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HistoPathology > [P] Week 1: Cell Injury, Cell Death, and Adaptations - Part 2 > Flashcards

[P] Week 1: Cell Injury, Cell Death, and Adaptations - Part 2 Flashcards

1
Q

THE FOUR ASPECTS OF DISEASE

  • Cause of disease
  • Has two factors, genetic and acquired
A

Etiology

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2
Q

THE FOUR ASPECTS OF DISEASE

  • Sequence of events in the response of cells or tissues to the etiologic agent
  • Initial stimulus to the ultimate manifestation of the disease
A

PATHOGENESIS

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3
Q

THE FOUR ASPECTS OF DISEASE

Structural alterations in cells or tissues characteristic of a disease or diagnostic of an etiologic process

A

Molecular and Morphologic Changes

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4
Q

THE FOUR ASPECTS OF DISEASE

  • its components contains: genetic, biochemical, and structural changes in cells and tissues
  • Lead to the clinical manifestations (symptoms and signs) of disease
  • Progress (clinical course and outcome)
A

Functional Deragnements and Clinical manifestation

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5
Q

Match

Injurious Stimulus:
1. Altered Physiological Stimuli & Some Non-Lethal Injurious Stimuli
2. Increased Demand and Increased Stimulation
3. Decreased Nutrients and Decreased Stimulation
4. Chronic Irritation (Physical or Chemical)

Cellular Response
A. Cellular Adaptations
B. Metaplasia
C. Atrophy
D. Hyperplasia, Hypertrophy

A
  1. A
  2. D
  3. C
  4. B
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6
Q

Match

Injurious Stimulus:
1. Reduced Oxygen Supply, Chemical Injury, Microbial Infection
2. Acute and Transient
3. Progressive and Severe (including DNA Damage
4. Metabolic Alterations (Genetic or Acquired) and Chronic Injury
5. Cumulative Sublethal Injury Over Long Life Span

A. Intracellular Accumulations; Calcification
B. Cell Injury
C. Cellular Aging
D. Irreversible Injury, Cell Death (Necrosis or Apoptosis)
E. Acute Reversible Injury, Cellular Swelling, or Fatty Change

A
  1. B
  2. E
  3. D
  4. A
  5. C

`

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7
Q

ADAPTATIONS OF CELLULAR GROWTH & DIFFERENTIATION

Reversible changes in response to changes in environment:

A
  • Size
  • Number
  • Phenotype
  • Metabolic Activity
  • Functions of Cells
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8
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

what are the cellular responses to stress and noxious stimuli?

A

Hypertrophy, Hyperplasia, Atrophy, and Metaplasia

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9
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

  • Increase in size of cells, increase in organ size
  • NO new cells, just larger cells
  • Affects cells incapable of proliferation
  • Synthesis of more structural components
  • Can be pathologic or physiologic
A

Hypertrophy

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10
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

  1. Hypertrophy of ____ organelles
  2. ____ show hypertrophy of (ER) in hepatocytes
  3. Increase amount of ____ to detoxify the drugs
A
  1. subcellular
  2. Barbiturates
  3. cytochrome P-450
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11
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

  • Increase in number of cells in an organ or tissue
  • Usually resulting in increased mass of the organ or tissue
  • Affects cells capable of dividing
  • Can occur with hypertrophy, can be triggered by same stimulus
  • Can be physiologic or pathologic
  • Mechanisms: Result of growth factor–driven proliferation of mature cells
A

Hyperplasia

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12
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

what are the physiologic hyperplasia

A
  • Hormonal Hyperplasia – increases the functional capacity of a tissue when needed
  • Compensatory Hyperplasia – increases tissue mass after damage or partial resection
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13
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

  • Most commonly caused by excess hormones or growth factors acting on target cells
  • Ex: Endometrial Hyperplasia, Benign Prostatic Hyperplasia
A

Pathologic Hyperplasia

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14
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

  • Reduced size of an organ or tissue resulting from a decrease in cell size AND number
  • Can be physiologic or pathologic
A

Atrophy

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15
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

  • Reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type
  • It often represents an adaptive response in which one cell type that is sensitive to a particular stress is replaced by another cell type that is better able to withstand the adverse environment
A

Metaplasia

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16
Q

CELLULAR RESPONSES TO STRESS & NOXIOUS STIMULI

The most common epithelial metaplasia is?

A

columnar to squamous, as occurs in the respiratory tract in response to chronic irritation

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17
Q

AN OVERVIEW OF CELL INJURY AND CELL DEATH

Early stages or mild forms of injury; the functional and morphologic changes are reversible if the damaging stimulus is removed

A

Reversible Cell Injury

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18
Q

AN OVERVIEW OF CELL INJURY AND CELL DEATH

Continuing damage becomes irreversible; cell cannot recover and dies

A

Cell Death

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19
Q

AN OVERVIEW OF CELL INJURY AND CELL DEATH

Hallmarks of Reversible Injury:
1. reduced ____ ____ with resultant depletion of energy stores in the form of adenosine triphosphate (ATP)
2. ____ ____ caused by changes in ion concentrations and water influx

A
  1. oxidative phosphorylation
  2. cellular swelling
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20
Q

CELL DEATH: NECROSIS VS. APOPTOSIS

Characterized by:
- Severe damage to membranes
- Lysosomal enzymes enter cytoplasm and digest the cell
- Cellular contents leak out

Always a pathologic process

A

Necrosis

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21
Q

CELL DEATH: NECROSIS VS. APOPTOSIS

Characterized by:
1. Nuclear dissolution
2. Fragmentation of the cell without complete loss of membrane integrity
3. Rapid removal of the cellular debris

Serves many normal functions and is not necessarily associated with cell injury

A

Apoptosis

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22
Q

FEATURES OF NECROSIS AND APOPTOSIS

Cell Size: Enlarged (swelling)

Nucleus: Pyknosis, karyorrhexis, karyolysis

Plasma Membrane: Disrupted

Cellular Contents: Enzymatic digestion; may leak out of cell

Adjacent Inflammation: Frequent

Physiology or Pathologic Role: Invariably pathologic (culmination of irreversible cell injury)

A

necrosis

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23
Q

FEATURES OF NECROSIS AND APOPTOSIS

Cell Size: Reduced (shrinkage)

Nucleus: Fragmentation into nucleosome-size fragments

Plasma Membrane: Intact; altered structure, especially orientation of lipids

Cellular Contents: Intact; may be released in apoptotic bodies

Adjacent Inflammation: No

Physiology or Pathologic Role: IOften physiologic, means of eliminating unwanted cells; may be pathologic after some forms of cell injury, especially
DNA damage

A

Apoptosis

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24
Q

CAUSES OF CELL INJURY

What are the causes of cell injury

A
  • Oxygen Deprication
  • Physical Agents
  • Chemical Agents and Drugs
  • Infectious Agents
  • Immunologic Reactions
  • Genetic Derangements
  • Nutritional Imbalances
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25
Q

Reversible cell injury is characterized by functional and structural alterations in?

A

early stages or mild forms of injury
which are correctable if the damaging stimulus is removed

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26
Q

REVERSIBLE CELL INJURY

what are the 2 feautes of Reversible Cell injury?

A
  • Cellular Swelling
  • Fatty Change
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27
Q

MORPHOLOGY OF REVERSIBLE CELL INJURY

the first manifestation of almost all forms of injury to cells

A

Cellular Swelling

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28
Q

ULTRASTRUCTURAL CHANGES IN REVERSIBLE CELL INJURY

what are the ultrastrucutal changes that take place in a cell injury?

A
  • Plasma membrane alterations
  • Mitochondrial changes
  • Dilation of the ER, with detachment of polysomes; intracytoplasmic myelin figures may be present
  • Nuclear alterations, with disaggregation of granular and fibrillar elements
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29
Q
  • Denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell; may take hours
  • a pathologic process that is the consequence of severe injury
A

Necrosis

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30
Q
  • characterized by denaturation of cellular proteins, leakage of cellular contents through damaged membranes, local inflammation, and enzymatic digestion of the lethally injured cell
  • leakage of intracellular proteins through damaged plasma membranes and ultimately into the circulation is the basis for blood tests that detect tissue-specific cellular injury
A

Necrosis

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31
Q

MORPHOLOGY OF NECROSIS

What are the morphologic features of necrosis?

A
  • increased eosinophilia
  • glassy homogeneous appearance
  • cytoplasm becomes vacuolated; appears moth-eaten
  • myelin figures - whorled phospholipid precipitates derived from damaged cell membranes
  • calcification of fatty acid residues results in the generation of calcium soaps - calcified dead cells
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32
Q

NUCLEAR CHANGES IN NECROSIS

Due to nonspecific breakdown of DNA:

  • faded basophilia of chromatin
  • loss of DNA due to degradation by endonucleases
A

Karyolysis

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33
Q

NUCLEAR CHANGES IN NECROSIS

Due to nonspecific breakdown of DNA:

  • also seen in apoptotic cell death
  • nuclear shrinkage and increased basophilia
  • chromatin condenses into a solid, shrunken basophilic mass
34
Q

NUCLEAR CHANGES IN NECROSIS

Due to nonspecific breakdown of DNA:

pyknotic nucleus undergoes fragmentation

A

Karyorrhexis

35
Q

What are the patterns of tissue necrosis

A
  1. Coagulative Necrosis
  2. Liquefactive Necrosis
  3. Gangrenous Necrosis
  4. Caseous Necrosis
  5. Fat Necrosis
  6. Fibrinoid Necrosis
36
Q

Identify the patterns of tissue necrosis

Histomorphologic Features:
- Architecture of dead tissues is preserved
- Firm texture of affected tissues
- Denaturation of structural proteins and enzymes, proteolysis is blocked
- Eosinophilic, anucleate cells
- Necrotic cells removed by phagocytosis
- Ischemia may lead to coagulative necrosis of the supplied tissue in all organs except the brain
- Infarct-localized area of coagulative necrosis

A

Coagulative Necrosis

37
Q

Identify the patterns of tissue necrosis

Histomorphologic Features:
- Digestion of the dead cells
- Liquid viscous mass
- Necrotic material frequently creamy yellow (Pus - presence of dead leukocytes)
- Seen in focal bacterial or fungal infections (Accumulation of leukocytes liberating enzymes; CNS hypoxia – manifest as liquefactive necrosis)

A

Liquefactive Necrosis

38
Q

Identify the patterns of tissue necrosis

  • Non-specific pattern of cell death
  • Digestion of the dead cells
  • Generally associated with the lower leg (Lost blood supply = necrosis (i.e., coagulative necrosis) Wet Gangrene – bacterial infection superimposed with liquefactive necrosis)
A

Gangrenous Necrosis

39
Q

Identify the patterns of tissue necrosis

Histomorphologic Features:
- Cheese-like, friable white appearance of the area
- Collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border
- Most often in foci of tuberculous infection
- This appearance is characteristic of a focus of inflammation known as a granuloma

A

Caseous Necrosis

40
Q

Identify the patterns of tissue necrosis

  • Not a specific pattern
  • Focal areas of fat destruction (Release of activated pancreatic lipases into pancreas and peritoneal cavity)
A

Fat necrosis

41
Q

Identify the patterns of tissue necrosis

  • Special form of vascular damage usually seen in immune reactions involving blood vessels
    -* Complexes of antigens and antibodies* deposited in arterial walls
  • Fibrinoid - bright pink and amorphous immune complexes with fibrin that has leaked out of vessels
A

Fibrinoid Necrosis

42
Q

check mo na mechanism of cell injury

A

okay? okay

43
Q

MECHANISMS OF CELL INJURY

Cell Injury may be imparted by?

A
  1. Depletion of ATP
  2. Mitochondrial Damage
  3. Influx of Calcium & Loss of Calcium Homeostasis
  4. Accumulation of Oxygen-Derived ree Radicals or Oxidative Stress
  5. Defects in Membrane Permeability
  6. Damage to DNA and Proteins

check niyo nalang illustration

44
Q

KEY CONCEPTS: MECHANISMS OF CELL INJURY

Failure of energy-dependent functions leading to reversible injury and ultimately necrosis.

A

ATP Depletion

45
Q

KEY CONCEPTS: MECHANISMS OF CELL INJURY

ATP depletion results in failure of energy-dependent functions, leading to necrosis; may also cause leakage of mitochondrial proteins that trigger apoptosis.

A

Consequence of Mitochondrial Damage?

46
Q

KEY CONCEPTS: MECHANISMS OF CELL INJURY

It may affect plasma, lysosomal, and mitochondrial membranes, typically culminating in necrosis.

A

Increased Permeability of Cellular Membranes

47
Q

KEY CONCEPTS: MECHANISMS OF CELL INJURY

What does the accumulation of Damaged DNA and Misfolded Proteins trigger?

A

It triggers apoptosis.

48
Q

KEY CONCEPTS: MECHANISMS OF CELL INJURY

What is the effect of Accumulation of ROS (Oxidative Stress)?

A

It causes covalent modification of cellular proteins, lipids, and nucleic acids.

49
Q

KEY CONCEPTS: MECHANISMS OF CELL INJURY

What is the impact of Influx of Calcium?

A

It activates enzymes that damage cellular components and may also trigger apoptosis.

50
Q

KEY CONCEPTS: MECHANISMS OF CELL INJURY

Accumulation of misfolded proteins in the ER activates adaptive mechanisms for cell survival; if repair capacity is exceeded, it triggers apoptosis.

A

Occurs during Unfolded Protein Response & ER Stress?

51
Q

type of cell death that is induced by a tightly regulated suicide program in which cells destined to die activate intrinsic enzymes that degrade the cells’ genomic DNA and nuclear and cytoplasmic proteins

52
Q

Apoptosis

TOF

Cell death by this pathway does NOT elicit an inflammatory reaction

53
Q

APOPTOSIS IN PHYSIOLOGIC SITUATIONS

Death by apoptosis is a ____ ____ that serves to eliminate cells that are no longer needed, or as a mechanism to maintain a constant number of various cell populations in tissues

A

normal phenomenon

54
Q

APOPTOSIS IN PHYSIOLOGIC SITUATIONS

Apoptosis is important in what following physiologic situations?

A
  • Removal of supernumerary cells
  • Involution of hormone-dependent tissues
  • Cell turnover in proliferating cell populations
  • Elimination of potentially harmful self-reactive lymphocytes
  • Death of host cells that have served their useful purpose

check nalang yung extra info

55
Q

APOPTOSIS IN PATHOLOGIC CONDITIONS

Apoptosis eliminates cells that are injured ____ ____ WITHOUT eliciting a host reaction, thus limiting collateral tissue damage

A

beyond repair

56
Q

APOPTOSIS IN PATHOLOGIC CONDITIONS

Death by apoptosis is responsible for loss of cells in a variety of pathologic states, what are those?

A
  • DNA Damage
  • Accumulation of Misfolded proteins
  • Infections

please check the transes for more informations

57
Q

Enumerate the morphologic features of apoptosis

A
  1. Cell shrinkage
  2. Chromatin Condensation
  3. Cytoplasmic Blebs and Apoptotic Bodies
  4. Phagocytosis of apoptotic cells or cell bodies
58
Q

MORPHOLOGIC FEATURES OF APOPTOSIS

  • Cell size is reduced, the cytoplasm is dense and eosinophilic, and the organelles, although relatively normal, are more tightly packed
  • This contrasts with necrosis, in which an early feature is cell swelling, not shrinkage
A

Cell Shrinkage

59
Q

MORPHOLOGIC FEATURES OF APOPTOSIS

  • This is the most characteristic feature of apoptosis
  • The chromatin aggregates peripherally, under the nuclear membrane, into dense masses of various shapes and sizes
  • The nucleus itself may break up into two or more fragments
A

Chromatin Condensation

60
Q

MORPHOLOGIC FEATURES OF APOPTOSIS

The apoptotic cell first shows extensive surface membrane blebbing, which is followed by fragmentation of the dead cells into membrane-bound apoptotic bodies composed of cytoplasm and tightly packed organelles, with or without nuclear fragments

A

Cytoplasmic Blebs and Apoptotic Bodies

61
Q

MORPHOLOGIC FEATURES OF APOPTOSIS

  • Usually accomplished by macrophages
  • The apoptotic bodies are rapidly ingested by phagocytes and degraded by the phagocyte’s lysosomal enzymes
A

Phagocytosis of Apoptotic Cells or Cell Bodies

62
Q

MECHANISMS OF APOPTOSIS

Apoptosis results from the activation of enzymes called caspases; 2 distinct pathways converge on caspase activation, what are the pathway?

A
  • MITOCHONDRIAL (INTRINSIC) PATHWAY
  • EXTRINSIC (DEATH RECEPTOR-INITIATED) PATHWAY
63
Q

MECHANISMS OF APOPTOSIS

  • Responsible for apoptosis in most physiologic and pathologic situations
  • Results from increased permeability of the mitochondrial outer membrane with consequent release of death-inducing (pro-apoptotic) molecules from the mitochondrial intermembrane space into the cytoplasm
A

Mitochondrial (intrinsic) Pathway

64
Q

MECHANISMS OF APOPTOSIS

  • Initiated by engagement of plasma membrane death receptors which are members of the tumor necrosis factor (TNF) receptor family that contain a cytoplasmic domain involved in protein-protein interactions
A

Extrinsic (Death Receptor-Initiated) Pawthway

65
Q

a process in which a cell eats its own contents

66
Q
  • It involves the delivery of cytoplasmic materials to the lysosome for degradation
  • is an evolutionarily conserved survival mechanism whereby, in states of nutrient deprivation, starved cells live by cannibalizing themselves and recycling the digested contents
  • is implicated in many physiologic states (e.g., aging and exercise) and pathologic processes
67
Q

STEPS IN AUTOPHAGY

Nucleation and formation of an isolation membrane, also called a ____; the isolation membrane is believed to be derived from the ER, though other membrane sources such as the plasma membrane and mitochondria may contribute

A

Phagophore

68
Q

STEPS IN AUTOPHAGY

Formation of a vesicle, called the ____, from the isolation membrane, inside which intracellular organelles and cytosolic structures are sequestered

A

autophagosome

69
Q

STEPS IN AUTOPHAGY

Maturation of the autophagosome by fusion with lysosomes, to deliver ____ ____ that degrade the contents of the autophagosome

A

digestive enzymes

70
Q
  • One of the manifestations of metabolic derangements in cells
  • These accumulations may be located in the cytoplasm, within organelles (typically lysosomes), or in the nucleus
  • They may be composed of substances that are synthesized by the affected cells or are produced elsewhere
A

Intracellular Accumulations

71
Q

INTRACELLULAR ACCUMULATIONS

There are four main mechanisms leading to abnormal intracellular accumulations, what are those?

A
  1. Inadequate removal of a normal substance secondary to defects in packaging and transport, e.g., hepatic steatosis
  2. Defects in folding, packaging, transport, or secretion of endogenous substances
  3. Failure to degrade a metabolite due to inherited enzyme deficiencies, e.g., lysosomal storage diseases
  4. Deposition and accumulation of an abnormal exogenous substance when the cell has neither the enzymatic machinery nor the transport ability
72
Q

Provide the mechanism of intracellular accumulations

A
  1. Abnormal metabolism
  2. Defect in protein folding, transport
  3. Lack of enzyme
  4. Ingestion of indigestible materials
73
Q

the abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other mineral salts

A

Pathologic Calcification

74
Q

There are two forms of pathologic calcification, enumerate those

A
  1. Dystophic calcification
  2. Metastatic Calcification
75
Q

PATHOLOGIC CALCIFICATION

  • When the deposition occurs locally in dying tissues
  • it occurs despite normal serum levels of calcium and in the absence of derangements in calcium metabolism
A

dystrophic calcification

76
Q

PATHOLOGIC CALCIFICATION

  • the deposition of calcium salts in otherwise normal tissues
  • it almost always results from hypercalcemia secondary to some disturbance in calcium metabolism
A

metastatic calcification

77
Q

PATHOLOGIC CALCIFICATION

  • Encountered in areas of necrosis
  • Almost always present in atheromas
  • Aging or damaged heart valves
  • Calcium salts appear macroscopically as fine, white granules or clumps, often felt as gritty deposits
  • Tuberculous lymph node is virtually converted to stone
A

Dystorphic Calcification

78
Q

PATHOLOGIC CALCIFICATION

Hypercalcemia
- Increased PTH
- Destruction of bone tissue
- Vitamin D-related disorders
- Renal failure

Principally affects interstitial tissues of the gastric mucosa, kidneys, lungs, systemic arteries, and pulmonary vein

A

Metastatic Calcification

79
Q

Progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of cellular and molecular damage due to the effects of exposure to exogenous influences

A

Cellular Aging

80
Q

Established by a regulated process
- Decreased cellular replication
- Accumulation of metabolic and genetic damage

A

Cellular Aging

HistoPathology (18 decks)

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