pathology (wk 2) Flashcards

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1
Q

what are haematogenous pigments?

A

pigments that are derived from the haemoglobin molecule within erythrocytes (includes haemoglobin, haemosiderin, bilirubin, and haematoidin, haematin, porphyrin)

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2
Q

what is the haemoglobin molecule composed of?

A

four subunits of the protein “globin, each of which is folded about a molecule of “haeme” (a tetraphyrrolic ring with a central atom of iron)

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3
Q

what is the main organ in charge of removing old or damaged red blood cells?

A

the spleen - it has splenic macrophages that are able to recognise old and damaged red blood cells and remove them from the circulation via phagocytosis

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4
Q

haemolysis is a pathological process - what does it mean?

A

the destruction of red blood cells before they reach the end of their lifespan (eg haemolytic diseases - where large numbers of red blood cells are damaged)

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5
Q

what is extravascular haemolysis?

A

the same as normal RBC removal (takes place in the spleen, macrophages involved etc) but with excessive levels of red blood cells being taken out

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6
Q

what is the globin from haemoglobin used for after haemolysis?

A

the globin is converted into amino acids in the macrophage which can be reused for protein synthesis

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7
Q

what two components do does haemoglobin break down into in the splenic macrophage?

A

heme and globin

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8
Q

how is haemosiderin formed?

A

golden brown granules formed from the iron from heme binding with ferritin

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9
Q

how is bilirubin formed?

A

a yellow pigment made from the non-iron part of the heme from the haemoglobin (this then goes to the liver)

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10
Q

what is intravascular haemolysis?

A

the red blood cells rupture within the circulatory system, releasing haemoglobin directly into the plasma

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11
Q

what is haemoglobinaemia?

A

a symptom of intravascular haemolysis - the haemoglobin from the ruptured RBC’s stains the plasma pink

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12
Q

what is haemoglobinuria?

A

pink pee due to haemoglobin released from intravascular haemolysis passing through the kidneys and staining the urine

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13
Q

What are the pigmented breakdown products formed during extravascular haemolysis?

A

haemosiderin and bilirubin

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14
Q

If you measure the PCV (packed cell volume) from an animal with marked extravascular haemolysis, what would the reading show?
a. Increased PCV
b. Normal PCV
c. Decreased PCV

A

c. Decreased PCV - with extravascular haemolysis there is destruction of large numbers of RBC’s, leading to haemolytic anaemia

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15
Q

What is the main pigmented substance released during intravascular haemolysis?

A

haemoglobin

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16
Q

The consequence of massive intravascular haemolysis is visible discoloration of the plasma and leakage of haemoglobin in the urine - what are the terms for these conditions?

A
  • haemoglobinaemia (pink plasma)
  • haemoglobinurea (pink urine)
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17
Q

What condition will be present in an animal with massive intravascular haemolysis?
a. Muscle atrophy
b. Anaemia
c. Diarrhoea
d. Bruising

A

b. Anaemia - too much RBC spontaneous explosion

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18
Q

the accumulation of large amounts of haemosiderin in macrophages is known as ____ and may be seen when there is a systemic overload of iron - is it….?
a. haemosiderosis
b. haemotoidin
c. hematin

A

a. haemosiderosis (iron deposits in tissues overload)

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19
Q

the bright yellow pigment derived from haemosiderin that is mostly deposited in tissues with haemorrhages (but doesn’t contain Fe itself)… is it:
a. haemosiderosis
b. haemotoidin
c. hematin

A

b. haemotoidin

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20
Q

a brown - black pigment formed by oxidation of haemoglobin (contain iron in the ferric state). this pigment can be found in formalin fixed tissues when the formalin solution was not prepared properly and in tissues affected with certain parasites…. is it:
a. haemosiderosis
b. haemotoidin
c. hematin

A

c. hematin

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21
Q

what happens to bilirubin once it’s made in the macrophage?

A

it’s released into the blood in unconjugated form and couples with albumin - then goes to liver where it’s detached from albumin and conjugated. from there to the bile duct to the small intestine, where it’s now colourless and called urobilinogen (most goes out in faeces, some gets reabsorbed into the urine and makes it yellow)

22
Q

what is jaundice (otherwise known as icterus?)

A

where the tissues of the body are abnormally yellow due to a high concentration of bilirubin in the blood and tissues

23
Q

what are the different colours around a bruise due to?

A

the presence of haemoglobin and it’s breakdown products - haemosiderin and bilirubin

24
Q

what is pre-hepatic jaundice?

A

haemolysis sourced bulk bilirubin, either extravascular or intravascular (note that haemoglonaemia and haemoglobinurea are only seen with intravascular)

25
Q

what is hepatic jaundice?

A

bilirubin buildup due to liver failure - hepatocytes are unable to conjugate and excrete bilirubin like normal

26
Q

what is post-hepatic jaundice?

A

obstructive - build up of conjugated bilirubin due to a blockage of the bile duct

27
Q

post-hepatic jaundice (obstructive): occurs when there is obstruction to the excretion of conjugated bile due to blockage of the bile duct system. This obstruction, which is also known as cholestasis, can be classified as either…

A
  1. extra-hepatic: where the obstruction if in the large bile duct that drains from the liver eg gallstones
    or
  2. intra-hepatic: when there is an obstruction of the tiny bile canaliculi between hepatocytes
28
Q

is bilirubin conjugated in…
a. the macrophage
b. the hepatocyte

A

b. the hepatocyte (initially unconjugated)

28
Q

what are the three decreased formation of melanin conditions?

A

albinism, vitiligo, acquired hypopigmentation

29
Q

what is albinism?

A

a genetically induced condition where no melanin is produced by melanocytes within the whole body - commonly due to an inherited deficiency of the the enzyme tyrosinase

30
Q

what is vitiligo?

A

an immune - mediated attack to melanocytes or keratinocytes leading to depigmented areas in the skin and hair

31
Q

what is acquired hypopigmentation?

A

can be associated with hormone imbalances, a local loss of melanocytes due to physical trauma or chemical injury e.g freeze branding, or due to dietary copper deficiency producing generalised hypopigmentation

32
Q

the three increased formation of melanin conditions?

A

acquired melanosis, congenital melanosis, melanocytic neoplasia

33
Q

what is acquired melanosis?

A

eg suntan - ultraviolet light stimulates an increase in melanin production in exposed skin

34
Q

what is congenital melanosis?

A

(think birthmarks, black marks on dogs gums etc) occurs when melanocytes don’t distribute evenly during embryonic development leading to discrete focal areas of hypopigmentation - these hypopigmented lesions have no clinical significance

35
Q

what is melanocytic neoplasia?

A

refers to a group of growths (neoplasia, cancer) that originates from melanocytes - eg skin cancer

36
Q

what is anthracosis?

A

accumulation of carbon particles (and other dusts) in the lungs and lymph nodes - common in animals living in heavily polluted urban areas (peppered looking lungs, grey/black lymph nodes)

36
Q

what’s wrong with cow no. 4?

A

nothing - it has carotenoid pigmentation of the subcutaneous fat tissue (Carotenoid pigments are present in plants (especially leafy green plants) and can give a yellow orange discolouration to plasma and adipose tissue especially in horses and Jersey dairy cattle. This colour change needs to be differentiated from jaundice.)

37
Q

what is fatty change?

A

abnormal accumulation of triglycerides in parenchymal (functional) cells of organs

38
Q

excessive fat accumulation in the liver (fatty liver) is caused by what three mechanisms?

A
  1. increased fat mobilisation (occurs after starvation etc)
  2. decreased metabolism of fat within hepatocytes
  3. reduced transport of fat out of hepatocytes
    *basically when the lipid metabolism pathway in the picture stops working
39
Q

which fatty liver mechanism occurs after starvation (particularly in obese individuals), with pregnancy toxaemia/ketosis in last gestation ewes carrying twins (“twin lamb disease; sleepy sickness”), with ketosis in high producing dairy cows in early lactation, and in animals with diabetes mellitus (due to increased carbohydrate metabolism due to lack of insulin)?
1. increased fat mobilisation
2. decreased metabolism of fat
3. reduced transport of fat

A
  1. increased fat mobilisation - occurs after starvation
40
Q

which fatty liver mechanism occurs within hepatocytes eg due to abnormal mitochondrial function, pregnancy toxaemia in ewes, alcoholism in humans, and after toxic damage to hepatocytes?
1. increased fat mobilisation
2. decreased metabolism of fat
3. reduced transport of fat

A
  1. decreased metabolism of fat
41
Q

which fatty liver mechanism occurs outside of hepatocytes, often due to decreased synthesis of apoprotein, eg in starvation or protein malnutrition?
1. increased fat mobilisation
2. decreased metabolism of fat
3. reduced transport of fat

A
  1. reduced transport of fat
42
Q

fatty liver - numerous small globules of fat around a central nucleus. is it?
a. acute (recent) fatty change
b. chronic (long standing) fatty change

A

a. acute (recent) fatty change

43
Q

fatty liver - the globules coalesce into one or more globules, which may displace the liver towards the of the cell. is it?
a. acute (recent) fatty change
b. chronic (long standing) fatty change

A

b. chronic (long standing) fatty change - often diseased

44
Q

which mechanism is most likely to lead to fatty liver with ketosis/pregancy toxaemia, starvation of obese animal, diabetes mellitus, high fat diet?
a. increased input to liver
b. decreased output of liver

A

a. increased input to liver

45
Q

which mechanism is most likely to lead to fatty liver with toxins damaging the liver and protein malnutrition?
a. increased input to liver
b. decreased output of liver

A

b. decreased output of liver

46
Q

which substance accumulation can occur with certain metabolic abnormalities in skeletal muscle, with ___ storage diseases in various organs and in the liver with diabetes mellitus or in dogs with an endocrine disease called hyperadrenocortisism?
1. glycogen
2. proteins
3. amyloid

A
  1. glycogen
47
Q

which substance accumulation can occur in the proximal renal tubular epithelial cells in animals with severe, chronic kidney disease?
1. glycogen
2. proteins
3. amyloid

A
  1. proteins
48
Q

which abnormal substance accumulation can occur due to misfolded proteins and that can accumulate locally or throughout the body - in animals the latter results from chronic inflammatory diseases, some cancers etc?
1. glycogen
2. proteins
3. amyloid

A
  1. amyloid