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Transfusion > Pigments and lipids > Flashcards

Pigments and lipids Flashcards

1
Q

what is perls staining used for and

A

detects the presence of iron

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2
Q

what is an artefact

A

deposits produced as result of a chemical reaction in tissue

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3
Q

define Endogenous

A

haematogenous or autogenous

produced within the tissue and have physiological function or are a by- product of normal metabolic process

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4
Q

define Exogenous

A

gain access to body accidentally with no physiological function. Usually minerals, enter by inhalation or implantation in skin during industrial exposure.

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5
Q

what are the artefact pigments ?

A

formalin
malarial
mercury
dichromate

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6
Q

what is formalin pigment and how is it removed

A

brown/black deposit following fixation in acid

formalin, especially seen in haemorrhagic tissue. Removed with picric acid

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7
Q

how is formalin pigment formed

A

Formalin pigment is formed from haemoglobin by the action of formaldehyde at acid pH (prevented by short fixations in neutral buffered formalin). In and around blood vessels

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8
Q

what is malarial pigment

A

similar to formalin pigment, formed in/near RBC’s

with parasite.

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9
Q

how is malarial pigment formed

A

Malarial pigment, brown/black pigment occurs in parasitic infection (such as Plasmodium malariae). In and around blood vessels. Left over from the metabolism of haemoglobin by the malarial parasite

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10
Q

what is mercury pigment

A

black deposit formed with fixatives containing

Mercury. Removed with iodine/hypo

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11
Q

how is mercury pigment formed

A

Mercury pigment can develop when mercuric chloride is incorporated into fixatives

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12
Q

What are dichromate deposits

A

yellow/brown deposits after potassium
dichromate fixation and insufficient washing prior to dehydration. Removed
with acid alcohol

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13
Q

how are dichromate deposits formed

A

Dichromate deposits can form after fixation with potassium dichromate containing fixatives and insufficient washing to remove any excess fixative

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14
Q

what are the three types of pigments and how do we differentiate between them

A

Endogenous - related to the cell as have physiological function (eg might always see them around the nucleus)

Artefact - non-related to cells so will be present everywhere

Exogenous- enter body via airways/skin

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15
Q

what is Lipofuscin

A

yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion. Aging or ‘wear-and-tear’ pigments

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16
Q

what are the two types of endogenous pigments

A

haematogenous and non- haematogenous

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17
Q

what are haematogenous pigments

A

haemoglobin:
globin - protein part
heme - pigment part:

splits off into iron or bile pigments

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18
Q

where are bile pigments found

A

liver/gall bladder/spleen etc

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19
Q

what do bile pigments do

A

Follows breakdown of RBC’s and release of haemoglobin and iron removal, leaving biliverdin. Transported to liver by phagocytic cells, reduced to bilirubin.

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20
Q

what is Haematoidin and where is it seen

A

an orange-yellow pigment in the bile that forms as a product of hemoglobin; excess amounts in the blood produce the yellow appearance observed in jaundice

Haematoidin seen in spleen haemorrhagic areas, sometimes brain

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21
Q

what are the three bile pigments and what type of pigment are they

A

biliverdin, bilirubin, haematoidin

endogenous

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22
Q

what does the bile - obstructive jaundice look like in histology and how is this caused (in general)

A

Accumulation of pigments – bile

Often this is due to extrahepatic biliary tract obstruction

Bile may also accumulate in liver (called cholestasis) when there is hepatocyte injury

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23
Q

what does an H&E stain of bile - obstructive jaundice look like (colour)

A

Orange pigment in bile ducts in portal areas liver in H&E. Higher magnification of area more impacted by obstruction of bile ducts

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24
Q

on a bile - infarction slide what would you see

A

lysed hepatocytes

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25
Q

what is Cholestasis

A

bile accumulation in the liver

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26
Q

facts on Lipofuscin and what type of pigment is it

A

Oxidation of lipids. Normal in ageing process, abnormal in Vit E deficiency. Seen in heart, liver, adrenal, testis, neurones. Stained by Sudan Black, PAS, Schmorl’s, Long Zn

endogenous

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27
Q

facts on melanin and what type of pigment is it

A

Intra cellular, brown/black. Normal in skin, retina, brain, hair shafts. Pathologically in benign naevus cell tumours, malignant melanoma Demonstrated by Masson Fontana (black)

endogenous

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28
Q

steps in the formation of melanoma (phases and key points)

A
  • Benign Nevus - BRAF mutation
  • Dysplastic Nevus - CDKN2A & PTEN loss
  • Radial growth phase - CD1 increase, move from epidermis to dermis
  • Vertical growth phase - E-cadherin loss
  • Metastatic Melanoma - break basement membrane and move into cells, Distant metastases
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29
Q

what is a Nevus

A

birthmark or mole

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30
Q

what is iron stored as, where and in what state

A

Stored as haemosiderin in marrow and spleen in ferric (Fe+3) state

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31
Q

iron clour

A

fine brown

32
Q

what test demonstrates iron

A

Perl’s Prussian Blue reaction

33
Q

what is Haemosiderin

A

iron storage found in cells of tissues (not including that in circulating blood). The iron within deposits of hemosiderin is very poorly available to supply iron when needed

34
Q

what is Haemosiderosis

A

iron overload disorder resulting in the accumulation of haemosiderin

35
Q

what would a slide of haemosiderin in the kidney look like

A

Perls reaction (iron)

haemoglobin breakdown - blue present

36
Q

what are heart failure cells

A

hemosiderin-containing macrophages generated in the alveoli of patients with heart failure or chronic pulmonary edema, when the high blood pressure causes red blood cell to pass through the vascular wall (H&E)

37
Q

What tests distinguish calcium

A

Demonstrated by Von Kossa (black), Alizarin red (red)

38
Q

what is calcuim

A

Insoluble, inorganic salts in bone/teeth

39
Q

what does wilsons disease have abnormal levels of

A

copper

40
Q

Facts on copper

A

Normal constituent of many tissues, part of some of the oxidase enzymes.

Present in very small amounts.

Abnormal levels in Wilson’s disease, seen in liver cirrhosis, brain.

41
Q

three tests for copper and colours

A 
Demonstrated by Shikata Orcein (brown), 
Rubeanic acid (green/black),
Rhodanine stain (red, picture)
42
Q

one distinguishing feature in a patient with wilsons disease?

A

deposit of copper in cornea (visible as a brown ring on the edge of the cornea)

43
Q

what are uric acids and urates

A

Breakdown product of Purine metabolism, normally further broken down and excreted in urine

44
Q

what causes gout and how?

A

uric acids and urates:

they do not break down and remain as accumulations , becoming crystallised in tissue (joints) leading to chemical arthritis. Produce gouty “tophi”

45
Q

how is gout seen on a slide/what stain is used

A

Demonstrated by silver stains (black). Seen as birefringence in polarised light.

46
Q

what is Birefringent

A

Birefringent is the optical property of a material having a refractive index that depends on the polarization and propagation direction of light

(POLARISED LIGHT)

47
Q

what do uric acid “Tophi” look like on a slide

A

Needle-shaped crystals in surrounding fibrous tissue

48
Q

examples of Exogenous pigments

A

carbon and asbestos

49
Q

what is Carbon pigment (and facts) and what type of pigment is it

A

Most common of the pigments, seen in lungs of urban dwellers, smokers. Absorbed by phagocytes. No histological methods, easy to identify (site), may be confused with melanin

Exogenous

50
Q

what is Asbestos pigment (and facts) and what type of pigment is it

A

Long beaded fibres (silica), cause fibrosis, may lead to asbestosis and mesothelioma.
Fibres become coated in protein sheaths containing haemosiderin,

51
Q

histology staining for asbestos?

A

demonstrated by Perl’s Prussian Blue (asbestos bodies).

52
Q

histology staining for carbon

A

no histological methods

53
Q

what is coal workers lung called

A

anthracosilicosis

54
Q

what causes coal workers lung

A

The accumulation of carbon (anthracosis) and silica (silicosis) in the lungs from inhaled coal dust.

Pathogenesis particles are taken up by macrophages and they store them. Production of fibrogenic factors, toxic factors, and proinflammatory factors

55
Q

what are other names for coal workers lung disease

A

pneumoconiosis or silicoanthracosis.
Pathogenesis particles are taken up by macrophages and they store them. Production of fibrogenic factors, toxic factors, and proinflammatory factors

56
Q

pathogenesis in detail of coal workers lung disease

A
  1. silica/coal/asbestos enters alveolar and taken up my macrophage

Results-

2a. Recruitment and activation of inflammatory cells (IL-6, TNF-a) etc causing more toxic factors to be released
2b. Toxic factors (proteases, O2, free radicals) released and cause lung injury - fibrosis
2c. Fibrogenic factors (TNF-a, fibronectin) recruit fibroblasts and collagen production - fibrosis

57
Q

what does an asbestos body look like in histology

A

dumbell shaped body

58
Q

what 3 things do asbestos bodies cause in the alveolar

A

interstitial fibrosis
pleural fibrosis
pleural plaque

59
Q

define lipids

A

naturally occurring fats and fat-like substances, usually insoluble in water, but soluble in fat-solvents

60
Q

what do lipids look like in histology

A

big clear blobs

61
Q

what enzymes break down lipids

A

bile salts, esterases, lipases

62
Q

true or false - fats are essential for the absorption of vitamins

A

true - except for B group

63
Q

what are fat cells called

A

adipocytes

64
Q

what are the classification of lipids

A

simple lipids
compound lipids
derived lipids
hydrocarbons

65
Q

examples of simple lipids

A

neutral lipids and waxes

66
Q

examples of compound lipids

A

Phospholipids, Cerebrosides

67
Q

examples of derived lipids

A

Fatty Acids, Alcohols

68
Q

examples of hydrocarbons

A

Carotenoids

69
Q

what are the different ways we can identify lipids in histology

A
  1. solubility
  2. examination by polarised lipids
  3. reduction by osmium tetroxide
  4. demonstration by other fat soluble dyes (lysochromes)
  5. other staining and histochemical methods
70
Q

what is an oval fat body and where are they observed

A

A cell body filled with fat droplets and no visible nucleus

(degenerated renal epithelial cells) are often observed in nephrotic syndrome of any origin

71
Q

what do lipids look like when they have been reduced by osmium tetroxide

A

dark/black blobs

72
Q

name some lysochromes (fat soluble dyes)

A

Sudan VI
Sudan black
Oil Red O - red/pink blobs
Nile blue

73
Q

what does lysochrome mean

A

fat soluble dyes

74
Q

what is Lipidoses

A

lipid storage disease:

a disorder of lipid metabolism; abnormal levels of certain fats accumulate in body. They are classified by the enzyme defect or the type of lipid involved (e.g. Sphingolipidoses)

75
Q

what is lipidoses an end product of

A

enzyme problem - genetic

76
Q

where does lipidoses usually occur

A

Majority in Central Nervous System (e.g. Ganglion cells in rectum

77
Q

what are the limitations of lab technique staining for lipids

A

Physical properties of lipids – change from “norm” of reaction (pure lipids stain differently from mixtures)

Melting points – 370C = fluid in body, solid in section, therefore may or may not stain or react with reagents

Transfusion (6 decks)

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