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Unit 2 > 10-8a Acute Inflammation > Flashcards

10-8a Acute Inflammation Flashcards

1
Q

What is acute inflammation?

A

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

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2
Q

What does inflammation do?

A

Rid host of initial cause of injury

Remove necrotic cells and tissues

Initiate the process of tissue repair

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3
Q

What are the cardinal signs of inflammation?

A

redness, heat, swelling, pain, loss of function

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4
Q

What drug blocks the enzyme that produces Prostaglandin E2?

A

non-steroidal anti-inflammatories

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5
Q

What does the mediator Prostaglandin E2 do?

A

sensitizes n. receptors to pain signals

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6
Q

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

A

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

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7
Q

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

A

platelets (thrombocytes): clotting

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

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8
Q

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

A

sentinel cells
resident macrophages
dendritic cells
mast cells

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9
Q

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

A
  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
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10
Q

what are cytokines?

A

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

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11
Q

What do cytokines do?

A

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

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12
Q

What are histamines?

A

released primarily by mast cells; vascular response

vasodilation, increased capillary permeability

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13
Q

What are prostaglandins and leukotriens?

A

other mediators that are produced in response to cytokines

contribute to vasodilation, pain, and platelet activation

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14
Q

What is hemostasis?

A

immediate response to traumatic injury to prevent blood loss

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15
Q

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

A

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

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16
Q

What do activated platelets do?

A

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

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17
Q

what is fibrin? What does it do?

A

a mesh network that stabilizes the clot

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

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18
Q

What are the five steps of inflammation?

A

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

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19
Q

How is injury recognized?

A

recognized by immune cells

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20
Q

What can trigger an inflammatory response?

A

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

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21
Q

What cells initally detect injury?

A

leukocytes in blood stream and sentinel cells in the tissue

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22
Q

What happens after the injury is recognized by immune cells?

A

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

23
Q

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

A

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)

24
Q

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

A

vascular changes

cellular changes

25
Q

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

A

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

26
Q

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

A

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

27
Q

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

A

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

28
Q

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

A

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

29
Q

How is the damaged tissue removed?

A 
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
30
Q

How is inflammatory response regulated?

A

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

31
Q

How does inflammation resolve?

A

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

32
Q

What does a progression of injury lead to?

A

chronic inflammation
fibrosis
scar tissue = poor recovery of function

33
Q

what is an abscess?

A

walled-off inflammation and pus accumulation

results in loss of function/scarring

34
Q

what is pus?

A

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

35
Q

What can go wrong with inflammation?

A

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

36
Q

What does too little inflammation involve?

A

Infections go unchecked

Wounds/tissues don’t heal

37
Q

What does misdirected inflammation involve?

A

Against self tissues in autoimmune diseases

38
Q

What does Inflammation in response to normally harmless substances involve?

A

Hypersensitivity and allergies

39
Q

When is Inflammation is excessively prolonged or repetitive?

A

chronic inflammation

40
Q

Key things to look for in acute inflammation examination:

A

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

41
Q

History questions for acute inflammation?

A

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

42
Q

Tests and measures for acute inflammation?

A

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

Edema assessment

43
Q

What is edema?

A

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

44
Q

What are signs for edema?

A

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

45
Q

Why is edema a problem?

A

Interferes with movement (lower neuromuscular control and ROM)

May indicate health problem: Tissue injury, DVT, heart failure, liver kidney failure

46
Q

What are the types of edema?

A

Inflammatory
Non-Inflammatory/pitting edema
Effusion

47
Q

Describe Inflammatory Edema

A

a) Assoc. with red, hot, painful

b) Due to trauma, infection, or inflammatory reaction

48
Q

Describe non-inflammatory/pitting edema

A

a) Variety of causes

b) Indentation left behind when touched

49
Q

Describe Effusion edema

A

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

50
Q

What info do you need to describe edema?

A

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

51
Q

Prognosis for acute inflammation?

A

How long should acute inflammation last?

If no change in signs and symptoms in 1-2 weeks, consider: Repeated injury?Another source of inflammation?

52
Q

Intervention for acute inflammation

A

Goal = manage inflammation, promote healing

POLICE
Protection
Optimal Loading
Ice
Compression
Elevation
53
Q

What is the purpose of inflammation?

A

look up

Unit 2 (29 decks)

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