WRITTEN REPORT

(Week 7)

Responses to Acute and Chronic Alterations/

Problems and its Pathophysiologic Basis in
Metabolism and Endocrine

Prepared and submitted by: Kyla R. Comoso, Jenerose D. Dante, Reinz Lei
Andrean Donayre, Reimann Sam Valdez.
BSN 3-A
 Responses to Acute and Chronic Alterations/ Problems and its Pathophysiologic Basis in
Metabolism and Endocrine
Topics
B. Nutritional -Metabolic Patterns/Responses to Altered Endocrine Function
1. Hyperfunction
2. Hypofunction
• Thyroid Gland
• Parathyroids
• Adrenal Glands
• Pituitary Glands
• Pancreas- Diabetes Mellitus

Learning Objectives

At the end of the 1 hour and 30 minutes discussion, the learners/ students
will be able to:

1. Determine various nutritional -metabolic patterns/responses in altered endocrine function

2. Develop understanding on hyperfunction and hypofunction of various glands in the
endocrine system.
3. Demonstrate knowledge on alterations of thyroid, parathyroid, adrenal, pituitary and
pancreas in terms of their etiology, risks factors, signs and symptoms, pathophysiology,
diagnostic tests, treatment, management and nursing responsibilities
B. Nutritional -Metabolic Patterns/Responses to Altered Endocrine Function

The endocrine system plays a critical role in maintaining homeostasis by regulating metabolism,
growth, reproduction, and energy balance through the secretion of hormones. Hyperfunction of
endocrine glands occurs when these glands produce excessive amounts of hormones, leading to
systemic disruptions in metabolic and nutritional patterns. This report explores the anatomy,
pathophysiology, clinical presentation, diagnostic approaches, treatment options, and nursing
responsibilities related to endocrine hyperfunction, with a focus on hyperthyroidism, Cushing’s
syndrome, and hyperinsulinism. Additionally, the prevalence of these conditions at international,
national, and local levels (Davao Region) is discussed.

1. HYPERFUNCTION
Hyperfunction of endocrine glands occurs when these glands produce excessive amounts of
hormones, leading to systemic disruptions in metabolic and nutritional patterns.
Thyroid Gland
Hormones Produced: Thyroxine (T4) and Triiodothyronine (T3).
Functions:
Regulate Metabolism: T3 and T4 control the body's metabolic rate, influencing how quickly the
body uses energy.
Energy Production: They help convert food into energy.
Growth and Development: Essential for normal growth, brain development, and bone
maintenance.
Body Temperature: Help maintain normal body temperature.

Heart and Muscle Function: Influence heart rate and muscle strength.
Hyperfunction (Hyperthyroidism):
Excessive T3 and T4 production leads to symptoms like:

• Increased metabolic rate

• Weight loss
• Heat intolerance
• Rapid heart rate (tachycardia)
• Anxiety and tremors.
Adrenal Glands

Hormone Produced: Cortisol (primary glucocorticoid).

Functions:

Stress Response: Cortisol helps the body respond to stress by increasing blood sugar levels and
suppressing non-essential functions (e.g., immune response).

Metabolism: Regulates carbohydrate, fat, and protein metabolism.

Immune Function: Modulates inflammation and immune responses.

Blood Pressure: Helps maintain blood pressure by regulating fluid balance.

Hyperfunction (Cushing’s Syndrome):
Excessive cortisol production leads to symptoms like:

• Central obesity (fat accumulation in the abdomen and face).

• Hyperglycemia (high blood sugar).
• Muscle weakness.
• Hypertension (high blood pressure).
• Thinning skin and easy bruising.

Pancreas
Hormone Produced: Insulin.
Functions:

• Blood Sugar Regulation: Insulin helps cells absorb glucose from the bloodstream,
lowering blood sugar levels.
• Energy Storage: Promotes the storage of glucose as glycogen in the liver and muscles.
• Fat and Protein Metabolism: Facilitates the storage of fats and the uptake of amino acids
into cells.

Hyperfunction (Hyperinsulinism):
Excessive insulin production leads to symptoms like:
Hypoglycemia (low blood sugar).
 Sweating, tremors, and confusion.

Hunger and irritability.

In severe cases, seizures or loss of consciousness.

Pathophysiology
Hyperfunction results from:
Tumors: Benign or malignant growths in endocrine glands (e.g., thyroid adenoma, pituitary
adenoma).
Autoimmune Disorders: Graves’ disease, where antibodies stimulate the thyroid to produce
excess hormones.
Genetic Mutations: Affecting hormone production or regulation.
Excessive Stimulation: Overproduction of trophic hormones (e.g., ACTH in Cushing’s disease).
Excess hormones disrupt metabolic processes, leading to symptoms such as:
Increased metabolic rate (hyperthyroidism).
Hypertension and hyperglycemia (Cushing’s syndrome).
Hypoglycemia (hyperinsulinism).

Risk Factors
Genetic Predisposition: Family history of endocrine disorders.
Autoimmune Diseases: Graves’ disease, Hashimoto’s thyroiditis.
Dietary Factors: Iodine excess or deficiency (thyroid disorders).
Lifestyle Factors: Obesity, chronic stress, sedentary lifestyle.
Medications: Long Term glucocorticoid use (Cushing’s syndrome).
Signs and Symptoms
The clinical presentation of hyperfunction varies depending on the affected gland:
Hyperthyroidism:
Weight loss, tachycardia, heat intolerance, tremors, exophthalmos (bulging eyes), and goiter.
Cushing’s Syndrome:
Moon face, buffalo hump, central obesity, hypertension, hyperglycemia, thin skin, and muscle
weakness.
Hyperinsulinism:
 Hypoglycemia, sweating, confusion, irritability, and seizures.

Diagnostic Tests
Accurate diagnosis of hyperfunction involves:
Blood Tests
Thyroid function tests (TSH, T3, T4).
Cortisol levels (Cushing’s syndrome).
Insulin and glucose levels (hyperinsulinism).
Imaging
Ultrasound, CT, or MRI to identify tumors or gland enlargement.
Biopsy
For suspicious thyroid or adrenal nodules.
Stimulation/Suppression Tests:
Dexamethasone suppression test (Cushing’s syndrome).

Treatment Options
Management of hyperfunction depends on the underlying cause and severity:
1. Medications:
Antithyroid drugs (e.g., methimazole for hyperthyroidism).
Cortisol inhibitors (e.g., ketoconazole for Cushing’s syndrome).
Beta Blockers to manage symptoms like tachycardia.
2. Radioactive Iodine Therapy:
For hyperthyroidism to destroy overactive thyroid tissue.
3. Surgery:
Thyroidectomy (hyperthyroidism).
Adrenalectomy (Cushing’s syndrome).
Pancreatectomy (insulinomas).
4. Lifestyle Modifications:
Low Iodine diet (hyperthyroidism).
Stress management and regular followup.
8. Nursing Responsibilities
Nurses play a critical role in managing patients with endocrine hyperfunction:
PreOperative Care:
Educate patients about the procedure and expected outcomes.
Monitor vital signs and symptoms.
PostOperative Care:
Monitor for complications (e.g., hypocalcemia after thyroidectomy).
Administer medications as prescribed.
Patient Education:
Dietary modifications (e.g., low iodine diet for hyperthyroidism).
Importance of medication adherence and followup.
Emotional Support:
Address anxiety and concerns related to chronic illness.

Prevalence
International:
Hyperthyroidism affects 12% of the global population.
Cushing’s syndrome is rare, with an incidence of 0.72.4 cases per million annually.
National (Philippines):
Thyroid disorders are common, particularly in iodine deficient areas.
Local (Davao Region):
Limited local data, but thyroid disorders are likely prevalent due to dietary and environmental
factors.

Summary
Endocrine hyperfunction disrupts metabolic and nutritional balance, leading to significant
clinical manifestations. Early diagnosis and treatment are essential to prevent complications and
improve patient outcomes. Nurses play a vital role in patient education, monitoring, and support,
ensuring holistic care for individuals with endocrine disorders. Increased awareness and
screening programs are needed, particularly in high-risk populations, to address the burden of
these conditions.
2.HYPOFUNCTION
What is hypofunction?
Hypofunction of an endocrine gland can result from understimulation by the pituitary whether
due to intrinsic pituitary dysfunction or understimulation of the pituitary by the hypothalamus. It
originates within the peripheral gland itself which can result from congenital or acquired disorders
(including autoimmune disorders, tumors, infections, vascular disorders, and toxins) (Young,
2022).
Causes:
• Genetic disorders (e.g., Cretinism)
• Diseases or Disorders (e.g., renal disease)
• Drugs (e.g., Amiodrane)
Hypofunction of Thyroid Gland
Overview of the Thyroid gland
The thyroid gland, located in the anterior neck just below
the cricoid cartilage, consists of 2 lobes connected by an
isthmus. Follicular cells in the gland produce the 2 main
thyroid hormones:
• Tetraiodothyronine (thyroxine, T4)
• Triiodothyronine (T3)

These hormones act on cells in virtually every body tissue

by combining with nuclear receptors and altering
expression of a wide range of gene products. Thyroid
hormone is required for normal brain and somatic tissue development in the fetus and neonate,
and, in people of all ages, thyroid hormone regulates protein, carbohydrate, and fat metabolism.
T4 has minimal hormonal activity, but its long half-life (8 days) serves as a reservoir or
prohormone for T3. T4 is converted (in most tissues) to T3, the active form that binds to nuclear
receptors, and to reverse T3 (rT3), an inactive form of thyroid hormone without metabolic activity.
Levels of rT3 increase in certain diseases. The Parafollicular cells (C cells) in the thyroid secrete
the hormone calcitonin, which is released in response to hypercalcemia and lowers serum calcium
levels
Synthesis and Release of Thyroid Hormones
The synthesis of thyroid hormones requires iodine. Iodine, ingested
in food and water as iodide, is actively concentrated by the thyroid
and converted to organic iodine (organification) within follicular
cells by thyroid peroxidase. The follicular cells surround a space
(follicle) filled with colloid, which consists of thyroglobulin, a
glycoprotein containing tyrosine within its matrix. Tyrosine in
contact with the membrane of the follicular cells is iodinated at 1
(monoiodotyrosine) or 2 (diiodotyrosine) sites and then coupled to produce the 2 forms of thyroid
hormone.
• Diiodotyrosine + diiodotyrosine → T4
• Diiodotyrosine + monoiodotyrosine → T3

T3 and T4 remain incorporated in thyroglobulin within the follicle until the follicular cells take up
thyroglobulin as colloid droplets. Once inside the thyroid follicular cells, T3 and T4 are cleaved
from thyroglobulin. Free T3 and T4 are then released into the bloodstream, where they are bound
to serum proteins for transport. The primary transport protein is thyroxine-binding globulin (TBG),
which has high affinity but low capacity for T3 and T4. TBG normally carries approximately 75%
of bound thyroid hormones.
Approximately 0.3% of total serum T3 and 0.03% of total serum T4 are free and in equilibrium
with bound hormones. Only free T3 and free T4 are available to act on the peripheral tissues. Most
circulating T3 is produced outside the thyroid in peripheral tissues by monodeiodination of T4.
Only one fifth of circulating T3 is secreted directly by the thyroid.
All reactions necessary for the formation and release of T3 and T4 are controlled by thyroid-
stimulating hormone (TSH), which is secreted by pituitary thyrotropic cells. TSH secretion is
controlled by a negative feedback mechanism in the pituitary: Increased levels of free T4 and T3
inhibit TSH synthesis and secretion, whereas decreased levels increase TSH secretion. TSH
secretion is also influenced by thyrotropin-releasing hormone (TRH), which is synthesized in the
hypothalamus. The precise mechanisms regulating TRH synthesis and release are unclear,
although negative feedback from thyroid hormones inhibits TRH synthesis.

Disorders Related to Hypofunction of Thyroid Glands

The presence of thyroid disease is associated with metabolic abnormalities due to the effects of
thyroid hormones on nearly all major metabolic pathways Chiu et al. (2024).
Hypothyroidism is a condition due to thyroid hormone deficiency. It occurs at any age but is
particularly common among older adults, where it may present subtly and be difficult to recognize.
Hypothyroidism may be:
• Primary hypothyroidism
• Secondary hypothyroidism
• Subclinical Hypothyroidism

Primary Hypothyroidism
In primary hypothyroidism, the thyroid gland cannot produce adequate amounts of thyroid
hormone. The most prevalent etiology of primary hypothyroidism is an iodine deficiency in iodine-
deficient geographic areas worldwide. Autoimmune thyroid diseases are the leading causes of
hypothyroidism in the iodine-sufficient regions. Hashimoto thyroiditis is the most commonly seen
etiology in the US and has a strong association with lymphoma. Hypothyroid etiology can be
influenced locally by iodine fortification and the emergence of new iodine-deficient areas.
Other Causes:
• Medications including amiodarone, thalidomide, oral tyrosine kinase inhibitors (eg,
sunitinib, imatinib), stavudine, interferon, bexarotene, perchlorate, rifampin, ethionamide,
phenobarbital, phenytoin, carbamazepine, interleukin-2, and lithium.
• Thyroid surgery
• Radiotherapy of the head or neck area
• The use of immune checkpoint inhibitors (eg, anti-CTLA-4 and anti-PD-L1/PD-1 therapy)
has been associated with both primary and secondary hypothyroidism

Goiter
Patients with IDD most commonly present with
goiter. Is an enlarged thyroid gland that causes
swelling in the neck. There are various possible
causes, but it can be a sign that the thyroid gland
is producing too much or too little thyroid
hormone.

Causes
• Iron deficiency
The most common cause of goiters is the lack of iodine in the diet. The thyroid needs iodine to
create thyroid hormones, which regulate metabolism.
• Hypothyroidism
Hypothyroidism is the result of an underactive thyroid gland. When the gland produces too little
thyroid hormone, it is stimulated to produce more, leading to swelling. This usually results from
Hashimoto’s thyroiditis, a condition in which the body’s immune system attacks its own tissue and
causes inflammation of the thyroid gland.
• Hyperthyroidism
Hyperthyroidism, or an overactive thyroid gland, is another cause of goiters. In people with this
condition, the thyroid produces too much thyroid hormone. This usually happens as a result of
Graves’ disease, an autoimmune disorder where the body’s immunity turns on itself and attacks
the thyroid gland, causing it to swell.
Other causes:
• Smoking: Thiocyanate in tobacco smoke interferes with iodine absorption and can cause
enlargement of the thyroid gland.
• Hormonal changes: Pregnancy, puberty, and menopause can affect thyroid function.
• Thyroiditis: Inflammation caused by infection, for example, can lead to goiter.
• Lithium: This psychiatric drug can interfere with thyroid function.
• Too much iodine: This can trigger a swollen thyroid.
• Radiation therapy: This also can trigger a swollen thyroid, particularly when administered
to the neck.
• Thyroid cancer: This is more common in females.
Symptoms
Hyperthyroidism, or an overactive thyroid, can cause symptoms such as:
• nervousness
• palpitations
• hyperactivity
• increased sweating
• heat hypersensitivity
• fatigue
• increased appetite
• hair loss
• weight loss
Hypothyroidism, or an underactive thyroid, can cause symptoms such as:
• an intolerance to the cold
• constipation
• forgetfulness
• personality changes
• hair loss
• weight gain
Types
• Multinodular goiter: In this common condition, multiple nodules develop in the thyroid.
 • Diffuse smooth goiter: This occurs when the entire thyroid swells. These goiters are
associated with overactive and underactive thyroid glands.
• Retrosternal goiter: This type of goiter can grow behind the breastbone. This can constrict
the windpipe, neck veins, or esophagus, and sometimes requires surgery.
Diagnosis
• A healthcare professional may diagnose a goiter through a physical examination of the
neck, palpating for swelling. They may ask the person to swallow while feeling for a goiter.
• Thyroid function tests are blood tests that measure levels of thyroid-stimulating hormone
(TSH) and thyroxine. A carefully controlled feedback mechanism means that TSH
stimulates the thyroid to produce more thyroxine, while T4 tells the thyroid to stop
producing as much thyroxine.
With an overactive thyroid, TSH levels are low or non-existent, and T4 levels are high. In
people with underactive thyroid, the reverse is true. TSH levels are high and T4 levels are
low. In some cases, such as suspected Graves’ disease, healthcare professionals may test
for another hormone, triiodothyronine.
They may also recommend special tests, such as:
• Radioactive iodine scan: This provides a detailed picture of the gland following an injection
of radioactive iodine.
• Ultrasound scan: This assesses the gland and the size of the goiter.
• Fine-needle aspiration: A doctor may perform a biopsy to remove a sample of cells from
within the gland if, for example, they suspect cancer.
Treatment
Most simple goiters are preventable through adequate intake of iodine, which is added to table salt
in many countries. A range of iodine supplements are also available in health stores.
• Hypothyroidism
In cases caused by an underactive thyroid, or hypothyroidism, treatment is a synthetic replacement
of thyroid hormone. A doctor will gradually increase the dosage of synthetic thyroxine (T4) until
their measurements indicate that the person’s normal thyroid function has been restored.
• Hyperthyroidism
In goiters caused by an overactive thyroid, or hyperthyroidism, treatment aims to counter the
excess hormone production. For instance, antithyroid drugs, such as thionamide drugs, gradually
reduce excessive hormone levels. Another option is radioactive iodine to decrease thyroid function
and stop hormone production.
• Goiter surgery
Doctors will reserve surgery to reduce the size of the swelling for cases where the goiter is causing
troublesome symptoms, such as difficulty breathing or swallowing. Surgeons will usually perform
thyroidectomies, the removal of part or all of the thyroid gland, when the person is under general
anesthetic.

Cretinism
Is an iodine deficiency disorder associated with insufficient
thyroid hormone activity occurring during fetal, infant or
childhood phases.
Types of Cretinism:
Congenital Cretinism
It can be caused due to a defect in the genes encoding various
enzymes involved in thyroid hormone synthesis such as
thyroglobulin, iodotyrosine deiodinase and also thyroid-
stimulating hormone (TSH). This type of hypothyroidism is also called congenital hypothyroidism,
non-goitrous (CHNG).
Endemic Cretinism
This type of cretinism often occurs in children who live in the geographical settings where iodine
is deficient and it is not corrected by either supplementing iodine or thyroid hormone to regain
normal thyroid hormone levels during early life.
a. Neurological cretinism – It is characterized by the following conditions:
• Retarded growth
• Deaf-mutism
• Motor spasticity
• Severe mental retardation with a squint
b. Myxedematous cretinism– It is characterized by the following conditions:
• Retarded growth.
• Incomplete maturation of facial expression.
 • Thickened and dry skin.
• Small and dry hair, eyelashes and eyebrows.
• Mental retardation of comparatively lesser intensity to neurological cretinism.
• Delayed sexual maturation.
Causes
• Lack of thyroid gland and failure of the thyroid gland to produce thyroid hormone
(congenital cretinism or congenital iodine deficiency syndrome).
• Iodine deficiency in the diet (Endemic cretinism).
Signs and Symptoms
• Generally characterized by stunted growth and mental retardation.
• Short stature (dwarfism).
• Mild neurological impairment with reduced muscle tone and coordination.
• Hearing and speech defects.
• Unable to maintain posture and balance with characteristic walking style.
• Myxoedema.
• Enlargement of the thyroid gland (goitre).
• The sparseness of hair and nails.
• Voice will be deep and hoarse.
• Retardation of sexual attributes.
• Thickened skin.
• Enlarged tongue.
• Protruded abdomen.
• Umbilical hernia.
• Delayed tendon reflexes.
• Decreased Intelligent quotient (IQ).
Diagnosis
• Congenital cretinism with severe hypothyroidism can be identified by antenatal screening
test in the first month of life.
• Technetium (Tc– 99m pertechnetate) thyroid scan.
 • Radioactive Iodine (RAIU) test (to differentiate between the congenital absence and a
defect in the organification process).
• Postnatal – Blood spot test such as Guthrie’s test.
• Elevated serum Thyroid binding globulin (TBG) and TSH level.
• Elevated serum T3 and low T4 level.
Treatment
• Once diagnosed, treatment should be started within 1-2 weeks of life.
• Treatment should be started before the onset of symptoms, if developmental abnormalities
and mental retardation start to appear, it will not reverse even with thyroid hormone
replacement therapy.
• The recommended dose is 10 to 15 μg per kg of body weight. The dose should be increased
as the age progresses.
• Everyday treatment with thyroxine should be initiated as early as possible as mental
retardation that has ensued already is only partially reversible. With early treatment,
physical development and growth can be revived and mental retardation can be checked.
Secondary Hypothyroidism
Also known as central hypothyroidism, is caused by a defect in the hypothalamic-pituitary axis
secondary to any of the following:
• Neoplastic, infiltrative, inflammatory, genetic, or iatrogenic disorders of the pituitary or
hypothalamus.
• Pituitary tumors
• Tumors compressing hypothalamus
• Sheehan syndrome
• Thyroid-releasing hormone (TRH) resistance
• TRH deficiency
• Lymphocytic hypophysitis
• Radiation therapy to the brain
• Medications (eg, dopamine, prednisone, or opioids)
Subclinical Hypothyroidism
Characterized by an elevated serum of TSH in patients with absent or minimal symptoms of
hypothyroidism and normal serum levels of free thyroxine (T4). Subclinical thyroid dysfunction
is relatively common; it occurs in approximately 15% of older females and 10% of older males
(1), particularly in those with underlying Hashimoto thyroiditis.

Hashimoto thyroiditis
Hashimoto thyroiditis is chronic autoimmune inflammation of the thyroid with lymphocytic
infiltration. It is believed to be the most common cause of primary hypothyroidism in North
America and is several times more prevalent among females. Incidence increases with age and in
patients with chromosomal disorders, including Down syndrome, Turner syndrome, and
Klinefelter syndrome. A family history of thyroid disorders is common.
Hashimoto thyroiditis, like Graves disease, is sometimes associated with other autoimmune
disorders, including Addison disease (adrenal insufficiency), type 1 diabetes mellitus,
hypoparathyroidism, vitiligo, premature graying of hair, pernicious anemia, systemic rheumatic
diseases (eg, rheumatoid arthritis, systemic lupus erythematosus, Sjögren syndrome), celiac
disease, and type 2 polyglandular deficiency syndrome (Schmidt syndrome—a combination of
Addison disease with hypothyroidism secondary to Hashimoto thyroiditis and/or type 1 diabetes
mellitus). There may be an increased incidence of thyroid tumors, rarely thyroid lymphoma.
Pathologically, there is extensive infiltration of lymphocytes with lymphoid follicles and scarring.
Signs and Symptoms
• Painless enlargement of the thyroid or fullness in the throat
• Nontender goiter that is smooth or nodular, firm, and more rubbery than the normal thyroid.
• Fatigue
• Cold intolerance
• Weight gain
Diagnosis
• Thyroxine (T4)
• Thyroid-stimulating hormone (TSH)
• Thyroid autoantibodies
• Thyroid ultrasonography
Testing consists of measuring T4, TSH, and thyroid autoantibodies. Early in the disease, T4 and
TSH levels are normal and there are high levels of thyroid peroxidase antibodies and, less
commonly, of antithyroglobulin antibodies. Thyroid ultrasonography should be done if there are
palpable nodules. Ultrasonography often reveals that the thyroid tissue has a heterogeneous,
hypoechoic echotexture with septations that form hypoechoic micronodules, and there may be
reduced vascularity of the gland.
Treatment
• Thyroid hormone replacement
Occasionally, hypothyroidism is transient, but most patients require lifelong thyroid hormone
replacement, typically levothyroxine 75 to 150 mcg orally once a day.
Prevalence
According to Chiu et al. (2024), globally, the prevalence of metabolic syndrome (MS)- a group of
conditions that increase the risk of heart disease, stroke, and type 2 diabetes, in the general
population, ranges from 12.5% to 31.4. In the Philippines, the prevalence of MS in the general
population ranges from 11.9% to 51.0%. Furthermore, according to a recent retrospective cross-
sectional local study in the Philippine General Hospital, Manila, Philippines, it was found out that
36.19% of their patients had the condition. Moreover, the Philippine Thyroid Diseases Study
(PhilTiDeS 1) showed that thyroid dysfunction was more common among women. The national
prevalence of thyroid function abnormalities is 8.5%, true hypothyroidism and subclinical
hypothyroidism have the prevalence rates of 0.4% and 2.2%, respectively.
Pathophysiology
The most common cause of hypothyroidism is the inability of the thyroid gland to produce a
sufficient amount of thyroid hormone; however, less commonly, pituitary and hypothalamus
impairment may also result in thyroid dysfunction. The hypothalamus secretes thyrotropin-
releasing hormone (TRH) that stimulates the pituitary gland to produce thyroid-stimulating
hormone (TSH). Thyroid-stimulating hormones stimulate the thyroid gland to produce and secrete
mainly T4, approximately 100 to 125 nmol daily, and smaller quantities of T3. The half-life of T4
is 7 to 10 days, and eventually, T4 is converted to T3 peripherally by 5'-deiodination. Negative
feedback on the production of TRH and TSH is exerted primarily by T3 and, to some extent, T4.
Alteration in the structure and function of any of these organs or pathways can result in
hypothyroidism. Additionally, the decline in the production of T4 results in an increase in the
secretion of TSH by the pituitary gland, causing hypertrophy and hyperplasia of the thyroid
parenchyma, thereby leading to increased T3 production (Patil et al., 2024).
Signs and Symptoms of Hypothyroidism
Symptoms and signs of primary hypothyroidism are often subtle and insidious. The most common
presenting symptoms are fluid retention and puffiness, especially periorbitally, tiredness, cold
intolerance, and mental fogginess.
Various organ systems may be affected with many possible signs and symptoms, including:
• Metabolic: Cold intolerance, modest weight gain (due to fluid retention and decreased
metabolism), hypothermia
• Neurologic: Forgetfulness, paresthesias of the hands and feet (often due to carpal tunnel
syndrome caused by deposition of proteinaceous ground substance in the ligaments around
the wrist and ankle); slowing of the relaxation phase of deep tendon reflexes
• Psychiatric: Personality changes, depression, dull facial expression, dementia or frank
psychosis (myxedema madness)
• Dermatologic: Facial puffiness; myxedema; sparse, coarse and dry hair; coarse, dry, scaly
and thick skin; carotenemia, particularly notable on the palms and soles (caused by
deposition of carotene in the lipid-rich epidermal layers); macroglossia due to deposition
of proteinaceous ground substance in the tongue
• Ocular: Periorbital swelling due to infiltration with the mucopolysaccharides hyaluronic
acid and chondroitin sulfate, droopy eyelids because of decreased adrenergic drive
• Gastrointestinal: Constipation
• Gynecologic: Heavy menstrual bleeding or secondary amenorrhea
• Cardiovascular: Slow heart rate (a decrease in both thyroid hormone and adrenergic
stimulation causes bradycardia), enlarged heart on examination and imaging (partly
because of dilation but chiefly because of pericardial effusion; pericardial effusions
develop slowly and only rarely cause hemodynamic distress)
• Other: Pleural or abdominal effusions (pleural effusions develop slowly and only rarely
cause respiratory or hemodynamic distress), hoarse voice, and slow speech.
Diagnostic
Serum thyroid-stimulating hormone measurement is the most sensitive test for diagnosing
hypothyroidism. In primary hypothyroidism, there is decreased feedback inhibition of the intact
pituitary, and serum TSH is always elevated, whereas serum free T4 is low. In secondary
hypothyroidism, free T4 and serum TSH are low (sometimes TSH is normal but with decreased
bioactivity)
Hypothyroid Screening Recommendations
While there are no universal guidelines on screening the public for thyroid disease, the American
Thyroid Association recommends that screening be performed every 5 years, beginning at the age
of 35 years. Individuals at high risk for hypothyroidism include the following:
• Women older than 60 years
• Pregnant women
• Patients with a prior history of head and neck irradiation
• Patients with autoimmune disorders or type 1 diabetes
• Positive thyroid peroxidase antibodies
• Family history of thyroid disorders
Prognosis
Without treatment, hypothyroidism may have a risk of high morbidity and mortality and can
eventually lead to coma or even death. In children, failure to treat hypothyroidism can result in
severe mental retardation. A leading cause of death in adults is heart failure. Most patients have a
good prognosis with treatment, and the symptoms usually reverse in a few weeks or months.
Complications
Severe hypothyroidism may present as myxedema coma, and it is an endocrine emergency. Prompt
recognition and early treatment in the intensive care unit (ICU) are essential, and even then,
mortality may reach 25% to 60% of the affected cases. Myxedema crisis should be suspected in
cases where there is encephalopathy, hypothermia, seizures, hyponatremia, hypoglycemia,
arrhythmias, cardiogenic shock, respiratory failure, and fluid retention. Factors leading to an
increased risk of myxedema crisis include inadequate doses of thyroid hormone, interruption in
treatment, undiagnosed hypothyroidism, or the presence of acute illness such as sepsis, perhaps
due to increased metabolic demands. Supportive therapy should be provided in the intensive care
unit with fluid and electrolyte management, ventilator support, and vasopressors, as well as
treatment of hypothermia and any underlying coexisting acute illnesses.
Treatment and Management for Hypothyroidism
Hypothyroidism is primarily treated with levothyroxine monotherapy.
Various thyroid hormone preparations are available for replacement therapy, including synthetic
preparations of T4 (levothyroxine), T3 (liothyronine), combinations of the 2 synthetic hormones,
and desiccated porcine thyroid extract. Levothyroxine is preferred; the usual maintenance dose is
75 to 150 mcg orally once a day, depending on age, body mass index, and absorption (for pediatric
treatment, see Hypothyroidism in Infants and Children). In young or middle-aged patients who are
otherwise healthy, the starting dose of levothyroxine can be 100 mcg or 1.7 mcg/kg orally once a
day.
In patients with heart disease, therapy is begun with low doses of levothyroxine, usually 25 mcg
once a day. The dose is adjusted every 6 weeks until maintenance dose is achieved. The
maintenance dose may need to be increased in patients who are pregnant. Dose may also need to
be increased if medications that decrease T4 absorption or increase its metabolic clearance are
administered concomitantly. The dose used should be the lowest that restores serum TSH levels to
the midnormal range (though this criterion cannot be used in patients with secondary
hypothyroidism). In secondary hypothyroidism the dose of levothyroxine should achieve a free T4
level in the midnormal range.
Surgery
A. Total Thyroidectomy (Complete Removal of Thyroid)
Total thyroidectomy is a surgical procedure that removes the entire thyroid gland. Since the thyroid
produces essential hormones (T3 and T4) that regulate metabolism, patients require lifelong
thyroid hormone replacement therapy (levothyroxine) after the procedure.
Indications:
• Severe goiter (enlarged thyroid) causing difficulty breathing/swallowing.
• Thyroid cancer (most common surgical reason).
• Refractory Hashimoto’s thyroiditis (rare but severe cases).
• Multinodular goiter with compressive symptoms.
Effect on Hypothyroidism:
• Leads to permanent hypothyroidism, requiring lifelong levothyroxine replacement therapy.
B. Partial (Subtotal) Thyroidectomy
Partial or subtotal thyroidectomy is a surgical procedure that removes a portion of the thyroid
gland, leaving some thyroid tissue intact. This allows the remaining gland to continue producing
hormones, reducing the risk of lifelong hypothyroidism compared to a total thyroidectomy.
Indications:
• Large benign thyroid nodules causing symptoms.
• Hyperthyroidism (Graves' disease) that does not respond to medications or radioiodine
therapy.
Effect on Hypothyroidism:
• May or may not develop hypothyroidism, depending on the remaining thyroid function.
C. Thyroid Lobectomy (Hemi-Thyroidectomy)
Thyroid lobectomy, also known as hemi-thyroidectomy, is a surgical procedure that removes one
lobe (half) of the thyroid gland while preserving the other half. This allows the remaining thyroid
tissue to continue producing hormones, reducing the need for lifelong thyroid hormone
replacement therapy.
Indications:
• Suspicious thyroid nodules requiring biopsy/removal.
• Unilateral goiter or small thyroid cancers.
Effect on Hypothyroidism:
• Some patients develop mild hypothyroidism if the remaining lobe does not compensate.
D. Parathyroidectomy (Parathyroid Removal)
Parathyroidectomy is a surgical procedure to remove one or more of the parathyroid glands, which
are small glands located behind the thyroid. These glands regulate calcium levels in the blood by
producing parathyroid hormone (PTH).
Indications:
• Secondary hyperparathyroidism due to chronic hypothyroidism.
• Parathyroid adenomas or hyperplasia affecting calcium metabolism.
Effect on Hypothyroidism:
• Not directly related, but may worsen metabolic imbalances.
Perioperative Care in Hypothyroid Patients
A. Preoperative Care
1. Assess Thyroid Function:
• Check TSH, Free T3, Free T4 levels.
• Optimize thyroid hormone levels with levothyroxine therapy if needed.
2. Cardiac Evaluation:
• Hypothyroid patients have bradycardia (slow heart rate) and risk of heart failure.
• ECG and echocardiogram may be required in severe cases.
3. Anesthesia Precautions:
• Hypothyroidism increases sensitivity to anesthetics, requiring careful dosing.
• Risk of airway obstruction due to goiter or swollen tissues.
4. Manage Electrolyte Imbalances:
• Check for low sodium (hyponatremia) and low glucose in severe cases.
• Ensure normal calcium and vitamin D levels, especially in parathyroid surgery.
5. Control Coexisting Conditions:
• Obesity, diabetes, or metabolic syndrome may worsen surgical risks.
• Correct anemia (common in hypothyroidism).
B. Intraoperative Care
1. Anesthesia Considerations:
• Use low-dose sedatives due to increased drug sensitivity.
• Careful airway management if there is a large goiter.
2. Monitor Temperature & Blood Pressure:
• Hypothyroidism increases risk of hypothermia during surgery.
• Maintain stable blood pressure to prevent hypotension and shock.
3. Prevent Myxedema Crisis (Severe Hypothyroid Emergency)
• Rare but life-threatening condition triggered by surgery.
• Symptoms: Low heart rate, confusion, respiratory failure, coma.
• Treat with IV thyroid hormone (levothyroxine) and supportive care.
C. Postoperative Care (After Surgery)
1. Monitor for Hypothyroidism Symptoms
• If the entire thyroid is removed → Start levothyroxine replacement therapy immediately.
• Adjust dose based on TSH and Free T4 levels after 6-8 weeks.
2. Monitor Calcium Levels (If Parathyroids Are Affected)
• Hypocalcemia (low calcium) can occur after total thyroidectomy due to parathyroid gland
damage.
• Symptoms: Numbness, muscle cramps, tetany (severe spasms).
• Treat with calcium and vitamin D supplements if needed.
3. Pain & Wound Care:
• Mild throat pain and swelling are common after thyroid surgery.
• Avoid heavy lifting and strenuous activity for 1-2 weeks.
4. Monitor for Surgical Complications:
• Bleeding or hematoma (risk of airway obstruction).
• Hoarseness or voice changes (due to recurrent laryngeal nerve injury).
• Infection (rare, but monitor for fever or pus at the incision site).
Long-Term Management After Thyroid Surgery
• Patients who undergo a total thyroidectomy require lifelong thyroid hormone replacement.
• Regular follow-ups with TSH tests (every 6-12 months) to adjust levothyroxine dosage.
• Maintain iodine & selenium intake for optimal thyroid function (if partial thyroid remains).

PARATHYROID

Parathyroid Gland
The parathyroid glands are four small glands located on the
posterior surface of the thyroid gland in the neck. Their
primary function is to regulate calcium and phosphorus levels
in the blood through the secretions of parathyroid hormone
(PTH). The levels of PTH and serum calcium are inversely
proportional. At low serum calcium levels, PTH, in
conjunction with vitamin D, works at many sites in the body
to mobilize calcium stores and increase calcium absorption
and reabsorption. Both calcium and vitamin D provide
negative feedback to the parathyroid glands; as calcium and vitamin D levels increase, they bind
receptors at the parathyroid glands and inhibit the production and release of PTH.
Hypofunction: Hypoparathyroidism
Hypoparathyroidism is an uncommon endocrine abnormality in which parathyroid gland
dysfunction causes parathyroid hormone deficiency. Subsequently, this absence or decreased level
of parathyroid hormone results in hypocalcemia, hyperphosphatemia, and increased
neuromuscular irritability.

Pathophysiology
Hypoparathyroidism is a condition characterized by insufficient secretion of parathyroid
hormone (PTH), leading to disturbances in calcium, phosphate, and bone metabolism. Normally,
PTH regulates calcium homeostasis by increasing calcium reabsorption in the kidneys, stimulating
calcium release from bones, and promoting calcium absorption in the intestines via activation of
vitamin D. In hypoparathyroidism, reduced PTH levels result in hypocalcemia (low blood calcium
levels) and hyperphosphatemia (high phosphate levels), which can cause neuromuscular
irritability, tetany, and cardiac arrhythmias. The deficiency may be due to autoimmune destruction,
surgical removal of the parathyroid glands (post-thyroidectomy or parathyroidectomy), genetic
disorders, or magnesium imbalances affecting PTH secretion.
Without adequate PTH, calcium levels drop, impairing nerve conduction and muscle
contraction, leading to symptoms such as tetany, muscle cramps, seizures, and paresthesia
(numbness and tingling in extremities). Chronic hypocalcemia may result in cataracts, brittle nails,
dry skin, and neuropsychiatric symptoms like depression or confusion. The lack of PTH also
reduces calcium resorption from bones, potentially leading to osteosclerosis (abnormally dense
bones). In severe cases, prolonged hypocalcemia can cause laryngospasm or cardiac complications
such as prolonged QT interval, increasing the risk of arrhythmias. Management focuses on calcium
and vitamin D supplementation to maintain normal calcium levels and prevent complications.

Causes of hypoparathyroidism
The most common cause of hypoparathyroidism is removal of or accidental injury to the
parathyroid glands during surgery to the neck.
Other causes include:
 • autoimmune conditions, where the body mistakenly attacks its own tissues – such
as Addison's disease and pernicious anaemia
• being born without parathyroid glands or with glands that don't work properly – for
example, people with the inherited genetic disorder DiGeorge syndrome can have
underdeveloped parathyroid glands
• radiotherapy to treat throat or neck cancer
• low blood magnesium levels – for example, because of alcohol misuse
Risk Factors
Factors that can increase the risk of developing hypoparathyroidism include:
• Recent neck surgery, particularly if the thyroid was involved
• A family history of hypoparathyroidism
• Having certain autoimmune or endocrine conditions, such as Addison's disease — which
causes a decrease in the hormones the adrenal glands produce
Signs and symptoms
• a tingling sensation (paraesthesia) in your fingertips, toes and lips
• twitching facial muscles
• muscle pains or cramps, particularly in your legs, feet or tummy
• tiredness
• mood changes, such as feeling irritable, anxious or depressed
• dry, rough skin
• coarse hair that breaks easily and can fall out
• brittle fingernails
• abnormal heart rhythms
Diagnostic tests
Blood Test: To determine the parathyroid hormone, calcium, phosphorus, creatinine, magnesium
Urine Test: To determine how much calcium the kidneys are releasing.
Electrocardiogram: To determine heart rhythms
Management
The goal of treatment is to restore the calcium and mineral balance within the body.
Oral calcium carbonate and vitamin D supplements are usually life-long therapy. Blood levels are
measured regularly to make sure that the dose is correct. A high-calcium, low-phosphorous diet is
recommended.
In the event of a life-threatening attack of low calcium levels or tetany (prolonged muscle
contractions), calcium is administered by intravenous (IV) infusion. Precautions are taken to
prevent seizures or larynx spasms. The heart is monitored for abnormal rhythms until the person
is stable. When the life-threatening attack has been controlled, treatment continues with medicine
taken by mouth.

Nursing Responsibilities
➢ Monitor serum calcium levels regularly to prevent hypocalcemic crises
➢ Observe for tetany, muscle cramps, numbness, tingling and Chvostek`s/Trosseau`s sign,
which indicates hypocalcemia
➢ Monitor for cardiac arrythmias, as hypocalcemia affects heart function
➢ Encourage a high-calcium, low phosphorus diet
➢ Promote adequate hydration to prevent kidney stones.
➢ Encourage stress management since emotional stress can trigger symptoms

ADRENAL GLAND

Adrenal gland is also known as suprarenal glands, are

small, triangular-shaped glands located on top of both
kidneys. It produces hormones that help regulate your
metabolism, immune system, blood pressure, response to
stress and other essential functions.

An adrenal gland is made of two main parts:

• The adrenal cortex is the outer region and also the largest part of an adrenal gland. It is
divided into three separate zones: zona glomerulosa, zona fasciculata and zona reticularis.
Each zone is responsible for producing specific hormones.
 • The adrenal medulla is located inside the adrenal cortex in the center of an adrenal gland.
It produces “stress hormones,” including adrenaline.
These two parts are enveloped in an adipose capsule that forms a protective layer around an
adrenal gland.

Hypofunction of Adrenal Glands

Adrenal insufficiency is an endocrine disorder that happens when the adrenal gland doesn’t
produce enough hormones, particularly mineralocorticoids like aldosterone, glucocorticoids like
cortisol, and androgens like testosterone.
Adrenal insufficiency can be primary or secondary:
• Primary adrenal insufficiency. This is known as Addison's disease. It occurs when the
adrenal glands are damaged. They don’t make enough of the hormones cortisol and
aldosterone. This condition is rare. It may occur at any age.
• Secondary adrenal insufficiency. This starts when the pituitary gland doesn’t make
enough of the hormone ACTH (adrenocorticotropin). As a result the adrenal glands don’t
make enough cortisol.

Who are at risk?

Addison’s disease can affect people of all age groups, but it’s most common in people 30 to 50
years old. People who have autoimmune polyendocrine syndrome, a rare, inherited condition in
which your immune system mistakenly attacks many of your tissues and organs, are much more
likely to have Addison’s disease. Your mucous membranes, adrenal glands and parathyroid glands
are commonly affected by this syndrome, though it can affect other types of tissues and organs.
People who have the following autoimmune disease are also at higher risk of developing the
autoimmune (most common) form of Addison's disease:
• Type 1 diabetes
• Pernicious Anemia
• Graves` Disease
• Chronic Thyroiditis
With Addison’s disease, the damage to your adrenal glands usually happens slowly over time, so
symptoms occur gradually. Symptoms vary from person to person.
Symptoms of Addison’s disease include:
• Steadily worsening fatigue (most common symptom).
• Patches of dark skin (hyperpigmentation), especially around scars and skin creases and on
your gums.
• Abdominal pain.
• Nausea and vomiting.
• Diarrhea.
• Loss of appetite and unintentional weight loss.
• Muscle pain, muscle spasms and/or joint pain.
• Dehydration.
• Low blood pressure, which can cause lightheadedness or dizziness upon standing.
• Changes in mood and behavior, such as irritability, depression and poor concentration.
• A craving for salty food.
• Low blood sugar (hypoglycemia)
Diagnostic tests
To determine Addison’s disease, healthcare provider may order the following tests:
• Blood tests: To measure the levels of sodium, potassium, cortisol and ACTH in your blood.
• ACTH stimulation test: This test measures your adrenal glands’ response after you’re
given a shot of artificial ACTH. If your adrenal glands produce low levels of cortisol after
the shot, they may not be functioning properly.
• Insulin-induced hypoglycemia test: to determine if your symptoms are due to problems
with your pituitary gland (secondary adrenal insufficiency) instead of your adrenal glands.
This test measures blood sugar (glucose) levels before and after the injection of fast-acting
insulin, which should lead to a drop in blood sugar (hypoglycemia) and a rise in cortisol.
• Imaging test: CT scans of the abdomen to check the size of the adrenal glands and look
for tumors, bleeding and other abnormalities
Treatment
Addison's disease treatment involves taking medicines to correct the levels of steroid hormones
that the body isn't making enough of. Some treatments include corticosteroid medicines taken by
mouth such as:
 • Hydrocortisone (Cortef), prednisone (Rayos, Prednisone Intensol) or methylprednisolone
(Medrol) to replace cortisol. These medicines should be taken on a schedule. This helps
mimic the changes in cortisol levels the body typically goes through over 24 hours.
• Fludrocortisone acetate to replace aldosterone.
Nursing Responsibilities
➢ Monitor vital signs and symptoms such as hypotension, dehydration and electrolytes
imbalance
➢ Ensure proper corticosteroid and mineralocorticoid therapy, monitor for side effects
➢ Encourage oral fluids, administer IV fluids as needed
➢ Educate the patient on recognizing early signs of adrenal crisis
➢ Recommend a proper diet, regular meals to prevent hypoglycemia and stress management
techniques

PITUITARY GLAND
What is the pituitary gland?
The pituitary gland, also known as hypophysis, produces hormones
that enable other glands in the body to function. It is located at the
base of the brain. The gland is attached to the hypothalamus, which
is a part of the brain that affects the pituitary gland, by nerve fibers
and blood vessels. It sits in its own little chamber under your brain
known as the sella turcica.
It is also often called as the “master gland,” because it controls the
functions of many of the other endocrine glands such as the thyroid,
adrenals, and gonads. It plays a vital role in regulating various endocrine functions by secreting
hormones that influence growth, metabolism, and reproduction.
Anatomy
Where is the pituitary gland located?
Your pituitary gland is located at the base of your brain, behind the bridge of your nose and
directly below your hypothalamus. It sits in an indent in the sphenoid bone called the sella
turcica.
What are the parts of the pituitary gland?
Your pituitary gland has two main parts, or lobes: the anterior (front) lobe and the posterior
(back) lobe. Each lobe has different functionality and different types of tissue.
The anterior pituitary, the larger of the two lobes, consists of hormone-secreting epithelial
cells and is connected to your hypothalamus through blood vessels.
The posterior pituitary consists of unmyelinated (lacking a casing of fatty insulation) secretory
neurons and is connected to your hypothalamus through a nerve tract.
How big is the pituitary gland?
A healthy pituitary gland weighs less than one gram (less than one paperclip) and is about the
size of a pea or kidney bean.
The anterior pituitary lobe is bigger than the posterior lobe and accounts for about 80% of the
total weight of your pituitary gland.
Functions of the pituitary gland
Each lobe of the pituitary gland makes certain hormones.
Anterior lobe
The mnemonic FLATPEG to remember the hormones that the anterior lobe secretes:
F- FSH (follicle-stimulating hormone which regulates the ovaries and testes)
L- LH (luteinizing hormone which regulates the ovaries or testes)
A- ACTH (adrenocorticotropic hormone which regulates the adrenal glands )
T- TSH (thyroid-stimulating hormone which regulates the thyroid gland )
P- Prolactin (to stimulate milk production in the female breast)
E- Endorphins (the “feel good” hormone, alleviates pain, lowers stress)
G- Growth hormone
Posterior lobe
• ADH, or antidiuretic hormone, also known as vasopressin, is produced in the
hypothalamus and stored in the pituitary gland; it increases absorption of water by the
kidneys. It also increases blood pressure)
• Oxytocin (to contract the uterus during childbirth and stimulate the release of milk during
breastfeeding)
Conditions and Disorders
What conditions and disorders are related to the pituitary gland?
Several conditions can affect or are affected by your pituitary gland’s function. When the
pituitary gland is acutely or chronically disrupted, it can significantly affect metabolism and
homeostasis, primarily through its interactions with target organs and hormones. Since your
pituitary gland and hypothalamus work together so closely, if one of them becomes damaged, it
can affect the hormonal function of the other.
Signs and symptoms of Pituitary Disorders:
Specific symptoms often depend on the disorder and hormone affected. A tumor’s location and
size play roles, too. Common symptoms include:
• Anxiety or depression
• Diabetes
• Hair loss
• High blood pressure
• Irregular menstrual periods
• Unexpected breast milk production
• Low energy or low sex drive
• Stunted growth or unusual growth spurts
• Unexplained weight gain
• Vision changes
Problems and Alterations of the Pituitary Gland Relating to Hypofunction:
Hypopituitarism
Hypopituitarism is a condition in which there’s a lack of one, multiple or all of the hormones
your pituitary gland makes.
Most cases of hypopituitarism involve one hormone deficiency. A deficiency in two or more of
the pituitary hormones is called panhypopituitarism. This typically happens after pituitary
surgery or brain radiation.
Hypopituitarism is most often caused by some type of damage to your pituitary gland or
hypothalamus.
A. Pituitary (Hypophysial) Crisis / Acute Pituitary Insufficiency
1. Cause: This can result from a sudden insult such as pituitary apoplexy (hemorrhage or
infarction in the pituitary, often in the presence of an existing adenoma), head trauma, or
 abrupt withdrawal of exogenous steroids (leading to acute adrenal insufficiency if ACTH
secretion was suppressed).
2. Pathophysiologic Changes:
o Decreased ACTH → sudden drop in cortisol production by adrenal glands →
severe hypotension, shock, and possible adrenal crisis.
o Decreased TSH → low thyroid hormone levels, although effects develop more
gradually than the adrenal issues.
o Decreased GH → affects glucose metabolism and muscle/fat distribution (usually
not the most acute issue).
o Decreased ADH release (if posterior pituitary or hypothalamic input is affected)
→ diabetes insipidus (polyuria, polydipsia, hypernatremia).
3. Clinical Presentation:
o Sudden headache (especially with pituitary apoplexy)
o Visual disturbances (due to pressure on optic chiasm)
o Signs of acute adrenal insufficiency: severe hypotension, fatigue, confusion,
potential shock
o Electrolyte imbalances: hyponatremia, hyperkalemia (especially if cortisol is
significantly deficient)
B. Chronic Hypopituitarism
1. Cause: Slow-growing pituitary tumors (often adenomas), autoimmune inflammation, or
previous surgery/radiation to the pituitary region can gradually reduce pituitary hormone
production.
2. Pathophysiologic Changes:
o Gradual deficiency in one or more of the anterior pituitary hormones (ACTH,
TSH, GH, LH, FSH, prolactin).
o ACTH deficiency → chronic secondary adrenal insufficiency (fatigue, low blood
pressure, poor stress response).
o TSH deficiency → secondary hypothyroidism (weight gain, cold intolerance,
bradycardia, fatigue).
o GH deficiency (in children) → short stature; (in adults) → changes in body
composition, poor muscle mass, dyslipidemia.
 o Gonadotropin deficiency (LH, FSH) → amenorrhea, infertility, reduced libido,
osteoporosis (long term).
3. Clinical Presentation:
o Progressive fatigue, weakness, weight changes
o Menstrual irregularities, infertility
o Decreased libido, erectile dysfunction
o Reduced tolerance for stress and infections
C. Chronic SIADH
While SIADH can present acutely, it may also become chronic due to ongoing ectopic ADH
production or persistent pituitary/hypothalamic abnormalities. Over time, chronic fluid retention
and recurrent hyponatremia episodes can cause cognitive and neurologic disturbances if not
managed.
D. Diabetes Insipidus (DI)
1. Cause: Inadequate ADH production (Central DI), typically from chronic pituitary or
hypothalamic damage (tumors, trauma, autoimmune).
2. Pathophysiologic Changes:
o Lack of ADH action in the kidney → inability to concentrate urine → massive
polyuria, polydipsia, potential hypernatremia if fluid intake does not keep up.
3. Clinical Presentation:
o Chronic dehydration if fluid intake is inadequate
o Significant thirst, nocturia
o Electrolyte imbalances (e.g., hypernatremia) if water losses are extreme
Hypopituitarism: Chronic deficiencies in pituitary hormone production can result from
various causes, including tumors, infiltrative diseases, or autoimmune conditions. The
clinical manifestations depend on the specific hormones that are deficient:
o Growth Hormone (GH) Deficiency: Leads to decreased muscle mass, increased
fat mass, and reduced quality of life.
o Adrenocorticotropic Hormone (ACTH) Deficiency: Results in secondary
adrenal insufficiency, characterized by fatigue, weight loss, and hypoglycemia.
o Thyroid-Stimulating Hormone (TSH) Deficiency: Causes secondary
hypothyroidism, presenting with fatigue, weight gain, and cold intolerance.
 o Gonadotropin Deficiency (LH and FSH): Leads to hypogonadism, resulting in
menstrual irregularities in women and decreased libido and erectile dysfunction in
men.
The pathophysiology involves the loss of trophic stimulation to target endocrine
glands, leading to decreased hormone production and subsequent metabolic
disturbances.
2. Pituitary Adenomas: These are benign tumors of the pituitary gland that can cause
hormonal hypersecretion or hyposecretion, depending on their type and size. For
instance, a prolactinoma secretes excess prolactin, leading to galactorrhea and
reproductive dysfunction. Non-functioning adenomas may cause hypopituitarism by
compressing normal pituitary tissue. The pathophysiologic basis involves either the
overproduction of specific hormones or the mass effect of the tumor compressing
adjacent structures.
Specific conditions that involve a deficiency of a pituitary hormone include:
• Growth hormone deficiency: This condition happens when your pituitary doesn’t
release enough growth hormone (GH). In children, it causes a lack of growth and
development and delayed puberty. In adults, it causes metabolic issues.
• Central diabetes insipidus: This condition happens when your pituitary doesn’t release
enough antidiuretic hormone (ADH, or vasopressin). This causes your body to produce
too much urine (pee), and it isn’t able to retain enough water.
• Central hypogonadism: This condition happens when your pituitary doesn’t release
enough luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This causes
issues with sexual function and development and fertility.
• Central adrenal insufficiency: This condition happens when your pituitary doesn’t
release enough ACTH. It causes your body to be unable to release cortisol.
• Central hypothyroidism: This condition happens when your pituitary doesn’t release
enough thyroid-stimulating hormone (TSH). It causes low thyroid hormone levels.
Treatment of hypopituitarism involves replacing the lacking hormones and monitoring the levels
through blood tests.
Nursing and Clinical Considerations
• Assessment: Monitor vital signs, fluid balance, electrolyte levels, and blood glucose
levels. Watch for signs of endocrine crises.
• Medication Management: Patients may require hormone replacement therapies (e.g.,
glucocorticoids, levothyroxine, desmopressin for DI) or medications to control excess
hormone production (e.g., somatostatin analogs for acromegaly, dopamine agonists for
prolactinomas).
• Education and Lifestyle: Teach patients about medication adherence, recognizing signs
of hormone imbalance (e.g., changes in energy, weight, thirst, or mood), and the
importance of regular follow-ups and lab tests.
• Long-Term Monitoring: Chronic conditions like acromegaly or hypopituitarism require
lifelong monitoring for complications.
Healthcare Treatment
What kind of healthcare provider treats pituitary gland issues?
Endocrinologists typically treat pituitary gland issues.
An endocrinologist is a healthcare provider who specializes in endocrinology, a field of medicine
that studies conditions related to your hormones. An endocrinologist can diagnose endocrine
(hormone) conditions, develop treatment and management plans for them and prescribe
medication.
If you have a pituitary gland issue, such as a pituitary adenoma, that’s affecting structures in your
brain and/or requires surgery, you’ll also need to see a neurosurgeon.
How do healthcare providers diagnose pituitary gland issues?
Since your pituitary gland releases hormones directly into your bloodstream, healthcare
providers often rely on blood tests to measure pituitary hormone levels.
If you have irregular hormone levels, your provider may also order imaging tests, such as a CT
scan or MRI scan, to evaluate your pituitary gland for any issues. Typically, providers order a
dedicated pituitary MRI to see your pituitary gland and stalk more clearly.

Care
How do I keep my pituitary gland healthy?
The best way to keep your pituitary gland healthy is to protect your head. Head injuries
and traumatic brain injuries (TBIs) can damage your pituitary gland, which can cause it to
release too little or excess hormones.
Things you can do to try to prevent head and brain injuries include:
• Wear a seat belt every time you drive or ride in a vehicle.
• Practice safe driving.
• Wear a helmet when you partake in certain activities, such as riding a bike or motorcycle
and playing contact sports.
• Take steps to prevent falls, especially if you’re at a greater risk for them. This can include
strength and balance exercises, removing obstacles and tripping hazards in your home,
using a walking aid and making sure you have clear vision.
• If you have children, make living and play areas safe for them.
When should I see my healthcare provider about my pituitary gland?
If you experience symptoms of a pituitary adenoma and/or hormonal imbalance, it’s important to
talk to your healthcare provider. They can run some tests to see if something is wrong with your
pituitary gland.
If you’ve recently experienced a traumatic brain injury (TBI), your provider will likely want to
monitor the function of your pituitary gland to make sure it’s working properly and wasn’t
damaged from the injury.
Summary
Your pituitary is a tiny but powerful gland. Since it’s responsible for several different hormones
that affect many aspects of your body and health, it can be difficult to pinpoint if certain symptoms
are a result of issues with your pituitary gland or something else. If you’re ever experiencing new
or concerning symptoms, it’s important to talk to your healthcare provider. They can usually run
some simple tests to assess your health.

PANCREAS
Anatomy and Physiology of the Pancreas
The pancreas is a vital organ located behind the stomach, playing dual roles in the body's
endocrine and exocrine systems. Its endocrine function involves the secretion of hormones like
insulin and glucagon, which regulate blood glucose levels. Insulin, produced by beta cells in the
islets of Langerhans, lowers blood glucose by facilitating cellular uptake, while glucagon raises
blood glucose by promoting glycogen breakdown in the liver. The exocrine function involves the
production of digestive enzymes that aid in the digestion of proteins, fats, and carbohydrates in
the small intestine.
Pathophysiology of Diabetes Mellitus
Diabetes mellitus is a group of metabolic disorders characterized by chronic hyperglycemia
resulting from defects in insulin secretion, insulin action, or both. The main cause of diabetes
varies by type. But no matter what type of diabetes you have, it can lead to excess sugar in the
blood. Too much sugar in the blood can lead to serious health problems. The two primary types
are:
1. Type 1 Diabetes Mellitus (T1DM): This is an autoimmune condition where the body's
immune system attacks and destroys the insulin-producing beta cells in the pancreas,
leading to an absolute insulin deficiency. The exact cause is unknown, but genetic and
environmental factors are believed to play roles. Without sufficient insulin, glucose
accumulates in the bloodstream, leading to hyperglycemia.
2. Type 2 Diabetes Mellitus (T2DM): This form is characterized by insulin resistance,
where the body's cells do not respond effectively to insulin, combined with a relative
insulin deficiency. Initially, the pancreas compensates by producing more insulin, but
over time, beta cell function declines, leading to hyperglycemia. Factors contributing to
T2DM include genetics, obesity, physical inactivity, and poor diet.
To understand diabetes, it's important to understand how the body normally uses glucose.
How insulin works
Insulin is a hormone that comes from a gland behind and below the stomach (pancreas).
• The pancreas releases insulin into the bloodstream.
• The insulin circulates, letting sugar enter the cells.
• Insulin lowers the amount of sugar in the bloodstream.
• As the blood sugar level drops, so does the secretion of insulin from the pancreas.
The role of glucose
Glucose — a sugar — is a source of energy for the cells that make up muscles and other tissues.
• Glucose comes from two major sources: food and the liver.
• Sugar is absorbed into the bloodstream, where it enters cells with the help of insulin.
 • The liver stores and makes glucose.
• When glucose levels are low, such as when you haven't eaten in a while, the liver breaks
down stored glycogen into glucose. This keeps your glucose level within a typical range
Prevalence in the Philippines
Diabetes is a significant health concern in the Philippines. As of 2021, an estimated 4.3 million
Filipinos were diagnosed with diabetes, with an additional 2.8 million cases undiagnosed.
Diabetic retinopathy is a leading cause of preventable blindness in the country, and diabetic
nephropathy accounts for 38% of renal disease cases.
Risk Factors
• Non-Modifiable:
o Genetics: Family history of diabetes increases risk.
o Age: Risk increases with age, particularly after 40.
• Modifiable:
o Obesity: Excess body weight, especially central obesity, is a major risk factor.
o Physical Inactivity: Sedentary lifestyle contributes to insulin resistance.
o Diet: High intake of processed foods, sugary beverages, and low fiber intake
increase risk.
o Hypertension and Dyslipidemia: Associated with increased risk of T2DM.
Signs and Symptoms
• Common to Both Types:
o Polyuria (frequent urination)
o Polydipsia (increased thirst)
o Polyphagia (increased hunger)
o Unexplained weight loss
o Fatigue
o Blurred vision
o Slow-healing wounds
• Specific to T1DM:
o Rapid onset of symptoms
o Presence of ketones in urine
• Specific to T2DM:
o Gradual onset of symptoms
o Frequent infections
 o Areas of darkened skin (acanthosis nigricans)
Diagnostic Tests
• Fasting Plasma Glucose (FPG): Measures blood glucose after an overnight fast.
• Oral Glucose Tolerance Test (OGTT): Assesses blood glucose before and after
consuming a glucose-rich drink.
• Hemoglobin A1c (HbA1c): Reflects average blood glucose levels over the past 2-3
months.
• Random Plasma Glucose Test: Measures blood glucose without regard to last meal.
Treatment
• Lifestyle Modifications:
o Diet: Emphasis on balanced meals with appropriate carbohydrate counting.
o Exercise: Regular physical activity to improve insulin sensitivity.
o Weight Management: Achieving and maintaining a healthy weight.
• Pharmacotherapy:
o Insulin Therapy: Essential for T1DM and sometimes required for T2DM.
o Oral Hypoglycemic Agents: Such as metformin, sulfonylureas, and DPP-4
inhibitors for T2DM.
o GLP-1 Receptor Agonists: Enhance insulin secretion and suppress glucagon
release.
Surgical Interventions
• Bariatric Surgery: Considered for obese patients with T2DM to improve glycemic
control.
• Pancreas Transplantation: Option for selected patients with T1DM, particularly those
undergoing kidney transplantation.
Nursing Responsibilities
• Patient Education: Instruct patients on blood glucose monitoring, insulin injection
medication administration, recognizing signs of hypo- and hyperglycemia, managing
blood sugar.
• Lifestyle Counseling: Support dietary planning, encourage physical activity, and
promote weight management.
• Monitoring: Regular assessment of blood glucose levels and vital signs.
• Care management: Ensure patients follow up with their care team, help patients
identify and treat life-threatening complications like diabetic ketoacidosis, provide
psychological support and care, and help patients feel hopeful and secure
 References

Boucai, L. (2024). Overview of Thyroid Function - Endocrine and Metabolic Disorders. MSD
Manual Professional Edition. https://www.msdmanuals.com/professional/endocrine-and-
metabolic-disorders/thyroid-disorders/overview-of-thyroid-function
BYJU'S. (2024). Cretinism: Meaning, Causes, Symptoms, Congenital and Endemic Cretinism.
BYJUS. https://byjus.com/neet/cretinism/
Cando, L. F. T., Quebral, E. P. B., Ong, E. P., Catral, C. D. M., Relador, R. J. L., Velasco, A. J. D.,
Alcazar, R. M. U., Reyes, N. a. L., Pilotin, E. J. B., Ornos, E. D. B., Paz-Pacheco, E., &
Tantengco, O. a. G. (2024). Current status of diabetes mellitus care and management in the
Philippines. Diabetes & Metabolic Syndrome Clinical Research & Reviews, 18(2),
102951. https://doi.org/10.1016/j.dsx.2024.102951
Chiu, H. H., Villanueva, E. I., Larrazabal, R. Jr., Arcellana, A. E., & Jimeno, C. (2024).
Characteristics and Prevalence of Metabolic Syndrome among Adult Filipinos with
Hypothyroidism: A Cross-sectional Study. Journal of the ASEAN Federation of Endocrine
Societies, 39(1), 53–60. https://doi.org/10.15605/jafes.039.01.13
Diabetes - Symptoms and causes. (n.d.). Mayo Clinic. https://www.mayoclinic.org/diseases-
conditions/diabetes/symptoms-causes/syc-20371444
Fletcher, J. (2023, February 16). How is the pancreas involved in diabetes?
https://www.medicalnewstoday.com/articles/325018?utm
How do healthcare providers diagnose hypoparathyroidism? (2019, June 26).
https://www.nichd.nih.gov/.
How do healthcare providers diagnose hypoparathyroidism? (2019c, June 26).
https://www.nichd.nih.gov/.https://www.nichd.nih.gov/health/topics/hypopara/conditioni
nfo/diagnosed
Hyperparathyroidism - Diagnosis & treatment - Mayo Clinic. (2022b, May 17). Mayo Clinic.
https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/diagnosis-
treatment/drc-20356199
Hyperparathyroidism - Symptoms & causes - Mayo Clinic. (2022, May 17). Mayo Clinic.
https://www.mayoclinic.org/diseases-conditions/hyperparathyroidism/symptoms-
causes/syc-20356194
Hypoparathyroidism - Symptoms & causes - Mayo Clinic. (2022, May 11). Mayo Clinic.
https://www.mayoclinic.org/diseases-conditions/hypoparathyroidism/symptoms-
causes/syc-20355375
Hypoparathyroidism. (n.d.). UCLA Health. https://www.uclahealth.org/medical-
services/surgery/endocrine-surgery/patient-resources/patient-education/endocrine-
surgery-encyclopedia/hypoparathyroidism
Hypopituitarism. (2021, June 17). Johns Hopkins Medicine.
https://www.hopkinsmedicine.org/health/conditions-and-diseases/hypopituitarism
Lee, S. L. (2024, December 12). Iodine Deficiency Clinical Presentation: History and Physical
Examination. Medscape.com; Medscape. https://emedicine.medscape.com/article/122714-
clinical#b4
Lewis, J. L., III. (2024, October 9). Hyperparathyroidism. MSD Manual Professional Edition.
https://www.msdmanuals.com/professional/endocrine-and-metabolic-
disorders/parathyroid-disorders/hyperparathyroidism
Lofrese JJ, Basit H, Lappin SL. Physiology, Parathyroid. [Updated 2023 Jul 17]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK482510/
MacGill, M. (2020, October 16). Everything you need to know about a goiter.
Medicalnewstoday.com; Medical News Today.
https://www.medicalnewstoday.com/articles/167559#diagnosis
Patil, N., Rehman, A., & Jialal, I. (2024, February 18). Hypothyroidism. PubMed; StatPearls
Publishing. https://www.ncbi.nlm.nih.gov/books/NBK519536/
Pituitary gland. (2021, August. Johns Hopkins Medicine.
https://www.hopkinsmedicine.org/health/conditions-and-diseases/the-pituitary-gland
Professional, C. C. M. (2024, December 19). Pituitary gland. Cleveland Clinic.
https://my.clevelandclinic.org/health/body/21459-pituitary-gland Understanding Pituitary
Disorders | Brain Institute | OHSU. (n.d.). https://www.ohsu.edu/brain-
institute/understanding-pituitary-disorders
Young, W. (2022). Overview of Endocrine Disorders - Endocrine and Metabolic Disorders. MSD
Manual Professional Edition. https://www.msdmanuals.com/professional/endocrine-and-
metabolic-disorders/principles-of-endocrinology/overview-of-endocrine-disorders