Week 2 - Pathology Flashcards

1
Q

What 4 cells make up the innate immune system?

A

1) Macrophages
2) Neutrophils
3) Eosinophils
4) Basophils

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2
Q

Macrophages:

The 3 ways they function?

A

1) Phagoctytosis of pathogens
2) Present antigens to T cells
3) Produce cytokines

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3
Q

Neutrophils:

The 2 ways they function?

A

1) Phagocytosis of pathogens

2) Release hyrdrolytic enzymes

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4
Q

Eosinophils:

The 3 ways they function?

A

1) Degranulation onto surface of parasites
2) Produce inflammatory cytokines
3) Phagocytosis of antigen-antibody complex

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5
Q

Basophils:

The 2 ways they function?

A

1) Release chemotactic cytokines

2) Interact with IgE to cause local inflammatory response

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6
Q

What 4 proteins make up the Innate immune response?

A

1) Antibodies
2) Cytokines
3) Complement
4) Inflammatory mediators

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7
Q

What are the 3 cell types that make up the Adaptive immune system?

A

Lymphocytes:

1) B-cells
2) CD4+ (T-cells)
3) CD8+ (T-cells)

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8
Q

How do CD4+ cells function?

A
  • Recognises antigens on MHC proteins produced by Antigen presenting cells
  • Produce cytokines to activate macrophages and inflammation
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9
Q

How do CD8+ cells function?

A

Directly kill pathogens

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10
Q

How do B-cells function?

A
  • Antibody production

- Stimulation of CD4+ cells

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11
Q

What are the 3 main functions of Antibodies?

A

1) Opsonisation (makes pathogens easier to phagocytose)
2) Activate complement proteins
3) Neutralise toxins and pathogens

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12
Q

What are the 4 functions of Complement proteins?

A

1) Promote inflammation
2) Opsonisation of pathogens
3) Insertion of MAC (Membrane attack complexes) onto pathogen membranes
4) Cytolysis (killing of pathogens)

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13
Q

Class 1 MHC present to what cells?

A

CD8 T cells

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14
Q

Class 2 MHC present to what cells?

A

CD4 T cells

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15
Q

What are the 4 types of Antibodies?

A

1) IgM
2) IgA
3) IgG
4) IgE

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16
Q

How does the IgM Antibody function?

A
  • Part of the primary immune response
  • Low affinity
  • Activate complement proteins
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17
Q

How does the IgA Antibody function?

A

Neutralises pathogens

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18
Q

How does the IgG Antibody function?

A
  • Secondary immune response
  • High affinity
  • Activates complement proteins
  • Opsonises pathogens
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19
Q

How does the IgE Antibody function?

A
  • Involved in allergy response

- Bind to mast cells (resulting in histamine release)

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20
Q

What is the primary immune response?

A
  • First response to a pathogen
  • Mainly IgM mediated
  • Lower affinity (i.e. less effective)
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21
Q

What is the secondary immune response?

A
  • Later onset than primary
  • Mostly IgG mediated
  • Higher affinity (i.e. more effective)
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22
Q

What are the 3 categories of immune system dysfunction?

A

1) Hypersensitivity
2) Autoimmune
3) Immunodeficiency

23
Q

What are the 2 types of autoimmunity?

A

1) Organ specific ( e.g. T1DM)

2) systemic (e.g. Rheumatoid arthritis)

24
Q

What are the 4 types of Hypersensitivity?

A

1) Type 1 - Immediate/atopic
2) Type 2 - Cytotoxic/Antibody dependent
3) Type 3 - Immune complex
4) Type 4 - Cell mediated

25
Q

What is Type 1 hypersensitivity?

A
  • Immediate/atopic
  • Occurs immediately
  • Mediated by IgE binding to mast cells
  • Increased severity on repeated exposure
26
Q

Give 3 examples of Type 1 hypersensitivity conditions

A

1) Asthma
2) Eczema
3) Hay fever

27
Q

How does Type 1 hypersensitivity work?

A
  • Antigen presented to CD4 cells resulting in IgE production

- IgE binds to mast cells and leads to degranulation (release of histamines, prostglandins and inflammatory cytokines)

28
Q

What effect does Type 1 hypersensitivity have on tissue?

A

1) Early phase (occurs within minutes) - smooth muscle contraction and increased vascular permeability due to histamine and prostglandins)
2) Late Phase (hours to days) - T-cells recruited resulting in sustained smooth muscle contraction and tissue remodeling

29
Q

What type of hypersensitivity is Anaphylaxis?

A

Type 1

30
Q

What is the pathology of Anaphylaxis?

A
  • A Severe and systemic Type 1 hypersensitivity
  • Widespread degranulation of mast cells resulting in
    widespread vascular permeability which leads to closure of airways due to swelling and loss of circulatory volume (Shock)
31
Q

What is Type 2 Hypersensitivity?

A
  • Antibodies attack human cells directly. (an autoimmune disease)
  • Mostly IgG/IgM mediated
32
Q

Name 3 diseases that are categorised as Type 2 Hypersensitivity

A

1) Bullous pemphigoid
2) Grave’s disease
3) Drug associated haemolysis

33
Q

What is Bullous Pemphigoid?

A
  • Type 2 Hypersensitivity

- Formation of blisters

34
Q

What is Type 3 Hypersensitivity?

A
Immune complexes (IgG/IgM) bind to a soluble antigen which then aggregate in small blood vessels.
- This causes occlusion, complement activation and inflammation.
35
Q

Name 2 diseases that are categorised as Type 3 Hypersensitivity

A

1) Rheumatoid arthritis

2) Systemic lupus erthematosus (SLE)

36
Q

What is Type 4 Hypersensitivity?

A
  • Cell mediated (lymphocytes)
  • Delayed Type Hypersensitivity (several days after exposure)
  • Lymphocytes are sensitised to own cells and directly attack them
37
Q

Name 2 diseases that are categorised as Type 4 Hypersensitivity

A

1) Type 1 diabetes

2) Hashimoto’s thyroiditis

38
Q

Give an example of 3 organ specific autoimmune conditions

A

1) T1DM
2) Myasthenia Gravis
3) Addison’s disease

39
Q

Give an example of 3 systemic autoimmune conditions

A

1) Rheumatoid arthritis
2) Systemic Lupus (SLE)
3) Multiple Sclerosis

40
Q

Outline the Pathophysiology of T1DM

A
  • Autoimmune destruction of pancreatic beta cells

- Leads to insulin deficiency

41
Q

Outline the Pathophysiology of Myasthenia Gravis

A
  • Syndrome of fatiguable muscle weakness

- IgG against acetylcholine receptor preventing signal transduction

42
Q

Outline the Pathophysiology of Rheumatoid arthritis

A
  • Chronic, auto-inflammatory autoimmune disease
  • IgM directed against IgG (this is called Rheumatoid factors)
  • Aggregate in synovial fluid and other tissue
  • This leads to inflammation.
43
Q

Give 5 signs associated with Rheumatoid arthritis

A

1) Pulmonary fibrosis and nodules
2) pericarditis
3) Soft tissue nodules
4) small vessel vasculitis
5) Joint pain/deformities

44
Q

What is the pharmacological management of autoimmune diseases?

A

1) Immunosuppression (steroids etc)

2) Biologic therapies (Infliximab, Etanercept etc)

45
Q

What is Inflammation?

A
  • Physiological response to tissue injury

- Has vascular and cellular components

46
Q

Name 4 causes of inflammation

A

1) Infection
2) Tissue necrosis (burns, radiation etc)
3) foreign materials
4) Immune reactions

47
Q

What are the 5 main features of inflammation?

A

1) Redness (vessels dilate)
2) Heat (increased blood flow)
3) Pain (stimulation of pain receptors)
4) Swelling (fluid accumulates)
5) Loss of function (due to selling and pain)

48
Q

There are 5 steps in the Inflammatory process, what are they?

A

1) Vascular changes
2) Extravasation
3) Leukocyte activation
4) Removing offending agent
5) Termination

49
Q

Inflammatory process:

What occurs during vascular changes?

A
  • Vasodilation
  • Increased vascular permeability
  • Vascular congestion
  • Endothelial activation
50
Q

Inflammatory process:

What occurs during Extravasation?

A
  • Margination
  • Rolling
  • Adhesion
  • Migration
  • Fuck learning it in more detail
51
Q

Inflammatory process:

What occurs during leukocyte activation?

A
  • Toll like receptors on leukocytes recognise pathogen

- Activates T cells/CD4/CD8 cells to go to work

52
Q

Inflammatory process:

What occurs during the removal of the offending agent?

A
  • Phagocytosis (WBC’s) leading to killing/degradation of pathogen
53
Q

Inflammatory process:

What occurs during termination?

A
  • Removal of stimulus

- Short neutrophil life