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Pathology basic > Chapter 3, inflammation and Repair > Flashcards

Chapter 3, inflammation and Repair Flashcards

1
Q

Define inflammation?

A

a response of vascularized tissues to infections and tissue damage that brings cells and molecules of host defense from the circulation to the sites where they are needed, to eliminate the offending agents.
damaged cells secrete mediators such as (cytokines).

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2
Q

acute and chronic inflammation, differences.

A
  • acute inflammation: develops within hours and is of short duration. Edema results
  • Chronic inflammation: longer duration and is associated with more tissue destruction, lymphocytes and macrophages, the proliferation of blood vessels and fibrosis.
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3
Q

what are the external manifestations of inflammation (cardinal signs)?

A

-Heat (calor in latin)
-redness (rubor)
-swelling (tumor)
-pain (dolor)
-loss of function (functio laesa)
both excessive and defective inflammation can be harmful.

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4
Q

define scarring?

A

the residual defects with connective tissue due to missing cells that had been eliminated due to an inflammation

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5
Q

when is inflammation terminated?

A

it is terminated when the offending agent is eliminated. the cytokines are degraded and anti-inflammatory substances are released.

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6
Q

stimuli that will trigger inflammation?

A

-Infections (bacterial, viral, fungal, parasitic)
the morphologic pattern of the response can be useful in identifying its etiology.
-tissue necrosis
-foreign bodies (dirt, splinters, sutures)
-immune reactions

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7
Q

what type of receptor is used to detect infectious pathogens?

A

toll like receptors (TLR)

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8
Q

what do Toll like receptors recognize?

A

pathogen-associated molecular patterns (PAMP). once recognized the cell secrete:
cytokines that induce inflammation, anti-viral cytokines and cytokines and membrane proteins that promote lymphocyte activation.

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9
Q

what are the sensors of cell damage?

A

cytosolic receptors that recognize molecules that are liberated or altered as a consequence of cell damage.
they are called DAMPS, (Damage associate molecular patterns)
-uric acid (product of DNA breakdown)
-ATP (released from damaged mitochondria)
-reduced cytosolic (K+) due to membrane damage.
-DNA (when is leaves the nucleus into the cytosol)

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10
Q

the 5 steps of inflammation?

A

“the 5 R’s”

  • recognition of the injurious agent
  • recruitment of leukocytes
  • removal of the agent
  • regulation (control) of the response
  • resolution (repair).
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11
Q

Acute inflammation 3 components?

A

1-dilation of small vessels increasing blood flow
2-increased permeability of vessels, enabling proteins and leukocytes to leave circulation
3-emigration of the leukocytes from the microcirculation their accumulation as the site of injury.
phagocytes and other sentinel cells in thee tissues recognize the presence of the foreign or abnormal substance and release mediators to initiate the above processes.

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12
Q

what is exudation?

A

the increased permeability of the vessels in response to inflammation resulting in fluid and proteins and blood cells from the vessel.

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13
Q

what is exudate?

A

an extravascular fluid that has a high protein concentration and contains cellular debris indicating an inflammatory reaction.

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14
Q

what is Transudate?

A

a fluid with low protein content, little or no cellular material, and low specific gravity. Ultrafilatrate of blood do to osmotic imbalance.

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15
Q

Define edema?

A

an excess of fluid in the intersitial tissue or serous cavities; it can be either an exudate or a transudate

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16
Q

Define Pus (purulent exudate)

A

an inflammatory exudate rich in leukocytes (mostly neurtophils) the debris of dead cells, and in many cases microbes.

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17
Q

what causes the redness and heat at the site of inflammation?

A

Histamine causing vasodilation.

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18
Q

what is the result of the loss of fluid during inflammation.

A

slower blood flood, high RBC concentration in small vessels, increased viscosity.
RESULT: engorgement of small vessels jammed with slowly moving RBC (vascular congestion)
ERYTHEMA: localized redness of the involved tissue.

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19
Q

what increases vascular permeability?

A
  • Retraction of endothelial cells (histamine, bradykinin, leukotrienes
  • Endothelial injury (leakage can last hours until vessel is repaired).
  • increased transcytosis in endothelial cells.
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20
Q

What is lymphangitis

A

-secondary inflammation of the lymphatics

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21
Q

What is lymphadenitis?

A

inflammation of the lymph nodes that enlarge.
red streaks near a skin wound is a telltale sign of an infection as the streaking follows the course of the lymphatic channels (indicating lymphangitis)

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22
Q

most important leukocytes for inflammation?

A

the ones capable of phagocytosis; neutrophils and macrophages.
Neutrophils respond faster.
Macrophages respond slower but longer action. Macrophages aid repair by secreting growth factors.

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23
Q

How does strong activation of leukocytes can cause “collateral damage”

A

leukocytes emit substances that help destroy the microbes and clean up necrotic tissues can affect healthy ones as well.

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24
Q

what are the 3 things that happen when leukocytes encounter and infection?

A
  • adhesion to endothelium
  • leukocyte migration through endothelium
  • chemotaxis of leukocytes
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25
Q

the process of leukocytes adhesion?

A

RBC flow in the center of a vessel and WBC near the vessel wall. If hemodynamic conditions change (such as during inflammation) WBC are moved even closed to vessel wall and can detect changes in it, such as increased in adhesion molecules. They roll along the inner wall until they find a place to bind tightly.

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26
Q

cytokines cause the expression of what on endothelial wall?

A

Integrins and selectins.
Selectins: rolling
Interginrs: tight adhesion

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27
Q

3 types of selectins? (their expression increases during inflammation).

A

E-selectin (endothelial cells)
P-selectin (platelets)
L-selectin (leukocytes)
Ligands for them are sialic acid-containing oligosaccharides bound to glycoprotein backbones.

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28
Q

mediators for selectin activation?

A

Histamine or thrombin: P-selectin expression increases

IL-1 and TNF (tumor necrosis factor) causes E-selectin and ligand for L-selectin to be expressed on endothelium.

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29
Q

what tissues produce cytokines during encounters with microbes and dead cells?

A

macrophages, dendritic cells, mast cells, and endothelial cells.

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30
Q

what is expressed on the surface of leukocytes in respect to adhesion?

A

L-selection on tips of microvilli

Ligands for E- and P-selectin

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31
Q

how are integrins activated?

A

Intergirns are expressed on luekoyctes plasma membranes in a low-affinity form and do not adhere to their specific ligands until the leukocytes are activated by chemokines secreted by cells in the site of inflammation.

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32
Q

name the ligands for integrins on the endothelium?

A
  • intercellular adhesion molecule-1 (ICAM-1)
  • Leukocyte function-associated antigen-1 (LFA-1)
  • Macrophage-1 antigen (Mac-1)\
  • Vascular cell adhesion molecule-1 (VCAM-1) which binds to the intergrin very late antigen-4 (VLA-4)
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33
Q

the process of leukocyte migration through endothelium?

A

Transmigration of leukocytes occurs in postcapillary venules (greater retraction of endothelial cells).
PECAM-1 (platelet endothelial cell adhesion molecule-1) on the surface of endothelium and platelets assist in migration as does chemokines.
the basement membrane is pierced by the secretion of collagenases.

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34
Q

after transmigration of leukocytes, chemotaxis is driven by?

A
  • bacterial products
  • cytokines (chemokine family)
  • components of the complement system (c5a)
  • products of the lipoxygenases pathway of arachidonic acid (LTB4) leukotriene B4
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35
Q

on what receptor does the chemoattractants act on and what are their effects?

A

they act on 7TM (G-proteins) on leukocytes causing polymerization of actin resulting in increased amounts at the leading edge of the cell and localization of myosin filaments at the back.

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36
Q

what type of cells are present at the site of infection at 6-24 hours and 24-48 hours?

A 
6-24h = neutrophils
24-48h = macrophages (derived from monocytes) replace neurtophils and they can proliferate in the tissue
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37
Q

what do anti-inflammatory drugs do?

A

Block TNF (tissue necrosis factor) which is one of the major cytokines in leukocyte recruitment.

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38
Q

3 steps of phagocytosis?

A
  • recognition and attachment of to-be ingested particle
  • engulfment with subsequent formation of a phagocyte vacuole.
  • killing or degradation of the ingested material.
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39
Q

types of receptors for leukocytes to recognize microbes?

A

-Mannose receptors; binds terminal mannose and fucose residues of glycoprotein and glycolipids that re found on microbial cell walls whereas mammalian glycoproteins and gycolipids contain terminal sialic acid or N-acetlygalactosamine.
-scavenger receptors (ingest LDL and microbes)
OPSONIZATION enhances phagocytosis

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40
Q

process of engulfment with respect to phagocytosis?

A

the phagocyte extends cytoplasm (pseudoppods) around particle and form a phagosome that fuses with lysosomes, ROS and reactive nitrogen species are used along with lysosomal enzymes.
phagocyte may release some granules contents into ECM possibly damaging nearby cells.

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41
Q

what makes ROS in lysosomes?

A

phagocyte oxidase; uses NADPH to reduce oxygen.
mutlicomponent enzyme that assembles on the phagosomal membrane.
H2O2 with myeloperoxidase (MPO) enzyme uses Cl to make hypochlorite (found in bleach).

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42
Q

leukocytes also release ROS which causes what problem?

A

ROS may also be released extracellularly accounting for the tissue damage during inflammation.

43
Q

what enzymes defend against ROS?

A
  • superoxide dismutase
  • catalase
  • glutathione peroxidase
44
Q

what does nitrogen oxide synthase do?

A

make NO from arginine to maintain vascular tone.

45
Q

Name the 2 granular WBCs

A

Neutrophils and monocytes have granules packed with enzymes and anti-microbial proteins.
the secreted proteases are kept in check by anti-proteases in the serum and tissue fluids (a1-anti-trypsin is the most important).

46
Q

what are NETs? (neutrophil extracellular traps)

A

neutrophils secrete their own nuclear chromatin to make a fibrillar network that concentrate anti-microbial substances at site of infection to prevent spreading of microbes by trapping them in the fibrils.

47
Q

Instances when the leukocytes cause injury.

A
  • normal reaction suffers collateral damage
  • autoimmune disease (attacks own cells)
  • host “hyper-reacts” against usually harmless environmental substances (asthma)
48
Q

inflammatory response termination process?

A

inflammation response ends when the offending agents are removed because the mediators are secreted in bursts in response to the stimulus and have short half-lives. The neutrophils themselves also have short half-lives.

49
Q

major cell types to produce mediators of acute inflammation?

A
  • macrophages
  • dendritic cells
  • mast cells
50
Q

INFLAMMATION MEDIATORS:

Vasoactive amines: histamine and serotonin, effects and production.

A
  • Serotonin is made mostly by mast cells located near vessels. But also basophils, platelets
  • stored in granules and released during physical injury such as trauma, cold or heat
  • binding of antibodies to mast cells also causes release.
51
Q

INFLAMMATION MEDIATORS:

Arachidonic acid metabolites effects and production.

A

arachidonic acid is made by prostaglandins and leukotrienes. the eicosanoids are made via lipoxigenase path (leukotrienes and lipoxins) and cyclooxygenases (prostaglandins)

52
Q

Prostaglandins production and effects.

A

made by mast cells, macrophages, endothelial cells, made by cycloxygenases COX-1 and COX-2.
designated by PGD, PGE, PGF, PGG and PGH subscripts designate the number of double bonds.

53
Q

effects of PGD2 and PGE2?

A

made by mast ells causes vasodilation and increases the permeability of postcapillary venules (edema results)

54
Q

effects of TXA2?

A

made by platelets via thromboxane synthase making TXA2 which causes platelet-aggregating agent and vasoconstrictor, promoting thrombosis.

55
Q

PGIs effects and formation?

A

made by vascular endotherlium via prostacyclin synthase causing vasodilator and a potent inhibitor of platelet aggregation.

56
Q

outside of local effects what do prostaglandins do?

A

involved in the pathogenesis of pain and fever.

PGE2 makes the skin hypersensitive to painful stimuli, and causes fever during infections.

57
Q

Leukotrienes effects?

A

made by leukocytes and mast cells via lipoxygenase; causes vascular reaction and leukocyte recruitment.

58
Q

Lipoxins effect?

A

made from arachidonic acid by the lipoxygenase path they suppress inflammation by inhibit leukocyte recruitment.

59
Q

Name Cyclooxygenase inhibitors

A

Aspirin and ibuprofen

nonsteroidal anti-inflammatory drugs (NSAIDS) that pain and fever.

60
Q

Name lipoxygenase inhibitors

A

zileuton, used to treat asthma.

61
Q

name corticosteroids inhibitors

A

a broad-specturm anti-inflammatory agents that reduce genes encoding COX-2 phospholipase A2, proinflammatory cytokines.

62
Q

Leuukotriene receptor antagonists?

A

Montelukast that block leukotriene receptors, used to treat asthma.

63
Q

Cytokine and chemokines are made by?

A

activated lymphocytes macrophages and dendritic cells, endothelial, epithelial and connective tissue cells.

64
Q

TNF and IL-1 roles?

A

leukocyte recruitment by promoting adhesion of leukocytes to endothelium and their migration through vessels.

  • activated macrophages and dendritic cells make them
  • TNF made by T-lymphocytes and mast cells and some epithelial cells produce IL-1 as well.
65
Q

actions of TNF and IL-1

A
  • endothelial activation (increased expression of endothelial adhesion molecules)
  • Activation of leukocytes (augments responses of neutrophils to bacteria.
66
Q

TNF effects on the body?

A

promotes lipid and protein catabolism and by suppressing appetite. Resulting weight loss, muscle atrophy.

67
Q

Systemic acute-phase response of IL-1 and TNF?

A

IL-1 and TNF induce fever and have been implicated in the pathogenesis of the systemic inflammatory response syndrome (SIRS) resulting in disseminated bacterial infection (Sepsis)

68
Q

how are chemokines catagorized?

A

by the position of their cysteine residues (C)
C-X-C chemokines, C-C, C, and CX3C.
they function in chemotaxis AND to maintain certain tissue architecture, such as T and B lymphocytes in discrete areas of the spleen and lymph nodes.

69
Q

what is the complement system?

A

a collection of soluble proteins and their membrane receptors that function mainly in host defense against microbes and in pahtologic inflammatory reactions.

70
Q

3 pathways of the complement system;

A

1 the classic pathway (antibodies bind to microbe)
2 the alternative pathway (microbes surface triggers it)
3 the lectin pathway (mannose-binding lectins activate C1)

71
Q

effects of the complement system?

A
  • inflammation C5a, C4a, C3a stimulate histamine release
  • Opsonization and phagocytosis via C3b to cell wall
  • Cell lysis: C5bC6789 forms the MAC (membrane attack complex that forms pores in cells.
72
Q

regulatory proteins function?

A

the complement system is tightly controlled by cell-associated and circulating regulatory proteins that inhibit the production or remove fragments that deposit on cells.

73
Q

name some complementary regulatory proteins

A
  • C1 inhibitor (blocks 1st protein of classic path)

- Decay accelerating factor (DAF) and CD59 (DAF inhibits C3 convertases and CD59 inhibits MAC formation)

74
Q

Hereditary angioedema is caused by deficiency in?

A

C1 inhibitor

75
Q

where does the connection between inflammation and coagulation exist?

A

with the Thrombin activated protease-activated receptors (PAR) expressed on leukocytes but PAR has a more clear role in platelets causing their aggregation.

76
Q

what does kallikrein enzyme do?

A

it cleaves a plasma glycoprotein precursor, high-molecular-weight kininogen to produce bradykinin which increases vascular permeability and causes contraction of smooth muscle and vasodilation and pain.

77
Q

define Serous inflammation

A

exudation of cell-poor fluid into spaces created by injury to surface epithelia or into body cavities lined by the peritoneum, pleura or pericardium.

78
Q

define fibrinous inflammation

A

leakage of fluid from the vessels allowing proteins such as fibrinogen to leave it.

79
Q

define purulent (suppurative) inflammation, Abscess

A

purulent inflammation is characterized by the production of pus an exudate consisting of neutrophils the liquefied debris of necrotic cells and edema fluid caused by bacterial infection that cause liquefactive tissue necrosis.

80
Q

Define Ulcers

A

a local defect or excavation of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflamed necrotic tissue. they are a result of inflammation exist on or near a surface.

81
Q

3 outcomes of inflammation

A

1: complete resolution (success in eliminating damage)
2: Healing by connective tissue replacement (scarring or fibrosis) with substantial destruction of tissue not able to regenerate causing connective tissue to grow into area of damage
3: Chronic inflammation

82
Q

causes of chronic inflammation

A
  • persistent infections
  • Hypersensitivity disease (autoimmune, allergic)
  • prolonged exposure to toxic agent
83
Q

what cells make up the mononuclear phagocyte system?

NOTE: monocytes go on to make macrophages

A

Macrophages are diffusely found in connective tissue.

  • liver kupffer cells
  • spleen and lymph nodes
  • CNS microglial cells
  • Lungs alveolar macrophages
84
Q

is the method of migration of monocytes into tissue the same as neutrophils?

A

YES, monocytes in circulation have a half life of 1 day

macrophages can last years.

85
Q

2 pathways of macrophage activation

A

1: Classical macrophage activation
- – use TLR (toll like receptors) engaged by microbial products, which induce ROS and lysosomes production.
2: alternative macrophage activation
- – induced by IL-4 and IL-13 make by T-lymphocytes. this pathway function is for tissue repair and healing.

86
Q

roles of macrophages in inflammation

A
  • they secrete mediators of inflammation such as cytokines (TNF, IL-1, chemokines)
  • Macrophages display antigens to T-lyphocytes
87
Q

3 different CD4+ T cells that secrete different cytokines and their effects on inflammation
(the role of lymphocytes in inflammation)

A
  • TH1 cells make IFN-gamma (classic path activation macrophage)
  • TH2 cells secrete IL-4, IL-5, and IL-13 (alternative macrophage activation)
  • TH17 secrete IL-17 (induce secretion of chemokines for neutrophils recruitment)
88
Q

how does T-lyphocytes and macrophages cause a positive feedback during inflammation?

A

macrophages present antigens to lyphocytes which get activated and secrete cytokines that which recruit and activate macrophages promoting more antigen presentation.

89
Q

Define granulomatous inflammation

A

a form of chronic inflammation characterized by collections of activated macrophages often with T lymphocytes and sometimes associated with central necrosis.

  • immune granulomas (t-cell mediated immune response)
  • foreign body granulomas (response to inert foreign bodies)
90
Q

what causes the fever?

A

pyrogens, the increase in body temperature is caused by prostaglandins. Exogenous pyrogens like LPS cause leuocytes to release cytokine such as IL-1 and TNF called endogenous pyrogens so stimulate cycloxygenase to make prostaglandins. In the hypothalamus PGE2 stimulate the production of neurotransmitter.

91
Q

what are Acute-phase proteins?

A

plasma proteins mostly synthesized in the liver whose plasma concentrations may increase 100x as part of the response to inflammatory stimuli

  • CRP (C-reactive protein) (act as opsonins)
  • serium amyloid A (SAA) (act as opsonins)
  • fibrinogen (causes erythrocyte sedimentation)
92
Q

what is Leukocytosis?

A

cytokine TNF and IL-1 cause bone marrow to accelerate leukocytosis.
prolonged infection can cause bone marrow precursor proliferation caused by increased production of colony-stimulating factors.

93
Q

Repair of damage tissues occurs by 2 types of reaction…

A
  • regeneration by proliferation of residual (uninjured cells)
  • and maturation of tissue stem cells and the deposition of connective tissue to form a scar.
94
Q

define Labile tissues
stable tissues
permanent tissues

A
  • Labile tissues: cells constantly lost and replaced (skin, bone marrow)
  • Stable tissues: in G0 phase but can divide when needed
  • permanent tissues: nervous, muscle tissue that cannot divide.
95
Q

what cells give off growth factors at the site of injury?

A

extracellular matrix, macrophages, but some epithelial and stromal cells also make these factors.

96
Q

what factors are responsible for regeneration of the liver?

A

cytokines and IL-6 made by kupffer cells and growth factors such as Hepatocyte growth factor (HGF).

97
Q

steps of scar formation?

A
  • hemostatic plug formation
  • inflammation as platelets release chemokines to recruit neurtophils and then monocytes.
  • M1 macrophages clear microbes and necrotic tissue, M2 macrophages promote repair.
98
Q

steps of vessel formation?

A
  • NO (vasodilation) increased permeability via VEGF
  • separation of pericytes from the abluminal surface and breakdown of the basement membrane to allow formation of a vessel sprout.
  • endothelial cells migrate to area of tissue injury
  • proliferation of endothelial cells behind the leading “tip”
99
Q

why are new vessels formed via angiogenesis leaky?

A

the incomplete interendothelial junctions and because VEGF that drives angiogenes also increases permeability.

100
Q

2 steps of the deposition of connective tissue and fibroblast activation.

A
  • migration and proliferation of fibroblasts into the site of injury
  • deposition of ECM proteins produced by these cells, mediated by TGF-B. Matrix metalloproteinases (MMP) balanced with their inhibitors (TIMPs) tissue inhibitors of metalloproteinases.
101
Q

what occurs during the remodeling phase of scar connective tissue?

A

the switching from type 3 to type 1 collagen.

102
Q

define Hypertrophic scar?

A

raised scar due to excessive amounts of collagen accumulation.
A KELOID is formed if it grows beyond the boundaries of the original wound with no regression.

103
Q

Define Contracture?

A

contraction of a wound that may inhibit the movement of joints such as the palm.

104
Q

Define Fibrosis

A

term is used to denote the excessive deposition of collagen and other ECM components in a tissue.
TGF-B is involved

Pathology basic (11 decks)

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