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Inflammation Flashcards

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1
Q

What are the 4 main causes of inflammation?

A

Physical, Chemical, Infective, Immunologic

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2
Q

What are the physical causes of inflammation?

A

Trauma, Heat or cold, Radiation

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3
Q

What are the chemical causes of inflammation?

A

Acid, Organic poisons

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4
Q

What are the infective causes of inflammation?

A

Bacteria, Viruses, Parasites

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5
Q

What are the Immunologic causes of Inflammation?

A

Ag-Ab, Cell-mediated

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6
Q

What are the harmful effects of inflammation?

A

Edema, Deformity, Hypersensitivity Reaction

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7
Q

What are the s/sx of inflammation?

A

Calor, Rubor, Tumor, Dolor, Functio laesa

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8
Q

Is there edema in Acute inflammation?

A

Yes

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9
Q

Is there edema in Chronic inflammation?

A

No

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10
Q

What are the predominant cells in Acute inflammation?

A

PMNs (Neutrophils)

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11
Q

What are the predominant cells in Chronic Inflammation?

A

Lymphocytes, Plasma cells, Macrophages, Fibroblasts

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12
Q

In what Inflammation will you find Fibrosis/ new blood vessels?

A

in Chronic Inflammation

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13
Q

Where does knowledge of chronic inflammation often come from?

A

Often from animal studies

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14
Q

Where does knowledge of Acute inflammation often come from?

A

Often based on human exposure

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15
Q

What are the mechanisms of inflammation?

A
  1. Vasodilation
  2. Exudation
  3. Emigration of cells
  4. Chemotaxis
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16
Q

What are the events in Acute inflammation?

A
  1. Neurologic Events
  2. Hemodynamic Events
  3. Cellular Events
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17
Q

Where do the magnitude of events in acute inflammation depend on?

A
  1. Severity of Injury
  2. Immune Status
  3. Temperature
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18
Q

What are the neurologic events of inflammation?

A
  1. Initial Vasoconstriction

2. Gradual Vasodilation

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19
Q

What are the hemodynamic changes that occur in inflammation?

A
  1. Transient Vasonconstriction
  2. Persistent progressive Vasodilation
  3. Progressive Vasodilatation
  4. Slowiing or Stasis
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20
Q

How many seconds do mild and severe injury undergo transient vasoconstriction?

A

Mild - 3-5 sec

Severe - 5 minutes

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21
Q

What causes Dolor and Rubor?

A

Vasodilatation

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22
Q

What happens in progressive vasodilatation?

A

There is elevation of local hydrostatic pressure

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23
Q

What happens when there is elevation of local hydrostatic pressure in inflammation?

A

There would be transudation of fluid into extracellular space and swelling

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24
Q

What happens in the slowing and stasis phase of hemodynamic changes?

A

There is increased concentration of red cells, increasing also blood viscosity

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25
What is the hallmark of early hemodynamic change?
Rubor and Dolor
26
What are the Mechanisms of Increased Capillary Permeability?
1. Endothelial Cell Contraction 2. Direct Endothelial Injury 3. Leukocyte-mediated endothelial injury via release of toxic oxygen species and proteolytic enzymes 4. Increased transcytosis 5. Leakage from regenerating capillaries
27
What is the hallmark of acute inflammation?
Increased vascular permeability leading to exudates
28
How do leukocytes move peripherally in inflammation?
During Slowing and stasis of blood flow, leukocytes assume more peripheral position along endothelial surface
29
What is Margination?
Occurs as leukocytes localize to the outer margin of the blood flow adjacent to the vascular endothelium
30
What is the specific gravity of exudates?
> 1.02
31
What is the specific gravity of Transudates?
32
What is the protein content of Exudates?
> 1.5 g/dL
33
What is the protein content of Transudates?
34
What are the cellular events that occur in Inflammation?
1. Extravasation | 2. Phagocytosis
35
What are the steps in the Extravasation of leukocytes?
1. Margination 2. Rolling 3. Pavementing 4. Adhesion 5. Diapedesis 6. Chemotaxis
36
What is the definition of pavementing?
It is where leukocytes line the endothelial surface
37
What are the 4 classes of adhesion molecules?
1. Selectins 2. Immunoglobulins 3. Integrins 4. Mucin-like glycoproteins
38
In what stages of extravasation will selectins predominate?
Rolling to adhesion
39
In what stages of extravasation will Integrins predominate?
Adhesion to Transmigration
40
What are the types of selectins?
E, P, L
41
What are the functions of E-selectins?
They bind to CHO groups of granulocytes, Monocytes, Memory T-cells
42
Where are E-selectins found?
They are found in endothelial cells
43
What are the functions of P-Selectins
They bind Neutrophils, T-lymphocytes, Monocytes
44
Where are P-selectins found?
Endothelium and Platelets
45
What are the functions of L-Selectins?
They bind to CD34, Sialyl-Lewis that are upregulated on endothelium by cytokines at injury sites
46
How are CD34, Sialyl-Lewis upregulated?
They are regulated by cytokines (TNF, IL-1) at injury sites
47
What are the cytokines that upregulate CD34, Sialyl-Lewis?
TNF, IL-1
48
Where are Immunoglobulin Adhesion Molecules expressed?
Endothelial Cells
49
What are the adhesion molecules expressed in endothelial cells?
Intercellular Adhesion Molecule (ICAM-1), Vascular Cell Adhesion Molecule (VCAM-1)
50
What is the role of immunoglobulin class adhesion molecule?
It acts as a ligand to integrins
51
What are the adhesion molecules expressed in Leukocytes that bind immunoglobulins?
Integrins
52
What are the integrins found in leukocytes?
LFA-1, Mac-1, VLA-4
53
Where does ICAM-1 bind?
LFA-1/ Mac-1
54
Where does VCAM-1 bind?
VLA-4
55
What is diapedesis?
Transmigration of leukocyte across the endothelium
56
What is involved in Transmigration?
Ig CD31/ PECAM / Platelet Endothelial Cell Adhesion Molecule 1
57
What are the chemotactic factors?
1. Bacterial products 2. Complement Components (C5a) 3. Arachidonic acid metabolites (LTB4) 4. Cytokines (IL-8)
58
How does chemotaxis occur?
1. Chemotactic agents bind surface receptors 2. This induces calcium mobilization 3. This also leads to assembly of cytoskeletal contractile elements
59
What are the steps of phagocytosis?
1. Recognition and attachment 2. Engulfment 3. Microbial killing and degradation
60
What does recognition in phagocytosis involve?
Mannose Receptors and Scavenger Receptors
61
What are the functions of Mannose receptros and Scavenger Receptors?
Recognition and attachment where there is binding and ingestion of microbes
62
What are the stages of engulfment?
1. Formation of Phagosome 2. Formation of Phagolysosome 3. Degranulation
63
What are the two types of microbial killing?
1. Oxygen-dependent microbial killing | 2. Oxygen-independent microbial killing
64
What are the mediators involved in Oxygen dependent microbial killing?
H2O2- myeloperoxidase and halide system
65
What are the mediators involved in oxygen-independent microbial killing?
1. BPI (Bactericidal Permeability Increasing Protein) 2. Lysozyme 3. Lactoferrin 4. MBP (Major Basic Protein) 5. Defensins
66
What is the mechanism of H2O2- Myeloperoxidase and Halide System?
Oxidative Burst (most effective)
67
What are the defects involved in microbicidal activity?
Deficiency in NADPH oxidase
68
What will happen if there is deficiency of NADPH oxidase?
There is less generation of superoxide, no oxidative burst (chronic granulomatous disease)
69
What are the functions of inflammation?
1. Destroy 2. Isolate 3. Initiate Repair
70
What are the types of inflammatory cells?
1. Neutrophils 2. Monocytes-Macrophage 3. Lymphocytes 4. Eosinophils 5. Plasma Cells 6. Basophils 7. Mast Cells
71
How long will neutrophils be prominent in inflammation reaction?
6 - 24hrs
72
How long will neutrophils be prominent in pseudomonal infections?
2-4 days
73
What cells will predominate in viral infections?
Lymphocytes
74
What cells will predominate in hypersensitivity reactions?
Eosinophils
75
What is a pus?
Exudate rich in neutrophils and parenchymal cell debris
76
When will neutrophils be replaced with macrophages?
1-2 days
77
When will lymphocytes predominate?
Viral Infections, chronic inflammations
78
How do lymphocytes participate in inflammation?
1. Lymphocyte binds with antigen 2. Lymphocyte activation 3. Production of lymphokines 4. Stimulation of monocyte chemotaxis + activate macrophages 5. Macrophages produce monokines 6. Monokines influence T and B-cell function
79
What situations will eosinophils participate in?
1. Allergic Reactions | 2. Parasitic Infestations
80
What do Eosinophil granules contain?
Major Basic Protein (MBP)
81
What is the function of MBP in Eosinophils?
1. It is toxic to parasites and cause lysis of epithelial cells 2. Causes tissue damage in hypersensitivity reactions
82
What are Mast Cells?
Specialized Cells with cytoplasmic granules such as histamine
83
When is histamine released by mast cells?
It is released in response to inflammatory reactions, particularly type I hypersensitivity reactions
84
What are chemical mediators?
1. May or may not utilize specific receptor 2. Signal target cells to release effector molecules, amplifying or inhibiting response 3. Tightly regulated
85
What are some chemical mediators of Vasodilation?
Prostaglandins, Nitric Oxide
86
What are the chemical mediators for increasing vascular permeability?
1. Vasoactive amines 2. C3a, C5a 3. Bradykinin 4. Leukotrienes 5. PAF
87
What are examples of vasoactive amines?
Histamine, Serotonin
88
What are chemical mediators for chemotaxic leukocytic activation?
C5a, LTB, Cytokines (IL-8)
89
What are the cells that release histamine?
Mast cells, Basophils, Platelets, anaphylotoxins, Cytokines, Neuropeptides, Leukocyte-derived histamine-releasing peptides
90
What are the cells that release serotonin?
Platelets
91
What are the cells that release lysosomal enzymes?
Neutrophils, Macrophages
92
What are examples of preformed mediators in secretory granules?
Histamine, Serotonine, Lysosomal Enzymes
93
What are mediators that are newly synthesized in inflammation?
1. Prostaglandin 2. Leukotrienes 3. Platelet-activating factors 4. Activating oxygen Species 5. Nitric Oxide 6. Cytokines
94
What cells synthesize prostaglandins?
All leukocytes, platelets, epithelial cells
95
What cells synthesize leukotrienes?
All leukocytes
96
What cells synthesize Platelet-activating factors?
All leukocytes, epithelial cells
97
What cells synthesize Activated oxygen species?
All leukocytes
98
What cells synthesize Nitric Oxide?
Macrophages
99
What cells synthesize Cytokines?
Lymphocytes, Macrophages, Basophils
100
What systems are activated when Factor XII is activated?
1. Kinin System | 2. Coagulation / Fibrinolysis System
101
What chemical mediators come from complement activation?
C3a, C5a, C3b, C5b-9
102
Which complements are anaphylatoxins?
C3a, C5a, C3b
103
Which complement is involved in membrane attack complex?
C5b-9
104
What are the chemical mediators that cause fever?
IL-1, IL-6, TNF, Prostaglandins
105
What are the chemical mediators that cause Pain?
Prostaglandins, Bradykinin
106
What are the chemical mediators involved in tissue damage?
Neutrophil and Macrophage products Lysosomal Enzymes Oxygen metabolites Nitric Oxide
107
What are the functions of Histamine?
Vasodilation and venular endothelial cell contraction | Junctional widening
108
What triggers the release of serotonin?
Platelet aggregation
109
What is the action of serotonin in inflammation?
Vasodilation similar to histamine
110
In which part of the platelets are serotonins stored?
Dense-body granules of platelets
111
What is the mechanism of action of Steroids in inflammation?
It inhibits the production of arachidonic acid by inhibition of phospholipases
112
What are the two pathways of arachidonic acid metabolism?
Cyclooxygenase ( cyclic endoperoxide) pathway | Lipooxygenase Pathway
113
What are the two inhibitors of cyclooxygenase pathway?
Aspirin and Indomethacin
114
What are the metabolites of Cyclooxygenase pathway?
Thromboxane (TxA2), Prostacyclin (PGI2), Prostaglandins D2, E1, E2, I2
115
What is the function of Thromboxane?
Vasoconstriction, Platelet Aggregation
116
What is the function of Prostacyclin?
Vasodialtion, Inhibits platelet aggregation
117
What is the function of Prostaglandins?
Vasodilation and increases vascular permeability
118
What are the metabolites of Lipooxygenase pathway?
Leukotrienes C4, D4 and E4
119
What are the functions of Leukotrienes C4, D4, E4?
Vasoconstriction, Bronchoconstriction, Increased Vascular Permeability
120
What are some examples of cytokines?
IL-1 and tumor necrosis factor (TNF, Cachectin)
121
What are the functions of cytokines?
They mediate immunologic response and inflammation
122
What do cytokines induce?
Acute phase responses
123
What are examples of plasma proteases?
Kinins, Fibrin split products, complements
124
What initiates the kinin system?
Hageman factor (factor IIa)
125
What does the kinin system cause?
Vascular permeability Arteriolar dilatation Non-Vascular smooth muscle contraction (bronchial smooth muscle) Pain
126
What inactivates the Kinin System?
Kininases (rapid)
127
How is the Complement System Activated?
It is activated via classic (C1) or alternative (C3) pathways
128
What is generated in the complement system?
MAC/ C5b-9
129
What is the function of MAC/ C5b-9?
They punch holes in microbe membranes
130
What are the functions of anaphylatoxins?
Degranulates basophils and mast cells
131
What will anaphylatoxins cause?
Vasodilation, Vascular permeability, Mast cell degranulation
132
What complement increases phagocytosis
C3b, which is an opsonin
133
Other than chemotaxis, what is another function of C5a?
It increases integrin activity leading to adhesion and activation of leukocytes
134
What secretes C5a?
Macrophages
135
What are the functions of LTB4?`
Chemotaxis, Leukocyte adhesion and activation
136
What are the 3 outcomes of inflammation?
1. Complete resolution 2. Healing by scarring or fibrosis 3. Progress to Chronic Inflammation
137
What is an abscess?
Localized collection of pus buried in tissue, organ or confined space
138
How is there localized collection of pus in Abscess?
There is formation of a fibrous wall that is inaccessible to circulation
139
What are the Hereditary defects that impair acute inflammatory response?
1. Deficiency of complement components | 2. Defects in neutrophils
140
What are the deficient complement components in hereditary defects that impair acute inflammatory response?
C2, C3, C5
141
What are the defects in neutrophils?
1. Chronic granulomatous disease of childhood 2. Myeloperoxidase deficiency 3. Chediak-Higashi syndrome
142
What is Chronic granulomatous disease of childhood?
It is an X-linked disorder where there is deficient activity of NADPH oxidase
143
What is Myeloperoxidase deficiency?
It is sometimes associated with recurrent infections but is often of little clinical consequence
144
What is the Chediak- Higashi Syndrome?
An autosomal recessive disorder marked by presence of abnormal WBC
145
What are the clinical manifestations of Chediak-Higashi Syndrome?
Neutropenia, Albinisim, Cranial and Peripheral Neuropathy Tendency to repeat infections
146
What are the morphologic patterns of acute inflammation?
``` Serous Inflammation Fibrinous Suppurative or Purulent Membranous Ulcer ```
147
What is a serous inflammation?
Fluids Predominate | Accumulation of Serum or secretions of mesothelial cells lining peritoneal, pleural and pericardial cavities (effusion)
148
What are some examples of Serous Inflammation?
Skin Blister and TB Pleuritis
149
What is Fibrinous Inflammation?
There is more of: Plasma Proteins (Fibrinogen) Fibrin
150
What will Fibrinous Inflammation manifest in microscope?
Thread-like or solid amorphous eosinophilic coagulum
151
What are diseases with Fibrinous Inflammation?
Bread and butter Pericarditis | Meningitis
152
What is Suppurative or Purulent Inflammation?
Pus formation, e.g. Abscess
153
What is Membranous Inflammation?
Necrosis of mucosa and inflammatory exudate remain attached as surface membrane
154
What are diseases with membranous Inflammation?
Diptheria, membranous enterocolitis
155
What are Ulcers?
Local defect / excavation of the surface of an organ produced by sloughing of inflammatory necrotic tissue
156
What are the three ways in which chronic inflammation occurs?
Persistent infection by intracellular microorganism Prolonged exposure to non-degradable toxic substances Autoimmunity
157
What will persistent infection by intracellular microorganisms lead to?
Delayed hypersensitivity reaction leading to formation of granulomaas
158
What are diseases of non-degradable toxic substances?
Asbestosis Silicosis Atherosclerosis
159
What are examples of autoimmune disorders?
Rheumatoid Arthritis | SLE
160
What are the histologic hallmarks of inflammation?
Mononuclear Cell Infiltration Proliferation of Fibroblasts and small Blood Vessels Increased Connnective Tissue (Fibrosis) Tissue Destruction
161
What are the two Patterns of Chronic Inflammation?
Non-granulomatous | Granulomatous
162
What are Non-granulomatous Inflammation?
Diffuse proliferation of chronic inflammatory cells, Fibroblasts and Collagen
163
What are the Chronic Inflammatory Cells?
Macrophages, Lymphocytes, Plasma Cells
164
What are Granulomatous Inflammations?
Formation of Granulomas - Focal/ nodular collections of epithelioid cells, usually surrounded by a rim of lymphocytes, multinucleate giant cells, with or without casesous necrosis
165
What are the two types of granulomas?
1. Foreign body granuloma | 2. Immune Granuloma
166
What are Foreign body granulomas?
Foreign body large enough to produce phagocytosis by a single macrophage. Does not incite any specific inflammatory or immune response
167
What is Immune Granuloma?
Insoluble particles that induce cell-mediated immune response
168
How does granulomas arise?
It involves activation of macrophages by interactions with T lymphocytes
169
What are steps of activation of macrophages by interactions with T lymphocytes?
1. Macrophage present poorly digestible antigen to CD4 + lymphocytes. 2. Release of Cytokines (interferon) 3. Monocyte Transforms to Macrophages to Epithelioid and giant cells
170
What are the causes of granulomatous inflammation?
Infectious agents Inorganic Metals and dusts Unknown
171
What are examples of bacterial granulomatous inflammations?
TB, SY, Leprosy, Cat-Scratch Disease
172
What are Examples of Fungal granulomatous inflammation agents?
Cryptococcus, Coccidioides immitis
173
What is a parasitic disease that would cause granulomatous inflammation?
Schistosomiasis
174
What granulomatous inflammation has an Unknown Etiology?
Sarcoidosis
175
What are the systemic effects of inflammation?
Fever | Changes in the peripheral blood
176
What are the changes in the peripheral blood as a systemic effect of inflammation?
Leukocytosis Increased Acute Phase Proteins Increased ESR Increased Blood Coagulability
177
What are acute phase proteins?
CRP, Fibrinogen, Serum Amyloid A protein (SAA)

Pathology (5 decks)

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