Cellular response to stress

Hyperplasia and Hypertrophy

 Introduction
• Normally cells perform within a narrow range of
structure and function. When faced with excess
demands, to maintain their viability, the cells
respond by calling upon their functional reserve.
Changes of this nature are called cellular
adaptations.

• Cellular adaptations may involve changes in growth

or differentiation. Cells can also adapt by storing
abnormal amounts of substances (intracellular
accumulation).

• Cellular adaptation is feasible to a certain extent

only. When the inciting stimulus is excessive, the
cell dies.
 Types of Cellular Adaptations
Adaptations involving Cellular Growth
Excessive Growth
• Hyperplasia
• Hypertrophy
Decreased Growth
• Developmental: Agenesis/Hypoplasia
• Acquired: Atrophy

Adaptations involving Cellular differentiation

- Metaplasia
- Certain forms of dysplasia

Intracellular accumulations
Of normal substances
- Lipids, Proteins, glycogen
Of abnormal substances
- Of Endogenous or Exogenous origin
 Certain Confusing Terms
• Dysplasia: The term when used in context of neoplastic
disorders, refers to constellation of abnormalities that include
loss of uniformity of individual cells as well as loss in their
architectural orientation.

• Dystrophy: It is a disorder, usually congenital, of structure or

function, of an organ or tissue due to abnormal nutrition.

• Dyscrasia: A term generally used by hematologists and refers

to a blood disorder of uncertain etiology.

• Dysostosis: Defective ossification of fetal cartilage.

• Aplasia: lack of development of an organ

• Agenesis: Absence of an organ due to failure of appearance of

the primordium of an organ during embryonic development

• Hypoplasia: Incomplete or underdevelopment of an organ.

 Hyperplasia
• Definition: An increase in number of cells of an organ or a
tissue resulting in increased volume of the organ or tissue is
called hyperplasia.

• An organ can undergo hyperplasia only when it is composed of

labile or stable cells.

• Organs/tissues that readily show hyperplasia:

– liver, kidney, fibrous tissue, endothelium, surface epithelial cells

and hemopoietic tissue.

• Organs/tissues with moderate capacity for hyperplasia:

– bone, cartilage, smooth muscle of bvs and uterus, solid glandular

epithelium

• Organs/tissues that cannot undergo hyperplasia:

– neurons and cardiac muscle fibers

 Causes of Hyperplasia
Physiological
• Hormonal:
– Breast enlargement during pregnancy, lactation and puberty
– Enlargement of uterus during pregnancy
• Compensatory:
– Liver and kidney enlargement after partial resection.
Pathological
• Hormonal:
– Endometrial hyperplasia,
– Fibrocystic disease,
– Graves disease etc.
• Non-hormonal:
– Lymphoid hyperplasia in infections,
– Vascular and connective tissue hyperplasia during wound healing,
– Hyperplasia of erythroid tissue in chronic anemia,
– Hyperplasia of skin, GI and respiratory epithelium when
chronically irritated
Hyperplasia of Endometrium
Gingival Hyperplasia
Prostatic Hyperplasia
Lymphoid
Hyperplasia
presenting as
cervical
lymphadenopathy
Prostatic Hyperplasia
 Mechanism of Hyperplasia
• It is caused due to increased production
of GFs, GF receptors or because of
increased activation of intracellular
signaling pathways.

• All these influences induce

transcription factors that result in
cellular proliferation.

• In some cases, stem cells are recruited

to form new cells.
 Hypertrophy
Definition: Increase in size of the cell without
increase in number is called hypertrophy

Physiological Hypertrophy
• Increased muscle mass in weight lifters
• Hypertrophy of uterus during pregnancy
• Breast hypertrophy during lactation

Pathological Hypertrophy
• Cardiac hypertrophy seen in HT and valvular heart ds.
• Hypertrophy of urinary bladder as seen in BPH and
urinary strictures
Gross specimen of Heart showing Hypertrophy
Cardiac Hypertrophy
 Mechanism of Hypertrophy
• Genes encoding for TFs (like c-fos and c-jun) and
GFs (like TGF-ß and IGF-1) are induced.

• Increased synthesis of cellular proteins and

filaments.

• Synthesis of fetal form of the protein instead of adult

form may occur.

• Some genes that are silent in post natal life may get
re-expressed.