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Foundations 2 > Wound healing > Flashcards

Wound healing Flashcards

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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
What happens when you produce less collagen?
aging, wrinkles
26
Vit. C def leads to swollen gums, bleeding, poor wound healing?
Scurvy
27
Sx: Aut dom mut. in Collagen I (two types), brittle bones, multiple factors, loose joints, hearing loss, poor teeth, blue sclera?
Osteogensis Imperfecta
28
How does blue Sclera happen?
Lack of collagen so eye lining is thin-so white part of eye is thin so you can see underlying veins --thus blue
29
heterogeneity due to defective collagen synth. of skin, joints and blood vessels
Ehlers-Danlos Syndrome
30
Sx: Hyperextensible skin, joint instability (hypermobile), easy bleeding and bruising, abnormal wound healing, vessel wall degeneration (heart valves --weak)
Ehlers-Danlos Syndrome
31
Types of Ehlers-Danlos Syndrome
Classical: Type V collagen Vascular: Type III collagen (organ rupture, valve prolapse, most severe, blood vessel wall not sturdy)
32
Describe Elastin?
insoluble, tropoelastin, little hydroxyproline no hydroxylysine
33
What links Elastin molecules?
Desmosine and isodesmosine
34
What is Fribrillin 1?
Scaffolding protein thats around elastin coded by FBN1 and binds and sequesters TGF-B
35
What is elastin fibers broken down by?
Elastase
36
What happens when you have alpha-1-antitrypsin def.?
Lungs have holes (emphysema) as bombarded with neutrophils elastase; (similar featuresalso seen in smoking
37
Mut. in FBN1 leads to?
Marfan syndrome and excess TGF-B so decreased elasticity
38
Sx: (wingspan> height) Dolichostenmelia, arachnodactyly, scoliosis, hyperflexibility, inverted sternum, pectus excavatum
Marfan syndrome
39
Sx: Eyes: ectopia lens, CV: aneurysms, aortic dissection --mitral valve prolapse and spontanrous pneumothorax
Marfan Syndrom
40
Most severe cause of death in Marfan syndrome
Mitral valve prolapse
41
What is loose connective tissue?
loosely arranged fibers, much ground subs, most abundant type; holds organs in place, allows for movement of nutrients and ions to cells
42
Example loose connective tissue?
Lamina propria: GI Tract, have immune cells, immediately below epithelial.
43
What is dense irregular connective tissue? Where is it?
few cells, irregularly arranged cells, submucosa of GIT, and reticular layer of dermis
44
What is dense regular connective tissue? where is it?
densely packed, parallel, organized fibers, few cells; tendons, ligaments, aponeuroses
45
Permanent cells of connective tissue?
Fibroblasts, myofibroblasts, macrophages, mast cells
46
Most numerous cells in connective cells? What do they do?
Fibroblasts secrete fibers, ground substance, MMPs, and GFs
47
Express alpha-smooth muscle actin contraction; necessary for secondary intention
myofibroblasts
48
Cells with granules that secrete histamine, heparin
Mast cells
49
Marked by tryptase, key cell for Type I hypersensitivity (allergy and asthma) and make and relase growth factors, cytokines and enzymes
Mast cells
50
Participate in innate and adaptive immunity, phagocytize foregin material, blood, and dead cells
Macrophages or histiocytes
51
Present antigens and also release cytokines, GFs, enzymes for inflammation and wound healing
Macrophages or histiocytes
52
What is ground substance?
gel-like and viscous, occupies space between cells and fibers and made up of proteoglycans, glycosaminoglycans and adhesive glycoproteins
53
Glycosaminoglycans (GAGs) are able to pull water due to?
sulfates that make them negatively charged (heparin, chondriotin, keratin, dermatan)
54
What does hylauronic acid (Glycosaminoglycans) do?
Backbone for proteoglycans, large and lubricant--shock absorbs
55
Developmental delay, corneal clouding, distinct face, hepatosplenomegaly, claw hands, autosomal recessive, accumulation of mucopolysaccharides
Hurler syndrome
56
aggressive behavior, dev. delays, accumulation of mucopolysaccharides, X-Recessive
Hunter Syndrome
57
What are proteoglycans?
(100 sulf-GAGs+ core proteins) core proteins attached to GAGs and hyaluronic acid, negatively charged and large--have various functions
58
adhesive glycoprotein that has cell- ECM binding
Fibronectin
59
Proteins involved in linking fibronectin, laminin?
integrins, type IV collagen, heparin and fibrin
60
adhesive glycoprotein that has cell- basement membrane binding
laminin
61
adhesive glycoprotein that modulate cell-ecm
Tenascin
62
adhesive glycoprotein that bind to osteocytes and integrin receptor on osteoclasts
osteopontin
63
Fibers of connective tissues
Collagen (I), reticular (heavily sugared Collagen III) and elastin fibers (elastin and fibrillin)
64
What does collagen do?
Tensile strength and wound healing
65
What does reticular do?
support system for organs
66
What does elastic fibers do?
stretchy, capable of elastic recoil--rubber band
67
What does VEGF do in angiogenesis?
Loosen endothelial junctions and increase vascular permeability
68
What happens during angiogenesis as stalk EC and tip EC form?
Extracellular matrix degrade, pericyte detach, matrix-bound angiogenic molecules (MMp) release and the tip migrates due to VEGF and Notch
69
Examples of pro-angiogenic mediators?
VEGF, bFGF, PDGF, IL-8, HGF (hepatocyte), PIGF (placental)
70
How can proangiogenic factors induce angiogensis?
directly or indirectly (through inflammatory cells or pericytes)
71
Examples of anti-angiogenic mediators?
Thrombospondin, interferon a/b, angiostatin, endostatin
72
What is the angiogenic switch?
A balance of activators and inhibitors of angiogenic process that are stimulated in either direction if a certain threshold is passed
73
How is angiogenic switch turned on?
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
Why is angiogenic regulation important to study?
Health(development and wound healing), disease (therapeutic implications for disease).
75
What's the role of blood vessels in tumor?
for growth and metastasis
76
Characteristics of blood vessels in tumor?
increased in number; disorganized and 'tortuous', extremely permeable (endothelial junctions not tight); coverage of basement membrane and pericyte is abnormal).
77
Anti-angiogenic concept?
Starvation hypothesis: treatment with angiogenic inhibitor will allow the vessel to regress and tumour shrinks
78
Strategies for anti-angiogensis therapy?
reduce activators (expression/production); bioavailability, signaling; or increase inhibitors (production or exogenous addtition)
79
Examples of antoangiogenic agents classification?
VEGF blocking agents; small molecule RTKIs; Endogenous inhibitors
80
Problems with anti-angiogenesis therapy?
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
Side effects of VEGF therapy?
wound healing complication, female reproductive cycle and abnormal fetal development
82
Type of wounds
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
Phases of repair
Hemostasis and inflammation; proliferation, remodeling
84
Hemostasis is?
Platelets being activated, plug damage vessles with fibrin, and releasing alpha granules (growth factor, cytokines)
85
Why is inflammatory phase important?
hemostasis, clear debris and foregin material, destory pathogen and stimulate subsequent healing
86
What are signs of inflammation?
Redness (erythema) , heat (vasodilation), swelling (edema) and pain
87
How is inflammation regulated?
pro-inflammatory mediators when pathogen or damage detected: relase cytokines, histamines, lipids, plasma proteins
88
Positive effects of inflammation?
prevent infection, clear debris and dead cells, growth factor
89
Negative effects of inflammation?
proteases and ROS--damage, so delayed healing and promote fibrosis
90
What is involved in reepithilzation? What is required?
keratinocytes; proliferation, migration and differentiation (all induced by growth factors)
91
What are mediators of proliferative phase?
growth factors
92
What growth factors stimulate keratinocytes?
EGF, KGF, TGF-alpha
93
What dissolves ECM?
Metalloproteinases and proteases
94
After keratinocytes migrate, do they differentiate to fully functional stratified epidermis?
Yes. (tope) Corneal layer, granular, spinous and basal)
95
Why do wounds not heal?
defective keratinocytes migration and insufficent angiogensis/ischemia, defective granulation and fibroblasts activity, persistent inflammation, and infection
96
ulcers by uncontrolled diabetes, peripheral neurapathy
Diabetic foot ulcers
97
Ulcer caused by not enough venous blood flow and found on lower leg between knee and ankle (commonly)
Venous Stasis ulcers
98
ulcers caused by prolonged unrelieved pressure and around tailbone, hips, heels, and elbows
Pressure ulcers (decubitus ulcers/bedsores)
99
Which phase does angiogenesis take place of wound healing?
proliferative
100
hypoxia and inflammation induces pro-angiogenesis through which growth factors?
VEGF, PDGF, and FGF-2
101
what growth factors timulate fibroblast proliferation, migration, and collagen production?
TGF-beta, PDGF, and FGF-2
102
what does amount of scar tissue depends on?
ratio of matrix production to matrix degredation
103
When does fibrosis happen?
When ECM synthesis is greater than degredartion
104
What happens if TIMPs increases (tissue inibitor of metalloproteinases)
MMPs does not destory matrix: so, scar and fibrosis
105
problems with scars?
70% strength of skin, psychosocial, reduce joint mobility, interfere with organ function
106
excessive scar that extends beyond initial injury, hard to treat, in asians and african american
keloids
107
Raised red scar, along orginal wound
hypertrophic scars
108
tightening of skin that effects underlying muscles and tendens--inelastic ecm instead of normal
contractures
109
What happens in lung fibrosis?
no gas exchange--death
110
What disrupts balance of collagen synth and degr.?
inflammation--resulting in fibrosis
111
liver regeneration?
compensatory hyperplasia
112
What is in a scar tissue?
disorganized and Excess collagen, less strengthm loss of appendages (hair follicles), loss of function and psychosocial problems

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