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LUIV [HS 202] Patho Exam > Trans 1- Cell adaptation > Flashcards

Trans 1- Cell adaptation Flashcards

1
Q

the study (logos) of disease (pathos)

A

Pathology

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2
Q

Disease is due to cellular abnormalities:

A

o Altered ability to proliferate
o Dysfunction
o Disturbed homeostasis

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3
Q

Cells react to adverse stimuli by:

A 
o Cellular adaptation
§ Hypertrophy
§ Hyperplasia
§ Atrophy
§ Metaplasia
o Reversible injury
o Irreversible injury and cell death
o Apoptosis
o Necrosis
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4
Q

Types of cellular adaptation

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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5
Q

response to hormonal or

endogenous influences

A

physiologic

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6
Q

response of the cell to injurious

stimuli which enable them to escape injury

A

pathologic

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7
Q

are continuously cycling

A

skin cells

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8
Q

are stable and will go to G1 if needed.

“Prometheus and his liver regeneration.”

A

Hepatocytes

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9
Q

are permanent cells and non-dividing. They cannot regenerate.

A

Heart muscles and Neurons

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10
Q
  • Increase in the number of cells

* Encountered in cells which are capable of dividing

A

Hyperplasia

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11
Q

Hyperplasia is encountered where

A

epithelium
blood cells
connective tissues

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12
Q

In hyperplasia, these are PHYSIOLOGIC if normal stressor

A

o Breasts in pregnancy

o Menstrual endometrium

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13
Q

In hyperplasia, these are PATHOLOGIC if normal stressor

A

o ACTH from pituitary adenoma

o High estrogen

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14
Q

• Increase in the size of cells due to an increase in the
cellular contents
• Encountered in cells which are not capable of or have
limited capacity to divide

A

Hypertrophy

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15
Q

Hypertrophy is encountered where

A

in myocytes and skeletal muscles

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16
Q

In hypertrophy, these are PHYSIOLOGIC if normal stressor

A

Skeletal Muscles with Exercise

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17
Q

In hypertrophy, these are PATHOLOGIC if normal stressor

A

Hypertensive cardiomegaly

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18
Q

Histological Comparisons between Pregnancy and Normal Uterus

A

Pregnancy has bigger cells compared to the Normal Uterus

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19
Q

A normal heart weighs

A

250 g

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20
Q
  • Decrease in the size of a previously normal cell

* Not hypoplasia, Cells under hypoplasia never developed to begin with.

A

Atrophy

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21
Q

In atrophy, these are PHYSIOLOGIC if normal stressor

A

non-pregnant uterus and

brain in senility

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22
Q

In atrophy, these are PATHOLOGIC if normal stressor

A

loss of stimulus (blood, innervation, endocrine, disuse, mechanical compression

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23
Q

Poliio virus affects

A

anterior motor neurons

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24
Q

Gyri become smaller, sulci become wider

A

Atrophy Normal Brain

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25
Q

More fat rather than beefy-looking

A

Skeletal Muscle Atrophy

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26
Q

Renal atrophy due to atherosclerosis or incidental cancer

A

renal atrophy

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27
Q

Change of Epithelium from one to another in an abnormal
location (Chronic cervicitis, Chronic bronchitis, Barrett Esophagus).
Gastro-esophageal junction demarcation is not clear.
Due to reflux.

A

Metaplasia

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28
Q

from squamous epithelium of normal esophagus to the glandular type along the gastroesophageal junction

A

Glandular metaplasia

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29
Q

• Not an adaptive response
• Limbo/grey area between normal and neoplastic tissue
• Alteration in the size, shape and organization of the
cellular components of a tissue
• Disorganized, haphazard cellular growth
• Like metaplasia, reflects persistence of injurious
influences and may regress
• Pre-neoplastic, step before cancer.

A

Dysplasia

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30
Q

Normal cellular constituent

A

water, lipids, proteins, carbohydrates

31
Q

may be acquired or congenital in origin (ex. lysosomal storage diseases)

A

enzymatic defects

32
Q

foreign material engulfed by macrophages, cell cannot degrade the substance nor transport it to other sites (ex. carbon particles, silica)

A

Exogenous deposition

33
Q

accumulations that appear as rounded, eosinophilic

droplets in the cytoplasm

34
Q

homogenous, glassy, pink appearance

A

mallory hyaline

35
Q

Steatosis (fatty change) resulting from abnormal

metabolism

36
Q

Fat accumulation is frequent in liver but also occurs in

A

heart, muscle and kidney

37
Q

major organ in fat metabolism

38
Q

Fat appearance

A

Gross: with progressive accumulation, the liver
enlarges and becomes increasingly yellow

In extreme instances, it may weigh 2 to 4 times
normal and be bright yellow, soft and greasy

Microscopic: small vacuoles around nucleus ->
join together to create cleared spaces, pushing
the nucleus to the cell’s periphery -> cells may
rupture and the enclosed fat globules will
coalesce to form fatty cysts

39
Q

exogenous deposition of pigments

§ phagocytosed by dermal macrophages

40
Q

most common, air pollutant

41
Q

accumulations blacken the organ (e.g. of the lungs, lymph nodes)

A

athracosis

42
Q

Picked up by macrophages in alveoli and

transported to regional lymph nodes

43
Q

Wear-and-tear pigment

A

Lipofuscin

44
Q

§ Yellow brown, finely granular cytoplasmic, often
perinuclear pigment
§ From lipid peroxidation and free radical injury

A

Lipofuscin

45
Q

may be pathologic (as in melanoma) or

physiologic

46
Q

Endogenous source is hemolysis

47
Q

elevated circulating iron, asymptomatic

A

hemosiderosis

48
Q

symptomatic

A

Hemochromatosis

49
Q

accumulation of copper in vital organs

A

Wilson’s disease

50
Q

Copper deposits in the cornea manifests as

A

Kayser-Fleischer ring

51
Q

bile-stained liver; also presents with nodularities which are hallmarks of liver cirrhosis

A

Cholestasis

52
Q

Bile deposition in brain

A

kernicterus

53
Q

results to deposition of bile in different parts of the body

A

Hyperbilirubinemia

54
Q
  • Controlled breakdown of cells in response to DNA damage or as part of normal growth and development
  • Greek: “falling off” or falling away”
  • Chromatin condensation and fragmentation
  • No inflammation
  • Ultrastructurally, clumping chromatin is better visualized
55
Q

catalytically active cysteine aspartic acid proteases (caspases)

A

initiation

56
Q

Apoptosis mechanism

A

o Intra and extracellular pathways
o Caspases cleave DNA
o DNA fragments are phagocytosed

57
Q

Stimuli: Hypoxia toxins

A

Coagulation Necrosis

58
Q

Stimuli: Physiologic and pathologic factors

59
Q

Histologic Appearance: Cellular Swelling

A

Coagulation Necrosis

60
Q

Histologic Appearance:
Single cells
Chromatin condensation
Apoptotic bodies

61
Q

DNA breakdown: Random, diffuse

A

Coagulation Necrosis

62
Q

DNA breakdown: Internucleosomal

63
Q

Mechanisms:
ATP depletion
Membrane injury
Free radical change

A

Coagulation necrosis

64
Q

Mechanisms:
Gene activation
Endonucleases
Proteases

65
Q

Tissue reaction: Inflammation

A

Coagulation Necrosis

66
Q

Tissue reaction:
No inflammation
Phagocytosis of apoptotic bodies

67
Q

Uncontrolled breakdown of cells due to injury

68
Q
  • Most common form
  • Protein is denatured, less enzymatic breakdown
  • More eosinophilic cytoplasm, less basophilic nucleus
  • Preserved architecture
  • Most organs
  • e.g. Acute myocardial infarction
A

Coagulative Necrosis

69
Q

o More enzymatic breakdown
o Occurs in lipid-rich, low-protein tissue (e.g. brain)
o Architecture is lost

A

Liquefactive necrosis

70
Q

o Can be enzymatic (as in pancreatitis) or traumatic

o Gross appearance: soapy white deposits

A

Fat necrosis

71
Q

o “Cheesy” appearance (resembling cream cheese or
kesong puti); classic description of tuberculosis
§ Not evident for all cases of TB
o Architecture not distinct microscopically; presents with
granuloma

A

Caseous necrosis

72
Q

o With pus

o e.g. renal abscess, brain abscess

A

Suppurative necrosis

73
Q

o Complication of coagulative, caseous, or liquefactive
necrosis
o Normal serum calcium and calcium metabolism

A

Dystrophic

74
Q

o Hypercalcemia

o Abnormal calcium metabolism

A

Metastatic

LUIV [HS 202] Patho Exam (5 decks)

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