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Examen

NUSCTX 10 MIDTERM 3 EXAM QUESTIONS WITH COMPLETE ANSWERS

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NUSCTX 10 MIDTERM 3 EXAM QUESTIONS WITH COMPLETE ANSWERS

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NUSCTX 10 MIDTERM 3 EXAM
QUESTIONS WITH COMPLETE
ANSWERS
bone remodeling - ANSWER--bone mass is maintained by continual degradation of
existing bone and synthesis of new bone
-good bone structure is matrix formed
-this remodeling facilitates: adjustment to new strength of level, adjustment to new
shape, replacement of degrading matrix (collagen and proteoglycan) during normal
turnover

osteomalacia - ANSWER--disease marked by softening of the bone caused by
calcium and vitamin D deficiency
-organic bone matrix normal but not calcified
-matrix > calcium

key players in bone remodeling - ANSWER-1. osteoblasts: cells that produce
protocollagen and proteoglycans that constitute the "matrix" of bone (vitamin c
involved in pro collagen synthesis; they respond to changes via Vit D receptors)
2. osteocytes: osteoblasts that become entrapped in polymerizing collagen fibers
3. osteoclasts: act to degrade bone

*vitamin D involved in all

intestinal functions of calcitriol - ANSWER--primary role of VD is to maintain blood
calcium levels
-Calcitriol: hormone produced from Vitamin D3 is the only hormone that can induce
the intestine to absorb dietary Ca
-without VD and its conversion into calcitriol, dietary Ca ++ absorption by the
intestine is severely impaired

calcium absorption - ANSWER-1. High concentrations of calcium allow absorption by
passive diffusion
2. Low to moderate concentrations of calcium require active transport. Vitamin D
turns on the synthesis of calcium transport proteins
3. Calcium transport proteins shuttle calcium from the lumen across the mucosal cell
4. A calcium pump that requires energy moves calcium from the mucosal cells to the
bloodstream

parathyroid hormone (PTH) - ANSWER-A hormone of the parathyroid gland that
regulates the metabolism of calcium and phosphorus in the body
-PTH roles: helps with reabsorption of Ca by kidney, release of Ca from bone,
increases absorption of Ca from intestine
-PTH does not conserve P

,regulation of blood calcium levels and PTH increase of blood calcium - ANSWER-1a.
low blood calcium levels cause PTH and Vitamin D3 to mobilize calcium from the
bone
1b. PTH also: reduces calcium excretion by the kidneys and stimulates kidney
synthesis of Vitamin D3
1c. Vitamin D3 stimulates intestinal calcium absorption
2. high blood calcium levels cause increased synthesis of the hormone calcitonin
which promotes calcium deposits in bones to help blood calcium levels return to
normal

regulation of blood calcium levels with Calcitonon - ANSWER--high blood calcium
causes the release of calcitonin from the thyroid gland: calcitonin inhibits calcium
release from bone and PTH stimulates calcium release from bone
-low blood calcium causes the release of PTH from the parathyroid gland: PTH
promotes calcium reabsorption by the kidney, PTH stimulates the activation of
vitamin D by the kidney, and active vitamin D increases intestinal calcium
reabsorption

Calcitonin moderates effects of PTH - ANSWER--Calcitonin is secreted by the
thyroid gland when plasma and Ca are high
-calcitonin reduces plasma Ca by: reducing osteolytic activity, reducing formation of
new osteoclasts, and increasing osteoblast activity

calcium balance - ANSWER-1. The intestines increase absorption of calcium from
the intestine.
2. The kidneys prevent its loss in the urine (some lost in sweat)
3. The bones release more calcium into the blood.

VD toxicity - ANSWER--megadoses through supplementation
-hypercalcemia: elevated blood calcium concentrations that can lead to calcification
of tissues (kidney stones)
-plasma Ca is the mediator for muscle contraction, neurotransmission and blood
clotting which effects bone structure
-hypocalcemia --> tetany --> death --> soft-tissue Ca --> hypocalcemia

functions of phosphorus - ANSWER--bone mineralization
-energy transfer (ATP, ADP, GTP)
-phospholipids
*85% of body phosphate is in bone, 1% in plasma

Sources of plasma calcium and phosphorus - ANSWER-- Ca from food: dairy
products, tofu, green leafy vegetables
-Ca from P: ubiquitous (don't need to take supplements), deficient only if low energy
and protein intakes
-adults need: 1g/day of each
-bone modeling: important source for both

Vitamin E forms - ANSWER--Antioxidant that protects cell membranes from free
radical oxidation
-8 compounds

, -Dietary sources: plant oils and nuts

VE deficiency - ANSWER-- Deficiency is rare, can occur in diseases of fat
malabsorption and premature infants
- Hemolytic anemia: too few red blood cells
because the membranes rupture
- Neuromuscular dysfunction

Vitamin K forms - ANSWER--necessary for blood clotting and bone formation
-synthesized by gut bacteria
-dietary sources: green vegetables and plant oils

the role of VA in vision - ANSWER--Helps maintain cornea (retinoic acid)
-Involved in conversion to light energy into nerve impulses in the rod cells of the
retina (retinal)

VA deficiency - ANSWER-- Occurs when in sufficient VA intake or protein deficiency
- Night blindness
- Increased mortality from infectious disease
- Xerophthalmia
- Keritinization

*consuming the right amount of Vitamin A is crucial

VA toxicity - ANSWER-- Occurs when VA is in excess of binding proteins and
damages cells
- Retinoid supplements are typically 750-1500 μg and many foods are fortified
- Increased bone fractures and osteoporosis
- Birth defects
- Excess β-carotene can lead to skin discoloration but is not toxic

Roles of VD in the body - ANSWER-- The active form of VD is a hormone, which
regulates gene transcription
- Maintains blood concentrations of calcium and phosphorous
- Regulates cell proliferation and differentiation
- Immune function

Factors affecting VD synthesis in the body - ANSWER--latitude
-season
-time of day
-skin pigmentation
-sun exposure
-sunscreen use

vitamin D forms - ANSWER--body can synthesize from cholesterol and UV light
-VD2 (ergocalciferol) in plant sources and supplements
-VD3 (cholecalciferol) in animal source foods and human body
-VD2 is less biologically active than VD3
-VD-binding-protein required for transport in blood

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31 de marzo de 2025
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