Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ESA2 - Mechanisms Of Disease > Healing And Repair > Flashcards

Healing And Repair Flashcards

1
Q

Define regeneration

A

Growth of cells and tissues to replace lost structures following injury, provided the stem cells are still intact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are labile cells? Give 3 examples

A
  • Cells which are continuously proliferating throughout life to replace lost/damaged cells
  • e.g. Surface epithelia of the epidermis, bone marrow, columnar epithelia of the gut mucosa and uterus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Can stable tissues undergo regeneration?

A
  • Yes, cells remain in the quiescent G0 phase of the cell cycle and can re-enter in response to stimuli and undergo rapid division
  • e.g. Parenchymal cells of the liver, kidney and pancreas, mesenchymal cells, fibroblasts, macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why can permanent tissues not regenerate?

A
  • Cells leave the cell cycle permanently and cannot undergo mitotic division in postnatal life, as the tissues contain no stem cells that can replace damaged tissue
  • e.g. cardiac myocytes cannot regenerate following infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the replication pattern in stem cells

A
  • ASYMMETRIC

- Following mitosis, one of the daughter cells remains a stem cell and the other differentiates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why can stem cells proliferate indefinitely without senescence? Are there any other cells which are capable of this?

A
  • Stem cells produce TELOMERASE which maintains the length of the telomeres during continuous mitotic division (telomeres are shortened during each division until they become a critical length and cells undergo apoptosis)
  • Cancer cells can also produce telomerase and can replicate indefinitely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the difference between totipotent, multipotent and unipotent cell types?

A
  • Totipotent cells can differentiate into ANY cell type e.g. embryonic stem cells
  • Multipotent cells can produce several different types of cells within the same lineage e.g. haematopoietic cells
  • Unipotent cells can only differentiate into a SINGLE cell type e.g. epithelia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give 2 instances where a fibrous scar may form

A
  • If collagen framework of tissue is destroyed
  • If there is ongoing chronic inflammation
    (Cells cannot be replaced at an effective rate to exceed cell loss, resulting in formation of a fibrous scar)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the process of fibrous repair (granulation tissue formation)

A
  • Phagocytosis of necrotic debris
  • Proliferation of endothelial cells, forming small capillaries (angiogenesis, stimulated by VEGF)
  • Proliferation of fibroblasts/myofibroblasts which form granulation tissue (collagen and GAGs) and cause wound contraction
  • Scar maturation (becomes less vascular and shrinks due to contraction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name 4 diseases which affect collagen synthesis

A
  • Scurvy (vitamin C deficiency)
  • Ehler’s Danlos syndrome (lysyl oxidase deficiency)
  • Osteogenesis imperfecta (type I collagen deficiency)
  • Alport syndrome (type IV collagen deficiency)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the symptoms of osteogenesis imperfecta

A
  • Deficiency in type I collagen causes bones to be brittle and extremely fragile and prone to fractures
  • Type 1 OI have blue sclerae, as the lack of collagen in the sclera makes them appear translucent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the pathophysiology of Ehler’s Danlos syndrome

A
  • Deficiency in lysyl oxidase so collagen is unable to form stable cross links so lack tensile strength
  • Skin is hyperextensible and joints are hypermobile as a result and wound healing is poor
  • Rupture of colon, cornea and large arteries is not uncommon due to lack of tensile strength of collage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why might patients with Alport syndrome present with haematuria?

A
  • Deficiency in type IV collagen which affects the basement membrane in the glomerulus of the kidney (Bowman’s capsule)
  • Dysfunction of the membrane causes filtration of RBCs which would normally not enter filtrate and are therefore present in the urine
  • This may progress to kidney failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 3 examples of how cells can communicate via local mediators or hormones

A
  • Autocrine (cell responds to signals that they themselves produce)
  • Paracrine (cells respond to signals produces by adjacent cells within the local vicinity, often a different type)
  • Endocrine (cells respond to hormones produced by endocrine organs which travel in the bloodstream to distant target cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are growth factors?

A
  • “Local polypeptide hormones” coded for by proto-oncogenes and act on cells via paracrine signalling over short distances
  • Bind to specific receptors and stimulate/inhibit cell proliferation and angiogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give 4 examples of growth factors and their associated actions

A
  • EGF (mitogenic for epithelia, hepatocytes and fibroblasts)
  • VEGF (induces vasculogenesis, role in angiogenesis of tumours, chronic inflammation and wound healing)
  • PDGF (migration and proliferation of fibroblasts, monocytes and smooth muscle cells)
  • TNF (induces fibroblast migration and proliferation, secretion of collagenase)
17
Q

What is contact inhibition? Name 2 important proteins involved in this

A
  • Normal cells (when isolated) replicate until they are touching other cells and then stop
  • Involves expression of adhesion molecules (cadherins which bind cell-cell, integrins which bind cell-stroma)
  • Adhesion molecules are abnormally expressed in cancer cells, allowing them to invade surrounding tissues
18
Q

When does healing by primary intention occur?

A

Incisional, closed, non-infected wounds with opposed edges and minimal loss of connective tissue scaffold

19
Q

What are the 5 stages of healing by primary intention?

A
  • Haemostasis (severed arteries contract and space fills with clotted blood)
  • Inflammation (neutrophils and leucocytes invade to kill of any bacteria present)
  • Migration of cells (macrophages migrate and remove neutrophils; release cytokines which attract fibroblasts and endothelial cells)
  • Regeneration (epithelial cells proliferate and granulation tissue invades the space; angiogenesis progresses)
  • Scarring and maturation (vascular channels regress, leaving an excess of fibrous tissue which matures)
20
Q

When does healing by secondary intention occur?

A

Excisional or infected wounds with a large amount of tissue loss and unopposed edges

21
Q

Describe the process of healing by secondary intention

A
  • Inflammation (more intense response as infection is likely)
  • Granulation tissue (abundant and fills open wound; grows in from the margins)
  • Wound contraction (myofibroblasts contract into centre to close the wound)
  • Scar formation (substantial but depends on the size of wound, no skin appendages present and skin is often thinner)
22
Q

Explain the stages involved in fracture healing

A
  • Haematoma formation and migration of macrophages
  • Macrophages secrete cytokines which attract fibroblasts which secrete ECM of granulation tissue and osteoprogenitor cells
  • Fibroblasts differentiate into chondroblasts which lay down hyaline cartilage, forming a fibrocartilaginous callus (procallus)
  • Endochondral ossification of cartilage forming woven bone. Osteoblasts lay down new woven bone which forms lamellar bone
  • Bone remodelling in response to mechanical stress and normal outline is restored
23
Q

Name 5 local factors which may impair wound healing

A
  • Blood supply
  • Local infection
  • Size, location and type of wound
  • Denervation
  • Presence of foreign bodies or necrotic tissue
24
Q

Name 5 systemic factors that affect wound healing

A
  • Age
  • Diabetes/Obesity
  • Malignancy due to cachexia
  • Drugs e.g. Steroids
  • Vitamin deficiency/malnutrition
25
Q

What are the complications of fibrous repair?

A
  • Formation of fibrous adhesions or replacement of parenchymal tissue with fibrous, which can compromise organ function
  • Distortion of tissue architecture e.g. cirrhosis
  • Keloid scar formation
  • Wound dihisence
  • Excessive scar contraction (cause strictures or fixed flextures)
26
Q

Describe the process of healing following a myocardial infarction

A
  • Cardiac myocytes are permanent cells which cannot proliferate and undergo regeneration
  • Damaged myocardium undergoes fibrous repair and scar tissue is formed
27
Q

Why is healing of cartilage poor?

A

Lacks blood supply, lymphatic drainage and innervation

28
Q

Describe 2 instances where permanent cells may be replaced by supporting cells

A
  • CNS - damaged neurones are replaced by glial cells via process of gliosis
  • Skeletal muscle - damaged myocytes are reinforced by satellite cells which fuse with existing muscle fibres and cause hypertrophy
29
Q

Describe the healing of a peripheral neve

A
  • Severed axons undergo Wallerian degeneration
  • Proximal stumps sprout and elongate and use Schwann cells from the distal stump to guide them back (grow 1-3mm/day)
  • May require surgery if the axon ends are unopposed

ESA2 - Mechanisms Of Disease (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions