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Pathology Exam 2 > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

Characteristics of acute inflammation

A

redness, swelling, heat, pain, loss of function

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2
Q

First step of acute inflammation

A

vasoconstriction followed immediately by vasodilation - increased vascular flow and caliber

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3
Q

Vasodilation following trauma results in

A

warmth and redness and edema

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4
Q

Vasodilation causes __________ in hydrostatic pressure and

A

increase; protein poor fluid enters tissue

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5
Q

Vascular permeability

A

endothelial cells separate (due to shrinkage and high hydrostatic pressure) allowing leakage into ECS

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6
Q

Initially the fluid leaked into the ECS is _________ in protein content, then becomes ______

A

low/poor, high/rich

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7
Q

High protein fluid in the ECS causes

A

increased osmotic pressure causing more fluid to accumulate

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8
Q

Pain receptors are triggered by

A

released chemical mediators

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9
Q

Immediate transient response

A

Mild tissue injury; within5-10min; lasts 15-30min; mediated by histamine; involves small-medium venules

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10
Q

Immediate sustained response

A

severe injury; endothelial necrosis; lasts for days; involves venues and capillaries

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11
Q

Delayed prolonged response

A

delayed by hours-days; response to burns, X-ray damage, UV damage, bacterial toxins, Type IV hypersensitivity

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12
Q

Primary cellular mediator of acute inflammation

A

segmented neutrophils

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13
Q

neutrophils engulf

A

bacteria, cellular debris, and immune complexes

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14
Q

neutrophils breakdown engulfed materials by

A

phagosomes + lysosome (hydrolytic and proteolytic enzymes)

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15
Q

Prolonged inflammation may result from

A

segmented neutrophil’s releasing lysosomal enzymes and toxic free radicals (toxic)

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16
Q

Margination

A

attracting segmented neutrophils to the endothelial lining of vessels where they congregate by PAVEMENTING

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17
Q

Adhesion

A

neutrophils adhere to endothelial cells via adhesion molecules

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18
Q

Emigration - how does a neutrophil traverse the blood vessel

A

insert pseudopods between endothelial cell tight junctions, squeeze through and exit via developing gaps in the basement membrane

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19
Q

How long after injury do segmented neutrophils first appear in extravascular tissue?

A

6-24hrs

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20
Q

Monocytes emigrate to the injury site once they have

A

become activated

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21
Q

How long after injury do monocytes first appear in extravascular tissue?

A

24-48hrs

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22
Q

Chemotaxis definition

A

unidirectional movement of cells along a chemical gradient toward an attractant/chemotactic factor

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23
Q

Chemotactic factors include

A

bacterial products, components of the complement system (C5a), and leukotriene B4

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24
Q

What percentage of the leukocyte receptors must be bound by chemotactic factors in order for activation and migration to occur

A

20%

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25
Q

The motion (chemotaxis) is facilitated by

A

pseudopod formation + pulling with actin-myosin filaments

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26
Q

What acts as a mediator in the interaction of contractile elements and cell movement

A

intracellular Ca2+

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27
Q

Chemokinesis definition

A

accelerated random locomotion of cells - not related to migration along a specific gradient

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28
Q

How does a neutrophil recognize cell debris or bacteria in the ECS?

A

opsonization by serum factors

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29
Q

2 key opsonins

A

IgG (subtypes 1 and 3) and complement factor C3b

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30
Q

In order to phagocytose debris, neutrophil and macrophage receptors bind/are specific for

A

Fc fragment of IgG or DIRECTLY bind to C3b following its activation

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31
Q

How does a neutrophil engulf bacteria/debris?

A

sends out cytoplasmic extensions/pseudopods which envelop bacteria and trap it in a vesicle

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32
Q

Phagosome

A

engulfed debris contained in a vesicle within the cell

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33
Q

Degradation of material within the phagosome occurs by

A

fusion of a lysosome and phagosome and degranulation releasing lysosomal digestive enzymes and free radicals

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34
Q

Phagolysosome

A

lysosome + phagosome fusion

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35
Q

Leakage of free radicals or phagolysosomal digestive enzymes contribute to

A

further injury (cellular or regional)

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36
Q

2 Oxygen dependent bactericidal mechanisms

A

break down of material within a lysosome that requires OXYGEN: Hydrogen peroxide-Myeloperoxidase Halide System, Myeloperoxidase Independent System

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37
Q

Hydrogen peroxide-Myeloperoxidase Halide System in PMN granules

A

(requires O2) uses the enzyme myeloperoxidase to destroy bacteria

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38
Q

Myeloperoxidase catalyzes

A

H2O2 + halide (Cl-) = HOCl- which acts as an antimicrobial and oxidant

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39
Q

Myeloperoxidase Independent System

A

use free radicals formed by alternative enzymes to kill bacteria

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40
Q

Myeloperoxidase Independent System is predominantly used by

A

macrophages and myeloperoxidase deficient segmented neutrophils

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41
Q

Oxygen Independent Bactericidal Mechanisms include:

A

Bactericidal permeability increasing protein (BPI), Lysozyme, Lactoferrin, Major Basic Protein

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42
Q

Major Basic Protein is produced by

A

Eosinophils and toxic to parasites

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43
Q

What may efflux from a neutrophil and cause further tissue damage?

A

lysosomal enzymes, oxygen-derived metabolites, and products of arachidonic acid metabolism

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44
Q

Release of effluxed material from neutrophils may be due to:

A

regurgitation during phagocytosis, reverse endocytosis, cytotoxic release, heterolysis

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45
Q

Defective leukocytes result in

A

impaired acute inflammatory response

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46
Q

Causes of defective leukocytes include

A

decreased numbers of circulating leukocytes, defects in adherence mechanisms, defects in migration/chemotaxis

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47
Q

Leukocyte defects in migration/chemotaxis may be due to:

A

intrinsic leukocyte abnormalities, defective production of chemotactic factors, inhibition of chemotactic factors, suppressed leukocyte locomotion, defective phagocytosis, defective microbiocidal activity, mixed defects in leukocyte function

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48
Q

Leukocyte defects in microbiocidal activity include

A

decreased hydrogen peroxide production, myeloperoxidase deficiency, G-6-PD deficiency

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49
Q

Vasoactive amines role

A

released in response to injury and cause immediate vasodilation and increased blood vessel permeability in acute inflammation, they also mediate IgE immune response

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50
Q

Vasoactive amines include:

A

histamine and serotonin (5-hydroxytryptamine)

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51
Q

Vasoactive amines are produced by

A

mast cells, basophils, and platelets

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52
Q

Vasoactive amine stimuli:

A

physical factors (heat, trauma), immune reactions (IgE factors), C3a, C5a (compliment anaphylotoxins), histamine releasing factors (neutrophils, monocytes, platelets), IL-1

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53
Q

complement system’s role

A

increase vascular permeability, mediate chemotaxis, facilitate opsonization and lysis of microbial organisms

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54
Q

2 complement cascades

A

Classic (fast) and alternative (slow)

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55
Q

Complement components of acute inflammation

A

C3a, C5a, C3b, iC3b, C5b-9

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56
Q

C3a and C5a role

A

increase vascular permeability, anaphylotoxins (stimulate mast cells and platelets to release histamine), chemotactic to neutrophils, basophils, eosinophils, and monocytes, mediate leukocyte adhesion to bv’s, activate lipoxygenase/arachidonic acid pathways in PMNs and macrophages

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57
Q

C3a and C5a effects on mast cells and platelets

A

stimulate the release histamine (anaphylotoxins)

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58
Q

C3a and C5a act as chemotactic factors to

A

neutrophils, basophils, eosinophils, and monocytes

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59
Q

C3a and C5a activate which pathways in neutrophils and macrophages

A

lipoxygenase/arachidonic acid pathways

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60
Q

Which compounds of the complement system mediate leukocyte adhesion to blood vessel endothelium?

A

C3a and C5a

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61
Q

C3b and iC3b role

A

act as opsonins for neutrophils, macrophages, and eosinophils

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62
Q

C5b-9 role

A

Membrane Attack Complex: direct lytic action on bacteria, injures parenchymal cells stimulating arachidonic acid metabolism and producing ROS metabolites

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63
Q

What initiates the classical complement pathway?

A

an immune complex binds C1 and activates it

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64
Q

What initiates the alternative complement pathway?

A

microbial surface polysaccharides interact with C3

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65
Q

the kinin system produces

A

bradykinin

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66
Q

bradykinin’s role

A

increases vascular permeability, causes smooth muscle contraction in the INITIAL vasoconstriction, subsequent vasodilation and pain

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67
Q

Is bradykinin a chemotactic factor?

A

NO

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68
Q

Are C3a and C5a chemotactic factors?

A

YES

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69
Q

The coagulation cascade’s main role in acute inflammation is to

A

activate the Hageman Factor

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70
Q

Downstream to the Hageman factor, fibrinogen is converted to fibrin, releasing

A

fibrinopeptides

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71
Q

Fibrinopeptides role

A

increase blood vessel permeability and act as chemotactic factors for leukocytes

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72
Q

Downstream to the Hageman factor, plasminogen is converted to _______ by ____________

A

PLASMIN by plasminogen activator or Kallikrein and

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73
Q

Kallikrein

A

converts plasminogen to plasmin

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74
Q

Plasmin’s role

A

Fibrinolysis (fibrin to fibrinopeptides), activation of Hageman factor (subsequently produces bradykinin), cleaves C3 to C3a

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75
Q

Arachidonic acid is derived from

A

dietary sources or produced by the metabolism of linoleic acid into arachidonic acid

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76
Q

Phospholipase A2 converts

A

linoleic acid to arachidonic acid

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77
Q

Steroids effect

A

steroids inhibit phospholipase and therefore prevent arachidonic acid synthesis

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78
Q

Arachidonic acid metabolites are formed by

A

esterification of phospholipids via the 5-lipoxygenase or cyclooxygenase pathways

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79
Q

Arachidonic acid metabolites produced by the COX pathway

A

Thromboxane (TXA2), Prostacyclin (PGI2), Prostaglandins (PGD2, PGE2, and PGF2)

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80
Q

Thromboxane (TXA2) role

A

promote platelet aggregation and cause vasoconstriction

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81
Q

Prostacyclin (PGI2) role

A

inhibit platelet aggregation and cause vasodilation

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82
Q

Prostaglandins (PGD2, PGE2, and PGF2) role

A

cause vasodilation and potentiate edema

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83
Q

Aspirin and Indomethacin have what effect on arachidonic metabolism

A

they are COX1 and COX2 inhibitors and they inhibit PROSTAGLANDIN production (preventing TXA, PGI, and Prostaglandins)

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84
Q

Lipoxygenase pathway

A

converts arachidonic acid into leukotrienes with the enzyme: lipoxygenase

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85
Q

Leukotriene B4 role

A

Chemotactic, stimulates aggregation of leukocytes

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86
Q

Leukotrienes C4, D4, and E4 role

A

Vasoconstriction, bronchospasms, increased vascular permeability

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87
Q

Segmented neutrophils contain _________ and ___________ granules

A

primary and secondary

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88
Q

Degranulation follows

A

phagocytosis and involves fusion of lysosome and phagosome

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89
Q

Neutrophil granule contents cause

A

bacterial lysis and breakdown of debris when released into phagolysosomes

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90
Q

Primary granules of neutrophils contain:

A

Myeloperoxidase, lysozyme, bactericidal factors, cationic proteins, acid hydrolyses, elastases

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91
Q

Secondary granules of neutrophils contain:

A

lactoferrin, lysozyme, alkaline-phosphatase, leukocyte adhesion molecules and collagenase

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92
Q

If lysosome granules leak into the ECS

A

further increase in vascular permeability, increased chemotaxis, and additional tissue damage

93
Q

ROS may cause

A

damage to endothelial cells, inactivate anti-proteases, injure tumor cells, RBCs, and parenchymal cells

94
Q

ROS may be inactivated by

A

anti-oxidants

95
Q

Platelet activating factor (PAF) is released by

A

IgE sensitive basophils

96
Q

Platelet activating factor (PAF) role

A

cause release of histamine and serotonin, vasoconstriction, bronchoconstriction (vasodilation/increased perm. at low concentrations), increased adhesion, leukocyte chemotaxis, degranulation, stimulation of oxidative burst

97
Q

Acute inflammation chemical mediators of pain

A

Prostaglandins and Bradykinin

98
Q

IL-1 is produced by what cell type

A

ALL cells

99
Q

IL-1 is produced in response to

A

endotoxins, trauma, immune reaction, and inflammation

100
Q

Tumor Necrosis Factor is released by what cell type

A

Stimulated macrophages

101
Q

Tumor Necrosis Factor role

A

induction and synthesis of adhesion molecules (PGI2 and PAF) and stimulation of coagulation cascade

102
Q

Cytokines involved in acute inflammation

A

TNF, IL-1, IL-6, Chemokines

103
Q

IL-1 and TNF have what acute phase reaction effects

A

fever, fatigue, decreased appetite, increased acute phase proteins, shock, neutrophilia

104
Q

IL-1 and TNF have what effects on endothelial cells

A

increased: leukocyte adhesion, PGI production, coagulation cascade, production of IL-1, IL-8, IL-6, PGDF

105
Q

IL-1 and TNF have what effects on fibroblasts

A

increased: proliferation, collagen synthesis, collagenase, protease, PGE synthesis

106
Q

Growth Factors that play a role in acute inflammation include:

A

EGF, TGF-alpha, Hepatocyte GF, platelet derived GF, vascular endothelial GF, FGF, TGF-beta

107
Q

TGF-beta’s role

A

growth inhibition of epithelial cells, fibrinogenic agent, anti-inflammatory, enhance immune function

108
Q

Vasodilators of acute inflammation:

A

prostaglandins, NO, and histamine

109
Q

Mediators of increased permeability in acute inflammation:

A

Histamine, serotonin, C3a and C5a, Leukotrienes C4, D4, and E4, PAF, Substance P (neuropeptide)

110
Q

Mediators of Chemotaxis, Leukocyte recruitment and activation in acute inflammation include:

A

TNF, IL-1, chemokines, C3a and C5a, Leukotriene B4, bacterial products

111
Q

Mediators of fever in acute inflammation:

A

IL-1, TNF, prostaglandins

112
Q

Mediators of pain in acute inflammation:

A

prostaglandins and bradykinin

113
Q

Mediators of tissue damage in acute inflammation:

A

lysosomal enzymes of leukocytes, ROS, NO

114
Q

Lymphangitis

A

inflammation of the lymphatic vessel when bacteria gain access

115
Q

Lymphadenitis

A

inflammation of lymph nodes if bacteria gains access

116
Q

Bacteremia/Sepsis

A

bacterial infection gains access to blood

117
Q

Mononuclear phagocyte system includes which cells

A

monocytes and macrophages

118
Q

Monocytes

A

defense mechanism against bacteria in the blood

119
Q

Macrophages

A

defense mechanism against bacteria in the tissues

120
Q

Monocytes and macrophages produce what chemical mediators of acute inflammation

A

neutrophil proteases, chemotactic factors, arachidonic acid metabolites, ROS, complement, coagulation factors, growth factors, cytokines, PAF, and interferon

121
Q

Chronic inflammation occurs as

A

sequela to acute inflammation, repeated episodes of acute inflammation, low grade inflammation from a long standing injury (persistent intracellular infection or toxins, autoimmune reactions)

122
Q

Major cellular components of chronic inflammation

A

macrophages, lymphocytes, plasma cells, eosinophils, fibroblasts

123
Q

Tissue changes involved in chronic inflammation

A

tissue destruction, vascular proliferation, fibrosis

124
Q

In chronic inflammation, monocytes play what role

A

they arrive at the injury site by chemotaxis, become activated into macrophages, divide and remain localized at site

125
Q

In chronic inflammation, progressive tissue damage occurs via

A

continued cell stimulation and release of chemical inflammatory mediators

126
Q

Plasma cells contribute to chronic inflammation by releasing

A

antibodies (derived from B cells)

127
Q

Lymphocytes contribute to chronic inflammation by releasing

A

lymphokines, which serve as chemotactic factors for more monocytes/macrophages

128
Q

Eosinophils contribute to chronic inflammation by releasing

A

Major basic protein (parasitic infections) and mediate IgE immune reactions

129
Q

Neutrophils contribute to chronic inflammation by

A

persisting in low numbers at injury site

130
Q

Granuloma

A

specialized form of chronic inflammation characterized by an area containing lymphocytes, plasma cell, macrophages, and multinucleate giant cells

131
Q

Cell types involved in granuloma formation

A

lymphocytes, plasma cell, macrophages, and multinucleate giant cells

132
Q

Caseating Granuloma

A

central area of caseating necrosis with a peripheral rim of lymphocytes, macrophages, and Langahns giant cells

133
Q

Disease processes generally associated with caseating granulomas

A

Tuberculosis, fungal infections

134
Q

Cell types involved in caseating granuloma formation

A

lymphocytes, macrophages, and Langahns giant cells

135
Q

Non-caseating Granuloma

A

Granuloma lacking the caseating necrotic center

136
Q

Disease processes generally associated with non-caseating granulomas

A

Sarcoidosis, Fungi, Brucellosis, Leprosy, foreign body reaction, cat scratch disease, syphilis, and parasites

137
Q

Serous inflammation produces

A

thin, cloudy, watery fluid produced

138
Q

Serous inflammation is generally found

A

in body cavities (pleural spaces, peritoneum)

139
Q

Fibrinous Inflammation produces

A

response composed of fibrin and plasma proteins

140
Q

Fibrinous Inflammation is generally found

A

in body spaces and potential spaces (pericardial, pleural, peritoneal)

141
Q

Suppurative/Purulent Inflammation is generally found

A

surfaces of epithelial or mesothelial structures and underlying tissue

142
Q

Suppurative/Purulent Inflammation predominant cell type

A

segmented neutrophils (acute process)

143
Q

Suppurative/Purulent Inflammation produces

A

pus (pyogenic), acute inflammatory exudate

144
Q

Abscess

A

cavity containing pus surrounded by tissue

145
Q

Ulceration

A

sloughing or shedding of the epithelial cells and underlying tissue that are infiltrated by inflammatory cells

146
Q

Acute ulcers contain primarily what cell type

A

segmented neutrophils

147
Q

Chronic ulcers contain primarily what cell type

A

macrophages, lymphocytes, plasma cells, fibroblasts

148
Q

During inflammation, fever is generated by

A

IL-1 and TNF effects on thermoregulatory center of the brain

149
Q

During inflammation, rigors is characterized by

A

shaking chills during fever, especially associated with bacteremia, viremia, parasitemia

150
Q

Acute phase reactions include:

A

fever, rigors, appetite suppression, sleep changes, protein degradation, hypotension, hematologic effects, and release of acute phase proteins

151
Q

IL-1 and TNF cause what hematological change

A

Left shift: an increase in the percentage of immature segmented neutrophils “Neutrophilic Leukocytosis” due to a stimulation of neutrophil release from bone marrow

152
Q

Leukocytosis

A

WBC count over 10,000

153
Q

Acute Phase proteins include

A

C reactive protein, Serum amyloid A, Complement factors, Coagulation factors

154
Q

C reactive protein role

A

bind to phosphocholine expressed on the surface of dead or dying cells (and some types of bacteria) in order to activate the complement system

155
Q

Serum amyloid A role

A

recruitment of immune cells to inflammatory sites, and the induction of enzymes that degrade extracellular matrix

156
Q

Irreversibly damaged cells must be replaced by

A

new cells and supporting tissue matrix

157
Q

Labile Cells

A

capable of mitotic division throughout life

158
Q

Labile cells include:

A

epithelial, splenic, lymphoid, and hematopoietic cells

159
Q

In order for epithelial cells to replicate there must be

A

an intact basement membrane

160
Q

Stabile Cells

A

Normally only replicate under specific stimuli

161
Q

Stabile cells include:

A

parenchymal, mesenchymal, and vascular endothelial cells

162
Q

In order for stabile cells to replicate there must be

A

intact basement membrane

163
Q

Permanent cells

A

limited (if any) ability to replicate

164
Q

damaged permanent cells

A

are replaced by scar tissue

165
Q

Permanent cells include:

A

neurons, skeletal muscle, and myocardium

166
Q

Granulation tissue

A

formed by the regenerative process through which injured or necrotic tissue is gradually replaced and repaired (angiogenesis, macrophage localization, edema, collagen deposition)

167
Q

Angiogenesis following irreversible tissue damage steps:

A

enzyme degradation of endothelial cell basement membrane of parent vessel, migration of endothelial cells to inflamed tissue, endothelial proliferation, endothelial maturation

168
Q

Edema occurs in granulation tissue due to

A

high permeability of parent vessel and new developing vessels

169
Q

Fibroblasts play what role in granulation formation

A

collagen formation to provide structure to repaired tissues

170
Q

Collagen’s role

A

increase strength and stability of the tissue undergoing repair

171
Q

Granulation tissue has a high number of __________ and a low number of ___________

A

high number of macrophages; low number of segmented neutrophils, eosinophils, and lymphocytes

172
Q

Primary Union

A

clean with straight margins which can easily be approximated (larger wounds require sutures)

173
Q

The first 24 hours a primary union wound is infiltrated with

A

neutrophils

174
Q

Within 24-48 hours a primary union wound is infiltrated with

A

epithelial cells from adjacent tissue (re-epithelialization) and macrophages

175
Q

By 72 hours, segmented neutrophils have been replaced by

A

macrophages

176
Q

By 72 hours, primary union wounds are

A

almost entirely composed of granulation tissue with marked neovascularization

177
Q

By 2 weeks, primary union wounds are

A

completely replaced by collagen

178
Q

Secondary Union

A

large gaping wounds in which the margins cannot be approximated, requiring significant re-epithelialization and stromal repair

179
Q

Secondary Union wounds include

A

trauma, burns, infarctions, ulcerations, and large surface wounds (lacerations)

180
Q

Granulation tissue in a secondary wound appears as

A

pink, moist granular surface within the wound

181
Q

Cicatrization

A

scar formation by collagen in secondary union wounds

182
Q

Fibrosis

A

collagen deposition (scaring) involving non-epithelial/parenchymal tissue

183
Q

Fibrous Adhesions

A

collagen deposition (scaring) involving mesothelial surfaces of viscera

184
Q

Collagen is constantly remodeled, it may take ______ for final remodeling process

A

9-12 mo

185
Q

Hypertrophic Scars

A

excessive production and deposition of collagen in a developing scar, resulting in a keloid

186
Q

Keloid

A

large nodular mass within a developing scar

187
Q

Competence Factors

A

prepare cells for mitotic division

188
Q

Progression Factors

A

stimulate cell division

189
Q

EGF is a

A

progression factor

190
Q

Platelet derived GF (PDGF) is a

A

competence factor

191
Q

PDGF is released with activation of

A

platelets, macrophages, endothelial cells, smooth muscle cells, and tumor cells

192
Q

PDGF’s role in healing

A

stimulate migration and proliferation of fibroblasts and smooth muscle

193
Q

FGF’s role in healing

A

stimulate angiogenesis

194
Q

TGF-alpha’s role in healing

A

bind EGF receptors stimulating EGF release

195
Q

TGF-beta’s role in healing

A

inhibits growth of parenchymal cells; inhibits macrophages; chemotactic for fibroblasts and mediates collagen production

196
Q

IL-1’s role in healing

A

chemotactic for fibroblasts; increases collagen and collagenase synthesis

197
Q

TNF’s role in healing

A

chemotactic for fibroblasts; increases collagen and collagenase synthesis

198
Q

Contact inhibition

A

cells grow until coming into contact with each other

199
Q

Surface receptors

A

recognize extracellular matrix proteins

200
Q

Collagenization

A

the FINAL mechanism of healing

201
Q

Tropocollagen

A

main unit of all types of collagen, 3 attached alpha chains cross-linked for tensile strength

202
Q

Skin contains predominantly Type ___ collagen

A

Type I

203
Q

Granulation tissue initially contains predominantly Type ___ collagen

A

Type III

204
Q

Following remodeling, granulation tissue contains predominantly Type ___ collagen

A

Type I

205
Q

Non-collagen components of the ECM

A

elastin, laminin, proteoglycans, fibronectin

206
Q

Primary union wounds have ____% of their original strength if sutures are used

A

70-80

207
Q

Primary union wounds have ____% of their original strength when sutures are removed

A

10

208
Q

How long would it take to regain 70-80% of strength in a primary union wound

A

3 months

209
Q

How long would it take to regain 100% of strength in a primary union wound

A

6-12 months

210
Q

Wound Dehiscence

A

Delayed wound healing: opening of a partially healed wound (large wounds with sutures prematurely removed, infection, or tensile pressure)

211
Q

For PMN adhesion, neutrophil _________ receptors bind to endothelial ______ receptors

A

Sialyl-Lewis X (PMN); Selectins (endothelial)

212
Q

For PMN transmigration, neutrophil _________ receptors bind to endothelial ______ receptors

A

Integrins (PMN); CAM (Endothelial)

213
Q

What cells may be present at both acute and chronic inflammatory sites?

A

macrophages

214
Q

Cell type indicative of early acute inflammation

A

segmented neutrophil

215
Q

Chemical Mediator involved in DIRECT bacterial lysis

A

C5b-9

216
Q

Segmented neutrophils leave blood vessels by

A

emigration through tight junctions

217
Q

Healing by primary union involves

A

approximation of wound margins (with or without sutures)

218
Q

Local Causes of delayed wound healing

A

Infection, inadequate blood supply, forge in body, type of tissue

219
Q

Systemic causes of delayed wound healing

A

Old age, poor nutrition, bleeding disorder, diabetes, Hypertension, Atherosclerosis, Collagen-Vascular Disease, NSAID or steroid use

220
Q

Eosinophils are increased under what conditions

A

Parasitic infections, allergic reactions, hypersensitivity reactions, and some chronic inflammation

221
Q

Erythema and warmth is indicative of

A

increased vascular flow (vasodilation)

222
Q

Example: Red streaks in the skin from the site of infection on the arm extending to the axilla

A

lymphangitis

223
Q

Swelling in acute inflammation is due to

A

increased vascular permeability, increased hydrostatic pressure, followed by increased TISSUE oncotic pressure

224
Q

Acute wound with thick yellow pus

A

acute inflammatory exudate

225
Q

Acute wound with thick yellow pus, but surround by tissue and enclosed within a cavity

A

abscess

226
Q

Main function of the neutrophil in a pyogenic acute infection

A

to kill G(+) and G(-) bacteria via phagocytosis

227
Q

Anaphylatoxin Chemical Mediators

A

C3a and C5a

228
Q

Opsins for phagocytosis

A

IgG (Fc fragment), C3b

229
Q

You get slapped in the face and your face turns red, feels warm, and throbs, but this goes away in 30 min, this is an example of

A

Immediate transient response

Pathology Exam 2 (2 decks)

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