Acute Inflammation And Inflammatory Mediators

Front 1

What is acute inflammation?

Back 1

Immediate response of vascular tissues to injurious agent

Front 2

What are the characteristic cells of acute inflammation?

Back 2

Neutrophils (PMNs, polys)

Front 3

What are the three main features of acute inflammation?

Back 3

1. Vascular dilation
2. Vascular structural changes to allow plasma proteins to exudate
3. Endothelial cells allow neutrophil adhesion and extravasation

Front 4

What are the four types of acute inflammation?

Back 4

1. Suppurative (infectious)
2. Post-injury (noninfectious)
3. With abscess formation
4. Pseudo-membranous

Front 5

What are the features of acute pseudo-membranous inflammation?

Back 5

--causes include infections, toxins, ischemia
--forms a membrane over organ or tissue made of necrotic epithelial cells, fibrin, neutrophils, platelets and bacteria
--it's not a true membrane, it lifts off easily

Front 6

What are the three features of subacute inflammation?

Back 6

1. Slightly longer duration of clinical inflammatory state
2. Eosinophils in infiltrate
3. Varying components of neutrophils, lymphocytes and macrophages

Front 7

What are the 3 phases of acute inflammation?

Back 7

1. Initiation (injury, structural changes, WBC emigration)
2. Amplification (both soluble mediators and cellular systems are activated and amplified)
3. Termination (specific inhibition or dissipation of mediators)

Front 8

What are the 3 possible outcomes of an inciting stimulus to acute inflammation?

Back 8

1. Resolution without scarring
2. Abscess and then resolution with scarring
3. Chronic inflammation

Front 9

How does acute inflammation differ from chronic in terms of changes to the stroma?

Back 9

Acute shows minimal stromal change, just some cellular separation due to edema; chronic shows cellular proliferation and fibrosis.

Front 10

What is the effect of vasodilation in acute inflammation?

Back 10

Vasodilation causes a decreased rate of blood flow. The slower blood pools, giving the neutrophils in it more time to adhere to endothelium and extravasate.

Front 11

What adhesion molecules are involved in the rolling stage of leukocyte extravasation?

Back 11

The selectins, P and E selectin on endothelium and L selectin on leukocytes.

Front 12

What adhesion molecules are involved in the adhesion and transmigration stages of leukocyte extravasation?

Back 12

On endothelium, I-CAM and V-CAM (intracellular and vascular cellular adhesion molecules, which are immunoglobulin-like); and on leukocytes, integrins.

Front 13

What is "margination?"

Back 13

An event in the initial stage of leukocyte extravasation during which the slowed blood flow causes the WBCs to fall out of the central blood current and collect around the vessel walls in contact with the endothelium.

Front 14

What is "pavementing?"

Back 14

A term for the histological appearance of endothelium completely lined with adhering (but not yet extravasated) WBCs.

Front 15

Where does leukocyte diapedesis (extravasation) usually occur?

Back 15

In the venules, except in the lung where it happens in the capillaries, too.

Front 16

What are the 4 main WBC actions that occur in acute inflammation?

Back 16

1. Margination/pavementing
2. Emigration/extravasation
3. Chemotaxis
4. Phagocytosis

Front 17

What are the 3 steps in phagocytosis?

Back 17

1. Attachment and recognition
2. Engulfment
3. Killing and degradation

Front 18

Name 4 ways in which adhesion molecules act as inflammatory mediators.

Back 18

1. Promote WBC adhesion
2. Promote diapedesis
3. Aid in chemotaxis
4. Facilitate phagocytosis

Front 19

What are Weibel-Palade bodies?

Back 19

Storage organelles in edothelial cells that contain von Willebrand Factor (vWF), P-selectin, and certain chemokines.

Front 20

How is P-selectin induced on endothelium?

Back 20

It is redistributed to the cell surface from storage in the Weibel-Palade bodies after stimulation by thrombin, histamine, and platelet activating factor (PAF).

Front 21

How is E-selectin induced in endothelial cells?

Back 21

Via stimulation with interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF-a).

Front 22

What are the 5 classic signs of inflammation?

Back 22

1. Redness
2. Swelling
3. Heat
4. Pain
5. Loss of function

Front 23

What are the 8 signs and symptoms of acute inflammation?

Back 23

1. Fever
2. Listlessness
3. Malaise
4. Loss of appetite
5. General disability
6. Headache
7. Leukocytosis
8. Non-specific elevation in serum proteins

Front 24

What is a "left shift?"

Back 24

If one considers a scale of leukocyte maturity on which cellular maturity increases from left to right, a left shift is when the bone marrow releases more cells from the left end of the scale (that is, more immature leukocytes or band cells) in order to combat acute stress or inflammation.

Front 25

Name the 7 characteristics of inflammatory mediators.

Back 25

1. All made by cells
2. Some are preformed and stored
3. Some are newly made in response to injury
4. Some circulate as precursors
5. They bind to specific receptors on target cells
6. Have autocrine, paracrine or endocrine function
7. Controlled by inactivators

Front 26

Name the 3 ways to control inflammatory mediators.

Back 26

1. Sequestration in organelles
2. Leave them in precursor form
3. Use inactivators

Front 27

What are some examples of inactivators of inflammatory mediators?

Back 27

--kinases
--histaminases
--C1 or C3 inactivator
--antioxidants
--antiproteases
--chemotactic factor inactivators

Front 28

Describe vasoactive amine inflammatory mediators.

Back 28

--serotonin and histamine
--preformed and stored in mast cells, basophils and platelets
--released by degranulation
--cause immediate increases in vascular permeability
--inactivated by histaminase

Front 29

Name 5 stimuli for the release of vasoactive amines.

Back 29

1. Physical injury
2. IgE
3. C5a
4. Cationic proteins
5. Neuropeptides

Front 30

What is the complement system?

Back 30

A cascade system of enzymatic proteins that is activated during acute inflammation because of (a)signals from necrotic cells, (b)antigen-antibody complexes, (c)endotoxins from gram-negative bacteria, or (d)products of the coagulation or fibrinolytic systems.

Front 31

Name the important components of the complement system.

Back 31

--C3: critical control point
--C3a and C5a: "anaphylotoxins" capable of releasing histamine; also, chemotactic for neutrophils, increase permeability
--C5-C9: together form Membrane Attack Complex, an active agent of complement lysis

Front 32

What is the kinin system?

Back 32

Made up of peptides of 9-11 amino acids, it is a group of plasma inflammatory mediators that is activated by coagulation Factor XII. Bradykinin is its most important factor for vascular permeability and pain mediation.

Front 33

What is the coagulation system?

Back 33

A cascade made up of proenzymes that are converted to enzymes, with the end result being the conversion of fibrinogen into fibrin, a major component of the acute inflammatory exudate and blood clots.

Front 34

What is Hagemann Factor?

Back 34

Also known as coagulation Factor XII, it is activated by ECM materials, such as basal lamina and by bacterial enzymes, and it activates the kinin, coagulation and fibrinolytic systems.

Front 35

What is the fibrinolytic system?

Back 35

The system that breaks fibrin down into its degradation products, which may have local effects on vascular permeability.

Front 36

Name some important cytokines.

Back 36

--IL-1
--IL-2
--TNF-a
--TNF-b
--Colony-stimulating factors (CSFs)
--Chemokines

Front 37

What is nitric oxide?

Back 37

A potent vasodilator produced constituitively by endothelial and neuronal cells via nitric oxide synthase, which can rapidly increase it when stimulated by calcium influx. It is inducible, via TNF-a or interferon gamma (INF-gamma), in macrophages and is involved in the pathogenesis of septic shock.