Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > Calcium dysregulation > Flashcards

Calcium dysregulation Flashcards

1
Q

What hormones control serum calcium?

A

Increase:
-Vit D
-Parathyroid hormone (PTH)

Decrease:
-Calcitonin

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

How is Vitamin D metabolised?

A

-Vit D3 (inactive) comes from sunlight and from the Vit D2 from our diet
- Vit D3 is first hyroxylated in the liver via the enzyme 25-hydroxylase to form 25(OH)cholecalciferol
- 25(OH)cholecalciferol is then hydroxylated in the kidney via the enzyme 1 alpha-hydroxylase to form 1,25(OH)2 cholecalciferol (ACTIVE VIT D= CALCITRIOL)
-There is a neg feedback loop- calcitriol decreases transcription of 1 alpha-hydroxylase

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

What are the effects of calcitriol on the kidney?

A

-Increases calcium reabsorption
-Increases phosphate reabsorption

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

What are the effects of calcitriol on the small intestine?

A
  • Increases phosphate absorption
  • Increases calcium absorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the effects of calcitriol on the bones?

A

-Increased osteoblast activity

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

What are the effects of PTH on the kidenys?

A

Increased Ca2+ reabsorption
Increased phosphate excretion
Increased 1-a-hydroxylase activity
(Which leads to an increase in 1,25 (OH)2D3/ calcitriol synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the effects of PTH on the intestines?

A

-Increases calcium absorption
-Increases phosphate absorption

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

What are the effects of PTH on the bones?

A

-Increased calcium reabsorption from bone- stimulates osteoclast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What effect does FGF23 have?

A

“Regulates serum phosphate”
1. FGF23 inhibits the sodium phosphate co transporter present on epithelia of proximal tubule
2. Less reabsorption of phosphate
3. Lowers serum phosphate
4. Also inhibits calcitriol production (indirectly decreases the phosphate absorbed via this pathway)

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

What are the presentations of hypocalcaemia?

A

Low calcium= sensitises excitable tissues
C: convulsions (seizure)
A: arrhythmias (irregular heart rhythms)
T: tetany (heart contracts but can’t relax- usually v. painful)
s
Go numb: paraesthesia- hands, mouth, feet, lips go numb/ tingly

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

How do we diagnose hypocalcaemia?

A
  1. Chvosteks’ sign – facial paresthesia
  2. Trousseau’s sign – carpopedal (hands) spasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of hypocalcaemia?

A

Low PTH levels = hypoparathyroidism
* Surgical – neck surgery
* Auto-immune
* Magnesium deficiency
* Congenital (agenesis, rare)- born without PTH
Low vitamin D levels
* Deficiency – poor
diet/malabsorption, lack of UV
light, impaired production (renal
failure)

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

What are the presentations of hypercalcaemia?

A

High calcium= Reduced neuronal excitability
“bones, stones, abdominal moans and psychic groans”
Stones – renal effects
* Nephrocalcinosis – kidney stones, renal colic
Abdominal moans - GI effects
* Anorexia, nausea, dyspepsia, constipation, pancreatitis
Psychic groans - CNS effects
* Fatigue, depression, impaired concentration, altered mentation, coma
(usually >3mmol/L)

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

What are the causes of hypercalcaemia?

A
  1. Primary hyperparathyroidism
    * Too much PTH
    * Usually due to a parathyroid gland adenoma
    * No negative feedback - high PTH, but high calcium
  2. Malignancy
    * Bony metastases produce local factors to activate
    osteoclasts
    * Certain cancers (eg squamous cell carcinomas)
    secrete PTH-related peptide that acts at PTH
    receptors
  3. Vitamin D excess (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the relationship between PTH and calcium?

A

As calcium levels fall, PTH increases (to restore this)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 3 types of hyperparathyroidism? What are there causes?

A
  1. Primary (parathyroid adenoma- makes too much PTH)
  2. Secondary (normal physiological response to low calcium)
  3. Tertiary (chronic/prolonged renal failure and chronic/prolonged vit D deficiency)
17
Q

How does primary hyperparathyroidism present?

A
  • Parathyroid adenoma producing too much PTH
  • Calcium increases, but no negative feedback to PTH due to autonomous PTH secretion from parathyroid adenoma
  • High calcium= Low phosphate – increased renal
    phosphate excretion but inhibition of sodium/phosphate co-transporter in kidney; more phosphate loss than reabsorbed
  • High PTH (not suppressed by hypercalcaemia)
    Untreated hyperparathyroidism has risks
    of
  • Osteoporosis
  • Renal calculi (stones)
  • Psychological impact of
    hypercalcaemia – mental function,
    mood
18
Q

How do you treat primary hyperparathyroidism?

A

Parathyroidectomy is treatment of
choice for primary hyperparathyroidism

19
Q

How does secondary hyperparathyroidism present?

A

Secondary hyperparathyroidism is a normal physiological response to hypocalcaemia
* Calcium will be low or low/normal
* PTH will be high (hyperparathyroidism)
secondary to the low calcium
* This is different from primary
hyperparathyroidism where calcium is high

20
Q

The issue of secondary hyperparathyroidism is the low calcium- what causes this?

A

Most common cause of secondary hyperparathyroidism is vitamin D deficiency *Commonly - diet, reduced sunlight
Less common, but important =
renal failure – can’t make calcitriol
in renal failure

21
Q

How do you treat secondary hyperparathyroidism?

A

Vitamin D replacement
* In patients with normal renal function
* Give 25 hydroxy vitamin D
* Patient converts this to 1,25 dihydroxy vitamin
D via 1a hydroxylase
* Ergocalciferol 25 hydroxy vitamin D2
* Cholecalciferol 25 hydroxy vitamin D3
* In patients with renal failure - inadequate 1a
hydroxylation, so can’t activate 25 hydroxy
vitamin D preparations
*Give Alfacalcidol - 1a hydroxycholecalciferol

22
Q

How does tertiary hyperparathyroidism present?

A

RARE
1. Constant low calcium levels caused by:
-chronic/ prolonged renal failure
-chronic/ prolonged vit D deficiency (can’t make calcitriol)
2. PTH increases (hyperparathyroidism)
3. Overtime due to the contant increase in PTH, parathyroid tissues undergo hypertrophy
4. Glands enlarged- hyperplasia- start to do their own thing- autonomous PTH secretion

23
Q

How do you treat tertiary hyperparathyroidism?

A

Treatment is parathyroidectomy

Endocrinology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions