CH 37 Thyroid and Parathyroid Agents
THE THYROID GLAND
❑ Located in the middle of the neck, it surrounds the
trachea like a shield
❑ Vascular gland with two lobes
❑ Produces: thyroid hormone and calcitonin
STRUCTURE AND FUNCTIONS
❑ It is made up of cells arranged in circular follicles
❑ Parafollicular cells 🡪 cell found around the
follicle of the thyroid gland
❑ The center of each follicle is composed of colloid
tissue in which thyroid hormones produced by the
gland are stored
❑ Removes iodine from the blood, concentrates it,
and prepares it for attachment to tyrosine
❑ Calcitonin 🡪 affects calcium levels and acts to
balance the effects of the parathyroid hormone
(PTH), parathormone
❑ Thyroid hormones:
A. Thyroxin or tetraiodothyronine (T4)
🡪 give in synthetic from levothyroxine
🡪 produced more
B. Triiodothyronine (T3)
🡪 synthetic form liothyronine
❑ Thyroid hormone regulates:
o Rate of Metabolism
o Heat production and body temp
o O2 consumption and cardiac output
o Blood volume
o Enzyme system activity
o Metabolism of carbohydrates, fats and
proteins
o Growth and development (reproductive and
nervous system)
CONTROL
❑ Production and release is regulated by anterior
pituitary hormone called thyroid stimulating
hormone (TSH)
❑ TRH 🡪 TSH 🡪 thyroid 🡪 thyroid hormones
❑ High levels of thyroid hormones sends negative
feedback message to pituitary to decrease TSH
release and TRH release
❑ Low levels of thyroid hormone stimulates release of
TRH🡪 TSH
THYROID DYSFUNCTION
❑ Involves underactivity (hypothyroidism) and
overactivity (hyperthyroidism)
❑ Read Box37.1 drug therapy across lifespan
HYPOTHYROIDISM
❑ Lack of sufficient levels of thyroid hormones to
maintain a normal metabolism
❑ Pathophysiological states:
o Absence of thy thyroid gland
o Lack of iodine in diet
o Lack of functioning thyroid tissue due to
tumor or autoimmune disease
o Lack of TSH due to pituitary disease
o Lack of TRH related to tumor or disorder of
hypothalamus
❑ Most common type of thyroid dysfunction
❑ Signs include fatigue and obesity
❑ Cretinism 🡪 a condition in children born without
thyroid gland
❑ Myxedema 🡪 sever adult hypothyroidism;
develop gradually as thyroid stops functioning;
develop as a result of autoimmune thyroid disease
(Hashimoto disease), viral infection, or over
treatment with antithyroid, or removal of thyroid
HYPERTHYROIDISM
❑ Occurs when excessive amounts of thyroid
hormones are produced and released in circulation
 ❑ Graves’ disease 🡪 autoimmune disease; most
common cause of hyperthyroidism
❑ Goiter 🡪 enlargement of thyroid gland; effect of
hyperthyroidism; overstimulation of TSH
❑ Treated with surgical removal of thyroid, radiation,
drug treatment that blocks T4
THYROID AGENTS
A. Levothyroxine (Synthroid, Levoxyl, Levothroid)
o Synthetic salt of T4
o Most frequently used replacement hormone
because of it predictable bioavailability and
reliability
B. Desiccated thyroid (Armour Thyroid and others)
o Prepared from dried animal thyroid and contains
T3 and T4
o Inexpensive
C. Liothyronine (Cytomel, Triostat)
o Synthetic salt of T3
D. Liotrix (thyrolar)
o Synthetic preparation of T4 and t3 in standard
4:1 ratio
THERAPEUTIC ACTIONS AND INDICATIONS
❑ Increase metabolic rate of body tissues, increase
consumption, respiration, HR, growth and
maturation, metabolism of CH, PRO, FAT
❑ Indicated for treatment of thyroid toxicity,
formation of goiter, thyroid overstimulation during
pregnancy
❑ Not approved for weight loss
PHARMACOKINETICS
❑ Well absorbed in GI and bound to serum proteins
❑ Deiodination of drug occurs in liver, kidney, other
body tissues
❑ Elimination primarily in bile
❑ Does not cross placenta and seems no effect on
fetus
❑ Should not be stopped during pregnancy
❑ Enter breast milk
CONTRAINDICATIONS AND CAUTION
❑ Allergy
❑ Acute thyrotoxicosis
❑ Acute myocardial infarction
❑ Liothyronine and liotrix🡪 increased cardiac effects
and anxiety
❑ Caution in:
o Lactation
o Hypoadrenal conditions (Addison’s)
ADVERSE EFFECTS
❑ Thyroid function should be checked annually
❑ Skin rxn and loss of hair often seen in children
❑ Cardiac stimulation
❑ CNS effects
❑ Difficulty swallowing and esophageal atresia (water
is strongly recommended to alleviate this effect)
DRUG TO DRUG INTERACTION
❑ +cholestyramine =decreased absorption (take 2hrs
apart)
❑ +oral anticoagulants =increased effectiveness
(dose of anticoagulant should be decreased)
❑ + digitalis glycosides = decreased effectiveness
❑ Theophylline clearance is decreased in hypothyroid
states
NURSING RESPONSIBILITIES
❑ Administer a single dose before breakfast each day
❑ Administer with full glass of water
❑ Monitor response carefully when beginning therapy
❑ Monitor cardiac response
❑ Arrange periodic blood tests of thyroid function

B.
ANTITHYROID AGENTS
🡪 block production of thyroid hormone and treat
hyperthyroidism
THERAPEUTIC ACTIONS AND INDICATIONS
A. Thioamides
❑ Lower thyroid hormone (TH) levels by preventing
formation of TH in thyroid cells
❑ Inhibit conversion of T4 to T3 at cellular level
❑ Treatment of hyperthyroidism
❑ Propylthiouracil (PTU) and Methimazole (Tapazole)
❑ Well absorbed in GI and concentrated in thyroid
❑ Methimazole ( onset 30-40; peak 60) cross
placenta and PTU low potential of crossing
❑ Adverse effects: Drowsiness, lethargy Bradycardia,
nausea, skin rash
❑ PTU adverse effects: nausea, vomiting, GI
complaints, severe liver toxicity
❑ Methimazole adverse effects: less GI effects; bone
marrow suppression
❑ PTU + oral coagulants = increase risk of bleeding
❑ PTU + theophylline, propranolol, digitalis = change
in serum levels, change in effects of PTU as patient
moves to hyperthyroid to euthyroid state
Iodine solutions
❑ High doses of iodine block formation of TH
❑ Cause thyroid cells to be oversaturated with iodine
❑ Radioactive iodine (sodium iodide I131) is taken up
by thyroid cells, then destroyed by beta-radiation
❑ Reserved for patients who are not candidates for
surgery, woman who can’t be pregnant, elderly
❑ Strong iodine solution , potassium iodide (Iosat,
thyrosafe, thyroshield), sodium iodide I131
❑ Rapidly absorbed in GI and widely distributed
throughout body fluids
❑ Taken orally and have rapid onset (effects in 24 hrs
and peak 10-15 days)
❑ Effects are short lived; may precipitate further into
thyroid enlargement and dysfunction
❑ Sodium iodide I131 category X and reserved for 30
yrs older patients
❑ Cross placenta and breastmilk
❑ adverse effects: hypothyroidism, iodism, staining of
teeth, skin rash, goiter
❑ +anticoagulants, theophylline, digoxin, metoprolol,
and propranolol = metabolism of these drugs
changes
NURSING RESPONSIBILITIES
❑ Administer propylthiouracil 3x a day around the
clock
❑ Give iodine solution through straw
❑ Monitor response carefully and arrange periodic
blood tests
❑ Monitor for signs of iodism
THE PARATHYROID GLANDS
🡪 4 very small froups of glandular tissue located at
the back of the thyroid gland
🡪 Produce PTH🡪 regulator of serum calcium
STRUCTURE AND FUNCTIONS
❑ Parafollicular cells of the thyroid gland produce
calcitonin which responds to high Ca levels to
lower serum levels
❑ PTH actions:
o Stimulation of osteoclasts or bone cells to
release calcium from the bone
o Increased intestinal absorption of Ca
o Increased Ca reabsorption from the kidneys
o Stimulation of cells in the kidney to produce
calcitriol (active form of vitamin D) which
stimulated intestinal transport of Ca into blood
CONTROL
❑ Serum levels of Ca just be maintained at 9 & 11
mg/dl
❑ Calcium levels rise 🡪 calcitonin is stimulated & PTH
is blocked 🡪 block bone resorption and enhance
bone formation 🡪 Ca serum is absorbed in bone
❑ Magnesium affects PTH secretion by mobilizing Ca
and inhibiting release of PTH when conc. Rise or
fall
❑ Increased serum phosphate stimulates parathyroid
activity
❑ Renal tubular phosphate resorption is balanced by
Ca secretion into urine, drops serum Ca,
stimulating PTH
PARATHYROID DYSFUNCTIONS
HYPOPARATHYROIDISM
❑ Absence of PTH results in low Ca levels
(hypocalcemia) and hypoparathyroidism
❑ Accidental removal of parathyroid during thyroid
surgery
❑ Treatment consist of Ca and vitamin D therapy
(anti hypocalcemic agents)
HYPERPARATHYROIDISM
❑ Excessive production of PTH increases serum Ca
(hypercalcemia) and hyperparathyroidism
❑ Caused by parathyroid tumor or genetic disorder
❑ Primary hyperparathyroidism occurs in women 60
and 70 yrs of age
❑ Secondary hyperparathyroidism occurs in chronic
renal failure
❑ Pseudo Rickets (renal fibrocystic osteosis or
renal rickets) 🡪 occurs as a result of phosphorus
retention (hyperphosphatemia), 🡪 increase
stimulation of parathyroid glands and increased
PTH
❑ Paget’s disease 🡪 genetically linked; overactive
osteoclasts that eventually replaced by enlarged
and soften bony structures
❑ Postmenopausal osteoporosis 🡪 dropping
estrogen levels allow calcium to be pulled out of
bone, resulting in a weakened and honey combed
bone structure
PARATHYROID AGENTS
ANTIHYPOCALCEMIC AGENTS
A. Teriparatide (forteo)
❑ PTH genetically engineered from E.coli bacteria
using rDNA technology
❑ Increase bone mass in postmenopausal women
and men with primary or hypogonadal
osteoporosis who are high risk for fracture
B. Parathyroid hormone (Natapara)
 ❑ Help control Ca level in patients with ❑ Dry mouth
hypoparathyroidism ❑ Constipation
C. Calcitriol (rocaltrol) ❑ Anorexia
❑ Most commonly used form of Vitamin D ❑ Severe hypocalcemia or hypercalcemia (parathyroid
hormone)
THERAPEUTIC ACTIONS AND INDICATIONS ❑ CNS effects
❑ Vitamin d compounds regulate absorption of Ca
from S.intestine, mineral resorption in bone and DRUG-DRUG INTERACTIONS
reabsorption of phosphate from renal tubules ❑ + magnesium-containing antacids = risk of
❑ Working with PTH and calcitonin, vitamin D works hypermagnesemia
as a hormone ❑ +cholestyramine or mineral oil = reduced
❑ Increase serum Ca levels and decrease serum absorption (separate between 2 hrs)
phosphate ❑ +digoxin = digoxin toxicity
❑ Indicated for management of hypocalcemia in p/t NURSING RESPONSIBILITIES
with chronic renal dialysis and for ❑ monitor calcium conc. Before and periodically
hypoparathyroidism ❑ nutritional consultation

PHARMACOKINETICS
❑ Calcitriol
o well absorbed in GI and widely distributed
o Stored in liver, fat, muscle , skin and bones
o Hepatic metabolism; excreted in bile
❑ Teriparatide
o SQ injection everyday
o Absorbed in SQ tissue; peak in 3 hrs
o Serum Ca levels will decline after 6 hrs and
return to baseline in 16-24 hrs
o Metabolized in liver; excrete kidney
❑ Parathyroid hormone
o Daily SQ injection
o Peak in 5-30 mins half-life 3 hrs
ANTIHYPERCALCEMIC AGENTS
CONTRAINDICATIONS AND CAUTION
A. Bisphosphates
❑ Allergy
❑ Act to slow or block bone resorption 🡪 lower Ca
❑ Hypercalcemia or Vitamin d toxicity
❑ Don’t inhibit normal bone formation and
❑ Pregnancy and lactation
mineralization
❑ Caution in history of renal stones
❑ Treatment of Paget’s disease and of postmenuposal
❑ Teriparatide 🡪 limit in postmenopausal women who
osteoporosis in women
have osteoporosis may cause osteo sarcoma
❑ Alendronate 🡪 is used to treat osteoporosis in
ADVERSE EFFECTS
men
❑ Metallic taste
❑ Nausea and vomiting
 ❑ Zoledronic acid 🡪 Prevent new fractures and ❑ Injection or nasal spray
treat multiple myeloma or documented bone ❑ Peak 40 mins and duration 8-24 hrs
metastases from solid tumors ❑ Contraindication:
❑ Well absorbed in S.intestine o Pregnancy and lactation
❑ Do not undergo metabolism o Allergy with salmon or fish products
❑ Excreted unchanged in urine o Caution in renal dysfunction or pernicious
❑ Slow onset and long duration anemia
❑ Contraindications and cautions: ❑ Adverse effect
o Hypocalcemia o Flushing of hand and face,
o Allergy o Skin rash
o Pregnancy and lactation(specially alendronate) o Nausea and vomiting
o Renal dysfunction o Urinary frequency
o Alendronate, ibandronate, risedronate 🡪 take o Local inflammation at site of injection
30 minutes before any food or beverage and NURSING RESPONSIBILITIES
p/t must remain upright for 30 minutes ❑ Ensure adequate hydration
o Zoledronic acid 🡪 caution in aspirin sensitive ❑ Arrange concomitant vitamin D, calcium
asthmatic patients; given IV infusion every 2 supplements and hormone replacement id used in
yrs for osteoporosis postmenopausal osteoporosis
o Ibandronate 🡪 available one-a -month ❑ Rotate injection and monitor site for calcitonin
formulation and IV prep for use when oral
drug can’t be taken
❑ Adverse effects:
o Headache, nausea, and diarrhea
o Increase bone pain in Paget’s disease
o Esophageal erosion (alendronate, ibandronate,
risedronate) if patient didn’t stay upright or 30
minutes
o Femoral shaft fractures (5 yrs use )
❑ Drug to drug interactions
o + antacids, calcium products, iron, or multiple
vitamins = Oral absorption is decreased
o +aspirin = Gi distress
B. Calcitonin (calcitonin salmon)
❑ Hormones secreted by the thyroid to balance
effects of PTH
❑ Inhibits bone resorption, lowers serum ca levels,
increase excretion of phosphate, Ca, and Na from
kidney
❑ Metabolized in tissues to inactive fragments;
excreted in kidney
❑ Cross placenta and affect fetus & Inhibit lactation