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Pathology 1 > Ch. 2&3 Inflammation and Repair > Flashcards

Ch. 2&3 Inflammation and Repair Flashcards

1
Q

What is inflammation?

A

The reaction of BVs, leading to accumulation of fluid and leukocytes in extravascular tissues

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2
Q

What are the components of inflammation (WBCs) in order of %?

A

Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils (Never Let Monkeys Eat Bananas)

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3
Q

What is the function of a neutrophil?

A

First responder, used in ACUTE inflammation. Bacterial or fungal infections. Increased activity and death => PUS

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4
Q

When are lymphocytes more common?

A

Chronic inflammation

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5
Q

What are lymphocytes?

A

T cells and B cells

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6
Q

What are monocytes and what is their function?

A

Long-lived phagocytes, present pathogen parts to T cells

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7
Q

What do monocytes become in tissues?

A

Macrophages

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8
Q

When are eosinophils used?

A

Parasite and allergic responses

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9
Q

When are basophils used?

A

Allergic and antigen responses - release HISTAMINE

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10
Q

What do basophils become in tissues?

A

Mast cells

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11
Q

What is the life span of an RBC?

A

120 days

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12
Q

What is the life span of a WBC?

A

days - years

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13
Q

What is the life span of a platelet?

A

8 days

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14
Q

What does a lymphocyte become in tissues?

A

Plasma cell

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15
Q

Onset of acute vs chronic inflammation?

A

Acute = Rapid onset Chronic = Slower onset

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16
Q

Duration of acute vs chronic inf.?

A

Acute = short duration Chronic = Longer duration

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17
Q

Which type of inflammation has edema?

A

Acute

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18
Q

What is the predominant WBC involved in acute inf.?

A

Neutrophils

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19
Q

Which type of inflammation has new blood vessels, fibrosis, and tissue necrosis?

A

Chronic inflammation

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20
Q

What are the predominant WBCs involved in chronic inf.?

A

macrophages and lymphocytes

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21
Q

What is fibrosis?

A

Space occupying lesion (SOL) on cellular/molecular level

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22
Q

What are the signs/symptoms of acute inflammation?

A

Redness (rubor), Heat (calor), Swelling (tumor), Pain (dolor), Loss of function (functio laesa)

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23
Q

What are the 3 main vascular changes in acute inflammation?

A
  1. Vascular dilation and increased blood flow 2. Extravasation and deposition of plasma fluid and proteins (edema) 3. Leukocyte emigration and accumulation in the site of injury
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24
Q

What is the normal avg. colloid osmotic pressure in a capillary?

A

25 mmHg

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25
Q

What is the avg. colloidal osmotic pressure in a capillary during acute inflammation?

A

20 mmHg

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26
Q

Why does colloidal osmotic pressure drop during acute inflammation?

A

Protein leakage across venule

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27
Q

What is the net result of decresed colloidal osmotic pressure?

A

Excess of extravasated fluid

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28
Q

What causes oncotic pressure?

A

Concentration of proteins increases in capillaries, pushing fluid out. Increased concentration of proteins in venules “suck” proteins back in

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29
Q

What controls arteriole pressure?

A

Precapillary sphincters

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30
Q

What happens when precapillary sphincters relax in acute inflammation?

A

Hyperemia

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31
Q

What is a Rouleaux?

A

Stacking of RBCs

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32
Q

What is neutrophil margination?

A

Pushed to outside of bloodstream due to RBC rouleaux

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33
Q

What is the process of Leukocyte extravasation?

A
  1. Margination 2. Pavementing (Rolling -> Tight binding -> Diapedesis) 3. Extravascular migration
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34
Q

What is the relation of Rouleaux to ESR?

A

Directly correlated - increased rouleaux = increased ESR

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35
Q

What initiates Leukocyte rolling?

A

P-Selectin and E-Selectin on endothelial cells

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36
Q

What causes Leukocyte binding?

A

Expression of endothelial adhesion molecules like ICAM-1 (by TNF and IL-1) and increased aviditiy of integrins on Leukocytes (by chemokines)

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37
Q

What causes leukocyte migration after diapedesis?

A

Chemokines

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38
Q

How are microbes destroyed by macrophages?

A
  1. Recognition and attachment 2. Engulfment 3. Microbe ingested in phagosome 4. Fusion of phagosome with lysosome => phagolysosome 5. Killing of microbes by lysosomal enzymes (ROIs and NO)
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39
Q

How are microbicidal reactive Oxygen intermediates produced within phagocytic vesicles?

A

Cytoplasmic oxidases, membrane oxidases, and myeloperoxidase

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40
Q

What are the 2 groups of mediators of inflammation?

A

Plasma derived and cell derived

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41
Q

What type of inflammation mediator is histamine?

A

Cell derived - biogenic amine

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42
Q

What is histamine released from?

A

Platelets and mast cells

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43
Q

What does histamine induce in endothelial cells?

A

Retraction - creates gaps => increased permeability

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44
Q

Why does histamine have short action (immediate transient reaction)?

A

Inactivated by histaminase

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45
Q

What Vitamin stabilizes mast cells?

A

Vitamin C (acute bolus of ascorbic acid when having a reaction)

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46
Q

What is bradykinin?

A

Plasma protein derived from kininogen

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47
Q

What enzyme is used to make bradykinin?

A

Kallikrein

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48
Q

What is kallikrein activated by?

A

Hageman factor

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49
Q

What does Hageman factor act on besides kallikrein?

A

Clotting and fibrinolytic systems of blood

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50
Q

What does bradykinin do?

A

Similar actions to histamine - also induces pain.

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51
Q

What are the preformed chemical mediators in secretory granules?

A

Histamine, serotonin, lysosomal enzymes

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52
Q

What are the newly synthesized chemical mediators of inf.?

A

PGs, Leukotrienes, Platelet-activating factors, Activated oxygen species, Nitric oxide, cytokines

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53
Q

What are the chemical mediators that are activated by Hageman factor?

A

Bradykinin, coagulation/fibrinolysis system

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54
Q

What are the chemical mediators that are activated by complement?

A

C3a, C3b, C5a, C5b (MAC attack)

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55
Q

What is the complement system?

A

Group of plasma proteins produced by liver, circulating in inactive form

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56
Q

How is complement activated?

A

Classical or alternative pathways

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57
Q

What does complement activation lead to?

A

formation of biologically active fragments, intermediate complexes, and MAC attack complex

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58
Q

What are the 4 main functions of activated complement derivatives?

A
  1. Opsonization 2. Anaphylaxis 3. Chemotaxis 4. Cell lysis
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59
Q

What is opsonization?

A

Flagging of antigens for macrophages to recognize

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60
Q

What is anaphylaxis?

A

Histamine release with increased vessel wall permeability

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61
Q

What is chemotaxis?

A

migration of leukocytes

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62
Q

How does complement cause cell lysis?

A

Through action of MAC - makes cell membranes “leaky”

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63
Q

3 steps of phagocytosis of bacteria?

A
  1. Attachment of opsonized bacterium to PMN 2. Engulfment of bacterium 3. Formation of phagocytic vacuole
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64
Q

How is arachidonic acid derived?

A

From phospholipids through the action of phospholipases

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65
Q

Two pathways which further metabolize arachidonic acid?

A

Lipoxygenase pway, Cyclooxygenase pway

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66
Q

5 types of arachidonic acid derivatives?

A

Leukotrienes, Lipoxins, Thromboxane, Prostacyclin, Prostaglandins

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67
Q

What do leukotrienes control?

A

chemotaxis, vascular permeability, bronchospasms

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68
Q

What do lipoxins control?

A

vasodilation, inhibition of neutrophil chemotaxis, monocyte adhesion

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69
Q

What does thromboxane control?

A

platelet aggregation, thrombosis

70
Q

What does prostacyclin control?

A

Opposes the effects of thromboxane - antagonist to clot formation

71
Q

What does prostaglandin control?

A

smooth muscle contraction

72
Q

Acute-phase inflammation effects of TNF/IL-1?

A

Fever, increase sleep, decrease appetite, increase acute-phase proteins, hemodynamic effects, neutrophilia

73
Q

Long term endothelial effects of TNF/IL-1?

A

Increased leukocyte adherence, Increased PGI synthesis, increased procoagulant activity, decreased anticoagulant activity, increased IL-1, IL-6, IL-8, PDGF

74
Q

Fibroblast effects of TNF/IL-1?

A

Increased proliferation, Increased collagen synthesis (=> FIBROSIS), Increased collagenase, Increased protease, Increased PGE synthesis

75
Q

Leukocyte effects of TNF/IL-1?

A

Increased cytokine secretion (IL-1, IL-6)

76
Q

What is the pathogenesis of fever?

A

IL-1/TNF change the basal body temp to a higher set point

77
Q

What is eNOS?

A

endothelial Nitric Oxide Synthase

78
Q

What is iNOS?

A

Inducible Nitric Oxide Synthase

79
Q

What effect does eNOS have on endothelial cells of BVs?

A

Local effect - relaxes smooth muscle => vasodilation (increased blood flow => more WBCs)

80
Q

What does long-term TNF production cause?

A

Cachexia

81
Q

When is iNOS activated?

A

When need to initiate microbial destruction - iNOS makes Nitric Oxide in macrophages

82
Q

What type of granule is lactoferrin?

A

Specific granule

83
Q

What type of granule is lysozyme?

A

Specific granule

84
Q

What type of granule is Alkaline phosphatase?

A

Specific granule

85
Q

What type of granule is type IV collagenase?

A

Specific granule

86
Q

What type of granule is Leukocyte adhesion molecule?

A

Specific granule

87
Q

What type of granule is plasminogen activation?

A

Specific granule

88
Q

What type of granule is phospolipase A2?

A

Specific granule OR azurophil granule

89
Q

What type of granule is myeloperoxidase?

A

Azurophil granule

90
Q

What type of granule is lysozyme - bactericidal factors?

A

Azurophil granule

91
Q

What type of granule is cationic protein?

A

Azurophil granule

92
Q

What type of granule is acid hydrolase?

A

Azurophil granule

93
Q

What type of granule is elastase?

A

Azurophil granule

94
Q

What type of granule is nonspecific collagenase?

A

Azurophil granule

95
Q

What type of granule is BPI?

A

Azurophil granule

96
Q

What type of granule is defensin?

A

Azurophil granule

97
Q

What type of granule is cathepsin G?

A

Azurophil granule

98
Q

Events in resolution of inflammation?

A
  1. return to normal vascular permeability 2. drainage of edema and proteins into lymphatics or by pinocytosis into macrophages 3. phagocytosis of apoptotic neutrophils and necrotic debris 4. disposal of macrophages
99
Q

What cell type has a central role in resolution of inflammation?

A

Macrophage

100
Q

What do macrophages produce to initiate process of repair?

A

Growth factors

101
Q

What is serous inflammation?

A

Early stage of most inflammations. Clear, non-viscous fluid

102
Q

Examples of serous inflammation?

A

Viral infection of skin vesicles (eg Herpesvirus), joint swelling in RA, eczema, skin burn (blister)

103
Q

What is effusion?

A

Fluid secreted from lining of peritoneal, pleural, or pericardial cavities - trapped in compartment

104
Q

What is fibrinous pericarditis?

A

deposits of fibrin on pericardium

105
Q

What is purulent inflammation?

A

Pus from dead/dying neutrophils

106
Q

What is an abscess?

A

Purulent inflammation encapsulated beneath tissue

107
Q

What is a sinus (in inflammation)?

A

Purulent inflammation can escape to surface

108
Q

What is a fistula?

A

Connection from one place to another

109
Q

What is a granuloma?

A

Lymphocytes, epithelioid cells, and multinucleated giant cells

110
Q

What are epithelioid cells?

A

Macrophages that resemble epithelial cells - line up around area of inflammation and wall it off

111
Q

What is granulomatous inflammation characteristic of?

A

tuberculosis (caseous necrosis)

112
Q

At what point does a monocyte become a macrophage?

A

When it leaves bloodstream/enters tissues

113
Q

When does a macrophage become activated?

A

In tissues

114
Q

What cytokine secreted by T cells activates macrophages?

A

Interferon(IFN)-gamma

115
Q

Non-immune activators of macrophages?

A

endotoxin, fibronectin, chemical mediators

116
Q

What are microglia and where are they located?

A

Macrophages in the CNS

117
Q

What are Kupffer cells and where aer they located?

A

Macrophages in liver

118
Q

Where are alveolar macrophages located?

A

Lungs

119
Q

What are osteoclasts and where are they located?

A

Macrophages in bone

120
Q

What are sinus histocytes and where are they located?

A

Macrophages in spleen and lymph nodes

121
Q

Products made by macrophages that cause tissue injury/destruction?

A

Toxic oxygen metabolites, proteases, neutrophil chemotactics, coagulation factors, AA metabolites, Nitric Oxide

122
Q

Products made by macrophages that cause fibrosis?

A

Growth factors (PDGF, FGF, TGF-beta), Fibrogenic cytokines, angiogenesis factors, “remodeling” collagenesis

123
Q

3 characteristic histologic features of chronic lung inflammation?

A
  1. collection of chronic inflammatory cells 2. destruction of parenchyma 3. replacement by connective tissue (FIBROSIS)
124
Q

3 steps of macrophage amplification?

A
  1. recruitment 2. division 3. immobilization
125
Q

Chronic inflammation effects?

A

SLIDE 67 activated lymphocytes and macrophages influence each other, and release inflammatory mediators that affect other cells

126
Q

Wound healing vs regeneration?

A

Healing = wound healing or fibrosis Regeneration = renewing tissues (epidermis, GI epithelium) or compensatory growth (liver/kidney)

127
Q

What is the cell cycle?

A

G1 -> S -> G2 -> M -> cell division -> permanent cells OR quiescent cells (G0)

128
Q

What are quiescent cells?

A

Stable cells, focus on normal functions instead of generation but are capable of reentering cell cycle. In G0 phase

129
Q

Can permanent cells (neurons, cardiac myocytes) reenter the cell cycle?

A

NO

130
Q

What are the differentiation factors for pluripotent bone marrow stromal cells?

A

Myo D, myogenin, VEGF, FGF2, Sox9, CBFA1, PPAR-gamma

131
Q

What does myo D or myogenin cause pluripotent cell to differentiate into?

A

Myotube

132
Q

What does VEGF or FGF2 cause pluripotent stromal cells to differentiate into?

A

endothelial cells

133
Q

What does Sox9 cause pluripotent stromal cells to differentiate into?

A

Chondroblasts

134
Q

What does CBFA1 cause pluripotent stromal cells to differentiate into?

A

Osteoblasts

135
Q

What does PPAR-gamma cause pluripotent stromal cells to differentiate into?

A

Fat cell

136
Q

What is autocrine signaling?

A

Target sites on same cell

137
Q

What is paracrine signaling?

A

Target sites on adjacent cells

138
Q

What is endocrine signaling?

A

Target sites on distant cells - signals enter bloodstream

139
Q

What is the general signaling pathway used in tissue regeneration?

A

Ligand binds to target cells, causes cascade of enzymes ->->-> turn on transcription/translation processes for repair

140
Q

What does binding of growth factor to tyrosine kinase receptors cause?

A

Receptor dimerization and autophosphorylation of tyrosine residues

141
Q

How does liver regenerate after partial hepatectomy?

A

Enlargement of remaining lobe without regrowth of removed lobe

142
Q

Cytokines that prime quiescent hepatocytes?

A

TNF, IL-6

143
Q

Growth factors that act on primed hepatocytes to make them progress through cell cycle?

A

HGF, TGF-alpha

144
Q

Adjuvants for liver regeneration?

A

Norephinephrine, insulin, thyroid hormone, growth hormone

145
Q

Major components of basement membrane?

A

Type IV collagen, laminin, proteoglycans

146
Q

Components of Interstitial Matrix?

A

Fibrillar collagens, elastin, proteoglycan and hyaluronan

147
Q

What vitamin is needed for HO-ization in collagen synthesis?

A

Vitamin C

148
Q

What reaction needs to happen for collagen to twist properly while being synthesized?

A

Hydroxylation

149
Q

What are focal adhesion complexes?

A

protein aggregates that include vinculin, paxillin, and talin

150
Q

What do focal adhesion complexes bind to?

A

ECM components (fibronectin and laminin)

151
Q

Process of angiogenesis from bone marrow?

A

endothelial precursor cells (EPCs) mobilized from bone marrow and migrate to site of injury/tumor growth. Once there, EPCs differentiate and form mature network by linking w/ existing vessels

152
Q

Process of angiogenesis from pre-existing vessels?

A

endothelial cells become motile and proliferate to form capillary sprouts.

153
Q

What stimulates matrix metalloproteinases?

A

PDGF, EGF, TNF/IL-1

154
Q

What inhibits metalloproteinases?

A

TGF-beta, steroids

155
Q

How are metalloproteinases activated?

A

Plasmin

156
Q

What do metalloproteinases do?

A

Break down collagen/debris

157
Q

What do TIMPs do?

A

block metalloproteinases with specific tissue inhibitors

158
Q

What mineral are MMPs dependent on?

A

Zinc

159
Q

What are the phases of wound healing?

A

Inflammation, granulation tissue, wound contraction, remodeling

160
Q

What are the three intentions of wound healing?

A

Primary, Secondary, Tertiary

161
Q

When is wound healing considered primary intention?

A

wound edges directly next to each other (eg surgical incisions)

162
Q

When is wound healing considered secondary?

A

Wider, not clean edges

163
Q

Does scarring occur with primary intention healing?

A

Minimal

164
Q

Does scarring occur with secondary intention healing?

A

Yes - granulation

165
Q

What is delayed primary closure?

A

tertiary intention - wound is purposely left open

166
Q

What is a keloid?

A

excess collagen deposition in the skin forming a raised scar

167
Q

What causes “cauliflower ear”?

A

Chronic tissue damage to ears

168
Q

What does persistent stimulus (chronic inflammation) cause?

A

Activation of macrophages/lymphocytes => Growth factors, cytokines, decreased metalloproteinase activity => increased collagen synthesis/decreased collagen degradation => FIBROSIS diagram slide 98

169
Q

What is tissue regeneration?

A

Restitution of normal structure

170
Q

What is tissue healing?

A

Scar formation, organization of exudate

171
Q

What is tissue fibrosis?

A

Tissue scar

Pathology 1 (6 decks)

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