Practice 6

1. In integumentary system, keratinocytes are one of their major cells. Discuss the
molecular composition and physiological significance of keratinocytes in the
epidermis. (5 Marks)

Keratinocytes are the predominant cell type of epidermis and originate in the
outermost layer of the skin. This cell undergoes a process called keratinisation where
the keratin is synthesised. Keratinocytes are also responsible for the formation of the
epidermal water barrier by secreting lipids. The molecular composition of the
keratinocytes is keratin proteins, desmosomes and lipids. Keratin proteins are the
primary component of keratinocytes. Keratin protein is made of structural proteins
that form intermediate filaments. The differences between the types of keratin can be
varied by their expressions on the different layers of the epidermis. Next is the
desmosomes. Desmosomes are the structures that connect the keratinocytes tightly to
each other. This component provides strength and resistance to mechanical stress. The
lipids are the products of the secretion and production of keratinocytes. For example,
ceramides are used to form the skin’s barrier function. The barrier is important to
prevent further water loss and protect the overall cell from pathogens from outside.

The physiological significance of the keratinocytes is the barrier function.

Keratinocytes contribute to the formation of the skin barrier which is in the outermost
layer of the epidermis. The stratum corneum which is composed of layers of dead
keratinized cells which can be found in the outer layer of the epidermis acts as a
protective barrier against pathogens and dehydration. The keratinocytes are also
important for wound healing. There is regeneration of the epidermis layers when there
are any injuries or wounds on the skin. Keratinocytes proliferate and migrate to cover
the damaged areas and repair them which leads to the healing process of the wound.
2. There are 3 factor to determine a human skin color. One of common skin color
are related with melanin, which is the color of yellow until dark skin color.
Explain in detail the role of melanocytes in skin pigmentation and how variations
in melanin production contribute to different skin tones. (10 Marks)

Deeper down in the epidermis right at the base of the later, is the melanocytes.
Melanocytes are star-shaped and produce the important pigment melanin. Melanin is
produced inside spere-like throughout the melanocyte. The spheres are called
melanosomes. Chemical reactions inside melanosomes turn the amino acid tyrosine
into melanin. The proportion of two main forms of melanin produced a reddish-
yellow type versus a black-brown type. The total amount of melanin in each
melanosome and the number of melanosomes in the epidermis all vary from person to
person and determine their skin colour. For the melanin to function as it is, the
melanosomes need to be transported to the keratinocytes.

Exposure to ultraviolet radiation from the sun stimulates melanocytes to produce

more melanin. The melanin inside the melanosome absorbs the ultraviolet energy
from the sunlight reducing the amount of ultraviolet radiation that reaches the
nucleus, in particular, the DNA inside the nucleus. When ultraviolet radiation
increases, more melanosomes are delivered to keratinocytes. The tanning response is
an example of how melanocytes respond to UV exposure by producing more melanin
leading to darker skin tone.

While the number of melanocytes is relatively consistent among individuals of

different ethnic backgrounds, the distribution and density of melanocytes can vary.
The variation in melanocyte activity and distribution across skin contributes to the
diversity of skin tones. Genetic factors play a significant role in determining the type
and amount of melanin produced by melanocytes. Different populations around the
world have evolved specific genetic variations that influence skin pigmentation. The
regulation of melanin production is influenced by various genes, with one of the key
players being the melanocortin 1 receptor (MC1R) gene. Genetic variations in these
genes can lead to differences in the type and amount of melanin produced,
contributing to individual variations in skin colour. Different ethnic groups exhibit
characteristic skin tones due to their genetic makeup and evolutionary adaptations to
their respective environments. Populations from regions with high levels of UV
radiation, such as near the equator, often have darker skin to provide better protection
against the harmful effects of UV rays
3. Integumentary system is capable to synthesis a vitamin D from natural source.
Analyze the adaptive mechanisms of the integumentary system in response to UV
radiation, highlighting the role of melanin and vitamin D synthesis.

One of the primary responses to UV radiation is the increased production of melanin,

the pigment responsible for skin colour. UV rays cause the production of melanin
which is a chemical in the skin. This is the skin’s first defence against UV radiation.
When skin cells are damaged by the UV, melanocytes release a dark pigment called
melanin. Melanin can absorb UV light so the body uses melanin as a kind of UV
shield. Melanin effectively blocks the UV rays from our DNA. When the skin is
exposed to the sun, melanin production increases. Melanin absorbs and dissipates UV
radiation, preventing it from penetrating deeper layers of the skin. Exposure to UV
radiation stimulates melanocytes, the cells that produce melanin, to increase melanin
synthesis. This adaptive mechanism results in tanning, which provides some degree of
protection against further UV damage. A tan is a sign that your skin is trying to keep
UV rays from damaging your skin. But melanin isn’t able to completely stop skin
damage from UB radiation. Vitamin D is synthesised in response to UV radiation.
While excessive UV exposure can be harmful, moderate exposure is essential for the
synthesis of vitamin D in the skin. Vitamin D is crucial for calcium absorption and
bone health. When the skin is exposed to UV light, the UV rays react with an enzyme
called 7-dehydrocholestrol. This reaction creates pre-vitamin D. Then, the pre-vitamin
D rearranges its structure to form vitamin D.
4. Explain in detail THREE (3) mechanism of skin bleeding. With a suitable
diagram, illustrate the cellular and molecular components involved in the
homeostatic response to skin bleeding, emphasizing the role of platelets and
clotting factors. (10 Marks).
The skin bleeding mechanism starts with vasoconstriction. The smooth muscle in the
wall of the vessel will constrict to reduce the blood flow to the injured area when a
blood vessel is injured. This response is called vasoconstriction. Vasoconstriction
minimizes the blood loss that happens because of the injured vessel. The blood loss is
being minimized by decreasing the diameter of the blood vessel. This rapid and
temporary response provides the needed time for the other homeostatic mechanisms
to take place. Moving to the second hemostatic mechanism of the skin bleeding which
is the primary hemostatic which also can be called the platelet plug formation.
Platelets that circulate in the blood stick to the damaged tissue and get activated which
means more platelets can recruit more platelets to form a platelet plug. This is to stop
blood loss from the damaged area. After vasoconstriction, the platelets adhere to the
exposed collagen fibres at the injured area. Collagen when it gets exposed, triggers
platelet activation. The nearby platelets become sticky when the platelets release
chemicals causing them to adhere to each other. This forms a plug that seals small
breaks in the injured blood vessel. Platelet plugs can also be called white thrombus.
The last mechanism of the skin bleeding is the coagulation. Coagulation is the most
complex phase of hemostasis of the skin bleeding. Coagulation involves a cascade of
events which leads to a stable formation of blood clots. intrinsic and extrinsic
pathways converge at the activation of Factor X, along with other factors, converting
prothrombin into thrombin. Thrombin converts fibrinogen into fibrin threads fibrin
threads weave through the platelet plug to form a more stable red thrombus or blood
clot. The clot serves as a more permanent seal for the damaged blood vessel.
5. Explore the cellular and molecular components involved in the homeostatic
response to burning, emphasizing the role of recovery for 1 st degree and 2nd
degree burning factors. (5 Marks)

The inflammatory response. In the cellular components, the neutrophils and

macrophages which are immune cells migrate to the site of injury engulfing the debris
and pathogens and the mast cells in the molecular components release histamines
which trigger vasodilation and increase the permeability of blood vessels whereas in
the molecular components, cytokinesis and chemokines signal the recruitment of
immune cells and the prostaglandins contribute to the inflammation and pain.
Furthermore, the vasodilation and increased permeability. The endothelial cells in the
cellular components respond to inflammatory signals by relaxing and increasing
permeability. As in the molecular components, the nitric oxide causes vasodilation
while the vascular endothelial growth factor induces angiogenesis. The next recovery
burn factor is fibroplasia and collagen deposition. In the cellular components, the
fibroblasts produce collagen and other extracellular matrix components. The
transforming growth factor beta stimulates collagen synthesis and the platelet-derived
growth factor promotes cell migration and angiogenesis.
6. Internal and external bleeding normally will be control by our body hemostasis.
Explain in detail the significance of the fibrinolysis process in the resolution of a
blood clot formed during the homeostatic response to skin bleeding. Discuss the
specific enzymes involved and their actions. (15 Marks).

The fibrinolysis starts with fibrin structure. Fibrin is a fibrous protein that forms a
mesh during the coagulation process. This mesh, along with platelets, creates a stable
clot to seal the wound and prevent excessive bleeding. Next is the plasminogen
activation. Plasminogen is an inactive precursor present in the fibrin clot. It is
incorporated into the fibrin mesh during clot formation. The conversion of
plasminogen to its active form, plasmin, is a key step in fibrinolysis. Then, the
plasmin activation. Plasminogen activation is catalyzed by activators such as tissue
plasminogen activator (tPA) and urokinase plasminogen activator (uPA). Tissue
plasminogen activator is released by endothelial cells and is considered a primary
activator in fibrinolysis. The fourth step is plasmin action. Once activated, plasmin
acts as a protease, cleaving fibrin into smaller fragments called fibrin degradation
products (FDPs) or fibrin split products. Plasmin is highly effective in breaking the
cross-linked fibrin structure, leading to the dissolution of the clot. The last step is the
fibrinolysis regulation. The fibrinolysis process is tightly regulated to prevent
excessive clot breakdown and potential bleeding complications. Plasmin activity is
controlled by plasminogen activator inhibitors (PAIs), which regulate the activity of
tPA and uPA. Alpha-2-antiplasmin is a crucial inhibitor that directly inhibits free
plasmin.
The significance of the fibrinolysis process is restoration of blood flow. Fibrinolysis
helps in breaking down the fibrin clot, allowing the restoration of normal blood flow
in the affected blood vessels. This is essential to maintain the circulation of blood and
oxygen to tissues. Moreover, it prevents the thrombosis. Fibrinolysis plays a crucial
role in preventing the inappropriate formation of blood clots within the vascular
system, a condition known as thrombosis. If clots persist beyond their necessary
function, they can lead to complications such as embolism or other vascular disorders.
Last but not least is the tissue repairing and healing. By resolving the blood clot,
fibrinolysis contributes to the overall tissue repair and healing process. Once bleeding
is under control, the removal of the clot allows for subsequent tissue regeneration
7. Bone modeling is one of negative feedback of human body. By use a suitable
diagram, illustrate and explain in detail the concept of bone remodeling as a
dynamic process in maintaining skeletal homeostasis, considering the activities of
osteoblasts and osteoclasts (10 Marks).
The bone remodelling starts with activation. The process begins with the activation of
bone remodelling. Various stimuli, such as mechanical stress, hormonal signals, or
microdamage in the bone, trigger the need for remodelling. Signals, such as
mechanical stress or hormonal changes, trigger the activation of osteoclasts and
osteoblasts. This is the initial phase of bone remodelling. The second step is
 resorption or bone resorption. Osteoclasts, specialized cells derived from monocytes
and macrophages, are activated and migrate to the site of remodelling. Osteoclasts
secrete enzymes and acids that break down and dissolve the mineralized bone matrix.
Calcium and phosphate are released into the bloodstream during this resorption phase.
After resorption, there is a reversal phase during which the bone undergoes a
transition from resorption to formation. This phase involves the recruitment of cells
known as osteoblasts. Osteoclasts are replaced by osteoblasts. The third step is the
bone formation. Osteoblasts, bone-forming cells, deposit new bone matrix onto the
resorbed surface. This matrix is initially unmineralized and is composed mainly of
collagen. Osteoblasts produce osteoid, a protein-rich material that serves as a
framework for the deposition of minerals. the next step is continued by
mineralization. Calcium and phosphate ions in the osteoid matrix gradually
mineralize, forming hydroxyapatite crystals and turning the osteoid into mature,
mineralized bone tissue. Last but not least is the quiescence step. Following the
formation phase, some osteoblasts become embedded in the bone matrix and become
osteocytes. Osteocytes are relatively inactive but play a role in sensing mechanical
strain and signalling for further remodelling if needed.

8. Homeostasis of human body is close related with a hormonal mechanism.

Differentiate the role of the regulatory hormones and growth factors in the
homeostasis of bone fracture repair. Discuss how factors like parathyroid
hormone and bone morphogenetic proteins influence the healing process. (15
Marks)
 Two regulatory hormones are involved in the homeostasis of bone fracture repair
which are the parathyroid hormone and the calcitonin. The parathyroid hormone
(PTH) is produced by the parathyroid glands and plays a vital role in calcium
homeostasis. It helps regulate calcium levels in the blood by stimulating the release of
calcium from bones when blood calcium is low. Next is the calcitonin. Calcitonin is
produced by the thyroid gland and opposes the action of PTH by promoting calcium
deposition in bones.
Just like the regulatory hormones, two different growth factors are involved in the
homeostasis of bone fracture repair. They are bone morphogenetic proteins and
insulin-like growth factors. The bone morphogenetic proteins (BMPs) are growth
factors that belong to the transforming growth factor-beta (TGF-β) superfamily where
they hold a crucial role in bone formation and repair. The next growth factor is the
insulin-like growth factor (IGF). Insulin-like growth factor is a growth factor that
plays a role in cell growth, differentiation, and development.
As for the healing process, the parathyroid hormone (PTH) stimulates the activity of
osteoclasts, which are cells responsible for breaking down bone tissue. This process is
known as bone resorption. Osteoclasts, under the influence of PTH, break down the
mineralized bone matrix, releasing calcium into the bloodstream. This is essential for
maintaining systemic calcium homeostasis and providing the necessary mineral
resources for the bone repair process. PTH promotes bone remodelling by influencing
the balance between bone resorption and bone formation. PTH also indirectly
supports the subsequent bone formation phase while it stimulates osteoclasts to break
down bone.
As for the healing process of bone morphogenetic proteins (BMPs), BMPs play a
crucial role in the early stages of bone fracture repair by promoting the differentiation
of mesenchymal stem cells into osteoblasts. Mesenchymal stem cells are precursor
cells that have the potential to become various cell types, including bone-forming
osteoblasts. BMPs induce the expression of genes associated with osteogenesis,
leading to the production of extracellular matrix proteins and the formation of a
cartilaginous callus at the site of the fracture. By enhancing osteoblast activity and
promoting the synthesis of bone matrix components, BMPs contribute to the
acceleration of bone formation and the eventual remodelling of the callus into mature
bone tissue.

9. Evaluate the impact of vitamin D on calcium regulation in the skeletal system.

Discuss how vitamin D influences calcium absorption in the intestines and its role
in bone health. (5 Marks)
 Vitamin D plays a vital role in calcium regulation in the skeletal system of a human’s
body. First of all, for the calcium absorption in the intestines. There are two processes
involved which are the stimulation of calcium absorption and the active form of
vitamin D. In the stimulation of calcium absorption, vitamin D enhances calcium
absorption in the small intestines. During the absence of vitamin D, the efficiency of
calcium absorption decreases significantly in the intestines. Vitamin D also stimulates
the synthesis of calcium-binding proteins in the intestinal cells. Next is the active
form of vitamin D. Calcitriol, the active form of vitamin D plays an important role
when it binds to vitamin D receptors in the intestines promoting the expression of
proteins which facilitates the active transport of calcium across the intestinal lining.
As for bone health, there are three processes: calcium homeostasis, bone
mineralization and prevention of rickets and Osteomalacia. For calcium homeostasis,
the skeletal system serves as a reservoir for calcium in the body. A correct amount of
vitamin D is essential to maintain calcium homeostasis ensuring a balance between
absorption in intestines, calcium release from the bones and the calcium excretion by
the kidneys. Continuing with bone mineralization. Bone mineralization is the process
of incorporating minerals especially calcium into the bone matrix which is why
vitamin D is vital in bone mineralization. The strength and integrity of the bones are
the results of proper mineralization.

10. Lacked some mineral such as calcium, magnesium, phosphate and other types of
minerals cause some disease to our body. Explain the effects of hormonal
imbalances on the homeostasis of calcium ions and other minerals and compared
a condition such as hyperparathyroidism and hypoparathyroidism and their
impact on bone health.
(15 Marks).

The parathyroid hormone (PTH) is one of the hormones that undergo hormonal
imbalances in the homeostasis of calcium ions. PTH is released by the parathyroid
glands in response to low blood calcium levels. The effect of imbalance can be seen in
two different cases. First of all, hyperthyroidism happens because of excess PTH.
Hyperthyroidism leads to an increase in the release of calcium from bones which can
be called bone resorption weakening the bone structures. This enhances the
reabsorption of calcium in the kidneys which can result in elevated blood calcium
levels and hypercalcemia. The second case is hypoparathyroidism which occurs
because of insufficient PTH. Hypoparathyroidism reduces the release of calcium from
bones and decreases the reabsorption of calcium in the kidneys. This can lead to
decreased blood calcium levels and hypocalcemia. Hypocalcemia where the calcium
levels in the blood are low, can lead to muscle cramps, spasms, and increased
neuromuscular excitability.

The next hormonal imbalance includes calcitonin. Calcitonin is produced by the

thyroid glands and acts in opposition to PTH. It is released in response to high blood
calcium levels and works to lower them. The effects of imbalances in calcitonin are
less common, but if they are present, they can affect calcium homeostasis by
influencing bone resorption and deposition. Effects on Bones of calcitonin is that
calcitonin promotes the deposition of calcium into bones, inhibiting bone resorption.
It helps regulate the storage of calcium in the bones.

Furthermore, vitamin D. Vitamin D is essential for the absorption of calcium and

phosphate from the intestines. Vitamin D deficiency is the effect of imbalance.
Vitamin D deficiency reduces the absorption of calcium and phosphate from the
intestines and impairs bone mineralization. This can lead to conditions like rickets in
children and osteomalacia in adults. The effects on bones of vitamin D imbalance is
that the vitamin D promotes the absorption of dietary calcium and phosphate from the
intestines, contributing to bone mineralization and strength.

Hypoparathyroidism is an uncommon condition that happens when the parathyroid

glands produce abnormally low levels of parathyroid hormone (PTH) and calcium
levels fall below normal. The PTH is a key to regulating and maintaining a balance
between two minerals in the body which are calcium and phosphorus. So the low
production of PTH in hypoparathyroidism leads to low levels of calcium in the blood
and an increase of phosphorus in the blood. Hypoparathyroidism symptoms include
muscle cramps, spasms, and neurological issues due to low calcium levels.
Hypoparathyroidism is usually treated with a special form of vitamin D (calcitriol)
and with calcium tablets. Careful monitoring is required to optimize the dosages.
Hyperparathyroidism occurs when the parathyroid glands create high amounts if
parathyroid hormone in the bloodstream even though calcium levels are higher than
normal. These parathyroid glands are located behind the thyroid at the bottom of the
neck and are about the size of a grain of rice. There are two types of
hyperparathyroidism. In primary hyperparathyroidism, an enlargement of one or more
of the parathyroid glands causes overproduction of parathyroid hormone. Secondary
hyperparathyroidism occurs due to another disease that first causes low calcium levels
in the body. Over time, increased parathyroid hormone levels occur as the body fights
to keep the calcium level up in the standard range. Hyperparathyroidism may cause
fatigue, weakness and kidney stones. Hyperparathyroidism may be treated with
surgery to remove overactive glands or medications to control calcium levels