Acute and Chronic Inflammation Flashcards

1
Q

What are the four cardinal signs of inflammation?

A

Calor, Rubor, Tumor, Dolor, Functio Lasea

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2
Q

what are the main cells involved with acute inflammation?

A

neutrophils

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3
Q

what are the main cells involved with chronic inflammation?

A

monocytes/macrophages and lymphocytes

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4
Q

what is the abnormal stimulus for inflammation recognized by?

A

epithelial cells, dendritic cells, phagocytes

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5
Q

Which 2 receptors are involed in inflammation?

A

Toll like Receptors: located in plasma membrane, when activated release cytokines (TNF); Inflammasome: cytoplasmic complex recognizing parts of dead cells, triggers activation of caspase-1 which activates IL-1 which recruits leukocytes

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6
Q

which 2 mediators are responsible for vasodilation?

A

histamine and nitric oxide, leads to stasis and margination of leukocytes

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7
Q

which 2 mediators are responsible for endothelial cell contraction?

A

histamine and bradykinin

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8
Q

Histamine causes:

A

vasodialtion and vascular permeability

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9
Q

nictric oxide causes:

A

vasodilation

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10
Q

bradykinin causes:

A

vasodilation and increased permeability and pain

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11
Q

what is transudate?

A

not enough proteins, kidneys are not functioning, fluids leak out, non-inflammatory process, due to increased hydrostatic pressure, low specific gravity

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12
Q

what is exudate?

A

more significant damage, causes inflammation, fluid AND protein leakage, high specific gravity–high protein!, caused by alteration in normal vessel permeability

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13
Q

what are the steps for acute inflammation?

A

margination, rolling, adhesion, transmigration, chemotaxis

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14
Q

which mediators aid in rolling and loose adhesion?

A

P and E selectin

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15
Q

which mediators on leukocytes provide stable attachment?

A

integrins

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16
Q

which are the two cytokines most likely secreted during inflammation?

A

IL-1 and TNF

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17
Q

what is diapedesis?

A

movement of leukocytes through the vessel wall (cells squeeze through the vessel wall)

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18
Q

what chemokine drives transmigration?

A

CD31 (PECAM1)

19
Q

what is the term for crossing the vessel wall and migrating towards injury site?

A

chemotaxis

20
Q

what are the components of chemotaxis?

A

bacterial products, chemokines, complement, leukotrienes

21
Q

when are leukocytes activated?

A

after recruitment to the site of injury!

22
Q

what activate leukocytes?

A

microbes, necrotic tissue, mediators

23
Q

result of leukocyte activation?

A

phagocytosis, intracellular destruction, release of substances that destroy dead tissue and microbes

24
Q

how do leukocytes recognize microbes?

A

via IgG, C3b (opsonins), these are ready to coat microbes and mark microbes as a targets

25
what are the specific species that degrade microbes within the phagolysosome?
ROS (Reactive Oxygen Species)
26
what two cytokines activate endothelial cells?
IL-1 and TNF
27
What are the subtypes of acute inflammation?
serious, fibrinous, suppurative, ulcer
28
serous inflammation
mildest form of acute inflammation, outpouring of thin fluid (protein-poor) from plasma or serosal cavity linings, ex: peritoneal, pleural, or pericardial effusions, (congestive heart failure), skin BLISTER form burn, viral infection or trauma
29
fibrinous inflammation
occurs secondary to more serious injury, larger vascular leaks, passage of fibrinogen, conversion to fibrin, affects linings: meninges, pericardium, pleura, peritoneum, examples: fibrinous pericarditis from uremia, fibrinous pleuritis overlying a pulmonary infarct
30
supporative inflammation
when large numbers of neutrophils are present, along with necrotic cells, edema and bacteria=PUS, occurs with Staphylococcus, abscesses, acute appendicitis, acute bronchopneumonia
31
ulcer
local defect, surface of organ or tissue, sloughing of surface covering and necrotic inflammatory tissue, examples: peptic ulcer, skin ulceration
32
what is chronic inflammation caused by?
persistent infections diff to eradicate-TB, syphillis, leprosy, prolonges exposure to toxic agents, immune-mediated inflammatory disease (RA, SLE)
33
in chronic inflammation, what cells persist?
macrophages!
34
when are eosinophils activated in chronic inflammation?
in parasitic infection and IgE mediated inflammation (allergies), major basic protein--toxic to parasites and epithelial cells
35
which cells are central to allergic reactions?
Mast cells
36
what is granulomatous Inflammation?
distinctive pattern of inflammation that contains macrophages with epithelioid appearance, develop multinucleate giant cells via IFN-y, surrounding lymphocytes, and fibrosis, caused from TB (central caseous necrosis),
37
what is fever caused by?
pyrogens (IL-1 and TNF), PGE2 (stimulates hypothalamus to reset at higher temp)
38
when acute-phase proteins are elevated what are they stimulated by?
IL-6
39
what else is a systemic effect of inflammation?
increased leukocytes!!
40
neutorphilia indicates
bacterial infection
41
lymphocytosis indicates
viarl infections
42
eosinophilia indicates
allergies, asthma, parasitic infections
43
leukopenia indicates
typhoid, rickettsiae, some protozoans