Inflammation Flashcards

1
Q

What is Inflammation?

A

Response of local vascular tissue to injury.

Inflammation is a normal response in defense and healing.

(If persistent and chronic, it is pathologic)

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2
Q

What is vascular tissues?

A

Vascular tissue is tissue which responds to injury.

Made up of three elements:
1. Vessels
2. Blood
3. Blood cells

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3
Q

Describe Acute Inflammation?

A

Early response to injury
Short duration (hrs - days)
Localize & removes agent of injury
Precedes IR (immune response)

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4
Q

Describe Chronic Inflammation?

A

Longer duration (wks - yrs)
Self-perpetuating cycle

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5
Q

What are the two responses to accute inflammation?

A
  1. Vacular Response
  2. Cellular Response
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6
Q

Describe the Vascular Response to A. Inflm?

A
  1. Injury leads to stat vasoconstriction (brief) at a local level. This is the nero response to keeps bleeding to a minimum.
    i. Leukocytes, Mast Cells, & Platelets release chemical mediators (de-granulate)
    ii. Histamine & Prostaglandins released - affect nerves and blood vessels on a local level causing…
  2. Vasodilation resulting in…
  3. Increase permeability
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7
Q

Histamine: What are the two essential functions?

A
  1. Increase the permeability of the cell wall. (In addition to the normal trancapillary exhange, you now have larger gaps which allow more/larger things to move out. Eg - O2, Nitrogen)
  2. Increase in capillary dilation
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8
Q

What is vasodilation?

A

Increased blood flow to do dilation of capiliary and permeability of cell wall.

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9
Q

What is Hyperemia?

A

Increase in blood flow from vasodilation.

Signs of hyperemia - Redness, Swelling, and Increased Blood Flow

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10
Q

Prostaglandin?

A

Does both the functions of histamine PLUS:
Causes Pain

Consider them as a local hormone, produced in many tissues, do different things depending where they occur

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11
Q

What is Rouleau?

A

The stacking of erythrocytes which slows blood flow in vasulature.

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12
Q

Describe the Cellular Response of A. Inflm?

A
  1. Chemotaxis of neutrophils and WBC’s to site of injury
  2. Margination of Endothelium (Pavementing). Assisted by adhesion molecules
  3. Diapedesis/Emigration of defense cells into tissue cells. Objective to localize and removal of debris.
  4. Phagocytosis of cell debris & foreign particles
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13
Q

5 Signs of Local Inflammation?

A
  1. Redness (erythema)
  2. Swelling
  3. Warmth
  4. Pain
  5. Loss of Fx (may not be present)
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14
Q

What is exudate?

A

Comprised of: i) fluid ii) protiens iii) blood cells

Fx: is to carry out healing cells and proteins into tissues
Exudate is an increase of fluid causing a dilute of toxins

Note: exudate expands, needing space it pushes out other cells causing swelling. The tissue stretch causes pain and immobility.

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15
Q

Name the 5 types of exudate?

A
  1. Serous
  2. Purulent/Suppurative
  3. Hemorrhagic
  4. Fibrinous
  5. Membranous
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16
Q

Exudate: Serous

A

Watery, Clear - Pink, Low in Proteins and Cells
Associated with acute inflammation.

17
Q

Exudate: Purulent/Suppurative

A

Pus! Contains WBC (neutrophils) and necrotic cells.
Thick, cloudy, smells bad (infected!)
Associated with severe acute inflammation.

18
Q

Exudate: Hemorrhagic

A

Major component is RBC’s (Erythrocytes), appears red.
Associated with severe injury, severed blood vessels.

19
Q

Exudate: Fibrinous

A

High in fibrinogen. Creates a sticky mesh.
Not common.

20
Q

Exudate: Membranous

A

Mucous Membrane
Necrotic Cells in Fibropurulent Exudate
(fibro = fibers, purulent = puss)

21
Q

4 Clinical Signs of Inflammation

A
  1. Headache
  2. Fatigue
  3. Malaise (general feeling of unwell)
  4. Fever
22
Q

Fever: What are the benefits?

A

Enhances phagocytosis and the Immune Response
Inhibits growth and reproduction of pathogens

23
Q

Pathogenesis of Fever?

A

Exogenous pyrogens (from outside the body):
i) induce host cells to produce fever-producing mediators. Stimulation of a cascade of production of endogenous pyrogens (released by body called IL1 + IL6 (Interleukin), and TNF (tumor necrosis factor).
ii) increases the set point by binding to the receptor at the hypothalamic receptor, mediated by PGE3 (prostaglandin).
iii) resulting in the temp set point adjusted upwards via cAMP (adenosene monophosphate, internal cellular messenger which helps PGE2 bind)

Note: if a fever develops in an absence of infection, there is no exogenous pyrgens. Eg. Anemia which causes excessive cell breakdown makes additional sourse of pyrogens instead.

24
Q

C-reative Protein
(CRP)

A

Produced by the Liver, in response to inflammation.
Serum marker for inflammation.
Persistant elevated levels is likely marker for cardio disease and atherosclerosis.

25
Q

Tx of Inflammation

A
  1. Cold (vasoconstriction - dec blood flow - dec blood loss - dec hydrostatic pressure - less exudate) = Less swelling
  2. i) Elevation (inc difficult for blood to reach - dec blood flow - dec hydrostatic pressure - dec exudate) = Decrease swelling.
    ii) Pressure (inc external pressure - oppose hydrostatic pressure - dec in exucate) = Decrease swelling.
  3. Heat (inc local vasodilation - in blood flow) = stimulates phagocytosis
  4. NSAID’s (dec prostaglandin synthesis) = Decreas pain
  5. Steroidal Anti-Inflammatory Drugs (decrease cap permeability, dec WBC, dec release of prostaglandins & histamine)