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The Endocrine System > Calcium Homeostasis and Disorders of Metabolism > Flashcards

Calcium Homeostasis and Disorders of Metabolism Flashcards

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1
Q

In which 3 ways can serum calcium be increased?

A
  1. Gut absorption
  2. Bone resorption
  3. Kidney reabsorption
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2
Q

Which receptor will serum calcium act on in order to self regulate its level?

A

Calcium sensing receptor (CaSR)

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3
Q

Stimulation of the CaSR will inhibit production of which hormone?

A

Parathyroid hormone (PTH)

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4
Q

What is the overall action of parathyroid hormone?

A

Increase serum calcium

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5
Q

In which 3 key ways does PTH increase serum calcium?

A
  1. Resorption of bone
  2. Reabsorption by the kidneys
  3. Absorption from the gut
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6
Q

Which vitamin is useful in calcium homeostasis?

A

Vitamin D3

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7
Q

What roles does vitamin D3 have on calcium homestasis?

A
  1. Increases calcium uptake from the gut
  2. Increases bone mineralisation (also increases resorption)
  3. Potentially reduces PTH activity
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8
Q

In which ways will hypercalcaemia acutely present?

A
  1. Thirst
  2. Dehydration
  3. Confusion
  4. Polyuria
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9
Q

In which ways will hypercalcaemia acutely present?

A
  1. Myopathy
  2. Osteopenia
  3. Fractures
  4. Depression
  5. Hypertension
  6. Abdominal pain (pancreatitis, ulcers, renal stones)

Stones, groans, bones and psychic moans

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10
Q

What is the most important test to do in someone with suspected hypercalcaemia?

A

PTH

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11
Q

If a patient has hypercalcaemia and high albumin, what will urea levels be like in the following circumstances?

a) Dehydration
b) Cuffed sample

A

a) Raised urea
b) Normal urea

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12
Q

If a patient has hypercalcaemia and normal/low albumin what are the 3 main things to consider?

A
  1. Familial hypocalciuric hypercalcemia (FHH)
  2. Primary/tertiary hyperparathyroidism
  3. Bone pathology
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13
Q

How may a bone pathology be differentiated from either FHH or primary/tertiary hyperparathyroidism in a patient with hypercalcaemia and low/normal albumin?

A

PTH (and phosphate) levels

(PTH is low and phosphate is high in such patients with bone pathology)

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14
Q

If a patient has primary/tertiary hyperparathyroidism or FHH, what levels are both phosphates and PTH expected to be?

A

PTH - Normal/high

Phosphates - Normal/low

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15
Q

How may primary/tertiary hyperparathyroidsm and FHH be differentiated biochemically?

A
  1. Primary/tertiary hyperparathyroidsm - High urine Ca2+
  2. Familial hypocalciuric hypercalcemia - Low urine Ca2+

(Both conditions have hypercalcaemia, normal/low albumin, normal/high PTH and normal/low phosphates)

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16
Q

What are the key biochemical markers which suggest a general bone pathology as the cause of hypercalcaemia?

A
  1. Hypercacaemia
  2. Normal/low albumin
  3. Low PTH
  4. High phosphates
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17
Q

When considering a bone pathology as the cause of hypercalcaemia, what 3 things would a high ALP suggest as the cause?

A
  1. Bone metastasis
  2. Sarcoidosis
  3. Thyrotoxicosis
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18
Q

When considering a bone pathology as the cause of hypercalcaemia, what 3 things would a low ALP suggest as the cause?

A
  1. Myeloma
  2. Vitamin D excess
  3. Milk-alkali syndrome
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19
Q

What causes milk-alkali syndrome?

A
  1. Excess dietary milk or alkali (e.g. dyspepsia)
  2. Excess calcium supplementation (e.g. in post-menopausal women)
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20
Q

What are the main causes for hypercalcaemia?

A
  1. Primary hyperparathyroidism
  2. Malignancy
  3. Drugs - vitamin D, thiazides
  4. Granulomatous disease - sarcoidosis, TB
  5. Familial hypocalcuric hypercalcaemia
  6. Tertiary hyperparathyroidism
  7. High calcium turnover - bedridden, thyrotoxic, Paget’s etc
  8. Dehydration
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21
Q

Primary hyperparathyroidsm has which 3 key biochemical abnormalities?

A
  1. Raised serum calcium
  2. Raised (or inappropriately normal) serum PTH
  3. Increased urine calcium excretion

(such abnormalities would also present with tertiary hyperparathyroidsm)

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22
Q

In which 3 main ways can malignancies induce hypercalcaemia?

A
  1. Parathyroid hormone release protein (PTHrp) release
  2. Metastatic bone destruction
  3. Osteoclast activating factors
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23
Q

How is acute hypercalcaemia treated?

A
  1. Fluids 0.9 saline 4-6L in 24hrs
  2. Loop diuretics once rehydrated
  3. Bisphosphonates
  4. Steroids (rarely used, e.g. sarcoidosis)
  5. Salmon calcitonin (rarely used)
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24
Q

How are the parathyroid glands imaged?

A

Sestamibi scintigraphy scan

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25
What are the treatment menthods for primary hyperparathyroidsm?
1. Surgery 2. Cinacalcet
26
How does cinacalet work?
Acts on CaSR as a calcimemetic Calcium levels are negatively regulated
27
What is secondary hyperparathyroidism?
**Excess PTH** secretion in response to **hypocalcaemia** (this is usually as a result of chronic kidney disease leading to excessive calcium loss) **Hyperplasia** of the parathyroid glands is usually implicated
28
Secondary hyperparathyroidism involves: a) High/Low calcium levels b) High/Low PTH levels
a) Low calcium levels b) High PTH levels
29
Which genetic syndromes can result in hyperparathyroidism?
1. MEN 1 and 2 2. Familial hyperparathyroidism
30
What is the reference interval for serum calcium?
2.2-2.6 mmol/L
31
Familial hypocalciuric hypercalcaemia is usually associated with a _____ hypercalcaemia
Familial hypocalciuric hypercalcaemia is usually associated with a **mild** hypercalcaemia
32
Pseudohypercalcaemia is usually associated with people with \_\_\_\_\_\_\_\_\_\_\_
Pseudohypercalcaemia is usually associated with people with **dehydration**
33
Why does pseudohypercalcaemia occur?
1. Increased serum albumin 2. Increased calcium required to bind to albumin 3. Free serum levels remain roughly the same due to increased production (this occurs in **dehydration** as albumin becomes more concentrated)
34
Why is calcium useful at normal levels in relation to nerve cells?
It helps to stabilise the resting potential preventing sodium influx
35
What symptoms may hypercalcaemia cause related to nerve cells and why?
1. Slower or absent reflexes 2. Slow muscle contraction (constipation, generalised muscle weakness) High extracellular calcium makes sodium channels in nerve cells **less likely** to open so depolarisation does not occur as easily
36
What are the two key effects of hypercalciuria?
1. Deydration (water excreted with calcium) 2. Kidney stones (calcium oxalate kidney stones - dehydration + hypercalciuria)
37
How does hypercalcaemia affect a ECG?
1. AV block 2. Bradycardia 3. Short QT interval 4. Osborn "J" waves
38
Why are loop diuretics useful for the treatment of hypercalcaemia but thiazide diuretics can cause or worsen the condition?
Thiazide diuretics promote calcium reabsorption Loop diuretics prevent calcium reabsorption in the loop of Henle - so then it can be excreted
39
What are the main symptoms and signs of hypocalcaemia?
1. Paresthesia (fingers, toes and perioral regions) 2. Muscle cramps (tetany) 3. Muscle weakness 4. Fatigue 5. Broncho/laryngospasm 6. Fits
40
Which two clinical signs suggest hypocalcaemia?
1. Chvostek's sign 2. Trousseau sign
41
Describe Chvostek's sign
Twitching of facial muscles on ipsilateral side after tapping over facial nerve
42
Describe Trousseau's sign
Carpopedal spasm induced by inflating a blood pressure cuff over systolic values for 3 minutes
43
What ECG change is seen with hypocalcaemia?
Long QT interval
44
What are the main causes for hypocalcaemia?
1. Hypoparathyroidism 2. Vitamin D deficiency (osteomalacia or Rickets) 3. Chronic renal failure
45
What are the key causes of hypoparathyroidism?
1. Congenital absence of parathyroid glands (DiGeorge syndrome) 2. Destruction or removal of glands 3. Autoimmune conditions 4. Hypomagnesaemia (required for PTH synthesis) 5. Idiopathic 6. Low vitamin D
46
How can acute hypocalcaemia treated?
IV calcium gluconate 10ml of 10% over 10 minutes
47
How can hypocalcaemia be treated long term?
1. Calcium supplements 2. Vitamin D supplements
48
What are the key causes of hypomagnesaemia?
1. Alcohol 2. Thiazide diuretics, PPIs 3. GI illness 4. Pancreatitis 5. Malabsorption
49
In pseudohypoparathyroidism there are low _______ levels yet elevated ________ levels
In pseudohypoparathyroidism there are low **calcium** levels yet elevated **PTH** levels
50
Why does pseudohypoparathyroidism occur?
Genetic defect (GNAS 1) (PTH resistance due to dysfunctional G protein alpha subunit)
51
What is pseudo-pseudohypoparathyroidism?
Pseudohypoparathyroidism, yet with normal calcium levels (patients can change from both conditions)
52
Osteomalcia and Rickets disease can both be caused by what?
1. Dietary calcium or vitamin D deficiency 2. Malabsorption 3. Chronic renal failure 4. Lack of sunlight 5. Drugs (e.g. anticonvulsants)
53
How does osteomalacia clinically present?
1. Low calcium 2. Muscle wastign and proximal myopathy 3. Dental defects - caries and enamel problems 4. Bone tenderness, fractures and deformities
54
What are Loosers zones?
Deficiency fractures Associated with osteomalacia or Rickets Transverse lucenies than travel partway through bone usually at right angles
55
Why does chronic kidney disease cause secondary hypoparathyroidism?
There is a vitamin D deficiency (cannot be metabolised by kindneys to active form)
56
What is vitamin D resistant Rickets?
X-linked hypophosphataemia
57
Which mutations may induce X-linked hypophosphataemia?
PHEX or FGF23
58
What is bone comprised of?
1. Collagen (mainly type 1) 2. Calcium phosphate (hydroxyapatite)
59
How much of the body's calcium is held in the following locations? ## Footnote a) Skeleton b) Extracellularly c) Intracellularly
a) 99% b) 0.99% c) 0.01%
60
In which two forms does extracellular calcium come in?
Free and bound
61
The regulation of serum calcium levels is brought about in which three main ways?
1. Parathyroid hormone 2. Calcitonin 3. Vitamin D
62
Which effects does parathyroid hormone have on calcium and phosphate levels and kidney function?
1. Calcium levels increase 2. Phosphate levels decrease 3. Vitamin D activation is promotoed in the kidney
63
Parathyroid hormone increases ________ activity in bones
Parathyroid hormone increases **osteoclastic** activity in bones
64
What effects does vitamin D have regarding calcium homeostasis?
1. Increased serum calcium 2. Increased serum phosphate 3. Bone resorption increased
65
When is calcitonin released?
Severe hypercalcaemia
66
How does calcitonin lower serum calcium?
1. Inhibits osteoclasts 2. Decreases calcium and phosphate absorption from intestines 3. Decreases calcium reabsorption from kidneys 4. Serum calcium is moved to bone
67
Why does serve hypocalcaemia sometimes cause asphyxiation?
There is unreleived contraction of respiratory muscles
68
Why is there increased risk of fractures and osteoporosis in patients with hyperparathyroidism?
Increased PTH causes an increase in serum calcium and a **decrease in skeletal calcium** (and phosphates)
69
What are the three main subdivisions of hyperparathyroidism?
1. Primary 2. Secondary 3. Tertiary
70
Describe primary hyperparathyroidism
Due to overactive thyroid * Increased PTH * Increased serum calcium
71
Describe secondary hyperparathyroidism
A physiological response to low calcium * Increased PTH * Decreased serum calcium
72
Describe tertiary hyperparathyroidism
Autonomous parathyroid after mnay years of secondary * Increased PTH * Increased serum calcium
73
What is the recommendation for all patients with primary hyperparathyroidism?
High fluid intake Avoid foods high in calcium and vitamin D
74
What causes hypoparathyroidism?
A lack of cells in the parathyroid gland producing PTH
75
What are the two subdivisions of hypoparathyroidism?
1. Genetic (e.g. DiGeorge syndrome) 2. Acquired (e.g. autoimmune, malignancy)
76
What will serum calcium, PTH and phosphates appear like in hypoparathyroidism?
1. Decreased calcium 2. Decreased PTH 3. Increased phosphates
77
Why is there increased incidence of fractures in patients with hypocalcaemia despite increased calcium deposition within the bones?
There are abnormalities in bone remodelling
78
Pseudohypoparathyroidism develops for which reason?
Resistance to PTH due to a genetic abnormality in the receptor
79
What will serum calcium, PTH and phosphate appear like in pseudohypoparathyroidism?
1. Decreased calcium 2. Increased PTH 3. Increased phosphate
80
What are the key complications of pseudohypoparathyroidism?
1. Subcutaneous calcification 2. Mental retardation 3. Blunting of 4th metacarpal (brachydactyly) 4. Obesity 5. Bone abnormalities
81
For which reasons may vitamin D deficiency develop?
1. Lack of sunlight absorption 2. Lack of absorption (poor diet or malabsorption e.g. Coeliac) 3. Problems with activation in kidney or liver
82
Decreased vitamin D caused a decreased absorption of what from the intestines?
Calcium and phosphates
83
Why does a lack of vitamin D induce bone resorption and decreased bone mineralisation?
Decreased calcium absorption from the intestine causes **increased PTH** secretion to compensate
84
Rickets is a condition affecting __________ that is induced due to a deficiency in \_\_\_\_\_\_\_\_\_\_\_
Rickets is a condition affecting **children** that is induced due to a deficiency in **vitamin D**
85
Why do children with Rickets present with genu varum?
Body weight causes bending of soft bones
86
What is the condition involving soft skull bones associated with Rickets called?
Craniotabes
87
Which condition is similar to Rickets yet occurs in adults?
Osteomalacia
88
Osteomalacia will often present with ______ and ________ tenderness, __________ fractures, yet rarely bone \_\_\_\_\_\_\_\_\_\_\_
Osteomalacia will often present with **bone** and **muscle** tenderness, **pathological** fractures, yet rarely bone **deformities**

The Endocrine System (35 decks)

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