IAH Flashcards

(135 cards)

1
Q

Name an autoimmune disease affecting

a) Kidneys
b) IgE on basement membrane
c) Thyroid
d) B cells
e) Salivary glands

A

a) Goodpastures syndrome
b) Bullous pemphigoid
c) Graves disease
d) SLE, MS
e) Sjogren’s

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2
Q

What type of disease is Bruton’s X-linked agammaglobulinemia?

A

Immunodeficiency

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3
Q

What causes Bruton’s?

A

Defect in B cell receptor signalling so B cell deficiency resulting in decreased Ig

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4
Q

How does Bruton’s affect Ig levels?

A

B cell deficiency so low Ig

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5
Q

Why is Bruton’s more common in boys?

A

Girls have 2 copies of the X chromosome so can be a carrier, boys only have one X chromosome from the mother so if the mother is a carrier the boy will have it

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6
Q

What surface molecule is expressed on T helper cells only?

A

CD4

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7
Q

What surface molecule is expressed on all T cells?

A

CD3

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8
Q

What microorganism causes Karposi’s sarcoma, pneumonia and B cell lymphoma?

A

Characteristic of AIDS

HIV1 (HIV2 but less severe)

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9
Q

What bacteria causes pneumonia in AIDS?

A

P. Jirovecci

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10
Q

How do commensal bacteria help prevent infections?

A

Prevent pathogen from gaining an ecological foothold

Stimulate colonic epithelial cells to from a balanced state = physiological inflammation
Compete with pathogens for nutrients, attachment sites and living space
Secrete bactericidal products e.g. FA from propionibacterium and lactic acid from lactobacilli

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11
Q

What bacteria causes infection at burns?

A

P. aeruginosa

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12
Q

What makes burns susceptible to infection?

A

Opportunistic infection
Moist surface
Vascular damage
Lots of nutrients like haem

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13
Q

Function of CD4 on actual membrane?

A

Binds antigen presented on MHC II
If activated by BCR it an activate B cell differentiation
Co-stimulatory factor - activates CD8 cells

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14
Q

Describe structure of granuloma

A

Central area of infected macrophages surrounded by outer layer of CD4 TH1 cells

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15
Q

What cytokine is secreted by lymphocytes in the granuloma, what is the effect?

A

Th1 cells secrete IL-2 to promote T cell proliferation and IFN gamma to activate macrophages

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16
Q

What causes granulomas to form?

A

Mycobacterium resisting bactericidal attempts of macrophages

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17
Q

Function of CD8 Tc cells

A

Control infection by directly killing infected cells

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18
Q

How do Tc cells cause cell death?

A

Release of cytotoxins to induce apoptosis

Interaction of FasL and Fas on target - apoptosis

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19
Q

What cells form from the myeloid and lymphoid lineage?

A

WBC
Myeloid = granulocytes (neutrophils, basophils, eosinophils, monocyte, mast cell)
Lymphoid = B cell, T cell, NK cell, ILC

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20
Q

Acute rejection

A
Type IV (T cell mediated) hypersensitivity reaction
Alloreactions in transplant rejection (recipients T cells attack the transplant alloantigen (HLA) or graft vs host disease (when T cells transplanted they react to host alloantgien (HLA))
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21
Q

Hyperacute rejection

A

Type II hypersensitivity caused by ABO or HLA mismatch

Pre-existing antibodies bind to graft = endothelial damage

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22
Q

What can increase the risk of hyper acute rejection?

A

Pre-existing anti-HLA antibodies e.g. pregnancy, multiple blood transfusion, past transplantation

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23
Q

How is hyper acute rejection circumvented?

A

Serological testing and antigen cross matching

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24
Q

Chronic rejection

A

Type III hypersensitivity reaction (immune complexes)
Donor-specific alloantibodies bind HLA not he surface on the graft, recruit inflammatory cells
Arteriosclerosis, fibrosis, hypo perfusion, loss of function

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25
Other than HIV what causes karposis Sarcoma
HHV8
26
Use of monoclonal antibodies?
Target specific antigens target cancer molecules target host immune response to boost performance identify size and location of tumour
27
Function of CD3 receptor on T cells?
Generates signal to activate signal transduction pathways once the binding has occurred
28
Function of CD28 receptor on T cells?
On surface of T cells interact with co-stimulatory molecules
29
What activates TLR4? | Where is it found?
LPS | Membrane bound
30
What activates TLR3? | Where is it found?
Ds viral RNA | Endoplasm
31
Function of a) Th1 b) Th2 c) Treg d) Th17 e) TFH
a) Activation of macrophage b) Mast cell activation c) Suppression of immune system d) Re-enforcement of inflammation e) activate B cells in lymph
32
How are CD8 cells activated?
Presentation of antigen on MHC class I molecule, CD3 then sends signal for signal transduction = release of cytotoxic release
33
What type of cell is MHC class I presented on?
Virally infected cells
34
Function of a) IL1 and TNF b) IL6 c) IL12 d) IL8 e) IL17
a) pro-inflammatory b) Lymphocyte activation and increased Ig production c) NK and T cell differentiation d) chemokine release (neutrophil migration) e) Th17 activation
35
Length of phases in HIV graph a) symptomatic phase b) non-symptomatic phase
a) 4-8 weeks (flu-like symptoms) | b) 2-12 years (reduction in CD4 equal to production of CD4 = fluctuations of virus in plasma
36
What disease results in the inability to class switch the Ig molecules, and what is the aetiology of this disease?
Common variable immune deficiency | Limited to IgA
37
What cells produce AMPs?
``` Paneth cells Neutrophils (alpha defensins) Epithelial cells (beta defensins) ```
38
How do AMPs kill pathogens?
Ampipathetic properties = insert into membrane and disrupt pore formation = lysis
39
Name a virus that lays dormant in B cells? Which disease does this cause?
Epstein-Barr virus | In immunosuppressed individuals EBV can re-activate and cause B cell lymphoma
40
How does herpes simplex evade the immune response?
``` Virally encoded Fc receptor blocks effector functions of antibodies bound to virally infected cells Virally encoded complement receptor blocks effector functions of complement Blocks MHC class I presentation = no activation of Tc cells ```
41
How does p. gingivalis and mycobacterium tuberculosis evade the immune response
P. gingivalis = releases proteases that digest antibodies | Mycobacterium = phagocytosed but highly resistant to proteolysis/lysosome fusion = no MHC II presentation
42
Cause of cell necrosis in Granuloma formation?
Centre of granuloma cut off from blood supply, cells die through anoxia and excessive macrophage lytic enzymes = necrosis
43
2 disease caused by mycobacterium?
TB and leprosy
44
What tissue does HSV first infect? Which tissue does it become latent in? Why? Treatment?
Epithelial Neurones (trigeminal ganglia) - very few MHC class I (so there isn't an immune response within- = evade immune system Aciclovir
45
Structure and function of Peyers patch?
Within the SI M cell on surface which samples antigens Antigens activate DC cells which present antigen to cells within the germinal centre of lymph nodes
46
Function of germinal centre of lymph node?
generate new cells - B and T cell activation
47
Mast cell a) function b) contents c) activation
a) degranulation releases inflammatory mediators (histamine) b) granules containing histamine c) Cross linking of IgE (by antigen binding) causes degranulation
48
Identification of monocyte? Function? % of cells made up of monocytes
Large cell, kidney bean nucleus Pre-cursor for macrophage. Circulates in the blood 2-10%
49
Candida albicans identification
Budding/hyphae form
50
Function of B cell antigen transport?
Present to T cells | Affinity mature
51
How do B cells change during life?
Somatic recombination V region recombinase Junctional diversity
52
Function of neutrophil?
Professional phagocyte Release pro-inflammatory cytokines Release AMP, ROS, NO
53
Function of MAC?
Form pits in membrane = lysis
54
Function of fibroblasts in inflammation?
Formation of scar tissue
55
Type I hypersensitivity?
Immediate | IgE mediated = Mast cells release pro-inflammatory cytokines
56
3 causes of haemolytic anaemia (type II reaction)
Penicillin hypersensitivity Autoimmune haemolytic anaemia Blood group incompatibility
57
Example of type II autoimmune reaction?
Pemphigus vulgaris | Autoimmune haemolytic anaemia
58
Example of type III autoimmune reaction?
Rheumatoid arthiritis
59
Example of type IV autoimmune reaction?
T1DM (autoantigens = beta cell antigen) | Chron's (autoantigen = antigens of microbial microbiota)
60
Atopy
Allergy with genetic predisposition (e.g. hay fever)
61
Example of type I hypersensitivity?
Anaphylactic shock Eczama Asthma
62
Type III reaction
Formation of immune complex that invade tissues and causes inflammation and destruction
63
Pus?
Dead/dying neutrophils
64
Polymorphism? | Example?
Genetic variation = different forms within the population | MHC
65
Which receptor has holotypes associated with autoimmune disease?
TCR | If they don't have central tolerance
66
Hypermutation effect
Mutations in B cells to produce Ig with higher affinty
67
SCID? | Causes?
Severe combined immunodeficiency Defects in T cell development = no T cells, antibodies, memory Caused by mutations in genes for cytokine signalling e.g. Il2 receptor
68
HHV8 | Consequence
Herpes simplex virus 8 | Highly prevalent in HIV patient = enlargement of lymph nodes
69
What Ig component recognises LPS?
Constant region (Fc)
70
What Ig component is most polymorphic?
Antigen binding site
71
What cell surface molecule recognises LPS?
TLR4
72
What is rearranged after a primary immune response?
Random recombination of gene segments to produce diversity in the antigen binding sites
73
Consequence of excessive tissue exudates
Neutrophils | Chronic inflammation and tissue destruction
74
What cells secrete performs?
NK
75
Most abundant WBC in healthy peripheral tissue?
Neutrophil
76
What WBC is low in chemotherapy patients?
Neutrophil
77
What is the consequence of S. pyogenes infection?
Strep throat = sore throat
78
What component of the immune response is mostly involved in S. pyogenes infection?
IgA
79
What is the general consequence of pyogenic bacterial?
Production of pus
80
How do streptococci evade the immune system?
Polysaccharide capsule
81
What cell surface receptor helps distinguish between active and naive T cells?
IL2 receptors
82
Cytokine associated with a) TH1 b) TFH c) Treg d) Th17
a) IFN gamma b) IL4 c) IL-10 d) IL-17
83
Example of a) type IV hypersensitivity b) type III c) type II d) type I
a) Chronic asthma b) serum sickness c) blood group incompatibility d) allergic rhinitis (hay fever)
84
Anatomical structure tonsils protect?
Larynx and back of throat
85
What cell synthesise IgA in the mouth and where are they located?
Plasma cells | Salivary glands
86
Where are the antigens that stimulate the production of IgA taken up in the body and where have they likely originated?
In the gut (M cells of peyer's patch) | Antigens probably come form mother
87
Difference between classical and alternative pathway
``` classic = C-reactive protein or antibody presentation Alternative = pathogen surface causes activation ```
88
Clinical consequence of complement deficiency?
More infections from extracellular bacteria like staphylococcus or pyogenic bacteria
89
2 cytokines that induce vascular changes associated with inflammation and their target?
IL1 and TNF | Endothelial cells of BV
90
3 social and/or demographic factors influencing the pattern of infectious disease?
``` Availability and infrastructure to healthcare Travel availability Poverty Porous borders Insolation/heirachy ```
91
Genetic basis fro antigenic shift and drift and how the outbreaks differ?
``` Drift = point mutation (gradual) = seasonal variation and limited epidemics Shift = recombination between strains = widespread infection (pandemics), jump between species = no immune response ```
92
Other than herpes simplex name another disease caused by re-actiavtion of latent herpes virus and name the virus responsible. What 2 locations of the body are the lesions commonly manifested?
Herpes Zoster = shingles | Skin of torso and head and neck
93
How does T. palladium evade antibody recognition?
Coated in fibronectin
94
Function of staphylococcal enterotoxins on T cells?
Superantigens = bind MHC and TCR independent of antigen specificity = polyclonal T cell response = excessive release of cytokines = toxic shock syndrome = apoptosis
95
Aetiology of primary immunodeficiencies>
Genetic mutation
96
Clinical consequence of B cells deficiency?
Increase infections from extracellular bacteria e.g. S/ pneumonia
97
Causes fo secondary immunodeficiency?
``` Immune senecence (age and nutrition) Trauma (burns, surgery) Drugs (immunosuppressants) Tumours (CLL) Infection (HIV) ```
98
Why is it difficult to gauge true extent of HIV infection?
Many asymptotic carriers that don't know they are HIV +
99
3 properties that compromise host immune response giants HIV?
High mutation rate, genetic variability, latency
100
Mode of anti-viral nucleoside analogues?
Interfere with viral transcription from viral RNA to viral cDNA
101
Other than nucleoside analogue, 2 other anti-HIV drugs?
Reverse transcription inhibitors and protease inhibitors
102
HAART? Advantages? Disadvantages?
highly active antiretroviral therapy Combination of anti-viral drugs = good when some viruses have resistance to some drugs Lifelong treatment (need gets rid of viral load), expensive, serious side effects
103
What elements of immune response mediate autoimmune disease?
Autoantibodies and autoimmune T cells
104
2 autoimmune disease involving CNS
MS | Myasthenia gravis
105
3 autoimmune disease of endocrine system
Graves T1DM Addisons
106
Autoimmune disease effecting exocrine gland
Sjogrens
107
3 lines of evidence that autoimmune disease have heritable element
Association with HLA genotype Run in families Different susceptibility of mice with different genetics High concordance in twin studies
108
Why are autoimmune disease often characterised by deficiency disorder to compromised function?
Often involve tissue destruction
109
3 autoimmune disease with oral manifestations?
Sjogrens, SLE, pemphigus vulgaris
110
Why are autoimmune diseases unequally distributed between sexes?
Endocrine effect | Imprinting
111
Allergen encountered through a) inhalation b) injection c) ingested d) contacted
a) pollen b) drugs c) food d) plants/synthetics
112
Immune mediators of a) Type I hypersensitivity b) Type II c) Type III d) Type IV
a) IgE b) IgG c) IgG d) T cells
113
Red patch often associated with wheal and flare?
Erythema
114
2 cells involved in type I hypersensitivity?
Mast cell | Plasma cell
115
Another name for atopic dermatitis?
Eczema
116
Management of type I hypersensitivity?
Anti-histamines Avoidance Desensitisation
117
Properties of Ig produced by memory B cells?
Class switched and high affinity to antigen
118
Properties of good vaccine preventing viruses entering cells of vaccinated individuals?
Induce neutralising antibodies
119
Properties of good vaccine helping responses against intra-cellular pathogens in vaccinated individuals?
Induce protective T cells
120
3 Practical difficulties with vaccinations by injection?
Needs a professional Expensive Equipment disposal problems
121
Reasons many populations remain unvaccinated?
Need for refrigeration | Need for skilled workers
122
3 manufacturing processes for antigen element of vaccine?
Killed Live attenuated Recombinated Purified
123
What is the challenge in developing vaccines against encapsulated bacteria?
By themselves they only provide and inadequate thymus independent immune response so a conjugated capsular vaccine is need to provide an environment for T cell differentiation
124
What 2 vaccines administered by mucosal route?
Polia and influenza
125
Why are adjuvants needed?
Purified antigens don't elicit an innate immune response, adjuvants promote a better immune response
126
Possible consequence of endocrine function of developing child of mother with Graves?
Hyperthyroidism as autoantibodies are passively transferred through placenta. Stimulate TSH receptor = more thyroid hormones release
127
Why does London have a higher incidence of certain infectious disease than other parts of the country?
Varied and dynamic population Variable disease exposure Variable immunity
128
Factors that may compromise the effectiveness of vaccination programmes?
Reduced uptake (fear, apathy) Expense Mutation of live attenuated viruses Shift in herd immunity
129
Other than organ transplantation, identify 4 further tissues commonly transplanted?
Cornea, blood, bone marrow, heart valves
130
Organ least likely to be rejected as a result of imperfect tissue matching?
Liver
131
Allotransplantation Xenotransplatation Autotransplatation
Between same species Between different species Within individual
132
Universal donor and universal recipient, why?
``` O = donor = no ABO antigens so cannot be recognised as non-self AB = no A or B antibodies so will not mount an immune response ```
133
Visible symptom of graft vs host disease?
Skin rash
134
3 features of rejected organ?
Swollen Hameorrhage Necrosis
135
Whta function of T cells do immunosuppressants target?
Cytokine secretion