adaption

1. Lecture: The «Compensation-adaptation reactions. Reparative regeneration».
Injury of tissue may result in cell death and tissue destruction. When the tissue has been damaged
during the inflammatory process or in other ways of injury, but the body itself is still alive, the tissue
will heal itself. There is two main process of healing:
1. regeneration – it is healing by proliferation of parenchymal cell, results in complete restoration
of the original tissues
2. repairing - it is healing by proliferation of connective tissue elements resulting in fibrosis and
scarring.
Types of regeneration:
1. Physiological regeneration it is permanent renewal of cells, tissue and organs.
2. Reparative regeneration (restoration) it is renewal of the damaged tissue by the analogical structures.
3. Restructive (pathologic) regeneration it is renewal of the damaged tissue by the analogical or by
other tissues.
PHYSIOLOGICAL REGENERATION (PR).
It is the process of replacement that occurs due to physiologic necrosis (erytrocytes, mucosa). There is
a complete transmission of genetic material during the process of cell division.
Levels of regeneration:
1. molecular-membrane
2. cellular
3. tissue-organ
It is the process of realization of the genetic program, that is secures differentiation of new cells and
apoptosis of the old one.
REPARATIVE REGENERATION (RR) – type of HEALING.
Healing is the body response to injury in an attempt to restore normal structure and function.
Variants of RR:
1. Complete (restitution) – replacement of injured cells by cells of the same type.
2. Incomplete with regenerative hypertrophy (substitution with hypertrophy)
According to the ability to regenerate there are three types of cells.
1. Labile cells – multiply throughout the life under normal physiologic condition. It is surface
epithelial cells of:
- epidermis
- alimentary tract
- respiratory tract
- urinary tract
- vagina
- cervix
- uterine endometrium
- haemopoetic cells of bone marrow, lymph nodules and spleen
2. Stable cells – lose their ability to proliferate after adolescence but return their capacity to
multiply under stimuli throughout adult life. It is parenchymal cells of:
- kidneys
- liver
- adrenal glands
- mesenchymal cells of smooth muscles
3. Permanent cells - lose their ability to proliferate around the time of birth:
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2. - neurons of nervous system
- skeletal muscles cells
- heart muscles cells
Levels of RR:
1. Cellular – bones, epidermis, mucosa, connective tissue, endothelium, hemopoetic system,
lymphoid tissue
2. Intracellular – myocardium, skeletal muscles, ganglious, CNS
3. Mixed – liver, kidneys, lungs, pancreas, endocrine organs, smooth muscles, VNS
HEALING BY PRIMARY INTENTION
A well-approximated surgical wound is the ideal situation for wound healing. Since the edges are close
together and held tight by sutures and fibrin, and there is little necrosis and hopefully no infection, the
healing is by primary union or first intention.
Timetable for "the best possible wound":
minutes: Fibrinogen from the severed vessels is activated via one or the other arms of the clotting
cascade, forms a meshwork, and stops the bleeding. The meshwork also contains platelets.
24 hours: Epithelial cells are regenerating from the edges of the wound surface.
3 days: The fibrin meshwork is extensively invaded by macrophages. Granulation tissue is appearing
at the edges of the incisions. A thin layer of epithelial cells now covers the wound surface.
5 days: Granulation tissue fills the entire wound, and there is abundant collagen.
2 weeks: Fibroblasts continue to multiply, and collagen continues to accumulate.
4 weeks: The overlying epidermis is now normal, though it will not re-grow adnexal structures.
Capillary involution and scar contraction is well underway, and the red scar is turning white.
HEALING BY SECONDARY INTENTION
Most wounds do not conform to the above ideal. There is a larger fibrin meshwork (a scab, rich in red
cells), more inflammation, possibly infection, more granulation tissue, and more spectacular wound
contraction.
When epidermis grows underneath some of the fibrin meshwork, the edges of the scab loosen. When
re-epithelialization is complete, the scab falls off.
As surface epithelium grows into crevices (i.e., down suture tracks, etc.), it excites excessive
fibroblastic activity. This is why there's more scarring where the sutures were.
Scarring by secondary intention always produces some deformity.
1. crippling contarcture
2. exuberant granulations
3. keloids - disfiguring scars with excessive collagen production
PATHOLOGIC REGENERATION or REPAIRING
Repair – is the replacement of injured tissue by fibrous tissue (substitution).
Forms:
1. hyporegeneration
2. hyperregeneration
3. metaplasia
REPAIR BY CONNECTIVE TISSUE
A few hours after injury, there is already evidence of connective tissue repair. Fibroblasts become
active and begin to proliferate, and buds ("angioblasts") sprout from the damaged capillaries.
The fibroblasts produce ground substance, fibronectin, and type III collagen; later they will produce
type I collagen for the mature scar. Of course, there are plenty of macrophages (to keep the new tissue
clean) and mast cells.
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3. The new tissue is called granulation tissue ("immature scar", etc.), and the fibrin meshwork is said to
be undergoing organization..
If any repair by fibrous tissue occurs, there will be a scar. Depending on the site, scar tissue may be
called:
1. "cicatrix",
2. "fibrosis",
3. "adhesions",
4. "gliosis",
5. "fibroplasia"
OUTCOMES OF REPARATIVE and PATHOLOGIC REGENERATION:
1. Complete renewal of structure and function of the damaged organ at:
а) shallow and small damage
б) inlaid damage of endothelium without violation of basal membrane
в) damage of epithelium of ducktal of canals.
Localization:
- cornea of eyes
- epithelium of any organ
- skin
- kidney, lungs, after the inlaid damage of alveolus, endothelium, epithelium of kidney canals.
2. Substitution – incomplete structural renewal of the damaged organ. There is partial or complete
renewal of function of organs, only at the ordinary physical loading. Arises up after:
- deep and vast damages
- heart attacks and necrosis
- festering-destructive processes
- micotical (fungi’s) process
- haematoma or hemorrhage in the serosis cavity
- damage of vessels, canals, channels with destruction of their basal membranes
- inlaid necrosis of the specialized structures
- deep ulcers, penetrable in the muscular layer of hollow organ.
Variants of renewal after the infarcts and strokes:
1. Substitution in heart by the connecting tissue or gliofibrosis in brain.
2. Cyst of brain, chronic aneurism of heart.
3. Renewal of functions.
Variants of substitution in other organs:
1. hearth sclerosis or cirrhosis of organ.
2. formation of cyst.
3. cavity – at destroying of content through the natural opening
4. incapsulation
5. formation of swish
6. formation of joints in serozis cavities and their partial or complete obliteration
7. ossification
8. scar obliteration conclusion channels > hydronefrozis, hydrotsefaliya, hydrotsele, retentsion
cysts (cavity into organ from violation of destroying of secret)
9. cicatrisation of wounds – primary pull, second pull, cicatrisation under scab, crawling of
epithelium, inflammation in wound with subsequent its clearing.
TISSUE-ORGAN LEVEL of DIFFERENTIATION.
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4. It is observed in the damaged organs.
Processes:
1. Renewal of population of cells.
2. Reparative angiogenesis.
3. Renewal of architectonics of stroma.
4. Renewal of specific architectonics of stroma
The beginning of process: initiation of process by macrophages and lymphocytes > synthesis of
interleukins.
Reparative angiogenesis – flows intensively during the first 5 days > saved endothelium is activated
and migrate to the basal membranes, on a new place they divide and forms similarity of capillary tube.
Reparative regeneration of cambial cells – this is cellular reparation.
In the process of reparations of stroma there is fibroklaziya – destruction of fibroblasts. Kelloid scars
are formed at violation of fibroklaziya.
COMPENSATION-ADAPTATION PROCESSES.
Adaptation – this aggregate of physiological processes, that is secures adaptation of cells and organs to
the changing terms.
Compensation – compensation of defects of organ and its adaptation.
Morphology of accommodation:
1. Apoptosis – elimination of surplus of cells
2. Aplasia is the complete failure of an organ to form.
3. Atresia is the complete failure of the lumen, or a portion of the length of the lumen, to form
where it should in a hollow organ.
4. Hypoplasia is the failure of an organ to grow to normal size.
5. Malformation: something was shaped wrong since before birth.
6. Deformation: something used to be well-formed, but its shape was permanently altered, other
than by being cut apart.
7. Atrophy: Shrinkage in the size of the cell by loss of cell substance, without the cell actually
dying. When many cells each become smaller, the organ itself becomes smaller.
8. Hypertrophy: Increase in the sizes of cells, and hence the size of the organ.
9. Hyperplasia: An increase in the number of cells in a tissue or organ. When an organ by
increasing the number of its cells. This may be physiologic, or pathologic.
Examples: The female breast at puberty -- under the influence of estrogens -- and during
pregnancy and lactation (additional hormones). The male breast in cirrhosis or estrogen therapy
or in some boys at puberty ("gynecomastia") -- all reflect estrogens action.
10. METAPLASIA: "(Adaptive) substitution of one type of adult or fully differentiated cell for
another type of adult (or fully differentiated) cell". "A reversible change in which one adult cell
type replaced by another adult cell type.". "Conversion of a differentiated cell type into
another" .
Examples:
Replacement of airway pseudostratified mucin-producing ciliated columnar epithelium
by stratified squamous epithelium (cigaret smokers -- "to protect our delicate tissues
from the harsh effects of smoke").
11. DYSPLASIA ("atypia", "atypical hyperplasia", "pre-cancer", etc.): "Bad growth". This implies
a very abnormal epithelium with "loss of uniformity of the individual cells, as well as a loss of
their architectural orientation". This includes "atypical hyperplasia" and "atypical metaplasia"
as well as the unfortunately-named newer term "intra-epithelial neoplasia". Unqualified,
"hyperplasia" and "metaplasia" imply the tissue cells look normal. In dysplasia, they look
distinctly abnormal, and the changes resemble those seen in cancer cells. These weird changes
are called ANAPLASIA.
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