Endocrine Disorders- Outline

Thyroid Adrenal
Hypothyroid (Hashimoto’s) • HPA review
• Hyper – Cushing
Hyperthyroid (Grave’s)
• Hypo- Addison
Parathyroid
Anterior Pituitary
Hyperparathyroid • Anterior pituitary review
Hypoparathyrod • Hyper GH- acromegaly
Posterior Pituitary
• Posterior pituitary review
• Hypo ADH- diabetes insipidus
• Hyper ADH- SIADH
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The topics listed on this outline will be covered over two classes.

Key References
Bichet, D. (2023, April). Arginine vasopressin deficiency (central diabetes insipidus): Treatment.
UpToDate.
Byrne, D. (2023). Nursing Management: Musculoskeletal Conditions. Dickinson, In J. Kwong, C.
Reinisch, J. Tyerman, S. Cobbett, D. Hagler, M. Harding, & R. Dottie (Eds.), Medical surgical nursing
in Canada: Assessment and management of clinical problems (5th Canadian ed., pp. 1642- 1664).
Elsevier Canada.
Canadian Society of Endocrinology and Metabolism. (2019). Understand the gland. Choosing Wisely
Canada, from https://choosingwiselycanada.org/toolkit/understand-the-gland/
Goltzman, D. (2024, June). Clinical manifestations of hypocalcemia. UpToDate.
Lacroix, A. & Raff, H. (2024, April).Dexamethasone suppression tests. UpToDate.
Melmed, S. & Katznelson, L. (2023, April). Treatment of acromegaly. UpToDate.
Morin, et al. (2023). Clinical practice guideline for management of osteoporosis and fracture
prevention in Canada: 2023 update. CMAJ, 195(39), E1333–E1348.
https://doi.org/10.1503/cmaj.221647
Nieman, L. (2024, August). Establishing the cause of Cushing's syndrome. UpToDate.
Nieman, L. & Desantis, A. (2024, October). Treatment of adrenal insufficiency in adults. UpToDate.
Shared Health Manitoba. (n.d.). ACTH stimulation test. Shared Health Manitoba.
https://apps.sbgh.mb.ca/labmanual/test/view?seedId=2162
Sterns, R. (2024, May). Pathophysiology and etiology of the syndrome of inappropriate antidiuretic
hormone secretion (SIADH)
Ross, D. (2024, May). Myxedema coma. UpToDate.
Ross, D. (2024, July). Graves' hyperthyroidism in nonpregnant adults: Overview of treatment.
UpToDate.
Wulf, N. & Kapusnik-Under, J. (2022). Radiology study: Iodine allergy is a myth. Patient Safety &
Quality Healthcare. https://www.psqh.com/analysis/radiology-study-iodine-allergy-is-a-myth/

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 Medication List
• Cushing syndrome
• Hypothyroidism: Hormone replacement
• levothyroxine • Addison: cortico and mineralo steroids
• hydrocortisone
• Hyperthyroid: thioamide antithyroid drugs
• fludrocortisone
• methimazole
Other corticosteroids:
• Hyperparathyroid
• dexamethasone
• bisphosphonates
• methylprednisolone
• alendronate
• Acromegaly: Somatostatin analogue:
• pamidronate
• octreotide
• selective estrogen receptor modulator
• raloxifene • Diabetes insipidus: Antidiuretic hormone
analogues:
• Hypoparathyroid
• desmopressin
• calcium gluconate
• magnesium sulphate

This is the full list for parts one and two.

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 Thyroid Hormone
Review

TSH release

Thyroid hormones induce gene transcription and protein synthesis in target cells, which:
1. Increases basal metabolic rate (BMR), which increases ATP and heat production – TH
plays important role in maintenance of body temperature
2. Enhances actions of epinephrine and norepinephrine by stimulating up-regulation of β-
adrenergic receptors. This enhances sympathetic responses (e.g. increased HR, SV, and
MAP)
3. Regulate development and growth of nervous tissue and bones. Thyroid hormone
deficiency during fetal development, infancy, or childhood causes severe mental
retardation and stunted bone growth.

Because thyroid hormones influence metabolic rate, the manifestations align with this-
making it easier to remember!

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 Thyroid disorders

• The most common causes of both hyper and hypothyroid disorders are
autoimmune (Hashimoto thyroiditis; Graves disease)

Hypothyroidism (Hashimoto’s) Hyperthyroidism (Graves)

↓ metabolic processes ↑metabolic processes
-fatigue, bradycardia, constipation, -nervousness, tachycardia, diarrhea,
weight gain, dry skin, brittle hair weight loss, fine hair, diaphoresis, heat
and nails, cold intolerance intolerance

Myxedema crisis Thyroid storm

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Some acquired causes include:

• imbalances in iodine intake (low= hypothyroid, excess= hyperthyroid)
• medications (recall that amiodarone can cause both hyper and hypothyroidism)

There is also a condition known as congenital hypothyroidism present at birth. It is more

common in resource-poor nations as the most common cause is iodine deficiency.
• Newborns should be screened for this condition as there may be no symptoms at birth
and if not treated early and consistently, it leads to intellectual disability.

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 Diagnosing Thyroid Disorders

• plasma levels of thyroid stimulating hormone (TSH)

• plasma free T4
• plasma thyroxine (T4) total
• plasma triiodothyronine (T3)
• thyroid antibodies in the blood can be measured to
assist in the diagnosis of autoimmune thyroid diseases
(Hashimoto).
• When a pt’s levels are within normal limits, this is called
being “euthyroid”
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Measurement of TSH is considered the most sensitive method from evaluating thyroid disease.
1. TSH normal – No further testing performed

2. TSH high = evidence of HYPOthyroidism. Free T4 added to determine the degree of

hypothyroidism.
• For pts already taking levothyroxine for treatment of hypothyroid the TSH level
ALONE can be used to determine if the tx is therapeutic, a Free T4 is not needed.
When levothyroxine is first started, TSH is checked at 6 weeks and titrated based on
levels. Once at target, retest at 4 to 6 months and then annually if they remain
within the goal range.

3. TSH low = evidence of HYPERthyroidism. Free T4 and T3 added to determine the degree of
hyperthyroidism.
**This can be confusing for students! Remember that TSH’s job is to STIMULATE the release of
thyroid hormone based on a negative feedback system.
• if we have too little thyroid hormone (HYPO) TSH levels go up in order to stimulate the
thyroid gland to “work harder”.
• if we have too much thyroid hormone (HYPER) then TSH levels go down to reduce stimulation
of the thyroid gland.

Usually in Hashimoto's disease, the immune system produces an antibody to thyroid peroxidase
(TPO), a protein that plays an important part in thyroid hormone production and this can be
measured if necessary (but usually is not).

Canadian Society of Endocrinology and Metabolism. (2019). Understand the gland. Choosing Wisely Canada, from
https://choosingwiselycanada.org/toolkit/understand-the-gland/

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 Diagnostics Specific to Hyperthyroid
Disorders
• Radioiodine uptake test –only relevant to hyperthyroidism
• radioactive iodine ingested which will be taken up by the thyroid
gland
• images examined to see degree of uptake to determine cause

• Thyrotropin receptor antibodies — can determine the etiology of

hyperthyroidism. Graves' disease is caused by autoantibodies to the
TSH (thyrotropin) receptor. May be used in pts who cannot take
radioactive iodine (e.g., pregnant)

Radioiodine uptake test –only relevant to hyperthyroidism in pts who present evidence of
nodular thyroid disease

The test: done in the radiology department-

-The patient is given radioactive iodine (liquid or capsule form) to swallow.
-The thyroid uptake will begin several hours to 24 hours later (often at least 4hrs after iodine
was swallowed)
-“measurements” are taken using a camera-it will take pictures which correlate directly to
the amount of iodine taken up by the thyroid

HIGH IODINE UPTAKE = excess hormone is actively being produced in the gland
LOW= indicates the gland is no longer producing high levels of thyroid hormone. So, the
elevated levels are either from inflammation and destruction of thyroid tissue with release of
existing hormone into the circulation or there is an extrathyroidal source of thyroid hormone
(where there is functioning thyroid tissue existing outside of the thyroid gland).

Pt considerations: Pregnancy and breastfeeding are absolute contraindications to

radionuclide imaging.

Misconception alert: It used to be believed that being allergic to shellfish meant a person
was allergic to iodine, but this has been disproven and iodine is not generally considered an
allergen (i.e., you cannot develop a true iodine allergy). However, some people do have
radiocontrast hypersensitivity reactions and anaphylaxis has occurred.

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 Treatment: Hypothyroidism
Class: synthetic hormone *Take on empty
stomach & not
Common: levothyroxine (Synthroid®) with other meds
Other drugs in this class: liothyronine (synthetic T3), liotrix (synthetic
T3 and T4)

Mechanism of Action: Synthetic T4 (thyroxine), which increases

metabolic rate (protein, carbohydrate, and lipid metabolism), increases
utilization and mobilisation of glycogen stores, promotes
gluconeogenesis, and stimulates protein synthesis.

Administer as a single daily dose, preferably on an empty stomach, 30-60 minutes before
breakfast if possible. *However, consistency is most important: Take at the same time every
day, maintaining consistency with regards to type of foods if taking with meals. This ensures
consistent absorption and the ability to accurately titrate dosing.

• Food Interactions: Certain foods like soybean flour, soybean infant formula,
cotton seed, walnuts, and dietary fiber may decrease levothyroxine absorption.

• Medication Interactions: Do not administer within 4 hours of calcium- or iron-

containing products, bile acid sequestrants, or other medications. Ideally, take
levothyroxine at least one hour before any other types of medications.

• Enteral Tube Feeds: If administered with enteral tube feeds, hold tube feeds for 30-60
minutes before and after levothyroxine administration to avoid reduced bioavailability.

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 Levothyroxine: Nursing Implications
Side Effects: most often occur d/t supratherapeutic levels (too much
drug= iatrogenic HYPERthyroidism)
• tachycardia and hypertension, and therefore: angina in those at risk
• insomnia, anxiety/nervousness, tremors
• heat intolerance, diaphoresis, weight loss
Use with caution in:
• recent MI
How might altering the pt’s
• uncorrected adrenal insufficiency BMR affect other medications?
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Cautionary Considerations:
• Recent Myocardial Infarction (MI): Use with caution in patients who have had a recent MI
due to the risk of increasing myocardial oxygen demand.

• Uncorrected Adrenal Insufficiency: Contraindicated in patients with uncorrected adrenal

insufficiency. The increased metabolic rate associated with thyroxine replacement increases
cortisol requirements, which cannot be met in the presence of adrenal insufficiency,
potentially leading to adrenal crisis.

Effects of Starting Levothyroxine on Existing Specific Medications

• insulin: requirements may increase due to increased counterregulatory activity
• digoxin: drug:drug interaction can lead to a decrease in digoxin levels (subtherapeutic)
• warfarin: monitor INR, levothyroxine may potentiate warfarin effects, increasing INR

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 Acute complications of hypothyroidism
Myxedema Crisis (coma): usually develops due to a combination of undertreated
hypothyroidism and a precipitating factor (see list below).
Manifestations: hyponatremia, hypoglycemia, hypothermia, hypotension, bradycardia,
hypoventilation and altered level of consciousness
Management
• Continuous cardiac monitoring
• Maintain MAP >65 mm Hg- IV fluid resuscitation, vasopressors
• Maintain ventilation- may require mechanical ventilation
• Dextrose infusion
• Passive warming
• IV levothyroxine loading dose then q 8h
• IV hydrocortisone until adrenal insufficiency ruled out 9

Myxedema “coma” can occur as the culmination of severe, longstanding hypothyroidism or

be precipitated by an acute event in a poorly controlled hypothyroid patient. Loss of
consciousness (coma) is a very late manifestation of untreated myxedema crisis, so “coma” is
a bit of a misnomer.

Common precipitating factors:

• Infection
• MI
• severe cold exposure
• Trauma
• sedating meds *opioids*

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 Treatment : Hyperthyroidism
Class: thioamide antithyroid drugs Adjunct
therapy:
Common: Methimazole (Tapazole®) Beta blockers

Other drugs in this class: propylthiouracil

Mechanism of Action: Inhibits synthesis of thyroid hormones by
blocking the oxidation of iodine in the thyroid gland, therefore ↓T4
and T3. It does not inactivate T4 and T3 that is already circulating.
Other options:
• radioiodine
• surgery
10

Three treatments for hyperthyroidism:

• thioamide antithyroid drugs- must be taken consistently and have potential side-effects.
Often used at the time of diagnosis to help quickly reduce thyroid levels in patients with
significant symptoms, or who are at risk for serious negative effects from increased
metabolic rate (e.g., pts with cardiovascular disease). After several weeks of treatment
with these meds and the patient is euthyroid, the pt may choose radioiodine treatment.

• beta blockers: administered as soon as the diagnosis of hyperthyroidism is made, even

before obtaining a definitive diagnosis as to the etiology of the thyrotoxicosis. Goal is to
reduce HR < 90 while avoiding hypotension.

• radioiodine (thyroid ablation)- taken by capsule (or sometimes a liquid) the iodine is
taken up by the thyroid gland and results in extensive tissue damage. Pt will need to take
levothyroxine replacement therapy for the rest of their lives once ablation complete.

• surgery (thyroidectomy)-rarely used (1% of pts)

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 Methimazole: Nursing Implications
• supratherapeutic levels lead to iatrogenic hypothyroidism
Serious adverse effects:
• hepatoxicity
• aplastic anemia (pancytopenia)- increased risk if the patient is also
taking other drugs that result in myelosuppression
Common side effects:
• nausea, vomiting, diarrhea (may take with food)
• rash, hives, and other dermatological reactions
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Although rare, it can cause aplastic anemia due to bone marrow suppression. This
results in a decrease in all blood cells:
- Anemia
- Leukopenia (neutropenia)
- Thrombocytopenia

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 Acute complications of hyperthyroidism
Thyroid storm (thyrotoxicosis)
• tachycardia, hypertension, hyperthermia, seizures, delirium, coma
Management
• beta blocker
• thioamide (antithyroid)
• iodine solution to block the release of thyroid hormone
• corticosteroids to reduce T4-to-T3 conversion, reduces flushing
(promotes vasomotor stability), and possibly treat an associated
relative adrenal insufficiency
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Precipitating factors:
• abruptly stopping antithyroid drugs
• surgery (especially in thyroid area)
• trauma
• infection
• acute iodine load (including amiodarone
• post-partum

Remember that when metabolic rate increases, we need stress hormones to respond
accordingly. In thyroid storm, the metabolic rate increases to extreme levels which means
the pt may have “normal” cortisol levels, but they are not “high enough” to offset the
increased metabolism which leads to a “relative” adrenal insufficiency.

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 Parathyroid disorders

Responsible for the

regulation of calcium
and phosphate levels.

13

The overall effect of PTH secretion is to increase serum calcium concentration and decrease
the level of serum phosphate.

A decrease in serum-ionized calcium level stimulates PTH secretion. PTH acts directly on the
bone to release calcium by stimulating osteoclast activity. PTH also acts on the kidney to
increase calcium reabsorption while phosphate reabsorption is decreased (i.e. increased
phosphate excretion).

Phosphate and magnesium concentrations also affect PTH secretion.

• An increase in serum phosphate level decreases serum calcium level by causing
calcium-phosphate precipitation into soft tissue and bone, which indirectly
stimulates PTH secretion.
• Hypomagnesemia in persons with normal calcium levels acts as a mild stimulant to
PTH secretion; however, in persons with hypocalcemia, hypomagnesemia
decreases PTH secretion.

Therefore, primary hyperparathyroidism increases serum calcium levels and

hypoparathyroidism decreases serum calcium levels.

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 Parathyroid disorders
Affect calcium and phosphate balance
HYPERCALCEMIA

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In PD1 we spoke about the importance of using lab results to diagnose electrolyte
imbalances. The key is knowing who is at risk for which imbalances and ensure these
electrolytes are being monitored. However, nurses are also expected to be familiar with the
key symptoms of certain imbalances. In the case of calcium imbalances, this is a favourite
focus for NCLEX-prep products.

Symptoms typically listed related to hypercalcemia include:

• Polyuria
• LOC changes (delirium)
• N&V and constipation
• lethargy, depressed reflexes, and muscle weakness
• bone pain (if associated with conditions of accelerated bone loss such as cancers affecting
bone).
• arrhythmias

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 Primary Hyperparathyroidism (H-PTH)
Primary- tumor leads to excess PTH release that is not responsive to
normal negative feedback signal
• Hypercalcemia
• Hypophosphatemia
Diagnosis:
Elevated PTH along with hypercalcemia
Secondary- most commonly associated with chronic kidney disease
CKD) due to decreased excretion of phosphate and decreased
absorption of calcium from the GI tract. Referred to as CKD mineral and
bone disorder (CKD-MBD)
15

There are different causes of H-PTH, but we will only be looking at the primary form in this
course which is usually the result of parathyroid adenomas. Secondary H-PTH is commonly
associated with chronic kidney disease (you will learn more about this link next term). There
is also tertiary H-PTH, but this is too rare to bother discussing.

In primary hyperparathyroidism the tumor causes increased PTH secretion that does not
respond to the usual negative feedback systems (elevated serum calcium should DECREASE
PTH release). This is why elevated PTH combined with hypercalcemia supports
hyperparathyroidism.

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 Treating parathyroid disorders
hyperparathyroidism
Primary- surgery to remove tumor
Priority concerns in the post operative period
• Maintenance of airway (have tracheostomy kit at bedside)
• Hypocalcemic crisis (tetany, seizure, laryngospasm). Monitor calcium levels closely
and report early signs of respiratory compromise:
• Dyspnea
• Stridor (high pitched wheezing)
• Drop in oxygen saturation
• Inability swallow (drooling)
Medical management:
• Calcimimetics: cinacalcet
• Bisphosphonates*
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Parathyroidectomy
Two distinct potential causes of airway compromise exist in the immediate post-operative
period:
1. Because the parathyroid gland is located in front of the trachea, post-operative
swelling/hematoma formation can lead to compression of the airway.
• Altering the MD to evidence of tracheal compression is the best way to prevent
life-threatening airway occlusion.

2. Post-operatively the pt is also at risk for hypocalcemic crisis which poses a risk for airway
compromise due to laryngeal spasm.
• Monitoring pt’s calcium levels closely and alerting the MD to decreases early is the
best way avoid hypocalcemic crisis (post-op parameters will usually be provided)

• Keeping an emergency tracheotomy kit at bedside is typically part of post-op care.

However, ideally, we want to identify airway issues early enough, so this invasive
intervention is not needed!

Medical management
If the patient cannot have surgery or the cause of hyperparathyroidism is not a tumor,
medications can be used to balance calcium and phosphate levels. Although calcimimetics
are first line for hyperparathyroidism, we will not examine this class closely as it is not
common.

Bisphosphonates are commonly used for tx of other conditions such as osteoporosis and for
patients with cancer who have increased bone resorption and hypercalcemia, so this class of
medication is explored on the next few slides.

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 Hyper-PTH causes Secondary Osteoporosis
Osteoporosis is characterized by low bone mass and increased skeletal
fragility. A clinical diagnosis of osteoporosis may be made in the
presence of:
• Fragility fracture, particularly at the spine, hip, wrist, humerus, rib,
and pelvis OR
• T-score ≤-2.5 bone mineral density (BMD) measurement by dual-
energy x-ray absorptiometry (DXA)

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We are popping in a bit more info about osteoporosis in general here to avoid repetition
related to the testing and treatments for bone loss as these are the same for H-PTH and
osteoporosis associated with aging- but the patho is different, so here is a very brief
overview.

Primary Osteoporosis
• Old bone is being resorbed faster than new bone is being made, causing the bones to lose
density, becoming thinner and more porous.
• Bone tissue can be normally mineralized in osteoporosis, but the mass (density) of bone is
decreased and the structural integrity of trabecular bone is impaired.
• Increases the risk for fragility factures (sometimes called pathological fracture). Common
fracture sites are spine, femoral neck, and wrist.

Risk factors:
• Postmenopausal females are at highest risk due to estrogen deficiency but older males
also at increased risk.
• Other factors, such as inadequate dietary calcium intake, lack of weight-bearing exercise,
and sarcopenia (muscle mass loss associated with aging)

Diagnosis: Based on the following criteria:

• bone mineral density (BMD) of 2.5 or more standard deviations below the peak bone
mass (i.e., T-score ≤ −2.5) Measured using DXA scan (sometimes spelled DEXA)
• 50 years and older and have sustained a low-trauma hip, vertebral, humerus or pelvic
fracture after the age of 40 years
• absolute fracture risk of 20% or more over the next 10 years, using a fracture risk
assessment tool

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 Prevention of Osteoporosis
• Good nutrition and physical activity through a lifetime can reduce risk
(i.e., don’t wait for menopause!)
• Calcium and vitamin D supplements
• Weight bearing, resistance, and functional (e.g., improving balance)
exercise
• Avoiding smoking

18

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 Treatment: Bisphosphonates
Class: Bisphosphonates
Common: Alendronate (Fosamax®) (oral)
Other common: Pamidronate (IV)
Indication: osteoporosis, bone loss r/t cancer, hypercalcemia of cancer,
Paget disease
Mechanism of Action: decreases the rate of bone resorption (by
inhibiting osteoclasts) leading to an indirect increase in bone mineral
density = prevents bone loss which also lowers serum calcium levels

19

Paget’s disease is a chronic, progressive genetic disease that leads to osteolytic and
osteoblastic activity. The disorganized reformation of bone that is structurally
abnormal and prone to fracture. Patients may also experience bone pain, arthritis,
and deformities.

19
 Bisphosphonates: Nursing Implications

Side Effects
• hypocalcemia
• bone*, joint, muscle pain, nausea, and dyspnea (worse with IV forms
like pamidronate)
• esophageal erosion- dyspepsia, nausea, GERD (oral forms only)

Take in the morning before eating with cup of water

Pt should remain sitting up for 30 mins post administration
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For oral alendronate:

• Administer first thing in the morning and ≥30 minutes before the first food or other
medication(s) of the day.
• Take with plain water. Do not take with mineral water.
• Avoid calcium-containing products at the time of administration
• Sit upright (not to lie down) for ≥30 minutes to reduce esophageal irritation

Serial bone mineral density (BMD) should be evaluated at baseline and every 1 to 3 years on
treatment

Pamidronate IV is more commonly used to treat hypercalcemia of malignancy (such as when

the patient has bone metastasis).
• IV forms should be administered slowly and the pt must be well hydrated to reduce the
nephrotoxic effects of the medication.
• Pts often complain of having flu-like symptoms after IV bisphosphonates.
*Although bone pain may be increased temporarily with administration, the overall effect of
bisphosphonates is the reduction of bone pain.

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 Selective Estrogen Receptor Modulators (SERM)
• Common: Raloxifene (Evista)
• Indications: to prevent or treat OP, prevention of breast cancer in high-
risk postmenopausal women with OP, safety not established for men
• MoA: Stimulates estrogen receptors on bone thus reducing resorption
of bone and increases bone density.
• Black box warnings: hx of DVT or CVD as can be prothrombotic
• Drug interactions: Lowered absorption of levothyroxine

Raloxifene acts like an estrogen agonist in the bone to prevent bone loss and has estrogen
antagonist activity to block some estrogen effects in the breast and uterine tissues, reducing
the cancer-related risks associated with classic hormone replacement therapy.

Increased risk of venous thromboembolism (VTE): Increased risk of deep vein thrombosis
and pulmonary embolism. Women with active or past history of VTE should not take
raloxifene.

Cardiovascular disease: Increased risk of death due to stroke in postmenopausal women

with documented coronary heart disease.

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 Hypoparathyroidism
1. Injury during thyroid surgery (75%)
2. Secondary to other medical condition/treatments (25%)
• Damaged by autoimmune disease
• Damaged by radiation
• Genetic defects

Diagnosis: PTH is low with a low calcium level in absence of

hypomagnesemia

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Hypomagnesemia – Hypomagnesemia causes hypocalcemia by inducing PTH

resistance or deficiency. It is therefore a reversible cause of hypocalcemia associated
with low or inappropriately normal PTH. Hypocalcemia should resolve within minutes
or hours after restoration of normal serum magnesium concentrations if
hypomagnesemia was the cause of the hypocalcemia. Therefore, this is a differential
diagnosis that must be ruled out when a pt has low Ca and low PTH.

22
 Manifestations of Hypocalcemia
Trousseau sign (BP cuff
inflated = carpal spasm)

Chvostek’s sign (tap

cheek = twitch)

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Here’s a big long list of complications r/t hypocalcemia…but what is most important? Say it
with us…”Know who is at risk for hypocalcemia and monitor lab results carefully so treatment
can be started BEFORE these effects occur!”

Neuromuscular irritability (Tetany)

Paresthesia (peri-oral, extremities)
Muscle twitching
Trousseau's sign
Chvostek's sign
Seizures
Laryngospasm
Bronchospasm

Cardiac
Prolonged QT interval
Hypotension
Heart failure
Arrhythmia

Goltzman, D. (2023, Oct 02). Clinical manifestations of hypocalcemia. UpToDate

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 Hypoparathyroidism: Treatment
Calcium gluconate- IV used in urgent/emergent situations
Indication: severe hypocalcemia, Mg toxicity, CCB or BB OD, hyperkalemia*
MoA: replaces Ca, which is essential for muscle contraction and
neurotransmission.
• Maximum rate 200 mg/min (usually infused over at least 1 hour)
➢Rapid infusion can result in dysrhythmias and hypotension
➢Central line is preferred (vesicant)
➢If given peripherally, must ensure site is healthy/patent (we will discuss actions
to take if extravasation of a vesicant medication occurs in Module 5)

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Usually, treatment of hypoparathyroidism will include oral calcium and vitamin D

supplements, but here we are focusing on IV calcium gluconate as it is a medication you may
encounter for a variety of clinical conditions.

You may have learned in Pharm and Diagnostics 1 about using calcium IV for pts with
hyperkalemia. *Remember, this is only to offset the effects of hyperkalemia on the resting
membrane potential and stabilize cardiac conduction. The calcium will not alter the
potassium level, so the pt will require a separate treatment to lower K+ levels.

Due to its stabilizing effects on myocardial cells, calcium gluconate is also used to help
counter the effects of BBs and CCBs on cardiac condition.

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 Hypomagnesemia: Treatment
Magnesium sulfate: IV replacement, anti-dysrhythmic
Indication: ventricular dysrhythmias, pre-eclampsia, refractory asthma
attack
MoA: slows neuromuscular and myocardial conduction
• Doses range from 1-6 grams depending on severity of symptoms.
Maximum rate is 150 mg/minute (in non-emergent situations, rate is 1
g/hr)
➢Rapid infusion can result in bradycardic dysrhythmias, hypotension,
respiratory depression

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As mentioned, having a very low Mg level can mimic hypo-PTH. To correct hypomagnesemia-
obviously we give magnesium.

Magnesium decreases acetylcholine in motor nerve terminals and acts on myocardium by

slowing the firing rate of SA node and prolonging conduction time to stabilize excitable
membranes. This is why it is also indicated in:
• Ventricular tachycardia
• Pre-eclampsia: a condition of pregnancy characterized by hypertension and proteinuria
and can lead to seizures and organ hypoperfusion.

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