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General Pathology > Unit 2 > Flashcards

Unit 2 Flashcards

1
Q

What is inflammation?

A

a protective response involving host cells, blood vessels, and proteins and other mediators that is intended to eliminate the initial cause of cell injury, as well as the necrotic cells and tissues resulting from the original insult, and to initiate the process of repair

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2
Q

How does inflammation accomplish its protective function?

A

diluting, destroying, or otherwise neutralizing harmful agents. Removes dead and injured cells and initiates tissue repair

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3
Q

The goal of the inflammatory reaction is to bring which cells to the site of infection or tissue damage?

A

Leukocytes and plasma proteins

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4
Q

What are the two types of inflammation?

A

Acute and or chronic

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5
Q

Which system transports leukocytes and plasma proteins to the infection site?

A

Circulatory system

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6
Q

Inflammation does have its downside however, It can cause secondary damage to normal tissue via

A

Virulent microbes, prolonged chronic infections and via innapropiate immune response

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7
Q

When injure or infection is detected, what happens?

A

Macrophages, dendritic cells and or mast cells secrete cytokines and attract plasma proteins to regulate or induce inflammation

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8
Q

What are the five steps of inflammation?

A

recognie the injury, recruit leukocytes, remove agents via phagocytosis, regulate the response and resolve/repair tissue

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9
Q

What are the cardinal signs of inflammation?

A

Rubor, calor, tumor, dolor, and functio laesa

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10
Q

Inflammations are typically, _____ (self limiting) when the pro inflammatory mediators are inactivated and the antiinflammatory mediators are activated

A

Short lived

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11
Q

What is an acute inflammation?

A

an inflammation that has a rapid onset and could last anywhere between minutes and days

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12
Q

what are the signs of acute inflammation?

A

Systemic signs, edema, neutrophils infiltrate cells, but no fibrosis

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13
Q

What is chronic inflammation?

A

Insidious form of inflammation and usually has an onset of days to years. It shows few systemic signs such as angiogenesis and fibrosis

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14
Q

In accute inflammation, in which day is the neutrophil activity most prevalent?

A

first day

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15
Q

In chronic inflammation which day/days has more monocyte and macrophage activity?

A

Day 2

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16
Q

What are the stimuli for accute inflammation?

A

infection, trauma, ischemia, necrosis, foreign bodies, and hypersensitivity reactions

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17
Q

What do leukocytes and plasma proteins do after they are stimulated (in acute inflammation)?

A

destroy microbes and celullar debris

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18
Q

What are the components of acute inflammation?

A

Vascular changes and leukocyte recruitment + activation

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19
Q

How do cells recognize harmful agents?

A

pattern recognition receptors

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20
Q

What are pattern recognition receptors?

A

Macrophages, dendritic cells and mast cells that recognize non-self molecular patterns

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21
Q

What are the two types of pattern recognition receptors?

A

Toll like receptors and inflammasome

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22
Q

What type of infections pathogens are recognized by Toll like receptors and where are they located?

A

All types of infectious pathogens and they are located in the plasma membrane

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23
Q

What type of pattern receptor recognizes products of dead cells and crystals and where is it located?

A

Inflammasome and they are located in the cytoplasm

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24
Q

Usually vessels alter to allow better flow and permeability of ____ and proteins to ____

A

Cells and proteins to target tissues

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25
Q

What does vasodilation entail?

A

Increase in blood flow

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26
Q

What could vasodilation cause during inflammation?

A

Erythema and calor in target area

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27
Q

What would an increase in permeability cause in inflammation?

A

An increase in fluid transport to target tissue

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28
Q

An increase in viscosity or stasis would cause _____ to collect along the vascular wall and then ______into tissue. This process is known as _____

A

Leukocytes, migrate, diapedesis

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29
Q

An increase in permeability would reverse osmotic gradient and then would fill the interstitial space with fluid causing what?

A

Edema

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30
Q

What are the mechanisms for increasing permeability?

A

Endothelial cell contraction , endothelial necrosis, and leakage from angiogenesis

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31
Q

What is the most common mechanism for increasing permeability in vessels?

A

endothelial contraction

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32
Q

What does endothelial contraction lead to and how does it dlead to it?

A

leads to intercellular gaps in postcapillary venules by binding histamine to specific receptors

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33
Q

What does endothelial necrosis entail?

A

basically vascular leakage by burns and or infections. This damage persists until repaired

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34
Q

What does leakage from angiogenesis entail?

A

vessel sprouts remain leaky until proliferating endothelial cells mature sufficiently to form intercellular junctions.

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35
Q

inflammation, lymph flow is increased and helps drain ___ ____ leukocytes, and cell debris from the extravascular space.

A

Edema fluid

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36
Q

What is lymphadenopathy?

A

A general disorder of lymph nodes

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37
Q

What is lympadenitis?

A

Inflammation of the lymph node leading to an increase in size

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38
Q

What is lymphangitis?

A

inflammation of the lymphatic channel

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39
Q

What do leukocytes actually do when delivered to target tissue?

A

Kill microbes, remove celullar debris. It also may lead to injury of the inflammation is prolonged or excessive

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40
Q

What are the 4 steps toward leukocyte recruitment?

A

(1) margination and rolling along the vessel wall; (2) firm adhesion to the endothelium; (3) transmigra- tion between endothelial cells; and (4) migration in inter- stitial tissues toward a chemotactic stimulus

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41
Q

What happens during margination and rolling?

A

Basically the RBC push the leukocytes out of the central canal and into the walls of endothelium causing them to interact with it by accumulating (margination) Once the endothelial cells are activated they express adhesion molecules to which the leukocytes attach and detach and sort of tumble (rolling)

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42
Q

What protein mediates Margination and rolling?

A

Selectins

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43
Q

Which protein mediates firm adhesion?

A

Integrins

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44
Q

What happens when leukocytes adhere to endothelium walls and start rolling?

A

they detect changes in the endothelium and can thus start the next step of repair once change is detected

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45
Q
A

Chemotaxis

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46
Q

Leukocyte activation results in the enhancement of the following functions:

A

Phagocytosis, destruction of phagocytosed molecules, liberation of substance

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47
Q

The process through which Leukocytes bind and ingest most microorganisms and dead cells by means of specific surface receptors is known as

A

Phagocytosis

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48
Q

What are opsonins?

A

receptors that recognize host proteins and coat microbes to tag them for phagocytosis

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49
Q

What are the most import ant opsonins?

A

Antibodies of the immunoglobulin G (IgG) class, break- down products of the complement protein C3, and plasma carbohydrate-binding lectins called col- lectins

50
Q

Leukocyte induced tissue injury in inflammation occurs because _____ ____ ____ cant distinguish between tissues

A

White blood cells

51
Q

In certain infections that are persistent such as tuberculosis the autoimmune response does ____ than the ______

A

more damage; microbe

52
Q

An example of tissue injury due to leukocytes might be an infarct. In this situation what may happen due to inflammation?

A

it may prolong and exacerbate the injurious con- sequences of the ischemia, especially upon reperfusion

53
Q

What are the 3 possible outcomes of inflammation?

A

Resolution: Regenation and repair, Chronic inflammation ,and/or scarring

54
Q

What happens during Resolution of inflammation?

A

the injured tissue is capable of regenerating, the usual outcome is restoration to structural and functional normalcy

55
Q

When structural and functional normalcy in the cell are being restored what must occur?

A

neutralization, decay, or enzymatic degradation of the various chemical medi- ators; normalization of vascular permeability; and ces- sation of leukocyte emigration, with subsequent death (by apoptosis) of extravasated neutrophils.

56
Q

Phagocytes and lymphatic drainage of lymph are both key players in this outcome of inflammation because they eliminate detritus from the “battlefield”

(actual quote from the book )

A

Resolution

57
Q

(after restoration of normalcy) Leukocytes secrete _______ that initiate the subsequent repair process, in which new blood vessels grow into the injured tissue to provide nutrients

A

cytokines

58
Q

What stimulates the proliferation of fibroblasts and collagen being layed down in order to fill defects ?

A

growth factors

59
Q

If inflammation still persists due to the offending tissue not being removed and exceeding the capacity for adaptability of the cell, inflammation persists in a more insidious fashion. this is also known as

A

Chronic inflammation

60
Q

What is scarring?

A

type of repair after substantial tissue destruction or when inflammation occurs in tissues that do not
regenerate, in which the injured tissue is filled in by connective tissue.

61
Q

What is fibrosis?

A

In organs in which extensive connec- tive tissue deposition occurs in attempts to heal the damage or as a consequence of chronic inflammation. This process can significantly impede function

62
Q

What are the morphologic patterns of acute inflammation?

A

Serous, Fibrinous, suppurative or purulent and ulcerative

63
Q

What is serous inflammation?

A

characterized by the outpour- ing of a watery, relatively protein-poor fluid that, depend- ing on the site of injury, derives either from the plasma or from the secretions of mesothelial cells lining the perito- neal, pleural, and pericardial cavities.

64
Q

What is fibrinous inflammation?

A

occurs as a consequence of more severe injuries, resulting in greater vascular perme- ability that allows large molecules (such as fibrinogen) to pass the endothelial barrier.

65
Q

What is characteristic of fibrinous inflammation?

A

Fibrinous exaudate

66
Q

What is suppurative inflammation?

A

Localized infection of pus-forming organishs such as Staph. aureus

67
Q

What is an abscess?

A

A focal collection of pus that may be caused by seeding of pyogenic organ- isms into a tissue or by secondary infections of necrotic foci

68
Q

What do abscesses typically have?

A

a central, largely necrotic region rimmed by a layer of preserved neutrophils with a surrounding zone of dilated vessels and fibroblast proliferation indicative of attempted repair.

69
Q

what is ulcerative inflammation?

A

a local defect, or excavation, of the surface of an organ or tissue that is produced by necrosis of cells and sloughing (shedding) of necrotic and inflammatory tissue

70
Q

Where are ulcers most commonly encountered?

A

the mucosa of the mouth, stomach, intestines, or genito- urinary tract and the subcutaneous tissues of the lower extremities in older persons who have circulatory disturbances predisposing affected tissue to extensive necrosis.

71
Q

What are two others types of inflammation?

A

Granolumatous or pseudomembranous

72
Q

What is a granulomatous inflammation?

A

A pattern of chrnoinc inflammation caused by activated macrophages and lymphocytes that wall off an area

73
Q

The most common type of granulomatous inflammation?

A

TB

74
Q

What kind of Granulomas are caused by TB?

A

Caseating granulomas

75
Q

inflammatory mediators may be produced locally by cells at the site of inflammation, or may be derived from circulating inactive precursors that are acti- vated at the site of inflammation (True or false?

A

True

76
Q

How do most mediators of inflammation act?

A

By binding to specific receptors on different target cells

77
Q

What are the types of cell derived inflammatory mediators?

A

Vasoactive amines, arachidonic acid metabolites, Cytokines, Reactive oxygen species, Lysosomal enzymes, and neuropeptides

78
Q

When are vasoactive amines activated and where do they come from?

A

They are activated during acute inflammation and they are derived from mast cells, platelets,endotheliums and WBCs

79
Q

What are the two types of vaso active amine inflammatory mediator?

A

Histamine and serotonin

80
Q

When is histamine released?

A

In response to physical injury (trauma/heat), Immune response dealing with IgE antibodies, in response to anaphylotoxins, leukocyte derived histamine releasing proteins, neuropeptides, and certain cytokines

81
Q

What does histamine cause?

A

Vasodilation and increases vascular permeability

82
Q

What is serotonin?

A

a preformed vasoac- tive mediator found within platelet granules

83
Q

when is serotonin released?

A

during platelet aggregation

84
Q

What does serotonin induce?

A

vasoconstriction during clotting

85
Q

What are Arachidonic acid metabolites?

A

Products derived from the metabolism of AA also known as Eicosanoids

86
Q

Where do Acid metabolites come from?

A

Leukocytes, mast cells, endothelial cells and platelets

87
Q

What do prostaglandins and leukotrienes do?

A

They are vasodilators and contribute to pain and fever caused by inflammation. They are also chemotaxis

88
Q

NSAIDs are medications that affect ______ ______ and reduce pain and fever due to that

A

Prostaglandin synthesis

89
Q

What are lipoxins?

A

A type of Metabolite that inhibits chemotaxis

90
Q

What do cytokines do?

A

Increase WBC production and contribute to Adhesion and well as migration

91
Q

where do cytokines come from?

A

Mast cells, endothelial cells, macrophages

92
Q

What are the most important cytokines?

A

Il-1 and 6, TNF and chemokines

93
Q

Where do ROS’s come from?

A

Neutrophils and macrophages

94
Q

What do ROS do?

A

Kill and degrade microbes

95
Q

What is an example of an ROS and whats its function?

A

Nitric oxide. It is a vasodilator and microbe killer

96
Q

Where do lysosomal enzymes come from and what do they do?

A

They come from neutrophils and monocytes and they kill microbes and degrade tissue

97
Q

What do neuropeptides do?

A

Initiate inflammation, transmit pain and regulate vascularity

98
Q

What are the plasma protein derived mediators of inflammation?

A

Complement proteins, coagulation proteins and kinin system

99
Q

What do complement proteins do?

A

They are plasma proteins and are very important in opsonization and inflammation.

They are vasodilators and increase vascular permeability

They help WBC get to where they need to go

100
Q

What are coagulation proteins?

A

Proteins that come from the liver (hageman factor) and are activated by Exposed collagen or platelets

101
Q

What do coagulation proteins stimulate?

A

Complement system, the kinin system, and clotting

102
Q

What do coagulation proteins activate?

A

Thrombin which leads to clotting

103
Q

What does the Kinin system lead to ?

A

Bradykinin production it is a vasodilator and it increases vascular permeability

104
Q

What is chronic inflammation?

A

inflammation of prolonged duration (weeks to years) in which continuing inflammation, tissue injury, and healing, often by fibrosis, proceed simultaneously

105
Q

How may chronic inflammation arise?

A

Persistent infection by microbes that are hard to eradicate, Immunesuppression (aids), hypersensitivity reactions

106
Q

What is chronic inflammation characterized by?

A

Mononuclear leukocyte cells are there after or around 48 hours, tissue destruction and fibrosis, and angiogenesis and repair

107
Q

What are the dominant cells at the site of chronic inflammation?

A

Macrophages

108
Q

What are the functions of macrophages?

A
  • Eliminate microbes & dead cells

* Initiate angiogenesis & fibrosis

109
Q

What are macrophages activated by during chronic inflammation?

A

Endotoxis, cytokines and foreign bodies

110
Q

What is another chronic inflammatory cell which sustains chronic inflammation and relate to adaptive and innate immunity?

A

Lymphocytes

111
Q

What could stimulate lymphocytes?

A

Bacterial/viral infxns., autoimmune rxns (RA)

112
Q

What is a classically activated macrophage?

A

macrophages that produce lysosomal enzymes, NO, and ROS, all of which enhance their ability to kill ingested organisms, and secrete cytokines that stimulate inflammation

113
Q

What is an alternative activated macrophage?

A

the macrophages that are not actively microbicidal; instead, their principal role is in tissue repair. They secrete growth factors that promote angiogenesis

114
Q

What are the systemic effects of inflammation?

A

Production of cytokines causes Acute Phase reactions and fever

115
Q

What is an acute phase reaction?

A

A reaction in which we experience malaise, elevated heart rate, elevated blood presure, anorexia, somnolecne and anhidrosis

116
Q

What causes fever?

A

Pyrogens related to prostaglandin synthesis

117
Q

When we have a high C reactive protein what does that mean?

A

C reactive protein is usually a telltale sign of inflammation

118
Q

What is leukocytosis?

A

elevated count of WBCs and is extremely common with bacterial infeactions

119
Q

During leukocytosis there is an elevated number of immature cells and they tend to

A

Shift to the left

120
Q

What are leukemoid reactions?

A

Reactions that mimic leukemia in which the blood leukocyte is very high commonly happens in TB

121
Q

What is leukopenia?

A

too low WBC count (HIV/AIDS, chemotherapy)

General Pathology (10 decks)

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