MET EOYS9 Flashcards
Which of the following raises serum calcium levels if infection (for example of sarcoidosis or TB) occurs?
A
B
C
Which of the following raises serum calcium levels if infection (for example of sarcoidosis or TB) occurs?
A: macrophage
B: neutrophil
C: lymphocyte
The most important regulator of serum phosphate levels is
OPG
RANKL
FGF23
1,25(OH)D
The most important regulator of serum phosphate levels is
OPG
RANKL
FGF23
1,25(OH)D
What effect does increasing FGF23 have on:
Serum phosphate levels [1]
Phosphate excretion [1]
1a hydroxylase activity [1]
High FGF23:
* increase fractional phosphate excretion
* Reduce serum phosphate levels
* Reduce 1α-hydroxylase activity
Elevated FGF-23 levels increase fractional phosphate excretion, reduce serum phosphate levels, and reduce 1α-hydroxylase activity
which reduces 1,25(OH)₂D₃ formation thereby increasing parathyroid hormone (PTH) secretion
Which of the following secretes FGF-23
osteoblast
osteoclast
chondrocyte
osteocyte
Which of the following secretes FGF-23
osteoblast
osteoclast
chondrocyte
osteocyte
Explain what happens when have hypercalcemia and diabetes? [2]
Nephrogenic Diabetes Insipidus:
* Ca2+ binds to CaSR in nephrone, which down regulates NaKCL2 symporter
* Renal stones & Renal failure due to XS Ca2+ in urine
Primary hyperparathyroidism can lead to the development of
Osteomalacia
Osteoarthirtis
Osteoporosis
Osteosarcoma
Primary hyperparathyroidism can lead to the development of
Osteomalacia
Osteoarthirtis
Osteoporosis
Osteosarcoma
(PTH) removes calcium from bones (that is what it does), all patients with a parathyroid problem will eventually develop thin bones. Bones with osteoporosis due to parathyroid problems can ache and hurt because the PTH is actively destroying the bone. Bones with osteoporosis are fragile bones which are much more susceptible to fractures and breaks.
Parathyrodism diagnosis
Explain the mechanism of a MIBI scan [1]
The parathyroid scan uses the radioisotope, technetium-99m sestamibi (or MIBI), which is injected into the body and absorbed by the overactive parathyroid mitochondria.
State the vertebral levels for each of the following:
Iliohypogastric [1]
Ilioinguinal [1]
Genitofemoral [1]
Iliohypogastric: L1
Ilioinguinal: L1
Genitofemoral; L1 & L2
Which type of diuretic may be used to treat kidney stones?
Loop diuretics
Thiazide like diuretics
K sparing diuretics
Carbonic anhydrase inhibitors
Which type of diuretic may be used to treat kidney stones?
Loop diuretics
Thiazide like diuretics: cause hypercalcemia
K sparing diuretics
Carbonic anhydrase inhibitors
Explain the importance of Ca2+ in cardiac AP [1]
How does low
Calcium is involved in maintaining the plateau phase:
- Na in
- Ca out.
Extracellular Ca2+: blocks the voltage gated Na channels in the cardiac cell membrane.
Low Ca2+ levels: less blockade of VGNaCs = tachyarrhythmias
What is the effect of Ca2+ binding to Ca2+ sensing receptor on parathyroid? [3]
Ca2+ binds to Ca2+ sensing receptor on parathyroid. Causes:
* Reduces PTH secretion
* Increases breakdown of stored PTH in vesicles
* Suppresses transcription of PTH gene.
Why does PTH cause an increase in phosphate excretion?
Bone is broken down to release Ca2+, but also P is released
Therefore the kidney needs to excrete P to compensate
Which areas of nephron cause reabsorbtion of Ca2+ dependently / independently of PTH? [3]
PCT: independent
LoH: independent
DCT: PTH dependent
Explain how Ca2+ is reabsorbed at PCT [2]
At PCT:
- independent of PTH
- Driven by NaKCl2 channel causing a voltage gradient paracellularly which Ca2+ flows (coupled with Na+ reabsorbtion)
Explain how Ca2+ is reabsorbed at LoH [2]
Driven by voltage gradient: Para/transcellular
Coupled with Na+ reabsorbtion: NKCC2 channel
Why do thiazide diuretics raise serum calcium?
Increase Ca2+ reabsorbtion into the blood / raises Ca2+ serum levels:
- Blocks Na/Cl symporter on luminal side
- This drops the Na conc. In tubular cell
- This creates Na diffusion gradient
- Na diffusion increases from capillary into tubular
cell - across Na/Ca exchanger -> takes Na into cell and transports Ca2+ into blood. -> increase in blood Ca levels.
Effect of PTH on:
- NaPi transporters (and therefore P reabsorbtion)? [1]
- Vit. D activation? [1]
- PCT GNG? [1]
- Na/H20/HCO3- reabsorbtion? [1]
- Down-regulation of NaPi transporters: Reduced phosphate reabsorption
- Vitamin D Activation Stimulation of 25(OH) D3 –> 1,25(OH)2 D3 (inactivates 1,25-dihydroxyvitamin D)
- Proximal tubule gluconeogenesis
- Inhibits sodium/water/bicarbonate reabsorption via effects on Na/H exchanger and Na/K ATPase
The conversion of vit. D to WHAT is regulated? [1]
The conversion of vit. D to WHAT is unregulated? [1]
What are the enzymes used for each? [2]
Conversion of vit D to 25(OH)D in the liver is an unregulated process, under the action of p450 enzymes. The half life of 25(OH)D is 2-3 weeks.
The conversion of vit D to 1,25(OH)D is highly regulated, via 1αhydroxylase
How does negative feedback of activation of vitamin D receptor work?
In most cells there is a negative feedback inhibition: activation of the VDR inhibits the action of 1α hydroxylase (which converts vit D to active form), therefore reducing the amount of activated vitamin D able to bind to the VDR.