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HCT lab Module 1.2 > HCT lab module 1.2 > Flashcards

HCT lab module 1.2 Flashcards

1
Q

A protective response, designed to remove the organism of both the initial cause of cell injury

(e. g. microbes, toxins) and the consequences of such injury (e.g. necrotic cells and
tissues) .

A

Inflammation

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2
Q

The local response of living mammalian tissues to injury due to any agent that disturb the normal steady state.

A

inflammation

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3
Q

A dynamic process, evolving through several

phases that last from a few minutes to days or even months and years.

A

inflammation

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4
Q

Inflammation of sudden onset and short duration

A

acute inflammation

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5
Q

Inflammation lasts a long time

A

chronic inflammation

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6
Q

[T or F] Inflammation occurs only in multicellular organisms that are capable of mounting a neuromuscular and cellular response to injury

A

True

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7
Q

[T or F] Inflammation occurs only in living tissues.

A

True

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8
Q

[T or F] The inflammatory response is not closely intertwined with the process of repair.

A

false

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9
Q

4 cardinal signs of inflammation

State both roman and english name:

A

✓ rubor (redness)
✓ tumor (swelling);
✓ calor (heat); and
✓ dolor (pain)

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10
Q

Who presented the 4 cardinal signs of inflammation? When was it introduced?

A

Roman writer Celsus in 1st century A.D.

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11
Q

Fifth sign of inflammation added by Virchow

A

functio laesa (loss of function)

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12
Q

[T or F] The word inflammation means flaming.

A

False - burning

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13
Q

is of short duration (lasting less than 2weeks) and represents the early body reaction, resolves quickly and is usually followed by healing.

A

Acute inflammation

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14
Q

is of longer duration and occurs either after the causative agent of acute inflammation persists for
a long time, or the stimulus is such that it induces chronic inflammation from the
beginning.

A

Chronic Inflammation

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15
Q

the type of chronic inflammation in which

during the course of the disease, there are acute exacerbations of activity.

A

chronic active inflammation

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16
Q

The three major components of acute inflammation are:

A

✓ alterations in vascular caliber that lead to an increase in blood flow;
✓ structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation; and
✓ emigration of leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent

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17
Q

The major manifestations of acute

inflammation, compared to normal.

A

1 , Vascular dilation and increased blood flow (causing erythema and warmth);
2, extravasation and extravascular deposition of
plasma fluid and proteins(edema);
3, leukocyte emigration and accumulation in the site of injury.

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18
Q

Acute inflammatory response process can be divided into two:

A

I. Vascular events

II. Cellular events

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19
Q

The earliest response to tissue injury is the alteration in the microvasculature

  • alterations include: hemodynamic changes and changes in vascular permeability
A

Vascular events

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20
Q

earliest features of inflammatory response result from changes in the vascular flow and calibre of small blood vessels in the injured tissue.

A

Hemodynaic Changes

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21
Q

Progression of hemodynamic changes:

A
  1. Transient vasoconstriction
  2. Persistent progressive vasodilation
  3. local hydrostatic pressure
  4. Slowing or stasis
  5. Leukocyte margination
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22
Q

occur immediately irrespective of the type of
injury. Mild form injury, the blood flow may be reestablished in 3-5 seconds, and in more
severe injury, the vasoconstriction may last for about 5 minutes.

A

Transient vasoconstriction

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23
Q

involves mainly the arterioles, but to a
lesser extent, affects other components of the microcirculation like venules and
capillaries. This can be seen within half an hour of injury.

  • results in increased blood volume, which is responsible for the redness and warmth at the site of acute inflammation.
A

Persistent progressive vasodilation

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24
Q

results in transudation of fluid into the extracellular space. This is responsible for the swelling at
the local site of acute inflammation.

A

local hydrostatic pressure

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25
Q

causes increased concentration of

red cells raising blood viscosity.

A

Slowing or stasis

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26
Q

also known as the peripheral orientation of

leukocytes (mainly neutrophils) along the vascular endothelium.

A

Leukocyte margination

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27
Q

The leukocytes briefly sticks to the vascular endothelium before moving and migrating through the gaps between the endothelial cells and into extravascular space.

A

Emigration

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28
Q

In and around the inflamed tissue, there is accumulation of edema fluid in the interstitial
compartment which comes from blood plasma by escaping through the endothelial wall
of the peripheral vascular bed.

A

Altered Vascular Permeability

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29
Q

Filtrate of blood plasma without changes in

endothelial epermeability

A

Transudate

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30
Q

Edema of inflamed tissue associated with

increased vascular permeability

A

Exudate

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31
Q

Characterizes a Non-inflammatory edema

A

Transudate

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32
Q

Characterizes an inflammatory edema

A

Exudate

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33
Q

protein content: Low (less than 1g/dL); mainly albumin, low fibrinogen; hence no tendency to coagulate

A

Transudate

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34
Q

Protein content: High 2.5-3.5 g/dL), readily coagulates due to high content of fibrinogen and other coagulation factors

A

Exudate

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35
Q

Glucose Content: Same as in plasma

A

Transudate

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36
Q

Protein content: Low (less than 60 mg/dL)

A

Exudate

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37
Q

Specific gravity: Low (<1.015)

A

Transudate

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38
Q

Specific gravity: High (>1.018)

A

Exudate

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39
Q

pH: >7.3
pH: <7.3

A

Transudate

Exudate

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40
Q

Few cells, mainly mesothelial cells and
cellular debris

Example is edema in congestive heart failure

A

Transudate

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41
Q

Many cells, inflammatory as well as
parenchymal

Purulent exudate such as pus

A

Exudate

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42
Q

[T or F] In acute inflammation, normally non-permeable endothelial layer of the microvasculature becomes leaky

A

true

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43
Q

The mechanisms of increased vascular permeability are

Hint: 5 mechanisms

A
  1. Contraction of endothelial cells (contraction)
  2. Retraction of endothelial cells (retraction)
  3. Direct injury to endothelial cells (direct injury)
  4. Endothelial injury mediated by
    leukocytes (Endothelial injury by leukocytes)
  5. Leakiness in neovascularisation (leakiness)
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44
Q

most common mechanism of increased leakiness that affects venules exclusively
while capillaries and arterioles remain unaffected

A

Contraction of endothelial cells

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45
Q

It is mediated by the release of histamine, bradykinin and other chemical mediators.

A

Contraction of endothelial cells.

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46
Q

The response begins immediately after injury, usually reversible, and for short duration only
(15-30 minutes).

A

Contraction of endothelial cells

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47
Q

In this mechanism, there is structural reorganization of the cytoskeleton of endothelial cells that causes reversible retraction at the intercellular junctions.

A

Retraction of endothelial cells

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48
Q

This change affects venules and is mediated by cytokines like interleukin-1 (IL-1) and tumor necrosis factor (TNF)-α.

A

Retraction of endothelial cells

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49
Q

The onset of response takes 4-6 hours after injury and lasts for 2-4 hours or more (somewhat delayed and prolonged leakage).

A

Retraction of endothelial cells

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50
Q

Example of such immediate transient leakage is mild thermal injury of skin of forearm.

A

Contraction of endothelial cells

51
Q

The example of this type of response

exists in vitro experimental work only

A

Retraction of endothelial cells

52
Q

results to cell necrosis and appearance of
physical gaps at the sites of detached
endothelial cells

A

Direct injury to endothelial cells

53
Q

The increased permeability may either appear immediately after injury and last for several hours or days (immediate sustained leakage), or may occur after a delay of 2-12 hours and last for hours or days (delayed prolonged leakage).

A

Direct injury to endothelial cells

54
Q 
The examples of immediate sustained
leakage are severe bacterial infections
while delayed prolonged leakage may
occur following moderate thermal
injury and radiation injury.
A

Direct injury to endothelial cells

55
Q
  • Occurs mainly in venules
  • Induced by histamine. NO. other mediators
  • Rapid and short-lived (minutes)
A

Retraction of endothelial cells

56
Q
  • Occurs in arterioles, capillaries, venules
  • Caused by burns, some microbial toxins
  • Rapid, may be long-lived (hours to days)
A

Direct injury to endothelial cells/ Endothelial injury

57
Q

Adherence of leukocytes to the
endothelium at the site of inflammation
may result in activated leukocytes
which release proteolytic enzymes and toxic oxygen species causing this and increased vascular easiness affects mostly venue and is a late response.

A

Endothelial injury mediated by

leukocytes

58
Q
  • Occurs in venules, pulmonary capillaries
  • Associated with late stages of inflammation
  • Long-lived (hours)
A

Endothelial injury mediated by
leukocytes/LEUKOCYTE-MEDIATED
VASCULAR INJURY

59
Q
  • Occurs in venules

* Induced by VEGF

A

Leakiness in neovascularisation/INCREASED

TRANSCYTOSIS

60
Q

The cellular phase of inflammation consists of 2 processes:

A

exudation of leukocytes

phagocytosis

61
Q

most important feature of inflammatory response.

consists of normal axial flow, margination of pavementing, rolling and adhesion, and emigration and diapedesis

A

Exudation of Leukocytes

62
Q

In acute inflammation,

___________________ comprise the first line of body defense, followed later by monocytes

A

polymorphonuclear neutrophils (PMNs)

63
Q

Due to slowing and
stasis, the central stream of cells widens and peripheral plasma zone becomes
narrower due to loss of plasma by exudation. This is called?

A

margination

64
Q

Neutrophils of the central column come close to the vessel wall

A

pavementing

65
Q

consists of central stream of cells comprised by leukocytes and RBCs and peripheral cell-free layer of plasma close to the vessel wall

A

Normal axial flow

66
Q

substances responsible for Rolling and Adhesion

A

Selectins, integrins and immunoglobulin gene superfamily adhesion molecule (ICAM)

67
Q

Peripherally marginated and pavemented neutrophils slowly roll over the endothelial
cells lining the vessel wall

A

Rolling phase

68
Q

The transient bond between

the leukocytes and endothelial cells becomes firmer

A

Adhesion phase

69
Q

neutrophils lodged between the endothelial
cells and basement membrane cross the basement membrane by damaging it locally
with secreted collagenases and escape out into the extravascular space

(damage is repaired immediately)

A

Emigration

70
Q

[T or F] Neutrophils are the dominant cells in acute inflammatory exudate in the first 24 hours,
and monocyte-macrophages appear in the next 24-48 hours.

A

True

71
Q

[T or F] neutrophils are short-lived (24-48 hours) while monocyte-macrophages survive much longer

A

True

72
Q

passive phenomenon where RBCs are being forced out either by raised hydrostatic pressure or may escape through the endothelial defects left after emigration of leukocytes.

-gives hemorrhagic appearance to the
inflammatory exudate.

A

Diapedesis

73
Q

Defined as locomotion oriented along a chemical gradient.

A

Chemotaxis

74
Q

[T or F] In Chemotaxis, Both exogenous and

endogenous substances can act as chemoattractants.

A

True

75
Q

agents that act as potent chemotactic substances or chemokines for neutrophils:

A
  • Leukotriene B4 (LT-B4)
  • Components of complement system (C5a and C3a)
  • Cytokines (Interleukins, IL-8)
  • Soluble bacterial products (formylated peptides)
76
Q

a product of lipooxygenase pathway of arachidonic acid metabolites

A

Leukotriene B4 (LT-B4)

77
Q

Aside from neutrophils, other inflammatory cells respond and participate in inflammation and there are also chemokines for them. State the examples:

A
  • eotaxin chemotactic for eosinophils

- NK cells for recognizing virally infected cells,

78
Q

Defined as the process of engulfment of solid particulate material by the cells.

A

Phagocytosis

79
Q

The cells engulfing of solid particulate material are called:

A

Phagocytes

80
Q

2 main types of phagocytes:

A 
Polymorphonuclear neutrophils (PMNs) 
Macrophage
81
Q
A

Polymorphonuclear neutrophils (PMNs) which appear early in acute inflammatory
response
2. Circulating monocytes and fixed tissue mononuclear phagocytes, commonly known as
macrophage

81
Q

Type of phagocyte which appear early in acute inflammatory response

A

Polymorphonuclear neutrophils (PMNs)

82
Q

[type of phagocyte] other term for macrophage

A

Circulating monocytes and fixed tissue mononuclear phagocytes

83
Q

Proleolytic enzymes produced by neutrophils and macrophages which degrade collagen and extracellular matrix.

hint: [mnemonic] LPCELPGA

A

lysozyme, protease, collagenase, elastase, lipase, proteinase, gelatins, and acid hydrolyses.

84
Q

Stages of phagocytosis

A

A, Opsonization of the particle.
B, Pseudopod engulfing the opsonized particle.
C, Incorporation within the cell (phagocytic vacuole)
and degranulation.
D, Phagolysosome formation after fusion of lysosome of the cell.

85
Q

[recognition and attachment] Phagocytosis is initiated by the expression of surface receptors on macrophages which recognize microorganisms: __________ and __________

A

mannose receptor and scavenger receptor

86
Q

[recognition and attachment] The process of
phagocytosis is further enhanced when the microorganisms are coated with specific
proteins called:

A

Opsonins

87
Q

[recognition and attachment] establish a bond between bacteria and the cell membrane of phagocytic cell.

A

Opsonins

88
Q

After a particle is bound to phagocyte receptors, extensions of the cytoplasm
(pseudopods) flow around it, and the plasma membrane pinches off to form a vesicle
(phagosome) that encloses the particle. The phagosome then fuses with a lysosomal
granule, resulting in discharge of the granule’s contents into the phagolysosome.

A

Engulfment

89
Q

[killing and degradation] The microorganisms being killed by antibacterial substances are degraded by _________.

A

Hydrolytic enzymes

90
Q

[T or F] The substances acting as chemical mediators of inflammation may be released from the cells, the plasma, or damaged tissue itself.

A

True

91
Q

The substances acting as chemical mediators of inflammation is broadly classified into to groups, this are:

A

mediators released by cells

mediators originating from plasma

92
Q

Cell-derived mediators

A
  1. Vasoactive amines (Histamine, 5 hydroxytryptamine, neuropeptides)
  2. Arachidonic acid metabolites (Eicosanoids)
    • Metabolites via cyclo-oxygenase pathway (prostaglandins, thromboxane A2, prostacyclin
    resolvins)
    • Metabolites via lipo-oxygenase pathway (5-HETE, leukotrienes, lipoxins)
  3. Lysosomal components (from (PMNs, macrophages)
  4. Platelet activating factor
  5. Cytokines (IL-1, TNF-a, TNF-B, IFN-ɣ, chemokines)
  6. Free radicals (Oxygen metabolites, nitric oxide)
93
Q

Plasma-derived mediators (Proteases)

A

Products of:

  1. The kinin system
  2. The clotting system
  3. The fibrinolytic system
  4. The complement system
94
Q

[T or F] The cells participating in acts and chronic inflammation are stationary leukocytes, plasma cells and tissue macrophages.

A

False - circulating

95
Q

Commonly called as neutrophils or polymorphs

A

Polymorphonuclear Neutrophils (PMNs)

96
Q

Contain granules in their cytoplasm (contains proteases, myeloperoxidase, lysozyme,
esterase, aryl sulfatase, acid and alkaline phosphatase, and cationic proteins.

A

Polymorphonuclear Neutrophils (PMNs)

97
Q

These cells comprise 40-70% of circulating leukocytes and their number is increased in
blood (neutrophilia) and tissues in acute bacterial infections

A

Polymorphonuclear Neutrophils (PMNs)

98
Q

Functions:
✓ “Initial phagocytosis” of microorganisms as they form the first line of body defense in
bacterial infection.
✓ “Engulfment” of antigen-antibody complexes and non-microbial material
✓ “Harmful effect” of neutrophils in causing basement membrane destruction of the
glomeruli and small blood vessels.

A

Polymorphonuclear Neutrophils (PMNs)

99
Q

These are larger than neutrophils but are fewer in number, comprising 1-6% of total blood
leukocytes

A

Eosinophils

100
Q

Granules in the cytoplasm contain a variety of enzymes, of which major basic protein
and eosinophil cationic protein are the most important which have bactericidal and toxic
action against helminthic parasites

A

Eosinophils

101
Q

conditions where eosinophils are increased:

A

✓ allergic conditions;
✓ parasitic infestations;
✓ skin diseases; and
✓ certain malignant lymphomas

102
Q

comprise about 1% of circulating leukocytes

A

Basophils (Mast Cells)

103
Q

These cells contain coarse basophilic granules in the cytoplasm and a polymorphonuclear
nucleus.

A

Basophils (Mast Cells)

104
Q

These granules are laden with heparin and histamine

A

Basophils (Mast Cells)

105
Q

Have receptors for IgE and degranulate when cross-linked with antigen

A

Basophils (Mast cells)

106
Q

Functions:
✓ In immediate and delayed type of hypersensitivity reactions; and
✓ release of histamine by Ig-E sensitized basophils.

A

Basophils (Mast cells)

107
Q

Next to neutrophils, these cells are the most numerous of the circulating leukocytes
(20-45%).

A

Lymphocytes

108
Q

They have scanty cytoplasm and consist almost entirely of nucleus

A

Lymphocytes

109
Q

Function:
✓ In tissues, they are dominant cells in chronic inflammation and late stage of acute
inflammation.
✓ In blood, their number is increased (lymphocytosis) in chronic infections like
tuberculosis.

A

Lymphocytes

110
Q

These cells are larger than lymphocytes with more abundant cytoplasm and eccentric
nucleus which has cart-wheel pattern of chromatin

A

Plasma cells

111
Q

inflammatory cells normally not seen in peripheral blood.

A

Plasma cells

112
Q

[T or F] There is an interrelationship between plasmacytosis and hyperglobulinemia

A

True

113
Q

These cells are most active in antibody synthesis

A

Plasma cells

114
Q

plasma cells are increased in conditions like:

A

✓ prolonged infection with immunological responses (e.g. syphilis, rheumatoid arthritis,
tuberculosis);
✓ hypersensitivity states; and
✓ multiple myeloma

115
Q

This cell system includes cells derived from 2 sources with common morphology, function
and origin

A

Mononuclear-Phagocyte System (Reticuloendothelial System)

116
Q

Mononuclear-Phagocyte System (Reticuloendothelial System) is derived from 2 sources. What are they?

A

Blood monocytes

Tissue macrophages

117
Q

These comprise 4-8% of circulating leukocytes

A

Blood monocytes

118
Q 
[Mononuclear-Phagocyte System (Reticuloendothelial System)] source of the cell system which includes the following]
• Macrophages in inflammation
• Histiocytes in connective tissues
• Kupffer cells in liver cells
• Alveolar macrophages in lungs
• Osteoclasts in the bones
• Microglial cells of the brain
• Langerhans’ cells/dendritic histiocytes of the skin
• Mesangial cells of glomerulus
A

Tissue macrophages

119
Q

These are the scavenger cells of the body as well as participate in immune system of the body

A

Mononuclear-Phagocyte System (Reticuloendothelial System)

120
Q

Functions:
✓ Phagocytosis
✓ Macrophages on activation by lymphokines

A

Mononuclear-Phagocyte System (Reticuloendothelial System)

121
Q

In chronic inflammation, when the macrophages fail to deal with particles to be removed,
they fuse together and form multinucleate ________.

A

Giant cells

122
Q

Giant cells observed in inflammation:

A

✓ Foreign body giant cells
✓ Langhans’ giant cells
✓ Touton giant cells
✓ Aschoff giant cells

123
Q

Giant cells observed in tumors:

A

✓ Anaplastic cancer giant cells
✓ Reed-Sternberg cells
✓ Giant cell tumor of the bone

HCT lab Module 1.2 (1 decks)

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