immunology Flashcards

1
Q

what is a granuloma?

A

an organised collection of activated macrophage + lymphocytes
- non-specific inflammatory response triggered by diverse antigenic agents or by inert foreign materials
- results in activation of T lymphocytes + macrophages
- failure of removal of the stimulus results in persistent production of activated cytokines

–> end result = organised collection of persistently activated cells

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

ifferential diagnosis of lung granuloma

A

sarcoidosis
myobacterial disease - Tb, leprosy
silicosis + other dust diseases
chronic stage of hypersensitivity pneumonitis
foreign bodies

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

presentation of antibody deficiencies

A

recurrent bacterial infections - resp, GI (viral less common)

antibody mediated autoimmune diseases
- idiopathic thrombocytopenia
- autoimmune haemolytic anaemia

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

common primary antibody deficiencies

A

common variable immune deficiency (CVID)

selective IgA deficiency

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

common variable immune deficiency (CVID)

A

low IgG, IgA + IgM
- causes most unknown

recurrent bacterial infections - esp resp
often assoc with autoimmune disease

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

selective IgA deficiency

A

VERY COMMON!!
2/3rd individuals asymptomatic *
other1/3rd -> recurrent resp infections

genetic component, but cause unknown

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

differential diagnosis of recurrent bacterial infections + hypogammaglobulinaemia

A

primary = antibody deficiency

secondary
- protein loss - nephrotic syndrome, protein losing enteropathy
- failure of protein synthesis - lymphoproliferative disorder (CLL, myeloma, NHL)

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

natural killer cells

A

innate-immunity feature to eliminate cancer cells
lack MHC molecules on surface
“natural” -> no need for antigen specificity

no long term memory

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

natural killer cell defects

A

predisposes to recurrent VZV, HSV, CMV, HPV NK cells

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

innate recognition of invaders

A

“toll- like receptors” (TLRs)
- respond to “PAMPS” (pathogen-assoc molecular patterns)

-> expressed on phagocytes + dendrites as built in burglar alarm for microbes - activation triggers proinflammatory cytokines + type 1 interferon secretion

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

what can TLR dysfunction cause?

A

(toll-like receptors -> built in burglar alarm)

can lead to immunodeficiency (too little) or autoimmunity (too much)

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

TLR activators use?

A

(toll-like receptors -> built in burglar alarm)

are used to boost immunity (“anti-skin cancer creams”) - imiquimoid

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

TNF-alpha

A

block pro-inflammatory cytokines
TNF-alpha is an immediate-early “fire alarm” signal in response to many stressors (microbes, stress, chemicals)

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

“biologic” drugs

A

MOST are artificial antibodies that block the bodys own proteins - so they act just like “passive immunisation” + have to be injected every couple of weeks

since they are normal proteins, their metabolism is NOT dependent on the liver/renal function - NO generic renal or hepatic toxicity

these are foreign protein, so the immune system on form antibodies against them

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

types of transplant rejection

A

hyperacute rejection
acute cellular rejection
acute vascular rejection
chronic allograft failure

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

hyperacute transplant rejection

A

time = mins-hrs
pathology = thrombosis+necrosis, tye 2 hypersensitivity

mechnism = preformed antibody + complement fixation
treatment = none

17
Q

acute cellular transplant rejection

A

time = 5-30days
pathology = cellular infiltration, type IV hypersensitivity

mechanism = CD4 + CD8 T cells
treatment = immunosuppresion

18
Q

acute vascualr transplant rejection

A

time = 5-30days
pathology = vasculitis, type II hypersensitivity

mechanism = de novo antibody + complemtent fixation
treatment = immunosupression +++

19
Q

chronic allograft failure (transplant rejection)

A

time = >30days
pathology = fibrosis, scarring

mechanism = immune + non-immune mechanism
treatment = minimise drug toxicity, hypertension, hyperlipidaemia

20
Q

what does vaccination produce?

A

memory in B cells + Tcells

longlived memory B cells are genereated during primary immune responses that can survive for many years - even after antigen has been eliminated
- memory B cells rapidly re-activate in response to a second encounter with that specific antigen

(clonal expansion, differentiation into plasma cells, antibody production)

21
Q

what does vaccination stimulate?

A

rare naive T cells
indices a strong T-cell response in 14-21days

some become effector T cells which
- mostly die by apoptosis in absence of persisting antigen
- small number become MEMORY T CELLS + are maintained at low frequency

22
Q

impact of memory on antibody production in primary vs secondary infection

A

primary = IgM first responds, then eventually IgG (clinical disease between these)

secondary = IgG kicks in before IgM + clinical features aborted

23
Q

pros + cons of inactivated vaccines

A

pros -> quick + easy
- made quick, good antibody response, easy to store

cons -> not very potent
- require boosters (no clonal expansion + titres diminish over time)

24
Q

examples of inactivated vaccines

A

whole cell vaccines
- polio, Hep A
- rabies, cholera

fractional vaccines
- subunit - Hep B, influenza, pertussis, HPV, anthrax

toxoids - diptheria, tetanus

pure polysaccharide vaccines - haemophilus influenza type B

25
Q

pro / cons of live attenuated vaccines

A

pros
- all relevant effector mechanism elicited (antibody, AND activated T cells)
- localised, strong response
- usally only one single dose required

cons
- safety - may revert virulence, infection in immunocompromised
- must be stored/handled carefully

26
Q

examples of live attenuated vaccines

A

viruses
- measles, mumps, rubella (MMR)
- chickenpox
- yellow fever
- rotavirus
- smallpox
- polio

bacterial - BCG, oral typhoid

27
Q

DNA/RNA vaccines

A

DNA or RNA which directs the assembly of the antigenic protein inside the host cell

  • can be given as “naked” DNA/RNA or packaged into a virus which then infects the host cells, instructing the cells to assemble the antigenic protein
28
Q

DNA/RNA vaccine pros/cons

A

pros
- can be v potent
- easier to make than protein vaccines
- can be applied to target mutated proteins found in cancer (so calle d”neo-antigens”)

cons
- may require complex cold-chain
- so far no long term experience

29
Q

examples of DNA/RNA vaccines

A

against covid19
- moderna vaccine (RNA)
- biontech vaccine (RNA_
- oxford vaccine (adenovirus)

30
Q

virus like particles (VLP) vaccines

A

empty shells (capsids) made from viruses that look like the real virus but have no DNA/RNA

31
Q

virus like particle (VLP) vaccines pros/cons

A

pros
- non-infectious
- v potent, one dose required
- activates both T + B cell responses

cons
- complex manufacture
- must be stored/handled carefully

32
Q

examples of VLP vaccines

A

against papillomavirus assoc cancers
- cervarix, gardasil

against Hep B - engerix