Wound healing Flashcards by Quennie Ann Silverio

used spiritual and physical

methods of wound care

2000 B.C: Sumerians

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

Babylonian time

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– first to differentiate infected and non-infected wounds

Egyptians

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

absorbent, and _____ as barrier

honey; lint; grease

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

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classified Acute vs Chronic wounds

Greeks

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shown importance of moisture

to wound healing

200 A.D. - Galen

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

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

1818-1865

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Germs introduced

to wound cause infections

Louis Pasteur

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Discovery of phenol for soaking instruments

Joseph Lister

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antiseptic

dressings using gauze + iodoforms

Robert Wood Johnson

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led to the development of polymeric

dressings.

1960-1970

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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)

WOUND

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PHASES OF WOUND HEALING

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

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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
_______

“HEMOSTASIS”

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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
__________

fibrin clot

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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
________________

“INFLAMMATORY PHASE”

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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: ________

PROLIFERATION

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First action is to stop bleeding by formation of clot and

activation of

coagulation cascade

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serves as the scaffolding of or cellular

infiltration

Fibrin Clot

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

24 to 48

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causes the migration of your white

blood cells, PMN’s

PDGF

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• 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

Polymorphonuclear Leukocytes (PMNs )

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• 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

Macrophages

• 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.

T Lymphocytes

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

Collagen III and fibronectin

It is only when the deposition of _____that the | wound starts to have the tensile strength

collagen I

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

VEGF

• 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

PROLIFERATIVE PHASE

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

Fibroblasts and endothelial cells PDGF.

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

Collagen

KNOWN FACTORS THAT HINDERS WOUND | HEALING

o Infection | o Foreign bodies

is the major component | of extracellular matrix in skin

Collagen type 1

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

Collagen type 3

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

Glycosaminoglycan

The major glycosaminoglycans present in | wounds are _________

dermatan and chondroitin | sulfate.

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

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

MATURATION AND REMODELING

early matrix | scaffolding

Fibronectin & Collagen Type III

is the final matrix

Collagen Type I

__________increases | resistance from enzymatic digestion

Fibril Formation and Cross linking

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

Fibrillin

• 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.

EPITHELIALIZATION

____ divide and migrate to bridge defect | followed layering of cells then keratinization.

basal cells

Stimuli for re-epithelialization:

• 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

Re-epithelialization starts from______and the layer | of epithelial cells hair follicle

stratum Basale

• 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

WOUND CONTRACTION (function of remodeling)

Wounds that heal in a predictable manner and | time frame

ACUTE WOUND

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

CHRONIC WOUND

• Closed primarily after surgery (clean wounds)

Primary Intention Healing (Primary closure)

• 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)

Secondary Intention Healing

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.

Tertiary Intention Healing (Delayed primary Closure)

``` • 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 ```

CLASS I

• 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

CLASS II

• 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)

CLASS III

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

CLASS IV

If the infection is up to subcutaneous tissue

Superficial incisional SSI

From facia to deep muscles

Deep incisional SSI

If infection extends into the abdominal space or an | organ

Organ/Space SSI

GIT failure of healing:

Dehiscence, Leaks and Fistulas

GIT Too much healing:

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

greatest tensile strength and suture | holding capacity

Submucosal Layer

achieves a watertight seal from luminal | side of bowel

Serosal Layer

Requirements for adequate anastomosis:

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

greater risk of leaks, lower | incidence of stenosis

Everting sutures-

- fewer leaks, higher incidence of | stenosis

Inverting sutures

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)

Neuropraxia

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)

Axonotmesis

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)

Neuronotmesis

3 Crucial steps in Nerve Healing

• 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

Regulators of Nerve Healing:

* Growth Factors * Cell Adhesion Molecules * Non-neuronal cells and receptors

soft callus formation

3-4 days

mineralization of soft callus and conversion to bone

1-3 months hard callus

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

Hematoma | phase

(excess callus reabsorbed and | marrow recanalized)

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

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

CARTILAGE

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)

CARTILAGE

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

Superficial injury

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

Deep injury

• 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

TENDONS AND LIGAMENTS

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

Oxygen is an important cofactor for collagen synthesis | during _________

hydroxylation

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

STEROIDS

Steroid: Effects may be reversed by administration of

Vitamin A

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

CHEMOTHERAPEUTIC DRUGS

– decreased inflammatory | response (25,000 to 100,000IU/day)

Vitamin A Deficiency

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

Zinc Deficiency

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

Diabetes Mellitus

T or F Use smallest possible suture that will hold wound edges

presence of host response in reaction to | deposition and multiplication of bacteria

Infection

• 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

HYPERTROPHIC SCAR

Wound healing Flashcards

(92 cards)