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PATHOLOGY > M1: Acute & Chronic Inflammation > Flashcards

M1: Acute & Chronic Inflammation Flashcards

0
Q

Cell death

A

Necrosis

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1
Q

Protective response to rid the initial cause of cell injury. Complex reactions of both blood vessels and leukocytes.

A

Inflammation

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2
Q

Fluid portion of the blood

A

Plasma

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3
Q

Body’s principal defenders against foreign invaders

A

Plasma proteins, Circulating leukocytes & Tissue phagocytes “PCT”

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4
Q

Protein is primarily synthesized in what organ

A

Liver

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5
Q

Triggers the vascular & cellular reaction

A

Soluble factors

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6
Q

Blood component, polymorphonuclear cell, responsible for Acute Inflammation.

A

Neutrophil

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7
Q

Blood component responsible for Chronic Inflammation

A

Macrophage & Leukocyte

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8
Q

Primarily from B Lymphocytes

A

Plasma cells

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9
Q

Elimination of offending agent is achieved by

A

Termination of Inflammation

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10
Q

Blood component that has a short lifespan in tissues

A

Leukocytes

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11
Q

Repair of damage tissue/cell. Example is abrasion of skin.

A

Regeneration

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12
Q

Filling of the defect with fibrous tissue

A

Scarring

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13
Q

Produce by fibroblast

A

Collagen

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14
Q

Hardening of the blood vessels

A

Atherosclerosis

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15
Q

Cardinal signs of an Infection

A

Rubor, Tumor, Calor, Dolor & Functio Laesa

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16
Q

Cardinal sign: redness

A

Rubor

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17
Q

Cardinal sign: pain

A

Dolor

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18
Q

Cardinal sign: loss of function

A

Functio Laesa

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19
Q

Cardinal sign: heat

A

Calor

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20
Q

Cardinal sign: swelling

A

Tumor

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21
Q

Rapid host response that serves to deliver leukocytes and plasma proteins. Early onset, involving fluid exudation and polymorphonuclear cell immigration.

A

Acute Inflammation

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22
Q

Two main components of Inflammation

A

Vascular wall response & Inflammatory response

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23
Q

Later onset and longer duration involving lymphocytes and macrophages, with blood vessels proliferation and fibrosis.

A

Chronic Inflammation

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24
Q

Calor is due to

A

Vascular dilatation

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25
Q

Rubor is due to

A

Vascular dilatation & Congestion

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26
Q

Tumor is due to

A

Increased vascular permeability

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27
Q

Dolor is due to

A

Mediator release

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28
Q

Functio laesa is due to

A

Pain, Edema, Tissue injury or scar

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29
Q

Three major components of Acute Inflammation: 1. Alterations in _____________, leading to increased blood flow.

A

Vascular caliber

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30
Q

Three major components of Acute Inflammation: Structural changes in the ________, permitting plasma proteins and leukocytes to leave the circulation to produce inflammatory ________.

A

Microvasculature. Exudates.

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31
Q

Three major components of Acute Inflammation: ___________ from blood vessels and accumulation of the site of injury with activation.

A

Leukocyte emigration

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32
Q

Stimuli for Acute Inflammation

A

Tissue necrosis, Infection & Microbial toxin “TIM”

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33
Q

Detects bacteria

A

Toll-like Receptors

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34
Q

Tissue necrosis is due to

A

Ischemia

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35
Q

Produced by cells deprived of O2 & activates transcription of many genes involved in inflammation

A

Hif 1A

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36
Q

Reactions of Blood Vessels in Acute Inflammation

A

BV, Leukocytes & Termination “BLT”

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37
Q

Pathological term for leaky

A

Vascular Permeability

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38
Q

Is excess fluid in interstitial tissue or body cavities

A

Edema

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39
Q

Is an inflammatory, extravascular fluid with cellular debris and high protein concentration. Specific gravity of 1.020 or more.

A

Exudate

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40
Q

Is excess, extravascular fluid with low protein content. It is essentially an ultrafiltrate of blood plasma resulting from elevated fluid pressures or diminished plasma osmotic forces. Specific gravity of 1.012 or less.

A

Transudate

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41
Q

Is a purulent inflammatory exudate rich in neutrophils and cell debris

A

Pus

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42
Q

Normal fluid exchange in vascular beds depends on an intact

A

Endothelium

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43
Q

Normal fluid exchange are modulated by two opposing factors

A

Hydrostatic pressure & Plasma colloid osmotic pressure

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44
Q

Causes fluid to move into the capillaries

A

Plasma colloid osmotic pressure

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45
Q

Causes fluid to move out of the circulation

A

Hydrostatic pressure

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46
Q

Yellowish & Turbid. Escape of fluid, CHONs & cells from the vascular system into the interstitial tissue or body cavities. Inflammatory edema. Increase protein with cellular materials.

A

Exudate

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47
Q

Increase HP & Decrease OP causing transudate

A

Edema

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48
Q

Clear, less hazy & cloudy. Non inflammatory edema. Decreased protein. Little or non cellular material. An ultrafiltrate plasma.

A

Transudate

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49
Q

One of the earliest manifestations of Acute Inflammation. Increase blood flow. Followed by Increase permeability of the microvasculature.

A

Vasodilation

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50
Q

Mediates Vasodilation

A

Histamine & Nitric Oxide

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51
Q

Lining of a vessel

A

Endothelium

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52
Q

Increases when there is vasodilation

A

Hydrostatic pressure

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53
Q

Combination of vascular dilation and fluid loss leads to

A

Increased blood viscosity & concentration of RBCs

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54
Q

Slow movement of erythrocytes

A

Stasis

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55
Q

Vascular congestion

56
Q

Increased Vascular Permeability: _________ of venule endothelium to form intercellular ______.

A

Contraction. Gaps.

57
Q

Contraction of venule endothelium is due to these chemical mediators

A

Histamine, Bradykinin & Leukotrienes “HBL”

58
Q

Contraction of venules/endothelial cells that occur rapidly after injury and is recersible transient. 15-30mins.

A

Immediate-transient response

59
Q

Increased Vascular Permeability: Direct _______ injury.

A

Endothelial

60
Q

Causes endothelial cell necrosis and detachment that affects venules, capillaries and arterioles

A

Sever necrotizing injury

61
Q

Recruited neutrophils may contribute to the injury through

A

Reactive Oxygen Species “ROS”

62
Q

Seen in late appearing sunburn

A

Prolonged delayed response

63
Q

Inflammation of the lymphatics. Secondary inflamed. Red streaks.

A

Lymphangitis

64
Q

Inflammation of the lymph nodes. Draining LN. Enlarged & painful lymph nodes. May be due to lymphoid follicle and sinusoidal phagocyte hyperplasia.

A

Lymphadenitis

66
Q

Increased Vascular Permeability: Increased ________.

A

Transcytosis

67
Q

Transendothelial channels form by interconnection of vesicles derived from the

A

Vesiculovacuolar organelle

68
Q

Induce vascular leakage by increasing the increasing the number of these channels

A

Vascular Endothelial Growth Factor (VEGF)

69
Q

Increased Vascular Permeability: _______ from new blood vessels.

70
Q

Endothelial proliferation and capillary sprouting result in leaky vessels

A

Angiogenesis

71
Q

Represent a secondary line of defense when local inflammatory responses cannot contain an infection

A

Mononuclear Phagocyte System

73
Q

Increased transport of fluids & proteins

A

Transcytosis

74
Q

In Acute Inflammation, this predominates during the first 6-24 hours.

A

Neutrophil

75
Q

In Acute Inflammation, this replaces the neutrophil after 24-48 hours.

76
Q

Journey of Leukocytes from the vessel lumen to the interstitial tissue.

A

Extravasation

77
Q

Extravasation Steps: in the lumen; _________, _________ & __________ to endothelium.

A

Margination, Rolling & Adhesion

78
Q

Extravasation Steps: Migration; ________ & ________.

A

Endothelium & Vessel wall

79
Q

Extravasation Steps: Tissue toward a ________ stimulus.

A

Chemotactic

80
Q

Process of leukocytes redistribution peripheral position of leukocytes along the endothelial surface.

A

Margination

81
Q

Individual & then rows of leukocytes adhere transiently to the endothelium.

82
Q

A chemical mediator that induces expression. Trigger adhesion molecules.

83
Q

Examples of Cytokines

A

TNF, IL-1 & Chemokines “TIC”

84
Q

These are adhesion molecules which mediates initial rolling

85
Q

Found at the surface. Mediates firm adhesion which is commonly seen in neutrophil.

86
Q

Induce endothelial expression of Ligands

A

TNF & IL-1

87
Q

Ligand of endothelial cells for VLA-4 & B1 Integrins

88
Q

Ligand of endothelial cells for LFA & B2 Integrins

89
Q

Express Integrin in low affinity state

90
Q

Firm adhesion of Leukocytes to adhesion molecules which then activate & bind to rolling leukocyte. An example is Cytokine.

A

Chemokines

91
Q

Transmigration

A

Diapedesis

92
Q

Diapedesis is mediated by

A

PECAM-1 (Elastase)

93
Q

Pierce the basement membrane by secreting collagenase

A

Leukocytes

94
Q

Epithelial lining of Endothelium

A

Simple squamous epithelial cells

95
Q

Directs specific binding location. Locomotion oriented along a chemical gradient. Both exogenous & endogenous substances can act as chemoattractants.

A

Chemotaxis

96
Q

Leukocyte responsible for viral infection

A

Lymphocytes

97
Q

Leukocyte responsible for hypersensitivity

A

Eosinophil

98
Q

Responsible for Antibody production

A

Plasma cell

99
Q

Source of cytokines

A

Macrophages

100
Q

Recognizes components of microorganisms

101
Q

Recognize short bacterial peptides. Activation of respiratory burst.

A

G-protein coupled receptors

102
Q

Process of coating a microbe to target it for ingestion which makes it easier to engulf microorganisms.

A

Opsonization

103
Q

Major macrophage activating cytokine. Secreted by natural killer cells reacting to microbes & by antigen activated T lymphocyte.

A

Interferon-Ÿ

104
Q

Coats the microbes. IgG antibodies. Mannan-binding lectin & C3B complement Proteins.

105
Q

Steps in Phagocytosis

A

Recognition, Engulfment & Degradation/Killing “RED”

106
Q

Extension of the cytoplasm

A

Pseudopods

107
Q

Encloses the particle

108
Q

Phagosome fuses with a lysosomal granule

A

Phagolysosome

109
Q

Killing & Degradation is done by

110
Q

Converts H2O2 to hypochloride which a potent antimicrobial agent

A

MPO in presence of Halide

111
Q

Most efficient bacteriocidal system of neutrophils

A

H2O2-MPO-Halide

112
Q

Converted to Hydroxyl radical which is another powerful destructive agent

113
Q

Produced from Arginine which is for microbial killing

A

Nitric Oxide

114
Q

Free harmful radical

A

Peroxynitrite

115
Q

OCl stands for

A

Hypochlorite

116
Q

ONOO stands for

A

Peroxynitrite

117
Q

O2’ stands for

A

Superoxide Anion

118
Q

Defects in phagolysosome function

A

Chedial Higashi Syndrome

119
Q

Defects in microbicidal activity & in genes encoding components of phagocyte oxidase

A

Chronic Granulomatous Disease

120
Q

Acquired deficiencies due to radiation & chemotherapy

A

Bone marrow suppression

121
Q

From mast cell, basophil & platelets. Causes dilation of arterioles a d increases the permeability of venules.

A

Vasoactive Amine: Histamine

122
Q

Stimulates when platelets aggregate after contact with collagen, thrombin, adenosine diphosphate and antigen-antibody complexes.

123
Q

Main source of serotonin

124
Q

Exposed when there is blood vessel injury

A

Subendothelial collagen

125
Q

Converts fibrinogen to fibrin

126
Q

Examples of Arachidonic Acid metabolites

A

Prostaglandin, Leukotrienes & Lipoxins “PLL”

127
Q

Endothelium-derived relaxing factor. Endogenous mechanism for controlling inflammatory response.

A

Nitric Oxide

128
Q

C3A & C5A are examples of

A

Anaphylatoxins

129
Q

Deposition of Collagen

130
Q

Morphologic Patterns of AI: ________ of small blood vessels.

A

Dilatation

131
Q

Morphologic Patterns of AI: _________ of blood flow.

132
Q

Morphologic Patterns of AI: Accumulation of _______ & _______ in the extravascular tissue.

A

Leukocytes & Fluid

133
Q

Marked by outpouring of thin fluid derived from plasma or secretions of mesothelial cells

A

Serous Inflammation

134
Q

Other term for Thin fluid

135
Q

From a 2nd degree burn or viral infection

A

Skin blisters

136
Q

Development of exudate in large vascular leaks. Inflammation in the lining of body cavities. May be removed by __________.

A

Fibrinous Inflammation. Fibrinolysis.

137
Q

Production of pus consisting neutrophils, liquefactive necrosis and edema fluid.

A

Suppurative/Purulent Inflammation

138
Q

Pyogenic bacteria is due to what microorganism

139
Q

Localized collections of purulent inflammatory tissue caused by suppuration in a tissue, organ or a confined space.

140
Q

Local defect or excavation of the surface an organ or tissue that is sloughing.

PATHOLOGY (2 decks)

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