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Human Diseases > W1 3 Inflammation > Flashcards

W1 3 Inflammation Flashcards

1
Q

What are the 5 cardinal signs of inflammation?

A

Heat, redness, swelling, pain, loss of function

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2
Q

What is inflammation?

A

A host response to eliminate microbes and injured cells

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3
Q

What are the 2 broad types of inflammation?

A

Acute and chronic

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4
Q

Features of acute inflammation

A

Has a fast onset. Mainly neutrophils infiltrate. Tissue injury is usually mild and self-limited. Prominent local and systemic signs.

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5
Q

Features of chronic inflammation.

A

Slow onset. Lymphocytes and plasma cells infiltrate. Often severe and progressive tissue injury. Less local and systemic signs.

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6
Q

What is the innate immune system?

A

Where particular inflammatory cells can respond to infection in a non-specific way. Tends to occur quickly within minutes or hours and mainly comprises neutrophils. (Links to acute inflammation)

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7
Q

What is the adaptive immune system?

A

Mainly mediated by B and T cells and plasma cells. Occurs hours or days after infection. Overlaps with chronic inflammation.

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8
Q

How does initiation of acute inflammation occur?

A

Recognition of infectious organisms and/or damaged cells leads to release/activation of chemical mediators of inflammation.
This can resolve the problem but also cause damage to surrounding tissues.

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9
Q

What cells recognise infectious organisms in acute inflammation?

A

Mechanisms of recognition:
Cell mediated: macrophages, dendritic cells, mast cells, epithelial cells
Plasma protein-derived: complement system

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10
Q

Describe the extracellular mechanism of recognition (of acute inflammation) (image pg17)

A

TLR can bind to bacterial cell wall components, mediating an intracellular signalling pathway. Similarly, other receptors like lectin can identify particular components of pathogens and elicit intracellular pathways. Pathogens are either recognised in cytoplasm or engulfed by vesicles. End result is the secretion of inflammatory cytokines, promoting further inflammation. Principally is TNF.

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11
Q

Describe the inflammasome pathway recognition of acute inflammation (image pg17)

A

Intracellular complex that can recognise components of pathogens. Result is the production of interleukin-1, a powerful promoter of acute inflammation (like TNF).

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12
Q

Give some cell-derived chemical mediators of inflammation

A

Histamine, PGs, leukotrienes, ROS, NO, cytokines, chemokines

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13
Q

Give some examples of plasma protein-derived chemical mediators of inflammation

A

Complement, linings, proteases activated during coagulation

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14
Q

What are the 2 major examples of inflammatory cytokines and what are they produced by?

A

Tumour necrosis factor (TNF) and interleukin-1 (IL1) are mainly produced by macrophages

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15
Q

What are the effects of inflammatory cytokines?

A

Endothelial activation
Leukocyte activation
Systemic effects

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16
Q

Describe how inflammatory cytokines cause endothelial activation (pg18 image)

A

They increase expression of cell adhesion molecules on endothelial cells and allows them to grab hold of inflammatory cells that are circulating in the blood into the area of inflammation.
Endothelial cells produce cytokines in response to TNF and IL1, amplifying the inflammatory response.
Increase vascular permeability of endothelial cells, so allows fluid to accumulate in the area, dilating effects of toxins and pathogens, allowing cells ready access

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17
Q

How do inflammatory cytokines activate leukocytes?

A

TNF and IL1 activate leukocytes to form IL1, IL6 and chemokines

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18
Q

What is the complement system activated by? (Pg19 image)

A

Directly by a microbe
Lectin pathway
Classical pathways (antibody association)

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19
Q

How does the activation of the complement system cause inflammation? (Pg19)

A

Can be mediated by the production of chemokines which recruit inflammatory cells to the area of inflammation
C3b is an opsonising function - binds to pathogen and allows macrophages to phagocytose them
Can be damaging to microbes by forming membrane attack complex (MAC), which punches a hole in the organism and causes it to fragment

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20
Q

What are the vascular changes in inflammation?

A

Vasodilatation, leakage of plasma proteins and oedema, migration of neutrophils from systemic circulation into tissue

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21
Q

Histological appearance of acute inflammation

A

Pg20
Congested dilated capillary with numerous neutrophils migrating through the wall into the surrounding oedematous tissues. Scattered macrophages present in the stroma.

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22
Q

How do leukocyte’s migrate? Pg20

A

Neutrophil and inflammatory cells will be recruited from the systemic circulation from lumen of blood vessels into the tissue by interacting with the endothelium
Inflammatory cytokines like TNF and IL1 cause the increased expression of lymphocyte recruitment molecules on the surface of endothelial cells. These include the selectins which allow the leukocytes to roll and transiently attach onto receptors, and the integrins which form stronger bonds between leukocyte and endothelial cells.
Once these inflammatory cells have anchored onto the endothelium, they are able to migrate through the barrier of the endothelium into the underlying tissue, where they can then exert their effects to deal with the infections present.

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23
Q

What are the elements of leukocyte activation?

A

Phagocytosis
Release of extracellular effectors (ROS, enzymes, NETs)
Amplification of the inflammatory response

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24
Q

What are NETs?

A

Neutrophil extra-cellular traps
Neutrophils extrude their DNA into the extracellular environment, creating a mesh which embeds to bacteria

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25
Q

When does disease associated with acute inflammation occur?

A

Disease occurs when inflammatory response is excessive or inappropriate for the stimulus, due to damage of host tissues by the inflammation.

26
Q

Give examples of diseases associated with acute inflammation

A

Acute appendicitis, acute meningitis, dental abscess

27
Q

What is pus?

A

A collection of neutrophils, oedema fluid and necrotic debris

28
Q

What are the systemic effects of acute inflammation?

A

Fever
Elevated levels of acute-phase proteins
Leukocytosis

29
Q

How does fever occur from acute inflammation?

A

Cytokines lead to increase in COX activity
Increased prostaglandins reset the target temperature in the hypothalamus

30
Q

How do elevated levels of acute-phase proteins occur from acute inflammation?

A

CRP, serum amyloid A and fibrinogen (markers of inflammation)
Function as opsonise by binding pathogens, facilitating phagocytosis.
Fibrinogen binds to RBCs leading to increased ESR

31
Q

How does leukocytosis occur from acute inflammation?

A

Cytokines cause increased production of white blood cells (mainly neutrophils) from the bone marrow

32
Q

What is an abscess?

A

Localised collection of pus in a cavity formed by disintegration of tissues

33
Q

Antigen presentation to T cells can occur by MHC class I or MHC class II molecules. Explain MHC class I molecules.

A

Expressed by all nucleated cells
Display antigens synthesised in the cytoplasm eg viral antigens
Interact with CD8+ cytotoxic T-cells

34
Q

Antigen presentation to T cells can occur by MHC class I or MHC class II molecules. Explain MHC class II molecules.

A

Expression restricted to antigen presenting cells: dendritic cells, macrophages, B-cells
Display antigens synthesised outside the cell eg bacterial antigens
Interact with CD4+ helper T-cells

35
Q

Describe T cell activation, migration and effects (pg23)

A

CD4+ T cells responding to a particular antigen derived from a bacteria engulfed from an APC
CD8+ T cell responding to an intracellular pathogen, eg virus
Results in the profile ration of CD4 and CD8 T cells, which travel in the blood to the area of inflammation:
- CD8 cells interact directly with infected cells in target organ, causing direct cell death
- CD4 T cells interact with local cells, particularly macrophages and cause cytokines production
Cytokines can cause secondary effects

36
Q

What are the effector functions of CD8+ T-cells (pg25)

A

Killing of the host cell by 2 distinct pathways
- Fas/Fas ligand pathway
- Granzyme/perforin pathway
Both result in cascade activation leading to apoptosis

37
Q

What are the effector functions of CD4+ T cells (pg25 table!)

A

APCs cause a variety of T helper subsets which can respond to a variety of pathogens
TH2 also promotes fibrosis

38
Q

How does IFN-y drive the M1 macrophage response?

A

Activated macrophages produce a host of enzymes which allow enhanced phagocytosis and killing of bacteria and fungi, and also release of inflammatory mediators including IL-1, amplifying the effect of inflammation.

39
Q

What happens in the absence of IFN-y?

A

M2 macrophage response - in the absence of interferon and presence of other ILs, we can get differently activated macrophages which produce anti-inflammatory cytokines and factors promoting fibrosis.

40
Q

What does B-cell activation result in? (T-cell independent - less common)

A

Direct binding of microbial antigens to B-cell receptor

41
Q

What does B-cell activation result in (T-cell dependent - stronger activation)

A

Internalisation of antigen bound to BCR
Presentation of antigen in MHC class II molecule
Recognition by activated CD4+ helper T-cell (stimulate a TH1 response with immunoglobulin production)

42
Q

What is the main function of B-cells?

A

To form immunoglobulins

43
Q

What are the functions of immunoglobulins?

A

Neutralise microbial toxins
Facilitate phagocytosis through opsonisation, similar to complement
Cause direct cell death
Activation of the complement system

44
Q

History of chronic inflammation

A

Progression from acute inflammation
De novo chronic inflammation
Re-exposure to a previously encountered antigen

45
Q

What is a hypersensitivity reaction?

A

An exaggerated adaptive immune response leading to tissue injury and disease

46
Q

What are causes of hypersensitivity reactions?

A

Microbial antigens
Self antigens (autoimmunity)
Environmental antigens eg pollen

47
Q

Classify Type I-IV hypersensitivity reactions

A

Type I - immediate
Type II - antibody mediated
Type III - immune complex-mediated
Type IV - T-cell mediated

48
Q

Give examples of type I hypersensitivity reactions and state whether it’s acute or chronic inflammation

A

Anaphylaxis, allergies, asthma
Acute/chronic

49
Q

Give examples of type II hypersensitivity reactions and state whether it’s acute or chronic inflammation

A

AHA, goodpasture syndrome
Acute/chronic

50
Q

Give examples of type III hypersensitivity reactions and state whether it’s acute or chronic inflammation

A

Lupus, vascularised, glomerulonephritis
Acute/chronic

51
Q

Give examples of type IV hypersensitivity reactions and state whether it’s acute or chronic inflammation

A

Type I diabetes, tuberculosis, rheumatoid arthritis
Chronic

52
Q

Describe the first phase of a Type I hypersentivity reaction

A

Sensitisation:
- immune system begins to recognise an allergen and cause an abnormal response to an allergen
- allergen is recognised as foreign by B and T cells
- TH2 response, producing IgE
- IgE binds to mast cells

53
Q

Describe the second phase of a type I hypersensitivity reaction

A

Re-exposure to the same allergen
- immediate activation of mast cells, releasing inflammatory mediators
- (particularly histamine, resulting in inflammation)
- cytokines also released which cause further inflammation within a few hours

54
Q

Describe type II hypersensitivity reactions

A

Mediated by antibodies, causing disease by inappropriate activation. Maybe by phagocytosis or chemotaxis and inflammation, or direct action of antibodies on particular receptors.

55
Q

What happens in Type III hypersensitivity reactions? PIC PG30

A

Antibodies form complexes with antigens. These can get stuck and bound onto cells, particularly endothelial cells in blood vessels, causing inflammation in blood vessels, and can cause diseases like kidney diseases like glomerulitis.

56
Q

What happens in a type IV hypersensitivity reaction? (PG30) (most important)

A

Abnormal adaptive immune response to either an infection, allergen, or self antigen
Production of CD4+ cells in response to this which elicits an abnormal inflammatory response that damages the tissues (if cytokine mediated = delayed-type hypersensitivity)
If mediated by CD8+ T cells, there is direct cell death

57
Q

What is granulomatous inflammation?

A

A specific pattern of type IV (delayed-type) hypersensitivity. Only a limited number cause this. Important to recognise.

58
Q

Characteristics of granulomatous inflammation (images pg31/32)

A

Aggregate of epithelioid macrophages +/- giant cells
Typically a collar of lymphocytes
Little phagocytise activity

59
Q

What are the causes of granulomatous inflammation?

A

Infection (eg tuberculosis)
Foreign body (eg cholesterol, sutures)
Drugs
Unknown (eg sarcoidosis)

60
Q

How do granulomas come about? (Pg31)

A

By the TH1 response, producing TNF and IFN-y. IFN-y drives proliferation of macrophages which are activated but unsuccessfully phagocytose the antigen,
So they are epitheloid macrophages, which have a low phagocytes activity, surrounded by lymphocytes around the edge

Human Diseases (75 decks)

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