General surgery ppt - PG

1. Parathyroid gland
DR CARUNYA MANNAN

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
Superior parathyroid glands - inferior thyroid
artery
Also supplied by branches of the superior
thyroid artery in 15 to 20
 Inferior parathyroid glands - inferior thyroid
artery

6. 1. Low circulating serum calcium concentrations stimulate the parathyroid glands to secrete PTH, which mobilizes calcium
from bones by osteoclastic stimulation
2. PTH also stimulates the kidneys to reabsorb calcium
3. PTH stimulates convertion of 25-hydroxyvitamin D3 (produced in the liver) to the active form 1,25-dihydroxyvitamin D3,
which stimulates GI calcium absorption
4. 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
 Little 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, subperiosteal 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
 No further dissection and no frozen section
 If no adenoma found, 4 gland exploration
-Norman J, et al, 1997

32. 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

33. 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)

34. Intraoperative parathyroid hormone testing
Introduced 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

35. 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.

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

37. Thank You!