Disorders of the parathyroid gland

• Hyperparathyroidism
• overactivitiy of the parathyroid gland
• Primary
– parathyroid gland adenoma
Secondary
– carcinoma, hyperplasia, ectopic PTH producing tumors
• - results in high serum calcium level and bone
demineralization.
• -elevated parathormone levels, hypercalcemia,
hypophosphatemia
• Pathophysiology- a parathyroid adenoma can
produce excessive PTH despite normal serum
calcium causing abnormalities.
 Clinical Features:
The two major sites of potential complications are the bones and
the kidneys.
-hypercalcemia-decrease neuromuscular excitability(9-11mg/dl)
(4.5-5.5meq/L), WEAKNESS, COMA, ARRYTHMIAS(HEARTBLOCK)
-hypophosphatemia- (2.2- 4.8 mg/dl)irritability, seizure
Symptoms:
Fatigue and muscle weakness, lethargy
Skeletal pain and tenderness, bone deformities result in fracture
Constipation
Cardic dysrhythmias, hypertension
The kidneys may have renal stones (nephrolithiasis) or diffuse
deposition of calcium-phosphate complexes in the parachyma
(nephrocalcinosis).
 Diagnosis
1. serum calcium elevated(8-11mg/dl)
2. Serum phosphate decreased(2.2- 4.8 mg/dl)
3. Parathyroid hormone elevated(12-68pg/ml)

Radiograph:
Plain X-ray of hands can be diagnostic showing
bone resorption usually on the radial surface
of the distal phalanx and generalzed
osteopenia.
 Medications Used in Treatment of hyperparathyroidism
1. Calcitonin
-If calcitonin inhibits bone resorption by opposing the effects
of parathyroid hormone, thus it decreases skeletal calcium
release and increase renal clearance of calcium.
• 200 IU nasally/day (alternating nares)
• Decrease pain with acute vertebral compression fracture
2. Bisphosphenates – (Fosamax)
– Inhibit osteoclast-mediated bone resorption thereby
increasing total bone mass.

These drugs increase bone mass and reduce the incidence of

vertebral and nonvertebral fractures (even in women who
already have fractures).

– Side effects – anorexia, weight loss, gastritis

Medications Used in Treatment of hyperparathyroidism
• 3.Gallium nitrate-antihypercalcemia
• 4. Lasix- to promote excretion of calcium
• 5. Estrogen
– It also decrease bone resorption and can be given to
postmenopausal women with primary hyperparathyroidism using
medical therapy
• SURGERY
• 1. parathyroidectomy- removal of one or more of the
parathyroid glands
• Post operative care:
• 1. monitor for respiratory distress have tracheostomy set at
hand, suction and oxygen
• 2. position fowlers position, watch out for edema that signals
bleeding
• 3. Watch out for hypocalcemic crisis- increase NMI(tetany,
laryngospasm)
• 4. Administer calcium supplement and vitamin D as ordered
 Nursing management
• 1. Increase fluid intake- to prevent renal
stones
• 2. Watch out for hypertension and cardiac
dysrhythmias- cardiac monitoring
• 3. MIO
• 4. watch out for signs of renal stones
• 5. Administer normal saline as prescribed to
maintain hydration(sodium enhances
excretion of calcium.)
 Hypoparathyroidism
Deficient secretion of PTH which manifests
itself biochemically by hypocalcemia,
hyperphospatemia diminished or absent
circulating PTH and clinically the symptoms of
neuromuscular hyperactivity.
Causes:
1. Accidental removal of parathyroid gland
2. Following thyroidectomy
3. Idiopathic hypoparathyroidism
– Circulating antibodies for the parathyroid glands
and the adrenals are frequently present.
 Other causes of chronic hypocalcemia other than
hypoparathyroidism

• Dietary deficiency of vitamin D or calcium

• Decreased intestinal absorption of vitamin D
or calcium due to primary small bowel
disease, short bowel syndrome, and post-
gastrectomy syndrome.
• Drugs that cause rickets or osteomalacia such
as phenytoin, phenobarbital, cholestyramine,
and laxative.
A. Pathophysiology
B. - reduce PTH production slows bone reabsorption
decreases serum calcium that leads to, increase
neuromuscular irritability
C. Clinical Features:
D. Neuromuscular symptoms
– Parathesia, carpopedal spasm
– Tetany, dysrythmias (muscle twitching)
– Hyperventilation
– Laryngospasm, dysphagia
– Hypotension
– Convulsion (More common in young people and it can take
the form of either generalized tetany followed by
prolonged tonic spasms or the typical epileptiform
seizures.
– Signs of latent tetany
• Chvostek sign
• Trousseau sign
• Extrapyramidal signs (due to basal ganglia calcification)-
cataract and brain damage
 Laboratory findings
• 1. decrease serum calcium
• 2. serum parathyroid hormone low
• 3. increase phosphate level
• Emergency Treatment for Hypocalcemia
• 1. Calcium should be given parenterally till
adequate serum calcium level is obtained and then
vitamin D supplementation with oral calcium
should be initiated.
• - calcium carbonate, calcium gluconate, lactate
• -vitamin D (calciferol, calcitriol)
• PARATHORMONE REPLACEMENT THERAPY
 Disorders of the Adrenal glands
• Cushing syndrome
• - cause by hypersecretion of adrenal cortex hormones.
• Cause:
• 1. Pituitary tumor of the pituitary gland
• 2. Excessive release of ACTH by the pituitary gland result from
faulty release of Corticotropin releasing factor (CRF) from the
hypothalamus.
• 3. Most endogenous types are due to Bilateral Adrenal
Hyperplasia due to ACTH secretion by pituitary adenoma.
• 4. chronic use of glucocorticoid. (Steroid therapy)
 Assessment findings
• 1. altered fat distribution(truncal obesity with thin
arms and legs, buffalo hump)-gluco&mineralo
• 2. moonface, edema--glucocorticoids
• 3. hypertension- mineralocorticoids
• 4. hyperglycemia- gluco (anti-insulin)
• 5. osteoporosis- gluco
• 6. low resistance to infection,poor would healing-
gluco
• 7. hypokalemia- mineralo
• 8. muscle wasting, weakness- gluco
• 9. hirsutism, acne(masculinization of women)-due to
increase androgens and estrogen
• 10. mood swings , irritability- estrogen
• 11. Impotence, amenorrhea- estrogen, androgens
 Laboratory findings
• 1. serum potassium decrease, increase sodium
• 2. increase glucose, decrease serum calcium
• 3. increase WBC
• 4. elevated level of ACTH
• Nursing management:
• 1. Monitor V/S especially blood pressure, MIO,
weight.
• 2. Protect from trauma, injury-hypocalcemia
• 3. Administer steroid inhibitors- decrease cortisol
production can cause drowsiness
• - aminoglutethimide
• -mitotane, ketoconazole
 4. Surgery
• 1. Adrenalectomy- hormonal replacement is
required after the surgery
• Monitor for addisonian crisis after surgery
• 2. hypophysectomy for pituitary tumor
• a. Post-operatively, the cotton sponges should
remain in your nose until removed by the surgeon.
Put client in fowlers position to promote venous
drainage
• b. You must not blow your nose after this type of
operation. Doing so could disrupt the healing
process and lead to cerebrospinal fluid leak or
other problems(check presence of glucose). A
small amount of bloody or mucous-type drainage
from the nose is expected.
• c. Pain medication
• d. Watch out for other complications
• e. Check MIO, if urine output is above 900ml/2hrs
this indicate diabetes insipidus
 Disorders of the Adrenal glands
• Addisons disease(adrenal insufficiency)
• - hyposecretion of adrenal cortex
hormones(glucocorticoids, mineralocorticoids and
sex hormones)
• Causes:
• 1. autoimmune disorders
• 2. neoplasm
• 3. adrenalectomy
• 4. fungal infection
• 5. tuberculosis
• Secondary adrenal insufficiency is associated with
• 1. suppression of the hypothalamic pituitary from
exogenous steroid use.
 Assessment findings-everything is low and slow except
potassium
• Adrenal hypofunction results in adrenal hormones results in
various fluids, electrolytes and metabolic disturbances.
• Clinical manifestation:
• 1. fatigue, muscle weakness, arthalgias, weight loss
• 2. anorexia, nausea & vomiting—hyperkalemia(decrease
aldosterone-sodium loss and fluid loss)
• diarrhea, abd pain
• 3. hypotension(dec. ability to constrict-dec. sympathetic
activity in the blood vessel), dehydration—sodium loss
• 4. hypoglycemia– due to decrease glucocorticoids
• 5. menstrual changes-amenorrhea, impotence for men—due
to hyposecretion of sex hormones(testosterone and estrogen)
• 6. SHOCK
 Assessment findings
6. Hyperpigmentation- hyposecretion of adrenal cortex
triggers MSH hormone

7. Decrease alertness and confusion

8. Addisonian crisis:- life threatening cause by acute
adrenal insufficiency, precipitated by stress,
infection, trauma or surgery
A. profound hypotension
B. extreme weakness, hypoglycemia
C. dehydration, hyponatremia--shock
D. hyperthermia
 Laboratory findings
• 1. decrease serum glucose(60-115mg/dl)
• 2. sodium level decrease (135-148 meq/L)
• 3. potassium level increase(3.5-5.5meq/L)
• Nursing management:
• 1. Monitor blood glucose and potassium
• -weight, V/S, MIO
• 2. Administer glucocorticoids and mineralocorticoids as
ordered
• - celestone(betamethasone)
• - cortistan(cortisone)
• - decadron(dexamethasone)
• - medrol( methylprednisone)
• - florinef (fludrocortisone)- mineralocorticoids
 Nursing intervention during steroid therapy(hormonal
replacement)
• 1.Monitor retention of sodium and water that may cause
elevation of BP-steroid may elevate the BP
• 2. monitor weight, edema, MIO
• 3. avoid exposure to infection-steroid may mask the signs
• 4. steroids can decrease potassium and calcium
• 5. administer steroids after meals or with milk cause can
lead to gastric irritation. Monitor gastric bleeding
• 6. monitor blood glucose level
• 7. steroids enhance metabolism
• - diet should be high protein and carbohydrates
• - high potassium, low sodium- prevents hypernatremia
and water retention
• -increase vitamin D & weight bearing exercise
• 8. dose should be tapered and not stop abruptly to
prevent addisonian crisis
 Nursing intervention during steroid therapy(hormonal
replacement)
• 9. Monitor side effects:
• - hyperglycemia
• - hypokalemia
• - hypocalcemia
• - sodium and water retention, edema
• - increase susceptibility to infection
• - gastric irritation
• - mood swings
• - altered fat distribution(truncal obesity with thin
arms and legs, buffalo hump)
 Contraindication of steroid therapy
• 1. diabetic clients
• 2. ongoing infection esp fungal mask the signs
of infection
• 3. when use with nsaids increase risk of
gastrointestinal ulcerations
• 4. barbiturates, rifampicin decrease the effect
of prednisone
 Addisonian crisis management
• 1. Administer glucocorticoid/IV(solu cortef)
• 2. Administer IVF to combat dehydration
• 3. GCS, MIO, V/S
• 4. Monitor electrolytes(sodium, potassium,
glucose level)
• 5. protect from infection
• 6. bedrest
 Posterior pituitary dysfunction
• - Diabetes insipidus- undersecretion of ADH
results in dilute urine production
• Causes:
• 1. posterior pituitary destruction from tumor
• 2. vascular accidents/head injury
• 3. certain medications- interfere with ADH
secretions(phenytoin, alcohol, lithium)
• Pathophysiology- decrease ADH or vasopressin
secretions leads to inability of the kidney tubules
to conserve water
Pathophysiology
 Assessment findings
• 1. increase urine output- 5-20L/day-diluted
• 2. nocturia
• 3. extreme thirst
• 4. weight loss
• 5. can lead to hypovolemia-dehydration
• Laboratory findings:
• 1. serum sodium levels are elevated and plasma
osmolality(276-295 mOsm/kg)
• 2. water deprivation test- demostrates inability
of the kidneys to concentrate urine despite
increase plasma osmolality level
 Nursing management
• 1. Administer ADH replacement- vasopressin,
desmopressin—conserve renal water by increasing
urine osmolality(80-1300mOsm/L) and decreasing
urine flow rate.
• - can be administered intranasally
• -IM route must be deep
• - watch out for water intoxication(drowsiness,
weight gain)
• 2. Replace fluids as indicated to prevent
dehydration
• 3. Monitor potassium and sodium.
 Syndrome of inappropriate anti diuretic
hormone(SIADH)
• - over secretion of ADH results in excessive water
conservation.
• Causes:
• 1. overuse of vasopressin therapy
• 2. pharmacologic agents( chemotherapeutic
agents, opioids)
• 3. head injury
• 4. stimulation cause by hypoxia
• Pathophysiology: excess vasopressin leads to
retention of water leads to dilutional hyponatremia
 Assessment findings
• 1. decrease urine output
• 2. weight gain
• 3. signs of hyponatremia(headache, confusion,
lethargy, seizures, coma)- delayed deep tendon
reflex
• Laboratory test:
• 1. serum ADH increase
• 2. hyponatremia(dilutional)
• 3. serum osmolality decrease
 Nursing management
• 1. Administer medications
• - furosemide
• - demeclocycline, lithium-makes the kidney less
sensitive to ADH
• 2. Restrict fluid intake
• 3. assess mental status
 Pheochromocytoma
• - a tumor that originates from the adrenal
medulla
• - usually benign
• - it stimulates hypersecretion of
cathecholamines(epinephrine and
norepinephrine)
• - can lead to 5 h’s(hypertension, headache,
hyperhidrosis, hypermetabolism, hyperglycemia)
 Laboratory findings
• Vanillylmandelic acid test(VMA test)- metabolite of
epinephrine
• - VMA test requires 24 hour urine specimen
• - avoid coffee, tea, chocolate, banana, vanilla, aspirin
cause it can alter the test.
• Nursing management:
• 1. Watch out for hypertensive crisis- can lead to CVA,
cardiac arythmias, MI.
• - bed rest
• - fowlers position during hypertensive attack, change
position slowly
• - avoid stimulants
• - administer alpha adrenergic blocking agents- clonidine
• - adrenalectomy
 Thank You!

Newborn Screening