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Year 3 > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the signs and symptoms of anaphylaxis?

A

Airway and breathing- bronchospasm, wheezing, tongue swelling, stridor, hoarse voice
Circulation- vasodilation, tachycardia, hypotension, cardiac arrest
Neurological- feeling faint, decreased cerebral blood flow, confusion, light headedness, feeling of impending doom
GI- pain, vomitting, diarrhoea, smooth muscle contraction.
Skin-Itching due to histamine and bradykinin release.

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2
Q

Name some common allergens.

A 
Pollen
Food
Medications
Blood donations
Latex
Anaesthetics
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3
Q

What are the mediators of Type 1 hypersensitivity reactions?

A

IgE, mast cell degranulation

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4
Q

What are the mediators of Type 2 hypersensitivity reactions?

A

IgG, IgM, complement

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5
Q

What are the mediators of Type 3 hypersensitivity reactions?

A

IgG, complement

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6
Q

What are the mediators of Type 4 hypersensitivity reactions?

A

T cells

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7
Q

Give examples of Type 1 hypersensitivity reactions.

A 
Asthma
Atopy- dermatitis/ eczema
Anaphylaxis
Allergic rhinitis
Food allergy
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8
Q

Give examples of Type 2 hypersensitivity reactions.

A

Grave’s disease
Incompatible transfusions
Autoimmune hemolytic anaemia
TTP

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9
Q

Give examples of Type 3 hypersensitivity reactions.

A

Arthus reaction
Serum sickness
SLE
RA

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10
Q

Give examples of Type 4 hypersensitivity reactions.

A

Contact dermatitis
Mantoux test
Coeliac
TB

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11
Q

What are the 4 key antibiotics given in Tuberculosis infections?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

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12
Q

What are the side effects of the 4 antibiotics used in TB?

A

Rifampacin- Dark urine, hepatotoxicity, decreased effectiveness of the oral contraceptive pill

Isoniazid- Peripheral neuropathy- Vit B6 given alongside, clumsiness/ unsteadiness

Pyrazinamide- Gout

Ethambutol- Eye damage- colour blindness and vision loss

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13
Q

Which components of the immune system are involved in response to viral infections?

A

INF alpha and beta
Cytotoxic T cells
Natural killer cells

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14
Q

Which type of T helper cell is involved in Autoimmunity, inflammation, intracellular pathogens?

A

Th1

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15
Q

What is released from mast cells?

A

Histamine
Prostaglandins
Leukotreines
Tryptase

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16
Q

What are the effects of mast cell mediators?

A

Vasodilation and tachycardia
Increased vessel permeability
Gland secretion
Bronchoconstriction

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17
Q

Which allergy usually appears first in life?
Rhinitis
Asthma
Dermatitis and food allergy

A

Dermatitis and food allergy

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18
Q

What genetic defect may there be for atopic dermatitis to occur?

A

Filaggrin defect= membrane disruption

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19
Q

What are the signs and symptoms of immediate (<1 hour) drug reactions?

A 
Vomit and diarrhoea
Tachycardia, hypotension
Wheeze, stridor
Urticaria (hives), angioedema
Loss of consciousness
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20
Q

What are the signs and symptoms of delayed (>1 hour) drug reactions?

A

Myalgia and arthralgia
Fever
GI upset
Itching and rash

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21
Q

How can a suspected Penicillin allergy be investigated?

A

Blood tests: look for eosinophils, plateles, haemolytic anaemia
Measure Tryptase: after 2 hours (peak) and 24 hours- this represents mast cell degranulation

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22
Q

What is Chronic Spontaneous Urticaria?

A

NOT anaphylaxis or allergy
Itching and rash, slow to resolve
Can have panic attack and angioedema

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23
Q

What is a biphasic anaphylaxis reaction?

A

2 episodes 1-8 hours apart

Mast cells refill and degranulate again

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24
Q

How soon after exposure does anaphylaxis usually occur?

A

Within 60 minutes

Later onset = less severe

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25
Q

What are the potential differential diagnoses for anaphylaxis?

A

Vocal cord dysfunction
Chronic urticaria
Hypotension due to shock, sepsis, blood loss, MI
Syncope. faint- but would appear white not blue

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26
Q

How is anaphylaxis managed?

A

ABCDE
Adrenalin IM 0.5mls (1:1000) repeat after 5 mins if no improvement
High flow oxygen
Fluid challenge (500-1000mls) for hypotension
Bronchodilator
Supportive management to prevent a biphasic reaction eg. Corticosteroids, anti histamines

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27
Q

In mastocytosis, which blood test level is always raised?

A

Tryptase

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28
Q

What is positive selection and where does it occur?

A

In the thymic cortex, imposed by cortical epithelial cells.

Developing T cells which recognise self peptide on MCH can continue maturing.

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29
Q

What is negative selection and where does it occur?

A

In the cortico-medullary junction of the thymus.

Developing T cells which have autoreactive TCRs are removed via apoptosis.

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30
Q

What are 2 examples of peripheral tolerance?

A
  1. Immune privelege- physical barries eg BBB, cells in testes express Fas which induces apoptosis in any T cells.
  2. TReg cells- downregulate immune responses
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31
Q

How can loss of tolerance occur (3 methods)?

A
  1. Immune priveledge lost eg. penetrating eye injury
  2. Failure of TReg cells
  3. Molecular mimicry- eg. Rheumatic fever may follow infection with Haemolytic strep
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32
Q

What can predispose to autoimmunity?

A

Female sex
Autoantibodies
HLA class DQ2 and DQ8

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33
Q

Which HLA classes are associated with coeliac disease?

A

HLA DQ2 in 95%

HLA DQ8

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34
Q

When should coeliac disease be suspected?

A

Diarrhoea, weight loss, anaemia

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35
Q

What are the key histological features of coeliac disease?

A

Villous atrophy
Crypt hyperplasia
Raised intra epithelial WBCs

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36
Q

What are the risk factors for rheumatoid arthritis?

A 
Smoking
Female
HLA DR4
CCP autoantibodies
Lung infections
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37
Q

What blood results/ antibodies will be found in rheumatoid arthritis?

A

CRP Raised
RF Raised
CCP autoantibodies
C3 and C4 Raised

NO dsDNA antibodies, ANA low

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38
Q

What are the key features of rheumatoid arthritis?

A

Symmetrical polyarthritis
Synovial joints of hands and feet
Morning stiffness

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39
Q

What systemic features may be present in rheumatoid arthritis?

A

Necrotising granulomas
Vasculitis
Atherosclerosis

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40
Q

How does rheumatoid arthritis appear on Xray?

A

Loss of joint space
Soft tissue swelling
Joint deformity

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41
Q

What is the treatment for Rheumatoid Arthritis?

A

Immunosuppression: Steroids
NSAIDs
Anti TNFalpha eg. Infliximab

42
Q

What will be found on a urine dip in a patient with SLE?

A

Protein and blood

SLE can lead to nephrotic syndrome, due to kidneys being blocked with immune complexes

43
Q

What blood results/antibodies will be found in a patient with SLE?

A

ANA high
dsDNA high
ENA (extractable nuclear antigens) Sm and RNP

CRP normal/ low
C3 and C4 low (no acute phase response)

44
Q

What is the treatment for SLE?

A

Immunosuppression- NSAIDs, hydroxychloroquinine, Azathiaprine, Methotrexate
Anti B cells (Rituximab/Belimumab)

45
Q

What are some of the key clinical features of SLE?

A 
Malar rash
Discoid rash
Malaise
Fatigue
Alopecia
Raynaud's
Oral/ nasal ulcers
Synovitis
Serositis
46
Q

What blood results/ antibodies will be found in vasculitis?

A

CRP high
ESR high
ANCA antibodies (pANCA in Microscopic Polyarteritis, cANCA in Wegener’s Granulomatosus)

47
Q

What is vasculitis?

A

Autoimmune condition
Autoantibodies against neutrophil enzymes, leads to neutrophil activation and damage to small blood vessels, and acute renal syndromes.

48
Q

What is the treatment for vasculitis?

A

Steroids
Cyclophosphamide
Anti B cell (Rituximab, Belimumab)

49
Q

What is Antiphospholipid Syndrome?

A 
Where antiphospholipid antibodies cause:
Recurrent abortions
Arterial or venous thrombi
Pre-eclampsia
Migraine
Stroke

Is associated with SLE or can present alone

50
Q

Which autoantibodies are found in antiphospholipid syndrome?

A

Anti-Cardiolipin

51
Q

Which autoantibodies are found in SLE?

A

ANA

Anti dsDNA

52
Q

Which autoantibodies are found in Primary Biliary Cholangitis?

A

AMA

53
Q

Which autoantibodies are found in Goodpastures disease?

A

Anti GBM

54
Q

Which autoantibodies are found in Rheumatoid arthritis?

A

Anti CCP

55
Q

What does scleroderma result in?

A

Skin, blood vessel and muscle changes

Collagen deposition

56
Q

What is CREST?

A

A syndrome due to Scleroderma:

C-Calcium deposition
R- Raynaud's
E-Oesophageal reflux
S- Sclerodactyly (skin thickening)
T- Telangiectasia (spider veins)
57
Q

What are the main types of innate immunodeficiency?

A
  1. Neutrophil defect
  2. Complement defects
  3. NK defects
  4. Cytokine/ TLR defects
  5. Splenectomy
58
Q

What are the main types of adaptive immunideficiency?

A
  1. B cell/ antibody defects

2. T cell defects

59
Q

How do neutrophil defects present?

A

Neutropenic sepsis; bacterial or fungal infection WITHOUT pus

60
Q

What are the causes of neutrophil defect?

A

Drugs- chemo
Leukaemia
Adhesion defect eg. LFA-1 deficiency
Respiratory burst defect eg. Chronic Granulomatous Disease

61
Q

What treatments are used for neutrophil defect?

A

G-CSF

Antifungals, Antibiotics

62
Q

How do patients with a splenectomy usually present?

A

Septicaemia

Infection with pneumococcus, meningococcus and malaria

63
Q

Which Ig in the spleen normally opsonises encapsulated bacteria?

A

IgM

64
Q

What is the treatment for patients who have had a splenectomy?

A

Penicillin prophylaxis

Vaccination: Meningococcus C, Haem B and Pneumococcal

65
Q

How do patients with NK defects present?

A

Viral infections eg. CMV, Herpes Zoster

66
Q

How do patients with complement (C3) defects present?

A

Pyogenic infections

67
Q

How do patients with complement (C5-9) defects present?

A

Neisseria or meningitis infections

68
Q

How do patients with complement (C1,2,4) defects present?

A

Immune complex diseases

69
Q

How do patients with Cytokine/TLR defects present?

A

Recurrent intracellular bacterial infections eg. Atypical mycobacterium avium

70
Q

How do patients with B cell/ Antibody defects present?

A
  1. Pneumonia, sinusitis, otitis
  2. Campylobacter (diarrhoea), Strep pneumonia, Haem influenza
  3. Pyogenic infections from encapsulated and non encapsulated bacteria
  4. Diarrhoea and malabsoprtion
  5. Aged 4 or 5 months
71
Q

What are the causes of B cell defects?

A
  1. Genetic (present >6 months of age) in males
  2. BTK deficiency
  3. B cell malignancy eg. CLL
  4. HIV
  5. Immunosuppression
72
Q

How can B cell defects be diagnosed?

A

Serum Igs and electrophoresis
Paraprotein?
Lymphocyte count will be normal (as B cells only count for 10%)
Give vaccines- eg. HIb and Meningitis and look for immune response

73
Q

How can B cell defects be treated?

A

Replace Igs

Antibiotics

74
Q

When does a T cell defect present in a patient?

A

Presents from birth- with failure to thrive, and opportunistic infections.

75
Q

What is Di Georg’es Syndrome?

A

A type of T cell defect; due to defective thymus.

Presents with opportunistic infections: Candida, EBV, P.Carini

76
Q

What are the features of Di George’s syndrome?

A

Small jaw
Abnormal ears
Cleft palate
Lymphopenia

77
Q

What is the commonest cause of CD4 cell deficiency?

A

HIV

78
Q

Which infections do HIV patients get?

A
  1. Intracellular: TB, Salmonella, Pneumocystis
  2. Viruses: Kaposi’s sarcoma, CMV, EBV
  3. Encapsulated bacteria- pneumonia
  4. Fungi and yeast- Candida, cryptococcus
  5. Protozoa- Pneumocystis, cryptosporidiosis, toxoplasmosis
79
Q

What is a likely cause of a chest infection in a HIV patient?

A

Pneumocystis (fungi)

80
Q

Which type of T helper cell is involved in secreting regulatory cytokines and restricting co-stimulatory availability for other T cells?

A

Treg

81
Q

Which type of T helper cell is involved in protection against extracellular helminths, promoting B cell class switching to IgE and involved in allergy and asthma?

A

Th2

82
Q

Which type of T helper cell is involved in protection against fungi, extracellular bacteria, autoimmunity and epithelial barriers?

A

Th17

83
Q

Which interferons are most important for protection against viruses?

A

IFN aplha and beta

84
Q

Which interferons are most important for protection against intracellular (non viral) infections?

A

IFN gamma

85
Q

Which cytokines are important in protection against parasitic infections?

A

Il 4 and Il5

Secreted frorm Th2 cells

86
Q

Which cells are the main phagocytes for extracellular bacteria?

A

Neutrophils

87
Q

What is the most common antibody deficiency?

A

IgA deficiency

88
Q

In Hyper IgM syndrome, there are low levels of which 2 antibody classes?

A

Low IgG and IgA

Presents with Pneumocystis and Crptosporidiosis

89
Q

BTK deficiency presents around what age?

A

6 months

90
Q

The autoantigen 21 hydroxylase is found in which condition?

A

Addison’s

91
Q

What % of RA patients have both RF and anti CCP in their serum?

A

70%

92
Q

Which antibody is most useful for predicting SLE disease severity?

A

Anti dsDNA

93
Q

60-70% patients with CREST have which antibodies?

A

Anti centromere

94
Q

Sjogrens syndrome patients usually have dry what?

A

Dry eyes

Dry mouth

95
Q

Which autoantibodies are present in Sjorgens syndrome?

A

ENA Ro and La

96
Q

Which cytokine is linked with IgE production?

A

Interleukin 4

97
Q

What are the effects of histamine?

A

Increased blood flow
Increased permeability
Itching due to nerve stimulation
Smooth muscle contraction

98
Q

Eosinophils are attracted to which cytokine?

A

Interleukin 5

99
Q

Asthma, hayfever and eczema are associated with which subset of T helper cells?

A

Th2

100
Q

Give an example of a H1 receptor antagonist drug.

A

Loratidine

Cetirizine

Year 3 (22 decks)

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