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NeuroEndocrine 3 > Regulation of Calcium and Phosphate > Flashcards

Regulation of Calcium and Phosphate Flashcards

1
Q

what is the biological form of Ca+

A

Free ionized Ca2+

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2
Q

What happens with Hypocalcemia

A

decrease in plasma Ca concentration

hyperreflexia
spontaneous twitching
muscle cramp and tingling and numbness

Indicators: Chvostek sign: twitching of facial muscles after tapping on facial nerve

Trousseau sign: carpopedal spasm upon inflation of a blood pressure cuff

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3
Q

What happens in hypercalcemia

A

increase in plasma Ca concentration

Decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, coma

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4
Q

How does calcium concentrations affect the membrane excitabillity

A

Hypocalcemia:

  • reduces activation threshold for Na channels making it easier to evoke a AP
  • increase in membrane exictabillity (more AP)
  • production of tingling and numbness

Hypercalcemia:

  • decrease in membrane excitabillity
  • nervous system becomes depressed and reflex responses are slo
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5
Q

How can Acid base abnormalities alter ionized Ca concentration

A

Albumin binds free calcium and H+

therefore the acidic the more H+ bound to ALbumin meaning more free floating Ca (increase concentration)

More basic the more Ca bound to albumin therefore a lower free floating Ca concentrations (hypocalcemia)

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6
Q

What is the relationship between Calcium and phosphate

A

Extracellular concentration of P is inversely related to that of Ca

Extracellular concentration of P is regulated by the same hormones that regulate Ca concentration

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7
Q

Where is PTH synthesized, how and secreted and what is its main function

A

chief cells of the Parathyroid gland synthesized on ribosomes as PreproPTH then cleaved to ProPTH and the finally cleaved in golgi to PTH and is packaged in secretory granules

used to regulate the concentration of Calcium and Phosphate in the plasma

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8
Q

what is the stimuli for PTH secretion

A

a decrease in Plasma concentration

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9
Q

What causes inhibition of PTH synthesis and secretion

A

hich concentration in Plasma Concentration

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10
Q

WHat happens in chronic Hypercalcemia

A

decrease in synthesis and storage of PTH that leads to an increase breakdown of stored PTH and release of inactive PTH fragments into circulation

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11
Q

what happens in chronic Hypocalcemia

A

AN increase in synthesis and storage of PTH that cases hyperplasia of the parathyroid gland (secondary hyperparathyroidism)

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12
Q

WHat happens if an individual has hypomagnesemia

A

chronic Mg depletion as in alcoholism

inhibition of PTH synthesis storage and secretion

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13
Q

How does PTH act on the bone, Kidney, and intestine

A

BOne: increase bone resorption

Kidney: increase Ca reabsorption, decrease Pi reabsorption
increase urinary cAMP

Intestine: Increase Ca absorption indirectly via vitamin D

all of these increase Plasma Ca concentrations

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14
Q

What is Vitamin D

A

Cholecalciferol

is a prohormone
steroid hormone (in active form)
it is physiologically inactive
Must be hydoxylated to be active

regulated by negative feedback mechanisms

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15
Q

what is the process of converting Vitamin D to active form

A

in liver Cholecalciferol converted to 25-OH-cholecalciferol then in the renal proximal tubule it is converted to 1,25-OH-Cholecalciferol

this is the active form and is done by CYP1a hydroxylase

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16
Q

where are the PTH receptors located on bone and what is PTH short term and long term actions on bone
howw does Vitamin D compare

A

PTH receptors located on osteoblasts

short term actions: Bone formation

Long term action: increase bone resorption (indirect action on osteoclasts mediated by cytokines released from osteoblasts)

vitamin D acts simularly to PTH

17
Q

Summary of factors important in bone formation: M-CSF

A

Macrophage colony stimulating factor

induce stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and finally mature multinucleated osteoclasts

18
Q

Summary of factors important in bone formation: RANKL

A

receptor activator for NF-kB ligand

cell surface protein produced by osteoblasts, bone lining and apoptotic osteocytes
-primary mediator of osteoclast formation

19
Q

Summary of factors important in bone formation: RANK

A

Cell surface protein receptor on osteoclasts and osteoclast precursors

20
Q

Summary of factors important in bone formation:OPG

A

osteoprotegerin

soluable protein produced by osteoblasts that inhibits the RANKL/RANK interaction

21
Q

How does PTH and Vitamin D affect RANKL

A

increases RANKL and decreases OPG

22
Q

Summary of PTH actions on the kidney

A

Stimulates 1a hydroxylase to activate Vitamin D

stimulates Ca reabsorption by the thick ascending limb of heneles loop and the distal tubule

Inhibits P reabsorption by proximal nephrons (represses NPT2a expression)

23
Q

process of Vitamin D on intestinal calcium absorption

A

1,25 dihydroxy Vitamin D changes transcription to make TRPV6 channel to allow for Calcium to enter from the intestine

from their Calbindin binds and then uses 3 Na from the intersitial space to get Calcium into the blood stream

24
Q

Summary of how Vitamin interacts with Ca and P in the small intestine, bone, kidney and Parathyroid gland

A

Small intestine: increases Ca and P absorption

Bone: sensitizes osteoblasts to PTH
regulates osteoid production and calcification

Kidne: Promotes P reabsorption byy proximal nephrons (stimulates NPT2a)

Parathyroid gland:
Directly inhibits PTH gene expression
Directly stimulates CaSR gene expression

25
Q

WHat is the role of calcitonin

A

decrease Ca and P concentration

does this by inhibiting bone resorption
-decreases the activity and number of osteoclasts

it does this if there is a high level of Calcium in the plasma

26
Q

How does thyroid tumors and thyroidectomy affect calcitonin

A

decrease in thyroidectomy
increase in a thyroid gland

overall no change in Ca from this though

27
Q

How does Estradiol 17B affect Ca levels

A

stimulates intestinal Ca absorption and renal tubular Ca reabsorption

promotes the survival of osteoblasts and apoptosis of osteoclasts favoring bone formation over resorption

28
Q

How do adrenal glucocorticoids affect Ca

A

Cortisol promotes bone resorption and renal Ca wasting and inhibit intestinal Ca absorption

patients treated with high levels of cortisol can induce osteoprosis

29
Q

Primary Hyperparathyroidism: PTH levels, Ca levels, P levels and Vitamin D, Treatment and characteristics

A

high PTH
High Ca
Low P
High Vitamin D

patients have hypercalciuria stones
increase bone resorption
constipation groans

treat ment is parathyroidectomy

30
Q

Secondary Hyperparathyroidism: PTH levels, Ca levels, P levels and Vitamin D, Treatment and characteristics

A

Renal failure: high PTH
low Ca
high P
low Vitamin D

Vitamin D deficiency:
High PTH
low Ca
low P
low vitamin D
31
Q

Hypoparathyroidism: PTH levels, Ca levels, P levels and Vitamin D, Treatment and characteristics

A

Low PTH
Low Ca
High P
low Vitamin D

causes are thyroid or parathyroid surgery
autoimmune or congenital

muscle cramping
seizures
poor teeth
numbness in hands and mouth

oral calcium and active form of vitamin D

32
Q

Pseudohypoparathyroidism type 1a PTH levels, Ca levels, P levels and Vitamin D, Treatment and characteristics

A

Albright hereditary osteodystrophy

high PTH
low Ca
high P
low Vitamin D

inherited autosomal dominant where the Gs for PTH in bone and kidney is defective
hypocalcemia and hyperphosphatemia develop
short stature
short neck
obesity
subcutaneous calcifications
shortedned metatarslas and metacarpals

33
Q

Humoral hypercalcemia of malignancy PTH levels, Ca levels, P levels and Vitamin D, Treatment and characteristics

A

low PTH
high Ca
low P
low Vitamin D

PTHrelated peptide produced by tumor and this peptide will bind and activate same receptor as PTH
high PTHrP levels
increase urinary cMP, Pi, Ca

34
Q

Familial Hypocalciuric hypercalcemia PTH levels, Ca levels, P levels and Vitamin D, Treatment and characteristics

A

FHH

normal to high PTH
High serum Ca
low Urine Ca
normal P
normal Vitamin D

mutation that inactivates CaSR in the parathyroid glands and in the ascending limb of the kidney

35
Q

what does the CaSR gene do

A

activated by levels of vitamin D and Ca but will inhibit the release of PTH from the Parathyroid hormone

36
Q

What are the two types of congenital Rickets

A

Congenital disorders:
-Pseudovitamin D deficient rickets or vitamin D dependant rickets type 1 (decrease in 1 alpha hydroxylase)

-Pseudovitamin D deficient rickets or vitamin dependant rickets type II (decrease in viramin D receptor)

lead to insufficient Ca and P and stunted growth and skeletal deformities

37
Q

Osteomalacia

A

Vitamin D deficiency in adults
due to malnutrition, gastrointestinal disorder, inadequate sun exposure

bone pain and muscle weakness
bone tenderness
fracture
muscle spasms and positive chvosteks sign

38
Q

Treatment of osteoprosis

A

PTH

Bisphosphonates
estrogen
Calcitonin
RANKL inhibitors

NeuroEndocrine 3 (17 decks)

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