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Chapters 1-9 - Robbins Pathologic Basis of Disease, 9th Edition > 3 - Inflammation and Repair > Flashcards

3 - Inflammation and Repair Flashcards

1
Q

What is the purpose of inflammation?

A

To bring cells and molecules of host defense from the circulation to a site of tissue damage to remove the offending agents.

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2
Q

What are the two main participants in inflammation?

A

Blood vessels and leukocytes

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3
Q

Do leukocytes have short or long life spans in tissues?

A

Short

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4
Q

What are the cardinal signs and symptoms of inflammation?

A

Rubor (redness), calor (heat), tumor (swelling), dolor (pain), functio laesa (loss of function)

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5
Q

What family of receptors senses the presence of foreign microbes?

A

Toll-like receptors (also, circulating antibodies and complement)

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6
Q

Intracellular sensors can sense what molecules that indicate possible damage to the cell?

A

ATP (indicating mitochondrial leakage), low potassium (indicating cellular leakage), uric acid (indicating DNA breakdown), DNA (indicating nuclear leakage)

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7
Q

Damage sensors in the cell trigger the formation of what structure?

A

The inflammasome

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8
Q

What does the inflammasome produce?

A

Interleukin-1

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9
Q

What are the general steps of inflammation?

A

(1) Recognition of the injurious agent, (2) recruitment of leukocytes, (3) removal of the agent, (4) regulation of the response, (5) resolution and repair

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10
Q

What are the three major components of acute inflammation?

A

Dilation of small blood vessels, increased permeability of the microvasculature, migration of the leukocytes to the damaged tissues

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11
Q

Why do blood vessels dilate in inflammatory situations?

A

To increase blood flow to the area and slow down the blood flow

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12
Q

What is the principle inflammatory mediator leading to vasodilation?

A

Histamine (and also kinins)

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13
Q

What do endothelial cells increase expression of during the inflammatory response?

A

Adhesion molecules (for leukocyte attachment)

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14
Q

What is the most common method increased vascular permeability? What are other methods?

A

Endothelial cell shrinkage (increasing the interendothelial space); direct endothelial damage and necrosis, vascular endothelial growth factor

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15
Q

What vessels proliferate during inflammatory responses?

A

Blood and lymph vessels

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16
Q

Define lymphangitis. Define lymphadenitis.

A

Lymph vessel inflammation; lymph node inflammation

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17
Q

What is the cause of the red streaks seen coming from an infected wound?

A

Lymphangitis

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18
Q

What are the three steps of leukocyte migration in the blood vessel lumen?

A

Margination, rolling, and adhesion (all to activated endothelium)

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19
Q

What adhesion molecules assist leukocytes in the rolling phase?

A

Selectins

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20
Q

What adhesion molecules assist leukocytes in the adhesion phase?

A

Integrins

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21
Q

What is the name of the process by which leukocytes leave the blood vessel? What molecules assist in this process?

A

Diapedesis (also known as transmigration); PECAM-1 and CD31

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22
Q

When does chemotaxis occur?

A

After diapedesis when a leukocyte has entered the tissue space

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23
Q

What are the three principal chemokines involved in chemotaxis?

A

Interleukin-8, C5a, and leukotriene B4

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24
Q

What is the first responder in acute inflammation? What leukocyte will replace the first responder within 24-48 hours?

A

Neutrophils (more abundant, quicker, short half-life); macrophages (less abundant, slower, longer half-life, can proliferate in tissues)

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25
Q

What three drugs are especially effective in interfering with tumor necrosis factor and inhibiting harmful inflammation?

A

Etanercept, infliximab, adalimumab

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26
Q

What happens to the leukocytes post-chemotaxis once they reach the site of injury?

A

(1) They recognize the offending agents (toll-like receptors); (2) they become activated and phagocytic

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27
Q

What are the three steps of leukocyte phagocytosis?

A

Recognition, engulfment, and killing (or degradation)

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28
Q

What leukocyte receptors identify bacteria but not host cells?

A

Mannose receptors

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29
Q

What combines with the phagosome containing a phagocytosed bacteria or other agent within the leukocyte?

A

A lysosomal granule (containing reactive oxygen species and degradation enzymes)

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30
Q

How are foreign microbes killed within the body?

A

Mainly reactive oxygen species (the respiratory burst within the phagolysosome)

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31
Q

What type of nitric oxide synthase is implicated in ROS formation?

A

Inducible NOS (iNOS)

32
Q

What enzymes do neutrophil lysosomes contain?

A

Lysozyme, hydrolytic enzymes, myeloperoxidase, and lactoferrin

33
Q

What are neutrophil extracellular traps?

A

Fibrillar networks released by neutrophils to trap microbes and kill them with antimicrobial substances

34
Q

What substances are released to limit and end inflammation?

A

Lipoxins, transforming growth factor-beta, interleukin-10

35
Q

What are some of the principal mediators of inflammation?

A

Vasoactive amines (e.g. histamine and serotonin), prostaglandins, leukotrienes, cytokines, and complement

36
Q

What are the sentinel cells of inflammation?

A

Mast cells, dendritic cells, macrophages

37
Q

What are the products of cyclooxygenase degradation of arachidonic acid?

A

Arachidonic acid –> Prostaglandin G2 –> Prostaglandin H 2–> Prostacyclin (prostaglandin I2) + Thromboxane A2 + Prostaglandins D2 and E2

38
Q

What are the products of 5-lipooxygenase degradation of arachidonic acid?

A

Hydroperoxide (5-HPETE) –> Leukotriene A4 –> Leukotriene B4 + C4 + D4 + E4 AND Hydroperoxide (5-HPETE) –> Lipoxin A4 + B4 (antiinflammatory)

39
Q

Why do COX-2 inhibitors increase the risk of adverse cardiovascular events?

A

They inhibit prostacyclin formation but leave thromboxane A2 formation untouched

40
Q

What benefits do COX-2 inhibitors show?

A

Decreased renal and gastrointestinal damage

41
Q

Of which molecules do corticosteroids decrease gene expression?

A

COX-2, phospholipase A2, iNOS, interleukin-1, TNF

42
Q

What are the principal types of exudate?

A

Serous, purulent, fibrinous

43
Q

Define ulcer.

A

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

44
Q

What are the potential outcomes of acute inflammation?

A

Resolution, fibrosis, and progression to chronic inflammation

45
Q

How long does chronic inflammation last?

A

Weeks to months

46
Q

What processes coexist in chronic inflammation?

A

Inflammation, tissue damage, and tissue repair

47
Q

What are some causes of chronic inflammation?

A

Persistent infections, hypersensitivity disorders, prolonged exposure to toxic agents

48
Q

What morphological changes characterize chronic inflammation?

A

Mononuclear cell infiltrate (macrophages and lymphocytes), tissue destruction, attempts at tissue healing (angiogenesis and fibrosis)

49
Q

Which cell is the major actor in chronic inflammation?

A

The macrophage

50
Q

What does classical activation cause macrophages to do? What does the alternative activation cause macrophages to do?

A

Microbicide; tissue repair

51
Q

What is granulomatous inflammation? What is its purpose as a form of chronic inflammation?

A

Granulomatous inflammation is a form of chronic inflammation characterized by collections of activated macrophages, often with T lymphocytes, and sometimes associated with central necrosis; a cellular attempt to contain an offending agent that is difficult to eradicate.

52
Q

What are the two types of macrophages seen in granulomas?

A

The activated macrophages may develop abundant cytoplasm and begin to resemble epithelial cells and are called epithelioid cells. Some activated macrophages may fuse, forming multinucleate giant cells.

53
Q

What are the two main types of granuloma?

A

Foreign body granulomas and immune granulomas

54
Q

What is a foreign body granuloma?

A

Typically, foreign body granulomas form around materials such as talc (associated with intravenous drug abuse), sutures, or other fibers that are large enough to preclude phagocytosis by a macrophage and do not incite any specific inflammatory or immune response.

55
Q

What is an immune granuloma?

A

Immune granulomas are caused by a variety of agents that are capable of inducing a persistent T cell-mediated immune response.

56
Q

What is the name of the collective signs and symptoms of the systemic effects of inflammation?

A

The acute-phase response

57
Q

Which cytokines are the principal mediators of the acute-phase response (systemic effects of inflammation)?

A

TNF, IL-1, IL-6, interferons

58
Q

What are the principal effects of the acute-phase response (systemic effects of inflammation)?

A

Fever, C-reactive protein, leukocytosis, and (in severe cases), septic shock

59
Q

What family of factors causes proliferation of hematopoietic stem cells in the bone marrow?

A

Colony-stimulating factors

60
Q

Which parenchymal organ has remarkable regenerative capacity? It can grow back after loss of what percentage of its cells?

A

The liver; 90%

61
Q

Which parenchymal organs have partial regenerative capacity?

A

The lungs, adrenal glands, thyroid, and pancreas

62
Q

How does the liver regenerate?

A

The proliferation of remaining hepatocytes and the regeneration from progenitor cells

63
Q

What are the steps of scar formation?

A

Angiogenesis, granulation tissue formation, remodeling of the scar tissue

64
Q

What role do macrophages play in tissue repair?

A

They phagocytize debris from the wound and secrete growth factors and cytokines to promote tissue growth

65
Q

Describe the process of angiogenesis.

A
66
Q

How is new connective tissue deposited in scar formation?

A

Fibroblasts migrate to the area and release ECM (transforming growth factor-beta is the most important cytokine in this process)

67
Q

Define healing by first intention (or primary union).

A

Healing when the injury involves only the epithelial layer

One of the simplest examples of this type of wound repair is

the healing of a clean, uninfected surgical incision approximated by surgical sutures.

68
Q

Define healing by second intention (or secondary union).

A

When cell or tissue loss is more extensive, such as in large

wounds, abscesses, ulceration, and ischemic necrosis

(infarction) in parenchymal organs, the repair process

involves a combination of regeneration and scarring.

69
Q

Carefully sutured wounds have what percentage of the strength of normal skin?

A

~70%

70
Q

After suture removal (1 week later), what percentage of the strength of unwounded skin does the healing skin have?

A

10%

71
Q

What percentage of unwounded skin strength does the healing skin have after 3 months?

A

70-80% (there will likely be no substantial improvement beyond that)

72
Q

What is the condition of an organ upon excessive deposition of collagen and scar tissue?

A

Fibrosis

73
Q

If a scar is raised due to excess collagen deposition, what is it called?

A

A hypertrophic scar

74
Q

If a scar grows outside the boundaries of a wound and does not regress, what is it called?

A

A keloid (more common in African-American patients)

75
Q

What is it called when excessive granulation tissue is deposited and it rises above the skin (disrupting reepithelialization)?

A

Exuberant granulation (must be removed by cautery or surgery to allow skin healing)

76
Q

Although contraction is an important part of the healing process, what is an excessive amount if contraction called? (often seen in burn patients)

A

A contracture

77
Q

What are two types of complication in wound healing when insufficient granulation or scar tissue is laid down?

A

Dehiscence (wound rupture) or ulceration

Chapters 1-9 - Robbins Pathologic Basis of Disease, 9th Edition (9 decks)

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