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MOD 2 Quiz 1 > Autoimmune disorders and review of immuno > Flashcards

Autoimmune disorders and review of immuno Flashcards

1
Q

Things to protect the GI epithelium?

A 
single epithelium
mucus
antimictobial made peptides
commensal bacteria (competes)
Peyer's patches
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2
Q

Shigella infection?

A

Gram neg rods, non motile and passed person to person by fecal-oral route
they survive in the stomach acids, reach and penetrate the mucus via M calls, then invade and destroy adjacent epithelial cells

Dendritic cells take up antigen travel to follicles and lymph nodes to activate T cells and B cells are also stimulated and antibody produced

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3
Q

Antibody production does what?

A

prevents further bacteria invasion and CD8+ T cells kill infeced cells

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4
Q

Mechanisms that help prevent lymphocyte mediated autoimmune disease?

A 
central intolerance (clonal deletion)
peripheral intolerance (anergy, deletion, suppression)
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5
Q

T cell activation?

A

the initiating agent or primary self antigen is unknown for many of these disease
genetics often contribute to the development of disease or susceptibilty, and for many of them HLA genes play a role

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6
Q

Immunologic mechanisms of joint disease?

A

T cell activation
Excess Immune complex formation
HLA genes play a role in many of them

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7
Q

autoimmune in this study?

A

sytemic lupus erthematosus
rehumatoid arthritis
juvenile idiopathic arthritis
reactive arthritis

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8
Q

lab results lupus?

A 
low hemoglobin
low WBC count
high CRP
high ESR (sed rate)
negative for RF
low level complement
positive for autoantibodeis andi-ds DNA, DAT (antobodies for erthyroctyres)
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9
Q

SLE?

A

is a complex autoimmune disease involving chronic systemic inflammation
multiple organ systems are usually involved

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10
Q

Major immuno features with SLE?

A

anti-nuclear antibody (ANA)
antibody against ds DNA
immune complex depositis in skin and kidneys
other autoantibody

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11
Q

major clin manifest systemic lupus erythematous?

A 
hematologic (always)
arthritis
skin
fever
renal
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12
Q

rash with SLE?

A

butterfly rash

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13
Q

Make the self antigens?

A

genetic susceptible indicidual– undergoes an environmental trigger, cause t cell driving force, IgG autoantibody production (also from other cellular immune defects)– autoantibody mediated clinical manifest

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14
Q

main genes for genetic susceptible?

A

MHC class I, complement

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15
Q

Antinuclear antibody most common in SLE?

A

against double stranded DNA and the nuclear Smith antigen are most specific for SLE

(histones second)

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16
Q

Diagnose SLE?

A

antinuclear antibody patterns on immunofluorescence
add patient serum to fix
predomiance of antigen bound but antibody makes the pattern

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17
Q

antiphospholipid antibodies (aPLA)

A

some SLE patients develop these, can affect coagulation and endothelium
promotes thrombus formation, platelet aggregation, and are asssociated with fetal loss
(antiphospholipid syndrome)

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18
Q

Rheumatoid arthritis?

A

chronic, inflammatory disease of the joints with varying degrees of systemic involvement

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19
Q

major immuno features of RA?

A

RF, anti-citrullinated protein antibody (ACPA), and immune complexes
inflammtory infiltrate into the joints
HLA associations
small joints (hands, wrists, ankles)

20
Q

Rheumatoid nodules?

A

raised firm extensor surfaces, derived from necrotic blood vessels

21
Q

Diagnose RA?

A

morning stiff, 3 or more joints, hand joints, symmetric, nodules, serum RF (ACPA more specific) radiologic changes

22
Q

key factors to RA?

A

genetic factors and environmental triggers
citrullination of proteins and immune response to them (ACPA)
inflammtory reactions occur within the joints fueled by adaptive immune responses
production of other autoantibodies

23
Q

HLA associated with RA?

A

HLA-DRB1

24
Q

cytokines involved with RA?

A

IL-1, IL-6, TNF

25
Q

IL-6?

A

activates luekocytes, B cell differentiation, active phase response

26
Q

TNFalpha?

A

induce production of proinflammatory cytokines
stimulates and activates endothelial cells, lead to further recruit of cells within the joint
stimulates cells within joint to break down the matrix wihich surrounds them
stimulates macrophages to produce matric metallo-proteinases and free radicals

27
Q

IL-1?

A

activates leukocytes, endothelial cells, fibroblasts, osteoclasts

28
Q

IL-17?

A

helps activate fibroblasts, chrondrocytes, recruit neutrophils

29
Q

early changes in RA?

A

inflammatory cells in the joint, neutrophils (fluid), lymph (membrane)

30
Q

middle stages of RA joint destruction?

A

synovium thickens
prolferative fibroblast
erosion of bone

31
Q

Late stages of RA joint destruction?

A

hyperplastic expanding vascular pannus

32
Q

Vascular pannus?

A

fibroblast like synovial cells, lymphocytes, macrophages, and other cell types releasing a number of proinflammatory cytokines and destructive enzymes

33
Q

bone resorption?

A

neurovascularization and an environment which promotes growth and activity of osteoclasts

34
Q

Systemic conseuqneces of RA?

A 
shortedend life span
increase risk of CV disease
fatigue
reduced cognitive function, osteoporosis
increased risk of lymphoma
increased risk of inflammatory and fibrotic lung disease
35
Q

Junvenile Idiopathic Arthritis? (JIA)

A

hetergenous group of autoimmune diseases of unknown etiology, under 16 yo, chronic arthritis, often larger joints (knee)

36
Q

characteristics of JIA?

A

HLA associations
ANA+ in 40 % of patients
+- for RF
activated CD4+ T cells and inflammtory cytokines

37
Q

Histo JIA?

A

thickened hyperplastic

synovium that is highly vascular and contains a dense infiltrate of inflammatory cells- T cells, macrophages, and DCs

38
Q

criteria for JIA?

A

age of onset <16 yo
arthritis in 1 or more joints, swelling or effusion, (limit motion, tenderness or pain on motion, heat)
symptoms present for 6 wks or longer
type of onset classified one of many
exclusion of other forms of junvile arthitis
involve hip
can resemble RA (poly)

39
Q

classify JIA?

A

oligoarticular, polyarticular, systemic (Stills disease), psoriatic junveille idopathic arthritis, enthesitis related arthritis

40
Q

Reactive arthritis?

A

seronegative spondlyoarthropathy (neg for RA)
triggered by enteric or urogential infections (Chlamydia tachomatis, Salmonella, Shigella, Yersinia)
peak onset 15-35
HLA-B27
not autoimmune related, molecular mimicry

41
Q

Systemic (still’s disease)?

A

fever spikes predictable pink rash, abdomen, extremities, hepatosplenomegaly, lympadenopathy

42
Q

HLA associations?

A

SLE- anti-nuclear antibody aganist ds DNA
RA- HLA-DRB1
JIA- HLA assocations
Reative arthritis- HLA-B27

43
Q

Reiter’s syndrome?

A

triad, one presentation of reactive arthritis

44
Q

Ankylosing Sondylitis?

A

chronic inflammatory disease of sacroiliac joint, vertebrae, entheses
Low back pain +- anterior uveitis (inflamme uvea)
lesions are painful and tender to the touch

45
Q

Common sites of ankylosing sponylitis?

A

insetion of achilles tendon and of the plantar fascia on the calcaneus

46
Q

characteristics of ankylosing sponylitis?

A

HLA-B27+, RF neg

xray findings and positive Schober’s test

MOD 2 Quiz 1 (9 decks)

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