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Pharmacology: year 3 > Bone and Mineral Health > Flashcards

Bone and Mineral Health Flashcards

1
Q

the site of new bone growth?

A

epiphyseal plate

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2
Q

function fo osteoblasts

A

build bone

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3
Q

function of osteoclasts

A

break down bone

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4
Q

as we age what happens to our bone mass?

A

after the ages of 35-60 we lose 0.5-1% of bone per year

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5
Q

Why is Ca2+ necessary?

A

for muscle contraction(heart), for cell signaling, bone support

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6
Q

Where do we get Ca2+ from?

A

diet and bone

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7
Q

what happens if the plasma doesn’t have enough Ca2+ in it?

A

it will absorb from bone

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8
Q

what is necessary for bone absorption?

A

Vitamin D

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9
Q

What are the forms of vitamine D, what is the one usually refereed to?

A

D2 - dietary vitamin D
D3 - sunlight vitamin D

D3

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10
Q

what process do the kidneys aid in?

A

converting calcifediol to calcitrol

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11
Q

what happens in kidney failure?

A

we need to take calcitrol as body can’t do the conversion itself

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12
Q

what are the 3 means that vitamin D increases plasma Ca2+

A
  1. mobilixing from bone
  2. reabsoprtion by kidnerys (less excreted in urine)
  3. absorption from intestines (through diet and supllments)
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13
Q

what does PTH do?

A

allow for the creation of calcitriol in the kidenys

  1. mobilization from bone
  2. promotes reabsorption from the kidneys
  3. stimulates ysnthesis of calcitriol
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14
Q

How do vitamin D and PTH interact?

A

a negative feedback loop in order to prevent too much blood in the bone

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15
Q

what is the role of calcitonin?

A

the opppsoite

decrease plasma calcium, decrease reabsorption in kidneys

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16
Q

what is osteoporposis?

A

when bone reabsorption exceed depoistion

so the osteoclasts break down bone and mobilize calcium to plasma

leading to low mineral density - and increasing fracture risk

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17
Q

what are some risk factors for osteoporosis?

A

older age, inadequate calcium intake, genetics, smoking, hormones

18
Q

what is the role of estrogen and osteoporosis?

A

estrogen is a protective factor

19
Q

what are some other diseases of bone growth and calcium metabolism?

A

Rickets

osteomalacia

Paget’s disease

hypoparathyroidism and hyperparathyroidism

20
Q

what hormones negatively effect bone growth? what’s happening?

A

Glucocorticosteroids (prednisone) - weaker bones

  • decrease calcium absorption, thus increasing PTH
  • decreased calcium absorption in kidneys
  • decreased osteoblast activity
  • increased osteoclast activity
21
Q

what hormone positively impacts bone growth? how?

A

gonadal steroids (testosterone) - stronger bones

  • decreased osteoclast activity, increasing osteoclast apoptosis, decreased osteoblast apoptosis
21
Q

What are the three kinds of calcium supplements?

A

Calcium gluconate (IV), calcium carbonate (PO), calcium citrate (PO)

22
Q

what are calcium supplements used to treat?

A

osteoporosis, hypoparathyroidism, elctrolyte imbalances

23
Q

what is the MOA of calcium supllments?

A

increase bone and minaeral density/ strenth

24
what are the SE of calcium supp?
GI disturbances (carbonte cause more constipation then citrate), kidney stones
25
what is impoartnte to know about doisng calcium supp?
only 500 mg of elemntal calcium can be absorbed at once (so per dose)
26
what are vitamin D supps used to treat?
osteoporosis, hypoparathyroidism, rickets/osteomalacia
27
what is a common vit D supp that requires a prescription?
calcitriol ( reserved for those in kidney failure)
28
what is the MOA of vit D supps?
they increase intestinal calcium absorption
29
what are the SE of vit D supps?
usually none can cause hypercalcemia
30
What is the main drug class used to treat osteoporosis?
bisphosphates
31
MOA of bisphosphates
they inhibit the mevalonate pathway whihc leads to osteoclast apoptosis
32
what are typical and extreme side effects of bisphosphates?
nausea, vomiting, diarrhea, esophageal erosion atypical femoral fracture, osteonecrosis of the jaw
33
in femal patienst what drugs can be used for osteoporosis trement?
hormone replacement therapy (HRT) (estrogen + progesterone) selective estrogen receptor partial agonist/antagonist (raloxifene)
34
how does homone replacment therapy work/MOA and it's side effects
MOA - increase osteoclast apoptosis and increase osteoblasts lifespan side effects - increase risk of breat cancer, increased cardiovascular risk, breat tenderness, uterine bledding, venous thrombosis
35
how does selective estrogen receptor modulators (SERMs) therapy work/MOA and it's side effects
MOA- estrogen partial agonist and antagonist agonist in bone and CV tissue anatagonist in mammaliary tissue and uterine tissue. thus combats cancer risk increase sosteoclasts apoptosis and increase osteoblast activity SE- hot flashes and venous thrombosis
36
Denusomab MOA and SE
MOA- a monoclonal antibody that binds RANKL and inhibits osteoclasts development and reduces their function/survival SE - musculoskeletal pain, hypocalcemia, skin rxn
37
Teriparatide MOA and SE
PTH analog - injected once daily SC MOA - promotes bone anabolism (forming new bone), by reducing osteoclast activity and increasing osteoblast activity However, remember that PTH increases bone breakdown (catabolism) so apparently intermittent exposure to PTH actually increases osteoblast activity and more then osteoclast thus one daily injection lead to bone growth SE- hypotension, hypercalcemia, musculoskeletal pain
38
What is calcitonin used to treat?
osteoporosis, pagets and hypercalcemia
39
Calcitonin MOA and SE
calcitonin decreases bone reabsorption by decreasing osteoclast activity so there is less plasma Ca2+ SE- facial flushing, NVD

Pharmacology: year 3 (5 decks)

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