ANATOMY OF PARATHYROID GLAND

The parathyroid glands are four pea-sized glands located on the thyroid gland in the neck. Occasionally, a person is born with one or more of the parathyroid glands embedded in the thyroid, in the thymus, or located elsewhere around this area. In most such cases, however, the glands function normally.

Though their names are similar, the thyroid and parathyroid glands are entirely different glands, each producing distinct hormones with specific functions. The parathyroid glands secrete PTH, a substance that helps maintain the correct balance of calcium and phosphorus in the body. PTH regulates the level of calcium in the blood, release of calcium from bone, absorption of calcium in the intestine, and excretion of calcium in the urine.

When the level of calcium in the blood falls too low, the parathyroid glands secrete just enough PTH to restore the blood calcium level.

HYPOPARATHYROIDISM

DEFINITION

• Result is form abnormally low PTH levels. The most common cause is damage to or removal of the parathyroid glands during thyroiddectomy. The lack of  circulating PTH causes hypocalcemia and an elevated blood phosphate level.

What is the causes of hypoparathyroidism??

• i) Acquired hypoparathyroidism
• Damage or removal of parathyroid glands. 

• ii) Hereditary hypoparathyroidism
• Parathyroid glands not present at birth or they don't work properly.

• iii) Autoimmune disease
•  Antibodies against the parathyroid tissues.

• iv) Extensive cancer radiation treatment 
•  Face or neck, radioactive iodine treatment for hyperthyroidism.

• v) Low levels of magnesium in blood
• Disturb function of parathyroid glands.

RISK FACTOR OF HYPOPARATHYROIDISM

• Recent neck surgery, particularly if the thyroid was involved
• A family history of hypothyroidism 
• Having certain autoimmune or endocrine conditions, such as Addison's disease

PHATOPHYSIOLOGY 

• Hypoparathyroidism occurs when the body does not have enough circulating parathyroid hormone (PTH) or decrease action of PTH it can either cause a decrease in serum calcium levels (hypocalcemia) and increase in serum Phosphorus levels (hyperphosphatemia) .
• The calcium and phosphorus have a reciprocal relationship in the body.
•  Although the majority of cases of hypoparathyroidism are due to hypocalcemia.

CLINICAL MANIFESTATION OF HYPOPARATHYROIDISM 

• Musculoskeletal system
• Muscle spasms
• Facial grimacing 
• Carpopedal spasms 
• Tetany and convulsions
• Integumentary system 
• Brittle nails 
• Hair loss
• Dry scaly skin
• Gastrointestinal system
• Abdominal cramps
• Malabsorption
• Cardiovascular system
• Arrhythmias
• Central nervous system
• Paresthesias ( lips, hand , feet) 
• Anxiety, depreassion and irritability
• Hyperactive reflexes
• Psychosis 
• Increase intracranial pressure

DIAGNOSTIC TEST 

• Blood test
• Blood elevated serum calcium 
• Increased serum  phosphate
• Elevated PTH levels
• Urine test
•  Elevated urinary cyclic adenosine monophosphate.

TREATMENT FOR HYPOPARATHYROIDISM

Treatment of hypoparathyroidism focuses on increasing calcium levels. Intravenous gluconate is given immediately to reduce tetany. Long term therapy includes supplemental calcium, increased dietary calcium, and vitamin D therapy.

COMPLICATION

• Tetany 
• Cramps like spasms to your hands and fingers may be prolonged and painful.
• Paresthesias
• Characterized by sensory symptoms of add, tingling sensations in the tongue, lips, fingers and feet.
• Loss of consciousness with convulsion 
• Malformation of the teeth 
• Impaired kidney function
• Heart arrhythimias and fainting

NURSING MANAGEMENT

• .      Care of postoperative patients who have undergone thyroidectomy, parathyroidectomy, or radical neck dissection is directed toward detecting early signs of hypocalcemia and anticipating signs of tetany, seizures, and respiratory difficulties.
• .      Calcium gluconate is kept at the bedside with equipment necessary for emergency IV administration. If the patient requiring administration of calcium gluconate has a cardiac disorder, is subject to dysrhythmias, or is receiving digitalis, the calcium gluconate is administered slowly and cautiously.
• .       Calcium and digitalis increase systolic contraction and also potentiate each other; this can produce potentially fatal dysrhythmias. Consequently, the cardiac patient requires continuous cardiac monitoring and careful assessment.

HYPERPARATHYROIDISM

DEFINITION

• Hyperparathyroidism means the parathyroid glands produce too much PTH. this causes blood calcium levels to rise (hypercalcaemia) and blood phosphorus levels to fall (hypophosphataemia).

WHAT ARE THE CAUSES OF HYPERPARATHYROIDISM?

1. Primary Hyperthyroidism 

• i . Single Parathyroid adenoma
• This is the most common cause of primary hyperparathyroidism. There is a benign  (non- cancerous) tumor of one of your parathyroid glands. this causes more parathyroid hormone to be released by the parathyroid gland. 
• ii. Hyperplasia affecting more than one parathyroid gland
• This is most common for most other causes of primary hyperparathyroidism. 
• Hyperplasia means that their is enlargement of a parathyroid gland. It usually affects more than one gland at the same time.

• iii. Parathyroid carcinoma
• Very rarely primary hyperparathyroidism is caused by cancer (carcinoma) in one of the parathyroid glands.

2. Secondary Hyperparathyroidism 

Secondary hyperparathyroidism  is caused by other or disease that are affecting your body.  The raised levels of parathyroid hormone are appropriate due to your low blood calcium level. some cause include

• i. Kidney disease
• Most common cause of secondary hyperparathyroidism. occurs in the person with pro long term kidney dialysis because of kidney failure, because of kidney failure the blood calcium level can be become low and stay low.
• ii. Vitamin D deficiency 
•  Another common cause vitamin D deficiency causes a long-standing  low level of calcium in the blood.
• iii. Gut ( intestinal ) malabsorption.
• These are various disease that can affects your gut and prevent the calcium that you eat from being absorb into your blood . 
• This can cause the blood calcium level to become low and stay low.

3. Tertiary Hyperparathyroidism

• This type of hyperparathyroidism  occurs as a result of prolonged secondary of  hyperparathyroidism. the condition  low blood calcium level and the secondary hyperparathyroidism has been treated.The parathyroid gland continue produce  large amounts of parathyroid hormone.
• This because they start to act by autonomously and are no longer sensitive to the blood calcium level.
• They are not switched off when blood calcium level rises.this result in a high calcium level in your blood.

RISK FACTOR OF HYPERPARATHYROIDISM.

• Family history with hyperparathyroidism 
• Women who has gone through menopause
• Prolonged severe calcium or vitamin D deficiency
• Radiation treatment for cancer that exposed to the neck.
• Kidney disease
• Family history of Multiple Endocrine Neoplasia 

PATHOPHYSIOLOGI OF HYPERPARATHYROIDISM. 

• Hyperparathyroidism are asymptomatic. When symptom occurs, they are related to hypercalcemia and various musculoskeletal, renal and gastriointestinal manifestations. 
• Bone absorption result in pathologic fractures, while elevated calcium level alter neural and muscular activity, leading to muscle weakness and atrophy.
• Proximal renal tubule function is altered, and metabolic acidosis , renal calculi formation , and polyuria occur.  

CLINICAL MANISFESTATION OF HYPERPARATHYROIDISM. 

• Musculoskeletal system 
• Bone pain ( back, joints, shins )
• Pathologic fractures ( women)
• Muscle weakness
• Muscle atrophy
• Renal Effects 
• Renal calculi
• Polyuria
• Polydipsia
• Gastrointestinal System 
• Abdominal pain
• Peptic ulcer
• Pancreatitis
• Nausea
• Constipation
• Cardiovascular system
• Arrhythmias
• Hypertension
• Central Nervous System
• Paresthesias 
• Depression
• Psychosis
• Metabolic Effects
• Acidosis 
• Weight loss

DIAGNOSTIC TEST.

• Blood test
• Serum total calcium, phosphorus, Alkaline phosphatase , Parathyroid hormone ( PTH )
• Urine test
• Their will check for calcium, Quantitative,and  phosphorus. 
• Function Test
• Ellsworth - Horward excretion test (  PTH infusion test ) , Urinary cyclic adenosine  monophosphate ( cAMP )

TREATMENT FOR HYPERPARATHYROIDISM.

• Medical treatment:
• Focuses on decreasing the elevated serum calcium levels. the mild hypercalcemia are urged to drink fluids and keep active. they should avoid immobilization, thiazide diuretic, large doses of vitamin A and D, antacid containing calcium, and calcium supplements.
• For severe hypercalcemia requires hospitalization and intensive treatment with intravenous saline . Medication to inhibit bone reabsorption and reduce hypercalcemia, such as pamidronate(Aredia), alendronate(Fosamax), and zoledronate(Zometa) it is a short term treatment and may relieve bone pain.
• Surgical treatment:
• Removal of the parathyroid gland affected by  hyperplasia or edenoma treats primary hyperparathyroidsm called parathyroidectomy. 

COMPLICATION OF HYPERPARATHYROIDISM.

• Osteoporosis 
• The loss of calcium often result in osteoporosis.
• Cardiovascular diseeas
• High calcium levels are associated with cardiovascular condition, such as  hypertension and certain of heart disease.
• Kidney stones
• The excess of calcium in the blood may cause small, hard deposits of calcium and other substances to form in the kidney.
• Neonatal hyperparathyroidism 
• Severe and untreated hyperthyroidism in pregnant mother may cause dangerously low level of calcium in newborn.

NURSING MANAGEMENT OF HYPERPARATHYROIDISM.

• Obtain baseline serum potassium, calcium , phosphate and magnesium levels before treatment
• Provide at least 3 liters of fluid per day, including cranberry or prune juice , to increase urine acidity and help prevent calculus formation.
• Take safety precaution to minimize the risk for injury from fall.
• schedule care to allow the patient with weakness as much rest as possible.
• provide comfort measures to alleviate bone pain.

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