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MSK LCRS > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

List the biochemical features of primary hyperparathyroidism

A

High calcium
High PTH

High or NORMAL alkaline phosphatase

LOW phosphate

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2
Q

List the biochemical features of secondary hyperparathyroidism

A

High PTH

Low calcium
Low or normal phosphate

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3
Q

List the biochemical features of Paget’s disease

A

High alkaline phosphatase

NORMAL calcium
NORMAL phosphate

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4
Q

List the biochemical features of osteomalacia

A

Low vitamin D
Low phosphate

Low or normal calcium

HIGH PTH
High alkaline phosphatase

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5
Q

List the biochemical features of osteoporosis

A

Normal calcium
Normal phosphate
Normal alkaline phosphatase

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6
Q

List the biochemical features of bone metastases

A

High calcium
High phosphate
High alkaline phosphatase

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7
Q

What actions does PTH have on the kidney? State how it has its effects on phosphate and where it has its effects on calcium.

A

Calcitriol formation
Calcium resorption in distal tubule
Phosphate excretion (blocks the sodium phosphate transporter)

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8
Q

How many amino acids does PTH contain?

A

84 amino acids

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9
Q

PTH is dependent upon which ion and who is this particularly bad for?

A

Dependent upon Mg

Bad for alcoholics

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10
Q

What’s the half life of PTH?

A

8 minutes!

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11
Q

What else activates the PTH receptor and when is it released?

A

PTHrP
(parathyroid hormone related peptide)

Released in pregnancy to supply calcium to the milk

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12
Q

How does the parathyroid hormone monitor levels of calcium?

A

Via the calcium sensing receptor

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13
Q

What effect does PTH have on bone?

A

Increased cortical bone resorption due to:

PTH binds to receptors on osteoblasts and stimulates RANKL production.

This increases osteoclast stimulation and resorption.

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14
Q

Primary HPT is more common in males or females and at what age?

A

Females (3:1)

Aged 50, after menopause

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15
Q

List four causes of primary hyperparathyroidism

A

Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid cancer
Familial syndromes

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16
Q

List three familial syndromes causing primary hyperparathyroidism

A

MEN 1
MEN 2A
HPT-IT

17
Q

What are the symptoms of primary hyperparathyroidism?

A

High calcium

Therefore:
Stones - renal colic, nephrocalcinosis, chronic renal failure
Moans - pancreatitis, dyspepsia, constipation, nausea, anorexia
Groans - depression, impaired concentration, drowsiness, coma

Also:
Thirst
polyuria 
Tiredness
Fatigue
Muscle weakness
18
Q

Why does primary HPT cause polyuria?

A

High serum calcium stops potassium, recycling in the loop of Henle, which in turns prevents the Na/Cl/K cotransporter from working, thus leading to diuresis.

19
Q

What are the downstream effects of calcitriol in the intestine?

A

Increased calcium and phosphate absorption

via TRPV6 and calbindin

20
Q

Where in the gut is calcium mostly absorbed, and through what type of transport?

A

Duodenum/jejunum
Colon

Passive paracellular linear transport (60%)
Active transport (40%)
21
Q

What is the effect of vitamin D on bone?

A

Maintains calcium in bone (increases osteoblast differentiation and bone formation)

(also works with PTH to increase calcium and phosphate release from bone if needed via RANKL and osteoclasts)

22
Q

What is the effect of Vitamin D on the kidney?

A

Increased calcium reabsorption from distal tubule via TRPV5, calbindin

23
Q

Vitamin D causes the production of what from the bone? Name the type of cell which produces this.

A

FGF-23 from osteoblasts in long bones

24
Q

What are the effects of FGF-23?

A

Inhibits sodium phosphate transporter in the proximal convoluted tubule
Also provides negative feedback to decrease calcitriol synthesis

25
Q

What are the symptoms of rickets?

A

Bone pain and tenderness (axial)
Muscle weakness
Lack of play

26
Q

What are the signs of rickets?

A

Myopathy
Hypotonia
Short stature
Tenderness on percussion

27
Q

What are the causes of vitamin D deficiency?

A

Small bowel malabsorption
Pancreatic insufficiency
Liver/kidney problem
Drugs e.g. phenytoin/phenobarbitone

28
Q

What are the rare hereditary causes of rickets?

A

Type 1 - 1 alpha hydroxylase deficiency

Type 2 - Defective vitamin D receptor

29
Q

Name three causes of rickets which cause chronically high levels of fibroblast growth factor

A

X-linked hypophosphatemic rickets (XLHR)

Autosomal dominant hypophosphatemic rickets (ADHR)

Oncogenic osteomalacia (mesenchymal tumours)

30
Q

What is X-linked hypophosphatemic rickets caused by?

A

Mutations in PHEX (phosphate-regulating endopeptidase)

31
Q

How does X-linked hypophosphatemic rickets present?

A 
In toddlers, with: 
Hypophosphatemia
Leg deformity
Enthesopathy 
Dentin anomalies
32
Q

Explain the problem in autosomal dominant hypophosphatemic rickets

A

Cleavage site of FGF-23 is mutated, therefore you get high levels of FGF-23

33
Q

When does ADHR present?

A

Age of onset is variable

34
Q

Explain oncogenic osteomalacia

A

Mesenchymal tumours produce FGF-23 which stops 1 alpha hydroxylase and causes phosphaturia

Therefore you get low phosphate and calcium, causing decreased mineralisation and osteomalacia

35
Q

What is the most common cause of damage to the proximal convulted tubule?

A

Fanconi syndrome

36
Q

What are the causes of Fanconi syndrome?

A

Multiple myeloma
Heavy metal poisoning
Drugs
Congenital diseases

37
Q

What drugs can cause Fanconi syndrome?

A

Tenofovir

Gentamycin

38
Q

What congenital diseases cause Fanconi syndrome?

A

Wilsons disease

Glycogen storage diseases

39
Q

What is Wilson’s disease?

A

A genetic disorder where excess copper builds up in the body

MSK LCRS (8 decks)

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