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Chapter 2 Flashcards

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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
lymphangitis
inflammation of a lymphatic channel
26
lymphandenitis
inflammation of a lymph node, increase in size
27
lymphandenopathy
general disorder of lymph nodes
28
what cells are predominately found in acute inflammation in the first 24-48 hours? following that time period?
24-48 hours=neutrophils | after= monocytes/macrophages and lymphocytes
29
what are collectins?
plasma carbohydrate-binding lectins which bind to microbial cell wall sugar groups
30
what are the possible outcomes of acute inflammation?
1- resolution 2- chronic inflammation 3- scarring
31
what are the morphologic patterns of inflammation?
1- serous inflammation 2- fibrinous inflammation 3-suppurative (purulent) inflammation 4-ulcerative inflammation
32
what are the characteristics of serous inflammation?
serum accumulates below epidermis serous effusion skin blister: burn, virus, toxin
33
what are the characteristics of fibrinous inflammation?
- severe injury - increased vascular permeability--allows large molecules to enter - fibrin rich exudate --->fibrin-rich scar - characteristic of peritoneum, pleura cavity and pericardial sac
34
what are the characteristics of suppurative (purulent) inflammation?
localized infection of pus-forming organism staph. aureus Abscess- localization of pus pus= collection of neutrophils, necrotic tissue, edema
35
what are the characteristics of ulcerative inflammation?
- near an organ or tissue surface - local defect - produced by necrosis of cells and sloughing of necrotic and inflammatory tissue - peptic ulcers, aphthous ulcer
36
what is granulomatous inflammation?
a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages with scattered lymphocytes. -sarcoidosis, Crohn disease, against certain microbes
37
How do mediators get to inflammation?
1- produced locally by the cells at site of inflammation | 2- derived from circulating inactive precursors that are activated at the site of inflammation
38
how do most mediators act?
by binding to specific receptors on different target cells
39
What type of inflammation are vasoactive amines associated with?
acute
40
what are two examples of vasoactive amines?
serotonin and histamine
41
where are vasoactive amines stored?
in mast cells, platelets, WBC's and endothelium
42
What is histamines action as a mediator?
vasodilation, increased permeability
43
what is serotonins action as a mediator?
vasoconstriction during clotting
44
what's another name for an arachadonic acid metabolite?
eicosanoids
45
increased synthesis of eicosanoids means (inc/dec) inflammation?
increased
46
what are the major sources of arachadonic acid metabolites?
WBC's, mast cells, endothelial cells and platelets
47
What drugs block prostaglandin synthesis? what's the result?
NSAIDS, decreased pain
48
what are prostaglandins and leukotrienes involved with?
vascular reactions, pain and chemotaxis
49
what are lipoxins?
anti-inflammatory mediators which inhibit neutrophil chemotaxis and adhesion to endothelium serve as endogenous antagonists of leukotrienes
50
What are the traits of cytokines?
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
What cells produce ROS and what are they used for?
neutrophils and macrophages microbial killing and adhesion Increase inflammatory mediators!
52
what is nitric oxide used for?
microbial killing and vasodilation
53
what are characteristics of lysosomal enzymes of leukocytes?
neutrophils, monocytes microbial killing tissue degradation
54
what are neuropeptides?
initiate inflammatory responses transmit pain signals ex: substance P
55
what are the plasma protein-derived mediator systems?
1- complement system 2-coagulation system 3- kinin system
56
What are the main characteristics of the complement system of plasma protein-derived mediators?
- 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
what controls the activation of complement mediators?
cell-associated and circulating regulatory proteins | protects normal cells from inappropriate damage
58
what is the protein synthesized by the liver that is activated by collagen, basement membrane or platelets? What systems does it, in turn, activate?
``` Hageman factor in the coagulation system of inflammation mediation 1-kinin system 2-clotting systems 3-fibrinolytic system 4-complement system ```
59
which system of plasma protein-derived mediators leads to the formation of bradykinin? what are the effects of bradykinin?
kinin system - increased vascular permeability, vasodilation - pain when injected - activates thrombin, increases clotting (thrombosis)
60
what are the typical causes of chronic inflammation?
- persistent injury/infection: TB, IBD, silica - immunosuppression- AIDS, transplant recipients - hypersensitivity reactions
61
what are the characteristics of chronic inflammation?
- mononuclear lymphocyte infiltration (macrophages, lymphocytes, platelets) - tissue destruction, fibrosis - angiogenesis
62
what is the dominant cell type in chronic inflammation? what is their job, generally? when are they first at the 'scene' of inflammation?
-macrophages -phagocytosis, initiate angiogenesis and fibrosis 48 hours
63
what classically activates macrophages? | what is their main job?
- endotoxins - T cell-derived signals - cytokine IFN-gamma - foreign bodies KILLLLLLLLLLL and secrete more cytokines to inc. inflammation
64
what alternatively activates macrophages? | what is their main job?
cytokines other than IFN-gamma they're produced by T lymphocytes, mast cells, eosinophils tissue repair,
65
what cells help sustain chronic inflammation?
lymphocytes
66
what causes of inflammation recruit lymphocytes?
bacterial/viral infections, autoimmune, parasites, hypersensitivities
67
what causes of inflammation recruit eosinophils?
parasites and IgE (allergies)
68
what do mast cells respond to? what do they release? are they part of acute or chronic inflammation?
- sentinel cells - atopic allergies - release histamine and ARA metabolites, increase inflammation - key role in anaphylactic shock - Both acute and chronic
69
what is granulomatous inflammation?
- a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages with scattered lymphocytes. - walls off the offending agent
70
when do granulomas form?
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
what are the most important mediators of the acute-phase rxn?
cytokines TNF, IL-1 and IL-6
72
what are symptoms and signs of acute-phase rxns?
``` increased BP and HR malaise anorexia somnolence anhidrosis ```
73
what substance is fever a response to? how does that substance work?
pyrogens | stimulates prostaglandin synthesis in the hypothalamus-->increasing T set point
74
what stimulates production of acute-phase proteins?
cytokines--> IL-6
75
what are two of the most common acute-phase proteins?
CRP (C-reactive protein) and fibrinogen
76
what is an ESR and how is it used?
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
what is leukocytosis and when is it found?
- 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
what are leukemoid reactions?
- extremely high blood leukocyte count (40-100k/microL) | - found with chronic inflammation (clostridium difficile, TB)
79
what is leukopenia?
- decreased leukocytes - <4000/microL - occurs in HIV/AIDS, chemo, radiation
80
What term is used to describe the extensive collagen deposition that occurs in the lungs, kidneys, liver and myocardium?
fibrosis
81
what causes fibrosis in the lungs, liver and kidney?
chronic inflammation
82
what causes fibrosis in the myocardium?
ischemic necrosis/ infarction | or extensive inflammation due to ischemia-reperfusion injury
83
what stimulates cellular proliferation? what two things determine the adequacy of the repair process?
growth factors 1- production of growth factors 2-ability of cells to divide in response to the factors
84
what phase of the cell cycle are nondividing cells in?
G0 or G1
85
what regulates the speed of the cell cycle?
cyclins
86
what determines the base population of a cell type in a tissue?
1-cell proliferation 2-cell death by apoptosis 3-emergence of new differentiated cells from stem cells
87
physiologic cell proliferation is in response to..
tissue damage
88
pathologic cell proliferation is in response to...
genetic changes
89
why are there checkpoints? what occurs there?
- quality control | - DNA repair, apoptosis, senescence
90
what molecules slow down the cell cycle? what pushes it past that 'speed bump' (suppresses aforementioned molecule)?
CDKI's | GF's
91
what controls cyclins?
cyclin-dependent kinases
92
what are the characteristics of labile tissues? | whats an example?
- continuously dividing - readily regenerate - replaced by stem cells (require preservation) - hematopoietic cells and surface epithelia (GI tract, skin)
93
what are the characteristics of stable tissues? examples?
- terminal differentiation (stuck in G0) - limited replication (only in response to injury) - ex: solid organs (liver, kidney, pancreas)
94
what are the characteristics of permanent tissue? examples?
- terminally differentiated - CANT replicate - injuries = permanent = scar tissue - ex: neurons, myocardium
95
many tissues have a combination of all three tissue types except which two?
neurons and myocardium
96
what are the two important properties of stem cells?
1-self renewal capacity | 2-asymmetric replication

Pathology (2 decks)

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