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2013/2014 > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

Functions of Inflammation

A

Defend against and stop aggression. Clean up by products via phagocytosis. Repair damaged tissues.

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2
Q

Two main characteristics of acute inflammation

A

Interstitial edema and accumulation of neutrophils.

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3
Q

Histological appearance of neutrophils

A

Multilobar nucleus. More than 3 usually. Lavender cytoplasm and purple nuclei.

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4
Q

Characteristics of chronic inflammation

A

Many mononuclear cells that include lymphocytes, plasma cells, macrophages. Granulation tissue, angiogenesis, fibrosis.

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5
Q

Histological appearance of plasma cells

A

Long, have epically located nucleus.

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6
Q

Appearance of lymphocytes

A

Round nucleus with little cytoplasm.

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7
Q

3 major components of acute inflammation

A
  1. Vascular alterations leading to increased blood flow. 2. Microvasculature alterations that allow proteins and neutrophils to leave circulation and produce an inflammatory exudate. 3. Diapedesis and accumulation of neutrophils.
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8
Q

Clinical signs of inflammation

A

Calor Rubor Tumor Dolor and Functio Laesa

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9
Q

What does vascular permeability do in acute inflammation?

A

Endothelial cells become leaky, either by direct injury or by chemical mediators. Protein rich fluid escapes into interstitial space (edema).

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10
Q

Why does vascular stasis occur in acute inflammation?

A

Because vascular dilation and exudation occur. Congestion also occurs to give inflammatory cells maximum time to collect and move into tissue.

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11
Q

Mechanisms of endothelial permeability

A

Endothelial retraction, where cytoskeleton reorganizes. Also contraction, but not sure about the difference. Direct endothelial injury and neutrophil mediated endothelial injury too.

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12
Q

Cellular events in acute inflammation

A

Margination, rolling, and adhesion of the leukocytes. Transmigration across endothelium. Migration through interstitial tissue towards chemotactic stimulus.

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13
Q

Selectin

A

Surface molecule that mediates cell attachment and rolling along endothelial cells. Sialyl Lewis X on cells binds to selectins on endothelium. Promoted by histamine, thrombin. P, E, and L selectin (platelets, endothelial cells, leukocytes).

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14
Q

Integrin

A

Expressed on endothelial cells. Their affinity is increased by chemokines.

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15
Q

PECAM

A

Platelet endothelial cell adhesion molecule, facilitates migration.

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16
Q

How do neutrophils know where to go in interstitium?

A

Follow chemotactic gradient. Usually molecules like leukotrienes, chemokines, complement fragments, which bind to neutrophils, produce secondary messengers, and cause pseudopod movement.

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17
Q

What happens when neutrophil arrives?

A

Phagocytosis or degranulation

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18
Q

What happens when offending agent is engulfed?

A

Oxygen dependent killing (myeloperoxidase, which takes hydrogen peroxide and halogenates it). Oxygen independent killing (major basic protein, defensins, lysozyme).

19
Q

Neutrophil induced tissue injury

A

Neutrophils can also degranulate, releasing free radicals and lysosomal enzymes into the extracellular space. Can cause chronic inflammation if persistent.

20
Q

How can acute inflammation resolve?

A

Macrophages engulf neutrophil and tissue debris causing complete resolution. Abscess can form. Healing and scarring can occur, or progression to chronic inflammation.

21
Q

Purulent

A

Exudate with prominent neutrophils

22
Q

Suppuritive

A

Purulent exudate with tissue necrosis

23
Q

Abscess

A

Localized collection of pus

24
Q

Fibrinous

A

Exudate containing fibrin due to leakage of proteins from blood vessels with increased permeability and activation of the coagulation cascade.

25
Q

Ulcer

A

Surface defect of an organ secondary to sloughing off of necrotic tissue

26
Q

Two sources of chemical mediators of inflammation

A

Cells and blood plasma (synthesized in liver)

27
Q

Cellular mediators of inflammation

A

Histamine, prostaglandins, Leukotrienes

28
Q

Plasma derived mediators of inflammation

A

Hageman Factor (Kinin system), complement proteins

29
Q

Histamine Source and Function

A

Released by mast cells and basophils. Among the first mediators to be released in an inflammatory response. Causes vasodilation and increased vascular permeability.

30
Q

Arachidonic Acid Metabolites, Function?

A

Cyclooxygenases (prostaglandins and thromboxanes), and Lipooxygenases (leukotrienes and lipoxins). Short range signaling agents.

31
Q

How is platelet activating factor released?

A

From mast cells and other leukocytes. Causes platelet aggregation and other things.

32
Q

What are the major inflammatory cytokines?

A

TNF and IL-1. Activate endothelial cells. Also involved in septic shock.

33
Q

Hageman Factor

A

AKA clotting factor XII. Initiates the kinin, clotting, finbrinolytic, and complement cascades.

34
Q

Bradykinin

A

Generated from Kallikrein. Involved in blood vessel dilation, increased permeability, pain.

35
Q

Kallikrein effect on Hageman Factor?

A

Profound amplifier!

36
Q

Intrinsic Clotting System

A

Results in the activation of thrombin, which leaves fibrinogen to fibrin. Thrombin also causes increased leukocyte adhesion to endothelium.

37
Q

Chronic Inflammation

A

Prolonged duration, active inflammation, tissue destruction, healing, all happening simultaneously

38
Q

How does chronic inflammation occur?

A

Persistent acute inflammation, persistent infection, prolonged exposure to toxic substances, autoimmune disease.

39
Q

Appearance of eosinophils

A

Bilobed nucleus with eosinophilic granules

40
Q

Do macrophages appear more in chronic or acute inflammation?

A

Chronic!

41
Q

Why does fibrosis occur in chronic inflammation?

A

Because macrophages induce fibroblast activity.

42
Q

Appearance of macrophages

A

Large, kidney shaped nucleus, blue cytoplasm.

43
Q

Granulomatous Inflammation Appearance

A

Epithelioid Macrophages surrounded by a collar of leukocytes. Central necrosis. Giant cells in the center.

2013/2014 (23 decks)

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