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SURGERY > Wound healing > Flashcards

Wound healing Flashcards

1
Q

used spiritual and physical

methods of wound care

A

2000 B.C: Sumerians

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2
Q

they were the ones
who first documented the process of
wound healing mostly based on spiritual
concepts

A

Babylonian time

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3
Q

– first to differentiate infected and non-infected wounds

A

Egyptians

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4
Q

1650 B.C. – Use of ______ as antibacterial, _____ as

absorbent, and _____ as barrier

A

honey; lint; grease

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5
Q

Edwin Smith Surgical Papyrus, a copy of
a much older document, describes at
least___ different types of wounds.

A

48

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6
Q

classified Acute vs Chronic wounds

A

Greeks

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7
Q

shown importance of moisture

to wound healing

A

200 A.D. - Galen

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8
Q

T or F
epithelialization rate increases by 50% in
a moist wound environment when
compared to a dry wound environment

A

T

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9
Q

Discovery of Antiseptics (Soap &
Hypochlorite)
o Ignaz Philipp Semmelweis, a Hungarian
obstetrician, noted that the incidence of
puerperal fever was much lower if
medical

A

1818-1865

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10
Q

Germs introduced

to wound cause infections

A

Louis Pasteur

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11
Q

Discovery of phenol for soaking instruments

A

Joseph Lister

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12
Q

antiseptic

dressings using gauze + iodoforms

A

Robert Wood Johnson

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13
Q

led to the development of polymeric

dressings.

A

1960-1970

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14
Q

any break in the integrity of the epithelial lining
e.g. skin or mucosal linings will start cascade of
events that will repair damage (does not occur
one after the other, they overlap)

A

WOUND

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15
Q

PHASES OF WOUND HEALING

A

o Hemostasis & Inflammation
o Proliferative Phase
o Maturation & Remodeling
o Epithelialization & Wound Contraction

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16
Q

The exposure of factors underneath the
epithelium, usually fibrin that triggers the
migration of platelets there and trigger the
coagulation cascade – and that part is the first
part of wound healing which is called
_______

A

“HEMOSTASIS”

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17
Q

first thing you can do to stop the bleeding
is to apply direct pressure because hemostasis
which is the normal function of the body would
attempt to stop the bleeding by platelet
aggregation and formation of what you called
__________

A

fibrin clot

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18
Q

the platelet secretes some co-factors
leading to the migration of the inflammatory cells
into the site of injury. And usually this are heralded
first with your neutrophils, white blood cells which
secretes further other factors that leads to the
migration of macrophages and later on
lymphocytes. This is what you call now the
________________

A

“INFLAMMATORY PHASE”

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19
Q

The macrophages that have migrated there will
secrete factors that will attract now your fibroblast
which heralds now the next part of the wound
healing: ________

A

PROLIFERATION

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20
Q

First action is to stop bleeding by formation of clot and

activation of

A

coagulation cascade

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21
Q

serves as the scaffolding of or cellular

infiltration

A

Fibrin Clot

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22
Q

In first two phases which are the hemostasis and
inflammation, this happens relatively fast, they
usually overlap with each other in first ___ hours

A

24 to 48

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23
Q

causes the migration of your white

blood cells, PMN’s

A

PDGF

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24
Q

• First infiltrating cells (24-48 hrs.)
• Phagocytes for bacteria and debris (initial
protectors)
• Major source of cytokines and collagenases
• TNF-α3 which may have a significant influence on
subsequent angiogenesis and collagen synthesis
• As the aforementioned cells appear, what they
secrete also increase.
• Collagen I ® Fibronectin ® Collagen III

A

Polymorphonuclear Leukocytes (PMNs )

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25
Q

• Second group of inflammatory cells (48-96 hrs. post
injury) infiltrating cells
• They produce most of the factors for wound
healing
• Phagocytes (more efficient) synthesize O2 (free)
radicals and nitric oxide
• Recruits and activates other cells via cytokines
and growth factors
• Regulate cell proliferation, matrix synthesis and
angiogenesis

A

Macrophages

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26
Q

• Less numerous than macrophages (1 week
post injury)
• Their presence is not fully understood because no
significant function has been identified
• Effects on modulation of wound environment
• Bridge the transition from inflammatory to
proliferative phase (modulate the wound
environment)
• They act like a marker that this wound is now going
to proliferative phase from inflammatory phase
• Role not fully defined possible effects on
modulation of wound environment.

A

T Lymphocytes

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27
Q

are the first collagen fibers
that are being deposited. They do not provide tensile
strength but they provide the lattice work or the
deposition of the mix group of collagen which is your
collagen I

A

Collagen III and fibronectin

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28
Q

It is only when the deposition of _____that the

wound starts to have the tensile strength

A

collagen I

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29
Q

leads to the migration of endothelial cell to
trigger angiogenesis which is an important phase to
herald now the start of the proliferative phase

A

VEGF

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30
Q

• Early phase of healing
• Collagen synthesis (function of fibroblasts) and
Angiogenesis (function of endothelial cells)
• From 4th to 12th day post injury (during this time,
wound tensile strength starts to occur and
increase with time).
• Fibroblast migration due to PDGF (from
macrophage)
• Endothelial cells migrate, replicate and form new
capillary tubules due to cytokines. TNF, TGF, &
VEGF

A

PROLIFERATIVE PHASE

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31
Q

•___ are the last cell
populations to infiltrate the healing wound, and
the strongest chemotactic factor for fibroblasts is
_____

A

Fibroblasts and endothelial cells

PDGF.

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32
Q

the most abundant protein in
the body, plays a critical role in the
successful completion of adult wound
healing.

A

Collagen

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33
Q

KNOWN FACTORS THAT HINDERS WOUND

HEALING

A

o Infection

o Foreign bodies

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34
Q

is the major component

of extracellular matrix in skin

A

Collagen type 1

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35
Q

which is also normally present in
skin, becomes more prominent and
important during the repair process

A

Collagen type 3

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36
Q

comprise a large portion
of the “ground substance” that makes up
granulation tissue

A

Glycosaminoglycan

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37
Q

The major glycosaminoglycans present in

wounds are _________

A

dermatan and chondroitin

sulfate.

38
Q

Fibroblasts synthesize these compounds,
increasing their concentration greatly during
the first __ weeks of healing

A

3

39
Q

• Reorganization of previously synthesized collagen
• Begins during fibroblastic phase
• Balance between collagenolysis and collagen
synthesis
• Collagen is broken down by Matrix
Metalloproteinases (MMP)

A

MATURATION AND REMODELING

40
Q

early matrix

scaffolding

A

Fibronectin & Collagen Type III

41
Q

is the final matrix

A

Collagen Type I

42
Q

__________increases

resistance from enzymatic digestion

A

Fibril Formation and Cross linking

43
Q

a glycoprotein secreted by fibroblasts, is
essential for the formation of elastic fibers found in
connective tissue.

A

Fibrillin

44
Q

• Proliferation and migration of epithelial cells adjacent to
the wound (alongside wound healing)
• Begins at day 1 of injury.
• Marginal basal cells divide and migrate to bridge defect
followed layering of cells then keratinization.

A

EPITHELIALIZATION

45
Q

____ divide and migrate to bridge defect

followed layering of cells then keratinization.

A

basal cells

46
Q

Stimuli for re-epithelialization:

A

• Loss of contact inhibition (contact inhibition is when cells
are attached to each other, the cells stop dividing)
• Exposure to matrix proteins (Fibronectin)
• Cytokines form mononuclear cells

47
Q

Re-epithelialization starts from______and the layer

of epithelial cells hair follicle

A

stratum Basale

48
Q

• Reduces the size of the wound (to heal faster)
• Role of myofibroblast (they approximate the cells
better and they decrease the size of the wound)
• Possess a cytoskeletal structure containing alpha
smooth muscle actin in bundles (Stress Fibers)
• Present from day 6 to day 15 of wound healing. Cells
undergo apoptosis after 4 weeks
• Fibroblast also contract wounds by movement of cells
with reorganization of the cytoskeleton.
• Starts as early as the second week

A

WOUND CONTRACTION (function of remodeling)

49
Q

Wounds that heal in a predictable manner and

time frame

A

ACUTE WOUND

50
Q

• Wounds that failed to progress through the
orderly process of healing.
• Wounds that have not healed in 3 months

A

CHRONIC WOUND

51
Q

• Closed primarily after surgery (clean wounds)

A

Primary Intention Healing (Primary closure)

52
Q

• Healing by granulation (reddish-pinkish tissue
on top of the wound)
• Fibroblast continue to lay down collagen, try to
cover the defect and the tissue formed here is
called granuloma.
• Its an indication that healing is already taking
place.
• Takes a long time (months)

A

Secondary Intention Healing

53
Q

Closing the wound predisposed the wound for infection
• Leaving the subcutaneous layer and skin open
for few days.
• Fatty layer appears and when the area appears
pinkish (meaning no infection is there), closing
can be done.

A

Tertiary Intention Healing (Delayed primary Closure)

54
Q 
• Clean wounds 
• Remove eye/insert transplant
• Total knee
• the chances for infection are below 1%
• body cavities are not involved 
• Body cavities involved e.g. breast hernia, 
thyroid
A

CLASS I

55
Q

• Clean- contaminated wound
• Removal of tonsils and adenoids
• Cystoscopy, stone removal
• bacterial count is very low because only normal
flora are the contaminants
• infection rate is 5%
• e.g. gallbladder cystic duct, urinary bladder,
stomach, vehicular accidents- ruptured urinary
bladder

A

CLASS II

56
Q

• Contaminated wounds
• accidental wound (trauma)
• higher bacterial load (gross contamination)
• expected higher infection rate of 10-15% (15-
25% in other books)
• e.g. fecal rupture (colon)

A

CLASS III

57
Q

• Dirty infected wounds (signs of inflammation
already)
• Drainage of abdominal mass
• E.g. diabetic foot ulcer, bedsores, delayed
operation of ruptured appendicitis.

A

CLASS IV

58
Q

If the infection is up to subcutaneous tissue

A

Superficial incisional SSI

59
Q

From facia to deep muscles

A

Deep incisional SSI

60
Q

If infection extends into the abdominal space or an

organ

A

Organ/Space SSI

61
Q

GIT failure of healing:

A

Dehiscence, Leaks and Fistulas

62
Q

GIT Too much healing:

A 
Stricture Formation (scar 
formation), Bowel Stenosis, Adhesions (in serosa 
attachment of the intestines)
63
Q

greatest tensile strength and suture

holding capacity

A

Submucosal Layer

64
Q

achieves a watertight seal from luminal

side of bowel

A

Serosal Layer

65
Q

Requirements for adequate anastomosis:

A 
irements for adequate anastomosis: 
• Tension free 
• Adequate Blood Supply (very important)
• Adequate nutrition (amino acids, proteins)
• Free of Sepsis/Infection
66
Q

greater risk of leaks, lower

incidence of stenosis

A

Everting sutures-

67
Q
  • fewer leaks, higher incidence of

stenosis

A

Inverting sutures

68
Q

focal demyelination (contusion of
the nerve, nabugbog na nerve; but if nerve cell are
still intact, axons are still intact, there may be
temporary loss of function but they recover
immediately; common in thyroid surgery)

A

Neuropraxia

69
Q

axonal interruption but preserved
Schwann Cell (because of trauma there is a break
in your axons but the covering-the Schwann cells;
since Schwann cells is intact, the axons that have
been torn underneath can regenerate and grows;
this occurs longer but there is recovery; more
severe injury, temporary loss of function)

A

Axonotmesis

70
Q

complete nerve transection (So
axon (nerve) and Schwann cells (nerve sheath) are
damage, for the patient to regain function you have
to put them back together and when you try to
suture nerves back together, you are not suturing
axon, you are suturing the covering, which is your
Schwann cells or your nerve sheath to allow the
axons underneath to grow over each other)

A

Neuronotmesis

71
Q

3 Crucial steps in Nerve Healing

A

• Survival of nerve cell bodies (in the brain and spinal
cord; if damaged no regeneration can happen)
• Regeneration of axons growing across transected
nerve to distal stump
• Migration and connection of regenerating nerve
ends to nerve ends of target organ (to preserve
normal function in the end organ

72
Q

Regulators of Nerve Healing:

A
  • Growth Factors
  • Cell Adhesion Molecules
  • Non-neuronal cells and receptors
73
Q

soft callus formation

A

3-4 days

74
Q

mineralization of soft callus and conversion to bone

A

1-3 months

hard callus

75
Q

does not lead to
the formation of your clot but leads to the
formation of your soft callus which is essentially
granulation tissue around the bone edges and
inflammatory cells

A

Hematoma

phase

76
Q

(excess callus reabsorbed and

marrow recanalized)

A

Remodeling phase

o Affected by cytokines and growth factors –
bone morphogenic proteins (BMP)
o Other growth factors: PDGF, TGF, TNF, FGF

77
Q

Consists of cells (chondrocytes) surrounded by an
extracellular matrix made up of several proteoglycans,
collagen fibers, and water

A

CARTILAGE

78
Q

Mainly avascular (do not have blood supply), nutrition
from Perichondrium (covering of the cartilage; provides
blood supply) through diffusion (through capillaries
present there; blood supply dependent on adjacent
organs)

A

CARTILAGE

79
Q

cartilage: no inflammatory
response, inadequate healing, incomplete
overall regeneration, persistent structural
defects (ear injuries)

A

Superficial injury

80
Q

– involves underlying bone and soft
tissue, associated hemorrhage allows
inflammation, granulation tissue formation,
reformation of hyaline cartilage, structural
integrity restored.

A

Deep injury

81
Q

• treat like bones and cartilage (we have to immobilize
them before using them)
• subjected to lacerations, rupture and contusions
• Damaged ends usually separated due to the mobility
of bone or muscles

A

TENDONS AND LIGAMENTS

82
Q

T or F
main characteristic that distinguishes the healing of
fetal wounds from that of adult wounds is the lack of
scar formation.

A

T

83
Q

Oxygen is an important cofactor for collagen synthesis

during _________

A

hydroxylation

84
Q

Inhibits inflammatory phase of wound healing
(angiogenesis, neutrophil and macrophage migration,
fibroblast proliferation)

A

STEROIDS

85
Q

Steroid: Effects may be reversed by administration of

A

Vitamin A

86
Q

• Inhibits cell proliferation and protein synthesis
• Use is delayed for at least 2 weeks postinjury
(clinically, 6-8 weeks)

A

CHEMOTHERAPEUTIC DRUGS

87
Q

– decreased inflammatory

response (25,000 to 100,000IU/day)

A

Vitamin A Deficiency

88
Q

decreased fibroblast proliferation,
decreased collagen synthesis, impaired overall wound
strength, delayed epithelialization

A

Zinc Deficiency

89
Q

Decreased inflammation,
angiogenesis and collagen synthesis compounded by
associated neuropathy and vasculopathy

A

Diabetes Mellitus

90
Q

T or F

Use smallest possible suture that will hold wound
edges

A

T

91
Q

presence of host response in reaction to

deposition and multiplication of bacteria

A

Infection

92
Q

• Above skin level and stay within confines of the
original wound (during remodeling phase) ex. CSstays in original incision, normal healing
• Often regress over time
• Occurs across areas of tension and flexor surfaces
• Increased occurrence when epithelialization
>21days
• Lesions initially erythematous and raised, becomes
pale and flatter with over time

A

HYPERTROPHIC SCAR

SURGERY (6 decks)

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