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14 Cards in this Set
- Front
- Back
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Calcium distribution |
-stored mainly in bones and teeth (99%) as hydroxyapatite crystals, the remaining 1% is distributed between intracellular and extra cellular environments - normal range of serum calcium is between 8.6 and 10.4 mg/dL - half is bound to proteins, 90% to albumin and 10 to globulin and the other half is free not bound protein - free calcium is ionized, 10% form complexes with phosphorus or carbonate to become salt - normal range of free calcium is between 4.6 to 5.2 mg/dL - total calcium depends on calcium linked to proteins - if there is a change in protein intake there is a change in total calcium but total ionized calcium stays the same - pH of blood has an effect on total calcium levels - metabolic acidosis: decrease in protein binding and increase in ionized calcium - metabolic alkalosis: increase in protein binding and decrease in ionized calcium |
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How the concentration of extra cellular calcium is maintained? |
- daily intake of 1g, 350mg active absorption, overall gain = 100mg/day - extracellular calcium is filtrated by the kidney then reabsorbed again - 100mg of calcium is lost in urine, we gain calcium from diet and lose it by kidney= system in balance - vitamin D is essential for intestinal calcium absorption, it increases the expression of transmembrane channels that allow calcium to be absorbed by the gut |
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Calcium homeostasis |
- calcium sensing receptors are used to regulate trans-epithelial calcium transport - when there is an increase in calcium levels in blood, there will be an increase in excretion of calcium by the kidney and a reduction in PTH secretion to reduce the amount of calcium mobilized by the bone - when calcium is reduced, there is reduced calcium excretion by kidney and increased secretion of PTH to mobilize calcium from bone, produce vitamin D and absorb calcium through the gut |
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PTH in calcium homeostasis |
- control of calcium levels in the blood - at the level of the kidney: increase in reabsorption of calcium, synthesis of calcitriol (vitamin D), acts at the level of the gut to facilitate the absorption of calcium and phosphorus from the diet - increase in excretion of phosphate - at the level of the bone: increase bone reabsorption by activation of osteoblasts to increase calcium mobilization by the bones - PTH stimulates the differentiation of precursor osteoblasts into fully differentiated osteoblasts and they increase the absorption of bone at the surface which increases the level of calcium and phosphorus in the blood |
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Vitamin D in calcium and phosphorus homeostasis |
- major source of vitamin D: sunlight, when skin is exposed= produces precursor of vitamin D: CHOLECALCIFEROL The active vitamin D is calcitirol - precursor has to be activated |
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Hypocalcemia |
- reduction in total serum calcium concentration below the normal range 8.8 mg/dL in the presence of normal plasma proteins concentrations - symptoms depend on severity and rapidity of onset hypocalcemia Hypocalcemia is severe when calcium levels are below 7.5 - pseudohypocalcemia= total calcium levels can be low because the calcium bound to proteins is low. The correct calcium levels are calculated from the concentration of serum calcium and albumin concentration needs to be used (when patient is at risk of hypoalbuminia, hypovolemia or hepatic disease) Ph can interfere with the count of calcium and we also need to take into account analytical errors in the lab (15%). |
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Reasons for hypocalcemia |
- hypoparathyroidism: important to differentiate low PTH from high PTH. There are conditions when hypocalcemia is related to hypoparathyroidism and the most frequent is post-surgical hypoparathyroidism For example: neck surgeries Other rare conditions - auto immune hypoparathyroidism - infiltration of parathyroid glands - damage to parathyroid gland -rare genetic disorders |
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Hyperparathyroidism |
- high PTH levels associated with hypocalcemia - deficiency in vitamin D - rare condition: PTH resistance resulting from pseudohypoparathyroidism which is a miss ensue mutation in PTH gene - hypomagnesinia caused by diuretic drugs can cause PTH resistance - drugs that cause hypocalcemia are inhibitors of bone resorption such as biphosphanates used in patients with osteoporosis |
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Hypoparathyroidism |
- hypocalcemia with low levels of PTH = hypoparathyroidism and low levels of vitamin D - hypoparathyroidism is a rare endocrine disease characterized by hypocalcemia, low PTH - chronic hypoparathyroidism when it lasts more than a year - transient hypoparathyroidism = parathyroid glands start to produce PTH appropriately after some months - the most frequent cause is neck surgery (goiter or Graves’ disease) - autoimmune hypoparathyroidism Example: autoimmune polyglandular syndrome type I: condition caused by a mutation in AIRE, involved in autoimmune control - association with more endocrine diseases: Addison’s disease (hypocortisolism), diabetes mellitus 1, alopecia, hypogonadism - genetic conditions: pseudohypoparathyroidism 1a, 1b and 2 |
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Acute hypocalcemia |
First symptoms - perineal and distal paresthesia - we need to prevent severe conditions that lead to tetany - if calcium is very low, patients can have tetanus crisis meaning a total spasm of face, limb muscles, cardiovascular manifestations, seizures and laryngeal spasms |
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Chronic hypocalcemia |
-neurological alterations: - personality disorders - cognitive deficits - calcifications of the basal ganglia - extra-pyramidal motor disorders -increased intracranial pressure - pupil edema in the eye: - it can cause a cataract due to calcification alteration of the skin or appendages leading to dry skin, fragility, alopecia and nail dystrophy Renal failure, nephrocalcinosis and nephrolithiasis |
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Detecting low levels of calcium |
- Trosseau sign: need a sphyngmomanometer, you inflate the machine for 5mins to cut arterial blood flow to the arm and if there is a painful spasm, the patient is positive to hypocalcemia - chovstek sign: as a patient relaxes the face, tap the facial nerve anterior to the ear lobe and the corner of the mouth, a positive response is the twitching of the lip and a spasm of all facial muscles depending on severity of hypocalcemia |
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Acute hypocalcemia treatment |
- primary goal: control symptoms If hypocalcemia is severe, we administer calcium through IV and check levels every 4-6 hours If patient is asymptomatic and concentration of calcium is higher (7.5mg/dL) we stop IV and start oral administration Conclusion: therapeutic goal is to control symptoms and increase calcium levels |
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Chronic hypocalcemia treatment |
- keep patients asymptomatic - avoid under-treatment and over-treatment - the treatment is: salt of calcium and vitamin D (activated: calcitriol) - calcitriol has a low therapeutic window= risk of over treatment leading to hypercalcemia and hyperphosphatemia or the risk of under-treatment leading to hypocalcemia - new therapy for hypoparathyroidism patient: administration of PTH full hormone, very expensive |
