This document discusses parathyroid tumors and calcium regulation by the parathyroid hormone (PTH). It covers primary, secondary, and tertiary hyperparathyroidism, their causes, symptoms, and treatments. Key points include: - PTH levels are regulated by calcium levels through a feedback loop involving the calcium sensing receptor. - Primary hyperparathyroidism is usually caused by a parathyroid adenoma and is often asymptomatic. Surgery is the only cure. - Secondary hyperparathyroidism is caused by chronic kidney disease or vitamin D deficiency and leads to hyperplasia of all four parathyroid glands. It can be managed medically but may require surgery. - Tert

1. DR ZEESHAN ALI
PARATHYROID TUMORS

2. CALCIUM –PTH
 Feed back regulation
 Sigmoid curve PTH-Calcium curve
 Calcium sensing receptor CSR
 ‘Set point’ ---shifting right with Lithium,CRF
--- shifting left with early renal failure
 PTH is secreted intermittently so normocalcaemia
can be found! T1/2 = 2mins
 Vit D deficiency can also lead to normocalcaemia

3. Manifestation of hypercalcaemia
 Muscle weakness
 Muscle and bone aches and pains
 Depression
 Constipation
 Tiredness
 Peptic ulceration
 Pancreatitis
 Renal impairment
 Nephrogenic diabetes insipidus
 Nephrolithiasis
 Shortened QT interval
 Band keratopathy
 Thirst and polyuria

4. Causes of hypercalcaemia
 Hyperparathyroidism
 Disseminated malignancy
 Vitamin D intoxication
 Milk-alkali syndrome
 Drug therapy (lithium, calcium antacids, calcium
replacement therapy)
 Familial hypercalcaemic hypocalciuria
 Granulomatous disease (sarcoidosis, tuberculosis)
 Immobilization
 Thyrotoxicosis
 Adrenal insufficiency

5. Types of hyperparathyroidism
 Primary hyperparathyroidism
 Secondary hyperparathyroidism
 Tertiary hyperparathyroidism
 Familial hyperparathyroidism
 Parathyroid carcinoma

6. PRIMARY
HYPERPARATHYROIDISM

7.  Adenoma and PTHrP ( PTH)
 Bones,stones,groans,psychic moans
 found mostly during workup of
osteopenia,osteoporosis and nephrolithiasis
 Osteitis fibrosa cystica is a condition of chronic
disease (usually with 2ndary and tertiary )
 Usually present in 60s
 2:1 female to male
 24 hrs urinary calcium is used
Adenoma has equal frequency in superior and
inferior glands!

8.  Treatment include medical and surgical BUT
surgery is curative
 In symptomatic pts decision is simple
 In asymptomatic NIH criteria used
 Less then 50 years old
 Unable to be effectively followed up
 Serum calcium >1.0 mg/dL above the normal range
 Urinary calcium >400 mg/24 hours
 30% decrease in renal function
 Complications of HPT: nephrocalcinosis,
osteoporosis (T-score o2.5 s.d. at lumbar spine, hip
or wrist)
 Severe psychoneurologic disorder

9. SECONDARY
HYPERPARATHYROIDISM

10.  Chronic PTH stimulus but relieved on removing
the stimulus
 Causes
 CRF
 Vit D def
 Intestinal malabsorption
 CCF
 HTN
 Parenteral nutrition
 Lithium
When nothing adds up than think LITHIUM!
( urinary Calcium,no stones, PTH)

11.  Four glands hyperplasia happens
 Sometimes adenoma can also form or a nodular
hyperplasia happens
Biopsy glands!
 Renal disease treated by phosphate binders
,calcitriol --- subtotal parathyroidectomy

12. TERTIARY
HYPERPARATHYROIDISM

13.  Refractory secondary hyperparathyroidism
 Set point irreversibly shifted to right
 Subtotal parathyroidectomy (leave 20-30gm)
Think when renal transplant doesn’t get PTH level
down!
Think when dialysis is not bringing PTH down!
Think when PTH high, in spite withdrawing lithium !
During operation wait 25 min (not 10 min) to draw
PTH for 50% reduction after removal of gland to
rule out any remaining glands!

14. FAMILIAL
HYPERPARATHYROIDISM

15.  Sporadic still a more common cause
 FAMILIAL HYPERCALCAEMIC
HYPOCALCIURIA
 AUTO DOMINANT MILD HYPER PTH
 NEONATAL SEVERE HYPER PTH
 MEN 1
 MEN 2A
 HPT JAW SYNDROME
 FAMILIAL ISOLATED HYPER PTH
HPT JAW SYND – related to carcinoma of PTH!
Subtotal resection will n
As polyclonal proliferatio
Tumor based, so
subtotal resection
will cure
asymptomatic

16. PARATHYROID CARCINOMA

17.  < 1%
 High incidence in Japan and Italy
 45—51 yrs
 More symptomatic
 Radiation exposure be a cause
 Cyclin D1 on chromosome 31,Rb genes, p53
genes
 radioresistant
Treatment _ enbloc resection + hemithyroidectomy
Deaths of these pts are due to hypercalcemia!

18. PARATHYROID LOCALIZATION

19. PREOPERATIVE
 Scintigraphy – Tc99m sestamibi(double phase
scan)
_ substraction technique via I 123
..best mode
 Doppler Ultrasound _ for ectopic glands
 FDG PET _ for ectopic glands
 MRI /CT scan
 Venous sampling
Experience surgeon can identify 95% of glands: all
above means 80%!

20. INTRAOPERATIVE
 GAMMA PROBE
 METHYLENE BLUE
 FROZEN SECTION
 INTRAOPERATIVE PTH (ioPTH)
 Expensive
 A measure of success of procedure
 Donot work well in hyperplasia situation
 Sample at T0,T5 and T10
 50% decrease in value means success

21. ANATOMY

22.  Encapsulated ,brown ,softer than thyroid and LN
 5-7mm in max dia
 Surrounded by a layer of fatty tissue

23. TECHIQUES OF
PARATHYROIDECTOMY

24.  Targeted approach … gamma probe for adenoma
only aided by ioPTH
 Four gland exploration … in glandular hyperplasia
aided by frozen section and ioPTH

25. PRINCIPLES OF GLAND SEARCH

26.  Superior gland _
 deep to RLN and inf throid artery at retrothyroid
area
 Within 1cm of cricothyroid
 Deep to cricothyroid
 Darker body with vessel inside a fat
 Inferior gland
 Region of Thyrothymic tract(Medial to RLN)
 Tracheoesophageal groove
 Within thymus
 Within thyroid
 Mediastinum
 Lateral to carotids
 Pyriform fossa

27.  Thymic exploration
 80 % rule – explore the opposite thymus if adenoma
found within one thymus
 Thyroid exploration
 For subcapsular or intraglandular PT --- ioPTH is
used to find the side
 1st thorough search frm hyoid to superior
mediatinum
 Than excise lower 2/3rd thyroid or do lobectomy
 Dice on table and find the missing PT
Look other side when cant find gland in normal
location at first!
No search after finding an adenoma if only one gland
is missing!
No search after bilateral exploration,bilateral thymic

28. AUTOTRANSPLANTATION AND
CRYOPRESERVATION

29.  Autotransplant in hyperplasia cases
 60mg diced in 15-20 1 cubic mm pieces in non-
dominant brachioradialis marked with ligaclips
 Rest cryopreserved for failure cases

30. MANAGEMENT OF
HYPOCALCAEMIA

31.  TEMPORARY THRESHOLD SHIFT( nerves and
muscle are accustomed to high calcium :so pt
become symptomatic)
 HUNGRY BONE SYND ( fall in PTH causes bone
to take in calcium)
days
 Temporary hypoparathyroidism
weeks
 Permenant hypoparathyroidism
>3 months
Only symptomatic hypocalcemia be treated !
If not resolving check magnesium!

32. MANAGEMENT OF ACUTE
HYPERCALCAEMIA

33.  Life threatening condition (confusion-coma)
 > 3.5 mmol/l
 Rehydrate with NaCl
 Loop diuretics
 Calcitonin will buy 72 hrs
 Steriods (decrease vit D conversion)
 Gallium and mithramycin (cytotoxic to osteoclast)
 Bisphosphonate main stay
treatment but slow onset
pamidronate 28 days lasting
effect
Will buy minutes

34. LATEST TRENDS

35.  ENDOSCOPIC TECNHIQUES VIA AXILLARY
ROUTE
 MINIMALLY INVASIVE USING GAMMA PROBE
 DE VINCI METHOD

36. THANK YOU