Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BRS Y2 > rheumatoid and other inflammatory arthritis > Flashcards

rheumatoid and other inflammatory arthritis Flashcards

1
Q

degenerative osteoarthritis distinguishing features- inflammation/non-inflammatory? onset?
what is in synovial fluid?
CRP?
WCC?

A

little-no inflammation
slow onset
sterile
CRP/WCC normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

immune mediated distinguishing features- inflammation/non-inflammatory? onset?
what is in synovial fluid?
CRP?
WCC?

A

inflammation
subacute onset
sterile with inflammatory cells
CRP high
WCC normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

crystal arthritis distinguishing features- inflammation/non-inflammatory? onset?
what is in synovial fluid?
CRP?
WCC?

A

inflammation secondary to crystals
rapid onset
synovial fluid analysis: sterile, crystals, inflammatory cells
CRP high
WCC normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

septic arthritis distinguishing features- inflammation/non-inflammatory? onset?
what is in synovial fluid?
CRP?
WCC?

A

inflammation secondary to inflammation
rapid onset
synovial fluid analysis: inflammatory cells/bacteria
CRP/WCC both high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is synovitis

A

inflammation of synovial membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

RA is synovial inflammation. Where are synovium found

A

-proximal inter-phalangeal joint synovitis
-extensor tenosynovitis
-olecranon bursitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

RA overview. Sex, age?
Key features? What’s seen in radiographs? What can be detected in blood?

A

Sex bias F:M ~2:1
Age of onset 30-50s

Key features:
Chronic arthritis
Polyarthritis
Pain, swelling and early morning stiffness in and around joints

joint damage - ‘joint erosions’ on radiographs

Auto-antibodies usually detected in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

RA- genetic/environmental aetiology

A

genetic
-twin studies - higher concordance in monozygotic than dizygotic =mix of genetic and environment (as there are still dizygotic)

environmental-
smoking
microbiome
p.gingivalis
poor oral health
contribute to ACPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

RA- genetics-
WHAT is the strongest genetic risk factor and what has GWAS found?

A

Strongest genetic risk factor = HLA-DR

GWAS- polygenic- cumulative genetic burden rather than 1 variant determines risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how to do GWAS

A

-Compare allelic frequencies at specific SNP between cases vs controls
-Repeat across the genomes for millions of SNPs
-Identify the SNPs associated with disease risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

implications of HLA genetic associations: HLA class 1

A

HLA A,B,C
present on all cells- cells present peptide in association with HLA class 1 to CD8 killer T cells

HLA-B27: Ankylosing spondylitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

implications of HLA genetic associations: HLA class 2

A

HLA D
Expressed on APC
APC present peptide associated with HLA class 2 to CD4 helper T cells

(HLA-DR4 in RA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

RA VS OA

A

RA: prolonged morning stiffness and inactivity stiffness

OA: pain worse with activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

RA extra-articular features

A

Systemic inflammation
Fatigue (v common)
Fever
Weight loss

Organ-specific
Subcutaneous nodules
Lung disease
episcleritis
Vasculitis-> digit ischaemia
Neuropathies
Felty’s syndrome – triad of splenomegaly, leukopenia and RA
Amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rheumatoid arthritis: subcutaneous nodules what are they

A

fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue

Associated with:
Severe disease/RF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where can subcutaneous (rheumatoid) nodules be found

A

hands

elbow/ulnar border of forearm

17
Q

what happens to RA synovium and how

A

Synovium becomes a proliferated mass of tissue (pannus) due to:
Neovascularisation
Lymphangiogenesis

Inflammatory cells:
activated B and T cells
mast cells
activated macrophages

18
Q

what is seen in a healthy synovial membrane

A

macrophage-like (type A synoviocyte)

fibroblast-like (type B synoviocyte) cells

type I collagen

Functions: maintenance of synovial fluid

19
Q

what is cytokine imbalance seen in RA

A

Excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)

20
Q

RA: TNF-a effect from action

A

Inflammatory cell recruitment, angiogenesis, lymphangiogenesis -> Pannus formation

Matrix metalloproteases -> Cartilage loss

Osteoclast activation -> Bone loss (erosions, osteopenia)

21
Q

RA investigations

A

bloods:
high ESR/CRP
Normocytic anaemia= high PLT

Autoantibodies=
RF (binds to IgG)
Anti-CCP antibodies

22
Q

what does anti-CCP antibodies stand for

A

anti-cyclic citrullinated protein antibodies

23
Q

RA pharmacological treatment

A

First line
Combination DMARD therapy:
Methotrexate + hydroxychloroquine +/- sulfasalazine
PLUS
IM or short course of oral steroids

24
Q

if disease is still active- second line for RA treatment:

A

Biological therapies
cytokines target
1. anti-TNFa-infliximab
2. IL-6 receptors Inhibitor (tocilizumab)

lymphocyte target
3. B cell depletion- rituximab
4. blocking T cell co-stimulation: abatacept

25
Q

what is DMARDs.

A

disease modifying anti-rheumatic drugs

immunomodulatory drug that halts/slows disease progression

26
Q

steroids (glucocorticoids)

A

when glucocorticoids binds to glucocorticoid receptor (in cytoplasm), steroid-GR complex translocates to the nucleus and binds DNA response elements, affecting transcription

27
Q

regular objective measurement of disease activity

A

disease activity score 28

DAS28 score = composite of
no. of tender joints,
no. of swollen joints,
patient visual analogue score (VAS),
ESR (or CRP)

28
Q

effects of rituximab. What it targets, how to take, what it does, side effects

A

ab against the B cell antigen-CD20.
IV infusions (x2), 2 weeks apart.
Rapid peripheral B cells depletion.
Usually repopulate after ~6-9 months
Side effects: infusion reactions, infection, hypogammaglobulinaemia

29
Q

how abatacept work

A

T cells require 2 signals to activate:
1)MHC + peptide on APC binding to TCR on T cell.
2)CD80 on APC binding to CD28 on T cell

Abatacept blocks signal 2

30
Q

psoriatic arthritis presentation and common IL pathway

A

Scaly red plaques on extensor surfaces (eg elbows)

some- joint inflammation
-dominant pathogenic pathway=IL17-IL23

see: nail pitting/onycholysis

31
Q

psoriatic arthritis clinical presentation and additional manifestations

A

clinical presentations:
- asymmetrical affecting IPJs
-Enthesitis

But also can manifest as:
-Spinal and sacroiliac joint inflammation
-Oligoarthritis of large joints
-Symmetrical involvement of small joints (rheumatoid pattern

32
Q

reactive arthritis- cause and symptoms

A

-sterile inflammation in joints following infection elsewhere in body

infection-urogenital/GI

symptoms
Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

33
Q

reactive arthritis - common in? onset of symptoms?

A

young adults with HLA-B27 and environmental trigger (e.g. Salmonella infection)

Symptoms follow 1-4 weeks after infection

34
Q

difference between septic arthritis and reactive arthritis

A

septic
synovial culture=positive
AB therapy=yes (IV)
joint lavage=yes

reactive
synovial fluid culture=sterile
AB therapy-no
joint lavage-no

BRS Y2 (60 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions