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Neuroendocrine Exam 3 > Calcium And Phosphate Homeostasis > Flashcards

Calcium And Phosphate Homeostasis Flashcards

1
Q

Ca+ in the body is found Where

A

99% bone and teeth 1% ICF Rest in ECF and Plasma

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2
Q

Ca+ is found HOW in what form

A

ACTIVE= Ca+2 (50%) 40% protein bound 60% ultra-filterable——10% anions attached to another ion , 50% Ionized ca+2

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3
Q

During Aging Ca+

A

Ca+2 absorption is decreased from food and such

=BONE gets reabsorbed faster then new bone can be made since Ca+2 is needed and not taken in sufficiently from food= osteoporosis, osteopenia

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4
Q

Hypocalcemia:

And symptoms

and signs

A

low Ca+2 in plasma

hyperreflexia, spntaneous twitching, muscle cramp, tingling and numbness

Chnostek sign=facial muscels twitch, when tap on facial nerve

Trousseau Sign= spasm of wrist and forarm when BP cuff is put on arm

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5
Q

Hypercalcemi:

Symptoms

A

high plasma Ca+2

shorter QT interval, constipation, low appetite, polyuria, muscle weakness, hyporeflexia, lethargy

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6
Q

Plasma Ca+2

A

ECM Ca+2

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7
Q

Low Ca+2 plasma

A

lowers threthhold for activation of NA+ channels to open

easier to get AP

=spontaneous AP made

=Hopocalcemic TETANY

(tingling, numbness-sensory neurons, spontaneous muscle twitches-motor neurons)

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8
Q

High Ca+2 plasma

A

harder to get AP , farther from threshold

Depressed NS and refelxes are slowed

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9
Q

Change form of Ca+2 found how:

A
  1. change [plasma protein] =increase plasma proteins-> increase Ca+2
  2. change [anion] = increase phosphate concentration –> lower ionized Ca+2
  3. change acid base abnormalities =change amount of Ca+-ALBUMIN–> ionized Ca+2 changes
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10
Q

Acidemia

A

high amounts of free ionized Ca+2 due to lower amounts of ALBUMIN

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11
Q

Alkalemia

A

decrease in free ionized Ca+2 due to high ALBUMIN, and usually due to HYPOCALCEMIA

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12
Q

HOW CA+2 ENTERS ECF

HOW CA+2 LEAVES ECF

(in GI, Bone, Kidneys)

A

GI: absorbed with VitD

(also secreated into the GI, and excreted)

BONE: resoption by osteoclasts, VitD +PTH

(Deposited also on bone)

KIDNEY:

Reabsorption with PTH

(Filtered into the kidney also)

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13
Q

Bone remodeling

A

no net gain or loss of Ca+2, deposited=resopted

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14
Q

Kidneys EXcrete how much Ca+2

A

as much as absorbed by the GI

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15
Q

P and Ca+2 relationship

A

inversily related

high P = low Ca+2

P: highest in bone85%, then ICF15%, then Plasma1%

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16
Q

PTH Cycle/Pathways of Ca and P

A
  1. parathyroid glands make and secrete PTH by chief cells
  2. PTH = DECREASE Ca+2

PTH = INCREASE P

(high ECM Ca+2—-I PTH synthesis) since Ca+2 binds to CaSR and signals inhibition if PTH synthesis and secretion

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17
Q

when is PTH secreted

A

low Ca+2 in plasma

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18
Q

PTH H. characteristics

A

peptide

pre-pro-PTH—-> Pro-PTH—–> PTH in the GOLGI—> packaged into secratory granules

INCREASE RANKL, and DECREASE OPG

Binds to a GPCR

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19
Q

PTH in chronic Hypercalcemia

A

very low amounts of PTH synthesis and storge

=higher breakdown of stored PTH fragments released into the blood

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20
Q

PTH in chronic hypocalcemia

A

hgih levels of PTH made

= hyperplasia of parathyroid glands

= hyperparathyroidism

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21
Q
  1. During Low Ca+2, there is an increase in PTH, this causes WHAT
A
  1. Bone: incresed resorption of Ca+2 to ECF
  2. Kidney: decreased P reabsorption

increased Ca+2 reabsorption to ECF

increased cAMP in urine

  1. GI: increase absorption of Ca+2 with Vit D also to ECF
  2. CA+2 INCREASES TO NORMAL
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22
Q

VITAMINE D

A

increases P and Ca+2 in ECF = mineralization of new bone

decreases PTH

Vit D =STERIOID H.

(Cholecalciferon)- prohormone from diet and modified from sun

1, 25= active

24.25 = inactive

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23
Q

Kidney 1alpha-hydroxylase

A

inhibited by ca+2 and Vit D

24
Q

Where are PTH receptors located

A

Osteoblasts

25
Q

short-term, intermittent PTH

A

binds to osteoblasts to cause BONE FORMATION

for osteoporosis Tx

26
Q

Long-term or continuous PTH

A

increase BONE RESORPTION causing osteoblasts to activate Osteoclasts

+ VIT D does the same

27
Q

Bone resorption by PTH mechanism

A
  1. PTH or Vit D binds to Osteoblasts (PTHR)
  2. Osteoblasts secrete RANKL (also made by apoptotic osteoclasts + inhibits OPG secretion
  3. RANKL —> RANK receptor on osteoclasts
  4. Bone resorption
28
Q

OPG

A

secreted by osteoblasts

—–I RANKL by binding to it and preventing it from binding to RANK receptor

=Bone formation

29
Q

PTH in the kidney mechanism

A
  1. PTH binds to GPCR
  2. ATP—> cAMP
  3. cAMP activates protein kinase + excreted in urine
  4. protein kinase phosphorylates NPT (nephron Phosphate Transporter)
  5. —-I Pi reabsorption into the tubule

(+ increase Ca+2 reabsorption)

  1. excess P excreted in the urine
30
Q

Vit D action in SI, Bone, Kidney, parathyroid Gland

A

SI= Increase Ca+2, and P

Bone = increase affintiy of PTH to osteoblasts (increase RANKL)

regulates calcification

Kidney= increase P reabsorption by NPT

Parathyroid Gland= —-I PTH gene

activate CaSR gene (increase ICF CA+2)

31
Q

low Ca+2, how does PTH and Vit D act

A

Increase PTH

increase CYP1-alpha

increase:

  1. 1,25(OH)2 VIT D (slowest)
  2. Bone turnover
  3. Ca+2 reabsorption in bone and P excretion in the kidneys
  4. VIT D will increase: Ca+2 absorption by SI and P reabsorption by Kidneys
32
Q

Calcitonin mechanism

“RISING CA+2 STIMULUS”

A
  1. HIGH Ca+2 stimulated calcitonin
  2. increase ca+2 bone deposition

decrease kidney uptake (reabsorption) of Ca+2

  1. lowers Ca+2 in blood
33
Q

“FALLING CA+2 STIMULUS”

A
  1. low Ca+2
  2. PTH is released from the parathyroid gland
  3. *increase Ca+2 resorption from bones

*increase reabsorption of Ca+2 in kidneys

+ activate Vit D

  1. Vit D absorption of Ca+2 in SI
34
Q

Calcitonin role

A

lower blood Ca+2 and P

binds to Osteoclasts to inhibit them

LONG TERM REGULATION of plasma CA+2

35
Q

Thyroidectomy vs Tyroid tumors

A

X calcitonin= however no effect on Ca+2 reuptake

HIGH Calcitonin= however no effect on Ca+2 excretion or bone formation

36
Q

calcitonin functions

and where does it bind

A
  1. —–I bone resorption= decrease Ca+2 and P
  2. binds to Osteoclast to inhibit their function

it is stimulated when Ca+2 is high

ACUTE

37
Q

Estradiol-17B function

A

CA+2 absorption in GI

CA+2 Reabsorption in Kindey

SURVIVAL of osteoblasts

bone formation in bone

38
Q

Adrenal Glucocorticoids (cortisol) function on Ca+2

A

Bone resporption

Ca+2 excretion in kidney

Ca+2 inhibited absorption in GI

can cause osteoporosis if prolonged steriod of cortisol is used

39
Q

Primary Hyprtparathyroidism

A

Hypercalcinuria stones= increased PTH-> increased bone resorption—> stones and constepation groans

Tx: parathyroidectomy

(also increases P excretion, Ca+2 absorption and reabsorption, increased activation of VIT D)

HIGH, Vit D, Ca+2, PTH

40
Q

Secondary Hyperparathyroidism

A

prolonger PTH =

  1. Renal Failure: low vit D, high P
  2. Vit D deficiency (low P)

—-> LOW CA+2

41
Q

Hypoparathyroidism

Causes

and Tx

A

low PTH= low vitD activation, low Ca+2, high P

(Thyroid/parathyroid surgery, Autoimmune disease)

Tx: oral Ca+2 with active VitD

42
Q

where is Vit D activated

A

Kidneys

25(OH)D3——> 1,25(OH)2D3

43
Q

Hypoparathyroidsim

Sx:

A

Sx: muscel cramp, spasm

numbness or tingling, buring, around mouth

mental deficiency

poor teeth

seizures

44
Q

Albright Hereditary Osteodystrophy (Psudohypoparathyroidism type 1a)

cause

A

Gs of the PTH R. is defective in bone and kindey

no cAMP

No bone resorption, no CA+2 reabsorption

LOW CA+2 HIGH P, PTH

=Hypoparathyroidism and Hyperphosphatemia

45
Q

Albright Hereditary Osteodystrophy (Psudohypoparathyroidism type 1a)

Sx:

A

Sx: short neck, obesity, subcutaneous calcification, short finges

46
Q

Humoral Hypercalcemia of malignancy

A

PTHrP(PTH related peptide) made by tumors

= similar to PTH —> type 1 PTH R.

HIGH Ca+2 reabsorptiona, resorption, absorption,

LOW P, PTH, vitD

same only slightly different from hyperparathyroidism

47
Q

Familial Hypocalcinuric Hypercalcemia (FHH)

A

mutation inactivate CaSR in parathyroid = no inhibition of PTH exocytosis

LOW CA+2

Hypocalcinuria (low in urine)

Hypercalemia (high in blood)

48
Q

Vit D inhibits what and activates what in the parathyroid

A

—–I PTH

—–> CaSR

49
Q

Rickets- Osteomalacia

A

X: VitD metabolism

active vitD cant be formed (no 1-alpha-hyroxylase)

GI problems, Renal failure, LOW P and CA+2

Growth failure skeletal probs(children)

Xnew bones+ soft bones: Osteomalcia (adults)

50
Q

Psudovitamin D-deficient rickets TYPE 1 vs TYPE 2

A

TYPE 1: X in 1-alpha-hydroxylase

TYPE 2: X in vitD receptor

51
Q

Osteomalacia

A

LOW VIT D

GI disorder or bad nuttrition or low sun exposure

bone pain after gastric bypass surgery

Muscle weakness, fractures, cramps, + Chevostek’s sign, tingling and numbness

HIGH PTH, LOW Ca+2, P, cAMP

52
Q

+ Chevostek’s sign

A

CN7 causes muscle twitching

=Hypocalcemia

53
Q

When bone mass increases and decreases

A

steap increase: 0-30yo

men—> slow decrease

women—-> high decrease at 50yo

male is higher at all times

54
Q

Osteoporisis Tx:

A

PTH anabolic therapy

Antiresorptive therapy: Bisphosphonated, ESTROGEN, CALCITONIN, DENOSUMAB (RANKL inhibitor)

55
Q

Vit D cycle

A

Neuroendocrine Exam 3 (18 decks)

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