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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
corticosteroids for treatment of hypercalcemia
used in vitamin D intoxication, granulomatous diseases, and hematologic malignancies - decreases production of 1,25(OH)2D
26
dialysis for treatment of hypercalcemia
for those with renal failure or no response to other measures
27
secondary hyperparathyroidism
PTH secreted in response to a perceived low calcium concentration
28
what stimulates PTH secretion in secondary hyperparathyroidism?
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
how to treat secondary hyperparathyroidism as a result of vit D deficiency
replace with ergo or cholecalciferol
30
how to treat secondary hyperparathyroidism as a result of renal disease
low phosphate diet, phosphate binders, replacement with 1,25 vit D and dialysis
31
tertiary hyperparathyroidism
as a result of the parathyroid glands becoming autonomous after prolonged secondary hyperparathyroidism
32
how does tertiary hyperparathyroidism different from secondary?
problem lies in the gland oversecreting (like primary) | unlike secondary, serum calcium is elevated (low or normal in secondary)
33
hypocalcemia
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
signs and symptoms of hypocalcemia
``` neuromuscular irritability (paresthesias, spasms) CNS (seizures, electroencephalographic abnormalities, increased intracranial pressure) cardiovascular (prolonged QT, heart block, CHF) abnormalities of teeth, fingernails, skin, hair ```
35
causes of hypocalcemia
hypoparathyroidism, parathyroid hormone resistance, vit D deficiency, vit d resistance, chronic renal failure, hyperphophatemia, antiresorptive agents, osteoblastic metastases, acute pancreatitis
36
labs for hypocalcemia
check albumin (see if calcium may actually be normal magnesium phosphorus levels (high in chronic renal failure) creatinine (high in chronic renal failure)
37
MCC hypocalcemia
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
treatment of secondary hyperparathyroidism from CRD (chronic renal disease)
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
hypoparathyroidism
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
25-hydroxyvitamin D as a pharmacologic agent: when used and what are teh drugs?
used in vit. d deficiency (low calcium and phosphorus, high PTH, low urine calcium) drugs: cholecalciferol (D3) and ergocalciferol (D2)
41
which is more efficacious: cholecalciferol or ergocalciferol
cholecalciferol (D3)
42
treatment of acute hypocalcemia
calcium gluconate IV - may need vit D orally if it persists
43
hypophosphatemia treatment
usualyl a genetic disorder - treat by replacing phosphorus and calcitriol
44
treatment for osteoporosis
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
side effects of bisphosphonates (DRONATES)
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
zoledronate and boniva
IV bisphosphonates given once a year (zoledronate) or every 3 months (boniva) - bypass GI tract
47
raloxifene
SERMs (used for osteoporosis and also breast cancer treatment)
48
alendronate, risdronate, ibandronate
bisphosphonates
49
why is calcitonin (salmon calcitonin) no longer recommended for use in osteoporosis?
cancer concerns
50
teriparatide
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
bisphosphonates
reduce osteoclast bone resportion with an increase in BMD and decrease in fracture risk
52
denosumab
RANK ligand inhibitor (prevents differentiation of osteoclasts) - antiresorptive -can be given at any GFR
53
side effects of denosumab
very well tolerated - skin infectiosn and hypocalcemia
54
paget's disease of bone
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
treatment of paget's disease
1. bisphosphonates (decrease osteoclasts and impair mineralization of new bone) includes pamidronate (3 hours), alendronate, risedronate 2. calcitonin
56
osteogenesis imperfecta
heritable disorder of type I collagen | -causes osteopenia, recurrent fractures, skeletal deformity, blue sclera
57
treatment of osteogenesis imperfecta
orthopedic, rehabilitative, dental interventions | -bisphosphonate therapy to prevent fracture
58
what is the function of calcitonin and where is it made
decrease serum calcium levels - made by C cells in the thyroid *increases phosphate excretion like PTH (everything else is opposite PTH)
59
what is responsible for causing the compressive strength of bone? tensile strength?
compressive strength: hydroxyapatite (Ca, Ph, OH) | tensile strength: type I collagen
60
what enzyme makes active vit D?
1 alpha hydroxylase
61
what is PTH effect on phosphate?
increase excretion
62
where is phosphate reabsorbed?
proximal tubule
63
which malignancies cause PTHrP to raise calcium levels?
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
what is an example of a calcimimetic?
sensipar
65
phosphate binders mechanism
binds to free phosphate so that phosphate does not cause release of PTH and does not bind to calcium
66
labs for hypocalcemia due to chronic renal failure
phosphorus, PTH, and creatinine levels are high becuase the kidney normall excretes phosphorous and creatinine
67
side effects of SERMs
increased risk of endometrial cancer (estrogen decreases osteoclast activity though yay!)

ABBEY MSII Unit 5 (8 decks)

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