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Pathology - Allergic Contact Dermatitis
There are numerous crucial features to this classic, delayed, cell-mediated (Type IV) hypersensitivity reaction. This process requires prior exposure to the sensitizer, most often poison ivy or poison oak in the United States. Upon exposure, the plant antigen is picked up by Langerhans cells, which migrate to lymph nodes and transmit the processed antigen via major histocompatibility complex (MHC) class II molecules to CD4 + T lymphocytes. These T cells develop into T-helper type 1 lymphocytes, which proliferate and enter the blood circulation. With re-exposure by presentation of the same particular antigen, the sensitized T lymphocytes produce cytokines, most notably interferon-gamma (IFN-γ), which mediates the local inflammatory response involving activated macrophages, natural killer cells, and CD8 + T cells. The clinical skin manifestations typically present 48 to 72 hours after contact, which is diagnostic of the delayed hypersensitivity reactions. Metals such as nickel and chromium are also capable of generating contact dermatitis and can typically present as a pruritic rash around the neck or wrist due to jewelry.
There are numerous crucial features to this classic, delayed, cell-mediated (Type IV) hypersensitivity reaction. This process requires prior exposure to the sensitizer, most often poison ivy or poison oak in the United States. Upon exposure, the plant antigen is picked up by Langerhans cells, which migrate to lymph nodes and transmit the processed antigen via major histocompatibility complex (MHC) class II molecules to CD4 + T lymphocytes. These T cells develop into T-helper type 1 lymphocytes, which proliferate and enter the blood circulation. With re-exposure by presentation of the same particular antigen, the sensitized T lymphocytes produce cytokines, most notably interferon-gamma (IFN-γ), which mediates the local inflammatory response involving activated macrophages, natural killer cells, and CD8 + T cells. The clinical skin manifestations typically present 48 to 72 hours after contact, which is diagnostic of the delayed hypersensitivity reactions. Metals such as nickel and chromium are also capable of generating contact dermatitis and can typically present as a pruritic rash around the neck or wrist due to jewelry.
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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 - 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 - Hirsutism
Hirsutism refers to excessive hair development in regions of the body where terminal hair does not ordinarily occur or is limited. It is most typically seen in women in whom aberrant hair growth takes on a pattern of masculine hair growth. This issue is a medical symptom rather than an illness and should be investigated appropriately. Hirsutism can be induced by either an increase level of androgens or an oversensitivity of hair follicles to androgens. Symptoms of aberrant hair growth may be accompanied by additional indicators of enhanced androgenic circulation, such as deepening of the voice, increased muscular mass, or cystic acne. Increased circulating levels of insulin in women may contribute to hirsutism, as high insulin levels stimulate ovarian theca cells to produce androgens. In addition, excessive doses of insulin may act at IGF-1 receptors in these same cells, resulting in increased androgen synthesis. Evaluation of this disorder comprises serum FSH level, free cortisol, 21-alpha hydroxylase deficiency, human growth hormone, fasting blood sugar, and hemoglobin A1c to check for PCOS, adrenocorticosteroid excess, congenital adrenal hyperplasia, acromegaly, and insulin resistance, respectively. Imaging of ovaries and adrenal glands may be indicated in some instances. Careful examination of drugs is also necessary, as hirsutism can be seen as a side effect of various medications including phenytoin, aldomet, metoclopramide, danazol, oral contraceptives, or phenothiazines.
Hirsutism refers to excessive hair development in regions of the body where terminal hair does not ordinarily occur or is limited. It is most typically seen in women in whom aberrant hair growth takes on a pattern of masculine hair growth. This issue is a medical symptom rather than an illness and should be investigated appropriately. Hirsutism can be induced by either an increase level of androgens or an oversensitivity of hair follicles to androgens. Symptoms of aberrant hair growth may be accompanied by additional indicators of enhanced androgenic circulation, such as deepening of the voice, increased muscular mass, or cystic acne. Increased circulating levels of insulin in women may contribute to hirsutism, as high insulin levels stimulate ovarian theca cells to produce androgens. In addition, excessive doses of insulin may act at IGF-1 receptors in these same cells, resulting in increased androgen synthesis. Evaluation of this disorder comprises serum FSH level, free cortisol, 21-alpha hydroxylase deficiency, human growth hormone, fasting blood sugar, and hemoglobin A1c to check for PCOS, adrenocorticosteroid excess, congenital adrenal hyperplasia, acromegaly, and insulin resistance, respectively. Imaging of ovaries and adrenal glands may be indicated in some instances. Careful examination of drugs is also necessary, as hirsutism can be seen as a side effect of various medications including phenytoin, aldomet, metoclopramide, danazol, oral contraceptives, or phenothiazines.
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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 - 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.
