Inflammation and Healing Flashcards

(39 cards)

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
Collagen Production
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
Wound Contraction
pulls edges of site together for smaller area of scar myofibroblasts have contractile properties and pull good skin together can have contracture
27
Contractures
uncontrolled wound contraction | inc resistance to passive stretch
28
Neovascularization/ Angiogenesis
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
Maturation/ Remodeling
modifies scar tissue into its mature form
30
Maturation Response
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
Induction Theory
scar mimics tissue its healing
32
Tension Theory
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
1st phase EPAs
cryo, compression, iontophoresis, laser, TENS, e-stim
34
2nd phase EPAs
inc BF - heat, diathermy | inc cell metab - laser, estim, US*
35
3rd phase EPAs
US*, laser, CPM, traction, NM e-stim
36
Acute Infla
sequence of healing continuous and within expected time frame
37
Chronic Inflammation
delay in processs because repeat trauma, poor perfusion/oxygenation, immune response to foreign material or RA
38
local factors to wound healing
``` type/size/location wound dimension infection vascular supply external forces movement ```
39
Systemic factors of wound healing
age disease medications nutrition - smoking