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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.
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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 -Primary Amenorrhea
This patient has primary amenorrhea — no beginning of menses in a female older than 16 years. This disorder may occur with or without other indicators of puberty and most usually happens as a result of anatomic, hormonal, or genetic abnormality. Anatomic causes include congenital lack of the uterus or vagina, presence of vaginal septum or imperforate hymen, blocked/narrowed cervix, or Müllerian agenesis. Hormonal reasons include pituitary (LH, FSH), ovarian malfunction, or androgen insensitivity. Genetic abnormalities include Turner’s syndrome (45 XO). If secondary sex traits are not present, gonadotropins (FSH, LH) are tested first. If levels are low, hypogonadotropic hypogonadism is present. If FSH and LH are excessive (hypergonadotropic hypogonadism), unresponsiveness of tissues (premature ovarian failure or Turner’s syndrome) is suspected. If secondary sex traits are present (as in the patient in the vignette), ultrasonography assessment of pelvic organs is indicated. If appropriate pelvic architecture is present, uterine outflow blockage is suspected. If aberrant pelvic morphology is identified, this may imply androgen insensitivity throughout fetal life or Müllerian agenesis.
This patient has primary amenorrhea — no beginning of menses in a female older than 16 years. This disorder may occur with or without other indicators of puberty and most usually happens as a result of anatomic, hormonal, or genetic abnormality. Anatomic causes include congenital lack of the uterus or vagina, presence of vaginal septum or imperforate hymen, blocked/narrowed cervix, or Müllerian agenesis. Hormonal reasons include pituitary (LH, FSH), ovarian malfunction, or androgen insensitivity. Genetic abnormalities include Turner’s syndrome (45 XO). If secondary sex traits are not present, gonadotropins (FSH, LH) are tested first. If levels are low, hypogonadotropic hypogonadism is present. If FSH and LH are excessive (hypergonadotropic hypogonadism), unresponsiveness of tissues (premature ovarian failure or Turner’s syndrome) is suspected. If secondary sex traits are present (as in the patient in the vignette), ultrasonography assessment of pelvic organs is indicated. If appropriate pelvic architecture is present, uterine outflow blockage is suspected. If aberrant pelvic morphology is identified, this may imply androgen insensitivity throughout fetal life or Müllerian agenesis.
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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.
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Symptoms and Signs – Differential Diagnosis of Complement deficiency
Congenital e.g. C1 esterase (C1 inhibitor) deficiency (normal C3, reduced C4)
Acquired
Reduced C3 and C4:
SLE, mixed cryoglobulinaemia
Subacute bacterial endocarditis
Serum sickness
Increased Loss/reduced synthesis: malnutrition, nephrotic syndrome, burns, liver failure
Reduced C3
Mesangiocapillary glomerulonephritis, partial lipodystrophy
Gram -ve (endotoxic) shock
Increased C3 and/or C4
Acute phase response
Congenital e.g. C1 esterase (C1 inhibitor) deficiency (normal C3, reduced C4)
Acquired
Reduced C3 and C4:
SLE, mixed cryoglobulinaemia
Subacute bacterial endocarditis
Serum sickness
Increased Loss/reduced synthesis: malnutrition, nephrotic syndrome, burns, liver failure
Reduced C3
Mesangiocapillary glomerulonephritis, partial lipodystrophy
Gram -ve (endotoxic) shock
Increased C3 and/or C4
Acute phase response
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Symptoms and Signs – Differential Diagnosis of Reduced Consciousness
Hypoglycaemia
Hypoxia: cardiac arrest, shock (hypovolaemic, septic), respiratory failure
Infection: meningitis, encephalitis
Inflammation (demyelination)
Toxic: drugs e.g. opiates, alcohol, anxiolytics, antidepressants
Trauma (head injury)
Tumour (increased intracranial pressure)
Vascular: intracranial haemorrhage/infarction
Metabolic: liver failure, renal failure, electrolyte (Na+, K+, Ca2+, Mg2+)
disturbances, endocrinopathies e.g. myxoedema coma, vitamin deficiencies
(e.g. thiamine, B12), hypothermia
Hypoglycaemia
Hypoxia: cardiac arrest, shock (hypovolaemic, septic), respiratory failure
Infection: meningitis, encephalitis
Inflammation (demyelination)
Toxic: drugs e.g. opiates, alcohol, anxiolytics, antidepressants
Trauma (head injury)
Tumour (increased intracranial pressure)
Vascular: intracranial haemorrhage/infarction
Metabolic: liver failure, renal failure, electrolyte (Na+, K+, Ca2+, Mg2+)
disturbances, endocrinopathies e.g. myxoedema coma, vitamin deficiencies
(e.g. thiamine, B12), hypothermia
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Symptoms and Signs – Differential Diagnosis of Constipation
Diet: low fibre, inadequate fluid intake
Drugs: opiates, anticholinergics (tricyclics, phenothiazines), iron
Immobility
Old age
Surgical/gastrointestinal:
Anorectal disease (fissure, stricture, rectal prolapse)
Intestinal obstruction (strictures, e.g. IBD, cancers, diverticulosis, pelvic mass,
e.g. fibroids)
Irritable bowel syndrome
Post-operative
Endocrine: hypothyroidism, hypercalcaemia, hypokalaemia, porphyria, lead
poisoning
Neurological/neuromuscular: autonomic neuropathy, spinal/pelvic nerve injury,
scleroderma, Hirschsprung's disease, Chagas' disease
Diet: low fibre, inadequate fluid intake
Drugs: opiates, anticholinergics (tricyclics, phenothiazines), iron
Immobility
Old age
Surgical/gastrointestinal:
Anorectal disease (fissure, stricture, rectal prolapse)
Intestinal obstruction (strictures, e.g. IBD, cancers, diverticulosis, pelvic mass,
e.g. fibroids)
Irritable bowel syndrome
Post-operative
Endocrine: hypothyroidism, hypercalcaemia, hypokalaemia, porphyria, lead
poisoning
Neurological/neuromuscular: autonomic neuropathy, spinal/pelvic nerve injury,
scleroderma, Hirschsprung's disease, Chagas' disease
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Symptoms and Signs – Differential Diagnosis of Corneal opacification
Corneal ulcer, keratitis
Anterior uveitis (iritis)
Acute angle closure glaucoma
Corneal ulcer, keratitis
Anterior uveitis (iritis)
Acute angle closure glaucoma
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Pathology - Osteomalacia
Osteomalacia may arise from vitamin D insufficiency. In metabolic bone disease there is decreased bone density and diminished bone strength. In osteomalacia the problem is restricted to loss of bone mineralization, but in osteoporosis there is also loss of the collagenous bone matrix. Vitamin D is essential for appropriate mineralization of bone by osteoblasts with calcium phosphate (hydroxyapatite) crystals. Inadequate vitamin D in children causes the irreversible bone abnormalities of rickets, and in adults it causes osteomalacia. Vitamin D is generated in the skin following exposure to UV-B radiation and is also present in the diet. Activation of vitamin D involves 25-hydroxylation in the liver and final conversion to 1,25-(OH)2 D3 (cholecalciferol) in the kidney, under the supervision of PTH. The patient is at great risk for vitamin D insufficiency due to his very restricted diet and avoidance of sunshine. Vitamin D is necessary for appropriate intestinal uptake of calcium and phosphate. Vitamin D insufficiency in this patient accounts for low serum calcium and phosphate levels. Pseudofractures are anomalies detected on radiographs as the periosteum thickens as a healing reaction to an adjacent area of bone demineralization. There are other probable causes of osteomalacia. One example is a mesenchymal tumor type, which releases phosphaturic substances such as fibroblast growth factor-23 (FGF-23), leading to phosphate deficit and bone disease. In children hereditary types of rickets can occur from mutations in either the 1-alpha hydroxylase enzyme for vitamin D activation (rickets type 1), or in the vitamin D receptor (rickets type 2).
Osteomalacia may arise from vitamin D insufficiency. In metabolic bone disease there is decreased bone density and diminished bone strength. In osteomalacia the problem is restricted to loss of bone mineralization, but in osteoporosis there is also loss of the collagenous bone matrix. Vitamin D is essential for appropriate mineralization of bone by osteoblasts with calcium phosphate (hydroxyapatite) crystals. Inadequate vitamin D in children causes the irreversible bone abnormalities of rickets, and in adults it causes osteomalacia. Vitamin D is generated in the skin following exposure to UV-B radiation and is also present in the diet. Activation of vitamin D involves 25-hydroxylation in the liver and final conversion to 1,25-(OH)2 D3 (cholecalciferol) in the kidney, under the supervision of PTH. The patient is at great risk for vitamin D insufficiency due to his very restricted diet and avoidance of sunshine. Vitamin D is necessary for appropriate intestinal uptake of calcium and phosphate. Vitamin D insufficiency in this patient accounts for low serum calcium and phosphate levels. Pseudofractures are anomalies detected on radiographs as the periosteum thickens as a healing reaction to an adjacent area of bone demineralization. There are other probable causes of osteomalacia. One example is a mesenchymal tumor type, which releases phosphaturic substances such as fibroblast growth factor-23 (FGF-23), leading to phosphate deficit and bone disease. In children hereditary types of rickets can occur from mutations in either the 1-alpha hydroxylase enzyme for vitamin D activation (rickets type 1), or in the vitamin D receptor (rickets type 2).
