Calcium, Phosphate And Magnesium Flashcards

1
Q

What the plasma concentrations of calcium, phosphate and magnesium?

A

Ca= 1.3

Ph= 1.3

Mg= 1.1

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2
Q

What is the difference in the distribution of these ions in the EC and IC compartments?

A

Ca mainly in the extracellular compartment

Ph and mg are similar distributed between the EC and IC compartment

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3
Q

What regulatory roles are calcium, phosphate and magnesium involved in?

A
Calcium:
Cell signalling and 2nd messenger 
Neurotransmitter and hormone release 
Exocytosis of proteins 
Muscle contraction 
Blood clotting 
Biomineralisation 

Phosphate:
Integral component of DNA and RNA
ATP
Phosphate groups can be added or deleted from proteins

Magnesium 
DNA and protein synthesis 
Oxidative phosphorylation 
Enzyme function 
Ion channel regulation 
Neuromuscular excitability
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4
Q

What hormones are involved the metabolism of these minerals?

A

PTH

Vitamin D

FGF-23

PTHrP

CT (calcitonin)

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5
Q

Which organ acts as the main regulator of these minerals homeostasis? How can it adapt its function to maintain homeostasis?

A

Kidney
NOTE: Ca/Mg sensory receptor in particular

Can decrease or increase the filtered load depending on whether there is a hypo or hyper state

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6
Q

What implications would impaired renal function have on levels of calcium, magnesium and phosphate in the body?

A

Would lead to impaired reabsorption and increased excretion

I.e. loss of homeostasis

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7
Q

How is vitamin D related to GIT calcium absorption?

A

Calcitrol (1,25-OH VD3) acts on ileum cell nuclei to cause transcription of Calbindin which acts to form Calbindin-Ca2+ complex to aid with transportation of Ca2+ from microvilli and into vesicles

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8
Q

Which parts of the nephron is associated with the absorption of the different minerals? Why is this clinically significant?

A

PCT= Ca + Phos primarily

DCT= Mg

Need to be aware that electrolyte imbalance might occur with the use of certain diuretics depending on which part of the nephron they target

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9
Q

What form of calcium regulates feedback mechanisms? What factors can influence this levels of this form of calcium?

A

Free ionised calcium

Decreased ph= increased Ca2+
Increased ph= decreased Ca2+

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10
Q

Why is it important to know the albumin concentration of a patient if you want to measure their calcium levels?

A

The concentration of free calcium depends on the concentration of albumin

Calcium concentrations need to be corrected to account for the fact that for 0.02mmol/L calcium binds to each gram of albumin

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11
Q

What are the causes of hypocalcaemia?

A

CDK and AKI

Vit D deificiency

Hypoparathyroidism

Acute pancreatitis

Magnesium deficiency i.e. Mg is a cofactor for PTH

Artefact i.e. wrong test tube (EDTA is a chelating agent which may lead to apparent hypocalcaemia)

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12
Q

Why is hypocalcaemia commonly associated with acute pancreatitis?

A

High levels of pancreatic lipase breakdown lipids to free fatty acid which accumulate in abdominal cavity and act to CHELATE calcium

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13
Q

What is the homeostatic response to low Ca2+ levels?

What feedback mechanism prevents excess PTH release?

A

Parathyroid gland detects low levels and secretes PTH
PTH:
-stimulates osteoclasts to increase bone resorption= Ca2+ and PO4 released
-stimulates 1-alpha hydroxylase production in the kidney which acts to convert 25(OH)D3 to 1,25(OH)D3
-1,25(OH)D3 acts on bone to stimulate release of FGF23 to decrease PO4 reabsoprtion and feeds back to parathyroid gland to prevent excess PTH release and acts on gut to increase Ca2+ and PO4 absorption

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14
Q

What is the homeostatic response to high calcium levels?

A

Calcitonin released from thyroid gland to decrease calcium reabsorption in kidney and decrease PO4 reabsorption

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15
Q

What are the 2 conditions associated with vitamin D deficiency? How are they different?

A
Rickets= affects growing bone 
osteomalacia= affects adult skeleton 

Due to lack of mineralisation of osteoid

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16
Q

What are the causes of vitamin D deficiency? How can it be treated?

A

Impaired availability of vit D

Impaired liver hydroxylation or renal hydroxylation

End organ insensitivity to vit D metabolites

Vit D replacement through diet or sunlight

17
Q

How can glucocorticoids cause vitamin D deficiency?

A

Inhibit intestinal vit D dependent calcium absorption

18
Q

Why might surgery or radiotherapy targeting the thyroid gland lead to hypocalcaemia?

A

Can lead to iatrogenic damage to parathyroid glands which results in decreased PTH production

19
Q

How might someone with hypocalcaemia present?

A

Asymptomatic

Neuromuscular symptoms are fairly common
I.e. pins and needles or spasm due to nerve irritations

20
Q

What tests are done to differentiate between the different causes of hypocalcaemia?

A

Biochemical test to look at PTH and PO4

21
Q

What conditions are indicate by the following test results?

  1. Increased PTH + decreased PO4
  2. Increased PTH + PO4
  3. Decreased PTH + increased PO4
A

1.
Vitamin D deficiency due to malabsorption or liver disease
Acute pancreatitis
Drugs I.e. Bisphosphonates

2.
CKD
Tumour lysis 
Early rhabomyolysis 
Pseudohypoparathyroidism 
3.
Reduced parathyroid function
Hypomagnesemia 
Drugs 
Neonatal hypocalcaemia due to maternal hypercalcaemia 
AI
Surgery
22
Q

How can you treat hypocalcaemia?

A

IV calcium= acutely ill w/ neuromuscular symptoms
Oral calcium= mildly symptomatic/asymptomatic

Treat underlying cause:
VD replacement
1,25 D3 products for hypoparathyroidism

23
Q

What causes hypercalcaemia?

A

Primary hyperparathyroidism

Malignancy

24
Q

What are the different causes of primary and secondary hyperparathyroidism?
How can you differentiate between the 2?

A

Primary:
Increased PTH secretion due to adenoma or parathyroid hyperplasia

Secondary:
Renal failure
Vitamin D deficiency

High calcium in primary
Low calcium in secondary

25
What are clinical features of hypercalcaemia?
``` Thirst Polyuria Constipation Aches and pain Anxiety + depression Confusion Coma Renal stones Osteoporosis Pancreatitis ```
26
Why is it important to identify malignancy-associated hypercalcaemia early?
Acts as poor prognostic signs and can lead to life saving therapy being put in place
27
What are the mechanisms behind malignancy associated hypercalcaemia?
Humoral hypercalcaemia i.e. PTHrP secreting tumour Bone invasion Immobilisation Parathyroid carcinoma
28
How can malignancy associated hypercalcaemia be treated?
Aggressive IV hydration IV bisphosphonates +/- calcitonin Manage renal failure if associated
29
What are the main causes of hypophosphataemia?
Increased renal excretion GIT malabsorption Cellular shifts
30
What are the clinical consequences of hypophosphataemia?
Asymptomatic Neuromuscular disturbance
31
How is hypophosphataemia treated?
Oral phosphate tablet if low IV phosphate polyfusor if more significant
32
What are the causes of hyperphosphataemia?
Decreased renal excretion due to renal failure or hypoparathyroidism
33
What are the symptoms of hyperphosphataemia?
Acute Tetany i.e. seizures and hypotension Chronic Secondary hyperparathyroidism i.e. can present with soft tissue calcification
34
What is the main cause of Mg deficiency?
GI causing malabsorption | I.e. associated with alcoholism
35
How does hypomagnesemia present?
Non-specific lethargy Weakness Increase neuromuscular excitability i.e. tremors or carpopedal spasm, muscle cramps, tetany Cardiac arrhythmias i.e. A tachycardia + VT
36
What are distinct features of Gitelmen syndrome?
Hypomagnesium and renal magnesium wasting
37
How would you treat hypomagnesemia? When is IV magnesium indicated?
Oral magnesium glycerophosphate tablets <0.5mmol/L= IV magnesium sulphate 50% solution
38
What are the causes and presentation of magnesium excess?
Acute renal failreu Severe diabetic ketoacidosis Addison’s disease Supplements Loss of deep tendon reflexes Increased PR interval which can lead to MI (when Mg >2.0 mmol/L)
39
How are patients with severe mineral imbalance monitored?
Fluid intake and output Daily weight to see if fluid accumulating ECG to look for arrhythmias Renal function and electrolytes tested daily (U&E, LFT, Ca, Mg, Phos, Bicarbonate, Cl)