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GEN PATHOLOGY > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Study of structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease

A

Pathology

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2
Q

Four Aspects of Disease Process

A
  • Etiology
  • Pathogenesis
  • Morphologic Changes
  • Clinical Manifestations
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3
Q

Functional and Structural Alterations in EARLY Stages of MILD forms of Injury

A

Reversible injury

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4
Q

Two features of reversible injury

A
  • Generalized cell swelling
  • Fatty change
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5
Q

Earliest manifestation in reversible injury due to hydropic change or vacuolar degeneration

A

Cell swelling

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6
Q

Two principal types of cell death

A
  • Necrosis
  • Apoptosis
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7
Q

A consequence of severe injury (ischemia, physical/ chemical injury, etc.)

A

Necrosis

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8
Q

In Necrosis, is there increased basophilia or eosinophil?

A

Increased eosinophilia

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9
Q

Nuclear change in necrosis

A
  • Karyolysis
  • Pyknosis
  • Karyorrhexis
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10
Q

Refers to cell shrinking

A

Pyknosis

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11
Q

refers to cell fragmentation

A

Karyorrhexis

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12
Q

refers to faded basophilia of cell

A

karyolysis

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13
Q

Patterns of Tissue Necrosis

A

Coagulative
Gangrenous
Liquefactive
Caseous
Fat
Fibrinoid

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14
Q

Architecture of dead tissue is
preserved for a span of at least
some days

A

Coagulative N.

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15
Q

Injury denatures both structural and enzymatic proteins

A

Coagulative N.

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16
Q

commonly used in clinical practice and usually applied to a limb (e.g. lower leg), that has lost its blood supply

A

Gangrenous N.

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17
Q

digestion of the dead cells, resulting in transformation of the tissue into a viscous
liquid

A

Liquefactive N.

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18
Q

Encountered most often in
foci of tuberculous infection
“Cheese-like”

A

Caseous N.

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19
Q

Results from release of activated pancreatic lipases

A

Fat N.

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20
Q

Fatty acids + Calcium = ?

A

Fat saponification

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21
Q

Special form of vascular damage usually seen in immune reactions involving
blood vessels

A

Fibrinoid N.

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22
Q

Bright pink and amorphous appearance

A

Fibrinoid N.

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23
Q

Type of Cell Death induced by tightly regulated suicide program

A

Apoptosis

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24
Q

Removal of supernumerary cells and Involution of hormone-dependent tissues on hormone withdrawal

A

Apoptosis (Physiologic situation)

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25
Q

Acute inflammatory response is to ? ; Immune response is to ?

A

neutrophils, lymphocytes

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26
Q

Apoptosis in Pathologic condition

A

Dna damage, Accumulation of misfolded proteins, infections

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27
Q

Apoptosis morphologic changes

A

Cell shrinkage, chromatin condensation, Cytoplasmic blebs and apoptotic bodies, phagocytosis of apoptotic cells

28
Q

Mechanism of apoptosis results from activation of?

A

Caspase

29
Q

Phase/ mechanism of Apoptosis

A

Initiation phase (activation of caspase)
Execution phase (cellular fragmentation)

30
Q

Other mechanisms of cell death

A
  • Necroptosis
  • Pyroptosis
  • Ferroptosis
31
Q
  • Hybrid of necrosis and apoptosis
  • Programmed Necrosis
  • Caspase-Independent Programmed
    Cell Death
A

Necroptosis

32
Q

Inflammasome increased over caspase, releases interleukin-1.

A

Pyroptosis

33
Q

Triggered when excessive intracellular levels of iron or ROS overwhelm the glutathione-dependent antioxidant defenses

A

Ferroptosis

34
Q
  • cell eats its own contents
  • delivery of cytoplasmic materials to the lysosome for degradation.
A

Autophagy

35
Q

Single unpaired electron in an outer
orbit

A

Free radicals

36
Q
  • Increased production or decreased
    scavenging of ROS
A

Oxidative stress

37
Q

Generation of free radicals:

A

Respiration
U-v light, x-rays
Inflammation

38
Q

Removal of free radicals

A

antioxidants
storage and transport proteins
enzymes acting as scavengers of free radicals

39
Q

Generated from H2O by hydrolysis

A

‘OH

40
Q

Inactivation of ‘OH

A

Conversion to H2O by glutathione peroxidase

41
Q

Pathologic effects of ‘OH

A

Most reactive oxygen-derived free radical

42
Q

Adaptation of cellular growth and development

A
  • Hypertrophy
  • Hyperplasia
  • Metaplasia
  • Atrophy
43
Q

Increase in cell size

A

Hypertrophy

44
Q

Mechanisms of hypertrophy

A

Mechanical sensor
Signaling pathways
Growth factor
Transcription factor

45
Q

Increase in number of cells

A

Hyperplasia

46
Q

Decreased workload of an organ or tissue causes?

A

Atrophy

47
Q

Inadequate Nutrition (Cachexia) results to?

A

Atrophy

48
Q

Mechanisms of Atrophy

A
  • Decreased protein synthesis
  • Increased protein degradation
49
Q

REVERSIBLE Change from one differentiated cell type (epithelial or mesenchymal) to another

A

Metaplasia

50
Q

Barrett esophagus metaplasia

A

Squamous to Columnar

51
Q

2 types of metaplasia

A

Epithelial and Mesenchymal

52
Q

Mechanisms of metaplasia

A
  • Reprogramming of local tissue stem cells
  • Colonization by differentiated cell populations from adjacent sites
  • Stimulated by signals
53
Q

in metaplasia mechanism, the signals are stimulated by?

A

Cytokines
Growth factors
Extracellular Matrix

54
Q

Lipids may develop these kind of pathology:

A
  • Atherosclerosis
  • Xanthomas
  • Cholesterolosis
  • Niemann-Pick disease (type C)
55
Q

Rounded, eosinophilic droplets, vacuoles, or aggregates in the cytoplasm

A

Proteins

56
Q

Causes of Protein accumulation

A
  • Reabsorption droplets in Proximal Renal Tubules
  • Excessive secretion of NORMAL Protein (Russell bodies)
  • Defective Intracellular Transport and Secretion of Proteins
  • Accumulation of cytoskeletal proteins
  • Aggregation of abnormal proteins
57
Q

Hyaline Change: Observed in Intracellular hyaline

A
  • Russell Bodies
  • Alcoholic Hyaline
  • Reabsorption Droplets
58
Q

Hyaline Change: Observed in extracellular hyaline

A
  • Collagenous fibers in Old Scars
  • Arteriolar wall in Kidneys with Hypertension and DM
59
Q

Glycogen in cells are due to

A
  • Excessive intracellular deposits
  • Abnormalities in either glucose or glycogen metabolism
60
Q

In morphology, these are Colored substances, Endogenous or exogenous

A

Pigments

61
Q

examples of exogenous pigments and how it is viewed under microscope

A
  • Carbon or coal dust (most common)
    (lungs - anthracosis)
    (Skin - tattooing)
  • No inflammatory response
62
Q

examples of endogenous pigments

A
  • lipofuscin (lipochrome or wear and tear pigment)
63
Q

Only endogenous brown-black pigment

A

Melanin

64
Q

Other black pigment

A

Homogentisic acid (alkaptonuria)

65
Q

Hemoglobin-derived, golden yellow to brown in color

A

hemosiderin

66
Q

Abnormal tissue deposition of calcium salts

A

Pathologic calcification

67
Q
A

GEN PATHOLOGY (1 decks)

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