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Life Sciences - Sem 2 > 0.3 Acute Inflammation > Flashcards

0.3 Acute Inflammation Flashcards

1
Q

What are the mechanisms behind the four signs of inflammation?

A

Heat + Redness = increased blood flow

Swelling = vascular leakage / exudate

Pain = Increased sensitivity of pain receptors (hyperalgesia)

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2
Q

What are the differences between oedema, exudate, and pus?

A

Oedema = accumulation of fluid extravascularly in tissues

Exudate = oedema fluid with high protein content

Pus = Exudate containing viable and dead neutrophils, cel debris, microorganisms, proteins, lipids, DNA etc

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3
Q

What is the difference between purulent and suppuration?

A

Purulent = adjective form of pus

Suppuration = formation of pus

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4
Q

What are the 3 major components of acute inflammation in the order they occur?

A
  1. Dilation of small vessels = incread blood flow
  2. Increased microvascular permeability = plasma proteins and leukocytes leave circulation
  3. Emigration of leukocytes into extravascular tissue = accumulation in the focal area of injury
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5
Q

What are the 3 components of microcirculation?

A
  1. Arterioles
  2. Capillaries
  3. Post-capillary venules (PCV)
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6
Q

How does vasodilation cause hyperaemia in acute inflammation?

A

Normally, only some capillaries will transport blood

When inflamed, capillary beds open allowing ALL capillaries to transport blood in order to keep up with the increased blood flow from ateriolar and venular dilatation

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7
Q

Injury / infection causes the formation of vasoactive mediators and chemotactic factors. How do they lead to the formation of exudate in acute inflammation?

A
  1. Vasoactive mediators cause vasodilation and endothelial contraction = hyperaemia + increased hydrostatic pressure + increases vascular permeability in proteins
  2. Chemotactic factors activate neutrophils and increase adhesion molecules on endothelium = neutrophil margination and migration
  3. Hyperaemia + increased hydrostatic pressure + increased vascular permeability + neutrophil migration = fluid movement = exudate
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8
Q

Why is the exudation of fluid, plasma proteins, and neutrophils important?

A

Fluid = dilution of toxins + increase lymph flow

Plasma proteins = antibodes, complement system components + fibrin system components

Neutrophils = destruction of microorganisms

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9
Q

What changes in vascular flow occur during acute inflammation?

A
  1. Vasodilation = earliest manifestation
  2. Increased permeability of microvasculature
  3. Vascular congestion
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10
Q

What are the key characteristics of vasodilation?

A

Induced mostly by histamines in vascular smooth muscles

Affects arterioles first and subsequently capillary beds

Increased blood flow results in heat + redness

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11
Q

What is the difference between transudate and exudate?

A

Transudate = before increased microvasculature permeability, protein poor

Exudate = after increased microvasculature, permeability, outpouring of protein rich fluid

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12
Q

What are the key characteristics of vascular congestion?

A

Increased viscosity of blood = stasis (slow moving blood)

Results in loss of fluid and increased vessel diameter (engorgement)

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13
Q

Vascular leakage can occur for two reasons. What are they?

A
  1. Retraction of endothelial cells as a result of acute inflammation
  2. Endothelial injury (via burns, microbial toxins, or cholesterol)
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14
Q

What are the characteristics of endothelial cells caused vascular leakage?

A
  1. Induced by histamines + other mediators
  2. Results in opening of endothelial spaces to allow passage of neutrophils and exudate etc
  3. Occurs rapidly and is short lived (minutes)
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15
Q

What are the characteristics of endothelial injury caused vascular leakage?

A
  1. Endothelial cell necrosis + detachment from severe injury
  2. Rapid, but may be long-lived (hours to days)
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16
Q

The acute inflammatory response is stereotypic. What does this mean?

A
  1. No individuality in response, it is non-specific
  2. There will ALWAYS be exudation + neutrophil extravasation
  3. It will ALWAYS lead to one or more of the following: pus (sometimes), chronic inflammation (rarely), or resolution + healing
17
Q

What are the steps for emigration of WBC via leukocyte-endothelial interaction?

A
  1. Leukocytes are activated
  2. Rolling (leukocyte progression via blood flow is slowed by endothelial cells)
  3. Firm adhesion (via integrins)
  4. Diapedesis (squeezing of WBC) in response to tissue derived chemoattractants (gradient)
18
Q

What role do selectins and integrins play in the emmigration of WBCs?

A

Selectins + integrins = adhesion molecules

Selectins = connect respective ligand between leukocyte + endothelial cell to slow leukocyte progression

Integrins = activated by chemokines to create high affinity state in leukocyte, forming a stable adhesion with endothelial cells

19
Q

What is the difference between polynuclear and mononuclear cells in terms of inflammation

A

Polynuclear = acute inflammation

Mononuclear = chronic inflammation

Polynuclear ALWAYS BEFORE mononuclear

20
Q

What is the function of polymorphnuclear neutrophils in acute inflammation?

A

Short lived cells (~5 days in circulation, 2 hours in tissue)

Role = phagocytose + kill bacteria

Result = bystander injury of cells and ECM via radicals, proteinases, and myeloperoxidase

Accumulates in vast numbers = pus

21
Q

What are 4 systemic changes in inflammation?

A
  1. Leukocytosis = above normal WBC count in CSF (CSF = bone marrow leukocyte production)
  2. Fever (IL-1, TNF + IL-6 = peripheral vasoconstriction + shivering
  3. Elevated acute phase proteins in respnse to IL-1, TNF, and IL-6
  4. Malaise / Nausea
22
Q

What are acute phase proteins (APPs)?

A

Proteins that change their serum concentration by >25% in response to inflammatory cytokines

23
Q

Inflammatory cytokines cause changes in acute phase proteins (APPs). What four factors do these changes affect?

A
  1. Coagulation
  2. Antibacterial properties
  3. Proteinase inhibition
  4. Metal metabolism
24
Q

What are the three morphological types of acute inflammation?

A
  1. Suppurative (pus formation / abscess)
  2. Serous (voluminous clear fluid produced / cellulitis)
  3. Fibrinous (fibrin deposited on a surface / pericarditis)
25
Q

What role do prostaglandins play in acute inflammation?

A

Prostaglandins work alongside inflammatory mediators (histamine, bradykinin etc) to sensitise pain receptors

The reason why inflammation is painful

26
Q

What are the four possible outcomes for acute inflammation?

A
  1. Recover / resolution
  2. Ulceration (with/without pus)
  3. Abscess (necrosis followed by healing)
  4. Progression to chronic inflammation

Life Sciences - Sem 2 (27 decks)

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