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2 - MOD > deck_579813 > Flashcards

deck_579813 Flashcards

1
Q

Define regeneration

A

The replacement of dead or damaged cells by functional differentiated cells

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2
Q

Describe the characteristics of stem cells

A

Limitless differentiation in theoryDaughter cells either remain as stem cells (maintains pool) or differentiate into specialised cell typesReplace lost or damaged cells in tissues

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3
Q

Define unipotent

A

Can only produce one type of differentiated cellE.g. Epithelial cells

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4
Q

Define Multipotent

A

Can produces several types of differentiated cellsE.g. Haematopoetic cells in bone marrow– erythrocytes, neutrophils, B-cells etc

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5
Q

Define totipotent

A

Can produce any type of cellsE.g. Embryonic stem cells – blastocyst

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6
Q

Give the regeneration ability of Labile cells

A

epithelial or haematopoietic cellsnormal state is active cell division: G1 – M – G1usually rapid proliferation

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7
Q

Give the regeneration ability of Stable cells

A

hepatocytes, osteoblasts, fibroblastsResting state (G0) is normal state speed of regeneration variable

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8
Q

Give the regeneration ability of Permanent cells

A

Neurones, cardiac myocytesUnable to divide - G0

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9
Q

What factors control cell regeneration?

A
  1. Growth Factors2. Contact between basement membrane and adjacent cells
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10
Q

Describe the characteristics of growth factors and how they control regeneration

A
  • Promote proliferation in the stem cell population- Extracellular signals transduced into the cell- Promote expression of genes controlling cell cycle- Can be proteins or hormones (EGF, PGDF, oestrogen, testosterone) ** Have a kinase property to phosphorylate intracellular signals **Autocrine, paracrine and endocrine signals from many cell types : inflammatory , mesenchymal etc
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11
Q

Describe how contact between basement membranes and adjacent cells controls regeneration.

A

Signalling through adhesion molecules between cellsinhibits proliferation in intact tissue‘Contact inhibition’Loss of contact promotes proliferation** these mechanisms are deranged in cancer **

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12
Q

Define Fibrous Repair

A

The replacement of functional tissue 
by scar tissue

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13
Q

When does fibrous repair occur?

A
  1. After necrosis in labile or stable cells and the collagen framework is destroyed 2. After necrosis of permanent cells
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14
Q

What are the key components of fibrous repair? What are these components known as?

A

Cell migrationBlood vessels - angiogenesisExtracellular matrix production & remodelling– GRANULATION TISSUE

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15
Q

What types of cells are present in fibrous repair?

A

INFLAMMATORY CELLS (depends on the circumstances)- Phagocytosis of debris – neutrophils, macrophages- Chemical mediators – lymphocytes & macrophagesENDOTHELIAL CELLS- Angiogenesis** FIBROBLASTS AND MYOFIBROBLASTS **- Extracellular matrix proteins e.g. collagen- Wound contraction- Most important components

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16
Q

What is the purpose of granulation tissue?

A

– Initiates fibrous repair– restores the contour of the skin (prevents a “dent” in the middle of the wound– allows for a good supply due to leaky capillaries from angiogenesis

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17
Q

What is “Proud Flesh”?

A

Where the granulation tissue appears above the plane of the skin

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18
Q

What are the non-cellular components of granulation tissue?

A

Collagen, ground substance components, extracellular matrix proteins

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19
Q

Describe the components that make up the extracellular matrix

A

MATRIX GLYCOPROTEINS– Organise and orientate cells, support cell migratione.g. Fibronectin, laminin, Tenascin,…PROTEOGLYCANS– Matrix organisation, cell support, regulate availablity of growth factorse.g. Heparan sulphate proteoglycan, …ELASTIN – Provides tissue elasticity

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20
Q

What is angiogenesis and why is it necessary?

A

The development of new blood vessels. – Blood supply is vital to wound healing– Provides access for inflammatory cells and fibroblasts and delivers of oxygen and other nutrients– Preexisting blood vessels sprout new vessels

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21
Q

What controls angiogenesis?

A

Proangiogenic growth factorse.g. Vascular endothelial growth factor

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22
Q

Describe the process of angiogenesis.

A
  1. Endothelial proteolysis of basement membrane2. Migration of endothelial cell via chemotaxis3. Endothelial proliferation4. Endothelial maturation and tubular remodelling5. Recruitment of periendothelial cells
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23
Q

What are the functions of the extracellular matrix?

A
  1. Supports and anchors cells2. Separates tissue compartmentse.g. basement membrane3. Sequesters growth factors4. Allows communication between cells5. Facilitates cell migration
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24
Q

Describe collagen

A

– Most abundant protein in animals– Provides extracellular framework– Composed of triple helices of various polypeptide alpha chains– Fibrillar collagens: I – III e.g. dermis, bone etc– Amorphous collagens: IV-VI e.g. BM– Remodelled by specific collagenases (slow remodelling)

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25
Q

Describe the process of collagen synthesis

A

Polypeptide alpha chains synthesised in EREnzymatic modification steps including vitamin C dependent hydroxylationAlpha chains align and cross-link to form procollagen triple helixSoluble procollagen is secretedAfter secretion procollagen cleaved to give tropocollagenTropocollagen polymerises to form fibrilsBundles of fibrils form fibresSlow remodelling by specific collagenases

26
Q

What are some defects involving collagen?

A

Vitamin C Deficiency – ScurvyEhlers-Danlos syndromes (defective conversion of tropocollagen to collagen)Osteogenesis imperfectaAlport syndrome

27
Q

Describe Vitamin C deficiency

A

– Inadequate Vit C dependent hydroxylation causes formation of defective collagen– Lacks strength, vulnerable to enzymatic degradation, particularly affects collagens supporting blood vessels –> Haemorrhage, skeletal changes in infants

28
Q

Give a general overview of the mechanism of fibrous repair

A
  1. Inflammatory cells infiltrate2. Clot is replaced by granulation tissue3. Maturation of fibrous tissue
29
Q

Describe the process of inflammatory cells infiltrating

A

Blood clot formsAcute inflammation occurs around the edgesIn chronic inflammation,macrophages and lymphocytes infiltrate and neutrophils digest the clot

30
Q

Describe how the clot is replace by granulation tissue

A
  1. Angiogenesis occurs – Capillaries and lymphatics sprout and infiltrate2. Myo/fibroblasts migrate and differentiate.Extracellular matrix is produced by myo/fibroblasts, collagen in synthesised and the number of macrophages is reduced
31
Q

Describe the maturation process in fibrous repair

A

Comparatively long-lastingCell population falls and collagen increases, matures and remodelsMyofibroblasts contract which causes a reduction in the volume of defectVessels differentiate and are reducedLeft with a fibrous scar

32
Q

How is fibrous repair controlled?

A

Chemotaxis controls influx of inflammatory cells2. Angiogenesisangiogenic cytokines are produced by platelets in response to hypoxia e.g. vascular endothelial growth factor and fibroblast growth factor3. Fibrosispro-fibrotic cytokines are produced by macrophages, e.g. IL1, TNF alpha, TGF beta…

33
Q

Describe primary intention healing

A

Have an incised wound with apposed edgesMinimal clot and granulation tissueEpidermis regenerates whilst the dermis undergoes fibrous repair— essentially only for surgical wounds, maybe a sharp cut by glass– sutures are removed at 10 days and the wound has ~ 10% of its normal strength

34
Q

Describe the process of healing by primary intention

A

There is a transition from granulation tissue to scar tissueLoss of contact inhibition leads to the proliferation of epithelial cells (releases epithelial growth factors)Maturation of scar continues up to 2 years.Minimal contraction & scarring leads to good strengthRisk of trapping infection which can lead to abscesses

35
Q

When does healing by secondary intention occur?

A

Occurs with an infarct, abscess or any large wound

36
Q

What are the difference between healing by primary and secondary intentions?

A

In secondary intention:– Have unapposed wound edges– Large clot dries to form a ‘scab’ or ESCHAR– Epidermis regenerates from the base up.– Repair process produces much more GRANULATION TISSUE

37
Q

Outline the characteristic of healing by secondary intention

A

Produces more contraction to reduce volume of defect (myofibrils)Produces a larger scar; not necessarily weakerTakes longer

38
Q

Describe the process of bone healing

A
  1. Haematoma forms from ruptured vessels within marrow cavity and periosteum2. Organising haematoma provides framework for ingress of macrophages, endothelial cells fibroblasts and osteoblasts3. Necrotic tissue removed by phagocytosis and capillaries develop4. Specialised mixture of cells is called callus which is a framework letting bone be laid down as cartilage (irregular woven bone)5. External callus provides splint-like support6. Woven bone is replaced by more organised lamellar bone7. Lamellar bone is remodelled in the direction of mechanical stress
39
Q

Describe local factors which will influence would healing

A
  1. Type, size, location of wound2. Apposition, lack of movement– Skin wounds, bone fractures, severed nerves3. Blood supply: Arterial, Venous4. Infection: Suppuration, Gangrene, Systemic5. Foreign material: dirt, glass, sutures, necrotic tissue6. Radiation damage
40
Q

Describe general factors which influence wound healing

A
  1. Age2. Drugs (n.b. steroids) and hormones3. General dietary deficiencies e.g. protein4. Specific dietary deficiencies– Vitamin C – alpha chain hydroxylation– Essential amino acids5. General state of health– chronic diseases e.g. diabetes, rheumatoid arthritis etc.6. General cardiovascular status
41
Q

Give some complications of repair

A

Insufficient fibrosis Excessive fibrosisAlcoholic cirrhosisExcessive contraction

42
Q

Describe insufficient fibrosis

A

Not enough fibrous repair takes place which can cause:Wound dehiscence (wound ruptures along surgical suture) hernia and ulcerationRisk factors:Obesity, elderly, malnutrition, steroids, trauma after surgery

43
Q

When does excessive fibrosis occur?

A

Cosmeti scarring, keloid scars, cirrhosis and lung fibrosis

44
Q

Describe alcoholic cirrhosis

A

Nodular growth of hepatocytes occurs which are separated by fibrous tissue– it impairs the bile flow to the biliary tree as well as vascular flow throughout the kidney

45
Q

Describe excessive contraction

A

Myofibroblast constrict the wound too much which causes tubes and channels to be obstructed, causing strictures. – it can also limit the movement of joints if the contracture occurs over a joint

46
Q

In what type of people does poor healing occur?

A

Elderly, diabetics, sufferers of chronic illness, people taking steroids

47
Q

What type of healing occurs in cardiac muscle?

A

Fibrous repair –are permanent cells so cannot divide/regenerate

48
Q

How do peripheral nerves regenerate?

A

There is degeneration of the nerve proximal to severing as well as of the distal nerve back to the previous node of ranvier. – the axon can grow back as the neurone extends across the gap.

49
Q

What factors must be present in order for the nerve regeneration to be successful?How much can a peripheral nerve regenerate in a day?

A
  1. Calcium influx will promote resealing2. Alignment must be correct in order for function to be restored– 1mm per day
50
Q

What type of nerve injury is preferable?

A

Sharp cut compared to a crush injury – axons will grow back more effectively and efficiently

51
Q

What occurs with acute and chronic damage to the liver?What damage occurs in chronic liver disease?

A

Acute damage –> RegenerationChronic damage –> Cirrhosis as regeneration is distorted by fibrosis– Liver tissue is replaced by nodule of hepatocytes which are surrounded by fibrosis. Tissue lacks normal vasculature and bile drainage.

52
Q

What determines the ability for the liver to regenerate?

A

The amount of damage to the hepatocyte architecture– hepatocytes can regenerate but the hepatocyte architecture cannot regenerate–The imbalance between hepatocyte regeneration and the ability to regenerate architecture leads to cirrhosis and nodules.

53
Q

Why must particular care be taken with thinner patients?

A

They are more susceptible to pressure sores (non-healing ulcers) – caused by a compromised nutrient and oxygen supply

54
Q

What types of fractures can you get?

A

Green-stickSpiralOpen or closedComminuted – bone has broken in multiple pieces

55
Q

What type of repair occurs in the brain?

A

Cells do not have a regenerative capacityUndergoes liquefactive necrosis to remove dead or damaged cellsA rim of gliosis will form around the damaged area instead of repair of scar tissue forming. Formed from proliferating glial cells.

56
Q

Why do glioses form in the brain?

A

Dont have fibroblasts or collagen in the brain so scar tissue can’t form. If scar formation did occur, the contraction of the wound would cause even more damage.

57
Q

What repair occurs in smooth muscle?

A

Permanent tissue. Will be replaced by a scarVascular smooth muscle has some, limited, regeneration

58
Q

What repair occurs in skeletal muscle?

A

It has limited regenerative capacity due to satellite cells

59
Q

What is acute tubular necrosis?

A

Death of tubular cells which transport urine to teh ureters and absorb 99% of water passing through them. Have localised necrosis of epithelial lining of the tubules.

60
Q

What are the two types of acute tubular necrosis?

A

Ischaemic and toxic ATN

61
Q

When can regeneration occur in acute tubular necrosis?

A

If the basement membrane is still intact

62
Q

Describe the process of repair in cardiac tissue

A

Necrotic area becomes replaced by scar tissue as are permanent cells. 1. Infarct becomes eosinophillic with intracellular oedema 2. Acute inflammatory response occurs and neutrophils invade between dead cardiac cells3. Dead fibres are replaced by granulation tissue4. Collagenous scar forms, end result is a white infarct

2 - MOD (18 decks)

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