. Chronic pyelonephritis often has an insidious onset. The patients present with clinical picture of chronic renal failure or with symptoms of hypertension.
Chronic obstructive PN may be insidious in onset or may present the clinical manifestations of acute recurrent PN with back pain, fever, frequent pyuria, and bacteriuria.
Infections of the lower urinary tract
Infections in the lower urinary tract are predisposed by obstruction and stasis.
Lower urinary tract infection is usually due to Gram-negative coliform bacilli, e.g. E. coli and Proteus, which are normally in the large bowel; because they have a short urethra, women are particularly prone to developing ascending infections.
In men, lower urinary tract infection is usually associated with structural abnormalities of the lower urinary tract and stasis due to obstruction.
Diabetes mellitus also predisposes to infection.
Morphology
The pelvicalyceal system is dark reddish brown as a result of acute inflammation of the usually smooth creamy mucosal lining due to bacterial infection.
The kidney is also congested and some small scattered abscesses are present in the cortex and medulla (acute pyelonephritis).
Obstruction of the drainage of urine from the kidney causes hydronephrosis.
Obstruction, one of the most important consequences of disease of the lower urinary tract, may occur at any place in the tract: renal pelvis (calculi, tumors), pelviureteric junction (stricture, calculi, extrinsic compression), ureter (calculi, extrinsic compression -pregnancy, tumor, fibrosis), bladder (tumor, calculi); urethra (prostatic hyperplasia or carcinoma, urethral valves, urethral stricture).
If obstruction occurs in the urethra, the bladder develops dilatation and secondary hypertrophy of muscle in its wall. This predisposes to development of out pouching of the bladder mucosa (diverticulae).
If obstruction occurs in a ureter, there is dilatation of the ureter (megaureter), with progressive dilatation of the renal pelvicalyceal system, termed hydronephrosis. Fluid entering the collecting ducts cannot empty into the renal pelvis and there is intrarenal resorption of fluid. At this stage, if the obstruction is relieved, renal, function returns to normal. However, if obstruction persists, there is atrophy of renal tubules, glomerular hyalinization, and fibrosis. As an end-stage, the renal parenchyma becomes severely atrophic and renal function is permanently impaired.
Urinary tract obstruction also predisposes to infection and stone formation.
Urolithiasis
Urolithiasis or formation of urinary calculi at any level of the urinary tract is a common condition. It is estimated that approximately 2% of the population experiences renal stone disease at sometime in their life with male-female ratio of 2:1.
Renal calculi are characterized clinically by colicky pain (renal colic) as they pass down along the ureter and manifest by hematuria.
Sites of formation. Two suggestions have been made:
1. Precipitates form in the collecting tubules and pass into renal pelvis where they enlarge.
2. Deposits are formed in the lymphatic vessels of the renal papillae and are extruted into the renal pelvis.
Types of Urinary Calculi
There are 4 main types of urinary calculi:
Calcium stones. Calcium stones are the most common comprising about 75% of all urinary calculi. They may be pure stones of calcium oxalate (50%) or calcium phosphate (5%), or mixture of calcium oxalate.
Mixed (Struvite) stones. About 15% of urinary calculi are made of magnesium-ammonium-calcium phosphate, often called struvite. “'Staghorn stone” which is a large, solitary stone that takes the shape of the renal pelvis where it is often formed is an example of struvite stone.
Uric acid stones. Uric acid calculi are radiolucent unlike radio-opaque calcium stones. Uric acid stones are smooth, yellowish-brown, hard and often multiple.
Cystine stones. Cystine stones are small, rounded, smooth and often multiple. They are yellowish and waxy. They are seen in heritable tubular transport defects causing cystinuria.
Complications: pyelonephtitis, hemorrhage, hydronephrosis.
Hydronephrosis
Hydronephrosis is the term used for dilatation of renal pelvis and calyces due to partial or intermittent obstruction to the outflow of urine.
Hydroureter nearly always accompanies hydronephrosis
Hydronephrosis may be unilateral or bilateral.
Unilateral hydronephrosis. This occurs due to some form of ureteral obstruction at the level of periureteric junction (PUJ). The causes are:
Intraluminal, e.g. a calculus in the ureter or renal pelvis.
Intramural, e.g. congenital PUJ obstruction, atresia of ureter, inflammatory stricture, trauma, neoplasm of ureter or bladder.
Extramural, e.g. obstruction of upper part of ureter by inferior renal artery or vein, pressure on ureter from outside such as carcinoma cervix, prostrate, rectum, colon or cecum and retroperitoneal fibrosis.
Bilateral hydronephrosis. This is generally the result of some form of urethral obstruction but can occur from the various causes listed above if the lesions involve both sides.
Congenital, e.g. atresia of the urethral meatus, congenital posterior urethral valve.
Acquired, e.g. bladder tumor involving ureteric orifices, prostatic enlargement, prostatic carcinoma and prostatitis, bladder neck stenosis, inflammatory or traumatic urethral stricture and phimosis.
Morphology
The kidneys may have moderate to marked enlargement.
Initially, there is extrarenal hydronephrosis characterised by dilatation of renal pelvis medially in the form of a sac.
Eventually, the dilated pelvi-calyceal system extends deep into the renal cortex so that a thin rim of renal cortex is stretched over the dilated calcyes and the external surface assumes tabulated appearance. This advanced stage is called as intrarenal hydronephrosis.
The wall of hydronephrotic sac is thickened due to fibrous scarring and chronic inflammatory cell infiltrate.
Cystic disease of the kidney
There are several cystic diseases of the kidney, some of which produce renal failure by causing disturbance of renal structure. Importantly, some conditions are heritable.
Adult polycystic disease is inherited in an autosomal dominant trait, generally becoming clinically manifest in adult life. Increasingly, disease is detected in childhood, with family screening and ultrasound examination.
Cysts develop and progressively enlarge over a number of' years, but remain asymptomatic until the number and size of the cysts is so great that the patient becomes aware of abdominal masses.
At about the same time, the replacement and compression of functioning renal parenchyma by the cysts leads to slowly progressive impairment of renal function, and patients develop chronic renal failure and hypertension.
Patients with adult-type polycystic renal disease may also develop cysts in the liver, lung and pancreas. There is an association with berry aneurysms of the cerebral arteries, which, with development of hypertension, predisposes to intracranial hemorrhage.
Infantile polycystic disease is uncommon and is encountered at birth. Children develop severe renal failure, with compression of the lungs due to massive enlargement of the kidneys.
Simple renal cysts are the most common form of renal cystic disease and must be distinguished from the congenital types discussed above. They are widely held to be acquired abnormalities, incidence increasing with age. They contain clear, watery fluid and have a smooth lining.
Simple cysts may be single or multiple and vary in size, generally being no larger than 5-6 cm. They have no effect on renal function, but may rarely become infected or develop hemorrhage.
Acquired cystic disease is seen in kidneys left in situ while patients are treated by dialysis or transplantation for chronic renal failure. The kidney is converted into a mass of large cysts. Hemorrhage into cysts is common, leading to bloodstained contents.
Chronic renal failure
Nephrosclerosis is morphologic basis of chronic renal failure.
Uremia is a syndrome encompassing a group of clinical and biochemical sings derived essentially from the retention of waste products and the failure to control fluid and electrolyte balance.
Uremia is final stage of chronic renal failure, which is characterised by
Hypernitrogenemia.
Metabolic acidosis (accumulation of sulphates, phosphates, and organic acids).
Hyperkaliemia, hypercalcemia.
Anemia.
Depression of immunological reaction. Infections are common and will in turn affect renal function.
Arterial hypertension.
Hemorrhagic syndrome (petechias, hemorrhagic erosions and ulcer in mucosa).
Fibrinous inflammation:
a) Fibrinous pericarditis (“cor vilosum”).
b) “Uremic pneumonitis” with pleural exudates.
c) Uremic gastritis, enteritis, colitis.
d) Edema of lungs.
The prognosis of final stage renal failure has been greatly improved by dialysis, renal transplantation.
GENITAL TPACT DISEASES
Diseases of Cervix
The cervix is an important site of pathology, particularly in women of reproductive age.
The ectocervix is covered by squamous epithelium, and the endocervical canal is covered by mucus-secreting columnar epithelium, which shows glandular down growth.
At various stages in a woman’s reproductive life, the junction between the squamous and columnar epithelium migrates into the convexity of the ectocervix, then back into the endocervical canal. This squamocolumnar junction is the seat of most of the epithelial diseases that occur in the cervix.
Cervical erosion (endocervicosis)
It represents an unfolding and eversion of the distal endocervix into an ectocervix. The term “cervical ectopia” is preffered.
Etiology: increased uterine bulk, in pregnancy, hormonal stimulation.
According to duration the endocervicosis classified:
Simple endocervicosis is characterized by metaplasia of the squamous epithelium into columnar epithelium without proliferation of reserve cells, presence of the cervical glands in ectocervix and papillary formation.
Progressive endocervicosis is characterised by proliferation of reserve cells and presence of the various size glands. Zone transformation is dilated.
Healing endocervicosis is characterized by recovery of normal structure of ectocervix or formation of Naboti’s cysts. Due to impairment of differentiations the dysplasia can take place.
Dysplasia
Dysplasia refers as cervical intraepithelial neoplasia (CIN) and it has 3 grades of differentiation:
CIN 1 or mild dysplasia: cells of basal third have high nucleocytoplasmic ratio and pleomorphic nuclei.
CIN 2 or moderate dysplasia: basal cells occupy lower half of squamous epithelium.
CIN 3 or severe dysplasia or cancer in situ: almost complete loss of stratification, loss of polarity of the cells, variation in nuclear size with increase in nuclear/cytoplasmic ratio and mitotic figures.
Cervicitis
Cervicitis may be specific and non-specific.
Acute and chronic cervicitis results from infection by any number of microorganisms, particulary Streptococcus, staphylococcus, or Enterococcus, and, less commonly, Neisseria gonorrhoeae and Chlamydia trachomatis.
Some of these microorganisms are sexually transmitted, whereas others may be introduced by foreign bodies, such as residual fragments of tampons and pessaries.
Purulent inflammation is a clinical sign of acute cervicitis. The inflamed cervix becomes congested and edematous.
Since biopsy samples from the cervix frequently exhibit some degree of nonspecific chronic inflammation, the diagnosis of chronic cervicitis should be made only when numerous lymphoid cells are present. Leukoplakia may develop (it means the white patches of hyperkeratosis).
Diseases of Endometrium
Dysfunctional Bleeding
Dysfunctional uterine bleeding is denned as abnormal bleeding in the absence of an organic lesion of the endometrium.
It is one of the most common gynecologic disorders of women of reproductive age, but one that is still poorly understood.
The bleeding may be due to anovulatory cycles related to excessive and prolonged estrogenic stimulation.
Without ovulation, a corpus luteum does not develop and progesterone is not secreted.
The endometrium, therefore, fails to proceed through the normal secretory phase, and an abnormal menstrual cycle results.
Organic lesions of the uterus must be excluded before the diagnosis of dysfunctional bleeding can be made. Examples of organic disorders are carcinoma, hyperplasia, polyps, endometritis, and complications of intrauterine or ectopic pregnancy.
Anovulatory Bleeding
Anovulatory bleeding is the most common form of dysfunctional uterine bleeding, particularly during adolescence and the climacteric period.
It is believed that estrogen maintains the stromal fluid turgescence that supports the blood vessels.
Anovulatory bleeding is caused by a fall in estrogen levels, which results in loss of fluid from the stroma and hence loss of vascular support. The vascular collapse leads to compression of the vessels, which in turn leads to stasis, thrombosis, infarction, and hemorrhage.
On microscopic examination the glands are disordered and appear crowded because of severe stromal necrosis and collapse of the proliferative endometrium.
Abnormalities of the Normal Menstrual Cycle
Dysfunctional bleeding may also be associated with abnormalities of the normal menstrual cycle.
Ovulatory oligomenorrhea (cycle longer than 45 days) is almost always due to a long follicular phase and may be the prelude to ovarian failure.
Ovulatory polymenorrhea, in which cycles are less than 18 days in length, is caused by short follicular phases (seen generally in adolescence) or short luteal phases (inadequate luteal phase). The latter may be due to defects in factors that maintain the corpus lutein.
Endometritis
Acute endometritis
This is almost confined to infection associated with partirition and abortion.
A mixed bacterial flora, pyococci, coliform organisms and proteus are usual.
Suppurative inflammation is usual.
Presence of polymorphonuclear leukocytes, results when an infection ascends from the cervix.
Curettage is both diagnostic and curative because it removes the necrotic tissue that serves as the nidus of infection.
Complications may follow endometritis: myometritis, parametritis, salpingitis, peritonitis, subsequent tubal blockage and infertility.
Pyometra, pus in the endometrial cavity, is associated with any lesion that causes cervical stenosis, such as a tumor or scarring from surgical treatment (conization) of the cervix. Long-standing pyometra may be associated with the development of squamous cell cancer of the endometrium.
Chronic endometritis
Chronic endometritis is usually associated with recent gestation, pelvic inflammatory disease, intrauterine contraceptive devices (IUD) use, and retained products of conception after an abortion or delivery, menstrual irregularities, but is also found in women who are being investigated for infertility.
Chronic endometritis may be caused by gonococcal or chlamydial infection, or tuberculosis.
Clinically, patients usually complain of bleeding, pelvic pain, or both.
Histologically: stroma infiltrated by plasma cells and lymphocytes; glands small and infrequent; epithelium atrophied.
Hyperplasia of endometrium
Endometrial hyperplasia usually results with conditions of prolonged estrogen excess and can lead to metrorrhagia (uterine bleeding at irregular intervals), menorrhagia (excessive bleeding with menstrual periods), or menometrorrhagia.
It is classified into following 3 types:
Simple hyperplasia (cystic glandular hyperplasia) is characterised by the presence of large and cystically dilated, varying-sized glands, which are lined by atrophic epithelium. Simple endometrial hyperplasias can cause bleeding, but are not thought to be premalignant.
Adenomatous hyperplasia (complex hyperplasia without atypia). This shows distinct proliferative pattern. The glands are increased in number, exhibit variation in size and are irregular in shape. Multiple layers of tall columnar epithelial cells with large nuclei, which have not lost basal polarity, line the glands and there is no atypia. Adenomatous hyperplasia is premalignant.
Atypical hyperplasia (complex hyperplasia with atypia) is characterised by the presence of atypical cells in the hyperplastic epithelium. The glands are enlarged and irregular with columnar cells that have some atypia (loss polarity, large size, irregular and hyperchromic nuclei, prominent nuclei, and altered nucleocytoplasmic ratio).
Endometriosis
When endometrial glands and stroma are found outside the uterus, the condition is known as endometriosis.
Up to 10% of women may have this condition. It can be very disabling and painful, even when just a few foci are present.
Typical locations for endometriosis may include: ovaries, uterine ligaments, rectovaginal septum, pelvic peritoneum, fallopian tubes and laparotomy scars. Endometriosis may even be found at more distant locations such as appendix and vagina.
Grossly, in areas of endometriosis the blood is darker and gives the small foci of endometriosis the gross appearance of "powder burns". Such areas of endometriosis can be seen and obliterated by cauterization via laparoscopy. Sometimes the old dark brown blood collects over time from repeated hemorrhage in a cystic space in the ovary and produces a so-called “chocolate cyst” (endometriotic cyst).
Histologically: foci of endometrial glands and stroma, old or new hemorrhage, hemosiderin-laden macrophages and surrounding zone of inflammation and fibrosis.
Diseases of Fallopian tubes
Acute and chronic salpingitis usually results from an ascending infection from the lower genital tract.
The most common causative organisms are E. coli, N. gonorrheae, Chlamydia, and Mycoplasma. Clostridia perfringens and various other anaerobes are less commonly encountered.
A fallopian tube damaged by prior infection is particularly susceptible to reinfection.
Acute Salpingitis
The host responds with a brisk granulocytic infiltrate and vascular engorgement, and edema of the involved tubal layers ensues. As the lumen fills with granulocytes, the tube distends and pyosalpinx develops.
Chronic Salpingitis
Chronic salpingitis usually results from repeated episodes of acute salpingitis.
The acute episodes, particularly those associated with chlamydial infection, may be asymptomatic.
Complications may be caused by either destruction of epithelium or deposition of fibrin on the mucosal plicae; the fibrin bridges cause the plicae to adhere to one another.
Fibrinous adhesions between the serosa and surrounding peritoneal surfaces may organize into thin, fibrous adhesions (“violin string” adhesions).
In severe chronic salpingitis, the adhesions may be dense and the fimbria adhere to each other to form a blunted; clubbed end.
Ovarian involvement leads to the formation of a tubo-ovarian abscess.
The consequence of the blocked lumen may be a hydrosalpinx or pyosalpinx. Because of destruction of the tubal epithelium and fibrosis, chronic salpingitis may lead to infertility and ectopic pregnancy.
Diseases of Ovaries
Ovarian changes of functional origin.
1. Follicilar cysts are cysts arising from Graafian follicles and are lined by granulosa cells, with an outer coat of thecal cells. They filled with clear serous fluid and may attain a diameter up to 2 sm. They may be single or multiple. Multiple follicular cysts, usually small, are associated with endometrial hyperplasia.
2. Luteal cysts are cysts from which the granulosa cells have disappeared, leaving cysts surrounded by luteinised tissue. Cysts are typically 2-3 cm in diameter, with a thick, yellow lining of luteinized granulosa cells. There is continued production of progesterone, resulting in menstrual irregularity.
3. Theca lutein cysts are usually seen as multiple bilateral cysts, up to 1 cm in diameter, filled with clear fluid. They are caused by high levels of gonadotropin, which precipitates follicle development (e.g. in hydatidiform mole and drug treatment).
4. Polycystic ovary disease (Stein-Leventhal Syndrome) is associated with obesity, hirsutism, oligomenorrhea, anovulation, and infertility.
The pathogenesis of this syndrome is still uncertain. Patients have a persistent anovulatory state, high level of estrogen, low level of progesteron with high levels of circulating androgen produced by the ovary. The high estrogen levels may cause endometrial hyperplasia and increase the risk of development of endometrial carcinoma.
The ovaries are usually involved bilaterally and are at least twice the size of the normal ovary. They are grey-white color and studded with multiple small bluish cysts just beneath the cortex.
Histologically. The outer cortex is thick and fibrous. The subcortical cysts are lined by prominent luteinised theca cells and represent follicles in various stages of maturation but there is no evidence of corpus lutein.
Obstetric pathology
Pre-eclampsia and eclampsia
Pre-eclamptic toxemia syndrome is characterised by hypertension, proteinuria and peripheral edema.
Seen particularly in association with multiple pregnancies, primigravidae and women over the age of 35 years.
Most cases are mild, with the blood pressure under 100 mmHg diastolic and no proteinuria; in severe cases the diastolic pressure is consistently above 100 mmHg, and there is proteinuria and severe peripheral edema.
A feature of pre-eclampsia is reduced placental blood flow; this may lead to fetal hypoxia in late pregnancy, particularly during labour, with increased risk of perinatal mortality. The fetus may also suffer intrauterine growth retardation and have low birth weight.
Placental ischemia takes place.
In the kidney, endothelial cells become swollen, with deposition of fibrin in glomeruli, leading, to proteinuria. If untreated, severe hypertension and intravascular coagulation occur with development of cerebral ischemia and fits.
Eclampsia is now a fare complication of pregnancy. Patients develop severe systemic disturbance, rapid and sustained rise in blood pressure, shock, anuria and fits.
Complications and causes of death: patients develop disseminated intravascular coagulation, with widespread occlusion of blood vessels, fibrinoid necrosis of vessel wails, and, in fatal cases, widespread microinfarcts in brain, liver, kidney and other organs.
Ectopic Pregnancy
Ectopic pregnancy refers to any gestation that develops outside the endometriun.
Over 95% occur in the tube (ampullary implantation, interstitial implantation and tubal wall).
Ovarian pregnancy is presumed to result from the rare fertilization and trapping of the ovum within the follicle just at the time of its rupture.
Abdominal pregnancies may develop when the fertilized ovum drops out of the fimbriated end of the tube.
Etiology of tubal pregnancy: salpingitis, leading to partial blockage of the tube; in women fitted with intrauterine contraceptive devices, endometriosis. Other factors are peritubal adhesions owing to appendicitis, leiomyomas, and previous surgery.
In all abnormal locations, the fertilized ovum undergoes its usual development with the formation of placental tissue, amniotic sac, and fetus, and the host implantation site develops decidual changes and syncytio-trophoblasts.
Abdominal pain is the most common symptom.
The appearance of ectopic pregnancy resembles that of placenta increta and percreta of the uterus. Because the tubal mucosa has a limited ability to undergo decidualization, the trophoblast readily penetrates the mucosa and wall, a situation, which results in an abnormal implantation.
The wall of the fallopian tube is thin and unless the ectopic pregnancy is discovered, the wall usually ruptures by the 12th week of gestation.
Tubal rupture with subsequent hemorrhage is a life-threatening complication.
The direction of rupture varies:
Rupture into the lumen of the tube and leakage into perinatal cavity (tubal abortion). Exceedingly rarely the whole pregnancy – ovum and placental tissue – aborts into peritoneal cavity where it reimplants. Usually development is limited and the fetus dies.
Rupture directly into the peritoneal cavity. If the implatation is interstitial, there may be a further complication – damage to the uterine arteries with arterial bleeding.
Rupture into the broad ligament lead to extraperitoneal hematoma.
Gestational Trophoblastic Disease
The clinical term “gestational trophoblastic disease” include of hydatidiform mole (complete and partial mole), invasive mole, gestational choriocarcinoma, and placental site trophoblastic tumor.
Hydatidiform Mole
1. Complete type.
In complete hydatidiform mole, grossly swollen chorionic villi, which resemble a bunch of grapes, show varying degrees of trophoblastic proliferation.
There is no embryo.
Complete mole results from fertilization of an egg in which the maternal chromosomal material has been lost or inactivated by a single sperm with a 23X set of chromosomes, which duplicate to 46XX.
The embryo dies at an early stage before the placental circulation has developed, and chorionic villi then contain few, if any, blood vessels.
Complications of complete hydatidiform mole include uterine hemorrhage, coagulopathy, uterine perforation, trophoblastic embolism, and infection. The most important complication is the development of choriocarcinoma.
2. Partial type.
In partial hydatidiform mole two populations of chorionic villi exist, some of which show hydropic swelling.
Trophoblastic proliferation is focal and usually less pronounced than in the complete mole.
In partial hydatidiform mole, unlike complete mole, there is frequently an associated embryo.
Partial hydatidiform mole is generally the result of fertilization of an egg by two paternal sets of chromosomes, with the maternal chromosomes remaining. This results in triploidy.
The fetus associated with a partial mole usually dies at approximately 10 weeks of gestation, and the mole is aborted shortly thereafter.
Microscopically, partial hydatidiform mole resembles complete mole, being composed of seemingly normal small villi along with villi that have accumulated considerable fluid. Blood vessels are typically found within the chorionic villi and contain fetal (nucleated) red blood cells. The villous outlines commonly have a scalloped appearance.
It is difficult to determine the relative frequency of complete and partial moles, since the entity of partial mole has only recently been recognized. Partial moles have a lower malignant potential than complete moles.
3. Invasive type.
The invasive mole, also called chorioadenoma destruens, is a hydatidiform mole that has invaded the underlying myometrium.
Uterine perforation from the locally infiltrative disease is the major complication.
Theca lutein cysts (hyperreactio luteinalis) may occur with any form of trophoblastic disease and may be prominent with invasive moles.
Microscopically, invasive moles show less hydropic change than complete moles; trophoblastic proliferation is usually prominent.
Benign diseases of the breast
Fibrocystic disease
Fibrocystic disease is the most common disorder of the female breast.
The cause of fibrocystic disease is uncertain. Most believe that it is due to disturbances of cyclical ovarian estrogen and progesterone levels, accompanied by altered responsiveness of breast tissues in women approaching the menopause.
Fibrocystic change is characterized by hyperplastic overgrowth of components of the mammary unit, i.e. lobules, ductules and stroma.
In this condition there are four characteristic features, and the form, which the disease takes varies according to the relative proportions of these features:
1. Fibrosis. This is mainly an increase in the amount of collagen rather a true growth of fibrous tissue.
2. Adenosis.
This is an increase in the number of lobules and in the size of existing lobules.
Sclerosing adenosis (fibroadenomatoid hyperplasia or fibroadenosis) is localised condition, which may simulate carcinoma.
There is proliferation of acini and stroma, and mitotic activity can be marked but there is no danger of malignancy.
This presents as palpable thickening and nodularity of breast tissue, but may also result in the development of single breast lumps.
3. Cyst formation.
Cysts are a prominent component, increasing in incidence with the approach of the menopause.
Obstruction of ducts leads to dilatation on the ducts and acini.
They range in size from those detectable only by histology to palpable lesions I-2 cm in diameter.
Histologically: cysts are lined by flattened epithelium derived from the lobular-ductal unit and are filled with watery fluid. As some carcinomas of the breast may be associated with cysts, it is not safe to assume that a lesion is benign because it has a fluid-filled cyst. The lining epithelium may show apocrine metaplasia.
4. Fibrocystic change.
Epithelial hyperplasia is the most important component because it forms a link between simple proliferation and malignant change.
Macroscopically, areas of fibrocystic changes appear as firm, rubbery replacement of breast tissue, in which cysts may be visible.
There are many histological variations within fibrocystic disease, such as:
Proliferation of myoepithelial layer;
Proliferation of ductal epithelium forming an irregular network (atypical ductal hyperplasia);
Uniform proliferation of acinar epithelium without acinar expansion (atypical lobular hyperplasia).
Fibroadenoma
Fibroadenoma is a bening nodular proliferation, now considered to be a component of fibrocystic changes and not a true neoplasm. The fibroadenoma is therefore best regarded as a form of hormone-dependent nodular hyperplasia, rather than a true benign tumor.
Fibroadenoma presents as a mobile lump in the breast of young women.
Macroscopically, fibroadenomas are typically 1-3 cm in diameter, appearing as firm, rubbery, well-circumscribed, elastic consistency, glistening, greish cut surface.
Histologically:
Small acinar and duct structures resembling normal brest.
Fibrous tissue arranged around acini.
Epithelium forms clefts: these are due to pressure from the projecting fibrous tissue.
Diseases of male genitalia
Prostatitis may be acute, chronic and granulomatous types.
Acute prostatitis
Acute prostatitis is characterised by acute focal or diffuse suppurative inflammation of the prostate.
It occurs most commonly due to ascent of bacteria from the urethra, less often by descent from the upper urinary tract or bladder, and occasionally by lymphogenous or hematogenous spread from a distant focus of infection.
The infection may occur spontaneously or may be a complication of urethral manipulation such as by catheterization, cystoscopy, etc.
Macroscopically, the prostate is enlarged, swollen and dense. Cut section shows multiple abscesses and foci of necrosis.
Histologically, the prostatic acini are dilated and filled with neutrophilic exudate. There may be diffuse acute inflammatory infiltrate. Edema, hyperemia and foci of necrosis frequently accompany acute inflammatory involvement.
Chronic prostatitis
Macroscopically, the prostate may be enlarged, fibrosed and shrunken.
Microscopically, the diagnosis of chronic prostatitis is made by foci of lymphocytes, plasma cells, macrophages and neutrophils within the prostatic substance. Prostatic calculi and foci of squamous metaplasia in the prostatic acini may accompany inflammatory changes.
Granulomatous prostatitis is a variety of chronic prostatitis, probably caused by leakage of prostatic secretions into the tissue, or could be of autoimmune origin. Macroscopically, the gland is firm to hard, giving the clinical impression of psoriatic carcinoma on rectal examination. Microscopically, the inflammatory reaction consists of macrophages, lymphocytes, plasma cells and some multinucleated giant cells.
Bening prostatatic hyperplasia (Nodular hyperplasia)
Nodular prostatic hyperplasia has been suggested by some as precursor for development of prostatic cancer.
Morphology
Macroscopically:
The enlarged prostate is nodular, smooth and firm.
The appearance on cut section varies depending upon whether the hyperplasia is predominantly of the glandular or fibromuscular tissue.
In primarily glandular benign nodular hyperplasia the tissue is yellow-pink, soft, honey-combed, and milky fluid exudes.
In mainly fibromuscular benign nodular hyperplasia the cut surface is firm, homogeneous and does not exude milky fluid.
The hyperplastic nodule forms a mass mainly in the inner periurethral prostatic gland so that the surrounding prostatic tissue forms a false capsule, which enables the surgeon to enucleate the nodular masses.
Microscopically:
Hyperplasia of all tissue elements in varying proportions - glandular, fibrous and muscular take place.
Glandular hyperplasia predominates in most cases and is identified by exaggerated intra-acinar papillary infoldings with delicate fibrovascular cores.
Fibromuscular hyperplasia when present as dominant component appears as aggregates of spindle cells forming an appearance akin to fibromyoma of the uterus.
Complications
Chronic retention of urine.
Cystitis and pyelonephritis.
Hydronephrosis.
Bladder stone.
Gynecomastia of male breast
Gynecomastia of male breast is most commonly idiopathic, but may be a sign of underlying endocrine disturbance.
The male breast is normally rudimentary and inactive, consisting of fibroadipose tissue containing atrophic mammary ducts.
Enlargement of the male breast, which is termed gynecomastia, may be unilateral (70% of cases) or bilateral.
In most cases it is idiopathic. Other causes include: Klinefelter’s syndrome. Estrogen excess (cirrhosis, puberty, adrenal tumor, exogenous estrogens), gonadotropin excess (testicular tumor), prolactin excess (hypothalamic or pituitary disease), drug-related (spironolactone, chlorpromazine, digitalis).
Macroscopically, there is enlargement of the breast as a firm, raised, rubbery mass beneath the nipple.
ENDOCRINE PATHOLOGY
The endocrine system consists of a highly integrated and widely distributed group of organs whose primary function is the control of homeostases.
All peripheral endocrine glands (thyroid, adrenal, pancreas, sexual, parathyroid) are closely connected with each other as well as with the central endocrine glands (pituitary, epiphysis) and neuronal (hypothalamus).
All diseases of the endocrine system are divided into 1) congenital, 2) acquired.
They may be represented by
1. Hypofuniction.
2. Hyperfunction.
3. Dysfunction.
In this case, dystrophy, atrophy, dysplasia, sclerosis and tumors may develop.
A practical classification of endocrine pathology is based on the damage of the main (primary) gland. The most frequent are endocrinopathy of
1. Pituitary body.
2. Adrenal glands.
3. Thyroid gland.
4. Pancreas.
5. Parathyroid gland.
6. Sexual glands.
Diseases of pituitary body
Diseases of pituitary body may occur the symptoms of hyperpituitarism or hypopituitarism.
Hyperpituitarism is characterised by oversecretion of one or more of the pituitary hormones due to the development of a hormone- secreting pituitary adenoma. The most frequent diseases of pituitary body associated with hyperfunction are Itsenko-Cushing disease, acromegaly, and gigantism.
1. Itsenko-Cushing disease.
Itsenko-Cushing disease occurs in adenomas from basophilic cells of anterior lobe of the pituitary or adenocarcinoma in rare cases. Increased ACTH production causes cortex hyperplasia as well as increased production of glucocorticoids.
It results in obesity of face and body, elevation of arterial pressure, diabetes mellitus, and sexual gland dysfunction. Osteoporosis, nephrolithiasis and chronic pyelonephritis may also develop.
The disease should be differentiated from Itsenko-Cushing syndrome. Its clinical manifestations (so called Cushingoid) are the same as in the disease (obesity of the upper part of the body), but the other signs are not clearly marked.
The causes of these states are adrenals damage (tumor of zona fasciculata), the administration of hormones (cortisole, prednisolone, hydrocortisone).
2. Acromegaly and gigantism
Excess of STH stimulates all mesenchymal derivatives (bones, cartilages, connective tissue).
If the disease occurs in adults, it is called acromegaly (the bones does not grow but ears, nose, lower jaw, feet and hands enlarge). The term “acromegaly” means increased growth of extremities.
If the disease occurs in prepubertal boys and gerls, it is called gigantism.
The other glands also involve by the process (goiter, atrophy of insulin apparatus of pancreas, thymus and epiphysis hyperplasia, adrenal cortex hyperplasia, sexual glands atrophy occur).
Hypopituitarism is characterised by less secretion of one or more of the pituitary hormones due to destraction of the anterior lobe (by metastases, ischemic necrosis) and the development of a nonsecretory adenoma or others tumors. The most frequent diseases of pituitary body associated with hypofunction are hypophyseal nanism, cerebro-hypophyseal cachexia, and diabetes insipidus.
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