Inflammation and Wound Healing

Question 1

Define inflammation

Answer 1

A non-specific, predictable response to injury that is dynamic by evolving through phases.

Question 2

Causes of injury resulting in inflammation

Answer 2

Chemical agents, physical force, living microbes, any endogenous/exogenous pathologic stimuli

Question 3

Inflammation of sudden onset, short duration

Answer 3

Acute

Question 4

Inflammation lasting a long time

Answer 4

Chronic

Question 5

Is inflammation protective or harmful

Answer 5

Both, generally beneficial until uncontrolled

Question 6

How does inflammation protect and harm the body with TB?

Answer 6

Protective granular enclosure, which then erodes pulmonary vessels (mass bleeding)

Question 7

What is a common clinical sign of TB granuloma erosion?

Answer 7

Hemoptysis

Question 8

How is injury determined to be delivered postmortem?

Answer 8

Inflammation only occurs in living tissues.

Question 9

What is PRISH?

Answer 9

5 cardinal signs of inflammation; pain, redness, immobility (loss of function), swelling, heat

Question 10

What is the body’s first response to injury?

Answer 10

Circulatory changes–vasoconstriction (brief), followed by vasodilation

Question 11

What mechanical action manipulates circulatory changes?

Answer 11

Smooth muscle cells on arterioles, acting as sphincters.

Question 12

What is the cause of redness, swelling, and heat in injured tissue?

Answer 12

Arteriole relaxation, allowing blood to rush into capillaries.

Question 13

What stimulates changes in arterioles?

Answer 13

Mechanoreceptors stimulated by source of injury that then stimulate nerves acting on smooth muscle.

Question 14

What is edema?

Answer 14

Plasma filtration through capillary and venule walls into tissue space by pressure secondary to vasodilation.

Question 15

What is hemoconcentration?

Answer 15

Higher concentration of formed elements as plasma escapes dilated vessels.

Question 16

What is a “Rouleaux” formation?

Answer 16

Concentrated RBCs stack, impeding and slowing blood flow.

Question 17

What is “pavementing”?

Answer 17

WBCs attach to the edge of blood vessel endothelium (aka margination) near site of injury.

Question 18

How do WBCs marginate?

Answer 18

By developing elongated protrusions on their surface cytoplasm, becoming sticky.

Question 19

What is the role of interleukins during inflammation?

Answer 19

They serve as soluble inflammatory mediators present in the blood that activate the surface components of WBCs and endothelial cells.

Question 20

Where are interleukins found most concentrated?

Answer 20

At the site of inflammation.

Question 21

What are interleukins a derivative of?

Answer 21

Platelets and WBCs.

Question 22

What is possibly the most important trigger in the release of inflammatory mediators?

Answer 22

Adhesion of WBCs to the endothelial cells.

Question 23

Once adhesion of WBCs to endothelial cells takes place, what prevents them from moving?

Answer 23

Platelets form a clot, which promotes fibrin, which anchors WBCs.

Question 24

What is the term for WBCs to squeeze through endothelial gap junctions and enter the tissue space?

Answer 24

Emigration.

Question 25

What factors allow emigration?

Answer 25

Increased permeability of capillaries and venules; fluid leakage that carries WBCs.

Question 26

What is the most common WBC during acute inflammation?

Answer 26

Neutrophils (PMNs)

Question 27

Which cells join PMNs during the first 24 hours after injury?

Answer 27

Monocytes.

Question 28

What are monocytes a progenitor for?

Answer 28

Macrophages.

Question 29

What is the lifespan of PMNs?

Answer 29

2-4 days

Question 30

Which cells emigrate as PMNs die off during subacute and chronic inflammation?

Answer 30

Macrophages, lymphocytes, and plasma cells.

Question 31

What is the role of pseudopods on the surface of PMNs?

Answer 31

Help identify bacteria as foreign once at the site of injury.

Question 32

T or F: Inflammation has specificity to certain stimuli.

Answer 32

F, it is an all or nothing phenomenon (i.e. burns don’t deliver bacteria, but PMNs still arrive).

Question 33

Attraction of PMNs to bacteria, dead/dying cells, and activated compliment is called what?

Answer 33

Chemotaxis; PMNs follow a gradient until they reach the source of inflammation.

Question 34

Once PMNs arrive at a site, what prompts phagocytic activity?

Answer 34

Complement C3b and the Fc portion of IgG opsonize (tag) the pathogen with opsens (lollipops).

Question 35

How does phagocytosis of bacteria by WBCs take place?

Answer 35

Opsonins attach “lock and key” to PMN pseudopods; PMN membrane attaches to bacteria cell wall; Invagination of bacteria; Granuloma formed around bacteria w/in cell; Acid hydrolases break down bacteria cell wall (neutralize).

Question 36

How do many PMNs die in their fight with bacteria?

Answer 36

Following invagination, granules from PMNs are discharged into the lumen, killing the bacteria and the PMN.

Question 37

What is pus?

Answer 37

Dead/dying PMNs and tissue debris form a viscous yellow fluid.

Question 38

What are purulent or suppurative inflammations?

Answer 38

Inflammation events dominated by pus formation.

Question 39

Inflammation typically produces what two important clinical findings?

Answer 39

Fever and leukocytosis.

Question 40

Definition of fever?

Answer 40

A typical response to acute inflammation caused by an endogenous pyrogen, resulting in elevation of body temp exceeding 37 deg C.

Question 41

Which two substances act on the thermoregulator centers in the hypothalamus during fever?

Answer 41

Interleukin-I (IL-1) and Tumor Necrosis Factor (TNF).

Question 42

How is a fever mediated?

Answer 42

PMNs and macrophages release pyrogens (IL-2 and TNF), which release prostaglandins in the hypothalamic center.

Question 43

What is the MOA for antipyretics?

Answer 43

Block the release of prostaglandins by pyrogens.