inflammation Flashcards
what are the clinical signs and symptoms of inflammation?
- redness
- swelling
- heat
- pain
how does vascularity change during acute inflammation?
- vasodilation
- increased vascular permeability
what do the changes in vascularity (during ACUTE inflammation) cause?
promote:
fluid (edema) and inflammatory cell accumulation
in the tissue
vasodilation results in the relaxation of ________ arterioles
pre-capillary
what is vasodilation mediated by during acute inflammation/
Mediated by:
- NO
- PGs
- Histamine
what is transudate?
Low protein content, low specific gravity fluid
when is non-inflammatory transudate present? what about inflammatory transudate?
Non-inflammatory - intact endothelium
Inflammatory – early endothelial contraction
what is exudate?
High protein content, high specific gravity fluid
what are the types of exudate? (theres 3 types)
Fibrinous – high protein, few cells
Purulent – high protein, many cells
Sanguineous – high protein, blood
T/F: the occurrence of transudate fluid is a result of fluid and protein leakage
FALSE- thats exudate
transudate is just fluid leakage
___________ contractions lead to an immediate increase in permeability
endothelial contractions
____________ is a delayed response (develops 4-6 hours after injury) and causes further vascular permeability
endothelial retraction
what mediates endothelial contraction?
PAF, histamine, bradykinin, leukotrienes
what mediates endothelial cell retraction following DIRECT endothelial injury?
IL-1, TNF, IFN-gamma
_________ is mediated by the injurious agent, or by ROS/enzymes from NEUTROPHILS
direct endothelial injury
what substances are secreted by injured cells to increase the pain perception during inflammation?
Bradykinin
PGE2
the fever (“heat”) associated with inflammation is associated with what cellular molecules?
IL-1
TNF
PGE2
what changes are seen in activated endothelial cells during inflammation? (4 changes)
1) Produce PGI2 and NO (vasodilation)
2) Contraction / retraction
3) Increase expression of adhesion molecules
4) Increase synthesis of mediators
what molecules facilitate leukocyte Adhesion?
- integrins
1) ICAM
2) VCAM
Emigration or transmigration of leukocytes is mediated by ___________
PECAM
__________ is the movement along a concentration gradient of chemotactic factors
chemotaxis
the _________ of leukocytes is driven by physical forces (stasis)
margination
list the chemotactic factors involved in PMN recruitment
1) PAF (potent)
2) LTB4 (potent)
3) Chemokines
4) Bacterial lipids and peptides
5) C5a
6) Fibrin degradation products
what molecules will mediate attachment during phagocytosis?
opsonins on target cells: IgG, C3b, collectins
these interact with Fc receptors on neutrophil
how does lysosomal degradation occur?
by fusion of engulfed target with the phagosome
what substances are released by the phagocyte during “oxygen bursts”
superoxide, hydrogen peroxide, hypochlorous radical
__________ is an enzyme active in the creation of HOCl (hypochlorous radical)
Myeloperoxidase
the presence of _________ defines acute inflammation
neutrophils
neutrophils begin to accumulate at the site of injury within ______ hours
6-24
neutrophils infiltrate tissue in response to tissue ________
necrosis
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
________ cells replace PMNs, usually beginning within 48 hours
Monocytes (macrophages and histiocytes)
T/F: the half-life of neutrophils is much longer than monocytes
FALSE
monocytes can last for months, while PMN’s last only days
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
repairwhat 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)
a ______ is characterized by diffuse, permeative infiltration of neutrophils with edema
cellulitis
a ______ is characterized by localized area of liquefactive necrosis
abscess
a ______ is characterized by an erosion of an epithelial surface exposing underlying connective tissue
ulcer
how does the length of time for chronic vs. acute inflammation differ?
acute inflammation: 10-14 days
vs.
chronic: months to years
_______ inflammation is innate whereas ______ inflammation relies upon specific, adaptive immune system
acute, chronic
T/F: although both acute and chronic inflammation can be reversible, only acute inflammation can be fatal
false- BOTH can be reversible and fatal
causes for chronic inflammation include:
- Persistent infections
- Prolonged exposure to a toxic agent
- Immune-mediated inflammatory disease
______________ inflammation is often associated with tissue repair that induces fibrosis.
non-specific chronic inflammation
Granulomatous Inflammation is linked to what condition?
Linked to the delayed-type IV hypersensitivity immune reaction
what 4 cell types are associated with chronic inflammation?
1) lymphocytes
2) macrophages
3) plasma cells
4) eosinophils
Epithelioid (activated) histiocytes are often present in what form of inflammation?
Granulomatous Inflammation
during a granulomatous inflammatory event, ____________ coalesce to form multinucleated giant cells Langhans or foreign body type).
Epithelioid histiocytes
how does a site with granulomatous inflammation (a granuloma) heal?
by fibrosis
Older granulomas develop a rim of _________ and _______
fibroblasts and connective tissue
what bacterial infections are characterized by granuloma formation?
tuberculosis, cat-scratch fever
what types of fungal infections lead to granulomas?
coccidioidomycosis, histoplasmosis
sarcoidosis, Crohn’s disease are both characterized by ________ inflammation
Granulomatous
_________ is released by physical injury, or antigen binding to IgE, C3a and C5a, cytokines.
Histamine
cyclo-oxygenase and lipo-oxygenase are important enzymes in the formation of what mediators?
Prostaglandins (cyclo) and leukotrienes (lipo)
While prostaglandins generally cause vasodilation, ______________ causes vasoconstriction
thromboxane A2
thromboxane A2 promotes platelet aggregation, while ____________ inhibits platelet aggregation
prostacyclin
what cell types are “labile” (continuously dividing)?
hematopoietic cells, surface epithelium
parenchymal cells, smooth muscle cells, and fibroblasts are all considered ________ in respect to their proliferation rate
stable
what types of cells are “permanent”, meaning they do not proliferate?
neurons, cardiac muscle
what is the primary cause of delayed healing?
infection
healing by ___________ is characterized by more inflammation and granuloma tissue formation
healing by secondary intention
what causes the wound contraction during healing by a secondary intention?
Wound contraction due to myofibroblasts
