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Flashcards in Chapter 17 Deck (53):

A) Type I hypersensitivities involve what type of antibody? [IgE mediated Type I hypersensitivity video]

Ige which binds to mast cells or basophils


B) What is sensitization? [Figure 17.1]

begins when a allergen induces antibody response.
IgE begins to be produced by the B cells and then the IgE molecules then attatch to basophils and mast cells and so when an allergen come in contact it illicits a response


C) What is the process of degranulation?

when spegific 2 mast cell's IgE's sense an allergen then they will come together and cross link. This results in histamine and other inflamatory mediators.


D) What causes the classic allergy symptoms?

degranulation: histamine= vaso dialations and bronchiolconstriction


E) What are hives? How is it identified? When do they occur?[Figure 17.2]

urticara: characterized by wheel(swelling) and flare(redness)
mast cells degranulate releaseing histamine causing the swelling


F) What are the symptoms of hay fever and when does it occur?

rhinitis: itching, teary eyes, sneezing. from airborne antigens


G) What causes asthma? How is it treated?

degranulation and release inflamatory mediators into the lower respiratory system. These mediators incled leukotrines and prostoglandins which cause bronchospasms and increased mucous production.
Treatment: Bronchodialators ie cortison like steroids. anti IgE therapy for prevention


H) What is systemic anaphylaxis and what can cause it?

antigen enters blood stream and spread throughout. the IgE's on basophils release their inflamatory mediators into blood stream resulting in a bp drop.
bee stings, peanuts, and penicillin injections.


I) What is Immunotherapy used for?

alters immune responses and decrease the negative feedback.


J) What is desensitization and how does it work?[Figure 17.3]

injecting people with the diluted allergen and slowly increase it. This helps IgG's to form and out compete the IgE's.


K) What is the medication omalizuMab used for?

prevents IGE's from binding to mast cells. this causes the IgG's toFc portion of the IgE's which prevents them from attatching to mast cells and basophils.


L) What are rhuMab’s?

q ????


A) What happens during a type II hypersensitivity reaction?

this is when the antibodies react with molecules on the surface of the cell and triggers it's destruction by compliment system or cytotoxicity . autoimmune diseases, transfusion reactions, and hemolytic disease


C) What happens during a transfusion reaction?

The antigens of others blood are attacked by antibodies and result in killing the rbs's wich release hemoglobin and peices of cells can cause clotts resulting in fever,damaging kidney, along with respiratory and digestive problems


D) How are blood types cross-matched in a clinical setting? [Table 17.2}

blood of donor mixed with recipient and if clumping they will not match


E) How is the Rh antigen different from the ABO system?

the rh negative do not have natural antibodies to rh antigens. These develop when they are exposed to rh positive cells.


F) When can a Rh-negative women become sensitized to the Rh antigen?

during childbirth(placenta ruptures) the babies rh positive antigens


G) What is Hemolytic disease of a newborn and how does it happen? [Figure 17.4]

when a infant's mother has developed rh antibodies an so blood passed through the placenta will attack the baby


H) When is the medication RhoGAM used?

This is anti rh antibodies. injected during pregnancy and shortly after the babay is born.. the anti rh antibodies bind to the rh positive erythrocytes that may have entered the mothers blood stream preventing cells from initiating immune response.


A) What are immune complexes and what do they cause? [Figure 17.5 and Immune Complex Type 3 Hypersensitivity video]

cause type 3 hypersensitivities.
consisting of IgG or IgM antibodies bound to a soluable antigen. These are removed by phagocytes wich Fc receptors lines with the Fc region on antigen.


B) What is disseminated intravascular coagulation and what causes it?

When the large immune complexes form a clot and then and block small blood vessels leading to organ failure.


C) What is the Arthus reaction?

localize immune complex reaction. this results in swelling and pain. ie when people get swelling at site of injection of vaccination


D) What is serum sickness?

caused by passive immunization.
when person is given antibodies from an animal and body recognizes antigens in serum and from enough complexes to result in fever,arthritis and kidney damage


A) What causes delayed-type hypersensitivity? [Delayed Type hypersensitivity video]

(type 4 hypersensitivities) antigen specific t cell responses. cell mediated reactions occure between 2-3 days following exposure to antigen


B) What is the tuberculin skin test? What does it test for? [Figure 17.6]

detects latent tb infections. they inject small an=mount of tb antigens under skin. The T cells will gather in area and release cytokines resulting in swelling.


C) What does delayed-type hypersensitivity cause when it happens with a chronic infection?

the t cells kill the microbes, but the release of cytokines released danaging the hosts tissues . ie leporacy the damaged sensory nerves


D) What causes contact dermatitis? [Figure 17.7 and 17.8]

when t cells respond to small molecules that penetrate the skin. Causing rash and sometimes blisters.


E) Why do you not have a skin reaction after first exposer

because this is when it is being "memorized by the T cells"


A) What is an allograft and when is it used?

tissues of donor and recipeint are not genetically identical. the main difference is on the mhc. initiating an immune response


B) What are isografts and why are they preferable?

grafts from identical sibling. this is close to their own mhc and so it doesn't illicit a response


C) What are xenografts?

grafts from animals ie pigs


D) What happens when a tissue is rejected?

a cell mediated immunilogical response. Involving many steps involveing Tc cells and NK cells.


E) How are immunosuppressive drugs used to minimized rejections and what are the risks?

They help supress t cell proliferation. they interfere with cell signaling this prevents clonal selection and expansion of activated t cells.


A) When does an autoimmune disease occur and what may cause it? [Table 17.3]

when body fails ot eliminate cells that recognize self cells. this results in attacking auto antigens.


B) What is type 1 diabetes mellitus and what are the symptoms?

organ specific autoimmune disease. Tc cells destroy beta pancreatic cells( which produce insulin) This results in increased blood levels of glucose. increasing thirst and urination.


C) What is grave’s disease and what are the symptoms? [Figure 17.9]

Organ specific autoimmune disease that attacks the thyroid. antibodies are generally focused on the receptors for TSH. This stimulates the thyroid to produce more hormones. This results in a goiter.


D) What is systemic lupus erythematosus and what are the symptoms?

systemic which results in symptoms that result in joint pain, rashes, and damage to the organs.


E) What is myasthenia gravis and what are the symptoms?

systemic and results in nerve transmission in muscles. The antibodies bind to acetylcholine receptors blocking transmission.


F) What is rheumatoid arthritis and what are the symptoms? [Figure 17.10]

antibodies target collegen in ct. T cells release cytokines leading to inflamation. They also from immune complexes further damaging the joint.


G) How can you treat autoimmune disease?

antiinflamatory and immunosuppressive drugs


1) How do you induce tolerance?

when you give a pill orally with the antigen so the so immune system learns to tolerate it. This decreases reactivity of the immune system to a specific antigen.


A) When do immunodeficiencies arise?

when body cannot make, or sustain an immune response.


B) What is the difference between primary and secondary immunodeficiencies? [Table 17. 4]

Primary: results from genetic defect, or enviromental factors that lead to developmental abnormalities.
Secondary: aquired as a result of an infection or stress like malnutrition.


C) What do primary immunodeficiencies affect?

b, t, nk,phagocytes and compliment systems.


1) What are the consequences of a IgA deficiency?

repeated bacterial infections.


2) What is SCID? What are the symptoms?

sever combined imunodeficiency.
when stem cells in bone marrow do not produce b or t cells. they die of infection at a young age.


3) What is DiGeorge syndrome and what are the characteristics?

This results from thymus not developing and so t cells cannot mature there. results in heart and blood vessel abnormalities. low set ears, small mouth and wide set eyes.


4) What is Chronic granulomatous disease and what caused it?

this is when phagocytes fail to produce h202 and other products of O2 metabolism. These are unable to kill some organisms such as catalase positive staph aureus


5) What is Chediak-Higashi disease?

phagocytic defect. the lysosomes in the phagocyte lack certain enzymes and therefore cannot destroy the phagosized material.


6) What happens to individuals lacking early and late components of the complement system?

Early: may develop imunne complex diseases because the components of the compliment system help clear out the complexes
Late: can have reocurrent Nissiera infections because they are typically destroyed by Mac's. If they lack important control protiens aka inhibitors can cause uncontroled complement activation causing fatal tissue swelling


D) How do secondary immunodeficiencies occur?

from malignancies, old age, pregnancy, and certain infections. ie. leporacy, syphilis, malaria all effect T cell polulation


1) Which is the most serious and widespread?

AIDS. which destroys Th cells


2) How does cancer affect immunity?

in lymph system. They cause the multiplication of immunoglobulin. this focuses system on working on this instead of making the others as well