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Foundations 2 > Wound healing > Flashcards

Wound healing Flashcards

1
Q

what are labile cells?

A

Little time in G0 and are in skin, lungs, GIT, GUT

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2
Q

What are stable cells?

A

Need to be injured in order to be simulated, in liver, kidney tubules, mesenchymal tissue

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3
Q

What are permanent cells?

A

Do not replace with functional tissue but rather with scar that impedes function–in neurons, cardiac muscle, skeletal muscle

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4
Q

Secreted by platelets and macrophages; stimulates vascular remodeling (vasodilation and vascular permeability, fibroblasts growth and fibroblast production of collagen I and III

A

Platelet derived Growth Factor (PDGF)

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5
Q

What clinical outcome in woundhealing gone crazy is PDGF involved in?

A

hypertrophic scars and keloid

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6
Q

Stimulates angiogensis and fibrosis (through SMADs) and inhibit proliferation of other cells (leading to inflammation)

A

Transforming Growth Factor-Beta (TGF-B)

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7
Q

Released by platelets at first and then by leukocytes, macrophages, fibroblasts and keratinocytes

A

TGF-B

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8
Q

What are the general roles of FGF?

A

chemotaxis, wound healing, angiogenesis, collagen production

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9
Q

What do FGF1&2 do?

A

stimulate angiogenesis and enhance fibroblasts activity, and controls skeletal development

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10
Q

What does FGF7 do?

A

cell proliferation

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11
Q

What happens when there is mutation in FGFR3?

A

Achondroplasia ( due to overgrowth of immature chondrocytes)

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12
Q

Stimulates angiogensis for wound healing, embryogenesis, collateral circulation (compensation when capillaries are blocked)

A

Vascular Endothelial Growth Factors (VEGF)

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13
Q

Cell proliferation through RTK and mut related to cancer

A

Epidermal Growth Factor (EGF)

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14
Q

What is connective tissues made up of?

A

Cells (fibroblasts and myofibroblasts, mast cells, macrophages), ground substance (proteoglycans, adhesive glycoproteins) and fibers

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15
Q

Important role of Vit. C in collagen production?

A

Hydroxylation of Proline and lysine

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16
Q

Where is type I collagen found in? necessary for?

A

Bone, skin, tendons, cornea; wound healing (last stage)

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17
Q

Where is type II collagen found?

A

cartilage, vitreous humor, nucleus pulposus

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18
Q

Where is type III collagen found? also called? necessary for?

A

Blood vessels, fetus uterus, reticular fibers; reticulin; early found healing/granulation tissue

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19
Q

Where is type IV collagen found?

A

Basement membrane (basal lamina) and lens

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20
Q

Where does Hydroxylation, Glycosylation and triple helix formation of collagen take place?

A

rough ER

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21
Q

What is collagen transcribed as?

A

Preprocollagen

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22
Q

How do you form insoluble tropocollagen and where does it take place?

A

cleave the terminal region and it takes place extracellularly

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23
Q

How do lysine and hydroxylysine crosslink in tropocollagen?

A

Lysyl oxidase and copper–leads tot collagen fibrils formation

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24
Q

autoimmune attack on collagen IV chain, hemorhage in lungs and kidney (hemoptosis –cough blood– and hematuria)

A

Goodpasture’s disease

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25
Q

What happens when you produce less collagen?

A

aging, wrinkles

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26
Q

Vit. C def leads to swollen gums, bleeding, poor wound healing?

A

Scurvy

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27
Q

Sx: Aut dom mut. in Collagen I (two types), brittle bones, multiple factors, loose joints, hearing loss, poor teeth, blue sclera?

A

Osteogensis Imperfecta

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28
Q

How does blue Sclera happen?

A

Lack of collagen so eye lining is thin-so white part of eye is thin so you can see underlying veins –thus blue

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29
Q

heterogeneity due to defective collagen synth. of skin, joints and blood vessels

A

Ehlers-Danlos Syndrome

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30
Q

Sx: Hyperextensible skin, joint instability (hypermobile), easy bleeding and bruising, abnormal wound healing, vessel wall degeneration (heart valves –weak)

A

Ehlers-Danlos Syndrome

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31
Q

Types of Ehlers-Danlos Syndrome

A

Classical: Type V collagen
Vascular: Type III collagen (organ rupture, valve prolapse, most severe, blood vessel wall not sturdy)

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32
Q

Describe Elastin?

A

insoluble, tropoelastin, little hydroxyproline no hydroxylysine

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33
Q

What links Elastin molecules?

A

Desmosine and isodesmosine

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34
Q

What is Fribrillin 1?

A

Scaffolding protein thats around elastin coded by FBN1 and binds and sequesters TGF-B

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35
Q

What is elastin fibers broken down by?

A

Elastase

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36
Q

What happens when you have alpha-1-antitrypsin def.?

A

Lungs have holes (emphysema) as bombarded with neutrophils elastase; (similar featuresalso seen in smoking

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37
Q

Mut. in FBN1 leads to?

A

Marfan syndrome and excess TGF-B so decreased elasticity

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38
Q

Sx: (wingspan> height) Dolichostenmelia, arachnodactyly, scoliosis, hyperflexibility, inverted sternum, pectus excavatum

A

Marfan syndrome

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39
Q

Sx: Eyes: ectopia lens, CV: aneurysms, aortic dissection –mitral valve prolapse and spontanrous pneumothorax

A

Marfan Syndrom

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40
Q

Most severe cause of death in Marfan syndrome

A

Mitral valve prolapse

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41
Q

What is loose connective tissue?

A

loosely arranged fibers, much ground subs, most abundant type; holds organs in place, allows for movement of nutrients and ions to cells

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42
Q

Example loose connective tissue?

A

Lamina propria: GI Tract, have immune cells, immediately below epithelial.

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43
Q

What is dense irregular connective tissue? Where is it?

A

few cells, irregularly arranged cells, submucosa of GIT, and reticular layer of dermis

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44
Q

What is dense regular connective tissue? where is it?

A

densely packed, parallel, organized fibers, few cells; tendons, ligaments, aponeuroses

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45
Q

Permanent cells of connective tissue?

A

Fibroblasts, myofibroblasts, macrophages, mast cells

46
Q

Most numerous cells in connective cells? What do they do?

A

Fibroblasts secrete fibers, ground substance, MMPs, and GFs

47
Q

Express alpha-smooth muscle actin contraction; necessary for secondary intention

A

myofibroblasts

48
Q

Cells with granules that secrete histamine, heparin

A

Mast cells

49
Q

Marked by tryptase, key cell for Type I hypersensitivity (allergy and asthma) and make and relase growth factors, cytokines and enzymes

A

Mast cells

50
Q

Participate in innate and adaptive immunity, phagocytize foregin material, blood, and dead cells

A

Macrophages or histiocytes

51
Q

Present antigens and also release cytokines, GFs, enzymes for inflammation and wound healing

A

Macrophages or histiocytes

52
Q

What is ground substance?

A

gel-like and viscous, occupies space between cells and fibers and made up of proteoglycans, glycosaminoglycans and adhesive glycoproteins

53
Q

Glycosaminoglycans (GAGs) are able to pull water due to?

A

sulfates that make them negatively charged (heparin, chondriotin, keratin, dermatan)

54
Q

What does hylauronic acid (Glycosaminoglycans) do?

A

Backbone for proteoglycans, large and lubricant–shock absorbs

55
Q

Developmental delay, corneal clouding, distinct face, hepatosplenomegaly, claw hands, autosomal recessive, accumulation of mucopolysaccharides

A

Hurler syndrome

56
Q

aggressive behavior, dev. delays, accumulation of mucopolysaccharides, X-Recessive

A

Hunter Syndrome

57
Q

What are proteoglycans?

A

(100 sulf-GAGs+ core proteins) core proteins attached to GAGs and hyaluronic acid, negatively charged and large–have various functions

58
Q

adhesive glycoprotein that has cell- ECM binding

A

Fibronectin

59
Q

Proteins involved in linking fibronectin, laminin?

A

integrins, type IV collagen, heparin and fibrin

60
Q

adhesive glycoprotein that has cell- basement membrane binding

A

laminin

61
Q

adhesive glycoprotein that modulate cell-ecm

A

Tenascin

62
Q

adhesive glycoprotein that bind to osteocytes and integrin receptor on osteoclasts

A

osteopontin

63
Q

Fibers of connective tissues

A

Collagen (I), reticular (heavily sugared Collagen III) and elastin fibers (elastin and fibrillin)

64
Q

What does collagen do?

A

Tensile strength and wound healing

65
Q

What does reticular do?

A

support system for organs

66
Q

What does elastic fibers do?

A

stretchy, capable of elastic recoil–rubber band

67
Q

What does VEGF do in angiogenesis?

A

Loosen endothelial junctions and increase vascular permeability

68
Q

What happens during angiogenesis as stalk EC and tip EC form?

A

Extracellular matrix degrade, pericyte detach, matrix-bound angiogenic molecules (MMp) release and the tip migrates due to VEGF and Notch

69
Q

Examples of pro-angiogenic mediators?

A

VEGF, bFGF, PDGF, IL-8, HGF (hepatocyte), PIGF (placental)

70
Q

How can proangiogenic factors induce angiogensis?

A

directly or indirectly (through inflammatory cells or pericytes)

71
Q

Examples of anti-angiogenic mediators?

A

Thrombospondin, interferon a/b, angiostatin, endostatin

72
Q

What is the angiogenic switch?

A

A balance of activators and inhibitors of angiogenic process that are stimulated in either direction if a certain threshold is passed

73
Q

How is angiogenic switch turned on?

A

Inflammation (deliver pro-angiogenic mediators by inflammatory cells), Hypoxia–sense of low oxygen by HIF (Hypoxia-inducible factor) and stimulation of pro-angiogenic mediator production.

74
Q

Why is angiogenic regulation important to study?

A

Health(development and wound healing), disease (therapeutic implications for disease).

75
Q

What’s the role of blood vessels in tumor?

A

for growth and metastasis

76
Q

Characteristics of blood vessels in tumor?

A

increased in number; disorganized and ‘tortuous’, extremely permeable (endothelial junctions not tight); coverage of basement membrane and pericyte is abnormal).

77
Q

Anti-angiogenic concept?

A

Starvation hypothesis: treatment with angiogenic inhibitor will allow the vessel to regress and tumour shrinks

78
Q

Strategies for anti-angiogensis therapy?

A

reduce activators (expression/production); bioavailability, signaling; or increase inhibitors (production or exogenous addtition)

79
Q

Examples of antoangiogenic agents classification?

A

VEGF blocking agents; small molecule RTKIs; Endogenous inhibitors

80
Q

Problems with anti-angiogenesis therapy?

A

High cost, modest overall survival advantage, side effects, resistance (but can target other pro-angiogenic pathways at the same time: eg pericyte and endothelial cells).

81
Q

Side effects of VEGF therapy?

A

wound healing complication, female reproductive cycle and abnormal fetal development

82
Q

Type of wounds

A

chronic (no heal in 30 days, poor nutrition, diabetes, age)
acute (surgery and trauma, heal)
Abrasion : superficial scrape of skin
Laceration: deep cut (stab)
Puncture: penetrates (nail or gunshot)
Avulsion: complete or partial tear of skin +tissue
Contusion: underlying skin becomes bad (blunt force trauma)

83
Q

Phases of repair

A

Hemostasis and inflammation; proliferation, remodeling

84
Q

Hemostasis is?

A

Platelets being activated, plug damage vessles with fibrin, and releasing alpha granules (growth factor, cytokines)

85
Q

Why is inflammatory phase important?

A

hemostasis, clear debris and foregin material, destory pathogen and stimulate subsequent healing

86
Q

What are signs of inflammation?

A

Redness (erythema) , heat (vasodilation), swelling (edema) and pain

87
Q

How is inflammation regulated?

A

pro-inflammatory mediators when pathogen or damage detected: relase cytokines, histamines, lipids, plasma proteins

88
Q

Positive effects of inflammation?

A

prevent infection, clear debris and dead cells, growth factor

89
Q

Negative effects of inflammation?

A

proteases and ROS–damage, so delayed healing and promote fibrosis

90
Q

What is involved in reepithilzation? What is required?

A

keratinocytes; proliferation, migration and differentiation (all induced by growth factors)

91
Q

What are mediators of proliferative phase?

A

growth factors

92
Q

What growth factors stimulate keratinocytes?

A

EGF, KGF, TGF-alpha

93
Q

What dissolves ECM?

A

Metalloproteinases and proteases

94
Q

After keratinocytes migrate, do they differentiate to fully functional stratified epidermis?

A

Yes. (tope) Corneal layer, granular, spinous and basal)

95
Q

Why do wounds not heal?

A

defective keratinocytes migration and insufficent angiogensis/ischemia, defective granulation and fibroblasts activity, persistent inflammation, and infection

96
Q

ulcers by uncontrolled diabetes, peripheral neurapathy

A

Diabetic foot ulcers

97
Q

Ulcer caused by not enough venous blood flow and found on lower leg between knee and ankle (commonly)

A

Venous Stasis ulcers

98
Q

ulcers caused by prolonged unrelieved pressure and around tailbone, hips, heels, and elbows

A

Pressure ulcers (decubitus ulcers/bedsores)

99
Q

Which phase does angiogenesis take place of wound healing?

A

proliferative

100
Q

hypoxia and inflammation induces pro-angiogenesis through which growth factors?

A

VEGF, PDGF, and FGF-2

101
Q

what growth factors timulate fibroblast proliferation, migration, and collagen production?

A

TGF-beta, PDGF, and FGF-2

102
Q

what does amount of scar tissue depends on?

A

ratio of matrix production to matrix degredation

103
Q

When does fibrosis happen?

A

When ECM synthesis is greater than degredartion

104
Q

What happens if TIMPs increases (tissue inibitor of metalloproteinases)

A

MMPs does not destory matrix: so, scar and fibrosis

105
Q

problems with scars?

A

70% strength of skin, psychosocial, reduce joint mobility, interfere with organ function

106
Q

excessive scar that extends beyond initial injury, hard to treat, in asians and african american

A

keloids

107
Q

Raised red scar, along orginal wound

A

hypertrophic scars

108
Q

tightening of skin that effects underlying muscles and tendens–inelastic ecm instead of normal

A

contractures

109
Q

What happens in lung fibrosis?

A

no gas exchange–death

110
Q

What disrupts balance of collagen synth and degr.?

A

inflammation–resulting in fibrosis

111
Q

liver regeneration?

A

compensatory hyperplasia

112
Q

What is in a scar tissue?

A

disorganized and Excess collagen, less strengthm loss of appendages (hair follicles), loss of function and psychosocial problems

Foundations 2 (15 decks)

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