Brainscape's Knowledge GenomeTM

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


See full index

Clinical Biochemistry: Introduction to Clinical Biochemistry > Calcium, Phosphate and Magnesium > Flashcards

Calcium, Phosphate and Magnesium Flashcards

1
Q

What are functions of Calcium?

A
  • Bone growth and remodeling
  • Secretion (exocytosis)
  • Excitation-contraction coupling
  • Stabilization of membrane potentials
  • Enzyme co-factor (e.g. in blood coagulation)
  • Second messenger – intracellular signalling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the different forms of calcium?

A
  • Calcium is in the skeleton (reservoir)
  • Serum Calcium 2.20 – 2.60 mmol/L
  • Ionised calcium 1.1-1.3 mmol/L: 45% exists in ionised form (physiologically active form), 45% bound to proteins (predominantly albumin), 10% complexed with anions (citrate, sulphate, phosphate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is calicum reported as adjusted calcium and calcium?

A

Ionised calcium difficult to measure

  • ABG machine
  • Calcium electrode
  • Not readily available
  • Dependent on pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are benefits and limitations of reporting adjusted Calcium?

A

Benefits

  • Accounts for changes in albumin. This is useful when a decrease in albumin may mask hypercalcaemia.

Limitations

  • Interpret with caution in extremes of pH. Acidosis decreases binding. Alkalosis increases binding
  • Conversely not useful in very low albumin states <20g/L. The body regulates unbound calcium and in low protein states ACa may be inaccurate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are common mechanisms of Hypercalcaemia?

A

Increased GI absorption

  • Elevated Vitamin D: Excess exogenous (therapeutic), Excess endogenous (e.g. sarcoidosis), Elevated PTH, Hypophosphataemia
  • Milk-alkali syndrome

Increased bone resorption

  • Increased net bone resorption (Elevated PTH, Malignancy)
  • Increased bone turnover (Paget’s disease, Hyperthyroidism)

Decreased bone mineralisation

  • Elevated PTH
  • Aluminium toxicity

Decreased urinary excretion

  • Elevated Vitamin D
  • Elevated PTH
  • Elevated PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are common mechanisms of Hypocalcaemia?

A

Decreased GI absorption

  • Poor dietary intake
  • Vitamin D deficiency (Poor dietary intake of Vit DMalabsorption) leading to low absorption of calcium
  • Decreased conversion of Vitamin D (Liver failure, Renal failure, Low PTH, Hyperphosphataemia) leading to low absorption of calcium

Decreased bone resorption/Increased bone mineralisation

  • Hypoparathyroidism
  • PTH resistance (pseudohypoparathyroidism)
  • Vitamin D deficiency
  • Hungry bone syndrome
  • Osteoblastic metastases

Increased urinary excretion

  • Low PTH (Thyroidectomy, I-131 treatment, Autoimmune hypoparathyroidism
  • PTH resistance
  • Vitamin D deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are aetiologies of Hypercalcaemia?

A
  • Primary hyperparathyroidism (99% ambulant patients): Single adenoma (80%), Hyperplasia (15%), Double adenoma (2%), Carcinoma (<1%)
  • Malignant disease (99% of ill patients): Metastases and myeloma, PTHrp secreting, Lymphoma, PTH secreting (v. rare)
  • Vitamin D excess
  • Tertiary hyperparathyroidism
  • Hyperthyroidism
  • Familial hypocaliuric hypercalcaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the signs and symtpoms of Hypercalcaemia?

A
  • Nausea
  • Depression
  • Mental Disturbances
  • Constipation
  • Renal Failure
  • Renal Stones
  • Polyuria
  • Soft Tissue Calcification
  • Peptic Ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the Parathyroid related aetiologies of Hypocalcaemia?

A
  • Parathyroid agenesis (Isolated, Part of complex developmental anomaly eg DiGeorge Syndrome)
  • Parathyroid destruction (Surgery, Radiation, Infiltration eg Haemochromatosis, Wilson’s)
  • Autoimmune (Isolated, Polyglandular)
  • Reduced parathyroid function (PTH gene defects, Hypomagnesaemia, Neonatal hypocalcaemia, Hungry bone disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the aetiologies of non-parathyroid causes of Hypocalcaemia?

A
  • Vitamin D deficiency
  • Vitamin D resistance
  • Altered vitamin D metabolism eg phenytoin, ketoconazole
  • PTH resistance (Pseudohypoparathyroidism, Magnesium deficiency)
  • Bisphosphonates
  • Acute pancreatitis
  • Acute rhabdomyolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are signs and symptoms of Acute Hypocalcaemia?

A
  • Tetany
  • Carpopedal spasm
  • Muscles cramps
  • Seizures – all types
  • Prolonged QT interval on ECG
  • Bronchospasm
  • Laryngospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are signs and symptoms of Chronic Hypocalcaemia?

A
  • Ectopic calcification eg in basal ganglia causing extrapyramidal neurological symptoms
  • Cataract
  • Papilloedema
  • Abnormal dentition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are functions of Phosphate?

A
  • Formation of high energy compounds e.g. ATP, creatinine phosphate
  • Formation of second messengers e.g. cAMP, inositol phosphates
  • Component of: DNA/RNA, Phospholipid membranes, Bone
  • Phosphorylation (activation/inactivation) of enzymes
  • Intracellular anion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the Distribution of Phosphate?

A
  • 85% is within the skeleton and teeth
  • 14% is located within the cells
  • Only 1% is present in the extracellular fluids

Present as organic (phosphoproteins, phospholipids) and inorganic (phosphate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are causes of Hyperphosphataemia?

A

Pseudohyperphosphataemia

  • Haemolysed specimen
  • Myeloma
  • Delayed separation / Old sample

Increased Phosphate Input

  • IV PO4
  • Rectal PO4
  • Cell death (Tumour lysis syndrome, Rhadbomyolysis, Malignant hyperpyrexia, Heat stroke)

Reduced phosphate excretion

  • Reduced eGFR (Acute renal failure, Chronic renal failure)

Increased renal tubule reabsorption

  • Physiological (Recovery from Vit D def, Lactation)
  • Pathological (Reduced PTH or PTH resistance, Vitamin D toxicity, Thyrotoxicosis, Acromegaly)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is required to exclude Hypocalcaemia?

A
  • EDTA contamination
  • Multiple transfusions with citrated blood products
17
Q

What is the causes of Hypophosphataemia?

A

Inadequate phosphate absorption

  • Low dietary intake (very rare)
  • Phosphate binders (dialysis patients)
  • Phosphate binding antacids (rare due to new therapies for peptic ulcers)

Abnormal urinary phosphate loss

  • Primary and secondary hyperparathyroidism
  • Osmotic diuresis e.g. hyperosmolar hyperglycameic state
  • Diuretics
  • Fanconi syndrome
  • Genetic conditions e.g.X-linked hypophosphataemia

Shifts of phosphate from extracellular fluid into cells

18
Q

What can causes shifts of phosphate from extracellular fluid into cells?

A

<1% in extracellular space

Recovery from DKA

  • Treatment with insulin causes phosphate to move back into cells

Refeeding syndrome

  • Starving or chronically malnourished are refed or given IV glucose
  • Carbohydrates stimulate insulin which drives phosphate and glucose intracellularly
  • Cells switch to anabolic state resulting in further depletion

Respiratory alkalosis

  • Activating phosphofructokinase which stimulates intracellular glycolysis

Increased muscle intake

Hepatic encephalopathy

Salicylate toxicity

Acute leukaemia

  • Rapid growing malignancies may consume phosphate preferentially
19
Q

What is FGF23?

A
20
Q

What are the functions of Magnesium?

A
  • Cofactor for 300+ enzymes
  • Mg-ATP complex is substrate for many ATP requiring enzymes
  • Critical role for DNA replication, transcription and translation
  • Maintenance of structure of ribosomes, nucleic acids and some proteins
  • Interacts with calcium
  • Affects permeability of excitable membranes and their electrical properties (ECF depletion of Mg causes hyperexcitability)
21
Q

What are symptoms of Hypomagnesaemia?

A
  • Loss of appetite
  • Nausea and vomitting
  • Fatigue
  • Weakness & numbness
  • Tingling
  • Muscle cramps
  • Seizures
  • Personality changes
  • Hypokalaemia
  • Hypocalcaemia
22
Q

What are symptoms of Hypermagnesaemia?

A
  • Non-specific symptoms include nausea, vomiting and flushing
  • Neuromuscular symptoms - Blockage of neuromuscular transmission
  • Conduction system symptoms (Mild decrease in blood pressure, Higher concentrations lead to symptomatic hypotension, Heart block >7mmol/L)
  • Hypocalcaemia
23
Q

What are causes of Hypomagnesaemia?

A

Decreased intake +/- absorption

  • Starvation (protein calorie malnutrition), Malabsorption syndrome, Prolonged gastric suction, Inadequate parenteral nutrition,

Loss from body

  • Extra renal, Diarrhoea, Laxative abuse, Gut fistula, Excessive lactation (rare)

Miscellaneous

  • Acute pancreatitis, Multiple transfusions, Insulin therapy, Hungry bone syndrome

Renal

  • Alcoholism, Interstitial nephropathy, Diuresis (e.g. DKA, post ATN), Drugs e.g. loop diuretics, cis-platinum (65-75% reabsorbed in Loop of Henle), Hypercalcaemia, RTA, Bartter’s syndrome, Gitelman’s, Endocrine (e.g. hypoparathyroidism, primary hyperaldosteronism, hyperthyroidism), K depletion, PO4 depletion, Post renal Tx, Primary renal Mg wasting
24
Q

What are causes of Hypermagnesaemia?

A
  • Impaired renal function
  • Large Mg load: IV Contamination, Post cardiac surgery, Pre-eclampsia (used to decrease neuromuscular excitability), Enema/laxative abuse
  • Excessive tissue breakdown
  • Lithium therapy (decrease renal excretion)
  • Hypothyroidism
  • Addison’s disease
  • Familial hypocalciuric hypercalcaemia
25
Q

What are the effects of hypermagnesaemia?

A
  • Cardiac conduction is affected at concentration >2.5-5.0 mmol/L
  • Very high concentrations >7.5 mmol/L cause respiratory paralysis and cardiac arrest

Significant hypermagnesaemia is uncommon as readily excreted in urine

Clinical Biochemistry: Introduction to Clinical Biochemistry (11 decks)

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