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Hpct > LEC5 - INFLAMMATION > Flashcards

LEC5 - INFLAMMATION Flashcards

1
Q

The word inflammation from the Latin

A

inflammare
(to set on fire)

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2
Q

according to him, inflammation is not a disease but only a protective response

A

john Hunter, Scottish surgeon in 1793:

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3
Q

Inflammation is a protective response involving:

A
  • host cells
  • blood vessels
  • proteins and
  • other mediators
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4
Q

host cell are involved if the inflammation is ?

A

acute or chronic

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5
Q

A response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host
defense from the circulation to the sites where they are needed, in order to eliminate the offending agents

A

inflammation

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6
Q

The word inflammation from the Latin

A

inflammare (to set on
fire)

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7
Q

he profound the 4 signs of inflammation - cardinal signs

A

o Rubor – redness
o Tumor – swelling
o Calor – heat
o Dolor – pain

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8
Q

*These signs are hallmarks of acute inflammation

A

o Rubor – redness
o Tumor – swelling
o Calor – heat
o Dolor – pain

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9
Q

he Added the 5th sign “Functio leasa” of inflammation

A

Rudolf Virchow (19th century)

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10
Q

he says that Inflammation is not a disease but a stereotypic response
that has salutary effect on its host

A

John Hunter (1793)

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11
Q

she Discovered the process of phagocytosis

A

Elie Metchnikoff (1880s)

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12
Q

in order to clear up or eliminate the initial cause of inflammation is through the process of

A

phagocytosis

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13
Q

2 etiology of inflammation

A

exogenous and endogenous

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14
Q

exogenous causes of inflammation

A

physical agents
chemical agents
biological agents

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15
Q

endogenous causes of inflammation

A

circulation disorders
enzyme activation
metabolic products deposals

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16
Q

Physical agents of inflammation

A

o Mechanic agents:
o Thermal agents:

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17
Q

under the physical agents, give example of mechanical agents

A

fractures, foreign, sand

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18
Q

under the physical agents, give example of thermal agents

A

burns or freezing

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19
Q

example of chemical agents

A

toxic gases, acids, bases

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20
Q

example of biological agents

A

microorganism

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21
Q

an endogenous causes, give example of circulation disorders

A

thrombosis, infarction, hemorrhage

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22
Q

an endogenous causes, give example of enzyme activation

A

acute pancreatitis

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23
Q

an endogenous causes, give example of metabolic deposals

A

uric acid, urea, cholesterol

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24
Q

all intracellular accumulation will fall in what category of exogenous causes of inflammation??

A

metabolic product deposals

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25
Q

CHANGES IN INFLAMMATION

A
  • Tissue damage
  • Cellular – vascular response
  • Metabolic changes (external manifestation)
  • Tissue repair
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26
Q

in acute inflammation, what are the cellular infiltrate

A

neutrophils

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27
Q

in chronic inflammation, what are the cellular infiltrate

A

Monocytes/macrophages
and lymphocytes

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28
Q

ACUTE

Tissue injury,
fibrosis

A

Usually
mild &
self-limited

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29
Q

CHRONIC

Tissue
injury,
fibrosis

A

Often severe and
progressive

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30
Q

ACUTE

Local &
systemic
signs

A

Prominent

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31
Q

CHRONIC

Local &
systemic
signs

A

Less prominent;
may be subtle

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32
Q

ACUTE INFLAMMATION

It is characterized by

A

o Exudation of fluids and plasma proteins (edema fluid)
o Emigration of neutrophilic leukocytes to the site of
injury

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33
Q

a type of inflammation that is An immediate and early response to an injurious agent

A

ACUTE INFLAMMATION

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34
Q

the cardinal sign is also called as

A

the external manifestation of acute inflammation

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35
Q

cardinal sign

Due to dilation of small blood vessels within
damaged tissue (cellulitis)

A

REDNESS
(RUBOR)

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36
Q

cardinal sign

Results from increased blood flow (hyperemia)
due to regional vascular dilation

A

HEAT (CALOR)

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37
Q

cardinal sign

Due to the accumulation of fluid in the
extravascular space.

A

SWELLING
(TUMOR)

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38
Q

CARDINAL SIGNs

Results from the stretching & destruction of
tissues due to inflammatory edema

A

PAIN (DOLOR)

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39
Q

CARDINAL SIGNS OF ACUTE INFLAMMATION

inflamed area is inhibited by pain
Severe swelling may physically immobilize the
tissue

A

LOSS OF
FUNCTION

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40
Q

Chemicals of acute inflammation (mediators)

A

Bradykinins
Prostaglandins
Serotonin

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41
Q

Chemicals of acute inflammation (mediators)

function of bradykinins

A

contribute for blood vessel dilation

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42
Q

Chemicals of acute inflammation (mediators)

function of prostaglandin

A

vascular and systemic reaction

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43
Q

Chemicals of acute inflammation (mediators)

function of serotonin

A

happy hormones

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44
Q

EVENTS OF ACUTE INFLAMMATION

A

VASCULAR CHANGES
CELLULAR EVENTS

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45
Q

VASCULAR CHANGES in acute inflammation

A
  • Increase in blood flow (vasodilation)
  • To bring cells and proteins to
    the site of injury
  • By vasodilation and increased
    vascular permeability
    (vascular leakage) by the
    chemical mediators especially
    histamine
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46
Q

CELLULAR EVENTS of acute inflammation

A
  • Recruitment of leukocytes
  • Activation of leukocytes
    leading to the process
    of destruction of
    invaders and production
    of mediators
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47
Q

Stages of Vascular response

A

(1) Vascular dilation and
increased blood flow
(2) extravasation and deposition
of plasma fluid and proteins
(edema)
(3) leukocyte (mainly
neutrophil) emigration and
accumulation in the site of injury.

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48
Q

the vascular dilation and increased blood flow will cause

A

causing erythema and
warmth

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49
Q

Mechanism of Vascular response

A

Vasoconstriction
vasodilation of arterioles and venules
stasis of blood flow
oozes protein-rich fluid into
extravascular tissues.
exudates clinically appears as
swelling. (edema)

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50
Q

Stages of Margination

A

Rolling
Pavementing

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51
Q

is a peripheral positioning of white cells along the endothelial
cells.

A

Margination

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52
Q

rows of leukocytes tumble slowly along the
endothelium

A

Rolling

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53
Q

endothelium can be lined by white cells the binding of leukocytes with endothelial cells is facilitated by cell
adhesion molecules

A

Pavementing

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54
Q

Transmigration of
leukocytes through the process of

A

Diapedesis

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55
Q

The movement of leukocytes
by extending pseudopodia
through the vascular wall.

A

Diapedesis

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56
Q

Stages of cellular
response

A

Margination
Transmigration
chemotaxis
phagocytosis

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57
Q
  • unidirectional attraction of leukocytes from vascular channels
    towards the site of inflammation within the tissue space
    guided by chemical gradients.
A

Chemotaxis

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58
Q

The important chemotactic factors for neutrophils

A

(C5a)
* leukotriene B4
*cytokines (IL-8)

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59
Q

(C5a) is composed of

A

complement system, bacteria and mitochondrial products of
arachidonic acid metabolism:

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60
Q

is the process of engulfment and
internalization by specialized cells of particulate material.

A

Phagocytosis

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61
Q

Phagocytic cells

A
  • polymorphonuclear leukocytes (neutrophiles),
    *monocytes
  • tissue macrophages.
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62
Q

Leukocyte recruitment is a multi-step process consistin

A

§ loose attachment to and rolling on endothelium (mediated by selectins);

§ firm attachment to endothelium (mediated by integrins)

§ migration through interendothelial spaces

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63
Q

Steps of the inflammatory response (5Rs)

A
  • Recognition of the injurious agent - etiology of the inflammation
  • Recruitment of leukocytes
  • Removal of the agent
  • Regulation (control) of the response
  • Resolution (repair
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64
Q

Defects in Leukocyte Function can be either ___ and ___

A

acquired and inherited

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65
Q

lead to increased susceptibility to infections, which may be recurrent
and life-threatening

A

Defects in Leukocyte Function

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66
Q

acquired disease in defect of leukocyte function

A

bone marrow suppresion
radiation, chemo therapy
diabetes, malignancy, sepsos, chronic dialysis

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67
Q

genetic causes of leukocyte disorder

A

leukocyte adhesion deficiency 1
leukocyte adhesion deficiency 2
chronic granulomatous disease
x linked
autosomal recessive
myeloperoxidase deficiency
chediak-higashi syndrome

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68
Q

defect in bone marrow suppression, tumor, radiation and chemotheraphy

A

production of leukocytes

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69
Q

defect in leukocyte function in diabets, maklignancym sepsis and chronic dialysis

A

adhesion and chemotaxis

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70
Q

defect in leukocyte for anemia, sepsis, diabetes, and malnutrition

A

phagocytosis and microbicidal activity

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71
Q

defect in leukocyte function wherein there’s defect in adhesion because of the mutations in B chain of CD 11/ CD18 integrins

A

leukocyte adhesion deficiency 1

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72
Q

a defect in leukocyte function wherein there’s a decreased oxidative burst

A

chronic granulomatous disease

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73
Q

defect in leukocyte function wherein there’s defect in adhesion because of the mutations in fucosyl transferase required for synthesis of sialated ologosaccharide (receptor for selectisn)

A

leukocyte adhesion deficiency 2

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74
Q

a defect in leukocyte function wherein there’s a phagocyte oxidase (membrane component)

A

x linked

75
Q

a defect in leukocyte function wherein there’s a phagocyte oxidase (cytoplasmic components )

A

autosomal recessive

76
Q

a defect in leukocyte function wherein there’s a decreased in microbial killing because of defective MPO-H2O2 system

A

myeloperoxidase deficiency

77
Q

a defect in leukocyte function wherein there’s a decreased leukocyte function because of the mutations affecting protein involved in lysosomal embrane traffic

A

chediak-higashi syndrome

78
Q

Three steps in Phagocytosis

A

(1) recognition and attachment of the
particle to the ingesting leukocyte
(2) engulfment, with subsequent
formation of a phagocytic vacuole
(3) killing and degradation of the
ingested material

79
Q

The outcome of acute inflammation

A

*Elimination of the noxious stimulus
*Decline of the reaction
* Repair of the damaged tissue,
* Persistent injury resulting in chronic inflammation.

80
Q

Persistent injury resulting in

A

chronic inflammation.

81
Q

Outcomes of acute
inflammation:

A

resolution,
healing by scarring (fibrosis),
chronic inflammation

82
Q

example of causes of acute inflammation

A

infarction
bacterial infection
toxins
trauma

83
Q

according to the diagram what are the characteristic or component of acute inflammation

A

vascular changes
neutrophil recruitment
mediators

84
Q

according to the diagram what are the characteristic or component of chronic inflammation

A

angiogenesis
mononuclear cell infiltrate
fibrosis (scar)

85
Q

healing in acute inflammation will result to

A

clearance of injurious stimuli
clearance of mediators and acute inflammatory cells
replacement of injured cells
normal function

86
Q

if an acute inflammation result to pus formation or abscess, it will then heal as a ___

A

fibrosis

87
Q

healing in chronic inflammation will result to

A

fibrosis - loss of function

88
Q

Morphological Feature of AI

A

*Serous inflammation
*Fibrinous inflammation
*Suppurative (purulent) inflammation

89
Q

is characterized by the outpouring of a watery, relatively
protein-poor fluid that, depending on the site of injury,

A

*Serous inflammation

90
Q

*Fluid in a serous cavity is called an

A

effusion

91
Q

resulting in greater vascular permeability allows large molecules such as fibrinogen to pass the endothelial barrier

A

fibrinous inflammation

92
Q

a ____ is a characteristic of inflammation in the lining of body cavities

A

fibrinous exudate

93
Q

a fibrinous exudate came from the lining of body cavities such as

A

meninges, pericardium, pleura

94
Q

manifested by the presence of large amounts of purulent exudate (pus)

A

*Suppurative (purulent) inflammation

95
Q

*Suppurative (purulent) inflammation consist of what cells

A

onsisting of neutrophils, necrotic cells, and edema fluid.
* (e.g., staphylococci)

96
Q

are focal collections of pus that may be caused by seeding of
pyogenic organisms into a tissue

A

abscesses

97
Q

secondary infections of necrotic foci

A

Abscesses

98
Q

is a local defect, or excavation, of the surface of an organ or tissue
that is produced by necrosis of cells and sloughing (shedding) of
inflammatory necrotic tissue

A

ulcer

99
Q

highest immigration of cells

A

abscess

100
Q

cell derived mediators

A

histamine
serotonin
prostaglandins
leukotrienes
platelet-activating factor
reactive oxygen species
nitric oxide
cytokines
neuropeptides

101
Q

a cell derived preformed mediators in secretary granules

A

histamine
serotonin

102
Q

source of histamine

A

mast cells, basophilic, platelets

103
Q

source of serotonin

A

platelets

104
Q

mediators in vasodilation

A

prostaglandins
nitric oxide
histamine

105
Q

mediators for increased vascular prmeabilty

A

histamine and serotonin
bradykinin
c3a and c5a
leukotrienes
PAF
susbtance P

106
Q

is inflammation of prolonged duration

A

chronic inflammation

107
Q

in which active inflammation, tissue injury, and healing proceed
simultaneously.

A

Chronic inflammation

108
Q

chronic inflammation is characterized by:

A

◦ Infiltration with mononuclear cells
◦ macrophages,
◦ lymphocytes,
◦ plasma cells
◦ Tissue destruction,
◦ Repair, involving new vessel proliferation (angiogenesis) and fibrosis

109
Q

the dominant cells of chronic inflammation

A

Macrophages

110
Q

lungs macrophage is called as

A

alveolar macrophage

111
Q

central nervous system macrophage

A

(microglial cells),

112
Q
  • spleen and lymph nodes macrophage
A

( sinus histiocytes),

113
Q

a chronic inflammatory cell that develops from activated b lymphocyes and produces antbodies

A

plasma cells

114
Q

a chronic inflammatory cells that are characteristically found in inflammatory sites around parasitic infections or as part of immune reactions

A

eosinophil

115
Q

what Ig is eosinophil associated with

A

IgE

116
Q

a chronic inflammatory cells that is distributed in connective tissues throughout the body, and they can participate in both acute and chronic inflammatory responses

A

mast cells

117
Q

This involves a diffuse
accumulation of
macrophages and
lymphocytes at site of
injury that is usually
productive with new
fibrous tissue
formations

A

Nonspecific chronic
inflammation:

118
Q

Classification of chronic inflammation

A

Nonspecific chronic
inflammation:
specific chronic inflammation (granulomatous inflammation)

119
Q

characterized by the presence of
granuloma.

A

Specific inflammation
(granulomatous inflammation):

120
Q

is a microscopic aggregate of
epithelioid cells.

A

granuloma

121
Q

cell is an activated
macrophage, with a modified
epithelial cell-like appearance.
The epitheloid cells can fuse
with each other & form
multinucleated giant cells.

A

Epithelioid

122
Q

The ___ can fuse
with each other & form
multinucleated giant cells.

A

epithelioid cells

123
Q

is a distinctive pattern of chronic
inflammation characterized by
aggregates of activated
macrophages that assume an
epithelioid appearance

A

*Granulomatous inflammation

124
Q

a typucal granuloma resulting from infection with mycobacterium tuberculosis showing central caseous necrosis

A

granulomatous inflammation

125
Q

Two types of giant cells

A

Foreign body-type giant cell
Langhans giant cells

126
Q

a type of giant cell which have irregularly scattered nuclei in
presence of indigestible materials.

A

Foreign body-type giant cells

127
Q

a type of giant cell in which the nuclei are arranged peripherally in a horse shoe patter which is seen typically in tuberculosis and sarcoidosis

A

Langhans giant cells

128
Q

Types of granulomas

A

Foreign body granuloma
Immune granulomas

129
Q

granulomas are initiated by inert fore

A

Foreign body granuloma

130
Q

*Antigen presenting cells (macrophages)
engulf a poorly soluble inciting agent.

A

Immune granulomas

131
Q

*Macrophage inhibitory factor helps to
localize activated macrophages and
epitheloid cells

A

Immune granuloma

132
Q

Major causes of
granulomatious inflammation

A

Bacterial
fungal
helminthic
protozoal
chlamydia

133
Q

Bacterial cause of granulomatous inflammation

A

Tuberculosis, Leprosy, Syphilis, Cat scratch
disease, Yersiniosis

134
Q

fungal cause of granulomatous inflammation

A

Histoplasmosis, Cryptococcosis,
Coccidioidomycosis, Blastomycosis

135
Q

helminthic cause of granulomatous inflammation

A

Schistosomiasis

136
Q

protozoal case of granulomatous inflammation

A

Leishmaniasis, Toxoplasmosis

137
Q

chlamydia case of granulomatous inflammation

A

Lymphogranuloma venerum

138
Q

SYSTEMIC EFFECTS OF
INFLAMMATIONS

A

*a. Fever
*b. Endocrine & metabolic responses
*c. Autonomic responses
*d. Behavioral responses
*e. Leukocytosis
* f. Leukopenia
*g. Weight loss

139
Q

restoration of tissue architecture and function
after an injury

A

Tissue repair

140
Q

Tissue Repair occurs in

A

– Regeneration of injured tissue
– Replacement by connective tissue (scarring) - Usually, tissue repair involves both processes

141
Q

Tissue Repair involves

A
  • cell proliferation-
    interaction between cells and extracellular matrix
142
Q

Mechanisms regulating cell
populations

A

Cell numbers can be altered by:
§ increased or decreased rates
of stem cell input
§ cell death due to apoptosis

Changes in the rates of
proliferation or differentiation

143
Q

Processes in the proliferation of cells

A
  1. DNA replication
    2.Mitosis
144
Q

Cellular Proliferation

divided into three groups

A

*. Continuously dividing (labile) tissues
** Stable tissues
** Permanent tissues

145
Q

mechanism of labile tisues

A

** Cells are continuously proliferating
** Can easily regenerate after injury
** Contain a pool of stem cells

146
Q

example of Continuously dividing (labile) tissues

A

bone marrow, skin, epithelium

147
Q

*Cells have limited ability to proliferate
*Limited ability to regenerate
*Can proliferate if injured

A

Stable tissues

148
Q

Stable tissues examples

A

Examples: liver, kidney, pancreas

149
Q

Cells can’t proliferate
*Can’t regenerate
* injury always leads to scar

A

Permanent tissues

150
Q

Permanent tissues examples

A

: neurons, cardiac muscle

151
Q

Three phases in granulation -
tissue

A

Phase of inflammation
Phase of demolition
ingrowth of granulation tissue

152
Q

3 phases of granulation

A

inflammatory exudate, platelet aggregation and fibrin
deposition.

153
Q

what happen in phase of demolition

A

*The dead cells liberate their autolytic enzymes.
*There is an associated macrophage infiltration.

154
Q

what happen in Ingrowth of granulation tissue

A

proliferation of fibroblasts and an ingrowth of new blood
vessels into the area of injury, with a variable number of
inflammatory cells.

155
Q

is a mechanical
reduction in the size of the defect

A

Wound contraction

156
Q

esults in much faster healing,
*If ___________ is prevented, healing is slow
and a large scar is formed.

A

contraction

157
Q

have the capacity to stimulate cell division and
proliferation

A

Growth factors

158
Q

Sources of Growth Factors:

A
  1. Platelets, activated (TGF)
    *2. Damaged epithelial cells, (EGF)
    *3. Circulating serum growth factors,
    *4. Macrophages, (angiogenic factor)
    *5. Lymphocytes recruited to the area of injuryowth Factors:
159
Q

The main phases of cutaneous wound
healing:

A

*Inflammation
*Formation of granulation tissue
*ECM remodeling

160
Q

*___ is the network that surrounds cells

A

ECM

161
Q
  • Two forms of ECM
A

interstitial matrix and basement membrane

162
Q

interstitial matrix componnt

A

fibrillar collagen
elastin
proteoglycan and hyaluronan

163
Q

It provides mechanical support to tissues

A

ecm

164
Q
  • It acts as a substrate for cell growth and the formation of
    tissue microenvironments.
A

ECM

165
Q

It regulates cell proliferation and differentiation

A

ecm

166
Q

_____ stimulate cells through cellular integrin
receptors.

A

fibronectin and laminin

167
Q

__bind growth factors and display them at high
concentration, and

A

proteoglycans

168
Q

An intact ECM is required for tissue regeneration

true or false

A

true

169
Q

healing of the epidermis

A

regeneration

170
Q

(healing of the dermis

A

repair by scarring

171
Q

Two patterns of healing

A

. Healing by first intention
Healing by second intention

172
Q

Occurs in small wounds that close
easily

A

healing by first intention

173
Q

Healing by first intention
(primary union)

_____ predominates
over fibrosis

A

epithelial regeneration

174
Q

healing by first intention

By 24 hours

A
    • clot forms
    • neutrophils come in
    • epithelium begins to regenerate
175
Q

healing by first intention

By 3-5 hours

A
    • macrophages come in
    • granulation tissue is formed
  • new blood vessels
  • fibroblasts
    • collagen begins to bridge incision
    • epithelium increases in thickness
176
Q

healing by first intention

By weeks later

A
    • granulation tissue gone
    • collagen is remodeled
    • epidermis full, mature
    • eventually, scar forms
177
Q

larger wounds that have gaps between wound margins

A

Healing by second intention
(secondary union)

178
Q

Fibrosis predominates over epithelial regeneration

A

healing by second intentoin

179
Q

Healing is slower, with more inflammation and
*granulation tissue formation, and more scarring

A

Healing by second intention
(secondary union)

180
Q

*Local Factors

A

*> Type, size, and location of the wound
* > Vascular supply
* > Infection
* > Movement
* > Ionizing radiation

181
Q

Systemic Factors

A

circulatory statius
infection
metabolic status
Nutritional deficiencies

182
Q

Complications of Wound Healing

A

infection
deficient scar formation
excessive scar formation

183
Q

Excessive Scar Formation will form

A

Keloid Formation
Hypertrophic Scar

184
Q

Deficient Scar Formation will lead to

A

Wound Dehiscence
Ulceration

Hpct (18 decks)

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