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Pathology I > 4: cellular adaptations and accumulations > Flashcards

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
Q

estrogen/progesterone imbalance

A

endometrial hyperplasia (pathological)

26
Q

benign prostatic hyperplasia

A

pathologic hyperplasia: over exuberant mitotic activity due to androgens

27
Q

graves disease

A

diffuse hyperplasia of the thyroid

28
Q

mechanism of hyperplasia

A

result of growth-factor-driven proliferation of mature cells & in some cases by increased output of new cells from tissue stem cells

29
Q

6 common causes of atrophy

A
  • disuse (decreased workload)
  • denervation
  • senile (decreased blood supply)
  • inadequate nutrition
  • loss of endocrine stimulation
  • increased pressure
30
Q

mechanism of atrophy

A

decreased prtn synthesis and increased prtn degradation in cells

31
Q

observe increased number of autophagic vacuoles and membrane-bound residual bodies like lipofuscin

A

atrophy

32
Q

characteristics of a brain with alzheimers

A

widened sulci
narrowed gyri
particularly in the frontal region

33
Q

reversible change in which one differentiated cell type is replaced by another cell type

A

metaplasia

34
Q

bronchi in smoker: replacement of ciliated columar cells with stratified squamous epithelial cells

A

metaplasia - more rugged, def. in Vit. A, loose mucocilliary escalator

35
Q

most common metaplasia

A

columnar to squamous

36
Q

barrett’s esophagus

A

metaplasia of normal squamous mucosa in esophagus to columar mucosa in esophagus due to chronic heart burn usually

37
Q

formation of cartilage, bone or adipose tissue in tissue that does not usually contain these elements

A

connective tissue metaplasia

38
Q

bone formation in muscle after intramuscular hemorrhage

A

connective tissue metaplasia

39
Q

disordered growth, most commonly seen in squamous epithelial cells following chronic injury

A

dysplasia

40
Q

observations in dysplasia

A
  • enlargemet, irregular borders, hyperchromasia of individual cell nuclei
  • disordered arrangement in epithelium
41
Q

HPV

A

dysplastic cervix

Pathology I (12 decks)

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