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Endocrine

Week 7

TermDefinition
Anterior pituitary hormones ACTH (corticosteroid synthesis), GH (somatotropin: growth, carbs, protein, fat metabolism), FSH (ovarian maturation), LH (ovulation, testosterone production), Prolactin (milk production), TSH (stimulates T3 and T4)
Hypopituitarism (pituitary gland) patho Hyposecretion of anterior pituitary hormones disrupts hormone release from adrenal cortex, thyroid, and gonads (affects widespread body functions)
Hypopituitarism causes rare disorder (gradual onset), tumor or hypothalamic damage, increased ICP (head trauma, CNS infection, brain tumor), postpartum hemorrhage
Hypopituitarism symptoms weakness, fatigue, decreased appetite, weight loss, sensitivity to cold, swollen facial features / body
ACTH Deficiency (Hypopituitarism ) leads to decreased glucocorticoids and mineralocorticoids , leading to decreased aldosterone and loss of sodium/water in the kidneys. LEADS TO CIRCULATORY COLLAPSE FROM SEVERE HYPOTENSION
TSH deficiency (Hypopituitarism) results in severe decrease in metabolism, affecting all body functions and impairs med metabolism
Management of Hypopituitarism fluid replacement, manage osteoporosis (vit D / calcium). Restore hormones to normal levels (take HRT in morning to mimic normal daily hormone release)
Hyperpituitarism patho Hormone production/hypersecretion of anterior pituitary hormones causes dysfunction
Manifestations of Hyperpituitarism elevated TSH: increased metabolic rate, weight loss, exophthalmos. Gonadotropins: altered sexual and reproductive function. Prolactin: hypogonadism, galactorrhea, increased body fat
Hyperpituitarism diagnosis hormone levels, electrolytes, CT/MRI (for suspected tumor)
Hyperpituitarism management strict IandO, check electrolytes, treat symptoms (hyperglycemia, HTN), decrease secretion of hormones (dopamine agonists), somatostatin analogs inhibit release of GH . Surgery: transsphenoidal hypophysectomy/adenectomy
Post op management of Hyperpituitarism surgery Monitor for ICP, CSF leak, diabetes insipidus, meningitis; LOOSE MUSTACHE DRESSING. No nose blowing 2-4weeks, sneeze with mouth open, no straws, no heavy lifting/bending, no vigorous exercise, no swimming/flying
Antidiuretic hormone (Vasopressin) made in hypothalamus and stored/released by posterior pituitary gland. Can cause DI or SIADH
Diabetes Insipidus patho Deficiency of ADH; results in large volumes of very dilute urine (polyuria).
SIADH patho too much ADH; increased water reabsorption which leads to increased intravascular volume and hyponatremia due to dilution
Central DI most common type of DI; problem with synthesis, transport or release of ADH. Causes include a brain tumor, brain surgery, head trauma, infections of CNS
Nephrogenic DI kidneys do not respond to ADH commonly due to nephrotoxic meds, hypercalcemia, renal disease
Dipsogenic DI thirst mechanism dysfunction due to damage to hypothalamus or pituitary. Not related to abnormal levels of ADH aka primary DI
Gestational DI enzymes from placenta interfere with kidney's ability to process ADH and is usually temporary. Reverses after pregnancy is over
SIADH causes Small cell carcinoma (lung), CNS disorders such as head injury, stroke, infection; meds (chemo, NSAIDs, psychotropics), COPD positive pressure ventilation
Symptoms of DI Polyuria (4 to 20 liters a day), dilute urine, polydipsia (excessive thirst), dehydration (tachycardia, hypotension, shock), hyponatremia, irritability, confusion, decreased LOC, coma. High sodium/hematocrit
symptoms of SIADH low urine output, concentrated/dark urine, edema, weight gain, pulmonary edema (dyspnea, increased WOB), N/V, muscle cramping and twitching, resp depression, lethargy, confusion, seizures, coma
Urine osmolality Number of dissolved particles per kg of water. Counts all solutes and is a direct indicator of the kidney's ability to concentrate / dilute urine (range is 300-900)
Urine specific gravity Density or weight of urine compared to pure water. Reflects total solute concentration plus the size/weight of the solutes (1.010 - 1.030 range)
DI Diagnosis serum and urine electrolytes, serum and urine osmolality, urine specific gravity (less than 1.005), CT/MRI of head, water deprivation test. HIGH AND DRY BLOOD AND LOW AND DILUTE URINE
Water deprivation test for DI assesses the kidney's ability to concentrate urine (differentiates central from nephrogenic DI). Strict NPO first, weight patient and monitor urine osmolality q1hr. Step 2 is desmopressin admin with increase in CDI with no increase seen with NDI
SIADH diagnosis serum and urine osmolality/electrolytes, hyponatremia, high ADH levels, scant/concentrated urine (diluted blood)
DI management IV fluids (based on sodium: dextrose 5% in water or 1/2 NS), do not rapidly overcorrect sodium. Desmopressin (synthetic analog of ADH given SQ, intranasal, PO), decreases Na
SIADH management Treat hyponatremia (severe gets 3% saline IV thru central line); fluid restriction, vasopressin receptor antagonists, diuretics, declomycin (increases water excretion), seizure precautions
Adrenal insufficiency Insufficiency of cortisol (regulates carb, fat, protein metabolism and suppresses immune and stress response), aldosterone (promotes sodium and water reabsorption, facilitates potassium excretion)
Primary adrenal insufficiency Addison's disease: adrenal cortex is damaged (usually due to autoimmune disease), other include TB/trauma, adrenalectomy, cancer, infection; must take hormones for life
Secondary adrenal insufficiency Occurs due to problems with pituitary gland. ACTH tells the adrenal cortex to release cortisol, can occur when chronic corticosteroids are stopped suddenly or due to a tumor/trauma to gland
Exogenous Corticosteroid Therapy Risks 2 week use: abrupt discontinuation may trigger acute adrenal crisis. 4-5 weeks: chronic corticosteroids creating negative feedback
Diagnosis of adrenal insufficiency Serum ACTH is less than 100 (primary), serum electrolytes: hyponatremia and hyperkalemia (from decreased aldosterone), morning serum cortisol, CRH stim test (tested at baseline and after synthetic admin), insulin tolerance, CT, MRI, labs
Adrenal insufficiency management VS, weight, I and O, stressors, heart monitor (hyperkalemia), safety, neuro checks, labs, cortisol replacement: hydrocortisone sodium succinate or dexamethasone
Complications of adrenal insufficiency Dehydration, hyponatremia, hyperkalemia, hypoglycemia, acute adrenal insufficiency (adrenal crisis - emergency)
Addisonian Crisis Severe hypoglycemia, electrolyte imbalances, weakness, severe headache/pain, confused irritable, hypotension, shock. Immediately stabilize with IV glucocorticoids, fluids, electrolytes, stress-free
Cushing's too much cortisol that can occur due to chronic corticosteroids, adrenal tumor or a non-pituitary ACTH secreting tumor
Cushing's s/s hyperglycemia, fluid retention, hypokalemia, abnormal fat distribution, decreased muscle mass, impaired immunity (destroys lymphocytes), thin arms/legs, truncal obesity, moon face, join pain, fragile skin, buffalo hump, depression, brain fog, ED
Diagnosis of cushing's serum electrolytes, cortisol urine test (24 hr urine), overnight dexamethasone suppression test (1 mg at 11 pm, labs at 8am), ACTH level, CT/MRI
Management of cushing's BP (HTN), skin assessment, fatigue, screen for depression, heart monitor, ongoing labs, bone scans, pain assessment
Cushing's complications osteoporosis / pathological fractures, acute adrenal crisis, hyperglycemia, GI bleeding, HTN, hypokalemia (life threatening dysrhythmias)
Treatment of Cushing's guided by cause; mifepristone (blocks effects of cortisol), pasireotide (inhibit ACTH secretion), osilodrostat (inhibit enzyme in cortisol synthesis), chemo/radiation, surgery, corticosteroids
Conn's syndrome patho primary aldosteronism with too much aldosterone released. Leads to sodium and water retention, HTN, hypokalemia, and usually due to an adenoma (non cancerous tumor)
Management of Conn's sodium restriction, potassium repletion, manage HTN with meds, adrenalectomy, monitor adrenal insufficiency postop, life-long glucocorticoid replacement
Pheochromocytoma Catecholamine secreting tumor (epi/norepi), diagnosed w/ 24 hr urine collection. Treatment is surgical removal (adrenalectomy). Watch for HTN crisis (labetalol), stroke, MI, dysrhythmias, alpha blockers(phenoxybenzamine), high BGL. No stimulants/amines
Adrenalectomy management monitor for electrolyte and glucose imbalance, postop hemorrhage, s/s of adrenal insufficiency, decreased urine output, plan for managing stress, glucocorticoids and/or mineralocorticoids, medical alert bracelet / emergency kit with glucocorticoids
Hypothyroidism causes Damaged thyroid cells (autoimmune, iodine deficiency, meds), thyroid removed, congenital, pituitary or hypothalamus malfunction
Hypothyroidism symptoms SLOWER:fatigue, weight gain, cold intolerance, hoarse voice, possible goiter, slow speech memory impairment, brain fog, depression, dry hair/skin, loss of outer 3rd of eyebrow, brittle nails, SOB, exercise intolerance, sleep apnea, low libido, irr periods
Hypothyroidism myxedema From increased deposition of glycosaminoglycans in cells and tissues. Causes osmotic edema and fluid collection (generalized nonpitting edema)
Diagnosis of hypothyroidism Increased TSH, decreased T3/T4, antibodies present with autoimmune disease, ultrasound (underlying cause/eval gland)
Complications of hypothyroidism Myxedema coma, fluid/electrolyte imbalances, hypothermia, hypotension, bradycardia, hypoglycemia, hyponatremia, slow med metabolism (sensitive to sedatives/narcotics)
Treatment of hypothyroidism Replace thyroid hormone levothyroxine (Synthroid) and supportive measures. Start at low dose and increase PRN; lifelong med
Management of hypothyroidism Monitor O2, serum Ca (low if thyroid removal), skin (turn freq), VS (low), daily weight, bowel function (constipation)
Causes of hyperthyroidism Graves' disease (autoimmune - most common), nodules, thyroiditis, iodine (too much/little)
Diagnosis of hyperthyroidism Primary: T3/T4 excess secretion. Secondary: TSH excess from anterior/posterior pituitary. Tertiary: TRH excess from hypothalamus. Labs and thyroid scan done
Hyperthyroidism symptoms elevated HR, afib, thyroid bruit, heat intolerance, increased gastric activity/appetite, weight loss, fatigue, nervousness, insomnia, light or absent period, hair loss, exophthalmos, goiter
Thyrotoxicosis / thyroid storm excessive thyroid hormone activity; MED EMERGENCY. Resp compromise / cardiac collapse. Increased HR, fever, HTN(sys), abd pain, tremors, LOC changes
Treatment for thyroid storm Airway management, fluid resuscitation, antithyroid meds, beta blockers, glucocorticoids, cooling blanket, seizure precautions, cardiac monitoring
Hyperthyroidism management Monitor electrolytes, decrease stress, skin and eye care, monitor IandO, monitor heart/VS, daily weight
Meds for hyperthyroidism Propylthiouracil (PTU), methimazole (Tapazole), Lithium carbonate (Lithonate)
Hyperthyroidism radioiodine therapy Private room, sign on door, staff wear dosimeter to measure exposure, rotate staff, limit direct contact with pt 30min/8 hr, no pregnant staff, encourage pt to do ADLs
Thyroidectomy management Priority: airway, hemorrhage. Hypocalcemia (watch for muscle spasms and nerve damage to larynx), semi fowlers, oral suction at bedside, humidified air, hormone replacement therapy
Hypoparathyroidism causes removal of glands, congenital (DiGeorge syndrome), secondary to iodine therapy for hyperthyroidism, autoimmune (DM or adrenal insufficiency - reversible)
Hypoparathyroidism patho HYPOCALCEMIA due to lack of PTH (primary disorder associated with this disorder)
Hypoparathyroidism symptoms decreased Ca, tetany (muscle cramps, carpopedal spasm), positive Chvostek and Trousseau signs, paresthesia of hands/feet, numbness/tingling of mouth, seizures, prolonged QT, hypotension, dysrhythmias, bone pain, skeletal deformities
Management of hypoparathyroidism Raise Ca levels (IV calcium gluconate/chloride. admin slowly with cardiac disease pt), monitor Ca/albumin/magnesium/phosphate
Hyperparathyroidism patho overactive parathyroid glands raise blood Ca levels as PTH acts on the bone, kidney and intestines. Primary: parathyroid adenomas; secondary: chronic renal failure
Symptoms of hyperparathyroidism may have no symptoms, lethargy, confusion, muscle weakness, fatigue, generalized bone pain, polyuria, anorexia, constipation, prolonged PR/short QT, abd pain (peptic ulcer disease)
Complications of hyperparathyroidism renal stones, fractures, loss of bone density, HTN, arrythmias
Diagnosis of hyperparathyroidism Direct measurement of PTH (intact), Ca (high), albumin, phosphorus levels
Hyperparathyroidism treatment increase fluid intake, IV normal saline to prevent renal calculi, decrease calcium and avoid thiazide diuretics
Diabetes type II patho modifiable factors are cause, insulin resistance (increased urine, thirst, hunger, fatigue, renal insufficiency, infection, visual issues), High A1C diagnosis. oral agents to lower resistance.
Diabetic Ketoacidosis patho Insulin deficiency, fat break down, ketone production, metabolic acidosis, counter resp hormones, severe hyperglycemia. Blood pH less than 7.35. Develops quickly
DKA symptoms initial presentation similar to DM, progresses to dehydration, hyper/hypokalemia, hypovolemia, hyponatremia. Late: hypotension, tachycardia, Kussmaul resp, fruity breath, abd pain, N/V, lethargy, coma
Treatment for DKA IVF isotonic NS, monitor potassium prior to insulin, cardiac monitor
Hyperosmolar Hyperglycemic State (HHS) hyperglycemia, hyperosmolality, severe dehydration without ketoacidosis. BGL above 600, higher mortality rate than DKA. Develops slowly. Shallow respirations seen
Diagnosis of HHS BGL above 600, serum osmolality above 320, serum pH above 7.4, bicarb above 15, altered LOC.
Treatment of HHS IVF, airway management, IV insulin. Monitor for cardiac arrythmias and hypovolemia
Created by: user-2007851
 

 



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