Wound Healing Flashcards
Which of the following regarding the inflammatory (reactive) phase is TRUE?
(1) It occurs immediately after injury.
(2) It includes hemostasis, but not removal of necrotic tissue
(3) There is decreased vascular permeability
(4) TGF beta causes activation of proteases and prevents scar tissue formation.
(1) Hemostasis occurs immediately after injury.
TGF-beta is activated during the inflammatory (Reactive phase). Its function is to:
cause inhibition of proteases; scar tissue formation occurs.
The reparative process with re-epithelialization, matrix synthesis and neovascularization to relieve the ischemia of the trauma itself.
(1) Inflammatory (reactive) phase
(2) proliferative phase
(3) Maturational phase
(1) proliferative phase
The proliferative phase occurs as
(1) acute responses of hemostasis and inflammation continue
(2) There is scaffolding and angiogenesis
(3) Two weeks post-wounding and angiogenesis 3 - 7 days.
The proliferative phase occurs as (2) there is scaffolding and angiogenesis.
The lag phase of the proliferative phase is characterized by:
(1) the absence of fibroblasts
(2) is over 7 days in length.
(3) The time for undifferentiated mesenchymal cells to differentiate into specialized fibroblasts.
(3) The time for undifferentiated mesenchymal cells to differentiate into specialized fibroblasts.
Wound contraction occurs during the
(1) Inflammatory (Reactive) phase
(2) proliferative phase
(3) maturational phase
(3) maturational phase
The maturational phase involves wound contraction. This results from:
myelofibroblasts
T/F: tensile strength of a scar is 30% less than that of normal tissue.
True.
Wound strength increases rapidly within ____ and plateaus up to 1 year.
Wound strength increases rapidly within 1 - 6 weeks and plateaus up to 1 year.
Around the third day of a post-wound, the major cell type present is:
(1) neutrophils
(2) macrophages
(3) fibroblasts
(2) macrophages
Fibroblasts peak post-wounding
(1) day 2
(2) day 3
(3) day 5
Fibroblasts peak post-wounding (3) day 5.
The provisional matrix is composed of:
(1) fibrin
(2) fibrinogen
(3) fibronectin
(4) All of these
(4) ALl of these.
The end result of the provisional matrix is:
collagen
The predominant component of the inflammatory phase is
fibronectin
As the inflammatory phase breaks down, the majority of collagen that is the FINAL result is:
collagen type 1
Matrix metalloproteinases are downregulated by:
TGF-beta
The activation of plasminogen results in
matrix degradation and facilitates cell migration.
The most common type of collagen (the type of collagen found in skin and bone) is:
type 1 collagen
Early wound healing is characterized by increased expression of:
(1) type 1 collagen
(2) type 2 collagen
(3) type 3 collagen
(3) type 3 collagen
Scurvy is a result of vitamin C deficiency. When vitamin D is deficient, there is prevention of:
There is prevention of proline hydroxylation and the formationf unstable triple helices.
Osteogenesis imperfecta occurs when there is deletion of one pro-collagen allele. The resut is:
pro-alpha collagen chains do not form.
Ehlers-Danlos syndrome produces mutations affecting:
type 3 collagen
Covalent linking of lysine residues provides tensile strength found in:
the collagen of tendons.
T/F: Marfan syndrome is a gene muation in fibrillin formation.
True.
Hypertrophic scars:
(1) remain in the confines of the wound
(2) do not regress spontaneously
(3) Have the same histology as normal scars
Hypertrophic scars (1) remain in the confines of the wound.
Keloid scars are the result of irreversible activation of:
TGF-beta
T/F: keloid scars can be prevented and are refractory to medical and surgical intervention.
True.
A patient presents with a hypertrophic scar. The treatment that can cause contracture and functional impairment:
(1) silicones and pressure therapy
(2) intra-lesional corticosteroid injections
(3) 5-fluorouracil, bleomycin, verapamil
(4) early surgery
(4) early surgery for hypertrophic scars can lead to contracture and functional impairment.
Unlike acute wound fluid, chronic wound fluid has higher levels of:
(1) IL-1
(2) IL-6
(3) TNF-alpha
(4) All of these
(4) All of these
The most common cause of healing delay is:
(1) infection
(2) ischemia
(3) vitamin and mineral deficienies
(4) exogenous drugs
(1) infection
A wound will not heal by any means if the bacterial count exceeds:
10^5 organisms per gram of tissue OR if beta hemolytic streptococci are present.
The substance that stimulates phagocytosis and collagenase and therefore prevents construction of the ECM:
endotoxins
Diabetes mellitus contributes to delayed wound healing due to:
(1) the basement membrane of capillaries is thickened, causing decreased perfusion in the microenvirnoment.
(2) There is an attenuated inflammatory response
(3) All of these
(3) All of these
Endarteritis obliterans causes atrophy, fibrosis and delayed tissue repair. Angiogenesis is not initiated. This results from:
ionizing radiation
T/F: elderly patients are more likely to have surgical wound ruptures and delayed healing.
True.
Hypoalbuminemia delays wound healing if the concentration is LESS than
2.0 g/dl.
The vitamin deficiency that causes impairment of TGF-beta receptors:
(1) Vitamin C
(2) vitamin A
(3) vitamin K
(2) Vitamin K
Which of the following medications decreases TGF beta?
(1) chemotherapeutic agents
(2) tamoxifen
(3) steroids
(2) Tamoxifen
Which of the following mediations impairs fibroblast proliferation and collagen synthesis, and its effects are reversible with vitamin A?
(1) chemotherapeutic agents
(2) tamoxifen
(3) steroids
(3) steroids
Appendicitis is an example of a condition that should be closed via:
(1) primary intention
(2) secondary intention
(3) tertiary intention
(3) tertiary intention
Oxygen dressings are conducive for
fibroblast proliferation and formation of granulation tissue.
Hyperbaric oxygen therapy is used for:
(1) bacterial infections (clostridia or gas gangrene)
(2) decompression sickness (scuba divers)
(3) split thickness skin grafts
(4) All of these
(4) All of these
Ischemia or tissue hypoxia results when the PO2 is less than
30 mmHg.
Inhalation of oxygen lasts for 2 - 4 hours after termination of therapy and induces synthesis of:
endothelial cell NO synthease as well as angiogenesis.
Which of the following is an indication for hyperbaric therapy?
(1) split thickness skin grafts
(2) uncontrolled pneumothorax
(3) current or recent treatment with bleomycin or doxorubicin
(4) treatment with disulfiram
(1) split thickness skin grafts
Negative pressure wound therapy works by:
the removal of chronic edema, leading to an increase in blood flow and stimulation of granulation tissue. This can be used for acute, subacute and chronic wounds. There are faster healing times with fewer associated complications
The transition from scarless to scarring repair occurs
The transition from scarless to scarring repair occurs near the end of the second trimester and the beginning of the third.
Fetal fibroblasts differ from the adult fibroblasts – early gestation fetal human fibroblasts have increased prolyl hydroxylase activity which falls off to adult levels after
Fetal fibroblasts differ from the adult fibroblasts – early gestation fetal human fibroblasts have increased prolyl hydroxylase activity which falls off to adult levels after 20 weeks gestation.
Tenascin: this is an inhibitor of
Tenascin: this is an inhibitor of FIBRONECTIN, which rises earlier and returns to normal more rapidly in the fetus. IT allows cells to migrate and fully epithelialize the wound more rapidly. There is decreased healing time.
Fetal wound healing shows decreased inflammatory response:
there is a LACK of neutrophil infiltration with decreased infiltration of endogenous immunoglobulins. There is decreased macrophages and difference in their temporal appearance in fetal wounds.
Fetal wound healing presents with:
(1) high TGF-beta and FGF-2
(2) PDGF in fetal wounds disappears more rapidly than in adult wounds.
(3) There is an abundance of growth factors.
(4) Absent pluripotent stem cells.
Fetal wound healing presents with (2) PDGF in fetal wounds disappears more rapidly than in adult wounds.
Epidermal Replacements:
(1) created by the expansion of patient-derived cells in the laboratory until enough cell mass is generated to be transferred to the wound.
(2) It is subject to rejection.
(3) There may be a 2 to 3 week delay to generate enough tissue to cover a defect.
(4) These do not require a well-vascularized dermal bed.
Epidermal Replacements:
(1) created by the expansion of patient-derived cells in the laboratory until enough cell mass is generated to be transferred to the wound.
(3) There may be a 2 to 3 week delay to generate enough tissue to cover a defect.
