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Pathology I > Inflammation review > Flashcards

Inflammation review Flashcards

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1
Q

what is the purpose to inflammation?

A

set up the immune system, set up regeneration response and deliver proteins needed to neutralize the injurious agent or infection and promote regeneration and healing

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2
Q

Inflammation definition

A

localized reaction of living vascularized tissue to injury

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3
Q

What are the components to inflammation?

A
  1. ) Vascular response: increased blood flow by vasodilation
    - > increased vascular permeability
  2. ) Cellular response:
    - cell migration-> cell attachment and diapedesis, evolution of cellular response
    - phagocytosis
    - cytokine synthesis
    - healing, regeneration, immune response
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4
Q

if you have high C reactive protein, what is more likely?

A

high percentage of having a fatal heart attack

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5
Q

steps in the inflammatory response

A
  1. ) damaged tissue release histamines-> increasing blood flow to area
  2. ) histamines cause capillaries to leak, releasing phagocytes and clotting factors into the wound
  3. ) Phagocytes engulf bacteria, dead cells, cellular debris
  4. ) platelets move out of the capillary to heal the wound area
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6
Q

what are the cells resident to tissue?

A

a. ) Mast cells- release histamine on tissue injury
b. ) Tissue macrophages: release cytokines, particularly in response to infectious agents
c. ) endothelial cells: mediate responses between tissue and blood supply
d. ) Parenchymal cells: signal inflammation on death or injury

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7
Q

what are the migrating cells?

A

a. ) neutrophils- phagocytosis
b. ) Monocytes: mature into macrophages in tissue and play central role in phagocytosis, elaboration of inflammatory signals, mediation of immune response, and initiation of tissue healing
c. ) lymphocytes: respond to antigens and direct antigen-specific reactions such as immunoglobulin synthesis and cytotixic T cells
d. ) eosinophils: respond to mast cell activation in allergic, parasitic diseases
e. ) platelets- initiate inflammatory signals on activation

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8
Q

what are the cardinal signals to inflammation?

A

Rubor, Tumor, Calor, Dolor, and functio laesa (loss of function)

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9
Q

what causes the rubor and Calor with inflammation?

A

increased blood flow resulting from vasodilation

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10
Q

what causes the tumor (swelling) with inflammation?

A

increased vascular permeability resulting from passage of fluid from blood to tissue

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11
Q

what causes the pain with inflammation?

A

edema and local mediators irritate nerves

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12
Q

what causes the loss of function with inflammation?

A

swelling and pain

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13
Q

what is the 1st phase of inflammation?

A

initiation of inflammation/signal augmentation

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14
Q

what is the 2nd phase of inflammation?

A

Vascular/hemodynamics-> increased blood flow and increased vascular permeability

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15
Q

what is the 3rd phase of inflammation?

A

Inflammatory Cell Phase

  • acute
  • subacute
  • chronic
    resolution: return to homeostasis
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16
Q

what acts to control inflammation?

A

local production of inflammatory mediators

  • inflammatory mediators act on local vascular endothelium to cause vasodilation and increased vascular permeability
  • mediators also act to signal phagocytes in the blood to be activated and migrate into the tissue
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17
Q

how quick to neutrophils respond to inflammation?

A

1st, 24-48 hours

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18
Q

why are neutrophils first?

A

adhesion molecules on the endothelium cells are first are more specific for neutrophils and then later change for macrophages

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19
Q

what is second to arrive at a site of inflammation?

A

macrophages, 48-96 hours

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20
Q

what is third to arrive at a site of inflammation?

A

lymphocytes, after 72 hours

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21
Q

what can initiate inflammation?

A
  1. ) tissue injury: trauma, necrosis, toxins, heat, radiation, enzymes
  2. ) infectious agents: direct tissue injury, toll-like receptors
  3. ) immune responses: immune complexes, antibodies, compliment activation
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22
Q

What is the primary role of the vascular changes associated with inflammation?

A
  • allow the delivery of needed components with are in very large supply in the blood
  • take place mainly in post capillary venules
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23
Q

what role do endothelial cells play in the vascular changes associated with inflammation?

A

play a central role in control of circulation, vascular permeability and coagulation

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24
Q

what is stasis?

A

early mediators act to cause vasodilation-> increased blood flow leads to rubor and calor-> as vessel dilates-> rate of flow slows

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25
NO and prostaglandins aid in what process?
vasodilation
26
what causes the red line seen with inflammation?
local vasodilation due to direct injury- red line extrusion
27
what causes the wheal response seen with inflammation?
increased permeability leading to a pale swelling | pale because edema separates epidermis from dermal vascular layer
28
what causes the flare response seen with inflammation?
wide spread vasodilation due to axon reflex
29
what is axonal flare?
-local release of histamine causes a reflexive dilation of arterioles in the immediate area-> results from stimulation of nerves supplying the arteriole smooth muscle
30
what is the mechanism behind stasis?
dilation of vessels with increased amount of blood-> opening up and filling of capillary beds-> congestion of venous efflux system-> hemoconcentration and slowing of blood flow (aids clotting)-> decreased "axial flow" and increased contact between cells and vascular wall
31
when does the vascular permeability as a result of inflammation occur?
during the first minutes of inflammatory response histamine activates endothelial cells lining capillaries (which usually have tight junctions)-> cells contract and open up the junctions-> fluid and serum proteins pass through-> tissue edema
32
what are the components of increased vascular permeability?
1. ) increased hydrostatic pressure-> increased blood flow, hemoconcentration, stasis 2. ) increased colloid osmotic forces-> fluid follows protein that leaks in between endothelial cells 3. ) activation of endothelial cells-> increased spaces between the endothelial cells 4. ) increased pinocytosis-> move fluid through the endothelial cell
33
what is transudate fluid?
denotes passage of fluid across a vascular wall without passage of proteins - due to increased hydrostatic pressure alone (ex: congestive heart failure) or decreased serum albumin (ex: cirrhosis, nephrotic syndrome) - NO protein, cells or particulate cross wall
34
what is exudate fluid?
protein passes from intravascular space into extracellular fluid-> high specific gravity, protein, cells and particulate matter
35
what does exudate fluid denote?
an active inflammatory process or injury | -reflects increase in vascular permeability
36
transudate properties?
specific gravity: < 1.012 protein: < 3% particulate matter: +
37
exudate properties?
specific gravity: > 1.020 protein: > 3% particulate matter: +++
38
what are mediators of increased vascular permeability?
early on: histamine amplification: kinin, C3a, C5a (anaphylatoxins) maintenance: prostagladins and interleukins
39
what is the immediate transient nature of vascular permeability?
15-30 minutes-> formation of endothelial gaps in venules-> mediates by histamine, bradykinin, leukotrienes, substance P-blocked by anti-histamine
40
what is the delayed transient nature of vascular permeability?
delayed prolonged leakage, hours to days - cytoskeletal reorganization (minutes to hours) (venules)-prostaglandins and cytokine production - leukocyte-mediated endothelial injury (venule)
41
immediate sustained transient nature of vascular permeability?
direct damage to endothelial cells | -all levels of vascular are affected
42
what components are about of the cellular phase of inflammation?
1. activation of inflammatory cells 2. emigrations of leukocytes 3. phagocytosis 4. initiation of immune responses 5. initiation and control of healing/regeneration
43
activation of cells consist of?
inactive cells become activated at sites of inflammation - local mediators and signals result in-> change in cell adhesion, cell migration, phagocytosis, synthesis of new mediators - mostly receptor-mediated via specific ligands
44
what are some common secondary messenger mechanism in cell activation?
- release of Ca - release of arachidonic acid and synthesis of a.a. metabolites - new protein synthesis - release of paracrine and autocrine inflammatory mediators - gene transcription - cell proliferation
45
what is essential in order for cell migration to occur?
activation of cells by locally produced inflammatory mediators-> promotes adherence and migration of phagocytes into tissue -cells activated express new adhesion molecules
46
how are phagocytes delivered to area of inflammation?
``` increased blood flow increased vascular permeability vascular stasis and slowing of blood flow local production of chemotactic factors local production of activation cytokines ```
47
in cell migration, what happens first?
migration of neutrophils predominates (day 0-1)-> then monocytes move in to greatly increase the population of macrophage
48
what is the mechanism behind the cell migration phase?
cell activation is mediated by binding of mediators to specific cell-surface receptors-> results in expression of new adhesion molecules, gene transcription (synthesis of cytokines), and activation of the cytoskeleton (cell movement)-> cell-cell and cell-extracellular matrix interactions are mediated by cell surface adhesion molecules-> activation results in movement along chemotactic gradient (to pull cell in one direction)
49
what is cellular emigration?
- occurs along the endothelium of post-capillary venules - activation of both leukocytes and endothelial cells alters cell adherence - chemotactic factors promote leukocyte activation and induce chemotaxis along a gradient - cells crawl through spaces between endothelial cells by pulling themselves into the extracellular matrix - infiltrate evolves over time-> 1st neutrophils, then macrophages, then lymphocytes
50
what is the process of emigration of neutrophils
reduced axial flow-> migration cells roll along endothelium because of weak adhesion molecules expressed on the PMN's (selectins)-> with more time more selectins are expressed because of local inflammatory molecules-> PMN's slow even more-> eventually activated PMN and activated endothelial cells express integrin adhesion molecules which result in firm adhesion of PMN to the endothelium
51
what activates the increased adhesion of neutrophil to EC's?
local inflammatory mediators
52
what do LTB4, C5a, and histamine do?
activate endothelial cells to express P-selectin which is stored in weibel palade granules
53
what do IL-1 and TNF do?
- induce the expression of E-selectin after several hours | - also activate the expression of ICAM on EC's that bind the integrin molecule on PMN's
54
what does IL-8 do?
chemotactic for neutrophils and induces conformational changes to enhance the binding of PMN integrins to endothelial cells
55
what is the process of diapedesis(crawling thru wall) and chemotaxis?
once firmly adhered-> PMN crawl between the endothelial cells into the tissue-> cells pull themselves along the extracellular matrix towards a chemical signal (chemotactic factor)
56
what is REQUIRED in order for directional movement?
chemotactic gradient
57
what are some major chemotactic molecules for PMN's?
- IL-8 (CXCL-8) made by macrophages - LTB4 made by neutrophils - C5a - bacterial products
58
what is the evolution of cell migration?
first minutes to hours-> vasodilation, edema first 6-24 hours-> neutrophils after 24 hours-> monocytes replenish and expand the macrophage population (24-72 hours both neutrophil and macrophages) after 72 hours-> lymphocytes begin to congregate (only macrophages and lymphocytes
59
besides migration and chemotaxis, what else do leukocytes do?
- synthesize more mediators - increase phagocytosis-> mediated by receptors for bacterial products, opsonins IgG/Fc receptor, C3b/CR1, mannose-binding lectin, C-reactive protein, toll-like receptor - increase oxidative mechanisms for killing
60
what do macrophages also do besides phagocytize bacteria and debris?
secrete chemical mediators to promote healing and regeneration
61
what are the two reactions by which macrophages kill bacteria?
- NADPH-dependent oxidases: oxygen radicals and hydrogen peroxide - Myeloperoxidase (azurophilic granules): + halide ion-> hyperchlorous acis - respiratory burst - NO production
62
which way of killing bacteria is the most efficient?
Myeloperoxidase
63
what are some oxygen independent ways of killing bacteria?
bacterial permeability increasing protein lysozyme lactoferrin major basic protein
64
what plays the major role of deciding whether or not to resolve inflammation?
macrophages
65
what are the characteristics of acute inflammation?
- few days - primarily neutrophils in days 0-2 - macrophages and lymphocytes predominate after day 2 - if no further injury occurs or if infection is controlled-> inflammation resolved - any injured tissue undergoes regeneration
66
what are the characteristics of chronic inflammation?
- persistent injury or infectious agent - beyond 4 days to many days, weeks, months - macrophages and lymphocytes predominate - persistent cell activation and cytokine production - chronic tissue damage with fibrosis and scarring

Pathology I (8 decks)

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