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Metabolic endocrinology > Ca metabolism > Flashcards

Ca metabolism Flashcards

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1
Q

Is there a circadian rhytms for thyroid hormone

A

We have confirmed that in humans there is a circadian rhythm of TSH with a peak level occurring at around 02:40 h and levels remaining above the mesor from 20:20–08:20 h

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2
Q

How regulation of calcium with PTH/D3 occurs

A
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3
Q

Regulation of calcium via calcitonin

A
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4
Q

Do we know the role of calcitonin

A

No, uncertain

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5
Q

What are remedies for rickets

A

Fish liver oil

Sun exposure

UV-irradiation of certain foods

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6
Q

Roles of Ca

A
  • v Major structural component of the skeleton
  • Blood clotting (cross-linking of fibrin)
  • Regulation of enzyme activities (induction of conformational changes or co-factor)
  • “Second messenger” of hormones signals .Release from endoplasmic reticulum
  • Membrane excitability

v Secretion of hormone/neurotransmitters
v Action potential

  • Muscle contraction

v Triggered by the release of Ca++ from the
sarcoplasmic reticulum.

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7
Q

Where the most Ca is found and how extracellular Ca can be regulated

A

Extracellular and
Intracellular Ca++
levels are tightly
regulated

Skeleton 99%

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8
Q

Disequilibrium between bound and unbound
Ca++ causes ___

A

tetany

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9
Q

what is alkalosis

A

Hyperventilation
reduces the partial
pressure of CO2. Less
H2CO3 is produced and
H+ falls → alkalosis

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10
Q

How hyperventilation and tetany are connected

A

v Hyperventilation
reduces the partial
pressure of CO2. Less
H2CO3 is produced and
H+ falls → alkalosis
v To compensate H+ is
released from serum
proteins. The negatively
charged protein binds
Ca++

Reduction in free serum Ca++ → tetany (spasm of skeletal muscle)
v similarly, blood transfusions in which citrate is the anti-coagulant can
cause tetany (due to Citrate chelating Ca++)

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11
Q

How many thyroid glands are there

A

4

Can be 5 th in 15% of people

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12
Q

What cells produce PTH and when PTH is release

A

v Chief cells (and oxyphil cells)
produce Parathyroid Hormone
(PTH)
v PTH is released in response to
low levels of ionized Ca in ECF

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13
Q

Calcitonin action

A

Reduces serum Ca

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14
Q

Half life for PTH, how it is cleaved

A

v Highly conserved
v Short half-life
v 2-4 min
v Cleaved into two
fragments (amino and
carboxy terminus)

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15
Q

How chief cells react on Ca concentration in the blood

A

calcium sensing receptor (CaR) located on Chief
cell membrane of chief cells detect ECF Ca++

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16
Q

Ca receptros are ___ receptros and couple with

A

Ca receptors on the parathyroid
cells
vSeven-transmembrane domain
receptor
v Coupled with G-protein complex
vHighly conserved

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17
Q

What happens to parathyroid cells with Ca concentration alteration

A

v Concentration- dependent
conformation alteration

vHigh Ca concentrations –
Decreased cAMP and increased IP3
vLow Ca concentrations – Increased
cAMP and decreased IP3

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18
Q

v PTH functions to
regulate calcium
levels via its actions
on three target
organs___

A

– the bone,
kidney, and gut.

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19
Q

How PTH influences bones

A

PTH increases the
resorption of bone
by stimulating
osteoclasts and
promotes the
release of calcium
and phosphate into
the circulation.

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20
Q

Mineral content of bones

A

v 99% of total Ca+2
v 90% of total PO4-3
v 50% of total Mg+2

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21
Q

Cells in bone

A

v Osteoprogenitor cells
v Osteoblasts
v Osteocytes
v Osteoclasts

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22
Q

Organic matrix of bone: composition

A

v Collagen (90-95%)
v Proteoglycans
v Glycoproteins
v Lipids

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23
Q

Osteobalsts function

A

v1mg of osteocalcin
binds 17 mg of
hydroxyapatite
vSerum level is indicator
of bone growth.

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24
Q

Osteonectin function

A

vBinds collagen and
hydroxyapatite
vMay serve as nucleator
for calcium deposition
in the bone.

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25
structure of bone
26
Describe osteoblast differentiation
27
Bone formation process describe
28
Turn-over Ca2+ in bone is \_\_\_per year in infants and 18% in adults
100%
29
Bone remodelling is performed by
Carried out by bone modeling units: osteoclasts dissolve bone followed by osteoblasts that lay down new bone
30
Factors regulating remodeling
Mechanical factors v Hormonal factors induced by PTH v Paracrine factors (i.e. IGF-II produced by osteoblasts) may act on neighboring osteoblasts and osteoclasts
31
Osteoclasts are derived from
``` from monocytes (Bone marrow, gives rise to macrophages). ```
32
How ostoclasts are attached to bone
via integrins and form tight seal
33
How osteoclast reach acid pH
Proton pumps (H+ dependent ATPases) move from endosomes to the cell membrane where they pump out H+ v Acid pH (~ 4.0) dissolves hydroxyapaptite; acid proteases break down collagen
34
What pyridinoline indicates
(collagen breakdown product) in urine is an index of bone resorption activity
35
How many nuclei are there in osteoclasts
Multiple
36
Why osteoclasts are tightly bound to bone matrix
Permitting acid from ruffled apical membrane to resort the bone
37
Bone remodelling and its hormonal control
38
What inhibits osteoclast activity
Calcitonin
39
What stimulates osteoblast activity
PTH, calcitriol, PGE2 (prostaglandin E) act on osteoblast to produce osteoclast-activating factors that stimulate resoprtion by osteoclast
40
How PTH influencec renal system
PTH also increases renal reabsorption of Ca from 33 urine and inhibits reabsorption of phosphate
41
What is the difference between PTH and PTHrP
Parathyroid Related Protein (PTHrP) similar structure to PTH and can bind to PTH receptor but produced by many tissues in fetus and adult
42
Function for PTHrP
required for normal development as a regulator of the proliferation and mineralization of chondrocytes and regulator of placental Ca++ transport usually acts in paracrine fashion but overexpression by tumour cells can produce severe hypercalcemia by activating PTH receptor
43
How many receptors for PTH and can PTHrP bind to it
2 G protein coupled receptors for PTH PTHR-1 binds PTH and PTHrP with equal affinity PTHR-2 binds only PTH receptors have different tissue distributions PTHR-1 is located in bone and kidney tissues
44
What is oteopetrosis
vOsteopetrosis: “marble bone” vIncrease in bone density due to defective osteoclasts – bones become more brittle and are prone to fracture
45
Osteoporosis is
``` vExcess osteoclast function vFrequent fractures (areas with trabecular bone: distal forearm, vertebral body, hip) ```
46
What is involutional osteoporosis
vLoss of bone density with age
47
Do women has an increased bone loss?
48
How estrogen downregulates osteoclast activity and what happens with menopause and can estrogen therapy help with it
49
What is primary hyperthyroidism
Primary hyperparathyroidism is characterized by increased parathyroid cell proliferation and PTH secretion which is independent of calcium levels. Etiology unknown, but radiation exposure, and lithium implicated, associated with loss of tumor suppressor genes (MENIN) MEN1 and MEN 2A Enlargement of a single gland or parathyroid adenoma in approximately 80% of cases, multiple adenomas or hyperplasia in 15 to 20% of patients and parathyroid carcinoma in 1% of patients
50
Signs and symptoms of primary hyperparathyroidism
51
Hypoparathyroidism may originate from Problems with PTH may arise from
-failure to secrete PTH, v altered responsiveness to PTH, Vit. D deficiency or v a resistance to Vit. D problems with PTH may arise from: v surgery v familial causes v autoimmune disorders v idiopathic causes
52
Major clinical symptoms of hypothyroidism and treatment
major clinical symptom is increased neuromuscular excitability (tetany) treatment: Calcium + Vitamin D
53
Treatment for hypercalcaemia
calcitonin
54
Is calcitonin physiologically important?
Overproduction of calcitonin (tumors of the parafollicular cells of the thyroid) → no phenotypic consequences v Thyroidectomy → no phenotypic consequences
55
Is there only one calcitonin
From the same gene as calcitonin neuronal cells can produce calcitonin gene related protein may act as a neurotransmitter v CGRP also acts as very potent vasodilator via GPCR receptor
56
Vitamin D defects leads to
vDeficiency leads to bone defects and the disease “rickets”, which causes bone deformations and loss of calcium and phosphate from the bones
57
How vitamin D can be formed from the skin
vVitamin D can be formed in the skin from 7-dehydrocholesterol in a photochemical reaction requiring sunlight. vVitamin D is converted in the liver and kidney to a hormone that regulates calcium uptake.
58
How vitamin D is synthesized ( the form that is added to food)
Vitamin D2 is a pharmaceutical product made by irradiating ergosterol (present in some plants). Used in food fortification such as margarine and milk
59
what are the main circulating derivatives of vitamin D
Main circulating derivatives are 25-OHcholecalciferol (made in the liver; 3-30 ng/ml) and calcitriol (made in the kidney; 20-60 pg/ml)
60
Vitamin D binding protein binds what type of protein
Vitamin D binding protein present in the serum binds 25-OH-cholecalciferol and to a lesser extent calcitriol
61
All physiological effects appear to be due to what form of vitamin D
calcitriol
62
Calcitriol: where is the receptor and what is the function
63
How vitamin D promotes Ca absorption
Calcitriol promotes active Ca2+ uptake in the intestine by maintaining a Ca2+ gradient v Uptake of calcium→binding to myosin/calmodulin complex→ move to the bottom of the microvilli driven by differential binding to proteins → free Ca2+ in cytoplasm is released by exocytosis or pumps v Calcitriol induces synthesis of the calbindin protein→ binds Ca2+→ maintenance of the Ca2+ gradient by mopping up all the free at the bottom of the microvilli.
64
Interaction of PTH and vitamin D in controlling plasma calcium
65
How can you get vitamin D deficiency and what diseases will occur
vinadequate sunlight, nutrition or malabsorption (up to 50-60 % of elderly expecially if institutionalized) vcause abnormal mineralization of bone and cartilage vRickets (children) vOsteomalacia (adults)
66
How vitamin D toxicity can occur, symptoms and treatment
Overdose either therapeutically or accidently Symptoms: weakness, lethargy, headaches, nausea, polyureia due to hypercalcemia and hypercalciuria – may lead to ectopic calcification etc. (kidneys, blood vessels, heart, lungs, skin) with chronic overuse v Treatment: reduced calcium intake and (Vit. D), rehydration and cortisol (antagonizes action of Vit. D on gut absorption of calcium) + time (slowly cleared from the body)

Metabolic endocrinology (9 decks)

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