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Pathology 1 > Cellular growth/differentiation & Regeneration and Repair > Flashcards

Cellular growth/differentiation & Regeneration and Repair Flashcards

1
Q

Anaplasia

A

total loss of differentiation as might occasionally be seen in malignant neoplasms
More than just an increased N/C ratio, the nucleus

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2
Q

Congenital / Developmental Change: Hypoplasia and Agenesis

A
  • Hypoplasia – defective formation or incomplete development of a part
  • Agenesis – absence/failure of formation
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3
Q

Pathological definition of Repair

A

deposition of collagen and other extracellular matrix components, causing the formation of scar
• “patches rather than restores”

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4
Q

Pathological definition of Regeneration

A

proliferation of cells and tissues to replace lost structures
• restores

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5
Q

What are the 5 overlapping processes involved in tissue repair.

A
  • Hemostasis – Plts, coagulation
  • Inflammation – PMNs, macrophages, lymphocytes, mast cells
  • Regeneration – stem cells and differentiated cells (part of proliferation phase)
  • Fibrosis – macrophages, granulation tissue (fibroblasts, angiogenesis), type II collagen (part of proliferation phase)
  • Remodeling–macrophages,fibroblasts, converting collagen III to I
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6
Q

Inflammatory Phase

A
  • Redness, swelling, pain, heat & inflammation
  • Capillary permeability increases & fluid moves in
  • Phagocytic cells come in to prevent infection and release GF
  • GF’s recruit fibroblasts, which marks beginning of the proliferative phase
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7
Q

Proliferative Phase

A
  • Begun by fibroblasts that secrete collagen and cause angiogenesis
  • This leads to epithelialization, and causes granulation tissue to form
  • Plasma leaks in, and epithelialization is the last of this stage
  • Here a new surface area, similar to the old one, is formed
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8
Q

Remodeling Phase

A
  • Remodeling begins after 3 weeks, and continues 6 moths or longer (tensile strength can be 70-80% at end of 3 months)
  • Synthesis and lysis of collagen occurs simultaneously
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9
Q

Wound Healing - Primary Intention

A 
Primary Intention (primary union)
• Regeneration
• Edges are approximated
• eschar (scab)
• Epidermal cells proliferate under scab
• Dermal healing is by routine scarring
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10
Q

Wound Healing - Second Intention (secondary union)

A
  • Occurs with failure of first intention t
  • poor apposition or dehiscence
  • Foreign material
  • Extensive necrosis
  • Infection
  • More fibrin, more granulation tissue
  • Wound contraction
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11
Q

Wound healing - Tertiary Intention

A
  • Surgical

* Sutures are placed later to help approximate the tissue

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12
Q

Etiology of scar formation:

A
  • When resolution fails in acute inflammation
  • Ongoing necrosis and chronic inflammation (eg.chronic hepatitis cirrhosis)
  • When cell necrosis cannot be repaired (eg.myocardial infarction)
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13
Q

Stages of scar formation

A

• Bleeding
• Preparation – removal of inflammatory debris and necrotic tissue by phagocytes
• Granulation tissue (highly vascularized
connective tissue)
• Fibronectin produced by fibroblasts

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14
Q

Granulation Tissue

A
  • Formed by fibroblasts and vascular endothelial cells.
  • Grossly it has a pink, soft, grainy appearance.
  • It is often edematous
  • Eventually it is converted to a pale avascular scar composed of fibroblasts, dense collagen III, fragments of elastic tissue and other ECM.
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15
Q

Repair - Scar

A
  • Collagenation – tensile strength
  • Collagen produced by fibroblasts
  • Maturation – pale/lacking circulation
  • Contraction and strengthening
  • Myofibroblasts contract early
  • Collagencontracts in late scars (type III becomes type I)
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16
Q

Factors causing defective scar forming

A

Deficiencies of vitamin B2, C, bioflavonoids and Zinc

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17
Q

Angiogeneisis

A

formation of new blood vessels (also called neovascularization)
• Branching of adjacent vessels
• Recruitment of endothelial progenitor cells
• From bone marrow

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18
Q

The collagen triple helix.

A

The individual α chains are left-handed helices with approximately three residues per turn. The chains are in turn coiled around each other following a right-handed twist. The hydrogen bonds which stabilize the triple helix (not shown) form between opposing residues in different chains (inter-peptide hydrogen bonding) and are therefore quite different from α helices which occur between amino acids located within the same polypeptide

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19
Q

Collagen Types:

A

(over 29) In the remodeling phase, type III collagen is laid down in granulation tissue, then converted to type I collagen

20
Q

Type I

A

Most common, and is the strongest as it is located in bones, skin, tendons, fascia, cornea, teeth and mature scars.

21
Q

Type II

A

little bit less strength seen in cartilage, vitreous humor, and nucleus pulposus

22
Q

Type III

A

is even weaker as it is present in granulation tissue, embryonic tissue, uterus, blood vessels, and keloids.

23
Q

Type IV

A

is the weakest is it only supports a row of epithelial cells as it’s found only in basement membranes.

24
Q

Hydroxylation of collagen is mediated by vitamin C. What cofactor is required? What is cross-linking performed by?

A

Cross-linking of collagen is performed by lysyl oxidase; Copper is a required cofactor

25
Q

What causes scurvy?

A

Vitamin C deficiency
• First affects collagen with highest hydroxyproline content, such as that in blood vessels
• Early symptom then is bleeding gums

26
Q

What is Ehlers-Danlos (ED) Syndrome?

A

Defect in collagen synthesis or structure
• Nine different types
• ED type IV is a defect in type III collagen

27
Q

Osteogenesis Imperfecta

A

• Defect in collagen type I

28
Q

Other Extracellular Matrix Components

A

• Elastic fibers: Elastin proteins are aligned on a
fibrillin framework; Defects in fibrillin framework; Defects in fibrillin are found in Marfan syndrome
• Adhesion molecules: Fibronectin; Laminin
• Proteoglycans and glycosaminoglycans: Heparan sulfate and Chondroitin sulfate

29
Q

What charge does the basement membrane have?

What is it comprised of?

A

net negative charge

  • Collagen type IV
  • Proteoglycans (heparin sulfate) • Laminin
  • Fibronectin
30
Q

Regeneration Overview: Healing and Regeneration

A

Different tissues have different regenerative capacities
• Healing – replacement by connective tissue
• Regeneration – Repair of injured tissue by parenchymal cells of the same type

31
Q

Stem Cell Overview

How are they distinguished?

A

Stem cells have the potential to develop into many different cell types in the body during early life and growth
• internal repair system, dividing without limit to replenish other cells
• stem cell divides to either stem cell or another specialized type
Distinguished from other cell types by two important characteristics:
• unspecialized cells capable of renewing themselves through cell division, sometimes after long periods of inactivity
• Under certain physiologic or experimental conditions, they can be induced to become tissue- or organ-specific cells with special functions

32
Q

Stem cells—three general properties:

A
  • They are capable of dividing and renewing themselves for long periods
  • They are unspecialized
  • They can give rise to specialized cell types.
33
Q

3 types of Stem Cells: Based on Proliferative Potential

A
  • Labile cells
  • Stable cells
  • Permanent cells
34
Q

Labile Cells

A

continuously dividing (Epidermis, mucosal epithelium, GI tract epithelium etc.)

Regenerate through life
• Examples: Surface epithelial cells (skin and
mucosal lining cells)
• Hematopoietic cells, stem cells, etc.

35
Q

Stable cells

A

low level of replication (Hepatocytes, renal tubular epithelium, pancreatic acini)

  • Replicate at a low level throughout life
  • Have the capacity to divide if stimulated by some initiating event
  • Examples: Hepatocytes, Proximal tubule cells, Endothelium
36
Q

Permanent cells

A

never divide (Nerve cells, cardiac myocytes, skeletal mm)

Few stem cells and/or differentiated cells with the capacity to replicate
• Very low level of replicative capacity
• Examples: Neurons, Cardiac Muscle

37
Q

Cell cycle: 5 phases of cell cycle

What regulates the transition between the phases?

A
  1. G0 (Quiescent phase)
  2. G1 (Pre synthetic phase)
  3. S (phase of DNA synthesis)
  4. G2 (premitotic growth phase)
  5. M (mitotic phase)
    • Transition between the phases regulated by cyclins and CDKs (cyclin dependent kinases)
    • kinases phosphorylate proteins, form mitotic spindles, cause dissolution of nuclear membranes and chromosome condensation
    - CDK inhibitors like TP53 are important for buying time for DNA repair, or to induce apoptosis if the DNA cannot be repaired.
38
Q

Repair in Specific Organs - Liver

A
  • Mild injury: repaired by regeneration of hepatocytes, sometimes with restoration of normal pathology
  • Severe or persistent injury causes formation of regenerative nodules that may be surrounded by fibrosis, leading to hepatic cirrhosis
39
Q

Repair in Specific Organs - Brain

A
  • Neurons are thought not to regenerate

* Microglia remove debris and astrocytes proliferate, gliosis

40
Q

Repair in Specific Organs - Heart

A

• Damaged heat muscle cannot regenerate, so the heart heals by fibrosis

41
Q

Repair in Specific Organs - Lung

A

• Type II pneumocytes replace both type I and type II pneumocytes after injury

42
Q

Repair in Specific Organs – Peripheral Nerves

A
  • Distal Part of the axon degenerates

* Proximal part regrows slowly using axonal sprouts to follow Schwann cells to the muscle

43
Q

Three Stages of Fracture Healing

A
  • Procallus – provides anchorage, but no structural rigidity
  • Fibrocartilagenous callous
  • Osseous callous
44
Q

Greenstick Fracture

A

In this particular fracture, the periosteum will need to be broken so that the fracture does not heal at an angle

45
Q

Comminuted Fracture

A

Will need ORIF or more likely, an external fixator

Pathology 1 (6 decks)

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