Disorders of immune response Flashcards
Innate vs Adaptive Immunity
- Innate (born with) e.g. skin, mucous membranes
Able to recognize self/non-self
Reacts to microbes
Leukocytes, macrophages, NKC
Complement system:
- Assist antibodies and phagocytes to destroy pathogens
2. Adaptive Responds to antigens -Infection -Tumor cells -Transplanted cells
B-cells (type of wbc) secretes antibodies
Cytotoxic T-cells act directly on infected cells
Hypersensitivity
- Excessive or inappropriate activation of the immune response
- The body is damaged by the immune response, rather than by the antigen (often called allergen)
Type I Hypersensitivity
- Commonly called “allergic reactions”
- Systemic or anaphylactic reactions
- Local or atopic reactions
examples:
-Rhinitis (hay fever)
-Food allergies
-Bronchial asthma
-Hives
-Atopic dermatitis
Anaphylaxis
- Systemic response to the inflammatory mediators released in type I hypersensitivity
- Histamine, acetylcholine, kinins, leukotrienes, and prostaglandins all cause vasodilation
-Acetylcholine, kinins, leukotrienes, and prostaglandins all can cause bronchoconstriction
Type II Hypersensitivity
- Cytotoxic
- IgG or IgM attack antigens on cell surfaces
1. Results in cell lysis (opsonization) - Transfusion reactions
- Rh disease (hemolytic disease of the newborn)
- Drug reactions
2. Results in inflammatory process - glomerulonephritis, transplant rejection
3. Results in cell dysfunction - Graves disease (TSH stimulated = hyperthyroidism)
- Myasthenia Gravis (acetylcholine or receptors blocked)
Type III Hypersensitivity
-Circulating inactive antigen + antibody immune complex
-Immune complexes deposit on walls of blood vessels and activate complement
-Blood vessels are damaged
Eg:
-Autoimmune vasculitis
-Glomerulonephritis
-Systemic lupus erythemoatosus (SLE)
-Serum sickness
Type IV Hypersensitivity
1. Cell-mediated: sensitized TH1 cells attack antigen and cell damaged as a result Occurs even if pathogen not harming cell E.g. some types of hepatitis 2. Direct cell-mediated cytotoxicity - Viral reactions 3. Delayed-type hypersensitivity -Tuberculin test -Allergic contact dermatitis
Autoimmune Diseases: Self tolerance, Central tolerance, Peripheral tolerance
Self-tolerance is ability to differentiate self from non-self
Maintained by
-Central tolerance which deletes T&B cells (in thymus; in bone marrow)
-Peripheral tolerance which deletes activated T&B cells.
If immune system is unable to differentiate, body tissues are destroyed
Immunodeficiency Disorders: Primary and aquired
- Primary (congenital or inherited)
-B-cell deficiencies
-T-cell deficiencies
CD4 helper
CD8 cytotoxic
-Combined immunodeficiencies - Acquired (more common)
AIDS
Acquired Immunodeficiency Syndrome (AIDS)
- Caused by Human Immunodeficiency Virus (HIV) attacking CD4 T lymphocytes
- Attaches to CD4 T cell receptors
- Enters cell
- Attaches own RNA to cell’s DNA
- Uses cells energy to reproduce more viruses
What does AIDS result in?
Results in:
- Profound immunosuppression
- Malignancies
- Opportunistic infections
- Wasting
- CNS degeneration
Human Immunodeficiency Virus (HIV) Transmission
-Transmitted by blood/body fluids
-Pre-ejaculate, semen, vaginal fluid (not saliva or urine)
-Breast milk (30-40% of cases)
-Blood to blood contact
-Contaminated needles
-Transfusions
-During pregnancy or birth
-In-utero (15-20%)
-During labor and delivery (45-50%)
Occupational exposure uncommon
Stage 1 of HIV infection
Stage 1: Primary infection phase
- Signs of systemic infection 1-4 weeks post exposure
- fever, fatgue, myalgia, sore throat, night sweats, GI issues, lymphadenopathy, maculopapular rash, h/a
- Last 7-10 days
- Rapid viral replication decreases CD4 t-cell count
- Most contagious during “window period” for 1-6 months prior to seroconversion
Stage 2 of HIV infection
Stage 2: Latent period (approx. 10 years)
- No signs and symptoms
- Virus replicates
- CD4 T-cell count decreases
- Possible lymphadonopathy
Stage 3 of HIV infection
Stage 3: Overt AIDS
- T-cell count low
- Death in 2-3 years without treatment
