Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Transition SB > Immunology > Flashcards

Immunology Flashcards

1
Q

what are features suggestive of immunodeficiency

A

SPUR

Serious infections
Persistent infections
Unusual infections
Recurrent infections

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

what are other features suggestive of a primary immune deficiency

A 
Weight loss or failure to thrive
Severe skin rash (eczema)
Chronic diarrhoea
Mouth ulceration
Unusual autoimmune disease
Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are conditions associated with secondary immune deficiency

A 
extremes of life - ageing, premature
HIV
Measles 
Immunosuppressive Tx
Anti-cancer Tx
Cancer of immune system - lymphoma, leukaemia, myeloma
Mets
Malnutrition
DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the commonest form of severe combined immunodeficiency

A

X-linked SCID

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

what causes SCID

A

mutation of IL2 receptor

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

what does the mutation in SCID results in

A

In inability to respond to cytokines

  • failure of T cell and NK cell development
  • production of immature B cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the number of T/B cells seen in X-linked SCID

A

Very low or absent T cells

Normal or increased B cells

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

presentation of severe combined immunodeficiency

A 
Unwell by 3 months of age
Persistent diarrhoea
Failure to thrive
Infections of all types
Unusual skin disease 
FX of early infant death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the IL12-gIFN network pathway

A
  1. macrophage infection with bacteria
  2. produces IL12
  3. IL12 induces T cells to secrete gIFN
  4. gIFN feeds back to macrophages and neutrophils
  5. stimulates production of TNF
  6. activates NADPH oxidase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what happens is there is no TNF

A

no functional granuloma

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

what is a granuloma

A

organised collection of activated macrophages and lymphocytes

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

what causes a granuloma to be formed

A
  1. inflammatory response triggered
  2. activation of T lymphocytes and macrophages
  3. failure of removal of stimulus
  4. persistent production of activated cytokines
  5. granuloma formed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are examples of conditions where granulomas are formed

A 
Sarcoidosis
TB
Leprosy 
Silicosis 
Foreign bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are antibody mediated autoimmune diseases

A

Idiopathic thrombocytopaenia

Autoimmune haemolytic anaemia

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

what are common variable immune deficiencies

A

Low IgG, IgA and IgM

Recurrent bacterial infections, esp. respiratory

Often associated with autoimmune disease

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

what is a relatively common antibody deficiency

A

Selective IgA deficiency

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

what are Sx of selective IgA deficiency

A

1/3rd have recurrent resp tract infections

2/3rd are asymptomatic

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

Ddx of recurrent bacterial infections AND hypogammaglobulinaemia

A

Antibody deficiency

Protein loss i.e. nephrotic syndrome

Failure of protein syntheses e.g. myeloma, lymphoma, CLL

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

what are the classifications of hypersensitivity reactions

A

Type I: Immediate hypersensitivity (IgE-mediated allergy)
Type II: Direct cell killing: antibody mediated
Type III: Immune complex mediated (example: SLE)
Type IV: Delayed type hypersensitivity

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

what organ secretes complement proteins

21
Q

what is lysis

A

direct killing of bugs by punching holes in it

22
Q

what is the function of natural killer [NK] cells

A

kill cells that lack MHC – molecules on surface

23
Q

what is meant by the term ‘natural’ in NK cells

A

no need for antigen specificity

24
Q

why couldn’t we just have NK cells

A

they have no long term memory

25
what immune system are NK cells part of
innate immunity
26
what receptors are seen on the cells that are part of the innate immunity
toll-like receptors [TLR]
27
why are TLR important
expressed on phagocytes and dendrites as built-in burgler alarm for microbes activation causes pro-inflammatory cytokines and type 1 Interferon secretion
28
what can TLR dysfunction cause
immunodeficiency (too little) or autoimmunity (too much)
29
what treatment activates TLR to boost immunity and through which number receptor
imiquimod, activating TLR7/8
30
what blocks pro-inflammatory cytokines
TNF inhibitors
31
what is the job of TNF-alpha
secreted as an immediate-early ‘fire alarm’ signal in response to many stressors
32
what are the 4 types of transplant rejection
hyperacute rejection acute cellular rejection acute vascular rejection chronic allograft failure
33
hyperacute rejection = time, pathology, mechanism, Tx
T - mins to hours P - thombosis & necrosis, Type II hypersensitivity M - preformed antibody and complement fixation Tx - none
34
acute cellular rejection = time, pathology, mechanism, Tx
T - 5 to 30 days P - cellular infiltration, Type IV hypersensitivity M - CD4 and CD8 T cells Tx - immunosuppresion
35
acute vascular rejection = time, pathology, mechanism, Tx
T - 5 to 30 days P - vasculitis, Type II hypersensitivity M - De novo antibody and complement fixation Tx - immunosuppresion
36
chronic allograft failure = time, pathology, mechanism, Tx
T - > 30 days P - fibrosis, scarring M - Immune and non-immune mechanisms Tx - minimise drug toxicity, hypertension, hyperlipidaemia
37
how do vaccinations work
produce memory in B cells and T cells
38
how does vaccinations work on T cells
simulates rare naive T cells induces a strong T-cell response in 14–21 days some become effector T cells which = - mostly die by apoptosis in absence of antigen - Smaller no. become memory T cells maintained at low frequency
39
what antibody quickly rises first in primary infection
IgM | - gone by 14 dyas
40
what antibody rises steadily and decreases slowly in primary infection
IgG | - takes years to decrease
41
what antibody is there more of in secondary infection
IgG however, get the same rapid rise and fall in IgM
42
what are key features of inactivated vaccines
Cannot replicate Generally not as effective as live vaccines Immune response primarily antibody based (not T cells) Antibody titer may diminish with time Require multiple doses to stimulate immune response
43
advantages of inactivated vaccines
Can be made quickly (prevent epidemics) Elicit good antibody responses Easy to store; No refrigeration required Usually safe
44
disadvantages of inactivated vaccines
Doesn’t stimulate clonal expansion of B and T cells Require multiple and booster injections Require adjuvants to improve immunogenicity
45
what are examples of inactivated vaccines
whole cell vaccines - polio, hep A, cholera, rabies fractional vaccines - influenza, hep B, diptheria, tetanus
46
adv of live attenuated vaccine
All relevant effector mechanisms elicited (antibody, activated T cells) Localised, strong response Usually only one single dose required
47
disadv of live attenuated vaccines
safety - may cause infection in immunocompromised fragile - must be stored carefully
48
examples of live attenuated vaccine
``` measles mumps rubella yellow fever MMR jab BCG ```

Transition SB (5 decks)

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