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5 -PATHOLOGYYYY > INFLAMMATION AND HEALING > Flashcards

INFLAMMATION AND HEALING Flashcards

1
Q

CARDINAL SIGN :

A

Rubor (redness)
Tumor (swelling)
Calor (heat)
Dolor (pain)

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2
Q

redness

A

RUBOR

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2
Q

swelling

A

tumor

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2
Q

pain

A

dolor

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3
Q

heat

A

calor

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3
Q

The earliest acceptable definition
of inflammation was given by —-
as the process that occur in a living tissue when it is injured provided that the injury is not of such a degree as to at once destroy its structure and vitality.

A

Bourdon-Sanderson

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3
Q

Is a protective mechanism in that protective factor such as
antibodies, complement and phagocytic cells normally confined to the
bloodstream gain access at localized tissue sites to destroy foreign invaders.

A

Inflammation

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4
Q

purpose Inflammation

A
  • is to minimize the effect of the irritant or injury
    *to heal the damaged tissue and
    *restore the affected tissues to normal
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5
Q

The etiology of inflammation varies and includes both living and nonliving agents such as:

A

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

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6
Q

described much of the descriptions on the initial inflammatory
reactions in 1882.

A

Conheim

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7
Q

the initial response involves the endothelia of capillary bed

A

(arteriole, venule, intercommunicating vessels and the true
capillaries)

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8
Q

After an initial arteriolar constriction, there occur sustained

A

dilatation of all small blood vessels

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9
Q

The overload of venous drainage
leads to passive congestion that also contributes to

A

vasodilation

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10
Q

Leucocytes then begin to
appear in the marginal plasma
stream of the venule (called

A

margination

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11
Q

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

A

adherence

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12
Q

Progressively, more leucocytes
adhere to the walls until the luminal
surface of the wall become covered
with a layer of leucocytes (called

A

pavementing

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13
Q

Two phases of increased vascular permeability:

A

*immediate phase lasting less than an hour
*prolonged phase that last for 3-4
hours or longer if the stimulus persists
*third phase that last for several days,
although delayed in onset has been described to occur in sunburns

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14
Q

in tissues is accomplished by pseudopodia into the intercellular junction of endothelial cells, enlarging their opening and
squeezing through.

A

migration

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15
Q

All leucocytes have similar migration capacity, but neutrophils and eosinophils,
commonly called

A

polymorphs or granulocytes

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15
Q

What attract the leucocytes to migrate to the injured site are
chemical mediators of inflammation and this process is called

A

chemotaxis

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15
Q

are usually first, and could move
through fibrin and past tissue cells to their destination

A

polymorphs or granulocytes

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15
Q

Accumulations of such
cells may reach a peak in about 4 hours although this may vary based on the
stimuli.

A
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16
Q

i. Red blood cells, unlike leucocytes, have no a —-
they may take the advantage of the holes created by leucocytes and leak
passively into the injured area.

A

amoeboid capabilities

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16
Q

influence the previously discussed changes in vascular caliber and permeability, as well as chemotaxis of leucocytes.

A

Chemical mediators

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16
Q

The central feature of inflammation is the

A

infiltration of leucocytes to the
site of injury

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17
Q

as coined in the early ‘90s to distinguish such chemical messengers from hormones and neurotransmitter substances.

A

autacoid

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18
Q

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

A

autacoid

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19
Q

those coming from the outside such as
bacterial products and toxins.

A

Exogenous mediators

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20
Q

Endogenous mediators –these are synthesized by the body and may
be:

A

➢Plasma derived –
➢ Cell or Tissue derived –

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21
Q

Plasma derived – coming from the three major mediator producing systems in the plasma as
*coagulation-fibrinolytic
system,
*kinin system, and
complement system

A
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22
Q

*may be performed and stored as
granules in cells (e.g., histamine and cationic proteins) or
*newly synthesized by cells (e.g., interleukin, leukotriene, and platelet
activating factor).

A

Cell or Tissue derived

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23
Q

generated by consequent or multiple enzymic
steps involving sequential activation of molecules by limited proteolysis
(e.g., mediators formed by the complement and coagulation-fibrinolytic
systems)

A

Peptide mediators

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24
Q

– collectively called eicosanoids,

A

Lipid mediators

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25
Q

these are derived from the action of phospholipase to membrane phospholipids through the arachidonic acid pathways (lipooxygenase and cyclooxygenase
pathways)

A

Lipid mediators

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26
Q

e arachidonic acid pathways (

A

(lipooxygenase and cyclooxygenase
pathways)

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27
Q

Most of the biologically active mediators of inflammation are derived from
the systems in the plasma

A

Kinin, Coagulation-Fibrinolytic, and Complement
systems
and that of eicosanoids.

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28
Q

Effects of Autacoids

Vasodilation and Hyperemia.

A

most potent are as follows: Histamine released from mast cells and basophils;
Bradykinin, Prostaglandin E1 and E2, Leukotriene B4, C3 and C5 fragments of
complement, and Thromboxane.

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29
Q

The mediators that increase the permeability of the
microvasculature includes Histamine, Serotonin, Bradykinin, Kallikrein, Platelet
Activating Factor, Lymphokines, Anaphylatoxin (C3 and C5 fragment of
Complement), Leukotriene B4, C4 and D4, 5-HPTES (5-hydroperoxy
eicosatetranoic acid), and fibrin degradation products.

A

Vasopermeability

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30
Q

Mediators that attract neutrophils in
an inflammatory response includes C5a fragment of Complement, Leukotriene
B4, Bacterial toxins, and Platelet Aggregating Factor.

A

Leucocyte Emigration and Chemotaxis.

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31
Q

Mediators that attract neutrophils in
an inflammatory response includes

A

C5a fragment of Complement,
Leukotriene
B4, Bacterial toxins, and
Platelet Aggregating Factor.

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32
Q

he chemotactic agents
acting on monocytes and macrophages include

A

C5a fragment of Complement,
Leukotriene B4,
Bacterial toxins,
Cationic protein fractions of neutrophils,
Lymphokines, and
Fibrin degradation products

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33
Q

Lymphocytes are attracted
mainly by

A

Lymphokines

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33
Q

eosinophils are attracted by e

A

chemotactic factor of anaphylaxis (ECF-A) derived from mast cells, and
prostaglandin D2

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33
Q

Types of Exudates

A
  1. Serous exudates
  2. Fibrinous exudates
  3. Hemorrhagic exudates
  4. Purulent or Suppurative exudates
  5. Catarrhal exudates
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33
Q

this is primarily a clear fluid that is low in protein that
exudes from serosal or mucosal surfaces following mild irritation.

A

Serous exudates

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33
Q

The most common example is that seen in cases of “runny nose” where a clear fluid leaks from the nostrils following irritation.

A
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33
Q

these exudates usually occur in severe vascular injuries where a fluid rich in fibrinogen is produced.

A

Fibrinous exudates

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33
Q

In severe mucosal
damage where the epithelia are lost, the fibrin that accumulates may become
tightly adherent to the underlying tissue forming what is known as a

A

diphtheritic membrane or pseudomembrane.

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33
Q

The term “diphtheritic” applies to fibrinous
organization of any necrotic exudates on a mucosal surface

A
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33
Q

When the body and organ surfaces have fibrinous exudates, the fibrous
organization of the exudates forms what is called

A

adhesion

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33
Q

This is commonly seen in mucosal and serosal surfaces, most notably in the intestines, pleura, peritoneum, and synovial
membranes.

A

. Fibrinous exudates –

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33
Q

Sometimes it is
called

A

sanguineous exudates

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33
Q

when red blood cells are the predominating cellular component, the exudates are called hemorrhagic exudates.

A

Hemorrhagic exudates

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33
Q

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

A

serosanguineous exudates.

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33
Q

Microscopically,
fibrin is viewed as solid clumps of long delicate eosinophilic strands.

A
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33
Q

– these exudates are characterized by
the production of pus (suppuration) which is a thick creamy fluid composed of a
large number of viable and dead polymorphs.

A

Purulent or Suppurative exudates

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34
Q

The exudates are fluid because of
the hydrolytic enzymes produced and released by the leucocytes.

A
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35
Q

In avian
species, since their heterophils lack the hydrolytic enzymes, purulent exudates
are semi-solid compared to the fluid nature of the exudates seen in mammals.

A
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36
Q

are characteristically associated with certain types of pyogenic bacteria (pus-forming).

A
37
Q

When the exudates are admixed with mucus, the term

A

mucopurulent

37
Q

if it is
admixed with fibrin.

A

fibrinopurulent

38
Q

e is a viable collection of pus within
or beneath the epidermis of the skin,

A

pustule

39
Q

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

A

abscess

40
Q

; it may spread along fascial planes and subcutaneous tissues and
is called

A

cellulitis or phlegmonous inflammation;

40
Q

The fates of an
abscess vary: It may rupture at a surface through a tract called a s

A

sinus or
fistulous tract;

41
Q

it may become encapsulated
and contained within fibrous tissue as a cold abscess that is slowly resorbed later;
or it may branch out sending various tracts to nearby surfaces to release the
developing fluid pressure. Pus contained in body cavities is called

A

empyema

42
Q

occur on mucus membranes and mucosal surfaces of
the alimentary tract, respiratory, and reproductive tract. T

A

Catarrhal exudates –

43
Q

These cells are the first to migrate at the site of inflammation
attracted by chemotactic factors, especially when bacteria are present at the site
of inflammation.

A

Neutrophils

43
Q

When admixed with pus, the exudates are c

A

mucopurulent exudates

44
Q

Cells in Inflammatory Exudates

A

Neutrophils
Eosinophils
Basophils
Lymphocytes
Plasma cells
Monocytes and Macrophages

45
Q

They are aggressively phagocytic but have a short life span of
24-48 hours

A
46
Q

The released lysosomal
enzymes from dead neutrophils help
liquefy cellular debris and fibrin as a
prelude to repair. These enzymes
include

A

alkaline phosphatase,
lysozymes,
myeloperoxidase,
betaglucoronidase,
alpha-mannosidase and
proteinase

47
Q

In purulent inflammation, the liquid nature
of pus is due to the liquefactive effects
of these enzymes.

A
48
Q

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

A

Eosinophils

49
Q

They are prominent in certain
parasitic infections and in allergic
reactions.

A
50
Q

Antigen-antibody
complexes strongly attract these
cells. They are consistently found in
some granulomas (e.g., eosinophilic
granuloma in cats), in eosinophilic
myositis in dogs, and in the meninges
of pigs in cases of salt poisoning

A
51
Q

Considered as the circulating form of mast cells, their number in
circulation is very low.
play an important role in hypersensitivity
reactions, where they produce histamine

A

Basophils

52
Q

They are more commonly seen in chronic
inflammation, and more importantly in viral
infections.

A

Lymphocytes

52
Q

Lymphocytes are associated
with the host’s immune response and are
often present in lesions around small blood
vessels where they form a cuff c

A

perivascular cuffing.

52
Q

Formed from transformed B-lymphocytes, they produce antibodies and their presence in an inflammatory site reflects a subacute or chronic process.

A

Plasma cells

53
Q

The formation of mature plasma cells from
lymphocytes requires about

A

4-5 days.

54
Q

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

A

Monocytes and Macrophages.

54
Q

Monocytes are considered the
circulating form of macrophages (also called

A

histiocytes

55
Q

On the site of inflammation, macrophages formplump aggregates of macrophages,

A

epithelioid cells

55
Q

which are large multinucleated cells formed by the fusion of macrophages.

A

giant cells

55
Q

There are several
types of giant cells, but the more commonly encountered types are the

A

foreign body giant cell and
Langhan’s type giant cell.

56
Q

is a large cell with multiple nuclei arranged centrally

A

Foreign body giant

57
Q

is of a similar size and frequently oval in shape with nuclei arranged peripherally in a horseshoe arrangement.

A

e Langhan’s type

58
Q

Found during repair phase, fibroblast form fibrous tissues

A

Fibroblast

58
Q

They multiply rapidly at site and secrete globular protein that precipitate as
macromolecular collagen fibers in the interstitium.

A
58
Q

Acute Inflammation is sometimes called
n because of
the numerous tissue and plasma factors that pours into the inflammatory site.

A

exudative inflammation

58
Q

Classification

A

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

58
Q

Microscopically, the acute lesions have some classic features as hyperemia, fluid
and cellular exudations.

A
58
Q

Chronic Inflammation occurs when the injurious stimuli persist over a long
period. It is often called

A

proliferative inflammation

59
Q

Chronic inflammation may take
several forms as
where an ulcer is not repaired

A

chronic ulceration

59
Q

where there is fibrous encapsulation of pus

A

chronic abscessation

59
Q

Chronic inflammation

A

chronic ulceration
chronic abscessation
chronic granulomatous inflammation

60
Q

is a term used to describe small nodular lesions of chronic inflammation that has a caseous center walled off by epithelioid cells, macrophages and fibroblasts.

A

granuloma

61
Q

Granulomas are associated with certain etiologic agents such as foreign bodies
(e.g., asbestos bodies), fungi, and bacteria (e.g., tubercle bacilli).

A
62
Q

inflammatory lesions are
usually small and surrounded by normal tissue.

A

Focal

63
Q

If it is well demarcated, the lesion
is said to be

A

discrete

64
Q

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

A

diffuse focal

65
Q

lesions represent several scattered foci of inflammation.

A

Multi-focal

65
Q

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

A

locally extensive.

65
Q

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

A

Diffuse

66
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

67
Q

are produced from the reduction of oxygen by
inflammatory cells, particularly during respiratory burst of phagocytic cells. Also,
damage to cellular membranes could lead to the production of these extremely
toxic products

A
68
Q

such as singlet oxygen, superoxide, hydrogen anion,
hydrogen peroxide, and hydroxyl radicals cause damage to tissues by reacting
with cellular membranes generating a series of lipid peroxides, lipid
hydroperoxides, and aldehydes that in turn damages membrane proteins such
as transport proteins.

A
69
Q

is essentially a protective mechanism of the body enabling it to
react to various noxious agents and localize them.

A
70
Q

Clinical Correlations
These reactions include the following:

A

Fever
Changes in blood cell composition
Reactive changes in organs or tissues.
Changes in circulating enzyme levels

71
Q

are substances that induce fever, and these include endogenous
pyrogens released from neutrophils and monocytes.

A

Pyrogens

71
Q

In events of inflammation, the hypothalamus is depressed by circulating pyrogens and the body thermostat is set at a higher level.

A
71
Q

A fairly constant accompaniment of inflammation, fever or pyrexia is the
rise in body temperature.

A

Fever

72
Q

the fever increased fluid loss
sufficient to cause sodium depletion, circulatory and renal failure.

A
72
Q

It can also
increase metabolism and cause excessive protein breakdown when prolonged.

A
73
Q

Depending on the cause of inflammation,
there may be clinically detectable changes in the blood cell composition.

A

Changes in blood cell composition.

74
Q

. Total
leucocyte counts may either be increased (leukocytosis) due to increased
mobilization from the peripheral pool and increased production in the bone
marrow, o

A
75
Q

may be decreased (leucopenia) when bone marrow production is
depressed.

A
76
Q

These changes are part of the
inflammatory reactions and include fibrosis, reactive hyperplasia (increase in
cellular components) of the draining lymph nodes, and degenerative changes in
the affected organ or tissue as result of toxic substances.

A

Reactive changes in organs or tissues.

77
Q

Depending on the organ involved, some
enzymes could be detected to have increased levels in the plasma.

A

Changes in circulating enzyme levels.

78
Q

two processes of healing:

A

healing by repair
healing by regeneration.

79
Q

occur at sites where there is only minimal loss of tissue, inflammation is moderate, and the tissue defect is closely apposed such
as a cut or surgical wound.

A

Healing by first intention

80
Q

The process involved in healing by second intention, also called healing
by
is similar to healing by first intention

A

granulation

80
Q

Regeneration 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

Healing by Regeneration

80
Q

is derived from its gross
appearance that is pink, soft
and granular (

A
80
Q

When inflammation is complete and has successfully eliminated the
noxious agent, repair by resolution follows. However, this could only occur when
there is minimal damage.

A

Repair by Resolution

80
Q

This tissue that fill-in the
gap is called

A

granulation tissue

80
Q

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

A

Labile cells

80
Q

These include the cells of the epithelial surfaces, lymphoid and hematopoietic
cells.
Included among the epithelial surfaces are the epidermis, lining of the buccal cavity, gastrointestinal tract, respiratory tract, genital tract, and the duct lining of most organs.

A
81
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, and possibly equal that of the
entire lifespan of the individual.

A

Stable cells

81
Q

In cases where there is incomplete resolution of inflammation, repair by
organization follows.
Fibroblasts and capillary loops proliferate and fill the gap, and progressive fibrosis develops. Inflammation may or may not be actively proceeding.
This leaves the tissue to remain scarred creating permanent
structural and functional damage.

A
82
Q

This includes the parenchymal cells of all
glands in the body such as the liver, pancreas, salivary glands, kidney
tubular epithelia, glands of the skin, the mesenchymal cells of the body
and their derivatives (e.g., fibroblast, chondroblast, osteoblast, and
adipose tissue), endothelial cells, and smooth muscle cells.

A
83
Q

Axonal damage, the nerve cells are
capable of replacing severed axonal processes provided that the pre-
existing pathway of the degenerated axon is followed, otherwise, the regrowth may give rise to mass of tangled fibers sometimes called

A

“amputation or traumatic neuroma”

83
Q

these cells cannot regenerate and therefore damage
to these cells represents permanent loss. It includes neurons, skeletal and
cardiac muscle cells.

A

Permanent cells

83
Q

Two aberrations could occur in either of the first or second intention repair
process. First, there may occur accumulation of excessive amounts of collagen
giving rise to a protruding tumor-like scar tissue known as

A

keloid

84
Q

Second, there may be excessive formation of granulation
tissues that protrudes above the level of injury. This is known as e

A

exuberant
granulation or proudflesh.

85
Q

Factors Influencing Healing

A
  1. Tissue involved
  2. Vascularity
  3. Protective covering
  4. Nutrition
  5. Hormones
  6. Age
  7. Magnitude of injury
  8. Presence of infection
  9. Presence of nerve supply
86
Q

This would determine whether the healing process is through repair, regeneration, or a combination of both

A

Tissue involved

86
Q

an adequate blood supply is essential for the inflammatory
process and the ensuing healing.

A

Vascularity

87
Q

Avascular areas do not heal and is a
feature of certain fractures such as the neck of femur, and ulna and carpal
scaphoid where avascular necrosis often result with non-union of
structures.

A
88
Q

the initial blood clot that covers the area of injury is essential for repair. Removal of which delays the healing process.

A

Protective covering

89
Q

Vitamin C and vitamin D are essential for the healing process for they involved in polymerization and thus maturation of collagen.
In avitaminosis C, healing may be completely absent

A

Nutrition

90
Q

thyroid hormones are necessary for healing for they regulate
metabolic activities.

A

Hormones

91
Q

the presence of adequate sensory nerve
supply is essential for healing, and its absence delays the healing process
for some unknown reasons

A

Presence of nerve supply –

91
Q

the continued presence of infectious particles,
including foreign bodies retards the healing process

A

Presence of infection

91
Q

– injured tissues from young subjects heal more easily than geriatric
animals.

A

Age

91
Q

– the degree of injury determines whether healing by
repair is by first or second intention, or whether regeneration is possible.

A

Magnitude of injury

5 -PATHOLOGYYYY (4 decks)

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