Non-Diabetic Endocrine Disorders Lecture Notes PDF

NUR 3111 Non-Diabetic Endocrine Disorders  Module 2: Non-Diabetic Endocrine Disorders Major Hormone-Secreting Glands of The Endocrine System Endocrine System Overview Hormones Chemical transmitters that regulate and integrate body functions by acti...

NUR 3111 Non-Diabetic Endocrine Disorders  Module 2: Non-Diabetic Endocrine Disorders Major Hormone-Secreting Glands of The Endocrine System Endocrine System Overview Hormones Chemical transmitters that regulate and integrate body functions by acting on local or distant target sites Help regulate organ function in concert with the nervous system, helping to finely regulate control of organ functions  Hypothalamus and Pituitary Glands Source Hormone Major Action Hypothalamus Releasing and inhibiting hormones Controls release of pituitary Corticotropin-releasing hormone (CRH) hormones Thyrotropin-releasing hormone (TRH) Growth hormone-releasing hormone (GHRH) Anterior Growth hormone (GH) Stimulates growth of bone and pituitary muscle; promotes protein synthesis and fat metabolism; decreases carbohydrate metabolism Adrenocorticotropic hormone (ACTH) Stimulates synthesis and secretion of adrenal cortical hormones Thyroid-stimulating hormone (TSH) Stimulates synthesis and secretion of thyroid hormones Posterior Antidiuretic hormone (also called vasopressin) Increases water reabsorption by pituitary kidney  Pituitary: GH The Pituitary; The Master Gland  Pituitary: GH Hypopituitarianism/Pituitary Insufficiency Hyposecretion of one or more pituitary hormones Many etiologies (tumor, infarction, trauma, radiation of pituitary are some) Area of the pituitary impacted determines hormone deficiencies Panhypopituitarianism, loss of all pituitary hormones, is rare. Collaborative care Treat cause Replace deficient hormones Educate patient about replacement hormones and signs and symptoms of hormone deficiencies and excesses.  Pituitary: GH Pituitary Tumors Almost all benign Oversecretion of Growth Hormone Giantism Acromegaly Oversecretion of ACTH Cushing’s (discussed with adrenal disorders) Undersecretion of all pituitary hormones Comprises 90% of pituitary tumors Tumors don’t produce hormones Tumors destroy the rest of the pituitary (can’t release hormones) Results in hypopituitarianism (one cause of this disorder)  Pituitary: Posterior Pituitary: Antidiuretic HormoneADH Disorders (ADH/Vasopressin) DI: Diabetes Insipidus Insufficient ADH (“don’t pee hormone”) SIADH: Syndrome of Inappropriate Antidiuretic Hormone Excess ADH (“don’t pee hormone”)  DI Pituitary: Problem Insufficient ADH (renal form not addressed) ADH Causes Head trauma Neurosurgery Radiation of pituitary area of brain Infections of CNS Tumor Clinical Thirst Manifestations Profound urine output (>250 mL/h) Very dilute urine Hypovolemia signs and symptoms High serum osmolality High serum sodium Low urine osmolarity Collaborative Treat cause (head injury, infection, etc.) Care Replace ADH (desmopressin, a synthetic vasopressin); usually long term Fluid replacement I and O/daily weights Education Medication: including adverse effects Prevention of complications Emergency measures Wear medical ID at all times  SIADH Pituitary: Problem Excess ADH ADH (cont.) Causes Head trauma Neurosurgery Radiation of pituitary area of brain Infections of CNS Malignant cells (esp. lung) can manufacture and secrete ADH Disorders of the lungs (pneumonia, pneumothorax, for example) Medications Thiazide diuretics Tricyclic antidepressants Phenothiazines Clinical Neurological symptoms of hypervolemia Manifestations Decreased urine output Concentrated urine Hypervolemia signs and symptoms Low serum osmolality Low serum sodium, including signs and symptoms of hyponatremia High urine osmolality Collaborative Care Treat cause (head injury, infection, etc.) Slow replacement of sodium with hypertonic saline Loop diuretics (furosemide/bumetanide) Fluid restriction I and O/daily weights Close monitoring of neurologic status Seizure precautions in some patients Careful skin care with edema Ongoing SIADH is rare  DI SIADH Pituitary: Problem Insufficient ADH (renal form not addressed) Excess ADH ADH Causes Head trauma Head trauma (cont..) Neurosurgery Neurosurgery Radiation of pituitary area of brain Radiation of pituitary area of brain Infections of CNS Infections of CNS Tumor Malignant cells (esp. lung) can manufacture and secrete ADH Disorders of the lungs (pneumonia, pneumothorax, for example) Medications Thiazide diuretics Tricyclic antidepressants Phenothiazines Clinical Manifestations Thirst Neurological symptoms of hypervolemia Profound urine output (>250 mL/h) Decreased urine output Very dilute urine Concentrated urine Hypovolemia signs and symptoms Hypervolemia signs and symptoms High serum osmolality Low serum osmolality High serum sodium Low serum sodium, including signs and symptoms of Low urine osmolarity hyponatremia High urine osmolality Collaborative Care Treat cause (head injury, infection, etc.) Treat cause (head injury, infection, etc.) Replace ADH (desmopressin, a synthetic vasopressin); Slow replacement of sodium with hypertonic saline (3%) usually long term Loop diuretics (furosemide/bumetanide) Fluid replacement (hypotonic saline or D 5W Fluid restriction I and O/daily weights I and O/daily weights Education Close monitoring of neurologic status Medication: including adverse effects Seizure precautions in some patients Prevention of complications Careful skin care with edema Emergency measures Ongoing SIADH is rare Wear medical ID at all times  Pituitar y Hypophysectomy  Definition  Partial or completed removal of pituitary  Indications  Pituitary tumors  Diabetic retinopathy  Metastatic breast or prostate cancer  Approach  Craniotomy  Transphenoidal (most common)  Pituitar Hypophysectomy (cont.) y http://img.tfd.com/mk/H/X2604-H-51.png Hypophysectomy (cont..)  Pituitar Hypophysectomy y (cont…) Postop care for transphenoidal hypophysectomy Monitor for target organ deficiencies Elevate HOB 30 degrees to decrease pressure Treat headache No tooth brushing; clean mouth with gauze pads and swabs Don’t blow nose, cough, sneeze Observe for CSF leak from nose Clear drainage Drainage positive for glucose Elevate HOB Call MD immediately Long term patient education plan Hormone replacement Break  Thyroid Thyroid Disorders  Thyroid Thyroid Hormones Hypothalamus produces thyrotropin-releasing hormone (TRH) which stimulates the pituitary to release thyroid stimulating hormone (TSH) TSH stimulates thyroid to release thyroid hormones T3 (four iodine atoms in each molecule) T4 (three iodine atoms in each molecule) Calcitonin Released in response to high serum calcium Reduces plasma calcium by increasing its deposition in bone When you think about thyroid, think about metabolism. Thyroid  Thyroid Hypothyroidism: TSH, T3, and T4 Pituitary problem: inadequate release of TSH (thyroid stimulating hormone Results in a failure of thyroid being stimulated to release thyroid hormones Levels in serum Low TSH Low T3, T4 This is secondary hypothyroidism Thyroid problem TSH released from pituitary Sick thyroid doesn’t respond Pituitary doesn’t “see” rise in thyroid hormones, so increases TSH levels in an effort to stimulate the thyroid further Levels in serum High TSH Low T3, T4 This is primary hypothyroidism  HYPOTHYROIDISM Thyroid Pathology Insufficient production of thyroid hormone – slowing of metabolism (cont.) Common Form Hashimoto’s thyroiditis (autoimmune destruction of thyroid); post treatment for Graves dz. Manifestations: Cold intolerant General Lethargic Weak Weight gain Forgetful Depression CNS Muscle exhaustion Slowed cognition Poor short-term memory Slowed speech/flat affect Decreased DTRs HEENT Dull, expressionless Dry, thin hair Dry, coarse, scaly skin Periorbital edema Thick puffy skin on face +/- goiter Hearing loss (1/3) CV Bradycardia Elevated cholesterol Atherosclerosis Coronary artery disease (for long-standing hypothyroidism, at risk for acute coronary syndrome Left ventricular dysfunction GI Decreased bowel sounds Constipation/impaction Anorexia (but weight gain) Fluid retention  HYPOTHYROIDISM Thyroid Pathology Insufficient production of thyroid hormone – slowing of metabolism (cont..) Common Form Hashimoto’s thyroiditis (autoimmune destruction of thyroid) Reproductive Female: Heavy, prolonged periods Irregular menses Infertile Male: Impotence Both: decreased libido Labs Low T3 & T4, high TSH in primary Low T3 & T4, low TSH in secondary (pituitary) Increased cholesterol, triglycerides (CV disease/HF risks and incidence increases) Management Hormone replacement (levothyroxine) Low calorie, high fiber diet Meds for constipation Extremes of Disease Myxedema/Myxedema Coma: Decompensation of poorly/undertreated patient Trauma, tumors, sedatives, narcotics and exposure to cold can alter the need for hormones, precipitating a crisis At risk for acute coronary syndrome  Thyroid Hyperthyroidism Low TSH High T3, T4 (overproduction of thyroid hormones suppresses production of TSH  Thyroid HYPERTHYROIDISM (cont… Pathology Overproduction of thyroid hormone – excessive stimulation of metabolism and excessive heat production ) Common Form Grave’s Disease (autoimmune disorder) most common, thyroiditis, goiter, benign tumor Manifestations: Heat intolerant HOT General Nervous, hyperactive Malnourished/weight loss Insomnia CNS Uncoordinated, muscle weakness and wasting Irritability/poor concentration (can’t focus) Fine tremors Emotional lability Increased DTRs HEENT Exophthalmos (bulging eyes) Fine, soft hair Excessive sweating Eyelid lag and stare Flushed, warm CV Tachycardia Bounding pulse Palpitations Atrial fibrillation Left ventricular hypertrophy and/or heart failure  HYPERTHYROIDISM Thyroid Pathology (cont….) Overproduction of thyroid hormone – excessive stimulation of metabolism and excessive heat production Common Form Grave’s Disease (autoimmune disorder) most common; thyroiditis; goiter; benign tumor GI Increased bowel sounds Diarrhea, abdominal pain Voracious appetite (but weight loss) Reproductive Female: Decreased menses Amenorrhea – no periods Male: Impotence, loss of libido Both: decreased sexual development Labs Increased T3 & T4 Decreased TSH Management Antithyroid drugs (propylthiouracil, methimazole) Beta blockers (control HR, arrhythmias, BP) Radioactive iodine treatments Thyroidectomy (remember parathyroid and Ca++ loss!) Extremes of Disease Thyroid storm: attenuated signs of hyperthyroidism Hypertensive crisis, severe tachycardia/arrhythmias, severely malnourished, high fever At risk for acute coronary syndrome  Thyroid Exophthalmos  Thyroid Thyroid Tumors If enlargement is large enough to cause visible swelling in the neck, it is referred to as a goiter (hypertrophy of thyroid gland) Benign or malignant Iodine deficient goiter Results from inadequate intake of iodine Rare in the US because of iodized salt More common in third world countries May recede with correction of iodine level (most often, iodized salt May require surgery Nodular goiter Some malignant, some benign Some result in hyperthyroidism Most will require thyroidectomy  Thyroid Goiters (Enlarged Thyroid Gland)  Thyroid Thyroidectomy Definition: removal of the thyroid gland (partial or total) Indications Patients unable to take antithyroid medications Large goiters Thyroid cancer Noncancerous thyroid nodules Postop care Monitoring Careful, frequent of calcium levels and for signs and symptoms of hypocalcemia (damage or inadvertent damage to parathyroid glands) Airway obstruction (postop swelling) Infection Bleeding (may have a drain, such as a JP, to collect blood) Begin with liquid nutrition and advance as tolerated Elevate HOB Pain management Teaching If total (and in some partial) thyroidectomy, patient will need levothyroxine for life Signs and symptoms of both hypo and hyperthyroidism; signs and symptoms of hypocalcemia Signs and symptoms of infection Persistent hoarseness Thyroid (cont…..)  Parathyro Parathyroid Disorders id  Parathyro id Parathyroid Hormone (PTH) Essential in calcium and phosphorous regulation Low serum calcium stimulates release of PTH Bones demineralize, raising calcium and phosphorus levels Kidneys excrete phosphorous and produce vitamin D (helps with absorption of calcium in the intestines) High serum calcium suppresses PTH release Bones reabsorb calcium  Parathyr Physiology of Calcium and Phosphorous oid Low Serum Calcium High Serum Calcium PTH Release stimulated Release inhibited Vitamin D Production stimulated by increase in PTH Synthesis suppressed by decreased PTH Calcitonin Very low level secretion Secretion stimulated by high serum calcium Intestinal absorption of Enhanced because of vitamin D impact on Low uptake calcium intestines (is reabsorbed into bones) Release of calcium and Stimulated by increase in PTH and Decreased due to low PTH and vitamin D phosphate from bone vitamin D levels Renal excretion of phosphate Stimulated by PTH (because of inverse Decreased due to low PTH levels relationship between calcium and phosphorous) Response Normal calcium and phosphate levels Low intestinal absorption; increased renal excretion (prevents hypercalcemia)  Parathyr Parathyroid Disorders oid Hypoparathyroidism Hyperparathyroidism (cont.) Problem Inadequate production of PTH resulting in Overproduction of PTH results in bone hypocalcemia demineralization Increased absorption of calcium by kidneys and intestine Causes Inadvertent damage or removal of parathyroid Primary: glands (thyroidectomy most common) Tumor of parathyroid gland (usually benign) Lithium Secondary: Renal failure because kidneys can’t filter phosphorous into urine Cancers that release a form of PTH (lung, for example) Clinical manifestations Signs and symptoms of hypocalcemia – may Usually asymptomatic be life-threatening Marked elevation in calcium Bone wasting Pathological fractures Tissue calcification Urinary stone formation Collaborative care Monitor serum calcium and vitamin D levels Treat cause (surgery, treat cancer) Replace calcium and vitamin D levels po or IV Medication Drink large volumes of water Exercise to strengthen bones Break (2)  Adrenal s Adrenal Disorders  Adrenal s Adrenal Cortex Hormones: Corticosteroids: stress adaptation Glucocorticosteroids: released in response to ACTH Cortisol Influence glucose metabolism Increase glucose level Mobilize fat stores Break down protein Long term negative effects Suppress the immune system Breaks down bone Mineralocorticosteroids: Released in a small part as a result of ACTH Primary release is in response to angiotensin II Aldosterone Stimulates renal reabsorption of sodium and water Stimulates renal filtration of potassium Androgens Sex hormones, mainly male Medullary hormones include epinephrine (beta) and norepinephrine (alpha) …  CUSHING’S DISEASE/SYNDROME Adrena ls Etiology Syndrome: Adrenal gland tumors (benign or malignant) Prolonged administration of corticosteroid drugs Malignant tumors that secrete ACTH Disease: Pituitary tumor: excess ACTH secreted, so excess cortisol released from adrenals Pathophysiology of Redistribution of fat to abdomen (leading to abdominal striae), face and upper back; high cortisol levels weight gain Insulin action blocked (hyperglycemia) Bone formation inhibited (osteoporosis) Hirsutism in women Antiinflammatory actions suppress normal response to illness, injury with poor wound healing Elevation of blood pressure (etiology not fully understood)  CUSHING’S DISEASE/SYNDROME Adrena Clinical Truncal obesity with thin arms, legs ls Manifestations Moon face (cont.) Buffalo hump Bruising/Petechiae: caused by increase protein metabolism resulting in capillary fragility Masculinization of women, amenorrhea Acne Hypertension Immunosuppression because of excess of cortisol: susceptible to infection Muscle weakness Emotional lability Labs: Hyperglycemia, hypokalemia, leukocytosis Collaborative Care Adrenalectomy for adrenal tumors and then provide steroid replacement therapy Hypophysectomy for pituitary tumors Treat tumors releasing ACTH With inoperable pituitary tumor: meds that inhibit cortisol release BP: Aldactone (inhibits aldosterone release) Potassium replacement if potassium-sparing Aldactone isn’t enough to manage potassium loss Treat hyperglycemia, hypertension  Adrenal s Cushing’s  Steroid Therapy and Cushing’s Syndrome (prednisone, hydrocortisone) Prolonged administration of corticosteroids can result in Cushing’s syndrome. Intravenous Oral Occasionally, inhaled Gradually withdraw any corticosteroid therapy Use the lowest dose that is effective  ADDISION’S Etiology Adrenalectomy/adrenal destruction Illness or stress in patient with adrenal disease Abrupt w/d of steroids after prolonged use Pathophysiology Primary: adrenals not functioning; autoimmune destruction most common Secondary: pituitary dysfunction or decreased production of ACTH - low cortisol levels (glucocorticoid) - low aldosterone levels (mineralocorticoid) - low estrogen/testosterone (androgens)  ADDISION’S Clinical Anorexia Manifestations Nausea, vomiting, diarrhea, abdominal pain Weakness, fever Hyperpigmentation of skin/bronze color (ACTH stimulates melanocyte production) Orthostasis, dehydration (low aldosterone decreases sodium and water, thus volume) Labs: Lack of aldosterone: - decreased plasma aldosterone - hyponatremia - hyperkalemia Hypovolemic: - decreased catecholamines - decreased peripheral tone (vasodilation) Hypoglycemic: - decreased cortisol levels leading to gluconeogenesis  ADDISION’S (cont.) Adrena ls Collaborative Treat cause (cont..) Care Replace deficient hormones: glucocorticoids, mineralocorticoids Stress management Maintain fluid status Manage electrolytes Addisonian or Cause: insufficient levels of corticosteroids in the face of increased need: trauma, stress, infection, Adrenal Crisis surgery are examples Manifestations: hypotension/shock, severe abdominal pain, high fever, confusion, hyponatremia, hyperkalemia, hypoglycemia, high WBCs. Treat with steroids and treat manifestations (such as shock) Adrena ls (cont… ) Corticosteroid Therapy and Addisonian Crisis (prednisone, hydrocortisone) In corticosteroid therapy, the adrenal gland’s ability to produce corticosteroids is suppressed. With abrupt withdrawal of corticosteroid therapy, the adrenal glands cannot immediately meet the body’s need for these substances The outcome can be adrenal crisis and may be life-threatening Always withdraw corticosteroid therapy slowly and gradually  Break (3) End of Lesson