third round

Question 1

a. What are the three phases of Type I sensitivity reactions?

Answer 1

a. Sensitization i. 1st exposure to allergen ii. Produce IgE b. Activation i. 2nd exposure to same allergen ii. Induce granulation of the cells iii. Atopy or anaphylax

Question 2

b. What is atopy?

Answer 2

a. Atopy a) Any chronic local allergy such as hay fever or asthma b) 10-30% of population c) Some people last a liftime d) Localized reaction and symptoms i) Smooth muscle contraction and vasodilation only occurs in specific tissue ii) Affectus mucous membrane of upper resp. tract (coughing) iii) Lower resp tract (wheezing) iv) Conjunctiva of the eye (watery eyes v) Nasal mucosa (runny nose/sneezing vi) Food allergies One. Contraction of smooth muscle within GI tract Two. Can cause vomiting (upper GI tract) Three. Diarrhea (lower GI tract) vii) SKIN REACTIONS One. Hives First. Body ending up at skin where masTcells degranulate and cause a local rash

Question 3

c. What is anaphylaxis? What are the clinical types?

Answer 3

a. 2 clinical types a) Cutaneous i) Wheal and flare inflammatory reactin to the local injection of allergen b) Systemic i) Physiological events similar to atopy One. Strength and response greatly amplified b. My lead to death in 15 minutes from completel airway blockage a) When smooth muscle contraction occurs in the resp or GI tract, may cause difficulty breathing and spotaneous incontinence b) Vasodilation causes blood pressure to drop

Question 4

d. What treatments are available for anaphylaxis response?

Answer 4

a. Epinephrine a) Counteracts effects of histamine and other mediators by relaxing the smooth muscle contraction and reducing vascular permeability b) Increased cardiac output- prevents vascular collapse c) Increased c-AMP levels in masTcells to block further degranulation

Question 5

e. What is the mechanism of type II hypersensitivity?

Answer 5

a. IgG and IgM directed against Tcell surfaces or tissue antigens b. Bring about damage to the target Tcell via: a) Classical complement cascade b) Opsonization c) ADCC (natural killer cells) antibody dependent cytotoxic cells

Question 6

f. During incompatible blood transfusions, is a good example of a type II reaction, T/F

Answer 6

a. True

Question 7

g. How do transfusion reactions cause destruction? e.g. Type O receiving blood from type A donor

Answer 7

a. Hemolysis b. Opsonization c. Increased phagocytosis

Question 8

h. What are some minor blood groups?

Answer 8

a. MN b. Duffy c. Kell d. Rhesus

Question 9

a. Why could the attack of incompatible blood transfusion be fatal?

Answer 9

a. IgM attack incompatible blood b. Trigger hemolytic reaction–> intravascular lysis of RBC’s c. Leads to hemoglobinuria i. Clog up kidney and lead to tubular necrosis –> may lead to kidney failure ii. May affect liver metabolism lead to nausea fever and chills d. May lead to anemia and jaundice

Question 10

b. What could be a treatment for incomptabile blood trasnfusion reaction?

Answer 10

a. Halting transfusion b. Drugs to remove hemoglobin from blood c. Begin another transfusion with correct type

Question 11

c. What percentage of humans carry Rh factor?

Answer 11

a. 85%

Question 12

d. What is hemolytic disease of the newborn? Or erythroblastosis?

Answer 12

a. When mother has a first response to Rh antigen from first born b. When second born shows Rh antigen, mother is ready with Rh antibodies and IgG from mother crosses into fetal and does complement agaisnt newborns blood

Question 13

e. What are the symptoms of erythorblastosis?

Answer 13

a. High number of immature necleated RBC b. Anemia c. Jaundic d. Enlarged spleen and liver

Question 14

a. When is antiserum injected to immunized mother of Rh+ fetus passively?

Answer 14

a. 28-32 weeks and again within 72 hours after parturition

Question 15

b. What is type III hypersensitivity ?

Answer 15

a. When exposure to a profuse quantity of soluble antigens stimulate the production of large quantities of antibodies and formation of antibody-antigen complex b. Deposition in the basement membrane of epthelial tissue activation of complement result in damaging inflammation response

Question 16

c. What are some types of immune complex disease?

Answer 16

a. Glomerulonphritis i. Post streptococcal infection ii. Lymph deposits of immune complex iii. Complement activation attracts neutrophils 1) Starts inflammaotry process b. Infective endocarditis i. In heart c. Rheumatoid arthritis, systemic lupus erythematous and scleroderma i. Autoimmune that can be considered hypersensitivity type III

Question 17

a. What kind of reaction does arthus reaction resemble?

Answer 17

a. Late phase of Type I hypersensitivity

Question 18

b. What are some exmamples of arthus reaction?

Answer 18

a. Farmers lung b. Pigeon fanciers disease c. Allergic bronchopulmonary aspergilosis

Question 19

c. What is serum sickness?

Answer 19

a. Repeated injejctions b. Eg. Horse serum to treat tetanus

Question 20

a. What is type IV delayed hypersenstivity?

Answer 20

a. Cell mediated b. Eg. Organ rejection c. Ag specific Tcells become sensitized (DTH cells) i. These cells will produce cytokines that attract and activate mononuclear cells (monocytes and macrophages) 1) To area of invasion that cause tissue damage d. Starts 24h-72 hrs after contact with antigen

Question 21

b. What are the two types of delayed type Iv hypersensitivity

Answer 21

a. Contact hypersensitivity i. Sensitation with simple molecules ii. Poison oak, etc iii. Caused by CD8 cyotoxic Tcells that attack skin cells which are displaying foreign antigens b. Tuberculin type hypersensitivity i. Micro organism Ag ii. CD4 positive helper Tcells and macrophages that are attracted to injection site

Question 22

c. How does a patient get tested for mycobacterium exposure?

Answer 22

a. Patient is injected with a small ammount of tuberculin intradermally i. Little reactin in first few hours ii. If over 48-72 hours redness develops iii. If skin test converst from negative to positive suggests that patient has been recently infected