hypersensitivities Flashcards

1
Q

what are autoimmune diseases a type of ?

A

hypersensitivity

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2
Q

what are hypersensitivities ?

A

when the immune system has an over reaction , the harmful immune responses are what produce tissue injury and may cause serious disease.

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3
Q

how many hypersensitivities are there ?

A

four

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4
Q

what do type one to three immediate hypersensitivity all involve ?

A

involve antibodies

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5
Q

what does type four delayed hypersensitivity not involve ?

A

antibodies

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6
Q

type 1 ?

A

IgE mediated

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7
Q

Type II ?

A

IgG mediated

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8
Q

Type III ?

A

immune complex mediated hypersensitivity

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9
Q

Type IV ?

A

cell mediated

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10
Q

what is type I induced by ?

A

allergens

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11
Q

can type I be genetically predisposed ?

A

yes

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12
Q

what can the cutaneous reactions involve ?

A

on the skin include urticaria which is a rash and this can occur in minutes

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13
Q

pathological reactions ?

A

oedema which is swelling , vasodilation which is when the blood vessels relax , smooth muscle contraction and anaphylaxis ( Lack of oxygen supply due to contraction of smooth muscle)

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14
Q

how is type one transferred ?

A

by serum and IgE

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15
Q

what are the effector cells ?

A

mast cells and basophils that contain granules

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16
Q

what are the secreated mediators ?

A

mast cell mediators such as histamine , vasoactive amine lipid mediators and cytokines.

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17
Q

why does the mast cell degranulate ?

A

the IgE antibody and antigen cross link.

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18
Q

what are type II ( IgG) and Type III ( immune complex ) induced by ?

A

antigens that induce IgG and IgM. These antigens can be anything from food , self antigens and even viral antigens

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19
Q

what are the cutaneous reactons ?

A

arthus reaction which is a hypersensitivity reaction that occurs several hours to days following the exposure and is marked by the formation of antigen-antibody complexes accompanied by localized inflammation, pain, redness, and sometimes tissue destruction.

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20
Q

what are the pathological responses ?

A

necrotizing vasculitis is an inflammation of blood vessel walls

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21
Q

How is it transferred ?

A

by serum and complement fixing IgG and IgM

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22
Q

what are the effector cells ?

A

neutrophils and monocytes

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23
Q

what are the secreated mediators

A

products of the complement activation

24
Q

give a of disease due to type II hypersensitivity ?

A

haemolytic disease of the newborn

25
Q

describe it ?

A

the Rh- mother gives birth to a Rh+ baby with a Rh+ father. The mothers IgG antibody crosses the placenta and responds to the RBC on the baby to destroy them. This destruction of the RBC releases viral toxins which affect the brain. Considerable enlargement of the liver and spleen associated with erythrocyte destruction caused by maternal anti-erythrocyte antibody in the fetal circulation.

26
Q

what is ADCC ?

A

antibody dependent cellular cytotoxicity

27
Q

how can the haemolytic disease be prevented ?

A

administering Rhogam at the time of delivery

28
Q

what is type II mediated by ?

A

immune complexes and resulting complement activation.

29
Q

what do the complement products elicit ?

A

localised vasodilation and attract neutrophils.

30
Q

when are lytic enzymes released ?

A

due to frustrated phagocytosis

31
Q

what is frustrated phagocytosis ?

A

a phagocyte fails to engulf its target, these toxic agents can be released into the environment .

32
Q

how is tissue damage occured ?

A

by the complement membrane attack complex

33
Q

when does serum sickness occur ?

A

immune complexes are deposited throughout the body so type III

34
Q

type IV does not involve antibodies , what instead ?

A

proteins and haptens as well as specific activation of T cells

35
Q

what is the cutaneous reaction and how long.

A

contact hypersensitivty and one to two days so longer than type I , II and III

36
Q

what is the patholgocial reactions ?

A

perivascular cellular infiltration and oedema occurs

37
Q

how is it transferred ?

A

lymphocytes

38
Q

effector cells ?

A

CD4+ T cells and activated macrophages

39
Q

secreated mediators ?

A

cytokines such as TNF alpha and IFN gamma

40
Q

summary of hypersensitivty ?

A

are inflammatory reactions within the humoral or cell-mediated branches of the immune system. Lead to extensive tissue damage and even death. Reactions are classified into four main types according to the mechanism that induces them. Each type generates characteristic effector molecules and clinical manifestation.

41
Q

what is an allergy a type of ?

A

hypersensitivity

42
Q

defintion of allergy ?

A

disease following a response by the immune system to an otherwise innocuous antigens.

43
Q

when is IgE produced ?

A

following a Th2 response

44
Q

effect of IgE ?

A

IgE binds to high affinity receptor FceRI on mast cells, basophils and eosinophils. This triggers degranulation of mast cells, basophils and eosinophils and release of mediators and cytokines. This degranulation occurs only when the antigen arrives and crosslinks with the antibody.

45
Q

why can type I hypersensitive reactoins occur ?

A

so that parasite killing can occur

46
Q

where are mast cells most abundant ?

A

near the body surface

47
Q

what do mast cells contain ?

A

granules

48
Q

role of mast cells ?

A

provide alert to the immune system and provide a rapid response

49
Q

what are mast cells important for controlling ?

A

bacterial infection and parasites

50
Q

what are the features of an allergen that promote the induction of an allergy ?

A
  • Protein
  • Enzymatically active
  • Low dose
  • Low molecular weight
  • Highly soluble
  • Stable
  • MHC class II binding peptides
51
Q

effects of degranulation of mast cells ?

A
Smooth muscle contraction 
Increased vascular permeability 
Vasodilation 
Platelet aggregation 
Eosinophil chemotoaxins 
Mucus secretion 
Circulatory collapse – heart attack
52
Q

how can you treat type I hypersensitivites with epinepthrine ?

A

Anaphylactic reactions are treated with epinephrine ( shot adrenaline).

53
Q

bronchodilators ?

A

relax the constricted airways during an asthma attack

54
Q

anti histamines ?

A

reduce urticaria induced by mast cell and eosinophil degranulation

55
Q

cromolyn ?

A

blocks production and release of mediators such as histamine

56
Q

topical and systemic corticosteroids ?

A

suppress chronic inflammation associated with asthma and eczema

57
Q

desensitisation ?

A

injection of increasing doses of allergen which switches off response .