Parathyriod disordesr seminar by abd.ppt

Parathyroid disorder

1. Parathyroid
disorders
By Dr. Osman Sadig Bukhari

2. Parathyroid disorders include:
1-Hyper parathyroidism Hyper calcaemia
2-Hypo parathyroidism Hypo calcaemia
Parathyroid gland is important
in Calcium metabolism through
parathyroid hormone (PTH)

3. Parathyroid hormone (PTH)
-4 parathyroid glandsposterior to the
thyroid gland
-PTHis a single chain polypeptide of 84
amino acids secreted from chief cells of
the parathyroid gland
-Important actions of PTH are on:
-Thebone
-Vit D metabolism
-Small intestine
-Renal tubules
-Calcitoninopposes the actions of PTH

4. Actions of PTH
PTH increases plasma Caby:
1-Bone resorption by osteoclastic activity
2-Enhances intestinal absorption of Ca
3-Increases synthesis of Vit D3
4-Increases renal tubular re absorption
of Ca
5-Increases excretion of PO4

5. PTH PTH
-ve feed back
Kidney
Plasma Ca
Bone
Small intestine
Parathyroid gland

6. Hyperparathyroidism
1-Pry:-single adenomas (> 80%)
-multiple adenomas
-diffuse hyperplasia of all glands
-Parathyroid carcinoma is rare
serum PTH & Ca are raised.
2-2ry:-due to hypertrophy of all glands 2ry to
hypocalcaemia :
-renal failure
-Vit D deficiency
raised serum PTH.Ca is low or normal

7. 3-tertiary: due to autonomous parathyroid
hyperplasia after longstanding
2ry hyperparathyroidism
serum PTH, Ca & P are raised
4-Ectopic: e.g Bronchogenic Ca secrete PTH
like proteins

8. Primary hyper parathyroidism
-commonest parathyroid disorder
-prevalence: 1 in 800
-F>M
-90% in those over 50 years
-50% with biochemical evidence of hyper
parathyroidism are asymptomatic
Clinical features are due to hypercalcaemia
OR bone disease
Features of hypercalcaemia:
-non specific symptoms (A,N,V, constipation
and Wt loss; polyuria, polydipsia; tiredness,
drowsiness, poor conc, memory loss & depress)

9. -renal calculi, nephrocalcinosis, renal
impairment poor urine conc, hypokalaemia,
hyperchloremic acidosis
-corneal calcification
-ectopic calcification in arterial walls & soft
tissues
-HT, PU, myopathy & pruritus.
Features of bone disease:
Due to osteitis fibrosa cystica with bone
-pains
-tenderness
-fractures
-deformity

10. Investigations:
-biochemistry: ( ser Ca, P & PTH)
-Radiological: resorption of terminal
phalanges, pepper-pot appearance of the
skull, nephrocalcinosis, soft tissue
calcification
-imaging for tumour localization
Treatment:
-Treatment of hypercalcaemia
-Surgery

11. Other causes of hypercalcaemia
1-Malignancies
-Multiple myeloma
-Bone metastasis
2-Excessive of Vit D
-Iatrogenic
-Granulomas e.g sarcoidosis
-Excess Ca intake e.g milk-alkali syndr
3-Thyrotoxicosis & Addison’s (usually mild)
4-Drugs: thiazides, Vit A, lithium
5-Long term immobility
6-familial

12. Investigation of hypercalcaemia
1-fasting serum Ca & P
2-serum PTH
3-renal function, usually normal
4-protein electrophoresis to exclude MM
5-serum T4 &TSH
5-serum cortisol & synacthen test to exclude
Addison’s
6-serum ACE in the diagnosis of sarcoidosis
7-hydrocortisone suppression test; suppression
of serum Ca in sarcoidosis & in Vit D related

13. 8-imaging:
-plain abd for renal calculi
-sub periosteal erosions in middle & terminal
phalanges
-DXA bone density
-parathyroid U/S, CT & scan
Treatment of hypercalcaemia
-treat the underlying cause
-high fluid intake
-? calcitonin

14. -There is no effective medical TR in Pry
hyper parathyroidism; Surgery in pts with
renal stones & impaired renal fn, bone
involvement, marked hyper-calcaemia,
previous episodes of severe acute hyper Ca -
Treatment of acute hypercalcaemia
(Anorexia, vomiting, polyuria, nocturia, dehydration
and altered consciousness)
1-adequate hydration
2-IV biphosphonates for hyper Ca of
malignancy
3-IV calcitonin of little use
4-IV hydrocortizone& prednisolone 30-60 mg

15. Hypocalcaemia
Causes:
1-Chronic renal failure & hyper phosphataemia
2-Hypo parathyroidism:
-thyroid surgery; usually transient
-idiopathic: rare AI diseases often
accompanied by vitiligo, other AI diseases
and cutaneous moniliasis.
-congenital (DiGeorge syndrome): mental
impairment, cataract, calcified basal ganglia

16. 3-Pseudohypoparathyroidism: end organ
resistance to PTH associated with short
stature, short metacarpals, S/C calcification
and sometimes intellectual impairment.
Pseudo-pseudohyperparathyroidism = No
abn of Ca metabolism
4-Vit D deficiency & Vit D resistance
Osteomalacia/ rickets
5-Drugs: calcitonin & biphosphonates
6-Acute pancreatitis, citrated massive BT, low
plasma albumin & malabsorption

17. Clinical features :
1-N/M irritability & neuropsychiatric manifest
paraesthesiae, cirumoral numbness, cramps,
anxiety, tetany followed by convulsions,
laryngeal strider, dystonia & psychosis
2-Chvostek’s & Trousseau’s signs are signs of
latent hypocalcaemia
3-papilloedema & prolonged QT interval in
severe hypocalcaemia

19. Investigations:
1-renal fn tests
2-serum PTH level, serum Ca & P levels
3-parathyroid Abs
4-serum level of 25 OH Vit D
5-X ray metacarpals

20. Treatment:
1-IV Ca gluconate for severe cases with tetany
2-one alpha Vit D + Ca supplements with
frequent check of serum Ca .
3-PTH ? Needs frequent dose & Abs formation
against it.

21. Tetany
It is due to increased peripheral nerve
excitability due to :
1-hypocalcaemia
2-alkalosis
Mg depletion is a possible contributing factor
specially in malabsorption.
1-Hypocalcaemia from any cause
2-Alkalosis: -repeated vomiting
-hyperventilation
-excessive oral intake of alkalis
-Pry hyperaldosteronism; rare

22. Clinical features:
1-Children:
carpopedal spasm/ stridor/ convulsions
2-Adults:
peripheral & circumoral tingling/ painful
carpopedal spasm. Stridor & fits are rare
3-Latent tetany is recognized by:
a-Trousseau’s sign
b-Chvostek's sign.

23. Management:
1-Control of tetany by IV Ca gluconate 20 ml
of 10% slowly. If no response give Mg as
well.
2-Correction of alkalosis by NS in persistent
vomiting; if not effective with adequate doses
add ammonium chloride 2 g over 4 hrs.
Inhalation of 5% CO2 or re breathing exp air.
3-Treatment of the cause