This document discusses hirsutism, excessive hair growth in women. It defines different types such as hypertrichosis, hirsutism, and virilization. Hirsutism specifically refers to male-pattern hair growth in women, such as on the face and abdomen. The causes of hirsutism include excess androgen (male hormone) production from the ovaries or adrenal glands in conditions like polycystic ovarian syndrome. The document provides details on evaluating hirsutism through hormonal testing of testosterone, DHEAS, and 17-hydroxyprogesterone levels. It also discusses the pathophysiology and genetic factors involved in polycystic ovarian syndrome, the most common cause of
This document discusses hirsutism, which is defined as excessive terminal hair growth in male pattern areas of the body in women. It outlines several potential causes of hirsutism including polycystic ovary syndrome (PCOS), adrenal or ovarian tumors, and congenital adrenal hyperplasia. The document describes evaluating a patient for hirsutism through history, examination, and laboratory tests. Potential treatment approaches are also summarized, including ovarian suppression with oral contraceptives or progestins, adrenal suppression with glucocorticoids, and the use of antiandrogens.
Diagnostic approach to a case of Hirsutism RANJANDASH12
Hirsutism, or excessive body hair in women, can have significant psychosocial impacts. It is important to distinguish normal variations from true hirsutism through a diagnostic approach involving history, clinical evaluation, and biochemical testing. This helps determine if the cause is ovarian or adrenal hyperandrogenism, which may indicate conditions like PCOS, CAH, or tumors. A thorough workup is needed to identify treatable causes and rule out serious underlying pathology while alleviating psychological distress.
This document provides an overview of hirsutism. It begins with definitions of terms like hirsutism, virilization, and hypertrichosis. It then discusses the causes of hirsutism, which can include polycystic ovary syndrome (PCOS), ovarian tumors, adrenal tumors, and other conditions. The document reviews approaches to clinical evaluation and investigations for hirsutism, including the Ferriman-Gallwey scoring system. It provides guidelines on tests to measure androgens and rule out conditions like congenital adrenal hyperplasia. Overall, the document provides a comprehensive review of hirsutism, including its definition, causes, evaluation, and treatment guidelines.
This document provides an overview of the evaluation and treatment of hirsutism. It discusses the definitions, pathogenesis, causes, clinical evaluation, investigations, and treatment of hirsutism. The major causes of hirsutism include polycystic ovary syndrome (PCOS), non-classical congenital adrenal hyperplasia, and androgen-secreting tumors. Clinical evaluation involves assessing hirsutism severity using the Ferriman-Gallwey score and checking for signs of hyperandrogenism or other disorders. Laboratory investigations can include tests of androgen and gonadotropin levels, and further testing may be needed depending on symptoms and signs. Treatment aims to reduce hair growth
This document summarizes key aspects of hair growth and disorders of excessive hair growth or hirsutism. It discusses the typical hair follicle cycle and differences between vellus and terminal hair. Common causes of hirsutism include polycystic ovary syndrome (PCOS), congenital adrenal hyperplasia, and androgen-secreting tumors. Evaluation involves assessing degree of hair growth and signs of virilization, with lab tests to identify underlying etiology. Treatment aims to suppress androgens and may include weight loss, oral contraceptives, antiandrogens like spironolactone, and sometimes surgery or medication targeting the specific hormone excess.
This document discusses the clinical approach and management of hirsutism and virilism. It defines hirsutism as excessive hair growth in androgen-dependent areas, while virilism is a more severe form involving additional masculine features. The clinical approach involves assessing a patient's history and examination findings to determine the severity and underlying cause. Management aims to remove excess hair, suppress androgens, and remove their source. Treatment options depend on the site of androgen overproduction and may include oral contraceptives, antiandrogens, cosmetic treatments like bleaching or laser, and surgery to remove tumors.
This document discusses androgen excess in females (hirsutism). It begins by defining hirsutism and virilization. It then covers the biology of hair growth and the roles of androgens and estrogens. It discusses the sources and metabolism of androgens in females. The main causes of hirsutism discussed are physiological puberty/pregnancy/menopause), idiopathic, ovarian (PCOS, tumors), and adrenal (CAH, tumors). The evaluation of hirsutism involves history, exam, and lab tests of hormones like testosterone and DHEA. Key tests aim to identify the underlying cause and assess for conditions like PCOS, tumors, CAH
This document discusses hirsutism, which is defined as excessive terminal hair growth in male pattern areas of the body in women. It outlines several potential causes of hirsutism including polycystic ovary syndrome (PCOS), adrenal or ovarian tumors, and congenital adrenal hyperplasia. The document describes evaluating a patient for hirsutism through history, examination, and laboratory tests. Potential treatment approaches are also summarized, including ovarian suppression with oral contraceptives or progestins, adrenal suppression with glucocorticoids, and the use of antiandrogens.
Diagnostic approach to a case of Hirsutism RANJANDASH12
Hirsutism, or excessive body hair in women, can have significant psychosocial impacts. It is important to distinguish normal variations from true hirsutism through a diagnostic approach involving history, clinical evaluation, and biochemical testing. This helps determine if the cause is ovarian or adrenal hyperandrogenism, which may indicate conditions like PCOS, CAH, or tumors. A thorough workup is needed to identify treatable causes and rule out serious underlying pathology while alleviating psychological distress.
This document provides an overview of hirsutism. It begins with definitions of terms like hirsutism, virilization, and hypertrichosis. It then discusses the causes of hirsutism, which can include polycystic ovary syndrome (PCOS), ovarian tumors, adrenal tumors, and other conditions. The document reviews approaches to clinical evaluation and investigations for hirsutism, including the Ferriman-Gallwey scoring system. It provides guidelines on tests to measure androgens and rule out conditions like congenital adrenal hyperplasia. Overall, the document provides a comprehensive review of hirsutism, including its definition, causes, evaluation, and treatment guidelines.
This document provides an overview of the evaluation and treatment of hirsutism. It discusses the definitions, pathogenesis, causes, clinical evaluation, investigations, and treatment of hirsutism. The major causes of hirsutism include polycystic ovary syndrome (PCOS), non-classical congenital adrenal hyperplasia, and androgen-secreting tumors. Clinical evaluation involves assessing hirsutism severity using the Ferriman-Gallwey score and checking for signs of hyperandrogenism or other disorders. Laboratory investigations can include tests of androgen and gonadotropin levels, and further testing may be needed depending on symptoms and signs. Treatment aims to reduce hair growth
This document summarizes key aspects of hair growth and disorders of excessive hair growth or hirsutism. It discusses the typical hair follicle cycle and differences between vellus and terminal hair. Common causes of hirsutism include polycystic ovary syndrome (PCOS), congenital adrenal hyperplasia, and androgen-secreting tumors. Evaluation involves assessing degree of hair growth and signs of virilization, with lab tests to identify underlying etiology. Treatment aims to suppress androgens and may include weight loss, oral contraceptives, antiandrogens like spironolactone, and sometimes surgery or medication targeting the specific hormone excess.
This document discusses the clinical approach and management of hirsutism and virilism. It defines hirsutism as excessive hair growth in androgen-dependent areas, while virilism is a more severe form involving additional masculine features. The clinical approach involves assessing a patient's history and examination findings to determine the severity and underlying cause. Management aims to remove excess hair, suppress androgens, and remove their source. Treatment options depend on the site of androgen overproduction and may include oral contraceptives, antiandrogens, cosmetic treatments like bleaching or laser, and surgery to remove tumors.
This document discusses androgen excess in females (hirsutism). It begins by defining hirsutism and virilization. It then covers the biology of hair growth and the roles of androgens and estrogens. It discusses the sources and metabolism of androgens in females. The main causes of hirsutism discussed are physiological puberty/pregnancy/menopause), idiopathic, ovarian (PCOS, tumors), and adrenal (CAH, tumors). The evaluation of hirsutism involves history, exam, and lab tests of hormones like testosterone and DHEA. Key tests aim to identify the underlying cause and assess for conditions like PCOS, tumors, CAH
Hirsutism _ excesive terminal hair growth in the women on a male pattern distribution-face, body(sexual hear,androgendependent)-common in PCOS
Hypertricosis_ can involve of vellus, lanugo, nonpigmanted hair and terminal hear occupying the entire body surface including the face ( androgen independent disorder)- congenital, caused by drugs, hypothyroidism, anorexia nervosa
Virilization _ production of androgens in women is extremely high (presence of clitoromegaly,alopecia- balding, deepening of the voice- bariphonia, male body habitus)-usually caused by androgen producing tumors, CAH
Acne _ du to hyperceratosis and occlusion of duct of sebaceum gland plus inflammation( multifactoral, androgendependent)
Acanthosis nigricans _ skin grey- brown ,velvety appearance mainly in the neck, axillae,vulva and groin (local hyperpigmentation of skin on specific area-marker of hyperinsulinemia/insulinresistance)
Includes physiological skin changes in pregnancy, specific dermatoses such as intrahepatic cholestasis of pregnancy, polymorphic eruption of pregnancy (pruritic urticarial papules and plaques of pregnancy - PUPP), pemphigoid gestationalis and atopic eruption of pregnancy, as well as non-specific dermatoses ranging from infections, infestations, inflammations and immune disorders.
Powerpoint made by Dr. Jerriton, second year MD post graduate in DVL, SVMC, Pondy.
Hirsutism is excessive hair growth in a male pattern in women. It is caused by excess androgen levels which can be from the ovaries, adrenals, or obesity. Diagnosis involves assessing androgen levels and ruling out conditions like PCOS. Treatment focuses on reducing androgen levels through weight loss, medication to suppress androgen production/action, or removal of hair. Common medications are combined oral contraceptives, spironolactone, flutamide, and finasteride which block androgen receptors or reduce conversion of testosterone to DHT. Laser and electrolysis can permanently remove excess hair.
This document discusses seborrheic dermatitis, a chronic papulosquamous skin condition characterized by yellowish, waxy, branny scaling along areas with sebaceous glands like the scalp, face, and trunk. It commonly affects infants under 3 months of age and adults between 40-70 years old. While the exact cause is unknown, factors like sebum production, microbial effects of Malassezia fungi, and genetic and environmental factors may play a role. The document describes the various clinical presentations in infants and adults and treatments involving topical antifungals, corticosteroids, keratolytics, and systemic antifungals.
This document discusses hirsutism, defined as excessive hair growth in androgen-dependent areas. It covers the physiology of hair growth and androgens, etiologies including PCOS and adrenal/ovarian tumors, diagnosis via Ferriman-Gallway scoring and lab tests, and treatments such as oral contraceptives, GnRH agonists, and androgen receptor antagonists like spironolactone and cyproterone acetate.
This document discusses hyperandrogenism and hirsutism in women. It provides information on:
- Androgens are hormones that stimulate hair growth and their normal levels in women. Common causes of increased androgens include PCOS, tumors, and CAH.
- Clinical manifestations of excess androgens include hirsutism, acne, and alopecia. Hirsutism is assessed using the Ferriman-Gallwey scale.
- PCOS is the most common cause of hirsutism. It is characterized by chronic anovulation, menstrual irregularities, and polycystic ovaries on ultrasound. Increased LH levels lead to elevated androgens
Androgenetic alopecia (AGA) is a nonscarring progressive miniaturization of the hair follicle in genetically predisposed men and women, usually in a specific pattern distribution.
Multifactorial and polygenetic etiology.
Clinical features:
-History of hair loss is -
long standing
slowly progressing reduction of hair density, diameter
Miniaturization of hair
Diminished anagen hair and increased telogen hair
-Pattern of hair loss in male:
Hamilton- Norwood type: recession of frontal hair line, latter followed by a vertex thinning with progression until top of the scalp is completely bald.
-Pattern of hair loss in female:
Centrofrontal hair loss with preservation of frontal hair line
(Ludwig type) {figure - left}
Christmas tree pattern {figure- right}
-Family history of AGA often positive
In female
signs of hyperandrogenism should be evaluated
gynecological history
progesterone containing pills
-To exclude other causes history should be taken regarding-
Thyroid disease,
Surgery, infection in last 6months to 1 year
Drug history
Iron deficiency
Smoking
UV exposure
Hair color, cosmetics use.
Allergic contact dermatitis
Treatment:
Androgenic alopecia is naturally progressive , so main strategy is to prevent progression and increase hair density.
1.Topical minoxidil:
2% for female and 5% spray for male 1 ml twice daily or half cup foam once daily.
There is transitory telogen shedding within first 8 weeks observed.
Response should be assessed after 6 months.
If response occurs, will be continued as main stay of treatment.
2.Finasteride oral ad Dutasteride oral
1 mg finasteride per day prevents progression of AGA .
0.5 mg daily dutasteride is alternative.
Combination of topical minoxidil and finasteride is good option
Response evaluated after 6 months . not indicated in women. Contraindicated in pregnant and child bearing female.
3.Antiandrogen and estrogenic drugs:
Given in hyperandrogenism in female. Not indicated in male.
Spironolactone 100-200 mg daily
Cyproterone acetate can be used
4.Hair transplantation
5.Low-level laser therapy
6.Miscellaneous: low level of evidence.
Platelet rich plasma therapy and microneedling
Herbal preparations
Topical melatonin
Nutritional supplement of- biotin, copper, zinc, aminoacids, micronutrients
The document discusses hyperandrogenism and virilization. It begins by defining androgens and their effects on male characteristics. It then discusses the relationships between hormones and the sources of androgens. Several conditions are covered that can cause hyperandrogenism and virilization including polycystic ovary syndrome (PCOS), Cushing's syndrome, congenital adrenal hyperplasia, and androgen-secreting tumors. The signs, symptoms, causes, and pathophysiology of each condition are described. Laboratory tests and ultrasound are discussed for evaluating patients. Lastly, a case scenario is presented of a woman with irregular periods and potential diagnosis of PCOS is discussed.
The document discusses male infertility, including:
- Spermatogenesis normally takes place in the testes and involves the production of millions of sperm daily.
- Common causes of male infertility include problems with sperm production in the testes, obstruction of the ducts that sperm pass through, hormone imbalances, genetic defects, illness, injury, and lifestyle factors.
- Evaluating male infertility involves assessing medical history, physical exam, semen analysis, and may include hormone testing, imaging of the reproductive organs, and genetic testing to identify underlying causes.
This document discusses polycystic ovarian syndrome (PCOS) and its impact on fertility. It notes that PCOS is the most common cause of infertility in women. The document covers the etiology, signs and symptoms, diagnostic criteria and tests, and treatment options for PCOS. It emphasizes that PCOS is associated with insulin resistance and an increased risk of conditions like diabetes and heart disease. Lifestyle changes including diet and exercise are recommended as first-line treatment, especially for overweight patients. Medications like metformin can also help address insulin resistance and related issues.
Primary amenorrhea is defined as no menstrual periods by age 16. Investigations into primary amenorrhea depend on whether secondary sex characteristics are present or absent. Causes can be physiological, pathological, anatomical, endocrinological, or chromosomal. Common causes include hypothalamic or pituitary disorders, chromosomal abnormalities like Turner's syndrome, congenital adrenal hyperplasia, androgen insensitivity syndrome, or müllerian agenesis. Treatment depends on the underlying cause but may include hormone replacement therapy, vaginal dilation, vaginoplasty, or gonadectomy.
This document provides information on evaluating and treating delayed puberty. It defines delayed puberty and discusses the main causes, which include constitutional delay of puberty, hypogonadotropic hypogonadism, and hypergonadotropic hypogonadism. Evaluation involves assessing medical history, physical exam including Tanner staging, lab tests of hormone levels, bone age, and imaging if needed. Treatment depends on the underlying cause, and may include observation, sex hormone therapy, or treating any underlying medical conditions.
PCOS is the most common endocrinopathy affecting about 5% of reproductive aged women. It is characterized by androgen excess, menstrual irregularity, and polycystic ovaries. While androgen excess in women has been recognized since ancient times, PCOS was first identified and named by Stein and Leventhal in 1935. PCOS is considered a complex, heterogeneous disorder that is likely caused by both genetic and environmental factors. Common features include hyperandrogenism, polycystic ovaries, and insulin resistance. Treatment focuses on managing symptoms like hirsutism, amenorrhea, and infertility and may include lifestyle changes, oral contraceptives, antiandrogens, insulin sensitizers, and fertility treatments.
Melasma| Melasma and its Treatment| Facial Pigmentation| Post-Pregnancy Pigm...Dr. Rajat Sachdeva
Melasma, Pigmentation on facial skin, most commonly occur on the face of female and in Dark Skin Races.
Treatment for melasma, Sun protection, avoid waxing, Tretinoin, Hydroquinone, Corticosteroid, Azeloic Acid, Glycolic Acid, Chemical Peels, Microdermabrasion, Laser Intensed Pulse Light,
Telogen effluvium is a form of nonscarring, diffuse hair shedding caused by systemic stress that pushes a large number of hairs into the telogen or resting phase at the same time. This results in increased shedding when the hairs enter the anagen or growth phase. It can affect both sexes and any age. While it typically affects the scalp, only hair loss from the scalp causes symptoms. Telogen effluvium is usually self-limiting and resolves on its own within 3-6 months, though chronic cases can last over 12 months. Treatment focuses on identifying and removing the underlying cause of stress while reassuring patients.
1) Infertility is defined as the failure to conceive after 12 months of regular unprotected intercourse. The doctor discusses evaluating male factor infertility through history, physical exam, semen analysis, and tests of sperm function.
2) Semen analysis involves assessing physical parameters like volume, pH, and viscosity. Under the microscope, technicians evaluate sperm count, motility, viability, and morphology. Normal ranges are defined for each parameter.
3) Abnormal results in semen analysis can indicate problems from pre-testicular to post-testicular levels, with various treatable causes like genetic factors, infections, or obstructions. A comprehensive evaluation of male fertility aims to identify underlying issues affecting conception.
Biochemistry of Hair fall, A complete review of hair fall cause, Types, Current methods of treatment, Natural methods of treatment,
for more detail text see :https://iiopinion.blogspot.in/2017/01/hair-fall-scientific-way-of-treatment.html
The document discusses three cases of patients presenting with acanthosis nigricans. Acanthosis nigricans is a skin condition linked to insulin resistance and hyperinsulinemia, often seen in obese individuals. It is characterized by thickening and darkening of the skin in body folds and creases. The best treatment is weight loss and exercise to reduce blood insulin levels and correct the underlying endocrinological abnormality.
Developmental anomalies of the reproductive system can occur when the mullerian duct system is disrupted during development in the embryo. The mullerian ducts normally differentiate to form the fallopian tubes, uterus, cervix, and upper vagina. A wide range of anomalies are possible, from complete absence of the uterus and vagina to minor uterine abnormalities. The classification system from the American Fertility Society categorizes mullerian duct anomalies into classes based on dysgenesis of the ducts or disorders involving vertical fusion of the ducts.
This document discusses intrauterine growth restriction (IUGR), including definitions, incidence, classification, etiology, diagnosis, complications, prevention, treatment, and management. Some key points:
- IUGR refers to failure of a fetus to reach its growth potential, putting it at risk of morbidity and mortality. SGA refers to weight below 10th percentile for gestational age.
- Incidence of IUGR is 3-5% of pregnancies. Perinatal mortality is 8-10 times higher for growth restricted fetuses.
- Etiology includes fetal, maternal, and placental factors like infections, vascular problems, and placental insufficiency.
- Diagnosis involves clinical
Hirsutism _ excesive terminal hair growth in the women on a male pattern distribution-face, body(sexual hear,androgendependent)-common in PCOS
Hypertricosis_ can involve of vellus, lanugo, nonpigmanted hair and terminal hear occupying the entire body surface including the face ( androgen independent disorder)- congenital, caused by drugs, hypothyroidism, anorexia nervosa
Virilization _ production of androgens in women is extremely high (presence of clitoromegaly,alopecia- balding, deepening of the voice- bariphonia, male body habitus)-usually caused by androgen producing tumors, CAH
Acne _ du to hyperceratosis and occlusion of duct of sebaceum gland plus inflammation( multifactoral, androgendependent)
Acanthosis nigricans _ skin grey- brown ,velvety appearance mainly in the neck, axillae,vulva and groin (local hyperpigmentation of skin on specific area-marker of hyperinsulinemia/insulinresistance)
Includes physiological skin changes in pregnancy, specific dermatoses such as intrahepatic cholestasis of pregnancy, polymorphic eruption of pregnancy (pruritic urticarial papules and plaques of pregnancy - PUPP), pemphigoid gestationalis and atopic eruption of pregnancy, as well as non-specific dermatoses ranging from infections, infestations, inflammations and immune disorders.
Powerpoint made by Dr. Jerriton, second year MD post graduate in DVL, SVMC, Pondy.
Hirsutism is excessive hair growth in a male pattern in women. It is caused by excess androgen levels which can be from the ovaries, adrenals, or obesity. Diagnosis involves assessing androgen levels and ruling out conditions like PCOS. Treatment focuses on reducing androgen levels through weight loss, medication to suppress androgen production/action, or removal of hair. Common medications are combined oral contraceptives, spironolactone, flutamide, and finasteride which block androgen receptors or reduce conversion of testosterone to DHT. Laser and electrolysis can permanently remove excess hair.
This document discusses seborrheic dermatitis, a chronic papulosquamous skin condition characterized by yellowish, waxy, branny scaling along areas with sebaceous glands like the scalp, face, and trunk. It commonly affects infants under 3 months of age and adults between 40-70 years old. While the exact cause is unknown, factors like sebum production, microbial effects of Malassezia fungi, and genetic and environmental factors may play a role. The document describes the various clinical presentations in infants and adults and treatments involving topical antifungals, corticosteroids, keratolytics, and systemic antifungals.
This document discusses hirsutism, defined as excessive hair growth in androgen-dependent areas. It covers the physiology of hair growth and androgens, etiologies including PCOS and adrenal/ovarian tumors, diagnosis via Ferriman-Gallway scoring and lab tests, and treatments such as oral contraceptives, GnRH agonists, and androgen receptor antagonists like spironolactone and cyproterone acetate.
This document discusses hyperandrogenism and hirsutism in women. It provides information on:
- Androgens are hormones that stimulate hair growth and their normal levels in women. Common causes of increased androgens include PCOS, tumors, and CAH.
- Clinical manifestations of excess androgens include hirsutism, acne, and alopecia. Hirsutism is assessed using the Ferriman-Gallwey scale.
- PCOS is the most common cause of hirsutism. It is characterized by chronic anovulation, menstrual irregularities, and polycystic ovaries on ultrasound. Increased LH levels lead to elevated androgens
Androgenetic alopecia (AGA) is a nonscarring progressive miniaturization of the hair follicle in genetically predisposed men and women, usually in a specific pattern distribution.
Multifactorial and polygenetic etiology.
Clinical features:
-History of hair loss is -
long standing
slowly progressing reduction of hair density, diameter
Miniaturization of hair
Diminished anagen hair and increased telogen hair
-Pattern of hair loss in male:
Hamilton- Norwood type: recession of frontal hair line, latter followed by a vertex thinning with progression until top of the scalp is completely bald.
-Pattern of hair loss in female:
Centrofrontal hair loss with preservation of frontal hair line
(Ludwig type) {figure - left}
Christmas tree pattern {figure- right}
-Family history of AGA often positive
In female
signs of hyperandrogenism should be evaluated
gynecological history
progesterone containing pills
-To exclude other causes history should be taken regarding-
Thyroid disease,
Surgery, infection in last 6months to 1 year
Drug history
Iron deficiency
Smoking
UV exposure
Hair color, cosmetics use.
Allergic contact dermatitis
Treatment:
Androgenic alopecia is naturally progressive , so main strategy is to prevent progression and increase hair density.
1.Topical minoxidil:
2% for female and 5% spray for male 1 ml twice daily or half cup foam once daily.
There is transitory telogen shedding within first 8 weeks observed.
Response should be assessed after 6 months.
If response occurs, will be continued as main stay of treatment.
2.Finasteride oral ad Dutasteride oral
1 mg finasteride per day prevents progression of AGA .
0.5 mg daily dutasteride is alternative.
Combination of topical minoxidil and finasteride is good option
Response evaluated after 6 months . not indicated in women. Contraindicated in pregnant and child bearing female.
3.Antiandrogen and estrogenic drugs:
Given in hyperandrogenism in female. Not indicated in male.
Spironolactone 100-200 mg daily
Cyproterone acetate can be used
4.Hair transplantation
5.Low-level laser therapy
6.Miscellaneous: low level of evidence.
Platelet rich plasma therapy and microneedling
Herbal preparations
Topical melatonin
Nutritional supplement of- biotin, copper, zinc, aminoacids, micronutrients
The document discusses hyperandrogenism and virilization. It begins by defining androgens and their effects on male characteristics. It then discusses the relationships between hormones and the sources of androgens. Several conditions are covered that can cause hyperandrogenism and virilization including polycystic ovary syndrome (PCOS), Cushing's syndrome, congenital adrenal hyperplasia, and androgen-secreting tumors. The signs, symptoms, causes, and pathophysiology of each condition are described. Laboratory tests and ultrasound are discussed for evaluating patients. Lastly, a case scenario is presented of a woman with irregular periods and potential diagnosis of PCOS is discussed.
The document discusses male infertility, including:
- Spermatogenesis normally takes place in the testes and involves the production of millions of sperm daily.
- Common causes of male infertility include problems with sperm production in the testes, obstruction of the ducts that sperm pass through, hormone imbalances, genetic defects, illness, injury, and lifestyle factors.
- Evaluating male infertility involves assessing medical history, physical exam, semen analysis, and may include hormone testing, imaging of the reproductive organs, and genetic testing to identify underlying causes.
This document discusses polycystic ovarian syndrome (PCOS) and its impact on fertility. It notes that PCOS is the most common cause of infertility in women. The document covers the etiology, signs and symptoms, diagnostic criteria and tests, and treatment options for PCOS. It emphasizes that PCOS is associated with insulin resistance and an increased risk of conditions like diabetes and heart disease. Lifestyle changes including diet and exercise are recommended as first-line treatment, especially for overweight patients. Medications like metformin can also help address insulin resistance and related issues.
Primary amenorrhea is defined as no menstrual periods by age 16. Investigations into primary amenorrhea depend on whether secondary sex characteristics are present or absent. Causes can be physiological, pathological, anatomical, endocrinological, or chromosomal. Common causes include hypothalamic or pituitary disorders, chromosomal abnormalities like Turner's syndrome, congenital adrenal hyperplasia, androgen insensitivity syndrome, or müllerian agenesis. Treatment depends on the underlying cause but may include hormone replacement therapy, vaginal dilation, vaginoplasty, or gonadectomy.
This document provides information on evaluating and treating delayed puberty. It defines delayed puberty and discusses the main causes, which include constitutional delay of puberty, hypogonadotropic hypogonadism, and hypergonadotropic hypogonadism. Evaluation involves assessing medical history, physical exam including Tanner staging, lab tests of hormone levels, bone age, and imaging if needed. Treatment depends on the underlying cause, and may include observation, sex hormone therapy, or treating any underlying medical conditions.
PCOS is the most common endocrinopathy affecting about 5% of reproductive aged women. It is characterized by androgen excess, menstrual irregularity, and polycystic ovaries. While androgen excess in women has been recognized since ancient times, PCOS was first identified and named by Stein and Leventhal in 1935. PCOS is considered a complex, heterogeneous disorder that is likely caused by both genetic and environmental factors. Common features include hyperandrogenism, polycystic ovaries, and insulin resistance. Treatment focuses on managing symptoms like hirsutism, amenorrhea, and infertility and may include lifestyle changes, oral contraceptives, antiandrogens, insulin sensitizers, and fertility treatments.
Melasma| Melasma and its Treatment| Facial Pigmentation| Post-Pregnancy Pigm...Dr. Rajat Sachdeva
Melasma, Pigmentation on facial skin, most commonly occur on the face of female and in Dark Skin Races.
Treatment for melasma, Sun protection, avoid waxing, Tretinoin, Hydroquinone, Corticosteroid, Azeloic Acid, Glycolic Acid, Chemical Peels, Microdermabrasion, Laser Intensed Pulse Light,
Telogen effluvium is a form of nonscarring, diffuse hair shedding caused by systemic stress that pushes a large number of hairs into the telogen or resting phase at the same time. This results in increased shedding when the hairs enter the anagen or growth phase. It can affect both sexes and any age. While it typically affects the scalp, only hair loss from the scalp causes symptoms. Telogen effluvium is usually self-limiting and resolves on its own within 3-6 months, though chronic cases can last over 12 months. Treatment focuses on identifying and removing the underlying cause of stress while reassuring patients.
1) Infertility is defined as the failure to conceive after 12 months of regular unprotected intercourse. The doctor discusses evaluating male factor infertility through history, physical exam, semen analysis, and tests of sperm function.
2) Semen analysis involves assessing physical parameters like volume, pH, and viscosity. Under the microscope, technicians evaluate sperm count, motility, viability, and morphology. Normal ranges are defined for each parameter.
3) Abnormal results in semen analysis can indicate problems from pre-testicular to post-testicular levels, with various treatable causes like genetic factors, infections, or obstructions. A comprehensive evaluation of male fertility aims to identify underlying issues affecting conception.
Biochemistry of Hair fall, A complete review of hair fall cause, Types, Current methods of treatment, Natural methods of treatment,
for more detail text see :https://iiopinion.blogspot.in/2017/01/hair-fall-scientific-way-of-treatment.html
The document discusses three cases of patients presenting with acanthosis nigricans. Acanthosis nigricans is a skin condition linked to insulin resistance and hyperinsulinemia, often seen in obese individuals. It is characterized by thickening and darkening of the skin in body folds and creases. The best treatment is weight loss and exercise to reduce blood insulin levels and correct the underlying endocrinological abnormality.
Developmental anomalies of the reproductive system can occur when the mullerian duct system is disrupted during development in the embryo. The mullerian ducts normally differentiate to form the fallopian tubes, uterus, cervix, and upper vagina. A wide range of anomalies are possible, from complete absence of the uterus and vagina to minor uterine abnormalities. The classification system from the American Fertility Society categorizes mullerian duct anomalies into classes based on dysgenesis of the ducts or disorders involving vertical fusion of the ducts.
This document discusses intrauterine growth restriction (IUGR), including definitions, incidence, classification, etiology, diagnosis, complications, prevention, treatment, and management. Some key points:
- IUGR refers to failure of a fetus to reach its growth potential, putting it at risk of morbidity and mortality. SGA refers to weight below 10th percentile for gestational age.
- Incidence of IUGR is 3-5% of pregnancies. Perinatal mortality is 8-10 times higher for growth restricted fetuses.
- Etiology includes fetal, maternal, and placental factors like infections, vascular problems, and placental insufficiency.
- Diagnosis involves clinical
This document provides a differential diagnosis for primary amenorrhea, which is the absence of menstruation by age 16. It lists various potential etiologies categorized as anatomic abnormalities of the genital tract, hypergonadotropic hypogonadism indicating gonadal failure, and hypogonadotropic hypogonadism where the hypothalamus-pituitary axis is affected. It further discusses an approach to evaluating a patient with primary amenorrhea through history, exam, and targeted laboratory and imaging tests to arrive at a diagnosis and guide treatment.
The document provides an overview of forceps delivery. It discusses the history of forceps development from ancient times through modern innovations. It then covers the various types and classifications of forceps, as well as the techniques for low/outlet, mid, and aftercoming head forceps applications. Potential complications of forceps delivery are also mentioned, including disengagement of the head, cord prolapse, and cranial injuries.
This document discusses human papillomavirus (HPV), including its structure, types, life cycle, and role in cervical cancer. Key points include:
- HPV is a small, non-enveloped virus with circular double-stranded DNA. Over 100 types exist, with about 30 causing genital infections.
- Types are classified as low, intermediate, or high risk based on cancer-causing potential. High-risk HPV 16 and 18 cause most cervical cancers.
- HPV spreads through sexual contact and can cause genital warts or remain asymptomatic. Persistent infection can lead to cervical pre-cancer.
- The virus infects epithelial cells and hijacks the host cell cycle to replicate.
This document discusses pregnancy and diabetes. It notes that the prevalence of diabetes among pregnant women is rising. Pregnancy causes insulin resistance and hormonal changes that can lead to gestational diabetes if the pancreas cannot keep up. Good control of blood sugar levels is important for the health of both the mother and baby by avoiding complications like macrosomia. Screening and treatment involve monitoring blood sugar, medical nutrition therapy, exercise, and potentially insulin treatment. Close monitoring is needed throughout pregnancy and delivery.
This document discusses various categories of drugs and their potential teratogenic effects. It notes that Category A drugs have no risk, Category B have no risk in animal studies but inadequate human studies, Category C have potential risks that may outweigh benefits, Category D have proven risks but benefits may outweigh, and Category X are contraindicated. It provides numerous examples of specific drugs that fall into each category and potential fetal effects, such as heart defects from ACE inhibitors, limb defects from retinoids, and hearing loss from aminoglycosides. It emphasizes careful consideration of risks and benefits for the mother and fetus.
This document outlines the protocol for antenatal clinic visits. It recommends that pregnant women have at least 4 checkups - in the first, second, and third trimesters and between 36 weeks and term. The first visit includes registration, history taking, examinations, and basic investigations. Subsequent visits monitor weight, blood pressure, fetal growth and position. Investigations are repeated as needed. The protocol advises on nutrition, rest, medication, symptoms to report, and maternal risk factors identified during antenatal care.
1. Blocked nose or rhinitis occurs in 30% of pregnant women usually in the third month of pregnancy and lasts 1-2 months after delivery.
2. Symptoms include blocked nose, sneezing, runny nose, and nasal itching caused by increased blood flow and hormones like estrogen and progesterone.
3. Treatment options include topical steroid sprays, nasal decongestants, antihistamines, and antibiotics as needed. Surgery is generally postponed until after delivery.
This document discusses sexuality and sexual dysfunction. It covers several topics including the definition of sexuality, factors that influence women's sexual function, models of the female sexual response cycle, physiology of sexual desire and arousal, and risk factors and causes of sexual dysfunction. It also discusses how various medical conditions, drugs, and obstetrics-gynecology problems can influence sexual function.
This document discusses the management of the third stage of labor. It describes signs that the placenta is separating, including the uterus becoming more mobile. It recommends controlled cord traction using the Brandt-Andrews technique to deliver the placenta within 20 minutes to reduce blood loss. If the placenta is not delivered by this method, manual removal may be necessary, especially if there is morbid adherence of the placenta. An injection of syntometrine after delivery can also help reduce postpartum hemorrhage risk. The fundus and blood loss should be monitored after delivery to ensure no placenta fragments are retained.
Surgical management of pph at tertiary centerdrmcbansal
This document provides information on the surgical management of postpartum hemorrhage (PPH) at a tertiary care center. It discusses the definition, causes, incidence, and risk factors of PPH. The key points are:
1. PPH is a leading cause of maternal mortality worldwide, responsible for nearly 30% of maternal deaths in India. Delay in seeking or receiving care contributes to higher mortality.
2. The major causes of PPH are uterine atony (70% of cases), lacerations (20%), and retained placental tissue (10%). Morbidly adherent placentas like placenta accreta are also discussed.
3. Active management of the
This document discusses pulmonary embolism (PE). PE occurs in about 10% of maternal mortality cases and has an incidence of 1 in 7,000 pregnancies. 70% of women who develop PE have a pre-existing deep vein thrombosis (DVT). Massive PE leads to right heart failure and hemodynamic instability when over 50% of the pulmonary arteries are blocked. Investigations to diagnose PE include lung scans, MRI, pulmonary angiography and echocardiography. D-dimer and coagulation tests can also help in diagnosis, while chest X-rays and ECG may show signs of PE. PE treatment focuses on anticoagulation to prevent further clots.
This document summarizes the bioactivity involved in preterm labor. It discusses how preterm labor follows the same four phases of parturition as term labor. Over 50% of preterm births are spontaneous without preterm premature rupture of membranes (PPROM). Factors like genetics, infection, malnutrition, and behavior can increase the risk of preterm delivery. The document then examines the specific mechanisms involved in PPROM, spontaneous preterm labor, uterine overdistension, maternal-fetal stress response, and intrauterine infection that can all contribute to preterm labor initiation.
The document summarizes the key events and hormonal changes that occur during the different phases of the menstrual cycle. It describes how the ovaries, pituitary gland, and endometrium change during the menstrual, proliferative, secretory, and pregnancy phases of the cycle. The hormones estrogen, progesterone, FSH, LH, and hCG are discussed in terms of how they regulate the development and shedding of the endometrium each month.
1) Vacuum and forceps deliveries are indicated for maternal exhaustion, prolonged second stage of labor, or fetal distress.
2) Proper technique using mnemonics like "ABCDEFG" are important to safely perform instrumental deliveries and minimize complications.
3) Potential maternal complications include vaginal lacerations and trauma, while fetal risks include scalp injuries, cephalohematomas, and rarely intracranial hemorrhage. Forceps carry higher risks than vacuum extraction.
1. Cancer of the vulva accounts for 1-5% of all genital cancers and commonly presents as squamous cell carcinoma in elderly women.
2. Staging of vulvar cancer ranges from Stage 0 (preinvasive lesions) to Stage IV (distant metastasis). Treatment depends on staging and may include surgery, radiation, chemotherapy, or a combination.
3. Prognosis depends on factors like tumor size, grade, lymph node involvement, and completeness of excision, with 5-year survival rates ranging from 90% for Stage I to 15% for Stage IV disease.
This document provides information on the normal female pelvis and contracted pelvis. It describes the boundaries, diameters, and planes of the true and false pelvis as well as the pelvic inlet, cavity, and outlet. It discusses anatomical landmarks like the sacral promontory, pubic bones, and ischial spines. Common causes of a contracted pelvis like rickets are mentioned. The Caldwell-Moloy classification system divides pelves into gynecoid, anthropoid, android, and platypelloid types based on transverse diameters.
The document discusses the history and debate around pain relief during childbirth. Originally, some clergy argued that pain relief interfered with God's will. However, Queen Victoria's painless birth using anesthesia influenced public acceptance. The document then describes various pharmacological (parental drugs, inhalational agents, regional blocks) and non-pharmacological (hypnosis, water birth, massage, music) methods for pain relief during labor and their benefits, risks, and mechanisms of action. Regional blocks like epidurals provide effective relief but require medical expertise and monitoring. Non-drug methods like hypnosis, water birth and massage can also help reduce a woman's pain and stress during labor.
This document discusses induction and augmentation of labor. It begins with an introduction that defines induction of labor as artificially stimulating uterine contractions before the onset of labor. Augmentation refers to stimulating inadequate spontaneous contractions.
It then covers the structures and physiology of the cervix and changes during pregnancy. This includes how collagen, elastin, and other components are reorganized to allow for cervical ripening and dilation during labor.
The document also discusses pre-requisites for labor induction like assessing gestational age and fetal wellbeing. It covers methods of assessing cervical status using Bishop's score and variants. The main body of the document will cover methods of cervical ripening and labor induction.
The document discusses hirsutism, which is the abnormal growth of hair in a male pattern on female skin. It defines hirsutism and differentiates it from hypertrichosis and virilization. It covers the causes of hirsutism including conditions like PCOS and tumors. The document outlines the approach to diagnosis through history, exams, and tests. It also discusses the treatment options for hirsutism which aim to control androgens through methods like oral contraceptives, antiandrogens like spironolactone, and laser hair removal.
This document discusses various types and causes of hair loss. It begins by classifying hair loss as scarring vs nonscarring, and diffuse vs localized. Nonscarring hair loss can be caused by telogen effluvium (the most common cause), anagen effluvium, androgenetic alopecia, etc. Triggers of telogen effluvium include stress, medical conditions, nutritional deficiencies, and certain drugs. Evaluation involves history, examination including pull test and trichogram, and basic lab tests. Treatment focuses on identifying and removing triggers when possible as well as medications for specific conditions like minoxidil for androgenetic alopecia.
Secondary amenorrhea is the absence of menses for more than three cycles or six months in women who previously had menses. Pregnancy is the most common cause. The document outlines the step-by-step process for evaluating secondary amenorrhea, including ruling out pregnancy, assessing medical history, performing a physical exam, basic lab tests, and follow-up testing and evaluation if initial results require further investigation. Treatment options are provided for common causes like hyperprolactinemia, ovarian failure, hyperandrogenism, and Asherman's syndrome.
Hirsutism is defined as excessive hair growth in a male pattern in women. It is caused by increased androgen levels and the most common causes are idiopathic hirsutism and polycystic ovary syndrome. Virilization refers to hirsutism accompanied by other signs of androgen excess like acne, balding and deepening of the voice. Investigations aim to determine the cause of excess androgen levels and treatment options include lifestyle changes, cosmetic hair removal techniques, oral contraceptives, anti-androgens and metformin. Hirsutism can negatively impact quality of life and mental health.
This document discusses the anatomy, physiology, and common conditions of hair and nails. It begins by classifying hair types and describing the hair growth cycle. It then discusses specific hair and nail conditions like alopecia areata, androgenetic alopecia, telogen effluvium, hirsutism, hypertrichosis, nail changes due to trauma or systemic disease, and nail infections. Throughout, it provides details on causes, presentations, courses, treatments, and differentials for each condition.
Primary hypogonadism is caused by testicular dysfunction resulting in low testosterone and sperm production. It can be caused by genetic conditions like Klinefelter syndrome, infections, trauma, or chemotherapy/radiation exposure. Physical exam may show small, soft testes and low body hair with high FSH and LH levels. Treatment is testosterone replacement therapy. Secondary hypogonadism results from pituitary or hypothalamic dysfunction, with proportionate low testosterone and sperm production and low or normal FSH and LH levels.
This document discusses excess hair growth. It defines terms like hirsutism, which refers to masculine hair growth patterns in women caused by excess androgen levels. Hypertrichosis refers to generalized increased hair growth all over the body. There are three main causes of excess hair growth: congenital (inherited hair growth patterns), topical (stimulation or friction causing increased growth), and systemic (caused by normal or abnormal hormonal changes). Normal systemic causes include puberty, pregnancy, and menopause, while abnormal causes can be endocrine disorders.
This document discusses androgenic alopecia (pattern hair loss) in adolescents. It notes that the condition can occur as early as age 6 and commonly presents between ages 13-15. Causes include decreased hair follicle size and replacement of terminal hairs with smaller vellus hairs due to interactions between androgens and androgen receptors in hair follicles. Treatment options for adolescents are limited since finasteride and minoxidil are only approved for adults, though low-dose finasteride and minoxidil have shown efficacy. Further evaluation of treatments is needed in adolescents to ensure safety and efficacy.
The document discusses polycystic ovary syndrome (PCOS), the most common cause of hyperandrogenism in women. PCOS is characterized by oligo- and/or anovulation, clinical or biochemical signs of hyperandrogenism, and polycystic ovaries. The pathogenesis involves both genetic and environmental factors like obesity that can increase androgen production and LH levels. Diagnosis is based on meeting at least two of three criteria: irregular periods, clinical or biochemical signs of hyperandrogenism, and polycystic ovaries. Treatment focuses on weight loss, regulating menstrual cycles, reducing hirsutism, and managing related health risks like diabetes.
Hair is an important part of who we are. The average person has 5 million hairs (100,000 – 150,000 are on the scalp). Blonds usually have more hair (about 140,000 hairs), brunettes have slightly higher than average hair (about 105,000 hairs), and redheads have a little less than average (about 90,000 hairs). Hair is composed of keratin, the same protein that nails and the outer layer of skin is made of. Hairs are produced by a small structure underneath the skin called the hair follicle.
Hair follicles are formed while we are still a fetus, and after we are born no new follicles are produced. Hair growth is often regulated by hormones within the body. At puberty, certain male hormones trigger the growth of pubic, underarm, and beard hairs. They can also trigger the start of genetic male pattern hair loss.
Each hair grows in a series of phases. In the growth phase, the hair is continually growing for up to five years. At the end of the growth cycle, there is a transitional phase where the hair does not grow and begins to change into the third phase. The third phase is the resting phase. During this phase, the follicle is no longer growing, and at the end the old hair is pushed out, then the cycle starts over and a new growth phase starts. This happens repeatedly throughout our lives, and is why even people unaffected with hair loss lose 50-100 hairs per day.
In people affected with genetic hair loss, there appears to be a higher number of hormone receptors in the areas of the scalp with hair loss. In most people affected by hair loss, male hormone levels are the same as in normal people, but because there are more receptors in the balding areas of the scalp they are affected as if their hormone levels were higher than normal. Researchers are still working on how the presence of a certain male hormone, Dihydrotestosterone (DHT), causes damage to follicles in people with genetic hair loss. As the follicles are damaged, the hairs grown are thinner and the growth cycles are shorter with each new growth cycle, until eventually no hair or a small, miniaturized hair is all that can be produced. As more and more hairs become smaller and more miniaturized, the person appears balder.
Genetic hair loss causes about 95% of all hair loss. Another main cause is an autoimmune condition known as Alopecia Areata (patchy hair loss), Alopecia Totalis (loss of all hair on the head), and Alopecia Universalis (loss of all hair on the body). Researchers are also working on a treatment for this condition. Other causes include hair loss due to side effects of medication, stress, or dietary deficiency.
The document summarizes research on skin manifestations of endocrine disorders. Two studies found that hirsutism and acanthosis nigricans are reliable signs of polycystic ovary syndrome in women, and that post-adolescent males with acne have higher rates of insulin resistance. The document also reviews other conditions like Cushing's disease, hypothyroidism, and congenital adrenal hyperplasia that can cause skin abnormalities through excess androgen production. It provides details on evaluating and treating patients with skin signs of endocrine disorders.
Telogen effluvium is a nonscarring, noninflammatory form of hair loss caused by an abnormal number of hairs entering the telogen or resting phase after a physiologic or emotional stressor. It presents with diffuse shedding of scalp hair three to five months after the inciting event. The diagnosis is usually made based on history and clinical findings. No treatment is needed as it is self-limited, usually resolving within six months once the underlying stressor is removed.
Disorders of Sex Development (DSD) can occur when sexual development does not follow the typical path from female or male. The presentation discusses DSD, including causes like genetic factors, hormone imbalances, and syndromes. Evaluation involves medical history, physical exam, imaging, labs, and biopsy to determine chromosomal, gonadal and genital characteristics. Management considers gender assignment, surgery, hormones, counseling, and the child's potential for future sexual/reproductive functions and quality of life. Religious and cultural perspectives must also be considered in treatment.
This document defines and discusses three types of abnormal hair growth: superfluous hair growth (unwanted hair), hirsutism (male-pattern hair growth in females caused by excess androgens), and hypertrichosis (overall excessive body hair in both sexes due to genetic factors). Hirsutism occurs in specific male-pattern areas and can be treated with electrolysis, while hypertrichosis involves dense hair growth over the entire body that is not usually treated with electrolysis.
This document summarizes male reproductive anatomy and function. It describes how the testes produce sperm and sex hormones, regulated by LH and FSH from the pituitary gland. Androgens produced by Leydig cells mediate male sexual development and function. Spermatogenesis requires FSH and androgens. The document also discusses evaluating Leydig and Sertoli cell function, puberty, causes of delayed puberty like constitutional delay or hypogonadism, and conditions like Klinefelter's and Turner's syndromes.
This document discusses disorders of sex development (DSD), including normal human sexual differentiation and various DSD conditions. It covers genetic, gonadal, ductal, and genital differentiation disorders. The most common types are 46,XX DSD (such as congenital adrenal hyperplasia) and 46,XY DSD (including androgen insensitivity syndrome and 5-alpha-reductase deficiency). Evaluation, management, counseling considerations, and the Islamic view on DSD treatment are also summarized. The goal is to quickly and correctly assign gender to improve quality of life and relieve family concerns.
This document discusses disorders of sex development (DSD), including normal sexual development and various DSD conditions. It covers the genetic, gonadal, ductal, and genital aspects of human sexual differentiation. The major types of DSD discussed are 46,XX DSD, which includes congenital adrenal hyperplasia, and 46,XY DSD, which includes androgen insensitivity syndrome and 5-alpha-reductase deficiency. Evaluation, investigations, management considerations, counseling, and the Islamic view on DSD management are also summarized.
Diffuse hair loss in women is a common complaint that requires a systematic evaluation. The diagnosis involves a detailed history, scalp examination, hair pull test, blood tests, and sometimes a scalp biopsy. Hair follicle cycling is influenced by internal and external factors, and all types of hair loss except scarring alopecia represent disorders of this cycle. The main differential diagnoses for diffuse female hair loss are telogen effluvium, female pattern hair loss, diffuse alopecia areata, dystrophic anagen effluvium, and psychogenic pseudoeffluvium. Trichoscopy can help differentiate between these conditions by examining hair characteristics. A thorough evaluation is needed since the causes of diffuse female hair loss can
This document discusses cervical intraepithelial neoplasia (CIN), a precancerous condition affecting the cervix. It provides a historical background of CIN and describes the grading system used (CIN 1-3). Risk factors for CIN include HPV infection and early sexual activity. CIN results from abnormal cell growth in the cervix due to HPV infection. Progression from CIN to invasive cancer depends on the grade, with higher grades having greater risk. Diagnosis involves Pap testing, colposcopy, and HPV testing.
Mullerian duct anomalies occur due to abnormal development of the paired mullerian ducts in females during embryological development. The three main phases of mullerian duct development are organogenesis, fusion, and septal resorption. When one or more of these phases are disrupted, it can lead to mullerian duct anomalies such as a bicornuate or septate uterus. Mullerian duct anomalies are diagnosed using imaging modalities like ultrasound, MRI, and hysterosalpingography which allow visualization of the uterine cavity and identification of the specific anomaly present. The most common anomalies include septate uterus, bicornuate uterus, and arcuate uterus.
This document provides information on convulsions during pregnancy. It discusses the different causes of convulsions including eclampsia, epilepsy, infections, tumors, and electrolyte imbalances. Eclampsia is defined as new-onset seizures in a woman with preeclampsia after 20 weeks of gestation. The incidence of eclampsia is higher in developing countries. Magnesium sulfate is the primary treatment for preventing seizures in eclampsia. Management of eclampsia involves controlling blood pressure, delivering the fetus, and preventing further seizures and complications. Epilepsy during pregnancy can increase risks for the fetus but does not necessarily contraindicate breastfeeding with proper monitoring and treatment.
This document provides an overview of assisted reproductive techniques (ART) such as in vitro fertilization (IVF). It discusses the history and definitions of ART and infertility. The major ART procedures described include IVF, gamete intrafallopian transfer, zygote intrafallopian transfer, and intracytoplasmic sperm injection. The document outlines the typical steps of an IVF cycle including ovarian stimulation, oocyte retrieval, fertilization, embryo culture, and transfer. It also discusses factors that influence the success of ART such as maternal age and ovarian reserve.
This document discusses bio activity related to preterm labour. It begins by explaining how uterine quiescence is maintained during pregnancy similarly to term labour, but preterm birth carries risks of neonatal morbidity and mortality. Over 50% of preterm births are idiopathic, while 25% involve preterm premature rupture of membranes (PPROM). The structure and composition of fetal membranes is described in detail. Increased matrix metalloproteinase activity and decreased tissue inhibitor of metalloproteinases lead to inappropriate degradation of the extracellular matrix of fetal membranes, which can cause membrane rupture and preterm birth.
This document discusses USG images taken in the third trimester of pregnancy. It was written by Prof. M.C. Bansal, who has served as the founder principal and controller of Jhalawar Medical College And Hospital in Jhalawar as well as the principal and controller of Mahatma Gandhi Medical College And Hospital in Sitapura, Jaipur. The USG images presented are from Donald School Textbook on Ultra Sonography-1 and William's Obstetrics Textbook for further reference on the topic.
The document discusses wound healing and classification. It describes the phases of wound healing as inflammatory, proliferative, and remodeling. The inflammatory phase begins immediately after wounding and lasts 2-3 days, involving vasoactive amines, growth factors, and inflammatory cells. The proliferative phase lasts from days 3 to 3 weeks, involving fibroblast activity, collagen production, angiogenesis, and re-epithelialization. The remodeling phase begins during proliferation and lasts up to 2 years, involving collagen remodeling and maturation. Healing is classified as primary intention for clean wounds or secondary intention for infected wounds. Factors like age, obesity, smoking, and malnutrition can affect wound healing.
This document discusses various assisted reproductive technologies (ART) such as in vitro fertilization (IVF), gamete intrafallopian transfer (GIFT), and zygote intrafallopian transfer (ZIFT). It provides a brief history of ART and describes techniques like ovarian stimulation protocols, oocyte retrieval, fertilization, embryo culture, and preimplantation genetic diagnosis. Potential indications for ART include tubal factor infertility, endometriosis, and male factor infertility. Success rates are influenced by factors like maternal age and ovarian reserve.
Flow charts for gynaecological conditionsdrmcbansal
This document contains flow charts and diagrams summarizing the diagnosis and management of various gynecological conditions. It includes flow charts for abnormal uterine bleeding, infertility workup, sexual dysfunction, abnormal sexual development, chronic pelvic pain, cervical cancer screening and interpretation, endometrial cancer management, and ovarian cancer treatment. The charts provide an overview of the evaluation and treatment pathways for different gynecological issues.
This document discusses reproductive hormones and their functions. It begins by listing the major endocrine glands and the hormones they produce, including the hypothalamus, pituitary gland, adrenal glands, thyroid gland, pancreas, ovaries, and testes. It then discusses steroid hormones in more detail, describing their basic structures. The rest of the document focuses on estrogen, including its synthesis in the ovaries, metabolism, mechanisms of action, effects on various body systems, common pharmaceutical preparations, clinical uses, and potential side effects.
Organizing an obstetrical critical care unit drmcbansal
The document discusses the need for organizing an obstetrical critical care unit. It notes that 0.5-1% of obstetrical admissions require intensive care, decreasing mortality by 10 times. An obstetrical ICU requires a multidisciplinary team including skilled obstetricians, intensivists, respiratory therapists, trained nursing staff, and clinical pharmacists to provide specialized care for critically ill pregnant patients. The nursing staff in particular requires high-risk obstetric training and a 1:1 nurse to patient ratio is recommended. Protocols and guidelines should be established to ensure standardized, quality care is provided across the multidisciplinary team.
Endocrinology --- control of parturitiondrmcbansal
1. The document discusses various factors involved in maintaining uterine quiescence during pregnancy and initiating labor. It describes how progesterone, relaxin, corticotropin-releasing hormone (CRH), prostaglandins, and other factors work to keep the uterus relaxed.
2. As term approaches, placental signals activate the fetal hypothalamic-pituitary-adrenal axis, increasing cortisol and estrogen production. Falling progesterone levels and rising estrogen allow the uterus to become responsive to contraction stimuli.
3. Uterine contractions in labor involve increased expression of contraction proteins, calcium signaling, and interactions between actin and myosin fibers in myometrial cells. Gap junctions and surface
This document discusses ultrasound examination in pregnancy. It provides information on using ultrasound for diagnostic and screening purposes in different trimesters. In the first trimester, ultrasound can be used to date the pregnancy, detect fetal anomalies, confirm intrauterine pregnancy, and detect ectopic pregnancies or nuchal lucency. Structures like the gestational sac, yolk sac, fetal pole, and heartbeat can be visualized on ultrasound as the pregnancy progresses in the first trimester. Crown rump length is an accurate method for measuring and dating the fetus early in the first trimester.
This document provides information about sexually transmitted infections (STIs). It discusses the definitions and differences between STIs and STDs. It also lists some of the most common bacterial, viral, parasitic and fungal STIs such as chlamydia, gonorrhea, herpes, HIV, and trichomoniasis. The document discusses transmission routes, risk factors, prevalence rates among different age groups, and potential complications of untreated STIs. It also describes some common signs and symptoms of STIs for both males and females.
Imaging in obstetrics & gynaecology part 2drmcbansal
This document discusses ultrasound examination in pregnancy. It provides information on using ultrasound for diagnostic and screening purposes in different trimesters. In the first trimester, ultrasound can be used to date the pregnancy, detect fetal anomalies, confirm intrauterine pregnancy, and detect ectopic pregnancies or nuchal lucency. Structures like the gestational sac, yolk sac, fetal pole, and heartbeat can be visualized on ultrasound as early as 5-6 weeks of gestation. The crown rump length is an accurate way to date the fetus from 6-12 weeks. An increased nuchal translucency between 11-14 weeks may indicate anomalies like aneuploidies or structural defects.
The document discusses the use of MRI in assessing female pelvic organs and genitourinary conditions. MRI provides detailed images of the uterus, ovaries, and surrounding tissues. It can accurately diagnose adenomyosis, uterine anomalies, and characterize fibroids and ovarian cysts. MRI is also useful for staging cervical, endometrial, and ovarian cancers by identifying the extent of tumor invasion and spread to nearby organs or lymph nodes. Due to its safety during pregnancy, MRI can also evaluate obstetric complications and differentiate between benign and malignant tumors that may complicate pregnancy.
The document discusses lasers and their use in gynecology. It provides background on the history and development of lasers, including how they work using stimulated emission and have properties of monochromaticity, directionality, coherence, and a quantum nature. It then discusses the specific applications and effects of lasers in gynecological surgery, noting they are useful surgical tools but require carefully designed studies to understand long-term benefits. Lasers can be used to vaporize, coagulate, or photodisrupt tissue depending on the energy density or fluence applied.
This document discusses sexuality and sexual dysfunction. It begins by defining sexuality as the right to pursue a satisfying and safe sexual life. It then discusses factors that modulate women's sexual function, including hormones, neurotransmitters, and environmental and neuroendocrine interactions. It provides models of women's sexual response cycles and discusses desire, arousal, and orgasm. It also discusses various medical conditions and psychological factors that can influence sexual function and cause sexual dysfunctions in women. The document recommends treatment approaches such as sex education, psychotherapy, medical treatments, and lifestyle modifications to address female sexual dysfunctions.
This document discusses pulmonary tuberculosis in pregnant women. It notes that 30% of global TB cases are in India, and 5% of pregnant women have active TB disease. It outlines symptoms of TB in pregnancy like fatigue, fever, and cough. It discusses evaluating and treating TB in pregnancy, including using directly observed therapy. Side effects on the fetus are considered minimal. Vaginal delivery is generally safe while avoiding certain drugs. Breastfeeding is also generally recommended while taking precautions if the mother has active TB.
This document discusses trauma during pregnancy, its types and management. It begins by describing common causes of trauma like motor vehicle accidents, falls, burns and domestic violence. It then discusses complications of trauma during specific periods of pregnancy. Trauma increases risks of abortion, preterm birth, placental abruption and fetal distress. Motor vehicle crashes are a leading cause while falls commonly occur at home. Management involves stabilizing the mother through aggressive resuscitation since fetal outcomes depend on maternal condition. Investigations may be conducted after weighing risks to fetus from radiation exposure.
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
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2. EXCESSIVE HAIR
GROWTH
IT MAY BE EITHER
HYPERTRICHOSIS—Excess of hair
growth all over the body.
HIRSUTISM—Male type sex hair
growth in females.
VIRILIZATION—Excess sex hair growth
and other hyper androgenic effects on
female genitalia and body.
3. 3
DEFINITION
HYPERTRICHOSIS : REFERS TO HAIR
DENSITY OR LENGTH BEYOND THE
ACCEPTED LIMITS OF THE NORMAL
FOR THE PARTICUALR AGE,RACE
OR SEX.
• The excess hair may be generalised or
localised and may consist of lanugo,
vellus or terminal hair.
• It is frequently associated with the use
of medication such as antiepileptics
4. Inherited types
CONGENITAL HYPERTRICHOSIS
LANUGINOSA – confluent generalised over
growth of silvery blonde to grey lanugo hair
at birth or early infancy, autosomal dominant,
associated dental anomalies.
AMBRAS syndrome- longer thicker hair more
over the face,ears and shoulders, facial
dysmorphism and dental anomalies.
CONGENITAL GENERALISED
HYPERTRCHOSIS – X linked dominant
4
7. 7
DEFINITION
HIRSUTISM : APPEARANCE OF
EXCESSIVE COARSE
(TERMINAL)HAIR IN A PATTERN NOT
NORMAL IN THE FEMALE
Definition highlights the abnormal
distribution of excess hair growth ,such
as facial ,chest or upper abdomen.
11. 11
DEFINITION
VIRILIZATION : REFERS TO CONCURRENT
PRESENTATION OF HIRSUTISM WITH A
BROAD RANGE OF SIGNS SUGGESTIVE
OF ANDROGEN EXCESS,SUCH AS
ACNE,
FRONTOTEMPORAL BALDING,
DEEPENING OF THE VOICE ,
A DECREASE IN BREAT SIZE
CLITORAL HYPERTROPHY
12. 12
INCREASED MUSCLE MASS
AMENORREA / OLIGOMENORRHEA
Virilization is seen less frequently than
hirsutism and may reflect a severe underlying
pathologic condition ,such as Male sex
hormone producing Ovarian / adrenal tumors
Hirsutism and virilization are closely
interlinked and hirsutism may actually be the
first manifestation of a condition that
ultimately will lead to virilization if left
untreated
15. 15
BASIC FACTS ABOUT
HAIR
Each hair follicle develops at about 8-10wks of
gestation as a derivative of epidermis.
Number of hair follicles is set from birth
Hair grows from a individual hair follicle that are
part of a pilosebaceous gland unit
Main difference between sexes is the degree of
differentiation of the hair
Human hair growth is continuous
Hair grows in a mosaic pattern(in a given area ,hair
are in different stages of development)
16. 16
BASIC FACTS ABOUT
HAIR
Some condition may cause a high level
of synchrony between the growth cycles
of hair ,leading to the appearance of
either massive hair loss (alopecia)or
excess hair for a limited period of time
17. 17
BASIC FACTS ABOUT
HAIR
Growth cycle of the Hair: ACT
Anagen : Growth phase,85- 90 % of the life
cycle
Catagen : rapid involution Phase
Telogen : Quiescent phase
The growth phase or the anagen phase is
primarily influenced by disorders that
stimulate hair growth as well as therapeutic
modalities.
18. 18
BASIC FACTS ABOUT
HAIR
Three types of Hair :
Lanugo : Body hair seen in the fetus and
newborn
Vellus : Fine adult hair covering the body
Terminal hair : Thick pigmented hair of scalp
and pubic area
Thickness of the terminal hair varies form one
individual to other depending upon genetic,
and possibly nutritional
19. 19
BASIC FACTS ABOUT
HAIR
Androgen sensitive hair : depend upon
androgen input for hair growth.
Face,neck,chest,abdomen,axillary,upper
arms ,inner thighs and pubic hair,+ part
of the scalp hair.
Less Androgen independent :
Forearms ,hands .lower legs
23. The production rate of
testosterone in the
normal female is
0.2 to 0.3 mg/day
Normal total testosterone
concentration in serum
is below 0.8ng/ml
23
26. 26
PRESENTATION OF
HIRSUTISM
Hirsutism alone is the greatest
challenge,patients usually go to dermatologist
Hirsutism wIth acne is frequently develop in
teenage girls
Hirsutism with ovulatory disorders comes
mostly to gynecologist
Hirsutism with virilization requires immediate
work-up
27. 27
CAUSES OF HIRSUTISM
Excess androgen production
Relative circulating androgen excess
and low binding globulins
Excess end organ response
Patient perception
28. 28
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
Source of androgen :
Exogenous
Endogenous (most common)
Two primary endogenous sources :
Adrenal glands
Ovaries
29. Mechanism of excessive
hair growth
Main stimulus- Testosterone
Testosterone – binds – androgen
receptors
29
Activation of
5 alpha reductase
DHT
TERMINAL HAIR
ANDROSTENEDION
35. Tumor related causes of
hirsutism
Tumors of the ovaries and the adrenal glands secrete excess
hormones including androgen.
Ovarian tumors Adrenal tumors
Granulosa -theca cell tumors Adrenal adenoma
Arrhenoblastoma Adrenal carcinoma
Gonadoblastomas
Lipoid cell tumors ACTH secreting tumors
Dysgerminoma
Brenner's tumor
35
36. 36
COMMON CAUSES OF ECTOPIC ACTH SECRETION
Small cell carcinoma of the lung 50%
Endocrine tumors of foregut origin 35%
Thymic carcinoid
Islet cell tumor
Medullary carcinoma thyroid
Bronchial carcinoid
Pheochromocytoma 5%
Ovarian tumors 2%
37. Miscellaneous causes of
hirsutism
Functional adrenal hyperandrogenism
Hypereactio luteinalis of pregnancy - transient increase
in androgen levels during pregnancy
Thecoma of pregnancy - Transient androgen secreting
tumor during pregnancy
True hermaphroditism - condition where both male and
female internal sex organs are present
37
38. Genetics
There are very obvious family and racial
differences in hirsutism patients. In
some women, the skin is very sensitive
to even low levels of androgens and
their follicles produce primarily terminal
(coarse and dark) hair.
38
39. 39
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
ADRENAL ANDROGEN EXCESS
May be linked to genetically determined
steroid synthesis enzyme deficiency
Malignant adrenal neoplastic process
Other conditions like Cushing’s syndrome
40. 40
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
ADRENAL ANDROGEN EXCESS
Three recognised adrenal enzyme deficiencies :
21 alpha Hydroxylase defieiency
11-beta-Hydroxylase deficiency
3-beta-ol-dehydrogenase deficiency
Classical forms are usually presented in
prenatal or neonatal period as ambiguous
genitalia in female
Nonclassic forms are linked with hirsutism
41. The enzyme deficiency causes
reduction in end-products,
accumulation of hormone
precursors & increased ACTH
production.
The clinical picture reflects the
effects of inadequate production
of cortisol & aldosterone and the
increased production of
androgens & steroid metabolites.
41
44. 44
In less severe forms (late onset CAH)
Genitalia is normal at birth.
Precocious pubic hair &
Clitoromegaly
Excess facial or body hair appear
later in childhood, often accompanied
by tall stature
GIRLS WITH CAH
Varying virilizing symptoms
ranging from oligomenorrhea
to hirsutism and infertility
45. 45
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
21-alpha-Hydroxylase deficiency:
Most common ,<1% to >10%
Prevalence depends on ethnic
origin(common in slavs,1/50 Hispanics 1/40,
ashkenazi jews 1/27
Cushing’s syndrome :Hirsutism with weight gain
and growth retardation as the primary
manifestation,with acne and other cutaneous
problems
48. 48
DISORDERS OF EXCESS
ANDROGEN PRODUCTION
OVARIAN ORIGIN
Most common cause is
POLYCYSTIC OVARIAN SYNDROME
Other
Neoplastic ovarian disease
49. PCOS
In 70-80 % cases of hirsutism
5-10% of women in reproductive age
Fulfills the Rotterdam criteria
Hyperandrogenism
Amenorrhoea /oligomenorrhoea
USG features of PCOD
Anovulation
Infertility
Obesity
49
51. Increased ovarian androgen biosynthesis in the
polycystic ovary syndrome results from abnormalities
at all levels of the hypothalamic–pituitary–ovarian
axis. The increased frequency of luteinizing hormone
(LH) pulses in the polycystic ovary syndrome appears
to result from an increased frequency of
hypothalamic gonadotropin-releasing hormone
(GnRH) pulses.
The latter can result from an intrinsic abnormality in
the hypothalamic GnRH pulse generator, favoring the
production of luteinizing hormone over follicle-
stimulating hormone (FSH) in patients with the
polycystic ovary syndrome, in whom the
administration of progesterone can restrain the rapid
pulse frequency
51
52. . By whatever mechanism, the relative increase in
pituitary secretion of luteinizing hormone leads to an
increase in androgen production by ovarian theca
cells.
Increased efficiency in the conversion of androgenic
precursors in theca cells leads to enhanced
production of androstenedione, which is then
converted by 17 -hydroxysteroid dehydrogenase (17 )
to form testosterone or aromatized by the aromatase
enzyme to form estrone. Within the granulosa cell,
estrone is then converted into estradiol by 17.
52
53. . Numerous autocrine, paracrine, and endocrine factors
modulate the effects of both luteinizing hormone and
insulin on the androgen production of theca cells; insulin
acts synergistically with luteinizing hormone to enhance
androgen production. Insulin also inhibits hepatic synthesis
of sex hormone–binding globulin, the key circulating
protein that binds to testosterone and thus increases the
proportion of testosterone that circulates in the unbound,
biologically available, or "free," state. Testosterone inhibits
and estrogen stimulates hepatic synthesis of sex
hormone–binding globulin. The abbreviation scc denotes
side-chain cleavage enzyme, StAR steroidogenic acute
regulatory protein, and 3 -HSD 3 -hydroxysteroid
dehydrogenase. Solid arrows denote a higher degree of
stimulation than dashed arrows.
53
55. Normal ranges
Total testosterone 20-80 ng/dl
Free testosterone 0.3-1.9 ng/dl
Bioavailable testosterone 0.8- 10 ng/dl
Free androgen index ( T/SHBG x 100)
Androgen producing tumor > 200 ng/dl
55
The Testosterone
level
56. 56
RELATIVE ANDROGEN
EXCESS AND SHBG
<3 % TESTOSTERONE IS FREE
Mostly bound to Sex hormone binding
globuline(SHBG)
Dcrease in SHBG leads to Excess free
Testosterone
Causes of Reduced SHBG :
PCOS(Chronic anovulation) and
Obesity
57. 57
EXCESS REPONSIVITY
TO ANDROGEN
TESTOSTERONE
5-ALPHA –
REDUCTASE
DIHIDROTESTOSTERONE
Excessive response of the receptor to DHT(may be
due to mutation of the highly polymorphic region in
gene of the receptor located on X Chromosome
Over activity of the 5-alpha-reductase (Type –1 and
Type 2,type –1 is involved in hirsutism )
TARGET CELLS
RECEPTOR
59. 59
BASIC APPROACH TO
THE DIAGNOSIS OF
HIRSUTISM AND
VIRILIZATION
SYMPTOMS AND HISTORY
SIGNS
PHYSICAL EXAMINATION
INVESTIGATION
60. 60
APPROACH TO
DIAGNOSIS
Patient may present with ovulatory problems
and hirsutism may not be reported
There may be normal hair pattern but patient
complains about hirsutism
Evident virilization should investigated at
once
61. 61
APPROACH TO
DIAGNOSIS
Careful history regarding the timing of
onset and chronological progression
Precocious puberty with androgen
excess suggests adrenal enzyme
defect
Family history : androgen excess
disorders
62. 62
APPROACH TO
DIAGNOSIS
Physical examination
Establish presence of hirsutism and
quantifying it
Presence of acne and virilization and
rule out hypertrichosis
Skin hyperpigmentation,acanthosis
nigricans suggests insulin
resistance.Often associated with PCOD
63. 63
APPROACH TO
DIAGNOSIS
Measurement of weight and height and
blood pressure: defects relates to
adrenal enzyme defects
Galactorrhoea
Tanner staging : Hirsutism before
Tanner stage 3 to 4 is alarming and
suggests a serious pathology
Visual genital examination for virilization
64. 64
APPROACH TO
DIAGNOSIS
Degree and extent
FERRIMAN GELLWAY SCORE
score
Quantifies the extent of hair growth in 9
most androgenic sensitive sites
Hair growth is graded 0-4 at each site
Score of 8 or more (max 36) indicates
hirsutism
66. 66
APPROACH TO
DIAGNOSIS
INVESTIGATION:
FOR VIRILIZATION :
Work-up focuses of the identification on the
source of androgen excess
Rule out exogenous androgen
Evidence of endogenous androgen excess:
Serum total testosterone
Serum dehydroepiandrosterone sulfate
(DHEAS)
68. 68
Any age
Rapid onset
Hirsutes++
Virilism+
Amenorrhoea
DHEAS ↑↑(>700µg/100ml)
T- normal or ↑
Dexa suppression test- negative
IVP
CT-scan
MRI
Any age
Rapid onset
Hirsutes++
Virilism+
Amenorrhoea
T- ↑( >200 ng/100ml)
DHEAS- normal
Sonography
Laparoscopy
biopsy
ADRENAL TUMOR OVARIAN TUMOR
69. 69
APPROACH TO
DIAGNOSIS
INVESTIGATION :
HIRSUTISM: Goal is to rule out serious
potential life threatening conditions and gain
information that helps in treatment
Evaluation of Androgen excess:
Testosterone ,total preferred
DHEAS
In selected cases : 17-OHP(fasting morning
sample)
70. 70
APPROACH TO
DIAGNOSIS
Evaluation of accompanying medical disorder
Ovulation disorder :FSH,LH
Thyroid dysfunction:TSH
Hyperprolactinemia :PRL
Other investigations ( inselected cases)
Androgen production :Androstenedione,
3-alpha Androstenediol glucuronide
Provocative tests : Corticotropin stimulation
tests,Insulin resistance determination
71. Differentation of
hyperandrogenism
71
Diagnosis Menstrual Total DHAS LH 17OHP Sourse of
Pattern Testoste- Androgen
rone
PCOS Irregular Elevated mildly Elevated Normal OVARY
elevated
CAH Irregular Elevated Often Usually Markedly Adrenals
Normal Normal elevated
Idiopatic Regular Normal Normal Normal Normal Skin
hirsutism
74. 74
THERAPEUTIC OPTIONS
BASIC STEPS OF MANAGEMENT OF
HIRSUTISM ARE:
DEFINE THE PROBLEM
QUANTIFY THE DEGREE OF HIRSUTISM
INDENTIFY THE PATHOPHYSIOLOGY
CORRECT THE PROBLEM,WHETHER
ACUTE OR CHRONIC
DEFINE SUCESSWITH THE PATIENT
FOLLOW UP
76. 76
THERAPEUTIC OPTIONS
GENERAL MEASURES :
Eliminating causative factors
Optimizing weight Weight Reduction
Associated with reduction of hyperinsulinemia
and androgen excess.BMI should not be > 25
Manage hair
Bleaching Cutting or shaving
Electrolysis Laser epilation
78. Removal of the
source
78
Adrenal or ovarian tumour – surgically
treated
Cushing disease –
Adrenalectomy
Radiation to pituitary
Removal of ACTH producing tumor
Iatrogenic cases – Offending drug to
be stopped
79. 79
THERAPEUTIC OPTIONS
Management of excess ovarian androgen
production :
Standard therapy is :combined E+P,most
commonly OCs
It reduces ovarian androgen production
It increases SHBG
It induces competition at the cellular level for
binding to the androgen receptor
80. 80
THERAPEUTIC OPTIONS
Choice of OC
EE + Norgestimate approved in USA
Cyproteroneacetate used as progesterone
component in Ocs
Cyproterone acetate:
A progestin that also has strong antiandrogenic
action.
Inhibits gonadotrophin secretion and interferes with
androgen action on target organs by competing for
androgen receptors
Dosage- 100mg from D5-D14 with ethinyloestradiol
30µg, from D 5 to D25
81. OVARIAN SUPPRESSION BY LONG
ACTING GnRH ANALOGUE
Can be used for functional ovarian
androgen overproduction and even for
malignant condition
But to be used for long with back-up
Treatment is expensive and results are
inconsistent
Use is reserved for patients resisting to
initial therapy.
81
82. 82
THERAPEUTIC OPTIONS
Long acting GnRH analogues used
But there is doubt that this therapy will
be beneficial over Ocs
INSULIN SENSITIZING AGENTS:
For PCO with acanthosis nigicans
Commonly used agent is : Metformin and
Troglitazone,Pioglitazone,Rosiglitazone
83. 83
Drosperinone in PCOS
CLINICAL BENEFITS
Helpful in treatment of Hirsutism
Excellent cycle control
Decreases acne
No weight gain.
METABOLIC BENEFITS
No effect on carbohydrate metabolism
No deterioration in the glycemic and insulinemic
response to glucose load.
No effect on serum lipid concentration.
Safe for long term use
84. 84
THERAPEUTIC OPTIONS
MANAGEMENT OF EXCESS
ADRENAL ANDROGEN PRODUCTION
Metabolic correction of the
disorder,usually with exogenous
steroids
Dexamethasone,mostly used,But
LIMITED ROLE
85. Glucocorticoids
85
Mode of action
Suppress pituitary adrenal axis -
suppression of
endogenous ACTH secretion
Use –
In adrenal or mixed adrenal and
ovarian hyperandrogenism
86. Glucocorticoid Dosage Frequency
Hydrocortisone 10-20 mg Twice daily
Prednisone 2.5-5 mg Nightly or
a
alternate days
Dexamethasone 0.25-0.50 mg Nightly
86
Glucocorticoid preparations used in
monotherapy & combined with antiandrogens
87. 87
THERAPEUTIC OPTIONS
Management directed to the target organ
and cells
Competition with Androgen
receptors:Spironolactone,Flutamide,
Ketoconazole,Cyproterone acetate
5-alpha reductase Inhibitors
:Finasteride
88. 88
CPA
50-100 mg/day on menstrual cycle days
5-15 with ethinyl estradiol 20-35 mg on days 5-25
Spironolactone
100-200 mg/day (given in divided doses twice daily)
Finasteride
2.5-5 mg/day
Flutamide
250-500 mg/day (high dose)
62.5 to - <250 mg (low dose)
DOSES
89. 89
THERAPEUTIC OPTIONS
androgen receptors
competitors
SPIRONOLACTONE:
Best studied and as Gold standard
Mechanism :Androgen receptors blockade
Suppression of Androgen biosynthesis
Increased metabolic clearance of teststerone
( Testosterone Estrogen )
50-200 mg/day in two divided doses
Spironolactone + OC is well established
regimen
90. 90
THERAPEUTIC OPTIONS
androgen receptors
competitors
FLUTAMIDE :
Blocks the androgen receptors
Decreases androgen production
May have therapeutic value in cases of
PCOS
Usually used with Ocs
KETOCONAZOLE:
Equally effective but danger of liver toxicity
Last resort of treatment.
91. CIMETIDINE= 300mg BD
LEAST POTENT ANDROGEN
RECEPTOR BLOCKER
Clinical reports disappointing.
CLINICALLY NOT EFFECTIVE.
91
92. Recent
Eflornithien: vaniqua (13.9% cream)
US FDA approved
It irreversibly inhibits ornithine decarboxylase
(ODC), an enzyme that catalyzes the rate-
limiting step for follicular polyamine synthesis,
which is necessary for hair growth.
Improvement occurs gradually over a period
of 4-8 weeks or longer.
Most reported adverse reactions consisted of
minor skin irritation. 92
93. 93
THERAPEUTIC OPTIONS
SELECTING BEST THERAPY:
Correct underlying medical problem
Correct thyroid/hyperprolactinemia
PCO :oral contraceptives
Ocs + spironolactone is usually the choice
75 –80% patients shows response
Atleast 6 months is needed for evidence of
response
94. Cosmetic treatments for
Hirsutism
94
Bleaching - can cause irritation, purities, skin
discoloration
Shaving - Shaving does not lead to worsening of
hirsutism and is a good short-term solution
for
facial hair.
- Does not affect the rate or duration of
anagen phase, or diameter of hair
- But yields a blunt tip – illusion of thicker hair
Plucking, Waxing - scarring, folliculitis,
hyperpigmentation
Depilatory creams - Irritant dermatitis
Electrolysis - painful, erythema, inflammation,
scarring
Laser
95. 95
THERAPEUTIC OPTIONS
If response is seen in 6 months then
treatment should be continued for
further 6 months and in most cases for
number of years
96. 96
Hirsutism is a symptom of underlying
cause
Commonest cause is PCO
Progression may hint to diagnosing
tumor
Treatment – Medicines/ Cosmetic
To summarise