NR507 Midterm Study guide
Study online at https://quizlet.com/_gv6yqb
1. What is Type 1 reaction mediated by?: IgE
*inflammation r/t mast cell degranulation
2. What are the local symptoms of Type 1 reaction?: itching, rash
3. What are systemic reactions of Type 1?: wheezing
4. What is the most dangerous form of type 1 reaction?: anaphylactic reaction
*systemic response-hypotension, severe bronchoconstriction
*epinephrine to reverse effects
5. What kind of reaction is type 2?: cytotoxic reaction-tissue specific
*machrophages are primary effector cells involved
*can cause tissue damage or alter function
6. What are examples of type 2 hypersensitivity?: Graves' disease
transfusion reaction
7. What happens in a transfusion reaction?: incompatible blood type causes
cell/tissue damage
*erythrocytes are destroyed by agglutination or complete-mediated lysis
8. In Graves' disease TSI's mimic what?: the action of TSH, binding to the recep-
tors on thyroid cells
*binding stimulates production and release of excessive thyroid hormones (T3-T4)
even in absence of TSH
9. What are key characteristics of Graves' disease?: autoantibody mediat-
ed-caused by IgG targeting TSH receptors
stimulatory not cytotoxic- involves cell overstimulation
10. What are common symptoms of Graves disease?: increased metabolism,
sweating, tremors, bulging eyes (exophthalmos)
11. What type of hypersensitivity as type 3?: Immune complex mediated-com-
plexes formed in blood and are deposited in various tissues
12. How is type 3 triggered?: when soluble antigens (foreign proteins, drugs,
microbial components) combine with antibodies -primarily IgG/IgM- form immune
complexes
13. What does type 3 reaction lead to?: inflammation and tissue damage
14. Where do type 3 immune complexes typically deposit themselves?: bl
vessel walls, joints, glomeruli, tissues with small vessels
* kidneys, lungs, skin, joints
15. What is the difference between type 2 and type 3?: Type 2- organ specific,
binds to cell surface
type3-not organ specific-bind to the soluble antigen outside cell surface that was
released into blood or body fluids, then deposited into tissue
16. What are type 3 axample?: RA-deposited into joints
SLE- deposit in organs that cause tissue damage
, NR507 Midterm Study guide
Study online at https://quizlet.com/_gv6yqb
17. What happens in SLE flare-up?: new or current symptoms worsen often trig-
gered by stress, infection, sunlight, hormonal changes, certain medications
18. What symptoms are associated with SLE flare up?: joint pain, fatigue, skin
rash, kidney dysfunction, fever, chest pain
19. How can SLE flare ups be managed?: Use sunscreen, manage stress, avoid
certain medications
20. What are medications for SLE management?: NSAIDS, steroids, immunosu-
pressive agents, antimalarials, biologics
21. What are lifestyle and support mechanisms for SLE?: regular monitoring,
sun protection, healthy lifestyle
22. What is alloimmunity?: general term used to describe individuals immune
system reaction against antigens on the tissues of other membranes
example-neonatal disease where maternal immune system becomes sensitized
against expressed by the fetus
-transplant rejection
-transfusion reaction
23. Describe type 4 hypersensitivity: delayed response
does not involve antigen/antibody complexes liek type 1,2,3
24. What is an example of type 4?: poison ivy
25. what is the difference between type 1 vs type 4 rash reaction?: type 1-atopic
dermatitis usually characterized by widely distributed lesions
type 4- contact dermatitis (delayed hypersensitivity) consists of lesions only at the
site contact with the allergen
26. What is the key determinant in determining type 1 vs type 4 rash: 1-
immediate
4- delayed several days followings i.e. poison ivy
27. How do you treat type 4 rash: topical steroid
*epi for type 1 anaphylaxis
*antihistamines act on H1 receptors
*type 4 reaction does not involve mast cells and H1 receptors
*ABX not appropriate for allergic reaction
28. What is primary immunodeficiency?: are result of single gene defect
*something lacking in immune system itself
*b-lymphocyte deficiency is one of the most severe forms
29. What is secondary immunodeficiency?: complication of some other physio-
logic condition or disease
*malnutrition is most common cause worldwide, preganancy, eating disorders
*i.e-HIV pt gets pneumocystis carinii
Study online at https://quizlet.com/_gv6yqb
1. What is Type 1 reaction mediated by?: IgE
*inflammation r/t mast cell degranulation
2. What are the local symptoms of Type 1 reaction?: itching, rash
3. What are systemic reactions of Type 1?: wheezing
4. What is the most dangerous form of type 1 reaction?: anaphylactic reaction
*systemic response-hypotension, severe bronchoconstriction
*epinephrine to reverse effects
5. What kind of reaction is type 2?: cytotoxic reaction-tissue specific
*machrophages are primary effector cells involved
*can cause tissue damage or alter function
6. What are examples of type 2 hypersensitivity?: Graves' disease
transfusion reaction
7. What happens in a transfusion reaction?: incompatible blood type causes
cell/tissue damage
*erythrocytes are destroyed by agglutination or complete-mediated lysis
8. In Graves' disease TSI's mimic what?: the action of TSH, binding to the recep-
tors on thyroid cells
*binding stimulates production and release of excessive thyroid hormones (T3-T4)
even in absence of TSH
9. What are key characteristics of Graves' disease?: autoantibody mediat-
ed-caused by IgG targeting TSH receptors
stimulatory not cytotoxic- involves cell overstimulation
10. What are common symptoms of Graves disease?: increased metabolism,
sweating, tremors, bulging eyes (exophthalmos)
11. What type of hypersensitivity as type 3?: Immune complex mediated-com-
plexes formed in blood and are deposited in various tissues
12. How is type 3 triggered?: when soluble antigens (foreign proteins, drugs,
microbial components) combine with antibodies -primarily IgG/IgM- form immune
complexes
13. What does type 3 reaction lead to?: inflammation and tissue damage
14. Where do type 3 immune complexes typically deposit themselves?: bl
vessel walls, joints, glomeruli, tissues with small vessels
* kidneys, lungs, skin, joints
15. What is the difference between type 2 and type 3?: Type 2- organ specific,
binds to cell surface
type3-not organ specific-bind to the soluble antigen outside cell surface that was
released into blood or body fluids, then deposited into tissue
16. What are type 3 axample?: RA-deposited into joints
SLE- deposit in organs that cause tissue damage
, NR507 Midterm Study guide
Study online at https://quizlet.com/_gv6yqb
17. What happens in SLE flare-up?: new or current symptoms worsen often trig-
gered by stress, infection, sunlight, hormonal changes, certain medications
18. What symptoms are associated with SLE flare up?: joint pain, fatigue, skin
rash, kidney dysfunction, fever, chest pain
19. How can SLE flare ups be managed?: Use sunscreen, manage stress, avoid
certain medications
20. What are medications for SLE management?: NSAIDS, steroids, immunosu-
pressive agents, antimalarials, biologics
21. What are lifestyle and support mechanisms for SLE?: regular monitoring,
sun protection, healthy lifestyle
22. What is alloimmunity?: general term used to describe individuals immune
system reaction against antigens on the tissues of other membranes
example-neonatal disease where maternal immune system becomes sensitized
against expressed by the fetus
-transplant rejection
-transfusion reaction
23. Describe type 4 hypersensitivity: delayed response
does not involve antigen/antibody complexes liek type 1,2,3
24. What is an example of type 4?: poison ivy
25. what is the difference between type 1 vs type 4 rash reaction?: type 1-atopic
dermatitis usually characterized by widely distributed lesions
type 4- contact dermatitis (delayed hypersensitivity) consists of lesions only at the
site contact with the allergen
26. What is the key determinant in determining type 1 vs type 4 rash: 1-
immediate
4- delayed several days followings i.e. poison ivy
27. How do you treat type 4 rash: topical steroid
*epi for type 1 anaphylaxis
*antihistamines act on H1 receptors
*type 4 reaction does not involve mast cells and H1 receptors
*ABX not appropriate for allergic reaction
28. What is primary immunodeficiency?: are result of single gene defect
*something lacking in immune system itself
*b-lymphocyte deficiency is one of the most severe forms
29. What is secondary immunodeficiency?: complication of some other physio-
logic condition or disease
*malnutrition is most common cause worldwide, preganancy, eating disorders
*i.e-HIV pt gets pneumocystis carinii
