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42 Cards in this Set
- Front
- Back
in what conditions is PTH secreted?
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low serum Ca, increased PO4, severe hypomagnesemia
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what are the hormones involved in regulation Ca, PO4, Mg levels in the body?
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PTH
Vit D Calcitonin phosphatonins |
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PTH actions on kidney, bone, intestine?
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kidney: gets rid of PO4 in PT; increase Ca reabsorption and incrase active Vit D in DCT
bone: increase bone resorption intestine: indirectly increease Ca and P absorption by increasing conversion to active vit D |
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what does cinacalcet do?
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increases sensitivity of CSR to calcium (used to tx secondary hyperparathyroidism like in chronic kidney dz)
remember what CSR is? in hypercalcemia, CSR activates to cause more excretion of Ca |
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what is the vitamin D synthesis pathway?
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vit D3 from sun or diet --> 25 HCC (via 25-hydroxylase in liver) --> 1,25 DHCC (via 1 hydroxylase in kidney)
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what is 1-hydroxylase enzyme activity (and thus active vit D) increased by?
decreased by? |
inc by low P, low Ca, low calcitriol (=active vit D), inc PTH
dec by high levels of active vit D (neg feedback) |
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what are the actions of vit D in the intestines, bone, PTH gland, kidneys?
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Intestine:- increase Ca, Mg and P reabsorption
Bone:- increase mineralization and enhance osteoclast activity (PTH required for Vitamin D effect on bone) PTH gland:- Provides feedback to PTH gland - inhibit PTH secretion Kidney:- Increased renal excretion of phosphate and decreased renal excretion of calcium maintains Ca-Pi balance |
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what is useful in tx of hypercalcemia?
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calcitonin
Opposite effect on serum calcium as PTH - Inhibits osteoclast-mediated bone resorption -zIncreases renal excretion of calcium |
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what is the normal level of calcium in serum?
-ionized ca? |
9-10.4 mg/dL
ionized= 4.8-5.2 mg/dL |
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where is most of the calcium in the body?
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in the bone! (99%)
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what is the definition of hypocalcemia?
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total serum Ca < 9.0 mg/dl
ionized calcium <1.2 mmol/L (nl=1.2-1.3) |
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what are causes of hypocalcemia?
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1) No PTH
-Hypo PTH, hypomagnesemia 2) Ineffective PTH (generally Vit D related) -Vit D deficiency, malfunction -Intestinal malabsorption Ca 3) PTH overwhelmed Hyperphosphatemia (e.g. tumor lysis and rhabdomyolysis) -- PO4 will bind to Ca in the blood; so if you control PO4, you'll bring Ca back up |
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what are teh clinical presentation of hypocalcemia?
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1) Neuromuscular (causes muscle contraction)
-Tetany, Trousseau’s and Chvostek’s signs -Seizures, neuropsychiatric changes 2) Cardiovascular -Prolonged QT interval, arrhythmias, hypotension, heart failure 3) Ectodermal (rare) Coarse scaly skin, cataracts |
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tx of hypocalcemia
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- correct underlying dz process
- IV calcium (Ca gluconate > Calcium chloride) - oral calcium (calcium citrate, ca- acetate, ie tums) - give vit D (to inc gut absorption of Ca) |
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what is the definition of hypercalcemia?
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total serum Ca >10.4 mg/dl
ionized Ca >1.3 mmol/L Calcium always has to be linked to protein when you discuss it?? |
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what are the causes of hypercalcemia?
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Bone (hyperPTH, tumor, acidemia, immobilization, vit A)
GI absorption (Vit D, sarcoid, milk-alkali syndrome) Renal (ARF/immobilization, thiazide diuretics, familial hypercalcemia) |
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how does hypercalcemia present?
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1) Cardiovascular
Vasoconstriction, Hypertension, short QT interval on EKG 2)Gastrointestinal Ulcers, constipation, pancreatitis 3) Neuropsychiatric Lethargy, obtundation, psychosis muscle weakness 4) Extraskeletal calcifications Dermal, ocular, vascular (with infarction), visceral organs |
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________ ___________ is the most common cause of hypercalcemia in all patients
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primary hyperparathyroidism
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T or F. Thiazide diuretics are useful for hypercalcemia therapy.
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F. Loop diuretics are useful, but not thiazide!!
thiazide diuretics would make hypercalcemia worse! the blockade of na/cl cotransporter causes an increase in the functioning of the na/ca antitransporter which is reabsorbing Ca's and leads to hypercalcemia. |
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hypercalcemia related to _______ is the most common in hospitalized patients.
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malignancy
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what is the most important initial tx for hypercalcemia?
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aggressive volume replacement (But be careful in management of pts with CHF -- don't want them to have too much fluid)
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65 year old man with multiple myeloma presents with altered mental status and serum calcium of 10 mg/dL. Serum albumin is 1.2 mg/dL.
Is he hypercalcemic? |
remember Ca is always linked to protein, so you have to correct for hyperalbumic state.
Calcium is bound to albumin. Ionized calcium level may be elevated if albumin level is low. Formula: Normal calcium range changes 0.8 mg/dL for each gram that albumin changes from 4. Serum albumin 1.2, down 2.6 from 4.0. His normal Ca should be 10-(2.6x0.8)=8 mg/dL. Thus, his serum calcium of 10 is equivalent to a calcium of 12 in a patient with normal albumin. so YES, he is hypercalcemic (If there’s not enough protein in serum to bind Ca, then it will become ionized…not all of this Ca will stay in the serum and thus, total levels will decrease (although level of ionized Ca relative to normal will be elevated)) |
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65 year old man with multiple myeloma presents with altered mental status and serum calcium of 10 mg/dL. Serum albumin is 1.2 mg/dL. On exam, he is volume depleted.
How do you make his calcium level decrease? |
Replete patient’s vascular volume with saline. This will slow proximal nephron absorption of sodium and calcium. Also, volume repletion decreases TAL absorption of calcium.
Once patient volume replete, give furosemide with sufficient saline, so patient does not become volume depleted. Furosemide further decreases TAL calcium absorption. |
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what's the big diff in PO4 vs Ca homeostasis?
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most of hte PO4 that we take in is excreted by kidney (so this is very important for pts with kidney dz).
most Ca is excreted in stool (2/3), kidney (1/3) |
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which regulation hormone inhibits phosphorus reabsorption? where does it act?
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PTH; acts on proximal tubule
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An intoxicated, malnourished 45 yo patient with known alcoholism is brought to the ER by the police. He is given glucose containing fluids, vitamins, and admitted to general medicine. The next morning he is found to have hyperphosphatemia, rhabdomyolysis, and acute renal failure. What happened?
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The patient was probably phosphate depleted due to poor dietary intake, and had relatively low insulin levels. When he was given glucose containing solutions, his insulin levels rose, phosphate moved into cells, dropping serum phosphate to dangerously low levels
Rhabdomyolysis developed due to hypophosphatemia Rhabdomyolysis released intracellular phosphate, so subsequently, serum phosphate levels rose. |
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where are most of the cations (Ca, Mg, PO4) in the body: tissue or serum?
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tissue (so serum levels are NOT reflective of total body stores)
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what's the main diff of Mg reabsorption from Ca and PO4?
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most of it is taken up in the thick ascending limb of Henle -- 60% (Ca and PO4 is taken mostly up in the PT == check this!!
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etiology and presentation of hypomagnesemia
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etiology
- malnutrition, alcoholism, GI malabsorption - renal wasting after cisplatin, amphotericin B, cyclosporin presentation: - muscle weakness, tremors, fasciculations, arrhythmias -neuropsychiatric changes - hypocalcemia, hypokalemia |
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tx of hypomagnesemia
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- replace by IV or IM supplements
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etiology and presentation of hypermagnesemia
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etiology
- iatrogenic (pre-eclampsia), esp if renal failure present (can't excrete Mg) - Mg containing antacids in ESRD pts presentation: - low: thirst, nausea, vomiting, - mid: hypotention!! - high: coma, resp paralysis manifestations |
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tx of hypermagnesemia
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- IV calcium gluconate
- loop diuretics, hemodialysis |
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A weak patient is found to have hypokalemia and hypocalcemia refractory to potassium and calcium supplements. What’s going on?
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Magnesium is a necessary substrate or cofactor for important enzymes such as ATPase, GTPase, phospholipase C, adenylate cyclase and guanylate cyclase, which are important for renal transport of calcium and potassium.
Persistent hypocalcemia and hypokalemia may result from hypomagnesemia. Treatment consists of giving all three cations. |
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what is phosphatonins
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hormone that makes body get rid of phosphorus (nl physiology is not clear)
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what does acidemia do to serum ionized Ca levels?
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increases ionized Ca (vice versa for alkalosis --> would dec ionized Ca)
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what are the renal manifestations of hypercalcemia?
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1)ARF
-Vasoconstriction and decreased renal plasma flow and GFR 2) Volume depletion -Inhibition of Na reabsorption and inability to concentrate urine 3) K and Mg losses due to Na wasting |
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tx of hypercalcemia
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1) optimize renal excretion of Ca (by correcting vol depletion, loop diuretics -- not thiazides!!)
2) inhibit bone resorption with calcitonin and biphosphonates |
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what are some causes of hyperphosphatemia?
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- tumor lysis, rhabdomyolysis
chronic renal failure (leading to inability to excrete PO4) hypo-PTH cathartics |
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what are 3 consequences of hyperphosphatemia?
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- hypocalcemia
- Ca-Pi deposits in blood vessels, soft tissues, visceral - secondary hyperparathyroidism (eg. in chronic kidney dz) |
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tx of hyperphosphatemia
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-correct underlying dz
-oral phosphate binding agents (calcium and non-calcium based binders) |
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what are some causes of hypophosphatemia?
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cellular shifts:
- glucose infusion after starvation - common in severe alcoholism renal losses: - elevated PTH -renal tubular defect malabsorption (malnutrition, alcoholism) vitamin D deficiency (can't absorb Pi in the intestines anymore) |
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tx of hypophosphatemia?
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oral
- milk, cheese, eggs - Na and K phosphate suplements IV (Na or K phosphate salts) - only use in emergencies bc can cause severe and symptomatic hypocalcemia |