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Yr 3 - Core Conditions > Locomotor > Flashcards

Locomotor Flashcards

1
Q

What is osteoarthritis?

A

Disorder of synovial joints, which occurs when damage triggers repair processes leading to structural change within a joint (progressive and degenerative joint disorder)

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2
Q

What are the most commonly affected joints by osteoarthritis?

A

knees, hips, hands

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3
Q

Which cells are involved in the breakdown of cartilage seen in osteoarthritis?

A

Chrondrocytes

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4
Q

How are chondrocytes involved in osteoarthritis?

A

Over time, continuous ‘wear’/trauma to joint causes local inflammation and stimulation of chondrocytes to release degradative enzymes

These enzymes break down collagen and proteoglycan; destroys articular cartilage

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5
Q

When the articular cartilage is destroyed by chondrocytes in osteoarthritis, what is exposed?

A

Subchrondral bone

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6
Q

How does the exposure of subchondral bone play a role in osteoarthritis?

A

Over time, cartilage thins which leads to exposure of subchondral bone which causes subchondral sclerosis

Continuous remodelling of subchondral bone forms subchondral cysts and osteophytes → leads to loss of joint space

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7
Q

Risk factors for osteoarthritis?

A
  • Increasing age
  • Female sex
  • Obesity
  • Articular congenital deformities/trauma to joint (less common)
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8
Q

What are the 3 criteria required for a diagnosis of osteoarthritis?

A
  1. >/= 45 y/o AND;
  2. Has activity related joint pain AND;
  3. Has either no morning related joint stiffness or morning stiffness that lasts no longer than 30 minutes
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9
Q

How does movement affect pain in OA vs inflammatory arthritis?

A

OA → worse on movement

Inflammatory → pain tends to improve on movement

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10
Q

Describe morning stiffness in OA vs inflammatory arthritis

A

OA → not prolonged (usually <20 minutes)

Inflammatory → morning stiffness is prolonged (>30 minutes)

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11
Q

Give some signs seen in OA

A
  • Reduced active and passive range of movement (2ary to pain)
  • May have a fixed deformity
  • Joint swelling but it shouldn’t be particularly hot or red
  • Tenderness over joint lines
  • Crepitus on movement
  • Cervical lordosis
  • Joint effusion (patellar tap)
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12
Q

Give some signs seen in the hands in OA

A
  • Sparing of MCP joints
  • Bony enlargement of PIP joints → Bouchard’s nodes
  • Bony enlargement of DIP joints → Heberden’s nodes
  • Squaring of 1st carpometacarpal joint (base of thumb)
  • Reduced functional movement (e.g. reduced grip strength)
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13
Q

Which joints in the hand are typically spared in OA?

A

MCP joints

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14
Q

Describe inflammatory markers in OA

A

CRP/ESR are typically normal in osteoarthritis

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15
Q

What is 1st line imaging in OA?

A

xray

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16
Q

Give the 4 typical signs seen on an xray in OA

A
  • Loss of joint space
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts
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17
Q

Conservative management for OA?

A
  • Education and advice about condition
  • Exercise: muscle strengthening and general aerobic fitness
    • Avoid weight bearing exercise though as can accelerate progression of disease
  • Weight loss (if overweight/obese)
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18
Q

Give the stepwise analgesic management of OA

A
  • 1st line: Topical NSAIDs (particularly effective for pain from OA)
  • 2nd line: Paracetamol and topical NSAID
  • 3rd line: Oral NSAID, paracetamol and topical capsaicin
  • 4th line: Opioid, NSAID, paracetamol and topical capsaicin
  • Intra-articular corticosteroid injection can be offered for acute exacerbation of pain (consists of steroid and local anaesthetic)
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19
Q

What is arthroplasty?

A

Joint replacement

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20
Q

What is athrodesis?

A

Fusion of joint

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21
Q

What is the analgesic ladder?

A
  • Step 1 → Non-opioid analgesics e.g. NSAIDs +/- adjuvant therapy
  • Step 2 → Weak opioids (hydrocodone, codeine, tramadol) +/- non-opioid analgesics +/- adjuvant therapy
  • Step 3 → Potent opioids (morphine, methadone, fentanyl, oxycodone, buprenorphine, tapentadol, hydromorphone, oxymorphone) +/- non-opioid analgesics +/- adjuvant therapy
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22
Q

What is gout?

A

A disorder of purine metabolism characterised by raised uric acid levels in the blood (hyperuricaemia) and the deposition of monosodium urate crystals in joints and other tissues.

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23
Q

What are tophi?

A

Deposits of monosodium urate crystals in the skin in people with longstanding hyperuricaemia

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24
Q

What are tophi pathognomonic for?

A

Gout

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25
Q

What is the most common inflammatory arthritis?

A

Gout

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26
Q

Prevalence of gout in developed vs less developed countries?

A

Developed countries have much higher prevalence than less developed countries

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27
Q

What is the single most important risk factor for gout?

A

Hyperuricaemia

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28
Q

Give some non-modifiable risk factors for gout

A
  • Male gender
  • FH of gout
  • Increasing age (>50 y/o) – Gout in <30 y/o suggests renal/enzymatic disorders (genetic)
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29
Q

Give some modifiable risk factors for gout

A
  • Obesity
  • Hypertension
  • Diabetes
  • CKD
  • Metabolic syndrome
  • Medications – thiazide diuretics, ACEi and aspirin
  • Alcohol
  • Menopause
  • Dyslipidaemia
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30
Q

What medications can cause gout?

A

Thiazide diuretics, ACEi and aspirin → all raise uric acid levels

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31
Q

The triggering of acute gout flares is often due to what?

A

Increased production of uric acid, either through digestion of protein or increased cell turnover and protein degradation:

  • Seafood & organ meats/protein binges – eating lots of high protein food raises levels of uric acid
  • Chemotherapy – increases cell breakdown
  • Trauma & surgery – increases cell breakdown
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32
Q

Pathophysiology of gout?

A

Precipitation of uric acid crystals within the joint leading to an acute inflammatory response.

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33
Q

Is it more common for gout to be caused by an under excretion of urate or an over production of urate?

A
  • 90% under-excretors of urate
  • 10% over-producers of urate
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34
Q

What conditions is gout seen more commonly in?

A
  • Hyperparathyroidism
  • Down’s syndrome
  • Sarcoidosis
  • Chronic renal disease
  • Severe psoriasis
  • Hypertension
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35
Q

3 most common gout complications?

A
  • Kidney damage
  • Joint damage
  • Bone loss
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36
Q

What are the 3 most important differentials of monoarthropathy?

A
  • Septic arthritis
  • Crystal arthropathy – gout/pseudogout (non-urate crystal-induced arthropathy)
  • Inflammatory arthritis – rheumatoid arthritis, seronegative arthritis
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37
Q

What is pseudogout?

A

Pseudogout → non-urate crystal-induced arthropathy

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38
Q

What should be excluded in any patient presenting with a hot swollen joint, especially if they are systemically unwell?

A

Septic arthritis

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39
Q

Which joint is typically affected in acute attacks of gout?

A

1st MTP joint (big toe

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40
Q

What characterises acute gout attacks?

A
  • Sudden, severe attacks of pain, swelling, redness and tenderness in the joint
  • Asymmetric joint distribution
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41
Q

Signs seen in acute gout attack?

A
  • Arthritis (swelling, redness, warmth, and pain on passive movement) typically of 1st MTP joint (although any joint can be affected)
  • Tophi (white lumps under skin formed from urate crystals)
  • Tachycardia as a transient sympathetic response to the pain of an acute attack
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42
Q

1st line investigation in gout?

A

(Note - investigations are usually not performed in typical gout presentation)

Arthrocentesis with synovial fluid aspiration

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43
Q

What result of the arthrocentesis would confirm a gout diagnosis?

A

Needle shaped monosodium urate crystals with negative birefringence confirm gout and differentiate it from pseudogout

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44
Q

In arthrocentesis in suspected gout, why should fluid be sent for gram stain and culture?

A

To rule out septic arthritis

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45
Q

A serum uric acid can be measured in gout to confirm hyperuricaemia. When should this be done?

A

Measured at least 2 weeks after acute attack

N.B. gout can develop with serum uric acid levels within the normal range

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46
Q

Describe joint space in gout xray

A

Normal

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47
Q

Give the 1st line NSAID used in the pharmacological management of gout?

A

Indomethacin

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48
Q

Is aspirin indicated in gout?

A

no → contraindicated as reduces uric acid excretion

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49
Q

Why is aspirin contraindicated in gout?

A

Do not use aspirin, because it can alter uric acid levels and potentially prolong and intensify an acute attack.

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50
Q

Lifestyle changes in gout?

A
  • Reduction of alcohol consumption
  • Reduction of purine-based foods – meats, seafood
  • Weight loss
51
Q

1st line choice for urate lowering therapy in gout?

A

Allopurinol

52
Q

When should allopurinol be given after an attack?

A

Allopurinol should be commenced at a low dose at least 2 weeks following an attack → otherwise may worsen the acute episode

53
Q

Starting or increasing urate lowering therapy can itself cause a gout flare. . For this reason, the first 3-6 months of urate lowering therapy are often covered with what drug?

A

NSAIDs or colchicine until the effective dose is reached

54
Q

What is septic arthritis?

A

Infection and inflammation of one or more joints by a pathogenic infectious agent

55
Q

What is the most common organism causing septic arthritis?

A

Staphylococcus aureus

56
Q

What is the 2nd most common organism causing septic arthritis?

A

Streptococcus pneumoniae

57
Q

Neisseria gonorrhoea (gonococcus) typically causes septic arthritis in which patient population?

A

Young, sexually active patients

58
Q

Give some other pathogens causing septic arthritis

A
  • Staphylococcus aureus
  • Streptococcus pneumoniae
  • Neisseria gonorrhoea (gonococcus)
  • Mycobacterium tuberculosis (gram negative organisms)
  • MRSA: nursing home residents, patients recently discharged from hospital, patients with leg ulceration or indwelling catheters
  • Streptococcus pyogenes, Haemophilus influenza and E. coli: less common bacterial causes
59
Q

Give some risk factors for septic arhtitis

A
  • Immunosuppression
  • PMH of joint disease e.g. rheumatoid arthritis, OA
  • Prosthetic joint
  • Pathogen access e.g. IVDU, intra-articular corticosteroid injections
60
Q

What is the most common route of spread of pathogens in septic arthritis?

A

Haematogenous spread from distant abscesses, wounds, respiratory tract infections, STIs etc

61
Q

How can previous joint disease facilitate haematogenous spread of pathogens?

A

Neovascularisation

62
Q

Septic arthritis can also be due to direct inoculation or contiguous spread from local infection. Give examples of both

A

Direct inoculation → joint infections, arthrocentesis, arthroscopic surgery, trauma, foreign objects, infected wounds

Contiguous spread from local infection → osteomyelitis, septic bursitis, abscesses

63
Q

Define contiguous

A

sharing a common border; touching.

64
Q

Pathophysiology behind septic arthritis

A
  • 1) Bacterial colonisation: bacteria enter and colonise joint space (facilitated by increased levels of adhesion proteins from previous joint inflammation)
  • 2) Immune response: synovial cells and macrophages detect PAMPs and induce immune response, recruiting macrophages, T cells and B cells (underlying joint disease impairs the phagocytic and bactericidal properties of healthy synovial cells and fluid)
  • 3) Acute inflammatory response: host factors released (pro-inflammatory cytokines which recruit more immune cells, and histamine from mast cells which stimulates vasodilation and increases vascular permeability)
  • 4) Bacterial factor release: toxins, enzymes, adhesins and cell wall proteins are released into joint space (exacerbate immune response causing more severe inflammation and contributing to articular destruction)
  • 5) Bone and cartilage necrosis: articular destruction from immune response, bacterial factors and resulting increase in intra-articular pressure compresses blood supply to joint
65
Q

Main complications of septic arthritis?

A
  • Osteomyelitis
  • Sepsis
  • Arthritis
  • Ankylosis fusion
  • Death
66
Q

Mortality rate or septic arthritis?

A

10%

67
Q

Incidence of septic arthritis in prosthetic joints vs native joints?

A

Prosthetic joint infection is an important complication of joint replacement and has a higher incidence (10x) than in native joints

68
Q

Main differentials of septic arthritis?

A
  • Gout (previous history, symptoms in foot joints) → fluid shows urate crystals that are negatively birefringent of polarised light
  • Pseudogout → fluid shows calcium pyrophosphate crystals that are rod-shaped intracellular crystals positively birefringent of polarised light
  • Reactive arthritis → typically triggered by urethritis or gastroenteritis and associated with conjunctivitis
  • Haemarthrosis → bleeding into joint
69
Q

What criteria is used in diagnosing septic arthritis?

A

Kocher criteria

70
Q

Symptoms of septic arthritis?

A
  • Hot, painful, swollen joint
  • Restricted movement
  • Fever & rigors (systemically unwell)
71
Q

Most common joint affected by septic arthritis?

A

Knee

72
Q

Signs seen in septic arthritis?

A
  • Look: swelling & erythema
  • Feel: warmth, joint pain & tenderness (knee flexion especially when intra-articular space is reduced), joint effusion
  • Move: reduced active and passive range of motion, reduced function (ability to walk)
73
Q

1st line investigation in septic arthritis?

A

Joint arthrocentesis for synovial fluid aspiration

74
Q

Appearance of joint fluid in septic arthritis?

A

Yellow/green (resembles pus)

75
Q

Other potential investigations in septic arthritis?

A
  • Blood culture
  • Urinalysis → raised nitrites in UTIs
  • Swabs → presence of N. gonorrhoea
  • Bloods: FBC, CRP/ESR, blood culture, U&Es, LFTs
  • Imaging: x-ray, ultrasound, MRI
76
Q

Management of septic arthritis?

A
  • SEPSIS 6 if suspected
  • Immediate empirical Abx therapy → IV flucloxacillin
  • Urgent joint aspiration (for investigation and symptom relief)
77
Q

Typical 1st line empirical Abx therapy in septic arthritis?

A

Flucloxacillin plus rifampicin is often first line

78
Q

Typical 1st line empirical Abx therapy in septic arthritis in pencillin allergic patients?

A

Vancomycin plus rifampicin for penicillin allergy, MRSA or prosthetic joint

79
Q

Typical 1st line empirical Abx therapy in septic arthritis in patients with prosthetic joints?

A

Vancomycin plus rifampicin for penicillin allergy, MRSA or prosthetic joint

80
Q

What is rheumatoid arthritis?

A

An autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa.

81
Q

RA is a symmetrical polyarthritis. What does this mean?

A

symmetrical (bilateral) and affects multiple joints

82
Q

Is RA more common in men or women?

A

Women

83
Q

What age does RA typically present at?

A

Typically develops in middle age (40-60) but can present at any age

84
Q

What 2 genes may be implicated in RA?

A
  • HLA DR4 – a gene often present in RF positive patients
  • HLA DR1 – a gene occasionally present in RA patients
85
Q

What 2 major autoantibodies are implicated in RA?

A
  1. Rheumatoid factor (RF)
  2. Cyclic citrullinated peptide antibodies (anti-CCP)
86
Q

What is rheumatoid factor? How does it cause disease?

A
  • An autoantibody presenting in around 70% of RA patients
  • Targets the Fc portion of the IgG antibody – this causes activation of the immune system against the patient’s own IgG, causing systemic inflammation
  • RF is normally IgM
87
Q

Is anti-CCP or RF more sensitive and specific to RA?

A

anti-CCP

88
Q

When do anti-CCP Abs tend to develop?

A

Anti-CCP antibodies often pre-date the development of rheumatoid arthritis and give an indication that a patient will go on to develop RA at some point

89
Q

How does RA typically present? (i.e. joints and symptoms)

A
  • Typically presents with a symmetrical polyarthropathy of the distal joints (MCP and PIP joints) of the hands, wrists and feet
  • Key symptoms:
    • Pain
    • Swelling & redness & warmth
    • Stiffness
  • Systemic symptoms:
    • Fatigue
    • Weight loss
    • Flu like illness
    • Muscle aches & weakness
90
Q

Which joints are typically spared in RA? What disease can this help differentiate it from?

A

DIP joints are typically spared → can help differentiate from psoriatic arthritis which can present in a very similar fashion

91
Q

How is pain in RA affected by movement?

A

worse after rest but improves with activity (unlike OA)

92
Q

Describe morning stiffness in RA

A

morning stiffness typically prolonged (>30 mins)

93
Q

Which joints are commonly affected in RA?

A
  • PIPJs
  • MCPJs
  • Wrist and ankle
  • MTPJs
  • Cervical spine
  • Large joints e.g. knees, hips, shoulders
94
Q

Give some hand signs seen in RA

A
  • Z shaped deformity to the thumb
  • Swann neck deformity (hyperextended PIP with flexed DIP)
  • Boutonniere’s deformity (hyperextended DIP with flexed PIP) – due to injury to tendon that straightens middle joint of finger
  • Ulnar deviation of the fingers at the knuckle (MCPJs)
95
Q

RA can present as an acute monoarthritis or palindromic rheumatism. What is the latter?

A

Recurrent, short-lived (hours to days) episodes of arthritis (pain, stiffness, swelling) in different joints that resolve.

96
Q

How can RA affect the cervical spine?

A
  • Atlantoaxial subluxation occurs in the cervical spine
  • Subluxation can cause spinal cord compression and is an emergency
97
Q

What 3 investigations can be done in RA?

A
  • Check rheumatoid factor (RF)
  • IF RF negative, check anti-CCP antibodies
  • Inflammatory markers e.g. CRP, ESR
98
Q

Which DMARD is often 1st line in the management of RA?

A

Methotrexate

99
Q

NICE guidelines for DMARDs in RA:

A
  • 1st line → monotherapy with methotrexate, leflunomide or sulfasalazine
    • Hydroxychloroquine can be considered in mild disease and is considered the ‘mildest’ anti-rheumatic drug
  • 2nd line → Use 2 of these in combination
  • 3rd line → Methotrexate plus a biological therapy (usually a TNF inhibitor e.g. adalimumab)
  • 4th line → Methotrexate plus rituximab
100
Q

Why do pregnant women tend to have an improvement in symptoms in RA

A

Due to the higher natural production of steroid hormones.

101
Q

How does methotrexate work?

A

Works by interfering with the metabolism of folate and suppressing certain components of the immune system.

102
Q

What is prescribed alongside methotrexate?

A

Folic acid

103
Q

Notable side effects of methotrexate?

A
  • Mouth ulcers and mucositis
  • Liver toxicity
  • Bone marrow suppression and leukopenia (low WCCs)
  • Teratogenic
104
Q

What occurs in a prolapsed intervertebral disc?

A

Outer fibres of the intervertebral disc are injured and the nucleus pulpous (soft inner bit) ruptures out of its enclosed space. The prolapsed disc can enter the spinal canal, squashing the spinal cord but more frequently the spinal nerves.

105
Q

Causes of a prolapsed intervertebral disc?

A
  • Sudden prolapse due to excessive pressure:
    • Falling from height and landing on buttocks
    • Bending forwards and lifting object
  • Weakening of outer fibres of disc e.g. repetitive minor injuries
106
Q

In which part of the spine do intervertebral disc prolapses most commonly occur?

A

in the lumbar spine and cervical spine (less commonly in the thoracic spine)

107
Q

A prolapsed disc can cause problems via which 2 mechanisms?

A
  1. Direct pressure → disc that has ruptured into the spinal canal or intervertebral foramen can put pressure on spinal nerves or spinal cord (e.g. cauda equina syndrome)
  2. Chemical irritation → the core material of the disc can cause a chemical irritation of the nerve roots and result in inflammation of the nerves
108
Q

Symptoms of a prolapsed disc?

A
  • Severe:
    • Loss of control of bladder and/or bowels
    • Numbness in genital area
    • Impotence (men)
  • Numbness, pins & needles, tinging in one or both arms/legs
  • Pain behind the shoulder blade(s) or in the buttock(s)
  • Pain running down one or both arms/legs
  • Weakness
109
Q

What is the most accurate test in prolapsed disc?

A

MRI

110
Q

What is the most accurate test in diagnosing a prolapsed disc?

A

MRI

111
Q

What is cauda equina syndrome?

A

Characterised by compression of the cauda equina (a collection of nerve roots which extend beyond the termination of the spinal cord at level L1, to exit the spinal column in the lower lumbar and sacral region)

112
Q

What is the most common cause of cauda equina syndrome?

A

Lumbar disc herniation at L4/L5 and L5/S1 level

113
Q

Clinical features of cauda equina syndrome?

A
  • Lower back pain
  • Altered bilateral radicular pain
  • Saddle anaesthesia – often manifesting as an inability to feel toilet paper when wiping
  • Bladder and bowel disturbance – constipation/retention/incontinence
114
Q

How does saddle anaesthesia typically manifest?

A

often manifesting as an inability to feel toilet paper when wiping

115
Q

Management of cauda equina syndrome?

A

Aim to surgically decompress within 48 hours

116
Q

What is the most common cause of back pain in adults?

A

Mehanical

117
Q

Sciatica can cause back pain. Sciatica involves the irritation of the sciatic nerve. What are the nerve roots of the sciatic nerve?

A

L4-S3

118
Q

Causes of sciatica?

A

herniated disc, spinal stenosis, spondylolisthesis

119
Q

Symptoms of sciatica?

A
  • Unilateral pain from buttock radiating down back of thigh to below knee or feet – ‘electric ‘or ‘shooting pain’
  • Paraesthesia (pins and needles)
  • Numbness
  • Motor weakness
  • Reflexes may be affected
120
Q

What is bilateral sciatic a red flag for?

A

cauda equina syndrome

121
Q

Give some causes of back pain

A
  • Mechanical
  • Sciatica
  • Cauda equina
  • Spinal stenosis
  • Spinal fracture
  • Ankylosing spondylitis
  • Spinal infection
  • Cancer
122
Q

Give some red flags for back pain

A
  • Cauda equina syndrome → motor deficits, sensory deficits (e.g. saddle anaesthesia), new urinary retention/incontinence, new faecal incontinence
  • Spinal fracture → history of trauma
  • Cancer → weight loss, unremitting pain
  • Spinal infection → systemic symptoms, TB, IVDU, diabetes
123
Q

What are the 5 most common cancers to metastasise to bone?

A

(BLT with a Kosher Pickle):

B – Breast

L – Lung

T – Thyroid

K – Kidney

P – Prostate

Yr 3 - Core Conditions (33 decks)

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