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AC1 > Immunology > Flashcards

Immunology Flashcards

1
Q

What factors make up the adaptive immune system?

A

B lymphocytes

T lymphocytes

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2
Q

What are categories of primary immunodeficiency?

A 
Phagocyte deficiencies (innate cell-mediated immunity)
Complement deficiencies (innate humoral immunity)
Severe combined immuno-deficiencies (adaptive cell-mediated 
immunity)
Predominantly antibody deficiencies (adaptive humoral immunity)
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3
Q

What are categories of secondary immunodeficiency?

A

Hyposplenism / Asplenism
Haematological malignancies
HIV / AIDS

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4
Q

What can cause Immunosuppression?

A 
Steroids & other immunosuppressive drugs
Cytotoxic chemotherapy (for malignancies)
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5
Q

What factors make up the innate immune system?

A 
Epithelial barriers
Phagocytes
Dendritic cells
Complement 
Acute phase proteins
NK cells
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6
Q

What is Chronic Granulomatous Disease (CGD)?

A

Multiple possible defects (most frequently X-linked)
Phagocytes unable to destroy ingested microbes due to a lack of oxidative burst to produce free radicals
Excessive granuloma formation occurs instead

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7
Q

What are clinical features of chronic granulomatous disease?

A

Eecurrent & persistent infections: pneumonia, skin infections, abscesses (skin & internal), septic arthritis and osteomyelitis

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8
Q

What investigations can be used to diagnose chronic granulomatous disease?

A

Nitroblue-tetrazolium (NBT) test: microscopy (normal phagocytes reduce NBT to a dark pigment)
Dihydrorhodamine (DHR) test: flow cytometry (normal phagocytes reduce DHR to a fluorescent pigment)
Genetic analysis to identify exact genetic defect

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9
Q

What are treatment options for chronic granulomatous disease?

A

Early diagnosis and treatment of any infections
Prophylactic antibiotics (co-trimoxazole and imidazoles)
Recombinant IFN-gamma (70% less infections)
Bone marrow / stem cell transplantation (curative)

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10
Q

Describe the process of phagocytosis

A

Chemotaxis and adherence of microbe to phagocyte
Ingestion
Formation of a phagosome
Fusion of phagosome with a lysosome to form phagolysosome
Digestion of ingested microbe by enzymes
Formation of residual body containing indigestible material
Discharge of waste materials

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11
Q

What is Common Variable Immunodeficiency (CVID)?

A

Multiple possible defects (not X-linked)
Hypogammaglobulinaemia (IgG, usually IgA, possibly IgM)
Lack of antibodies to neutralise & opsonise pathogens
Severe, persistent, unusual and recurrent infections, autoimmune, malignant, enteric and lymphoid disorders

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12
Q

What are clinical features of common variable immunodeficiency?

A

Streptococcus pneumoniae (LRTIs and sepsis)
Haemophilus influenzae (URTI/LRTIs and meningitis)
Neisseria meningitidis (meningitis)
Otitis media (Pseudomonas)
Bronchiectasis
Sever, persistent, unusual or recurrent infections

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13
Q

What investigations can be done to diagnose common variable immunodeficiency?

A

Reduced immunoglobulins on simple blood test
Decreased IgG always, deceased IgA usually, decreased IgM in ~50%
Normal B lymphocyte count, but immature types

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14
Q

What are treatment options for common variable immunodeficiency?

A

Early diagnosis and treatment of any infections
Prophylactic immunoglobulin transfusions (IV every 3-4 weeks or SC every week) immunoglobulin reactions can occur (serum sickness)

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15
Q

What is serum sickness?

A

Flu-like symptoms (but no respiratory component)
Possible thrombotic events or anaphylaxis
Reaction to immunoglobulin treatment

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16
Q

What can be causes of Hyposplenism or asplensim?

A

Congenital
Post-surgical (after trauma)
Atrophy (after infarcts from thrombosis or sickle cell disease)
Functional (malignancy, coeliac disease or IBD)

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17
Q

What is the risk with hypo/asplensim? Which groups of people are at particular risk?

A

Increased risk of severe infection with encapsulated bacteria Strep. pneumoniae, H. influenza, N. meningitides)
Higher risk of malaria and babesiosis
Age 50, poor response to vaccination, previous invasive pneumococcal infection, haematological malignancy, other immunosuppression

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18
Q

What are clinical features of Hyposplenism?

A

Respiratory tract infection possibly with sepsis

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19
Q

What investigations can be done to diagnose Hyposplenism?

A

Spleen function assessed by imaging (USS)

Blood films show Howell-Jolly bodies in erythrocytes (Nuclear DNA Remnants)

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20
Q

What are treatment options for Hyposplenism?

A

Prevention with vaccination & antibiotics
UK Green Book (Immunisation against Infectious disease)
Pneumococcal, Hib, meningococcal and flu vaccines (with measurement of serological response)
Phenoxymethlypenicillin (oral) if high-risk
Strict malaria prophylaxis and bite avoidance measures
Patient education on early treatment of infections

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21
Q

What is HIV?

A

Aquired through sex, blood transfusions, iatrogenic
Infects Th lymphocytes (CD4 cells)
CD4

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22
Q

What are clinical features of HIV/AIDS?

A 
Non-specific seroconversion illness after 2-4 weeks
Latency for ~10 years before AIDS develops
Cerebral toxoplasmosis
PML (progressive multi focal leukoencephalopathy) due to JC virus
HSV ulcers (chronic)
Pneumocystis pneumonia (recurrent)
Tuberculosis
Intestinal cryptosporidiosis
Cryptococcal meningitis
CMV retinitis
Oesophageal candidiasis
Pneumococcal pneumonia 
Atypical mycobacterial infection
Intestinal isosporiasis
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23
Q

What investigations can be done to diagnose HIV?

A

Low lymphocytes / high immunoglobulins
HIV tests (serology & antigen-detection)
CD4 count / HIV viral load

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24
Q

What are treatment options for HIV?

A

Initially targeted at opportunistic infections
Prophylaxis against infections where possible (eg. toxoplasmosis, cryptococcosis, pneumocystis pneumonia, mycobacterium avium complex)
Anti-retroviral combination drugs, typically 3-4 given for life

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25
Q

What is the prognosis of HIV and AIDS?

A

AIDS without treatment: death in 1-3 years

HIV with treatment: almost normal life expectancy

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26
Q

What are clinical features of Immunosuppression caused by steroids and other drugs?

A

All cause risk of new infections
Steroids: risk of CMV reactivation
Methotrexate, azathioprine, cyclosporine: increase risk of lymphoma
Anti-TNF drugs: re-activation of TB

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27
Q

What is neutropenic sepsis?

A

Development of fever, often with other signs of infection in a patient with an abnormally low neutrophil count
Absolute neutrophil count

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28
Q

What molecules are involved in neutrophil recruitment to a site of injury?

A

Selectins on neutrophils and endothelium allow rolling

At sites of injury, integrins are expressed and cause adhesion of the neutrophils

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29
Q

What organisms can cause neutropenic sepsis?

A

Bacteria: Staph aureus, E. Coli, Pseudomonas aeruginosa
Fungi: after prolonged neutropenia, Difficult to diagnose, Antifungals added if fever does not respond to antibiotics

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30
Q

What is the empirical treatment for neutropenic sepsis?

A

Tazobactam-piperacillin (Tazocin)
Vancomycin (If no response at 48 hours and lines in)
Antifungal: Voriconazole/Amphotericin B (If no response at 72 hours)

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31
Q

20 year old, lots of chest infections as a child, was tested for cystic fibrosis – neg, Bad acne as a teenager, Recurrent skin abscess. Chronic cough, Persistent lymphadenitis. Burkholderia cepacia infection isolated. DHR not oxidised by neutrophils, so no shift in DHR fluorescence. What is the likely diagnosis?

A

Chronic granulomatous disease

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32
Q

What can be common causative organisms and clinical manifestations in chronic granulomatous disease?

A

Recurrent bacterial infections: Pneumonia, Abscesses, Lymphadentiis, Osteomyelitis, Bacteraemia
Predominant organisms: Staphylococcus aureus, Burkholdia (Pseudomonas) cepacia, Serratia marcescens

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33
Q

23 yr old woman has everal episodes of pneumococcal pneumonia and sinusitis. She has seronegative polyarthritis, chronic intermittent diarrhoea but colonoscopy normal. Low levels of IgG and IgA, what is the likely diagnosis?

A

Common variable immunodeficiency

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34
Q

What are clinical manifestations of common variable immunodeficiency?

A 
Infections 
Hematologic or organ-specific autoimmunity
Chronic lung disease 
Bronchiectasis 
Gastrointestinal inflammatory disease 
Malabsorption 
Granulomatous disease 
Liver disease/hepatitis
Non Hodskins Lymphoma
Other cancers
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35
Q

What infections may be common in someone with common variable immunodeficiency?

A

Sino-pulmonary: Bacterial (pneumococcal, haemophilus)
Chronic giardia
Infective complications of chronic lung diseases: Bronchiectasis, obstructive airways disease

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36
Q

35 year old woman, Cough and shortness of breath, No response to course of amoxicillin, seen by dermatology for dermatitis, Referred to haem because of persistent lymph nodes
O2 sats – 94% fall to 82% on climbing stairs, WCC normal, CRP 65, CD4 count 12, Sputum – Pneumocystis jirovecii PCR pos. What is the diagnosis?

A

HIV

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37
Q

What investigations should be used to identify common immunodeficiencies?

A

Full blood count
Immunoglobulins
Serum complement
HIV testing

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38
Q

What phases do T cells go through from being immature to maintenance?

A

Initiation: APC presents antigen to T cell
Clonal expansion
Contraction
Maintenance

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39
Q

By what mechanism do B cells adapt to recognise new antigens?

A

Somatic hypermutation
Programmed process of mutation affecting variable regions of immunoglobulin genes but only affects individual immune cells

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40
Q

What are immature B cells called?

A

Centroblasts
Which become centrocytes
Which become plasma cells or memory B cells

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41
Q

Where are the antigens which b and T cells target?

A

B cells: extracellular

T cells: intracellular

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42
Q

What types of immunosuppressive drugs are there?

A

Corticosteroids
Cytotoxic drugs
T cell suppressant
Antibody/biologics

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43
Q

What is membranous glomerulonephritis?

A

Commonest in adult
Autoantibodies against the phospholipase A2 receptor 1 in the basement membrane
Immune complex formation in the glomerulus
Triggers membrane attack complex on glomerular epithelium causing it to become leaky

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44
Q

What is minimal change disease?

A 
Commonest in children
T / B cell dysfunction
Glomerular permeability factor
Proteinuria and oedema 
Lacks evidence of pathology on light microscopy
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45
Q

What is the first line treatment for minimal change disease? And how does it work?

A

Prednisolone: inhibitors transcription factors so reduced cytokine production, therefore reduced clonal expansion of t helper cells
Ubiquitous expression of corticosteroid receptor
Interrupts multiple steps in immune activation
Inhibit antigen presentation (Innate)
Inhibit cytokine production and proliferation of lymphocytes (Adaptive)

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46
Q

What are some autoimmune indications for plasma exchange?

A

Severe vasculitis
Good pasture’s disease: antibodies attack basement membrane in lungs and kidneys
Gillian Barre syndrome: antibodies against myelin/nerve axons in PNS
Myasthenia gravis: antibodies against ACh receptor
Antibody mediated transplant rejection

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47
Q

What are Sirolimus and Everolimus? And what is their mechanism of action?

A

mTOR inhibitors
Block cell cycle progression in G1
Blocks IL2 mediated activation of T & B cells
Reduced clonal proliferation of T cells

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48
Q

What are side effects of mTOR inhibitors?

A

Hypertriglyceridaemia
Hypercholesterolaemia
Pneumonitis
Oral ulcers

49
Q

What are advantages of mTOR inhibitors?

A

Reduce cancer risk

Not nephrotoxic

50
Q

What is Rituximab and what is its mechanism of action?

A

Monoclonal antibody against surface determinant on B-cells (CD20)
B cell depletion

51
Q

What are side effects of Rituximab?

A

Neutropenia
Hypogammaglobulinemia
Reactivation of latent infections

52
Q

What is alemtuzumab?

A

Monoclonal antibody to cell determinant CD52

T cell depletion

53
Q

What are side effects of alemtuzumab?

A

Leukopenia

Infection

54
Q

What is infliximab? What is its mechanism of action?

A

Antibody against TNF-alpha
Reduction of pro-inflammatory cytokines, leukocyte migration and activation
Subsidence of inflammation

55
Q

What are side effects of infliximab?

A 
Infusion reactions
Neutropenia
Infections (TB)
Demyelinating disease
Heart failure
Cutaneous reactions
Malignancy
Induction of autoimmunity
56
Q

In what conditions might you use infliximab as treatment?

A

RA, IBD, Psoriasis and Ankylosing spondylitis

57
Q

What is Behçet’s disease?

A

Immune mediated small vessel systemic vasculitis
Mucous membrane ulceration and ocular problems
Recurrent oral aphthous ulcers, genital ulcers, uveitis

58
Q

What is an antigen?

A

Substance capable of generating an immune response

59
Q

What is immunological tolerance?

A

Unresponsiveness of immune system to an antigen, induced by previous exposure to that antigen

60
Q

What is autoimmunity?

A

Immune response to self-antigens due to a failure of immunological tolerance

61
Q

When specific lymphocytes encounter antigen for the first time they may be…?

A

Activated leading to an immune response

Inactivated or destroyed leading to tolerance

62
Q

What is a tolerogen?

A

Antigen which induces tolerance

63
Q

What is an immunogen?

A

Antigen which induces an immune response

64
Q

What role does infection play in loss of immune tolerance?

A

Allows bystander activation of auto-reactive cells

Molecular mimicry

65
Q

What fates do lymphocytes have which would react to self antigens in a healthy person?

A

Deleted
Inactivated
Undergo a change in their specificity

66
Q

Where can self tolerance be induced?

A

Central: B cells in bone marrow, T cells in thymus

Peripheral

67
Q

Describe central immunological tolerance to self antigens

A

Induced in immature lymphocytes in generative lymphoid organs. B cells in bone marrow, T cells in Thymus
If cells react to self antigens: Apoptosis: Cell deletion
Change in receptor until no longer self reactive (B Cells)
Develop into regulatory T cells (CD4+ Cells), Mature and enter peripheral circulation, where peripheral tolerance will cause cell to undergo: anergy, deletion or suppression

68
Q

Antigens that lymphocytes encounter in generative organs are…?

A

Self antigens

External antigens are not usually found in generative lymphoid organs but remain in peripheral lymphoid tissue

69
Q

Describe peripheral immunological tolerance to self antigens

A

Mature lymphocytes
Deletion: Induction of apoptosis in self-reactive lymphocytes
Anergy: Render self-reactive lymphocytes incapable of reacting antigen upon re-exposure
Suppression: T Regulatory Cells suppress self-antigen specific lymphocytes

70
Q

Describe clonal deletion

A

CD4+ T cells which show high avidity self-reactivity are

negatively selected in the thymus

71
Q

What are the determinants of negative selection in clonal deletion?

A

Presence or absence of self-antigen in thymus, determined by autoimmune regulator (AIRE) protein (transcription factor) whichcontrols expression of thymic epithelial cells which express tissue restricted antigens (major proteins from elsewhere in body)
Affinity of T-Cell Receptor (TCR) for antigen. High affinity = increased chance deletion

72
Q

What is anergy as a mechanism of peripheral tolerance?

A

Exposure of CD4+ T cells to antigen in absence of co- stimulation or innate immunity leads to CD4+ T cells becoming incapable of reacting to that antigen

73
Q

What 2 signals are required for T cell activation? What happens if these are not present?

A

T cell receptor binding Ag presented on MHC
Recognition of co-stimulators by CD28
If this is absent, prolonged stimulation by antigen will lead to anergy
Co-stimulators are only expressed on antigen presenting cells when then are activated e.g. by innate immunity or inflammation

74
Q

What are the 2 main inhibiting receptors which regulate T cell responses?

A

CTLA-4: Member of CD28 family, expression up-regulated in T cells exposed to antigen and terminates continued activation of these cells. Expressed on regulatory cells and mediates suppressive function. Acts to block T cell receptor signalling and reduce availability of co-stimulatory molecules on APC
PD-1: Binds to ligand on APC and inactivates the T Cells

75
Q

Where is CTLA 4 important in inhibiting T cells?

A

Centrally

76
Q

Where is PD-1 important in inhibiting T cells?

A

Peripherally

77
Q

What does suppression by regulatory T cells lead to inhibition of?

A

Effector T Cell production
B Cell production
NK Cell production

78
Q

What does generation of regulatory T cells require?

A

Cytokines, especially Il-2 (promotes differentiation into T-regs)

79
Q

What do regulatory T cells do?

A

Produce immunosuppressive cytokines
Reduce ability of APCs to stimulate T Cells
Consumption of Il-2 (necessary growth factor for other cell populations)

80
Q

What are important factors in CD8+ T cell tolerance?

A

Co-stimulation presence or absence
Inhibitory receptors: PD-1
T-Reg cells can control activation

81
Q

By what processes does central B cell tolerance occur?

A

Deletion
Receptor editing: non-self antigen specificity is reached
Anergy: Occurs if cells recognise self-antigen weakly

82
Q

By what processes does peripheral B cell tolerance occur?

A

In the absence of T Helper Cells
Apoptosis
Anergy (via engagement of inhibitory receptors)

83
Q

What type of course do autoimmune diseases often follow?

A

Chronic, progressive, relapsing and remitting

84
Q

What immune abnormalities can lead to autoimmunity?

A

Defective tolerance or regulation
Abnormal display of self antigens
Inflammation or an initial immune response

85
Q

What abnormalities can occur, leading to defective tolerance or regulation?

A 
Imbalance between lymphocyte activation and control due to:
Defects in negative selection
Defects in reg T cells
Defects in apoptosis
Inadequate function of inhibitory cells
86
Q

What abnormalities might occur which result in an abnormal display of self antigens?

A

Increased expression
Structural changes
Exposure of hidden antigens

87
Q

How can inflammation lead to autoimmunity?

A

Activate APC, therefore enabling co-stimulation and activation not anergy of self recognising lymphocytes

88
Q

Describe autoimmunity as a polygenic multifactorial disease

A

Inheritance of multiple genetic polymorphisms contributing to susceptibility: Some disease specific, Some generic for autoimmune disease
Contribution of variable environmental factors

89
Q

Which autoimmune conditions are associated with HLA-B27?

A

Ankylosing spondylitis, reactive arthritis

90
Q

Which autoimmune condition is associated with HLA-DR2?

A

Systemic lupus erythematosus (SLE)

91
Q

Which autoimmune conditions are associated with HLA-DR3?

A

Atoimmune hepatitis, Sjögren’s syndrome, T1DM, SLE

92
Q

Which autoimmune conditions are associated with HLA-DR4?

A

Rheumatoid arthritis, T1DM

93
Q

What infections can trigger autoimmune conditions?

A

Streptococcal infection → rheumatic fever
urethritis or gastroenteritis → reactive arthritis
Campylobacter gastroenteritis → Guillain–Barré syndrome

94
Q

How can infection lead to autoimmune conditions?

A

Molecular mimicry

95
Q

What chemicals can lead to autoimmune disorders?

A

Anti-convulsants or antibiotics →drug-induced lupus

Halothane (general anaesthetic) →liver necrosis

96
Q

What autoimmune condition can result from a teratoma?

A

Autoimmune encephalitis

97
Q

Exposure of self antigens in which protected sites could lead to autoimmune destruction?

A

Eye

Testes

98
Q

What is the significance of autoimmune conditions being mainly B cell mediated?

A

Easier to diagnose (eg. antibody detection tests)

Can occur in utero (eg. neonatal thyrotoxicosis, neonatal lupus)

99
Q

What types of hypersensitivity reactions can cause autoimmune conditions?

A

Type 2: Antibody mediated e.g. Graves
Type 3: Immune-complex mediated e.g. SLE
Type 4: T-cell mediated

100
Q

How can antibodies lead to autoimmune conditions?

A

Antibodies bind to antigens on cells: cause recruitment of inflammatory cells and tissue injury
Can cause abnormal cellular function e.g. Graves’
Antigen-antibody complexes forming in circulation: induce vascular inflammation with ischaemia to associated tissue

101
Q

How can immune complexes lead to autoimmune conditions?

A

Ag (self or foreign) and Ab complex deposit in tissues and induces inflammation
Amount of complex deposited in a tissue is determined by nature of the complex and characteristic of the blood vessels

102
Q

How can T cell mediated autoimmunity lead to disease?

A

Trigger inflammation leading to tissue injury

103
Q

How can cytokines lead to autoimmune disease?

A

Immune-mediated inflammation (TH 1 and 17) via secretion of cytokines that recruit and activate leukocytes
Delayed hypersensitivity: Activation of CD4+ T cells with inflammation 24-48 hrs after challenge

104
Q

What would you measure levels of to confirm Graves’ disease?

A

TSH receptor

105
Q

What would you measure levels of to confirm Hashimoto’s thyroiditis?

A

Thyroid peroxidase

106
Q

What would you measure levels of to confirm Rheumatoid arthritis?

A

Rheumatoid factor

107
Q

What would you measure levels of to confirm SLE?

A

ANA and dsDNA

108
Q

What would you measure levels of to confirm Sjögren’s syndrome?

A

ANA

109
Q

What would you measure levels of to confirm Coeliac disease?

A

Anti-gliadin and anti-endomysial

110
Q

What would you measure levels of to confirm Primary biliary cirrhosis?

A

ANA and AMA (anti mitochondrial antibodies)

111
Q

What would you measure levels of to confirm chronic autoimmune hepatitis?

A

SMA (smooth muscle antibodies) and LKM-1 (liver kidney microsomal type 1)

112
Q

What would you measure levels of to confirm Wegeners granulomatosis?

A

c-ANCA (anti neutrophil cytoplasmic antibody)

113
Q

What is Wegeners granulomatosis?

A

Form of vasculitis that affects small vessels in organs

Lung and kidney damage

114
Q

What are the most prevalent autoimmune conditions?

A

Graves’ disease

Rheumatoid arthritis

115
Q

What may be clinical features of anti phospholipid syndrome?

A

thrombophilia

recurrent miscarriages

116
Q

List some symptoms of systemic lupus erythematosus

A

Systemic : malaise, fever, weight loss
Skin : rash, photosensitivity, vasculitis, hair loss
CNS : cerebral lupus, transverse myelitis
Heart : pericarditis, Libman-Sacks endocarditis
Lungs : pleural effusions, pulmonary fibrosis
Kidneys : glomerulonephritis
Blood : anaemia, leukopenia, thrombocytopenia, 2° anti phospholipid syndrome
Other : 2° Sjögren’s syndrome, arthralgia, non-deforming arthritis

117
Q

Describe the pathogenesis of SLE

A

Susceptibility genes: b and T cells specific to self nuclear antigens
External triggers: defective clearance of apoptotic bodies so increased burden of nuclear antigens
Anti nuclear antibodies: form complexes which are endocytosed and stimulate B cells, resulting in high levels of anti nuclear IgG production

118
Q

What investigations results would you expect in SLE?

A

FBC =↓Hb (chronic/haemolytic),↓WCC,↓Plts
ESR : raised
CRP : moderately raised
ANA : 95% sensitivity
dsDNA : 50% sensitivity & 99% specificity
anti-cardiolipin (phospholipid) antibodies

119
Q

What treatment is given for SLE?

A

Sun-avoidance / sun screens
Steroids : as for other autoimmune rheumatological disorders
NSAIDs : as for other autoimmune rheumatological disorders
DMDs : hydroxychloroquine, azathioprine (anti-proliferative), cyclophosphamide (anti-proliferative)
mAbs : rituximab (anti-CD20 on B lymphocytes)

AC1 (18 decks)

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