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General Pathology > Cell Adaptations & Accumulations > Flashcards

Cell Adaptations & Accumulations Flashcards

1
Q

Define atrophy

A

Decreased size and/or number of cells after it reached its normal size (decrease in number and size of organelles).

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2
Q

Define Hypoplasia

A

tissues or organs that are smaller than normal because they never developed completely.

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3
Q

What are the mechanisms of atrophy?

A

Apoptosis and autophagy

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4
Q

Define Autophagy

A

Autophagy: Cells consume their own damaged organelles, as a housekeeping function, to remain alive.

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5
Q

What are the causes of atrophy?

A
  1. Nutrient deprivation (lack of adequate blood flow)
  2. Loss of hormonal stimulation,
  3. Decreased workload (disuse atrophy)
  4. Denervation (especially in skeletal muscle)
  5. Compression (adjacent to neoplasms or other masses)
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6
Q

Insert atrophy images here

A
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7
Q

Define hypertrophy and give an example.

A
  • Increase in size and volume of a tissue or an organ due to increase in cell size
  • Increase in size or number of organelles
  • Ex: Heart and skeletal muscle (cells are postmitotic and incapable of replication)
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8
Q

What are the causes of hypertrophy?

A

Increased workload.

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9
Q

Define hyperplasia. How can this occur?

A
  • Increase in number of cells

* This response can occur only in a cell population that is capable of mitosis (epithelial cells respond quickly)

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10
Q

What is the difference between Hyperplasia and Neoplasia?

A

Differs from neoplasia because subsides if the stimulus is removed.

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11
Q

What are the causes of Hyperplasia?

A
  • Hormonal stimulation (mammary glands and endometrium during lactation and gestation, respectively)
  • Iodine deficiency leading to thyroid hyperplasia (goiter)
  • Idiopathic: nodular hyperplasia in spleen, liver, adrenals in older dogs
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12
Q

Hypertrophy image

A
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13
Q

What happens as a result of iodine deficiency?

A

The thyroid needs iodine to function properly. Lack of iodine –> thyroid responds with hyperplasia to capture and try to produce thyroid hormone. Without iodine, pituitary gland will release a lot of TSH –> Hyperplasia of follicular cells in colloid.

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14
Q

Hyperplasia image

A
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15
Q

Define metaplasia. Give an example

A

Change of cell type of the same germ line. Usually decrease in function associated with change of cell type.
Ex: Squamous epithelial → Columnar epithelial, translational epithelial —> squamous epithelial

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16
Q

What can Metaplasia act as? Give examples.

A

Metaplasia can act as a protection mechanism in response to chronic injury.
Examples:
1. Squamous metaplasia of trachea and bronchi in smokers can lead to full neoplastic transformation
2. Vitamin A deficiency: Squamous metaplasia.
3. Chronic regurgitation can lead to intestinal (columnar) metaplasia of the esophagus and predispose to esophageal tumor. (Barrett’s esophagus) neoplastic.

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17
Q

Metaplasia image

A
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18
Q

Define dysplasia. Give an example

A

Implies an abnormality in formation of a tissue.

E.g. renal and hip dysplasia

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19
Q

What is the definition of dysplasia when it is applied to epithelium? What is it caused by?

A
  • When applied to epithelium, dysplasia implies a disorganized cells varying in size, shape, with nuclear pleomorphism and increased mitotic figures.
  • Always pre-neoplastic
  • Induced by chronic injury such as UV radiation, viruses
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20
Q

Dysplasia image

A
21
Q

List all of the types of intracellular accumulations.

A 
• Intracellular
	◦ Lipids
	◦ Glycogen
	◦ Proteins
	◦ Viral inclusion bodies
	◦ Lead inclusions
22
Q

List all of the types of extracellular accumulation

A
  1. Amyloid
  2. Fibrinoid change
  3. Cholesterol
  4. Urate trophi
23
Q

Define lipidosis.
What is this process also called?
Where does this occur? What happens as a result?

A

Lipidosis is the accumulation of lipids within parenchymal cells.
It is also called steatosis.
Develops in many tissues, but because the liver is important to lipid metabolism, hepatic lipidosis is common.

24
Q

Any defect in these steps (3) leads to lipid accumulation:

A

Uptake, Catabolism, Secretion

25
Q

What are the causes of hepatic lipidosis?

A

Increased delivery of fatty acids to the hepatocyte
◦ Starvation in overweight animals
◦ High fat diet
◦ Diabetes mellitus (increased mobilization from fat stores)
Decreased mobilization of lipids from hepatocytes
◦ Suppression of fatty acid oxidation: Hypoxia, any other cell damage
◦ Suppression of apoprotein synthesis and impaired release of lipoproteins from hepatocytes: Toxins such as Aflatoxins

26
Q

Lipidosis image

A
27
Q

In homeostasis, where is glycogen stored? In metabolic abnormalities?

A

Homeostasis: Glycogen is stored in hepatocytes and skeletal muscle.

Metabolic Abnormalities: Glycogen accumulates is a result of Diabetes mellitus and canine hyperadrenocorticism.

Also in glucocorticoid therapy (exogenous source)

28
Q

Glycogen accumulation image

A
29
Q

Histologically, proteins are?

A

Eosinophilic (pink to orange to red in an H&E

30
Q

When is the term “hyaline” used when referring to proteins? Give examples

A

• When it has a homogenous, eosinophilic and translucent appearance the term “hyaline” is used
Example:
◦ Hyaline droplets in the apical cytoplasm of proximal renal tubular epithelial cells in protein-losing nephropathy.
◦ Mott cells have cytoplasmic hyaline globules (Russell bodies): they are immunoglobulins. Mott cells are plasma cells containing immunoglobulins.

31
Q

Protein resorption droplets

A
32
Q

Define viral inclusion bodies

A

Viral inclusion bodies are proteins produced by viral replication

33
Q

What is the difference between a DNA virus and an RNA virus? Give examples

A

◦ DNA viruses produced Intranuclear inclusion bodies (Herpesvirus, Adenovirus, Papilloma)
◦ RNA viruses produced Intracytoplasmic inclusion bodies (Rabies)

34
Q

What are the exceptions to the definition of viral inclusion bodies?

A

• Exceptions:
◦ Poxviruses are DNA and produce cytoplasmic inclusion bodies.
◦ Distemper virus (Morbillivirus, family Paramyxoviridae) produce both cytoplasmic and nuclear inclusion bodies.

35
Q

Viral inclusion image

A
36
Q

What happens in some cases of lead poisoning? What stains are ideal for this type of case?

A
  • In some cases of lead poisoning, intranuclear inclusion develop in renal tubular epithelial cells.
  • The inclusions are a mixture of lead and protein.
  • More easily observed with acid-fast stain (Ziehl–Neelsen) than H&E
37
Q

Lead inclusion image

A
38
Q

Define amyloid.

A

• Misfolding disorder of soluble and functional proteins, converting them into insoluble and nonfunctional aggregates

39
Q

Where can amyloids be deposited?

A

• It can be deposited in any tissue but is commonly found in the liver, kidney, and vessel’s wall

40
Q

What are the mechanisms of amyloidosis?

A
  • Propagation of misfolded proteins that serve as a template for self- replication
  • Accumulation of misfolded proteins due to failure to degrade them.
  • Genetic mutations that promote misfolding of proteins (Alzheimer’s and Huntington’s disease).
  • Protein overproduction because of abnormality or proliferation in the synthesizing cell (Plasma cell neoplasia).
41
Q

How is amyloidosis classified?

A
  • Amyloid can be classified by the biochemical identity of protein
  • AA (systemic, derived from serum amyloid A)
  • AL (localized, derived from immunoglobulin light chains)
  • Hereditary or familial AA
  • Histologically similar
42
Q

Describe AA Amyloidosis

A

• Serum amyloid A (AA) is produced by hepatocytes in cases of chronic inflammation
• Systemic deposition of serum AA (fibrillar protein)
• Commonly deposited in the kidney (renal glomeruli) and Liver (space of Disse)
• Hereditary or familial forms of AA Amyloidosis
◦ Shar-Pei dogs and Abyssinian cats
◦ Renal medullary interstiium +++, rather than renal glomeruli

43
Q

Describe AL Amyloidosis

A
  • Localized form of amyloidosis
  • Derived from immunoglobulin light chains
  • Commonly deposited adjacent to plasma cell tumors
  • Nasal amyloidosis in horses (conjunctiva might be affected)
44
Q

Amyloidosis image

A
45
Q

Define fibrinoid change

A
  • Leakage of plasma proteins into the wall of a blood vessel.
  • Septic or immune-mediated vasculitis.
46
Q

Fibrinoid change iamge

A
47
Q

Where does cholesterol form?

What does it induce?

A
  • Form in tissue at sites of chronic hemorrhage and in atherosclerosis
  • Induce inflammatory response
48
Q

Atherosclerosis image

A
49
Q

Define urate trophi.
In what species does this occur in?
What can it lead to?

A

• Deposition of crystals of uric acid in cases with hyperuricemia (renal disease or dehydration)
- Birds, primates, reptiles

General Pathology (2 decks)

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