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General Pathology > Cell Injury and Cell Death > Flashcards

Cell Injury and Cell Death Flashcards

1
Q

Define Pathology:

A

the study of disease

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2
Q

Define Etiology:

A

origin or cause of disease (the why)

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3
Q

Define Pathogenesis:

A

steps/mechanisms in development of a
disease (the how)

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4
Q

Define Pathophysiology:

A

the functional changes associated with
or resulting from disease (the what happens in the body
because of the disease)

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5
Q

Define Prognosis:

A

the likely course/outcome of a disease

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6
Q

Define Sequela(e):

A

pathologic conditions resulting from a disease

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7
Q

Cells actively change in response to the
“____” in their environment to maintain a ____

A

stress, steady state (homeostasis)

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8
Q

Sources of stress can be _______ or _______

A

Endogenous (inside the body), Exogenous (outside environment)

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9
Q

Examples of endogenous stress:

A
  • Hypoxia - oxygen deficiency
  • Immunologic reactions
  • Genetic defects
  • Aging
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10
Q

Examples of exogenous stress:

A
  • Physical agents - trauma, hot, cold, radiation
  • Chemicals and drugs
  • Microbiologic agents (bacteria, viruses etc.)
  • Nutritional imbalances
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11
Q

What are the three kinds of tissue in terms of proliferative capacity?

A

Continuously dividing tissues, Stable Tissues, and Permanent Tissues

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12
Q

What is another name for Continuously dividing tissues?

A

labile tissues

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13
Q

What are examples of Continuously dividing tissues?

A

skin, oral cavity, vagina, cervix, exocrine ducts,
GI tract

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14
Q

What is another name for stable tissues?

A

quiescent

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15
Q

What is stable tissue?

A

A type of tissue that only divide in response to injury/stimulus

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16
Q

What are examples of stable tissues?

A

endothelial cells, fibroblasts, smooth muscle, most solid organs (kidney, pancreas, liver)

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17
Q

What is permanent tissue?

A

A type of tissue that does not proliferate after birth having become fully mature or terminally
differentiated

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18
Q

What are examples of permanent tissues?

A

neurons, cardiac muscle, skeletal muscle

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19
Q

Four types of cellular response/adaptation?

A

Hyperplasia, Hypertrophy, Atrophy, and Metaplasia

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20
Q

The four types of cellular response/adaptation can respond to both ______ or ______ stress

A

normal, pathologic

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21
Q

Define Hyperplasia

A

production of new cells from stem cells

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22
Q

Define Hypertrophy

A

increase in cell size (in non-dividing
cells)

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23
Q

Define Atrophy

A

decrease in cell size and number

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24
Q

Define Metaplasia

A

adult cell changes into another cell type

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25
Q

What happens to cells that can’t adapt?

A
  • Reversible injury (non-lethal)
  • Irreversible injury (cell death): Necrosis or apoptosis
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26
Q

Where can hypertrophy and hyperplasia occur together in the body?

A

(uterus)
or if in non-dividing cells then only
hypertrophy occurs

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27
Q

Hypertrophy and hyperplasia can be ______ or ______

A

physiologic, pathologic

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28
Q

Match one letter with one number:
A) physiologic Hyperplasia:
B) physiologic Hyperplasia + hypertrophy:
C) pathologic Hyperplasia:
D) pathologic Hypertrophy:

1) uterus during pregnancy
2) cardiac
3) breast during puberty or pregnancy
4) endometrial hyperplasia, benign prostatic
hyperplasia

A

A-3
B-1
C-4
D-2

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29
Q

(T/F) Pathologic hypertrophy/hyperplasia is an uncontrolled process

A

False. These are controlled processes (different than a neoplasm which shows uncontrolled growth)

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30
Q

What causes atrophy?

A

decreased hormone stimulation, blood
supply/nutrition, workload, innervation, or aging

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31
Q

How are proteins degraded?

A
  • Cytoskeleton broken down by proteasomes (Ubiquitin-proteasome degradation)
  • Cellular components are “self-eaten” (autophagy). Autophagic vacuoles of cellular components fuse with lysosomes leading to hydrolytic breakdown. Used to survive when nutrients are scarce
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32
Q

What is metaplasia?

A

A technically reversible response to “stress”
where one adult cell type turns into another cell
type (reprogramming of stem cells)

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33
Q

What are two example of metaplasia?

A
  • Smokers: respiratory epithelium → squamous
    epithelium, which can turn to cancer
  • Gastric reflux: squamous epithelium →
    gastric/intestinal epithelium (Barrett esophagus),
    which can progress to cancer
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34
Q

What are two other examples of metaplasia?

A
  • Vitamin A deficiency can cause metaplasia
    because it is essential for differentiation of
    specialized epithelial surfaces (e.g. conjunctiva).
    When lacking, this squamous lining begins to
    keratinize which can lead to blindness
    (keratomalacia)
  • Mesenchymal (connective tissue) cells can
    undergo metaplasia usually reacting to
    pathologic stress. Ex. muscle tissue changing to
    bone after trauma (myositis ossificans)
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35
Q

Injury occurs when stress ______ the cell’s adaptive ability

A

exceeds

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36
Q

Degree of injury depends on stress _____, _____ and _____

A

type, severity and cell type affected

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37
Q

What is ischemia? hypoxemia?

A
  • ischemia (decreased blood supply to tissues),
  • hypoxemia (low concentration of blood oxygen)
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38
Q

Decreased O2 impairs ___________ → decreased ____ production → cell ______

A

oxidative phosphorylation, ATP, injury

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39
Q

Define an ischemic shock

A

generalized drop in blood pressure causing poor
tissue perfusion

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40
Q

When does hypoxemia occur?

A
  • High altitude- decreased PaO2
  • Hypoventilation- increased PaCO2 results in decreased PaO2
  • Diffusion defect (e.g. thicker barrier in pulmonary fibrosis)
  • Blood bypasses the lung (e.g. shunt) or oxygenated air can’t reach the blood (e.g. when the lung collapses)
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41
Q

Decreased O2 carrying capacity arises with _______ loss or altered affinity for O2

A

hemoglobin (Hb)

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42
Q

Three examples of decreased O2 carrying capacity

A

Anemia, Carbon monoxide poisoning, and Methemoglobinemia

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43
Q

Define Anemia

A

(decrease in RBC mass)- PaO2 and SaO2 are normal

44
Q

Define Carbon monoxide poisoning

A

CO binds Hb better than O2

45
Q

Define Methemoglobinemia

A

Iron in heme is oxidized to Fe3+ which can’t bind O2

46
Q

Four Mechanisms leading to cell injury

A
  • ATP depletion and production of reactive oxygen species (ROS) in mitochrondria
  • Ca2+ influx into the cytoplasm
  • Cell membrane damage (plasma, mitochondrial
    and lysosomal)
  • DNA damage and protein misfolding
47
Q

Explain ATP depletion

A
  • Na/K+ pump stops working- leads to ↑ sodium and water in cytosol → cell swelling (including ER-ribosome detachment → decreased protein synthesis)
  • Ca2+ pump stops working- leads to ↑ Ca2+ in cytosol
  • Switch to anaerobic glycolysis → lactic acid buildup lowers pH → denatures protein and precipitates DNA
48
Q

What is the effect of reactive oxygen species (ROS)?

A
  • Peroxidized lipids → membrane damage
  • Oxidation of DNA → mutations
  • Oxidation of protein → protein breakdown/misfolding
49
Q

How are reactive oxygen species (ROS) made?

A

Made during mitochondrial respiration due to
imperfect reaction of O2 to H2O which forms
superoxide (O2-)

50
Q

Free radicals and ROS decay spontaneously and
are broken down by:

A
  • superoxide dismutase (superoxide to H2O2 )
  • glutathione peroxidases (in cytoplasm) and catalase (in peroxisomes) convert H2O2 to water
51
Q

__________ block free radical formation or scavenge them

A

Antioxidants

52
Q

Examples of antioxidants

A

(vitamins A, E, C and β-carotene)

53
Q

Ischemia causes release of intracellular _____
stores into the ______ then later ______ across
the plasma membrane

A

Ca2+, cytosol, influx

54
Q

Elevated cytosolic Ca2+: (two effects)

A
  • activates enzymes which damage membranes,
    proteins, DNA and ATP
  • can also induce apoptosis by activation of caspases and increasing mitochondrial permeability
    (cytochrome c release)
55
Q

Plasma membrane damage leads to: (two effects)

A
  • cytosolic enzymes leaking into serum (e.g. cardiac troponin)
  • Calcium influx
56
Q

Mitochondrial membrane damage leads to: (two effects)

A
  • Loss of electron transport chain
  • Cytochrome c leaking into cytosol (activates
    apoptosis)
57
Q

Lysosome membrane damage leads to: (two effects)

A

hydrolytic enzymes leaking into the cytosol which
are activated by high intracellular calcium

58
Q

Cell __________ and _________ are altered with cellular swelling

A

morphology (appearance), function

59
Q

Define hydropic degeneration

A

accumulation of water droplets in cytoplasm. Causes organ to appear pale/swollen

60
Q

Define fatty change

A

(degeneration) in cells involved in fat
metabolism- lipid vacuoles in cytoplasm. Causes
organ to appear yellow/greasy

61
Q

In _____________, if stimulus is removed, tissues return to normal

A

Reversible Injury

62
Q

Two predictors of Irreversible injury:

A
  • Cell can no longer make ATP (ATP levels drop)
  • Membranes lose their integrity
63
Q

(T/F) In irreversible stress, cells lose their function as a result of change in their morphology

A

False. Cells lose their function long before they
change morphology or die

64
Q

What is the main histologic change in cell death?

A

the loss of the nucleus

65
Q

Three forms of nuclear loss

A

condensation (pyknosis)
fragmentation (karyorrhexis)
dissolution (karyolysis)

66
Q

What are the two mechanisms of cell death?

A

necrosis and apoptosis

67
Q

Define necrosis

A

Death of a group of cells → release of
cellular contents → acute inflammatory
response

68
Q

What are the three gross patterns of necrosis?

A
  • Coagulative- most common form
  • Liquefactive
  • Caseous
69
Q

Characteristics of coagulative Necrosis

A

Cell shape and organ structure preserved due to
coagulation of proteins but nucleus disappears

70
Q

Example of coagulative necrosis

A

Pattern seen with ischemic infarction (obstruction of blood leading to cell/tissue death) of any organ except the brain

71
Q

What color/shape is tissue with coagulative necrosis?

A

Area of infarcted tissue is pale (i.e. called “white”) and often wedge-shaped (pointing to focus of vascular occlusion)

72
Q

When does coagulative necrosis tissue appear red?

A

“Red” infarction arises if blood re-enters a loosely
organized tissue (e.g. pulmonary or testicular
infarction)

73
Q

Characteristics of liquefactive Necrosis

A

Necrotic tissue that becomes liquefied;
enzymatic lysis of cells and protein results in
liquefaction

74
Q

Two examples of liquefactive Necrosis

A
  • Brain infarction- proteolytic enzymes from microglial cells liquefy the brain.
  • Abscess- proteolytic enzymes from neutrophils liquefy tissue.
75
Q

Characteristics of gangrenous Necrosis

A

Coagulative necrosis that resembles mummified
tissue (dry gangrene)

76
Q

Example of gangrenous Necrosis

A

Characteristic of ischemia of the lower limb and
GI tract

77
Q

When does “wet gangrene” occur?

A

If superimposed infection of dead tissues
occurs, then liquefactive necrosis ensues (wet
gangrene)

78
Q

Characteristics of caseous necrosis

A
  • Soft and friable with “cheese-like”
    appearance
  • Tissue architecture is replaced by defined
    foci of granulomatous inflammation
    (contain granulomas)
79
Q

Example of caseous necrosis

A

Tuberculosis or deep fungal infections

80
Q

Characteristics of fat necrosis

A

Focal areas of fat destruction from trauma or
enzymatic breakdown

81
Q

Example of fat necrosis

A

Acute pancreatitis releases pancreatic enzymes

→ break down membranes and fats of
adjacent adipose tissue in the peritoneum
→ fatty acids released combine with calcium
to form chalky white areas (fat saponification)

82
Q

Characteristics of fibrinoid necrosis

A

Necrosis of a vessel wall leading to leakage
of fibrin and other proteins into the wall
which stains bright pink on H&E

83
Q

Example of fibrinoid necrosis

A

Immune reactions (vasculitis) and malignant hypertension

84
Q

Define apoptosis

A

ATP-dependent “programmed” cell death of single or small groups of cells

85
Q

Apoptosis eliminates: (four types of cells)

A
  • Unneeded structures- embryogenesis, stopping the immune response
  • Old, non-functional cells- intestine turnover, menstrual cycle
  • Potentially harmful cells- virus-infected, cancer cells
  • Cells with DNA damage that can’t be repairedradiation, drugs etc.
86
Q

Steps of apoptosis

A
  • Initiated by caspases which activate
    endonucleases (degrade DNA) and proteases
    (degrade cytoskeleton)
  • As the dying cell shrinks, the cytoplasm
    becomes more eosinophilic and the nucleus
    condenses and fragments
  • Fragments of the cell break off with intact cell
    membranes
  • Phagocytes engulf the fragments
  • Little to no inflammatory response
87
Q

Apoptosis can be _______ or _______

A

Intrinsic (mitochondrial), Extrinsic (Death Receptor)

88
Q

Explain the intrinsic (mitochondrial) Pathway of apoptosis

A

Cell injury, DNA damage or lack of growth
signals
→ a decrease in BCL-2 protein family (antiapoptotic)
→ which allows cytochrome c to leak from the
mitochondria into the cytoplasm
→ activates caspases leading to apoptosis

89
Q

Explain the extrinsic (Death Receptor) Pathway of apoptosis

A
  • Cells express “death” receptors [TNF
    receptor family and Fas (CD95)]
  • Fas ligand (FasL), mainly on activated T
    cells, binds to Fas and activates caspases
    leading to apoptosis
90
Q

(T/F) Intracellular accumulation is always harmful to the cell

A

False. Abnormal amounts of substances can
accumulate due to injury, which can be
harmless or can impair cellular function

91
Q

How does substance accumulate in the cell?

A
  • Inadequate removal of normal substance from
    cell (e.g.- fatty change)
  • Genetic or acquired defect in protein folding or
    transport
  • Enzyme deficiency leads to accumulation of
    metabolites (storage diseases)
  • Accumulation of exogenous substances (e.g.
    carbon pigment)
92
Q

Pigments can be ________ or ________

A

exogenous, endogenous

93
Q

Example of an exogenous pigment

A

Carbon- most common exogenous pigment. In
coal dust and urban air. Aggregates in the lung
(anthracosis)

94
Q

__________ is a brownish-yellow complex of lipid and protein

A

Lipofuscin “wear and tear”

95
Q

Background of lipofuscin, origin and accumulation site?

A
  • derived from previous free radical damage of
    membranes.
  • accumulates with age or atrophy in heart, liver and brain (a lot of it causes “brown atrophy”)
96
Q

Characteristics of melanin

A

brown/black pigment made by
melanocytes (epidermis and mucosal
surfaces) that screens against UV damage

97
Q

Characteristics of hemosiderin

A

golden yellow/brown, hemoglobin-derived pigment present where there is excess of iron

98
Q

What is pathologic Calcification?

A

Abnormal tissue deposition of calcium salts

99
Q

Pathologic Calcification in dead or dying tissue is called:

A

“dystrophic calcifications”
serum calcium is normal

100
Q

Pathologic Calcification in normal tissue is called:

A

“metastatic calcifications”
almost always caused by elevated calcium (hypercalcemia)

101
Q

Hypercalcemia is caused by:

A
  • Renal failure
  • Increased parathyroid hormone (PTH)
  • Bone destruction
  • Vitamin D disorders
102
Q

Cell aging is regulated by:

A

a limited number of genes and pathways

103
Q

Cell aging results from:

A

progressive decline in life span and function of cells

104
Q

Why do cells age?

A
  • Accumulation over time of unrepaired DNA damage
  • Decreased cellular replication- after a fixed number of divisions all cells stop dividing (replicative senescence) because of telomere shortening
  • Defective proteins- ↓ production, defective folding and repair
  • Increasing inflammation
105
Q

How can cell aging be slowed?

A

Calorie restriction and physical activity slow aging

General Pathology (32 decks)

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