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Immunology ESA 4 > Key facts > Flashcards

Key facts Flashcards

1
Q

What does a type 1 Hypersensitivity reaction involve?

A

Allergy - IgE mediated mast cell activation to cause release of histamine

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2
Q

What does a type 2 Hypersensitivity reaction involve?

A

Antibody mediated IgM and IgG reaction to cell-bound antigens

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3
Q

What does a type 3 Hypersensitivity reaction involve?

A

Antibody mediated IgM and IgG response to soluble antigen complexes

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4
Q

What does a type 4 Hypersensitivity reaction involve?

A

Macrophage and T-cell (cell-mediated) response to environmental antigens aka Delayed

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5
Q

Name the first phase of hypersensitivity reactions and what happens

A

Sensitivity - first exposure, memory effector cells activated - no clinical manifestation

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6
Q

What is the second phase of a hypersensitivity reaction?

A

Effector phase - second exposure leads to reaction

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7
Q

Name 5 Type 2 Hypersensitivity diseases

A
  • Pernicious anaemia
  • Graves disease
  • HDN
  • Myasthenia gravis
  • Goodpastures
  • Transfusion reaction to blood
  • Immune thrombocytopenic purpura
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8
Q

What blood group is the universal donor?

A

O

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9
Q

What blood group is the universal acceptor?

A

AB

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10
Q

What does HDN lead to?

A

Jaundice - yellow sclera, skin, pale stools, dark urine

Mental retardation, seizures - “kernicterus”

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11
Q

What is the treatment for HDN?

A

RhoGAM - given to mum during first birth

It is Anti-D - binds to the Rhesus D antigen, stops induction of an immune reaction and so no sensitisation can occur

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12
Q

What antigen is Rhesus +ve?

A

D-antigen

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13
Q

What is the diagnostic test for HDN and what does it involve?

A

Coombs test

Test either baby’s blood for antibodies attached to blood cells or mother’s serum for anti-D antibodies

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14
Q

Describe the pathophysiology of Myasthenia Gravis

A

Antibodies bind AcH receptors - cannot be activated

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15
Q

What are the symptoms of Myasthenia Gravis?

A

Muscular weakness + fatigue
Diplopia
Ptosis
Limited ocular movements

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16
Q

Name a treatment for Myasthenia Gravis and its type

A

Pyridostigmine

AcHesterase inhibitor

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17
Q

Name a side-effect of Pyridostigmine

A

SLUDGE

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18
Q

What can happen to a baby if the mother has Myasthenia Gravis?

A

When born, can have IgG that passed through the placenta and so temporarily can have symptoms

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19
Q

Name 3 treatments of Type 2 Hypersensitivity reactions

A
  • Plasmapheresis
  • AcHesterase inhibitor
  • Splenectomy - ITP
  • Correct metabolism eg. In Graves
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20
Q

Describe the pathophysiology of Graves disease

A

TSH receptor antibody binding causes excess Thyroid hormone release

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21
Q

Name 5 symptoms of Graves disease

A
  • Lid lag
  • Exophthalmos
  • Pre-tibial Myxedema - non-pitting oedema of the skin
  • Heat intolerance
  • Tachycardia
  • Weight loss
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22
Q

Name 3 diseases that Plasmapheresis could help with and what it is

A
  • Graves
  • Goodpastures
  • Myasthenia Gravis
    Plasma separated from blood, containing IgG
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23
Q

Describe Type 3 Hypersensitivity in detail

A

IgG and IgM form complexes with soluble antigens
Small complexes can be cleared by RE system and large by C3b
However, intermediate/low-affinity antigens cannot be sorted by either
These then deposit in organs and cause damage eg. RA
This can also occur if there is complement deficiency - cannot clear large either

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24
Q

What can happen if there is complement (C3b) deficiency in a Type 3 Hypersensitivity reaction?

A

Cannot clear large immune complexes

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25
Q

Describe how damage occurs to an organ with an immune complex deposited within it

A

Immune complexes are deposited
C3b attaches
Neutrophils recruited, which cause degranulation

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26
Q

Name 3 diseases caused by Type 3 hypersensitivity reactions

A
  • RA - Rheumatoid factor (IgG) deposited
  • Glomerulonephritis (infectious cause) eg. Hepatitis B -> post-infection, bacteria form immune complexes
  • SLE
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27
Q

Name an important feature about SLE and pregnancy

A

Commonly causes miscarriage

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28
Q

Why is a Type 4 hypersensitivity reaction referred to as “Delayed”?

A

Occurs only 24-72 hours after exposure

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29
Q

Describe the pathophysiology of a Type 4 immune reaction

A

Sensitisation phase: TH1 cells developed to antigen by APC presentation
Effector phase: Macrophages activate and try to attack antigen - however, they cannot clear it eg. Tb - leads to massive interferon/cytokine release
Cytotoxic as recruits TH2 (T killer cells)

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30
Q

Name 5 diseases caused by Type 4 hypersensitivity reactions

A
  • Contact: Nickel
  • Granulomatous: Tb/Sarcoidosis
  • Tuberculin: Mantoux test for Tb epithelial reaction
  • Diabetes mellitus type 1 - attack of pancreatic B cells
  • Hashimoto’s
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31
Q

Name 2 treatments for Type 3 and 4 hypersensitivity reactions

A

Corticosteroids - Prednisolone

Steroid-sparing agents: Azothioprine

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32
Q

What antibody type can pass across the placenta?

A

IgG

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33
Q

Why does an ABO mismatch between mother and child not cause HDN?

A

ABO antibodies are IgM

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34
Q

What is the treatment for a type 1 hypersensitivity reaction?

A

Adrenaline injection to prevent systemic mast cell activation

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35
Q

Give an example of a seasonal and perennial allergen

A

Seasonal: Pollen
Perennial: Dust mites

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36
Q

Describe the pathophysiology of Type 1 Hypersensitivity reactions in relation to antibody response

A

TH2 response via IL-4, 5, 13
IgE production by B cells that then binds to mast cells, which then migrate to cell surface
These then degranulate and release histamine etc. on SECOND EXPOSURE ONLY
Leads to IgE cross linking and histamine release

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37
Q

What interleukins are involved in a Type 1 Hypersensitivity reaction?

A

IL-4, 5, 13

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38
Q

Name 3 factors of western culture leading to the Hygiene hypothesis/ Microbial dysbiosis - what do these lead to?

A

Small family sizes, high antibiotic use, good sanitation

Alters body microbiome diversity

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39
Q

Where are mast cells most commonly found?

A

At mucosal surfaces eg. in GI tract, skin etc.

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40
Q

Name 3 mast cell mediators

A

Histamine, leukotrienes, platelet-activating factor

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41
Q

Name 2 skin manifestations of allergic reactions

A
  • Urticaria

- Angioedema

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42
Q

Describe Urticaria

A

Reddening of the skin caused by mast cell activation in the epidermis - histamine/cytokine activation

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43
Q

Describe Angioedema

A

Swelling of lip/eyes/tongue/URT due to activation of mast cells within the deep dermis - histamine and bardykinin

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44
Q

What is anaphylaxis?

A

Systemic activation of mast cells

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45
Q

What are the symptoms of anaphylaxis? (5)

A 
Hypotension
CVS collapse
Generalised urticaria
Angioedema
Breathing problems
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46
Q

Describe how adrenaline acts as a treatment for anaphylaxis

A

Timesaver, not lifesaver

  • Reverses vasodilation and reduces oedema
  • Reverses airway obstruction
  • Increases CO
  • Inhibits mast cell activation
47
Q

Name 4 treatments for Type 1 Hypersensitivity reaction other than adrenaline

A
  • Oral desensitisation immunotherapy
  • Anti-IgE
  • Anti-histamine
  • Corticosteroids
48
Q

Define food allergy

A

Hypersensitivity to food that can lead to disease

49
Q

What is the definition of an allergen?

A

Any substance that can stimulate an IgE immune response or a cellular immune response (either)

50
Q

What is the definition of Atopy?

A

Tendency to produce IgE antibodies in response to ordinary exposure to potential allergens

51
Q

Name 5 presentations of allergy

A
  • Allergic rhinitis
  • Allergic conjunctivitis
  • Asthma
  • Eczema
  • Urticaria
52
Q

Describe the allergic march

A

Early age: Food allergy and eczema most dominant
School age: Asthma
Later age: Rhinitis most common allergy (pollen food allergy)

53
Q

What is important to note about milk allergy?

A

It can present many weeks after first ingested

54
Q

Name the two types of milk allergy presentation

A
  • Immediate IgE mediated onset - anaphylaxis symptoms

- Delayed onset (more common) - mostly GI symptoms

55
Q

Name 3 major allergens

A

Celery
Crustaceans
Gluten

56
Q

What is the difference between food allergy and intolerance?

A

Food allergy = immune response causing an adverse health effect
Food intolerance = adverse health effect not involving an immune response

57
Q

Name two types of adverse reaction to foods

A
  • Non-immune mediated - intolerance

- Immune mediated - allergy

58
Q

Name two types of immune mediated reactions to food (allergies)

A

IgE and non-IgE

59
Q

Give 2 examples of food intolerances

A

Lactose intolerance

Caffeine (overdose)

60
Q

Describe the differences between IgE mediated and non-IgE mediated allergies

A

IgE = immediate onset, Non-IgE = delayed (days)
IgE = Presentation - based on age of onset, Non-IgE = early childhood
IgE will often resolve later than non-IgE

61
Q

Name 4 IgE mediated allergy symptoms

A 
Pruritus, erythema
Urticaria
Angioedema
Respiratory - blocked/rhinitis
Hypotensive
62
Q

Name 4 non-IgE mediated allergy symptoms

A

Eczema
Mostly GI:
GORD, loose stools, constipation, blood in stools, abdominal pain

63
Q

What is the most common IgE food allergy in adults?

A

Pollen food syndrome - pruritus and mild oedema in the oral cavity associated with raw fruit and vegetables

64
Q

Describe the food allergy march (not the allergic march)

A

Infancy: Milk, eggs, peanuts
Childhood: Wheat, fish
Adults: Food pollen syndrome

65
Q

Describe how food can be processed to reduce allergic-ness

A
  • Heat it - milk, egg, apples

- Processing to destroy epitopes

66
Q

Describe “cross-reactivity”

A

Can be allergic to cows milk and also to goat’s milk

Also with pollen and fruit and vegetables

67
Q

What is acute viral urticaria?

A

A non-allergic cause of urticaria - usually children

Caused by flu and leads to excess histamine release

68
Q

Name the food allergy tests

A
  • Skin-prick test

- IgE serum test

69
Q

Describe the skin-prick test

A

Allergen injected into skin layer - becomes red and swollen

Will have a control for normal reaction based on width - can test multiple allergens at the same time

70
Q

Describe the IgE serum allergy test

A

Serum taken from patient and added to allergen - check IgE reaction

71
Q

Name 3 types of replacement milk in infants for milk allergy

A
  • Extensively hydrolysed formula
  • Amino acid formula
  • Soya
72
Q

How would you tell the difference between non-IgE mediated milk allergy and lactose intolerance?

A
  • Non-IgE = constipation, abdo pain, food refusal

- Lactose intolerance = explosive diarrhoea, bloating, flatulence

73
Q

Describe the 4 steps of management of food allergies

A

Allergy testing
Diet advice - avoid foods
Desensitisation therapy
Oral food challenge form

74
Q

Describe Sjorgens syndrome

A

Autoantibody Type 4 disease causing dry eyes, mouth and arthritis

75
Q

Name the two classifications of autoimmune disease

A
  • Organ specific - Type 2

- Non Organ-specific - Type 3

76
Q

Describe 5 diagnosis criteria for autoantibodies

A
  • Presence of autoantibodies that correlate with disease severity
  • Autoantibodies at tissue area
  • Transfer of autoantibodies to a healthy host causes disease
  • Clinical benefit from immunotherapy
  • Family history
77
Q

What is a primary autoantibody?

A

The primary antibody is one that binds directly to the antigen.

78
Q

What is a secondary autoantibody?

A

A secondary antibody binds with a primary antibody that is directly attached to the target antigen.

79
Q

Name 3 examples of primary antibodies

A
  • Anti-TSHR antibodies in Graves
  • Anti-AcH in Myasthenia
  • Anti-GBM in Goodpastures - affects both lung and kidney
80
Q

Name 4 examples of secondary antibodies

A
  • Anti-nuclear in SLE
  • Anti-parietal in Pernicious - reliable diagnostic tool
  • Anti-thyroid peroxidase in Hashimotos
  • Anti-RF in RA - only useful in females below 30
81
Q

Define the “specificity” of an autoantibody

A

% of people who do not have the disease that the test excludes

82
Q

Define the “sensitivity” of an autoantibody

A

% of people with the disease the test identifies

83
Q

Name 4 IgGs that can be passed to babies in pregnancy

A

Myasthenia gravis
Graves
ITP
SLE

84
Q

How does autoimmunity become an autoimmune disease?

A

Thymic tolerance breaks down, Treg cells do not work, autoreactive B cells are activated

85
Q

List some systemic causes of autoimmune diseases

A
  • Hormones - women more affected
  • Infectious factors post-infection - M protein from Strep Pyogenes causing rheumatic fever
  • Drugs
  • Genetic factors
86
Q

Name 4 treatments for Type 4 Hypersensitivity reaction

A 
Immunosuppressive drugs:
- Corticosteroids - prednisolone/hydrocortisone
- Anti-metabolites (methotrexate)
- Azothiaprine
Anti-inflammatory drugs
87
Q

Describe the pathophysiology of SLE

A

Cellular remnants post-apoptosis end up in blebs.
These blebs are usually phagocytosed, but in SLE they are done so poorly. They are transferred to lymphoid tissues and presented by APCs and presented to T cells, which activate B cells to produce antibodies against self.

88
Q

Describe the epidemiology of SLE

A

Female, black

89
Q

Name 6 symptoms of SLE

A

Hands: Raynaud’s, joint pains, swelling, hand rash
Sweater: Alopecia, proximal muscle weakness, mouth ulcers, rash, chest pain, photosensitivity

90
Q

What is the autoantibody for Lupus called?

A

ANA positive

91
Q

What would be visible on examination of a patient with SLE?

A
  • Alopecia
  • Malar rash
  • Swelling of hands
92
Q

Name 4 treatments for SLE

A

Education about sunscreen/lifestyle
DMARDs - Azothioprine, hydroxychloroquine
Steroids - prednisolone
Severe: IV cyclophosphamide

93
Q

What is a common complication of Lupus?

A

Renal disease

Systemic lupus erythematous nephritis - ESRD eventually

94
Q

What type of renal damage does SLE cause?

A

Nephrotic syndrome

95
Q

What type of immunoglobulin is Rheumatoid factor?

A

IgG

96
Q

What causes damage in rheumatoid arthritis?

A

Overproduction of TNF-a following RF attack on the synovium of the joint

97
Q

How is rheumatoid arthritis diagnosed?

A

X-ray, not RF test

98
Q

What are the 4 signs that would be visible on an X-ray for RA?

A
  • Loss of joint space
  • Periarticular osteopenia
  • Marginal bony erosions
  • Subluxation
99
Q

Name 4 treatments of RA

A

DMARDs - Hydroxychloroquine

Steroids - prednisolone

100
Q

How do the treatments for RA work to slow down RA?

A

Block TNF-a and IL-6

101
Q

Name 3 non-articular manifestations of RA

A

Lungs: Rheumatoid nodules - scarring
Sjogren’s: Dry eyes, dry mouth
Anaemia of chronic disease

102
Q

Name 5 symptoms of Graves disease

A
  • Exophthalmos
  • Tibial Myxedema
  • Lid lag
  • Tachycardia
  • Sweating
  • Weight loss
  • Heat intolerance
103
Q

Name 2 treatments for Graves disease

A
  • Carbimazole - anti-thyroid

- Plasmapheresis

104
Q

Name 5 symptoms of Hashimotos disease

A
  • Alopecia
  • Weight gain
  • Weakness
  • Cold intolerance
  • Swollen thyroid (goitre)
105
Q

How would Hashimoto’s be diagnosed?

A

Raised TSH (since keeps trying to stimulate)

106
Q

Name 1 treatment of Hashimoto’s disease

A

Levothyroxine

107
Q

How does Carbimazole work?

A

Inhibits thyroid peroxidase

108
Q

Name the key enzyme of the Thyroid

A

Thyroid peroxidase

109
Q

How is a hybridoma formed?

A

Immunise an animal, harvest B cells from spleen, immortalised (fused with myelomas)

110
Q

How do MABs work?

A

Bind cell-surface receptor and activate or block signalling
Cause cell-death:
- Antibody dependent cell cytoxicity
- Complement dependent cytotoxicity

111
Q

What is Lymphoma?

A

Cancer of the lymphocytes (b or t cells)

112
Q

What are the B symptoms of Lymphoma?

A

Night sweats, weight loss

113
Q

What receptor do lymph nodes express that is a target for Lymphoma treatment?

A

CD20

114
Q

Name 3 monoclonal antibodies and what they treat

A

Rituximab - Lymphoma
Herceptin - inhibition of HER-2 signalling, breast cancer
Abciximab - glycoprotein 2/3a inhibitor - anti-platelet

Immunology ESA 4 (1 decks)

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