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Respiratory > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the major hallmarks of immune deficiency?

A 
SPUR
Serious infections
Persistent infections
Unusual infections
Recurrent infections
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2
Q

What are the cells and proteins in the innate immune system?

A

Cells

  • Macrophages
  • Neutrophils
  • Mast cells
  • Natural Killer Cells

Proteins

  • Compliment
  • Acute Phase Proteins
  • Cytokines
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3
Q

What are the cells and proteins in the acquired immune system?

A

Cells

  • B lymphocytes
  • T lymophocytes

Proteins
- Antibody

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4
Q

What are the 3 functions of the innate immune system?

A

Rapid clearance of microorganisms
Stimulates the acquired immune response
Buys time while the acquired immune system is mobilized

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5
Q

What are the main phagocytes?

A

Neutrophils

Monocyte/Macrophages

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6
Q

What are the main functions of the phagocytes?

A

Initiates and amplifies the inflammatory response.
Scavenges cellular and infectious debris
Ingests + kills microorganisms
Produces inflammatory molecules that regulate other components of the immune system
Resolution and Repair

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7
Q

What are Phagocytes most important in defence against?

A

Bacteria and Fungi

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8
Q

What might reccurent infections tell you about a patient’s phagoctes?

A

There is a deficiency.

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9
Q

What are the 4 types of organisms that may give rise to infection in a patient with phagocyte deficiencies?

A

Common - (Staph Aureus)
Unusual - (Burkholderia cepacia)
Mycobacteria - (TB and atypical mycobacteria)
Fungi - (Candida, Aspergillus)

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10
Q

What is reticular dysgenesis?

A

Failure of stem cells to differentiate along myeloid lineage. (Failure to produce neutrophils)

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11
Q

What are two specific conditions that lead to failure of neutrophil maturation?

A

Kostmann syndrome - (severe congenital neutropaenia)

Cyclic neutropaenia - (Episodic neutropaenia every 4-6 weeks)

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12
Q

Does recticular dysgenesis allow for the production of T/B-Lymphocytes + Natural Killer Cells?

A

No.
Recticular dysgenesis halts productions before stem cells can become a common lymphoid progenitor OR a common myeloid progenitor.

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13
Q

Does Kostmann syndrome allow for the production of Monocytes and Neutrophils?

A

NO.
Kostmann syndrome halts production of neutrophils. Howevrer sufferers can still create monocytes and all the lymphoid profenitor things (Lymphocytes and NKCs)

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14
Q

What would be the classic clinical presentation of Kostmann Syndrome?

A

Reccurent bacterial infections
Systemic or localised infection
(WITHIN 2 WEEKS AFTER BIRTH)

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15
Q

What definitive treatments could you give a child with Kostmann Syndrome?

A

Stem cell transplant

Granulocyte colony stimulating factor (G-CSF) - (specific growth factor to assist maturation of neutrophils

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16
Q

What are the supportive treatments for Kostmann Syndrome?

A

Prophylactic antibiotics

Prophylactic antifungals

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17
Q

What is the mortality % of children with Kostmann Syndrome in the first year without definitive treatment?

A

70%!

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18
Q

What are upregulated in the blood supply at sites of infection to stimulate neutrophil adhesion and migration into tissues

A

Endothelial Adhesion Markers

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19
Q

What is the condition when phagocytes are unable to identify Endothelial Adhesion Markers and what would happen?

A

Leukocyte adhesion deficiency.

failure of neutrophil adhesion and migration.

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20
Q

Is Leukocyte adhesion deficient a primary or secondary immunodeficiency?

A

RARE primary. (From birth)

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21
Q

What would be the clinical presentation of Leukocyte adhesion deficiency?

A

Marked leukocytosis

Localized bacterial infections that are difficult to detect.

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22
Q

What is the difference between direct and indirect recognition of a Pathogen by a phagocyte?

A

Indirect uses opsonins which act as binding enhancers on the surface of the phagocyte.

Direct binds directly

23
Q

Name the different types of opsonin.

A

Complement C3b, IgG antibody and C-reactive protein.

24
Q

What could cause defective phagocytosis?

A

Defect in opsonin receptors.

Defect of complement or antibody production (decreased efficiency of opsonisation)

25
Q

What is chronic granulomatous disease?

A

Failure of oxidative killing mechanisms.

26
Q

What are the main causes of Chronic granulomatous disease?

A

Absent respiratory burst

  • Deficiency of intracellular killing mechanism of phagocytes
  • inability to generate oxygen free radicals
  • Impaired killing of intracellular micro-organisms

Inability to clear organisms

  • Failure to degrade chemoattractants and antigens
  • persistant accumulation of neutrophils, activated macrophages and lymphocytes
27
Q

What are the main clinical presentations of Chronic Granulomatous Disease?

A 
Recurrent deep bacterial infections - (Staphylococcus, Aspergillus, Pseudomonas capacia. Mycobacteria, atypical mycobacteria)
Recurrent fungal infections
Failure to thrive
Lymphadenopathy + hepatosplenomegaly
Granuloma formation
28
Q

What is the investigation of choice for chronic granulomatous disease?

A

Nitroblue Tetrazolium test (NBT)

(feed patient neutrophils source of Ecoli
Add dye sensitive to H2O2
if H2O2 is roduced by neutrophils, dye changes colour)

29
Q

What are the supportive and definitive treatments of chronic granulomatous disease?

A 
Supportive
 - prophylactic antibiotics + antifungals
Definative
 - Stem cell transplantation
 - Gene therapy
30
Q

What is the problem with intracellular organisms?

A

They hide from the immune system by locating within cells.
(e.g. Salmonella, Chlamydia, Rickettsia)

Some hide in immune cells! (e.g. Mycobacteria)

31
Q

What does an infection with mycobacteria (TB) lead to to allow the body to fight it when the mycobacteria is within a macrophage?

A

Activates IL12 - gIFN network

Interleukin12 (IL12) is released by infected macrophage.
IL12 induces T cells to secrete gamma interferon (gIFN)
gIFN feeds back to macrophages + neutrophils
Stimulates TNF production
Activates NADPH oxidase
Stimulates oxidative pathways.

32
Q

What would a defect in the IL12 - gIFN axis cause?

A

Patient with sucseptability to intracellular bacteria

e.g. Mycobacteria + Salmonella

33
Q

Why are anti-TNF drugs, used in the treatment of inflammatory diseases sometimes contraindictive?

A

Can lead to reactivation of latent Tuberculosis!

MIND = BLOWN

34
Q

What investigation would allow you to check the mobilisation of phagocytes from bone marrow?

A

FBC

35
Q

What investigation would you use to check oxidative killing?

A

NBT

36
Q

What would be the aggressive management of an infection in a patient with phagocyte deficiency?

A

Infection prophylaxis
Oral/intravenous antibiotics
Surgical draining of abscesses

37
Q

What is the definitive treatment for a patient with phagocyte deficiency?

A

Bone marrow transplantation

Specific treatment for Chronic granulomatous disease - (e.g. gIFN therapy)

38
Q

At what stage does the acquired immune system begin to respond to infection?

A

> 96 hours after innate begins.

39
Q

Where do pre-T cells originate?

A

They arise from haematopoetic stem cells in bone marrow.

40
Q

What happens to pre-T cells in the Thymus?

A

Maturation and selection takes place.

10% of cells survive and enter the circulation and reside in lymph nodes and secondare ymphoid follicles.

41
Q

What do CD4+ T lymphocytes do?

A

Provide costimulatory signals - (activate CD8+ T lymphocytes and naive B cells)
Produce cytokines
Regulate other lymphocytes and phagocytes.

Recognise peptides on HLA Class II molecules.

42
Q

What do CD8+ T lymphocytes do?

A

Recognise peptides in association HLA Class I.
Directly kills cells - (Produces pore-forming perforin, triggers apoptosis of the target, Secrete cytokines (e.g. IFNy))
Important in defence against viral infections and tumours.

43
Q

Where do B lymphocytes arise from?

A

Haemopoetic stem cells in bone marrow

44
Q

Where would you find mature B lymphocytes?

A

Bone marrow
lymphoid tissue
spleen

45
Q

What is severe combined immunodeficiency?

A

Failure to produce lymphocytes.

46
Q

How would a patient present with severe combined immunodeficiency?

A 
Unwell by 3 months
persistent diarrhoea
failure to thrive
infections of all types (SPUR)
skin diseases
Family history of early infant death.
47
Q

Why do children with severe combined immunodeficiency not usually present before 3 months?

A

Because the maternal IgG protects them in the first 3 months of life but their immune system has not matured enough to fight infections.

48
Q

What would you expect the levels of T cells, B cells and lymphoid tissue to be like in a child with SCID?

A

Very low or absent T cells
Normal or increased B cells
Poorly developed lymphoid tissue + thymus

49
Q

What is DiGeorge syndrome?

A

Developmental defect of the 3rd/4th pharyngeal pouch.

50
Q

What would you expect in a child with DiGeorge syndrome?

A

Fucked from the ears to the heart.

NO T cell maturation site

51
Q

what levels of cells would you see in DiGeorge syndrome?

A

Absent or decreased number of T cells
Normal or increased B cells (Low IgG, IgA, IgE)
Normal NK cells

52
Q

What would be a consequence of Bruton’s X-linked hypogammaglobulinaemia?
(Failure to produce mature B cells)

A

No circulating B cells
No plasma cells
No circulating antibody after first 6 months

53
Q

What is common variable immune deficiency?

A

A problem with IgM B cells differentiating causing low IgG, IgA, and IgE

54
Q

why am i doing this?!

A

Coz it’s shite.

Respiratory (12 decks)

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