By Linda Self Assessment and Management of Patients with Endocrine Disorders.

By Linda Self

Assessment and Management of Patients with Endocrine Disorders

Glands of the Endocrine SystemHypothalamusPosterior PituitaryAnterior PituitaryThyroidParathyroidsAdrenalsPancreatic isletsOvaries and testes

HypothalamusReleasing and inhibiting hormonesCorticotropin-releasing hormoneThyrotropin-releasing hormoneGrowth hormone-releasing hormoneGonadotropin-releasing hormoneSomatostatin-=-inhibits GH and TSH

Anterior PituitaryGrowth Hormone--Adrenocorticotropic hormoneThyroid 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

Posterior PituitaryAntidiuretic Hormone

Oxytocin—contraction of uterus, milk ejection from breasts

Adrenal CortexMineralocorticoid—aldosterone. Affects sodium

absorption, loss of potassium by kidney

Glucocorticoids—cortisol. Affects metabolism, regulates blood sugar levels, affects growth, anti-inflammatory action, decreases effects of stress

Adrenal androgens—dehydroepiandrosterone and androstenedione. Converted to testosterone in the periphery.

Adrenal MedullaEpinephrine and norepinephrine

serve as neurotransmitters for sympathetic system

ThyroidFollicular cells—excretion of triiodothyronine (T3)

and thyroxine (T4)—Increase BMR, increase bone and calcium turnover, increase response to catecholamines, need for fetal G&D

Thyroid C cells—calcitonin. Lowers blood calcium and phosphate levels

ParathyroidParathyroid hormone—regulates serum calcium

Pancreatic Islet cellsInsulin

Glucagon—stimulates glycogenolysis and glyconeogenesis

Somatostatin—decreases intestinal absorption of glucose

Kidney1, 25 dihydroxyvitamin D—stimulates calcium

absorption from the intestineRenin—activates the RAASErythropoietin—Increases red blood cell production

OvariesEstrogenProgesterone—inportant in menstrual cycle,*maintains

pregnancy,

TestesAndrogens, testosterone—secondary sexual

characteristics, sperm production

ThymusReleases thymosin and thymopoietinAffects maturation of T lymphocetes

PinealMelatoninAffects sleep, fertility and aging

ProstaglandinsWork locallyReleased by plasma cellsAffect fertility, blood clotting, body temperature

AssessmentHealth history—energy level, hand and foot size

changes, headaches, urinary changes, heat and cold intolerance, changes in sexual characteristics, personality changes, others

Physical assessment—appearance including hair distribution, fat distribution, quality of skin, appearance of eyes, size of feet and hands, peripheral edema, facial puffiness, vital signs

Diagnostic EvaluationSerum 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 pituitary

Suppression tests—tests negative feedback systems that control secretion of hormones from the hypothalamus or pituitary.

Disorders of the PituitaryPituitary TumorsEosinophilic tumors may result in gigantism or in

acromegaly. May suffer from severe headaches, visual disturbances, decalcification of the bone, endocrine disturbances

Basophilic tumors may cause Cushing’s syndrome w/features of hyperadrenalism, truncal obesity, amenorrhea, osteoporosis

Chromophobic tumors—90% of pituitary tumors. Present with lowered BMR, obesity, somnolence, scant hair, low body temp, headaches, visual changes

Growth hormone deficiency in childhood will result in primary dwarfism.

Pituitary Tumors—Assessment and Diagnostic Findings

H&PVision testsCT, MRISerum levels of pituitary hormones, others

Diabetes InsipidusDeficiency of ADHExcessive thirst, large volumes of dilute urineCan occur secondary to brain tumors, head

trauma, infections of the CNS, and surgical ablation or radiation

Nephrogenic DI—relates to failure of the renal tubules to respond to ADH. Can be related to hypokalemia, hypercalcemia and to medications (lithium demeocycline)

ManifestationsExcessive thirstUrinary sp. gr. of 1.001.1.005

Assessment and Diagnostic FindingsFluid 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 hypotensive

Trial of desmopressin and IV hypertonic salineMonitor serum and urine osmolality and ADH levels

Pharmacologic 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

SIADHExcessive 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 diuretics

Meds can either affect the pituitary or increase sensitivity to renal tubules to ADH

Management: eliminate cause, give diuretics (Lasix), fluid restriction, I&O, daily wt., lab chemistries

SIADHRestoration of electrolytes must be gradualMay use 3% NaCl in conjunction with Lasix

ThyroidT3 and T4Need iodine for synthesis of hormones—excess will

result in adaptive decline in utilization called the Wolf-Chaikoff mechanism

Thyroid is controlled by TSH Cellular 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

ThyroidInspect glandObserve for goiterCheck TSH, serum T3 and T4T3 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 accuracy

T3 more accurate indicator of hyperthyroidism according to text

ThyroidAntibodies 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 uptake

Thyroid scan—helps determine the location, size, shape and size of gland. “Hot” areas (increased function) and “cold” areas (decreased function) can assist in diagnosis.

Nursing 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

HypothyroidismMost common cause is Hashimoto’s thyroiditisCommon 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

ManifestationsFrom mild symptoms to myxedemaMyxedema –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

Pharmacologic 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

Management in MyxedemaCautious fluid replacementGlucose to restore to normal glycemic levelsAvoid rapid overheating due to increased oxygen

demands but keep warmMay give levothyroxine intravenously

With recovery,Modify activityHigh fiber foodsHome health for follow-up

HyperthyroidismExtreme form is Grave’s diseaseCaused by thyroiditis, excessive amount thyroid

hormone, abnormal output by immunoglobulinsIs more common in women

Manifestations of hyperthyroidismThyrotoxicosis—nervousness, irritable, apprehensive,

palpitations, heat intolerance, skin flushing, tremors, possibly exophthalmos

Have an increased sensitivity to catecholaminesCan occur after irradiation or presence of a tumor

Assessment and DiagnosisThyroid thrill and or bruit may be present Thyroid may be enlargedDecreased TSH, increased free T4 and an increased

radioactive iodine uptake

ManagementReduce thyroid hyperactivity—usually use radioactive

iodine, antithyroid meds or surgery)Beta blockersCan be relapse with antithyroid meds

Pharmacologic TherapyIrradiation with administration of radioisotope iodine

131—initially may cause an acute release of thyroid hormones. Should monitor for thyroid storm

S/S of thyroid storm—high fever. Tachycardia, delirium, chest pain, dyspnea, palpitations, weight loss, diarrhea, abdominal pain

Management 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

Antithyroid MedicationsPTU—propylthiouracil—blocks synthesis of

hormones Tapazole (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 teeth

Dexamethazone—suppresses release of thyroid hormones

Surgical ManagementReserved for special circumstances, e.g. large goiters,

those who cannot take antithyroid meds, or who need rapid normalization

Subtotal thyroidectomyBefore surgery, give PTU until s/s of hyperthyroidism

have disappearedIodine may be used to decrease vascularity

Nursing ManagementReassurance r/t the emotional reactions experiencedMay 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.

Parathyroid 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)

Manifestations 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

Assessment and Diagnostic FindingsPersistent elevated calcium levelsElevated serum parathormone levelBone studies will reveal decreased densityDouble antibody parathyroid hormone test is used to

distinguish between primary hyperparathyroidism and malignancy

Ultrasound, MRI, thallium scan, fine needle biopsy also can be used to localize cysts, adenomas, or hyperplasia

ManagementRecommended 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

Hypercalcemic crisisSeen with levels greater than 15mg/dLCan 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 calcium

Give calcitonin or mithramycin to decrease serum calcium levels quickly

HypoparathyroidismSeen 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

Clinical 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

Assessment and Diagnostic FindingsTrousseau’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

Management of HypoparathyroidismRestore 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.

Management of HypoparathyroidismKeep 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

Adrenals--PheochromocytomaUsually benign tumorOriginates from the chromaffin cells of the adrenal

medullaAny age but usu. Between 40-50 years oldCan be familial10% are malignantMay be associated with thyroid carcinoma or

parathyroid hyperplasia or tumor

Clinical ManifestationsHeadache, 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

Assessment and Diagnostic FindingsAssociated 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 testing

Clonidine suppression test—in normal individual, would block catecholamine release

Imaging studies

ManagementBedrestElevated HOBICUNiprideCalcium channel blockers and Beta blockers Surgical management (manipulation of the tumor can

cause excessive release of catecholamines)Steroid therapy if adrenalectomy performedHypotension and hypoglycemia can occur post-op

Addison’s DiseaseAdrenocortical insufficiencyAutoimmune or idiopathic atrophyCan be caused by inadequate ACTH from pituitaryTherapeutic use of steroids

ManifestationsMuscle weaknessAnorexiaDark pigmentationHypotensionHypoglycemiaLow sodium levelsHigh potassium levelsCan result in Addisonian crisis

Addisonian crisisCirculatory shockPallor, 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

Assessment and Diagnostic FindingsEarly 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

ManagementRestore circulatory status—fluids, steroidsMay 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

Cushing’s SyndromeResults from excessive adrenocortical activityMay 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

Manifestations of Cushing’s syndrome

Cataracts, glaucomaHypertension, heart failureTruncal obesity, moon face, buffalo hump, sodium

retention, hypokalemia, hyperglycemia, negative nitrogen balance, altered calcium metabolism

Decreased inflammatory responses, impaired wound healing, increased susceptibility to infections

Osteoporosis, compression fracturesPeptic ulcers, pancreatitisThinning of skin, striae, acneMood alterations

Assessment and Diagnostic FindingsOvernight 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

Medical 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.

Primary Aldosteronism or Conn’s Syndrome

Excessive aldosterone secondary to adrenal tumor retain 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

Assessment and Diagnostic FindingsHigh sodiumLow potassium levelHigh serum aldosterone levelLow renin levelAldosterone excretion rate after salt loading is

diagnostic for primary aldosteronismRenin-aldosterone stimulation test

Management

Surgical removal of tumorCorrect hypokalemiaUsual postoperative care with abdominal surgeryAdminister steroidsFluidsMonitoring of blood sugarControl of hypertension with spironolactone

Corticosteroid TherapyHydrocortisone--CortisolCortisone--CortatePrednisone--DeltasonePrednisolone-PreloneTriamcinolone--KenalogBetamethasone--CelestoneFludrocortisone (contains both mineralocorticoid and

glucocorticoid) Florinef

IndicationsRAAsthmaMSCOPD exacerbationsLupusOther autoimmune disordersDermatologic disorders

DosingLowest doseLimited durationBest time to give dose is in early morning between 7-8

amNeed to taper off med to allow normal return of renal

function

Side Effects of SteroidsHypertension, thrombophlebitis, accelerated

atherosclerosisIncreased risk of infectionGlaucoma and corneal lesionsMuscle wasting, poor wound healing, osteoporosis,

pathologic fracturesHyperglycemia, steroid withdrawal syndromeMoon face, weight gain, acne

Case 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 10-15 minutes.

Routine hematology and chemistry studies are wnl and chest xray and ECG are normal.

What is your impression?What labs would you draw?

Case 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?

Case 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 8.4-10.1)

Phosphorus is 2.4 (reference range is 2.5-4.5)What is your diagnosis?

Case 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?

Case 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?