Inflammation Flashcards

1
Q

What is Inflammation?

A
  • Latin, Inflamatio, to set on fire
  • Biological reaction to noxious stimuli such as microbes, burns and trauma
  • Fundamentally protective process but may potentially be harmful leading to tissue injury
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2
Q

What are the two types of inflammation?

A
  • Acute inflammation
  • Chronic Inflammation
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3
Q

What are the 5 clinical signs of acute inflammation

A
  • Rubor (redness)
  • Tumour (Swelling)
  • Calor (Heat)
  • Dolor (Pain)
  • Functio Laesa (Loss of function)
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4
Q

What is acute inflammation?

A
  • Rapid host response to deliver leucocytes and plasma proteins such as antibodies to the sites of infection or tissue injury
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5
Q

Acute inflammation protects the body from further injury in response to what?

A
  • Infections
  • Trauma (blunt or penetrating)
  • Burns/frostbite (thermal and chemical)
  • Allergic reactions
  • Tissue necrosis
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6
Q

How fast does acute inflammation occur and last?

A
  • Occurs immediately and lasts hours-days
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7
Q

What reactions does acute inflammation consists of?

A
  • Consists of vascular and cellular reactions
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8
Q

What are the three major components of acute inflammation? Explain them

A
  • Vascular dilation- to increase blood flow
  • Structure changes - in the microvasculature to allow plasma proteins and leukocytes to leave the circulation
  • Emigration - of the leukocytes from the microvasculature, their accumulation in the injury site and their activation to eliminate the offending agent
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9
Q

What happens in Vascular reaction

A
  • Vessel dilation and increased blood flow
  • Leakage of plasma fluid and protein
  • Leukocyte emigration and accumulation in the site of injury
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10
Q

What happens in vessel dilation and what is its purpose

A
  • One of the earliest signs of acute inflammation - quick
  • To increase blood flow
  • Results in heat and redness (hyperaemia)
  • Induced by the actions of several mediators on VSM: Histamine, Bradykinin, NO
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11
Q

What are the 3 mediators of vascular reactions?

A
  • Histamine
  • Bradykinin
  • Nitric Oxide
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12
Q

What is the source and function of Histamine

A
  • Source: Mast cells, basophils, platelets
  • Function: Arteriole dilation, increased of venous permeability
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13
Q

What is the Source and Function of Bradykinin

A
  • source: kinin system
  • Function: Vasodilation, increase vascular permeability, pain
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14
Q

What is the source and function of Nitric oxide

A
  • Source: Endothelial cells
  • Function: Vasodilatation
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15
Q

What happens in Increased vascular permeability (leakage)

A
  • A hallmark of acute inflammation
  • Allow plasma fluid and protein to escape from the circulation into extracellular tissue
  • The cause of oedema
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16
Q

Explain the mechanisms of Increased vascular permeability

A
  • Endothelial cell contraction to increase intracellular spaces
  • Endothelial cell injury and detachment
  • Increased transport of fluid and protein through the endothelial cells
17
Q

What is Leukocyte recruitment?

A
  • Movement of leukocytes from vessel lumen to interstitial tissue is called extravasation
18
Q

What happens in extravasation

A
  1. Leukocyte adhesion to endothelium
    - Endothelial adhesion molecules: P-selectin, E-selectin, CD34, ICAM-1, VCAM-1
  2. Leukocyte migration through endothelium
  3. Chemotaxis of leukocytes
    - A process that leukocytes emigrate toward the site of injury driven by substances called chemoattractants
19
Q

What are the Cellular components of the Acute inflammation?

A
  • Leukocytes - some act as phagocytes; others release enzymatic granules
  • Migration of these leukocytes is a critical step of inflammation
  • Initially phagocytic cells - neutrophils followed by monocytes
  • Produce inflammatory mediators that maintain the inflammatory response
20
Q

What is Chemotaxis?

A
  • A process that leukocytes are attracted by chemotactic agents tot eh site of injury once outside of the blood vessel
21
Q

Name Chemoattractants

A
  • Exogenous: bacterial products
  • Endogenous: complement components, cytokines, products of lipoxygenase pathway (leukotriene B4)
22
Q

Explain Leucocyte recognition through leukocyte receptors

A
  • Receptor for microbial products: Toll-like receptors (TLRs)
  • G protein-coupled receptors: Recognise short bacterial peptides containing N-formyl methionyl residues
  • Receptors for opsonins: Examples of opsonins - antibodies, complements, lectins
  • Receptor for cytokines: INF
23
Q

What is Phagocytosis?

A
  • Removal of the offending agents
24
Q

Explain Phagocytosis

A
  1. Recognition and attachment
  2. Engulfment
    - Engulfed particle fuses with lysosome to form phagolysosome
    - Degranulation
  3. Killing
    - ROS (oxidative burst generated by NADPH oxidase)
    - Other lysosomal enzymes
25
Q

Name Acute inflammatory cytokines

A
  • TNF-alpha
  • IL-1
  • IL-6
  • chemokines
26
Q

What is the sources for TNF-alpha?

A
  • Macrophages, mast cells, T lymphocytes
27
Q

What is the sources for IL-1?

A
  • Macrophages, endothelial cells, epithelial cells
28
Q

What is the sources for IL-6?

A
  • Macrophages, other cells
29
Q

What is the sources for Chemokines?

A
  • Macrophages, endothelial cells, T lymphocytes, mast cells, other cells
30
Q

Name 4 Morphological patterns for acute inflammation

A
  • Fibrinous
  • Purulent
  • Serous
  • Ulcerative
31
Q

What is Fibrinous? (Morphological patterns)

A
  • Characterised by fibrinous exudate which can lead to scar formation and limitation of function
32
Q

What is Purulent? (Morphological patterns)

A
  • Pus filled fluid consisting of neutrophils and dead cells, typically caused by staphylococcal infections
33
Q

What is Serous? (Morphological patterns)

A
  • Copious effusion of non-viscous serous fluid. Typical example is skin blister
34
Q

What is Ulcerative? (Morphological patterns)

A
  • Necrotic loss of tissue from the surface, exposing lower layers leading to formation of an ulcer
35
Q

What are the outcomes of acute inflammation?

A
  • Complete resolution: injury is limited or short-lived, with little tissue damage
  • Healing by connective tissue replacement (fibrosis): Substantial tissue damage, fibroblasts grow into the area of damage
  • Progression to chronic inflammation