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WOUND HEALING > WOUND HEALING > Flashcards

WOUND HEALING Flashcards

1
Q

TGF Alpha cell origin

A

macrophages

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2
Q

TGF beta cell origin

A

platelet alpha granules
Macrophages
fibroblast \ keratinocyte

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3
Q

EGF

A

platelet alpha granules

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4
Q

IL 1 cell origin

A

macrophage

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5
Q

IL 2 cell origin

A

T. lymphocyte

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6
Q

what cells or critical and what cells are not critical for wound healing

A

neutrophils NOT needed for wound healing

macrophages ARE required further wound healing

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7
Q

effects smoking on wound healing

A

decreased metalloproteinase
decrease a white cell taxis
microvascular vasoconstriction

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8
Q

Vitamin supplementation proven to help wound healing

A

vitamin A. 25,000 international units IV-given to counteract steroid use

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9
Q

maximum dose of lidocaine

A

4.5/5 mg per kilogram without epi

7 mg per kilogram with epi

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10
Q

Maximum dose of bupivacaine

A
  1. 5 mg per kilogram without epi

3. 5 mg per kilogram with epi

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11
Q

Avastin effects on wound healing

A

prevent angiogenesis

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12
Q

rapamycin effect and wound healing

A

“Seroliumus”
do not use of recent wound - prevent neointimal hyperplasia
(Used to coat cardiac)

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13
Q

retention of tensile strength of catgut

A

7 days

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14
Q

retention of tensile strength of chromic

A

14 days

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15
Q

retention of tensile strength of polyglycolic acid

A

“Vicryl “
14-30 days
dissolve by hydrolysis

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16
Q

polypropylene trade name

A

Prolene

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17
Q

retention of tensile strength of polydioxanone and trade name

A

PDS

2 months

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18
Q

what is Marlex mesh made out of

A

polypropylene

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19
Q

Why venous ulcers found with air found

A

medial malleolus

Cockett veins communicate saphenous

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20
Q

diabetic foot pathology

A

collapse of midfoot resulting Charcot foot

plantar prominence of metatarsals

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21
Q

went home improved use of PDGF

A

foot ulcers

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22
Q

with his best preparation of iodine for wound care

A

Cadexomer iodine
elemental iodine
“Iodosorb”
absorbs exudate from wound to promote sterile environment
One a few topical antimicrobial supported by random -controlled trials

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23
Q

cell that get everything started for wound healing

A

platelets

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24
Q

at what time. In wound healing are PMNs predominant cell

A

day 3

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25
Q

what type of collagen was made down in the proliferative phase of wound healing

A

type III

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26
Q

whitish type III collagen converted to an wound healing

A

converted to type I collagen

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27
Q

first choice at and management of keloid scar

A

silicone sheet

Second choice inject with steroid

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28
Q

with family of local anesthetic can cause methemoglobinemia

A

Amides:
lidocaine
Marcaine

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29
Q

2 examples of Ester local anesthetic

A

procaine

Chloral procaine

30
Q

what is treatment of methemoglobinemia

A

methylene blue

31
Q

Symptoms of methemoglobinemia

A

decreased oxygen saturation

32
Q

Marcaine toxicity treated with

A

Intralipid

33
Q

and in wound healing cuff all G. warehouse are metalloproteinases seen

A

principle pathology and AAA

increase was smoking

34
Q

name complications that are being monitored with system based medicine

A 
PE
DVT
Central line infection
Sternal wound
Ventilator acquired pneumonia
CHF
Surgery site infection
Wrong site surgery
35
Q

pathophysiology of venous ulcer

A

venous pressure increases to the point of decreased perfusion pressure ultimately limits arterial inflow

36
Q

most common organisms associated with cholecystectomy wound infection

A

staph aureus

37
Q

definitive diagnosis with necrotizing fasciitis

A

excess skin

Intraoperatively she easily delaminated from the digital dissection excised until this stops

38
Q

for perforated appendicitis and kids how is skin incision managed

A

closed!

NOT in adults

39
Q

The textbook management of fluctuance in postoperative wound without surrounding erythema and cellulitis

A

I&D only

NO antibiotics

40
Q

antibiotics for necrotizing pancreatitis?

A

NO!

NO imipenem!

41
Q

Xigris

A

TAKEN OFF THE MARKET!
Recombinant protein C
BLEEDING complication
protein C is endogenous anticoagulant and clotting cascade

42
Q

Pathophysiology of Coumadin causing skin necrosis

A

inhibits protein C (endogenous anticoagulant) before the vitamin K dependent clotting factors are inhibited-paradoxical HYPER coagulable

43
Q

Pathophysiology of factor V Leiden deficiency

A

Factor V Leiden is required to activate protein C causes patient to be HYPERCOAGULABLE

44
Q

best management to avoid seroma

A

Close suction drain

45
Q

number of days when peak number of fibroblasts

A

6

46
Q

functional macrophage in wound

A

peak number of macrophages 40-96 hours post injury

Most cubital roll is activation and improvement of other cells side of times and growth factors

releases TGF beta and the VEGF , and for a growth factor, endothelial growth factor

Also involved in phagocytosis and a, angiogenesis

47
Q

First cell to migrate into wound

A

PMN

48
Q

Type I collagen

where it is found what is function

A

Major component of extracellular matrix and skin

49
Q

Type III collagen

A

transformed into a type I collagen with wound maturity

50
Q

Tensile strength of completely healed wound approaches the strength uninjured tissue at what time.

A

Never

51
Q

time it take for reepithelialization-complete repair of external barrier in a well approximated surgical wound

A

2 days! in superficial wound such as skin grafts and second-degree burns

The Unless large wound with significant epidermal and dermal defect

52
Q

TGF beta

A

released by macrophages

Angiogenesis

also released by:
platelet alpha granules
fibroblast \ keratinocyte

53
Q

Ehlers-Danlos syndrome

Inheritance and findings

A

autosomal dominant most common
fibronectin and lysyl hydroxylase
laxity of skin and joints or graft possible abnormal clotting studies

54
Q

protein abnormality and Marfan syndrome

and clinical findings

A

FIBRILIN
(Also defect and collagen type III)
myopia, scoliosis, AAA, ligament laxity

Hernias

55
Q

protein defective in osteogenesis imperfecta-describe syndrome

A

collagen type I (also defect in Ehlers-Danlos syndrome along with fibronectin)

SCARRING IS NORMAL

Skin hyper distensible with increased bruisability and dermal thinning

 presentation:
Can be fatal,
Brittle bones
Osteopenia
Decreased muscle mass
Hernias
Ligament laxity

4 major types:

56
Q

Acrodermatis enteropathica

A

pediatric condition from
Inability to absorb sufficient zinc from breast milk
fracture and faint uptake in intestine

sphincter deficiency associated with him. Granulation tissue
think is also cofactor for being a polymerization reverse transcutaneous

impaired wound healing, pustular dermatitis,

Treat with zinc orally curative for wound healing

57
Q

With layer of intestine has greatest tensile strength

A

SUBMUCOSA

58
Q

Which structures of the gastrointestinal tract lack serosa

A

esophagus
Rectum
Retroperitoneal portions of the colon

59
Q

primary mechanism from which bowel anastomosis leak 5-7 days after surgery

A

increased collagenolysis

60
Q

pathophysiology of bowel healing

A

initial watertight characteristic dependent on fibrin seal on the serosa

Decreased marginal strength in the first week due to collagenolysis that far exceeded collagen symphysis

61
Q

Supplementation of which amino acid may improve wound healing

A

arginine
fibroplasia related
may enhance wound collagen deposition

62
Q

Vascular pathology seen with Ehlers-Danlos syndrome

A

spontaneous arterial venous fistula

small blood vessels are friable may develop aneurysms, varicosities, arteriovenous fistulas,

63
Q

Clinical findings suspicious for Ehlers-Danlos syndrome in child

A

Recurrent hernia, coagulopathy, platelet abnormality and low coagulation factor levels

64
Q

name defects seen with Ehlers-Danlos syndrome

A

Defects:
type III (and I) collagen
fibronectin
lysyl hydroxylase

65
Q

epidermolysis bullosa

A

3 types

Impairment of adhesion with the epidermis and basement membrane her dermis

Causes blisters and minimal trauma

Nutritional status compromised because of oral erosions and esophageal obstruction

Treatment may include esophageal dilation, gastrostomy tube

66
Q

Which phase of healing is most affected by exogenous corticosteroids

A

Initial phase of so migration and angiogenesis

Reduces collagen symphysis and one strength

Most deleterious effect therefore is 3-4 days post injury

Inhibit inflammatory phase of wound healing:
Angiogenesis
Neutrophil migration
Macrophages migration
Fibroblastic proliferation
Release  lysis normal enzymes

also inhibits epithelialization and contraction with increased rate of wound infection regardless of time of administration

67
Q

Pathophysiology of vitamin C deficiency

A

Failure and collagen symphysis
Failure of collagen cross-linking

Vitamin C required for Prolene and glycine conversion to hydroxy Prolene and hydroxy lysine

Possible associated impairment of neutrophil function-increased wound infection

Nonsmoker without trauma needs only 60 mg a day

Trauma and the smoker may need one to 2 g of a

68
Q

vitamin A dose IV

A

25,000 mg - 100,000 mg

69
Q

how does vitamin a work to help wound healing

A

counteract steroids

Increases inflammatory response and wound probably related to life his Lysosomal membrane

increases macrophages that increase collagen symphysis

Direct increase of collagen production and epidermal growth factor receptors

Also helpful for diabetics tumor formation radiation

70
Q

marjolin’s ulcer

A

malignant transformation of chronic ulcer

Seen in any chronic wound

Over turned wound edges

71
Q

metallic pronation to have what functioned biochemically

A

initiate collagen degradation

pile of collagen in AAA with smokers

72
Q

severe cases of hidradenitis suppurativa in the groin treated how

A

rotational flap

WOUND HEALING (1 decks)

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