PARATHYROID GLAND FUNCTION AND DISORDERS
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The document discusses the parathyroid gland from a historical, anatomical, physiological, and pathological perspective. It covers topics such as: - The historical discoveries of the parathyroid gland from 1849 to 1925. - The embryology and surgical anatomy of the parathyroid gland. - The physiology of calcium homeostasis and the role of parathyroid hormone (PTH). - Various parathyroid disorders including hypoparathyroidism, primary hyperparathyroidism, secondary hyperparathyroidism, and tertiary hyperparathyroidism. - Diagnostic tests and surgical management options for parathyroid disorders, including parathyroidectomy.
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PARATHYROID GLAND FUNCTION AND DISORDERS
- 1. PARATHYROID GLAND Dr. Abhijeeth D Sakaria PG resident Dept of General Surgery SIMS & RC
- 2. TABLE OF CONTENT Historical Aspects Surgical anatomy & embryology Physiology Parathyroid disorders Management
- 3. Historical Background 1849: Sir Richard Owen 1880: Ivar Sandstorm 1891: Eugene Gley 1905: Mac Callum 1925: Fleix Mandl
- 4. Embryology
- 6. PHYSIOLOGY
- 8. HYPOPARATHYROIDISM Inadeqate PTH secretion Cause- Post surgical, Trauma to the gland. Features- Trousseau Chvostek Other variants: Congenital hypoparathyroidism, Pseudohypoparathyroidism Treatment
- 10. PRIMARY HYPERPARATHYROIDISM Enlarged abnormal gland → High PTH →High ca2+. Risk factors: Radiation to head and neck MEN 1 syndrome MEN 2A syndrome Parathyroid Carcinoma Clinical presentation:
- 12. Physiologic secretion of PTH by the parathyroid glands in response to hypocalcemia. usually managed medically, until they become refractory to medical treatment, then subtotal parathyroidectomy is done. SECONDARY HYPERPARATHYROIDISM
- 13. TERTIARY HYPOPARATHYROIDISM Advanced form of secondary hyperparathyroidism Causes: CRF Post renal Transplant Biochemical values: Hypercalcemia Normal PTH Life threatening & need surgical intrevention
- 14. PERSISTENT HYPERPARATHYROIDISM Hypercalcaemia persists after 1st neck exploration. Preop investigations, operative findings, & pathology must be reviewed. Cause: missed adenoma, ectopic PT gland. Treatment: Removal of the gland.
- 15. RECURRENT HYPERPARATHYROIDISM Hypercalcaemia after >12months of initial curative operation Cause: Missed pathology at 1st operation Hyperplasia in auto transplanted tissue Parathyromatosis Development of 2nd adenoma
- 17. HYPERCALCEMIC CRISIS Significantly elevated serum calcium level with end organ dysfunction Causes: Malignancy PHPT Clinical Features Treatment: Initially-medical Definitive- Surgical
- 18. CALCIPHYLAXIS Syndrome of: Vascular calcification Thrombosis Skin necrosis
- 19. CALCIPHYLAXIS Causes: 1. ESRD 2. Non uremic calciphylaxis: • PHPT • Alcoholic liver cirrhosis • Breast Ca treated with Chemo • Rheumatiod Arthritis Diagnosis: Skin biopsy, Bone Scintigraphy Treatment: Subtotal Parathyroidectomy
- 20. PARATHYROID CARCINOMA Rare Age: 4-5th decade Clinical features: Uncontrolled hypercalcaemia Renal failure Cardiac Arrhythmias Hoarsness of voice Treatment: Parathyroidectomy
- 22. INVASIVE STUDIES
- 23. MANAGEMENT- PARATHYROIDECTOMY Indications in PHPT:
- 24. BILATERAL NECK EXPLORATION Visualization of all four glands with subsequent removal of one or more abnormal gland. Indications: Surgeon preference Failure of focused exploation known/ intraop identified hyperplsia High suspicion of multigland disease Associated with higher rate of transient hypocalcemia
- 27. MINIMALLY INVASIVE PARATHYRIODECTOMY Also known as Focoused Parathyroidectomy. Done through a small incision of 3-4cm. Advantages: smaller incision Shorter operative period Lower rates of transient hypocalcemia.
- 28. OPERATIVE ADJUNCTS Intraoperative PTH monitoring - helps confirm that there is no residual hyperfunctioning parathyroid tissue. Intraoperative frozen section analysis Indocyanine green dye and near-infrared autofluorescence Others: USG, Bilateral jugular venous sampling, radio-guided parathyroidectomy using gamma probe, Recurrent laryngeal nerve monitoring.
- 29. RECENT ADVANCES Endoscopic parathyroidectomy. Co2 insufflation through small cervical incision Complication: Hypercarbia, Sub cut. Emphysema Video assisted Parathyroidectomy high cosmetic satisfaction Robotic Parathyroidectomy
- 30. POSTOPERATIVE MANAGEMENT Observation for neck hematoma, features of hypocalcemia, Patient are educated on symptoms of hypocalcemia 25(OH)D level to be rechecked at 3months Calicum levels rechecked on POD1, 2weeks, and 6months after surgery.
- 31. COMPLICATIONS Transient hypocalcemia (5-47%). Permanent Hypoparathyroidism (0-3%). Recurrent laryngeal nerve injury (<1%). Neck hematoma (0.3%). Wound infection.
Editor's Notes
- 1. Curator of London Zoological Gardens, Provided first accurate description of normal parathyroid gland after autopsy examination of an Indian rhinoceros. 2. Medical student in Uppsala, Sweden, named GLANDULAE PARATHYROIDEAE. 3., Gley, a physiologist, documented the function of parathyroid gland, i.e association of tetany with PT glands. 4. Mac Callum described their role in calcium metabolism, demonstrated tht administration of calcium/PTH could reverse / prevent post op tetany 5. First successful parathyroidectomy, on 38yr old man, who had severe bone pain secondary to osteitis fibrosa cystica. Condition improved dramatically, but died after 7yrs due to reccurent HPT or renal failure. 6.1929: Barr, bulger and dixon- “hyperparathyroidism” 7.1951-leonard skeggs-autoanalyzers-rapid serum analysis & diagnose hypercalcemia. 8. Purification & isolation of PTH by Auerbach first & Rasmussen later 9.irvin 1990-IOPTH
- A. View of pharynx of an 8-10 mm embryo. B. Shows location of thyroid, parathyroid, and thymic tissues in 13-14mm embryo. 80% normal Superior PT glands are found near the posterior aspect of upper and middle thyroid lobes @ level of cricoid cartilage. 1% them cn be seen in paraesophageal or retroesophageal space. Ectopic superior PT are rare, but cn be seen in middle or posterior mediastinum or aortopulmonary window. Inferior parathyroid have longer descent, which makes their anatomic position more variable. As high in neck at the upper carotid sheat & as low in the mediastinum as pericardium. In spite of so much variability they are mostly found near the inferior pole of corresponding thyroid lobe.
- (84%- four), (13% > four), (very few -three). OVOID in shape, 5x3x2mm in SIZE, 35-40gm each in WEIGHT. Superior: dorsal to RLN @ level of cricoid cartilage. Inferior: ventral to RLN. Appear: yellow tan to reddish Blood supply: Inferior thyroid artery, branch of thyrocervical trunk from subclavian artery. Each gland has its own end arterial branch. Alternatively superior PT glands can be supplied by Superior thyroid artery in 20% cases. Venous: Superior, middlie, inferior thyroid veins, drain into internal jugular vein, innominated & brachiocephalic veins. LN: deep cervical & paratracheal LN. Nerve: Superior & Cervical sympathetic ganglia. Vasomotor. Not secretomotor, Endocrine secretion of PTH is conntrolled hormonally.
- 115 aa- prepro PTH....subsequently cleaved to 84aa PTH. Secreted by Parathyroid cheif cells in response to low serum calcium. Plasma half life : 3-5mins, but can vary from 1-21mins. exerts action on target organs by binding to PTH receptors (bone, kidney, GI, CVS, CNS, breast skin, pancreatic tissues. and leads to release of intracellular calcium stores.
- Calcium is tranported in blood bound to plasma protiens (45%-largely to albumin), small anions such as Phosphate or citrate (15%), or in free ionised state (40%). Total Serum calcium: 8.5-10.2mg/dl. Free ionised ca (4.6-5.2mg/dl). Intracellular calcium : Important second messenger regulating cell division, motility, membrane trafficking & secretion. Extracellular calcium: Exication contraction coupling in muscle tissues, Synaptic transmission in nervous system, coagulation, and secretion of other hormones. In kidney: Increased calcium resorption at ascending limb of LOH & DCT, and increased renal production of 1,25 Dihydroxy Vit D3. In bones: 2 phases: 1. Immediate Phase: Mobilizes calcium from redialy available skeletal stores in equilibrium with extracellular fluid. 2. Slow: release of calcium & phosphate through bone resorption. In intestines: increases calcium & phosphate absorption. Vit D, from diet or dermal synthesis, which travels to liver then to kidney.
- Circumoral tingling, numbness, paraesthesia, carpopedal spasm, stridor. Trousseau: BP cuff >20mmhg SBP for 3-5min leads to carpopedal spasm: Flexion @ Wrist, MCP, with Extension at IP joint with Adduction of 5digits. feet are extended and adducted. chvostek sign: When facial nerve is tapped at angle of jaw, facial muscle on the same side of the face contract due to hyper excitibility of nerve. AKA WEISS SIGN. Rx: Oral ca, vit d supplements. Congenital: rare cause, Born without adequate parathyroid tissue - DiGeorge syndrome (micro deletions in chr. 22q11.2) CHD, Palate defects, Facial anomalies, infections.. Pseudo: Body fails to respond to PTH. Type 1a- Albright hereditary osteodystrophy ( shorth 4th & 5th metacarpels, with rounded facies with TSH resistance, 1b-biochemicaly same, but lacks phenotype. associated with methylation defect. Type 2- inherent abnormalities in calcium regulation.
- Pts develop a new set point of n one or more PT gland. Stones: flank pain, frequent urination, kidney stones. Bones: bone pain, curving of spine, fractures, Groans: confusion, dementia, depression & memory loss Moans: abdominal pain, constipation, decreased appetite, nausea, vomiting, Peptic Ulcer Disease. men1a: symmetrical enlargement Men 2a: asymmetrical enlargement.
- The increase in serum PTH leads to a higher rate of bone resorption, with resultant cortical bone loss; markers of bone turnover, such as urine hydroxyproline excretion, are increased in patients with low serum 25(OH)D (<30 nmol/liter). Chronic renal failure leads to hyperphosphatemia and decreased renal conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, resulting in reduced intestinal calcium absorption, with subsequent hypocalcemia and stimulation of PTH. The mechanism by which uremic hyperparathyroidism develops is multifactorial and involves (1) mutations in calcium-sensing receptors, (2) alterations in calcium set-points, (3) decreased metabolic clearance of PTH, and (4) increased phosphate retention. Regardless of the cause of secondary hyperparathyroidism, hyperplasia of all parathyroid glands develops. However, in contrast to patients with PHPT, less than 1% of patients with uremic secondary HPT require surgical intervention.
- Long standing chronic renal failure Persistent autonomous secretion of PTH after renal transplantation. (loss of response to serum calcium levels leads to four gland hyperplasia with autonomous activity. Assymetrical parathyroid glands. Subtotal parathyroidectomy.
- S.Ca- >14mg/dl (3.5mmil/Litre) Such life threatening hypercalcemia is a medical & surgical emergency. C/F; Consitutional (Fatigue) , Neurological(Depression, confusion, obtundation), GI(Constipation, abd pain), Renal findings( oliguria/anuria) , hypovolemia, hyperkalemia) Med: Aggressive fluid correction(200ml/hr) Diuretics (inhibit Ca absorption) Dialysis Glucocorticoid( hydrocort- 200-400mg/day x 5 days) Calcitonin 100u bisphophonate Surgical: urgent parathyroidectomy once Ca level decreases.
- AKA. Calcific Uremic Arteriolopathy Results in Chronic non healing ulcer. Seen in pts who are on hemodylasis or recent kidney transplant.
- Skin biopsyL=: Small arterial calcification Bone scintigraphy: Increase tracer accumulation in soft tissue. Aggressive Subtotal parathyroidectomy
- TOTAL PARATHYROIDECTOMY
- NON INVASIVE USG: PT adenoma is Hypoechoic, Accuracy is operator dependent, Mediastinal PT lesion can be missed. Sestamibi SPECT: Accumulate in mitochondria, Abnormal PT glands have abundant mitochondria 4DCT: 4th dimension is the time, Differentiate perfusion characteristic between hyperfunctioning PT & surrounding structure. MRI : mainly used in pregnant ladies PET: focal tracer uptake, has high sensitivity
- SVS: Cathetrization of common femoral vein to obtain baseline PTH, followed by SVS from small venous branches of neck & mediastinum. 2times more from baseline: positive Indication: Persistent & recurrent HPT.
- Multi gland disease: Sec, Tertiary HPT, Lithium induced HPT, Familial HPT)
- Anesthesia: GA Position: supine with neck extended. Incision: horizontal crease 5-6cm incision just caudal to cricoid cartilage. Adr. can be injected into superficial fascia to reduce bleeding while raising flaps 60ml of 1 in 400000 adr.' upper flap:upto thyroid cartilage (subplatysmal) Lower flp: sternoclavicular joint, suprasternal notch, avoid injuring ant jugular veins- air embolism deep fascia incised vertically, strap muscles retracted (strenohyoid, omohyoid in outer plane, sternothyroid in deeper plane). one side of neck is chosen for exploration, and is maintained lateral to thyroid.
- Thyroid gland is mobilized to identify the parathyroid adenoma. Parathyroid having adenoma is mobilized which is close to recurrent laryngeal nerve. End artery of the parathyroid is identified and ligated. Adenoma is separated from adjacent thyroid tissue using gauze dissection. then confirmed with adjuncts which is disscussed later.
- Can be performed under local or general anesthesia. consists of focoused dissection, limited to one gland.
- IOPTH: While local practices vary, PTH levels are drawn at the following time points: (1) preincision (at a date prior to surgery or prior to starting the operation on the day of surgery); (2) preexcision (after exposing an abnormal gland but prior to ligating the blood supply to the gland); (3) 5 minutes after gland removal; and (4) 10 minutes after gland removal. Based on the Miami Criteria, a more than 50% decline in PTH at 10 minutes following parathyroid gland removal compared to the highest baseline level, either the preincision or preexcision, suggests cure and the procedure can be terminated. Dual criteria are commonly used to decide when to stop parathyroid exploration, which requires a more than 50% PTH decrease from the preincision level plus a final PTH that is within the normal range.
- Patients at an increased risk for postoperative bleeding such as those on anticoagulation or hemodialysis or with a known coagulopathy should be considered for overnight observation. Symptoms of hypocalcemia include acral and perioral numbness and paresthesias, muscle cramping, and weakness, and are treated with intravenous calcium gluconate and/or oral calcium carbonate with or without vitamin D supplementation, postoperatively. Patients with profound hypocalcemia may experience tetany with carpopedal spasm or trismus.
- Hungry bone: Metabolic syndrome, prolonged hypocalcemia, hypophosphatemia , & hypomagnesemia, following parathyroidectomy. The condition results from sudden decrease in PTH, resulting in increased uptake by bones.