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Emily Phase 2a > Musculoskeletal & Rheumatology > Flashcards

Musculoskeletal & Rheumatology Flashcards

1
Q

What are the features of inflammatory pain?

A

Inflammatory :
- pain eases with use
- stiffness, >30 mins in morning
- swelling, synovial +/- bony
- hot + red
- young
- joint distributions = hangs and feets
- responds to NSAIDs

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2
Q

What are the features of degenerative pain?

A
  • pain increases with use
  • stiffness, not prolonged
  • swelling, none, bony
  • not clinically inflamed
  • older people
  • joint distribution = 1st CMC J, DIP J, knees
  • less convincing response to NSAIDs
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3
Q

What are the patterns of bone pain?

A

pain at rest and night
- tumour, infection, fracture

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4
Q

What are the patterns of pain in inflammatory joint pain?

A

Pain and stiffness in joints in the morning, at rest and with us

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5
Q

What are the patterns of pain in osteoarthritits?

A

pain on use,
at end of day

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6
Q

What are the patterns of pain in neuralgic?

A

Pain + paraesthesia in dermatomal distribution worsened by specific activity

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7
Q

What are the patterns of pain in referred pain?

A

Pain unaffected by local movement

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8
Q

Define osteomyelitis.

A

Bone - marrow - inflammation
- infection localized to bone

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9
Q

What is the epidemiology of osteomyelitis?

A
  • increasing incidence of chronic osteomyelitis
  • bimodal age distribution

young = haematogenous osteomyelitis
older = diabetes, peripheral vascular disease

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10
Q

What are the 3 pathways in osteomyelitis of pathogens infecting the bones?

A

bacteria gets into the bone by:
1) direct innoculation into the bone = wound, trauma, surgery
2) continugous spread of infection to bone = spreads to adjacent soft tissue and joints, older adults, DM
3) Haematogenous seeding = pathogen in one part of the bone carried via blood to another weal part, children, mono-microbial

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11
Q

What host factors are risk factors for osteomyelitis?

A

Behavioral factors
i.e. risk of trauma

Vascular supply
Arterial disease
Diabetes mellitus
Sickle cell disease

Pre-existing bone / joint problem
Inflammatory arthritis
Prosthetic material inc arthroplasty

Immune deficiency
Immunosuppressive drugs
Primary immunodeficiency

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12
Q

What bones are most likely affected in Osteomyelitis?

A

Adults = vertebra - clavicle, pelvis
Children = long bones

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13
Q

Why in adults is osteomyelitis more likely to affect vertebra?

A

With age the vertebrae become more vascular, making bacterial seeding of the vertebral endplate more likely

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14
Q

Why are long bones in children more likely to be affected in osteomyelitis?

A

In metaphysis
- blood flow is slower
- endothelial basement membranes are absent
- The capillaries lack or have inactive phagocytic lining cells
- High blood flow in developing bones in children

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15
Q

Which other groups of people have a higher risk of getting osteomyelitis?

A
  1. People who inject drugs (PWD / IVDU)
    younger, more often clavicle and pelvis
  2. People with risk factors for bacteremia
    central lines, on dialysis
    sickle cell disease,
    urinary tract infection, urethral catheterization
    Similar factors as those for infective endocarditis
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16
Q

What are steps of the pathogenesis of osteomyelitis?

A
  1. inflammatory exudate in the marrow
  2. increased intramedullary pressure
  3. extension of exudate into the bone cortex
  4. rupture through the periosteum
  5. interruption of periosteal blood supply causing necrosis
  6. leaves pieces of separated dead bone
  7. new bone forms here
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17
Q

What is the acute phase of osteomyelitis?

A

Bacteria reach the bone and start to proliferate. This alerts immune cells and they try and fight off the infection.
The immune cells release chemicals that cause local bone destruction and usually this is effective

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18
Q

What is chronic osteomyelitis?

A

If the lesion is not that extensive, and there’s viable bone the osteoblasts and the osteoclasts begin to repair the damage over a period of weeks.

However, in some cases, the process turns into a chronic osteomyelitis - lasting months to years.

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19
Q

What are the signs of osteomyelitis?

A

Systemic:
Fever, rigors, sweats, malaise

Local:
tenderness, warmth, erythema, and swelling
PLUS any of
draining sinus tract
deep / large ulcers that fail to heal despite several weeks treatment*
non-healing fractures

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20
Q

What are the symptoms of osteomyelitis?

A

Onset - several days.
dull pain at site of OM
- may be aggravated by movement.
fever
erythema
muscle aches

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21
Q

What are the investigations for osteomyelitis?

A

Laboratory tests:
Acute = high WCC
Chronic = can have normal WCC
Raised inflammatory markers = CRP but can be normal

Imaging:
plain radiographs
MRI
CT (alternative to MRI)
Nuclear Bone scan if metalwork makes CT/MRI impossible

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22
Q

What is the gold standard test for osteomyelitis?

A

MRI- will show bone marrow oedema and abscesses

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23
Q

When can you use an X-ray as an investigation osteomyelitis?

A

in chronic osteomyelitis

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24
Q

What can be identified in an MRI for osteomyelitis?

A
  • bone marrow oedema from 3-5 days
  • Delineates cortical, bone marrow and soft tissue inflammation
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25
Q

What are the diagnosis differentials in OM?

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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26
Q

What is the treatment for osteomyelitis?

A
  1. 6 weeks of flucloxacillin, possibly with rifampicin or fusidic acid added for the first 2 weeks
  2. Clindamycin if penicillin allergy
  3. Vancomycin in MRSA

Chronic requires 3 months of antibiotics

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27
Q

What are the more radical treatments for osteomyelitis?

A
  1. Surgical
    Debridement
    Hardware placement or removal
  2. Antimicrobial therapy
    Initial broad spectrum empirical therapy “start SMART”
    - S. aureus or MRSA?
    - gram-negative organisms?
    - Special population: IVDU/HbSS?
    Tailored to culture and sensitivity findings -
    - “then FOCUS”.
    Bone penetration of drug
    Prolonged duration
    - unreliable antibiotic penetration into bone if vascular disease
    - shorter duration possible if all infected bone resected
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28
Q

What are the features and managment of TB osteomyelitis?

A
  • May be slower onset
  • Systemic symptoms
  • Epidemiology is different from pyogenic OM
  • Blood Culture less useful
  • Biopsy essential:
    prolonged mycobacterial culture
    Caseating Granolumata on histology
    Induced sputum may help (sometimes occult pulmonary TB)
  • Longer treatment 6 months (oral instead of IV)
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29
Q

What are the usual microrganisms that cause OM?

A

Staphylococcus aureus,

coagulase-negative staphylococci,
aerobic gram-negative bacilli (30%)

Others:
Streptococci (skin, oral)
Enterococci (bladder, bowel)
Anaerobes (bowel)
fungi,
Mycobacterium tuberculosis

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30
Q

What acute and chronic changes occur in the histopathology of OM?

A

Acute changes:
Inflammatory cells
Oedema
Vascular congestion
Small vessel thrombosis

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

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31
Q

What are the clinical features for OM in hip, vertebra or pelvis?

A

pain but few other signs

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32
Q

What are the clinical features for OM in Vertebral: lumbar > thoracic > cervical?

A
  • Posterior extension - epidural and subdural abscesses or even meningitis.
  • Extension anteriorly or laterally can lead to paravertebral, retropharyngeal, mediastinal, subphrenic, retroperitoneal, or psoas abscesses
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33
Q

What are the clinical features for OM in joints?

A

(can also present as septic arthritis.)

when infection breaks through cortex resulting in discharge of pus into the joint (knee, hip, and shoulder).

More common in infants due to patent transphyseal blood vessels and immature growth plate

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34
Q

What are the complications of osteomyelitis?

A

Septic arthritis - if infection spreads to joints

Growth disturbance in children and adolescents

Amputations

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35
Q

What is the most common microorganism to cause joint infection?

A

staphylococcus aureus

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36
Q

What happens to prednisolone dose on being admitted into hospital with an infected joint?

A

double the dose

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37
Q

What is septic arthritis?

A

An infection of 1 or more joints caused by pathogenic inoculation of microbes.

(infection within a joint)

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38
Q

What is the epidemiology of septic arthirits?

A
  • 2-8 cases in 100,000
    more common in Rheumatoid arthritis
    M =F
    prosthetic joint infection > native joint infection
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39
Q

What is gonoccocal arthiritis?

A
  • joint inflammation occurs within disseminated gonococcal infection
  • affects multiple joints = polyarticular compared to septic
  • maculopapular = pustular rash
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40
Q

What are the risk factors for a septic joint?

A

Any cause for bacteraemia
Direct/ penetrating trauma
Local skin breaks/ ulcers
Damaged joints/ undelrying joint disease
IV drug user
prosthetic joint

Immunosuppression (including steroids only)
Elderly
Rheumatoid arthritis (or other immune-driven disease)
Diabetes

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41
Q

What are the typical clinical presentations of septic joints?

A

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

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42
Q

What is the most important investigation in septic joints?

A

Aspirate and send fluid for culture

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43
Q

What are the first line investigations for septic arthritis?

A

FBC
Elevated CRP and ESR
Blood cultures
Plain x-ray

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44
Q

What is a the most common location of septic arthritis?

A

Knee
- normally only one joint is affected

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45
Q

What is the scoring criteria used for septic arthritis?

A

Kocher criteria a score of 2 suggests 40% likelihood and score of 3 suggest 93%

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46
Q

What is the treatment for septic arthritis?

A

Empirical therapy = flucloxacillin plus rifampicin is first-line

Penicillin allergy = clindamycin

Suspected or confirmed MRSA = vancomycin

Gonococcal arthritis or gram-negative infection = cefotaxime or ceftriaxone

Continue for 3-6 weeks

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47
Q

What is the prognosis for septic arthritis?

A

Mortality from septic arthritis ranges from 10 to 20% with treatment,

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48
Q

What are the pathways of infection for a prosthetic joint?

A

Local = been there since surgery, symptoms occur quickly
Haematogenous spread = takes longer to present

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49
Q

What is the gold standard investigation for prosthetic joint diagnosis?

A

Aspiration
- identifies organisms
- must be done with patient off antibiotics for at least 2 weeks

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50
Q

What are the aims of prosthetic joint infection treatment?

A
  • eradicate sepsis
  • relieve pain
  • restore function
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51
Q

What is the treatment for prosthetic joint infection?

A
  1. Antibiotic suppression = will NOT eliminate sepsis
  2. Debridement and retention of prosthesis = for acute infections
  3. Excision arthroplasty = cutting tissue away within the joint to allow it to move again
  4. One stage exchange arthroplasty = remove + add in new prothesis in same surgery
  5. Two stage exchange arthroplasty = remove and wait to do reconstruction
  6. Amputation
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52
Q

What is the most likely causative microorganism for upper limb joint inflammation?

A

Propionibacteria
- 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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53
Q

What causes joint inflammation?

A
  1. Inflammatory arthritis:
    Rheumatoid arthritis
    Seronegative spondyloarthritis
    - Psoriatic
    - Ank Spond
    - Reactive Arthritis
    - Enteropathic – Crohns and Ulcerative Colitis related
    Crystal arthrits – gout and pseudogout
  2. septic arthritis
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54
Q

What is the epidemiology of RA?

A
  • F>M
  • smokers
  • middle aged
  • family history
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55
Q

What are the key features of RA?

A

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

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56
Q

What are the key features of seronegative/inflammatory arthritis?

A
  • Asymmetrical big joints, with spinal involvement
  • More common in men
  • Associated symptoms = Inflammatory bowel, or GI infection, eye inflammation and psoriasis
  • Nail involvement predicts arthritis in patients with psoriasis
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57
Q

What are the key features of psoriatic arthritis?

A

RA like
Distal interphalangeal involvement (OA more common)
Mutilans - rare
Dactylitis – sausage digit / toe
Asymetrical large joints + spine

CRP may not be significantly raised

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58
Q

What is psoriatic Arthritis?

A

An inflammatory arthritis associated with psoriasis. Can vary in severity from mild stiffening and soreness in the joint or the joint can be completely destroyed arthritis mutilans

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59
Q

What % of people with psoriasis will develop psoriatic Arthritis?

A

10-20% and it usually occurs within 10 years of developing the skin change

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60
Q

What is the pathophysiology of psoriatic Arthritis?

A

It has a strong genetic component and although not fully understood the activation of CD8+ T cells is thought to play a crucial role

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61
Q

What are the signs of psoriatic Arthritis?

A

Joint tenderness and warmth
Dactylitis: swelling of the whole digit (sausage fingers)
Enthesitis: Inflammation of the tendons
Plaques of psoriasis on the skin
Pitting of the nails
Onycholysis (separation of the nail from the nail bed)

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62
Q

What are some other complications of psoriatic Arthritis?

A

Eye disease
Aortitis
Amyloidosis

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63
Q

What are the different patterns in which psoriatic Arthritis can present?

A

not a single pattern of affected joints like osteoarthritis or rheumatoid:

Symmetrical polyarthritis presents similarly to rheumatoid arthritis and is more common in women. The hands, wrists, ankles and DIP joints are affected.

Asymmetrical pauciarthritis affecting mainly the digits (fingers and toes) and feet. Pauciarthritis describes when the arthritis only affects a few joints.

Spondylitic pattern is more common in men.

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64
Q

What is used to screen patients who have psoriasis for arthritis?

A

PEST screening tool
Patients are asked about: joint pain, swelling, nail pitting

Can also use the CASPAR criteria

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65
Q

What are some x-ray changes seen in psoriatic Arthritis?

A
  1. Periostitis- thickened and irregular outline of the bone
  2. Ankylosis- where bones are joined together
  3. Pencil-in-cup appearance- the classic x-ray change to the digits is the “pencil-in-cup appearance”.
    - central erosions of the bone beside the joints
    - appearance of one bone in the joint being hollow and looking like a cup whilst the other is narrow and sits in the cup.
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66
Q

What are the key features of the 2 types of crystal arthritis?

A

Typically acute intermittent episodes joint inflammation

  1. Gout (6x more common in men = MC type)
    feet, ankles, knees, elbows, hands
    Hyperuricaemia
    Risks – beer, renal impairment, diuretics, aspirin, FH (affect how kidney deals with uric acid)
  2. Pseudogout – 3 x more common in women
    calcium pyrophosphate crystals deposits
    wrists, knees, hands
    Typically on background of OA
    Chondrocalcinosis on xray
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67
Q

What are the key features of ostesoarthritis?

A

NOT INFLAMMATORY (would be sudden onset)

Usually slow onset – months to years
Typically weight bearing joints DIPs, PIPs, thumb bases, big toes
Minimal early morning stiffness (gelling)
No variability to joint swelling
Normal CRP
Clear changes on xray

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68
Q

What are the differences between inflammatory and osteoarthritis?

A

Inflammatory
- happen at any age
- rapid onset
- symmetrical
- small joints of hand and feet
- stiffness worse in mornings
- fatigue, fever, night sweats

Osteoarthritis:
- later in life
- slow onset, years
- initially asymmetrical, polyarthritis
- weight bearing joints
- stiffness <1 hour + worse at end of day

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69
Q

What is gout?

A

A type of crystal arthritis which is associated with chronically high levels of uric acid. Urate crystals are deposited in the joint causing it to become hot swollen and painful

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70
Q

What happens to uric acid levels in Gout in an acute flare up?

A

Normal
- as the uric acid is in the joints not the blood
- if measured when not having a flareup then the uric acid levels would be high

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71
Q

What is the pathophysiology of Gout?

A
  1. Uric acid formed as a breakdown product of purines
  2. uric acid has a limited solubility in the blood and when there is too much uric acid it can become a urate ion and bind to sodium
  3. this forms urate crystals which deposit in areas with slow blood flow the joints and kidney tubules
  4. The immunological reaction initiated to try and remove them, leads to acute pain and swelling

( Only ‘Curable’ form of inflammatory arthritis)

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72
Q

What causes an increase of uric acid intake?

A
  • beer
  • diet = red meat, shellfish, offal, purine rich
  • sweetened soft drinks (fructose shares renal uric acid transporter)
  • conditions leading to increased cell turnover (haematological malignancy + psoriasis)
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73
Q

Why does alcohol increase risk of gout?

A

Beer / lager / stout equally bad
All rich in guanosine and then converted into uric acid
Small increased risk with spirits
No increased risk with wine

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74
Q

What will affect the output of uric acid?

A
  • Renal impairment (any cause)
  • Drugs:
    Low dose aspirin reduces renal clearance by 10%
    Diuretics – worse with higher dose
    Cyclosporin, TB drugs, theophyllines

Genetics – affects renal clearance of uric acid
Fructose – shares renal uric acid transporter

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75
Q

How will Gout first present?

A

Sudden acute swollen big toe

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76
Q

Risk factors for Gout?

A

Renal impairment
Beer
Diuretics
Aspirin
Family History
Fructose

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77
Q

What joints are typically affected in acute gout?

A

1st MTPJ 90%
Midfoot, ankle, knee, wrist, elbow hand
Periarticular involvement - Olecranon bursitis
Systemic features can occur

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78
Q

What are the investigations for Gout?

A

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

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79
Q

What are the 4 clinical phases if Gout is untreated?

A

 asymptomatic hyperuricemia,
 acute/recurrent gout,
 intercritical gout,
 chronic tophaceous (uric acid deposits in the skin) gout

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80
Q

What are the x-ray signs of gout?

A

Joint space maintained
Lytic lesions
Punched out erosions
Sclerotic borders with overhanging edges

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81
Q

What is the treatment for acute Gout?

A
  1. NSAID (short course) - unless Renal failure, Peptic Ulcer Disease, Some pts with asthma
  2. Colchicine - 500ug 2-3 times daily
  3. Corticosteroids - Intra-articular, Oral - low dose (5-10mg short course)

Other analgesics don’t work!! (as don’t deal with inflammation)

  1. advice about lifestyle
  2. ensure patient knows to return if further attacks
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82
Q

What is the indication and treatment for long term Gout?

A

Indication:
1. Recurrent attacks
2. Evidence of tophi or chronic gouty arthritis
3. Associated renal disease
4. Normal serum Uric acid cannot be achieved by life-style modifications

Medication:
1. Allopurinol – Xanthine Oxidase Inhibitor
2. Febuxostat – more potent Xanthine Oxidase Inhibitor
3. Benzbromarone / Probencid – if allergic / intollerant

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83
Q

What is the aim of gout treatment?

A

Aim of chronic gout management is to reduce Uric acid below <300 umol/l

  • Start at 100mg allopurinol and increase every 2-4 weeks until target met.
  • Engage patient in this – more likely to comply and make lifestyle modification
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84
Q

What is used to prevent gout?

A

Lifestyle management and a Xanthine oxidase inhibitor

First-line Allopurinol
Second-line Febuxostat

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85
Q

What are the complications of Gout?

A

Disability and misery
Tophi (punched out erosions)
Renal disease:
Calculi 10 -15%
Chronic urate nephropathy
Acute urate nephropathy (cytotoxics)

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86
Q

What is pseudogout?

A

Is a form of inflammatory arthritis caused by the deposition of calcium pyrophosphate crystals in the synovium

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87
Q

What are risk factors of pseudogout?

A

Hyperparathyroidism
Hemochromatosis
Hypomagnesaemia
Hypophosphatemia
Wilson’s disease
Acromegaly

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88
Q

Describe the pathophysiology of pseudogout?

A

Deposition of calcium pyrophosphate triggers synovitis with the knee, shoulder and wrist most commonly being affected

Can be acute or chronic

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89
Q

What will joint aspiration for pseudogout show?

A

No bacterial growth
Calcium pyrophosphate crystals
Rhomboid shaped needles
Positive birefringent of polarised light

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90
Q

What would an x-ray of pseudogout show?

A

Chondrocalcinosis is the classic x-ray change in pseudogout. It appears as a thin white line in the middle of the joint space caused by the calcium deposition. This is pathognomonic (diagnostic) of pseudogout.

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91
Q

At what point is an X-ray useful for investigating RA?

A

only 6 months after onset would you see an abnormal X-ray

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92
Q

What is the prognosis of RA?

A

if treated within ‘window of opportunity’ can control disease and prevent damage

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93
Q

What is the clinical presentation of RA?

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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94
Q

What are some signs of rheumatoid arthritis?

A
  • Z shaped deformity to the thumb
  • Swan neck deformity
  • Boutonnieres deformity- due to a tear in the central slip of the extensor components of the finger. This means when they try to straighten their finger it cause it to bend and flex
  • Ulnar deviation of the fingers at the knuckles
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95
Q

What are some extra-articular manifestations of rheumatoid arthritis?

A

Pulmonary fibrosis
Anaemia
Cardiovascular disease - pericardial effusion
Amyloidosis
Bronchiolitis obliterans (inflammation causing small airway destruction**
Felty’s syndrome (RA, neutropenia and splenomegaly)
Sjogren’s syndrome
Subcutaneous nodules
Peripheral sensory neuropathy
Episcleritis (redness + pain of sclera)

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96
Q

What is found in a physical examination of RA?

A
  • struggle to form a fist
  • doesn’t involved DIP joint
  • symmetrical
  • deformity unusual at presentation
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97
Q

What are the investigations for RA?

A

CRP (+/- ESR) raised

Rheumatoid Factor
- Falsely positive in 10-15% population
- 70% of patients with RA are positive

Anti-CCP (cyclic citrullinated peptide)
- Almost never falsely positive
- 70% of patients with RA are positive
- Selects the subset of patients with most aggressive disease

Joint X-rays

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98
Q

What is the main aim of treatment of RA?

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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99
Q

What is the diagnostic criteria for rheumatoid arthritis?

A

Comes from the American college of rheumatology
1. The joints involved (more and smaller joints score higher)
2. Serology
3. Inflammatory markers
4. Duration of symptoms longer or less than 6 weeks

Score is added up and a score of greater than 6 indicates rheumatoid arthritis

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100
Q

Who is considered to have the worst prognosis with rheumatoid arthritis?

A

younger onset
Male
Presence of RF and anti-CCG

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101
Q

What is treatment of RA?

A
  1. DMARD treatment = methotrexate, sulphasalazine, leflunomide, hydroxychloroquine
  2. referral to physio, OT
  3. escalate to biologic treatment if resistant disease e.g. anti-TNF, rituximab, JAK inhibitors
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102
Q

What is the first-lie monotherapy for rheumatoid arthritis?

A

Any one of methotrexate, leflunomide or sulfasalazine

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103
Q

What second line therapy for rheumatoid arthritis?

A

Two of methotrexate, leflunomide or sulfasalazine

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104
Q

What is third line treatment for rheumatoid arthritis?

A

Methotrexate plus a TNF inhibitor e.g., infliximab

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105
Q

What is fourth line treatment for rheumatoid arthritis?

A

Methotrexate plus rituximab (monoclonal antibody)

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106
Q

What is the mechanism of action for Methotrexate?

A

(DMARD)
- competitively inhibits dihydrofolate reductase > inhibits folate synthesis
- 100,000 times greater affinity than dihydrofolate

(Must give 5mg of Folic Acid ONCE weekly not on the same day as Methotrexate)

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107
Q

What is used to monitor rheumatoid arthritis?

A

CRP levels and DAS28

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108
Q

What is the leading cause of death in rheumatoid arthritis?

A

Accelerated atherosclerosis leading to cardiovascular disease

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109
Q

Describe the pathophysiology of rheumatoid arthritis

A
  1. Environmental triggers cause modification of self-antigens e.g., arginine is converted to citrulline in type 2 collagen.
  2. Due to susceptibility due to genes the immune cells cannot differentiate between self and non-self antigen.
  3. This causes an inflammatory response and cytokines Interferon gamma, IL-17, TNF, Il-1 and IL6 are secreted
  4. This creates a pannus (thick synovial membrane). This damages the cartilage, soft tissue and bones. The cytokines can also escape and affect multiple organ systems
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110
Q

What are two autoantibodies that are found in rheumatoid arthritis?

A
  1. Rheumatoid factor =
    - 70% of patients with rheumatoid arthritis.
    - It targets the Fc portion of the IgG antibody.
    - This causes activation of the immune system against own IgG antibodies.
    - RF is mainly IgM antibodies
  2. Cyclic citrullinated peptide antibodies (anti-CCP antibodies) =
    - target citrullinated proteins.
    - This forms immune complexes which can accumulate and activate the complement system.
    - Often found before development of rheumatoid arthritis
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111
Q

What is the typical presentation of rheumatoid arthritis?

A

Symmetrical polyarthritis: (on both sides of body)

Pain, swelling and stiffness in the small joints of the hands and feet. The onset can be rapid or over months to years

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112
Q

What type of joint problems are NSAIDs most useful for?

A

usually helpful for most inflammatory causes of pain

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113
Q

What type of joint problems are colchicine most useful for?

A

crystal arthritis

114
Q

What are the 2 types of connective tissue disease?

A
  1. inherited
    - Marfans’ syndrome
    - Ehler Danlos syndrome (super stretchy skin + hypermobile joints)
  2. autoimmune
    - SLE
    - Sjogren’s syndrome
    - systemic sclerosis
    - dermatomyositis
115
Q

What are the features of auto-immune connective tissue diseases?

A

Pathology: inflammation leading to scarring in organs affected
- can lead to organ failure
- any system can be affected

116
Q

Epidemiology of SLE?

A

Afro-Carribean and Asian
Women (14-64 years)
Genetic association: HLA DR2/DR3, C4 A null allele (low C4)

117
Q

What is systemic lupus erythematosus?

A

Is a chronic systemic autoimmune condition (type III hypersensitivity) due to a complex interplay between genetic and environmental factors.

It often takes a relapsing-remitting course. This results in chronic inflammation

118
Q

Why is SLE got the word erythematosus in it.

A

It refers to the typical red malar rash that occurs across the face.
It is more common in women and Asians

119
Q

What are the leading causes of death in SLE?

A

Cardiovascular disease
Infections

120
Q

What are some environmental triggers of SLE?

A

UV light
Smoking
EBV
Sex hormones

121
Q

Describe the pathophysiology of SLE?

A
  1. Environmental triggers e.g., UV light causes cell death. Due to genetic factors there is reduced clearance of these cellular debris
  2. genetics - play a further role as the immune system of these patients do not recognise the cellular debris as self so they attack them forming antibody-antigen complexes which get deposited in different tissues activating the complement pathway (type III hypersensitivity)
122
Q

What are the antibodies found in SLE called?

A

Anti-nuclear antibodies

123
Q

What are the symptoms of SLE

A

Fatigue
Weight loss
Joint and muscle pain
Fever
Photosensitive malar rash. Get’s worse with sunlight and is butterfly shaped across the cheeks
Hair loss
Mouth ulcers
Shortness of breath

124
Q

What are some investigations for SLE?

A

Antibodies
FBC will show anaemia of chronic disease
C3 and C4 levels will be low
Increased CRP and ESR
Renal biopsy to asses for lupus nephritis

125
Q

What are the two main antibodies to screen for in SLE?

A
  1. Anti-nuclear antibodies (ANA):
    - 85% positive
    - The initial step in testing for SLE.
    - Antinuclear antibodies can be positive in healthy patients and with other conditions (e.g. hepatitis).
  2. Anti-double stranded DNA (anti-dsDNA):
    - is specific to SLE, meaning patients without the condition are very unlikely to have these antibodies.
    - 70% of patients
126
Q

What are some complications of SLE?

A

CVD
Infections
Pericarditis
Lupus nephritis
Recurrent miscarriage

127
Q

What is the treatment for SLE?

A

NSAIDs
Steroids (prednisolone)
Anti-malarials = Hydroxychloroquine first line for mild
Topical = Sun cream for malar rash

128
Q

What are some biological therapies for SLE?

A

Rituximab = targets B cells
Belimumab = targets B-cell activating factor

129
Q

What is Raynaud’s phenomenon?

A
  • blood vessels go into a temporary spasm
  • block blood flow
  • affected area goes to white, then blue and then red as the bloodflow returns
130
Q

What is systemic sclerosis?

A

An autoimmune inflammatory and fibrotic connective tissue disease. It affects the skin in all areas and also the internal organs

131
Q

What are the two main patterns of disease in systemic sclerosis?

A
  1. Limited cutaneous systemic sclerosis
  2. Diffuse cutaneous systemic sclerosis
132
Q

What is Limited cutaneous systemic sclerosis?

A

Used to be called CREST syndrome. (sleroderma)

C- calcinosis
R- Raynaud’s phenomenon
E- oEsophageal dysmotility
S- Sclerodactyly (tightening of skin)
T- Telangiectasia (spider veins)

133
Q

What is diffuse cutaneous systemic sclerosis?

A

Includes the CREST symptoms but also has systemic features

Cardiovascular e.g., CAD and hypertension-
Lung problems e.g., pulmonary hypertension and fibrosis
Kidney problems causes glomerulonephritis and a condition called scleroderma renal crisis

134
Q

What is Telangiectasia?

A

Telangiectasia are dilated small blood vessels in the skin. They are tiny veins that have dilated. They have a fine, thready appearance.

135
Q

What is Oesophageal dysmotility?

A

Oesophageal dysmotility is caused by connective tissue dysfunction in the oesophagus. This is commonly associated with swallowing difficulties, acid reflux and oesophagitis

136
Q

What is Scleroderma renal crisis?

A

An acute condition where there is a combination of severe hypertension and renal failure.

137
Q

What are the antibodies associated with systemic sclerosis?

A
  1. Antinuclear antibodies (ANA) = positive in most
  2. Anti-centromere antibodies = most associated with limited cutaneous systemic sclerosis.
  3. Anti-Scl-70 antibodies = most associated with diffuse cutaneous systemic sclerosis. They are associated with more severe disease.
138
Q

What test would you perform on someone with Raynaud’s to check for systemic scleropathy?

A

Nailfold capillaroscopy- examines the health of the peripheral capillaries.
micro-haemorrhages indicate systemic sclerosis

139
Q

What is used to treat Raynaud’s phenomenon?

A

Nifedipine

140
Q

What are the features of Dermatomyositis/polymyositis?

A

muscle and skin affected - rash + muscle weakness
- no cure but treatment to reduce symptoms

141
Q

What are the different types of vasculitis?

A

Giant cell arteritis = large vessel

Polyarteritis nodosa = medium vessel

ANCA associated vasculitis (includes granlomatosis + eosinophilic granulomatosis w/ polyangitis) = small vessels

142
Q

What is the pathophysiology of vasculitis?

A
  1. Primary (idiopathic autoimmune) or secondary (drugs, infection) trigger
  2. activate immune cells infiltrate into vessel wall
  3. direct damage stimulates vascular smooth muscle remodelling
  4. leads to ischaemia, infarction, aneurysm
143
Q

What are the two classification models for vasculitis?

A
  1. by vessel size
  2. Consensus classification (Chapel-Hill) = hybrid of vessel size, pathophysiology + underlying cause
144
Q

What is antiphospholipid syndrome?

A

A disorder associated with antiphospholipid antibodies where the blood becomes prone to clotting as the patient is in a hypercoagulable state.

It presents with a variety of clinical features characterised by thromboses and pregnancy related morbidity

145
Q

What condition is associated with APS?

A

Systemic lupus erythematous in 20-30% of cases

146
Q

Describe the pathophysiology of APS

A

Antiphospholipid antibodies can cause thrombosis by binding to the phospholipid on the surface of cells such as endothelial cells, platelets and monocytes.

Once they bind to these cells it can result in thrombosis formation and/or miscarriage. They tend to affect cerebral and renal vessels

147
Q

What things do Antiphospholipid antibodies cause?

A

C- Coagulation defects
L- livedo reticularis - lace-like purplish discolouration of skin
O- Obstetric issues e.g., miscarriage
T- Thrombocytopenia (low platelets)

CLOT

148
Q

What are some of the venous complications of APL?

A

DVT
PE

149
Q

What are the arterial complications of APL?

A

Stroke
MI
Renal thrombosis

150
Q

What are the pregnancy related complications of APL?

A

Recurrent miscarriage
Still birth
Preeclampsia

151
Q

What is another complication of APL?

A

Libmann-Sacks endocarditis:
- is a type of non-bacterial endocarditis
- growths (vegetations) on the valves of the heart.
- The mitral valve is affected. It is associated with SLE and antiphospholipid syndrome.

152
Q

What is another complication of APL?

A

Libmann-Sacks endocarditis:
- is a type of non-bacterial endocarditis
- growths (vegetations) on the valves of the heart.
- The mitral valve is MC affected. It is associated with SLE and antiphospholipid syndrome.

153
Q

How would you make a diagnosis for APL?

A

Diagnosis would be made when there is a history of thrombosis or pregnancy related complications plus the presence of:

Lupus anticoagulant antibodies
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

The presence of them needs to be persistent positive test more than 12 weeks apart

–

154
Q

How would you treat APL?

A

Long term warfarin with an INR range of 2-3

Pregnant women are put on low molecular weight heparin plus aspirin

155
Q

What are polymyositis and dermatomyositis?

A

Autoimmune disorders where there is inflammation in the muscles.

Polymyositis refers to chronic inflammation of the muscles. Dermatomyositis is a connective tissue disorder where there is chronic inflammation of the skin and muscles

156
Q

What is the key enzyme for diagnosing polymyositis and dermatomyositis?

A

The creatine kinase blood test. It is an enzyme that is found inside muscle. Inflammation of the muscles can lead to the release of it.

157
Q

Other than polymyositis and dermatomyositis what can cause creatine kinase levels to rise?

A

Rhabdomyolysis
Acute kidney injury
Myocardial infarction
Statins
Strenuous exercise

158
Q

What can cause polymyositis and dermatomyositis?

A

They can be caused by an underlying malignancy. This makes them paraneoplastic syndromes

159
Q

What cancers are most associated with polymyositis and dermatomyositis?

A

Lung
Breast
Ovarian
Gastric

160
Q

What are the symptoms of polymyositis and dermatomyositis?

A

Muscle pain, fatigue and weakness
Occurs bilaterally and typically affects the proximal muscles
Mostly affects the Shoulder and pelvic girdle
Develops over weeks

161
Q

What are the skin features of polymyositis and dermatomyositis?

A

Polymyositis occurs without skin features

Gottron lesions (erythematous macules over elbows/knees)
Photosensitive rash on back shoulders and neck
Purple rash on face and eyelids
Periorbital oedema
Subcutaneous calcinosis

162
Q

What is the antibody found in polymyositis?

A

Anti-Jo-1

163
Q

What are the two antibodies found in dermatomyositis

A

Anti-Mi-2 antibodies
Anti-nuclear antibodies

164
Q

How would you diagnose polymyositis and dermatomyositis?

A

Clinical presentation
Elevated creatine kinase levels
Autoantibodies

165
Q

What is the gold standard test for polymyositis and dermatomyositis?

A

Muscle biopsy

166
Q

What is the management for polymyositis and dermatomyositis?

A

Patients should be assessed for underlying cancer
Corticosteroids are first line
Then immunosuppressants
Then infliximab

167
Q

What is osteoporosis/osteopenia?

A

Osteoporosis is a condition where there is a reduction in the density of the bones.

Osteopenia refers to a less severe reduction in bone density than osteoporosis. Reduced bone density makes bone less strong and more prone to fractures.

168
Q

What can cause osteoporosis?

A

Primary disease
Malignancy
Endocrine dysfunction
COPD
IBD
CLD
CKD
Reduced skeletal loading = if skeleton not being used it will increase bone resorption

169
Q

What are the risk factors for developing osteoporosis?

A

S- Steroid use (can increase cortisol = ⬆️ bone resorption + osteoblast apoptosis)
H- Hyperthyroidism, hyperparathyroidism (⬆bone turnover)
A- Alcohol and tobacco use (poisons osteoblasts)
T- Thin = not exercising/using skeleton enough
T- Testosterone decrease
E- early menopause- oestrogen is protective
R- renal or liver failure
E- Erosive/inflammatory bone disease
D- dietary e.g., reduced Ca2+, malabsorption, diabetes

170
Q

Why does bone mass decrease as we get older?

A

Osteoclasts are responsible for the breakdown of bone and osteoblasts are responsible for the formation. As we age osteoclast activity is increased however this is not matched by osteoblast activity

The peak mass we reach as young adults is key a higher peak bone mass can be protective

171
Q

What percentage of women over 50 will have a fracture due to osteoporosis?

A

50%

172
Q

Pathophysiology of osteoporosis

A

Reduced bone strength + fall = fracture

reduced bone strength caused by:
- reduced bone mineral density
- reduced bone quality (reduced bone turnover + architecture)

173
Q

How can a fall in levels of oestrogen cause bone mass to decrease?

A

Oestrogen deficiency leads to an increased rate of bone loss. It is key to the activity of bone cell receptors found on osteoblasts, osteocytes, and osteoclasts.

It is thought that osteoclasts survive longer in the absence of oestrogen and there is an arrest of osteoblastic synthetic architecture

resorption > formation

174
Q

How can glucocorticoids cause a reduction in bone mass?

A
  • They cause an increased turnover of bone.
  • Prolonged use can result in reduced turnover state however the synthesis is affected resulting in bone mass reduction
175
Q

How does trabecular archictecture change with ageing?

A

Decrease in trabecular thickness, more pronounced for non load-bearing horizontal trabeculae

  • Decrease in connections between horizontal trabeculae (falls put more strain on vertical so preserve vertical connections more)
  • Decrease in trabecular strength and increased susceptibility to fracture
176
Q

What is the symptom of osteoporosis and where is this most likely to occur?

A

There is an increased frequency of fractures.

The most common ones include, vertebral crush fracture, and those of the distal wrist (Colles’ fracture) and proximal femur

177
Q

What is the FRAX tool?

A

It gives a prediction of the risk of a fragility fracture over the next 10 years

It involves the inputting of information such as age, BMI, co-morbidities, smoking, family history and if done you can enter a bone mineral score from a DEXA scan

178
Q

What do the results of the FRAX tool give?

A

It gives the result as a percentage probability of a:

Major osteoporotic fracture
Hip fracture

179
Q

What is the prognosis of osteoporosis fractures?

A

20% die within one year of post hip fracture
- usually in elderly so makes them very immobile

180
Q

What is used to assess bone mineral density?

A

DEXA scan

181
Q

What is a DEXA scan and what does it measure?

A

It stands for dual-energy x-ray absorptiometry.
- low radiation dose

It assess how much radiation is absorbed by the bones indicating how dense the bone is.
- measures important fracture sites

The measurement is usually taken from the Hip
(lumbar spine, proximal femur + distal radius MC)

182
Q

What are the T and Z scores of a DEXA scan and which one is more clinically relevant?

A

T-score: represents the number of standard deviations compared with the mean for a healthy young adult

Z-score: represents the number of standard deviations the bone density falls below a person for their age

T-score is more relevant

183
Q

What do the different T-scores represent?

A

More than -1 = Normal

-1 to -2.5 = Osteopenia

Less than -2.5 = Osteoporosis

Less than -2.5 plus a fracture = Severe Osteoporosis

184
Q

What is the management for someone who has had a FRAX score without a DEXA scan?

A

Low risk- reassure
Medium risk- offer DEXA scan and recalculate the risk with the results
High risk: offer treatment

185
Q

What are some lifestyle management/light treatment for mild osteoporosis/osteopenia?

A
  • Activty and exercise
  • Weight control
  • Reduce alcohol/stop smoking
  • calcium supplementation with vitamin D = in patients at risk of fragility fractures with an inadequate intake of calcium.
    (An example of this would be Calcichew-D3, which contains 1000mg of calcium and 800 units of vitamin D (colecalciferol).)

Patients with an adequate calcium intake but lacking sun exposure should have vitamin D supplementation.

186
Q

What is the first line treatment for someone at high risk of a fracture?

A
  1. Bisphosphonates - they interfere with osteoclast activity reducing their activity
    E.g.
    Alendronate 70mg once weekly
    Riseronate 35mg once weekly
    Zoledronic acid 5 mg once yearly (intravenous)
187
Q

What pathway to bisphosphonates work on?

A

HMG-CoA pathway

same as statins but a different part of it

188
Q

What are the side effects of bisphosphonates?

A

Reflux and oesophageal erosions. They are taken 30 minuets before food to prevent this

Osteonecrosis of the jaw and external auditory canal

189
Q

What are some other treatment options for osteoporosis?

A

Denosumab = is a monoclonal antibody that works by blocking the activity of osteoclasts.
- rebound increase of bon turnover when stopped, making bones even weaker than before

Strontium ranelate = is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction.

Raloxifene = is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus.

Hormone replacement therapy = should be considered in women that go through menopause early.

190
Q

What is an anabolic treatment for osetoporosis?

A

Teriparatide - increase bon density + improves trabecular structure

  • very expensive
191
Q

How should people be monitored who have osteoporosis or who are at risk of getting it?

A

Low risk patients should have a follow up within 5 years

Patients being treated should have a repeat FRAX and DEXA after 3-5 years and a treatment holiday if BMD has improved (this is 18months to 3 years of treatment before a repeat assessment)

192
Q

What is osteoarthritis?

A

Progressive synovial joint damage resulting in structural changes, pain and reduced function

193
Q

What is the epidemiology of osteoarthritis?

A

More common in women
Most common form of arthritis
8.75 million people over 45 with it in the UK

194
Q

What are the risk factors for developing osteoarthritis?

A

Age
high BMI
Joint injury or trauma
Excessive stress for exercise or certain occupations

195
Q

What gene is related to an increased risk of osteoarthritis?

A

COL2A1- collagen type 2 gene

196
Q

Describe the pathophysiology of osteoarthritis?

A

It is classified as non-inflammatory however inflammatory mediators play a role as inflammatory cytokines interrupt the normal repair of cartilage damage.

Cartilage is lost and joint space narrows this causes bone on bone interaction.

197
Q

What are the chemical mechanisms which cause osteoarthritis?

A

Metalloproteinases = secreted by chondrocytes degrade the collagen and proteoglycan

IL-1 and TNF-alpha = stimulate metalloproteinase production and inhibit collagen production

Deficiency in growth factors such as insulin-like growth factor impairs matrix repair

Gene susceptibility has a 35-60% influence

198
Q

What areas are most affected by osteoarthritis?

A

Knees
Hips
Sacro-ileac joints
Cervical spine
Wrist
base of thumb (carpometacarpal)
finger joints (interphalangeal)

199
Q

What are the signs of osteoarthritis?

A

Heberden’s nodes = swelling in the distal interphalangeal joints

Bouchard’s nodes = swelling in the proximal interphalangeal joint

Weak grip

Reduced range of motion

200
Q

What are the symptoms of osteoarthritis?

A

Joint pain
Mechanical locking
giving way
Crepitus - crunching sensation when moving joint

201
Q

How can a diagnosis of osteoarthritis be made?

A

If someone is over 45 and has typical activity related pain with no morning stiffness or stiffness lasting less than 30 minuets

202
Q

What are the 4 key x-ray changes found in osteoarthritis?

A

L- Loss of joint space
O- Osteophytes
S- Subchondral sclerosis increased density of bone along the joint line
S- Subchondral cysts (fluid filled holes in the bone)

203
Q

What is the management for osteoarthritis?

A

Patient education lifestyle changes such as weight loss and physiotherapy

Oral paracetamol and topical NSAIDs or topical capsaicin (chilli pepper extract - reduce substance P, pain transmitter to nerves)

Intra-articular steroid injection (don’t use these I’ve had loads and they destroy your joint even more)

Joint replacement

204
Q

What is rheumatoid arthritis?

A

A chronic systemic inflammatory disease. It leads to a deforming and symmetrical inflammatory arthritis of the small joints which progress to involve larger joint and other organs such as the skin and lungs

205
Q

What genes are implicated in rheumatoid arthritis?

A

HLA-DR1
HLA-DR4
They are both crucial in activating T-cells

206
Q

What are some environmental causes of rheumatoid arthritis?

A

Smoking
Other pathogens e.g., bacteria

207
Q

What are spondyloarthropathies?

A

A group of related chronic inflammatory conditions. They tend to affect the axial Skelton adn share similar clinical features.

208
Q

What are the shared clinical features of spondyloarthropathies?

A

Rheumatoid factor negative
HLA-B27 positive
Pathology in the spine
Asymmetrical inflammation of an entire joints = Sausage fingers
Extra-articular manifestations

209
Q

When should you suspect spondyloarthropathies?

A

S- Sausage digit
P- Psoriasis
I- inflammatory back pain
N- NSAIDs illicit a good response
E- Enthesitis inflammation where tendon meets joint (plantar fasciitis)
A- Arthritis
C- Crohn’s/colitis/CRP
H- HLA-B27
E- eye uveitis

210
Q

What is ankylosing spondylitis?

A

A chronic progressive inflammatory arthropathy. It mainly affects the spine and cause progressive stiffness and pain.

Ankylosis= abnormal stiffening and immobility of a joint due to the fusion of a bone

211
Q

What is epidemiology of ankylosing spondylitis?

A

More common in males
Most commonly presents in teens/20s
Women present later and are underdiagnosed
90% are HLA-B27 positive

212
Q

What is the pathology of ankylosing spondylitis?

A

There is lymphocyte and plasma infiltration with local erosion of bone at the attachments of the intervertebral and other ligaments.

Inflammation of these tendons/ligaments when they heal they heal with new bone formation

213
Q

What are the key presentations of ankylosing spondylitis?

A

Symptoms tend to occur gradually over 3 months
-Lower back pain stiffness and sacroiliac pain in the buttock region.

The pain and stiffness is worse with rest and improves with movement it is worse at night and morning and improves throughout the day

214
Q

What are some other signs and symptoms of ankylosing spondylitis?

A

Weight loss and fatigue
Chest pain
Anaemia
Heart block
Pulmonary fibrosis
Aortitis inflammation of the aorta

Note that any of the SPINEACHE symptoms may be present

215
Q

What would the first line investigations for ankylosing spondylitis be?

A

FBC normocytic anaemia
CRP and ESR elevated
Genetic testing for HLA-B27
X-ray (MRI if x-ray of the spine is normal may show bone marrow oedema)

216
Q

What would an x-ray for ankylosing spondylitis show?

A
  1. Bamboo spine- calcification of ligaments
  2. Syndesmophytes - areas of boney growth where the ligament normally inserts into the bone.
  3. Ossification - structures such as ligaments turn into bone like tissue
  4. Fusion - seen in facet joints, sacroiliac joints and costovertebral joints
217
Q

What is the test used to asses mobility in the spine and help to diagnose ankylosing spondylitis?

A

Schober’s test

218
Q

What is Schober’s test?

A

Have the patient stand straight. Find the L5 vertebrae. Mark a point 10cm above and 5cm below this point (15cm apart from each other). Then ask the patient to bend forward as far as they can and measure the distance between the points.

If the distance with them bending forwards is less than 20cm, this indicates a restriction in lumbar movement and will help support a diagnosis of ankylosing spondylitis.

219
Q

What are the treatments of ankylosing spondylitis?

A

NSAIDs
Steroids
TNF-alpha infliximab
Monoclonal antibodies targeting IL-7 (secukinumab)

220
Q

What are the complications of ankylosing spondylitis?

A

Vertebral fractures
Osteoporosis
Aortitis
Restrictive lung disease
Heart block

221
Q

What is reactive arthritis (Reiter syndrome) ?

A

It refers to synovitis occurring due to a recent infective trigger. This is an autoimmune response to infection elsewhere in the body

222
Q

What is the epidemiology of reactive arthritis?

A

30-50 fold increase if someone is HLA-B27 positive
Women less commonly affected
Mainly occurs in adults

223
Q

What can cause reactive arthritis?

A

Gastroenteritis- Salmonella, shigella
Sexually transmitted disease- chlamydia, Gonorrhoea

224
Q

How does an infection cause reactive arthritis?

A

Immune system is responding to the recent infection. This results in antibodies and inflammation that also affect the joints

It presents a lot like septic arthritis without infection at site of the bone it is somewhere else in the body

225
Q

What is the key presentation of reactive arthritis?

A

Acute, asymmetrical monoarthritis typically in lower leg (knee).
Can also present with triad of: Urethritis, arthritis and conjunctivitis

Can’t see, pee or climb a tree

226
Q

What are some other signs and symptoms of reactive arthritis?

A

Iritis - swelling and irritation of eye

Keratoderma blennorrhagia - painless, red, raised plaques and pustules

Circinate balanitis - dermatitis of the head of the penis

-Mouth ulcers

227
Q

What are the investigations for reactive arthritis?

A

Aspirate joints to rule out septic arthritis/Gout
Infectious serology
Sexual health review/ask about diarrhoea if present do a stool sample

228
Q

How should you treat reactive arthritis?

A

If patient presents with acute, warm, swollen and painful joint
- Hot joint policy - presume patient has septic arthritis until its excluded
= Antibiotics
= Aspirate joint - MCS & crystal examination

229
Q

What is the prognosis of reactive arthritis?

A

Most cases resolve within 6 months

230
Q

What is fibromyalgia?

A

Widespread chronic pain

231
Q

What are the risk factors for developing fibromyalgia?

A

female
Middle age
Genetics
Environmental e.g., child abuse, low household income divorced

232
Q

What causes fibromyalgia?

A

It is a problem with how the brain receives pain signals. Most patients have low levels of serotonin which is involved in inhibiting pain signals and elevated levels of substance P which increase pain signals

This together is though to paly a role in the hypersensitivity towards pain. Therefore the patient may perceive pain more readily compared to other people. The pain can be affected by lots of things e.g., sleep and emotions

233
Q

What are the key presentations of fibromylagia?

A

Allodynia- pain in response to non-painful stimuli

Hyperaesthesia- exaggerated perception of pain to mild stimuli

234
Q

What are the general symptoms of fibromyalgia?

A

Widespread pain that is aggravated by stress, cold and activity
Extreme tiredness
Sleep disturbance
Low mood
Poor concentration and headaches

235
Q

How would you diagnose fibromyalgia/

A
  • Chronic pain that has been present for at least 3 months
  • Widespread pain - involved left and right sides, above and below waist, and the axial skeleton.
  • Palpate tender point sites - severe pain in 3 to 6 different areas of your body, or you have milder pain in 7 or more different areas
  • No other reason for symptoms has been found

ALL INVESTIGATIONS WILL BE NORMAL

236
Q

What are the differentials for fibromyalga?

A

Rheumatoid arthritis
Chronic fatigue
Hypothyroidism
SLE
Polymyalgia rheumatica (PMR)
High calcium
Low vitamin D
Inflammatory arthritis

237
Q

What are the pharmacological: treatments for fibromyalgia?

A
  • Amitriptyline - tricyclic antidepressant
  • Serotonin-norepinephrinereuptake inhibitors (SNRIs) e.g. duloxetine

Help by elevating serotonin and norepinephrine levels.

  • Anticonvulsants like pregabalin and gabapentinwhich slow nerve impulses can help with sleep problems.
238
Q

What is Sjogren’s syndrome?

A

An autoimmune condition that affects the exocrine glands. It leads to symptoms such as dry mouth, eyes and vagina

239
Q

What are the two types of Sjogren’s syndrome?

A

Primary SS: where the condition occurs in isolation

Secondary SS; where the condition occurs with SLE or rheumatoid arthritis

240
Q

What other autoimmune conditions can cause Sjogren’s syndrome?

A

Hepatitis
PBC
Graves’ disease
Antiphospholipid syndrome

241
Q

What are the two main antibodies implicated in Sjogren’s syndrome?

A

Anti-Ro
Anti-La

242
Q

What is the Schirmer test for Sjogren’s syndrome?

A

Involves inserting a folded piece of filter paper under the lower eyelid with a strip hanging out over the eyelid

This is left for 5 minuets and the distance travelled along the strip is measured. Anything less than 10mm is significant

243
Q

What are the complications of Sjogren’s syndrome?

A

Eye infections
Oral problems such as cavities and candida infections
Vaginal problems such as candidiasis and sexual dysfunction

244
Q

What other organs can be affected by Sjogren’s syndrome?

A

Pneumonia and bronchiectasis
Non-Hodgkin’s lymphoma
Peripheral neuropathy
Vasculitis
Renal impairment

245
Q

What is the management for Sjogren’s syndrome?

A

Artificial tears
Artificial saliva
Vaginal lubricants
Hydroxychloroquine is used to halt the progression of the disease.

246
Q

What is vasculitis?

A

Inflammation of a blood vessel. It is characterised by the presence of an inflammatory infiltrate and destruction of vessel walls

247
Q

What are the types of vasculitis that affect the large vessels?

A

Giant cell arteritis
Takayasu’s arteritis

248
Q

What are the types of vasculitis that affect the medium sized vessels?

A

Polyarteritis nodosa
Kawasaki disease

249
Q

What are ANCA+ types of vasculitis that affect the small vessels?

A

Microscopic polyangiitis
Wegener’s granulomatosis
Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)

250
Q

What are the ANCA- types of vasculitis that affects the small vessels?

A

Henoch-schonlein purpura

251
Q

What are the blood tests done for vasculitis?

A

Anti neutrophil cytoplasmic antibodies (ANCA)

There are two types of blood test p-ANCA (anti-MPO) and c-ANCA (anti-PR3).

p-ANCA are positive in: Microscopic polyangiitis and Churg-Strauss syndrome
c-ANCA are positive in Granulomatosis with polyangiitis

252
Q

What is Giant Cell Arteritis (GCA)?

A

It is vasculitis of the medium and large arteries. It is the most common form of systemic vasculitis that affects and adults.

It usually affects branches of the carotid artery

253
Q

What are the risk factors for developing GCA?

A

Age usually over 50
Female
Caucasians
Polymyalgia rheumatica associated in 50% of cases

254
Q

What causes GCA and what arteries are affeceted?

A

It is a granulomatous vasculitis. Arteries become inflamed and thickened and there is a narrowed vascular lumen and can obstruct blood flow.

Cerebral arteries are particularly affected.:
- Superficial temporal: headache and scalp tenderness
- Mandibular: Jaw claudication
- Ophthalmic artery: visual loss due to retinal ischaemia

255
Q

What are the signs of GCA?

A

Superficial temporal artery tenderness
Absent temporal pulse
Reduced visual activity

256
Q

What are the symptoms of GCA?

A

Main symptom is headache that us unilateral and around forehead and temple.
Irreversible painless complete sight loss
Jaw claudication
Scalp tenderness may be noticed when brushing hair

257
Q

What are the systemic symptoms of GCS?

A

Fever
Muscle aches
Fatigue
Weight loss
Loss of appetite
Peripheral oedema

258
Q

What are the investigations for GCA?

A

ESR a value of greater than 50mm/h makes up 1 of the 5 criteria

Definitive diagnosis- is made doing a temporal artery biopsy:
- presence of Multinucleated giant cells. (negative results don’t rule out GCA due to presence of skip lesions)

259
Q

What is the treatment of GCA?

A

Corticosteroids 40-60mg IV methylprednisolone

Oral aspirin to prevent ischaemic cranial complications

260
Q

What are the complications of GCA?

A

Aortic aneurysms
Glucocorticoid toxicity
Vision loss
Cerebrovascular accident

261
Q

What is the ongoing management for GCA?

A
  • Once the diagnosis is confirmed they will need to continue high dose steroids (40-60mg) until the symptoms have resolved.
  • They then need to slowly wean off the steroids.
  • This can take several years. This is a similar process to managing polymyalgia rheumatica.
262
Q

What is Granulomatosiswith polyangiitis (Wegener’s granulomatosis)?

A

A multi-system disorder of unknown cause characterised by necrotising granulomatous inflammation

263
Q

What causes Granulomatosiswith polyangiitis (Wegener’s granulomatosis)?

A

B-cells mistakenly target their antibodies to granules made by a person’s own neutrophils.

These are ‘cytoplasmic anti-neutrophilic cytoplasmic antibodies’ or c-ANCAs.

Once they are bound to the neutrophil it causes free radical release which damages nearby cells

264
Q

What are the symptoms of Granulomatosiswith polyangiitis (Wegener’s granulomatosis)?

A

It affects the respiratory tract and the kidneys.

Nose bleeds
Sinusitis
Crusty nail secretions
Saddle shaped nose
Cough
Wheeze
Haemoptysis
glomerulonephritis

265
Q

What is the treatment for Granulomatosiswith polyangiitis (Wegener’s granulomatosis)?

A

Steroids combined with cyclophosphamide

Methotrexate and azathioprine usually used for maintenance

266
Q

What is polyarteritis nodosa?

A

Polyarteritis nodosa (PAN) is a medium vessel vasculitis. It is most associated with hepatitis B but can also occur without a clear cause or with hepatitis C and HIV.

It affects the medium sized vessels in locations such as the skin, gastrointestinal tract, kidneys and heart. This can cause renal impairment, strokes and myocardial infarction.

It is associated with a rash called livedo reticularis. This is a mottled, purplish, lace like rash.

267
Q

What is Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)?

A

Eosinophilic granulomatosis with polyangiitis used to be called Churg-Strauss syndrome and is still often referred to by this name. It is a small and medium vessel vasculitis.

It is most associated with lung and skin problems, but can affect other organs such as kidneys.

It often presents with severe asthma in late teenage years or adulthood. A characteristic finding is elevated eosinophil levels on the full blood count.

268
Q

What is the histology of RA nodules?

A

a central area of fibrinoid necrosis surrounded by a palisade layer of histiocytes and peripherally by a zone of loose connective tissue

269
Q

How do dairy products affect gout?

A

Dairy products increase excretion of uric acid by the kidneys

270
Q

How is arthritis different in SLE and RA?

A

RA = shape change and bone erosions

SLE = shape change but no erosions so hands can be pushed back into normal position

271
Q

What is the difference in X-rays for osteoarthritis and RA?

A

OA
LOSS
- loss of joint space
- osteophytes (bony lumps)
- subchondral sclerosis
- subchondral cysts

RA
LESS
- loss of joint space
- eroded bone
- soft tissue swelling (subcutaneous nodules)
- soft bone (osteopenia)

272
Q

What is the 1st line treatment for SLE?

A

anti-malarials = hydroxychloroquine

273
Q

What is the most common organism to infect a hip replacement?

A

Coagulase negative staphylococcus

274
Q

What description of joint pain would support a diagnosis of inflammatory back pain?

A

Pain across the costochrondral joints

275
Q

What are the gene associations for different MSK conditions?

A

HLA-DR4 = RA
HLA-DR7 = phospholipid syndrome
HLA-DR2 = SLE
HLA-DR5 = RA
HLA-DR8 = ankylosing spondylitis

276
Q

What is Scabies?

A

Scabies is a parasitic skin infection characterized by superficail burrows, intense pruritis and secondary infections

277
Q

What is the aetiology of Scabies?

A

Sarcoptes Scabiei
- transmitted by skin to skin contact

278
Q

What are the

A

Pruritis
burrows
papules
- found on flexor surfaces of wrist, finger webs, elbows, axillary folds, areola of breast in women and genital of males

scabies dig into skin at skin folds

279
Q

What is the treatment for Scabies?

A

1st: Permethrin 5%
2nd: Malathion 0.5%

Close contacts: treated same way even if asymptomatic

280
Q

What is the mechanism of action for allopurinol?

A
  • xanthine oxidase inhibitor
  • xanthine oxidase metabolises xanthine into uric acid
  • lowers plasma uric and precipitation of uric acid in joints

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