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Pathology - Exam 1 > Cell Injury, Death, and Adaptation > Flashcards

Cell Injury, Death, and Adaptation Flashcards

1
Q

Etiology definition

A

Origin of a disease - including underlying causes and modifiers
The initiating event and its related risk factors
Why a disease occurs

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2
Q

Pathogenesis definition

A

Development of disease, from molecular/cellular changes to functional and structural abnormalities
The transition from normal to abnormal
How a disease occurs

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3
Q

Cell injury results from what?

A

Disruption of one or more components that maintain viability

Induces a cascade of effects

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4
Q

What can happen following cell injury?

A

It may be reversible
May result in cell adaptation
May lead to cell death

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5
Q

What happens if cell injury is mild/transient?

A

It is reversible and things can go back to normal

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6
Q

What happens if cell injury is severe/progressive?

A

Can cause irreversible injury

Cell death

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7
Q

What are the two types of cell death

A 
Necrosis = death
Apoptosis = programmed death
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8
Q

What happens if cell death does not occur properly?

A

Can get sarcomas, carcinomas, cancers

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9
Q

Clinical Expression definition

A

Several steps removed from morphologic changes that are preceded by the biochemical changes associated with cell injury

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10
Q

What are different causes of cell injury - from the Patient’s persepective?

A 
Hypoxia
Infectious agents
Physical injury
Chemicals/drugs
Immune response
Genetric abnormalities
Nutritional imbalance
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11
Q

Hypoxia

A

Lack or decrease of Oxygen

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12
Q

T/F - Hypoxia effects all cells equally

A

False - some cells are more sensitive to hypoxia than others, ie: heart and brain

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13
Q

What are the major targets that cause cell injury/death

A

Cell membrane
Mitochondria
Cell proteins
DNA/RNA

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14
Q

How can a disruption in cell membrane cause cell injury/death?

A

Disrupts the balance between electrolytes, cations, protein/enzyme balance

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15
Q

How can a disruption of the mitochondria cause cell injury/death?

A

Impairs the cell’s ability to get energy

Function drops off rapidly

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16
Q

How can a disruption of cell proteins cause cell injury/death?

A

Don’t get enzymes and structural proteins needed for function

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17
Q

How can a disruption of DNA/RNA cause cell injury/death?

A

May take a while for the problem to manifest

Cell lacks an ability to get information

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18
Q

What are the different cell injury mechanisms?

A 
ATP depletion
Generation of ROS
Loss of Ca+2 homeostasis
Altered membrane permeability
Mitochondrial damage
DNA and protein damage
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19
Q

What is the Hypoxia-Ischemia model of cell damage, and what causes it?

A

Decreased (hypoxia) or no (anoxia) oxygen due to:

  • Impaired absorption of oxygen
  • Decreased blood flow (Ischemia)
  • Disease of blood or blood vessels
  • Inadequate oxygenation of the blood
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20
Q

How does Hypoxia-Ischemia lead to decreased energy production?
What does the decrease in energy lead to?

A

Decreased oxygen impairs oxidative phosphorylation in the mitochondria
-Reduced ATP reduces the ability of the plasma membrane to maintain homeostasis, leading to a net gain of solute and an isosmotic gain in cytoplasmic water

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21
Q

Decreased energy leads isosmotic gain in water leads to what?

A
  • Cell swelling with formation of cell surface blebs
  • Swelling of the mitochondria
  • Dilation of the ER
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22
Q

Dilation of the ER leads to what?

A

Detachment of ribosomes from RER and dissociation of polysomes and a decrease in protein synthesis

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23
Q

Reduced Oxidative phosphorylation leads to what?

A

Increased glycolysis, producing lactic acid and inorganic phosphates which decreases intracellular pH, leading to chromatin clumping`

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24
Q

Hypoglycemia

A

Reduced substrate for ATP producing results similar to the Hypoxia-Ischemia model

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25
Q

T/F - ROS are normally generated

A

True - they’re generated by normal endogenous oxidative reactions in the plasma membrane, mitochondria, cytoplasm, and peroxisomes

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26
Q

Generation of too many ROS are associated with what?

A 
Inflammation
Oxygen toxicity
Chemicals
Irradiation
Aging
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27
Q

What are the different types of ROS?

A 
Superoxide (O2*)
Hydrogen Peroxide (H2O2)
Hydroxyl Radicals (OH*)
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28
Q

Superoxide

A

O2*

Produced by auto-oxidation in the mitochondria and by cytosplasmic oxidases

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29
Q

Hydrogen Peroxide

A

H2O2

Produced by auto-oxidation in the mitochondria and by cytoplasmic oxidases

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30
Q

How are Superoxides (O2*) inactivated?

A

Spontaneously
OR
By superoxide dismutase (SOD) to form H2O2

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31
Q

How is Hydrogen Peroxide inactivated?

A

By glutathione peroxidase and catalase

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32
Q

Hydroxyl Radicals

A

OH*
Generated by hydrolysis of water by ionizing radiation and H2O2 by the Fenton reaction that utilizes transitional metals (such as Fe++ or Cu++)

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33
Q

How do ROS damage cells?

A

Lipid Peroxidation
Protein Fragmentation
Single strand breaks in DNA

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34
Q

Lipid Peroxidation

A

Oxygen radical comes in and causes the lipids to become radical lipid peroxides
These radical species can react with other species and disrupt the membrane and cause issues with the membrane products

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35
Q

What are the major sites of DNA damage via ROS?

A

Thymidine and Guanine

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36
Q

What are the Intracellular antioxidant systems to reduce the effects of ROS?

A

SOD
Catalase
Glutathione Peroxidase

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37
Q

What are the Extracellular antioxidant systems to reduce the effects of ROS?

A

Vitamins E, A, and C
Glutathione and Cysteine
Serum proteins that reduce/bind iron (transferrin, ferritin) and copper (ceruloplasmin) needed to catalyze the formation of ROS

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38
Q

What maintains Cytoplasmic Ca++

A

Protein sequestration in the cytoplasm, Mitochondria, and ER

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39
Q

Increased levels of Ca++ will cause what?

A

It will activate various degradative enzymes, such as:

  • Phospholipases
  • Proteases
  • Endonucleases
  • ATPase
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40
Q

What are some ‘other’ causes of cell membrane injury?

A 
Complement C5-C9 membrane attack complex
Cytotoxic T and NK cells - perforin
Virus
Bacterial endotoxins and exotoxins
Drugs
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41
Q

Reversible Cell Injury

A

aka Sub-lethal Cell Injury
Acute in nature
Occurs when the cell cannot maintain normal homeostasis due to cell injury of short duration and minimal intensity

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42
Q

What are some common causes of Reversible Cell Injury?

A

Toxins
Infectious Agents
Hypoxia
Thermal Injury

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43
Q

What are the morphological changes associated with Reversible Cell Injury

A

Plasma membrane injury that leads to increased intracellular Na+ that leads to an isosmotic gain in water
Organelles and cells swell, and the organ may appear pale and swollen

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44
Q

What occurs first, Biochemical alterations of morphologic changes?

A

Biochemical alterations

45
Q

The degree of cell injury is determines by what?

A
  • Physiological state of the cell
  • Intensity of insult
  • Duration of insult
  • Number of exposures to the insult
46
Q

What are the different outcomes that can occur from a cell injury?

A

1) It reverses
2) Results in a cell adaptation
3) Leads to cell death - necrosis or apoptosis

47
Q

What are different types of cellular adaptations?

A

Changes in cell number, size, or differentiation

Cellular adaptations associated with abdnormal accumulations

48
Q

T/F - There is one biochemical event that equates with cell death

A

False - There is no single biochemical event that equates with cell death

49
Q

What are the two types of cell deaths

A

Necrosis

Apoptosis

50
Q

What gets released after cell death?

A

Cellular constituents get released into the extracellular environment

51
Q

What morphologic changes occur in necrosis?

A

Cell Swelling
Protein denaturation; yielding a glassy, homogenous pink staining cytoplasm
Organelle breakdown may result in vacuoled cytoplasm
Nuclei changes: karylosis, pyknosis, karyorrhexis, or total loss
Inflammation

52
Q

What are the different morphologic types of necrosis

A

Coagulative Necrosis
Liquefactive Necrosis
Caseous Necrosis
Fat Necrosis

53
Q

Coagulative Necrosis

A

Most common form
Cytoplasmic proteins are coagulated
Nucleus is lost, but the eosinophilic outline of the cell is retained for a short time prior to being removed by inflammatory response

54
Q

Liquefactive Necrosis

A

The tissue is totally digested by the release of lysosomal enzymes during the acute inflammatory response
Often associated with focal bacteria or fungal infections (abscesses and wet gangrene)
Also seen in the CNS
Fills with pus

55
Q

Caseous Necrosis

A

Associated with M. tuberculosis
The tissue has a white and “cheesy” appearance on gross examination
Microscopically characterized by amorphous pink granular material within a ring of granulomatous inflammation and loss of tissue architecture

56
Q

Fat Necrosis

A

Common in trauma to the breast or in cases of pancreatitis

Adipose tissue has a chalky white-yellow gross appearance

57
Q

What is the type of Necrosis dependent on?

A

The patterns of enzymatic degredation of cells and ECM
The type of necrotic debris
Bacterial products when present

58
Q

T/F - Apoptosis is the same as Necrosis

A

False - It is a morphologically distinct, gene directed form of individual cell death

59
Q

What are some morphologic features of apoptosis?

A

Cell shrinkage
Chromatin condensation followed by fragmentation
Apoptotic body formation
Phagocytosis of the apoptotic bodies without a significant inflammatory response

60
Q

When is apoptosis useful?

A

Normal cell turnover
Embryogenesis
Immune function

61
Q

What diseases/pathology cause excessive Apoptosis?

A 
AIDS
Ischemia
Neurodegenerative diseases
Myelodysplasia
Toxin-induced liver injury
62
Q

What diseases/pathology inhibit apoptosis?

A

Cancer
Autoimmune diseases
Viral diseases

63
Q

What are the mechanisms of Apoptosis?

A

1) Intrinsic program - Mitochondria
2) “Death signals” - Fas-ligand binding to Fas receptor (extrinsic)
3) Removal of trophic signals (hormones)
4) ROS, radiation, toxins
5) Effect of Cytotoxic T-cells

64
Q

What are the two pathways to control and integrate

A

1) Direct Signaling (Fas-ligand, TNF binding)

2) Regulation of mitochondrial permeability

65
Q

Bcl-2 gene family

A

Serve as an ‘on/off switch’ that regulate membrane permeability of the mitochondria (Bcl-2, Bax, Bak)

66
Q

What do Bcl-2 and Bcl-x products do?

A

Inhibit apoptosis

67
Q

What do Bax and Bak gene products do?

A

Stimulate apoptosis

68
Q

What happens when Cytochorme-C is released from the outer mitochondrial membrane?

A

It disrupts Bcl-2, and therefore favors apoptosis

69
Q

Capspases

A

Apoptosis signaling pathways converge on an autocatalytic proteolytic cascade of capspaces
Their substrates include: cytoskeletal and nuclear matrix proteins, DNase, and transcription proteins

70
Q

What does the mitochondrial release of Ca do?

A

Activates various enzymes the execute apoptosis

  • Transglutaminases cross-link cytoplasmic proteins
  • Endonucleases cleave DNA at the linker regions between nucleosomes
71
Q

What removes cell fragments that underwent apoptosis?

A

Phagocytosis by neighboring cells and macrophages

Little or no inflammation associated

72
Q

What stimulates each type of cell death?

A 
Apoptosis = Physiologic and pathologic
Necrosis = hypoxia and toxins
73
Q

What is the morphology of Apoptosis v Necrosis?

A

Apoptosis

  • Single cells
  • Shrinkage
  • Condensed chromatin
  • Intact plasma membrane
  • Apoptotic bodies

Necrosis

  • Multiple cells
  • Lysed plasma membrane
  • Organelle disruption
74
Q

What are the mechanisms of DNA destruction in Apoptosis v Necrosis?

A

Apoptosis

  • ATP dependent
  • Gene activation and endonuclease mediated DNA fragmentation

Necrosis

  • ATP independent
  • Random, Diffuse, Free radicals, Membrane injury
75
Q

What are the tissue reactions of Apoptosis v Necrosis?

A

Apoptosis

  • Minimal inflammaiton
  • Phagocytosis of Apoptotic bodies

Necrosis
-Inflammation

76
Q

Chronic (sub-lethal) cell injury leads to what?

A

Adaptations

77
Q

What are the different types of cellular adaptations?

A 
Atrophy = diminishment of cells and functionality
Hypertrophy = Increase in size
Hyperplasia = Increase in number
Metaplasia = Intracellular accumulations
78
Q

What occurs alongside cell atrophy?

A

Concurrent decrease in organ size and/or funciton

79
Q

What can cause Atrophy?

A 
Decreased workload
Loss of innervention
Decreased blood supply
Inadequate nutrition
Decreased hormonal stimulation
Aging
Local pressure
80
Q

What is the morphologic appearance of atrophic cells

A

Shrunken

Reduction in structural components

81
Q

Hypertrophy

A

Increase in cell size and is associated with an increase in functional capacity

82
Q

What can accompany cellular hypertrophy?

A

Tissue and/or organ size may increase
AND
It may be accompanied by an increase in cell number (hyperplasia)

83
Q

What are the different etiologies of hypertrophy?

A

Response to trophic signals (hormonal)

Response to increased functional demand

84
Q

What are the types of trophic signaling that lead to cellular hypertrophy?

A

Normal/Physiologic (ie smooth muscle hypertrophy in pregnant uterus)
Abnormal/Pathologic (ie, exogenous anabolic steroids leading to muscle hypertrophy, and increased TSH leading to a goiter)

85
Q

What are some examples of hypertrophy to response of increased functional demand?

A

Muscle hypertrophy - skeletal muscles get bigger with exercise or myocardial cell hypertrophy due to increased pumping workload

86
Q

Hyperplasia

A

Increase in the number of cells in a tissue or organ
May involve the proliferation of epithelial and.or stromal cells
May increase the risk for subsequent neoplastic transformation

87
Q

Hyperplasia is stimulated by what

A

Trophic factors (hormones and cytokines/GF)

88
Q

What are some examples of hormones stimulating hyperplasia

A

Endometrial glandular cells during the normal menstrual cycle
Gynecomastia (hyperplasia of breast in men) secondary to estrogen treatment of prostate cancer
Erythrocyte hyperplasia can follow extopic production of erythropoeitin renal cell carcinoma

89
Q

Metaplasia

A

One adult cell type is replaced by another adult cell type in response to chronic stress

90
Q

Intestinal metaplasia

A

Replacement of normal epithelium with goblet cells and other intestinal mucosa-type cells
-due to prolonged exposure to reflux gastric contents

91
Q

Squamous metaplasia

A

Conversion of normal columnar epithelium to stratified squamous epithelium
Examples include
-respiratory tract in response to smoking
-Ductal epithelium of various glands due to vitamin A deficiency
-Cervix in response to various agents

92
Q

Mechanisms of intracellular accumulations include what?

A

Abnormal metabolism
Lack on an enzyme
Abnormal protein folding or transport
Ingestion of indigestible matieral

93
Q

What are the different types of lipid accumulation

A

Steatosis

Cholesterol

94
Q

What things can accumulate in cells

A

Normal constituents (H2O, lipids, proteins, carbs)
Abnormal substances - either endogenous or exogenous
Pigments
Calcium

95
Q

Steatosis

A

An abnormal accumulation of triglycerides within parenchymal cells of the liver, heart, kidney, and skeletal muscle

96
Q

What is the etiology of Steatosis

A 
Obesity
Diabetes
EtOH
Anorexia
Toxins
Protein malnutrition
97
Q

Gross appearance of Steatosis

A

Enlarged, yellow liver

98
Q

Microscopic appearance of Steatosis

A

Hepatocytes contain clear cytoplasmic vacuoles that displace the nucleus

99
Q

Cholestrol accumulation

A

Accumulates primarily in macrophages (foam cells)

100
Q

Cholesterol accumulation in skin

A

In the subepithelial macrophages forming a Xanthoma

101
Q

Cholestrol accumulation in vessels

A

In Atheromas of atherosclerosis

102
Q

Protein accumulation histology

A

Eosinophilic cytoplasmic droplets, vacuoles, or aggregates

103
Q

What are some examples of protein accumulation

A

a1-anti-trypsin deficiency - impaired folding due to a gene mutation
Mallory bodies - impaired secretion due to improper folding or precipitation
Neurofibrilary triangles in Alzheimer’s disease

104
Q

What are the different types of pigment accumulation?

A

Exogenous pigement

Endogenous pigment

105
Q

What are examples of exogenous pigments

A

Carbon accumulated in macrophages

Tattoos

106
Q

What are examples of endogenous pigments

A

Lipofuscin
Melanin
Hemosiderin
Bilirubin

107
Q

Lipofuscin

A

“Wear-and-tear” brown-yellow granular pigment

A lipoprotein complex due to ROS peroxidation of membranes

108
Q

Melanin

A

Balck-brown pigment

Produced by melanocytes by accumulated in adjacent epidermal cells and in macrophages

Pathology - Exam 1 (9 decks)

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