metab iv adrenal)

8/2/2019 Metab IV Adrenal)

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Hormones


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Anterior Pituitary Disorders

Acromegaly

Excessive growth hormone (GH)


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Risk factors

None

Etiology

Anterior Pituitary adenoma; abnormalhypothalamic function (rare)

May demonstrate hyperglycemia; inacromegaly, GH level remains increased.


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Diagnostic Procedures

X-ray

x-ray of the skull may show thickening of thebones and enlargement of the nasal sinuses

x-rays of the hands show thickening of the

bones under the fingertips and swelling of thetissue around the bones

Blood Test

The diagnosis is confirmed by blood tests,which usually show high levels of both growthhormone and insulin-like growth factor


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CT Scan

usually done to look for abnormal growths inthe pituitary gland

Because acromegaly is usually present forsome years before being diagnosed, a tumoris seen on these scans in most people.


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Clinical Manifestations

excessive production of growth hormone begins betweenthe ages of 30 and 50, long after the growth plates of thebones have closed

Bones become deformed rather than elongated

Facial features become coarse, and the hands and feetswell

Overgrowth of the jawbone (mandible) can cause the jawto protrude (prognathism).

Cartilage in the voice box (larynx) may thicken, making thevoice deep and husky.

The ribs may thicken, creating a barrel chest.

Joint pain The tongue may enlarge and become more furrowed

Coarse body hair, which typically darkens, increases asthe skin thickens


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The sebaceous and sweat glands in the skin enlarge,producing excessive perspiration and often an offensive bodyodorThe heart usually enlarges, and its function may be so

severely impaired that heart failure occursSometimes a person feels disturbing sensations andweakness in the arms and legs as enlarging tissues compressthe nervesNerves that carry messages from the eyes to the brain may

also be compressed, causing loss of vision, particularly in theouter visual fieldsThe pressure on the brain may also cause severe headaches.irregular menstrual cyclesProduction of breast milk even though not breastfeeding(galactorrhea) because of either too much growth hormone ora related increase in prolactinAbout one third of men who have acromegaly develop erectiledysfunctionLife expectancy is reduced in people with untreatedacromegaly


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Radiation therapy

involves the use of supervoltage irradiation

This treatment may take several years tohave its full effect, however, and oftenresults in later deficiencies of other pituitaryhormones, as normal tissue is often also

affected


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Drug therapy

Also used to lower growth hormone levelsbromocriptine (Parlodel) and other drugs that act likedopamine

somatostatin, the hormone that normally blocks

growth hormone production and secretion octreotide (Sandostatin) which only have to be given

about once a month

These drugs are effective in controlling acromegaly in

many people as long as they continue to be taken(they do not provide a cure)


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Gigantism

excessive secretion of growth hormone duringchildhood, before the closure of the bone

growth plates

excess growth hormone causes overgrowth ofthe long bones and very tall stature.


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Causes

benign pituitary gland tumor If excessive secretion of growth hormone

occurs after normal bone growth has stopped,the condition is known as acromegaly

The vertical growth in height that marks thiscondition is also accompanied by growth inmuscles and organs, which makes the child

extremely large for his or her age. Thedisorder can also delay puberty

Gigantism is very rare


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Manifestations: Excessive growth during childhood

Frontal bossing and a prominent jaw

Thickening of the facial features

Disproportionately large hands and feet with thickfingers and toes

Increased perspiration

Weakness

Secretion of breast milk

Irregular menstruation

Headache

Delayed onset of puberty

Double vision or difficulty with peripheral vision


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Exams and Tests

increase in insulin growth factor-I (IGF-I) levels failure to suppress serum growth hormone (GH)

levels after an oral glucose challenge (maximum 75g)

CT or MRI scan of the head showing pituitary tumor

High prolactin levels Other hormone levels may be low due to damage to

the pituitary, including thyroid hormone, testosterone(boys), stradiol (girls), or cortisol.


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Treatment In pituitary tumors with well-defined borders, surgery is the

treatment of choice and is curative is about 80% of cases. For situations in which surgery cannot completely remove

the tumor, medication is the treatment of choice. The mosteffective medications are somatostatin analogs (such asoctreotide or long-acting lanreotide), which reduce growthhormone secretion.

Dopamine agonists (bromocriptine mesylate, cabergoline)have also been used to reduce growth hormone secretion,but these are generally less effective.

Radiation therapy has also been used to normalize growthhormone levels. However, it can take 5-10 years for the fulleffects to be seen and is almost always associated with

deficiencies in other pituitary hormones. In addition,radiation has been associated with learning disabilities,obesity, and emotional changes in children. Most expertswill use radiation only if surgery and medication fail.


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Possible Complications The development of secondary sexual

characteristics may be delayed.

Surgery and radiation can both lead todeficiencies in other pituitary hormones,causing hypothyroidism, adrenal insufficiency,hypogonadism, and (rarely) diabetes

insipidus.


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Dwarfism

the result of the disproportionate growth of the skeleton.In most cases, dwarfism is genetically determined. We

refer to those affected as "Little People." A dwarf is a person of short stature - under 4 10 as an

adult.

More than 200 different conditions can cause dwarfism.A single type, called achondroplasia, causes about 70

percent of all dwarfism. Achondroplasia is a genetic condition that affects about

1 in 25,000 people. It makes arms and legs short incomparison to the head and trunk. Other geneticconditions, kidney disease and problems withmetabolism or hormones can also cause short stature.

Dwarfism itself is not a disease. However, there is agreater risk of some health problems. With propermedical care, most people with dwarfism have active

lives and live as long as other people


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Etiology

Family history and parent's stature are usually notrelevant to the child's dwarfism.

genetic mutations at the moment of conception random combination of two recessive genes that may

have been dormant for generations


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Signs and Symptoms

In general, the disorders are divided into twobroad categories.

Disproportionare dwarfismProportionate dwarfism


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Disproportionate dwarfism

If body size is disproportionate, some parts ofthe body are small and others are of averagesize or above-average size. Disorders causingdisproportionate dwarfism inhibit the

development of bones.Characteristics: The person has an average-size trunk and very short

limbs, but some people may have a very short trunkand shortened (but disproportionately large) limbs.

The other common characteristic of these disorders isthe head being disproportionately larger than thebody.


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Almost all people with disproportionate dwarfismhave normal intellectual capacities. Rareexceptions are usually the result of a secondary

factor, such as excess fluid in the brain(hydrocephalus).

About 70 percent of all people with dwarfismhave a disorder called chondroplasia, which

causes disproportionately short stature. Thisdisorder usually results in:


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An adult height of approximately 4 feet

An average-size trunk Short arms and legs, with particularly short upper

arms and legs

Short fingers, often with a wide separation between

the middle and ring fingers Limited mobility at the elbows

A disproportionately large head, with a prominentforehead and flattened bridge of the nose

Progressive development of bowed legs (genuvarum) Progressive development of swayed lower back

(lordosis)


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Proportionate dwarfism

A body is proportionately small if all parts of the body

are small to the same degree and appear to beproportioned like a body of average stature.

Proportionate dwarfism results from medicalconditions present at birth or during early childhood

that limit overall growth and development. Therefore,the head, trunk and limbs are all small but of averageproportions relative to each other.

Most of these disorders are uncommon, and signs

and symptoms of the disorders vary greatly. A fewdisorders causing proportionate dwarfism result inmental retardation.


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Growth hormone deficiency is a relativelycommon cause of proportionate dwarfism. It

occurs when the pituitary gland fails toproduce an adequate supply of growthhormone, which is essential for regularchildhood growth. Signs and symptoms

include:Height below the fifth percentile on standardpediatric growth charts

Slowed growth before age 5

Periods of little or no change in height

Adult height usually less than 5 feet

Delayed or no sexual development duringadolescence


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Intervention

The orthopaedic effects of dwarfism requirecomplex reconstructive surgery and extensive

physical therapy. Much like the severeaccident victim, surgery on Little Peopleinvolves bone grafts, fusions, steel screws,pins and plates, then months of physical

therapy to regain even the most basic functionlike walking.


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Nursing Management

Families of Little People sacrifice greatly toimprove the quality of their children's lives.Medical bills, transportation, multiplehospitalizations and operations, and months

spent in casts can take their toll emotionally,economically, and physically on the entirefamily

provide the family with the support they needto endure these trying times, knowing thattheir goals are attainable and worthwhile


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Hypergonadism

A clinical state resulting from enhanced

secretion of gonadal hormones. A condition of increased hormone production

before puberty, which produces precocioussexual development in both sexes.


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Causes

Male: Unknown causes, testicular tumors, andpituitary tumors.

Female: primarily due to idiopathic causes.

Uncommon causes include ovarian andadrenal tumors.

Diagnosis

Confirmed by positive clinical history bloodtesting for evidence of elevated sexhormones.


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Male

Onset of puberty usually occurs around age

13 with Hypergonadism, this development occurs

before age 10

Signs of precocious sexual developmentinclude:

growth of a beard and pubic hair

enlargement of the penis and the testes

Rapid growth of muscle and bone leads to earlyuniting of the epiphyses and a premature stoppageof growth in the long bones.


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Female

In the female, onset of puberty, usually occursaround the age of 10

with hypergonadism, this development occursbefore age 8.

Signs of precocious sexual developmentinclude:

onset of menarche

appearance of pubic and underarm hair

breast enlargement

Ovarian development renders the individual fertile,making pregnancy possible.


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Hypogonadism

condition more prevalent in males in whichthe production of sex hormones and germ

cells are inadequate.


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Boys: Hypogonadism most often shows up as an

abnormality in boys during puberty

Kallmann's syndrome is a birth defect in thebrain that prevents release of hormones andappears as failure of male puberty.

The childhood disease- Mumps, if acquired

after puberty, can infect and destroy thetesticlesa disease called viral orchitis


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Ionizing radiation and chemotherapy, trauma,several drugs (spironolactone, a diuretic andketoconazole, an antifungal agent), alcohol,

marijuana, heroin, methadone, andenvironmental toxins can all damage testiclesand decrease their hormone production.


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Females:

Female problems in puberty are not causedby too little estrogen. Even female

reproductive problems are rarely related to asimple lack of hormones, but rather tocomplex cycling rhythms gone wrong. All theproblems with too little hormone happen

during menopause, which is a normalhypogonadism.


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Manifestations The penis may be small, the testicles undescended

(cryptorchidism) or various degrees of "feminization"of the genitals may be present.

Besides the tissue changes generated by hormonestimulation, the only other symptoms relate to sexualdesire and function. Libido is enhanced bytestosterone, and male sexual performance requiresandrogens. The role of female hormones in female

sexual activity is less clear, although hormonesstrengthen tissues and promote healthy secretions,facilitating sexual activity.


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Treatment:

Replacement of missing body chemicals.

Estrogen replacement is recommended for nearly allwomen after menopause for its many beneficialeffects.

Estrogen can be taken by mouth, injection, or skinpatch. It is strongly recommended that the otherfemale hormone, progesterone, be taken as well,because it prevents overgrowth of uterine lining and

uterine cancer.

Testosterone replacement is available for males whoare deficient


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Posterior Pituitary Disorders

Posterior pituitary dysfunction include specificdisorders involving oversecretion orundersecretion of ADH.

Diabetes Insipidus, caused by undersecretion ofADH, results in excessive dilute urine production.

Syndrome of Inappropriate ADH (SIADH),involving oversecretion of ADH, results inexcessive water conservation.


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Etiology

Diabetes Insipidus

Posterior pituitary destruction of tumors

Vascular accidents

Surgery or hypothalamic damage

Certain drugs that interfere with ADHsecretion or action (e.g., phenytoin, alcohol,

lithium carbonate) Nephrologenic diabetes insipidus, familial or

arising from various renal disorders


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SIADH

Central nervous system disorders

Stimulation due to hypoxia or decreased leftatrial filling pressure

Overuse of vasopressin therapy

Ectopic ADH production associated withsome cancers

Nausea or narcotic use, which can stimulateADH secretion


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Pathophysiology

Diabetes Insipidus occurs when injury to theposterior pituitary gland causes a decrease invasopressin, also known as ADH, secretion oran inability of the kidney tubules to respond toADH.

In SIADH, the basic pathologic disturbancesare excessive ADH activity, with water

retention and dilutional hyponatremia, andinappropriate urinary excretion of sodium inthe presence of hyponatremia.


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Assessment Findings


Diabetes Insipidus

Profoundly increased output (5-20 L/day)

Nocturia

Extreme thristWeight loss

Possible tachycardia, hypotension, andweakness


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SIADH

Decreased urine output

Weight gain

Altered mental status (e.g. headache, confusion,lethargy, seizures, and coma in severehyponatremia)

Delayed deep tendon reflex


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Laboratory and diagnostic study findings

Diabetes InsipidusPlasma osmolality and serum sodium levels areelevated

Water (fluid) deprivation test demonstratesinability of the kidneys to concentrate urinedespite increased plasma osmolality and lowplasma vasopressin level.Vasopressin test demonstrates that the kidneyscan concentrate urine after administration ofADH; this differentiates central (pituitary orhypothalamic) from nephrogenic diabetesinsipidus.


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Nursing Management

Provide general nursing care for diabetesinsipidus and SIADH.

Assess dehydration, skin turgor, and mucousmembranes.

Provide meticulous skin and mouth care.

Monitor serum electrolyte levels, including sodium

and potassium.


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Provide specific nursing care for diabetesinsipidus.

Administer prescribed medications, which

may include ADH replacements. Replace fluids as indicated. Assess for and

report any illness, injury, or other problemthat could prevent adequate fluid intake.

Encourage the client to drink fluids inresponse to thirst. For some unknownreason, the client craves ice cold water.


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Provide specific nursing care for SIADH.Administer prescribed medications, which mayinclude Furosemide (Lasix), to preventconcentration of urine

Regularly assess mental status.


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Thyroid Gland Disorders

Hypothyroidismstate of insufficient serum thyroid hormone

prevalent in persons between 40 and 50 years old

at least twice as common in women as it is in men.


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Manifestations

prolonged jaundice after birth, or dry wrinkled skin, aswollen face and tongue that causes noisy respirationand an open mouth that drools

fingers may be broad, and a small hernia at the bellybutton is quite common

baby is usually listless, slow-moving, constipated, anda slow feeder

older children who develop hypothyroidism suddenlystop growing


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Risk Factor

Age, weight, and medical history

Women are more likely to develop thedisease after age 50; men, after age 60

Obesity

family history

history of high cholesterol levels

autoimmune diseases as lupus, rheumatoidarthritis, or diabetes mellitus


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Etiology

Primary Hypothyroidism results frompathologic changes in the thyroid glandcaused by: Autoimmune thyroids

Thyroidectomy Radioactive iodine therapy Antithyroid medication therapy

Secondary Hypothyroidism results from

failure of the pituitary gland to secreteadequate TSH, possibly because of atumor, surgical removal, or irradiation.


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Laboratory and diagnostic study findings Thyroid function tests reveal decreased T4 and T3

levels

Serum TSH test reveal increased TSH (primary).

Serum antibody tests detects presence of antithyroidantibodies (autoimmune)

Blood studies reveal elevated cholesterol andcreatine phosphokinase


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Pathophysiology

Inability of the thyroid gland to secrete sufficient

amounts of thyroid hormone, (thyroxine regulatessuch essential functions as heart rate, digestion,physical growth, and mental development, aninsufficient supply of this hormone)

1. leads to decreased cellular metabolic activities2. decreased oxygen consumption

3. decreased heat production

these actions produce mild to marked effects in all

organ systems, can slow life-sustaining processes,damage organs and tissues in every part of the body,and lead to life-threatening complications.

Assessment


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AssessmentClinical Manifestations Sluggishness, lethargy, depression, apathy, fatigue,

and exercise intolerance Memory impairment Muscle aches, numbness and tingling of hands Cold intolerance Constipation

Weight gain and decreased appetite Menstrual irregularities, infertility, and decreased

libido Dry skin, brittle nails and dry hair Possible goiter Delay in muscle contraction and relaxation of tendon

reflexes Bradycardia

M d


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Myxedema coma

extreme complication of hypothyroidism in whichpatients exhibit multiple organ abnormalities andprogressive mental deterioration

refers to the swelling of the skin and soft tissuethat occurs in patients who are hypothyroid

Myxedema coma occurs when the body'scompensatory responses to hypothyroidism areoverwhelmed by a precipitating factor such asinfection.

The cardinal manifestation of myxedema coma isa deterioration of the patient's mental status.


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Myedema coma

Hypotension

Hypoventilation

HypothermiaStupor, possibly progressing to coma

N i M t


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Nursing Management

Provide Pharmacotherapy

Administer prescribed medications, which mayinclude T4

Keep in mind that a client with hypothyroidism isvery sensitive to narcotics, anesthetics, and

sedatives; drug degradation is delayed, andrespiratory depression can develop.

Instruct the client and family members orsignificant others in the prescribed medication

regimen, including purpose dosage schedule, andsigns of overreplacement and underreplacement.


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Administer fluids cautiously, because the clientmay not be able to excrete a heavy water load.If the client has hypoglycemia, infuse aconcentrated source of glucose

Provide relief of constipation, as indicated.

Prevent vascular collapse in a hypothermicclient. Refrain from aggressive rewarming.

Institute respiratory assistance whennecessary.

Implement infection-prevention measures.


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Hyperthyroidism

metabolic imbalance resulting from excessivethyroid hormone production

Graves disease- most common form The incidence of Graves disease is greatest

between the ages of 30-40 and is higheramong women than men.


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Etiology

Autoimmune dysfunction is the most commoncause of Graves disease; autoantibodiesapparently mimic TSH, leading tohypersecretion of thyroid hormones.

Genetic factors seem to play a role. Other possible causes include:

Toxic nodular goiter

Exposure to iodine

TSH-secreting pituitary tumor (rare)Thyroiditis, which may be acute, subacute, orchronic (ie, Hashimoto disease)


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Pathophysiology

Excessive secretion of thyroid hormone- leadsto:

increased metabolic rateexcessive heat production

increased responsiveness to catecholamines

these actions lead to profound changes inmany organ systems.


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Assessment Findings


Nervousness, irritability, hyperactivity, emotionalexcitability, and decreased attention span

Weakness, easy fatigability, and exercise

intoleranceHeat intolerance

Weight change (loss or gain) and increasedappetite

Insomnia and interrupted sleepFrequent stools and diarrhea


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Menstrual irregularities and decreased libido

Warm, sweaty, flushed skin with a velvety-smoothtexture and spider telangiectasias

Tremor, hyperkinesias, and Hyperreflexia

Exophthalmos, retracted eyelids, and staring gaze

Hair loss

Goiter

Bruits over the thyroid gland


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Thyroid storm:

Hyperthermia, Hypertension, Delirium,Vomiting and abdominal pain,

Tachyarrhythmias


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Laboratory and Diagnostic Study Findings

Serum thyroid function test reveal increased T4 andT3 levels.

Radioactive iodine uptake test shows an increaseduptake.

Serum TSH assay reveals a nondetectable TSH level.

Thyroid scan reveals increased function (i.e., hotareas) in the thyroid gland.

Nursing Management


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Nursing Management

Administer prescribed medications

Assist the client and family members or significant

others in exploring treatment options. Include familymembers or significant others because the clientsattention span deficit may impair retention ofinformation. Options include:

Pharmacotherapy with drugs that interfere with thyroidhormone synthesis of release

Radioactive iodine therapy permanently limits thyroidhormone secretion by destroying thyroid tissue.Hypothyroidism, requiring lifelong replacement therapy

usually develops at some point after this treatment.Surgery (subtotal or total thyroidectomy). The thyroidlevels must be lowered preoperatively to prevent thyroidstorm; lifelong replacement therapy may be necessary.


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Prevent Injury

Maintain Normothermia


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Provide post-operative care, if appropriate.Support the head and avoid tension on sutures.

Monitor for complications and intervene asindicated. Hemorrhage requires the nurse to assess the

surgical dressing and sides and back of neck forbleeding.


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Parathyroid Gland Disorders

Hyperparathyroidism

overproduction of PTH, resulting in high bloodcalcium levels and bone demineralization

may be primary or secondary Primary hyperparathyroidism is a common

condition, usually occurring after age 60 andaffecting women more often than men.


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Etiology

Primary HyperparathyroidismAbout 80% of cases are linked to a single

adenoma of the parathyroid gland; the remainingcases are caused by parathyroid hyperplasia.

Secondary hyperparathyroidism results from anadaptive increase in PTH secretion associated

with problems involving chronic hypocalcemia.

Assessment Findings


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Assessment Findings


Although hyperparathyroidism may beasymptomatic, it may produce the followingsigns and symptoms:

Fatigue, muscular weakness, and listlessness

Height loss and frequent fracturesRenal calculi

Anorexia, nausea, abdominal discomfort, andconstipation

Memory impairment

Polyuria and polydipsia

Back and joint pain

Hypertension


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Laboratory and Diagnostic Study Findings Total and ionized serum calcium levels are elevated

Serum and phosphate levels are decreased

Urinalysis identifies hypercalciuria andhyperphosphaturia

Radiograph or bone densitometry detects bonedemineralization

PTH levels are elevated Parathyroid scan possibly detects abnormal findings


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Nursing ManagementProvide preoperative care.Prepare the client for surgical treatment of primaryhyperparathyroidism, which ,may includeadenoma removal and hyperplastic gland

resection.Force fluids to prevent dehydration, constipation,and kidney stone formation.Reduce added calcium by eliminating over-the-counter antacids, which may contain calcium;thiazide diuretics, which interfere with renalcalcium excretion; and excessive intake of dairyproducts.


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Provide postoperative care, which is similar tothat for thyroidectomy.

As indicated, provide aggressive calciumsupplementation after surgery to compensate

for hungry bone syndrome. Observe the client

for symptoms of hypercalcemia (e.g., nausea,vomiting, headache, mental confusion,anorexia).

Assess for renal calculi; report hematuria orflank pain as necessary.


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Take measures to protect the client frominjury.

Assist with the activities of daily living and

ambulation as necessary.Encourage weight bearing to reducecalcium loss from the bones.

Teach strategies to minimize falls, which

may lead to fractures.


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Provide relief of constipation as indicated; prunejuice, stool softeners, physical activity, andincreased fluids help prevent constipation.

Monitor nutritional status, and intervene asnecessary. Advise the client to avoid a diet withrestricted or excess calcium.

Reinforce the health care follow-up scheduled.


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Hypoparathyroidism

PTH deficiency characterized by

hypocalcemia, hyperphosphatemia, andneuromuscular hyperexcitability.


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Etiology iatrogenic, caused by accidental removal of or

trauma to parathyroid glands during thyroidectomy,parathyroidectomy, or radical head or neck surgery.

autoimmune genetic dysfunction (affects more

women than men). A reversible form may be associated with

hypomagnesemia, which interferes with PTHsecretion.

A Fi di


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Assessment Findings


Anxiety and irritability

Numbness, tingling, and cramps in extremities

Dysphagia

Photophobia Evidence of neuromuscular hyoerexcitability,

such as positive Chvostek and Trousseausigns, carpopedal spasms, bronchospasms,

laryngeal spasms, arrhythmias, andconvulsion


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Laboratory and diagnostic study findingsTotal and ionized serum calcium levels are low.

Serum phosphate level is elevated.

Serum PTH level is low.

Nursing Management


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Administer prescribed medications, which includecalcium and vitamin D supplements.

Intervene for lie-threatening tetany as indicated.

Administer intravenous calcium gluconateto prevent calcium depletion.

Be alert for possible laryngeal spasm andresulting respiratory obstructions; keep atracheostomy set available.

Institute seizure precautions. Providepadded side rails and bite block at

bedside.Minimize environmental stimuli.

After the crisis resolves, closely monitorcalcium levels. Keep intravenous calcium

gluconate in the clients room.


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Provide care in chronic hypoparathyroidism.

high calcium and low phosphorus diet

Milk, milk products, and egg yolks must beavoided because they are high in phosphorus.

Administer vitamin D and magnesiumsupplementation, as indicated. In clients

receiving magnesium, observe for symptoms ofhypermagnesemia (i.e., hypotension, respiratorydepression, muscle weakness, and confusion.)

Administer oral calcium preparations to

supplement the diet.


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Provide client and family teaching about themedication regimen, including purpose,dosage schedule, and signs and symptoms ofhypocalcemia and hypercalcemia. Inform theclient that the dosage will be adjustedperiodically based on the laboratory findings.

Adrenal Glands Disorders


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Adrenal Glands Disorders

Cushing Syndrome involves excessive production of

adrenocortical hormones, primarily cortisol but

also androgens and mineralocorticoids. Theincident is higher in women than in men.


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Etiology

The most common cause of CushingSyndrome is bilateral adrenal hyperplasia (i.e.,Cushing disease).

Other causes include: Adrenal adenomas and carcinoma

Ectopic ACTH production by tumors in otherorgans, such as the lungs and pancreas.

Glucocorticoid therapy

Assessment Findings

Clinical Manifestations depend on the


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Clinical Manifestations depend on theadrenocortical hormones involved and mayinclude:

Weight gain and altered fat distribution (e.g., centralobesity with round [moon] face and buffalo hump.

Muscle weakness, proximal muscle wasting, and fatigue

Frequent infections and poor wound healing

Symptoms of hyperglycemia Mental status changes and mood swings

Menstrual disturbances, such as amenorrhea

Diminished libido

Skin changes, such as striae, bruises, acne, andthinning of scalp hair

Hypertension

Hirsutism

Susceptibility to compression fractures

Edema


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Laboratory Findings Serum potassium level is decreased.

Serum glucose level is elevated.

WBC count reveals depressed eosinophiland lymphocyte counts.

Diurnal variation plasma levels revealelevated plasma cortisol and 24-hour urine

cortisol results.


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Results for the 24-hour urinary free cortisollevel and 24-hour urine collection for 17-

hydrocorticosteriods and 17-ketosteroids areelevated.

Selected radiographic and axial CT studiesmay determine the site if ectopic ACTH

production

N i M t


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Nursing Management

Administer prescribed medications, which mayinclude adrenocortical steroid inhibitors.Take measures to protect the client from injuryand infection.

Assess skin integrity regularly. Avoid agents that can damage skin (e.g., tape,

strong soaps) Promote good hygiene. Modify the environment to remove or minimize

hazards.


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Prepare the client for surgery, if indicated. Keep in mindthat any treatment modality can cause temporary

adrenal insufficiency. Procedures may include:Adrenalectomy, if the cause is adrenaladenoma

Transsphenoidal hypophysectomy, if the cause

is pituitary adenomaTumor resection

Encourage the client and family to ask questions andverbalize concerns about disease pathology, body

image, treatment, and mental status.


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Addison disease

a primary adrenal hypofunction due tohyposecretion of adrenal cortex hormones.


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Etiology

Addison Disease can result from:

An autoimmune process

Hemorrhage into the adrenal gland

Adrenalectomy

Neoplasm

Fungal infection

Tuberculosis


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Assessment Findings

Clinical Manifestations Addison disease

Gastrointestinal complaints such as anorexia,nausea, vomiting, abdominal pain, and diarrhea

Fatigue, muscle weakness, and arthralgias Decreased alertness and confusion

Weight loss

Dry skin, decreased body hair, and possible

increased pigmentation with excessive ACTHstimulation


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Addisonian (adrenal) CrisisHypotension

Rapid, weak pulse

Rapid respiratory rate

Pallor and extreme weakness

Hyperthermia


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Laboratory and Diagnostic Study Findings Suggestive Findings

Serum blood glucose is decreased.

Serum sodium level is decreased.

Serum potassium level is increased.

WBC cell count is increased.

Definitive Findings

Serum cortisol levels are decreased.ACTH stimulation test reveals a low to normalcortisol response.

N i M t


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Nursing Management

Administer prescribed medications, whichmay include glucocorticosteroids andmineralocorticosteroids.

Provide immediate treatment for an

addisonian crisis. Treatment includesintravenous fluid, glucose, and electrolytes.Corticosteroid replacement andvasopressors may be administered. The

client must avoid exertion.


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Help prevent adrenal crisis. Instruct the client to take precautions to

avoid unnecessary activity and events that

may be stressful. Ensure that hospitalized, acutely ill clients

on a long-term glucocorticoid therapyreceive additional doses to compensate for

stress.


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Provide client and family teaching.

Discuss hormone therapy, including its purpose,side effects, duration, symptoms of abnormalities toreport to health care manager, and the need toinform all health care providers about the steroid

replacement therapy. If overreplacement of glucocorticoids is indicated,

inform the client about the purpose of therapy andpossible side effects, such as cushingoidappearance, weight gain, acne, hirsutism, peptic

ulcer, diabetes mellitus, osteoporosis, infection,muscular weakness, mood swings, cataracts, andhypertension.


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Pheochromocytoma a tumor that is usually benign and originiates

from the chromaffin cells of the adrenal

medulla.


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peak incidence is ages 20-50 years 10% of the tumors are bilateral; 10% are

malignant

stimulates hypersecretion of catecholamines(epinephrine and norepinephrine)

SNS overactivity causing the five Hs:

hypertension, headache, hyperhidrosis,

hypermetabolism, hyperglyclemia

Diagnostic Exams


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Total Plasma Catecholamine Concentration

the client should lie supine and rest for 30minutes

butterfly needle is inserted 30 minutes beforeblood specimen is collected (to prevent elevation

of catecholamine levels by the stress ofvenipuncture)

normal values:Epinephrine: 100 pinogram/ml (590 pmol/L)

Epinephrine: 100 to 550 pinogram/ml (590-3240pmol/L)


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Clonidine Suppression Test

Clonidine (Catapress) a centrally actingadrenergic blocker suppresess the release ofcatocholamines.

in pheochromocytoma, clonidine does not

suppress the release of catecholamines Normal response: 2-3 hours after a single oral

dose of clonidine, the total plasmacatecholamine value decreases at least 40%

from the clients baseline.


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CT scan, MRI, and Ultrasound to localize the pheochromacytoma


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Collaborative Management

Medical Management Bed rest, head of bed elevated during episode

of hypertension, tachycardia, and anxiety toprovide orthostatic decrease in BP.

Pharmacologic therapy

Phentolamine (Regitine)

Sodium Nitroprusside (Nipride) to lower BP quickly


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Surgery Adrenalectomy

Removal of single glands requires

corticosteroid therapy for the first few days orweeks postoperatively

Bilateral removal requires lifetimecorticosteroid therapy


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Nursing Management Teaching the Client Self-Care

Emphasize the importance of periodic follow-up

care.Provide instructions on corticosteroid therapy.

Teach the client and family on how to measure theclients BP.


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End of Chapter!

metab iv adrenal)

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