Adrenal Gland, Thyroid, Pancreas, and Pituitary Gland Overview
Introduced by: Lauren Milam, MSN, RN
Key Topics: Glucose and Hormonal Regulation
Exemplars of Conditions Related to Hormonal Regulation
Diabetes Types 1 & 2
Hypos and Hyperglycemia
Metabolic Syndrome
Starvation
Hypo/hyperthyroidism
Cushings’ Syndrome
Addison’s Disease
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Diabetes Insipidus (DI)
Learning Objectives
List the laboratory tests used to diagnose Type 1 and Type 2 diabetes and metabolic syndrome.
Recognize the complications of uncontrolled diabetes and untreated metabolic syndrome.
Describe the pathological mechanisms causing Type 1 and Type 2 diabetes.
Identify signs and symptoms of Type 1 diabetes and Type 2 diabetes.
Identify risk factors for Type 1 diabetes, Type 2 diabetes, and metabolic syndrome.
Differentiate between diseases associated with hyperfunction versus hypofunction of the pituitary, thyroid, and adrenal glands.
Recognize hormones originating in the anterior and posterior pituitary glands.
Explain the hypothalamus-pituitary-hormone axis and feedback system.
Hormone Cell-to-Cell Communication
Paracrine Pathway: Hormones secreted from one cell act on nearby cells.
Autocrine Pathway: Cells produce hormones that act on themselves.
Endocrine Pathway: Hormones secreted into blood travel to distant cells.
Synaptic Pathway: Neurotransmitters travel along the axon to synapses to act on nearby neurons.
Neuroendocrine Pathway: Neurohormones produced in neurons enter the bloodstream to influence distant targets.
Hypothalamus & Pituitary Interaction
Roles: The hypothalamus produces releasing/inhibiting hormones acting on the pituitary gland to stimulate the release of pituitary hormones.
Hypothalamic Hormones:
Corticotrophin-Releasing Hormone
Dopamine
Growth Hormone-Releasing Hormone
Somatostatin
Gonadotrophin-Releasing Hormone
Thyrotrophin-Releasing Hormone
Posterior Pituitary Hormones: Oxytocin and Antidiuretic Hormone (ADH, Vasopressin) produced in hypothalamus, stored in the posterior pituitary until secreted.
Pituitary Gland Functions:
Master Gland: Regulates other glands in the body.
Comprised of Anterior and Posterior sections, each with unique functions.
Blood Regulatory Influences on the Pituitary
Blood levels regulate:
Releasing Hormones:
Thyrotropin-Releasing Hormone (TRH)
Corticotropin-Releasing Hormone (CRH)
Gonadotropin-Releasing Hormone (GnRH)
Growth Hormone-Releasing Hormone (GHRH)
Components: Nerve axons, blood vessels, hormones (e.g. Estrogen, Testosterone, etc.).
Disorders of Pituitary Function
Hypothalamus: (grape sized gland) Produces ADH & Oxytocin, communicates with anterior pituitary via a portal system.
Pituitary Size: Pea-sized, referred to as "Hypophysis".
Two portions; each with unique functions
Anterior: Oxytocin, Vasopressin
Posterior: TSH, ACTH, LH, FSH, GH, Prolactin
Major Pituitary Hormones and Their Functions
ACTH (Adrenocorticotropic Hormone): Stimulates release of corticosteroids.
GH (Growth Hormone): Triggers growth.
TSH (Thyroid Stimulating Hormone): Stimulates thyroid gland activity.
FSH (Follicle Stimulating Hormone): Stimulates ovarian follicles and seminiferous tubules.
LH (Luteinizing Hormone): Stimulates androgen (testosterone) production.
Prolactin: Stimulates milk production, primarily from anterior pituitary.
ADH (Antidiuretic Hormone): Regulates water balance, released from posterior pituitary.
Oxytocin: Stimulates uterine contractions and milk letdown during lactation.
Hypopituitarism: Growth Hormone Deficiency
Effects: Inhibits somatic growth, primarily affects hypothalamus.
Primary site of dysfunction appears to be in the hypothalamus
Signs and Symptoms: Short stature, obesity, immature facial features, delayed puberty, hypoglycemia, seizures, and insulin resistance.
Evaluation of Growth Hormone Deficiency & Replacement
Methods:
Family history
Growth patterns & health history
Definitive diagnosis bases of radioimmunoassay of plasma GH levels
Hand x-rays to evaluate growth potential vs. ossification
Endocrine studies to detect deficiencies
Family history
Growth patterns & health history
Definitive diagnosis bases of radioimmunoassay of plasma GH levels
Hand x-rays to evaluate growth potential vs. ossification
Endocrine studies to detect deficiencies
Prognosis for GH Deficiency Treatment
Success Rate: GH replacement therapy effective in 80% of cases.
Growth Rate: Typically 3.5-4 cm/yr, increasing to 8-9 cm/yr after treatment initiation.
Factors Influencing Response: Age, treatment length, frequency and dosage of treatment, and amount of GH receptors.
Challenges: Costly treatment ($20,000 - $30,000/year), need for family support and preparation for daily injections.
Pituitary Hyperfunction & Clinical Manifestations
Growth Hormone Overproduction: Can lead to overgrowth during childhood (before epiphyseal closure) or acromegaly in adulthood (after closure).
Main Symptoms: Excessive height, proportions in growth, facial features typical of acromegaly.
• Reach heights of 8 feet or more
• Vertical growth + increased muscle
• Weight generally in proportion to
height
• Excess GH after epiphyseal closure is
called acromegaly
• Typical facial features
Diagnostic Evaluations & Management of Pituitary Disorders
Causes: May be due to adenoma (non-cancerous tumor) in anterior pituitary.
Treatment Options: Radiologic studies, endocrine studies, surgical intervention if necessary, radiation, hormone replacement therapy post-surgery.
Diabetes Insipidus (DI)
Description: Main disorder of posterior pituitary due to hyposecretion (lack of) of ADH leading to uncontrolled diuresis.
Etiology: Genetic (familial or idiopathic) or secondary causes like trauma, tumors, CNS infection, or aneurysm.
Clinical Manifestations of Diabetes Insipidus & Treatment
Key Symptoms: (Cardinal signs) Polyuria (excessive urination) and polydipsia (excessive thirst), often leading to dehydration.
FIRST sign is ofter enuresis (involuntary urination)
The urine is highly dilute with a low specific gravity. Loss of fluids leads to serum hyperosmolality and severe dehydration. Shock and death can occur in untreated.
Infants: Often present with irritability, improved with water but not with milk.
Treatment: Hormone replacement therapy with vasopressin (DDAVP, nasal spray or IV), requires lifelong treatment.
Cardinal signs:
SIADH Pathophysiology (OPPOSITE of DI)
Condition: Caused by hypersecretion of ADH leading to low sodium (hyponatremia), fluid retention, and hypotonicity.
Symptoms: Anorexia, nausea/vomiting, irritability, personality changes which vanish with decreased ADH levels.
Diagnosis: Hyponatremia with serum sodium <135 mEq/L, hypotonicity (plasma osmolality <280 mOsm/kg), decreased urine volume, high urine sodium content.
Management: Monitor intake/output, restrict water, protect against seizures, administer hypertonic saline in severe cases, and potentially use ADH-antagonistic medications.
SIADH increases water retention with the nephrons
Diabetes Insipidus vs. SIADH
DI Characteristics: High urinary output, low levels of ADH, usually presenting with hypernatremia, indicates dehydration.
SIADH Characteristics: Low urinary output, high levels of ADH, usually presenting with hyponatremia, indicates overhydration.
Common Symptoms: Both conditions present excessive thirst.
Thyroid Function
Regulation: Thyroid hormone controls basal metabolic rate and secretes T3 (Triiodothyronine) and T4 (Thyroxine).
Conditions: Patients may experience hypothyroidism or hyperthyroidism, possibly has a disturbance in TSH secretion.
Hypothyroidism
Types: Congenital (during fetal development) and Acquired (due to various causes such as autoimmune reactions, iodine deficiency, etc.).
Manifestations: Low metabolic rate, fatigue, cold intolerance, weight gain, constipation, and skin changes like dry skin, sparse hair, and periorbital edema.
Treatment: Lifelong replacement therapy with levothyroxine (T4).
Congenital hypothyroidism occurs during fetal development and results in thyroid gland underdevelopment, insufficient synthesis of thyroid
hormone, or problems with TSH secretion. In utero, maternal T4 crosses the placenta; therefore, the newborn appears unaffected at birth.
If the child is untreated after birth, the lack of thyroid hormone production and secretion results in intellectual disability and impaired growth
Acquired hypothyroidism can result from (1) deficient thyroid hormone synthesis; (2) destruction of the thyroid gland; or (3) impaired TSH or TRH secretion.
Common causes of acquired hypothyroidism include autoimmunity, iodine deficiency, surgical removal of or radiation therapy to the thyroid gland, medications that destroy the thyroid gland, and genetic defects that affect the thyroid hormones. Hashimotos is an autoimmune cause more common in females
Hyperthyroidism (Graves' Disease)
Characteristics: Common cause is Graves' disease, characterized by enlargement of the thyroid gland and exophthalmos.
Onset: Peak incidence between ages 12-14 but can be congenital.
Diagnosis: Based on elevated T3 and T4 levels and suppressed TSH.
Clinical Manifestations of Hyperthyroidism
General Symptoms: High metabolic rate, weight loss, heat intolerance, diarrhea, tachycardia, tremors, and goiter (enlargement of thyroid).
Exophthalmos: Protrusion of eyeballs often seen in Graves' disease due to TSH-sensitized antibodies. This protrusion is usually bilateral and results from the interaction of TSH- sensitized antibodies interacting with fibroblast antigens found in extraocular muscles and tissues. The interaction results in lymphocyte infiltration, edema, and fibroblast accumulation, which displaces the eyeballs forward. Exophthalmos often persists despite treatment of hyperthyroidism.
Thyroid Storm
Condition: A hyperthyroid crisis due to sudden hormone release, can be life-threatening, especially in adults.
Triggers: Infection, surgery, or discontinuation of antithyroid medications.
Management: Anti-thyroid drugs and propranolol for symptomatic treatment.
Nursing Considerations for Thyroid Disorders
Care: Monitor for signs of both hyper and hypothyroidism, prepare clients for quiet environments with rest periods, help family cope, ensure adequate dietary intake for metabolic needs, and manage medication side effects.
Disorders of Adrenal Function
Hormones: Adrenal cortex secretes glucocorticoids, mineralocorticoids, and sex steroids. Adrenal medulla secretes catecholamines.
Conditions: Adrenal problems may lead to dysfunctions like Cushing syndrome and adrenal insufficiency (Addison's disease).
Pheochromocytoma
Description: Adrenal tumor producing catecholamines; often benign and may require extensive surgery or hormone therapy post-removal.
Cushing Syndrome
Definition: Excessive free cortisol in the circulation, potentially reversible following steroid withdrawal.
Etiology: Long-term corticosteroid therapy, pituitary tumors, adrenal tumors, or ectopic ACTH production.
Clinical Presentation of Cushing Syndrome
Signs: Weight gain, excessive body hair, buffalo hump, moon face, striae on skin, fatigue, and poor wound healing.
Management: Surgery, radiation, and hormone replacement therapy as required.
Acute Adrenocortical Insufficiency
Description: Also known as an adrenal crisis, leading to life-threatening symptoms like hypotension and shock.
Causes: Often autoimmune destruction of adrenal cortex leading to comprehensive loss of steroid hormone production.
Chronic Adrenocortical Insufficiency: Addison's Disease
Symptoms: Gradually onset after 90% adrenal tissue loss; treated with hydrocortisone infusions initially, followed by oral steroid replacements.
Pancreatic Hormone Function
Islets of Langerhans:
Alpha Cells: Produce glucagon.
Beta Cells: Produce insulin.
Delta Cells: Produce somatostatin to regulate insulin and glucagon.
Starvation Effects on Hormonal Regulation
Metabolic Sources: In starvation, glucose availability reduces; gluconeogenesis from muscle protein breakdown occurs.
Hormonal Response: Insulin suppressed, while glucagon, cortisone, epinephrine, and growth hormone levels increase to adapt metabolism towards fat usage and ketone production.
Diabetes Mellitus Type 1
Characteristics: Results from total or partial insulin deficiency due to beta cell destruction, often presenting in childhood or adolescence.
Pathophysiology: Inability for cells to uptake glucose leads to hyperglycemia; excess glucose spills into urine, with proteins being utilized as an energy source instead.
Diagnostic Tests for Type 1 Diabetes
Tests: Blood glucose, fasting glucose, glucose tolerance test, hemoglobin A1c and urinalysis to assess glucose and ketone levels, and diagnose diabetes based on specific thresholds.
Signs and Symptoms of Type 1 Diabetes
Clinical Manifestations: Polyuria, nocturia, glucosuria, polydipsia, dry mouth, weight loss, fatigue, and blurred vision.
Pathophysiologic Process: Hyperglycemia creates osmotic diuresis leading to dehydration, stimulates thirst, and prompts hunger due to cell starvation.
Diabetic Ketoacidosis (DKA)
Condition: Occurs when glucose isn’t available, leading to ketone production and resultant metabolic acidosis.
Manifestations: Kussmaul respirations (hyperventilation) with an acetone odor due to high ketone levels.
Treatment of DKA
Management Focus: Stabilizing glucose levels, correcting acidosis, fluid, and electrolyte replacement to improve tissue perfusion.
Treatment for Type 1 Diabetes
Essential Elements: Insulin therapy, glucose monitoring, dietary management, and handling of acute illness and DKA management.
Hypoglycemia
Definition: A state of low blood glucose presenting with weakness or pallor; common in type 1 diabetes due to insulin therapy.
Management: Simple carbohydrates to quickly elevate blood glucose and prevent brain deprivation.
Comparison of Type 1 and Type 2 Diabetes
Type 1: Cannot be prevented or cured; absolute insulin deficiency usually from autoimmune causes.
Type 2: Preventable through lifestyle change; insulin resistance or insufficient production more common, often noticed post-40 years of age.
Type 2 Diabetes Overview
Mechanism: Insulin resistance often leading to hyperglycemia; symptoms can include polydipsia, fatigue, and long-term complications like neuropathy.
Metabolic Syndrome
Definition: Associated with insulin resistance, characterized by obesity, high triglycerides, low HDL, hypertension, and heart disease.
Importance: Screening essential for patients with type 2 diabetes to understand full metabolic implications.
Long-Term Complications of Diabetes Mellitus
Microvascular Issues: Nephropathy and retinopathy.
Macrovascular Complications: Include neuropathy, increased infection risk, and cardiovascular diseases.
Patient Education for Diabetes Management
Key Areas: Understanding diabetes, meal planning, insulin therapy details, glucose monitoring, recognizing hypoglycemia/hyperglycemia, and support systems.
Clinical Presentation of Diabetes Mellitus vs. Insipidus
Diabetes Mellitus: Characterized by polyphagia, blurred vision, hyperglycemia, and dependence on insulin.
Diabetes Insipidus: Primarily presents with excessive urination without glucose, related to ADH deficiency.
Endocrine Study Guide Chart Overview
Major Hormones and their Glands:
Growth Hormone (GH) → Anterior Pituitary
Antidiuretic Hormone (ADH) → Posterior Pituitary
T3, T4 → Thyroid
Cortisol → Adrenal
Insulin → Pancreas