Allergies and Sensitivities

Question 1

What type of hypersensitivity is an atopic allergy?

Answer 1

Type 1 Hypersensitivity

Question 2

What is the main difference between an allergic reaction and an autoimmune reaction?

Answer 2

The stimulus for autoimmune hypersensitivities are internal and come from within the body/made by by body. An allergic reaction stems from an external allergen.

Question 3

Type IV hypersensitivities are mediated by what immune cells?

Answer 3

T cells

Question 4

Types I-III hypersensitivities are mediated by what immune cells?

Answer 4

B Cells

Question 5

What inflammatory mediators are released by mast cells?

Answer 5

histamine, prostaglandin, leukotrienes and cytokines

Question 6

In a type I hypersensitivity, what cells are activated by the immunogen?

Answer 6

Mast cells

Question 7

What lies on the surface of mast cells to recognise immunogens and trigger degranulation?

Answer 7

IgE antibodies

Question 8

What antibody is usually released first from B-effector cells?

Answer 8

IgG

Question 9

What cytokine is released by CD4+ (Th) cells and what is it’s relevance in type I hypersensitivity reactions?

Answer 9

IL-4, stimulates B cells to produce IgE instead of IgG.

Question 10

How can mast cells affect the gastrointestinal system?

Answer 10

Inflammatory mediators act on the smooth muscle causing cramps, vomiting and diarrhoea.

Question 11

What is urticaria?

Answer 11

raised, itchy rash (often called hives)

Question 12

What is the name for the swelling deep in the subcutaneous tissue that can occur alongside urticaria?

Answer 12

Angioedema

Question 13

What life-threatening emergency condition can arise from a type I hypersensitivity reaction?

Answer 13

Anaphylactic shock

Question 14

What changes in the bronchial walls happen to cause bronchoconstriction?

Answer 14

Inflammation causing thickening, smooth muscle contraction (narrowing airway) and excess mucus production

Question 15

Describe the effect of Th1 and Th2 cells on each other

Answer 15

Th1 cells release IL-10 which inhibits Th1 activation. Th1 release IF-gamma which inhibits the proliferation of Th2.

Question 16

What is the mechanism of action for anti-histamine drugs?

Answer 16

Blocks histamine at H1 receptors on vascular, respiratory and gastro-intestinal epithelium.

Question 17

What happens on a molecular level to cause a type II hypersensitivity reaction?

Answer 17

Small molecules of the immunogen bind to cell surfaces, producing modified structures that are recognised as foreign by the immune system. The cells are then destroyed by the immune response.

Question 18

What antibodies are elevated in a type II hypersensitivity reaction?

Answer 18

IgG and/or IgM

Question 19

Haemolytic disease of the newborn is an example of what type of hypersensitivity?

Answer 19

II

Question 20

What is Goodpasture’s syndrome?

Answer 20

A type II hypersensitivity where antibodies are present against a subtype of type IV collagen found in the basement membrane of alveoli and glomeruli. The autoimmune reaction results in renal dysfunction and haemoptysis.

Question 21

What mechanism causes a Type II hypersensitivity?

Answer 21

Antibody-antigen complexes are not destroyed by the complement system or phagocytosis. They are deposited on the walls of blood vessels, synovial membranes or the glomerular basement membrane. This triggers the classic complement pathway and the inflammatory cells cause tissue damage.

Question 22

Pernicious anaemia is what type of hypersensitivity?

Answer 22

II

Question 23

Rheumatoid arthritis is what type of hypersensitivity?

Answer 23

III

Question 24

“Delayed hypersensitivity” is what type?

Answer 24

IV

Question 25

Contact dermatitis is what type of hypersensitivity and how long will it take for symptoms to develop from exposure?

Answer 25

IV, 24-72 hours

Question 26

Which type of hypersensitivity occurs in minutes?

Answer 26

I

Question 27

What are eicosanoids and give two examples?

Answer 27

20 carbon fatty acids, leukotrienes and prostaglandins

Question 28

Describe a feature of eicosanoids which makes them good pro-inflammatory mediators

Answer 28

Unstable and broken down quickly so they act locally for a short-time after their release

Question 29

What acid is stored within the plasma membrane (as the hydrophobic tails of phospholipids) and used to create eicosanoids?

Answer 29

Arachidonic acid

Question 30

What type of receptors are leukotriene and prostaglandin receptors?

Answer 30

GPCRs

Question 31

What is the molecular target of NSAIDs and why is this relevant in asthma?

Answer 31

Cyclo-oxygenase (COX), an enzyme that hydrolyses arachidonic acid into prostaglandins. This could facilitate the hydrolysis of arachidonic acid into leukotrienes instead which could precipitate an asthmatic reaction.

Question 32

What type of COX is inhibited by NSAIDS like aspirin, ibuprofen and naproxen and why is this relevant for side effects?

Answer 32

They are non-selective, but mainly inhibit COX-1, this enzyme is involved in creating prostaglandins that affect stomach and kidney functions, which makes COX 1 inhibitors more likely to cause nephrotoxicity and stomach ulcers.

Question 33

Why are COX-2 selective inhibitors not used more often?

Answer 33

They increase the incidence of MI

Question 34

What is the first enzyme involved in the pathway from arachidonic acid to leukotrienes?

Answer 34

5-lipoxygenase