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Extra Stage 2 > IAH SSA > Flashcards

IAH SSA Flashcards

1
Q

Nuclei shapes:

A

T cell nucleus - round;

monocyte - heart shaped;

neutrophil - blobby (irregular);

plasma cell - bottom of the cell (fills a large proportion of the cell)

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2
Q

Which region of the Ig binds to the neutrophil

A

Fc receptor

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3
Q

MS

A

Myelin sheath attach

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4
Q

Myasthenia gravis

A

Results from antibodies that block or destroy nicotinic acetylcholine receptors at the junction between the nerve and muscle

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5
Q

Pemphigus vulgaris

A

Epidermal desmosomes. Type II hypersensitivity.

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6
Q

Bullous pemphigoid

A

Attacks basal epidermis

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7
Q

HIV graph of CD4 cells, viral proteins and ab levels in serum:

A

Peak at the start is acute HIV syndrome - asymptomatic or flu like symptoms
2-12 years - latency - asymptomatic
2-3 years afterwards is full blown AIDs -> death; symptomatic
4-8 weeks is innate response but then

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8
Q

Autoimmune diseases that affect: Kidneys

A

Good pasture’s

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9
Q

Autoimmune diseases that affect: IgE on basement membrane

A

bullous pemphigoid

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10
Q

Autoimmune diseases that affect: Thyroid

A

Hashimoto’s, Grave’s disease

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11
Q

Autoimmune diseases that affect: b cells

A

Systemic lupus

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12
Q

Autoimmune diseases that affect: Salivary glands

A

Sjrogen’s

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13
Q

Autoimmune diseases that affect: Acid and receptor

A

associated with gout

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14
Q

What receptors are on T cells

A

TCR
CD4 (helper T cells) or CD8 (cytotoxic T cells)
IL-2 (in differentiated cells)
CD28 - co-stimulatory molecule on naive T cells
CD3 - co receptor that helps activate both CD4 and CD8 cells

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15
Q

Toll-like receptor

A

Receptors in the innate system
Can be intracellular or extracellular to detect for different pathogens
3,7,9 are intracellular receptors
The rest are extracellular

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16
Q

MHC molecules what they bind to

A

they bind to ag that has been processed in the proteasome and then present this to the adaptive immune system

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17
Q

How antibody levels are affected in Bruton’s disease

A

X linked agammaglubulinemia

Tyrosine kinase is affected resulting in immature B cells

Impact on Ig production

No ability to class switch

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18
Q

What would the levels of IgM and IgG be in the this disease?

A

no mature B cells produced; lack of antibodies. IgM levels would be ok

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19
Q

name the two steps before CD8 kills virus infected cell

A

Class I MHC presents antigen to CD8 cell. 2nd signal comes from CD28 co receptor.

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20
Q

Type 4 hypersensitivity

A

delayed type hypersensitivity that involves T cells

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21
Q

after HIV What microorganisms cause Kaposi’s sarcoma, pneumonia and B cell lymphoma?

A

HIV and AIDs cause these conditions as secondary infections arising from reduced immune response

Kaposi’s sarcoma - HHV8

B cell lymphoma - EBV

Pneumonia - S. pneumoniae

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22
Q

How do commensal bacteria help to prevent infection?

A

outcompete, secrete toxins which damage adjacent organisms which may be pathogens

23
Q

What factor mean burns are more susceptible to infections

A

more nutrients like haem, dead tissues prevent immune response reaching colonisation and proliferation sites

24
Q

Function of CD4 on the membrane

A

co stimulatory factor; assists in MHC class II recognition.

25
Q

What lymphocyte is present in granulomas; what cytokine does it secrete; what other cell is involved:

A

Multinucleated macrophages with TH1 cells; cytokines secreted are IFN-gamma and IL-2

26
Q

The process of CD8 cytotoxicity

A

Activated in secondary lymphoid tissue, recognises viral infected cells by MHC I, TCR, peptide interactions and releases cytotoxins which perforate cell membrane and instructs apoptosis. Then secrete IFN-gamma to attract macrophages

27
Q

Name two cells which produce antimicrobial peptides

A

paneth cells (alpha defensins) and NK cells

28
Q

How do antimicrobials kill pathogens

A

disruption of peptidoglycan layer or other form of bacteria specific action

29
Q

Herpes simplex virus, which tissue does it infect first? Which tissue does it become latent in?

A

First infects epithelial tissues and then becomes latent in the trigeminal ganglion. Treated with aciclovir to varying degrees of effectiveness

30
Q

Virus that lays dormant in B cells and what disease does it cause

A

Epstein Barr virus, glandular fever progressing to B cell lymphoma in some patients

31
Q

What type of hypersensitivity is it when T cells are involved?

A

Type IV e..g chronic asthma

32
Q

In granuloma formation what causes cell necrosis?

A

dead and dying macrophages release lytic enzymes which damage surrounding tissues

33
Q

What are the two diseases caused by mycobacterium

A

TB and leprosy

34
Q

What is SCID?

A

lack of functioning T cells and therefore B cells which cannot be activated by t helper cells

35
Q

What is ADA? -

A

autorecessive disorder metabolic disorder that causes immunodeficiency. The main symptoms of ADA deficiency are pneumonia, chronic diarrhea, and widespread skin rashes. Affected children also grow much more slowly than healthy children and some have developmental delay. Most individuals with ADA deficiency are diagnosed with SCID in the first 6 months of life.

36
Q

What Ig component recognises LPS? -

A

variable region

37
Q

Which Ig component is most polymorphic?

A

variable region

38
Q

What haplotype is most associated with autoimmune disorders? -

A

HLA

39
Q

What causes granulation tissue?

A

a diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds (most importantly the superoxide radical due to defective phagocyte NADPH oxidase) used to kill certain ingested pathogens.

40
Q

MHC - myeloid and non-myeloid

A

Myeloid - megakaryocytes, erythrocytes, granulocytes, monocyte, macrophages im sure :neutrophil, dendritic cell too

Lymphoid - T cells, B cells, NK cells (ILC)

41
Q

Outline hyper acute rejection

A

Type II hypersensitivity
HLA class I mismatch
IgG binds to transplant resulting in agglutination

42
Q

Addison’s disease

A

dark mucosal pigmentation (oral manifestation); primary adrenal disease -> hypocorticolism

43
Q

Kidney rejection:

A

hyper acute - type II hypersensitivity caused by pre exisiting abs binding to the graph.
Chronic - type III hypersensitivity. Immune complexes between Ab and HLA.

44
Q

Cells and cytokines involved in fungal infections

A

NK, macrophage, TH1, IFN-gamma, IL-12

45
Q

How tumour antibodies are used

A

Monoclonal antibodies are used to target specific molecules e.g. cancer cells (rituximab kills B cells), host immune system to boost response or identification of size and location of the tumour

46
Q

Hypersensitivities:

A

Type I - acute immediate reaction - mast cells; IgE - histamine release
Type II - surface antigens
Type III - Immune complexes
Type IV - delayed response; T cells

47
Q

HIV graph of CD4 cells, viral proteins and antibody levels in serum?

A

infection- enters via CD4 receptor and CCR5 co receptor

seroconversion- HIV antibodies produced and HIV can be detected in the blood

symptomatic- macrophage and dendritic cells first to be infected
- switches to T cell infection later in the disease - symptomatic

full blown aids- hiv kills T cells quicker than they can be replaced- full blown aids

48
Q

immune response to HIV

A

acute viraemia- increase om viral particles after infection- flu like symptoms

activation of anti-HIV specific immune responses

  • cytotoxic cells
  • anti HIV antibodies (seronversion)

assymptoamtic phase- latent

49
Q

What disease class is Brutons why is It , much more common in males

A

primary immune deficiecny
• Failure of B-cell receptor signalling (B cell receptor is an immunoglobulin expressed on the surface rather than being secreted) – get issues with cell development
Do not prduce mature B cells, leading to lack on Ig in bloodstream.
can’t class switch I think

  • Recurrent infections with extra-cellular pyogenic bacteria e.g. Streptococcus pneumoniae
  • Chronic infections with poliovirus, HBV or HCV

X-linked, much more common in males

50
Q

In granuloma formation what causes cell necrosis?

A

Dead/dying macrophages release lytic enzymes which damage surrounding tissue.

51
Q

kidney rejection

A

1st phase of rejection - hyperacute rejection

•Type II hypersensitivity (antibodies recognise antigens on the surface of cells)
•Pre-existing antibodies (IgG) to non-self antigens bind vascular endothelium of transplant and activate complement causing endothelial damage and haemorrhage of graft due to ABO or HLA Class I antigen mismatch
Anti-HLA antibodies may arise as the result of pregnancy, multiple blood transfusions and previous transplants

Type 4 hypersensitivity

  • immune response by one individual to the alloantigens of another caused by alloreactive T-cells
  • with kidney you just get a rejected kidney but wihen bone marrow translated can get GVHD- T cells attack the recipient’s tissues and there is a potentially fatal graft vs host reaction

Chronic - Type III hypersensitivity reaction
• Immune complexes between Ab and HLA molecules
• Fibrosis  key feature of chronic rejection
immune effectors can enter the wall of the artery and inflict damage

52
Q

• Graph about class switching ie. IGm to IgG

A
  1. Isotype switching from IgM to IgG- better immune response with more coverage. Increased affinity- stronger at the same concentration!!
53
Q

Tumour antigens and therapeutic strategies

A

• Monoclonal antibodies to target specific antigens

  • Target cancer molecules: killing of B-cells in lymphoma (Rituximab)
  • Target host immune system to boost performance: checkpoint inhibitor drugs (e.g. ipilmumab)
  • identify size and location of tumour (conjugated to radioactive isotope

Extra Stage 2 (14 decks)

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