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Pathology 1 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

How is inflammatory exudate formed?

A

Inflammatory exudate due to increased vessel permeability containing salts, water, small plasma proteins (fibrinogen)

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2
Q

What are leukocytes?

A

Neutrophils, monocytes & lymphocytes expressing l-selectin ligands on endothelium

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3
Q

How is a chemoattractant gradient formed?

A

Chemoattractants formed at site of infection /injury and diffuse into adjacent tissue forming a gradient

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4
Q

What are the signs of acute inflammation?

A

Redness due to increased blood flow (hyperaemia) to injury site
Swelling from fluid accumulation due to increased vessel permeability
Heat from increased blood flow and metabolic activity
Pain as release of pain mediators and pressure on nerve ends
Loss of function from excessive swelling and pain

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5
Q

Which factors prevent tissue healing?

A

Infection, Diabetes, Old Age, poor general health & nutrition
Protein / vitamin C deficiency
Drugs - corticosteroids
Extensive inury & haemorrhage, poor vascular supply
Foreign bodies, pressure, torsion, movement on wound edges (dehiscence)

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6
Q

Why is acute inflammation described as a local response?

A

All the symptoms and effects take place in the affected tissue

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7
Q

What is the role of selectins in acute inflammation?

A

Mediate rolling of neutrophils, expressed by activated endothelium

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8
Q

Which factors favour tissue regeneration?

A

Minimal destruction & cell death
Quick removal of dead tissue and foreign material
Immobilisation of wound edges
Fast infection clearance

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9
Q

What are the 5R’s of acute inflammation?

A 
Recognition of injury 
Recruitment of leukocytes 
Removal of injurious agents 
Regulation and closure of inflammatory response 
Resolution / Repair of affected tissue
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10
Q

Which tissues have no regeneration ability?

A

Permanent tissues
neurons, myocardium, skeletal muscle
Heal with fibrosis, scarring and loss of function

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11
Q

What is haemorrhagic exudate?

A

Exudate formed when blood vessel rupture or trauma RBCs predominate

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12
Q

What is neutrophil chemotaxis?

A

Movement of cells through tissue, towards inflamed site guided by chemoattractants

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13
Q

What would be the consequence if no acute inflammation occurred?

A

There would be no infection control

Impaired wound and no tissue healing

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14
Q

Which tissues have an immediate regeneration ability?

A

In stable tissues
If in normal state quiescent cells are in G0/G1, injury leads to cell division, they may regenerate when injured
e.g. liver, kidney, pancreas, endothelial cells, fibroblasts
If an extensive injury, scarring is prevalent

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15
Q

What are the main features of fibrinuous exudate?

A
  • Fibrin deposition derived from fibrinogen in plasma
  • Large vascular leaks: fibrinogen exits blood entering
    tissues
  • serous cavities : meningis, pleura & pericardium
  • Can lead to scarring if not cleared as fibroblasts ->
    collagen
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16
Q

What is the role of leukocytes?

A

Endothelial leukocytes bind to ligands on neutrophils
Low affinity interaction is disrupted by blood flow, causing repetitive binding and detaching
Rolling (mediated by sleectins) slows down

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17
Q

What is the purpose of acute inflammation?

A

Alters the body , limiting spread of infection / injury to rest of the body
Protects injured site from further infection by eliminating dead cells / tissues
Creates a healing environment

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18
Q

How is acute inflammation terminated?

A

Via antimicrobial mechanisms, inflammatory mediators
Not specific to microbes / dead tissues
Normal tissues can get damaged during inflammation - termination is vital

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19
Q

How is Sepsis caused?

A

In rare cases, systemic inflammatory reaction scan lead to sepsis which is a form of systemic inflammatory response syndrome (SIRS)
- can be widespread and have severe manifestations

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20
Q

Describe the vascular events of acute inflammation

A
  1. Vasodilation of small vessels due to histamine /
    serotonin release by injured cells, mast cells &
    macrophages
  2. Increased blood flow to injured area results in an influx
    of WBCs, fluid, oxygen, and nutrients
  3. Increased vessel permeability (microvessels) due to
    endothelial contractions results in fluid containing cells
    leakage into injured tissue
  4. Endothelial cells activated increasing adhesion
    molecules
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21
Q

What systemic manifestations can occur during acute inflammation?

A

Fever

  • Endogenous pyrogens (IL-1, TNF-α)
  • Exogenous pyrogens (microbial components)

Neutrophilia

  • G-CSF stimulation of bone marrow
  • > replenishes dead neutrophils
  • > release immature neutrophils

Acute Phase reactants

  • C-reactive proteins (CRP), fibrinogen, complement, serum Amyloid A protein (SAP)
  • produced in liver
  • induced by IL-6, IL-1 and TNF-α
  • > increased fibrinogen leads to RBC stacking, erythrocyte sedimentation rate increases
22
Q

What other types of inflammatroy responses are there?

A

Eosinophils (allergies, parasite infections)

Lymphocytes (viral infections)

23
Q

Outline steps of neutrophil recruitment

A
  1. migration & rolling
  2. Integrin activation by chemokines
  3. Firm adhesion to endothelium
  4. Transmigration through endothelium into tissues
  5. Chemotaxis to inflamed site
24
Q

Give examples of neutrophil chemoattractants

A 
Chemokines IL-8
Complement components C5a
Leukotriene B4 (LTB4)
Bacterial components :
(peptides containing N-formylmethionine-leucine-phenylalanine lipids)
25
Q

What is the overall effect of acute inflammation on the vascular system?

A

Leukocytes & plasma proteins leave vessels and enter inflammation site to deal with damage / infection

26
Q

Which molecules are involved in neutrophil recruitment?

A

Adhesion molecules:

  • Selectin
  • Leukocytes
  • Immunoglobulin super family cell adhesion molecules (CAMs)
27
Q

How are integrins activated by chemokines?

A
  • Endothelial contact slows neutrophil rolling
  • Neutrophils express integrins LFA-1
  • integrins in low affinity configuration have no ligand
    binding
  • activated endothelial cells produce / bind chemokines
  • chemokines bind to neutrophils via receptors
28
Q

Describe the key features of purulent exudates in inflammation

A
  • Pus - many leukocytes, dead cells and microbes
  • pyogenic bacteria e,g, straphylococci
  • acute appendicitis
  • Abscess: localised collection of purulent inflammation
29
Q

Why does the composition of cells at the inflammation site change over time?

A

Neutrophils are short lived and die in tissues after 24 hours
Monocytes survive longer and proliferate, differentiating into macrophages
- use similar mechanism to leave blood -> tissue
inflamed

30
Q

How is acute inflammation triggered?

A

Infections
- Bacteria, viruses, parasites, fungi, toxins

Tissue damage by:

  • Physical agents: frost bite, burns, radiation (Ionising/UV)
  • Chemical agents: chemical burns, irritants
  • Mechanical activity and Ischemia: trauma, tissue crush, reduced blood flow

Foreign Bodies
- splinters, sutures, dirt, swallowed bones , dentures

31
Q

What enzymes are carried in neutrophile granules?

A

Specific granules (small)
- lysozymes, collagenase, gelatinase, lactoferrin, alkaline-
phosphatase

Azurophil granules (larger)
- myeloperoxidases, lysozymes, defensin, acid hydrolases,
proteases, (cathepsin G, elastases, collagenases, and
proteinase-3)

32
Q

Describe what happens once inflammation is resolved

A

-> recruited cells die, inflammatory mediators are
degraded
-> regulatory & tissue repair mechanisms are activated
-> lost tissue is replaced via cell regeneration /
connective tissue

33
Q

What is an exudate?

A

Any fluid that is filtered from the circulatory system into lesions or areas of inflammation

34
Q

What is acute inflammation?

A

Relatively non-specific, innate immune response, activated in response to several tissue injuries

35
Q

Which tissues have a high regeneration ability?

A

Epithelial cells in skin, airway, gut, & blood cells

Labile tissues divide continuously sometimes providing perfect regeneration with no scarring

36
Q

Outline the cellular events during acute inflammation

A
  1. migration and accumulation of cells (neutrophils initiate
    it), involving complex process of exit from blood
    vessels
  2. Removal of pathogens / injured & dead cells by
    neutrophils phagocytosing pathogens and dead
    tissues. Neutrophils die quickly creating pus
  3. Migration & accumulation of monocytes which
    differentiate into macrophages
    Phagocytosis -> clearance of injured site
    TGF-β release factors promote tissue repair
37
Q

What is Abscess?

A

Mass of necrotic tissue caused by pyogenic bacteria

If not drained / reabsorbed, abscess can become chronic

38
Q

What is the result of integrin activation?

A

Leads to high affinity configuration
- integrins bind to endothelium ligands
- integrin ligands (ICAM-1, VCAM-1) are induced by IL-1
and TNF-α
=> leads to firm adhesion of neutrophils to endothelium

39
Q

Describe serous exudate

A
  • few cells and no microbes
  • fluid from plasma or is secreted by mesothelial cells
  • serous cavities: pleura, peritonium and pericardium
  • skin blisters, present in burns and viral infections
40
Q

How does tissue repair occur by replacement?

A

Injured tissue is replaced by connective tissue
Scarring alters tissue function
TGF-β released by macrophages promoting fibrosis

41
Q

What are the outcomes of inflammation?

A

Complete resolution
- affected tissue is restored to it’s normal state

Repair
- lost tissue is replaced by connective tissue (scarring /
fibrosis)

Chronic inflammation
- arises when acute inflammation can’t be resolved

42
Q

What are the different types of inflammatory exudates?

A

Serous
Purulent
Fibrinuous
Haemorrhagic

43
Q

How does neutrophil recruitment occur in acute inflammation?

A

Its a multi step process involving adherence to luminal surface of endothelium and migration through vessel wall

44
Q

How does tissue scarring occur?

A

Normal tissue is only restored if the residual tissue is structurally intact
If there’s extensive damage affecting the structure, incomplete regeneration and scarring can occur

45
Q

How does neutrophil transmigration occur?

A

Neutrophils migrate through inter-endothelial spaces, passing through vessel walls and enter tissue
Chemotaxis towards inflamed site

46
Q

How is complete resolution achieved?

A

Via removal of the damaging agent
Injured tissue is replaced by cells of the same type
There is no change in tissue structure or function

47
Q

Name the different acute inflammation mediators

A 
1. Vasoactive amines (histamines, serotonin)
    antihistamine drugs (H1 receptor antagonists)
  1. Lipid derived mediators (from arachidonic acid)
    • prostaglandins: PGE2, PGD2, prostacyclin,
      thromboxane
    • leukotriens: LTC4, LTD4, LTE4) lipoxygenases
    • lipoxins are anti-inflammatory (lipoxygenase pathway)
    • COX inhibitor drugs
    • lipoxygenase inhibitors
  2. Inflammatory cytokines - interleukins
    IL-1, IL-6, TNF-α
  3. Chemokines IL-8
  4. Complement C3a, C5a
  5. Other kinins (bradykinin) neuropeptides
    • corticosteroid drugs inhibit transcription of
      inflammatory genes
48
Q

How long does acute inflammation last?

A

Rapid response (mins/hrs) to tissue injury lasting a short while (hrs/days)

49
Q

How is neutrophil transmigration guided?

A

Chemotaxis guided by gradient of chemoattractants

50
Q

What are NETs?

A

Neutophil extracellular traps
- mesh of chromatin containing antimicrobial molecules to
trap microbes

51
Q

What is transudate?

A

Fluid leaks due to altered osmotic / hydrostatic pressure

Vessel permeability is normal

52
Q

What are the 2 types of selectin involved in acute inflammation?

A

P-selectin: performed granules

E-selectin: Induced by IL-1, TNF-α producing cytokines by macrophages, mast cells, and endothelium at inflammation site

Pathology 1 (20 decks)

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