4: cellular adaptations and accumulations Flashcards

1
Q

new but altered steady state

A

adaptation

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2
Q

is adaptation reversible?

A

yes

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3
Q

responses of cells to normal stimulation by hormones or endogenous chemical mediators

A

physiologic adaptation

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4
Q

allow cell to modulate their environment and escape injury

A

pathologic adaptation

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5
Q

weight lifter example

A

physiological hypertrophy of skeletal muscle cells

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6
Q

pregnant uterus example

A

physiological hypertrophy and hyperplasia

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7
Q

cardiac enlargement that occurs w/ hypertension or aortic valve disease

A

pathologic hypertrophy

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8
Q

enlargement of cardiac muscle cells following MI (death of surrounding myocytes)

A

pathologic hypertrophy

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9
Q

concentric hypertrophy of left ventricle

A

hypertension

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10
Q

boxcar nuclei

A

hypertrophy of cardiac muscle nucleus and cytoplasm

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11
Q

increased production of cellular proteins

A

hypertrophy

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12
Q

signals for hypertrophy (3)

A
mechanical (stretch)
vasoactive agents (alpha-adrenergic agonists)
growth factors (TGF- beta)
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13
Q

transcription factors for hypertrophy

A

Myc
Fos
Jun

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14
Q

Induction embryonic/fetal genes

A

cardiac alpha-actin

ANF

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15
Q

what 3 major changes are seen in hypertrophy

A
  • induction of embryonic/fetal genes
  • increased synthesis of contractile proteins
  • increased production of growth factors
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16
Q

what effect does increased induction of embryonic/fetal genes have

A
  • increased mechanical performance

- decreased work load

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17
Q

fetal isoforms contract more ….

A

slowly (more energy efficient)

18
Q

hyperplasia

A

increase in the number of cells

19
Q

increase in functional capacity of a tissue when needed

A

hormonal hyperplasia

20
Q

female breast at puberty and during pregnancy

A

hormonal hyperplasia example

21
Q

proliferative endometrium

A

hormonal hyperplasia

- estrogen builds it up, progesterone sloughs it off

22
Q

increased tissue mass after damage or resection

A

compensatory hyperplasia

23
Q

resected liver begins to regenerate in as little as 12 hrs

A

compensatory hyperplasia

24
Q

excessive hormones or growth factors acting on target cells

A

pathologic hyperplasia

25
estrogen/progesterone imbalance
endometrial hyperplasia (pathological)
26
benign prostatic hyperplasia
pathologic hyperplasia: over exuberant mitotic activity due to androgens
27
graves disease
diffuse hyperplasia of the thyroid
28
mechanism of hyperplasia
result of growth-factor-driven proliferation of mature cells & in some cases by increased output of new cells from tissue stem cells
29
6 common causes of atrophy
- disuse (decreased workload) - denervation - senile (decreased blood supply) - inadequate nutrition - loss of endocrine stimulation - increased pressure
30
mechanism of atrophy
decreased prtn synthesis and increased prtn degradation in cells
31
observe increased number of autophagic vacuoles and membrane-bound residual bodies like lipofuscin
atrophy
32
characteristics of a brain with alzheimers
widened sulci narrowed gyri particularly in the frontal region
33
reversible change in which one differentiated cell type is replaced by another cell type
metaplasia
34
bronchi in smoker: replacement of ciliated columar cells with stratified squamous epithelial cells
metaplasia - more rugged, def. in Vit. A, loose mucocilliary escalator
35
most common metaplasia
columnar to squamous
36
barrett's esophagus
metaplasia of normal squamous mucosa in esophagus to columar mucosa in esophagus due to chronic heart burn usually
37
formation of cartilage, bone or adipose tissue in tissue that does not usually contain these elements
connective tissue metaplasia
38
bone formation in muscle after intramuscular hemorrhage
connective tissue metaplasia
39
disordered growth, most commonly seen in squamous epithelial cells following chronic injury
dysplasia
40
observations in dysplasia
- enlargemet, irregular borders, hyperchromasia of individual cell nuclei - disordered arrangement in epithelium
41
HPV
dysplastic cervix