Atrophic processes in cystic fibrosis
In cystic fibrosis, atrophy is most often secondary in nature. It develops against the background of excretory duct obstruction by thick, viscous secretions, as well as due to progressive proliferation of connective tissue.
Pancreatic involvement In early childhood, the morphological picture may be minimal, but as the patient grows older, stones form and fibrosis increases. In older children and adult patients, complete atrophy of the exocrine part of the gland is observed. The parenchyma is replaced by adipose and fibrous tissue, among which only preserved islets of Langerhans are visualized. It is important to note that the endocrine apparatus atrophies extremely rarely: clinical manifestations of diabetes mellitus are recorded in no more than 5% of patients.
Changes in other organs
- Salivary glands: There is progressive dilation of the ducts, squamous metaplasia of the epithelial lining, and marked atrophy of the glands themselves resulting in fibrosis. An exception may be the parotid glands, which are of the serous type, lack mucous-producing cells, and are therefore less susceptible to these changes.
- Intestines (meconium ileus): Due to the accumulation of thick dark-green meconium, a sharp dilation of the loops of the small intestine occurs. The villi of the mucous membrane are compressed, and the epithelial cells become flattened and atrophic.
Atrophy in organs of the male reproductive system
Atrophic changes in the testes often lead to irreversible consequences for a man's reproductive health. In pathological anatomy, several classic examples of such lesions are distinguished.
Cryptorchidism (undescended testis) Pathological changes in the ectopic testis begin already in early childhood. There is a pronounced developmental delay of the spermatogenic epithelium. The seminiferous tubules gradually transform into dense cords formed by hyalinized connective tissue with a thickened basement membrane. The volume of the stromal component increases, and the Leydig cell population decreases. As atrophy progresses, the testis becomes dense and significantly decreases in size.
Complications and outcomes of cryptorchidism:
- Infertility. Develops not only in bilateral but also in unilateral lesions (in the second, normally descended testis, the differentiation of germ cells is also disrupted and their number decreases).
- Malignant transformation. In the atrophied ectopic testis, the risk of developing malignant tumors (malignancy) increases manifold.
- Associated pathologies: inguinal hernias and frequent trauma to the testis when it is retained in the inguinal canal.
Orchitis and epididymo-orchitis Acute inflammation (for example, as a complication of mumps) is accompanied by pronounced edema, mononuclear infiltration, and small focal hemorrhages. This leads to microcirculation disorders and the formation of testicular tissue infarctions. The natural outcome of such damage is deep atrophic and sclerotic processes, which also result in male infertility.
Local atrophic changes in chronic inflammation
Long-standing purulent-necrotic processes have a destructive effect on surrounding tissues, causing their thinning and degradation.
A classic example is chronic hematogenous osteomyelitis. The disease develops as a consequence of the acute form and is characterized by the formation of intraosseous abscesses, sequestration of necrotic bone areas, and active periosteal bone formation.
In addition to gross deformation of the bone itself and periosteal sclerosis, adjacent soft tissues are involved in the pathological process. Pronounced scar changes develop in them, fistulous tracts are formed for the discharge of small bone sequestra, and the skin directly above the focus of inflammation becomes thinned and atrophic.
Among the severe systemic complications of such prolonged purulent inflammation (in addition to local atrophic and scarring changes), secondary amyloidosis, pathological fractures, false joints, bleeding from fistulas, and even the appearance of tumors in the affected area are distinguished.
To remember the main outcomes of testicular atrophy in cryptorchidism, use the acronym BMI: Barrenness (Infertility), Malignancy, Inflammation/trauma.
Class and exam questions
Does pancreatic atrophy in cystic fibrosis necessarily lead to the development of diabetes mellitus?
No. In cystic fibrosis, complete atrophy of the exocrine part of the gland occurs, but the endocrine part (islets of Langerhans) persists among the fibrous and adipose tissue. Clinical signs of diabetes occur in no more than 5% of patients.
Why is testicular atrophy dangerous when it fails to descend into the scrotum (cryptorchidism)?
Progressive atrophy of the ectopic testis leads to irreversible infertility. In addition, in such altered tissues, the risk of malignancy—the development of a malignant neoplasm—is significantly higher.
What is the outcome of testicular infarctions occurring against the background of severe orchitis?
Impaired blood supply and subsequent infarctions of the testicular tissue result in pronounced atrophic and sclerotic processes. The main clinical outcome of this condition is male infertility.
What else to study on this topic
- Pathogenesis and morphological picture of chronic hematogenous osteomyelitis
- Bronchopulmonary complications of cystic fibrosis: formation of bronchiectasis and pneumosclerosis
- Meconium ileus and meconium peritonitis: macro- and microscopic changes
- Infectious mononucleosis: involvement of lymphoid tissue, liver, and spleen
- Pathological anatomy of viral CNS infection using poliomyelitis as an example
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