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Phase1c Medicine > Msk > Flashcards

Msk Flashcards

1
Q

What is osteoarthritis?

A

Asymmetrical degenerative synovial joint disease

Cartilage destruction exceeds repair causing pain and instability

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2
Q

What are the primary causes of osteoarthritis?

A 
Obese
Older
Female
Occupation
Post menopausal
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3
Q

What is secondary osteoarthtiis?

A

Inflammatory -Rh Septic arthritis

Congenital -DDh

Metabolic

Altered joint architecture- and acquires more joint damage

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4
Q

What is the presentation of osteoarthritis?

A

Morning stiffness for approximately 15 minutes

Joint pain - Gradual onset, worse on activity, better with rest

High-use or weight bearing joints - hip, knee, or DIP, PIP , 1st CMC, wrist

(Late) - Night pain, instability , deformity, loss of function

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5
Q

What are the common examination findings for osteoarthritis?

A

Crepitus - bone surfaces grinding against each other

Effusion, erythema

Squaring (Base of thumb)

Heberden’s and bouchard’s nodes

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6
Q

What does a plain X-ray reveal in osteoarthritis?

A

Loss of join space (joint space narrowing)
Osteophytes
Subarticular sclerosis
Subchondral cysts

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7
Q

What is the first-line management for osteoarthritis?

A

oral paracetamol/topical NSAIDs, topical capsaicin (Stepwise analgesia
Oral NSAID + PPI
Opiates

Joint replacement
Intra-articular steroids

Lifestyle - physiotherapy

occupational therapy

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8
Q

What is co-prescribed with NSAIDs?

A

Proton pump inhibitor

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9
Q

What is rheumatoid arthritis?

A

Autoimmune, chronic (>6 weeks) and progressive inflammation of synovial lining, tendon sheaths and bursa

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10
Q

What genes are associated with rheumatoid arthritis?

A

HLA DR4, DR1

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11
Q

How is rheumatoid arthritis diagnosed?

A

Clinical diagnosis

Symmetrical polyarthritis _ extraarticular manifestations

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12
Q

What is polyarthritis?

A

> 4 joints

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13
Q

What is the presentation of rheumatoid arthritis?

A

Pain and stiffness in hands and wrists

  • Worst in the morning, resolves over the course of the day
  • Fatigue
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14
Q

What examination findings is seen in rheumatoid arthritis?

A

Swan-neck deformity
Ulnar deformation
Swelling and tenderness

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15
Q

Which joints are commonly affected in rheumatoid arthritis?

A

Wrist, ankle, MCP, PIP and MTP

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16
Q

What joints are commonly spared in rheumatoid arthritis?

A

Distal interphalangeal joints

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17
Q

What are the chronic signs seen in rheumatoid arthritis?

A

Z-deformity of the thumb - hyperextension of the IP joint and fixed flexion and subluxation of MCP joint

Ulnar deviation at the MCP

Radial deviation at the wrist

Swan-neck deformity - DIP is flexed

Boutonniere’s deformity - Permanent flexion of PIP joint and overextension of DIP joint

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18
Q

What are the extra-articular signs in rheumatoid arthritis?

A

Rheumatoid nodules

-Episcleritis, slceritis

Secondary Sjogren’s/Sicca

  • Lymphandenopathy
  • Pericarditis
  • Carpal tunnel syndrome
  • Pulmonary fibrosis/pleuritis/bronchiolitis obliterans
  • Tenosynovitis, bursitis

Felty’s syndrome - triad of Rheumatoid arthritis, splenomegaly and neutropenia

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19
Q

What is Felty’s syndrome?

A

Felty’s syndrome - triad of Rheumatoid arthritis, splenomegaly and neutropenia

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20
Q

What investigations are performed in RH Arth?

A

Rheumatoid factor - IgM antibody

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21
Q

What is rheumatoid factor?

A

IgM antibody targeting the Fc portion IgG antibody- immune activation

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22
Q

What is the most sensitive marker for diagnosing rheumatoid arthritis?

A

Anti-CCP

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23
Q

What indicates aggressive and severe rheumatoid disease?

A

Positive antibodies and raised inflammatory markers (Associated with worse prognosis)

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24
Q

What are the urgent referral indications in rheumatoid arthritis?

A

Small joints of hands, feet and multiple joints

Sx >3 months

Persistent synovitis

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25
Q

What is the acute management for rheumatoid arthritis?

A

Short course steroids for acute flares

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26
Q

What is the management for rheumatoid arthritis?

A

NSAIDs and COX-2 inhibitors co-prescribed with PPI

DMARDs

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27
Q

Which DMADs are prescribed in rheumatoid arthritis?

A

Methorexate, Sulfasaazline
Anti-TNFs
Rituximab (Consider TB)

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28
Q

What are the four common forms of seronegative spondyloarthropathies?

A

Psoriatic arthritis
Enteropathic arthritis
Ankylosing spondylitis
Reactive arthritis

Common factors
Male > female
No Rh factor
HLA-B27

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29
Q

Which gene is implicated in seronegative spondys?

A

HLA-B27

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30
Q

What skeleton is affected in ankylosing spondylitis?

A

Axial skeleton

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31
Q

What is ankylosing spondylitis?

A

Chronic progressive inflammatory arthropathy of axial skeleton

-Peripheral joints, entheses (tendon/ligament attachments) and extra-articular sites

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32
Q

What is the presentation of ankylosing spondylitis?

A

Pain and stiffness of lower back and hips upon waking

Better on physical activity

Entheses - plantar asciitis

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33
Q

What extra-articular manifestations are present in ankylosing spondylitis?

A

Anterior uveitis
Apical lung fibrosis
Aortic regurgitation
+Psoriasis, IBD sx

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34
Q

What are the late changes seen in ankylosing spondylitis?

A

Kyphosis
Loss of lumbar lordosis
Neck extension

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35
Q

What specific tests are performed in ankylosing spondylitis?

A

Schober’s test - lumbar motility (Point-point reduced distance increase)

Tragus to wall

Stress tests - Gaenslen;s - sarcoiliac joint pain

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36
Q

What radiological investigations are performed in ankylosing spondylitis?

A

X-ray

MRI

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37
Q

What is revealed in an X-ray for ankylosing spondylitis?

A

SI joint - symmetrical bilateral sacroiliitis

Subchondral erosions, sclerosis

Bamboo spine

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38
Q

What is reactive arhtritis?

A

Sterile, seronegative joint inflammation in response to extra-articular infection

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39
Q

Why does reactive arthritis occur?

A

Initial activation of immune system by microbial antigen stimulates AI reaction affecting skin, eyes and joints

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40
Q

What is Reiter’s syndrome?

A

Arthritis, urethritis, conjunctivitis

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41
Q

What is the presentation of reactive arthritis?

A

Painful, swollen, unilateral joint inflammation

Associated with past infective history (Related symptoms)

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42
Q

What are the extra-articular manifestations of reactive arthritis?

A

Keratoderma blenorrhagicum

Reiter’s

Circinate balanitis - painless ulcers/plaques

Oral ulcers - painless cystitis/prostatitis

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43
Q

What is the presentation of septic arthritis?

A

Acute monoarthritis

Hot, swollen, erythematous joint with restriction of movement

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44
Q

What is the acute presentation of gout?

A 
Acute mono-arthritis
1st MTP (Podagra)
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45
Q

What is the acute presentation of pseudogout?

A

Acute monoarthritis
Large joints - knee
Polyarticular (chronic)

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46
Q

What are the causes of septic arthritis?

A

Caused by current infection
Haematogenous spread of direct inoculation

Staph aureus >30 years
Neisseria gonorrhoea <30 years

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47
Q

What is the most common organism for causing septic arthritis in <30 years?

A

Neisseria gonorrhoea

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48
Q

What is the most common organism for causing septic arthritis >30 years?

A

Staph aureus

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49
Q

What factors can precipitate gout?

A

Trauma, infection
Monosodium urate crystals
- Hyperuricaemia - inceased intake (purine foods), increased production - tumour lysis syndrome or decreased excretion
High alcohol intake

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50
Q

What type of crystals are deposited in pseudogout?

A

Calcium pyrophosphate crystals

-HyperPTH, hypoPO4, hypoMg, metabolic

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51
Q

What are the risk factors for gout?

A 
Alcohol
High purine diet
Obesity
Male
Diuretics
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52
Q

What are the risk factors for pseudogout?

A

RFs: Elderly, female

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53
Q

What crystals are seen in gout?

A

Negatively birefringent needle-shaped crystals

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54
Q

What crystals are see in psuedogout?

A

Positively birefringent rhomboid-shaped crystals

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55
Q

What XR findings are seen in gout?

A

Rat-bite erosions

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56
Q

What XR findings are seen in pseudogout?

A

Chondrocalcinosis

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57
Q

What is the management for septic arthritis?

A

Empirical IV Abx for 2 weeks + 4 weeks oral ABx

-Cover S.aureus and streptococcous

Stop any biologic therapies (12 months of forever for prosthetic joint)

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58
Q

What is the management for acute gout attacks?

A

NSAIDs
Colchicine (anti-mitotic)
Corticosteroids

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59
Q

What is the prophylactic treatment for gout?

A

Allopurinol

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60
Q

What is the management for psuedogout?

A

Intra-articular steroids

NSAIDs or colcichine

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61
Q

What is osteomyelitis?

A

Infection of bone due to haematogenous spread

  • IVDU
  • Immunosuppression
  • Diabetes

Contiguous spread - cellulitis or localised infection

Direct inoculation - penetrating injury, ulcers, surgery

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62
Q

What is the most common cause of osteomyellitis?

A

Staph aureus

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63
Q

In patients w sickle cell disease which type of osteomyelitis is common?

A

Salmonella

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64
Q

What is the presentation of osteomyellitus?

A 
Non-specific pain in affected area
Fever
Malaise
Rigors
Ski lesions, sore throat

Localised erythema, swelling and warmth
-Reduced ROM of affected join
Discharge associated with wound/ulcer

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65
Q

What are the investigations for osteymyelltiis?

A

Bloods - raised WCC, ESR/CRP

MRI - see darkening, periosteal thickening

Bone culture - Causative organism

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66
Q

What is the management for ostemyellits?

A

High dose IV ABx empirical Abx then adapt to cultured organism
Surgical debridement - biofilm

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67
Q

What is ankylosing spondylitis?

A

A seronegative chronic inflammatory arthropathy affects preferentially the axial skeleton and large proximal joints

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68
Q

What type of arthritis is associated with ankylosing spondylitis?

A

Seronegative

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69
Q

Which gene is associated with ankylosing spondylitis?

A

HLA-B27 gene

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70
Q

Which joints are predominantly affected in ankylosing spondylitis?

A

Spine and sacroiliac joints

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71
Q

Where does the inflammation begin in ankylosing spondylitis?

A

At the entheses (where ligaments attach to the vertebral bodies)

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72
Q

Which vertebrae are affected in ankylosing spondylitis?

A

Lumbar vertebrae

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73
Q

What shape are the vertebral bodies in ankylosing spondylitis?

A

Squaring

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74
Q

What are syndesmophytes in ankylosing spondylitis?

A

Bridging the margins between adjacent vertebrae + fusion

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75
Q

What is the long course of ankylosing spondylitis presentation?

A

Kyphosis, neck hyper-extension and spino-cranial ankyloses

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76
Q

What is the initial presentation of ankylosing spondylitis?

A

Lower back pain and sacroiliac pain

Disturbed sleep

Progressive loss of spinal movement

Pleuritic chest pain (Due to costovertebral joint involvement)

Heel pain (Due to plantar fasciitis)

Non-specific symptoms - Malaise and fatigue

Blindness due to acute iritis

Pain pattern

  • Worse in the morning
  • Better with activity
  • Worse when resting
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77
Q

Describe the pain profile associated with ankylosing spondylitis

A

Better with activity

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78
Q

What are the examination features of ankylosing spondylitis?

A

Hyper-extended neck

Loss of lumbar lordosis

Flexed hips and knees

Reduced range of spinal movement (particularly hip rotation)

Reduced lateral spine flexion

Tenderness over sacroilliac joints

Later stages

  • Kyphosis
  • Spinal fusion
  • Question-mark posture
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79
Q

What are the extra-articular manifestations of ankylosing spondylitis?

A 
Anterior uveitis
Apical lung fibrosis
Achilles' tendinitis
Amyloidosis
Aortic regurgitation
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80
Q

What is the Schober’s test?

A
  • Two fingers are placed on the patients back about 10 cm apart.
  • The patient is instructed to bend over
  • The distance between the two fingers should increase by >5 cm on forward flexion. Reduced movement  Suggests ankylosing spondylitis.
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81
Q

What is the first-line investigation for ankylosing spondylitis?

A

Radiograph - Reveals Vertical syndesmophytes

And Bamboo spine appearance

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82
Q

What additional test should be performed in ankylosing spondylitis?

A

Lung function tests to assess for mechanical ventilatory impairment due to kyphosis

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83
Q

What is the first-line management for ankylosing spondylitis?

A

NSAIDs (Naproxen)

  • Analgesia
  • Intra-articular corticosteroid injection (peripheral joint)
  • Sulfasalazine or methotrexate
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84
Q

What DMARDs are used for severe ankylosing spondylitis?

A

TNF-alpha inhibitors (Adalimumab and etanercept) for severe disease

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85
Q

What is reactive arthritis?

A

Characterised by sterile arthritis occurring after an extra-articular infection particularly urogenital (e.g., Chlamydia trachomatis) and gastrointestinal (e.g., Salmonella, Shigella, campylobacter).

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86
Q

What urogenital infection is commonly associated with reactive arthritis?

A

Chlamydia trachomatis

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87
Q

What is the epidemiology of reactive arthritis?

A
  • 20x more common in males

* Age of onset: 20-40 years

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88
Q

What is the presentation of reactive arthritis?

A

Urethritis

Arthritis, low back pain (Due to sacroiliitis), painful heels and conjunctivitis

Arthritis

  • Assymmetrical oligoarthritis
  • Affects the lower extremiites
  • Sausage shape digits

Circinate Balanitis

  • Scaling red patches on the glans
  • Painless

Signs of conjunctivitis
-Anterior uveitis- Painful red eye

Keratoderma blennorrhagia
-Brownish-red macules
found on the soles and palms.

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89
Q

What blood investigations are carried out in reactive arthritis?

A 
Bloods
•	FBC
•	High ERS and CRP
•	HLA-B27 testing
•	ANA and Rheumatoid factor negative
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90
Q

What urine dipstick test would reveal reactive arthritis?

A

Urine

• Screen for chlamydia trachomatis

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91
Q

What would a plain X-ray reveal in reactive arthritis?

A

Evidence of asymmetrical sacroiliitis and enthesitis (Especially of the Achilles’ tendon).

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92
Q

What is the first-line management for reactive arthritis?

A

Symptomatic relief
-NSAID - Naproxen/ibuprofen/indomethacin

Corticosteroid- Prednisolone

Ongoing or chronic reactive arthritis
-Sulfalazine 500mg OD

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93
Q

Define rheumatoid arthritis

A

A chronic inflammatory systemic disease characterised by symmetrical deforming peripheral polyarthritis and extra-articular manifestations.

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94
Q

What are the common joints affected in rheumatoid arthritis?

A

• Polyarthritis: Swelling of small joints of the hand and wrists (MCP, PIPs and MTP joints).

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95
Q

Which antibody is associated with rheumatoid arthritis?

A 
Anti-CCP
Rheumatoid factor (IgM antibody)
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96
Q

What is the typical presentation of rheumatoid arthritis?

A

Symmetrical, swollen, painful and stiff small joints of hands and feet
-Morning stiffness

Joint pain -Polyarthritic involvement including large and small joints

Swelling

Morning stiffness >1 hour - improves motility

Impaired function

-Affects peripheral joints symmetrically

systemic symptoms: Fever,fatigue, weight loss, pericarditis, pleurisy

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97
Q

What are the early signs of rheumatoid arthritis?

A
  • Spindling of fingers
  • Swelling of MCP and PIP or MTP joints- Symmetrical.
  • Warm, tender joints
  • Reduction in range of movement
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98
Q

What are the late signs of rheumatoid arthritis?

A
  • Symmetrical deforming arthropathy.
  • Radial deviation of the wrist
  • Swan-neck deformity1
  • Boutonniere deformity2
  • Z deformity of the thumb
  • Trigger finger (Inability to straighten the finger, tendon nodule papule)
  • Tendon rupture
  • Wasting of small muscles of the hand
  • Palmar erythema.
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99
Q

What is a swan-neck deformity in rheumatoid arthritis?

A

In a swan neck deformity, the PIP joint is hyperextended with flexion at the distal interphalangeal (DIP) joint.

100
Q

What is a Boutonniere deformity?

A

In a boutonniere deformity, there is flexion the PIP joint with hyperextension of the DIP joint.

101
Q

Why does ulnar deviation occur in rheumatoid arthritis?

A

Ulnar deviation of fingers because of subluxation. Inflammation of the MCP joints causes the fingers to become dislocated. The tendons pull on the dislocated joints, the fingers tend to drift towards the ulnar side.

102
Q

Boutonniere’s and swan-neck deformities are associated with what type of arthritis?

A

Rheumatoid arthritis

103
Q

What extra-articular features are associated with rheumatoid arthritis?

A

Subcutaneous nodules - Central area of fibrinoid necrosis surrounded by histocytes

Vasculitis

Occular inflammation -episcleritis

Neuropathies

Amyloidosis

Lung diseae

Felt’s syndrome

104
Q

What is Felt’s syndrome?

A

Triad of splenomegaly, leukopenia and rheumatoid arthritis

105
Q

Which finger joint is particularly affected in rheumatoid arthritis within the hand?

A

The proximal-interphalangeal joint

106
Q

What do rheumatoid nodules suggest?

A

presence confirms diagnosis of rheumatoid arthritis and invariably associated with rheumatoid factor

107
Q

What is a severe complication of vasculitis?

A

Digital ischaemia

108
Q

Which ANA is highly-specific for rheumatoid arthritis?

A

Anti-CCP antibodies

109
Q

What type of anaemia is associated with rheumatoid arthritis?

A

Anaemia of chronic disease

110
Q

What investigation should be performed on suspected rheumatoid to differentiate it from septic arthritis?

A

Joint aspiration

111
Q

What X-ray features are associated with rheumatoid arthritis?

A 
BONDS
Bone erosions
Osteopenia - Low bone mineral density 
Narrowing of join space
Deformity
Soft tissue swelling
112
Q

What investigation is performed to detect synovitis in rheumatoid arthritis?

A

Ultrasound

113
Q

Bony erosions and osteopenia is more associated with what type of arthritis?

A

Rheumatoid arthritis

114
Q

What does joint space narrowing indicate in rheumatoid arthritis?

A

Indicates articular cartilage loss

115
Q

What is the 1st-line management for rheumatoid arthritis?

A

Methotrexate in combination with hydroxychloroquine (DMARDs)

116
Q

What is the 2nd line management for rheumatoid arthritis?

A

Biological therapies (offer potent and targeted strategies)

117
Q

What is the short-term management for acute exacerbations of rheumatoid arthritis?

A

Glucocorticoid therapy (Prednisolone)

118
Q

What type of drug is inflixiimab?

A

Biologics

-Anti-TNF

119
Q

What is osteoarthritis?

A

Age-related degenerative synovial joint disease when cartilage destruction exceeds repair, causing pain and disability.
• Deterioration of cartilage in joints results in bone rubbing together, and creating stiffness, pain, and improved movement.

120
Q

What are the commonly affected joints in osteoarthritis?

A

DIP, thumb, carpometacarpal joints, knees

121
Q

What is the presentation of osteoarthritis?

A 
Joint pain and discomfort – Localised to knee or hip.
•	Use-related
•	Pain on movement and crepitus
•	Worse at end of day
•	Background pain at rest
•	Stiffness or gelling after inactivity lasting <1 hour.
•	Difficulty with certain movements
•	Feelings of joint instability
•	Restriction walking, climbing stairs
•	Systemic features are usually absent
122
Q

What examination findings are present in osteoarthritis?

A

• Local joint tenderness
• Bony swellings along joint margins
- Heberden’s nodes: Distal interphalangeal joint
- Bouchard’s nodes: Proximal interphalangeal joint.
• Crepitus and pain during joint movement
• Restriction of range of joint movement
• Joint effusion

123
Q

What are Herbden’s nodes?

A

Bony swellings along the distal interphalangeal joint

124
Q

What are Bouchard’s nodes?

A

Bony swellings along the proximal interphalangeal joint

125
Q

What does a joint X-ray reveal in osteoarthritis?

A

Loss of joint space (Narrowing)

Osteophytes

Subchondral cysts

Subarticualr slcerosis

126
Q

What is the first-line management for osteoarthritis?

A

Paracetamol, codeine, NSAIDs, cox-2 inhibitors

Topical NSAIDs

Intra-articular injections for symptomatic relief

127
Q

What is septic arthritis?

A

Septic arthritis is an acute joint inflammation resulting from intra-articular infection.
• Can deteriorate a knee within 24 hours.
• Predominantly affects the knee.

128
Q

What is the aetiology of septic arthritis?

A

– In most cases, there is systemic infection allowing for haematogenous spread.
• Monoarthritis (Single joint affected)
• Consider septic arthritis in a patient presenting with acute pain, red hot and swelling of joint, particularly if fever.

129
Q

What are the risk factors for septic arthritis?

A
  • Immunosuppressed patients, pre-existing joint damage, and intravenous drug use (IVDU).
  • Recent orthopaedic procedures
  • Osteomyelitis
  • Diabetes mellitus
  • Rheumatoid arthritis
  • Chronic renal failure
  • Prosthetic joints – infection here is particularly difficult to treat
  • Alcoholism
130
Q

What are the common causative organisms for septic arthritis?

A
  • Staphylococcus aureus

* TB

131
Q

What is the common causative organism for 16-40 in septic arthritis?

A

• Neisseria gonorrhoeae

132
Q

What is the presentation of septic arthritis?

A
  • Sudden onset
  • Fever
  • Excruciating joint pain
  • Joint redness, swelling and loss of joint function
  • Usually a monoarthropathy (affecting one large joint)
  • Tuberculous arthritis develops more slowly and is more chronic.
133
Q

What are the examination findings for septic arthritis?

A
  • Painful, hot, swollen
  • Immobile joint
  • Erythema
  • Severe pain prevents passive movement
  • Pyrexia
134
Q

What is the first-line investigations for septic arthritis?

A

URGENT: Joint aspiration
• In infective arthritis, the aspirate will be grossly purulent.
• Send synovial fluid for MC&S  Microscopy to exclude crystal arthritis.
- PCR used if suspected viral aetiology.

135
Q

What does an FBC reveal in septic arthritis?

A

Raised WCC and neutrohils

High CRP and ESR

136
Q

What is the first-line management for septic arthritis?

A

Emergency: Temporary joint immobilisation with a splint + Analgesia.
• URGENT: Surgical lavage and intravenous antibiotics – Symptomatic relief.

137
Q

What is gout?

A

Gout: A disorder of uric acid metabolism causing recurrent bouts of acute arthritis caused by deposition of monosodium urate crystals in joints, and soft tissues and kidneys.
• Tophi around the joints and potential joint destruction.
• Affects the first toe (Podagra), foot, ankle, knee, fingers, wrist, and elbow.

138
Q

What are the crystals associated with gout?

A

Monosodium urate crystals

139
Q

What describes the involvement for the first toe in gout?

A

Podagra

140
Q

What are the risk factors for gout?

A

The main metabolic disturbance is hyperuricaemia- High plasma urate (>6.8mg/dL).
• Monosodium urate crystals deposit in joints leading to inflammation and pain.
This may be caused by:
• Increased urate intake or production
• Increased dietary intake of purines – Shellfish, anchovies, red meat.
• Increased nucleic acid turnover – Lymphoma, leukaemia, psoriasis.
• Increased synthesis of urate – Lesch-Nyhan Syndrome.

Decreased renal excretion 
•	Idiopathic
•	Dehydration
•	Alcohol excess
•	Drugs (Ciclosporin, alcohol, loop diuretics)
•	Renal dysfunction.
141
Q

What is the most common joint affected in gout?

A

Typical presents with an acute monoarthropathy with severe joint inflammation >50% occur at the metatarsophalangeal joint of the big toe (Podagra).
• A sensation of the toe is on fire.

142
Q

What are tophi?

A

Urate deposits (Tophi) in the pinna, tendons, joints, and renal disease

143
Q

What is the acute presentation of gout?

A
  • Sudden excoriating monoarticular pain – Usually affecting the metatarsophalangeal joint of the great toe (Podagra).
  • Symptoms peak at 24 hours (Rapid-onset 10+ severity).
  • They resolve spontaneously over 7-10 days
  • Sometimes acute attacks can present with cellulitis, polyarticular or periarticular involvement.
  • Attacks are often recurrent
  • Patients are symptom-free between attacks.
  • Joint stiffness, warm, swollen and tender
144
Q

What investigations are performed in gout?

A

Synovial fluid aspirate

Bloods - FBC, U&Es, urate, ESR

AXR/KUB film

145
Q

What does a synovial fluid aspirate reveal in gout?

A

Negatively birefringent needle-shaped crystals

146
Q

What is the first-line management for an acute attack of gout?

A

Acute attack: NSAIDs. Colchicine if NSAIDs are contraindicated.
• Intra-articular corticosteroids
• Intramuscular ACTH for difficult cases.

147
Q

What is the prophylactic management for gout?

A

Allopurinol (Xanthine oxidase inhibitor)

148
Q

What is the advice for gout?

A

Reduce meat

Alcohol intake

149
Q

What are the complications for gout?

A

Renal failure, urate urolithiasis, urate nephropathy, secondary infection, or ulceration of tophi.

150
Q

What is pseudogout?

A

Pseudogout is defined as arthritis associated with the deposition of calcium pyrophosphate dihydrate (CPPD) crystals in the joint cartilage.

151
Q

What crystals are associated with pseudogout?

A

calcium pyrophosphate dihydrate

152
Q

What are the causes of pseudogout?

A
  • Haemochromatosis
  • Hyperparathyroidism
  • Hypomagnesaemia
  • Hypophosphatasia
153
Q

What is the examination for crystal arthropathy (Pseudogout)?

A

Painful, swollen joint (knee, ankle, shoulders, elbow and wrist)

154
Q

Which joints are affected in pseudogout?

A

Knee
Shoulders
Elbow and wrist

155
Q

What investigation findings are associated with pseudogout?

A
  • High WCC in acute attacks (>2 x 109/L
  • High ESR
  • Blood culture – To exclude septic arthritis
156
Q

What is the diagnostic investigation for pseudgout?

A

Joint aspiration of synovial fluid

157
Q

What does a joint aspiration reveal in pseudogout?

A

Positively-birefringent rhomboid brick-shaped crystals

158
Q

What does a plain radiograph reveal in pseudogout?

A

Chondrocalcinosis

159
Q

What is the first-line management for pseudogout?

A

Joint aspiration and intra-articular steroids

NSAIDs for alangesia

160
Q

What is SLE?

A

A multi-system autoimmune disease manifests as a multi-site inflammation that affects several organs.
• Associated with autoantibodies directed against components of the cell nucleus (Nucleic acids, and proteins) – predominantly affects the joints, skin and kidneys

161
Q

What class of antibodies is associated with SLE?

A

Anti-nuclear antibodies (ANA)

162
Q

What is the presentation for SLE?

A
  • Serositis – Pleuritis or pericarditis
  • Oral ulcers
  • Arthritis (Non-erosive)
  • Photosensitivity
  • Bloods (Haemolytic anaemia/leukopenia/thrombocytopenia).
  • Renal disease (Urine casts/proteinuria).
  • ANA
  • Immunological disorder (anti-dsDNA/anti-Sm/Anti-phospholipid)
  • Neurological disease (Psychosis/seizures)
  • Malar rash
  • Discoid rash
163
Q

What ANA antibody is associated with SLE?

A

Anti-double stranded DNA antibodies

164
Q

What type of hypersensitivity reaction is SLE?

A

Type 3 hypersensitivity

165
Q

What is the general presentation for SLE?

A

General Symptoms
• Fever
• Fatigue
• Weight loss
• Lymphadenopathy
• Splenomegaly
• Raynaud’s Phenomenon – Numbness of fingers/toes in cold. Intermittent vasospasm of digits.
- Vasospasm – Blanching of the digit
- Cyanosis as static venous blood deoxygenates
- Reactive hyperaemia – Transient increase in organ blood flow as a response to occlusion.
• Oral ulcers
• Skin rash
- Malar Rash
• Discoid lupus (Red scaly patches)
• Atypical rashes (Photosensitivity, vasculitis, urticaria purpura)

166
Q

What rash is associated with SLE?

A

Malar rash

167
Q

Which antibody is associated with Sjogren’s syndrome?

A

Anti-RO anti-LA

168
Q

Which antibodies are associated with drug-induced lupus?

A

Anti-histones

169
Q

What TB drug can induce lupus?

A

Ionazid

170
Q

What causes anti-phospholipid syndrome in sle?

A

• Anti-cardiolipin/phospholipid  Primary anti-phospholipid syndrome – associated with an increased risk of arterial and venous thrombosis in SLE.

171
Q

What renal investigations are performed in SLE?

A

• Measure urine protein (Urine protein: Creatinine ratio) [uPCR).
• Albumin
• eGFR
N.B: In renal disease, the immune complexes accumulate within the glomerular membrane – glomerulonephritis.
• Increase in ACR
• Proteinuria is increasing as indicated by a decrease in serum albumin.

• Measure urine protein (Urine protein: Creatinine ratio) [uPCR).
• Albumin
• eGFR
N.B: In renal disease, the immune complexes accumulate within the glomerular membrane – glomerulonephritis.
• Increase in ACR
• Proteinuria is increasing as indicated by a decrease in serum albumin.

172
Q

What is a measure of disease Activity in SLE?

A

Immune complexes activate the complement cascade, depleting C3/C4 in active lupus associated with high levels of anti-dsDNA antibodies.
• A drop in complement C3 corresponds to SLE activity.

173
Q

What is the first-line management for SLE?

A

Hydroxychloroquine

174
Q

What is the acute management for SLE?

A

• Maintenance Therapy – Glucocorticoids (Methylprednisolone, prednisolone) – used in acute settings.

175
Q

Which immunomodulatory agents are indicated in SLE?

A

• Immunomodulatory agents – Methotrexate, azathioprine, mycophenolate – Considered in patients with a life-threatening disease or unresponsive to hydroxychloroquine.

176
Q

What is Reiter’s syndrome?

A

Arthritis
Conjunctivitis
Urethritis

177
Q

What is osteomyelitis?

A

Osteomyelitis is an inflammatory condition of bone caused by an infecting organism (predominantly by Staphylococcus aureus or Group A streptococcus),
• Leading to necrosis and new bone formation – can be acute, subacute, or chronic.

178
Q

What is the most common causative organism for osteomyelitis?

A

Staphylococcus aureus or Group A streptococus

179
Q

What are the risk factors for osteomyelitis?

A
  • Diabetes
  • Immunosuppression
  • IV drug use
  • Prostheses
  • Sickle-cell anaemia
180
Q

What is the presentation of Osteomyelitis?

A

• Pain in the affected area (is worsened by physical activity or percussion to the affected area).
• Fever
• Malaise
• Rigours
• Limp or reluctance to weight-bear.
• History of preceding skin lesion, sore throat, trauma, or operation.
N.B: Infants may not show localising signs.

181
Q

What are the examination findings for osteomyelitis?

A
  • Localised erythema
  • Tenderness
  • Swelling
  • Warmth
  • Painful/limited movement of the affected limb
  • Seropurulent discharge from an associated wound or ulcer.
182
Q

What investigations are performed for confirming osteomyelitis?

A

FBC - WCC is raised (Low specificity for osteomyelitis)

Blood culture - perform prior to administering ABx

ESR - Raised]

Swabs of wound or discharge

Radiograph

183
Q

What radiograph findings are found in osteomyelitis?

A

Shows periosteal thickening, osteopenia, soft-tissue swelling

Vertebral osteomyelitis - rarefication of single vertebral body

Bone destruction

184
Q

What is the management for osteomyelitis?

A

Suspected Sepsis  Follow SEPSIS 6 Protocol.
• Aim to take blood cultures before commencing antibiotic therapy
• Commence intravenous antibiotic therapy within 1 hour if the patient is at high risk.

1st-line ABx therapy (Flucloaxcillin/Vancomycin within 1 hour)

185
Q

What ABx is administered for adults with osteomyelitis?

A

Flucloxacillin/Vancomycin

186
Q

What ABx is administred for children with osteomyelitis?

A

Cefazolin or cefuroxime

187
Q

What ABx is given for MRSA?

A

IV vancomycin

188
Q

What is osteoporosis?

A

Osteoporosis is defined as a reduced bone mineral density (>2.5 standard deviations below peak bone mass, T-score >2.5)  Results in bone fragility and increased fracture risk.
• Reduced bone mass

189
Q

What fractures are associated with osteoporosis?

A

Fragility fractures

  • Crush fractures of vertebrae
  • Cortical bone affected
  • Stress fractures
190
Q

What are the risk factors for osteoporosis?

A
  • Age
  • Family history
  • Low BMI (<22)
  • Low calcium intake
  • Smoking
  • Lack of physical exercise
  • Low exposure to sunlight
  • Alcohol abuse
  • Late menarche
  • Early menopause
  • Hypogonadism
  • Rheumatoid arthritis.
  • Steroid use of >5mg of prednisolone.
191
Q

Which drugs can increase the risk of developing osteoporosis?

A

Corticosteroids, heparin, SSRIs, anti-epileptics, PPIs, glitazones, aromatase inhibitors.

192
Q

What is the presentation of osteoporosis?

A

Characteristic fractures
• Neck of the femur (After minimal trauma)
• Vertebral fractures (Leading to loss of height, stooped posture, and acute back pain on lifting).
• Colle’s fracture (Of the distal radius after falling on an outstretched hand).
• Impaired vision
• Impaired gait, imbalance, and lower-extremity weakness.

193
Q

What is the first-line investigation for osteoporosis?

A

1st-line investigations
• Dual-energy x-ray absorptiometry (DXA)
• Z score is adjusted for age, gender and ethnic factors

T > -1.0 = Normal
-1.0 to -2.5 = Osteopenia

194
Q

What T-score is diagnostic for osteoporosis?

A
195
Q

What is the first-line management for osteoporosis?

A

Bisphosphonate therapy

Vitamin D and calcium supplementation

196
Q

What therapies are available for osteoporosis is bisphosphonate therapy is contraindicated or not-tolerated?

A

Denosumab

Strontium Ranelate and Raloxifene

197
Q

What is Denosumab?

A

Denosumab is a monoclonal antibody inhibiting the activation and maturation of osteoclasts.

198
Q

What is polymyalgia rheumatica?

A

An inflammatory rheumatological syndrome that manifests as pain and morning stiffness involving the neck, shoulder girdle and pelvic girdle in individuals >50 years.

199
Q

Which disorder co-exists with polymyalgia rheumatica?

A

Temporal arteritis

200
Q

Which joints are affected in PMR?

A

Neck
Shoulder girdle
Pelvic girdle

201
Q

Describe the onset of PMR?

A

Rapid onset within one month

202
Q

PMR responds to which drug?

A

Corticosteroids

203
Q

What is the presentation of PMR?

A

Aching, morning stiffness in the proximal limb muscles

Shoulder/hip stiffness with associated inflammatory pain persisting for more than one hour

Low-grade fever

Reduced appetite

Weight loss

Malaise

204
Q

What blood investigations are performed for the diagnosis of PMR?

A

ESR >40 mm/hr

CRP - elevated

205
Q

What is the first-line management for PMR?

A

Corticosteroid (Prednisolone)

Calcium + Vitamin D + Bisphosphonate

206
Q

What investigation should be performed in patients to screen for complications due to PMR treatment?

A

DEXA scan in those with high fracture risk.

207
Q

What is the cause of osteomalacia?

A

Osteomalacia refers to the incomplete mineralisation of mature organic bone matrix (osteoid) following growth plate closure.
• Secondary to Vitamin-D deficiency  Decreased bone mineral content.

208
Q

What are the main causes of osetomalacia?

A

• Vitamin D deficiency
- Malabsorption (Coeliac disease)
- Lack of sunlight
- Diet
• Chronic kidney disease
- Renal tubular acidosis – Loss of phosphate leads to osteomalacia due to failed reabsorption.
- Renal osteodystrophy – Develops whereby a renal failure leads to reduced 1-25, dihydroxycholecalciferol production (phosphate rises)
• Drug-induced e.g., anticonvulsants (Phenytoin, and carbamazepine).
• Inherited: Hypophosphatemic rickets (Vitamin-D resistant rickets).
• Liver disease: E.g., cirrhosis
• Cadmium poisoning

209
Q

What is the presentation of osteomalacia in children?

A
  • Bowing of the legs
  • Knock knees
  • Wrist swelling
  • Swelling of the costochondral junctions
  • Skull softening
  • Delayed tooth eruption
210
Q

What gait is associated with osteomalacia?

A

Waddling gait

211
Q

What is the presentation of adult osteomalacia?

A

Diffuse bone pain and tenderness

Proximal muscle weakness

Fractures - especially femoral neck

212
Q

What is the management of osteomalacia?

A

Vitamin D supplementation

213
Q

Define psoriatic arthritis

A

An inflammatory arthritis associated with psoriasis and is classified as a seronegative spondyloarthropathy; often precedes the development of skin lesions.

214
Q

What is the presentation of psoriatic arthritis?

A

Symmetrical polyarthritis

Sacroillitis

Distal interphalangeal joint disease

• Arthritis mutilans (severe deformity fingers/hand, telescoping fingers).
• Psoriatic skin lesions
• Periarticular disease
- Tenosynovitis and soft tissue inflammation resulting in:
- Enthesitis: Inflammation at the site of tendon and ligament insertion – Achilles tendonitis, plantar fasciitis.
- Tenosynovitis: Of the flexor tendons of the hands
- Dactylitis: Diffuse swelling of a finger or toe

• Nail changes

  • Pitting
  • Onycholysis
215
Q

What nail changes are associated with psoriatic arthritis?

A

Pitting

Onycholysis

216
Q

What X-ray appearances are seen in psoriatic arthritis?

A

Pencil in the cup appearance

Periostitis

Erosive changes and new bone formation

217
Q

What is the first-line management for psoriatic arthritis?

A

NSAID

Usterkinumab

218
Q

What is the definition of polyarteritis nodosa?

A

A form of systemic vasculitis that affects medium-sized vessels

219
Q

What is the presentation of polyarteritis nodosa?

A 
Fever
Unintentional weight loss
Myalgia
Arthralgia
Mononeuritic multiplexx
Paraesthesia
Muscle tenderness
Abdominal pain 
Skin manifestations
-Skin ulcers, bullous or vesicular eruptions
-Diastolic blood pressure >90 mmHg
220
Q

What investigation findings are consistent with polyarteritis nodosa?

A
  • CRP – An acute-phase protein that is elevated in inflammatory conditions.
  • ESR – Raised
  • FBC – Normocytic anaemia, elevated WBC and raised platelet count
  • Complement – Reduced
221
Q

What is the management of polyarteritis nodosa?

A

Oral prednisolone + DMARD (Cyclophosphamide, azathioprine)

222
Q

What is systemic sclerosis?

A

An autoimmune connective tissue disease characterised by the production of autoantibodies and the overproduction of collage

-Fibrosis of the skin and organs -Raynaud’s

223
Q

What autoantibodies are associated with systemic slcerosis?

A

ANA
Anti-centromere
Anti-topoisomerase I

224
Q

What is limited cutaneous systemic sclerosis characterised by?

A

Limited cutaneous systemic sclerosis is characterised by skin fibrosis of the fingers (Sclerodactyly).

It does not affect the upper arms, upper legs or trunk

225
Q

What is CREST syndrome?

A 
Calcinosis
Raynaud's phenomenon
Oesophageal dysmotility
Sclerodactyly
Telangiectasia
226
Q

What is the presentation of systemic sclerosis?

A

• Raynaud’s phenomenon (RP)
- Describes an exaggerated reaction to low temperatures, resulting in vasospasm of small arterioles and arteries – decreasing blood flow to the skin.
- Characterised by colour induced change of the fingers: White  Blue  Red (Well demarcated).
• Dysphagia
• GORD
• Dilated nailbed capillaries
• Bright shiny skin of hands, feet

227
Q

What does an echocardiogram reveal in systemic sclerosis?

A

Demonstrates right heart enlargement

228
Q

What is the first-line management for systemic sclerosis?

A

ACEi and hydration

Captopril, enalapril

Non-renal crisis
Smoking cessation, exercise, physiotherapy

229
Q

What is the management of Raynaud’s phenomenon?

A

Calcium channel blockers - nifedipine and nicardipine

230
Q

Wha is dermatomyositis?

A

An idiopathic autoimmune inflammatory disorder characterised by myopathy with a distinctive cutaneous eruption.

231
Q

What is the distinctive feature of dermatomyositis?

A

• Symmetrical, proximal muscle weakness and characteristic skin lesions

232
Q

What is the presentation of dermatomyositis?

A

• Gottron’s papules
- Macular erythematous patches over the dorsal surface of the hands, especially over the metacarpophalangeal and proximal interphalangeal joints.
• Heliotrope rash with or without periorbital oedema.
- Symmetrical distribution
• Macular violaceous erythema
- V-sign: Distribution in ‘v’ of the neck and upper chest indicating photo distribution.
- Shawl Sign: Distribution in the nape, posterior shoulders, and upper back.
• Periungal erythema, nail-fold capillary dilation, cuticular overgrowth.
• Mechanics hands: Hyperkerataosis, scaling and fissuring of palms of hands.
• Proxximal muscle weakness
- Onset of muscle weakness is subacute
- Symmetrical (Difficulty getting out of chair, climbing stairs, combing hair).
• Photosensitivity
• Poikiloderma vasculare atrophicans
• Pruritus
• Fatigue and malaise
• Dyspnoea
• Weight loss

233
Q

Which serum marker is raised in dermatomyositis?

A

Creatine kinase

234
Q

What is the diagnostic investigation for dermatomyositis?

A

Muscle biopsy - perivascular or inter-fascicular inflammation - endothelial hyperplasia

235
Q

What antinuclear antibody is raised in dermatomyositis?

A

Jo-1 antibodies

236
Q

What is the management for acute flares of dermatomyositis?

A

Intravenous corticosteroid

  • Methylprednisolone
  • Intravenous immunoglobulin (IVIG)
237
Q

What is the definitive management of dermatomyositis?

A

Methotrexate, azathioprine, rituximab

238
Q

What is Sjogren’s syndrome?

A

Sjogren’s syndrome is characterised as an autoimmune disorder affecting the exocrine glands resulting in:

239
Q

What are the main features of Sjogren’s syndrome?

A

Dry mucosal surfaces
Diminished lacrimal and salivary gland secretion (Sicca complex)

Characterised by dry eyes and dry mouth

240
Q

What is the presentation of Sjogren’s syndrome?

A 
•	Fatigue
•	Dry eyes
•	Dry mouth 
•	Vasculitis
-	Skin rash 
-	Single episode of vasculitis skin disease 
•	Dental caries 
-	Destruction around the necks of the teeth and even on the labial and incisal surfaces. 
•	Vaginal dryness
•	Arthralgia
•	Raynaud’s 
•	Sensory polyneuropathy
•	Recurrent episodes of parotitis
241
Q

What auto-antibodies are raised in Sjogren’s syndrome?

A

Anti-RO
Anti-LA
Rheumatoid factor

242
Q

What test is performed to measure tear formation in sjogren’s?

A

Schirmer’s test

243
Q

What is the management of Sjogren’s syndrome?

A

Pilocarpine (Cholinergic agonist) stimulates saliva production

Artificial saliva and tears

244
Q

What is Takayasu arteritis?

A
  • Affects the aorta and major branches
  • Subclavian – Upper limb claudication
  • Carotid- CNS disease
  • Renal- hypertension
245
Q

What is giant-cell arteritis?

A
  • Inflammation of cranial vessels:
  • Temporal  Headaches/tenderness
  • Artery to masseters  Jaw claudication
  • Ophthalmic/retinal/posterior ciliary arteries  Visual loss
  • Raised ESR CRP + Abnormal temporal artery on USS.
    N.B: Management  High dose 60mg OD Prednisolone before biopsy and tocilizumab for severe relapsing disease.
246
Q

What mare the features of Wegener’s granulomatosis?

A
  • Upper airway involvement/Saddle nose
  • Kidney involvement – Glomerulonephritis
  • Pulmonary involvement with large nodules

Phase1c Medicine (11 decks)

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