Module 2 Chapter 12 Flashcards
Immunodeficiency
One or more parts of the immune system are working improperly. Increases susceptibility to illnesses that the normally working immune system would have fought off.
Primary immunodeficiency disorders
Congenital (developed during birth)
or
Inherited (passed on from parents to offspring)
Secondary immunodeficiency disorders
Develop later in life due to various pathophysiologic processes.
Briefly describe:
1. Innate Immunity
2. Adaptive Immunity
- Innate Immunity - the body’s first line of defense against invading organisms. Composed of the epithelial cells, leukocytes (monocytes, macrophages, neutrophils, eosinophils, DC, NK cells). The complement system which plays a large role in innate and adaptive immunity. Slow down the spread of the infection and spread word to the adaptive immune system that something is going on.
- Adaptive Immunity - the body’s second (last) line of defense. A slower but more efficient and effective form of immunity. Further split into the humoral and cell-mediated portions. The humoral portion is run by B-lymphocytes which work to produce 2 subsets - one for making antibodies and another for memory. The cell mediated portion relies on T-cells to carry out it’s functions.
What are some ways that secondary immunodeficiency disorders can develop?
- Malnutrition
- Infection
- Cancer
- Immunosuppressive therapy (steroids or transplant rejection medicines)
Complement System Disorders
1. What parts of the cascade can be affected?
2. Clinical manifestations
- Any part of the complement system cascade can be affected. If C3 is affected, this causes the greatest decline in function due to all 3 complement system pathways (lection, classical, and abnormal) relying on this guy.
- The clinical manifestations seen with complement disorders depends on what part of the pathway is affected. Ones listed in the reading are: Neisseria gonorrhoeae, N. meningitidis, hemolytic uremic syndrome, and adult-onset-macular degeneration.
Hereditary Angioneurotic Edema
1. Cause?
2. Symptoms?
- An inherited complement system disorder that results due to a deficiency of C1.
- These deficiencies result in the release of vasoactive substances that increase vascular permeability. This results in spontaneous development of deep tissue pockets of localized tissue swelling. This swelling can occur pretty much anywhere but is especially dangerous when it involves the upper airway. Commonly preceded by the appearance of erythema marginatum (macular nonpruritic rash).
Hypersensitivity Reaction
The mechanisms of the immune system that work to protect the body can also go overboard leading to the body being damaged. Hypersensitivity is defined as an abnormal and excessive response of the immune system that results in host tissue damage or injury.
Type 1 Hypersensitivity Disorders
1. Mediator
2. What sets this hypersensitivity reaction off? Common examples?
3. How does it present?
4. What cells are involved and what are their functions?
- These reactions are mediated by IgE. IgE is found in small amounts in the body and plays a role in allergic and inflammatory processes.
- Type 1 hypersensitivity reactions are initiated in response to an antigen (allergen). The reactions can be in response to environmental (dust, dander, pollution), medical, or pharmaceutical (drug allergies) means.
- Type 1 reactions presentation depend on the portal of entry. For instance, if an allergen comes in contact with the skin - contact dermatitis can result. If the allergen is consumed or is inhaled this can result in a systemic response which is more dangerous and can be life threatening.
- Cells:
A. B - lymphocytes - Produce specific antibodies. Typically make IgM and IgG antibodies but when stimulated by the CD4 cells in response to exposure to an allergen, switch the production to IgE cells.
B. CD4 cells - CD4 cells are directed to differentiate into T1H or T2H. T1H differentiation is directed by DC and macrophages. T2H is differentiation is directed by mast cells.
C. Mast cells - contain histamine and heparin which the IgE molecules stimulate the release of.
What role do B - lymphocytes play in type 1 hypersensitivity reactions?
B - lymphocytes - Produce specific antibodies. Typically make IgM and IgG antibodies but when stimulated by the CD4 cells in response to exposure to an allergen, switch the production to IgE cells.
CD4 cells differentiation during type 1 hypersensitivity reactions. What do these newly differentiated cells do?
CD4 cells - CD4 cells are directed to differentiate into T1H or T2H. T1H differentiation is directed by DC and macrophages. T2H is differentiation is directed by mast cells.
T1H - tell B-lymphocytes to produce IgM and IgG.
T2H - tell B-lymphocytes to produce IgE.
Mast cells/ Basophils in type 1 hypersensitivity reactions
Mast cells - contain histamine and heparin which the IgE molecules stimulate the release of.
Phases of Type 1 hypersensitivity reactions
1. Time frame
2. Symptoms
Primary phase -
1. Begins 5-30 minutes after exposure and subsides roughly 60 minutes later.
2. Characterized by the sterotypical signs of anaphylaxis - vasodilation, smooth muscle spasm, vascular damage.
Secondary phase -
1. 2-8 hours after resolution of the primary phase, can last days
2. Mucosal edema, secretions, WBC infiltration, bronchospasm
Type 2 hypersensitivity reactions
Anti-body mediated Disorders.
IgM and IgG antibodies attack antigens on a specific cell type. This attack results in the cells death or dysfunction. This can result in the body producing antibodies that destroy its own cells.
Can be seen as the cause of many autoimmune disorders.
Type 3 Hypersensitivity reactions
IgG and IgM molecules bind with free floating antigens, forming complexes. These complexes activate the complement system which damages nearby tissue damage. Can result in altering of blood flow, increased vascular permeability, and damage to nearby tissues. Serum sickness. Arthus reaction.
