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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
Q

PMNs

A

Neutrophils, polymononuclear cells

26
Q

nitric oxide

A

Chemical Mediator of Inflammation, released from macrophages and endothelial cells. Involved in tissue destruction and vasodilation.

27
Q

Chemical mediators of inflammation that increase vascular permeability

A

bradykinin, C3a, C5, histamine, serotonin, PAF, prostaglandins, leukotrienes

28
Q

Chemical mediators of inflammation – Vascular dilators

A

bradykinin, histamine, serotonin, prostaglandin, NO

29
Q

Chemical mediators of inflammation – Vascular constrictors

A

PAF

30
Q

Chemical mediators of inflammation – Smooth Muscle Contractors

A

bradykinin

31
Q

Chemical mediators of inflammation – pain elicitors

A

bradykinin and prostaglandin

32
Q

Chemical mediators of inflammation – histamine release

A

C3, C5, IL1, IL8

33
Q

Chemical mediators of inflammation – opsonization promotor

A

C3a

34
Q

Chemical mediators of inflammation – Chemotaxis mediators

A

C5, C3, IL1, leukotriene B4, prostaglandins, PAF

35
Q

Chemical mediators of inflammation – platelet aggregation promoters

A

thromboxane A2

36
Q

Chemical mediators of inflammation – platlet aggregation inhibitors

A

prostacyclin

37
Q

Chemical mediators of inflammation – Fever inducers

A

IL1, IL6, TNF

38
Q

Chemical mediators of inflammation – Tissue destroyers

A

NO

39
Q

Chemical mediators of inflammation – increased WBC releasors

A

IL1, TNF

40
Q

Chemical mediators of inflammation – increased WBC production

A

CSFs

41
Q

Acute Inflammation outcomes

A

complete resolution, suppuration/abscess formation, progression to chronic inflammation, repair

42
Q

granulomatous inflammation

A

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
Q

laboratory dx of inflammation

A
  • Leukocytosis (more bands–immature leukocytes, seen in chronic inflammation)
  • CRP– ACUTE phase reaction, increased WBCs
  • ESR - acute inflammation, non specific marker for infection
44
Q

primary intention wound healing

A

put it back together - cleanly incised and reapproximated

45
Q

secondary intention

A

let it heal openly - granulates in

46
Q

tertiary intention

A

delayed primary closure, avoids infection

47
Q

Phases of wound healing

A

1) inflammation
2) epitheliazation
3) collagen synthesis
4) Scar Maturation
5) organization

48
Q

Cell Injury

A 
PGOCNIi
physical
genetic
oxengation
chemical
nutrition
infectious
immunological
49
Q

reversible cell injury

A

cell swells b/c NA/K pump is impaired, ER swells, mitochondria swells, chromatin clumps

50
Q

irreversible cell injury

A

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
Q

hypoxia vs. hypoxemia

A

hypoxia is decreased oxygen for body tissue, hypoxemia is decreased oxygen availability to blood

52
Q

induction

A

one group of cells changes the behavior of another group of cells

53
Q

Types of necrosis

A 
"coagulation of liquid fat results in lawsuit cases"
Coagulative
liquefactive
caseous
fat
also: 
gummatous
hemorrhagic
fibrinoid
fat saponification
wet gangrene
dry gangrene
54
Q

coagulative necrosis

A

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
Q

liquefactive necrosis

A

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
Q

caseous necrosis

A

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
Q

fat necrosis

A

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
Q

Gummatous necrosis, hemorrhagic necrosis, and fibrinoid necrosis

A

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
Q

anaplasia

A

reversion of cells to an earlier state

60
Q

wet/dry gangrene

A

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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