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Musculoskeletal System > Inflammatory arthritis > Flashcards

Inflammatory arthritis Flashcards

1
Q

What are the main characteristics of inflammatory arthritis?

A
  1. Heat/ Warmth
  2. Redness/ Erythema
  3. Pain
  4. Swelling
  5. Morning stiffness - usually gets better after a while
  6. Systemic symptoms (malaise, wt loss, fever etc.)
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2
Q

Why is it important to differentiate between inflammatory and non - inflammatory types?

A
  1. Inflammatory is potentially more serious
  2. Many inflammatory arthritis have systemic manifestations
  3. Early recognition and intervention improves outcome
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3
Q

What are some causes of acute/ self limiting inflammatory arthritis?

A
  1. Infections e.g Parovirus B19 or Streptococcus, mycoplasma
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4
Q

Name some chronic inflammatory arthritis

A
  1. Rheumatoid arthritis
  2. Spondyloarthropathies e.g Psoriatic arthritis and Axial SpA
  3. Crystal arthritis
  4. Connective tissue disease (SLE, Scleroderma)
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5
Q

What is the history/examination of inflammatory arthritis?

A
  1. Age
  2. Sex
  3. Mode of onset
  4. Severity of joint inflammation (intensity, number of swollen joints)
  5. Temporal pattern of joint involvement
  6. Distribution of joint involvement
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6
Q

What are the laboratory investigations in polyarthritis?

A
  • FBC
  • ESR or CRP
  • RF, ANA, anti- CCP, HLAB27
  • Uric acid
  • Synovial fluid analysis
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7
Q

What does sclerosis mean?

A

Subchondral bone formation due to loss on cartilage - shows increased bone density on radiographs

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8
Q

What are radiographical erosions?

A

Bone destruction

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9
Q

What are some causes of polyarticular pain?

A
  • Hyper & Hypothyroidism
  • Hyperparathyroidism
  • Multiple sclerosis (malignancy)
  • Chronic Pain syndromes (Fibromyalgia)
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10
Q

What is the Norfolk arthritis register (NOAR)

A

A register of patients who are over the age of 16 and present with 2 or more swollen joint. Their Sympotms usually lasts for 4+ weeks

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11
Q

What are the aims of NOAR?

A
  1. Identify risks factors for the development of IP (inflammatory polyarthritis) and RA
  2. To establish the incidence of IP and RA
  3. To identify predictors of outcome in IP and RA
  4. To measure the burden of illness
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12
Q

Rheumatoid arthritis is (asymmetrical/symmetrical) and affects ….. of hands and feet

A
  1. Symmetrical

2. Small joints

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13
Q

What is the clinical presentation of RA?

A
  1. Insidious (70%)
  2. Additive - starts with one joint then expands to others
  3. Small joint involvement (MCP, PIP, MTP, and wrist)
  4. Uveitis, Rheumatoid nodules
  5. Could me palindromic, polymyalgia
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14
Q

What are the classification criteria for RA?

A
  • Morning stifness lasting more than 1 hour
  • Arthritis is more that 3 joints for 6 weeks
  • Hand involvement for 6 weeks
  • Symmetry
  • Nodules
  • Radiographic erosions
  • Positive rheumatoid facor
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15
Q

What is the rheumatoid factor made up of?

A

An IgG + Anti-IgG (IgM) component

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16
Q

What happens after IgG and IgM bind in RA?

A
  1. Complement is activated2. 2. Inflammatory cytokines released
  2. They damage cartilage, destroy bone and produce inflammation
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17
Q

In what other conditions is rheumatoid factor also found in?

A
  • Sjogren’s Syndrome
  • SLE
  • JIA
  • Hepatitis
  • TB
  • Chronic bronchitis
  • Normal finding in older people
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18
Q

What predicts RA?

A

Anti - CCP (anti-cyclic citrullinated peptide) - autoantibody that works against normal antibodies.

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19
Q

What predicts RA?

A

Anti - CCP (anti-cyclic citrullinated peptide) - levels can reflect response to treatment

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20
Q

Where are citrullinated proteins found on?

A

In the inflamed synovium

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21
Q

How common are erosions in RA?

A

40-73% of patients develop X-ray erosions within the first year

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22
Q

Males are more likely to develop RA? True or False

A

FALSE

- Women are more affected

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23
Q

What is the overall prevalence of RA?

A

0.8 - 1 %

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24
Q

What are some risk factors of RA?

A
  • Smoking
  • Obesity
  • Immunisation
  • Blood transfusion
  • Previous termination of pregnancy
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25
Q

Vitamin C and Vitamin E can be effective in preventing RA? True or False

A

TRUE

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26
Q

The prevalence of RA is high in Pima Indians. What is the percentage

A

5 -6%

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27
Q

RA is more common in ages above 30? True or False

A

TRUE

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28
Q

What are the treatments given to RA patients and in what cases are they administered?

A

Mild - NSAIDs
Moderate - DMARDs
Severe - Combination therapy (steroids)
Very severe - Biological therapy

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29
Q

How is the disease activity measured?

A

Through the disease activity score ( 28 joints are assessed)

  • tender joint score
  • swollen joint score
  • ESR levels
  • General Health assessment
    (patient tells us how active they think their disease is)
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30
Q

Name 3 DMARDs

A
  1. Salazopyrine
  2. Hydroxychloroquine
  3. Leflunomide
  4. Methotrexate
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31
Q

What are some predictors of a poor prognosis?

A
  • RF positive
  • Anti - CCP positive
  • Rheumatoid nodules
  • HAQ score
  • Poor grip strength
  • High number of swollen joints
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32
Q

What do biologic agents for RA include?

A
  • Anti - TNF
  • Rituximab
  • Abatacept
  • JAK inhibitors (high cost drugs)
  • Tocilizumab
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33
Q

When can patients be administered biological agents for RA?

A

When they didn’t respond to 2 or more DMARDs including methotrexate

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34
Q

What are some surgical treatments for RA?

A
  • Arthroplasty
  • Repair of tendon rupture
  • Synovectomy (rarely done now - tissue surrounding a joint is removed)
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35
Q

Why is it important to treat RA early?

A
  • reduces risk of long - term outcomes
  • could lead to complete loss of mobility
  • could lead to bone destruction
  • could have other systematic effects
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36
Q

What is enteropathic arthritis?

A
  • HLA B27 athropathy
  • behaves like AS
  • associated with Crohn’s disease and spondylitis (inflammatory bowels disease)
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37
Q

In enteropathic arthritis, the arthritis and gut symptoms are usually linked. True or False

A

TRUE

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38
Q

Where does enteropathic arthritis usually present?

A

Asymmetrical large joints

- also some dactylitis and uveitis

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39
Q

How many people in the population are affected by psoriasis?

A

1-3% of patients

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40
Q

What is the prevalence of psoriasis and does it affect males and females equally?

A
  • 0.67%

- Yes, it affected males and females equally

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41
Q

Nail lesions/ nail pitting is a very common way to predict psoriatic arthritis. True or false

A

TRUE

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42
Q

What are the main presentations of psoriatic arthritis?

A
  • usually asymmetrical
  • DIP joint involvement usually
  • Rash (usually vesicular)
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43
Q

What are the main treatment types for psoriatic arthritis?

A
  • NSAIDs
  • DMARDs
  • Biological therapy
  • JAX Inhibitors
  • Physio and Education
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44
Q

When can a person be administered biologics?

A
  • if they have 3 or more tender & 3 or more swollen joints
  • if they haven’t responded to 2 DMARDs
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45
Q

What is enthesitis?

A

Inflammation at the point where a tendon or ligament insert into the bone

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46
Q

What are some radiographic changes seen in psoriatic arthritis?

A

Pencil in cup deformity

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47
Q

In Axial spondylitis where does the inflammation start?

A
  • In the sacroiliac joints and then it moves up the spine
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48
Q

What is the clinical criteria for diagnosis AS?

A
  • Low back pain and stiffness for more than 3 months (improves with exercise)
  • Limitation of motion of the lumbar spine in both the sagittal and frontal planes
  • Limitation of chest expansion
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49
Q

What are some radiographic features of AS?

A
  • Bone marrow edema (swelling caused by fluid)

- Sacroiliitis with pain and stiffness + new bone formation

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50
Q

Ankylosing spondylitis is the term given to patients who have inflammation of specifically the SIJ first. TRUE or FALSE

A

TRUE

- usually patients with ankylosing present with radiographic disease and spinal changes

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51
Q

Axial Spondylitis is the term given to patients who have general inflammation of the spine. TRUE or FALSE

A

TRUE

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52
Q

Name some clinical features of AS

A
  1. Gradual onset
  2. Early morning stiffness
  3. Improves with movement
  4. Usually starts at a younger age
  5. Responds well to NSAIDs
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53
Q

Name some treatments for AS

A
  1. Physiotherapy
  2. NSAIDs, biologics
  3. DMARDs for peripheral joints only
  4. Monitoring of disease activity
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54
Q

All AS patients have a radiographic disease. True or False

A

FALSE

- not all AS patients present with spinal changes

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55
Q

What are some other systematic symptoms associated with SpA?

A
  • uveitis
  • anemia
  • Weight loss
  • Psoriasis
  • inflammatory back pain
  • Crohn’s disease
  • Dactylitis
  • Enthesitis
  • Osteoporosis
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56
Q

What investigations are used to diagnose AS?

A
  • FBC, ESR AND CRP
  • X -Ray SIJ, Spine
  • MRI
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57
Q

What is the definition of reactive arthritis?

A

A sterile joint inflammation that develops after a distant infection

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58
Q

What are some triggering infections of ReA?

A
  • Throat
  • Urogenital (chlamydia, Neisseria)
  • GI tracts (salmonella, shigella etc.)
  • Meningococci, streptococci
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59
Q

Females are more affected by ReA than men. TRUE OR FALSE

A

FALSE

Males and females are equally affected.

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60
Q

What age group is usually affected by ReA?

A

Young adults aged 20 - 40

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61
Q

Is the HLA B27 gene involved in reactive arthritis?

A

Yes it is, reactive arthritis tends to be more severe if HLA B27+

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62
Q

What is the first line management in treating ReA?

A

Test for septic arthritis first!!

- aspirate joint

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63
Q

What are some clinical features of ReA?

A
  • history of infection up to 2 weeks before

- family history

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64
Q

Name 3 systemic symptoms of ReA

A
  • Malaise
  • Fatigue
  • Fever
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65
Q

Reactive arthritis usually affects larger joints and is asymmetrical - true or false

A

true

66
Q

What should you look out for when examining patients with reactive arthritis

A
  • Redness/ erythema
  • Swelling
  • Temperature (warmth)
67
Q

State 3 extra- articular msk manifestations associated with ReA

A
  1. Tenosynovitis - (inflammation of tendon sheath)
  2. Enthesopathy
  3. Plantar Fasciitis (pain at bottom of foot)
68
Q

What investigations should you take for ReA?

A
  • gram stain
  • polarised light microscopy
  • culture from (faeces, urine, throat, blood/serology)
  • X-rays
  • autoantibody screen
69
Q

How is reactive arthritis managed?

A
  • Analgesia
  • NSAIDs
  • Steroids
  • Antibiotics (if infection is still present)
  • Splinting
70
Q

State some prognosis of ReA

A
  • self - limiting in weeks
  • some back pain
  • Arthralgia
  • Synovitis
  • usually good prognosis
71
Q

What are the main triggers for inflammation?

A
  • Infections
  • Tissue necrosis
  • Foreign bodies
  • Immune reactions
72
Q

What are some features of acute inflammation?

A
  • Immediate response
  • Non specific (innate immunity)
  • Edema and neutrophils in tissue
73
Q

Inflammatory cells allow plasma proteins and fluid to exit blood vessels and to enter interstitial space. TRUE or FALSE

A

TRUE

74
Q

What is a virulence factor?

A
  • trigger acute inflammation

- molecules that help pathogens to colonize tissues and cause infection

75
Q

What are PAMPS? (Pathogen associated molecular patterns)

A
  • trigger acute inflammation

- small molecules with conserved patterns that are shared across many different pathogens

76
Q

What are DAMPS? (Damage associated molecular patterns)

A
  • intercellular proteins released when a cells plasma membrane is injured or a cell dies - trigger inflammation too
77
Q

What are DAMPS and PAMPS recognized by?

A

Pattern recognition receptors

  • cell surface receptors on various leukocytes
  • begin inflammatory response
78
Q

What is the function of IL-1?

A

Recruitment of leukocytes

79
Q

What are the 5 steps of inflammation?

A
  1. Recognition of injurious agent
  2. Recruitment of leucocytes
  3. Removal of the agent
  4. Regulation of the response
  5. Resolution
80
Q

What is the role of cytokines?

A

Proteins that are secreted my main dendritic cells, activated lymphocytes and macrophages
- regulate immune reaction
s (orthokrene, parakrene and

81
Q

Name 5 mediators of acute inflammation

A
  1. Hageman factor
  2. Complement system
  3. Mast cells
  4. Arachidonic acid metabolites
  5. Toll - like receptors
82
Q

What is the Hageman factor (Factor 12)

A
  • It is a clotting factor

- triggers fibrin formation through activation of Factor 11

83
Q

What is the intrinsic clotting pathway activated by?

A

The Hageman factor

84
Q

Where is the Factor 12 produce?

A

Liver

85
Q

How is the hageman factor activated?

A 
By contact (coming into contact with pathogens/microbes/ yeast/ parasites)
OR coming into contact with glass and medical apparatus
86
Q

What is the function of anaphylatoxins? (C3a, C4a, C5a)

A
  • causes histamine to be released from mast cells

- C5a is a chemotactic and activation agent for neutrophils, monocytes, eosinophils and basophils

87
Q

What is the function of histamine

A

Histamine is involved in the inflammatory response and has a central role as a mediator of itching.

88
Q

What is the function of histamine

A

Histamine increases the permeability of the capillaries to white blood cells and some proteins = more accessibility to pathogens

89
Q

C5b, C6, C7, C8 and C9 (membrane attack complex) flood the cell with water and ions which causes lysis. TRUE or FALSE

A

TRUE

90
Q

Why are mast cells important in inflammation?

A

Because they’re membranes contain pre-made granules that can be immediately released = immediate reaction

91
Q

Where are mast cells found?

A
  • distributed throughout connective tissues
92
Q

How are mast cells activated?

A
  • complement proteins (C3, C5a)
  • tissue trauma
  • cross linking of cell surface IgE by antigen
93
Q

What happens when a mast cell becomes activated?

A
  • granules are released

- vasodilation of arterioles - increased vascular permeability

94
Q

Where are arachidonic acid metabolites derived from?

A

Membrane phospholipids

95
Q

What is prostaglandin E2 responsible for?

A

Pain and Fever

96
Q

What is prostaglandins, IL- 1 and TNF responsible for?

A

Fever

97
Q

Where are leukotrienes produced and what is their function?

A
  • vasoconstriction
  • bronchospasm
  • vascular permeability
98
Q

Where are leukotrienes produced and what is their function? (LTC4, LTD4, LTE4)

A
  • vasoconstriction
  • bronchospasm
  • vascular permeability
99
Q

What is LTB4 responsible for?

A

Neutrophil attraction and activation

100
Q

Steroids are not anti - inflammatory agents. TRUE OR FALSE

A

FALSE

101
Q

Where are toll - like receptors found?

A

On the cells of innate immune cells e.g macrophages and dendritic cells
- on some adaptive immunity cells e.g lymphocytes

102
Q

What are toll like receptors activated by?

A
  • PAMPS
103
Q

What do granules do?

A

They contain enzymes that break down pathogens and reduce inflammation

104
Q

What is acute cellulites caused by?

A

Bacterial infection

105
Q

What does

  1. Rubor
  2. Calor
  3. Dolor
  4. Tumor
  5. Functio Laesa
A
  1. Rubor - redness
  2. Calor - heat
  3. Dolor - pain
  4. Tumor - swelling
  5. Functio laesa - loss of function
106
Q

What causes rubor and color?

A
  • vasodilation causing increased blood flow

- this is due to the relaxation of arteriolar smooth muscle

107
Q

Why do patients get pyrexia related to inflammation?

A
  • pyrogens (proteins from gram - negative bacteria) cause macrophages to release IL -1 and TNF = increases COX activity in the hypothalamus
  • COX produces prostaglandins = temperature raised
108
Q

What is swelling caused by?

A
  • leakage of fluid from post - capillary venules into interstitial space (exudate)
109
Q

What inflammatory mediators cause pain?

A
  • bradykinin and PGE2 sensitise sensory nerve endings
110
Q

What cells arrive first during inflammation?

A

Neutrophils

111
Q

State 3 roles of neutrophils

A
  1. Margination (cells marinate from centre of flow to the periphery of the venule)
  2. Rolling - neutrophils roll along the endothelial surface
  3. Adhesion - neutrophils adhere to the walls of the endothelium to move through them with the help of integrins
  4. Transmigration and chemotaxis
  5. Phagocytosis
  6. Destruction of pathogens
  7. Resolution
112
Q

What are integrins

A

Integrins are the principal receptors used by animal cells to bind to the extracellular matrix.

113
Q

Name 2 outcomes of inflammation

A
  • resolution and healing

- abscesses formation

114
Q

When do macrophages peak?

A

2-3 days after inflammation begins

115
Q

What is the role of macrophages?

A

Phagocytosis

116
Q

Rheumatoid arthritis is managed by the MDT and methotrexate is an MDT drug. TRUE OR FALSE

A

TRUE

117
Q

What are the effects of bradykinin?

A
  • Vasodilation
  • Increased vascular permeability
  • Pain
118
Q

Name 3 causes of chronic inflammation

A
  1. Persistent infection ( e.g myobacteria, parasites and fungi)
  2. Autoimmune disease
  3. Foreign material
  4. Carcinoma
119
Q

What are the main inflammatory cells

A
  • Macrophages
  • Lymphocytes
  • Plasma cells
120
Q

What is the dominant cell in most chronic inflammatory reactions?

A

Macrophages

121
Q

Where are macrophages derived from

A
  • haematopoietic stem cells and circulate as monocytes
122
Q

Where are monocytes found in?

A
  • connective tissue
  • liver (kupffer cells)
  • spleen
  • lymph nodes (sinus histocytes)
  • central nervous system
123
Q

The half-life of monocytes is about a day whereas the lifespan of tissue macrophages is several months or years. TRUE OR FALSE

A

TRUE

124
Q

Where are T-lymphocytes produced?

A

Bone marrow as progenitor T-cells but further developed in the THYMUS

125
Q

TCR complex does not recognise antigen presented on MHC molecules. TRUE OR FALSE

A

FALSE - IT DOES

126
Q

Where are B - lymphocytes produced

A

Bone marrow

127
Q

After immunoglobulin gene rearrangement what do B-lymphocytes turn into?

A

Naive B-Cells that express IgM and IgD

128
Q

What do antigens bind to that cause maturation of plasma cells

A

IgM or IgD

129
Q

What type of protein are IgM or IgD?

A

Antibodies

130
Q

What are the characteristics of plasma cells seen under a microscope?

A
  • oval shape

- larger than neutrophils and rbc

131
Q

What is granulomatous inflammation?

A

Inflammation that deals with tricky pathogens

Associated with foreign material, Crohn’s disease or Cat scratch disease, sarcoidosis

132
Q

Define granuloma

A

Collection of activated macrophages/epithelioid histocytes

133
Q

What are epithelioid histocytes

A

Macrophages that resemble epithelial cells

134
Q

Granulomas can be non caseating or caseating. What does that mean?

A

Non - caseating: Non- necrotizing granulomas

Caseating - necrosis involving dead cells with no nuclei and debris (cheese like necrosis)

135
Q

What is sarcoidosis?

A
  • abnormal collection of granulomas usually in the lungs, skin or lymph nodes
136
Q

What is the early stage of wound healing?

A
  • transition from acute inflammation
137
Q

The inflammatory phase of healing includes

A

coagulation - platelets cells , neutrophils and macrophages

138
Q

What is the function of platelets during wound healing?

A
  • Clot formation

- As they degranulate they release growth factors that initiate proliferation of undamaged cells

139
Q

When does healing start?

A

When inflammation begins occurs via regeneration and repair

140
Q

What does the ability to regenerative depend on?

A

depends on the regenerative capacity of the cell

141
Q

What are the three types tissues can be divided into based on regenerative capacity?

A
  • Labile - have stem cells that continuously cycle to regenerate tissue
  • Stable - cells are usually inactive but can re -enter the cell cycle to regenerate tissue when necessary
  • Permanent - lack of significant regenerative potential (e.g skeletal muscle)
142
Q

Define repair

A

Replacement of damaged tissue with a fibrous scar - occurs when regenerative cells are lost e.g deep skin cut

143
Q

Granulation tissue formation is the second phase of repair. TRUE OR FALSE

A

FALSE - It is the initial phase

144
Q

What does granulation tissue comprise of?

A

Proliferated capillaries providing nutrient, fibroblasts and myofibroblasts (cause wound contraction)

145
Q

What is regeneration and repair mediated by?

A
  • Paracrine signalling by growth factors (macrophages secrete growth factors)
146
Q

Interaction of growth factors with receptors results in …..(1)……. and ……..(2)

A
  1. Gene expression

2. Cellular growth

147
Q

What are the functions of transforming growth factor -beta?

A

Fibroblasts growth and inhibition of inflammation

148
Q

What mediator causes growth of endothelium, smooth muscle and fibroblasts?

A
  • Platelet derived growth factor
149
Q

What is angiogenesis?

A

When new blood vessels form from pre-existing vessels

150
Q

What are the 4 phases of wound healing

A
  1. Coagulation phase (involves neutrophils etc.)
  2. Inflammatory phase
  3. Proliferative/granulation tissue phase
  4. Remodelling phase (myofibroblasts begin to remodel extracellular matrix)
151
Q

What are growth factors needed for?

A

Recruitment of epithelial cells

152
Q

What happens during primary intention of wound healing?

A
  • wound edges brought together - leads to minimal scarring
153
Q

What happens during the secondary intention of wound healing?

A
  • edges are not brought together
  • granulation tissue fills the gap
  • myofibroblasts contract the wound
    > scar forms
154
Q

What is the difference between a hypertrophic and keloid scar?

A

Hypertrophic - excess scar production local to wound

Keloid - excess scar production that is larger than wound

155
Q

Name 3 factors that can delay healing

A
  1. Vitamin C deficiency
  2. Copper deficiency
  3. Zinc deficiency
  4. Foreign bodies
  5. Ischaemia
  6. Diabetes
  7. Malnutrition
156
Q

What causes hypersensitivity reactions?

A
  • Autoimmune diseases
  • Reactions against environmental antigens
  • Reactions against microbes
157
Q

What is lyme disease?

A

A bacterial infection that can be spread to humans by infected ticks

158
Q

What are the clinical features of lyme disease

A
  • skin reaction: erythema migrans (rash)(looks like a bulls eye)
  • Peripheral neuropathy (nerve damage outside cns)
  • Lymphocytic meningitis
  • Cranial nerve palsies (loss of function of cranial nerve)
  • Late disease: arthritis affecting larger joints
159
Q

How do you diagnose lyme disease?

A
  • mostly clinical
  • antibody detection is frequently negative
  • Immunofluorescence or ELISA can give false positive reaction for many other conditions
160
Q

How do you manage lyme disease

A

Medication
- doxycyline
- amoxicillin
for minimum 28 days

161
Q

How can you prevent lyme disease?

A
  • protective clothing

- insect repellents in tick-infested areas

162
Q

What are the seronegative features of RA?

A
  • IBD
  • Uveitis
  • Psoriasis
  • Spinal symptoms

Musculoskeletal System (14 decks)

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