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Part 3 – PM3A > (PM3A) Hypersensitivity > Flashcards

(PM3A) Hypersensitivity Flashcards

1
Q

What is hypersensitivity and autoimmunity?

A

(1) Damage caused by adaptive immune mechanisms

(2) No hazard can be identified

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2
Q

What is the difference between autoimmunity and hypersensitivity?

A

The source of the antigen:

  • (1) Internal = autoimmunity
  • (2) External = hypersensitivity

Effector mechanism:
- Could be antibody type or T lymphocytes/ cells

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3
Q

What are the types of antibody in effector mechanisms?

A

(1) Binding + blocking
(2) Histamine
(3) Phagocytosis

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4
Q

How are hypersensitivity reactions classified?

A

Classification table

Class 1-4

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5
Q

How does the mediation of class 1-3 compare to that of 4 in hypersensitivity reactions?

A

1-3 = B cell mediated

4 = T cell mediated

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6
Q

Which class of hypersensitivity is most common?

A

Class 1

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7
Q

What is the effector mechanism for hypersensitivity class 1 reactions?

A

IgE antibody on mast cells

e.g. hayfever/ asthma/ anaphylaxis

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8
Q

What is the effector mechanism for hypersensitivity class 2?

A

IgM + IgG antibody-mediated cell killing

e.g. mismatched blood transfusion/ haemolytic anaemia of a newborn

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9
Q

What is the effector mechanism for hypersensitivity class 3?

A

IgG antibody immune complexes

e.g. serum sickness/ long-term mAb use

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10
Q

What is the effector mechanism for hypersensitivity class 4?

A

T cells (lymphocytes)

e.g. contact dermatitis

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11
Q

What are some triggers of hypersensitivity class 1 responses?

A

(1) Tree pollen
(2) Grass pollen
(3) Flower pollen
(4) Medicines
(5) Latex
(6) Dust mites
(7) Rodents
(8) Birds
(9) Insect bites

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12
Q

Which receptor is present on the outside of mast cells?

A

IgE

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13
Q

What is a sentinel?

A

Another name for a mast cell

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14
Q

What is contained within mast cells?

A

Histamine granules

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15
Q

What triggers histamine release from mast cells?

A

Parasite antigen recognition

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16
Q

What are some common signs and symptoms of a hypersensitivity class 1 response?

A

(1) Swelling
(2) Sneezing
(3) Vasodilation
(4) Itching
(5) Sudden death

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17
Q

Why are mast cells considered antigen specific?

A

Presence of IgE antibodies on surface

Able to recognise parasitic antigens

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18
Q

When are mast cells considered part of adaptive immunity?

A

When they are coated with IgE

To be able to recognise antigens

19
Q

How is hayfever a hypersensitivity reaction?

A

(1) Allergen in upper respiratory tract/ eyes

(2) Itching + sneezing

20
Q

How is asthma a hypersensitivity reaction?

A

(1) Allergen in lower respiratory tract
(2) Causes air vessel constriction
(3) Shortness of breath + wheezing

21
Q

How is anaphylaxis a hypersensitivity reaction?

A

(1) Triggering of sufficient mast cells at the same time
(2) Causes systemic vasodilation
(3) Catastrophic BP drop
(4) Death

22
Q

How may an antigen of a class 1 hypersensitivity reaction?

A

(1) Removal of antigen – diaries to log when symptoms occur, e.g. removal of foods from diet/ pet from environment
(2) Skin prick test

23
Q

What is a skin prick test?

A

(1) Drop of liquid purified antigen on skin
(2) Introduce a tiny prick
(3) Small enough to only let a small amount in for a local effect
(4) Must have adrenaline present in case of allergic reaction

24
Q

What is the normal role of IgG and IgM in class 2 hypersensitivity reactions?

A

Killing pathogens

25
Q

What does ‘complement’ do?

A

Punches holes in cell membranes of pathogens

26
Q

How is drug-induced anaemia caused?

A

(1) Drug attaches to red blood cells (erythrocytes)
(2) Antibodies bind to drug
(3) Lyses red blood cells
(4) Causes anaemia

27
Q

What is an example of a high affinity hapten-type reaction?

A

Drug-induced anaemia

28
Q

What are some common drugs that cause drug-induced anaemia?

A

(1) Cephalosporins
(2) Penicillin
(3) Tetracycline

29
Q

What is the normal role of IgG in class 3 hypersensitivity reactions?

A

Neutralising bacterial toxins + viruses

30
Q

What is a class 3 hypersensitivity reaction?

A

Binding of IgG antibodies to bacterial toxins

31
Q

How is antivenom made?

A

(1) Venom taken from snake
(2) Injected into horses
(3) Serum taken from horse is the ‘antivenom’

(4) Can be infused into patient following snakebite
- IF type of snake is known

32
Q

What is likely to occur if large concentrations/ continued use of antivenom occurs?

A

Patient may develop immunity to antivenom (serum sickness)

(Production of antibodies)

Formation of immune complexes

33
Q

What is serum sickness?

A

High levels of antibody

In response to foreign antibody

Systemic inflammatory problems

34
Q

What is a modern alternative to antivenom?

A

Monoclonal antibodies

mAb

35
Q

What type/ class of hypersensitivity is relevant when considering use of monoclonal antibodies?

A

Type/ class 3 hypersensitivity

36
Q

How is hypersensitivity to antivenoms been largely resolved?

A

Monoclonal antibodies

Fully human rather than from horse

37
Q

How are monoclonal antibodies synthesised?

A

(1) Isolation of DNA of a single antibody molecule from millions of B cells
(2) Use of machinery (bioreactor) to upscale production
(3) Injection of pure antibody

38
Q

What are some common examples of antigen target for monoclonal antibodies?

A

(1) Human TNF

(2) Human HER2 receptor

39
Q

What is passive immunisation?

A

Transfer of antibodies into the body

40
Q

What are some disadvantages of antivenom?

A

(1) Horse proteins
(2) Multiple types of antibody
(3) Made in animals

41
Q

What is an example of a class 4 hypersensitivity reaction?

A

Allergic contact dermatitis

42
Q

What is class 4 hypersensitivity?

A

T helper cells

Trigger inflammation

In response to microbial peptides

43
Q

What is delayed-type hypersensitivity?

A

Type/ class 4 hypersensitivity

44
Q

What is the slowest type/ class of hypersensitivity?

A

Type/ class 4

Part 3 – PM3A (28 decks)

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