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Adv Patho > Autoimmune Diseases > Flashcards

Autoimmune Diseases Flashcards

1
Q

What factors are at play that can influence susceptible genes?

A

1: infection
* increased activation of T cells can cause them to accidentally mistaken self
* virus can add protein to tissue membrane
* microbes may have same amino acid sequence as self proteins
2: injury
* alter display of self antigen
* release of molecules like DNA

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2
Q

The T cells and B cells do not recognize the intercellular self antigens
aka they don’t recognize the inside of the cell as self

CD4 cells activate=B cells activate to produce autoantibodies against the intercellular products

These products are deposited through circulation in skin, kidneys, brain, heart, spleen, lungs, GI and joints=causes inflammation=IFN alpha overproduction=opsonization and phagocytosis of RBC, WBC, platelets

A

Systemic Lupus Erythematosus

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3
Q

What is ANA?

A

antinuclear antibodies; created by B cells to target the intracellular components that they do not recognize as self
in the diseases Lupus

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4
Q

What is a diagnostic used to dx Lupus?

A

antibodies to the double stranded DNA (dsDNA) or the Smith (Sm) antigen

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5
Q

What disease primarily affects the ductal epithelia cells of the lacrimal glands and salivary glands ultimately cause sing dryness of mouth and eyes?

A

Sjogren’s Syndrome

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6
Q

CD4 T cells do not recognize self lacrimal and salivary glandular cells because loss of tolerance in the CD4 population or the response against known or unknown antigens expressed in the gland

this causes B cells to secrete antibodies against the lacrimal and salivary glands
T and B cells aggregate and blocks glands
activates CD8
=inflammation=induces apoptosis=atrophy, fibrosis, dysfunction

A

Sjogren’s Syndrome

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7
Q

What is the long term affects of systemic sclerosis (scleroderma)?

A

fibrosis of the dermis and subcutaneous tissue, macro vascular disease, CREST Syndrome (calcinosis, raynauds, esophageal dysmobility, sclerodactyly, telangiectasia)

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8
Q

What are anticentromere antibodies and DNA toposomerase I antibodies and what do they indicate?

A

1: anticentromere antibodies indicate limited scleroderma
2: DNA toposomerase I antibodies indicte diffuse scleroderma

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9
Q

CD4 T cells respond to unknown antigens in the skin=cytokines=inflammation=activate mast cells, macrophages, platelets=upregulation of fibroblasts->secrete excessive amounts of collagen=excessive fibrosis
endothelial injury, endothelial proliferation, fibrosis, and narrowing=tissue ischemia
B cell activation

ex: fibrosis of lung, GI, heart, kidney

A

Systemic Sclerosis (Scleroderma)

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10
Q

membrane attack complex, CD4 T cell, and B cell deposition in microvascular around myocytes

microvascular is damaged by the inflammatory response=myocyte injury and necrosis occurs

=inflammatory and lymphocytic infiltration around blood vessels in muscle

A

Dermatomyositis

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11
Q

What are the clinical manifestations of dermatomyositis?

A

proximal muscle weakness, elevated CK from muscle degeneration, IL 1, TNFa constitutional symptoms

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12
Q

What are the B cell constitutional symptoms?

A

fatigue, fever, night sweats, wt loss

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13
Q

Classic purple rash around the eyelids and periorbital edema is associated with…

A

dermatomyositis

when the inflammatory and lymphocytic infiltration around blood vessels in muscles occurs

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14
Q

CD4 differentiates into Th1 and Th2
Th2 stimulates activation of CD8 T cells and macrophages
=inflammation, lymphocytic infiltration round muscle fiber=proximal muscle weakness, elevated CK from muscle degeneration, IL 1 and TNFa constitutional symptoms

A

Polymyositis/Inclusion-Body Myositis (focus is the myocyte)

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15
Q

What autoimmune disease does not have genetic predisposition?

A

inflammatory myopathies

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16
Q

The genetic predisposition in ankylosing spondylitis is…

A

HLA-B27

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17
Q

T cell activation against unknown axial antigen=antibodies against axial joint elements primarily sacroiliac joint, apophyseal joint and vertebral ligaments=inflammation=erosion of articular cartilage and bone=repair leads to calcification and ossification with bony outgrowths
symptoms: progressive low back pain, stiffness, decreased spinal mobility, increased kyphosis, diminished normal convex curve of lower spine

A

Ankylosing Spondylitis

18
Q

What diagnostics are used for Ankylosing Spondylitis?

A

radiology: osseous bridging between the vertebrae, calcification of discs
increased sediment rate
disease can extend to peripheral joints and eyes

19
Q

Antigen Antibody complexes are deposited in the sub endothelium of blood vessels of skin, joints, and kidneys=inflammation=cell injury
autoantibodies are directed against neutrophil cytoplasm=neutrophils release ROS and proteolytic enzymes=injure cel

A

Non-Infectious Vasculitis

20
Q

In non-infectious vasculitis, what autoantibody is positive?

A

ANCA (anti-neutorphil cytoplasmic antibody)

21
Q

CD4 T cell response to unknown antigen-Th2 activates B cells->antibodies RF
RF target IgG ‘self’
complexes are deposited in the synovial membranes=inflammation=injury to tissue
synovial cell activation and proliferation->secrete cytokines, fibroblasts activate, proliferation and secretion of cytokines, secretion of matrix metalloproteinases

causes IL 1 and TNFa constitutional symptoms

A

RA

22
Q

Why are RF antibodies not essential in RA?

A

Not everyone with RA test positive for RF

23
Q

What are the cytokines that are secreted by macrophages that are important in RA?

A

IL 1, IL 6, TNFa, IL 8, IL 17

24
Q

How does destruction of cartilage and bone occur in RA?

A

1 cartilage: fibroblasts activation and proliferation cause secretion of protease which destroy cartilage and bone. This forms scar tissue that immobilizes joint. inflammation stimulates synovial-lining cell proliferation=chondrocytes attack cartilage=synovium becomes hyper plastic and grows over cartilage=this causes pannus (fibrovascular growth) that causes further cartilage reabsorption

2 bone: CD4 and synovial cells activate osteoclasts that cause bone destruction

25
Q

What are the IL 1 and TNFa constitutional symptoms

A

fever, malaise, fatigue, wt loss, diaphoresis, anemia, vasculitits

26
Q

Increased production or decreased excretion of what acid causes gout?

A

uric acid

27
Q

What is a product of purine metabolism?

A

uric acid

28
Q

Why does gout occur in distal joints usually?

A

because lower body temperature

29
Q

What disease occurs as a result of imbalance between hyaline cartilage matrix synthesis and matrix degradation that causes cartilage erosion?

A

OA

30
Q

The patho of OA

A

1 Matrix
*the synthesis of matrix is defective=apoptosed
*increased matrix degradation=increased breakdown of collagen
2 Cell injury
*release of TNFa and IL1=inflammaiton=loss of smooth cartilage surface and loss of cartilage and bone hardening and articulating bone deformity and degeneration

31
Q

What disease occurs because of the misfolding of proteins?

A

Amyloidosis

32
Q

Patho of Amyloidosis…

A

amloid forms from abnormal folding of protein and failure to degrade abnormal protein=aggregation=deposited between cells in various tissues and organs=pressure and atrophy of adjacent tissue and cells disrupting normal function

33
Q

Common forms of amyloid…

A

those made by immunoglobulin light chains
those synthesized by liver during inflammation
this found in Alzheimer’s Disease (AB amyloid)

34
Q

Primary immune deficiencies

A
  • are manifested between 6 months and 2 years of age by recurrent bacterial infections
  • genetically determined by the effect of lymphocytes
35
Q

Diagnostic tests used for HIV/AIDS

A

rapid antibody test
ELISA test: tests for the presence of antibodies against HIV-1 and HIV-2 antigen
Western Blot Test: tests for antibodies against HIV-1 and HIV-2 capsid and core protein antigen

36
Q

Patho of HIV/AIDS

A
  • core of virus is inserted into the CD4 cell
  • core is then uncoated and viral RNA released to target cell’s cytoplasm
  • enzyme reverse transcriptase converts RNA into cDNA
  • cDNA enters the nucleus
  • when T cell is activated the DNA of HIV will make copies of mRNA
  • mRNA goes to cytoplasm where it is spliced =genomic RNA
  • it then binds with proteins and buds through the host cell=leads to CD4 cell death
37
Q

What cells can HIV/AIDS invade besides CD4?

A

macrophages because they have a receptor for CD4
*when CD4 cells are low the macrophages are more vulnerable (macrophages are usually harder to get to because they are in the tissues and protected by host defenses)

38
Q

When are the antibodies of the HIV/AIDS virus detectable?

A

seroconversion to antibodies are detectable in the blood by 3-7 weeks

39
Q

In the latency period, what cell begins to kill CD4 cells that are infected by the HIV/AIDS virus?

A

CD8 T cells, but because the decline in CD4 cells the CD8 cells decline as well because the CD4 are no longer available to activate them

40
Q

The marked decline in CD4 T cell count characterize the HIV infection due to…

A
  • HIV mediated destruction of the CD4 cells
  • CD8 destruction of infected CD4 cells
  • apoptosis of unaffected CD4 cells because of toxicity of viral proteins to the CD4 cell
41
Q

What happens to the B cells and platelets in HIV infection?

A

B cells
*more globulins are produced against the HIV
*increased circulating immune complexes
*depressed response to new antigens (immunosuppresssed)
Platelets
*CD4 receptors on megokarocytes are targeted by the HIV virus and ultimately destroyed by the antibodies

42
Q

What cytokine in particular is associated with severe wasting syndrome in patients with advanced HIV/AIDS disease?

A

TNF

Adv Patho (11 decks)

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