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AY Respiratory > Immunology > Flashcards

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)

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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
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3
Q

2 classifications of immunodeficiencies

A

Primary (rare)

Secondary (common)

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4
Q

2 branches of the immune system

A

Innate

Acquired

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5
Q

Cells in the innate immune system

A

Macrophages
Neutrophils
Mast cells
NK cells

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6
Q

Proteins of innate immune system

A

Complement
Acute phase protein
Cytokines

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7
Q

Function of innate immune system

A

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

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8
Q

Cells in the acquired immune system

A

B lymphocytes

T lymphocytes

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9
Q

Proteins in the acquired immune system

A

Antibody

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10
Q

Function of acquired immune system

A

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

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11
Q

Examples of phagocytes

A

Neutrophils

Monocytes/Macrophages

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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

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13
Q

Clinical features of phagocytes deficiencies

A

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

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14
Q

Where are phagocytes found

A

Bone marrow or within tissues

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15
Q

What is Kastmann syndrome?

A

Rare autosomal recessive disorder

Severe chronic neutropenia

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16
Q

Clinical presentation of Kastmann syndrome

A 
Infections (0 - 2 weeks old)
Fever
Irritability 
Oral ulcers 
Failure to thrive
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17
Q

Treatment of Kastmanns syndrome

A 
Supportive 
- prophylaxis antibiotics & antifungals 
Definitive 
- stem cell transplant 
G-CSF
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18
Q

What is leukocyte adhesion deficiency?

A

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

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19
Q

Clinical features of leukocyte adhesion deficiency

A

Marked leukocytos

Localised infections - difficult to detect

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20
Q

What causes chronic granulomatous disease?

A

Failure of oxidative killing mechanisms

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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
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22
Q

Investigation for chronic granulomatous disease

A

NBT test

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23
Q

Treatment of chronic granulomatous disease

A 
Supportive 
- prophylactic antibiotics/anti-fungals
Definitive 
- stem cell,transplant 
- gene therapy
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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

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25
Q

Examples of intracellular organisms

A

Salmonella
Chlamydia
Rickettsia

26
Q

What network defends against intracellular organisms?

A

IL12- gIFN network

27
Q

Brief summary of IL12-gIFN network

A

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
Q

Causes of defects in IL12-gIFN network

A

Single gene defects

  • gIFN receptor deficiency
  • IL12 deficiency
  • IL12 receptor deficiency
29
Q

Treatment of phagocyte deficiencies

A 
Supportive 
- prophylaxis 
- oral/IV antibiotics 
- surgical drain of abscess
Definitive 
- bone marrow transplant 
- gIFN therapy 
- gene therapy
30
Q

4 organisms that the immune system tackles

A

Viruses (e.g. Influenza)
Bacteria (e.g. Staph/Strep)
Protozoa (e.g. Amoeba)
Worms (e.g. Guinea worm)

31
Q

Where do lymphocytes mature?

A

Thymus gland

32
Q

Where is the thymus gland?

A

Just in front of the heart in the mediastinum

33
Q

How is lymph returned to the systemic circulation?

A

Thoracic duct

34
Q

What does the thoracic duct join with?

A

Left subclavian vein

35
Q

What does IL-1 do?

A

Causes fever and activates lymphocytes

36
Q

What does Il- 6 do?

A

Causes fever, stimulates the liver to produce acute phase proteins such as CRP, activates lymphocytes and promotors antibody production

37
Q

What does IL-8 do?

A

Causes neutrophil Chemotaxis

38
Q

What does IL-12 do?

A

Activates NK cells and TH1 cells (important for intracellular infections)

39
Q

What does TNF-alpha do?

A

Increases vascular permeability to allow immune cells to reach tissues

40
Q

What do IL-4, IL-5 and IL-13 do?m

A

Promote IgE production and eosinophilic reactions inpatients with allergies

41
Q

What does gamma interferon do?

A

Activates cell mediated immunity in viral infections

42
Q

What does IL-10 do?

A

Has an anti inflammatory affect

43
Q

What do co stimulators molecules do?

A

Encourage activation of the adaptive immune system

44
Q

How are dendritic cells involved in antigen presentation?

A

Carry digested antigens to lymph nodes

Present to TH0 cells with MHC II complexes

45
Q

What can TH0 cells differentiate into?

A

TH1 and TH2

46
Q

How are hypersensitivity reactions classed?

A

Type I: immediate hypersensitivity
Type II: direct cell killing
Type III: Immune complex mediated
Type IV: delayed type hypersensitivity

47
Q

Summary of the path ophthalmology of allergic reactions

A

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
Q

What is sodium cromoglycate?

A

Mast cell stabiliser

49
Q

Mechanism of action of anti-histamines

A

H1 receptor antagonists

Block affects of histamines

50
Q

Example of leukotriene receptor antagonist

A

Montelukast

51
Q

Action of adrenalin in anaphylaxis

A

Acts on B2 adrenergic receptors to constrict arterial smooth muscle
Increases blood pressure limiting vascular leakage
Dilates bronchial smooth muscle

52
Q

Key feature of Type II hypersitivity reaction

A

Antibody binds to cell surface antigen

53
Q

4 actions of complement

A

Chemotaxis (recruits neutrophils and macrophages)
Solubilisation (of immune complexes)
Direct killing (of encapsulated bacteria - MAC punches hole)
Opsonisation (tomato ketchup)

54
Q

Clinical example of type II hypersensitivity reaction

A

Blood donor rejection

55
Q

What is plasmapheresis?

A

Cell separator to remove pathogenic antibody

56
Q

Example of type III hypersensitivity reaction

A

Farmers lung
Pigeon fanciers lung
Systemic lupus erythematosus (SLE)

57
Q

Examples of type IV hypersensitivity

A

Nickel hypersensitivity

58
Q

Management of sarcoidosis

A

NSAIDS (for acute onset)
Systemic corticosteroids
- block T cell activation
- block macrophage activation

59
Q

Diseases characterised by type IV hypersensitivity and granuloma formation

A

Sarcoidosis
Tuberculosis
Leprosy (some forms)
Berylliosis, silicosis and other dust diseases
Chronic stage of hypersensitivity pneumonitisis

60
Q

Types of transplant rejection

A

Hyperacute rejection
Acute cellular rejection
Acute vascular rejection
Chronic allograft failure

61
Q

Treatment for transplant rejection

A

Immunosuppressive

AY Respiratory (11 decks)

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