module 2 review questions Flashcards
Define hypersensitivity.
An altered immunologic response to an antigen that results in disease or damage to the individual
What are two alternate names for Type I sensitivity?
Allergic reactions and immediate hypersensitivity
Describe the mechanism of a Type I response, including the sensitizing exposure and the re-exposure (including the immediate and longer-term response)
Sensitizing exposure:
Upon encountering allergen for first time and with help of T helper 2 cells, B lymphocytes differentiate into plasma cells which produce IgE
IgE spends a very short time in bloodstream, as the Fc portion (stem) rapidly binds to mast cells
When enough IgE has bound, the person is “sensitized” to antigen
Reexposure
Immediate response – symptoms occur 5-30 mins after exposure
When the antigen enters the system for this second time, it can bind to the arms of the IgE which is bound to the mast cells
Mast cell degranulation > histamine > inflammation
Longer-term response:
Begins 8-12 hours later, lasts 24-36 hours
Mast cells generate leukotrienes, prostaglandins, chemokines and cytokines -> further inflammation and other local and systemic effects occur
What are 3 actions of histamine?
Vasodilation, increase permeability, bronchoconstriction
Where are the antigens located that react with the antibodies in a Type II response?
Fixed on the surface of various body cells or specific tissues
Where are the antigens initially located that react with the antibodies in a Type III response?
Formed in circulation
Describe the mechanism of each of the following two types of Type IV hypersensitivity, and be familiar with examples of each: a. Delayed hypersensitivity b. Direct cell mediated cytotoxicity
Both start with: the antigen is ingested by an antigen presenting cell which is then transported to a lymph node and presents the antigen to helper T 1 cells
Delayed hypersensitivity:
Helper T 1 cells are activated, proliferate and migrate back to tissues, releasing inflammatory cytokines
This attracts monocytes to area -> macrophages
Macrophages release lysosomal enzymes & ROS -> tissue destruction
Example: tuberculin skin test
Direct cell mediated cytotoxicity
The first steps are the same as with delayed type, but once the helper T 1 cells are activated:
The helper T 1 cells then activate cytotoxic T cells
Cytotoxic T cells travel throughout the body, directly destroying body cells displaying the antigen
Example: type 1 diabetes
Name 3 areas of the body where the effects of mast cell degranulation can be significant. Describe the effects in each area and relate these to the signs and symptoms that occur in each area.
Gastrointestinal tract
Effects: Increased fluid secretion, increased peristalsis
Signs/symptoms: Vomiting & diarrhea
Airways
Effects: Decreased diameter, increased mucus secretion
Signs/symptoms: congestion and blockage of airways (wheezing, coughing), swelling and mucus secretion in nasal passages
Blood vessels
Effects: increased blood flow, increased permeability
Signs/symptoms: increased fluid in tissues causing increased flow of lymph to lymph nodes, increased cells and protein in tissues, increased effector response in tissue
Describe the signs and symptoms (“S&S”) of allergic rhinitis.
Sneezing, itching, watery nasal discharge
Severe attacks lead to systemic symptoms (general malaise) but afebrile (no fever)
What are the treatments for allergic rhinitis?
Antihistamines, decongestants, nasal corticosteroids, allergen avoidance if known
What is involved in a “skin test” for this type of allergy?
Can be performed to determine which compounds are allergens (affected people can then hopefully avoid the allergen)
Describe the mechanism behind desensitization therapy.
Minute quantities of antigen are injected in increasing doses over a long period of time, with the hope of developing IgG against the allergen to neutralize it so that it can’t bind to IgE and produce allergic response
What part of this mechanism can cause anaphylactic shock?
Inflammatory mediators can cause massive systemic vasodilation and increased capillary permeability leading to anaphylactic shock
Describe the symptoms of anaphylaxis (There are 3 systems involved).
Itchy rash, flushed skin
Laryngeal edema, wheezing / difficulty breathing
Low blood pressure and tachycardia
Identify the primary treatment and describe what two actions this treatment has. (anaphylaxis)
Injection of epinephrine
Relaxes smooth muscle in bronchioles producing bronchodilation
Contracts smooth muscle in vessels (= vasoconstriction) to restore blood pressure
What other treatments can be given for anaphylaxis? (There are 3)
Administration of intravenous fluids
Corticosteroids: potent inhibitors of inflammatory process
antihistamines
Describe the signs and symptoms of bronchial asthma.
Recurrent episodes of wheezing, breathlessness, chesst tightness and coughing, particulary at night or early in the morning
What is the difference between an extrinsic and an intrinsic trigger for bronchial asthma?
Extrinsic = type I response to environmental allergens (pollen, animal dander)
Intrinsic = (non-type I immune mechanisms) respiratory infections, cold air, emotional stress
Describe the acute phase response of bronchial asthma. (This should be a very familiar mechanism.)
Usual type I reaction, leading to bronchoconstriction, edema of airway walls and increased mucous production
Describe the late phase response of bronchial asthma: a. Why does it occur at a later time? b. What compounds are synthesized and released by the mast cells? What do they do? c. What inflammatory cells are summoned to the area and what do they do?
Mast cells continue to synthesize inflammatory compounds (but this takes time)
Prostaglandins and leukotrienes released by mast cells cause the same, but more pronounced, effects as histamine in the acute phase response
Cytokines released by mast cells summon eosinophils and neutrophils that release compounds, damaging tissue (airway fibrosis and permanent narrowing) airway hyperresponsiveness develops
What two types of drugs are given for quick relief of an asthma attack?
Bronchial dilators (those that cause relaxation and those that oppose constriction), through inhalation, bring relief within 30 mins
Corticosteroids, given orally or parenterallym oppose the late-phase response
Be familiar with the types of drugs given for long-term treatment of asthma.
Anti-inflammatories (corticosteroids) to decrease airway hyperresponsiveness
Agents to stabilize mast cells (I.e. decrease their degranulation)
Smooth muscle relaxants
Leukotriene modifiers
By which two hypersensitivity reactions are autoimmune reactions usually caused?
Usually type II or type III
Describe two possible mechanisms for an autoimmune disease.
Release of sequestered antigens
Places in the body that are not drained by the lymph system do not release self-antigens that the immune system can learn to ignore. If an injury later releases these self-antigens into the body, an immune reaction can occur which could then damage the tissue from which the antigen came
Molecular minicry
Infection with organism possessing Ag close in structure to a self-antigen
Individual becomes infected with pathogen. Unfortunately, an antigen on the pathogen that the immune system has learned to recognize closely resembles a protein in the body. Immune system now attacks body protein (which has now become a “self-antigen”)
Describe SLE: a. two self-antigens that are molecular (what type of hypersensitivity would this be?) b. three self-antigens that are cellular (what type of hypersensitivity would this be?) c. the most characteristic self-antigens d. be familiar with signs and symptoms (easier to remember if you relate the mechanism of the hypersensitivity to the S&S) e. treatment
Nucleic acids, coagulation proteins (antibody complex with them, and then are deposited in tissues, causing inflammation (type III)
Lymphocytes, platelets, erythrocytes (basically all of the formed elements, since the antigen are part of the cell surface, type II)
Nucleic materials (nucleic acids, histones)
Tend to affect all body systems, and include swollen, painful joints, a “butterfly rash” on face, or body rash (that increases with sun exposure), inflammation of various area (glomerulonephritis)
No cure. NSAIDs can be used to suppress inflammation and oain. Immunosuppressive drugs can be used in more serious instances
Identify and explain the type of hypersensitivity reaction on which the alloimmune response involved with the ABO blood grouping is based.
Every cell of the body has numerous compounds on the surface of the cell that are unique in structure for each individual
Carbohyrdate chains on RBC that are part of the ABO blood grouping system
Because these chains can cause the production of antibody in those individuals whose RBC do not possess them, they are antigens
If such an event occurred, the RBC would be attacked by the immune system of the recipient and be destroyed (type II)
Describe the influence of HLA’s/MHCI’s on tissue transplantation.
Of great influence in the recognition of foreign tissue are the MHCl proteins that occur on every nucleated cell
Genetic information to produce these proteins is carried on chromosome 6, and there are hundreds of different alleles, which means no 2 humans will have exactly the same structure for HLAs
Because this information is inherited, the more closely related 2 people are, the closer in structure there HLA’s will be
Before a transplant occurs, the tissue of the donor and recipient must be tissue typed to ensure as close a match as possible
The poorer the HLA match, the more likely the recipient’s immune system will react to the transplanted tissue
Describe graft vs. host disease (2 characteristics that make it possible), and in which type of transplant it most often occurs.
When the transplanted tissue contains components of the donprs immune system that recognize the recipient’s tissue as foreign, and attack it && recipient is usually immunocompromised, so their immune system can’t fight back effectively
Bone marrow transplants
Describe immunodeficiency and differentiate between primary and secondary.
Failure of the immune system to function normally, resulting in increased susceptibility to infection
Primary: congenital – caused by genetic defect
Secondary: acquired – caused by cancer, infection, aging
What is the main clinical manifestation of immunodeficiency?
Recurrent severe infections
identify the usual cause of a PID, and describe the 5 main classes of PID.
Immediate: appear within the first 2 years
Progressive: appearing in 20-30 years
B lymphocyte
No circulating antibodies or sometimes only one class of antibody affected
T lymphocyte
Low cell-mediated immunity
Because helper T cells are important to B cell function, there is also a low level of circulating antibodies
Sometimes only a defect in defense against a particular pathogen
Combined (both B & T cells deficient)
Most severe is SCIDs: few lymphocytes, no antibodies, reduced thymus
Bare lymphocyte syndrome: no MHC-I or MHC-II molecules therefore no way for cells to interact. Death usually occurs before 5
Complement
Most severe is C3 deficiency – involved in all pathways of complement protein production. Increased risk for infection with encapsulated bacteria
Phagocyte (neutrophils. Macrophages)
Defects of phagocyte number, function or both
Increased risk for infection by bacteria
Describe the treatments for B cell deficiency, lymphocyte deficiency, and SCID.
B cell deficiency: regular infusions of gamma-globulins (antibody rich plasma)
Lymphocyte deficiency & SCID: replacement of stem cells through implantation with stem cell rich tissue (bone marrow)
Define secondary immune deficiencies and give one example.
Are acquired: complication of other pathophysiologic conditions & diabetes mellitus
How is HIV transmitted?
Blood, semen, vaginal fluids and breast milk
Why does the HIV virus cause AIDS?
HIV destorys helper T cells, required for development of plasma and cytotoxic T cells (therefore, essential for both humoral and cell mediated immunity)
What are the early stage symptoms of HIV infection?
Flu-like symptoms which disappear however, virus is multiplying in lymph nodes and person is infective
How is AIDS diagnosed? (Be familiar with common opportunistic infections and malignancies, especially one example of an opportunistic infection, and one example of a malignancy.)
With symptoms that include atypical infections and cancers and chronic disease syndromes
Opportunistic infections: PCP – a fungal microbe found in lungs of healthy individuals
Malignancies: kaposi sarcoma - viral induced skin cancer
How is HIV infection treated?
Mainly target mechanisms of viral transmission and replication. Cannot cure disease as HIV can incorporate into DNA of host cells, where antimicrobial agents cannot be effective. Treat secondary infections
Why is HIV infection difficult to treat and why is a vaccine unlikely?
HIV is as variable as the influenze virus
What are 3 reasons for the poor antigenic response of the elderly?
Cells of immune system not able to proliferate as rapidly
Total number of T cells is maintained, but they have decreased cytotoxicity
Antibody production is also decreased
Therefore, not as many immune cells, and the ones that are present don’t function as vigorously
Define the following terms: allergy, allergen, anaphylaxis, immediate vs. delayed hypersensitivity reaction, autoimmune response, alloimmune response, urticaria, pruritus
Allergy: refers to hypersensitivity to environmental antigens
Allergen: an antigen involved in an allergic response
Pruritus: symptom of itching
Urticaria: a localized pruritic skin disruption characterized by wheals and hives
