Hypoparathyroidism: Nursing

Hypoparathyroidism: Nursing

NUR 229 module IV

NUR 229 module IV

Diabetes insipidus: Nursing process (ADPIE)
Syndrome of inappropriate antidiuretic hormone (SIADH): Nursing process (ADPIE)
Hypothyroidism: Nursing process (ADPIE)
Hyperthyroidism: Nursing process (ADPIE)
Thyroid nodules and thyroid cancer: Pathology review
Increased intracranial pressure (ICP): Nursing
Acute kidney injury (AKI): Nursing process (ADPIE)
Dialysis care: Nursing
Chronic kidney disease (CKD): Nursing
Hyperpituitarism: Nursing
Hypopituitarism: Nursing
Hyperparathyroidism: Nursing
Hypoparathyroidism: Nursing
Hypernatremia
Medications for thyroid disorders: Nursing pharmacology
Medications for growth hormone disorders: Nursing pharmacology
Medications affecting the parathyroid glands: Nursing pharmacology
Cushing syndrome and Cushing disease: Nursing
Glucocorticoids and mineralocorticoids: Nursing pharmacology
Adrenal insufficiency (Addison disease): Nursing
Physical assessment - Neurological system: Nursing
Head injury: Nursing
Traumatic brain injury: Pathology review
Spinal cord injury (SCI): Nursing
Brain tumors: Nursing
Physical assessment - Cranial nerves: Nursing
Meningitis: Nursing process (ADPIE)
Encephalitis: Nursing
Shock - Neurogenic: Nursing
Brown-Séquard syndrome: Year of the Zebra
Guillain-Barré syndrome: Nursing
Hyponatremia
Endocrine system anatomy and physiology
Anatomy of the thyroid and parathyroid glands
Medications for antidiuretic hormone (ADH) disorders: Nursing pharmacology
Thyroid hormones
Thyroid eye disease (NORD)
Cortisol
Hyperkalemia
Hydrocephalus: Nursing process (ADPIE)
Epidural and subdural hematoma: Nursing
Altered level of consciousness (LOC): Nursing

Notes

HYPOPARATHYROIDISM

KEY POINTS
NOTES
DEFINITION
  • Low parathyroid hormone (PTH)

PHYSIOLOGY
  • PTH produced by parathyroid glands
  • PTH maintains calcium within range
    • Low calcium
      • PTH increases
      • Increase bone resorption
      • Increase gut absorption
      • Increase kidney reabsorption
    • High calcium
      • PTH decreases
      • Increased deposition in bone
      • Increased excretion from kidney

CAUSES AND RISK FACTORS
  • Causes
    • Any condition that damages parathyroid glands
      • Iatrogenic
      • Thyroidectomy
      • Autoimmune destruction
      • Functional causes
      • Idiopathic
  • Risk factors
    • Neck surgery or radiation therapy
    • Injury to neck
    • Family history of parathyroid disorder or autoimmune disease

PATHOPHYSIOLOGY
  • PTH levels fall below normal
  • Bone resorption, vitamin D activation, and calcium reabsorption inhibited
    • Hypocalcemia
  • Neurons become more excitable

SIGNS AND SYMPTOMS
  • Associated with hypocalcemia
  • Photophobia
  • Mental status changes
  • Tetany
  • Paresthesia
  • Bronchospasm
  • Laryngospasm
  • Arrhythmias
  • Chvostek sign
  • Trousseau sign

DIAGNOSIS
  • History
  • Physical assessment
  • Laboratory tests

TREATMENT
  • Long-term
    • Oral calcium supplements
    • Oral vitamin D
  • Short-term
    • IV calcium
    • Treat complications

MANAGEMENT OF CARE
  • Goals of care
    • Prevent complications
    • Provide supportive care
  • Assess vital signs and signs of hypocalcemia
  • Review laboratory results
  • Ensure emergency equipment at bedside
    • Notify HCP
      • Dyspnea
      • Stridor
  • Assess cardiac status
    • Report to HCP
      • Arrhythmias
      • Hypotension
  • Monitor for signs of hypocalcemia
  • Monitor for neurological irritability
    • Institute seizure precautions
    • Report to HCP
      • Seizure activity
  • Administer calcium gluconate as prescribed
    • Ensure antidote available
  • Ensure patent IV access
    • Monitor for extravasation
  • Monitor calcium levels

PATIENT AND FAMILY TEACHING
  • Explain condition, plan of care, and how to safely self-administer medications
  • Eat diet high in calcium and low in phosphorus; avoid foods with oxalic acid
  • Report to HCP
    • Signs of hypocalcemia

Transcript

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Hypoparathyroidism is a condition characterized by low blood parathyroid hormone, or PTH for short, which ultimately results in hypocalcemia, or low blood calcium levels, as well as hyperphosphatemia, or high blood phosphate levels.

Now, PTH is produced by four small glands called the parathyroid glands. These glands lie in the neck, being stuck to the back surface of the thyroid gland. The main function of PTH is keeping the levels of calcium within the normal range. For example, when calcium levels are low, PTH boosts bone resorption, which causes the release of calcium and phosphate from the bone into the bloodstream. In addition, PTH activates vitamin D, which in turn increases calcium and phosphate absorption from the gut. PTH also stimulates calcium reabsorption and phosphate excretion from the kidney. On the other hand, high calcium levels cause the secretion of PTH to fall, which increases the deposition of calcium in bones and the excretion of calcium by the kidneys.

Alright, now hypoparathyroidism can be caused by anything that damages the parathyroid glands. The most common cause is iatrogenic where surgery or radiation therapy for another condition also injures the parathyroid glands. Thyroidectomy is a good example since when a part of the thyroid is removed, the parathyroids will often be removed or damaged also. Hypoparathyroidism may also be caused by autoimmune destruction mediated by autoantibodies. Next, there are the functional causes like hypomagnesemia where the parathyroid glands will function poorly when magnesium level is low. However the glands are not damaged, so when hypomagnesemia is corrected, the hypoparathyroidism will resolve. Finally, hypoparathyroidism can be idiopathic, meaning that the cause is unknown.

Now, risk factors of developing hypoparathyroidism include neck surgery or radiation therapy; and serious injury to the neck, like during a car crash or by strangulation; as well as a family history of parathyroid disorder or autoimmune diseases.

Regardless of the underlying cause and type of hypoparathyroidism, when PTH levels fall below normal, they result in inhibition of bone resorption, as well as vitamin D activation, and calcium reabsorption from the kidneys. These changes add up to finally cause hypocalcemia, as well as hyperphosphatemia.

Now, many organs and tissues throughout the body depend on normal calcium levels to function properly. This is especially important in nerve transmission in the heart, muscles, and brain. As a result, hypocalcemia makes the neurons more excitable.

Okay, so in clients with hypoparathyroidism, signs and symptoms are typically associated with hypocalcemia. These can include photophobia, as well as mental status changes, which can range from anxiety, irritability, and confusion to psychosis, and in severe cases, even seizures. In addition, the increased neuromuscular excitability may result in tetany, which is characterized by involuntary muscle contractions leading to severe muscle cramps, most often involving the hands and feet, but severe cases can even involve the respiratory muscles, leading to difficulty breathing; clients with hypocalcemia can also present with paresthesia, or a feeling of tingling or numbness, typically around the mouth or in the hands and feet. In addition, hypocalcemia may lead to bronchospasm, laryngospasm, and even cardiac arrhythmias. Finally, hypocalcemia may manifest as two clinical signs; Chvostek sign and Trousseau sign. A positive Chvostek sign describes an ipsilateral contraction of facial muscles upon percussing the facial nerve; whereas a positive Trousseau sign describes an involuntary contraction of the muscles in the hand and wrist upon compressing the upper arm with a blood pressure cuff.

The diagnosis of hypoparathyroidism starts with history and physical assessment, followed by laboratory tests showing decreased blood levels of PTH, hypocalcemia, and hyperphosphatemia, as well as hypomagnesemia, and vitamin D deficiency, in addition to increased urine levels of cyclic adenosine monophosphate, or cAMP for short.