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UNMC_ Pathophysiology II Exam II.
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UNMC: Pathophysiology II Exam II4 Types of Immune Alterations - ANS-Exaggerated, misdirected against host's own
cells, Directed against beneficial foreign tissues, and Deficiency
Hypersensitivity - ANS-- Autoimmunity is when the body starts to think of its own
antigens as foreign.
- Isoimmunity is when the body reacts against tissues of other members of the same
species.
4 Types of Hypersensitivity - ANS-- Type I: IgE mediated allergic reactions / allergies
- Type II: tissue-specific / blood transfusion reactions
- Type III: immune complex mediated reactions / antigen antibody form and deposit
tissues
- Type IV: cell mediated reactions / involve T cells and macrophages
Allergy/Anaphylaxis - ANS-- Rapid immune response with re-exposure to an antigen.
Systemic - ANS-1. Bronchial construction/edema (life threatening)
2. Skin/itching (pruritis)/erythema
3. GI - abdominal cramps, vomiting, diarrhea
4. Mucous membranes - increased secretions
5. Vasculature - increased vascular permeability + vasodilation (life threatening)
Systemic Lupus Erythematosus (SLE) - ANS-chronic, autoimmune, multi-system
inflammatory disease.
- Most activity is Type III hypersensitivity, some Type IV
- Antigen antibody complexes form and deposit in vessel walls
- Step 1: B cell activates the IgG, which targets and attacks the DNA on the vessel walls
- Step 2: The T helper cells add to the stimulation of the B cells
- Step 3: Macrophages also attack the DNA on the vessel walls
- Step 4: The IgG attack red blood cells along with the DNA
- Step 5: The T suppressor cells are not very good at slowing down this process
- Clinical Manifestations: arthritis of peripheral joints, vasculitis/photosensitivity, renal
disease, anemia, and CV disease - pericarditis
Rheumatoid Arthritis - ANS-autoimmune, inflammatory joint disease / destruction of
synovial membrane
- Type III and Type IV hypersensitivity
, - Normal antibodies become autoantibodies (IgM + IgG) and attack antigens on cell
membrane
- Clinical Manifestations:
o Early: synovitis and systemic manifestations of inflammation (minor)
o Then, start to get stiffness and tenderness of the joints
o Late: pain, deformity, loss of function, rheumatoid nodules, ulnar drift
Immune Deficiencies - ANS-deficient, impaired function to immune response /
congenital and acquired
- Congenital (Primary): genetic - immune cells improperly developed
- Acquired (Secondary): associated physiologic conditions - PG, infancy, elderly, chronic
illness, malnutrition / Iatrogenic deficiencies / trauma / stress
HIV/AIDS (Acquired Immune Deficiency Syndrome):
- viral disease (a retrovirus) - HIV-1 carries its genetic coding in RNA / infects and
depletes a portion of immune suppressor cells (cells with CD-4 receptors) and helper T
cells and then starts to attack macrophages and cytotoxic T cells.
Step 1: Glycoprotein (gp120) binds to CD-4 T cell.
Step 2: Chemokee aids in binding of gp120.
Step 3: Viral RNA is converted into DNA (with help - Reverse Transcriptase, Integrase,
and Protease enzymes)
Step 4: DNA is inserted and integrates into helper T cell DNA and takes over the cell
Spreads to other cells in three ways - ANS-1. Remain latent (no spread)
2. New HIV particles bud out
3. Lysis of cell with release of particles
Four Possible Conditions - ANS-1. Serologically negative: but can have virus without
antibodies produced or detected yet.
2. Serologically positive: but asymptomatic detachable antibodies, but no real symptoms
3. Early stages of HIV disease: symptoms but not AIDS
4. AIDS: serious clinical symptoms or malignancies and often less than 200 T helper
cells.
Clinical Manifestations - ANS-1. Serologically negative: high risk groups, ability to
unknowingly transmit virus, and most are asymptomatic
2. Serologically positive: 20% can remember experiencing flu or mono like illnesses
3. Early stages of HIV disease: chronic lymphadenopathy, night sweats, recurrent
fevers, flu-like, fatigue, anorexia, weight loss, and diarrhea
4. AIDS: opportunistic infections and malignancies
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