Chapter 2: Inflammation and Repair Flashcards Preview

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Flashcards in Chapter 2: Inflammation and Repair Deck (102):
1

What are some functions of inflammation?

-Kills and eliminates infective microbes
-Removes dead/injured cells
-Initiates tissue repair

2

What are some examples of leukocytes?

-Lymphocytes
-Monocytes
-Neutrophils
-Eosinophils
-Basophils

3

What is the difference between granulocytes and agranulocytes?

Granulocytes: acute inflammatory cells, fast acting, and contain granules
Agranulocytes: slow acting, but last a long time. Do not contain granules

4

This process is fundamental to healing (eliminates infection and damaged tissue), attracts immune cells, and may cause secondary damage to normal tissue.

Inflammation

5

What types of cells detect injury or infection?

Macrophages, dendritic cells, and mast cells

6

When an injury or infection is detected what do immune cells typically do?

Secrete cytokines and attract plasma proteins, which induces/regulates inflammation

7

What are the five steps of inflammation?

-Recognize the injury/microbe
-Recruit leukocytes
-Remove agent (phagocytosis)
-Regulate (control) response
-Resolution and tissue repair

8

What are the cardinal signs of inflammation?

-Rubor: redness
-Calor: heat
-Tumor: swelling
-Dolor: pain
-Functio laesa: loss of function

9

This type of inflammation has a rapid onset and lasts for minutes to days. It has systemic signs, edema, neutrophils, and no fibrosis.

Acute inflammation

10

This type of inflammation has an insidious onset and lasts for days to years. It it is characterized by angiogenesis, fibrosis and few systemic signs. Macrophages, lymphocytes, and plasma cells are also present.

Chronic inflammation

11

What are some stimuli of acute inflammation?

Infection, trauma, ischemia, necrosis, foreign bodies, and hypersensitivity reactions.

12

What are the components of acute inflammation?

-Vascular changes
-Leukocyte recruitment and activation

13

This pattern recognition receptor of acute inflammation recognizes all types of infectious pathogens and is located in the plasma membrane.

Toll-like receptors

14

This pattern recognition receptor of acute inflammation recognizes products of dead cells (uric acid, ATP) and crystals. It is located in the cytoplasm.

Inflammasome

15

What are some of the vascular changes associated with acute inflammation?

1. Immediate vasoconstriction (few seconds)
2. Vasodilation
3. Increased permeability of fluid leading to increased viscosity and diapedesis

16

What is diapedesis?

Transmigration of leukocytes into the cell.

17

What are the mechanisms of increased permeability during acute inflammation?

-Endothelial contraction
-Endothelial necrosis
-Leakage from angiogenesis

18

What does exudate mean?

Protein-rich

19

What does transudate mean?

Protein-poor

20

Which associated with inflammation, exudate or transudate?

Exudate

21

This term is used to describe an increase in lymphatic drainage. It may transport microbes or cellular debris.

Edema

22

This is a general disorder of the lymph nodes.

Lymphadenopathy

23

This is an inflammation of lymph nodes, increase in size.

Lymphadenitis

24

This is an inflammation of the lymphatic channel.

Lymphangitis

25

What are the five steps of leukocyte recruitment?

1. Margination and rolling (selectins)
2. Firm adhesion to endothelium (integrins)
3. Transmigration between endothelial cells
4. Chemotaxis toward target tissue

26

Which leukocytes predominates acute inflammation?

For the first 48 hours neutrophils dominate

27

This is an immunoglobulin G (IgG) and is a component of phagocytosis. They target/label a cell for destruction and enhance macrophage binding and breakdown.

Opsonins

28

What is the process of targeting/ labeling a cell for destruction?

Opsonization

29

Once activated, do white blood cells distinguish tissues?

No. This results in secondary tissue injury

30

An area of tissue necrosis, ischemia-repurfusion injuries, and hypersensitivity reactions (allergies, autoimmune conditions) all have the complication of what?

Leukocyte-induced tissue injury

31

What are some of the outcomes of acute inflammation?

-Resolution (regeneration and repair): minimal injury
-Chronic inflammation: failure to remove the offending agent
-Scarring (fibrosis): severe injury, unable to regenerate

32

What are the four types of inflammation?

Serous, fibrinous, suppurative (purulent), and ulcerative

33

This type of inflammation is characterized by serum accumulating within or below the epidermis. It usually produces a blister.

Serous

34

This type of inflammation is caused by a severe injury and is characterized by a large amount of vessel permeability, which allows large molecules out of circulation and the formation of fibrin-rich exudate and scars. Primarily occurs in the pericardial sac, peritoneum, and pleural cavity.

Fibrinous

35

This type of inflammation is characterized by a localized infection of pus-forming organisms (Staph. aureus). A pus-filled abcess usually forms.

Suppurative (purulent)

36

This type of inflammation usually occurs near an organ or tissue surface and characterized by a shedding of necrotic tissue. Peptic ulcers and aphthous ulcers are good examples.

Ulcerative

37

This is a pattern of chronic inflammation characterized by a collection of macrophages walling off an area of damage that could not be removed. Tuberculosis is the most common cause of this inflammation.

Granulomas

38

Of all the conditions that can causes granulomas, what is the only condition that causes caseating granulomas?

Tuberculosis

39

What are the cell-derived (at the affected tissues) mediators of inflammation?

-Vasoactive amines
-Arachidonic acid metabolite
-Cytokines
-Reactive oxygen species
-Lysosomal enzymes
-Neuropeptides

40

Examples of these cell-derived mediators of inflammation include mast cells, platelets, endothelium, and white blood cells. .

Vasoactive amines

41

What are the two main substances associated with vasoactive amines?

Histamine (vasodilation/increase in permeability) and Serotonin (vasoconstriction during clotting)

42

These cell-derived mediators of inflammation are produced by white blood cells and include prostaglandins, leukotrienes, and lipoxins.

Arachidonic acid metabolites

43

These arachidonic acid metabolites are involved with vasodilation, pain, fever, bronchospasm, and chemotaxis.

Prostaglandins and leukotrienes

44

These arachidonic acid metabolites are rare and inhibit chemotaxis (anti-inflammatory).

Lipoxins

45

These cell-derived mediators of inflammation increase white blood cell production, adhesion, and migration. They are produced by mast cells, endothelial cells, and macrophages.

Cytokines

46

These cell-derived mediators of inflammation are primarily produced by neutrophils and macrophages. They are used to kill and degrade microbes and a prime example is nitric oxide, which is used in vasodilation and microbial killing.

Reactive oxygen species

47

This cell-derived mediator of inflammation is produced by neutrophils and monocytes and is used in microbial killing and tissue degradation.

Lysosomal enzymes

48

This cell-derived mediator of inflammation initiates inflammation, transmits pain, and regulates vascular tone/permeability. They best example of this is substance P.

Neuropeptides

49

What are the three plasma protein-derived mediators of inflammation?

-Complement proteins
-Coagulation proteins
-Kinin system

50

This plasma protein-derived mediator of inflammation is involved with opsonization and the membrane attack complex. They vasodilate and increase permeability.

Complement proteins

51

This plasma protein-derived mediator of inflammation are from the liver and activated by exposed collagen or platelets. They are involved with clotting.

Coagulation proteins

52

This plasma protein-derived mediator of inflammation leads to bradykinin production. It is also involved with vasodilation and increased vascular permeability.

Kinin system

53

This is prolonged inflammation or unresolved acute inflammation due to persistent infection, immunosuppression, or hypersensitivity reactions

Chronic inflammation

54

What three things characterize chronic inflammation?

-Mononuclear leukocyte cells
-Tissue destruction and fibrosis
-Vessel production and repair

55

These are the dominant cells at the site of chronic inflammation. They eliminate microbes/dead cells, initiate angiogenesis/fibrosis, and are activated by endotoxins, cytokines, and foreign bodies.

Macrophages

56

These cells are involved with innate and adaptive immunity. They sustain chronic chronic inflammation.

Lymphocytes

57

What are the two types of macrophage activation?

-Classically activated
-Alternatively activated

58

This type of macrophage activation is brought on by microbes, endotoxins, and cytokines (INF-y). It results in microbicidal actions, and inflammation.

Classically activated

59

This type of macrophage activation is brought on by cytokines (not INF-y), mast cells, and eosinophils. It results in tissue repair/fibrosis and anti-inflammatory effects

Alternatively activated

60

What are some of the systemic effects inflammation?

-Acute-phase reactions
-Leukocytosis
-Leukemoid reactions
-Leukopenia

61

What types of conditions would be considered an acute-phase reaction to inflammation?

Malaise, increased heart rate, increased blood pressure, anorexia, fever (protaglandins), elevated plasma proteins (CRP and erythrocyte sedimentation rate)

62

This is an increase in blood leukocyte count (15-20 k/uL) and very common with bacterial infections.

Leukocytosis

63

This is an extremely large increase in blood leukocyte count (40-100 k/uL), mimics leukemia, and is involved with chronic inflammation.

Leukemoid reactions

64

This is a decrease in blood leukocyte count (<4000 k/uL) and is consistent with HIV/AIDS, chemotherapy, and radiation therapy.

Leukopenia

65

What are some repair mechanisms for tissue injury?

Regeneration and Scarring

66

This repair mechanism replaces damaged cells with new ones bringing the tissue to "pre-injury status". Injury is typically mild.

Regeneration

67

This repair mechanism is characterized by the deposition of fibrotic connective tissue due to severe structural damage and an inability for cells to proliferate. Injury is typically severe

Scarring

68

What three things does tissue homeostasis require?

-Cellular proliferation
-Apoptosis
-Stem cell differentiation

69

Cellular proliferation is tightly controlled and stimulated by what? What coordinates proliferation?

Growth factors; injured cells, stem cells, and vessels

70

What are the two types of cellular proliferation?

Physiologic and Pathologic

71

Describe physiologic cellular proliferation?

-Well-regulated proliferation
-Tissue repair, adaptations to stress
-Preserves normal cellular functions

72

Describe pathologic cellular proliferation?

-Result of genetic alterations
-Unregulated proliferation
-Neoplasia (tumor growth)

73

What promotes entry into the cell cycle (proliferation/ G0-->G1)?

Growth factors

74

These are regulators of the cell cycle.

Cyclins (gatekeepers)

75

What are the two types of cyclin that influence the cell cycle?

-Cyclin-dependent kinase (CDK) enzymes
-CDKIs: slow down the cell cycle
*growth factors inhibit CDKIs

76

What are the three types of cells that have an intrinsic proliferative capacity?

-Labile
-Stable
-Permanent

77

These cells that have an intrinsic proliferative capacity are continuously dividing and are typically found in epithelia and hematopoietic cells.

Labile

78

These cells that have an intrinsic proliferative capacity are typically in a quiescent state (G0), have limited replication, and are typically found in solid organs (kidney, liver, pancreas).

Stable

79

These cells that have an intrinsic proliferative capacity are terminally differentiated, injury is irreversible, and are typically classified as neurons, skeletal, and cardiac muscles.

Permanent

80

What are the two properties of stem cells?

-Self-renewal capacity (undifferentiated)
-Asymmetric replication (some cells differentiate while others do not)

81

In terms of regeneration and healing, what do growth factors do?

-Stimulate growth control genes
-Ignore cell cycle checkpoints
-Prevent apoptosis

82

What types of cells produce growth factors?

-Macrophages and lymphocytes at the site of inflammation
-Stromal or parenchymal cells in response to injury

83

What are the general functions of growth factors?

Stimulate:
-cellular proliferation/repair
-cellular migration
-cellular differentiation

84

What are growth factor signaling mechanisms?

Autocrine: acts on secreting cells
Paracrine: acts on adjacent cells
Endocrine: systemic, via the circulatory system

85

It is a network of proteins that surrounds cells and acts as structural support, storage (H2O, minerals, GF), and a regulator of cellular proliferation and movement. It is constantly remodeling.

Extracellular matrix (ECM)

86

This is one type of extracellular matrix that is found between cells in connective tissues (no specific shape) and is produced by fibroblasts.

Interstitial matrix

87

This is one type of extracellular matrix that is a type of specialized membrane found around cavities and organ surfaces. It is produced by epithelium and looks like a "chicken wire" mesh

Basement membrane

88

What are the three components of the extracellular matrix?

-Fibrous proteins
-Water-hydrated gels
-Adhesive glycoproteins

89

This component of the ECM functions to strengthen it. Examples include collagen and elastin.

Fibrous proteins

90

This component of the ECM provides resilience and lubrication. Examples include hyaluronan and proteoglycans.

Water-hydrated gels

91

This component of the ECM connects elements of the ECM to other cells (cellular adhesion). Examples include fibronectin, laminin, integrins, and selectins.

Adhesive glycoproteins

92

This occurs when repair cannot be achieved by regeneration due to severe damage, chronic/prolonged injury, or terminally differentiated cells

Scar formation (fibrosis)

93

What are the steps of scar formation?

-Angiogenesis
-Fibroblast migration and proliferation
-Collagen deposition (scar)
-Remodeling (lifetime)

94

What are the steps of angiogenesis?

-Vasodilation
-Pericyte separation
-Endothelial migration and proliferation
-Capillary remodeling
-Development and maturation of: pericytes, smooth muscles, and basement membrane

95

These enzymes breakdown collagen, require zinc ions as a cofactor, and are produced by fibroblasts, macrophages, etc.

Matrix metalloproteinase (MMPs)

96

What are some factors that influence tissue repair?

-Infection
-Nutritional deficiency
-Glucocorticoids
-Poor perfusion
-Etc.

97

This term is used to describe an excessive deposition of collagen. Exuberant granulation tissue is laid down resulting in a raised scar beyond the boundaries of the wound.

Keloid

98

Healing of skin wounds is a combination of what two things?

Epithelial regeneration and fibrosis

99

What are the phases associated with the healing of a skin wound?

-Inflammation
-Granulation tissue
-ECM deposition and remodeling

100

This type of healing is brought upon by an incision, in a sterile field, uninfected, and sutured. There is minimal cellular death and greater epithelial regeneration compared to fibrosis.

Healing by first intention (primary union): healing is done in about one month

101

This type of healing is brought upon by a large wound with necrotic tissue and intense inflammation. Abundant scar tissue formation occurs and there is prominent wound contraction (myofibroblasts)

Healing by second intention (secondary union): healing lasts >6 weeks

102

After sutures are removed from an injury what is the strength of that wound compared to normal tissue? After the 1st month? After 3 months?

10%; 70%; 80%
-injured tissue never reaches its previous strength after healing.