Inflammation and Healing Flashcards

1
Q

Erythrocytes

A

RBCs
do not migrate to injury
ROLE: O2 transport
Hemoglobin specifically transports the O2

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2
Q

Leukocytes

A

WBCs migrate to the injury
clear debris - PHAGOCYTOSIS to prep for healing
each one is specialized for a task in early or later stages of inflammation

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3
Q

Monocyte becomes Macrophage once out of capillary WBC

A

PHAGOCYTOSIS - eating dead stuff
prominent in CHRONIC inflammation
come and go quickly in acute inflammation
too many is BAD = chronic infla

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4
Q

Lymphocyte WBC

A

bacteria killer - come and go within 1-2 days
if chronic it sticks around
too many is bad = chronic infla

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5
Q

Eosinophil

A

if high count - scary
allergic reaction or parasite infection
too many is bad = chronic

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6
Q

Neutrophil

A

bacteria killer - come and go in a couple of days

acute inflammation/ NL

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7
Q

Basophil

A
acute inflammation/ NL
releases histamine (inc BF to area)
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8
Q

Mast Cells

A

found in CT (not blood)
releases HISTAMINE/Heparin in response to tissue injury and infla
present in NL infla process

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9
Q

Platelets

A

1st cells to injury site and promote blood clotting
even come to site when skin is intact
PDGF - platelet derived growth factor creates PRP (platelet rich plasma) which can be injected into injury to speed up healing process

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10
Q

Chemotactic Signaling

A

platelets send out chemical messages than an injury is present
the signal is PDGF

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11
Q

Fibroblasts **

A

Spew Collagen**
found in CT and forms collagen fibers
Good - but too much is not always good
EPA’s inc their activity: US/laser

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12
Q

Inflammation

A

1-6 days
prepares the wound for healing to occur
some EPAs try to trigger/restart this process

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13
Q

Inflammation Signs

A

heat, pain, swelling, redness, loss of function

Resolve QUICKLY! prevent chronic inflammation

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14
Q

Vascular Inflammation Response

A

Brief VC (5-10min) to not lose blood
VD and inc permeability to clean up and bring troops
Extravasation, Histamine, Hageman Factor, Bradykinin, Prostaglandin

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15
Q

Extravasation

A

the process of a leukocyte migrating form the vessel to the tissue

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16
Q

Histamine = VD

A

VD**
released by Mast, plateets and basophils
VD to inc vascular permeability leading to edema

17
Q

Hageman Factor (clot factor XII)

A

enzyme found in blood that helps to stop local bleeding

18
Q

Bradykinin

A

mediated the inflammatory process
inc VD**
maybe some pain regulation

19
Q

Prostaglandin

A

attracts leukocytes
chemotactic signaling - attracts WBCs (troops)
pain - receptors sensitized

20
Q

Hemostatic Inflammation Response

A

limit local bleeding and fluid drainage
seal damaged vessels
platelets - 1st to promote clot and PDGF
collect fibrin and collagen to help clot

21
Q

Cellular Inflammation Response

A

Mast and platelets release chemotactic agents to attract leuk. Destroy neutrophils to break down fibers, mediate immune response, macrophage - phagocytose and attract fibroblasts

22
Q

PT goals with Inflammation

A

Protect area and Prevent Inflammation

23
Q

Proliferation

A

“Fibroblastic Phase”
rebuilds damaged tissue and strengthen the wound
4 steps: epithelialization, collagen production, wound contraction, neovascularization/angiogenesis

24
Q

Epithelialization

A

if open wound - reestablishment of epidermis, provides protection, healthy cells migrate to cover wound

25
Q

Collagen Production

A

fibro eat Ca and spew collagen which is thin, weak, unorganized (type III) which tolerates early and controlled movement.
Day 12 type III is replaced by type I which is more mature and stronger - still unorganized

26
Q

Wound Contraction

A

pulls edges of site together for smaller area of scar
myofibroblasts have contractile properties and pull good skin together
can have contracture

27
Q

Contractures

A

uncontrolled wound contraction

inc resistance to passive stretch

28
Q

Neovascularization/ Angiogenesis

A

Development of new bld vsls to area helps healing and supply of O2 and nutrients
Form a capillary loop which is weak and often immob helps protect these was they grow
pink/bright red

29
Q

Maturation/ Remodeling

A

modifies scar tissue into its mature form

30
Q

Maturation Response

A

collagen reabsorbed if off direction
longest phase up to 1 yr
changes in size, form, strength of scar (become white)
Type I coll replace type III need O2 - also need a balance between synthesis of new and lysis of III

31
Q

Induction Theory

A

scar mimics tissue its healing

32
Q

Tension Theory

A

internal and external stressed placed on area determine final structure
tension during healing can inc tensile strength
immobilization reduces tensile strength and collagen structure

33
Q

1st phase EPAs

A

cryo, compression, iontophoresis, laser, TENS, e-stim

34
Q

2nd phase EPAs

A

inc BF - heat, diathermy

inc cell metab - laser, estim, US*

35
Q

3rd phase EPAs

A

US*, laser, CPM, traction, NM e-stim

36
Q

Acute Infla

A

sequence of healing continuous and within expected time frame

37
Q

Chronic Inflammation

A

delay in processs because repeat trauma, poor perfusion/oxygenation, immune response to foreign material or RA

38
Q

local factors to wound healing

A
type/size/location
wound dimension
infection
vascular supply
external forces
movement
39
Q

Systemic factors of wound healing

A

age
disease
medications
nutrition - smoking