Cell Adaptations & Accumulations

Question 1

Define atrophy

Answer 1

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

Question 2

Define Hypoplasia

Answer 2

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

Question 3

What are the mechanisms of atrophy?

Answer 3

Apoptosis and autophagy

Question 4

Define Autophagy

Answer 4

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

Question 5

What are the causes of atrophy?

Answer 5

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)

Question 6

Define hypertrophy and give an example.

Answer 6

• 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)

Question 7

What are the causes of hypertrophy?

Answer 7

Increased workload.

Question 8

Define hyperplasia. How can this occur?

Answer 8

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

Question 9

What is the difference between Hyperplasia and Neoplasia?

Answer 9

Differs from neoplasia because subsides if the stimulus is removed.

Question 10

What are the causes of Hyperplasia?

Answer 10

• 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

Question 11

Define metaplasia. Give an example

Answer 11

Change of cell type of the same germ line.
Ex: Squamous epithelial → Columnar epithelial, translational epithelial —> squamous epithelial

Question 12

What can Metaplasia act as? Give examples.

Answer 12

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.

Question 13

Define dysplasia. Give an example

Answer 13

Implies an abnormality in formation of a tissue.
E.g. renal and hip dysplasia

Question 14

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

Answer 14

• 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

Question 15

List all of the types of intracellular accumulations.

Answer 15

• Intracellular
◦ Lipids
◦ Glycogen
◦ Proteins
◦ Viral inclusion bodies
◦ Lead inclusions

Question 16

List all of the types of extracellular accumulation

Answer 16

1. Amyloid
2. Fibrinoid change
3. Cholesterol
4. Urate trophi

Question 17

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

Answer 17

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.

Question 18

What are the causes of hepatic lipidosis?

Answer 18

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

Question 19

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

Answer 19

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)

Question 20

Histologically, proteins are?

Answer 20

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

Question 21

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

Answer 21

• 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.

Question 22

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

Answer 22

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

Question 23

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

Answer 23

• 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

Question 24

Define amyloid.

Answer 24

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

Question 25

Where can amyloids be deposited?

Answer 25

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

Question 26

What are the mechanisms of amyloidosis?

Answer 26

• 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).

Question 27

How is amyloidosis classified?

Answer 27

• 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**

Question 28

Describe AA Amyloidosis

Answer 28

• 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

Question 29

Describe AL Amyloidosis

Answer 29

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

Question 30

Fibrinoid change iamge

Question 31

Where does cholesterol form?
What does it induce?

Answer 31

• Form in tissue at sites of chronic hemorrhage and in atherosclerosis (thickening/hardening of arteries caused by a buildup of plaque in the inner lining of an artery).
• Induce inflammatory response

Question 32

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

Answer 32

• Deposition of crystals of uric acid in cases with hyperuricemia
- Birds, primates, reptiles

• May lead to renal disease or dehydration