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Pathology - Endometriosis
Endometriosis can manifest with a triad of symptoms that includes dysmenorrhea (painful menses), dyspareunia (pain during intercourse), and dyschezia (pain on defecation). The condition is primarily caused by reflux of blood and endometrial cells from the uterus through the fallopian tubes into the abdominal cavity. Other causes have also been postulated, including coelomic metaplasia and hematogenous spread. Dyschezia arises secondary to endometrial cell implants in the rectouterine pouch of Douglas. The implants act as normal endometrial cells and undergo cyclical alterations according to systemic hormone balance variations, regardless of the implant location.
Laparoscopy is the current gold standard for diagnosis because it permits viewing of the endometrial implants.
Menstrual periods can be regulated with oral contraceptives and discomfort can be eased with anti-inflammatory medications.
Endometriosis can manifest with a triad of symptoms that includes dysmenorrhea (painful menses), dyspareunia (pain during intercourse), and dyschezia (pain on defecation). The condition is primarily caused by reflux of blood and endometrial cells from the uterus through the fallopian tubes into the abdominal cavity. Other causes have also been postulated, including coelomic metaplasia and hematogenous spread. Dyschezia arises secondary to endometrial cell implants in the rectouterine pouch of Douglas. The implants act as normal endometrial cells and undergo cyclical alterations according to systemic hormone balance variations, regardless of the implant location.
Laparoscopy is the current gold standard for diagnosis because it permits viewing of the endometrial implants.
Menstrual periods can be regulated with oral contraceptives and discomfort can be eased with anti-inflammatory medications.
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Pathology - Spontaneous Abortion
This patient may clinically diagnosed with threatened abortion . Her indications and symptoms may suggest that there is impending spontaneous abortion (miscarriage), which follows from fetal demise in utero . Approximately 80% of spontaneous abortions occur with the first 12 weeks. Miscarriage is generally linked with bleeding into the decidual membrane and local tissue necrosis. The typical natural process that follows is detachment of the ovum/fetus from the endometrium, which drives uterine contraction and expulsion of the products of conception. Approximately 30% of all pregnancies are lost after implantation has occurred, with two-thirds of these being clinically silent, prior to diagnosis of a pregnancy. Most usually there is a fetal chromosomal defect and in half of the cases there is a “ blighted ovum ” (missing fetus). Chromosomal mistakes become less likely when loss happens later in pregnancy.
Risk factors include maternal age, type 1 DM, progesterone shortage, and hypothyroidism, with weak associations to smoking, alcohol, diet, and environmental pollutants; infections are an uncommon cause of miscarriage. Uterine anomalies including fibroids in the endometrial area or other anatomical uterine defects may have a role. The condition of incompetent cervix resulting in protrusion of membranes into the vagina may be a symptom of later miscarriage and is surgically treated with cerclage. Recurrent miscarriage is defined if three or more consecutive pregnancy losses before 20 weeks occur. Autoimmune or alloimmune (against another person) variables may be implicated.
This patient may clinically diagnosed with threatened abortion . Her indications and symptoms may suggest that there is impending spontaneous abortion (miscarriage), which follows from fetal demise in utero . Approximately 80% of spontaneous abortions occur with the first 12 weeks. Miscarriage is generally linked with bleeding into the decidual membrane and local tissue necrosis. The typical natural process that follows is detachment of the ovum/fetus from the endometrium, which drives uterine contraction and expulsion of the products of conception. Approximately 30% of all pregnancies are lost after implantation has occurred, with two-thirds of these being clinically silent, prior to diagnosis of a pregnancy. Most usually there is a fetal chromosomal defect and in half of the cases there is a “ blighted ovum ” (missing fetus). Chromosomal mistakes become less likely when loss happens later in pregnancy.
Risk factors include maternal age, type 1 DM, progesterone shortage, and hypothyroidism, with weak associations to smoking, alcohol, diet, and environmental pollutants; infections are an uncommon cause of miscarriage. Uterine anomalies including fibroids in the endometrial area or other anatomical uterine defects may have a role. The condition of incompetent cervix resulting in protrusion of membranes into the vagina may be a symptom of later miscarriage and is surgically treated with cerclage. Recurrent miscarriage is defined if three or more consecutive pregnancy losses before 20 weeks occur. Autoimmune or alloimmune (against another person) variables may be implicated.
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Pathology - Ectopic Pregnancy
Ectopic means any implantation outside of the uterine cavity. The incidence of ectopic pregnancy is 2% of first time pregnancy.
Ninety-five percent of instances occur in the uterine tube, although implantation can also occur in the cervix, cesarean section scars, peritoneum, or ovary. Approximately 70% of tubal implantations occur in the dilated ampulla, which is the most common location of fertilization. Prior tubal injury is the most important risk factor for ectopic pregnancy.
Six percent of maternal deaths are attributable to ectopic pregnancy and occur from tubal rupture and bleeding. The patient in the vignette is hemodynamically stable at this moment and is unlikely to develop a rupture. The absence of a uterine pregnancy in the presence of serum hCG, which is produced from trophoblast tissue, implies an ectopic implantation. The finding of only slowly increasing hCG levels, which would ordinarily double every 2 days early in pregnancy, together with low levels of progesterone secretion, offers a sensitive and specific diagnosis. Treatment may be surgical to remove the products of conception, or alternatively a pharmacological technique to induce abortion can be utilized; methotrexate is a folate antagonist that interrupts rapid cell division to produce abortion of the pregnancy.
Ectopic means any implantation outside of the uterine cavity. The incidence of ectopic pregnancy is 2% of first time pregnancy.
Ninety-five percent of instances occur in the uterine tube, although implantation can also occur in the cervix, cesarean section scars, peritoneum, or ovary. Approximately 70% of tubal implantations occur in the dilated ampulla, which is the most common location of fertilization. Prior tubal injury is the most important risk factor for ectopic pregnancy.
Six percent of maternal deaths are attributable to ectopic pregnancy and occur from tubal rupture and bleeding. The patient in the vignette is hemodynamically stable at this moment and is unlikely to develop a rupture. The absence of a uterine pregnancy in the presence of serum hCG, which is produced from trophoblast tissue, implies an ectopic implantation. The finding of only slowly increasing hCG levels, which would ordinarily double every 2 days early in pregnancy, together with low levels of progesterone secretion, offers a sensitive and specific diagnosis. Treatment may be surgical to remove the products of conception, or alternatively a pharmacological technique to induce abortion can be utilized; methotrexate is a folate antagonist that interrupts rapid cell division to produce abortion of the pregnancy.
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Pathology - Preeclampsia Syndrome
Preeclampsia syndrome is characterized for a first term pregnancy as a systolic pressure greater than 140 or diastolic pressure greater than 90 after 20 weeks’ gestation plus the presence of proteinuria. mother hypertension is a significant cause of mother and newborn morbidity and mortality. Risk factors include obesity, African American ethnicity, and first pregnancy. The pathophysiology is hypothesized to include an early stage in which there is incomplete invasion of maternal uterine arteries by the trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that induce endothelial injury in the mother. Subsequent problems develop on a range of severity and can span numerous organ systems. Platelet aggregation and activation cause release of thromboxane A2 leading to vasospasm that drives high blood pressure. In severe circumstances platelet depletion can occur. Increased endothelial permeability leads to protein leak, which in this case is evidenced by proteinuria and pitting edema in the extremities. Pulmonary edema is observed in this case generating rales and shortness of breath.
In severe situations, hemolysis and vascular blockage may also occur, for example, in the liver or brain. The state of eclampsia is defined if the mother suffers tonic–clonic seizures and is associated with bad outcomes. Initial treatment involves blood pressure medication but timely delivery of the fetus is important if signs of severe preeclampsia develop; birth is usually curative.
Preeclampsia syndrome is characterized for a first term pregnancy as a systolic pressure greater than 140 or diastolic pressure greater than 90 after 20 weeks’ gestation plus the presence of proteinuria. mother hypertension is a significant cause of mother and newborn morbidity and mortality. Risk factors include obesity, African American ethnicity, and first pregnancy. The pathophysiology is hypothesized to include an early stage in which there is incomplete invasion of maternal uterine arteries by the trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that induce endothelial injury in the mother. Subsequent problems develop on a range of severity and can span numerous organ systems. Platelet aggregation and activation cause release of thromboxane A2 leading to vasospasm that drives high blood pressure. In severe circumstances platelet depletion can occur. Increased endothelial permeability leads to protein leak, which in this case is evidenced by proteinuria and pitting edema in the extremities. Pulmonary edema is observed in this case generating rales and shortness of breath.
In severe situations, hemolysis and vascular blockage may also occur, for example, in the liver or brain. The state of eclampsia is defined if the mother suffers tonic–clonic seizures and is associated with bad outcomes. Initial treatment involves blood pressure medication but timely delivery of the fetus is important if signs of severe preeclampsia develop; birth is usually curative.
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Pathology - Nephrolithiasis
This condition most usually manifests as in the vignette, with patients complaining of relatively quick onset of acute flank discomfort spreading to the front of the abdomen on the affected side. While there are some established risk factors for development of renal calculi such as usage of certain medications (hydrochlorothiazide), certain medical disorders (gout, hypercalcemia), or excessive dietary consumption of oxalate (tea, spinach, others), most of the time the etiology is unclear. Evaluation of stone type (struvite vs. calcium oxalate vs. other) can help to identify likely causation in some cases. Stones form in the kidney and migrate down the ureters and eventually expelled in the urine or eliminated using ultrasonic lithotripsy if too large to pass through the ureter. Clinical findings include hematuria, which may be gross or microscopic and systemic signs of illness (fever, nausea, chills), which may occur as a result of acute urinary blockage. Males are afflicted more regularly; repeated episodes are prevalent and can progress to tubular scarring and ultimately renal parenchymal involvement and irreversible kidney disease.
This condition most usually manifests as in the vignette, with patients complaining of relatively quick onset of acute flank discomfort spreading to the front of the abdomen on the affected side. While there are some established risk factors for development of renal calculi such as usage of certain medications (hydrochlorothiazide), certain medical disorders (gout, hypercalcemia), or excessive dietary consumption of oxalate (tea, spinach, others), most of the time the etiology is unclear. Evaluation of stone type (struvite vs. calcium oxalate vs. other) can help to identify likely causation in some cases. Stones form in the kidney and migrate down the ureters and eventually expelled in the urine or eliminated using ultrasonic lithotripsy if too large to pass through the ureter. Clinical findings include hematuria, which may be gross or microscopic and systemic signs of illness (fever, nausea, chills), which may occur as a result of acute urinary blockage. Males are afflicted more regularly; repeated episodes are prevalent and can progress to tubular scarring and ultimately renal parenchymal involvement and irreversible kidney disease.
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Pathology - Urinary Tract Infection
Pyelonephritis is a result of ascending infection from the lower urinary tract. Bacteria enter the urinary tract at the urethra and rise to the bladder, ureters, and kidneys. There are some mechanisms to restrict bacterial development, including acidic urine pH. However, females are more prone to developing UTIs due to the shorter urethral length and proximity of the urethral meatus to the vaginal introitus and anus.
Once the infection reaches the kidneys, it can spread hematogenously and produce signs of sepsis and eventually septic shock if left untreated. Therefore, patients should be hospitalized and treated with empiric intravenous antibiotics until the microorganism sensitivities are identified from the urine culture. The presence of nitrites in the urine suggests the presence of nitrate-reducing bacteria, whereas the presence of leukocyte esterase shows white blood cells in the urine. It is crucial to highlight that patients can have a UTI without the presence of nitrites in the urine if the infection is secondary to a bacterium that does not decrease nitrates.
Pyelonephritis is a result of ascending infection from the lower urinary tract. Bacteria enter the urinary tract at the urethra and rise to the bladder, ureters, and kidneys. There are some mechanisms to restrict bacterial development, including acidic urine pH. However, females are more prone to developing UTIs due to the shorter urethral length and proximity of the urethral meatus to the vaginal introitus and anus.
Once the infection reaches the kidneys, it can spread hematogenously and produce signs of sepsis and eventually septic shock if left untreated. Therefore, patients should be hospitalized and treated with empiric intravenous antibiotics until the microorganism sensitivities are identified from the urine culture. The presence of nitrites in the urine suggests the presence of nitrate-reducing bacteria, whereas the presence of leukocyte esterase shows white blood cells in the urine. It is crucial to highlight that patients can have a UTI without the presence of nitrites in the urine if the infection is secondary to a bacterium that does not decrease nitrates.
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Pathology - HELLP Syndrome
HELLP syndrome is a severe type of preeclampsia/eclampsia characterized by Hemolysis, Elevated Liver enzymes, and Low Platelet count. The pathogenesis is likely to entail inadequate invasion of maternal uterine arteries by the early trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that cause extensive endothelial injury in the mother. Platelet aggregation occurs at locations of endothelial damage, resulting in platelet depletion. Activation of platelets induces release of thromboxane A2 leading to vasospasm that is inadequately countered by endothelial relaxant factors and prostacyclin due to loss of endothelium. Deposition of fibrin also occurs in the lumens of tiny arteries, which increases shearing forces on red cells and promotes hemolysis (notice elevated LDH levels).
Obstruction of hepatic sinusoids with fibrinlike deposits accounts for local necrosis and hepatocellular damage (notice increased liver enzymes). Vascular obstruction within the liver creates a buildup of pressure and in this instance subcapsular hematoma is observed on ultrasonography; this process may even terminate in liver rupture. Treatment may include glucocorticoids to advance fetal lung maturation, although timely delivery of the fetus is necessary. Unlike preeclampsia syndrome, delivery may not result in immediate resolution of maternal symptoms after the HELLP syndrome has established.
HELLP syndrome is a severe type of preeclampsia/eclampsia characterized by Hemolysis, Elevated Liver enzymes, and Low Platelet count. The pathogenesis is likely to entail inadequate invasion of maternal uterine arteries by the early trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that cause extensive endothelial injury in the mother. Platelet aggregation occurs at locations of endothelial damage, resulting in platelet depletion. Activation of platelets induces release of thromboxane A2 leading to vasospasm that is inadequately countered by endothelial relaxant factors and prostacyclin due to loss of endothelium. Deposition of fibrin also occurs in the lumens of tiny arteries, which increases shearing forces on red cells and promotes hemolysis (notice elevated LDH levels).
Obstruction of hepatic sinusoids with fibrinlike deposits accounts for local necrosis and hepatocellular damage (notice increased liver enzymes). Vascular obstruction within the liver creates a buildup of pressure and in this instance subcapsular hematoma is observed on ultrasonography; this process may even terminate in liver rupture. Treatment may include glucocorticoids to advance fetal lung maturation, although timely delivery of the fetus is necessary. Unlike preeclampsia syndrome, delivery may not result in immediate resolution of maternal symptoms after the HELLP syndrome has established.
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Pathology - Menopause
This symptoms occurs in women, most commonly in late fifth or early sixth decade of life. The diagnosis is most typically made clinically when a women of this age range ceases to have menstrual cycles for a straight 12-month time frame. Menopause is the outcome of a natural decline in ovarian production of estrogen and progesterone, clinically noticeable as a woman begins to experience more erratic and unpredictable menstrual cycles and ceases releasing viable eggs each month. While this decline in hormone production occurs across years (perimenopausal era), eventually menses will halt for 12 months or more at which time menopause is stated to have happened. Menopause that happens before the age of 40 and owing to extrinsic causes such as hysterectomy or chemotherapy is termed to be premature. Decreased hormone production in menopause is responsible for the common symptoms experienced by most women, including hot flashes (thought to be due to hypothalamic dysregulation), vaginal dryness and dyspareunia (due to atrophic changes in tissues supported by estrogen), and sleep abnormalities (thought to be due to loss of estrogenic effects on nervous tissue responsible for sleep/wake regulation).
Laboratory assessment of this disorder is usually not essential. If examined, blood FSH level will be significantly elevated as a result of pituitary reaction to low circulating estrogen levels.
This symptoms occurs in women, most commonly in late fifth or early sixth decade of life. The diagnosis is most typically made clinically when a women of this age range ceases to have menstrual cycles for a straight 12-month time frame. Menopause is the outcome of a natural decline in ovarian production of estrogen and progesterone, clinically noticeable as a woman begins to experience more erratic and unpredictable menstrual cycles and ceases releasing viable eggs each month. While this decline in hormone production occurs across years (perimenopausal era), eventually menses will halt for 12 months or more at which time menopause is stated to have happened. Menopause that happens before the age of 40 and owing to extrinsic causes such as hysterectomy or chemotherapy is termed to be premature. Decreased hormone production in menopause is responsible for the common symptoms experienced by most women, including hot flashes (thought to be due to hypothalamic dysregulation), vaginal dryness and dyspareunia (due to atrophic changes in tissues supported by estrogen), and sleep abnormalities (thought to be due to loss of estrogenic effects on nervous tissue responsible for sleep/wake regulation).
Laboratory assessment of this disorder is usually not essential. If examined, blood FSH level will be significantly elevated as a result of pituitary reaction to low circulating estrogen levels.
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Pathology - Dysfunctional Uterine Bleeding
Dysfunctional uterine bleeding ( DUB) is identified clinically following meticulous history and physical examination and appropriate laboratory test. DUB is caused by hormonal abnormalities in the hypothalamic–pituitary axis in the absence of obvious anatomical or biological disease. Most typically, DUB is related with anovulatory conditions occurring at the extremes of reproductive age, such as early puberty and perimenopause. In certain cases, women do not correctly develop and release a mature egg. Without appropriate ovulation, a corpus luteum does not form and progesterone levels are lowered, producing practically constant estrogen production and subsequent thickening of the uterine lining. Menstruation is sometimes delayed; when it occurs, it can be heavy and lengthy. This condition has been connected with psychological stress, fast weight gain or loss, other endocrinopathies, neoplasms, and medication use. Mechanisms of DUB are generally unknown and often, no specific cause is recognized. Laboratory assessment includes blood hemoglobin level; LH, FSH, prolactin, and TSH levels; evaluation for pregnancy; and androgen profile, if clinically needed. Evaluation of endometrial thickness using pelvic ultrasonography may be indicated in some cases. Symptoms of weariness mentioned in the patient in the vignette above may be attributed to anemia/low hemoglobin from repeated excessive blood loss during protracted menses. The term used to describe severe menstrual bleeding is menorrhagia. Metrorrhagia is used to characterize frequent (more often than every 28 days) bleeding or bleeding in between menstrual cycles.
Dysfunctional uterine bleeding ( DUB) is identified clinically following meticulous history and physical examination and appropriate laboratory test. DUB is caused by hormonal abnormalities in the hypothalamic–pituitary axis in the absence of obvious anatomical or biological disease. Most typically, DUB is related with anovulatory conditions occurring at the extremes of reproductive age, such as early puberty and perimenopause. In certain cases, women do not correctly develop and release a mature egg. Without appropriate ovulation, a corpus luteum does not form and progesterone levels are lowered, producing practically constant estrogen production and subsequent thickening of the uterine lining. Menstruation is sometimes delayed; when it occurs, it can be heavy and lengthy. This condition has been connected with psychological stress, fast weight gain or loss, other endocrinopathies, neoplasms, and medication use. Mechanisms of DUB are generally unknown and often, no specific cause is recognized. Laboratory assessment includes blood hemoglobin level; LH, FSH, prolactin, and TSH levels; evaluation for pregnancy; and androgen profile, if clinically needed. Evaluation of endometrial thickness using pelvic ultrasonography may be indicated in some cases. Symptoms of weariness mentioned in the patient in the vignette above may be attributed to anemia/low hemoglobin from repeated excessive blood loss during protracted menses. The term used to describe severe menstrual bleeding is menorrhagia. Metrorrhagia is used to characterize frequent (more often than every 28 days) bleeding or bleeding in between menstrual cycles.
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Pathology -Secondary Amenorrhea
In secondary amenorrhea the female patient has had normal menstruation that has ended for some reason.
The most prevalent reason for secondary amenorrhea is pregnancy, and this should be examined in all patients, even if sexual activity is denied. After pregnancy has been ruled out, TSH and prolactin levels should be evaluated, as hypothyroid conditions and hyperprolactinemia are typical reasons of monthly irregularity or cessation. Other causes include excessively low levels of gonadotropins (pituitary tumor) or abnormally high levels of these same hormones (hypergonadotropic hypogonadism found in ovarian failure). Two common causes of normogonadic secondary amenorrhea include outlet blockage and PCOS. Outflow obstruction may develop owing to uterine scarring from infection, obstructive polyps, or cervical stenosis. PCOS is the most common cause of hyperandrogenic chronic anovulation disease. While the primary etiology of PCOS is uncertain, insulin insensitivity is thought to have a role. Hypothalamic amenorrhea is a disorder linked with anomalies in GnRH secretion and disruption of the hypothalamic–pituitary–ovarian axis. The syndrome is commonly induced by extreme weight loss, activity, or stress and may be found in female athletes with lower than normal percentage of body weight. The mechanism of how stress or weight loss impacts GnRH secretion is unknown. Menses will normally return if a healthy body weight is achieved.
In secondary amenorrhea the female patient has had normal menstruation that has ended for some reason.
The most prevalent reason for secondary amenorrhea is pregnancy, and this should be examined in all patients, even if sexual activity is denied. After pregnancy has been ruled out, TSH and prolactin levels should be evaluated, as hypothyroid conditions and hyperprolactinemia are typical reasons of monthly irregularity or cessation. Other causes include excessively low levels of gonadotropins (pituitary tumor) or abnormally high levels of these same hormones (hypergonadotropic hypogonadism found in ovarian failure). Two common causes of normogonadic secondary amenorrhea include outlet blockage and PCOS. Outflow obstruction may develop owing to uterine scarring from infection, obstructive polyps, or cervical stenosis. PCOS is the most common cause of hyperandrogenic chronic anovulation disease. While the primary etiology of PCOS is uncertain, insulin insensitivity is thought to have a role. Hypothalamic amenorrhea is a disorder linked with anomalies in GnRH secretion and disruption of the hypothalamic–pituitary–ovarian axis. The syndrome is commonly induced by extreme weight loss, activity, or stress and may be found in female athletes with lower than normal percentage of body weight. The mechanism of how stress or weight loss impacts GnRH secretion is unknown. Menses will normally return if a healthy body weight is achieved.
