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Block 3 Week 5 > Keef; PTH gland Ca and phosphate > Flashcards

Keef; PTH gland Ca and phosphate Flashcards

1
Q 
What makes this happen:
nerve excitability
transmitter release
muscle contraction
enzyme cofactor
bone
A

Calcium

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2
Q 
What makes this happen:
phosphoproteins
buffering pH
DNA, RNA
Bone
A

phosphorus

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3
Q

DO we have more calcium in the cell or outside?

Do we have more phosphorus in the cell or outside?

A 
in cell
in cell (wayyy more phosphoruse than calcium in cell though)
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4
Q

Is ther a lot of variation in calcium levels?

How about in phosphorus?

A

NO

Yes

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5
Q

Where are phosphorus and calcium regulated?

A

kidneys
bone
GI tract

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6
Q

Do you absorb the majority of your calcium?

A

you excrete the majority of it (85%), you absorb about 300 mg

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7
Q

What happens to the calcium you asborb?

A

the majority is placed into the extracellular fluid where it will be distributed. It will either be excreted into urine, placed into bone, or put into cells. THe majority is placed into bone where it will be in equilibrium

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8
Q

What happens to phosphate when you eat it?

A

about 1/3 is excreted and 2/3rds absorbed. The 2/3rds that where absorbed is placed into the extracellular space where it will be in equilibrium with skeleton, excreted into urine , or placed into soft tissue

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9
Q

Once calcium gets absorbed into the intestines what needs to happen?

A

calbindin will bind it to regulate it. Bound calcium will not affect intracellular calcium concentrations.

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10
Q

How do we get calcium in and out of the intestinal cell into the blood?

A

calcium will go into the cell passively but needs active transport out of the cell in the duodenum and jejunum.

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11
Q

In the duodenum and jejunum, when calcium needs to leave the cell to enter the blood stream, how does it do this?
How does calcium transport work in the illeum?

A

via and Ca/H atpase or a Ca/Na exchange

Paracellularly (so no energy)

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12
Q

How do you get phosphate in and out of the lumen of the intestine into the blood?
How do you get phosphate in kidney and out to blood?

A

Active transport into cell via Na, phosphate exchanger and then passive into the blood

Active transport into the cell and then passive into the blood.

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13
Q

explain calcium processing in the kidney

A

(passive into kidney cell, and active into the blood)
70% of calcium passes paracellulary (passive) in proximal tubule
The rest is abosrbed trabscellular via TRP channels and then placed into blood via ca/Na exchanger or CaATPase.

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14
Q

What does PTH do to calcium?

A

stimulates calcium reabsorption by stimulating Gs protein->PKA->tripp channels-> increase calcium reabsorption

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15
Q

How does vit D effect calcium reabsorption?

A

Vit D will stimulate transcription of calbinindin and Tripp channels to allow for quicker and easier reabsorption

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16
Q

What does PTH do to calcium and what does it do to phosphate?

A

stimulates Ca reabsorption

Inhibits phosphate reabsorption

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17
Q

What percent of phosphate is excreted in the kidney?

What percent of calcium is excreted in the kidney?

A

10%

1%

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18
Q

How is phosphate absorbed, paracellularly or transcellularly?

A

alll is transcellularly!

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19
Q

What is the composition of mature compact bone?

A

collagen fibers, calcium salts (hydroxyapatite crystals), canaliculi, cell processes, bone cells

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20
Q

Do minerals take up more volume of bone,or make up more weight of the bone?

A

makes more weight (50%)

volume (25%)

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21
Q

HOw do we make osteoblasts?

How do we make osteoclasts?

A

osteoprogenitor cells->ostebolasts

monocyte precursors-> fusion-> osteoclasts

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22
Q

PTH stimulates the (blank) to release MCSF which causes stem cells to become osteoclasts precursors->osteoclats

A

osteoblasts

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23
Q

PTH stimulates the osteoblasts to release (blank) which causes stem cells to become (blanK) precursors, which will become osteoclasts

A

MCSF

Osteoclasts

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24
Q

When is PTH released?

A

when there isnt enough calcium

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25
Q

When vitamin D is activated, what is it called?

What does it do?

A

calcitriol

stimulates PTH

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26
Q

What bone disorder is this:

increased osteoid and mineral

A

osteopetrosis

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27
Q

What bone disorder is this:

soft bones, demineralization, rickets in children

A

osteomalacia

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28
Q

What bone disorder is this:

decreased osteoid and mineral

A

osteoporosis

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29
Q

What are some drugs used in treatment of osteoporosis?

A

Bisphosphates, calcitonin, estrogen-> inhibit osteoclasts

PTH stimulates Osteoblasts

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30
Q

Why do a lot of older women get osteoporosis?

A

because they lack estrogen which inhibits osteoclasts

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31
Q

How do you rapidly regulate plasma calcium?

A

non-hormonally
via protein bound calcium and
Ca exchange with bone

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32
Q

How do you regulate plasma calcium in the long term?

A

hormonally

via PTH, Calcitriol, calcitonin (CT)

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33
Q

WHere are parathryoid glands located?

A

on the back of the thyroid gland

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34
Q

What releases PTH?

And how do these cells release this?

A

chief cells

chief cells have calcium sensors, when low they release PTH.

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35
Q

When you have decreased magnesium and increased phosphate what will happen to PTH?

A

you will get increased release

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36
Q

Is calcitonin essential for life?

A

no

37
Q

What releases calcitonin?

A

thyroid gland C Cells/parafolicular cells

38
Q

When is calcitonin release stimulated?

A

when you have high levels of calcium (remember calcitonin tones down calcium)

39
Q

Whih is more important in the regulation of calcium, PTH or CT?

A

PTH

40
Q

What is the normal range for PTH?

A

10-55 pg/ml

41
Q

What does calcitonin do to osteoclast activity?

What does PTH do to osteoclast activity?

A

inhibits (also increases Ca excretion in the kidneys)

stimulates

42
Q

What is the second most important regulator of calcium?

A

activate vit D (calcitriol)

43
Q

What is the most important step in activating vit D?

A

coverting 25-hydroxycolacacliferol to calcitriol in the kidney

44
Q

Since the kidneys are so important for activating vit D, what happens if you have kidney failure?

A

you need supplements

45
Q

What makes 25, hyroxyvit D so much less active than 1,25 hydroxy vit D?

A

an extra OH makes it more active

46
Q

Where does calcitriol work?

A

modulates calcium and phosphate in bone, kidneys and intestine

47
Q

How can you stimulate 25-hydroxvit D 1 aplha hydroxylase (the step to convert 25 hydroxy to calcitriol)?

A

via low levels of Phosphate

low levels of Calcium

48
Q

What will calcitriol do in bone?
in intestine?
In kidney?

A

bone- increase Ca and phosphate mobilization
intestine- increase calcium and phosphate absorption
kidney- decrease phosphate and calcium excretion

49
Q

Since PTH and calcitriol have opposing effects on phosphate excretion, which will win out?

A

PTH (you will get increased phosphate excretion)

50
Q

(blank) makes the intestine absorb more calcium and phosphate i.e increases the abosrpiton of Ca and Phosphate SO very important

A

Vit D

51
Q 
What will these do:
PTH
Calcitriol
Insulin
Androgens
GH
Growth factors
A

stimulate bone formation

52
Q 
What will these do:
PTH
Calcitriol
Thyroid hormone
corticosteroids
prostaglandins
growth factors
A

Stimulate bone resorption

53
Q

What will calcitonin and estrogen do?

A

inhibit bone resorption

54
Q

What will corticosteroids do?

A

inhibit bone formation

55
Q

(blank) is essential for life, and can result in death by hypocalcemic tetany if you dont have it.

A

PTH

56
Q

What are the symptoms of lack of PTH

A

CATS

convulsions, arrhythmias, tetany, numbness

57
Q

How come hypocalcemia causes tetany?

A

reduced Ca depolarizes membrane and activates sodium channel in nerve and muscle

58
Q

What does PTH stimulat?

A

increase Ca reabsorption in Kidney, increases active Vit D in kidney

59
Q

What does PTH inhibit?

A

Phosphate reabosrption

60
Q

What does activated Vit D inhibit?

A

itself (negative feedback)

61
Q 
What do these result in:
hypoparathyroidism
pseudohypoparathyroidism
osteomalacia/rickets
chronic renal failure
A

hypocalcemia

62
Q

What do these result in:
vit D intoxication
Pri. hyperparathyroidism

A

hypercalcemia

63
Q

(blank) inhibits abnormal calcification.

A

inorganic phosphate

64
Q

(blank) breaks down pyrophosphate favoring bone remodeling.

A

alkaline phosphatase (TNAP)

65
Q

(blank) have a lot of alkaline phosphatase.

A

osteoblasts

66
Q

(blank) enhances the ability of mineral to be deposited in the bone, this is an indicator that bone remodeling is going on and high PTH activity.

A

alkaline phosphatase

67
Q

What is the most common cause of hypoparathyroidism?

A

injury during head and neck surgery

68
Q

If you have hypoparathyroidism then what will happen?

A

you will have decreased PTH which will lead to*

hypocalcemia, hyperphosphatemia, decreased PTH

69
Q

What is the treatment for hypoparathroidism?

A

give calcium

vit D supplements

70
Q

What results when you have pseudohypoparathyroidism?

A

Lack of response to PTH**
hypocalcemia
hyperphosphatemia
increased PTH

71
Q

What results when you have osteomalacia/rickets?

A

softening of bone due to loss of calcium (maybe lack of vit D)**
Hypocalcemia, decreased Vit D, hypophosphatemia, increased PTH

72
Q

PTH and bone resorption have what kind of relationship?

A

direct

73
Q

So explain the mechanism of rickets/osteomalacia

A

calcium absorption into intestine is diminished
This triggers PTH-> increased bone resorption (taking calcium out of bone), but this isn’t enough so you have decreased Plasma Ca levels and decreased phosphate levels. THe increased PTH will result in high alkaline phosphate levels

74
Q

How do you detect if someone has rickets?

A

increased alkaline phosphate

75
Q

What is the overall result of osteomalacia/rickets?

A

hypocalcemia
hypophosphatemia
increased PTH
increased Alkaline Phosphatase

76
Q

What happens when you have chronic renal failure?

A

lack of kidney means lack of vit D.

which results in decreased calcium reabsorption and therefore increased PTH and decreased Plasma Calcium

77
Q

What is the overall result of chronic renal failure?

A 
hypocalcemia
hyperphosphatemia
increased PTH
increased Alkaline phosphatase
Brittle bones
78
Q

Hypocalcemia is often associated with elevated phosphate levels except in one case which is (blank).

A

osteomalacia/rickets

79
Q

What happens when you have vit D intoxication?

A

decreased PTH and increased plasma Ca

increased Phosphate reabsorption and increased mineral deposits where they shouldn’t be

80
Q

What is the overall effect of vit D intoxication?

A

hypercalcemia
hyperphosphatemia
decreased PTH
increased calcium in urine

81
Q

What happens when you have primary hyperparathyroidism?

A

increased PTH-> increased bone resorption-> increased plasma calcium->decreased phosphate, brown tumors will result

82
Q

What is the overall effect of primary hyperparathyroidism?

A

hypercalcemia
hypophosphatemia
Increased PTH
calcium in urine

83
Q

(blank) inhibits PTH release and calcium reabsorption from the kindey

A

calcium sensing mechanism

84
Q

(blank) stimulates calcium channels in nephron via Gs/cAMP/PKA pathway.
(blank) inhibits calcium channels in nephron via other mechanisms (Gq/G11)

A

PTH

CaSR

85
Q

In kidneys you have calcium sensing receptors(CaSR) when it senses calcium it will (blank) calcium reabsorption.

A

inhibit

i.e. you have too much calcium so you want to excrete it

86
Q

(blank) protects tissues from excess calcium in extracellular fluids

A

CaSR

87
Q

What does CTAL do?

A

inhibits Ca and Mg reabsorption in kidney

88
Q

(blank) is an autosomal dominant disease caused by an inactivation mutation of the calcium-sensing receptors (CaSR).

A

FHH

89
Q

In FHH,
What happens to PTH release?
What happens to Ca excretion?
What will happen to plasma Ca levels?

A

PTH will continue to be released
Ca excretion will decrease
Plasma Ca levels will increase

Block 3 Week 5 (7 decks)

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