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HYPERPARATHYROIDISM

GROUP 4 PRESENTATION

objectives
Define hyperparathyroidism
Explain causes of hyperparathyroidism
Describe the pathophysiology of
hyperparathyroidism
Mention clinical manifestations of
hyperparathyroidism
Explain the medical and nursing management

Definition
Hyperthyroidism is a disorder of the parathyroid
gland.
It is referred to as excessive production of
parathyroid hormones (PTH) by the parathyroid
gland characterized by decalcification of bones
and formation of kidney stones which contains
calcium.
This disorder is characterized by high levels of
calcium ions in blood due to excessive bone
decalcification.

Location of Parathyroid glands

TYPES OF HYPERPARATHYROIDISM

Hyperparathyroidism is divided into three


types
1. Primary hyperparathyroidism
2. Secondary hyperparathyroidism
3. Tertiary hyperparathyroidism

Primary hyperparathyroidism
Occurs too-three times more in women than men
and children.
It is often common in people aged 60-70 years of
age
ETIOLOGY
Primary hyperparathyroidism is a result of an
abnormality of the parathyroid glands
Adenoma
(non-cancerous
growth)
on
the
parathyroid gland is the most cause.
Hyperplasia which is simply enlargement of the

Etiology contd
Malignant tumors (cancerous)
Genetics- inherited traits from parents that
cause the disorder

Secondary hyperparathyroidism
Occurs due to other conditions that lowers serum
calcium levels.
Therefore the Low levels of calcium levels
stimulates excess secretion of parathyroid gland
hormones and multiplication of the parathyroid
gland hormones in a process to composite for
the lowered calcium levels

Factors that contribute to Sec Hyperparathyroidism


Severe calcium deficiency as a result of
low calcium in diet
Malabsorption from the GIT
Severe vitamin D deficiency
Active vitamin D help in the absorption of calcium
from the gut. Exposure to sunlight help the skin to
produce inactive vitamin D.
Some vit D is absorbed from the GI tract

Factors contributing to sec hyperparathyroidism


contd
Chronic renal failure
Kidneys are responsible for converting inactive
vit D into active vitamin D
Kidney failure implies that the kidneys will fail to
convert precursor D vitamin into its active form
and thus leading to Malabsorption of calcium
from the GI tract

PATHOPHYSIOLOGY OF HYPERPARATHYROIDISM
Parathyroid glands respond to low serum calcium
levels by releasing PTH. PTH increases serum calcium
levels through direct action on bone and the kidneys
and indirectly in the GIT.
PTH stimulates osteoclasts to reasorpt bone and
mobilize calcium into the blood.
In the kidneys, PTH acts to reduce calcium excretion
and stimulates synthesis of active vitamin D, which
stimulates calcium absorption in the gastrointestinal
tract
In their normal state, the glands function to keep

Pathophysiology contd
Sustained hypocalcaemia leads to cellular
replication and increased mass of the glands.
Adenomas, malignant tumors and hyperplasia
result into increased mass of the parathyroid
gland this in turn result in excess production of
the parathyroid hormone, PTH results in excess
bone decalcification.
Kidney failure result in inactivation of vitamin D
which is responsible for absorption of calcium in
the GIT, as such low calcium absorption result in
increased production of PTH which decalcifies

PRIMARY HYPERPARATHYROIDISM
In primary hyperparathyroidism, an abnormality
of the parathyroid gland causes inappropriate,
PTH production.
The cause of primary hyperparathyroidism
ordinarily is hypertrophy (hyperplasia) or a tumor
on one or more of the parathyroid gland.
such tumors occur much more frequently in
women than in men and children, mainly
because pregnancy and lactation stimulates the
parathyroid gland to secrete PTH to decalcify
calcium from the mothers bones for neonate

SECONDARY
HYPERPARATHYROIDISM

In secondary hyperparathyroidism, high levels of


PTH occur as a compensation for hypocalcaemia
rather than a primary abnormality of the
parathyroid gland.
This contrast with primary hyperparathyroidism
which is associated with hypertrophy of the
parathyroid gland.
Secondary hyperparathyroidism can be caused
by
calcium deficiency,

Elevated parathyroid hormones result in an


elevation of serum calcium levels which
cause widespread organ dysfunction.
Symptoms include anorexia, nausea,
vomiting, polydipsia (abnormally great thirst
as a symptom of disease or psychological
disturbance), polyuria, lethargy, and with
extreme hypercalcemia, coma and death.
Decalcification of bones result in weak bones
that easily break (fracture)

Functions of calcium
Bone mineralization
Muscle contraction
Skeletal
Cardiac
Smooth muscle
Blood clotting
Nerve impulse transmission

CLINICAL MANIFESTAIONS
Fragile bones that easily fracture
Kidney stones
Excessive urination and thirst
Abdominal pain
Tiring easily and fatigue
Depression and forgetfulness
Bone and joint pains
Frequent complaints of feeling ill without apparent cause
Nausea, vomiting and loss of appetite
constipation

Diagnosis of Hyperthyroidism
History taking
Ask for the following signs and symptoms
oWeight loss, weakness, joint pains, alterations
in neural activities such us forgetfulness and
changes in heart beat i.e. palpitations,
Blood test
Check for levels of parathyroid hormones and
calcium levels
Physical examination
Check for tenderness in bones, heart

Diagnosis contd
Urine test- for urine calcium levels and kidney
functioning
Neck ultra sound- to check for size of the glands
Magnetic resonance imaging-to check for size of the
glands
Bone density scanning-to check for osteoporosis

Bone scanning for osteoporosis

Normal bone

Hyperparathyroidism / bone osteoporosis

Management of
Hyperparathyroidism
MEDICAL MANAGEMENT
Calcimimetics
These are a group of drugs that mimic or act as
natural calcium in serum.
They induce negative feedback mechanism by
inhibiting
the
production
of
Parathyroid
hormones by the parathyroid glands.

Medical management contd


Hormone Replacement therapy
Hormones such us calcitonin is administered.
Calcitonin help to control calcium levels by
antagonizing the actions of parathyroid gland
and parathyroid hormones.
It decreases osteoclastic activity
Bisphosphonate
Examples are alendronates
Prevents loss of calcium from bones

SURGERY-PARATHYROIDECTOMY
Surgical procedure to remove part of the
parathyroid gland or tumors and any other
growth on the parathyroid gland.
NOTE: if all four glands are affected three
glands are removed leaving one to continue
functioning

NURSING MANAGEMENT
Hydration-provide at least 3 liters of fluids per
day to help prevent calcium accumulation in the
kidneys and formation of kidney stones
Take safety precautions to minimize risk of
injury from fall
Encourage patient to rest due to muscle and
bone weakness
Observe patient for signs of muscle, joint and
bone pain and monitor effectiveness of
analgesics
Provide comfort measures

Possible complication of
hyperparathyroidism

The most significant complication of


hyperparathyroidism is HYPERCALCAEMIA
Complications associated with hypercalcaemia are
Sinus bradycardia
Increase in the degree of a heart block
Cardiac arrhythmia
Hypertension
Pancreatitis
Peptic ulcer disease
Nephrolithiasis

references
AMERICAN FAMILY PHYSICIAN-VOLUME 69,
NUMBER 2 / JANUARY 15, 2004 website.
www.aafp.org/afp
American Family Physician-Volume 72, Number 4
August 15, 2005
JOURNAL OF BONE AND MINERAL RESEARCHVolume 6, Supplement 2, 2012 Mary Ann Lie
Bert, Inc., Publishers
Brunner and suddarths textbook of medical
surgical nursing twelfth edition