Thyroid And Parathyroid Glands Flashcards
Mention manifestation of primary hyperparathyroidism
is a disease of bones, stones and abdominal groans. It is characterized by hypercalcemia and hypophosphatemia.
*The bones soften and deform as their mineral salts are replaced by fibrous connective tissue. Multiple bone cysts are present (Osteitis fibrosa cystica).
*Formation of renal stones because of excess ca salts being filtered through the kidneys leading to renal colic and hematuria. Deposition of Ca2+ salts within kidney tissue (nephrocalcinosis) with marked reduction in tubular and glomerular function leading to renal failure.
Gastrointestinal disorders e.g. peptic ulcer (as prolonged hypercalcemia has stimulatory effect on gastric acid secretion), which may contribute to peptic ulcer. Also, acute pancreatitis may occur due to activation of trypsinogen by excess Ca2+. Nausea, vomiting and constipation (due to decreased intestinal motility) may occur (abdominal groans). Hypercalcemia decreases neuromuscular excitability which can be manifested by skeletal
muscle weakness, decreased alertness, and poor memory. Cardiac arrhythmias (shortening of QT interval).
What are causes of hyperparathyroidism
Primary Parathyroid gland tumour (parathyroid adenoma).
Secondary (compensatory hypertrophy): e.g. Vitamin D deficiency & renal failure (due to phosphate retention & inability of the kidney to activate vitamin D) resulting in severe loss of calcium from the bones.
What are the immediate and delayed effects of PTH on bone
Immediate effect
This effect begins within minutes and continues for hours.
PTH🍃 stimulates membrane bound Ca² pumps, thus ↑ permeability of the osteoblastic- osteocytic bone membrane to Ca2+. So the amorphous Ca2+ (soluble, non-crystallized, labile Ca pool) is transferred from bone fluid into plasma.
B) Delayed (chronic) effect:
This takes days to weeks.
PTH increases the🍃 number and activity of osteoclasts, which break down the hydroxyapatite crystals (insoluble, crystallized, stable Ca2+ pool) leading to localized dissolution of bone and release of Ca2+ into plasma (= osteoclast activation).
What is the mechanism of action of PTH
PTH is a hydrophilic hormone which binds mainly to a G protein coupled receptors activating adenylyl cyclase, increasing intracellular cAMP.
Compare between labile and stable pool
What are the forms of ca in bone
✓(Labile pool<1%)It is also termed non crystallized, soluble, amorphous calcium (which is physicochemical equilibrium with ECF and readily exchangeable).🌸 This is the site of rapid action of PTH on bone.
✓Stable pool (>99%):
It is in the form of insoluble hydroxyapatite crystals (which is mobilized from bone by the action of osteoclasts).
🌸This is the site of delayed action of PTH on bone.
Mention regulation of PTH
When plasma Ca2+ level is high, PTH secretion is inhibited and Ca² is deposited in bones. When plasma Ca2+ is low, PTH secretion is increased.
PTH is increased by:
a) ⇓ Ionized plasma calcium level.
b)↓ Plasma Mg2+ level.
c) ⇓ 1,25-dihydroxy cholecalciferol.
d) ↑ Plasma PO4 level.
What is the action of PTH on kidney
PTH directly stimulates* reabsorption of calcium and magnesium in distal convoluted tubules and *excretion of phosphate in proximal convoluted tubules of kidney.
*PTH also increases the formation of 1, 25-dihydroxycholecalciferol (active vitamin D3 = calcitriol).
Mention action of PTH on intestine
PTH increases absorption of calcium by intestinal tract. This action of PTH on intestine is indirect via vitamin D3, as PTH increases the formation of calcitriol by kidney
Vitamin D3 in turn increases calcium absorption from intestine (through ↑ production of calcium binding proteins in intestinal mucosa called calbindin D).
TTT OF hyperparathyroidism
Surgical removal of the tumor in primary hyperparathyroidism. Treatment of the cause in secondary hyperparathyroidism.
What are causes of hypoparathyroidism
The most common cause is accidental removal or injury of parathyroid glands (3 glands at least) during thyroid surgery (thyroidectomy) leading to hypocalcemic tetany.
▸ Pseudohypoparathyroidism: a receptor disease in which the tissues fail to respond to the hormone (end organ resistance), commonly due to defective Gs protein with subsequent decrease in cAMP concentration.
Why hypocalcemia causes tetany
A decrease in free ca increases Na permeability
RMP closer to threshold so the peripheral nerve fibers become so excitable and begin to discharge spontaneously==>tetanic muscle contraction
What are the causes of hypocalcemia
Causes of hypocalcemia:
1) Hypoparathyroidism.
2) Renal failure.
3) Alkalaemia (decrease ionized Ca²*).
4) Vitamin D defficiency.
Compare between manifest and latent tetany
✓Manifest tetany
Appear during rest when the blood
Ca²-level decreases below 7mg
Muscular twitches and attacks of tonic & colonic contractions leading to generalized convulsions suffocation
In between attacks muscles are♠ stiff showing carpopedal spasm
✓Latent tetany
When the blood Ca++ level is from 7-8.5 mg%.
a Tetanic contractions are absent at rest but appear in certain situations (stress,hyperventilation, pregnancy).
★Latent tetany could become manifest by Provocative tests
What are Provocative tests for latent tetany
🌿Trousseau’s sign:
Occlusion of circulation of forearm by sphygmomanometer for few minutes causes ischemia of peripheral nerves resulting in flexion of wrist and thumb with extension of fingers.
🌿chvostek sign
Tapping over the facial nerve at angle of the jaw causes quick contraction of facial muscles.
TTT of hypocalcemic tetany
🌻Manifest tetany (acute hypocalcemia): an Calcium gluconate is given by slow intravenous injection.
🌻Latent tetany (chronic hypocalcemia):
Diet rich in calcium and oralcalcium,
Active vitamin D3 supplementation.
