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General Pathology > Chapter 1: Cell injury, Cell Death, and Adaptations > Flashcards

Chapter 1: Cell injury, Cell Death, and Adaptations Flashcards

1
Q

This is the study of disease (suffering).

A

Pathology

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2
Q

This term refers to the origin of disease (“why”).

A

Etiology

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3
Q

This term refers to the steps in development of disease (“how”).

A

Pathogenesis

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4
Q

What is the purpose of cellular adaptations to stress?

A

To attempt to preserve viability and function

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5
Q

What are some cellular adaptations to stress?

A

Hypertrophy, Hyperplasia, Atrophy, and Metaplasia

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6
Q

The ability for a cell to adapt may be exceeded. This results in either ____ or ____ cell injury.

A

Reversible; Irreversible

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7
Q

These are observable characteristics or traits.

A

Phenotype

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8
Q

If a normal cardiac myocyte is subjected to an increased load through pressure, how will it adapt?

A

It will undergo hypertrophy

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9
Q

If a normal cardiac myocyte is subjected to an increased load through pressure and is unable to adapt what will happen?

A

It can swell, undergo steatosis, and eventually die

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10
Q

This term refers to the accumulation of fat within a damaged cell.

A

Steatosis

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11
Q

This is a cellular adaptation characterized by an increase in the size of the cells/organ. No new cells are created.

A

Hypertrophy

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12
Q

What does hypertrophy result from?

A

Overloading or and increase in growth factors

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13
Q

What is a physiologic cause of hypertrophy?

A

Lifting weights

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14
Q

What is a pathologic cause of hypertrophy?

A

Hypertension

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15
Q

This is a cellular adaptation characterized by an increase in the number of cells and an increase in growth factor.

A

Hyperplasia

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16
Q

What is a physiologic example of hyperplasia?

A

The female breast or the liver

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17
Q

What is a pathologic example of hyperplasia?

A

Human papillomavirus (wart/verruca)

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18
Q

Does hyperplasia respond to the body’s control mechanisms over growth?

A

Yes

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19
Q

This is a cellular adaptation characterized by a reduction in cell size (organ) and reduced function.

A

Atrophy

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20
Q

During atrophy, cells decrease in size which results in a ____ in protein synthesis and ____ in protein breakdown.

A

Decrease; Increase

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21
Q

What are some causes of atrophy?

A
  • Disuse (immobilization)
  • Ischemia: decrease in blood/nutrients
  • Denervation
  • Endocrine disruption
  • Aging (senile)
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22
Q

When cerebral tissue atrophies what happens to the gyri and sulci?

A

The gyri narrow and the sulci widen

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23
Q

This is a cellular adaptation and is characterized by the reversible replacement of one mature cell type by another.

A

Metaplasia

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24
Q

When does metaplasia occur?

A

It is an adaptation to prolonged stressors, such as smoking.

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25
Q

What is the risk of metaplasia?

A

Malignant transformation

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26
Q

This occurs when the stressors exceed the adaptive ability or cells or directly induce abnormalities.

A

Injury

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27
Q

What are the two types of cellular injury?

A

Reversible and irreversible (death)

28
Q

This type of cellular injury is transient and mild. It results in cellular swelling, steatosis, and there is no damage to the membranes or nucleus.

A

Reversible cellular injury

29
Q

Can a cell recover from a reversible cellular injury?

A

Yes, if the stressor is removed

30
Q

This type of cellular injury is prolonged and severe. It results in mitochondrial dysfunction or disturbed membranes.

A

Irreversible cellular injury

31
Q

What two things can happen to a cell that has undergone an irreversible cellular injury?

A

Necrosis or apoptosis

32
Q

This type of cellular death is always pathological and inflammatory. It can be caused by trauma, toxin, or ischemia.

33
Q

This type of cellular death is physiological/pathological and non-inflammatory. It can be caused by a decrease in growth factors or damage to DNA/proteins.

34
Q

What are the nuclear changes of necrosis?

A

Karyolysis, pyknosis, karyorrhexis

35
Q

This is a nuclear change of necrosis and is characterized by a dissolution of chromatin due to the action of DNAases and RNAases.

A

Karyolysis (nuclear fading)

36
Q

This is a nuclear change of necrosis and is characterized by the DNA condensing into a shrunken basophilic mass.

A

Pyknosis (nuclear shrinkage)

37
Q

This is a nuclear change of necrosis and is characterized by the pyknotic nuclei membrane rupturing and the nucleus undergoing fragmentation.

A

Karyorrhexis (nuclear fragmentation)

38
Q

What are the morphologic patterns of tissue necrosis?

A
  • Coagulative (gangrenous)
  • Liquefactive
  • Caseous
  • Fat
  • Fibrinoid
39
Q

This type of necrosis is due to vascular occlusion, which results in the death of tissue and solid organ infarction. The tissue structure is preserved, firm.

A

Coagulative necrosis (ischemic necrosis)

40
Q

This is a type of coagulative necrosis found in an extremity. It can be caused by peripheral vascular disease in people who have diabetes or atherosclerosis.

A

Gangrenous necrosis (dry, wet, gas)

41
Q

This is a type of necrosis where dead cells are completely digested and a liquid viscous mass forms. It can be caused by infections or hypoxia in the CNS.

A

Liquefactive necrosis

42
Q

This type of necrosis has a “cheese-like” appearance. It is enclosed within a distinctive border and is typical of tuberculosis infections.

A

Caseous necrosis

43
Q

This is a walled-off accumulation of macrophages.

44
Q

This type of necrosis is characterized by the local destruction of fat. Its gross morphology is chalky white.

A

Fat necrosis

45
Q

What are some causes of fat necrosis?

A

Acute pancreatitis and trauma to a breast.

46
Q

This type of necrosis is due to autoimmune reactions and requires light microscopy to identify. Immune complexes and fibrin are deposited into the arterial walls, which weakens them and increases the risk of aneurysm.

A

Fibrinoid necrosis

47
Q

What are some conditions that may result in fibrinoid necrosis?

A

-Polyarteritis nodosa (affects the coronary artery)
-Systemic lupus erythematosus (affects the renal vessels)
-Malignant hypertension (high blood pressure)
Transplant rejections

48
Q

This term is used to describe programmed/regulated cellular death. It occurs in unneeded or irreparable cells and involves enzymatic breakdown of DNA and cytoplasmic proteins. Inflammation does not occur in this process.

49
Q

This type of apoptosis occurs with embryonies (gill slits, webs), endometrium, breasts, immune cells, and normal cell populations.

A

Physiologic apoptosis

50
Q

This type of apoptosis occurs in DNA damaged cells, misfolded proteins, and viral infections. It may accompany atrophy.

A

Pathologic apoptosis

51
Q

During apoptosis, what does the activation of caspases lead to?

A

Cellular fragmentation

52
Q

This apoptotic pathway involves the decrease of GF, DNA damage, misfolded proteins, and an increase in mitochondrial membrane permeability.

A

Mitochondrial (intrinsic) pathway

53
Q

Which caspase is activated in the mitochondrial (intrinsic) pathway?

54
Q

This apoptotic pathway involves the binding of surface molecules to “death receptors”. This pathway eliminates self-reactive lymphocytes or virus infected cells.

A

Death receptor (extrinsic) pathway

55
Q

Which caspase is activated in the death receptor (extrinsic) pathway?

56
Q

This process involves the lysosomal digestion of cellular components (“self-eating”). It is used as a survival mechanism when nutrients are low or it is used to get rid of misfolded proteins.

57
Q

What are the mechanisms of cellular injury?

A
  • Depletion of ATP
  • Mitochondrial damage
  • Influx of calcium
  • Oxidative stress
  • Defects in membrane permeability
  • DNA and protein damage
58
Q

Myocardial infarction and cerebral infarct are conditions that result from what type of cellular injury?

A

Ischemia-reperfusion injury

59
Q

This type of chemical (toxic) injury is due to a combination with cellular organelles.

A

Direct chemical injury

60
Q

This type of chemical (toxic) injury is due to a conversion of chemicals resulting in the creation of reactive metabolites.

A

Indirect chemical injury

61
Q

What are some mechanisms of intracellular accumulation?

A
  • Abnormal metabolism
  • Defective protein folding/transport
  • Defective or absent enzyme(s)
  • Ingestion of indigestible materials
62
Q

This is the abnormal accumulation of lipids in a cell. This can be due to toxins, malnutrition, diabetes, obesity, etc.

A

Fatty change (steatosis)

63
Q

This type of calcification occurs through cellular injury/aging and most often occurs in necrotic cells.

A

Dystrophic calcification

64
Q

This is an autosomal dominant mutation that is characterized by dysfunctional soft tissue repair and trauma to a tissue resulting in heterotopic ossification.

A

Fibrodysplasia ossificans progressiva

65
Q

This type of calcification is characterized by the accumulation of Ca in normal tissues. It most often occurs in vessels, kidnys, lungs, and G.I. mucosa.

A

Metastic calcification

66
Q

What are some characteristics of cellular aging?

A
  • DNA damage
  • Replicative senescence
  • Defective protein homeostasis
67
Q

These conditions are characterized by an accelerated aging process.

A
  • Progeria (mortality around teens)

- Werner syndrome

General Pathology (7 decks)

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