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pharm unit 5 > parathyroid > Flashcards

parathyroid Flashcards

1
Q

how much of the skeleton is cortical bone?

A

80%

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2
Q

where is cortical bone found?

A

int he shafts of long bone

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3
Q

what does cortical bone provide us with?

A

mechanical support and protective functions for the hematopoietic system.

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4
Q

where is trabecular bone

A

at the ends of long bones, ribs, vertebral bodies, pelvic.

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5
Q

what does trabecular bone do?

A

serves the metabolic functions of the skeleton.

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6
Q

where do osteoblasts come from? what do they do?

A

mesenchymal system. bone forming cell. responsible for making osteoid and its subsequent mineralization

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7
Q

where do clasts come from and what do they do>

A

hematopoietic system and are a modified macro. they are responsible for break down.

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8
Q

osteocytes?

A

they are osteoblasts that have been caught in the mineralized matrix. play a role in mobilizing minerals.

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9
Q

OPG

A

osteoprotegerin. when expressed inhibits physiological and pathological breakdown of bone.

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10
Q

RANKL and RANK

A

involved in the osteoclastic activation

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11
Q

bone formation markers

A

alk phos and osteocalcin

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12
Q

bone breakdown markers

A

TRAP (serum), NTx/CTx (serum and urine)

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13
Q

What controls the release of PTH

A

serum calcium levels. when low PTH is secreted.

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14
Q

what does PTH do?

A

defends against hypocalcemia. stimulation of bone resorption by clasts. renal reabsorption of Ca and Mg. inhibition of reabsorption of Ph and Bicarb. stimulation of Vitamin D production.

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15
Q

is the activation of osteoclasts by PTH direct or indirect?

A

it is indirect, there is no PTH receptor on the clast. just on the blasts.

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16
Q

does PTH enhance the intestinal reabsorption of Ca2?

A

indirectly through activation of Vitamin D.

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17
Q

what percentage of calcium is ionized

A

50

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18
Q

what percentage of calcium is protein bound

A

40.

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19
Q

what percentage of ca is complexed

A

10

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20
Q

what effect does acidosis have on the calcium level?

A

increases it because it releases it from albumin binding.

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21
Q

what is the correction formula for calcium

A

Cca = Mca + 0.8 (4 - Malb)

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22
Q

where is ca absorbed

A

in the intestines, duodenum and jejunum.

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23
Q

what is the main determinant of intestinal absorption

A

activated Vitamin D

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24
Q

what affects the absorption of Ca

A

ceoliac, bypass, malabsorption, low Vit D.

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25
Q

where are the main sources of ca loss?

A

urine and feces.

26
Q

what enhances reabsorption of ca in the kidney

A

PTH, PRPrP, alkalosis, thiazides, reabsorption of sodium

27
Q

what decreases the reabsorption of Ca

A

acidosis, loops, saline diuresis and low PTH

28
Q

what increases the retention of phos

A

low PTH/hypoPT, low calcium. hypophos

29
Q

who gets dietary phosphate deficiency?

A

RARE. alcoholics, and people taking large amounts of aluminum containing antacids.

30
Q

where do we get Mg from

A

green vegetables and meats. 40% is absorbed from the intestine.

31
Q

what can cause hypoMg

A

loop diuretics and cisplatin.

32
Q

what are the most common causes of hypercalcemia

A

hyperparaT, or malignancy.

33
Q

what is the first step in a calcium workup?

A

PTH levels.

34
Q

what is the most common source of hyerPTH

A

solitary adenoma 80%

35
Q

how common is parathyroid carcinoma

A

extremely rare.

36
Q

what is the most common presentation of hypercalcemia when looking at Ca and PTH

A

low PTH, high calcium

37
Q

what is suggestive of familial hypocalciuric hypercalcemia

A

when the calcium clearance is less than 0.01.

38
Q

what is the causes of FHH

A

lack of the calcium sensor function

39
Q

what is milk alkali syndrome

A

consumption of large amounts of ca in the context of an alkali substance -TUMS.

40
Q

treatment for mild hyperCa

A

advise patient to increase fluid intake and moderate Ca diet. discontinue meds that cause high ca

41
Q

treatment for moderate hyperCa.

A

often requires direct measures to lower the calcium in the blood stream.

42
Q

what medications cause retention of calcium

A

thiazides and lithium.

43
Q

treatment for severe hyperCa

A

needs immediate treat. FLUIDS. bisphosphonates, calcitonin, corticosteroids, and dialysis

44
Q

why give fluids in severe hyper Ca

A

because hypercal causes dehydration. loops can be given to increase the calcium excretion. must be careful though.

45
Q

what is the corner stone treatment?

A

bisphosphonates. bind calcium immediately lowering the levels in most patients. this is the mainstay treatment.

46
Q

what does calcitonin do for hypercalcemia

A

mild, yet rapid effect for lowering the serum calcium. increases the renal excretion.

47
Q

what is the downfall of calcitonin

A

within 2-3 days there is down regulation and tachyphalaxis

48
Q

how do corticosteroids work for hyperCa and which diseases do they work the best on?

A

they will decrease the production of VIT D. work best in vitamin D intox, granulomatous and malignancy.

49
Q

what are the common causes of hypoPT

A

agenesis, surgical destruction, altered production of PTH, pseudohypoPT.

50
Q

what is low vitamin D classically associated with?

A

osteomalacia and rickets.

51
Q

how does low vitamin D present

A

hypocalcemia and hypophosphatemia.

52
Q

osteoporosis?

A

caused by increases in the rate of bone remodeling with more osteoclastic activity than osteoblastic. increase in the bone fragility and increase risk of fractures.

53
Q

bisphosphonates

A

reduce osteoclastic bone resorption. increase bone mineral density and decrease bone turnover markers. they also reduce fracture risk.

54
Q

side effects of bisphosphonates

A

GI irritation and esophageal.

55
Q

SERMs

A

estrogen like compounds that decrease bone resorption.

56
Q

SERMs side effects

A

hot flashes and DVT

57
Q

calcitonin

A

unique effect on the vertebral fractures as an analgesic. given through the nostrils as an inhalant. inhibits osteoclast resorption.

58
Q

side effects of calcitonin

A

rhinitis. minimal

59
Q

triparatide

A

PTH analog. unique anabolic agent. given in short subcutaneous bursts has the ability to only activate blasts and increase BMD and decrease fractures. only given as alternative. only the first part of the molecule.

60
Q

side effects of triparatide

A

transient hyperCa. also has a black box warning for osteosarcoma.

61
Q

denosumab

A

antibody that works as a RANK ligand inhibitor. antiresorptive agent that works on osteoclasts.

62
Q

pagets disease

A

increased alk phos with a increased bone metabolism. results in enlarged bone. presents as localized bone pain. initiated by osteoclast bone reposition and then a compensatory bone formation resulting in a disorganized mosaic. look to the pelvis, spine, femur, tibia, skull. formation and resorption markers are typically elevated. bone deformation, pain, hearing loss, fractures, osteosarcoma.

pharm unit 5 (12 decks)

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