Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypercalcemi:

Symptoms

A

high plasma Ca+2

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Plasma Ca+2

A

ECM Ca+2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

High Ca+2 plasma

A

harder to get AP , farther from threshold

Depressed NS and refelxes are slowed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acidemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Alkalemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bone remodeling

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Kidneys EXcrete how much Ca+2

A

as much as absorbed by the GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

P and Ca+2 relationship

A

inversily related

high P = low Ca+2

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when is PTH secreted

A

low Ca+2 in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

PTH in chronic hypocalcemia

A

hgih levels of PTH made

= hyperplasia of parathyroid glands

= hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Kidney 1alpha-hydroxylase

A

inhibited by ca+2 and Vit D

24
Q

Where are PTH receptors located

A

Osteoblasts

25
short-term, intermittent PTH
binds to osteoblasts to cause BONE FORMATION for osteoporosis Tx
26
Long-term or continuous PTH
increase BONE RESORPTION causing osteoblasts to activate Osteoclasts + VIT D does the same
27
Bone resorption by PTH mechanism
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
OPG
secreted by osteoblasts -----I RANKL by binding to it and preventing it from binding to RANK receptor =Bone formation
29
PTH in the kidney mechanism
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) 6. excess P excreted in the urine
30
Vit D action in SI, Bone, Kidney, parathyroid Gland
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
low Ca+2, how does PTH and Vit D act
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
Calcitonin mechanism "RISING CA+2 STIMULUS"
1. HIGH Ca+2 stimulated calcitonin 2. increase ca+2 bone deposition decrease kidney uptake (reabsorption) of Ca+2 3. lowers Ca+2 in blood
33
"FALLING CA+2 STIMULUS"
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 4. Vit D absorption of Ca+2 in SI
34
Calcitonin role
lower blood Ca+2 and P binds to Osteoclasts to inhibit them LONG TERM REGULATION of plasma CA+2
35
Thyroidectomy vs Tyroid tumors
X calcitonin= however no effect on Ca+2 reuptake HIGH Calcitonin= however no effect on Ca+2 excretion or bone formation
36
calcitonin functions and where does it bind
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
Estradiol-17B function
CA+2 absorption in GI CA+2 Reabsorption in Kindey SURVIVAL of osteoblasts bone formation in bone
38
Adrenal Glucocorticoids (cortisol) function on Ca+2
Bone resporption Ca+2 excretion in kidney Ca+2 inhibited absorption in GI can cause osteoporosis if prolonged steriod of cortisol is used
39
Primary Hyprtparathyroidism
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
Secondary Hyperparathyroidism
prolonger PTH = 1. Renal Failure: low vit D, high P 2. Vit D deficiency (low P) ----\> LOW CA+2
41
Hypoparathyroidism Causes and Tx
low PTH= low vitD activation, low Ca+2, high P (Thyroid/parathyroid surgery, Autoimmune disease) Tx: oral Ca+2 with active VitD
42
where is Vit D activated
Kidneys 25(OH)D3------\> 1,25(OH)2D3
43
Hypoparathyroidsim Sx:
Sx: muscel cramp, spasm numbness or tingling, buring, around mouth mental deficiency poor teeth seizures
44
Albright Hereditary Osteodystrophy (Psudohypoparathyroidism type 1a) cause
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
Albright Hereditary Osteodystrophy (Psudohypoparathyroidism type 1a) Sx:
Sx: short neck, obesity, subcutaneous calcification, short finges
46
Humoral Hypercalcemia of malignancy
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
Familial Hypocalcinuric Hypercalcemia (FHH)
mutation inactivate CaSR in parathyroid = no inhibition of PTH exocytosis LOW CA+2 Hypocalcinuria (low in urine) Hypercalemia (high in blood)
48
Vit D inhibits what and activates what in the parathyroid
-----I PTH -----\> CaSR
49
Rickets- Osteomalacia
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
Psudovitamin D-deficient rickets TYPE 1 vs TYPE 2
TYPE 1: X in 1-alpha-hydroxylase TYPE 2: X in vitD receptor
51
Osteomalacia
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
+ Chevostek's sign
CN7 causes muscle twitching =Hypocalcemia
53
When bone mass increases and decreases
steap increase: 0-30yo men---\> slow decrease women----\> high decrease at 50yo male is higher at all times
54
Osteoporisis Tx:
PTH anabolic therapy Antiresorptive therapy: Bisphosphonated, ESTROGEN, CALCITONIN, DENOSUMAB (RANKL inhibitor)
55
Vit D cycle

Neuroendocrine Exam 3 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions