Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology > Immunology > Flashcards

Immunology Flashcards

1
Q

Primary immune deficiency

A

inherited cause of immune compramise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Secondary immune deficiency

A

due to any other cause e.g. infection (HIV), malignancy, mmalnutrition, drugs (steroids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Physiological immune deficiency

A
  • neonates
  • pregnancy
  • old age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Constitutive physical barriers of the immune system (3)

A
  1. commensal bacteria
  2. mucous surfaces
  3. epithelial barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Deficiency of epithelial barrier?

A

Burns - high risk of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Deficiency of mucosal barriers?

  • organs affected (2)
  • genetic risk factor
A

IgA deficiency

  • lungs, GI tracts - recurrent infections
  • caucasian population
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Deficiency of commensal bacteria?

  • when
  • common infections (2)
A
  • after broad spectrum Abx
    1) candida albicans
    2) C.diff
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cells of innate immune system (7)

A
  1. Macrophages
  2. neutrophils
  3. eosinophils
  4. monocytes
  5. basophils
  6. NK cells
  7. dendritic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How the innate immune system works (7)

A
  1. Innate immune cells are produced in bone marrow, and circulate in blood to be able to migrate to tissues
  2. cytokines and chemokines detect site of infection and activate endothelium
  3. Toll-like and Mannose recpetors detect pathogen at infection site
  4. PAMPs recognise pathogen by responding to proteins on their bacterial sugars
  5. Fc receptors recognise immune complexes
  6. inflammatory chemokines and cytokines recruit phagocyte by
    a) increasing vascular permeability
    b) attracting phagocytes
  7. Oxidative and Non-oxidative killing of pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Oxidative Killing

A

mediated by reactive oxygen species (superoxides and hydrogen peroxide) generated by action of the NADPH oxidase complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Non-oxidative killing

A

mediated by bacteriocidal enzymes such as lysozyme

the lysosome and phagocyte come together to form a phagolysosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Opsonisation

  • what
  • mediators
A

“making the pathogen tasty”
binding of pathogen and phagocyte in order to kill pathogen
facilitated by opsonin
mediated by antibodies, Fc receptors and acute phase proteins e.g. CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Common bacterial pathogens in recurrent infections? (2)

A
  1. staph aureus

2. mycobacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Common fungal pathogens in recurrent infections? (2)

A
  1. C.albicans

2. Aspergillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Types of phagocyte deficiency (3)

A
  1. recruitment of phagocytes
  2. find & catch organism
  3. kill organism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Reticular Dysgenesis

  • what
  • inheritance pattern
  • enzyme mutation
  • lab findings
  • outcome
A
  • Severe form of Severe Combined Immunodeficiency (SCID)
  • failure of stem cells to differentiate down myeloid/lymphoid lineage leading to a complete absence of granulocytes
  • autosomal recessive
  • adenylate kinase 2 (AK2)
  • absolute deficiency in neutrophils, leukocytes, monocytes, platelets
  • fatal without BMT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Kostmann Syndrome

  • what
  • inheritance pattern
  • mutation
  • Nitroblue test of oxidative killing (NBT)
  • neutrophil count
  • leukocyte adhesion markers
A
  • severe congenital neutropenia
  • autosomal recessive
  • HAX1 protein
  • NBT neg
  • absent neutrophil count
  • leukocyte adhesion markers NORM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cyclic Neutropenia

  • what
  • inheritance pattern
  • mutation
A
  • cyclic neutropenia every 4-6weeks
  • autosomal dominant
  • neutrophil elastase ELA-2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Leukocyte Adhesion Deficiency LAD1

  • what
  • mutation
  • presentation
  • lab findings
  • treatment
A
  • failure to express leukocyte adhesion markers therefore neutrophils are unable to get to site of infection
  • B-2 integrin subunit of CD18 in LAD1
  • Neonatal bacterial infection
  • HIGH neutrophil count
  • bone marrow transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

LAD2

A
  • rare
  • associated with
    a) growth restriction
    b) mental retardation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chronic Granulomatous Disease

  • pathophysiology (5)
  • investigation
  • inheritance pattern
A
  1. deficiency in NADPH oxidase
  2. inability to generate oxygen free radical s
  3. excessive inflammation due to high neutrophil/macrophage recruitment
  4. granuloma formation
  5. lymphadenopathy + hepatosplenomegaly
  • Nitroblue test of oxidative killing (NBT) - abnormal
    Dihydrorhodamine test - abnormal
  • x-linked
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

IFN gamma receptor deficiency

  • what
  • cytokines involved
  • outcome
A
  • defect of interaction between macrophages and other cells (T cells)
  • IL12 & IFNgamma
  • susceptibility to mycobacterial infections, salmonella, TB and GBS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Common infections associated with chronic Granulomatous Disease (7)

A 
PLACESS
Pseudomonas
Listeria
Asperigillus
Candida
E coli
Staph aureus
Serratia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Inflammatory cytokines (4)

A

IL-1
IL-12
TNF
IL-6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Non-inflammatory cytokines (2)
IL-10 | TGF-beta
26
Neutrophil
Polymorphonuclear cells capable of phagocytosing pathogens and killing by oxidative and non-oxidative mechanisms
27
NKC
Lymphocytes that express inhibitory receptors capable of recognising HLA class I molecules and have cytotoxic capacity
28
Dendritic Cell
Immature cells are adapted for pathogen recognition and uptake whilst mature cells are adapted for antigen presentation to prime T cells
29
Macrophage
Derived from monocytes and resident in peripheral tissues
30
Complement Classical Pathway - which proteins? - main protein and function - dependant on? - causes
- C1, C2, C4 - C1 provides binding site on Ab - immune response - formation of immune complexes Ab/antigen
31
MBL Pathway - which proteins - protein function - causes
- MBL - MBL direct binding to microbial carbohydrates - links in classical pathway via C2, C4
32
Complement Alternative Pathway - which proteins? - protein function - factors involved
- C3 - C3 directly binds to bacterial cell wall - B, I , P
33
C3
Cleavage of this protein may be triggered via the classical, MBL or alternative pathways
34
C1
Binding of immune complexes to this protein triggers the classical pathway of complement activation
35
C9
Part of the final common pathway resulting in the generation of the membrane attack complex
36
MBL
Binds to microbial surface carbohydrates to activate the complement cascade in an immune complex independent manner
37
Classical pathway deficiency - common protein affected - association - why - test
- C2 - SLE - Classical pathway is repsonsible fro removing immune complexes, these build up in SLE in skin, joints, kidneys - CH50
38
MBL deficiency - common or rare? - significant when?
- very common (30%) | - significant is another immune impairment present e.g. chemo/HIV
39
Alternative pathway deficiency - common factor involved - susceptible to infections caused by which microbes? (4) - test
- Factor B - ENCAPSULATED bacteria 1. N menigitides 2. Strep pneumoniae 3. H influenzae 4. GBS - AP50
40
Terminal Pathway Deficiency - what - why - associations (2) - susceptible to infections? (4) - tests
- lack of C3, 5, 6, 7, 8, 9 so severe susceptibility to bacterial infections - cannot form MAC to kill bacteria - 1. glomerulonephritis 2. connective tissue disease - ENCAPSULATED bacteria 1. N menigitides 2. Strep pneumoniae 3. H influenzae 4. GBS - CH50 & AP50
41
Membranoproliferative nephritis and bacterial infections
C3 deficiency with presence of nephritic factor
42
Meningococcus meningitis with family history of sibling dying of same condition aged 6
C9 deficiency
43
Severe childhood onset SLE with normal levels of C3 and C4
C1q deficiency
44
Recurrent infections when receiving chemotherapy but previously well
MBL deficiency
45
Characteristics of the adaptive immune system (4)
1. wide repertoire of antigen receptors 2. specificity 3. clonal expansion 4. immunological memory
46
Primary lymphoid tissues (2)
1. Bone marrow | 2. Thymus
47
Secondary lymphoid tissue (3)
1, Lymph nodes 2. MALT 3. Spleen
48
Where does B cell maturation occur?
Bone marrow
49
Where does T cell maturation occur?
Thymus
50
T Cell Maturation (5)
1. arise from haemopoetic stem cells 2. exported as immature cells to the THYMUS 3. Mature T lymphocytes leave thymus and enter circulation 4. Reside in secondary lymphoid tissue 5. T cell receptor interacts with HLA molecule on APC
51
Which HLA Class do CD4+ T cells interact with?
Class II
52
Which HLA Class so CD8+ T cells interact with?
Class I
53
Three types of T Cell tolerance ?
1. Low affinity for HLA - to avoid inadequate reactivity 2. Intermediate affinity for HLA - positive selection for 10% cells 3. High affinity for HLA - to avoid autoreactivity
54
CD4+ T Cell subsets (5)
1. Th1 2. Th17 3. Treg 4. TFh 4. Th2
55
Th1 (2)
1. Help CD8 T cells and macrophages | 2. Subset of cells that express CD4 and secrete IFN gamma and IL-2
56
Th17
Help neutrophil recruitment | Enhance generation autoantibodies
57
Treg (2)
1. Regulate IL-10/TGF beta expressing | 2. Subset of lymphocytes that express Foxp3 and CD25
58
TFh (2)
1. Support the germinal centre on the lymph node 2. Play an important role in promoting germinal centre reactions and differentiation of B cells into IgG and IgA secreting plasma cells
59
Th2
T helper cells
60
CD8+ T cells (5)
1. cytotoxic T cells 2. recognise HLA Class I peptides 3. kill cells directly 4. produce cytokines INFgamma and TNFalpha 5. important defence against viral infections & tumours
61
CD8+ T Cells
Express receptors that recognise peptides usually derived from intracellular proteins and expressed on HLA class I molecules
62
Antigen encounter in germinal centre of LN (4)
1. CD4+ T cell is primed by dendritic cell 2. CD4+ T cell helps IgM B cell differentiation 3. B cell proliferation 4. Isotype switching to IgG, IgE, IgA
63
What area of the immunoglobulin recognises the antigen?
Fab antigen binding region on both the heavy and light chain
64
What is the effector area of the immunoglobulin?
Fc region of the heavy chain
65
Antibody function (3)
1. identification of toxins and pathogens - Fab 2. Interaction with other immune cells to remove pathogens - Fc 3. Defence against bacteria
66
B Cell Memory (4)
1. reduced time between antigen exposure and antibody production 2. increased titre of antibody produced 3. IgG antibodies dominate 4. can be independant of CD4+ T cells
67
Pre B Cells
Exist within the bone marrow and develop from haematopoietic stem cells
68
IgA
Divalent antibody present within mucous which helps provide a constitutive barrier to infection
69
IgG secreting plasma cells
Cell dependent on the presence of CD4 T cell help for generation
70
IgM secreting plasma cells
Are generated rapidly following antigen recognition and are not dependent on CD4 T cell help
71
Common infections in Lymphocyte deficiencies - bacterial (2) - fungal (2) - viral - malignancy
``` Bacterial 1) mycoplasma 2) salmonella Fungal 1) Pneumocystis 2) Crytosporidium Viral - CMV Early malignancy ```
72
Age of presentation of SCID and WHY?
>3/12 | Prior to this protected by maternal IgG that CAN cross placenta
73
Most common form of SCID? Mutation? Pathogenesis (4)
X-linked IL-2 receptor 1. IL-2 receptor shared by numerous interleukins 2. Inability to respond to cytokines 3. T Cell and NK cell development is arrested 4. Formation of immature B cells
74
Di George syndrome - what - symptoms - chromosomal abnormality - laboratory findings
``` - developmental defect of pharyngeal pouch C- cardiac abnormalities A- abnormal facies T - thymic aplasia C- cleft palate H - hypocalcemia 22 - 22q11.2 deletion - reduced numbers of T cells due to thymic immaturity ```
75
Most common type of Bare Lymphocyte Syndrome?
Type II
76
Regulatory proteins involved in BLS? (2)
1. Regulatory Factor X | 2. Class II transactivator
77
BLS Type I
defect in expression of MHC Class I therefore profound deficiency in CD8+ T Cells
78
BLS Type II
defect in expression of MHC Class II therefore profound deficiency in CD4+ T Cells
79
Association with BLS?
Sclerosing cholangitis
80
Severe recurrent infections from 3 months,CD4 and CD8 T cells absent, B cell present, IgM present, IgA and IgG absent
X-linked SCID
81
Young adult with chronic infection with Mycobacterium marinum
IFN gamma receptor deficiency
82
Recurrent infections in childhood, abnormal facial features, congenital heart disease, normal B cells, low T cells, low IgA and IgG
Di George syndrome
83
6 month baby with two recent serious bacterial infections. T cells present – but only CD8+ population. B cells present. IgM present but IgG absent
Bare Lymphocyte Syndrome Type II
84
Bruton's hypogammaglobulinaemia - inheritance pattern - defect - lab finding
X-linked B cell tyrosine kinase Lack of mature B cells
85
Selective IgA Deficiency - who - what infections? (2) - 70%?
- caucasian - resp and GI - asymptomatic
86
Hyper-IgM Syndrome - what (2) - mutations (4) - lab findings - who - common infection
- disruption in T/B Cell communication - failure of antibody class swtichinh 1. CD40 Ligand 2. CD40 3. AICDA 4. CD154 - HIGH IgM, abesent IgG/IgE/IgA - boys - pneumocystis carinii
87
Common variable immune deficiency - what - presentation (3) - lab findings
- defect in B cell differentiation of unknown cause 1. failure to thrive 2. recurrent infections 3. autoimmune & granulomatous diseasae - LOW IgG/IgE/IgA
88
Adult with bronchiectasis, recurrent sinusitis and development of atypical SLE
Common variable immune deficiency
89
Recurrent bacterial infections in a child, episode of pneumocystis pneumonia, high IgM, absent IgA and IgG
X-linked hyper-IgM syndrome due to CD40 ligand mutation
90
1 year old boy. Recurrent bacterial infections. CD4 and CD8 T cells present. B cells absent, IgG, IgA, IgM absent
Bruton's hypergammaglobulinaemia
91
Recurrent respiratory tract infections, absent IgA, normal IgM and IgG
IgA deficiency
92
Type I hypersensitivity reaction - immunoglobulin - process (6) - how long? - symptoms (7)
- IgE 1. crosslinking of IgE on mast cells 2. degranulation of mast cells 3. release of histamine 4. recruitment of neutrophils 5. increased blood vessel permeability 6. inflammation - within minutes, up to 2 hours 1. angioedema 2. urticaria 3. rhinoconjunctivits 4. wheeze 5. diarrhoea 6. vomiting 7. anaphylaxis
93
Anaphylaxis
a severe, systemic allergic reaction
94
Types of anaphylaxis
1. IgE mediated e.g. peanut, penicillin, bites 2. Non-IgE mediated e.g. NSAIDs, IV contrast - both result in mast cell degranulation
95
Management of Anaphylaxis (8)
``` ABCDE 100% O2 elevate legs IM Adrenaline 500mcg Inhaled bronchodilators IC Hydrocortisone 100mg IV Chlorphenamine 10mg IV Fluids ```
96
Type I Hypersensitivity Reactions (5)
1. Atopic dermatitis 2. Food allergy 3. Oral allergy syndrome 4. Allergic rhinitis 5. Acute urticaria
97
Type IV Hypersensitivity - onset - mediated
Delayed hypersensitivity - 24-48 hours - T Cell mediated
98
Examples of Type IV Hypersensitivity (4)
1. T1DM 2. Multiple sclerosis 3. RA 4. Crohn's disease
99
Type II Hypersensitivity - mediated by - results in
- IgM IgG | - IgG/IgM reacts with self antigen and results in tissue damage, receptor blockade/activation
100
Type III Hypersensitivity - mediated by - pathphysiology - association - examples (4)
- IgG/IgM - immune complex mediated damage - underlying Hep C 1. SLE 2. Mixed essential cryoglobinaemia 3. Serum sickness 4. Polyarteritis Nodosa
101
Serum Sickness - what - pathophysiology (4) - type of hypersensitivity reaction - Abx - Symptoms (7) - Onset
- reaction to proteins in antiserum 1. formation of immune complexes 2. that activate complement and 3. infiltrate vessels causing inflammation 4. small vessel vasculitis - Type III Sx rashes urticaria arthralgia lymphadenopathy fever malaise confusion - 7-12 days
102
Sjogren's Syndrome - what - who (2) - symptoms (3) - test
- chronic autoimmune disease against exocrine glands - M>F >40years 1. dry eyes- xerostomia 2. keratoconjunctivitis sicca 3. parotid or salivary gland enlargement - Schirmer test
103
IPEX Syndrome - what - who (2) - symptoms 4)
``` I - immmune dysregulation P - polyendocrinopathy E - enteropathy X - X-linked - male children ```
104
Human immunoglobulin therapy - use - where from? - which diseases? (4)
- post exposure prophylaxis - screened human donors 1. Tetanus 2. Rabies 3. Varicella zoster 4. Primary antibody deficiencies
105
Anti T Cell monoclonal antibodies - use (3) - examples (3)
1. during active transplant rejection 2. prevention of rejection 3. RA if anti-TNF have failed 1. Muromonab-CD3 2. Basiliximab 3. Abatacept
106
Use of recombinant cytokines (2) | - examples (3)
1. boost immune response to cancer 2. boost immune response to specific pathogens IFN alpha IFN beta IFN gamma
107
Uses of IFNalpha (3)
1. Hep C 2. Karposi's sarcoma 3. CML
108
Uses of IFNbeta
relapsing MS
109
Uses of IFNgamma
chronic granulomatous disease
110
Ipilimubab - what - mechanism - example of use
- immune booster - blocks CTLA4 to allow T cell activation - melanoma
111
Pembrolizumab - what - mechanism - example of use
- immune booster - blocks PD-1 to allow T cell activation - melanoma
112
uses of corticosteroids (5)
1. auto-immune 2. allergic disorders 3. auto-inflammatory disorders 4. transplantation 5. malignant disease
113
Mechanism of corticosteroids (4)
1. inhibits phospholipase A2 2. Reduces prostaglandin synthesis 3. Inhibits phagocyte migration and function 4. Inhibits lymphocyte function and promotes apoptosis
114
Side effects of corticosteroids (10)
``` C - cataracts U - ulcers S - skin; bruising, thinning, striae H - hypertension, hirsuitism, hyperglycemia I - infection N - necrosis of femoral head G - glaucoma O - obesity, osteoporosis I - immunosuppression D - diabetes ```
115
Anti-proliferative agents - target - cells affected - examples (3) - side effects (4)
- inhibit DNA synthesis - rapid turnover 1. Cyclophosphamide 2. Mycophenolate mofetil 3. Azathioprine 1. Bone marrow suppression 2. infection 3. malignancy 4. teratogenicity
116
Cyclophosphamide - mechanism of action - uses (2)
- alkylates guanine base of DNA 1. multi-system connective tissue disease 2. vasculitis with end-organ damage
117
Azathioprine - mechanism of action - uses (3) - side effect
- blocks de novo purine synthesis 1. auto-immune disease 2. auto-inflammatory disease 3. transplantation - hepatotoxicity
118
Myclophenolate mofetil - mechanism of action - uses (3) - side effects (2)
- blocks de novo nucleotide synthesis 1. Autoimmune disease 2. vasculitis 3. transplantation 1. bone marrow suppression 2. herpes
119
Plasmapharesis - what - uses (3)
- removal of pathogenic antibody by treating patients own plasma and then reinfusing - type II antibody mediated hypersensitivity reactions 1. Goodpasture's 2. Myasthenia Gravis
120
Inhibitors of Cell signalling - mechanism (2) - examples (3)
- inhibits calcineurin - therefore downregulates IL-2 expression 1. Tacrolimus 2. Ciclosporin 3. Sirolimus
121
Side effects of Ciclosporin (6)
1. gingical hypertrophy 2. DM 3. nephrotoxicity 4. neurotoxicity 5. hypertension 6. dysmorphism
122
Rituximab - mechanism of action - result - use
Anti-CD20 Decreases B cells Lymphoma
123
Methotrexate - mechanism of action - result - uses (3) - side effects (2)
- inhibitis dihydrofolate reductase DHFR - decreases DNA synthesis 1. RA 2. psoriasis 3. Crohn's 1. teratotoxicity 2. hepatotoxicity
124
Basiliximab - mechanism of action - result - use
Anti-CD25 Inhibits T cell proliferation Prophylaxis for allograft rejection
125
Abatacept - mechanism of action - result - use
CTLA4-Ig fusion protein Reduces T cell activation RA
126
Natalizumab - mechanism of action - result - use (2)
Antibody to alpha4 subunit Inhibits T cell migration 1. relapsing-remitting MS 2. Crohn's
127
Efalizumab - mechanism of action - result - use
Antibody to CD11a Inhibits T cell migration Psoriasis
128
Tocilizumab - mechanism of action - result - use
Antibody to IL-6 Reduces macrophage, T cell and B cell activation RA
129
Alemtuzumab - mechanism of action - result - use
Antibody to CD52 Lymphocyte depletion CLL
130
Anti-cytokines - what - examples (5) - uses (4)
TNF-alpha 1. Infliximab 2. Adalimumab 3. Certolizumab 4. Golimumab 5. Etanercept Uses 1. RA 2. AS 3. Psoriasis 4. IBD
131
Denosumab - mechanism of action - result - use
RANK ligand inhibitor inhibits RANK mediated osteoclast differentiation OA
132
Three stages of Transplant rejection
1. Recognition 2. Activation 3. Effector function
133
Most relevant proteins in transplant recognition
1. ABO blood antigens | 2. HLA coded by chromosome 6 on MHC
134
Where are ABO antigens expressed?
1. RBCs | 2. endothelial lining of blood vessels in transplanted organ
135
Where is HLA Class I expressed?
A, B, C | ALL cells
136
Where is HLA Class II expressed?
DR, DQ, DP | expressed by APCs and cells under stress
137
What's special about HLA?
Highly polymorphic as there are hundreds of alleles for each locus so any two people are unlikely to have the same two alleles
138
Where is most of the variability in HLA?
peptide groove
139
Maximum number of HLA mismatches allowed in transplantation?
6
140
Direct recognition?
Donor APC presents antigen and/or MHC to recipient T cells | Acute rejection
141
Indirect recognition?
Recipient APC presents donor antigen to recipient T cells | Chronic rejection
142
Phases of transplant rejection (3)
Phase 1 - recognition of foreign antigens Phase 2 - T cell activation Phase 3 - effector phase
143
Effector phase of rejection (5)
1. T cells proliferate 2. T cells produce cytokines 3. Activate CD8+ cells 4. Provide help for antibody production 5. Recruit phagocytic cells
144
What type of hypersensitivity reaction is rejection?
Type IV
145
Symptoms of rejection 1. general 2. kidney 3. liver 4. lung
1. fever, tenderness 2. rise in creatinine, fluid rentention, HTN 3. deranged LFTs, coagulopathy 4. breathlessness, pulmonary infiltrate
146
How to investigate transplant rejection?
Biopsy - check for acute cellular reaction - infiltration of cells - tubular function
147
Time scale of acute rejection? | - pathology
weeks - months | cellular infiltrate
148
Time scale of chronic rejection? | - pathology
months - years | fibrosis & vasculopathy
149
Prevention of rejection (3)
1. AB/HLA matching 2. Screening for anti-HLA antibodies 3. Immunosuppression
150
screening for HLA antibodies? (3)
1. cytotoxicity assays 2. flow cytometry 3. solid phase assays
151
HLA matching is very important in...? (2)
1. Kidney | 2. BMT
152
Graft versus host disease? - onset - symptoms
donor cells attacks hosts days-weeks rash, D&V, bloody stool, jaundice
153
Treatment of antibody-mediate damage? (2)
1. Plasma exchange | 2. IVIg
154
Common opportunistic infections post-transplant? (3)
1. CMV 2. BK virus 3. pneumocystis carini
155
Post-transplantation's malignancies? (2)
1. Karposi's sarcoma | 2. EBV
156
What kind of virus is HIV?
RNA retrovirus
157
HIV Lifecycle (7)
1. Targets CD4+ T helper cells 2. Reverse transcription & DNA synthesis 3. Integration (viral DNA + host DNA) 4. viral transcription 5. viral protein synthesis 6. assembly of virus & release of virus 7. maturation
158
HIV-1 co-receptors used to enter target cells? (2)
CCR5 | CXCR4
159
Transmission of HIV (3)
1. Sexual - mucosal surfaces contain dendritic cells 2. Vertical - mother to child through birth or via breast milk 3. Blood - transfusion, sharing needles
160
Where does HIV bind to?
gp120- intial binding | gp41 - conformational change
161
Immune response to HIV-1 (3)
1. Innate 2. Adaptive 3. Aquired
162
Innate response to HIV (4)
1. Non-specific activation of macrophages, NK cells, complement 2. stimulation of dendritic cells by TLR 3. release of chemokines & cytokines 4. inflammation
163
Adaptive response to HIV - neutralising antibodies (2) - non-neutralising antibodies (1)
neutralising 1. anti-gp120 2. anti-gp41 | non-neutralising 1. anti-p24 gag IgG
164
Acquired response to HIV - which cells? - chemokines (3) - how?
CD8+ Tcells MIP-1a, MIP-1b, RANTES prevent HIV entry into CD4+ T cells
165
How does HIV-1 damage the immune response? (5)
1. Infected CD4+ T cells are killed by CD8+ T cells 2. Infected CD4+ T cells are anergised 3. CD4+ T cells are unable to prime CD8+ T cells so T cell cell memory is lost 4. Infected monocytes or dendritic cells are killed by the virus 5. quasispecies are produced as reverse transcriptase is error-prone
166
Development from HIV-1 to AIDS?
8-10 years
167
Prediction of disease progression?
viral load
168
Rapid progressors - development from HIV-1 to AIDS
2-3 years
169
Long-term non-progressors?
stable CD4+ counts and no symptoms after 10 years
170
AIDS CD4+ T cell count?
171
Screening test fro HIV?
anti-HIV antibody detected by ELISA
172
Confirmation test by HIV?
Anti-HIV antibody detected by Western Blot
173
How long is the incubation period to seroconvert?
10 weeks
174
HIV treatment?
HAART - highly active anti-retroviral therapy | = 2 non-nucelotide reverse transcriptase inhibitors + protease inhibitor
175
Limitations of HAART? (5)
1. doesn't eradicate latent HIV-1 2. fails to restore T cell responses 3. high pill burden 4. toxicities 5. adherence
176
HAART during pregnancy?
Zidovudine - reduces transmission to newborn from 26% to 8%
177
8 week vaccinations (7)
1. Diphtheria 2. Tetanus 3. Whooping cough 4. Polio 5. H.influenzae B 6. Pneumococcal 7. Rotavirus
178
1 year vaccinations (4)
1. H.influenzae B 2. Men C 3. Pneumococcal 4. MMR
179
best vaccine?
activate both B and T cell memory
180
Antigen presenting cells (4)
1. Macrophages 2. B lymphocyte 3. Langerhans cells 4. Dendritic cell
181
Cell mediated response - t cell - cytokines involved (3)
Th1 Cell | IL-2, IFN-gamma, TNF
182
Humoral response - t cell - cytokines involved (3)
Th2 cell | IL-4, IL-5, IL-6
183
T Memory cells a) central memory cells - where - express - produce b) effector memory cells - where - express - produce
a) central memory cells - LNs and tonsils - CCR7+ CD62L- - IL-2 b) effector memory cells - liver, lungs, gut - CCR7- CD62 low - IFN-gamma, perforin
184
Live vaccine - advantages (2) - disadvantages (2) - examples (3)
``` Ads 1) lifelong immunity 2) cross-reaction against different strains Disads 1) reversion to virulence 2) careful in ID patients Examples - polio, MMR, BCG ```
185
Inactivated vaccine - advantages (4) - disadvantages (2) - examples (3)
``` Ads -1) easy storgae 2) cheaper 3) safe in ID patients 4) no reversion to virulence Disadvs 1) repeated boosters required 2) shorter immunity ``` Examples - Diphtheria, tetanus, Hep B
186
Adjuvants used in vaccines? - why - example
acts as a depot to increase immune response by slow release of the antigen without altering its specificity - ALUM, CpG

Pathology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions