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EMS MOD > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

what is a hypersensitivity reaction?

A

reaction that is produced by the normal immune system that is directed against innocuous antigens in a pre-sensitised host

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2
Q

who determined the four stages and classifications of hypersensitivity?

A

Coombs and Gell in 1963 types I-IV

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3
Q

which cells are involved in hypersensitivity?

A

dendritic cells - circulate and sample environment and present to T and B cells
antibodies - specific to particular protein sequences
macrophages - clear out rubbish in immune system
T and B cells - produce cytokines for communication in immune system

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4
Q

what is a Type I hypersensitivity?

A

it is an IgE mediated mast cell and basophil degranulation

it is the release of preformed and de novo synthesised inflammatory mediators

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5
Q

what are the clinical features of type I?

A

fast onset, weal and flare, mild, moderate or severe

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6
Q

what is the primary response of type I?

A

degranulation and release of histamine, proteases and chemotactic factors

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7
Q

what is the secondary response of type I?

A

release of leukotrienes, prostaglandins, eosinophils

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8
Q

what cell has a central role in the type I?

A

there is a central role for the Th2 t helper cell

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9
Q

how is the mast cell adapted for this?

A

it has preformed mediators such as histamine and IgE receptors on it’s surface

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10
Q

what happens once the antibodies and antigens connect?

A

the antibodies on the mass cells will connect to antigen with at least two antibodies, and cross link. This signals mast cells to throw out granules and releases histamine

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11
Q

what do cytokines do?

A

cytokines will cause the B cells to proliferate into IgE plasma cells

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12
Q

what are signs of inflammation?

A

flushing, urticaria, cutaneous and oral pruritus (itching), abdo pain/nausea/vomiting, runny nose and sneezing

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13
Q

how can this be treated?

A

antihistamines, and nasal spray

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14
Q

what are the effects of histamine?

A

swelling, inflammation, higher HR and blood clots, gastric acid secretion, dilation of blood vessels, bronchoconstriction, increased permeability of capillaries and adrenaline release

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15
Q

what is moderate to severe hypersensitivity reaction?

A

it is anaphylaxis. It is a medical emergency and is an acute, potentially life threatening, IgE mediated systemic hypersensitivity reaction

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16
Q

what are the hallmarks of anaphylaxis?

A

diffuse urticaria and angiodema

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17
Q

what are the symptoms of anaphylaxis?

A

hoarseness, cough, shortness of breath, wheezing and cyanosis (respiratory arrest), severe abdo pain, diarrhoea, nausea and vomiting, hypotension

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18
Q

why do we get allergies?

A

components of the immune system respond to parasitic infection are also involved in allergic response. The system has developed to produce a rapid tissue based response to re-infection. Lack of infectious drive is a contributory factor in allergic disease. It is a combination of genetic (genetic predisposition) and environmental factors.

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19
Q

which cell identifies the allergen?

A

dendritic cell and presents it to naive T cell which has a specific receptor recognising the antigen

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20
Q

The T cell differentiated into Th2 cells and secrete what?

A

cytokines IL-4 and IL-3 - act as signals to naive B cells

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21
Q

what do naive B cells become and how are they adapted?

A

memory B cells and they have specific IgEs recognising the allergen on further exposure

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22
Q

these memory B cells remain in the system for what reason?

A

they continue to produce ABs for further exposure

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23
Q

what is the dual allergen exposure hypothesis?

A

we have early cutaneous exposure to food protein through disrupted skin barriers which leads to allergen sensitisation. Oral exposure leads to tolerance. There are additional theories that relate to environmental factors such as vitamin D for the immunological mechanisms important in preventing food allergens and establishing oral tolerance.

24
Q

what did the LEAP study show?

A

that allergies can still develop despite early primary and secondary prevention strategies and that oral exposure can also increase sensitisation

25
Q

why does genetics influence allergies?

A

can have a tendency to have an allergy if family also have it but not always the case. There are polygenic diseases, cytoline gene cluster for interleukins etc and therefore this is for susceptibility and not sufficient for the disease alone.

26
Q

what if the atopic march saying?

A

eczema and food allergies tend to decrease over age - there is a general connection between allergies.

27
Q

how would you diagnose an allergy?

A

you would use histroy, a specific antibody test (IgE), an intradermal test, oral challenge test

28
Q

what do you need to make sure of before conducting a skin prick test?

A

that the patient has not been on antihistamines recently, and wait 15 minutes for result - over 3mm

29
Q

why do you use a control in the skin prick test?

A

to make sure they have no reacted to the skin prick itself

30
Q

which layer of the skin does the intradermal tesing injection go into?

A

into the dermis - lower layer of the skin

31
Q

what is the CRD?

A

when you find different parts of the allergen and find specific IgE

32
Q

what is the atopic triad?

A

eczema, asthma and rhinitis

33
Q

how would you treat rhinitis?

A

antihistamines and nasal steroids

34
Q

what are the immediate symptoms of asthma due to?

A

IgE mediated - damage to airways due to late phase response

35
Q

what is asthma?

A

its a disease of inflammation and hyperactivity of the small airways

36
Q

what is another word for eczema?

A

atopic dermatitis - there is also contact (allergic or non-allergic)

37
Q

what is used to treat eczema?

A

topical steroids and moisturisers

38
Q

what is a type II hypersensitivity reaction?

A

cytotoxic - IgG and IgM AB response against self or foreign antigen at cell surface

39
Q

what is activated in type II?

A

there is complement activation, phagocytosis and ADCC

40
Q

what are the clinical features of type II?

A

the onset in minutes to hours, with cell lysis and necrosis - common antigens are penicillin and there are diseases that result in type II hypersensitivity such as Goodpasture’s nephritis or a blood transfusion reaction

41
Q

what is the basis of a blood transfusion reaction?

A

there is incorrectly matched blood. The patient’s APCs will detect the foreign antigen and present it to B cells which will make ABs. These will activate the complement cascade and have cytotoxic action, and via the classical pathway make a MAC attack complex. Therefore there is inflammation and cell lysis and haemolysis

42
Q

how does the complement pathway come about?

A

C1 binds IgG and IgM and the cascade follows. C3 activation results in opsonisation and the MAC.

43
Q

what is the type III hypersensitivity?

A

it is immune complex. It uses IgG and IgM against a soluble antigen for immune complex deposition - attach and form a complex - nets which get trapped in blood vessels - vasculitis - irritation of blood vessels and leaking

44
Q

what are the clinical features of immune complex?

A

the onset of 3-8 hours and vasculitis

45
Q

what is the traditional cause of type III?

A

serum sickness and associated diseases are SLE

46
Q

what are the differences between type II and III?

A

different targets - II is not an immune complex, it is attached to a cell and III is a soluble antigen that makes a complex

47
Q

why should we have self tolerance?

A

T and B cells that recognise own antigens should be excluded in the secondary lymphoid organs - if not then autoimmunity results

48
Q

what is the basis of SLE?

A

we have no self tolerance - we recognise our own antigens from damaged cells - failure to filter out at the secondary lymphoid organs - complexes are not cleared easily from body and get stuck to vessel walls - inflammation

49
Q

what is a key blood test for SLE and why?

A

test for C3 and 4 as they are used up in large amounts once C1 has bound the AB. C3a makes chemokines and C4a and 5a make anaphylotoxins.

50
Q

what happens in vasculitis?

A

high concentration of complexes in kidneys due to the filtering, plasma is then filtered into synovial fluid to the joints

51
Q

what is a type IV hypersensitivity reaction?

A

delayed - antigen specific T cell mediated cytotoxicity

52
Q

what are the clinical features of type IV?

A

onset of 48-72hrs with erythema in duration

53
Q

what are common antigens for type IV?

A

metals, tuberculin test and poison ivy

54
Q

what disease is associated with type IV?

A

contact dermatitis

55
Q

what happens with poison ivy?

A

allergen goes through the skin and is picked up by dendritic cells. T cells release chemicals communicating with immune system and IL-2 is released. Machrophages all migrate to contact site - delayed as longer to recruit T cells

EMS MOD (28 decks)

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