Week 2, 3, & 4 – Endocrine Problems
PITUITARY GLAND
 Posterior pituitary hormones
o Anti-diuretic hormone: promotes water
retention in kidney tubules
 Anterior pituitary hormones
o Growth hormones (GH): promotes
growth by stimulating protein anabolism
and fat mobilization
o Adrenocorticotropic hormone (ACTH):
promotes development and secretion in
the adrenal glands
o Thyroid stimulating hormone (TSH): stimulates the synthesis and secretion of
target hormones
DISORDERS OF THE ANTERIOR PITUITARY GLAND
GROWTH HORMONE EXCESS
 Excess growth hormone production
 Stimulates growth of bones and soft tissue
 Excess production after epiphyseal plates close
 Overproduction
o Usually caused by a benign adenoma in the brain
o In ADULTS  will cause hyperglycemia through insulin antagonism and
mobilization of glucose and free fatty acids
MANIFESTATIONS
 Gigantism  in childhood
 Acromegaly  in adulthood
o Enlargement and thickening of hands and feet
o Enlargement of bony and soft tissue on face and head with skin changes
o CV changes due to hyperglycemia
o 3 P’s of hyperglycemia  polydipsia, polyphagia, polyuria
o Can lead to oral/pharyngeal changes and sleep apnea
o Can get increased intracranial pressure  neuro changes =
o * Physiologic changes cannot be reversed *
DIAGNOSTIC STUDIES
 History and physical
 Serum GH test  blood test
 Glucose tolerance test
 MRI to identify tumor or CT
 Ophthalmologic changes
MANAGEMENT
 Surgery  excision of adenoma and/or hypophysectomy (surgical removal of pituitary
gland)  transsphenoidal (across sphenoid sinus)
 Radiation  secondary treatment plan when surgery is not successful
o Also used preoperatively
 Drug therapy  medications to reduce GH levels as primary treatment or adjunct
o Octreotide is most common (reduces GH)
o Does not take away the tumor
CONCERNS OF SURGERY
 *** Infection
o *** Increased ICP from swelling
o *** Place in high fowlers
o If ICP causes brain herniation  severe medical emergency
 *** Leaking CSF
o Test for glucose  CSF has glucose, snot does not
o Halo effect  will see a circle of RBC on the tissue dressing
NURSING PROCESS
 Assessment
o Assess for symptoms of abnormal tissue growth and evaluate changes in physical
size
 Implementation
o Pre and post op care
o Nothing in the nose
o No blowing the nose
 Acute intervention
o Knowledge about surgical interventions
o Pre-operatively  nose drops, mouth care and breathing, pain control, activity
o Post-operatively  analgesia, **neurological checks, hormone replacement
(lifelong ADH, cortisol, and thyroid hormone needed)
o Complications

Testing CSF leaks for glucose

Diabetes insipidus (DI)

Syndrome of inappropriate antidiuretic hormone (SIADH)
POSTERIOR PITUITARY GLAND PROBLEMS
 Antidiuretic hormone (ADH): produced in response to low fluid status
o Works with renin, angiotensin, and aldosterone
 Syndrome of inappropriate antidiuretic hormone (SIADH)  over production or oversecretion of ADH
 Diabetes insipidus  underproduction or under-secretion of ADH
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)
 Occurs when low ADH is released despite NORMAL or LOW plasma osmolarity with
DECREASED urine output
 Still producing ADH when not needed
 Causes:
o *** Malignant tumors of the lungs
o Head injuries, CV injuries, Guillain-Barre syndrome
o Positive pressure ventilation
PATHOPHYSIOLOGY
 ** Serum osmolarity should be 285-295 mmol/kg***
ASSESSMENT
 General manifestations of fluid volume excess
 Clinical manifestations:
o Headache
o Weight gain without edema
o Progressive altered level of
consciousness – can get seizures
o Small amounts of amber coloured
urine – because kidneys are retaining
the water
o Dilutional hyponatremia
DIAGNOSTICS
 High urine osmolarity and high specific
gravity (1.005-1.030)
 Low serum osmolarity
 Decreased Hct, Hgb, BUN, and serum sodium
 Water load test: send a bolus of 0.9 NaCl 
less than 50% of fluid bolus excreted and
urine does not become more dilute
o Fluid bolus does not dilute the urine
COLLABORATIVE MANAGEMENT

Treat the cause

Stop meds that stimulate ADH release

Restore normal fluid volume and osmolality GRADUALLY
o Mild (Na >125)  fluid restriction, loop diuretics (watch for hypokalemia)

Normal sodium 135-145
o Severe (Na <120) and/or seizures present:

Hypertonic (3-5%) saline given SLOWLY on an IV pump  must be
prepared by pharmacy

Sodium level cannot be corrected too quickly because it will cause
fluid to shift again

Fluid restriction to 500cc a day

Watch for signs of cerebral swelling  headaches, altered LOC
NURSING MANAGEMENT

VS, I&O, *** daily weight  tells fluid volume status

Urine specific gravity  should be 1.003-1.005

Signs of hyponatremia

Heart and lung sounds – Indicative of overload (S3, crackles)

*** Head of bed flat or at 10°  enhances venous return  gets picked up by
baroreceptors  decreases ADH production

Seizure precautions  pad bed rails

Oral hygiene (very dry)
MEDICATION MANAGEMENT

IV hypertonic saline (3%)

Demeclocycline (declomycine) – antibiotic, phenytoin (Dilantin) – antiseizure, or lithium
may be used to inhibit the action of ADH on the renal tubules
o Need to watch people taking lithium for bipolar very frequently because its
causes increased output

Diuretics (furosemide) to eliminate excessive fluid

K+ replacement may be necessary due to loop diuretics
DIABETES INSIPIDUS

Polyuria, polydipsia, NO POLYPHAGIA

Group of conditions associated with deficiency of production or secretion of ADH or
decreased renal response to ADH

Results from excessive loss of water caused by hyposecretion of ADH OR the kidney’s
ability to respond to ADH (unable to retain water)

*** Subsequent polyuria (4-30L in 24 hours) can lead to severe dehydration if the client
does not replace the lost water

CENTRAL DIABETES INSIPIDOUS: usually caused by damage to pituitary gland or
hypothalamus from surgery, tumour, illness (ex: meningitis), inflammation, or head
injury
o Damage disrupts normal production, storage, and release of ADH

NEPHROGENIC DIABETES INSIPIDOUS: occurs as a result of a defect in the kidney
tubules
o Making ADH but unable to respond to it
o This makes the kidneys unable to respond to ADH
o Defect may due to inherited disorder or a common kidney disorder
o Can occur with lithium and tetracycline
NURSING ASSESSMENT

Main assessment
o Excretion of LARGE quantities of urine (520L/day) with very low specific gravity
(<1.005) and low urine osmolarity (<100
mOsm/kg)
o Elevated serum osmolality (>295 mOsm/kg)

Signs and symptoms
o Polydipsia, polyuria, fatigue, weight loss, constipation
o Hypotension, tachycardia, hypovolemic shock
o May have signs of hypernatremia  seizures, coma
DIAGNOSTIC TESTS

Serum sodium > 145 mEq/L

Elevated BUN

Elevated serum osmolality > 295
mOsm/L

HCT elevated

Increased urine output +++

Vasopressin test  give synthetic ADH
(vasopressin) to see if UO decreases
o if it does decrease, you can
confirm it is DI

Water deprivation test
o Pre-test weight, serum, and
osmolality
o Measurements reported hourly until urine osmolality exceeds 800 mOsm/L or
5% of body weight is lost or urine specific gravity does not increase
COLLABORATIVE MANAGEMENT

Assess high-risk patients, monitor for:
o I&O, daily weights
o Specific gravity
o Monitor electrolytes
o Neurologic checks for signs and symptoms of cerebral edema/increased ICP
o Assessment for signs and symptoms of pulmonary edema  ex: crackles


In case the increased fluid leads to overload
Correct fluid volume deficit
o Use hypotonic solutions (.45% NS or dextrose 5%)
o Rate of volume replacement determined by volume of urine output and
insensible losses

Administer exogenous ADH replacement for central DI
o Vasopressin/desmopressin  synthetic ADH
o Frequent fluid and electrolyte monitoring is suggested

Administer ADH potentiator as prescribed for nephrogenic DI
o Chlorpropamide stimulate the release of ADH from pituitary gland and enhances
its effect at the renal tubule
o Thiazide diuretics (helps renal tubules respond to ADH) and sodium restriction
o NSAIDs  improves response to ADH

Monitor for complications
o Coma
o Hypovolemic shock
o Thromboembolism due to increased osmolarity of the blood

Risk for pulmonary embolism
DISORDERS OF THE THYROID GLAND
HYPERTHYROIDISM

Excessive secretion of thyroid hormone from the thyroid gland leading to increased:
o BMR, cardiovascular, GI, and neuromuscular function, weight loss and heat
intolerance, thyroid hormone affects metabolism of facts, carbs, and protein
ETIOLOGY & PATHOPHYSIOLOGY

Increased synthesis and release of thyroid hormones

*** Grave’s disease  most common

Toxic nodular goiters (enlargements)

Pituitary tumours  effects release of TSH

Thyroid cancer

Thyroiditis

Excessive dose of supplemental thyroid hormone

Excessive levothyroxine

Precipitating factors
o Insufficient iodine supply  thyroid
needs certain amount of iodine

Thyroid will enlarge and overproduce thyroid hormones
o Infections  inflammation
o Stressful life events interacting with genetic factors
o Grave’s disease accounts for 75% of cases

Antibodies are developed to the TSH receptor

May progress to destruction of thyroid tissue  lead to hypothyroidism
GRAVE’S DISEASE

Autoimmune disease of unknown etiology

Diffuse thyroid enlargement and excessive thyroid hormone secretion

Excessive T3, T4, and free T4
DIAGNOSTIC TESTS

Elevated serum T3, T4, and free T4  through blood test

Decreased TSH
o If problem is in the thyroid, TSH will be low

Positive RAI uptake scan (from nuclear medicine)
o Scan thyroid, take blood and mix with RAI, then re-scan the gland
o Looking for how much iodine is up taken
o Enlargement  will uptake a lot more

Thyroid scan
NURSING ASSESSMENT

Exophthalmos
o Impaired drainage from orbit increasing fat and edema in retroorbital tissues
o Eyeballs forced outward or protrude
o Corneal surfaces become dry and irritated
o Need to sit up to encourage drainage

Cardiovascular system
o Systolic hypertension
o Increased CO
o Arrythmias (tachycardia at rest)

Can lead to atrial fibrillation
o Cardiac hypertrophy

GI system – everything is sped up
o Increased appetite, thirst
o Weight loss
o Diarrhea
o Splenomegaly
o Hepatomegaly

Integumentary system
o Warm, smooth, moist skin
o Thin, brittle nails and hair
o Hair loss
o Clubbing of fingers
o Diaphoresis
o Vitiligo (like MJ)

Musculoskeletal assessment
o Fatigue
o Muscle weakness
o Proximal muscle wasting
o ** Dependent edema (sacral area)
o Osteoporosis

Nervous system
o Fine tremors
o Insomnia
o Lability of mood, delirium  calm to manic very fast
o Inability to concentrate

Reproductive system
o Menstrual irregularities
o Amenorrhea
o Decreased libido, impotence
o Gynecomastia in men  breast development
o Decreased fertility

Intolerance to heat

Increased sensitivity to stimulant drugs  no caffeine

Elevated basal temp  low-grade fever due to increased BMR
COLLABORATIVE MANAGEMENT

Drug therapy
o Antithyroid drugs – propylthiouracil (PTU) and methimazole (Tapazole)

Inhibit synthesis of thyroid hormones

Improvement begins in 1-2 weeks

Continued 6 months to a year
o Iodine – Lugol’s solution

Useful with other antithyroid drugs in preparation for thyroidectomy or
treatment of crisis

Large doses rapidly inhibit the synthesis of T3 and T4 and block their
release into circulation
o Beta-adrenergic blockers  treat the HTN and HR – slow HR down (does not
treat the thyroid)

Symptomatic relief of thyrotoxicosis resulting from beta-adrenergic
receptor stimulation

Metoprolol (Lopressor) or Propanol (Inderal) administered with other
antithyroid agents

Used in conjunction with other antithyroid medications
o Radioactive Iodine Therapy (RAI)

Damages or destroys thyroid tissue

Delayed response 2-3 months

Treated with antithyroid drugs and beta-blocker before and during first 3
months of RAI


May cause dryness and irritation of mouth and throat

Can lead to hypothyroidism

Cannot be around pregnant women or children
Surgical therapy
o Indicated for those

Unresponsive to drug therapy

With large goiters causing tracheal compression  can lead to airway
obstruction

With possible malignancy (cancer)
o Prep for thyroidectomy

Teach DB&C

Instruct client to hold hands behind the neck

Instruct client on self-administration of prescribed anti-thyroid
medications (PTU, iodine) prior to surgery

PTU will inhibit release of thyroid hormones  if not, all
hormones will get dumped in blood and cause a thyroid storm

Iodine will reduce vascularity  risk for thyroid storm and
hemorrhage
o Take radioactive iodine with a straw so that it does not
damage teeth
o Minimally invasive therapy  endoscopic thyroidectomy

Appropriate for small modules with no malignancy

Less scarring, pain, and recovery time
o Subtotal thyroidectomy

Removal of significant portion of the thyroid

90% removed to be effective

If too much removed, regeneration will not occur  leads to
hypothyroidism

Need to monitor parathyroids  they control calcium
o Postoperative care

Pain control

Administer non-salicylate antipyretics as prescribed for fever

Monitor for hemorrhage  check behind neck for bleeding

Protect incision

Promote patent airway  monitor hoarseness, consider tracheostomy

Prevent tetany  low calcium (damaged parathyroid) can compromise
airway from muscle rigidity and tight vocal cords


Chvostek sign  tap facial nerve – twitching

Trousseau sign  BP cuff inflated – hand cramping

** RR does not accurately tell patency of airway
Assess for laryngeal nerve damage
COMPLICATIONS

Thyrotoxic crisis (Thyroid storm)
o Acute, rare condition where all manifestations are heightened
o Life-threatening emergency
o Presumed causes  infection, trauma, manipulation of thyroid gland
o Manifestations

Severe tachypnea

Shock

Hyperthermia

Restlessness, agitation, seizure

Abd pain, N, V & D

Coma
o Treatment and therapy

Reduce thyroid hormone levels and clinical manifestations

Therapy aimed at fever reduction, fluid replacement, and management of
stressors

Can give high dose iodine to reduce thyroid hormone levels
HYPOTHYROIDISM
ETIOLOGY & PATHOPHYSIOLOGY

Results from insufficient circulating thyroid hormone

Can be primary or secondary (pituitary)

May also be transient to thyroiditis

Discontinuation of thyroid hormone therapy

Primary hypothyroidism
o Congenital defects
o Hashimotos disease (opposite to Grave’s)  autoimmune process in which
thyroid antibodies and lymphocytes destroy thyroid tissue
o Thyroiditis  due to a bacterial or viral infection

Secondary hypothyroidism
o Outside of the gland (ex: pituitary tumour)

In post thyroidectomy patients and those with known hypothyroidism, secondary
hypothyroidism results from inadequate medication therapy

Iodine deficiency is the most common cause worldwide and is most prevalent in iodinedeficient areas

In places where iodine intake is adequate, the primary cause in the adult is atrophy of
the gland  *** very common in older adults
CLINICAL MANIFESTATIONS

Depends on the length of time and severity of the lack of thyroid hormone

The thyroid gland gradually enlarges forming a goiter in an attempt to secrete more
thyroid hormone  thinks it will make more hormones if it is bigger
DIAGNOSTIC TESTS

Decreased T4 and free T4

Normal T3 initially

Increased TSH levels  to make more thyroid hormone

Elevated cholesterol and triglycerides, anemia, and increased creatinine kinase

Primary  problem in thyroid gland  not producing enough thyroid hormone 
pituitary senses this and produces more TSH

If TSH goes up after injections of TRH, the problem is in the hypothalamus
o TRH normally made by hypothalamus  if injection of TRH causes increases in
TSH, it is clear that the problem is that the hypothalamus is not making TRH
o TRH tells the pituitary to produce more TSH  TSH goes to the thyroid gland
NURSING ASSESSMENT

Health history
o Changes in BP
o Anemia
o Family history of CHF, thyroid disorders
o Immigration from area deficient in iodine
o Arrythmias  atrial fibrillation

Cardiovascular system
o Increased capillary fragility
o Decreased rate and force of contraction
o Cardiac hypertrophy, distant heart sounds
o Anemia
o Tendency to develop CHF, angina, and MI  because of
high cholesterol and triglyceride levels

Integumentary system
o Dry, thick, inelastic, cold
o Thick, brittle nails
o Dry, sparse, coarse hair
o Pallor
o Myxedema – puffy face

when proteins and other substances accumulate in the interstitial space,
interstitial fluid increases, causing myxedema


Symptoms include change in composition of dermis and other tissues
Nervous system
o
NS signs often missed because they resemble aging
o Apathy
o Lethargy, fatigue, slowed mental status
o Forgetfulness
o Hoarseness
o Slow, slurred speech
o Stupor, coma
o Anxiety and depression

Reproductive system
o Prolonged menstrual periods or amenorrhea
o Decreased libido
o Infertility
NURSING ASSESSMENT

Increased susceptibility to infection

***Sensitivity to narcotics, barbiturates, anesthesia  careful of dosing because of the
inability to break down (need less than normal)

Cold intolerance

Goiters
COLLABORATIVE MANAGEMENT

Administer replacement hormones
o Give medication in morning one hour before food intake or two hours after
o Levothyroxine (Synthroid)  must be in the morning – when BMR is highest


Must be careful of interactions (ex: calcium supplements)

Must take with water for absorption
Provide comfort measures
o Adjust environment with blankets
o Shivering unnecessarily increases O2 consumption

Evaluate cardiac and nutritional status
o Encourage intake of 2000cc of water daily (if no CHF) and a high fibre diet

Keep alert for life-threatening complications  ex: myxedema coma

Client education
o Thyroid preparations potentiate the effects of some common drug groups

Antidepressants

Digitalis compounds

Anticoagulants  check INR
COMPLICATIONS

Myxedema coma
o Can be precipitated by infection, drugs, cold, or trauma – due to stress
o Characterized by subnormal temperature, hypotension, and hypoventilation
o Mental sluggishness
o Drowsiness
o Lethargy that progresses gradually or suddenly to impairment of consciousness
of coma
o ABC  support airway, breathing, and circulation
o Acute intervention

Client with myxedema coma often requires mechanical respiratory
support and cardiac monitoring

Administer thyroid hormone replacement therapy and other meds IV

Monitor core temp as client is often hypothermic

Assess vitals, I&O, and visible edema
PARATHYROID GLANDS

The sole purpose of the parathyroid glands is to control serum calcium within a range of
2.25-2.74

Works independently of other glands

Increase in PTH = increase in calcium, decreased in PTH = decrease in calcium

As blood filters through, they detect how much calcium is present and release
parathyroid hormone accordingly
HYPERPARATHYROIDISM

Increased levels of parathyroid hormone (PTH)

Causes increased serum calcium levels

REMEMBER  “moans, groans, stones, and bones, and psychological overtones” = high
serum calcium
ETIOLOGY/PATHOPHYSIOLOGY

Causes:
o Primary  parathyroid gland tumor – in the gland itself
o Secondary  compensatory response to other disease states that cause
hypocalcaemia – outside the gland

Vit D deficiency, chronic renal failure
o Tertiary  hyperplasia of parathyroid glands, loss of negative feedback –
continued release


Kidney transplant patients
Result:
o Hypercalcemia and hypophosphatemia – calcium and phosphate move in the
opposite direction

Increased bone resorption (calcium coming out of bones)  osteoporosis

Hypercalciuria  calculi

Increased GI absorption
CLINICAL MANIFESTATION

Same as hyperglycemia:
o Muscle weakness, pathological fracture
o Constipation
o Emotional disorder
o Fractures
o Kidney stones

Complications:
o Severe osteoporosis, fractures
o Renal failure and kidney stones
o Cardiac dysrhythmias
DIAGNOSTIC TESTS

PTH levels

Elevated serum calcium levels > 2.75 mmol/L

Low serum phosphate levels < 0.9 mmol/L

24-hour urine – hypercalciuria

CT, MRI, to find adenoma
NURSING MANAGEMENT

Collaborative care:
o Surgery  most effective for primary and secondary – 95% success rate

Leads to rapid reduction of Ca levels
o Nonsurgical treatment – for non-surgical candidates

Dietary measures

Phosphorus supplements

Fosamax, Evista, Actonel  for treatment of osteoporosis

Should stay upright after taking dose
o Post-op monitoring  hemorrhage (check behind the neck), signs and symptoms
of hypocalcaemia (Chvostek and Trousseau)
o Give IV fluids to lower calcium levels
HYPOPARATHYROIDISM
ETIOLOGY AND PATHOPHYSIOLOGY

State of decreased parathyroid hormone production or activity

Very uncommon

Most common cause  iatrogenic (caused by improper treatment)
o Damage to vasculature during neck surgery
o Damage or removal at time of thyroid or parathyroid surgery
o Congenital
SIGNS & SYMPTOMS

Same as low serum calcium
o Hyperexcitability of nervous system

Tetany, muscle spasms, laryngospasms

Tingling of lips and fingers

Chvostek’s and Trousseau’s signs

Anxiety
DIAGNOSTICS

Decreased serum calcium and PTH levels

Increased serum phosphate levels
NURSING MANAGEMENT

Collaborative care:
o Treat acute hypocalcaemia with IV

SLOW calcium infusion (through central line) with EKG monitoring
o Long term management

Vit D and calcium

Possible magnesium

Rocaltrol, calciferol

High calcium diet
DISORDERS OF THE ADREANAL GLAND

Adrenal Cortex:
o Hyperfunction  Cushing syndrome
o Hypofunction  Addison’s disease

Adrenal Medulla
o Pheochromocytoma

ACTH comes from pituitary and stimulates adrenals to produce corticosteroids
CUSHING’S SYNDROME
ETIOLOGY AND PATHOPHYSIOLOGY

Caused by excess of corticosteroids, particularly glucocorticoids

Most common cause  iatrogenic (HC administered) administration of exogenous
corticosteroids
o Ex: prednisone  used for Addison’s, RA, lupus, transplant

85% of endogenous (inside body) is due to ACTH-secreting pituitary
tumors

Other causes  adrenal tumours and ectopic ACTH production by
tumours outside hypothalamic-pituitary-adrenal axis

Key feature  moon face
CLINICAL MANIFESTATIONS

Hyperglycemia  bc of glucocorticoids (may need insulin)

Protein wasting  can cause swelling

Loss of collagen  thin tissue, can bruise easily

Delayed wound healing  from hyperglycemia

Mood disturbances  labile moods

Insomnia, irritability, psychosis

Seen more commonly in adrenal carcinomas:
o Women  menstrual disorders and hirsutism (hair
growth on face and body)
o Men  gynecomastia and impotence

Purplish red striae on abdomen, breast, or buttocks  changes in tissue from excess
cortisol

Can get hypokalemia
DIAGNOSTIC STUDIES

Plasma cortisol levels may be elevated with loss of diurnal variation

CT and MRI are used for tumor localization

24-hour urine for free cortisol

Other findings but not diagnostic of Cushing’s
syndrome:
o Agranulocytosis  low WBC (risk for
infection)
o Lymphopenia
o Eosinopenia
o ***Hyperglycemia
o Glycosuria  spilling glucose into urine
o Hypercalciuria
o Osteoporosis  calcium comes out of bones

Hypokalemia and alkalosis seen in ectopic ACTH syndrome and adrenal carcinoma

Plasma ACTH may be low, normal, or elevated depending on the problem

High or normal ACTH levels indicate ACTH-dependent Cushing’s disease

Low or undetectable ACTH levels indicate adrenal or exogenous etiology
COLLABORATIVE MANAGEMENT

Ectopic ACTH-secreting tumours managed by treating primary neoplasm

Drug therapy indicated when surgery is contraindicated

Goal is inhibition of adrenal function

Medications to suppress cortisol secretion by the adrenal cortex
o Mitotane

Suppresses cortisol production


Alters peripheral metabolism of cortisol

Decreases plasma and urine corticosteroid levels
Medications that inhibit cortisol synthesis
o Metyrapone
o Ketoconazole
o Aminoglutethimide

Cortisol replacement therapy post-operatively
o Radiation therapy to the pituitary gland
o Single or bilateral adrenalectomy

If developed during use of corticosteroid:
o Gradually discontinue
o Reduction of dose
o Conversion to alternate day regimen – helps keep hypothalamus-pituitaryadrenal system awake
o Avoids potentially life-threatening adrenal insufficiency
NURSING MANAGEMENT

Wear medic-alert bracelet at all times

Avoid exposure to stress, extremes of temp, and infections  requires different dose
o Body cannot increase cortisol on its own in response to stress

If their body needs extra, they cannot create that
o Increase steroid for dental procedures (physiological stressor)
o If steroid is not increased, it can lead to Addisonian crisis
ADDISON’S DISEASE
ADRENOCORTICAL INSUFFICIENCY

Primary cause  Addison’s disease – in pituitary

Secondary cause:
o Lack of pituitary ACTH secretion
o Outside of the gland
ETIOLOGY AND PATHOPHYSIOLOGY

All 3 classes of adrenal corticosteroids are decreased in Addison’s disease
o Glucocorticoids
o Mineralocorticoids – ex: aldosterone
o Androgens

Infarction

Fungal infections

AIDS

Metastatic cancer

Iatrogenic Addison’s
o May be due to adrenal hemorrhage
CLINICAL MANIFESTATIONS

does not become evident until 90% of adrenal cortex is destroyed

slow onset

Progressive weakness, fatigue, weight loss, anorexia

Skin hyperpigmentation
o Areas exposed to sun
o Pressure joints, over joints, in creases
o Bronze skin
NURSING ASSESSMENT

Orthostatic hypotension

Hyponatremia and hyperkalemia  LIFE THREATENING
o Hyponatremia because of the aldosterone – losing sodium

Nausea and vomiting

Secondary adrenocortical hypofunction
o Signs and symptoms common with Addison’s – lack hyperpigmentation

Risk for life-threatening Addisonian crisis

Severe manifestations of glucocorticoid and mineralocorticoid deficiencies
o Hypotension, tachycardia  shock
o Dehydration
o Hyponatremia

Circulatory collapse  often unresponsive to usual treatment

Low blood volume  blood vessels constrict to increase BP  diverts blood flow away
from GI tract

GI manifestations  severe vomiting, diarrhea, abd pain

Pain in lower back or legs
DIAGNOSTIC STUDIES

Subnormal levels of cortisol

Levels fail to rise over basal levels with ACTH stimulation test

Abnormal lab findings
o *** hyperkalemia, hyponatremia, hypoglycemia
o Urine levels of cortisol are low
o Anemia
o Increased BUN  dehydration

ECG
o Peaked T waves from hyperkalemia

CT, MRI
o Localize tumours or identify calcifications
or enlargement
COLLABORATIVE MANAGEMENT

Hydrocortisone  most commonly used replacement therapy

Glucocorticoid dosage must be increased during times of stress to prevent Addisonian
crisis

Treatment directed at:
o Shock management  large volumes of NS and D5 are administered to reverse
hypotension and electrolyte imbalances

High dose hydrocortisone replacement IV
NURSING MANAGEMENT

Acute intervention
o Assess VS and signs of fluid and electrolyte imbalances every 30-40 minutes to 4
hours for the first 24 hours
o Take daily weight
o Administer corticosteroid therapy diligently – on time
o Protect against infection

Medications
o Mineralocorticoids given once in the morning
o Glucocorticoids given once in the morning

2/3 given in the morning  when cortisone goes up

1/3 given later in the day
o Long-term care includes need for:

Extra medication

Stress management

Teach signs and symptoms of corticosteroid deficiency and excess

Carry emergency kit with IM hydrocortisone, syringes, and instructions for use
PHEOCHROMOCYTOMA
ETIOLOGY AND PATHOPHYSIOLOGY

Rare condition

Tumor of the adrenal medulla

Excessive production of catecholamines  epinephrine and norepinephrine

Causes:
o Adrenal gland tumor
o Drugs that inhibit catecholamine reuptake – tricyclic antidepressants and cocaine

Results in severe HTN from vasoconstriction
o If untreated, may lead to:

Diabetes mellitus

Cardiomyopathy

Death
CLINICAL MANIFESTATIONS

Clinical features include:
o Severe episodic HTN > 200 mmHg
o Severe, pounding headache
o Tachycardia with palpitations
o Profuse sweating
o Abdominal or chest pain – heart is working very hard

Diagnosis is often missed  syndrome comes and goes
DIAGNOSTIC STUDIES

Measurement of urinary catecholamine metabolites (metanephrines) in a 24hr urine
collection  most reliable

Measure plasma catecholamine

CT, MRI to localize tumours
COLLABORATIVE MANAGEMENT

Surgical removal of tumour

CCBs (ex: nifedipine) to control BP and help with angina

Sympathetic blocking agent may decrease BP and decrease symptoms of catecholamine
excess

BBs to decrease dysrhythmias, BP, and angina

Monitor BP closely

Make client as comfortable as possible

Monitor glucose