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Pathophysiology, exam 1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Concept of the nature of disease

A

May be thought of as a reaction of a cell or group of cells to an injury

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2
Q

Possible disruptions caused by cell injury

A

Disruption of chemical processes or direct damage to components of the cell

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3
Q

Eight categories of injury

A
  1. Hypoxia
  2. Chemical
  3. Physical
  4. Infectious
  5. Immunologic
  6. Genetic
  7. Nutritional
  8. Degenerative
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4
Q

What happens to living cells when injured?

A

They change structure and function.

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5
Q

What happens with prolonged injury?

A

Clinically apparent as physical signs and symptoms

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6
Q

Describe in words the chart of general categories of cell reactions.

A

A normal cell in homeostasis undergoes stress and adapts. If there is an inability to adapt or a homeostatic cell undergoes injurious stimulus, it becomes injured. If the injury is mild, it is reversible and can continue to homeostasis. If the injury is severe/progressive, the injury is irreversible and the cell will either die or undergo apoptosis.

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7
Q

Example of early physiologic response to exercise to maintain homeostasis

A

Tachycardia

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8
Q

Definition of cell adaptation

A

Process by which cells change in size, number, and appearance in response to changes in the cell environment

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9
Q

What types of changes can occur with cell adaptation?

A

Either physiologic or pathologic changes may occur

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10
Q

Definition of hyperplasia

A

Increase in the number of cells

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11
Q

Example of physiologic hyperplasia

A

Increase in the number of glandular breast tissue during pregnancy

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12
Q

Example of pathologic hyperplasia

A

Abnormally high levels of estrogen in circulation can cause abnormal proliferation of the endometrium

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13
Q

Definition of hypertrophy

A

Increase in the size of a cell because of increased cellular substance

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14
Q

Physiologic example of hypertrophy

A

Muscle fibers become bigger for an athlete who repeatedly lifts weights

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15
Q

Pathologic example of hypertrophy

A

Patient with systemic hypertension will increase cardiac muscle mass because heart must work harder to overcome vascular resistance (cardiac muscle loses ability to become mitotic)

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16
Q

Definition of atrophy

A

Decrease in the size of a cell because of loss of cellular substance

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17
Q

Physiologic example of atrophy

A

Decreased estrogen ultimately results in atrophic uterus; decrease in number and size of myometrium

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18
Q

Pathologic example of atrophy

A

Muscles will atrophy when leg is placed in a plaster cast for a broke bone

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19
Q

Common example of atrophy

A

Normal atrophy over time of brain in elderly patients

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20
Q

Definition of metaplasia

A

Substitution of one type of an adult cell for another type of adult cell

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21
Q

Clinical example of metaplasia

A

Normal trachea and bronchi are lined by ciliated columnar epithelium, but chronic irritation of the respiratory epithelium by cigarette smoking may cause replacement of columnar cells by stratified squamous cells

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22
Q

Two features of irreversible injury to a cell

A

Non-repairable mitochondrial dysfunction

Profound membrane dysfunction

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23
Q

What part of the cell is affected first?

A

Function

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24
Q

Four vulnerable biochemical systems

A
  1. Mitochondria
  2. Cellular calcium
  3. Integrity of membranes
  4. Integrity of genetic material
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25
Q

What happens with increased numbers of reactive oxidative species (ROS)?

A

Damage to lipids, proteins, and DNA

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26
Q

What increases the number of free ROS?

A

Mitochondrial damage

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27
Q

What two downstream effects are mediated by the increase of calcium entry into the cell?

A

Increase in mitochondrial permeability and activation of multiple cellular enzymes

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28
Q

What happens with plasma membrane damage?

A

Loss of cellular components

29
Q

What happens with damage to the lysosomal membrane?

A

Enzymatic digestion of cellular components

30
Q

What happens with protein misfolding or DNA damage?

A

Activation of pro-apoptotic proteins

31
Q

Describe what happens with cessation of ATP production (three main processes)

A

Amount of sodium in the cell increases due to non-functioning Na/K ATPase pumps. Sodium is osmotically active and pulls water into the cell, causing swelling of the cell.
No oxidative respiration can occur, increasing the amount of lactic acid produced. This decreases the pH of the cell and causes chromatin clumping.
Ribosomes detach from the endoplasmic reticulum, decreasing protein synthesis and increasing fat deposition.

32
Q

What happens with permeability of injured cells, and how can this be of clinical importance?

A

Membrane permeability is altered and allows for intracellular enzymes to leak from the cell into vascular compartments. These levels can be measured with lab tests to diagnose injury.

33
Q

Definition of free radical

A

A free radical is an atom or group of atoms which have a single unpaired electron in the outer orbit. They are chemically unstable and very reactive with components of the cell

34
Q

Why is free radical damage so concerning?

A

Free radical damage causes a chain reaction; when the free radicals combine with other molecules, they create more free radicals

35
Q

Common free radical in the past

A

Carbon tetrachloride (CCl4)

36
Q

What happened with CCl4?

A

It was converted to CCl3 in hepatocytes, which oversteps the ability of the superoxide dysmutase to combat the ROS of CCl3, causing cell death in the liver.

37
Q

What organelles/processes are affected by CCl3?

A

ER membranes, protein synthesis, lipid export, mitochondria, and plasma membranes

38
Q

Explain reperfusion injury.

A

Cells start to get reperfused and “wake up,” causing more free radical production, as well as infiltration of white blood cells that also release free radicals as a “protective” mechanism.

39
Q

Morphology of reversible cell injury (5)

A
  1. Cellular swelling
  2. Steatosis
  3. Myelin figures
  4. Endoplasmic reticulum swelling
  5. Membrane blebs
40
Q

What are myelin figures?

A

Little clumps of protein and lipid that form in the cytoplasm

41
Q

What is eosinophilia?

A

Manifestation of cellular injury; cells appear more red on slides.

42
Q

What causes eosinophilia?

A

Less uptake of blue dye because the ER is not functioning, so more pink dye is taken up by the cytoplasm

43
Q

What characterizes necrosis?

A

Presence of leukocytes infiltrating dead tissue from adjacent living tissue

44
Q

What causes morphologic changes in cells after necrosis?

A

Enzymatic breakdown of cell and denaturation of proteins

45
Q

Common descriptive terms used for the histological patterns of necrosis

A
  1. Coagulation necrosis
  2. Liquifactive necrosis
  3. Caseous necrosis
  4. Enzymatic fat necrosis
  5. Gangrene
46
Q

Describe coagulation necrosis.

A

Pattern of necrosis associated with severe ischemia, usually in solid organs like the heart and kidney

47
Q

Histological pattern of coagulation necrosis

A

Ghost-like remnants of intact cells which lack nuclei; cell outline is preserved and cytoplasm stains intense pink.

48
Q

Macroscopic description of coagulation necrosis

A

Firm tissue in early stages

49
Q

Examples of coagulation necrosis

A

Myocardial infarct, renal infarct

50
Q

Three classic histologic signs of coagulation necrosis

A
  1. No nuclei
  2. No cellular components
  3. More red
51
Q

Describe liquefactive necrosis

A

Pattern of necrosis often associated with bacterial infections

52
Q

Microscopic observations of liquefactive necrosis

A

Bacteria release enzymes causing a rapid loss of cellular structure and a collection of liquid, amorphous debris. Ring of neutrophils surrounds the necrotic tissue

53
Q

Macroscopic observations of liquefactive necrosis

A

Creamy yellow material usually housed in an ABSCESS

54
Q

What type of histological pattern of necrosis is exhibited by the brain?

A

Liquefactive necrosis ONLY

55
Q

Describe caseous necrosis

A

Associated with an inflammatory reaction called a “granuloma.”

56
Q

Histological description of caseous necrosis

A

Amorphous granular debris in the center of granulomatous cell reaction

57
Q

Macroscopic description of caseous necrosis

A

Soft, white, friable; looks like cheese curds

58
Q

Describe enzymatic fat necrosis

A

Cell death in the pancreas and adjacent fat

59
Q

How does enzymatic fat necrosis occur?

A

Damage to the pancreas causes release of the pancreatic enzymes that then start breaking down peripancreatic fat

60
Q

What also happens when pancreatic enzymes are released into the abdomen?

A

Large amount of calcium released by dead cells, which causes calcium soap formation when calcium combines with fat

61
Q

Describe gangrene

A

Clinical term that represents ischemic necrosis in the extremity, bowel, or gallbladder

62
Q

Describe wet gangrene

A

Bacteria contaminates dying tissue and superimposes liquifactive necrosis

63
Q

Describe apoptosis

A

Regulated pattern of cell death characterized by nuclear condensation and fragmentation coupled with fragmentation of cytoplasm into “apoptotic bodies”

64
Q

Is there an inflammatory reaction with apoptosis

A

No

65
Q

What happens to the cells that underwent apoptosis?

A

Recognized and removed by phagocytes

66
Q

Ischemic injury to the central nervous system from right internal carotid arterial occlusion suffered by a 72 year old man will result in what pattern of necrosis?

A

Liquefactive

67
Q

Which are the major mechanisms which result in membrane damage typical for a reperfusion injury following myocardial ischemia in a 68 year old woman?

A

Reactive oxygen species

68
Q

An endocervical biopsy in a 23 year old woman demonstrates the presence of squamous epithelium (not columnar epithelium). What process has occurred?

A

Metatrophic changes

Pathophysiology, exam 1 (6 decks)

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