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Unit 2 > BIOMED 10/8a Acute Inflammation > Flashcards

BIOMED 10/8a Acute Inflammation Flashcards

1
Q

what is acute inflammation

A
  • vascular response to promote healing
  • latin for set on fire
  • response to infection and damage that brings cells and molecules to the damaged tissue
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2
Q

Goals of acute inflammation

A

-rid the hose of initial cause of injury
-remove necrotic cells and tissue
-initiate repair
(inflammation>proliferation>maturation)

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3
Q

Cardinal Signs of inflammation

A
  • Redness
  • Heat
  • Swelling
  • Pain
  • Loss of Function
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4
Q

How does acute inflammation stimulate or trigger pain?

A

prostaglandin E2 sensitizes specialized nerve endings to effect bradykinin and other pain mediators

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5
Q

drug that blocks the enzyme that produces prostaglandin E2

A

NSAIDS

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6
Q

How does acute inflammation cause loss of function?

A

pain and swelling limit the following:

  • strength
  • ROM
  • neuromotor control (afferent signals from damage around tissue/joint go to spinal cord and motor cortex that work to decrease the motor drive to that joint)
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7
Q

How does inflammation work?

A 
Turn On Inflammation
1. Recognition of injury 
2. Recruitment of leukocytes
3. Removal of injurious agent and damaged tissue
Turn Off Inflammation
4. Regulation of the response 
5. Resolution
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8
Q

How does recognition of an injury work?

A
  1. Injury is recognized by immune cells
    - Sentinel cells in tissues
    - Leukocytes in blood stream
  2. After recognized, go through phagocytosis
  3. Then mediators are produced
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9
Q

Define injury

A

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

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10
Q

cells in the blood

A
  • Plasma (Proteins, Water - 91%, other solutes)

- Formed Elements (Platelets and leukocytes combined 1%, and erythrocytes > 90%)

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11
Q

Platelets

A

Thrombocytes

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12
Q

White Blood Cells

A

Leukocytes

  • Neutrophils
  • Monocytes (in blood), Macrophages (in tissues)
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13
Q

sentinel cells

A

“sense that something is wrong and they go tell”

  • Resident Macrophages (live in tissue)
  • Dendritic Cells (have dendrites)
  • Mast Cells (live in the tissue and early warning sign)
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14
Q

Key features of Sentinel Cells

A
  1. Receptors on the cell surface that sense the invading microbes and recognize biproducts of cellular necrosis of tissue
  2. Bind, ingest, and phagocytize microbes and necrotic tissue
  3. **release cytokines and other inflammatory mediators (most important - inflammatory mediators that are signals sent out to bloodstream to recruit leukocytes from the blood stream to the tissue)
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15
Q

Cytokines

A
  • Most important cytokines are histamines, prostaglandins, and leukotrienes
  • signaling molecules secreted by immune cells in response to injury/infection that induce the immune response
  • can upregulate or downregulate the inflammatory process as the inflammation process proceeds
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16
Q

Pro-inflammatory cytokines induce

A
  1. Fever
  2. Inflammation
  3. Tissue Destruction
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17
Q

anti-inflammatory cytokines induce

A

suppression of pro-inflammatory cytokine signals

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18
Q

histamines

A
  • regulate inflammation
  • released by mast cells
  • increase vasodilation
  • increase capillary permeability
19
Q

Prostaglandins and leukotrienes

A
  • produced in response to cytokines

- regulatory roles in vasodilation, pain, and platelet activation

20
Q

hemostasis

A
  • immediate response to traumatic injury to prevent blood loss
  • damaged endothelial cells release MEDIATORS that cause:
    1. vasoconstriction
    2. activation of platelets
21
Q

Platelet activation in hemostasis

A
  1. adhere to lesion/each other
  2. attract other platelets
  3. initiate coagulation cascade and the end product is fibrin
22
Q

what is fibrin

A
  • mesh network that stabilizes a clot

- fibronectin provides initial scaffolding for infiltrating cells and ECM components

23
Q

how is injury recognized?

A
  • Sentinel Cells in tissue and leukocyts in blood stream sense and recognize damage
  • receptors on cell surface/interior recognize molecules (released by damaged tissue - ATP, DNA, low K+)
  • Phagocytosis of microbes and necrotic tissue
  • Production and release of mediators (amines, cytokines, prostaglandins, leukotrienes, and bradykinins) trigger recruitment
24
Q

what is the process of leukocyte recruitment into the tissue?

A
  1. Vascular changes
    - predominant, heat, redness, swelling
  2. Cellular changes
25
Q

vascular changes that cause recruitment of leukocytes into the tissue

A
  1. cytokines and inflammatory mediators act on the endothelial cells of the BVs in the tissue and cause
    - Vasodilation: main driver is histamines that increase BF to the area, but decrease velocity
    - Vessel permeability: causes edema after endothelial cell retraction yields small pores on the surface
    - Vascular Stasis: results from increased BF, decreased velocity, and increased hemoconcentration; accounts for warmth and redness; facilitates extravasation of leukocytes into tissue
26
Q

cellular changes caused that trigger recruitment of leukocytes into the tissue

A
  1. Activation: integrin receptors grab onto surface proteins of WBCs and activate them to slowemdown
  2. Extravasation of WBCs (roll, adhere, migrate)
  3. Chemotaxis - WBCs are drawn to area of injury
27
Q

Removal of injurious agent and damaged tissue

A
  1. First Wave = neutrophils (still upregulating inflammation)
  2. Second Wave = macrophages (anti-inflammatory that begin down regulation)
28
Q

process that entails the first wave of removal of injurious agents

A
  • neutrophils ingest and destroy microbes, necrotic tissue through phagocytosis
  • they create a reactive oxygen and reactive nitrogen species
  • the release cytokines before death to call in macrophages
  • then they die quickly through apoptosis
29
Q

after apoptosis of neutrophils, what happens to the second wave of cells?

A
  • macrophages enter and phagocytize remaining microves, necrotic tissue, and dead neutrophils
  • they “clean up” the mess made by the damage and the neutrophils
  • they produce anti-inflammatory cytokines thatbegin the downregulation of inflammation
30
Q

after removal or injurious agent, what happens?

A

Regulation of the response - collateral damage if there was no regulation.

  • once activated, leukocytes have SHORT HALF LIVES.
  • anti-inflammatory signals activate to stimulate down regulation of inflammation (lymphocytes are an example)
31
Q

after regulation of the response what happens?

A

Resolution

  • leukocyte activation triggers proliferation and migration of fibroblasts (not immune cells, but cells that make new tissues)
    1. fibroblasts produce collagen and ECM comps
    2. main cell of proliferative phase
32
Q

what can go wrong with inflammation?

A
  1. too little inflammation - infections unchecked, or wounds/tissues don’t heal
  2. misdirected inflammation - against self tissues in autoimmune disease (rheumatoid arthritis)
  3. inflammation in response to normally harmless substances (allergies)
  4. inflammation tthat is excessively prolonged or repetitive (chronic inflammation)
33
Q

what happens when the resolution phase is off?

A

we get chronic inflammation and see a lot more formation of scar tissue which leads to poor recovery and function

  • repeated stimuli
  • repeated injurious agents
  • bacterial pathway that’s hard to remove
  • autoimmune disease
34
Q

what is pus?

A

bacterial invasions that lead to neutrophils to phagocytize then macrophages come in to eat dead neutrophils and the result is pus

35
Q

what is abscess

A

area of inflammation that is walled off and we get lots of scarring

36
Q

what is the Physical therapist’s role with inflammation?

A
  • History questions
  • tests and measures
  • prognosis and acute inflammation
  • intervention and acute inflammation
37
Q

what are important history questions to ask in regards to inflammation?

A
  1. has this happened before?
  2. how long has this been like this?
  3. MECHANISM OF INJURY
    - traumatic
    - atraumatic
  4. pain?
    - location?
    - impact on function?
    - motions that provoke pain?
    - type of pain? Dull, ache, shooting
    - severity of pain (0-10 0 is no pain, 10 is the worst pain)
    - what makes it better
  5. SOB?
  6. Dizziness?
38
Q

Tests and measures to complete with inflammation?

A
  1. assessment of function - anterior drawer, ROM, strength, larger functions like gait, standing, cutting, etc.
  2. assessment of edema
39
Q

what is edema?

A

fluid in interstitial space (space that surrounds the cells and blood vessels where the ECM and ground substance are - part of the tissue that is not cells and blood vessels)

40
Q

how do you asses edema?

A
  • increased girth at the body part
  • tight, shiny skin
  • indentation of skin under clothing
  • weepind/leaking fluid
  • interferes with movement, NMS control, can be painful
  • may indicate a health problem (DVT/diabetes)
  • different kinds of edema
41
Q

what are the different types of edema?

A
  1. inflammatory: red, hot, painful
  2. non-inflammatory or pitting: variety of causes, indentation left on skin
  3. Effusion: excess fluid in enclosed space, joint effusion or pleural effusion
42
Q

what information do we want when completing tests and measures on patients with inflammation?

A
  • location (limb/tissue, unilateral/bilateral)
  • duration (acute/chronic)
  • inflammatory vs pitting (press firmly for 5 seconds and rate from 1-4 based on indentation lasting time)
  • amount (girth/volumetric)
43
Q

prognosis and acute inflammation

A
  • acute inflammation should last for days or weeks
  • is this a repeat?
  • is there another source?
44
Q

intervention for acute inflammation

A

-manage inflammation and promote healing
-POLICE
Protection
Optimal Loading
Ice
Compression
Elevation

Unit 2 (31 decks)

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