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HistoPathology > [P] Week 2: Inflammation and Repair - Part 2 > Flashcards

[P] Week 2: Inflammation and Repair - Part 2 Flashcards

1
Q

Enumerate the steps of phagocytosis

A
  1. Recognition and Attachment
  2. Engulfment
  3. Killing and Degradation
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2
Q

STEPS OF PHAGOCYTOSIS

Involves the recognition and attachment of the particle to be
ingested by the leukocyte

A

Recognition and Attachment

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3
Q

STEPS OF PHAGOCYTOSIS

this receptors enable phagocytes to bind and ingest microbes

A

Mannose receptors, scavenger receptors, and receptors
for various opsonins

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4
Q

STEPS OF PHAGOCYTOSIS

Consists of the extension of the cytoplasm around the particle, and the plasma membrane pinches off to form an intracellular vesicle called the PHAGOSOME, which encloses the particle.

A

Engulfment

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5
Q

STEPS OF PHAGOCYTOSIS - Engulfment

The phagosome then fuses with a lysosomal granule, which discharges its contents into the?

A

PHAGOLYSOSOME

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6
Q

STEPS OF PHAGOCYTOSIS

Involves the killing of the microbe and degradation of the
ingested material

A

Killing and degradation

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7
Q

STEPS OF PHAGOCYTOSIS

Killing of microbes is accomplished by? enumerate

A
  • Reactive oxygen species (ROS)
  • Reactive nitrogen species (mainly derived from and nitric oxide (NO))
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8
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

produced by the rapid assembly and activation of a multicomponent oxidase nicotinamide adenine dinucleotide phosphate (NADPH) oxidase which oxidizes reduced NADPH and, in the process, reduces oxygen to superoxide anion–making it highly reactive

A

Reactive Oxygen Species

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9
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

superoxide from the NAPDH oxidization can be converted to?

A

hydrogen peroxide

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10
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

Hydrogen peroxide may not efficciently kill microbes, so it should be combined with?

A
  • myeloperoxidase (MPO)
  • Halide (such as chloride to convert to HCl)
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11
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

give an example of an ROS

A

hydrogen peroxide myeloperoxidase (H2O2-MPO) halide system

most potent bactericidal system of the neutrophils

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12
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

a soluble gas produced from arginine by the action of nitric oxide
synthase (NOS), also participates in microbial killing.

A

Reactive Nitrogen Species: Nitric Oxide

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13
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

what are the three types of NOS

A
  • endothelial nitric oxide synthase (eNOS)
  • neuronal nitric oxide synthase (nNOS)
  • inducible nitric oxide synthase (iNOS)
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14
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

constitutively expressed at low levels, and the NO they generate functions to maintain vascular tone and as neurotransmitter, respectively

A

eNOS and nNOS

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15
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

This NO is type that is involved in microbial killing, is induced when macrophages are activated by cytokines.

A

iNOS

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16
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

in macrophage what is the mechanism of NO so that it will attack and damage the microbe

A

NO reacts with a superoxide to
generate the highly-reactive free radical PEROXYNITRITE

NO + Superoxide = Peroxynitrite

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17
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

Granules, may be categorized as?

A
  • Smaller specific (secondary) granules
  • Larger azurophilic (primary) granules
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18
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

this granule contains the:

lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, alkaline phosphatase

A

Secondary granules

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19
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

this granule contains the:

myeloperoxidase, bactericidal proteins such as lysozymes and defensins, acid hydrolases, and a variety of neutral proteases such
as elastase, cathepsin G, non-specific collagenase, and
proteinase 3

A

Primary granules

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20
Q

STEPS OF PHAGOCYTOSIS - Killing and degradation

this granule contains the:

defencins, cathelicidins, lysozyme, lactoferrin, and the major basic
protein, which is usually present in eosinophils

A

Other microbicidal granule

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21
Q

This mechanism are present in order to combat the action of these free radicals

A

Antioxidant Mechanism

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22
Q

Antioxidant Mechanism may be in the form of?

A
  • Superoxide dismutase
  • Catalase
  • Glutathione peroxidase
  • Ceruloplasmin
  • Transferrin
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23
Q

Extracellular fibrillar networks that provide a high concentration of antimicrobial substances at sites of
infection and trap microbes, helping to prevent their spread

A

NEUTROPHIL EXTRACELLULAR TRAPS (NETs)

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24
Q

LEUKOCYTE-MEDIATED TISSUE INJURY

Leukocytes are important causes of injury to normal cells and tissues under several circumstances:

As part of the normal defense reaction against infectious
microbes, when ____ tissues suffer collateral
damage

A

Adjacent

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25
Q

LEUKOCYTE-MEDIATED TISSUE INJURY

Leukocytes are important causes of injury to normal cells and tissues under several circumstances:

In some infections that are difficult to eradicate, such as tuberculosis, and certain viral diseases, the ____ ____ ____ contributes more to the pathology that does the microbe itself.

A

prolonged host response

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26
Q

LEUKOCYTE-MEDIATED TISSUE INJURY

Leukocytes are important causes of injury to normal cells and tissues under several circumstances:

When the inflammatory response is inappropriately directed against host tissues, as in certain _____ _____

A

Autoimmun diseases

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27
Q

LEUKOCYTE-MEDIATED TISSUE INJURY

Leukocytes are important causes of injury to normal cells and tissues under several circumstances:

When the host reacts excessively to against usually harmless environmental substance, as in ____ ____, including asthma

A

Allergic diseases

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28
Q

OTHER FUNCTIONAL RESPONSES OF ACTIVATED LEUKOCYTES

Activated leukocytes play several other roles in host defense, enumerate

A
  1. Produce Cytokines (either amplify or limit inflammatory reactions)
  2. Produce Growth Factors (stimulate the proliferation of endothelial cells and fibroblasts and the synthesis of collagen, and enzymes that remodel connective tissues.)
  3. Production of Th17 (IL-17) cells (induces the secretion of chemokines that recruit other leukocytes)
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29
Q

KINDLY CHECK

A

CLINICAL EXMPALES OF LEUKOCYTE INJURY, ACUTE AND CHRONIC PLEASE LANG

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30
Q

DEFECT IN LEUKOCYTE FUNCTIONS (GENETIC)

Match

  1. Leukocyte adhesion def 1
  2. Leukocyte adhesion def 2
  3. Chronic granulomatous disease
  4. MPO def
  5. Chediak Higashi syndrome

A. Mutations in fucosyl transferase
B. Decrease oxidative burst
C. Mutations in B chain of CD11/CD18 integrins
D. Mutations affecting protein involved in lysosomal membrane traffic
E. Defective MPO H2O2 system

A
  1. C
  2. A
  3. B
  4. E
  5. D
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31
Q

DEFECT IN LEUKOCYTE FUNCTIONS (ACQUIRED

Match

  1. Bone marrow suppression
  2. Diabetes, malignancy, sepsis, chronic dialysis
  3. Leukemia, anemia, sepsis,
    diabetes, malnutrition

A. Adhesion and Chemotaxis
B. Phagocytosis and Microbicidal activity
C. Production of Leukocyte

A
  1. C
  2. A
  3. B
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32
Q

DEFECTS IN LEUKOCYTE FUNCTION

defect in phagolysosome function seen in?

A

Chediak-Higashi syndrome

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33
Q

DEFECTS IN LEUKOCYTE FUNCTION

Inherited defects in ____ ____ like in chronic granulomatous disease wherein there is inherited defects in
the genes encoding components of phagocyte oxidase

A

microbicidal activity

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34
Q

DEFECTS IN LEUKOCYTE FUNCTION

may lead to marrow suppression

A

Acquired deficiencies

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35
Q

DEFECTS IN LEUKOCYTE FUNCTION

cells in tissue that serve important functions in initiating acute inflammation.

A

Mast cells and macrophages

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36
Q

DEFECTS IN LEUKOCYTE FUNCTION

defect of integrins and selectin ligands which may lead to recurrent bacterial infection.

A

Inherited defect in leukocyte adhesion

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37
Q

TERMINATION OF ACUTE INFLAMMATORY RESPONSE

When the cells were able to control the infection, there must be a?

A

termination of the inflammatory response

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38
Q

TERMINATION OF ACUTE INFLAMMATORY RESPONSE

Note that inflammation is a?

A

DOUBLE-EDGED SWORD

(it is protective but it can also cause damage to the normal cells or tissues)

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39
Q

TERMINATION OF ACUTE INFLAMMATORY RESPONSE

nfammation declines after the offending agents are
removed simply because the mediators of inflammation: ENUMERATE

A
  • Are produced in rapid burst as long as the stimulus persists
  • Have short half-lives
  • Are degraded after their release (easily destroyed)
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40
Q

TERMINATION OF ACUTE INFLAMMATORY RESPONS

it should produce what anti-inflammatories?

A
  • anti-inflammatory lipoxins
  • anti-inflammatory cytokines
  • anti-inflammatory lipid mediators
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41
Q

MEDIATORS OF INFLAMMATION

substances that initiate
and regulate inflammatory reactions.

A

Inflammatory mediators

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42
Q

MEDIATORS OF INFLAMMATION

Mediators are generated either from?

A

cells or from plasma
proteins.

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43
Q

MEDIATORS OF INFLAMMATION

this mediator are produced in response to active stimuli

A

Active mediators

44
Q

MEDIATORS OF INFLAMMATION

TOF

One mediator can stimulate the release of another mediator

A

eurt

45
Q

MEDIATORS OF INFLAMMATION

TOF

Mediators vary in their range of cellular suspect

A

False

cellular target not suspect

46
Q

MEDIATORS OF INFLAMMATION

Once activated and released from the cell, most of these mediators are?

A

Short lived

47
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

Histamine

A

Source: Mast cells (predominant), basophils, platelets

Action: Vasodilation, increased
vascular permeability,
endothelial activation

48
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

Prostaglandins

A

Source: Mast cells and leukocytes

Actions: Vasodilation, pain, fever

49
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

Leukotrienes

A

Source: Mast cells and leukocytes

Action: Increased vascular permeability, chemotaxis, leukocyte adhesion and activation

50
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

Cytokines
(TNF, IL-1)

A

Source: Macrophages,
endothelial cells, mast cells

Action: Local endothelial activation, fever/pain/anorexia/hypotension, decreased vascular resistance

51
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

Chemokines

A

Source: Leukocytes, activated macrophages

Action:Chemotaxis, leukocyte
activation

52
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

PAF

A

Source: Leukocytes, mast cells

Action: Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation,
oxidative burst

53
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

Complement
(C5a, C3a,
C4a)

A

Source: Plasma (produced in liver)

Action: Leukocyte chemotaxis and activation, vasodilation

54
Q

ACTION OF PRINCIPAL MEDIATORS

Give the source and action of the mediators:

Kinins

A

Source: Plasma (produced in liver)

Action: Increased vascular permeability, smooth muscle contraction, vasodilation, pain

55
Q

this mediators are normally sequestered in intracellular granules and can be rapidly secreted by granule exocytos or are synthesized de novo

A

Cell-derived mediators

56
Q

CELL-DERIVED MEDIATORS

  • Important action in blood vessels
  • First mediators to be released
A

Vasoactive Amines: Histamine and Serotonin

57
Q

CELL-DERIVED MEDIATORS - Vasoactive Amine

▪ Mostly coming from mast cells; basophil, platelet

A

Histamine

58
Q

CELL-DERIVED MEDIATORS - Vasoactive Amine

Stimuli that may trigger the secretion of this mediator:
- Physical injury
- Binding of antigen to IgE antibodies displayed on the surfaces of mast cell
- Fragments of complement (anaphylatoxin) C3a & C5a
- Histamine releasing protein derived from leukocytes
- Neuropeptides (substance P)
- Cytokines (IL-1, IL-8)

A

Histamine

59
Q

CELL-DERIVED MEDIATORS - Vasoactive Amine

this mediator causes dilatation of arterioles and increased permeability of venules

A

Histamine

60
Q
A
61
Q

CELL-DERIVED MEDIATORS - Vasoactive Amine

Histamine vasoactive effects are mediated mainly via binding to?

A

H1 receptors on microvascular endothelial cells

62
Q

CELL-DERIVED MEDIATORS - Vasoactive Amine

It is a vasoconstrictor, but the importance of this action in inflammation is unclea

A

Serotonin (5-hydroxytryptamine)

63
Q

CELL-DERIVED MEDIATORS - Vasoactive Amine

A preformed vasoactive mediator present in platelets and certain neuroendocrine cells

A

Serotonin (5-hydroxytryptamine)

64
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

AA converted by action of enzymes to produce?

A

prostaglandin and leukotrien

65
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

AAis a 20-carbon polyunsaturated fatty acid that is derived from?

A

dietary sources or by synthesis from a precursor molecule, linoleic acid

66
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

AA-derived mediators, also called

A

eicosanoids

67
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

AA-derived mediators, also called eicosanoids, are synthesized by two major classes of enzymes:

A
  • Cyclooxygenases (which generate prostaglandins)
  • Lipoxygenases (which produce leukotrienes and lipoxins
68
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

Match

Action:
1. Vasodilation
2. Vasoconstriction
3. Increase Vascular permeability
4. Chemotaxis, and leukocyte adhesin

Eicosanoid:
A. Leukotriene B4, HETE (Hydroxyeicosatetraenoic acid)
B. Thromboxane A2, leukotrienes C4, D4, E4
C. PGI2 (prostacyclin), PGE1, PG32, PGD2
D. Leukotrienes C4, D4, E4

A
  1. C
  2. B
  3. D
  4. A
69
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

▪ Produced by mast cells, macrophages, endothelial cells and other cells
▪ They are generated by the actions of two cyclooxygenases, called COX-1 and COX-2.

A

Prostaglandins (PGs

70
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

Prostaglandin are involved in pathogenesis of ____ and ____ in inflammation.

A

Pain and Fever

71
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

produced in leukocytes and mast
cells by the action of lipoxygenase and are involved in vascular and smooth muscle reactions and leukocyte recruitment

A

Leukotrienes

72
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

Secreted mainly by ____, forming leukotrienes
and lipoxines

A

leukocytes

73
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

There are three different lipoxygenases, ____being the predominant one in neutrophils

A

5-lipoxygenase

74
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

This enzyme converts AA to 5 hydroxyeicosatetraenoic acid, which is chemotactic for neutrophils and is the precursor of the leukotrienes

A

lipoxygenases

75
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

hoiw many lipoxygenases lead to production of lipoxins?

A

12 lipoxygenases

76
Q

CELL-DERIVED MEDIATORS - Arachidonic Acid (AA) Metabolites

inhibitors of inflammation inhibiting
leukocyte recruitment & cellular components of inflammation

A

Lipoxins

77
Q

Enumerate the Pharmocologic inhibitors of prostaglanding and leukotrienes

A
  1. Cyclooxygenase inhibitors
  2. Lipoxygenase inhibitors
  3. Corticosteroids
  4. Leukotriene receptor antagonists
78
Q

Pharmocologic inhibitors of prostaglanding and leukotrienes

Enumerate what Cyclooxygenase inhibitors inhibits

A

COX-1 and COX-2

79
Q

Pharmocologic inhibitors of prostaglanding and leukotrienes

Are broad spectrum antiinflammatory agents that reduce the transcription of genes encoding many proteins involved in inflammation

A

Corticosteroids

80
Q

Produced mainly by macrophages, lymphocytes and dendritic cells

A

Cytokines

81
Q

Cytokines

serve critical roles in leukocyte recruitment by promoting adhesion of leukocytes to endothelium and their migration through blood vessels.

A

TNF (tumor necrosis factor) and IL-1

82
Q

Are a family of small (8 to 10 kDa) proteins that act primarily as chemoattractants for specific types of leukocytes.

A

Chemokines

83
Q

What are the 4 major groups of chemokines, they are arranged according to the arrangement of cysteine (C) residues in the proteins

A
  1. C-X-C chemokines
  2. C-C chemokines
  3. C chemokines
  4. CX3C chemokines:
84
Q

OTHER MEDIATORS OF INFLAMMATION

  • Phospholipid derived mediator that may cause platelet aggregation, vasoconstriction,bronchoconstriction
  • A variety of cell types, including platelets, basophils, mast cells, neutrophils, macrophages, and endothelial cells,can elaborate PAF in both secreted and cell-bound forms
A

Platelet Activating Factor (PAF)

85
Q

What are the three outcomes of acute inflammatory

A
  1. Complete resolution
  2. Healing by connective tissue replacement
  3. Progress to chronic
86
Q

Enumerate the morphologic patterns of Acute inflmmation

A
  1. Serous Inflammation
  2. Fibrinous inflammation
  3. Purulent Inflammation and abscesses
  4. Ulcers

`

87
Q

morphologic patterns of Acute inflmmation

  • Outpouring of a thin fluid from plasma or secretions.
  • Accumulation of fluid in cavities called effusion.
A

Serous inflammation

88
Q

morphologic patterns of Acute inflmmation

fibrinogen pass out of the blood, and fibrin is formed and deposited in the extracellular space.

A

Fibrinous inflammation

89
Q

morphologic patterns of Acute inflmmation

Purulent inflammation is characterized by the production of pus

A

Purulent Inflammation and abscesses

`

90
Q

morphologic patterns of Acute inflmmation

A local defect, or excavation, of the surface of an organ or tissue

A

ulcers

91
Q

Causes of Chronic inflammation

A

a) Persistent infections
b) Immune mediated inflammatory response
c) Allergic dose
d) Prolonged exposure to potentially toxic agents

92
Q

MORPHOLOGIC FEATURE of chronic inflammation

A
  • Infiltration with mononuclear cells
  • Tissue destruction
  • Attempts at healing by connective tissue replacement of damaged tissue
93
Q

CELLS AND MEDIATORS OF CHRONIC INFLAMMATION

Enumerate the cells

A
  1. Macrophage
  2. Lymphocytes
  3. B Cells or Plasma Cells
  4. Eosinophils
  5. Mast cells
  6. Neutrophils

recall nalang kayo sa hema, diko na iddump info dito

94
Q

It is a form/pattern of chronic inflammation characterized by
collections of activated macrophages, often with T lymphocytes, and sometimes associated with necrosis

A

Granulomatous Inflammation

95
Q

Consisting of a microscopic aggregation of macrophages that are transformed into epithelium like cells, surrounded by a collar of mononuclear leukocytes, pricipally lymphocytes

A

GRANULOMA

96
Q

Granulomatous Inflammation

are activated macrophages, which forms epithelioid cells (resembles epithelial cells) and it is surrounded by inflammation — lymphocytes

A

Granuloma

97
Q

CLASSIFICATION OF GRANULOMA

Incited by relatively inert foreign bodies, like sutures, which induce inflammation in the absence of T cell-mediated immune responses.

A

Foreign Body Granuloma

98
Q

CLASSIFICATION OF GRANULOMA

  • They are caused by a variety of agents that are capable of inducing a persistent T cell-mediated immune response.
  • Inciting agent is poorly degradable or particulate
  • An example is granuloma in TB
A

Immune Granuloma

99
Q

SYSTEMIC EFFECTS OF INFLAMMATIO

Inflammation, even if localized, is associated with cytokineinduced systemic reactions that are collectively called the?

A

acute-phase response

100
Q

CLINICAL AND PATHOLOGIC CHANGES OF ACUTE PHASE RESPONSE

pyrogens that act by stimulating prostaglandin synthesis); LPS-exogenous; IL1, TNF-endogenou

A

Fever

101
Q

CLINICAL AND PATHOLOGIC CHANGES OF ACUTE PHASE RESPONSE

CRP, fibrinogen, serum amyloid A protein

A

Acute phase proteins

102
Q

CLINICAL AND PATHOLOGIC CHANGES OF ACUTE PHASE RESPONSE

a common feature of inflammatory
reactions, especially those induced by bacterial infections.

A

Leukocytosis

103
Q

CLINICAL AND PATHOLOGIC CHANGES OF ACUTE PHASE RESPONSE

In the clinics, we may observe on the patients what presentation?

A

increase pulse rate & bp,
and decrease sweating

104
Q

DEFECTIVE OR EXCESSIVE INFLAMMATION

results mainly in increased susceptibility to infection, delayed healing

A

Defective inflammation

105
Q

DEFECTIVE OR EXCESSIVE INFLAMMATION

Most common cause is leukocyte deficiency due to replacement of the bone marrow by leukemias and
metastatic tumors and suppression of the marrow by therapies for cancer and graft rejection

A

Defective inflammation

106
Q

DEFECTIVE OR EXCESSIVE INFLAMMATION

  • may lead to allergies and autoimmune diseases
  • It is the underlying cause of many human diseases
A

Excessive inflammation

107
Q
A

HistoPathology (10 decks)

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