STEPTRACKERGENERAL PRINCIPLES | PATHOLOGY | HIGH-YIELD REVIEW

Growth Adaptations

Cells adapt to stress before they are injured — name the change, its trigger, and whether it can lead to cancer.

FOCUS ON
Metaplasia vs dysplasia is the tested pair. Metaplasia swaps one mature cell type for another and is reversible; dysplasia is disordered growth on the road to carcinoma. Whether a tissue can divide decides hypertrophy vs hyperplasia.
ADAPTATION
WHAT CHANGES · MECHANISM
KEY RULES
CLASSIC EXAMPLES
Hypertrophy
↑ cell size
More proteins, filaments and organelles per cell via gene activation and ↑ protein synthesis. No new cells.
The only way permanent tissues (cardiac, skeletal muscle) grow. Often accompanies hyperplasia in dividing tissues.
LV hypertrophy in hypertension · skeletal muscle with exercise · gravid uterus (with hyperplasia)
Hyperplasia
↑ cell number
Stem cells divide in response to hormones or growth factors.
Only in labile and stable tissues. Pathologic hyperplasia may progress to dysplasia — except BPH, which carries no cancer risk.
Endometrial hyperplasia (unopposed estrogen) → endometrial carcinoma risk · BPH · psoriasis · breast in pregnancy
Atrophy
↓ size and number
Loss of stimulus → apoptosis (↓ number) + ubiquitin–proteasome breakdown of cytoskeleton and autophagy (↓ size).
Causes: ↓ hormones, disuse, denervation, ↓ blood supply, malnutrition, pressure. Autophagic residual bodies leave lipofuscin.
Disuse muscle after casting · renal cortex in hydronephrosis · cerebral atrophy · thymus with age
Metaplasia
cell type A → cell type B
Stem cells reprogrammed to make a cell type better suited to the stress.
Reversible if stress removed; persistent stress → dysplasia → carcinoma. Exception: apocrine metaplasia of breast — no added cancer risk.
Barrett esophagus (squamous → columnar with goblet cells) · smoker's bronchus (ciliated columnar → squamous) · vitamin A deficiency · myositis ossificans
Dysplasia
disordered growth
Pleomorphism, hyperchromasia, ↑ nuclear:cytoplasmic ratio, loss of polarity and maturation.
Usually arises from longstanding hyperplasia or metaplasia. Mild–moderate may regress; full-thickness = carcinoma in situ; breaching basement membrane = invasive carcinoma.
CIN of cervix · dysplasia in Barrett · actinic keratosis
Aplasia / hypoplasia
developmental
Aplasia: failure of cell production during embryogenesis. Hypoplasia: ↓ production → small organ.
Developmental terms — not responses of a mature organ to stress.
Unilateral renal agenesis (aplasia) · streak ovaries in Turner syndrome (hypoplasia)
Mesenchymal metaplasia
connective tissue → bone
Fibroblasts in injured soft tissue form bone.
Benign; shows on x-ray as soft-tissue calcified mass — do not mistake for osteosarcoma.
Myositis ossificans after muscle trauma

Mechanism — the stress continuum

Stress ↑Hormones, workload, irritants
→
AdaptHypertrophy · hyperplasia
→
Persistent irritantMetaplasia
→
DysplasiaDisordered, still reversible early
→
CarcinomaIn situ → invasive (BM breached)

Stress ↓ runs the other way: atrophy. If the stress exceeds what adaptation can handle, the cell moves to injury (page 1.02).

Can the tissue divide?

TISSUE TYPE
EXAMPLES
GROWS BY
Labile
Bone marrow, skin, GI epithelium, hair follicles
Hyperplasia (continuously cycling)
Stable
Hepatocytes, proximal tubule, periosteum, smooth muscle
Hyperplasia when stimulated (G0 → G1)
Permanent
Neurons, cardiac myocytes, skeletal muscle, RBCs, lens
Hypertrophy only; injury → scar

How it's tested

COMMON CONFUSIONBPH and endometrial hyperplasia are both hyperplasia, but only endometrial hyperplasia raises cancer risk.
THE TRAPThe vignette describes "intestinal-type columnar cells with goblet cells in the distal esophagus" and never says metaplasia. Or it asks how the heart enlarges — "increased number of myocytes" is wrong.
YOUR APPROACHAsk in order: did size, number or type change? Is the change orderly (adaptation) or disordered (dysplasia)? Is the basement membrane intact?

If you see… think…

Chronic GERD + columnar cells with goblet cells → Barrett metaplasia (adenocarcinoma risk)
Smoker's bronchial biopsy with squamous lining → squamous metaplasia
Night blindness, dry eyes, Bitot spots → vitamin A deficiency (keratinizing metaplasia)
Obese woman, postmenopausal bleeding → endometrial hyperplasia from unopposed estrogen
Thick LV wall in long-standing hypertension → hypertrophy
Thin renal cortex above an obstruction → pressure atrophy
Calcified mass in thigh muscle weeks after trauma → myositis ossificans
Full-thickness atypia, basement membrane intact → carcinoma in situ
Golden-brown perinuclear pigment in aged heart → lipofuscin (atrophy, autophagy)