UNIT 8 Nursing management of patients with disorders of endocrine system
π§ Review of Anatomy and Physiology of the Endocrine System
π Definition of Endocrine System:
The endocrine system is a network of glands that produce and secrete hormones directly into the bloodstream to regulate the bodyβs growth, metabolism, development, tissue function, reproduction, mood, and homeostasis.
βοΈ Major Characteristics of the Endocrine System:
π§ͺ Feature
π‘ Description
π Regulation
Maintains long-term processes like growth and development
𧬠Hormone-based
Uses chemical messengers called hormones
π§ Close integration with nervous system
Works with hypothalamus to coordinate body functions
β³ Slower but prolonged response
Compared to nervous system (which is faster but short-lived)
π§ββοΈ Major Endocrine Glands and Hormones:
π¬ Gland
π Location
π Hormones Secreted
π Function
Hypothalamus
Brain (below thalamus)
CRH, TRH, GnRH, GHRH, Somatostatin
Regulates pituitary gland
Pituitary (Master Gland)
Base of brain
Anterior: GH, TSH, ACTH, FSH, LH, PRL Posterior: ADH, Oxytocin
β Endocrine system controls long-term body functions through hormones β Hormones act on specific target organs via receptors β Maintains homeostasis, growth, metabolism, stress response, and reproduction β Feedback mechanisms maintain hormonal balance β Disorders often arise due to hormone deficiency or excess
To identify signs and symptoms of hormonal imbalances, determine functional changes, evaluate the impact on body systems, and guide effective nursing and medical interventions.
π I. Health History Collection
1. 𧬠General Information:
Age, sex, weight changes
Chief complaints: fatigue, weight loss/gain, polyuria, polydipsia, etc.
To identify dysfunction in hormone production, regulation, or target tissue response and to detect systemic effects of endocrine imbalance. Assessment helps in early detection, accurate diagnosis, and effective management.
ποΈ I. Comprehensive Health History
A detailed history provides critical clues about the type and extent of hormonal dysfunction. Use open-ended and focused questions.
π§Ύ A. Chief Complaint (CC):
Ask the patient: β‘οΈ βWhat brings you here today?β
Reflexes (hyperreflexia in hyperthyroidism, slow in hypothyroidism)
Orientation, memory, behavior
Neuropathy (numbness, tingling in diabetes)
Seizures (hypocalcemia)
β€οΈ G. Cardiovascular and Respiratory:
Palpitations, irregular heart rhythms
Chest pain or breathlessness
Heart sounds (pericardial effusion in hypothyroidism)
𧬠H. Abdominal Examination:
Distension (ascites in Cushingβs)
Liver enlargement (fatty liver in diabetes)
Adrenal mass (pheochromocytoma)
πΊ I. Reproductive and Genitourinary:
Amenorrhea or oligomenorrhea
Erectile dysfunction
Infertility
Changes in libido
π III. Functional and Diagnostic Assessment (Reviewed by Nurse):
π Test
Purpose
β Blood glucose (FBS/RBS/HbA1c)
Diabetes diagnosis/control
β Thyroid profile (TSH, T3, T4)
Thyroid dysfunction
β Cortisol (AM/PM)
Adrenal function
β ACTH stimulation test
Adrenal insufficiency
β Serum electrolytes
NaβΊ, KβΊ, CaΒ²βΊ imbalance
β MRI/CT
Tumors (pituitary, adrenal)
β Urine tests
24-hr catecholamines, ketones
π§· Key Points:
β Always correlate subjective complaints with objective findings β Endocrine disorders can have multi-systemic effects β assess holistically β Monitor trends in weight, energy levels, mental state, and skin/hair changes β Early detection and documentation help prevent complications like thyroid storm, myxedema coma, or adrenal crisis β Nurses play a critical role in ongoing monitoring, patient education, and early warning sign identification
π¦ Disorders of the Thyroid Gland
π Overview of the Thyroid Gland:
The thyroid is a butterfly-shaped gland located anterior to the trachea in the neck.
It secretes:
T3 (Triiodothyronine)
T4 (Thyroxine)
Calcitonin (involved in calcium regulation)
Controlled by the HypothalamicβPituitaryβThyroid Axis:
Hypothalamus β TRH
Pituitary β TSH
Thyroid β T3 & T4
β οΈ Common Disorders of the Thyroid Gland:
π Disorder
β¬οΈ/β¬οΈ Function
π‘ Description
Hypothyroidism
β
Underactive thyroid hormone production
Hyperthyroidism
β
Overactive thyroid hormone production
Goiter
Variable
Enlargement of the thyroid gland
Thyroiditis
β or β
Inflammation of the thyroid gland
Thyroid nodules/cysts
Variable
Lumps in the thyroid; benign or malignant
Thyroid cancer
Variable
Malignancy of thyroid tissue
π§ͺ 1. Hypothyroidism
β Definition:
A condition in which the thyroid gland fails to produce sufficient T3 and T4, slowing down body metabolism.
π― Causes:
Autoimmune (e.g., Hashimotoβs thyroiditis)
Iodine deficiency
Post-thyroidectomy or radioactive iodine treatment
Congenital (cretinism)
Drug-induced (e.g., lithium, amiodarone)
π§ Signs & Symptoms:
Fatigue, weight gain, cold intolerance
Constipation, depression, dry skin, brittle hair
Bradycardia, slow reflexes
Menstrual irregularities
Myxedema (severe form)
π¬ Diagnosis:
β TSH, β T3 & T4 (Primary hypothyroidism)
β TSH, β T3 & T4 (Secondary hypothyroidism)
Thyroid antibodies in autoimmune cases
π Management:
Hormone replacement: Levothyroxine
Lifelong therapy with regular monitoring
π₯ 2. Hyperthyroidism
β Definition:
Excess production of thyroid hormones, accelerating metabolic rate.
Watch for hypocalcemia (Trousseauβs & Chvostekβs signs)
Voice changes (recurrent laryngeal nerve damage)
πΉ Patient Education:
Lifelong medication adherence
Signs of under/overdose
Importance of follow-up and monitoring
Diet: Avoid goitrogens (e.g., cabbage, soy) in iodine-deficient patients
β οΈ Complications of Untreated Thyroid Disorders:
π Disorder
π¨ Complication
Hypothyroidism
Myxedema coma (life-threatening)
Hyperthyroidism
Thyroid storm (acute crisis)
Goiter
Tracheal compression
Thyroid cancer
Metastasis, airway obstruction
Thyroid surgery
Hypocalcemia, voice changes
π§· Key Points:
β Thyroid gland regulates metabolism, growth, and calcium balance β Disorders include hypo-, hyperthyroidism, goiter, nodules, thyroiditis, and cancer β Diagnosis is based on hormone levels, imaging, and biopsy β Treatment includes medications, radioactive iodine, or surgery β Nursing care focuses on assessment, monitoring complications, post-op care, and education
π¦ Hypothyroidism
π Definition:
Hypothyroidism is a clinical condition that results from the underproduction of thyroid hormones (T3 and T4) by the thyroid gland, leading to a slowing of metabolic processes in the body. It may be mild (subclinical) or severe (myxedema).
β οΈ Causes of Hypothyroidism:
πΉ A. Primary Hypothyroidism
(Problem is in the thyroid gland itself) Most common form.
π¨ Cause
π Details
Autoimmune thyroiditis
Hashimotoβs thyroiditis β most common in developed countries
Iodine deficiency
Most common cause globally (especially in endemic regions)
Thyroid surgery
Partial or total thyroidectomy
Radioactive iodine therapy
Used for hyperthyroidism, can cause thyroid damage
Congenital hypothyroidism
Born without a fully functioning thyroid
Drugs
Lithium, amiodarone, interferon-alpha
Infiltrative diseases
Sarcoidosis, hemochromatosis affecting thyroid
πΉ B. Secondary Hypothyroidism
(Problem in the pituitary gland)
π¨ Cause
π Details
Pituitary tumors
Compress or destroy TSH-secreting cells
Pituitary surgery/radiation
Causes hormonal imbalance
Sheehanβs syndrome
Postpartum pituitary infarction
πΉ C. Tertiary Hypothyroidism
(Problem in the hypothalamus)
π¨ Cause
π Details
Hypothalamic tumors
Interfere with TRH production
Trauma/inflammation
CNS infections, radiation injury
πΉ D. Other Causes:
Severe illness (euthyroid sick syndrome)
Resistance to thyroid hormone (rare genetic condition)
𧬠Types of Hypothyroidism:
π·οΈ Type
π Description
Primary Hypothyroidism
Most common; due to direct failure of the thyroid gland
Secondary Hypothyroidism
Due to insufficient TSH secretion from the pituitary
Tertiary Hypothyroidism
Due to lack of TRH secretion from the hypothalamus
Congenital Hypothyroidism
Present at birth; can cause cretinism if untreated
Subclinical Hypothyroidism
Mild; β TSH but normal T3 & T4 levels; asymptomatic or subtle signs
Overt Hypothyroidism
Full-blown symptoms with β TSH and β T3/T4 levels
Myxedema
Severe, life-threatening hypothyroidism with altered mental status, hypothermia, and multi-organ failure
π Pathophysiology of Hypothyroidism:
π§ Disruption in the HypothalamicβPituitaryβThyroid (HPT) Axis:
Normally:
Hypothalamus secretes TRH β Stimulates pituitary to release TSH β TSH stimulates thyroid to produce T3 & T4.
In hypothyroidism:
Due to gland failure, TSH may rise (in primary) but T3/T4 remains low.
π» Reduced Thyroid Hormone Production:
Decreased T3 (active) and T4 levels β Slow down cellular metabolism.
π’ Slowing of Metabolic Processes:
Reduced oxygen consumption and heat production
Decreased energy utilization, protein synthesis, lipid metabolism
π Feedback Mechanism Disrupted:
Low T3/T4 β Pituitary increases TSH in primary hypothyroidism
In secondary/tertiary, both TSH and T3/T4 are low
β οΈ Systemic Effects:
Cardiovascular: Bradycardia, low cardiac output
Nervous system: Slowed cognition, depression
GI: Slowed motility β constipation
Renal: Reduced GFR β fluid retention
Skin: Dryness, thickening
Hematologic: Anemia due to reduced erythropoietin
π¨ Signs and Symptoms of Hypothyroidism:
π System
π§Ύ Clinical Features
π‘οΈ General
Fatigue, cold intolerance, weight gain despite poor appetite
πββοΈ Skin/Hair
Dry, coarse skin; brittle nails; hair thinning or loss; puffy face
Monitor vitals, prevent complications, educate on medication adherence, and promote self-care.
β Complication to watch for:
Myxedema coma β medical emergency with altered mental status, hypothermia, and organ failure
β Patient Education:
Take medication on an empty stomach
Avoid drug interactions (e.g., calcium, iron)
Never stop medication abruptly
Regular follow-up is essential for dose adjustment
π₯ HYPERTHYROIDISM
π Definition:
Hyperthyroidism is a condition in which the thyroid gland overproduces thyroid hormones β T3 (triiodothyronine) and T4 (thyroxine) β leading to a hypermetabolic state that affects multiple body systems.
π It is the opposite of hypothyroidism and causes an overall increase in body metabolism.
β οΈ Causes of Hyperthyroidism:
π Cause
π Description
Gravesβ Disease (Autoimmune)
Most common cause; body produces TSH receptor antibodies (TRAb) that overstimulate the thyroid
Toxic Multinodular Goiter
Presence of multiple autonomously functioning thyroid nodules secreting excess hormone
Toxic Adenoma
A single benign tumor (nodule) producing excess thyroid hormone
Thyroiditis
Inflammation of the thyroid causing leakage of hormones (e.g., subacute, postpartum thyroiditis)
Excessive Iodine Intake
High iodine (e.g., contrast agents, amiodarone) can trigger hormone overproduction in susceptible individuals
Warm, moist skin; fine hair; thinning hair; flushed face
π Musculoskeletal
Muscle weakness, especially proximal muscles (e.g., thighs, shoulders)
βοΈ Reproductive
Menstrual irregularities (amenorrhea or oligomenorrhea), infertility
π« Respiratory
Shortness of breath, dyspnea on exertion
π€ Others
Sleep disturbances, hyperactivity, restlessness
π₯ Thyroid Storm (Thyrotoxic Crisis): A life-threatening emergency with extreme symptoms: high fever, severe tachycardia, altered mental state, and multi-organ failure.
π§ͺ Diagnosis of Hyperthyroidism:
π¬ Test
π Purpose / Interpretation
β TSH (Thyroid-Stimulating Hormone)
β Suppressed (low) in primary hyperthyroidism
β Free T3 and T4
β Elevated levels confirm diagnosis
β Thyroid Stimulating Immunoglobulins (TSI)
β Positive in Graves’ disease (autoimmune)
β Radioactive Iodine Uptake (RAIU) Test
High uptake in Gravesβ, low in thyroiditis
β Thyroid Scan
Identifies hot (functioning) or cold (non-functioning) nodules
β Ultrasound of Thyroid
Assesses size, nodules, vascularity
β ECG
May show atrial fibrillation, tachycardia
β CBC, LFT, Electrolytes
Baseline health and to assess effects of hyperthyroidism or related treatment
Monitor for hypothyroidism, teach lifelong hormone replacement if needed
π¦ GOITER
π Definition:
A Goiter is an abnormal enlargement of the thyroid gland, which is located in the front of the neck, just below the Adamβs apple. It may occur with normal, increased, or decreased thyroid function (euthyroid, hyperthyroid, or hypothyroid states).
π£οΈ A goiter may or may not be visible but can sometimes cause difficulty in swallowing or breathing if large enough.
β οΈ Causes of Goiter:
π Cause Category
π‘ Examples
Iodine Deficiency
Most common worldwide cause; leads to decreased hormone production and increased TSH stimulation
Expresses reduced anxiety and improved quality of life
β οΈ COMPLICATIONS OF GOITER
If a goiter is left untreated or poorly managed, especially when large or toxic, it can lead to several local, systemic, and endocrine-related complications:
𧨠1. Compressive Complications
π¨ Complication
π Description
Tracheal compression
Causes dyspnea, stridor, or airway obstruction
Esophageal compression
Leads to dysphagia (difficulty swallowing)
Recurrent laryngeal nerve compression
Hoarseness or voice changes
Superior vena cava syndrome
Rare; large retrosternal goiters may compress great vessels
π₯ 2. Thyroid Functional Complications
π₯ Type
π Description
Hypothyroidism
In long-standing or autoimmune goiters (e.g., Hashimotoβs)
Hyperthyroidism (Toxic Goiter)
Seen in Gravesβ disease, toxic multinodular goiter
Thyroid storm
Life-threatening complication of toxic goiter if unmanaged
𧬠3. Malignant Transformation
Some cold nodules in multinodular goiter may be malignant
β Complications: Compression of nearby structures, thyroid dysfunction, malignancy, and post-surgical complications.
𧬠THYROIDITIS
π Definition:
Thyroiditis is a general term for inflammation of the thyroid gland, which may be acute, subacute, or chronic in nature. It may result in hypothyroidism, hyperthyroidism, or transient thyroid dysfunction, depending on the type and stage of inflammation.
β οΈ The inflammation may be infectious, autoimmune, post-viral, drug-induced, or radiation-related.
β οΈ Causes of Thyroiditis:
π Cause Category
π Examples
Autoimmune
Hashimotoβs thyroiditis, postpartum thyroiditis
Viral (post-viral)
Subacute (De Quervainβs) thyroiditis after upper respiratory infections
Bacterial (infectious)
Acute suppurative thyroiditis from bacterial invasion
Drugs
Amiodarone, interferon-alpha, lithium
Radiation-induced
After radioactive iodine therapy or external beam radiation
Trauma or surgery
Injury to the thyroid gland
Postpartum hormonal changes
Postpartum thyroiditis due to immune reactivation
Genetic
Certain HLA types predispose to autoimmune thyroiditis
Reassure that many forms (e.g., subacute, postpartum) are self-limiting
Discuss importance of follow-up for long-term monitoring
π V. Evaluation Criteria (Expected Outcomes)
Pain is reduced or controlled
Thyroid hormone levels return to normal range
No signs of airway obstruction or infection
Patient demonstrates understanding of disease and medication regimen
Patient participates actively in follow-up and self-monitoring
β οΈ COMPLICATIONS OF THYROIDITIS
Complications of thyroiditis depend on the type, severity, and duration of the condition. If left untreated or poorly managed, thyroiditis can lead to significant health issues.
π₯ 1. Hypothyroidism (Most Common)
Especially in Hashimotoβs thyroiditis
May be permanent, requiring lifelong levothyroxine therapy
Occurs after destruction of thyroid follicles
β οΈ 2. Hyperthyroidism (Thyrotoxic Phase)
Seen in early stages of subacute, silent, and postpartum thyroiditis
Can cause cardiac complications like palpitations, atrial fibrillation, and heart failure if severe
π· 3. Thyroid Storm (Rare)
A medical emergency seen in uncontrolled thyrotoxic phase
High fever, tachycardia, altered mental status
Requires ICU management
π¦ 4. Abscess Formation and Sepsis
In acute suppurative thyroiditis (bacterial origin)
Risk of airway obstruction, neck cellulitis, or septicemia
β Thyroid cysts are often benign; tumors may be benign or malignant β FNA biopsy is the gold standard for evaluation of thyroid nodules β Papillary carcinoma is the most common and has excellent prognosis β Early diagnosis and treatment reduce risk of complications β Total thyroidectomy + RAI + levothyroxine is standard in many thyroid cancers β Nurses play a key role in airway management, voice monitoring, calcium assessment, and patient education
π§ Disorders of the Parathyroid Gland
π Overview of the Parathyroid Gland:
The parathyroid glands are four small glands located behind the thyroid gland.
They secrete parathyroid hormone (PTH), which is vital for regulating calcium and phosphate balance in the blood.
PTH increases blood calcium levels by:
Stimulating bone resorption
Enhancing calcium reabsorption in kidneys
Promoting activation of Vitamin D, which increases intestinal absorption of calcium
π Major Disorders of the Parathyroid Gland:
π¬ Disorder
β¬οΈ/β¬οΈ PTH
π Description
Hyperparathyroidism
β PTH
Excessive secretion of PTH leading to hypercalcemia
Hypoparathyroidism
β PTH
Inadequate secretion of PTH causing hypocalcemia
Pseudohypoparathyroidism
Normal or β PTH
Genetic condition where tissues are resistant to PTH
β οΈ 1. Hyperparathyroidism
π Definition:
A condition where one or more parathyroid glands secrete excess PTH, leading to elevated blood calcium levels (hypercalcemia) and bone demineralization.
π― Causes:
Type
Cause
Primary
Parathyroid adenoma (most common), hyperplasia, or carcinoma
Observe for signs of hypocalcemia (muscle twitching, tetany)
Ensure seizure precautions if calcium is critically low
Provide calcium-rich diet and limit high-phosphate foods
Educate on lifelong therapy, medication adherence, and emergency signs
β οΈ 3. Pseudohypoparathyroidism
π Definition:
A rare genetic disorder in which body tissues are resistant to PTH, despite normal or elevated hormone levels.
𧬠Pathophysiology:
PTH is produced normally, but target tissues donβt respond, causing hypocalcemia and hyperphosphatemia.
Symptoms:
Similar to hypoparathyroidism: tetany, muscle cramps
Short stature, round face, developmental delays
Known as Albright hereditary osteodystrophy
Diagnosis:
β PTH
β Calcium
β Phosphate
Genetic testing
Management:
Calcium and vitamin D supplementation
Symptom management and genetic counseling
π§· Key Points on Parathyroid Disorders
β Parathyroid glands regulate serum calcium and phosphate via PTH β Hyperparathyroidism causes hypercalcemia, kidney stones, bone loss β Hypoparathyroidism causes hypocalcemia, tetany, muscle spasms β Surgery (thyroidectomy) is the most common cause of acquired hypoparathyroidism β Famous signs in hypocalcemia: Trousseauβs and Chvostekβs signs β Medical management includes calcium, vitamin D, bisphosphonates, calcimimetics β Nursing role involves calcium monitoring, seizure precautions, and patient education
βοΈ HYPOPARATHYROIDISM
π Definition:
Hypoparathyroidism is a rare endocrine disorder characterized by inadequate secretion or action of parathyroid hormone (PTH), resulting in hypocalcemia (low blood calcium) and hyperphosphatemia (high blood phosphate).
π§ Since PTH plays a critical role in maintaining calcium homeostasis, its deficiency leads to neuromuscular excitability, muscle cramps, tetany, and seizures.
β οΈ Causes of Hypoparathyroidism:
π― Cause
π Description
Surgical (most common)
Accidental removal or damage of parathyroid glands during thyroidectomy, parathyroidectomy, or neck surgery
Autoimmune
Autoimmune destruction of parathyroid tissue, often part of Autoimmune Polyendocrine Syndrome (APS)
Congenital/Genetic
Developmental absence or hypoplasia of parathyroid glands (e.g., DiGeorge syndrome)
Radiation-induced
Radiation therapy to neck region damaging parathyroid glands
Infiltrative diseases
Hemochromatosis, Wilsonβs disease, granulomas involving the parathyroids
Magnesium deficiency or excess
Affects PTH secretion and function
𧬠Types of Hypoparathyroidism:
π Type
π Description
Acquired Hypoparathyroidism
Most common; occurs after surgery or radiation
Autoimmune Hypoparathyroidism
Due to autoantibodies against parathyroid glands; may be isolated or part of APS-1
Congenital Hypoparathyroidism
Present at birth; e.g., DiGeorge syndrome (22q11 deletion)
Idiopathic Hypoparathyroidism
Cause unknown; diagnosis of exclusion
Pseudohypoparathyroidism
Rare genetic disorder where PTH is present but target tissues are resistant to it (not true hormone deficiency)
𧬠Pathophysiology of Hypoparathyroidism:
π» Decreased PTH Secretion or Action:
In hypoparathyroidism, parathyroid hormone (PTH) is either absent, decreased, or ineffective (e.g., in pseudohypoparathyroidism).
β Disrupted Calcium Regulation:
PTH normally maintains calcium levels by:
Stimulating bone resorption
Increasing renal calcium reabsorption
Promoting activation of vitamin D β increases intestinal calcium absorption
Without PTH, all these processes decrease, leading to hypocalcemia.
Hyperparathyroidism is a condition characterized by excessive secretion of parathyroid hormone (PTH) by one or more of the parathyroid glands, leading to elevated blood calcium levels (hypercalcemia) and low phosphate levels (hypophosphatemia).
π§ PTH regulates calcium and phosphate. Excess PTH results in increased bone resorption, renal calcium reabsorption, and intestinal calcium absorption, causing hypercalcemia.
Look for Trousseauβs and Chvostekβs signs, tingling around mouth/fingers
Airway observation
Watch for signs of swelling, stridor, or respiratory distress
Voice changes
May indicate recurrent laryngeal nerve injury
Pain management
Provide analgesics and reassure patient
IV calcium gluconate at bedside
Keep ready for emergency hypocalcemia
Patient positioning
Keep in semi-Fowlerβs to reduce swelling and aid breathing
π§βπ« IV. Patient and Family Education
π° Hydration: Drink plenty of fluids to prevent stones
π₯¦ Diet: Follow dietary advice (may vary by type and treatment phase)
π Medication adherence: Take prescribed calcium-lowering meds or supplements regularly
π§ͺ Lab monitoring: Regular testing of calcium, PTH, vitamin D, and renal function is essential
π§ Signs to report: Confusion, muscle twitching, bone pain, or signs of kidney stones
ποΈ Follow-up: Lifelong monitoring may be required, especially after surgery
π V. Evaluation Criteria (Expected Outcomes)
Serum calcium and phosphate levels maintained within normal range
Patient remains free from fractures, kidney stones, and neurological symptoms
Patient demonstrates knowledge of disease and treatment plan
Patient reports improved comfort, energy, and mobility
No signs of hypocalcemia or hypercalcemia crisis post-surgery
β οΈ COMPLICATIONS OF HYPERPARATHYROIDISM
If left untreated or poorly managed, hyperparathyroidism can lead to multi-system complications due to persistently high calcium levels and bone demineralization.
𦴠1. Skeletal Complications:
Osteoporosis and osteopenia
Bone pain, fragility fractures, especially in the spine and long bones
Osteitis fibrosa cystica (rare): bone lesions, cysts due to extreme bone resorption
π 2. Renal Complications:
Nephrolithiasis (kidney stones) from hypercalciuria
Nephrocalcinosis (calcium deposits in kidneys)
Progressive renal insufficiency or chronic kidney disease (CKD)
π 3. Cardiovascular Complications:
Hypertension
Arrhythmias due to altered calcium-potassium balance
Shortened QT interval on ECG
Vascular and valvular calcification (especially in secondary hyperparathyroidism)
π« 4. Neurological and Psychiatric Complications:
Cognitive impairment, memory loss
Depression, anxiety
Fatigue, lethargy
Seizures (rare, usually from very high calcium levels)
π½οΈ 5. Gastrointestinal Complications:
Peptic ulcers, constipation, nausea, and pancreatitis
π§ͺ 6. Postoperative Complication: Hypocalcemia
“Hungry bone syndrome”: sudden drop in calcium post-parathyroidectomy due to rapid bone remineralization
Requires urgent calcium supplementation
π§· KEY POINTS ON HYPERPARATHYROIDISM
β Definition: Excess production of PTH by the parathyroid glands, causing hypercalcemia and hypophosphatemia
β Common Causes:
Primary: Parathyroid adenoma (most common)
Secondary: Chronic kidney disease, vitamin D deficiency
Tertiary: Autonomous PTH secretion after prolonged secondary hyperparathyroidism
β Classic Symptoms Mnemonic: “Bones, Stones, Groans, and Moans” β Bone pain, kidney stones, GI upset, and neuropsychiatric symptoms
β Diagnosis:
β Serum calcium, β PTH, β phosphate
Bone density scan (DEXA), sestamibi scan, renal ultrasound
β Medical Treatment:
Hydration, loop diuretics, bisphosphonates, calcimimetics, vitamin D
β Surgical Treatment:
Parathyroidectomy (minimally invasive, subtotal, or total with autotransplantation)
β Nursing Role:
Monitor calcium levels
Watch for signs of hyper- and hypocalcemia
Educate on diet, hydration, medications, and follow-up
β Complications:
Bone loss, kidney stones, cardiac arrhythmias, neuropsychiatric changes, and post-op hypocalcemia
π§ MYXEDEMA
π Definition:
Myxedema is a severe and advanced form of hypothyroidism, characterized by the accumulation of mucopolysaccharides in the skin and other tissues, causing non-pitting edema, especially in the face, hands, and feet.
𧬠It represents the end-stage of untreated or poorly managed hypothyroidism.
In extreme cases, it may lead to myxedema comaβa life-threatening emergency.
π― Causes of Myxedema:
π Cause
π Description
Untreated or long-standing hypothyroidism
Most common cause
Autoimmune thyroiditis (Hashimotoβs disease)
Destruction of thyroid tissue
Post-thyroidectomy
Without adequate hormone replacement
Radiation therapy
To neck or thyroid
Drug-induced
Lithium, amiodarone, antithyroid medications
Pituitary or hypothalamic failure
Secondary or tertiary hypothyroidism
Severe illness/infection in hypothyroid patients
Triggers myxedema crisis
π§Ύ Types of Myxedema:
π Type
π Description
Primary Myxedema
Due to direct thyroid gland failure (e.g., autoimmune destruction)
Secondary Myxedema
Due to pituitary failure β β TSH secretion
Tertiary Myxedema
Due to hypothalamic dysfunction β β TRH β β TSH
Myxedema Coma
Life-threatening complication of severe untreated hypothyroidism, often precipitated by infection, surgery, or trauma
π¬ Pathophysiology:
π Severe deficiency of thyroid hormones (T3, T4)
π Slowing of metabolic rate in all body systems
π₯ Accumulation of glycosaminoglycans (mucopolysaccharides) in interstitial tissues β non-pitting edema
π§ Depression of neurological and cardiovascular function
βοΈ Hypothermia, hypoventilation, bradycardia, hyponatremia β can progress to coma and death
π¨ Signs and Symptoms:
β οΈ System
π Symptoms
General
Fatigue, lethargy, cold intolerance, weight gain, puffy face
Skin
Dry, coarse skin, non-pitting edema (face, hands, feet), pale appearance
Hair & Nails
Hair thinning, loss of outer third of eyebrows, brittle nails
Watch for shallow breathing, provide oxygen if needed
Administer medications
Levothyroxine as prescribed; monitor effects
Prevent skin breakdown
Turn frequently, keep skin clean and moisturized
Nutritional support
Encourage warm fluids, fiber-rich diet
Patient education
Lifelong hormone therapy, signs of overdose (palpitations, sweating), need for follow-up
Emergency preparedness
Recognize signs of myxedema coma; keep IV access ready for emergencies
β οΈ Complications:
Myxedema coma (life-threatening)
Hypothermia
Hypoglycemia
Cardiac arrhythmias or heart failure
Respiratory failure
Hyponatremia-induced seizures
Permanent cognitive decline if untreated
π§· Key Points Summary
β Myxedema is a severe, life-threatening stage of hypothyroidism β Caused by untreated thyroid disease, surgery, radiation, drugs, or autoimmune destruction β Classic features: Puffy face, cold intolerance, bradycardia, dry skin, lethargy β Myxedema coma is a medical emergency β needs IV T3/T4, steroids, fluids, and intensive care β Diagnosed by β T3/T4, β TSH (in primary) and clinical symptoms β Managed by lifelong hormone replacement (levothyroxine) β Nurses play a vital role in early detection, medication administration, monitoring, and education.
π§ CRETINISM (CONGENITAL HYPOTHYROIDISM)
π Definition:
Cretinism is a condition of severe hypothyroidism present at birth or in early infancy, resulting in stunted physical growth and delayed mental development. It occurs due to deficiency or absence of thyroid hormones (T3, T4) during critical developmental periods.
If untreated, it leads to permanent intellectual disability, growth failure, and multiple system complications.
𧬠Causes of Cretinism:
π― Cause
π Description
Congenital absence of thyroid gland (athyreosis)
No gland formed during fetal development
Ectopic thyroid gland
Thyroid tissue located outside normal position, poorly functioning
Thyroid dyshormonogenesis
Genetic defect in thyroid hormone production
Iodine deficiency (maternal or fetal)
Major cause in endemic areas
Maternal antithyroid drug use
Crosses placenta, suppresses fetal thyroid function
Maternal autoimmune disease
Antibodies cross placenta and attack fetal thyroid
π·οΈ Types of Cretinism:
Type
Description
Neurological Cretinism
Intellectual disability, deaf-mutism, spasticity; due to fetal hypothyroidism
Myxedematous Cretinism
Growth retardation, coarse features, hypothyroid signs; often from postnatal iodine deficiency
Sporadic Cretinism
Due to genetic or developmental defects; occurs in iodine-sufficient areas
Endemic Cretinism
Occurs in iodine-deficient populations; preventable with iodization
π¬ Pathophysiology:
β Thyroid hormones (T3, T4) during fetal/infant development
Leads to impaired brain myelination and synaptic development
Also causes delayed skeletal maturation and cartilage ossification
Affects basal metabolism, protein synthesis, and growth hormones
Results in mental retardation, short stature, skeletal deformities, and myxedematous features
π¨ Signs and Symptoms:
Often subtle at birth, become more apparent within first few months:
π§ Infant Symptoms:
Prolonged jaundice
Constipation
Poor feeding
Hoarse cry
Sleepiness, lethargy
Hypotonia (floppy baby)
Large fontanelles, wide sutures
Macroglossia (large tongue)
Puffy face, dry skin
Umbilical hernia
Poor growth and weight gain
πΆ Later in Untreated Children:
Stunted growth
Delayed milestones
Mental retardation
Deaf-mutism
Coarse facial features
Dry skin, brittle hair
Myxedematous face and extremities
π§ͺ Diagnosis:
Test
Findings
Neonatal screening (TSH, T4)
Elevated TSH, low T4 (done within 48β72 hours after birth)
Serum thyroid profile
β TSH (primary), β T3, β T4
Thyroid scan (scintigraphy)
Shows absence, ectopic, or hypoplastic gland
Thyroid ultrasound
Detects gland size and position
X-ray (bone age)
Delayed epiphyseal maturation
Genetic testing
In suspected inherited enzyme defects
π Medical Management:
Early treatment within the first 2 weeks of life is critical to prevent permanent damage.
Treatment
Purpose
Levothyroxine (T4)
Start as early as possible, lifelong therapy
Initial dose
10β15 mcg/kg/day (adjust based on labs)
Monitor
TSH, T4 every 2β4 weeks initially, then every 3β6 months
Supportive therapies
Speech therapy, physiotherapy, educational support for delays
βοΈ Surgical Management:
β Surgery is not indicated in cretinism. However, it may be used to treat:
Goiter or compressive thyroid cysts (rare in congenital cases)
Watch for signs of undertreatment (lethargy, poor growth)
Refer for therapy
Speech, occupational, and developmental therapy as needed
β οΈ Complications:
Irreversible intellectual disability if untreated
Growth retardation and short stature
Deaf-mutism
Delayed puberty
Skeletal deformities
Social and emotional difficulties
Poor school performance
π§· Key Points on Cretinism
β Cretinism = congenital hypothyroidism β Caused by thyroid dysgenesis, iodine deficiency, or maternal antibodies/drugs β Early signs: lethargy, constipation, macroglossia, poor growth β Newborn screening is essential for early detection β Start levothyroxine within 2 weeks of birth to prevent brain damage β No surgical treatment needed; focus on lifelong hormone replacement β Nurses must educate and support families for long-term management
𧬠Disorders of the Adrenal Gland
π₯ Overview of Adrenal Glands:
The adrenal glands are small, triangular glands located on top of each kidney.
Each gland has two parts:
Adrenal cortex (outer layer): Produces cortisol, aldosterone, and androgens
Addisonβs disease is a rare endocrine disorder characterized by destruction or dysfunction of the adrenal cortex, leading to deficiency of cortisol, and often aldosterone and androgens as well.
π§ It results in hypocortisolism, causing fatigue, weight loss, hypotension, and electrolyte imbalances.
𧬠Causes of Addisonβs Disease:
π Cause Category
π Examples
Autoimmune destruction (most common)
Autoimmune adrenalitis β often part of Autoimmune Polyendocrine Syndrome (APS)
Infections
Tuberculosis (most common cause globally), fungal infections (e.g., histoplasmosis), CMV, HIV
Adrenal hemorrhage/infarction
Due to anticoagulants, trauma, or sepsis (Waterhouse-Friderichsen syndrome)
Cushingβs Disease is a specific form of Cushingβs Syndrome caused by a pituitary adenoma (benign tumor) that secretes excess adrenocorticotropic hormone (ACTH), leading to overstimulation of the adrenal glands and increased production of cortisol.
π§ Cushingβs Syndrome is the general term for excess cortisol, regardless of cause. Cushingβs Disease refers specifically to pituitary-origin ACTH overproduction.
𧬠Causes of Cushing’s Disease:
π― Cause
π Description
Pituitary adenoma (ACTH-secreting)
Most common cause of Cushingβs disease (in ~70% of endogenous cases)
Ectopic ACTH-producing tumors (not Cushing’s Disease, but Cushing’s Syndrome)
Small cell lung cancer, pancreatic tumors
Exogenous corticosteroids (Cushingβs Syndrome)
Prolonged use of high-dose corticosteroids (e.g., prednisone, dexamethasone)
Congenital Adrenal Hyperplasia (CAH) is a group of inherited autosomal recessive disorders characterized by enzyme deficiencies in the adrenal cortex that impair the synthesis of cortisol, and sometimes aldosterone, leading to excess androgen production.
π§ CAH leads to adrenal hyperplasia due to increased ACTH stimulation, and can result in ambiguous genitalia, salt-wasting crisis, or early puberty, depending on the enzyme involved.
𧬠Causes:
π Cause
π Description
Genetic Mutation
CAH is caused by mutations in genes responsible for enzymes that synthesize adrenal hormones (mainly 21-hydroxylase deficiency)
Autosomal Recessive Inheritance
Both parents must carry a mutated gene
Enzyme Deficiencies
These impair cortisol (and/or aldosterone) synthesis, leading to:
Reduced negative feedback
β ACTH from pituitary
Adrenal hyperplasia
Excess androgen production (testosterone-like hormones)
π·οΈ Types of CAH (Based on Enzyme Deficiency):
Common in untreated or poorly controlled CAH, especially in females
Menstrual irregularities, anovulation, and PCOS-like features
π 6. Medication Side Effects (from Long-Term Steroid Use)
Cushingoid features if over-treated: weight gain, moon face, glucose intolerance
Osteoporosis, hypertension, and glucose abnormalities with long-term high-dose steroid use
π§· KEY POINTS ON CONGENITAL ADRENAL HYPERPLASIA (CAH)
β Definition: CAH is a group of inherited enzyme deficiencies affecting cortisol (and sometimes aldosterone) production β adrenal hyperplasia + excess androgens
β Most common cause: 21-hydroxylase deficiency
β Types:
Classic Salt-Wasting CAH β cortisol and aldosterone deficiency
Simple Virilizing CAH β cortisol deficiency, normal aldosterone
Non-Classic CAH β mild form, appears later in life
Confirm with newborn screening, hormone tests, and genetic testing
β Treatment:
Lifelong hydrocortisone, fludrocortisone, and salt supplementation
Surgical correction of genitalia (when needed)
Emergency care with stress dosing of steroids during illness
β Nursing Role:
Monitor growth, electrolytes, adherence
Educate on medications, stress dosing, and emergency response
Provide family counseling and emotional support
β Complications:
Adrenal crisis, growth issues, infertility, psychosocial problems, and steroid side effects
β‘ PHEOCHROMOCYTOMA
π Definition:
Pheochromocytoma is a rare, usually benign tumor that arises from the chromaffin cells of the adrenal medulla and produces excess catecholaminesβprimarily epinephrine (adrenaline) and norepinephrine (noradrenaline).
πΊ These hormones cause sudden or sustained episodes of hypertension, palpitations, sweating, and other fight-or-flight symptoms.
𧬠Causes:
π Cause
π Description
Genetic mutations (familial forms)
25β30% of cases are hereditary; mutations in genes such as RET, VHL, NF1, and SDH
Sporadic (non-hereditary)
Most common in adults, no family history
Associated syndromes
– Multiple Endocrine Neoplasia type 2 (MEN 2A & 2B)
Von Hippel-Lindau disease
Neurofibromatosis type 1 (NF1) | | Tumors outside adrenal gland (paraganglioma) | Arise from extra-adrenal chromaffin tissue; may also secrete catecholamines |
π·οΈ Types of Pheochromocytoma:
Type
Description
Adrenal Pheochromocytoma
Arises from the adrenal medulla (most common form)
Extra-adrenal Pheochromocytoma(Paraganglioma)
Arises from sympathetic ganglia outside the adrenal glandsβmay be abdominal, thoracic, pelvic
Benign Pheochromocytoma
Non-cancerous and confined to adrenal gland (majority of cases)
Malignant Pheochromocytoma
Rare; defined by metastasis to organs like bones, lungs, liver, or lymph nodes
Familial Pheochromocytoma
Occurs as part of hereditary syndromes (MEN 2, VHL, NF1); often bilateral or multiple tumors
𧬠Pathophysiology of Pheochromocytoma:
Tumor develops in chromaffin cells of the adrenal medulla or extra-adrenal sympathetic tissue (paraganglia).
These tumor cells overproduce catecholamines:
Epinephrine (adrenaline)
Norepinephrine (noradrenaline)
Occasionally dopamine
Excess catecholamines stimulate alpha- and beta-adrenergic receptors:
β¬οΈ Vasoconstriction β hypertension
β¬οΈ Heart rate and contractility β tachycardia
β¬οΈ Glycogenolysis β hyperglycemia
Intermittent or sustained secretion causes episodic or persistent hypertensive crises, potentially life-threatening if untreated.
High catecholamines can damage heart, kidneys, brain, and increase the risk of stroke or MI.
π¨ Signs and Symptoms of Pheochromocytoma:
Classic “Rule of 10s” (old teaching, less used now): 10% bilateral, 10% malignant, 10% extra-adrenal, 10% familial (now known to be ~30% familial)
π Classic Triad of symptoms:
Headache (severe, pounding)
Palpitations (with tachycardia)
Sweating (diaphoresis)
π§ Other Common Symptoms:
System
Symptoms
Cardiovascular
– Sudden or sustained hypertension (may be episodic)
Rare, but malignant pheochromocytomas can metastasize
Requires lifelong surveillance, especially in familial types
π§· KEY POINTS ON PHEOCHROMOCYTOMA
β Definition: Tumor of adrenal medulla or sympathetic ganglia that secretes excess catecholamines (epinephrine, norepinephrine)
β Classic Triad:
Headache
Palpitations
Sweating
β Other Signs:
Paroxysmal or sustained hypertension
Tremors, pallor, anxiety, hyperglycemia
β Diagnosis:
β Plasma/urine metanephrines
Imaging: CT/MRI, MIBG scan
β Preoperative Management:
Alpha-blocker (phenoxybenzamine) first
Then beta-blocker (after alpha-blockade)
Ensure volume expansion
β Definitive Treatment:
Laparoscopic or open adrenalectomy
β Postoperative Monitoring:
For hypotension, hypoglycemia, and adrenal insufficiency
β Complications:
Hypertensive crisis, stroke, arrhythmia, cardiomyopathy, and post-op adrenal shock
β Nursing Role:
Monitor vitals closely
Prevent triggers
Prepare patient for surgery and lifelong follow-up
Educate on medication adherence, genetic counseling, and emergency awareness
π§ͺ HYPERALDOSTERONISM
π Definition:
Hyperaldosteronism is a condition characterized by the excessive secretion of aldosterone, a mineralocorticoid hormone produced by the adrenal cortex, leading to sodium retention, potassium excretion, and hypertension.
π Aldosterone acts on the kidneys to conserve sodium and excrete potassium. Its overproduction causes volume overload, hypokalemia, and high blood pressure.
Metabolic alkalosis | | Cardiac arrhythmias | – Due to low potassium (e.g., premature beats, tachycardia) |
π§ͺ Diagnosis:
Test
Findings
Plasma aldosterone concentration (PAC)
β Elevated
Plasma renin activity (PRA)
β Suppressed (in primary)
Aldosterone-renin ratio (ARR)
β High ratio (>20:1) suggests primary hyperaldosteronism
Serum electrolytes
β Potassium, β Sodium, β Bicarbonate
24-hour urinary aldosterone
Confirms aldosterone excess
CT/MRI of adrenal glands
Detects adrenal adenoma or hyperplasia
Adrenal vein sampling (AVS)
Differentiates unilateral vs bilateral disease
Saline or fludrocortisone suppression test
Confirms autonomous aldosterone production
π Medical Management:
Treatment
Purpose
Mineralocorticoid receptor antagonists
(e.g., Spironolactone, Eplerenone)
– Block aldosterone effects
Used in bilateral adrenal hyperplasia and unilateral cases not suitable for surgery | | Antihypertensives | – Control BP if not normalized with spironolactone | | Potassium supplements | – Correct hypokalemia | | Low-sodium diet | – Helps control blood pressure |
βοΈ Surgical Management:
π― Definitive treatment for unilateral adrenal adenoma (Connβs syndrome)
Surgery
Description
Laparoscopic adrenalectomy
– Removal of the affected adrenal gland
Normalizes BP and potassium in most patients | | Bilateral hyperplasia | Surgery not preferred β medical management with spironolactone | | Post-op care | Monitor for hypotension, electrolyte shifts, and renal function changes |
β Primary cause: Adrenal adenoma (Connβs Syndrome), bilateral adrenal hyperplasia β Secondary cause: Due to β renin from conditions like renal artery stenosis, CHF
β Classic features:
Hypertension + Hypokalemia + Metabolic alkalosis
β Diagnosis:
β Aldosterone
β Renin (in primary)
CT scan, AVS, suppression tests
β Treatment:
Spironolactone or eplerenone
Adrenalectomy (if unilateral tumor)
Lifestyle: low-salt diet, potassium-rich food
β Nursing care:
Monitor BP, electrolytes
Educate on medication, diet, signs of crisis
Ensure adherence to follow-up and therapy
𧬠ADRENAL INSUFFICIENCY
π Definition:
Adrenal insufficiency is a condition in which the adrenal glands fail to produce adequate amounts of hormones, particularly cortisol (and sometimes aldosterone). Cortisol is essential for stress response, metabolism, immune function, and blood pressure regulation.
π In severe cases, it can lead to an Addisonian crisisβa life-threatening emergency.
Adrenal crisis during surgery/infection if not stress-dosed
π§· Key Points Summary:
β Adrenal insufficiency = β cortisol (Β± aldosterone) β Primary = adrenal gland problem β β ACTH, hyperpigmentation β Secondary = pituitary problem β β ACTH, no hyperpigmentation β Symptoms: fatigue, hypotension, salt craving, GI issues, electrolyte imbalances β Diagnosed via ACTH stimulation test, cortisol & ACTH levels β Treated with glucocorticoids, mineralocorticoids (if primary) β Crisis = emergency β needs IV hydrocortisone + fluids β Nurses monitor vitals, electrolytes, and teach lifelong steroid management
𧬠ADRENAL TUMORS
π Definition:
Adrenal tumors are abnormal growths that develop in the adrenal glands, which are located above each kidney and consist of two parts:
Adrenal cortex (outer part): produces cortisol, aldosterone, and androgens
Adrenal medulla (inner part): produces catecholamines (epinephrine and norepinephrine)
Tumors may be benign or malignant, functional (hormone-secreting) or non-functional.
𧬠Causes:
Cause
Description
Unknown (sporadic)
Most adrenal tumors are spontaneous and idiopathic
Genetic syndromes
– Multiple Endocrine Neoplasia (MEN) type 2
Li-Fraumeni syndrome
Beckwith-Wiedemann syndrome
Von Hippel-Lindau (VHL) disease
Neurofibromatosis type 1 (NF1) | | Adrenal hyperplasia | May develop into nodules or tumors | | Metastatic spread | Cancer from lung, breast, or kidney may spread to adrenal glands |
π·οΈ Types of Adrenal Tumors:
Tumor Type
Origin
Hormone Status
Common Names
Adenoma
Cortex
Functional or non-functional
Benign; may cause Cushingβs or Connβs syndrome
Adrenocortical carcinoma
Cortex
Often functional
Rare, aggressive
Pheochromocytoma
Medulla
Functional
Secretes catecholamines
Neuroblastoma
Medulla
Often non-functional
Common in children
Myelolipoma
Cortex
Non-functional
Benign, fatty tumor
Metastatic adrenal tumors
Secondary
Usually non-functional
From breast, lung, GI tract
π¬ Pathophysiology:
Uncontrolled cellular growth in the adrenal cortex or medulla forms a mass.
If functional, the tumor secretes excess hormones:
Recurrence or metastasis (especially in adrenocortical carcinoma)
Post-op complications: bleeding, infection, DVT
Psychosocial impact: from body changes, long-term medication use
π§· Key Points Summary:
β Adrenal tumors can arise from cortex or medulla, be benign/malignant, and functional/non-functional β Common types: adenoma, pheochromocytoma, adrenocortical carcinoma β Symptoms vary by hormone secretedβcortisol, aldosterone, androgens, catecholamines β Diagnosed via hormonal assays + imaging β Treatment includes surgery, hormone control, and lifelong follow-up β Nurses play a key role in preparing, monitoring, educating, and preventing crises
π§ DISORDERS OF THE PITUITARY GLAND
π Overview of the Pituitary Gland:
The pituitary gland, also known as the βmaster gland,β is a small pea-sized endocrine gland located at the base of the brain in the sella turcica. It is divided into:
Vital signs, neuro status, intake/output, signs of hormone imbalance
Post-op care
Prevent sneezing, coughing, straining; monitor for CSF leak (clear nasal discharge), DI signs
Hormonal therapy
Administer and monitor replacement hormones
Patient education
Lifelong hormone therapy, signs of crisis, when to seek help
Fluid balance
Especially in SIADH and DI
Emotional support
Coping with chronic illness, body image issues (e.g., acromegaly, Cushingβs)
β οΈ Complications:
Adrenal crisis, thyroid crisis
Pituitary apoplexy (hemorrhage/infarction of the gland)
Infertility, visual disturbances, depression
Water intoxication or dehydration (SIADH or DI)
Hypopituitarism after surgery or radiation
π§· Key Points Summary:
β Pituitary gland controls multiple endocrine functions β Disorders can be due to excess or deficiency of hormone secretion β Common conditions: Cushingβs disease, acromegaly, prolactinoma, DI, SIADH β Diagnosed via hormone levels, MRI, stimulation/suppression tests β Treated with medications, surgery, and lifelong hormone replacement β Nurses play a crucial role in monitoring, post-op care, and patient education
π§ ACROMEGALY
π Definition:
Acromegaly is a chronic hormonal disorder characterized by excessive secretion of growth hormone (GH) in adults (after the closure of epiphyseal growth plates), usually due to a pituitary adenoma. This results in progressive enlargement of bones and soft tissues, especially in the hands, feet, and face.
π§ In children, GH excess before epiphyseal closure causes gigantism, not acromegaly.
𧬠Causes of Acromegaly:
Category
Example
Pituitary causes (most common)
– GH-secreting pituitary adenoma (>95% cases)
Pituitary hyperplasia | | Non-pituitary (ectopic) GH/ GHRH secretion | – GH or GHRH-secreting tumors (e.g., lung or pancreatic tumors)
Carcinoid tumors | | Genetic or familial syndromes | – MEN type 1
McCune-Albright syndrome (rare) |
π·οΈ Types of Acromegaly:
Type
Description
Pituitary acromegaly
Due to benign adenoma of pituitary gland (most common form)
Ectopic acromegaly
Due to non-pituitary tumors secreting GH or GHRH (rare)
Familial acromegaly
Genetic syndromes with pituitary tumors (MEN1, AIP mutation)
Acromegaly + gigantism
Occurs if GH excess begins before and continues after puberty (rare overlap condition)
𧬠Pathophysiology:
A pituitary adenoma (GH-secreting tumor) or ectopic tumor secretes excess growth hormone (GH) in adults.
GH stimulates the liver and other tissues to produce insulin-like growth factor 1 (IGF-1), which is responsible for most of the growth-promoting effects.
Excess GH and IGF-1 lead to:
Overgrowth of bones and soft tissues (especially hands, feet, face)
Organomegaly (heart, liver, kidneys)
Metabolic changes like insulin resistance β diabetes
Increased cartilage and bone thickening, especially in skull, jaw, and vertebrae
Compression effects from the pituitary tumor may also affect nearby structures:
Optic chiasm β visual field defects
Normal pituitary β hypopituitarism
π¨ Signs and Symptoms of Acromegaly:
Slow onset; symptoms develop over years, often missed early.
𦴠Skeletal & Soft Tissue Changes:
Enlargement of hands and feet (rings/shoes donβt fit)
Demonstrates adherence to medications and follow-up
Reports improved coping and reduced stress
Free from postoperative or treatment-related complications
β οΈ COMPLICATIONS OF ACROMEGALY
Uncontrolled or late-diagnosed acromegaly can lead to serious systemic complications, many of which are irreversible without early intervention.
π§ 1. Neurological Complications:
Headaches due to tumor pressure
Bitemporal hemianopia from optic chiasm compression
Carpal tunnel syndrome from nerve compression
Peripheral neuropathy
β€οΈ 2. Cardiovascular Complications:
Hypertension (very common)
Cardiomyopathy β heart failure
Arrhythmias
Increased risk of stroke & sudden cardiac death
π¬ 3. Metabolic Complications:
Insulin resistance β Type 2 Diabetes Mellitus
Hyperlipidemia
Weight gain/obesity
𦴠4. Musculoskeletal Issues:
Joint pain, arthritis
Kyphosis, enlarged hands and feet
Osteoarthritis due to cartilage overgrowth
π 5. Respiratory Complications:
Obstructive sleep apnea due to soft tissue overgrowth in airway
Voice deepening and snoring
𧬠6. Reproductive & Endocrine Disorders:
Menstrual irregularities, infertility
Erectile dysfunction, decreased libido
Galactorrhea (if prolactin is elevated)
π§ͺ 7. Post-Treatment Complications:
Hypopituitarism (especially post-surgery or radiotherapy)
CSF leak or infection after transsphenoidal surgery
Adrenal or thyroid insufficiency if entire pituitary function is impaired
π§· KEY POINTS ON ACROMEGALY
β Definition: A hormonal disorder in adults due to excess GH secretion, usually from a pituitary adenoma β Key hormones involved: Growth hormone (GH) and IGF-1 β Classic signs:
Enlarged hands, feet, facial features
Joint pain, coarsened skin, voice deepening
Hypertension, diabetes, sleep apnea
β Diagnosis:
β IGF-1 levels, OGTT GH suppression test
MRI of pituitary gland
β Treatment:
Transsphenoidal surgery (first-line)
Somatostatin analogs, GH receptor antagonists
Radiotherapy if tumor is unresectable
β Nursing role:
Monitor for visual changes, blood sugar, BP
Post-op care to prevent CSF leak, DI
Provide psychosocial support and promote medication adherence
β Complications:
Diabetes, heart disease, neuropathy, sleep apnea, infertility, and hypopituitarism
π GIGANTISM
π Definition:
Gigantism is a rare endocrine disorder characterized by excessive secretion of growth hormone (GH)before the epiphyseal growth plates close (i.e., during childhood or adolescence), resulting in abnormally increased linear growth and tall stature.
π§ It is caused by the same mechanisms as acromegaly, but it occurs before puberty, leading to height >97th percentile for age and sex.
Support postoperative recovery and medication adherence
Prevent or detect neurological and metabolic complications
Provide psychological and developmental support
Educate family and patient about lifelong care and follow-up
ποΈ I. Nursing Assessment
Focus Area
Key Points
Growth and development
Monitor height, weight, bone age, pubertal status
Vital signs
Observe for hypertension, pulse irregularities
Vision assessment
Monitor for visual field defects (optic chiasm compression)
Neurological assessment
Watch for headache, behavior changes, signs of raised ICP
Musculoskeletal
Assess for joint pain, kyphosis, scoliosis
Psychosocial
Evaluate for low self-esteem, peer difficulties, or anxiety
π II. Common Nursing Diagnoses
Disturbed body image related to physical overgrowth
Chronic pain related to joint/muscle strain
Risk for injury related to impaired mobility or visual field changes
Ineffective coping related to chronic illness or abnormal appearance
Knowledge deficit regarding disease, treatment, and follow-up care
Risk for impaired growth and development related to hormonal imbalance
π§Ύ III. Nursing Interventions
πΉ A. Preoperative Care (If Surgery Planned):
Intervention
Purpose
Prepare child and family for transsphenoidal surgery
Reduce fear and increase cooperation
Monitor neurological signs, vision, and hormone levels
Establish baseline for comparison
Encourage psychological counseling/support groups
Help manage body image and emotional issues
πΉ B. Postoperative Care:
Intervention
Purpose
Monitor for CSF leak (clear nasal discharge), meningitis signs
Prevent life-threatening infections
Assess for diabetes insipidus
Monitor urine output and serum sodium levels
Monitor for hypopituitarism
Watch for fatigue, hypotension, growth failure post-op
Administer hormone replacements as prescribed
Prevent adrenal, thyroid, or gonadal insufficiency
Encourage rest and gradual activity
Prevent fatigue and reduce ICP risk
πΉ C. Long-term Nursing Care:
Intervention
Purpose
Educate on medication adherence (e.g., somatostatin analogs)
Promote hormone balance and tumor control
Schedule and reinforce regular follow-ups
Monitor IGF-1, GH levels, MRI imaging
Support nutritional and orthopedic management
Ensure joint protection and healthy weight
Promote school reintegration and peer acceptance
Help with developmental and social challenges
Provide family-centered education
Teach disease understanding, emergency signs, and home care routines
π IV. Evaluation Criteria (Expected Outcomes):
Patient maintains stable GH and IGF-1 levels
Shows normal or slowed growth velocity
Demonstrates improved self-esteem and coping skills
Verbalizes understanding of medication regimen and follow-up care
Remains free of postoperative or therapy-related complications
β οΈ COMPLICATIONS OF GIGANTISM
If left untreated or diagnosed late, gigantism can result in serious, sometimes lifelong complications due to prolonged GH and IGF-1 elevation, and structural abnormalities:
π§ 1. Neurological Complications
Headaches, due to tumor pressure
Bitemporal hemianopia from optic chiasm compression
Hydrocephalus (rare, if tumor is large and obstructive)
π 2. Cardiovascular Complications
Hypertension
Left ventricular hypertrophy β cardiomyopathy
Heart failure (a leading cause of death in untreated cases)
π¬ 3. Metabolic Complications
Insulin resistance and Type 2 Diabetes Mellitus
Hyperlipidemia
Obesity (in some cases)
𦴠4. Musculoskeletal Problems
Joint pain and early-onset osteoarthritis
Kyphosis, scoliosis, and bone deformities
Delayed closure of epiphyses β risk of fractures
π« 5. Respiratory Complications
Obstructive sleep apnea due to enlarged tongue, soft tissues
Reduced lung function due to chest wall deformity
𧬠6. Endocrine/Reproductive Issues
Delayed puberty, infertility, or menstrual irregularities
Hypopituitarism after surgery or radiation
Galactorrhea if prolactin is elevated
π§ 7. Psychological & Social Impact
Depression, anxiety, low self-esteem due to appearance
Social withdrawal, bullying in adolescence
Academic issues due to vision or neurological effects
π§· KEY POINTS ON GIGANTISM
β Definition: Overproduction of GH before epiphyseal plate closure β abnormally tall stature and tissue overgrowth β Cause: Most often due to GH-secreting pituitary adenoma in children/adolescents β Classic features:
Prolactinoma is a benign pituitary tumor that overproduces prolactin, the hormone responsible for breast development and milk production. It is the most common type of pituitary adenoma and can affect both females and males, with symptoms varying by sex and age.
πΊ High prolactin levels (hyperprolactinemia) suppress reproductive hormones β infertility, amenorrhea, and galactorrhea.
Vitals, vision changes, signs of hormone imbalance
Medication compliance
Ensure regular intake of dopamine agonists
Assess for side effects
Nausea, dizziness (from dopamine agonists)
Post-op care (if surgery)
Monitor nasal drainage (CSF leak), DI symptoms, neuro checks
Emotional support
Coping with infertility, body image, chronic disease
Patient education
Medication adherence, need for follow-up MRI/hormone testing, contraception during treatment (unless pregnancy is desired)
β οΈ Complications:
Vision loss from tumor growth
Infertility (reversible with treatment)
Bone demineralization from prolonged low estrogen/testosterone
Hypopituitarism (after surgery or tumor compression)
Pituitary apoplexy (sudden hemorrhage/infarction)
Medication side effects (nausea, orthostatic hypotension, psychiatric effects)
π§· Key Points on Prolactinoma
β Most common pituitary tumor, especially in women of reproductive age β Caused by prolactin-secreting pituitary adenoma β Symptoms: amenorrhea, galactorrhea, infertility, low libido β Diagnosed via β serum prolactin and MRI β Dopamine agonists (cabergoline, bromocriptine) are first-line therapy β Surgery is reserved for resistant or complicated tumors β Nurses play a key role in medication adherence, monitoring, and supportive care
π§ Diabetes Insipidus (DI)
π Definition:
Diabetes Insipidus (DI) is a rare disorder characterized by the excretion of large volumes of dilute urine (polyuria) and intense thirst (polydipsia) due to either a deficiency of antidiuretic hormone (ADH, also called vasopressin) or the inability of the kidneys to respond to ADH. Unlike diabetes mellitus, DI is not related to glucose metabolism.
ADH is normally secreted by the posterior pituitary gland and acts on the kidneys to conserve water. In DI, this mechanism fails, leading to excessive water loss and a risk of dehydration, electrolyte imbalance, and hypovolemia.
𧬠Causes:
The causes of DI can be divided into central (neurogenic), nephrogenic, gestational, and behavioral (dipsogenic) forms:
Central Diabetes Insipidus results from damage to the hypothalamus or posterior pituitary gland, leading to insufficient production or release of ADH. This damage may be due to:
Nephrogenic Diabetes Insipidus occurs when the kidneys are resistant to the action of ADH, even though it is present in normal or high amounts. Causes include:
Chronic kidney disease
Long-term use of certain drugs (especially lithium or demeclocycline)
Electrolyte imbalances such as hypercalcemia and hypokalemia
Congenital defects (mutations in ADH receptor or aquaporin-2 water channel genes)
Gestational Diabetes Insipidus is a temporary form of DI that occurs during pregnancy, typically in the third trimester. It is caused by the placenta producing an enzyme called vasopressinase, which breaks down ADH. This form usually resolves after delivery.
Dipsogenic Diabetes Insipidus, also called primary polydipsia, is caused by excessive water intake, which suppresses natural ADH secretion. It may occur in individuals with psychiatric disorders (such as schizophrenia) or damage to the hypothalamic thirst-regulating center.
π·οΈ Types of Diabetes Insipidus:
Central (Neurogenic) DI β Due to deficient production or secretion of ADH
Nephrogenic DI β Due to renal resistance to ADH
Gestational DI β Due to ADH degradation by placental enzymes during pregnancy
Dipsogenic DI β Due to compulsive or habitual water drinking, leading to ADH suppression
𧬠Pathophysiology:
The central feature of diabetes insipidus is the inability of the body to conserve water, leading to excessive loss of dilute urine (polyuria) and resulting in intense thirst (polydipsia).
Under normal circumstances, antidiuretic hormone (ADH), also called vasopressin, is released by the posterior pituitary gland in response to dehydration or high plasma osmolality. ADH acts on the renal collecting ducts, increasing their permeability to water, which allows water to be reabsorbed into the bloodstream and concentrates the urine.
In central DI, there is a deficiency in ADH production or release, often due to damage to the hypothalamus or pituitary gland. As a result, water is not reabsorbed by the kidneys, leading to excessive loss of water in urine.
In nephrogenic DI, ADH is produced in adequate amounts, but the kidneys do not respond to it. This leads to the same outcome: inability to concentrate urine and loss of free water.
In gestational DI, an enzyme produced by the placenta (vasopressinase) degrades ADH, reducing its effectiveness. In dipsogenic DI, excessive fluid intake suppresses the release of ADH, mimicking the symptoms of true DI.
As the kidneys fail to concentrate urine, patients develop polyuria (usually >3 L/day in adults), leading to dehydration, increased thirst, low urine osmolality, and in severe cases, electrolyte imbalances.
π¨ Signs and Symptoms:
The hallmark symptoms of DI are:
Polyuria: Excessive production of dilute urine (may exceed 5β10 liters per day in adults)
Polydipsia: Intense, unquenchable thirst (especially for cold water)
Nocturia: Frequent urination at night
Dehydration: Dry skin, dry mouth, dizziness, and fatigue
Weight loss: Due to fluid loss
Low urine specific gravity: <1.005
Hypotension and tachycardia: In severe dehydration
Constipation or dry mucous membranes: In chronic cases
Hypernatremia (β serum sodium): When water intake is inadequate to match losses
In infants or young children:
Irritability
Poor feeding
Vomiting
Fever
Failure to thrive
Seizures (due to electrolyte imbalance)
π§ͺ Diagnosis:
History and Clinical Examination:
History of excessive thirst and urination
Evaluation of risk factors: head trauma, surgery, medications, pregnancy
Laboratory Tests:
Serum sodium: Often elevated (hypernatremia)
Serum osmolality: High (>295 mOsm/kg)
Urine osmolality: Low (<300 mOsm/kg)
Urine specific gravity: Low (<1.005)
24-hour urine volume: Confirms polyuria (>3 liters/day in adults)
Water Deprivation Test:
Diagnostic gold standard
Patient is restricted from fluids for several hours under supervision
If urine remains dilute despite dehydration, it confirms DI
Desmopressin (DDAVP) is administered:
If urine becomes concentrated after DDAVP β Central DI
If no change β Nephrogenic DI
ADH (Vasopressin) Level:
May be low in central DI
Normal or high in nephrogenic DI
Imaging (MRI brain):
Used to evaluate pituitary or hypothalamic lesions, especially in central DI
π Medical Management:
The treatment of diabetes insipidus depends on its type (central, nephrogenic, gestational, or dipsogenic) and the underlying cause. The primary goals are to:
Control fluid balance
Reduce urine output
Normalize serum electrolytes
Treat the underlying disorder
β 1. Central Diabetes Insipidus:
Desmopressin (DDAVP):
Synthetic analog of ADH
Drug of choice for central DI
Administered intranasally, orally, or parenterally
Reduces urine output and restores normal fluid balance
Chlorpropamide or Carbamazepine:
Occasionally used in mild cases to stimulate ADH release
Rarely used now due to better options
Fluids:
Encourage oral fluids to prevent dehydration
IV fluids (e.g., D5W) in cases of severe dehydration or unconsciousness
β 2. Nephrogenic Diabetes Insipidus:
Thiazide diuretics (e.g., hydrochlorothiazide):
Paradoxically reduce polyuria by inducing mild volume depletion
Promotes proximal reabsorption of sodium and water
Low-sodium, low-protein diet:
Helps reduce urinary solute load
Indomethacin or NSAIDs:
Reduce urine volume by decreasing renal prostaglandin synthesis
Patient education and fluid restriction under monitoring
Treatment of underlying psychiatric disorder (if present)
π οΈ Surgical Management:
Surgery is not a primary treatment for most types of diabetes insipidus but may be needed in specific cases where the underlying cause is a structural lesion.
β Surgical Indications:
Pituitary or hypothalamic tumor (e.g., craniopharyngioma, adenoma):
May require transsphenoidal surgery
Often followed by radiotherapy
Postoperative patients may develop central DI and need lifelong desmopressin
Traumatic brain injury with pituitary damage:
If surgical decompression or CSF drainage is needed
Hydrocephalus or brain malformations:
Neurosurgical correction can relieve pressure and restore ADH function in some cases
β οΈ Post-Surgical Considerations:
Close monitoring for:
Polyuria or polydipsia
Electrolyte imbalances (especially sodium)
Signs of hypopituitarism
Lifelong hormone replacement therapy may be required after pituitary surgery
Monitor and maintain fluid and electrolyte balance
Prevent dehydration and hypovolemic shock
Promote adherence to medications and dietary modifications
Provide education about disease management and complications
Support emotional and psychological well-being
ποΈ I. Assessment
Monitor Intake and Output (I&O):
Record urine output hourly (may exceed 200β500 mL/hour)
Monitor for signs of polyuria and polydipsia
Vital Signs Monitoring:
Observe for hypotension, tachycardia, weak pulse (signs of dehydration)
Assess for Dehydration:
Dry mucous membranes
Poor skin turgor
Thirst and weakness
Weight loss
Monitor Neurological Status:
Altered sensorium due to hypernatremia or fluid deficit
Daily Weights:
Early indicator of fluid imbalance
Laboratory Monitoring:
Serum sodium and osmolality
Urine specific gravity (usually <1.005)
Blood glucose (to rule out diabetes mellitus)
π§Ύ II. Nursing Interventions
πΉ A. Fluid Management
Encourage oral fluids (preferably water) to prevent dehydration
Administer IV fluids (e.g., D5W or hypotonic saline) as ordered in cases of severe dehydration
Adjust fluid intake according to urine output
πΉ B. Medication Administration
Administer Desmopressin (DDAVP) as prescribed (oral, nasal spray, or IV)
Teach proper nasal spray technique if used at home
Administer thiazide diuretics or NSAIDs for nephrogenic DI under supervision
Monitor for side effects of all medications (e.g., hyponatremia due to over-treatment)
πΉ C. Nutrition and Electrolyte Balance
Monitor and correct electrolyte imbalances (e.g., sodium, potassium)
Provide a low-sodium, low-protein diet for nephrogenic DI patients if advised
Educate patient/family on hydration and dietary needs
π III. Patient and Family Education
Explain the nature of DI, its chronic course, and treatment options
Teach the importance of strict fluid balance monitoring
Instruct how to recognize early signs of dehydration or fluid overload
Educate about lifelong medication adherence (especially in central DI)
Stress the importance of regular follow-up visits and lab monitoring
π€ IV. Emotional and Psychosocial Support
Provide emotional reassurance and counseling
Address body image, fatigue, or lifestyle adjustment issues
Encourage participation in support groups, especially for chronic or genetic cases
π Evaluation (Expected Outcomes):
Maintains adequate hydration and stable vital signs
Exhibits normal serum sodium and osmolality
Demonstrates understanding of disease and self-care practices
Adheres to medication regimen and follow-up schedule
Remains free from complications like hypovolemic shock or seizures
β οΈ COMPLICATIONS OF DIABETES INSIPIDUS
If untreated or poorly managed, DI can lead to serious and potentially life-threatening complications due to excessive fluid loss and electrolyte imbalance:
Excessive water loss leads to elevated serum sodium levels
May cause:
Confusion
Seizures
Irritability
Coma (in severe cases)
π« 3. Hypovolemic Shock
Sudden drop in blood pressure due to fluid depletion
Life-threatening emergency
Signs: tachycardia, hypotension, cold extremities
π§ͺ 4. Electrolyte Imbalances
Hypernatremia, hypokalemia, or hypercalcemia
Can lead to cardiac arrhythmias or neuromuscular dysfunction
𧬠5. Growth and Development Issues (in children)
Poor growth or failure to thrive
Developmental delays if chronic DI is unrecognized
𧱠6. Complications of Treatment
Water intoxication or hyponatremia due to over-treatment with desmopressin
Nasal irritation or headache with DDAVP nasal spray
GI upset or hypotension from thiazide diuretics or NSAIDs
π KEY POINTS ON DIABETES INSIPIDUS
β Definition: A disorder characterized by excessive urine output (polyuria) and intense thirst (polydipsia) due to ADH deficiency or renal resistance to ADH.
β Main Types:
Central DI β due to β ADH secretion
Nephrogenic DI β due to renal resistance to ADH
Gestational DI β due to placental destruction of ADH
Dipsogenic DI β due to excess fluid intake suppressing ADH
β Key Symptoms:
Polyuria, polydipsia, nocturia
Dilute urine, low specific gravity
Signs of dehydration and hypernatremia
β Diagnosis:
Low urine osmolality, high serum osmolality
Water deprivation test + Desmopressin response
MRI to assess pituitary or hypothalamic abnormalities
β Treatment:
Desmopressin for central and gestational DI
Thiazide diuretics and low-sodium diet for nephrogenic DI
Behavioral therapy for dipsogenic DI
β Nursing Role:
Monitor I&O, hydration, vitals
Educate on medication use and follow-up
Prevent complications like dehydration and electrolyte imbalance
π¦ SIADH β Syndrome of Inappropriate Antidiuretic Hormone Secretion
π Definition:
SIADH is a condition characterized by the excessive release of antidiuretic hormone (ADH) despite normal or low plasma osmolality, leading to water retention, hyponatremia (low serum sodium), and dilutional hypo-osmolality.
In SIADH, the kidneys reabsorb too much water, causing:
Decreased urine output
Dilute blood (low serum osmolality)
Concentrated urine
π βToo much ADH = Too much water retained = Dilutional hyponatremiaβ
𧬠Causes of SIADH:
SIADH may result from various conditions that cause abnormal ADH production or enhance its effect. Causes are grouped into central, pulmonary, malignancy-related, drug-induced, and other categories:
π§ 1. Central Nervous System (CNS) Disorders
Head trauma
Brain tumors (especially pituitary or hypothalamic)
Meningitis, encephalitis
Stroke, subarachnoid hemorrhage
Post-neurosurgery
π« 2. Pulmonary Disorders
Pneumonia (especially viral or bacterial)
Tuberculosis
Acute respiratory failure
Mechanical ventilation
Positive pressure ventilation (stimulates ADH)
𧬠3. Malignancies (Paraneoplastic Syndrome)
Certain cancers can produce ectopic ADH, especially:
Small cell lung carcinoma (most common)
Pancreatic cancer
Prostate and bladder cancer
Leukemia and lymphoma
π 4. Drug-Induced SIADH
Many medications can stimulate ADH release or enhance its action:
Educate the patient and family about fluid restriction and treatment
ποΈ I. Assessment and Monitoring:
πΈ Fluid Intake & Output (I&O):
Maintain strict documentation of all oral and IV fluids
Monitor for decreased urine output
πΈ Daily Weights:
Weigh patient daily at the same time
Sudden weight gain = fluid retention
πΈ Vital Signs Monitoring:
Observe for hypertension, tachycardia, or hypothermia
Assess for signs of fluid overload (edema, crackles)
πΈ Neurological Assessments:
Monitor for changes in level of consciousness, confusion, headache, seizures
Be vigilant with sodium levels <125 mEq/L
πΈ Laboratory Values:
Monitor:
Serum sodium (Hyponatremia <135 mEq/L)
Serum osmolality (β <275 mOsm/kg)
Urine osmolality (β >100 mOsm/kg)
Urine sodium (β >40 mEq/L)
π§Ύ II. Nursing Interventions:
πΉ Fluid Restriction:
Limit fluid intake to 800β1000 mL/day (or as prescribed)
Offer ice chips, sugarless gum, or oral swabs for dry mouth
Instruct family to avoid bringing extra drinks to the patient
πΉ Medication Administration:
Administer diuretics, hypertonic saline, or vasopressin antagonists as prescribed
Monitor for overcorrection of sodium (rapid rise may cause central pontine myelinolysis)
Observe for side effects of medications (e.g., thirst, dizziness, GI upset)
πΉ Safety Measures:
Implement seizure precautions (padded side rails, oxygen, suction setup)
Assist with ambulation (risk of falls due to confusion, weakness)
πΉ Nutritional Support:
Provide high-sodium diet (if prescribed)
Educate on avoiding low-sodium foods during hyponatremia
Monitor swallowing ability if neurological status is altered
π III. Patient and Family Education:
Explain what SIADH is and why fluid restriction is important
Teach early symptoms of hyponatremia: nausea, headache, confusion
Emphasize importance of regular blood tests to monitor sodium
Instruct to avoid over-the-counter medications that may worsen SIADH (e.g., NSAIDs, certain antidepressants)
π IV. Evaluation (Expected Outcomes):
β Maintains normal serum sodium levels β Demonstrates neurological stability β Adheres to fluid restriction and medication plan β Verbalizes understanding of the condition and prevention strategies β Remains free from complications like seizures or coma
β οΈ COMPLICATIONS OF SIADH
When SIADH is not identified or properly managed, it can lead to serious complications, primarily due to dilutional hyponatremia and cerebral edema.
π§ 1. Neurological Complications
Cerebral edema (swelling of brain cells)
Headache, confusion, irritability
Seizures, coma, and even death in severe hyponatremia
Brainstem herniation (rare but fatal if sodium drops too rapidly)
π§ͺ 2. Electrolyte Imbalance
Persistent hyponatremia (<120 mEq/L)
May result in muscle cramps, weakness, or altered reflexes
β Definition: SIADH is the excess secretion of ADH, causing water retention, dilutional hyponatremia, and concentrated urine.
β Common Causes:
CNS disorders (e.g., head injury, tumor, stroke)
Lung diseases (e.g., pneumonia, TB)
Small cell lung cancer (ectopic ADH secretion)
Medications: SSRIs, anticonvulsants, chemo
β Key Features:
Low serum sodium & osmolality
High urine sodium & osmolality
No signs of fluid overload (euvolemic hyponatremia)
β Major Symptoms:
Early: nausea, headache, fatigue
Moderate: confusion, irritability
Severe: seizures, coma, respiratory arrest
β Diagnosis:
Based on labs, clinical picture, and rule out of other causes (adrenal, thyroid, renal)
β Treatment:
Fluid restriction (mainstay)
Hypertonic saline (for severe cases)
Loop diuretics, salt tablets, or vaptans
Treat underlying cause (e.g., infection, tumor, drug)
β Nursing Focus:
Monitor I&O, neuro signs, labs
Prevent complications
Educate on fluid restriction and medication adherence
β Complications:
Seizures, coma, central pontine myelinolysis, fluid overload
π¬ Diabetes Mellitus (DM)
π Definition & Causes
β Definition:
Diabetes Mellitus is a chronic metabolic disorder characterized by hyperglycemia (elevated blood glucose levels) due to:
Deficiency of insulin secretion,
Resistance to insulin action, or
Both.
Insulin is a hormone produced by the beta cells of the pancreas (Islets of Langerhans) that regulates glucose uptake into cells for energy. When insulin is inadequate or ineffective, glucose remains in the bloodstream, leading to persistent high blood sugar and disturbances in carbohydrate, fat, and protein metabolism.
π Chronic uncontrolled diabetes can affect the eyes, kidneys, nerves, heart, and blood vessels.
𧬠Causes of Diabetes Mellitus:
The causes vary by the type of diabetes but generally involve genetic, autoimmune, environmental, and lifestyle factors.
π 1. Type 1 Diabetes Mellitus (T1DM):
Autoimmune destruction of pancreatic beta cells β absolute insulin deficiency
Usually occurs in children or young adults
Can also be idiopathic (without a known cause)
Common Causes:
Autoimmune reaction (anti-GAD antibodies)
Genetic predisposition (HLA-DR3, DR4)
Viral infections (e.g., Coxsackievirus, mumps)
Family history of Type 1 DM
π΅ 2. Type 2 Diabetes Mellitus (T2DM):
Characterized by insulin resistance and relative insulin deficiency
Most common type, often seen in adults, but increasingly in children due to obesity
Common Causes:
Obesity, especially central (abdominal) obesity
Physical inactivity
Poor dietary habits (high-sugar, high-fat intake)
Genetic predisposition
Aging
History of gestational diabetes or polycystic ovarian syndrome (PCOS)
Ethnic background (e.g., South Asians, African Americans)
π‘ 3. Gestational Diabetes Mellitus (GDM):
Develops during pregnancy due to hormonal changes causing insulin resistance
Usually resolves after delivery, but increases risk of future T2DM
Causes/Risk Factors:
Hormones (placental lactogen, cortisol) interfere with insulin
Obesity during pregnancy
Family history of diabetes
Previous macrosomic baby
Advanced maternal age
π’ 4. Other Specific Causes (Secondary Diabetes):
Genetic defects: MODY (Maturity Onset Diabetes of the Young), mitochondrial mutations
π’ Types of Diabetes Mellitus (DM)
Diabetes mellitus is classified into several types based on its cause, age of onset, and pathophysiology. The four major types are:
1οΈβ£ Type 1 Diabetes Mellitus (T1DM) β Insulin-Dependent Diabetes
Caused by autoimmune destruction of pancreatic Ξ²-cells, leading to absolute insulin deficiency
Usually occurs in childhood or adolescence, but can occur at any age
Requires lifelong insulin therapy
Key Features:
Rapid onset
Weight loss despite increased appetite
Polyuria, polydipsia, polyphagia
Positive for autoantibodies (GAD, ICA)
Risk of diabetic ketoacidosis (DKA)
2οΈβ£ Type 2 Diabetes Mellitus (T2DM) β Non-Insulin-Dependent Diabetes
Caused by insulin resistance in body tissues and a relative insulin deficiency
Most common type (β90β95% of all diabetes cases)
Often associated with obesity, sedentary lifestyle, and genetic predisposition
Key Features:
Gradual onset
May be asymptomatic for years
Managed by diet, exercise, oral antidiabetics, and sometimes insulin
Increased risk of cardiovascular disease and complications
3οΈβ£ Gestational Diabetes Mellitus (GDM)
Glucose intolerance that develops during pregnancy, usually in the 2nd or 3rd trimester
Caused by placental hormones (e.g., hPL, cortisol) that create insulin resistance
Key Features:
Temporary but may recur in future pregnancies
Increases risk of Type 2 DM later in life
Associated with fetal complications (macrosomia, neonatal hypoglycemia)
4οΈβ£ Other Specific Types (Secondary Diabetes)
These are less common and occur due to specific causes:
πΉ A. Genetic Defects in Ξ²-cell Function:
MODY (Maturity Onset Diabetes of the Young)
Neonatal diabetes mellitus
πΉ B. Diseases of the Pancreas:
Chronic pancreatitis
Pancreatic cancer
Hemochromatosis
πΉ C. Endocrinopathies:
Cushingβs syndrome
Acromegaly
Pheochromocytoma
Hyperthyroidism
πΉ D. Drug- or Chemical-Induced Diabetes:
Long-term use of glucocorticoids
Thiazide diuretics
Antipsychotics
Immunosuppressants (e.g., tacrolimus)
πΉ E. Infections:
Congenital rubella
Cytomegalovirus
𧬠Pathophysiology of Diabetes Mellitus
π Overview:
Diabetes mellitus is marked by a deficiency of insulin or the bodyβs inability to use insulin effectively, leading to elevated blood glucose levels (hyperglycemia). The metabolic consequences affect carbohydrate, fat, and protein metabolism.
π· Type 1 Diabetes Mellitus (T1DM) β Pathophysiology:
Autoimmune reaction targets and destroys the Ξ²-cells in the pancreatic islets of Langerhans, where insulin is produced.
This leads to absolute insulin deficiency β the body cannot use glucose for energy.
Glucose accumulates in the bloodstream (hyperglycemia) and is excreted in urine (glycosuria), pulling water with it β polyuria and dehydration.
As glucose cannot enter cells:
The body uses fats for energy, producing ketone bodies β ketosis
If unchecked, this leads to diabetic ketoacidosis (DKA) β a life-threatening emergency.
π In T1DM, insulin is virtually absent, and patients are dependent on insulin injections for survival.
πΆ Type 2 Diabetes Mellitus (T2DM) β Pathophysiology:
Begins with insulin resistance: body cells (muscle, fat, liver) fail to respond to insulin properly.
The pancreas compensates by producing more insulin (hyperinsulinemia).
Over time, Ξ²-cell dysfunction develops, and insulin secretion declines.
The result is relative insulin deficiency and persistent hyperglycemia.
π In T2DM, insulin is present but not effectiveβeventually requiring medication or insulin.
π Common Effects in Both Types:
Hyperglycemia β cellular dehydration
Glycosuria β osmotic diuresis β polyuria and dehydration
Polydipsia β due to fluid loss
Polyphagia β due to glucose not entering cells
Weight loss β due to fat/protein breakdown
Chronic complications from glucose toxicity:
Eyes (retinopathy)
Kidneys (nephropathy)
Nerves (neuropathy)
Heart & vessels (coronary artery disease, stroke)
β Signs and Symptoms of Diabetes Mellitus
The classic symptoms result from persistent hyperglycemia, cellular glucose deprivation, and osmotic diuresis. Symptoms may vary slightly depending on Type 1, Type 2, or Gestational Diabetes.
π· Common Symptoms in Both Type 1 & Type 2:
Polyuria β Frequent urination due to glucose-induced osmotic diuresis
Polydipsia β Excessive thirst due to dehydration
Polyphagia β Increased hunger (glucose not entering cells)
Weight loss β Especially in Type 1, due to fat and protein breakdown
Fatigue and weakness β Due to energy depletion
Blurred vision β Due to fluid shifts in the eye lens
Slow wound healing β High sugar impairs immune and tissue repair functions
Tingling or numbness β Peripheral neuropathy in chronic diabetes
Recurrent infections β Especially skin, urinary tract, or genital infections
πΆ Type 1 Diabetes Specific:
Sudden onset of symptoms
Common in children or adolescents
More likely to present with diabetic ketoacidosis (DKA) (nausea, vomiting, fruity breath, abdominal pain, rapid breathing)
π΅ Type 2 Diabetes Specific:
Gradual onset; may remain undiagnosed for years
Often detected during routine blood tests
Frequently associated with obesity, hypertension, or dyslipidemia
π‘ Gestational Diabetes Specific:
Usually asymptomatic
May present with:
Excessive weight gain
Increased thirst or urination
Detected during routine prenatal screening
π§ͺ Diagnosis of Diabetes Mellitus
Diagnosis is based on blood glucose levels, either fasting, random, or after a glucose load, and HbA1c (glycated hemoglobin).
Support stress reduction, as it may elevate blood glucose
β οΈ IV. Preventing and Managing Complications
Hypoglycemia:
Administer 15g quick-acting carbohydrates (e.g., juice, glucose tablets)
Recheck sugar after 15 minutes
Prepare to give glucagon IM or IV dextrose in severe cases
Diabetic Ketoacidosis (DKA)/HHS:
Monitor vitals, blood gases, ketones, hydration
Prepare for IV fluids, insulin therapy, and electrolyte replacement
π V. Evaluation (Expected Outcomes):
β Maintains blood glucose within target range β Verbalizes understanding of disease and management β Demonstrates correct insulin/self-care technique β Shows no signs of complications β Adheres to diet, medication, and lifestyle changes
β οΈ COMPLICATIONS OF DIABETES MELLITUS
Diabetes, especially when poorly controlled, can lead to acute emergencies and chronic multi-organ damage.