1c continued

Question 1

Chemical mediators general overview a 4 groups according to function

Answer 1

All S&S of inflammation are produced by chemical mediators
1 vasoactive properties
2 activate complement (clotting and kinin)
3 Chemotactic factors
4 Direct affectation of tissue cells

Question 2

Histamine

Answer 2

Found preformed in mast, basophils and platelets.
Released from trauma or immune reactions (IgE binding)
First on scene
Binds to H1 (antihistamines often competitively antagonize H1)
Causes dilation of arterioles, and increases permeability of venules.
Considered principle mediator of immediate transient phase of increased vascular permability

Question 3

Histamine H1 receptors specifically

Answer 3

-Promote inflammation from vasodilation, increased vascular permeability (due to retraction of endothelial cells lining caps)
-Chemotaxis
-Prostaglandin synthesis
Smooth muscle effects are bronchoconstriction and vasodilation

Question 4

Histamine H2 receptors functions

Answer 4

Negative feedback (decrease histamine release) which reduces activity of lymphocytes and eosinophils, decreases neutrophil chemotaxis, decrease granulation of mast cells

Question 5

H2 location

Answer 5

Parietal cells of stomach mucosa which increase gastric secrtion

Question 6

Arachidonic acid two pathways

Answer 6

It is found in phospholipid bilayers and released by phospolipase A2. Release leads to
Cyclooxygenase pathway (prostaglandins and thromboxane) 
Lipoxygenase pathway (leukotrienes)

Question 7

Leukotrienes effects and pathway

Answer 7

Similar to histamine
Constricts pulmonary airway
Increase microvascular permability
From AA to lipoxygenase to leukotriens)

Question 8

Prostaglandins

Answer 8

Promotes and inhibits inflammation cell response
Induces vasodilation
Induces vasoconstriction
From AA to cyclooxygenase

Question 9

Thromboxane

Answer 9

From AA to cylcooxygenase pathway

Promotes platelet aggregation, vasodilation, bronchoconstriction

Question 10

Arachadonic acid metabolites

Answer 10

Lipoxygenase (leukotriene receptor antagonist) Leukotrienes

Cyclooxygenase (asprin NSAID) prostaglandin and thrombaxane

Question 11

Platelet Activating Factor

Answer 11

Lipid stored in membranes, induces platelet aggregation, activates neutrophils, chemotactic factor eosinophils

Question 12

Plasma Proteins Three interrelated systems

Answer 12

Clotting, complement, and kinin

Inactive and need to be triggered

Question 13

Clotting Cascade plasma proteins

Answer 13

Produces chemokines, expression of endothelial adhesion molecules, prostaglandin synthesis
Thrombin binds to PARs which triggers production of these plus PAF

Question 14

Complement system plasma proteins

Answer 14

Contribute by causing vasodilation, increasing vasc permeability, enhancing phagocyte activity, and forms Membrane Attack Complex MAC

Question 15

Kinin System plasma proteins

Answer 15

Release of bradykinin:
Increased vasc perm
Smooth muscle contraction
Vasodilation and incites pain when bound to nociceptors

Question 16

Cytokines

Answer 16

Proteins produced by many different cells which cause functional effects on other cell types
Examples tumor necrosis factor-a and interleukin-1
They are released by macrophages and cause a wide range of effects
There are several forms of interleukins

Question 17

Chemokines

Answer 17

Chemotactic cytokines

They are proteins that attract leukocytes and other inflammatory cells to site of injury

Question 18

Nitric oxide

Answer 18

Smooth muscle relaxation, platelet antagonism, reduction of leukocyte recruitment
Can be considered a mechanism that prevents cell stage of inflammation from going too far
Produced by many cells

Question 19

ROS

Answer 19

Produced during phagocytosis, released exogenously
Exogenous effects of ROS:
Increased vasc perm
Increased endothelial adhesion
Increasion expression of cytokines

Question 20

Exudates

Answer 20

Serious - watery fluids low in protein, a result of large amounts of plasma
Hemorrhagic - caused by vessel damage, or increased leaking of RBCs into tissue
Fibrinous - large amounts of fibrinogen (similar to a clot)
Membranous - develop on mucous membranes
Purulent - contains pus (degraded WBCs, proteins, tissue debris)

Question 21

Abscess

Answer 21

Localized inflammation with purulent (pus) exudate
Has a central necrotic core surrounded by a layer of neutrophils
POSSIBLY surronded by a layer of fibroblasts which would prevent anti-microbial agents from entering
This is why you often see abscess’ drained

Question 22

Ulceration

Answer 22

Localized inflammation with epithelial damage
Erosion of tissue
From trauma or vasc deficits

Question 23

Chronic inflammation

Answer 23

2 weeks + 
Not self-limiting, self-perpetuating
caused by:
recurrent acute inflammation
progressive acute
persisten low grade irritants

Question 24

Chronic inflammation is charactrized by

Answer 24

Influx of macrophages and lymphocytes as opposed to neutrophils in acute response
By build up of fibroblasts rather than exudate which leads to risk of scarring

Question 25

Nonspecific inflammation

Answer 25

Diffuse accumulation of macrophages and lymphocytes Continual chemotaxis fibroblast proliferation scar formation

Question 26

Granulomatous inflammation

Answer 26

Mass of macrophages surrounded by lymphocytes Insulting agent was poorly controlled by other inflam mechs CT eventually encapsulates mass Example would be TB

Question 27

Systemic manifestations

Answer 27

``` Body tries to control inflammation to local, if it does go systemic it is characterized by THREE features Acute-phase response WBC response Lymphadenitis (swollen members) Severe systemic is cytokine storm ```

Question 28

Acute phase response

Answer 28

``` From cytokines systemic Increased C reactive protein* Eleveated CSR* Skeletal muscle catabolism Negative nitrogen balance Fever, anorexia, somnolence, malaise ```

Question 29

WBC response in systemic

Answer 29

Bacterial infections produce increase in neutrophils Parasitic and allergic responses produce increase in eosinophils Viral infections produce decrease in neutro increase in lymphocytes

Question 30

Leukocytosis

Answer 30

increased WBC | decreased is leukopenia

Question 31

Lymphadenitis

Answer 31

Lymphs responsible for draining inflammation Either due to immunologic response to specific antigen or a generalized response to chemical medatiors in the inflammation

Question 32

Cytokine storm

Answer 32

Massive release of chemical mediators into body SIRS

Question 33

Tissue repair

Answer 33

Tissue regen - replacement with same cells | Fibrous tissue - replacement with CT (scar)

Question 34

Healing is regulated by

Answer 34

chemical mediators, ECM, and growth factors

Question 35

Growth factors

Answer 35

Hormone-like molecules interact with specific cell receptors, control proliferation, differentiation, metabolism of cells during healing process Also regulate inflammatory process, act as chemo attractants, stimulate angiogensis, help form ECM

Question 36

Cells involved in wound healing

Answer 36

``` Leukocytes Macrophages Epithelial cells CT (myofibros, angio, and fibro -blasts) Tissue rich in those ^ is granulation tissue ```

Question 37

Primary vs secondary intention

Answer 37

Small close wounds heal by primary | Large spaced out ones are secondary

Question 38

3 phases of wound healing

Answer 38

Inflammatory Proliferative Remodeling

Question 39

Inflammatory phase of healing

Answer 39

Prepares environment | Needs proliferation of chem mediators and growth factosr

Question 40

Proliferative Phase

Answer 40

Formulation of granulation tissue (fibro, myofibro, angioblasts) Epithelization also occurs (migration, prolif, and differentiation of epithelial cells at wound edges to form new layer)

Question 41

Remodeling phase of wound healing

Answer 41

Type 3 collagen replaced with Type 1, done to increase overall strength of wound

Question 42

Factors affecting wound healing

Answer 42

``` Nutrition Blood flow Impaired inflammatory or immune resonses Infecction Wound seperation Foreigners ```

Question 43

Complications of bad wound healing

Answer 43

``` Loss of founction Contractures (perm shortening of muscle or joint) and obstruction Adhesions Hypertrophic scar tissue (keloid -elevated scars) Ulcerations Wound dehiscence Infection Delayed healing ```