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Diseases of Parathyroid & Adrenal Glands
Omar Alaidaroos MSc, MD, FRCS
Associate Prof. of General Surgery
Parathyroid glands
• There are four, oval-shaped endocrine glands embedded in the posterior surface
of the thyroid gland
• Two superior glands: located near the superior
pole of the thyroid gland at the junction of cricoid
and thyroid cartilages.
• Two inferior glands: located in the area between
the inferior poles of the thyroid lobes and the
superior mediastinum
• Function: secretion of PTH in response to low calcium serum levels
• Effects of parathyroid hormone (PTH):
• Calcium:
• Increases blood calcium levels by directly stimulating osteoclasts to break down bone.
• Promotes calcium reabsorption by the kidneys
• Increases gastrointestinal calcium absorption by activating vitamin D
• Phosphate
• Inhibits proximal tubular reabsorption of phosphorus
• Arterial supply: Inferior thyroid arteries
• Venous drainage: Thyroid venous plexus
• Different cells of the parathyroid glands:
• Chief cells: secretion of parathyroid hormone
• Oxyphil cells
• Adipocytes
Causes:
Primary hyperparathyroidism :
is usually due to a parathyroid benign adenoma (75%) or parathyroid hyperplasia (20%). 1.0% have parathyroid carcinoma.
Secondary hyperparathyroidism:
is hyperplasia of the gland in response to hypocalcaemia (e.g. in chronic renal failure).
In tertiary hyperparathyroidism,
autonomous secretion of parathormone occurs when the secondary stimulus has been removed (e.g. after renal
transplantation).
MEN syndromes
(type I (parathyroid adenoma, pancreatic islet cell tumours, pituitary adenoma) and
type II (parathyroid adenoma, medullary thyroid cancer, phaeochromocytoma)
 Ectopic parathormone production (e.g. from small cell lung cancer).
Pathology:
Parathormone mobilizes calcium from bone,
enhances renal tubular absorption and,
with vitamin D, intestinal absorption of calcium.
The net result is hypercalcaemia.
Clinical features
Older women, >40 years of age.
Renal calculi or renal calcification – occurs in 20% of patients, polyuria (‘renal
stones’).
Bone pain or deformity, osteitis fibrosa cystica, pathological fractures (‘painful
bones’).
Muscle weakness, anorexia, intestinal atony, psychosis (‘psychic moans’).
Peptic ulceration and pancreatitis (‘abdominal groans’).
Salt-and-pepper-spots-in-skull
Epulis: resorption of the alveolar ridge so that the denture moves further into the vestibular mucosa, creating
an inflammatory fibrous hyperplasia
• Laboratory:
• High PTH
• Elevated serum Ca
• Low phosphate
• High Alkaline Phosphatase
• Low Mg
• High urinary Ca
Imaging
High-resolution ultrasound.
99mTc sestamibi scintigraphy ± sestamibi-single photon emission computed tomography (SPECT).
CT and MRI scanning.
DXA scans for bone density measurement in all patients with hyperparathyroidism.
Selective vein catheterization and digital subtraction angiography in patients in whom exploration has been unsuccessful.
• Radiology:
• DEXA: Wrist, spine, and hip
• KUB, IVP, CT (For renal stones)
Demeneralization of long bones , Pathological fracture
Laboratory
Elevated PTH in the setting of hypercalcaemia.
Serum calcium (specimen taken on three occasions with patient fasting, at rest and without a
tourniquet). Body Ca:
99% stored in the skeleton
1% is free
½ bound to proteins
½ is free ionized (Active)
Normal range 2.2–2.6 mmol/L. Calcium is bound to albumin and the level has to be ‘corrected’
when albumin levels are abnormal. •
May be decreased serum phosphate and elevated alkaline phosphatase
• Complications of parathyroidectomy:
• Post op. bleeding
• Hematoma:
• Pre tracheal (airway obstruction)
• pre- platysmal
• Nerve injury
• 1-2% permanent:
• Recurrent laryngeal (hoarseness)
• Superior laryngeal (loss of high pitched sound)
• Hypocalcemia
Management:
Treat hypercalcaemia if calcium levels very high (>2.88 mmol/L).
Patients with symptomatic PHPT are candidates for surgery: excise adenoma if present, remove 3.5 of 4
glands for hyperplasia.
Intraoperative rapid PTH assay facilitates minimally invasive parathyroidectomy under LA with >95%
success rate, i.e. return to normocalcaemia.
Asymptomatic or patients refuse or unfit for surgery: bisphosphonates (inhibit bone resorption),
calcimimetics (cinacalcet inhibits PTH secretion),
oestrogen-progestin in postmenopausal women, maintain moderate vitamin D and calcium intake
and encourage hydration (8 glasses of water/day).
• Surgical indication:
• Parathyroidectomy
• Excision
• Total with auto-transplantation
Hypoparathyroidism:
Is a rare condition characterized by hypocalcaemia due to reduced production of parathormone.
Hypoparathyroidism
 Primary (Congenital)
 Secondary (Acquired)
Iatrogenic (Surgery)
Autoimmune:
• Adrenal insufficiency
• Hashimoto’s
• Pernicious anemia
Causes
Post-thyroid or parathyroid surgery (‘hungry bone syndrome’) or neck irradiation.
Idiopathic (often autoimmune and presents in children or young adults).
Congenital enzymatic deficiencies (numerous syndromes).
Metal overload (e.g. iron (haemochromatosis or thalassaemia), copper (Wilson’s disease),
magnesium).
Pseudohypoparathyroidism (reduced sensitivity to parathormone).
Reduced serum calcium increases neuromuscular excitability.
Clinical features: Depend on the severity
Perioral paraesthesia, Periorbital, finger tips cramps, tetany.
Muscle weakness, fasciculation, and cramps
Tetany:
Chvostek’s sign: tapping over facial nerve
induces facial muscle contractions.
Trousseau’s sign: inflating BP cuff to above systolic pressure
induces typical main d’accoucheur carpal spasm.
Prolonged QT interval on ECG.
• Trousseau’s sign
• Inflation of BP cuff to 20 mmHg above the SBP
• Spasm of hand and forearm muscles
• Results in carpopedal spasm
Calcium and parathormone levels decreased.
Also measure vitamin D and magnesium.
Diagnosis:
Blood levels of ionized Calcium and PTH are low,
ECG: shows a lengthened Q–T interval
Treatment:
Asymptomatic
• Calcium supplements PO
Symptomatic:
• IV Calcium supplement, you have to correct magnesium as well
• Also known as suprarenal glands
• Endocrine glands that produce a variety of
hormones
• Each gland has an outer cortex and
an inner medulla
• The adrenal cortex is divided into 3 zones:
• Zona glomerulosa
• Zona fasciculata
• Zona reticularis
• Mineralocorticoids:
• Zona glomerulosa
• Produces aldosterone
• Helps in the regulation of blood pressure and electrolytes balance
• Na retention
• Water retention
• K+ excretion
• Glucocorticoids:
• Zona fasciculata
• Cortisol and cortisone
• Helps in the the regulation of the metabolism and immune
system suppression
• CORTISOL is responsible for control & metabolism of:
A. CHO (carbohydrates)
• Increases glucose formation
• Increases glucose release
B. FATS:
• Control of fat metabolism
• Stimulates fatty acid mobilization from adipose tissue
C. PROTEINS:
• Control of protein metabolism
• Stimulates protein synthesis in liver & protein breakdown in tissues
D. Others:
• Inflammatory and allergic response
• Immune system therefore increases the risk of infection
• ANDROGENS:
• Zona reticularis
• Produces androgens that are converted to fully functional sex
hormones in the gonads and other target organs
• Hormones which increases male characteristics via release of
testosterone
• Produced in anterior pituitary gland
• Individual biorhythms
• Highest in early morning
• Gradually decrease on the rest of the day
• Stress- Increases cortisol production
• It produces catecholamines
• Catecholamines produce a rapid response throughout the body
in stress situations
• Epinephrine, and Norepinephrine
• Cushing’s disease
• Cushing Syndrome
• Hyperaldosteronism “Conn’s Syndrome”
• Addison's disease
• Pheochromocytoma
• Secretion of cortisol from adrenal cortex
• 4 times more frequent in females
• Usually occurs at 35-50 years of age
• Causes:
• Endogenous
• Adrenal tumor
• Tumor of the anterior pituitary gland (Cushing’s disease)
• Hyperplasia (NAH)
• Ectopic ACTH
• Secreting tumor (e.g. lung, pancreas)
• Exogenous
• Excessive cortisone intake
• DIAGNOSIS:
• High Serum cortisol levels
• URINARY LEVELS OF STEROID METABOLITES
17-OHCS (hydroxycorticosteroid) (High)
17-KS (ketosteroid) (High)
• Hematology:
• WBCs (Decreased)
• Lymphocytes (Increased)
• Eosinophils (Decreased
• TREATMENT:
• Primary:
• Adrenalectomy (unilateral or bilateral)
• if bilateral, need hormone replacement for life
• Secondary
• Trans-sphenoidal removal of pituitary tumor
• Ectopic:
• Try to remove source of ACTH secretion
• Radiation to tumors
• Palliative drugs:
• MITOTANE (destroys tissue in adrenal cortex)
•“Conn’s Syndrome”
• Too much aldosterone secretion
• Usually caused by adrenal tumor
• SYMPTOMS & SIGNS:
• High Na and water retention
• HTN
• Low K+
• Usually no edema
• Diagnosis:
• High urinary K+
• High plasma aldosterone level with low plasma renin
• EKG changes
• CT scan
• Treatment:
• Control BP
• Using Aldactone which is aldosterone antagonist.
• Correct hypokalemia/hypernatremia
• K+ supplements+ low Na diet
• Partial or total adrenalectomy
• PRE-OP:
• Stabilize hormonally
• Correct fluid and electrolytes
• Cortisol PM before surgery, AM of surgery and during OR
• POST-OP:
• IV cortisol for 24 hours
• IM cortisol 2nd day
• PO cortisol 3rd day
• Poor wound healing (prophylactic antibiotics)
• If unilateral, then steroids gradually weaned because the other adrenal will take over in 6-
12 months.
• Hypofunction of adrenal cortex, leads to low levels of
• Glucocorticoids
•
• Mineralocorticoids (aldosterone)
• Androgens
• Rare, catecholamine-secreting tumor
• 10% is malignant
• SYMPTOMS & SIGNS:
• Classically, it manifests with the following characteristics:
• Headaches
• Palpitations
• Diaphoresis
• Severe hypertension/ related complications
• The following may also occur :
• Tremor
• Nausea
• Weakness
• Anxiety, sense of doom
• Epigastric pain
• Constipation
• Diagnosis:
• 24 hour urine-VMA
• Plasma metanephrine (metabolite of Epinephrine)
• CT/MRI to locate tumor/ (MIBG scan)
• Intervention:
• Alpha blocking agents
• Prazosin (Minipress) to decrease BP
• Beta blocking agents
• Inderal to control heart rate
• Sedatives
• Surgical resection of the tumor is the treatment of choice and usually cures the
hypertension
 An MIBG scan is commonly used for detection of neuroendocrine tumours, such as neuroblastoma and
phaeochromocytoma. It can also aid in the detection of carcinoid and medullary thyroid carcinoma
THANKS

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Diseases of parathyroid & adrenal glands

  • 1. Diseases of Parathyroid & Adrenal Glands Omar Alaidaroos MSc, MD, FRCS Associate Prof. of General Surgery
  • 2. Parathyroid glands • There are four, oval-shaped endocrine glands embedded in the posterior surface of the thyroid gland • Two superior glands: located near the superior pole of the thyroid gland at the junction of cricoid and thyroid cartilages. • Two inferior glands: located in the area between the inferior poles of the thyroid lobes and the superior mediastinum
  • 3. • Function: secretion of PTH in response to low calcium serum levels • Effects of parathyroid hormone (PTH): • Calcium: • Increases blood calcium levels by directly stimulating osteoclasts to break down bone. • Promotes calcium reabsorption by the kidneys • Increases gastrointestinal calcium absorption by activating vitamin D • Phosphate • Inhibits proximal tubular reabsorption of phosphorus • Arterial supply: Inferior thyroid arteries • Venous drainage: Thyroid venous plexus • Different cells of the parathyroid glands: • Chief cells: secretion of parathyroid hormone • Oxyphil cells • Adipocytes
  • 4.
  • 5. Causes: Primary hyperparathyroidism : is usually due to a parathyroid benign adenoma (75%) or parathyroid hyperplasia (20%). 1.0% have parathyroid carcinoma. Secondary hyperparathyroidism: is hyperplasia of the gland in response to hypocalcaemia (e.g. in chronic renal failure). In tertiary hyperparathyroidism, autonomous secretion of parathormone occurs when the secondary stimulus has been removed (e.g. after renal transplantation). MEN syndromes (type I (parathyroid adenoma, pancreatic islet cell tumours, pituitary adenoma) and type II (parathyroid adenoma, medullary thyroid cancer, phaeochromocytoma)  Ectopic parathormone production (e.g. from small cell lung cancer).
  • 6.
  • 7. Pathology: Parathormone mobilizes calcium from bone, enhances renal tubular absorption and, with vitamin D, intestinal absorption of calcium. The net result is hypercalcaemia.
  • 8. Clinical features Older women, >40 years of age. Renal calculi or renal calcification – occurs in 20% of patients, polyuria (‘renal stones’). Bone pain or deformity, osteitis fibrosa cystica, pathological fractures (‘painful bones’). Muscle weakness, anorexia, intestinal atony, psychosis (‘psychic moans’). Peptic ulceration and pancreatitis (‘abdominal groans’).
  • 9.
  • 10.
  • 12. Epulis: resorption of the alveolar ridge so that the denture moves further into the vestibular mucosa, creating an inflammatory fibrous hyperplasia
  • 13. • Laboratory: • High PTH • Elevated serum Ca • Low phosphate • High Alkaline Phosphatase • Low Mg • High urinary Ca
  • 14. Imaging High-resolution ultrasound. 99mTc sestamibi scintigraphy ± sestamibi-single photon emission computed tomography (SPECT). CT and MRI scanning. DXA scans for bone density measurement in all patients with hyperparathyroidism. Selective vein catheterization and digital subtraction angiography in patients in whom exploration has been unsuccessful.
  • 15.
  • 16. • Radiology: • DEXA: Wrist, spine, and hip • KUB, IVP, CT (For renal stones) Demeneralization of long bones , Pathological fracture
  • 17.
  • 18. Laboratory Elevated PTH in the setting of hypercalcaemia. Serum calcium (specimen taken on three occasions with patient fasting, at rest and without a tourniquet). Body Ca: 99% stored in the skeleton 1% is free ½ bound to proteins ½ is free ionized (Active) Normal range 2.2–2.6 mmol/L. Calcium is bound to albumin and the level has to be ‘corrected’ when albumin levels are abnormal. • May be decreased serum phosphate and elevated alkaline phosphatase
  • 19. • Complications of parathyroidectomy: • Post op. bleeding • Hematoma: • Pre tracheal (airway obstruction) • pre- platysmal • Nerve injury • 1-2% permanent: • Recurrent laryngeal (hoarseness) • Superior laryngeal (loss of high pitched sound) • Hypocalcemia
  • 20. Management: Treat hypercalcaemia if calcium levels very high (>2.88 mmol/L). Patients with symptomatic PHPT are candidates for surgery: excise adenoma if present, remove 3.5 of 4 glands for hyperplasia. Intraoperative rapid PTH assay facilitates minimally invasive parathyroidectomy under LA with >95% success rate, i.e. return to normocalcaemia. Asymptomatic or patients refuse or unfit for surgery: bisphosphonates (inhibit bone resorption), calcimimetics (cinacalcet inhibits PTH secretion), oestrogen-progestin in postmenopausal women, maintain moderate vitamin D and calcium intake and encourage hydration (8 glasses of water/day).
  • 21. • Surgical indication: • Parathyroidectomy • Excision • Total with auto-transplantation
  • 22. Hypoparathyroidism: Is a rare condition characterized by hypocalcaemia due to reduced production of parathormone.
  • 23. Hypoparathyroidism  Primary (Congenital)  Secondary (Acquired) Iatrogenic (Surgery) Autoimmune: • Adrenal insufficiency • Hashimoto’s • Pernicious anemia
  • 24. Causes Post-thyroid or parathyroid surgery (‘hungry bone syndrome’) or neck irradiation. Idiopathic (often autoimmune and presents in children or young adults). Congenital enzymatic deficiencies (numerous syndromes). Metal overload (e.g. iron (haemochromatosis or thalassaemia), copper (Wilson’s disease), magnesium). Pseudohypoparathyroidism (reduced sensitivity to parathormone).
  • 25. Reduced serum calcium increases neuromuscular excitability.
  • 26. Clinical features: Depend on the severity Perioral paraesthesia, Periorbital, finger tips cramps, tetany. Muscle weakness, fasciculation, and cramps Tetany: Chvostek’s sign: tapping over facial nerve induces facial muscle contractions. Trousseau’s sign: inflating BP cuff to above systolic pressure induces typical main d’accoucheur carpal spasm. Prolonged QT interval on ECG.
  • 27. • Trousseau’s sign • Inflation of BP cuff to 20 mmHg above the SBP • Spasm of hand and forearm muscles • Results in carpopedal spasm
  • 28. Calcium and parathormone levels decreased. Also measure vitamin D and magnesium.
  • 29. Diagnosis: Blood levels of ionized Calcium and PTH are low, ECG: shows a lengthened Q–T interval Treatment: Asymptomatic • Calcium supplements PO Symptomatic: • IV Calcium supplement, you have to correct magnesium as well
  • 30. • Also known as suprarenal glands • Endocrine glands that produce a variety of hormones • Each gland has an outer cortex and an inner medulla • The adrenal cortex is divided into 3 zones: • Zona glomerulosa • Zona fasciculata • Zona reticularis
  • 31. • Mineralocorticoids: • Zona glomerulosa • Produces aldosterone • Helps in the regulation of blood pressure and electrolytes balance • Na retention • Water retention • K+ excretion
  • 32. • Glucocorticoids: • Zona fasciculata • Cortisol and cortisone • Helps in the the regulation of the metabolism and immune system suppression • CORTISOL is responsible for control & metabolism of: A. CHO (carbohydrates) • Increases glucose formation • Increases glucose release
  • 33. B. FATS: • Control of fat metabolism • Stimulates fatty acid mobilization from adipose tissue C. PROTEINS: • Control of protein metabolism • Stimulates protein synthesis in liver & protein breakdown in tissues D. Others: • Inflammatory and allergic response • Immune system therefore increases the risk of infection
  • 34. • ANDROGENS: • Zona reticularis • Produces androgens that are converted to fully functional sex hormones in the gonads and other target organs • Hormones which increases male characteristics via release of testosterone
  • 35. • Produced in anterior pituitary gland • Individual biorhythms • Highest in early morning • Gradually decrease on the rest of the day • Stress- Increases cortisol production
  • 36. • It produces catecholamines • Catecholamines produce a rapid response throughout the body in stress situations • Epinephrine, and Norepinephrine
  • 37.
  • 38. • Cushing’s disease • Cushing Syndrome • Hyperaldosteronism “Conn’s Syndrome” • Addison's disease • Pheochromocytoma
  • 39.
  • 40. • Secretion of cortisol from adrenal cortex • 4 times more frequent in females • Usually occurs at 35-50 years of age • Causes: • Endogenous • Adrenal tumor • Tumor of the anterior pituitary gland (Cushing’s disease) • Hyperplasia (NAH) • Ectopic ACTH • Secreting tumor (e.g. lung, pancreas) • Exogenous • Excessive cortisone intake
  • 41.
  • 42. • DIAGNOSIS: • High Serum cortisol levels • URINARY LEVELS OF STEROID METABOLITES 17-OHCS (hydroxycorticosteroid) (High) 17-KS (ketosteroid) (High) • Hematology: • WBCs (Decreased) • Lymphocytes (Increased) • Eosinophils (Decreased
  • 43. • TREATMENT: • Primary: • Adrenalectomy (unilateral or bilateral) • if bilateral, need hormone replacement for life • Secondary • Trans-sphenoidal removal of pituitary tumor • Ectopic: • Try to remove source of ACTH secretion • Radiation to tumors • Palliative drugs: • MITOTANE (destroys tissue in adrenal cortex)
  • 44.
  • 45. •“Conn’s Syndrome” • Too much aldosterone secretion • Usually caused by adrenal tumor • SYMPTOMS & SIGNS: • High Na and water retention • HTN • Low K+ • Usually no edema
  • 46.
  • 47. • Diagnosis: • High urinary K+ • High plasma aldosterone level with low plasma renin • EKG changes • CT scan • Treatment: • Control BP • Using Aldactone which is aldosterone antagonist. • Correct hypokalemia/hypernatremia • K+ supplements+ low Na diet • Partial or total adrenalectomy
  • 48. • PRE-OP: • Stabilize hormonally • Correct fluid and electrolytes • Cortisol PM before surgery, AM of surgery and during OR • POST-OP: • IV cortisol for 24 hours • IM cortisol 2nd day • PO cortisol 3rd day • Poor wound healing (prophylactic antibiotics) • If unilateral, then steroids gradually weaned because the other adrenal will take over in 6- 12 months.
  • 49. • Hypofunction of adrenal cortex, leads to low levels of • Glucocorticoids • • Mineralocorticoids (aldosterone) • Androgens
  • 50.
  • 51. • Rare, catecholamine-secreting tumor • 10% is malignant • SYMPTOMS & SIGNS: • Classically, it manifests with the following characteristics: • Headaches • Palpitations • Diaphoresis • Severe hypertension/ related complications
  • 52. • The following may also occur : • Tremor • Nausea • Weakness • Anxiety, sense of doom • Epigastric pain • Constipation
  • 53.
  • 54.
  • 55. • Diagnosis: • 24 hour urine-VMA • Plasma metanephrine (metabolite of Epinephrine) • CT/MRI to locate tumor/ (MIBG scan) • Intervention: • Alpha blocking agents • Prazosin (Minipress) to decrease BP • Beta blocking agents • Inderal to control heart rate • Sedatives • Surgical resection of the tumor is the treatment of choice and usually cures the hypertension  An MIBG scan is commonly used for detection of neuroendocrine tumours, such as neuroblastoma and phaeochromocytoma. It can also aid in the detection of carcinoid and medullary thyroid carcinoma

Notas do Editor

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