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Flashcards in Parathyroid Pathology Deck (21)
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What is a "chief cell" in the parathyroid and what is its job?

It secretes parathyroid hormone (PTH) and regulates the free (ionized) calcium in the blood.


How does PTH increase the activity of bone osteoclasts?

It first activates the osteoblasts, which activates the osteoclasts, which will reabsorb calcium AND phosphate from the bone (note, however, that this is not "free" calcium as it will be bound to phosphate).


How does PTH induce Ca reabsorption in the small bowels?

PTH turns Vit D in its active form, which induces the small bowel to reabsorb calcium AND phosphate.


What function does PTH have in the kidney?

It increases Ca reabsoprtion, but also increases phosphate EXCRETION. This is the only pathway of PTH that actually increases the ionized Ca levels because the other 2 ways also reabsorb phosphate in addition to Ca.


What is "Primary hyperthyroidism?"

Excess PTH due to a disorder of the parathyroid gland itself. This can happen in 3 ways.


What is the most common cause of Primary hyperthyroidism?

Over 80% due to parathyroid adenoma, but can also be caused by a carcinoma or a sporadic hyperplasia randomly.


What is "Parathyroid adenoma?" How does it present?

Benign neoplasm of the parathyroid involving only one gland, and is usually asymptomatic hypercalcemia.


What are the consequences of increased PTH or hypercalcemia?

Nephrolithiasis of the calcium oxalate kind, Nephrocalcinosis, CNS disturbances, Constipation, Peptic Ulcer DIsease, and acute pancreatitis. Also Osteitis Fibrosa Cystica.


What is "Nephrocalcinosis?"

The most common variant of metastatic calcification (where calcium deposits in tissues) where the calcium deposits in kidney tubules.


What is Osteitis Fibrosa Cystica?

A consequence of the high PTH, resulting in scarring and cyst formation, sometimes hemmorhage of the bone.


What are the lab findings of Primary hyperparathyroidism?

Increased serum PTH, calcium, and alkaline phosphatase, decreased serum phosphate, increased urinary cAMP


Why do we see increased cAMP in the urine in primary hyperparathyroidism?

When PTH binds to its receptor in the kidneys, that receptor is a Gs receptor, which will activate the adenyl cyclase pathway resulting in the creation of cAMP. This cAMP can get into the urine and be detected in lab tests.


Why do we see increased serum alkaline phosphatase in primary hyperparathyroidism?

PTH receptors are present in osteoblasts not osteoclasts, so increased PTH will first activate the osteoblasts which lays down bown formation. For this to happen there needs to be an alkaline environment, which is achieved via alkaline phosphatase. Once bone is laid down, then the osteoclasts can come and reabsorb the bone (idea is the reabsorption is more than the depositon so we have an overall "activation" of osteoclasts due to PTH.


What causes secondary parathyroidism?

Increase in PTH due to something extrinsic to the parathyroid gland, most commonly chronic renal failure.


How would renal insufficiency trigger secondary parathyroidism?

Messed up renal function means less ability to do its functions, which includes excretion of phosphate. Less phosphate excreted means more remains in the blood, which means more phosphate binds to free Ca in the blood, and this reduction of free Ca will be detected by all 4 PTH glands. As a result, they will secrete a ton of PTH resulting in hyperparathyroidism.


What are the associated lab findings of secondary hyperparathyroidism?

Increased PTH, however decreased serum Ca (because that is what is causing the increased PTH secretion in the first place), increased serum PTH (because kidney isnt doing its job) and increased alkaline phosphatase (due to increased osteoblast activity which later means increased osteoclast activity).


What are 3 causes of Hypothyroidism?

Autoimmune damage, surgical excision (of maybe the thyroid being removed but the parahtyroid gland gets removed by accident), and DiGeorge syndrome.


What is DiGeorge Syndrome?

Failure of development of the 3rd and 4th pharyngeal pouch.


What are clinical manifestations of Hypothyroidism?

Numbness and tingling esp around the perioral region, muscle spasms (tetany). All this is due to decreased PTH which in turn means decreased serum calcium.


What is pseudohypoparathyroidism and what are the lab findings?

The Parathyroid is fine and it is secreting PTH but the organs are not responding to the PTH. Therefore the lab will show decreased free serum calcium but increased PTH.


What is one possible reason for the end organ resistance of PTH seen in pseudohypoparathyroidism? What else is seen in patients that have this defect?

An AD defect in the Gs proteins, so even though the PTH is binding the Gs is failing to activate the adenyl cyclase pathway to generate the cAMP which is the secondary messenger to mediate the effects of PTH. These patients also have a short stature and short 4th and 5th digits.