Calcium Flashcards

1
Q

Normal Serum Ca

A

Normal = 9.5 mg/dl (8.5-10)

  • 45% bound to albumin
  • 10% in complexes w/ phosphate or carbonate
  • 45% free or ionized
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2
Q

Ca Sources and Absorption

A
  • Intake = 1000 mg but only 150-200 absorbed (proximal SI - duodenum and jejunem)
  • Dark green leafy vegetables, dairy, almonds, soy, fortified foods (cereal, OJ, etc)
  • Supplements - most common is Ca carbonate (w/ food need acid) OR Ca citrate (do NOT need food)
  • Aided by activated Vit D (1,25 dihydroxyvitamin D) but also some passive absorption
  • 1st Hydroxylation - in liver @ 25
  • 2nd Hydroxylation - in kidney @ 1 (regulated by PTH and FGF-23)
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3
Q

PTH Regulation and 5 Roles

A
  • PTH - cleaved into PTH 1-34 (main effects)
  • Mainly regulated by serum Ca conc - Ca-sensing receptor on parathyroids sense free Ca++ (dec serum Ca++ - secrete PTH v. inc serum Ca++ - binds receptors - inhibits PTH secretion and dec levels of PTH mRNA)
  • Actions
    1- Stim 1,25 Vit D production in kidney
    2- Stim Ca reabsorption in tubules
    3- Block phosphate reabsorption in tubules
    4- Activates osteoclasts for resorption ACUTELY and osteoblasts SUBACUTE/CHRONICALLY
    5- Activate Ca transport indirectly in intestine via 1,25 Vit D
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4
Q

FHH and ADHH

A
  • Familial Hypocalciuric Hypercalcemia (FHH) - inactivating mutation of Ca sensing receptor - higher set point
  • Auto Dom Hypocalcemic Hypercalciuria (ADHH) - lower set pt
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5
Q

Kidney Ca Control

A
  • 65% reabsorbed in proximal tubule (not tightly regulated) - coupled to Na and water transport
  • 35% delivered to cortical TAL and distal tubules - reabsorbed there under regulation of PTH (very tightly regulated)
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6
Q

Hypocalcemia Value + Signs/Symptoms

A

<2 SD below mean in lab (usually 8.5) - must check albumin and Mg

ALL SIGNS DUE TO HYPEREXCITABILITY (dec mem threshold)

  • Neuro - fatigue, seizures, peri-oral numbness/tingling, basal ganglia or intra-cerebral calcifications
  • Cardio - prolonged QT –> arrhythmias
  • MSK - twitches, cramping, tetani
  • GI - cramping
  • Pulm - bronchospasm
  • Eyes - cataracts
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7
Q

Chvostek and Trousseau’s Signs

A

Chvostek’s Sign - twitch facial muscles when tap facial nerve w/ reflex hammer (only helpful if no sign at baseline)

Trousseau’s Sign - spasms of forearm w/ BP cuff > systolic

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8
Q

How does the body respond to hypocalcemia acutely and chronically?

A
  • Acute - parathyroids sense dec free Ca –> inc PTH (min) –> 2 acute effects
    • 1- Inc Ca reabsorption / dec Ca excretion in kidney
    • 2- Stimulate osteoclasts (net release of Ca into serum)
  • In few days … elevated PTH –> inc 1,25 Vit D synthesis (takes few days) which inc Ca absorption in gut
  • If not corrected … chronic elevated PTH –> delayed activation of osteoblasts too so restore Ca balance from bone; maintain Ca by dec excretion and hyper-absorption
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9
Q

Hypoparathyroidism

A
  • Low free Ca w/ low PTH, often high phosphorous, low 1,25 Vit D –> lower absorption, low bone turnover (no net losses or gains), PTH not stimulating kidneys so “open faucet” - more Ca given - more Ca in urine
  • Causes - surgery, autoimmune, infiltration
    (hemochromatosis, Wilson’s), congenital
  • Tx - Ca supplement and 1,25 Vit D (calcitrol), monitor urinary Ca
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10
Q

Vit D Def

A
  • Diagnosed by low 25 OH Vit D
  • Results from malabsorption, inadequate skin exposure, dec activation (liver or renal disease), genetics (mutations in hydroxylases or Vit D receptors)
  • Reduced levels –> mineralization defects in bone
    • Rickets in kids
    • Osteomalacia in adults
  • Lab Patterns = low Vit D, low absorption, high PTH secondary to low Ca –> inc bone resorption and will try to inc 1,25 Vit D (not successful b/c substrate to low) and max reabsorption of Ca in kidneys
  • Tx - Vit D supplements; use 1,25 Vit D if end-stage renal disease OR hypoparathyroidism (cannot activate on own)
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11
Q

Magnesium Def

A
  • More common in hospitalized patients (malabsorption or inc losses of Mg in urine from diuretics and IV fluids, can also be due to alcoholism or cisplatinin for chemo)
  • Co-factor for PTH; low Mg –> inhibition of PTH secretion and dec PTH effects on target organs (kidney and bone)
  • Tx - oral Mg replacement (some GI upset)
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12
Q

Pancreatitis

A
  • Causes - duct obstruction, alcohol, meds, trauma
  • Mild to severe hypocalcemia is a poor prognostic factor
  • Mechanism - pancreatic lipase released into peritoneal space –> digests triglycerides –> free FAs (neg charge) which bind Ca (pos charge) –> insoluble FA-Ca salts (soaps)
  • Chronically causes malabsorption of Ca and Vit D
  • Tx
    - Ca replacement by IV if acute
    - Resolves w/ resolution of pancreatitis
    - Ca and Vit D replacement if chronic
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13
Q

Hypercalcemia Value (+ correction)

A
  • Definition - > 2 SD above normal of lab; about 10.2-10.5; no grading criteria
  • Generally, 12-14 mild; > 14 severe
  • Correct for albumin
  • Corrected Total Ca = Meas Ca + .8 (4- meas albumin)
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14
Q

How does the body respond to hypercalcemia acutely and chronically?

A
  • Acute - parathyroids sense inc Ca –> no PTH –> dec Ca reabsorption in kidneys ands dec bone resorption
  • Chronic - body adapts by re-coupling bone resorption and formation; fall in 1,25 Vit D –> dec absorption in gut and still excreting more Ca in urine
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15
Q

Hypercalcemia Signs and Symptoms

A

(all related to inc depolarization threshold across cell - dec response to chemical and neural stimuli)

  • Neuro - fatigue, obtunded, comatose (influenced by rate of onset, age, baseline mental status)
  • Renal - polyuria and inc thirst/dehydration; Ca inhibits water reabsorption by osmotic diuresis; Ca inhibits ADH effect on distal nephron –> nephrogenic DI + Ca-phos deposits in interstitium or Ca stones
  • Cardio - Shorter Q-T intervals, Ca-phos deposits in conduction system, vasoconstrict in response to diuresis
  • MSK - weakness b/c dec contractility
  • GI - constipation, ileus (hypoactive smooth muscle), deposits in pancreas –> pancreatitis
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16
Q

2 Types of Malignancy Related Hypercalcemia (+ tx of both)

A

1- Secretion of PTHrP –> “humoral hypercalcemia of malignancy”

- PTHrP is similar to PTH - causes some inc in phosphorous excretion and inc Ca reabsorption in kidney
- But does not stimulate 1,25 Vit D
- Inc resorption --> inc Ca and phosphorpous in serum but PTHrP causes inc phos excretion --> low or normal serum phos

2- Skeletal mets –> cytokine mediated osteoclast bone destruction
- NO bone formation (all resorption), high or normal serum phosphate (b/c no PTHrP to inc phosphorous excretion when there is inc serum phosphorous from bone breakdown)

  • Tx - treat underlying malignancy; acute bisphosphonates; IV fluids
17
Q

Sarcoidosis

A
  • Granulomas have macrophages –> make 1,25 Vit D –> hyper-absorption of Ca in gut
  • Lab Patterns
    • Dec PTH in response, inc Ca excretion (kidney overwhelmed even though inc Ca reabsorption)
  • Tx - GCs (steroids inhibit macrophages)
18
Q

Milk Alkali Syndrome

A
  • Cause - consumption of large amount of Ca (4,000 to 20,000 a day)
  • Passive absorption of Ca overwhelms defense mechanisms against hypercalcemia (kidney cannot clear)
  • Lab Patterns
    • Absorb much more, PTH down-reg to compensate –> dec 1,25 Vit D, bone not affected, high urinary Ca as you try to get rid of it
19
Q

Types of Familial Hypercalcemia

A
  • FHH - most common
  • MEN1, MEN2A
  • Hyper-parathyroidism-Jaw Tumor Syndrome
  • Familial Isolated Primary Hyperparathyroidism

ALL AUTO DOM