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Year 1 POM > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A
  • Inflammation is non-specific response to cellular injury
  • Designed to remove the cause and conseuqnce of injury
  • Complex tightly regulated process
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2
Q

What are the causes of inflammation?

A
  • Pathogens
  • Allergents
  • Autoantigens
  • Physcial damage
  • Extreme temperature
  • Non-apoptotic cell death
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3
Q

What are disease causing inflammation?

A
  • Infection
  • Autoimminity
  • Hyoersensitivity
  • Trauma
  • Fibrotic disease
  • Cancer
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4
Q

What are the cell types in inflammation?

A
  • Epithelial cells
  • Endothelial cells
  • Neutrophils
  • Macrophages
  • Lymphocytes
  • Eoisingphils
  • Mast cells
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5
Q

What is acute inflammation?

A
  • Inflmmation is rapid response non-specific response to cellular injury
  • Change in local blood flow - structural changes in microvasculature - recruitment/accumulation of immune cells and proteins
    1. Steady state
    2. Damage
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6
Q

What is damage in acute inflammation?

A
  1. Inflammatory signals: nonapoptoic cell death, detection of forge in in material
  2. Vasodilators rebased: histmaine, nitric chide
  3. Vascular changes: increased permeability, dilation, reduced flow, plasma leakage
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7
Q

What are examples of soluble mediators?

A
  1. Histamine
  2. Prostaglandins
  3. Cytokines (TNF, IL-1)
  4. Chemokines
  5. Complement (C5a, C3a, C4a)
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8
Q

Describe histamine

A

Principle Source: mast cells, basophils, platelets

Actions: vasodilation, increased vascular permeability, endothelial activation

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9
Q

Describe prostaglandins

A

Principle Source: mast cells, leukocytes

Actions: vasodilation, pain, fever

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10
Q

Describe cytokines (TNF, IL-1)

A

Principle Source: macrophages endothelial cells, mast cells

Actions: endothelial activation (adhesion meoclules), fever, malaise, pain, anorexia, shock

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11
Q

Describe chemokines

A

Principle Source: leukocytes, activated macrophages

Actions: chemotaxis, leukocytes activation

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12
Q

Describe complement (C5a, C3a, C4a)

A

Principle Source: plasma (produced in the liver)

Actions: leukocytes chemotaxis and activation vasodilation (mast cell stimulation), opsonisation

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13
Q

What is exudate?

A

Fluid proteins cells that have seemed out of a blood vessel

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14
Q

What is immune cell recruitment?

A

-Recruitment and inflammation signals at the site of manage e.g. chorines produced
-Chemokines diffuse out to form a gradient
-Leukocyytes expressing complementary chemokine receptors receptors migrate toward the chemokine source
E.G. Chemokine: CXCL8 otherwise known as IL-8
Receptors: CXCR1 and CXCR2, g-coupled 7-transmembrane proteins
Cell type: Neutrophils. Often the first cell type recruited to the site of inflammation

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15
Q

What happens during neutrophil extravasation?

A
  1. Chemoattraction: cytokines - endothelial upregualtion of adhesion molecules e.g. selections
  2. Rolling adgension: carbohydrate ligands in a low affinity state on neutrophils bind selectness e.g. PSGL1 (selectin P ligand) binds P and E-selectins
  3. Tight adhesion: chemokine promote low to high affinity switch in integrins LFA-1, Mac-1 – enhance binding to ligands e.g. ICAM-1/2
  4. Transmigration: - Cytoskeletal re-arrangement and extension of pseudopodia. Mediated by PECAM interactions on both cells.
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16
Q

What is the function of a neutrophil at sight of inflammation?

A
  1. Pathogen recognition: e.g. use of TLR4 and CD14 to identify lipopolysaccharides (LPS) present in gram-negative bacteria
  2. Pathogen clearance: phagocytosis, netosis
  3. Cytokine secretion: recruitment and activation of other immune cells
  4. Phagocytosis: -Large particles engulfed into membrane bound vesicles (phagosomes)-Phagosome fuses with lysosome (vesicles containing enzymes e.g. elastase and lysozyme) -> phagolysosome -Ractive oxygen species (ROS) – phagocyte NADPH oxidase -Antimicrobial peptides – e.g. defensins.
17
Q

What is the resolution of acute inflammation?

A
  1. Pathogen recognition: Immune cells (e.g. neutrophils) and antimicrobials (e.g. antibodies) will infections or particulates.
  2. Short half life: -Neutrophils (especially activated) have a rapid half-life-inflammatory mediators are turned over rapidly
  3. Macrophages: -Clear apoptotic cells -Produce anti-inflammatory mediators
  4. Repair/wound healing: -Covered in the after online material (seals any gaps in membrane)
18
Q

What are the reasons for chronic inflammation?

A

Chronic inflammation: e.g. rheumatoid arthritis, asthma, glomerulonephritis, hepatitis, psoriases, MS, IBS

  1. Persistent inflammatory stimuli: persistent/prolonger infection e.g. YB, hepatitis B/C, persistent toxic simuli e.g. allergens, pollutes, unclear able particulates e.g. silica, autoimmunity e.g. self antigens
  2. Distinct immune cell infiltrate: inflammatory macropages, T cells and other lymphocytes, plasma (antibody secreting) cells
  3. Viscous cycle: no clearance of inflammatory agent, bystander tissue destruction, concurrent repair processes (fibrosisi and abiogenesis)
19
Q

What are the good and bad parts of macrophages?

A
  • Can recruited as monocytes to the site of inflammation but ALSO tissue resident
  • GOOD: phagocytic, cytotoxic, anti-inflammatory (e.g. TGF-beta, IL-10), wound repair
  • BAD: cytotoxic, inflammatory, pro-fibrotic
20
Q

What are T cell lymphocytes?

A
  • Innate and adaptive immune cells work together
  • T cells in inflammation
  • pro-inflammatory (e.g. TNF, IL-17, IFN-γ)
  • Cytotoxic (e.g. granzymes, perforin)
  • Regulatory (e.g. TGF-β)
21
Q

What are B cell lymphocytes?

A
  • Generate plasma cells that secrete antibody.
  • Protective, clearing infection
  • Inflammatory, driving reactions against self
  • Can either be local to inflammatory site, or operate remotely
22
Q

What is part of granulomatous inflammation?

A
  • Granulomatous inflammation: e.g. TB, leprosy, foreign body granuloma, tumour reactions, sarcoidosis, Crohn’s disease
  • Chronic inflammation with distinct pattern of granuloma formed
  • Aggregation of activated macrophages and a barrier designed for clearance
  • Triggered by strong T cell responses
  • Resistant agents (e.g. mycobacterium tumour)
  • Granuloma: ball of activated lymphocytes and macrophages
  • Giant cells: fused macrophages with horseshoe-shaped nuclei
23
Q

What are the features of acute inflammation?

A
  • Immediate onset; lasts a few days
  • Vasodilation, increased vascular permeability, leukocyte response
  • Neutrophil predominate
  • Histamine release
  • Prominent necrosis
  • Outcomes include: complete resolution / progression to chronic inflammation
24
Q

What are the features of chronic inflammation?

A
  • Delayed onset: may last weeks, months or years
  • Persistent inflammation, ongoing tissue injury, attempts at healing
  • Monocytes/macrophages predominate
  • Ongoing cytokine release
  • Prominent scarring
  • Outcomes include: scarring / loss of function
25
Q

What are the possible positive outcomes of acute and chronic inflammation?

A

clear inflammatory agent, removed damaged cells, restore normal tissue function

26
Q

What are the possible negative outcomes of acute and chronic inflammation?

A

excess tissue damage, scarring, loss of organ function-organ failure

27
Q

What does wound healing lead to?

A

Leads to extracellular matrix (e.g. collagen) deposition

28
Q

What are the consequences of inflammation?

A
  • Broncho-pneumonia
  • Scarring
  • Wound healing in sensitive tissue
29
Q

What are key features of chronic inflammation?

A
  • cytokines
  • caused by persistent damage (e.g. persistent infection, autoimmunity)
  • form Granulation tissue
30
Q

What are the histology of chronic inflammation?

A

Lots of macrophages, lymphocytes and plasma cells

31
Q

What is the difference between chronic and acute inflammation with onset?

A

Acute:
-Immediate onset; lasts a few days
Chronic:
-Delayed onset; may last weeks, months or years

32
Q

What is the difference between chronic and acute inflammation with vascular?

A

Acute:
-Vasodilation, increased vascular permeability, leukocyte response
Chronic:
-Persistent inflammation, ongoing tissue injury, attempts at healing

33
Q

What is the difference between chronic and acute inflammation with histology?

A

Actue:
-neutrophils predominate
Chronic:
-Monocytes/macrophages predominate

34
Q

What is the difference between chronic and acute inflammation with release?

A

Acute:
-Histamine release
Chronic:
-Ongoing cytokine release

35
Q

What is the difference between chronic and acute inflammation with prominence?

A

Acute:
-Prominent necrosis
Chronic:
-Prominent scarring

36
Q

What is the difference between chronic and acute inflammation with outcome?

A 
Acute: 
-Complete resolution 
-Progression to chronic inflammation 
Chronic: 
-Scarring 
-Loss of function

Year 1 POM (39 decks)

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