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Pathophysiology 1 > Cell Injury, Adaptation and Death > Flashcards

Cell Injury, Adaptation and Death Flashcards

1
Q

What are the main types of stressors that affect the body

A

Pathologic- Negative change in the body (ischemia)
Physiologic- Encounter in Normal Healthy Life (Pregnancy)

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2
Q

What are the 3 ways a cell responds to stress

A

Adaptation
Injury
Cell Death

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3
Q

Of the 3 ways cells respond to stress, which one is a reversible change in response to the stress

A

Adaptation

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4
Q

Of the 3 ways cells respond to stress, which one is reversible (as long as you stop the stress) but could also be irreversible and lead to cancer if the stress continues

A

Injury

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5
Q

Of the 3 ways cells respond to stress, which one is irreversible making the cell no longer able to function in its intended capacity due to prolonged stress of the cell

A

Cell Death

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6
Q

Cellular adaptations are a responses to stresses on cells that are reversible, what are the different types of cellular adaptations

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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7
Q

Cellular adaptations are a responses to stresses on cells that are reversible, which adaptation is an increase in the size of the cell

A

Hypertrophy

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8
Q

Cellular adaptations are a responses to stresses on cells that are reversible, which adaptation is an increase in the overall number of cells and often occurs with Hypertrophy

A

Hyperplasia

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9
Q

Cellular adaptations are a responses to stresses on cells that are reversible, which adaptation is a decrease in the size of the cell

A

Atrophy

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10
Q

What causes the cellular adaptation of atrophy to occur

A

Lack of use
Lack of nutrients (O2, Macros)

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11
Q

Cellular adaptations are a responses to stresses on cells that are reversible, which adaptation is a complete change in phenotype (function or the way a cell looks)

A

Metaplasia

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12
Q

This condition is an increase in cell size that can occur with Hyperplasia, some examples of physiological adapations that can occur are muscle mass increase in body builders and uterus size in pregnancy

A

Cellular Hypertrophy

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13
Q

Cellular Hypertrophy is an increase in cell size that can occur with Hyperplasia, what are some examples of Pathologic adaptations that can occur

A

LVH- Increases the risk of heart failure

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14
Q

This condition is an increase in the numbers of cells due to excess hormone stimulation and often occurs with Hypertrophy, some physiologic adaptations are breast growth at puberty and liver regeneration

A

Cellular Hyperplasia

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15
Q

This condition is an increase in the numbers of cells due to excess hormone stimulation and often occurs with Hypertrophy, some examples of Pathologic adaptations that occur are Endometrial and Prostatic Hyperplasia

A

Cellular Hyperplasia

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16
Q

This type of adaptation is a reduction in size of an organ/tissue (dec in cell size and/or # of cells), some examples of Physiologic adaptations are Embryonic structures and the uterus after childbirth

A

Atrophy

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17
Q

This adaptation is a reduction in size of an organ/tissue (dec in cell size and/or # of cells), In pathological cases it causes __________

A

Atrophy

Skeletal Muscle atrophy from disuse
Cachexia (poor nutrition)
Decreased Blood Supply
Nerve innervation lost

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18
Q

What type of cellular adaptation is a change in cell type in order to adapt to stress, the new cell type is able to withstand the stress.

A

Metaplasia

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19
Q

This type of cellular adaptation commonly occurs in epithelial cells, is potentially reversible but could also lead to dysplasia/malignancy if left untreated

A

Metaplasia

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20
Q

T/F Could Metaplastic cellular adaptations revert back to normal cells if the stressor is removed?
What about dysplastic

A

Metaplastic-can be reverted back if stressor is removed
Dysplastic- mild may revert but severe is typically irreversible

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21
Q

What type of cellular adaptation is a disordered proliferation (growth), is non-neoplastic but can be pre-cancerous, occurs in epithelial tissues and is usually preceded by hyperplasia or metaplasia

A

Dysplasia

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22
Q

What are the steps for cells to go from normal to Malignant

A

Normal–> Metaplasia/Hyperplasia–> Dysplasia —-> (Benign/Malignant)

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23
Q

An example of metaplasia is in the respiratory tract in smokers:
_________ epithelium—-> _________ epithelium

A

Columnar
Squamous

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24
Q

What are the four causes of cellular injury

A

-Capacity for adaptation is exceeded (pushed beyond capabilities)
-Exposure to toxic/injurous agents (Smoking/Chemotherapy)
-Deprived of nutrients (Glucose and O2—> Brain, O2—> Heart)
-Mutations disrupt metabolism (malfunctions in enzyme production and prevent breakdown of toxins)

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25
Q

Is cellular injury reversible

A

To a point, the longer the tissue is stressed, less likely to reverse

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26
Q

What are the four mechanisms of cellular injury

A

-Calcium-mediated damage
-Mitochondrial Damage
-ATP depletion
-Free radicals

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27
Q

What mechanism of cell injury shows an influx of calcium (sign of injury) across cell membranes and cause a release of CA2+ from intracellular stores, this activating enzymes that destroy the cell

A

Calcium-Mediated Damage

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28
Q

During Calcium-mediated cellular damage, the influx of Ca2+ turns on what cellular enyzmes

A

Phospholipase
Protease
Endonuclease
ATPase

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29
Q

The activation of the following cellular enzymes during calcium-mediated cellular damage does damage to what structures
Phospholipase
Protease
Endonuclease
ATPase

A

Phospholipase- Phospholipids—-> Membrane damage
Protease- Disrupt of membrane & cytoskeletal proteins—> Membrane Damage
Endonuclease—–> Nuclear Damage
ATPase—–> decrease ATP

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30
Q

During Calcium-mediated cellular damage, the influx of Ca2+ turns off what

A

Mictochondrial permeability transition——-> Decrease ATP

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31
Q

What mechanism of cell injury shows a failure of oxidative phosphorylation and depletion of ATP

A

Mitochondrial damage

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32
Q

What are some causes of mitochondrial damage

A

Toxins
ETOH
Some medication

33
Q

What are the two end results for the tissue during mitochondrial damage

A

Necrosis
Apoptosis

34
Q

Which end result during mitochondrial damage is a messy process that increases inflammation and results in purulent discharge

A

Necrosis

35
Q

Which end result during mitochondrial damage is more of a planned process, is much cleaner and is carried out by WBC

A

Apoptosis

36
Q

What mechanism of cell injury is a result of loss of membrane pumps and protein synthesis

A

ATP Depletion

37
Q

What is the purpose of the membrane pumps (Na+, K)

A

Keep things in homeostasis

38
Q

What type of cell injury is caused by a molecule with an unpaired electron

A

Free radical

39
Q

What is a normal byproduct of metabolism and also a result of external sources (x-rays, ozone, cigarette smoking, air pollutants, industrial chemicals)

A

Free radicals

40
Q

What are some enzymes that work to inactivate free radicals

A

Catalase
Superoxide Dismutase
Glutathione peroxidase

41
Q

Catalase converts H2O2 into what

A

H2O2—-> H2O + O2

42
Q

Superoxide Dismutase (SOD) converts O2* to what

A

O2*—> SOD—> H2O2—> H2O + O2

43
Q

Glutathione Peroxidase converts *OH to what

A

*OH—-> H2O2—-> H2O + O2

44
Q

What happens to a cell if it isn’t killed during apoptosis

A

It becomes auto-immune

45
Q

What are free radical scavengers

A

Antioxidants

46
Q

What are some examples of antioxidants

A

Vitamin E, A, C and glutathione

47
Q

What genetic condition has a limited use of glutathione and is triggered by fava beans, sulfa drugs, infection

A

G6PD

48
Q

What condition has a limited supply of glutathione and when triggered generates ROS that further depletes glutathione and in turn free radicals damage RBC

A

G6PD

49
Q

What is the difference between free radicals and reactive oxygen species

A

Free radicals- molecule with an upaired electron that does damage to cells
ROS- an “antioxidant” that neutralizes (inactivates) free radicals

50
Q

What is a programmed cellular death that is non-inflammatory, the cell activates its own enzyme to destroy cells and the cell is consumed by phagocytes (macrophages)

A

Apoptosis

51
Q

Does the membrane remain intact during apoptosis

A

Yes

52
Q

Embryogenesis, hormone withdrawal, DNA damaged cells, abnormal cells and infected cells (especially viral) are all examples of what type of cell death

A

Apoptosis

53
Q

What is an inflammatory cell death in which the membrane is destroyed (lysis), enzymes and the contents leak out and the cell nucleus undergoes changes

A

Necrosis

54
Q

___________ cell death
Inflammatory
membrane damage
Many cells affected
Always pathological
Harmful

A

Necrosis

55
Q

___________ cell death
Non-inflammatory
Intact membranes
Single cell affected
Can by physiological
harmful but also planned

A

Apoptosis

56
Q

What physiological conditions are the loss of growth factor signaling a mechanism of apoptosis for

A

Embryogeneis
Turnover of proliferative tissues (intestinal epithelium, lymphocytes in bone marrow and thymus)

57
Q

What physiological condition is a decreased hormone levels lead to reduced survival signals a mechanism of apoptosis for

A

Involution of hormon-dependent tissues (endometrium)

58
Q

What physiological condition is a loss of survival signals as stimulus for leukocyte activation is eliminated a mechanism of apoptosis for

A

Decline of leukocyte numbers at the end of immune and inflammatory responses

59
Q

Which form of apoptosis is responsible for most physiologic and pathologic situations. Growth factor withdrawal, DNA damage (free radicals), and Protein misfolding stimulate BH3 receptors, effecting Bcl-2 effectors that induce the mitochondria to release cytochrome c and other apoptotic proteins that activate capase ultimately leading to nuclear fragmentation and formation of apoptotic bodies.

A

Intrinsic Apoptosis

60
Q

Which form of apoptosis is due to death receptors triggering apoptosis. Most of these are members of the tumor necrosis factor (TNF) receptor family. The prototypic death receptors are Type I TNF and Fas , these receptor-ligand interactions stimulate adaptor proteins in the cell that then activate capase that ultimately lead to nuclear fragmentation and formation of apoptotic bodies.

A

Extrinsic Apoptosis

61
Q

What are the different types of tissue necrosis

A

Coagulative
Liquefactive
Gangrenous
Caseous
Fat
Fibrinoid

62
Q

Categorize tissue injuries based on the type of necrosis they experience

A
63
Q

Which type of tissue necrosis is seen in infarctions and ischemia, the tissue architecture is preserved but the injury denatures structural proteins and enzymes—> blocking proteolysis of dead cells. Two types pale and hemorrhagic

A

Coagulative

64
Q

Which type of tissue necrosis is the tissue considered gelatin-like

A

Coagulative

65
Q

This type of coagulative necrosis is when dense tissue prevents spread of blood (solid organs- heart, kidney, spleen, (except brain))

A

Pale infarction

66
Q

This type of coagulative necrosis is when blood leaks into loosely organized tissue (pulmonary, testicular)

A

Hemorrhagic

67
Q

Which type of tissue necrosis is when the tissue is considered viscous

A

Liquefactive

68
Q

Which type of tissue necrosis is seen in focal bacterial and, occasionally, fungal infections developing abcesses and in brain infarction, the tissue becomes liquified and lysolomal enzyme digest tissue

A

Liquefactive

69
Q

This type of liquefactive necrosis is when microglial enzymes liquify brain tissue

A

Brain Infarct

70
Q

This type of liquefactive necrosis is neutrophillic proteolyic enzymes liquify parenchyma

A

Abcesses

71
Q

Which type of tissue necrosis is caused by ischemia of limb or bowle and has two types Dry and Wet

A

Gangrenous

72
Q

Which type of gangrenous necrosis is when black-shrunken tissue as a result of ischemia, causing coagulative necrosis

A

Dry

73
Q

Which type of gangrenous necrosis is when black-shrunken tissue as a result of ischemia is superimposed with a bacterial infection causing both coagulative and liquefactive necrosis and becomes soft, swolled, purulent and foul smelling

A

Wet

74
Q

Do dry gangrenous limbs self amputate?

A

Yes

75
Q

Which type of tissue necrosis is seen in tuberculosis and fungal infections, the friable necrotic tissue develops a “cheese-like” appearance

A

Caseous

76
Q

Which type of tissue necrosis is the result of the digestion of the cell membrane

A

Caseous

77
Q

Which type of tissue necrosis is seen in Malignant HTN, Vasculitis and Auto-immune disorders, creates necrotic damage to blood vessel walls which then deposit proteins (including fibrin) in the cell wall , resulting in a bright pink appearance

A

Fibrinoid

78
Q

Which type of tissue necrosis is characteristic of trauma (in breast tissue) or lipase release (pancreatitis), is the destruction of fat tissue and results in saponification (when fatty acids combine with calcium to produce chalky whie areas

A

Fat

79
Q

Does fibrin make the vessel walls more rigid and susceptible to rupture

A

Yes

Pathophysiology 1 (1 decks)

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