NUR 2390 endocrine
Study Notes for Pharmacology - Endocrine System
Overview of Endocrine System
**Key Hormones and Glands: **
Grouped under various glands, including:
Pituitary Gland (Master Gland)
Thyroid
Parathyroid
Adrenal Glands
Hormones include: Growth Hormone (GH), Thyroid Stimulating Hormone (TSH), Adrenocorticotropic Hormone (ACTH), Prolactin, Oxytocin, Anti-Diuretic Hormone (ADH)
Pituitary Gland
Description:
Often referred to as the "Master Gland" because it controls other endocrine glands.
Location: Directed by the hypothalamus and divided into two lobes:
Anterior Lobe:
Secretes:
Growth Hormone (GH) – Stimulates growth in tissues and bones
Thyroid Stimulating Hormone (TSH) – Acts on the thyroid gland
Adrenocorticotropic Hormone (ACTH) – Stimulates adrenal gland
Gonadotropins (Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH)) – Affect testosterone and estrogen production in testes and ovaries
Posterior Lobe:
Secretes:
ADH – Acts on kidneys and blood vessels
Hormonal Regulation
Negative Feedback Loop:
Endocrine glands operate using a negative feedback loop:
If conditions in the body change from a set point, corrective mechanisms are activated until conditions return to that set point.
Growth Hormone (GH)
Production and Regulation:
Hypothalamus:
Secretes Growth Hormone-Releasing Hormone (GHRH) – Stimulates PITUITARY to release GH
Secretes Growth Hormone-Inhibitory Hormone (GHIH) – Inhibits GH release from PITUITARY
Action of GH:
Promotes growth of bones, muscle, and body tissues/organs (no specific target gland)
Deficiencies:
In Childhood:
Leads to short stature syndrome; GH replacement can improve short stature syndrome if administered before epiphyses close.
Prevents pituitary dwarfism (different from primordial dwarfism)
In Adulthood:
Short stature syndrome / pituitary dwarfism may become permanent; characterized by doll facies, obesity, high-pitched voice, muscle atrophy.
Patients with chronic illness (e.g., HIV) or muscle-wasting diseases may benefit from GH administration.
Illicit use seen in bodybuilding and strength training.
Growth Hormone Replacement Therapy
Somatropin:
Identical amino acid sequence to Human Growth Hormone (HGH)
Administration: Not orally (destroyed by GI enzymes), subcutaneous (SQ) or intramuscular (IM) (not IV)
Costly treatment
Long-term effects on insulin secretion leading to diabetes mellitus (DM).
Not to be used with corticosteroids.
Not effective for growth deficiency caused by Prader-Willi syndrome.
Side Effects of Somatropin:
Includes:
Paresthesias, arthralgia, myalgia, edema, headache
Glucose fluctuations, hypothyroidism, hematuria
Flu-like symptoms
Adverse Reactions:
Seizures, increased intracranial pressure, leukemia
Somatrem:
Similar to somatropin but with an extra amino acid.
Growth Hormone Excess
Causes:
Most commonly a pituitary tumor.
Consequences:
May lead to Gigantism or Acromegaly.
Treatment Options:
Removal or radiation of the tumor
Bromocriptine (Dopamine agonist) - reduces GH production
Pegvisomant (blocks GH action)
Octreotide (somatostatin agonist - suppresses GH release)
Note: Treatments are costly, and GI side effects are common.
Thyroid Gland
Function:
Regulates metabolic rate.
Hormonal Regulation:
Hypothalamus secretes Thyrotropin-Releasing Hormone (TRH) → stimulates PITUITARY to release TSH → stimulates thyroid to secrete T3 (triiodothyronine) and T4 (thyroxine).
Hypothyroidism:
Underactive thyroid results in low T3 and T4 levels.
Consequences: Increased TRH and TSH as negative feedback.
Hyperthyroidism:
Overactive thyroid leads to high T3 and T4 levels.
Consequences: Decreased TRH and TSH as negative feedback.
Iodine and Thyroid Function
Importance:
Iodine is essential for the production of T3 and T4
Consequences of Deficiency:
Leads to thyroid dysfunction and goiter.
Goiter
Primary Cause:
Iodine deficiency is the most common cause, leading to enlarged thyroid trying to capture more iodine for hormone production.
Other Causes:
Graves' Disease
Hashimoto's Thyroiditis
Nodules or thyroid cancer
Thyroid Dysfunction Causes
Primary: Issues with the thyroid itself (more frequent).
Indications: Thyroid dysfunction reflects inverse relationship with TSH:
Hypothyroid = LOW T3/T4 & HIGH TSH
Hyperthyroid = HIGH T3/T4 & LOW TSH.
Secondary: Tumor or issue with pituitary affecting TSH release.
Causes and Treatment of Hypothyroidism
Primary Causes:
Thyroid gland disorder - frequent; indicated by low T3/T4 and elevated TSH (could be due to Hashimoto’s, excessive therapy, surgery).
Treatment:
Synthetic T3/T4 replacement (Levothyroxine (T4) most common).
Liothyronine (T3) for rapid severity treatment.
Secondary Causes:
Pituitary issues - indicated by low TSH and low T3/T4 levels.
Treatment: Address pituitary issue (e.g., surgery).
Symptoms of Hypothyroidism
Common symptoms:
Lethargy, apathy, memory impairment, emotional changes, slow speech, cold intolerance, thick dry skin, weight gain.
Severe cases: MYXEDEMA coma.
In children: Leads to Cretinism (stunted growth).
Drug Therapy for Hypothyroidism
Uses: Treatment for hypothyroidism, myxedema, and cretinism.
Levothyroxine Sodium:
Pregnancy Category: A
Drug interactions: Increased effects of anticoagulants and decreased effects of antidiabetics.
Side effects include headache, nausea, vomiting, diarrhea, cramps.
Contraindicated in thyrotoxicosis, myocardial infarction, severe renal disease.
Caution advised in patients with cardiovascular disease.
Adverse reactions: Tachycardia, hypertension, palpitations, life-threatening thyroid crisis, angina, dysrhythmias.
Pharmacokinetics of Levothyroxine Sodium
Mechanism: Increases metabolic rate and oxygen consumption.
Pharmacodynamics:
Absorption: PO 50-75% (must be taken on an empty stomach).
IV onset: 6-8 hours; PO peak: 24-48 hours; duration: up to 1-3 weeks.
Distribution: 99% protein-bound, excreted in bile and feces.
Hyperthyroidism
Primary Causes:
Usually Graves' Disease (hyperfunction of the thyroid).
Symptoms: Rapid pulse, weight loss, excessive perspiration, heat intolerance, nervousness, irritability, exophthalmos.
Severe Cases: Thyroid Storm (life-threatening).
Treatment Options: Surgery, radioactive iodine, medications to inhibit secretion.
Secondary Causes: Pituitary issues secreting too much TSH.
Drug Therapy for Hyperthyroidism
Thiourea Derivatives:
Reduce thyroid hormone production (e.g., PTU, Methimazole).
Side effects mimic hypothyroid symptoms.
Prolonged use can cause goiter due to increased TSH secretion.
Antidiuretic Hormone (ADH)
Production: Produced in the posterior pituitary.
Function: Promotes water reabsorption from renal tubules, maintaining fluid balance in the body.
ADH Abnormalities
Deficiency: Leads to Diabetes Insipidus - increases urine production (diuresis), fluid loss, dehydration, hypotension, electrolyte disturbances.
Excess: Leads to Syndrome of Inappropriate Antidiuretic Hormone (SIADH) - causes water retention, fluid overload, CHF exacerbation, hyponatremia.
Treatment for Diabetes Insipidus
Replacement Therapy:
Vasopressin (Pitressin) - IM, SQ, or intranasal; serious side effect is hyponatremia; contraindicated in severe renal disease.
Desmopressin acetate (DDAVP) - used similarly, also indicated for nocturnal enuresis.
Parathyroid Glands
Function: Secrete Parathyroid Hormone (PTH), regulating calcium levels.
Mechanism of Action:
PTH secretion increases when serum calcium decreases.
Enhances osteoblast activity, calcium resorption from renal tubules and intestines (via Vitamin D).
Parathyroid Abnormalities
Deficiency (Hypoparathyroidism):
Caused by damage to glands or low magnesium; leads to hypocalcemia.
Excess (Hyperparathyroidism):
Usually due to malignancy; causes hypercalcemia.
Treatment for Hypoparathyroidism
Calcium Supplementation:
Calcitriol (Vitamin D analogue) enhances calcium absorption; Ergocalciferol enhances sodium and phosphorus absorption.
NATPARA - recombinant human PTH therapy available SQ.
Calcitriol Action and Pharmacokinetics
Use: Treats hypoparathyroidism and manages hypocalcemia in chronic renal failure.
Pharmacokinetics:
Absorption (PO) forms are effective, onset 2-6 hours, peak 10-12 hours, half-life around 3-8 hours, mainly excreted in feces.
Calcitonin
Thyroid Hormone: Besides T3 and T4, also produced by the thyroid to regulate calcium levels.
Released in response to increased serum calcium levels, stimulates osteoclast activity and calcium deposition.
Treatment for Hyperparathyroidism
Surgery: Partial/total parathyroidectomy is preferred.
Medications for hypercalcemia:
Salmon-derived calcitonin, intranasally (only if no fish allergy); adverse effects include hypocalcemia, tetany.
Cinacalcet - reduces PTH secretion, helps slow bone destruction.
Bisphosphonates assist with osteoporosis management.
Adrenal Glands Overview
Structure: Comprised of adrenal cortex and adrenal medulla.
Function: Produce glucocorticoids (e.g., cortisol) and mineralocorticoids (e.g., aldosterone).
Glucocorticoids (Cortisol)
Function: Affected by ACTH release; influences carbohydrate, protein metabolism, muscle activity.
Common Effects: Antiinflammatory, antiallergic, antistress impact, but long-term use increases side effects (e.g., fluid retention).
Common Drugs: Prednisone, methylprednisolone, dexamethasone.
Prednisone Overview
Uses: Decrease inflammation; immunosuppressant for various conditions.
Cautions:
Numerous drug interactions (e.g., with digoxin).
Side effects include hypertension, mood changes, weight gain, and serious complications like GI hemorrhage.
Corticosteroid Effects
Short-term vs Long-term Effects:
Long-term use leads to adrenal atrophy, necessitating careful tapering of doses.
Addison’s Disease
Description: Adrenal insufficiency leading to severe symptoms, requiring steroid therapy for life.
Cushing Syndrome
Description: Caused by overproduction of cortisol, usually due to pituitary or adrenal tumors; symptoms often parallel those of steroid therapy side effects.