Diseases of Immunity ppt patho exam 2

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What are the three causes of hypersensitivity diseases?

1.) autoimmunity 2.) rxn against microbes (maybe prolonged exposure to something 3.) rxn against enviromental antigens (all of us are exposed to these but only some people react to them, they are usually harmless antigens ex. Pollin)

mechanisms of immunologically mediated disorders

Type I hypersensitivity is mediated by ____ directed against specific antigens (allergens)

immunoglobulin E (IgE)

Primary mediators of type I hypersensitivity include ___, ___, ___ and ____.

histamine, adenosine, heparin and proteases

Secondary mediators of type I hypersensitivity include ____, ___, ____ and ____.

leukotrienes (which are 10x more potent than histamine), prostaglandin D2, platelet-activating factor, and cytokines

Anaphylaxis, allergies, and bronchial asthma are all prototype disorders of type ___ hypersensitivity

I

In type I hypersensitivity, both primary and secondary mediators cause ___, ____ and ____.

vascular permeability, smooth muscle contraction, and prolonged inflammation

Hypersensitivity can cause ___ and ___ reactions

local (ex. Bee sting) and systemic (ex. Anaphylactic response)

Type on hypersensitivity

Mast cells in hypersensitivity

Type II hypersensitivity is mediated by _____.

antibodies (our own body reacting to our body)

With Type II hypersensitivity, antibodies are directed against target antigens on the surface of cells or orther tissue components. This leads to _____.

inflammation

What are the three kinds of Type II hypersensitivity?

1.) complement-dependent reactions 2.) antibody-dependent cell-mediated cytotoxicity 3.) antibody-mediated cellular dysfunciton

Type 2 hypersensitivity

List the five reactions of complement-dependent Type II reactions.

1.) transfusion rxns 2.) erythroblastosis fetalis 3.)autoimmune hemolytic anemia, agranulocytosis or thrombocytopenia 4.) drug rxns 5.) pemphigus vulgaris

Type III Hypersensitivity is ______-mediated

immune complex (antigen-antibody)

What are the three mechanisms of Type III hypersensitivity?

1.) antigen-antibody complexes 2.) activates complement in tissues at site of trapping of complexes 3.) accumulation of polymorphonuclear leukocytes

With type III hypersensitivity, mediated injury can be ____ or ____.

systemic; localized

What are the three phases of type III hypersensitivity?

1.) complex formed btw antigen and antibody 2.) complex deposits in tissue 3.) this triggers recruitment of PMNs (inflammatory rxn)

Type IV hypersensitivity is _____ mediated

cell (also known as delayed)

Typer IV hypersensitivity is mediated by ____ or ____ cells

T; CD4

Type IV hypersensitivity causes the recruitment of _____

macrophages (CD8 cells)

Type IV hypersensitivity can cause _____.

cytotoxicity

TB (and other mycobacteria), fungi, protozoa, parasites, sarcoidosis, contact skin sensitivity and transplant rxns can all cause type ___ hypersensitivity.

IV

What are the two types of Type IV hypersensitivity?

1.) delayed-type hypersensitivity 2.) direct cell cytotoxicity

Delayed-type hypersensitivity is mediated by ___ cells

CD4

Direct cell cytotoxicity is mediated by ___ cells

CD8

In delayed-type hypersensitivity, CD4 T cells are activated and then differentiate into _____.

Th 1 (T-helper) cells

Delayed-type hypersensitivity activates ____ and ____

macrophages and TNF (which add more to the inflammation process ex. PPD test, contact dermatitis)

If delayed-type hypersensitivity is not resolved it can cause _____.

chornic inflammation--> multinucleated giant cells

______ is when perivascular CD4 T-cells infiltrate is replaced by macrophages over a 2-3 week time period and turn into epithelioid cells (large, flat, eosinophilic -> multinucleated giant cells)

granulomatous inflammation (ex. Poison ivy)

Epitheliod cells are surrounded by _____.

lymphocytes

What mediates Type I hypersensitivity

IgE antigens (e.g. mast cells--> histamine)

anaphylaxis, angioedema and atopic allergy are examples of

Type 1 (immediate)

How fast do Type I hypersensitivities occur

1 hour

Type I hypersensitivity is also known as ______

Immediate

Type II hypersensitivity is also known as ______

Cytotoxic Antibody Reaction

Type II hypersensitivity is mediated by_____ and _____ antigens

IgG (more important) IgM

reactions to transfusion, Rh incompatibility and Hashimoto's thyroditis are examples of

Type II (cytotoxic antibody reaction)

Type III hypersensitivity is also known as _______

immune complex reaction

How fast does Type III hypersensitivity occur

1-3 weeks after exposure

SLE, erythema nodsum and RA are examples of ______

Type III (immune complex reaction)

Type III hypersensitivity should be associated with_____

antigen-antibody complex deposits in tissue

Type IV hypersensitivity is also known as ____

delayed type

Type IV hypersensitivity should be associated with_____

cellular response

Type IV hypersensitivity is mediated by _______

T-lymphcytes to specific antigens

PPD and contact dermatitis are examples of this hypersensitivity

Type IV (delayed type)

How fast does Type IV hypersensitivity occur

2-7 days post-exposure

Which type of hypersensitivity involves MHC

Type IV (delayed type)

MHC (stands for?)

major histocompatibility complex)

What is the role of MHC?

Once a pathogen is engulfed and broken down into peptides the MHC is activated and results in antigen presentation so the T-cell can recognize infected cells

________reactions to _________is the cause of certain human disease

immune; self-antigens (presence of antigens alone is not pathologic)

__________reactions cause systemic disease

cell-mediated

APC's (Stands for?)

antigen presenting cell

describe the general process of tissue injury due to autoimmune disease

The individual has self-reactive lymphocytes which binds to their own cells activating APC's thus causing an increase of lymphocytes into tissue which leads to tissue injury

of systemic lupus erythematous (SLE)

failure to maintain self-tolerance

Lupus affects ________in the _____or______decade of life

females; 2nd/3rd

what are the 11 criteria for classification of SLE

malar rash, discoid rash, photsensitivty, oral ulcers, arthritis, serosis, renal disorder, neurologic disorder (seizures or psychosis), hematologic disorder, immunologic disorder or antinuclear antibody

is characterized by the destruction of articular carlage and bone

RA

A 16-year-old black female presents to her primary care physician with symptoms of fatigue, musculoskeletal pain, and a facial rash. On examination she is noted to be thin with malar skin changes. No other abnormality is found

SLE

A 52-year-old woman presents with a 2-month history of bilateral hand and wrist pain, and swelling in her fingers. She has also recently noted similar pain in the balls of her feet. She finds it hard to get going in the morning and feels stiff for hours after waking up. She also complains of increasing fatigue and is unable to turn on and off faucets or use a keyboard at work without a significant amount of pain in her hands.She also presents with leg ulcers that have been chronic and has ulnar deviation of the hands bilaterally. She denies any infections before or since her symptoms started

RA

pathologic changes that begin in ligmentous attachments to bone; frequently involves SI joints

Seronegative spondyloarthropathies

A 45-year-old woman presents with fatigue and a history of positive anti-nuclear antibodies. She has had recurrent sensation of sand/gravel in eyes and dry mouth every day for more than 3 months.

sjogren's syndrome

the pathogenesis of sjogrens syndrome

B-cell hyperactivity

genetic factors of sjogren's syndrome

HLA association

what are the two groups of systemic sclerosis (SS)

diffuse and limited scleroderma

widespread skin involvement and rapid progression of early visceral involvment

diffuse SS

skin involvment is confined to fingers/face, visceral involvement occurs late, presents with CREST

limited scleroderma SS

Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and telangiectasia

CREST syndrome

calcinosis

calcium deposits in the skin

raynaud's phenomenon

spasm of blood vessels in response to cold/stress

esophageal dysfunction

acid reflux and decrease in motility of esophagus

sclerodactyly

thickening and tightening of the skin on the fingers and hands

telangiectasias

diallation of capillaries causing red marks on surface of skin

what is the next step in the immune response after mast cells and macrophages are recruited

release of fibroblast growth and chemotactic factors or endothelial cell injury

Heliotrope rash associated with_______

dermatomyositis

characterized by decreased antibodies, T/B-cells, phagocytes or complements

primary immunodeficiency

Ex of decreased T-cells

Thymic aplasia, DiGeorge's syndrome

Ex of decreased antibodies

X-linked hypgammaglobulinemia

characterized by old age, chronic malnutrition, widespread malignancy, metabolic (DM, liver failure...), drugs, splenectomy or HIV

Secondary immunodeficiency

RNA retrovirus

HIV

which type of HIV is more prevalent in our geographic location?Africa?

HIV 1; HIV2

Name some high risk groups of HIV

risky sex, IV drug users, homosexual, transfusion pts, and hyperphiliacs

what cells are affected mainly by HIV infection

CD4 cells

how is HIV transmitted

body fluids, mother to fetus

HIV is a ______ retrovirus

RNA

HIV-2 is prevelent in

Africa

HIV-1 is prevelent

US

HIV is transmitted via

Bodily Fluids, vertical transmissions

HIV High Risk groups include

IV drug users, homosexuals, transfusions, hemopheliacs

HIV affects ______ cells

CD-4

With HIV you can test for a ________

Viral Load

In HIV _____ binds to ______

gp120/CD-4

In HIV after binding to CD-4 gp41 ________

penetrates the membrane

HIV _____ off of cell

buds

HIV clinical latency is considered a CD-4 of greater than _______

200

Three phases of HIV

Early acute, clinical latency, crisis phase

AIDS defining diseases include (6)

toxoplasmosis, candidiasis, salmonella, kaposi's sarcoma, non-hodgkin's lymphoma, TB

Amyloidosis

most common amyloid

AL (amyloid light chain)

plasma cells and immunoglobin light chain)

AA (amyloid-associated)

non-immunoglobulin synthesized in the liver

cerebral lesion of alzheimer disease

Nonspecific complaints of amyloidosis

weakness, fatigue, initial weight loss, renal involvement (proteinuria-nephrotic syndrome), hepatomegaly, splenomegaly, cardiac abnormalities (arrhythmias

Dx of Amyloidosis

biopsy, and congo red staining

Catagorized as "systemic amyloidosis" (5)

Immunocyte dyscrasias (primary), reactive systemic (secondary), hemodialysis, hereditary (familial mediterranean fever or familial amyloidotic neuropathies), systemic senile

catagorized as "localized amyloidosis" (3)

Senile cerebral, endocrine (medullary carcinoma of thyroid, islet of langerhans), isolated atrial amyloidosis

disease associated with immunocyte dyscrasias with amyloidosis

multiple myeloma and other monoclonal B-cell proliferations

disease associated with reactive systemic amyloidosis

chronic inflammatory conditions

disease assoc w/ hemodialysis associated amyloidosis

chronic renal failure

disease assoc w/ senile cerebral amyloidosis

alzheimer disease

disease assoc. w/ islet of langerhans

type 2 diabetes

Immunocyte dyscarasias fibril protein

AL

Reactive systemic amyloidosis fibril protein

AA

Hemodialysis associated major fibril protein

Senile Cerebral Fibril protein

Familial mediteranean fever fibril protein

AA

Insoluble Fibrils

stimulus------soluble precursor

AL Protein

Carcinogen-----monoclonal B lymphocyte proliferation----plasma cells-----immunoglobulin light chains (limited proteolysis)

AA Protein

chronic inflammation ----macrophage activation----interleukins 1 and 6----- liver cells----SAA protein (limited proteolysis)

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