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gen path- exam 1 > inflammation > Flashcards

inflammation Flashcards

(62 cards)

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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
how does lysosomal degradation occur?
by fusion of engulfed target with the phagosome
26
what substances are released by the phagocyte during "oxygen bursts"
superoxide, hydrogen peroxide, hypochlorous radical
27
__________ is an enzyme active in the creation of HOCl (hypochlorous radical)
Myeloperoxidase
28
the presence of _________ defines acute inflammation
neutrophils
29
neutrophils begin to accumulate at the site of injury within ______ hours
6-24
30
neutrophils infiltrate tissue in response to tissue ________
necrosis
31
how do neutrophils react once they reach the site of injury? (hint: they can do 2 things)
- Undergo apoptosis after phagocytosis and digestion. | - Release reactive oxygen species and lysosomal enzymes
32
________ cells replace PMNs, usually beginning within 48 hours
Monocytes (macrophages and histiocytes)
33
T/F: the half-life of neutrophils is much longer than monocytes
FALSE monocytes can last for months, while PMN's last only days
34
what are the functions of monocytes? (theres a shit-ton of them)
``` Phagocytosis Antigen presentation Cytokines Enzymes Plasma proteins MPO - ROS NO, Prostaglandins Factors of healing and repair ```
35
what are some "other" cell types (besides PMN's and monocytes) that are involved in injury/inflammation? what role do they play?
a) Lymphocytes, plasma cells b) Eosinophils (allergic reactions, parasitic infections) c) Mast cells – surface IgE (release histamine)
36
a ______ is characterized by diffuse, permeative infiltration of neutrophils with edema
cellulitis
37
a ______ is characterized by localized area of liquefactive necrosis
abscess
38
a ______ is characterized by an erosion of an epithelial surface exposing underlying connective tissue
ulcer
39
how does the length of time for chronic vs. acute inflammation differ?
acute inflammation: 10-14 days vs. chronic: months to years
40
_______ inflammation is innate whereas ______ inflammation relies upon specific, adaptive immune system
acute, chronic
41
T/F: although both acute and chronic inflammation can be reversible, only acute inflammation can be fatal
false- BOTH can be reversible and fatal
42
causes for chronic inflammation include:
1. Persistent infections 2. Prolonged exposure to a toxic agent 3. Immune-mediated inflammatory disease
43
______________ inflammation is often associated with tissue repair that induces fibrosis.
non-specific chronic inflammation
44
Granulomatous Inflammation is linked to what condition?
Linked to the delayed-type IV hypersensitivity immune reaction
45
what 4 cell types are associated with chronic inflammation?
1) lymphocytes 2) macrophages 3) plasma cells 4) eosinophils
46
Epithelioid (activated) histiocytes are often present in what form of inflammation?
Granulomatous Inflammation
47
during a granulomatous inflammatory event, ____________ coalesce to form multinucleated giant cells Langhans or foreign body type).
Epithelioid histiocytes
48
how does a site with granulomatous inflammation (a granuloma) heal?
by fibrosis
49
Older granulomas develop a rim of _________ and _______
fibroblasts and connective tissue
50
what bacterial infections are characterized by granuloma formation?
tuberculosis, cat-scratch fever
51
what types of fungal infections lead to granulomas?
coccidioidomycosis, histoplasmosis
52
sarcoidosis, Crohn’s disease are both characterized by ________ inflammation
Granulomatous
53
_________ is released by physical injury, or antigen binding to IgE, C3a and C5a, cytokines.
Histamine
54
cyclo-oxygenase and lipo-oxygenase are important enzymes in the formation of what mediators?
Prostaglandins (cyclo) and leukotrienes (lipo)
55
While prostaglandins generally cause vasodilation, ______________ causes vasoconstriction
thromboxane A2
56
thromboxane A2 promotes platelet aggregation, while ____________ inhibits platelet aggregation
prostacyclin
57
what cell types are "labile" (continuously dividing)?
hematopoietic cells, surface epithelium
58
parenchymal cells, smooth muscle cells, and fibroblasts are all considered ________ in respect to their proliferation rate
stable
59
what types of cells are "permanent", meaning they do not proliferate?
neurons, cardiac muscle
60
what is the primary cause of delayed healing?
infection
61
healing by ___________ is characterized by more inflammation and granuloma tissue formation
healing by secondary intention
62
what causes the wound contraction during healing by a secondary intention?
Wound contraction due to myofibroblasts

gen path- exam 1 (10 decks)

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