Chapter 2: Inflammation and Repair Flashcards
(102 cards)
1
Q
What are some functions of inflammation?
A
- Kills and eliminates infective microbes
- Removes dead/injured cells
- Initiates tissue repair
2
Q
What are some examples of leukocytes?
A
- Lymphocytes
- Monocytes
- Neutrophils
- Eosinophils
- Basophils
3
Q
What is the difference between granulocytes and agranulocytes?
A
Granulocytes: acute inflammatory cells, fast acting, and contain granules
Agranulocytes: slow acting, but last a long time. Do not contain granules
4
Q
This process is fundamental to healing (eliminates infection and damaged tissue), attracts immune cells, and may cause secondary damage to normal tissue.
A
Inflammation
5
Q
What types of cells detect injury or infection?
A
Macrophages, dendritic cells, and mast cells
6
Q
When an injury or infection is detected what do immune cells typically do?
A
Secrete cytokines and attract plasma proteins, which induces/regulates inflammation
7
Q
What are the five steps of inflammation?
A
- Recognize the injury/microbe
- Recruit leukocytes
- Remove agent (phagocytosis)
- Regulate (control) response
- Resolution and tissue repair
8
Q
What are the cardinal signs of inflammation?
A
- Rubor: redness
- Calor: heat
- Tumor: swelling
- Dolor: pain
- Functio laesa: loss of function
9
Q
This type of inflammation has a rapid onset and lasts for minutes to days. It has systemic signs, edema, neutrophils, and no fibrosis.
A
Acute inflammation
10
Q
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.
A
Chronic inflammation
11
Q
What are some stimuli of acute inflammation?
A
Infection, trauma, ischemia, necrosis, foreign bodies, and hypersensitivity reactions.
12
Q
What are the components of acute inflammation?
A
- Vascular changes
- Leukocyte recruitment and activation
13
Q
This pattern recognition receptor of acute inflammation recognizes all types of infectious pathogens and is located in the plasma membrane.
A
Toll-like receptors
14
Q
This pattern recognition receptor of acute inflammation recognizes products of dead cells (uric acid, ATP) and crystals. It is located in the cytoplasm.
A
Inflammasome
15
Q
What are some of the vascular changes associated with acute inflammation?
A
- Immediate vasoconstriction (few seconds)
- Vasodilation
- Increased permeability of fluid leading to increased viscosity and diapedesis
16
Q
What is diapedesis?
A
Transmigration of leukocytes into the cell.
17
Q
What are the mechanisms of increased permeability during acute inflammation?
A
- Endothelial contraction
- Endothelial necrosis
- Leakage from angiogenesis
18
Q
What does exudate mean?
A
Protein-rich
19
Q
What does transudate mean?
A
Protein-poor
20
Q
Which associated with inflammation, exudate or transudate?
A
Exudate
21
Q
This term is used to describe an increase in lymphatic drainage. It may transport microbes or cellular debris.
A
Edema
22
Q
This is a general disorder of the lymph nodes.
A
Lymphadenopathy
23
Q
This is an inflammation of lymph nodes, increase in size.
A
Lymphadenitis
24
Q
This is an inflammation of the lymphatic channel.
A
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.
