Cell Adaptations: Intracellular & Extracellular Accumulations Flashcards

1
Q

Atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia are all ways cells may __________ to sub lethal injury

A

Adapt

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2
Q

Decreased size and/or number of cells after reaching normal size; decrease in number and size of organelles

A

Atrophy

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3
Q

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

A

Hypoplasia

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4
Q

What are apoptosis and autophagy?

A

Mechanisms of atrophy where cells consume their own damaged organelles as a housekeeping function to remain alive

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5
Q

What are some factors that cause atrophy? (Multiple answers)

A
  • Nutrient deprivation (lack of adequate blood flow)
  • Loss of hormonal stimulation
  • Decreased workload (disuse atrophy)
  • Denervation (especially in skeletal m.)
  • Compression (adjacent to neoplasms or other masses)
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6
Q

What is adrenocortical atrophy, and what does it cause?

A

Destruction (atrophy) of the adenohypophysis that causes a loss of hormonal stimulation

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7
Q

Increase in size and volume of a tissue or an organ due to increase in cell size; increase in size or number of organelles; caused by increased workload

A

Hypertrophy

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8
Q

Why are heart and skeletal muscle prone to hypertrophy?

A

Their cells are post-mitotic and incapable of replication

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9
Q

Increase in the number of cells; can only occur in cell populations capable of mitosis; subsides if stimulus removed

A

Hyperplasia

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10
Q

What are some causes and examples of hyperplasia?

A
  • Hormonal stimulation (mammary glands & endometrium during lactation/gestation)
  • Iodine deficiency (thyroid hyperplasia/goiter)
  • Idiopathic (modular hyperplasa in spleen, liver, or adrenal cortex in older dogs)
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11
Q

Change of cell type of the same germ line (such as squamous epithelial to columnar epithelial); can be a protection mechanism responding to chronic injury, but may be pre-neoplastic

A

Metaplasia

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12
Q

What happens during squamous metaplasia of the trachea and bronchi and smokers?

A

Loss of cilia/goblet cells, leading to a decrease in mucocilliary clearance capabilities

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13
Q

Squamous metaplasia of mucosal glands occurs as a result of which type of deficiency?

A

Vitamin A deficiency

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14
Q

Intestinal metaplasia of the esophagus that predisposes the animal to an esophageal tumor (caused by chronic regurgitation)

A

Barrett’s esophagus

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15
Q

An abnormality in the formation of a tissue; when applied to epithelium, implies disorganized cells varying in size and shape, with nuclear pleomorphism and increased mitotic figures; pre-neoplastic, induced by chronic injury

A

Dysplasia

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16
Q

Lipids, glycogen, proteins, viral inclusion bodies, and lead inclusions are all _____________ accumulations

A

Intracellular

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17
Q

Amyloid, fibrinoid change, cholesterol, and urate tophi (gout) are all ______________ accumulations

A

Extracellular

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18
Q

Accumulation of lipids within parenchymal cells; very common in the liver

A

Lipidosis (steatosis)

19
Q

Normal lipid metabolism consists of uptake, catabolism, and secretion, but what happens if there is a defect in one or more of these steps?

A

Lipid accumulation

20
Q

Starvation in overweight animals, high fat diet, and diabetes mellitus are all causes of…

A

Hepatic lipidosis due to increased delivery of fatty acids to hepatocytes

21
Q

Suppression of fatty acid oxidation (via hypoxia/other cell injury) and suppression of apoprotein synthesis and impaired release of lipoproteins from hepatocytes (via toxins) are both causes of…

A

Hepatic lipidosis caused by decreased mobilization of lipids from hepatocytes

22
Q

What is the general gross appearance of a liver affected by diffuse hepatic lipidosis?

A

Swollen (high rupture risk), yellow, greasy/friable texture

23
Q

What is the microscopic appearance of hepatic lipidosis?

A

Swollen hepatocytes, sharply defined vacuoles, nucleus displaced to periphery

24
Q

Stored in hepatocytes and skeletal muscle; accumulates during metabolic abnormalities (such as diabetes mellitus and canine hyperadrenocorticism)

25
What is the gross appearance of glycogen accumulation (in the liver)?
Swollen, pale brown, mottled appearance
26
What is the microscopic appearance of glycogen accumulation?
Clear cytoplasmic vacuoles; cells irregular sized, exist in multiples, have indistinct outlines, and nuclei not marginated (generally)
27
What is a prominent histological characteristic of proteins?
Eosinophilia (Extra note: the term “hyaline” is used when proteins have a homogenous, eosinophilic, and translucent appearance)
28
Plasma cells containing cytoplasmic hyaline globules (also called Russell bodies) that are also immunoglobulins
Mott cells
29
Proteins produced by viral replication
Viral inclusion bodies Extra note: DNA virus = INTRANUCLEAR inclusion bodies (herpesvirus) RNA virus = INTRACYTOPLASMIC inclusion bodies (rabies) (Generally - there are exceptions)
30
What are two exceptions from the norm for viral inclusion body production?
- Poxviruses (DNA, but produce cytoplasmic inclusion bodies) - Distemper virus (produces both types of inclusion bodies)
31
In some cases of lead poisoning, _______________ inclusion develops in renal tubular epithelial cells. These inclusions are a mixture of lead and _________.
Intranuclear; protein
32
Which stain is best to use in order to see lead inclusions?
Acid-fast (Ziehl-Neelsen) stain
33
Protein-misfolding disorder of soluble and functional proteins, converting them into insoluble and non-functional aggregates; commonly found in liver, kidney, and vessel walls
Amyloid
34
What are the mechanisms of amyloidosis? (4 mechanisms)
- 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 - Protein overproduction due to abnormality/proliferation in synthesizing cell
35
What is the gross appearance of amyloidosis?
Increased tissue/organ size, paleness, yellow/orange coloration in areas of amyloid accumulation
36
What is the microscopic appearance of amyloidosis?
Amorphous, pale eosinophilic (hyaline), extracellular material, atrophy of adjacent cells; stains red with Congo Red stain, bright green birefringence in polarized light
37
How is amyloidosis classified?
Based on biochemical identity of protein (all are histologically similar) AA = systemic, derived from serum amyloid A AL = localized, derived from Ig light chains Hereditary or familial AA
38
Production of serum amyloid A by hepatocytes in cases of chronic inflammation (most common in wildlife); amyloids commonly deposited in renal glomeruli in kidneys and space of Disse in liver
AA amyloidosis
39
Localized amyloidosis derived from Ig light chains; commonly deposited adjacent to plasma cell tumors
AL amyloidosis
40
Amyloidosis that affects Shar-Pei dogs and Abyssinian cats; targets renal medullary interstitium rather than renal glomeruli
Hereditary/familial AA amyloidosis
41
__________ change refers to a leakage of plasma proteins into the wall of a blood vessel - septic or immune-mediated vasculitis
Fibrinoid (Plasma proteins = fibrin Ig)
42
Forms acicular clefts in tissue at sites of chronic hemorrhage and in atherosclerosis; induces inflammatory response (MQs often seen surrounding the clefts)
Cholesterol
43
Deposition of atheroma (plaque made of cholesterol clefts, MQs, and cellular debris) in a vessel wall
Atherosclerosis
44
Deposition of crystals of uric acid in cases with hyperuricemia (renal disease or dehydration) seen in birds, primates, and reptiles; articular and visceral gout
Urate tophi