Secondary Hyperparathyroidism (SHPT) and Tertiary Hyperparathyroidism (THPT)

by Carlo Raj, MD

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    Let’s talk about secondary hyperparathyroidism. What does this mean to you? It means that the parathyroid glands are responding to decreased calcium. So, what happened first? A decrease in calcium. The decrease in calcium will then trigger the parathyroid from releasing the parathyroid versus primary. The main causes include… well, most common would be, let’s say your patient has diabetic nephropathy, may result in chronic renal failure. So, therefore, you walk into a dialysis clinic and each one of those patients is experiencing renal failure. When renal failure is taking place, each one of those patients sitting on their thrones, you know for a fact, is Vitamin D deficient because the kidneys aren’t working properly, don’t have 1-alpha hydroxylase activation, Vitamin D is not properly formed or active Vitamin D is not formed; the calcitriol not being present may result in osteomalacia or decreased calcium. That decrease in calcium may then trigger secondary hyperparathyroidism. Our discussion in nephrology took us through what may then happen when there is renal failure. Now, because the kidneys aren’t working properly and you have too much PTH, the PTH does not work on the kidney whatsoever because the kidney’s dead. It’s going to go to the bone and start destroying it, but we do not call this osteitis fibrosa cystica, do we? What do we call this? Renal osteodystrophy. Every single patient in a dialysis clinic is receiving some form of calcium because for a fact you know that with chronic renal failure, the patient will be deficient of Vitamin D or calcium. Increased serum phosphorus binds with calcium. Why is phosphate even elevated in a patient with renal failure? Important beyond belief, right? Because the kidneys are dead. If the kidneys are dead... remember normally, what does PTH do with the phosphate in...

    About the Lecture

    The lecture Secondary Hyperparathyroidism (SHPT) and Tertiary Hyperparathyroidism (THPT) by Carlo Raj, MD is from the course Parathyroid Gland Disorders.

    Included Quiz Questions

    1. Decreased alpha hydroxylase activity
    2. Increased active vitamin D
    3. Decreased serum phosphorus
    4. Increased serum calcium
    5. Decreased PTH
    1. Calcium deposition in tissues of the body
    2. Paraneoplastic syndrome
    3. Secondary hyperparathyroidism
    4. Renal osteodystrophy
    5. Vitamin D deficiency
    1. Increased phosphate
    2. Increased PTH
    3. Decreased or normal phosphate
    4. Increased alkaline phosphatase
    5. Decreased serum calcium
    1. Autonomously increased PTH secretion due to secondary hyperplasia
    2. PTH secretion that is dependent on levels of calcium but does not respond to vitamin D levels
    3. Parathyroid hormones that surge PTH secretion and then become quiescent
    4. PTH secretion that responds to negative feedback from bound instead of free serum calcium
    5. PTH secretion that responds to signals from kidney but not to serum electrolyte levels

    Author of lecture Secondary Hyperparathyroidism (SHPT) and Tertiary Hyperparathyroidism (THPT)

     Carlo Raj, MD

    Carlo Raj, MD

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