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THYROID HORMONES DISORDERS
• Thyroid Hormones• 1. Grave’s Disease = an autoimmune disorder
that causes growth of thyroid and hypersecretion of thyroid hormones, with no negative feedback
• 2. Cretinism = hyposecretion of T3/T4 during fetal life and infancy.
• 3. Myxedema = hyposecretion during adulthood.• 4. Simple goiter: Enlarged thyroid due to low
iodine levels
HYPERTHYROIDISMHYPERTHYROIDISM• Hyperthyroidism
– Etiology/pathophysiology
•Also called Graves’ disease•Grave’s disease-(exopthalmic goiter, toxic diffuse goiter, thyrotoxicosis)- hyperactive thyroid gland, overproduction of T3 and T4.
•Overproduction of the thyroid hormones•Exaggeration of metabolic processes•Causes can be stress, pregnancy, infection, genetic, autoimmune disorder.
•5x more common in women, peak age 30-40.
HYPERTHYROIDISMHYPERTHYROIDISM– Clinical manifestations/assessment
• Edema of the anterior portion of the neck(Thyroid enlargement)• Exophthalmos: (protrusion of eyeballs due to periorbital edema
which can lead to blindness). • Inability to concentrate; memory loss• Hoarseness• Increased appetite• Weight loss• Nervousness: mild to severe• Vitals signs elevatedI(Elevated temperature, Tachycardia;
hypertension)• Dysphagia, hoarseness, jittery, weight loss, intolerance to heat,
profuse sweating, hyperactivity.• Insomnia• Warm, flushed skin• Amenorrhea• Diaphoresis• Hand tremors
HYPERTHYROIDISMHYPERTHYROIDISM– Medical management/nursing interventions
•Medications–Propylthiouracil–Methimazole
•Meds given orally over a long period of time.•Radioactive iodine:Radiation- destroys overactive thyroid cells but permanently hormone secretion.
•Subtotal thyroidectomy•Cool, quiet, non-stressful environment.•Diet- high calorie, vitamins and mineral supplements, high CHO, between meal snacks. Avoid tea and cola.
•Encourage fluids. Assess swallowing functions.
HYPERTHYROIDISMHYPERTHYROIDISM• Treatment continue:
•Protect eyes- patches, eye drops, artificial tears.•Avoid aspirin- will increase hormone.•Surgery- thyroidectomy, removes 5/6 of the thyroid gland; assures prolonged remission. Done if drugs and radiation are ineffective.
•Pre-op- Lugol’s solution; a solution of elemental iodine and potassium iodide in water mix with fruit juice to mask the taste. Main reason- decrease incidence of hemorrhage due to decreased thyroid vascularity(vessels that carry or circulate fluids, such as blood, lymph, or sap, through the body )
HYPERTHYROIDISMHYPERTHYROIDISM• Postoperative
– Check airway patency. Keep neck still, avoid coughing/talking X 48 hrs
– Check voice Q 2-4 hrs- laryngeal nerve may be damaged– Check for bleeding- check dressing (side and back of
neck, top of shoulders) internal and external bleeding.– Voice rest; voice checks( Use written communication.)
– Avoid hyperextension of the neck: Semi-Fowler’s position. Don’t hyperextend neck. Prepare suction machine and tracheostomy set at the bedside.
– Assess for tetany– Chvostek’s and Trousseau’s signs: Signs of
Hypocalcemia:– Assess for thyroid crisis
HYPERTHYROIDISMHYPERTHYROIDISM• Post-op Continue:• Check return of swallowing and
coughing reflex before giving anything by mouth.
• Diet- clear, cool liquid, high calorie.
• Maintain a quiet environment, limit
visitors.• Post-op complications- tetany and
thyroid crisis- due to inadvertent removal of parathyroid glands. Absence of PTH results to hypocalcemia (numbness and tingling of fingers, toes and corners of mouth).
HYPERTHYROIDISMHYPERTHYROIDISM• Post-op complications-• Carpopedal spasms- spasms of wrist
and feet.• Chvostek’s sign- spasms of facial
muscles when facial nerve is tapped. • Trousseau’s sign- carpal spasm
induced by BP cuff.• Hypocalcemia and hypomagnesemia-
can lead to convulsions or cardiac dysrhythmias.
• Laryngeal spasms- due to hypocalcemia, use tracheostomy set.
THYROID CRISIS THYROID CRISIS (THYROTOXICOSIS)(THYROTOXICOSIS)
• Post-op complications-• A rare post-op complication of thyroid surgery Occurs within 12 hours post-op, characterized
by oversecretion of T3 and T4 followed by release of epinephrine.
• Maybe caused by :infection, extreme stress, diabetic ketoacidosis or trauma due to manipulation during surgery.
• S/S: exaggerated signs of hyperthyroidism, fever up to 106 F, tachycardia, severe HTN, n&v, restlessness, delirium, heart failure and death.
THYROID CRISIS THYROID CRISIS (THYROTOXICOSIS)(THYROTOXICOSIS)
• Emergency treatment: IV fluids, sodium iodide, corticosteroids, antipyretics, oxygen, sedatives, cardiotonics.
• Diagnosis:–Thyroid hormone levels–RAUI (radioactive iodine uptake test)- oral
administration of radioactive iodine, then blood level is checked 2,6 and 24 hrs later to measure how much isotope has been removed from the blood stream. Check for allergy, obtain consent, no radiation precaution needed.
THYROID CRISIS THYROID CRISIS (THYROTOXICOSIS(THYROTOXICOSIS))
• Nursing diagnosis:• Hyperthermia, risk for• Nutrition imbalance, less than body
requirements• Swallowing, impaired• Breathing pattern, ineffective• Disturbance in self esteem• High risk for injury
HYPOTHYROIDISM
1. Cretinism = hyposecretion of T3/T4 during fetal life and infancy. 2. Myxedema = hyposecretion during adulthood.
HYPOTHYROIDISMHYPOTHYROIDISM• Thyroid gland secrets
inadequate hormones, caused by disease of the thyroid g. itself (primary) or pituitary condition (secondary) resulting to low TSH resulting to low metabolism.
• Common in women and age group 40-50.
• Causes include: surgery, radiation, tumor.
HYPOTHYROIDISMHYPOTHYROIDISM• Cretinism- congenital
hypothyroidism during infancy and childhood. Total absence of T4.
• S/S usually do not appear until 6-12 wks of age for bottle-fed infants and after weaning for breast-fed.
• S/S include inactivity, retarded physical and mental growth, anemia, thick, dry and mottled skin.
HYPOTHYROIDISMHYPOTHYROIDISM• S/S: children look obese, short
and stocky because skeletal growth is more inhibited than tissue growth.
• Medical management/nursing interventions– Medications
• Synthroid• Levothyroid• Proloid• Cytomel
– Symptomatic treatment
HYPOTHYROIDISMHYPOTHYROIDISM• Myxedema- severe
hypothyroidism in adult.• Affects women 5X more than
men; common age 30-60 y.o.• S/S: low v/s, intolerance to cold,
impaired thought processes, low libido, thin hair, brittle nails, low energy, enlarged facial features, mask-like face, enlarged hands and feet.
• Monitor for signs of angina.• Diagnosis
– Physical exam and history.
– Low T3 and T4, high TSH.
HYPOTHYROIDISMHYPOTHYROIDISM
• Treatment:– Hormone replacement (Synthroid, Levothyroid,
Cytomel) PO in AM. Dose gradually increase until desired dose is acquired. Taken for the rest of patient’s life
– Regulate room temperature.
– Monitor/ prevent constipation- use stool softeners, increase fluids, high fiber diet, high protein, low calorie diet. Adequate iodine intake (iodized salt, fish, milk, eggs).
DISORDERS OF THE THYROID AND
• Simple goiter– Etiology/pathophysiology
• Enlarged thyroid due to low iodine levels• Enlargement is caused by the accumulation of colloid in the thyroid follicles
• Usually caused by insufficient dietary intake of iodine• Goiter- visible swelling of the neck. • Toxic goiter- swelling + hyperthyroidism
– Clinical manifestations/assessment
• Enlargement of the thyroid gland• Dysphagia• Hoarseness• Dyspnea
– Medical management/nursing interventions
• Potassium iodide• Diet high in iodine• Surgery—thyroidectomy
SIMPLE GOITERCONTINUE:
• Endemic (iodine-deficient) goiter- geographic areas with low iodine supply (Great Lakes). Also called simple or colloidal.
• Swelling is the result of thyroid g. compensation due to low iodine supply. May result to tracheal compression if severe.
SUMMARY(THYROID HORMONES DISORDER)
1.Cretinism = hyposecretion of T3/T4 during fetal life and infancy.
a. dwarfism & mental retardation;
b. prevention = newborn testing;
c. treatment = oral thyroid therapy.
2. Myxedema = hyposecretion during adulthood.
a. edema, slow heart rate, low body temp, dry hair & skin, muscular ,weakness, lethargy, weight gain;
b. Oral thyroid hormones reduce symptoms.
3. Grave’s Disease = an autoimmune disorder that causes growth of thyroid and hypersecretion of thyroid hormones, with no negative feedback.
a. enlarged thyroid (2-3x larger);
b. peculiar edema of the eyes (bulging);
c. treatment = surgical removal, use of radioisotopes to destroy some of the thyroid. and anti-thyroid drugs to block synthesis of the hormones.
4. Simple goiter: Enlarged thyroid due to low iodine levels
Medical management: Iodine Diet.
THYROID THYROID TUMORSTUMORS
LETS WATCH THIS
THYROID TUMORSTHYROID TUMORS• Cancer of the thyroid
– Etiology/pathophysiology
•Malignancy of thyroid tissue; very rare
– Clinical manifestations/assessment
•Firm, fixed, small, rounded mass or nodule on thyroid
– Medical management/nursing interventions
•Total thyroidectomy•Thyroid hormone replacement• If metastasis is present: radical neck dissection; radiation, chemotherapy, and radioactive iodine
TYPES OF THYROID CANCER
• There are four types of thyroid cancer, and some are more common than others.– Papillary and/or mixed papillary/follicular ~ 78%
– Follicular and/or Hurthle cell ~ 17%
– Medullary ~ 4%
– Anaplastic ~ 1%
• Thyroid cancer affects women two to three times more than men. Besides what appears to be a hormonal or gender connection, the causes of thyroid cancer are, for the most part, not known.
1. 1. PAPILLARY CANCER • Papillary cancer is the most common type of
cancer, perhaps because papillaries are quite common in the thyroid gland. Papillary cancer mostly involves one side of the thyroid and sometimes spreads into the lymph nodes. The cure rate is very high.
Papillary adenocarcinoma- begins in childhood or early adult, can metastasize to lymph nodes if untreated.
• Family hx and radiation exposure increase risk.
2.2. FOLLICULAR ADENOCARCINOMA
• Follicular cancer, the second most common type of thyroid cancer, is somewhat more malignant than papillary. The thyroid gland is comprised of follicles which produce thyroid hormones that are essential for growth and development of all body tissues. This cancer doesn't usually spread to the lymph nodes, but it may spread to arteries and veins of thyroid gland and more distantly (lung, bone, skin, etc), though that is uncommon. Follicular cancer is more common in older people. Again, the long -term survival rate is high.
• Encapsulated and feels elastic and rubbery..• S/S: swelling, hyperthyroidism.• Dx: needle biopsy, physical exam, ultrasound,
thyroid scan.
FOLLICULAR CANCER CONTINUE:
• Treatment:• SSKI (saturated solution of potassium iodide)-
corrects iodine imbalance by depressing TSH.• Surgery- thyroidectomy
• Post-op interventions: observe for s/s of bleeding (check dressing, shoulders and back of neck). Semi- Fowlers position. Tracheostomy set at bedside.
• High-calorie diet. Instruct patient to minimize talking as much as possible. Teach patient to support neck with his hands to prevent stress on incision
THYROID CANCERTHYROID CANCER
• Complications of surgery: edema, hemorrhage, injury to laryngeal nerve (ask pt. to speak post-op), injury to parathyroids resulting to hypoparathyroidism (numbness and tingling sensation around the mouth, Chvostek’s sign, Trosseous sign, tetany).
• NANDA: Ineffective breathing pattern; impaired swallowing; anxiety; alteration in comfort: pain.
3. MEDULLARY THYROID CANCER
• Medullary thyroid cancer is the third most common type of thyroid cancer, and usually originates in the upper central lobe of the thyroid. It spreads to the lymph nodes earlier than papillary or follicular cancers. It differs from papillary and follicular cancer, however, in that it does not arise from cells that produce thyroid hormone, but instead from C cells. These C cells make the hormone calcitonin. This type of cancer can run in families, and also has a good cure rate.
4. ANAPLASTIC• Anaplastic is the rarest and most serious
thyroid cancer. It can spread early to lymph nodes, thus usually the cause for a visit to the doctor is a mass in the neck. It also is the form of thyroid cancer most likely to spread to other organs beyond the thyroid or lymph nodes. This type of thyroid cancer is more common in those over 65 and in men. Long-term survival rates are far less than for the other three types of cancer.
THYROIDITISTHYROIDITIS• Immune system attacks the thyroid gland.
Maybe acute (bacterial), subacute )viral) or chronic.
• Common in women in their 50’s.• Presents as painful neck swelling lasting 1-2
months then disappears without residual effect.• S/S: symmetrical swelling, pain, overlying skin
is red and warm, dysphagia, irritability, weight loss, chills, fever.
• Tx: aspirin to control inflammation; antibiotics if bacterial.
THYROIDITISTHYROIDITIS• Hashimoto’s disease- chronic thyroiditis in
women 30-50 years old.• Not accompanied by pain or fever. Thyroi
activity is low. Maybe hereditary.• If untreated, could lead to hypothyroidism.• Rx: reduce thyroid size of thyroid and
prevent myxedema- thyroid hormone therapy. Antibiotics, steroids, analgesics.
• Dx: leukocytosis, high T3 and T4• Prognosis: good with compliance with
lifelong meds.
PARATHYROID PARATHYROID DISORDERSDISORDERS
HYPERPARATHYROIDISM– Etiology/pathophysiology
•Overactivity of the parathyroid, with increased production of parathyroid hormone, PTH excess results to hypercalcemia caused by adenoma of the parathyroid gland, or as a response to hypocalcemia caused by Vit. D deficiency or chronic renal failure.
•Hypertrophy of one or more of the parathyroid glands
– Clinical manifestations/assessment
•Hypercalcemia•Skeletal pain; pain on weight-bearing•Pathological fractures•Kidney stones•Fatigue, Drowsiness•Nausea, Anorexia
HYPERPARATHYROIDISMHYPERPARATHYROIDISM• Dx:
– high calcium and low phosphorus serum level.– 24 hr urine specimen- high calcium– Xray- calcium loss from bones– MRI, CT scan- evaluate parathyroid glands for
tumors
• Medical management/nursing interventions– Removal of tumor– Removal of one or more parathyroid glands
• Can result to hypercalcemic crisis which is a life-threatening condition.
HYPERPARATHYROIDISMHYPERPARATHYROIDISM• Treatment:• Surgical removal of parathyroid gland for
primary type• Increased fluid intake, encourage mobility,
limit calcium intake (milk, etc), encourage prune juice and stool softeners.
• NANDA– Activity intolance– Constipation– High risk for injury– Altered nutrition: less than body requirements
HYPOPARATHYROIDISM– Etiology/pathophysiology
• Decreased parathyroid hormone• Decreased serum calcium levels, high phosphate level in the
blood. • Inadvertent removal or destruction of one or more parathyroid
glands during thyroidectomy• Most common cause- inadequate secretion of PTH following
surgical removal of parathyroid glands during thyroidectomy, parathyroidectomy, radical neck dissection or trauma.
– Clinical manifestations/assessment• Neuromuscular hyperexcitability• Involuntary and uncontrollable muscle spasms• Tetany, seizures • Laryngeal spasms• Stridor• Cyanosis• Parkinson-like syndrome• Chvostek’s and Trousseau’s signs
HYPOPARATHYROIDISMHYPOPARATHYROIDISM• Dx:
– Positive Troussau’s or Chvostek’s signs– Hypocalcemia, hyperphosphatemia and bone
calcification in x-rays
• Medical management/nursing interventions– Calcium gluconate or calcium chloride IV– Vitamin D for Ca absorption– Manipulate environment- reduce noise, sudden drafts,
bright lights. Seizure precaution.– Post-op- Ca gluconate IV at bedside, cardiac monitoring– Diet- high calcium, low phosphorus. Limit milk intake due
to its high phosphorus content.– Gelusil, amphogel- given after meals to bind phosphate
and promote excetion thru the GI tract
HYPOPARATHYROIDISMHYPOPARATHYROIDISM
• NANDA• Ineffective airway clearance due to laryngeal
spasm• Self-care deficit r/t cramping• High risk for injury
DISORDERS OF THE ADRENAL
GLANDS
What are adrenal gland disorders?
• What are adrenal gland disorders?
• Adrenal gland disorders occur when the adrenal glands don’t work properly. Sometimes, the cause is a problem in another gland that helps to regulate the adrenal gland. In other cases, the adrenal gland itself may have the problem. The NICHD conducts and supports research on many adrenal gland disorders. Some examples include
Adrenal gland disorders • ADDISON’S DISEASE- Inadaquate amounts of
glucocorticoids and mineralocorticoids• Cushing's Syndrome - Cushing’s syndrome
happens when a person’s body is exposed to too much of the hormone cortisol
• Congenital Adrenal Hyperplasia - Congenital adrenal hyperplasia is a genetic disorder of adrenal gland deficiency
• Pituitary Tumors - The pituitary gland is located in the brain and helps to regulate the activity of most other glands in the body, including the adrenal glands
ADDISON’S DISEASEADDISON’S DISEASELets watch This
• Adrenal hypofunction (Addison’s disease)– Etiology/pathophysiology
• Adrenal glands do not secrete adequate amounts of glucocorticoids and mineralocorticoids
•May result from– Adrenalectomy
– Pituitary hypofunction
– Long-standing steroid therapy
• Addison’s is primary disease- from atrophy, cancer of the adrenal cortex, fungal infection or TB.
• Secondary- adrenalectomy, pituitary hypofunction, long-term steroid therapy
ADDISON’S DISEASEADDISON’S DISEASE– Clinical manifestations/assessment– The symptoms of Addison's disease develop insidiously, and it
may take some time to be recognized. • Related to imbalances of hormones, nutrients, and electrolytes• Nausea; anorexia• Postural hypotension• Headache• Disorientation• Abdominal pain; lower back pain• Anxiety• Darkly pigmented skin and mucous membranes• Weight loss• Vomiting • Diarrhea• Hypoglycemia• Hyponatremia• Hyperkalemia• Assess for adrenal crisis
DX• Routine investigations may show.• Hypercalcemia • Hypoglycemia, low blood sugar (worse in children
due to loss of glucocorticoid's glucogenic effects) • Hyponatraemia (low blood sodium levels), due both
to a deficiency in Aldosterone (a mineralocorticoid) dependant Sodium retention and also the effect of Corticotropin-releasing hormone to stimulate secretion of ADH
• Hyperkalemia (raised blood potassium levels),
ADDISON’S DISEASEADDISON’S DISEASE
Treatment•Restore fluid and electrolyte balance•Replacement of adrenal hormones•Diet high in sodium and low in potassium•In case of Adrenal crisis:IV corticosteroids in a solution of saline and glucose
Treatment• Maintenance• Treatment for Addison's disease involves replacing the missing
cortisol, sometimes in the form of hydrocortisone tablets, or prednisone tablets in a dosing regimen that mimics the physiological concentrations of cortisol. Treatment must usually be continued for life. In addition, many patients require fludrocortisone as replacement for the missing aldosterone. Caution must be exercised when the person with Addison's disease becomes unwell with infection, has surgery or other trauma, or becomes pregnant. In such instances, their replacement glucocorticoids, whether in the form of hydrocortisone, prednisone, prednisolone, or other equivalent, often need to be increased. Inability to take oral medication may prompt hospital attendance to receive steroids intravenously. People with Addison's are often advised to carry information on them (e.g. in the form of a MedicAlert bracelet) for the attention of emergency medical services personnel who might need to attend to their needs.
Adrenal crisis-• Crisis
• 1.Standard therapy involves intravenous injections of glucocorticoids and large volumes of intravenous saline solution with dextrose, a type of sugar. This treatment usually brings rapid improvement.
• 2.When the patient can take fluids and medications by mouth, the amount of glucocorticoids is decreased until a maintenance dose is reached.
ADDISON’S DISEASEADDISON’S DISEASE• Addison crisis- medical emergency-
– fever, cyanosis, shock, pallor, rapid, weak pulse, low BP.
• Primary and secondary forms basically have the same symptoms,Crisis may occur suddenly or gradually
• First sign is darkening of the skin (bronzed skin)• Fatigue, dry skin, n&v, anorexa, tachycardia,
salt craving, postural hypotension, vertigo, severe headache, weight loss, diarrhea, hypoglycemia (may occur 5-6 hrs after eating)
• Dx:• Decreased glucose level, low Na, high K, low
aldosterone,.
ADDISON’S DISEASEADDISON’S DISEASE• Treatment• Adrenal crisis- immediate rx is to combat shock,
restore circulation, give fluids, monitor v/s• Emergency rx- IV corticosteroids and
antibiotics (Florinef- synthetic corticosteroids)• Diet- high Na and CHON, low K• Nursing care: I&O, daily weight, v/s, maintain a
quiet env’t., protect from infection, administer glucocorticoids and mineralocorticoids, increase fluids, 5-6 small meals a day to control hypoglycemia
ADDISON’S DISEASEADDISON’S DISEASE
• Teaching- medications, report any illness to the MD, avoid infection, eliminate stress, medicalert bracelet
• Corticosteroid therapy- anti-inflammatory, anti-stress. Keep BP elevated, maintain glucose level as steroids cause it to increase
ADDISON’S DISEASEADDISON’S DISEASE• May cause pituitary and
adrenal gland suppression and changes in CNS function- such effects maybe disabling or dangerous.
• Dosage frequently altered to avoid untoward effects
• Ardrenal cortex suppression may persist for up to a year after a 2-wk steroid therapy
ADDISON’S DISEASEADDISON’S DISEASE• Adverse effects more likely to occur
with long term therapy: peptic ulcer, osteoporosis, infection, euphoria, mood changes and psychological dependence.
• Nsg. Diagnosis– Infection, risk for– Fluid volume deficit– Altered nutrition, less than body requirements– Activity intolerance– Prognosis- fair with long term therapy
CUSHING’S SYNDROMECUSHING’S SYNDROMELets watch this
Cushing's syndrome• Cushing's syndrome is a hormone disorder caused
by high levels of cortisol in the blood. This can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH) or CRH Cushing's disease refers to one specific cause of the syndrome, a tumor (adenoma) in the pituitary gland that produces large amounts of ACTH, which in turn elevates cortisol. It is the most common cause of Cushing's syndrome, responsible for 70% of cases excluding glucocorticoid related cases
CUSHING’S SYNDROMECUSHING’S SYNDROME• Adrenal hyperfunction; opposite of Addison’s disease• 3x more common in women.• Excess amounts of glucocorticoids,
mineralocorticoids and sex homone• Etiology/pathophysiology
– Plasma levels of adrenocortical hormones are increased– Hyperplasia of adrenal tissue due to overstimulation by the
pituitary gland– Tumor of the adrenal cortex– Adrenocorticotropic hormone (ACTH) secreting tumor
outside the pituitary– Overuse of corticosteroid drugs
CUSHING’S SYNDROMECUSHING’S SYNDROME• S/S- buffalo hump, thin extremities, weight gain,
weakness, delayed wound healing, osteoporosis, female hirsutism, deepened voice, susceptible to infection.
• Clinical manifestations/assessment– Moonface– Buffalo hump– Thin arms and legs– Hypokalemia; proteinuria– Increased urinary calcium excretion– Susceptible to infections– Depression– Loss of libido
CUSHING’S SYNDROMECUSHING’S SYNDROME• Clinical manifestations/assessment
– Ecchymoses and petechiae– Weight gain– Abdominal enlargement– Hirsutism in women– Menstrual irregularities– Deepening of the voice
• DiagnosisDiagnosis• Physical exam, plasma cortisol level, skull x-ray, 24- hr.
urine, CT scan, MRI, ultrasound• Hypokalemia, hyperglycemia, elevated ACTH,
hypernatremia
CUSHING’S SYNDROMECUSHING’S SYNDROME• Medical management/nursing interventions
– Treat causative factor• Adrenalectomy for adrenal tumor• Radiation or surgical removal for pituitary tumors
– Lysodren X 3 months- – Low-sodium, high-potassium diet
• DietDiet- • low Na, low calories, low CHO, • high K• Skin care, I&O, diuretics, Nizoral, Cytadern,
Mitotane
CUSHING’S SYNDROMECUSHING’S SYNDROME• NandaNanda• Activity intolerance r/t weakness and
immobility• Self-care deficits• Impaired skin integrity• Ineffective individual coping
• Prognosis- depends whether the tumor is benign or malignant
pheochromocytoma• A pheochromocytoma or phaeochromocytoma
(PCC)– Etiology/pathophysiology
• Chromaffin cell tumor; usually found in the adrenal medulla• Causes excessive secretion of epinephrine and norepinephrine
– Clinical manifestations/assessment• Hypertension, kidney damage, tachycardia, polyuria,
hyperglycemia, headache, intolerance to heat, tremors, nausea
– Diagnosis• 24 hr urine, MRI, ultrasound, CT scan, IVP
– Medical management/nursing interventions• Surgical removal of tumor
PHEOCHROMOCYTOMAPHEOCHROMOCYTOMA• Tx:• Surgery• Diet without stimulants (coffee, tea)• Vasopressors, corticosteroids replacement
• Nanda:• Activity intolerance• Anxiety and fear
• Prognosis- depends on tumor size and characteristics
Conn's syndrome
HYPERALDOSTERONISM HYPERALDOSTERONISM (CONN’S SYNDROME)(CONN’S SYNDROME)
• Conn's syndrome is an Aldosterone-Producing Adenoma (APA). Conn's syndrome is named after Jerome W. Conn (1907–1994 )
• Hypersecretion of aldosterone by the adrenal cortex; maybe caused by a benign or malignant tumor
• Results to hypernatremia and hypokalemia
• Kidneys unable to concentrate or acidify urine
• S/S:
• Headache, polyuria, polydipsia, HTN, paresthesia, chills, fever, muscle weakness
HYPERALDOSTERONIHYPERALDOSTERONISM (CONN’S SM (CONN’S SYNDROME)SYNDROME)
• Dx:• Low K, high Na, increased urine pH, x-ray,
CT, MRI• Tx:• Surgical removal of the tumor• I&O, diet high in K and low in Na• Spinorolactone- K-sparing diuretic • Regular weights, observe for edema
Adrenalectomy
• Adrenalectomy is the surgical removal of one or both (bilateral adrenalectomy) adrenal glands. It is usually advised for patients with tumors of the adrenal glands. The procedure can be performed using an open incision or laparoscopic technique
ADRENALECTOMYADRENALECTOMY• Maybe performed for Cushing’s syndrome,
Conn’s syndrome that’s caused by a tumor, and pheochromocytoma
• Abdominal or side incision under 12th rib• Protect pt. from infection• Corticosteroids replace hormones no longer
supplied by adrenal glands. No replacement needed if surgery is unilateral
• Maintain serum glucose level• Provide rest, reduce stress
