosphonates and HRT and denosumab

Anabolic teriparatide

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26
Q

What are Bisphosphonates/

A

Cheap effective and well studied, oral daily or weekly IV they stop cholesterol syntheses it disables osteoclasts

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27
Q

What is denosumab?

A

They interact with RANKL by binding it its very responsive big rebound when you stop it

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28
Q

What is teriparitide?

A

It is a bone resorbing activator quite like a hormone contraindicated in previous bone cancer or radio treatment in bones

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29
Q

What is characteristic of inflammatory joint pain?

A

heat redness swelling pain and loss of function. swollen joint compressible and tender worst in morning of after rest, longer than 30 mins stiffness can be intermittent and consonant

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30
Q

What are good things for patients to notice?

A

Swelling stiffnes and pain on squeezing

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31
Q

What are characteristics of rheumatoid artheritis?

A

familial smoking, more common in females, middle ages very common, no spinal involvement small joints of hands symetrically nevere DIP only PID MCP bad prognosis for big joint involvement can be intermittent migratory or additive

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32
Q

What are characteristics of rheumatoid artheritis?

A

familial smoking, more common in females, middle ages very common, no spinal involvement small joints of hands symetrically nevere DIP only PID MCP bad prognosis for big joint involvement

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33
Q

What are characteristics of Psoriatic arthritis?

A

like RA but get DIP joint involvement get dactylitis, asymmetrical large joints and spine CRP may not be raised significantly

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34
Q

What are characteristics of Psoriatic arthritis?

A

like RA but get DIP joint involvement get dactylitis, asymmetrical large joints and spine CRP may not be raised significantly

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35
Q

What are the characteristics of osteoarthrits?

A

Is slow onset months to years, DIP PIP thumb bases big toes and big joints, minimal early morning stiffness clear changes on Xrays

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36
Q

What are the characteristics of crystal arthristis?

A

intermitent episodic, big toe often feet ankles kneees elbows hands, hyperuricaemia, 6x in men, can e from beer renal imparment diuretics aspirin Family history, pseudogout is more common in women often in wrists knees and hands often in OA backcround and see chondrocalcinosis on Xray

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37
Q

What to look at with arthritis to start diagnosis?

A

Inflammation, joint pattern associated symptoms/risks and tests like xray RF

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38
Q

What are principals of RA treatment?

A

Early diagnosis (2-3months), reduce inflammation

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39
Q

What is the rumatology mantra?

A

inflammation*time=damage so reduce inflammation aASAP

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40
Q

What happens in RA joint?

A

Inflamed membrane overproduces produces Pannus and this dammages joint

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41
Q

How is RA treatment?

A

surpess inflamation DMARDS methotrexate sulpathalasine and can block inflammation wiht biological treatments to stop inflammatory cytokines NSAIDS can help Colchicine for crystal arthritis

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42
Q

How is RA treatment?

A

surpess inflamation DMARDS methotrexate sulpathalasine and can block inflammation wiht biological treatments to stop inflammatory cytokines NSAIDS can help Colchicine for crystal arthritis

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43
Q

Why is OA important?

A

Very common

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44
Q

What is Osteoarthritis?

A

age related dynamic reacton pattern of a joint to use and dammage. It is inflammatory but not just wear and tear but driven by mechanical forces it is degredation of joint and da

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45
Q

What are risk factors for OA?

A

traumatic insult to joint,neuromuscular function decline not, common in under 45. usually female increase after menopause, genetic predisposition get less in hip and les in hand. obesity can cause problem but not directly from weight fat tissue is proinflammatory, occupation manual labour farming and football, local trauma, inflammatory arthritis, abnormal biomechanics

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46
Q

What are the symptoms of osteoarthritis?

A

pain not always though functional impairment on walking and activities of daily living

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47
Q

What are the radiological features of arthritis?

A

Joint space narrowing osteophyte formation, suchondral sclerosis, subchondral cysts and abnormalites of bone contour first and last are not specific

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48
Q

WHat are the radiological features of arthritis?

A

Joint space narrowing osteophyte formation, suchondral sclerosis, subchondral cysts and abnormalites of bone contour first and last are not specific

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49
Q

What are heberdens nodes and buchards nodes?

A

heberdoens isbony growths in DIP and buchards are in PIP

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50
Q

In the knee where does OA start?

A

medial compartment of the knee

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51
Q

Where are you likely to get hip pain?

A

In the groin not the lateral part of the hip very often

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52
Q

Where are you likely to get hip pain?

A

In the groin not the lateral part of the hip very often

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53
Q

What is erosive/ inflammatory OA?

A

subset of OA strong inflammatory component can treat with RA treatments

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54
Q

How is OA managed?

A

Non-medical - patient education activity to exercise activity and exercise weight loss physiotherapy, occupational therapy footwear orthoses walking aids
Medical- pain relief, topical NSAIDs (avoid oral) gels patches paracetamol FMARDs in inflammatory OA
Surgical managment arthroscopy, only for loose bodies, osteotomy to increase ROM, arthropasty, fusion

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55
Q

What are indications of arthroplasty?

A

uncontrolled especially at night and significant limitation of function patient age is a consideration for some surgeons

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56
Q

What are indications of arthroplasty?

A

uncontrolled especially at night and significant limitation of function patient age is a consideration for some surgeons

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57
Q

What are common multisystem diseases?

A

Infection, auto-immune connective tissue diseases, metabolic diseases, endocrine diseases, cancer

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58
Q

What is marfans?

A

AD disease, long fingers toes, chest deformities dilated aorta high arch pallate anddislocated eye

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59
Q

What is ehler danlos syndrome?

A

Joint hypermobility and skin elasticity

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60
Q

What are features of autoimmune connective tisue diseases?

A

Inflammation and scaring in multiple organs, can present with organ failure sometimes asyptomatic,

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61
Q

What is butterfly rash?

A

specific to marfans but nt always present

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62
Q

What is butterfly rash?

A

specific to marfans but nt always present

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63
Q

What is the pathogenesis for SLE?

A

Inflamation that lead

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64
Q

How can SLE present?

A

Dermatology, rashes, Rheymatology inflammatory arthritis, Nephrology nephritis cardiology Acute MI pericarditis respiratory pleural effusion, Neurologue numerous,

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65
Q

How can skin be affected in lupus?

A

Acute malar butterfly rash, photosensitive, discord rash, subacute lupus rash, moth ulcers alopecia.

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66
Q

How does SLE affect jints?

A

Symmetrical less proliferative less

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67
Q

How can SLE affect neuro?

A

can have very many conditions that it can cause including mood disorders and MS lie symptoms

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68
Q

How is blood in SLE?

A

Pancytopenia

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69
Q

What are autoantibodies to test for SLE?

A

Antinuclear antibodies which are nonspecific for lupus, double stranded DNA antibodies specific and also rheumatoid factor

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70
Q

How is lupus managed?

A

No cure chronic? UV protection patient education and support, assess their flairups anf immunological assessment check organ function and assess for dammage, assess phospholipid antibodies, good liaison with other specialists,

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71
Q

How is lupus managed?

A

No cure chronic? UV protection patient education and support, assess their flairups anf immunological assessment check organ function and assess for dammage, assess phospholipid antibodies, good liaison with other specialists,

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72
Q

What are drug treatments on drugs?

A

No treatment, topical suncream steroids cytotoxic NSAIDs(avoidance) Antimalarials for rash treatment, steroids and anticoaguland drugs and Bell disruption.

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73
Q

What is Raynaud’s phenomenon?

A

Whitness from vasoconsticiton, then blue from hypoxia then goes red when vasodilatationcan be primary or secondary to systemic scleosis SLE or mixed connective tissue disease vibrating things

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74
Q

What is systemic sclerosis?

A

Vasculopathy excessive collagen deposition and inflammation. there are several classifications

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75
Q

What are symptoms of systemic sclerosis?

A

joint calcium deposis necrosis at the end of the fingers, dilated capilliaries, oesophageal distension

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76
Q

How to test for systemic sclerosis/

A

lots of different types of antibodies

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77
Q

What are the treatments for systemic sclerosis?

A

pysical protection for ranauds, vasodilators, GORD PPIs renal crisis ACE inhibition. Can’t do much for them other than symptomatic treatment

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78
Q

WHat is primary SJogren’s syndrome?

A

Dry eyes mouth arthrisis rashes neurological featers vasculatis renal tbulular acidosis

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79
Q

WHat an cause secodary sjorgrens?

A

SLE

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80
Q

How to test for primary Sjogren’s?

A

Biopsy of salivary gland, and antibodies

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81
Q

How to treat Sjogren’s?

A

Tear saliva replaceent hydroxychloroquine for myalgia etc

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82
Q

What are Dermatomyosits and polymyositis?

A

rashes and muscle weakness, lungs can be affected often present with cancers

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83
Q

How is dermatomyositis and polymyositis treated?

A

Steroids and

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84
Q

What defines MSK health?

A

Do activities you would like without symptoms.

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85
Q

What are modifieable risk factors for MSK?

A

Vitamin D/ Calcium levels, Obesity, physical activity, injury prevention

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86
Q

Where is prevention for MSK diseases imrportant?

A

During pregnancy, child healh adult health and generally

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87
Q

What should mothers do during pregnancy to safeguard their child’s bone health?

A

Smoking diet Vit D

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88
Q

What can you do in children for MSK problem prevention?

A

Physical activity, diet for bone density and healthy body weight

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89
Q

How is physical activity related to MSK health/

A

Bidirectional relation with health and exercise. Low activity can cause MSK problems, but low activity can be as a result of poor MSK health

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90
Q

What is multimorbidity in MSK?

A

Painful MSK conditions are linked to poor mental health especially anxiety and depression

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91
Q

How can physical activity advice be used in clinical consultations?

A

Brief interventions are good. Moving medicine has 1 minute consultation. Ask if they know that being more active can help their condition, explain that it can help take control and wond hurt them. Invite them to come and discuss more or get involved

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92
Q

What are signs of a joint infection?

A

Painful swollen red hot joint, High white cell count neutrophils, CRP can be up, ESR can be higher, need to take aspiration from the joint, blood cultures,

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93
Q

What does infected synovial fuid look like?

A

Cloudy discoloured fluid. Usually it should be transparent and slightly yellow

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94
Q

What is most common native joint infection bacteria others?

A

S. Aureus, streptococi, e coli, Can depend on history consideration eg recent UTI,IV drug users

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95
Q

What should be done in joint infection?

A

antibiotics double steroids to avoid adrenal crisis, stop other immunosupression. if not clearing can aspirate the joint

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96
Q

What is difficulty with antibiotics and joint inflammation?

A

doesn’t usually get into the joints, can be injected directly

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97
Q

Where are septic joint arthritis most comon?

A

prosthetic joint infection is more common usually in over 65yrs

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98
Q

What to watch out for in joint infection?

A

Immunocompromised patients can often have odd organisms, such as TB or Fungi

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99
Q

What is change in septic joint arthritis in children?

A

Used to have haemophillus but now vaccinated against it

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100
Q

What is Gonococcal arthritis?

A

Can afect multiple joints, and can be associated with rash causes pain before visible,

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101
Q

What to do if aspiration negative?

A

Synovial biopsy, blood cultures and swabs in rest of body

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102
Q

What are risk factors of septic joints?

A

Any cause for bacteraemia, direct penetrating trauma local skin outbreaks dammaged joints, Diabetes, Older, immunosuppressed

103
Q

What is overall management of joint?

A

Always aspirate long antibiotics guided by aspiration, long course antibiotics 6 weeks minimum, can rest splints and physio and stop immunosuppression of possible

104
Q

How common is prosthetic joint infection?

A

quite rare but happens lots as we do operations a lot

105
Q

What are consequences of joint infection?

A

Destruction of tissue and loss of limbs and life threatenting

106
Q

What usually cause prosthetic joint infections ?

A

Gram positive cocci including Saureas the rest are gram negative can be from skin often

107
Q

How to treat prosthetic joint infections prevention ?

A

Prevent them as much as possible, laminar flow theatre low staff, sterile hoods facemasks, double gloving, antibiotics during surgery, antibiotic cement,

108
Q

Hoe to diagnose joint prosthetic ifection?

A

History of joint, risk factors since operation pain in the joint, X eays FBC ESR CRPmicrobiological culture

109
Q

How useful are inflammatory markers in oint infection?

A

CRP ESR if raised likely it is infected of both low 90% not infected. IF several CRP and ESR are raised to 80% have it. Alpha defensin can see this from immune rsponse to joint infection 95% accurate

110
Q

How is best way to conform diagnosis of prosthetic joint infection?

A

aspiration of the joint have to be off 2 weeks antibiotics.

111
Q

What are aims of treating prosthetic joint infection?

A

eradicate sepsis relive pain restore function

112
Q

What are treatement options to prosthetic joint infection?

A

Antibiotic, debridement and retention of prosthesis, Excision of athroplasty, one stage exchange arthroplasty two stae exchange athroplaty and finally amputation

113
Q

When in antibiotics used to treat prosthetic joint infection?

A

Unfit for surgery, low virulence, poor cover on joint, multiple joints. will not cure

114
Q

What is debridement?

A

replaceing parts take out soft tissues infected, not for chronic infection or loose joints,

115
Q

When is excision arthroplasty used?

A

high risk patients get a poor outcome functionally

116
Q

what is gold standard prosthetic joint infection treatment?

A

Exchange arthroplasty, remove all dead and infected tissue, replace joint and check for sensitivity at all stages

117
Q

What is one stage exhange?

A

debridement new cemented prosthesis local and systemic antibiotics, 85% sucess

118
Q

What is a new problem especially in upper limb problems?

A

Propionibacteria only waits up hard to culture and detect with standart techniques

119
Q

What is osteomyelitis?

A

Infection localisted to bone

120
Q

What is epidemiology of osteomyelitis?

A

Bimodal in young children and old patients after operations or Diabetes and PVD increasingly seeing chronic osteomyelitis

121
Q

What are ways for osteomyelitis to happen?

A

Direct innoculation of infection into the bone, contagious spread of infection from adjacent joints and soft tissues, common after surgery or chronic ucers les commonly haematogenous seeding where long children get it in long bones and in vertibrae in adults

122
Q

How common are bone and soft tissue tumours?

A

rare bit often secondary tumours and are usually to provide symptomatic control and survival

123
Q

Where do bone cancers/tumours happen?

A

Quite variable depending on the type of bone cancers

124
Q

What are risk factors for bone malicancy?

A

Genetic conditions redinobblastoma pagets disease radiotherapy

125
Q

What are red flag bone cancer symptoms?

A

Pain swelling weiht loss night sweats pathalogical fracture previous malignancy and bone pain in children, lump present loss of function,

126
Q

How to investigate bone cancer?

A

Blood tests FBC U+E Ca2+ Alk phos parathyroid to look at bone matabolism
X-rays, US CT for assessing bone quality and solid tumours MRI for reactive soft tisue changed and bone marrow, Bone scan for skeletal metastases

127
Q

What is a zone of transition?

A

Reliable indicator on if osteolytic lesion is benign or malignant, if ther is narrow zone it showes slow growth of tumour

128
Q

What can a CT scan show you about bone cancer?

A

Intramedullary or extramedilliary, assess soft tissue cortex involvment cystic or solid

129
Q

When is PET scan done?

A

In rare tumours used to see where tumour is

130
Q

what are tumour markers?

A

identify trypes of tumours they are molecules produced when there are cancers

131
Q

What is important to estabilish in bone cancer?

A

Benign or malignant, primary secondary, where is it are there multiple lesions local soft tissue sread or distant lystic or blastic, how much of cortex is eroded

132
Q

What are the most common metastasise that end up in the bone?

A

Prostate breast, lungs thyroid and kidneys often to the spine

133
Q

What are the benign bone/ cartilage. cystic/ fibrous toumours?

A

bone(Osteoid osteoma, Osteochondroma,osteoblastoma Enchondromas, Giant cell tmours, Osteocalstoma

134
Q

What are osteochondromas?

A

outgrowth of metaphysis of long bones covered by cartilaginous cap stops growing after puberty surgical excision if symptomatic Commonly affect males under 25, often around knee hip and scapular

135
Q

What are the factors that can increase risk of joint infection?

A

trauma, arterial supply sickle cell diseae diabetes mellitus, pre-existing bone problems inflammatory arthritis or immunosupresion

136
Q

Where is haematogenous osteomyelitis common?

A

In adults usually over 50 vertebrae clavicle and pelvis more commonly than vertebrae, in children often in long bones more than vertibrae

137
Q

Why is long bone OM more common in children?

A

Blood flow is high to netapgysis in children as is devloping

138
Q

What are the histological changes in OM?

A

inflammatory cells, oedema, vascular congestion, small vessel thrombosis, in chronic get necrotic bone and new bone formation neutrophil exuadates

139
Q

What are the symptoms of OM?

A

several days onset dull pain at the site of infection, fever rigors sweats malaise, tenderness warmth erythema and swelling can present as septic arthritis

140
Q

How is OM diagnosed?

A

High WCC chronic can be normal, MRI or CT or nuclear bone scan, raised inflammatory markers bone biopsy and blood cultures

141
Q

How is osteomyelitis treated?

A

Surgical debridement, hardware placement or removal tailored sensitivity antibiotics,

142
Q

What is TB osteomyelitis?

A

Slower onset systemic symptomes takes longer to treat harder to diagnose

143
Q

What are malignant bone tumours?

A

Osteosarcoma, chondrosarcome fibrosarcoma

144
Q

What is osteoid osteoma?

A

Benign bone forming lesion in young patients often in proximal femur, tibial diaphysis spine often self limiting osteoblasts affect diaphysis small nidus

145
Q

What is osteoblastoma?

A

Rare bone producing tumour, not self limiting get bone destruction surrounded by reactive new bone from osteoblastss axial skeleton form large nidus

146
Q

What is osteosarcoma?

A

Spindle cell neoplasms that produce osteoid, there are types associated with a mutation from osteoblasts often in metastasis often in adolecents, associated with retinal blastoma

147
Q

What is secondary osteosarcoma?

A

Secondary to padgets disease, irradiation and fibrous dysplasia

148
Q

How is osteosarcoma treated?

A

Chemotherapy but has poor prognosis

149
Q

What is giant cell tuours?

A

bone trauma and radiation make more likely arise from osteoclasts, often in epiphysis and can become mallignant

150
Q

What is ewings sarcoma?

A

neuroectodermal cells, mutations, formation of ewingsarcome aprotein stopping cells differentiating

151
Q

What are chondrosarcomas?

A

From chondrocytes often affect pelvis and femur and humerus usually in medulla

152
Q

What are some specific presentations of bone cancers?

A

osteoid osteoma is worst at night, osteochrondroma and osteoblastoma cause neurological symptoms like limb weakness, numbness avascualr necrosis.
pumonary symtoms as often metastisise to there

153
Q

What are special Xray findings in bone cancers?

A

Solit lump undereriostium can be in benign tumours producing bone, in faster growth get onion skin or periosteal reaction lamellated in ewings sarcoma osteosarcoma and osteomyelitis, Sunburst sharpeys fibres ossify, codmans triangle when tumour grows rapidly but steadily so only edges of periostium ossify. eccentric lytic soap bubble appearance on giant cell tumours

154
Q

On X-ray for bone cancer what are the things to look for?

A

location size, cortical irregularity, periosteal reaction, soft tissue involvement pattern of bone destruction

155
Q

Why look at bone with MRI?

A

Better for marrow contents differentiation of benign and malignent tumours

156
Q

What are the bone forming cancers?

A

Osteoma osteoid osteoma osteoblastoma and osteosarcoma

157
Q

What are the cartilate forming cancers?

A

Chondroma osetochondroma, Chondropastoma and malignand is chondrosarcoma

158
Q

What are osteolytic cancers?

A

Giant cells, benign osteoclastoma malignant osteoglastoma

159
Q

What are most common benign bone tumours?

A

enchondromas

160
Q

What is vasculitis?

A

Rare multi-system diseases characterised by inflammation of blood vessels classifed by vessel size and common features

161
Q

What is the most common vasculitis?

A

Giant cell arthrteritis

162
Q

What is the pathophysiology of vasculitis?

A

they lose differentiation of media and adventitia nucleated cells in adventitia . ideopathic autoimmune process or drugs, infection and autoimmune diseases can cause vasculitis.Immune cells enter the wall and cause vascular cell remodelling and causes weakening and occlusion of blood vessels and ischaemia infarction and aneurism.

163
Q

How can vasculitis be classified?

A

By vessel size, consensus clasification that are on vessel size and pathophysiology

164
Q

What are ANCA asscociated vasculitis?

A

antineutrophil cytoplasmic antibody.

165
Q

What size vessels are ANCA vasculitis associated with?

A

smaller vessels including veins

166
Q

What is epidemiology of Giant cell vasculitis?

A

Older age over 50, most common in white and scandinavian countries

167
Q

What are the symptoms of vasculitis?

A

Cranial GCA Large vessel GCA that mimic cancer presentation temproal headach and scalp ache facial and lingual artery involvement causing painful jaw or tonugue, visual symptoms, polymyalgia fever malaise, limb claudication.

168
Q

What are complications of giant cell arteritis?

A

Strokes and blindness from retinal artery occlusion visual outcomes are poor

169
Q

What can help negative features of headache that aren’t GCA?

A

Vomiting Raised intracranial presure, acute localised clinical signs, fever (infection)

170
Q

what can differentiate inflammatory from Degernerativ artheritis?

A

Inflam vs Degen
Pain eases with use vs worsens with use
Redness and hot vs no inflammation
Sweling with les likely boney vs alwasy boney
Stiffness after inactivity for significant time vs not prolongued
patietns usually young with history of psoriasis vs older or occumpation related
hands and feet vs thrum DIPJ and knees
responds to NSAIDs vs not

171
Q

What is important about bone pain?

A

Pain at rest and at night from tumour infection or fracture

172
Q

Where might you get Rhematoid arthritis?

A

hands and feet neck and other synovial joints

173
Q

Where might osteoarthritis present?

A

In big joints knees big toe thum DICP hips spine

174
Q

Where can psoraitic arthritis affect?

A

All joints and finger toes swelling and pain at tentons

175
Q

What is ESR?

A

Erythrocyte sedimentation rate. faster rate more inflammationor infection. It rises very slowly over days or weeks and remains hight ofr a while

176
Q

What can affect false positive sin ESR?

A

increases in age, obesity femaile racial difference South east asian, high cholesterol anaemia

177
Q

What is CRP/

A

Acute phase protein when get inflammation and infectioon in response to IL6, falls and rises rapidly

178
Q

What is sponyloarthrits/

A

A Group of disease including Anylosing spondylitis, Reactive arthritis, Enteropathic arthritis, Psoriatic arthrits, Undifferentiated SpA, acute anterior Uveitis (iritis) Juvenile idiopathic arthritis

179
Q

What is HLA B27?

A

Tissue type and is a protein on all cells exccept RBC which is part of MHC antigent presenting

180
Q

Why is HLA B27 improtant?

A

Varies in prevalence around the world

181
Q

How can B27 be used?

A

most peple with Ankylosisn sponylitis have it but not all do and therre are a lot who have it that dont have disease

182
Q

What are the ideas of B27 involvement?

A

Misfolding protein causes activation of inflamation

183
Q

What are generic features of spondyloarthrits?

A

inflammatory back pain and khyphosis, psoriatic rashes around joints, infammation of achillies tendon, Uvitis acute anterior red inflamed painful photophoic , swollen joints

184
Q

What is SPINACHE a way for remembering?

A 
For all spondylosing arthritis.
Sausage digits
Psoriasis
Inflammatory back pain
Nsaids response
Enthesitis
Arthrits
Crohn's Colitis CRP
HLA B27
Eye (uveitis)
185
Q

What is Ankylosing spondylitis?

A

Bamboo spine, Axial spobdyloarthritis, get syndesmophytes calcium growing on the front of the spine, sacroilitis joint fusion

186
Q

What is inflammatory back pain?

A

usually young, back pain for a while months or years, gets better with exrcise worse with rest, night time in second half of night alternating buttock pain

187
Q

What are the staes of Axial spondyloarthrits?

A

Xray undetectable 10 years of change based on MRI findings at this point then if have Xray changes it is progressed

188
Q

What are the treatments for Spondylosingarthrits?

A

only IV biologival drugs anti -TNF and IL-17 IL-23 blockers

189
Q

What is psoriatic arthrits?

A

arthritis associated with psoriasis. all joints including DIPJ, have nail changes, can get dactylitis,

190
Q

What is arthritis Mutilans?

A

A damaging agressive form of arthritis that causes rapid deformity

191
Q

What is reactive arthritis?

A

Arthritis typically 2 days to 2 weeks post infection get sterile Urethritis, Conjunctivitis keratoderma blenorrhagica.

192
Q

How is peripheral arthritis managed?

A

With biologic and oral DMARDS methotrexate, mild immunosupressive

193
Q

What is enteropathic arthritis?

A

Inflammatory arthrits associated with Crohns’ Ulcerative collits flairups can be separate or together

194
Q

What are the problems with treating Enteropathic Arthrits

A

some drugs for joints affect the bowels negatively Vedilizumab, but some do something for one but not other or some like DMARDs work for both

195
Q

What are the principals ofr ortopaedics?

A

Improve pain reduce disability a

196
Q

What happens during fractrue treatment?

A

4 R’s Resucitate, (C) ABC
Reduce move the joint to where it should be
Retain to fix the joint in place internally or externally
Rehabilitate

197
Q

How to present orthopaedic X-ray?

A

Always start with Who when what adequacy always need 2 views ABC alignment - dislocation Bone - fractures Cartilage- widened joint, Soft tissue- sweelling effusion

198
Q

How to describe the fracture?

A

which bone, intra or extra articular, position pattern, Transverse/ oblique spiral, condition comminuted, segmental, impacted Displacement length alignment Translation Angulation Rotation

199
Q

What is a crystal?

A

Homogenous solid stable hard high density it can form in the kidney or in joints

200
Q

What are the types of crystal arthritis?

A

Gout urate crystals, pseudogout pyrophosphate crystal

201
Q

What is the history of gout?

A

Sudden onset hot swollen joing excruciatingly painful joint

202
Q

Where does gout usually affect?

A

Big toe, ankle, foot, knee, finger , elbow, wrist.

203
Q

How can gout become cronic?

A

Large crystals that don’t go away, can then become chronic but can be treated

204
Q

What is epidemiology of gout?

A

More in men than women until after menopause, south east asians phillipino when out of countires

205
Q

What is the key enzymes involved in uric acid crystals formation?

A

Xanthine oxidase

206
Q

What is the pathophysiology of gout?

A

Uric acid in serum above its saturation point which can cause crystals to form

207
Q

What are causes of high uric acid?

A

Too much in, Alcohol -beer, fructose sweetened drinks excess meat shellfish offal, yeast extract, myeloproliferative disease, psoriasis tumour lysis syndrome
Too little out Renal impairment, thiazide diuretics, low dose aspirin, tacrolimus, ciclosporin, ethambutol, pyrazinamide

208
Q

What syndrome is involved in gout?

A

Metabolic syndrome which includes High BP Type 2 DM heart disease and lipit problems

209
Q

What can trigger an attack of gout?

A

Direct trauma to the joint, intercurrent illness alcohol ofr shellfish binge, surgery, dehydration most are spontaneous starting treatment

210
Q

What are investigatins for gout?

A

Routine bloods inflammatory expect rasied ESR and CRP, Uric acid levels but not always helpful as could all be in joint at time of attack, confirmation by joint aspiration needle shapes negatively birefringent, Xrays nondianostic

211
Q

What are acute treatments for gout?

A

NSAIDs not in renal impairment, Colchicine diarrhoea side effects, Prednisolone to control pain

212
Q

How is gout treated chronicly?

A

Lifestyle advice, Allopurinol Febuxostat which are xanthine oxidase inhibitors to stop uric acid production. What is target? less than 300 in serum keep eye on kidney function for febuxostat check liver function

213
Q

What is pseudogout?

A

Linked with osteoarthritis

214
Q

What are risk factors for pseudogout?

A

Haemochromotosis, hyperparathyroidsim,

215
Q

What is investigation for pseudogout?

A

Routine bloods Iron PTH PO4 Mg TSH, inflammatory markers, Uric acid, Joint aspiration rhomboid shaped crystals, X-ray

216
Q

What is treatment of pseudogout?

A

NSAIDSs, Colchisine prednisolone.

217
Q

What is treatment chronic for pseudogout?

A

Low does prednisolone and sometimes others but no real effective treatment

218
Q

Where can neck pain radiate?

A

Down arm and skull

219
Q

Which rheumatological conditions commonly have extra articular manifestations?

A

Rheumatoid arthritis, SLE, GOUT, Gonnococcal arthritis

220
Q

What extraarticular presentations can Rheumatoid arthritis affect?

A

Eyes (uvitis anterior), Cervical spine, skin, pericarditis back of knee

221
Q

What extra-articular manifestations are present in lupus?

A

face (mallar rash), buccal mucosa ulcers, heart pericarditis and andocarditis, kidney nephritis, hotosensitivity, neuro, clots pancytopenia

222
Q

Where are extraarticular Manifestations of gout?

A

Skin tophi in earlobes achillies tendon

223
Q

What can cause septic arthritis?

A

Gonorrhoea

224
Q

Can Chlamydia cause septic arthritis?

A

No but can cause reactive arthritis

225
Q

What is ANA?

A

Autoantibodies for the nucleus components, reported as titre for dilution to become undetectable. If positive he dilution doesn’t matter for severity

226
Q

What is drug-induced lupus?

A

Causes lupus like symptoms from Hydralazine, Procainamide isoniaszid

227
Q

How is ANA used in drug induced lupus?

A

All have ANA so it is good for ruling out it is 100% sensitive

228
Q

How good is ANA for SLE?

A

98-100% have it so good for rulling out generally it is sensitive but not specific

229
Q

How is ANA used for Scroderma Sjogren’s Dermatomtositis or RA?

A

40% have it so less useful but can still be used

230
Q

Why is ANA not specific?

A

There are many diseases which can have it as well as the one you are considdering and also some normal people have it without disease

231
Q

What are ANA patterns?

A

To see what types of antibodies they are

232
Q

What test(s) are specific for SLE?

A

Anti-dsDNA (absent in drug induced and correlates with SLE activity so serial mesureuses are good and Anti-Smith antibodies just for confirmation

233
Q

What are specific ANAs?

A

They are certain types of ANA that can be specific for certain types of disease

234
Q

What are some specific ANAa/

A

anti-histone for drug induced, anti-centromere limited scleroderma, anti RNA polymeraseIII sceroderma kidney, Anti SCL-70 antitopioisomerase I systemic sclerosis

235
Q

What are sedimentation factors?

A

fibrinogen and immunoglobulin and rouleaux formation.

236
Q

What can increase ESR?

A

Inflammation, Infection, Anaemia, Macrocytosis, Multiple myeloma, Ealdensctrom macroglobulineria

237
Q

What can decrease ESR?

A

Hyperviscosyty syndrome, polycythemia sickle cell microcytosis, sherpocytosis

238
Q

Why are ESR and CRP good?

A

Acute inflammatry levels, They indicate severity of inflammation and respond to treatment ESR takes longer to respond

239
Q

What are secondary causes of OA?

A

Joint trauma, prior inflamatory arthritis, metabolic disorders(haemochomotosis, Paget disease Ocronosis) endocrine disorders Collagen defects others Osteoporosis or osteonecrosis

240
Q

What is pathophysiology of OA?

A

Injured chondrcytes, then get proliferation of chondrocytes and secrete inflam mediators collagenase, protease, proteoglycans, causeing remodelling and chronic inflammation and losss of cartilate and subcondral bone changes

241
Q

What are Heberdan’s nodes?

A

bony nodules in the Distal interphalangeal joints osteophytes

242
Q

What are bouchards nodes?

A

bony nodules in the proximal interphalangeal joints osteophytes

243
Q

What are OA blood tests?

A

All normal but some can be positive as they are not 100% specific

244
Q

What are the joint fluid analysis of OA?

A

Increased volume, transparent, yellow slightly high WBC generaly lymphocytes negative cultrue

245
Q

What can you see in radiology of OA?

A

Asymmetrical change, Subchondral scerosis, osteophytes, Joint space narrowing bone enlargement

246
Q

What are extra-articular manifestations of RA?

A

Scleritis, Baker cyst, Anaemia of chronic disease, Carpal tunnel syndrome, Pancarditis ans pericarditis, basal fibrosis of lungs, scleritis and episcleritis, atlantoaxial subluxation,

247
Q

What indicates agressive RA?

A

RF and anti CCP

248
Q

What is a Pannus?

A

Type of extra growth in your joints that can cause pain, swelling and damage to your bones and joint tissues

249
Q

What does high sensitivity test mean?

A

If its negative you are very unlikely to have the disease. The true positive is very high compared to false negative

250
Q

What does high specificity mean?

A

If it is positive

251
Q

What are the main uses for ANA test?

A

100% drug induced have it highly sensitive, 98%-100% SLE have it also for Mixedconnective tissue disease. for sceroderma sjorgren dermatomyositis and polymyosistis it is much lower. For rheumatoid arthritis only 40% of patients are ANA +

252
Q

What does high sensitivity mean in terms of predict vaule?

A

High sensitivity is high negative predict value, meaning if its negative it rules out the disease

253
Q

Why is ANA not specific?

A

It isnt for a sepecific disease

254
Q

Is positive ANA a useful thing?

A

Not neccessarily negative is more importatnt

Phase 2 mine (13 decks)

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