Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Meded Path Lectures > Immuno 1 > Flashcards

Immuno 1 Flashcards

1
Q

Cells of the innate immune system

A

Polymorphic - Neutrophils, eosinophils, basophils
Monocytes/Macrophages
Natural Killer Cells
Dendritic Cells

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

Soluble components of the innate immune system

A

Complement
Acute phase proteins
Cytokines/Chemokines

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

Fc Receptors

A

Polymorphic cells of innate system use Fc receptors to recognise pathogenic antigens

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

Dendritic Cells

A

Present antigens to lymph nodes

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

NK Cells

A

Destroy cells not expressing HLA 1

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

Oxidative Killing

A

NADPH catalyses formation of reactive oxygen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Non-Oxidative Killing

A

Lysosome action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Macrophage action

A

Phagocytose pathogens and present processed antigens to T cells to activate adaptive response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Complement - Classical pathway

A

Activated by Ag-Ab Complexes

C1,2,3 activates C3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complement - Mannose Binding Lectin

A

Recognises microbial cell surface carbohydrates (mannose)
C4,C2
Activates C3

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

Complement - Alternative Pathway

A

Recognises bacterial cell wall

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

Complement - Common Pathway

A

C3 activates C5-C9 which form the Membrane Attack Complex

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

Components of the adaptive immune response

A

B Cells - humoral
T Cells - Cellular
Cytokines
Chemokines

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

T cell classification

A

All have CD3
CD4 - Helper T Cells
CD8 - Cytotoxic T Cells

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

Primary Lymphoid Organs

A

Bone Marrow

Thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Secondary Lymphoid Organs

A

Spleen
Lymph Nodes
Mucosal Associated Lymphoid Tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T Cell Selection

A

Positive Selection -> Intermediate affinity for HLA, no affinity/too high affinity are destroyed

Negative Selection -> Cells with affinity for tissue self antigens are destroyed

Affinity for HLA I -> CD8+
Affinity for HLA II -> CD4+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

B Cell selection

A

No recognition of self in bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

B Cell proliferation

A

T Cell-Independent = B Cells secrete IgM

Germinal Centre Reaction = Dendritic Cells prime CD4+ T cells which present antigens to B cell, leading to proliferation, somatic hypermutation and isotype switching to IgG, A, E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Types of primary immunodeficiencies

A

Innate
Adaptive
Complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Deficiencies in neutrophil production

A

Kostmann Syndrome
Cyclic Neutropenia
Treatment = G-CSF (Granulocyte colony stimulating factor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Kostmann’s Syndrome

A

Autosomal Recessive
HAX 1 Protein
G-CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cyclic Neutropenia

A

Autosomal Dominant
Episodic Neutropenia every 4-6 Weeks
Mutation in ELA 2
G-CSF

24
Q

Deficiencies in Leukocyte migration

A

Leukocyte Adhesion Deficiency

25
Leukocyte Adhesion Deficiency
CD11a/18 is usually expressed on neutrophils, but is deficient here. usually binds ICAM-1 on endothelial cells Neutrophils cannot exit bloodstream, hence high neutrophil count, no pus formation Delayed Umbilical Cord Sloughing
26
Leukocyte Adhesion Deficiency Treatment
Haematopoietic Stem Cell transplant
27
Deficiencies in Oxidative Killing
Chronic Granulomatous Disease
28
Chronic Granulomatous Disease
NAPDH Oxidase deficiency leads to failure to produce reactive oxygen species = impaired killing Granuloma Formation Lymphadenopathy Hepatosplenomegaly Lots of Pus Susceptible to catalase positive organisms
29
Chronic Granulomatous Disease treatment
IFN-y
30
Chronic Granulomatous Disease infections
Catalase positive organisms (since these are killed by oxidative killing) ``` Pseudomonas Listeria Aspergillus Candida E Coli Staph A Serratia ```
31
Test for chronic granulomatous disease
Nitroblue Tetrazolium Hydrogen Peroxide = yellow to blue = normal Dihydrhodamine Flow Cytometry test DHR to Fluorescent rhodamine in presence of hydrogen peroxide. Fluorescent = normal
32
Cytokine Deficiency
IL12, IL12R, IFNy, IFNyR deficiency Usually needed for macrophage-T cell communication Infection with intracellular organisms such as mycobacteria and salmonella
33
T Cell - Macrophage Communication
Macrophages produce IL-12, which stimulate T Cells to produce IFN-y, which induce TNF activation and formation of free radicals
34
Classical Pathway Deficiencies
C1q/r/s, C2, C4 deficiency C2 = common = SLE Severe skin disease Lots of infections
35
MBL pathway deficiencies
30% heterozygous 6-10% no MBL Increased risk of infection if other immune impairment, ie. prematurity, chemo, HIV, Ab deficiency
36
Common Pathway Deficiency
``` C3, C5-9 Risk of N. meningitidis * S. pneumoniae H. influenzae ``` Low CH50 and low AP50
37
Why does SLE cause complement deficiency?
Lupus causes production of Ab-Ag immune complexes | These consume C3/C4 = low complement, despite there not being a primary complement deficiency
38
Why do nephritic factors cause complement deficiency?
Auto-Abs against complement associated with glomerulonephritis and partial lipodystrophy
39
Complement deficiency investigations
C3 levels C4 levels CH50 (classical) levels AP50 (alternative) levels
40
Management of Complement Deficiency
Screening family members Prophylactic Abx Vaccination against encapsulated bacteria Aggressive treatment of active infections
41
Alternative Pathway Deficiencies
Factors B, I, P | Infections with encapsulated bacteria
42
Active vs Severe SLE complement levels
``` Active = Low C4, Normal C3 Severe = Low C3, Low C4 ```
43
Lymphoid pregenitors deficiency
Severe Combined Immunodeficiency Reticular Dysgenesis X Linked SCID ADA Deficiency
44
Reticular Dysgenesis
Autosomal Recessive Adenylate Kinase 2 mutation = 0 production of lymphocytes, neutrophils, monocytes, platelets Most severe SCID
45
X-Linked Severe Combined Immunodeficiency Disorder
y-chain IL-2 mutation Poor cytokine response No T cells, NK cells, immature B cells Only boys
46
Adenosine Deaminase Deficiency
Needed for lymphocyte metabolism Low B,T,NK Peg-ADA
47
Lymphoid pregenitor deficiency management
Stem Cell transplant
48
T Cell maturation deficiency
Di George Syndrome
49
Di George Syndrome
Defect of development of pharyngeal pouch 22q11.2 Deletion CATCH 22 ``` Cardiac abnormalities (TOF) Abnormal facies Thymic aplasia* Cleft palate Hypocalcaemia ``` 22 = chromosome
50
Di George Investigation findings
``` Low T Normal B Low IgG Better with age 22q11.2 deletion ```
51
Di George Management
Thymic Transplant (to quadriceps)
52
Deficiency due to CD4/8 T cell selection
Bare lymphocyte syndrome MHC gene expression defect Class I = Type I = no CD8 Class II = Type II = No CD 4 = Low IgG, IgA, IgE
53
Deficiency in B Cell development
Bruton's X-Linked a-gammaglobulinaemia Defect in B cell tyrosine Kinase gene B cells cannot mature No IgG after 3 months No lymph nodes/tonsils IV Ig treatment
54
immunoglobulin defects
Selective IgA Deficiency | Combined Variable Immune Deficiency
55
Selective IgA Deficiency
1:600 2/3 asymptomatic 1/3 recurrent resp tract infections (IgA = mucosal membranes)
56
Combined Variable Immune Deficiency
Low IgA,G,E Resp + GI Infections Autoimmune disease, granulomatous disease
57
Defect in class switching
Hyper IgM Syndrome CD40-L defect in T cells on Xq26 = T cell defect leading to no T cell stimulation of B Cell maturation = no class switching = high IgM, no others

Meded Path Lectures (15 decks)

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