- Published on
Pathology - Male Hypogonadism
The disorder is caused by insufficient testosterone release from the testes. Congenital causes of male hypogonadism include the chromosomal abnormalities Klinefelter’s syndrome (47, XXY plus variants) and mutations such as those in Kallmann syndrome that result in the loss of GnRH secreting neurons. The patient in this example has a past history of normal fertility, indicating he has an acquired etiology of hypogonadism.
Inadequate testosterone levels account for loss of libido, erectile dysfunction, decreased muscle mass, weariness, and depression. Severe chronic cases may also result in loss of facial, body, and pubic hair. The condition can be classified as hypogonadotropic (normal or low LH, as in this example) or hypergonadotropic (high LH due to primary testicular failure and loss of negative feedback on LH secretion). This patient has no clear identifiable cause of hypogonadism such as pituitary disease, hypothyroidism, granulomatous disease, or adverse drug reaction but rather has a functional reason related to obesity, aging, and chronic ill health. Testosterone levels normally fall 1–2% every year at the age of 40 years and the aromatase activity of adipose tissue converts testosterone to estrogen. Testosterone replacement usually restores virility, but its usage must be balanced against the increased risk of cardiovascular events, and it should not be used while active prostate cancer is present.
The disorder is caused by insufficient testosterone release from the testes. Congenital causes of male hypogonadism include the chromosomal abnormalities Klinefelter’s syndrome (47, XXY plus variants) and mutations such as those in Kallmann syndrome that result in the loss of GnRH secreting neurons. The patient in this example has a past history of normal fertility, indicating he has an acquired etiology of hypogonadism.
Inadequate testosterone levels account for loss of libido, erectile dysfunction, decreased muscle mass, weariness, and depression. Severe chronic cases may also result in loss of facial, body, and pubic hair. The condition can be classified as hypogonadotropic (normal or low LH, as in this example) or hypergonadotropic (high LH due to primary testicular failure and loss of negative feedback on LH secretion). This patient has no clear identifiable cause of hypogonadism such as pituitary disease, hypothyroidism, granulomatous disease, or adverse drug reaction but rather has a functional reason related to obesity, aging, and chronic ill health. Testosterone levels normally fall 1–2% every year at the age of 40 years and the aromatase activity of adipose tissue converts testosterone to estrogen. Testosterone replacement usually restores virility, but its usage must be balanced against the increased risk of cardiovascular events, and it should not be used while active prostate cancer is present.
- Published on
Pathology - Erectile Dysfunction
Two mediators in penile tumescence are nitric oxide (NO) and cyclic guanosine monophosphate (GMP). Tactile stimulation of the penis leads in the firing of neurons that transfer impulses based on feeling. This produces secretion of NO which has a vasodilatory effect, allowing corpora cavernosa to engorge with blood. Cyclic GMP also has a vasodilatory impact. Disorders that alter brain function, such diabetes, can influence a patient’s ability to obtain an erection. There are various more factors that can cause erectile dysfunction that should be considered: psychogenic disorders, drug use, vasculopathy, and endocrine abnormalities. With psychogenic difficulties, patients still tend to have morning tumescence after waking from REM sleep. The current gold standard treatment is oral phosphodiesterase inhibitors, which function by inhibiting the breakdown of cyclic GMP.
Two mediators in penile tumescence are nitric oxide (NO) and cyclic guanosine monophosphate (GMP). Tactile stimulation of the penis leads in the firing of neurons that transfer impulses based on feeling. This produces secretion of NO which has a vasodilatory effect, allowing corpora cavernosa to engorge with blood. Cyclic GMP also has a vasodilatory impact. Disorders that alter brain function, such diabetes, can influence a patient’s ability to obtain an erection. There are various more factors that can cause erectile dysfunction that should be considered: psychogenic disorders, drug use, vasculopathy, and endocrine abnormalities. With psychogenic difficulties, patients still tend to have morning tumescence after waking from REM sleep. The current gold standard treatment is oral phosphodiesterase inhibitors, which function by inhibiting the breakdown of cyclic GMP.
- Published on
Pathology - Benign Prostatic Hyperplasia
Symptoms are related to involvement of the periurethral prostatic tissue; alternatively, prostate tumors might be asymptomatic if they start in the peripheral prostatic tissue. Dihydrotestosterone (DHT) causes hyperplasia of the glandular cells. Estrogen also has a role by upregulating androgen receptors.
5-Alpha-reductase inhibitors like as finasteride, which prevent synthesis of DHT from testosterone in stromal cells, can be utilized in the treatment of BPH. Irregular and nodular prostates should undergo biopsy to rule out prostate cancer.
It is vital to note that PSA might be increased in BPH and prostatitis.
Symptoms are related to involvement of the periurethral prostatic tissue; alternatively, prostate tumors might be asymptomatic if they start in the peripheral prostatic tissue. Dihydrotestosterone (DHT) causes hyperplasia of the glandular cells. Estrogen also has a role by upregulating androgen receptors.
5-Alpha-reductase inhibitors like as finasteride, which prevent synthesis of DHT from testosterone in stromal cells, can be utilized in the treatment of BPH. Irregular and nodular prostates should undergo biopsy to rule out prostate cancer.
It is vital to note that PSA might be increased in BPH and prostatitis.
- Published on
Pathology - Prostatitis
Acute bacterial prostatitis, can be owing to an ascending infection from the urethra or can be caused to urine reflux into the prostatic ducts. The microorganisms are usually gram-negative bacteria, and sepsis can occur if left untreated. Patients with indwelling catheters or history of sexually transmitted infections are at greater risk. This patient has a history of benign prostatic hyperplasia, which causes constriction of the urethra as it passes through the prostate gland to reach the bladder. This produces secondary blockage of urinary flow with possible stasis of urine and reflux into the prostatic ducts. Bacteria can proliferate and induce inflammation, leading to prostatodynia.
Treatment consists mostly of empiric antibiotics such as fluoroquinolones until urine culture sensitivities are discovered.
Acute bacterial prostatitis, can be owing to an ascending infection from the urethra or can be caused to urine reflux into the prostatic ducts. The microorganisms are usually gram-negative bacteria, and sepsis can occur if left untreated. Patients with indwelling catheters or history of sexually transmitted infections are at greater risk. This patient has a history of benign prostatic hyperplasia, which causes constriction of the urethra as it passes through the prostate gland to reach the bladder. This produces secondary blockage of urinary flow with possible stasis of urine and reflux into the prostatic ducts. Bacteria can proliferate and induce inflammation, leading to prostatodynia.
Treatment consists mostly of empiric antibiotics such as fluoroquinolones until urine culture sensitivities are discovered.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
- Published on
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.
