HYPERCALCEMIA

Definition:
Hypercalcemia is characterized by serum calcium value greater than 10.2
mg/dL or 2.6 mmos/L.

Mild Hypercalcemia - usually causes no apparent symptoms if the rise of

calcium level is chronic over a long period of time.
Moderate Hypercalcemia -
Acute Hypercalcemia -

(Treatment options depend on the severity and cause of hypercalcemia,

mild cases may only require lifestyle modification or increasing fluid
intake. In more severe cases or when complications arise, medical
interventions such as IV fluids, medication to lower calcium, or
addressing the underlying cause may be necessary.)

Disease Relevant to Hypercalcemia:

(This condition can occur due to various factors such as excessive intake
of calcium or vitamin D, immobilization, certain medications [thiazide
diuretics, thophylline intoxication, digitalis toxicity], Vit A and D
intoxication, hormonal imbalances or underlying medical conditions)

Hyperparathyroidism is a medical condition characterized by the over-activity

of the parathyroid glands, resulting in excessive production of parathyroid hormone
(PTH). Increased bone resorption (In primary hyperparathyroidism one or more of
the parathyroid glands become enlarged and produce excess PTH which stimulates
osteoclasts that leads to increased bone resorption) Enhanced intestinal absorption
(PTH also acts on the intestines to increase calcium absorption from dietary sources,
thus elevated PTH increases calcium absorption in he intestines) Impaired renal
calcium excretion (The kidneys play a vital role in maintaining calcium balance by
filtering and excreting excess calcium from the blood. PTH inhibits renal tubular
reabsorption of calcium, promoting its excretion in urine. However in
hyperparathyroidism, the kidneys become less responsive to the PTH’s inhibitory
effect on calcium reabsorption leading to reduced excretion of calcium and
exacerbating hypercalcemia) Increased conversion of vitamin D (PTH stimulates the
conversion of inactive vitamin D/calcidiol into its active form/calcitriol in the
kidneys. Calcitriol enhances intestinal absorption of calcium. In hyperparathyroidism,
increased PTH levels results in higher calcitriol production leading to enhanced
intestinal absorption of calcium)

Malignancies refer to the presence of cancerous cells or tumors in the body. These
abnormal cells have the ability to invade nearby tissues and spread to other parts of
the body. Local osteolytic activity (Some cancers such as multiple myeloma and
metastatic tumors can directly invade bone tissue. This tumors secrete factors that
stimulates osteoclasts therefore increasing bone resorption) Parathyroid hormone
related protein (PTHrP) production (Certain malignancies including lung cancer can
produce a hormone called PTHrP which mimics the action of PTH. BY binding the
same receptors as PTH, PTHrP increases releas of calcium from bones and enhances
renal absorption of calcium) Ectopic production of calcitriol (Calcitriol is responsible
in regulating calcium absorption from the intestines. Some malignancies, particularly
lymphomas and certain types of solid tumors like ovarian cancer, can produce
calcitriol or its analogs. Excessive calcitriol leads to increased intestinal absorption
and enhances renal reabsorption of calcium) Bone metastases (When cancer spreads
to the bones through metastasis, it can disrupt normal bone remodeling processes.
Tumor cells stimulates osteoclast activity while inhibiting osteoblast function
therefore increasing bone resorption.) Cytokine release (inflammatory cytokines can
be produced by certain malignancies such as renal cell carcinoma and breast cancer.
These cytokines promote osteoclast activation and bone rsorption)

Nursing Diagnosis:

Nursing Interventions:
 Encourage patient to increase mobility/frequent ambulation
 Encourage pt. To increase fluid intake (fluid containing sodium
should be given unless contraindicated as it assist in calcium
excretion)(2.8-3.8 L)
 Encourage adequate fiber diet
 Implement safety precautions
 Monitor ECG

Medical Management:
- aims include decreasing the serum calcium level and reverse the process
causing hypercalcemia. Treating underlying cause is essential.
 Administer IV fluids (0.9% NaCl) - to dilute serum calcium level and
increase urinary calcium excretion by inhibiting reabsorption of
calcium. (IV Phosphate) - cause a reciprocal drop in serum calcium.
 Furosemide - increases calcium excretion together with diuresis
 Calcitonin - lower serum calcium level; particularly useful for pts
with heart disease or kidney injury who cannot tolerate large sodium
loads; reduces bone resorption, increases calcium & phosphorous
deposition in the bones; increases urinary excretion of calcium &
phosphorous.
 For pts with CANCER, treatment is directed as controlling the
condition: surgery, chemotheraphy or radiation therapy.
 For pts. with hyperparathyroidism partial parathyroidectomy.
 For pts. With sarcoidosis, myelomas, lumphomas, and leukemias,
Corticosteroids may be used to decrease bone turnover and tubular
reabsorption.
 Some biophosphonates (e.g., pamidronate disodium [Aredia],
ibandronate sodium [boniva]) inhibit osteoclast activity. IV forms can
 cause: fever, transient leukopenia, eye inflammation, nephrotic
syndrome, and jaw osteonecrosis.
 Mithramycin, a cytotoxic antibiotic inhibits bone resorption;
thrombpcytopenia, nephrotoxicity, rebound hypercalcemia when
discontinued and hepatotoxicity.
 Inorganic Phosphate salts can be given orally/NGT (in form of
phospho-soda/neutra-phos), rectally (retention enemas) or IV(use
with caution may cause severe calcification in various tissues,
hypotension, tetany and acute kidney injury.

LAB RESULTS/DIAGNOSTIC FINDINGS

 Serum calcium level is greater than 10.2 mg/dL(2.6 mmol/L).
 Cardiovasclar changes may include a variety of dysrhythmias (e.g.,
heart block) and shortening of the QT interval and ST segment.
 Double-antibody PTH test (used to differentiate between
hyperparathyroidism and malignancy as cause of hypercalcemia)
(PTH level is increased in primary/secondary hyperparathyroidism
and supressed in malignancy)
 Xrays may reveal bone changes if pt has hyperglycemia secondary to
malignancy, bone cavitations, or urinary calculi.
 Urine calcium may be normal or elevated in hyperparathyroidism and
hypercalcemia caused by malignancy.
PATHOPHYSIOLOGY
The parathyroid gland releases PTH (parathyroid hormone) [stimulates
osteoclast which are cells in the bones that are responsible for the
breakdown of bone tissues or bone resorption that then releases calcium
from the bone to the blood] if there is increase release of PTH it results to
enhanced bone resorption and then increases calcium in the blood. The
high calcium level in the blood can alter balance across cell membrane.
[High calcium levels in the blood can disrupt balance across cell
membranes by interfering with ion channel function, this disruption
affects affects various tissues and organs including the bones and GI
tract] Bone, excess calcium to blood, loss of calcium in the bone
[increased PTH stimulates bone resorption therefore the calcium from the
bone is released to the blood stream] Bone weakness [as calcium plays an
essential role in maintaining strength and structure of the bone, and is
required for both osteoclast and osteoblast activity.] Bone pain, muscle
weakness and fatigue [the weakened bones are more susceptible to
fractures and microfractures which can cause significant pain and
discomfort, also it may not be able to provide adequate support for the
muscles resulting to muscle weakness.] GI Tract, Increased vitamin D
+ calcium rich food [Vitamin D enhances absorption of dietary calcium
from the intestines and promotes reabsorption in the kidneys] Increased
parathyroid hormone [an increase in vit d and calcium intake can cause an
increased release of of PTH due to its roles in regulating calcium
absorption, bone resorption and renal absorption] Contractility of GI soft
tract muscle [when PTH levels rise, it stimulates the release of calcium
from bone tissues into the bloodstream. This triggers the contraction of
smooth muscles in the GI tract to have decreased motility and transit time
of food. Also, increased PTH has shown to decrease gastric acid secretion
and inhibit gastric emptying.] Then increased calcium in the blood affect
the kidneys [kidneys play a crucial role in maintaining calcium balance in
the body by regulating its reabsorption and excretion. Then it can impair
renal function by interfering with normal filtration process in the kidneys
as high calcium causes damage to the renal tubules, which is responsible
for filtering waste products from the blood and reabsorbing essential
substances.] Calcium inhibits insertion of aquaporin channels in
collecting duct membranes [aquaporins are proteins that facilitate the
movement of water across cell membranes. In collecting ducts of the
kidney aquaporin is responsible for reabsorption of water and solutes
including calcium from urine back into the bloodstream. When aquaporin
channels are inhibited it impairs the ability of water to be reabsorbed
from the urine. It increases flow rate of urine through the collecting ducts
resulting in a decreased contact time between the urine and renal tubules
which reduces opportunity for calcium ions to be reabsorbed back into
the bloodstream = hypercaluria, which then increases release of PTH as a
compensatory mechanism. CONCLUSION: Disruption of of water
absorption and impairment of calcium reabsorption] Increased calcium
[hypercaluria, which then increases release of PTH as a compensatory
mechanism] Hard to filter calcium [Then it can impair renal function by
interfering with normal filtration process in the kidneys as high calcium
causes damage to the renal tubules, which is responsible for filtering
waste products from the blood and reabsorbing essential substances.]
KIDNEY STONES [increased urinary calcium excretion can contribute
to the formation of kidney stones (calcium oxalate stones most common
type of kidney stones) especially if it is combine with other substances in
the urine such as oxalate.] Less water reabsorption in renal vasculature,
More water in tubule filtrates = Polyuria and Polydypsia [it means that
more water remains in the filtrate instead of being reabsorbed back into
the bloodstream, as a result a larger fluid volume reaches the collecting
ducts in the kidney and continues through the urinary system, as a result a
larger volume of urine is produced and excreted from the body =
polyuria. The increased urine output resulting from excess water in the
tubules leads to dehydration and stimulates thirst receptors in the brain to
compensate for the excessive fluid loss]
 PATHOPHYSIOLOGY

The modifiable factors associated with hypercalcemia are Increased

vitamin D, DIET, LIFESTYLE, UNDERLYING DISEASE
(HYPERPARATHYROIDISM AND MALIGNANCIES)

HYPERCALCEMIA, it starts in the PARATHYROID GLAND The

parathyroid gland releases PTH (parathyroid hormone) [stimulates
osteoclast which are cells in the bones that are responsible for the
breakdown of bone tissues or bone resorption that then releases calcium
from the bone to the blood] if there is increase release of PTH it results to
enhanced bone resorption and then increases calcium in the blood. The
high calcium level in the blood affects various tissues and organs
including BONE, KIDNEY AND THE GI TRACT.

WHAT HAPPENS IN THE BONE?

Bone, excess calcium to blood, loss of calcium in the bone [increased
PTH stimulates bone resorption therefore the calcium from the bone is
released to the blood stream] Bone weakness [as calcium plays an
essential role in maintaining strength and structure of the bone, and is
required for both osteoclast and osteoblast activity.] Bone pain, muscle
weakness and fatigue [the weakened bones are more susceptible to
fractures and microfractures which can cause significant pain and
discomfort, also it may not be able to provide adequate support for the
muscles resulting to muscle weakness.]

WHAT HAPPENS IN THE GI TRACT?

GI Tract, Increased vitamin D + calcium rich food [Vitamin D
enhances absorption of dietary calcium from the intestines and
promotes reabsorption in the kidneys] Suppressed activity at
myoneural junction [also known as the neuromascular junction, is the
point of communication between a nerve cell or neuron and transmits
signals from the nerve system to the muscles, allowing them to contract
and relax. Calcium ions are involved in the release of neurotransmitters,
acethylcholine, from the nerve ending at the junction. However, excess
calcium in the blood, it can disrupt this process by inhibiting the release
of acethylcholine leading to decrease in signal transmission at the
myoneural junction = there is reduction in muscle contraction and
activity.] Decreased contraction in smooth muscle [Smooth muscle
tone decreases due to hypercalcemia leading to constipation. The reduce
contraction slow down the movement of food through the Digestive
System resulting in difficulty passing of stool]
WHAT HAPPENS IN THE KIDNEY?

High solute in ECF, High solvent in ICF [The elevated calcium in the
blood results in an increased concentration of calcium in the filtrate. This
high concentration of solute hinders movement of water through osmosis.
AS a result, less water is reabsorbed from the filtrate back to the
bloodstream] Inhibition of water and solute reabsorption [
Hypercalcemia is a medical condition characterized by an abnormally
high level of calcium in the blood. This condition can have various
effects on the body, including the suppression of activity at the myoneural
junction, leading to decreased tone in smooth and striated muscle. This
can result in symptoms such as constipation and loss of appetite.

The myoneural junction, also known as the neuromuscular junction, is the

point of communication between a nerve cell (neuron) and a muscle cell.
It is responsible for transmitting signals from the nervous system to the
muscles, allowing them to contract and relax. Calcium plays a crucial role
in this process.

In hypercalcemia, the elevated levels of calcium interfere with the normal

functioning of the myoneural junction. Calcium ions are involved in the
release of neurotransmitters, such as acetylcholine, from the nerve
endings at the junction. These neurotransmitters bind to receptors on the
muscle cells, triggering muscle contraction