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Pathology > Chapter 2 - Cell Injury > Flashcards

Chapter 2 - Cell Injury Flashcards

1
Q

Mild cell injury (Cellular stress)

A

Induces cells to alter and adapt without dying, due to disruption of cellular homeostasis

  • An interruption or alteration of cell function
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2
Q

Reactions to injury or cellular stress

A
  • May be reversible or irreversible
  • May result in recovery, adaptation or death
  • Vary with: 1.) Injury type
    2. ) Duration and severity of injury
    3. ) Type of cell
    4. ) Current state or health of the cell
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3
Q

Functions of the cell most vulnerable to injury

A

From immediate to long term…

  • Aerobic respiration: the most important energy source, no oxygen = no ATP
    (Hypoxia - most common injury cause)
  • Cell membrane integrity
  • Enzyme and structural proteins synthesis
  • Genetic integrity
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4
Q

Intracellular accumulations

A

Require mild injury or stress for at least a few weeks

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5
Q

Acute mild injury or stress

A
  • Intracellular edema

- Steatosis

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6
Q

Intracellular edema

A

Water accumulation (hydrophobic change = cloudy swelling)

  • Due to interference with cellular metabolism > decreased ATP > sodium potassium pump failure > loss of selective permeability of cell membrane > influx of sodium and water into cell
  • Reversible if source of stress is removed early enough; if not, this will eventually result in death
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7
Q

Steatosis

A

Fat accumulation (“fatty change” or “fatty degeneration”)

  • Interference in cellular metabolism may result in: decreased export of fat from cell or increased production of fat
  • Reversible if source of stress is removed early enough; if not will eventually result in cell death
  • Chronic alcoholism: fatty liver due to stress of alcohol consumption
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8
Q

Chronic mild injury or stress

A
  • Cholesterol accumulation
  • Protein accumulation
  • Glycogen accumulation
  • Pigment accumulation
  • Calcification
  • Hyaline deposits
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9
Q

Cholesterol accumulation

A

The most extensive and damaging accumulation

  • First appears in macrophages and smooth muscle cells in arterial wall
  • Later accumulates into large, extracellular pools in the arterial wall
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10
Q

Protein accumulation

A

Proteins are misfolded and nonfunctional

  • Alpha 1 anti-trypsin deficiency: genetic degeneration with protein clumps in hepatocytes
  • Mallory bodies: protein clumps due to alcoholic liver disease
  • Alzheimer disease: neuronal protein plaque accumulations
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11
Q

Glycogen accumulation

A

Storage form of glucose in the liver and muscles

  • Diabetes: high blood glucose causes liver and kidney cells to be stuffed with glycogen
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12
Q

Pigment accumulation

A

Soluble, visible substances

  • Lipofuscin
  • Melanin
  • Carbon
  • Hemosiderin and ferritin
  • Bilirubin
  • Tattoos
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13
Q

Lipofuscin

A

Residue of worn out organelles (“wear and tear” pigment)

  • Golden brown granules are most common pigment accumulation
  • Result of aging or long term, low-grade cell stress
  • Brain neurons, myocardial muscles cells, and hepatocytes
  • Usually does not interfere with cell function
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14
Q

Melanin

A

Normal pigment, usually good

  • Normal body pigment, brown granule a basal cells in epidermis
  • Increased deposit seen with:
    • excess sun
    • various metabolic skin diseases, or tumors (melanoma)
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15
Q

Carbon

A
  • Acquires as dust from the environment (exogeneous)
  • Black granules
  • Deposits and lung are called anthracosis (not due Bacillus anthracis)
  • Usually doesn’t interfere with cell function
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16
Q

Hemosiderin and ferritin

A

Iron storage molecules

  • Important and hemoglobin and iron metabolism
  • Dark brown granules
  • Deposits and lungs are called hemosiderosis
    • May indicate there is underlying disease
    • May interfere with cell function or cause cell death
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17
Q

Bilirubin

A

“Red” bile: orange or yellow color

  • Break down product of hemoglobin from dying RBC’s
  • Processed and excreted by the liver
  • Excess amounts in tissue result in a yellow color (jaundice or icterus)
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18
Q

Tattoos

A

Ink pigments into skin where dermal macrophages (Langerhan cells) engulf and persist for a lifetime

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19
Q

Calcification

A

Calcium compounds and tissue

  • Normal in bones and teeth
  • Abnormal calcification
    • Dystrophic calcification: deposits in damaged or dead tissue
    • Metastatic calcification: deposits in living tissue due to cancer disorder
20
Q

Hyaline deposits

A

A collective term meaning anything that looks pink in structureless (amorphous) under the microscope

  • Fibrin, collagen, amyloid (starch-like)
21
Q

Adaptations to mild injury or stress

A
  • Atrophy
  • Hypertrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia
  • Anaplasia
22
Q

Atrophy

A

Decrease cell size

  • Cell or organ loses substance in and attempt to survive changing circumstances
  • Causes: • Disuse atrophy - not used
    • Loss of innervation (EMS won’t prevent, only slows down atrophy)
    • Diminished blood supply (ischemia)
    • Loss of endocrine simulation
    • Chronic inflammation
23
Q

Hypertrophy

A

Increase cell size, not number of cells

  • Usually from increased functional demand “compensatory hypertrophy”
    • Skeletal muscles in a bodybuilder
    • Heart in patient with hypertension (systematic)
    • Kidney enlargement following removal of other kidney
  • Hormonal stimulation: breast enlargement after delivery due to prolactin
24
Q

Hyperplasia

A

Increase number of cells

  • Usually from increased functional demand
    • Skin callus: following repeated use or trauma
    • Uterine smooth muscle: during pregnancy
    • Increased liver cells following loss of liver tissue
  • Hormonal stimulation: thyroid gland following stimulation by the pituitary
25
Q

*** Note on hypertrophy and hyperplasia

A

Frequently occur together if cells have the ability to divide

  • Cardiac muscle cells don’t divide, so they can only hypertrophy
  • Both are controlled processes that don’t stop when stimulus ceases
26
Q

Metaplasia

A

Change of cell type

  • Change from one mature cell type to another mature cell type
  • Usually a change from a more sensitive cell type to a better able to survive a particular stress
  • Like dysplasia it is reversible if irritation is removed
27
Q

Dysplasia

A

Disarrangement of cells, usually associated with epithelia

  • Replacement abnormal cells with abnormal, usually following chronic irritation
  • First stage in development of malignancy
  • Reversible if irritation is removed
28
Q

Anaplasia

A

Formation of malignant tumors or neoplasms (not benign tumors)

  • Tissue organization breaks down beyond dysplasia or metaplasia
  • Undifferentiated cells: do not resemble tissue of origin (nonfunctional)
    • Benign tumor show slight anaplasia if cells are semi-differenciated
  • Uncontrolled cell division: density dependent cell division lost
  • Irreversible
29
Q

Typical cancer progression

A

Normal > dysplasia > anaplasia

30
Q

Lung cancer progression

A

Normal > metaplasia > dysplasia anaplasia

31
Q

Connective tissue cancers progression

A

Normal > anaplasia

  • No warning
32
Q

Severe injury and cell death

A
  • Autolysis

- Necrosis

33
Q

Autolysis

A

Self digestion, when the whole body is dead

  • Cell damage leads to release of interest cellular enzymes > break down adjacent structures
  • Usually refers to sell death in the context of an individual, cell death in a dead body
34
Q

Necrosis

A

Pathological cell death, localized

  • Coagulation necrosis
  • Liquefication necrosis
  • Caseous necrosis
  • Fat necrosis
35
Q

Coagulation necrosis

A

Makes tissue more solid than normal

  • Cells are dead but overall cell outlines remain intact for a while, nuclei don’t show
    • Often called a “ghost town” appearance
    • Eventually dead cells are removed by the body’s clean up system and replaced by scar tissue
  • Infarct
36
Q

Infarct

A

Ischemic death usually resulting from a loss of blood supply

  • Most common cause of coagulation necrosis
  • Myocardial infarction
37
Q

Liquefication necrosis

A

Dead tissue rapidly dissolves into fluid, eventually cleaned up and leaves a hole

  • Suppurative (pus forming) bacterial infections (abscesses, boils, puss)
  • Death of tissue with powerful hydrolytic enzymes (brain infarction)
38
Q

Caseous necrosis

A

Dead tissue becomes crumbly amorphis debris “cheese like”

  • Usually result of infection by organisms that elicit a granulomatous inflammatory response (tuberculosis)
39
Q

Fat necrosis

A

Result of damage by lipase (pancreatic enzyme) associated with “pancreatic ez”

  • Lipase breaks triglycerides into fatty acids
  • Fatty acids combine with calcium to make chalky “soaps” (saponification: one form of dystrophic calcification)
  • Calcium soaps can be visible on radiographs, mimic calcium deposits in breast cancer
  • Fatty tissues die and become firm, white, and chalky
40
Q

Biologic aging

A
  • Aging

- Apoptosis

41
Q

Aging

A

Normal physiological process distinct from disease

  • Cell lifespan
  • Telomere
  • Progeria
42
Q

Cell lifespan

A

Have about 50 generations

43
Q

Telomere

A

Cap of nucleotides on the end of each DNA strand
• Each replication: telomere loses a few nucleotides, like a clock ticking
• Telomere gone: cell no longer replicates and dies

44
Q

Progeria

A

Rapid aging disease, “early geriatrics”, increased speed with high stress

45
Q

Apoptosis

A

Normal, physiologic, planned cell death

  • Epidermis: cells are genetically programmed to commit suicide after a few days
  • GI tract: epithelial cells are actively dividing to replace cells programmed to die

Pathology (6 decks)

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