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Y2S2 VETS2007 theory > Inflammation acute > Flashcards

Inflammation acute Flashcards

1
Q

Inflammation general

A

occurs in living vascularised tissue
Cause acne be exogenous or endogenous
Response purpose = diluting/inactivating bio or chemical toxins, killing microbes, foreign material, necrotic tissue and neoplastic cells, degrading forming materials, providing wound healing factors.
Brings leukocytes _ plasma proteins circulating around the blood to the site of tissue damage.

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2
Q

Typical inflammatory reaction (5) steps

A

Host cells and molecules recognise offending agent
Leukocytes and plasma proteins arrive at the location
Leukocytes and proteins are activated and working together destroy and eliminate the offending substance
The reaction is controlled an terminated
Damaged tissue is repaired

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3
Q

List some issues with the inflammatory reaction when it is misdirected (4)

A
  1. Autoimmune disease
  2. Neuro degenerative disorders
  3. Allergies
  4. Neoplastic processes (cancer promoting as the inflammation factors/components can cause DNA damage in specific genes and cell proliferation )
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4
Q

Cardinal signs of inflammation

A 
Rubor
Calor
Tumour
Dolor
functio leasa

Signs are typically more prominent in acute inflammation than in chronic inflammation and many of these are consequences of the local vascular changes initiated by inflammation

Redness (rubor) and heat (calor) due to increased blood flow to inflamed site with vasodilation
Swelling (tumour) is caused by the accumulation of fluid in extravascular
Pain (dolar) is due to release of chemicals that stimulate nerve endings
Loss of fx (functio leasa) things that destroy foreign invaders and other causes of inflammation have an intrinsic ability to injure normal tissues with secondary loss of fx

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5
Q

Pattern of inflammation: acute vs chronic

A

Acute - main features are exuding of fluid and plasma proteins and leukocytic emigration, principally neutrophils followed by rapid repair and healing.

Chronic- longer duration and it is associated histologically with presence of lymphocytes and macrophages, the proliferation of blood vessels, fibrosis and tissue necrosis

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6
Q

Cells involved in the acute ad chronic inflammatory response and why these are the cells are in this order

A

Acute
neutrophils predominate during first 6-24hrs
Monocytes 24-48hrs
Reasoning for the process above- more numerous in blood = neutrophils, respond more rapidly to chemokine and they may attach more firmly to adhesion molecules on endothelial cells,

But neutrophils are short lived and undergo apoptosis after 24-48hrs, whereas monocytes survive longer

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7
Q

Explain variations with inflammation cellular patterns

A

Pseudomonas organism —> neutrophils predominate over 2-4 days.
Viral infections —> lymphocytes arrive first
Parasitic infections consists of eosinophils
Allergies —> mast cells and eosinophils maybe the main type

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8
Q

Explain the initiators of the inflammation

A

Innate immune system has numerous PRRs (pattern recognition receptors)—> recognise = PAMPS (Pathogen-associated molecular patterns)

Sentinel cells - macrophages ( express PRRs)

When macrophages PRRs detect microbial product = cascade of reactions in the cell

Activated macrophage —> inside cell synthesise and release pro inflammatory cytokines —> these then signal other inflammatory ells and blood vessels in the area

Example of studied PRRs activated by PAMPs are the toll-like receptors (TLRs) a family that detects bacteria, viruses, fungi and protozoa

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9
Q

Explain sterile inflammation

A

Instead of bacterial it is trauma, physical and chemical injury, foreign bodies or inappropriate products of adaptive immunity

DAMPSs or alarmins these activate the macrophages

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10
Q

How do DAMPS work?

A

Derived from normal proteins and metabolites found in the cytoplasm or nucleus of host cells which are released after necrosis.

Therefore the extracellular presence of these molecules indicates cellular injury in the vicinity- Numerous PRRs specifically recognize DAMPs leading to the same activation and signalling cascade as that occurring with PAMPs

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11
Q

Three major components of acute inflammation (3)

A
  1. Dilation of small vessels= increased blood flow
  2. Increased permeability of microvasculature enabling plasma proteins to leave the circulation
  3. Emigration of leukocytes from the microcirculation to focus of injury + activation to eliminate the offending agent
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12
Q

When an individual encounters an injurious agent, such as an infectious microbe or dead cells

A

phagocytes that reside in all tissues try to eliminate these agents
Cytokines + lipid messenger + mediators of inflammation —> release phagocytes and other sentinel cells to those areas
Some of the mediators act on small blood vessel in area promoting efflux of plasma and recruitment of circulating leukocyte

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13
Q

Reactions of blood vessels in acute inflammation

A

Change blood flow + permeability to allow plasma proteins + leukocytes leave—> circulation into—> infection site

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14
Q

Explain exudation

A

The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities is known as exudation

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15
Q

Explain an exudate

A

An exudate is an extravascular fluid that has a high protein concentration and contains cellular debris

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16
Q

Most of the changes observed in the early stage of the vascular reaction are mediated by

A

histamine and other chemical compounds released by inflammatory cells, mainly mast cells, that are widely distributed in the normal connective tissue

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17
Q

Explain the two steps of acute inflammation response to injury

A
  1. Begins vasodilation (widening of blood vessels) = increase blood volume —> the increase diameter =. Slow velocity blood
    the slowing of blood means leukocytes principally neutrophils begin to accumulate along the vascular endothelial surface ( this the first step)
  2. Increase in vascular permeability
    allowing fluid and plasma proteins into interstitial tissue (exudate process)
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18
Q

What is margination

A

As stasis develops, leukocytes (principally neutrophils) begin to accumulate along the vascular endothelial surface—a process called margination 


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19
Q

Explain the importance of plasma protein in exudate

A

not only important for diluting the inciting agent, but some of them have an active role in removing and immobilizing them

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20
Q

Immunoglobulins are important?

A

for improving phagocytosis (opsonisation), activating the complement system and directly inactivating some organisms

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21
Q

The complement system

A

The cascade to the MAC

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22
Q

Fibrinogen is an important plasma protein in exudates

A

that polymerizes in extravascular spaces to form fibrin. Polymerized fibrin confines the stimulus to an isolated area, has chemotactic properties and induces blood clot formation, as well as forms a framework for fibroblast and endothelial cell migration during the initial stage of wound healing

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23
Q

Mechanisms of increased vascular permeability (3)

A

In healthy tissue protein -rich flow stays in the vessel due to endothelial cells intercellular tight junctions

  1. Endothelial gaps can occur
  2. Direct injury to endothelial cells
  3. Increased transcytosis induced by VEGF
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24
Q

Explain how endothelial gaps occur

A

by contraction of endothelial cells or reorganisation of cytoskeletal microtubule and microfilament proteins within endothelial cells

occurs most the time in postacapullary venues
Transient (15-30mins)
Histamine part of chemical mediators

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25
Q

Explain direct injury to endothelial cells (2) and lx

A

injury - detachment of the cell from the underlying basement membrane occurs quickly by thermal injury, radiation, bacterial cytotoxins

. Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction.

It affects arterioles, capillaries and postacapillary venules

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26
Q

Explain normal leukocyte movement

A

Flow rapidly in the blood

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27
Q

Explain the recruitment of leukocytes (4 steps)

A

This processes purpose is to move leukocytes from the vascular lumen to extravascular space where issues usually are

Step

  1. Margination and rolling along the vessel wall
  2. Firm adhesion to the endothelium
  3. Transmigration between endothelial cells
  4. Migration in interstitial tissues toward a chemotactic stimulus

Cytokines influence these processes

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28
Q

Explain leukocyte Rolling ( the selectins)

A

Traveling leukocytes are slowed down by brief binding of selectin to their ligands.
L selectins on leukocytes
P selectins on endothelial + platelets
E selectins on endothelial cells

29
Q

Explain leukocyte stable adhesion

A

Leukocyte - B2 integrin molecules <-binds-> ICAM1 (inter cellular adhesion molecule)

leukocyte had to be stimulated to express B2 integrin molecules
4 B2 interns with identical B subunit (CD18)

30
Q

Explain LAD

A

Leukocyte adhesion deficiency
cattle, Dog (Irish setters) and humans
No B2 integrin expression
= normal fx neutrophils but impaired passage across vascular walls
Therefore —> infections cannot be cleared
Hallmark = lesion has no neutrophils but they are in the blood vessels

31
Q

Explain leukocyte Diapedesis

A

Diapedesis = the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.

Leukocytes going through the endothelial layer
Mediated by
Endothelial cell adhesion molecule 1
Junctional adhesion molecules JAMs

32
Q

L - selectin

A

Expressed by leukocytes for rolling

33
Q

P-selectin

A

Expressed by endothelial cells and platelets for rolling

34
Q

E-selectin

A

expressed by endothelial cells for rolling

35
Q

B2 integrin

A

Expressed by leukocytes for ‘stable adhesion’

36
Q

ICAM-1

A

expressed by endothelial cells for ‘stable adhesion’

37
Q

PECAM1

A

Expressed by endothelial cells/leukocytes for’ diapedesis

38
Q

JAMs

A

Expressed by endothelial cells/leukocytes for’ diapedesis

39
Q

Define chemotaxis

A

Locomotion along a chemical gradient

40
Q

Leukocytes chemotaxis steps

A
  1. Chemoattractants on Plasma membrane extend pseudopods to region of greatest chemotactic
  2. The pseudopoda then pulled the whole cell towards that direction

These influence inflammatory cells
Influenced by the complement system

41
Q

What stimulates leukocyte?

A

Exogenous or endogenous stimuli

This often occurs at a site of infection or tissue necrosis.

42
Q

Leukocytes’ defensive functions at the site of inflammation (3)

A

Phagocytosis
Liberation of substances
Production of mediators

43
Q

Explain leukocytes phagocytosis 3 steps

A
  1. Recognition and attachment
  2. Engulfment —> formation of phagocytic vacuole
  3. Intracellular destruction by phagosomes ( ROS and nitrogen species and lysosomal enzymes)
44
Q

Explain liberation of substances that destroy extracellular microbes and dead tissues of leukocytes

A

Largely the same as the phagocytic vesicles, but contained within leukocytes granules

45
Q

List the three chemical mediators of acute inflammatory response

A
  1. Histamine
  2. The complement cascade
  3. Arachidonic acid metabolites
46
Q

Explain histamine

A

Stored in
mast cells, basophils + platelets

Stimulated to be released by
IgE
C3a
C5a
Heat
Cold
Substance P
ATP
Products from leukocytes
Fx/effect (mediator of inflammattion)
Vasodilation
Increased vascular permeability 
Pain
Itch
Neural reflexes 
Bronchial contraction
Eosinophilic chemotaxis

Duration and onset
effect immediate = within minutes
Lasting 30-90mins

47
Q

Explain the complement cascade

A

The molecules are produced by the liver
cascade all form the AMC
Classical = antigen-antibody
Alternative pathway = LPS Gram -ve and polysaccharides from fungal cell wall
Lectin pathway = mannose-binding lectins to microbial product

C3a nd C5a - influence mast cells to release histamines and other mediators

48
Q

Arachidonic acid metabolites

A

Arachidonic acid = poly unsaturated fatty acid ltx = plasma membrane

Inflammation occurs = cell membrane is injured = lipids in there are rapidly rearranged = arachidonic acid is released + several active lipid mediators are produced.

Producing autacoids

Three COX isoenzymes
COX1
COX2
COX3

49
Q

What are autacoids

A

Metabolites acting as local hormones and short -lived and most important ones are prostaglandins and leukotrienes produced by the cycloxygenase and lypooxygenase enzyme pathways.

50
Q

Explain COX 1

A

Is constitutively expressed and present in almost all tissues

51
Q

Explain COX 2

A

Induced by exogenous and endogenous stimuli and occurs locally in sites of inflammation

52
Q

Explain COX 3

A

Recently discovered COX3

Expressed in cereal cortex of dogs and humans

53
Q

Explain the general action of Aspirin, naproxen, ibuprofen etc

A

Inhibit arachonic acid metabolites produced by cox 1 and cox 2 pathways

54
Q

Morpholoigcal patterns of acute inflammation (4)

A
  1. Serous inflammation
  2. Catarrhal inflammation
  3. Fibrinous inflammation
  4. Suppurative inflammation
55
Q

Explain serous inflammation morphology

A

Ltx = hypersecretion of inflamed serous glands
thermal injury to skin or acute allergic response

Process = the watery fluid leaks from the small gaps between endothelial cells and from hypersecretion of inflamed serous glands

Stx = watery fluid accumulation with
low concentration of plasma proteins
No to low numbers of leukocytes

Grossly looks like

  1. Excessive clear to slightly yellow watery fluid leaking from the tissue on cut section
  2. Forms raised fluid-filled vesicles
56
Q

Explain Catarrhal inflammation morphology

A

Secretion or accumulation of a thick gelatinous fluid containing abundant mucus and muffins from mucous membrane

Ltx
Occurring in ltxs of tissue with abundant goblet cells and mucous glands

Grossly —> surface or cut surface of affected tissue may be covered with or contain a slightly opaque thick fluid

57
Q

Explain fibrinous inflammation

A

Accumulation of fluid with high concretion of plasma proteins and low number of leukocytes

Cause = servere endothelial cell injury

Fibrinogen leaks from capillaries and postcapullary venues and polymerises outside of the vessels to fibrin ( homogenous and hypereosinophilic protein)

Ltx most common —> infection microbes and in serous membranes of the body cavities.

Grossly
- the surface of affected tissues are red and covered with thick , stringy, elastic, white-grey to yellow exudate

58
Q

Explain Suppurative inflammation

A

fluid accumulation —> high concentration of plasma proteins and high number of leukocytes, predominantly neutrophils.

Commonly known as pus
Most commonly causes by bacteria

59
Q

Systemic effects of an acute inflammatory response (7)

A 
Loss of appetite
Leathery
Muscular wasting (Cachexia)
Haemodynamic changes (shock)
Fever
Leukocytosis
Alterations to acute phase proteins
60
Q

Explain how fever is inducedWhat mediates systemic effects of acute inflammation

A

mediated by the systemic release of TNFα, IL1 and IL6 by activated leukocytes

Others effects serve to conserve energy and mobilize resources to aid in the resource-expensive process of inflammation (anorexia, lethargy, cachexia)

61
Q

Explain how fever is induced

A

Exogenous —> LPS
Endogenous —> IL1, and TNF (Tumour Necrosis Factor)
Then Pyrogens stimulate prostaglandin synthesis in hypothalamus = increased production of neurotransmitters = reset the temperature set-point at a higher level

62
Q

Explain the hypothesis of the benefits of a fever (8)

A

May induce heat shock proteins = these then enhance lymphocyte response to microbial antigens
Increased expression of some cytokines
Enhanced phagocytosis
Increased T cell proliferation
Inhibition of growth of some microbes
Induction or iron-sequestering proteins
Enhanced interferon-stimulated responses
Increased motility and activation of some leukocytes

63
Q

What is leucocytosis

A

Increased number of leukocytes circulating in the blood

64
Q

Explain the acute inflammation leukocytosis generally

A

Primary a neutrophillia reaction.

This occurs because accelerate release of cells from the bone marrow post mitotic reserve pool (neutrophils with mature cells)

Compared to prolonged infection there is depletion of bone marrow store of mature cells and proliferation of precursors in the bone marrow cause increased production of CSFs (colony-stimulating factors).

It is one of the most important clues a veterinarian has in gauging whether the animal’s clinical signs stem from an inflammatory process, especially if the site of inflammation is not immediately evident.


65
Q

Acute phase proteins

A

-plasma proteins —> synthesised in liver ( plus = leukocytes, adipocytes, heart, GI tract, kidney)

these increase during inflammation
Concentration rises very quickly
peak 24-48hrs
10-100 times normal serum concentrations

The increased synthesis of these molecules is upregulated cytokines as IL16, IL1 or TNF

Eg major in dogs, rabbits pigs and primates is C-reactive protein (CRP)
fx = bind to certain components of surface of bacteria, parasites or damaged cells enhancing their clearance

Other APPs are serum amyloid A, haptoglobin, fibrinogen, ceruloplasmin

66
Q

List possible outcomes of acute inflammation (3)

A

The following are based on
severity of tissue damage
Ability of cells to regenerate
Physical or biologic features of the case of injury determine these outcomes

1 Resolution
2 Scarring occurs
3 Actor to chronic transition occurs

67
Q

Explain how a resolution can become the outcome of an acute inflammation.

A

Correct sequence
Macrophage and lymphatic vessels remove the exudate
Inciting agent is eliminated
Connective tissue is intact and provides support fro regeneration of epithelial cells

68
Q

Explain how scarring can become the outcome of an acute inflammation.

A

Severe tissue destruction
Inflammatory injury involves tissues that are incapable of regeneration
Or
Abundant fibrin exudate

69
Q

Explain how a transitioning to chronic can become the outcome of an acute inflammation.

A

Acute response cannot resolve, because of persistence of injurious agent or to some interference with normal process of healing

Y2S2 VETS2007 theory (12 decks)

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