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002 - Pathology - (02) - Inflammation > (04) Lecture 4 > Flashcards

(04) Lecture 4 Flashcards

1
Q

(Regeneration)

1-2. What are the two requirements?

A
  1. cell population capable of proliferation (labile or stable cells)
  2. intact connective tissue framework
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2
Q

(First intention healing)

  1. are wound margins directly or improperly apposed?
  2. how fast of healing?
A
  1. directly
  2. rapid
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3
Q

(Second Intention Healing)

  1. What type of apposition and wound margins?
  2. Fibrin and later connective tissue fill defect… but what?
  3. imperfect basis for epithelizaiton
A
  1. improper
  2. angiogenesis and ECM synthesis/degradation in haphazard fashion
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4
Q

(Repair by Fibrosis - scar or diffuse organ fibrosis)

  1. Inflammation –> ?
  2. Proliferation and migration of what two cell types?
  3. angiogenesis
  4. Synthesis of what?

5 Tissue remodeling via what?

  1. wound contraction via what?
  2. wound strengthening
A
  1. removal of dead cells
  2. parenchymal cells and connective tissue cells
  3. extracellular matrix (ECM)
  4. matrix metalloproteinases
  5. myofibrocytes
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5
Q

(Angiogensis)

  1. recruitment of EC progenitor cells from what?
  2. Angiogenesis from what?
  3. 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
  1. bone marrow
  2. pre-existing vessels
  3. many mesenchymal cells (hypoxia); endothelial cells
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6
Q

(Re-epitheliazation)

  1. lateral movement of epithelial cell at margin towards what?
  2. requires what?
  3. Growth factors for epithelial cells (eg EGF)
  4. factors stimulating what?
A
  1. centerof wound
  2. underlying basement membrane
  3. differentiation
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7
Q

(ECM - extracellular matrix)

  1. principally produced by what three things?
  2. Main component of what?
  3. composed of what two things?
  4. What on the cell surface bind to fibronectin and laminin?
  5. Contains certain growth factors
A
  1. fibroblasts, chondroblasts, and osteoblasts
  2. connective tissue
  3. fibers and ground substance (form basal membranes and interstitial matrices)
  4. cell adhesion molecules (such as integrins and cadherins)
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8
Q

(ECM)

(Ground substance)

  1. composed of what?
  2. hyaluronic acid –> ?
  3. also?

(Fibers)

1-3. what three kinds of fibers?

A
  1. proteoglycans and glycosaminoglycans (GAGs)
  2. viscous gel (joints, nucleus, matrix of migrating cells)
  3. hydrated gel (heparansulfate, chondritinsulfate, etc..)
  4. collagenous (are widespread)
  5. elastic (elastin and fibrillin) (eg lungs and arteries)
  6. reticular (collagen III) scaffold in liver, bone marrow, and lymphoid tissue
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9
Q

(ECM)

  1. constant remodeling by action of what two things?

(Damage of ECM in initial injury)

2-3. due to what two things?

  1. Fibroblast proliferation controlled by what two things?
A
  1. matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMP)
  2. physical
  3. enzymatic (MMPs - from fibroblasts, neutrophils, and macrophages)

(but remember damage necessary for migration…)

  1. growth factor and cytokines (esp TGF-b)
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10
Q

(Fibroblastic Stimuli)

1-2. What are the two?

A
  1. Growth factors (PGDF, TGF-b, FGF)
  2. cellular source (platelets, macrophages, endothelial cells)
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11
Q

(Fibroblasts and ECM: TGF-b)

  1. What is the most important GF involved in inflammatory fibrosis?

(say if TGF-b increases or decreases)

  1. fibroblast migration and prolifeation
  2. synthesis of fibronectin and collagen
  3. degradation of ECM by MMPs
A
  1. TGF-B!!! (don’t forget this)
  2. increased
  3. increased
  4. decreased
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12
Q

(Granulation Tissue)

  1. the hallmark of what?

2-4. What are the three components?

A
  1. healing
  2. fibroblasts
  3. small blood vessels
  4. macrophages
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13
Q

(Granulation tissue cont)

  1. special type of what?
  2. result of what kind of inflammation?
  3. Why can it be problematic?
A
  1. connective tissue
  2. chronic due to continuing stimulation of would healing (eg due to continued mechanical irritation)
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14
Q

(granulation tissue cont)

(immature granulation tissue)

  1. numerous what?
  2. vascular sprouts in orderly or disorderly orientation?
  3. proliferating blood vessels run parallel or perpendicular to fibroblasts/collagen? which run how relative to wound to wound surface?

(Mature granulation tissue)

  1. what is it like?
A
  1. angioblasts (embryonic mesenchymal tissue from which blood cells and blood vessels arise)
  2. orderly
  3. perendicular; parallel
  4. high density of collagenous fibers with few vessels (and few inflammatory cells)
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15
Q

(Wound Contraction and Strength)

(Contraction)

  1. Are large wounds able to shrink?
  2. Facilitated by what?

(Strength)

  1. collagen synthesis > or < collagen degradation?
  2. structureal modifications in what?
A
  1. yes
  2. myofibroblasts (derived from fibroblasts, contractile features)
  3. >
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16
Q

(Organ Fibrosis)

  1. Replacement of parenchyma by what?
  2. collagen synthesis due to what? must be greater than what?
  3. increasing loss of function of organ
  4. What is primary fibrosis?
  5. secondary fibrosis?
A
  1. fibrotic stroma (multifocal or diffuse)
  2. growth hormone and cytokine exposure; collagen degradation by MMPs
  3. 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
  1. alteration: damage of tissue by injurious stimulus
  2. exudation (of blood components) - liquid and corpuscular/cellular
  3. proliferation - immigtaion and proliferation of cells and ECM
20
Q

(Inflammation)

(Necrotizing Inflammation)

(Pathogenesis)

  1. 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
  1. parenchymal organs
  2. musculature
  3. mammary gland
  4. tubular organs
22
Q

(Necrotizing INflammation)

  1. macroscopic and microscopic finding - similar to what?

(Sequela)

  1. in tubular organs?
  2. in parenchymal organs?
A
  1. necrosis
  2. removal or necrotic tissue –> ulcer
  3. scarring or sequester formation
23
Q

(Serous Inflammation)

  1. presence of what?

(Pathogenesis)

  1. relatively mild tissue and vascular injury with leakage of what from vasculature? leads to what?
  2. cell damage with what?
A
  1. exudate (colorless to slightly yellowish; serum-derived fluid)
  2. small molecular weight compounds; interstitial edema/serous effusions
24
Q

(Serous Inflammation)

  1. When does it occur?
  2. transitional (early) phase afte more injurious stimulation
  3. in periphery (spatial) after more injurious stimulation…(?)
  4. infection with what?
  5. What else?
A
  1. mild injurious stimuli (mild trauma and burns (blisters), plant and insect bites)
  2. epitheliotropic viruses (eg feline herpesvirus)
  3. hypersensitivity (anaphylaxis (type 1) and autoimmune disease of the skin (type 2))
25
Q

(Serous Inflammation)

(Where does it occur?)

  1. transepithelial leakage into body cavities lined by what?
  2. transepithelial leakage into tubular organs (+ what else?) leads to what?
  3. intraepithelial leads to what? which lead to what? which can lead to what or what?
A
  1. single layer of serosa (mesothelial cells)
  2. mucin from goblet cells; catarhal inflammation
  3. blisters; rupture; either erosion on moist surface (mucous membrane) or crust on dry surface (skin)
26
Q

(Serous Inflammation: Where does it occur?)

(Interstitial)

  1. edema
  2. what is accumulation of large quantity of clear fluid in interstitium with cavity formation?
  3. 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
  1. seroma (resembles hematoma)
27
Q

(Serous Inflammation)

(Histology)

(Acute)

  1. how’s it look?

(Chronic)

  1. what do you see?
A
  1. no unequivocal inflammatory lesions (tissue may look edematous)

002 - Pathology - (02) - Inflammation (6 decks)

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