Republic of the Philippines

CENTRAL MINDANAO UNIVERSITY

COLLEGE OF NURSING
University Town, Musuan, Maramag, Bukidnon

E-mail: nursing@cmu.edu.ph

HYPERPARATHYROIDISM
In Partial Fulfillment of the Requirements in
NCM 74: CARE OF CLIENTS WITH PROBLEMS IN NUTRITION, AND
GASTROINTESTINAL, METABOLISM AND ENDOCRINE, PERCEPTION,
AND COORDINATION.
(ACUTE AND CHRONIC)

BSN 3 – B
PEPITO, MARK ALBERT L.
SANCHEZ, DIXIE LOUISE E.
Reporters

CLINICAL INSTRUCTOR
NEDA JOY L. ESPINA, MAN, LPT, RN

February 2022
Table of Contents

Page
PRELIMINARIES
Table of Contents 2
INTRODUCTION 3
Definition 3
Statistics 4
Types of Hyperthyroidism 4
CONCEPT MAP 4
Etiology of the disease 5
Risk factors 5
Pathophysiology (Disease process) 6
Clinical Manifestations 7
Nursing Diagnoses 7
Nursing Management 8
Health Teaching/Education 10
Pharmacological Management 11
Medical Management 12
Diagnostic Tools 13
Prognosis 14
TEST QUESTIONS 15
REFERENCES 16

Page 2 of 16
Introduction
1. Hyperparathyroidism.

 Excessive production of parathyroid hormone by the parathyroid glands

characterized by decalcification of bone and the formation of kidney stones, which
contain calcium (Brunner & Suddarth’s, 2001). The secretion of parathyroid
hormone is regulated directly by the
plasma concentration of ionized
calcium. The main effects of
parathyroid hormone are to increase
the concentration of plasma calcium
by increasing the release of calcium
and phosphate from bone matrix,
increasing calcium reabsorption by
the kidney, and increasing renal
production of 1, 25-dihyroxyvitamin D-3 (calcitriol), which increases intestinal
absorption of calcium. Thus, overproduction of parathyroid hormone results in
elevated levels of plasma calcium. Parathyroid decreasing serum phosphate levels.
Hyperparathyroidism is usually subdivided into primary, secondary, and tertiary
hyperparathyroidism.
2. Statistical data.
2.1 Primary hyperparathyroidism. Primary hyperparathyroidism (PHPT) is a
relatively common endocrine disorder, with prevalence estimates of one to seven
cases per 1000 adults. It is believed to be the most common cause of hypercalcemia,
predominantly affecting elderly populations and women two to three times as often
as men.
2.2 Secondary hyperparathyroidism. Secondary hyperparathyroidism is
common among patients with vitamin D deficiency and chronic kidney disease. Since
about half of the world population is vitamin D deficient, and about 1/7 have CKD,
it is important to understand the condition in depth.
2.3 Tertiary hyperparathyroidism. The incidence in patients in whom the
disease appears or progresses after kidney transplantation (tertiary
hyperparathyroidism) is 6% to 7%. The indication for surgery is often failure of the
pharmacologic therapy as a result of poor patient compliance during dialysis, with
worsening of uremic osteodystrophy.
3. Hyperparathyroidism is characterized as.
3.1 Primary Hyperparathyroidism. Excessive secretion of PTH due to a disorder of
the parathyroid glands resulting in abnormal calcium homeostasis.

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 3.2 Secondary Hyperparathyroidism. Hypocalcaemia due to non-parathyroid
disorders leads to chronic PTH hypersecretion, typically as a result of vitamin D
deficiency and/or chronic kidney disease (CKD).
3. 3 Tertiary Hyperparathyroidism. Autonomous secretion of PTH unrelated to
serum calcium concentration in patients with long – standing secondary
hyperparathyroidism resulting in hypercalcemia. Some authorities reserve the term for
secondary hyperparathyroidism that persist after successful renal transplantation.
A. CONCEPT MAP HYPERPARATHYROIDISM

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4. Etiology of the disease.
4.1 Primary Hyperparathyroidism.
 Parathyroid gland adenoma. A non-cancerous growth (adenoma) on a gland is
the most common cause.
 Hyperplasia & multiple adenoma. Enlargement of two or more parathyroid
glands accounts for most other cases.
 MEN type 1 & 2. Have a rare, inherited disorder, such as multiple endocrine
neoplasia, type 1, which usually affects multiple glands.
4.2 Secondary Hyperparathyroidism.
 Chronic kidney disease. The kidneys convert vitamin D into a form that the body
can use. If the kidneys work poorly, useable vitamin D may decline and calcium
levels drop, causing parathyroid hormone levels to go up. Chronic kidney failure is
the most common cause of secondary hyperparathyroidism. In some people with
long-term end-stage kidney disease, the parathyroid glands enlarge and begin to
release PTH on their own, and PTH does not go down with medical management.
This is called tertiary hyperparathyroidism, and people with this condition may
require surgery to remove parathyroid tissue.
 Vitamin D Deficiency. Vitamin D helps maintain appropriate calcium levels in the
blood. It also helps digestive system absorb calcium from the food.
 Malnutrition.
4.3 Tertiary Hyperparathyroidism.
 Persistent secondary hyperparathyroidism. In some people with long-term
end-stage kidney disease, the parathyroid glands enlarge and begin to release PTH
on their own, and PTH does not go down with medical management. This is called
tertiary hyperparathyroidism, and people with this condition may require surgery to
remove parathyroid tissue.
5. Risk factors.
5.1 Predisposing Factors.
 Older women who are post-menopausal. Women are more likely to get the
condition than men.
 Women of Age (50 – 60 years old). Age is associated with hyperparathyroidism.
5.2 Precipitating Factors.
 Radiation Therapy. Treatment for other neck cancers can affect the parathyroid
gland.
 Nutritional Deficiencies. Severe, ongoing vitamin D or calcium deficiencies can
trigger hyperparathyroidism.
 Lithium Use. Lithium, a drug used to treat bipolar disorder, can affect calcium
levels.

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6. Pathophysiology of the disease.
6.1 Primary hyperparathyroidism.
 In primary hyperparathyroidism due to adenomas, the normal feedback on
parathyroid hormone production by extracellular calcium seems to be lost,
resulting in a change in the set point. However, this is not the case in primary
hyperparathyroidism from parathyroid hyperplasia. An increase in the cell numbers
is probably the cause.
 The chronic excessive resorption of calcium from bone caused by excessive
parathyroid hormone can result in osteopenia. In severe cases, this may result in
osteitis fibrosa cystica, which is characterized by subperiosteal resorption of the
distal phalanges, tapering of the distal clavicles, salt-and-pepper appearance of
the skull, and brown tumors of the long bones. This is not commonly seen now. In
addition, the chronically increased excretion of calcium in the urine can predispose
to the formation of renal stones.
 The other symptoms of hyperparathyroidism are due to the hypercalcemia itself
and are not specific to hyperparathyroidism. These can include muscle weakness,
fatigue, volume depletion, nausea and vomiting, and in severe cases, coma and
death. Neuropsychiatric manifestations are particularly common and may include
depression, confusion, or subtle deficits that are often characterized poorly and
may not be noted by the patient (or may be attributed to aging). Increased calcium
can increase gastric acid secretion, and persons with hyperparathyroidism may
have a higher prevalence of peptic ulcer disease. Rare cases of pancreatitis have
also been attributed to hypercalcemia.
6.2 Secondary hyperparathyroidism.
 Secondary hyperparathyroidism results from a chronic stimulus of the parathyroid
gland to release parathyroid hormone. Parathyroid hormone release is increased
in the setting of hypocalcemia and hyperphosphatemia and is decreased by
fibroblast growth factor 23 (FGF-23).
 Parathyroid hormone acts on bone to release calcium into the blood and activates
1 alpha hydroxylation in the kidney to form 1,25-dihydroxvitamin D, which in turn
increases calcium absorption in the gastrointestinal tract. The rise in calcium
detected by the calcium-sensing receptor on the parathyroid gland reduces the
stimulus for parathyroid hormone excretion.
 Calcium and phosphorous homeostasis is tightly regulated between bone, the
kidney, and the parathyroid gland. Key modulators of calcium and phosphorous
include FGF-23, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and parathyroid
hormone. FGF-23 is released from bone due to increasing serum phosphorus levels
and acts in the kidney to increase phosphorous excretion and decrease 1 alpha
hydroxylation of 25-hydroxyvitamin D. FGF-23, along with serum phosphorous,
also decreases parathyroid hormone secretion, to maintain calcium and

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 phosphorous balance. In CKD, stages 3-5 (eGFR < 59 mL/min), FGF-23 levels
increase, initially leading to phosphaturia and decreased parathyroid hormone
excretion. As the CKD progresses, there is a resistance in the kidney and
parathyroid gland to FGF-23 and a deficiency in the kidney of 1 alpha hydroxylation
of vitamin D, both of which contribute to reduced phosphorous excretion. The
deficiency of 1,25-dihydroxyvitamin D, along with the decreased phosphorus
excretion, results in hypocalcemia and hyperphosphatemia, thereby maintaining
stimulation of parathyroid hormone synthesis and parathyroid gland hyperplasia.
6.3 Tertiary hyperparathyroidism.
 Tertiary disease is characterized by the development of autonomous hypersecretion
of parathyroid hormone causing hypercalcemia. The etiology is unknown but may
be due to monoclonal expansion of parathyroid cells (nodule formation within
hyperplastic glands). A change may occur in the set point of the calcium-sensing
mechanism to hypercalcemic levels. Four-gland involvement occurs in most patients.
The Pathophysiology of tertiary hyperparathyroidism is observed most commonly in
patients with chronic secondary hyperparathyroidism who have been on dialysis
therapy for years. The hypertrophied parathyroid glands enlarge over time and
continue to oversecrete parathyroid hormone, despite serum calcium levels that are
within the reference range or even elevated. In these cases, the hypertrophied
glands become autonomic and cause hypercalcemia, even after withdrawal of
calcium and active vitamin D therapy. They also may become resistant to
calcimimetic treatment. This type of tertiary disease is particularly dangerous
because the phosphate level is often elevated. If the calcium value multiplied by the
phosphate value yields a high product, diffuse calcinosis may occur.
7. Clinical Manifestations.
 Fatigue.
 Muscle Weakness.
 Vomiting.
 Hypertension.
 Bone or joint pain.
 Polyuria.
 Nephrolithiasis.
8. Nursing Diagnoses.
8.1 Fatigue. Fatigue r/t decreased metabolic energy production and increased
energy requirements.
8.2 Muscle Weakness. Impaired physical mobility r/t decreased strength and
endurance.
8.3 Vomiting. Imbalanced nutrition: less than body requirements r/t inability to
absorb nutrients secondary to inability to ingest foods.
8.4 Hypertension. Risk for decreased cardiac output.

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 8.5 Bone or joint pain. Acute pain r/t physical mobility aeb crying, facial grimaces,
irritability and reports of a decreased ability to perform ADLS because of discomfort.
8.6 Polyuria/Excessive urination. Deficient fluid volume r/t compromised
endocrine regulatory mechanisms.
8.7 Nephrolithiasis. Impaired urinary elimination r/t stimulation of the bladder by
calculi, renal or urethral irritation aeb urgency and frequency.
9. Nursing Management.
9.1 Fatigue r/t decreased metabolic energy production and increased energy
requirements.
 Monitor vital signs.
 Allow patient adequate rest periods, schedule activities for periods when the
client has the most energy.
 Encourage patient to do whatever possible such as self - care, walking within
war premises and interacting with family.
 Instruct methods to conserve energy such as sitting when doing daily care
or other activities, combining and simplifying activities and taking frequent
short rest periods during activities.
 Assist patient in self-care needs and with ambulation if needed.
9.2 Impaired physical mobility r/t decreased strength and endurance.
 Encourage the patient to do as much as they can.
 Medicate for pain.
 Schedule activities around rest periods. Consider energy-saving techniques.
 Provide passive ROM.
 Promote proper nutrition and hydration.
 Provide positive reinforcement during activity.
 Help patient in accepting limitations.
 Help patient develop sitting balance and standing balance.
 Reinforce principles of progressive exercise, emphasizing that joints are to
be exercised to the point of pain not beyond.
9.3 Imbalanced nutrition: less than body requirements r/t inability to absorb
nutrients secondary to inability to ingest foods.

 Note the patient's weight and monitor trends.

 Monitor for signs of malnutrition.
 Offer oral fluids as tolerated in small increments and consider patient
preferences.
 Provide calorie-dense foods.
 Anticipate intravenous fluid administration in severe cases of dehydration.
 Emphasize the importance of the timing of antiemetic medications.

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  Anticipate the need for enteral feedings if the patient is unable to eat after
24 to 48 hours.
 Eliminate strong odors during meal time.

9.4 Risk for decreased cardiac output.

 Assess vital signs, focusing on blood pressure and pulses and record.
 Thoroughly check the patient's laboratory results such as blood cell counts,
ABGs, electrolytes and cardiac marker studies.
 Help the patient to plan alternate periods of rest and activity.
 Advise the patient to limit intake of food high in sodium and cholesterol.
 Encourage patient to be vigilant in the intake of his maintenance
medications.

9.5 Acute pain r/t physical mobility aeb crying, facial grimaces, irritability and reports
of a decreased ability to perform ADLS because of discomfort.

 Assess the client's description of pain.

 Assess the client's previous experiences with pain and pain relief.
 Identify factors or activities that seem to precipitate acute episodes.
 Determine the client's emotional reaction to chronic pain.
 Medicate for pain before activity and exercise therapy.
 Provide for adequate rest periods.
 Provide/instruct patient to take prescribed analgesics or anti - inflammatory
medications such as acetaminophen.

9.6 Deficient fluid volume r/t compromised endocrine regulatory mechanisms.

 Monitor intake and output.

 Monitor for increased thirst (polydipsia).
 Weigh daily.
 Monitor urine specific gravity.
 Monitor serum and urine osmolality.
 Monitor urine and serum sodium levels.
 Monitor serum potassium.
 Monitor for signs of hypovolemic shock (e.g., tachycardia, tachypnea, and
hypotension).
 Allow the patient to drink water at will.
 Provide easily accessible fluid source, keeping adequate fluids at bedside.
 Administer medications as prescribed.
 If vasopressin is given, monitor for water intoxication or rebound
hyponatremia.

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 9.7 Impaired urinary elimination r/t stimulation of the bladder by calculi, renal or
urethral irritation aeb urgency and frequency.

 Record intake and output and characteristics of urine.

 Determine patient's normal voiding pattern and note variations.
 Encourage the patient to walk if possible.
 Promote sufficient intake of fluids.
 Strain all urine. Document any stones expelled and send to laboratory
analysis.
 Observe for changes in mental status, behavior or level of consciousness.
 Check laboratory studies (electrolytes, BUN, CR).
 Obtain urine for culture and sensitivities.
 Irrigate with acid or alkaline solutions as indicated.

10. Health teaching/Health Education of the disease.

 Educate patients about prescribed medications.

Rationale: Patients will be more willing to take medications when they have
good information about what to expect.
 Educate patients regarding the importance of periodic laboratory
and radiologic testing.
Rationale: In doing this procedure, it provides early detection and diagnosis
of disease to individualized treatment plans based on a patient’s condition.
 Monitor patient’s how much calcium and vitamin D she/he gets in
his/her diet.
Rationale: Restricting dietary calcium intake isn't advised for patients with
hyperparathyroidism. The daily recommended amount of calcium for adults
ages 19 to 50 and men ages 51 to 70 is 1,000 milligrams (mg) of calcium a
day. That calcium recommendation increases to 1,200 mg a day for women
age 51 and older and men age 71 and older. The daily recommended amount
of vitamin D is 600 international units (IUs) of vitamin D a day for people
ages 1 to 70 and 800 IUs a day for adults age 71 and older. Talk to your
doctor about dietary guidelines that are appropriate for you.
 Instruct & educate patient the importance of drinking plenty of
fluids.
Rationale: Drinking enough fluids, mostly water, will have to produce nearly
clear urine to lessen the risk of kidney stones.
 Instruct patient to exercise regularly.
Rationale: Regular exercise, including strength training, helps maintain
strong bones. Talk to your doctor about what type of exercise program is
best for you.

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  Instruct patient not to smoke.
Rationale: Smoking may increase bone loss as well as increase your risk of
a number of serious health problems. Talk to your doctor about the best
ways to quit.
 Educate patient and instruct them to avoid calcium-raising drugs.
Rationale: Certain medications, including some diuretics and lithium, can
raise calcium levels. If you take such drugs, ask your doctor whether another
medication may be appropriate for you.
 Instruct patient to avoid excessive loss of body fluids (e.g.,
dehydration), prolonged bed rest or inactivity, and high calcium diet.
Rationale: This can increase blood calcium levels.
 Instruct patient to consume a moderate amount of vitamin D (400
to 600 international units, or 10 to 15 micrograms, daily).
Rationale: Vitamin Deficiency can stimulate PTH secretion and bone
resportion and should be avoided.

11. Pharmacological Management.

11.1 Fatigue r/t decreased metabolic energy production and increased energy
requirements.
 Corticosteroids. Provides relief for inflamed areas of the body.
11.2 Impaired physical mobility r/t decreased strength and endurance.
 OTC Pain Relievers (Ibuprofen, Acetaminophen). Pain killers.
 Levothyroxine (Synthetic thyroid hormone). Hormone replacement
therapy after surgery.
11.3 Imbalanced nutrition: less than body requirements r/t inability to absorb
nutrients secondary to inability to ingest foods.
 Antiemetic. Treatment for nausea and vomiting.
11.4 Risk for decreased cardiac output.
 ACE's. Lowers blood pressure by relaxing blood vessels as well as decrease
in blood volume, which leads to lower blood pressure and decreased oxygen
demand from the heart.
 CCBs. Drugs used to lower blood pressure. They work by preventing calcium
from entering the cells if the heart and arteries. Calcium causes the heart
and arteries to squeeze (contract) more strongly. By blocking calcium,
calcium channel blockers allow blood vessels to relax and open.
11.5 Acute pain r/t physical mobility aeb crying, facial grimaces, irritability and
reports of a decreased ability to perform ADLS because of discomfort.
 Calcimimetics. Drug that mimics calcium circulating in the blood. The drug
may trick the parathyroid glands into releasing less parathyroid hormone.
The drug is sold as cinacalcet (Sensipar).

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 Take note: Some doctors may prescribe cinacalcet to treat primary
hyperparathyroidism, particularly if surgery has not successfully cured the
disorder or a person is not a good surgery candidate.
Side effects: Joint and muscle pain, diarrhoea, nausea, and respiratory
infection.
 Biophosphonates. Prevents the loss of calcium from bones and ay lessen
osteoporosis caused by hyperparathyroidism.
Side effects: Low blood pressure, fever, vomiting. This treatment does not
address the underlying problems with the parathyroid glands.
11.6 Deficient fluid volume r/t compromised endocrine regulatory mechanisms.

 Desmopressin. Helps to control increased thirst and too much urination

due to these conditions, and helps prevent dehydration.

11.7 Impaired urinary elimination r/t stimulation of the bladder by calculi, renal or
urethral irritation aeb urgency and frequency.

 Analgesic. Pain reliever, or pain killer.

 Alpha blockers. Lowers blood pressure by preventing a hormone called
norepinephrine from tightening the muscles in the walls of smaller arteries
and veins. As a result, the blood vessels remain open and relaxed. This
improves blood flow and lowers blood pressure. Because alpha blockers also
relax other muscles throughout the body, these medications can help
improve urine flow.
 Calcium channel blockers. Drugs used to lower blood pressure. They
work by preventing calcium from entering the cells if the heart and arteries.
Calcium causes the heart and arteries to squeeze (contract) more strongly.
By blocking calcium, calcium channel blockers allow blood vessels to relax
and open.

12. Medical Management.

12.1 Fatigue r/t decreased metabolic energy production and increased energy
requirements.
 Hydration Therapy.
12.2 Impaired physical mobility r/t decreased strength and endurance.
 Hydration Therapy.
 Occupational Therapy.
 Parathyroidectomy and/or Tumor Resection (for carcinomas in the
parathyroid).
12.3 Imbalanced nutrition: less than body requirements r/t inability to absorb
nutrients secondary to inability to ingest foods.
 Hydration Therapy

Page 12 of 16
  Parathyroidectomy and/or Tumor Resection (for carcinomas in the
parathyroid).
12.4 Risk for decreased cardiac output.
 Bed rest
 Parathyroidectomy and/or Tumor Resection (for carcinomas in the
parathyroid).
12.5 Acute pain r/t physical mobility aeb crying, facial grimaces, irritability and
reports of a decreased ability to perform ADLS because of discomfort.
 Parathyroidectomy and/or Tumor Resection (for carcinomas in the
parathyroid)
12.6 Deficient fluid volume r/t compromised endocrine regulatory mechanisms.
 Bed rest
 Parathyroidectomy and/or Tumor Resection (for carcinomas in the
parathyroid).
12.7 Impaired urinary elimination r/t stimulation of the bladder by calculi, renal or
urethral irritation aeb urgency and frequency.
 Hydration Therapy.
 Percutaneous Nephrolithotomy.
 Parathyroidectomy and/or Tumor Resection (for carcinomas in the
parathyroid).
13. Diagnostic tools.
 X – RAY, CT SCAN, MRI. Scans can identify blockages caused by excess calcium
and any bone fractures.
 Bone densitometry. Also called dual-energy x-ray absorptiometry, DEXA, DXA,
uses a very small dose of ionizing radiation to produce pictures of the inside of the
body (usually the lower or lumbar, spine and hips) to measure bone loss. It is
commonly used to diagnose osteoporosis, to assess an individual’s risk for
developing osteoporotic fractures.
 Blood test. Measures levels of calcium, vitamin D, parathyroid hormone and to
see how well the kidneys are working.
 Urine test. (Urine dipstick, Urinalysis, Urine Microscopy). Helps to determine how
severe the condition is and whether the kidney problems are the cause. The
primary health care provider will check the urine to see how much calcium it
contains.
 Hormone level studies. Hormone replacement therapy may help bones retain
calcium.
 Serum urea, Cystatin C, Creatinine, Electrolytes, cMAP. Detection for any
abnormality level.
 Abdominopelvic CT, UTZ, KUB X – ray. Only performed prior to surgery to
determine the exact location of the abnormal glands.

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  Intravenous pyelogram. Imaging test used to look at the kidneys and ureters.
14. Prognosis.
14. 1 If treated…
A. Primary hyperparathyroidism:

 If treatment is necessary, surgery is the commonly used treatment. Surgical

procedures involve removing enlarge parathyroid glands or tumors on the glands.
 Calcimimetics, which acts like calcium in the blood. These drugs can trick patient's
glands into making less PTH.
 Bisphosphonates, which keep the patient's bone from losing calcium.
 Hormone replacement therapy can help bones hold on to calcium.

B. Secondary hyperparathyroidism:

 Treatment involves bringing PTH level back to normal by treating the underlying
cause. Methods of treatment include taking prescription vitamin D for severe
deficiencies and calcium and vitamin D for chronic kidney failure.
 Certain medications and dialysis if patient has chronic kidney failure.

C. Tertiary hyperparathyroidism:

 The high blood calcium levels may be controlled with a drug, cinacalcet.
 Definitive treatment is surgery, which involves partial or total removal of the
parathyroid glands (parathyroidectomy).

13.2 If not treated…

 Osteoporosis. The loss of calcium often results in weak, brittle bones that fracture
easily.
 Kidney stones. Too much calcium in the blood may lead to too much calcium in
the urine, which can cause small, hard deposits of calcium and other substances to
form in the kidneys.
 Cardiovascular disease. Although the exact cause-and-effect link is unclear, high
calcium levels are associated with cardiovascular conditions such as high blood
pressures and certain types of heart disease.
 Neonatal hypoparathyroidism. Severe, untreated hyperparathyroidism in
pregnant women may cause dangerously low levels of calcium in newborns.

Page 14 of 16
PEPITO, Mark Albert L. BS – NURSING 3B

SANCHEZ, Dixie Louise E. Medical – Surgical Nursing 2

HYPERPARATHYROIDISM QUESTIONS

1. What usually leads to electrolyte imbalances if patient has excessive levels of

circulating PTH?
a. Hypernatremia & hypokalemia
b. Hyperkalemia & hypophosphatemia
c. Hypercalcemia & hypophosphatemia
d. Hypocalcemia & hypercalcemia
2. What certain electrolytes do parathyroid gland regulate?
a. Calcium & phosphorus
b. Sodium & magnesium
c. Potassium & sodium
d. Calcium & potassium
3. Patients with long-term end-stage kidney disease, the parathyroid glands enlarge
and begin to release PTH on their own, and PTH does not go down with medical
management.
a. Hyperparathyroidism
b. Primary hyperparathyroidism
c. Secondary hyperparathyroidism
d. Tertiary hyperparathyroidism
4. What causes the condition of patient having secondary hyperparathyroidism?
a. Persistent secondary hyperparathyroidism
b. Chronic kidney disease
c. Chronic kidney disease & Vitamin D deficiency
d. Hyperplasia & multiple adenoma
5. In what condition of the patient that definitive surgery is opted, which involves
partial or total removal of parathyroid gland (parathyroidectomy)?
a. Hyperparathyroidism
b. Primary hyperparathyroidism
c. Secondary hyperparathyroidism
d. Tertiary hyperparathyroidism

Page 15 of 16
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