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5
74

Management of Menorrhagia

 
Dr Ben Savage
about 12 years ago
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5
58

Polycystic Ovarian Syndrome

I made this ppt several years ago, so some of the information may be outdated...  
AMIT ABRAHAM
about 9 years ago
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5
230

Pre-Eclampsia and Hypertensive Disease in Pregnancy

Based on presentation I gave as a medical student doing Obstetrics and Gynaecology in 2009. More details pertaining to each slide are in the Notes sections.  
Tariq Shafi
over 8 years ago
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5
114

Rh isoimmunisation

This is a very rare condition in the field of obstetics. This will be useful for both undergraduate and post graduate students of obstetrics.  
chaduvula
about 7 years ago
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5
161

Development of Male vs. Female Genitalia (USMLE Tutorial)

http://www.usmlesuccess.net A look at the way by which males and females develop their genitalia while in utero - very high-yield USMLE material. Grab your F...  
YouTube
almost 8 years ago
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5
80

Demystifying Medicine: Sexually Transmitted Diseases

Includes the presentation of patients, pathology and diagnosis.  
YouTube
over 7 years ago
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5
182

A Guide to Preeclampsia: Hand-drawn Tutorial

All credit for this video goes to professor May. If there is anything on it that sounds inspirational, it most likely came from her.  
YouTube
about 7 years ago
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5
76

Pre-Eclampsia Management

 
thewomens.r.worldssl.net
almost 7 years ago
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5
19

Recurrent miscarriage: psychological and relational consequences for couples.

Psychol Psychother. 2006 Dec;79(Pt 4):585-94.  
ncbi.nlm.nih.gov
over 6 years ago
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5
123

Gestational Diabetes: Detection, Management and Implications

These pages are best viewed with Netscape version 3.0 or higher or Internet Explorer version 3.0 or higher. When viewed with other browsers, some characters or attributes may not be rendered correctly.  
journal.diabetes.org
over 6 years ago
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5
34

Obstetrics - Umbilical Artery Doppler

When to use and how to interpret an umbilical artery doppler  
youtube.com
over 5 years ago
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4
105

Advanced cervical cancer and renal failure

A presentation for palliative care and oncology  
James Harper
about 13 years ago
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4
79

Balanced Translocation

A fictional case based presentation themed around Christmas to explain the significance of Balanced Translocations in Miscarriage.  
Alison Teo
almost 11 years ago
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4
202

Diagnostic Testing for Bacterial STDs and UTIs

This is a chart including testing information to differentiate between different bacteria causing STDs and UTIs. It also includes urine dipstick testing. Pink is gram negative bacteria and blue is gram positive. The document is in word format so it can be changed and updated as needed.  
A Wallace
over 7 years ago
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4
101

Gestational Diabetes and Diabetes in Pregnancy

Resistance to insulin is a normal physiological response in pregnancy, thought to be induced by maternal hormones.  However, in some women, this is severe enough to result in gestational diabetes. In these women, there is reduced ability of the pancreas to produce enough insulin to overcome the insulin resistance.   Gestation diabetes is defined as - Any hyperglycaemia with first onset or presentation during pregnancy    
almostadoctor.com - free medical student revision notes
almost 8 years ago
Foo20151013 2023 2njk5o?1444774020
4
1355

LWW: Case Of The Month - April 2013

This month’s case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e, with 15% off using the discount code: MEDUCATION. The case below is followed by a quiz question, allowing you a choice of diagnoses. Select the one letter section that best describes the patient’s condition. The Case A 28-year old woman has an unremarkable pregnancy through her first 28 weeks of gestation, with normal weight gain and no serious complications. She has no previous history of diabetes, hypertension of other systemic disease before or during her current pregnancy. During her 30-week checkup, her blood pressure measures 128/85, and she complains about feeling slightly more “bloated” than usual with swelling in her legs that seems to get more uncomfortable as the day goes on. Her obsterician recommends that she get more bed rest, stay off her feet as much as possible and return for evaluation in one week. At the one-week follow-up, the patient presents with noticable”puffiness” in her face, and a blood pressure of 145/95. She complains she has been developing headaches, sporadic blurred vision, right-sided discomfort and some shortness of breath. She has gained more than 10 lb (4.5kg) in the past week. A urinalysis on the patient revelas no glucose but a 3+ reading for protein. Her obstetrician decides to admit her immediately to a local tertiary care hospital for further evaluation. Over the next 24 hours, the patient’s urine output is recorded as 500mL and contains 6.8 grams of protein. Her plasma albumin level is 3.1 g/dl, hemacrit 48%, indirect bilirubin 1.5mg/dl and blood platelets=77000/uL, respectively. Her blood pressure is now 190/100. It is decided to try to deliver the foetus. The expelled placenta is small and shows signs of widespread ischmic damage. Within a week of delivery, the mother’s blood pressure returns to normal, and her oedema subsides. One month later, the mother shows no ill effects of thos later-term syndrome. Question What is the clinical diagnosis of this patient’s condition and its underlying pathophysiology? A. Gestational Hypertension B. Preeclampsia C. Gestational Diabetes D. Compression of the Inferior Vena Cava Answer The correct answer is "B. Preeclampsia". The patient’s symptoms and laboratory findings are consistent with a diagnosis of Preeclampsia, which is a condition occurring in some pregnancies that causes life-threatening organ and whole body regulatory malfunctions. The patient’s negative urine glucose is inconsistent with gestational diabetes. Gestational hypertension or vena caval compression cannot explain all of the patient findings. The patient has three major abnormal findings- generalised oedema, hypertension and proteinuria which are all common in preeclampsia. Although sequalae of a normal pregnancy can include water and salt retention, bloating, modest hypertension and leg swelling (secondary to capillary fluid loss from increased lower limb capillary hydrostatic pressure due to compression of the inferior vena cava by the growing foetus/uterus), oedema in the head and upper extremities, a rapid 10 pound weight gain and shortness of breath suggests a generalized and serious oedematous state. The patient did not have hypertension before or within 20 weeks gestation (primary hypertension) and did not develop hypertension after the 20th week of pregnancy with no other abnormal findings (gestational hypertension). Hypertension with proteinuria occurring beyond the 20th week of pregnancy however is a hallmark of preeclampsia. In addition, the patient has hemolysis (elevated bilirubin and LDH levels), elevated liver enzyme levels and thrombocytopenia. This is called the HELLP syndrome (HELLP = Hemolysis, Elevated Liver enzymes and Low Platelets.), and is considered evidence of serious patient deterioration in preeclampsia. A urine output of 500 ml in 24 hours is 1/2 to 1/4 of normal output in a hydrated female and indicates renal insufficiency. Protein should never be found in the urine and indicates loss of capillaries integrity in glomeruli which normally are not permeable to proteins. The patient has substantial 24 urine protein loss and hypoalbuminemia. However, generally plasma albumin levels must drop below 2.5 gm/dl to decrease plasma oncotic pressure enough to cause general oedema. The patient’s total urinary protein loss was insufficient in this regard. Capillary hyperpermeability occurs with preeclampsia and, along with hypertension, could facilitate capillary water efflux and generalized oedema. However myogenic constriction of pre-capillary arterioles could reduce the effect of high blood pressure on capillary water efflux. An early increase in hematocrit in this patient suggests hemoconcentration which could be caused by capillary fluid loss but the patient’s value of 48 is unremarkable and of little diagnostic value because increased hematocrit occurs in both preeclampsia and normal pregnancy. PGI2, PGE2 and NO, produced during normal pregnancy, cause vasorelaxation and luminal expansion of uterine arteries, which supports placental blood flow and development. Current theory suggests that over production of endothelin, thromboxane and oxygen radicals in preeclampsia antagonize vasorelaxation while stimulating platelet aggregation, microthrombi formation and endothelial destruction. These could cause oedema, hypertension, renal/hepatic deterioration and placental ischemia with release of vasotoxic factors. The patient’s right-sided pain is consistent with liver pathology (secondary to hepatic DIC or oedematous distention). Severe hypertension in preeclampsia can lead to maternal end organ damage, stroke, and death. Oedematous distension of the liver can cause hepatic rupture and internal hemorrhagic shock. Having this patient carry the baby to term markedly risks the life of the mother and is not considered current acceptable clinical practice. Delivery of the foetus and termination of the pregnancy is the only certain way to end preeclampsia. Read more This case is by David R Bell PhD, co-author of Medical Physiology: Principles for Clinical Medicine, 3e (ISBN: 9781451110395) For more information, or to purchase your copy, visit: http://tiny.cc/Rhoades4e. Save 15% (and get free P&P) on this, and a whole host of other LWW titles at (lww.co.uk)[http://lww.co.uk] when you use the code MEDUCATION when you check out! About LWW/ Wolters Kluwer Health Lippincott Williams and Wilkins (LWW) is a leading publisher of high-quality content for students and practitioners in medical and related fields. Their text and review products, eBooks, mobile apps and online solutions support students, educators, and instiutions throughout the professional’s career. LWW are proud to partner with Meducation.  
Lippincott Williams & Wilkins
almost 9 years ago
Foo20151013 2023 1u6up6r?1444774235
4
137

Keep on Truckin’

Shattered. Third consecutive day of on-calls at the birth centre. I’m afraid I have little to show for it. The logbook hangs limply at my side, the pages where my name is printed await signatures; surrogate markers of new found skills. Half asleep I slump against the wall and cast my mind back to the peripheral attachment from which I have not long returned. The old-school consultant’s mutterings are still fresh: “Medical education was different back then you see....you are dealt a tough hand nowadays.” I quite agree, it is Saturday. Might it be said the clinical apprenticeship we know today is a shadow of its former self? Medical school was more a way of life, students lived in the hospital, they even had their laundry done for them. Incredulous, I could scarcely restrain a chuckle at the consultant’s stories of delivering babies while merely a student and how the dishing out of “character building” grillings by their seniors was de rigeur. Seldom am I plied with any such questions. Teaching is a rare commodity at times. Hours on a busy ward can bear little return. Frequently do I hear students barely a rotation into their clinical years, bemoan a woeful lack of attention. All recollection of the starry-eyed second year, romanced by anything remotely clinical, has evaporated like the morning dew. “Make way, make way!...” cries a thin voice from the far reaches of the centre. A squeal of bed wheels. The newly crowned obs & gynae reg drives past the midwife station executing an impressive Tokyo drift into the corridor where I stand. Through the theatre doors opposite me he vanishes. I follow. Major postpartum haemorrhage. A bevy of scrubs flit across the room in a live performance of the RCOG guidelines for obstetric haemorrhage. They resuscitate the women on the table, her clammy body flat across the carmine blotched sheets. ABC, intravenous access and a rapid two litres of Hartmann’s later, the bleeding can not be arrested by rubbing up contraction. Pharmacological measures: syntocinon and ergometrine preparations do not staunch the flow. Blood pressure still falling, I watch the consciousness slowly ebb from the woman’s eyes. Then in a tone of voice, seemingly beyond his years, the reversely gowned anaesthetist clocks my badge and says, “Fetch me the carboprost.” I could feel an exercise in futility sprout as I gave an empty but ingratiating nod. “It’s hemabate....in the fridge” he continues. In the anaesthetic room I find the fridge and rummage blindly through. Thirty seconds later having discovered nothing but my general inadequacy, I crawl back into theatre. I was as good as useless though to my surprise the anaesthetist disappeared and returned with a vial. Handing me both it and a prepped syringe, he instructs me to inject intramuscularly into the woman’s thigh. The most common cause of postpartum haemorrhage is uterine atony. Prostaglandin analogues like carboprost promote coordinated contractions of the body of the pregnant uterus. Constriction of the vessels by myometrial fibres within the uterine walls achieves postpartum haemostasis. This textbook definition does not quite echo my thoughts as I gingerly approach the operating table. Alarmingly I am unaware that aside from the usual side effects of the drug in my syringe; the nausea and vomiting, should the needle stray into a nearby vessel and its contents escape into the circulation, cardiovascular collapse might be the unfortunate result. Suddenly the anaesthetist’s dour expression as I inject now assumes some meaning. What a relief to see the woman’s vitals begin to stabilise. As we wheel her into the recovery bay, the anaesthetist unleashes an onslaught of questions. Keen to redeem some lost pride, I can to varying degrees, resurrect long buried preclinical knowledge: basic pharmacology, transfusion-related complications, the importance of fresh frozen plasma. Although, the final threat of drawing the clotting cascade from memory is a challenge too far. Before long I am already being demonstrated the techniques of regional analgesia, why you should always aspirate before injecting lidocaine and thrust headlong into managing the most common adverse effects of epidurals. To have thought I had been ready to retire home early on this Saturday morning had serendipity not played its part. A little persistence would have been just as effective. It’s the quality so easily overlooked in these apparently austere times of medical education. And not a single logbook signature gained. Oh the shame! This blog post is a reproduction of an article published in the Medical Student Newspaper, February 2014 issue.  
James Wong
almost 8 years ago
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4
295

2nd Trimester Scanning Guide

A guide to confirming dating of pregnancy, fetal normality/abnormality, placental localisation and AF volume.  
slideshare.net
over 6 years ago