Basic knowledge for 5th year medical students

1. DISEASE OF PARATHYROID GLANDS
Dr. Mohammed Hajhamad,
MB.ChB. (MUST - Egypt), M.S (UKM - Malaysia)
Department of Surgery
International Medical School
Management and Science University
1

2. HISTORY
 1849 Sir Richard Owen provided 1st accurate
description of normal parathyroid glands after
examining Indian Rhinoceros
2

3. HISTORY
 1879 Anton Wölfer described tetany in a patient
after total thyroidectomy
 Ivar Sandström a Swedish medical student
grossly and microscopically described parathyroid
glands
3

4. HISTORY
 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
4

5. PARATHYROIDS
 The parathyroid glands are
usually embedded between the
posterior border of the thyroid
gland and its fibrous capsule.
 At times, the parathyroids may
be intrathyroidal.
 They measure 6 x4x2 mm in
maximum diameter and weigh
25-40 mg each.
 Number of glands can vary from
4-6
5

6. PARATHYROID GLAND, PHYSIOLOGY
 Calcium & Phosphate Metabolism
 Distribution & Balance of Ca & PO4
 Hormones involved
 Parathyroid Hormone
 Calcitonin
 Vit. D
6

7. PARATHYROID HORMONE (PTH)
 A peptide hormone that increases plasma Ca2+.
by:
 Mobilization of Ca2+ from bone
 Enhancing renal reabsorption
 Increasing intestinal absorption (indirect)
7

8. PARATHYROID HORMONE RAISES BLOOD CA
BY ACTING ON 3 ORGANS:
 Bone: main effect- stimulates osteoclasts  bone
breaks down  Ca released
 Intestines: increases uptake of Ca from intestine
 Kidney: stimulates reabsorption of Ca at kidney
tubules.
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9. PARATHYROID HORMONE
Actions (to increase plasma calcium):
 increasing osteoclastic resorption of bone.
 increasing intestinal absorption of calcium.
 increasing synthesis of 1,25-(OH)2D3.
 increasing renal tubular reabsorption of calcium.
 increasing excretion of phosphate.
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10. PTH FUNCTION
10

11. CALCITONIN
 a thyroid hormone
 produced by C-cells
 physiological effects
are antagonist to
those of PTH
 rapid acting, short
term regulator of
plasma Ca levels
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12. CALCITONIN LOWERS BLOOD CA
o Stimulates osteoblasts, inhibits osteoclasts
o Causes removal of Ca from plasma to calcify new bone
o Lowers plasma Ca (opposes PTH)
12

13. VIT. D
 Derived from irradiation of 7-dehydrocholesterol in
skin by UV rays
 Causes Ca absorption from intestinal tract
 Active form of this hormone is 1,25-
dihydroxycholecalciferol (calcitriol)
13

14. ACTIVE VITAMIN D (CALCITROL) IS MADE IN 3
STEPS BY DIFFERENT ORGANS
 The skin uses ultraviolet sunlight to make vitamin D3
(cholecalciferol) from cholesterol
 The vitamin D3 is converted to 25-Hydroxycholecalciferol in the
liver
 Stimulated by PTH
 The 25-Hydroxycholecalciferol is made into calcitriol (1, 25-
Dihydroxycholecalciferol) in the kidney
 Stimulated by PTH
 The main effect of calcitriol is to increase intestinal absorption
of Ca
14

15. HYPERPARATHYROIDISM
 Affects approximately 100,000 patients a year
 Primary hyperparathyroidism occurs in 0.1 to 0.3%
of the general population and is more common in
women (1:500) than in men (1:2000).
 Primary hyperparathyroidism is characterized by
increased parathyroid cell proliferation and PTH
secretion which is independent of calcium levels.
15

16. HYPERPARATHYROIDISM
 Etiology unknown, but radiation exposure, and
lithium implicated, associated with MEN1, and
MEN 2A
 Enlargement of a single gland or parathyroid
adenoma in approximately 80% of cases,
multiple adenomas or hyperplasia in 15 to 20%
of patients and parathyroid carcinoma in 1% of
patients 16

17. CLINICAL FEATURES
 Kidney stones, painful bones, abdominal groans, psychic
moans, and fatigue overtones.
 Kidney stones calcium phosphate and oxalate
 Osteopenia, osteoporosis, and osteitis fibrosa cystica, is
found in approximately 15% of patients with PHPT.
 Increased bone turnover .
 Peptic ulcer disease, pancreatitis
 Psychiatric manifestations such as florid psychosis,
obtubdation, coma, depression, anxiety, fatigue 17

18. HYPERPARATHYROIDISM
 Hypercalcemia can be from other sources. Intact
PTH measurement and elevated PTH level very
sensitive for hyperparathyroidism
18

19. IMAGING
 In the early stages there is demineralisation, with
subperiosteal erosions and terminal resorption in
the phalanges.
 A 'pepper-pot' appearance :lateral X-rays of the
skull.
 Reduced bone mineral density, resulting in either
osteopenia or osteoporosis. And is assessed by
DEXA
 In nephrocalcinosis, scattered opacities within the
renal outline.
 There may be soft tissue calcification in arterial
walls, soft tissues of the hands and the cornea.
19

20. IMAGES
Source: http://uwmsk.org/residentprojects/hpth.html
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21. PRE-OPERATIVE LOCALIZATION
 The predictive value of ultrasonography,
 CT scan and / or Magnetic resonance imaging
 Thallium-technetium dual isotope scintigraphy
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22. 22

23. SURGERY
 Bilateral neck exploration is “gold standard”
 With pre-operative imaging techniques can have
minimally invasive focused surgery towards
adenoma
 Can have 99-Tc Sestamibi timed within 3 hours of
surgery to intra-operatively localize parathyroid
adenoma using hand held geiger probe
 Can have sequential Sestamibi scan and repeat
technetium injection 10 minutes prior to surgery
 In this setting intra-operative PTH level testing
questionable
23

24. PARATHYROID CARCINOMA
 1% of cases of primary hyperparathyroidism
 15% of patients have lymph node
metastases and 33% have distant
metastases at presentation.
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25. PARATHYROID CARCINOMA
 Bilateral neck exploration, with en bloc
excision of the tumor and the ipsilateral
thyroid lobe.
 Modified radical neck dissection is
recommended in the presence of lymph
node metastases
25

26. SECONDARY HYPERPARATHYROIDISM
 In pts with chronic renal failure
 Deficiency of 1,25-dihydroxy vitamin D as a result
of loss of renal tissue, low calcium intake,
decreased calcium absorption, high phosphate
level and abnormal parathyroid cell response
 Normally treated medically
26

27. SECONDARY HYPERPARATHYROIDISM
 Surgical treatment is indicated and
recommended for patients with
 Bone pain,
 Pruritus, and a calcium-phosphate product >=70,
 Ca greater than 11 mg/dl with markedly elevated PTH
 Calciphylaxis
 Progressive renal osteodystrophy,
 Soft-tissue calcification
27

28. TERTIARY HYPERPARATHYROIDISM
 Long standing renal failure after renal transplant
 autonomous parathyroid gland function and tertiary HPT.
 Can cause problems similar to primary hyperparathyroidism
 Operative intervention
 symptomatic disease
 autonomous PTH secretion persists for more than 1 year
after a successful transplant
 subtotal or total parathyroidectomy with autotransplantation
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29. POST OPERATIVE COMPLICATIONS
 Hypocalcemia (Chvostek’s and Trousseau’s
sign)
 Vocal cord paralysis after RLN injury
29

30. HYPOPARATHYROIDISM
 Deficient secretion of PTH which manifests itself
biochemically by hypocalcemia, hyperphospatemia
diminished or absent circulating iPTH and clinically
the symptoms of neuromuscular hyperactivity.
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31. HYPOPARATHYROIDISM
 Surgical hypoparathyroidism – the commonest
 After anterior neck exploration for thyroidectomy,
abnormal parathyroid gland removal, excision of a neck
lesion.
 It could be due to the removal of the parathyroid glands
or due to interruption of blood supply to the glands.
Causes:
31

32. HYPOPARATHYROIDISM
 Idiopathic hypoparathyroidism
 A form occuring at an early age (genetic origin) with
autosomal recessive mode of transmission “multiple
endocrine deficiency –autoimmune-candidiasis
(MEDAC) syndrome”
 “Juvenile familial endocrinopathy”
 “Hypoparathyroidism – Addisson’s disease –
mucocutaneous candidiasis (HAM) syndrome”
Causes:
32

33. HYPOPARATHYROIDISM
 Idiopathic hypoparathyroidism
 Circulating antibodies for the parathyroid glands and the
adrenals are frequently present.
 Other associated disease:
 Pernicious anemia
 Ovarian failure
 Autoimmune thyroiditis
 Diabetes mellitus
Causes:
33

34. HYPOPARATHYROIDISM
 Functional hypoparathyroidism
 In patients who has chronic hypomagesaemia of various
causes.
 Magnesium is necessary for the PTH release from the glands
and also for the peripheral action of the PTH.
Causes:
34

35. MAJOR CAUSES OF CHRONIC HYPOCALCEMIA OTHER
THAN HYPOPARATHYROIDISM
 Dietary deficiency of vitamin D or calcium
 Decreased intestinal absorption of vitamin D or
calcium due to primary small bowel disease,
short bowel syndrome, and post-gastrectomy
syndrome.
 Drugs that cause rickets or osteomalacia such as
phenytoin, phenobarbital, cholestyramine, and
laxative.
35

36. MAJOR CAUSES OF CHRONIC HYPOCALCEMIA OTHER
THAN PARATHYROPRIVAL HYPOPARATHYROIDISM
 States of tissue resistance to vitamin D
 Excessive intake of inorganic phosphate compunds
 Psudohypoparathyroidism
 Severe hypomagnesemia
 Chronic renal failure
36

37. HYPOPARATHYROIDISM
A. Neuromuscular
 The rate of decrease in serum calcium is the major
determinant for the development of neuromuscular
complications.
Clinical Features:
37

38. HYPOPARATHYROIDISM
A. Neuromuscular
 Parathesia (sensation of numbness or tingling on the skin)
 Tetany
 Hyperventilation
 Adrenergic symptoms
 Convulsion (More common in young people and it can
take the form of either generalized tetany followed by
prolonged tonic spasms or the typical epileptiform
seizures.
 Signs of latent tetany
 Chvostek sign (nilateral spasm of the oris muscle is initiated by
a slight tap over the facial)
 Trousseau sign
 Extrapyramidal signs (due to basal ganglia calcification)
Involuntary movements, Tremors and rigidity
Clinical Features:
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39. HYPOPARATHYROIDISM
B. Other clinical manifestation
1. Posterio lenticular cataract
2. Cardiac manifestation:
3. Prolonged QT interval in the ECG
4. Resistance to digitalis
5. Hypotension
6. Refractory heart failure with cardiomegally can
occur.
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40. HYPOPARATHYROIDISM
B. Other clinical manifestation
3. Dental Manifestation
Abnormal enamel formation with delayed or absent
dental eruption and defective dental root formation.
4. Malabsorption syndrome
Presumably secondary to decreased calcium level
and may lead to steatorrhoea with long standing
untreated disease.
40

41. HYPOPARATHYROIDISM
 In the absence of renal failure the presence of
hypocalcaemia with hyperphosphataemia is virtually
diagnostic of hypoparathyroidism.
 Undetectable serum iPTH confirms the diagnosis or
it can be detectable if the assay is very sensitive.
Diagnosis:
41

42. HYPOPARATHYROIDISM
 The mainstay of treatment is a combination of oral
calcium with pharmacological doses of vitamin D or
its potent analogues.
 Phosphate restriction in diet may also be useful with
or without aluminum hydroxide gel to lower serum
phosphate level.
Treatment:
42

43. EMERGENCY TREATMENT FOR HYPOCALCAEMIC
Calcium should be given parenterally (IV) till adequate
serum calcium level is obtained and then vitamin D
supplementation with oral calcium should be initiated.
Tetany:
43

44. EMERGENCY TREATMENT FOR HYPOCALCAEMIC
In patients with hypoparathyroidism and severe
bone disease who undergo successful
parathyroidectomy hypocalcaemia may be
severe and parenteral calcium infusion with later
supplementation with oral calcium and vitamin D.
Hungry bone syndrome:
44

45. CLINICAL SCENARIO-
PARATHYROID GLAND
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46. CASE # 01
 A 43-year-old male is admitted to the emergency
room for severe pain in his left flank, radiating to the
groin. The pain is intermittent and initiated after
running a marathon on a hot summer day. The
patient is asked for a urine specimen and blood is
detected in the urine. He is hydrated and additional
diagnostic procedures are done. Laboratory values
show an increased plasma calcium of 12 mg/dL,
and increased plasma intact PTH values of 130
pg/mL.
46

47. CASE # 02
 A 73-year-old woman is admitted to the hospital
following a bout of severe vomiting and generalized
weakness. Initial laboratory values reveal increased
plasma calcium levels. The referring physician tells
you that she has breast cancer and her bone scan
indicates metastasis to bone.
47

48. CASE # 03
 A postmenopausal patient is referred for
asymptomatic hypercalcemia and history of
repeated episodes of urolithiasis (kidney stones).
Blood laboratory values reveal increases in intact
PTH, 1,25(OH)2D, and markers of bone resorption.
Neck ultrasound revealed a mass below the right
lobe of the thyroid gland.
48

49. CASE # 04
 A 35-year-old woman undergoes a thyroidectomy
for papillary serous thyroid cancer. The surgeon
suspects that the parathyroid glands have been
removed. Which of the following findings is most
likely to be seen in the patient 1 week
postoperatively?
 A. Coma
 B. Constipation
 C. Esophagitis
 D. Muscle spasms and tetany
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50. YOUR BRAIN
BEFORE AFTER
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