Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Pigments, Infiltrates > Flashcards

Pigments, Infiltrates Flashcards

1
Q

What are 3 things an increase in pigment cause?

A

Anthracosis, melanosis, lipofuscin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are 2 things a decrease in pigment causes?

A

Albinism, acquired depigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are 2 types of normal cells producing pigment and what species are they found in?

A

Chromatophores -> birds, fish, reptiles

Melanin -> birds, mammals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are 3 types of chromatophore?

A

Xanthophore, erythrophore, iridophore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is intracellular accumulation?

A

Accumulation of abnormal amounts of substance -> can be normal but excessive or abnormal (endogenous or exogenous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are 2 causes of intracellular accumulations?

A

Inherited or acquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are 3 types of abnormal intracellular accumulations? (what do they do)

A
  1. Normal excessive -> rate of metabolism not enough to remove
  2. Normal or abnormal endogenous accumulation -> accumulates due to defect in its metabolism, packaging or transortation
  3. Abnormal exogenous -> accumulates eg carbon inhalation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is an example of a disorder caused by exogenous pigements? What is the histology associated with this?

A

Anthracosis -> accumulation of carbon in lungs + lymph nodes

Carbon phagocytosed by macrophages and cant be degraded

Histology -> fine blue/black granules in macrophages in airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are 2 examples of a disorder caused by endogenous pigements?

A

Melanosis (excess) and albinism (deficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What enzyme is associated with albinism and how do acquired deficiencies occur?

A

Tyrosinase

Can get acquired deficiency due to copper deficiency not allowing enzyme to function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is melanosis and what are the types?

A

Generalised -> Induced by UV

Localised -> lung, liver, meninges, maternal caruncles - angus cattle have melanin everywhere

Congenital naevi -> dermal accumulations of melanoblasts (moles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does soft tissue calcinosis form?

A

Cacinogenic plants contain steroidal glycoside - this hydrolyses and has vitamin D3 activity

Creates excessive Ca2+ binding protein -> increases GIT absorption -> hypercalcaemia + soft tissue calcificiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does lipid accumulation occur and where is it most common?

A

Liver (also in kidney and skeletal muscle)

Causes large lipid vacuoles in parenchymal cells and pale liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does accumulation of protein cause?

A

Resorption droplets in proximal convoluted tubules of the kidney -> proteinuria (brown colour due to haemoglobin) -> hyaline droplets in cytoplasm of those cells

Or excessive normal secretion causes immunoglobulins in plasma cells (russell bodies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does glycogen accumulation cause?

A

Hepatocytes and respiratory epithelium in newborns -> cells with central nucleus and clear cytoplasm

Liver will be pale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are 2 lipopigments?

A

Ceroid and Lipofuscin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are lipopigments derived from?

A

Lipid-peroxidation products of membrane polyunsaturated FA’s - accumulate in lysosomes in cells which do not divide (neurons, muscle, skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does ceroid accumulation result from and cause?

A

Results from peroxidation of fat deposits

Yellow pigment

Ovine white liver disease - ceroid accumulates in hepatocytes then sinusoidal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes accumulation of lipofuscin and what does it cause?

A

Derived from lipid peroxidation of membrane unsaturated FA -> accumulation in lysosomes of cells that dont divide (neurons, muslce, skin)

Yellow brown granular pigment - does not affect cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is lipofuscin accumulation associated with?

A

Aging -> generation of free radicals as byproducts of metabolism

Prevented by vitamin E -> inhibits peroxidation by incorporating into lipid bilayer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is lipofuscinosis?

A

In dogs -> brown dog gut

Gut smooth muscle atrophy and myocyte cytoplasm full of lipofuscin

22
Q

What is haemosiderin and how does it form?

A

Yellow brown granular pigment containing ferric iron (Fe3+) mostly derived from breakdown of haemoglobin

  • erythrocyte phagocytosis after haemorrhage
  • Haemolytic anaemias and ovine mycoplasma ovis infection
23
Q

Where does haemosiderin accumulate?

A

Macrophages, sites of haemorrhage or fixed marcophages in hepatocytes/spleen/renal tubular cells

24
Q

What does haemosiderin cause grossly?

A

Brown discolouration of tissue

25
Q

How is excess Fe dealt with?

A

No mechanism to excrete, only can be scavenged (can get toxicity)

26
Q

What is hepcidin and what does it do?

A

Peptide hormone produced by the liver
Inhibits Fe transport by binding to + degrading fe2+ channel ferroprotin on enterocytes, hepatocytes and macrophages

Controls intake and release from cells

27
Q

What are 3 steps of haemoglobin breakdown?

A
  1. Globin chains degraded to aa and reutilised for protein synthesis
  2. Fe converted to ferritin -> may accumulate as haemosiderin
  3. Haeme -> biliverdin -> free bilirubin (in resident tissue macrophages)

Happens in bruise/spleen

28
Q

How is bilirubin excreted?

A

Hepatocytes convert free bilirubin to conjugated bilirubin (soluble and non-toxic)

Conjugated bilirubin excreted in bile and discharged into the intestine

29
Q

What is icterus and what does it result from?

A

Jaundice -> accumulation of bilirubin

30
Q

What are 3 types of jaundice?

A

Haemolytic (prehepatic)
Toxic (Hepatic)
Obstructive (post-hepatic)

31
Q

What do birds and reptiles do that differs to mammals in regard to bilirubin?

A

They make biliverdin and excrete it (only small amount of bilirubin as lipid based antioxidant)

32
Q

How do fetuses get rid of bilirubin?

A

Through the placenta (lipid based)

Couldnt get rid of biliverdin as it is water based

33
Q

What is haemolytic icterus?

A

Pre-hepatic jaundice
Increased breakdwon of erythrocytes -> may be haemoglobinaemia, haemoglobinuria and increase in unconjugated bilirubin in the blood

Hepatic system overloaded

34
Q

What happens in hepatic icterus?

A

Hepatic jaundice
damage to hepatocytes canot conjugate or excrete bilirubin -> increased free bilirubin in blood with no evidence of haemolysis

May be increased urobilinogen as may not be re-excreted by damaged liver

35
Q

What is obstructive icterus?

A

Obstruction of excretion of conjugated bilirubin due to blockage of bile ducts

Increased conjugated bilirubin in blood
Reduced serum and urine urobilinogen with pale faeces

36
Q

What is amyloidosis and what are the two broad types?

A

Amyloid proteins abnormally deposited in organs or tissue

15 types classified by protein precursors from which amyloid fibril is derived

Pattern of amyloid can be systemic (vessels affected) or localised

37
Q

What are 3 types of systemic amyloidosis?

A

Primary amyloidosis

Amyloid protein: light chains

Reactive amyloidosis

38
Q

what is primary amyloidosis?

A

Associated with multiple myeloma

Malignant plasma cells synthesise excessive immunoglobulin light chains

39
Q

What is amyloid protein light chain amyloidosis?

A

Accumulate in tissue and pass in urine

40
Q

What is reactive amyloidosis?

A

Associated with chronic inflammation autoimmune disease

A persistent systemic acute phase response - extra serum amuloid A or inflammatoru proteins deposit in tissues

41
Q

What are the types of renal amyloidosis?

A

If in renal glomeruli -> protein loss in urine

If interstitial amyloidosis in medulla -> glomerulus is working but cannot concentrate urine

42
Q

What is feline pancreatic amyloidosis?

A

Islet amyloid polypeptide secrete by beta islet cells along with insulin -> insulin disrupted

43
Q

What happens in Alzheimers?

A

Cerebral cortex gets foci of degenerate axons and neurites surrounding core of amyloid fibrils

44
Q

How do crystals form?

A

Ingested by plants containing oxalate - accumulate of calcium oxalate crystals mostly in kidney tubules and sometimes CNS

45
Q

What is gout?

A

Uric acid or urate crystals deposited in tissues

46
Q

What is pathological calcification and what are two types?

A

Dystrophic mineralisation - found in areas of necrosis wher Ca precipitates

Metastatic mineralisation - normal tissues with hypercalcaemia - destriuction of bone, increase PTH secretion, renal failure + vitamin D toxicity

47
Q

How do lysosomal storage diseases happen?

A

Partial or lack of lysosomal hydrolase -> substrates stored

Mostly autosomal recessive

47
Q

How do lysosomal storage diseases happen?

A

Partial or lack of lysosomal hydrolase -> substrates stored

Mostly autosomal recessive

48
Q

what is alpha mannosidosis and how does it start?

A

Autosomal recessive a-mannose deficiency in lysosomes

Mannose containing oligosaccharides accumulate + neurons + epithelial cells vacuolated

Aquired by toxic plants containing swainsonine that inhibits a mannosidase

49
Q

What is glycogenoses?

A

Glycogen accumulates in lysosomes of skeletal and cardiac muscle, liver and CNS

Swollen + vacuolated cytoplasm

Inherited deficinecy of lysosomal a,1,4-glucosidase

50
Q

What is galactocerebrosidosis

A

Cell leukodystrophy of cairn terriers and poll dorset

Deficnecy of enzyme -> accumlation of galacotocerebrosides in myelin sheath

= decrease myelin formation

Lipid accumulates in oligodendroglia and globoid cells in perivascular areas in CNS

Pathology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions