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Immunology Flashcards

1
Q

Most effective public health intervention after clean drinking water

A

Vaccination

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2
Q

Impact of memory on antibody production

A

IgM is the first antibody against an infection followed by a delayed IgG response. However this leads to clinical manifestation of the disease. Memory helps in the production of IgG prior to IgM being produced with clinical features being absorbed

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3
Q

What mediates secondary antibody response

A

Long lived plasma cells residing in bone marrow that continually secrete antigen specific antibodies IgG

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4
Q

Characteristics of memory B and T cells

A

Memory cells are present in greater numbers than original lymphocyte. CD8+ T cells can kill antigen immediately upon stimulation and CD4+ can produce cytokines immediately (overall faster response). Memory cells also have enhanced properties of cell adhesion and chemotaxis

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5
Q

Vaccination vs immunisation

A

Immunisation is an individual developing immunity/memory to a disease, natural and induced.
Vaccination is deliberate administration of antigenic material to produce immunity to disease

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6
Q

Active vs passive immunity

A

Active immunity is protection produced by persons own immune system whereas passive immunity is protection transferred from another person or animal

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7
Q

What are adjuvants in immunisation

A

Adjuvants are a mixture of inflammatory substances required to stimulate an immune response to coadministered peptides, proteins or carbohydrates. Ex: Aluminium hydroxide

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8
Q

Sabin or Salk polio vaccine

A

Salk - Inactivated and safe however expensive and doesn’t provide herd immunity, injection route
Sabin - Oral, easy to administer however there is a risk of reversion to virulent form

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9
Q

Source of passive immunity

A

Naturally acquired from mother - transplacental transport of maternal IgG in third trimester. Breast milk, especially colostrum contains IgA important for colonisation of infant gut tract
Therapeutic - Pooled normal human immunisation, hyperimmune globulin

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10
Q

What are pooled normal immunoglobulins

A

Transfer of antibodies from an unrelated individual, previously used for protection against Hep A

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11
Q

What is hyperimmune globulin

A

Administered after specific exposure, antibodies from an individual known to have high anitbody level against specific pathogen. Ex: Rabies or snake venom anti-toxin

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12
Q

Are there too many vaccines to be taken?

A

Approx. 16 vaccines by the time you’re 18. Antigen burden today is less than 50 years ago (no smallpox vaccine, no whole cell pertussis vaccine)

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13
Q

Hallmarks of immune deficiency

A

SPUR -
Serious infection - Unresponsive to antibiotics (oral)
Persistent infection - Chronic infections
Unusual infection - Unusual site or organism
Recurring infection - Two major or one major one minor

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14
Q

Other features suggestive of primary immune deficiency

A

Weight loss, failure to thrive, severe skin rash (eczema), chronic diarrhoea, mouth ulceration, family history, unusual autoimmune disease

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15
Q

Types of immunodeficiency

A

Primary - Inherited

Secondary - Acquired

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16
Q

What are phagocytes

A

Neutrophils and Monocytes/Macrophage

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17
Q

Primary defect causing failure of stem cells to differentiate along myeloid lineage

A

Reticular dysgenesis - Most severe form of Severe Combined Immunodeficiency (SCID) causing lack of innate and adaptive immune system.

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18
Q

What is Kostmann’s syndrome

A

Myelopoiesis causing congenital form of neutropenia. Recurrent systemic or localised bacterial infections within 2 weeks after birth.

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19
Q

Mangement of Kostmann syndrome

A

Supportive - Prophylactic antibiotics or antifungals
Definitive - Stem cell transplantation or granulocyte colony stimulating factor (G-CSF)which assists neutrophil maturation

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20
Q

Underlying pathology of patient with recurrent infections, high neutrophil blood count with no pus formation

A

Leukocyte adhesion deficiency, failure to recognise markers expressed on endothelial cells

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21
Q

What is leukocyte adhesion deficiency

A

Genetic defect in leukocyte integrins (CD18). Results in failure of neutrophil adhesion and migration. Leads to marked leukocytosis and localized bacterial infection that are difficult to detect

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22
Q

Types of PRR

A

PRR - Pathogen Recognition Receptor

Toll like receptor, scavenger and lectin receptor

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23
Q

What are opsonins

A

Molecules that act as binding enhancers for the process of phagocytosis. Ex: Complement protein C3b, IgG and C-reactive protein (CRP)

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24
Q

Indirect recognition by phagocytes

A

Phagocytes have receptors -
Fc receptors for antibodies bound to antigen
CR-1; Complement receptor 1 that bind to complement fragments bound to antigen

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25
Q

What can be defects in phagocyte function

A

Can be a defect in opsonisation molecules or receptors expressed on phagocytes

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26
Q

Disease causing deficiency of intracellular killing mechanism of phagocytes

A

Chronic granulomatous disease, failure of phagocyte killing mechanism. They can’t form reactive oxygen compound (ROS/RNS) due to defective phagocyte NADPH oxidase used to kill certain ingested pathogens.

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27
Q

Commonest deficiency in chronic granulomatous disease

A

Deficiency of p47phox component of NADPH oxidase

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28
Q

Features of chronic granulomatous disease

A

Recurrent deep bacterial and fungal infection
Failure to thrive
Lymphadenopathy, hepatosplenomegaly
Granuloma formation

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29
Q

Lab test for chronic granulomatous disease

A

Nitroblue tetrazolium test (NBT)

Patients are fed E.coli with dye sensitive to hydrogen peroxide. If this is produced by neutrophils, it changes colour

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30
Q

Treatment of chronic granulomatous disease

A

Supportive -
Prophylactic antibiotics and antifungals
Definitive -
Stem cell transplant, gene therapy

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31
Q

Host response to infection with mycobacterium such as TB

A

These are intracellular pathogens and infect macrophages. These infected macrophage are stimulated to produce interleukin 12 (IL-12) which induces Th1 cell proliferation and secretion on INF-gamma. This feeds back onto neutrophils and macrophages to stimulate production of TNF. NADPH oxidase is stimulated to activate the oxidative pathways.

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32
Q

Decfects in the IL12 : INFgamma axis are associated with

A

Susceptibility to intracellular bacteria

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33
Q

How can oxidative function of phagocytes be assessed

A

NItroblue Tetrazolium Test (NBT)

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34
Q

NBT test in congenital neutropenia

A

Absent due to few/no neutrophils

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35
Q

Life of a T-lymphocyte

A

T-lymphocytes arise from haematopoetic stem cells in the bone marrow. They are exported as immature cells to the thymus where they mature. They proliferate and mature and reside in secondary lymphoid follicles and lymph nodes.

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36
Q

CD4+ T lymphoctyes function

A

Immunoregulatory function -
Provide co-stimulatory signals to naive B cells and activation of CD8+ T lymphocytes.
Recognise peptides on MHC Class II molecules (APC cells only)
Produce cytokines

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37
Q

Function of CD8+ T lymphocytes

A

Specialised cytotoxic cells that kill by -
Formation of pore - perforin
Triggering apoptosis
Secrete cytokines - Interferon-Gamma
Recognise peptides in association with MHC Class I

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38
Q

What cells do B cells arise from

A

Haematopoetic stem cells

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39
Q

Example of haematopoetic stem cells disease

A

Reticular dysgenesis, corrected with bone marrow transplant

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40
Q

Example of disease of lymphoid precursors

A

Severe combined immunodeficiency

Failure of production of T and B lymphocytes from lymphoid progenitor cells

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41
Q

Clinical phenotype of SCID

A

Failure to thrive, SPUR, persistent diarrhoea, unusual skin disease, family history of early infant death

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42
Q

What is hypogammaglobulinaemia

A

Reduction in all types of gamma globulins, including antibodies that help fight infection. May be congenital or due to medication

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43
Q

Most common form of severe combined immunodeficiency (SCID)

A

X-linked SCID, mutation of IL-2 receptors. Results in inability of T cell and NK cell development as well as production of immature B cells

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44
Q

What IL is important to T cell development and what can it’s deficiency cause

A

IL-2, hence IL-2 receptor deficiency such as in X linked SCID, T lymphoctye numbers are low

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45
Q

Clinical phenotype of severe combined immunodeficiency

A

Low T lymphocyte numbers
Normal or increased B cells
Poorly developed lymphoid tissue and thymus

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46
Q

Treatment of SCID

A

Prophylactic - Avoid infections, prophylactic antibiotics and antifungals. Antibody replacement with intravenous immunoglobulins
Definitive - Stem cell transplant from sibling for HLA (or) stem cell transplant

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47
Q

How are T lymphocytes formed

A

By thymopoiesis, thymocytes are haematopoietic stem cells that differentiate into mature T lymphocytes.

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48
Q

How can DiGeorge syndrome lead to immunodeficiency

A

Developmental defect of 3/4th pharyngeal pouch causing failure of thymic development. This leads to T-cell deficiency.

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49
Q

Blood count in DiGeorge syndrome

A

Absent or decreased T cells
Normal or increased B cells -
Poor antibody response to pathogens
Normal NK cells

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50
Q

Management of DiGeorge syndrome

A

Correct metabolic/cardiac abnormality
Prophylactic antibiotics
Early and aggressive treatment of infection
Immunoglobulin replacement

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51
Q

Investigating T lymphocyte deficiencies

A

First line -
White cell count and differential, serum immunoglobulins, quantification of lymphocyte sub populations
Second line -
Functional test of T cell activation and proliferation
Additional tests of lymphocyte lineage
HIV test

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52
Q

What test is essential in T lymphocyte deficiency

A

HIV test

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53
Q

What infections are less common in B cell deficiency

A

Viral infections

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54
Q

Most common primary immunodeficiency disease (PIDD)

A

People with this disorder have absent levels of blood protein called immunoglobulin A (IgA)

55
Q

What is common variable immune deficiency (CVID)

A

Immune disorder characterized by recurrent infection and low antibody levels, especially IgA, IgG and IgM

56
Q

Investigating B cell deficiencies

A 
1st line -
Total white cell count and differential 
Serum/urine immunoglobulin
2nd line - 
Quantitation of B and T lymphocytes
Specific antibody response to pathogen
57
Q

Management of B cell deficiencies

A

Aggressive treatment of infection
Immunoglobulin replacement
Stem cell transplant

58
Q

What are hypersensitivity reactions

A

Immune response that results in bystander damage to self tissues. Due to exaggerated immune mechanism

59
Q

Gel and Coomb’s classification

A

Type 1 - Immediate hypersensitivity (IgE)
Type 2 - Direct cell killing (IgG and IgM)
Type 3 - Immune complex mediated
Type 4 - Delayed type hypersensitivity (T lymphocyte)

60
Q

What is an allegy

A

IgE-mediated antibody response to to external antigen (allergen)

61
Q

Animal dander is?

A

Protein found on saliva. Animals like their hair. This hair is shed, causing an allergic response

62
Q

Why is prevalence of allergies increasing

A

Hygiene hypothesis - Improved sanitation and decreased incidence of infectious disease has resulted in a world that is too clean

63
Q

Patient prone to allergies -

Isolated environment, single child, clean environment, affluent, sterile environement

A

Due to hygiene hypothesis

64
Q

Which Th helper cells proliferation causes allergies

A

Differentiation into Th2 cells which is responsible for antibody mediated immunity instead of cell-mediated immunity

65
Q

Pathophysiology of allergic disease

A

CD4+ T cells are stimulated by allergens. This causes it to be stimulated into Th2 cytokine producing cells. These B cells produce IgE antibodies. Th2 cells also stimulate differentiation and stimulation of mast cells and eosinophils

66
Q

How do mast cells orchestrate inflammatory cascade

A

Increase blood flow, contraction of smooth muscles, increase vascular permeability, increase secretions at mucosal surface

67
Q

Mast cell in allergic reactions

A

Mast cells express Fc receptors for antibodies on their surface. On first encounter, B cells produce IgE which clear the specific antigen. Allergen is cleared and residual IgE antbodies bind to circulating mast cells via Fc receptors. Once the allergen is reencountered, the allergen binds to IgE coated mast cells. This disrupts cell membrane cause release of vasoactive mediators such as histamine and tryptase. Cytokine and leukotriene transciption is increased

68
Q

Clinical features of allergic disease

A

Urticaria, angioedema, asthma, allergic rhinitis, conjunctivitis, anaphyaxis

69
Q

What is urticaria

A

Skin rash or hives, red patches

70
Q

What is angioedema

A

Localised swelling of subcutaneous tissues or mucous membrane

71
Q

Is angioedema pitting

A

No, self limiting too and not itchy unless with urticaria

72
Q

Allergy history taking

A

What is meant exactly by allergy, allergens involved, previous investigation for allergy, history of allergic disease, elimination of trigger made difference to symptoms

73
Q

Investigations for allergies

A 
Elective investigations -
Skin prick test
Challenge test
Quantitate IgE
During acute anaphylactic episode -
Evidence of mast cell degranulation by serum mast cell tryptase level
74
Q

Management of IgE mediated allergic disorder

A

Block mast cell activation -
H1 receptor antagonist - Loratidine and cetrizine
Leukotriene receptor antagonist - Montelukast
Corticosteroids - Anti-inflammatory by blocking formation of platelet activating factor, prostaglandins and cytokines

75
Q

How can anaphylaxis be treated

A

Adrenaline syringe called Epipen -
Works on B2 adrenergic receptors to constrict arterial smooth muscle. Increase blood pressure, limiting vascular leakage. Dilated bronchial smooth muscle, decreasing airflow obsctruction

76
Q

Immunotherapy to anaphylaxis

A

Controlled exposure to increasing amounts of allergen.

77
Q

What is type 2 hypersensitivity

A

Antibody to cell surface antigen

78
Q

What is complement activation by antibody

A

20 proteins produced by liver present in circulation as inactive molecules. When triggered, they activate other proteins in a biological cascade

79
Q

Function of complement activation

A

C3 which is the eventual product helps in chemotaxis, solubilization, opsonisation, formation of membrane attack complex which directly kills encapsulated bacteria

80
Q

What are anaphylatoxins

A

Complement protein fragments such as C3a, C5a and C4a

81
Q

How do anaphylatoxins regulate immune process through negative feedback

A

Fragments of complement proteins can dissolve the immune complexes that triggered them switching off the process of complement activation

82
Q

What Ig class is involved in type 2 hypersensitivity direct cell killing

A

IgG

83
Q

Patient with high number of immature red blood cells (reticulocytes), low mature RBC. Blood test such as smear test done shows high bilirubin and low protein called heptoglobulin.

A

Autoimmune haemolytic anaemic (AIHA)

84
Q

Treatment for autoimmune haemolytic anaemia

A

Corticosteroids or splenectomy

85
Q

Type 2 hypersensitivity reaction if donor blood isn’t compatible with recipient

A

Acute haemolytic transfusion reaction (AHTR)

Recipient will have preformed antibodes that cause complement mediated lysis of transfused RBC

86
Q

A woman in her early 30s presents with acute fatigue and breathlessness. Two days earlier she was prescribed penicillin for a UTI. She has take the same antibiotic before with no problems. She was found to be pale and mildly jaundiced. Tests showed evidence of RBC destruction.

A

Penicilin-induced immune haemolytic anaemia
Tests to find RBC/Penicillin complex
Penicillin acts as a hapten here, combines with RBCs to elicit production of antibodies

87
Q

Type 2 hypersensitivity management

A

Plasmapheresis -
Removal of pathogenic antibody, patient blood is removed via cell separator
Immunosuppression -
Rebound antibody production limits efficacy to plasmapheresis. Given potent immunosuppressive agent to switch off B cell production of antubody

88
Q

What is type 3 hypersensitivity reaction

A

Antibody to soluble antigen

89
Q

Pathophysiology of type 3 hypersensitivity

A

In excess antigen, antibody binds together forming small immune complexes. These are trapped in small blood vessels, joints and glomeruli

90
Q

Pathophysiology of farmers lungs

A

Antigens such as mouldy hay deposit in lungs. These stimulate antibody formation. The antibody form immune complexes with antigen. This activates complement and attracts inflammatory cells such as neutrophils. These degranulate causing endothelial cell basement membrane damage.

91
Q

What is acute hypersensitivity pneumonitis

A

Immune complexes are deposited in the walls of the alveoli and bronchioles causing inflammation

92
Q

Acute vs chronic hypersensitivity pneumonitis

A

Acute hypersensitivity pneumonitis is mediated by type 3 where chronic is not

93
Q

Explain clinical feature of acute hypersensitivity pneumonitis - pyrexia

A

Antibody complex travels to the hypothalamus, affecting the thermoregulatory center. Hence, we get pyrexia

94
Q

Management of type 3 hyersensitivity reactions

A

Avoid triggers
Corticosteroids - Decrease inflammation
Immunosuppression - Decrease antibody production

95
Q

What are corticosteroids

A

Synthetic glucocorticoids

96
Q

What is type 4 hypersensitivity mediated by

A

T cell

97
Q

Pathophysiology of type 4 hypersensitivity

A

Generation of primed effect Th1 cells and memory T cells upon initial sensitisation to antigen
Subsequent exposure leads to activation of previously primed T cells, recruitment of macrophage/lymphocytes/neutrophils and release of proteolytic enzymes causing persistent inflammation.

98
Q

Main cells of type 4 hypersensitivity

A

Th1 cells

99
Q

What mediates sarcoidosis

A

Type 4 hypersensitivity reaction. Presence of granulomas due to an allergic response to an unknown antigen

100
Q

What is autoimmunity

A

Presence of immune response against self tissue/cells

101
Q

What is IPEX syndrome

A

Immune dysregulation polyendocrinopathy enteropathy and x-linked inheritance syndrome -
The rare genetic disorder causing immune dysregulation. There is overwhelming systemic autoimmunity

102
Q

Symptoms of IPEX

A

Severe infections, intractable disease, eczema, early onset diabetes mellitus, autoimmune manifestations

103
Q

Treatment of IPEX

A

Hematopoietic stem cell transplantation (HSCT)
Immunosuppresive drugs
Parenteral nutrition

104
Q

Pathogenesis of IPEX

A

Mutation in FOXP3 gene which is essential for the development of T cells. Condition is x-linked

105
Q

A young male infant with intractable diarrhoea, gut villous atrophy and failure to thrive

A

Consider genetic checkup for FOXP3 gene causing IPEX syndrome.

106
Q

The function of regulatory T cells

A

Suppress hyper-reactive T cells by secreting TGF-beta and IL-10

107
Q

What does mutation in FOXP3 gene cause

A

Loss of function in regulatory T cells, losing inhibition of T cell activation - IPEX syndrome

108
Q

Types of tolerance mechanisms in the body

A

Central tolerance -
Deletion of self-reactive lymphocytes in primary lymphoid tissue
Peripheral tolerance -
Inactivation of self-reactive lymphocytes in peripheral tissues that escape central tolerance by Tteg cells

109
Q

Human leukocyte antigen classes

A

All nucleated cells express Class 1 on the cell surface

Specialized antigen-presenting cells express additional Class 2 molecules

110
Q

What is molecular mimicry

A

T cells with cross-reactive TCRs are activated by peptides donated by pathogens that resemble or are identical to endogenous peptides. This leads to aberrant immune activation against self antigen triggered by presence of foreign antigen that shares molecular or antigenic properties with self P

111
Q

Pathogenesis of rheumatic fever after streptococcal infection

A

Streptococcal cell wall stimulates antibody response against M protein. Some antibodies cross-react with heart tissue, which has structurally similar proteins, causing rheumatic fever

112
Q

Mechanisms of autoimmunity

A

Molecular mimicry
Antigen sequestration -
A sequestered antigen is released from the lens/sperm/etc that are not ordinarily available for recognition by the immune system. This release might occur due to trauma or infection
Toxic shock syndrome -
Production of superantigens during an invasive streptococcus infection or a localized staphylococcus infection

113
Q

Leading cause of hyperthyroidism

A

Grave’s disease, auto-antibodies are generated that bind to thyroid stimulating hormone (TSH) receptor. Type 2 hypersensitivity autoimmune disease

114
Q

Autoimmune disease affecting the lungs and kidney

A

Auto-antibodies attack the basement membrane in lungs and kidneys. This leads to glomerulonephritis and pulmonary haemorrhage.

115
Q

Type 3 hypersensitivity autoimmune disease

A

Systemic lupus erythematosus (SLE) -

Preformed immunocomplexes deposit in various vascular beds and cause injury at these sites.

116
Q

Prevalence of SLE

A

Higher in females (90%), peak onset of 20-30 years and strong genetic desposition

117
Q

Common symptoms of SLE

A

Photo-sensitivity, butterfly rash, arthritis, poor circulation in fingers and toes

118
Q

Pathogenesis in SLE

A

Infection or UV radiation leads to increase ROS production. Mutations in Mac-1 integrin decreases phagocytosis which alters clearance in SLE. These apoptotic bodies degenerate, potentially releasing auto-antigens. This leads to immune complex formation which may deposit in small vessels

119
Q

Example of Type 4 autoimmune conditions

A

Insulin-dependant diabetes mellitus
Rheumatoid arthritis
Multiple sclerosis
Coeliac disease

120
Q

Natural antibiotics produced by epithelial cells

A

Defensins and cathelicidins

121
Q

Why does white cell count rise in bacterial infection

A

Cytokines released cause an increase in maturation and release of neutrophils from bone marrow

122
Q

What is an abscess

A

Localized collection of pus

123
Q

What causes swelling during an inflammation

A

Leaking of plasma and cells into tissue space

124
Q

Interactions within lymph nodes

A

Dendritic cells with T cells
T cells with B cells
B cells with macrophages
Plasma cells

125
Q

When do local lymph nodes start to enlarge

A

3-4 days after initial injury

126
Q

What is septic shock

A

Failure of normal inhibitory mechanisms to control inflammatory response -
Excessive production of proinflammatory cytokines by macrophages - hypotension/hypovolaemia/tissue oedema
Uncontrolled neutrophil activation -
Release of proteases and ROS damages endothelial cells causing vascular injury and increase capillary permeability
Direct activation of coagulation pathway -
Combines with endothelial cell disruption to form clots with damaged vessels

127
Q

Treatment of lymphangitis

A

Empirical antibiotics such as Amoxicillin

Rehydration and close monitoring

128
Q

What type of hypersensitivity is anaphylaxis

A

Type 1 - IgE mediated

129
Q

Common clinical manifestations of anaphylaxis

A

Urticaria, angioedema, stridor due to laryngeal obstruction, dyspnoea

130
Q

Treatment of anaphylaxis

A

Oxygen by mask
Adrenaline to act on B2 receptors -
Vasoconstriction to increase blood pressure/decrease leaking and bronchodilation
IV anti-histamine (Piriton)
Oppose mast cell released histamine
Nebulised bronchodilators - Improve O2 delivery
IV corticosteroids - Systemic anti-inflammatory
Takes 30 mins to peak, important in preventing rebound
IV fluids - Increase circulating blood volume and hence blood pressure

131
Q

Type 1 hypersensitivity and food allergies

A

Type 1 hypersensitivity to latex can cross-react with latex containing foods

132
Q

Chronic granulomatous disease test

A

Nitro-blue test; When there is an NADPH oxidase defect, the phagocyte is unable to make reactive oxygen species or radicals required for bacterial killing. As a result, bacteria may thrive within the phagocyte. The higher the blue score, the better the cell is at producing reactive oxygen species.

133
Q

Feature of CVID

A

Reduced CD27 memory B cell numbers

Respiratory (26 decks)

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