Growth Adaptations

Question 1

Generally HYPERTROPHY (Increase in SIZE) + HYPERPLASIA (Increase in CELL NUMBER from stem cells) occur simultaneously. What is the exception?

Answer 1

Exception = PERMANENT TISSUES (Cardiac myocytes, skeletal muscle, nerve) do NOT have stem cells
ONLY undergo HYPERTROPHY (no hyperplasia)

Question 2

Biopsy of the heart shows an INCREASED THICKNESS of the LV wall. What is the mechanism of this?

Answer 2

LV HYPERTROPHY

Since hyperplasia is NOT possible in permanent tissues

Question 3

Give an example of PHYSIOLOGIC HYPERPLASIA. An example of PATHOLOGIC HYPERPLASIA.

Answer 3

PHYSIOLOGIC HYPERPLASIA: Polyclonal, reversible, regulated (Uterine SM during pregnancy)
PATHOLOGIC HYPERPLASIA: Monoclonal, irreversible, unregulated (Endometrial hyperplasia -> Dysplasia -> Cancer)

Question 4

PATHOLOGIC HYPERPLASIA increases the risk of cancer as it can progress to dysplasia. What is the one exception to this principle?

Answer 4

BENIGN PROSTATIC HYPERPLASIA

Does NOT increase the risk of PROSTATE CANCER

Question 5

What are the 2 mechanisms of ATROPHY? What is the underlying process(es) of each mechanism?

Answer 5

DECREASE IN CELL NUMBER - Apoptosis

DECREASE IN CELL SIZE -
Process 1: Ub-proteasome degradation pathway [Cytoskeletal IMF get tagged with ubiquitin and directed to proteasomes for degradation]
Process 2: Autophagy [Cellular components become autophaged in intracellular vacuoles -> Fuse with lysosomes -> Hydrolytic enzymes breakdown components]

Question 6

What are the 3 types of epithelium that can generally undergo METAPLASIA (change in cell type due to a change in stress)?

Answer 6

SQUAMOUS (Keratinizing or non-keratinizing)
COLUMNAR
UROTHELIAL (i.e. TRANSITIONAL)

Question 7

Generally metaplasia can increase the risk of CANCER (e.g. BARRETTS esophagus). What is the metaplasia of BARRETT’S?

Answer 7

Acid-induced METAPLASIA:
Nl Lower 1/3 of esophagus = Non-keratinized squamous epithelium
ACID-induced metaplasia = Non-ciliated, mucinous, columnar cells + goblet cells

Question 8

What is the major exception to the rule that Metaplasias increase the risk of cancer development?

Answer 8

APOCRINE METAPLASIA = Fibrocystic change of the breast that does NOT increase the risk of cancer dvlm

Question 9

What are 4 pathologies that VitA Deficiency can result in?

[Think eye, heme-onc, metaplasia, breast pathology]

Answer 9

1. NIGHT BLINDNESS - Loss of VitA on ROD receptor (Rods responsible for NIGHT + PERIPHERAL vision)
2. ACUTE PROMYELOCYTIC LEUKEMIA - t(15;17) disrupts retinoic acid receptor -> Blocks myeloblast (neutrophils, eosinophils, basophils) maturation -> PANCYTOPENIA
3. KERATOMALACIA
4. PERIDUCTAL MASTITIS: SMOKERS -> Relative Vit A deficiency -> Loss of maintenance of highly specialized epithelium of the lactiferous ducts -> columnar luminal cells become squamous metaplasia -> keratin plug -> periductal mastitis

Question 10

What are the 4 functions of VitA? What are the associated pathologies with a deficiency/disruption of each function

Answer 10

1. Maintains specialized epithelium of conjunctiva (GOBLET CELL/COLUMNAR EPITHELIUM) to maintain its transparency -VitA deficiency = KERATOMALACIA (white spot on eye rather than transparent conjunctiva)
2. Differentiation of ROD receptors for night and peripheral vision - VitA deficiency = NIGHT BLINDNESS
3. Maturation of myeloblasts into NEUTROPHILS/EOSINOPHILS/BASOPHILS - VitA receptor disruption [t(15;17)] = ACUTE PROMEYLOCYTIC LEUKEMIA
4. Maintenance of highly specialized epithelium of BREAST LACTIFEROUS DUCTS = PERIDUCTAL MASTITIS (Female smokers)

Question 11

What type of METAPLASIA is seen with KERATOMALACIA with VitA deficiency?

Answer 11

Nl CONJUNCTIVAL EPITHELIUM = Goblet cells/columnar epithelium
METAPLASIA CONJUNCTIVAL EPITHELIUM = Keratinizing squamous epithelium

Question 12

What is MYOSITIS OSSIFICANS?

Answer 12

Metaplastic change of skeletal muscle usually after trauma

Trauma -> Skeletal muscle CT undergoes inflammation and healing -> Changes to BONE

Question 13

METAPLASIA OF SKELETAL MUSCLE TO BONE

Answer 13

MYOSITIS OSSIFICANS

Question 14

What is dysplasia? What are 2 methods of developing dysplasia? Provide a classic example for each.

Answer 14

DYSPLASIA = disorganized proliferation of PRE-CANCEROUS CELLS (e.g. CIN)
METHOD 1: Pathological hyperplasia - Endometrial hyperplasia -> Endometrial dysplasia -> Endometrial carcinoma
METHOD 2: Metaplasia (Barret’s esophagus) -> Dysplasia -> Adenocarcinoma (distal 1/3 of esophagus)

Question 15

What differentiates DYSPLASIA/METAPLASIA from CARCINOMA?

Answer 15

METAPLASIA or HYPERPLASIA -> DYSPLASIA are REVERSIBLE - remove inciting stress
CARCINOMA is IRREVERSIBLE

Question 16

What is the classic example of AGENESIS (failure to develop)?

Answer 16

UNILATERAL RENAL AGENESIS

Question 17

What is the classic example of HYPOPLASIA (Decreased cell production during embryogenesis)? In association with a chromosomal disorder

Answer 17

STREAK OVARY with TURNER SYNDROME