Bones Flashcards
what is the role of vitamin D in the body?
vitamine D aids in calcium absorption in the gut
What is the most immediate effect of PTH on calcium homeostasis?
A. Decrease bone formation
B. Increase phosphate excretion in kidneys
C. decrease calcium excretion in urine
D. Promote intestinal calcium absorption
B and C
Rationale: The fastest action of PTH is in the kidneys, where it increases calcium reabsorption and decreases phosphate reabsorption (Slide 10).
KNOW PTH is released in response to low calcium
Why does PTH increase bone resorption, and why does calcitonin decrease it?
A.
PTH increases bone resorption by directly stimulating osteoblasts,
Calcitonin decreases it by suppressing vitamin D activation.
B.
PTH increases bone resorption by enhancing RANKL expression on osteoblasts,
Calcitonin decreases it by inhibiting osteoclast attachment via G-protein coupled receptors.
C.
PTH increases bone resorption by increasing calcium absorption in the gut,
Calcitonin decreases it by promoting osteoblast differentiation.
D.
PTH increases bone resorption by reducing phosphate levels,
Calcitonin decreases it by activating osteoblast calcium uptake.
Answer: B
Rationale:
PTH acts indirectly by increasing RANKL expression on osteoblasts, which binds to RANK on osteoclast precursors, stimulating their differentiation and activity → increased bone resorption (Slide 7, 10).
Calcitonin binds to GPCRs on osteoclasts, leading to their detachment from bone and reduced activity → decreased bone resorption (Slide 35).
what does bone homeostasis depend on?
osteoclasts (bone reabsorption) and osteoblasts (bone building, anabolic)
recall that the bones are in a cocnstant state of being remodellef to maintain structure and function
What is the primary role of RANKL in bone remodeling?
A. Promotes osteoblast proliferation
B. Inhibits osteoclast differentiation
C. Stimulates osteoclast differentiation and activity
D. Inhibits calcium and phosphate resorption from bone
C
Rationale: RANKL is secreted by osteoblasts and binds to RANK on osteoclast precursors, promoting differentiation and bone resorption (Slide 7).
whatis the effect of osteoblasts binding to RANK?
binding stimulates osteoclasts differentiation, bone reabsorption and the release of Calcium adn phosphorus into the serum (bc osteoclasts absrob bones)
What effect does calcitonin have on bone metabolism?
A. Increases osteoblast activity
B. Promotes calcium absorption in the gut
C. Inhibits osteoclast-mediated bone resorption
D. Enhances PTH secretion
Inhibits osteoclast-mediated bone resorption
Calcitonin acts on osteoclasts to reduce bone resorption (Slide 5, 35).
Why is calcitonin administered via nasal spray or injection?
A. It acts locally on nasal receptors
B. It is deactivated in the liver
C. It is not absorbed orally
D. It requires parenteral activation
Calcitonin is a peptide and not absorbed via the GI tract, so it’s given nasally or parenterally (Slide 35).
Which of the following best describes the negative feedback relationship between calcium and parathyroid hormone (PTH)?
A.
Low serum calcium suppresses PTH secretion through inhibition of the parathyroid gland.
B.
High serum calcium stimulates PTH secretion to promote calcium reabsorption.
C.
High serum calcium inhibits PTH secretion, reducing calcium release from bone.
D.
Low serum calcium increases calcitonin, which then suppresses PTH secretion.
Answer: C
Rationale:
When serum calcium levels are high, this provides negative feedback to the parathyroid glands, inhibiting PTH secretion. This reduces bone resorption and stabilizes serum calcium (Slide 9, 14).
Which form of vitamin D is considered biologically active?
A. Cholecalciferol
B. Ergocalciferol
C. 25-hydroxyvitamin D
D. 1,25-dihydroxyvitamin D
D
Rationale: 1,25-dihydroxyvitamin D (calcitriol) is the active form, produced in the kidneys (Slide 13).
when a person is exposed to sunlight (ultraviolet B), what are the following forms of vitamin D that form? list the correct sequence in order:
previtamin D (cholececalciferol-D3), 7-dehydrocholesterol,
7 dehydro, then previtamin D
How do 25-hydroxy-vitamin D [25(OH)D] and calcitriol [1,25-dihydroxy D] differ in their roles and activation pathways?
A.
25(OH)D is the active form synthesized in the kidney,
while 1,25(OH)₂D is the storage form produced in the liver.
B.
25(OH)D is the inactive precursor made in the skin,
while 1,25(OH)₂D is the active form converted in the gut.
C.
25(OH)D is the major circulating storage form synthesized in the liver,
while 1,25(OH)₂D (calcitriol) is the biologically active form generated in the kidney.
D.
25(OH)D is the bone-resorbing form that increases PTH release,
while 1,25(OH)₂D suppresses calcium absorption from the gut.
Answer: C
Rationale:
25(OH)D is the main circulating and storage form, synthesized in the liver (Slide 13).
1,25(OH)₂D (calcitriol) is the biologically active form, generated in the kidney via 1α-hydroxylase, and enhances intestinal calcium absorption (Slides 13–14).
How are vitamin D and calcium levels in the blood physiologically connected?
A.
Vitamin D increases phosphate excretion, which leads to a decrease in calcium absorption.
B.
Vitamin D inhibits parathyroid hormone (PTH) release, preventing calcium from entering the bloodstream.
C.
Vitamin D promotes intestinal absorption of calcium, helping to raise and maintain blood calcium levels.
D.
Vitamin D stimulates osteoblast activity, which removes calcium from the blood to build bone.
Vitamin D promotes intestinal absorption of calcium, helping to raise and maintain blood calcium levels.
Vitamin D (specifically, calcitriol) enhances calcium absorption from the gut, helping to elevate and maintain serum calcium levels. This also contributes to a negative feedback loop that reduces PTH secretion once calcium is sufficient (Slide 14).
what is the role of 1α-hydroxylase?
it is an enzyme made by the kidney that activates vitamin D, and leads to increased calcium reabsorption in the gut
restored Ca2+ provides negative feedback to the parathyroid glands, discontinuing PTH
What defines hypercalcemia?
A. Serum calcium < 8.8 mg/dL
B. Serum calcium = 10.4 mg/dL
C. Serum calcium > 10.4 mg/dL
D. Serum calcium < 7.0 mg/dL
✅ Answer: C
Rationale: Hypercalcemia is defined as serum calcium >10.4 mg/dL (Slide 23).
recall that normal calcium levels are between 8.8 and 10.4mg/dL
Why are adequate calcium levels and optimal vitamin D concentrations essential for bone density and bone metabolism?
A.
They directly suppress osteoblast activity, allowing bones to harden properly.
B.
They stimulate calcitonin release, which increases bone resorption to strengthen bone.
C.
They promote calcium storage in fat tissue, reducing blood calcium fluctuations.
D.
They support bone mineralization and remodeling by ensuring calcium availability and absorption.
: D
Rationale:
Calcium is the key mineral for bone mineralization, and vitamin D ensures its absorption from the gut and availability in the blood. Both are essential for maintaining bone density and healthy remodeling processes (Slide 19).
Chvostek’s or Trousseau’s signs are linked what levels of calcoum concentration in the body?
linked to hypocalcemia
seizuresm cardiomyopathy, and congestive heart failure are linked to calcium ______. while muscle cramps, paresthesia and Chvostek’s or Trousseau’s signs are linked to ______
calcium defficiencies, clinical signs of hypocalcemia
Hypocalcemia can be categorized into PTH deficiency (hypoparathyroidism) and secondary hyperparathyroidism. How do they differ?
hypoPARAthyroidism causes low PTH levels
- due to destruction of the parathyroid glands or abnormal parathyroid development
- low PTH levels
secondary:
- relative to vitamin D deficiency
- increased PTH
Which of the following best describes the most common underlying mechanism leading to hypercalcemia?
A. Overproduction of vitamin D leading to increased calcium renal excretion and reduced bone resorption
B. Decreased parathyroid hormone secretion causing increased osteoblast activity and reduced plasma calcium
C. Excessive parathyroid hormone production or malignancy increasing bone resorption and serum calcium levels
D. Chronic calcium deficiency triggering compensatory calcium release from bone via calcitonin secretion
Excessive parathyroid hormone production or malignancy increasing bone resorption and serum calcium levels
due to excessive PTH production
According to the lecture, what is the main treatment approach for hypercalcemia?
A. Oral calcium supplements and vitamin D
B. Loop diuretics and calcitonin
C. Intravenous hydration and bisphosphonates
D. Parathyroid hormone and potassium supplements
Intravenous hydration and bisphosphonates
how do biphosphonates affect the bones?
it causes decreased bone reabsorption and reduced calcium levels
Osteoporosis primarily results from which of the following?
A. Enhanced osteoblast activity due to elevated calcium intake
B. Decreased bone resorption and increased bone formation
C. Imbalance favoring bone resorption over bone remodeling
D. Suppression of osteoclast activity through PTH overproduction
Osteoporosis arises from increased resorption relative to formation, leading to reduced skeletal mass.
Which of the following best explains how estrogen deficiency contributes to increased bone resorption in postmenopausal osteoporosis?
A. Estrogen deficiency increases calcium absorption, promoting osteoblast apoptosis and reducing bone density
B. Reduced estrogen suppresses IL-7, decreasing T-cell activation and inhibiting osteoclast activity
C. Estrogen deficiency increases IL-7, which activates T-cells to release IL-1, IL-6, and TNF-α, promoting osteoclast formation
D. Estrogen deficiency enhances calcitonin release, stimulating osteoblast function and decreasing bone resorption
C correctly describes the inflammatory pathway: Low estrogen → ↑ IL-7 → T-cell activation → ↑ IL-1, IL-6, TNF-α → osteoclast formation → bone resorption.
The other options contain misleading elements (like increased calcitonin or suppressed IL-7) that are not supported by the lecture content.
how does estrogen increase osteoclast formation?
low estrogen causes the increase of inflammatory factor, such as the rankl/rank signalling pathway (becomes activated). this leads to osteoclast formation
what is the role of biphosphonates?
a. anticatabolic/antiresortive therapy
b. anabolic thterapy
c. increase osteroclast formation
d. decreases osteoclast formation
they are an anticatabolic antiresortive therapy that decreases osteroclast fromation by binding with high affinity to the mineral matrix of the bone
how do biphosphonates, like alendronate, work when inhibitng osteoclast formation?
A. prevents the RANKL/RANK signalling pathway, which inhibit osteoclast formation
B. activate GPCR’s on osteroclasts, which reduces the number of osteoclasts attatched to the bones, increasing BMD
C. stimulates growth and formation of oteoblasts
D. oxygen in the the group have high affinity for Ca2+, inhibiting osteoclast reabsorption of the bone
oxygen in the the PHOSPHONATES have high affinity for Ca2+, inhibiting osteoclast reabsorption of the bone
*biphosphonates bind to bone before osteoclasts and when osteoclasts try o reabsorb the bone, they reabsorb the biphosphonates instead, which kills them
a- refers to Denosumab
b- is for calcitonin
c- is for Teriparatide
Denosumab and SERMS both affect the RANKL pathway in bone reabsorption, how do they differ?
A. Denosumab suppresses osteoblasts to reduce RANK production; SERMs bind to RANKL and directly prevent osteoclast maturation
B. Denosumab activates estrogen receptors on osteoclasts; SERMs block RANKL directly to prevent osteoclast differentiation
C. Denosumab increases calcitonin secretion to reduce RANKL activity; SERMs inhibit RANK signaling by acting as estrogen antagonists in bone
D. Denosumab directly binds RANKL to prevent its interaction with RANK; SERMs activate estrogen receptors to inhibit RANKL expression
Denosumab directly binds RANKL to prevent its interaction with RANK; leading to osteoclast differentiation and low function
SERMs have anticatalbolic effects that activate Era estrogen receptors to inhibit RANKL expression
D
a drug that binds to G-protin receptors on osteoclasts, which causes osteocast detatchement from the reabsorptive lacuna
a. biphodphonates
b. Denosumab
c. SERMS
d. calcitonin
e. Teriparatide
calcitonin is responsible for osteoclass deattatchment from the bone
a drug that stimulates bone growth and formation by increasinf osteoblast activity:
a. biphodphonates
b. Denosumab
c. SERMS
d. calcitonin
e. Teriparatide
Teriparatide
