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18 Cards in this Set
- Front
- Back
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What are the three things controling calcium homeostasis?
How do they work, generally speaking? |
PTH, calcitonin, and 1,25-dihydroxyvitamin D
modulate cal¬cium levels by affecting its absorption in the intestine, its re¬absorption from the bony skeleton, and its excretion by the kidneys. |
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PTH, which is secreted into the circulation as the intact hormone and as carboxyterminal fragments, which do not bind PTHR
- what clears PTH? - what clears the carboxyterminal fragments? What part of the structure gives it it's biological activity? |
liver and renal
just renal --> thus accumulates in blood w/ decreasing renal fx 1-34 aa residues in N-terminal; b/ PTH-R |
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What activates the CaSR (Ca sensing receptor) in the Parathyroid? Effect?
- where else does the CaSR exist? - effect & triggers there? What does PTH b/ to PTH-R do intracellularly? |
low Ca, high PO4 (via lowering concentration of free Ca ions), Epinephrine, and nt's.
- secretes PTH. - 'C' cells (parafollicular cells) in thyroid - Calcitonin secretion in response to hypercalcemia, ^Mg, Glucagon, pentagastrin, and catecholamines - ^^cAMP |
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What is the effect of PTH b/ to PTH-R in the following tissues?
- bone - kidney (3) - GI tract |
- Osteoblasts secrete RANK ligand --> recruits osteoclasts --> bone resorption.
- \PT phosphate reabsorption; ^Ca resorption from the distal nephron. **25(OHD) --> 1,25(OH)D3 - 1,25(OH)D3 enhances absorbtion of Ca. |
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Where are calcitonin receptors found? Effect?
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osteoclasts - direct inhibition of osteoclastic bone resorption
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How does 1,20(OH)D activate transcription?
Actions in the following places: - bone - GI tract - kidney Pharmacological lvls of vit D cause what in the bone? |
through Vitamin D receptor (VDR) in the nucleus.
- enhance mineralization of osteoid both directly and by increasing calcium and phosphate - The hormone also stimulates the absorption of calcium and phosphate in the intestinal tract - increases Ca resorption and PO4 resorption. Actually causes bone resorption. |
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Pt presents to the clinic w/ anorexia, N&V, constipation, abdominal pain, pancreatitis.
Pt complains of fatigue, weakness and on PE you note hyporeflexia. Pt states that their eyes have a gritty sensation, and on PE you can see band keratopathy. Pt is hypertensive, has arrhythmias, and SHORT QT. Also complains of polyuria. Pt is likely deficient in which electrolyte? Chronically or Acutely? |
Ca, chronically.
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What can be the result of severe acute hypercalcemia?
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obtundation, coma, arrhythmias, cardiac failure, or acute renal insufficiency.
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Which vitamin D levels are measured in a lab work up of calcium homeostasis issues?
What other labs are done? |
25(OH)D
calcium, 24hr urine calcium, phosphate, PTH, alk phos, thyroid hormone, and renal fx tests. |
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What is the easy to remember shorthand sx list for hyperparathyroidism?
What is the most common sporadic etiology? Genetic forms? (3) What can this be secondary to? What is the most 'tricky' variant of this dz? |
serendipity stone moans groans bones.
adenoma [chief cell hyperplasias] - MEN I: pituitary, pancreas, paraT... cells can't cycle. - MEN IIa: paraT, medullary carcinoma thyroid, pheo. [constit. actv of osteoblast recep] - factitious PTH signal. renal failure --> secondary hyperparathyroidism. normocalcemic! 1,25(OH)D deficiency, some osteomalacia. |
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What happens to PTH lvls in the hypercalcemia of malignancy? Why?
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they get suppressed!
a tumor is secreting something else (analog, TNF, RANK ligand) that is activating the cascade w/o PTH, so PTH gets suppressed by negative feedback. |
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Answer if the following can cause hyperC. Then explain how, if they can.
- thyrotoxicosis - adrenal insufficiency - pheo - VIPoma |
- direct effect of thyroxine on bone to increase osteoclast activity, possibly TSH-R as a tonic inhibitor of osteoclastogenesis
- contraction of volume vs no glucocorticoid to oppose 1,25D action - vol contract, adrenergic change in PTH set point. - volume contraction. |
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Which drugs can cause hypercalcemia?
What is milk-alkali syndrome? |
Vit A, D, thiazide diuretics, Li.
combo of increased gut Ca abs w/ decreased excretion due to renal dysfunction. |
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What can macrophages produce in Granulomatous dz?
What is Familial hypocalciuric hypercalcemia (FHH)? |
1,25(OH)D
Ca-R abnormality causes problems w/ calcium sensing in kidney and paraT. |
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Pt presents with Extrapyramidal sx, convulsions, and irritability. Also has muscle cramps. Pt has prolonged QT and signs of CHF. Pt also has defective mineralization, rickets (children) and osteomalacia (adults). Lenticular cataracts and abnormal dental eruptions are also noted.
electrolyte issue? |
Hypocalcemia.
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What are 6 general causes of hypocalcemia?
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HypoparaT syndrome
Vit D deficiencies Acute pancreatitis Hungry bone syndrome Factitious (hypoalbuminemia) Hypermagnesemia |
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What is pseudohypoparathyroidism?
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end organs are resistant to PTH.
- TI: lack of cAMP actv - TII:normal cAMP, but the defect is post-receptor. |
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What can anticonvulsants cause re: Vitamin D?
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Vitamin D deficiency.
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