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inflammation, necrosis, etc. > ham > Flashcards

ham Flashcards

1
Q

exudate

A

fluid released from the body with a high concentration of protein, cells, or solid debris

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2
Q

exudation

A

pathological oozing of fluids, usually as a result of inflammation

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3
Q

transudate

A

fluid that passes through a membrane, ultrafiltrate of plasma

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4
Q

transudation

A

oozing of a fluid through pores or interstices

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5
Q

pus

A

protein rich fluid rich in leukocytes and parenchymal cell debris

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6
Q

edema

A

excess fluid in interstitial areas / body cavities from exudate and transudate

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7
Q

effusion

A

escape of fluid into a part of the body (pleural effusion)

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8
Q

sequence of vascular flow changes in acute inflammation

A

1) initial brief vasoconstriction to limit blood loss
2) vasodilation to increase blood flow, which results in calor, rubor, allows cells needed for repair to reach site more easily
3) increased vascular permeability due to increased capillary pressure, resulting in escape of exudate and ultimately, edema

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9
Q

signs of acute inflammation

A

Dolor, Calor, Rubor, Tumor, Functio Lasae

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10
Q

Cellular events leading to emigration of leukocytes to site of injury

A 
Leuckocyte extravasion:
Marge Rolls Along a Track
Marginization
Rolling
Adhesion
Transmigration

then chemotaxis - leukocytes move towards injury following chemical signals “chemoattractants”

phagocytosis - macrophage follows chemical gradient to source

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11
Q

Vasoactive Amines

A

Preformed Chemical Mediators of Inflammation, preformed and released quickly from mast cells (histamine) and platelets (serotonin)

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12
Q

Histamine

A

Vasoactive amine - chemical mediator preformed and released from mast cells that causes vasodilation and increases vascular permeability

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13
Q

Serotonin

A

Vasoactive amine - chemical mediator pre-formed and released from platelets that causes vasodilation and increases vascular permeability

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14
Q

Bradykinin

A

Chemical Mediator of inflammation, preformed in the plasma, increases vascular permeability, causes vasodilation, causes smooth muscle contraction, elicits pain

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15
Q

Complement System

A

Chemical Mediators of Inflammation; preformed in the plasma, includes C3a and C5a

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16
Q

C3a

A

Part of the complement system, promotes histamine release, mediates chemotaxis, promotes opsonization

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17
Q

C5a

A

Mediates chemotaxis, promotes histamine release

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18
Q

Arachidonic acid metabolites

A

Chemical Mediators of Inflammation located on the lipid membrane and formed via the cyclooxygenase and lipooxygenase pathways

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19
Q

Prostaglandins

A

Chemical Mediator of Inflammation, an arachidonic acid metabolite. Promotes vasodilation, increases vascular permeability, mediates chemotaxis.

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20
Q

Thromboxane

A

Chemical Mediator of Inflammation, an arachidonic acid metabolite. Promotes platelet aggregation

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21
Q

Prostacyclin

A

Inhibits platelet aggregation

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22
Q

Leukotrienes

A

Chemical Mediator of Inflammation, arachidonic acid metabolites. Mediates chemotaxis and increases vascular permeability.

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23
Q

Cytokines

A

Chemical Mediator of Inflammation General term for family of proteins produced by many cell types to mediate the function of other cell types.
IL1-mediates chemotaxis, induces fever, induces WBC release, promotes histamine release
IL6-induces fever
IL8-promotes histamine release
TNF-Induces fever, induces WBC release from marrow
p-Colony stimulating factors - increase WBC production

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24
Q

Platelet Activating Factor

A

PAF - Chemical Mediator of Inflammation. Released from mast cells, PMN (neutrophils)

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25
PMNs
Neutrophils, polymononuclear cells
26
nitric oxide
Chemical Mediator of Inflammation, released from macrophages and endothelial cells. Involved in tissue destruction and vasodilation.
27
Chemical mediators of inflammation that increase vascular permeability
bradykinin, C3a, C5, histamine, serotonin, PAF, prostaglandins, leukotrienes
28
Chemical mediators of inflammation -- Vascular dilators
bradykinin, histamine, serotonin, prostaglandin, NO
29
Chemical mediators of inflammation -- Vascular constrictors
PAF
30
Chemical mediators of inflammation -- Smooth Muscle Contractors
bradykinin
31
Chemical mediators of inflammation -- pain elicitors
bradykinin and prostaglandin
32
Chemical mediators of inflammation -- histamine release
C3, C5, IL1, IL8
33
Chemical mediators of inflammation -- opsonization promotor
C3a
34
Chemical mediators of inflammation -- Chemotaxis mediators
C5, C3, IL1, leukotriene B4, prostaglandins, PAF
35
Chemical mediators of inflammation -- platelet aggregation promoters
thromboxane A2
36
Chemical mediators of inflammation -- platlet aggregation inhibitors
prostacyclin
37
Chemical mediators of inflammation -- Fever inducers
IL1, IL6, TNF
38
Chemical mediators of inflammation -- Tissue destroyers
NO
39
Chemical mediators of inflammation -- increased WBC releasors
IL1, TNF
40
Chemical mediators of inflammation -- increased WBC production
CSFs
41
Acute Inflammation outcomes
complete resolution, suppuration/abscess formation, progression to chronic inflammation, repair
42
granulomatous inflammation
a conglomeration of macrophages cluster together to wall of infectious material from the rest of the body. Granulomas may form as a result of the inability of phagocytes to digest foreign material or continued irritant stimulus.
43
laboratory dx of inflammation
- Leukocytosis (more bands--immature leukocytes, seen in chronic inflammation) - CRP-- ACUTE phase reaction, increased WBCs - ESR - acute inflammation, non specific marker for infection
44
primary intention wound healing
put it back together - cleanly incised and reapproximated
45
secondary intention
let it heal openly - granulates in
46
tertiary intention
delayed primary closure, avoids infection
47
Phases of wound healing
1) inflammation 2) epitheliazation 3) collagen synthesis 4) Scar Maturation 5) organization
48
Cell Injury
``` PGOCNIi physical genetic oxengation chemical nutrition infectious immunological ```
49
reversible cell injury
cell swells b/c NA/K pump is impaired, ER swells, mitochondria swells, chromatin clumps
50
irreversible cell injury
cell membrane integrity is lost, ER swells and lyses, ribosomes lost, lysosomes rupture, and nuclear changes occur karolysis (dissolution of chromatin) -pyknosis (nuclear shrinkage) karyorrhexis (membrane rupture/fragmentation)
51
hypoxia vs. hypoxemia
hypoxia is decreased oxygen for body tissue, hypoxemia is decreased oxygen availability to blood
52
induction
one group of cells changes the behavior of another group of cells
53
Types of necrosis
``` "coagulation of liquid fat results in lawsuit cases" Coagulative liquefactive caseous fat ``` ``` also: gummatous hemorrhagic fibrinoid fat saponification wet gangrene dry gangrene ```
54
coagulative necrosis
Cells are dead, but maintain outline/form, so the tissue maintains its architecture. Cell has no nucleus and cytoplasm appears pink. Cell death resulting from hypoxia (aside from brain cells) leads to coagulative necrosis. Physical presentation: gangrene; skin appears firm, pale, as if “cooked.”
55
liquefactive necrosis
Cell loses its outline/shape and becomes “liquidy.” Bacterial and some fungal infections lead to liquefactive necrosis. When brain cells become hypoxic, they suffer liquefactive necrosis. Cell loses structure b/c lysosomal organisms are present & quickly break down necrotic cells. Physical Presentation: Thick yellowish fluid/pus is present.
56
caseous necrosis
Cell loses its outline/form & tissue loses its architecture. Macrophages and lymphocytes surround the cell (called granulomatous inflammatory border). Caseous Necrosis occurs in TB infections. Presentation: Soft, “cheesy,” yellow, whitish areas are present.
57
fat necrosis
Affects fat cells; cell maintains its outline/form and a blue layer of Calcium forms around the cell. Neutrophils, lymphocytes, and macrophages surround the cell. Fat necrosis necrosis occurs in the pancreas & in fatty tissue (breast, abd. subcutaneous adipose tissue). Presentation: white, chalky areas are seen (these white/chalky areas are called “saponification”).
58
Gummatous necrosis, hemorrhagic necrosis, and fibrinoid necrosis
gummatous - firm, rubbery dead tissue, original archetecture not preserved, seen in only spirochete infections (syphillis) hemorrhagic- occurs when drainage of a tissue is blocked & becomes backed up with blood and unable to perfuse (testicular torsion) fibrinoid - necrosis that affects blood vessel walls
59
anaplasia
reversion of cells to an earlier state
60
wet/dry gangrene
dry - black, dry, shrivelled tissue with distinct difference between healthy and not wet- swollen, red, dark, liquified tissue, foul odor from bacteria, border hard to discern

inflammation, necrosis, etc. (1 decks)

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