• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/19

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

19 Cards in this Set

  • Front
  • Back
Rheumatoid arthritis is classified as what type of hypersensitivty disease?
-Type III
Rheumatoid factor IgG complexes lead to systemic vasculitis

Type 4
-unknown synovial joint antigen leads to joint inflammation and destruction
Mixed Essential cryoglublinemia:
autoantigen and consequence
patients needs to be in?
another form of?
clinical findings due to?
-Rheumatoid factor IgG complex leading to systemic vasculitis

-cold
-vasculitis
-immune complex lodges in places-->red patches of skin
Type 4 Cell Mediated Diseases?
Type I diabetes
-pancreatic B-cell antigen
-Bcell destruction and inability to produce insulin

RA

Multiple Sclerosis
-myelin, proteolipid protein, myelin oligodendrocyte, glycoprotein
-leads to brain invasion by CD4 Tecells, muscle weakness, other neuro sx
type I diabetes mechanism?

why isnt it a type II hypersensitivty?
-CD8-t-cell recognizes and kills B-cells so no insulin can be made
-glucagon and somatostatin are still produced by alpha nad B cells

-tho Abs do form against beta cells...the predominant method of destruction of Beta cells is by lysing them w/ CD8
Type I diabetes Alleles
-HLA typing:
-DR3/DR4 alleles
Rheumatoid Arthritis Mechanism

Type of hypersensitivty?
-unknown trigger sets up initial focus of inflammation in synovial membrane attracting leukocytes into tissue

-autoreactive CD4-Tcells are able to leak through endoothelial to activate macrophages leading to production of pro-inflammatory cytokines and sustained inflammation

-cytokines(IL-6, TNF-a) induce production of MMP and Rank-L by fibroblast

-MMPs attack tissues. Activation of bone destroying osteoclast resulting in joint destruction

-starts as Type IV but evnetually shows Type III and II
RA
-defined by?
-effects?
-Key articular pathologic features?
metric inflammatory polyarthritis
-affects small joints of the hand

-Pannus Formation
-synovial swelling, inflammation
-cartilage loss and bone ersoions
-joint damage and loss of fxn

Osteoclast activation
-bone erosions
-joint damage
Multiple Sclerosis mechanism
-unknown trigger leads to inflammation in brain and BBB
-area becomes permeable to leukocytes and blood proteins
-T-cells specific for CNS antigen and which were activated in the peripheral lymphoid tissues re-encounter antigen present on microglia or dendritic cells in brain-target the the gray matter of the brain

-inflammatory rxn in brain due to mast-cell activation, complement activation, antibodies and cytokines

-demyelination of neuorns

-diagnosed by plaque formation
Multiple Sclerosis findings?
-white spot lesions showing demylenation in myelin stain.
-Abs in the CNS-diagnosis but no primary mediator
Systemic autoimmune diseases?
-RA
-Scleroderma
-Systemic Lupus Erythematosus/primary sjorgen's syndrome
Scleroderma

characterized by?
pathophysiology/mechanism?
diagnosis?
involves which systems
two groups?
type of hypersensitivty?
-excessive fibrosis due to fibroblast activation to myofibroblast throughout the body

-Injury-->endothelial dyfxn-->T-cell entry-->Cd4 cells respond to unidentified antigen-->release of cytokines-->active macrophages, fibroblasts, mast cells-->activated fibroblast which-->fibrosis
B cells also activated

-Antibodies...do not mediate pathogensis

-GI tract most common, musculoskeletal, joints, lungs, kidenys, heart

-Diffuse: initial widespread skin involvement with rapid progression and early visceral involvment

-limited: CREST-mild skin involvement up to elbows or knees, visceral later.
Calcinosis, Raynaud's phenomenon, Esophageal dysfunction, Sclerodactyly, and Telangiectasias


-Type IV initially but develop Abs-complex later(Type III)
SLE
-type of disease? Etiology?
-pathogensis?
-common organs affected?
-systemic autoimmune, unknown etiology affecting multple organ systems

-defective clearance of nuclear antigens released from apoptotic cells and failure of T/B cell tolerance to these self antigens

-common organs affected
-kidney, skin/oralmucosa, joints, CNS, spleen, heart
SLE
role of antibodies?
-type of hypersensivity?
-dammage tissues directly or through immune complex deposits

-Production of autoantibodies to various componenets of the cell or ANA(antinuclear Abs)
-ex. DNA, Histones, Non-histone proteins bound to RNA, Nucleolar Ag

-Production of autoantibodies to surface antigen in BLOOD CELLS

-Production of autoantibodies to proteins complexed with PHOSPHLIPIDS(lupus anticoagulaants)

-Type III then Type II
What is the major problem/issue with SLE
-kidney involvement/renal failure
-ANA(antinuclear ab) complexes in glomeruli that evoke inflammatory response
SLE skin pattern?reflects?
worsted by?
caused by?
-butterly malor rash
- areas with more vasculariztion
-UV rays
-Deposition of IgG-immune complex in skin at dermoepidermal jxn
Common target of SLE
leads to?
-small painful lesions on buccal mucosa and roof
-oral lesions erupt with flares in the disease and go away when episode is over
Sjogrens
-definition
-pathophysiology and possible reasons?
-Ab's role
-major targets?
-usually accompanied by?
-autoimmune lymphocytic(primarily CD4, Bcells) infiltration of exocrine glands(primarily salivary glands and lacrimal glands) resulting in glandular damage and subsequent dysnfxn/loss of fxn

-autoimmune T-cell rxn against an unknown self-antigen(loss of tolerance)
-immune rxn against antigens of a virus that infects the tissues

-Abs aid in diagnosis but do not contribute to pathogenesis

-ductal epithelial cells of glands

-accompanying autoimmune disorder such as RA(MHCII alleles predispose)
Sjogren Syndrome
clinical features
-dry mouth: decreased saliva production with increased risk for dental caries
-dry eyes : diminsied tear production
-Dry tracheobronchial mucosa: decreased oropharyngeal aand upper respiratory secretions
-Dry skin and vaginal mucosa
-salivary gland enlargement
-pancreatic exocrine dysfxn
Amyloidosis
-defined by?
-classes of amyloidosis
-Deposits and the types of diseases assoicated with them?
is amyloidosis a autoimmune disease?
-variety of proteinaceous materials abnormally deposited in tissue interstitium

-reactive systemic
-localized
-heredofamilial
-endocrine
-amyloid of aging

-AL-amyloid light chain-multiple myeloma
-AA-amyloid-associated-chronic inflammatory states
-AB- alzheimers-beta amyloid sheets/tangles

-no, its an accumulation of protein due to systems autoimmune disease
-