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MOD Midterm > Chapter 3: Acute Inflammation II > Flashcards

Chapter 3: Acute Inflammation II Flashcards

1
Q

What are the four most important mediators of acute inflammation?

A

1) vasoactive amines 2) lipid products (prostaglandins and leukotrienes) 3) cytokines 4) products of complement activation

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2
Q

what are the two major vasoactive amines?

A

histamine and serotonin

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3
Q

what are the first mediators to be released during inflammation?

A

histamine and serotonin

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4
Q

what is the richest source of histamine/ where is histamine stored?

A

in mast cell granules

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5
Q

how is histamine released from mast cells?

A

released by mast cell degranulation in response to to a variety of stimuli

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6
Q

what are the different stimuli that can cause release of histamine by mast cell degranulation?

A

1) physical injury (such as trauma), cold and heat 2) binding of antigen to IgE antibodies displayed on the surfaces of mast cells (hypersensitivity reactions and skin testing) 3) products of complement called anaphylatoxins

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7
Q

what is the function of histamine?

A

it causes dilation of the arterioles (smooth muscle) and increases the permeability of venules

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8
Q

what is histamine considered to be?

A

the principal mediator of the immediate transient phase of increased vascular permeability

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9
Q

How are the vasoactive effects of histamine mediated?

A

mainly via binding to receptors on microvascular endothelial cells

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10
Q

what are the lipid mediators and what are the produced from?

A

prostaglandins and leukotrienes –> produced from arachidonic acid

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11
Q

when do we produce arachidonic acid?

A

when you break down cell membranes by phospholipases

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12
Q

what are the two main “arms” of arachidonic acid?

A

cyclooxygenase and 5-Lipoxygenase

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13
Q

what does cyclooxygenase lead to?

A

prostaglandin G2, Prostaglandin H2, prostacyclin PGI2, Thromboxane A2, and PGD2/PGE2

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14
Q

what is the effect of prostacyclin/ PGI2?

A

it causes vasodilation and inhibits platelet aggregation

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15
Q

what is the effect of thromboxane A2?

A

it causes vasoconstriction and promotes platelet aggregation

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16
Q

what is the effect of PGD2/ PGE2?

A

it causes vasodilation, increased vascular permeability, and leukocyte chemotaxis

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17
Q

How can you inhibit the cyclooxygenases?

A

using a COX-1 and COX-2 inhibitor, aspirin, or indomethacin

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18
Q

what comes from 5-Lipoxygenase?

A

5-HPETE, Leukotriene C4, Leukotriene D4, and Leukotriene E4

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19
Q

What does 5-HPETE lead to?

A

5-HETE, which leads to chemotaxis

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20
Q

what do leukotrienes C4, D4, and E4 all lead to?

A

bronchospasm and increased vascular permeability

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21
Q

besides 5-HETE, what else can 5–HPETE lead to?

A

12-Lipoxygenase

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22
Q

what can 12-lipoxygenase lead to?

A

Lipoxin A4 and Lipoxin B4

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23
Q

what is the function of lipoxin A4 and B4?

A

they inhibit neutrophil adhesion and chemotaxis (they are considered the stop signals in inflammation)

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24
Q

how can you inhibit leukotriene production/ 5-lipoxygenase production?

A

use a 5-lipoxygenase inhibitor (Zileuton)

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25
Q

how can you treat bronchospasm and increased vascular permeability caused by leukotrienes?

A

use a leukotriene receptor antagonist (Zafirlukast and Montelukast)

26
Q

What two cytokines serve a critical role in leukocyte recruitment and by how?

A

TNF and IL-1; by promoting adhesion of leukocytes to endothelium and their migration through vessels

27
Q

the actions of TNF and IL-1 contribute to what?

A

the local and systemic reactions of inflammation

28
Q

What has been remarkably effective in the treatment of chronic inflammatory diseases; and what are some examples of these diseases?

A

TNF antagonists; RA and also psoriasis

29
Q

what is one of the complications seen with TNF antagonists?

A

patients become susceptible to mycobacterial infection, reflecting reduced ability of macrophages to kill intracellular microbes

30
Q

what can be used to treat juvenile arthritis?

A

anti-IL-6 receptor

31
Q

what can be used to treat psoriasis?

A

anti- IL-17

32
Q

what are the two main functions of chemokines?

A

inflammatory chemokines and homeostatic chemokines

33
Q

the complement system function in what type of immunity for defense against microbial pathogens?

A

both innate and adaptive immunity

34
Q

What is the critical step in the tightly controlled complement activation cascade?

A

the proteolysis of the third (and most abundant) component C3

35
Q

cleavage of C3 can occur by one of three pathways. What are these pathways?

A

Classical, lectin pathway (MBL), and alternative pathway

36
Q

what is the classical pathway triggered by?

A

when C1 binds to an antibody (usually IgM or IgG) that has combined with antigen

37
Q

what is the alternative pathway triggered by?

A

microbial surface proteins and other substances in the absence of antibody

38
Q

how is the lectin pathway triggered?

A

it binds to carbohydrates on microbes and then directly activates C1

39
Q

All 3 complement pathways lead to the activation of what specifically?

A

an active enzyme called C3 convertase, which splits C3 into two functionally distinct fragments (C3a and C3b)

40
Q

What are the 3 main functions of complement/ C3b?

A

opsonization and phagocytosis, stimulation of inflammatory reactions, and complement-mediated cytolysis (MAC formation)

41
Q

the activation of complement is tightly controlled by what?

A

cell-associated and circulatory proteins: C1 inhibitor, DAF and CD59, and Complement Factor H

42
Q

what can inherited deficiencies of complement proteins cause?

A

increased susceptibility to infections

43
Q

deficiencies of regulatory proteins can cause what?

A

a variety of disorders such as macular degeneration and hemolytic uremic syndrome resulting from excessive complement activation

44
Q

what is the complication associated with the inherited deficiency of a C1 inhibitor?

A

hereditary angioedema

45
Q

what is the complication associated with the inherited deficiency of DAF/ CD59?

A

paroxysmal nocturnal hemoglobinuria (PNH)

46
Q

What are the 4 different morphologic patterns of acute inflammation?

A

serous inflammation, fibrinous inflammation, purulent (suppurative) inflammation/ abscess, and Ulcer

47
Q

what is serous inflammation marked by?

A

the exudation of cell-poor fluid (transudate) into spaces created by cell injury or into body cavities lined by the peritoneum, pleura, or pericardium (i.e. effusion)

48
Q

when does a fibrinous exudate develop?

A

when vascular permeability allows large molecules such as fibrin to pass out of the blood

49
Q

what is a fibrinous exudate characteristic of?

A

inflammation in the lining of body cavities, such as the meninges, pericardium, and pleura

50
Q

what happens if the fibrin is not removed?

A

over time it may stimulate the ingrowth of fibroblasts and blood vessels and thus leading to scarring (a process called organization)

51
Q

what is another name for fibrin?

A

Factor Ia

52
Q

what is fibrin?

A

a fibrous, non-globular protein involved in the clotting of blood

53
Q

how is fibrin formed?

A

by the action of the protease thrombin on fibrinogen which causes it to polymerize

54
Q

what does the polymerized fibrin and platelets form?

A

a hemostatic plug or clot over a wound site

55
Q

what is purulent inflammation characterized by?

A

the production of pus, an exudate consisting of neutrophils, the liquified debris of necrotic cells, and edema fluid

56
Q

what are abscesses?

A

localized collections of pus

57
Q

what is the most frequent cause of purulent (suppurative) inflammation?

A

infection with bacteria that cause liquefactive tissue necrosis, such as staphylococci

58
Q

what are pus producing pathogens referred to as?

A

pyogenic bacteria

59
Q

what is an ulcer?

A

a local defect or excavation of the surface of an organ or tissue that is produced by the sloughing (shedding) or inflamed necrotic tissue

60
Q

where are ulcers most commonly encountered?

A

the mucosa of the mouth, stomach, intestines, or GI tract; the skin and subcutaneous tissue of the lower extremities in older person who have circulatory disturbances

61
Q

acute inflammatory reactions typically have one of three outcomes, what are these outcomes?

A

resolution, fibrosis, or chronic inflammation

MOD Midterm (22 decks)

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