Growth Adaptations Flashcards

1
Q

Basic Principles of Growth Adaptations

A

Baseline: Organ is in homeostasis w/ physiologic stress placed on it

Increase, decrease or change in stress on the organ leads to growth adaptations.

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2
Q

Hyperplasia vs. Hypertrophy

A

Both: Increased Stress → Increased Size

Hyperplasia: More cells
Hypertrophy: Bigger cells

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3
Q

Mechanism of Hypertrophy

A

Make more cytoskeleton & organelles via:

Gene Activation
Protein Synthesis
Production of Organelles

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4
Q

Mechanism of Hyperplasia

A

Production of new cells from stem cells

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5
Q

Gravid Uterus: Hyperplasia or Hypertrophy?

A

Both!

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6
Q

Permanent Tissues

A

No Stem Cells
Only Undergo Hypertrophy

3 Types:
Cardiac Myocytes
Skeletal Muscle
Nerve Tissue

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7
Q

Pathologic Hyperplasia

A

Dysplasia, cancer

Example: Endometrial hyperplasia

Exception: BPH (does not have an increased risk of cancer)

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8
Q

Atrophy

A

Decreased Stress → Decreased Size

Smaller Cells (Ubiquitination or Autophagy)

OR

Fewer Cells (Apoptosis)

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9
Q

Ubiquitination

A

Ubiquitin marks IFs
Proteosome destroys ubiquitinated structures
Cytoskeleton reduces
Cell shrinks

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10
Q

Autophagy

A

Vacuoles form

Vacuoles fuse w/ lysosomes

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11
Q

Metaplasia

A

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

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12
Q

Barrett’s Esophagus Metaplasia

A

Normal esophagus:
Squamous epithelium
Sharp demarcation between esophagus (squamous) & stomach (columnar)

Reflux → Metaplasia of esophagus
Squamous → Columnar, nonciliated, mucinous
New cells handle acid better

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13
Q

Apocrine Metaplasia

A

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.

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14
Q

Myositis Ossificans Metaplasia

A

Trauma → Skeletal Muscle Inflammation → Bone Formation in skeletal muscle

Seen as opacity in muscle or X-Ray

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15
Q

Radiologic difference between Myositis Ossificans and an Osteosarcoma

A

Myositis Ossificans if:
Adjacent bone is normal
There is a separation between lesion and adjacent bone.

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16
Q

3 Types of Epithelium

A

Squamous (Keratinizing or Not)
Columnar
Transitional (Almost exclusively seen in the context of urothelium)

17
Q

Mesenchymal Tissues

A

AKA Connective Tissues:

Bone
Blood Vessels
Cartilage
Fat

18
Q

Apocrine Tissue

A

Exocrine Tissue that behaves very specifically

Membrane buds off into lumen
Secreting cell loses cytoplasm with each secretion
Seen in breast tissue

19
Q

Vitamin A Deficiency Leads To:

A
Night Blindness (Nyctalopia)
Keratomalacia (Conjunctival Thickening)
Immune Deficiency (Cells stuck in blast phase)
20
Q

Malignant Cause of Vitamin A Deficiency

A

Acute Promyelocytic Leukemia

15:17 Translocation
Involves retinoic acid receptor
Too many cells trapped in blast phase
Can treat with ATRA

21
Q

Vitamin A - Uses

A

Maturation of immune cells beyond blast phase

Maintenance of specialized epithelium

22
Q

ATRA

A

All Trans-Retinoic Acid

Binds Retinoic Acid receptor
Allows immune cells to mature

23
Q

Dysplasia

A

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)

24
Q

Example of Dysplasia

A

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

25
Q

Aplasia

A

Failure of cell production during embryogenesis

Example:
Unilateral renal agenesis

26
Q

Hypoplasia

A

Decrease in cell production during embryogenesis
Leads to small organs

Example:
Streak ovary in Turner Syndrome