Brainscape's Knowledge GenomeTM

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


See full index

Inflammation > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What codes for genetic predisposition to RA

A

HLA DR4 serotype

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

How does smoking cause RA

A

Cigarettes cause citrullination of proteins - post translational modification by which arginine is converted to citrulline. Citrullination is a normal process, required for skin formation

In RA, an abnormal autoimmune response develops against citrullinated peptide->anti-cyclic citrilinated protein antibodies
Shared epitope predispose to the development

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

What is the synovial immunology of RA

A

Adaptive and innate immune pathways integrate. T cells releasing cytokines which are pro-inflammatory. T cells activating B cells which become plasma cells that release anti-CCP antibodies. In joint lining, innate cells like macrophages (cytokine) and neutrophils (reactive oxygen intermediates) causing damage and inflammation. Activation of the cell within the lining of the join: chondrocytes, fibroblasts, osteoclasts. These activations cause tissue remodelling and damage.

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

What do osteoclasts do in RA

A

Osteoclasts are the major driver of bony erosion in rheumatoid - causes breakdown and degradation of bone.

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

What are the joint signs of RA

A

Polyarthritis: tender, swollen, stiff, painful

Symmetrical involvement:
Hands - MCP/PIP joints
Feet - MTP joints
Variable large joints involved

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

How is RA diagnosed

A 
Rheumatoid factor (antibody factor of IgM): classically red cells or latex particles. Currently nephelometry or ELISA
anti-CCP antibody: uses ELISA, more specific than RF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is swan neck deformity

A

hyperextension of PIJ and flexion of DIJ

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

What is boutonniere defeformity

A

PIJ (flexion) bent towards the palm and DIJ (hyperextension) is bent away

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

How does RA invovle the spine

A

Lower lumbar spine and thoracic spine is rarely involved.
Atlas and Axis: erosion can occur at odontoid peg. Can cause forward movement of atlas over axis, causing the head to move forward - can cause cord compression.

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

Define RA nodules

A

RA nodules are often painless. CCP and rheumatoid factor positive.
Nodules can occur in the chest - rheumatoid lung disease. Can also cause fibrosis of the lungs - pulmonary fibrosis (long standing RA).

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

What is necrotising slceritis

A

repeated sclerosis which can cause perforation of the sclera

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

What is methotrexate

A

Analogue of folic acid

Inhibits enzyme dihydrofolate reductase (DHFR) reducing folinic acid -> affects purine and pyrimidine metabolism

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

What are the adverse effects of methotrexate

A

nausea, bone marrow suppression, hepatoxicity, pneumonitis (inflammation of the lungs, presenting with SOB and fever), embryotoxic

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

What are TNF inhibitors

A

monoclonal abx that bind to cytokine TNF. Currently have 5 different TNF inhibitors - Infliximab, Adalimumab (pens given sc), Golimumab, Certolizumab pegol, Etanercept

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

What is IL-6

A

most abundant cytokine within RA synovium. Drives acute phase response, mediates chemokine driven lymphocyte trafficking, induction of RANK-L (activates osteoclasts) through JAK/STAT signalling.

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

What is rituximab

A

(also treats non-Hodgkin’s lymphoma): monoclonal abx that targets the CD20 molecule expressed on the surface of B cells - depletion of B cell. Efficacy persists long after drug clearance. Only effective in seropositive px

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is tocilizumab

A

(given sc) binds to IL-6 receptor, preventing IL-6 binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is SLE diagnosed

A

ANA, anti-dsDNA, anti-Sm, antiphospholipid Abs, low complement, direct Coomb’s test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What extractable antibodies are found in lupus

A

Antibodies to Ro/SSA = photosensitivity
Sm = SLE specific
RNP = Raynaud’s/overlap
La/SB = neonatal lupus

In severe lupus with multisystem disease, prevalence of anti-DNA is 70-80%

20
Q

What are the ESR and CRP marker levels in lupus

A

If ESR 100 with CRP 0 = Lupus or related autoimmune disease
CRP>100 in a lupus patient = infection
Cytopenia
Low complement C3/C4

21
Q

What are the causes of lupus

A

Environment -> sunlight, drugs (only curable form of lupus) and chemicals, viruses (EBV in paediatric onset lupus)
Genetic -> defective apoptosis (all nuclear antigens become expressed on cell surface in normal apoptosis, but lupus patients fail to clear away the apoptotic bodies)

22
Q

What is the pathogenesis ofl upus

A

Autoantigens are processed by follicular dendritic cells in the germinal centre where they are presented to autoreactive B cells. This interaction under the influence of T1 interferons leads on to autoantibody producing plasma B cells -> immune complexes formed between auto-antibodies and antigen. Immune complexes bind to tissue to initiate vascular inflammation and lupus nephritis.

23
Q

What are the risk factor for lupus

A

female hormones, genetics, drugs, ethnic origin (African and Asian ancestry), environmental factors
Disease onset after menarche in women, decline in disease activity with menopause (oestrogen plays a role)

24
Q

What is discoid lupus

A

lesions in chest, face, trunk and back (just pure discoid px very rarely develop SLE)

25
Q

What is subacute cutaneous lupus

A

all have anti-Ro antibodies

26
Q

What is Jaccoud’s arthritis

A

full normal function of hands (differs from RA) - tendonitis

27
Q

What is lupus vasculitis

A

cutaneous vasculitis. Small vessel vasculitis: splinter haemorrhages, digital infarcts, palpable purpura, vasculitis ulcer, urticarial vasculitis

28
Q

What is Libman-Sacks endocarditis

A

(development of verrucous vegetation, but it is a sterile endocarditis): affects the mitral valve (treated with warfarin, abx, and corticosteroids)

29
Q

What is neuropsychiatric lupus

A

psychosis (hallucinations), seizures, strokes, psychological disorders, transverse myelitis (inflammation of the spinal cord, similar to MS)

30
Q

What is lupus nephritis

A

asymptomatic proteinuria, nephrotic syndrome, renal failure, rapidly progressive glomerulonephritis, dysmorphic/fragmented red cells, granular casts
Consider renal biopsy unless contraindicated

31
Q

How is lupus nephritis diagnosed

A

low C3 and C4, high anti-dsDNA antibodies

32
Q

What is the treatment for lupus

A

NSAIDs are contraindicated due to increased cardiovascular events from lupus
Hydroxychloroquine (first line of treatment), Mepacrine (anti-malaria drug) - main stay of treatment. Downregulates cytokines. Takes 3 months to work. Long term use well tolerated including pregnancy. Decreases risk of cardiac neonatal lupus. Reduce relapse rate and risk of renal flares. Improves lipid and glucose profiles. Thromboprophylaxis.
Smoking reduces anti-malaria efficacy

33
Q

What do positive APAs inidcate

A

Anticardiolpin antibodies (aCL), Lupus anticoagulant (LA), anti-beta2 glycoprotein 1 antibodies. If triple positive, more likely to detect obstetric and clotting problems.

34
Q

What are the signs of cerebral APS

A

Headache, cognitive dysfunction, ischaemic stroke, transient ischaemic attacks, acute ischaemic encephalopathy, amaurosis fugas, chorea

35
Q

How is APS treated in pregnancy

A

No thrombosis í careful monitoring; aspirin
Previous maternal thrombosis -> heparin + aspirin
Recurrent embryonic loss (<10 weeks) -> heparin + aspirin; low dose aspirin
Late fetal death/IUGR/severe pre-eclampsia -> heparin + aspirin
Postpartum -> 6/52 heparin

36
Q

What is secondary raynuad’s

A

Asymmetrical, thumb often affected, macroscopic nailfold capillary loops, digital infarcts, autoantibodies. 95% predictive of CTD, SLE, systemic sclerosis

37
Q

What is scleroderma

A

diffuse cutaneous systemic sclerosis. Anti-Scl 70: DNA topoisomerase I and anti-RNA polymerase I, III

38
Q

What is crest syndrome

A

limited cutaneous systemic sclerosis: anti-centromere antibodies. More likely to have pulmonary hypertension.

39
Q

What is dermatomyositis

A

Dermatomyositis (DM) is a rare inflammatory muscle disease that leads to destruction of muscle tissue usually accompanied by pain and weakness.

40
Q

What is acute anterior uveitis

A

Inflammation of the middle layer of the eye, causing eye pain and changes to vision. Very similar genetically SpA. HLA-B27 very strong link with both uveitis and SpA. Differs from conjunctivitis with pain.

41
Q

What is psoriatic arthritis

A

DIP and PIP synovitis, asymmetric oligoarthiritis, dactylitis (whole digit inflammation, which is not present in RA)

42
Q

What is ankylosing spondylitis

A

Ankylosing spondylitis is a HLA-B27 associated spondyloarthropathy. It typically presents in males (sex ratio 3:1) aged 20-30 years old.

43
Q

What are the signs of ankylosing spondylitis

A 
reduced lateral flexion
reduced forward flexion
reduced chest expansion
Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
and cauda equina syndrome
44
Q

What is psoriasis

A

presents with red, scaly patches on the skin although it is now recognised that patients with psoriasis are at increased risk of arthritis and cardiovascular disease.

45
Q

What is psoriatic arthropathy

A

Psoriatic arthropathy correlates poorly with cutaneous psoriasis and often precedes the development of skin lesions. Around 10-20% percent of patients with skin lesions develop an arthropathy with males and females being equally affected
Treat as RA

46
Q

What is the genetic association of psoriasis

A

associated HLA-B13, -B17, and -Cw6. Strong concordance (70%) in identical twins

47
Q

What is the immunology of psoriasis

A

abnormal T cell activity stimulates keratinocyte proliferation. There is increasing evidence this may be mediated by a novel group of T helper cells producing IL-17, designated Th17. These cells seem to be a third T-effector cell subset in addition to Th1 and Th2

Inflammation (12 decks)

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