Disorders of the Immune Response, chap 16 Flashcards
Innate Immunity: “natural immunity”
> Early rapid response (min-hrs). First line of defence
> physical, chemical, molecular, and cellular defenses that are in place bfr infection
> able to recognize self/non-self
> reacts to microbes (bc these are non-self)
> skin, mucous membrane, phagocytic leukocytes** (neutrophils and macrophages), specialized lymphocytes (NK cells), and several plasma proteins.
> complement system- assists antibodies and phagocytes to destroy pathogens
Adaptive Immunity:
> second major immune defense.
> responds less rapid, but more effectively to : infection, tumor cells, transplanted cells
> uses focused recognition of each foreign agent
> B-cell (type of WBC)- secretes antibodies
T-cell- directed by B-cell activity.
Hypersensitivity
> excessive or inappropriate activation of the immune response
> the body is damaged by the body rather than the antigen (often called allergen)
–cell death that shouldn’t have happened. The bodies response damages the body
Type 1 Hypersensitivity
Allergic, Anaphylaxis, Atopy
“allergic rxn”
> systemic or anaphylactic reactions
> local or atopic reactions:
- Rhinitis
- Food
- Bronchial asthma
- Hives
- Atopic Dermatitis - hives and eczema
Anaphylaxis
Type 1 hypersensitivity
Systemic response to the inflammatory mediators released in type 1 hyper
– Histimine, acetylcholine, kinins, leukotrines, and prostaglandins cause = vasodilation and decreased BP.
– acetylcholine, kinins, leukotrines, and prostaglandins cause = bronchoconstriction
Tx: epinephrine
Type 2 hypersensitivity
AntiBody
- -Cytotoxic- toxic to that cell
- IgG or IgM attack antigens on cell surfaces
- Results in Cell Lysis (opsonization)
- - ABO blood incompatibility (transfusion reaction)
- - Rh disease (hemolytic disease of new born)
- - drug reaction - Results in Inflammatory Process
- - Glomerulonephritis, transplant rejection - Results in Cell Dysfunction
- - Graves disease- over active thyroid
- - Myasthenia Gravis- acetacholine or receptor blocked. muscle weakness with out atrophy
Type 3 Hypersensitivity
Immune Complex
Circulating inactive antigen + antibody immune complex – causes deposit on walls of blood vessels and activate complement
> Immune complexes deposit on the walls of blood vessels and activate complement = Inflammation
> Blood vessels are damaged
Ex.
–Autoimmune vasculitis- inflam of blood vessel
– Glomerulonephritis
– Systemic Lupus Erythematosus (SLE)- autoimmune attacks healthy tissue
– Serum sickness- drug reaction
Type 4 Hypersensitivity
Delayed
does not involve antibodies
Cell-mediated: Sensitized TH1 cells attack antigen and cell damaged as a result
– occurs even if pathogen is not harming cell
– ex. some types of hepatitis
2 types:
- Direct cell-mediated cytotoxicity
- - viral infections - Delayed-Type Hypersensitivity
- -TB test
- - Allergic contact dermatitis. ex. poison ivy
Autoimmune Diseases
Self-tolerance is ability to differentiate self from non-self
– Maintained by “central tolerance” which deletes T and B cells (in thymus and bone marrow)
–Maintained by “peripheral tolerance” which deletes activated T and B cells
If immune system is unable to differentiate, body tissues are destroyed
Immunodeficiency Disorders
- Primary- (congenital or inherited)
- -B-cell deficiencies
- - T-cell deficiencies: CD4 helper and CD8 cytotoxic
- - Combines Immunodeficiency’s - Acquired (more common)
- - AIDS
Acquired Immunodeficiency Syndrome (AIDS)
Caused by Human Immunodeficiency Virus (HIV) which attacks the CD4 T cell receptors.
> HIV attaches to the CD4 T-cell receptors
enters the cell
attaches own RNA to cells DNA
uses cells energy to reproduce more virusus
AIDS results in: 5
- Profound Immunosuppression
- Malignancies
- Opportunistic infections
- Wasting
- CNS degeneration
Human Immunodeficiency Virus (HIV):
Transmitted by blood/body fluids:
> pre-ejaculate, semen, vag fluid (not saliva or urine)
> breast milk 30-40%
> blood to blood contact :
– needle sharing
– transfusions
– During pregnancy or birth: in-urtero 15-20% and during labor/delivery 45-50%
> Occupational exposure uncommon
Stages of HIV:
Stage 1 : Primary infection phase
> signs of systemic infection 1-4 weeks post exposure
- -fever, fatigue, sore throat, night sweats, GI issues, lymphadenopathy, muscular rash, ha
- -lasts 7-10 days
> Rapid viral replication decreases CD4 t-cell count
Seroconversion: Immune system responds and antibodies against HIV appear 1-6 months and have started to develop the antibodies
***Most contagious during “window period” for 1-6 months prior to seroconversion
Stages of HIV:
Stage 2 : Latent Period
> aprox 10 years > no signs and symp >virus is replicating > CD$ count drops >possible lymphadenopathy
