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Ms. Amandeep Kaur
Nursing Tutor
MMCON
Parathyroid Glands
Four or more small glands embedded on posterior surface
of thyroid gland.
Each gland is about the size of a grain of rice (weighs
approximately 30 milligrams and is 3-4 millimeters in
diameter).
Produces Parathormone (PTH).
Regulates calcium and phosphate levels in an inverse
relationship.
Calcium levels major controlling factor of PTH secretion.
Parathyroid Glands
PARATHYROID FUNCTION
• Parathormone, the protein hormone from the
parathyroid glands, regulates calcium and
phosphorus metabolism.
• Increased secretion of parathormone results in
increased calcium absorption from the kidney,
intestine, and bones, thereby raising the blood
calcium level.
• Some actions of this hormone are increased by
the presence of vitamin D.
CONT…
• Parathormone also tends to lower the blood
phosphorus level.
• Excess parathormone can result in markedly
elevated levels of serum calcium, a potentially
life-threatening situation.
• When the product of serum calcium and serum
phosphorus (calcium ×phosphorus) rises,
calcium phosphate may precipitate in various
organs of the body and cause tissue calcification.
CONT…
The serum level of ionized calcium regulates
the output of parathormone.
Increased serum calcium results in decreased
parathormone secretion, creating a negative
feedback system.
Functions oF Parathormone
hyPerParathyroidism
Over activity of one or more of the parathyroid
glands.
Incidence-
Greatest numbers after 60 years
Females> males (2:1)

Hyperparathyroidism
Hyperparathyroidism, which is caused by
overproduction of parathyroid hormone by the
parathyroid glands, is characterized by bone
decalcification and the development of renal
calculi (kidney stones) containing calcium.
Hyperparathyroidism-
Classifications
Primary- related to secreting tumor of the
parathyroid gland.
Hyperplasia
Adenoma
 Develops when the normal regulatory relationship
between serum calcium levels and parathyroid
hormone secretion is interrupted.
 Primary hyperparathyroidism is related to no
injury, just a parathyroid gone bad.
CONT…
Increased calcium in the kidneys = kidney
stones; increased calcium in the small
intestines = gastrointestinal upset; increased
bone resportion occurs, this means there is
increased bonde demineralization, bone
damage, osteoporosis.
These symptoms are part of what is known as
the moans and groans, stones and bones.
Hyperparathyroidism-
Classifications
Secondary- occurs when the glands are hyperplastic because of
malfunction of another organ system. Usually the cause is renal
failure or hyperphosphotemia.
Compensatory response to chronic hypocalcemia.
 Vit D deficiency
 Malabsorption
 Result of renal failure
 Hyperphosphatemia
Pathophysiology
Normal function of PTH is to increase bone reabsorption,
thereby maintaining proper balance of calcium and
phosphorus ions in the blood
Excessive circulating PTH leads to bone damage,
hypercalcemia, and kidney damage
Clinical Manifestations
 Skeletal disease ( backache, joint pain, bone pain, pathologic
fracture of spine, ribs and long bones).
 Renal involvement ( polyuria, polydipsia, appearance of sand ,
gravel, or stones in the urine, azotemia, hypertension).
 GI manifestations (thirst, nausea, anorexia, constipation,
abdominal pain, peptic ulcer, GI bleeding, and pancreatitis).
 Psychiatric manifestations (listlessness, lethargy, fatigue,
depression, memory loss, confusion, stupor, coma, depression,
paranoia are sometimes associated with high ca levels).
Clinical Manifestations
 Decreased neuro-muscualar irritability.
 Decreased deep tendon reflexes.
Muscle weakness and atrophy.
Hyperparathyroidism- Assessment
1. Decreased deep tendon reflexes.
2. CNS changes-headache, drowsiness, fatigue.
3. Muscle weakness & atrophy.
Hyperparathyroidism- Assessment
Diagnostic Tests-
Increased serum Calcium (>5.2mEq/l)
Decreased serum Phosphate (<4.5 mg/dl)
Increased serum PTH levels.
X-Rays - bone demineralization.
Ultrasound or MRI of glands.
Medical/Surgical Management
Hyperparathyroidism- Medical
Management
 Goal is to lower severely elevated calcium levels.
 Long term management of hypercalcemia with drugs
to increase bone reabsorption of calcium.
Hyperparathyroidism- Medical/Surgical
Management
Secondary Disease
 Calcium supplements
 Vitamin D
Tertiary Disease
 Phosphate Binders
 Amphogel, Basaljel
 Tums
Surgical Management
PARATHYROIDECTOMY:-
Removal of the parathyroid glands
or parathyroid tumors.
Parathyroid disorders
High risk for injury R/ted to demineralisation of
bones resulting in pathologic fractures.
- Prevent accidents ( keep bed in low position, use
side rails, help with ambulation).
- Space activities, plan rest periods.
- Encourage weight bearing 30mins/day to promote
bone rebuilding.
- Avoid high-impact activities or sports.
- Home should be cleared of articles that can increase
risk of falling such as throw rugs/carpet.
Impaired urinary elimination related to renal
involvement secondary to hypercalcemia and
hyperphosphaturia resulting in urolithiasis, painful
urination, hematuiria and spasms.
Encourage fluids ( 2-3000ml /day)
 Prevent urolithiasis ( cranberry juice helps in making urine
more acidic which helps in preventing renal stone
formation as calcium is more soluble in acidic urine than in
alkaline urine)
Imbalanced nutrition less than body requirements
related to anorexia resulting in decreased food intake
and wt loss.
Low calcium diet to correct hypercalcemia
 Antacids for clients with peptic ulcer
 Diet high in calories without dairy products
Constipation r/ted adverse effects of hypercalcemia on
GI tract resulting in decreased frequency of stools and
painful defecation.
 Add fiber to diet
Increase fluid intake
Use stool softeners or laxatives
Knowledge Deficit Related to Dietary Changes
Low calcium diet
Limit milk products
Risk For Renal Stones
Increase fluid intake (2-3000ml/day)
Encourage cranberry or prune juice
Assess for:-
 flank pain
 hematuria
Nursing management of surgical client
 Monitor for post-op complications:-
 Hemorrhage, airway obstruction, recurrent injury
to laryngeal nerve.
 Eat foods high in calcium.
 Encourage ambulation as soon as after surgery as weight
bearing exercises speeds recalcification
Parathyroid disorders
Hypoparathyroidism
Deficiency of PTH due to hyposecretion of Parathyroid
glands
Serum calcium levels are abnormally low, serum phosphate
levels are abnormally high and tetany may develop.
Incidence-
Women are more prone than men
 Incidence related to thyroid surgery
Hypoparathyroidism
CAUSES-
Iatrogenic i.e.- treatment induced (removal of viable
parathyroid tissue)
 Surgery ( accidental removal during thyroidectomy.
 Infarction of parathyroid glands because of an
inadequate blood supply to the glands during
surgery.
 Trauma.
 Idiopathic- autoimmune disorder.
Assessment
Physical Assessment-
Acute Hypoparathyroidism
 Positive CHVOSTEK SIGN (spasms of facial
muscle after a tap over the facial nerve signifying
facial nerve hyperirritability) and TROUSSEAU
SIGNS (Spasm of wrist and hand after compression
of upper arm as by BP cuff.)
 Hyperactive Deep Tendon Reflexes
 Paresthesia:- Numbness and tingling of fingers
Hypoparathyroidism- Assessment
Chronic Hypoparathyroidism
Lethargy, weakness, fatigue
Thin , patchy hair
Brittle nails
Dry scaly skin
Personality changes
Cataracts
Permanent Brain Damage
Hypoparathyroidism- Assessment
Diagnostic Tests-
Decreased serum Calcium(<4.8mEq/l)
Increased serum Phosphate (>1.75mEq/l)
Low PTH levels
Decreased Urine Calcium
Ophthalmic exam : calcification of lens
Radiograph- increased bone density of Skull
Hypoparathyroidism- Medical Management
Active Form of Vit D-to maintain Ca WNL
Rocaltrol
Hytakerol (Dihydortachysterol)
IV Calcium -
10% Calcium Chloride or Calcium Gluconate
Emergency Treatment
Supplemental Calcium
Oral
Dietary
 Address seizures and laryngeal spasms ( ca gluconate,
tracheostomy set )
 Parathyroid hormone replacement

Hypoparathyroidism - Nursing Management
Knowledge Deficit of Dietary Management/
Medications
High calcium, low phosphate
 avoid milk and cheese (high in phosphorus).
 Calcium rich food: Beans, Almonds, 7 dark green
leafy vegetables(spinach).
Discuss medications and ensure compliance with
treatment.
Cont….
High risk for injury: muscle tetany related to
hypocalcemia
- Assess chvostek and trousseau signs
-Assess for twitching, numbness and tingling,
-Seizures
-Safety precautions for seizures
-Maintain patent airway, keep trach set at bedside
-Keep ampoule of IV calcium at bedside
Parathyroid disorders

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Parathyroid disorders

  • 2. Parathyroid Glands Four or more small glands embedded on posterior surface of thyroid gland. Each gland is about the size of a grain of rice (weighs approximately 30 milligrams and is 3-4 millimeters in diameter). Produces Parathormone (PTH). Regulates calcium and phosphate levels in an inverse relationship. Calcium levels major controlling factor of PTH secretion.
  • 4. PARATHYROID FUNCTION • Parathormone, the protein hormone from the parathyroid glands, regulates calcium and phosphorus metabolism. • Increased secretion of parathormone results in increased calcium absorption from the kidney, intestine, and bones, thereby raising the blood calcium level. • Some actions of this hormone are increased by the presence of vitamin D.
  • 5. CONT… • Parathormone also tends to lower the blood phosphorus level. • Excess parathormone can result in markedly elevated levels of serum calcium, a potentially life-threatening situation. • When the product of serum calcium and serum phosphorus (calcium ×phosphorus) rises, calcium phosphate may precipitate in various organs of the body and cause tissue calcification.
  • 6. CONT… The serum level of ionized calcium regulates the output of parathormone. Increased serum calcium results in decreased parathormone secretion, creating a negative feedback system.
  • 8. hyPerParathyroidism Over activity of one or more of the parathyroid glands. Incidence- Greatest numbers after 60 years Females> males (2:1) 
  • 9. Hyperparathyroidism Hyperparathyroidism, which is caused by overproduction of parathyroid hormone by the parathyroid glands, is characterized by bone decalcification and the development of renal calculi (kidney stones) containing calcium.
  • 10. Hyperparathyroidism- Classifications Primary- related to secreting tumor of the parathyroid gland. Hyperplasia Adenoma  Develops when the normal regulatory relationship between serum calcium levels and parathyroid hormone secretion is interrupted.  Primary hyperparathyroidism is related to no injury, just a parathyroid gone bad.
  • 11. CONT… Increased calcium in the kidneys = kidney stones; increased calcium in the small intestines = gastrointestinal upset; increased bone resportion occurs, this means there is increased bonde demineralization, bone damage, osteoporosis. These symptoms are part of what is known as the moans and groans, stones and bones.
  • 12. Hyperparathyroidism- Classifications Secondary- occurs when the glands are hyperplastic because of malfunction of another organ system. Usually the cause is renal failure or hyperphosphotemia. Compensatory response to chronic hypocalcemia.  Vit D deficiency  Malabsorption  Result of renal failure  Hyperphosphatemia
  • 13. Pathophysiology Normal function of PTH is to increase bone reabsorption, thereby maintaining proper balance of calcium and phosphorus ions in the blood Excessive circulating PTH leads to bone damage, hypercalcemia, and kidney damage
  • 14. Clinical Manifestations  Skeletal disease ( backache, joint pain, bone pain, pathologic fracture of spine, ribs and long bones).  Renal involvement ( polyuria, polydipsia, appearance of sand , gravel, or stones in the urine, azotemia, hypertension).  GI manifestations (thirst, nausea, anorexia, constipation, abdominal pain, peptic ulcer, GI bleeding, and pancreatitis).  Psychiatric manifestations (listlessness, lethargy, fatigue, depression, memory loss, confusion, stupor, coma, depression, paranoia are sometimes associated with high ca levels).
  • 15. Clinical Manifestations  Decreased neuro-muscualar irritability.  Decreased deep tendon reflexes. Muscle weakness and atrophy.
  • 16. Hyperparathyroidism- Assessment 1. Decreased deep tendon reflexes. 2. CNS changes-headache, drowsiness, fatigue. 3. Muscle weakness & atrophy.
  • 17. Hyperparathyroidism- Assessment Diagnostic Tests- Increased serum Calcium (>5.2mEq/l) Decreased serum Phosphate (<4.5 mg/dl) Increased serum PTH levels. X-Rays - bone demineralization. Ultrasound or MRI of glands.
  • 19. Hyperparathyroidism- Medical Management  Goal is to lower severely elevated calcium levels.  Long term management of hypercalcemia with drugs to increase bone reabsorption of calcium.
  • 20. Hyperparathyroidism- Medical/Surgical Management Secondary Disease  Calcium supplements  Vitamin D Tertiary Disease  Phosphate Binders  Amphogel, Basaljel  Tums
  • 21. Surgical Management PARATHYROIDECTOMY:- Removal of the parathyroid glands or parathyroid tumors.
  • 23. High risk for injury R/ted to demineralisation of bones resulting in pathologic fractures. - Prevent accidents ( keep bed in low position, use side rails, help with ambulation). - Space activities, plan rest periods. - Encourage weight bearing 30mins/day to promote bone rebuilding. - Avoid high-impact activities or sports. - Home should be cleared of articles that can increase risk of falling such as throw rugs/carpet.
  • 24. Impaired urinary elimination related to renal involvement secondary to hypercalcemia and hyperphosphaturia resulting in urolithiasis, painful urination, hematuiria and spasms. Encourage fluids ( 2-3000ml /day)  Prevent urolithiasis ( cranberry juice helps in making urine more acidic which helps in preventing renal stone formation as calcium is more soluble in acidic urine than in alkaline urine)
  • 25. Imbalanced nutrition less than body requirements related to anorexia resulting in decreased food intake and wt loss. Low calcium diet to correct hypercalcemia  Antacids for clients with peptic ulcer  Diet high in calories without dairy products
  • 26. Constipation r/ted adverse effects of hypercalcemia on GI tract resulting in decreased frequency of stools and painful defecation.  Add fiber to diet Increase fluid intake Use stool softeners or laxatives Knowledge Deficit Related to Dietary Changes Low calcium diet Limit milk products
  • 27. Risk For Renal Stones Increase fluid intake (2-3000ml/day) Encourage cranberry or prune juice Assess for:-  flank pain  hematuria
  • 28. Nursing management of surgical client  Monitor for post-op complications:-  Hemorrhage, airway obstruction, recurrent injury to laryngeal nerve.  Eat foods high in calcium.  Encourage ambulation as soon as after surgery as weight bearing exercises speeds recalcification
  • 30. Hypoparathyroidism Deficiency of PTH due to hyposecretion of Parathyroid glands Serum calcium levels are abnormally low, serum phosphate levels are abnormally high and tetany may develop. Incidence- Women are more prone than men  Incidence related to thyroid surgery
  • 31. Hypoparathyroidism CAUSES- Iatrogenic i.e.- treatment induced (removal of viable parathyroid tissue)  Surgery ( accidental removal during thyroidectomy.  Infarction of parathyroid glands because of an inadequate blood supply to the glands during surgery.  Trauma.  Idiopathic- autoimmune disorder.
  • 32. Assessment Physical Assessment- Acute Hypoparathyroidism  Positive CHVOSTEK SIGN (spasms of facial muscle after a tap over the facial nerve signifying facial nerve hyperirritability) and TROUSSEAU SIGNS (Spasm of wrist and hand after compression of upper arm as by BP cuff.)  Hyperactive Deep Tendon Reflexes  Paresthesia:- Numbness and tingling of fingers
  • 33. Hypoparathyroidism- Assessment Chronic Hypoparathyroidism Lethargy, weakness, fatigue Thin , patchy hair Brittle nails Dry scaly skin Personality changes Cataracts Permanent Brain Damage
  • 34. Hypoparathyroidism- Assessment Diagnostic Tests- Decreased serum Calcium(<4.8mEq/l) Increased serum Phosphate (>1.75mEq/l) Low PTH levels Decreased Urine Calcium Ophthalmic exam : calcification of lens Radiograph- increased bone density of Skull
  • 35. Hypoparathyroidism- Medical Management Active Form of Vit D-to maintain Ca WNL Rocaltrol Hytakerol (Dihydortachysterol) IV Calcium - 10% Calcium Chloride or Calcium Gluconate Emergency Treatment Supplemental Calcium Oral Dietary  Address seizures and laryngeal spasms ( ca gluconate, tracheostomy set )  Parathyroid hormone replacement 
  • 36. Hypoparathyroidism - Nursing Management Knowledge Deficit of Dietary Management/ Medications High calcium, low phosphate  avoid milk and cheese (high in phosphorus).  Calcium rich food: Beans, Almonds, 7 dark green leafy vegetables(spinach). Discuss medications and ensure compliance with treatment.
  • 37. Cont…. High risk for injury: muscle tetany related to hypocalcemia - Assess chvostek and trousseau signs -Assess for twitching, numbness and tingling, -Seizures -Safety precautions for seizures -Maintain patent airway, keep trach set at bedside -Keep ampoule of IV calcium at bedside

Editor's Notes

  1. Increase Ca reabsorption from kidney and PO4 excretion Increase resorption of Ca and PO4 from bone Increase Ca and PO4 from intestines
  2. Primary hyperparathyroidism is related to no injury, just a parathyroid gone bad. Signs and symptoms include the presence of kidney stones, hypercalcemia, and bone demineralization. This client is at risk for kidney stones. The calcium is taken from bones and intestines and kidney and transported to the blood as a result of increased PTH. Hyperparathyroidism yields increased calcium levels in the blood. The increased calcium in the other organs puts the organ at risk for development of calculi or stones. Increased calcium in the kidneys = kidney stones; increased calcium in the small intestines = gastrointestinal upset; increased bone reabsorption occurs, this means there is increased bone demineralization, bone damage, osteoporosis. These symptoms are part of what is known as the moans and groans, stones and bones. Refer to pg 1210
  3. Remember what a secondary disorder means’ that it is a result of some other organ insult. Usually the cause is renal failure of hyperphosphotemia. In renal failure, there is a decreased GFR, so there is increased phosphorus. Phosphorus and calcium are inversely related therefore caclium decreases. When calcium is decreased the parathyroid thinks it needs to pump itself up and more PTH is released in an attempt to increase the levels of calcium. It may also occur secondary to a nutritional disorder. Vitamin D deficiency or malabsorption problems can contribute to nutritional imbalance. The body attempts to compensate for this imbalance which leads to the parathyroid trying to increase calcium levels. (Vitamin D and malabsorption have relate to calcium).
  4. Moans and groans, stones and bones is described in more detail on page 1210 Moans: pscyh manifestations- lethargy, gatigue, depression, memory loss, pscyhoses, neuroses, paranoia, confusion, stupor, coma Groans: constipation, nausea, vomiting, ulcers ,indigestion, pancreatitis Stones: renal stones, uremia, polydypsia, polyuria Bones: arthritis, osteomalacia, osteitis
  5. Lasix, furosemide is a loop diuretic. It promotes calciuria, that’s a good thing when the calcium level is too high, you’d want to get rid of it. DO NOT give this patient a thiazide diuretic as these diuretics promote calcium RETENTION in the kidneys. HCTZ, hydrochlorothiazide is a common thiazide diuretic.
  6. IF the hyperparathyroidism is caused by a nutritional deficit of calcium or vitamin D, then those substances need replacing. IF the hyperparathyroidism is of a primary nature, then vitamin D and calcium need to be reduced in the client’s diet so as not to further increase the calcium level. Keep the scenarios straight as to when to supplement or restrict vitamin D and calcium. If it’s PRIMARY hyperparathyroidism, then the diet needs to be low in calcium and vitamin D. Otherwise, supplements of vitamin D and calcium need to be given. IF, the cause is hyperplasia of the parathyroid or a decreased response to calcium levels, meaning that with an increased or normal calcium, the parathyroid doesn’t know when to shut-up, then phosphate binders are given. Remember phosphorus and calcium exist in inverse relationship (most of the time). Increase the phosphorus, the calcium will decrease. Bind the phosphorus, then calcium will stop decreasing.
  7. Cranberry and prune juice increase urine acidity and thereby decrease the formation of kidney stones Straining the urine is done to detect gravel or stones of the renal kind. Pain associated with renal calculi has been likened to childbirth or worse than childbirth, be kind to the patient with renal calculi
  8. This often occurs as an inadvertent removal during a thyroidectomy. The parathryoids are right behind the thyroid glands, the proximity so close that an accidental removal of the parathyroid (one or more) may occur.
  9. Signs and symptoms of tetany may be so severe as to cause laryngospasm, laryngeal edema and obstruction, and/or dyspnea. Hence, the need for a tracheostomy set, intubation equipment, including suction and oxygen.
  10. Increased bone density is seen on radiograph as calcium is stuck in the bones, instead of the fair share going into the bloodstream.
  11. Hypocalcemia = tetany = death, this is an emergency situation (as Mrs. Brock)