THE

PARATHYROID
GLANDS
Anatomic and Physiologic Overview
Anatomic and Physiologic Overview
 Specific Disorders of the
Parathyroid Glands

HYPERPARATHYROIDISM
caused by overproduction of
parathormone characterized by bone
decalcification & development of
renal calculi containing
Calcium
 Types of Hyperparathyroidism
a. Primary hyperparathyroidism
hyperplasia or tumor of one of the
parathyroid glands
b. Secondary hyperparathyroidism
gland enlargement due to chronic
hypocalcemia
 Types of Hyperparathyroidism

c. Tertiary hyperparathyroidism
parathyroid glands are enlarged & do
not respond to changes in serum Ca
levels, usually associated w/ chronic
renal failure
Pathophysiology
 Clinical Manifestations
• May be asymptomatic/symptomatic
• Apathy
• Fatigue
• Muscle weakness
• n/v
• Constipation
• HPN
• Cardiac dysrhythmias
Increase in Ca – produces a decrease in excitation
potential of nerve and muscle tissue
Formation of renal stones – r/t increased urinary
excretion of Ca & Ph, occurs in 55% of pts. w/
primary hyperparathyroidism
Renal damage – results from the precipitation of
Ca phosphate in the renal pelvis & parenchyma,
w/c causes renal calculi, obstruction,
pyelonephritis, & renal failure
MS symptoms:
May be caused by demineralization of the bones or
by bone tumors composed of benign giant cells
resulting from overgrowth of osteoclasts
Skeletal pain & tenderness esp. of back & joints
Pain on weight-bearing
Pathologic fxs, deformities, shortening of body
stature
Bone loss attributable to risk for fracture
 Assessment & Diagnostic Findings

Primary hyperparathyroidism – is
diagnosed by persistent elevation of
serum calcium levels & elevated
concentration of parathormone
RIA – for parathormone are sensitive &
differentiate primary
hyperparathyroidism from other causes
of hypercalcemia
Double-antibody parathyroid hormone test
– is used to distinguish b/w primary
hyperparathyroidism & malignancy as a
cause of hypercalcemia

UTZ, MRI, Thallium scan, & fine-needle

biopsy – used to evaluate the function of
the parathyroids & to localize the
parathyroid cysts, adenomas, or
hyperplasia
 Medical Management

 Recommended treatment of primary

hyperparathyroidism is surgical removal
of abnormal parathyroid tissue
(parathyroidectomy)
 Hydration therapy
daily fluid intake of 2000 ml or
more is encouraged
cranberry juice – lowers urinary
pH
avoid thiazide diuretics - decrease
renal excretion of Ca &
further elevate serum Ca levels
(hypercalcemic crisis) – instruct to
avoid dehydration
 Mobility
walking or use of a rocking chair (for
those w/ limited mobility) – bones
that are subjected to normal stress
give up less Ca
avoid bed rest – increases Ca excretion
& risk for renal calculi
oral phosphatase – lower the serum
Ca level, long-term use is not
recommended because of risk of ectopic
Ca phosphate deposition in soft tissues
 Diet & Medications
avoid diet w/ restricted or excess Ca
(if w/ coexisitng peptic ulcer) –
antacids & CHON feedings
anorexia – improve appetite
constipation – prune juice, stool
softeners, & physical activity,
increase fluid intake (common
post-operatively)
 Nursing Management

• Awareness of the course of the disorder

& an understanding approach by the
nurse may help the patient and family
deal with their reactions & feelings

• close monitoring for life-threatening

complications of the tx
 Complications: Hypercalcemic crisis

• Characterized by extreme elevation of

serum Ca levels >15 mg/dl (3.7 mmol/L)
result in neurologic, cardiovascular & renal
symptoms
tx: rehydration, diuretic agents to promote
renal excretion of excess Ca, & phosphate
therapy to correct hypophosphatemia &
decrease serum Ca levels by promoting Ca
deposition in bone & reducing GI
absorption of Ca
• Cytotoxic agents (mithramycin),
calcitonin, & dialysis may be used in
emergency situations to decrease serum
Ca levels quickly
• combination of calcitonin &
corticosteroids (in emergencies) – to
reduce serum Ca level by increasing Ca
deposition in bone
• biphosphonates – etidronate,
pamidronate to dec serum Ca levels
 HYPOPARATHYROIDISM
 inadequate secretion of
parathormone after interruption of the
blood supply or surgical removal of
parathyroid gland tissue during
thyroidectomy, parathyroidectomy, or
radical neck dissection
 results in increased blood phosphate
(hyperphosphatemia) and decreased
blood Ca levels
In the absence of parathormone, there is
decreased intestinal absorption of dietary Ca
& decreased resorption of Ca from bone &
through the renal tubules
Decreased renal excretion of phosphate causes
hypophosphaturia, & low serum Ca levels
result in hypocalciuria
 Clinical Manifestations
• Tetany
• Bronchospasm, laryngeal spasm,
carpopedal spasm (flexion of the elbows
& wrists & extension of the
carpophalangeal joints & dorsiflexion of
the feet)
• Dysphagia, photophobia, cardiac
dysrhythmias, & seizures
• Anxiety, irritability, depression, delirium
• ECG changes & hypotension may occur
 Assessment & Diagnostic Findings

(+) trousseau’s sign – is positive when

carpopedal spasm is induced by
occluding the blood flow to the arm for 3
minutes w/ BP cuff
(+) Chvostek’s sign – is positive when a
sharp tapping over the facial nerve just in
front of the parotid gland & anterior to
the ear causes spasm or twitching of the
mouth, nose & eye
• Tetany develops at serum Ca levels of
5 to 6 mg/dl (1.2 to 1.5 mmol/L) or
lower
• Serum Ph – increased
• X-ray of bone – increased density;
calcification of the subcutaneous or
paraspinal basal ganglia of the brain
 Medical Management
• Goal of therapy: to increase s. Ca level to
9-10 mg/dl (2.2-2.5 mmol/L) & eliminate
symptoms of hypoparathyroidism &
hypocalcemia
• Administration of IV Calcium gluconate,
sedative agents (pentobarbital)
• Parenteral parathormone – to tx acute
hypoparatyhroidism w/ tetany;
monitored for allergic reactions
• Environment: free of noise, drafts, bright
lights, or sudden movement
• Tracheostomy or mechanical ventilation,
bronchodilating medications – for
respiratory distress
• Oral tabs – Ca gluconate
Al H3O gel/Al CO3 (Gelusil, Amphojel)
– administered after meals to bind
phosphate & promote its excretion
through the GIT
• Vit. D preps – enhance Ca absorption
from GIT
 Nursing Management
 Care of postoperative pts – detecting
early signs of hypocalcemia &
anticipating signs of tetany, seizures, &
respiratory difficulties
 Ca gluconate kept at bedside, w/
equipment necessary for IV
administration; caution w/ pt w/ cardiac
d/o & is receiving digitalis, given slowly &
cautiously (inc. systolic contraction)
THE ADRENAL GLANDS
Anatomic & Physiologic Overview
 Anatomic & Physiologic Overview

• Adrenal medulla – function as part of the

ANS
stimulation of preganglionic sympathetic
nerve fibers, w/c travel directly to the
cells of the adrenal medulla, causes
release of the catecholamine hormones
epi & norepi
- regulates catabolism of stored fuels to
meet caloric needs
- prepares the body to meet a challenge
(fight-or-flight response)
- causes decreased blood flow to tissues
that are not needed in emergency
situations (GIT)  (cardiac/skeletal
muscle
- induce release of free fatty acid,
increase BMR, & elevate blood glucose
level
• Adrenal Cortex – makes it possible to
adapt to stress of all kinds
w/o this, severe stress would cause
peripheral circulatory failure, circulatory
shock & prostration
 Glucocorticoids – are so-called for
their influence on glucose metabolism:
increased hydrocortisone secretion
(elevates bld. glucose level)
- inhibit inflammatory response to tissue
injury & suppress allergic manifestation
- S/E: dev’t of DM, osteoporosis, peptic
ulcer, increased protein breakdown
resulting in muscle wasting & poor
wound healing, & redistribution of body
fat
 Mineralocorticoids:
• Has major effect in electrolyte
metabolism
• Act on renal tubular & GI epithelium to
cause increased Na ion absorption in
exchange for excretion of K or
Hydrogen ions
 Adrenal Sex Hormone (Androgens)
• dev’t of secondary characteristics
• stimulate protein synthesis and inhibit
protein breakdown, enhancing the
growth of muscle and bone tissue in
the developing male
• May also secrete small amounts of
male & female sex hormones
 Adrenocortical Insufficiency (Addison’s
Disease)

 Occurs when adrenal cortex function is

inadequate to meet the pt’s need for
cortical hormones
 Autoimmune or idiopathic atrophy
 Surgical removal of both adrenal glands
& infection of AG (TB & histoplasmosis)
 Inadequate secretion of ACTH = dec.
stimulation of AC
 Use of corticosteroids (suppress
function of adrenal cortex)
 Clinical Manifestations

• Muscle weakness, anorexia, GI

symptoms, fatigue, emaciation, dark
pigmentation of the mucous membrane
& the skin (knuckles, knees, & elbows),
hypotension, low bld. Glucose, low s. Na,
high s. K levels
• mental status changes: depression,
emotional lability, apathy, & confusion
• w/ disease progression & acute
hypotension, addisonian crisis develops
• Characterized by cyanosis, classis signs of
circulatory shock: Pallor, apprehension,
rapid & weak pulse, rapid respirations, &
low BP
• h/a, nausea, abd. Pain, diarrhea
confusion, restlessness
 Assessment & Diagnostic Findings

• Early morning serum cortisol (<165

nmol/L) & plasma ACTH
• Primary insufficiency (>22.0 pmol/L)
• Decreased levels of glucose & Na, Inc.
level of K & inc. WBC count
• Confirmed by low levels of adrenocortical
hormones in the blood or urine &
decreased serum cortisol levels
 Medical Management

• Administering fluids & corticosteroids,

monitoring v/s, placing pt in recumbent
position
• Hydrocortisone (Solu-Cortef) given IV
followed by 5% dextrose in NS
• Vasopressor for hypotension (persistent)
• Antibiotics
 Nursing Management

• Assess the patient – especially BP & PR,

skin color/turgor, wt changes, muscle
weakness, fatigue, precipitating factor
• Monitoring & Managing Addisonian
Crisis
• Monitor s/s indicative of Addisonian
crisis: Shock
• Avoid physical & psychological stressors
(avoiding overexertion, cold, infection,
emotional distress)
• IV administration of fluid, glucose,
electrolytes (Na), replacement of missing
steroid hormones, vasopressors
Restoring Fluid Balance
Improve Activity Tolerance
- maintain a quiet, non-stressful env’t

Promoting home & community-based care

- teaching patients self-care – explicit
verbal & written instructions – how &
when to use the injection, inform other
health care providers, wearing a medic
alert bracelet, & carry information at all
times about the need for corticosteroids
- need to know the signs of excessive or
insufficient hormone replacement

Continuing care
Referral for home care to assess pt’s
recovery, monitor hormone replacement, &
evaluate stress in the home, assess the pt &
family’s knowledge about the medication
therapy & dietary modifications