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41 Cards in this Set
- Front
- Back
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what's the PTh blocker?
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calcitonin
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Glucocorticoids build bone
They a) maintain osteoBlast activity b) block osteoClast activity |
a) maintain osteoBlast activity
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Calcitonins builds bone
They a) maintain osteoBlast activity b) block osteoClast activity |
b) block osteoClast activity
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Estrogens builds bone
They a) maintain osteoBlast activity b) block osteoClast activity |
both
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4 things that cause hypercalcemia
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1. Primary HYPER-Parathyroidism
2. Malignancy 3. Benign Familial HYPER-Calcemia 4. Medications/Vitamin Excess |
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KEY PHYSICAL SIGNS:
Primary HYPER-Parathyroidism (2) |
1. Band Keratopathy-across the cornea
2. Subperiosteal Bone Resorption (aka. Osteitis Fibrosa Cystica)- Causes a classic moth-eaten appearance to the phalangeal cortex on finger x-rays due to prolonged PTH excess. |
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Primary HYPER-Thyroidism
LAB DIAGNOSIS |
High Ca+ and
High PTH |
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IF, patient has SYMPTOMATIC PRIMARY HYPER-PARATHYROIDISM, ie. Kidney-stones , low bone density…,
WHAT DO YOU DO NEXT? |
SURGICAL REMOVAL OF ADENOMA
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HYPER-Calcemia of Malignancy
3types? |
1. Myeloma- produces Osteoclast Activation Factor (OAF) that Breaks down Bone.
2, Solid Tumors-produce PTH-rp 3. Bone Metastasis-50% of all elevated calcium & malignancy; produce Local Osteoclast activation substance. |
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BOARDS< BOARDS< BOARDS (but not a test question.)
Hypercalcemia from HCTZ is never greater than what value? |
11.0
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What if you have a Calcium sensor problem where you have high Ca but normal PTH?
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Benign Familial HYPERcalcemia-
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What does Lithium do to cause hypercalcemia?
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increases the THRESHOLD at which increasing Calcium stops the PTH.
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First thing to treat hypercalcemia
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Immediately give 3-4Liters of Normal Saline
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What's next?
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Furosemide (Lasix-LOOP diuretic)- but NEVER until the patient is Hydrated.
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Why not thiazides?
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Furosemide PROMOTES Calciuria; while Thiazides INHIBIT Ca+
excretion. (it gets rid of [reabsorbs] stones) |
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Your hypercalcemic pt has been treated with hydration and diuretics. There are still symptoms. What do you do next?
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PAMIDRONATE-a bisphosphonate which interferes with bone resorption in areas of high turnover
Standard for cancer pts/ with symptoms, etc. |
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Your hypercalcemic pt is treated with hydration, a loop, and (prn) bisphosphonate. What now?
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look at phosphates. correct low PO4
adjust diet (lower Ca) |
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5 causes of hypocalcemia
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1. DECREASED PTH SECRETION
2. VITAMIN D Deficiency - common “locked Inn” 3. Loss of Calcium 4. Acute Hyperphosphatemia 5. PseudoHypoParathyroidism |
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What's a HOnDA?
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HTN, Obese, DM, Acidotic
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Your hypocalcemic, hyperphosphatemic pt needs a new name. What is it?
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hypo-parathyroidic
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Your Hypo-PTH pt has acute tetany. What do you do?
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Give IMMEDIATE IV CaGluconate (10ml) slowly-
Also, give Magnesium |
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Your Hypo-PTH pt has tetany all the time over and over. What do you do?
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1. Oral Ca+ +/- Vitamin D to goal of 8.5-9.0 mg/dL
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Most common cause of hypo-PTH
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Post-Surgical removal of the Thyroid gland and inadvertently remove the Parathyroids.
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3 major bone disorders
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Osteoporosis-
Osteomalacia- Paget’s Disease |
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Describe mineral to matrix ratio of osteoporosis.
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normal mineral:matrix ratio
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Why do we think we might be able to effectively treat osteomalacia?
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deficiency of Vitamin D or Phosphorus that alters the formation of hydroxyapatite.
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treatment of Paget's disease.
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suppression of bone resorption with calcitonin or bisphosphonates.
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A kid has psueudofractures, listlessness, irritability and bowed legs. How do you tell the diff b/w abuse and rickets?
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rickets is bilateral
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If you suspect vit D deficiency, what test do you run?
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25-(OH)-D3 levels if suspect deficiency; NOT 1,25-
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MEN 1 - WERMER Syndrome
REMEMBER “PPP” = |
Pituitary, Parathyroid, Pancreas
Anterior Pituitary, Parathyroid and Pancreatic Islet Cell Neoplasia |
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Comment on blood sugar and calcium in MEN 1
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HYPOglycemia and HYPERcalcemia
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Known as SIPPLE SYNDROME
Prior known as MEN 2A REMEMBER “TPP” - |
THYROID, PHEOCHROMOCYTOMA, PARATHYROID HYPERPLASIA
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Chromosome 11
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MEN 1 - WERMER Syndrome
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Chromosome 10
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SIPPLE SYNDROME
Prior known as MEN 2A |
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KEY to MEN II
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COMBO OF MEDULLARY THYROID CARCINOMA (hyperplasia of the calcitonin producing cells) AND PHEOCHROMOCYTOMA
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Hallmark of MENII is
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consistent elevation of serum Calcitonin.
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LIFE EXPECTANCY of MENII =
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60 YEARS OLD
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how is MEN II like MEN III (2b)
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Medullary Thyroid Carcinoma, Pheochromocytoma
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How is MEN II diff from MEN III
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MEN III has ABNORMAL PHYSICAL APPEARANCES
-dysfiguring neuromas of the lips and mouth -Marfan like habitus |
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Is there Parathyroid HYPERPLASIA
in MEN III? |
no
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LIFE EXPECTANCY of MEN III
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30 YEARS OLD
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