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NYCPM Pathology > Cellular Injury > Flashcards

Cellular Injury Flashcards

1
Q

hypertrophy

A

increase in size of an organ or tissue due to an increase in the size of cells.

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2
Q

hypertrophy is characterized by

A

an increase in protein synthesis and size and number of organelles.

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3
Q

two examples of cellular adaptation to increased workload

A

increase in skeletal muscle mass associated with exercise.

enlargement of the left ventricle of heart in hypertensive heart disease.

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4
Q

hyperplasia

A

increase in the size of an organ or tissue caused by an increase in the NUMBER of cells.

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5
Q

example of hyperplasia

A

glandular proliferation in the breast during pregnancy.

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6
Q

some tissue undergo hyperplasia and hypertrophy

A

during pregnancy, uterine enlargement is caused by both hypertrophy and hyperplasia of the smooth muscle cells in the uterus.

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7
Q

After an abnormality ceases (increased functional/energy/work demand, tissue injury), what happens is

A

reduced cell size and cell number.

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8
Q

Tissues that lack a stem cell reservoir cannot undergo

A

hyperplasia. They can ONLY undergo hypertrophy (skeletal muscle, brain and spinal cord).

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9
Q

aplasia

A

failure of cell production

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10
Q

during fetal development, aplasia results in

A

agenesis, absence of an organ due to failure of production.

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11
Q

later in life, aplasia can be caused by

A

permanent loss of precursor stem cells in proliferative tissues, such as the bone marrow.

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12
Q

atrophy

A

decrease in the size of an organ or tissue resulting from a decrease in the mass of pre-existing cells.

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13
Q

atrophy results most often from

A

disuse, nutritional or oxygen deprivation, diminished endocrine stimulation, aging and denervation.

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14
Q

during atrophy, stem cell reserve is

A

intact

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15
Q

atrophy is often marked by the presence of

A

autophagic granules, vacuoles contining debris from degraded organelles.

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16
Q

metaplasia

A

the replacement of one differentiated tissue by another.

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17
Q

metaplasia examples

A

squamous metaplasia
osseous metaplasia
myeloid metaplasia

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18
Q

squamous metaplasia

A

the replacement of columnar epithelium at the squamocolumnar junction of the cervix by squamous epithelium.

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19
Q

places where squamous metaplasia occurs

A

cervix
respiratory epithelium
endometrium
pancreatic ducts.

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20
Q

true or false: squamous metaplasia is reversible

A

true

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21
Q

osseous metaplasia

A

the formation of new bone at sites of tissue injury. Cartilaginous metaplasia may also occur.

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22
Q

myeloid metaplasia

A

proliferation of hematopoietic tissue in sites other than the bone marrow, such as the liver or spleen.

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23
Q

reversible cell injury

A

pathologic changes reversible with removal of stimulus.

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24
Q

in reversible cell injury, if stimulus is persistent but not too intense, cells may

A

undergo adaptation to survive.

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25
Q

irreversible cell injury

A

pathologic changes permanent and lead to cell death.

26
Q

2 patterns of cell death

A

necrosis

apoptosis

27
Q

necrosis

A

more common in response to exogenous stimulus (heat, trauma, infection, toxins, ischemia).

28
Q

signs of necrosis

A

swelling, denaturation/coagulation of proteins, breakdown of organelles, cell ruptures and leaks.

29
Q

necrosis is associated with

A

inflammation.

30
Q

apoptosis

A

activation of internal suicide program (i.e. embryogenesis, viral infections, critically mutated cells).

31
Q

apoptosis entails

A

a carefully orchestrated assembly of cellular components designed to eliminate unwanted cells with minimal disruption of surrounding tissue.

32
Q

apoptosis is NOT associated with

A

inflammation.

33
Q

causes of cellular injury

A 
oxygen deprivation (hypoxia)
physical agents
chemical agents and drugs
infectious agents
immunologic reactions
genetic derangements
nutritional imbalances
34
Q

3 causes of oxygen deprivation (hypoxia)

A

ischemia (loss of blood supply)
inadequate oxygenation (cardiorespiratory failure)
loss of O2 carrying capacity of blood (anemia, CO)

35
Q

3 mechanisms of cell injury

A

hypoxic injury
free radical injury
chemical injury

36
Q

causes of hypoxic cell injury result from

A

cellular anoxia or hypoxia, which, in turn, results from various mechanisms, including:
ischemia (most common), anemia, and CO poisoning, decreased perfusion of tissues, and poor oxygenation of blood.

37
Q

what happens during the early stages of hypoxic cell injury?

A

lack of O2 affects the mitochondria, resulting in decreased oxidative phosphorylation and ATP synthesis.

38
Q

consequences of decreased ATP availability

A
  1. Failure of cell membrane pump, swelling of organelles.
  2. Disaggregation of ribosomes and failure of protein synthesis.
  3. Stimulation of phosphofructokinase activity.
39
Q

cellular swelling (hydropic change) is characterized by

A

the presence of large clear vacuoles in the cytoplasm.

40
Q

cellular swelling signifies

A

reversible injury

41
Q

irreversible, high amplitude swelling is characterized by

A

marked dilation of the inner mitochondrial space.

42
Q

stimulationof phosphofructokinase activity results in

A

increased glycolysis, accumulation of lactate, and decreased intracellular pH.

43
Q

what happens during the late stages of hypoxic cell injury?

A

Membrane damage to plasma, lysosomal and other organelle membranes with loss of membrane phospholipids.

formation of myelin figures and cell blebs.

44
Q

what myelin figures look like

A

whorl like structures (think fingerprint)

45
Q

In cell death, the point of no return is marked by

A

irreversible damage to cell membranes, leading to massive calcium influx, extensive calcification of the mitochondria and cell death.

46
Q

free radicals

A

molecules with a single unpaired electron in the outer orbital.

47
Q

generation of free radicals occurs by

A

normal metabolism

oxygen toxicity, such as in the alveolar damage that can cause the adult respiratory distress (ARDS).

Drugs and chemicals

reperfusion after ischemic injury

48
Q

normally, free radicals are degraded by

A

intracellular enzymes (glutathione peroxidase)

exogenous and endogenous antioxidants (vitamins A, C, E, transferrin)

spontaneous decay

49
Q

CCl3 is

A

toxic to cells. It is the result of CCl4 being processed.

50
Q

The diffusion of CCl3 results in

A

lipid peroxidation of intracellular membranes. It includes

Disaggregation of ribiosomes (decreased protein synthesis)

plasma membrane damage (caused by products of lipid peroxidation in the smooth ER).

51
Q

steatosis

A

the accumulation of intracellular parencymal triglycerides.

52
Q

steatosis is most frequently in the

A

liver, heart and kidney.

53
Q

steatosis results from an

A

imbalance among the uptake, utilization and secretion of fat caused by 4 mechanisms.

54
Q

4 mechanisms that cause steatosis

A
  1. increased transport of triglycerides or fatty acids to affected cells.
  2. decreased mobilization of fat from cells, most often mediated by decreased production of apoproteins required for fat transport.
  3. decrease use of fat by cells
  4. overproduction of fat in cells.
55
Q

fatty change is linked to the

A

disaggregation of ribosomes and consequent decreased protein synthesis caused by failure of ATP production in CCl4 injured cells.

56
Q

hyaline change describes a

A

characteristic (homogeneous, glassy, eosinophilic) appearance in hematoxylin and eosin secretions, caused most often by nonspecific accumulations of proteinaceous material.

57
Q

examples of exogenous pigments

A 
carbon (anthracosis)
silica
iron dust
lead (plumbism)
silver (argyria)
58
Q

melanin is produced within

A

melanocytes and transferred to basal keratinocytes.

59
Q

decreased melanin pigmentation is observed in

A

albinism and vitiligo. Both conditions associated with a decrease or absence of melanocytes.

60
Q

bilirubin is the catabolic product of

A

heme moiety of hemoglobin and myoglobins.

61
Q

various pathologic conditions, accumulates and stains the blood, sclerae, mucosae and internal organs, producing a yellowish discoloration called

A

jaundice

NYCPM Pathology (4 decks)

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