Javern M.

Supnet RN

1. Describe primary and secondary endorcrine disorders

Answer:

Endocrinopathies are classified as primary, secondary, or tertiary. Primary endocrine disease inhibits
the action of downstream glands. Secondary endocrine disease is indicative of a problem with the
pituitary gland. Tertiary endocrine disease is associated with dysfunction of the hypothalamus and its
releasing hormones.

Endocrine disorders can result from

A. Dysfunction originating in the peripheral endocrine gland itself (primary disorders)

B. Understimulation by the pituitary (secondary disorders)

C. Overstimulation by the pituitary (secondary disorders)

D. Rarely, because of abnormal tissue response to hormones (usually hypofunction).

In general, most endocrine pathology involves either the overproduction or the underproduction of
a hormone. Overproduction of a given hormone may be caused by hyperplasia of the organ that
produces the hormone, by a neoplastic process, or by some combination of the two processes.
Underproduction of a given hormone, in contrast, may be caused by either destruction of the gland
that produces the hormone or by conditions that deprive an endocrine organ of its normal trophic
influence. Also primary diseases are diseases that originate within the gland in question (e.g., primary
hyperthyroidism is due to a defect in the thyroid gland), and secondary diseases represent change in
one organ as a result of disease in another organ (e.g., secondary hyperthyroidism may be due to a
TSH-secreting pituitary adenoma).

2. List effects of excessive secretion of growth hormone on different organ/systems

Answer:

Growth Hormone (Somatotropin)

Growth hormone is a protein hormone of about 190 amino acids that is synthesized and secreted by
cells called somatotrophs in the anterior pituitary. It is a major participant in control of several
complex physiologic processes, including growth and metabolism. Growth hormone is also of
considerable interest as a drug used in both humans and animals.

Physiologic Effects of Growth Hormone

A critical concept in understanding growth hormone activity is that it has two distinct types of effects:
  Direct effects are the result of growth hormone binding its receptor on target cells. Fat cells
(adipocytes), for example, have growth hormone receptors, and growth hormone stimulates
them to break down triglyceride and supresses their ability to take up and accumulate
circulating lipids.

 Indirect effects are mediated primarily by a insulin-like growth factor-I (IGF-I), a hormone
that is secreted from the liver and other tissues in response to growth hormone. A majority
of the growth promoting effects of growth hormone is actually due to IGF-I acting on its
target cells.

Effects on Growth

Growth is a very complex process, and requires the coordinated action of several hormones. The
major role of growth hormone in stimulating body growth is to stimulate the liver and other tissues to
secrete IGF-I. IGF-I stimulates proliferation of chondrocytes (cartilage cells), resulting in bone growth.
Growth hormone does seem to have a direct effect on bone growth in stimulating differentiation of
chondrocytes.

Metabolic Effects

Growth hormone has important effects on protein, lipid and carbohydrate metabolism. In some
cases, a direct effect of growth hormone has been clearly demonstrated, in others, IGF-I is thought to
be the critical mediator, and some cases it appears that both direct and indirect effects are at play.

 Protein metabolism: In general, growth hormone stimulates protein anabolism in many

tissues. This effect reflects increased amino acid uptake, increased protein synthesis and
decreased oxidation of proteins.

 Fat metabolism: Growth hormone enhances the utilization of fat by stimulating triglyceride
breakdown and oxidation in adipocytes.

 Carbohydrate metabolism: Growth hormone is one of a battery of hormones that serves to

maintain blood glucose within a normal range. Growth hormone is often said to have anti-
insulin activity, because it supresses the abilities of insulin to stimulate uptake of glucose in
peripheral tissues and enhance glucose synthesis in the liver.

The effect of excessive secretion of growth hormone is also very dependent on the age of onset and is
seen as two distinctive disorders:

 Giantism is the result of excessive growth hormone secretion that begins in young children
or adolescents. It is a very rare disorder, usually resulting from a tumor of somatotropes. One
of the most famous giants was a man named Robert Wadlow. He weighed 8.5 pounds at
birth, but by 5 years of age was 105 pounds and 5 feet 4 inches tall. Robert reached an adult
weight of 490 pounds and 8 feet 11 inches in height. He died at age 22.
  Acromegaly results from excessive secretion of growth hormone in adults, usually the result
of benign pituitary tumors. The onset of this disorder is typically insideous, occurring over
several years. Clinical signs of acromegaly include overgrowth of extremities, soft-tissue
swelling, abnormalities in jaw structure and cardiac disease. The excessive growth hormone
and IGF-I also lead to a number of metabolic derangements, including hyperglycemia.

3. Discuss the clinical features of follicle stimulating hormone and lutenizing hormones

Answer:

Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are called gonadotropins because
stimulate the gonads - in males, the testes, and in females, the ovaries. They are not necessary for
life, but are essential for reproduction. These two hormones are secreted from cells in the anterior
pituitary called gonadotrophs. Most gonadotrophs secrete only LH or FSH, but some appear to
secrete both hormones.

As described for thyroid-simulating hormone, LH and FSH are large glycoproteins composed of alpha
and beta subunits. The alpha subunit is identical in all three of these anterior pituitary hormones,
while the beta subunit is unique and endows each hormone with the ability to bind its own receptor.

Physiologic Effects of Gonadotropins

Physiologic effects of the gonadotrophins are known only in the ovaries and testes. Together, they
regulate many aspects of gonadal function in both males and females.

Luteinizing Hormone

In both sexes, LH stimulates secretion of sex steroids from the gonads. In the testes, LH binds to
receptors on Leydig cells, stimulating synthesis and secretion of testosterone. Theca cells in the ovary
respond to LH stimulation by secretion of testosterone, which is converted into estrogen by adjacent
granulosa cells.

In females, ovulation of mature follicles on the ovary is induced by a large burst of LH secretion
known as the preovulatory LH surge.Residual cells within ovulated follicles proliferate to form
corpora lutea, which secrete the steroid hormones progesterone and estradiol. Progesterone is
necessary for maintenance of pregnancy, and, in most mammals, LH is required for continued
development and function of corpora lutea. The name luteinizing hormone derives from this effect of
inducing luteinization of ovarian follicles.

Follicle-Stimulating Hormone

As its name implies, FSH stimulates the maturation of ovarian follicles. Administration of FSH to
humans and animals induces "superovulation", or development of more than the usual number of
mature follicles and hence, an increased number of mature gametes.

FSH is also critical for sperm production. It supports the function of Sertoli cells, which in turn support
many aspects of sperm cell maturation.

FHS LH

FEMALE A. stimulates ovary to produce A. stimulates ovary to produce

steroids steoroids

ovary will produce estradiol

during follicular phase and
progesterone during luteal B. surge at midcycle triggers
phase ovulation
C. luteinizing hormone turns the
B. Surge at midcycle, with LH, follicle into the
triggers ovulation corpeus luteum by triggering
ovulation

MALE A. stimulates Sertoli cells to A. stimulates Leydig cells to

produce androgen-binding produce testosterone
protein (ABP), thereby
stimulating spermatogenesis

B. testosterone provides
negative feedback to anterior
B. FSH also stimulates Sertoli pituitary and hypothalamus
cells to produce inhibin, which
provides negative feedback to
the anterior pituitary to
decrease FSH secretion
In the female:

Estrogen:

 Negative feedback:
o occurs during follicular phases when estrogen levels are still low.
 Postive feedback:

o occurs at high concentrations near the end of the follicular phase, estrogen
becomes a positive inducer of the anterior pituitary
o positive feedback triggers the anterior pituitary to release more FSH and LH
o more FSH and LH cause the ovary to produce more estrogen
o the ensuing LH surge is responsible for ovulation

Progesterone:

 stimulate secretory and vascular activity of the endometrium, preparing for implantation of
an embryo
 secreted by the corpus luteum, after ovulation
 when corpus luteum regresses, progresterone levels fall

o new vasculature in endometrium regresses and the tissue sloughs off.

4. Describe diabetes insipidus include the following:

Etiology - Diabetes insipidus is an uncommon disorder that causes an imbalance of fluids in the body.
This imbalance makes you very thirsty even if you've had something to drink. It also leads you to
produce large amounts of urine. The hypothalamus produces a hormone called vasopressin, an
antidiuretic hormone (ADH) that tells the kidneys how much fluid to absorb from the bloodstream.
This normally results in a lower amount of urine produced. When there is damage to the
hypothalamus (Central diabetes insipidus, or CDI) or the kidneys are not able to respond to the
vasopressin (Nephrogenic diabetes insipidus or NDI), the kidneys do not know when to stop removing
fluid from the body, even if the body is already dehydrated. This results in the patient feeling
extremely thirsty, which prompts them to drink more fluids, and therefore, secrete more dilute urine.
A. Signs and Symptoms

Signs and symptoms of diabetes insipidus include:

 Extreme thirst

 Producing large amounts of diluted urine

 Frequent need to get up to urinate during the night

 Preference for cold drinks

Young child with diabetes insipidus may have the following signs and symptoms:

 Heavy, wet diapers

 Bed-wetting

 Trouble sleeping

 Fever

 Vomiting

 Constipation

 Delayed growth

 Weight loss

Pathophysiology - Electrolyte and volume homeostasis is a complex mechanism that balances the
body's requirements for blood pressure and the main electrolytes sodium and potassium. In general,
electrolyte regulation precedes volume regulation. When the volume is severely depleted, however,
the body will retain water at the expense of deranging electrolyte levels.

The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic
and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules
down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland where it is
stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the
ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the
cortex. The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water
permeability in the collecting ducts and distal convoluted tubule, specifically it acts on proteins called
aquaporins which open to allow water into the collecting duct cells. This increase in permeability
allows for reabsorption of water into the bloodstream, thus concentrating the urine.

Diagnostics - In order to distinguish DI from other causes of excess urination, blood glucose levels,
bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can
reveal a high sodium level (hypernatremia as dehydration develops). Urinalysis demonstrates a dilute
urine with a low specific gravity. Urine osmolarity and electrolyte levels are typically low.

A fluid deprivation test helps determine whether DI is caused by:

1. excessive intake of fluid ( e.g: psychogenic polydipsia.)

2. a defect in ADH production
3. a defect in the kidneys' response to ADH

This test measures changes in body weight, urine output, and urine composition when fluids are
withheld and as dehydration occurs. The body's normal response to dehydration is to concentrate
urine and conserve water, so urine becomes more concentrated and urination becomes less frequent.
Those with DI continue to urinate large amounts of dilute urine in spite of not drinking any fluids.
Sometimes measuring blood levels of ADH during this test is also necessary.

Water deprivation test

This test confirm the diagnosis and help determine the cause of diabetes insipidus . you will be asked
to stop dinking water for several hour before test ,then we measure the changes in urine output and
its body weight.

Vasopressin or Desmopressin test

This test is helpful to distinguished between central and nephrogenic diabetes insipidus.

Reduction of urine output and increases urine osmolarity , then ADH is deficient.

B. Medical Intervention

Answer:

Fluid replacement
Most patients with diabetes insipidus (DI) can drink enough fluid to replace their urine losses. When
oral intake is inadequate and hypernatremia is present, replace losses with dextrose and water or an
intravenous (IV) fluid that is hypo-osmolar with respect to the patient’s serum. Do not administer
sterile water without dextrose intravenously, as it can cause hemolysis. To avoid hyperglycemia,
volume overload, and overly rapid correction of hypernatremia, fluid replacement should be provided
at a rate no greater than 500-750 mL/h. A good rule of thumb is to reduce serum sodium by 0.5
mmol/L (0.5 mEq/L) every hour. The water deficit may be calculated on the basis of the assumption
that body water is approximately 60% of body weight.
Desmopressin and other drugs
In patients with central DI, desmopressin is the drug of choice. A synthetic analogue of antidiuretic
hormone (ADH), desmopressin is available in subcutaneous, IV, intranasal, and oral
preparations. Generally, it can be administered 2-3 times per day. Patients may require
hospitalization to establish fluid needs. Frequent electrolyte monitoring is recommended during the
initial phase of treatment.

In central DI, the primary problem is a hormone deficiency; therefore, physiologic replacement with
desmopressin is usually effective. Use a nonhormonal drug for central DI if response is incomplete or
desmopressin is too expensive.

Monitoring
Monitor for fluid retention and hyponatremia during initial therapy. Follow the volume of water
intake and the frequency and volume of urination, and inquire about thirst. Monitor serum sodium,
24-hour urinary volumes, and specific gravity. Request posthospitalization follow-up visits with the
patient every 6-12 months. Patients with normal thirst mechanisms can usually self-regulate.

Dietary measures
No specific dietary considerations exist in chronic DI, but the patient should understand the
importance of an adequate and balanced intake of salt and water. A low-protein, low-sodium diet can
help to decrease urine output.

Postoperative Setting
After pituitary surgery, patients should undergo continuous monitoring of fluid intake, urinary output,
and specific gravities, along with daily measurements of serum electrolytes. In patients who develop
DI, administer parenteral desmopressin every 12-24 hours, along with adequate fluid to match losses.

Nursing Intervention

Answer:

Nursing Interventions and Rationales

1. Monitor I & O, daily weights, and polydipsia. Weight loss will occur with excessive

fluid loss. Thirst can be an indicator of fluid balance.

2. Monitor for signs / symptoms of hypovolemia. Excess fluid loss results in decreased

circulatory volume. Early detection and intervention can prevent hypovolemic shock

from occurring.
 3. Monitor for signs of hypotension and provide education and assistance with

ambulation. Dehydration and hypernatremia can cause the blood pressure to drop

which may result in dizziness or weakness with position changes. Assist patient

when standing or walking to prevent falls and injury. Educate patient to make slow

changes in position.

4. Encourage hydration and provide easy access to fluids; administer IV fluids if

necessary

A. Hypotonic- D5W or 0.45% sodium chloride

B. Isotonic – NS (0.9% sodium chloride) if hemodynamically unstable

If the patient has intact thirst, offer plenty of fluids to prevent dehydration. If the patient cannot

orally tolerate fluids, initiate IV fluids.

5. Monitor labs / electrolyte balance

A. Serum and urine osmolality

B. Serum and urine sodium levels

C. Serum potassium

Excess fluid loss results in the body excreting potassium and retaining sodium. This results in too

much sodium and too little potassium in the blood.

6. Provide easy access to bathroom. Frequent urination can be frustrating for the

patient. Provide easy access for voiding including urinal or bedside commode as

appropriate.

7. Prevent injury and initiate fall precautions. Frequent trips to the bathroom can

increase the risk of falls. Provide assistance as needed with ambulation, especially if

patient has confusion, muscle cramps or muscle weakness from electrolyte

imbalance.

8. Assess for skin integrity, apply skin barriers as needed. Polyuria may lead to bouts of

incontinence and increase the risk of skin breakdown. Apply barriers and

precautions as necessary to avoid redness or excoriation.

5. Compare and Contrast the hypo and hyper state of thyroid function.
Answer :

A. Hyperthyroidism - (overactive thyroid) occurs when your thyroid gland produces too much
of the hormone thyroxine. Hyperthyroidism can accelerate your body's metabolism, causing
unintentional weight loss and a rapid or irregular heartbeat.

Symptoms

 Unintentional weight loss, even when your appetite and food intake stay the same or increase

 Rapid heartbeat (tachycardia) — commonly more than 100 beats a minute

 Irregular heartbeat (arrhythmia)

 Pounding of your heart (palpitations)

 Increased appetite

 Nervousness, anxiety and irritability

 Tremor — usually a fine trembling in your hands and fingers

 Sweating

 Changes in menstrual patterns

 Increased sensitivity to heat

 Changes in bowel patterns, especially more frequent bowel movements

 An enlarged thyroid gland (goiter), which may appear as a swelling at the base of your neck

 Fatigue, muscle weakness

 Difficulty sleeping

 Skin thinning

 Fine, brittle hair

Graves' ophthalmopathy

Sometimes an uncommon problem called Graves' ophthalmopathy may affect your eyes, especially if
you smoke. This disorder makes your eyeballs protrude beyond their normal protective orbits when
the tissues and muscles behind your eyes swell. Eye problems often improve without treatment.

Signs and symptoms of Graves' ophthalmopathy include:

 Dry eyes

 Red or swollen eyes

 Excessive tearing or discomfort in one or both eyes

 Light sensitivity, blurry or double vision, inflammation, or reduced eye movement

 Protruding eyeballs

Causes

Thyroid gland

Hyperthyroidism can be caused by a number of conditions, including Graves' disease, Plummer's

disease and thyroiditis.

Your thyroid is a small, butterfly-shaped gland at the base of your neck, just below your Adam's apple.
The thyroid gland has an enormous impact on your health. Every aspect of your metabolism is
regulated by thyroid hormones.

Your thyroid gland produces two main hormones, thyroxine (T4) and triiodothyronine (T3), that
influence every cell in your body. They maintain the rate at which your body uses fats and
carbohydrates, help control your body temperature, influence your heart rate, and help regulate the
production of protein. Your thyroid also produces a hormone that helps regulate the amount of
calcium in your blood (calcitonin).

Reasons for too much thyroxine (T4)

Normally, your thyroid releases the right amount of hormones, but sometimes it produces too much
T4. This may occur for a number of reasons, including:
  Graves' disease. Graves' disease is an autoimmune disorder in which antibodies produced by
your immune system stimulate your thyroid to produce too much T4. It's the most common
cause of hyperthyroidism.

 Hyperfunctioning thyroid nodules (toxic adenoma, toxic multinodular goiter or Plummer's

disease). This form of hyperthyroidism occurs when one or more adenomas of your thyroid
produce too much T4. An adenoma is a part of the gland that has walled itself off from the rest
of the gland, forming noncancerous (benign) lumps that may cause an enlargement of the
thyroid.

 Thyroiditis. Sometimes your thyroid gland can become inflamed after pregnancy, due to an
autoimmune condition or for unknown reasons. The inflammation can cause excess thyroid
hormone stored in the gland to leak into your bloodstream. Some types of thyroiditis may
cause pain, while others are painless.

Risk factors

Risk factors for hyperthyroidism include:

A. A family history, particularly of Graves' disease

B. Female sex

C. A personal history of certain chronic illnesses, such as type 1 diabetes, pernicious anemia and
primary adrenal insufficiency

Hyperthyroidism can lead to a number of complications:

A. Heart problems. Some of the most serious complications of hyperthyroidism involve the
heart. These include a rapid heart rate, a heart rhythm disorder called atrial fibrillation that
increases your risk of stroke, and congestive heart failure — a condition in which your heart
can't circulate enough blood to meet your body's needs.

B. Brittle bones. Untreated hyperthyroidism can also lead to weak, brittle bones (osteoporosis).
The strength of your bones depends, in part, on the amount of calcium and other minerals they
contain. Too much thyroid hormone interferes with your body's ability to incorporate calcium
into your bones.

C. Eye problems. People with Graves' ophthalmopathy develop eye problems, including bulging,
red or swollen eyes, sensitivity to light, and blurring or double vision. Untreated, severe eye
problems can lead to vision loss.

D. Red, swollen skin. In rare cases, people with Graves' disease develop Graves' dermopathy. This
affects the skin, causing redness and swelling, often on the shins and feet.
 E. Thyrotoxic crisis. Hyperthyroidism also places you at risk of thyrotoxic crisis — a sudden
intensification of your symptoms, leading to a fever, a rapid pulse and even delirium. If this
occurs, seek immediate medical care.

B. Hypothyroidism - Hypothyroidism (underactive thyroid) is a condition in which your thyroid

gland doesn't produce enough of certain crucial hormones.

Hypothyroidism signs and symptoms may include:

 Fatigue

 Increased sensitivity to cold

 Constipation

 Dry skin

 Weight gain

 Puffy face

 Hoarseness

 Muscle weakness

 Elevated blood cholesterol level

 Muscle aches, tenderness and stiffness

 Pain, stiffness or swelling in your joints

 Heavier than normal or irregular menstrual periods

 Thinning hair

 Slowed heart rate

 Depression

 Impaired memory

 Enlarged thyroid gland (goiter)

Hypothyroidism results when the thyroid gland fails to produce enough hormones. Hypothyroidism
may be due to a number of factors, including:

 Autoimmune disease. The most common cause of hypothyroidism is an autoimmune disorder

known as Hashimoto's thyroiditis. Autoimmune disorders occur when your immune system
 produces antibodies that attack your own tissues. Sometimes this process involves your thyroid
gland.

 Over-response to hyperthyroidism treatment. People who produce too much thyroid

hormone (hyperthyroidism) are often treated with radioactive iodine or anti-thyroid
medications. The goal of these treatments is to get thyroid function back to normal. But
sometimes, correcting hyperthyroidism can end up lowering thyroid hormone production too
much, resulting in permanent hypothyroidism.

 Thyroid surgery. Removing all or a large portion of your thyroid gland can diminish or halt
hormone production. In that case, you'll need to take thyroid hormone for life.

 Radiation therapy. Radiation used to treat cancers of the head and neck can affect your
thyroid gland and may lead to hypothyroidism.

 Medications. A number of medications can contribute to hypothyroidism. One such medication

is lithium, which is used to treat certain psychiatric disorders. If you're taking medication, ask
your doctor about its effect on your thyroid gland.

Hypothyroidism may result from one of the following:

 Congenital disease. Some babies are born with a defective thyroid gland or no thyroid gland. In
most cases, the thyroid gland didn't develop normally for unknown reasons, but some children
have an inherited form of the disorder. Often, infants with congenital hypothyroidism appear
normal at birth. That's one reason why most states now require newborn thyroid screening.

 Pituitary disorder. A relatively rare cause of hypothyroidism is the failure of the pituitary gland
to produce enough thyroid-stimulating hormone (TSH) — usually because of a benign tumor of
the pituitary gland.

 Pregnancy. Some women develop hypothyroidism during or after pregnancy (postpartum

hypothyroidism), often because they produce antibodies to their own thyroid gland. Left
untreated, hypothyroidism increases the risk of miscarriage, premature delivery and
preeclampsia — a condition that causes a significant rise in a woman's blood pressure during
the last three months of pregnancy. It can also seriously affect the developing fetus.

 Iodine deficiency. The trace mineral iodine — found primarily in seafood, seaweed, plants
grown in iodine-rich soil and iodized salt — is essential for the production of thyroid hormones.
Too little iodine can lead to hypothyroidism, and too much iodine can worsen hypothyroidism
in people who already have the condition.

6. Discuss the pathophysiology of Graves’ Disease

Answer:

Graves’s Disease results from the production of thyroid-stimulating immunoglobulins (TSI) by

stimulated B lymphocytes. These immunoglobulins bind to the thyroid stimulating hormone (TSH)
receptor to mimic the action of TSH, resulting in follicular cell growth, an increase in vascularity and
the excessive synthesis and secretion of thyroud hormone.

Auto antibodies (TSI, TBII, TGI) target and bind to TSH receptors > Antibodies act like TSH
(thyrotropin), causing excessive release of t3 and t4 into the blood. > This spike in Thyroid hormone
release, cause TSH level to decrease (negative feedback) > Exopthalmos is caused by antibodies
attacking the eye muscle fibroblasts, forcing a change into adipose tissue. > The resulting adipose
tissue builds up, exerting a pressure behind eyes. > Pressure build up constricts draining veins,
resulting edema. > The increases in appetite and weight loss, the heat intolerance and diaphoresis,
are caused by the Thyroid hormones increasing the Basal Metabolic Rate. > Hyperactivity and
Fatigability occurs as Thyroxine overstimulates the motor end plate of the neuromuscular junction.

7. Discuss the pathophysiology of Cushing syndrome

Answer :

Normally, The hypothalamus secretes corticotropin releasing hormone or (CRH) which stimulates the
Pituitary gland to secretes Adrenocorticotropic hormone or (ACTH). ACTH stimulates adrenal cortex
and releases corticosteroids (Cortisoland aldosterone and sex hormoes) this is what we called
negative feedback.

In Cushing’s we have increase secretion of cortisol After production the cortisol is carried to different
parts of the body by cortisol binding protein, almost 90% of cortisol binds to these (CBG) protein and
has a bioavailability of 60% to 100%. Synthetic corticosteroids have varying bioavailability and
potency, but all affect similar pathways. It is a catabolic hormone which is released under stressful
conditions. The excess of cortisol results in an increased rate of gluconeogenesis, glycogenolysis and
increases insulin resistance. Cortisol is a steroid hormone, and it directly affects the transcription and
translation of enzyme proteins involved in the metabolism of fats, glycogen, proteins synthesis and
Kreb's cycle. It promotes the production of free glucose in the body, elevating glucose levels, while
simultaneously increasing insulin resistance. The destruction of protein yields amino acids which are
used in gluconeogenesis. The prolonged catabolism of proteins causes purplish striae of the torso,
osteoporosis and poor wound healing. All these processes involve collagen which is a three amino
based protein. High cortisol levels also cause immune disruptions; this hormone leads to a decrease in
lymphocyte levels and increases the neutrophils. It causes detachment of marginating pool of
neutrophils in the bloodstream and increases the circulating neutrophil levels although there is no
increased production of the neutrophils. This mechanism explains the typical picture of raised TLC
where there is decreased lymphocyte number and increased neutrophils.