CELLULAR ADAPTATIONS HIGH YIELD Flashcards

1
Q

pathology encompasses what aspects of the discipline?

A

etiology
pathogenesis
morphology
clinical signs and symptoms

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2
Q

cells react to adverse influences by?

A

adapting

sustaining reversible/irreversible injury and dying

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3
Q

what is the affect of increased workload and cell injury on myocytes?

A

adapted myocyte leading to hypertrophy

irreversibly injured myocyte leading to cell death

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4
Q

atrophy causes?

A
decreased workload
loss of innervation
decreased blood supply
inadequate nutrition 
loss of endocrine stimulation
aging
pressure
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5
Q

what is the mechanism of atrophy?

A

decreased protein synthesis, so increased protein degradation

increased autophagy

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6
Q

cellular protein degradation occurs mainly by _____?

A

ubiquitin proteasome pathway

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7
Q

three principles that describe the morphology of atrophy?

A

loss of cellular constituents
autophagic vacuoles
residual bodies

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8
Q

what are the causes of hypertrophy?

A

increased functional demand

physiologic (uterus in preg)

pathologic (LVD)

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9
Q

what are the mechanisms of hypertrophy affecting the heart?

A

mechanical: stretch
trophic: soluble mediators that stimulate cell growth via gene activation, i.e- switch from adult to fetal contractile protein

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10
Q

the affect of morphology on hypertrophy?

A

fragmentation and loss of myofibrillar contractile elements known as degenerative changes which can lead to cardiac failure

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11
Q

cause for hyperplasia?

mechanisms?

A

physiologic(hormonal) and pathologic

mostly due to hormonal imbalances estrogen/progesterone

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12
Q

what are the causes of metaplasia?

A

chronic irritation
chronic inflammation

based on principle: replacement of cells sensitive to stress with those better able to withstand it

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13
Q

smoking is an example of chronic inflammation due to metaplasia that results in columnar respiratory epithelium being replaced by what cells?

A

squamous cells

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14
Q

what is the mechanism of metaplasia?

A

result of reprogramming of stem cells from cytokines, GFs, ECM components not from phenotype changes of the differentiated cell

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