10-8a Acute Inflammation

Question 1

What is acute inflammation?

Answer 1

response of vascularized tissues to infection and damage that brings cells and molecules of host defense from the circulation to sites where they are needed

Question 2

What does inflammation do?

Answer 2

Rid host of initial cause of injury

Remove necrotic cells and tissues

Initiate the process of tissue repair

Question 3

What are the cardinal signs of inflammation?

Answer 3

redness, heat, swelling, pain, loss of function

Question 4

What drug blocks the enzyme that produces Prostaglandin E2?

Answer 4

non-steroidal anti-inflammatories

Question 5

What does the mediator Prostaglandin E2 do?

Answer 5

sensitizes n. receptors to pain signals

Question 6

What is a consequence to tissues swelling around a joint in regards to loss of function?

Answer 6

Pain and swelling limit strength, loss of motion, and neuromotor control

afferent signals go to the spinal cord and motor cortex to decrease motor drive

Question 7

What are the key players in the blood (immune cells) for acute inflammation response?

Answer 7

platelets (thrombocytes): clotting

WBCs (leukocytes): neutrophils and monocytes (in blood)/macrophages (in tissues

Question 8

What are the tissue (immune) cells related to acute inflammatory response? What are the three types?

Answer 8

sentinel cells
resident macrophages
dendritic cells
mast cells

Question 9

What are the three key features of sentinel cells that make them useful for acute inflammatory response?

Answer 9

1. receptor on the cell surface that detect invading microbes and the biproducts of cellular necrosis (via receptors)
2. bind, ingest, and phagocytize microbes and necrotic tissue
3. release cytokines and other inflammatory that recruit mediators from blood

Question 10

what are cytokines?

Answer 10

signaling mol. produced mostly by leukocytes that respond to injury and infection by inducing/modulating immune response

Question 11

What do cytokines do?

Answer 11

either up-regulate pro-inflammatory processes (fever, inflammation, tissue, destruction) or
suppress pro-inflammatory signals

Question 12

What are histamines?

Answer 12

released primarily by mast cells; vascular response

vasodilation, increased capillary permeability

Question 13

What are prostaglandins and leukotriens?

Answer 13

other mediators that are produced in response to cytokines

contribute to vasodilation, pain, and platelet activation

Question 14

What is hemostasis?

Answer 14

immediate response to traumatic injury to prevent blood loss

Question 15

What do damaged endothelial cells release? What do they cause?

Answer 15

mediators that cause vasoconstriction, platelet activation, and fibrin clot formation

Question 16

What do activated platelets do?

Answer 16

stick to RBCs, each other, and the vessel wall
attract other platelets
initiate coagulation cascade = fibrin production
platelet activation + fibrin = clot

Question 17

what is fibrin? What does it do?

Answer 17

a mesh network that stabilizes the clot

later on, fibrin mesh network provides scaffolding for infiltrating cells that eventually produce new tissue

Question 18

What are the five steps of inflammation?

Answer 18

Recognition of injury
Recruitment of leukocytes (sentinel cells would be overwhelmed if not)
Removal of injurious agents and damaged tissue
Regulation to prevent collateral tissue damage
Resolution

Question 19

How is injury recognized?

Answer 19

recognized by immune cells

Question 20

What can trigger an inflammatory response?

Answer 20

trauma, necrotic tissue, infection by pathogens or foreign bodies, maladaptive immune response

Question 21

What cells initally detect injury?

Answer 21

leukocytes in blood stream and sentinel cells in the tissue

Question 22

What happens after the injury is recognized by immune cells?

Answer 22

receptors detect either invading microbes or necrotic tissue mols.

phagocytosis of invading pathogens/breaking down of necrotic tissues

recognition results in the production of mediators (histamines, cytokines, prostaglandins, leukotrienes etc.) that trigger recruitment

Question 23

What are the vascular changes that cause recruitment of WBCs to tissue?

Answer 23

Cytokines and inflammatory mediators act on endothelial cells (that have receptors) of local blood vessels that cause:
increased vasodilation

increased vessel permeability

vascular stasis (less movement)

Question 24

What are the two stages of recruitment of WBCs to the tissues?

Answer 24

vascular changes

cellular changes

Question 25

What causes vasodilation of vessels during immune response? What are the effects of vasodilation of the vessels?

Answer 25

histamine and other mediators released by mast cells cause relaxation of the vessel ^ blood flow to the area decreases the velocity of blood flow

Question 26

What does endothelial cell retraction cause (in response to sentinel cell messages)?

Answer 26

the endothelial cells move away from one another and causes pore formation > leaking of fluid (plasma) and proteins out of vessel (edema)

Question 27

What causes vascular stasis? What does it account for? What does it facilitate?

Answer 27

vasodilation slows blood flow pore formation causes more concentrated blood (leaking of plasma) = hemoconcentration redness and warmth in the tissue facilitates WBC movement out of blood into the tissue

Question 28

How are WBCs recruited to the tissue cellularly? What happens once they enter the endothelium?

Answer 28

activated platelets and cytokines prod. by mast cells act on the endothelial cells of the vessel, which express receptors (proteins) on the surface that grab onto proteins on the WBCs flowing in the vessel cytokines produced by mast cells and activated platelets turn on leukocytes extravasation: WBCs start to slow down and roll along the surface of the vessel; then they adhere to the vessel wall and migrate through the endothelium chemotaxis: Once in tissue, leukocytes migrate to area of injury

Question 29

How is the damaged tissue removed?

Answer 29

``` 1st wave: neutrophils Ingest and destroy microbes and damaged tissues through phagocytosis (create reactive O2 and N species), die quickly (few hours) via apoptosis, and can have collateral damage to healthy surrounding tissues if these reactive species aren't regulated 2nd wave: Macrophages phagocytize remaining microbes, necrotic tissue, and dead neutrophils, “clean up” mess made by damage and neutrophils, and produce anti-inflammatory cytokines that begin to down-regulate inflammation ```

Question 30

How is inflammatory response regulated?

Answer 30

leukocytes have short-half lives anti-inflammatory signals activated to down-regulate inflammation (lymphocytes play a role) *shift from pro-inflammatory cytokine signals to anti-inflammatory cytokine signals*

Question 31

How does inflammation resolve?

Answer 31

Leukocyte activation triggers proliferation and migration of fibroblasts (repair tissues): produce collagen and extracellular matrix components and are the main cell of proliferative phase

Question 32

What does a progression of injury lead to?

Answer 32

chronic inflammation fibrosis scar tissue = poor recovery of function

Question 33

what is an abscess?

Answer 33

walled-off inflammation and pus accumulation | results in loss of function/scarring

Question 34

what is pus?

Answer 34

phagocytized neutrophils/microbes by macrophils = pus indication of immune response largely bacterial ivasion

Question 35

What can go wrong with inflammation?

Answer 35

Too little inflammation Misdirected inflammation Inflammation in response to normally harmless substances Inflammation is excessively prolonged or repetitive

Question 36

What does too little inflammation involve?

Answer 36

Infections go unchecked | Wounds/tissues don’t heal

Question 37

What does misdirected inflammation involve?

Answer 37

Against self tissues in autoimmune diseases

Question 38

What does Inflammation in response to normally harmless substances involve?

Answer 38

Hypersensitivity and allergies

Question 39

When is Inflammation is excessively prolonged or repetitive?

Answer 39

chronic inflammation

Question 40

Key things to look for in acute inflammation examination:

Answer 40

Redness? Warmth? Swelling? Impact on movement and gait? Vigor of inflammatory response > reflects degree of injury

Question 41

History questions for acute inflammation?

Answer 41

When and how did this happen? Assess pain: Location, intensity, aggravating/relieving factors

Question 42

Tests and measures for acute inflammation?

Answer 42

Assessment of function, if region stable: Ankle movements (ROM, Strength) and Gait Edema assessment

Question 43

What is edema?

Answer 43

fluid in the interstitial space (everything surrounding cells and vessels)

Question 44

What are signs for edema?

Answer 44

increased girth of body part, tight/shiny skin, indentation of skin under clothing, weeping/leaking

Question 45

Why is edema a problem?

Answer 45

Interferes with movement (lower neuromuscular control and ROM) May indicate health problem: Tissue injury, DVT, heart failure, liver kidney failure

Question 46

What are the types of edema?

Answer 46

Inflammatory Non-Inflammatory/pitting edema Effusion

Question 47

Describe Inflammatory Edema

Answer 47

a) Assoc. with red, hot, painful | b) Due to trauma, infection, or inflammatory reaction

Question 48

Describe non-inflammatory/pitting edema

Answer 48

a) Variety of causes | b) Indentation left behind when touched

Question 49

Describe Effusion edema

Answer 49

a) Excess fluid in enclosed space i) Joint effusion = fluid in joint capsule ii) Pleural effusion = fluid in pleural space

Question 50

What info do you need to describe edema?

Answer 50

1) Location (unilateral/bilateral) a) Limb/tissue b) Unilateral vs. bilateral 2) Duration Acute = days to weeks Chronic = weeks to months/years 3) Inflammatory vs. pitting a) Are other signs present? b) Pitting? Scale 4) Measure amount a) Girth measurements vs. volumetric

Question 51

Prognosis for acute inflammation?

Answer 51

How long should acute inflammation last? | If no change in signs and symptoms in 1-2 weeks, consider: Repeated injury?Another source of inflammation?

Question 52

Intervention for acute inflammation

Answer 52

Goal = manage inflammation, promote healing ``` POLICE Protection Optimal Loading Ice Compression Elevation ```

Question 53

What is the purpose of inflammation?

Answer 53

look up