Inflammation Overview Flashcards
Name the four typical signs of inflammation.
redness
swelling
heat
pain
How do formed cells communicate with the vasculature?
mediators
What are the two main events that occur with acute inflammation?
- Vascular changes + mediators
2. Cellular events + mediators
What are some common mediators that are present with acute inflammation?
IL-1
TNF-alpha
IL-6
“I Like, I Like TiNy, aCUTE things”
With acute inflammation there is a(n) ______ in vascular permeability.
increase
Increased vascular permeability will promote fluid leakage (edema) and cell accumulation. Which cells are the first to arrive at the site of injury?
PMNs
What are the effects of vasodilation?
- relaxation of pre-capillary arterioles
- engorgement of capillary beds with redness/warmth
What are three mediators associated with vasodilation?
Nitric Oxide
Prostaglandins
Histamine
What is transudate?
a type of fluid that accumulates with inflammation
- low protein
- low specific gravity
How does exudate differ from transudate?
Exudate has a HIGH protein content and HIGH specific gravity
Transudate has a LOW protein content and LOW specific gravity
Is exudate associated with “early endothelial contraction?”
NO, exudate is seen later.
*transudate is associated with early endothelial contraction in the case of inflammatory processes: the endothelium contracts but is still intact (not separating)
True or False: Transudate can be inflammatory or non-inflammatory.
True
What are three forms of exudate?
- Fibrinous
- Purulent
- Sanguineous
Describe fibrinous exudate.
high protein
few cells
Describe purulent exudate.
high protein many cells (PMNs)
Describe sanguineous exudate.
high protein
presence of blood
In a normal vessel, the hydrostatic pressure is slightly higher but relatively equal to the ________.
colloid osmotic pressure
Transudate is associated with an increase in ______ pressure.
hydrostatic pressure (plus decreased colloid osmotic pressure=fluid leakage)
What are the three mechanisms of increased vascular permeability?
- Endothelial contraction
- Endothelial retraction
- Direct injury
Which mechanism of increased vascular permeability is delayed (develops in 4-6 hours) and sustained for 24 hours or more?
Endothelial REtraction
Which mechanism of vascular permeability occurs immediately and is reversible?
Endothelial CONtraction
Which mechanism of vascular permeability is either immediate OR delayed and is sustained?
Direct injury (detachment/necrosis/non-lethal injury)
Endothelial ________ is mediated by PAF, histamine, bradykinin, and leukotrienes.
CONtraction
Endothelial ________ is mediated by IL-1, TNF, and IFN-gamma.
REtraction
Endothelial ________ is mediated by ROS/enzymes from PMNs.
injury
Pain symptoms of acute inflammation are mediated by _____ and ______.
bradykinin
PGE2
“P and B: P-ain is B-ad”
Fever from acute inflammation is mediated by _____, ______, and _____.
IL-1
TNF
PGE2
“fever P.I.T”
True or False: Infectious agents, hypoxia, and inflammatory mediators will activate endothelial cells.
True
Do “activated endothelial cells” increase or decrease the expression of adhesion molecules?
increase
Activated endothelial cells will produce PGI2 and ______ which results in vasodilation.
Nitric Oxide (NO)
What are the five leukocyte actions that follow activation?
- Margination
- Rolling
- Adhesion
- Transmigration
- Chemotaxis
Which mediators are involved in leukocyte rolling?
selectins
Which two integrins are involved in leukocyte adhesion?
ICAM
VCAM
________ is integral to leukocyte emigration or transmigration (allows neutrophils to pass through gaps in endothelial cells)
PECAM
Cellulitis is caused by ______ cells moving into tissues.
White Blood
What are the four stages of phagocytosis/digestion?
- Attachment
- Engulfment
- Degranulation
4 Oxidative burst
Oxidative burst occurs within a ________.
phagolysosome
True or False: There are multiple mechanisms of intracellular killing by leukoctyes that are non-respiratory.
True
ex. lysozyme, major basic protein, defensins, bactericidal permeability-increasing protein
The presence of _____ defines acute inflammation.
neutrophils
What cell type is responsible for apoptosis, responds to necrosis, and releases ROS?
neutrophil
Edema activity peaks after ______ hours.
10 to 12 (then drops)
PMN activity peaks after ______ hours.
24 hours (then drops)
Macrophage/Monocyte activity peaks after ______ and then remains within tissue for _____.
2 to 3 days
months
What are the functions of activated macrophages?
- P hagocytosis
- R OS
- A ntigen presentation
- N itric Oxide and prostaglandins
- C ytokines and plasma proteins
- E nzymes and factors of healing/repair
“They PRANCE in to clean up the mess”
What are the three “later stage” inflammatory cells?
lymphocytes (immune function) eosinophils (allergy, parasite) mast cells (histamine)
What are the three different patterns of inflammation?
- Abscess
- Cellulitis
- Ulcer
What is cellulitis?
diffuse tissue infiltration by PMNs, with edema
What is an abscess?
a LOCALIZED collection of PMNs and degradation of tissues (liquefactive necrosis: center filled with pus)
What is an ulcer?
erosion of epithelium with exposure to the underlying connective tissue
Compare the duration of acute inflammation to that of chronic inflammation.
Acute: days - weeks
Chronic: days - years
What is the location of acute inflammation?
localized
What is the location of chronic inflammation?
maybe systemic
Is there an immune response for acute inflammation?
No
Is there an immune response for chronic inflammation?
Yes
Is acute inflammation reversible? Chronic?
Acute: often reversible
Chronic: maybe
Which cells are most prevalent in acute inflammation?
PMNs
Which cells are most prevalent in chronic inflammation?
macrophages and lymphocytes
What are the two types of chronic inflammation?
- non-specific
2. granulomatous
True or False: Tissue destruction leading to fibrosis is common in chronic inflammation.
True
What is another (more common) name for “fibrosis?”
scarring
_______ is a common cause of chronic inflammation.
Infection (Tuberculosis)
Why is acute inflammation of the lung more life threatening than chronic inflammation of the lung?
the alveoli fill with PMNs
Which cells of chronic inflammation are seen histologically as “mostly nucleus?”
lymphocytes
Which cells of chronic inflammation are seen with “eccentric nuclei?”
plasma cells
Which cells of chronic inflammation are filled with many small red granules?
eosinophils
What are the four causes of granulomatous (chronic type) inflammation?
- Inorganic matter (sutures)
- Bacterial infection (TB)
- Parasitic infection (toxoplasmosis)
- Uncertain etiology (sarcoidosis, Crohn’s disease)
Which inflammatory mediators will increase vascular permeability? (5)
histamine bradykinin leukotrienes PAF Complements C5a and C3a
Which three mediators are involved in vasodilation?
histamine
NO
Prostaglandins
Which mediators are involved in chemotaxis/opsonization?
C5a and C3a
PAF
Leukotriene B4
Which chemical mediators are highly involved with pain potentiation?
bradykinin
prostaglandins
IL-1
TNF
Which chemical mediators increase fever associated with inflammation?
IL-1
TNF
Prostaglandins
Prostaglandins will vasodilate; whereas, its opposite _______ will vasoconstrict.
Thromboxane A2
Prostaglandins and leukotrienes are derived from ______.
arachidonic acid
- ->cyclo-oxygenase = prostaglandins
- ->lipoxgenase = leukotrienes
What is a “labile” cell? Give examples.
continuously dividing (regrowable)
- hematopoietic cells
- surface epithelium
What is a “stable” cell? Give examples.
some replicative activity
- parenchymal cells
- smooth muscle cells
- fibroblasts
What is a “permanent” cell? Give examples.
nonproliferative, not regenerative
- neurons
- cardiac muscle
First Intention healing occurs within ______ days.
3 to 5
Second Intention healing occurs within _______, and is accompanied by _______ shrinkage.
1 to 3 weeks
myofibroblastic
_______ effect wound healing such as: epithelial proliferation, monocyte chemotaxis, fibroblast proliferation, angiogenesis, collagen synthesis
Growth Factors
What is the primary cause of delayed wound healing?
infection
Other than infection, what are some additional factors that would affect wound healing?
- nutrition
- steroid therapy
- mechanical factors
- poor tissue perfusion (diabetes, atherosclerosis)
