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Endocrine > Calcium levels > Flashcards

Calcium levels Flashcards

1
Q

What is the normal values of total calcium levels?

A

Normal serum or plasma total calcium should be 2.13 to 2.63 mmol/L

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2
Q

What is the definition of ‘Total calcium’ levels?

A

Total calcium is a measurement of the total amount of calcium in the bloodstream.

It includes both the ionized (free, active) calcium and the calcium that is bound to proteins, primarily albumin.

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3
Q

What is the role of calcium bound proteins?

A
  1. Protein-bound calcium is inactive and not readily available for physiological processes.
  2. It is a reservoir for calcium that can be released when needed
  3. Approximately 40-45% of total calcium is bound to proteins, with the majority bound to albumin.
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4
Q

What is the definition of Ionised calcium levels?

A
  1. Ionised calcium measures the concentration of free, biologically active calcium ions in the blood.
  2. These ions are not bound to proteins and are physiologically active
  • onized calcium does not consider the calcium bound to proteins. It measures only the unbound calcium ions.
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5
Q

What is the normal value of ionised calcium levels?

A

1.15 to 1.27 mmol

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6
Q

How is calcium absorbed in the kidneys;
via : Proximal tubule?

A
  1. Via passive diffusion (mostly)
  2. Na+/Ca2+ exchanger
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7
Q

How is calcium absorbed in the kidneys;
via : Thick ascending limb of the distal convulated tubule?

A
  1. Calcium reabsorbtion via passive diffusion 2nd to sodium-K+- Cl-2 contransporter
    * Na/K/Cl cotransporter actively transports Na+/K+/Cl-
    * Resulting in passive calcium reabsorbtion
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8
Q

How is calcium absorbed in the kidneys;
via : Distal conv tubule

A

Regulated via the parathyroid hormone

    • Stimulates the reabsorption of calcium in the DCT
    • Increases the expression of calcium channels in the apical membranes of the tubule cells
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9
Q

How is calcium absorbed in the kidneys;
via : Collecting ducts

A

Enhanced by vitamin D (active calcitriol)
* Enhances calcium reabsorption / facilitates the transport of calcium absorption

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10
Q

What is the most common cause of hypercalcaemia?

A

Primary Hyperparathyroidism
- 85% of cases are due to a single adenoma of one of the parathyroid glands

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11
Q

What are the main causes of hypercalacemia?

A
  1. Excessive bone resorption
    * Hyperparathyroidism - increased osteoclastic bone resorption
    * Thyrotoxicosis - thyroid mediated increase in bone resorption
  2. Malignancy
    - bone involvement via tumor or ectopic PTH secretion
  3. Excess vitamin D
    - stimulates increased intestinal and renal resoption of calcium
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12
Q

Which drugs can cause hypercalcaemia and how?

A
  1. Thiazide diuretics -increase calcium reabsorption in the distal convulated tubules of the kidneys
  2. Lithium - increases renal calcium reabsorption and stimulates PTH secretion
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13
Q

What are clinical features of hypercalcaemia : Renal

A
  1. Renal stones : calcium oxolate stones
  2. Hypercalcuria
  3. Polyuria and Polydipsia
  4. Renal failure
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14
Q

What are clinical features of hypercalcaemia : Neurological

A
  1. Absent reflexes
  2. Lethargy
  3. Confusion, depression, irritability
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15
Q

What are clinical features of hypercalcaemia : GI

A
  1. Constipation
  2. Nausea, vomiting and abdominal pain
  3. Peptic ulcer disease
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16
Q

What are clinical features of hypercalcaemia : CVS

A
  1. Arrythmia e.g. Bradycarda
  2. Shortened QT interval
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17
Q

What are clinical features of hypercalcaemia : MSK

A
  1. Generalised muscle weakness
  2. Bone pain suggests metastases in long bone
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18
Q

Common malignancies that can lead to hypercalcaemia?

A
  1. Multiple myeloma
  2. Leukaemia
  3. Lung cancer
  4. Breast cancer

When malignancies cause hypercalcaemia, the tumor is typically very advanced

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19
Q

What investigations are indicated in hypercalcaemia?

A
  1. serum calcium: elevated
  2. parathyroid hormone: elevated or inappropriately normal despite high calcium.
  3. 24-hour urine calcium : elevated
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20
Q

What is the management of hypercalcaemia?

A
  1. Loop diuretics - inhibit calcium reabsorption
  2. Glucocorticoids - decrease GI calcium absorption
  3. Bisphosphonates or calcitonin - inhibit osteoclasts, prevent bone resorption
  4. Dialysis
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21
Q

What are the causes of hypocalcaemia?

A
  1. Hypoparathyroidism
    Main cause of hypocalcaemia
    * It is often caused by accidental removal of all the parathyroid glands during surgery or radiation-induced parathyroid destruction.
  2. Low Vitamin D - via diet, reduced sun exposure
    * Reduces absorption of calcium from the intestines and kidneys
  3. Hypomagnesaemia
  4. A history of repeated blood transfusions
    * e.g. chronic anaemia, or defects of iron metabolism (e.g., haemochromatosis) or copper metabolism (e.g., Wilson’s disease),
    * suggest an infiltrative process in the parathyroid glands.
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22
Q

How does hypomagnesia cause hypocalcaemia?

A
  • Interferes with the secretion and action of PTH.
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23
Q

What are the causes of hypomagnesaemia?

A

Hypomagnesaemia generally occurs as a;

*primary disorder *
* that is secondary to defects in intestinal absorption and renal absorption

secondary disorder
* due to nutritional deficiency
as seen in patients with chronic alcoholism.

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24
Q

Which drugs cause hypocalcaemia?

A
  1. proton-pump inhibitors
  2. bisphosphonates,
  3. glucocorticoids,
  4. anticonvulsants
25
Q

What are the investigations in hypocalcaemia?

A
  • Serum total calcium concentration & ionised calcium
  • Albumin
  • Magnesium
  • Serum intact parathyroid hormone level.
  • Renal function
  • Alkaline phosphatase
  • 25-hydroxyvitamin D;
  • 24-hour urine calcium and creatinine
  • Amylase and/or lipase levels should be checked in patients with abdominal pain
26
Q

What are the clinical features of hypocalcaemia?

A
  1. Paresthesia
    Chronic numbness and tingling in the fingertips, toes, and perioral region
  2. Abdominal pain + hypocalcaemia Consider acute pancreatitis.
  3. Chronic diarrhoea with steatorrhoea / intestinal disease, e.g. Crohn’s disease or chronic pancreatitis,
    * malabsorption of calcium or vitamin D
27
Q

Which symptoms indicate acute management of hypocalcaemia?

A
  1. cardiac hyperexcitability, tetany, hypotension, seizures, mental confusion, and carpopedal spasms
  2. not necessarily to return the calcium level to normal
28
Q

What is the acute management of hypocalcaemia?

A
  1. IV 10% Calcium gluconate
    (preferred form of intravenous calcium because calcium chloride is more likely to cause local irritation)
  2. Electrocardiographic monitoring is recommended because dysrhythmias can occur if correction is too rapid.
  3. Treatment can be repeated until symptoms have cleared
29
Q

Why is digoxin contraindicated in hypercalcaemia?

A
  1. Risk serious arrhythmias in patients taking digitalis
  2. Hypercalcaemia can worsen digitalis toxicity
  3. Conversely, hypocalcaemia can also nullify the effects of digoxin
  • digoxin may be ineffective until serum calcium is restored to normal.
  1. ECG monitoring during intravenous calcium replacement is warranted in patients receiving digoxin therapy
30
Q

When is parathyroid hormone released?

A

Parathyroid gland, secreted ‘Parathyroid hormone’ - a polypeptide,

  1. in response to low levels of Calcium ions in the blood
  2. Increased Ca2+ levels serve as a negative feedback loop signalling the parathyroid gland to stop the release of PTH.
31
Q

What is the mechanism of action of the parathyroid hormone on the bones?

A

act on PTH receptors on osteoclasts to increase bone breakdown and release of calcium into the blood

32
Q

What are the sources of ‘Vitamin D’

A
  1. Intestine - absorbs precursors such as ergocalciferol and cholecalciferol from dietary sources
  2. Skin - exposure of skin keratinocyte exposure to UV light to produce vitamin D3 production
33
Q

What is the effect of PTH on the kidneys?

A
  1. PTH binds on proximal convoluted tubules —> inhibits sodium-phosphate co-transporter —> reduces sodium phosphate reabsorption —> increases urinary phosphate secretion
  2. PTH binds on receptors on principal cells of dital convoluted tubules —> upregulates sodium/calcium channel —> increases calcium reabsorption Intestines -
  3. PTH promotes vitamin D3 (Cholecalciferol) conversion by up regulating 1-alpha-hydroxylase enzyme which converts 25- hydroxycholecalciferol it to 1,25 - dihydroxycholecalciferol (calcitriol) aka active vitamin D in the proximal convoluted tubule
34
Q

What is the physiology of calcitriol production?

A
  1. Ergocalciferol, Cholecalciferol enters through the intestine
  2. Liver - hepatocytes add 25-hydroxylase
  3. 25-hydroxycholecalciferol produced then re enters blood
  4. Proximal convoluted tubule - 25-hydroxycholecalciferol —> 1-alpha-hydroxylase —> dihydroxycholecalciferol aka active vitamin D aka calcitriol
35
Q

What is the mechanism of action of active vitamin D on the body?

A
  1. Bone - acts synergistically with PTH
    * Osteoclast activity stimulation —> increases calcium concentration in the blood
    • Kidneys - stimulates Ca2+, phosphate reabsorption
    • Intestine - increases calcium and phosphate absorption
36
Q

What is the pathophysiology of hypoparathyroidism?

A
  1. Low PTH release resulting in a lack of action of the PTH to ;
    Reabsorb calcium from the urine
  2. Unable to generate active vitamin D in the kidneys to reabsorb calcium from the bone
  3. Lack of action on the kidneys to excrete phosphate ions
37
Q

What is the main etiology of ‘Hypoparathyroidism;

A

Inadvertent damage during thyroid surgery or intentional parathyroidectomy

38
Q

What are the other causes of hypoparathyroidism?

A
  1. Hypomagnesaemia :Low Mg2+ levels secondary to alcoholism can inhibit PTH release
    - Readily reverses by Mg2+ repletion
  2. Destruction of parathyroid tissues due to Haemochromatosis/Wilson’s disease/Radiation induced damage
39
Q

What are the risk factors of hypoparathyroidism?

A
  1. Hx of Neck surgery
  2. Chronic alcoholism
    - causes renal wasting of Mg2+ leading to hypomagnesaemia
  3. Malnutrition, malabsorption, Diarrhoea
    - Poor Mg2+ absorption
  4. Muscle twitches, spasms and cramps
    - Sx of hypocalcaemia
40
Q

What are the investigation results for hypoparathyroidism?

A
  1. Serum calcium
    - adjusted for albumin or ionised calcium
  2. Plasma intact PTH
  3. Serum albumin
    - low albumin gives a falsely low total serum calcium
  4. Serum magnesium and serum phosphate
  5. ECG
41
Q

What is the acute management of hypocalcaemia?

A
  • IV calcium gluconate with ECG monitoring
  • attaining an albumin-corrected serum total calcium of approximately 2 mmol/L (8 mg/dL) or serum ionised calcium of 1 mmol/L

Aim : acute relief of symptoms

42
Q

What is the management of chronic hypoparathyroidism?

A
  1. Oral calcium
  2. Calcitriol (biologically active form of vitamin D)
43
Q

What is the definition of primary hyperparathyroidism?

A

Autonomous overproduction of parathyroid hormone results in excess calcium metabolism
* Raised PTH
* Raised Calcium
* Low Phosphate

44
Q

What is the pathophysiology of ‘Primary Hyperparathyroidism’

A
  1. Low calcium levels normally stimulates PTH secretion whereas raised Ca2+ suppresses PTH secretion
  2. In Primary Hyper-PTH } PTH secretion is not suppressed by high calcium levels
  3. Excessive PTH leads to over-stimulation of bone resorption, excess production of Vitamin D
  4. Leading to HYPERCALCAEMIA
45
Q

What is the main cause of primary hyperparathyroidism?

A
  1. Single parathyroid adenoma : releases excess PTH hormone
    Accounts for 80% of cases of primary hyperparathyroidism
46
Q

What are the causes of primary hyperparathyroidism?

A
    • Inherited diseases - lead to hyper functioning parathyroid glands.
      * E.g. MEN syndrome
    • Parathyroid malignancies
      * Responsible for <1% of cases
    • External neck radiation
47
Q

Which drug causes hyperparathyroidism?

A

**Lithium therapy **
* Used in Bipolar disorder
* Lead to overstimulation of parathyroid plans by altering feedback inhibition of PTH secretion

48
Q

What is the management of primary hyperparathyroidism?

A
  1. Parathyroidectomy - Indicated in all patients with;
    * Symptomatic hyperparathyroidism
    * Target organ complications such as bone disease (osteoporosis) or renal involvement
  2. Vitamin D supplementation
    Bisphosphonates if osteoporosis is present
49
Q

What is the definition of secondary hyperparathyroidism?

A
  1. Parathyroid gland hyperplasia, excess parathyroid hormone secreted in response to** chronic hypocalcaemia**
  2. Impaired kidney function - kidneys do not filter phosphate properly into urine, make insufficient calcitriol
  • Altered calcium, phosphate levels -> increased parathyroid hormone levels -> bone resorption
50
Q

What is the definition of tertiary hyperparathyroidism?

A
  1. Develops in individuals with secondary hyperparathyroidism for many years
  2. often due to hyperplasia of parathyroid glands.
  3. Autonomous secretion of PTH separately from good calcium levels
51
Q

What are the clinical features of hyperparathyroidism?

A

Clinical features similar to those of hypercalcaemia
1. Renal stones : typical in hyperparathyroidism
‘Stones, throne, bones, groans and psychiatric overtones’

  1. Primary - slower muscle contraction caused by less excitable neurone secondary to hypercalcaemia
  2. Secondary - Bone resoption/renal osteodystrophy; calcification of blood vessels, soft tissues
  • Stone - Calcium-based kidney stones, gallstones
  • Thrones - toilet, polyuria, impaired sodium, water reabsorption
  • Bone - pain from chronic hormone, demineralisation
  • Groans - constipation, muscle weakness
  • Psychiatric overtones; depressed mood, confusion
52
Q

What are the lab results of : Primary hyperparathyroidism

A
  1. High total serum calcium (hypercalcaemia), low phosphate (hypophosphatemia)
  2. Raised ALP
  3. Raised PTH
  • Hypercalciuria from excess calcium loss through urine, may cause dehydration
  • Serum 25-hydroxyvitamin D
53
Q

What are the lab results of ; Secondary Hyperparathyroidism

A
  • Low calcium
  • High phosphate
  • Low vitamin D
  • High ALP
  • High Phosphate
54
Q

What are the lab results of ; Tertiary Hyperparathyroidism

A
  • Normal - High calcium
  • High PTH
  • Low vitamin D
55
Q

What are the X-ray findings in ‘Hyperparathyroidism’

A
  1. Pepperpot skull
  2. Osteitis fibrosa cystica
56
Q

What is the management of primary / tertiary hyperparathyroidism?

A

Calcimemetics

57
Q

What is the management of secondary hyperparathyroidism?

A
  1. Hyperphosphatemia - phosphate binders
  2. Vitamin D supplements
    Calcitriol, vitamin D analogs - suppress PTH levels
58
Q

What is the definitive management of hyperparathyroidism?

A

Surgery
Total parathyroidectomy

Endocrine (11 decks)

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