Chapter 2 Flashcards

1
Q

What is inflammation?

A

a protective response involving host cells, blood vessels and proteins and other mediators that is intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult and to initiate the process of repair.

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2
Q

What are the characteristics of acute inflammation?

A

rapid in onset
short duration (minutes to days)
fluid and plasma protein exudation
predominantly neutrophilic leukocyte accumulation

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3
Q

what are the characteristics of chronic inflammation?

A

longer duration (days to years)
lymphocytes and macrophages
vascular proliferation
fibrosis

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4
Q

what are the external signs of inflammation?

A
heat--calor
redness--rubor
swelling--tumor
pain--dolor
loss of fxn--functio laesa
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5
Q

who added the 5th cardinal sign of inflammation?

A

Rudolf Virchow, the ‘father of modern pathology’

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6
Q

what are the two major components of acute inflammation?

A

vascular changes–vasodilation and increased vascular permeability
leukocyte recruitment and activation

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7
Q

what are the two most important families of pattern recognition receptors?

A
  • Toll-like receptors (TLRs)

- inflammasome

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8
Q

what do TLRs sense? where are they found (on/in) a cell

A
  • products of bacteria, viruses and other pathogens.

- found on plasma membrane–sense environment

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9
Q

what do inflammasomes sense? where are they found (on/in) a cell?

A
  • products of dead cells, such as uric acid and extracellular ATP
  • activate caspase-1
  • found in a cell–sense cytoplasm
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10
Q

what is responsible for the redness and warmth characteristic of acute inflammation?

A

arteriolar vasodilation

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11
Q

what is stasis, as applied to acute inflammation?

A

the dilation of microvasculature causing blood to become more concentrated and viscous, decreasing circulation

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12
Q

what is margination?

A

the accumulation of leukocytes along the vascular endothelial surface as stasis develops.

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13
Q

what is exudate?

A

protein-rich fluid accumulation in vessels as water leaves the blood and enters the tissues due to osmotic pressure imbalance during increased vascular permeability

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14
Q

what is transudate

A

interstitial fluid accumulations caused by increased hydrostatic pressure, typically a consequence of reduced venous return.
low [protein] and few or no blood cells

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15
Q

which is normally found with acute inflammation, exudate or transudate?

A

exudate

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16
Q

what causes increased vascular permeability in acute inflammatory reactions?

A

1-endothelial cell contraction leading to intercellular gaps in postcapillary venules (MC)
2- endothelial injury
3-increased transcytosis
4-leakage from new blood vessels

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17
Q

what do leukocytes do?

A

1-ingest offending agents, kill bacteria, and other microbes

2-eliminate necrotic tissue and foreign substances

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18
Q

what cell types have surface receptors?

A

macrophages, mast cells, dendritic cells

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19
Q

what is diapedesis

A

when a cell goes out of circulation to get to target tissue during acute inflammation

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20
Q

what are the sequence of events in the recruitmentof leukocytes form the vascular lumen to the extravascular space?

A

1- margination and rolling along the vessel wall
2- firm adhesion to the endothelium
3-transmigration between endothelial cells
4-migration in interstitial tissues toward a chemotactic stimulus

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21
Q

Leukocyte activation results in the enhancement of what functions?

A

1- phagocytosis
2-intracellular destruction of phagocytosed microbes and dead cells
3-liberation of substances that destroy extracellular microbes and dead tissues
4- production of mediators

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22
Q

what is opsonization?

A

the process by which leukocytes recognize host proteins (opsonins) that coat microbes and target them for phagocytosis
-most important opsonins are antibodies of IgG class

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23
Q

what are the most important microbicidal substances for killing and degrading phagocytosed microbes?

A

ROS and lysosomal enzymes (esp. elastase)

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24
Q

when does scarring occur?

A

after substantial tissue destruction or after chronic inflammation

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25
Q

lymphangitis

A

inflammation of a lymphatic channel

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26
Q

lymphandenitis

A

inflammation of a lymph node, increase in size

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27
Q

lymphandenopathy

A

general disorder of lymph nodes

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28
Q

what cells are predominately found in acute inflammation in the first 24-48 hours? following that time period?

A

24-48 hours=neutrophils

after= monocytes/macrophages and lymphocytes

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29
Q

what are collectins?

A

plasma carbohydrate-binding lectins which bind to microbial cell wall sugar groups

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30
Q

what are the possible outcomes of acute inflammation?

A

1- resolution
2- chronic inflammation
3- scarring

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31
Q

what are the morphologic patterns of inflammation?

A

1- serous inflammation
2- fibrinous inflammation
3-suppurative (purulent) inflammation
4-ulcerative inflammation

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32
Q

what are the characteristics of serous inflammation?

A

serum accumulates below epidermis
serous effusion
skin blister: burn, virus, toxin

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33
Q

what are the characteristics of fibrinous inflammation?

A
  • severe injury
  • increased vascular permeability–allows large molecules to enter
  • fibrin rich exudate —>fibrin-rich scar
  • characteristic of peritoneum, pleura cavity and pericardial sac
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34
Q

what are the characteristics of suppurative (purulent) inflammation?

A

localized infection of pus-forming organism
staph. aureus
Abscess- localization of pus
pus= collection of neutrophils, necrotic tissue, edema

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35
Q

what are the characteristics of ulcerative inflammation?

A
  • near an organ or tissue surface
  • local defect
  • produced by necrosis of cells and sloughing of necrotic and inflammatory tissue
  • peptic ulcers, aphthous ulcer
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36
Q

what is granulomatous inflammation?

A

a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages with scattered lymphocytes.
-sarcoidosis, Crohn disease, against certain microbes

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37
Q

How do mediators get to inflammation?

A

1- produced locally by the cells at site of inflammation

2- derived from circulating inactive precursors that are activated at the site of inflammation

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38
Q

how do most mediators act?

A

by binding to specific receptors on different target cells

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39
Q

What type of inflammation are vasoactive amines associated with?

A

acute

40
Q

what are two examples of vasoactive amines?

A

serotonin and histamine

41
Q

where are vasoactive amines stored?

A

in mast cells, platelets, WBC’s and endothelium

42
Q

What is histamines action as a mediator?

A

vasodilation, increased permeability

43
Q

what is serotonins action as a mediator?

A

vasoconstriction during clotting

44
Q

what’s another name for an arachadonic acid metabolite?

A

eicosanoids

45
Q

increased synthesis of eicosanoids means (inc/dec) inflammation?

A

increased

46
Q

what are the major sources of arachadonic acid metabolites?

A

WBC’s, mast cells, endothelial cells and platelets

47
Q

What drugs block prostaglandin synthesis? what’s the result?

A

NSAIDS, decreased pain

48
Q

what are prostaglandins and leukotrienes involved with?

A

vascular reactions, pain and chemotaxis

49
Q

what are lipoxins?

A

anti-inflammatory mediators which inhibit neutrophil chemotaxis and adhesion to endothelium
serve as endogenous antagonists of leukotrienes

50
Q

What are the traits of cytokines?

A

1- recruit leukocytes
2-increase WBC production, adhesion, migration
3- produced by macrophages, mast cells and endothelial cells
4- Ex: TNF, IL-1, IL-6 and chemokines

51
Q

What cells produce ROS and what are they used for?

A

neutrophils and macrophages
microbial killing and adhesion
Increase inflammatory mediators!

52
Q

what is nitric oxide used for?

A

microbial killing and vasodilation

53
Q

what are characteristics of lysosomal enzymes of leukocytes?

A

neutrophils, monocytes
microbial killing
tissue degradation

54
Q

what are neuropeptides?

A

initiate inflammatory responses
transmit pain signals
ex: substance P

55
Q

what are the plasma protein-derived mediator systems?

A

1- complement system
2-coagulation system
3- kinin system

56
Q

What are the main characteristics of the complement system of plasma protein-derived mediators?

A
  • plasma proteins that opsonize particles (microbes) for phagocytosis
  • contribute to inflammation by vasodilation and increase permeability, WBC adhesion and chemotaxis
  • activates membrane attack complex (MAC) to ‘punch holes’ in microbe cell membranes
57
Q

what controls the activation of complement mediators?

A

cell-associated and circulating regulatory proteins

protects normal cells from inappropriate damage

58
Q

what is the protein synthesized by the liver that is activated by collagen, basement membrane or platelets? What systems does it, in turn, activate?

A
Hageman factor in the coagulation system of inflammation mediation
1-kinin system
2-clotting systems
3-fibrinolytic system
4-complement system
59
Q

which system of plasma protein-derived mediators leads to the formation of bradykinin? what are the effects of bradykinin?

A

kinin system

  • increased vascular permeability, vasodilation
  • pain when injected
  • activates thrombin, increases clotting (thrombosis)
60
Q

what are the typical causes of chronic inflammation?

A
  • persistent injury/infection: TB, IBD, silica
  • immunosuppression- AIDS, transplant recipients
  • hypersensitivity reactions
61
Q

what are the characteristics of chronic inflammation?

A
  • mononuclear lymphocyte infiltration (macrophages, lymphocytes, platelets)
  • tissue destruction, fibrosis
  • angiogenesis
62
Q

what is the dominant cell type in chronic inflammation?
what is their job, generally?
when are they first at the ‘scene’ of inflammation?

A

-macrophages
-phagocytosis, initiate angiogenesis and fibrosis
48 hours

63
Q

what classically activates macrophages?

what is their main job?

A
  • endotoxins
  • T cell-derived signals
  • cytokine IFN-gamma
  • foreign bodies

KILLLLLLLLLLL and secrete more cytokines to inc. inflammation

64
Q

what alternatively activates macrophages?

what is their main job?

A

cytokines other than IFN-gamma
they’re produced by T lymphocytes, mast cells, eosinophils

tissue repair,

65
Q

what cells help sustain chronic inflammation?

A

lymphocytes

66
Q

what causes of inflammation recruit lymphocytes?

A

bacterial/viral infections, autoimmune, parasites, hypersensitivities

67
Q

what causes of inflammation recruit eosinophils?

A

parasites and IgE (allergies)

68
Q

what do mast cells respond to? what do they release? are they part of acute or chronic inflammation?

A
  • sentinel cells
  • atopic allergies
  • release histamine and ARA metabolites, increase inflammation
  • key role in anaphylactic shock
  • Both acute and chronic
69
Q

what is granulomatous inflammation?

A
  • a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages with scattered lymphocytes.
  • walls off the offending agent
70
Q

when do granulomas form?

A

1-persistent T-cell responses to certain microbes (i.e. TB)
2-immune mediated inflammatory diseases (Chrons)
3- sarcoidosis–respond to inert foreign bodies

71
Q

what are the most important mediators of the acute-phase rxn?

A

cytokines TNF, IL-1 and IL-6

72
Q

what are symptoms and signs of acute-phase rxns?

A
increased BP and HR
malaise
anorexia
somnolence
anhidrosis
73
Q

what substance is fever a response to? how does that substance work?

A

pyrogens

stimulates prostaglandin synthesis in the hypothalamus–>increasing T set point

74
Q

what stimulates production of acute-phase proteins?

A

cytokines–> IL-6

75
Q

what are two of the most common acute-phase proteins?

A

CRP (C-reactive protein) and fibrinogen

76
Q

what is an ESR and how is it used?

A

erythrocyte sedimentation rate

  • fibrinogen binds to erythrocytes, causing them to stack. this test measures how long it takes erythrocytes to sediment at unit gravity, the stacks reaching the bottom quicker.
  • this is a simple test for inflammation levels
77
Q

what is leukocytosis and when is it found?

A
  • increased blood leukocyte count (15-20k/microliter)
  • caused by accelerated release of cells from bone marrow–>presence of circulating immature cells = ‘shift to the left’
  • occurs with bacterial/viral infxn (MC), allergies and parasites
78
Q

what are leukemoid reactions?

A
  • extremely high blood leukocyte count (40-100k/microL)

- found with chronic inflammation (clostridium difficile, TB)

79
Q

what is leukopenia?

A
  • decreased leukocytes
  • <4000/microL
  • occurs in HIV/AIDS, chemo, radiation
80
Q

What term is used to describe the extensive collagen deposition that occurs in the lungs, kidneys, liver and myocardium?

A

fibrosis

81
Q

what causes fibrosis in the lungs, liver and kidney?

A

chronic inflammation

82
Q

what causes fibrosis in the myocardium?

A

ischemic necrosis/ infarction

or extensive inflammation due to ischemia-reperfusion injury

83
Q

what stimulates cellular proliferation? what two things determine the adequacy of the repair process?

A

growth factors
1- production of growth factors
2-ability of cells to divide in response to the factors

84
Q

what phase of the cell cycle are nondividing cells in?

A

G0 or G1

85
Q

what regulates the speed of the cell cycle?

A

cyclins

86
Q

what determines the base population of a cell type in a tissue?

A

1-cell proliferation
2-cell death by apoptosis
3-emergence of new differentiated cells from stem cells

87
Q

physiologic cell proliferation is in response to..

A

tissue damage

88
Q

pathologic cell proliferation is in response to…

A

genetic changes

89
Q

why are there checkpoints? what occurs there?

A
  • quality control

- DNA repair, apoptosis, senescence

90
Q

what molecules slow down the cell cycle? what pushes it past that ‘speed bump’ (suppresses aforementioned molecule)?

A

CDKI’s

GF’s

91
Q

what controls cyclins?

A

cyclin-dependent kinases

92
Q

what are the characteristics of labile tissues?

whats an example?

A
  • continuously dividing
  • readily regenerate
  • replaced by stem cells (require preservation)
  • hematopoietic cells and surface epithelia (GI tract, skin)
93
Q

what are the characteristics of stable tissues? examples?

A
  • terminal differentiation (stuck in G0)
  • limited replication (only in response to injury)
  • ex: solid organs (liver, kidney, pancreas)
94
Q

what are the characteristics of permanent tissue? examples?

A
  • terminally differentiated
  • CANT replicate
  • injuries = permanent = scar tissue
  • ex: neurons, myocardium
95
Q

many tissues have a combination of all three tissue types except which two?

A

neurons and myocardium

96
Q

what are the two important properties of stem cells?

A

1-self renewal capacity

2-asymmetric replication