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Care - MOD 2024 > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

What 3 factors does the healing process depend on?

A

The type of tissue damaged
The extent of the injury
Underlying host factors

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2
Q

Why do we need tissue repair?

A
  • disease - deviation or interruption of normal structure and/or function
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3
Q

Parenchymal vs Stromal

A

Parenchymal tissue refers to the functioning cells of a body part, such as a
- hepatocyte or nephron or myocyte

Stromal tissue refers to the structural cells of a body part such as
- connective tissue or the ECM.

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4
Q

What are the 3 cell types?

A

Labile, Stable, and Permanent

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5
Q

Where do I find labile cells? What are they?

A

They are cells that continually reproduce/divide. They are often found in epithelial tissue, such as the skin, oropharynx, bone marrow and GI/GU tract.

  • hair, skin, mucosal membrane cells
  • bone marrow cells
  • epithelial cells - skin, oropharynx, GI and GU tract
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6
Q

Where do I find stable cells? What are they?

A

Stable cells normally stop dividing once growth ceases, but can regenerate.
- Usually found as hepatocytes or smooth muscle cells.
- walls of blood or gut vessels
- osteoblasts
They require a stromal framework for regeneration.

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7
Q

Where do I find permanent (fixed) cells? What are they?

A

Fixed cells that rarely regenerate or divide.
- Examples include neurons, heart, skeletal muscle cells, and RBCs.
- ocular lens

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8
Q

What is the ECM?

A

material secreted by cells through the body
surrounds and supports cells

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9
Q

What 4 categories make up the ECM - extracellular matrix?

A

Fibrous Structural Proteins
Water-hydrated gels
Adhesive glycoproteins
ground substance

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10
Q

What are the fibrous structural proteins of the ECM?

A

Collagen and elastin

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11
Q

What are the water-hydrated gels of the ECM?

A

Hyaluronan and proteoglycans

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12
Q

What are the adhesive glycoproteins of the ECM?

A

Fibronectin and laminin

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13
Q

What is ground substance?

A

It refers to the ECM except for fibrous proteins.

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14
Q

What is a basement membrane?

A

It is the underlying epithelial, endothelial, and smooth muscle cells;

separating the lining from the connective tissue.
- must be present before re-epithelialization can occur

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15
Q

What is the interstitial matrix?

A

It is the gel-like substance found between cells.

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16
Q

What are integrins and what are they used for?

A

They are integral/transmembrane proteins that allow for
- attachment to the ECM
- communication between the intracellular and extracellular environment.

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17
Q

What is granulation tissue?

A

It is the precursor to scar tissue.

It develops when there is a wound that can’t be resolved with regeneration alone.
- It is a highly vascularized tissue that is typically reddish, moist, soft, bumpy, and granular in appearance. It is very fragile and bleeds easily.
- new capillaries (angiogenesis), proliferating fibroblasts, and residual inflammatory cells

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18
Q

What is angiogenesis and what triggers it?

A

It is the generation of new blood vessels from existing blood vessels, triggered by the release of VEGF (vascular endothelial growth factor) from hypoxic cells.

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19
Q

What are the 4 steps of angiogenesis?

A
  1. Proteolytic degradation of parent vessel basement membrane by VEGF, leading to a capillary sprout.
  2. Migration of endothelial cells from parent vessel towards an angiogenic stimulus.
  3. Proliferation of endothelial behind the leading edge of migrating cells.
  4. Maturation of endothelial cells and vessel walls.
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20
Q

What are examples of conditions that cause angiogenesis?

A

Damaged or disrupted tissue
Cancerous lesions
Diabetic Retinopathy –> proliferation of too many new blood vessels can block normal transmission of light signals to retina which can cause vision quality loss

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21
Q

What makes scar tissue?

A

Fibroblasts

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22
Q

What does scar formation build on?

A

granulation tissue framework of new vessels and loose ECM

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23
Q

How does scar tissue initially form?

A

builds on granulation tissue framework of new vessels and loose ECM

fibroblasts emigrate to the area of injury and proliferate (Fibronectin, collagen, hyaluronan, and proteoglycans)
- ECM components as granulation tissue transitions to scar tissue

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24
Q

What are the initial ECM components secreted by fibroblasts?

A

Fibronectin, collagen, hyaluronan, and proteoglycans

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25
Q

What happens to scar tissue over time as it is constructed?

A

Increased collagen synthesis, diminished fibroblast proliferation, and diminishing new blood vessels.

vascular granulation tissue transitions to dense collagen fiber matrix
- usually pale due to loss of vascularization

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26
Q

When and why will angiogenesis regress?

A

over weeks-months as the tissue repair process resolves and extra blood flow is no longer needed

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27
Q

What mediators regulate the healing process?

A

ILs, IFNs, prostaglandins, and leukotrienes
- promote chemotaxis and leukocytes and fibroblasts, along with mediating the inflammatory response.

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28
Q

What are the 4 growth factors?

A

Vascular Endothelial Growth Factor (VEGF)
Platelet-Derived Growth Factor (PDGF)
Fibroblast Growth Factor (FGF)
Epithelial Growth Factor (EGF)

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29
Q

What are the effects of growth factors?

A
  • Mediate proliferation, differentiation, cell metabolism,
  • inflammatory response.
  • Promote chemotaxis of leukocytes and fibroblasts
  • Stimulate angiogenesis
  • Contribute to the generation of ECM
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30
Q

What are the stages of Healing and Tissue Repair?

A

Hemostasis: clotting and vascular response
Inflammation
Proliferation: Epithelial healing, contraction, and scar formation.
Remodeling: Scar remodeling

  • removal of debris –> restoration of structural integrity –> restoration of functional integrity –> remodeling of healed tissue
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31
Q

length of each stage of healing is significantly impacted on what ____?

A

What intention a wound is healing by

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32
Q

What are the 3 types of wound intention?

A

Primary: small, incision-like wounds with well-approximated edges that can be sutured easily. (narrow)

Secondary: large, crater-like wounds with greater loss of tissue. (necrotic areas, heart attack/stroke)

Tertiary: large wounds that are intentionally left open to drain or are infected and are then sutured at a later date. (contaminated wounds)

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33
Q

What are the stages of wound repair?

A

1.) inflammation and homeostasis
2.) removal of debris
3.) restoring structural integrity
— re-epitheliazation of wound
4.) restoring functional integrity
5.) remodeling

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34
Q

Describe the process of hemostasis

A
  1. Initial blood vessel constriction at the site (transient vasoconstriction)
  2. Increased platelet aggregation and attraction
  3. Thrombus forms to promote hemostasis and prevent entry of foreign agents.
  4. Following the blockage of the vessel injury, dilation and increased capillary membrane permeability can then occur.

Leukocytes neutralize foreign bodies and pathogens introduced into the tissue at the site of injury.

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35
Q

What removes debris?

A

Neutrophils and Macrophages
They remove foreign matter, extracellular debris, damaged fibrin, and cell fragments.

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36
Q

What additional things do macrophages do over neutrophils?

A

Macrophages also release growth factors to stimulate cell growth, attract fibroblasts, and help with angiogenesis.

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37
Q

When does proliferation in wound healing begin occurring?

A

Within 2 days (can last for weeks)

38
Q

What is the early form of the ECM called during proliferation?

A

Provisional matrix

39
Q

What is the purpose of provisional matrix?

A

Attracting and supporting fibroblasts, endothelial cells, and epidermal cells.
Provides the materials to start granulation tissue construction.

40
Q

How soon can granulation tissue begin forming?

A

Within 24 hours.

41
Q

What begins forming granulation tissue?

A

Fibrolasts begin secreting collagen and other components, as well as releasing growth factors to encourage the healing process.

42
Q

over time, granulation tissue regresses, leaving a framework for final product of repair called

A

re-epithelialization - new epithelial barriers form between wound and external environment

43
Q

What is the primary aim for restoring functional integrity

A

restore the functional integrity of parenchymal tissues

44
Q

What are the 3 healing outcomes of restoring functional integrity?

A

Resolution, Regeneration, and Replacement

45
Q

What kind of injury and cell types are seen in resolution?

A

very mild injury with minimal disruption (paper cut or biting tongue)
- rapid healing, minimal to no scarring

Labile cells –> quick to regenerate

46
Q

What kind of injury is seen in replacement?

A

production of scar tissue when regeneration is not possible
- seen with injuries to permanent cells, extensive or major injuries

47
Q

What cell types are seen in regeneration?

A

Labile or stable cell types. They can differentiate, proliferate, and do diapedesis (migrate)

48
Q

How soon can remodeling begin in uncomplicated wounds?

A

3 weeks - 6 months

49
Q

What will happen to remodeling time if injury or cut is on a cleavage line?

A

the body will heal faster and won’t have to do as much remodeling

50
Q

What occurs during remodeling?

A

continued remodeling of scar tissue
1. Collagenase enzymes remove collagen
2. Fibroblasts lay down new collagen
3. Reorientation of scar architecture to surrounding tissue to maximize tensile strength of wound.

51
Q

most wound do not regain …

A

full tensile strength of unwounded skin

52
Q

How much strength does a sutured wound have? After its removed?

A

70% once closed, 10% once removed.

53
Q

What is the most tensile strength wounds have after 3-6 months?

A

70-80%

54
Q

Why is secondary contraction common in large wounds?

A

Wounds often undergo contraction while in the remodeling phase if they are in an area that constantly stretches, such as at the base of the neck
- scar tissue is often smaller. than original wound
- can cause limited mobility and deformities

55
Q

What are all the complications that can occur during wound healing?

A

Ulcerations
Dehiscence
Keloids
Hypertrophic Scars
Adhesions
Proud Flesh

56
Q

What is an ulceration and what makes it hard to heal?

A

It is an open, crater-like lesion of skin or mucous membranes. Common to have necrotic epithelium with subepithelial inflammation.

It is difficult to heal because of poor perfusion and blood flow to that area, the patient’s limited inflammatory or immune response, and frequent colonization by microbes.

  • seen in diabetes or BR pts
57
Q

What is a dehiscence and what are the early/late causes of its formation?

A

It is a deficient scar formation, usually caused by a wound bursting at the site of injury before scarring finishes.
- decreased collagen formation

Early causes include mechanical stress (after suture removal)
- Later causes include deficient ECM or collagen formation, such as someone with Ehlers-Danlos Syndrome.

58
Q

What is a keloid and its risk factors?

A

Excessive collagen production at the site of injury which often exceeds margins of wound

Risk factors include darker pigmented skin, age 10-30, and family history of keloids.

59
Q

What is a hypertrophic scar?

A

Excessive collagen production at site of injury that stays within the margins of the wound.
- typically stays within wound margins (straight line)

60
Q

What can be used as a treatment for keloids?

A

corticosteroids to inhibit scar tissue

61
Q

What are adhesions and where are they normally found?

A

Inappropriate fibrous connections between injury and nearby tissues.

Commonly inhibits the movement of surrounding tissues.

Most commonly occurs in intra-abdominal surgeries.

62
Q

Why are adhesions difficult to treat?

A

Excision of an adhesion typically causes more scarring.

63
Q

What is proud flesh and how is it treated?

A

It is the excess production of granulation tissue and extends beyond the anatomical edges of the wound.

Prevents normal healing such as re-epithelialization from taking place

Treated with surgical removal and/or chemical cauterization.

64
Q

What factors affect wound healing?

A

Malnutrition
blood flow/oxygenation
immune/inflammatory response
infection
foreign bodies
age.

65
Q

6 important factors needed to prevent malnutrition

A

proteins - needed for mediation of inflammatory phase, fibroblast, proliferation, collagen synthesis, angiogenesis, and remodeling

Carbohydrates - needed for energy for WBCs and reduce use of proteins for energy

fats - needed for synthesis of new cells

vitamin C - needed for collagen synthesis (scar remodeling is an active process)

Vitamin A - needed for epithelialization, capillary formation, collagen synthesis (can also reduce anti-inflammatory effects of corticosteroids)

Zinc - needed for enzymes responsible for cell proliferation

66
Q

What does a deficiency in Vitamin C cause?

A

Collagen synthesis impairment.

67
Q

What does a deficiency in Vitamin A cause?

A

Epithelialization, capillary formation, and collagen synthesis impairment.

Can reduce the anti-inflammatory effects of corticosteroids.

68
Q

What does a deficiency in zinc cause?

A

It is required for the enzyme used in cell proliferation.

69
Q

What does a protein deficiency cause for inflammation?

A

Needed for the mediation of the inflammatory phase, fibroblast proliferation, collagen synthesis, angiogenesis, and remodeling.

70
Q

Why is blood important in healing?

A

supplies nutrients and cells to injury and removes waste products, toxins and pathogens

71
Q

Why is oxygen important in healing?

A

It is required for collagen synthesis and intracellular destruction of organisms by phagocytes (oxidation)

72
Q

What is the purpose of hyperbaric oxygen?

A

Hyperbaric oxygen is high pressure oxygen that is thought to improve the partial pressure of oxygen in the blood/plasma/tissue and improve the healing process.

73
Q

What conditions can impair inflammation/immune response?

A

Impaired perfusion to injury site
Impaired phagocytic function
Diabetes Mellitus
Corticosteroid Administration

74
Q

What is the effect of DM on inflammation?

A

Diminishes chemotaxis and phagocytosis
Impairs perfusion due to microvascular disease

  • limits WBC movement into the injured area
75
Q

What is the effect of Corticosteroids on inflammation and the immune response?

A

Decreased immune mediator production (via arachidonic pathway)
Decreased capillary permeability (limits vascular response)
Impaired phagocytosis
Inhibited fibroblast proliferation and function

76
Q

How do foreign bodies inhibit the healing process?

A

They prolong the inflammatory phase
They impair granulation tissue formation
They inhibit the proliferation of fibroblasts and deposition of collagen fibers
Contribute to pathogen invasion via becoming a reservoir and mechanical barrier to wound closure.

77
Q

Why are children bad at healing?

A

They have a greater capacity for healing but greater metabolic demands and may lack reserves for proper tissue repair

They also have an immature immune system and therefore a prolonged immune response.

78
Q

Why are old people bad at healing?

A

The elderly have decreased dermal thickness, collagen content in their skin, and elasticity of skin.

They produce less fibroblasts and less collagen.
They take longer to re-epithelialize their wounds and are more vulnerable to slower wound healing and chronic wounds.

79
Q

compare and contrast acute vs. chronic inflammation

A
80
Q

What are the two most common causes for chronic inflammation?

A

Persistent injury/infection (Ulcerations, pathogens, and foreign bodies)

Autoimmune conditions (RA, MS, systemic lupus erythematosus)

81
Q

What are ALL of the manifestations of chronic inflammation?

A

5 cardinal signs

systemic manifestations
-Fever
-malaise
-fatigue/weakness
-anemia (decreased RBCs)
-anorexia and weight loss

remission - diminished to absent symptoms

82
Q

What are the systemic manifestations of chronic inflammation?

A

Fever
malaise
fatigue/weakness
anemia (decreased RBCs)
anorexia and weight loss

83
Q

What causes anemia in chronic inflammation?

A

Prolonged inflammation –> increases Ferritin (body thinks iron increased because Ferritin increased so it stops producing iron) –> IL-6 production, which goes to the liver and makes more hepcidin, which reduces iron in the body by blocking and promoting breakdown of ferroportin

Ferroportin is an iron exporter, so reduced iron leads to reduced RBC formation (anemia)

84
Q

What inhibits the release of erythropoietin?

A

Il-1, TNF-alpha, and IFN-gamma
- they augment RBC phagocytosis

85
Q

Why do cancer cells proliferate? (cancer and inflammation)

A

They are classified as abnormal/damaged by the body and cause go into cellular distress.
- tumor cells have abnormal markers and often outgrow local supply of nutrients leading to cell distress and ischemia

They then release cytokines and cause angiogenesis and nutrients to come to them.

The release of more growth factors allow the cancer cells to expand and proliferate.

Proteases and remodeling of ECM can enhance the ability of tumor cells to grow and spread

86
Q

non-specific chronic inflammation

A

diffuse accumulation of macrophages and lymphocytes at site of injury –> release inflammatory mediators –> recruit new WBCs/fibroblasts
- cytokines produced by underlying cause lead to persistent chemotaxis of leukocytes and fibroblasts
- significant scar tissue formation - often replaces normal stromal and parenchymal tissues (ex: in pts with chronic damage to kidneys who have problems with HTN/DM)

loss of normal structure and function of tissue

87
Q

What is granulamatous inflammation?

A

They are nodular inflammatory lesions that encase substances not easily destroyed by usual inflammatory and immune responses (creates walls around it)
- foreign bodies
- pathogens

macrophages adapt to address insult
- giant cells
- epithelioid cells

Fibrous tissue eventually surrounds and encapsulates inflamed area
- macrophages phagocytize harmful substances within the granuloma, filling it with necrotic remains

88
Q

What commonly causes granulamatous inflammation?

A

Retained foreign bodies and certain bacterias, such as M. tub, syphilis, and fungal infections.

89
Q

Examples of foreign bodies

A

splinters, sutures, silica, and asbestos

90
Q

Examples of pathogens

A

mycobacterium tuberculosis (TB), syphilis, deep fungal injections

91
Q

Examples of giant cells

A

multinucleated, coalesced macrophages - surround large particles

92
Q

Examples of epithelioid cells

A

surround and contain offending agent and macrophages processing it

Care - MOD 2024 (16 decks)

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