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Kyla's Phase 2a Flashcards > Musculoskeletal & Rheumatology > Flashcards

Musculoskeletal & Rheumatology Flashcards

1
Q

Define osteoarthritis

A
  • Degenerative joint disorder
  • Wear and tear in the synovial joints
  • NOT INFLAMMATORY (RA = inflammatory)
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2
Q

Pathology of OA

A

Combination of genetic factors + overuse + injury
Imblance between:
* Cartilage wearing down
* Chondrocytes repairing it
* → leading to structural issues in the joints
Progressive loss of articular cartilage, underlying bone of synovial joints

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3
Q

Rx for OA

A
  • Obesity
  • Age >50yrs
  • Occupation
  • Trauma
  • Female
  • Family history
    • Mutations of cartilage building collagens (types II, IX, XI)
  • Inflammation
    • Increased proinflammatory cytokines (IL1, IL6, TNF)
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4
Q

What are the key presentations of OA?

A
  • Joint pain + stiffness
  • Worsens with activity - contrast to inflammatory arthritis that is worse in the morning
  • OA = leads to deformity + instability + reduced joint function
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5
Q

What is crepitus on movement? When does it occur?

A

Joint sounds + bone cracking
OA

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6
Q

Signs of OA

A
  • Bulky bone enlargement of joint
  • Restricted range of motion
  • Crepitus on movement (joint sounds + bone cracking)
  • Effusions (fluid) around the joint
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7
Q

What are the commonly affected joints in OA?

A
  • Hips
  • Knees
  • Sacro-iliac joints
  • Distal-interpharyngeal (DIP) joints in the hands
  • Carpometacarpal (CMC) joint at the base of the thumb
  • Wrist
  • Cervical spine (cervical spondylosis)
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8
Q

What is the mnemonic for the x-ray changes in OA?

A

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

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9
Q

What are the OA signs in the hands?

A
  • Heberden’s nodes (DIP joints)
    • (H for high)
  • Bouchard’s nodes (PIP joints)
    • (B for below)
  • Squaring at the base of the thumb (carpometacarpal joint)
  • Weak drip
  • Reduced range of motion
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10
Q

What are Heberden’s and Bouchard’s nodes and in which condition are they found?

A

Osteoarthritis
* Heberden’s node = DIP joints
* Bouchard’s nodes = PIP joints

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11
Q

What is the criteria of an OA diagnosis (without investigations)?

A
  • Over 45
  • Typical activity-related pain
  • No morning stiffness OR stiffness lasting LESS than 30 minutes
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12
Q

Ix for OA?

A

First line:
* X-ray of affected joints
* Inflammatory markers (serum CRP and ESR)

Other:
* Rheumatoid factor (negative)
* MRI of affected joints

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13
Q

DDx of OA

A
  • Gout
  • Pseudogout
  • Rheumatoid arthritis (RA)
  • Psoritatic arthritis
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14
Q

First line management for OA

A
  • Patient education + lifestye changes (weight loss, physiotherapy, occupational therapy + orthotics
  • Stepwise use of analgesia (symptom control)
    • Oral paracetamol + topical NSAIDs or capsaicin
    • ADD: Oral NSAIDs (+ PPI)
    • Opiates (codeine, morphine)
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15
Q

What is the second line Tx for OA?

A
  • Intra-articular steroid injections
    • Temporary reduction in inflammation + improve symptoms
    • Methylprednisole acetate
  • Joint replacement (severe cases)
    • Typically hips + knees
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16
Q

What is the corticosteroid used in the intra-articular injections in OA?

A

Methyprednisolone acetate

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17
Q

Name 2 complications of OA?

A
  • Functional decline + inability to perform activities of daily living
  • Spinal stenosis in cervical + lumbar OA
  • NSAID-related GI bleeding
  • Effusion
    • Arthrocentesis + corticosteroid injection and/or referral to rheumatology, should be considered
  • NSAID-related renal dysfunction
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18
Q

What is rheumatoid arthritis (RA)?

A
  • Autoimmune condition that causes chronic inflammation of the synovial lining of the joints + tendon sheaths and bursa
    • Inflammation of tendons (increase risk of tendon rupture)
  • Inflammatory arthritis
  • Synovitis = synovial inflammation
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19
Q

What pattern does RA present in?

A

Symmetrical + affects multiple joints = Symmetrical polyarthritis

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20
Q

What typical patient presents with RA?

A

Middle aged woman

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21
Q

What are the genetic associations in RA?

A
  • HLA DR1
  • HLA DR4 (often present in RF positive patinets)
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22
Q

Name the two auto-antibodies found in RA patients, and which is more sensitive + specific?

A
  • Rheumatoid factor (RF) (70% of RA patients)
  • Anti-cyclic citrullinated peptide antibodies (anti-CCP antibodies)
    • More sensitive + specific than RF
    • Often predates RA development
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23
Q

What are the key presentations of OA?

A
  • Symmetrical distal polarthropathy
    • Pain
    • Swelling
    • Stiffness
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24
Q

What is the onset like for RA?

A

Very varied!
* Very rapid (i.e. overnight)
* Over months to years

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25
Q

What are the systemic symptoms of RA?

A
  • Fatigue
  • Weight loss
  • Flu-like symptoms
  • Muscle aches + weakness
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26
Q

What is the difference in pain in RA (inflammatory arthritis) and OA (mechanical problem)?

A

RA: Worse after rest, improves with activity
OA: Worse with activity, improves with rest

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27
Q

If a patient presents with arthritis Sx, including affected distal interphalangeal joint (DIP), which arthritis is more likely?

A

OA
(DIP joint almost never affected in RA)

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28
Q

What are the joints in RA most commonly affected?

A
  • Proximal Interphalangeal Joints (PIP) joints
  • Metacarpophalangeal (MCP) joints
  • Wrist and ankle
  • Metatarsophalangeal joints
  • Cervical spine
  • Large joints can also be affected such as the knee, hips and shoulders
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29
Q

What auto-antibody is the most sensitive + specific found in RA?

A

Anti-CCP
(Anti-cyclic citrullinated peptide antibodies)

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30
Q

What are the signs in the hands in RA?

A
  • Palpitation of the synovium in around the joints when disease is active → ‘boggy’ feeling
  • Z-shaped deformity to the thumb
  • Swan neck deformity (hyperextended PIP + flexed DIP)
  • Ulnar deviation of the fingers at the knucke (MCP joints)
  • Boutonnieres deformity (hyperextended DIP + flexed PIP)
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31
Q

What are the thumb deformities seen in RA and OA?

A
  • OA → squaring of base of thumb
  • RA → Z-shaped deformity of thumb
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32
Q

What are the extra-articular manifestions that can be seen in RA patients?

A
  • Secondary Sjogren’s syndrome AKA sicca syndrome
  • Pulmonary fibrosis
  • Anaemia of chronic disease
  • Felty’s syndrome (RA, neurtopenia + splenomegaly)
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33
Q

What is the pattern of RA presention?

A

Symmetrical polyarthropathy affecting small joints

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34
Q

What are the first line Ix for RA

required to make a diagnosis alongside clinical presentations

A
  • RF → if neggy, check anti-CCP antibodies
  • ESR/CRP
  • X-ray of hands + feet
  • Ultrasound scan of joints
    • Evaluate + confirm synovitis
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35
Q

What is a RA diagnosis involve?

A

Diagnosis criteria for RA = American College of Rheumatology (ACR)
Patients are scored based on:

  1. The joints that are involved (more and smaller joints score higher)
  2. Serology (RF and anti-CCP)
  3. Inflammatory markers (ESR and CRP)
  4. Duration of symptoms (more or less than 6 weeks)

Scores are added up and a score greater than or equal to 6 indicates a diagnosis of rheumatoid arthritis.

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36
Q

What scoring system monitors the disease activity in RA?

A

DAS28 Score (Disease Activity Score) - assessment for 28 joints:
* Swollen joints
* Tender joints
* ESR/CRP result

(Monitoring disease activity + response to treatment)

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37
Q

What are the X-ray changes seen in RA?

A
  • Joint destruction + deformity
  • Soft tissue swelling
  • Periarticular osteopenia
  • Boney erosions
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38
Q

A RA patient complains of experiencing self-limiting short episodes of inflammatory arthritis - with joint pain + stiffness + swelling. It only lasted just over a day. What is this phenomenom called?

A

Palindromic rheumatism

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39
Q

DDx for RA

A
  • Psoriatic arthritis (PsA)
  • Infectious arthritis
  • Gout
  • Systemic lupus erythematosus
  • Osteoarthritis
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40
Q

Why do you monitor the DAS28 in RA?

A

Aim to reduce the dose to the ‘minimal effective dose’ that controls the disease

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41
Q

What are DMARDs and what are they used in?

A

Disease modifying Anti-rheumatic drugs
(Used in RA)

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42
Q

What is the course of treatment for RA?

A

First line: Methotrexate or sulfasalazine (hydroxychloroquine in mild dsease)
Second line: 2 DMARDs (methotrexate + sulfasalazine)
Third line: Methotrexate + infliximab
Fourth line: Methotrexate + rituximab

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43
Q

Biological therapies lead to what?

A

Immunosuppression

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44
Q

What are the complications of immunosuppressants?

A
  • Patients are prone to serious infections
  • Can lead to reactivation of dormant infections (TB + HepB)
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45
Q

What class of drug is infliximab?

A

Anti-TNF

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46
Q

What class of drug is rituximab?

A

Anti-CD20

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47
Q

What are the DMARDs used in pregnancy?

A
  • Sulfasalazine
  • Hydroxychoroquine
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48
Q

How does methotrexate work and what needs to be prescribed with it?

A
  • Methotrexate = works by interfering with the metabolism of folate + suppressing certain components of the immune system
  • Folic acid = prescribed with methotrexate (taken on a different day)
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49
Q

What are the major side effects of methotrexate?

A
  • Liver toxicity
  • Mouth ulcers + mucositis
  • Bone marrow suppression + leukopenia (low WBCs)
  • TERATOGENIC
    • Needs to be avoided prior to conception in mothers + fathers
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50
Q

Read: Complications of main drugs used in RA

A
  • Methotrexate: Bone marrow suppression and leukopenia and highly teratogenic
  • Anti-TNF medications: Reactivation of TB or hepatitis B
  • Rituximab: Night sweats and thrombocytopenia
  • Hydroxychloroquine: Nightmares and reduced visual acuity
  • Sulfasalazine: Male infertility (reduces sperm count)
  • Leflunomide: Hypertension and peripheral neuropathy
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51
Q

Name 2 complications of RA

A
  • Work disability
  • Increased joint replacement surgery
  • Increased coronary artery disease
  • Increased mortality
  • Carpal tunnel syndrome (CTS)
  • Methotrexate-related liver toxicity and lung involvement
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52
Q

Name the crystal athropathies

A
  • Gout
  • Pseudogout
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53
Q

Which sex is more likely to develop gout?

A

Male
(x5)

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54
Q

What are the Rx for gout?

A
  • Guanosine in beer
  • Diuretics
  • Male
  • Obesity
  • Renal impairment
  • Renal impairment
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55
Q

What causes of gout? (pathology)

A
  • Gout = crystal athropathy
  • Chronically high blood uric acid levels
  • Urate crystals = deposited → hot + swollen + painful
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56
Q

What are gouty tophi?

A

Subcutaneous deposits of uric acid

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57
Q

Where are gouty tophi most commonly found?

A

Typically affects small joints + connective tissues:
* Hands (DIP joints = most affected)
* Elbows
* Ears

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58
Q

If a patient presents with a single hot, swollen and painful joint. What is a possible diagnosis that is not septic arthritis?

A

Gout

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59
Q

What are the most common joints affected by gout?

A
  • Base of the big toe (metatarsopharyngeal joint)
  • Wrists
  • Base of thumb (carpometacarpal joints)

Larger joints:
* Knee
* Ankle

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60
Q

What are the two Ix for gout?

A
  • Aspiration of joint fluid (arthrocentesis with synovial fluid analysis)
    • No bacterial growth
    • Monosodium urate crystals
    • Negatively birefringment of polarised light
  • Joint x-ray
    • Lytic lesions in the bone
    • Punched out lesions
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61
Q

What are characteristics of synovial fluid analysis of gout?

A
  • Needle-shaped crystals
  • Negatively birefringment of polarised light
  • Monosodium urate crystals
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62
Q

What are the first to third line Mx options for gout?

A
  • First line: NSAID (unless renal impairment)
  • Second line: Colchicine (S/E diarrhoea)
  • Third line: Intra-articular or oral
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63
Q

What are the pharmacological and non-pharmacological options for gout prophylaxis?

A
  • Allopurinol = reduces uric acid level
  • Lifestyle changes:
    • Wt loss
    • Staying hydrated
    • Minimise alcohol consumption + purine-based food (meat + seafood)
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64
Q

What is a complication of gout?

A

Renal calculi!

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65
Q

Pseudogout is caused by which type of crystal?

A

Calcium pyrophosphate crystals

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66
Q

What is the typical patient that has pseudogout?

A

Older women
(Overlaps with OA)

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67
Q

What are two causes of pseudogout?

A
  • Direct trauma to the joint
  • Intercurrent illness
  • Surgery – especially parathyroidectomy
  • Blood transfusion, IV fluid
  • T4 replacement
  • Joint lavage
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68
Q

Rx for pseudogout?

A
  • Old age
  • Osteoarthritis
  • Hyperparathyroidism
  • Haemochromatosis
  • Hypophosphatemia
  • Diabetes
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69
Q

What is chrondrocalcinosis

A

Pseudogout

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70
Q

Typical presentation of pseudogout

A
  • Acute synovitis, acute hot + swollen joint or OA joint
  • (Severe joint pain, fever and stiffness)
  • Can affect multiple joints
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71
Q

What are the signs of pseudogout on an x-ray?

A

Similar osteoarthritis:
- L–Loss of joint space
- O–Osteophytes
- S–Subarticular sclerosis
- S–Subchondral cysts

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72
Q

What is the gold standard Ix for pseudogout

A

Aspiration of synovial fluid:
- No bacterial growth
- * Calcium pyrophosphate crystals
- * Rhomboid shaped crystals
- * Positive birefringent of polarised light

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73
Q

How do distinguish pseudogout from OA?

A
  1. Pattern of involvement – knee, wrists, shoulders, ankles, elbows
  2. Marked inflammatory component
  3. Superimposition of acute attacks

Septic arthritis = needs to be excluded

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74
Q

What are the management options for pseudogout?

A
  • Symptoms usually resolve themself
  • NSAIDs
  • Colchicine
  • Joint aspiration
  • Steroid injections (dexamethasone)
  • Oral steroids

Severe cases:
* Joint washout (athrocentesis)

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75
Q

What drug can you use for recurrent gout?

A

Allopurinol
(Reduces uric acid levels)

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76
Q

Name two forms of infective arthritis

A
  • Septic arthritis
  • Osteomyelitis
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77
Q

What is osteomyelitis?

A

Inflammation in a bone + bone marrow
(usually caused by bacterial infection)

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78
Q

What are the two types (/causes) of osteomyelitis?

A
  • Haematogenous contamination
    • = pathogen carried via blood → seeded into bone
  • Direct contamination (of bone)
    • = osteomyelitis at fracture site (or during an orthopaediac operation)
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79
Q

What bacteria is the most common cause of osteomyelitis?

A

Staphylcoccus aureus

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80
Q

Rx for osteomyelitis

A
  • Open fractures
  • Orthopaedic operations
    • (Perioperative prophylactic antibiotics used)
  • IV drug use
  • Immunosuppression
  • Diabetes (diabetic foot ulcer)
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81
Q

What is the typical presentation of osteomyelitis?

A

Non-specific → generalised Sx of infection
* Fever
* Lethargy
* Nausea
* Muscle aches

Inflammation (DR CT)
* Dolor (pain)
* Rubor (red)
* Calor (warm)
* Tumour (swelling)

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82
Q

What first line Ix would you perform if osteomyelitis is suspected?

A

First line:
* X-ray (cannot pick up early stages)
- Localised osteopenia(thinning of the bone)
- Destruction of areas of the bone
- Periosteal reaction(changes to the surface of the bone)
* Blood tests - raised inflammatory markers
- WBC, CRP, ESR
* Bone + blood cultures (stapylcoccus aureus) + antibiotic sensitivities

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83
Q

What is a diagnostic scan for osteomyelitis?

A

MRI scan

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84
Q

What are two differentials for osteomyelitis?

A
  • Septic arthritis
  • Reactive arthitis
  • Necrotising fasciitis
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85
Q

A patient presents with osteomyelitis, what is the treatment?

A
  • Surgical debridement of infected bone + tissues
    AND
  • 6 weeks of flucloxacillin
    • Alternatives: Clindamycin or Vancomycin (if MRSA)

Chronic osteomyelitis = requires 3 months or more of antibiotics

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86
Q

Complications of osteomyelitis

A
  • Infection recurrence
  • Fracture
  • Amputation
  • Joint stiffness
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87
Q

When should you suspect osteomyelitis?

A
  • Unwell child/immunocompromised patient with a limp
  • Chronic osteomyelitis in adults with a history of open fracture, previous orthopaedic surgery or a a discharging sinus
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88
Q

What is septic arthritis?

A
  • Infection within a joint (native or replacement)
  • Medical emergency! - the infection can quickly destroy the bone → cause systemic illness (10% mortality)
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89
Q

What are the 2 routes in which a pathogen can enter a joint and cause septic arthritis?

A
  • Haematogenous = bloodstream
  • Direct inoculation = from nearby infection/direct (e.g. open fracture
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90
Q

What are the two routes staphylococcus can cause osteomyelitis (infection of bone) and septic arthritis (infection of joint)?

A
  • Haematogenous = bloodstream
  • Direct inoculation = from nearby infection/direct (e.g. open fracture
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91
Q

Read: Pathology of septic arthritis

A

Infection of joint → endotoxin production → cytokine release → neutrophil attraction → inflammation → damage of joint structures

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92
Q

Septic arthritis is an important complication of what surgery?

A

Joint replacement
- 1% occurrence of straight forward hip or knee replacements
- Higher in revision surgery

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93
Q

What is the most common causative bacteria in septic arthritis?

A
  • Staphylococcus aureus (most common)
  • Escherichia coli(E. coli)
  • Neisseria gonorrhoea in sexually active individuals
  • Group A Streptococcus(most commonlyStreptococcus pyogenes)
  • Haemophilus influenza
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94
Q

Rx for septic arthritis?

A

Joints:
* Underlying joint disease
* Prosthetic/artificial joint, surgical procedure
* Osteomyelitis

Immunosuppression:
* Immunosuppressuin
* Age
* HIV
* Diabetes

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95
Q

A patient comes into A&E with a rapid onset of a hot, red, swollen and painful knee joint. They complain that its stiff and they have a reduced range of motion. They also have systemic syptoms of fever, lethargy and potentially spsis. What is a potential diagnosis?

A

Septic arthritis

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96
Q

When condition should you suspect, when a young patient presents with a a single acutely swollen joint.

A

Gonococcus specific arthritis

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97
Q

A patient with suspected septic arthritis has a synovial fluid aspiration and its cultured. It comes back as a gram-negative diplococcus. What is the casusative organism?

A

Neisseria gonorrhoea

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98
Q

Ix for septic arthritis

A
  • Synovial fluid aspiration:
    • Culture + sensitivies
    • Gram stain (and crystal/polarising microscopy)
    • WBC count
    • Joint fluid = may ve purulent (full of pus)
  • Blood culture (bc of haematogenous spread) - before antibotics
  • Inflammatory markers (ESR and CRP)
  • FBC (Raised WBC count)
  • Plain x-ray (not diagnostic)
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99
Q

DDx of septic arthritis

A
  • Gout
  • Pseudogout
  • Reactive arthritis - triggered by:
    • Urethritis
    • Gastroenteritis
    • Conjuctivitis (associated with)
  • Haemarthrosis (bleeding into the joint)
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100
Q

First line treatment of septic arthritis

A

Antibiotics (before sensitivities are known) - 3-6 weeks:
* First line: Flucloxacillin + rifampicin
* Vancomycin + rifampicin → penicillin, MRSA, prosthetic joint
- Clindamycin = an alternative

IV 2 weeks + oral 4 weeks

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101
Q

Complications of septic arthritis

A
  • Osteomyelitis (infection spread to surrounding bone)
  • Joint destruction (permanent irreversible damage)
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102
Q

What is osteoporosis?

A
  • Low bone density + micro-architectural defects in the bone tissue
  • Increased bone fragility + susceptibility to fracture
  • Low bone mass → bone fragility → increased fracture risk
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103
Q

What is osteopenia?

A

Less severe reduction in bone density than osteoporosis
* Osteopenia = precursor to osteoporosis
* Bone mineral density 1-2.5 standard deviations below young adult mean value

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104
Q

What is osteomalacia?

A
  • Poor mineralisaton (lack of calcium) → soft bones
  • Osteomalacia = adult form of rickets
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105
Q

What is the adult form of rickets?

A

Osteomalacia

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106
Q

What is the primary cause of osteoporosis?

A

Post-menopausal

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107
Q

What are the secondary causes of osteoporosis?

A

SHATTERED (increases bone turnover)
- S – steroid use (prednisolone)
- H – hyperthyroidism/hyperparathyroidism
- A – alcohol/smoking
- T – thin (low BMI)
- T – testosterone low
- E – early menopause
- R– renal or liver failure
- E – erosive/inflammatory bone disease e.g. RA, myeloma
- D – dietary calcium low

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108
Q

What should you thibk about when thinking about the Rx of osteoporosis?

A

Patient, disease, medication
* Patient:
- Older age
- Female (post-menopausal)
* Disease:
- Malabsorption (decreased Ca2+)
- Endocrine disorders (Cushing’s and hyperparathyroidism)
- Rheumatoid arthritis
* Medication:
- Long-term corticosteroids (prednisolone)
- SSRIs, PPIs

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109
Q

A post-menopausal women presents to A&E with a hip fracture. What could be an underlying disease?

A

Osteoporosis

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110
Q

Where are pathological fractures most likely to be in a patient with osteoporosis?

A
  • Vertebral colum
  • Ribs
  • Hips
  • Wrist
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111
Q

A patient presents with sudden back pain, spinal cord compression, cauda equina syndrome. O/E you see loss of height, hunched posture, kyphosis (curvature of spine). Possible diagnosis?

A

Compression fracture of the vertebral column secondary to osteoporosis

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112
Q

What is the first line and gold standard scan for osteoporosis?

A

DEXA scan
(Dual Energy X-ray Absorptiometry)

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113
Q

What soes a DEXA scan measure?

A

Bone mineral density (BMD)
(Key classifiction + management is osteoporosis)

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114
Q

What are the 2 scores that are given from a DEXA?

A
  • Z score: Number of standard deviations the patients bone density falls below the mean for their age.
  • T scores: Number of standard deviations below the mean for a healthy young adult their bone density is.
    • T SCORE = MORE IMPORTANT
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115
Q

Give the T scores + classifications for osteopenia, osteoporosis and sever osteoporosis

A
  • > -1 = normal
  • -1 to -2.5 = osteopenia
  • < -2.5 = osteoporosis
  • < - 2.5 plus fracture = severe osteoporosis
    (Measure in SDs below the mean for a healthy young adult)
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116
Q

What is the the FRAX tool used for?

A

Gives prediction of the risk of a fragility fracture over the next 10 years
* Major osteoporotic fracture
* Hip fracture
FRAX Tool = first step in assessing someone’s risk of osteoporosis

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117
Q

What information in used in the FRAX tool?

A
  • Bone mineral density (from DEXA scan)
    Variables:
  • Age
  • Sex
  • BMI
  • Previous fractures
  • Steroids
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118
Q

Name some lifestyle changes for osteoporosis

A
  • Avoiding falls
  • Activity and exercise
  • Maintain a healthy weight
  • Adequate calcium intake
  • Adequate vitamin D
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119
Q

First line management of osteoporosis

A
  • Oral bisphosphonates (alendronate)
  • Calcium + vitamin D supplemenation
    • (inhibits bone reabsorption)
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120
Q

Name some primary prevention from osteoporosis

A
  • Calcium-rich diet e.g. dairy or sardines, white beans
  • HRT – menopausal women
  • Corticosteroids – consider prophylactic bisphosphonates
  • Smoking + alcohol cessation
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121
Q

Name a vitamin D and calcium supplementation
(osteoporosis-related)

A

Calcichew-D3

122
Q

Why are bisphosphonates the first line medication in osteoporosis?

A

Reduce osteoclast activity
(Preventing reabsorption of bone)

123
Q

S/E of bisphophonates

A
  • Oesophageal reflux + erosions
  • Osteonecrosis of the jaw
124
Q

Symptoms of osteoporosis

A

Asymptomatic until fracture occurs

125
Q

Osteoporosis BMJ Summary:

A
  • Diagnosis based on history of prior fragility fracture or low bone mineral density, which is defined as a T-score ≤-2.5.
  • Fall prevention is first-line therapy.
  • Bisphosphonates are first-line pharmacological therapy for postmenopausal women and men.
  • In postmenopausal women, oestrogen is considered only for those at high risk for whom non-oestrogen medicines are inappropriate.
126
Q

What is kyphosis?

A

Curvature of the spine that causes the top of the back to appear more rounded than normal

127
Q

What is fibromyalgia?

A
  • Fibromyalgia = chronic pain syndrome - diagnosed by the presence of widespread body pain
  • Non-specifc muscular disorder - with unknown cause (AKA chronic persistent pain)
  • No signs of inflammation
    (Fibro = soft tissue)
    (Myalgia = muscle pain)
128
Q

Typical person with fibromyalgia

A

Middle aged female

129
Q

What are some risk factor/causes of fibromyalgia?

A
  • Genetic factors
  • Environmental factors (child abuse)
  • Negative emotions = can amplify pain
  • Associated with:
    • IBS
    • Chronic headache
    • Depression
    • Chronic fatigue syndrome
  • Family history
130
Q

What is the pathophysiology behind fibromyalgia?

A

Chronic condition of central sensitisation → hypersensitivity to pain + sleep disturbances
- Low serotonin → inhibits pain signals
- Raised substance P + nerve growth factor → increased pain signals

131
Q

A 50 y/o female patient presents with widespread muscle pain for over 3 months, shows no signs of inflammation and has a low threshold to pain. Possible diagnosis?

A

Fibromyalgia

132
Q

Describe the pain associated with fibromyalgia?

A
  • Widespread muscle pain
  • Low threshold to pain
    • Pain worsens with stress + cold weather + activity
  • Morning stiffness (less than an hour)
  • Headacge/diffuse abdominal pain
133
Q

What is ‘fibro-fog’?

A

Poor concentration + memory
(in fibromyalgia)

134
Q

Apart from widespread muscle pain, and fatigue, what are some other symptoms of fibromyalgia?

A
  • Numbness/tingling sensations
  • Sensitivity to sensory stimuli (e.g. bright lights, odoures, noises)
135
Q

How is a diagnosis of fibromyalgia made?

A

Strictly clinical (+ tests to exclude other pathologies)

136
Q

What is the diagnostic criteria for fibromyalgia?

A
  • Presence of chronic (>3 months) widespread body pain
  • Fatigue + sleep disturbance
  • Presence of pain in 11/18 palpitation sites
137
Q

What are some non-pharmacological treatments for fibromyalgia?

A
  • Education
  • CBT (manage pain)
  • Exercise
138
Q

What are some pharmacological treatments for fibromyalgia?

A

Antidepressants (inhibit pain by elevating serotonin + NE levels)
* TCA (amitriptyline)
* SNRI (duloxetine)

Anticonvulsants (slow nerve impulses + relieve sleep disturbances) - Gabapentin

NSAIDs (naproxen) = analgesic

139
Q

What is Sjogren’s syndrome?

A
  • Autoimmune condition that causes destruction of the exocrine glands
    • (esp lacrimal (tear) + salivary glands)
  • Leads to dry mucous membranes → dry mouth, dry eye, dry vagina
140
Q

What conditions can cause secondary Sjogren’s syndrome?

A
  • Rheumatoid arthritis
  • SLE
  • Other autoimmune conditions
141
Q

What are the genetic associations of sjogren’s syndrome?

A

HLA-DR8/DR3

142
Q

Name some associations with Sjogren’s syndrome

A
  • Gluten sensitivity
  • Associated with other autoimmune problems e.g. thyroid, RA, myasthenia gravis
  • More common in females
  • Associated with HLA-D8/DR3
  • Onset in 40s-50s
143
Q

What is primary Sjogren’s syndrome called?

A

Sicca syndrome

144
Q

A 60 y/o woman with RA presents with salivary gland enlargement, dry eyes, dry mouth (xerostomia), dryness of skin and vagina. She also has fatigue and joint pain. Possible diagnosis?

A

Sjogren’s syndrome

145
Q

A 60 y/o woman with RA presents with salivary gland enlargement, dry eyes, dry mouth (xerostomia), dryness of skin and vagina. She also has fatigue and joint pain. Possible diagnosis?

A

Sjogren’s syndrome

146
Q

You suspect Sjogren’s syndrome in a patient (symptoms of dry mucous membranes), what Ix do you perform?

A
  • Schirmer’s test (measures conjunctival dryness)
  • Anti-Ro (SS-A) and Anti-La (SS-B) antibodies
147
Q

Management of Sjogren’s syndrome

A
  • Hydroxychloroquine (halts disease progression)
  • NSAIDs + hydroxychloroquine (for athralgia + fatigue)
  • Artifical tears + saliva
148
Q

Complications of Sjogren’s sydnrome

A
  • Eye infections such as conjunctivitis and corneal ulcers
  • Oral problems such as dental cavities and candida infections
  • Vaginal problems such as candidiasis and sexual dysfunction
149
Q

Complications of Sjogren’s sydnrome

A
  • Eye infections such as conjunctivitis and corneal ulcers
  • Oral problems such as dental cavities and candida infections
  • Vaginal problems such as candidiasis and sexual dysfunction
150
Q

Define vasculitis

A

Inflammation of blood vessels
(Can affect any organ by causing destruction (aneurysm/rupture) or stenosis of a vessel)

151
Q

Name a vasculitis that effects the small, medium, large blood vessels

A
  • Small → Granulomatosis with polyangiitis
  • Medium → Polyarteritis nodosa
  • Large → Giant cell arteritis
152
Q

Name some conditions associated with vasculitis

A
  • Infective: Infective endocarditis
  • Non-infective:
    • Vasculitis with RA
    • SLE
    • Scleroderma
    • Goodpasture syndrome
153
Q

Breif pathology of vascultits

A

Inflammation + necrosis of blood vessels with → subsequent blood flow **
* Vessel wall destruction → perforation + haemorrhage into tissues
* Endothelial injury → thrombosis →ischaemia/infarction** of dependent tissues

Autoimmune diseases:
Direct method: Body mistakes endothelial layer of blood vessel for foreign pathogen → attacks
- Molecular mimicry: Immune system WBCs = mistake normal antigens of endothelial cells as foreign
- Medium, large-vessel vasculitides

Indirect method: Immune system attacks healthy cells near vascular endothelium → damages endothelial cells
- Small-vessel vasculatides (exception: Henoch-Schonlen purpura)

154
Q

Name some general vasculitis presentations

A
  • Purpura
    • Purple-coloured non-blanching spots (caused by blood leaking from the vessels under the skin)
    • Joint + muscle pain
    • Peripheral impairment
    • GI disturbance
    • Hypertension

Systemic manifestations:
* Fatigue
* Fever
* Weight loss
* Anorexia (loss of appetite)
* Anaemia

155
Q

General Ix for vasculitis

A
  • Inflammatory markers (CRP + ESR) = usually raised
  • Anti neutrophil cytoplasmic antibodies (ANCA)
    • c-ANCA (granulomatosis with polyangiitis)
    • p-ANCA

(Think c & p for CRP - vasculitis being an inflammatory condition)

156
Q

What is the general management for vasculitis?

A

Steroidscan be administered to target the affected area:
- Oral(i.e. prednisolone)
- Intravenous(i.e. hydrocortisone)

Immunosuppressants
- Cyclophosphamide
- Methotrexate
- Azathioprine
- Rituximab

157
Q

What sized blood vessels does giant cell arteritis affacet?

A

Systemic vasculitis of large + medium arteries

158
Q

Typical giant cell arteritis symptoms are associated with which arteries?

A

Temporal arteries

159
Q

What condition is giant cell arteritis associated with?

A

Polymyalgia rheumatica

160
Q

Which patients are most at risk of GCA?

A

White females over 50
(+ smoking and atherosclerosis)

161
Q

Pathology of giant cell arteritis

A
  • Arteries become inflamed, thickened and can obstruct blood flow
  • Cerebral arteries affected in particular e.g. temporal artery
  • Ophthalmic artery can also be affected potentially resulting in permanent or temporary vision loss
162
Q

A 52 y/o female patient complains of severe unilateral headache → typically around the temple + forehead and pain when eating (jaw claudification), and scalp tenderness (noticed when brushing her hair). Later she complains that her vision is becoming more blurry in one eye. Possible diagnosis?

A

Giant cell arteritis

163
Q

What are the three groups of symptoms of giant cell arteritis?

A

Pain:
- Severe unilateral headache → typically around the temple + forehead
- Scalp tenderness → noticed brushing hair
- Jaw claudication (pain when eating)

Visual changes:
- Blurred or double vision
- Irreversible painless complete sight loss can occur rapidly

Systemic symptoms:
- Peripheral oedema
- Muscle aches
- Fever
- Fatigue
- Weight loss + loss of appetite

164
Q

What first line and gold standard Ix are performed for giant cell arteritis?

A

First line:
* Duplex ultrasound of temporal arteries
* Bloods
- CRP + ESR (raised)
- FBC (may show normocytic anaemia + thrombocytosis)
- ANCA (negative)

Gold standard:
* Temporal artery biopsy (multinucleated giant cells)
- Necrotising arteritis

165
Q

What cells are found on a temporal artery biopsy for GCA?

A

Multinucleated giant cells

166
Q

Is giant cell arteritis ANCA positive or negative?

A

Negative

167
Q

Tx for giant cell arteritis

A
  • Corticosteroids immediately (prednisolone) - reduce risk of sight loss
  • Aspirin (decreases visual loss + strokes)
  • Proton pump inhibitor (omeprazole) - for gastric prevention while on steroids
168
Q

What is granulomatosis with polyangiitis?

A
  • Small vessel vasculitis → affectes respiratory tract + kidney
  • Necrotising, granulomatous vasculitis of arterioles, capillaries and post capillary venules

Remember it as the rule of C’s
- C in body (nose, upper resp. tract, kidneys),
- C-ANCA +, biopsy (Cross-section),
- Corticosteroids and Cyclophosphamide

169
Q

What antibodies are found in granulomatosis with polyangiitis?

A

cytoplasmic anti-neutrophil cytoplasmic antibodies (cANCA)
(B cells release them)

170
Q

Which 3 areas of the body does granulomatosis with polyasngiitis?

A
  • Nasal passage
  • Lung
  • Kidney
171
Q

Patient presents with a saddle-shaped nose, pleuritic chest pain, sinusitis and glomerulonephritis w/ hypertension. Possible diagnosis?

A

Granulomatosis with polyangiitis

172
Q

Ix for granulomatosis with polyangiitis

A
  • Urinalysis (haematuria)
  • CT chest (lung nodules)
  • Bloods
    • c-ANCA (positive)
    • ESR
    • LFTs
173
Q

Tx for granulomatosis with polyangiitis

A
  • Corticosteroid: Prednisolone
  • Immunosuppressant: Cyclophosphamide or rituximab
174
Q

Polyarteritis Nodosa affects which sized blood vessels?

A

Medium-sized blood vessels

175
Q

Which virus is associated with polyarteritis nodosa?

A

Hepatitis B

176
Q

What are some features of polyarteritis nodosa?

A
  • Systemic: Fever, fatigue, weight loss, myalgia/arthralgia
  • End organ ischaemic damage
  • Renal arteries → hypertension, acute/chronic kidney disease → haematuria, proteinuria
  • Coronary arteries → MI and HF
  • Skin arteries → skin lesions (e.g. uclers, purpura, erythematous nodules)
  • ********Mesenteric artery******** → mesenteric ischaemia → severe abdominal pain, GI bleeding
  • Neurological → Numbness, tingling, abnormal/lack of sensation + inability to move part of body

Just systemic and really vague!

177
Q

Ix for polyarteritis nodosa

A
  • Bloods
    • FBC (anaemia)
    • WBC (raised)
    • ESR and CRP (raised)
    • ANCA (negative)
  • Serologies - Hep B and C
  • Urinalysis (MSU)
    • Mild proteinuria (normal or elevated)
  • Angiography
    • Hepatic, mesenteric or renal vessels → show micro-aneurysms
    • ‘String of beads’ pattern along artery, spasms
178
Q

What appearnace does polyarteritis nodosa have on angiography?

A

‘Strings of beads’
(micro-aneurysms + focal narrowing)

179
Q

What form of vasculitis needs this Tx?:
* BP control (ramipril)
* Prednisolone + cyclophosphamide

A

Polyarteritis nodosa

180
Q

Patient presents with pathogical fractures and hearing loss. Potential diagnosis?

A

Paget’s disease

181
Q

What is systemic lupus erythematosus?

A

An inflammatory autoimmune connective tissue disease
(Systemic → affects multiple organs)
(Erythematosus → red malar rash (occurs across the face)

182
Q

Typical patient which SLE?

A

Young/middle-aged Asian woman

183
Q

SLE is characterised the presence of which antibodies?

A

Anti-nuclear antibodies (ANA)
(Leads to autoimmune inflammatory response)

184
Q

What type of hypersensitivity reaction occurs in SLE?

A

Type 3 hypersensitivity reaction

185
Q

What disease course does SLE present in?

A

Relapsing-remitting course
(with flares + improvements)

186
Q

A patient presents with hair loss, malar rash, splenomegaly, lymphadenopathy. They complain of SOB, joint pain and myalgia. Possible diagnosis?

A

SLE

187
Q

What two rashes are present in SLE?

A
  • Photosensitive malar rash
    • Butterfly shaped rash across nose - gets worse with sunlight
  • Discoid rash
    • Erythematous rasied patches
    • Atrophic scarring (older lesions)
188
Q

Signs of SLE?

A
  • Weight loss
  • Photosensitive malar rash (butterfly)
  • Discoid
  • Lymphadenopathy + splenomegaly
  • Raynaud’s phenomenon
  • Haematological
    • Anaemia (haemolytic, Coombs positive)
    • Thrombocytopenia
    • Neutropenia
    • Lymphopenia
189
Q

What are the symptoms of SLE?

A
  • Fatigue
  • Arthralgia (joint pain)
  • Myalgia (muscle pain)
  • Fever
  • SOB
  • Pleuritic chest pain
190
Q

Of the two auto-antibodies needed to diagnose SLE, which is the most sensitive and specific?

A
  • Anti-nuclear antibodies = sensitive
  • Anti-double-stranded DNA (ds)DNA = specific
191
Q

What are the Ix needed for SLE?

A
  • Autoantibodies
    • Antinuclear antibodies
    • Anti-dsDNA antibodies
  • FBC (normocytic anaemia of chronic disease)
  • ESR + CRP (raised in active inflammation)
  • Urine protein:creatinine ratio (proteinuria in lupus nephritis)
192
Q

What is a commmon secondary complication of SLE?

A

Antiphospholipid syndrome

193
Q

What is the diagnostic criteria for SLE?

A

Confirming presence of antinuclear antibodies (ANA) + number of clinical features suggestive of SLE

194
Q

DDx for SLE

A
  • Rheumatoid arthritis
  • Systemic sclerosis
  • Lyme disease
  • HIV
  • Cytomegalovirus
  • Glomerulonepheitis
  • Fibromyalgia
195
Q

Treatment of SLE?

A
  • NSAIDs
  • Prednisolone
  • Hydroxychloroquine (first line for mild SLE)
    • Or methotrexate

Severe cases:
* Biological therapies - Rituximab

Like most autoimmune conditions → anti-inflammatory + immunosuppressants

196
Q

Complications of SLE

A
  • Cardiovascular disease
  • Infection (secondary to immunosuppressants)
  • Anaemia of chronic disease
    • Chronic normocytic anaemia
  • Pericarditis
  • Pleuritis/pleurisy
  • Interstitial lung disease
  • Lupus nephritis
  • Neuropsychiatric SLE
  • Pregnancy complications
  • Venous thromboembolism
197
Q

What is scleroderma?

A

Hardening of the skin

198
Q

What is systemic sclerosis?

A

Autoimmune + fibrotic connective tissue disease
* Multi-system disease
* Involvement of the skin + Raynaud’s phenomenon occuring early

199
Q

What are the two main disease patterns in systemic sclerosis?

A
  • Limited cutaneous systemic sclerosis
  • Diffuse cutaneous systemic sclerosis
200
Q

Typical patient with systemic sclerosis/scleroderma?

A

Female 30-50

201
Q

What are the features of limited cutaneous systemic sclerosis?

A

CREST
* C - Calcinosis (deposition of Ca2+ under skin)
* R - Raynaud’s phenomenon
* E - oEsophageal dysmotility
* S -Slerodactyly (fibrosis of skin of digits)
* T - Telangiectasia (dilation of small blood vessels)

202
Q

What are the features of diffuse cutaneous systemic sclerosis?

A

CREST + many internal organs
* Cardiovascular problems
- Hypertension + coronary heart disease
* Lung problems
- Pulmonary hypertension + pulmonary fibrosis
* Kidney problems
- Glomerulonephritis

203
Q

What is scleroderma (systemic sclerosis) caused by?

A
  • Chronic autoimmune inflammation
  • Triggerd anticentromere antibodies (ACAs)
204
Q

What is an environmental risk factor for scleroderma?

A

Silica dust and solvents

205
Q

Pathology of scleroderma (/systemic sclerosis)

A

Chronic inflammatory autoimmune disease → results in widespread damage to small blood vessels + skin → fibrosis (FGF sensitivity)

206
Q

What des the skin look like in scleroderma?

A

Hardening of skin looks like:
* Shiney + tight + without normal folds
* Most notable on hands + face

207
Q

What are the 3 components of a scleroderma (systemic sclerosis)?

A
  • Clinical features
  • Antibodies
    • (L: ACA, D: Anti-Scl-70 antibodies)
  • Nailfold capillaroscopy
208
Q

What are the serum antibodies in limted and diffuse cutaneous systemic sclerosis?

A
  • Limited: Anti-centromere antibodies (ANAs)
  • Diffuse: Anti-Scl-70 antibodies
209
Q

What is nailfold capillaroscopy?

A

Abnormal capillaries, avascular areas and micro-haemorrhages indicate systemic sclerosis

210
Q

How do you differentiate between systemic sclerosis and primary Raynaud’s?

A

Nailfold capillaroscopy

Raynauds = normal nailfold capillaries

211
Q

What is the management of systemic sclerosis?

A

No cure → steroids + ocassionally immunosuppressants
* Prevention of renal crisis → ACEi (ramipril)
* Raynaud’s phenomenon → amlodipine (vasodilator)
* Generalised skin involvement → topical emollient

212
Q

Complications of scleroderma

A

Vascular + fibrosing complications
* Renal crisis
* Fibrosis of lungs, heart, GI tract
* Skin ulcers
* Secondary skin infection
* Malabsorptive diarrhoea, steatorrhoea, weight loss
* Cardiac arrhythmias

213
Q

A patient presents with non-specific symptoms (includeing fatigue), vague musculoskeletal complaints, diffuse swelling of hands, and Raynaud’s. Possible diagnosis?

A

Systemic sclerosis
(scleroderma)

214
Q

Read: Systemic sclerosis info

A

Systemic sclerosis (SSc), also known as scleroderma, is a multi-system, autoimmune disease, characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of auto-antibodies.

215
Q

What does seronegative refer to?

A

“Seronegative” refers to the fact that these diseases are negative for rheumatoid factor →indicating a different pathophysiological mechanism of disease than is commonly seen in rheumatoid arthritis

216
Q

What is a spondyloarthropathy or spondyloarthrosis?

A

Refers to joint disease of the vertebral column

217
Q

Name 4 spondylarthropathies

A
  • Ankylosing spndylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Enteric arthritis
218
Q

Give some features of of spondyloarthropathies

A
  • Group of autoimmune diseases
    • Axial inflammation → spine + sacroiliac joints
  • Asymmetrical peripheral arthritis
    -** Absence of RF** → hence ‘seronegative’
  • Strong association with HLA-B27
219
Q

What class surface antigen is Human Leucocyte Antigen (HLA B27)?

A

Class I surface antigen on antigen-presenting cell

220
Q

Why is HLA B27 linked to molecular mimicry?

A

Infection → immune response → infectious agent has peptides very similar to HLA B27 molecule → auto-immune response triggered against HLA B27

221
Q

What does SPINEACHE stand for?

A
  • Sausage digit (dactylitis) – inflammation of tendon sheaths and joints in fingers
  • Psoriasis
  • Inflammatory back pain
  • NSAID good response
  • Enthesitis (heel)
  • Arthritis
  • Crohn’s/Colitis/elevated CRP (CRP can be normal)
  • HLA B27
  • Eye (Uveitis)
222
Q

If you see:
* Inflammatory back pain
* Asymmetrical (large joint) arthritis
* Skin psoriasis
* Inflammatory bowel disease
* Inflammatory eye disease
What disease group should you think of?

A

Spondylarthritis

223
Q

What is ankylosing spondylitis?

A

Chronic progressive inflammatory arthritis of the vertebral facet joints in spine + ribcage → leading to new bone formation + fusion of the joints → BAMBOO SPINE

224
Q

Define the term ankylosis

A

Joint fusion

225
Q

What spondyloarthropathy is characterised by having a painful ‘bamboo spine’?

A

Ankylosing spondylitis

226
Q

When does ankylosing apondylitis normally ocuur?

A

Late teens/early 20s

227
Q

What genetic association do 88% of pateints with ankylosing spondylitis have?

A

HLA-B27
(MHC class I)

228
Q

What diseases are associated with ankylosing spondylitis?

A
  • Crohn’s
  • Ulcerative colitis
229
Q

What are the joints affacted in ankylosing spondylitis?

A
  • Vertebral column
  • Sacroiliac joints
230
Q

Pathology of ankylosing spondylitis

A

Inflammation = causes pain + stiffness in these joints → leads to fusion of the spine + sacroiliac joints → bamboo spine

231
Q

A 20 y/o male presents with:
* Lower back pain + stiffness
* Sacroiliac pain (in the buttick region)

The pain + stiffness:
* Worse with rest
* Improves with movement
* Pain = worse at night + morning → wakes up at night
* Stiffness = takes more than 30 mins to improve in the morning

Possible diagnosis?

A

Ankylosing sponylitis

232
Q

Characterise the stiffness in ankylosing spondylitis

A
  • Slow onset (more than 3 months)
  • Lower back stiffness
  • Improves with activity
  • Takes more than 30 minutes to improve
233
Q

Where is the pain in ankylosing spondylitis?

A
  • Lower back
  • Sacroiliac pain (buttock region)
234
Q

What sign is present in late stage ankylosing spondylitis?

A

Kyphosis of the thoracic + cervical spine
(can’t look up and see the sun)

235
Q

What are the signs and symptoms of ankylosing spondylitis?

A

Signs: SPINEACHE
Symptoms:
* Develop of 3 months
* Buttock/thigh pain
* Neck or back pain/stiffness
* Systemic symptoms (weight loss + fatigue)

236
Q

Name a couple of associations with ankylosing spondylitis

A
  • Systemic symptoms (wt loss + fatigue)
  • Chest pain
  • Enthesitis → plantar fasciitis + achilles tendonitis
  • Dactylitis
  • Anaemia
  • Aortitis
  • Heart block
  • Inflammatory bowel disease
237
Q

What is the diagnosis criteria for ankylosing spondylitis?

A
  • Patients with > 3 months back pain
  • Age at onset <45
  • Sacroiliitis (XR/MRI) + > 1 SPINEACHE feature
238
Q

Ix for ankylosing spondylitis

A
  • ** X-ray pelvic**
    • Sacroilitis
    • Bamboo spine
  • MRI (more sensitive)
  • Bloods
    • Raised CRP/ESR
    • HLA-B27 positive
  • Schober’s test
239
Q

What is the Schober’s test and when is it used?

A

Ankylosing spondylitis
(Less than 20cm → indicates restriction in lumbar movement)

Mark a point 10cm above and 5cm below L5 vertebrae (15cm apart from each other).

240
Q

Mx of ankylosing spondylitis

A
  • First line: NSAIDs (naproxen) + physiotherapy
  • Second line:
    • Steroids during flares
    • TNFa inhibitor (infliximab)
241
Q

What is a major complication of ankylosing spondylitis?

A

Vertebral fractures

242
Q

Patinet presents with back pain that is of insidious onset, is worse in the morning, and improves with exercise. Possible diagnosis?

A

Ankylosing spondylitis

243
Q

What is psoriatic arthritis?

A

Autoimmune chronic inflammatory arthritis associated with psoriasis (red scaly patches)

244
Q

What genetic association is linked to psoriatic athritis?

A

HLA-B27

245
Q

What is thought to be the cause of psoriatic arthritis?

A

Local trauma → induced dysregulated immune response → local tissue destruction
Koebner phenomenom

246
Q

Pathology of psoriatic arthritis

A

T-cell mediated attack of joints in perople with psoriasis

247
Q

What are the signs of psoriatic arthritis?

A
  • Plaques of psoriasis on the skin
  • Pitting of nails
  • Onycholysis (separation of the nail from the nail bed)
  • Dactylitis (inflammation of the full finger)
  • Enthesitis
248
Q

What joints are most commonly affected in psoriatic arthritis?

A

Peripheral arthritis in hands + feet

249
Q

What is the tool used to assess psoriatic arthritis?

A

PEST Tool
(Psoriasis Epidemiological Screening Tool)

250
Q

What factors does the PEST tool take into account?

A
  • Joint pain
  • Swelling
  • History of arthritis
  • Nail pitting
251
Q

First line Ix for psoriatic arthritis

A
  • ** PEST Tool**
  • Plain film **x-ray of hands + feet **
    • Erosion of DIP joint
    • ‘Pencil-in-cup’ deformity
  • Bloods
    • HLA-B27 positive
    • ESR/CRP (normal or elevated)
252
Q

What spondyloarthropathy is shows a ‘pencil-in-cup’ malformation in DIP joint on an x-ray?

A

Psoriatic arthritis

253
Q

What are some DDx of psoriatic arthritis?

A
  • Rheumatoid arthritis
  • Gout
  • Reactive arthritis
254
Q

What are the first and second line treatment options for psoriatic arthritis?

A

First line:
* NSAIDs (naproxen)
* DMARDs (sulfasalazine, methotrexate)
* Intra-articular corticosteroid injection (methylprednisolone acetate)

Second line:
* TNFa inhibitor (infliximab)

255
Q

Complications of psoriatic arthritis?

A
  • Eye disease (conjunctivitis)
  • Aortitis
  • Amyloidosis
  • Cardiovascular disease
  • Arthritis Mutilans
256
Q

What is arthritis mutilans?

A
  • Most severe form of psoriatic arthritis
  • Osteolysis (destruction) of the bones around the joints of the digits
  • Progressive shortening of the digit
257
Q

How do you diferentiate between psoriatic arthritis and RA?

A
  • Dactylitis is only present in psoriatic arthritis
  • Psoriatic arthritis is RF and anti-CCP negative
258
Q

Define reactive arthritis

A

Inflammatory arthritis - occurs after exposure to certain GI or GU infections

  • Typically causes acute monoarthritis → affecting a single joint in the lower limb (most often the knee)
  • Typically presents as:
    • Warm
    • Swollen
    • Painful joint
259
Q

Which spondylarthropathy can be remembered as ‘can’t see, pee or climb a tree’?

A

Reactive arthritis

260
Q

What causes reactive arthritis?

A
  • GI infection (diarrhoeal illness)
  • GU infection (STIs) - chlamydia
  • HLA-B27 linked
261
Q

What are the 3 features of reactive arthritis?
(Reiter’s syndrome)

A
  • Conjuctivitis (cant see)
  • Urethritis, circinate balantitis (cant pee)
  • Oligoarthritis (cant climb a tree)
262
Q

A patient develops arthritic symptoms in knee after testing positive for chlamydia 3 weeks ago. Possible diagnosis?

A

Reactive arthritis

263
Q

Ix for reactive arthritis

A
  • ESR/CRP (raised)
  • X-rays (asymmetrical sacroiliitis, enthesitis)
  • Joint aspiration (exclude septic arthritis)
  • Urogenital + stool cultures
    • STIs (NAAT)
  • RF and ANA negative
  • HLA-B27 (sensitivity + specificity are low)
264
Q

DDx for reactive arthritis

A
  • Septic arthritis
  • Gout
265
Q

Treatment of reactive arthritis
(first and second line)

A

First line:
* NSAID (naproxen)
* Corticosteroids (prednisolone)

Seond line:
* DMARD (sulfasalazine)

266
Q

Patients presents with fever, peripheral and axial arthritis, enthesitis (inflammation where tendons insert into bone), dactylitis (swelling of an entire finger or toe), conjunctivitis and iritis, and skin lesions including circinate balanitis and keratoderma blennorrhagicum. Possible diagosis?

A

Reactive arthritis

267
Q

Describe the arthritis aspect of reactive arthritis

A
  • Asymmetrical oligoarticular arthritis
  • Affects large joints of lower limb
268
Q

What is enteric arthritis?

A

Arthritis that occurs with IBD (Crohn’s and UC)

269
Q

What are the signs and symptoms of enteric arthritis?

A

GI:
* Abdomianl pain
* Blood in stool
* Diarrhoea
* Wt loss

Arthritis:
* Usually affects arms + legs
* Stiffness
* Swelling
* Tenderness of joints

270
Q

Ix of enteric arthritis

A
  • Arthrocentesis
  • Stool culture
  • Colonoscopy + biopsy
  • CRP/ESR
  • X-ray of affected joints
271
Q

Mx of enteric arthritis

A
  • DMARDs (methotrexate, sulfasalazine)
  • NSAIDs (naproxen)
  • Tumour necrosis factor alpha inhibitor (infliximab)
  • Physiotherapy
272
Q

What cancers metastasise to bone?

A

PoRTaBLe
* P = prostate
* R = renal
* T = thyroid
* B = breast
* L = Lung

273
Q

When should you consider cancers of the bone (metastasis)/ spinal metastases?

A

Patient presenting with back pain
(Or cauda equina)

274
Q

Define antiphospholipid syndrome

A
  • Associated with antiphospholipid (aPL) antibodies
  • Blood becomes hypercoagulable
  • Characterised by
    • Thrombosis (arterial or venous)
    • Recurrent miscarriage
    • aPL postive
  • Can be primary or secondary to an autoimmune condition (SLE)
275
Q

Pathology of antiphospholipid syndrome

A

Antiphospholipid antibodies (aPL) = bind to targets → induce hypercoagulable state

276
Q

Clinical presentation of antiphsophlipid syndrome

A

Major clinical features = result of thrombosis

Causes CLOTS:
- C - Coagulation defect
- DVT, PE; MI, stroke
- L - Livedo reticularis - lace-like purplish discolouration of skin
- O- Obstetric issues
- Miscarriage, pre-eclampsia, still birth
- T - Thrombocytopenia (low platelets)

277
Q

Criteria for antiphsopholipid syndrome

A
  • History of thrombosis /pregnancy complication
  • Peristent antibodies
278
Q

Ix for antiphospholipid syndrome

A
  • Serum antibodies
    • Anti-cardiolipin antibody test
    • Anti-B2-glycoprotein test
    • Lupus anticoagulant test
  • FBC (thrombocytopenia)
  • ANA or dsDNA (SLE)
279
Q

Name a differential for antiphosphlipid syndrome

A

Inherited thrombophilia

280
Q

Treatment for antiphospholipid syndrome

A
  • Management of risk factors of thrombosis (smoking etc)
  • LMWH (dalteparin)
  • Long term warfarin (INR 2-3)

Warfarin is contraindicated in pregnancy

281
Q

What is polymyositis?

A

Autoimmune chronic inflammation of muscles

282
Q

What is dermatomyositis?

A

Autoimmune connective tissue disorder - chronic inflammation of the skin + muscles

283
Q

What Rx for dermatomyositis and polymyositis?

A

Dermatomyositis:
- 60yrs
- Malignancy

Polymyositis:
- Autoimmune disease
- Chronic viral infection (HIV)

HLA-D8/DR3 appear to be at highest risk

284
Q

Pathology of dermatomyositis and polymyositis

A
  • Dermatomyositis – immune system attacks muscle and skin
  • Polymyositis – immune system attacks the muscles due to molecular mimicry
285
Q

Sx of polymyositis and dermatomyositis

A

Polymyositis:
* Symmetrical progressive muscle weakness and wasting affecting large and proximal muscles e.g. shoulders and hips

Dermatomyositis:
* Same as polymyositis
* Gottron’s sign = scaly erythematous plaques over knuckles
* Purple discolouration of eyelids

286
Q

Inflammation in muscle cells (myositis) leads to the release of which enzyme in the blood?

A

Serum creatinine kinase

287
Q

What is the first line and gold standrd Ix for polymyositis/dermatmyositis?

A

First:
* Bloods:
- Serum creatine kinase (elevated)
- Anti-nuclear antibody (ANA) (positive)
- Anti-Jo-1 antibodies
* Electromyography(EMG) (abnormal spontaneous activity)

Gold standard:
* Muscle biopsy
* Skin biopsy

288
Q

Management for dermatomyositis and polymyositis

A

First line:
* Corticosteroids (prednisolone)
* Physiotherapy + occupational therapy

Second line:
* Immunosuppressants (azathioprine)
* Infliximab

289
Q

How is polymyalgia rheumatica chacterised?

A

Chronic systemic rheumatic inflammatory disease
* Aching + morning stiffness in the neck, shoulder, pelvic girdle

290
Q

What are the core features of polymyalgia rheumatica?

A
  • Bilateral shoulder pain - may radiate to the elbow
  • Bilateral pelvic girdle pain
  • Worse with movement
  • Interferes with sleep
  • Stiffness for at least 45 mins in the morning
291
Q

What regions of the body are affected by polymyalgia rheumatica?

A
  • Neck pain
  • Shoulder girdle pain + stiffness
  • Pelvic girdle pain + stiffness
292
Q

What is a clinical diagnosis for polymyalgia based on?

A

Clincial presentation + response to steroids
(exclude other conditions)

293
Q

What is the treatment for polymyalgia rheumatica?

A

Prednisolone

294
Q

What condition is usually described by patients as ‘difficultulty rising from seated or prone ppositions’?

A

Polymyalgia rheumatica

295
Q

What genetic mutation is Marfan’s disease caused by?

A

Autosomal dominant inherited
(Fibrillin-1 gene)

296
Q

What are the features of Marfan syndrome?

A

Abnormal connective tissue
* Tall stature
* Long neck
* Long limbs
* Long fingers (arachnodactyly)
* High arch palate
* Hypermobility
* Pectus carinatum or pectus excavatum
* Downward sloping palpable fissures

297
Q

Ehlers-Danlos syndrome definition

A

The most common presenting complaint for hypermobile EDS is joint pain and hypermobility, however abnormalities in collagen make it a multi-system disorder leading to symptoms across multiple areas of the body:
* Hypermobility in joints4

298
Q

What is osteomalcia?

A
  • Soft bones from insufficient vitamin D
299
Q

How does osteomalacia present?

A

Weak bones, bone pain, muscle weakness and fractures.

300
Q

Treatment of osteomalacia

A

Vitamin D deficiency

301
Q

What is the lab investigation for Vitamin D?

A

Serum 25-hydroxyvitamin D

Kyla's Phase 2a Flashcards (11 decks)

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