My fellow medical students, interns, residents and attendings: I am not a medical student but an emeritus professor of Obstetrics and Gynecology at the University of Miami Miller School of Medicine, and also a voluntary faculty member at the Florida International University Herbert Wertheim College of Medicine. I have a great deal of contact with medical students and residents. During training (as student or resident), gaining confidence in one's own abilities is a very important part of becoming a practitioner. This aspect of training does not always receive the necessary attention and emphasis. Below I describe one of the events of confidence building that has had an important and lasting influence on my career as an academic physician. I graduated from medical school in Belgium many years ago. I came to the US to do my internship in a small hospital in up state NY. I was as green as any intern could be, as medical school in Belgium at that time had very little hands on practice, as opposed to the US medical graduates. I had a lot of "book knowledge" but very little practical confidence in myself. The US graduates were way ahead of me. My fellow interns, residents and attendings were really understanding and did their best to build my confidence and never made me feel inferior. One such confidence-building episodes I remember vividly. Sometime in the middle part of the one-year internship, I was on call in the emergency room and was called to see a woman who was obviously in active labor. She was in her thirties and had already delivered several babies before. The problem was that she had had no prenatal care at all and there was no record of her in the hospital. I began by asking her some standard questions, like when her last menstrual period had been and when she thought her due date was. I did not get far with my questioning as she had one contraction after another and she was not interested in answering. Soon the bag of waters broke and she said that she had to push. The only obvious action for me at that point was to get ready for a delivery in the emergency room. There was no time to transport the woman to the labor and delivery room. There was an emergency delivery “pack” in the ER, which the nurses opened for me while I quickly washed my hands and put on gloves. Soon after, a healthy, screaming, but rather small baby was delivered and handed to the pediatric resident who had been called. At that point it became obvious that there was one more baby inside the uterus. Realizing that I was dealing with a twin pregnancy, I panicked, as in my limited experience during my obstetrical rotation some months earlier I had never performed or even seen a twin delivery. I asked the nurses to summon the chief resident, who promptly arrived to my great relief. I immediately started peeling off my gloves to make room for the resident to take my place and deliver this twin baby. However, after verifying that this baby was also a "vertex" without any obvious problem, he calmly stood by, and over my objections, bluntly told me “you can do it”, even though I kept telling him that this was a first for me. I delivered this healthy, screaming twin baby in front of a large number of nurses and doctors crowding the room, only to realize that this was not the end of it and that indeed there was a third baby. Now I was really ready to step aside and let the chief resident take over. However he remained calm and again, stood by and assured me that I could handle this situation. I am not even sure how many triplets he had delivered himself as they are not too common. Baby number three appeared quickly and also was healthy and vigorous. What a boost to my self-confidence that was! I only delivered one other set of triplets later in my career and that was by C-Section. All three babies came head first. If one of them had been a breech the situation might have been quite different. What I will never forget is the implied lesson in confidence building the chief resident gave me. I have always remembered that. In fact I have put this approach in practice numerous times when the roles were reversed later in my career as teacher. Often in a somewhat difficult situation at the bedside or in the operating room, a student or more junior doctor would refer to me to take over and finish a procedure he or she did not feel qualified to do. Many times I would reassure and encourage that person to continue while I talked him or her through it. Many of these junior doctors have told me afterwards how they appreciated this confidence building. Of course one has to be careful to balance this approach with patient safety and I have never delegated responsibility in critical situations and have often taken over when a junior doctor was having trouble. Those interested, can read more about my experiences in the US and a number of other countries, in a free e book, entitled "Crosscultural Doctoring. On and Off the Beaten Path" can be downloaded at this link. Enjoy!
DR William LeMaire
over 6 years ago
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 8 years ago
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.
about 7 years ago
Following the implantation of the blastocyst into the endometrium of uterus, the embryo begins another important embryological process called gastrulation. Gastrulation is the formation of the three distinct germ layers - the ectoderm, the mesoderm and the endoderm. The ectoderm is the outermost layer of the developing embryo and it consists of cells that eventually give rise to the integumentary system (the outer skin, nails and hair) as well as the nervous system (central and peripheral system). The mesoderm is the middle layer of the developing embryo and it consists of cells that eventually give rise to the musculoskeletal system (bone, cartilage, skeletal muscle, cardiac muscle, smooth muscle), cardiovascular system (the heart and blood vessels), excretory system (kidneys) and reproductive system (gonads). The endoderm is the innermost layer of the developing embryo and it gives rise to the epithelial layer of the digestive tract, lungs, pancreas, bladder, liver as well as the thyroid gland, parathyroid gland and thymus.
almost 6 years ago
Amended from Wikipedia and other sources T.I Lemon Stage means spread Grade means histology Prostate cancer staging – spread of the cancer There are two schemes commonly used to stage prostate cancer. TMN and Whitmore Jewett Stage I disease is cancer that is found incidentally in a small part of the sample when prostate tissue was removed for other reasons, such as benign prostatic hypertrophy, and the cells closely resemble normal cells and the gland feels normal to the examining finger Stage II more of the prostate is involved and a lump can be felt within the gland. Stage III, the tumour has spread through the prostatic capsule and the lump can be felt on the surface of the gland. In Stage IV disease, the tumour has invaded nearby structures, or has spread to lymph nodes or other organs. Grading - Gleason Grading System is based on cellular content and tissue architecture from biopsies, which provides an estimate of the destructive potential and ultimate prognosis of the disease. TX: cannot evaluate the primary tumor T0: no evidence of tumor T1: tumor present, but not detectable clinically or with imaging • T1a: tumor was incidentally found in less than 5% of prostate tissue resected (for other reasons) • T1b: tumor was incidentally found in greater than 5% of prostate tissue resected • T1c: tumor was found in a needle biopsy performed due to an elevated serum PSA T2: the tumor can be felt (palpated) on examination, but has not spread outside the prostate • T2a: the tumor is in half or less than half of one of the prostate gland's two lobes • T2b: the tumor is in more than half of one lobe, but not both • T2c: the tumor is in both lobes but within the prostatic capsule • T3: the tumor has spread through the prostatic capsule (if it is only part-way through, it is still T2) • T3a: the tumor has spread through the capsule on one or both sides • T3b: the tumor has invaded one or both seminal vesicles • T4: the tumor has invaded other nearby structures It should be stressed that the designation "T2c" implies a tumor which is palpable in both lobes of the prostate. Tumors which are found to be bilateral on biopsy only but which are not palpable bilaterally should not be staged as T2c. Evaluation of the regional lymph nodes ('N') NX: cannot evaluate the regional lymph nodes • N0: there has been no spread to the regional lymph nodes • N1: there has been spread to the regional lymph nodes Evaluation of distant metastasis ('M') • MX: cannot evaluate distant metastasis • M0: there is no distant metastasis • M1: there is distant metastasis • M1a: the cancer has spread to lymph nodes beyond the regional ones • M1b: the cancer has spread to bone • M1c: the cancer has spread to other sites (regardless of bone involvement) Evaluation of the histologic grade ('G') Usually, the grade of the cancer (how different the tissue is from normal tissue) is evaluated separately from the stage; however, for prostate cancer, grade information is used in conjunction with TNM status to group cases into four overall stages. • GX: cannot assess grade • G1: the tumor closely resembles normal tissue (Gleason 2–4) • G2: the tumor somewhat resembles normal tissue (Gleason 5–6) • G3–4: the tumor resembles normal tissue barely or not at all (Gleason 7–10) Of note, this system of describing tumors as "well-", "moderately-", and "poorly-" differentiated based on Gleason score of 2-4, 5-6, and 7-10, respectively, persists in SEER and other databases but is generally outdated. In recent years pathologists rarely assign a tumor a grade less than 3, particularly in biopsy tissue. A more contemporary consideration of Gleason grade is: • Gleason 3+3: tumor is low grade (favorable prognosis) • Gleason 3+4 / 3+5: tumor is mostly low grade with some high grade • Gleason 4+3 / 5+3: tumor is mostly high grade with some low grade • Gleason 4+4 / 4+5 / 5+4 / 5+5: tumor is all high grade Note that under current guidelines, if any Pattern 5 is present it is included in final score, regardless of the percentage of the tissue having this pattern, as the presence of any pattern 5 is considered to be a poor prognostic marker. Overall staging The tumor, lymph node, metastasis, and grade status can be combined into four stages of worsening severity. Stage Tumor Nodes Metastasis Grade Stage I T1a N0 M0 G1 Stage II T1a N0 M0 G2–4 T1b N0 M0 Any G T1c N0 M0 Any G T1 N0 M0 Any G T2 N0 M0 Any G Stage III T3 N0 M0 Any G Stage IV T4 N0 M0 Any G Any T N1 M0 Any G Any T Any N M1 Any G Bladder T (Primary tumour) • TX Primary tumour cannot be assessed • T0 No evidence of primary tumour • Ta Non-invasive papillary carcinoma • Tis Carcinoma in situ (‘flat tumour’) • T1 Tumour invades subepithelial connective tissue • T2a Tumour invades superficial muscle (inner half) • T2b Tumour invades deep muscle (outer half) • T3 Tumour invades perivesical tissue: • T3a Microscopically • T3b Macroscopically (extravesical mass) • T4a Tumour invades prostate, uterus or vagina • T4b Tumour invades pelvic wall or abdominal wall N (Lymph nodes) • NX Regional lymph nodes cannot be assessed • N0 No regional lymph node metastasis • N1 Metastasis in a single lymph node 2 cm or less in greatest dimension • N2 Metastasis in a single lymph node more than 2 cm but not more than 5 cm in greatest dimension,or multiple lymph nodes, none more than 5 cm in greatest dimension • N3 Metastasis in a lymph node more than 5 cm in greatest dimension M (Distant metastasis) • MX Distant metastasis cannot be assessed • M0 No distant metastasis • M1 Distant metastasis. Grade Urothelial papilloma – non cancerous (benign) tumour •Papillary urothelial neoplasm of low malignant potential (PUNLMP) – very slow growing and unlikely to spread •Low grade papillary urothelial carcinoma – slow growing and unlikely to spread •High grade papillary urothelial carcinoma – more quickly growing and more likely to spread
over 7 years ago
Researchers have identified two proteins in a fetus' lungs responsible for initiating the labor process, providing potential new targets for preventing preterm birth. They discovered that the proteins SRC-1 and SRC-2 activate genes inside the fetus' lungs near full term, leading to an inflammatory response in the mother's uterus that initiates labor.
over 5 years ago
The normal position of the uterus is anteverted. In this position, the uterus is concave on the side of the bladder, and bends round to sit just above and behind the bladder. In a retroverted uterus, the uterus instead bends ‘backwards’ so that the concave side is posterior. About 20-30% of women have a retroverted uterus. Clinical features
almostadoctor.com - free medical student revision notes
almost 7 years ago
Labor and Delivery - Normal Uterine Contractions with Fetal Monitoring Strip. Depicts a relaxed uterus and dilated cervix followed by a contracted uterus. The third image shows a relaxed uterus. The fourth image shows the uterus contracting, and squeezing the baby toward the birth canal. The fifth and sixth illustrations picture a fetal monitor and its printout, graph with contractions and recovery periods.
Nucleus Medical Media
almost 7 years ago
Topics Today, I’ll discuss the inherent contraction patterns of the uterus as they vary throughout the menstrual cycle and the role that may play in sperm transport, infertility, endometriosis and contraception. Free Links: OBGYN-10 OBGYN-101 Gray Haired Note Brookside Associates Medical Education Division
Mike Hughey, MD
over 10 years ago
This is an inflammatory condition (often secondary to infection), affecting any part of the higher female reproductive system, e.g.; uterus, fallopian tubes, ovaries. Salpingitis – this term is sometimes used interchangeably with PID, but technically only refers to inflammation in the fallopian tubes. Endometritis Risk factors STD: Young age (16-24)
almostadoctor.com - free medical student revision notes
almost 7 years ago
The US Food and Drug Administration (FDA) issued a safety communication on 17 April urging doctors not to use laparoscopic power morcellation for hysterectomies or removal of uterine fibroids over concerns that the technique may spread uterine sarcomas beyond the uterus.1
almost 7 years ago
Genetic diagnostic technologies are rapidly changing the way medicine is practiced. Preimplantation genetic testing is a well established application of genetic testing within the context of in vitro fertilization cycles. It involves obtaining a cell(s) from a developing embryo in culture, which is then subjected to genetic diagnostic analysis; the resulting information is used to guide which embryos are transferred into the uterus. The potential applications and use of this technology have increased in recent years. Experts agree that preimplantation genetic diagnosis is clinically appropriate for many known genetic disorders. However, some applications of such testing, such as preimplantation genetic screening for aneuploidy, remain controversial. Clinical data suggest that preimplantation genetic screening may be useful, but further studies are needed to quantify the size of the effect and who would benefit most.
almost 6 years ago
Labor is a physiologic process during which the fetus, membranes, umbilical cord, and placenta are expelled from the uterus. Stages of labor Obstetricians have divided labor into 3 stages that delineate milestones in a continuous process.
over 5 years ago