Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > Immunology > Flashcards

Immunology Flashcards

1
Q

Hallmarks of immunodeficiency

A

Serious infections
Persistent infections
Unusual infections
Recurrent infections

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

Features suggestive of primary immune deficiency

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

Primary immunodeficiency

A

Rare

Hereditary

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

Secondary

A

Common
Acquired
Often subtle
Often involves more than one component of immune system

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

Conditions associated with secondary immune deficiency

A 
Ageing, Prematurity
Infection
Treatment interventions
Malignancy
Biochemical and nutritional disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phagocyte Deficiencies

A

Defects of phagocyte production, mobilisation and recruitment
Leukocyte Adhesion Deficiency
Defects of recognition
Failure of oxidative killing mechanisms

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

Failure of stem cells to differentiate into neutrophils

A

Primary defect: Recticular Dysgenesis

Secondary defect: After stem cell transplantation

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

Failure of neutrophil maturation

A

Kostmann syndrome

Cyclic neutropaenia

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

Recticular dysgenesis

A

Complete block in leukocyte development

Severe Combined Immuno Deficiency

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

Kostmann Syndrome

A

Defect in receptor or cytokine GCSF
Blocks neutrophil development
Autosomal recessive disorder
Severe chronic neutropaenia

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

Supportive treatments for kostmann syndrome

A

Prophylactic antifungals

Prophylactic antibiotics

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

Definite treatments for kostmann syndrome

A

Stem Cell transplantation

Granulocyte Colony Stimulating Factor

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

Leukocyte adhesion deficiency

A

Rare primary immunodeficiency
Caused by genetic defect in leukocyte integrins (CD18)
Failure to recognise activation markers expressed on endothelial cells

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

Markers of leukocyte adhesion deficiency

A

Localised deep tissue bacterial infections that are difficult to detect
Very high neutrophil count

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

Failure of oxidative killing mechanisms

A

Absent respiratory burst
Deficiency of the intracellular killing mechanism of phagocytes
Inability to generate oxygen free radicals
Failure to degrade chemoattractants and antigens
Persistent accumulation of neutrophils, activated macrophages and lymphocytes

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

Features of chronic granulomatous disease

A 
Recurrent deep bacterial infections
Recurrent fungal infections
Failure to thrive
Lymphadenopathy and hepatosplenomegaly
Granuloma formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Laboratory investigation of chronic granulomatous disease

A

NBT Test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment of chronic granulomatous disease

A

Prophylactic antibiotics
Prophylactic antifungals
Stem cell transplantation
Gene therapy

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

Investigations in phagocyte recruitment function

A

Full blood count & differential
Presence of pus
Expression of neutrophil adhesion molecules

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

Investigations in phagocyte recognition function

A

Chemotactic assays

Phagocytosis assays

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

Investigations in phagocyte killing function

A

NBT test of oxidative killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What drives immunoglobulin class switching?

A

CD4 cell

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

What is the first antibody secreted from the bone marrow?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Antibody functions

A

Antigen receptors (IgM and IgD)
Opsonisation (IgG)
Neutralisation (IgA)
Mast cell activation (IgE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How can the adaptive immune system go wrong?

A

Defects of hematopoietic stem cells
Defects of lymphoid precursors (SCID)
Failure of Thymic development
Disorders of T cell effector function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Clinical phenotype of severe combined immunodeficiency

A 
Unwell by 3 months of age
Persistent diarrhoea
Failure to thrive
Infection of all types
Unusual skin disease
Family history of early infant death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Causes of SCID

A

Deficiency of cytokine receptors
Deficiency of signalling molecules
Metabolic defects
Defective receptor arrangements

28
Q

X-linked SCID

A

Mutation of a component of the IL-2 Receptor
Results in inability to respond to cytokines
-Failure of T cell and NK cell development
-Production of immature B cells

29
Q

DiGeorge Syndrome

A

Failure of thymic development

Results in T cell immunodeficiency

30
Q

Phenotype of DiGeorge Syndrome

A 
Congenital heart defects
Cleft palate
Hypocalcaemia
Developmental delay
Psychiatric disorders
Oesophageal atresia
T cell lymphopaenia
31
Q

Laboratory results for DiGeorge Syndrome

A

Absent or decreased number of T cells
Normal or increased B cells
Normal NK cells numbers

32
Q

Disorders of T cell effector function

A

Cytokine production
Cytotoxicity
T-B cell communication
(IFNy deficiency, IL-12 deficiency)

33
Q

First line investigations of T cell deficiencies

A

Total white cell count and differential
Quantitation of lymphocyte subpopulations
Serum immunoglobulins

34
Q

Second line investigations of T cell deficiencies

A

Functional tests of T cell activation and proliferation
Additional tests of T lymphocyte lineage
HIV test

35
Q

Immune deficiencies affecting B lymphocytes

A

B cell maturation defects
Failure of TFH cell co-stimulation
Failure of IgA production (Selective IgA deficiency)
Failure of production of IgG (Common variable immune deficiency, Selective antibody deficiency)

36
Q

First line investigations of B cell deficiencies

A

Total white cell count and differential

Serum/ urine immunoglobulins

37
Q

Second line investigations of B cell deficiencies

A

Quantitation of B and T lymphocytes

Specific antibody responses to known pathogens

38
Q

Hypersensitivity Reaction

A

Immune response that results in bystander damage to the self
Usually exaggeration of normal immune mechanisms

39
Q

Type 1 Hypersensitivity reaction

A

Immediate hypersensitivity

40
Q

Type 2 hypersensitivity reaction

A

Direct cell killing

41
Q

Type 3 hypersensitivity reaction

A

Immune complex mediated

42
Q

Type 4 hypersensitivity reaction

A

Delayed type hypersensitivity

43
Q

What type of hypersensitivity reaction is allergic reaction?

A

Type 1: Immediate hypersensitivity

44
Q

Allergy

A

IgE-mediated antibody response to external antigen

45
Q

The ‘Hygiene Hypothesis’

A

Changes in microbial stimuli influences the maturation of the immune response
General decrease in infectious burden during early life
results in increased predisposition to allergic conditions during childhood

46
Q

Vasoactive substances produced by mast cells

A

Histamine, Tryptase, Heparin
Leukotrienes, prostaglandins
TNFa, IL-4

47
Q

The role of mast cells in allergic reactions

A

Express receptors for Fc region of IgE antibody on their surface
Release of vasoactive mediators (histamine, tryptase)
Increased cytokine and leukotriene transcription

48
Q

Mast cell stabilisers

A

Sodium cromoglycate
Stabilises mast cell membranes
Prevents release of inflammatory mediators

49
Q

Anti-histamine

A

H1 Receptor antagonists

Block biological effects of histamines

50
Q

Leukotriene receptor antagonists

A

Montelukast

Blocks effects of leukotrienes

51
Q

Adrenaline

A

Acts on B2 adrenergic receptors to constrict arterial smooth muscle

52
Q

Pathophysiology of direct cell killing (type 2)

A

Antibody binds to cell surface antigen

Results in activation of complement and opsonisation

53
Q

Functions of antibody

A

Activates B lymphocytes
Acts as opsonins
Mast cell degranulation
Causes antigen clumping and inactivation of bacterial toxins
Activates antibody dependent cellular activity
Activates complement

54
Q

Effects of complement activation

A

Chemotaxis
Solubilization of immune complexes
MAC-direct killing of bacteria
Opsonisation

55
Q

Which fragments of complement proteins released after activation increase permeability of blood vessels

A

Anaphylotoxins (C3a and C5a)

56
Q

Clinical examples of type 2 hypersensitivity

A

Acute haemolytic transfusion reaction

Drug induced haemolysis

57
Q

Blood type A

A

Surface antigen A

Anti-B antibodies

58
Q

Blood type B

A

Surface antigen B

Anti-A antibodies

59
Q

Blood type AB

A

Surface antigen A and B

Neither anti-A or anti-B antibodies

60
Q

Type O

A

Neither surface A or B antigens

Anti- A and anti-B antibodies

61
Q

Type 2 hypersensitivity management

A

Plasmapheresis

Immunosuppression

62
Q

Pathophysiology of type 3 hypersensitivity

A

Antibodies bind to soluble antigens forming small immune complexes
These are trapped in small blood vessels, joints and glomeruli

63
Q

Management of type 3 hypersensitivity reaction

A

(Avoidance)
Corticosteroids to reduce inflammation
Immunosuppression to decrease production of antibody

64
Q

Autoimmune diseases associated with delayed hypersensitivity reaction

A

Type 1 diabetes
Psoriasis
Rheumatoid arthritis

65
Q

Non-autoimmune diseases associated with delayed hypersensitivity reaction

A 
Contact dermatitis
Tuberculosis
Leprosy
Sarcoidosis
Cellular rejection of organ transplant
66
Q

Pathophysiology of type 4 hypersensitivity reaction

A

Initial sensitisation to antigen creates ‘primed’ generation of effector Th1 and memory T cells
Subsequent exposure activates previously primed T cells
Recruitment of macrophages, lymphocytes, neutrophils, proteolytic enzymes, inflammation…

67
Q

Management of type 4 hypersensitivity reaction

A

Watchful waiting
NSAIDS
Systemic corticosteroids

Respiratory (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions