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Y2 Clinical Pathology > Core clinical immunology > Flashcards

Core clinical immunology Flashcards

1
Q

What is allergy and hypersensitivity

A

Undesirable, damaging, discomfort-producing and sometimes fatal reactions produced by the normal immune system directed against innocuous antigens in a pre-sensitized host

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2
Q

What is the immune response to parasitic disease

A 
Increased levels of IgE
Tissue inflammation with:
-Eosinophil and mastocytosis
-Basophil infiltration
Presence of CD4+ T cells secreting:
-IL4, IL5 and IL13
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3
Q

What is the role of Th2 T cell

A

Multiple cytokine release
Innate inflammatory response
Drive for immunoglobulin production

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4
Q

What is rhinitis

A

Blocked/ runny/ itchy nose, sneezing often with eye symptoms (itching/burning/watery eyes, redness)

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5
Q

What are the two types of rhinitis and they’re causes

A

Allergic:

  • Seasonal (Pollen, moulds)
  • Perenial (House dust mite, animal dander)

Non-allergic (vasomotor, infective, structural, drugs, hormonal, polyps)

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6
Q

What is asthma

A

Disease of inflammation and hyper-reactivity of small airways
Immediate symptoms are IgE mediated
Damage to airways due to late phase response
Damaged airways are hyper reactive to non-allercic stimuli

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7
Q

What are the classifications of dermatitis

A 
Eczema
-Atopic
-Non-atopic
Contact dermatitis
-Allergic
-Non-allergic
Other types (discoid eczema, photosensitive dermatitis, seborrhoea dermatitis)
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8
Q

How are allergies diagnosed

A 
History
Specific IgE
Skin prick test (>2mm wheal)
Intra-dermal test
Graded challenge test
Basophil activation test
Component resolved diagnostic
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9
Q

What is a skin prick test

A

Prick skin and measure wheal formed

Positive if more than >2mm wheal

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10
Q

What is an intra dermal test

A

Inject into dermal layer of skin and look for increase in size of lump
Positive if increase by more the 3mm

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11
Q

What are the treatments for allergies

A 
Antihistamines
Steroids
Adrenaline
Avoidance
Immunotherapy
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12
Q

What is the mechanism of immunotherapy

A

Diverts immune response from Th2 to Th1 pathways

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13
Q

What are major food allergens

A 
Cow's milk
Egg
Legumes (peanuts, soybean, tree nuts)
Fish
Crustaceans/molluscs
Cereal grains
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14
Q

What are the clinical manifestations of adverse reactions to food

A 
Gastrointestinal:
-vomiting
-diarrhoea
-oral symptoms 
Respiratory (upper and lower)
-rhinitis
-bronchospasm
Cutaneous
-urticaria
-angioedema
-role of food in atopic dermatitis is unclear
Anaphylaxis
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15
Q

What is important in history of drug allergy

A

Indication for the drug
Detailed description of the reaction
Time between drug intake and onset of symptoms
Number of doses taken before onset
Aware of pharmacological effects and non-immunological ADR

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16
Q

What is the management of drug allergy

A

Intradermal testing
Graded challenge
Desensitization

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17
Q

What cells are involved in the innate immune system

A 
Macrophages
Dendritic cells
Mast cells
Neutrophils
Complement
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18
Q

What cells are involved in the adaptive immune system

A

T cells

B cells

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19
Q

What are the features of the innate immune system

A 
Pattern recognition against broad classes of antigen
No memory
No amplification
Little regulation
Fast response
Short duration
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20
Q

What are the features of the adaptive immune system

A 
Highly specific (T and B cell receptors)
Strong memory and amplification component
Many regulatory mechanisms
Slow response
Responses may last months- years
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21
Q

How do the immune systems interact

A
  • Innate cells directly detect and attack antigenic targets:
    • occurs at sites of infection
    • phagocytosis
  • -cytotoxicity
  • -inflammatory mediators and chemokine to attract other cells

-Dendritic cells present antigen to T cells

  • Cross talk between Dendritic cells, T cells and B cells:
    • Immune memory to determine specific learned responses
  • -Occurs in lymphoid tissues
  • Adaptive immune cells activate innate immune cells directing tissue inflammation to specific targets
    • T cell cytokines activate monocytes, macrophages
  • -B cell antibodies activate complement
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22
Q

What are the phagocytic cells of the innate immune system and what do they do

A

Neutrophils: eat and destroy pathogens
Macrophages: eat and destroy pathogens and produce chemokine to attract other immune cells
Dendritic cells: Eat and destroy pathogens and present antigen to adaptive immune system

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23
Q

What is the role of cytokines

A

Signal between different immune cells (innate to adaptive, adaptive to innate)

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24
Q

What are the roles of the complement components of the innate immune system

A

Directly attacks pathogens via alternative and lectin pathways
May be activated by adaptive immune system via antibodies

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25
Q

What are the roles of the histamine-producing cells

A 
Vasodilation 
Attract other immune cells
Defence against parasites 
Wound healing
Allergy and anaphylaxis
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26
Q

What do mast cells, basophils, eosinophils do

A

Produce histamine and other chemokine and cytokines

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27
Q

What do T cells do

A

Cause inflammation by inflammatory cytokines or by helping B cells make autoantibodies

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28
Q

What is the defining characteristic of autoimmunity

A

The adaptive immune system recognises and targets the body’s own molecules, cells and tissues

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29
Q

What are the characteristics of autoimmunity

A

T cells that recognise self antigens
B cells and plasma cells that make autoantibodies
Inflammation in target cells, tissues and organs is secondary to actions of T cells, B cells and antibodies

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30
Q

What are the characteristics of autoinflammation

A

Seemingly spontaneous attacks of systemic inflammation
No demonstrable source of infection as precipitating cause
Absence of high-titre autoantibodies and antigen specific autoreactive T cells
No evidence of auto-antigenic exposure

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31
Q

What is autoimmunity

A

Theoretical concept
Breakdown of self-tolerance
Many cells of the immune system have capacity for autoimmune functions
Overlap with normal immune functions such as anti-tumour immunity
Some people have autoantibodies without any symptoms

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32
Q

What is autoimmune disease

A

Distinct clinical entities
Environmental factors acting on favourable genetic background
Wide variety of pathogenic mechanisms between diseases
Autoimmunity leading to inflammation, organ dysfunction and damage

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33
Q

Where are T cells and B cells selected

A

T: thymus
B: bone marrow

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34
Q

What are some antigenic factors of autoimmunity

A

Infections that trigger autoimmune responses
Environmental triggers: UV light, smoking
Alterations in self-proteins that increase their immunogenicity

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35
Q

What are organ specific diseases

A

Affect a single organ
Autoimmunity restricted to autoantigens of that organ
Overlap with other organ specific diseases
Autoimmune thyroid disease is typical

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36
Q

What are systemic diseases

A

Affect several organs simultaneously
Autoimmunity associated with auto antigens found in most cells of the body
Overlap with other non-organ specific diseases
Connective tissue diseases are typical

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37
Q

What is Hashimoto’s thyroiditis

A

Destruction of thyroid by autoimmune process
Associated with autoantibodies to thyroglobulin and to thyroid peroxidase
Leads to hypothyroidism

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38
Q

What is Grave’s disease

A

Inappropriate stimulation of thyroid gland by anti-TSH-autoantibody
Leads to hyperthyroidism

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39
Q

What are some connective tissue diseases

A 
Systemic lupus erythematosus
Scleroderma
Polymyositis
Sjogrens syndrome
Ubiquitous antigens (components of cell nucleus) cause multi system inflammation
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40
Q

How is autoimmune disease spotted

A

Clinical history taken
Examination of patient
Perform blood testing

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41
Q

What is the meaning of sensitivity

A

Measure of how good the test is in identifying people with the disease

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42
Q

What is the meaning of specificity

A

Measure of how good the test is at correctly defining people without the disease

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43
Q

What are the types of diagnostic tests

A

Non specific: inflammatory markers

Disease specific: autoantibody testing, HLA typing

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44
Q

What are the non-specific markers of systemic inflammation

A 
ESR
CRP
Ferritin
Fibrinogen
Haptoglobin
Albumin
Complement
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45
Q

What are antinuclear antibodies (ANA)

A

Antibodies in the patient’s blood that bind to the cell nucleus

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46
Q

What is the function of the immune system

A

Protect the body from infection:

  • recognise pathogens
  • mount an immune response which requires cell-cell communication
  • Clear the pathogen which may require adaptive responses to changing pathogen
  • self-regulation which is important to minimise host damage
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47
Q

What is immunodeficiency

A

Clinical situations where the immune system is not effective enough to protect the body against infection

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48
Q

What is primary immunodeficiency

A

Inherent defect within the immune system - usually genetic

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49
Q

What is secondary immunodeficiency

A

Immune system affected due to external causes

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50
Q

What are secondary causes of immunodeficiency

A
  • Breakdown in physical barriers: cystic fibrosis
  • Protein loss: burns, protein loosing enteropathy, malnutrition
  • Malignancy: especially lymphoproliferative disease, myeloma
  • Drugs: Steroids, DMARDS, Rituximab, anti-convultants, myelosuppressive (chemotherapy)
  • Infection: HIV, TB
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51
Q

What are pathogen recognition receptors

A

Recognise pathogen associated molecular patterns which are unique to each pathogen
Phagocytes use PRRs to detect pathogens

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52
Q

What is an example of a pathogen associated molecular pattern

A

Lipopolysaccharide

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53
Q

What is a Toll like receptor

A

type of pathogen recognition receptor
TLR4 recognises lipopolysaccharide
TLR5 recognises flagellin

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54
Q

What is the result of lack of TLR3

A

Unable to recognise virus and can lead to recurrent HSV encephalitis

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55
Q

What is CRP

A

A marker of inflammation

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56
Q

How does IRAK4 and MyD88 deficiencies present

A

Recurrent bacterial infection especially streptococcus and staphylococcus - pneumonia, meningitis, arthritis
Poor inflammatory response
Susceptibility to infection decreases with age

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57
Q

How do you treat IRAK4 and MyD88 deficiencies

A

Prophylactic antibiotics, IV immunoglobulin if severe

58
Q

How does chronic granulomatous disease present

A

Recurrent abscesses: lung, liver, bone skin, gut
Infection by: Staphylococcus, Klebsiella, Serretia, Aspergillus, Fungi
It is X -linked so commonly presents in males

59
Q

How is chronic granulomatous disease tested

A

Function of macrophages
Rely on reduction (gain of electron)
Measure dihydrohodamine reduction using flow cytometry, on blood chart the curve should shift over time when the macrophages are working but it will stay the same if they have the disease.

Nitro blue tetrazolium dye reduction where healthy neutrophils should go purple

60
Q

What is immunomodulation

A

The act of manipulating the immune system using immunomodulatory drugs to achieve a desired immune response

61
Q

What will the therapeutic effect of immunomodulation

A

May lead to immunopotentiation, immunosuppression, or induction of immunological tolerance

62
Q

What are immunomodulators

A

Medicinal products produced using molecular biology techniques including recombinant DNA technology

63
Q

What are the classes of immunomodulators

A

Substances that are nearly identical to the body’s own key signalling proteins

Monoclonal antibodies

Fusion proteins

64
Q

What is immunopotentiation

A

Enhancement of the immune response by increasing the speed and extent of its development and by prolonging its duration

65
Q

What is passive immunisation

A

Transfer of specific, high titre antibody from donor to recipient
Provides immediate but transient protection

66
Q

What are the problems of passive immunisation

A

Risk of transmission of viruses

Serum sickness

67
Q

What are the types of passive immunisation

A 
Pooled specific human immunoglobulin
Animal sera (antitoxins and antivenins)
68
Q

What are the uses of passive immunisation

A 
Hep B prophylaxis and treatment
Botulism
VZV (pregnancy)
Diptheria
Snake bites
69
Q

What is active immunisation

A

To stimulate the development of a protective immune response and immunological memory

70
Q

What are the problems with active immunisation

A

Allergy to any vaccine component
Limited usefulness in immunocompromised
Delay in achieving protection

71
Q

What are agents of immunosuppression

A 
Corticosteroids
Cytotoxic agents
Anti-proliferative/ activation agents
DMARDs
Biological DMARDs
72
Q

What are the actions of corticosteroids

A

Decreased neutrophil margination
Reduced production of inflammatory cytokines
Inhibition phospholipase A2 (reduced arachidonic acid metabolites production)
Lymphopenia
Decreased T cells proliferation
Reduced immunoglobulins production

73
Q

What are the side effects of corticosteroids

A

Carbohydrate and lipid metabolism leading to diabetes and hyperlipidaemia
Reduced protein synthesis leading to poor wound healing
Osteoporosis
Glaucoma and cataracts
Psychiatric complications

74
Q

What are the uses of corticosteroids

A

Autoimmune diseases (CTD, vasculitis, RA)
Inflammatory diseases (Crohn’s, sarcoid, GCA/polymyalgia rheumatica)
Malignancies (lymphoma)
Allograft rejection

75
Q

What drugs target lymphocytes

A

Antimetabolites:

  • Azathioprine (AZA)
  • Mycophenolate mofetil (MMF)

Calcineurin inhibitors:

  • Ciclosporin A (CyA)
  • Tacrolimus (FK506)

M-TOR inhibitors:
- Sirolimus

IL-2 receptor mABs:

  • Basiliximab
  • Daclizumab
76
Q

What are the actions of Calcineurin inhibitors

A

CyA binds to intracellular protein cyclophilin
Tacromilus binds to intracellular protein FKBP-12

Prevents activation of NFAT
Factors which stimulate cytokines gene transcription

Reversible inhibition of T-cell activation, proliferation and clonal expansion

77
Q

What are the actions of sirolimus (rapamycin)

A

Macrolide antibiotic that binds to FKBP12 and insist mammalian target of rapamycin
Inhibits response to IL-2
Cell cycle arrests at G1-S phase

78
Q

What are the side effects of Calcineurin/ mTOR inhibitors

A 
Hypertension 
Hirsutism
Nephrotoxicity
Hepatotoxicity
Lymphomas
Opportunistic infections
Neurotoxicity
Multiple drug interactions
79
Q

What do antimetabolites do

A

Inhibit nucleotide synthesis

Azathioprine:

  • guanine anti-metabolite
  • rapidly converted into 6-mercaptopurine
Mycophenolate mofetil (MMF)
-prevents production of guanosine triphosphate

Impaired DNA production
Prevents early stages of activated T and B cells proliferation

80
Q

What are the side effects of cytotoxic drugs

A 
Bone marrow suppression 
Gastric upset
Hepatitis 
Susceptibility to infections
Cystitis
Pneumonitis
81
Q

What are the clinical uses of cytotoxic drugs

A

AZA/MMF:

  • Autoimmune diseases (SLE, vasculitis, IBD)
  • Allograft rejection

MTX:

  • RA, PSA, Polymyositis, vasculitis
  • GvHD in BMT

Cyclophosphamide:

  • Vasculitis (Wagner’s, CSS)
  • SLE
82
Q

What are examples of biologics

A 
Anti-cytokines (TNF, IL-6 and IL-1)
Anti-B cell therapies
Anti-T cell activation
Anti-adhesion molecules
Complement inhibitors
Check point inhibitors
83
Q

What are types of adoptive immunotherapy

A

Bone marrow transplant

Stem cell transplant

84
Q

What are the uses of adoptive immunotherapy

A

Immunodeficiencies
Lymphomas and leukaemia
Inherited metabolic disorders (osteoporosis)
Autoimmune diseases

85
Q

What are the immunomodulators used in allergies

A

Immune suppressants
Allergen specific immunotherapy
Anti-IgE monoclonal therapy
Anti-IL-5 monoclonal treatment

86
Q

What are the indications for allergen specific immunotherapy

A

Allergic rhinoconjunctivitis not controlled on maximum medical therapy
Anaphylaxis to insect venoms

87
Q

What are the mechanisms of allergen specific immunotherapy

A

Switching of immune response from Th2 (allergic) to Th1 (non-allergic)
Development of T regulatory cells and tolerance
Routes:
SC or sublingual for aero-allergens

88
Q

What are the side effects of allergen specific immunotherapy

A

Localised and systemic allergic reactions

89
Q

What are the innate defences

A

Skin (barrier, sebum, normal flora)
Mucous membranes (tears, urine flow, phagocytes)
Lungs (goblet cells, muco-ciliary escalator)
Interferons, complement, lysozyme, acute phase proteins
Normal commensal flora in gut

90
Q

What are qualitative and quantitative defects of neutrophils

A

Qualitative (lose ability to kill or chemotaxis)

Quantitative (less present)

91
Q

What is a neutropenic patient

A

When a patient has reduced neutrophils <0.5x10^9/L

92
Q

How are hypogammaglobulinaemias treated and what are they

A

Antibody problems

Treated using immunoglobulin

93
Q

What is the role of the spleen

A

Source of complement and antibody producing B cells, removes opsonised bacteria from blood

94
Q

How are infections investigated

A 
History and exam
Urgent diagnosis and treatment
Blood cultures
Respiratory samples
Other samples as systems suggest eg urine, serology samples - antibody/antigen
Radiology
Histopathology
95
Q

What are the general principles of prevention when managing infection in immunocompromised patients

A

Hand washing, aseptic technique, protective isolation, HEPA air filtration
Vaccines (avoid live in T cell deficient)
Prophylactic antimicrobials and passive immunoglobulin
Special diet

96
Q

What is SIRS and how will it present

A 
Systemic inflammatory response syndrome
Temp >38
Heart rate >90
Resp rate >20
WBC >12
97
Q

What is sepsis

A

SIRS and suspected focus of infection

98
Q

What is septic shock

A

Sepsis and low blood pressure (<90/60)

99
Q

What is the bufalo management

A 
Blood cultures (2 sets)
Urine output (catheterise)
Fluid (500ml IV saline/15mn)
Antibiotics 
Lactate (arterial blood gas)
Oxygen (15 l/min via reservoir face mask)
100
Q

What is cellulitis

A

Skin and soft tissue infection
Caused by gram positive cocci (staph aureus and strep pyogenes)
Treated with flucloxacillin

101
Q

What is necrotising fasciitis

A

A sever skin and soft tissue infection caused by a polymicrobial mix but usually involving streptococcus pyogenes

102
Q

How is necrotising fasciitis treated

A

Debridement
Meropenem
Clindamycin

103
Q

What is infective endocarditis

A 
Infection od heart valves
Many possible bugs
Most common:
-staph aureus
-streptococci
104
Q

How is infective endocarditis treated

A

6 weeks IV antibiotics depending on bug

105
Q

Why are people predisposed to brain abscess

A

Immunosuppression
HIV
Intravenous drug use
Endocarditis

106
Q

What is the treatment for a brain abscess

A

Drainage

ABx for 4+weeks based on bug

107
Q

What are the antibiotic rules during pregnancy

A

Beta lactams are the most well tolerated antibiotics and safe in pregnancy (penicillins, cephalosporins, meropenem)
Avoid in pregnancy:
-Quinolones (damage to cartilage)
-Trimethoprim (folic acid antagonist)
-Tetracyclins (deposits and stains bones/teeth)

108
Q

What is the difference between HLA and MHC molecules

A

HLA (human leukocyte antigens) are only found in humans whereas MHC (major histocompatibility complex) molecules are commonly found in many vertebrates

109
Q

What is HLA

A

A gene complex present in human chromosome 6 which encodes for both classes of MHC molecules

110
Q

What is the likelihood that siblings will have the same HLA molecules and why is that important

A

1 in 4 so an enormous registry is required for transplant which need an exact match (eg bone marrow)

111
Q

What are the characteristics of the two HLA classes

A

Class 1:

  • A, B, C
  • all cells except RBCs as no nucleus
  • Heavy chain and B2m

Class 2:

  • DR, DQ, DP
  • antigen presenting cells
  • heterodimer
112
Q

What are class 1 MHC molecules good at handling

A

Intracellular peptides

113
Q

What are class 2 MHC molecules good at handling

A

Foreign molecules that are endocytosed

114
Q

What is the purpose of MHC molecules

A

Part of defence against infection

115
Q

What starts the process of rejection of a transplant and what modulate the action

A

APCs of foreign cells of transplant migrate to the lymph nodes and thus start process of rejection
Complement, PRRs, innate immune cells all modulate rejection
CD4 T cells set up delayed hypersensitivity reactions

116
Q

What is an autologous cell

A

Manufactured as a single lot from the patient being treated

117
Q

What is an allogenic cell

A

Manufactured in large batches from unrelated donor tissues

118
Q

What is the purpose of HLA typing

A

A way to predict transplant rejection and minimise the chance of this occurring

119
Q

How are successful transplants achieved

A

Ensuring transplant material is as well matched as possible

T cells are suppressed using drug therapy to prevent a strong immune reaction

120
Q

What are the two types of HLA typing

A 
Serological - cell based
Molecular:
- Extraction of DNA
- Amplification 
- Detection of sequence polymorphisms (ie tissue types)
-- hybridisation to probes
-- sequencing
121
Q

What are the benefits of HLA testing

A

Less rejection episodes
Better graft survival
National kidney waiting lists so can work out the best match from register
Less sensitisation
Establish relationships (eg paternity testing)

122
Q

What happens in antibody detection

A

Screen regularly for antibodies to prevent hyper acute rejection pre- and post-transplant

123
Q

What is the complement dependent cytotoxicity test

A

CDC

Detects complement fixing IgG/ IgM HLA anf non-HLA using blood and serum

124
Q

What are the advantages of CDC

A

> 30 years experience

Inexpensive

125
Q

What are the disadvantages of CDC

A 
Limited sensitivity
Subjective
Non-complement fixing antibodies
Viable reagent supply and quality control
Non-HLA antibody interference
126
Q

What is Flow cytometry

A

Laser shines into cells

Fluorescent dyes are used and if antibodies are present then there is a shift in fluorescence

127
Q

What is lumina screening

A

Similar to flow cytometry but uses beads

Very sensitive

128
Q

What are the types of rejection

A

Acute antibody mediated rejection
Acute cellular rejection
Chronic antibody mediated rejection
Hyperacute rejection

129
Q

What is a hyper acute rejection

A

As soon as blood flows into transplanted organ, rejection process happens

130
Q

What is acute cellular rejection

A

T cell dependent
-use T cell immunosuppression
Directed against HLA molecules as the effect of HLA mismatch
Happens 7-10 days after transplant

131
Q

How are hyper acute rejection minimised

A

Blood group matched
HLA matched
Gal antibodies to lower species

132
Q

What is the function of complement

A

Should lyse foreign cells if the foreign cells are covered in antibody and will trigger the classical complement cascade

133
Q

How does complement deficiency present

A

C2, C4 deficiency:

  • SLE
  • Infections
  • Myositis

C5-C9 (which form membrane attack complex) deficiency:
-Presents with repeated episodes of bacterial meningitis (particularly Neisseria meningitis)

134
Q

What are some B cell defects

A

CVID
IgA deficiency
X linked hyper IgM syndrome
Transient hypogammaglobuliaemia of infancy
Secondary antibody deficiency due to drugs

135
Q

What are the results of B cell defects

A

Loss of antibody secretion
Usually leads to recurrent bacterial infection with pyogenic organisms
Treat with antibiotics then IV IgG for life
Most are very serious (except IgA deficiency)

136
Q

What is the treatment for antibody deficiency

A

Antibiotics

Immunoglobulin G replacement

137
Q

What are the results of T cell defects

A

More severe since B cells also need T cell help so even if there are B cells they won’t function
Symptoms are recurrent infection with opportunistic infections, bacteria, viruses, fungi (candida), protozoa (pneumocystis)

138
Q

What are some types of defects in T cells

A

SCID (severe combined immunodeficiency)

DOCK8 deficiency

139
Q

What is SCID

A 
Severe combined immunodeficiency
No T cells and suggestive history 
Paediatric emergency
Antibiotics, antivirals, antifungals
Asepsis
Haemopoietic stem cell transplant is the only cure
140
Q

What are the causes of SCID

A

Defect/ absence of critical T cell molecule (TCR, common gamma chain)
Loss of communication (MHC2 deficiency)
Metabolic (adenosine deaminase deficiency)

Y2 Clinical Pathology (11 decks)

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