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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Inflammation

A

Local response of vascularized tissue to stimuli that cause injury

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2
Q

Goals of inflammation

A

To isolate or contain
To remove causative agent
To achieve healing

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3
Q

Causes of Inflammation

A

Infection
Tissue necrosis
Foreign bodies
Immune reactions(hypersensitivity and autoimmune)

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4
Q

Hypersensitivity

A

Exaggerated response of the immune system

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5
Q

Autoimmune

A

Immune reaction on local antigens or self harm

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6
Q

How does the body recognize damaged cells and microbes

A

-Cellular Receptors for microbes
Intracellular or extracelluar- TLRs
-Sensor of cell damage
Through detecting molecules that are released from the intracytoplasmic compartment.- ATP, uric acid, nucleic acids
-Other cellular receptors- for antibodies and complement proteins.

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7
Q

Inflammation classified based on

A

Duration of lesion
Histologic appearance
Type of inflammatory cells

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8
Q

Increased blood flow

A

Hyperemia

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9
Q

Chemicals that induce pain

A

Bradykinin,serotonin, prostaglandins

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10
Q

Vascular phase

A

Brief vasoconstriction
Vasodilation
Vascular leakage

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11
Q

Cellular phase

A

Migration
Rolling and adhesion
Transmigration
Migration

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12
Q

Causes of vascular leakage

A 
Endothelial constriction or retraction
Endothelial injury(direct or lymphocyte mediated)
Increased transcytosis and angiogenesis
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13
Q

Cardinal signs of inflammation

A 
Redness
Heat
Pain
Swelling
Loss of function
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14
Q

Adhesion molecules

A

Selectins(p,e,l)
Immunoglobulin superfamily
Integrins
Mucin-like glycoproteins

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15
Q

IG superfamily and integrin interaction

A

ICAM-1 and VCAM-1 with VLA-4 and LFA-1

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16
Q

endothelium can be virtually lined by white cells an appearance called

A

Pavementing

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17
Q

Leukocyte activation

A

Prepares Archinidonic acid metabolites from plasma membrane
Prepare for oxidative burst
Regulate leukocyte adhesion to endothelial cells

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18
Q

Enhances phagocytosis

A

Opsonins

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19
Q

Steps of phagocytosis

A

Recognition and attachment
Engulfing
Killing or degrading

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20
Q

Major opsonins

A

Immunoglobulin G opsonin or Fc fragment of IG
Complementary system (C3b and C3bi)
Lectins or carbohydrate binding proteins

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21
Q

Phagocytosis receptors

A

Mannose and scavenger

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22
Q

Cell killing(phagocytosis)

A

Oxygen dependent

Oxygen independent

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23
Q

Oxygen dependent phagocytosis

A

Non myoperoxidase

Myoperoxidase

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24
Q

Non-myo peroxidase

A

H2O2 to OH-

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25
Q

Myoperoxidase

A

H2O2 to HOCL by halide ions and MYO enzymes

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26
Q

Oxygen independent

A 
Lysozymes
Bacterial permeability increasing protein
Lactoferrin
Defensins
Major basic proteins
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27
Q

Defects in leukocyte adhesion

A

LAD 1 AND 2 cause impaired healing and recurrent bacterial infection
LAD 1 because of B2 integrin deficiency which inhibits adhesion with VCAM and ICAM

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28
Q

Defects in phagolysosome

A

Chediak-Higashi syndrome
Neutropenia, defective granuloma tissue and delayed killing
Recurrent bacterial infection and giant granules

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29
Q

Defects in microbial activity

A

Chronic granulomatous disease
Defects in genes coding for NADPH oxidase
Infection in nares and gingivitis

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30
Q

Termination of acute inflammation due to

A

Short half life of mediators

Stop signals

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31
Q

Chemical mediators source

A

Plasma, leukocytes, macrophages, mast cells, platelets

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32
Q

Mediators kept in granules

A

Histamines
Serotonins
Lysosomal enzymes

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33
Q

De novo mediators

A 
Leukotrienes
Prostaglandins
Nitric oxide
ROS
cytokines
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34
Q

Plasma mediators

A 
Complement system(3a,3b,5a,5b-9)
Hageman factor (kinin, fibrosis)
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35
Q

Histamine found

A

Mast cells, platelets and basophils

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36
Q

Vasoamines

A

Histamines and serotonins

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37
Q

Histamine release stimulated by

A

Physical injury
Immune reactions, binding of IG E
Fragments of complement system known as anaphylatoxins(C3A, C5A)
Cytokines( IL-1 AND IL-8)

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38
Q

Histamine action

A

Vasodilation of arterioles

Increased vascular leakage of venules

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39
Q

PGE2

A

Fever and pain

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40
Q

PGD2

A

vascular permeability and vasodilation

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41
Q

TXA2

A

Vasoconstriction, aggregates platelets

Thromboxane

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42
Q

PGI2

A

Inhibits platelet aggregation and causes vasodilation

Prostacyclin

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43
Q

Arachindonic acid metabolite pathways

A

Cyclooxygenases

Lipooxygenases

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44
Q

Cyclooxygenase

A

Generate prostaglandins
Cox-1 constitutively expressed
Cox-2 during inflammation

45
Q

Lipooxygenase pathway

A

5-lipooxygenase -> 5- HETE -> leukotrienes

46
Q

Leukotriene b4

A

Chemotaxin

47
Q

Leukotriene C4,D4,E4

A

Broncospasm
Increased permeability
Vasoconstriction

48
Q

Lipotoxin

A

Trans cellular biosynthetic pathway

Inhibit Leukocyte recruitment and cellular component of inflammation

49
Q

Anti inflammatory substances for cyclooxygenase pathway

A

Aspirin and indomethacin affect prostaglandin generation

Glucocorticoid affect expression of PCLA2 and COX-1

50
Q

Platelet activating factor action

A

Vasodilation, increased permeability
Bronchiconstriction, vasoconstriction
Leukocyte chemotxin, aggregates platelet
Increased leukocyte adhesion

51
Q

Master cytokines

A

Tumor necrosis factor and interleukine 1

52
Q

Stimulus for master cytokines secretion

A

Physical injury
Immune complexes
Endotoxins
Microbial products

53
Q

Cachexia

A

a pathologic state characterized by weight loss & anorexia that accompanies some infections & neoplastic disease

54
Q

a pathologic state characterized by weight loss & anorexia that accompanies some infections & neoplastic disease

A

Cachexia

55
Q

Cachexia caused by

A

Sustained production of Tumor Necrosis Factor

56
Q

Action of master cytokines

A

Effect on endothelium(increase in adherence, procoagulant activity, increased interleukine production); fibroblast( increase in collagen synthesis, proliferation) and leukocyte( cytokine production)
Acute response reactions (fever, loss of appetite, shock, neutrophilia)

57
Q

Chemokine action

A

stimulate leukocyte recruitment in inflammation
control the normal migration of cells through various tissues

CXC and CC chemokines

58
Q

NO action

A 
Vasodilator
Signal transduction in neurons
Inhibit mast cell induced inflammation 
Microbicidal activity
Reduces platelet aggregation and adhesion
59
Q

Specific or primary lysosomes

A

MYO, acid hydroplane and neutral protease

60
Q

Azurophilic or secondary

A

Lysozymes, lactoferrins and collagenases

61
Q

effects of lysosomal contents are controlled by

A

system of anti proteases

62
Q

ROS

A

damage endothelium
Inhibit anti proteomes
Injure a variety of cells

63
Q

Antioxidants

A 
Ceruloplasmin
Transferrin
Superoxide dismutase
Catalase
Glutathione peroxidase
64
Q

The biologic functions of the complement system

A

Cell lysis by the MAC

Effects of proteolytic fragments of complement

65
Q

The kinin system generates vasoactive peptides from

A

plasma proteins called kininogens

66
Q

The kinin system generates vasoactive peptides from plasma proteins called kininogens by the action

A

specific proteases called kallikreins

67
Q

Bradykinin action

A

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

68
Q

Complete resolution if

A

the injury is limited or short-lived
there has been little tissue destruction
the damaged parenchymal cells can regenerate

69
Q

Healing by fibrosis if

A

There is substantial tissue destruction
the inflammatory injury involves tissues that are incapable of regeneration
there is abundant fibrin exudation

70
Q

Morphological patterns of acute inflammation based on

A

Severity
Site
Cause
Type of cell

71
Q

Serous inflammation

A

From blood serum or mesothelial secretion

Blisters from burn or viral infection

72
Q

Fibrinous inflammation cause

A

Increase in permeability

Increase in procoagulant stimuli

73
Q

Fibrinous inflammation course

A

Removal by fibrolysis

Scar formation or fibrosis

74
Q

Pus contents

A

A large number of living or dead leucocytes (pus cells)
Necrotic tissue debris
Living and dead bacteria
Edema fluid

75
Q

Suppurative inflammation characterized by

A

pus

76
Q

Types of suppurative inflammation

A 
Acute diffuse (phlegmonous) inflammation
Abscess formation
77
Q

Pyogenic membrane content

A

Layers of fibrin
Inflammatory cells
Granulation tissue

78
Q

Phegmonous or acute diffuse inflammation

A

characterized by diffuse spread of the exudate through tissue spaces caused by virulent bacteria(streptococci)

79
Q

Catarrhal inflammation example

A

Rhinitis in upper respiratory tract

80
Q

The basic elements of pseudomembranous inflammation

A

extensive confluent necrosis of surface epithelium

severe acute inflammation of the underlying tissues

81
Q

Pseudomembrane inflammation example

A

Dipthetric infection of the pharynx or larynx

Clostridium difficille infection in the large bowel

82
Q

Cause of chronic inflammation

A

Prolonged exposure to toxins
Persistent infections
Immune reaction(autoimmune and allergic)
Pathogenesis of other disease

83
Q

Chronic inflammation is characterized by

A

Infiltration with mononuclear cells
Tissue destruction
Attempts at healing by angiogenesis & fibrosis

84
Q

Complement system activation

A

Classical
Alternative
Lectin

85
Q

Macrophages activated by

A

Cytokines (eg IFN γ) secreted by sensitized T lymphocytes

Bacterial endotoxins

86
Q

products of activated macrophages

A

eliminate injurious agents
initiate process of repair (growth factors)
are responsible for tissue injury (reactive oxygen metabolites)

87
Q

Cells of chronic inflammation

A 
Lymphocytes 
Macrophages 
Plasma
Eosinophils- parasitic 
Mast cells
88
Q

Mononuclear phagocyte systems also called

A

Reticuloendothelial system

89
Q

IL-2 from macrophage activation

A

Promotes T lymphocyte response

90
Q

Non specific chronic inflammation

A

Suppurative inflammation
Diffuse accumulation of mononuclear cells
Formation of fibrous tissue

91
Q

Granulomatous inflammation

A

Activated macrophages, epitheliod cells and multinucleated giant cells

92
Q

Granuloma

A

Focal area of granulomatous inflammation

Accumulation of epitheliod cells in clusters surrounded by cuff of lymphocytes and occasional plasma

93
Q

Types of granuloma

A

Foreign body

Immune

94
Q

Foreign body granuloma

A

Inert foreign bodies
Doesn’t elicit an immune response
Example sutures

95
Q

Immune granuloma

A

Insoluble particles
Elicits cell mediated immune response
Example TB

96
Q

Causes of granulomatous inflammation

A

Bacteria, fungi, helminthic, Protozoa, chlamydia, inorganic material, idiopathic

97
Q

Bacterial cause of GMI

A

TB, leprosy, syphilis, Yersiniosis, cat scratch

98
Q

Fungal cause of GMI

A

Histoplasmosis, cryptococcosis, coccdiodomycosis, blastomycosis

99
Q

Helmenthic GMI

A

Schistosomiasis

100
Q

Protozoal GMI

A

Leishmaniasis and toxoplasmosis

101
Q

Chlamydia GMI

A

lymphogranuloma venerum

102
Q

Inorganic GMI

A

Berrylosis

103
Q

Idiopathic GMI

A

acidosis, Cohn’s disease, primary biliary cirrhosis giant cells

104
Q

Acute phase response

A 
Fever
Leukocytosis
Acute phase proteins
Increased pulse
Anorexia
Malaise
105
Q

Fever mechanism

A

Toxin induce cytokines release from leukocytes
IL-1 and TNF stimulate AA metabolism
Prostaglandin E2 released
PGE2 stimulates NTs in the hypothalamus
CAMP stimulation causes rise in temperature

106
Q

Acute phase proteins

A

C reactive
Fibrinogen
Serum Amyloid A

107
Q

C reactive protein

A

Binds to PC of PM on a dying cell and activates complementary system

108
Q

Fibrinogen

A

Sticks RBC together hence they sediment rapidly
Basis for measuring ESR
Indicator of acute phase response

109
Q

Serum amyloid A

A

Replaces Apollo protein A in HDL

Targets macrophages instead of liver cells

Pathology (8 decks)

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