module 2 review questions

Question 1

Define hypersensitivity.

Answer 1

An altered immunologic response to an antigen that results in disease or damage to the individual

Question 2

What are two alternate names for Type I sensitivity?

Answer 2

Allergic reactions and immediate hypersensitivity

Question 3

Describe the mechanism of a Type I response, including the sensitizing exposure and the re-exposure (including the immediate and longer-term response)

Answer 3

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

Question 4

What are 3 actions of histamine?

Answer 4

Vasodilation, increase permeability, bronchoconstriction

Question 5

Where are the antigens located that react with the antibodies in a Type II response?

Answer 5

Fixed on the surface of various body cells or specific tissues

Question 6

Where are the antigens initially located that react with the antibodies in a Type III response?

Answer 6

Formed in circulation

Question 7

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

Answer 7

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

Question 8

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.

Answer 8

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

Question 9

Describe the signs and symptoms (“S&S”) of allergic rhinitis.

Answer 9

Sneezing, itching, watery nasal discharge

Severe attacks lead to systemic symptoms (general malaise) but afebrile (no fever)

Question 10

What are the treatments for allergic rhinitis?

Answer 10

Antihistamines, decongestants, nasal corticosteroids, allergen avoidance if known

Question 11

What is involved in a “skin test” for this type of allergy?

Answer 11

Can be performed to determine which compounds are allergens (affected people can then hopefully avoid the allergen)

Question 12

Describe the mechanism behind desensitization therapy.

Answer 12

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

Question 13

What part of this mechanism can cause anaphylactic shock?

Answer 13

Inflammatory mediators can cause massive systemic vasodilation and increased capillary permeability leading to anaphylactic shock

Question 14

Describe the symptoms of anaphylaxis (There are 3 systems involved).

Answer 14

Itchy rash, flushed skin

Laryngeal edema, wheezing / difficulty breathing

Low blood pressure and tachycardia

Question 15

Identify the primary treatment and describe what two actions this treatment has. (anaphylaxis)

Answer 15

Injection of epinephrine

Relaxes smooth muscle in bronchioles producing bronchodilation

Contracts smooth muscle in vessels (= vasoconstriction) to restore blood pressure

Question 16

What other treatments can be given for anaphylaxis? (There are 3)

Answer 16

Administration of intravenous fluids

Corticosteroids: potent inhibitors of inflammatory process

antihistamines

Question 17

Describe the signs and symptoms of bronchial asthma.

Answer 17

Recurrent episodes of wheezing, breathlessness, chesst tightness and coughing, particulary at night or early in the morning

Question 18

What is the difference between an extrinsic and an intrinsic trigger for bronchial asthma?

Answer 18

Extrinsic = type I response to environmental allergens (pollen, animal dander)

Intrinsic = (non-type I immune mechanisms) respiratory infections, cold air, emotional stress

Question 19

Describe the acute phase response of bronchial asthma. (This should be a very familiar mechanism.)

Answer 19

Usual type I reaction, leading to bronchoconstriction, edema of airway walls and increased mucous production

Question 20

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?

Answer 20

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

Question 21

What two types of drugs are given for quick relief of an asthma attack?

Answer 21

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

Question 22

Be familiar with the types of drugs given for long-term treatment of asthma.

Answer 22

Anti-inflammatories (corticosteroids) to decrease airway hyperresponsiveness

Agents to stabilize mast cells (I.e. decrease their degranulation)

Smooth muscle relaxants

Leukotriene modifiers

Question 23

By which two hypersensitivity reactions are autoimmune reactions usually caused?

Answer 23

Usually type II or type III

Question 24

Describe two possible mechanisms for an autoimmune disease.

Answer 24

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”)

Question 25

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

Answer 25

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

Question 26

Identify and explain the type of hypersensitivity reaction on which the alloimmune response involved with the ABO blood grouping is based.

Answer 26

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)

Question 27

Describe the influence of HLA’s/MHCI’s on tissue transplantation.

Answer 27

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

Question 28

Describe graft vs. host disease (2 characteristics that make it possible), and in which type of transplant it most often occurs.

Answer 28

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

Question 29

Describe immunodeficiency and differentiate between primary and secondary.

Answer 29

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

Question 30

What is the main clinical manifestation of immunodeficiency?

Answer 30

Recurrent severe infections

Question 31

identify the usual cause of a PID, and describe the 5 main classes of PID.

Answer 31

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

Question 32

Describe the treatments for B cell deficiency, lymphocyte deficiency, and SCID.

Answer 32

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)

Question 33

Define secondary immune deficiencies and give one example.

Answer 33

Are acquired: complication of other pathophysiologic conditions & diabetes mellitus

Question 34

How is HIV transmitted?

Answer 34

Blood, semen, vaginal fluids and breast milk

Question 35

Why does the HIV virus cause AIDS?

Answer 35

HIV destorys helper T cells, required for development of plasma and cytotoxic T cells (therefore, essential for both humoral and cell mediated immunity)

Question 36

What are the early stage symptoms of HIV infection?

Answer 36

Flu-like symptoms which disappear however, virus is multiplying in lymph nodes and person is infective

Question 37

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.)

Answer 37

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

Question 38

How is HIV infection treated?

Answer 38

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

Question 39

Why is HIV infection difficult to treat and why is a vaccine unlikely?

Answer 39

HIV is as variable as the influenze virus

Question 40

What are 3 reasons for the poor antigenic response of the elderly?

Answer 40

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

Question 41

Define the following terms: allergy, allergen, anaphylaxis, immediate vs. delayed hypersensitivity reaction, autoimmune response, alloimmune response, urticaria, pruritus

Answer 41

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