Adaptation

Adaptation


The normal cell is able to handle normal physiologic demands, maintaining a steady state called homeostasis. More severe physiologic stresses and some pathologic stimuli may bring about a number of physiologic and morphologic cellular adaptations, during which new but altered steady states are achieved, preserving the viability of the cell and modulating its function as it responds to such stimuli

If the limits of adaptive response to a stimulus are exceeded, or in certain instances when the cell is exposed to an injurious agent or stress, a sequence of events follows that is loosely termed cell injury. Cell injury is reversible up to a certain point, but if the stimulus persists or is severe enough from the beginning, the cell reaches a "point of no return" and suffers irreversible cell injury and ultimately cell death.

Types of Adaptation:

1-Atrophy: is decrease in cell size by loss of cellular substances.

2-Hypertrophy: is increase size of cell and organ. Hypertrophy can be physiologic or pathologic and is caused either by increased functional demand or by specific hormonal stimulation

3-Hyperplasia: is increase in cells number. Hyperplasia and hypertrophy are closely related and often develop at same time in the tissue

Hyperplasia can be physiologic or pathologic .Physiologic hyperplasia is divided into hormonal hyperplasia and compensatory hyperplasia

Most forms of pathologic hyperplasia are instances of excessive hormonal or growth factor stimulation

4-Metaplasia: is reversible change in which one adult cell type(epithelial or mesenchymal) replaced by another cell type.



Examples

Testicular atrophy

Usually affecting any age group according to the cause

Causes:-

Chronic ischemia, trauma, tumor, radiation, infection and aging process

The patient presented with local pain and the most important complication is infertility.

Grossly (macroscopically)

Decrease testicular size

Diagnosis: by physical examination

Microscopically

1-decrease in the size of seminephrous tubules

2- no germinal cells within testicular tubule; however; sertolli cells are still easily identified.

3-the basement membrane of the tubules is thickened and stained pink ; a process called "hyalinization".

4-the interstitial tissue shows an increase deposition of fibrous tissue.


Benign prostatic hyperplasia (BPH)(Nodular hyperplasia)

Nodular hyperplasia(BPH), is an extremely common disorder in men over age 50. It is characterized by hyperplasia of prostatic stromal and epithelial cells, resulting in the formation of large, fairly discrete nodules in the periurethral region of the prostate

Incidence.

Histologic evidence of nodular hyperplasia can be seen in approximately 20% of men 40 years of age, a figure that increases to 70% by age 60 and to 90% by age 70

Clinical features

Symptoms of nodular hyperplasia, when present, relate to two secondary effects: (1) compression of the urethra (2) retention of urine in the bladder ,so patients experience frequency, nocturia, difficulty in starting and stopping the stream of urine, and dysuria (painful micturition). In many cases, sudden, acute urinary retention occure.

Macroscopically

In the usual case of prostatic enlargement, the prostate weights between 60 and 100 gm. On cross-section of the affected prostate, the nodules usually are fairly readily identified. They vary in color from yellow-pink to pale gray, and vary in consistency from soft to tough and from oozing fluid to not.

Microscopically

Microscopically, the hallmark of BPH is nodularity due to glandular proliferation or dilation and to fibrous or muscular proliferation of the stroma . Glandular proliferation takes the form of aggregations of small to large to cystically dilated glands, lined by two layers, an inner columnar and an outer cuboidal or flattened epithelium, based on an intact basement membrane. the epithelium is characteristically thrown up into numerous papillary buds and infoldings,


Thyroid Hyperplasia

The function of thyroid is controlled by hypothalamic-pituitary system by secretion of TSH which stimulate the thyroid follicles to secrete thyroxin which regulate the production of TSH by negative feed back mechanism, any condition disturbance this balance result in increased secretion of TSH or similar substance and result in thyroid hyperplasia, the most common cause is Graves disease which is the most common cause of hyperthyroidism.

Graves disease occurs in younger adult and more common in female than male , usually presented with decrease weight, increase appetite, tachycardia, palpitation, palmer sweating, tremor, exophthalmia, nervousness and etc.

Macroscopically

.symmetrical enlarged thyroid gland

.the gland is smooth and soft in consistency

.warm or hot due to increased vascularity

Microscopical features

-Thyroid follicles increased in number

-The follicular epithelial cells are tall and columnar and more crowding result in the formation of papillae, which project into follicular lumen

-decreased colloid which is pale with scalloped formation

-Proliferation of stroma and increased vascularity with lymphocyte infiltration


Endometrial hyperplasia(simple cystic glandular endometrial hyperplasia)

This condition occur due to prolong endometrium stimulation by excessive estrogen lead to both glandular and stromal hyperplasia.

Etiology

-Around menopause due to hormonal disturbance

-Estrogen secreted ovarian tumor

- female on estrogen therapy

Clinical features

- Irregular menstrual cycle.

-Heavy vaginal bleeding in perimenopausal female

-It rarely progressed to malignancy

Gross features

-Increased size and wt. of uterus

-Thickening of endometrium with fronds of hyperplastic endometrium.

Microscopical features

-Proliferation of endometrium glandular tissue

-Proliferation of glandular epithelial cells(multilayer of lining epithelium).

-dilation of endometrial gland, so it appear like tiny cyst scatter among normal looking endometrium gland

-Stroma proliferation which contain thin wall blood vessels and lymphocytes infiltration


Gastric metaplasia of the esophagus (Barrett Esophagus)

It is a complication of long standing gastroesophageal reflux. Barrett esophagus is defined as the replacement of the normal distal stratified squamous mucosa of the esophagus by metaplastic columnar epithelium containing goblet cells

Metaplastic columnar epithelium is thought to be more resistant to injury from refluxing gastric contents

Clinical features

Barrett esophagus usually present with features of gastroseophageal reflux such as heart burn, sour brash and rarely sever chest pain.

Microscopically

The esophageal squamous epithelium is replaced by metaplastic columnar epithelium