(04) Lecture 4 Flashcards
1
Q
(Regeneration)
1-2. What are the two requirements?
A
- cell population capable of proliferation (labile or stable cells)
- intact connective tissue framework
2
Q
(First intention healing)
- are wound margins directly or improperly apposed?
- how fast of healing?
A
- directly
- rapid
3
Q
(Second Intention Healing)
- What type of apposition and wound margins?
- Fibrin and later connective tissue fill defect… but what?
- imperfect basis for epithelizaiton
A
- improper
- angiogenesis and ECM synthesis/degradation in haphazard fashion
4
Q
(Repair by Fibrosis - scar or diffuse organ fibrosis)
- Inflammation –> ?
- Proliferation and migration of what two cell types?
- angiogenesis
- Synthesis of what?
5 Tissue remodeling via what?
- wound contraction via what?
- wound strengthening
A
- removal of dead cells
- parenchymal cells and connective tissue cells
- extracellular matrix (ECM)
- matrix metalloproteinases
- myofibrocytes
5
Q
(Angiogensis)
- recruitment of EC progenitor cells from what?
- Angiogenesis from what?
- VEGF - VEGF-R signalling… VEGF produced by what (triggered by what)? VEGF-R produced by what?
NEW VESSELS ARE LEAKY - NEW VESSELS NEED STABILIZATION
A
- bone marrow
- pre-existing vessels
- many mesenchymal cells (hypoxia); endothelial cells
6
Q
(Re-epitheliazation)
- lateral movement of epithelial cell at margin towards what?
- requires what?
- Growth factors for epithelial cells (eg EGF)
- factors stimulating what?
A
- centerof wound
- underlying basement membrane
- differentiation
7
Q
(ECM - extracellular matrix)
- principally produced by what three things?
- Main component of what?
- composed of what two things?
- What on the cell surface bind to fibronectin and laminin?
- Contains certain growth factors
A
- fibroblasts, chondroblasts, and osteoblasts
- connective tissue
- fibers and ground substance (form basal membranes and interstitial matrices)
- cell adhesion molecules (such as integrins and cadherins)
8
Q
(ECM)
(Ground substance)
- composed of what?
- hyaluronic acid –> ?
- also?
(Fibers)
1-3. what three kinds of fibers?
A
- proteoglycans and glycosaminoglycans (GAGs)
- viscous gel (joints, nucleus, matrix of migrating cells)
- hydrated gel (heparansulfate, chondritinsulfate, etc..)
- collagenous (are widespread)
- elastic (elastin and fibrillin) (eg lungs and arteries)
- reticular (collagen III) scaffold in liver, bone marrow, and lymphoid tissue
9
Q
(ECM)
- constant remodeling by action of what two things?
(Damage of ECM in initial injury)
2-3. due to what two things?
- Fibroblast proliferation controlled by what two things?
A
- matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMP)
- physical
- enzymatic (MMPs - from fibroblasts, neutrophils, and macrophages)
(but remember damage necessary for migration…)
- growth factor and cytokines (esp TGF-b)
10
Q
(Fibroblastic Stimuli)
1-2. What are the two?
A
- Growth factors (PGDF, TGF-b, FGF)
- cellular source (platelets, macrophages, endothelial cells)
11
Q
(Fibroblasts and ECM: TGF-b)
- What is the most important GF involved in inflammatory fibrosis?
(say if TGF-b increases or decreases)
- fibroblast migration and prolifeation
- synthesis of fibronectin and collagen
- degradation of ECM by MMPs
A
- TGF-B!!! (don’t forget this)
- increased
- increased
- decreased
12
Q
(Granulation Tissue)
- the hallmark of what?
2-4. What are the three components?
A
- healing
- fibroblasts
- small blood vessels
- macrophages
13
Q
(Granulation tissue cont)
- special type of what?
- result of what kind of inflammation?
- Why can it be problematic?
A
- connective tissue
- chronic due to continuing stimulation of would healing (eg due to continued mechanical irritation)
14
Q
(granulation tissue cont)
(immature granulation tissue)
- numerous what?
- vascular sprouts in orderly or disorderly orientation?
- proliferating blood vessels run parallel or perpendicular to fibroblasts/collagen? which run how relative to wound to wound surface?
(Mature granulation tissue)
- what is it like?
A
- angioblasts (embryonic mesenchymal tissue from which blood cells and blood vessels arise)
- orderly
- perendicular; parallel
- high density of collagenous fibers with few vessels (and few inflammatory cells)
15
Q
(Wound Contraction and Strength)
(Contraction)
- Are large wounds able to shrink?
- Facilitated by what?
(Strength)
- collagen synthesis > or < collagen degradation?
- structureal modifications in what?
A
- yes
- myofibroblasts (derived from fibroblasts, contractile features)
- >
16
Q
(Organ Fibrosis)
- Replacement of parenchyma by what?
- collagen synthesis due to what? must be greater than what?
- increasing loss of function of organ
- What is primary fibrosis?
- secondary fibrosis?
A
- fibrotic stroma (multifocal or diffuse)
- growth hormone and cytokine exposure; collagen degradation by MMPs
- without a known cause of injury (possibly genetic)
17
Q
make sure you look at his summary slides
A
18
Q
A
19
Q
(Inflammation)
(3 morphologically defined phases - with markedly variable expression)
1-3. What are they?
A
- alteration: damage of tissue by injurious stimulus
- exudation (of blood components) - liquid and corpuscular/cellular
- proliferation - immigtaion and proliferation of cells and ECM
20
Q
(Inflammation)
(Necrotizing Inflammation)
(Pathogenesis)
- massive and rapid tissue damage of tissue including vessels (inflammation is secondary)
2-4. What can cause this?
A
21
Q
(Necrotizing Inflammation)
1-4. where does it occur?
A
- parenchymal organs
- musculature
- mammary gland
- tubular organs
22
Q
(Necrotizing INflammation)
- macroscopic and microscopic finding - similar to what?
(Sequela)
- in tubular organs?
- in parenchymal organs?
A
- necrosis
- removal or necrotic tissue –> ulcer
- scarring or sequester formation
23
Q
(Serous Inflammation)
- presence of what?
(Pathogenesis)
- relatively mild tissue and vascular injury with leakage of what from vasculature? leads to what?
- cell damage with what?
A
- exudate (colorless to slightly yellowish; serum-derived fluid)
- small molecular weight compounds; interstitial edema/serous effusions
24
Q
(Serous Inflammation)
- When does it occur?
- transitional (early) phase afte more injurious stimulation
- in periphery (spatial) after more injurious stimulation…(?)
- infection with what?
- What else?
A
- mild injurious stimuli (mild trauma and burns (blisters), plant and insect bites)
- epitheliotropic viruses (eg feline herpesvirus)
- hypersensitivity (anaphylaxis (type 1) and autoimmune disease of the skin (type 2))
25
Q
(Serous Inflammation)
(Where does it occur?)
- transepithelial leakage into body cavities lined by what?
- transepithelial leakage into tubular organs (+ what else?) leads to what?
- intraepithelial leads to what? which lead to what? which can lead to what or what?
A
- single layer of serosa (mesothelial cells)
- mucin from goblet cells; catarhal inflammation
- blisters; rupture; either erosion on moist surface (mucous membrane) or crust on dry surface (skin)
26
Q
(Serous Inflammation: Where does it occur?)
(Interstitial)
- edema
- what is accumulation of large quantity of clear fluid in interstitium with cavity formation?
- Prolonged fluid accumulation in interstitium: fibrocyte stimulation –> fibroblast –> deposition of intracellular matrix (fibrosis/sclerosis/induration)
fuck it - what shitty notes… just read this slide
A
- seroma (resembles hematoma)
27
Q
(Serous Inflammation)
(Histology)
(Acute)
- how’s it look?
(Chronic)
- what do you see?
A
- no unequivocal inflammatory lesions (tissue may look edematous)
