PAPER

The Endocrine and Metabolic System

ENGLISH IN NURSING 1

CLASS: A-1

GROUP 6 MEMBERS:

Lailaturohmah Kurniawati 131411131016

Desy Indah Nur Lestari 131411131052

Kiki Ayu Kusuma 131411131070

Syarif Hidayatullah 131411131088

Niken Ariska Prawesti 131411133002

Bella Nabilla Wijaya K. 131411133020

Fasilitator : Yulis Setiya Dewi, S.Kep.,Ns.,M.Ng

NURSES EDUCATION STUDY PROGRAM

FACULTY OF NURSING
UNIVERSITAS AIRLANGGA
SURABAYA
2015
 PREFACE

First at all, we wanted to thank God for His love and grace.

Thanks to God for helping and giving us the chance to finish this
assignment on time. And I would like to thank Mrs.Yulis Setiya Dewi,
S.Kep.,Ns.,M.Ng. as the lecturer that always teaches us and give much
knowledge.

This assignment is the one of English task that composed of The endocrine
and metabolic system We realized this assignment is not perfect. But I hope it can
be useful for us. Critics and suggestion is needed here to make this assignment be
much better.

Hopefully, we, as a student in “Faculty of Nursing Airlangga University”

can work more professional by using English as the second language whatever we
done. Thank you.

Authors

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 CONTENTS
COVER ........................................................................................................... i
PREFACE ....................................................................................................... ii
CONTENTS .................................................................................................... iii
CHAPTER I INTRODUCTION................................................................... 1
1.1 Background .............................................................................................. 1
1.2 Problem Formulation ............................................................................... 2
1.3 Purposes ................................................................................................... 2
1.4 Benefits .................................................................................................... 3
CHAPTER 2 DISCUSSION .......................................................................... 4
2.1 Anatomy and Physiology of the Endocrine and Metabolic System ....... 4
2.2 Types and Classification of the Endocrine and Metabolic System ........ 11
CHAPTER 3 DIABETES MELLITUS ........................................................ 29
3.1 Definition of Diabetes Mellitus ............................................................. 23
3.2 Type of Diabetes Mellitus ..................................................................... 24
3.3 Etiology of Diabetes Mellitus ................................................................ 25
3.4 Clinical Appearance of Diabetes Mellitus .............................................. 31
3.5 Prevention and treatment of Diabetes Mellitus ...................................... 33
CHAPTER 4 CLOSING ................................................................................ 35
4.1 Conclusion ............................................................................................... 35
REFERENCES ............................................................................................... 36

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 CHAPTER 1

INTRODUCTION
1.1. Background

Endocrine system is found in humans, all the animals, both

vertebrates or invertebrates. Endocrine system of the nervous system

collectively known as super neuroendocrine systems that work together

cooperatively to maintain control and coordination functions in the body.

In general, the endocrine system work to handle a variety of physiological

functions of the body, among other metabolic activity, osmoregulasi,

digestion, growth, and reproduction. Endocrine system is a system of

glands that produce for substance to the body. Endocrine glands produce

the substance that remains outstanding and work in the body.

Ductless glands or channels clogged glands grouped together under

the name of endocrine organs, causes secretion made not leave the gland

through the channels, but directly into the blood circulation in the gland.

The word " endocrine " comes from the Greek meaning " secretion into ".

The main active substance of this internal secretion of the hormone called,

from the Greek word meaning " stimulate " . Some of the endocrine organ

produces a single hormone, whereas others again two or more types of

hormones : eg Pituitary gland produces several hormones that control the

activities of many other organs, which is the gland Pituitary gland is

depicted as " a leader glands of the body ".

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 Hormones are specific chemical compounds produced by certain

endocrine glands. local hormones and hormones are common. examples

of local hormones are : Acetylcholine is released by the ends of neurons

and neural parasimpatis frame. Secretin released by duedenum wall and

transported in the blood to rise toward penkreas secretion of the pancreas

and released in the intestine colesistocinin refined, transported to the gall

bladder gall bladder contractions that arise and pancreatic enzyme

secretion to arise.

1.2. Problem Formulation

As for the problems that will be discussed in this paper are :

1. How are anatomy and physiology of the endocrine and metabolic

system?

2. What are the function of the endocrine and metabolic system of the

human body ?

3. How are the type and classification of the endocrine and metabolic

system of the human body ?

4. What are etiology and clinical appearance of Diabetes Mellitus?

1.3. Purpose

1. Knowing and understanding the anatomy and physiology of the

endocrine and metabolic system of the human body

2. Knowing and understanding the function of the endocrine and

metabolic system of the human body

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 3. Knowing and understanding types and clasification of the endocrine

and metabolic system

4. Knowing and understanding etiology of Diabetes Mellitus

5. Knowing clinical appearances of Diabetes Mellitus

1.4 Benefits

1. Adding insight to students about the endocrine and metabolic

system
2. Increase student knowledge about the clinical appearances of the
endocrine and metabolic system (Diabetes Mellitus)
3. To inform about the endocrine and metabolic system and Diabetes
Mellitus

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 CHAPTER 2

DISCUSSION

2.1 Anatomy and Physiology of the Endocrine and Metabolic System

2.1.1 Anatomy and Physiology

The endocrine system is the regulatory system of the body. The

endocrine system is slower acting, but is very important in terms of health

and disease for its longer acting effects. It works through chemical

messengers called hormones. The endocrine system consist of glands and

hormones that each hormone has a particular function in the body. The

endocrine system is ductless. The glands of the endocrine system are

therefore often referred to as ductless glands. This means the substances

secreted by endocrine glands directly enter the circulatory system or act

directly on specific cells. In contrast, glands such as the salivary glands

secrete their chemicals into ducts. Each endocrine gland secretes one or more

hormones. These are chemical messengers that are typically steroids,

proteins, amino acids, or lipids.

Types of Formed from Examples

compound
Amines Amino acids Norepinephrine, epinephrine
Peptides Amino acids ADH, OT, TRH, SS, GnRH
Proteins Amino acids PTH, GH, PRL
Glycoproteins Proteins and FSH, LH, TSH
carbohydrates

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Steroids Cholesterol Estrogen, testosterone, aldosterone,
cortisol

Steroids are hormones that are built from cholesterol. Steroid

hormones are bound loosely to plasma proteins as they circulate in the blood.

They are lipid-soluble, and like all lipid-soluble substances they can easily

cross cell membranes. They target receptors on the nuclear membrane. Once

inside the nucleus, the steroid hormones turn specific genes on or off. This

results in new products being formed or new functions occurring. Examples

of steroid hormones are aldosterone, estrogen, progesterone, and testosterone.

One major difference between steroid hormones and protein hormones

is that proteins cannot easily cross the cell membrane. This means that these

hormones must have assistance to exert their effects. Receptors are structures

in the cell membranes of a target tissue that combine with a chemical such as

a hormone or drug to alter the functioning of the cell. Once the protein

hormone binds to receptors on the cell membrane, a “second messenger” is

activated. The best example of a second messenger is G-protein, which is the

second messenger that causes the needed changes in the cell. Examples of

hormones that are proteins include growth hormone secreted by the anterior

pituitary gland, calcitonin from the thyroid gland, and antidiuretic (ADH)

hormone from the posterior pituitary gland.

Yet another type of hormone is made up of amino acids, which are the

building blocks of proteins. These hormones also require a second messenger.

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 An example of an amino acid hormone is melatonin, which is secreted by the

pineal gland.

Lipids are the final category of hormones. As lipids, hormones are fat

soluble and easily cross the cell membrane, making a second messenger

unnecessary. Examples of lipid hormones are prostaglandins. They were first

discovered in the prostate gland, they are produced by many cells in the body

including the kidneys, heart, uterus, stomach, and even the brain. They

normally target receptors on nearby organs, so they do not travel through the

blood. The have a role in promoting inflammation, intensifying pain,

increasing fever, involved in smooth muscle contraction, glandular secretions,

and altering the immune response.

Gland Hormone Target Tissue Action Produced

Hypothalamus Antidiuretic Anterior lobe Is stored and released
(produces) hormone (ADH) of pituitary by posterior pituitary
Oxytocin (OT) gland
Anterior pituitary Growth hormone Most tissue in Promotes growth and
(GH) body tissue maintenance
Melanocyte Epidermis of Stimulates pigment
stimulating the skin regulation in
hormone (MSH) epidermis
Adrenocorticotropi Adrenal cortex Stimulates adrenal
c hormone (ACTH) cortex to produce its
hormone
Thyroid Thyroid gland Stimulates in thyroid
stimulating to produce its
hormone (TSH) hormones
Follicle stimulating Ovarian Stimulates ovaries to
hormone (FSH) follicles in produce ova and
female; estrogen; Stimulates
seminiferous testes to produce
tubules of sperm and
testis in male testosterone
Luteinizing Ovary in Stimulates ovaries foe

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 hormone female; testis ovulation and estrogen
(LH) in male production; Stimulates
testes to produce
testosterone
Prolactin (PRL) Mammary Stimulates the breasts
gland to produce milk;
Works with and
complements LH
Posterior pituitary Antidiuretic Kidney Stimulates the kidneys
hormone (ADH) to retain water
Oxytocin (OT) Uterus; Stimulates uterine
mammary contraction for labor
gland and delivery and milk
ejection from breast
Pineal body Melatonin Hypothalamus Regulates biological
clock; Linked to onset
of puberty
Thyroid T3 and T4 Most body Synthesize protein and
cells increase energy
production for all cells
Calcitonin Primarily bone Increases bone
calcium and decreases
blood calcium
Parathyroid Parathyroid Bone, kidney, Acts as antagonist to
hormone (PTH) digestive tract calcitonin; Decreases
bone calcium and
increases blood
calcium
Thymus Thymosin and Tissue Both hormones
thymopoietin involved in stimulate the
immune production of T
response lymphocytes
Adrenal cortex Aldosterone kidney Stimulates the body to
retain sodium and
water
Cortisol Kidney Decreases protein
synthesis; decreases
inflammation
Adrenal medulla Epinephrine and Heart, blood Prepare body for
norepinephrine vessels, liver, stress; increase heart
adipose rate, respiration, and
blood pressure
Pancreas (islet of Alpha cells- Liver Increases blood sugar;
Langerhans) glucagon Decreases protein
synthesis
Beta cells-insulin General, but Decreases blood

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 especially sugar; Increases
liver, skeletal protein synthesis
muscle,
adipose
Gonads: ovaries Estrogen and Most body Develop secondary
(female) progesterone cells, uterus, sex characteristics;
and breast female sex hormone
Testes (male) testosterone Most body Develops secondary
cells sex characteristics;
male reproductive
hormone

2.1.2 Activities are regulated or influenced the endocrine system include

1. Reproduction and lactation

2. Process of the immune system

3. Balance of acids and bases

4. Intake of fluid, the balance of intracellular and extracellular fluid volume

5. Metabolism of carbohydrates, proteins, fats and nucleic acids

6. Digestion, absorption and distribution of nutrients

7. Blood Pressure

8. Prisoners pressure

9. Adaptation to environmental changes

2.1.3 The function of endocrine system

1. Regulation of sodium and water balance and control of blood volume and

pressure

2. Regulation of calcium and phosphate balance to preserve extracellular

fluid concentrations required for cellular membrane intergrity and

intracellular signaling

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 3. Regulation of energy balance and control of fuel mobilization,

utilization, and storage to ensure that cellular metabolic demands are met

4. Coordination of the host hemodynamic and metabolic counterregulatory

responses to stress

5. Regulation of reproduction, development, growth, and senescence

6. Coordinate and integrate cellular activity within the whole body by

regulating cellular and organ function throughtout life and mantaining

homeostasis

2.1.4 Hormones

Each one is different in its chemical composition, structure, and action.

Despite the differences, there are similarities in these molecules.

a. Chemical nature of hormone

Chemically, hormones may be classified as either proteins or steroids.

All of the hormones in the human body, except the sex hormones and

those from the adrenal cortex, are proteins or protein derivatives. This

mean that their fundamental building blocks are amino acids. These

hormones must be administered by injection. Sex hormones and those

from the adrenal cortex are steroids, which are lipid derivatives. These

lipid-soluble hormones may be taken orally.

b. Mechanism of hormone action

Hormones are carried by the blood throughout the entire the

body, yet they affect only certain cells. The specific cells that respond

to a given hormone have receptor sites for that hormone. This is sort

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 of a lock-and-key mechanism. If a hormone fits the receptor site, then

there will be an effect. If a hormone and a receptor site do not match,

then there is no reaction. All the cells that have receptor sites for a

given hormone make up the target tissue for that hormone.

Receptor sites may be located on the surface of the cell

membrane or in the interior of the cell. The hormone-receptor reaction

on the cell membrane activates an enzyme within the membrane,

called adenyl cyclase, which difuses into the cytoplasm. Within the

cell, adenyl cyclase catalyzes the removal of phosphates from

adenosine triphosphate (ATP) to produce cyclic adenosine

monophosphate (cyclic AMP). The protein hormone, which reacts at

the cell membrane, is called the first messenger. Cyclic AMP, which

brings about the action attributed to the hormone, is called the second

messenger. This type of action is relatively rapid because the

precursors are already present and they just need to be activated in

some way.

c. Control of hormone action

A hormone may have profound effects on metabolic processes,

because of their potency, hormone secretion must be regulated within

very narrow limits to maintain homeostasis in the body. Some

endocrine glands secrete hormones in response to other hormones.

The hormones that cause secretion of other hormones are called tropic

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 hormone. A hormone from gland “A” causes gland “B” to secrete its

hormone.

A third method of regulating hormone secretin is by direct

nervous stimulation. A nerve stimulus causes a gland to secrete its

hormone. A physiologic example of this mechanism is the

sympathetic nerve stimulation of the adrenal medulla, which responds

by secreting epinephrine (adrenaline).

2.2 Types and Classification of the Endocrine and Metabolic System

1. Endocrine gland

Endocrine disorders are usually the result of “hypo” (too little) or

“hyper” (too much) secretion of hormone. Other endocrine disorders

include benign and malignant tumors. Tumors that are benign are

nonmalignant, which means they are not recurrent or progressive. Tumors

that are malignant are cancerous, harmful, or tend to produce death.

An example of a hyposecretion of a hormone is hypopituitarism.

When the anterior pituitary glands secretes too little growth hormone in

childhood, dwarfism may result. An example of hypersecretion of a

hormone is hyperthyroidism. When the thyroid secretes too much thyroid

hormone it may cause a condition called Graves’ disease.

Pheochromocytoma is a benign tumor of the adrenal medulla that can

cause an increase in epinephrine and a corresponding rise in blood

pressure.

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 Endocrine sytem diseases and conditions: quick reference guide

Hormone Hypo- or Hyper-Secretion Disease or Condition

GH (somatotropin) Hyposecretion (children) Dwarfism
Hypersecretion (children) Gigantism
Hypersecretion (adults) Acromegaly
ACTH Hyposecretion (adrenal Addison’s disease
cortex-cortisol)
Hypersecretion (adrenal Cushing’s syndrome
cortex-cortisol)
ADH Hyposecretion Diabetes insipidus
(dehydration)
Hypersecretion Edema, hypertension
T3 and T4 Hyposecretion Cretinism
(congenital/children)
Hyposecretion (adults)- Hypothyroidism and
severe cases myxedema
Hypersecretion Grave’s disease
Glucagon Hyposecretion Hypoglycemia
Hypersecretion Hyperglycemia
Insulin Hyposecretion Hyperglycemia (diabetes
mellitus)
Hypersecretion Hypoglycemia
(hyperinsulinism)

2. Pituitary gland

The pituitary gland is sometimes called the “master gland” because

it produces or secretes several different hormones and has an effect on

nearly every organ in the body. It also is called the hypophysis (Latin for

“beneath-grow”) because it is located at the base of the brain. It about the

size of a pea and is found a bony structure of the sphenoid bone called the

sella turcica (Latin for “Turkish saddle”) because of its shape. The pituitary

gland is located inferior to the optic chiasm. The nervous system, is a visual

pathway from the optic nerve of the eyes to the occipital lobe of the brain.

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 The pituitary gland is divided into anterior and posterior lobes. The

anterior lobe is called the adenohypophysis, it develops from oral ectoderm

in the roof of the mouth called Rathke’s pouch and secretes seven different

hormones. The posterior lobe is called the neurohypophysis, it develops

from nervous tissue in the brain and secretes two hormones.

a. Anterior pituitary (adenohypophysis)

Growth hormone (GH) is a protein hormone that targets virtually

every cell and tissue in the body. It is responsible for the growth seen in

childhood and an increase in mass of skeletal muscle and bones. It also

involved in repair of injured tissues. GH sometimes referred to as

somatotropin (soma=body, tropin=growth).

b. Melanocyte stimulating hormone (MSH)

Melanocyte stimulating hormone (MSH) is a peptide hormone that

targets the melanocytes and their organelles, melanosomes, which are

responsible for producing melanin, the protective pigment found in the

epidermis of the skin.

c. Adrenocorticotropic hormone (ACTH)

As the name suggests, adrenocorticotropic hormone (ACTH) has

the adrenal cortex as its target. It causes this portion of the adrenal gland to

secrete its hormones. Aldosterone and cortisol are the two major adrenal

cortical hormones. ACTH also affects the melanocytes in the skin and

increase pigmentation.

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d. Thyroid stimulating hormone (TSH)

Thyroid stimulating hormone (TSH) or thyrotropin is a peptide

hormone. It causes the release of thyroxine from the thyroid gland to

secrete thyroid hormone.

e. Follicle stimulating hormone (FSH)

Although the name follicle stimulating hormone (FSH) may

indicate that this is a hormone found in females, it is actually found in both

men and women. FSH stimulates the maturation of the ova in the female

and production of sperm in the male. It also causes increased production of

estrogen by the ovaries. FSH is a glycoprotein.

f. Luteinizing hormone (LH)

Luteinizing hormone (LH) is a glycoprotein that is important in

stimulating ovulation (release of mature ova from the ovary). LH causes

ovulation and the production and secretion of the female sex hormones

progesterone and estrogen. In the male, LH is sometimes called interstitial

cell stimulating hormone (ICSH) because it stimulates the interstitial cells

of the testes to produce and secrete the male sex hormone testosterone.

g. Prolactin (PRL)

Prolactin (PRL) or lactogenic hormone is the peptide responsible

for the production of milk by the mammary glands after the birth of the

infant and promotes to development of glandular tissue in the female

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 breast during pregnancy and stimulates milk. In males, prolactin helps

with the function of luteinizing hormone.

h. Antidiuretic hormone (ADH)

Antidiuretic hormone (ADH) is another peptide hormone and it is

secreted at the posterior pituitary (neurohypophysis). It helps the body

retain water (think “against diuresis or urination”) by increasing water

absorption by the kidneys. By increasing fluid volume, it increases blood

pressure. Depending on the situation, this may be a good or bad thing.

When blood pressure increases too much (hypertension), a category of

drugs called diuretics may be administered. They have the opposite effect

of ADH, causing an increase in excretion of urine and a decrease in blood

pressure.

i. Oxytocin (OT)

Oxytocin (OT) is a protein hormone that assists in childbirth by

increasing the force of contractions. It also causes milk ejection from the

breasts. Although it might seem that OT is strictly a “female” hormone, like

FSH it also has a role in the male body. It causes contraction of the prostate

and the vas deferens during sexual arousal and possibly facilitates sperm

motility.

3. Thyroid gland

The thyroid gland has two lobes and an isthmus (a narrow band of

tissue) that connects them. The thyroid is located in the front of the neck

15
 just inferior to the larynx (voice box) and easily palpable on a routine

physical examination. It is responsible for important functions that help

maintain homeostasis. It is also involved in several common diseases.

Some of these diseases have an autoimmune component and are seen more

frequently in women. When examining thyroid tissues under a microscope,

you will see follicles that appear as large spaces filled with a pinkish

substance (when stained with a special dye), which are the thyroid

hormones T3 and T4. Additional cells adjacent to the follicles, called

extrafollicular cells, are responsible for producing another thyroid hormone

known as calcitonin.

a. Thyroid hormone

Thyroid hormones are amino acid hormones. There are actually three

different thyroid hormones: triiodothyronine (T3), which has three iodine

molecules attached to it, tetraiodothyronine (T4), which has four iodine

molecules, and calcitonin. T3 is more active thanT4. Calcitonin is responsible

for moving calcium from the blood to the bone (the major reservoir for

calcium). It stimulates osteoblasts (immature bone cells) to produce new bone

tissue. Thyroid hormones are very important in homeostasis and are involved in

energy production, protein synthesis, and tissue repair.

b. Hypothyroidism

With hyposecretion of thyroid hormones the individual often

experiences slowing of the metabolism. Other symptoms may include dry skin,

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fatigue, cold intolerance, constipation, and difficulty getting pregnant. A

childhood (congenital) form of hypothyroidism is called cretinism. These

children often experience both mental and physical growth retardation.

c. Hyperthyroidism

Hyperthyroidism of thyroid hormones causes an overall increase in

metabolism. Symptoms include an increase in heart rate, heart palpitations,

nervousness, and insomnia (inability to sleep). The individual may also be heat

intolerant and have protruding eyeballs, a condition known as exophthalmos.

One form of hyperthyroidism is called Grave’s disease. Former Frist Lady

Barbara Bush suffers from Grave’s disease.

d. Thyroid tumors

The thyroid gland may develop both benign and malignant (cancerous)

tumors. The type of tumor determines the treatment chosen.

e. Calcitonin

Calcitonin is secreted by the parafollicular cells of the thyroid gland.

This hormone oppose the action of the parathyroid glands by reducing the

rate which calcium is released bone, by increasing the rate calcium

excretion by the kidneys, and by reducing calcium absorption in the

intestines. If blood calcium levels become too high, calcitonin is secreted

until calcium in levels decrease to normal.

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 Calcitonin hyposecretion results in less calcium going into bone,

possibly resulting in hypercalcemia (an increase in blood calcium levels).

Hypersecretion of calcitonin results in more calcium going into bone.

4. Parathyroid gland

The human body typically has four parathyroid gland, although some

people may have six. These glands are rather small and embedded in the

posterior aspect of the thyroid gland. They secrete parathyroid hormone,

which is the antagonist to calcitonin.

a. Parathyroid hormone (PTH)

Parathyroid hormone (PTH) is a polypeptide that stimulates osteoclasts

to help “break down” bone. When the bone is broken down, calcium

leaves the bone to enter the blood circulation. PTH also causes the

kidneys to conserve more calcium by stimulating the production of the

active form of Vitamin D. Vitamin D then includes synthesis of a

calcium-binding protein in intestinal epithelial cells that facilitates

efficient absorption of calcium into blood.

5. Adrenal gland

There are two adrenal gland in the body. Each is located on the

superior surface of one the kidneys. That is why the adrenal (“next to” the

kidneys) glands are sometimes called the suprarenal glands (“above” the

kidneys). Each adrenal gland has an inner portion called the medulla (a

term that you see in several different structure which means “inner”) and an

outer portion called the cortex. The medulla secretes hormones that are

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 considered neutrotransmitters. The nervous system that mimic the “flight or

fight” response of the sympathetic nervous system. The hormones of the

adrenal medulla are referred to as catecholamines. The adrenal cortex

secretes two categories of hormones mineralcorticoids and glucocorticoids

that are important in the regulation of minerals such as sodium and glucose,

respectively.

a. Adrenal medulla

The inner portion of the adrenal gland is the medulla and is responsible for

secreting two very important hormones. Epinephrine and norepinephrine

(adrenalin and noradrenalin, respectively) are released by the adrenal

medulla. These are amino acid hormones that prepare the body for

emergency situations. They are also released during times of physical or

emotional stress. They increase heart rate, breathing rate, and blood

pressure. The bronchioles are dilated to allow more air into the lungs and

peristalsis slows, so some of the target organs are the heart, lungs, and

arterioles (small arteries).

b. Adrenal cortex

Several hormones are secreted by the adrenal cortex. Aldosterone is one of

two that we will mention here. It is a steroid hormone classified as a

mineralcorticoid because it helps regulate the amount of sodium in the

body. It targets the tubules of the kidneys to increase retention of sodium.

There is a saying “where sodium goes, water follows”. When sodium is

retained by the body, water is also retained. This causes an increase in fluid

19
 volume and an increase in blood pressure. You may have noticed that when

you eat very salty foods, for example, you rings or shoes suddenly become

too tight.

6. Pancreas

The pancreas is located behind the stomach, so it is not palpable. The

pancreas is a “mixed” gland which means that it is both exocrine (about 80

to 90 percent) and endocrine (10 to 20 percent). The exocrine portion

secretes digestive enzymes such amylase, protease, and lipase. These

enzymes are secreted into the duodenum of the small intestine.

The endocrine pancreas is made up of groups of cells called the islets

of Langerhans. The two major cells, which secrete glucagon and beta cells,

which secrete insulin. These two hormones act as antagonists to each other,

meaning they create opposite effects. Glucagon increases blood glucose

levels and insulin does the opposite. As stated earlier, another example of

this concept is calcitonin, which increases bone calcium, and parathyroid

hormone, which decreases bone calcium.

a. Insulin

Insulin is peptide hormone that lowers blood glucose levels. Because it

also helps take up amino acids into cells, it facilitates protein synthesis.

Insulin is secreted by specialized cells called beta cells.

b. Glucagon

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 Glucagon is peptide hormone that raises blood glucose levels.

Therefore, it has the opposite effect of insulin. Glucagon is secreted by

specialized cells called alpha cells.

7. Thymus

The tymus lies in the space between the lungs called the mediastinum.

It reaches its maximum size by adolescence and then atrophies or involutes

(“turns in on itself”) as the body ages. It matures or processes the T

lymphocytes that are very important in immunity. It produces the hormone

thymosin.

a. Thymosin

Thymosin is a peptide hormone that is involved in the maturation of T

lymphocytes. Hyposecretion of thymosin may result in lack of

maturation of T lymphocytes and a decrease in immunity. Tumors are

rare, when they do occur they are often very aggressive.

8. Pineal gland

The pineal gland (pineal body) is located in the brain between the

cerebral hemispheres. At time it was thought that this was a vestigial organ,

which means over time it has lost its function. We now know that is not

true because we have identified the function of this gland: it produces

melatonin. Melatonin is an amino acid hormone that regulates circadian

rhythms or the body’s biological clock. In other words, it helps with the

awake-sleep cycle. Melatonin is also involved with the onset of puberty.

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9. Gonads

The general term for the male and female reproductive organs is

gonads. The female gonads are the ovaries and the male gonads are the

testes.

a. Female hormones

The ovaries of the female are located in the pelvic cavity and secrete

two important hormones, estrogen and progesterone. Estrogen is a

steroid hormone that is the main female sex hormone. It regulates the

menstrual cycle and is important in the development of female

secondary sex characteristics. Progesterone is also a steroid hormone

with many functions. It helps reduce anxiety and induce sleep, build

and maintain bone tissue, and it maintains the embryo and fetus during

pregnancy.

b. Male hormones

Testosterone is a steroid hormone responsible for the development of

the male reproductive organs. It is also responsible for male secondary

sex characteristics. These include more facial and chest hair, increased

muscle mass and bone density, and a deeper voice than females.

22
 CHAPTER 3

DIABETES MELLITUS

3.1 Definition of Diabetes Mellitus

Diabetes mellitus (DM) is a common chronic disease of adults

requiring continuing medical supervision and client self-care education.

Diabetes derives from a Greek word meaning ‘to siphon’, referring to the

increased output of urine. Mellitus derives from a Latin word meaning

‘sweet’. The two words together identify the disease as an outpouring of sweet

urine. Diabetes mellitus is a major endocrine disorder involving the islet cell

hormone. DM is a metabolic disorder with wide-ranging and serious effect,

many of which are life-threatening. It may occur in either of two forms, which

differ in pathogenesis but produce essentially similar metabolic derangements.

Diabetes mellitus (DM) is a group of metabolic disorders characterized

by a chronic hyperglycemic condition resulting from defects in insullin

secretion, insullin action or both. Permanent neonatal diabetes is caused by

glucokinase deficiency, and is an inborn error of the glucose-insullin signaling

pathway (Njolstad et al.,2003).

Diabetes mellitus (DM) is a group of diseases characterized by high

levels of blood glucose resulting from defects in insulin production, insulin

action, or both. The term diabetes mellitus describes a metabolic disorder of

multiple aetiology characterized by chronic hyperglycaemia with disturbances

of carbohydrate, fat and protein metabolism resulting from defects in insulin

secretion, insulin action, or both.

23
 The effects of diabetes mellitus include long–term damage,

dysfunction and failure of various organs. Diabetes mellitus may present with

characteristic symptoms such as thirst, polyuria, blurring of vision, and weight

loss. In its most severe forms, ketoacidosis or a non–ketotic hyperosmolar

state may develop and lead to stupor, coma and, in absence of effective

treatment, death.

3.2 Type of Diabetes Mellitus

There are types of diabetes mellitus :

a. Type 1 diabetes, also called insullin dependent diabetes mellitus

(IDDM), is caused by lack of insullin secretion by beta cells of the

pancreas. Type 1 diabetes mellitus is a catabolic disorder resulting in

hyperglicemia. It is characterized by the auto-immune distruction of

pancreatic beta-cells, islet cell antibody-mediated insulitis, and complete

insulinopenia. Approximately 95% of individuals with type 1 diabetes

demonstrate the presence of antigen specific markers that identify their

genetic susceptibility to the disorder. Heavy lymphocytic infiltrates

appear in and around islets. The number and size of islets are eventually

destroyed, leding to descreased insulin production and glucose

intolerance. Risk factors for type 1 diabetes may include autoimmune,

genetic, and environmental factors.

b. Type 2 diabetes, also called non-insullin dependent diabetes mellitus

(NIDDM), is caused by decreased sensitivity of target tissues to insullin.

It usually begins as insulin resistance, a disorder in which the cells do not

24
 use insulin properly. As the need for insulin rises, the pancreas gradually

loses its ability to produce insulin. Type 2 diabetes is associated with

older age, obesity, family history of diabetes, history of gestational

diabetes, impaired glucose metabolism, physical inactivity, and

race/ethnicity. African Americans, Hispanic/Latino Americans, American

Indians, and some Asian Americans and Native Hawaiians or Other

Pacific Islanders are at particularly high risk for type 2 diabetes. Type 2

diabetes is increasingly being diagnosed in children and adolescents.

3.3 Etiology of Diabetes Mellitus

People need untreated diabetes have high glucose, which occurs

because a person’s pancreas doesn’t make enough insulin or the muscle, fat,

and liver cells don’t respond normally to insulin or both. Diabtes is clasified

primaraly as type 1 or type 2. Both types are complex diseases associated with

genetic mutation as well as being realted to enviromental facts. Although, the

exact causes of diabetes is unknown, there are several factors that, when

present, place a person at greater risk for the development of diabetes. This

include:

1. A parent’s pr siblings with diabetes

2. Obesity

3. Age older than 45 years old

4. Certain ethnic group (articularly native American, black, latino)

5. History of diabetes during pregnancy (gestasional diabetes) are

delivering a neonative weighting more than 9lb (4,1 kg)

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 6. High blood pressure

7. High trigliceride level

8. High cholesterol level

3.4 Patofisiology of Types Diabetes Mellitus

1. Types 1 Diabetes Mellitus

The autoimmune destruction of pancreatic β-cells, leads to a

deficiency of insulin secretion which results in the metabolic

derangements associated with IDDM. In addition to the loss of insulin

secretion, the function of pancreatic α-cells is also abnormal and there is

excessive secretion of glucagons in IDDM patients. Normally,

hyperglycemia leads to reduced glucagons secretion, however, in patients

with IDDM, glucagons secretion is not suppressed by hyperglycemia

(Raju and Raju, 2010).

The resultant inappropriately elevated glucagons levels exacerbate

the metabolic defects due to insulin defi-ciency. The most pronounced

example of this metabolic disruption is that patients with IDDM rapidly

develop diabetic ketoacidosis in the absence of insulin administration.

Although insulin deficiency is the primary defect in IDDM, there is also a

defect in the administration of insulin. There are multiple biochemical

mechanisms that account for impairment of tissue’s response to insulin.

Deficiency in insulin leads to uncontrolled lipolysis and elevated levels of

free fatty acids in the plasma, which suppresses glucose metabolism in

peripheral tissues such as skeletal muscle (Raju and Raju, 2010). This

26
impairs glucose utilization and insulin deficiency also decreases the

expression of a number of genes necessary for target tissues to respond

normally to insulin such as glucokinase in liver and the GLUT 4 class of

glucose transporters in adipose tissue.

Raju and Raju (2010) explained that the major metabolic

derangements, which result from insulin deficiency in IDDM are impaired

glucose, lipid and protein metabolism which are explained in details as

follows:

a. Effect on glucose metabolism

Uncontrolled IDDM leads to increased hepatic glucose output. First,

liver glycogen stores are mobilized then hepatic gluconeogenesis is

used to produce glucose. Insulin deficiency also impairs non hepatic

tissue utiliza-tion of glucose. In particular in adipose tissue and

skeletal muscle, insulin stimulates glucose uptake. This is

accomplished by insulin mediated movement of glucose transporters

proteins to the plasma membrane of these tissues. Reduced glucose

uptake by peripheral tissues in turn leads to a reduced rate of glucose

metabolism. In addition, the level of hepatic glucokinase is regulated

by insulin. Therefore, a reduced rate of glucose phosphor-rylation in

hepatocytes leads to increased delivery to the blood. Other enzymes

involved in anabolic metabolic metabolism of glucose are affected by

insulin. The combination of increased hepatic glucose production and

reduced peripheral tissues metabolism leads to elevated plasma

27
 glucose levels. When the capacity of the kidneys to absorb glucose is

surpressed, glucosuria ensues. Glucose is an osmotic diuretic and an

increase in renal loss of glucose is accompanied by loss of water and

electrolyte. The result of the loss of water (and overall volume) leads

to the activation of the thirst mechanism (polydipsia). The negative

caloric balance, which results from the glucosuria and tissue

catabolism leads to an increase in appetite and food intake that is

polyphagia (Raju and Raju, 2010).

b. Effect on lipid metabolism

One major role of insulin is to stimulate the storage of food energy in

the form of glycogen in hepatocytes and skeletal muscle, following the

consumption of a meal. In addition, insulin stimulates hepatocytes to

synthesize and store triglycerides in adipose tissue. In uncontrolled

IDDM there is a rapid mobilization of triglycerides leading to

increased levels of plasma free fatty acids. The free fatty acids are

taken up by numerous tissue (except the brain) and metabolized to

provide energy. In the absence of insulin, malonyl COA levels fall, and

transport of fatty acyl-COA into the mitochondria increases.

Mitochondrial oxidation of fatty acids generates acetyl COA that can

be further oxidized in the TCA cycle. However, in heap-tocytes the

majority of the acetyl COA is not oxidized by the TCA cycle but is

metabolized into the ketone bodies (acetoacetate and b-

hydroxybutyrate). These ketone bodies are used for energy production

28
 by the brain, heart and skeletal muscle. In IDDM, the increased

availability of free fatty acids and ketone bodies exacerbates the

reduced utilization of glucose, furthering the ensuing hyperglycaemia.

Production of ketone bodies in excess of the body’s ability to utilize

them leads to ketoacidosis. A spontaneous breakdown product of

acetoacetate is the acetone that is exhaled by the lungs, which gives a

distinctive odor to the breath. Normally, plasma triglycerides are acted

upon by lipoprotein lipase (LPL) that requires insulin. LPL is a

membrane bound enzyme on the surface of the endothelial cells lining

the vessels, which allows fatty acids to be taken from circulating

triglycerides for storage in adipocytes (Raju and Raju, 2010). The

absence of insulin results in hypertriglyceridemia.

c. Effect on protein

Insulin regulates the synthesis of many genes, either positively or

negatively, which affect overall metabolism. Insulin has an overall

effect on protein metabolism, increasing the rate of protein synthesis

and decreasing the rate of protein degradation. Thus insulin deficiency

will lead to increased catabolism of protein. The increased rate of

proteolysis leads to elevated concen-tration of amino acids in plasma

(Raju and Raju, 2010). Glucogenic amino acids serve as precursors for

hepatic and renal glyconeogenesis, which further contributes to the

hyperglycaemia seen in IDDM.

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2. Types 2 Diabetes Mellitus

On the basis of oral glucose tolerance testing the essential elements

of NIDDM can be divided into four distinct groups:

a) Those with normal glucose tolerance.

b) Chemical diabetes (called impaired glucose tolerance).

c) Diabetes with minimal fasting hyperglycemia (fasting plasma glucose

less than 140 mg/dl).

d) Diabetes mellitus in association with overt fasting hyperglycemia

(fasting plasma glucose greater than 140 mg/dl).

The individuals with impaired glucose tolerance have

hyperglycemia inspite of having highest levels of plasma insulin,

indicating that they are resistant to the action of insulin. In the progression

from impaired glucose tolerance to diabetes mellitus, the level of insulin

declines indicating that patients with NIDDM have decreased insulin

secretion. Insulin resistance and insulin deficiency are common in the

average NIDDM patients (Holt, 2004). Insulin resistance is the primary

cause of NIDDM, however some researcher contend that insulin

deficiency is the primary cause because a moderate degree of insulin

resistance is not sufficient to cause NIDDM (Raju and Raju, 2010). Most

patients with the common form of NIDDM have both defects. Recent

evidence has demonstrated a role for a member of the nuclear hormone

receptor super family of proteins in the etiology of type 2 diabetes (Raju

and Raju, 2010). Relatively new classes of drugs used to increase the

30
 sensitivity of the body to insulin are the thiazolidinedione drugs. These

compounds bind to and alter the function of the peroxisome proliferators-

activated receptor g (PPARg). PPARg is also a transcription factor and

when activated, binds to another transcription factor known as the retinoid

x receptor (RXR). When these two proteins are complexed a specific set of

genes becomes activated. PPARg is a key regulator of adipocyte

differentiation; it can induce the differentiation of fibroblasts or other

undifferentiated cells into mature fat cells. PPARg is also involved in the

synthesis of biologically active compounds from vascular endothelial cells

and immune cells (Raju and Raju, 2010).

3.5 Clinical Appearance of Diabetes Mellitus

a. Type I DM

The manifestations of type I DM are the result of a lack of insulin

to transport glucose across the cell membrane into the cells. Glucose

molecules accumulate in the circulating blood, resulting in hyperglycemia.

Hyperglycemia causes serum hyperosmolarity, drawing water from the

intercellular spaces into the general circulation. The increased blood

volume increases renal blood flow and the hyperglycemia acts as an

osmotic diuretic. The resulting osmotic diuresis increases urine output.

This condition is called polyuria. When the blood glucose level exceeds

the renal threshold for glucose-usually about 10 mmol/L-glucose is

excreted in the urine, a condition called glucosuria. The decrease in

intracellular volume and the increased urinary output cause dehydration.

31
 The mouth becomes dry and thirst sensors are activated, causing the

person to drink increased amounts of fluid (polydipsia).

Because glucose cannot enter the cell without insulin, energy

production decreases. This decreases in energy stimulates hunger and the

person easts more food (polyphagia). Despite increased food intake, the

person loses weight as the body loses water and breaks down proteins and

fats in attempt to restore energy sources. Malaise and fatigue accompany

the decrease in energy. Blurred vision in also common, resulting from

osmotic effects that cause swelling of the lenses of the eyes.

Thus, the classic manifestations are polyuria, polydipsia and

polyphagia, accompanied by weight loss, malaise and fatigue. Depending

on the degree of insulin lack, the manifestations vary from slight to severe.

People with type I DM require exogenous insulin to maintain life.

b. Type II DM

The person with type II DM experiences a slow onset of

manifestations and is often unaware of the disease until seeking healthcare

for some other problem. The hyperglycemia in type II is usually not as

severe as in type I, but similar symptoms occur, especially polyuria and

polydipsia. Polyphagia is not often seen and weight loss is uncommon.

Other manifestations are also the result of hyperglycemia: blurred vision,

fatigue, paresthesia and skin infections. If available insulin decrease,

especially in times of physical or emotional stress, the person with type II

32
 DM may develop diabetic ketoacidosis (DKA), but this occurrence is

uncommon.

3.6 Prevention and treatment of Diabetes Mellitus

a. Prevention

1) Lifestyle interventions included diet and moderate-intensity physical

activity (such as walking for 2 1/2 hours each week).

2) Research studies have found that lifestyle changes can prevent or delay

the onset of type 2 diabetes among high-risk adults.

3) In the Diabetes Prevention Program, a large prevention study of people at

high risk for diabetes, the development of diabetes was reduced 58% over

3 years.

b. Treatment

Treatment of IDDM is predominantly by subcutaneous insulin

injection. The aim is restoration of glucose metabolism, so that its dietary

intake must be closely regulated and matched to insulin dose. This usually

means that meals must be taken at regularly timed intervals, with frequent

snacks between meals. Caloric levels are closely monitored for all food

intake. Foods in rich sugars are strictly limited because they release glucose

from the GI lumen into the blood more rapidly than insulin can cope with it.

Recently, battery-powered insulin infusion pumps have been increasingly

used. These provide a continuous insulin supply through a subcutaneous

needle or intravenously. They have their own set of complications (e.g.

battery failure or hypoglycemia from overdose) and are not indicated for all

33
IDDM patients. Transplantation of the pancreas is also being explored, but

the procedure is unlikely to become widespread because of immune rejection

complications.

In NIDDM, insulin is required much less often. In many cases, the loss

of excess weight provides a substantial correction of the problem. Moderate

exercise also promotes carbohydrate metabolism and can contribute to

normalization without drug therapy. If needed, one of several sulfonyl urea

preparations may be used to stimulate insulin release from beta cells. Other

drugs, which mimic the action of insulin, are finding increasing use in

NIDDM therapy.

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 CHAPTER 4

CLOSING
a. Conclusion

The endocrine system is the regulatory system of the body. The glands

of the endocrine system are therefore often referred to as ductless glands.

This means the substances secreted by endocrine glands directly enter the

circulatory system or act directly on specific cells. In contrast, glands such

as the salivary glands secrete their chemicals into ducts. Each endocrine

gland secretes one or more hormones. Endocrine systems are divided to

eight glands, andrenal gland, thymus gland, pancreas gland, parathyroid

gland, pineal gland, Gonad gland, pituitary gland, and thyroid gland.

Diabetes mellitus (DM) is a group of diseases characterized by high

levels of blood glucose resulting from defects in insulin production, insulin

action, or both. The term diabetes mellitus describes a metabolic disorder

of multiple aetiology characterized by chronic hyperglycaemia with

disturbances of carbohydrate, fat and protein metabolism resulting from

defects in insulin secretion, insulin action, or both. The Types of Diabetes

Mellitus is Type 1 (IDDM), and Type 2 (NIDDM).

The last, we as nurse sould be better to prevent of diabetes mellitus

than give treatment or medication.

35
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