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Y1 LCRS Endocrinology > 13 Role of Calcium Ions > Flashcards

13 Role of Calcium Ions Flashcards

1
Q

Q: How do we get the calcium we need? Abundance in body? What form of calcium is active?

A

A: diet should meet all Ca requirements (or supplements can be used)

Calcium is the most abundant metal in the human body (fifth most abundant element)

Only the free (unbound) Ca2+ is bioactive (in blood)

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2
Q

Q: What are the 3 forms of calcium found in blood? Include percentage and quantity. What is the total quantity? Which type does the homeostatic system respond to?

A

A: TOTAL BLOOD [Ca2+] ~2.5 mM

50% UNBOUND*** (IONIZED) ~1.25 mM

45% BOUND TO PLASMA PROTEINS ~ 1.13 mM

5% AS SOLUBLE SALTS (e.g. citrate, lactate) ~0.13mM

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3
Q

Q: Which 4 components are the main calcium handling parts of the body? Draw a diagram to represent.

A

A: REFER

gastro intestinal tract:

  • intake= ~1000mg/24h (we don’t need all of it usually)
  • faeces ~850mg/24h

->LARGER ARROW to blood
LARGE ARROW to kidneys

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4
Q

Q: What increases [Ca2+] in blood? (2) What decreases it?

A

A: [Ca2+] INCREASED BY:
- PARATHYROID HORMONE (PTH)
- active vitamin D3:
1,25 (OH)2 VITAMIN D3 (DIHYDROXY- CHOLECALCIFEROL, or CALCITRIOL)

[Ca2+] DECREASED BY:
- CALCITONIN hormone

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5
Q

Q: How are calcium levels in the blood detected? where? describe.

Specific to parathyroid gland?

A

A: calcium sensing receptors- found all over body

G protein coupled cell surface receptors

main role in parathyroid gland is to detect how much Ca is present-> can change how much PTH is released

won’t release much PTH if normal levels of Ca are detected but if levels drop= no longer bind to calcium sensing receptor = get large PTH release

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6
Q

Q: How is PTH originally made? What is the size of PTH and what type of hormone is it? What does it bind to? How does it act? (2)

A

A: Initially synthesized as protein pre-proPTH

PTH is a polypeptide of 84 aas (peptide H)

transmembrane G-protein linked receptors

Activation of adenyl cyclase, but also phospholipase C (PLC) - second intracellular messenger systems

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7
Q

Q: Which organs are affected by PTH? (3) How? Show on diagram. What’s the main target?

A

A: direct effect on bone***:

  • osteoclasts stimulated (break down)
  • osteoblasts inhibited (build up)
  • increased bone resorption (bone loss is favoured to supplement circulating levels)

direct effect on kidney:
-Increased Ca2+ reabsorption
-Increased PO43- excretion
-Stimulates 1a hydroxylase activity => Increased
1,25 (OH)2D3 synthesis (active vitamin D3)

1,25 (OH)2D3
synthesis (active vitamin D3) from kidneys stimulates SI

indirect effect on small intestine:

  • Increased Ca2+ absorption
  • Increased PO43- absorption (some degree)
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8
Q

Q: What are the actions of PTH?

A

A: direct effect on kidney:

  • Increased Ca2+ reabsorption
  • Increased PO43- excretion
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9
Q

Q: Summarise the effect of PTH on blood [Ca2+].

A

A: REFER

bone:
-increased Ca2+ mobilisation

kidneys:

  • Increased Ca2+ reabsorption (increased PO43-
    excretion) (-1,25 (OH)2D3)

1,25 (OH)2D3 stimulate small intestine
-Increased Ca2+ (and PO43- ) absorption

ALL = BLOOD increased [Ca2+]

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10
Q

Q: Draw a diagram showing the regulation of PTH. (6)

A

A: REFER

decreased plasma [Ca2+]
+
catecholamines from NS stimulate adrenergic receptors of the parathyroid glands (beta receptors)

=> increase parathyroid production of PTH

=> increase plasma [Ca2+’ concentration
+
synthesis of 1,25 (OH)2D3

negative feedback:

  • increased Ca back to para glands
  • activated vit D3 to para glands
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11
Q

Q: Describe the production of activated vitamin D3. Alternative names?

A

A: gain of vitamin d3/cholecalciferol from:

  • diet
  • in skin: UV acting on 7-dehydroCHOLESTEROL

25 HYDROXY-CHOLECALCIFEROL (25(OH)D3) synthesized in LIVER and stored in this form

action of 1a-hydroxylase (stimulated by PTH)

=> 1,25 DI-HYDROXY-CHOLECALCIFEROL (1,25(OH)2D3) synthesized in KIDNEYS = main BIOACTIVE form
(also known as CALCITRIOL)

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12
Q

Q: What are the actions of 1,25(OH)2D3?

A

A: direct effect on small intestine:

  • increased Ca2+ absorption (major action)
  • Increased PO4[3-] absorption

Ca2+ absorbed goes to bone= stored

small effect of 1,25(OH)2D3= on bone = increase osteoblast activity

small effect of 1,25(OH)2D3 on kidneys = Increased Ca2+ and PO43- reabsorption

Ca2+ reabsorbed goes to bone

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13
Q

Q: How does 1,25(OH)2D3 act on the small intestine? No binding protein?

A

A: causes calcium to enter enterocytes via transporter for them to be bound to binding proteins (1,25(OH)2D3 also increases activity of binding proteins)

binding protein- calcium complex enters blood via different transporters

without binding protein- could act as secondary signaller= not wanted

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14
Q

Q: What is fibroblast growth factor 23 involved in? In response to? Released from?

A

A: regulating phosphate- mainly stops PO4 reabsorption

high phosphate

bone osteocytes

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15
Q

Q: Draw a diagram showing phosphate reabsorption.

A

A: REFER- cell= eg kidney

Na+/PO4[3-] enters cell from lumen via Na+/PO4[3-] co transporter

PTH from blood enters cell and causes negative effect on co transporter

FGF23 does same (down regulates transporter)

calcitriol (activated vit D3) causes positive effect on FGF23 but vice versa= negative

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16
Q

Q: How is calcitonin synthesised? Size? What does it bind to? Actions? (2) What happens without it?

A

A: Synthesized as pre-procalcitonin

Calcitonin is 32 aa polypeptide

Binds to transmembrane G-protein linked receptor

Activation of adenyl cyclase or PLC as second messenger systems

can live

17
Q

Q: Draw a diagram showing calcitonin actions and regulation. (7)

A

A: REFER

increased plasma [Ca2+]
+
gastrin

promote parafollicular cells of thyroid to produce calcitonin

  1. bone: inhibits osteoclast activity
  2. kidneys: increased urinary excretion of Ca2+ (Na+, PO4[3-])

=> cause decreased plasma [Ca2+] (limited effect)

18
Q

Q: Name 3 endocrine causes of hypocalcaemia. Which is most common?

A

A: HYPOPARATHYROIDISM*** = not enough PTH produced

PSEUDOHYPOPARATHYROIDISM= inefficient PTH signalling although it is made- due to target organ resistance

VITAMIN D DEFICIENCY

19
Q

Q: Name and describe 2 symptoms of hypocalcaemia. What are they both?

A

A: tetany= condition marked by intermittent muscular spasms, caused by malfunction of the parathyroid glands and a consequent deficiency of calcium.

  • Trousseau’s sign (main d’accoucheur)= hand won’t relax
    <= increase pressure of inflation cuff to exaggerate effect of low Ca on muscle contractions
  • Chvostek’s sign
    <= hit nerves on side of head and get particular twitch
20
Q

Q: Name 3 causes of hypoparathyroidism.

A

A: IDIOPATHIC

HYPOMAGNESAEMIA= if you sense low magnesium levels -> body also correlates to high Ca levels -> PTH levels are suppressed

(SUPPRESSION BY RAISED PLASMA CALCIUM CONCENTRATION)= part of normal negative feedback

21
Q

Q: What is pseudohypoparathyroidism also known as? What is it? Cause? Summarise.

A

A: ALLBRIGHT HEREDITARY OSTEODYSTROPHY

-target organ resistance to PTH (multiple underlying causes).

Believed due to defective Gs protein (needed to increase cAMP intracellularly in response to PTH receptor activation)

cells don’t respond to PTH

22
Q

Q: Describe 4 features of pseudohypoparathyroidism.

A

A: - particular physical appearance (short stature, round face)

  • low IQ
  • subcutaneous calcification and various bone abnormalities (e.g. shortening of metacarpals)
  • associated endocrine disorders (e.g. hypothyroidism, hypogonadism)
23
Q

Q: What does vitamin D deficiency cause in children? adults? Clinical feature? resulting in? Children? Adults?

A

A: Rickets in children
Osteomalacia in adults

Clinical feature is the decreased calcification of bone matrix resulting in softening of bone

bowing of bones in children
adults= prone to fractures

24
Q

Q: Differential diagnosis. Complete table:

top:
plasma Ca | plasma PO4 | PTH

side:
HYPOPARATHYROIDISM
-
PSEUDO-HYPOPARATHYROIDISM
-
VITAMIN D DEFICIENCY
A

A: down up down
down up up
down down up

25
Q

Q: Name 3 endocrine causes of hyperglycaemia.

A

A: PRIMARY HYPERPARATHYROIDISM

TERTIARY HYPERPARATHYROIDISM

VITAMIN D TOXICOSIS

26
Q

Q: Describe the 3 types of hyperparathyroidism. Include cause, pathway and name. What is hyperparathyroidism?

A

A: PRIMARY HYPERPARATHYROIDISM

  • cause= adenoma
  • parathyroids-> increased PTH-> increased [Ca2+]
  • no negative feedback when Ca levels increase (adenoma is immune to it)

SECONDARY HYPERPARATHYROIDISM

  • cause= Low plasma [Ca] e.g. renal failure
  • parathyroids-> increased PTH-> unchanged [Ca2+] (target areas are not responding well)
  • body makes more PTH to try and get Ca high

TERTIARY HYPERPARATHYROIDISM

  • cause= Initial chronic low plasma [Ca]
  • parathyroids (autonomous)-> increased PTH-> increased [Ca2+]
  • no negative feedback when Ca levels increase

make too much PTH

27
Q

Q: Describe the mechanism of tertiary hyperparathyroidism. (3)

A

A: para thyroid glands are using to making lots of PTH to try and restore the initial chronic low [Ca2+] -> takes a long time to get Ca levels to where they need to be

eventually becomes autonomous -> even if corrected eg vit D3 supplements taken and Ca levels restored

get broken feedback
-so even when Ca levels are restored you get more PTH produced

28
Q

Q: What are the effects of excess PTH on the kidneys? (6)

A

A: parathormone

  • increased Ca reabsorption
  • increased PO4 excretion
  • Polyuria
  • Renal stones
  • Nephrocalcinosis
  • increased 1,25(OH)2D3 synthesis in kidneys
29
Q

Q: What are the effects of excess PTH on the gastrointestinal tract? (2)

A

A: -increased Gastric acid (can lead to.. below)

-Duodenal ulcers

30
Q

Q: What are the effects of excess PTH on bone? (5)

A

A: - decreased bone density

  • Bone lesions
  • Bone rarefaction
  • Fractures
  • promoting bone turnover (breakdown and liberation of Ca)
31
Q

Q: Give 2 symptoms of primary hyperparathyroidism

A

A: clubbing of fingers

Marked periosteal bone erosion in the terminal phalanges

Y1 LCRS Endocrinology (19 decks)

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