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PHY V > Ca And P Homeostasis > Flashcards

Ca And P Homeostasis Flashcards

1
Q

Cation with the highest concentration in the body? Where is it stored?

A

Ca2+

>99% of the body calcium is in the skeleton and other 1% is in other tissues and body fluids

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2
Q

Phosphorus

  1. T or F. It is present in every cell of the body.
  2. Location of storage?
A
  1. True!

2. 80% in the skeleton and 20% in other tissues and body fluids

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3
Q

The levels of Ca2+ and PO34- is regulated by 3 things:

A
  1. GI absorption and secretion (actually, more of absorption)
  2. Kidneys would also play a role in your Ca and P lvl (can inc or dec the reabs rate of Ca and P)
  3. Bone turnover wherein you have your bone formation (w/c lowers down Ca and P blood lvl) and bone resorption (break down bone increasing your Ca and P lvl)
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4
Q

Forms of Ca and P in the body?

A

Both Ca and P would exist in 3 forms:
1. Ionized/free (50%)
Majority of Ca2+ in the blood would exist in the ionized form. Impt bc this form is the active form or is the one responsible for the physiologic effects of Ca2+
IMPORTANT!!!

  1. Complexed
    Remaining 10%
    Complexed -> meaning Ca that is bound to other anions (e.g. PO4, SO4, HCO3, etc)
  2. Protein bound (40%)
    2nd most high conc
    This is the form of Ca that is bound to your plasma proteins (most impt one is your albumin)
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5
Q

Effect of the ff on Calcium levels:

  1. Hypoalbuminemia
  2. Acidemia
  3. Hyperalbuminemia
  4. Alkalemia
A

Conditions that can inc or dec your Ca2+ lvls
-Hypoalbuminemia (low lvls of albumin)
>protein bound Ca will dec and a concomitant effect of that is your free Ca would increase
>same is true for acidemia or acidosis (inc lvl of protons and these protons would displace your Ca2+ that is bound to your albumin) so as a result, your ionized Ca2+ would inc

Hyperalbuminemia
>If you have lots of albumin, Albumin will take Ca, lowering free ionized Ca
>same as alkalemia (dec protons on your blood causing more of free sites on Albumin where Ca can bind into so tataas si protein bound Ca)

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6
Q

What are calcitriopic hormones?

A
  1. PTH

2. 1,25-hydroxyvitamin D (Calcitriol)

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7
Q

T or F. Calcitonin is a calcitripic hormones?

A

F! It is also involved on calcium homeostasis but works opposite to the calcitriopic leading to lowering down Ca2+ lvl.

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8
Q

How do calcitriopic hormones maintain body Ca2+? P?

A

How our body maintains Ca2+
Note: PTH and Calcitriol, they would inc plasma Ca2+ lvl by
1. Inc bone resorption (facilitate the break down of your bone freeing up your Ca2+)
2. At the same time, at the lvl of kidneys, PTH and Calcitriol would inhibit the excretion of Ca2+ (or in other words, it inc reabs of ca2+)
3. At the lvl of small intestines, it’s only calcitriol that would exert its effect not PTH (so what happens, you inc the absorption of Ca2+)

For P:
1. Sa bones, both PTH and Calcitriol would still inc bone resorption thereby inc your plasma P lvl
2. At the lvl of kidneys, they would have opposing effects
>Si PTH would inhibit reabsorption at lvl of PCT (so it inc the excretion) and your calcitriol would inhibit excretion so opposing fx BUT between the 2, PTH would have greater effect than calcitriol so net effect of PTH is you inc P excretion even tho vit D is present
3. At lvl of small int, calcitriol would inc P absorption in the GIT

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9
Q
  1. Primary hormones that would prevent hypocalcemia?
  2. What secretes #1?
  3. Main sites of action of #1?
  4. Feedback on Vitamin D?
A

Parathyroid hormone

  • secreted by your gland (so it is located on the post aspect of thyroid gland)
  • specifically, it would be the principal/chief cells that would secrete your PTH
  • described as the primary hormone that would prevent hypocalcemia so it would inc your serum Ca2+ lvl
  • main sites of PTH action: kidneys and the bones (not the GI Tract)
  • (+) production of Vitamin D
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10
Q

Secretion and Regulation of PTH

A

One of the fx of PTH, inc synthesis of Vitamin D

This is the secretion of PTH by your chief cells

  • At the surface/PM of your chief cell, you have CSR (Ca-sensing receptor) receptor that detects Ca2+ lvl
    • At low lvls/absence of Ca2+, the receptor will not be activated so PTH will be secreted or exocytosed
    • But if we have increasing lvls of Ca, Ca2+ now will activate the receptor -> cascade of events which inhibits exocytosis of PTH (so PTH secretion dec when u have high lvls of Ca2+)
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11
Q

Half life of PTH?

A

2 minutes

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12
Q

T or F. PTH is a steroid hormone.

A

F!! Peptide hormone.

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13
Q

Relationship between serum PTH and PTH secretion/Free Ca2+ in the blood

A

Sigmoidal but inverse

Higher serum PTH -> lower Ca2+ in the blood/lower %PTH secretion

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14
Q

PTH receptor
>Where are these located?
>Effect

A

> PTHr
PTHrP
Parathyroid hormone-related peptide (may binding site)
expressed by kidneys and bones
Effect: Increase plasma Ca2+ lvls
Note: At the lvl of kidneys, you increase Vitamin D synthesis (specifically at the PCT)

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15
Q 
Vitamin D!
>Type of hormone
>Precursor
>Synthesized as? Where?
>Function
>Forms we get from diet
A

Vit D
-another calcitriopic hormone; steroid hormone
-precursor: 7-dehydocholesterol
-The Vit D we know is a prohormone (inactive). Once in our body, it will be conv to 1,25-dihydroxyvitamin D (aka 1,25-dihydroxycholecalciferol or Calcitriol)
-The precursor is synthesized in the basal layers of the skin
-Function: would target small int, kidneys, and bone
-The forms of Vit D we get from our diet, there are 2: Ergocal and Cholecal
>Plant source and the other one is animal source

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16
Q

Vitamin D synthesis?

A

> 7DHC sa skin to, once this is acted upon by UV rays/light what happens is this ring will open forming your cholecalciferol -> cholcal will be transported to the liver (so Vit D3 - liver)
same is true for dietary Vit D3 we get (once absorbed, it will utimately be transported to liver as well)
In the liver you have 25-hydroxylase which will hydroxylate your cholecal forming now your 25-hydroxycholecalciferol (this is still an inactive hormone). What will activate it is an enzyme found on your PCT sa kidneys (1-alpha hydroxylase, after action you get 1,25-Dihydroxyvitamin D (active hormone) -> you now have physiologic/biologic fx

There’s another pathway:

  • Which forms your 24,25-Hydroxylase
  • So your enzyme is 24-hydroxylase (a pathway that inactivates Vit D)
17
Q

Regulation of Vitamin D.
1. 24-hydroxylase

  1. PTH
  2. FGF-23
A

> Vit D exerts negative feedback by increasing synthesis of 24-hydroxylase which will exert a positive feedback on itself. This enzyme inactivates Vitamin D.

> Binding of PTH to the receptor increases transcription of 1-alpha-hydroxylase so you’ll form more of active Vitamin D. Vitamin D would exert a negative effect by inhibiting transcription of 1-alpha-hydroxylase so di over effect.

> FGF-23 is a hormone produced by osteocytes in the bone. One of its effect is to inhibit 1-alpha-hydroxylase synthesis.

18
Q

Vitamin D receptor

-Location

A

Vit D receptor

  • Vit D being a steroidal hormone is nonpolar so it can readily diffuse in the cell so its receptor is intracellular specifically for Vit D, a nuclear receptor (parang thyroid hormone)a
  • Vit D readily diffuses in nucleus and binds to NRs -> hormone + receptor complex will bind to specifc areas in DNA where it can inhibit/activate gene transcription resulting to the ff effects: Apoptosis, Anti-angiogenesis, differentiation, cell cycle arrest
19
Q

Which of these 3 hormones has an effect on your GI Tract - PTH, Calcitriol, or Calcitonin? How?

A

Epithelial Ca channels: TRPV5 & 6
Basolateral: PMCA or Na/Ca exchanger
NPT2Slide
—-
-Which of the 3 hormones has an effect on your GI Tract - PTH, Calcitriol, or Calcitonin? Calcitriol (Vit D lang) TATANUNGIN NIYA TO SA QUIZ HAHAHA
-Vit D increases the absorption of Ca and P
How? It would inc synthesis of the proteins necessary for absorption of these 2 ions
What are those transporters or proteins? Channels on the apical side (TRPV5/6), Calbindin (Calcium binding protein), and it would inc synthesis of proteins located in the basolateral membrane (Na/Ca exchanger: NCX), Ca ATPase (PMCA: Plasma Membrane Ca2+ ATPase)

For Phosphate, ganun din. Vit D would inc synthesis of proteins necessary for absorption of Phosphate:
>On apical side: Na/P symporter
>Basolateral side: Na/K pump, Phosphate transporter (yung question mark)

So the net effect of Vit D -> inc Ca and P absorption

20
Q

Renal handling of Ca2+ and Pi?

A

This slide is the summary of the fx of PTH and Vit D in the kidneys.
Note: PTH has 2 fx for Ca2+
>At lvl of PCT, PTH would decrease Ca2+ reabsorption.
>At lvl of thick ascending limb and DCT, PTH would inc Ca2+ reabs
-Bet the 2, the predominant effect of PTH would be sa DCT
>In terms of Phosphate, your PTH would dec P reabs at PCT and it would also inc Vit D synthesis at PCT

Vit D

  • has opposing effects to PTH (2 fx pala)
  • In terms of Ca2+ reabs, it is synergistic w/ PTH (same fx: reabs)
  • For Phosphate, opposing. Vit Di will enhance P reabs while DCT would dec. Bet the two, PTH would have a greater effect on your P reabsorption
21
Q

What is bone turnover?

A

Cyclic process of bone destruction (bone resorption) and bone deposition (new synthesis of bone matrix)

22
Q

How does bone resorption occur?

A

RANK: Receptor for activation of nuclear factor κB
OPGRANK: Receptor for activation of nuclear factor κB
OPG
-
Let’s start first w/ bone resorption
>What’s impt here is that your PTH hormone and Vit D would only exert their effect on osteoblast (your osteoblast would express receptor for PTH and Vit D. Not osteocyte nor osteoclast)
>So high lvls of Vit D sensitizes your osteoblast for your PTH (meaning mas nagiging sensitive siya for PTH) meaning to say, at lower amts of PTH, your PTH could bind to its receptor kay osteoblast
>Yun ginagawa ni Vit D (sensitizes your osteoblast for your PTH)

-Si PTH naman (high lvls) when it binds to your osteoblast would secrete several factors:
1. M-CSF (Monocyte-Colony Stimulating Factor) which causes the differentiation of your stem cell. Your SCs would become/dx into preosteoclast or osteoclast precursors which are special cells that would express receptors for 2 ligands: (a) IL-6 receptor and (b) RANK (receptor for activator of NFkB)
2. IL-6
3. RANKL (RANK Ligand)
Meaning to say these 2 would bind to their respective receptors. When your IL-6 and RANKL bind to their receptor, your preosteoclast would now dx into your multinucleated osteoclast. This multinucleated osteoclast is the mature osteoclast/the one that can perform its fxn which is bone resorption)

> So in other words, PTH and Vit D would indirectly promote formation of multinucleated osteoclast -> hence, bone resorption

> At low lvls of PTH, when PTH binds to the osteoblast, your osteoblast would secrete OPG (Osteoprotegerin: osteo = bone; protect), a factor that sequesters your ligand for RANK so that RANKL would not bind to RANK. So OPG will protect the bone from being resorbed

  • Osteoclast in the presence of RANKL would do the ff things:
    1. Activate proton pump (Pump out H+ ion into space and at the same time, pump out Cl ion so you now form HCl)
    2. Cause the exocytosis of lysosomes such that the lysosomal enzyme will now be present inside the space
    3. HCl + lysosomal enzymes will break down the matrix of the bone, freeing up the Ca2+ and P so nasisira siya
23
Q

Bone Mineralization

A

On the other side, your bone deposition (fxn of osteoblast) or Bone mineralization
-So your osteoblast would initially form an osteoid. It will release certain factors surrounding this area.
Factors: Pyrophosphate, AP, GPs. All of which would take Ca2+ and P from the blood and form your mineralized bone so magfform yan ng osteoid dito.

  • Eventually osteoblast will be surrounded by mineralized bone. Once it is surrounded, it will now become an osteocyte so si osteocyte wala na siya effect on bone deposition or bone resorption
  • Other factors that would increase your bone mineralization would be your mechanical stress but recent studies show that the presence of microfractures on the bone would cause the osteocytes to secrete a hormone, osteocalcin, w/c promotes bone deposition. (PERO WALA PA SA BOOK SO MECH STRESS NA LANG MUNA)
24
Q

Effect of Calciotropic Hormones on bones?

A

PTH

  • 1’ regulator of bone remodeling in adults
  • PTH/PTHrP receptor is found in osteoblasts ONLY
  • indirectly activates osteoclasts

Vitamin D

  • sensitizes osteoblasts for PTH
  • For coordination of osteoid production & calcification
  • VDr is found in osteoblasts ONLY
  • increases serum Ca2+/PO43- (eventually bone deposition)
25
Q

Integrated Physiologic Regulation of Ca2+ & Pi?

A
  • For example you have a low plasma Ca2+ so hypocalcemia, this will be detected by chief cells on parathyroid gland. Pag walang nagactivate sa CSR, you’ll have inc in PTH release -> PTH would have ff effects: (1) inc 1-alpha hydroxylase activity, (2) bone resorption and (3) inc Ca reabs (kidneys)
  • At the same time, you also increase your Vit D synth which will also inc bone resorption and inc dietary Ca2+ absorption
  • All of which the net effect is you inc Plasma Ca2+ lvl which exerts a negative effect on your Vit D synthesis and PTH secretion
26
Q

Calcitonin

  1. Type of hormone
  2. Secreted by?
  3. Secreted in response to?
  4. Greater or less effect on Ca2+ homeostasis? Why?
  5. Effects?
A

Calcitonin
-Also a PH
-secreted by thyroid gl
-Secreted in response to a VERY HIGH plasma Ca2+ lvl
-HOWEVER, it is not one of the main hormones that would regulate your Ca2+ bc its effect is longer or takes time unlike your PTH so it is not involved in minute to minute regulation (a fxn of PTH) so long term yung Calcitonin
-Effects:
Inhibiting bone resorption/osteoclasts activity
Increases renal Ca2+ excretion
Increases renal PO43- excretion
On Multinucleated Osteoclast
-Calcitonin, once it binds to the receptor on your osteoclast, it would inhibit bone resorption. All of these would be inhibited: proton pump, Cl- channel, exocytosis of lysosomes

27
Q

Effect of gonadal hormones on bone remodeling?

Relate to osteoporosis?

A
  • Promote bone formation and Calcium absorption
  • Promote apoptosis of osteoclasts

Osteoporosis
Dec estrogen lvl -> bone resorption becomes more predominant -> more porous bone

28
Q

Effect of glucocorticoids on bone remodeling?

A
  • GCs are produced by zone fasciculata
  • One of its effects: Elevated lvls of cortisol for long periods of time -> inhibit osteoblast dx & dec OPG release -> bone resorption -> osteoporosis
29
Q

Effect of FGF-23 on bone remodeling?

A
  • Produced by osteocytes
  • Inhibits both PO43- reabsorption (in PCT) and calcitriol synthesis
  • Stimulated by sustained high lvls of phosphate (hyperphosphatemia), PTH, and calcitriol
30
Q

Hypophosphatemia?

A

Increased Vit D synthesis -> Dec FGF-23

Net effect: inc serum Ca2+ and PO43- which will decrease PTH secretion leading to inc PO43- reabsorption so all in all tataas si serum PO43-

31
Q

What happens in Vit D deficiency?

A

> aka rickets (children) or osteomalacia (adults)
Deficient Vit D -> dec GI absorption of Ca2+ and Pi -> hypocalcemia -> inc PTH secretion -> inc Pi excretion -> low Pi/Ca2+ lvls -> Impaired bone formation & inc demineralization

When you have Vit D def, you’ll have a dec GI absorption of Ca2+ and P so you’ll have hypocalcemia. This dec in Ca will cause an inc in your PTH release. This inc in PTH release would inc your Ca and at the same time would inc your P secretion so onti na nga lang naabsorb mong P, you excrete more P pa resulting now to a low Phosphate to calcium ratio. When that happens, you have impaired bone formation and mineralization.

Take note: For bone deposition to occur, you must have normal lvls of both Ca2+ and P not just Ca2+ lang dapat parehas!

32
Q

Hyperparathyroidism?

A

-You have an inc PTH secretion. This will have the ff fx: Inc renal Ca reabs, bone resorption, and bc PTH inc Vit D synthesis, you’ll also have an inc GI Ca absorption so tataas ng tataas si Ca2+. Eventually when you have v high lvls of Ca2+, some of the Ca2+ will also be excreted in the urine so you have hypercalciuria and phosphaturia. Problem here is that when u have Ca and P in urine, they can precipitate so pwedeng magkaroon ng stones so you presentation of hyperparathyroidism, you can have: osteoporosis and nephrolithiasis (pabalik balik yung stones bc of this one)

33
Q

Hyperphosphatemia?

A

Inc blood P lvl -> would complex with your ionized Ca2+ -> resulting to decreased blood Ca2+ lvl -> secondary hyperparathyroidism

PHY V (12 decks)

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