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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
Myoperoxidase
H2O2 to HOCL by halide ions and MYO enzymes
26
Oxygen independent
``` Lysozymes Bacterial permeability increasing protein Lactoferrin Defensins Major basic proteins ```
27
Defects in leukocyte adhesion
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
28
Defects in phagolysosome
Chediak-Higashi syndrome Neutropenia, defective granuloma tissue and delayed killing Recurrent bacterial infection and giant granules
29
Defects in microbial activity
Chronic granulomatous disease Defects in genes coding for NADPH oxidase Infection in nares and gingivitis
30
Termination of acute inflammation due to
Short half life of mediators | Stop signals
31
Chemical mediators source
Plasma, leukocytes, macrophages, mast cells, platelets
32
Mediators kept in granules
Histamines Serotonins Lysosomal enzymes
33
De novo mediators
``` Leukotrienes Prostaglandins Nitric oxide ROS cytokines ```
34
Plasma mediators
``` Complement system(3a,3b,5a,5b-9) Hageman factor (kinin, fibrosis) ```
35
Histamine found
Mast cells, platelets and basophils
36
Vasoamines
Histamines and serotonins
37
Histamine release stimulated by
Physical injury Immune reactions, binding of IG E Fragments of complement system known as anaphylatoxins(C3A, C5A) Cytokines( IL-1 AND IL-8)
38
Histamine action
Vasodilation of arterioles | Increased vascular leakage of venules
39
PGE2
Fever and pain
40
PGD2
vascular permeability and vasodilation
41
TXA2
Vasoconstriction, aggregates platelets | Thromboxane
42
PGI2
Inhibits platelet aggregation and causes vasodilation | Prostacyclin
43
Arachindonic acid metabolite pathways
Cyclooxygenases | Lipooxygenases
44
Cyclooxygenase
Generate prostaglandins Cox-1 constitutively expressed Cox-2 during inflammation
45
Lipooxygenase pathway
5-lipooxygenase -> 5- HETE -> leukotrienes
46
Leukotriene b4
Chemotaxin
47
Leukotriene C4,D4,E4
Broncospasm Increased permeability Vasoconstriction
48
Lipotoxin
Trans cellular biosynthetic pathway | Inhibit Leukocyte recruitment and cellular component of inflammation
49
Anti inflammatory substances for cyclooxygenase pathway
Aspirin and indomethacin affect prostaglandin generation | Glucocorticoid affect expression of PCLA2 and COX-1
50
Platelet activating factor action
Vasodilation, increased permeability Bronchiconstriction, vasoconstriction Leukocyte chemotxin, aggregates platelet Increased leukocyte adhesion
51
Master cytokines
Tumor necrosis factor and interleukine 1
52
Stimulus for master cytokines secretion
Physical injury Immune complexes Endotoxins Microbial products
53
Cachexia
a pathologic state characterized by weight loss & anorexia that accompanies some infections & neoplastic disease
54
a pathologic state characterized by weight loss & anorexia that accompanies some infections & neoplastic disease
Cachexia
55
Cachexia caused by
Sustained production of Tumor Necrosis Factor
56
Action of master cytokines
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
Chemokine action
stimulate leukocyte recruitment in inflammation control the normal migration of cells through various tissues CXC and CC chemokines
58
NO action
``` Vasodilator Signal transduction in neurons Inhibit mast cell induced inflammation Microbicidal activity Reduces platelet aggregation and adhesion ```
59
Specific or primary lysosomes
MYO, acid hydroplane and neutral protease
60
Azurophilic or secondary
Lysozymes, lactoferrins and collagenases
61
effects of lysosomal contents are controlled by
system of anti proteases
62
ROS
damage endothelium Inhibit anti proteomes Injure a variety of cells
63
Antioxidants
``` Ceruloplasmin Transferrin Superoxide dismutase Catalase Glutathione peroxidase ```
64
The biologic functions of the complement system
Cell lysis by the MAC | Effects of proteolytic fragments of complement
65
The kinin system generates vasoactive peptides from
plasma proteins called kininogens
66
The kinin system generates vasoactive peptides from plasma proteins called kininogens by the action
specific proteases called kallikreins
67
Bradykinin action
increases vascular permeability causes contraction of smooth muscle dilation of blood vessels pain when injected into skin
68
Complete resolution if
the injury is limited or short-lived there has been little tissue destruction the damaged parenchymal cells can regenerate
69
Healing by fibrosis if
There is substantial tissue destruction the inflammatory injury involves tissues that are incapable of regeneration there is abundant fibrin exudation
70
Morphological patterns of acute inflammation based on
Severity Site Cause Type of cell
71
Serous inflammation
From blood serum or mesothelial secretion | Blisters from burn or viral infection
72
Fibrinous inflammation cause
Increase in permeability | Increase in procoagulant stimuli
73
Fibrinous inflammation course
Removal by fibrolysis | Scar formation or fibrosis
74
Pus contents
A large number of living or dead leucocytes (pus cells) Necrotic tissue debris Living and dead bacteria Edema fluid
75
Suppurative inflammation characterized by
pus
76
Types of suppurative inflammation
``` Acute diffuse (phlegmonous) inflammation Abscess formation ```
77
Pyogenic membrane content
Layers of fibrin Inflammatory cells Granulation tissue
78
Phegmonous or acute diffuse inflammation
characterized by diffuse spread of the exudate through tissue spaces caused by virulent bacteria(streptococci)
79
Catarrhal inflammation example
Rhinitis in upper respiratory tract
80
The basic elements of pseudomembranous inflammation
extensive confluent necrosis of surface epithelium | severe acute inflammation of the underlying tissues
81
Pseudomembrane inflammation example
Dipthetric infection of the pharynx or larynx | Clostridium difficille infection in the large bowel
82
Cause of chronic inflammation
Prolonged exposure to toxins Persistent infections Immune reaction(autoimmune and allergic) Pathogenesis of other disease
83
Chronic inflammation is characterized by
Infiltration with mononuclear cells Tissue destruction Attempts at healing by angiogenesis & fibrosis
84
Complement system activation
Classical Alternative Lectin
85
Macrophages activated by
Cytokines (eg IFN γ) secreted by sensitized T lymphocytes | Bacterial endotoxins
86
products of activated macrophages
eliminate injurious agents initiate process of repair (growth factors) are responsible for tissue injury (reactive oxygen metabolites)
87
Cells of chronic inflammation
``` Lymphocytes Macrophages Plasma Eosinophils- parasitic Mast cells ```
88
Mononuclear phagocyte systems also called
Reticuloendothelial system
89
IL-2 from macrophage activation
Promotes T lymphocyte response
90
Non specific chronic inflammation
Suppurative inflammation Diffuse accumulation of mononuclear cells Formation of fibrous tissue
91
Granulomatous inflammation
Activated macrophages, epitheliod cells and multinucleated giant cells
92
Granuloma
Focal area of granulomatous inflammation | Accumulation of epitheliod cells in clusters surrounded by cuff of lymphocytes and occasional plasma
93
Types of granuloma
Foreign body | Immune
94
Foreign body granuloma
Inert foreign bodies Doesn’t elicit an immune response Example sutures
95
Immune granuloma
Insoluble particles Elicits cell mediated immune response Example TB
96
Causes of granulomatous inflammation
Bacteria, fungi, helminthic, Protozoa, chlamydia, inorganic material, idiopathic
97
Bacterial cause of GMI
TB, leprosy, syphilis, Yersiniosis, cat scratch
98
Fungal cause of GMI
Histoplasmosis, cryptococcosis, coccdiodomycosis, blastomycosis
99
Helmenthic GMI
Schistosomiasis
100
Protozoal GMI
Leishmaniasis and toxoplasmosis
101
Chlamydia GMI
lymphogranuloma venerum
102
Inorganic GMI
Berrylosis
103
Idiopathic GMI
acidosis, Cohn’s disease, primary biliary cirrhosis giant cells
104
Acute phase response
``` Fever Leukocytosis Acute phase proteins Increased pulse Anorexia Malaise ```
105
Fever mechanism
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
Acute phase proteins
C reactive Fibrinogen Serum Amyloid A
107
C reactive protein
Binds to PC of PM on a dying cell and activates complementary system
108
Fibrinogen
Sticks RBC together hence they sediment rapidly Basis for measuring ESR Indicator of acute phase response
109
Serum amyloid A
Replaces Apollo protein A in HDL | Targets macrophages instead of liver cells

Pathology (8 decks)

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