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Phase 2a Lecture Notes > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Osteomyelitis

A

inflammatory condition of bone caused by an infecting organism, most commonly Staphylococcus aureus.

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2
Q

When to suscept acute osteomyelitis

A

Most commonly in an unwell child with a limp, or in an immunocompromised patient.

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3
Q

When to suscept chronic osteomyelitis

A

most commonly in adults with a history of open fracture, previous orthopaedic surgery, or a discharging sinus

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4
Q

Osteomyelitis- signs- acute

A

Systemic- Fever, rigors, sweats, malaise
Local- tenderness, warmth, erythema, and swelling

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5
Q

Osteomyelitis- signs- chronic

A

Systemic- Fever, rigors, sweats, malaise
Local- tenderness, warmth, erythema, and swelling
draining sinus tract
deep / large ulcers that fail to heal despite several weeks treatment (DM ulcer)
non-healing fractures

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6
Q

Native vertebral osteomyelitis- signs

A

Local back pain associated with systemic symptoms, paravertebral muscle tenderness and spasm

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7
Q

Osteomyelitis RFs

A

previous osteomyelitis
penetrating injury
intravenous drug misuse
diabetes

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8
Q

Osteomyelitis- investigations

A

FBC- may be raised WBC (chronic is normal)
ESR/ CRP- usually raised
Blood culture- to identify suitable antibiotic
Plain x-ray of affected area
MRI/ CT

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9
Q

Osteomyelitis- investigations- plain x ray

A

Chronic- cortical erosion,
periosteal reaction,
mixed lucency,
Sclerosis
sequestra
soft tissue swelling

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10
Q

Osteomyelitis- investigations- MRI

A

marrow oedema from 3-5 days
Delineates cortical, bone marrow and soft tissue inflammation

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11
Q

Osteomyelitis- investigations- definitive diagnosis

A

Bone biopsy- 2 samples
Positive blood cultures (50% of acute OM)

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12
Q

Osteomyelitis- differential diagnosis

A

Soft tissue infection (Cellulitis and erysipelas)
Charcot joint
Avascular necrosis of bone (Causes: steroid, radiation, or bisphosphonate use)
Gout (uric acid crystals in joint fluid / more acute presentation)
Fracture
Bursitis
Malignancy

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13
Q

Osteomyelitis- treatment

A

Surgical- Debridement or Hardware placement or removal
Antimicrobial therapy

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14
Q

Osteomyelitis- treatment- antimicrobial therapy

A

Initial broad spectrum empiric therapy
Tailored to culture and sensitivity findings
Bone penetration of drug
Prolonged duration (6 weeks<)

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15
Q

Routes of Osteomyelitis

A
  • Direct inoculation of infection into the bone
    trauma or surgery,
    poly/ monomicrobial
  • Contiguous spread of infection to bone
  • Haematogenous seeding- children (long bones)>adults (vertebrae), monomicrobial
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16
Q

Routes of Osteomyelitis- Contiguous spread of infection to bone

A

-from adjacent soft tissues and joints, polymicrobial or monomicrobial,
-older adults: DM, chronic ulcers, vascular disease, arthroplasties / prosthetic material

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17
Q

Osteomyelitis- typical microbe causes

A

Staphylococcus aureus,
coagulase-negative staphylococci,
aerobic gram-negative bacilli

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18
Q

Osteomyelitis- histopathology- acute changes

A

Inflammatory cells
Oedema
Vascular congestion
Small vessel thrombosis

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19
Q

Osteomyelitis- histopathology- chronic changes

A

neutrophil exudates
lymphocytes & histiocytes
Necrotic bone ‘sequestra’
new bone formation ‘involucrum’

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20
Q

Pathogenesis of OM – Host factors

A

Behavioural factors- risk of factors
Vascular supply- arterial disease, DM, sickle cell disease
Pre-existing bone/ joint problem
Immune deficiency

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21
Q

Periprosthetic joint infection

A

Infectious complication following total joint arthroplasty (TJA)

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22
Q

Periprosthetic joint infection- common causes of infection

A

Gram‐positive bacterium is still the most common pathogenic bacteria in PJI
Staphylococcus epidermidis and Staphylococcus aureus were the largest in number.

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23
Q

Periprosthetic joint infection- upper vs lower limb

A

Propionibacteria more sig problems in upper limb

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24
Q

Periprosthetic joint infection- upper limb and propionibacteria

A

They are colonisers of humans from the above the waist
Can even be shed by blinking the eyes
Therefore may represent more of a threat in upper limb prostheses and Spines

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25
Q

Septic arthritis

A

Consider in any acutely inflamed joint as it can destroy joint in 24 hrs and has high mortality rate (11%)
Inflammation may be less overt if immunocompromised or underlying joint disease
Commonly affect knee (>50%)

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26
Q

Septic arthritis RFs

A

Pre-existing joint disease (esp rheumatoid arthritis)
DM, CKD, immunocompromised, recent joint surgery, prosthetic joints, IV drug users, increased age (80<)

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27
Q

Septic arthritis- common organisms- native joints

A

Staph Aureus (DM)
Streptococci
Neisseria gonorrhoea (young, sexually active, MSM)
Anaerobes (DM)
Mycobacterium/ fungi- immunocompromised

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28
Q

Gonococcal Arthritis

A

Occurs with disseminated gonococcal infection
Fever, arthritis, tenosynovitis- multiple joints, small + large
Maclopapular- pustular rash (with both flat and raised parts)

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29
Q

Typical clinical presentation of septic joint

A

Painful, red, swollen, hot joint
Remember children may just not use it
Fever
90% monoarthritis- don’t rule out in polyarticular presentations
Knee > hip > shoulder

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30
Q

Septic arthritis- investigations

A

Urgent aspiration- synovial fluid microscopy, gram stain, culture + sensitivities and WBC- before starting antibiotic therapy unless urgent
Blood culture
Bloods- for baseline
Pain x ray- not urgent as not diagnostic but baseline investigation

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31
Q

Diagnostic investigation for septic arthritis

A

Urgent joint aspiration for synovial fluid for microscopy or culture

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32
Q

Septic arthritis- treatment

A

Long course antibiotics (>6 weeks) guided by aspiration results
Joint washout/ rpt’d aspiration until no recurrent effusion
Rest/ splint/ physio
Analgesia
Stop any immuno-suppression temporarily if possible

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33
Q

Septic arthritis- most common infecting organism overall (native joints)

A

Staph Aureus

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34
Q

Inflammatory Arthritis

A

New onset joint SWELLING- Synovial (compressible, tender), Often red, Warm to touch
Worst in morning / inactivity
Stiffness > 30 mins (usually longer)
Constant or intermittent

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35
Q

Inflammatory Arthritis- 3 Ss

A

Stiffness
Swelling
Squeezing- painful

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36
Q

Causes of Joint Inflammation

A

Inflammatory Arthritis
*RA
*Seronegative Spondyloarthritis
*Crystal arthrits – gout and pseudogout
Septic Arthritis

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37
Q

Causes of Joint Inflammation- Seronegative Spondyloarthritis examples

A

-Psoriatic
-Ank Spond
-Reactive Arthritis
-Enteropathic – Crohns and Ulcerative Colitis related

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38
Q

Rheumatoid Arthritis

A

Symmetrical small joints, hands wrists feet
Big joints involved later, bad prognostic sign if involved at presentation
No spinal involvement
1% of pop

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39
Q

Rheumatoid Arthritis- RFs

A

Middle age, female, family history, smoking

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40
Q

Seronegative Arthritis

A

Asymmetrical big joints, with spinal involvement
More common in men
Associated symptoms

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41
Q

Seronegative Arthritis
- Associated symptoms

A

-Inflammatory bowel, or GI infection, eye inflammation and psoriasis
-Nail involvement predicts arthritis in patients with psoriasis

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42
Q

Psoriatic Arthritis

A

RA like
Distal interphalangeal involvement
CRP may not be significantly raised

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43
Q

Crystal Arthritis (Gout/Pseudogout)

A

Typically acute intermittent episodes joint inflammation

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44
Q

Gout

A

6x more common in men
feet, ankles, knees, elbows, hands
Hyperuricaemia

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45
Q

Gout- RFs

A

beer, renal impairment, diuretics, aspirin, FH

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46
Q

Pseudogout

A

3 x more common in women
wrists, knees, hands
Typically on background of OA
Chondrocalcinosis on x ray

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47
Q

Osteoarthritis

A

Degenerative- slow onset – months to years
Typically weight bearing joints DIPs, PIPs, thumb bases, big toes

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48
Q

Osteoarthritis- signs

A

Pain and crepitus on movement and back ground ache at rest
Minimal early morning stiffness (gelling)
No variability to joint swelling
Normal CRP
Clear changes on xray

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49
Q

Arthritis- making a diagnosis

A

Is it inflammatory?
Which joint pattern?
Associated symptoms / risks
Tests- RF (Rheumatoid factors)/CCP+ (RA only), uric acid between attacks ?gout
-X rays

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50
Q

Arthritis-making a diagnosis- is it inflammatory

A

Visible joint swelling
Elevated CRP
Variable symptoms with flares

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51
Q

Arthritis-making a diagnosis- Associated symptoms / risks

A

Psoriasis (particularly with nail involvement)
Inflammatory eye / bowel symptoms
Family / Smoking history (RA)

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52
Q

Crystal Arthritis

A

commonest cause of acute joint swelling
Gout most common in men
Pseudogout in women

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53
Q

Gout

A

Caused by the deposition of monosodium urate crystals within joint
The immunological reaction initiated to try and remove them, leads to acute pain and swelling
Curable

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54
Q

Gout- causes of hyperuricaemia

A

Under excretion urate- genetic, drugs
Overproduction of urate- diet, alcohol, metabolic, proliferation

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55
Q

Gout pathogenesis

A

Hyperuricaemia > crystal formation + shedding > synovial cells > inflammatory response

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56
Q

Gout and Alcohol

A

Beer / lager / stout equally bad
All rich in guanosine
Small increased risk with spirits
No increased risk with wine

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57
Q

Gout RFs

A

Renal impairment
Beer
Diuretics
Aspirin
Family History
Fructose

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58
Q

Gout presentation

A

Acute episodes
Onset often at night
Resolve spontaneously (quicker with treatment)
Usually recur in a predictable pattern of joint involvement

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59
Q

Acute Gout – Most common joint effect

A

1st MTPJ (metatarsophalangeal joint- big toe joint) 90%

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60
Q

Gout- differential diagnosis

A

Septic Arthritis
Trauma
Calcium Pyrophosphate Arthritis
Rheumatoid Arthritis
(Osteoarthritis!)

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61
Q

Gout diagnostic investigation

A

arthrocentesis with synovial fluid analysis- shows negatively birefringent needle-shaped crystals under polarised light

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62
Q

Gout symptoms

A

severe joint pain, with swelling, effusion, warmth, erythema, and or tenderness of the involved joint

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63
Q

Gout other investigations

A

FBC (expect raised WCC)
U+E
LFT if concern re alcohol
Serum Uric Acid (often normal during acute attack)
CRP
Xray if recurrent episodes or concern re sepsis

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64
Q

Gout clinical course

A

> asymptomatic hyperuricemia,
acute/recurrent gout,
intercritical gout,
chronic tophaceous gout

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65
Q

Gout- acute treatment

A

High dose NSAID unless renal failure, peptic ulcer disease, com pts with asthma
If CI, use colchicine or corticosteroids
+ lifestyle advice

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66
Q

Gout- lifestyle advice

A

Alcohol
Diet
Weight loss
Adequate fluid intake

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67
Q

Gout- chronic treatment indications

A

Recurrent attacks
Evidence of tophi or chronic gouty arthritis
Associated renal disease
Normal serum Uric acid cannot be achieved by life-style modifications

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68
Q

Gout- chronic treatment

A

1st lines- Allopurinol – Xanthine Oxidase Inhibitor (urate-lowering drugs)
2nd line- Febuxostat – more potent Xanthine Oxidase Inhibitor
If CI, use probenecid or sulfinpyrazone (increase renal excretion of uric acid)

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69
Q

Gout- aims of treatment

A

Aim of chronic gout management is to reduce Uric acid below <300 umol/l
Increase allopurinol every 2-4 weeks until this is met
Engage patient in this – more likely to comply and make lifestyle modification

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70
Q

Chronic Gout – signs

A

Tophi- chunks of uric acid crystals that accumulate in and around joints

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71
Q

Gout – complications

A

Disability and misery
Tophi
Renal disease ie calculi

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72
Q

Rheumatology Mantra

A

Inflammation x time = damage
Inflammation reversible, but damage not

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73
Q

Rheumatoid arthritis- clinical presentation

A

Pain and Swelling of joints
- Typically small joints hands, wrists, forefeet
Early morning stiffness (often prolonged)
Sudden change in function
Intermittent, Migratory or Additive involvement

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74
Q

Rheumatoid arthritis- physical examination

A

Decreased grip strength / fist formation
Often subtle synovitis – MCPs, PIPs, MTPs, ankles
DIPs are spared
Usually symmetrical
Deformity unusual at presentation

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75
Q

Rheumatoid arthritis- investigations

A

rheumatoid factor (RF)- positive
Anti-cyclic citrullinated peptide (anti-CCP) antibody- positive
Radiographs show erosions
Ultrasonography show synovitis of the wrist and fingers

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76
Q

Rheumatoid factor (RF)

A

Autoantibodies frequently seen in patients with RA but can also be seen in hepatitis C, chronic infections, and other rheumatological conditions
60-70% of RA patients test positive

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77
Q

Anti-cyclic citrullinated peptide (anti-CCP) antibody

A

Positive in 70% of RA patients
Anti-CCP can be positive when RF is negative, and it seems to play more of a pathogenic role in the development of RA

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78
Q

Rheumatoid arthritis- investigations- X rays

A

Used as diagnostic, and prognostic tools, and to monitor therapy

Xray changes of RA
-Soft tissue swelling
-Periarticular osteopenia
-Joint space narrowing
-Bone erosion

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79
Q

Rheumatoid arthritis- X rays changes

A

-Soft tissue swelling
-Periarticular osteopenia
-Joint space narrowing
-Bone erosion

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80
Q

Rheumatoid arthritis- treatment aims

A

To suppress inflammation as completely and quickly as possible once diagnosis confirmed without making our patients ill
Improve symptoms, prevent/reduce damage, prevent premature mortality

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81
Q

Rheumatoid arthritis- treatment

A

Early use of DMARS improve outcomes
Referral to physio, OT, podiatry as indicated
Escalation to biologic treatment if resistant disease

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82
Q

Connective tissue disease- autoimmune example

A

Systemic lupus erythematosus (SLE)
Systemic sclerosis
Primary Sjögren’s Syndrome
Dermatomyositis/Polymyositis

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83
Q

Multi-system diseases- causes

A

Infections
Auto-immune connective tissue diseases
Metabolic diseases
Endocrine diseases
Cancer

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84
Q

Inherited Connective Tissue Diseases

A

Marfan’s Syndrome
Ehler Danlos Syndrome

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85
Q

Marfan’s Syndrome

A

being tall
abnormally long and slender limbs, fingers and toes (arachnodactyly)
heart defects
lens dislocation

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86
Q

Ehlers-Danlos syndromes (EDS)

A

Joint hypermobility
stretchy skin
fragile skin that breaks or bruises easily

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87
Q

Auto-immune connective tissue diseases features

A

Inflammation leading to scarring in organs affected- can lead to organ failure
Any system can be affected
Inflammation can be treated with immunosuppressive drugs, damage is irreversible

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88
Q

Systemic Lupus Erythematosus

A

Multisystemic autoimmune disease
Autoantibodies are made against a variety of autoantigens (ANA) which form immune complexes. Inadequate clearance of immune complexes result in host immune responses which cause tissue inflammation and damage

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89
Q

Systemic Lupus Erythematosus- prevalence

A

More common in women (90% of disease)
More common in Afro-Caribbeans and Asians
4/100 000/year
Genetic association

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90
Q

Systemic Lupus Erythematosus- Pathogenesis

A

Immune complex mediated> tissue damage

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91
Q

Systemic Lupus Erythematosus- clinical features

A

Remitting and relapsing illness of variable presentation and course
Often non-specific (malaise, fatigue, myalgia and fever) or organ specific

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92
Q

Systemic Lupus Erythematosus- LE specific skin conditions

A

Malar “butterfly” rash with sparing of the nasolabial folds- acute
Annular, Psoriasiform- Subacute
Discoid rash, Scarring alopecia, Lupus profundus- chronic
Photosensitive rash

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93
Q

Systemic Lupus Erythematosus- clinical features- organ specific

A

Rashes, Inflammatory arthritis, Nephritis/ nephrosis, renal failure, pericarditis, acute MI, pleural effusion, PE, Numerous neurology, Psychosis, oral ulceration, recurrent abortions, pregnancy complications, cytopenia, abnormal clotting

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94
Q

Systemic Lupus Erythematosus- arthritis

A

Symmetrical
Less proliferative than RA
Can be deforming
Non-erosive

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95
Q

Lupus nephritis

A

Hypertension, proteinuria, renal failure

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96
Q

Systemic Lupus Erythematosus- Auto antibodies

A

Anti-nuclear antibody: Not specific for lupus (screening test)
Double stranded DNA antibody: Specific

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97
Q

Systemic Lupus Erythematosus- Haematological Features

A

Anaemia (Haemolytic, Coombs positive)
Thrombocytopenia
Neutropenia
Lymphopenia

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98
Q

Systemic Lupus Erythematosus- Investigations

A

Antinuclear antibodies (not diagnostic, sign of connective tissue disease), double-stranded (ds)DNA, Smith antigen- positive
ECG/ Chest x-ray for pts presenting with cardiopulmonary symptoms
Urinalysis- to asses renal involvement
Bloods- FBC, U+E, ESR/CRP

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99
Q

Systemic Lupus Erythematosus- Investigations- bloods

A

FBC- anaemia, leukopenia, thrombocytopenia
U+E- elevated urea and creatinine
ESR/CRP- elevated, shows non-specific inflammation, think infection

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100
Q

Systemic Lupus Erythematosus- diagnosis

A

Think SLE when multi-system disorder and ESR is raised
Anti-dsDNA antibody titres
Complement- decreased C3+C4
Skin and renal biopsies can be diagnostic

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101
Q

Systemic Lupus Erythematosus- treatment aims

A

Low disease activity and prevention of flares in all organ systems may be the aim (as full remission is rare)

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102
Q

Systemic Lupus Erythematosus- general treatment

A

High factor sun block- UV protection
Hydroxychloroquine- reduces disease activity and improves survival
Patient education

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103
Q

Systemic Lupus Erythematosus- maintenance treatment

A

NSAIDs and Hydroxychloroquine for joint pain
Topical steroids for skin flares
Steroid sparing agents
Monoclonal antibodies for high disease activity

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104
Q

Systemic Lupus Erythematosus- flare treatment

A

Mild- Hydroxychloroquine and steroid
Moderate- DMARDs or mycophenolate
Severe- Urgent high dose steroids, mycophenolate (immunosuppressive), rituximab (monoclonal antibodies)

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105
Q

Raynaud’s problem

A

decreased blood flow to the fingers
Can be primary or secondary to other diseases

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106
Q

Raynaud’s problem- secondary

A

Connective tissue disease- systemic sclerosis, mixed connective tissue, SLE
Drugs
Vascular damage- atherosclerosis, frost bite, vibrating tools

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107
Q

Systemic sclerosis (SSc)

A

Vasculopathy, excessive collagen deposition, inflammation, auto-antibody production

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108
Q

Systemic sclerosis (SSc)- features

A

Scleroderma (skin fibrosis), internal organ fibrosis and microvascular abnormalities (ie Raynaud’s phenomenon)

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109
Q

Raynaud’s- management

A

Physical protection
Vasodilators (Nifedipine, Iloprost, Sildenafil, Bosentan)
Fluoxetine
Sympathectomy- surgery

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110
Q

Systemic sclerosis (SSc)- management

A

Prevention of renal crisis- (ACEi)
Early detection of pulmonary arterial hypertension- Annual echocardiograms and pulmonary function tests
Treatment of skin oedema
Treatment of pulmonary fibrosis

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111
Q

Sjögren’s Syndrome

A

Chronic inflammatory autoimmune disease
Primary or secondary to other disease
There is lymphocytic infiltration and fibrosis of exocrine glands
More common in men in 40s/50s

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112
Q

Sjögren’s Syndrome- secondary

A

SLE
Rheumatoid arthritis
Scleroderma
Primary billiary cirrhosis
Other auto-immune diseases

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113
Q

Primary Sjogren’s Syndrome- clinical features

A

Dry eyes/mouth
Arthritis
Rash
Neurological features
Vasculitis
ILD
Renal tubular acidosis
Strong association with gluten sensitivity
Increased risk of lymphoma

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114
Q

Primary Sjogren’s Syndrome- investigations

A

Positive ANA, RF, Ro and La
Negative ds DNA
Raised Immunoglobulins
Abnormal salivary glands on ultrasound
Sialadenitis on lip biopsy

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115
Q

Sjogren’s Syndrome- treatment

A

Tear and saliva replacement
Hydroxychloroquine for fatigue, myalgia, arthralgia, rashes
Corticosteroids/immunosuppressants for organ-threatening extra-glandular disease

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116
Q

Polymyositis

A

Rare condition characterized by insidious onset of progressive symmetrical proximal muscle weakness and autoimmune-mediated straited muscle inflammation, associated with myalgia +/- arthralgia
Lungs can be affected

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117
Q

Dermatomyositis

A

Myositis + skin signs

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118
Q

Dermatomyositis- skin signs

A

Macular rash
Lilac-purple rash on eyelids often with oedema
Nailfold erythema
Gottrons papules- roughened red papules over knuckles (also elbows and knees)

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119
Q

Dermatomyositis/Polymyositis- investigations

A

Muscle enzymes (CK) elevated
Antibody screen
EMG
Muscle/skin biopsy- diagnostic
Screen for malignancy (PET-CT)- Malignancy associated antibodies
Chest X ray, PFTs, High resolution CT lungs

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120
Q

Dermatomyositis/Polymyositis- management

A

Steroids
Immunosuppressive drugs

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121
Q

Spondyloarthropathy

A

Chronic inflammation condition, tend to affect the axial skeleton without a positive rheumatoid factor, hence seronegative with overlapping clinical manifestations and association with the gene HLA-B27

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122
Q

Spondyloarthropathy- examples

A

Ankylosing spondylitis, psoriatic arthritis, enteropathic arthritis, and reactive arthritis

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123
Q

Clinical features of Spondyloarthritis

A

inflammatory arthritis of the “axial skeleton”
enthesitis
acute anterior uveitis (irits)
peripheral arthritis
skin psoriasis
May also have (sub-clinical) inflammatory bowel disease

124
Q

Other clinical features of Spondyloarthritis- SPINEACHE

A

Sausage digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAID good reponse
Enthesitis (heel)
Arthritis
Crohn’s/ Colitis/ elevated CRP*
HLA B27
Eye (uveitis)

125
Q

HLA B27

A

human leukocyte antigen
-present in 90–95% of patients with ankylosing spondylitis, 60–90% of patients with reactive arthritis, 50–60% of patients with psoriatic arthritis or inflammatory bowel disease and spondylitis

126
Q

Human leukocyte antigens

A

Proteins that help the body’s immune system tell the difference between its own cells and foreign, harmful substances

127
Q

Inflammatory arthritis of the “axial skeleton”

A

Inflammatory arthritis of the spine/ rib cage and hips, which results in new bone formation and “fusion” of the vertebrae/ costovertebral / SIJ

128
Q

Enthesitis

A

inflammation of junction between ligament/ tendon and bone

129
Q

Acute anterior uveitis (irits)

A

inflammation of the anterior chamber of the eye

130
Q

Ankylosing Spondylitis (Axial Spondyloarthritis)

A

Chronic progressive inflammatory arthritis of the spine and rib cage – eventually leading to new bone formation and fusion of the joints (bamboo spine, Syndesmophytes, Sacroiliitis)
Typically starts in late teenage years/ 20s
Affects male and females equally

131
Q

Syndesmophytes

A

new bone formation and vertical growth from anterior vertebral corners

132
Q

Sacroiliitis

A

Sclerosis, erosions, loss of joint space
Fusion

133
Q

Ankylosing spondylitis- investigations

A

pelvic x-ray shows sacroiliitis
MRI shows bone marrow oedema
Spine x rays

134
Q

Ankylosing spondylitis- investigations- pelvic x ray

A

sacroiliitis

135
Q

Ankylosing spondylitis- investigations- MRI

A

bone marrow oedema on a T2-weighted sagittal short-tau inversion recovery image

136
Q

Ankylosing spondylitis- investigations- spinal x ray

A

show erosions, squaring, sclerosis, syndesmophytes or bridging syndesmophytes in the lumbar spine, bamboo spine (late disease)

137
Q

Final stage of Ankylosing spondylitis

A

Severe kyphosis (exaggerated, forward rounding of the upper back) of thoracic and cervical spine- patient unable to look ahead walking/ see the sun

138
Q

Ankylosing spondylitis- treatment

A

Physio and NSAIDs
Biologics- Anti TNF, IL-17 blockers
Small targeted molecules: JAK inhibitors

139
Q

Psoriatic Arthritis

A

PsA occurs in around 25% of patients with psoriasis
Chronic inflammatory MSK disease associated with psoriasis. It manifests with seronegative inflammatory arthritis commonly presenting with skin and nail lesions, peripheral arthritis, dactylitis, enthesitis, and spondylitis

140
Q

Psoriatic Arthritis vs rheumatoid arthritis

A

Psoriatic Arthritis can be differentiated from rheumatoid arthritis (RA) by several clinical features
-frequent oligoarticular or monoarticular initial pattern of joint involvement
-distal interphalangeal joint involvement
-Dactylitis (inflammation of a digit) and sacroiliitis are not observed in RA

141
Q

Hidden sites for psoriasis

A

under hair, nails, belly button

142
Q

Psoriatic Arthritis mamagement

A

Similar to RA
Early intervention with DMARDs + biologics

143
Q

Reactive Arthritis (ReA)

A

Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually gastro-intestinal or genital

144
Q

Reactive Arthritis (ReA)- associated infections

A

Gut associated infections- Salmonella, Shigella, Yersinia
Sexually acquired infection (NSU)- Chlamydia, Ureaplasma urealyticum

145
Q

Reactive Arthritis- classic triad

A

Arthritis- Typically 2 days to 2 weeks post infection
Conjunctivitis
(Sterile) urethritis (inflammation of urethra)

146
Q

Reactive Arthritis- associated skin lesions

A

Keratoderma blenorrhagica, Circinate Balanitis

147
Q

Reactive Arthritis- investigations

A

ESR/ CRP- elevated
ANA/RF- negative
Urogenital/ Stool cultures- negative
Arthrocentesis with synovial fluid analysis- negative
Imaging- sacroiliitis or enthesopathy

148
Q

Reactive Arthritis- treatment acute

A

NSAID- 1st line
Corticosteroid

149
Q

Reactive Arthritis- treatment chronic

A

DMARD

150
Q

Enteropathic Arthritis

A

Episodic peripheral synovitis occurs in up to 20%
of patients with Inflammatory bowel disease
Management tailored to treat both bowels and joints

151
Q

Enteropathic Arthritis- characteristics

A

Asymmetric lower limb arthritis
Usually reflects the disease activity
Remission generally related to suppression of bowel disease.

152
Q

Osteoarthritis

A

Most common condition affecting synovial joints
Age-related, dynamic reaction pattern of a joint in response to insult or injury- all tissues of the joint are involved and changes bone at joint margins
Typically primary but can be secondary to joint disease or other conditions (obesity, haemochromatosis, occupational)

153
Q

Osteoarthritis- tissue most affected

A

Articular cartilage

154
Q

Osteoarthritis- pathogenesis

A

Metabolically active and dynamic process
Mediated by cytokines (IL-1, TNF-α, NO)
Driven by mechanical forces

155
Q

Osteoarthritis- Main pathological feature

A

Loss of cartilage
Disordered bone repair

156
Q

Osteoarthritis- RFs

A

Age, Female preponderance (post menopause), genetic factors, obesity, occupation (manual labour= small joints of hands OA, Farming and OA of hips, footballs and OA of knee), local trauma, inflammatory arthritis, abnormal biomechanics

157
Q

Osteoarthritis and increased age

A

Due to: -Cumulative effect of traumatic insult
-Decline in neuromuscular function
Of all people aged over 65:
80-90% will have radiographic evidence of OA
50% will have symptoms of OA

158
Q

Osteoarthritis and obesity

A

Linear relationship between BMI and risk of hip and knee OA- Not thought to be due to mechanical factors
Also association with OA of non-weight-bearing joints – e.g. hand joints
Obesity is a low grade inflammatory state
Release of: IL-1, TNF, Adipokines (leptin, adiponectin)

159
Q

Osteoarthritis symptoms

A

Pain- may not present despite sig changes on X rays
Functional impairment- walking, activities of daily living

160
Q

Osteoarthritis signs

A

Alteration in gait
Joint swelling
Other joint abnormalities (limited range of movement, crepitus, tenderness, deformities)

161
Q

Osteoarthritis signs- joint swelling

A

Bony enlargement
Effusion
Synovitis (if inflammatory component)

162
Q

Osteoarthritis- Radiological features

A

Joint space narrowing
Osteophyte formation
Subchondral sclerosis
Subchondral cysts
Abnormalities of bone contour

163
Q

Osteoarthritis- Radiological features- LOSS

A

Loss of joint space
Osteophyte
Subchondral sclerosis
Subchondral cysts

164
Q

Osteoarthritis- Osteophyte formation

A

Bone spurs- bony lumps that grow on the bones in the spine or around joints

165
Q

Osteoarthritis- Subchondral sclerosis

A

thickening and hardening of bone that happens underneath cartilage in a joint

166
Q

Osteoarthritis- Subchondral cysts

A

fluid-filled space inside a joint that extends from one of the bones that forms the joint

167
Q

Osteoarthritis- investigations

A

Clinical diagnosis- activity-related joint pain, morning stiffness that lasts no longer than 30 minutes, >45 years of age
X-rays only considered if diagnosis is unclear or an alternative/additional diagnosis is suspected
Bloods- inflammatory markers- normal
No antibodies found

168
Q

DIP joint

A

Distal Interphalangeal Joint- located at the tip of the finger, just before the finger nail starts

169
Q

PIP joint

A

proximal interphalangeal joint- articulation between the proximal and middle phalanx in the hand

170
Q

CMC joint

A

carpometacarpal joint- base of the thumb where it meets the hand

171
Q

OA of the hands

A

Relapsing, remitting course over a few years
‘Nodal’ form has a strong genetic component
Often ‘inflammatory’ phase for each joint
Bony swelling and cyst formation
Reduced hand function

172
Q

3 compartments of knee that OA can affect

A

Medial (commonest)
Lateral
Patellofemoral

173
Q

Knee OA

A

Any may be affected in isolation or in combination
Without significant trauma, evolution very slow
Once established, often remains stable for years

174
Q

Erosive / inflammatory OA

A

Subset of OA
Strong inflammatory component
In addition to standard management, DMARD therapy (usually milder agents) often used

175
Q

Osteoarthritis- Loose body in the knee

A

Associated with ‘locking’ of knee
Bone or cartilage fragment
The only indication for arthroscopy in osteoarthritis

176
Q

Osteoarthritis- non-medical management

A

Patient education- Activity and exercise and Weight loss
Physio/ Occupational therapy
Footwear
Orthoses- external medical device for supporting joint
Walking aids- stick/ frame

177
Q

Osteoarthritis- Pharmacological management

A

Topical- NSAIDs, Capsaicin
Oral- Paracetamol, NSAIDs (with caution), Opioids
Transdermal patches- Buprenorphine, Lignocaine
Intra-articular steroid injections- role remains unclear

178
Q

Osteoarthritis- DMARDs

A

Role in inflammatory OA

179
Q

Osteoarthritis- surgical management

A

Arthroscopy (only for loose bodies)
Osteotomy
Arthroplasty
Fusion- (Usually ankle and foot)

180
Q

Osteoarthritis- Indications for arthroplasty

A

Uncontrolled pain (particularly at night)
Significant limitation of function
Age is considered

181
Q

Fracture treatment- 4 Rs

A

Resuscitate
Reduce
Retain
Rehab

182
Q

Orthopaedic X ray- ABCs

A

Alignment - Dislocation
Bone - Fractures
Cartilage – widened joint
Soft tissues – swelling, effusion

183
Q

Bone remodelling cycle

A

1.Resting
2.Resorption
3. Formation
4.Mineralisation

184
Q

Callus formation

A

1.Bleeding
2. Soft callus
3.Bony callus
4.Remodelling

185
Q

Direct bone healing

A

Gap <1mm
Absolute stability
Compression
Gap healing
No callus

186
Q

Indirect bone healing

A

Relative stability
Callus formation

187
Q

Aim of orthopaedic treatment

A

Improve pain
Reduce disability
Improve function

188
Q

Fracture considerations

A

Intra/Extra articular
Position
Pattern
Condition
Displacement

189
Q

Fracture- Intra/Extra articular

A

Intra-articular fracture — A fracture that extends into the joint
Extra-articular fracture — A fracture that does not extend into the joint

190
Q

Fracture- pattern

A

Transverse- fracture run horizontally perpendicular to your bone
Oblique- bone is broken at an angle
Spiral- bone is broken with a twisting motion, causing fracture line that wraps around your bone and looks like a corkscrew

191
Q

Fracture- condition

A

Comminuted- broken in three or more places
Segmental- broken in at least two places, leaving a segment of your bone totally separated by the breaks
Impacted- broken ends of the bone are jammed together by the force of the injury

192
Q

Fracture- Displacement

A

Length- has the length of the bone overall shortened
Alignment -Translation- movement of fractured bones away from each other
Angulation- two ends of the broken bone are at an angle to each other
Rotation- two ends of bone not on the same plane

193
Q

Osteoporosis

A

Systemic skeletal disease characterised by low bone mass
and microarchitectural deterioration of bone tissue, with a
consequent increase in bone fragility and susceptibility to
fracture

194
Q

Osteoporosis- RFs- SHATTERED

A

Steroid use
Hyperthyroidism/ parathyroidism/ calciuria
Alcohol and tobacco use
Thin (BMI< 19)
Testosterone decrease
Early menopause
Renal or liver failure
Erosive/ imflammatory bone disease
Dietary low Ca2+/malabsorption or DM

195
Q

Osteoporosis - epidemiology

A

18% of females >50
6% of males >50
>300,000 Osteoporotic fractures in UK each year

196
Q

Pathophysiology of fracture

A

-Trauma
-Bone strength (Bone mineral density, bone size, bone quality)

197
Q

Bone mass and age

A

Peak bone mass between 15-50
Decreases gradually with age for both M+F- menopause causes bone mass to decrease massively

198
Q

Common Osteoporotic fracture

A

Hip (most common)
Vertebrae
Colles’ (more common in women)

199
Q

Colles’ fracture

A

break in the radius close to the wrist

200
Q

Factors that affect bone mineral density

A

Peak bone mass, rate of bone loss

201
Q

Factors that affect bone strength

A

Bone size

202
Q

Factors that affect bone quality

A

Bone turnover, architecture, mineralisation

203
Q

Bone remodelling cycle

A

Quiescence> Resorption > Formation > Quiescence

204
Q

Postmenopausal osteoporosis

A

-Loss of restraining effects of oestrogen on bone turnover
-Preventable by oestrogen replacement
-Characterized by high bone turnover (resorption > formation), predominantly cancellous bone loss, microarchitectural disruption

205
Q

Postmenopausal osteoporosis- pathophysiology

A

Quiescence -> increased resorption -> insufficient formation Remodelling imbalance:
net loss of bone

206
Q

Osteoporosis- Changes in trabecular architecture with ageing

A
  • Decrease in trabecular thickness, more
    pronounced for non load-bearing
    horizontal trabeculae
  • Decrease in connections between
    horizontal trabeculae
  • Decrease in trabecular strength and
    increased susceptibility to fracture
207
Q

Osteoporosis- gold standard investigation

A

dual-energy x-ray absorptiometry (DXA)- bone mineral density (BMD) measurements diagnostic for osteoporosis

208
Q

Dual-energy x-ray absorptiometry (DXA)

A

Bone mineral density (BMD) is compared with that of a gender- matched, healthy young adult average.
The T score represents no SD the BMD is from the youthful average

209
Q

Dual-energy x-ray absorptiometry (DXA)- results

A

T score >0- better than reference
T score 0 to -1- no evidence of osteoporosis
T score -1 to -2.5- Osteopenia
T score < -2.5- osteoporosis (+fracture= severe osteoporosis)

210
Q

Osteopenia

A

Bone density is lower than the average adult, but not low enough to be diagnosed as osteoporosis, risk of later osteoporosis
Offer lifestyle advice

211
Q

Osteoporosis and inflammatory disease

A

Inflammatory cytokines increase bone resorption- ie RA, seronegative arthritis, connective tissue disease, inflammatory bowel disease

212
Q

Osteoporosis and endocrine disease

A

Thyroid hormone and parathyroid hormone
increase bone turnover
Cortisol increases bone resorption and induces (Cushing’s syndrome)
osteoblast apoptosis
Oestrogen/ testosterone control bone turnover

213
Q

Osteoporosis and reduced skeletal loading

A

Reduced skeletal loading increases resorption
o Low body weight
o Immobility

214
Q

Osteoporosis and drugs

A

Can be caused by certain drugs
* Glucocorticoids
* Depo-provera
* Aromatase inhibitors
* GnRH analogues
* Androgen deprivation

215
Q

Osteoporosis- drugs aims

A

Anti-resorptive- Decrease osteoclast activity and bone turnover
Anabolic- Increase osteoblast activity and bone formation

216
Q

Osteoporosis- Anti-resorptive drugs drugs

A

o Bisphosphonates
o HRT
o Denosumab

217
Q

Osteoporosis- Anabolic drugs drugs

A

o Teriparatide
o Romosozumab

218
Q

Osteoporosis- first line treatment

A

Bisphosphonates (typically oral alendronic acid)

219
Q

Bisphosphonates known side effect

A

Have to be taken with plenty of water while standing upright for >30 mins and wait 30 before eating/ drinking
Photosensitivity, GI upset, oesophageal ulcers- stop if any dysphagia, abdo pain

220
Q

Osteoporosis- Denosumab

A
  • Rapid acting and very potent anti-resorptive
  • Good fracture risk reduction
  • Rebound increase of bone turnover when stopped
221
Q

Osteoporosis- Teriparatide

A
  • PTH analogue
    Useful for people who have suffered more fractures after previous treatment, Increased risk of renal cancer
222
Q

Osteoporosis- HRT

A

Can prevent osteoporosis in post menopausal women, risk of breast cancer is slightly increased

223
Q

How do bones grow?

A

Most grow by getting longer and wider
Modeling is dominant process during skeletal growth- Subperiosteal, Endocortical, Trabecular

224
Q

Osteogenesis imperfecta

A

Commonest primary osteoporosis
Defects related to type 1 collagen
Mostly autosomal dominant inheritance
Low bone mass
Increased bone fragility
“brittle bone disease”

225
Q

Osteomalacia

A

Normal amount of bone but its mineral content is low (there is excess uncalcified osteoid and cartilage)

226
Q

Osteomalacia vs osteoporosis

A

Osteomalacia is low mineral content and normal amount of bone
Osteoporosis is normal mineral content and overall bone loss

227
Q

Osteomalacia and rickets

A

Rickets is the result of low mineral content during the period of bone growth
Osteomalacia is the result of this process after the fusion of the epiphyses

228
Q

Rickets- signs and symptoms

A

Growth retardation, hypotonia, apthay in infants
Once walking- knovk-kneed, bow-legged + deformities of the metaphyseal-epiphyseal joint (growth plate)
Features of low Ca2+

229
Q

Osteomalacia- signs and symptoms

A

Bone pain/ tenderness, fractures (esp femoral neck), proximal myopathy (waddling gait), due to low PO4- and vit D def

230
Q

Causes of Osteomalacia

A

Vit D deficiency, renal osteodystrophy (renal failure leads to 1,25(OH)2D deficiency), drug- induced, vit D resistance, liver disease, tumour

231
Q

Vitamin D and rickets

A

Defect of mineralisation of growing bone
Failure of apoptosis of hypertrophic chondrocytes
Accumulation of un-mineralised growth plate cartilage and un-mineralised osteoid in the rest of the skeleton

232
Q

Symptomatic vitamin D deficiency

A

Bowing of legs
Aches
Hypocalcaemia
Fits
Muscle weakness
Cardiomyopathy
Enamel hypoplasia
Fractures

233
Q

Radiological Features of Rickets

A

Cupping
Splaying
Fraying
Osteopaenia
Periosteal elevation

234
Q

Treatment of rickets

A

Treat underlying cause of rickets
ie vit D supplement for diet deficiency, vit D2 for malabsorption/ hepatic disease or calcitriol for vit D resistance or renal disease

235
Q

Phosphate absorption

A

Small intestinal absorption
Not often limited in diet
Absorb 60-65% dietary content
Can be absorbed passively or actively via stimulation from 1,25OH2vitamin D

236
Q

X-linked hypophosphataemic rickets

A

Inherited- due too defect in renal phosphate handling
Rickets develop in early childhood
Plasma PO4- is low

237
Q

X-linked hypophosphataemic rickets- treatment

A

Large dose of oral phosphate and calcritiol

238
Q

Hypophosphatasia

A

inherited disorder characterized by defective bone and teeth mineralization, and deficiency of serum and bone alkaline phosphatase activity

239
Q

Generalized Arterial Calcification of Infancy (GACI)

A

rare, life-threatening inherited. Disorder Patients develop calcifications and intimal proliferation in multiple arteries, often resulting in critical illness and death in utero or early infancy

240
Q

Skeletal dysplasia

A

category of rare genetic disorders that cause abnormal development of a baby’s bones, joints, and cartilage

241
Q

Achondroplasia

A

Commonest skeletal dysplasia 1 in 15-30 thousand
Diagnosis in early infancy
80% to average stature parents
Affects fibroblast growth factor receptor

242
Q

Achondroplasia- mean adult heights in US

A

131 cm males
124 cm females

243
Q

Achondroplasia- long bones

A

Disproportionately short-limbs
Bowing of legs and other malalignment
Ligamentous laxity

244
Q

Achondroplasia- complications

A

Spinal stenosis, lower extremity misalignment, Hydrocephalus, Cervicomedullary/ spinal cord Myelopathy

245
Q

Achondroplasia- treatments

A

Treatment for complications
Monitoring- X-rays to monitor the position of the spine and lower extremities. MRI scans of the brain and spine help doctors spot development of spinal stenosis,

246
Q

What is a crystal?

A

Homogenous solid
Stable, hard, high density
Strengthen the skeleton and remove excess ions

247
Q

Crystal pathology

A

Pathological in wrong sites
-Nephrolithiasis (kidney stones)
-Crystal arthropathies (gout, pseudogout)
Local inflammatory response leading to tissue damage

248
Q

Crystal arthropathies

A

Gout
-Urate crystals
Pseudogout
-Pyrophosphate crystals

249
Q

Gout

A

Sudden onset hot swollen joint
Excruciatingly painful

250
Q

Gout typical joint involvement

A

Big toe- 76%
Ankle/foot- 50%
Knee- 32%
Finger- 25%
Elbow/Finger- 10%

251
Q

Most common joint involvement- gout

A

Big toe

252
Q

Tophaceous gout

A

uric acid crystals form tophi of white growths that develop around the joints and tissues that gout has affected.
Most severe form of gout

253
Q

Tophi

A

often visible under the skin and tend to look like swollen nodule

254
Q

Gout Epidemiology

A

Commonest arthritis in men >40yrs
Rises in post-menopausal women- often related to identifiable trigger eg diuretics
More common in males

255
Q

Normal uric acid excretion

A

Uric acid produced by nucleic acids/purine metabolism
Usually excreted by kidneys

256
Q

Purine metabolism

A

Purine> Hypoxanthine> Xanthine (catalysed by Xanthine oxidase)> Uric Acid

257
Q

Gout pathophysiology- uric acid crystal formation

A

Uric acid not fully excreted by kidneys
Converted in to monosodium urate
Excess coalesces into crystals

258
Q

Urate serum levels

A

Serum saturation = 0.3mmol/l
Urate in solution
Serum levels > 0.36mmol/l
Risk of crystal deposition
Plasma concentration >0.42mmol/l
Supersaturation; crystal deposition very likely

259
Q

RFs for excess Urate in plasma

A

Too much urate consumed (diet, conditions that cause over–production of uric acid)
Too little urate excreted (renal impairment, drugs)

260
Q

RFs for Too much urate consumed

A

Alcohol – especially beer
Fructose sweetened drinks
Excess meat, shellfish, offal
Yeast extract
Myeloproliferative disease
Psoriasis
Tumour lysis syndrome
Lesch-Nyhan syndrome

261
Q

RFs for Too little urate excreted

A

Renal impairment
Thiazide diuretics
Low dose aspirin
Tacrolimus, ciclosporin
Ethambutol, pyrazinamide

262
Q

Dietary causes of gout

A

Excess consumption of: Alcohol – especially beer
Fructose sweetened drinks
Excess meat, shellfish, offal
Yeast extract

263
Q

Drug causes of gout

A

Thiazides – increase fluid excretion so remaining fluid more concentrated, also reduce kidney’s excretion of urate
Aspirin reduces uric acid excretion
Tacrolimus, ciclosporin reduce uric acid excretion

264
Q

Lesch-Nyhan syndrome and gout

A

x-linked recessive, neurological and behavioural abnormalities and over-production of uric acid

265
Q

Gout and metabolic syndrome

A

association with metabolic syndrome, diabetes, hypertension
Extra fat, body produces more insulin, makes it harder for kidneys to get rid of uric acid

266
Q

Hypertension and gout

A

Hypertension damages glomerulus, affects renal excretion of uric acid

267
Q

Gout triggers

A

Most are spontaneous
Direct trauma to the joint
Intercurrent illness
Alcohol or shellfish binge
Surgery
Dehydration

268
Q

Gout- diagnostic investigation

A

Arthrocentesis with synovial fluid analysis
shows high WBC, strongly negative birefringent needle-shaped crystals under polarised light

269
Q

Gout-Arthrocentesis with synovial fluid analysis

A

Diagnostic- Excludes septic arthritis and differentiates gout from pseudogout
shows high WBC and monosodium urate crystal (strongly negative birefringent needle-shaped crystals under polarised light)

270
Q

Gout- acute 1st line treatment

A

NSAIDs
Colchicine- (anti-inflammatory medicine for gout)
Prednisolone- corticosteroid

271
Q

Gout- chronic- 1st line treatment

A

Allopurinol- Lower uric acid levels

272
Q

Gout- chronic- treatment

A

Allopurinol (1st line)
Febuxostat
Xanthine oxidase inhibitors
Low dose colchicine, NSAID or corticosteroid for up to 6 months to prevent paradoxical risk of flare
Education

273
Q

Gout- chronic- aim of treatment

A

Lower uric acid levels

274
Q

Gout- acute- aim of treatment

A

Inhibit phagocyte activation and acute inflammation

275
Q

Pseudogout

A

Sudden onset hot swollen joint
Knees>wrists>shoulders>ankles>elbows
Resolution in 1-3 weeks
Calcium pyrophosphate (CPP) crystals

276
Q

Pseudogout- epidemiology

A

Predominantly a disease of the elderly
Chronic arthropathy overlap with OA

277
Q

Pseudogout- crystal type

A

Calcium pyrophosphate (CPP) crystals

278
Q

Pseudogout- diagnostic treatment

A

arthrocentesis with synovial fluid analysis
-positively birefringent rhomboid-shaped crystals under polarised light

279
Q

Pseudogout- arthrocentesis with synovial fluid analysis

A

Positively birefringent rhomboid-shaped crystals under polarised light

280
Q

Pseudogout RFs

A

Haemochromatosis
Hyperparathyroidism
Hypophosphatasia
Hypomagnesaemia
Hypothyroidism
Acromegaly

281
Q

Pseudogout- acute treatment

A

NSAIDs
Colchicine- (anti-inflammatory medicine for gout)
Prednisolone- corticosteroid

282
Q

Pseudogout- chronic treatment

A

LT low dose Prednisolone
LT low dose colchicine

283
Q

Typical gout presentation

A

acute with hot swollen joint(s)
Chronic with joint/tissue damage

284
Q

Crystal deposition in joints can trigger

A

acute inflammation
long term damage

285
Q

Vasculitis

A

inflammation of a blood vessel, which is characterised by the presence of an inflammatory infiltrate and destruction of the vessel wall

286
Q

Systemic Vasculitis

A

autoimmune disorders characterised by inflammation of blood vessels

287
Q

Giant cell arteritis

A

Granulomatous vasculitis of large and medium-sized arteries
It primarily affects branches of the external carotid artery
Common form of vasculitis in people aged 50 years or older

288
Q

Giant cell arteritis- key signs and symptoms

A

Presence of a new headache in someone with tenderness of the scalp, aching + stiffness, extremity claudication, jaw and tongue claudication
Partial/complete loss of vision (painless) in one or both eyes in up to 20% of patients

289
Q

Granulomatosis with polyangiitis

A

Systemic vasculitis that typically involves small and medium vessels.
Classic triad of upper and lower respiratory tract involvement and pauci-immune glomerulonephritis

290
Q

Granulomatosis with polyangiitis- key signs and symptoms

A

Upper + lower respiratory tract involvement, renal involvement
Common constitutional effects include fatigue, malaise, fever, night sweats, anorexia, and weight loss

291
Q

Antineutrophil cytoplasmic antibodies (ANCA) testing

A

attack healthy neutrophils. This can lead to a disorder called autoimmune vasculitis
strongly correlated with certain forms of vasculitis (like granulomatosis with polyangiitis)

292
Q

List key indications for antineutrophil cytoplasmic antibodies (ANCA) testing

A

Signs of inflammatory bowel syndrome
Signs of vasculitis

293
Q

Systemic vasculitis- investigations

A

Anti-neutrophil cytoplasmic auto-antibodies (ANCA)- positive, not diagnostic
Biopsy of affected tissue- may be misleading due to sampling error or immunosuppressive therapy

294
Q

Giant cell arteritis- diagnostic investigations

A

Vascular ultrasonography and/or a temporal artery biopsy

295
Q

Giant cell arteritis- treatment

A

Start treatment with a high-dose glucocorticoid immediately, even while awaiting confirmation of the diagnosis

296
Q

Granulomatosis with polyangiitis- treatment

A

Remission induction- high-dose corticosteroid
Remission maintenance- corticosteroids and immunomodulatory therapy

297
Q

Overview of treatment for systemic vasculitis

A

Dependent on specific diagnosis and on the severity of the clinical manifestations

298
Q

Complications of systemic vasculitis

A

Organ damage, blood clots and aneurysms, vision loss, infections

299
Q

Polymyalgia rheumatica

A

inflammatory rheumatologic syndrome that manifests as pain and morning stiffness involving the neck, shoulder girdle, and/or pelvic girdle in individuals older than age 50 years
Treat with 24 to 72 hours with low-dose prednisolone

300
Q

Polymyalgia rheumatica and giant cell arteritis

A

About 15% to 20% of patients with PMR have giant cell arteritis (GCA); 40% to 60% of GCA patients have PMR.

301
Q

Fibromyalgia

A

syndrome characterised by widespread pain in the body present for at least 3 months and is thought to be related to amplified pain signals in the spinal cord and brain
Aetiology is unknown

302
Q

Fibromyalgia- clinical diagnosis

A

No x-ray/lab test- diagnosis is strictly clinical based on clinical criteria- presence of chronic (>3 months), widespread body pain and associated symptoms such as fatigue and sleep disturbance

303
Q

Fibromyalgia treatment

A

Non-pharmacological therapies are the cornerstone to the management of fibromyalgia- patient education, self-management, physical activity, physio, Psychological interventions

304
Q

Polyarteritis nodosa

A

Necrotising inflammation of medium-sized or small arteries without glomerulonephritis or vasculitis in arterioles, capillaries, or venules

305
Q

Polyarteritis nodosa and Hepatitis B virus

A

Very rare since immunisation program
Short course of high-dose corticosteroids, followed by a combination of antiviral therapy and plasma exchange

306
Q

Non-HBV-related Polyarteritis nodosa treatment

A

Immunosuppression is the mainstay of treatment

307
Q

Paget’s disease of bone

A

chronic bone disorder that is characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone
This unbalanced process may lead to osseous deformities, altered joint biomechanics, nerve compressions, and pathological fracture

Phase 2a Lecture Notes (14 decks)

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