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SF quizzes > Wound Care > Flashcards

Wound Care Flashcards

1
Q

Which cell is highest in number in a healing wound after 5 days?

a) neutrophils
b) macrophages
c) keratinocytes
d) fibroblasts

A

b) macrophages

neutrophils within 24 hour

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2
Q

How many hours does early inflammation last for?

A

24 hours

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3
Q

How many hours does late inflammation last for?

A

48 hours

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4
Q

How many hours does proliferation last for?

A

72 hours

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5
Q

How long does the remodelling phase last?

A

Weeks to months

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6
Q

When is maximal collagen content first achieved in normal primary wound healing?

a) 3 weeks
b) 6 weeks
c) 12 weeks
d) 6 months

A

3 weeks

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7
Q

What percentage of maximal skin strength is achieved by 6 weeks?

a) 30%
b) 50%
c) 70%
d) 90%

A

70%

skin and scar never as strong as original dermis

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8
Q

Name 7 Local factors affecting wound healing

A
  • infection
  • tension
  • hematoma
  • vascular supply
  • edema
  • foreign body
  • neuropathy
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9
Q

Name 8 SYSTEMIC factors affecting wound healing

A
  • Steroids
  • Nutrition
  • Anemia
  • Immunosuppression
  • Diabetes
  • Renal/Hepatic Failure
  • Radiation
  • Smoking
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10
Q

Which of the following is the mechanism of steroid inhibition in wound healing?

a) increase angiogenesis
b) inhibit synthesis of pro-collagen
c) increased collagenase activity
d) increased macrophage production

A

Inhibits synthesis of pro-collagen

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11
Q

Systemic corticosteroids interfere with wound healing. There effect may be minimized by:

a) Vitamin A
b) Vitamin C
c) Vitamin E
d) Zinc

A

Vitamin A (25 000 IU per day)

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12
Q

In collagen synthesis, which two residues must be hydroxylated
for stability?

A

Proline and Lysine

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13
Q

What is the sequence of Collagen synthesis?

A

mRNA –> pre-procollagen –> hydroxylation (pro, lys) –> Procollagen Trimers –> excretion & cross linking (lysine & hydroxylysine)

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14
Q

Which vitamin is important in collagen synthesis/stability

A

Vitamin C (ascorbic acid)

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15
Q

Name the effect of nutritional protein deficiency

A

Immune response and poor collagen formation

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16
Q

Name the effect of nutritional Vtitamin C deficiency

A
  • Inhibits secretion of collagen by fibroblasts

- Required co-factor for hydroxylation and cross-linking for collagen synthesis

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17
Q

Name the effect of nutritional VITAMIN A deficiency

A

Impairs epithelial proliferation and differentiation

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18
Q

Name the effect of nutritional ZINC deficiency

A

Impairs function of enzymes, eg nucleic acid polymerases

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19
Q

What are the 3 types of wound healing?

A 
Primary intention
Secondary intention (prolonged inflammatory phase)
Tertiary intention (delayed primary)
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20
Q

Scar maturation process may last how long?

A

3 weeks to 2 years

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21
Q

In scan maturation, which type of collagen is replaced by another?

A

Type 3 collagen replaced with Type 1 (1:8)

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22
Q

What happens to vascularity during scar maturation?

A

Decreased vascularity

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23
Q

What percent of hospitalized patients in Canada have pressure ulcers (PU)?

A

9 and 25%

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24
Q

What kind of ulcer is responsible for more hospital admissions than any other complication of diabetes?

A

DM foot ulcers

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25
Q

At the TOH (The Ottawa Hospital), what is the frequency of all stages of PU? Stage 2 and up?

A

All stages = 14.3%

Stage 2 and up = 9.9%

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26
Q

What are the 3 concepts of wound healing?

A

1) moist wound healing
2) acute vs chronic wound healing
3) wound bed prep

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27
Q

What is the advantage of moist wound healing vs air dry?

A

Accelerates healing by 50% due to faster migration of epithelial cells.
(epithelial cells migrate on moist wound bed, instead of under a dry scab)

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28
Q

Name 3 other advantages to moist wound healing

A
  • allows autolytic debridement
  • decreases pain
  • wet to dry dressings peel off healing layers
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29
Q

Define acute wound healing

A

Wound that

  • passes in an orderly fashion through the phases of healing
  • closes in a predictable time frame
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30
Q

Define chronic wound healing

A

Wound that are

  • present for >3 months
  • fails to progress through the 4 phases of wound healing
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31
Q

In chronic wound healing, wounds are often stuck in which phase?

A

Phase 2 - Inflammatory phase

32
Q

What molecular processes predominate in a chronic wound?

A
  • WBC predominate and release MMP
  • MMP digest wound matrix faster than it can be laid down
  • Leaky capillaries (excess release of proteins that inactivate GF)
  • Fibroblasts stop responding to normal wound healing signals
33
Q

What contributes to the vicious cycle of chronic wound healing?

A

Continued release of MMP by stimulated WBC by local wound environment

  • bacteria
  • necrotic tissue
34
Q

What is the goal of wound bed prep?

A

Convert a chronic wound into an acute wound (allow normal healing)

35
Q

List the three pronged attack of a wound bed prep

A
  1. Debridement
  2. Decrease Bacterial Burden
  3. Manage wound exudate
36
Q

Name 4 methods of wound debridement

A
  • surgical
  • enzymatic
  • biological
  • lavage
37
Q

2 goals of debridement

A
  1. remove necrotic/infected tissue

2. allow proper wound staging

38
Q

Name 3 possible microbial states of a wound

A

Contamination (non-replicating organisms)

Colonization (presence of replicating organisms, no host imm response)

Infection (replicating organisms WITH host immune response)

39
Q

What formula depicts the presence of an infection?

A

Presence of Infection

= (#bacteria x virulence of bacteria)/host immune function

40
Q

What are subtle signs of wound infection?

A

Increased pain
Friable granulation tissue
Increased exudate
Wound deteriorates

41
Q

What is the wound “macro” environment?

Micro wound environment?

A

Treating the patient

Treating the wound

42
Q

Underlying cause for the Macro Environment, and its management

A

Arterial (bypass, amputate, angioplasty)
Venous (compression dressing, Sgx)
Diabetic (offload pressure, anti-diabetic meds)
Infection (Abx, debride)
Pressure (offload pressure, mattress, MYOcutaneous flap)

43
Q

How do you manage the Micro wound environment?

A

D.I.M.E

D - Debridement
I - Infection/inflammation
M - Moisture Balance
E - Edges of the wound

44
Q

What are the 3 rules of dressing selection?

A

1-No universal wound dressing

2-Must be appropriate for underlying cause

3-Re-assess dressing regularly, as process is dynamic and changes

45
Q

Mechanism of Action of Silver in dressings?

A

(Ionized silver)
Targets bacterial DNA
Disrupts proteins in cell membrane
Inhibits function of some bacterial enzyme

46
Q

What two dressings decrease bacterial load? (HOT)

A

Silver (acticoat) - bactericidal + broad spec MRSA/VRE

Iodosorb - broad spec, decreased foul odor

47
Q

Which dressings are Not recommended for decreased bacterial burden?

A 
Iodine solutions
Hygeol
Acetic acid
Topical abx
Peroxide
48
Q

What does Hydrogel do?

A

Moist wound healing (low exudate)
Autolysis
Decreases pain (when peeled off)

NOT recommended (wet to dry saline soaked gauze)

49
Q

For moderate to heavy exudate wounds, what is recommended?

A

Foam
Alginate
Hydrofiber
The VAC (negative pressure dressing)

NOT abdo pads

50
Q

Name the 4 wonders of wound care

A

VAC
Growth factors
Hyperbaric Oxygen chamber
Soft Tissue Substitutes

51
Q

How does the VAC work? (7 items)

A 
Improves blood flow
Granulation Tissue formation
Reduces edema
Decreases Bacteria
Controls exudate
Mechanically draws wound edges inward
Moist environment
52
Q

Name indications for hyperbaric oxygen

A

Gas Gangrene, Compartment Syndrome, Nec Fasc

Refractory osteomyelitis, Skin Grafts/Flaps, Diabetic ulcers

53
Q

Define hyperbaric oxygen

A

Breathing 100% oxygen at increased atmospheric pressures

54
Q

How does HBO2 work?

A 
1 Hyperoxygenation
2 Vasoconstriction
3 Angiogenesis
4 Fibroblast proliferation and collagen synthesis
5 Leukocyte oxidative killing
6 Toxin Inhibition (clostridium)
7 Antibiotic Synergy
55
Q

Which of the following statements is true regarding Osteogenesis Imperfecta?

1) Due to Mutation in Collagen Type 1
2) Due to defect in Elastin
3) Causes abnormal adhesion of the epidermis to basement membrane
4) Cases abnormal wound healing and skin elasticity

A

Mutation is Collagen Type 1

56
Q

Name the 4 types of OI

A

I- mild (AD)
II - extremely severe (AR)
III - Severe (AR)
IV - Undefined (AD)

57
Q

Define Cutis Laxa (Elastolysis)

A

Skin laxity
Fibulin or Elastin gene substitution
Degenerative changes in skin Elastin
?Increased elastase activity

58
Q

Define Epidermolysis Bullosa

A

Epidermins and dermis separate
Blistering/Skin erosion
Keratin/Collagen VII/Laminin

59
Q

Which 3 proteins are implicated in epidermolysis Bullosa?

A

Keratin
Collagen VII
Laminin

60
Q

Which of the following statements is/are true regarding Ehlers Danlos?

a) due to mutation in collagen
b) due to a defect in fibrillin
c) causes increased joint elasticity
d) causes abnormal wound healing and skin elasticity

A

a) due to mutation in collagen

61
Q

Ehlers Danlos can have abnormalities in which types of collagen?

A

I, III, V

62
Q

Which gene/protein is abnormal in Marfan Syndrome?

A

FBN1 gene = fibrillin protein

63
Q

List 3 features of marfan syndrome

A

Tall stature
Arachnodactyly (long and slim spider fingers)
MV prolapse, Aortic Regurg

64
Q

What are 2 possible wound healing complications?

A

Hypertrophic scarring

Scar contracture

65
Q

21M suffers a 8x10 cm partial thickness wound to Lt flank. After 2 weeks is has shrunk by 25%. Cells most responsible for this are?

a) neutrophils
b) macrophages
c) fibroblasts
d) myofibroblasts

A

myofibroblasts

66
Q

In which of the following ways do hypertrophic scars differ from normal scars?

a) increased ratio of Type 1 collagen to Type 3 collagen
b) increased water content
c) increased collagen concentration
d) decreased glycosaminoglycan content

A

c) increased collagen concentration

In fact Collagen type 3 is increased, so is collagenase
Normal Skin (I:III)  8:1
Hypertrophic scar 8:4
67
Q

Which of the following is UNTRUE about keloids?

a) histologically similar to hypertrophic scars
b) extend beyond the limits of the original wound
c) usually amenable to surgical excision
d) can be treated with steroid injection
e) radiation is mentioned only to be condemned

A

UNTRUE answer- generally amenable to surgical excision

68
Q

Name 5 risk factors for keloid/hypertrophic scars

A
  • Location (#1 ear, shoulder, midline scars)
  • Genetics (dark skin)
  • Race
  • Age 10-30
  • Delayed wound healing
69
Q

How can you manage hypertrophic scars?

A

Time, Pressure, Silicone Gel, Steroids

70
Q

Keloid scar management?

A 
Same as hypertrophic scars, but also includes
-radiation
-Imiquimod (aldera)
-Retinoic acid
?Excision
71
Q

What are the 4 stages of Wound healing?

A 
(C-I-P-R)
Coagulation
Inflammation
Proliferation
Remodelling
72
Q

What are the stages of wound healing?

A

CIPR

  • coagulation
  • inflammation
  • proliferation
  • remodelling
73
Q

How do steroids act in the setting of wound healing?

A

Inhibit

  • macrophage function
  • fibrogenesis
  • angiogenesis
74
Q

What is one bacteria that acetic acid works to eradicate?

A

Pseudomonas

Greenish/yellow discharge from wound

75
Q

Name 4 VAC Tips

A
  • black/white sponge does not have to touch wound edges (or sit right on regular skin)
  • dry and tape wet edges last
  • start suction even before completely sealed
  • you can never have too much tegaderm
76
Q

For normal wound healing, what 3 things do you advise patients to prevent a bad scar (after stitches are out)?

A

1) No tanning in the early phase
2) Pressure (scar massage)
3) Silicone gel/sheets

77
Q

Risks of injecting steroids (kenalog) into a scar?

A 
De-pigmentation
Fat atrophy (dent in skin)

SF quizzes (9 decks)

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