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Pathology > Cell Adaptation and Injury > Flashcards

Cell Adaptation and Injury Flashcards

1
Q

Hyperplasia

A

Hyperplasia: an increase in the number of cells in an organ or tissue

*typically a response to hormones and growth
factors

ex) breast with ducta; hyperplasia (additional layers of epithelium)

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2
Q

Forms of Cell Adaptation

A
  1. Hyperplasia
  2. Hypertrophy
  3. metaplasia
  4. atrophy
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3
Q

Hypertrophy

A

„ Hypertrophy: an increase in the size of individual cells due to increase in structural
components of cells

  • due to GFs and txn factors
    ex) gravid myometrium (note nuclei are spaced further apart)
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4
Q

Atrophy

A

Atrophy (cellular): decrease in cell size

  • due to increases in protein degradation-to-synthesis ratio
    ex) skeletal muscle with peripheral myofiber trophy
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5
Q

Metaplasia

A

„ Metaplasia: one adult cell type is replaced by another adult cell type

-chronic

Ex) mucosal (columnar) lining to squamous

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6
Q

Cell Adaptation: Intracellular Accumulations

Four general situations

A
  1. Normal endogenous: Abnormal metabolism
  2. Abnormal endogenous: Defect in protein folding and transport
  3. Normal Endogenous: Enzyme missing for metabolism
  4. Abnormal exogenous: lack machinery to digest it and get rid of it
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7
Q

Cell Adaptation: Intracellular Accumulations

  1. Lipids
A
  1. Lipids
    a) TGs in steatosis: round clear holes
    b) cholesterol: foamy cells (intracellular)
    c) atherosclerosis (extracellular): crystalline shards of clear areas
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8
Q

Cell Adaptation: Intracellular Accumulations

  1. Proteins
A
  1. Proteins
    - Little pink globules
    - amyloidosis
    * **usually extracellular
    * **can lead to pressure atrophy of adjacent cells
    * **ex) heart
    * **glassy pink
    * **Congo red stains it and is green under polarized light whereas collagen in white
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9
Q

Cell Adaptation: Intracellular Accumulations

  1. Hyaline Change
A

Descriptive Term of something really pink and glassy

“Russell Bodies”

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10
Q

Cell Adaptation: Intracellular Accumulations

  1. Glycogen
A

H&E: clear and frothy cytoplasmic vacuoles

PAS: hot pink

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11
Q

Cell Adaptation: Intracellular Accumulations

  1. Pigments
A
  1. Carbon
    - anthracosis: coal miners’ lungs
  2. Lipofuscin
    - wear and tear brown-yellow things
    - common in elderly hearts and livers
  3. Melanin
  4. Hemosiderin
    - looks similar to lipofuscin thus we stain it with Prussian Blue for iron
    - made of iron bound to ferritin
  5. Bilirubin (extracellular): in cananliculi in between hepatocytes
    - yellow pigment derived from hemoglobin (no iron)
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12
Q

Necrosis

A
  1. Pathologic
  2. Inflammatory
    - if tissue lives long enough
  3. Cell Swelling b/ can’t control osmolarity and water rushes in causing swelling
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13
Q

Apoptosis

A
  1. Pathologic or physiologic
  2. non-inflammatory
  3. Triggered by: GF withdrawal, DNA damage (radiation, toxins, free radicals), protein misfolding (ER stress)
  4. Cell Shrinkage
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14
Q

Phases of Apoptosis:

  1. Initiation Phase:
    a) intrinsic mitochondrial pathway
A
  • normally there is a GF survival signal that causes production of anti-apoptotic proteins which bind to Bcl-2/Bcl-x and they keep the mitochondrial pore closed
    a) lack of GFs + injury like radiation leads to DNA damage

b) activate BH3 proteins
- antagonize BCL2 channels

activate Bax/Bak channel

c) leakage of cytochrome C
- activate capsases (cysteine proteases)

d) apoptosis

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15
Q

Phases of Apoptosis:

  1. Initiation Phase:
    b) Extrinsic (death receptor pathway
A

a) FasL from T-cells attaches to the PM’s Fas Receptor
b) Cleaves procaspase8 into caspase 8
c) cascade of caspases
d) apoptosis

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16
Q

Phases of Apoptosis: Execution Phase

A

Same regardless of pathway

  • Caspases trigger activation of apoptotic enzymes, DNAases, proteases, etc.
  • bleb and broken into membrane bound fragments and phagocytosed by macrophages
17
Q

Causes of cell injury and death:

A

-„ Hypoxia/ischemia
„- Physical agents
„ -Chemical agents
„ -Infection
„ -Immunologic reactions and derangements
-„ Genetic derangements
„ -Nutritional deficiencies and imbalances

18
Q

Targets of Cell Injury

A
  • machinery for energy production
  • membranes
  • machinery for protein synthesis
  • genetic apparatus
19
Q

Mechanisms of Cell Injury:

1. Depletion of ATP

A

1) Failure of energy-dependent cell systems
„ *plasma membrane Na-K pump: intracellular Na+ buildup–>cell swelling

„ *calcium pump: influx of Ca2+
„
*protein synthesis

*protein folding

2) Increased glycolysis, leading to increased lactic acid, decreased pH and decreased
activity of enzymes

20
Q

Mechanisms of Cell Injury:

2. Mitochondrial Damage

A

*typically secondary to excess Ca2+, ROS, hypoxia

Results:

  1. mitochondrial permeability transition pore
    - destroys membrane potential needed to for making ATP
    - leads to necrosis
  2. Leakage of cytochrome c and others–>apoptosis
21
Q

Mechanisms of Cell Injury:

3. Loss of Ca2+ homestasis

A

*increased intracellular Ca2+
Results:
1. Increases mitochondrial permeability transition pore–>decreased ATP
2. Activates phospholipases, proteases–>membrane damage
3. endonucleases–>nuclear damage
4. ATPases

22
Q

Mechanisms of Cell Injury:
4. Oxidative Stress

  1. ROS
  2. patholigic Effects
  3. Sources of ROS
  4. Removal of Free Radicals
A 
*ROS and Free Radicals:
–hydroxyl radical ( •OH) 
– superoxide anion (O 2- •) 
– hydrogen peroxide (H2O2 ) 
– peroxynitrite (ONOO- )
  1. Pathologic Effects:
    a) lipid peroxidation of membranes: unsaturated lipid + ROS–>lipid radical–> propagation –> lipid peroxyl radicals

b) oxidative modification of proteins:
„ -disrupt active site of enzyme
„ -disrupt conformation of structural protein

c) lesions in DNA

  1. Sources
    – mitochondrial oxidative phosphorylation (normal)
    – radiant energy (e.g., UV rays, X-rays)
    – leukocytes during inflammatory response
    – metals (e.g., iron and copper)
    – nitric oxide
4. Removal of free radicals 
– antioxidant scavengers 
– transport proteins that bind reactive metals 
– enzymes: 
 „ superoxide dismutase 
 „ catalase 
 „ glutathione peroxidase
23
Q

Mechanisms of Cell Injury:
5. Defects in membrane permeability

  1. Causes
  2. Consequences
A

*occur in necrotic cell death, but not in apoptosis

1. Causes 
– damage by reactive oxygen species 
– decreased phospholipid synthesis secondary to 
low ATP 
– phospholipases activated by increased 
cytoplasmic Ca 2+ 
– detergent action of phospholipid breakdown 
products 
– cytoskeleton damage 
2. Consequences: 
– loss of ion potentials 
– loss of osmotic balance 
– loss of proteins and other metabolites 
– lytic enzyme release from lysosomes
24
Q

Mechanisms of Cell Injury:

6. DNA and protein Damage

A
  1. Free radicals damage DNA

2. Unfolded or misfolded proteins

25
Q

Morphologic changes:

Apoptosis

A
  1. Dark black fragments of DNA
  2. apoptotic bodies (little purple fragments) bleb out from cells
  3. note the lack of inflammation
26
Q

Morphologic changes:

A. necrosis

1) reversible
2) Irreversible

A

Robust neutrophilic infiltration

  1. Reversible
    a) EM Slide 93
    - loss of microvilli and blebbing
    - mitochondrial swelling
    - dilated endoplasmic reticulum
    b) LM Slides 94, 95
    - paler staining due to extra water in cytoplasm
    - steatosis
  2. irreversible
    a) EM
    - marked mitochondrial swelling
    - membrane discontinuity
    - myelin figures
    b) LM
    - nuclear pyknosis
    - karyolysis
    - loss of nuclei
    - fat necrosis with calcification
27
Q

Patterns of Tissue Necrosis: Coagulative

A

Slide 100-102

often in solid organs after ischemia
•
still see myocytes but most nuclei missing
•
lots of inflammation in between (but sometimes not due to ischemia)

We can tell the cells are necrotic but they look
•
the same-ish–we can ID the tissue

Can see more eosinophilia; loss of nuclei

28
Q

Patterns of Tissue Necrosis:

Liquefactive

A

Dead cells completely digested leaving only a viscous liquid

*usually bacterial and fungal infections; hypoxic injury in CNS

Slide 104: CNS infarct with cystic-like space remaining
after liquefactive necrosis

29
Q

Patterns of Tissue Necrosis: caseous

A

fungal/ •
mycobacterial
infections like TB

crumbly cheese •
texture

30
Q

Patterns of Tissue Necrosis: fat Necrosis

A

Areas of fat destruction usually with Calcium deposits and saponification (Ca2+ and fat make chalky white stuff)

*often associated with pancreatitis

31
Q

Patterns of Tissue Necrosis: Dystrophic Calcification

A

Deposition of Ca2+ salts in dying tissue

  • Occurs despite normal serum Ca2+
  • Stain deep purple (basophilic)
  • associated w/all four patterns of necrosis

Pathology (5 decks)

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