- Published on
Pathology - Endometritis
Acute endometritis is typically caused by trauma, Staphylococcus aureus, and Streptococcus species, and commonly occurs following childbirth or miscarriage.
Chronic endometritis is caused by granulomatous disease, chronic pelvic inflammatory disease (PID), postpartum or post-abortal conditions, and tuberculosis (TB).
Endometrium: Plasma cells, macrophages, and lymphocytes observed in the glandular lumen.
Acute: Manifests with inflammation and discomfort following delivery or miscarriage.
Chronic cases are characterized by abnormal vaginal bleeding, discomfort, discharge, and infertility.
Antibiotic treatment can help prevent secondary complications, such as salpingitis.
Endometrial polyps are growths made up of endometrial tissue seen inside the uterine cavity.
Fibroids typically manifest in women over 40 years old and can lead to uterine hemorrhage, but they are commonly noncancerous.
Acute endometritis is typically caused by trauma, Staphylococcus aureus, and Streptococcus species, and commonly occurs following childbirth or miscarriage.
Chronic endometritis is caused by granulomatous disease, chronic pelvic inflammatory disease (PID), postpartum or post-abortal conditions, and tuberculosis (TB).
Endometrium: Plasma cells, macrophages, and lymphocytes observed in the glandular lumen.
Acute: Manifests with inflammation and discomfort following delivery or miscarriage.
Chronic cases are characterized by abnormal vaginal bleeding, discomfort, discharge, and infertility.
Antibiotic treatment can help prevent secondary complications, such as salpingitis.
Endometrial polyps are growths made up of endometrial tissue seen inside the uterine cavity.
Fibroids typically manifest in women over 40 years old and can lead to uterine hemorrhage, but they are commonly noncancerous.
- Published on
Pathology - Endometriosis
The etiology is uncertain, but believed to result from a blend of genetic, hormonal, and immunological elements.
Affects 10% of women, typically aged 20 to 30.
Non-neoplastic nodules are abnormal growths of endometrial tissue found outside the uterus, commonly in the ovary, uterine ligaments, rectovaginal septum, and pelvic peritoneum. These nodules can lead to the formation of chocolate cysts on the ovaries due to cyclic bleeding of ectopic endometrial tissue.
Microscopic features include endometrial glands, endometrial stroma, and the presence of hemosiderin pigment.
Manifests as firm, detectable, ovarian masses on both sides, overall pelvic discomfort, painful menstruation (dysmenorrhea), and discomfort during sexual intercourse (dyspareunia); irregular menstrual cycles can result in infertility, which is the main concern for 30%-40% of individuals.
Therapy
Options for treatment include oral contraceptives, medroxyprogesterone, danazol, GnRH analogues such as leuprolide, and surgical excision or coagulation of the lesion.
Adenomyosis is a condition where endometriosis occurs within the myometrium, often causing uterine enlargement and irregular bleeding.
The etiology is uncertain, but believed to result from a blend of genetic, hormonal, and immunological elements.
Affects 10% of women, typically aged 20 to 30.
Non-neoplastic nodules are abnormal growths of endometrial tissue found outside the uterus, commonly in the ovary, uterine ligaments, rectovaginal septum, and pelvic peritoneum. These nodules can lead to the formation of chocolate cysts on the ovaries due to cyclic bleeding of ectopic endometrial tissue.
Microscopic features include endometrial glands, endometrial stroma, and the presence of hemosiderin pigment.
Manifests as firm, detectable, ovarian masses on both sides, overall pelvic discomfort, painful menstruation (dysmenorrhea), and discomfort during sexual intercourse (dyspareunia); irregular menstrual cycles can result in infertility, which is the main concern for 30%-40% of individuals.
Therapy
Options for treatment include oral contraceptives, medroxyprogesterone, danazol, GnRH analogues such as leuprolide, and surgical excision or coagulation of the lesion.
Adenomyosis is a condition where endometriosis occurs within the myometrium, often causing uterine enlargement and irregular bleeding.
- Published on
Pathology - Leiomyoma
The cause is unidentified, however genetic abnormalities have been detected in the cancerous cells.
The most prevalent non-cancerous growth in the female reproductive system.
Most frequently observed in women over the age of 40, with a higher occurrence rate among African Americans.
The pathology indicates the presence of many enlarged, irregular, and heterogeneous tumors located in the myometrium (intramural), beneath the endometrium (submucosal), or beneath the serosa (subserosal). The tumor is estrogen-sensitive, with its size increasing during pregnancy and reducing with menopause.
Microscopic findings include a whorled pattern of smooth muscle bundles, with uncommon mitoses in muscle cells. Cellular atypia and large cells may also be observed.
May be asymptomatic or may result in excessive menstruation with frequent periods.
Additionally linked to pelvic pressure, frequent urination (due to bladder compression), and infertility.
Laboratory results indicate iron deficiency anemia caused by blood loss.
Treatment involves hormonal medication such as oral contraceptive tablets to induce regression of endometrial tissue. Myomectomy, hysterectomy, or uterine artery embolization may be performed for big tumors.
Uterine fibroids, also known as leiomyomas, do not develop into leiomyosarcomas.
Leiomyosarcomas are irregular tumors that develop spontaneously and may extend from the cervix, characterized by fleshy tissue, necrotic regions, and hemorrhaging. Leiomyosarcomas are more common among African Americans, are cancerous, and can be treated with a mix of chemotherapy drugs.
The cause is unidentified, however genetic abnormalities have been detected in the cancerous cells.
The most prevalent non-cancerous growth in the female reproductive system.
Most frequently observed in women over the age of 40, with a higher occurrence rate among African Americans.
The pathology indicates the presence of many enlarged, irregular, and heterogeneous tumors located in the myometrium (intramural), beneath the endometrium (submucosal), or beneath the serosa (subserosal). The tumor is estrogen-sensitive, with its size increasing during pregnancy and reducing with menopause.
Microscopic findings include a whorled pattern of smooth muscle bundles, with uncommon mitoses in muscle cells. Cellular atypia and large cells may also be observed.
May be asymptomatic or may result in excessive menstruation with frequent periods.
Additionally linked to pelvic pressure, frequent urination (due to bladder compression), and infertility.
Laboratory results indicate iron deficiency anemia caused by blood loss.
Treatment involves hormonal medication such as oral contraceptive tablets to induce regression of endometrial tissue. Myomectomy, hysterectomy, or uterine artery embolization may be performed for big tumors.
Uterine fibroids, also known as leiomyomas, do not develop into leiomyosarcomas.
Leiomyosarcomas are irregular tumors that develop spontaneously and may extend from the cervix, characterized by fleshy tissue, necrotic regions, and hemorrhaging. Leiomyosarcomas are more common among African Americans, are cancerous, and can be treated with a mix of chemotherapy drugs.
- Published on
Pathology - Primary Hyperparathyroidism
Resulting from PTH adenoma, PTH hyperplasia, PTH carcinoma, or the secretion of PTH-like hormone by malignancies, particularly squamous cell bronchogenic carcinoma.
Linked to Multiple Endocrine Neoplasia Type I and Type IIA.
Pathology
Parathyroid gland: Parathyroid adenoma is a well-defined nodule consisting of homogeneous polygonal chief cells and a small number of bigger oxyphil cells.
Osseous tissue: Osteitis fibrosa cystica is characterized by cystic areas filled with fibrous tissue, known as brown tumors, due to heightened osteoclast activity.
Clinical Symptoms and Signs
Symptoms include bone discomfort from osteitis fibrosa cystica, nephrocalcinosis, peptic ulcers, constipation, weakness, altered mental status, and polyuria.
Laboratory results: Hypercalcemia, elevated PTH levels, elevated blood alkaline phosphatase, reduced serum phosphate.
Surgical excision of aberrant glands is recommended for individuals with renal failure, osteoporosis, or substantial hypercalcemia.
Additional causes of hypercalcemia include bone cancer, multiple myeloma, sarcoidosis, milk alkali syndrome, Paget disease of the bone, hyperthyroidism, and vitamin D toxicity.
Resulting from PTH adenoma, PTH hyperplasia, PTH carcinoma, or the secretion of PTH-like hormone by malignancies, particularly squamous cell bronchogenic carcinoma.
Linked to Multiple Endocrine Neoplasia Type I and Type IIA.
Pathology
Parathyroid gland: Parathyroid adenoma is a well-defined nodule consisting of homogeneous polygonal chief cells and a small number of bigger oxyphil cells.
Osseous tissue: Osteitis fibrosa cystica is characterized by cystic areas filled with fibrous tissue, known as brown tumors, due to heightened osteoclast activity.
Clinical Symptoms and Signs
Symptoms include bone discomfort from osteitis fibrosa cystica, nephrocalcinosis, peptic ulcers, constipation, weakness, altered mental status, and polyuria.
Laboratory results: Hypercalcemia, elevated PTH levels, elevated blood alkaline phosphatase, reduced serum phosphate.
Surgical excision of aberrant glands is recommended for individuals with renal failure, osteoporosis, or substantial hypercalcemia.
Additional causes of hypercalcemia include bone cancer, multiple myeloma, sarcoidosis, milk alkali syndrome, Paget disease of the bone, hyperthyroidism, and vitamin D toxicity.
- Published on
Pathology - Secondary Hyperparathyroidism
Primarily due to chronic renal insufficiency.
Parathyroid gland shows diffuse expansion due to hyperplasia of principal cells.
Pathophysiology: Reduced l,25-(OH)2 D3 generation from deteriorating kidney function leads to diminished intestinal calcium absorption resulting in hypocalcemia. This condition is additionally exacerbated by elevated calcium excretion from the impaired kidney, leading to higher parathyroid hormone (PTH) levels.
Clinical Symptoms and Signs
Osteoclastic bone disease with widespread distribution; metastatic calcification in soft tissues.
Laboratory results: Low calcium levels, elevated parathyroid hormone (PTH), elevated serum alkaline phosphatase, elevated serum phosphate.
Therapy
If the disease is severe, the aberrant glands will be surgically removed.
Phosphate binders and vitamin D supplementation.
Primarily due to chronic renal insufficiency.
Parathyroid gland shows diffuse expansion due to hyperplasia of principal cells.
Pathophysiology: Reduced l,25-(OH)2 D3 generation from deteriorating kidney function leads to diminished intestinal calcium absorption resulting in hypocalcemia. This condition is additionally exacerbated by elevated calcium excretion from the impaired kidney, leading to higher parathyroid hormone (PTH) levels.
Clinical Symptoms and Signs
Osteoclastic bone disease with widespread distribution; metastatic calcification in soft tissues.
Laboratory results: Low calcium levels, elevated parathyroid hormone (PTH), elevated serum alkaline phosphatase, elevated serum phosphate.
Therapy
If the disease is severe, the aberrant glands will be surgically removed.
Phosphate binders and vitamin D supplementation.
- Published on
Pathology - Hypoparathyroidism
The condition can be caused by surgical removal of the parathyroid glands, congenital lack of the parathyroid glands (as seen in DiGeorge syndrome), radioactive iodine therapy, or idiopathic autoimmune atrophy of the parathyroids.
Pathology
Gross finding: Slight reduction in the size of the gland.
Microscopic: Fibrotic tissue replaces main cells.
Hypocalcemia symptoms include tetany, prolonged QT interval on ECG, Trousseau sign, and Chvostek sign.
Laboratory results indicate low levels of calcium, reduced parathyroid hormone (PTH) levels, and elevated serum phosphate levels.
Therapy includes calcium and vitamin D supplements.
The condition can be caused by surgical removal of the parathyroid glands, congenital lack of the parathyroid glands (as seen in DiGeorge syndrome), radioactive iodine therapy, or idiopathic autoimmune atrophy of the parathyroids.
Pathology
Gross finding: Slight reduction in the size of the gland.
Microscopic: Fibrotic tissue replaces main cells.
Hypocalcemia symptoms include tetany, prolonged QT interval on ECG, Trousseau sign, and Chvostek sign.
Laboratory results indicate low levels of calcium, reduced parathyroid hormone (PTH) levels, and elevated serum phosphate levels.
Therapy includes calcium and vitamin D supplements.
- Published on
Pathology - Pseudohypoparathyroidism
Autosomal recessive condition causing a faulty PTH receptor.
Deficiency in Gs-a results in reduced connection between the PTH receptor and adenylate cyclase, causing the PTH receptor to be unable to activate the target cell.
The regulation of Gs-a is changed so that the target cell does not respond to PTH receptor stimulation.
Symptoms and signs
Hypocalcemia symptoms include tetany, extended QT interval on ECG, Trousseau sign, and Chvostek sign.
Pseudohypoparathyroidism is linked to Albright hereditary osteodystrophy, a group of diseases that involve pseudohypoparathyroidism, small stature, developmental delay, shortened fourth and fifth metacarpal and metatarsal bones, and obesity.
Laboratory results: Hypocalcemia, low PTH levels, elevated serum phosphate levels.
Therapy involves calcium and vitamin D supplements.
Autosomal recessive condition causing a faulty PTH receptor.
Deficiency in Gs-a results in reduced connection between the PTH receptor and adenylate cyclase, causing the PTH receptor to be unable to activate the target cell.
The regulation of Gs-a is changed so that the target cell does not respond to PTH receptor stimulation.
Symptoms and signs
Hypocalcemia symptoms include tetany, extended QT interval on ECG, Trousseau sign, and Chvostek sign.
Pseudohypoparathyroidism is linked to Albright hereditary osteodystrophy, a group of diseases that involve pseudohypoparathyroidism, small stature, developmental delay, shortened fourth and fifth metacarpal and metatarsal bones, and obesity.
Laboratory results: Hypocalcemia, low PTH levels, elevated serum phosphate levels.
Therapy involves calcium and vitamin D supplements.
- Published on
Pathology - Conn Syndrome
Resulting from aldosterone-secreting adrenocortical adenoma or hyperplasia.
Adrenal cortex: An adenoma is a single enclosed growth made up of consistent cortical cells that are packed with vesicles holding lipids.
Hyperplasia: increased cell growth in the zona glomerulosa.
Symptoms and signs
Hypertension, muscle weakness occasionally accompanied by tetany, headache, excessive urination, and increased thirst.
Laboratory results: Metabolic alkalosis, low serum potassium, reduced renin levels, elevated aldosterone levels.
Therapies
Adrenalectomy is recommended for unilateral adenoma, whereas spironolactone, a potassium-sparing diuretic, is prescribed for bilateral adrenal hyperplasia. Antihypertensive treatment should be used as necessary.
Secondary hyperaldosteronism is linked to conditions that cause the kidneys to detect a low effective circulation volume, such as renal ischemia, chronic renal failure, hepatic cirrhosis, congestive heart failure, or nephrotic syndrome. It is linked to elevated aldosterone levels caused by high renin levels.
Resulting from aldosterone-secreting adrenocortical adenoma or hyperplasia.
Adrenal cortex: An adenoma is a single enclosed growth made up of consistent cortical cells that are packed with vesicles holding lipids.
Hyperplasia: increased cell growth in the zona glomerulosa.
Symptoms and signs
Hypertension, muscle weakness occasionally accompanied by tetany, headache, excessive urination, and increased thirst.
Laboratory results: Metabolic alkalosis, low serum potassium, reduced renin levels, elevated aldosterone levels.
Therapies
Adrenalectomy is recommended for unilateral adenoma, whereas spironolactone, a potassium-sparing diuretic, is prescribed for bilateral adrenal hyperplasia. Antihypertensive treatment should be used as necessary.
Secondary hyperaldosteronism is linked to conditions that cause the kidneys to detect a low effective circulation volume, such as renal ischemia, chronic renal failure, hepatic cirrhosis, congestive heart failure, or nephrotic syndrome. It is linked to elevated aldosterone levels caused by high renin levels.
- Published on
Pathology - Cushing Syndrome
Hypercortisolism can be caused by iatrogenic cortisol injection, increased ACTH production by pituitary adenoma/hyperplasia (Cushing disease), adrenal cortical adenoma/carcinoma, or ectopic ACTH-secreting tumors (typically small cell bronchogenic carcinoma).
The pathophysiology of the adrenal gland is determined by its underlying cause. (1) Iatrogenic: Adrenocortical atrophy caused by medical treatment; (2) ACTH overproduction: Enlargement of lipid-rich cells in the zona fasciculata of both adrenal glands; (3) Adrenal adenoma: Small enclosed growth made up of uniform zona fasciculata cells; (4) Pituitary hyperplasia or adenoma (observed in Cushing disease): Accumulation of basophilic cells.
Clinical Symptoms and Signs
Truncal obesity, hypertension, moon facies, buffalo hump, muscular wasting, hyperglycemia from insulin resistance, skin alterations such purple abdomen striae and bruises, osteoporosis, hirsutism, mental state changes, immunological suppression, and central obesity.
Laboratory results: Elevated cortisol levels, atypical ACTH levels (lower in cases of iatrogenic and adrenal adenoma, higher in pituitary adenoma and ectopic ACTH secretion), hyperglycemia.
Clinical manifestations
Surgical removal of pituitary or adrenal adenoma, or ectopic ACTH-secreting tumors.
Therapies
The dexamethasone suppression test is utilized to identify the cause of Cushing's illness.
High doses of dexamethasone decrease cortisol levels in Cushing's disease from pituitary adenomas but do not modify levels in cases caused by ectopic ACTH-secreting tumors.
Hypercortisolism can be caused by iatrogenic cortisol injection, increased ACTH production by pituitary adenoma/hyperplasia (Cushing disease), adrenal cortical adenoma/carcinoma, or ectopic ACTH-secreting tumors (typically small cell bronchogenic carcinoma).
The pathophysiology of the adrenal gland is determined by its underlying cause. (1) Iatrogenic: Adrenocortical atrophy caused by medical treatment; (2) ACTH overproduction: Enlargement of lipid-rich cells in the zona fasciculata of both adrenal glands; (3) Adrenal adenoma: Small enclosed growth made up of uniform zona fasciculata cells; (4) Pituitary hyperplasia or adenoma (observed in Cushing disease): Accumulation of basophilic cells.
Clinical Symptoms and Signs
Truncal obesity, hypertension, moon facies, buffalo hump, muscular wasting, hyperglycemia from insulin resistance, skin alterations such purple abdomen striae and bruises, osteoporosis, hirsutism, mental state changes, immunological suppression, and central obesity.
Laboratory results: Elevated cortisol levels, atypical ACTH levels (lower in cases of iatrogenic and adrenal adenoma, higher in pituitary adenoma and ectopic ACTH secretion), hyperglycemia.
Clinical manifestations
Surgical removal of pituitary or adrenal adenoma, or ectopic ACTH-secreting tumors.
Therapies
The dexamethasone suppression test is utilized to identify the cause of Cushing's illness.
High doses of dexamethasone decrease cortisol levels in Cushing's disease from pituitary adenomas but do not modify levels in cases caused by ectopic ACTH-secreting tumors.
- Published on
Pathology - Primary Adrenocortical Insufficiency (Addison Disease)
Addison's disease is a kind of primary adrenocortical insufficiency.
Possible causes consist of autoimmune adrenalitis, TB infection, bilateral adrenal bleeding after trauma, surgery, or anticoagulant medication, amyloidosis, and metastatic neoplasms in the adrenal gland.
Pathology
Gross: Adrenal gland that has decreased in size due to atrophy.
Microscopic findings include a small number of cortical cells and the presence of lymphoid infiltration, which is characteristic of autoimmune adrenalitis.
Clinical Symptoms
Symptoms of reduced glucocorticoids include weakness, weariness, nausea, vomiting, and skin hyperpigmentation caused by elevated MSH production, a precursor molecule of ACTH.
Symptoms of reduced mineralocorticoids include low blood pressure, low blood sugar, high levels of potassium, and low levels of sodium.
Laboratory results indicate increased ACTH levels and decreased cortisol levels.
Treatment involves replacing glucocorticoids and mineralocorticoids.
Secondary adrenocortical insufficiency can result from pituitary or hypothalamic disorders that decrease ACTH production, including persistent glucocorticoid medication, malignancy, infection, or trauma. This condition resembles primary adrenocortical insufficiency but lacks hyperpigmentation due to reduced MSH levels.
Waterhouse-Friderichsen syndrome is characterized by sudden bilateral adrenal insufficiency resulting from hemorrhagic necrosis of the adrenal glands, typically triggered by disseminated intravascular coagulation (DIC) or meningococcemia.
Addison's disease is a kind of primary adrenocortical insufficiency.
Possible causes consist of autoimmune adrenalitis, TB infection, bilateral adrenal bleeding after trauma, surgery, or anticoagulant medication, amyloidosis, and metastatic neoplasms in the adrenal gland.
Pathology
Gross: Adrenal gland that has decreased in size due to atrophy.
Microscopic findings include a small number of cortical cells and the presence of lymphoid infiltration, which is characteristic of autoimmune adrenalitis.
Clinical Symptoms
Symptoms of reduced glucocorticoids include weakness, weariness, nausea, vomiting, and skin hyperpigmentation caused by elevated MSH production, a precursor molecule of ACTH.
Symptoms of reduced mineralocorticoids include low blood pressure, low blood sugar, high levels of potassium, and low levels of sodium.
Laboratory results indicate increased ACTH levels and decreased cortisol levels.
Treatment involves replacing glucocorticoids and mineralocorticoids.
Secondary adrenocortical insufficiency can result from pituitary or hypothalamic disorders that decrease ACTH production, including persistent glucocorticoid medication, malignancy, infection, or trauma. This condition resembles primary adrenocortical insufficiency but lacks hyperpigmentation due to reduced MSH levels.
Waterhouse-Friderichsen syndrome is characterized by sudden bilateral adrenal insufficiency resulting from hemorrhagic necrosis of the adrenal glands, typically triggered by disseminated intravascular coagulation (DIC) or meningococcemia.
