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General Pathology > Cell Adaptations: Intracellular & Extracellular Accumulations > Flashcards

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)

A

Glycogen

25
Q

What is the gross appearance of glycogen accumulation (in the liver)?

A

Swollen, pale brown, mottled appearance

26
Q

What is the microscopic appearance of glycogen accumulation?

A

Clear cytoplasmic vacuoles; cells irregular sized, exist in multiples, have indistinct outlines, and nuclei not marginated (generally)

27
Q

What is a prominent histological characteristic of proteins?

A

Eosinophilia

(Extra note: the term “hyaline” is used when proteins have a homogenous, eosinophilic, and translucent appearance)

28
Q

Plasma cells containing cytoplasmic hyaline globules (also called Russell bodies) that are also immunoglobulins

A

Mott cells

29
Q

Proteins produced by viral replication

A

Viral inclusion bodies

Extra note:
DNA virus = INTRANUCLEAR inclusion bodies (herpesvirus)
RNA virus = INTRACYTOPLASMIC inclusion bodies (rabies)
(Generally - there are exceptions)

30
Q

What are two exceptions from the norm for viral inclusion body production?

A
  • Poxviruses (DNA, but produce cytoplasmic inclusion bodies)
  • Distemper virus (produces both types of inclusion bodies)
31
Q

In some cases of lead poisoning, _______________ inclusion develops in renal tubular epithelial cells. These inclusions are a mixture of lead and _________.

A

Intranuclear; protein

32
Q

Which stain is best to use in order to see lead inclusions?

A

Acid-fast (Ziehl-Neelsen) stain

33
Q

Protein-misfolding disorder of soluble and functional proteins, converting them into insoluble and non-functional aggregates; commonly found in liver, kidney, and vessel walls

A

Amyloid

34
Q

What are the mechanisms of amyloidosis? (4 mechanisms)

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
  • Protein overproduction due to abnormality/proliferation in synthesizing cell
35
Q

What is the gross appearance of amyloidosis?

A

Increased tissue/organ size, paleness, yellow/orange coloration in areas of amyloid accumulation

36
Q

What is the microscopic appearance of amyloidosis?

A

Amorphous, pale eosinophilic (hyaline), extracellular material, atrophy of adjacent cells; stains red with Congo Red stain, bright green birefringence in polarized light

37
Q

How is amyloidosis classified?

A

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
Q

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

A

AA amyloidosis

39
Q

Localized amyloidosis derived from Ig light chains; commonly deposited adjacent to plasma cell tumors

A

AL amyloidosis

40
Q

Amyloidosis that affects Shar-Pei dogs and Abyssinian cats; targets renal medullary interstitium rather than renal glomeruli

A

Hereditary/familial AA amyloidosis

41
Q

__________ change refers to a leakage of plasma proteins into the wall of a blood vessel - septic or immune-mediated vasculitis

A

Fibrinoid

(Plasma proteins = fibrin Ig)

42
Q

Forms acicular clefts in tissue at sites of chronic hemorrhage and in atherosclerosis; induces inflammatory response (MQs often seen surrounding the clefts)

A

Cholesterol

43
Q

Deposition of atheroma (plaque made of cholesterol clefts, MQs, and cellular debris) in a vessel wall

A

Atherosclerosis

44
Q

Deposition of crystals of uric acid in cases with hyperuricemia (renal disease or dehydration) seen in birds, primates, and reptiles; articular and visceral gout

A

Urate tophi

General Pathology (10 decks)

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