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Dealing with Threats > Cell Injury 3 > Flashcards

Cell Injury 3 Flashcards

1
Q

What is considered to be “cellular suicide”?

A

apoptosis

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2
Q

Explain the physiologic process of apoptosis?

A

Involution after hormone withdrawal
elimination of self reactive lymphocytes
age-related thymic involution

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3
Q

Pathologically, what can lead to apoptosis?

A

viral infections
gland involution following duct blockage (mastitis)
accumulation of misfolded proteins
immune mediated

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4
Q

What is the difference between necrosis and apoptosis

A

cell death by cell membranes rupturing vs cell suicide which is tightly regulated

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5
Q

What do both apoptotic pathways lead to activation of?

A

caspase cascade

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6
Q

What is the caspase cascade?

A

culminates in DNA degradation and apoptosis

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7
Q

Explain what the extrinsic pathway of apoptosis does as far as binding goes

A

binding of cell surface death receptors
TNF family receptors - FAS

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8
Q

Increased mitochondrial permeability would lead to what?

A

intrinsic pathway

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9
Q

In response to increased mitochondrial permeability how does the intrinsic pathway of apoptosis respond?

A

release of pro-apoptotic molecules in cytoplasm - specifically cytochrome c

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10
Q

What are the characteristic morphological features associated with apoptosis?

A

cell shrinkage
condensed chromatin
cytoplasmic buds - apoptotic bodies
NO INFLAMMATION

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11
Q

In apoptosis, there is cell shrinkage. How does this differ from necrosis?

A

swelling and rupture vs shrinkage

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12
Q

How are apoptotic bodies taken care of?

A

eaten up by resident macrophages

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13
Q

What are the two abnormal mechanisms in which calcification occurs?

A

Dystrophic
Metastatic

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14
Q

Where does dystrophic calcification occur?

A

Areas of necrosis

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15
Q

Where does metastatic calcification occur?

A

occurs in normal tissue around body secondary to hypercalcemia

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16
Q

What are some examples that would lead to metastatic calcification?

A

renal failure
vitamin D toxicosis
Elevated PTH or PTHrp (primary hyperparathyroidism)
neoplastic bone destruction

17
Q

With cellular aging, what is there a decline in?

A

cell functionality/viability

18
Q

What is myocardial mineralization? In other words which type of mineralization is this related to?

A

dystrophic - secondary to myocardial necrosis

19
Q

What are common areas of mineralization and why?

A

Stomach, lung, kidneys - acid metabolism and mineral metabolism

20
Q

What does cellular aging occur due to? What does it lead to a reduction in?

A

progressive exposure to exogenous influences and accumulation of cellular damage
leads to reduced oxidative phosphorylation and reduced protein/nucleic acid synthesis

21
Q

Cellular aging has decreased cellular replications. Why is this important?

A

Progressive telomere shortening - once telomere reaches its stop signal the cell cannot function any more

22
Q

What is an instance where a cell will never die?

A

Telomerase activity in somatic cells have allowed for them to use telomerase to their advantage leading to neoplasia

23
Q

Why does intracellular accumulations occur?

A

Dysregulation of cellular metabolism

24
Q

What are 4 different instances in which intracellular accumulations would occur?

A

Normal product but inadequate removal leading to fatty changes in liver
Normal product but defective enzymatic removal leading to lysosomal storage dx
Abnormal product due to gene mutation
Abnormal exogenous substances such as carbon or silicon

25
Q

Explain the pathogenesis of Hepatic lipidosis such as seen in cats

A

accumulation of intracellular triglycerides due to increased supply of FFA or decreased metabolism/excretion of lipoproteins
mobilizing peripheral fat stores - liver cant keep up

26
Q

How can you reverse hepatic lipidosis in cats?

A

Get them to eat again

27
Q

What are examples of hepatic lipidosis?

A

early lactation dairy cows
obese animals suddenly off fed

28
Q

What are the morphological features of hepatic lipidosis grossly and histopathologically?

A

Gross - pale tan, friable/greasy
Histo - distinct, clear, smooth walled cytoplasmic vacuoles

29
Q
A
30
Q

What are exogenous and endogenous sources of abnormal intracellular accumulation of substances such as pigment?

A

exogenous - carbon, tattoo ink
endogenous - melanin, lipofusion, hematogenous pigments

31
Q

What are some causes of glycogen intracellular accumulation?

A

corticosteroids
diabetes melitus
glycogen storage diseases

Dealing with Threats (27 decks)

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