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Y1 TP2 Pathological Processes (topic 3 Onwards) > 4. Regeneration And Repair > Flashcards

4. Regeneration And Repair Flashcards

1
Q

Stem cell definition

A

• A stem cell is an undifferentiated cell that can:

  1. continuously divide – proliferation, duplication, replication
  2. differentiate into various other kind(s) of cell
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2
Q

2 characteristics of stem cells

A

Self renewal

Potency

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3
Q

Self renewal

A

capable of dividing and renewing themselves, to keep the source of regrowth

• Dauaghter cell can become exactly like the original stem cell
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4
Q

Potency

A

the capacity to differentiate into sdifferent kinds of specialized cell types for development and regeneration

• Daughter cell can proliferate further and differentiate into different cells
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5
Q

4 types of potency

A

Totipotent
Pluripotent
Multipotent
Unipotent

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6
Q

Totipotent

A
  • fertilised egg and the cells produced by the first few divisions
    • can differentiate into embryonic (to develop organs and tissues) and extraembryonic cell types (placenta)
    • they can construct a baby!
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7
Q

• Pluripotent:

A
  • the embryonic stem cells (ESC), descendants of totipotent cells, cells from inner mass of blastocyst
    • can differentiate into cells of any of the three germ layers or any tissues/organs.
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8
Q

• Multipotent:

A

• can produce a family of several types of cells (e.g. hematopoietic stem cells HSC differentiate into different blood cells, neural stem cells NSC into neurons and glia).

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9
Q

Unipotent

A
  • can produce (differentiate) only one cell type (lineage specific)
    • but have the property of self-renewal – specialised cells
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10
Q

4 types of stem cells

A

Embryonic stem cells
Adult (or tissue-specific) stem cells
Induced pluripotent stem cells (iPSC) (from somatic cell to stem cell)
Cord blood (umbilical) stem cells

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11
Q

Embryonic stem cells

A

• that exist only at the earliest stages of development

= Pluripotent

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12
Q

Adult (or tissue-specific) stem cells

A
  • that appear after fetal development and remain in our bodies throughout life
    • Multiple and uni potent
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13
Q

Induced pluripotent stem cells (iPSC) (from somatic cell to stem cell)

A
  • From specialised cell converted back to stem cells

* Pluripotent

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14
Q

Cord blood (umbilical) stem cells

A

Multipotent

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15
Q

2 roles of adult stem cells

A
  • Regernation = The adult stem cells constantly replace the used cells
    • Healing = The adult stem cells regrow for the regeneration and repair
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16
Q

Adult stem cells → Bone Marrow-Derived Stem Cells

A

• Bone marrow produces multipotent hematopoietic stem cells (labile)
○ Produce wbc, rbc and platelets
○ Directly involved in healing

• Other stem cells from bone marrow-EPC, - endothelial progenitor cells 
	○ ESC = endothelial cells, angiogenesis 
	○  MSC = fibroblasts
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17
Q

Skin stem cells

A
  • Epidermis –epidermal stem cells at the basal layer, hair follicle stem cell (labile)
    • Bottom of skin or bottom of hair follicles
    • Activate and grow to replace lost skin
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18
Q

GI epithelial stem cells

A

• –Intestinal mucosa –bottom of crypts (labile)

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19
Q

Hepatocyte stem cells

A

• –Liver –between hepatocytes and bile ducts (stable)

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20
Q

4 examples of adult stem cells in different tissues

A

Bone Marrow-Derived Stem Cells
Skin stem cells
GI epithelial stem cells
Hepatocyte stem cells

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21
Q

Ageing and stem cells

A

As age increases Ageing: stem cells decrease their ability of self-renewal and differentiation abilities

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22
Q

Regenerative capcity of cells

  • labile, stabile, permanent
A

Outside of cell cycle – cell can’t reproduce itself

LABILE = Some cells e.g. epidermis skin cells) are constantly going through cell cycle – these are labile cells

PERMANENT = Cardiac monocytes and neurons = permanent cells, come out of the cell cycle permanantly – will never go back into cell cycle

STABLE = remain quiescent but can be activated when stimulated and go back into cell cycle to proliferaet (hepatocyte)

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23
Q

Labile definition

A

continuously dividing cells/tissues

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24
Q

Stable definition

A

quiescent tissue, but cells can undergo rapid division in response to stimuli and can reconstruct the tissue of origin.

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25
Q

Permanaent definition

A

Non dividing

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26
Q

Example of labile tissues

A
  • e.g. skin epithelia, epithelia GI tract, haematopoietic tissue…:
    • normal state is active cell division: G1– M – G1
    • usually rapid proliferation for regeneration from active stem cells
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27
Q

Example of stable tissues

A
  • e.g. hepatocytes, osteoblasts, fibroblasts:
    • Resting state – G0 (quiescent mature cell and stem cells)
    • speed of regeneration variable
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28
Q

Example of permanent tissues

A
  • e.g. neurones, cardiac myocytes:
    • unable (?) to divide - G0 (terminally differentiated cells and no effective stem cells)
    • no effective generation
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29
Q

High regenerative capacity tissues

A
  • Skin
    • liver
    • Blood cels
    • Smooth muscle
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30
Q

moderate regenerative capacity tissues

A
  • Skelton muscle
    • Kidney
    • Bone
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31
Q

Low regenerative capacity tissues

A
  • heart
    • Cartilage/ tendons
    • Peripheral nerve
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32
Q

3 Factors controlling regeneration and repair mechanisms

A

Cell to cell communication
Growth factors
Cell-cell and cell-stroma contact

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33
Q

What is cell to cell communication

A

Uses:
• Local mediators (e.g. cytokines, growth factors-soluble signals)
• Systemic hormones (eg. growth hormone)
• Direct cell-cell or cell-stroma contact

Balance between stimulation and inhibition

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34
Q

What are the growth factors involved in wound healing

A
  • Polypeptides (local mediators and hormones)
    • Bind to that act on cell surface receptors, stimulate transcription of genes that regulate cell proliferation and other effects.
    • Determine if cell goes into cell cycle

Produced mostly by macrophages and other cells (local hormones)

Local hormones:
• Epidermal growth factor (EGF)-mitogenic for epithelial cells and fibroblasts
• Vascular endothelial growth factor (VEGF)-induces angiogenesis
• Platelet derived growth factor (PDGF)-causes migration and proliferation of fibroblasts
• Tumour necrosis factor (TNF)-induces fibroblast migration, fibroblast proliferation and collagenase secretion.

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35
Q

What is Cell-cell and cell-stroma contact

A

—> Signalling through adhesion molecules
• Connexion and Cadherins (adhesion junctions binding cells together) bind cells to each other
• Integrins bind cells to the extracellular matrix = binding can send signals

Effect-Contact inhibition-Inhibits cell proliferation

Balance between stimulation and inhibition

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36
Q

Regenerative medicine definition

A

—> application of stem cells

A process of replacing, engineering or regenerating cells, tissues or organs to restore or establish normal function.

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37
Q

2 examples of regenerative medicine

A

Cell therapy
• Original cells (blood transfusion…)
• Lab (ex vivo) expanded cells –> healing

Stem cell therapy
• Stem cells from embryo (e.g. cord blood…) from adult (bone marrow…) (FDA!)
• Induced stem cells from adult (FDA?)

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38
Q

Process of skin tissue regeneration for burn injury

A
  1. Get sample of healthy skin tissue
    1. Send to lab
    2. Lab – tissue digestion to isolate single cells (epithelial and stem cells)
    3. Expand these cells into millions of cells using proper medium
    4. Add cells to burn area = helps tissue regeneration
    5. Restore normal skin cells instead of scar
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39
Q

Cord blood stem cell treatment

A
  1. Cord blood contains several type of stem cells
    1. Many haemopoietic stem cells
    2. Llots of MCS mesenchymal stem cells that can give rise to several cell types – fibroblasts
    3. Fibroblasts are important in tissues
    4. Endotherlial progenitor cells – angiogenesis
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40
Q

Functions of MCS and other stem cells (when transplanted to the body)

A
  • Differentiate and replace the cells
    • Promote other cells regeneration
    • Rejuvenate aged stem cells
41
Q

Induced pluripotent stem cells (iPSC)

Formation and Uses

A
  1. Treat somatic cells with transcriptional factors (reprogramming factors)
    1. Reprogram somatic cells → stem cells = pluripotent cells
    2. = induced pluripotent cells

Uses:
• Personalized medicine/Precision medicine
• Overcome tissue rejection issue
• Drug test – which drugs are suitable to individuals
• Disease research

42
Q

Pros of stem cell use

A
  • Medical benefits-regeneration and repair
  • Diseases curing (including gene correction)
  • Research for human disease
  • Drug testing on human cells
43
Q

Cons of stem cell use

A
  • Uncertainty of long term effect-need research
  • Potential tumour growth = as stem cells proliferate alot
  • Tissue rejection
  • Ethical and legal aspects
44
Q

5 layers of blood vessels

A 
○ Tunica intima
Internal elastic lamina
○ Tunica media
External elastic lamina
○ Tunica externa
45
Q

Tunica intima

A
  • inner layer
    • thinnest
    • Single layer of endothelial cells
46
Q

Internal elastic lamina

A
  • Dense elastic membrane

* Sepreates tunica intima from media

47
Q

Tunica media

A
  • Thickest layer
    • Middle
    • Smooth mucle cells,
    • Elastic fibres
    • Connective tissues
48
Q

External elastic lamina

A

• Serperates tunica media from tunica adventita

49
Q

Tunica adventita

A
  • Outer layer
    • Connective tissue
    • Vessels and nerves
50
Q

Arteriosclerosis definition

A

○ hardening of arteries affecting the wall, thickens wall

51
Q

3 diseases included arteriosclerosis

A
  • Atherosclerosis – affect large and medium sized artery
  • Arteriolosclerosis – hardening of arterioles mainly kidney arterioles
  • Monkeberg’s disease – calcification in media of large arteries
52
Q

Atherosclerosis definition

A

• Is the accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries

* Degernative process slowly progressive
* Acuumulation of fatty material in blood vessels walls
* Affects medium and large arteries
53
Q

What is atherosclerosis characterised by?

A

•Characterized by intimal lesions called: atheroma, atheromatous or fibro-fatty plaques

54
Q

Pathogenesis of atherosclerosis

A

Endothelial injury causes:
• Platelet adhesion, platelet derived growth factor release, smooth muscle cell (SMC)proliferation and migration
• Accumulation of lipid, LDL oxidation, uptake of lipid by smooth muscle cells and macrophages
• Migration of monocytes (WBC and when inside the tissue –> macrophage) into intima
To form atherocsclerotic lesions

55
Q

. Conditions that lead to edothelial injury

A
  • Hyperlipidaemia
    • Hypertension
    • Smoking
    • Homocysteine
    • Hemodynamic factors
    • Toxins
    • Viruses
    • Immune reations
56
Q

Cause of atherosclerois

A

→ response to injury hypothesis

57
Q

Steps of Response to injury hypothesis (causing atherosclerosis)

A
  1. Injury to the endothelium (dysfunctional endothelium)
    1. Chronic inflammatory response
    2. Migration of SMC – smooth muscle cells from media to intima - activate macrophage
    3. Proliferation of SMC in intima - smc and macrophages engulf lipids → formation of fatty streak
    4. Excess production of Extra cellular Matrix- to support lesion and form fibrous cap
    5. Enhanced lipid accumulation’
    • Formation of the atheroscloretic plaque
    • Fibrofatty atheroma centre – dead cells in the centre due to lack of blood supply
    • Formation of fibrous cap – roof of lesion that encases it and prevents repture and release of contents
58
Q

3 intimal lesions in atherosclerosis

A
  • Formation of the atheroscloretic plaque
  • Fibrofatty atheroma centre – dead cells in the centre due to lack of blood supply
  • Formation of fibrous cap – roof of lesion that encases it and prevents repture and release of contents
59
Q

Main components of fibro-fatty plaque

A
  • Lipid containing macrophages
  • Extracellular matrix
  • Cells, Proliferating smooth muscle cells
60
Q

How to visually differentiate between artery and vein

A

• compare the thickness of the wall

61
Q

2 most important causes of endothelial dysfunction are:

Response to injury hypothesis

A
  1. Hemodynamic disturbances (HTN)
  2. Hypercholesterolemia

Inflammation is also an important contributor

62
Q

Lesions progression (progression of atherosclerosis)

A

Initial lesion – macrophages then migrate
Fatty streak – intracellular lipid accumulation
Intermeidate lession - intracellular lipid accumulation
Atheroma - intracellular lipid accumulation, core on extracellular lipid
Fibroatheroma – fibrotic/calcific layers
Compliacted lesion – haemorrhage and thrombosis

63
Q

Plaques

A

Fatty streaks can grow and become plaques

* White to yellow 
* Spots
* Fibrosis, necrosis 
* Vary from 0.3 to 1.5 cm in diameter, but can coalesce to form larger masses
* Extension of vessels into media and intima
64
Q

Microscopic features of atherosclerosis

Early changes

A
  • proliferation of smooth muscle cells
  • accumulation of foam cells
  • extracellular lipid
65
Q

Microscopic features of atherosclerosis

Later changes

A
  • fibrosis
  • necrosis
  • cholesterol clefts
  • +/- inflammatory cells
  • disruption of internal elastic lamina
  • damage extends into media
  • ingrowth of blood vessels
  • plaque fissuring
66
Q

Stable atherosclerotic plaque

A
  • Fibrous cap is thick, seperates lesion from lumen

* Necrotic core contains necrotic debris, red blood cells, cholesterol esters / clefts

67
Q

Vulnerable atherosclerotic plaque

A
  • Thin fibrous cap
    • Necrotic core superated from lumen by thin fibrous cap
    • thin cap fibroatheromas are considered to be vulnerable to rupture of the fibrous cap and sudden coronary artery
    • Cap may rupture and components may be released
68
Q

5 steps for forming vulnerable or stable plaques

A
  1. Normal aretery
    1. Endothelial dysfunction
    2. Fatty streak
    3. More fibrosis and matrix = fibro fatty plaque
    4. Weakness of cap may lead to vulnerable plaque
      • Risks of aneuysm and repture, accumulation by thrombus, critical stenosis
69
Q

Simple plaque

A
  • Raised yellow/white
  • Irregular outline
  • Widely distributed
  • Enlarge and merge
70
Q

Complicated plaque

A
  • Thrombosis
  • Haemorrhage into plaque
  • Calcification
  • Aneurysm formation
71
Q

Common sites of atherosclerosis

A

—> usually elastic arteries. Large and medium muscular arteries

  • Abdominal aorta
  • Coronaries
  • Popliteal artery
  • The internal carotid arteries
  • The vessels of the circle of Willis
72
Q

How can atherosclerosis cause clinical complications

A
  1. Progressive lumen narrowing due to high-grade plaque stenosis.
    • Because of lesion most of lumen has stenosis (70%) affect blood flow
  2. Acute atherothrombotic occlusion (key pathology)
    • Plaque ruptured, so components are released to blood strea
  3. Thrombus embolisation into the distal arterial bed
    • Fragmentation of material of atherosclerotic lesion
  4. Ruptured abdominal atherosclerotic aneurysm
    • Weakness of structure and stability of blood vessel walls
    • Lead to haemorrhage and death
73
Q

Clinical complications of atherosclerosis

A
  • Myocardial infarction (heart attack), ischaemic heart disease(IHD)
  • Cerebral infarction (stroke)
  • Aortic aneurysms
  • Mesenteric occlusion
  • Peripheral vascular disease (gangrene of the legs)
74
Q

Myocardial infarction - caused by atherosclerosis

A
  1. Blockage in artery
    1. Muscle damage
    2. Myocardial infarction
75
Q

Classical appearance of myocardial infarction

A

approximately 2–3 weeks in age shows the formation of granulation tissue characterized by loss of myocytes, neovascularization, loose collagen deposition, fibroblasts, and hemosiderin containing macrophages

76
Q

Cerebral infarction

A

—> blockages in cerebral artery

= liquefactive necrosis

77
Q

Intestinal infarction

A

• Marked dark red ischaemic small bowel

○ Due to bockage of main blood supply

78
Q

Peripheral vascular disease

A
  • When atherosclerosis affects popliteal, femoral or iliac artery
    • May end up with gangrene due to loss of blood supply
79
Q

Abdominal aoritc aneurysms

A
  • Localized enlargement of the abdominal aorta
    • Cause no symptoms except when ruptured —> severe complication
    • Occasionally, abdominal, back, or leg pain may occur
80
Q

Sacular aneurysm – looks like a sac

A
  • Complication = disecting, rupture inner layer of arterial wall so blood fills gap between 2 layers
    • Lumen of artery can be occluded
81
Q

Non modificable risk factors of atherosclerosis

A
  • Age = slowly progressive throughout adult life
  • Gender = women protected relatively before menopause due to loss of oestrogen
  • Genetic predisposition = Familial hyperlipidaemia
  • Genetically determined abnormalities of lipoproteins – defect in lipoprotein metabolism = high lipid level
  • Lead to early development of atherosclerosis
82
Q

Familial hyperlipidaemia

A

• Genetically determined abnormalities of lipoproteins – defect in lipoprotein metabolism = high lipid level
• Lead to early development of atherosclerosis
• Associated physical signs
• Argus = white grey ring around cornea of eye
• Tendon xanthomas = cholesterol deposits around knuckles
Xanthelasma = yellowish deposite of cholesterol under skin around eylids

83
Q

Modifiable risk factors - atherosclerosis

A
  • Hyperlipidaemia
  • Cigarette smoking
  • Alcohol
  • Infection
  • Hypertension
84
Q

Hyperlipidaemia

A
  • high plasma cholesterol associated with atherosclerosis
    • LDL most significant = bad one might lead to atherosclerosis
    • HDL protective = level increase with exercsise decrease with smoking
85
Q

Hypertension

A

• Mechanism uncertain on how it causes atherosclerosis
• Endothelial damage caused by raised pressure
‘

86
Q

Diabetes mellitus

A
  • DM also associated with high risk of ccerebrovascular and peripheral vascular disease.
  • Related to hyperlipidaemia and hypertension
87
Q

Cigarrette smoking

A

Powerful risk factor for ischaemic heart disease (IHD)

• Mode of action uncertain
-coagulation system
-increased platelet aggregation
• Increased inflamamtion, damage to blood vessel wall

88
Q

Alcohol consumption

A
  • > 5 units /day associated with increased risk of IHD
  • Alcohol consumption often associated with other risk factors. eg smoking and high BP but still an independent risk factor
89
Q

Infections that can cause atherosclerosis

A
  • Chlamydia pneumoniae
  • Helicobacter pylori
  • Cytomegalovirus
90
Q

Cells involved in atherosclerosis

A
  • Endothelial cells
  • Platelets
  • Smooth muscle cells
  • Macrophages
  • Lymphocytes
  • Neutrophils
91
Q

Endothelial cells

A
  • Key role in haemostasis
  • Altered permeability to lipoproteins
  • Production of collagen
  • Stimulation of proliferation and migration of smooth muscle cells
92
Q

Platelets

A
  • Key role in haemostasis

* Stimulate proliferation and migration ofsmooth muscle cells

93
Q

Smooth muscle cells

A
  • Take up LDL and other lipid to become foam cells

* Synthesise collagen and proteoglycans

94
Q

Macrophages

A
  • Oxidise LDL
  • Take up lipids to become foam cells
  • Secrete proteases which modify matrix
  • Stimulate proliferation and migration of smooth muscle cells
95
Q

Lymphocytes

A

• Stimulate proliferation and migration of smooth muscle cells

96
Q

Neutrophils

A

• Secrete proteases leading to continued local damage and inflammation

97
Q

Atherosclerosis - prevention

A
  • No smoking
  • Reduce fat intake
  • Treat hypertension
  • Not too much alcohol
  • Regular exercise/weight control

• BUT some people will still develop atherosclerosis

98
Q

Atherosclerosis interventions

A
  • Stop smoking
  • Modify diet – low fat diet, high fiber
  • Treat hypertension
  • Treat diabetes
  • Lipid lowering drugs
99
Q

Haemostasis

A

Clotting

Y1 TP2 Pathological Processes (topic 3 Onwards) (9 decks)

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