Acute inflammation Flashcards

1
Q

Define acute inflammation and what are some common causes?

A
immediate / early response to injury (mins-days)
Causes:
- infection (bacterial, viral etc)
- physical inflammation e.g. burns 
- chemical agent 
- immune response 
- tissue death 
Any form of tissue injury will induce acute inflammation
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2
Q

What are the consequences of acute inflammation?

A

can be beneficial e.g. bacterial killing, removal of dead tissue
can also be harmful - lung damage in pneumonia, kidney damage in acute pylonephritis
May precede chronic inflammation, healing and repair

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3
Q

What are the 2 main components of acute inflammation?

A

1) vascular response
- vasodilation (erytherma)
- odema - increased permeability
- leukocyte margination

2) inflammatory cell infiltration
- mainly neutrophils (1st line defence)
- macrophages (later stages)
- lymphocytes may also be involved

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4
Q

What happens during increased permeability?

A

protein-rich fluid escapes into extravascular space
increased concentration of RBCs = congestion
increased blood viscosity
reduced blood flow = stasis

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5
Q

What happens during leukocyte margination?

A

loss of axial streaming
first stage in process of leukocyte emigration - allows them to come into contact with endothelial lining
- the initial increase in blood flow leads to leukocyte margination

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6
Q

What are the phases of leukocyte margination?

A

1) margination = movement to periphery of blood vessels (mainly related to stasis)
2) rolling = transient weak binding to endothelium by selectins
3) adhesion = firm adhesion to endothelium by integrins
4) transmigration = movement into extravascular space by platelet endothelial cell adhesion molecule-1

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7
Q

What is involved in the control of leukocyte migration ?

A

interaction between leukocyte receptors and ligands on endothelial cells
- regulated by cytokines and chemokines

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8
Q

Define chemotaxis:

A

migration along chemical gradients

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9
Q

What are some examples of chemotactic substances?

A

bacterial products, complement components (C5a), leukotrienes, chemotactic cytokines (attract leukocytes and activate receptors)

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10
Q

What is the process of phagocytosis?

A

1) recognition and attachment of particle to leukocyte - opsonins
2) engulfment - pseudopods surround particle, form phagocytic vacuole
3) killing and degradation - production of ROS, release of lysosomal enzymes

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11
Q

What are the general aspects about the chemical mediators involved in acute inflammation?

A

may be locally produced or systemic
most act on specific receptors expressed on target cells 0 mediator function tightly regulated
others act in a non-specific manner

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12
Q

What are some different examples of suppurative (purulent) inflammation?

A

Pus

  • mainly neutrophils, necrotic cells and bacteria
  • complication of infection with pus forming bacteria - pyogenic (specific type of pus forming bacteria)

Abscess
- localised collection of pus

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13
Q

What are diseases with lymphocytes rather than neutrophils?

A

acute viral hepatitis - A, B, C
viral meningitis e.g. coxsackievirus, mumps
viral myocarditis e.g. coxsackievirus, echovirus

immune mediated diseases
- autoimmune hepatitis

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14
Q

What are the main inflammatory cells in viral myocarditis?

A

lymphocytes

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15
Q

What is the sequel of acute inflammation?

A

resolution - limited injury, return tissue to normal state
scarring/fibrosis - more extensive damage, tissues with limited capacity to regenerate, abscess formation
progression to chronic

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16
Q

What are the classic clinical features of acute inflammation?

A

1) heat (calor)
2) redness (rubor)
3) swelling (tumor)
4) pain (dolor)
HALLMARKS

17
Q

What is also apparent in acute inflammation?

A

raised WBC count - mainly neutrophils

  • particularly high pyogenic bacteria
  • also present in non-infective causes (myocardial infarction)
  • neutrophil rich leukocytosis in other body fluids

if rich in lymphocytes instead it is more likely to be a viral infection

18
Q

What are examples of hereditary defects in leukocyte function?

A

chronic granulomatous disease

19
Q

What are examples of acquired defects in leukocyte function?

A

leukaemia

20
Q

What is a broad spectrum anti-inflammatory treatment?

A

NSAIDs- inhibits cyclooxygenase enzymes involved in arachidonic acid production which produces prostaglandins

21
Q

What is a targeted anti-inflammatory treatment?

A

therapies blocking specific chemical mediators or receptor ligand interactions e.g. anti-TNF ab, anti-ICAM-1