Parathyroid gland

General surgery ppt - PG

1. Parathyroid gland Dr Carunya M annan

2. History 1849 - Sir Richard owen provided - 1st accurate description of normal parathyroid glands in Indian Rhinoceros 1879 Anton Wölfer described tetany in a patient after total thyroidectomy Ivar Sandström a Swedish medical student grossly and microscopically described parathyroid glands Calcium measurement possible in 1909 and association with parathyroids established 1925- 1st successful parathyroidectomy on 38 yr old man with severe bone pain secondary to osteitis fibrosa cystica

3. Location: Usually paired. less than 5 mm - size of a grain of rice or a lentil Weigh 35 to 50 milligrams Color - light yellow to reddish-brown Most - oval, bean shaped or spherical, variations such as teardrop, pancake, rod-like, sausage, and leaf shaped Occasionally - bi- lobated / multilobated Anatomy

4. Anatomy 4 parathyroid glands, two superior and two inferior glands Usually symmetric Development : Like thyroid gland, develop from endodermal thickening in floor of early pharynx and epithelium of 3rd and 4th gill slit pouches

5. BLOOD SUPPLY S uperior parathyroid glands - inferior thyroid artery Also supplied by branches of the superior thyroid artery in 15 to 20 I nferior parathyroid glands - inferior thyroid artery

6. Low circulating serum calcium concentrations stimulate the parathyroid glands to secrete PTH, which mobilizes calcium from bones by osteoclastic stimulation PTH also stimulates the kidneys to reabsorb calcium PTH stimulates convertion of 25-hydroxyvitamin D3 (produced in the liver) to the active form 1,25-dihydroxyvitamin D3, which stimulates GI calcium absorption High serum calcium concentrations have a negative feedback effect on PTH secretion.

7. Hyperparathyroidism Primary Hyperparathyroidism Normal feedback of Ca disturbed, causing increased production of PTH Secondary Hyperparathyroidism Defect in mineral homeostasis leading to a compensatory increase in parathyroid gland function Tertiary Hyperparathyroidism Hypercalcemia caused by autonomous parathyroid function after long-term hyperstimulation

8. Primary Hyperparathyroidism Pathology Single Adenoma 89% Double Adenoma 4% Hyperplasia 7% MENI, MENIIa 4% Non-MEN 3% Parathyroid Carcinoma <0.1% Hundahl , Cancer, 1999 Van Heerden , Surgery 1996

9. Parathyroid adenoma A single adenoma is found in 70-80% of primary hyperparathyroidism. Benign tumor. Unregulated release of PTH. Double adenoma in 4-5%

10. Parathyroid adenomas composed of fairly uniform, polygonal chief cells with small, centrally placed nuclei

11. Parathyroid hyperplasia Diffuse enlargement of all the parathyroid glands. Unregulated release of PTH. 10-15% of cases of primary hyperparathyroidism.

12. Parathyroid hyperplasia L ittle or no adipose tissue, but any or all cell types normally found in parathyroid are present. This is actually "secondary hyperparathyroidism" with enlarged glands as a consequence of chronic renal failure with impaired phosphate excretion. 12

13. Parathyroid carcinoma Less than 1% of cases of hyperparathyroidism

14. Other causes Multiple Endocrine Neoplasia Type 1 and 2 Abnormalities of thyroid, adrenal, and parathyroid glands Hyperplasia of the parathyroid glands Radiation therapy to the head and neck during childhood for benign diseases Familial hyperparathyroidism - rare

15. Secondary Hyperparathyroidism Occurs when the parathyroid glands become hyperplastic after long-term stimulation to release PTH in response to chronically low circulating calcium. Chronic renal failure, rickets, and malabsorption syndromes are the most frequent causes. High levels of PTH do not cause hypercalcemia because the primary problem is hypocalcemia. With long-term hyperstimulation, the glands eventually function autonomously and continue to produce high levels of PTH even if the chronic hypocalcemia has been corrected.

16. Hypercalcemia Malignancy-related -Solid tumor with metastases (breast) -Solid tumor with humoral mediation of hypercalcemia (lung, kidney) -Hematologic malignancies (multiple myeloma, lymphoma, leukemia) Endocrine diseases: Hyperthyroidism.Addisonian crisis.pheochromocytoma Granulomatous diseases : Sarcoidosis.T.B . Iatrogenic: Excessive intake of Vit D or calcium -Rx with lithium -Thiazide diuretics Associated with renal failure -Severe secondary hyperparathyroidism -Aluminum intoxication Familial hypocalcuric hypercalcemia -Milk-alkali Primary hyperparathyroidism and cancer account for 90% of cases of hypercalcemia

17. Stones Renal stones Nephrocalcinosis Polyuria Polydipsia Uraemia Bones Osteitis fibrosa with: -subperiosteal resorption - osteoclastomas - bone cysts Radiologic „osteoporosis” Osteomalacia or rickets Arthrithis Abdominal groans Constipation Indigestion, nausea, vomiting Peptic ulcer Pancreatitis Psychic moans Lethargy, fatigue Depression Memory loss Psychoses – paranoia Personality change, neuroses Confusion, stupor, coma Other Proximal muscle weakness Keratitis, conjunctivitis Hypertension Itching P-HPTH signs & symptoms Clinical featues

18. Investigations Intact PTH and chemistry panel PTH elevated (normally 0.15-1ng/ml ) despite elevated serum calcium Serum phosphate decreases/ Alkaline phosphatase elevated serum creatinine to evaluate for CRI/CRF Rule out lithium or thiazide use 24-hour urine calcium excretion Used to rule out familial hypocalciuric hypercalcemia Values below 100mg/24 hours or a calcium creatinine clearance ratio of <0.01 are suggestive of FHH XR-Skull: salt pepper appearance, s ubperiosteal erosion of radial side of middle phalanx . Osteitis fibrosa cystica . USG KUB , IVP or CT to evaluate for kidney stones

19. Treatment

20. Guidelines for recommendation for surgical treatment (from the 2002 NIH Workshop on Asymptomatic Primary Hyperparathyroidism): Patients with a serum calcium concentration of 1.0 mg/ dL or more above the upper limit of normal Patients with hypercalciuria Patients with a creatinine clearance that is 30 percent or lower than that of age-matched normal subjects Patients with bone density at the hip, lumbar spine, or distal radius that is more than 2.5 standard deviations below peak bone mass Patients who are less than 50 years old Patients in whom periodic follow-up will be difficult

21. Surgery Bilateral neck exploration is “gold standard” With pre-operative imaging techniques can have minimally invasive focused surgery towards adenoma

22. Pre-Operative Imaging- Localization High-resolution ultrasound Sensitivity 65-85% for adenoma; 30-90% for enlarged gland Results suboptimal in pts with multinodular thyroid disease, pts with short thick neck, ectopic glands (15-20%) May be useful in detecting sestamibi scan negative adenomas CT with contrast/thin section Sensitivity of 46-87% Good for ectopic glands in the chest MRI Sensitivity of 65-80% Good for ectopic glands Sestamibi 85-95% accurate in localizing adenoma in primary HPT Sestamibi -SPECT(single photone emission CT) Sensitivity 60% for enlarged gland and 98% for solitary adenomas

23. Tc-99m Sestamibi Scan Taken up by actively metabolizing tissues - salivary glands, thyroid, parathyroid glands Over time blood flow causes washout from thyroid and normal parathyroid glands delayed images show a discrete “hot spot” in 75-80% patients with primary HPT can be used to direct minimally invasive surgical approaches

24. Parathyroid Imaging - Tc-99m Sestamibi 45 min Anterior 45 min LAO 2 HR 2 HR submandibular gland thyroid lobe adenoma Delayed views

25. Right inferior pole parathyroid adenoma 15 min Ant 1 hr Ant 1 hr RAO adenoma

26. 15 min Ant 1 hr Ant Right superior parathyroid adenoma adenoma

27. Minimally Invasive Radioguided Parathyroidectomy (MIRP) Only in patients who localize by pre-op sestamibi scan (75% with primary HPT) Sestamibi scan performed 2-3 hours before exploration - timing crucial gamma probe used to find the “hottest” spot N o further dissection and no frozen section If no adenoma found, 4 gland exploration -Norman J, et al, 1997

28. MIRP - results 2 cm incision local w/ sedation, out-patient procedure 100% cure rate no complications mean operating time = 25 minutes re-operative cure rate = 100% -Norman J, 1997

29. Evolution of Surgery for Primary HPT Preoperative sestamibi in all patients with primary HPT: help decision whether to operate in selected patients localize adenoma to plan localized exploration Minimally invasive parathyroidectomy (MIP): 2-4 cm incision often w/ local + sedation out-patient procedure +/- IOPTH testing - biochemical confirmation Endoscopic removal of parathyroid gland(s)

30. Intraoperative parathyroid hormone testing I ntroduced 1993 Used to determine the adequacy of parathyroid resection When the PTH falls by 50% or more in 10 minutes after removal of a parathyroid tumor, as compared to the highest preremoval value, the test is considered positive and the operation is terminated

31. Treatment, Non-Surgical Avoid factors that can aggravate hypercalcemia: thiazide diuretic lithium volume depletion prolonged bed rest or inactivity high calcium diet Encourage physical activity to minimize bone resorption. Encourage adequate hydration.   Maintain a moderate calcium intake (1000 mg/day). Maintain moderate vitamin D intake.

32. Treatment, Non-Surgical   Monitoring Serum calcium every six months Serum creatinine, and bone density (hip, spine, and forearm) every 12 months

33. Thank You!