Adaptation to Stress: Alterations of Cell Growth and Differentiation

Atrophy vs. Aplasia

 Atrophy: Reduction in size of an organ or tissue due to decrease in cell size and number
o Retreat of the cell to a smaller size at which survival is still possible (can be
pathologic or physiologic)
 Aplasia: Absence of an organ due to failure of growth of the existing primordium
o Subtle difference from agenesis (absence of organ and primordium)
o Used in aplastic anemia (chronic primary hematopoietic failure)
Hypertrophy vs. Hyperplasia
 Hypertrophy: increase in size of cells cells have limited capacity to divide
o Ex. Hypertrophic LV: increase in size of myocardial cells in LV due to added
workload from HTN or valvular disease
o Ex. Hypertrophic Myometrium of Uterus during pregnancy

 Hyperplasia: increase in number of cells  adaptive response in cells capable of

replication
o Physiologic Stimuli: hormonal, compensatory (liver regrowing)
o Pathologic Stimuli: disturbed hormonal balance, wound healing, wart viruses
o If signals that cause it abate  hyperplasia disappears
o Can occur together with hyperplasia
Reversible vs. Irreversible Changes:
 Reversible Changes:
o Light microscopic changes
 Cell Swelling (hydropic change/vacuolar degeneration)
 Fatty Change  more lipid vacuoles
 Increased eosinophilic staining (pink)  part of progression to necrosis
o Ultrastructural Changes
 Plasma Membrane alterations (loosening, blebbing)
 Mitochondrial Changes (swelling, phospholipid rich densities)
 Dilatation of ER (ribosomes detach)
 Nuclear Condensation (chromatin clumping)
 Cytoplasm acquires myelin figures from damaged cell membranes

o Steatosis (Fatty Change in Liver) – can go back to normal by abstaining from EtOH
 Fatty Liver: double the size in gm, yellow color due to fat
  Irreversible Injury (Necrosis = Pathologic, Apoptosis = Not Always Pathologic)

o Apoptotic Body (Acidophilic Body with shrunken nucleus): viral hepatitis,

physiologic
o Necrosis:
 Coagulative: cell outlines preserved
 Liquefactive: cells dissolved
 Caseous: cheesy
 Fat Necrosis
 Fibrinoid
Progression of Inflammation (Acute, Chronic, Granulomatous)
 Coagulative Necrosis (MI)
 Tissue Repair and Healing Process in MI:N

Necrosis – pink acidophilic cells with no nucleus

Inflammation – neutrophils (multilobed nucleus and cytoplasmic granules) and
macrophage

Progression from Granulation Tissue to Fibrosis (tissue repair)

 Granulation Tissue – composed of fibroblasts and blood vessels
 Muscle tissue is not replaced
  Transmural Neutrophil Infiltrate – inside lumen and walls (gives pus like appearance)

Granulation Tissue vs. Granulomatous Inflammation (e.g. granuloma)

 Granulomatous Inflammation

o Characterized by:
 Aggregates of activated macrophages (epithelioid cells)
 Scattered lymphocytes
  Multinucleated giant cells (macrophages fuse)

 Caseous Necrosis (cheesy crumbly appearance)

o Caused by:
 T cell response to pathogens (tuberculosis)
 Immune mediated inflammatory disease (Crohn’s)
 Inert foreign bodies (splinters, sutures)
 Sarcoidosis
 Eosinophils (bilobed) – found in inflammatory sites around parasitic infections and IgE
immune mediated reactions = bright red granules
Repair of Tissue Injury:
 Inflammation (followed by adhesions)
  Granulation Tissue (repair tissue that results in scarring)

 Fibrosis – produce collagen and can lay down scar tissue + new blood vessels

Subtypes of Acute Inflammation:

 Acute Mi: Coagulative Necrosis
 Acute Pancreatitis: Necrosis from Released Enzymes
o Liquefactive Necrosis with Acute Inflammation (no preserved cell outlines, pale
and dropping out, neutrophil infiltrate)
 o Fat Necrosis – release of lipase
 Acute Bacterial Pneumonia: tissue injury with acute inflammation (abundance of
macrophages and neutrophils)
o Foci of acute inflammation with yellowish appearance (A)
o Abscess resulting from tissue injury and inflammation

Subtypes of Chronic Inflammation:

 Prolonged host response to constant stimulus (inflammation, injury, fibrosis proceed
simultaneously)
 Hallmarks: appearance varies by length/time of inflammation and what they phagocytize
 o Lymphocytes: B and T cell ratios vary

o Plasma Cells: from B Cells

o Macrophages: mature monocytes

Introduction to Metaplasia and Dysplasia