VPP 211: General Veterinary Pathology (1+1)

APLASIA, HYPOPLASIA AND ATROPHY

Aplasia

• Aplasia (Gr. A: Without; not; Plasia: Development; formation) is the complete failure of an organ to develop. This developmental disturbance occurs in the embryo or foetus in utero. In the place of the organ, rudimentary tissue of fat and connective tissue are present. The condition is incompatible with life when it involves vital organs like heart, brain etc.

Hypoplasia

It is the failure of an organ or tissue to attain its full normal adult size.

• Causes
  • Any injury occurring in late stages of development of fetus or neonates. e.g. Genetic mutation affects proper differentiation and migration of cells in embryo, virus causes hypoplastic changes; drug induced hypoplasia occurs through degeneration and necrotic changes.
  • Pathological changes: Organ will be smaller than adult size. The cells show alterations in lysosomes and inspissated protein in cytoplasm. The phagolysosomes increase in size with lipofuscin pigment.

Atrophy

• Atrophy is the decrease in the size (quantitative) or amount (numerical) of cells/tissues/organ after attaining full normal growth. Atrophy is representing adaptation to deficient nutrient supply, lack of stimulation and decreased work load. This may affect any organ or part of an organ.
• Atrophy can be broadly classified into physiological atrophy and pathological atrophy.

Physiological atrophy

• Involution of the organs can be observed as the age is advanced. Involution is the decrease in the size of the organ due to decrease in the number of cells, caused by apoptosis. e.g. Involution of thymus on attaining puberty, uterine involution after parturition (decrease in smooth muscle size and number)
• Senile atrophy: Atrophy of the organs occurs with ageing and reproductive organs like testis and ovaries are the first to show such changes. It is associated with loss of cells.

Left - Atrophy, Right - Sertoli cell tumour

Pathological atrophy

• Nutritional atrophy: This is due to starvation. Starvation of the tissue is caused by malnutrition, malabsorption, chronic infection, parasitism, neoplasia etc. Mismothering is also quoted in starvation atrophy in neonates. In starvation following depletion of glycogen and fat reserves, protein of the musculature and vital organs is lost, resulting in muscular wasting.
• Angiotrophic atrophy: Diminished blood supply (ischaemia, chronic passive congestion, anaemia) may lead to atrophic changes.
• e.g. Parasitic ischaemia caused by Strongylus larvae by the occlusion of femoral artery leads to atrophy of hind limb in horses. Hepatic atrophy can occur due to decreased portal venous blood flow. Chronic venous congestion results in centrilobular necrosis of liver due to inadequate oxygen and nutrition supplied to the hepatocytes.
• Disuse atrophy
  • Decreased work load: Decrease in the size of the body musculature due to inactivity as in the case of race horses.
  • Immobilization: Skeletal muscle atrophic changes can occur in plaster casted animals. In fracture, there will be decrease in the size of the myocytes.
• Neurotrophic atrophy: Decrease in the size of muscle fibres occurs if a nerve is severed or injured.
  • e.g. In horses, laryngeal muscle atrophy occurs due to the injury to left recurrent laryngeal nerve and shoulder muscle atrophy (sweening) occurs due to suprascapular nerve injury.
• Pressure atrophy: In space occupying lesions like tumours, abscesses etc., the neighboring tissues undergo atrophic changes mainly due to lack of nutrition from pressure ischemia.
• Endocrine atrophy: Prolonged steroid therapy leads to atrophy of zona fasciculata of the adrenal gland. Castration leads to atrophy of prostate. Hyperestrogenism associated with sertoli cell tumour results in seminiferous cell atrophy. Ovariectomy leads to uterine atrophy.

Pathogenesis

• In atrophy, the cells survive and are smaller in size with decreased function. There is imbalance between protein synthesis and degradation or loss of protein. That is excessive protein loss or degradation overproduction of proteins. Atrophy and atrophic changes can be attributed to autophagocytosis with destruction of cytoplasmic organelles like ribosomes, mitochondria and lysosomes and by ubiquitin-proteasome pathway wherein the proteins combine with ubiquitin, a cytosolic peptide and then it is destroyed (that is called proteasome).

Morbid/ gross changes

• Affected organs show decreased weight and volume, wrinkling of surface membrane and tortuous blood vessels too large for the volume of the tissue. Organs may be fibrosed and become firm. Fat shows serous atrophy (indicating starvation) i.e. clear/yellowish gelatinous material is seen in place of fat especially cardiac fat, renal fat etc.The organ may become soft and flabby and loss of tone and tissue colour.

Microscopic changes

• Cells are smaller than normal and decrease in number. Sometimes, complete disappearance of the cells is found. Adipocytes become smaller. Interstitial hyaluronic acid and mucopolisacharides are increased. Sometimes brown atrophy is encountered. Brownish discolouration is due to the membrane bound, indigested residual bodies in the cytoplasm.