ENDOCRINE SYSTEM Overview

The Endocrine System FNP IV - N 477
Ann Sparks Dr. Denise Wilson
Endocrine Anatomy & Physiology Overview

Hormonal regulation: primary means the body uses to communicate within itself Endocrine and nervous systems work together to regulate responses through body Secretion and mechanisms of action of hormones are an extremely complex system of integrated responses
The endocrine system has five general functions: Differentiation of the reproductive and central nervous systems in developing fetus Stimulation of sequential growth and development during childhood and adolescence Coordination of the male and female reproductive systems, making sexual reproduction possible Maintenance homeostasis throughout the lifespan Initiation of corrective and adaptive responses when emergency demands occur Hormones control these functions in three different types of communication: Autocrine within a cell Paracrine between local cells Endocrine between remote cells Although there are a wide variety of hormones and functions, they share certain characteristics: Hormones have specific rates and rhythms of secretion Hormones operate within feedback systems, either positive or negative (feedback loops)* Hormones affect only cells with appropriate receptors, causing specific functions Other organs affecting hormones: o Kidneys secrete hormones o Liver metabolizes hormones inactivating them and making them more water soluble for renal secretion Hormones can be classified several ways, according to: Structure - Water soluble versus Lipid soluble (See page 2) Gland of origin Target organ effects Chemical composition Not within the scope of this paper
(McCance, 655)
Hormone Transportation & Cellular Effects based on Hormone Structure

Structural Categories of Hormones
Structural Category WATER SOLUBLE Peptides (Overview know general idea) Examples (not an exhaustive list)
Unbound with a short -life
Glycoproteins
Polypeptides
Amines
Growth hormone Insulin Parathyroid hormone Prolactin Follicle-stimulating hormone Luteinizing hormone Thyroid-stimulating hormone Adrenocorticotropic hormone Antidiuretic hormone Melanocyte-stimulating hormone Endorphines Glucagon Hypothalamic hormones Lipotropins Calcitonin Epinephrine Norepinephrine
Bound to carrier or binding protein, therefore less free
LIPID SOLUBLE Steroids (cholesterol is a precursor for all steroids)
Estrogens Glucocorticoids (cortisol) Mineralcorticoids (aldosterone) Progestins (progesterone) Testosterone Leukotreines Prostacyclines Thromboxanes Thyroxine both thyroxine (T4) and triiodothyronine (T3)
Derivatives of arachidonic acid (autocrine or paracrine action)
Thyroid hormones
Water-soluble hormones have a high molecular weight and cannot diffuse across the cell wall/membrane. They interact with receptors on the outer cell wall. Lipid-soluble hormones can easily diffuse across the plasma membrane of the cell, interacting with the cytosolic and/or nuclear receptors, to even change genome transcription.
(McCance, 656-59)
The following organs are the principal glands of origin of hormonal regulation: In the HEAD: Hypothalamus Pineal gland or epithalamus (epiphysis)
(McCance, 419)
Pituitary gland (hypophysis) o Anterior pituitary o Posterior pituitary In the NECK: Thyroid gland Parathyroid glands Thymus Pancreas Adrenal glands o Adrenal cortex o Adrenal medulla
In the CHEST: In the ABDOMEN:
In the PELVIS/Perineum: Ovaries/Testes

(McCance, 656)
Target Organ Effects

Pineal gland or epithalamus (epiphysis) Produces the Serotonin derivative Melatonin direct effect on sleep/wake states o Increases during the stress response o release is suppressed by light and increased in the dark o receptors have been identified on lymphoid cells, such as T cells and B cells
(Macchi; McCance, 322, 419)
Hypothalamus The hypothalamus is responsible for the synthesis and release of hormones that regulate the pituitary gland. Stimulation or inhibition of the pituitary hormones elicits a specific cascade of responses in peripheral target glands. In response, these glands secrete 3
hormones that exert a negative feedback on other hormones in the hypothalamuspituitary axis.
(Chisholm-Burns, 702)
Hypothalamic Hormones:
Hormone Target Tissue Anterior Pituitary Anterior Pituitary Anterior Pituitary Anterior Pituitary Anterior Pituitary Anterior Pituitary Anterior Pituitary Anterior Pituitary Action Stimulates release of Thyroid Stimulating Hormone (TSH); Modulates prolactin secretion Stimulates Follicle stimulating hormone (FSH) and Luteinizing Hormone (LH) Inhibits release of Growth hormone (GH) and TSH Stimulates release of GH Stimulates release of adrenocorticotropic hormone (ACTH) and Beta-endorphin Inhibits synthesis of ACTH Stimulates secretion of GH, FSH, LH, and prolactin Stimulates secretion of prolactin
Thyrotropic Releasing Hormone (TRH) Gonadotropin releasing Hormone (GnRN) Somatostatin Growth-Hormone Releasing Hormone (GHRH) * Corticotropin-releasing Hormone (CRH) * Substance P Dopamine Prolactin Releasing Factors (PRF)
* Significant in steroid level/control
(McCance, 664)
H-P-A (Hypothalamic-Pituitary Axis) The H-P-A forms a highly important portion of the endocrine system. It affects: the thyroid gland the adrenal glands male & female reproductive glands somatic growth lactation (see table above) There is a direct connection between the hypothalamus and the pituitary by blood and nerve supply. Physical trauma, emotional stress and hypoglycemia cause corticotropin-releasing hormone (CRH) to increase stimulating increased amounts of ACTH released by the anterior pituitary stimulates increased release of glucocorticoids, primarily cortisol.
As cortisol increases, it produces negative feedback for the adrenals, pituitary and hypothalamus to slow production of their respective hormones. (McCance, 316, 66164, 1139; Fauci, 918; Wilson, 208-09)
WARNING:
Adrenal suppression (heavy or long-term steroid use): May cause hypercorticism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children or in patients receiving high doses for prolonged periods. HPA axis suppression may lead to adrenal crisis. Withdrawal and discontinuation of a corticosteroid should be done slowly and carefully. Caution is required when patients are transferred from systemic corticosteroids to inhaled products due to possible adrenal insufficiency or withdrawal from steroids. Patients receiving >20 mg per day of prednisone (or equivalent) are most susceptible. Prednisone taper schedule (other regimens also available): Day 1: 30 mg divided as 10 mg before breakfast, 5 mg at lunch, 5 mg at dinner, 10 mg at bedtime Day 2: 5 mg at breakfast, 5 mg at lunch, 5 mg at dinner, 10 mg at bedtime Day 3: 5 mg 4 times/day (with meals and at bedtime) Day 4: 5 mg 3 times/day (breakfast, lunch, bedtime) Day 5: 5 mg 2 times/day (breakfast, bedtime) Day 6: 5 mg before breakfast
(Great article on steroid details at Merck Manuals Online)
Posterior Pituitary Hormones Antidiuretic Hormone (ADH) increases water reabsorption and concentrates urine. Regulated by osmoreceptors of the hypothalamus. Mechanoreceptors in the left atrium, the carotid arteries and the aortic arch stimulate ADH secretion with fluid volume loss. Oxytocin responsible for uterine contraction and milk ejection, and some antidiuretic affect similar to ADH.
Anterior Pituitary Hormones: These hormones are secreted by the Anterior Pituitary: Corticotropin related hormones: o ACTH Stimulates the adrenal cortex to release cortisol Diurnal patterns highest ACTH before awakening (see also: adrenals) o Beta-lipoprotein o Melanocyte-stimulating hormone (MSH) o Related endorphins Somatomammotropins: GH and prolactin; Prolactin induces and maintains lactation, and decreases reproductive function (through suppression of gonadatropin releasing hormone). Glycoproteins: LH, FSH, and TSH (Fauci, 918-19; McCance, 661-65) Thyroid Gland controls the rates of metabolic processes throughout the body. Acetylcholine, catecholamines and other peptides directly affect secretory activity of the follicular cells and thyroid blood flow. Thyroid Hormone (TH) regulated through a negative feedback loop involving 5
o Hypothalamus, anterior pituitary, and the thyroid gland. Thyroid Stimulating Hormone (TSH) a glycoprotein hormone synthesized and stored in the anterior pituitary. o TSH is secreted by the anterior pituitary and binds with receptors on the thyroid gland causing An immediate increase in the release of stored thyroid hormones An increase in iodide uptake and oxidation An increase in thyroid hormone synthesis An increase in the synthesis and secretion of prostaglandins by the thyroid o When TH is secreted by the thyroid gland, it acts on the thyroid gland, the anterior pituitary to regulate further TH production. Thyroid hormones have a negative feedback effect and inhibit TRH and TSH with decreases TH synthesis and secretion. The thyroid gland is stimulated to produce thyroid hormone by pituitary TSH, by low serum iodide levels, or by drugs interfering with the thyroid glands uptake of iodide from the blood. Iodide is oxidized into iodine. 25% of ingested iodine is trapped by the thyroid gland. Thyroxine levels have a direct affect on the sinoatrial (SA) node electrophysiological function, causing tachyarrhythmias and increased force of contraction, when too high.
(Medcape News)
o The thyroid gland normally produces 90% T4 and 10% T3 T4 is converted to T3 in the tissues and T3 has the greatest metabolic effects. SUMMARY of the thyroid: thyroid hormones affect many body tissues, primarily by affecting growth and maturation. They bind with intracellular receptors and influence the genetic expression of specific proteins. They also affect cell metabolism by altering protein, fat, and glucose metabolism and, as a result, heat production, and oxygen consumption are increased. T3 stimulates the synthesis of proteins affecting cardiac contractility o Hyperthyroidism increased heart rate and cardiac output, and the development of cardiomyopathy. Also, osteopenia, hypercalcemia, and hypercalcuria. Thyroid hormones respiratory center o Severe hypothyroidism causes respiratory depression
(McCance, 665-68)
Parathyroid Glands control serum calcium levels through the parathyroid hormone (PTH). PTH is the single most important factor in the regulation of serum calcium levels. PTH acts directly on the bone and the kidneys o Bone At least two affects Removes calcium from the bone to maintain serum calcium levels
(see Ch 42 McCance)
o Kidney PTH acts on the distal and proximal tubules to increase the reabsorption of calcium and decrease the absorption of phosphorus, respectively. o PTH also decreases the proximal tubule reabsorption of bicarbonate PTH stimulates the synthesis of biologically active form of vitamin D, a potent stimulator of calcium and phosphate absorption in the intestine.
(McCance, 668)
Calcium and phosphate balance is regulated by PTH, Vitamin D, and Calcitonin o Low circulating calcium + PTH + low phosphate = renal activation of Vitamin D Vitamin D thereby: Increases intestinal absorption of calcium Enhances bone reabsorption of calcium Increases renal tubular reabsorption of calcium, increasing Ca+
(McCance, 107-08)
o PTH is inhibited by estrogen, therefore Post-menopausal women at risk for osteoporosis ERT reduces hypercalcemia slightly (McCance, 1098-99) Magnesium and phosphate levels also affect PTH secretion. o Hypomagnesemia in persons with normal calcium levels acts as a mild stimulant to PTH secretion o In hypocalcemia, the condition of hypomagnesemia decreases PTH secretion Primary metabolic chemicals of the parathyroid gland: PTH hormone, calcium, magnesium, phosphate, bicarbonate
Thymus Gland specialized primary lymphoid organ that acts with the bone marrow Driven by hormones to generate clonal diversity in adaptive immunity. Pancreas is both an endocrine gland that produces hormones and an exocrine gland that produces digestive enzymes. Endocrine function: Islets of Langerhans secrete glucagon and insulin, hormones that regulate much of the carbohydrate metabolism. (Three types of hormone cells) o Alpha cells secrete glucagon High glucose levels cause glucagon release to be inhibited Low glucose levels and sympathetic stimulation promote glucagon release, particularly in the liver Glucagon is a hormone that promotes the breakdown of glycogen in the liver to glucose, increasing the blood sugar. o Beta cells secrete insulin (an anabolic hormone) o Delta cells secrete somatostatin and gastrin Beta cells synthesize insulin from the precursor, proinsulin o Secretion of insulin is chemical, hormonal and neural controlled o Insulin secretion is promoted by increased blood glucose amino acids serum free fatty acids 7
gastrointestinal hormones parasympathetic stimulation of the beta cells o Insulin secretion diminishes in response to Low blood levels of glucose (hypoglycemia) High levels of insulin (through negative feedback to the beta cells)
(McCance, 669)
The Somogyi effect is when insulin-induced hypoglycemia triggers excess secretion of glucagon and cortisol, leading to a rebound hyperglycemia response by morning. (McCance, 714) Kidney involvement The kidney regulates the acid-base buffer system along with the respiratory system. It also responds to PTH in the vitamin D and calcium regulation. It also responds to ADH produced by the posterior pituitary (McCance, 111-13) See GenitoUrinary synthesis project by Maggie Adrenals o The adrenal cortex produces steroid hormones controlled by the hypothalamus and pituitary synthesized from cholesterol: (Chisholm-Burns, 687) o Glucocorticoids (inc.luding Cortisol) responsible for: Metabolism Carbohydrate metabolism Anti-inflammatory properties Growth suppression Influence levels of awareness and sleep patterns o High levels of cortisol and synthetic glucocorticoids suppress both CRH and ACTH and low levels stimulate their secretion. o Diurnal rhythms affect ATCH and cortisol levels ACTH peaks 3-5 hrs after sleep begins and declines throughout the day (cortisol levels highest just prior to awakening o Stress increases ACTH secretion resulting in increased cortisol o Mineralcorticoids Aldosterone Conserves sodium by acting on the sodium pump of cells Resultant excretion of potassium When K+ is increased, Aldosterone is released. (McCance, 103) o Adrenal androgens and estrogens sexual characteristics o The adrenal medulla produces catecholamines o Epinephrine (adrenaline) o Norepinephrine (noradrenaline) (McCance, 672-74) Ovaries/Testes Ovaries Female gonads: o Production of estrogen & progesterone o Androgens/testosterone to a lesser degree o Production of gametes ova (McCance 743-44) See Womens Health synthesis project by Ashley, Alyssa and Nelle Testes Male gonads: o Production of gametes sperm o Production of androgens/testosterone 8
o Testosterone is produced by the testes, and to a lesser degree, the adrenal glands produce testosterone and other androgens as well. _____________________________________

(McCance, 752-55)
Endocrine REVIEW OF SYSTEMS

General: weight variations __, fatigue __, weakness __, fever__, chills __, night sweats __, growth problems__, poor hygiene __, dietary iodine __, dietary supplements__, change in shoe or glove size __. Skin/integument: hair texture __, hair dryness __, unusual hair patterns __, nail changes __. Do you check your feet __, sores on feet __. skin lesions __, problems healing __. HEENT: o Head: shape/symmetry __, visual changes __, dry mouth __. Ptosis __, headache __ o Eyes: glasses __, contacts __; blurring __, diplopia __, visual loss __, last eye exam ________ o Mouth/throat/neck: hoarseness __, sore throat __, swollen neck __, goiter __, nodules__. change in voice tone __. Breasts: skin changes __, masses/lumps __, pain __, discharge __, SBE __ CV: chest pain __, HTN __, palpitations __, DOE __, orthopnea __, edema __, Last EKG _________ Resp: SOB __, Last CXR _____________________ GI: appetite __, N/V __, indigestion___, dysphagia __, diarrhea/constipation __, frequency of BMs_____, abdominal pain __, GU: urgency __, polyuria __, dysuria __, hematuria __, nocturia __, incontinence __, stones__, infections__. Genital: FEMALE HISTORY: General; sexual interest __, function __, problems___, menopause ___, hot flashes ___, night sweats ___, yeast infections___. Also see Womens Health synthesis projects by Ashley, Alyssa and Nelle MALE HISTORY: gynecomastia __, decreased testicular size __, testicular masses __ or pain ___, frequency of STE __, last CTE ___ General: libido/sexual interest ___, function ___, problems ____ Vascular: leg edema __, color/skin changes __. MSK: weakness __, pain __, decreased muscle mass __, exercise routine __, numbness ___, tingling __, history of fractures __. Neuro: dizziness __, weakness __, numbness__, loss of sensation __, tremor __. Endocrine: Heat/cold intolerance __, excessive sweating __, polyuria__, polydipsia __, polyphagia __, thyroid problems __, diabetes __, hormone therapy or oral contraceptives __. Psych/Sleep: mood __, anxiety__, depression __, memory problems __, sleep disturbances __, agitation __, conflict __. (Bickley) __________________________________________
Endocrine EXAMINATION:
VS: Full set: Note rate, rhythm, quality BP- ______________ ______/_____ Hgt (inches) _________________ - Growth patterns Wgt (kg/pounds) ____________ - Change from previous BMI ____________________________ - Change from previous GENERAL: stature/development __, musculature __, nourishment__, race __, dress __, hygiene __, affect/temperament __, habitus __,hair patterns __, any distress __, dress/hygiene __. 9
INTEGUMENTARY: skin dry__, cool/coarse/rough __ or warm, moist, soft/velvety skin __, pale or yellowish __, edema __, puffiness __, acanthosis nigricans ___ (nap of neck, axilla), eruptive xanthomas __, thin/brittle nails __, myxedema __, hair coarse/brittle __ or thin/fine __, hyperpigmentation __ striae __, skin atrophy __, purpura __, ecchymosis __, acne __, buffalo hump __. HEENT: HEAD/FACE: shape and size: moon face __, acromegaly features __, o Note flushing, edema or fullness, hair loss/alopecia __, eye brow distribution __. o Eyes: exopthalmos __, lid lag __, opacities __, retinal abnormalities __. MOUTH: candidiasis __, fruity breath __, spacing of teeth __, dental care __, dentures __, NECK: shape and size o Note thyroid fullness __, goiter __, thyromegally __, nodules __, masses __ BREAST: Be alert for discharge See Womens Health synthesis projects by Ashley, Alyssa and Nelle. Note skin of axilla __. HEART: Normal PMI, regular rate and rhythm, normal S1, S2, precordial movement LUNGS: no respiratory distress __, note quality of respirations __. ABDOMEN: shape __, scars __, BS __, consistency (soft/firm), tenderness __, masses __, guarding __, GU: hair distribution __, vaginal candidiasis __, secondary sexual development __. MALE: Normal Male Testes descended and of appropriate size. FEMALE: See Womens Health synthesis projects by Ashley, Alyssa and Nelle MSK: Muscle atrophy/weakness __; swelling __, gait normal symmetric muscle tone __. VASCULAR: pulses: carotid, radial, femoral, popliteal, posterior tibial, dorsalis pedis __; varicose veins __. NEUROLOGICAL: Mental status abnormalities __, normal strength and tone __. Reflexes __. PSYCH: Inappropriate affect __, behavior __, agitation__, tremulousness __. DEVELOPMENTAL: Inappropriate growth __, (Bickley) ____________________________________
Common Pathological conditions of the Endocrine system, Epidemiology, and Pharmacology, including clinical guidelines
(Select uncommon conditions also mentioned)
E Pituitary Tumors tumors secreting prolactin are the most common. GH and
ACTH tumors account for 10-15% of pituitary tumors. Pituitary adenomas are benign. Symptoms: headache, visual loss, diplopia, ptosis, facial sensory changes Testing: Common testing includes prolactin, insulin-like growth factor I (IGF-I), GH stimulation tests, 24-h urinary free cortisol, ACTH stimulation test, FSH, LH and menstrual history in women (testosterone in men), TSH, Free T4. Refer to endocrinologist for medical or surgical intervention 10
E Disorders of the Anterior Pituitary and Hypothalamus E
Pituitary apoplexy (bleeding or impaired blood supply): endocrine emergency severe headache, bilateral vision changes, opthalmoplegia, CV collapse, & loss of consciousness. It may result in hypotension, severe hypoglycemia, CNS hemorrhage and death. (Fauci, 917-19; Wikipedia)
E Pituitary Hormone Hypersecretion Syndromes

E Hyperprolactinemia Prolactin normally acts to develop breasts during pregnancy, post-partum milk production, and suppression of ovarian function during breastfeeding. Normally prolactin is elevated during pregnancy Pathologic elevation in women results in amenorrhea, galactorrhea, hirsutism and osteopenia (as a result of decreased estrogen), headaches, and macroadenomas can cause bitemporal hemianopsia (tunnel vision). Pathologic elevation in men results in hypogonadism, erectile dysfunction, impaired libido, oligospermia, diminished ejaculate volume. Prolactin-secreting adenomas: common cause of prolactin levels >100 mcg/L Some conditions and medications can cause an increase in prolactin:
Polycystic Ovarian Disease Renal Failure Primary hypothyroidism H2 Agonists Opiates Metoclopramide Tricyclic antidepressants Methyldopa Estrogens Antipsychotics (risperidone, chlorpromazine) SSRIs
Diagnosis: MRI may show pituitary adenoma surgical resection of tumor Treatment: Medications causing hyperprolactinemia should be discontinued Medications: dopamine agonist for microprolactinomas (Cabergoline or bromocriptine) Surgery or Radiation (Fauci, 919-20; Kemmann; McCance 691-92)
E Acromegally (and Giganticism) Growth Hormone (GH) - Most common cause: secretion by pituitary adenoma Giganticism begins as a child Excess GH when bone growth plates not yet calcified Extremely tall stature Acromegally begins as adult Excess GH after bone growth plates are calcified Pronounced facial features (A), forehead bossing, increase in shoe/glove size (B), deeper voice Cardiomyopathy, L ventricular hypertrophy, sleep apnea, diabetes Because of pulsitility of GH, Measuring GH isnt an appropriate diagnostic 11
Diagnosis = failure of GH suppression test Refer to endocrinology (Fauci, 919-21)
E Cushings See Adrenal gland E Non-functioning and gonadotropin-producing adenomas present with symptoms of 1 or more hormone deficiencies. E Hypopituitarism may be congenital, traumatic, neoplastic, infiltrative, vascular or infectious. Hormone replacement is indicated. (Fauci, 922)
E Diabetes Insipidus (DI): Too little ADH (i.e.: Vasopressin or AVP)

Arginine vasopressin (AVP) deficit in pituitary or decreased action in the kidney Multiple causes: head trauma, congenital/genetic, medications or metabolic conditions or renal damage. DI must be differentiated from other etiologies of polyuria (Fauci, 924) Symptoms: polyuria, polydipsia, also dehydration and hypernatremia may occur Urine output > 50ml/kg per day and urine osmolality < 300 mosmol/kg or specific gravity < 1.010. Primary DI may be treated with desmopressin (DDAVP). Nephrogenic DI may be treated with prostaglandin synthesis inhibitors (indomethacin) or a thiazide diuretic with amiloride + low sodium diet.
E SIADH (Syndrome of Inappropriate Antidiuretic Hormone): Too much ADH

Excessive or inappropriate production of arginine vasopressin (AVP) Multiple causes: neoplasm, head trauma, lung infection, vascular, neurogenic, congenital, metabolic, medications. Physiology: Normally, hyperosmolity and hypovolemia stimulate ADH secretion o Regulation of ADH release occurs from baroreceptors and neural input Pathology: Persistent ADH release without the physiological cues Symptoms: hyponatremia, hemodilution/water intoxication (headache, confusion, anorexia, nausea, vomiting, convulsions, coma). Drugs that can cause SIADH: Increase ADH production Potentiate ADH action
Antidepressants o TCs, MOAs, SSRIs Antineoplastics o Cyclophosphamide, vincristine Carbamazapine Neuroleptics o Thiothixene, thioridazine, haldol Vasopressin/DDAVP Carbamazepine Chlorpropamide, tolbutamide Cyclophosphmide NSAIDs Somatostatin & analogs Amiodarone Lists not exhaustive
12
Labs: low BUN, Creatinine, uric acid, albumin; serum Na < 130 mmol/L, plasma osmolality < 270 mmol/kg; urine likely hypertonic to plasma & urine Na often >20 mmol/L. Treatment: Fluids restricted to 500 mL less than urinary output. With severe Sx, hypertonic (3%) saline infused at </= 0.05 mL/kg body weight IV per minute. For further treatment, see Fauci, 924-25.
(Fauci, 924; McPhee, 844)
E Anxiety all patients should be screened for glucose, calcium, phosphate levels,
EKG and thyroid studies. Urine drug screen and urinary catacholamines may be required to exclude specific disorders. (Psychiatry On Call)
E Thyroid Gland disorders E
E Hypothyroidism:
Epidemiology high prevalence in areas of poor iodine intake. In the U.S. 1-3% of the population and it increases with age, with upwards of 5-20% of elderly affected.
(McPhee, 1061; Wilson, 2011)
Cause can be at any level of the production: hypothalamus TRH Ant. Pituitary TSH Thyroid T3 and T4. Etiology if in area of adequate iodine intake, causes are autoimmune or iatogenic. Primary hypothyroidism Deficient thyroid hormone secretion from thyroid. o High TSH, Low T3 and T4 o Autoimmune Hashimotos disease, Hepatitis C (McPhee, 1062) o Radiation o Medications: Lithium, Interferon, Amiodarone, and others o Genetic, autoimmune or idiopathic Secondary hypothyroidism pituitary or hypothalamic disease (tumors or trauma) o Low TSH, Low T3 and T4 in secondary hypothyroidism. Subclinical hypothyroidism normal thyroid hormone level (T3 and T4) with mild elevation of TSH. MAY have minor symptoms. Clinical (overt) hypothyroidism higher TSH, low free T4 Symptoms: lethargy, dry hair & skin, cold intolerance, hair loss, difficulty concentrating, mild weight gain with poor appetite, dyspnea, hoarse voice, muscle cramping, mennorrhagia. Clinical features: bradycardia, mild diastolic hypertension, prolonged relaxation of deep tendon reflexes, cool peripheral extremities, possibly palpable goiter or thyroid may be atrophic and non-palpable. Severe: Cardiomegaly with pericardial effusion, flat affect, periorbital puffiness, large tongue, pale/doughy, cool skin Myxedema crisis: Hypothermia and stuporous (myxedema coma), respiratory depression, rhabdomyolysis, acute kidney injury (can be caused by hypothermia, trauma, infection, or narcotics). (McPhee, 1064; Fauci, 926) 13
SCREENING: All newborns should be tested for congenital hypothyroidism between 2 and 4 days of age with TSH and Free T4. (U. S. Preventative Services Task Force) TSH at age 35 and at least every 5 years in adults. Also, there is an immediate indication in depression, anxiety, pregnancy, and throughout these conditions. Also, closer monitoring needed while on medications that can cause hypothyroidism.
(U. S. Preventative Services Task Force)
The ultrasensitive assay TSH is the most sensitive screening test for hypothyroidism. Also, it is most sensitive to detect subclinical thyroid excess or deficiency. Normal TSH = 0.4 4.0 mU/L High TSH = > 4.0 (inadequate amount of levothyroxine) Low TSH = < 0.4 (over-corrected with levothyroxine) (Wilson, 2008; 548) DIAGNOSTICS: Serum TSH High in primary hypothyroidism, but low in secondary hypothyroidism Free T4 (Thyroxine) decreased in all forms of clinical hypothyroidism, but normal in subclinical hypothyroidism Antithyroglobulin and antihyroperoxidase antibodies if autoimmune issue Thyroid scan (with radioactive isotopes) or thyroid ultrasound (Wilson, 2008; 64, 546-47) Lipid panel hypothyroidism causes a decreased ability to metabolize lipids. TREATMENT: T4 (levothyroxine):
Start low increase/change slow Before & After treatment for hypothyroid
TREATMENT (contd)

Adults < 60 y/o with no heart disease start with 50-100 mcg T4 (levothyroxine)/day Older adults or those with CAD 12.5 25 mcg of levothyroxine/day The dosage should be adjusted in 12.5 25 mcg increments every 6-8 weeks on the basis of TSH levels, until normal TSH levels are achieved. MEASURE TSH: every 6-8 weeks until stable; with significant illness; with other medication changes (See McPhee, 1065); at 6 months and then every 6-12 months, once stable. (McPhee, 1061-65) Patient Education: Take on an empty stomach, at the Bioavailability varies between same time daily. Food/other meds brands stick to one brand. TSH can decrease absorption. Take at should be drawn in 6-8 weeks if least 4 hours from brand is changed. Report S/Sx of hyperthyroid: cholestyramine palpitations, tremor, insomnia, FeSO4 diarrhea, heat intolerance or wgt sucralfate loss. calcium antacids Other drugs can interact with T4: notify practitioner of med changes 14
The Endocrine System FNP IV - N 477 REFER to ENDOCRINOLGY IF: Pediatric Unresponsive to therapy Pregnant High risk cardiac complications


Presence of goiter, nodule, or other structural change in the thyroid gland Presence of other endocrine disease
E Thyrotoxicosis (Hyperthyroidism)
EPIDEMIOLOGY: Prevalence rate of 2.7%. Less than 25% of hyperthyroid patients > 65 present with typical symptoms Routine screening essential. Primary Hyperthyroidism T3 and T4 levels are elevated and serum TSH levels are suppressed (Graves disease, Toxic Multinodular Goiter, Toxic Adenoma and Iodine excess). Thyroid destruction - T3 and T4 levels are elevated (subacute thyroiditis, silent thyroiditis, amiodarone, radiation). Secondary Hyperthyroidism - T3 and T4 levels are elevated (TSH-secreting pituitary adenoma, thyroid hormone resistance syndrome, human chorionic gonadatropin [hCG]-secreting tumors, gestational thyrotoxicosis) Table 26-5 on page 1067, McPhee gives causes for high T3, T4, and Low TSH level
E Graves disease
SYMPTOMS: Ophthalmopathy o Conjunctival edema o Exopthalmus o Conjunctivitis lag Restless, nervous, fidgety Irritability/anxious Fatigue/weakness Heat intolerance Memory problems Wgt loss w/ increased appetite Frequent BMs Oligomenorrhea Skin is warm & moist Fingernail separation from nail bed (Plummers nails) Tetany - rare Tachycardia Systolic HTN ex: 190/80 Systolic murmur Atrial fibrillation Fine tremor
Hyperreflexia Proximal muscle weakness Long-standing thyrotoxicosis osteoporosis Thyroid 2-3X normal size o Thyroid bruit/thrill may be present In subacute thyroiditis: o Tender thyroid o Thyroid enlargement o Referred pain to jaw or ear
DIAGNOSTICS: Serum TSH and Free T4. See diagnostic Algorithm in Fauci, p 929 COMPLICATIONS of hyperthyroidism: 15

Hypercalcemia Osteoporosis Decreased libido Erectile dysfunction Gynecomastia Cardiac arrythmias

Heart failure Thyroid crisis Ophthalmopathy Dermopathy
(Wilson, 2011)
TREATMENTS: Propanolol: 20-40 mg every 6 hours, or longer acting Beta-blocker: Atenolol (50 mg/d) for adrenergic symptoms (rapid HR, tremor, diaphoresis, anxiety) Methimazole or carbimazole: (10-20 mg bid-tid initially, titrated to 2.5-10 mg/d) inhibits thyroid hormone synthesis. Reduce dose as hyperthyroid resolves. Iodinated contrast agents (Iopanoic acid or ipodate sodium) Propylthiouracil (PTU): 100-200 mg q8h initially, titrated to 50 mg qd or bid. Safest in breast-feeding and pregnancy. Decrease dose as Free T4 level approaches normal. Radioactive iodine Used most often in the elderly. Can be used initially, or after 2 yrs of ineffective trial of antithyroid drugs. Also, the treatment of choice for toxic nodules. o Hypothyroid is often the result Thyroid surgery rarely indicated for Graves; not used in the elderly o Women < 45 y/o or pregnant o Nodular goiters o Malignancy o Risks: hypoparathyroidism (check calcium); laryngeal nerve damage Permanent hypothyroidism can occur Anticoagulation for patients in atrial fibrillation For Exopthalmus artificial tears; tape eyelids shut during sleep o Severe with chemosis, opthalmoplegia, or vision loss: Large doses of prednisone (40-80 mg/day) Opthamology referral for possible orbital decompression For Thyroid Storm: o Large doses of PTU (600 mg loading dose, PO, NG, or per rectum) See further treatment in Fauci, p 930 Patient teaching for PTU: Written instructions: Common side effects (1-4% of patients): rash, urticaria, fever, arthralgia. Rare but major side effects: Hepatitis C, agranulocytosis, Sx of agranulocytosis sore throat, fever, mouth sores Stop treatment pending a CBC to rule out agranulocytosis (Fauci, 929-30) Referrals: Endocrinology Cardiology Ultrasound and fine needle aspiration (FNA) repeat annually if benign 16
Recheck TSH and Free T4 in 3-6 weeks after starting medications o After stabilization recheck in 1 year (Fauci, 929; Wilson, 2011)
E Sick Euthroid Syndrome Any acute or severe illness can cause abnormal
TSH levels, even in the absence of underlying thyroid disease. Routine thyroid testing should be avoided in acutely ill patients unless a thyroid disorder is strongly suspected.
(Fauci, 931)
E Amiodarone may cause hypothyroidism or thyrotoxicosis. Elevated T4 (> 20 mcg/dL) or T3 (> 200 ng/dL), and suppressed TSH Elderly most often have cardiac manifestations o Heart failure o Angina o Atrial fibrillation o Complicated by myopathy, osteoporosis or depression
E Nontoxic Goiter Enlarged thyroid gland, women more common than men.

``
(Fauci, 931)
Perform Thyroid function tests to exclude thyrotoxicosis and hypothyroidism Substernal goiter should be evaluated w/ respiratory flow studies, CT or MRI
(Fauci, 931)
E Thyroid Neoplasms nodule may be benign 90%, or malignant 10%
Size: > 1 cm warrants follow-up + testing here are Red flags: Recent or rapid growth of a nodule or mass History of neck irradiation Lymph node involvement Hoarseness Fixation of the growth to surrounding tissues cold nodule on iodine uptake scan (indicative of non-functioning tissue) See diagram 26-6 Evaluations of thyroid nodules, McPhee, 1079 DIFFERENTIAL: Hypermetabolism without hyperthyroidism (Severe anemia, Leukemia, Polycythemia, Cancer) Phyeochromocytoma (hypermetabolism, tachycardia, profuse sweating) Acromegaly (tachycardia, diaphoresis, thyroid enlargement) Cardiac disease (atrial fib. angina, heart failure) Thyroid cancer Benign thyroid nodule Osteoporosis Diabetes Mellitus DIAGNOSIS of a thyroid nodule: TSH, T4, Free T4, T3 U/S criteria should be used to determine which 10- to 14-mm nodules should undergo Fine Needle Aspiration Biopsy (FNAB). (McCarty) 17
TSH low: Thyroid ultrasound looking for hot nodule, versus cold o Cold nodule is indicative of benign or malignant cancer TSH normal: Fine needle aspiration Cytopathology CT scan Algorithm for further Dx procedures in Fauci, p 933 (Fauci, 931-33)
E Adrenal Gland disorders E HYPERfunction of the adrenal gland E Cushings Syndrome (Hypercortisolism)
Manifestations of excessive corticosteroids. Most commonly, the cause of Cushings syndrome is from administration of glucocorticoids for therapeutic reasons. Cushings Disease 40% of Cushings disease cases result from hypersecretion of ATCH by the pituitary. Most often results from a small (<5mm) benign anterior pituitary adenomas (98% of cases). Ectopic sources can include tumors of the lung, thyroid, thymus, pancreas, or ovary, are 25% of Cushings Syndrome cases. Occurrence is at least 3X more common in women than men. (McPhee, 1111) Manifestations:, Increased insulin resistance causing glucose tolerance and diabetes mellitus. With Cushings syndrome, leukocytosis and relative granulocytosis and lymphopenia are present. Hypokalemia is also often present. Also, central obesity, hypertension, osteoporosis, psychological disturbances, acne, amenorrhea thin fragile skin, ecchymosis, purple striae, proximal myopathy, fat deposits in the face and intrascapular areas (moon face and buffalo hump), and virilization (masculine features brought on by androgens). Testing: In the hyperstimulation of the adrenals of Cushings, pituitary suppression does not prevent the hyperactive adrenal cortex from continuing to produce large amounts of cortisol. (Wilson, 208) Diagnosis of Cushings syndrome requires abnormal cortisol suppression in response to dexamethasone by the Dexamethasone suppression test (DST). 11PM: Dexamethasone 1mg PO 8AM: Serum Cortisol Normal: < 5 mcg/dL (140nmol/L SI u)
(McPhee, 1111; Wilson, 208-09)
Collaboration/referral required. Surgical excision required for tumors. Stress doses of glucocorticoids must be given pre- and postoperatively. (Fauci, 934)
E Aldosteronism Hypersecretion of the adrenal mineralcorticoid, aldosterone.

18
Primary Aldosteronism adrenal cause such as adrenal tumor or adrenal hyperplasia Secondary Aldosteronism extraadrenal stimulus such as renal artery stenosis or diuretic therapy Manifestations: Severe headache and diastolic hypertension. Edema will be absent unless the pt has CHF or renal disease. Hypokalemia may cause muscle weakness/fatigue, though levels may be normal in primary aldosteronism. Hypernatremia and metabolic acidosis may occur. Dx/Testing: The hypertension in conjunction with persistent hypokalemia in a nonedematous patient NOT receiving potassium-wasting diuretics is suspicious for diagnosis. If hypokalemia persists after two weeks of potassium supplementation, screening using serum aldosterone and plasma rennin to determine the ratio, should be performed. For proper testing of primary Aldosteronism D/C diuretics 3 weeks prior to testing Also, Beta-blockers and Dihyropyrodine Calcium Channel Blockers can interfere with Dx ACE-I and Alpha-blockers are less likely to alter testing results, such as verapamil, hydralazine, prazosin, doxazosin, and terazosin. (McPhee, 1116) Refer to endocrinologist for medical treatment of hyperplasia with sodium restriction and spironolactone, or surgical intervention for adenoma. (Fauci, 935)
E Syndromes of Adrenal Androgen excess in women

virilization increased androgen levels deepening voice, clitoromegaly, decrease in breast size, and hirsutism excessive male-pattern hair growth
(Fauci, 935, 955)
HYPOfunction of the Adrenal gland E Addisons Disease or Adrenocortical insufficiency

Occurs when >90% of the adrenal tissue is destroyed surgically, through a granulomatous disease, or by autoimmune mechanism, or other rare causes. Uncommon disorder: Chronic deficiency of cortisol, aldosterone, and adrenal androgens Etiology: TB is the leading cause of Addisons. Others that are more rare. Manifestations: fatigue/weakness, anorexia, nausea/vomiting, wgt loss, abdominal pain, cutaneous & mucosal pigmentation, irritability, hypotension, salt craving, and occasionally hypoglycemia. Routine labs may be normal, but serum Na+ may be reduced and serum K+ increased. Extracellular fluid depletion may accentuate hypotension. Diagnostics: Low plasma cortisol (< 3 mcg/dL) at 8:00AM is diagnostic, especially if with a simultaneous elevation of plasma ACTH (usually >200 pg/mL). WBC count: moderate neutropenia, lymphocytosis and elevated eos. Treatment: Hydrocortisone is the primary glucocorticoid replacement therapy. Mineralcorticoid supplementation is usually indicated for adrenal insufficiency. 19
The patient will need to learn to give own maintenance injections, and will require double the amount of steroids during illness. Refer to endocrinologist for treatment.
(Fauci, 936)
E Incidental Adrenal masses termed incidentalomas are commonly found on

abdominal CT or MRI scans, 70-80% of which are non-functional. Plan: Determine the functional status by measurement of the plasma free metanephrines to screen for pheochromocytoma Refer to Endocrinology See algorithm (Fauci, 937)
E Pancreatitis Acute Pancreatitis (Chronic Pancreatitis not covered in this paper)

Majority of cases are related to: Biliary tract disease (a passed gallstone, usually < 5 mm diam) Heavy alcohol intake
thiazides, enalapril, methyldopa, sulindac, procainamide, glucocorticoids, and others) Vasculitis Infections (mumps, cytomegalovirus) Peritoneal dialysis CABG ERCP Ciliac disease 15-25% of cases are truly idiopathic; the incidence of acute pancreatitis has increased since 1990. May be absent bowel sounds if associated ileus Fever (38.4 39.0 C) Tachycardia Hypotension/shock Pallor and/or cool, clammy skin Mild jaundice May have abdominal mass due to inflamed pancreas or pseudocyst Acute kidney injury early in the course of acute pancreatitis
E Pancreatic Disorders E
Other possible causes can include: Hypercalcemia Hyperlipidemia Abdominal trauma Drugs (valproic acid, tetracyclines, estrogen, tamoxifen, sulfonamides, Other possible causes (contd): Signs and Symptoms: Epigastric/abdominal pain of abrupt onset Steady, boring and severe Pain worse w/ walking, lying Pain better w/ sitting, leaning forward Oftent with radiation to the back, or left/right Nausea/vomiting usually present Weakness, diaphoresis, anxiety if severe attack Upper abdominal tenderness. Often w/o guarding, rigidity or rebound May be distention Assess severity: Ransom criteria Table 16-8 McPhee, 686
20

Sequential Organ Failure Assessment (SOFA) to assess injury to other organs Acute Physiology And Chronic Health Evaluation (APACHE II) assesses BUN, mental status, systemic inflammatory response, identifying high-risk pts Lab/Imaging: Grossly elevated amylase & lipase BUN, alkaline phos may be elevated Leukocytosis Abnormal coagulation tests Proteinuria Elevated serum creatinine Granular casts Plain radiographs of the abdomen Glycosuria (U/S not as useful) Hyperglycemia Unenhanced CT if Dx not certain Elevated serum bilirubin Differential: Acutely perforated duodenal ulcer High intestinal obstruction Acute cholecystitis Gastroenteritis Acute intestinal obstruction Ectopic pregnancy Leaking Aortic Aneurism Administration of opioids Renal colic After abdominal surgery Acute mesenteric ischemia Serum Amylase may also be elevated in Complications: Intravascular volume depletion Pancreatic abscess Ileus Pseudocysts Acute tubular necrosis (without Pancreatic ascites overt shock) Hemorrhage Some require dialysis Permanent diabetes mellitus Necrotizing pancreatitis Exocrine pancreatic insufficiency Fever, leukocytosis, shock, Chronic pancreatitis multiple organ failure ARDS Treatment: Mild Disease: NPO (allows pancreas to rest) bed rest For Severe Disease: ICU admit NG at low intermittent suction
(McPhee, 687-88)
E Diabetes Mellitus E
Persons Affected: 15.7 million people (5.9 percent of the U.S. population). 6.3 million (18.4 percent ) of the elderly (65 and over). 8.2 percent of people 20 and over. 10.8 percent of non-Hispanic blacks, 10.6 percent of Mexican-Americans, and 9.0 percent of American Indians. From 1990 to 1998, diabetes increased by 70 percent for people ages 30 to 39, by 40 percent for people ages 40 to 49, and by 31 percent for people ages 50 to 59.
(National Guideline Clearinghouse)
21
E DM I - Diabetes Mellitus Type I is an immune-mediated disease in over 90% of

cases, and idiopathic in about 10%. (McPhee, 1140) DM-I is insulin deficiency accompanied by ketosis when untreated. Catabolism occurs when circulating insulin is virtually absent and plasma glucagon is elevated as the pancreatic B cells fail to respond to all insulinogenic stimuli. Exogenous insulin is therefore required to reverse the catabolic state, prevent ketosis, reduce the hyperglucagonemia, and reduce blood glucose. Signs and symptoms Polyuria and polydipsia result of osmotic diuresis, causing loss of glucose, free water and electrolytes. Thirst and blurred vision result from the hyperosmolar state. Weight loss and weakness in the presence of polyphagia due to depletion of water, glycogen and triglycerides, causing reduced muscle mass as amino acids are diverted to form glucose and ketone bodies. Lowered plasma volume produces hypotension, while potassium losses and catabolism of muscle contribute to weakness. Parasthesias may present at diagnosis. These generally clear as insulin replacement restores glycemic levels. Treatment includes Insulin is required - absence of Beta cell function. Oral agents and incretins are ineffective. 1-2X daily insulin regimens are usually ineffective. At least 4 measurements of glucose and 4 insulin injections are necessary daily for tight control. A combination therapy of long-acting and short-acting insulin, so that there are not hyperglycemic episodes between treatments. Some may qualify for continuous glucose monitoring devices or insulin pumps In general 0.5-1.0 U/kg per day will be required, divided into multiple doses (Fauci, 944) Exercise is not safe when insulin is not available in the system. See Diagnostics, glucose monitoring, insulin, teaching, and clinical monitoring after DM II below.
(McPhee, 1140-1164)
E DM II
Over 90% of Diabetic patients in the U. S. have Diabetes Mellitus Type II. DM-II occurs predominantly in adults, but because of the obesity epidemic, there are an increasing number of children being diagnosed. (McPhee, 1142) DM-II is characterized by variable degrees of insulin resistance, impaired insulin secretion, and excessive hepatic glucose production. Glucose tolerance and DM increase in prevalence with age. Obesity is the greatest contributor to insulin resistance. (Fauci, 942) In 2002, ages 65+ prevalence was >16% while patients under 45 were at 1.2% 22
20 million people in the U.S. have prediabetes & most will be diabetic in 10 years DM in the >65 category is projected to increase by 56% between 2002 and 2020
(Ham, p 484-85)
Signs and Symptoms: Often can be asymptomatic years, and may be discovered on routine screening. Increased infections: Yeast and/or Skin Weight gain Retinopathy
Polyuria or enuresis Polyphagia Peripheral neuropathy Autonomic neuropathy Microalbuminemia
Clinical practice guidelines: A. Testing for Diabetes in Asymptomatic Patients Testing to detect type 2 diabetes and assess risk for future diabetes in asymptomatic people should be considered in adults of any age who are overweight or obese (body mass index [BMI] 25 kg/m2) and who have 1+ additional risk factors for diabetes. In those without these risk factors, testing should begin at age 45 years. If tests are normal, repeat testing carried out at least at 3-year intervals is reasonable. To test for diabetes or to assess risk of future diabetes, A1C, fasting plasma glucose (FPG), or 2-h 75-g oral glucose tolerance test (OGTT) is appropriate. In those identified with increased risk for future diabetes, identify and, if appropriate, treat other cardiovascular disease (CVD) risk factors.
B. Screening children and adolescents for DM II in primary care Children and adolescents in the population under consideration who are overweight and have any two other risk factors should be screened every three years for diabetes. Overweight is defined as body mass index (BMI) 85th percentile for age and gender using the 2000 CDC growth charts; weight for height >85th percentile, or weight >120% of ideal weight for height. Overweight plus any two of the following risk factors: 1st degree and/or 2nd degree relative with diabetes Race/ethnicity (Native American, African American, Latino, Asian, Pacific Islander, Native Alaskan) Signs of insulin resistance or conditions associated with insulin resistance: Acanthosis nigricans Hypertension Dyslipidemia Polycystic ovarian syndrome Maternal history of diabetes or gestational diabetes during the child's gestation
C. Medical Guidelines for Clinical Practice for Developing a DM comprehensive Care Plan Diagnosis Target children, adolescents, & adults with or at risk of developing DM 1. Elevated Glucose any of the following a. A1C 6.5% 23
b. Fasting Glucose 126 mg/dl (7.0 mmol/l) c. 2-h plasma glucose 200 mg/dl (11.1 mmol/l) during an oral glucose d. In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis:
tolerance test (OGTT): glucose load of 75 g glucose dissolved in water. a random plasma glucose 200 mg/dl (11.1 mmol/l).
(American Diabetes Asso)
2. Differentiate between Type I and Type II a. Based on clinical features and presence of ketonuria with glycosuria b. Measure ICA, GAD65, IAA, and ICA 512 antibodies if uncertain 3. Baseline Electrocardiogram (EKG) 4. Baseline Comprehensive Metabolic Profile (CMP) check kidney & liver function 5. Assessment and documentation of a. Family history and age of onset of any diabetic condition b. Include information about obesity and if insulin was required c. Cardiac risk factors including family history d. Smoking history e. Presence of hypertension, hyperlipidemia (including family history) and/or oral contraceptive use (McPhee, 1169) Screening/Prevention for pre-diabetes/impaired GT 1. Patients with Impaired Glucose Tolerance, Increased Fasting Glucose, or an A1C of 5.76.4% should be referred to an effective ongoing support program for weight loss of 510% of body weight and increase in physical activity to at least 150 min/week of moderate activity. 2. Follow-up counseling 3. In addition to lifestyle counseling, metformin may be considered 4. Monitoring for the development of diabetes in those with pre-diabetes should be performed every year. 5. Screening for depression Treatment/Management 1. Comprehensive treatment program 2. Multidisciplinary team approach 3. Patient self-management education (DSME) 4. Glucose monitoring - individualized 5. Goal of a HgbA1C at < 7.0% per ADA. American Association of Clinical endocrinologists recommends goal of 6.5% (Therapeutic Research Center) 6. Glucose control Hgb A1C monitoring (2-4 X annually). Every 6 mo if wellcontrolled (< 7.0), or every 3 mo if poorly controlled 7. Glucagon prescribed for all patients who have a risk of severe hypoglycemia 8. Fasting Lipid Profile and serum Creatinine (every 6mo) If on a lipid-lowering medication, such as a statin, monitor LFTs (liver enzymes) q6m 9. Influenza and pneumococcal immunizations 10. Pharmacotherapy (insulin, metformin, thiazolidinediones [TZD], sulfonylureas, pramlintide) 11. For those with BMI > 35 kg/m2, consider bariatric surgery 12. 150 min/wk moderate-intensity aerobic activity to 50-70% max HR based on age 24
13. PsychoSocial assessment and care 14. Screen & treat neuropathies (annual foot inspection, exercise, balance training, orthotics, tricyclic antidepressants, anticonvulsants, serotonin and norepinephrine reuptake inhibitors) Foot exam education Hx of foot ulcer or amputation multidisciplinary approach 15. Influenza and pneumococcal immunizations 16. Serum creatinine and estimated glomerular filtration rate (eGFR) 17. Retinal examination and treatment of retinopathy 90% prevalence within 10 yr. 18. Screen for nephropathy with a urine Microalbumin (annual) 19. Modification of cardiovascular risk factors Blood pressure control (Dietary Approaches to Stop Hypertension [DASH] diet, angiotensin-converting enzyme [ACE] inhibitors, angiotensin receptor blockers [ARBs], beta-blockers, calcium channel blockers). Blood pressure measurement (quarterly) GOAL: < 130/80 if no protenuria; < 125/75 if proteinuria If ACE-I, ARB, and/or diuretics used, monitor kidney function and K+ Note: ACE-I and ARBs are contraindicated in pregnancy Dyslipidemia control (statins, bile acid sequestrants, niacin and/or cholesterol absorption inhibitors) Assess FLP annually, unless low risk values are noted (then q 2 yr) Dietary saturated fat intake of <7% of total calories Reduce Trans fat intake Fasting Lipid Profile and serum Creatinine (q 6 m) If on a lipid-lowering medication, such as a statin, monitor LFTs q 6 m Screen for PAD: hx of claudication Consider ABI testing even if asymptomatic Smoking cessation education/counseling and support Consider anti-platelet therapy aspirin 75-162 mg/d Therapeutic lifestyle changes (medical nutrition therapy, regular exercise) Treat (+) microabluminuria by improving glucose, lipid control and adding an ACE-I or ARB (ACE-I only, per McPhee, p 1169) Asymptomatic coronary artery disease (measure coronary artery calcification, coronary imaging) Assessment for sleep related problem (obstructive sleep apnea, restless leg)
(American Diabetic Asso., Fauci, 946; National Guideline Clearinghouse)
Patients with DM-II may be managed with diet modifications and exercise alone, or in conjunction with oral glucose lowering agents, insulin, or a combination of oral agents and insulin. See oral agents and insulin products/classifications below.
*** Preferred Initial therapy for new diagnosis is Metformin because of its
efficacy (1-2% lowering of HgbA1C), known side effect profile, and low cost. It also:
Promotes mild weight loss Lowers insulin levels Improves FLP slightly Renal insufficiency Does not cause hypoglycemia as a monotherapy CHF Acidosis
Contraindications of Metformin are:
25
Liver disease or chronic ETOH If receiving XRay contrast Hypoxia Metformin should be stopped on the day of testing with a radiocontrast agent, and restarted 48 hours after testing is completed - nephrotoxic combo
(Fauci, 944; McCance, 1155; Therapeutic research Center)
Oral & Incretin Glucose Lowering Agents for DM II

Agent Biguinide Metformin/Glucophage *** Sulfonylureas Glimepiride Giipizide Glipizide (extended release) Glyburide Glyburide (micronized) Non-sulfonylurea Repaglinide Netaglenide Alpha-Glucosidase inhibitor Acarbose Miglitol Thiazolidinedione Rosiglitazone Pioglitazome GLP-1 Receptor Agonists ** Byetta exenatide SubQ ** Victoza liraglutide SubQ DPP IV inhibitor Sitagliptin 0.5-16 180-360 1-4 1-3 Daily dose, mg Doses/day Contraindications Cr > 1.5 men, or > 1.4 women, liver disease, CHF, IV contrast
500-2500
1-3 Renal/liver disease
1-8 2.5-40 5-10 1.25-20 0.75-12
1 1-2 1 1-2 1-2 Renal/liver disease
25-300 25-300
1-3 1-3 Liver disease/CHF
2-8 15-45 5-10mcg 0.6-1.2mg 100
1-2 1 Pancreatitis 2 1 1 Medulary Thyroid Cancer in pt or family low dose w/ renal failure (Fauci, 944)
Biguinides & Thiazolidinediones Lowers glucose by acting on liver, muscle, & adipose. Sulfonylureas and Non-sulfonylureas Stimulates insulin secretion by binding with the sulfonylurea receptor on the Beta cell in the pancreas. Alpha Glucosidase inhibitors Affects the absorption of glucose in the gut, delaying the absorption of carbohydrates and lowering postprandial glycemic excursion. Incretins (GLP-1 preparations are injectables) ** GLP-1 Receptor agonists prolongs the action of endogenously released GLP-1 (in the gut), stimulating insulin secretion, lowering glucose levels. Suppresses glucagon release by the pancreas and it has a lower risk of hypoglycemia than sulfonylureas.
26
DDP-IV inhibitors prolongs the action of endogenously released GLP-1 and GLP (in the gut), stimulating insulin secretion, lowering glucose levels. (McPhee, 1152-59) At the point where combination oral therapy is inadequate (HgbA1C running > 6.9), insulin is often started, particularly if the patients lifestyle modifications of diet and exercise are ineffective. Incretin Mimetics are a good option to investigate for DM-II before moving into insulin therapy. Byetta or Victoza are both supplied in pen/injectable form. Its contraindicated if there is a history of medullary thyroid carcinoma (pt or family) with pancreatic, gastroparesis, or renal insufficiency. Caution should be used in concurrent use of ACE-I. Glargine/Lantus insulin is a good starting point, since it has no peak activity and there is less possibility of hypoglycemia during the nighttime hours. (McPhee, 1161)
Pharmacokinetics of insulin preparations

Preparation Short-acting subq Lispro Aspart Glulsine Regular Intermediate-acting subq NPH Long-acting subq Detemir Glargine Insulin combinations - subq
75/25 - 75% protamine lispro, 25% lispro 70/30 - 70% protamine lispro, 30% aspart 50/50 - 50% protamine lispro, 50% lispro 70/30 - 70% NPH, 30% reg 50/50 - 50% NPH, 50% reg
Onset, in hrs < 0.25 < 0.25 < 0.25 0.5-1.0 1-4 1-4 1-4 Onset, In hrs
< 0.25 < 0.25 < 0.25 0.5-1.0 0.5-1.0 1.5 1.5 1.5 Dual Dual
Peak, in hrs 0.5-1.5 0.5-1.5 0.5-1.5 2-3 6-10 NA NA Peak, In hrs 3-4 3-4 3-4 4-6
Duration, in hrs
10-16 12-20 24 Duration, In hrs

Up to 10-16 Up to 10-16 Up to 10-16 10-16 10-16
(Fauci, 945)
When/How to start insulin in DM II: After lifestyle modification and other antihyperglycemic agents have failed. Insulin is considered after failed control of Hgb A1C < 7.0 with two oral agents. Adding a third agent is usually less effective, more expensive, and less tolerated than adding insulin. Start low and titrate steadily. Start at 0.15 0.2 units/kg body weight, long-acting insulin such as NPH or glargine (Lantus). 10 units q HS is typical . Increases (or decreases) are generally in 2 unit increments q 3 d with the goal FBS of 80-109 mg/dL If fasting glucose is > 180mg/dL, dose can be increased by 4 units q 3 d An oral agent may be continued if it remains effective. Short-acting insulin can be added at AC/meal-time, if Hgb A1C still > 7%. Have patient monitor glucose pre-breakfast and/or pre-dinner and record; report the results to the healthcare practitioner. 27
Office Visits: Adjust insulin weekly according to glucose levels until stable. Higher insulin doses are generally needed for DM II because of insulin resistance. See more at http://clinical.diabetesjournals.org/content/23/2/78.full See endocrinology consensus statement at http://www.aace.com/files/GlycemicControlAlgorithm.pdf
(Therapeutic Research Center)
Estimated Average Glucose based on Hgb A1C

A1C (%)
5 6 7 8 9 10 11 12
Est. Average Glucose (mg/dL)

97 126 154 183 212 240 269 298
For both DM-I and DM-II

Switching insulins: Prescribers newsletter http://www.albany.edu/sph/coned/sta/attachment_7.pdf Patient teaching Comprehensive initially, and then annually: Self-monitoring and treatment of the disease patient-focused goals Glucose monitoring at home + documentation Insulin replacement, or in DM-II, incretins and/or oral drugs that lower glucose levels if glucose levels can be maintained with oral meds. Medical nutrition therapy (annually) Proper diet balance high in a variety of vegetables and fiber with limited fats, sugar, sodium and simple carbohydrates. www.choosemyplate.gov If on insulin, carbohydrate counting - insulin bolus for each meal based on carbs. Limit protein intake if nephropathy to 0.8 g/kg body wgt. Daily Lipid management (McPhee, 1169) Exercise for improved metabolism (keep glucose available for hypoglycemia) Weight loss generally not needed in DM-I, but essential in DM-II for appropriate glycemic control. Foot care (proper shoes + daily examination) and dental care Eye exams, including dilated exam, (annually) Diabetic cataracts depends on duration and severity of hyperglycemia Diabetic retinopathy DM-I prevalence at 15 years with disease: 75-95% DM-II prevalence at 16 years with disease: 60% Diabetic glaucoma occurs in ~6% of persons with diabetes Prevention of infections Quit smoking 28
Blood pressure management (Ham, 490, Fauci, 1120) Routine office visits every 3 months during difficult control events and a minimum of every 6 months if well controlled. (McPhee, 1164) Complications of diabetes include: Ocular complications Diabetic Nephropathy Diabetic Neuropathy Poor wound healing Cardiovascular: CAD, PVD (McPhee, 1173)
Hospitalized patients due to changes in diet, stress, procedures, and other factors: Discontinue all oral glucose lowering medications Sliding scale regimen implemented on a QID AC/HS schedule, or continuous infusion of regular insulin A continuous infusion of 5% Dextrose should be administered when pt is NPO
E Dyslipidemias
(Fauci, 946-47; McPhee, 1173)
Can occur as a result of the following endocrine abnormalities: Hypothyroidism Diabetes Mellitus Glycogen storage abnormalities Pancreatic dysfunction Obesity Metabolic Syndrome Stress (Wilson, 2008) Correct underlying pathology and manage lipid levels See the guidelines for lipid management at: http://www.guideline.gov/content.aspx?id=24712&search=hypothyroidism Also see synthesis project for Cardiovascular disease by Kelli
E Metabolic Bone Disease Condition of decreased bone density E Osteoporosis Both bone matrix and mineral decreased
Fracture risk increased in spine, hip, pelvis and wrist from demineralization Serum PTH, calcium, phosphorus and alkaline phosphorus usually normal Serum 25-hydroxyvitamin D levels often low as a co-morbid condition Osteoporosis causes 1.5 million fractures annually in the U. S. Women more frequently affected than men due to postmenopausal osteoporosis Bone formation is often normal, but bone reabsorption is increase Estrogen deficiency (women) 29
Hormonal causes of osteoporosis:
The Endocrine System FNP IV - N 477 Androgen deficiency (men) Hormone excesses: Cushings syndrome Artificial corticosteroid admin Thyrotoxicosis Hyperparathyroidism Uncontrolled Diabetes Other medication causes: Excessive Vitamin D or A Heparin therapy SSRIs Rosiglitizone Genetic disorders: Type I collagen mutations
Ann Sparks Dr. Denise Wilson Idiopathic osteoporosis Marfan Syndrome Miscellaneous Causes: Celiac Disease Anorexia Nervosa Chronic hyponatremia Protein-calorie malnutrition Vitamin C deficiency Copper deficiency Liver disease Rheumatoid arthritis Immobilization Tobacco use Alcoholism Malignancy (esp. Multiple Myeloma)
Osteogenesis Imperfecta Symptoms: Asymptomatic until a fracture occurs. May have a backache or loss of height Laboratory findings: Serum calcium, phosphate, PTH normal Alkaline Phosphatase usually normal, but may be elevated following a fracture Vitamin D deficiency is common Serum hydroxyvitamin D to be evaluated on all who have low bone density < 20 ng/dL is frank deficiency; 20 30 ng/dL is moderate deficiency Testing for thyrotoxicosis, hypogonadism and celiac disease may be indicated Bone densitometry: DXA determines bone density of the lumbar spine and hip T Score results: per World Health Organization T score >/= -1.0 is normal T score 1.0 to 2.5 is osteopenia (low bone density) T score < - 2.5 is osteoporosis T score < - 2.5 with fracture is severe osteoporosis DXA recommended in postmenopausal women: q 5 yr for T score 1.0 to 1.5 q 3-5 years for T score 1.5 to 2.0 q 1-2 years for T score < - 2.0 Quantitative CT: more accurate in cases of arthritis and very tall or very short patients Differential: Osteopenia can be caused by osteomalacia (demineralization alone) or neoplasm such as myeloma or metastatic bone disease. Treatment: Calcium + Vitamin D: Calcium citrate (0.4 0.7 g elemental Ca+/d) or Calcium carbonate (1 1.5 g elemental Ca+/d) 30
Biophosphonates inhibits osteoclast bone-reabsorption Take in AM at least 40 minutes before food and remain upright Estrogen replacement therapy (ERT) if osteoporosis has occurred, ERT not effective. Selective estrogen modulators Teriparatide PTH analog Calcitonin
E Disorders of Male Reproduction E E Androgen Deficiency

Primary hypogonadism Testicular failure o Testosterone level low (AM level < 6.93 nmol/L [< 200 ng/dL]) o Gonadotropin levels high (LH and FSH) o Klinefelters Syndrome most common cause (extra X chromosomes) o Also caused by systemic disease, trauma or drugs/toxins causing testicular failure Secondary hypogonadism hypothalamic-pituitary defects o Testosterone level low o Gonadotropin levels also low Symptoms: Testicular abnormalities: Normal gonads during childhood, but during puberty they remain small or decrease in size during aging. In Klinefelters Syndrome, they are fibrous, firm and non-tender to palpation. Gynecomastia and decreased body hair. Decreased androgen-dependent events such as morning erections, sexual thoughts, and erections. Ennuchoidal proportions: arm span >2cm greater than height can occur prior to epiphyseal fusion. Treatment: Androgen replacement testosterone Daily transdermal patches (5-10 mg/d) or gel (50-100 mg/d), or Parenteral long-acting testosterone ester (100-200 mg testosterone enanthate at 1- to 3-week intervals) Contraindications of testosterone treatment: Class IV CHF, prostate CA, severe sleep apnea, severe lower urinary tract obstruction.
(Fauci, 947-48; McCance, 1123-24)
E Male infertility 25% of infertile couples are Male infertility related E Erectile Dysfunction the failure to achieve an erection, or failure to ejaculate,
or both. Affects 10-25% of middle-aged and elderly men. Failure to initiate (psychogenic, endocrinologic, or neurologic) Failure to fill (arteriogenic) 31
Failure to store adequate blood volume within the lacunar network (venoocclusive dysfunction) o Diabetic, atherosclerotic and drug-related causes account for >80% of causes of ED on older men. o Thiazide diuretics and beta-blockers are the most frequently implicated. Anti-depressant and anti-psychotic medications can cause problems. o Recreational drugs and disorders that affect the sacral spinal cord or the autonomic fibers to the penis may lead to ED
E Disorders of Female Reproduction E

See Womens Health synthesis project by Ashley, Alyssa and Nelle Additional Resources: Online journal: Endocrinology by The Endocrine Society. Found at http://endo.endojournals.org/site/collections
Sample Questions for the Endocrine System 1. Which of the following is most consistent with subclinical hypothyroidism? A. Elevated free thyroxine (T4) and thyroid-stimulating hormone (TSH) levels B. Normal free T4 and elevated TSH levels C. Elevated TSH and low free T4 levels 32
The Endocrine System FNP IV - N 477 D. Low TSH and free T4 levels

(Fitzgerald [2010], 237)
2. A fixed, painless thyroid mass accompanied by hoarseness and dysphagia should raise suspicion of 1. 2. 3. 4. Autonomously functioning adenoma Graves disease Hashimoto disease Thyroid malignancy
3. How do you know if a pediatric patient is most likely to be diagnosed with DM I rather than DM II? A. The blood glucose levels will run higher than in DM II. B. Metformin will be effective in controlling the patients HgbA1C. C. There will be a short history of significant symptoms including recent unexplained weight loss, ketonuria, and the classic polys of polydipsia, polyphagia, and polyuria. D. The HgbA1C will be 6.2%. E. The patient has a BMI of 43.2 (Fitzgerald [2011], 113) 4. For a 56 year-old male patient, you are adjusting the insulin because the AM fasting level is running too high, though the other blood sugars throughout the day are remaining mostly under 150. As you increase the HS NPH dose, you are NOT seeing an adequate response to an increase of NPH insulin at bedtime. What is could be the problem? A. The patient is having a bedtime snack that has too many calories and is too late in the evening. B. The patient is not taking the NPH insulin correctly. C. The patient could be having the Somogyi effect and actually be hypoglycemic during the night, and rebounding with hyperglycemia in the morning. D. All of the above. E. None of the above. (Fitzgerald [2010], 217)
5. Your 47 year-old female patient with Diabetes Type II has been well controlled on Metformin 500mg PO BID. She goes into the hospital for a cholecystectomy. What would you expect the treatment plan to include? A. Continued Metformin 500mg PO BID until she has to be NPO for surgery at midnight. Then resumption of the same dosage the following day after surgery when her 1800 kcal diet is resumed by advance diet as tolerated. B. Metformin discontinued and initiation of Glucotrol. C. Discontinuation of the Metformin and placed on a sliding scale regular insulin AC and HS (QID) for the hospital stay. D. None of the above. (Fauci, 947; Fitzgerald [2010], 217) 33
The Endocrine System FNP IV - N 477 6. Intervention in microalbuminuria for a person with DM includes
A. Improved glycemic control. B. Strict dyslipidemia control. C. Use of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. D. all of the above. (Fitzgerald [2010], 217) 7. Which of the following should be periodically monitored with the use of a biguanide? A. B. C. D. Creatine kinase (CK) Alkaline phosphatase (ALP) Alanine aminotransferase (ALT) Creatinine (Cr)
8. Osteoporosis is more common in individuals A. With Diabetes Type II B. On long-term systemic corticosteroid therapy C. Who are obese D. Of African ancestry
9. All of the following are common causes of secondary hypertriglyceridemia except: A. ACE inhibitor use B. Hypothyroidism C. Poorly controlled DM D. Excessive alcohol use
10. Untreated hypothyroidism can result in which of the following changes in the lipid profile? A. Increased HDL and decreased triglycerides B. Increased LDL and total cholesterol C. Increased LDL , total cholesterol and triglycerides D. Decreased LDL and HDL
_______________________________________________
Answer key: 1. B Subclinical hypothyroidism is diagnosed based on the presence of an elevated TSH level and normal free T4 level in the absence of or with minimal symptoms. An estimated 1% - 10% of the overall population to 20% in women 60 years and older. In men 74 years and older the prevalence has been reported as more than 15%. (Fitzgerald [2010], 239-41) 34
2. D A fixed mass is a red flag sign, along with dysphonia and dysphagia, that this could be a malignancy. Graves disease (thyrotoxicosis) is a type of hyperthyroidism with thyroid enlargement, exopthalmos, nervousness and heat intolerance. Hashimoto disease is an autoimmune disorder of the thyroid most often accompanied by a goiter. The risk of a thyroid nodule being malignant is about 5%. (Fitzgerald [2010], 239-41) 3. C DM-I is an autoimmune process involving beta cell destruction resulting in insulin deficiency. The onset is generally accompanied by hallmark symptoms of polys. Whereas DM-II is often symptom-free, diagnosed through routine screening that begins with insulin resistance. Oral agents are effective until insulin resistance occurs. (Fitzgerald [2011], 113) 4. D All of these answers are a possibility, but Somogyi effect can be overlooked and the insulin increased. This can be quite detrimental, because actually the problem is hypoglycemia during the night, with resulting secretion of glucagon and cortisol, driving the blood sugar into hyperglycemia by morning.
5. C Current recommendations are totally discontinuing Metformin during hospitalizations because of 1) the stress response of illness, 2) possible interactions with contrast media during testing, and 3) the risk of lactic acidosis in perioperative periods. (Fauci, 947; Fitzgerald [2010], 217) 6. D Microalbuminuria is considered a predictor of glomerular dysfunction associated with diabetic nephropathy. The condition can actually precede development of DM by 10 years. Tight glycemic and lipid controls, as well as management of the blood pressure <130/80 mm/Hg, is necessary to reduce further nephropathy. (Fitzgerald [2010], 220) 7. D Excreted by the kidney, metformin can become nephrotoxic, particularly with contrast media, causing the creatinine to become elevated. Metformin is contraindicated in a creatinine level equal to or greater than 1.4 mg/dL
(Chisholm-Burns, 656)
8. B Glucocorticoids play a significant role in bone remodeling. Bone formation is reduced through inhibition of osteoblasts. Patients receiving long-term glucocorticoids are at increased risk of fracture. (Chisholm-Burns, 864) 9. A ACE inhibitors do not contribute to high triglycerides. There is an excellent chart in McPhee. (McPhee, 1192) 35
10. C Screening for hypothyroidism in patients with hyperlipidemia is appropriate. Lab abnormalities with hypothyrodism often include increased LDL, total cholesterol and triglycerides. (McPhee, pps 1063, 1192)
REFERENCES American Association of Clinical Endocrinologists. (2009). AACE/ACE Consensus statement. Type 2 diabetes: Algorithm for glycemic control. Endocrine Practice. 15(6). Retrieved from http://www.aace.com/files/GlycemicControlAlgorithm.pdf 36
American Diabetes Association. (2010). Executive Summary: Standards of medical care in diabetes 2010. Diabetes Care. Jan 2010, 33(1). Retrieved from http://care.diabetesjournals.org/content/33/Supplement_1/S4.full Bickley, L.S. (2009). Bates guide to physical examination and history taking (10th ed.). South Asian Edition: New Dheli: Lippincott. Chisholm-Burns, M. A., Schwinghammer, T. L., Wells, B. G., Malone, P. M., Kolesar, J. M., & DiPiro, J. T. (2008). Pharmacotherapy: principles and practice. New York: McGraw-Hill. Epocrites.com PDA application (Program updated on April 1, 2012). Fauci, A. S., Braunwald, E., Kasper, D. L., Hauser, S. L., Longo, D. L., Jameson, J. L., & Loscalzo, J. (2009). Harrison's manual of medicine (17th ed.). New York: McGraw-Hill. Fitzgerald, M. A. (2010). Nurse Practitioner certification exam and practice preparation. (3rd Ed.). Philadelphia: F. A. Davis. Fitzgerald, M. A. (2011). Nurse Practitioner Certification Exam Review & advanced practice update. North Andover, MA: Fitzgerald Health Education Associates, Inc. Gutierrez, K. (2008). Pharmacotherapeutics: Clinical reasoning in Primary Care. St. Louis: Saunders. Ham, R. J., Sloane, P. D., Warshaw, G. A., Bernard, M. A., & Flaherty, E. (2007). Primary care geriatrics: A case-based approach (5th Ed.). Philadelphia: Elsevier Mosby. Hahn, R. K., Albert, L. J., & Reist, C. (2011). Psychiatry on call. Current Clinical Strategies. Kemmann, E. & Jones, J. R. (1983). Hyperprolactinemia and headaches. American Journal of Obstetrics and Gynecology. Mar 15; 145(6): 668-71. 37
Macchi M. & Bruce J. (2004). Human pineal physiology and functional significance of melatonin. Front Neuroendocrinol. 25(34): 17795. McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biologic basis for disease in adults and children (5th Ed.). St. Louis: Elsevier-Mosby. McCarty, C. R. & Stukenborg, G. J. (2008). Decision Analysis of Discordant Thyroid Nodule Biopsy Guideline Criteria. Journal of Clinical Endocrinological Metabolism. 93(8): 3037-3044. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2515085/ McPhee, S.J., & Papadakis, M.A. (2011). 2010 Current medical diagnosis & treatment (50th Ed.). New York: Lange Medical Books/McGraw-Hill. Medicalook (2012). Retrieved from http://www.medicalook.com/Hair_loss/Hirsutism.html Medscape News. (2009) Retrieved from http://www.medscape.com/viewarticle/717168_3 Merck Manual Online. Retrieved from http://www.merckmanuals.com/professional/lexicomp/prednisone.html National Guideline Clearinghouse. Standards of medical care in diabetes. II. Testing for diabetes in asymptomatic patients. Retrieved from http://www.guideline.gov/content.aspx?id=25328 National Guideline Clearinghouse. Clinical practice guideline: screening children and adolescents for type 2 diabetes mellitus in primary care. Retrieved from http://www.guideline.gov/content.aspx?id=3404 National Guideline Clearinghouse. American Association of Clinical Endocrinologists 38
medical guidelines for clinical practice for developing a diabetes mellitus comprehensive care plan. Retrieved from http://www.guideline.gov/content.aspx?id=34038 Agency for Healthcare Research and Quality. Improving care for diabetes patients through intensive therapy and a team approach. Retrieved from http://www.ahrq.gov/research/diabria/diabetes.htm Wikipedia (2012). Retrieved from http://en.wikipedia.org/wiki/Pituitary_tumor_apoplexy Wilson, D. D. (2008). McGraw-Hill's manual of laboratory & diagnostic tests. New York: McGraw-Hill. Wilson, D. D. (2011). Family Nurse Practitioner III N475 lecture. Normal, IL: Illinois State University. Therapeutic Research Center. (2008). Insulin use in patients with type 2 diabetes. Pharmacists Letter/Prescribers Letter 2008; 24(11): 241120. U. S. Department of Health and Human Services National Diabetes Education Program. Guiding principles for diabetes care: for health care professionals. (2009). U. S. Preventative Services Task Force. Screening for congenital hypothyroidism. Retrieved from http://www.uspreventiveservicestaskforce.org/uspstf08/conhypo/conhyprs.htm#s ummary U. S. Preventative Services Task Force. Screening for thyroid disease. Retrieved from http://www.uspreventiveservicestaskforce.org/3rduspstf/thyroid/thyrrs.htm
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ENDOCRINE SYSTEM Overview

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The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

Endocrine Anatomy & Physiology Overview

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

Hormone Transportation & Cellular Effects based on Hormone Structure

LIPID SOLUBLE Steroids (cholesterol is a precursor for all steroids)

Derivatives of arachidonic acid (autocrine or paracrine action)

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

In the CHEST: In the ABDOMEN:

In the PELVIS/Perineum: Ovaries/Testes

Target Organ Effects

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

* Significant in steroid level/control

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

Endocrine REVIEW OF SYSTEMS

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

E Disorders of the Anterior Pituitary and Hypothalamus E

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

E Pituitary Hormone Hypersecretion Syndromes

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

Diagnosis = failure of GH suppression test Refer to endocrinology (Fauci, 919-21)

E Diabetes Insipidus (DI): Too little ADH (i.e.: Vasopressin or AVP)

E SIADH (Syndrome of Inappropriate Antidiuretic Hormone): Too much ADH

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

E Thyroid Gland disorders E

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

Ann Sparks Dr. Denise Wilson

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

E Thyroid Neoplasms nodule may be benign 90%, or malignant 10%

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

E Aldosteronism Hypersecretion of the adrenal mineralcorticoid, aldosterone.

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

E Syndromes of Adrenal Androgen excess in women

HYPOfunction of the Adrenal gland E Addisons Disease or Adrenocortical insufficiency

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

E Incidental Adrenal masses termed incidentalomas are commonly found on

E Pancreatitis Acute Pancreatitis (Chronic Pancreatitis not covered in this paper)

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson

The Endocrine System FNP IV - N 477

Ann Sparks Dr. Denise Wilson