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General Veterinary Pathology > Inflammation & Healing > Flashcards

Inflammation & Healing Flashcards

1
Q

Inflammation

A
  • vascular and cellular responses of living tissue to injury
  • involves; blood, vessel, cell
  • purpose is to eliminate offending irritant/stimulant
  • reaction of living tissue to injury which comprises series of changes in the TERMINAL VASCULAR BED, and BLOOD, and TISSUE.
  • remove and repair
  • series of complex reactions by VASCULAR connective tissue elements in order to address injury
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2
Q

Causes of inflammation

A

° pathogenic microorganism
° chemical injuries
° mechanical and thermal injuries
° immune reactions

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3
Q

accumulation of fluid in the injured area (functions)

A
  • to dilute
  • to localize
  • to destroy
  • to remove
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4
Q

advantages of inflammation

A
  • protect the surrounding tissue by localizing and isolating the injured tissues
  • to neutralise and inactivate toxins
  • destroys and inhibit the growth of pathogenic microorganisms
  • prepares injured area for healing and repair.
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5
Q

disadvantages of inflammation

A
  • excessive scar formation
  • varying degrees of disabilities as a result of pain swelling
  • tissue compression, vessel rupture, hemorrhage
  • formation of cavities, sinus, fistula
  • aggregates inflammation by destruction of surrounding intact tissue
  • development of inflammatory diseases (hypersensitivity)
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6
Q

Cardinal Signs

A

° rubor (redness)
° tumor (swelling)
° calor (heat)
° dolor (pain)
° functio laesa

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7
Q

redness

A

rubor

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8
Q

swelling

A

tumor

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9
Q

heat

A

calor

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10
Q

pain

A

dolor

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11
Q

caused by vasodilation

A

rubor (redness)

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12
Q

fluid exudate, increase vascular permeability

A

tumor (swelling)

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13
Q

rapid inflow of warm blood thru dilated vessels

A

calor (heat)

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14
Q

vasoactive chemicals will be released

A

dolor (pain)

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15
Q

loss of function

A

functio laesa

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16
Q

vasoactive chemicals

A

histamine, serotonin

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17
Q

10 generalities of inflammatory response

A
  1. process
  2. living tissue
  3. series of events; overlapping into a continuum
  4. a response; requires initiation by some kind of stimulus
  5. response can be more harmful than the stimulus
  6. survival oriented
  7. fairly stereotype of any initiating stimuli
  8. always component of blood
  9. carefully coordinated defense mechanism essential to life
  10. complicated but understandable
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18
Q

escape of fluid and blood cells from the vascular system into the interstitial tissue

A

exudation

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19
Q
  • fluid with high protein concentration
  • high specific gravity increase 1.020
A

exudate

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20
Q
  • fluid with low protein content
  • specific gravity less than 1.012
  • ultra filtrate of blood plasma
  • result of hydrostatic imbalance across vascular endothelium
A

transudate

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21
Q

excess of fluid in the interstitial tissue/serous cavities

A

edema

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22
Q

purulent inflammatory exudate rich in leukocytes and parenchymal debris.

A

pus

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23
Q

cells involve in inflammation

A

° granulocytes
° agranulocytes
° plasma cells

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24
Q

example of granulocytes

A

✓ neutrophils
✓ eosinophils
✓ basophils

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25
Q
  • first to arrive in the site of inflammation
  • a phagocytic cells by releasing lytic lysosomal enzymes and some chemotactic factors
A

neutrophils

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26
Q

examples of lysosomal enzymes released by neutrophils

A

✓ myeloperoxidase
✓ acid hydrolysis
✓ lysosomes and muramidase
✓ cationic proteins

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27
Q
  • prominent in allergic reactions, parasitic infections
  • contains; lysosomal granules/enzymes, histamines
  • also a phagocytic cells
A

eosinophils

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28
Q

-least numerous
- shared common properties of mast cells
- secrete and release vasoactive amines/chemicals
- non phagocytic cells

A

basophils

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29
Q

not found in circulation but in tissues

A

mast cells

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30
Q

example of agranulocytes

A

monocyte and lymphocytes

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31
Q
  • peripheral blood phagocytes
  • becomes part of the tissue, then become macrophage
  • involved immune response as an antigen preventing cell
  • phagocytic cells
A

monocytes

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32
Q
  • found in tissues of all types of inflammation esp, after acute increase of neutrophils
  • derived from bone marrow stem cells thru hematopoiesis
  • both involved in cell mediated and humoral cell responses
A

lymphocytes

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33
Q

primary lymphoid organs

A

bone marrow

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34
Q

3 types of lymphocytes

A
  1. T-lymphocyte
  2. B-lymphocyte
  3. natural killer cells
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35
Q

70%. involved cell mediated lymphocytes

A

T-lymphocytes

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36
Q

derived from bursa

A

B-lymphocytes

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37
Q
  • formed by a process of maturation and deviation of B-lymphocytes into 2 distinct cells
A

plasma cells

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38
Q

2 distinct cells

A

memory cells and plasma cells

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39
Q

surface contains immunoglobulins + antibodies

A

plasma cells

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40
Q

macrophages (important component of immune system)

A

a. histiocytes
b. skin
c. liver
d. lungs
e. kidney
f. brain

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41
Q

connective tissue

A

histiocytes

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42
Q

skin

A

langerhan cells

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43
Q

liver

A

von kupffer cell

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44
Q

lungs

A

alveolar macrophages

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45
Q

brain

A

microglial cells

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46
Q

responsible for hemodynamic + vascular changes

A

vasoactive amines

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47
Q

histamines

A
  • stored in granules of mast cells
  • found in basophils and platelets
  • released by degranulation in response to various stimuli
  • once released, can cause vasoconstriction and vasodilation
  • cause increase vascular permeability of small veins and venules
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48
Q

mediators of inflammation

A

✓ protein
✓ peptides
✓ glycoproteins
✓ cytokines
✓ arachidonic acid metabolites
✓ nitric acid
✓ oxygen free radicals
✓ vasoactive amines

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49
Q

once activated, it will lead to formation BRADYKININ

A

kinin system

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50
Q

once plasma comes into contact with;

A
  • collagen
  • endotoxins
  • basement membrane proteins
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51
Q

proteases secreted serine proteins

A

kallikrein

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52
Q

most important mediators of inflammation process

A

complement system

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53
Q

serotonin

A
  • stored in GIT, CNS, dense granules of platelets
  • regulates almost all immune cells in response to inflammation following the activation of platelets
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54
Q

leukocytes substances (activation of inflammation)

A
  • hydrolytic enzymes
  • proteases
  • cationic proteins
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55
Q

lipid found in mast cells

A

Slow Reactive Substance of Anaphylaxis (SRSA)

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56
Q

biologically active substances produced by T-cells during immune reaction.

A

lymphokines

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57
Q

begins within 4-6 hours and can remain constant in appearance depending on the initiators for survival days

A

acute

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58
Q

may cover considerable time span between acute reaction and those in which evidence of chronicity apparent.

A

subacute

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59
Q
  • prolonged inflammation
  • caused by persistent agent
A

chronic

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60
Q

key features of chronicity

A
  1. caused by persistent inflammatory stimuli in which the host failed to completely rid in the tissue of invader
  2. inflammatory response is usually accompanied by an immune system due to persistence of invader
  3. highlighted by evidence of host tissue contribution in terms of reparative responses
  4. characterized histologically by both mononuclear cells infiltrates and by CT cells such as fibroblasts
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61
Q

Cellular Phase of Inflammation

A

° margination and pigmenting
° diapedesis
° chemotaxis
° phagocytosis

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62
Q

major event of inflammation

A

after injury

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63
Q

2 opposing forces in Inflammation

A

° hydrostatic pressure
° plasma colloid osmotic pressure

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64
Q

due to vasodilation

A

hydrostatic pressure

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65
Q

due to leakage of high protein fluid to interstitial resulting in marked net outflow and edema

A

plasma colloid osmotic pressure

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66
Q

3 patterns of increased in Inflammation

A
  1. immediate transient response
  2. immediate sustained reaction
  3. delayed prolonged leakage
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67
Q
  • elicited by chemical mediators such as histamine in mild injury
  • occurs as a result of construction in endothelium
A

immediate transient response

68
Q

caused by severe injury (endothelial necrosis)

A

immediate sustained reaction

69
Q

occurs after mild, moderate injury and due to direct injury to endothelium causing intracellular gaps

A

delayed prolonged leakage

70
Q

leukocyte exudation

A

✓ leukocyte adhesion
✓ immigration
✓ phagocytosis
✓ intracellular degradation of ingested particles
✓ extracellular release of leukocyte products

71
Q

occurs be of specific interactions complementary adhesion molecules present in leukocytes

A

leukocyte adhesion

72
Q

2 types of bactericidal mechanisms

A

✓ oxygen dependent mechanism
✓ oxygen independent mechanism

73
Q

oxygen dependent mechanism

A

✓ HOCl- Hypochlorous Acid
✓ HCI- Hydrogen Peroxide

74
Q

types of exudates

A
  1. serous
  2. cataract
  3. hemorrhage
  4. fibrinous
  5. suppurative
  6. granulomatous
75
Q

characterized by dominant vascular and cellular component

A

exudates

76
Q

implies a mild injury; serous fluids predominates

A

serous

77
Q

occurs in areas with mucous glands/secretions; predominated by mucous or cattarh.

A

catarrhal

78
Q

exudate predominated by RBC

A

hemorrhage

79
Q

predominated by fibrin and blood clot

A

fibrinous

80
Q

pus, mostly consist by neutrophils

A

suppurative

81
Q

predominates macrophages

A

granulomatous

82
Q

hageman factor - formation - bradykinin - kallikrein

A
83
Q

2 pathway

A

classical pathway and non-immunologic stimuli (such as bacterial toxins)

84
Q

for antigen antibody complexes

A

classical pathway

85
Q

how to activate;

A

activation- cleavage of complement C3 C5 which C3A into two pathways

86
Q

example of arachidonic acid metabolites

A

prostaglandin and leukotrienes

87
Q

potent vasodilators involved in edema formation by potentiating effects of histamines

A

prostaglandin

88
Q

produces pain potentiating the effect of bradykinin and act on yhe hypothalamic mechanism of fever production

A

prostaglandin E2

89
Q

inhibit platelet aggregation

A

PG12 (prostacycline)

90
Q

derived from lipoxygenase pathway

A

leukotrienes

91
Q

leukotrienes

A

✓ LTB4
✓ LTC4
✓ LTD4
✓ LTE4

92
Q

potent chemotactic agent for neutrophil and monocyte macrophages

A

LTB4

93
Q

-powerful stimulator of vascular permeability

A

LTC4 and LTD4

94
Q
  • 1000 times potency than histamines
  • cause vasoconstriction and bronchoconstriction
A

LTE4

95
Q

Distribution

A

° focal
° multi-focal
° locally extensive
° diffused

96
Q

what attract the leukocytes to migrate to the injured site are chemical mediators of inflammation and this process is called?

A

chemotaxis

97
Q

more leukocytes adhere to the walls until the luminal surface of the wall become covered with a layer of leucocytes called?

A

pavementing

98
Q

began to stick to the walls and adhere to it for longer periods called?

A

adherence

99
Q

leucocytes begin to appear in the marginal plasma stream of the venule

A

margination

100
Q

the etiology of inflammation varies includes both living and non-living agents such as;

A

bacteria, fungi, viruses, metazoan parasites, protozoa, immunologic injury, trauma, heat, cold, toxins or poisons and irradiation

101
Q

inflammation is a protective mechanism in that protective factor such as?

A

antibodies, complement and phagocytic cells

102
Q

purpose of inflammation

A

✓ to minimize the effect of the irritant or injury
✓ to heal the damaged tissue
✓ restore the affected tissues to normal

103
Q

2 phases of increased vascular permeability;

A

immediate phase (less than an hour)
prolonged phase (3-4 hrs)

104
Q

AGENTS THAT CAUSE ANAPHYLAXIS is numerous and include:

A

•venom or stings of biting insects
•vaccines
•variety of drugs
•food substances
•blood donors/blood products

105
Q

Clinical signs can be localized or generalized. Symptoms include:

A

✓restlessness and excitement

✓facial edema
✓pruritus on
✓affected area

✓salivation

✓lacrimation

✓vomiting

✓diarrhea

✓abdominal pains
✓dyspnea

✓cyanosis

✓shock

✓incoordination

✓convulsions

✓death

106
Q

T lymphocytes

A

✓helper T cells- CD4
✓Suppressor and cytotoxic T cells –CD8 or T8

107
Q

are tissue phagocytes

A

macrophages

108
Q

macrophages are important components of immune system

A

✓T cell activation
✓Macrophage activation
✓B cell activation

109
Q

Secretory functions of macrophage

A

✓release colony stimulating factor
✓release of alpha interferon
✓precursors of prostaglandins

110
Q

formed from macrophages and are often found together in
chronic lesions.

A

epithelioid and Giant cells

111
Q

Two types of giant cells are recognized

A
  1. langerhan cells
  2. foreign body giant cells
112
Q

the nuclei are arranged throughout the cell.

A

foreign body giant cells

113
Q

giant cell with nuclei around the periphery

A

langerhans cells

114
Q

chemotactic factors

A

Neutrophil (NCF)
-
Eosinophils (ECF)

115
Q

is an atom or molecule that is capable of independent existence
and has one or more unpaired electrons that make it highly reactive and
potentially cytotoxic

A

free radical

116
Q

inflammatory lesions are
usually small and surrounded by normal tissue.

A

focal

117
Q

lesions represent several scattered foci of inflammation

A

multi focal

118
Q

lesion involves a considerable are of tissue within an organ

A

locally extensive

119
Q

inflammatory lesions involve all of the tissue or the whole organ.

A

diffuse

120
Q

term used to describe small nodular lesions of chronic
inflammation that has a caseous center walled off by epithelioid cells

A

granuloma

121
Q

sometimes called exudative inflammation because of
the numerous tissue and plasma factors that pours into the inflammatory site

A

acute inflammation

122
Q

have some classic features as hyperemia, fluid and cellular exudations

A

acute lesions

123
Q

occurs when the injurious stimuli persist over a long period. It is often called proliferative inflammation

A

chronic inflammation

124
Q

traditionally classified on a time basis as acute, subacute, and chronic

A

inflammatory response

125
Q

They are less common than neutrophils, and arrive at the site of inflammation later than the polymorphs (granulocytes)

A

monocytes and macrophages

126
Q

Considered as the circulating form of mast cells, their number in
circulation is very low.

A

basophils

127
Q

are not phagocytic, and do not ordinarily migrate
during the acute phase of inflammation.

A

lymphocytes

128
Q

present in lesions around small blood
vessels where they form a cuff

A

perivascular cuffing

129
Q

they produce antibodies and their presence in an inflammatory site reflects a subacute or chronic process

A

plasma cells

130
Q

These cells are very much like neutrophils in that they have
granules containing an assortment of
enzymes, are phagocytic, and react
to stimuli similar to that of neutrophils

A

eosinophils

131
Q

Effects of Autacoids

A

• Vasodilation and Hyperemia.
• vasopermeability
• Leucocyte Emigration and Chemotaxis.

132
Q

are chemical messengers that act on vascular endothelia and leukocytes to contribute to an inflammatory reaction.

A

autacoids

133
Q

it influence the previously discussed changes in vascular caliber and permeability as well as chemotaxis of leukocytes

A

chemical mediators

134
Q

lipid mediators collectively called?

A

eicosanoids

135
Q

when coupled with a thin fluid where it imparts a red tinge color, the exudate are called?

A

serosanguineous exudates

136
Q

when the exudates are admixed with mucus the term is?

A

mucopurulent

137
Q

when exudates are admixed with fibrin

A

fibrinopurulent

138
Q

a viable collection of pus within of beneath the epidermis of the skin

A

pustule

139
Q

localized collection of pus, usually confined with a diphtheritic membrane or pyogenic membrane

A

abscess

140
Q

rupture at a surface through a tract

A

sinus or fistulous tract

141
Q

spread along fascial planes and subcutaneous tissues

A

cellulitis or phlegmonous inflammation

142
Q

pus contained in body cavities

A

empyema

143
Q

the principal element of catarrhal exudates are?

A

° secreted mucin
° admixed with neutrophils
° tissue debris
° fibrin and red blood cells

144
Q

when admixed with pus, the exudates are called?

A

mucopurulent exudates

145
Q

inflammatory lesions are usually small and surrounded by normal tissue

A

focal

146
Q

if it is well demarcated the lesion is said to be?

A

discrete

147
Q

if it blends well with the surrounding normal tissue, is said to be?

A

diffuse focal

148
Q

lesion represent several scattered foci odf inflammation

A

multi-focal

149
Q

if the lesion involves a considerable are of tissue within an organ, the lesion is said to be?

A

locally extensive

150
Q

inflammatory lesions involve all of the tissue or the whole organ

A

diffuse

151
Q

two processes of healing

A

repair and regeneration

152
Q

occur at sites where there is only minimal loss tissue

A

healing by first intention

153
Q

the process involved in healing by second intention also called?

A

healing by granulation

154
Q

the tissue that fill-in the gap and is beneath the coagula is called?

A

granulation tissue

155
Q

this could only occur when there is minimal damage. this type of repair is typified by what happens in the lungs.

A

repair by resolution

156
Q

where there is incomplete resolution of inflammation

A

repair by organization

157
Q

these cells continue to multiply throughout life to replace those shed or destroyed by normal physiological processes

A

labile cells

158
Q

they retain their latent capacity to regenerate, but do not actively replicate under normal circumstances because they have a survival time measured in terms of years

A

stable cells

159
Q

these cells cannot regenerate and therefore damage to these cells represents permanent loss

A

permanent cells

160
Q

implies that lost cells are replaced by cells of the same kind, and indicates cellular division of the remaining viable cells to take over the place of those lost from injury

A

regeneration

161
Q

two aberrations could occur in either of the first or second intention repair process. what are these two?

A

✓ keloid
✓ exuberant granulation or proudflesh

162
Q

may occur accumulation of excessive amounts of collagen giving rise to a protruding tumor-like scar tissue

A

keloid

163
Q

may be excessive formation of granulation tissues that protrudes above the level of injury

A

exuberant granulation or proudflesh

164
Q

Several factors that influences the healing process

A

✓ tissue involved
✓ vascularity
✓ protective covering
✓ nutrition
✓ hormones
✓ age
✓ magnitude of injury
✓ presence of infection
✓ presence of nerve supply

165
Q

these hormone are necessary for healing for they regulate metabolic activities

A

thyroid hormone

166
Q

delays healing for they interfere in with the maturation of collagen and in the on-going inflammatory process

A

corticosteroid

General Veterinary Pathology (23 decks)

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