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gen path- exam 1 > inflammation > Flashcards

inflammation Flashcards

1
Q

what are the clinical signs and symptoms of inflammation?

A
  • redness
  • swelling
  • heat
  • pain
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2
Q

how does vascularity change during acute inflammation?

A
  • vasodilation

- increased vascular permeability

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3
Q

what do the changes in vascularity (during ACUTE inflammation) cause?

A

promote:
fluid (edema) and inflammatory cell accumulation
in the tissue

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4
Q

vasodilation results in the relaxation of ________ arterioles

A

pre-capillary

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5
Q

what is vasodilation mediated by during acute inflammation/

A

Mediated by:

  • NO
  • PGs
  • Histamine
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6
Q

what is transudate?

A

Low protein content, low specific gravity fluid

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7
Q

when is non-inflammatory transudate present? what about inflammatory transudate?

A

Non-inflammatory - intact endothelium

Inflammatory – early endothelial contraction

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8
Q

what is exudate?

A

High protein content, high specific gravity fluid

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9
Q

what are the types of exudate? (theres 3 types)

A

Fibrinous – high protein, few cells

Purulent – high protein, many cells

Sanguineous – high protein, blood

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10
Q

T/F: the occurrence of transudate fluid is a result of fluid and protein leakage

A

FALSE- thats exudate

transudate is just fluid leakage

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11
Q

___________ contractions lead to an immediate increase in permeability

A

endothelial contractions

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12
Q

____________ is a delayed response (develops 4-6 hours after injury) and causes further vascular permeability

A

endothelial retraction

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13
Q

what mediates endothelial contraction?

A

PAF, histamine, bradykinin, leukotrienes

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14
Q

what mediates endothelial cell retraction following DIRECT endothelial injury?

A

IL-1, TNF, IFN-gamma

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15
Q

_________ is mediated by the injurious agent, or by ROS/enzymes from NEUTROPHILS

A

direct endothelial injury

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16
Q

what substances are secreted by injured cells to increase the pain perception during inflammation?

A

Bradykinin

PGE2

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17
Q

the fever (“heat”) associated with inflammation is associated with what cellular molecules?

A

IL-1

TNF

PGE2

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18
Q

what changes are seen in activated endothelial cells during inflammation? (4 changes)

A

1) Produce PGI2 and NO (vasodilation)
2) Contraction / retraction
3) Increase expression of adhesion molecules
4) Increase synthesis of mediators

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19
Q

what molecules facilitate leukocyte Adhesion?

A
  • integrins

1) ICAM
2) VCAM

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20
Q

Emigration or transmigration of leukocytes is mediated by ___________

A

PECAM

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21
Q

__________ is the movement along a concentration gradient of chemotactic factors

A

chemotaxis

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22
Q

the _________ of leukocytes is driven by physical forces (stasis)

A

margination

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23
Q

list the chemotactic factors involved in PMN recruitment

A

1) PAF (potent)
2) LTB4 (potent)
3) Chemokines
4) Bacterial lipids and peptides
5) C5a
6) Fibrin degradation products

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24
Q

what molecules will mediate attachment during phagocytosis?

A

opsonins on target cells: IgG, C3b, collectins

these interact with Fc receptors on neutrophil

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25
Q

how does lysosomal degradation occur?

A

by fusion of engulfed target with the phagosome

26
Q

what substances are released by the phagocyte during “oxygen bursts”

A

superoxide, hydrogen peroxide, hypochlorous radical

27
Q

__________ is an enzyme active in the creation of HOCl (hypochlorous radical)

A

Myeloperoxidase

28
Q

the presence of _________ defines acute inflammation

A

neutrophils

29
Q

neutrophils begin to accumulate at the site of injury within ______ hours

A

6-24

30
Q

neutrophils infiltrate tissue in response to tissue ________

A

necrosis

31
Q

how do neutrophils react once they reach the site of injury? (hint: they can do 2 things)

A
  • Undergo apoptosis after phagocytosis and digestion.

- Release reactive oxygen species and lysosomal enzymes

32
Q

________ cells replace PMNs, usually beginning within 48 hours

A

Monocytes (macrophages and histiocytes)

33
Q

T/F: the half-life of neutrophils is much longer than monocytes

A

FALSE

monocytes can last for months, while PMN’s last only days

34
Q

what are the functions of monocytes? (theres a shit-ton of them)

A 
Phagocytosis 
   Antigen presentation
   Cytokines
   Enzymes
   Plasma proteins
   MPO - ROS
   NO, Prostaglandins
   Factors of healing and
      repair
35
Q

what are some “other” cell types (besides PMN’s and monocytes) that are involved in injury/inflammation? what role do they play?

A

a) Lymphocytes, plasma cells
b) Eosinophils (allergic reactions, parasitic infections)
c) Mast cells – surface IgE (release histamine)

36
Q

a ______ is characterized by diffuse, permeative infiltration of neutrophils with edema

A

cellulitis

37
Q

a ______ is characterized by localized area of liquefactive necrosis

A

abscess

38
Q

a ______ is characterized by an erosion of an epithelial surface exposing underlying connective tissue

A

ulcer

39
Q

how does the length of time for chronic vs. acute inflammation differ?

A

acute inflammation: 10-14 days

vs.
chronic: months to years

40
Q

_______ inflammation is innate whereas ______ inflammation relies upon specific, adaptive immune system

A

acute, chronic

41
Q

T/F: although both acute and chronic inflammation can be reversible, only acute inflammation can be fatal

A

false- BOTH can be reversible and fatal

42
Q

causes for chronic inflammation include:

A
  1. Persistent infections
  2. Prolonged exposure to a toxic agent
  3. Immune-mediated inflammatory disease
43
Q

______________ inflammation is often associated with tissue repair that induces fibrosis.

A

non-specific chronic inflammation

44
Q

Granulomatous Inflammation is linked to what condition?

A

Linked to the delayed-type IV hypersensitivity immune reaction

45
Q

what 4 cell types are associated with chronic inflammation?

A

1) lymphocytes
2) macrophages
3) plasma cells
4) eosinophils

46
Q

Epithelioid (activated) histiocytes are often present in what form of inflammation?

A

Granulomatous Inflammation

47
Q

during a granulomatous inflammatory event, ____________ coalesce to form multinucleated giant cells Langhans or foreign body type).

A

Epithelioid histiocytes

48
Q

how does a site with granulomatous inflammation (a granuloma) heal?

A

by fibrosis

49
Q

Older granulomas develop a rim of _________ and _______

A

fibroblasts and connective tissue

50
Q

what bacterial infections are characterized by granuloma formation?

A

tuberculosis, cat-scratch fever

51
Q

what types of fungal infections lead to granulomas?

A

coccidioidomycosis, histoplasmosis

52
Q

sarcoidosis, Crohn’s disease are both characterized by ________ inflammation

A

Granulomatous

53
Q

_________ is released by physical injury, or antigen binding to IgE, C3a and C5a, cytokines.

A

Histamine

54
Q

cyclo-oxygenase and lipo-oxygenase are important enzymes in the formation of what mediators?

A

Prostaglandins (cyclo) and leukotrienes (lipo)

55
Q

While prostaglandins generally cause vasodilation, ______________ causes vasoconstriction

A

thromboxane A2

56
Q

thromboxane A2 promotes platelet aggregation, while ____________ inhibits platelet aggregation

A

prostacyclin

57
Q

what cell types are “labile” (continuously dividing)?

A

hematopoietic cells, surface epithelium

58
Q

parenchymal cells, smooth muscle cells, and fibroblasts are all considered ________ in respect to their proliferation rate

A

stable

59
Q

what types of cells are “permanent”, meaning they do not proliferate?

A

neurons, cardiac muscle

60
Q

what is the primary cause of delayed healing?

A

infection

61
Q

healing by ___________ is characterized by more inflammation and granuloma tissue formation

A

healing by secondary intention

62
Q

what causes the wound contraction during healing by a secondary intention?

A

Wound contraction due to myofibroblasts

gen path- exam 1 (10 decks)

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