Immunology Flashcards

1
Q

Hallmark of immune deficiencies

A

SPUR -
S - serious infections (unresponsive to oral antibiotics)
P - persistent infections (early structural damage, chronic infections)
U - unusual infections (unusual organisms or sites)
R - recurrent infections (2 minor or 1 major a year)

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

Other features of immune deficiency

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

2 classifications of immunodeficiencies

A

Primary (rare)

Secondary (common)

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

2 branches of the immune system

A

Innate

Acquired

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

Cells in the innate immune system

A

Macrophages
Neutrophils
Mast cells
NK cells

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

Proteins of innate immune system

A

Complement
Acute phase protein
Cytokines

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

Function of innate immune system

A

Rapid clearance of microorganisms
Stimulates acquired immune response
Buys time for acquired immune response

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

Cells in the acquired immune system

A

B lymphocytes

T lymphocytes

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

Proteins in the acquired immune system

A

Antibody

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

Function of acquired immune system

A

Adaptive response after exposure to antigen
Responsive to unlimited number of molecules
Immunological memory

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

Examples of phagocytes

A

Neutrophils

Monocytes/Macrophages

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

Functions of phagocytes

A

Initiation and amplification of inflammatory response
Scavenge for cellular and infectious debris
Produce inflammatory molecules which regulate other parts of IS
Resolution and repair

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

Clinical features of phagocytes deficiencies

A

Recurrent infections
May affect common or unusual sites
All types of bacteria and fungi

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

Where are phagocytes found

A

Bone marrow or within tissues

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

What is Kastmann syndrome?

A

Rare autosomal recessive disorder

Severe chronic neutropenia

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

Clinical presentation of Kastmann syndrome

A
Infections (0 - 2 weeks old)
Fever
Irritability 
Oral ulcers 
Failure to thrive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of Kastmanns syndrome

A
Supportive 
- prophylaxis antibiotics & antifungals 
Definitive 
- stem cell transplant 
G-CSF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is leukocyte adhesion deficiency?

A

Rare primary immunodeficiency
Caused by genetic defect
Results in failure of neutrophil adhesions and migration

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

Clinical features of leukocyte adhesion deficiency

A

Marked leukocytos

Localised infections - difficult to detect

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

What causes chronic granulomatous disease?

A

Failure of oxidative killing mechanisms

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

What are the features of chronic granulomatous disease?

A
Recurrent deep bacterial infections
Recurrent fungal infections
Failure to thrive
Lymphadenopathy & hepatosplenomegaly 
Granuloma formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Investigation for chronic granulomatous disease

A

NBT test

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

Treatment of chronic granulomatous disease

A
Supportive 
- prophylactic antibiotics/anti-fungals
Definitive 
- stem cell,transplant 
- gene therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why are intracellular organisms difficult for the immune system?

A

Hide from immune system by locating within cells
Can hide in immune cells (esp. macrophages)
Need specific strategies to clear infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Examples of intracellular organisms
Salmonella Chlamydia Rickettsia
26
What network defends against intracellular organisms?
IL12- gIFN network
27
Brief summary of IL12-gIFN network
Infected macrophages stimulated to produce Il12 IL12 induces T cells to produce gIFN gIFN feeds back to macrophage and neutrophils Stimulate TNF production Activate NADPH Stimulates oxidative pathways
28
Causes of defects in IL12-gIFN network
Single gene defects - gIFN receptor deficiency - IL12 deficiency - IL12 receptor deficiency
29
Treatment of phagocyte deficiencies
``` Supportive - prophylaxis - oral/IV antibiotics - surgical drain of abscess Definitive - bone marrow transplant - gIFN therapy - gene therapy ```
30
4 organisms that the immune system tackles
Viruses (e.g. Influenza) Bacteria (e.g. Staph/Strep) Protozoa (e.g. Amoeba) Worms (e.g. Guinea worm)
31
Where do lymphocytes mature?
Thymus gland
32
Where is the thymus gland?
Just in front of the heart in the mediastinum
33
How is lymph returned to the systemic circulation?
Thoracic duct
34
What does the thoracic duct join with?
Left subclavian vein
35
What does IL-1 do?
Causes fever and activates lymphocytes
36
What does Il- 6 do?
Causes fever, stimulates the liver to produce acute phase proteins such as CRP, activates lymphocytes and promotors antibody production
37
What does IL-8 do?
Causes neutrophil Chemotaxis
38
What does IL-12 do?
Activates NK cells and TH1 cells (important for intracellular infections)
39
What does TNF-alpha do?
Increases vascular permeability to allow immune cells to reach tissues
40
What do IL-4, IL-5 and IL-13 do?m
Promote IgE production and eosinophilic reactions inpatients with allergies
41
What does gamma interferon do?
Activates cell mediated immunity in viral infections
42
What does IL-10 do?
Has an anti inflammatory affect
43
What do co stimulators molecules do?
Encourage activation of the adaptive immune system
44
How are dendritic cells involved in antigen presentation?
Carry digested antigens to lymph nodes | Present to TH0 cells with MHC II complexes
45
What can TH0 cells differentiate into?
TH1 and TH2
46
How are hypersensitivity reactions classed?
Type I: immediate hypersensitivity Type II: direct cell killing Type III: Immune complex mediated Type IV: delayed type hypersensitivity
47
Summary of the path ophthalmology of allergic reactions
Production of specific IgE directed against antigen IgE allergen complex binds to mast cells via Fc receptors De granulation of mast cells Release of preformed and newly synthesised inflammatory molecules (e.g. histamine, leukotrienes)
48
What is sodium cromoglycate?
Mast cell stabiliser
49
Mechanism of action of anti-histamines
H1 receptor antagonists | Block affects of histamines
50
Example of leukotriene receptor antagonist
Montelukast
51
Action of adrenalin in anaphylaxis
Acts on B2 adrenergic receptors to constrict arterial smooth muscle Increases blood pressure limiting vascular leakage Dilates bronchial smooth muscle
52
Key feature of Type II hypersitivity reaction
Antibody binds to cell surface antigen
53
4 actions of complement
Chemotaxis (recruits neutrophils and macrophages) Solubilisation (of immune complexes) Direct killing (of encapsulated bacteria - MAC punches hole) Opsonisation (tomato ketchup)
54
Clinical example of type II hypersensitivity reaction
Blood donor rejection
55
What is plasmapheresis?
Cell separator to remove pathogenic antibody
56
Example of type III hypersensitivity reaction
Farmers lung Pigeon fanciers lung Systemic lupus erythematosus (SLE)
57
Examples of type IV hypersensitivity
Nickel hypersensitivity
58
Management of sarcoidosis
NSAIDS (for acute onset) Systemic corticosteroids - block T cell activation - block macrophage activation
59
Diseases characterised by type IV hypersensitivity and granuloma formation
Sarcoidosis Tuberculosis Leprosy (some forms) Berylliosis, silicosis and other dust diseases Chronic stage of hypersensitivity pneumonitisis
60
Types of transplant rejection
Hyperacute rejection Acute cellular rejection Acute vascular rejection Chronic allograft failure
61
Treatment for transplant rejection
Immunosuppressive