week 4- anaphalaxyis

Question 1

antigen

Answer 1

Antigen: (Ag) something that stimulates an immune response

Any molecule ~10 amino acids long: components of bacterial cell walls, chemicals (poison ivy sap), proteins

Question 2

allergen

Answer 2

Allergen: an antigen that causes an allergy

Question 3

Hypersensitivity:

Answer 3

abnormal & excessive response of activated immune system causing injury & damage to host tissues

Question 4

antibody

Answer 4

Antibody: (Ab) a family of defensive proteins the body makes when stimulated by an antigen (Ag)
Ab contains a receptor that specifically binds one Ag & not another
Different Ab isotypes exist: IgM, IgG, IgA, IgD, IgE

Question 5

allergy

Answer 5

Allergy: an IgE response to innocuous antigens (a type 1 hypersensitivity reaction)

Question 6

anaphalyaxis

Answer 6

exposures causes cross linkages form between IgE antibodies, bridging two IgE molecules
IgE receptors aggregate, stimulating signal transduction, causing mast cell degranulation

Question 7

Sensitisation stage

Answer 7

• On first exposure of antigen, plasma directs production of IgE antibodies which then attach to basophils and mast cells
• on second or third exposure IgE receptors aggregate this triggers mast cell degranulation and and histamine is released

Question 8

primary response

Answer 8

T2H cells (directing IgE maturation) also mobilise & activate mast cells, basophils & eosinophils

• This causes mast cell degranulation
• In Venule walls: mast cells release histamine causing leaky vessels

-Net result: fluid shift from worsening hypotension, further worsened by histamine-mediated nitric oxide (NO) release as histamine causes vasodilation, vascular leaking and smooth muscle contraction

Question 9

secondary response

Answer 9

-Secondary response: intense tissue infiltration by white blood cells (eosinophils), trying to aid immune system
-Acute and chronic mediators of inflammation released
Epithelial (tissue) damage due to inflammation
-Lipid mediators release
these come from arachidonic acid from degranulated mast cell membranes
-Arachidonic acid used to make leukotrienes & prostaglandins
Similar effect as histamine, but longer onset & prolonged effect

Question 10

mast cell degranulation

Answer 10

Vasoactive substances released
Vasodilation & ↑capillary permeability  hypotension (low BP)
Poor perfusion/hypoxia

Question 11

effects of histamine

Answer 11

• bhronchial constriction
• increased nitric oxide production
• relaxes vascular smooth muscle
• increased venule and cappilary permiability
• smooth muscle contraction

Lungs: fluid into alveoli
Airway: oedema (swelling), smooth muscle contraction

Question 12

SECONDARY RESPONSE SIMPLE

Answer 12

Secondary phase: typically occurs 2 – 8 hours after resolution of initial phase, can last several days
Sometimes may be significantly prolonged/only partially resolved
Due to lipid mediators & cytokines released from immune cells

RESULTS IN-

• intense infiltraion of tissues with eonisphils and other actue and chronic imflammatory cells.
• tissue destruction (epithelial cell damage)

Question 13

PRIMARY RESPONSE SIMPLE

Answer 13

Primary phase: commences 5 – 30 minutes post allergen exposure, subsides within 60 minutes
caused by mast cell degranulation & release of preformed OR enzymatically activated mediators
Key mediator: histamine!
RESULTS IN Vasodilstion, smooth muscle contraction (throat closing), vascular leakage

Question 14

type 1 hypersensitivity reaction- allergic reaction

Answer 14

T cells produce either type 1 or 2 helper cells- in this reaction type 2 helper cells are produced which causes b-cell to activate and develop into IgE antibody

Question 15

eosonophis

Answer 15

disease fighting wbc