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FD1 > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

What are the aims of inflammation?

A
  • Get rid of damaged or necrotic tissue
  • Remove microorganisms or other foreign material
  • Sets the scene for regeneration or repair of tissue
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2
Q

How can inflammation be harmful?

A
  • Hypersensitivities e.g. hay fever
  • Autoimmune reactions
  • Prolonged inflammation
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3
Q

What are the cardinal signs of inflammation?

A
  • Redness
  • Swelling
  • Heat
  • Pain
  • Loss of function
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4
Q

What are the 3 components of acute inflammation?

A
  • Increased blood flow
  • Increased vascular permeability
  • Leukocyte emigration
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5
Q

What are the stimuli for acute inflammation?

A
  1. Microorganisms (parasites, fungi, bacteria, viruses)
  2. Necrosis (Ischaemis, trauma, physical + chemical injury)
  3. Hypoxia (HIF-1alpha)
  4. Foreign bodies (cause trauma/ carry microbes)
  5. Hypersensitivity reactions/ autoimmune disease (self antigens)
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6
Q

How do blood vessels change in acute inflammation?

A

-they change in order to allow plasma proteins and cells out of circulation into the site of the stimulus

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7
Q

What is oedema?

A
  • release of excess fluid into tissue or body cavities

- pure fluid (a type of exudate)

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8
Q

What is exudation?

A
  • release of fluid and cells from the circulation
  • an extracellular fluid rich in protein and containing cells
  • high specific gravity
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9
Q

What is contained in pus (purulent exudate)?

A
  • rich in leukocytes (mainly neutrophils)
  • debris of dead cells
  • sometimes microbes
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10
Q

What are ultrafiltrates of plasma caused by?

A
  • caused by loss of osmotic pressure or high hydrostatic pressure
  • creates a transudate
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11
Q

What is a transudate?

A
  • low protein content
  • little or no cellular material
  • low specific gravity
  • e.g. liver/kidney disease
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12
Q

What happens in a normal blood vessel?

A
  • fluid squeezed out of the vessel
  • protein stays in the vessel
  • so the conc increases inside the vessel
  • this drags fluid back inside
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13
Q

What happens in the blood vessels if there is damage?

A
  • damage to the cells
  • endothelial cells told to contract/ gaps appear between them
  • the normal blood pressure will push fluid out
  • protein will also be pushed out due to gaps
  • oncotic pressure loss
  • net movement of fluid out of the vessel
  • becomes red, hot, inflamed
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14
Q

When does vasodilation occur? And what happens first?

A
  • when injury occurs- few seconds of vasoconstriction
  • follows by vasodilation
  • first arterioles dilate opening new capillary bed in the region
    - allows increased blood flow to the tissue
    - causes erythema (heat and redness) at site
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15
Q

What is vasodilation induced by?

A
  • histamine
  • nitric oxide (NO)
  • act on SM of vessels
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16
Q

What does increased vascular permeability allow?

A

-escape of protein-rich exudate into the tissue (oedema)

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17
Q

What are the 3 mechanisms that promote the increase in vascular permeability?

A
  1. Contraction of endothelial cells (increasing interendothelial spaces)
  2. Endothelial injury (necrosis and detachment)
  3. Increased transport through endothelial cells (transcytosis)

may all occur at the same time

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18
Q
  1. Contraction of endothelial cells (describe what happens)
A
  • increased space between the endothelial cells
  • most common mechanism
  • typically an immediate and transient response
  • occurs immediately after exposure to mediator
  • short lived (15-30 mins)
  • mediated by numerous chemical mediators e.g. histamine
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19
Q

Why can contraction of endothelial cells be delayed?

A
  • sometimes delayed with prolonged leakage
  • some forms of mild injury (e.g. after burns, irradiation)
  • vascular leakage begins after delay of 2 to 12 hrs, lasting for several hours/days
  • cause by contraction of endothelial cells/ mild endothelial damage
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20
Q
  1. Endothelial injury (describe)
A
  • direct damage to the endothelial cells leading to necrosis and detachment from basement membrane
    - happens in severe injury (burns)/ actions of endotheliotropic microbes
  • starts immediately after injury
  • sustained for several hours until damaged vessels are thrombosed
  • neutrophils can damage the endothelial cells whilst adhered during inflammation
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21
Q

What are endotheliotropic cells?

A

-microbe that target endothelial cells

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22
Q
  1. Transcytosis (descibe)
A
  • fluid and proteins transported through the endothelial cells
  • channels created by vesicles and vacuoles (vesiculovacuolar organelle) located near intercellular junctions allow the transport
  • mediators e.g. VEGF can promote transport by increasing number and size of channels
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23
Q

What is the role of fibrin in vascular permeability?

A
  • the plasma that leaves the vessel acts to dilute the stimulus of acute inflammation
  • Fibrinogen is one of the proteins which leaves the vessel in exudates
  • fibrinogen polymerises to form fibrin
  • fibrin:
    - stops the stimulus spreading into nearby tissue
    - allows leukocytes to target the the inciting cause of inflammation
    - assists in blood clotting
    - acts as scaffold for epithelial migration during wound healing
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24
Q

Fluid loss + increased vessel diameter =

A

slower blood flow

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25
Q

Increased concentration of red cells =

A

increased viscosity of blood

26
Q

What is stasis observed as?

A

vascular congestion

27
Q

Stasis:

A
  • allows leukocytes to accumulate on the vascular endothelium
  • endothelial cells are activated by mediators of inflammation, so express increased levels of adhesion molecules
  • leukocytes can then adhere to the endothelium and migrate through vessel wall
28
Q

What are the reactions of lymphatic vessels?

A
  • normally- drain the lymph and take it to lymph nodes
  • during inflammation: lymph flow increased, draining the oedema fluid, leukocytes and cells debris enter the lymph
  • they proliferate
  • Secondary inflam = lymphangitis
  • draining lymph nodes may become inflamed = lymphadenitis
  • lymph nodes increase in size too (due to hyperplasia of the lymphoid follicles = reactive/ inflammatory lymphadenitis
29
Q

What is lymphangitis?

A

secondary inflammation

30
Q

What is the draining of lymph nodes?

A

lymphadenitis

31
Q

What are the actions of leukocytes?

A
  1. Adhesion to the endothelium
  2. Migration across the vessel wall
  3. Migration to the stimulus
32
Q
  1. Adhesion to the endothelium (describe)
A
  • normally = red blood cells travel centrally and leukocytes travel peripherally
  • when blood flow slows and stasis occurs (inflammation) - leukocytes make contact with endothelial surface (margination)
  • start rolling along endothelium before adhering to endothelium
  • Adhesion between leukocytes + endothelial cell is by complementary adhesion molecules
  • Cytokines - enhance expression of the adhesion molecules
33
Q

What is margination?

A

-leukocytes make contact with endothelial surface

34
Q

what are selectins?

A

-proteins which mediate rolling

35
Q

Name the selectins

A
  • L-selectin (expressed on leukocytes)
  • E-selectin (endothelial cells)
  • P-selectin (platelets and endothelial cells)
36
Q

What do selectins bind to?

A

-ligands

37
Q

Ligands?

A

-sialylated oligosaccharides bound to mucin-like glycoprotein backbones

38
Q

What are selectins and their ligands expressed in response to?

A
  • cytokines
  • within a couple of hours of endothelial cells express E-selectin and the ligands for L-selectin
  • P-selectin is redistributed from its intracellular stores to cell surface
  • L-selectin is expressed on the tips of the microvilli of leukocytes, along with ligands for E and P selection
39
Q

What is the interaction between selectins and their ligands?

A

-low-affinity (allow rolling)

40
Q

What does rolling do?

A
  • slows down leukocytes

- allows stronger adhesion

41
Q

What is this mediated by?

A
  • integrins
  • ICAM-1 on endothelial cells bind to B2 integrins on neutrophils, monocytes and lymphocytes
  • VCAM-1 on endothelial cells bind to B1 integrins on eosinophils, monocytes and lymphocytes

this stops the rolling, reorganises cytoskeleton (so leukocyte spreads out)

42
Q

How do leukocytes migrate across the vessel wall?

A
  • moving through the endothelium = diapedesis

- predominatently in post-capillary (down a chemokine gradient)

43
Q

What mediates the transmigration/diapedesis?

A

-PECAM-1/ CD31

44
Q

What do the leukocytes adhere to when passing the endothelial cells?

A

-extracellular matrix in the connective tissue using integrins and CD44 to bind to matrix proteins

45
Q

Leukocyte adhesion deficiencies are characterised by:

A

-recurrent bacterial infections due to the inability of the leukocytes to perform any of the steps shown

46
Q

What is chemotaxis?

A

-migration of cells along a chemical gradient (used by leukocytes migrating towards sites of injury)

47
Q

Exogenous agents:

A

-Bacterial products (lipids, peptides)

48
Q

Endogenous agents:

A
  • cytokines
  • complement system
  • arachidonic acid metabolites
49
Q

What does downstream signalling alter?

A

-the cytoskeleton of leukocytes causing filopodia to move the cell in the direction of the stimulus, along the chemical gradient

50
Q

Name the receptors involved in recognition of foreign organisms and dead tissue

A
  • G protein- coupled receptors
  • Toll-like receptors (TLR’s)
  • Cytokine receptors
  • Opsonin receptors
51
Q

What are the 3 steps of phagocytosis?

A
  1. Recognition and attachment of the particle by the leukocyte
  2. Engulfment and formation of a phagocytic vacuole (phagosome) which fuses with lysosome
  3. Killing or degradation of the material by reactive oxygen species or lysosomal enzymes within phagolysosome
52
Q

2 types of mediators of acute inflammation?

A
  • cell derived

- plasma protein derived

53
Q

Name the cell derived mediators

A

(Vasoactive amines)

  • Histamine (in mast cell granules)
  • Seratonin (in platelets)
54
Q

Describe Platelet-Activating Factor (PAF)- cell derived mediator

A
  • Phospholipid derived mediator
  • can elicit most of the vascular and cellular reactions of inflammation
  • causes increased leukocyte adhesion to endothelium, chemotaxis, degranulation and the oxidative burst
  • increases synthesis of other mediators
55
Q

Describe ROS (cell derived mediator)

A
  • Oxygen derived free radicals
  • Superoxide anion, hydrogen peroxide and hydroxyl radical are the major species produced within cells
  • extracellular release = increase expression of chemokine, cytokines and endothelial leukocyte adhesion molecules (amplify inflammation response)
  • ROS in leukocytes- destroy phagocytksed microbes (damaging)
56
Q

Describe NO (cell derived)

A
  • produced by endothelial cells and macrophages
  • relaxes vascular SM, promoting vasodilation
  • Inhibitor of the cellular component of the inflammatory response
57
Q

Describe cytokines and chemokine (cell derived)

A
  • Cytokines:
    • TNF and IL1
    • produced by activated macrophages
  • Chemokines
    - chemoattractants for different leukocytes
58
Q

Describe neuropeptides (cell derived)

A
  • secreted by sensory nerves and leukocytes
  • substance P
  • sensory neurons can also produce other pro-inflammatory molecules
59
Q

What is the complement system?

A
  • group of plasma proteins triggered by antibody fixation or microbial antigens
  • cause inflammation, phagocytosis, cell lysis
60
Q

Name the plasma protein derived mediator

A

KININS

  • vasoactive peptides
  • bradykinin
61
Q

How does the body prevent excessive damage to the host?

A
  • half life of mediators is short and mediators rapidly degraded
  • Neutrophils have short half life and die by apoptosis within hours of release
  • switch from pro to anti inflammatory mediators:
    - Lipoxins
    - macrophages produce anti-inflammatory cytokines (TGF-B/IL-10)
    - Resolvins/ protectins
    - cholinergic discharge

FD1 (31 decks)

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