Assessment and Management of Patients With Endocrine Disorders

5/20/2018 Assessment and Management of Patients With Endocrine Disorders

1/78

By Linda Self

Assessment and Management of

Patients with Endocrine Disorders


2/78

Glands of the Endocrine System

Hypothalamus

Posterior Pituitary

Anterior Pituitary

Thyroid Parathyroids

Adrenals

Pancreatic islets

Ovaries and testes


3/78

Hypothalamus

Releasing and inhibiting hormones

Corticotropin-releasing hormone

Thyrotropin-releasing hormone

Growth hormone-releasing hormone Gonadotropin-releasing hormone

Somatostatin-=-inhibits GH and TSH


4/78

Anterior Pituitary

Growth Hormone--

Adrenocorticotropic hormone

Thyroid stimulating hormone

Follicle stimulating hormoneovary in female, spermin males

Luteinizing hormonecorpus luteum in females,

secretion of testosterone in males

Prolactinprepares female breasts for lactation


5/78

Posterior Pituitary

Antidiuretic Hormone

Oxytocincontraction of uterus, milk ejection from

breasts


6/78

Adrenal Cortex

Mineralocorticoidaldosterone. Affects sodiumabsorption, loss of potassium by kidney

Glucocorticoidscortisol. Affects metabolism,regulates blood sugar levels, affects growth, anti-

inflammatory action, decreases effects of stress

Adrenal androgensdehydroepiandrosterone andandrostenedione. Converted to testosterone in the

periphery.


7/78

Adrenal Medulla

Epinephrine and norepinephrine

serve as neurotransmitters for sympathetic system


8/78

Thyroid

Follicular cellsexcretion of triiodothyronine (T3)and thyroxine (T4)Increase BMR, increase bone and

calcium turnover, increase response to catecholamines,

need for fetal G&D

Thyroid C cellscalcitonin. Lowers blood calcium

and phosphate levels


9/78

Parathyroid

Parathyroid hormoneregulates serum calcium


10/78

Pancreatic Islet cells

Insulin

Glucagonstimulates glycogenolysis and

glyconeogenesis

Somatostatindecreases intestinal absorption of

glucose


11/78

Kidney

1, 25 dihydroxyvitamin Dstimulates calciumabsorption from the intestine

Reninactivates the RAAS

ErythropoietinIncreases red blood cell production


12/78

Ovaries

Estrogen

Progesteroneinportant in menstrual cycle,*maintains

pregnancy,


13/78

Testes

Androgens, testosteronesecondary sexualcharacteristics, sperm production


14/78

Thymus

Releases thymosin and thymopoietin

Affects maturation of T lymphocetes


15/78

Pineal

Melatonin

Affects sleep, fertility and aging


16/78

Prostaglandins

Work locally

Released by plasma cells

Affect fertility, blood clotting, body temperature


17/78

Assessment

Health historyenergy level, hand and foot sizechanges, headaches, urinary changes, heat and cold

intolerance, changes in sexual characteristics,

personality changes, others

Physical assessmentappearance including hair

distribution, fat distribution, quality of skin,

appearance of eyes, size of feet and hands, peripheral

edema, facial puffiness, vital signs


18/78

Diagnostic Evaluation Serum levels of hormones Detection of antibodies against certain hormones

Urinary tests to measure by-products (norepinephrine,metanephrines, dopamine)

Stimulation testsdetermine how an endocrine glandresponds to stimulating hormone. If the hormoneresponds, then the problem lies w/hypothalmus or

pituitary

Suppression teststests negative feedback systemsthat control secretion of hormones from thehypothalamus or pituitary.


19/78

Disorders of the Pituitary

Pituitary Tumors Eosinophilic tumors may result in gigantism or in

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

disturbances Basophilic tumors may cause Cushings syndrome

w/features of hyperadrenalism, truncal obesity,amenorrhea, osteoporosis

Chromophobic tumors90% of pituitary tumors.Present with lowered BMR, obesity, somnolence, scanthair, low body temp, headaches, visual changes


20/78

Growth hormone deficiency in childhood will result inprimary dwarfism.


21/78

Pituitary TumorsAssessment and

Diagnostic Findings

H&P

Vision tests

CT, MRI

Serum levels of pituitary hormones, others


22/78

Diabetes Insipidus

Deficiency of ADH

Excessive thirst, large volumes of dilute urine

Can occur secondary to brain tumors, head

trauma, infections of the CNS, and surgical

ablation or radiation

Nephrogenic DIrelates to failure of the renal tubules

to respond to ADH. Can be related to hypokalemia,

hypercalcemia and to medications (lithiumdemeocycline)


23/78

Manifestations

Excessive thirst

Urinary sp. gr. of 1.001.1.005


24/78

Assessment and Diagnostic Findings

Fluid deprivation testwithhold 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 saline

Monitor serum and urine osmolality and ADH levels


25/78

Pharmacologic Tx and Nursing

Management

DDAVPintranasal bid

Can 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 ADH

If renal in originthiazide diuretics, NSAIDs

(prostaglandin inhibition) and salt depletion may help

Educate patient about actions of medications, how toadminister meds, wear medic alert bracelet


26/78

SIADH

Excessive ADH secretion Retain fluids and develop a dilutional hyponatremia

Often non-endocrine in originsuch as bronchogeniccarcinoma

Causes: Disorders of the CNS like head injury, brainsurgery, tumors, infections or medications likevincristine, 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


27/78

SIADH

Restoration of electrolytes must be gradual

May use 3% NaCl in conjunction with Lasix


28/78

Thyroid

T3 and T4

Need iodine for synthesis of hormonesexcess 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 body

T3 is five times as potent as T4 Calcitoninsecreted in response to high levels of

serum calcium, increases deposition in the bone


29/78

Thyroid

Inspect gland

Observe for goiter

Check TSH, serum T3 and T4

T3 resin uptake test useful in evaluating thyroidhormone 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


30/78

Thyroid

Antibodies seen in Hashimotos, Graves and otherauto-immune problems.

Radioactive iodine uptake test measures rate of iodine

uptake. Patients with hyperthyroidism exhibit a high

uptake, hypothyroidism will have low uptake

Thyroid scanhelps determine the location, size,

shape and size of gland. Hot areas (increased

function) and cold areas (decreased function) can

assist in diagnosis.


31/78

Nursing Implications

Be aware of meds patient is taking (see list in text) thatcan affect accuracy of testing

Also be aware if patient is taking multivitamins and

food supplements


32/78

Hypothyroidism

Most common cause is Hashimotos thyroiditis

Common in those previously treated for hyperthyroidism

Atrophy of gland with aging

Medications like lithium, iodine compounds, antithyroid

meds can cause

Radiation treatments to head and neck

Infiltrative diseases like amyloidosis, scleroderma

Iodine deficiency and excess

Hypothalamic or pituitary abnormality

More common in women, especially over age 50


33/78

Manifestations

From mild symptoms to myxedema

Myxedemaaccumulation of mucopolysaccharides in

sc and interstitial tissues. Is the extreme form of

hypothyroidism. Can progress to shock.

S/Sfatigue, 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


34/78

Pharmacologic Management of

hypothyroidism

Levothyroxine is preferred agent

Dosage is based on TSH

Desiccated thyroid used infrequently due to

inconsistent dosing

Angina 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


35/78

Management in Myxedema

Cautious fluid replacement

Glucose to restore to normal glycemic levels

Avoid rapid overheating due to increased oxygen

demands but keep warm

May give levothyroxine intravenously

With recovery,

Modify activity

High fiber foods

Home health for follow-up


36/78

Hyperthyroidism

Extreme form is Graves disease

Caused by thyroiditis, excessive amount thyroid

hormone, abnormal output by immunoglobulins

Is more common in women


37/78

Manifestations of hyperthyroidism

Thyrotoxicosisnervousness, irritable, apprehensive,palpitations, heat intolerance, skin flushing, tremors,

possibly exophthalmos

Have an increased sensitivity to catecholamines

Can occur after irradiation or presence of a tumor


38/78

Assessment and Diagnosis

Thyroid thrill and or bruit may be present

Thyroid may be enlarged

Decreased TSH, increased free T4 and an increased

radioactive iodine uptake


39/78

Management

Reduce thyroid hyperactivityusually use radioactiveiodine, antithyroid meds or surgery)

Beta blockers

Can be relapse with antithyroid meds


40/78

Pharmacologic Therapy

Irradiation with administration of radioisotope iodine131initially may cause an acute release of thyroidhormones. Should monitor for thyroid storm

S/S of thyroid stormhigh fever. Tachycardia,

delirium, chest pain, dyspnea, palpitations, weight loss,diarrhea, abdominal pain

Management of thyroid stormoxygen, IV fluidswith dextrose, hypothermic measures, steroids to treatshock or adrenal deficiency, iodine to decrease outputof T4, beta blockers, PTU or Tapazole impedesformation of thyroid hormone and blocks conversionof T4 to T3


41/78

Antithyroid Medications

PTUpropylthiouracilblocks synthesis of hormones Tapazole (methimazole)blocks synthesis of

hormones. More toxic than PTU.

Sodium Iodide-suppresses release of thyroid hormone

SSKI (saturated solution of potassium chloride)

suppresses release of hormones and decreases

vascularity of thyroid. Can stain teeth

Dexamethazonesuppresses release of thyroidhormones


42/78

Surgical Management

Reserved for special circumstances, e.g. large goiters,those who cannot take antithyroid meds, or who need

rapid normalization

Subtotal thyroidectomy

Before surgery, give PTU until s/s of hyperthyroidism

have disappeared

Iodine may be used to decrease vascularity


43/78

Nursing Management

Reassurance r/t the emotional reactions experienced May need eye care if has exophthalmos

Maintain normal body temperature

Adequate caloric intake Managing potential complications such as

dysrhythmias and tachycardias

Educate about potential s/s of hypothyroidism

following any antithyroid tx.


44/78

Parathyroid Glands

Parathormone maintains sufficient serum calciumlevels

Excess calcium can bind with phosphate andprecipitate in various organs, can cause pancreatitis

Hyperparathyroidism will cause bone decalcificationand development of renal calculi

More common in women

Secondary hyperparathyroidism occurs in those with

chronic renal failure and renal rickets secondary toexcess phosphorus retention (and increased

parathormone secretion)

M if t ti f


45/78

Manifestations of

Hyperparathyroidism

May be asymptomatic Apathy, fatigue, muscle weakness, nausea, vomiting,

constipation, hypertension and cardiac dysrhythmias

Excess calcium in the brain can lead to psychoses

Renal lithiasis can lead to renal damage and even

failure

Demineralization of bones with back and joint pain,

pain on weight bearing, pathologic fractures Peptic ulcers and pancreatitis can also occur


46/78


Persistent elevated calcium levels Elevated serum parathormone level

Bone studies will reveal decreased density

Double antibody parathyroid hormone test is used todistinguish between primary hyperparathyroidism and

malignancy

Ultrasound, MRI, thallium scan, fine needle biopsy

also can be used to localize cysts, adenomas, orhyperplasia


47/78

Management

Recommended treatment for hyperparathyroidism issurgical removal

Hydration therapy necessary to prevent renal calculi

Avoid thiazide diuretics as they decrease renal excretion ofcalcium

Increase mobility to promote bone retention of calcium

Avoid restricted or excess calcium in the diet

Fluids, prune juice and stool softeners to preventconstipation

Watch for s/s of tetany postsurgically (numbness, tingling,carpopedal spasms) as well as cardiac dysrhythmias andhypotension


48/78

Hypercalcemic crisis

Seen with levels greater than 15mg/dL Can result in life-threatening neurologic,

cardiovascular and renal symptoms

Treatments 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


49/78

Hypoparathyroidism

Seen most often following removal of thyroid gland,parathyroid glands or following radical neck surgery

Deficiency of parathormone results in increased bone

phosphate and decreased blood calcium levels

In absence of parathormone, there is decreased

intestinal absorption of dietary calcium and decreased

resorption of calcium from bone and through kidney

tubules

Cli i l M if t ti f


50/78

Clinical Manifestations of

Hypoparathyroidism

Irritability of neuromuscular system Tetanyhypertonic muscle contractions , numbnes,

tingling, cramps in extremities, laryngeal spasm,

bronchospasm, carpopedal spasm ( flexion of the

elbows and wrists, dorsiflexion of the feet), seizures


51/78


Trousseaus signcan check with a BP cuff Chvosteks signtapping over facial nerve causes

spasm of the mouth, nose and eye

Lab studies may reveal calcium levels of 5-6 mg/dL or

lower

Serum phosphate levels will be decreased


52/78

Management of Hypoparathyroidism

Restore calcium level to 9-10 mg/dL May need to give IV calcium gluconate for immediate

treatment

Use of parathormone IV reserved for extreme

situations due to the probability of allergic reactions

Monitor calcium levels

May need bronchodilators and even ventilator

assistance Diet high in calcium and low in phosphorus; thus,

avoid milk products, egg yolk and spinach.


53/78

Management of Hypoparathyroidism

Keep calcium gluconate at bedside Ensure has IV access

Cardiac monitoring

Care of postoperative patients who have undergone

thyroid surgery, parathyroidectomy or radical neck

surgery. Be watchful for signs of tetany, seizures, and

respiratory difficulties


54/78

Adrenals--Pheochromocytoma

Usually benign tumor Originates from the chromaffin cells of the adrenal

medulla

Any age but usu. Between 40-50 years old

Can be familial

10% are malignant

May be associated with thyroid carcinoma or

parathyroid hyperplasia or tumor


55/78

Clinical Manifestations

Headache, diaphoresis, palpitations, hypertension May have hyperglycemia related to excess epinephrine

secretion

Tremors, flushing and anxiety as well

Blurring of vision

Feeling of impending doom

BPs exceeding 250/150 have occurred


56/78


Associated with the 5 Hshypertension, headache,hyperhidrosis, hypermetabolism and hyperglycemia

Urinary catecholamines and metanephrine are direct andconclusive tests

Serum epinephrine and norepinephrine levels will be

elevated Urinary vanillymandelic acid also diagnostic

Must avoid coffee, tea, bananas, chocolate, vanilla andASA, nicotine, amphetamines, decongestants before 24hurine testing

Clonidine suppression testin normal individual, wouldblock catecholamine release

Imaging studies


57/78

Management

Bedrest Elevated HOB

ICU

Nipride

Calcium channel blockers and Beta blockers

Surgical management (manipulation of the tumor can

cause excessive release of catecholamines)

Steroid therapy if adrenalectomy performed Hypotension and hypoglycemia can occur post-op


58/78

Addisons Disease

Adrenocortical insufficiency Autoimmune or idiopathic atrophy

Can be caused by inadequate ACTH from pituitary

Therapeutic use of steroids


59/78

Manifestations

Muscle weakness Anorexia

Dark pigmentation

Hypotension

Hypoglycemia

Low sodium levels

High potassium levels

Can result inAddisonian crisis


60/78

Addisonian crisis

Circulatory shock Pallor, apprehension, weak&rapid pulse, rapid

respirations and low blood pressure

Headache, nausea, abdominal pain and diarrhea

Can be brought on by overexertion, exposure to cold,

acute infection, decrease in salt intake


61/78


Early morning serum cortisol and plasma ACTH areperformed. 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


62/78

Management

Restore circulatory statusfluids, steroids May need antibiotics if infection precipitated crisis

May need lifelong steroid therapy and

mineralocorticoid therapy

May need additional salt intake

Check orthostatics

Daily weights

Aware that stressors can precipitate crises Medic alert bracelet or similar identification of history


63/78

Cushings Syndrome

Results from excessive adrenocortical activity May be related to excessive use of corticosteroid

medications or due to hyperplasia of the adrenal cortex

Oversecretion of corticosteroids can also be caused by

pituitary tumor

Can be caused by bronchogenic carcinoma or other

malignancy

Manifestations of Cushings


64/78

Manifestations of Cushing s

syndrome

Cataracts, glaucoma

Hypertension, heart failure

Truncal obesity, moon face, buffalo hump, sodiumretention, hypokalemia, hyperglycemia, negative

nitrogen balance, altered calcium metabolism Decreased inflammatory responses, impaired wound

healing, increased susceptibility to infections

Osteoporosis, compression fractures

Peptic ulcers, pancreatitis Thinning of skin, striae, acne

Mood alterations


65/78


Overnight dexamethasone suppression test frequentlyused for diagnosis

Administered at 11pm and cortisol level checked at8am

Suppression of cortisol to less than 5mg/dL indicatesnormal functioning

Measurement of plasma ACTH (radioimmunoassay) inconjunction with dexamethasone suppression test helpsdistinguish pituitary vs. ectopic sites of ACTH.

MRI, CT and CT also help detect tumors of adrenal orpituitary


66/78

Medical Management

If pituitary source, may warrant transphenoidalhypophysectomy

Radiation of pituitary also appropriate

Adrenalectomy may be needed in case of adrenalhypertrophy

Temporary replacement therapy with hydrocortisone orFlorinef

Adrenal enzyme reducers may be indicated if source ifectopic 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 Conns


67/78

Primary Aldosteronism or Conn s

Syndrome

Excessive aldosterone secondary to adrenal tumor retain sodium and excrete potassium

Results in alkalosis

Hypertensionuniversal sign of hyperaldosteronism

Inability of kidneys to concentrate the urine

Serum becomes concentrated

Excessive thirst

Hypokalemia interferes with insulin secretion thus willhave glucose intolerance as well


68/78


High sodium Low potassium level

High serum aldosterone level

Low renin level

Aldosterone excretion rate after salt loading is

diagnostic for primary aldosteronism

Renin-aldosterone stimulation test


69/78

Management

Surgical removal of tumor

Correct hypokalemia

Usual postoperative care with abdominal surgery

Administer steroids

Fluids

Monitoring of blood sugar

Control of hypertension with spironolactone


70/78

Corticosteroid Therapy

Hydrocortisone--Cortisol Cortisone--Cortate

Prednisone--Deltasone

Prednisolone-Prelone

Triamcinolone--Kenalog

Betamethasone--Celestone

Fludrocortisone (contains both mineralocorticoid and

glucocorticoid) Florinef


71/78

Indications

RA Asthma

MS

COPD exacerbations

Lupus

Other autoimmune disorders

Dermatologic disorders


72/78

Dosing

Lowest dose Limited duration

Best time to give dose is in early morning between 7-8

am

Need to taper off med to allow normal return of renal

function


73/78

Side Effects of Steroids

Hypertension, thrombophlebitis, acceleratedatherosclerosis

Increased risk of infection

Glaucoma and corneal lesions

Muscle wasting, poor wound healing, osteoporosis,

pathologic fractures

Hyperglycemia, steroid withdrawal syndrome

Moon face, weight gain, acne


74/78

Case Study 1

35 year old male presents with BP of 188/112 at ayearly physical exam. Previous exams noted bloodpressures of 160/94 and 158/92. On questioning,patient admits to twice a month episodes ofapprehension, severe headache, perspiration, rapid

heartbeat, and facial pallor. These episodes had anabrupt onset and lasted 10-15 minutes.

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

What is your impression? What labs would you draw?


75/78

Case Study 2

50 year old woman presents with enlargement of leftanterior 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 hota lot recently.

She is 58 tall and weighs 150#. Heart rate is 110 and

blood pressure is 110/76.

What might be this patients problem?

What lab tests might you draw?


76/78

Case study 3

48 year old woman with a past history of mentalillness presents with a new onset of bizarre psychoticbehavior. She had been well over the past two years.

She is 55 tall and weighs 138#. Her heart rate is 65,irreg and BP is 130/75. Exam is normal except that sheis confused to place, time and year. Patient c/o jointsaching 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?


77/78

Case Study 4

40 year old deeply tanned woman presents with a 6month 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, muscleweakness, 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?


78/78

Case Study #5

27 year old woman presents with depression, insomnia,increased facial fullness and recent increase in acne. Shehad an episode of depression and acute psychosis followinguncomplicated 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 infectionsrecently.

Heart rate is 90bpm, BP is 146/100. Her face is puffy andhas acne vulgaris. Thin extremities and with truncal obesity.

What are your suspicions?

What labs will you draw?

Assessment and Management of Patients With Endocrine Disorders

Documents

Transcript of Assessment and Management of Patients With Endocrine Disorders