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Foo20151013 2023 2njk5o?1444774020
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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
over 8 years ago
Foo20151013 2023 1nftkgk?1444774218
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Gin & Tonic Anyone?

It was a Saturday, about tea-time in the quaint village of Athelstaneford, East Lothian. Mrs Alexandria Agutter sat in her cottage, enjoying the delights of the late-summer evening with a glass of gin and tonic. She listlessly sipped from the rather generous pick-me up, no doubt chewing over the happenings of the day. Blast! The taste was much too bitter to her liking. She stood up. And promptly crumpled to the floor in a dizzied heap. It had not been five minutes when a fiery pain gripped her parched throat and in her frenzied turn she watched the bleary room become draped in a gossamery silk. How Dame Agatha would approve. But this is no crime novel, on that fateful day, 24th August 1994, poor Mrs Agutter immortalised herself in the history books of forensic medicine; she was the victim of a revered toxin and a vintage one it was too. She had unwittingly imbibed a G&T laced with a classic poison of antiquity. A clue from the 21st century: do you recall the first Hunger Games film adaption? Those inviting purple-black berries or as Suzanne Collins coined them ‘Nightlock’; a portmanteau of hemlock and Deadly Nightshade. True to the laters’ real life appearance those onscreen fictional fruits played a recurring cameo role. Deadly Nightshade is a perennial shrub of the family Solanaceae and a relative of the humble potato (a member of the Solanus genus). It is a resident of our native woodland and may be found as far afield as Europe, Africa and Western Asia. The 18th century taxonomist, Carl Linnaeus gave the plant an intriguing name in his great Species Plantarum. The genus Atropa is aptly named after one of the three Greek Fates, Atropos. She is portrayed shearing the thread of a mortal’s life so determining the time and manner of its inevitable end. The Italian species name belladona (beautiful woman) refers to the striking mydriatic effect of the plant on the eye. The name pays homage to Pietro Andre Mattioli, a 16th century physician from Sienna, who was allegedly the first to describe the plant’s use among the Venetian glitterati - ladies of fashion favoured the seductive, doe-eyed look. Belladona is poisonous in its entirety. It was from the plant’s roots in 1831, the German apothecary Heinrich F. G. Mein isolated a white, odourless, crystalline powder: it was (surprise, surprise) atropine. Atropine is a chiral molecule. From its natural plant source it exists as a single stereoisomer L-atropine, which also happens to display a chiral potency 50-100 times that of its D-enantiomer. As with many other anaesthetic agents it is administered as a racemic mixture. How strange that atropine now sits among the anaesthetist’s armamentarium, its action as a competitive antimuscarinic to counter vagal stimulation belies its dark history. It was a favourite of Roman housewives seeking retribution against their less than faithful husbands and a staple of the witch’s potion cupboard. Little wonder how belladona became known as the Devil’s plant. Curiouser still it’s also the antidote for other poisons, most notably the organophosphates or nerve gases. On account of its non-selective antagonism, atropine produces a constellation of effects: the inhibition of salivary, lacrimal and sweat glands occurs at low doses; dry mouth and skin are early markers. Pyrexia is a central effect exacerbated by the inability to sweat. Flushing of the face due to skin vessel vasodilatation. Low parasympathetic tone causes a moderate sinus tachycardia. Vision is blurred as the eye becomes dilated, unresponsive to light and accommodation is impaired. Mental disorientation, agitation and ataxia give the impression of drunkedness or a delirium tremens like syndrome. Visual hallucinations, often of butterflies or silk blowing in the wind, are a late feature. It was then that Mr Agutter, seemingly untroubled by the sight of his wife’s problematic situation, proceeded to leave a message with the local practitioner. How fortunate they were to have the vigilant locum check the answering machine and come round to the Agutter’s lodge accompanied by an ambulance crew. The attending paramedic had the presence of mind to pour the remainder of Mrs Agutter’s beverage into a nearby jam jar, while Mr Agutter handed over what he suspected to be the offending ingredient: the bottle of Indian tonic water. As it soon transpired there were seven other casualties in the surrounding countryside of East Lothian – all involving an encounter with tonic water. In fact by some ironic twist of fate, two of the victims were the wife and son of Dr Geoffry Sharwood-Smith, a consultant aneasthetist. Obviously very familiar with the typical toxidrome of anticholinergic agents, he was quick to suspect atropine poisoning. Although for a man of his position with daily access to a sweetshop of drugs, it was not something to draw attention to. Through no small amount of cunning had the poisoner(s) devised the plan. It was elegant; atropine is very bitter. So much so that it can be detected at concentrations of 100 parts per million (0.001%). Those foolish enough to try the berries of belladonna during walks in the woods are often saved by the berry’s sour taste. They are soon spat out. But the quinine in the tonic water was a worthy disguise. The lethal dose for an adult is approximately 90-130mg, however atropine sensitivity is highy variable. In its salt form, atropine sulfate, it is many times more soluble: >100g can be dissolved in 100ml of water. So 1ml may contain roughly tenfold the lethal dose. There ensued a nationwide scare; 50 000 bottles of Safeway branded Indian tonic water were sacrificed. Only six bottles had been contaminated. They had all been purchased, tops unsealed, from the local Safeway in Hunter’s Tryst. Superficially this looked like the handiwork of a psychopath with a certain distaste for the supermarket brand, and amidst the media furore, it did have some verisimilitude: one of the local papers received a letter from 25 year old, Wayne Smith admitting himself as the sole perpetrator. The forensic scientist, Dr Howard Oakley analysed the contents of the bottles. They all contained a non-lethal dose, 11-74mg/litre of atropine except for the Agutter’s, it contained 103mg/litre. The jam jar holding Mrs Agutter’s drink bore even more sinister results, the atropine concentration was 292mg/L. It would appear Mrs Agutter had in some way outstayed her welcome. But she lived. A miscalculation on the part of the person who had added an extra seasoning of atropine to her drink. According to the numbers she would have had to swallow a can’s worth (330ml) to reach the lethal dose. Thankfully she had taken no more than 50mg. The spotlight suddenly fell on Dr Paul Agutter. He was a lecturer of biochemistry at the nearby University of Napier, which housed a research syndicate specialising in toxicology. CCTV footage had revealed his presence at the Safeway in Hunter’s Tryst and there was eye witness evidence of him having placed bottles onto the shelves. Atropine was also detected by the forensic investigators on a cassete case in his car. Within a matter of two weeks he would be arrested for the attempted murder of his wife. Despite the calculated scheme to delay emergency services and to pass the blame onto a non-existent mass poisoner, he had not accomplished the perfect murder. Was there a motive? Allegedly his best laid plans were for the sake of a mistress, a mature student from Napier. He served seven years of a twelve year sentence. Astonishingly, upon his release from Glenochil prison in 2002, he contacted his then former wife proclaiming his innocence and desire to rejoin her in their Scottish home. A proposition she was not very keen on. Dr Agutter was employed by Manchester University as a lecturer of philosophy and medical ethics. He is currently an associate editor of the online journal Theoretical Biology and Medical Modelling. We will never know the true modus operandi as Dr Agutter never confessed to the crime. Perhaps all this story can afford is weak recompense for the brave followers of the Dry January Campaign. Oddly these sort of incidents never appear in their motivational testimonials. Acknowledgements Emsley J. Molecules of Murder. 2008, Cambridge, RSC Publishing, p.46-67. Lee MR. Solanaceae IV: Atropa belladona, deadly nightshade. J R Coll Physicians Edinb. March 2007; 37: 77-84. Illustrator Edward Wong This blog post is a reproduction of an article published in the The Medical Student Newspaper January issue, 2014 http://www.themedicalstudent.co.uk/  
James Wong
almost 8 years ago
Foo20151013 2023 1u6up6r?1444774235
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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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Heart disease kills more women than breast cancer

The Irish Heart Foundation has launched a campaign highlighting the dangers of heart disease for women.  
rte.ie
over 6 years ago
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watch

*Gynecologic Emergencies* Gynaecological emergencies are disease conditions of the female reproductive system that threaten the life of the woman, her sexual...  
youtube.com
about 6 years ago
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Women Entrepreneurs in Radiology

Carolyn C. Meltzer, MD, FACR shares a story from medical school in this snippet from the ACR 2015 session, "Entrepreneurial Women Leaders in Radiology."  
youtube.com
about 6 years ago
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Fibromyalgia

Fibromyalgia is a non-specific muscular disorder of unknown origin. It primarily affects insertions of tendons and associated soft tissues and presents with dull aching pains. It is much more common in women.  Epidemiology and Aetiology Cause is unknown Affects muscles rather than joints – although can often feel like joint pain Peak age of onset: 40-50 years M:F ratio 1:9  Pathology  
almostadoctor.com - free medical student revision notes
almost 8 years ago
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Booking, Screening & Antenatal Care

Much of the follow-up of pregnant women is carried out in the community, by midwifes at primary health care centres. The risk of death from pregnancy in the UK is roughly 1 in 20 000. Antenatal care is as much about educating women about pregnancy, childbirth and child care, as it is about providing for actual medical needs, particularly in the case of a first pregnancy. The exact measures will differ between NHS trusts, but below is a general outline of the type of care provided in pregnancy.    
almostadoctor.com - free medical student revision notes
almost 8 years ago
Foo20151013 2023 1njk26?1444774138
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Doctor or a scientist?

"One special advantage of the skeptical attitude of mind is that a man is never vexed to find that after all he has been in the wrong" Sir William Osler Well, it's almost Christmas. I know it's Christmas because the animal skeleton situated in the reception of my University's Anatomy School has finally been re-united with his (or her?) Christmas hat, has baubles for eyes and tinsel on its ribcage. This doesn't help with my trying to identify it (oh the irony if it is indeed a reindeer). This term has probably been one of the toughest academic terms I've had, but then when you intercalate that is sort of what you choose to let yourself in for. I used to think that regular readings were a chore in the pre-clinical years. I had ample amounts of ethics, sociology and epidemiology readings to do but this is nothing compared to the world of scientific papers. The first paper I had to read this term related to Glycosaminoglycan (GAG) integrity in articular cartilage and its possible role in the pathogenesis of Osteoarthritis. Well, I know that now. When I first started reading it felt very much like a game of boggle and highly reminiscent of high school spanish lessons where I just sat and nodded my head. This wasn't the end. Every seminar has come with its own prescribed reading list. The typical dose is around 4-5 papers. This got me thinking. We don't really spend all that much time understanding how to read scientific papers nor do we really explore our roles as 'scientists' as well as future clinicians. Training programmes inevitably seem to create false divides between the 'clinicans' and the 'academics' and sometimes this has negative consequences - one simply criticises the other: Doctors don't know enough about science, academics are out of touch with the real world etc... Doctors as scientists... The origins of medicine itself lie with some of the greatest scientists of all time - Herophilus, Galen, Da Vinci, William Harvey (the list is endless). As well as being physicians, all of these people were also respected scientists who regularly made contributions to our understanding of the body's mechanics. Albeit, the concept of ethics was somewhat thrown to the wind (Herophilus, though dead for thousands of years, is regularly accused of performing vivisections on prisoners in his discovery of the duodenum). Original sketches by William Harvey which proved a continuous circuit of blood being supplied and leaving the upper limb. He used his observations to explain the circulatory system as we know it today What was unique about these people? The ability to challenge what they saw. They made observations, tested them against their own knowledge and asked more questions - they wanted to know more. As well as being doctors, we have the unique opportunity to make observations and question what we see. What's causing x to turn into y? What trends do we see in patients presenting with x? The most simple question can lead to the biggest shift in understanding. It only took Semmelweiss to ask why women were dying in a maternity ward to give rise to our concept of modern infection control. Bad Science... Anyone who has read the ranting tweets, ranting books and ranting YouTube TED videos of academic/GP Ben Goldacre will be familiar with this somewhat over used term. Pseudoscience (coined by the late great Karl Popper) is a much more sensible and meaningful term. Science is about gathering evidence which supports your hypothesis. Pseudoscience is a field which makes claims that cannot be tested by a study. In truth, there's lots and lots of relatively useless information in print. It's fine knowing about biomarker/receptor/cytokine/antibody/gene/transcription factor (insert meaningless acronym here) but how is it relevant and how does it fit into the bigger picture? Science has become reductionist. We're at the gene level and new reducing levels of study (pharmacogenetics) break this down even further and sometimes, this is at an expense of providing anything useful to your clinicial toolbox. Increasing job competition and post-graduate 'scoring' systems has also meant there's lots of rushed research in order to get publications and citations. This runs the danger of further undermining the doctors role as a true contributor to science. Most of it is wrong... I read an article recently that told me at least 50% of what I learn in medical school will be proven wrong in my lifetime. That might seem disheartening since I may have pointlessly consumed ample coffee to revise erroneous material. However, it's also exciting. What if you prove it wrong? What if you contributed to changing our understanding? As a doctor, there's no reason why you can't. If we're going to practice evidence-based medicine then we need to understand that evidence and doing this requires us to wear our scientist hat. It would be nice to see a whole generation of doctors not just willing to accept our understanding but to challenge that which is tentative. That's what science is all about. Here's hoping you don't find any meta-analyses in your stockings. Merry Christmas.  
Lucas Brammar
about 8 years ago
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Goodbye fear and ego, hello better patient care

The best doctors in the world still have bad consultation. Sometimes you just start off on the wrong foot. The patient leaving in a floor of tears is usually an indication that this has just occurred. On one of my medical placements I witnessed one such consultation. A young woman in the early stages of her pregnancy had a per vaginal bleed and wanted a scan to see if the pregnancy was still ok. Medically speaking, a scan wasn’t indicated as the pregnancy was too early on to detect any changes. The doctors noted the “agenda” as they later remarked, and was not going to “play the game” and send the young woman for a scan. She was not happy about this. The doctor felt that he couldn’t have done more. Medically there was nothing he could offer to the woman other than advice to go home and wait a little while before repeating a pregnancy test. To me, there was lots that could have been done. This woman was scared and worried and a sympathetic ear and a tissue would have gone some way to making her feel better. The doctor I was with couldn’t see this. They were blind sighted by the repeated requests for a scan and slightly frustrated that the unhelpfulness of this was not being understood. When the young woman began to cry I was waiting for the doctor to hand over a tissue. “Any second now...” I thought, but it never happened. I wanted to give the woman a tissue and put my arm around her but that would have meant physically placing myself between the doctor and the patients and interrupting a consultation I wasn’t really a part of. But the truth is. I was a part of that consultation. I might not have been the doctor in charge but I was another person in that room who could have made that situation easier for that patient and I didn’t. Hours later, on my way home, I was still thinking about this. I felt I had let that woman down. I could see what she needed and I sat there and did nothing. After the consultation I immediately told the doctor what I thought. I felt that the patient had been let down. They took on what I said and mostly agreed with it. All egos were put aside in that frank conversation and the doctor genuinely reflected on how they could have done better in that situation. It wasn’t about me or the doctor. It was about the patient. As a medical student it is easy to feel in the way in the hospital environment or in a busy clinic. When the consultant is running behind, it takes a lot to ask the patients something or butt in and add something you think is relevant that in the end may turn out to be a very trivial thing. But at the end of the day, it is worth it if it means that there is a better out come for the patient because when all is said and done they are the ones we are doing this all for. I regret not handing that patient a tissue and it’s a mistake I hope never to repeat again.  
Salma Aslam
almost 8 years ago
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The Importance Of Clinical Skills

In the USA the issue of indiscriminate use of expensive, sophisticated, and time consuming test in lieu of, rather than in addition to, the clinical exam is being much discussed. The cause of this problem is of course multifactorial. One of the factors is the decline of the teaching of clinical skills to our medical students and trainees. Such problems seem to have taken hold in developing countries as well. Two personal anecdotes will illustrate this. In the early nineties I worked for two years as a faculty member in the department of ob & gyn at the Aga Khan University Medical School in Karachi, Pakistan. One day, I received a call from the resident in the emergency room about a woman who had come in because of some abdominal pain and vaginal bleeding. While the resident told me these two symptoms her next sentence was: “… and the pelvic ultrasound showed…” I stopped her right in her tracks before she could tell me the result of the ultrasound scan. I told her: “First tell me more about this patient. Does she look ill? Is she bleeding heavily? Is she in a lot of pain and where is the pain? What are her blood pressure and pulse rate? How long has she been having these symptoms? When was her last menstrual period? What are your findings when you examined her ? What is the result of the pregnancy test?”. The resident could not answer most of these basic clinical questions and findings. She had proceeded straight to a test which might or might not have been necessary or even indicated and she was not using her clinical skills or judgment. In another example, the resident, also in Karachi, called me to the emergency room about a patient with a ruptured ectopic pregnancy. He told me that the patient was pale, and obviously bleeding inside her abdomen and on the verge of going into shock. The resident had accurately made the diagnosis, based on the patient’s history, examination, and a few basic laboratory tests. But when I ran down to see the patient, he was wheeling the patient into the radiology department for an ultrasound. "Why an ultrasound?" I asked. “You already have made the correct diagnosis and she needs an urgent operation not another diagnostic procedure that will take up precious time before we can stop the internal bleeding.” Instead of having the needless ultrasound, the patient was wheeled into the operating room. What I am trying to emphasize is that advances in technology are great but they need to be used judiciously and young medical students and trainees need to be taught to use their clinical skills first and then apply new technologies, if needed, to help them to come to the right diagnosis and treatment. And of course we, practicing physicians need to set the example. Or am I old fashioned and not with it? Medico legal and other issues may come to play here and I am fully aware of these. However the basic issue of clinical exam is still important. Those wanting to read more similar stories can download a free e book from Smashwords. The title is: "CROSSCULTURAL DOCTORING. ON AND OFF THE BEATEN PATH." You can access the e book here.  
DR William LeMaire
over 7 years ago
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Shoulder Dystocia

Topics This afternoon, I’d like to talk about an important complication of delivery, called shoulder dystocia. Shoulder Dystocia… View Text Here Delivery of the Posterior Arm Video… View Free Video Here Commercial Links: Shoulder Dystocia Vide 5-Minute Vaginal Delivery Vide 5-Minute Episiotomy Video Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Shoulder Dystocia in the Global Library of Women’s Medicin Brookside Associates Medical Education Division  
Mike Hughey, MD
over 11 years ago
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Bartholin Cysts

Topics This morning, I’m talking about Bartholin cysts. Bartholin Cyst and Abscess… View Text Here Draining a Bartholin Cyst Video… View Free Video Here Commercial Links: 5-Minute Bartholin Cyst Vide 5-Minute Vulvar Biops 5-Minute Vulva Anatomy Video Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Simple Operations of the Vulva in the Global Library of Women’s Medicin Brookside Associates Medical Education Division  
Mike Hughey, MD
over 11 years ago
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HOUJC1 2009 | Case 5

ResearchToPractice.com/HOUJC109 – Case 5: 53yo woman with symptomatic, high-risk mantle-cell lymphoma treated with R-hyper-CVAD. Interviews conducted by Neil Love, MD. Produced by Research To Practice.  
Dr Neil Love
over 11 years ago
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VPB1_2010 | Case05

ResearchToPractice.com/VPB110 – A 54yo woman with bipolar disorder is diagnosed with a 1.6-cm, Grade III, strongly ER+, weakly PR+, HER2-, node- IDC and an Oncotype DX RS of 32. Interview conducted by Neil Love, MD. Produced by Research To Practice.  
Dr Neil Love
over 11 years ago
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How should Medical Students Interact with Social Media Networking Sites?

An award winning essay written for the Medical Women's Federation Conference on Social Media in Medicine 2012. The essay summarises some of the concerns over using social media in medicine, but also highlights some of the potential benefits.  
Dr. Luke Farmery
about 9 years ago