acute and chronic inflammation

Question 1

Rapid in onset (minutes)
Short duration (hours or a few days)
Exudation of fluid and plasma proteins (edema)
Emigration of leukocytes (neutrophils)

Answer 1

acute inflammation

Question 2

May follow acute inflammation
May be insidious in onset
Longer duration
Presence of lymphocytes and macrophages
Proliferation of blood vessels and fibrosis
Tissue destruction

Answer 2

chronic inflammation

Question 3

3 major components of acute inflammation

Answer 3

Alterations in vascular caliber
Structural changes in the microvasculature
Emigration of the leukocytes

Question 4

what are causes of acute inflammation?

Answer 4

infections
tissue necrosis
foreign bodies
immune reactions

Question 5

what is exudate?

Answer 5

Inflammatory extravascular fluid
High protein concentration
Specific gravity > 1.020
Usually due to  permeability

Question 6

what is transudate?

Answer 6

Fluid with low protein concentration (albumin)
Specific gravity < 1.012
Permeability usually not increased (due to a pressure response)

Question 7

what is the earliest manifestation of acute inflammation?

Answer 7

vasodilation

Question 8

what is the hallmark of acute inflammation?

Answer 8

increased vascular permeability

Question 9

what is the most common mechanism for vascular leakage?

Answer 9

contraction of endothelial cells

Question 10

what is called the immediate transient response?

Answer 10

contraction of endothelial cells

Question 11

contraction of endothelial cells are mediated by…

Answer 11

histamine
bradykinin
leukotriene
neuropeptide substance P

Question 12

what are the different mechanisms of increased vascular permeability?

Answer 12

contraction of endothelial cells (minutes)
endothelial injury (hours to days)
leukocyte mediated vascular injury (late stages of inflammation. hours)
transcytosis (occurs in venules and induced by VEGF)

Question 13

what is lymphangitis?

Answer 13

lymphatics secondarily inflammed

Question 14

what is lymphadenitis?

Answer 14

draining lymph nodes may be inflamed

Question 15

what are the stages of recruitment of leukocytes?

Answer 15

extravasation
margination
rolling
adhesion

Question 16

what kind of cells predominate during the first 6-24 hours of acute inflammation?

Answer 16

neutrophils

except if infected with peudomonas bacteria. In which case will be neutrophils for days

except if infected with viral infections. in which case lymphocytes would be first to arrive

Question 17

what kind of cells predominate during hours 24-48 of acute inflammation?

Answer 17

monocytes

Question 18

how is microbial killing done??

Answer 18

reactive oxygen species
reactive nitrogen species
can also occur from other stuff in granules
- elastase
- defensins
- cathelicidins
- lysozyme
-lactoferrin
- major basic protein
- bacteriacidal/permeability protein

Question 19

what are some functional responses of activated leukocytes?

Answer 19

stimulate proliferation of endothelial cells and fibroblasts
stimulate synthesis of collagen
stimulate enzymes that remodel connective tissues
drive the process of repair after tissue injury

Question 20

what happens in chediak higashi syndrome?

Answer 20

defective fusion of phagosomes and lysosomes causing susceptibility to infections
Abnormalities in melanocytes (leading to albinism)
Cells of the nervous system (associated with nerve defects)
Platelets (causing bleeding disorders)
Leukocyte abnormalities
Neutropenia (decreased numbers of neutrophils)
Defective degranulation
Delayed microbial killing

Question 21

what happens with chronic granulomatous disease?

Answer 21

Defects in bacterial killing
Render patients susceptible to recurrent bacterial infection
Inherited defects in the genes encoding components of phagocyte oxidase
Initial neutrophil defense is inadequate
Collections of activated macrophages that wall off the microbes
Aggregates called granulomas

Question 22

what are 2 major vasoactive amines?

Answer 22

histamine and serotonin

among the first mediators to be released during inflammation

Question 23

where can you find serotonin?

Answer 23

present in platelets
- stimulated when platelets aggregate

present in certain neuroendocrine cells in the GI tract

Question 24

what are the arachodonic acid metabolites?

Answer 24

prostaglandins
leukotrienes
lipoxins

derived from linoleic acid

Question 25

Arachodonic acid derived mediators (eicosanoids) are synthesized by these 2 enzymes…

Answer 25

cyclooxygenases - generate prostaglandins
lipoxygenases - produce leukotrienes and lipoxins

can bind to G protein coupled receptors
can mediate virtually every step of inflammation

Question 26

what produces prostaglandins?

Answer 26

by mast cells, macrophages, and endothelial cells

COX-1 and COX-2 is involved

Question 27

what are the most important prostaglandins in inflammation?

Answer 27

PGE2, PGD2, PGF2α, PGI2 (prostacyclin), and TxA2 (thromboxane)

Question 28

Actions of PGD2

Answer 28

vasodilation
increases permeability of post capillary venules
chemoattractant for neutrophils

Question 29

actions of PGF2

Answer 29

contraction of uterine and bronchial smooth muscles and small arterioles

Question 30

actions of PGE2

Answer 30

hyperalgesic
makes skin hypersensitive to pain stimuli
involved in cytokine induced fever during infections

Question 31

leukotrienes are produced by

Answer 31

lipoxygenase enzymes
secreted by leukocytes
chemoattractant for leukocytes
has vascular effects

Question 32

5 lipoxygenase

Answer 32

5-lipoxygenase 
Predominant one in neutrophils
Converts AA to 5-hydroxyeicosatetraenoic acid
Chemotactic for neutrophils
Precursor of the leukotrienes

Question 33

LTB4

Answer 33

Potent chemotactic agent and activator of neutrophils
Causes aggregation and adhesion of the cells to venular endothelium
Generation of ROS
Releases lysosomal enzymes

Question 34

Cysteinyl-containing leukotrienes C4, D4, and E4 (LTC4, LTD4, LTE4)

Answer 34

Intense vasoconstriction, bronchospasm and increased vascular permeability

Question 35

what do lipoxins do?

Answer 35

Inhibit leukocyte recruitment and the cellular components of inflammation
Inhibit neutrophil chemotaxis and adhesion to endothelium
inhibitors of inflammation
inverse to leukotrienes