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PATH > Inflammation and Wound Healing > Flashcards

Inflammation and Wound Healing Flashcards

1
Q

What is inflammation?

A

Protective response to cell injury

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2
Q

What are the five cardinal signs of inflammation?

A

Calor - heatRubor - redTumor - swellingDolor - painfulFunctio laesa - loss of function

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3
Q

What is the difference between transudate and exudate?

A

Transudate contains little protein and is found in early inflammation and exudate contains lots of protein and clots on exposure to air.

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4
Q

Name the bodily fluid, produced by the liver, which contains circulating clotting factors, fibrinogen, kininogens and complement proteins.

A

Plasma

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5
Q

Which cells of the body produce extra cellular matrix?

A

Fibroblasts

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6
Q

Amphiphilic

A

Cytoplasm which stains with both acidic and basic dyes

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7
Q

Neutrophils and eosinophils are examples of what type of cells?

A

Polymorphonuclear

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8
Q

Monocytes, basophils and lymphocytes are examples of which cell type?

A

Mononuclear

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9
Q

Bodily fluid found in created cavities, rich in neutrophils and cell debris.

A

Pus

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10
Q

Order these vascular changes in the correct order whilst regarding acute inflammation:1. Blood stasis2. Short lived vasoconstriction3. Vasodilation and increased blood flow

A

2,3,1

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11
Q

Increased permeability of capillary beds during acute inflammation leads what secondary effects?

A

Endothelial mediated leakage Protein leakage - altered oncotic pressureIncreased hydrostatic pressure - fluid into interstitium

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12
Q

What are the stages of acute inflammation?

A
  1. Vascular phase
    1. initial phase
    2. hypeaemia
  2. Exudative phase
  3. Migration of leukocytes
  4. Pyrexia
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13
Q

Describe the vascular phase of acute inflammation

A

Initial phase; transient

  • arteriole constriction (white line)
  • smooth muscle response

Hyperaemia; mins-days

  • arteriole and capillary dilation
  • chemical mediators
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14
Q

What happens in the vascular phase?

A

The pre-capillary sphincters open. Blood is diverted from the arterioles into the capillary beds.

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15
Q

Describe the exudative phase of acute inflammation

A

Exudate moves from the dilated capillaries into the tissues.

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16
Q

What is the inflammatory exudate composed of?

A
  • Fluids (water and electrolytes);containing salts and a high protein concentration; including immunoglobulins
  • Fibrin; a high molecular weight, filamentous, insoluble protein- osmotic gradient
  • Red blood cells and platelets
  • Neutrophil polymorphs; from the white blood cell population
  • Macrophages; phagocytic cells derived from blood monocytes
  • Lymphocytes
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17
Q

What allows the exudative phase to occur?

A

Endothelial cells contract, creating gaps between cells. This increases vascular permeability and allows protein rich fluid to move from blood into the tissue.
Caused by histamine released by mast cell.

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18
Q

What can endothelial contraction be caused by?

A
  • Histamine from mast cells
  • Physical damage - lysis
  • Toxic agents
  • Infection
  • Enzymes
  • Oxygen free radicals - leukocyte mediated
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19
Q

What can cause endothelial retraction? Which cell organelle is involved in this process?

A

Cytokines (IL1 and TNF)

Cytoskeleton

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20
Q

What are the five stages of the migration of leukocytes?

A
  • Instigation by cytokines
  • Leucocyte is lightly tethered to endothelium and rolls on selectins
  • Firm adhesion of leucocytes to endothelium via integrins
  • Transmigration of leukocytes through vessel wall
  • Migration through ECM and chemotaxis
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21
Q

What is meant by laminar blood flow?

A

Rolling of blood on endothelia but not attaching.

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22
Q

Name two breeds of animal which are know to suffer from LAD (leucocyte adhesion deficiency)

A

Irish Setter

Holstein cattle

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23
Q

Order these cell types/phases in the order of which they are seen in acute inflammation. and their approximate time scales of appearance.

  • Neurophils
  • Exudation
  • Macrophages
A
  1. Exudation
  2. Neutrophils - 6-24 hrs
  3. Macrophages - 24+ hrs
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24
Q

Give examples of chemotaxins?

A
  • Bacterial products; endotoxin
  • Fibrin degredation products
  • Complement derived factors
  • Cytokines, esp. lymphokines
  • Tissue breakdown products
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25
Q

What is the difference between exogenous and endogenous chemotaxins?

A

Exogenous are bacteria-derived (LPS) and endogenous are host-derived (complement c5a)

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26
Q

What are the functions of neutrophils?

A
  • Phagocytosis of microorganisms or foreigh material
  • Fusion of phagosome with lysosomes to kill or degrade material
  • Secreation and/or release of granules into exudate to enhance acute inflammatory response
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27
Q

If there are insufficient numbers of circulating neutrophils avaliable how does the body compensate? What phenomenon occurs?

A

Store of neutrophils, including some immature forms, are released from the bone marrow.

Left shift, release of band neutrophils

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28
Q

What do the structures in this image represent?

What is their function?

(Pseudopodia)

A

Pseudopodia

Cell migration and engulfment of bacteria

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29
Q

Give 5 cells that contain pyrogens?

A
  • Neutrophils; when they begin to phagocytose (also eosinophils and macrophages)
  • Gram negative organisms; cell walls continue pyrogens
  • Damaged tissue cells; necrosis releases pyrogens
  • Antigen-antibody complexes
  • Tumours; may release pyrogens, especially those that have metastasised. Central necrosis may also release pyrogens
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30
Q

Which mineral ion is vital for cell movement?

A

Ca2+

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31
Q

Describe the three phases of phagocytosis.

A
  1. Recognition and attachment - via PAMPs or opsonins
  2. Engulfment - Pseudopodia surround bacteria, forms phagosome (to phagolysosome)
  3. Killing and degrading - via free radicals (OH- OCl-) created by NAPH oxidase and myeloperoxidase.
32
Q

Myeloperoxidase is responsible for the creation of which free radical.

A

OCl-

33
Q

Why are neutrophils the first to arrive at a site of inflammation?

A

They cross the membrane quickest

34
Q

Which two chemical mediators are released with degranulation of mast cells?

Briefly discuss their role.

A

Histamine and Seratonin (5-HT)

Increase vascular permeability

35
Q

Categorise the following chemical mediators into these types; vasoactive amines, complement proteins, AA system molecules, kinin system molecules and clotting system molecules.

  1. Bradykinin
  2. Prostaglandin
  3. C5a
  4. Histamine
  5. Leucotreines
  6. Seratonin
  7. Thrombin
A
  1. VA - 4,6
  2. CP - 3
  3. AA - 2,5
  4. K - 1
  5. CF - 7
36
Q

What are the 6 types of acute inflammation?

Briefly describe them.

A
  1. Serous - Thin fluid, no proteins
  2. Catarrhal - serous inflammation of mucous membranes
  3. Fibrinous - Serous plus fibrin protein (clots)
  4. Diphtheritic - Necrosis of upper layers plus serous
  5. Haemorrhagic - RBC’s plus exudate
  6. Suppurative - Neutrophil dominated exudate
37
Q

What words can be used to describe distribution of acute inflammation?

Briefly describe their meaning.

A
  1. Focal - Single lesion
  2. Multifocal - Multiple distinct lesions
  3. Disseminated - Multifocal lesions throughout an organ
  4. Diffuse - Evenly spread lesions throughout an organ
38
Q

What are the three phases of chronic inflammation? Briefly describe each step.

A
  1. Active inflammation - infiltration of mononuclear cells
  2. Tissue destruction - leucocyte induced tissue injury
  3. Repair - angiogenesis, fibrosis and cell proliferation powered by growth factors
39
Q

What conditions are necessary to promote chronic inflammation?

A
  1. Persistent infection - hypersensitivity
  2. Prolonged irritation - FB, toxins
  3. Immune response - autoimmunity
40
Q

What type of cell is this? What types of characteristic feature do they produce in tissue?

What is their function?

A

Plasma cell

Russell bodies

Produce immunoglobulins

41
Q

Which cell types are characteristic of chronic inflammation?

A

Lymphocytes

Plasma cells

Macrophages

42
Q

Which chemokines are involved in active chronic inflammation?

How do the act?

A

IL1 and TNF released by macrophages activate lymphocytes which release IFN gamma which causes macrophage recruitment

43
Q

lymphocytes:

  1. life span?
  2. can they leave the tissues?
  3. appearance?
  4. how are T and B cells distinguished?
A
  1. 200 days
  2. yes, they circulate between the blood and tissues
  3. round cells with densely staining nucleus, thin rim of cytoplasm
  4. T - CD3, B - CD79a
44
Q

macrophages:

  1. appearance?
  2. what are they called in tissues?
  3. immature stage in the blood?
  4. what are the 3 functions?
A
  1. large round cells with round nucleus and abundant clear often vacuolated cytoplasm
  2. histocytes
  3. circulating monocytes - mature into macrophages
  4. phagocytosis, antigen presentation, stimulation of fibroplasia and fibrosis
45
Q

plasma cells:

  1. appearance?
  2. what are Russell bodies?
A
  1. round to oval shaped cells with an eccentric round nucleus and adundant purple cytoplasm
  2. activated plasma cells with abundant Ig
46
Q

2 subtypes of macrophages?

A
  1. epthelioid cells
    1. look like squamous ep cells
    2. may be binucleate
    3. primarily secretory
  2. giant cells
    1. multinucleated
    2. formed by the fusion of epithelioid cells or macrophages
47
Q

what causes a granulomatous inflammation?

what is the structure?

A
  1. organisms of a low virulence but great persistence in the tissues or by implanted foreign bodies
    1. central core containing irritant
    2. surrounding chronic inflammatory cells
    3. outer fibrous capsule
48
Q

Leukocyte mediated tissue injury is caused by release of what by leukocytes?

A

Lysosomal enzymes

Free radicals

AA metabolites

49
Q

Fibrosis

  1. What is it?
  2. What are the four phases of fibrosis?
A
  1. Replacement of lost tissue with collagen fibres
  2. Phases
    1. Angiogenesis - blood vessel formation
      1. basement membrane degraded
      2. migration of endothelium
      3. proliferation of endothelium
      4. periendothelial recruitment
    2. Fibroblast migration and proliferation
      1. VEGF allows fibrinogen and fibronectin put down
      2. Cytokines atimulate proliferation and migration
    3. ECM depositation
    4. Tissue remodelling
      1. Replacement of granulation tissue
50
Q
  1. What stimulates macrophages during the active stage of healing?
  2. What are they stimulated to do?
A
  1. Stimulated by the hypoxic conditions (low oxygen) of their surroundings to produce factors that induce angiogenesis.
  2. Also stimulate cells to re-epithelializethe wound, create granulation tissueand lay down a new extra-cellular matrix.
51
Q

What is the function of matrix metalloproteinases in fibrosis?

A
  1. Angiogenesis
  2. Cell migration
  3. Scar contraction
  4. Removal of damaged ECF
52
Q

Which molecules inhibit MMP’s?

A

TIMP’s

53
Q

The image below shows granulation tissue, what is represented by each of the different coloured arrows?

A

Black = macrophages

Green = fibroblasts

Red = lymphocytes

Blue = capillaries

+ tissue is very oedematus

54
Q

Regenerative healing of cells occurs with what characteristic of some cell types?

A

Labile or stable (non-permanent cell types)

GIT, epithelium, haemopoietic

55
Q

What is an abscess and under what conditions do they occur?

Draw its structure

A

Suppurative inflammation buried in tissue

They occur with low hyaluronidase bacteria which spread slowly and cause a strong local reaction.

56
Q

How does the histology of the capsule of an abscess differ from the outside to the inside?

A

Outside = old = fibre rich

Inside = younger = cell rich (capillaries and macrophages)

57
Q

Liquifaction

A

Complete loss of cellular structure

58
Q

“Loss of epidermis and basement membrane exposing the dermis”

A

Ulcer

59
Q

“Macrophage dominated chronic inflammation”

A

Granulomatous

60
Q

Compare the histological structure of Langerhans and foreign body giant cells.

A

Langerhans = peripheral nuclei

Foreign body = clusters of nucleus distributed throughout

61
Q

This pathogen is an example of one which creates multifocal granulomatous tissue within the lungs of the host.

A

Mycobacterium

62
Q

Frunculosis

A

Infected hair follicle

63
Q

Fibrosis

A

Replacement of lost tissue of collagen fibres

64
Q

What factors can affect wound healing?

A
  1. Local factors - foreign material, size, type etc
  2. Sytemic factors - nutritional or hormonal
  3. Deficient scar formed - ulceration, contractive, wound dehiscence
  4. Excessive repair componants - collagen, granulation tissue (proud flesh forms)
65
Q

Proud flesh

A

Excessive formation of granulation tissue

66
Q

Define healing by first intention.

A

A small deficit where wound edges are opposed, surgically brought together.

67
Q

Define healing by second intention.

A

A large spatial deficit where edges dont come together easily.

Wound is left to heal on its own.

68
Q

Outline the process of healing by first intention at:

  1. 24hrs
  2. 2-7 d
  3. 2-4 wks
  4. Months
A
  1. Blood clot forms, thickening of the epidermis, neutrophils appear.
  2. Epithelial cells grow along basement membrane. Neutrophils replaced by macrophages. Granulation tissue invades and fills space. fibroblasts appear and deposit collagen which bridges the wound.
  3. Inflammation has disappeared. Accumulation of collagen from fibroblasts causes a scar.
  4. Scar remodels and strengthens.
69
Q

Outline the process of healing by second intention at:

  1. 2-3days
  2. 1-2weeks
  3. 3-6weeks
  4. Months
A
  1. Blood clot with necrotic tissue. Neutrophils appear
    Larger defect in epidermis and dermis.
  2. Granulation tissue fills deficit. Epithelialisation begins at margins.
  3. Maturation of granulation tissue contraction of wound. Epithelialisation completes.
  4. Contraction of wound produces irregular scar. Loss of adnexae.
70
Q

Describe how wound strength changes over time after injury of the tissue.

A

Takes years of remodelling, can only regain

71
Q

Describe how scar remodelling increases tensile strength of scars.

A

Increases in size, and creates cross linking bonds to increase tensile strength of the scar.

72
Q

What are the functions of macrophages in chronic inflammation?

A
  • phagocytosis
  • antigen presentation [MHC II]
  • secretory function
    • proinflammatory (IL-1, TNF, PAF, PGs…)
    • procoagulatory
    • immune regulation
  • wound healing
  • regulation of monocyte and granulocyte pools
73
Q

Outline the characteristics of granulation tissue.

A
  • begins approx. 24 h after injury
  • visible from days 3-5 onwards
  • contains new small blood vessels and proliferating fibroblasts
  • oedematous
74
Q

Outline the procedure of fibrosis and briefly explain each step.

A
  1. Angiogenesis - penetration of new blood vessels into the site of inflammation (delivers cells and other factors)
  2. Migration and proliferation of fibroblasts
  3. ECM deposition - fibroblasts synthesis and put down collagen, continues for several weeks
  4. Remodelling of fibrous tissue - replaces granulation tissue with a scar
75
Q
  1. Migration and proliferation of fibroblasts in chronic inflammation is mediated by which growth factors?
  2. What is their outcome?
A
  1. VEGF
    1. Increases in vascular permeability, increased deposition of fibrinogen and fibronectin in ECM (Stroma for fibroblasts)
  2. GFs, IL-1, TNF
    1. Trigger fibroblast migration and proliferation from capillaries.
76
Q

Tissue remodelling in chronic inflammation is mediated by which factors?

A

MMP and their inhibitors TIMPs

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