Parathyroid disorders.pdf

PRESENTATION ON MANAGEMENT OF
PATIENTWITH PARATHYROID DISORDERS
MRS. JISHA SRIVASTAVA
1

OBJECTIVES
2
After the class the students will be able
Explain the structures and function of Parathyroid gland.
Explain the age affect on parathyroid gland.
Describe the definition, etiology, risk factors, pathophysiology,
medical management, surgical management and Nursing
management of Hyperparathyroidism.
Describe the definition, etiology, risk factors, pathophysiology,
medical management, surgical management and Nursing
management of Hypothyroidism.
List down the health education for Hyperparathyroidism and
Hypoparathyroidism.

ANATOMY AND PHYSIOLOGY
OF PARATHYROID GLAND

OF PARATHYROID GLANDS
Four parathyroid glands, two on the back of each lobe of the thyroid gland.
The hormone they produce is called parathyroid hormone (PTH), which is
an antagonist to calcitonin; it maintains normal blood levels of calcium
and phosphate.
Target organs of PTH are bone, small intestine and kidneys.
PTH increases the resorption of calcium and phosphate from the bones to
the blood, which raises their blood levels.
Absorption of calcium and phosphate from food in the small intestine is
also increased by PTH through its action of activating vitamin D
(calcitriol) in the kidneys.
PTH also increases the resorption of calcium by the kidneys and the
excretion of phosphate (more than is obtained from bones).
4

OF PARATHYROID GLANDS
Overall effect of PTH is to raise the blood calcium level and
lower the blood phosphate level.
Secretion of PTH is stimulated by hypocalcemia (a low blood
calcium level) and is inhibited by hypercalcemia.
PTH is probably the most important regulator of the blood
calcium level.
Calcium ions in the blood are essential for normal excitability of
neurons and muscle cells and for the process of blood clotting.
5

FUNCTION OF THE
PARATHYROID GLANDS
Parathyroid glands produce parathyroid hormone, which plays a
key role in the regulation of calcium levels in the blood.
Precise calcium levels are important in the human body, since
small changes can cause muscle and nerve problems.
Release of calcium by bones into the bloodstream
Absorption of calcium from food by the intestines
Conservation of calcium by the kidneys
Stimulates cells in the kidney to transforms weaker forms of
vitamin D into the form that is strongest at absorbing calcium
from the intestines
6

DEFINITION
Hyperparathyroidism (HPT) is the most common type of
parathyroid disease. In HPT, one or more glands are overactive.
As a result, the glands make too much PTH. This may result in
too much calcium in the blood—a condition
called hypercalcemia.
Hyperparathyroidism, a disorder caused by overactivity of one or
more of the parathyroid glands, is classified as primary,
secondary, or tertiary.
8

INCIDENCE
Primary hyperparathyroidism occurs two to four times
more often in women than in men and is most common
in patients between 60 and 70 years of age.
About 100,000 new cases of hyperparathyroidism are
detected each year in the United States.
The disease is rare in children younger than 15 years,
but the incidence increases tenfold between the ages of
15 and 65 years.
9

INCIDENCE
It usually occurs in clients older than 60 and affects
women twice as often as men, and clients with renal failure.
The overall incidence of hyperparathyroidism is 27 per
100.000.
Half of the patients diagnosed with hyperparathyroidism do
not have symptoms.
Secondary hyperparathyroidism, with manifestations
similar to those of primary hyperparathyroidism, occurs in
patients with chronic renal failure and so called renal rickets
as a result of phosphorus retention, increased stimulation of
the parathyroid glands, and increased parathyroid hormone
secretion
10

Adenoma or Hyperplasia
or a benign tumor of the
parathyroid glands.
Hereditary.
Some cancers can also make a
substance that mimics PTH and
causes hypercalcemia.
Serum calcium may be reduced
in kidney disease because of the
kidneys’ failure to activate
vitamin D 11
ETIOLOGY

Primary hyperparathyroidism develops when
the normal regulatory relationship between serum
calcium levels and parathyroid hormone (PTH)
secretion is interrupted.
12
CLASSIFICATION

Secondary hyperparathyroidism occurs when
the glands are hyperplastic because of malfunction
of another organ system. It is usually the result of
renal failure and cancers such as multiple myeloma,
Or carcinoma with bone metastasis.
Tertiary hyperparathyroidism occurs when PTH
production is irresponsible(autonomous) in clients
with normal or low Serum calcium levels
13
CLASSIFICATION

The normal function of
TH is to increase bone
resorption, thereby
maintaining the proper
balance of calcium and
phosphorus the blood.
Excessive circulating
PTH leads to bone
damage, hypercalcemia,
and kidney damage.
14
PATHOPHYSIOLOGY

Primary Hyperparathyroidism :
The severity of hypercalcemia reflects the quantity of hyper
functioning parathyroid tissue.
Excessive PTH stimulates transport or calcium into the
blood from the intestine, kidneys, and bone.
Nephrolithiasis is secondary to calcium phosphate kidney
stones and deposition of calcium in the soft tissues of the
kidney.
Pyelonephritis may complicate the nephrolithiasis. Bone
resorption related to hypercalcemia may develop.
15
PATHOPHYSIOLOGY

Secondary Hyperparathyroidism:
Chronic renal failure and hyperphosphatemia cause secondary
hyperparathyroidism.
As the glomerular filtration rate (GFR) decreases in chronic
renal failure, serum phosphorus levels rise, which causes the
serum calcium level to fall.
PTH secretion is stimulated. This increase decreases renal
tubular absorption of phosphorus, causing serum phosphorus
levels to return to normal.
As the GFR continues to decrease, PTH is secreted in increased
amounts to decrease tubular reabsorption of phosphorus and
maintain serum phosphorus level at or close to normal limits.
16
PATHOPHYSIOLOGY

Apathy, fatigue, muscle weakness, nausea,
vomiting, constipation, hypertension, and cardiac
dysrhythmias may occur; all are attributable to the
increased concentration of calcium in the blood.
Psychological manifestations may vary from
irritability and neurosis to psychoses caused by the
direct effect of calcium on the brain and nervous
system.
An increase in calcium produces a decrease in the
excitation potential of nerve and muscle tissue.
17
CLINICAL
MANIFESTATIONS

The formation of stones in one or both kidneys,
related to the increased urinary excretion of calcium
and phosphorus
Renal damage results from the precipitation of
calcium phosphate in the renal pelvis and parenchyma,
resulting in renal calculi (kidney stones), obstruction,
pyelonephritis, and renal failure.
19
CLINICAL
MANIFESTATIONS

Musculoskeletal symptoms accompanying
hyperparathyroidism may result from demineralization
of the bones or bone tumors composed of benign
giant cells resulting from overgrowth of osteoclasts.
The patient may develop skeletal pain and tender-
ness, especially of the back and joints; pain on
weight bearing; pathologic fractures; deformities;
and shortening of body stature.
20
CLINICAL
MANIFESTATIONS

Bone loss attributable to hyperparathyroidism
increases the risk for fracture.
The incidence of peptic ulcer and pancreatitis is
increased with hyperparathyroidism and may be
responsible for many of the gastrointestinal symptoms
that occur.
Hypercalcemia can cause serious problems, including:
osteoporosis, kidney stones, heart disease, high
blood pressure
21
CLINICAL
MANIFESTATIONS

Most people with primary HPT have no symptoms.
Some people experience mild symptoms, such as:
muscle weakness, fatigue, increased need for sleep,
depression, aches and pains in the joints and bones
Symptoms for people with more severe disease may
include: loss of appetite, nausea, vomiting,
constipation, confusion or impaired thinking and
memory, increased thirst and urination
22
CLINICAL
MANIFESTATIONS

In rare cases, two or more of the glands are
overactive. This is called hyperplasia.
HPT is most often diagnosed in people between the
ages of 50 and 60. Women are affected about three
times as often as men. Some people have HPT due to a
rare genetic disorder called familial hypocalciuric
hypercalcemia. This condition is typically benign and
does not require treatment.
kidney failure causes the parathyroid glands to
become overactive. This is called secondary HPT.
23
CLINICAL
MANIFESTATIONS

Primary
hyperparathyroidism is
diagnosed by persistent
elevation of serum
calcium levels and an
elevated level of
parathormone.
Radioimmunoassays
for parathormone are
sensitive and
differentiate primary
24
DIAGNOSTIC FINDINGS
S.
N
O
TEST NORMA
L
VALUES
FINDINGS
1 Parathyroid
hormone
25 pg/mL ↑ in primary
hyperparathyroidism
↓ in primary
hypoparathyroidism,
parathyroid trauma during
thyroid surgery
↑ in some cancers,
hyperparathyroidism ↓ in
hypothyroidism
↑ in hypoparathyroidism
↓ in hyperparathyroidism
2 Calcium 8.5–10.5
mg/dL
3 Phosphorus 2 . 4 – 4 . 7
mg/dL

An elevated serum calcium level alone is a nonspecific
finding because serum levels may be altered by diet,
medications, and renal and bone changes. Bone
changes may be detected on x-ray or bone scans in
advanced disease.
The double antibody parathyroid hormone test is used
to distinguish between primary hyperparathyroidism
and malignancy as a cause of hypercalcemia.
25
DIAGNOSTIC FINDINGS

Ultrasound, MRI, thallium scan, and fine-needle
biopsy have been used to evaluate the function of the
parathyroids and to localize parathyroid cysts,
adenomas, or hyperplasia.
Bone densitometry (DEXA, DXA): Bone
densitometry, also called DEXA or DXA, uses a very
small dose of ionizing radiation to produce pictures of
the inside of the body (usually the lower spine and
hips) to measure bone loss. DXA is simple, quick and
noninvasive.
26
DIAGNOSTIC FINDINGS

Ultrasound: Ultrasound imaging uses sound waves to
produce pictures of the inside of the body. Ultrasound is
safe, noninvasive, and does not use radiation.
Computed tomography (CT) - body: CT scans use a
combination of x rays and computer technology to
create three-dimensional (3-D) images. A CT scan may
include the injection of contrast material.
27
DIAGNOSTIC FINDINGS

HYPERCALCEMIC CRISIS
Acute hypercalcemic crisis can occur with extreme
elevation of serum calcium levels. Serum calcium
levels higher than 15 mg/dL (3.7 mmol/L) result in
neurologic, cardiovascular, and renal symptoms that
can be life-threatening.
28
COMPLICATIONS

Treatment includes rehydration with large volumes of
intravenous fluids, diuretic agents to promote renal
excretion of excess calcium, and phosphate therapy to
correct hypophosphatemia and decrease serum cal-
cium levels by promoting calcium deposit in bone and
reducing the gastrointestinal absorption of calcium.
Cytotoxic agents (mithramycin), calcitonin, and
dialysis may be used in emergency situations to
decrease serum calcium levels quickly .
29
COMPLICATIONS

The patient requires expert assessment and care to
minimize complications and reverse the life-threatening
hypercalcemia.
Medications are administered with care, and attention
is given to fluid balance to promote return of normal
fluid and electrolyte balance. Supportive measures are
necessary for the patient and family.
30
COMPLICATIONS

The recommended treatment of primary
hyperparathyroidism is the surgical removal of
abnormal parathyroid tissue.
In some patients without symptoms and with only
mildly elevated serum calcium levels and normal renal
function, surgery may be delayed and the patient
followed closely for worsening of hypercalcemia, bone
deterioration, renal impairment, or the development of
kidney stones.
31
MEDICAL
MANAGEMENT

Lowering severely elevated calcium levels and long-
term management of hypercalcemia with drugs to
increase bone resorption of calcium.
Serum calcium levels are lowered by hydration and
calciuria.
Hydration can be achieved with an infusion of normal
saline solution. Normal saline is the fluid of choice
because it both expands the volume and acts in the
kidney to inhibit the resorption of calcium.
32
MEDICAL
MANAGEMENT

Furosemide (Lasix), a loop diuretic, may also be used
to promote calciuria after rehydration has occurred..
A client with hypercalcemia should have a diet low in
calcium and vitamin D.
Drugs that inhibit bone resorption include plicamycin
(Mithracin), gallium nitrate (Ganite), phosphates, and
calcitonin.
Plicamycin is a chemotherapeutic drug that is effective
in lowering serum calcium levels.
MEDICAL
MANAGEMENT

The hypocalcemic effect occurs after 24 hours and
lasts about 1 to 2 weeks.
Gallium nitrate, a newer drug, is now being used more
often because it has even fewer side effects.
Glucocorticoids may be used to reduce hypercalcemia
by decreasing the gastrointestinal absorption of calcium.
Etidronate (Didronel) or calcitonin can be used to
decrease the release of calcium by bones.
34
MEDICAL
MANAGEMENT

Parathyroidectomy :Definitive treatment of primary
hyperparathyroidism is surgical removal of the gland
or glands causing hyper secretion of PTH.
Intraoperative, rapid parathyroid hormone assay
measurement affords the ability to ensure removal of
all hyper functioning parathyroid tissue.
Autotransplantation of the parathyroid glands is a
useful modality for the management of certain forms
of hyperparathyroidism and radical neck surgery.
35
SURGICAL
MANAGEMENT

After partial parathyroidectomy, it is possible to
transplant the remaining healthy parathyroid tissue to a
safer location, such as the brachioradial muscle of the
forearm.
Re-exploration of the neck in the future may cause
laryngeal nerve damage and influence complications
of the original surgery.
36
SURGICAL
MANAGEMENT

Transplantation procedures take some time to come
to full effect. In the meantime, he client must
supplement the diet with calcium and vitamin D to
prevent hypoparathyroidism and hypocalcemia.
If hyperparathyroidism is surgically treated early in
its Course, the chance of total recovery is good.
Bone pain may disappear within 3 days after removal
of parathyroid tissue, and bone lesions may heal
completely. unfortunately, serious renal disease might
not be reversible by parathyroid surgery.
37
SURGICAL
MANAGEMENT

Complications after parathyroidectomy are similar to
those following thyroidectomy and rarely Occur.
Hypocalcemia is a potentially life-threatening
complication even if some parathyroid glands are left
untouched because edema reduces their function. The
client may also experience respiratory distress related
to either to hemorrhage or to recurrent laryngeal nerve
damage.
The cure rate for primary hyperparathyroidism after
surgical removal is greater than 95%.
38
SURGICAL
MANAGEMENT

The nursing management of the patient undergoing
parathyroidectomy is essentially the same as that of a patient
undergoing thyroidectomy.
However, the previously described precautions about dehydration,
immobility, and diet are particularly important in the patient awaiting
and recovering from parathyroidectomy.
Although not all parathyroid tissue is removed during surgery in an
effort to control the calcium–phosphorus balance, the nurse closely
monitors the patient to detect symptoms of tetany (which may be an
early postoperative complication).
Most patients quickly regain function of the remaining parathyroid
tissue and experience only mild, transient postoperative
hypocalcemia.
39
NURSING
MANAGEMENT

Nursing Interventions
Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure.
Monitor central venous pressure (CVP), if available.
Investigate reports of chest pain or angina.
Assess pulse and heart rate while patient is sleeping.
Auscultate heart sounds, note extra heart sounds, development of gallops and
systolic murmurs.
Monitor ECG, noting rate and rhythm. Document dysrhythmias.
Auscultate breath sounds. Note adventitious sounds.
Monitor temperature; provide cool environment, limit bed linens or clothes,
administer tepid sponge baths.
40
RISK FOR DECREASED CARDIAC OUTPUT
RELATED TO DYSRHYTHMIAS DUE TO
INCREASED CALCIUM LEVEL IN THE BLOOD

Observe signs and symptoms of severe thirst, dry mucous membranes, weak or thready pulse,
poor capillary refill, decreased urinary output, and hypotension.
Record I&O. Note urine specific gravity.
Weigh daily. Encourage chair rest or bedrest. Limit unnecessary activities.
Note history of asthma and bronchoconstrictive disease, sinus bradycardia and heart blocks,
advanced HF, or current pregnancy.
Observe for adverse side effects of adrenergic antagonists: severe decrease in pulse, BP; signs
of vascular congestion/HF; cardiac arrest.
Administer IV fluids as indicated.
Administer medications as indicated:
Thyroid hormone antagonists: propylthiouracil (PTU), methimazole (Tapazole)
[beta]-blockers: propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard), pindolol
(Visken)
41
RISK FOR DECREASED CARDIAC OUTPUT
RELATED TO DYSRHYTHMIAS DUE TO
INCREASED CALCIUM LEVEL IN THE BLOOD

Monitor vital signs, noting pulse rate at rest and when active.
Note development of tachypnea, dyspnea, pallor, and cyanosis.
Provide for a quiet environment; cool room, decreased sensory
stimuli, soothing colors, quiet music.
Encourage patient to restrict activity and rest in bed as much as
possible.
Provide comfort measures: touch therapy or massage, cool
showers. Patient with dyspnea will be most comfortable sitting
in high Fowler’s position.
Provide for diversional activities that are calming, e.g., reading,
radio, television.
42
FATIGUE RELATED TO DISEASE CONDITION AS
EVIDENCED BY VERBALISATION OF OVERWHELMING
LACK OF ENERGY TO MAINTAIN THE USUAL
ROUTINE, DECREASED PERFORMANCE.

Assess the thinking process. Determine attention span, orientation to
place, person, or time.
Note changes in behavior.
Assess the level of anxiety.
Provide a quiet environment; decreased stimuli, cool room, dim lights.
Limit procedures and/or personnel.
Reorient to person, place, or time as indicated.
Present reality concisely and briefly without challenging illogical
thinking.
Provide clock, calendar, room with outside window; alter the level of
lighting to simulate day or night.
43
RISK FOR DISTURBED THOUGHT PROCESSES
RELATED TO PHYSIOLOGICAL CHANGES:
INCREASED CNS STIMULATION/ACCELERATED
MENTAL ACTIVITY

Monitor daily food intake. Weigh daily and report losses.
Encourage patient to eat and increase the number of meals and
snacks. Give or suggest high-calorie foods that are easily digested.
Provide a balanced diet, with six meals per day.
Avoid foods that increase peristalsis and fluids that cause diarrhea.
Consult with a dietitian to provide a diet high in calories, protein,
carbohydrates, and vitamins.
Administer medications as indicated: glucose, vitamin B
complex, insulin (small doses).
44
RISK FOR IMBALANCED NUTRITION: LESS THAN
BODY REQUIREMENTS RELATED NAUSEA/
VOMITING.

Observe behavior indicative of the level of anxiety.
Monitor physical responses, noting palpitations, repetitive movements, hyperventilation, insomnia.
Stay with the patient, maintaining a calm manner. Acknowledge fear and allow the patient’s behavior to
belong to the patient.
Describe and explain procedures, surrounding environment, or sounds that may be heard by the patient.
Speak in brief statements. Use simple words.
Reduce external stimuli: Place in a quiet room; provide soft, soothing music; reduce bright lights; reduce
the number of persons having contact with the patient.
Discuss with patient and/or SO reasons for emotional lability and/or psychotic reaction.
Reinforce the expectation that emotional control should return as drug therapy progresses.
Administer antianxiety agents or sedatives and monitor effects.
Refer to support systems as needed: counseling, social services, pastoral care.
45
ANXIETY RELATED TO PHYSIOLOGICAL FACTORS: HYPER METABOLIC
STATE AS EVIDENCED BY INCREASED FEELINGS OF APPREHENSION,
SHAKINESS, LOSS OF CONTROL

Review the disease process and future expectations.
Provide information appropriate to individual
situation.
Identify stressors and discuss precipitators to thyroid
crises: personal or social and job concerns, infection,
pregnancy.
Provide information about signs and symptoms
of hypothyroidism and the need for continuous follow-
up care.
46
DEFICIENT KNOWLEDGE RELATED TO LACK OF
EXPOSURE/RECALL AS EVIDENCED BY QUESTIONS,
REQUEST FOR INFORMATION

DEFINITION
Hypoparathyroidism is an uncommon condition in
which your body produces abnormally low levels of
parathyroid hormone (PTH). PTH is key to regulating
and maintaining a balance of two minerals in your body
calcium and phosphorus.
49

INCIDENCE
Hypoparathyroidism is diagnosed in women more often
than men. The incidence is related to thyroid surgery.
The incidence of temporary hypoparathyroidism after
total thyroidectomy ranges from 6.9% to 25%. The
incidence after subtotal thyroidectomy is 1.6% to 9%.
50

ETIOLOGY
Iatrogenic (treatment-induced) or idiopathic
(without a specific cause).
51

ETIOLOGY
Iatrogenic causes include accidental removal of the
parathyroid glands during thyroidectomy.
Infarction of the parathyroid glands because of an
inadequate blood supply to the glands during surgery
Strangulation of one or more of the glands by
postoperative scar tissue.
Health maintenance actions include monitoring of
PTH, calcium, and phosphorus levels.
52

ETIOLOGY
Calcium supplements are required for life to prevent
tetany.
In rare occurrences idiopathic hypoparathyroidism may
exist.
Like Graves' disease and Hashimoto's disease, it may be
an autoimmune disorder with a genetic basis.
Pseudohypoparathyroidism (Albright's hereditary
osteodystrophy) is an inherited form of
hypoparathyroidism that involves a lack of end-organ
responsiveness to PTH.
53

ETIOLOGY
Neck surgery.
Autoimmune disease.
Hereditary hypoparathyroidism.
Low levels of magnesium in your blood.
Normal magnesium levels are required for normal
production of parathyroid hormone.
Extensive cancer radiation treatment of face or
neck.
54

PATHOPHYSIOLOGY
PTH acts to increase bone resorption, which maintains
proper serum calcium levels.
PTH also regulates phosphate clearance by the renal
tubules, thereby maintaining the correct inverse balance
between serum calcium and serum phosphate levels.
Consequently when parathyroid secretion is reduced,
bone resorption slows, serum calcium levels fall, and
severe neuromuscular irritability develops.
55

PATHOPHYSIOLOGY
Calcifications form in various organs, Such as the eyes
and basal ganglia.
Without sufficient PTH, fewer phosphorus ions are
secreted by the distal tubules of the kidney, renal excretion
of phosphate falls, and serum phosphate levels rise.
The client may fully recover from the effects of
hypoparathyroidism if the conditions diagnosed early,
before serious complications begin. Unfortunately,
cataracts and brain calcification, once formed, are
irreversible.
56

PATHOPHYSIOLOGY
Symptoms of hypoparathyroidism are caused by a deficiency
of parathormone that results in elevated blood phosphate
(hyperphosphatemia) and decreased blood calcium
(hypocalcemia) levels.
In the absence of parathormone, there is decreased intestinal
absorption of dietary calcium and decreased resorption of
calcium from bone and through the renal tubules.
Decreased renal excretion of phosphate causes
hypophosphaturia, and low serum calcium levels result in
hypocalciuria.
Muscular hyper irritability Uncontrolled spasm, Hypo
calcemic Tetany.
57

CLINICAL
MANIFESTATIONS
Hypocalcemia causes irritability of the neuromuscular
system and contributes to the chief symptom of
hypoparathyroidism—tetany.
Tetany is a general muscle hypertonia, with tremor and
spasmodic or uncoordinated contractions occurring
with or without efforts to make voluntary movements.
Symptoms of latent tetany are numbness, tingling, and
cramps in the extremities, and the patient complains of
stiffness in the hands and feet.
58

CLINICAL
MANIFESTATIONS
In overt tetany, the signs include bronchospasm,
laryngeal spasm, carpopedal spasm (flexion of the
elbows and wrists and extension of the carpophalangeal
joints), dysphagia, photophobia, cardiac dysrhythmias,
and seizures.
Other symptoms include anxiety, irritability,
depression, and even delirium. ECG changes and
hypotension also may occur.
Tingling or burning in your fingertips, toes and lips.
59

CLINICAL
MANIFESTATIONS
Twitching or spasms of your muscles, particularly
around your mouth, but also in your hands, arms and
throat
Fatigue or weakness
Painful menstrual periods
Patchy hair loss, Dry, coarse skin, Brittle nails
Depression or anxiety
60

CLASSIFICATION
Acute Hypoparathyroidism :
Acute hypoparathyroidism is caused by accidental
damage to parathyroid tissues during thyroidectomy.
It is characterized by greatly increased neuromuscular
irritability, which results in tetany.
Clients with tetany experience painful muscle spasms,
irritability, grimacing, tingling of the fingers,
laryngospasm, and dysrhythmias.
Assessment also reveals Chvostek's and Trousseau’s
signs.
61

CLASSIFICATION
Chronic Hypoparathyroidism:
Chronic hypoparathyroidism is usually idiopathic, resulting in
lethargy; thin, patchy hair; brittle nails; dry, scaly skin; and
personality changes.
Ectopic or unexpected calcification may appear in the eyes and
basal ganglia.
Thus cataracts and permanent brain damage, accompanied by
psychosis or convulsions, may develop.
In addition, severe persistent hypocalcemia adversely affects the
heart, causing dysrhythmias and eventual cardiac failure.
The diagnosis of hypoparathyroidism is based on the following
physical examination findings related to hypocalcemia.
62

DIAGNOSTIC FINDINGS
Presence of Chvostek's sign , Trousseau’s sign , Hyperactive deep
tendon reflexes (DTRS): A positive Trousseau’s sign or a positive
Chvostek’s sign suggests latent tetany.
Trousseau’s sign is positive when carpopedal spasm is induced by
occluding the blood flow to the arm for 3 minutes with a blood
pressure cuff.
Chvostek’s sign is positive when a sharp tapping over the facial
nerve just in front of the parotid gland and anterior to the ear causes
spasm or twitching of the mouth, nose, and eye
Circumoral paresthesia
Numbness and tingling of fingers
63

COMPLICATIONS
Reversible complication.
Cramp like spasms of your hands and fingers that can be prolonged and painful,
or muscle pain and twitches or spasms of the muscles of your face, throat or
arms.
When these spasms occur in your throat, they can interfere with breathing,
creating a possible emergency.
feeling, in your lips, tongue, fingers and toes.
Seizures.
Malformed teeth, affecting dental enamel and roots, in cases when
hypoparathyroidism occurs at an early age when teeth are developing.
Problems with kidney function.
Heart arrhythmias and fainting, even heart failure.
64

COMPLICATIONS
Irreversible complications:
Stunted growth
Slow mental development in children
Calcium deposits in the brain, which can cause balance
problems and seizures
Clouded vision due to cataracts
65

PREVENTION
There are no specific actions to prevent
hypoparathyroidism. However, if you're scheduled
to have thyroid or neck surgery, talk to your
surgeon about the risk of damage to your
parathyroid glands during the procedure.
Test your calcium, parathyroid hormone and
vitamin D levels and have you begin
supplementation if needed before surgery.
66

PREVENTION
If you've had surgery involving your thyroid or
neck, watch for signs and symptoms that could
indicate hypoparathyroidism, such as a tingling or
burning sensation in your fingers, toes or lips, or
muscle twitching or cramping.
If they occur, your doctor might recommend
prompt treatment with calcium and vitamin D to
minimize the effects of the disorder.
67

MEDICAL
MANAGEMENT
The goal of therapy is to raise the serum calcium level to 9 to
10 mg/dL (2.2 to 2.5 mmol/L) and to eliminate the symptoms of
hypoparathyroidism and hypocalcemia.
When hypocalcemia and tetany occur after a thyroidectomy, the
immediate treatment is to administer calcium gluconate
intravenously.
Because of neuromuscular irritability, the patient with
hypocalcemia and tetany requires an environment that is free of
noise, drafts, bright lights, or sudden movement.
Tracheostomy or mechanical ventilation may become necessary,
along with bronchodilating medications, if the patient develops
respiratory distress.
68

MEDICAL
MANAGEMENT
The patient receiving parathormone is monitored closely for allergic
reactions and changes in serum calcium levels.
Because of neuromuscular irritability, the patient with hypocalcemia and
tetany requires an environment that is free of noise, drafts, bright lights, or
sudden movement.
Tracheostomy or mechanical ventilation may become necessary, along
with bronchodilating medications, if the patient develops respiratory
distress.
Therapy for the patient with chronic hypoparathyroidism is determined
after serum calcium levels are obtained.
A diet high in calcium and low in phosphorus is prescribed. Although
milk, milk products, and egg yolk are high in calcium, they are restricted
because they also contain high levels of phosphorus.
69

MEDICAL
MANAGEMENT
If this does not decrease neuromuscular irritability and seizure activity
immediately, sedative agents such as pentobarbital may be administered.
Parenteral parathormone can be administered to treat acute hypoparathyroidism with
tetany. The high incidence of allergic reactions to injections of parathormone,
however, limits its use to acute episodes of hypocalcemia. The patient receiving
parathormone is monitored closely for allergic reactions and changes in serum calcium
levels.
Because of neuromuscular irritability, the patient with hypocalcemia and tetany
requires an environment that is free of noise, drafts, bright lights, or sudden
movement. Tracheostomy or mechanical ventilation may become necessary, along
with bronchodilating medications, if the patient develops respiratory distress.
Therapy for the patient with chronic hypoparathyroidism is determined after serum
calcium levels are obtained. A diet high in calcium and low in phosphorus is
prescribed. Although milk, milk products, and egg yolk are high in calcium, they are
restricted because they also contain high levels of phosphorus.
70

MEDICAL
MANAGEMENT
Spinach also is avoided because it contains oxalate, which would form insoluble calcium
substances. Oral tablets of calcium salts, such as calcium gluconate, may be used to
supplement the diet. Aluminum hydroxide gel or aluminum carbonate (Gelusil, Amphojel)
also is administered after meals to bind phosphate and promote its excretion through the
gastrointestinal tract.
Variable dosages of a vitamin D preparation—dihydrotachysterol (AT 10 or Hytakerol),
ergocalciferol (vitamin D), cholecalciferol (vitamin D)—are usually required and enhance
calcium absorption from the gastrointestinal tract. The goal of treatment is to relieve
symptoms and to normalize levels of calcium and phosphorus in your body. A treatment
regimen usually includes:
Oral calcium carbonate tablets. Oral calcium supplements can increase calcium levels in
your blood. However, at high doses, calcium supplements can cause gastrointestinal side
effects, such as constipation, in some people.
71

MEDICAL
MANAGEMENT
Vitamin D. High doses of vitamin D, generally in the form of calcitriol, can help your
body absorb calcium and eliminate phosphorus.
Magnesium. If your magnesium level is low and you're experiencing symptoms of
hypoparathyroidism, your doctor may recommend that you take a magnesium
supplement.
Thiazide diuretics. If your calcium levels remain low even with treatment, thiazide
diuretics can help decrease the amount of calcium lost through your urine. However, some
people with hypoparathyroidism, including people who inherited the condition, shouldn't
take thiazide diuretics.
Parathyroid hormone (Natpara). The U.S. Food and Drug Administration has approved
this once-daily injection for treatment of low blood calcium due to hypoparathyroidism.
Because of the potential risk of bone cancer (osteosarcoma), at least in animal studies, this
drug is available only through a restricted program to people whose calcium levels can't
be controlled with calcium and vitamin D supplements and who understand the risks.
blood-calcium levels rise or fall
72

MEDICAL
MANAGEMENT
If you need immediate symptom relief, your doctor might recommend
hospitalization so that you can receive calcium by intravenous (IV)
infusion, as well as oral calcium tablets. After hospital discharge, you'll
continue to take calcium and vitamin D orally.
Your doctor will regularly check your blood to monitor levels of calcium
and phosphorus. Initially, these tests will probably be weekly to monthly.
Eventually, you'll need blood tests just twice a year.
Because hypoparathyroidism is usually a long-lasting disorder, treatment
generally is lifelong, as are regular blood tests to determine whether
calcium is at normal levels. Your doctor will adjust your dose of
supplemental calcium if your blood-calcium levels rise or fall
73

MEDICAL
MANAGEMENT
A diet high in calcium and low in phosphorus is
prescribed. Although milk, milk products, and egg
yolk are high in calcium, they are restricted because
they also contain high levels of phosphorus. Spinach
also is avoided because it contains oxalate, which
would form insoluble calcium substances.
74

Rich in calcium. This includes dairy products,
green leafy vegetables, broccoli and foods with
added calcium, such as some orange juice and
breakfast cereals.
Low in phosphorus. This means avoiding
carbonated soft drinks, which contain
phosphorus in the form of phosphoric acid, and
limiting meats, hard cheeses and whole grains
DIET
75

Tracheotomy or Mechanical ventilation may become
necessary, along with Broncho dilating medication if
patient develops respiratory distress.
Hormonal replacement therapy .
A loss of central or peripheral vision blindness or
changes in vision chronic eye pain
SURGICAL MANAGEMENT
76

Prevent Respiratory Arrest.
When caring for a client with severe hypoparathyroidism, always be prepared for laryngeal spasm and respiratory
obstruction.
Have an endotracheal tube, laryngoscope, and tracheostomy set available when caring for a client with acute tetany.
When a client is at risk for sudden hypocalcemia, as after thyroidectomy, an ampule of intravenous calcium carbonate is
usually kept at the bedsicde for immediate use if necessary.
When the intravenous tubing is removed, it is sometimes capped so that rapid venous access is available. Sometimes
clients are encouraged to ingest a ready source of calcium carbonate, such as Tums.
If hypocalcemia is transient after a thyroidectomy, it usually resolves as edema decreases. If it is chronic, the client is
usually able to manage the therapeutic regimen with minimal difficulty.
Monitor for signs of tetany and report immediately to RN or physician so treatment can be instituted quickly.
Make sure a tracheostomy set, endotracheal tube, and intravenous calcium are available for emergency use if
laryngospasm occurs.
Consult a dietitian for high-calcium diet teaching. The patient may need a lifelong high-calcium diet.
Teach the patient about the importance of diet and medication therapy, and follow-up laboratory test- ing. The patient
needs to understand self-care for follow-up at home.
INEFFECTIVE BREATHING PATTERN RELATED TO
HYPERVENTILATION AND LARYNGOSPASM CAUSED
BY NEUROMUSCULAR IRRITABILITY.
77

Interventions
Monitor vital signs, to assess elevating temperature, tachycardia, respiratory
distress.
Observe for nerve muscular irritability, e,g. numbness, paresthesias,
twitching.
Avoid restraining during seizures.
Keep side rails raised and padded.
Monitor serum calcium level.
Administer anticonvulsants as prescribed to control the seizures activity.
Ask for regular medical follow-up to monitor effectiveness of therapy and for
prevention of fatal complications.
RISK FOR INJURY: MUSCLE TETANY RELATED TO
DECREASED SERUM CALCIUM LEVELS.
78

Establish guidelines and goals of activity with the patient.
Evaluate the need for additional help at home.
Have the patient perform the activity more slowly, in a longer time
with more rest or pauses, or with assistance if necessary.
Gradually increase activity with active range-of-motion exercises in
bed, increasing to sitting and then standing.
Dangle the legs from the bed side for 10 to 15 minutes.
Refrain from performing nonessential activities or procedures.
Assist with ADLs while avoiding patient dependency.
Provide bedside commode as indicated.
ACTIVITY INTOLERANCE RELATED TO
WEAKNESS AND APATHY.
79

Ascertain healthy body weight for age and height. Refer to a dietitian for complete nutrition
assessment and methods for nutritional support.
Set appropriate short-term and long-term goals.
Provide a pleasant environment.
Promote proper positioning.
Provide good oral hygiene and dentition.
If patient lacks strength, schedule rest periods before meals and open packages and cut up food for
patient.
Provide companionship during mealtime.
Consider the use of seasoning for patients with changes in their sense of taste; if not
contraindicated.
Consider six small nutrient-dense meals instead of three larger meals daily to lessen the feeling of
fullness.
For patients with physical impairments, refer to an occupational therapist for adaptive devices.
RISK FOR IMBALANCED NUTRITION: LESS THAN
BODY REQUIREMENT (CALCIUM LEVEL) R/T
INADEQUATE CALCIUM DIET OR INTAKE.
80

Assist with treatment for underlying problems, such
as anorexia, brain injury/increased intracranial
pressure, sleep disorders, biochemical imbalances.
Reorient to time/place/person, as needed.
Have patient write name periodically; keep this
record for comparison and report differences.
Provide safety measures (e.g., side rails, padding, as
necessary; close supervision, seizure precautions), as
indicated.
DISTURBED THOUGHT PROCESSES RELATED TO
HYPOCALCEMIA INDUCED NEUROLOGIC
DYSFUNCTION
81

Discuss the importance of long-term management and follow-
up care, especially periodic checks of the patient's serum
calcium levels.
Advise the patient that long-term replacement therapy will be
necessary. Instruct him to take the medication as ordered and not
to discontinue it abruptly.
Instruct the patient to take calcium supplements with or after
meals and to chew the tablets well.
Encourage the patient to wear a medical identification bracelet
and to carry his medicatíon with him at all times
HEALTH EDUCATION
82

Teach the patient and his family to identify and report signs and
symptoms of hypercalcemia, tetany, and respiratory distress
Teach the patient protective measures to decrease stress and to
avoid fatigue and infection.
Advise the patient to follow a high- calcium, low-phosphorus diet.
Discuss foods high in calcium; for example, dairy products, salmon,
egg yolks, shrimp, and green, leafy vegetables.
Caution him to avoid high-phosphate foods, such as spinach,
rhubarb, and asparagus.
HEALTH EDUCATION
83

Parathyroid disorders can be controlled and the
manifestations reversed if they are discovered in a timely
manner and prompt and proper treatment is begun. You
are an important resource for these clients, who require
considerable education. You are also responsible for
closely monitoring any client who needs Surgery for the
parathyroid gland.
SUMMARY AND CONCLUSION
85

RESEARCH
scienti
fi
c reports
Joon Ho, Donggyu Kim, Ji-Eun Lee, Namki Hong, Byung Moon Kim, Dong Joon Kim, Jinkyong Kim, Cho Rok Lee, Sang-Wook Kang, Jong Ju Jeong, Kee-Hyun Nam, Woong Youn Chung & Yumie Rhee
Scienti
fi
c Reports
volume
12, Article number: 7058 (2022) Cite this article
• 301 Accesses
• 1 Altmetric
• Metrics
Parathyroid venous sampling for the preoperative localisation of parathyroid adenoma in patients with primary hyperparathyroidism
Abstract
Preoperative localisation studies are essential for parathyroidectomy in patients with primary hyperparathyroidism. If the location of abnormal
parathyroid glands cannot be identified through non-invasive studies, parathyroid venous sampling (PVS) may be employed. In this study, we
evaluated the utility of preoperative PVS in parathyroid surgery. Patients with primary hyperparathyroidism who underwent preoperative PVS at
Severance Hospital between January 2015 and June 2020 were identified. Patients for whom the results of non-invasive imaging studies were
inconsistent or negative underwent PVS. The results of PVS were compared with operative findings and pathologic results. For 14 patients, the
results of preoperative ultrasonography and 99mTc-sestamibi single-photon emission computed tomography (SPECT) were negative; for 20
patients, either the result of only one test was positive, or the results of the two tests were inconsistent. With respect to the lateralisation of diseased
adenoma, the results of PVS and pathological examination were inconsistent only for one patient in either group (total: 2/34 patients). This study
showed that PVS could be used effectively for preoperative localisation in patients with primary hyperparathyroidism in whom the location of
diseased parathyroid glands cannot be determined through non-invasive image studies.
Conclusions
PVS may have certain limitations, but it is an exact technique for the preoperative localisation of parathyroid lesions and diseased parathyroid
glands whose locations cannot be determined through non-invasive imaging studies. Therefore, PVS may be a sufficient complementary means
when the location of the diseased parathyroid cannot be confirmed by imaging tests such as US, SPECT, 4D-CT, and PET. Consequently, with the
use of PVS, it is possible to eliminate the need to perform operative bilateral neck exploration and enable the use of MIS, which is associated with
less invasiveness to patients.

BIBLIOGRAPHY
Brunner & suddarth’s, Medical-Surgical nursing,(2015) 10th edition, Page1743-47
Joyce.M.Black, Medical-Surgical nursing,(2020) 6th edition, Page 1687-1708
Williams.S. Linda,Understanding Medical Surgical Nursing, 3rd edition(2007),
page 678-690
Taylor Carol, Fundamentals of nursing(2010), 5th edition
Chintamani, Lewis Medical-surgical nursing,( 2011), 2nd edition,CBS Publications
Priscilla Lemonne, Medical Surgical Nursing, 2nd edition
https://accesspharmacy.mhmedical.com/data/interactiveguide/physexam/heent/
neckexamination.html
https://pubmed.ncbi.nlm.nih.gov/21250067/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858710/

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