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Faculty of Medicine - Benha University
Induction of ovulation oral injectable clomiphesne citrate letrozole GNT GnRH unilatral or bilateral ovarian drilling
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Recurrent pregnancy loss (RPL), also referred to as recurrent miscarriage or habitual abortion, is historically defined as 3 consecutive pregnancy losses prior to 20 weeks from the last menstrual period.
Managing recurrent pregnancy loss
Managing recurrent pregnancy loss
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Stage 0 no prolapse - Aa,Ba,Ap,Bp are all at -3 - C or D between tvl and < tvl -2 Stage I most distal portion > 1cm above level of hymen Stage II <1cm proximal to or distal to the plane of hymen Stage III >1cm below the plane of the hymen Stage IV complete eversion, distal portion at least (tvl -2 cm)
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Recurrent pregnancy loss is a significant redroductive medical problem, influencing 2%–5% of couples. ... Throughout the years, proof based medications, for example, surgical correction of uterine abnormalities or asprin and heparin for antiphospholipid syndrome have improved the results for couples with repetitive pregnancy loss.
Recurrent pregnancy loss Presentation by Dr.Laxmi Shrikhande
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gynaecology.Sec amenorrhea.(dr.hana)
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Induction of ovulation oral injectable clomiphesne citrate letrozole GNT GnRH unilatral or bilateral ovarian drilling
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muhammad al hennawy
Recurrent pregnancy loss (RPL), also referred to as recurrent miscarriage or habitual abortion, is historically defined as 3 consecutive pregnancy losses prior to 20 weeks from the last menstrual period.
Managing recurrent pregnancy loss
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Stage 0 no prolapse - Aa,Ba,Ap,Bp are all at -3 - C or D between tvl and < tvl -2 Stage I most distal portion > 1cm above level of hymen Stage II <1cm proximal to or distal to the plane of hymen Stage III >1cm below the plane of the hymen Stage IV complete eversion, distal portion at least (tvl -2 cm)
Classification & conservative surgeries for prolapse
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Recurrent pregnancy loss is a significant redroductive medical problem, influencing 2%–5% of couples. ... Throughout the years, proof based medications, for example, surgical correction of uterine abnormalities or asprin and heparin for antiphospholipid syndrome have improved the results for couples with repetitive pregnancy loss.
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In cases of Nulliparous prolapse or even patients deserving child bearing uterus preserving surgeries are done. Recently even for prolapse if women want to preserve uterus for variety of reasons ,with newer minimally invasive methods it is now gaining popularity.Larger studies and longer followup is required.
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5-year survival of GCP after radical procedures significantly depended on: 1) PT “early-invasive cancer”; 2) PT N0--N12; 3) Cell Ratio Factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) GC cell dynamics; 9) GC characteristics; 10) tumor localization; 11) anthropometric data; 12) surgery type. Optimal diagnosis and treatment strategies for GC are: 1) screening and early detection of GC; 2) availability of sufficient quantity of experienced abdominal surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunotherapy for GCP with unfavorable prognosis.
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Dr. Faiza delivers an insightful lecture on the distinguishing characteristics of skeletal, smooth, and cardiac muscles, offering a comprehensive understanding of their histology, physiological anatomy, electrophysiological properties, and contractile mechanisms. Through meticulous tabulation and comparison, she aims to equip learners with a detailed comprehension of the unique features and functionalities of each muscle type. Beginning with a detailed exploration of histological differences, Dr. Faiza outlines key distinctions such as multinucleation in skeletal muscle, mononucleation in smooth and cardiac muscles, and the presence of striations in skeletal and cardiac muscles. She meticulously elucidates the structural arrangement of each muscle type, highlighting their cellular morphology and organization within tissues. Transitioning to physiological anatomy, Dr. Faiza navigates through various aspects including innervation, level of control, initiation of contraction, and modification by hormones. By delineating the role of the somatic nervous system in skeletal muscle control, and contrasting it with the autonomic nervous system's influence on smooth and cardiac muscles, she offers a nuanced understanding of neural regulation in muscle physiology. Furthermore, Dr. Faiza delves into electrophysiological properties, elucidating the mechanisms underlying action potential generation, duration, and ionic basis in each muscle type. Through insightful analysis, she reveals how differences in action potential characteristics contribute to variations in muscle contraction speed, duration, and resistance to fatigue. Finally, Dr. Faiza meticulously examines the contractile mechanisms of skeletal, smooth, and cardiac muscles, shedding light on the sliding filament theory, mechanisms of calcium action, and speed of contraction. By comprehensively comparing these mechanisms, she provides learners with a deep understanding of the intricate processes governing muscle contraction and function. Through engaging presentation and meticulous analysis, Dr. Faiza's lecture serves as a valuable resource for students seeking a thorough understanding of the fundamental differences between skeletal, smooth, and cardiac muscles.
Difference Between Skeletal Smooth and Cardiac Muscles
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MedicoseAcademics
These are simplified slides discussing the regulation of cardiac output and venous return. Learning objectives: 1. Comprehend the determinants of cardiac output and factors affecting cardiac output 2. Comprehend the factors affecting stroke volume and heart rate and total peripheral resistance 3. Identify the factors regulating venous return 4. Discuss the causes of high and low output cardiac failure 5. Enlist the functions of veins and recognise the significance of venous reservoirs Study Resources: 1. Chapter 20, Guyton and Hall Textbook of Medical Physiology, 14th edition 2. Chapter 30 and 32, Ganong’s Review of Medical Physiology, 26th edition 3. Chapter 10, Human Physiology by Lauralee Sherwood, 9th edition 4. Physiology, Cardiac Output - StatPearls https://www.ncbi.nlm.nih.gov/books/NBK470455/
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Cardiac Output, Venous Return, and Their Regulation
MedicoseAcademics
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Amenorhea
1.
Amenorrhoea Prof. Aboubakr Elnashar Benha university hospital, Egypt elnashar53@hotmail.com Aboubakr Elnashar CONTENTS 1. INTRODUCTION 2. CLASSIFICATIONS 3. CAUSES 4. DIAGNOSIS 5. TREATMENT 5 Aboubakr Elnashar
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Sequence Of Menstruation CNS IV. Hypothalamus GnRh III. Ant. Pituitary FSH + LH II. Ovary E + P I. Uterus & outflow tract V. Others Aboubakr Elnashar 2. CLASSIFICATIONS • According to the onset: • Primary amenorrhea. • Secondary amenorrhea. • According to the cause: • Physiological. • Pathological • According to Hidden or apparent: • False amenorrhea (Crypto menorrhea). • True amenorrhea. • According to level of LH/FSH • Hypogonadptophic • Eugonadotrophic • Hypergonadotophic • These are complementary to each other Aboubakr Elnashar
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▪ Primary: ▪ Lack of menstruation by age ▪ 16 in the presence of 2ndry " sexual characteristics or ▪ 14 in their absence. ▪2ndary: ▪ Absence of menstruation for a time equivalent to a total of 3 previous cycles or 6 months. ±: diagnostic error & should be avoided. Aboubakr Elnashar Primary Amenorrhoea Aboubakr Elnashar
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2ndry Amenorrhoea Aboubakr Elnashar ▪ The commonest causes Primary Amenorrhoea ▪ Turner’s syndrome ▪ Abscent vagina ▪ Gn deficiency ▪ Constitutional delay Secondary Amenorrhoea ▪ Pregnancy ▪ PCOS ▪ Hyperprolactinemia ▪ POI Aboubakr Elnashar
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3. CAUSES I. Physiological causes •Pregnancy: must always be excluded. •Lactation. •Menopause. II. Iatrogenic causes •Progestagenic contraceptives: Depo-Provera", Mirena IUS*, Nexplanon*, POP. •Therapeutic progestagens •Continuous COCP use •GnRH analogues Aboubakr Elnashar Physiologic causes Aboubakr Elnashar
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Compartment II: Disorders of the Ovary Compartment I: Disorders of the Outflow Tract Compartment IV: Hypothalamic Disorders Compartment III: Disorders of the Anterior Pituitary Eugonadism Hypogonadotropic hypogonadism Hypogonadotropic hypogonadism Hypergonadotropic hypogonadism Normogonadotropic Hypogonadism(PCOD) Aboubakr Elnashar ▪ Pathological causes I. Anatomic: Genital tract outflow obstruction: ▪Congenital 1. Imperforate hymen 2. Transverse vaginal septum 3. Cervical stenosis 4. Agenesis of uterus & mulerian duct structures: sporadic or associated with AIS. ▪Acquired 1. Asherman's syndrome (intrauterine adhesions). 2. TB 3. Surgery II. Hormonal/Endocrinologic 1. Hpogonadotropic 2. Normogonadotropic 3. Hypergonadotropic Aboubakr Elnashar
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Speroff et al, 2020 Aboubakr Elnashar ❑Imperforate hymen ▪ Complaint 1. Cyclic abd. pain ▪ for almost a year with lack of menses ▪ colicky in nature 2. Vomiting 3. Urine retention 4. Severe back pain 5. Swelling of the lower abdomen Aboubakr Elnashar
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▪ Local ex. ▪ Bluish bulging imperforate hymen ▪ At the proper examining position ▪ U/S examination ▪ Cystic pelvic mass extending to the abdomen. ▪ Tender during examination ▪ Trans perineal U/S with trans rectal U/S confirm the thickness of the Hymen and the diagnosis. Aboubakr Elnashar ❑ Androgen Insensitivity Syndrome ▪Axillary&pubic hair do not develop or spare ▪{resistance to testosterone}. ▪46 XY ❑ Asherman Syndrome Aboubakr Elnashar
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II. Hormonal Aboubakr Elnashar I. Aboubakr Elnashar
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Aboubakr Elnashar MRI: pituitary macroadenoma (classic "snowman" appearance of the bi-lobed pituitary MRI: pituitary microadenoma (arrows).Coronal image. Aboubakr Elnashar
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II. Aboubakr Elnashar • NI (1990) ▪ Chronic anovulation. ▪ Cl and/or biochemical hyperandrogenism. Rotterdam (2003) 2 out of 3 ▪ Ch anovulation. ▪ Cl and/or biochemical hyperandrogenism. ▪ PCO on US AES (2006) AE-PCOS(2009) ▪ Cl and/or biochemical hyperandrogenism. ▪ Ovarian dysfunction (anovulation and/or PCO) ▪ Exclusion of related ovulatory or other androgen excess disorders (e.g., thyroid dysfunction, hyperprolactinemia, androgen-secreting neoplasms, or non classic adrenal hyperplasia) 8% 18% 12% Prevalence of PCOS Aboubakr Elnashar
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Aboubakr Elnashar ❑ Late onset congenital adrenal hyperplasia HLA Manifestations Incidence Subtype BW 14 Amenorrhea, Hirsutism +++ Late-onset BW 51 Virilization ++ Simple virilizing BW 47 Virilization, Salt loss + Salt-loosing Aboubakr Elnashar
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Centripetal obesity 79-97 Facial plethora 50-94 Glucose intolerance 39-90 Weakness, proximal myopathy 29-90 Hypertension 74-87 Psychological changes 31-86 Easy bruisability 23-84 Hirsutism 64-81 Oligomenorrhea or amenorrhea 55-80 Acne, oily skin 26-80 Abdominal striae 51-71 Ankle edema 28-60 Backache, vertebral collapse, fracture rare Clinical manifestations % ❑ Cushing syndrome Aboubakr Elnashar ❑ Crushing’s Syndrome Aboubakr Elnashar
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III. Aboubakr Elnashar ❑ Turner syndrome Turner’s stigmata ▪ Sexual infantilism ▪ Short stature ▪ Webbed neck ▪ Spaced nipples ▪ Cubitus valgus ▪ Shield chest ▪ Pigmented nevi ▪ Coarctation of aorta ▪ Renal anomaly ▪ Streak gonads Turner’s Karyotype XO XO/XX XXp- XXr Aboubakr Elnashar
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Aboubakr Elnashar Turner's S. Aboubakr Elnashar
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Mosaic (46-XX / 45-XO) (Classic 45-XO) Turner’s syndrome Aboubakr Elnashar 4. DIAGNOSIS I. History ▪Present 1. Sexual activity, risk of pregnancy 2. Type of contraceptive used. 3. Galactorrhoea 4. Androgenic symptoms: weight gain, acne, hirsutism 5. Menopausal symptoms: night sweats, hot flushes 6. Issues with eating or excessive exercise. ▪Past 1. Drug use: dopamine antagonists 2. Genital tract surgery: intrauterine instrumentation Aboubakr Elnashar
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II. Examination ▪General: 1. BMI <17/>30 2. Hirsutism 3. Stigmata of endocrinopathies: thyroid Turner's syndrome. 4. Evidence of virilization: deep voice, male pattern, balding, cliteromegaly 5. 2° sexual characteristics (Tanner staging). Aboubakr Elnashar ▪ Abdominal: ▪ Masses due to tumours ▪ Genital tract obstruction. ▪ Pelvic 1. Imperforate hymen 2. Blind ending vaginal septum 3. Absence of cervix and uterus. Aboubakr Elnashar
18.
▪ Progestin challenge test: ▪ (MPA 5mgX5d or P in oil 100 mg /3d X 3) ▪ +ve: Anovulation ▪ -ve: E + P: ▪ -ve: outflow or uterine failure → HSG, hysteroscopy, IVP & laparoscopy. ▪ +ve: Ovarian failure or pituitary-hypothalamic dysfunction. Aboubakr Elnashar Progesterone challenge test Bleeding No bleeding Chronic anovulation e.g PCOS Combined oestrogen & progesterone Bleeding No bleeding Ovarian failure Serum FSH Primary Secondary Uterine factor Aboubakr Elnashar
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▪ limitations. 1. Women with high androgen levels, (such as occurs with PCOS and CAH,) may have an atrophic endometrium and may fail to bleed. Specifically, up to 20% of women in whom estrogen is present will fail to bleed following progesterone withdrawal (Rarick, 1990) 2. Estrogen levels may fluctuate both in hypothalamic amenorrhea and in the early stages of ovarian failure: patients with these disorders may have at least some bleeding after progesterone withdrawal. Namely, menses may be observed after progesterone administration in up to 40% of women with hypothalamic amenorrhea due to stress, weight loss, or exercise and in up to 50% of women with POI (Nakamura, 1996). This bleeding derives from endometrium that grew prior to amenorrhea onset. ▪ Use of this test is best restricted to those situations in which accurate serum hormone measurements are unavailable. Aboubakr Elnashar II. Investigations: ▪ modified by patient history and physical examination. ▪Lab: ▪Pregnancy test. All reproductive-aged women with amenorrhea and a uterus are assumed pregnant until proven otherwise ▪Prolactin should always be tested ▪TSH ▪FSH/LH: ▪ inc in POF ▪ dec in hypothalamic causes ▪ not useful in PCOS ▪ Testosterone& (SHBG): most useful for PCOS. Aboubakr Elnashar
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▪Pelvic ultrasound: •congenital abnormalities •Asherman's syndrome •Haematometra •PCOS morphology •Physiological activity or endometrial atrophy in POF. ▪Karyotype if uterus absent or suspicion of Tumer's syndrome ▪Specific tests for endocrinopathies where there is clinical suspicion. Aboubakr Elnashar William gynecology, 2019) Aboubakr Elnashar
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Aboubakr Elnashar IHH = idiopathic hypogonadotropic hypogonadism Aboubakr Elnashar
22.
Aboubakr Elnashar Aboubakr Elnashar
23.
5. MANAGEMENT ▪Must be guided by the diagnosis and fertility wishes. ▪Obese or under wt: attain normal BMI. ▪Hyperprolactinaemia: Cabergoline or surgery ▪PCOS: Cyclical withdrawal bleeds (COCP ) ▪POI: HRT ▪Genital tract obstruction: ▪ cervical dilation ▪ hysteroscopic resection ▪ incision of hymen. ▪Endocrinopathies & tumours: TT ▪Major congenital abnormalities, AIS: multidisciplinary teams Aboubakr Elnashar Imperforate hymen Hymenotomy or curiciate incision Aboubakr Elnashar
24.
Thanks Aboubakr Elnashar Oligomenorrhoea Aboubakr Elnashar Aboubakr Elnashar
25.
DEFINE ▪Cycles are longer than 32 days ▪anovulation or intermittent ovulation. ❑Transient oligomenorrhoea common stress' or emotionally related causes usually self-limiting. Aboubakr Elnashar CAUSES ▪Similar to many of the causes of 2 º amenorrhoea: 1. PCOS is the commonest cause 2. Borderline low BMI. 3. Obesity without PCOS. 4. Ovarian resistance: anovulation e.g. incipient POF. is rare, but important, 5. Milder degrees of hyperprolactinaemia 6. Mild thyroid disease. Aboubakr Elnashar
26.
MANAGEMENT What does the patient want? Regular periods or fertility? 1. Provide reassurance. 2. Treat any underlying causes 3. It is not uncommon for no cause to be found, but serious pathology must be excluded. 4. Attain normal BMI (weight loss or gain as appropriate). Aboubakr Elnashar ▪Provide regular cycles: 1. COCP or cyclical progestagens 2. PCOS a minimum of 3 periods/yr {avoid the risk of endometrial hyperplasia due to unopposed oestrogen}. ▪Full fertility screening should be performed if ovulation induction is required Aboubakr Elnashar
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