Tissue Repair

4. TISSUE REPAIR
The body has many techniques for protecting itself from uninvited
“guests” or injury.

5. Tissue Repair
 Intact mechanical barriers such as the skin
and mucosae, the ciliary activity of epithelial
cells lining the respiratory tract, and a strong
acid (chemical barrier) produced by stomach
glands represent three defenses exerted at
the body’s external boundaries.

6. Tissue Repair
 When tissue injury occurs these barriers are
penetrated, this stimulates the body’s
inflammatory and immune responses, which
wage their battles largely in the connective
tissues of the body.

7. Tissue Repair
Inflammatory Response:
The inflammatory response is a relatively
nonspecific reaction that develops quickly
and occurs whenever and wherever tissues
are injured .Essentially, inflammation acts to
get rid of the harmful agent, prevent further
injury, and restore the tissue to a healthy
condition.

8. Tissue Repair
Immune Response:
The immune response, on the other hand, is
extremely specific, but takes longer to swing
into action.
Cells of the immune system, programmed to
identify foreign substances such as
microorganisms, toxins, and cancer cells,
mount a vigorous attack against specific
recognized invaders, either directly or by
releasing antibodies into the blood.

9. Steps of Tissues Repair
1.Inflammation sets the stage:
Let us briefly examine the inflammatory events
that tissue injury sets into motion.
 First , the tissue trauma causes injured tissue
cells, macrophages, mast cells, and others to
release inflammatory chemicals which causes
the capillaries to dilate and become very
permeable.

10. 1.Inflammation sets the stage:
 This allows white blood cells and plasma fluid
rich in clotting proteins, antibodies, and other
substances to seep into the injured area.
 Then the leaked clotting proteins construct a
clot, which stops the loss of blood, holds the
edges of the wound together, and effectively
walls in, or isolates, the injured area,
preventing bacteria, toxins, or other harmful
substances from spreading to surrounding
tissues.

11. 1.Inflammation sets the
stage:
 The part of the clot exposed to air quickly
dries and hardens , forming a scab.The
inflammatory events leave excess fluid, bits
of destroyed cells, and other debris in the
area.
 Most of this material is eventually removed
from the area via lymphatic vessels or
phagocytized by macrophages during the
repair process.

12. Tissue Repair

13. Tissue Repair

14. 2. Organization restores the
blood supply:
 During organization the blood clot is replaced
by granulation tissue.
 Granulation tissue; is a delicate pink tissue
composed of several elements.
 It contains capillaries that grow in from
nearby areas and lay down a new capillary
bed.

15. 2. Organization restores the
blood supply:
 Granulation tissue is actually named for these
capillaries, which protrude nublike from its
surface, giving it a granular appearance.
 These capillaries are fragile and bleed freely,
as demonstrated when someone picks at a
scab.
 Also present in granulation tissue are
proliferating fibroblasts that produce growth
factors as well as collagen fibers to bridge the
gap.

16. 2. Organization restores the
blood supply:
 Some of these fibroblasts have contractile
properties that pull the margins of the wound
together.
 As organization proceeds, macrophages
digest the original blood clot and the deposit
of collagen fibers continues.

17. 2. Organization restores the
blood supply:
 The granulation tissue, destined to become
scar tissue (a permanent fibrous tissue patch),
is highly resistant to infection because it
produces bacteria-inhibiting substances.

18. 3. Regeneration and fibrosis
effect permanent repair:
 During organization, the surface epithelium
begins to regenerate, growing under the
scab, which soon detaches.
 As the fibrous tissue beneath matures and
contracts, the regenerating epithelium
thickens until it finally resembles that of the
adjacent skin.

19. 3. Regeneration and fibrosis
effect permanent repair:
 The end result is a fully regenerated
epithelium, and an underlying area of scar
tissue.
 The scar may be invisible, or visible as a thin
white line, depending on the severity of the
wound.

20. Tissue Repair
 The above process described above follows of
a wound (cut,scrape,puncture) that breaches
an epithelial barrier.
 In pure infections (a pimple or sore throat),
healing is solely by regeneration.
 Only severe (destructive) infections lead to
scarring.

21. Capacity for regeneration
The capacity for regeneration varies widely
among the different tissues.
 Epithelial tissues regenerate extremely well,
as do bone, areolar connective tissue, dense
irregular connective tissue, and blood
forming tissue.
 Smooth muscle and dense regular connective
tissue have a moderate capacity for
regeneration.

22. Capacity for regeneration
 Skeletal muscle and cartilage have a weak
regenerative capacity.
 Cardiac muscle and the nervous tissue in the
brain and spinal cord have no functional
regenerative capacity ; hence they are
routinely replaced by scar tissue.

23. Scar Tissue
 In nonregenerating tissues and in
exceptionally severe wounds, fibrosis totally
replaces the lost tissue.
 Over a period of months, the fibrous mass
shrinks and becomes more and more
compact.
 The resulting scar appears as a pale , often
shiny area composed mostly of collagen
fibers.

24. Scar Tissue
 Scar tissue is very strong, but it lacks the
flexibility and elasticity of most normal
tissues.
 It cannot perform the normal function of the
tissue it has replaced.

25. Platelets
 Platelets are the smallest of the three major
types of blood cells.
 Platelets are only about 20% of the diameter
of red blood cells, the most numerous cell of
the blood. The normal platelet count is
150,000-350,000 per micro liter of blood, but
since platelets are so small, they make up just
a tiny fraction of the blood volume. The
principal function of platelets is to prevent
bleeding.

26. Platelet Production
Platelets are produced in the bone marrow, the
same as the red cells and most of the white
blood cells. Platelets are produced from very
large bone marrow cells called
megakaryocytes. As megakaryocytes develop
into giant cells, they undergo a process of
fragmentation that results in the release of over
1,000 platelets per megakaryocyte. The
dominant hormone controlling megakaryocyte
development is thrombopoietin (often
abbreviated asTPO).

27. Platelets structure
 Platelets are actually not true cells but merely
circulating fragments of cells.
 But even though platelets are merely cell
fragments, they contain many structures that
are critical to stop bleeding.
 They contain proteins on their surface that
allow them to stick to breaks in the blood
vessel wall and also to stick to each other.

28. Platelets structure
 They contain granules that can secrete other
proteins required for creating a firm plug to
seal blood vessel breaks.
 Also platelets contain proteins similar to
muscle proteins that allow them to change
shape when they become sticky.

29. Platelet Function
 Platelets serve three primary functions:
1) sticking to the injured blood vessel (called
platelet adherence).
2) attaching to other platelets to enlarge the
forming plug (called platelet aggregation).
3) providing support (molecules on the surface
of platelets are required for many of the
reactions) for the processes of the
coagulation cascade.

30. Platelet Function
 Platelets are not only the smallest blood cell, they
are the lightest. Therefore they are pushed out from
the center of flowing blood to the wall of the blood
vessel.
 There they roll along the surface of the vessel wall,
which is lined by cells called endothelium.
 The endothelium is a very special surface, likeTeflon,
that prevents anything from sticking to it.
 However when there is an injury or cut, and the
endothelial layer is broken, the tough fibers that
surround a blood vessel are exposed to the liquid
flowing blood.

31. Platelet Function
 It is the platelets that react first to injury.
 The tough fibers surrounding the vessel wall,
like an envelop, attract platelets like a
magnet, stimulate the shape change , and
platelets then clump onto these fibers,
providing the initial seal to prevent bleeding,
the leak of red blood cells and plasma
through the vessel injury.

32. Platelet Function

33. Clotting Cascade
Introduction:
 The process by which the body prevents
blood loss is referred to as coagulation.
Coagulation involves the formation of a blood
clot (thrombus) that prevents further blood
loss from damaged tissues, blood vessels or
organs.

34. Clotting Cascade
 This is a complicated process with a cellular
system comprised of cells called platelets that
circulate in the blood and serve to form a platelet
plug over damaged vessels.
 A second system based upon the actions of
multiple proteins (called clotting factors) that act
in concert to produce a fibrin clot.These two
systems work in concert to form a clot; disorders
in either system can yield disorders that cause
either too much or too little clotting.

35. Clotting Cascade
Process:
 When a break in a blood vessel occurs,
substances are exposed that normally are not in
direct contact with the blood flow.
 These substances (primarily collagen and von
Willebrand factor) allow the platelets to adhere
to the broken surface.
 Once a platelet adheres to the surface, it
releases chemicals that attract additional
platelets to the damaged area, referred to as
platelet aggregation.

36. Clotting Cascade
 These two processes are the first responses
to stop bleeding.
 The protein based system (the coagulation
cascade) serves to stabilize the clot that has
formed and further seal up the wound.

37. Factors
FactorVII:
Tissue factor and factorVIIa (the ‘a’ denotes the active form of the
factor)
Factor Xa, IIa , Ia:
Activate factor X, forming factor Xa.Factor Xa is then able to activate
prothrombin (also referred to as factor II) to form thrombin
(factor IIa). Thrombin converts fibrinogen to fibrin (factors I and
Ia respectively).
Factor XIII:
Fibrin forms a mesh that, in concert with the platelets, plugs the
break in the vessel wall. The fibrin mesh is further stabilized by
factor XIII, which sews up the clot (much like forming an intricate
network of cross-stitched strands of fibrin).

38. Factors
Factors that Accelerate Clot Formation:
FactorV and factorVIII accelerate the conversion of
factor X to factor Xa by factor IXa (this is done by
factorVIII) and accelerate the conversion of
prothrombin to thrombin as done by factor Xa.
Factors that Inhibit (Slow Down) Clot
Formation:
Protein C, protein S and thrombomodulin form a
complex (group of proteins) that can inactivate
factorVIII and factorV. The protein C, protein S and
thrombomodulin complex is activated by thrombin.

39. Factors
Antithrombin:
Antithrombin
(formerly called
antithrombin
III) serves to
block the
actions of
multiple
clotting factors
(called
inhibition).

41. Blood Groups
 Blood is a complex, living tissue that contains
many cell types and proteins. A transporter,
regulator, and defender, blood courses through the
body carrying out many important functions.

42. PROTEINS & BLOOD TYPES:
 Distinct molecules called
agglutinogens (a type of
antigen) are attached to the
surface of red blood cells.
 There are two different
types of agglutinogens, type
"A" and type "B".
 Each type has different
properties. The ABO blood
type classification system
uses the presence or absence
of these molecules to
categorize blood into four
types.

43. Four Type Of Blood

44. Blood Transfusion
 When conducting a blood transfusion, it is
important to carefully match the donor and
recipient blood types.
 If the donor blood cells have surface
molecules that are different from those of
the recipient, antibodies in the recipient's
blood recognize the donor blood as
foreign.
 This triggers an immune response
resulting in blood clotting.

45. Blood Transfusion
 If the donor blood cells have surface
molecules that are the same as those of
the recipient, the recipient's body will not
see them as foreign and will not mount an
immune response.

46. RH Factors
 Scientists sometimes
study Rhesus monkeys
to learn more about the
human anatomy.
 While studying Rhesus
monkeys, a certain
blood protein was
discovered.
 This protein is also
present in the blood of
some people. Other
people, however, do
not have the protein.
A+ A-
B+ B-
AB+ AB-
O+ O-

47. RH Factors
 The presence of the protein, or lack of
it, is referred to as the Rh (for Rhesus)
factor.
 If your blood does contain the protein,
your blood is said to be Rh positive
(Rh+). If your blood does not contain
the protein, your blood is said to be Rh
negative (Rh-).

48. HOMEOSTASIS

49. Everyday your body is affected
by many things

50. Is the way your body keep balance

51. Introduction
 Homeostasis is the property of a system that
regulates its internal environment and tends
to maintain a stable, relatively constant
condition of properties.
 All homeostatic control mechanisms have at
least three interdependent components for
the variable being regulated:
 The receptor
 The control center
 The effector

52. Three components of
Homeostasis

53. Positive feedback &
Negative feedback

54. Positive feedback
 Positive feedback is a mechanism by which an
output is enhanced.
 Positive feedback mechanisms are designed
to accelerate or enhance the output created
by a stimulus that has already been activated.

55. Negative feedback
Negative feedback mechanisms consist of
reducing the output or activity of any organ or
system back to its normal range of functioning.

56. Negative feedback

57. Thermal Balance

58. Body temperature
 Normal body internal temperature is 370C
 Temperatures above this:
denature enzymes and block metabolic
pathways
 Temperatures below this:
slow down metabolism and affect the brain
 We need to regulate internal body
temperature in order to provide the
optimum conditions for enzyme-catalyzed
reactions to be carried out.

59. Control of homeostasis
 When your body gets
too hot, your body
need cooling down by:
sweating, vasodilation,
etc…
 When your body gets
too cold, you also need
warming up by:
Shivering,
vasoconstriction, etc…

60. Glucose
Homeostasis

61. About glucose in the body
 Glucose is a monosaccharide which represents an essential
biological energy source, enabling the generation of ATP
following glycolysis
 Although many tissues can also use fats and protein as an
energy source, the brain and red blood cells can only use
glucose.
 Glucose is stored in the body, importantly in the liver, as
glycogen.

62. Circulating levels of glucose
 Circulating levels of glucose are controlled by
two enzymes, insulin and glucagon.
glucagoninsulin

63. High glucose levels
 In response to high glucose levels, pro-insulin is released from
pancreatic beta cells in the islets of Langerhans and is converted to
the active form in the blood.
 Insulin stimulates the uptake of glucose and storage in the tissues as
glycogen (glycogenesis).

64. Low glucose level
 In contrast, low glucose levels cause secretion of
pancreatic peptide hormone glucagon from alpha
cells.
 Glucagon promotes the conversion of liver glycogen
to glucose (glycogenolysis) and release of glucose
back into the blood.
 During starvation and intense exercise, glucose can
also be generated from non-carbohydrate precursors
(i.e. pyruvate, amino acids and glycerol), in a
process called gluconeogenesis.

66. Diabetes mellitus
 Disruption of glucose homeostasis is most
commonly studied in the field of diabetes
mellitus, a metabolic syndrome in which
patients do not produce suffi cient levels
of, or correctly respond to, insulin.

67. References
 Human Anatomy & Physiology, Fifth Edition,
Elaine N. Marieb, Chapter 4,Tissue:The
Living Fabric ;Tissue Repair, Page No. 138-140
 www.admin.med.uiuc.edu/hematology
 www.slideshare.com

68. Thank you
For listening to us