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HLTH3200 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation, the cause and the types

A

Inflammation:
- Response of vascularised tissues to infections and tissue damage
- Brings cells and molecules of host defence from circulation to sites where they are needed, to eliminate offending agents
Types:
- Acute (seconds to 2-3 days)
- Sub-Acute (2 weeks)
- Chronic (weeks to months)
Cause:
- Complex response to injurious agents that consist of vascular response, cellular reaction and systemic reaction

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2
Q

What are the main characteristic features of early acute inflammation

A
  • Immediate / rapid and early defensive response in host tissue to injury
  • Non-specific
  • Exudate: Inflammatory extravascular fluid / infiltrate, plasma liquid, plasma proteins, WBC, RBC, cellular debris
  • Causes changes in microcirculation
  • Exudation of fluid
  • Emigration of leukocytes
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3
Q

What are the 5 cardinal signs of acute inflammation

A
  • Heat: Vasodilation
  • Redness: Increased vascular permeability
  • Swelling: Leukocyte extravasation / release of chemicals
  • Pain: Leukocyte activation
  • Loss of function: Endothelial damage
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4
Q

What is vasodilation (acute inflammation)

A
  • Arteriolar Vasodilation
  • Increased blood flow
  • Erythema
  • Leads to heat loss across epidermis
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5
Q

What is increased vascular permeability (acute inflammation)

A
  • Endothelial cells involved in exudation of protein rich fluid into interstitium
  • Expansion of capillary bed facilitates this movement
  • Edema: Marked outflow of fluid and accumulation in interstitial tissue
  • Blood: Increased viscosity, vascular stasis which impedes outflow
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6
Q

What are the different classifications of fluids

A
  • Transudate: Fluid leakage due to increased hydrostatic / decreased osmotic pressure, ultra filtrate of plasma with little protein and few or no cells
  • Exudate: Extravascular fluid collection, rich in protein and cells, in inflammation, vascular permeability increases
  • Edema: Excess extravascular fluid in interstitial space, either transudate or exudate
  • Pus: Made up of neutrophils, necrotic cells and edema fluid
  • Serous: Transudate with mainly edema fluid and cells
  • Serosanguinous: Effusion containing RBC
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7
Q

What is leukocyte extravasation (acute inflammation)

A
  • Delivers delivers leukocytes from blood to site of injury
  • Involves adhesion receptor (selectins, Ig family, integrins and mucin-like glycoproteins)
  • Process: Margination, transmigration and migration
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8
Q

What is the process of leukocyte extravasation

A

Margination:
- Leukocytes adhere to endothelial cells of BV due to CAMs
- Selectins teacher neutrophils to endothelium, begin rolling
- Tighter binding through ICAMs through integrins
Transmigration:
- Leukocytes move across the endothelium
Migration:
- Movement of leukocytes into interstitial tissue
- Movement towards chemotactic stimuli
- Phagocytosis of microbes
- Leukocyte induced acute cytokine immediate response / induced endothelial expression of receptors

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9
Q

What is leukocyte activation

A
  • Recognition of microbes and mediators via phagocytic receptors
  • Lead to phagocytosis and production of ROS lysosomal enzymes
  • Lead to leukocyte activation and killing of microbes
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10
Q

What is the wheal and flare response

A
  • Triple Response: Histamine, saline and allergens
  • Reddening: Vasodilation
  • Flare: Red halo, hyperaemia
  • Wheal: Swelling, fluid accumulation
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11
Q

What are inducers of acute inflammation

A
  • Infections
  • Trauma
  • Physical and chemical agents
  • Foreign bodies
  • Tissue necrosis
  • Hypersensitivity reactions
  • Environmental / non-selfsubstances
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12
Q

What are systemic clinical signs of acute inflammation

A
  • Fever: Entry of pyrogens and release of prostaglandins
  • WBC Count: BM release / production, increased neutrophils, lymphocytes, neutropenia and high WBC
  • Plasma Proteins: Changes in plasma protein levels
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13
Q

What is the outcome of acute inflammation

A
  • Complete resolution
  • Abscess formation
  • Fibrosis (substantial tissue destruction, little regeneration, abundant fibrin exudation)
  • Progression to chronic inflammation
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14
Q

List the 4 morphological patterns of acute inflammation

A
  • Serous: Accumulation of excessive clear watery fluid, skin peritoneal, pleural / pericardial cavities, exudate w low plasma protein / cell content
  • Fibrinous: Increased fibrin / fibrinogen in vessel wall / extracellular spaces (pleura, pericardium), exudate w high plasma protein
  • Catarrhal: Inflammation of mucous membranes, airways / cavities, enlargement of epithelial cells, exudate of mucous / WBC
  • Purulent / Suppurative: Bacteria, pus / purulent w neutrophils, necrotic cells and edema
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15
Q

What are examples / nomenclature of acute inflammation

A
  • Appendicitis: Inflammation of the appendix
  • Cellulitis: Inflammation of skin
  • Meningitis: Inflammation of brain
  • Pneumonitis: Inflammation of lungs
  • Nephritis: Inflammation of kidney
  • Myocarditis: Inflammatory cardiomyopathy, inflammation of heart muscle
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16
Q

What are abcesses’

A
  • Localised collections of purulent inflammatory tissue
  • Defence reaction to bacteria
  • Abscess seals infected tissue from adjacent healthy cells
  • Central Region: Mass of necrotic leukocytes / tissue with zone of neutrophils
  • Outer Region: Vascular dilation, parenchymal / fibroblastic proliferation
  • Over Time: Replaced by connective tissue
  • Exudative purulent localised inflammation
17
Q

What is and the causes of chronic inflammation

A
  • Response of prolonged duration (weeks or months)
  • Inflammation, tissue injury, and attempts at repair coexist
  • Sum of responses mounted by tissue against a persistent injurious agent / aggressive stimuli
  • Persistent infections / long lasting infections
18
Q

List the four main causes of chronic inflammation

A
  • Persistant infections
  • Prolonged exposure
  • Autoimmunity
  • Non-resolution
19
Q

What are persistent infections and examples (chronic inflammation)

A
  • Persistent infections by microorganisms that are difficult to eradicate
  • Examples: Mycobacteria and certain viruses, fungi, and parasites
    Tuberculosis:
  • Systemic infectious disease
  • Caused by mycobacterium tuberculosis
  • Varying manifestations, creates tuberculous granuloma (caseation of necrosis)
  • Treated with antibiotics
20
Q

What is prolonged exposure and examples (chronic inflammation)

A
  • Prolonged exposure to potentially toxic agents (exogenous or endogenous)
    Silica:
  • Exogenous particulate
  • Causes silicosis when inhaled for prolonged periods - Inflammatory lung disease
    Hyperlipidaemia:
  • Excessive production and tissue deposition of endogenous cholesterol, triglycerides and other fats
  • Causing atherosclerosis of arterial wall
21
Q

What is autoimmunity (chronic inflammation)

A
  • Autoimmune diseases
  • Malfunction in immune system
  • Components of patient’s own body get attacked
  • Chronic tissue damage and inflammation
    Multiple Sclerosis:
  • Lesions (early / chronic)
  • Cause inflammation / demyelination
  • Contain activated T / B cells, macrophages and pro-inflammatory cytokines
  • Early: Mononuclear inflammatory cells
  • Chronic: Complete demyelination severe astrogliosis very little inflammation
    Allergies:
  • Type 1 hypersensitivity
  • Vasodilation and nerve irritation
22
Q

What is non-resolution (chronic inflammation)

A
  • Following acute inflammation
  • Chronic Leg Ulcer: Break in skin of leg allows air and bacteria to invade underlying tissue, leads to poor circulation and venous / arterial disease
23
Q

What is an example of specific chronic inflammation

A
  • Granulomatous inflammation
    Granuloma:
  • Nodular activated macrophages (0.5-2mm) surrounding a central core
  • Surrounded by a rim of lymphocytes, macrophages and some fibrosis
24
Q

What are the type of granulomas in the body

A

Foreign Body Granuloma:
- Particles too large to be phagocytosed
- Material is inert (doesn’t provoke immune response)
- Endo: Keratin, cholesterol
- Exo: Splinter, parasite
Immune Granuloma:
- Insoluble particles
- Capable of inducing cell mediate immune response
- Non-degradable antigens
Unknown Aetiology Granuloma:
- Crohn’s disease
- Portion of GIT
- Inflammation, clusters of neutrophils with crypts

25
Q

What is an example of unspecific chronic inflammation

A
  • Destruction of gastric / duodenal mucosa by H.pylori infection
  • Ulcerated surface (acute / chronic inflammatory cells)
  • Peritonitis, haemorrhage, fibrous scar
  • Inflammatory exudate
  • Fibrinoid necrosis
  • Granulation / fibrous tissue
26
Q

Briefly compare and contrast acute and chronic inflammation

A
  • Acute: Often resolution with tissue recovery, neutrophils, vascular damage, more exudation, little or no fibrosis, flush, flare and weal
  • Chronic: Often scarring and fibrosis with loss of function, macrophages and lymphocytes, new BV, no / less exudation, prominent fibrosis and little signs
27
Q

What are the morphological signs of chronic inflammation

A
  • Infiltration with mononuclear cells
  • Tissue destruction (persistent offending agent)
  • Attempt at healing (angiogenesis and fibrosis)
28
Q

What are the cardinal signs of chronic inflammation

A
  • Increased blood flow and increased capillary permeability
  • Accumulation of WBC continues, composition of cells changes
  • Tissue destruction (necrosis)
    Infiltration with mononuclear cells leads to immune response and phagocytosis

HLTH3200 (14 decks)

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