Presentation on theme: "Assessment and Management of Patients with Endocrine Disorders"— Presentation transcript:
1Assessment and Management of Patients with Endocrine Disorders By Linda Self
2Glands of the Endocrine System HypothalamusPosterior PituitaryAnterior PituitaryThyroidParathyroidsAdrenalsPancreatic isletsOvaries and testes
3Hypothalamus Releasing and inhibiting hormones Corticotropin-releasing hormoneThyrotropin-releasing hormoneGrowth hormone-releasing hormoneGonadotropin-releasing hormoneSomatostatin-=-inhibits GH and TSH
4Anterior Pituitary Growth Hormone-- Adrenocorticotropic hormone Thyroid stimulating hormoneFollicle stimulating hormone—ovary in female, sperm in malesLuteinizing hormone—corpus luteum in females, secretion of testosterone in malesProlactin—prepares female breasts for lactation
5Posterior Pituitary Antidiuretic Hormone Oxytocin—contraction of uterus, milk ejection from breasts
6Adrenal CortexMineralocorticoid—aldosterone. Affects sodium absorption, loss of potassium by kidneyGlucocorticoids—cortisol. Affects metabolism, regulates blood sugar levels, affects growth, anti- inflammatory action, decreases effects of stressAdrenal androgens—dehydroepiandrosterone and androstenedione. Converted to testosterone in the periphery.
7Adrenal Medulla Epinephrine and norepinephrine serve as neurotransmitters for sympathetic system
8ThyroidFollicular cells—excretion of triiodothyronine (T3) and thyroxine (T4)—Increase BMR, increase bone and calcium turnover, increase response to catecholamines, need for fetal G&DThyroid C cells—calcitonin. Lowers blood calcium and phosphate levels
10Pancreatic Islet cells InsulinGlucagon—stimulates glycogenolysis and glyconeogenesisSomatostatin—decreases intestinal absorption of glucose
11Kidney1, 25 dihydroxyvitamin D—stimulates calcium absorption from the intestineRenin—activates the RAASErythropoietin—Increases red blood cell production
12OvariesEstrogenProgesterone—inportant in menstrual cycle,*maintains pregnancy,
13TestesAndrogens, testosterone—secondary sexual characteristics, sperm production
14Thymus Releases thymosin and thymopoietin Affects maturation of T lymphocetes
15PinealMelatoninAffects sleep, fertility and aging
16Prostaglandins Work locally Released by plasma cells Affect fertility, blood clotting, body temperature
17AssessmentHealth history—energy level, hand and foot size changes, headaches, urinary changes, heat and cold intolerance, changes in sexual characteristics, personality changes, othersPhysical assessment—appearance including hair distribution, fat distribution, quality of skin, appearance of eyes, size of feet and hands, peripheral edema, facial puffiness, vital signs
18Diagnostic Evaluation Serum levels of hormonesDetection of antibodies against certain hormonesUrinary tests to measure by-products (norepinephrine, metanephrines, dopamine)Stimulation tests—determine how an endocrine gland responds to stimulating hormone. If the hormone responds, then the problem lies w/hypothalmus or pituitarySuppression tests—tests negative feedback systems that control secretion of hormones from the hypothalamus or pituitary.
19Disorders of the Pituitary Pituitary TumorsEosinophilic tumors may result in gigantism or in acromegaly. May suffer from severe headaches, visual disturbances, decalcification of the bone, endocrine disturbancesBasophilic tumors may cause Cushing’s syndrome w/features of hyperadrenalism, truncal obesity, amenorrhea, osteoporosisChromophobic tumors—90% of pituitary tumors. Present with lowered BMR, obesity, somnolence, scant hair, low body temp, headaches, visual changes
20Growth hormone deficiency in childhood will result in primary dwarfism.
21Pituitary Tumors—Assessment and Diagnostic Findings H&PVision testsCT, MRISerum levels of pituitary hormones, others
22Diabetes Insipidus Deficiency of ADH Excessive thirst, large volumes of dilute urineCan occur secondary to brain tumors, head trauma, infections of the CNS, and surgical ablation or radiationNephrogenic DI—relates to failure of the renal tubules to respond to ADH. Can be related to hypokalemia, hypercalcemia and to medications (lithium demeocycline)
23ManifestationsExcessive thirstUrinary sp. gr. of
24Assessment and Diagnostic Findings Fluid deprivation test—withhold fluids for 8-12 hours. Weigh patient frequently. Inability to slow down the urinary output and fail to concentrate urine are diagnostic. Stop test if patient is tachycardic or hypotensiveTrial of desmopressin and IV hypertonic salineMonitor serum and urine osmolality and ADH levels
25Pharmacologic Tx and Nursing Management DDAVP—intranasal bidCan be given IM if necessary. Every 24-96h. Can cause lipodystrophy.Can also use Diabenese and thiazide diuretics in mild disease as they potentiate the action of ADHIf renal in origin—thiazide diuretics, NSAIDs (prostaglandin inhibition) and salt depletion may helpEducate patient about actions of medications, how to administer meds, wear medic alert bracelet
26SIADH Excessive ADH secretion Retain fluids and develop a dilutional hyponatremiaOften non-endocrine in origin—such as bronchogenic carcinomaCauses: Disorders of the CNS like head injury, brain surgery, tumors, infections or medications like vincristine, phenothiazines, TCAs or thiazide diureticsMeds can either affect the pituitary or increase sensitivity to renal tubules to ADHManagement: eliminate cause, give diuretics (Lasix), fluid restriction, I&O, daily wt., lab chemistries
27SIADH Restoration of electrolytes must be gradual May use 3% NaCl in conjunction with Lasix
28ThyroidT3 and T4Need iodine for synthesis of hormones—excess will result in adaptive decline in utilization called the Wolf- Chaikoff mechanismThyroid is controlled by TSHCellular metabolism, brain development, normal growth, affect every organ in the bodyT3 is five times as potent as T4Calcitonin—secreted in response to high levels of serum calcium, increases deposition in the bone
29Thyroid Inspect gland Observe for goiter Check TSH, serum T3 and T4 T3 resin uptake test useful in evaluating thyroid hormone levels in patients who have received diagnostic or therapeutic dose of iodine. Estrogens, Dilantin, Tagamet, Heparin, amiodarone, PTU,steroids and Lithium can cloud the accuracyT3 more accurate indicator of hyperthyroidism according to text
30ThyroidAntibodies seen in Hashimoto’s, Grave’s and other auto-immune problems.Radioactive iodine uptake test measures rate of iodine uptake. Patients with hyperthyroidism exhibit a high uptake, hypothyroidism will have low uptakeThyroid scan—helps determine the location, size, shape and size of gland. “Hot” areas (increased function) and “cold” areas (decreased function) can assist in diagnosis.
31Nursing ImplicationsBe aware of meds patient is taking (see list in text) that can affect accuracy of testingAlso be aware if patient is taking multivitamins and food supplements
32Hypothyroidism Most common cause is Hashimoto’s thyroiditis Common in those previously treated for hyperthyroidismAtrophy of gland with agingMedications like lithium, iodine compounds, antithyroid meds can causeRadiation treatments to head and neckInfiltrative diseases like amyloidosis, sclerodermaIodine deficiency and excessHypothalamic or pituitary abnormalityMore common in women, especially over age 50
33Manifestations From mild symptoms to myxedema Myxedema –accumulation of mucopolysaccharides in sc and interstitial tissues. Is the extreme form of hypothyroidism. Can progress to shock.S/S—fatigue, hair loss, dry skin, brittle nails, numbness and tingling of the fingers, amenorrhea, weight gain, decreased heart rate and temperature, lassitude, cognitive changes, elevated cholesterol levels, constipation, hypotension
34Pharmacologic Management of hypothyroidism Levothyroxine is preferred agentDosage is based on TSHDesiccated thyroid used infrequently due to inconsistent dosingAngina can occur when thyroid replacement is initiated as it enhances effects of cardiovascular catecholamines (in pt. w/pre-existent CAD). Start at low dose.Hypnotics and sedatives may have profound effects on sensorium
35Management in Myxedema Cautious fluid replacementGlucose to restore to normal glycemic levelsAvoid rapid overheating due to increased oxygen demands but keep warmMay give levothyroxine intravenouslyWith recovery,Modify activityHigh fiber foodsHome health for follow-up
36Hyperthyroidism Extreme form is Grave’s disease Caused by thyroiditis, excessive amount thyroid hormone, abnormal output by immunoglobulinsIs more common in women
37Manifestations of hyperthyroidism Thyrotoxicosis—nervousness, irritable, apprehensive, palpitations, heat intolerance, skin flushing, tremors, possibly exophthalmosHave an increased sensitivity to catecholaminesCan occur after irradiation or presence of a tumor
38Assessment and Diagnosis Thyroid thrill and or bruit may be presentThyroid may be enlargedDecreased TSH, increased free T4 and an increased radioactive iodine uptake
39ManagementReduce thyroid hyperactivity—usually use radioactive iodine, antithyroid meds or surgery)Beta blockersCan be relapse with antithyroid meds
40Pharmacologic Therapy Irradiation with administration of radioisotope iodine 131—initially may cause an acute release of thyroid hormones. Should monitor for thyroid stormS/S of thyroid storm—high fever. Tachycardia, delirium, chest pain, dyspnea, palpitations, weight loss, diarrhea, abdominal painManagement of thyroid storm—oxygen, IV fluids with dextrose, hypothermic measures, steroids to treat shock or adrenal deficiency, iodine to decrease output of T4, beta blockers, PTU or Tapazole impedes formation of thyroid hormone and blocks conversion of T4 to T3
41Antithyroid Medications PTU—propylthiouracil—blocks synthesis of hormonesTapazole (methimazole)—blocks synthesis of hormones. More toxic than PTU.Sodium Iodide-suppresses release of thyroid hormoneSSKI (saturated solution of potassium chloride)– suppresses release of hormones and decreases vascularity of thyroid. Can stain teethDexamethazone—suppresses release of thyroid hormones
42Surgical ManagementReserved for special circumstances, e.g. large goiters, those who cannot take antithyroid meds, or who need rapid normalizationSubtotal thyroidectomyBefore surgery, give PTU until s/s of hyperthyroidism have disappearedIodine may be used to decrease vascularity
43Nursing Management Reassurance r/t the emotional reactions experienced May need eye care if has exophthalmosMaintain normal body temperatureAdequate caloric intakeManaging potential complications such as dysrhythmias and tachycardiasEducate about potential s/s of hypothyroidism following any antithyroid tx.
44Parathyroid GlandsParathormone maintains sufficient serum calcium levelsExcess calcium can bind with phosphate and precipitate in various organs, can cause pancreatitisHyperparathyroidism will cause bone decalcification and development of renal calculiMore common in womenSecondary hyperparathyroidism occurs in those with chronic renal failure and renal rickets secondary to excess phosphorus retention (and increased parathormone secretion)
45Manifestations of Hyperparathyroidism May be asymptomaticApathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension and cardiac dysrhythmiasExcess calcium in the brain can lead to psychosesRenal lithiasis can lead to renal damage and even failureDemineralization of bones with back and joint pain, pain on weight bearing, pathologic fracturesPeptic ulcers and pancreatitis can also occur
46Assessment and Diagnostic Findings Persistent elevated calcium levelsElevated serum parathormone levelBone studies will reveal decreased densityDouble antibody parathyroid hormone test is used to distinguish between primary hyperparathyroidism and malignancyUltrasound, MRI, thallium scan, fine needle biopsy also can be used to localize cysts, adenomas, or hyperplasia
47ManagementRecommended treatment for hyperparathyroidism is surgical removalHydration therapy necessary to prevent renal calculiAvoid thiazide diuretics as they decrease renal excretion of calciumIncrease mobility to promote bone retention of calciumAvoid restricted or excess calcium in the dietFluids, prune juice and stool softeners to prevent constipationWatch for s/s of tetany postsurgically (numbness, tingling, carpopedal spasms) as well as cardiac dysrhythmias and hypotension
48Hypercalcemic crisis Seen with levels greater than 15mg/dL Can result in life-threatening neurologic, cardiovascular and renal symptomsTreatments include: hydration, loop diuretics to promote excretion of calcium, phosphate therapy to promote calcium deposition in bone and reducing GI absorption of calciumGive calcitonin or mithramycin to decrease serum calcium levels quickly
49HypoparathyroidismSeen most often following removal of thyroid gland, parathyroid glands or following radical neck surgeryDeficiency of parathormone results in increased bone phosphate and decreased blood calcium levelsIn absence of parathormone, there is decreased intestinal absorption of dietary calcium and decreased resorption of calcium from bone and through kidney tubules
50Clinical Manifestations of Hypoparathyroidism Irritability of neuromuscular systemTetany—hypertonic muscle contractions , numbnes, tingling, cramps in extremities, laryngeal spasm, bronchospasm, carpopedal spasm ( flexion of the elbows and wrists, dorsiflexion of the feet), seizures
51Assessment and Diagnostic Findings Trousseau’s sign—can check with a BP cuffChvostek’s sign—tapping over facial nerve causes spasm of the mouth, nose and eyeLab studies may reveal calcium levels of 5-6 mg/dL or lowerSerum phosphate levels will be decreased
52Management of Hypoparathyroidism Restore calcium level to 9-10 mg/dLMay need to give IV calcium gluconate for immediate treatmentUse of parathormone IV reserved for extreme situations due to the probability of allergic reactionsMonitor calcium levelsMay need bronchodilators and even ventilator assistanceDiet high in calcium and low in phosphorus; thus, avoid milk products, egg yolk and spinach.
53Management of Hypoparathyroidism Keep calcium gluconate at bedsideEnsure has IV accessCardiac monitoringCare of postoperative patients who have undergone thyroid surgery, parathyroidectomy or radical neck surgery. Be watchful for signs of tetany, seizures, and respiratory difficulties
54Adrenals--Pheochromocytoma Usually benign tumorOriginates from the chromaffin cells of the adrenal medullaAny age but usu. Between years oldCan be familial10% are malignantMay be associated with thyroid carcinoma or parathyroid hyperplasia or tumor
55Clinical Manifestations Headache, diaphoresis, palpitations, hypertensionMay have hyperglycemia related to excess epinephrine secretionTremors, flushing and anxiety as wellBlurring of visionFeeling of impending doomBPs exceeding 250/150 have occurred
56Assessment and Diagnostic Findings Associated with the 5 H’s—hypertension, headache, hyperhidrosis, hypermetabolism and hyperglycemiaUrinary catecholamines and metanephrine are direct and conclusive testsSerum epinephrine and norepinephrine levels will be elevatedUrinary vanillymandelic acid also diagnosticMust avoid coffee, tea, bananas, chocolate, vanilla and ASA, nicotine, amphetamines, decongestants before 24h urine testingClonidine suppression test—in normal individual, would block catecholamine releaseImaging studies
57Management Bedrest Elevated HOB ICU Nipride Calcium channel blockers and Beta blockersSurgical management (manipulation of the tumor can cause excessive release of catecholamines)Steroid therapy if adrenalectomy performedHypotension and hypoglycemia can occur post-op
58Addison’s Disease Adrenocortical insufficiency Autoimmune or idiopathic atrophyCan be caused by inadequate ACTH from pituitaryTherapeutic use of steroids
59Manifestations Muscle weakness Anorexia Dark pigmentation Hypotension HypoglycemiaLow sodium levelsHigh potassium levelsCan result in Addisonian crisis
60Addisonian crisis Circulatory shock Pallor, apprehension, weak&rapid pulse, rapid respirations and low blood pressureHeadache, nausea, abdominal pain and diarrheaCan be brought on by overexertion, exposure to cold, acute infection, decrease in salt intake
61Assessment and Diagnostic Findings Early morning serum cortisol and plasma ACTH are performed. Will distinguish between primary and secondary adrenal insufficiency. In primary, will have elevated ACTH levels and below normal cortisol levels.If the adrenal cortex is not stimulated by the pituitary, a normal response to doses of exogenous ACTH (see text)Blood sugar levels and electrolyte values
62Management Restore circulatory status—fluids, steroids May need antibiotics if infection precipitated crisisMay need lifelong steroid therapy and mineralocorticoid therapyMay need additional salt intakeCheck orthostaticsDaily weightsAware that stressors can precipitate crisesMedic alert bracelet or similar identification of history
63Cushing’s Syndrome Results from excessive adrenocortical activity May be related to excessive use of corticosteroid medications or due to hyperplasia of the adrenal cortexOversecretion of corticosteroids can also be caused by pituitary tumorCan be caused by bronchogenic carcinoma or other malignancy
65Assessment and Diagnostic Findings Overnight dexamethasone suppression test frequently used for diagnosisAdministered at 11pm and cortisol level checked at 8amSuppression of cortisol to less than 5mg/dL indicates normal functioningMeasurement of plasma ACTH (radioimmunoassay) in conjunction with dexamethasone suppression test helps distinguish pituitary vs. ectopic sites of ACTH.MRI, CT and CT also help detect tumors of adrenal or pituitary
66Medical ManagementIf pituitary source, may warrant transphenoidal hypophysectomyRadiation of pituitary also appropriateAdrenalectomy may be needed in case of adrenal hypertrophyTemporary replacement therapy with hydrocortisone or FlorinefAdrenal enzyme reducers may be indicated if source if ectopic and inoperable. Examples include: ketoconazole, mitotane and metyrapone.If cause is r/t excessive steroid therapy, tapering slowly to a minimum dosage may be appropriate.
67Primary Aldosteronism or Conn’s Syndrome Excessive aldosterone secondary to adrenal tumorretain sodium and excrete potassiumResults in alkalosisHypertension—universal sign of hyperaldosteronismInability of kidneys to concentrate the urineSerum becomes concentratedExcessive thirstHypokalemia interferes with insulin secretion thus will have glucose intolerance as well
68Assessment and Diagnostic Findings High sodiumLow potassium levelHigh serum aldosterone levelLow renin levelAldosterone excretion rate after salt loading is diagnostic for primary aldosteronismRenin-aldosterone stimulation test
69Management Surgical removal of tumor Correct hypokalemia Usual postoperative care with abdominal surgeryAdminister steroidsFluidsMonitoring of blood sugarControl of hypertension with spironolactone
70Corticosteroid Therapy Hydrocortisone--CortisolCortisone--CortatePrednisone--DeltasonePrednisolone-PreloneTriamcinolone--KenalogBetamethasone--CelestoneFludrocortisone (contains both mineralocorticoid and glucocorticoid) Florinef
71Indications RA Asthma MS COPD exacerbations Lupus Other autoimmune disordersDermatologic disorders
72Dosing Lowest dose Limited duration Best time to give dose is in early morning between 7-8 amNeed to taper off med to allow normal return of renal function
73Side Effects of Steroids Hypertension, thrombophlebitis, accelerated atherosclerosisIncreased risk of infectionGlaucoma and corneal lesionsMuscle wasting, poor wound healing, osteoporosis, pathologic fracturesHyperglycemia, steroid withdrawal syndromeMoon face, weight gain, acne
74Case Study 135 year old male presents with BP of 188/112 at a yearly physical exam. Previous exams noted blood pressures of 160/94 and 158/92. On questioning, patient admits to twice a month episodes of apprehension, severe headache, perspiration, rapid heartbeat, and facial pallor. These episodes had an abrupt onset and lasted minutes.Routine hematology and chemistry studies are wnl and chest xray and ECG are normal.What is your impression?What labs would you draw?
75Case Study 250 year old woman presents with enlargement of left anterior neck. She has noted increased appetite over the past month with no weight gain, and more frequent bowel movements over the same period. Patient feels jittery at times, experiences palpitations and feels “hot” a lot recently.She is 5’8” tall and weighs 150#. Heart rate is 110 and blood pressure is 110/76.What might be this patient’s problem?What lab tests might you draw?
76Case study 348 year old woman with a past history of mental illness presents with a new onset of bizarre psychotic behavior. She had been well over the past two years.She is 5’5” tall and weighs 138#. Her heart rate is 65, irreg and BP is 130/75. Exam is normal except that she is confused to place, time and year. Patient c/o joints aching and of feeling fatigued.Lab tests reveal serum calcium level of 13.8mg/dL (reference range is )Phosphorus is 2.4 (reference range is )What is your diagnosis?
77Case Study 440 year old deeply tanned woman presents with a 6 month history of increasing fatigue. For the past three months she has suffered from recurrent URIs, poor appetite, abdominal cramps, fatigue and diarrhea. She has lost 25#. She has noted joint pains, muscle weakness, and has not menstruated for the past 3 months.Labs reveal blood glucose of 59, Na+ 130, K+ 6.0.What disorder do you expect?
78Case Study #527 year old woman presents with depression, insomnia, increased facial fullness and recent increase in acne. She had an episode of depression and acute psychosis following uncomplicated delivery of normal baby boy 9 months previously. Her menses have been irregular since their resumption after the birth (she is not breast feeding). Patient relates has had several vaginal yeast infections recently.Heart rate is 90bpm, BP is 146/100. Her face is puffy and has acne vulgaris. Thin extremities and with truncal obesity.What are your suspicions?What labs will you draw?