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Pathology > 2.2 Pigmentation and mineralisation > Flashcards

2.2 Pigmentation and mineralisation Flashcards

1
Q

Pigmentation can be:

A

exogenous or endogenous

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2
Q

exogenous pigmentation:

A

involves pigments from external environments
- accumulation of excess amounts of foreign pigments​ in the tissues
- enter via skin, lung, intestinal tract

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3
Q

endogenous pigmentation:

A

formed inside the body
- accumulation of excess amounts of normal pigments

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4
Q

Most common exogenous pigment?

A

carbon (anthracosis): usually inhaled, urban environmemnts

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5
Q

Carbon (anthracosis) process:

A

carbon –> lung parenchyma, macrophage –> ultimately tracheobronchial lymph nodes
- inert thus remains for life
ex: dog lung: 2nd hand smoke

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6
Q

Pulmonary anthracosis, inner city dog , london

A
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7
Q

Dust​ (pneumocoiniosis)

A
  • inhalation and retention of dust
  • small particles evade the mucociliary system of the nose/upper resp tract
  • Chronic irritation associated with pulmonary fibrosis and/or tumors​ ( mesotheliomas)
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8
Q

Carotenoids​ (lipochrome)

A
  • Fat-soluable yellow/orange
  • Plant orgin Incl beta-carotenes (Viatmin A)
  • Stain many normal tissues (adrenal cortex, testes CL, serum)
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9
Q

latrogenic:

A

tattoo - pigmentation loose dermis or macrophage
- tetracycline- based antibodies - exposure during the development of teeth and bone (yellow/brown)
- iron dextran injection (young piglets)

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10
Q

endogenous pigment examples:

A
  • melanin
  • blood/ bile pigments
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11
Q

Melanin:

A
  • skin, hair, iris
  • protective

Quantities affected​ by genetics:
- albinism
- UV light exposure
- chronic damage

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12
Q

Melanocytes

A

contain granules that​ synthesize melanin

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13
Q

Melanosis

A

cogenial accumulation in some tissues, in some species
ex: lung (ruminant, pigs)
meniges (sheep)

**organs affected may be condemned​ at meat inspection

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14
Q

It is known as the ‘wear and tear’ pigment

A

pigment lipofuscin

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15
Q

It is protective against ultraviolet damage to skin

A

This is melanin

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16
Q

It accummulates in the lungs secondary to pollution

A

This is anthracosis, where carbon accummulates in macrophage

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17
Q

Hyperpigmentaion is due to?

A

increased melanocytes or increased melanin production

ex: chronic skin disease, endocrine disease
ex: cushings

18
Q

Hyperpigmentation:

A
  • congenitial or hereditary or acquired via copper deficiency
  • chronic inflammation of skin –> leakage of melanin into dermis (melanin incontinence
  • autoimmune disease
19
Q

Melanoma

A

tumour of melanocytes
- grey horses (perineal)
dogs, cats (skin, mouth, digit, eye)
may be amelanotic

20
Q

blood/ bile pigments:

A

mainly hemoglobin (Hb), haemosiderin, bilirubin, and haematin​ derived from red blood cell pigment (haeme)

21
Q

Haemoglobin colour normally varies with?

A

oxygenation

22
Q

What happens to plasma in haemolytic diseases?

A

plasma becomes red, kidneys become dark red and urine red (hemoglobinuria​)

23
Q

Haemosiderin accumulates where​?

A

in vascular tissue (especially lung) in chronic congestion due to heart failure

  • RBCs lysed, phagocytosed by macrophage in alveoli “heart failure”
24
Q

Bilirubin:

A
  • yellow or yellow brown
  • ## remains of haeme (after iron removed and stored)
25
Q

Where is bilirubin​ found?

A

Found in macrophages at sites of erythrocyte breakdown
- accumulate thoughout body causes diffuse yellowing of tissues = icterus or jaundice

26
Q

icterus occurs with:

A
  • excess production
  • inadequate removal of bilirubin
27
Q

icterus =

A

jaundice

28
Q

Classifications of icterus:

A
  • pre-hepatic (hemolytic) icterus
  • Hepatic icterus
  • Post-hepatic (obstructive​) icterus
29
Q

pre-hepatic (hemolytic) icterus

A

excessive production of bilirubin due to hemolysis​
- increased unconjugated bilirubin in blood

ex: large haemorrhage into tissues or infection ( leptospirosis) immune mediated erthrycyte breakdown

30
Q

Hepatic icterus

A

hepatocyte damage ( decrease conjugation)
- increased unconjugated bilirubin in blood ( or both unconjugated and conjugated bilirubin​

ex: liver damage by chemical or toxic causes

31
Q

Post-hepatic (obstructive) icterus:

A

obstruction of bile excretion
- increased conjugated biliruben in blood

ex: obstruction of bile outflow by gall stone, tumour inflammation

32
Q

Mineralization:

A

calcification:
- dysrophic
- metastatic

crystal formation
- oxalate

33
Q

calcification:

A

deposition of Ca2+ salts in tissues other than bones and teeth

  • affected tissues white, gritty grandular

2 types:
- dystrophic
- metastatic

34
Q

Dystrophic calcification:

A

local deposition in degenerate or necrotic​ tissues
ex: granulomas (TB), dead parasites, Vitamins E/ Se deficiency

Normal serum Ca
Ca metabolism normal

35
Q

Dystrophic formation:

A

dead/dying cells no longer able to regulate Ca 2+ influx, start to accumulate

  • usually irreversible may casue organ dysfunction
  • indicates previous tissue damage
36
Q

Dystrophic Hitology:

A

irregular blue-purple gragments

37
Q

Matastatic calcification:

A
  • deposition of Ca2+ salts in otherwise NORMAL tissues
  • always​ results from high blood Ca2+ secondary to disturbed Ca metabolism
  • Increased scretion parathyroid hormone
  • bone destruction
  • vitamin d disorders
  • Morphology = dystrophic calcificatioj
38
Q

Hypercalcaemia due to hyperparathyroidism

A
  • Primary: rare (parathyroid tumours)
  • secondary: more common (ex: chronic renal disease or dietary imbalances of Ca and P
  • apparent: inappropriate secretion of parathyroid hormone related protein by malignat non-parathyroid tumours
39
Q

Renal seconadary hyperparathyroidism:

A

chronic renal failure cause retention of PO4- and loss of Ca2+
- increased parathyroid stimulation –> bone resorption also fibrous osteodystrophy (rubber jaw)

40
Q

Oxalate crystals:

A

ethylene ( antifreeze) poisoning, small animals
- sheep, cattle - ingestion of oxalate-containing plants
- absorption from GIT metabolism (liver) to toxic products
- filtered by glomeruli –> acute tubular necrosis
- RRuminants, also neuromuscular dysfunction due to Ca chelation

41
Q

Can oxalate crystals be seen in histological sections?

A

yes

Pathology (7 decks)

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