Pigmentation and Mineralization Flashcards
1
Q
Exogenous Pigments
A
- Involves accumulation of foreign pigments from external environment
- Enter via skin, lung, intestinal tract
2
Q
Carbon (anthracosis)
A
- Most common exogenous pigment.
- Usually inhaled, esp urban environments
- Carbon–> lung parenchyma, stored in macrophages–>ultimately tracheobronchial lymph nodes
- Inert thus remains for life, causes no real functional issues
- Histologically, carbon in lungs intra- or extra cellularly
3
Q
Dusts (pneumoconiosis)
(Exogenous Pigment)
A
Pneumoconiosis = inhalation & retention of dusts e.g. silicosis and asbestosis
Small particles, evade mucociliary system of nose/upper resp tract –> Chronic irritation–> Pulmonary fibrosis and/or tumours (mesotheliomas)
Asbestos fibres–> alveolar spaces- penetrates walls–> pleural space –> chronic irritation, can–> tumours
4
Q
Carotenoids
(Exogenous Pigments)
A
- Plant derived pigments. They have essential functions but in excess they can stain tissues, but need to be consumed!
- Horses & Channel Island cattle naturally have more of this present in their fat & CT–> yellowish appearance
- Horse fresh tissue. Fatter horses is very yellow, they just contain high levels of carotenoids
- Plant origin, incl β-carotenes (Vit A)- Fat-soluble–> yellow/orange fat
- Stain: many normal tissues (adrenal cortex, testes, corpus luteum,
- serum), animal products (egg yolks, butter)
• Not to be mistaken for icterus (jaundice)
5
Q
Iatrogenic
(Exogenous Pigments)
A
Iatrogenic
- Tattoos – pigments (incl C) loose in dermis or in macrophages
- Tetracycline-based antibiotics – use during development of teeth & bone–> discolours (yellow/brown)- Avoid giving puppies and kittens, young animals. Will stain their teeth.
- Iron dextran injections (young piglets)- can–> iron deposits in tissue
6
Q
Endogenous Pigments
(Melanin)
A
- Present in skin, hair, eyes (iris)
- Melanin granules are located above nucleus within cells of skin/ hair/ iris- shields nucleus from UV light
- Melanocytes contain granules (melanosomes) which synthesise melanin- Melanocytes are constantly producing melanin granules
- -get a little melanin cap, protecting nucleus from UV light. Tanning is either more melanocytes or melanin granules (melanin production)
- 1 melanocyte per every 10/20 epithelial cells, traffic granules to cells via dendrites
- Quantities affected by genetics (albinism), UV light exposure, chronic skin damage, copper deficiency (tyrosinase)
7
Q
Melanosis
A
- Congenital accumulation in some tissues, in some species (melanocytes migrate to wrong place)
- Instead of melanin collecting in the skin, melanocytes get lost embryonically and end up in unusual spaces. Lung, meninges. No pathological significance.. Just odd looking
- e.g. lung (ruminants, pigs), meninges (sheep).
- No functional relevance, not pathogenic
- Organs affected may be condemned at meat inspection
8
Q
Hyperpigmentation
A
- Due to ↑ melanocytes/ ↑ melanin production e.g. bilaterally pigmented= typical of endocrine diseases. (hyperadrenocorticism - “Cushing’s disease”)
- bilaterally symmetrical alopecia
- increased cortisol causes increased pigmentation of the skin
- down the abdomen, and down the legs
- classic for an endocrine disease
9
Q
Hypopigmentation
A
- Congenital/hereditary or acquired (Cu deficiency)
- Albinoism: congenital lack of tyrosinase enzyme. This is important in producing melanin. If you have a defect and the enzyme is defective, you have a congenital lack of melanin
- Can have a copper deficiency, this is also a co-factor for melanin production. See more often in farm animals. Can get pale skin, or pale eyes(pale spectacles)
- Chronic inflammation of skin –> disrupts basal layer of epidermis–> leakage of melanin into the dermis (‘melanin incontinence’)- Should just be forming melanin caps in the epidermis. can occur due to autoimmune diseases e.g. SLE (lupus), DLE- No black nasal pigmentation–> depigmented. Sign that it is an autoimmune disease
10
Q
Melanoma
A
- Tumour of melanocytes (Melanocytoma= benign, Melanoma= malignant)
- Usually start near peritoneum and then spread in horses
-In dogs/cats find around the mouth and eyes
- Grey horses (perineal melanomas that can spread as the animal ages), dogs, cat (skin, mouth- more often, digit, eye), May be amelanotic (skin cancer where cells don’t make melanin)
- amelanotic: just becasue a mass is not black (pigmented) does not mean it is not a melanoma. In becoming a tumor somethimes they undergo mutations that make them lose the ability to make melanin
11
Q
Haemoglobin
(Endogenous Pigments blood/bile)
A
Haemoglobin- Colour normally varies with oxygenation.
- In haemolytic diseases: plasma becomes red,
- kidneys –> stain dark red
- & urine–> red (haemoglobinuria)
- Distinguish between haemoglobinuria & haematuria: if free haemoglobin–> remains red when span
12
Q
Haemosiderin
(Endogenous Pigments- Blood/Bile)
A
- Intracellular protein-iron complex- Forms after trauma/ haemorrhage from splitting Hb. - Stored in protein complex, way for the body to recycle iron. Get the iron by lysing RBC’s
- Accumulates locally–> yellow-brown pigmentation of old bruises. -iron that is stored in macrophages in the tissue can stain yellow/brown/green
- Diffuse/excessive accumulations with ↑ RBC breakdown (haemolysis).
- Heart failure accumulation in vascular tissues (esp lung)- RBCs lysed, phagocytosed by macrophages in alveoli –>“heart failure cells”
- a lot of blood that gets pooled in the lungs can form an edema
- Get left with Haemosiderin. If you can find these Haemosiderin filled macrophages, you can find that the animal was undergoing heart failure at time or before death
- Can be distinguished using Perl’s Prussian blue stain- Melanin will not stain with this blue, but Haemosiderin will
13
Q
Bilirubin
(Endogenous Pigments- blood/bile)
A
- Jaundice
- bilirubin is a Yellow, or yellow-brown pigment
- Remains of haeme (after iron removed & stored)- Found in macrophages at sites of RBC breakdown-
This is what is left is the Haeme molecule that forms the bilirubin, taken away iron
- Accumulation throughout body –> diffuse yellowing of tissues= icterus/ jaundice
- Occurs with: Excess production (too many RBCs being lysed). Inadequate removal of bilirubin from the body
- Bilirubin stains bright green with Fouchet stain
- With this condition there are 3 potential routes to how this could have occured
14
Q
Classification of Jaundice
A
- normally: Unconjugated form of bilirubin= insoluble, has to be bound to albumin to travel in blood & trafficked to liver where conjugation occurs (Livers function is to conjugate bilirubin)–> s_olubilised by glucuronic acid so it can be excreted_, albumin no longer req.–> Vast majority goes to bile: gives it the green color! (Progressively excreted into small intestine, Bile aids in digestion! (lipids)). There is recycling of bile by enterohepatic circulation which returns to the liver and then a small component that becomes Stercobilin (final component in faeces)
- small amount is excreted from kidneys as urobilin
- Lesions can cause unconjugated/ conjugated bilirubin to build up in body, in either case, can–> jaundice
- in animals with these cases important to realize how much conjugated bilirubin there is vs. conjugated to tell which type it is
- More unconjugated= pre-hepatic, more conjugate (post-hepatic)
- Pre-hepatic (haemolytic) icterus-
- problems occuring before the liver
- Excessive production of bilirubin due to haemolysis–> ↑ unconjugated bilirubin in blood
- Also low albumin can be a rate limiting step as it needs to bind to be soluble
- Liver functioning normally, but conjugation rate isn’t quick enough so it accumulates- Overwhelms liver capacity to conjugate it- the bilirubin will then deposit in animals tissues making it look clinically jaundice
E.g. Large haemorrhage into tissues (e.g. intrabdominal from car accident) , or infectious (e.g. Leptospirosis, Babesiosis) or immune-mediated erythrocyte breakdown (AIHA)-autoimmunehemolytic anaemia: A LOT OF RBCs BEING BROKEN DOWN - Hepatic icterus
- Liver (Hepatocyte) damage (↓ conjugation)- may function a little but not sufficiently
- see ↑ unconjugated bilirubin in blood (& some conjugated bilirubin in blood) depending on liver capacity. E.g. Liver damage by chemical or toxic causes, hepatocellular tumour. chronic alcoholism –> damage to liver
- Post-hepatic (obstructive) icterus
- Obstruction of bile excretion
- ↑ conjugated bilirubin in blood
E.g. Obstruction of bile outflow by gall stone, tumour, inflammation
-Blocking of excretion of conjugated bilirubin in the blood, but liver is working normally
15
Q
Acid haematin
A
Black Spots
Annoying histological artefact. Brown/black granular. can occur in unbuffered formalin, formalin that has gone off or heated during transport, pH will drop and if it is below 6 you can get this acid haematin (between formalin and haemagloblin in the tissue)
- Acid in unbuffered formalin (pH < 6) (or gastric ulcers) binds with Hb–> pigment
- can see this in tissues as well with a lot of Hb and normal formalin (tissues with a lot of bood in them)
- Has to be distinguished from haemosiderin (use Perl’s Prussian Blue)
- Would get a Fouchet stain that is negative
19
Q
Dystrophic Calcification
A
occurs in degenerate or necrotic tissues. local depostion in degenerate or necrotic tissues
-Have irregularly fragmented, blue, material
- e.g. granulomas (TB), dead parasites, Vit E/Se deficiency (antioxidants) etc.
- Normal serum Ca (but may be accentuated by hypercalcaemia), Ca metabolism normal
- Formation: dead/dying cells no longer able to regulate their Ca2+ influx, so start to accumulate it
- Histo: irregular blue-purple fragments
- Usually irreversible- may indicate previous tissue damage & may affect organ function in severe cases
- Intervertebral disc degeneration & mineralisation can–> ↓ elastic–> prolapse. As animal ages the disks become more mineralised. Any impact or pressure can cause center to rupture or put pressure on nerve roots. Be aware of herniation
- White muscle disease, occurs in large ruminants, due to vitamin and selenium deficiency
-Build up of free radicals in heart and a deficiency of these nutrients leads to this mineralized dystrophic disease
22
Q
Gout
(Mineralisation- Crystal Formation)
A
Gout = deposition of sodium urate crystals in tissue. Occurs in birds, reptiles, (man).
-Rather uncommon, just see more in birds and reptiles ( and humans)
- Excess production/ insufficient excretion –> deposition of uric acid salt crystals (from purine metabolism)
- deposition of crystals when uric acid levels in blood exceed solubility
- Articular form (rare), birds & tortoises. Tophi with acute–> chronic inflammation
- Visceral form. More frequent. Serous membranes, esp pericardium
-In kidney crystals block tubules & ureter lumens
- Causes (sporadic): Vit A deficiency, Prior kidney damage, ↑ protein diet, Dehydration
- Diagnose usually P.M.
27
Q
Fouchet Stain
A
- Bilirubin stains bright green with Fouchet Stain
- fat becomes very yellow and may see liver become very yellow
- If there is an abnormal amount of bilirubin in the liver, can use the stain to be sure (since it could be mistaken for haemosiderin and melanin)
