Thrush- Immunological pathologies I

Question 1

what is type I hypersensitive reaction?

Answer 1

immediate type hypersensitivity. allergy that is IgE mediated

Question 2

what is type II hypersensitive reaction?

Answer 2

cytotoxic hypersensitivity. think Rh mismatch that leads to Ig-mediated complement activation

Question 3

what is type III hypersensitive reaction?

Answer 3

immune complex hypersensitivity. example would be serum sickness that results from Ag-Ab complexes

Question 4

what is type IV hypersensitive reaction?

Answer 4

delayed type hypersensitivity. example would be TB skin test that results from Tdth cells

Question 5

in allergies what happens during the sensitization phase?

Answer 5

exposure of antigen and the production of IgE. and binding to mast cells and basophils.

Question 6

in allergies what happens during the effector phase?

Answer 6

IgE binds allergen (antigen), crosslinking of IgE results in degranulation of the mast cell and the release of pharmacologically-active mediators

Question 7

can mast cells bind to multiple types of antibodies at once?

Answer 7

yes. the Fc-epsilon receptor of the mast cell can bind different types of antibodies

Question 8

how do B cells and mast cells differ?

Answer 8

Fc-epslion receptors in B cells only bind one type of antibody and mast cells can bind various types

Question 9

when an allergen binds to the IgE (antibodies) on a mast cell what phenomena is triggered?

Answer 9

crosslinking of IgE’s, which leads to degranulation of the mast cell

Question 10

once cross-linking takes place, what ion is mobilized and brought into the cell? and what does this ion lead too?

Answer 10

calcium influx.

calcium stimulates breakdown of arachidonic acids

Question 11

what are arachidonic acids broken down too?

Answer 11

LEUKOTRIENES and prostaglandins

Question 12

how do drugs like epinephrine and theophylline prevent the degranulation of mast cells?

Answer 12

they keep cAMP levels high, which prevents degranulation even if IgE’s have already undergone cross-linking

Question 13

do Th1 or Th2 cells lead to the production of IgE?

Answer 13

Th2

Question 14

what does IL-4 lead too? and what inhibits it?

Answer 14

it is a switch factor for IgE but can be prevented by IFN-gamma (comes from Th1)

Question 15

how do Th2 cells prevent Th1 cells from being produced?

Answer 15

by producing IL-10, because it inhibits IFN-gamma

Question 16

what does IFN-gamma (from Th1) activate?

Answer 16

macrophages, T cells and neutrophils

Question 17

what does IL-4 and IL-5 (from Th2) activate?

Answer 17

B cells, mast cells and eosinophils

Question 18

if a patient experiences an allergic reaction and blood serum is tested, what levels of tryptase would you expect to see? and what is the draw back?

Answer 18

increase levels of BETA tryptase (greater than 1 ng/mL).
it has a short half-life so it would need to be measured a few hours after the allergic reaction

Question 19

what are secondary molecules that are produced after a cross linking?

Answer 19

leukotrienes and cytokines

Question 20

what is 1000x more potent than histamine and increase vascular permeability and contraction of pulmonary smooth muscles?

Answer 20

leukotrienes

Question 21

what would you see in a patient that is experiencing a skin allergy?

Answer 21

wheel and flare reaction

Question 22

how does desensitization work during an allergy?

Answer 22

stimulate immune system to produce IgG instead of IgE

Question 23

what acts as an antibody and binds to IgE to prevent an allergic reaction?

Answer 23

anti-IgE therapy

Question 24

how would you detect allergen specific IgE?

Answer 24

radioimmunoassays

Question 25

what is type II hypersensitivity?

Answer 25

Ab-mediated cytotoxicity

Question 26

how does Ab-mediated cytotoxicity occur?

Answer 26

antibodies bind to cell surface, activate complement and the lead to cell lysis

Question 27

why are blood transfusion reactions a good example of type II hypersensitivity?

Answer 27

because if the wrong blood type is injected into an individual than the individuals body will produce antibodies to the mismatched foreign blood and activate complement lysis

Question 28

if a mother delivers an infant that has Rh, what would you be able to administer so that the mother doesn’t mount an immune response to Rh?

Answer 28

RhoGAM will bind to the Rh antigens from the infant so that the mother doesn’t mount an immune response

Question 29

lupus and serum sickness are considered examples of type III hypersensitivity. how do they cause damage to the body?

Answer 29

they still form Ag-Ab complexes, which is a good thing. but too many Ag-Ab complexes which causes bystander cell damage (kidney)

Question 30

in type III hypersensitivity is the antigen on the cell?

Answer 30

no. it is floating around… type II hypersensitivity has the antigen on the cell

Question 31

what is an arthus reaction?

Answer 31

a localized type III reaction (insect bite)

Question 32

how does serum sickness occur?

Answer 32

after a foreign serum is injected for a second time, a large immune complex is formed that leads to things like rash, arthritis, edema etc.

Question 33

what is delayed type (cell mediated) hypersensitivity?

Answer 33

type IV hypersensitivity

Question 34

does type IV hypersensitivity rely on influx of inflammatory cells and Th1 type cytokines?

Answer 34

yes. (Th1 cells best against intracellular infection)

Question 35

why is the tuberculin reaction (PPD injection) considered a type IV hypersensitivity?

Answer 35

memory Tdth cells present and become activated

Question 36

if a patient is exposed to poison oak, what type of hypersensitivity reaction would be mounted and why?

Answer 36

type IV, because oils from the oak bind to a protein to form a hapten like reaction