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Medicine > Immuno 2nd Year > Flashcards

Immuno 2nd Year Flashcards

1
Q

What is a type 1 hypersensitivity?

A

Allergic reaction

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2
Q

What are the immediate reactions with a type 1 hypersensitivity?

A

Local reactions: Ingested - GI symptoms, Inhaled - respiratory symptoms

Systemic reaction: agioedema, hypotension, tachycardia, broncho-constriction, haematochezia

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3
Q

What cells are involved in the type 1 hypersensitivity?

A

Mast cells - (IgE related)

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4
Q

What is the medical term for year round exposure to allergens?

A

Perennial exposure

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5
Q

What 3 interleukins are responsible for Type 1 hypersensitivity in the TH2 (T helper cells) response?

A

IL-4, IL-5, IL-13

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6
Q

What is the hygiene hypothesis and what does it mean?

A

Western lifestyle associated with a reduced infectious burden - hygiene hypothesis. Children exposed to animals, pets and microbes in the early postnatal period appeared to be protected against certain allergic diseases

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7
Q

Why are mucosal membranes and blood vessels affected in a type 1 hypersensitivity reaction?

A

The location of mast cells is in these areas and they have IgE on their surface so allergic reactions will cause local effects in these areas

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8
Q

What are the 4 mast cell mediators and what do they each do?

A

Tryptase - remodel connective tissue matrix but measured in the anaphylactic response

Histamine - toxic to parasites, increase vascular permeability, cause smooth muscle contraction

Leukotrienes C4, D4, E4 - cause smooth muscle contraction, increase vascular permeability, stimulate mucus secretion

Platelet-activating factor - attracts leukocytes, amplified production of lipid mediators, activates neutrophils, eosinophils and platelets.

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9
Q

What is happens on the 1st and subsequent exposures of an allergen causing an allergic response

A

Allergen 1st exposure - TH2 response
IgE - mediated triggering of mast cell - antigen specific IgE
No immediate response - sensitisation reaction here

Allergen 2nd exposure - IgE cross-linking = degranulation of mast cells, systemic exposure - systemic response

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10
Q

Allergic reaction leading to facial manifestations are called?

A

Angioedema

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11
Q

What are the systemic manifestations of allergic reaction and what symptoms are characterised by them?

A

Systemic: Hypotension/ cardiovascular collapse/ generalised urticaria - increased vascular permeability,
Angiodema - generalised vasodilation,
Breathing problems - bronchial constriction

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12
Q

How would you treat the abnormal adaptive immune response against the allergen (TH2 response, IgE, mast cell activation)?

A

TH2 response = allergen desensitisation (oral immunotherapy)

IgE = anti-IgE monoclonal antibody - good for chronic asthmatics and chronic urticaria

Mast cell activation = antihistamines, leukotriene receptor antagonists, corticosteroids

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13
Q

Define hypersensitivity

A

The antigen specific immune responses that are either inappropriate or excessive and result in harm to the host

Change in function or damage to the function of the host

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14
Q

What are the types of hypersensitivities and the causes of the response?

A

Type 1 - allergy
Type 2 - antibody mediated
Type 3 - immune complexes mediated
Type 4 - cell mediated (delayed) - environmental infectious agents and self antigens

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15
Q

What immunoglobulins are responsible for the 4 hypersensitivities?

A

Type 1 - IgE
Type 2 and 3 - IgG or IgM
Type 4 - IgM

Type 2 is organ specific disease - membrane bound

Type 3 IgG is soluble but when they complex they can get caught up in particular parts of the body and causes problems there

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16
Q

What are the 2 phases of hypersensitivity reactions?

A

Sensitisation phase - first encounter with antigen
Activation of APCs and memory effector cells.

Effector phase - pathologic reaction upon re-exposure to the same antigen and activation of the memory cells of the adaptive immunity

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17
Q

What happens in type 2 hypersensitivity within the following parameters:
Development time, Antibody involvement, Antigen location, Outcomes.

A 
Development time: 5-12hours
Antibody: IgG or IgM
Antigens: cell bound antigens
Exogenous: blood group antigens, rhesus D antigens
Endogenous: self antigen

Outcomes:
Tissue/ cell damage, physiological change

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18
Q

What antigen can cause haemolytic disease of the newborn?

A

Rhesus D

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19
Q

What antigens cause transfusion reactions?

A

ABO blood group system

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20
Q

What 2 mechanisms drive type 2 hypersensitivity?

A

Complement activation and antibody-dependent cell cytotoxicity

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21
Q

Name the 3 antibody-dependent cell cytotoxic diseases of type 2 hypersensitivity

A

1- Autoimmune haemolytic anaemia
2- Immune thrombocytopenia Purpura
3- Goodpasture’s syndrome

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22
Q

What immunoglobulin is responsible for the RBC lysis in incompatible blood transfusions?

A

IgM

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23
Q

Explain what happens in Rhesus D positive pregnant mothers and what is the treatment?

A

In Rhesus D negative pregnancy the problems are not immediate but in further pregnancies miscarriage occurs if the foetus also has rhesus positive RBC due to the antigen on the foetuses RBC.
A foetuses RBC can sometimes leak out of the foetal circulation and enter the maternal circulation. This results in the mother in the first ever rhesus positive pregnancy producing anti-rhesus antibodies due to the sensitisation process. If the woman becomes pregnant again with another rhesus positive foetus then her anti-Rh antibodies will cross the placenta and damage foetal RBC causing haemolytic disease of the newborn

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24
Q

What 2 diseases result from receptor blockade and stimulation that are part of type 2 hypersensitivity?

A

Graves disease - receptor stimulation - antibodies against the TSH receptor causing hyperthyroidism
Myasthenia gravis - receptor blockade - antibody against the ACh receptor causing reduced signal transmission

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25
Q

How could type 2 hypersensitivity be treated?

A

Plasmaphoresis - removal of circulating antibodies and inflammatory mediators
Anti-inflammatory drugs - complement activation
Splenectomy - reduced opsonisation and phagocytosis
IVIG - IgG degradation
Antithyriod surgery or drugs to block the TSH receptor
Replacement therapy - pyridostigmine - AChE blocker to increase amount of ACh in synaptic cleft

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26
Q

What is a type 3 hypersensitivity?

A

Complex mediated IgG soluble therefore when complexes are made this causes damage in the organ they end up in

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27
Q

How quickly can T3 hypersensitivity reactions occur?

A

3-8 hours

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28
Q

What immunoglobulins are responsible for T3 hypersensitivity?

A

IgG or IgM and antigens

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29
Q

What are the causes (antigens) for T3 hypersensitivity?

A

Soluble antigens - foreign (infection) or endogenous (self antigen)

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30
Q

What 3 factors affect T3 hypersensitivity immune complex pathogenesis and why?

A

Complex size - small and large are not a problem to deal with but intermediate sized ones can’t be cleared effectively

Host response - low affinity antibody and complement deficiency

Local tissue factors - haemodynamic factors and physicochemical factors

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31
Q

What are 3 diseases that are type 3 hypersensitivity reactions?

A

Rheumatoid arthritis - antigen is the Fc portion of IgG with articular and extraarticular features. Intertwined with episodes of inflammation and remission

Glomerulonephritis (infectious) - bacterial endocarditis or hepatitis B infection - immune complexes have a sustained production of antibodies leading to glomerulonephritis

SLE - antigen is the double stranded DNA in cells. Most prevalent immune complexes disease. Mainly women affected 9:1

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32
Q

What is a type 4 hypersensitivity?

A

Cell mediated or delayed - environmental infectious agents and self antigens. Involves lymphocytes and macrophages

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33
Q

How long does it take for type 4 hypersensitivity to react?

A

24-72 hours - delayed

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34
Q

What are the different subtypes of type 4 hypersensitivity reactions?

A

Contact hypersensitivity
Tuberculin hypersensitivity
Granulomatous hypersensitivity

35
Q

What is the pathophysiology of type 4 hypersensitivity?

A

Sensitisation phase - bacteria are seen by APCs and macrophages. They then inform the TH1 cells and the DTH cells.
Effector phase - TH1 cells inform the resting macrophages by TNF-beta and IFN-gamma which then causes them to become activated and then cause the local effects

36
Q

What is contact hypersensitivity and what is an example of it?

A

On skin contact with the antigen a reaction occurs 48-72hours post exposure with an epidermal reaction and requires endogenous proteins
Nickel, poison ivy, organic chemicals are examples

37
Q

What is granulomatous hypersensitivity?

A

Occurs 21-48 DAYS post exposure with resultant tissue damage. It is usually due to the inability for the body to remove the foreign material/ bacteria and so closes it off from the rest of the body. A granuloma is formed as a result. Central necrotic cord, surrounded by lots of Giant cells and T-cells.
Examples - TB, Leprosy, Schistosomiasis, Sarcoidosis

38
Q

What are examples of T4 hypersensitivity reactions to endogenous proteins?

A

Pancreatic beta cells - insulin dependent DM
Thyroid gland - hashimoto’s thyroiditis
Fc portion of IgG = rheumatoid arthritis

39
Q

Explain Hashimoto’s disease vs Grave’s disease immunologically?

A

Hashimoto’s disease - CD4 T-cells react with B cells and CD8 T cells to lead to necrosis and apoptosis of thyroid cells - leading to hypothyroidism. Plasma cells are activated by the CD4 cells and the CTL are activated CD8 T cells.
Grave’s disease - CD4 T cells activating B cells to produce antibodies against the TSH receptor causing activation

40
Q

How do we treat T3 and T4 hypersensitivity?

A

Anti-inflammatory drugs - NSAIDs, Corticosteroids, Steroid-sparing drugs - AZA, Mycophenolate, cyclophosphamide.
Monoclonal antibodies - B -cells and T-cells, cytokine network, APCs.

41
Q

What is allergy defined as?

A

Immunological hypersensitivity that can lead to a variety of different diseases via different pathomechanisms. This can be IgE mediated (e.g. peanut allergy) or non-IgE mediated (e.g. milk protein)

42
Q

What is an allergen?

A

Any substance stimulating the production of IgE or a cellular immune response. Usually a protein, but can be carbohydrates

43
Q

Define sensitivity

A

Normal response to a stimulus

44
Q

Define hypersensitivity

A

Abnormally strong response to a stimulus

45
Q

Define sensitisation

A

Production of IgE antibodies (detected by serum IgE assay or SPT) after repeated exposure to an allergen

46
Q

Define atopy

A

A tendency to produce IgE antibodies in response to ordinary exposure to potential allergens. Strongly associated with asthma, rhinitis, eczema and food allergy

47
Q

Define anaphylaxis

A

A serious allergic reaction with bronchial, laryngeal and cardiovascular involvement that is rapid in onset and can cause death

48
Q

Define food allergy

A

Immunologically mediated adverse reaction to food

49
Q

How does allergic rhinitis present?

A

Blocked/ runny nose, itchy nose, sneezing

50
Q

What is the trigger of allergic rhinitis?

A

Pollen, pets or HDM

51
Q

How does allergic conjunctivitis present?

A

Red, swollen, itchy, watery eyes

52
Q

How does asthma present?

A

Chest symptoms of wheeze, cough, SOB and tight chest

53
Q

How does atopic dermatitis eczema present?

A

Commonest chronic inflammatory skin disease with itch and excoriation

54
Q

How does urticaria (hives) present?

A

Acute/ chronic maculo-papular pruritic rash without or with angioedema

55
Q

How does insect allergy present?

A

Mainly to bee or wasp stings. Mild (local), Moderate (urticaria), Severe (anaphylaxis)

56
Q

How do drug allergies present?

A

Especially to antibiotics - anaphylaxis or hives or angioedema, rashes

57
Q

How does eczema prevalence change with age?

A

As age increases prevalence of asthma decreases

58
Q

How does food allergy prevalence change with age?

A

As age increases prevalence of food allergy decreases

59
Q

How does asthma prevalence change with age?

A

As age increases prevalence of asthma increases up until 26 when prevalence decreases

60
Q

How does rhino conjunctivitis prevalence change with age?

A

Increases rapidly with age

61
Q

What two allergies help predict future asthma prevalence?

A

Food allergy and eczema

62
Q

Before what age do milk allergies always present by?

A

12 months

63
Q

What are the 3 most common major allergens?

A

Celery, Cereals containing gluten, Crustaceans

64
Q

How can blood tests be used to determine food allergies?

A

IgE levels and levels of allergens can be detected in the blood

65
Q

What is the difference in symptom onset with IgE- mediated and non IgE-mediated food allergies?

A

IgE-mediated = immediate 5 to 30mins

Non IgE-mediated = delayed hours to days

66
Q

What is the difference in presenting age with IgE- mediated and non IgE-mediated food allergies?

A

IgE-mediated = variable - age of contact, all milk allergy by 1 year
Non IgE-mediated = infancy and early childhood, all milk allergy by 1 year

67
Q

What is the difference in natural history with IgE- mediated and non IgE-mediated food allergies?

A

IgE-mediated = milk and egg allergy can resolve, others persistent into adulthood
Non IgE-mediated = Resolve earlier than IgE and many by school age

68
Q

How does temperature affect cows milk allergy?

A

Casein is more heat resistant than whey
Forms bonds in food matrix to reduce availability and allergenicity
Up to 70% milk-allergic can tolerate baked milk (in wheat)

69
Q

How does temperature affect egg white allergy?

A

4 major proteins in egg white, all except ovomucoid heat labile
Well cooked eggs are much less allergenic than raw egg
Up to 70% of egg-allergic can tolerate baked egg (in wheat)

70
Q

How does temperature affect peanut allergy?

A

Allergenicity increased if dry roasted, decreased if boiled/fried

71
Q

How does temperature affect fish allergy?

A

Fish protein is very heat stable but canned tuna and salmon are significantly less allergenic

72
Q

How does temperature affect allergies to apples?

A

Apple proteins are very heat sensitive therefore patients with pollen food syndrome can eat processed apple

73
Q

What is another term for IgE mediated allergy?

A

Immediate-onset

74
Q

What is another term for Non-IgE mediated allergy?

A

Delayed-onset

75
Q

How does diagnosis verification work in allergy diagnosis?

A

Controlled oral food challenges

76
Q

How can immunoassays be used for detection of specific IgE?

A

ELISA-Plates, Western blots

1 - Allergen is adsorbed and immobilised to a solid phase
2 - Patient’s serum is added followed by incubation for 30-60minutes followed by several washing steps
3 - Allergen-bound IgE is detected by an enzymatically labelled anti-human IgE monoclonal antibody

77
Q

What are typical symptoms of lactose intolerance?

A

Bloating, flatulence, explosive diarrhoea

78
Q

How early can lactase be detected in the jejunal brush border and when do the levels rise then decrease?

A

Detection from 8 weeks gestation
Rise from 32 weeks to peak at birth
Activity decreases within months

79
Q

How many stages are there on the milk ladder?

A

4 stages

80
Q

On the milk ladder what stage has the most denatured/ lower protein dose and which has the least denatured/ higher protein dose?

A

Stage 1 - more denatured / lower protein dose - less allergenic
Stage 4 - less denatured / higher protein dose - more allergenic

81
Q

How are food induced anaphylaxis treated?

A

Adrenaline - EpiPen / Emerade

82
Q

What causes angioedema in allergic reactions?

A

Non-itchy swelling as histamine and bradykinin are released in the deep dermis - causing vasodilation and inc vascular permeability.

83
Q

How do you treat mast cell activation in allergies?

A

Antihistamines, leukotriene receptor antagonists, corticosteroids

Medicine (15 decks)

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