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Foundations of Medicine > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

Pathology

1
Q

Acute Inflammation

A

Immediate and early response to injury, designed to deliver leukocytes to site of injury

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2
Q

Diverticulitis

A

Inflammation of

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3
Q

Diverticulosis

A

A disease or condition

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4
Q

Causes of Inflammation

A
  1. Microbial Infection
  2. Hypersensitivity reactions
  3. Physical agents (trauma, radiation, heat injury)
  4. chemicals (corrosives, acids, bacterial toxins)
  5. Tumour necrosis (Secondary to ischaemia)
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5
Q

What are hypersensitivity reactions?

A

Excessive immune response -> Tissue damage

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6
Q

Microbial Infection includes…

A
  1. Bacterial endotoxins
  2. Bacterial exotoxins
  3. Viral intracellular multiplication
  4. organisms causing hypersensitivity reactions
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7
Q

Bacterial exotoxins

A

chemicals released by bacteria which stimulate inflammation

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8
Q

Bacterial endotoxins

A

Associated with bacterial cell walls, also stimulate inflammation

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9
Q

Viral intracellular multiplication

A

leading to cell death, debris then stimulates inflammation

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10
Q

Cardinal signs of acute inflammation and why

A
  1. Redness (rubor)- due to dilation of vessels
  2. Heat (calor)- due to increased blood flow
  3. Swelling (tumor)- due to accumulation of fluid & increase in inflammatory cells migrating to the area
  4. Pain (dolor)- due to physical distortion of tissue & release of chemical mediators (Bk, PGs)
  5. Loss of function (functio laesa)
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11
Q

Stages of Inflammation

A
  1. Release of chemical mediators
  2. Vasodilation
  3. Increased vascular permeability
  4. Fluid accumulation
  5. Cellular recruitment
  6. Phagocytosis
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12
Q

Components of Acute Inflammation

A
  1. Vascular changes
    -change in vessel calibre
    -Increase in vascular permeability
  2. Cellular events
    -formation of cellular exudate
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13
Q

Vascular Changes in Acute Inflammation

A
  1. Changes in vascular calibre
  2. Initial transient constriction
  3. Then vasodilation (can last 15m to several hours)
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14
Q

Exudation

A
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15
Q

Formation of cellular exudate

A

Accumulation of neutrophil polymorphs

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16
Q

Neutrophils characteristics

A
  1. can move
  2. can stick to opsonised microorganisms
  3. Phagocytosis
  4. can kill microorganisms
17
Q

How do neutrophils move?

A

-by contracting cytoplasmic microtubules
-Calcium ion dependent mechanism, chemotaxis in response to inflammatory chemicals

18
Q

How do neutrophils bind to opsonised microorganisms?

A

Once bacteria have encountered immunoglobulins or complement components, neutrophils can bind to them

19
Q

How do neutrophils kill?

A

A variety of intracellular methods to produce microbicidal agents
Eg, producing hydrogen peroxidase, to react with cytoplasmic myeloperoxidase

20
Q

Margination

A

Loss of intravascular fluid
Slowing of flow to the site

Allows neutrophils to marginate

21
Q

Adhesion

A

Also known as “pavementing”
Neutrophils adhere to vascular endothelium

Caused by interaction between paired adhesion molecules on the neutrophil and endothelial surfaces

22
Q

Emigration

A

Pass between endothelial cells
Through basal lamina and into adventitia

23
Q

Components of Acute Inflammation

A

-Cells: Endothelial and Inflammatory
-Chemical agents: cytokines, complement, histamine, PGs

24
Q

chemical mediators- early chemical events

A
  1. Histamine and thrombin are released by original inflammatory stimulus
    -These chemicals cause upregulation of P-selectin and platelet activating factor (PAF) on the endothelial cells
  2. Neutrophils start to roll along endothelial wall
    -Ligands on the neutrophil surface engage with the P-selectin on the endothelial cells

PAF docks with corresponding receptor on neutrophil and promotes expression of other molecules (LFA-1, MAC-1) – overall end result is firm neutrophil adhesion to endothelial surface

25
Q

Chemical mediators released by cells

A
  1. Histamine
  2. Lysosomal compounds
  3. Leukotrienes
  4. Prostaglandins
  5. Serotonin
  6. Chemokines
26
Q

Histamine…

A
  1. Causes vascular dilation and permeability
  2. Released mainly by mast cells
27
Q

Lysosomal compounds

A
  1. Lots of different functions, such as vascular permeability
  2. Some can stimulate histamine release from mast cells
  3. Released by neutrophils
28
Q

Leukotrienes

A
  1. Vasoactive properties
  2. Often made in neutrophils from arachidonic acid
29
Q

Prostaglandins

A
  1. Also derived from arachidonic acid
  2. Some cause increased vacular permeability
  3. Some cause platelet aggregation
  4. Released by lots of cell types
30
Q

Serotonin

A
  1. Vasoconstrictor
  2. Released by platelets
31
Q

Chemokines

A
  1. Family of chemicals which attract more white blood cells to site of inflammation
  2. Eg IL-8 attracts neutrophils
32
Q

Plasma factors- cascade system in plasma

A
  1. Coagulation system
  2. Kinins
  3. Fibrinolytic system
  4. Complement system
33
Q

Coagulation system

A

converts soluble fibrinogen into fibrin

34
Q

Kinins

A

Activated by coagulation factor XII
Bradykinin important peptide in mediating vasodilation, pain

Foundations of Medicine (6 decks)

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