Lecture 26 Flashcards

1
Q

Define the term dystrophic calcification:

A

usually associated with an area of necrosis – for example: I went out and played paintball got a spot of necrosis and ended up getting a mineral deposit in the tissue (no evidence of hypercalcaemia will be evident)

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2
Q

Define the term metastatic calcification:

A

many tissues of the body – not just focally defined, living tissues not dead ones and secondary to hypercalcemia in the blood

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3
Q

Explain the process of dystrophic calcification:

A
  1. Dead/dying tissues (can be intracellular or can be extracellular) (has to be a process occurring cell injury or cell death) 2. Calcium influx into the tissue (more likely if the blood supply is still intact) causing mitochondrial foci (have high levels of calcium) they then normally precipitate with PO42- from organic compounds 3. The elevated levels of Ca2+ causes saponification of cell membranes
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4
Q

Describe the histological appearance of dystrophic calcification:

A

appears to be basophillic

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5
Q

What is a stain that could be used to highlight the appearance of dystrophic calcification and how would this appear on a slide?

A

Von Kossa stain - would likely appear black on a histological slide

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6
Q

What is the process of metastatic calcification?

A
  1. Can be initiated by a wide variety of causes (see below) 2. Hypercalcaemia (or abnormal Ca2+ metabolism) 3. Large amounts of Ca2+ enters the cells 4. Precipitates in specific organelles (esp. mitochondria) 5. Occurs in normal tissue – common sites include: lung (alveolar septa), stomach (mucosa), kidney (tubular epithelium) and walls of small blood vessels
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7
Q

What are the causes of metastatic calcification (HARD IONS)?

A

H – hyperparathyroidism 1o/2o A – Addison’s disease R – Renal disease D – Vitamin D toxicosis (includes granulomatous) I – idiopathic O – osteolytic disease N – neoplasia (hypercalcemia of malignancy) S – spurious

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8
Q

Fill in the blanks in the diagram below:

A
  1. Increase PTH
  2. PTH
  3. Calcidiol
  4. Calcitriol
  5. Calcitriol
  6. Vitamin D
  7. Increased calcitriol formation, decreased calcium excretion
  8. Increased calcium absorption
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9
Q

Explain how primary parathyroidism occurs and provide an example of a cause:

A

Would be where we have a parathyroid gland tumour (e.g. parathyroid gland adenoma) so the PTH gland does not recognise the negative inhibition

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10
Q

How does secondary hyperparathyroidism occur and what is an example of an inciting cause?

A

An example would be parathyroid gland hyperplasia secondarily to renal failure. As a result of getting increased calcium excretion and decreased calcitriol formation we get decreased Ca2+ in blood. This results in increased PTH hormone. As a result of this the bones can become soft and pliable.

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11
Q

What is an example of pseudo-hyperparathyroidism?

A

An example of this is lymphoma, anal sac adenocarcinoma – these tumours are able to secrete parathyroid like hormone however they are not susceptible to negative feedback mechanisms from the serum calcium

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12
Q

How does osteolytic diseases cause increases in serum calcium?

A

A primary or metastic neoplasm causes osteomyelitis that leads to increased serum calcium

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13
Q

How does Vitamin D toxicosis cause metastatic neoplasm?

A

plants containing vitamin D analogues (Cholecalciferol rodenticide poisoning or a therapeutic overdose)

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14
Q

How does Milk-alkali syndrome (Burnett’s syndrome) causes metatastic calcification?

A

Antacid therapy CaCO3 = absorbable alkali or excess calcium intake (e.g. supplements for osteoporosis and dairy products) leads to increased calcium absorption

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15
Q

Why do sheep tend to develop post-mortem changes quicker than pigs?

A

Increased body temperature causes the changes to occur quicker

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