Growth Adaptations Flashcards
Basic Principles of Growth Adaptations
Baseline: Organ is in homeostasis w/ physiologic stress placed on it
Increase, decrease or change in stress on the organ leads to growth adaptations.
Hyperplasia vs. Hypertrophy
Both: Increased Stress → Increased Size
Hyperplasia: More cells
Hypertrophy: Bigger cells
Mechanism of Hypertrophy
Make more cytoskeleton & organelles via:
Gene Activation
Protein Synthesis
Production of Organelles
Mechanism of Hyperplasia
Production of new cells from stem cells
Gravid Uterus: Hyperplasia or Hypertrophy?
Both!
Permanent Tissues
No Stem Cells
Only Undergo Hypertrophy
3 Types:
Cardiac Myocytes
Skeletal Muscle
Nerve Tissue
Pathologic Hyperplasia
Dysplasia, cancer
Example: Endometrial hyperplasia
Exception: BPH (does not have an increased risk of cancer)
Atrophy
Decreased Stress → Decreased Size
Smaller Cells (Ubiquitination or Autophagy)
OR
Fewer Cells (Apoptosis)
Ubiquitination
Ubiquitin marks IFs
Proteosome destroys ubiquitinated structures
Cytoskeleton reduces
Cell shrinks
Autophagy
Vacuoles form
Vacuoles fuse w/ lysosomes
Metaplasia
Stress Change → Stem Cell Reprogramming → Cell Type Change
Most common in surface epithelium
Metaplastic cells handle new stress better (eg Barrett’s)
Reversible via removal of driving stressor (eg GERD → Barrett’s, GERD resolution → Return to normal epithelium)
Can progress to dysplasia & cancer (except Apocrine Metaplasia)
Can be due to Vitamin A Deficiency
Mesenchymal tissues can undergo metaplasia too
Barrett’s Esophagus Metaplasia
Normal esophagus:
Squamous epithelium
Sharp demarcation between esophagus (squamous) & stomach (columnar)
Reflux → Metaplasia of esophagus
Squamous → Columnar, nonciliated, mucinous
New cells handle acid better
Apocrine Metaplasia
Does not increase risk for cancer
Fibrocystic breast changes can be involved in increased risk for breast cancer, but the Apocrine Metaplasia, itself, is not.
Myositis Ossificans Metaplasia
Trauma → Skeletal Muscle Inflammation → Bone Formation in skeletal muscle
Seen as opacity in muscle or X-Ray
Radiologic difference between Myositis Ossificans and an Osteosarcoma
Myositis Ossificans if:
Adjacent bone is normal
There is a separation between lesion and adjacent bone.
3 Types of Epithelium
Squamous (Keratinizing or Not)
Columnar
Transitional (Almost exclusively seen in the context of urothelium)
Mesenchymal Tissues
AKA Connective Tissues:
Bone
Blood Vessels
Cartilage
Fat
Apocrine Tissue
Exocrine Tissue that behaves very specifically
Membrane buds off into lumen
Secreting cell loses cytoplasm with each secretion
Seen in breast tissue
Vitamin A Deficiency Leads To:
Night Blindness (Nyctalopia) Keratomalacia (Conjunctival Thickening) Immune Deficiency (Cells stuck in blast phase)
Malignant Cause of Vitamin A Deficiency
Acute Promyelocytic Leukemia
15:17 Translocation
Involves retinoic acid receptor
Too many cells trapped in blast phase
Can treat with ATRA
Vitamin A - Uses
Maturation of immune cells beyond blast phase
Maintenance of specialized epithelium
ATRA
All Trans-Retinoic Acid
Binds Retinoic Acid receptor
Allows immune cells to mature
Dysplasia
Disordered Cellular Growth
Proliferation of precancerous cells
Arises from longstanding pathologic hyperplasia (eg endometrial) or metaplasia (eg Barrett’s)
Reversible with removal of inciting stress
Stress Persists → Carcinoma (Irreversible)
Example of Dysplasia
CIN
CIN1 - LSIL: Mild dysplasia, basal 1/3 of cervix
CIN2 - HSIL: Moderate dysplasia, basal 2/3 of cervix
CIN3 - HSIL: Severe dysplasia, more than 2/3 of cervix
