Pathologic Calcification Flashcards

1
Q

What is pathologic calcification?

A
  • Abnormal deposition of Ca++ salts usually in form of phosphates and carbonates.
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2
Q

What is Dystrophic calcification?

A

When the deposition of abnormal calcium salts occur locally in dying tissue.

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3
Q

What causes Metastatic calcification?

A

Almost always result of hypercalcemia secondary to some disturbance in calcium metabolism.

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4
Q

What is the cause of this kind of calcification? Which is the abnormal lesion A or B?

A

Causes can be vitamin E / Selenium deficiency

There will be areas of normal adipose tissue (labeled A) and abnormal calcification ( usually on left ventricle (labeled b)

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5
Q

How can you tell if there is calcification when you make your incision? Where is the calcification in this histology slide?

A

You can tell when making your incision if there are calcium deposits because it will feel gritty in comparison to other areas.

The calcium deposits are the dark red areas in this slide.

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6
Q

What is occuring in these images? What is the causes of the lesions? Where can it be seen most commonly?

A

This is Metastatic calcification. Cases of Vitamin D toxicity can cause calcium deposition in organs causing metastatic calcification. You will see it most commonly in the intima of major vessels, and you will see raised, granular mineralization.

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7
Q

What can cause vitamin D toxicity?

A

Vitamin D toxicity, access to plants that are carcinogenic, that contains vitamin D analogs which can cause hypercalcemia due to excessive vitamin D.

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8
Q

Is Uremic gastritis Dystrophic or metastatic calcification?

A

Metastatic Caclification.

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9
Q

What is Uremic gastritis? What are causes of uremic gastritis?

A
  • Renal failure -> Secondary Hyperparathyroidism -> Hypercalcemia.
  • Uremia induces vasculitis -> this causes thrombosis in different tissues, including GI tract. This is called uremic gastritis. Sometimes this is the cause of lesions such as this in patients with renal failure.
  • This accumulation of urea, nitrogen products in blood of individual with renal failure will cause vasculitis in the mucosa of the stomach, mucosa of intestine, can lead to thrombosis/ ischemic damage to the tissue, which will cause degeneration/ necrosis and then dystrophic calcification.
  • Can also develop secondary hyperparathyroidism (which would lead to metastatic calcification.
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10
Q

What occurs with renal failure?

A

• Renal Failure:
◦ Retention of phosphates-> increased stimulation of parathyroid gland -> increase in parathyroid hormone -> stimulation of osteoclasts -> increased calcium absorption ( increased calcium level (aka hypercalcemia))

This can lead to dystrophic/ metastatic calcification

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11
Q

What is occuring in this image?

A

Uremic Gastritis

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12
Q

What is occuring in this image? What will you feel when palpating this area?

A

Uremic gastritis leading to gastric mineralization.

In this image you can see the mineralization of the mucosa of the intestines.
• You will feel hard tissue in the intestines, this would be deposition of calcium w/in intestinal lumen.

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13
Q

When can familial renal disease show signs

A

Familial renal disease can show signs at 2 years old.

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14
Q

What will you see with familial renal disease? What will you see on histology segments?

A

You can see congestion and hemorrhage, and inflammation. When the stain (von Koda) is done you can see increased calcium deposits within the mucosa. Could be dystrophic due to vasculitis and ischemia which leads to necrosis, or it could be metastatic due to secondary hyperparathyroidism.

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15
Q

What would a histological slide like the one below be showing?

A

Metastatic calcification

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16
Q

What is subpleural mineralization and where can this be seen? What is this a consequence of?

A

Y ou can see this sometimes in patients with renal failure,. Their could be areas of subpleurital mineralization. This is considered to be both metastatic/ dystrophic depending on the cause. Can be found on the inside of the ribs

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17
Q

What are the three categories of pigments and where are they formed?

A

Exogenous (formed outside the body)

Endogenous (formed inside the body)

Hematogenous (blood origin)

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18
Q

What are examples of exogenous pigments?

A
  • Carbon
  • Tattoos
  • Dusts
  • Carotenoids
  • Tetracyclin
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19
Q

What is anthracosis? What is its cause? Where can it be found? Is it clinically significant?

A
  • position of carbon particles is called anthrocosis
  • most common in lungs, bronchi, regional lymph nodes, ect.
  • From carbon deposition within these areas. Can be seen in areas with high air pollution. Can be seen on pleural surface.
  • Not clinically significant, but can be an indication of exposure to air pollution.
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20
Q

What is the most exogenous pigment and what can it lead to?

A

Carbon is the most exogenous pigment. Portal entry is usually by inhalation and can lead to black lungs. This is common in areas with substantial air polution.

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21
Q

What are tattoos used for in animals and what occurs to them after they are introduced to the body?

A
  • tattoos used to identify animals.
  • these pigments are phagocytized by macrophages while others remain free in the Dermis without eliciting an inflammatory response.
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22
Q

What are dusts? What are the conditions associated with it ?

A

Dusts. The condition associated with the inhalation and
retention inorganic dusts within the lungs is known as Pneumoconiosis

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23
Q

When the term dust is used, what are the stains that are typically used? What are the concerns with inhaling these substances?

A

This term is usually applied to the inhalation of silica
or asbestos (asbestosis) that may lead to significant
pulmonary fibrosis.

  • Silica crystals are birefringent under
    polarized light. Mild will not show any clinical significance.

You don’t see it often. (Sometimes when there is exposure of volcanic ash.

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24
Q

What are carotenoid pigments?

A
  • Fat soluable pigements of plant origin
  • Can be seen by over abundance of certain vitamin A precursors.
  • Can be seen in the adipose tissue. Due to consumption of feed with high level of pigment. Seen in horses and cattle.
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25
Q

What pigment can you see in this image?

A

Carotenoid pigments.

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26
Q

What is the concern/ what can occur with tetracycline based antibiotics? When should you avoid the administration of tetracycline?

A

When administered during the period of teeth development they
will be it deposited in the mineralizing dentin, enamel and
cementum, staining the teeth or portions of them yellow or
brown.
 high doses may induce enamel hypoplasia
Avoid the administration during pregnancy!

27
Q

What are the endogenous pigments?

A

Melanin

Lipofuscin/ Ceroid.

28
Q

What is melanin? What produces it? What can cause/ is a response of a general lack of melanin?

A

Pigment normally present in the epidermis,
responsible for skin color and hair color.

 Produced by melanocytes.

 Formed by the oxidation of tyrosine, which requires
tyrosinase (copper-containing enzyme).

 Lack of tyrosinase may lead to a general lack of
melanin, a metabolic inherited defect known as
albinism.

29
Q

What is occuring in this photo?

A

Albinism

30
Q

What is occuring in these photos?

A

Melanosis

31
Q

What is lipofuscin?

A

The aging pigment

32
Q

What are tan/ brown colored areas on this histological slide?

A

Lipofuscin

33
Q

Where can you see melanosis? What is the clinical implications?

A
  • Sometimes can be seen in young animals such as cattle/ pigs, sheep ect. You can also see it in the intima of the aorta, and in the brain.
  • This is presence of melanin in abnormal places.
  • Their is dark brown discoloration on the tissue. This is just accumulation of melanin outside the skin. No proliferation changes/ clinical significance.
34
Q

Where is the area of melanosis located in this image?

A

The leptomeninges

35
Q
A
36
Q

Where can lipofuscin be found? What does it look like? What can it do to surrounding tissue?

A
  • can be found in an aging animal. Can be seen in cardiac muscle, cardiac myocytes. Brown yellow granular tissue, that is next to nucleus.
  • Wear and tear pigment.
  • Can cause the destruction of organelles over time. This is usually not concerning. But will indicate age.
37
Q

Other than in cardiac muscle/ age, where can you see lipofuscin?

A

In neuronal tissue, you can see lipofuscin as well.

38
Q

What is ceroid?

A

Ceroid has a similar histochemical features to lipofuscin but is not age-related.
Small intestine a bit brown, this is the presence of ceroids. This can be a sign of vitamin E deficiency.

39
Q

What is occuring in the box in this image?

A

Ceroid -> associated to vitamin E deficiency and the ingestion of unsaturated fatty acids –brown discoloration of the tunica muscularis.

40
Q

What are hematogenous pigments?

A

Hemoglobin

Parasite

Hematin

Hemosiderin

Bilirubin

Porphyrins

41
Q

What is hemaglobin? What would you see in the mucus membranes of dogs that have adequate oxygen content? In the dogs who do not?

A

Hemoglobin is the normal red pigment of erythrocytes, responsible got oxygen transport.

  • Normal animal Pink MM
  • Cyanosis: Pale grey- Blue MM -> Decreased O2, CO2 may be carried instead
  • Anemia: Pale pink - White - > Decreased RBC count
42
Q

What is cyanide poisoning? What occurs? What color are the mm? What is a common cause of cyanide poisoning?

A
  • Cyanide binds to cytochrome oxidase, the enzyme responsible for oxidative phosphorylation -> leads to impaired cellular respiration within mitochondria -> tissues are unable to use the oxygen carried by the blood hemoglobin causing rapid death.
  • The arterial and venous blood in the poisoned individual appears brightly red.
  • Smoke inhalation is a common cause of cyanide poisoning during fires.
43
Q

What occurs in intravascular hemolysis? Where may this substance be secreted? What doe the color indicate?

A

In intravascular hemolysis Hb is released from lysed erythrocytes and stains the plasma pink.

 It may be excreted by the kidney staining it dark-red and the urine red (hemoglobinuria)

44
Q

What is occuring in these images?

A

Hemoglobin pigmentation

45
Q

What can be seen in this image?

A
  • Urinary bladder was filled with red urine ( patient with bovine babesiosis)
  • You can see increased bilirubin and since it is difficult to excrete it will accumulate in the tissues which gives the jaundice characteristic yellow color
46
Q

What is parasite hematin?

A

• Black tracks on surface of the liver, this is exhaust from the trematods you can find cystic lesions with trematode clusters. This is the result of breaking down hemoglobin in the area.

47
Q

What is the fluke infestation that could leave fluke exhaust?

A

• Fascilodis Minor ( fluke infestation)

48
Q

What is occuring in this image?

A

Fluke exhaust. Parasite hematin.

49
Q

What is hemosiderin? Where does it develop?

A

Golden-brown granular iron-containing pigment
(intracellular aggregates of ferritin) that originates
from the breakdown of erythrocytes.

 It develops within macrophages, particularly common
in the spleen, liver or within foci of hemorrhage.

50
Q

What is occuring in these images? What is causing the lesions?

A

Hemosiderin

  • can also be seen in the lungs of individuals with congestive heart failure.
  • when there is breakdown of erythrocytes, iron containing heme will stain.
51
Q

What is occuring in this image? What stain can be used to find hemosiderin? How will it stain?

A

Chronic pulmonary congestion and edema is occuring in a horse with CHF. Iron (Perl’s) stain can be used to find Hemosiderin-laden macrophages (“heart failure cells” -> siderophages). These cells will stain blue.

52
Q

What occurs in chronic pulmonary congestion?

A

• Blood will back up into the lungs, which will increase the hydrostatic pressure in the pulmonary vasculature. Left sided congestive heart failure patients can have dyspnea (especially at night), chest tightness.

53
Q

What are the consequences of left sided CHF?

A
  • Left sided congestive heart failure, since there is an area with stagnated poorly o2 blood, you end up with hypoxic damage to the alveoli. Their is also little foci of hemorrhage (micro hemorrhage).
  • RBC that go into alveoli will be phagocytized by alveolar macrophages, this will leave behind these brown intracytoplasmic pigment. This is called /hemosiderin.
54
Q

What is being indicated by the black arrows?

A

HE-stain, dark brown pigment within the cytoplasm of alveolar macrophages

55
Q

What is occuring in this image?

A

Chronic pulmonary congestion and edema, horse with congestive heart failure, H&E stained section

56
Q

What is bilirubin? Where is it derrived from? What color is it?

A
  • normal major pigment found in bile

 Derived from Hb but contains no iron (end product of
heme degradation)

 Yellow to brownish green pigment

57
Q

Will Iron be in bilirubin?

A

no iron, end product is from eme degradation.

58
Q

Where is bilirubin conjugated? Where is it excreted? Is there normally a high concentration in the plasma?

A

 Low concentrations are normal in plasma as a result of the
breakdown of senescent red blood cells.

 Bilirubin is conjugated in the liver and excreted in the bile

59
Q

What will occur with excessive bilirubin in the plasma?

A

Excessive amount of bilirubin in plasma will lead to
icterus (Jaundice)

yellow staining of tissues.

60
Q

What are the 3 classifications of icterus and examples of when each is found?

A
  • Pre-hepatic: IMHA ( common especially in dogs) Destruction of RBC. Will overwhelm the liver.
  • Hepatic Jaundice: Hepatosis dietetica - vitamin E/ selenium deficiency. In pigs this can be main presentation due to liver lesions. Jaundice is easily seen in the intima of the vessel wall.
  • Posthepatic: Any disease that occurs after the liver and causes impairment of function.
61
Q

What is occuring in this image? What pigment is causing it?

A

This is icterus or jaundice. It is caused by an increase in the bilirubin in plasma.

62
Q

What are porphyrins? What is another name for accumulation of this pigment and why?

A

Congenital erythropoietic porphyria of calves, cats and pigs is a rare inherited disorder caused by deficiency of uroporphyrinogen III cosynthetase. It affects RBC precursors and results in anemia. The disease is refer to as “pink tooth” because porphyrins accumulate in dentin and bones resulting in reddish teeth in young animals and dark brown teeth in older ones.

63
Q

What is occuring in this image?

A

Congenital Erythropoietic Polyphyria

64
Q

What will occur with urine that contains the pigments of Congenital Erythropoietic Porphyria?

A
  • Pigment is excreted in urine that if allowed to stand in light, develops a port-wine color due to photic activation of porphyrins

 Urine and tissues fluoresce blue-green in UV light