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PATHOLOGY <3 > Chapter 2 – Acute and Chronic Inflammation > Flashcards

Chapter 2 – Acute and Chronic Inflammation Flashcards

1
Q

____________ is a complex reaction in tissues that consists mainly of responses of blood vessels and leukocytes. The body’s principal defenders against foreign invaders are plasma proteins and circulating leukocytes (white blood cells), as well as tissue phagocytes that are derived from circulating cells.

A

Inflammation

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2
Q

is rapid in onset (typically minutes) and is of short duration, lasting for hours or a few days; its main characteristics are the exudation of fluid and plasma proteins (edema) and the emigration of leukocytes, predominantly neutrophils (also called polymorphonuclear leukocytes).

A

Acute inflammation

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3
Q

may follow acute inflammation or be insidious in onset. It is of longer duration and is associated with the presence of lymphocytes and macrophages, the proliferation of blood vessels, fibrosis, and tissue destruction

A

Chronic inflammation

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4
Q

Repair begins during _______________ but reaches completion usually after the injurious influence has been neutralized

A

inflammation

In the process of repair the injured tissue is replaced through REGENERATION of native parenchymal cells, by filling of the defect with fibrous tissue (SCARRING) or, most commonly, by a combination of these two processes (

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5
Q

In recognition of the wide-ranging harmful consequences of inflammation, the lay press has rather melodramatically referred to it as?

A

“the silent killer.”

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6
Q

the four cardinal signs of inflammation:

A

rubor (redness)

tumor (swelling)

calor (heat)

dolor (pain)

loss of function (functio laesa),
was added by Rudolf Virchow in the 19th century

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7
Q

discovered the process of phagocytosis by observing the ingestion of rose thorns by amebocytes of starfish larvae and of bacteria by mammalian leukocytes. [3] He concluded that the purpose of inflammation was to bring phagocytic cells to the injured area to engulf invading bacteria

A

Russian biologist Elie Metchnikoff

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8
Q

noted what is now considered an obvious fact: that inflammation is not a disease but a nonspecific response that has a salutary effect on its
host.

A

John Hunter

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9
Q

“The Doctor’s Dilemma,” in which one physician’s cure-all is to “stimulate the phagocytes

A

George Bernard Shaw

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10
Q

studying the inflammatory response in skin, established the concept that chemical substances, such as histamine (produced locally in response to injury), mediate the vascular changes of inflammation.

A

Sir Thomas Lewis

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11
Q

is a rapid host response that serves to deliver leukocytes and plasma proteins, such as antibodies, to sites of infection or tissue injury.

A

Acute Inflammation

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12
Q

Acute inflammation has three major components:

A

(1) alterations in vascular caliber that lead to an increase in blood flow

Vascular dilation and increased blood flow (causing (RUBOR) erythema and (CALOR) warmth);

(2) structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation

extravasation and extravascular deposition of plasma fluid and proteins (edema);

(3) emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent

leukocyte emigration and accumulation in the site of injury.

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13
Q

STIMULI FOR ACUTE INFLAMMATION

(bacterial, viral, fungal, parasitic) and microbial toxins are among the most common and medically important causes of inflammation

A

Infections

most important receptors for microbial products are the family of Toll-like receptors (TLRs)

which can detect bacteria, viruses, and fungi Engagement of these receptors triggers signaling pathways that stimulate the production of various mediators.

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14
Q

STIMULI FOR ACUTE INFLAMMATION

including ischemia (as in a myocardial infarct), trauma, and physical and chemical injury (e.g., thermal injury, as in burns or frostbite; irradiation; exposure to some environmental chemicals

A

Tissue necrosis from any cause

Several molecules released from necrotic cells are known to elicit inflammation; these include uric acid, a purine metabolite; adenosine triphosphate, the normal energy store; a DNA-binding protein of unknown function called HMGB-1; and even DNA when it is released into the cytoplasm and not sequestered in nuclei, as it should be normally

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15
Q

STIMULI FOR ACUTE INFLAMMATION

which often underlies cell injury, is also itself an inducer of the inflammatory response. This response is mediated largely by a protein called HIF-1α (hypoxia-induced factor-1α), which is produced by cells deprived of oxygen and activates the transcription of many genes involved in inflammation, including vascular endothelial growth factor (VEGF), which increases vascular permeability

A

Hypoxia,

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16
Q

STIMULI FOR ACUTE INFLAMMATION

(splinters, dirt, sutures) typically elicit inflammation because they cause traumatic tissue injury or carry microbes

A

Foreign bodies

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17
Q

STIMULI FOR ACUTE INFLAMMATION

also called hypersensitivity reactions) are reactions in which the normally protective immune system damages the individual’s own tissues

A

Immune reactions

The injurious immune responses may be directed against self antigens, causing autoimmune diseases, or may be excessive reactions against environmental substances or microbes. Inflammation is a major cause of tissue injury in these diseases

The term immune-mediated inflammatory disease is often used to refer to this group of disorders

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18
Q

The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities is known as

A

exudation

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19
Q

is an extravascular fluid that has a high protein concentration, contains cellular debris, and has a high specific gravity. Its presence implies an increase in the normal permeability of small blood vessels in an area of injury and, therefore, an inflammatory reaction

A

exudate

An exudate is formed in inflammation, because vascular permeability increases as a result of increased interendothelial spaces.

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20
Q

is a fluid with low protein content (most of which is albumin), little or no cellular material, and low specific gravity. It is essentially an ultrafiltrate of blood plasma that results from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability

A

transudate

A transudate is formed when fluid leaks out because of increased hydrostatic pressure or decreased osmotic pressure

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21
Q

denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate

A

edema

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22
Q

a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils), the debris of dead cells and, in many cases, microbes

A

Pus

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23
Q

Proliferation of blood vessels

is prominent during repair and in chronic inflammation

A

angiogenesis

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24
Q

is one of the earliest manifestations of acute inflammation; sometimes it follows a transient constriction of arterioles, lasting a few seconds

A

Vasodilation

first involves the arterioles and then leads to opening of new capillary beds in the area. The result is increased blood flow , which is the cause of heat and redness (erythema) at the site of inflammation. Vasodilation is induced by the action of several mediators, notably histamine and nitric oxide (NO), on vascular smooth muscle.

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25
Q

Vasodilation is quickly followed by ____________ with the outpouring of protein-rich fluid into the extravascular tissues

A

increased permeability of the microvasculature

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26
Q

The loss of fluid and increased vessel diameter lead to slower blood flow, concentration of red cells in small vessels, and increased viscosity of the blood. These changes result in dilation of small vessels that are packed with slowly moving red cells, a condition termed

A

STASIS, which is seen as vascular congestion (producing localized redness) upon examination of the involved tissue

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27
Q

hallmark of acute inflammation is increase ___________ leading to the escape of a protein-rich exudate into the extravascular tissue, causing edema

A

Increased Vascular Permeability (Vascular Leakage)

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28
Q

is the most common mechanism of vascular leakage and is elicited by histamine, bradykinin, leukotrienes, the neuropeptide substance P, and many other chemical mediators

A

Contraction of endothelial cells resulting in increased interendothelial spaces

Ω immediate transient response because it occurs rapidly after exposure to the mediator and is usually short-lived (15–30 minutes

Ω exposure to certain bacterial toxins), vascular leakage begins after a delay of 2 to 12 hours, and lasts for several hours or even days; this delayed prolonged leakage may be caused by contraction of endothelial cells or mild endothelial damage. Late-appearing sunburn is a good example of this type of leakage.

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29
Q

is the most common mechanism of vascular leakage and is elicited by histamine, bradykinin, leukotrienes, the neuropeptide substance P, and many other chemical mediators

A

Contraction of endothelial cells resulting in increased interendothelial spaces

Ω immediate transient response because it occurs rapidly after exposure to the mediator and is usually short-lived (15–30 minutes

Ω exposure to certain bacterial toxins), vascular leakage begins after a delay of 2 to 12 hours, and lasts for several hours or even days; this delayed prolonged leakage may be caused by contraction of endothelial cells or mild endothelial damage. Late-appearing sunburn is a good example of this type of leakage.

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30
Q

Direct damage to the endothelium is encountered in severe injuries, for example, in burns, or by the actions of microbes that target endothelial cells. [9] Neutrophils that adhere to the endothelium during inflammation may also injure the endothelial cells and thus amplify the reaction.

A

Endothelial injury, resulting in endothelial cell necrosis and detachment

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31
Q

Increased transport of fluids and proteins, through the endothelial cell is called

A

transcytosis

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32
Q

involve channels consisting of interconnected, uncoated vesicles and vacuoles called the______________ many of which are located close to intercellular junctions

A

vesiculovacuolar organelle

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33
Q

normally drain the small amount of extravascular fluid that has seeped out of capillaries

A

lymphatics

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34
Q

Inflamed lymph nodes are often enlarged because of hyperplasia of the ________

A

lymphoid follicles

is termed reactive, or inflammatory, lymphadenitis

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35
Q

lymphatics may become secondarily inflamed
For clinicians the presence of red streaks near a skin wound is a telltale sign of an infection in the wound. This streaking follows the course of the lymphatic channels and is diagnostic of

A

lymphangitis

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36
Q

painful enlargement of the draining lymph nodes, indicating

A

lymphadenitis.

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37
Q

The most important leukocytes. the ones capable of phagocytosis

A

neutrophils and macrophages

These leukocytes ingest and kill bacteria and other microbes, and eliminate necrotic tissue and foreign substances. Leukocytes also produce growth factors that aid in repair

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38
Q

ecruitment of Leukocytes to Sites of Infection and Injury

The journey of leukocytes from the vessel lumen to the interstitial tissue, called

A

extravasation

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39
Q

extravasation,

can be divided into the following steps

A
  1. In the lumen: margination, rolling, and adhesion to endothelium
  2. Migration across the endothelium and vessel wall
  3. Migration in the tissues toward a chemotactic stimulus
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40
Q

white cells assume a peripheral position along the endothelial surface. This process of leukocyte redistribution is called

A

margination

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41
Q

then rows of leukocytes adhere transiently to the endothelium, detach and bind again, thus

A

rolling on the vessel wall

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42
Q

cells finally come to rest at some point where they adhere firmly (resembling pebbles over which a stream runs without disturbing them).

A

adhesion

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43
Q

three types of selectins

A
  1. one expressed on leukocytes (L-selectin),
  2. on endothelium (E-selectin),
  3. one in platelets and on endothelium (P-selectin).

expression of selectins and their ligands is regulated by cytokines produced in response to infection and injury

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44
Q

counter Part for adhesion molecule?

P-selectin

A

Sialyl-Lewis X–modified proteins

Major Role
Rolling (neutrophils, monocytes, T lymphocytes)

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45
Q

counter Part for adhesion molecule?

E-selectin

A

Sialyl-Lewis X–modified proteins

Major Role

Rolling and adhesion (neutrophils, monocytes, T lymphocytes)

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46
Q

counter Part for adhesion molecule?

GlyCam-1, CD34

A

L-selectin [*]

Major Role

Rolling (neutrophils, monocytes)

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47
Q

counter Part for adhesion molecule?

ICAM-1 (immunoglobulin family)

A

CD11/CD18 (β2) integrins (LFA-1, Mac-1)

Major Role

adhesion, arrest, transmigration (neutrophils, monocytes, lymphocytes)

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48
Q

counter Part for adhesion molecule?

VCAM-1 (immunoglobulin family

A

VLA-4 (β1) integrin

Major Role

Adhesion (eosinophils, monocytes, lymphocytes)

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49
Q

Firm adhesion is mediated by a family of heterodimeric leukocyte surface proteins called

A

integrins

TNF and IL-1 induce endothelial expression of ligands for integrins, mainly vascular cell adhesion molecule 1 (VCAM- 1, the ligand for the VLA-4 integrin) and intercellular adhesion molecule-1 (ICAM-1, the ligand for the LFA-1 and Mac-1 integrins).

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50
Q

the process of leukocyte recruitment is migration of the leukocytes through the endothelium

A

called transmigration or diapedesis

Transmigration of leukocytes occurs mainly in post-capillary venules

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51
Q

After traversing the endothelium, leukocytes pierce the basement membrane, probably by secreting

A

collagenases, and enter the extravascular tissue

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52
Q

the leukocytes are able to adhere to the extracellular matrix by virtue of

A

of integrins and CD44 binding to matrix proteins

Thus, leukocytes are retained at the site where they are needed .

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53
Q

After exiting the circulation, leukocytes emigrate in tissues toward the site of injury by a process called ____________

which is defined as locomotion oriented along a chemical gradient. Both exogenous and endogenous substances can act as chemoattractants

A

chemotaxis

most common exogenous agents are bacterial products, including peptides that possess an N- formylmethionine terminal amino acid, and some lipids

Endogenous chemoattractants include several chemical mediators (described later): (1) cytokines, particularly those of the chemokine family (e.g., IL-8); (2) components of the complement system, particularly C5a ; and (3) arachidonic acid (AA) metabolites, mainly leukotriene B4 (LTB4).

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54
Q

The leukocyte moves by extending ___________ that pull the back of the cell in the direction of extension, much as an automobile with front-wheel drive is pulled by the wheels in front

A

filopodia

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55
Q

In most forms of acute inflammation neutrophils predominate in the inflammatory infiltrate during the first 6 to 24 hours and are replaced by monocytes in 24 to 48 hours

A

Several reasons account for the early appearance of neutrophils: they are more numerous in the blood, they respond more rapidly to chemokines, and they may attach more firmly to the adhesion molecules that are rapidly induced on endothelial cells, such as P- and E-selectins

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56
Q

Receptors for microbial products

A

Toll-like receptors (TLRs) recognize components of different types of microbes.

TLRs are present on the cell surface and in the endosomal vesicles of leukocytes (and many other cell types), so they are able to sense products of extracellular and ingested microbes

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57
Q

Leukocytes express receptors for proteins that coat microbes. The process of coating a particle, such as a microbe, to target it for ingestion (phagocytosis) is called

A

opsonization

substances that do this are opsonins

include antibodies, complement proteins, and lectins

enhancing the phagocytosis of particles is coating the particles with IGG antibodies specific for the particles, which are then recognized by the high-affinity Fcγ receptor of phagocytes, called FcγRI

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58
Q

the major macrophage-activating cytokine.

A

interferon-γ (IFN-γ),

Leukocytes express receptors for cytokines that are produced in response to microbes

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59
Q

Phagocytosis involves three sequential steps

A

(1) recognition and attachment of the particle to be ingested by the leukocyte;
(2) its engulfment, with subsequent formation of a phagocytic vacuole;
(3) killing or degradation of the ingested material

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60
Q

recognizes microbes and not host cells

A

mannose receptor

The macrophage mannose receptor is a lectin that binds terminal mannose and fucose residues of glycoproteins and glycolipids. These sugars are typically part of molecules found on microbial cell walls

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61
Q

were originally defined as molecules that bind and mediate endocytosis of oxidized or acetylated low-density lipoprotein (LDL) particles that can no longer interact with the conventional LDL receptor

A

Scavenger receptors

Macrophage scavenger receptors bind a variety of microbes in addition to modified LDL particles. Macrophage integrins, notably Mac-1 (CD11b/CD18), may also bind microbes for phagocytosis

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62
Q

plasma membrane pinches off to form a vesicle that encloses the particle

A

phagosome

During this process the phagocyte may also release granule contents into the extracellular space

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63
Q

Microbial killing is accomplished largely by

A

reactive oxygen species

reactive nitrogen species, mainly derived from NO

generation of ROS is due to the rapid assembly and activation of a multicomponent oxidase (NADPH oxidase, also called phagocyte oxidase), which oxidizes NADPH (reduced nicotinamide-adenine dinucleotide phosphate) and, in the process, reduces
oxygen to superoxide anion

the ROS are produced within the lysosome

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64
Q

In neutrophils, this rapid oxidative reaction is triggered by activating signals and accompanies phagocytosis, and is called

A

respiratory burst.

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65
Q

converts H2O2 to hypochlorite

A

the azurophilic granules of neutrophils contain the enzyme myeloperoxidase (MPO), which, in the presence of a halide such as Cl - , converts H2O2 to hypochlorite (OCl•, the active ingredient in household bleach

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66
Q

the most efficient bactericidal system of neutrophils

A

The H2O2-MPO-halide system

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67
Q

cationic arginine-rich granule peptides that are toxic to microbes

A

defensins,

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68
Q

antimicrobial proteins found in neutrophils and other cells

A

cathelicidins

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69
Q

produce a number of growth factors that stimulate the proliferation of endothelial cells and fibroblasts and the synthesis of collagen, and enzymes that remodel connective tissues

A

macrophages,

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70
Q

are induced by microbial products and cytokines, particularly IFN-γ, and are microbicidal and involved in potentially harmful inflammation

A

Classically activated macrophages

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71
Q

are induced by other cytokines and in response to helminths (not shown), and are important in tissue repair and the resolution of inflammation (and may play a role in defense against helminthic parasites

A

Alternatively activated macrophages

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72
Q

Clinical Examples of Leukocyte-Induced Injury

ACUTE

Cells and Molecules Involved in Injury?

ACUTE RESPIRATORY DISTRESS SYNDROME

A

Neutrophils

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73
Q

Clinical Examples of Leukocyte-Induced Injury

ACUTE

Cells and Molecules Involved in Injury?

Acute transplant rejection

A

Lymphocytes; antibodies and complement

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74
Q

Clinical Examples of Leukocyte-Induced Injury

ACUTE

Cells and Molecules Involved in Injury?

Asthma

A

Eosinophils; IgE antibodies

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75
Q

Clinical Examples of Leukocyte-Induced Injury

ACUTE

Cells and Molecules Involved in Injury?

Glomerulonephritis

A

Neutrophils, monocytes; antibodies and complement

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76
Q

Clinical Examples of Leukocyte-Induced Injury

ACUTE

Cells and Molecules Involved in Injury?

Septic shock

A

Cytokines

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77
Q

Clinical Examples of Leukocyte-Induced Injury

ACUTE

Cells and Molecules Involved in Injury?

Lung abscess

A

Neutrophils (and bacteria)

78
Q

Clinical Examples of Leukocyte-Induced Injury

CHRONIC

Cells and Molecules Involved in Injury?

Arthritis

A

Lymphocytes, macrophages; antibodies

79
Q

Clinical Examples of Leukocyte-Induced Injury

CHRONIC

Cells and Molecules Involved in Injury

Asthma

A

Eosinophils; IgE antibodies

80
Q

Clinical Examples of Leukocyte-Induced Injury

CHRONIC

Cells and Molecules Involved in Injury?

Atherosclerosis

A

Macrophages; lymphocytes?

81
Q

Clinical Examples of Leukocyte-Induced Injury

CHRONIC

Cells and Molecules Involved in Injury?

Chronic transplant rejection

A

Lymphocytes; cytokines

82
Q

Clinical Examples of Leukocyte-Induced Injury

CHRONIC

Cells and Molecules Involved in Injury?

Pulmonary fibrosis

A

Macrophages; fibroblasts

83
Q

the inability of the leukocytes to surround and ingest these substances

triggers strong activation, and the release of large amounts of lysosomal enzymes into the extracellular environment

A

(frustrated phagocytosis)

84
Q

genetic defects of integrins and selectin-ligands that cause leukocyte adhesion deficiencies types 1 and 2. The major clinical problem in both is recurrent bacterial infections.

A

Inherited defects in leukocyte adhesion

85
Q

disorder is CHÉDIAK-HIGASHI SYNDROME, an autosomal recessive condition characterized by defective fusion of phagosomes and lysosomes in phagocytes (causing susceptibility to infections), and abnormalities in melanocytes (leading to albinism), cells of the nervous system (associated with nerve defects), and platelets (causing bleeding disorders).

A

Inherited defects in phagolysosome function

86
Q

defects in bacterial killing and render patients susceptible to recurrent bacterial infection

results from inherited defects in the genes encoding
components of phagocyte oxidase, which generates O2-

A

Inherited defects in microbicidal activity

chronic granulomatous disease

87
Q

the most frequent cause of leukocyte defects

Acquired deficiencies

A

bone marrow suppression, leading to decreased production of leukocytes. This is seen following therapies for cancer (radiation and chemotherapy) and when the marrow space is compromised by tumors, which may arise in the marrow (e.g., leukemias) or be metastatic from other sites.

88
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Defective leukocyte adhesion because of mutations in β chain of CD11/CD18 integrins

A

GENETIC

Leukocyte adhesion deficiency 1

89
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Defective leukocyte adhesion because of mutations in fucosyl transferase required for synthesis of sialylated oligosaccharide (ligand for selectins)

A

GENETIC

Leukocyte adhesion
deficiency 2

90
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Decreased oxidative burst

A

GENETIC

Chronic granulomatous disease

91
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Phagocyte oxidase (membrane component)

A

GENETIC

X-linked

92
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Phagocyte oxidase (cytoplasmic components)

A

GENETIC

Autosomal recessive

93
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Decreased microbial killing because of defective MPO—H2O2 system

A

GENETIC

MPO deficiency

94
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Decreased leukocyte functions because of mutations affecting protein involved in lysosomal membrane traffic

A

GENETIC

Chédiak-Higashi syndrome

95
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Bone marrow suppression: tumors, radiation, and chemotherapy

A

ACQUIRED

PROBLEM in Production of leukocytes

96
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Diabetes, malignancy, sepsis, chronic dialysis

A

ACQUIRED

Problem in Adhesion and chemotaxis

97
Q

Defects in Leukocyte Functions

GENETIC or ACQUIRED

Leukemia, anemia, sepsis, diabetes, malnutrition

A

ACQUIRED

Problem in Phagocytosis and microbicidal activity

98
Q

cells resident in tissues also serve important functions in initiating acute inflammation. The two most important of these cell types are?

A

Ω mast cells
These cells release histamine, leukotrienes, enzymes, and many cytokines (including TNF, IL-1, and chemokines), all of which contribute to inflammation

Ω tissue macrophages.

These “sentinel” cells are stationed in tissues to rapidly recognize potentially injurious stimuli and initiate the host defense reaction

99
Q

mediators are normally sequestered in

A

intracellular granules and can be rapidly secreted by granule exocytosis (e.g., histamine in mast cell granules) or are synthesized de novo (e.g., prostaglandins, cytokines) in response to a stimulus

100
Q

The major cell types that produce mediators of acute inflammation are

A

platelets, neutrophils, monocytes/macrophages, and mast cells, but mesenchymal cells (endothelium, smooth muscle, fibroblasts) and most epithelia can also be induced to elaborate some of the mediators. Plasma-derived mediators (e.g., complement proteins, kinins) are produced mainly in the liver and present in the circulation as inactive precursors that must be activated, usually by a series of proteolytic cleavages, to acquire their biologic properties.

101
Q

the cytokine TNF acts on endothelial cells to stimulate the production of another

A

cytokine, IL-1, and many chemokines. The secondary mediators may have the same actions as the initial mediators but may also have different and even opposing activities. Such cascades provide mechanisms for amplifying—or, in certain instances, counteracting—the initial action of a mediator.

102
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Mast cells, basophils, platelets

A

Histamine

Vasodilation, increased vascular permeability, endothelial activation

103
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Platelets

A

Serotonin

Vasodilation, increased vascular permeability

104
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Mast cells,

leukocytes

A

Prostaglandins

Vasodilation, pain, fever

105
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Mast cells, leukocytes

A

Leukotrienes

ncreased vascular permeability, chemotaxis, leukocyte adhesion and activation

106
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Leukocytes

A

Reactive oxygen species

Killing of microbes, tissue damage

107
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Endothelium, macrophages

A

Nitric oxide

Vascular smooth muscle relaxation, killing of microbes

108
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Macrophages, endothelial cells, mast cells

A


Cytokines (TNF, IL-1)

Local endothelial activation (expression of adhesion molecules), fever/pain/anorexia/hypotension, decreased vascular resistance (shock)

109
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Leukocytes, mast cells

A

Platelet- activating

Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

110
Q

These are the PRINCIPAL SOURCES what CELL-DERIVED?

Leukocytes, activated macrophages

A

Chemokines

Chemotaxis, leukocyte activation

111
Q

PLASM A PROTEIN–DERIVED

Plasma (produced in liver)

A

Complement products (C5a, C3a, C4a)

Leukocyte chemotaxis and activation, vasodilation (mast cell stimulation)

112
Q

PLASM A PROTEIN–DERIVED

Plasma (produced in liver)

A

Increased vascular permeability, smooth muscle contraction, vasodilation, pain

113
Q

PLASM A PROTEIN–DERIVED

Plasma (produced in liver)

A

Proteases activated during coagulation

Endothelial activation, leukocyte recruitment

114
Q

TNF

A

tumor necrosis factor

115
Q

MAC

A

membrane attack complex;

116
Q

IL-1

A

interleukin-1

117
Q

The two major Vasoactive Amines

named because they have important actions on blood vessels,

A

Histamine and Serotonin

118
Q

mast cell release degranulation in response to a variety of stimuli,

A

(1) physical injury such as trauma, cold, or heat;
(2) binding of antibodies to mast cells, which underlies allergic reactions
(3) fragments of complement called anaphylatoxins (C3a and C5a);
(4) histamine-releasing proteins derived from leukocytes;
(5) neuropeptides (e.g., substance P); and (6) cytokines (IL-1, IL-8).

119
Q

causes dilation of arterioles and increases the permeability of venules. It is considered to be the principal mediator of the immediate transient phase of increased vascular permeability, producing interendothelial gaps in venules, as we have seen. Its vasoactive effects are mediated mainly via binding to H1 receptors on microvascular endothelial cells.

stored as preformed molecules in cells and are therefore among the first mediators to be released during inflammation

A

histamine

120
Q

is a preformed vasoactive mediator with actions similar to those of histamine. It is present in platelets and certain neuroendocrine cells, e.g. in the gastrointestinal tract, and in mast cells in rodents but not humans

A

Serotonin (5-hydroxytryptamine)

121
Q

Arachidonic Acid (AA) Metabolites

A

Prostaglandins, Leukotrienes, and Lipoxins

122
Q

is a 20-carbon polyunsaturated fatty acid (5,8,11,14-eicosatetraenoic acid) that is derived from dietary sources or by conversion from the essential fatty acid linoleic acid. It does not occur free in the cell but is normally esterified in membrane phospholipids

A

Arachidonic Acid (AA)

123
Q

Mechanical, chemical, and physical stimuli or other mediators (e.g., C5a) release AA from membrane phospholipids through the action of

A

phospholipase A2

activation of phospholipase A2 include an increase in cytoplasmic Ca 2+ and activation of various kinases in response to external stimuli

124
Q

are synthesized by two major classes of enzymes: cyclooxygenases (which generate prostaglandins) and lipoxygenases (which produce leukotrienes and lipoxins)

A

eicosanoids

125
Q

are produced by mast cells, macrophages, endothelial cells, and many other cell types, and are involved in the vascular and systemic reactions of inflammation. They are produced by the actions of two cyclooxgenases, the constitutively expressed COX-1 and the inducible enzyme COX-2.

A

Prostaglandins (PGs)

126
Q

Prostaglandins (PGs) that are most important ones in inflammation are?

A

PGE2,
the major prostaglandin made by mast cells

PGD2,
the major prostaglandin made by mast cellsPGF2α,

PGD2 is a chemoattractant for neutrophils

PGI2 (PROSTACYCLIN)
Vascular endothelium lacks thromboxane synthetase but possesses prostacyclin synthetase

TXA2 (THROMBOXANE),

platelets contain the enzyme thromboxane synthetase, and hence txa2 is the major product

127
Q

enzymes are responsible for the production of leukotrienes, which are secreted mainly by leukocytes, are chemoattractants for leukocytes, and also have vascular effects

A

lipoxygenase

128
Q

three different lipoxygenases

A

5-LIPOXYGENASE BEING the predominant one in neutrophils. This enzyme converts AA to 5-hydroxyeicosatetraenoic acid, which is chemotactic for neutrophils

129
Q

LTB4 is a potent chemotactic agent and activator of neutrophils, causing aggregation and adhesion of the cells to venular endothelium, generation of ROS, and release of lysosomal enzymes

A

go

130
Q

cysteinylcontaining leukotrienes

A

C4, D4, and E4 (LTC4, LTD4, LTE4)

cause intense vasoconstriction, bronchospasm (important in asthma), and increased vascular permeability. The vascular leakage, as with histamine, is restricted to venules

131
Q

are much more potent than is histamine in increasing vascular permeability and causing bronchospasm

A

Leukotrienes

132
Q

are inhibitors of inflammation from AA

A

lipoxins

The principal actions of lipoxins are to inhibit leukocyte recruitment and the cellular components of inflammation

inhibit neutrophil chemotaxis and adhesion to endothelium

133
Q

Action

; PGI2 (prostacyclin), PGE1, PGE2, PGD2

A

Vasodilation

134
Q

Action

; Thromboxane A2, leukotrienes C4, D4, E4

A

Vasoconstriction

135
Q

Action Leukotrienes C4, D4, E4

A

Increased vascular permeability

136
Q

Action

;Leukotriene B4, HETE

A

Chemotaxis, leukocyte adhesion

137
Q

HETE

A

hydroxyeicosatetraenoic acid

138
Q

include aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin. They inhibit both COX-1 and COX-2 and thus inhibit prostaglandin synthesis

A

• Cyclooxygenase inhibitors

aspirin does this by irreversibly acetylating and inactivating cyclooxygenases

139
Q

should be anti-inflammatory without having the toxicities of the nonselective inhibitors, such as gastric ulceration

A

COX-2 inhibitors

may increase the risk of cardiovascular and cerebrovascular events

impair endothelial cell production of prostacyclin, a vasodilator and inhibitor of platelet aggregation

140
Q

Lipoxygenase inhibitors

5-lipoxygenase is not affected by NSAIDs, and many new inhibitors of this enzyme pathway have been developed. Pharmacologic agents that inhibit leukotriene production (e.g. Zileuton) or block leukotriene receptors (e.g. Montelukast) are useful in the treatment of asthma.

A

Lipoxygenase inhibitors

141
Q

powerful anti-inflammatory agents may act by reducing the transcription of genes encoding COX-2, phospholipase A2, pro-inflammatory cytokines (such as IL-1 and TNF), and iNOS

A

• Broad-spectrum inhibitors include corticosteroids

142
Q

serve as poor substrates for conversion to active metabolites by both the cyclooxygenase and lipoxygenase pathways but are excellent substrates for the production of anti-inflammatory lipid products called RESOLVINS AND PROTECTINS

A

consumption of fish oil

143
Q

another phospholipid-derived mediator

causes vasoconstriction and bronchoconstriction, and at extremely low concentrations it induces vasodilation and increased venular permeability with a potency 100 to 10,000 times greater than that of histamine

also causes increased leukocyte adhesion to endothelium (by enhancing integrin-mediated leukocyte binding), chemotaxis, degranulation, and the oxidative burst

boosts the synthesis of other mediators, particularly eicosanoids, by leukocytes and other cells

A

Platelet-Activating Factor (PAF)

144
Q

Inactivation of antiproteases

with increased destruction of extracellular matrix. In the lung, such inhibition of anti-proteases contributes to destruction of elastic tissues, as in emphysema

A

α1-antitrypsin

145
Q

antioxidants

A

enzyme superoxide dismutase

catalase, which detoxifies H2O2

glutathione peroxidase, another powerful H2O2 detoxifier

copper-containing serum protein
ceruloplasmin

the iron-free fraction of serum transferrin

146
Q

a soluble gas that is produced not only by endothelial cells but also by macrophages and some neurons in the brain. It acts in a paracrine manner on target cells through induction of CYCLIC GUANOSINE

leading to a response, such as the relaxation of vascular smooth muscle cells

A

Nitric Oxide (NO)

147
Q

NO is synthesized from

A

L-arginine by the enzyme nitric oxide synthase (NOS

148
Q

three different types of NOS

A

endothelial (eNOS),

neuronal (nNOS), and

inducible (iNOS)
induced when macrophages and other cells are activated by cytokines (e.g., TNF, IFN-γ) or microbial products.

149
Q

reduces platelet aggregation and adhesion inhibits several features of mast cell–induced inflammation, and inhibits leukocyte recruitment.

A

NO

production of NO is thought to be an endogenous mechanism for controlling inflammatory responses

150
Q

are proteins produced by many cell types (principally activated lymphocytes and macrophages, but also endothelial, epithelial, and connective tissue cells) that modulate the functions of other cell types

A

Cytokines

151
Q

TNF

INACUTEINFLAMMATION

A

Macrophages, mast cells, T lymphocytes

Stimulates expression of endothelial adhesion molecules and secretion of other cytokines; systemic effects

152
Q

IL-1

INACUTEINFLAMMATION

A

Macrophages, endothelial cells, some epithelial cells

Similar to TNF; greater role in fever

153
Q

IL-6

INACUTEINFLAMMATION

A

ages, other cells

Systemic effects (acute-phase response)

154
Q

Chemokines

INACUTEINFLAMMATION

A

Macrophages, endothelial cells, T lymphocytes, mast cells, other cell types

Recruitment of leukocytes to sites of inflammation; migration of cells to normal tissues

155
Q

IL-12

CHRONIC INFLAMMATION

A

Dendritic cells, macrophages

Increased production of IFN-γ

156
Q

IFN-γ

CHRONIC INFLAMMATION

A

T lymphocytes, NK cells

Activation of macrophages (increased ability to kill microbes and tumor cells)

157
Q

IL-17

CHRONIC INFLAMMATION

A

T lymphocytes

Recruitment of neutrophils and monocytes

158
Q

are two of the major cytokines that mediate inflammation. They are produced mainly by activated macrophages.

can be stimulated by endotoxin and other microbial products, immune complexes, physical injury, and a variety of inflammatory stimuli

A

TNF and IL-1 are

most important actions in inflammation are their effects on endothelium, leukocytes, and fibroblasts, and induction of systemic acute-phase reactions ( Fig. 2-13 ). In endothelium they induce a spectrum of changes referred to as ENDOTHELIAL
ACTIVATION.

expression of endothelial adhesion molecules; synthesis of chemical mediators, including other cytokines, chemokines, growth factors, eicosanoids, and NO; production of enzymes associated with matrix remodeling

159
Q

The production of IL-1 is controlled by a multi-protein cellular complex, sometimes called the

A

“inflammasome

responds to stimuli from microbes and dead cells

160
Q

inherited autoinflammatory syndromes, the best known of which is familial Mediterranean fever

A

mutant proteins either constitutively activate the inflammatory caspases or interfere with the negative regulation of this enzymatic process. The net result is unregulated IL-1 production

161
Q

IL-1 and TNF (as well as IL-6) induce the systemic acute-phase responses associated with infection or injury

A

TNF also regulates energy balance by promoting lipid and protein mobilization and by suppressing appetite. Therefore, sustained production of TNF contributes to CACHEXIA, a pathologic state characterized by weight loss and anorexia that accompanies some chronic infections and neoplastic diseases

162
Q

primarily as chemoattractants for specific types of leukocytes

A

Chemokines

two main functions: they stimulate leukocyte recruitment in inflammation and control the normal migration of cells through various tissues

163
Q

chemokines have are classified into four major groups, according to the arrangement of the conserved cysteine (C) residues in the mature proteins

A

C-X-C chemokines (also called α chemokines) chemokines act primarily on neutrophils

164
Q

which include monocyte chemoattractant protein (MCP-1), eotaxin, macrophage inflammatory protein-1α (MIP-1α), and RANTES (regulated and normal T-cell expressed and secreted), generally attract monocytes, eosinophils, basophils, and lymphocytes but not neutrophils

A

C-C chemokines (also called β chemokines) have

165
Q

The C chemokines (e.g., lymphotactin) are relatively specific for lymphocytes.

A

C chemokines (also called γ chemokines)

166
Q

xists in two forms: the cell surface-bound protein can be induced on endothelial cells by inflammatory cytokines and promotes strong adhesion of monocytes and T cells, and a soluble form, derived by proteolysis of the membrane-bound protein, has potent chemoattractant activity for the same cells.

A

CX3C chemokines

fractalkine

167
Q

Neutrophils have two main types of granules

A

The smaller specific (or secondary) granules contain lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, and alkaline phosphatase.

The larger azurophil (or primary) granules contain myeloperoxidase, bactericidal factors (lysozyme, defensins), acid hydrolases, and a variety of neutral proteases (elastase, cathepsin G, nonspecific collagenases, proteinase
3). [40] Both types of granules can fuse with phagocytic vacuoles containing engulfed material, or the granule contents can be released into the extracellular space.

168
Q

Acid proteases

A

degrade bacteria and debris within the phagolysosomes, in which an acid pH is readily reached

169
Q

Neutral proteases

A

are capable of degrading various extracellular components, such as collagen, basement membrane, fibrin, elastin, and cartilage, resulting in the tissue destruction that accompanies inflammatory processes.

170
Q

Monocytes and macrophages

A

contain acid hydrolases, collagenase, elastase, phospholipase, and plasminogen activator. These may be particularly active in chronic inflammatory reactions.

171
Q

α1-antitrypsin,

A

major inhibitor of neutrophil elastase. A deficiency of these inhibitors may lead to sustained action of leukocyte proteases, as is the case in patients with α1-antitrypsin deficiency

172
Q

substance P and neurokinin A

A

belong to a family of tachykinin neuropeptides produced in the central and peripheral nervous systems. [69] Nerve fibers containing substance P are prominent in the lung and gastrointestinal tract. Substance P has many biologic functions, including the transmission of pain signals, regulation of blood pressure, stimulation of secretion by endocrine cells, and increasing vascular permeability

173
Q

consists of more than 20 proteins

cause increased vascular permeability, chemotaxis, and opsonization

A

complement system

174
Q

critical step in complement activation is the proteolysis of the third (and most abundant) component

A

Cleavage of C3

175
Q

Cleavage of C3 can occur by one of three pathways:

A

the classical pathway , which is triggered by fixation of C1 to antibody (IgM or IgG) that has combined with antigen

the alternative pathway, which can be triggered by microbial surface molecules (e.g., endotoxin, or LPS), complex polysaccharides, cobra venom, and other substances, in the absence of antibody

lectin pathway, in which plasma mannose-binding lectin binds to carbohydrates on microbes and directly activates C1.

THEY ALL LEAD TO THE FORMATION OF AN ACTIVE ENZYME CALLED THE C3 CONVERTASE, WHICH SPLITS C3 INTO TWO FUNCTIONALLY DISTINCT FRAGMENTS, C3A AND C3B.

C3a is released

C3b becomes covalently attached to the cell or molecule where complement is being activated

C3b then binds to the previously generated fragments to form C5 convertase

which cleaves C5 to release C5a and leave C5b attached to the cell surface

C5b binds the late components (C6–C9), culminating in the formation of the membrane attack complex (MAC, composed of multiple C9 molecules

176
Q

complement system fall into three general categories

A

Inflammation
ANAPHYLATOXINS
C3a, C5a, and, to a lesser extent, C4a are cleavage products of the corresponding complement components that stimulate histamine release from mast cells and thereby increase vascular permeability and cause vasodilation

Phagocytosis
C3b and its cleavage product iC3b (inactive C3b), when fixed to a microbial cell wall, act as OPSONINS and promote phagocytosis by neutrophils and macrophages, which bear cell surface receptors for the complement fragments

Cell lysis
The deposition of the MAC on cells makes these cells permeable to water and ions and results in death (lysis) of the cells.

177
Q

The intrinsic clotting pathway is a series of plasma proteins that can be activated by

A

Hageman factor (factor XII

XII), a protein synthesized by the liver that circulates in an inactive form. Factor XII is activated upon contact with negatively charged surfaces, for instance when vascular permeability increases and plasma proteins leak into the extravascular space and come into contact with collagen, or when it comes into contact with basement membranes exposed as a result of endothelial damage.

178
Q

thrombin, a product of clotting, promotes inflammation by engaging receptors that are called protease-activated receptors (PARs) because they bind multiple trypsin-like serine proteases in addition to thrombin

A

coagulation and inflammation can initiate a vicious cycle of amplification

interfering with clotting is a potential therapeutic strategy for the systemic inflammatory disease seen with severe, disseminated bacterial infections. This is the rationale for treating this disorder with the anticoagulant, activated protein C, which may benefit a subset of the patients

179
Q

are vasoactive peptides derived from plasma proteins, called kininogens, by the action of specific proteases called kallikreins

A

Kinins

Kallikrein itself is a potent activator of Hageman factor, allowing for autocatalytic amplification of the initial stimulus

180
Q

increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected into the skin

A

bradykinin

181
Q

XIIa is inducing fibrin clot formation, it activates the fibrinolytic system.

A

go

182
Q

plasminogen,

A

plasma protein that binds to the evolving fibrin clot to generate plasmin, a multifunctional protease

primary function of plasmin is to lyse fibrin clots, during inflammation it also cleaves the complement protein C3 to produce C3 fragments, and it degrades fibrin to form fibrin split products,

183
Q

Activated Hageman factor (factor XIIa

initiates four systems involved in the inflammatory response:

A

(1) the kinin system, which produces vasoactive kinins;
(2) the clotting system, which induces formation of thrombin, which has inflammatory properties;
(3) the fibrinolytic system, which produces plasmin and degrades fibrin to produce fibrinopeptides, which induce inflammation; and
(4) the complement system, which produces anaphylatoxins and other mediators.

Some of the products of this initiation —particularly kallikrein—can, by feedback, activate Hageman factor, resulting in amplification of the reaction.

184
Q

C3a and C5a can be generated by several types of reactions

A

(1) immunologic reactions, involving antibodies and complement (the classical pathway);
(2) activation of the alternative and lectin complement pathways by microbes, in the absence of antibodies; and
(3) agents not directly related to immune responses, such as plasmin, kallikrein, and some serine proteases found in normal tissue.

185
Q

Prostaglandins
Nitric oxide
Histamine

causes

A

Vasodilation

186
Q 
Histamine and serotonin
C3a and C5a (by liberating vasoactive amines from mast cells, other cells)
Bradykinin
Leukotrienes C4, D4, E4
PAF
Substance P

causes

A

Increased vascular permeability

187
Q 
TNF, IL-1
Chemokines
C3a, C5a
Leukotriene B4
(Bacterial products, e.g., N-formyl methyl peptides)

causes

A

Chemotaxis, leukocyte recruitment and activation

188
Q

IL-1, TNF
Prostaglandins

causes

A

Fever

189
Q

Prostaglandins
Bradykinin

causes

A

Pain

190
Q

Lysosomal enzymes of leukocytes
Reactive oxygen species
Nitric oxide

causes

A

Tissue damage

191
Q

Outcomes of Acute Inflammation

may have one of three outcome

A

Complete resolution.

resolution and is the usual outcome when the injury is limited or short-lived or when there has been little tissue destruction and the damaged parenchymal cells can regenerate

Healing by connective tissue replacement (fibrosis

incapable of regeneration, or when there is abundant fibrin exudation in tissue or serous cavities (pleura, peritoneum) that cannot be adequately cleared

ORGANIZATION

connective tissue grows into the area of damage or exudate, converting it into a mass of fibrous tissue—a process also called

Progression of the response to chronic inflammation

Acute to chronic transition occurs when the acute inflammatory response cannot be resolved, as a result of either the persistence of the injurious agent or some interference with the normal process of healing

PATHOLOGY <3 (2 decks)

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