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Foundations of Disease > Exam 1: Healing and Repair > Flashcards

Exam 1: Healing and Repair Flashcards

1
Q

Goal of Healing

A
  • Restore tissue architecture and function
    • Repair parenchymal tissues
    • Heal the surface
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2
Q

Repair Processes

A
  1. Regeneration
    • Cells that survive injury proliferate
      • Sometimes added by stem cells
    • Need cells that can proliferate
    • Need intact stroma & basement membrane
    • More normal/functional result
  2. Scar formation ⇒ CT deposition
    • Occurs if
      • Tissue incapable of complete restitution
      • Supporting structures severely damanged
    • Not normal but can provide enough stability to allow some function
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3
Q

Proliferative Capacity

A

3 groups:

  1. Labile cells
  2. Stable cells
  3. Permanent cells
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4
Q

Labile Cells

A
  • Continuously dividing tissues
  • Multiply throughout life
  • Can regenerate as long as stem cells preserved
  • Ex:
    • Epithelial surface cells
    • Lymphoid/hematopoietic cells
    • Epithelium of GI/GU tract
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5
Q

Stable Cells

A

“Quiescent cells”

  • Latent capacity to regenerate
  • Includes:
    • Parenchymal cells of kidney, liver, pancreas
    • Fibroblasts
    • Smooth muscle
    • Endothelial cells
    • Lymphocytes
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6
Q

Permanent Cells

A
  • Non-dividing tissues
  • Do not divide enough to regnerate
  • Includes:
    • Neurons
    • Cardiac muscle
    • Skeletal muscle
      • Satellite cells can help
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7
Q

Cell Proliferation

A

Driven by many growth factors:

  • Activated macrophages most important source
  • Cells use integrins to bind ECM proteins
    • Activate signaling pathways
    • Induce protein production ⇒ drives cell through cell cycle
    • Release blocks on cell cycle
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8
Q

Tissue Regeneration

Labile Cells

A
  • Tissue stem cells normal quiescent until needed
    • Due to soluble factors, cell-cell, and cell-ECM interactions
  • Most are not totipotent
    • Limited types of differentiated cells they can generate
  • Injury stimulates cells to divide and differentiate
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9
Q

Tissue Regeneration

Stable Cells

A

Ex. Liver:

  • Loss of liver tissue from infection, injury, surgery
  • Can adequately regenerate even if 90% is lost
  • Phases:
    1. Priming phase
      • Kuppfer cells make cytokines
      • Makes hepatocytes competent to receive & respond to growth factors
    2. Growth factor phase
      • Growth factors drive primed hepatocytes into cell cycle
      • Then non-parenchymal cells proliferate
        • Endothelial, Kuppfer, Stellate
    3. Termination Phase
      • Heptocytes exit cell cycle & return to quiescence
  • Progenitor cells can also be activated
    • Found in Canals of Hering
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10
Q

Scar Formation

Causes

A
  • Regeneration not enough for repair
    • Severe or chronic tissue injury
    • Damage to parenchymal cells, epithelial, CT frame
  • Injury of non-dividing cells
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11
Q

Scar Formation

Process

A
  • 3 key steps:
    1. Angiogenesis
    2. Deposition of CT ⇒ formation of granulation tissue
    3. Remodeling of CT
  • Macrophages important
    • Clear microbes/dead tissue
    • Provide growth factors
    • Secrete cytokines
  • Repair begins within 24 hours of injury
  • See granulation tissue in 3-5 days
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12
Q

Scar Formation

Timeline

A
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13
Q

Scar Formation

Area Preparation

A
  1. Immune system removes offending agent and inflammatory exudate
  2. Lysosomal enzymes liquefy debris
  3. Inflammatory response ends
  4. Fibroblasts recruited to begin remodeling
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14
Q

Scar Formation

Angiogenesis

A

Formation of blood vessels:

  1. Changes in hemodynamics
    • NO ⇒ vasodilation
    • Vascular endothelial growth factor (VEGF) ⇒ ↑ vascular permeability / promote angiogenesis
      • Contributes to edema in healing wounds
  2. Pericytes seperate from adluminal surface
    • Breaks down basement membrane
    • Allows formation of vessel sprout
  3. Endothelial cells
    • Migrate towards injury
    • Proliferate behind leading front (“tip”) of migrating cells
    • Remodel into capillary beds
  4. Periendothelial cells recruited to form mature vessels
    • Pericytes for capillaries
    • Smooth muscle cells for larger vessels
  5. Endothelial proliferation & migration suppressed
  6. Basement membrane deposited
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15
Q

Scar Formation

Granulation Tissue Formation

A
  • Highly vascularized CT composed of:
    • New capillaries
    • Infiltrating and proliferating fibroblasts
      • Produces loose CT
  • Pink/red and granular in gross appaerance
  • Occupies tissue defect until scar can mature
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16
Q

Scar Formation

Collagen Deposition

A
  • Two steps:
    • Fibroblasts migrate and proliferate into site of injury
    • Fibroblasts produce and deposit ECM proteins
  • Controlled by local cytokines
    • Mostly from M2 macrophages
      • TCF-β most important
  • Further ECM deposition ⇒ more distance between capillaries and fibroblasts
    • Less erythema
  • Some fibroblasts become myofibroblasts
17
Q

Scar Formation

CT Remodeling

A
  • Need balance between synthesis and degradation of ECM proteins
  • Done through remodeling
  • Matrix Metalloproteinases (MMPs)
    • Degrade collagen and other ECM components
      • Collagenases, gelatinases, stromelysins
    • Produced by many cell types
    • Must be activated by proteases at site of injury
    • Inhibited by specific Tissue Inhibitors of Matalloproteinases (TIMPs) made by mesenchymal cells
18
Q

Healing

Influencing Factors

A
  1. Infection
    • Prolongs inflammation & ↑ local injury ⇒ delays healing
  2. DM
  3. Glucocorticoids
    • Anti-inflammatory
    • ⊗ TGF-β production ⇒ weakens scar, ↓ fibrosis
  4. Nutritional status
    • Especially protein & Vit C deficiency
  5. Mechanical factors
    • ↑ local pressure or torsion ⇒ dehiscence
  6. Perfusion
    • Arteriosclerosis, DM
    • Obstructed venous drainage e.g. varicose veins
  7. Foreign body
  8. Tissue type
    • Only stable and labile cells capable of restoration
  9. Extent of injury
    • Need intact parenchyma/BM/stem cells
  10. Location of injury
    • Inflammation in tissue spaces ⇒ extensive exudates
      • Pleural, peritoneal, synovial
    • Exudates must be digested/reabsorbed by leukocytes
    • Can restore as long as there is not cellular necrosis
    • Large exudate can organize ⇒ granulation ⇒ scar
19
Q

Collagen Deposition

Effects of Nutrition

A
  • Type III collagen deposited initially in granulation tissue
  • Type III replaced by Type I collagen
    • Hydroxylation of lysine and proline needed to crosslink
      • Vit C required
      • Cu2+ is a co-factor for lysyl hydroxylase
    • Collagenase required for transition from Type III ⇒ Type I
      • Zn2+ is a co-factor
20
Q

First Intention Healing

Overview

A
  • Occurs through primary union
  • Wound edges are apposed
  • Primary mech ⇒ epithelial regeneration
    • Limited # of dead cells
    • Only minor discontinuites in BM
21
Q

First Intention Healing

Process

A
  • Day 1
    • Formation of fibrin clot ⇒ coagulation
    • Neutrophils arrive within 24 hours
  • Day 2
    • Epithelial cells from both edges migrate and proliferate along edges
    • Deposition of BM components
    • Thin epithelial layer closes the wound
  • Day 3
    • Neutrophils replaced by macrophages
      • Wound debrided
    • Fibroblasts arrive
      • Start collagen production
    • Epidermis covering wound now near normal thickness
  • Day 5
    • Peak of neovascularization
    • Granulation tissue filling incisional space
    • New vessels are leaky
  • Week 2
    • Fibroblast proliferation and collagen deposition continues
    • See fewer neutrophils, vessels, and edema
  • End of 1st month
    • Scar is cellular CT
    • Nearly no inflammatory cells
    • Covered by nearly normal epidermis
    • Dermal appendages in line of incision are lost
22
Q

Second Intention Healing

A
  • Occurs when wound edges are not in contact ⇒ tissue lost
  • Repair through a combo of regeneration and scarring
  • Characteristics
    • Slower
    • Larger fibrin clot
    • More exudate and necrotic debris
    • More intense inflammatory reaction
    • More granulation tissue
    • Accumulation of ECM and larger scar
    • Wound contraction can occur due to myofibroblasts
      • ↓ size of large skin defects to 5-10% of original by 6 weeks
    • More complications
23
Q

Wound Strength

A
  • 7 days s/p wound
    • 10% tensile strength
    • Low collagen content
  • 60-70 days s/p wound
    • 30% tensile strength
    • 100% collagen content
    • High ratio of Type III : Type I collagen
  • 3 months s/p wound
    • 70-80% tensile strength
    • 100% collagen content w/ remodeling and turnover
    • Inc. Type I : type III collagen ⇒ 85% of normal skin Type I
  • Never reaches 100% of tensile strength
24
Q

Fibrosis

Overview

A

Abnormal deposition of collagen in internal organs due to chronic disease.

  • Caused by persistent injurious stimuli
    • Chronic infections and/or immunological reactions ⇒ loss of tissue ⇒ attempt at repair
  • Develops in space occupied by inflammatory exudate
    • Ex. Organizing pneumonia
  • Results in organ dysfunction and/or organ failure
  • TGF-β ⇒ major cytokine involved
    • Collagen made by myofibroblasts in lung & kidney
    • Collagen made by stellate cells in liver
25
Q

Fibrosis

Examples

A
  • Cirrhosis of the liver
  • Systemic schlerosis (schleroderma)
  • Fibrosing disease of the lungs
  • End-stage kidney disease
  • Constrictive pericarditis
26
Q

Inadequate granulation tissue or scar formation can lead to…

A

wound dehiscence or ulceration

27
Q

Wound Dehiscence

A

“Rupture”

  • Most often seen with abdominal surgery
  • Due to increased abdominal pressure from vomiting or coughing
  • Creates mechanical stress on the wound
28
Q

Wound Ulceration

A
  • Due to inadequate vascularization during healing
  • Ex.
    • Ulceration in leg wounds with atherosclerotic peripheral vascular disease
    • Areas devoid of sensation in neuropathic ulcers
29
Q

Hypertrophic scars

A
  • Forms due to accumulation of excess collagen
  • Ex. thermal or traumatic injury
    • Involves deep layers of dermis
30
Q

Keloid

A
  • Scar tissue grows beyond boundaries of original wound without regression
  • Individuals can be predisposed
    • More common in African Americans
31
Q

Exuberant Granulation

A
  • Tissue protrudes above level of surrounding skin
  • Blocks re-epithelialization
  • Called ‘Proud Flesh”
  • May need to remove with cautery or surgical excision
32
Q

Desmoid

A

“Aggressive Fibromatosis”

  • Proliferation of fibroblasts
  • Can be neoplastic
33
Q

Wound Contraction

A
  • Part of normal healing
  • If exaggerated ⇒ see contractures and deformities of wound and surrounding tissues
  • Prone to develop on palms, soles, anterior thorax
  • Common after serious burns
    • Can compromise joint movement

Foundations of Disease (46 decks)

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