Chapter 10 Altered Immunity

Front 1

Alterations in immunity

Back 1

Excessive immune response

Deficient immune response

Front 2

Excessive immune response types

Back 2

Autoimmune disorders

Hypersensitivity

Front 3

Auto immune disorders is a general term used when ___. Caused by ___. Occurs due to __

Back 3

The immune system attacks your own cells

Genetic or environmental factors

Failure to recognize self-antigens

Front 4

Hypersensitivity is a ___ or is ___. Immune system may ___.

Back 4

Normal immune response that is excessive

Or is triggered by non-pathogenic antigens

Respond to a normally harmless substance

Front 5

Normally harmless substance the immune system may respond to

Back 5

Allergens

Front 6

Type 1 hypersensitivity is caused by

Back 6

Genetics

Front 7

Type 1 hypersensitivity is so known as ___ because ___.

Back 7

Immediate-type hypersensitivity

Signs and symptoms occur within 15-30 min if exposure to antigen or allergen

Front 8

Type 1 hypersensitivity is also called

Back 8

Anaplaxis or atopic hypersensitivity

Front 9

Type 1 hypersensitivity is mediated by

Back 9

IgE

Front 10

Type 1 hypersensitivity principal effecor cell

Back 10

Mast vekl

Front 11

Type 1 hypersensitivity pathogenesis:

First exposure

Second exposure

Release of

Back 11

First exposure to antigen caused production of IgE antibodies which are then out on the surface of mast cells

Second exposure may cause immediate degranulation of mast cells, which triggers an inflammatory response

Release of histamines and other chemical mediators

Front 12

Examples of Type 1 hypersensitivity (7)

Back 12

Allergic rhinitis

Allergic asthma

Atopic dermititis

Food allergy

Insect stings

Medications

Vaccines

Front 13

Allergic rhinitis+ caused by + Tx

Back 13

Nasal allergy

Caused by pollen spores, house dust mites, animal dander/feathers etc

Tx: anihistamines

Desensitization by low dose exposure

Front 14

What does low dose exposure do

Back 14

Causes the development of IgG which bind to allergens before they can bind to IgE and cause mast cell degranulation

Front 15

Anaphylaxis +occurs due to + Tx

Back 15

Life threatening form of Type 1 hypersensitivity

Occurs due to release of histamine

Epinephrine, antihistamines, oxygen, corticosteroids

Front 16

What does epinephrine do

Back 16

Constricts blood vessels and causes bronchodilation

Front 17

Type 2 hypersensitivity is also known as

Back 17

Cytotoxic or tissue specific hypersensitivity

Front 18

In Type 2 hypersensitivity Antibodies

Back 18

Attack antigens on the surface of specific cells or tissues activating complement if CMI cytotoxicity

Front 19

Type 2 hypersensitivity can occur within

Back 19

15-30 min of exposure but is usually much slower to develop

Front 20

Type 2 hypersensitivity is mediated by

Back 20

IgG or IgM Antibodies

Front 21

Type 2 hypersensitivity pathogenesis

Back 21

Then antigen antibody binding activates complement

IgG or IgM Antibodies bind to antigens located on the surface of cellsThen antigen antibody binding activates complementLysis of the cell with antigens occurs via complement or is phagocytized

cellsThen antigen antibody binding activates complementLysis of the cell with antigens occurs via complement or is phagocytized

Lysis of the cell with antigens occurs via complement or is phagocytized

Front 22

Examples of Type 2 hypersensitivity (8)

Back 22

ABO transfusion reaction

Hemolytic disease of newborns (Rh incompatibility)

Myasthenia gravis

Thyroiditis

Graves disease

Acute graft rejection

Autoimmune hemolytic anemia

Type 1 diabetes

Front 23

Myasthenia gravis

Back 23

Antibodies form that bind to acetylcholine receptors

Front 24

Gabe's disease

Back 24

Antibodies bind to TSH receptors

Front 25

Type 3 hypersensitivity is also known as

Back 25

Immune complex disorder or arthus reaction

Front 26

Type 3 hypersensitivity is when a ___ forms that is __. It is then __.

Back 26

Antigen-antibody complex forms that is insoluble. It is then deposited in tissues which then causes inflammatory reaction

Front 27

Type 3 hypersensitivity occurs (time)

Back 27

Hours after exposure

Front 28

Type 3 hypersensitivity mediated by

Back 28

IgG or IgM

Front 29

Type 3 hypersensitivity pathogenesis (5)

Back 29

°Antigen-antibody complex forms

°Complex becomes insoluble and precipitates out if blood and into tissue

°Triggers complement in the tissue which triggers inflammation

°Inflammation leads to tissue destruction, scarring, further attack against damaged tissue

°note that tissue damage is due to inflammation and infiltration of inflammatory cells

Front 30

Exapmles of Type 3 hypersensitivity (3)

Back 30

Systemic lupus erythematosus

Immune complex glomerulonephritis

Rheumatoid arthritis

Front 31

Systemic lupus erythematosus

Back 31

Antibodies develop to nuclear antigens (DNA and RNA)

Affects multiple organ systems: joint swelling, pain, skin lesions cardiac, renal, CNS involvement classic butterfly rash

Front 32

Type 4 hypersensitivity is also known as

Back 32

Delayed-type hypersensitivity or cell-mediated hypersensitivity

Front 33

Type 4 hypersensitivity mediated by

Back 33

Cells

Front 34

Type 4 hypersensitivity usually occurs

Back 34

24 hours to 14 days after exposure

Front 35

Delayed cell reaction in Type 4 hypersensitivity causes

Back 35

Tissue damage

Front 36

Type 4 hypersensitivity pathogenesis (3)

Back 36

°Antigen processed by presenting cell and presented to helper T cells

°Cytokines from helper T cells activate macrophages and stimulate cytotoxic T cells

°Macrophages and cytokines T cells migrate to area of antigen and cause cell destruction

Front 37

Examples of Type 4 hypersensitivity (5)

Back 37

Contact hypersensitivity

Tuberculin test

Chronic transplant rejection

Graft-virus-host disease

Granulomatous hypersensitivity

Front 38

Contact hypersensitivity is + slow to develop because+ causes

Back 38

Allergic response to a variety of plant oils, chemicals, ointments, clothing, cosmetics, dyes, adhesives

Slow to develop because happen must penetrate epidermis and combine with normal epidemiology protein to form Antigen

Erythems, edema, pruritus, blisters

Front 39

Tuberculin test

Back 39

Myoplasma tuberculosis antigen injected into dermis

Positive results indicate previous exposure to M. Tuberculosis enough to cause hypersensitivity reaction. Does not necessarily mean you have active TB

Front 40

Tx for chronic transplant rejection

Back 40

Immune suppressants

Front 41

Graft-verses-host disease +Ex

Back 41

Immune suppressed host attacked by T-lymphocyte from donor tissue

They attack host antigen as foreign

Ex bone marrow transplant

Front 42

Granulomatous hypersensitivity

Back 42

Caused by persistent antigen Macrophages are unable to destroy. Wall off Ag in connective tissue. Inflammatory cells form a mass called granuloma

Over time center of granuloma can undergo necrosis

Eventually fibroblasts produce collagen and make the granuloma fibrotic w/ scar tissue

Front 43

Immunodeficiency due to + first clinical indicators + in children

Back 43

Due to one or more components of immune system not functioning

Infections

In children first see as recurrent or untreatable infections

Front 44

Immunodeficiency 2 examples

Back 44

SCID severe combined immunodeficiency disorder

B-cell disorders

Front 45

SCID

Back 45

Lack of T-cells and sometimes also B-cells

Group of disorders

Genetically determined

Front 46

B-cell disorders

Back 46

Most common type is selective IgA deficiency

Prone to respiratory, GI and urinary tract infections

Front 47

HIV disease and AIDS

Front 48

Hallmark of Aids

Back 48

Loss if CD4 cells due to HIV infections

Front 49

Etiology of HIV

Back 49

HIV type 1- most common

HIV type 2- endemic in West Africa

Front 50

HIV is a ___virus meaning __

Back 50

Retrovirus

Contains RNA

Front 51

HIV infects (cells)

Back 51

CD4 (helper T-cells) and macrophages (they also have CD4 protiens but fewer than helper T-cells)

Front 52

Surface glycoprotein on HIV

Back 52

gp120

Front 53

gp120 binds to ___ and allow__

Back 53

CD4 protiens in CD4 cells and allows virus to enter cell

Front 54

Viral RNA ___ using __. This becomes __.

Back 54

Is transcribed into DNA,

Viruses reverse transcriptase enzyme

Spliced into host cells DNA

Front 55

DNA replicated

Back 55

Viral and host as viral is permanently appart of host DNA

Front 56

CDC classification matrix is based on

Back 56

CD4 levels

Clinical

Front 57

Catagories based on CD4 levels

Back 57

Category 1 >500/microL

Category 2 200-499/microL

Category 3 < 200/mircoL

Front 58

Clinical Categories

Back 58

A- Asymptomatic or generalized lymphadenopathy

B- symptoms of immune deficiency not serious enough to be in C

C- includes conditions listed in AIDS surveillance of CDC

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Persons in catagory _ or _ considered to have AIDS

Back 59

3 or C

Front 60

Treatment goal is

Back 60

To delay disease progression, maintain immune system function, decrease viral load and minimize clinical manifestations

Front 61

Opportunistic diseases are

Back 61

Treated individually with standard protocols

Front 62

HAART

Back 62

Highly Active Antiretroviral therapy

Uses combination of drugs

Front 63

Drugs aimed at stopping replication(4)

Back 63

°Nucleoside and ninnucleoside reverse transcriptase inhibitors

°Proteases inhibitors

°Fusion of entry inhibitors

°Integrates strand transfer inhibitors

Front 64

Proteases inhibitors

Back 64

Block enzymes essential for virus replication

Work later in infection

Front 65

Urticaria

Back 65

Hives

Front 66

Pruritus

Back 66

Itching

Front 67

Erythema

Back 67

Red skin

Front 68

Dyspnea

Back 68

Difficulty breathing

Front 69

Bronchial constriction

Back 69

Causes wheezing, coughing