Inflammation and Repair Flashcards

1
Q

Four cardinal signs of inflammation

A

Rubor (redness), Calor (heat), Tumor (swelling), Dolor (pain)

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2
Q

Characteristic cells of chronic inflammation

A

Lymphocytes, plasma cells, and macrophages

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3
Q

Chracteristic cells of acute inflammation

A

Platelets and neutrophils (PMNs)

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4
Q

How do arterioles react early in injury?

A

Transient vasoconstriction followed by vasodilation (hyperemia)

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5
Q

What is the primary site at which vasoactive mediators induce endothelial changes?

A

The post-capillary venule

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6
Q

Effusion

A

Excess fluid in cavities of the body

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7
Q

Difference between transudate and exudate

A

Transudate - low protein content (sg lt 1.015), exudate - high protein content (sg gt 1.015)

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8
Q

Give two classes of drugs that inhibit arachidonic acid metabolism

A

Corticosteroids and NSAIDs

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9
Q

How might corticosteroids inhibit arachidonic acid metabolism?

A

Induction of lipocortin, which inhibits PLA2, thus reducing generation of arachidonic acid

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10
Q

Platelet adherence, aggregation, and degranulation occurs when platelets come in contact with what?

A

Exposed collagen or thrombin

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11
Q

Platelet degranulation leads to release of what and what does it do (in this instance)?

A

Serotonin, a vasoactive mediator of acute inflammation

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12
Q

What stimulates histamine release from mast cells?

A

Anaphylatoxins (eg C3a and C5a)

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13
Q

The most important vasoactive mediators produced by endothelial cells

A

PGI2, NO, Endothelin

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14
Q

What causes endothelial cells to secrete increased amounts of procoagulant tissue factor?

A

Lipopolysaccharide or specific cytokines (e.g. IL-1)

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15
Q

How else is prostacyclin written?

A

PGI2

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16
Q

What is arachidonic acid generated from and by what enzyme?

A

Generated from Phosphatidyl Choline by Phospholipase A2

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17
Q

What regulator of vascular permeability do monocytes and macrophages secrete?

A

Platelet-activating factor (PAF)

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18
Q

What activates Hageman Factor (Factor 12)?

A

Negatively charged surfaces (e.g. basement membranes), proteolytic enzymes, and bacterial lipopolysaccharide

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19
Q

What does Hageman activate?

A

Plasma kallikreins (e.g. bradykinin)

20
Q

What complex is formed by activation of the complement system?

A

The Membrane Attack Complex

21
Q

What are the pathways which activate the complement system?

A

Classical, alternative, and high-mannos

22
Q

What triggers the classical complement pathway?

A

Binding of C1 complex proteins to immune complexes

23
Q

What effects do anaphylatoxins have on smooth muscle and vasculature?

A

Enhancement of smooth muscle contraction and increase in vascular permeability

24
Q

Opsonization

A

Process by which a specific molecule binds to the surface of a bacterium

25
Q

What is the purpose of opsonization

A

Enhances phagocytosis by coating target with an opsonin

26
Q

What are the three mechanisms by which leukocytes accrue at site of injury and what protein moderates each?

A

Margination (selectins), Emigration (integrins), Chemotaxis (C5a, Chemokines, Bacterial and Mitochondrial products)

27
Q

Examples of things that PMN receptors can bind

A

Fc portion of IgG and IgM, Complement components, Arachidonic acid metabolites, Chemotactic factors

28
Q

Three reactive oxygen metabolites which are used to kill phagocytosed bacteria

A

Superoxide anion, Hydrogen peroxide, Hypochlorus acid

29
Q

Oxygen-independent methods for killing phagocytosed bacteria

A

Lysosomal hydrolases, bactericicdal/permeability-increasing protein, defensins, lysozyme

30
Q

What type of cell responds specifically to parasitic infections and what other type of reaction is it found in?

A

Eosinophils. Also found in allergic reactions

31
Q

In what types of event is a chronic inflammatory response the first response (ie no acute inflammatory response)

A

Viral infections, automimmune disease, malignant tumors

32
Q

Principle cells of granulmous inflammation

A

Macrophages and lymphocytes

33
Q

Three types of granulomas

A

Foreign body giant granulomas, allergic granulomas, caseous granulomas (tb)

34
Q

Leukocytosis

A

Increase in number of circulating leukocytes, commonly accompanies acute inflammation

35
Q

Leukopenia

A

Decrease in circulating white cell count

36
Q

Characteristics of acute phase response

A

Fever, leukocytosis, decreased appetite, change in levels of acute phase proteins (eg C-reactive protein)

37
Q

What does granulation tissue consist of?

A

Fibroblasts, myofibroblasts, macrophages, and proliferating capillaries (endothelial cells)

38
Q

How long after injury does vascular proliferation start?

A

48 to 72 hours

39
Q

What is the rule of thumb for wound strength?

A

2 weeks = 20% strength

40
Q

What is the predominant collagen found in mature scars?

A

Type I

41
Q

Why is wound healing inadequate in scurvy?

A

Because collagen hydroxylation requires vitamin C

42
Q

What type of cell mediates wound contraction

A

Myofibroblast

43
Q

What protein present in clots can be cross-linked to bridge clots with tissues?

A

Plasma fibronectin

44
Q

Scar formation following spinal cord injury, which can prevent axon regeneration, is mediated largely by what type of cell?

A

Vascular pericytes

45
Q

Primary intention

A

Healing of wounds with apposed edges

46
Q

Secondary Intention

A

Healing of wounds without apposed edges