Inflammation Flashcards

1
Q

Ten Generalities about the Inflammatory Response

A

1.
It is a process, not a thing.
2.
It occurs only in living tissue.
3.
It is a series of events overlapping into a continuum.
4.
It is a response and therefore requires initiation by some kind of stimulus.
5.
The response can be more harmful than the initiating stimulus.
6.
It is survival oriented and does not object to scarring as an end result.
7.
It is fairly stereotyped irrespective of the initiating stimulus.
8.
It has most of its components in the blood, whereas injury is always in the tissues.
9.
It is a carefully coordinated defense mechanism essential to life.
10.
It is complicated, but understandable.

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2
Q

is the vascular and cellular responses of living tissue to injury.

It is the reaction of the living tissue to injury, which comprises a series of changes in the terminal vascular bed, in the blood, and in the connective tissues that tend to eliminate the offending irritant and to repair the damaged tissue.

Inflammation consists of a series of complex reactions by vascular and connective tissue
elements to a tissue injury.

A

Inflammation

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3
Q

A definition of inflammation is complicated because systemic effects that include malaise,
fever, leukocytosis metabolic disturbances and shock may accompany the local vascular and tissue reactions.
Inflammation is the directed tissue response to noxious and injurious external and internal
stimuli.

A
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4
Q

– (the toxic and injurious substances produced by microbes).
Included are bacteria, viruses, protozoa, fungi and parasitic metazoa.

A

Pathogenic microorganisms

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5
Q

– toxins, free radicals, drugs, acids, alkalis etc.

A

Chemical injuries

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6
Q

The following are general etiologic agents of inflammation.
1.
Pathogenic microorganisms – (the toxic and injurious substances produced by microbes).
Included are bacteria, viruses, protozoa, fungi and parasitic metazoa.
2.
Chemical injuries – toxins, free radicals, drugs, acids, alkalis etc.
3.
Mechanical and thermal injuries (physical) – burns, heat, irradiation, excessive cold as
well as trauma, blows, lacerations, pressure.
4.
Immune reactions – antigen-antibody complexes, hypersensitivity reactions, immune
depositions etc.

A
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7
Q

Functions of the Inflammatory Response
To minimize the effect of an irritant the injured tissue is the goal of inflammatory response. This
is done by accumulation of fluids and cells in the injured area. The overall plan for this fluids and
cells is to:

A

1.to dilute
2.to localize
3.to destroy
4.to remove

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8
Q

Advantages and Disadvantages of Inflammation
ADVANTAGES
1.
It protects the surrounding healthy tissue by localizing and isolating the injured or
infected tissue.
2.
Inflammatory processes neutralize and inactivate toxins.
3.
It destroys and inhibits the growth of pathogenic microorganisms.
4.
It readies the injured area for healing and repair by eliminating damaged tissue and
necrotic cell debris.
DISADVANTAGES
1.
It can result to excessive scar tissue formation as with keloids, contractures, adhesions etc.
2.
Varying degrees of disabilities as result of pain and swelling.
3.
Tissue compression, vessel rupture and hemorrhage.
4.
Formation of cavity, sinus and fistula.
5.
Aggravates inflammation by destruction of surrounding intact tissues.
6.
Development of inflammatory diseases such as glomerulonephritis, hypersensitivity illness.

A
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9
Q

INFLAMMATION Overview:
• Inflammation is the vascular and cellular responses of living tissue to
injury. Inflammation is the body’s response to tissue injury, infection, or
harmful stimuli.
• Purpose: It aims to eliminate the initial cause of cell injury, clear out damaged
cells and tissues, and establish a repair process.

A
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10
Q

Vascular Changes:

A

o Vasodilation: Increases blood flow to the affected area, causing redness
and heat.
o Increased Permeability: Allows proteins and leukocytes to leave the
bloodstream and enter the tissue, leading to swelling.

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11
Q

Cellular Response:

A

o Leukocyte Recruitment: White blood cells (leukocytes) migrate to the
site of injury.
o Phagocytosis: Leukocytes engulf and digest pathogens and debris.

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12
Q

Chemical Mediators:

A

o Cytokines and Chemokines: Signaling molecules that regulate the
inflammatory response.
o Acute Phase Proteins: Produced by the liver, these proteins enhance the
inflammatory response.

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13
Q

Clinical Signs of Inflammation:

A

o Redness (Rubor)
o Heat (Calor)
o Swelling (Tumor)
o Pain (Dolor)
o Loss of Function (Functio Laesa)

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14
Q

Outcomes of Inflammation:

A

o Resolution: Complete healing without any residual damage.
o Chronic Inflammation: Prolonged inflammation leading to tissue
damage and fibrosis.
o Abscess Formation: Collection of pus due to infection.
o Scarring: Replacement of normal tissue with fibrous tissue.

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15
Q

Cardinal Signs of Inflammation
Cornelius Celsus (30BC to 30 AD) formulated the 4 cardinal features of inflammation:
1. rubor
-
REDNESS
2. tumor
-
SWELLING
3. calor
-
HEAT
4. dolor
-
PAIN
Rudolf Virchow (1821-1902), the father of modern pathology added:
5. functio laesa
LOSS OF FUNCTION

A
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16
Q

is caused by vasodilatation.

A

Redness

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17
Q

results mainly from fluid exudates accumulation
consequent to increased vascular permeability

A

Swelling

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18
Q

sensation of ____ is attributable to rapid
inflow of warm blood through dilated vessels in an inflamed area

A

heat

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19
Q

Pain can be due to
distension/compression of tissue and factors such as release of vasoactive chemicals i.e. kinins,
histamines, metabolites and bradykinin contribute to pain.

A
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20
Q

added to prevent
using the part that hurts.

A

Loss of function

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21
Q

. The escape of fluid and blood cells from the vascular system into the interstitial tissue
or body cavities.

A

Exudation

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22
Q

. An inflammatory extravascular fluid that has a high protein concentration, much
cellular debris, and a specific gravity above 1.020

A

Exudate

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23
Q

. A fluid with low protein content and a specific gravity of less than 1.012. It is
essentially an ultra filtrate of blood plasma and results from hydrostatic imbalance across the
vascular endothelium.

A

Transudate

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24
Q

Development of Transudates and Exudates. A, Normal hydrostatic pressare (blue arrow) can lead to the outflow of thad, but this is counter balanced by the mean colloid osmotic pressure (green arrow), which attracts fluid to the vascular lumen, therefore the net flow of fluid acrow the vascular bed is minimal. B. A transudate forms when fluid leaks out because of increased hydrostatic pressure of decreased cumotic pressure along with increased permeability across the endothelial cell layer. C. An exudate forms in and damage to the endothelial laver inflammation because vascular permeability increases result of of increased interendothelial spaces

A
25
Q

. Denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an
exudates or a transudate.

A

Edema

26
Q

– also known as the polymorphonuclear cells (PMN’s) or pus cells, are cells of
cute inflammatory response. They are the first to arrive at the site of inflammation. Neutrophils
are phagocytic cell that subsequently destroys invading microbes by releasing lytic lysosomal
enzymes and formation of chemotactic factors. The lysosomal enzymes (present in the granules):

A

Neutrophils

27
Q

Neutrophils
are phagocytic cell that subsequently destroys invading microbes by releasing lytic lysosomal
enzymes and formation of chemotactic factors. The lysosomal enzymes (present in the granules):

A

a)
Myeloperoxidase
b)
Acid hydrolases
c)
Lysozome (muramidase)
d)
Cationic proteins

28
Q

– usually prominent in allergic reactions and parasitic migrations. Lysosomal
granules contains enzyme that degrade and neutralizes the action of potent vasoactive chemicals
e.g. histaminase degrades/inactivates histamines; arylsulfatase B, which inactivates SRS-A.
eosinophils are phagocytic.

A

Eosinophils

29
Q

– the least numerous of the granulocytes, basophils share common properties
with mast cells by their ability to secrete or to release vasoactive amines/chemicals. The granules
contain histamines, heparin and SRS-A. Basophils are non-phagocytic.

A

Basophils

30
Q

Monocytes – are peripheral blood phagocytes. Once in migrated in the tissues, monocytes
become part of the tissue macrophage. Monocytes are phagocytic and are involved in immune
response as an antigen-presenting cell.

A
31
Q

Lymphocytes – Lymphocytes are found in the tissues in all types of inflammation, especially
after the acute ingress of neutrophils. All lymphocytes are derived from bone marrow stem cells
and differentiate into lymphocytes in the primary lymphoid organs (i.e., thymus and bone
marrow). From there lymphocytes seed to secondary lymphoid organs i.e. lymph nodes, spleen,
tonsils, Peyer’s patches etc. They are the cells involved in both the cell mediated (CMI) and
humoral immune (HI) responses. Three types of lymphocytes are currently recognized the first
two are non-phagocytic.
a.)
T lymphocytes – thymic lymphocytes; found in the paracortical areas of lymph nodes;
comprise about 70% of peripheral lymphocytes; involved in CMI.
T cell surface marker = CD or cellular differentiation or T
i
Helper T cells – CD4 or T4; aids in humoral immunity
ii
Suppressor and cytotoxic T cells –CD8 or T8

A
32
Q

– bursua derived lymphocytes; involved in HI.
B cells are found in the paracotical areas of the lymph nodes and in the germinal centers of
lymphoid follicles.

A

B lymphocytes

33
Q

– are lymphocytes that are nondefinable by either B or T
cell criteria. They are phagocytcic and nonspecific

A

Null or natural killer (NK) cells

34
Q

__________ – formed by a process of maturation and division of
B lymphocytes into two
distinct cells: __________ and ______ Their presence indicates a humoral response. Surface
of plasma cells contain specific class of immunoglobulin or antibodies.

A

Plasma cells
memory cells and plasma cells.

35
Q

Macrophages – are tissue phagocytes; depending on their location, macrophages are
named accordingly:
histiocytes
-
connective tissues
Langerhans cells
-
skin
von Kupffer cells
-
liver
alveolar macrophages
-
lungs
mesangial cells
-
kidneys
microglial cells
-
brain
spleen/lymph nodes
-
free and fixed macrophages
pleura and peritoneum
-
macrophages
Macrophages are important components of the immune system.

A
36
Q

-
connective tissues

A

histiocytes

37
Q

-
skin

A

Langerhans cells

38
Q

-
liver

A

von Kupffer cells

39
Q

-
lungs

A

alveolar macrophages

40
Q

-
kidneys

A

mesangial cells

41
Q

brain

A
42
Q

-
free and fixed macrophages

A

spleen/lymph nodes

43
Q

-
macrophages
Macrophages are important components of the immune system.

A

pleura and peritoneum

44
Q

T cell activation
a.
____^^__ “present” processed antigens to T cells in conjunction
with _________________________________ molecules on the macrophage surface.
These steps are required in the sensitization and activation of T cells.
b.
Macrophages releases _____________, a substance that stimulates sensitized T cell
activation to ILL-2. The latter allows full T cell activation to proceed to and causes the
proliferation of various T cell subsets.

A

Macrophages
major histocompatibility complex (MHC)
interleukin-1 (IL-1)

45
Q

Macrophage activation
a.
T cells, once activated, cause the mobilization and metabolic activation
of macrophages by releasing various lymphokines.
b.
The activation of macrophages is immunologically specific.
c.
Activated macrophages prolong the inflammatory process and the cause tissue destruction
by releasing their highly irritative enzymes. The process also has a protective function, thereby
amplifying immune response.

A
46
Q

B cell activation
a.B cell activation requires _____, which is secreted by macrophages (and some other APC’s or
antigen presenting cells
b.
________requires that antibody on the B cell surface match its specific antigen.
Antigen on the macrophage surface serve this purpose.
c.
B cell activation is aided by the presence of _______.

A

IL-1
B cell activation
helper inducer T cells

47
Q

Secretory functions of macrophages:
.

A

1.Releases colony stimulating factor and tumor necrosis factor.
2.
Release of alpha interferon, which aids in blocking viral replication.
3.
Precursors of prostaglandins

48
Q

Healing and Repair:

A

1.
Resorption by phagocytosis
2.
Release of fibroblast proliferating factor
3.
Epithelioid and Giant Cells – are formed from macrophages and are often found together in
chronic lesions. Epithelioid cells resemble squamous epithelial cells and macrophages. Giant cells
form by the fusion of the cytoplasm of macrophages.

49
Q

Two types of giant cells are recognized:
a.
Langhan’s Cells – giant cell with nuclei around the periphery
b.
Foreign body giant cells – the nuclei are arranged throughout the cell.

A
50
Q

– giant cell with nuclei around the periphery

A

Langhan’s Cells

51
Q

the nuclei are arranged throughout the cell.

A

Foreign body giant cells –

52
Q

are responsible for hemodynamic and
vascular changes.

A

Vasoactive amines (i.e., histamines and serotonin)

53
Q

MEDIATORS OF INFLAMMATION
A. Vasoactive amines (i.e., histamines and serotonin) are responsible for hemodynamic and
vascular changes.
1. Histamine
a.
Source. Most of the body’s histamine is stored in the granules of mast
cells. Also found in basophils and platelets.
b.
Release. Histamine is released by degranulation in response to various stimuli such as,
physical factors (heat, cold, trauma, radiation), type 1 hypersensitivity reactions, C3a and C5a
(referred to as anaphylatoxins), and cationic lysosomal proteins.
c.
Actions
(1)
Once released, histamine causes direct vascular effect. Some degree of vasoconstriction
(which varies according to animal species) almost always occurs, followed by vasodilation (which
is the stage of observable hyperemia). Histamine also causes an increase in the vascular
permeability of small veins and venules.
(2)
Histamine also has been shown to be chemotactic for eosinophils.
2. Serotonin
a. Source. Most of the body’s serotonin is stored in the gastrointestinal tract and central nervous
system; a much smaller proportion exists in the dense granules of platelets.

A
54
Q

B.
Plasma factors
1. The kinin system, when activated, leads to the formation of bradykinin.
a. Generation of bradykinin. When plasma comes in contact with collagen, endotoxin, or
basement membrane proteins, a there is an activation of clotting factor XII (Hageman factor). This is followed sequentially by kallikrein formation, which then converts high molecular-weight
kininogen (HMWK) to bradykinin.
2. The complement system, an important mediator of the inflammatory process, contains 9 major
plasma proteins, termed complement components.
a. Activation of complement. Critical to the biologic action of the complement system is the
activation, or cleavage, of complement component C3, which forms C3a. This can occur in two
pathways.
1. In the classical pathway, circulating antigen-antibody complexes activate the system and by
successive steps of cleavage and combination, generate complement components C3a and C5a.
2. In the alternate pathway, nonimmuologic stimuli (e.g. bacterial endotoxin) activate the system
and lead to cleavage of C3.
b.Actions

Both C3a and C5a are chemotactic for neutrophils and play an important role in the
increased vascular permeability caused by histamine release from mast cells.

Following complement cascade activation (by either pathway), C5, C6, and C7 in
combination also become chemotactic.

C5b through C9 (termed the membrane attack sequence) appears to be involved in injury to
parenchymal cells. (C5b6789 – MEMBRANE ATTACK COMPLEX).

A
55
Q

, when activated, leads to the formation of bradykinin.

A

kinin system

56
Q

, when activated, leads to the formation of bradykinin.

A

kinin system

57
Q

The kinin system, when activated, leads to the formation of bradykinin.
a. Generation of bradykinin. When plasma comes in contact with collagen, endotoxin, or
basement membrane proteins, a there is an activation of clotting __________. This is followed sequentially by ______ formation, which then converts high molecular-weight
kininogen (HMWK) to______// .

A

factor XII (Hageman factor)
kallikrein
bradykinin

58
Q

The________ , an important mediator of the inflammatory process, contains 9 major
plasma proteins, termed complement components.

A

complement system

59
Q

Activation of complement. Critical to the biologic action of the complement system is the
activation, or cleavage, of complement component C3, which forms C3a. This can occur in two
pathways

A