Endocrine system

You might also like

Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 9

HYPOTHYROIDISM

DEFINITION
Hypothyroidism is a disorder in which thyroid gland is underactive and does not produce or
release enough thyroid hormones or thyroxin.
Classification
The types of hypothyroidism are classified according to their causes:
 Central hypothyroidism- There is a failure of the pituitary gland,
the hypothalamus, or both to stimulate production of thyroid hormones.
 Primary hypothyroidism - in primary hypothyroidism, the thyroid gland cannot
produce adequate amounts of thyroid hormone
 Secondary or pituitary hypothyroidism- The cause is entirely a pituitary
disorder in secondary hypothyroidism.
 Tertiary or hypothalamic hypothyroidism-This refers to the cause as a disorder of
the hypothalamus resulting in inadequate secretion of TSH due to decreased
stimulation of TRH.
CAUSES
 Inflammation of the thyroid gland, which damages the gland’s cells.
 Autoimmune diseases. The most common cause of hypothyroidism in adults is
autoimmune thyroiditis or Hashimoto’s disease.
 Atrophy of the thyroid gland. (The thyroid gland shrinks in size as a result of aging.)
 Radioactive iodine and thyroidectomy could also cause hypothyroidism.
 Medications such as lithium, iodine compounds, and antithyroid medications could
decrease the production of TSH.
 Iodine deficiency or excess- The imbalance in the iodine levels in the body also
affects the thyroid gland.
 Autoimmune or Hashimoto’s thyroiditis, in which the immune system attacks the
thyroid gland, is the most common example of this.
 Radiation of head , neck for treatment of head and neck cancers
INVESTIGATION
Physical examination -Typical clinical findings of hypothyroidism on examination may
include: Dry skin, Bradycardia, Cold peripheries, Stiff muscles, Hair loss, Hertoghe’s sign-
Hertoghe’s sign (also called Queen Anne’s sign), the loss of the outer third of the eyebrow, is
a rare sign of hypothyroidism.

Thyroid function tests- TSH, T3, T4


Thyroid antibodies. Results of testing by immunoassay techniques for antithyroid antibodies
are positive in Hashimoto’s thyroiditis
Medical Management
The primary objective in the management of hypothyroidism is to restore a normal metabolic
state by replacing the missing hormone.
 Pharmacologic therapy. Synthetic levothyroxine is the preferred preparation for
treating hypothyroidism and suppressing nontoxic goiters.
 Prevention of cardiac dysfunction
 Supportive therapy. Oxygen saturation levels should be monitored; fluids should
be administered cautiously; application of external heat must be avoided, and oral
thyroid hormone therapy should be continued.
Nursing Assessment
 Assessment of the thyroid from an anterior or posterior position.
 Auscultation of the lobes of the thyroid gland using the diaphragm of
the stethoscope if there are abnormalities palpated.
 Assess thyroid gland for firmness (Hashimoto’s) or tenderness (thyroiditis).
 Monitor the lab values
 Monitor the temperature
 Monitor respiratory rate, depth and rhythm
 Proper cardiac monitoring
 Monitor the serum cholesterol levels
Nursing Interventions
Promote rest. Space activities to promote rest and exercise as tolerated.
Protect against coldness. Provide extra layer of clothing or extra blanket.
Avoid external heat exposure. Discourage and avoid the use of external heat source.
Mind the temperature. Monitor patient’s body temperature.
Increase fluid intake. Encourage increased fluid intake within the limits of fluid
restriction.
Provide foods high in fiber.
Manage respiratory symptoms. Monitor respiratory depth, rate, pattern, pulse
oximetry, and ABG.
Maintain patent airway
Pulmonary exercises. Encourage deep breathing, coughing, and use of incentive
spirometry.
Orient to present surroundings. Orient patient to time, place, date, and events around
him or her.
Administer the medication as per doctor order
Provide emotional support
Avoid use of hypnotics, sedatives and analgesics agent
Diagnosis
 Activity intolerance related to fatigue and depressed cognitive process.
 Risk for imbalanced body temperature related to cold intolerance.
 Constipation related to depressed gastrointestinal function.
 Ineffective breathing pattern related to depressed ventilation.
 Disturbed thought processes related to depressed metabolism and altered
cardiovascular and respiratory status.
HYPERTHYROIDISM

DEFINITION
Hyperthyroidism is a hyperthyroid state resulting from hypersecretion of thyroid
hormones (T3 and T4). Hyperthyroidism is characterized by an increased rate of body
metabolism.
CAUSES
 Graves disease (most common cause of hyperthyroidism)
 Inflammation (thyroiditis) of the thyroid due to viral infections, some medicines, or
after pregnancy (common)
 Taking too much thyroid hormone (common)
 Noncancerous growths of the thyroid gland or pituitary gland (rare)
CLINICAL FEATURES
. The presenting symptoms are
 Anxiety
 Irritability
 More talkative
 Thin fine hair/hair loss
 Anxiety
 Hoarseness of voice
 Rapid heart rate (tachy cardia), palpitation and increased pulse pressure
 hypertension
 Progressive weight loss
 More appetite
 Muscle weakness
 tremors
 Skin warm to touch, flushed continuously with a characteristic of salmon color
 Inability to tolerate hot
 Diarrhoea
 Rapid breathing
 Anxiety
 Protrusion of eye balls (exophthalmos)
 insomnia
Patients with well developed hyperthyroidism exhibit a characteristic group of signs and
symptoms some time referred to as Thyrotoxicosis or thyroid storm. is a sudden
worsening of hyperthyroidism symptoms that may occur with infection or stress. Fever,
decreased mental alertness, and abdominal pain may occur. Immediate hospitalization
is needed.
DiagnosticEvaluation

 Thyroid-stimulating hormone (TSH) assay reveals a decrease in result


 Elevated Thyroxine (T4)
 Elevated Tri-iodothyronine (T3)
 Other Tests: 24-hr radioactive iodine uptake; thyroid autoantibodies;
antithyroglobulin; electrocardiogram (ECG)
Management
Medical Management
Treatment is directed toward reducing thyroid hyperactivity for symptomatic relief and
removing the cause of complications. Three forms of treatment are available:
Radioactive Iodine (131I)
131
 I is given to destroy the overactive thyroid cells (most common treatment in the
elderly).
 123I also have destructive effects on the thyroid gland
131
 I is contraindicated in pregnancy and nursing mothers because radioiodine crosses
the placenta and is secreated in breast milk.
Pharmacotherapy
The objective of pharmacotherapy is to inhibit hormone synthesis or release and reduce the
amount of thyroid tissue.
 Propylthiouracil (PTU) an antithyroid agent is given to return the patient to the
euthyroid (normal) state. PTU inhibits use of iodine by thyroid gland; blocks
oxidation of iodine and inhibitis thyroid hormone synthesis
 Methimazole (Tapazole) an antithyroid agent is given to return the patient to the
euthyroid (normal) state by inhibiting use of iodine by thyroid gland.
 Other Drugs: Beta-adrenergic blockers, corticosteroids, radioactive iodine
 Corticosteroids: dexamethasone (Decadron)
 Rationale: Provides glucocorticoid support. Decreases hyperthermia; relieves
relative adrenal insufficiency; inhibits calcium absorption; and reduces
peripheral conversion of T3 from T4. May be given before thyroidectomy and
discontinued after surgery.
 Digoxin (Lanoxin)
 Rationale: Digitalization may be required in patients with HF before [beta]-
adrenergic blocking therapy can be considered or safely initiated.
 Potassium (KCl, K-Lyte)
 Rationale: Increased losses of K+ through intestinal and/or renal routes may
result in dysrhythmias if not corrected.
 Acetaminophen (Tylenol)
 Rationale: Drug of choice to reduce temperature and associated metabolic
demands. Aspirin is contraindicated because it actually increases level of
circulating thyroid hormones by blocking binding of T 3 and T4 with thyroid-
binding proteins.
 Sedative, barbiturates
 Rationale: Promotes rest, thereby reducing metabolic demands and cardiac
workload.
 Furosemide (Lasix)
 Rationale: Diuresis may be necessary if HF occurs. It also may be effective in
reducing calcium level if neuromuscular function is impaired.
 Muscle relaxants.
 Rationale: Reduces shivering associated with hyperthermia, which can further
increase metabolic demands.
 Provide supplemental O2 as indicated.
 Rationale: May be necessary to support increased metabolic demands and/or
O2 consumption.
 Provide hypothermia blanket as indicated.
 Rationale: Occasionally used to lower uncontrolled hyperthermia (104°F and
higher) to reduce metabolic demands/O2 consumption and cardiac workload.
Surgery
Surgical treatment with thyroidectomy is no longer the preferred choice of therapy for
Graves’ disease but is an alternative therapeutic approach in some situations. In particular, it
is used for patients who cannot tolerate antithyroid drugs, have significant ophthalmopathy,
have large goiters, or cannot undergo radioiodine therapy.
Nursing Interventions
 Assess the vital signs, cardiac and respiratory function, ABG analysis and pulse
oximetry
 Provide adequate rest.
 Administer sedatives as prescribed.
 Provide a cool and quiet environment.
 Provide cool baths and cool or cold fluids.
 Obtain weight daily.
 Provide a high-calorie high protein diet.
 Encourage fluid intake
 Avoid the administration of stimulants.
 Administer antithyroid medications (propylthiouracil [PTU]) that block thyroid
synthesis, as prescribed.
 Administer iodine preparations that inhibit the release of thyroid hormone as
prescribed.
 Administer propranolol (INderal) for tachycardia as prescribed.
 Prepare the client for radioactive iodine therapy, as prescribed, to destroy thyroid
cells.
 Prepare the client for thyroidectomy if prescribed.
 Provide for diversional activities that are calming, e.g., reading, radio, television.
 Avoid topics that irritate or upset patient. Discuss ways to respond to these feelings
NURSING DIAGNOSIS
 Risk for Decreased Cardiac Output
 Fatigur related to hypermetabolic state
 Risk for Decreased Cardiac Output related to increased CNS stimulation
HYPERPARATHYROIDISM
DEFINITION
Hyperparathyroidism is a disorder caused by over secretion of parathyroid hormone (PTH) by one or
more of the four parathyroid glands. This disorder can disrupt calcium, phosphate, and bone
metabolism
TYPES OF HYPERPARATHYROIDISM
Hyperparathyroidism is classified into three groups: primary, secondary, or tertiary.
1. Primary hyperparathyroidism (most common type): a problem in which the parathyroid gland
is releasing too much PTH, even though there is enough calcium already in the blood. Most of
the time, this is caused by an adenoma (a non-malignant growth) of the parathyroid gland.
2. Secondary hyperparathyroidism occurs when the glands have become enlarged due to
malfunction of another organ system. Causes of secondary hyperparathyroidism include;
severe deficiency in vitamin D, severe deficiency in calcium, and chronic renal failure.
Chronic renal failure is the most common cause of secondary hyperparathyroidism.
3. Tertiary hyperparathyroidism is seen in dialysis clients who have chronic secondary
hyperparathyroidism. Dialysis clients who suffer from chronic renal failure lack the ability to
absorb and convert vitamin D into a form that can be used by the body. This decline in
vitamin D decreases the amount of calcium that can be absorbed.\
CLINICAL FEATURES
Fatigue
Weakness
Muscle weakness
Nausea
Vomiting
Constipation
Bone pain
Hypertension
Cardiac dysarrhythmias
Irritability and nervousness
Diagnosis
May include: Blood tests to check for calcium, phosphorus, magnesium and PTH levels; bone x-rays;
kidney scans; biopsy.

MEDICAL MANAGEMENT
 Bisphosphonates. Bisphosphonates prevent calcium loss from bones and improve bone
density. Examples of bisphosphonates include etidronate
(Didronel), alendronate (Fosamax®), zoledronicacid (Zometa®) and ibandronate (Boniva®).
 Calcimimetics. Calcimimetics act like calcium in tissues and tell parathyroid glands to
produce less PTH. Providers more often use them to treat secondary
hyperparathyroidism. Cinacalcet (Sensipar®) and etelcalcetide (Parsabiv®) are examples of
calcimimetics.
 Avoiding certain medications. Some medications, like thiazide diuretics and lithium, can
increase calcium levels.
 Dietary changes. provider might recommend getting a certain amount of calcium or vitamin
D through supplements or the foods you eat.
 Treatment for primary hyperparathyroidism is surgical removal of affected parathyroid gland,
 If secondary hyperparathyroidism is related to kidney disease eg nephrologist may
recommend: tic use, which mimics calcium circulating in the blood and may trick the
parathyroid glands into releasing less parathyroid hormone; limit protein intake and take
calcium supplements
 Other causes of secondary hyperparathyroidism require different treatments. eg, avoid foods
containing gluten if secondary hyperparathyroidism is from from celiac disease; take vitamin
D supplements if secondary hyperparathyroidism is from a vitamin D deficiency.
NURSING DIAGNOSIS
Risk for Injury related to bone demineralization and weakness.
Imbalanced Nutrition:
More Than Body Requirements related to increased calcium levels.
Risk for Impaired Renal Function related to potential kidney stone formation.
Knowledge Deficit regarding the management of hyperparathyroidism and hypercalcemia.
Nursing Mangement
Monitoring and Managing Electrolytes: Regularly monitor calcium and PTH levels and
administer medications to control hypercalcemia as prescribed.
Nutritional Support: Provide dietary counseling to manage weight and gastrointestinal
symptoms.
Fluid Management: Encourage adequate hydration to prevent kidney stones and assist in
maintaining kidney function.
Anxiety Reduction: Offer emotional support and counseling, especially for patients
undergoing surgery.

You might also like