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ABBEY MSII Unit 5 > Pharm: parathyroid and bone > Flashcards

Pharm: parathyroid and bone Flashcards

1
Q

what are the two types of bone

A

cortical (long bones) and trabecular (vertebral bodies, ribs, pelvis, end of long bones)

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2
Q

osteoclasts and osteoblasts

A

blasts build bone, clasts resporb

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3
Q

parathyroid hormone (PTH) secretion

A

secreted by 4 parathyroid glands - controlled by serum ionized calcium (when low, PTH stimulated)

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4
Q

actions of PTH

A

release Ca from bone, reabsorb Ca in kidneys, absorb Ca and PO4 in small intestine in order to maintain serum calcium levels

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5
Q

what are the 3 forms Ca circulates in?

A

ionized (50% - active form), protein bound calcium (albumin), complexed to bicarb, citrate, phos

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6
Q

what are phosphorus levels influenced by?

A

PTH and 1,25 (OH)2D

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7
Q

phosphorus reabsorption increased by

A

phosphate depletion, hypoparathyroidism, hypocalcemia

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8
Q

phosphorus excretion increased by

A

increased PTH, PTH4P, hypercalcemia, hypokalemia, hypomagnesemia, calcitonin, glucocorticoids and diuretics

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9
Q

magnesium and PTH

A

necessary for the release of PTH and for the action of the hormone of its target tissues

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10
Q

vitamin D active form

A

begins as biologically inert- needs 2 hydroxylations in the liver and kidney to become 25 (OH)D then active 1,25 (OH)2 D

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11
Q

what is the main effect of vitamin D

A

maintain normal serum calcium level by increasing intestinal absorption of dietary calcium and stimulating bone cells to become osteoclasts

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12
Q

what is renal production of 1,25 (OH)2D regulated by?

A

calcium levels through PTH and phosphorus

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13
Q

MCC hypercalcemia

A

hyperparathyroidism (primary - PTH is high or normal) or malignancy
also: FHH (familial hypocalcemic hypercalcemia), milk alkali syndrome, granulomatous diseases (by hydroxylation to make active vit D), medications (thiazides and lithium)

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14
Q

what is primary hyperparathyroidism caused by?

A

benign solitary adenoma 80%

4 gland hyperplasia

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15
Q

how is primary hyperparathyroidism diagnosed?

A

elevated calcium, elevated or normal PTH, low phosphorus, elevated urine calcium

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16
Q

what are signs and symptoms of primary hyperparathyroidism?

A

MOANS, GROANS, BONES, STONES, PSYCHIATRIC OVERTONES
CNS symptoms (lethargy, drowsiness, depression, confusion, coma)
neuromuscular (muscle weakness, hyporeflexia)
GI (nausea, vomiting, anorexia, constipation,)
renal (polyuria, polydipsia, impaired renal function)
cardiovascular (HTN, short QT, bradycardia)

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17
Q

treatment of hyperparathyroidism

A

cured when abnormal tissue is removed

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18
Q

what does PTH target?

A

cortical bone

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19
Q

when is primary hyperparathyroidism in the differential?

A

calcium greater than 1.0 mg/dL, creatinine clearance less than 60, age less than 50

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20
Q

medical treatment of primary hyperparathyroidism

A
  • adequate hydration and ambulation
  • moderate calcium intake (protect bones)
  • bisphosphonates (treat low bone density)
  • calcimimetics (reduce PTH and serum calcium levels by providing negative feedback)
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21
Q

treatment of hypercalcemia

A

mild (calcium less than 12) - may be asymptomatic, increase fluid intake and moderate calcium diet
moderate (12-14) intervention
severe (greater than 14) immediate treatment, poor prognosis if from malignancy

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22
Q

fluids for treatment of hypercalcemia

A

IV saline 4-6L
careful use of a loop diuretic (makes you lose Ca2+ - others don’t push out calcium) after adequate replacement to increase urinary calcium excretion and prevent volume overload

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23
Q

bisphosphonates for treatment of hypercalcemia

A

inhibit bone resportion (IV)

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24
Q

calcitonin for treatment of hypercalcemia

A

rapid effect of lowering calcium - increases urinary calcium excretion, inhibits bone resportion
-only good for acute setting (SC or IM)

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25
Q

corticosteroids for treatment of hypercalcemia

A

used in vitamin D intoxication, granulomatous diseases, and hematologic malignancies - decreases production of 1,25(OH)2D

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26
Q

dialysis for treatment of hypercalcemia

A

for those with renal failure or no response to other measures

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27
Q

secondary hyperparathyroidism

A

PTH secreted in response to a perceived low calcium concentration

28
Q

what stimulates PTH secretion in secondary hyperparathyroidism?

A
  1. renal disease: phosphate retention and lack of 1-alpha hydroxylase activity in failing kidney resulting in deficient 1,25(OH)2D
  2. at high concentrations, phosphorus directly stimulates PTH secretion
  3. Vit D deficiency
29
Q

how to treat secondary hyperparathyroidism as a result of vit D deficiency

A

replace with ergo or cholecalciferol

30
Q

how to treat secondary hyperparathyroidism as a result of renal disease

A

low phosphate diet, phosphate binders, replacement with 1,25 vit D and dialysis

31
Q

tertiary hyperparathyroidism

A

as a result of the parathyroid glands becoming autonomous after prolonged secondary hyperparathyroidism

32
Q

how does tertiary hyperparathyroidism different from secondary?

A

problem lies in the gland oversecreting (like primary)

unlike secondary, serum calcium is elevated (low or normal in secondary)

33
Q

hypocalcemia

A

parathyroid glands secrete PTH in relation to the serum calcium

  • hypocalcemic disorders can arise from destruction or failure of the parathyroid glands or inactivity of PTH at target tissues
  • categorized based upon low or elevated PTH levels
34
Q

signs and symptoms of hypocalcemia

A 
neuromuscular irritability (paresthesias, spasms)
CNS (seizures, electroencephalographic abnormalities, increased intracranial pressure)
cardiovascular (prolonged QT, heart block, CHF)
abnormalities of teeth, fingernails, skin, hair
35
Q

causes of hypocalcemia

A

hypoparathyroidism, parathyroid hormone resistance, vit D deficiency, vit d resistance, chronic renal failure, hyperphophatemia, antiresorptive agents, osteoblastic metastases, acute pancreatitis

36
Q

labs for hypocalcemia

A

check albumin (see if calcium may actually be normal
magnesium
phosphorus levels (high in chronic renal failure)
creatinine (high in chronic renal failure)

37
Q

MCC hypocalcemia

A

chronic renal failure - limited excretion of phosphorus and diminished hydroxylation of 1,25 vit D causes decreased calcium absorption from the cut and decreased mobilization from the bone causes PTH secretion

38
Q

treatment of secondary hyperparathyroidism from CRD (chronic renal disease)

A
  1. calcitriol or other vit D analogs (paracalcitol or doxercalciferol) (oral daily or IV several tiems a week)
  2. phosphate binders to reduce phosphorus levels (calcium carbonate, calcium acetate, sevelamer)
  3. calcimimetics (cinacalcet)
39
Q

hypoparathyroidism

A

clinical disorder when PTH produced is insufficient to maintain serum calcium levels or is unable to function properly at target tissues
-low calcium, elevated phosphorus, low PTH

40
Q

25-hydroxyvitamin D as a pharmacologic agent: when used and what are teh drugs?

A

used in vit. d deficiency (low calcium and phosphorus, high PTH, low urine calcium)
drugs: cholecalciferol (D3) and ergocalciferol (D2)

41
Q

which is more efficacious: cholecalciferol or ergocalciferol

A

cholecalciferol (D3)

42
Q

treatment of acute hypocalcemia

A

calcium gluconate IV - may need vit D orally if it persists

43
Q

hypophosphatemia treatment

A

usualyl a genetic disorder - treat by replacing phosphorus and calcitriol

44
Q

treatment for osteoporosis

A
  1. bisphosphonates to reduce osteoclast bone resportion with an increase in BMD and decrease in fracture risk
    include: alendronate, risedronate, ibandronate (DRONATES)
  2. SERMS (selective estrogen receptor modulators)
    include: raloxifene
  3. calcitonin (inhibits osteoclast resorption)
  4. teriparatide (PTH analog)
  5. denosumab (RANK ligand inhibitor - antiresorptive)
45
Q

side effects of bisphosphonates (DRONATES)

A

local GI irritation at the esophagus (need to be taken fasting in the morning) - burns holes in esophagus - need to sit up after taking

46
Q

zoledronate and boniva

A

IV bisphosphonates given once a year (zoledronate) or every 3 months (boniva) - bypass GI tract

47
Q

raloxifene

A

SERMs (used for osteoporosis and also breast cancer treatment)

48
Q

alendronate, risdronate, ibandronate

A

bisphosphonates

49
Q

why is calcitonin (salmon calcitonin) no longer recommended for use in osteoporosis?

A

cancer concerns

50
Q

teriparatide

A

anabolic agent (building bone) for osteoporsis - PTH analog

  • must be given in short bursts because blasts stimulate clasts - if short, clasts aren’t activated
  • reserved for patients at high risk of fracture because of black box warning of osteosarcoma
51
Q

bisphosphonates

A

reduce osteoclast bone resportion with an increase in BMD and decrease in fracture risk

52
Q

denosumab

A

RANK ligand inhibitor (prevents differentiation of osteoclasts) - antiresorptive
-can be given at any GFR

53
Q

side effects of denosumab

A

very well tolerated - skin infectiosn and hypocalcemia

54
Q

paget’s disease of bone

A

localized disorder of bone remodeling - increase in osteoclast mediated bone resorption and in bone formation causing disorganized bone at one or more sites
complications include hearing loss, fractures, increased risk of leeding, osteosarcoma

55
Q

treatment of paget’s disease

A
  1. bisphosphonates (decrease osteoclasts and impair mineralization of new bone)
    includes pamidronate (3 hours), alendronate, risedronate
  2. calcitonin
56
Q

osteogenesis imperfecta

A

heritable disorder of type I collagen

-causes osteopenia, recurrent fractures, skeletal deformity, blue sclera

57
Q

treatment of osteogenesis imperfecta

A

orthopedic, rehabilitative, dental interventions

-bisphosphonate therapy to prevent fracture

58
Q

what is the function of calcitonin and where is it made

A

decrease serum calcium levels - made by C cells in the thyroid
*increases phosphate excretion like PTH (everything else is opposite PTH)

59
Q

what is responsible for causing the compressive strength of bone? tensile strength?

A

compressive strength: hydroxyapatite (Ca, Ph, OH)

tensile strength: type I collagen

60
Q

what enzyme makes active vit D?

A

1 alpha hydroxylase

61
Q

what is PTH effect on phosphate?

A

increase excretion

62
Q

where is phosphate reabsorbed?

A

proximal tubule

63
Q

which malignancies cause PTHrP to raise calcium levels?

A
  1. squamous cell carcinoma of the lung
  2. renal cell carcinoma
  3. breast adenoma
    - PTH levels are low/undetectable because PTHrP is not being measured and this is what is inducing the hypercalcemia
64
Q

what is an example of a calcimimetic?

65
Q

phosphate binders mechanism

A

binds to free phosphate so that phosphate does not cause release of PTH and does not bind to calcium

66
Q

labs for hypocalcemia due to chronic renal failure

A

phosphorus, PTH, and creatinine levels are high becuase the kidney normall excretes phosphorous and creatinine

67
Q

side effects of SERMs

A

increased risk of endometrial cancer (estrogen decreases osteoclast activity though yay!)

ABBEY MSII Unit 5 (8 decks)

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