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Pathology > Cell Adaptations & Accumulations > Flashcards

Cell Adaptations & Accumulations Flashcards

1
Q

What are the 4 adaptive responses?

A
  1. hypertrophy
  2. hyperplasia
  3. atrophy
  4. metaplasia
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2
Q

What is hypertrophy?

A

increased size of cells result in increased organ size

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3
Q

What is hyperplasia?

A

increased number of cells result in increased organ size

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4
Q

What is atrophy?

A

shrinkage in cell size result in decreased decreased organ size

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5
Q

What is metaplasia?

A

an adult cell type is replaced with another adult cell type of the same tissue

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6
Q

What type of cells does hypertrophy work with?

A

differentiated (permanent) cells; muscle cells

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7
Q

What type of cells does hyperplasia work with?

A

labile cells; epithelial cells

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8
Q

What is compensatory hypertrophy?

A

following the removal of one kidney, with increased workload, the remaining kidney increases in size to compensate

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9
Q

What does hypertrophy usually respond to?

A

increased workload

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10
Q

What does hyperplasia usually respond to?

A
  • hormones
  • growth factors
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11
Q

Prolonged hyperplasia is a risk for what?

A

malignant transformation

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12
Q

What is the term for a decrease in cell number?

A

involution (apoptosis); losing tissues

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13
Q

Breast epithelial hyperplasia responds to what hormone?

A

estrogen

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14
Q

Prostatic epithelial hyperplasia responds to what hormone?

A

testosterone

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15
Q

Can benign prostatic hyperplasia become cancerous?

A

NEVER

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16
Q

A 1/3 partial hepatectomy can be regenerated by which adaptive response?

A

hypertrophy

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17
Q

A 2/3 partial hepatectomy be regenerated by which adaptive response?

A

hyperplasia

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18
Q

What is atrophy driven by?

A

loss of trophic factors

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19
Q

What is a unique characteristic of atropic cells?

A

reduce to lowest capacity to maintain survival mode; NOT DEAD

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20
Q

Where is physiologic atrophy seen?

A

in development/aging

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21
Q

Where is pathologic atrophy seen?

A

immobilization, ischemia, skinny leg syndrome

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22
Q

What is the earliest change in epithelial transitions?

A

from esophagus to stomach

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23
Q

Is there a change in size for metaplasia?

A

NO

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24
Q

What is the risk with metaplasia when the tissue is NOT suited?

A

malignant transformation

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25
Q

Where does metaplasia usually occur?

A

in areas of chronic inflammation

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26
Q

What type of cells does metaplasia work with?

A

epithelial

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27
Q

What is Barrett’s esophagus?

A

gastric simple columnar epithelium goes past junction into esophagus

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28
Q

In Barret’s esophagus, what happens in response to chronic acid reflux?

A

esophageal stratified squamous epithelium changes to mucus-secreting columnar epithelium

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29
Q

What is bronchial metaplasia?

A

columnar epithelium to stratified squamous epithelium

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30
Q

Bronchial metaplasia has an increased risk of what?

A

malignant transformation

31
Q

What is cervical metaplasia?

A

simple columnar epithelium changes to stratified squamous epithelium

32
Q

What is the endocervix?

A

lower portion of uterus

33
Q

Where in the cervix does cervical metaplasia occur?

A

endocervix

34
Q

What are examples of intracellular accumulations?

A
  • proteins
  • lipids
  • fats
  • metals
  • pigments
35
Q

Intracellular/extracellular accumulations may signal what?

A

damage or adaptation to stress by cells

36
Q

How does liver disease form in intracellular accumulations?

A

rate of metabolism is inadequate

37
Q

What are the mechanisms of intracellular accumulations?

A
  1. normal substance produced but rate of metabolism is inadequate
  2. normal accumulation d/t defect in metabolism, packaging, transport, or secretion
  3. gene mutation resulting in inactive metabolic enzyme
  4. gene mutation results in abnormal protein
38
Q

What is the inherited disorder associated with the accumulation of proteins?

A

alpha-1-antitrypsin disease (A1AT)

39
Q

What does alpha-1-antitrypsin disease (A1AT) arise from?

A

misfolded AAT proteins

40
Q

What occurs when the misfolded AAT proteins cannot be packaged/secreted?

A

causes damage/accumulation

41
Q

What is the disease associated with intracellular accumulations that code for alpha subunit lysosomal enzyme beta-hexosaminidase A?

A

Tay-Sachs disease

42
Q

What does Tay-Sachs disease inhibit?

A

complete digestion of gangliosides

43
Q

What are the 2 disorders associated with fat accumulation?

A
  • Reyes syndrome
  • acute fatty liver of pregnancy
44
Q

Reyes syndrome affects what organs in whom?

A

liver and brain in children/teenagers recovering from viral infection

45
Q

What is acute fatty liver of pregnancy?

A

mitochondrial dysfunction of fatty acids d/t deficiency of 3-hydroxyacyl-CoA dehydrogenase

46
Q

What does the accumulation of cholesterol contritbute to?

A

atherosclerosis

47
Q

What is iron from damaged RBCs stored by macrophages as?

A

ferritin

48
Q

How can ferritin be transported?

A

by transferrin via circulation to liver

49
Q

What is known as the undigestable hemosiderin?

A

end product of ferritin metabolic degradation

50
Q

What is hemochromatosis?

A

autosomal recessive disorder of iron absorption

51
Q

What disorder involves an increased uptake of iron in GI tract?

A

hemochromatosis

52
Q

What stain is associated with the accumulation of copper?

A

rhodanine stain

53
Q

What is the mechanism of copper excretion?

A

biliary tract

54
Q

What can chronic biliary obstruction lead to?

A

copper accumulation in hepatocytes

55
Q

What is the disease associated with the accumulation of copper?

A

Wilson’s disease

56
Q

What is Wilson’s disease?

A

autosomal recessive disease of inability to excrete copper from hepatocyte to bile tract

57
Q

Where do the toxic levels appear with the accumulation of copper?

A

liver and brain

58
Q

What are the endogenous pigments?

A
  • bilirubin
  • jaundice
  • lipofuscin
59
Q

What is bilirubin?

A

breakdown of heme moiety of hemoglobin and heme-containing enzymes

60
Q

What is lipofuscin?

A

wear and tear/aging pigment

61
Q

What are the exogenous pigments?

A

carbon particles and tattoos

62
Q

What are the 2 extracellular accumulations?

A

amyloidosis and pathologic calcification

63
Q

What is amyloidosis?

A

inherited and inflammatory disorder with extracellular deposition of misfolded fibrillar amyloid proteins

64
Q

What is the protein plaque found in Alzheimer and the most common form of amyloidosis?

A

alpha-beta

65
Q

Where is amyloid esophagus found?

A

in people who smoke or drink

66
Q

Where is amyloid kidney glomerulus found?

A

in people with diabetes

67
Q

What is pathologic calcification?

A

large intracellular calcific bodies in irreversibly injured mitochondria

68
Q

What are the 2 types of pathologic calcifications?

A

dystrophic and metastatic

69
Q

What is dystrophic calcification?

A

extracellular Ca in necrotic/chronically traumatized tissue

70
Q

Are the serum values for Ca normal in dystrophic calcification?

A

YES

71
Q

Is dystrophic calcification always localized?

A

YES

72
Q

When does metastatic calcification occur?

A

in conditions of high serum Ca levels with deposits of Ca salts in viable normal tissue

73
Q

What are the serum conditions like in metastatic calcification?

A

high

74
Q

What are some causes of hypercalcemia?

A
  • hypersecretion of parathyroid hormone
  • destruction of bone tissue
  • vitamin D poisoning
  • milk-alkali syndrome
  • uremia

Pathology (7 decks)

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