The tail of the caudate nucleus shows more degeneration than the body purchase generic avanafil on-line erectile dysfunction dsm 5, which is more involved than the head avanafil 200mg discount impotence while trying to conceive. Similarly, the caudal portion of the putamen is more degenerated than the rostral portion. Along the coronal (or dorsoventral) axis of the neostriatum, the dorsal neostriatal regions are more involved than the ventral ones (Fig. Along the medio-lateral axis, the paraventricular half of the caudate nucleus is more involved than the paracapsular half. In essence, the dorsal third of the rostral neostriatum is especially prone to degenerate in contrast to the relatively preserved ventral third, including the nucleus accumbens (Fig. Microscopically, degeneration is manifested by neuronal loss and reactive gliosis (Figure 29). Fibrillary astrogliosis parallels the loss of neurons along the caudo-rostral and dorsoventral striatal gradients of decreasing severity. The dorsal, medial field of the normal head of the caudate nucleus is remarkable for the presence of scattered neurons dispersed within a smooth, homogeneous neuropil (top). This illustrates the gradient of decreasing severity along the dorso-ventral axis of the neostriatum especially at this level. The distribution of neuronal loss in particular brain regions is more or less distinctive for each disease of this group. Prominent, ubiquitin-labeled, nuclear inclusions involving the neurons and scant glial cells. The excitotoxicity theory proposes that subpopulations of striatal medium- sized spiny projection neurons are hypersensitive to corticostriatal and thalamostriatal 76 glutamate, or excessive glutamate is released by these afferents, while striatal interneurons 13 are less affected. This over activation results in an influx of Na+ initially, which causes cell 2+ swelling, and then Ca , which appears to be necessary for neurodegeneration. Summary of neurodegenerative disease associated inclusions Disease Inclusion Composition Alzheimer’s disease Senile plaque Beta-amyloid, apoE Neurofibrillary tangles Tau, ubiquitin Hirano bodies Actin, actin-binding proteins Lewy body diseases Lewy body Alpha-synuclein, neurofilament, ubiquitin Pick’s disease Pick body Tau, ubiquitin Chromosome 17- Neurofibrillary tangles Tau linked dementias Glial tangles Tau Huntington’s disease Intranuclear inclusions Huntingtin, ubiquitin 13 M. Aronin, Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain, Science 277 (1997) 1990-1993. One principle that must be emphasized when one speaks of metabolic diseases of the nervous system is that of selective vulnerability. By this we mean that specific cell types or populations are more susceptible to a particular (metabolic) insult than others. It is best to consider these two conditions jointly, since their pathologic effects on the nervous system are almost identical. If the central nervous system is deprived of either oxygen or glucose for even short periods of time, neurons are rendered incapable of functioning and may die. The most common clinical setting for hypoxia is that of oligemic or ischemic hypoxia, produced by a reduction or absence of blood flow. There are infrequent instances, however, of hypoxic, anemic or histotoxic hypoxia in which blood flow is normal, but sufficient oxygen is not presented to neurons. The major acute change produced by hypoxia or hypoglycemia is that of individual neuronal necrosis, manifested histologically by cytoplasmic eosinophilia and nuclear pyknosis. If, as usually happens, blood flow is also compromised, then one may find evidence of both cytotoxic and even vasogenic edema. Specific neurons and regions of the central nervous system are more vulnerable to oxygen or glucose deprivation than others. Watershed zones are those areas between the terminations of the major cerebral arteries, and are typically parasagittal or lateral parieto-temporo-occipital in location. Permanent or residual clinical manifestations depend upon the extent and localization of the lesions. For the sake of this course, we will restrict ourselves to deficiencies of thiamine (vitamin B1) and cobalamin (vitamin B12). In the acute stage (Wernike’s disease), symptoms are characterized by confusion, ocular disturbances and ataxia. Its clinical recognition is important, since the prompt administration of thiamine will result in a dramatic reversal of the symptomatology. If thiamine deficiency persists, or if the patient has repeated bouts of thiamine deficiency, then neuronal loss may occur and the deficit will become irreversible. In this situation one usually finds 80 that patients also have defects in memory (amnestic syndrome), particularly in the retention of short-term memory, referred to as Wernicke-Korsakoff psychosis. Although Wernicke-Korsakoff disease is the most frequent form of the Korsakoff syndrome, any destructive lesion that bilaterally interrupts the limbic circuit may produce the same amnestic syndrome. Deficiency of vitamin B12 is most commonly seen as a result of the malabsorption syndrome in pernicious anemia. Pathologic changes in the spinal cord, brain, optic nerves and peripheral nerves may occur. Myelin sheaths of spinal cord white matter, particularly at the upper thoracic levels, are most vulnerable. These lesions are asymmetrical and involve the posterior columns and the postero- lateral aspects of the lateral funiculi. They are not restricted to specific tracts and are characterized histologically by a dramatic spongy change. At the ultrastructural level, this spongy change represents intramyelinic edema; that is, excessive fluid between myelin lamellae. With time, axons degenerate, oligodendrocytes are lost, astrocytes proliferate and macrophages appear. Some of the mitochondrial diseases, the "ragged-red fiber" disorders, are caused by mitochondrial genomic mutations, and show a maternal inheritance pattern. Those diseases related to deficiency of lysosomal enzymes often display conspicuous morphologic and biochemical manifestations of "storage" of specific chemical substances. Before discussing these, we will mention those that involve two other organelles: mitochondria and peroxisomes; with the exception of adreno-leukodystrophy, these do not qualify as "storage" diseases. Family history is often positive, and juvenile and adult onsets have been well documented. Neuropathologic lesions in this disease are distinctive and involve all levels of the nervous system. Involvement of the optic system, cerebral and cerebellar white matter, dentate nucleus, and spinal gray is frequently noted. Lesions, primarily of demyelinative type, in spinal roots, dorsal root ganglia, and peripheral nerve also have been reported. Hyperoxaluria I 82 Many of the above disorders have been known clinically and pathologically for years, but only recently have their etiologies been traced to peroxisomal abnormalities. Some (Zellweger) patients display an absence of peroxisomes, due to defects in peroxisome assembly; others (adreno-leukodystrophy) have normal appearing peroxisomes, but are deficient in certain specific peroxisomal functions. In adreno-leukodystrophy very long chain fatty acids are not admitted to the beta-oxidation system of the peroxisome, and demyelination occurs progressively as these fatty acids accumulate (see discussion above under Myelin Disorders). Cerebro-Hepato-Renal (Zellweger) Syndrome is characterized by dysmorphic features and the neonatal onset of profound hypotonia and seizures. This disease is the prototype of a new class of inherited metabolic diseases in which there is an absence of, or severe reduction in, peroxisomes.

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The first wave purchase avanafil with paypal erectile dysfunction injection medication, which started during the spring of 1918 generic avanafil 100 mg free shipping erectile dysfunction and diabetes type 1, was highly contagious but not particularly deadly. Symptoms in 1918 were so unusual that, initially, it was misdiagnosed as dengue fever, cholera, or typhoid (Barry 2004). In contrast to subsequent pandemics, most deaths during the 1918 pandemic were among young and healthy persons aged 15 to 35 years old, and 99 % of deaths occurred in people younger than 65 years. According to this investigation, the 1918 virus was not a reassortant virus (like those of the 1957 and 1968 pandemics), but more likely an entirely avian-like virus that adapted to humans. Patients with chronic underlying disease and pregnant women were particularly at risk of developing pulmonary complications (Louria 1957). The mortality impact was not even particularly severe compared to the severe epidemic in 1967–1968 (the last H2N2 epidemic), as well as two severe H3N2 epidemics in 1975–1976, and in 1980–1981 (Simonsen 2004). The death toll has been estimated to have been around 1 million, and in the United States, nearly 50 percent of all influenza-related deaths occurred in the younger population under 65 years of age. Sero-archaeological studies showed that most individuals aged 77 years or older, had H3 antibodies before they were exposed to the new pandemic virus (Dowdle 1999) and that pre-existing anti- H3 antibodies might have protected the elderly (> 77 years old) during the 1968 H3N2 pandemic. Since 1968, there has been only one episode – in 1976 – when the start of a new pandemic was falsely anticipated (Dowdle 1997, Gaydos 2006, Kilbourne 2006). Current Situation Major pandemics have occurred throughout history at an average of every 30 years and there is a general consensus that there will be another influenza pandemic. One possible candidate is the avian H5N1 strain which has become endemic in wild waterfowl and in domestic poultry in many parts of Southeast Asia, and is recently spreading across Asia into Europe and Africa. Recent research has shown that just ten amino acid changes in the polymerase proteins differentiate the 1918 influenza virus sequences from that of avian viruses, and that a number of the same changes Individual Impact 23 have been found in recently circulating, highly pathogenic H5N1 viruses (Taubenberger 2005). Human cases, first documented in 1997 (Yuen 1998), coincided with outbreaks of highly pathogenic H5N1 avian influenza in poultry. Very limited human-to-human transmission of the H5N1 strain was documented in healthcare workers and family members with contact (Katz 1999, Buxton Bridges 2000). Although H5 antibodies were detected in these groups, indi- cating infection with the virus, no cases of severe disease occurred. There are little data to show to what extent asymptomatic infection or mild clinical disease occur following infection with highly pathogenic avian H5N1 strains. The reason for this age distribution (exposure risk, disease reporting bias, intrinsic host issues, etc. Likewise, it is not known whether, and to what extent, genetic composition plays a role in the suscep- tibility and resistance to infection with H5N1 influenza virus (Promed 20060216. However, if we translate the death toll associated with the 1918 influenza virus to the current population, there could be 180 million to 360 million deaths globally (Osterholm 2005). Individual Impact The fate of an individual during an influenza outbreak, be it epidemic or pandemic, is variable. Among the others, clinical presentation varies from afebrile respira- tory symptoms mimicking the common cold, to febrile illnesses ranging in severity from mild to debilitating (Hoffmann 2006a), and may cause disorders affecting the lung, heart, brain, liver, kidneys, and muscles (Nicholson 2003). The clinical course is influenced by the patient’s age, the degree of pre-existing immunity, properties of the virus, smoking, co-morbidities, immunosuppression, and pregnancy (Nicholson 2003). Death mostly occurs as a consequence of primary viral pneumonia or of secondary respiratory bacterial infections, especially in pa- 24 Influenza 2006 tients with underlying pulmonary or cardiopulmonary diseases. The very young and the elderly usually have the highest risk of developing serious complications; how- ever, during pandemics, there is a mortality shift towards younger age groups (Simonson 1998). Once the virus enters a cell, it causes complex cytopathic effects, predominantly in the columnar epithelial cells, by shutting down the synthesis of host proteins. There are numerous individual factors associated with protection against or increasing the risk of a fatal outcome caused by a given influenza strain (Behrens and Stoll 2006), and genetic factors that affect host susceptibility are likely to play a role. Specific immunity against certain viral epitopes or some de- gree of cross-immunity may explain why people > 65 years were less affected by the 1918 pandemic. The unusual severity of H5N1 infection in humans was initially ascribed to multiple basic amino acids adjacent to the cleavage site, a feature characteristic of highly pathogenic avian influenza A viruses (Subbarao 1998). The presence of these basic amino acids renders the protein susceptible to proteases from many different types of tissues and allows extrapulmonary dissemination due to broadened tissue tropism (Yuen 2005). Another explanation may be that interferons are pivotal in preventing viral spread outside the respiratory tract and that H5N1 interferes with this innate defence against viral infection. The Virus Infectious diseases are the result of a conflict of interest between macroorganisms and microorganisms. Requirements for Success To become a pandemic strain, an influenza virus must comply with a series of re- quirements. It has to The Virus 25 • enter the human body and replicate there, • cause illness in humans, and • be easily transmittable between humans. In the current situation, the potential pandemic virus would have to compete with the al- ready circulating H3N2 and H1N1 strains. The prerequisite for success is good adaptation: adaptation to human cells; the ca- pability to take over the production machinery of the host cell to produce new off- spring; as well as making the individual cough and sneeze to spread the offspring viruses. The clue to success is virulence (Noah 2005, Obenauer 2006, Salomon 2006) – and novelty: if the virus is a true newcomer, most living human beings will have little or no protection at all. The new virus will have unlimited access to virtu- ally every human being and will find a feeding ground of > 6. The passing of powers from one reigning influenza subtype to a new one is called “antigenic shift” because the antigenic characteristics of the new virus need to shift dramatically to elude the immune system of virtually the entire mankind. Antigenic shift is a major change in the influenza A viruses resulting in new haemagglutinin and/or new neuraminidase proteins. This change may occur by: 1) reassortment of the segmented genome of two parent viruses, or 2) gradual mutation of an animal virus. For reassortment to take place, both the new pandemic candidate virus, nor- mally of avian origin, and an already circulating human virus, i. Inside the cell, genes from both viruses are reassembled in an entirely new virus (they don’t actually have sex, but for didactic purposes, this image might work quite nicely). Recent evi- dence with recombinant viruses containing genes from the 1918 pandemic virus shows that viruses expressing one or more 1918 virus genes were less virulent than the constellation of all eight genes together (Tumpey 2005). The 1918 virus was particular indeed: it appears that it was not the result of a reassortment of two ex- isting viruses, but an entirely avian-like virus that gradually adapted to humans in stepwise mutations (Taubenberger 2005). It is obviously tempting to speculate that the emergence of a completely new human-adapted avian influenza virus in 1918 (n=1) could be deadlier than the introduction of reassortant viruses in 1957 and 1968 (n=2), but such speculation is not scientific. Interestingly – and worryingly –, some amino acid changes in the 1918 virus that distinguish it from standard avian sequences are also seen in the highly pathogenic avian influenza virus strains of H5N1, suggesting that these changes may facilitate virus replication in human cells and increase pathogenicity (Taubenberger 2005). They are spherical or filamentous in structure, ranging from 80 to 120 nm in diameter (Figure 4 and 5). When sliced transversely, influenza virions resemble a symmetrical pepperoni pizza, with a circular slice of pepperoni in the 26 Influenza 2006 middle and seven other slices evenly distributed around it (Noda 2006). The domestic duck in Southeast Asia is the principal host of influenza A viruses and also has a central role in the generation and maintenance of the H5N1 virus (Li 2004). In Thailand, there was a strong association between the H5N1 virus and the abundance of free-grazing ducks and, to a lesser extent, native chickens and cocks, as well as wetlands, and humans. The virus is killed by heat (56°C for 3 hours or 60°C for 30 minutes) and common disinfectants, such as formalin and iodine compounds. Transmission Influenza is primarily transmitted from person to person via droplets (> 5 µm in diameter) from the nose and throat of an infected person who is coughing and sneezing (Figure 6).

In contrast Role of the Mesh Kits they report no post-operative Pelvic organ prolapse is often complications and acceptable associated with a global weakness outcomes with this newer of support structures and in generation allograft order avanafil 100 mg visa erectile dysfunction pump pictures. There remains very little Grade 1 They consist of an anterior and evidence for the use of mesh and posterior system discount avanafil 100 mg fast delivery erectile dysfunction young male. Sexual function is each side that are placed through often not reported in the literature the obturator foramina. The and those studies that do look at posterior kit has a central mesh this aspect of vaginal function, portion with bilateral arms that usually confne it to a number go through the buttock, traverse of short sentences with very the ischiorectal fossa and enter the little questionnaire-based data. The frst reports on a rise in dyspareunia of these devices to be launched following repair with synthetic was the Prolift System, marketed mesh. They superior arm is inserted in a similar have, however, been implemented fashion to the Posterior prolift and with very little data to support Apogee but in addition, it also their use. Author N Prosthesis Follow up Success Complications (months) Rust [1975] 12 Mersilene 9-42 100% Nil Symonds[1981] 17 Tefon 60-360 88% Nil Addison[1985] 56 Mersilene 6-126 89% Nil Timmons 163 Mersilene 9m – 18 99% Nil years Drutz[1987] 15 Marlex 3-93 93% 1 sepsis mesh removal Baker[1990] 59 Prolene 1-45 86% Nil Snyder[1991] 147 78 Gore -Tex 60 73% 4 mesh erosions 65 Dacron Creighton[1991] 23 Mersilene 3-91 91% 2 sinuses removal mesh Van Lindert[1993] 61 Gore-Tex 15-48? Failure number of signifcant long-term to recognise and repair an anal complications including faecal sphincter injury is one of the top incontinence, perineal pain and four reasons for complaint and dyspareunia. Johanson et al report that faecal incontinence related to only one third of women suffering sphincter injuries in the frst year with faecal incontinence sought after birth. If the included low parity, prolonged patient has had a instrumental frst and second stage, high birth delivery or if a large episiotomy weight, episiotomy and forceps was performed, she should be delivery. They analysed the same examined by an someone who data, applying multivariate logistic is experienced in the diagnosis progression analysis and only high of sphincter injury. If in doubt, birth weight and forceps delivery it is useful to ask the women to emerged as risk factors. Occiptoposterior postion “pill-roll” the sphincter with the also appears to be associated forefnger in the rectum and the with sphincter injury, with Wu et thumb in the vagina. This will al reporting a fourfold increase enable the clinician to detect compared to occipitoanterior any loss of sphincter bulk – again positions. The relationship suggesting an underlying third or between episiotomy and sphincter fourth degree tear. Overall, signifcant amount of uncertainty, 50% of third degree tears are it would be prudent to perform associated with episiotomy and the repair under anaesthesia. Fourth degree: a third degree tear with disruption of the anal The anal sphincter comprises: epithelium. A general or spinal the vaginal epithelium, perineal anaesthetic makes it much easier skin, perineal muscles and fascia to inspect the tissues and to but not the anal sphincter. The sphincter is usually more relaxed Third degree: disruption of the which makes it easier to retrieve vaginal epithelium, perineal skin, if the ends are retracted. The surgeon also has access 3a: partial tear of the external to better lighting and proper sphincter involving less than 50% instrumentation and often it is thickness. In addition to recommending an overlap technique, Monga Inexperience of the operator and Sultan also performed a signifcantly increases morbidity separate repair of the internal and may also predispose to anal sphincter and this may also litigation. In a trial by Repair of the sphincter following Fernando et al 24% of women who an acute obstetric injury has had an end-to-end repair reported undergone a signifcant change faecal incontinence compared over the past decade. The reported lower incidence in faecal urgency success rates with an overlapping and lower anal incontinence score technique are better, with in the overlap group. After the sphincter has been The torn muscle, including the repaired, the vaginal skin is closed internal and external sphincter, much like one would close an should always be repaired with episiotomy, making every effort to a monoflamentous delayed reconstruct the perineal body. The internal Every woman should be given anal sphincter should frst be antibiotics and stool softeners identifed and then repaired using following the repair. If it is a 3B, an overlap technique is probably better and this is done as follows: The ends of the torn muscle are identifed and clamped using Allis forceps. Whether an end-to-end or overlap technique is used, between three and four sutures are inserted and these are tied following insertion of all the sutures. They urogenital fstulae occur as a are described by their anatomical consequence of surgery, most location (Table: I) and can be commonly following abdominal classifed according to organ hysterectomy and more recently involvement, i. The of urogenital fstulae with the majority of urogenital fstulae remainder following urological, occur between the vagina and vascular and colorectal procedures. Clinic, 82% of cases were caused by Communication between the gynaecological surgery, followed lower urinary tract and the uterus by obstetric related fstulae in 8%, or cervix are rare (Figure: 1) 6% related to pelvic radiation and 4% following trauma. There are bleeding at the angles of the reports of cases presenting many vault, pelvic adhesions, a previous as fve years after therapy. It is caesarean section leading to imperative to investigate these diffculty in separating the bladder women for a possible recurrence peritoneum from the uterus, and of the malignancy. Uncommon causes Ureterovaginal fstulae occur most for urogenital fstulae include commonly with laparoscopic or vaginal foreign bodies, trauma abdominal hysterectomy, usually or a bladder calculus. Vesicouterine The exact prevalence is unknown Ureterovaginal but they are particularly common Ureterourerine in Africa and South Asia. The level at which the fetal head Urethrovaginal becomes impacted during labour Complex Fistulae determines the site of injury and Uretero-vesico-vaginal type of fstula. The Urogenital Fistulae urethra is involved in 28% of cases Surgery of obstetric related fstula with Obstetrical total urethral destruction in 5% of patients. Infection Foreign body Symptoms injury or ligation and tissue necrosis following ischaemia or Symptoms of fstulae vary infammation. A women who presents with fuid Urethrovaginal fstulae may leaking from her vagina following occur following surgery for pelvic surgery, should be suspected urethral diverticulae, anterior to have a fstula unless proven vaginal prolapse, stress urinary otherwise. In these women, a fstulae, usually present with foul smelling or persistent vaginal urinary leakage approximately one discharge often precedes the urine week following delivery (range day leakage. Unlike Ureterovaginal fstulae are also iatrogenic surgical fstulae which not infrequently associated are characterised by a discrete with febrile episodes. If there is injury, the pathophysiological extravasation of urine into the effects of obstructed labour abdominal cavity, patients may are wider and can result in a present with anorexia, nausea, broad range of injuries including vomiting, increasing abdominal neurapraxia, lower bowel pain, abdominal distension and dysfunction, muscle injury and postoperative ileus. The term should alert the physician not only “feld injuries” has been coined to to a possible ureterovaginal fstula, refer to this range of damage. A tampon is then and diagnostic investigation placed in the vagina and again as an outpatient is acceptable. If costovertebral angle tenderness, the tampon turns orange, a associated with ureteric injuries vesicouretric fstula is diagnosed. The pathognomonic fnding is Investigations the observation of urine leaking into the vagina on speculum The aims of the investigations examination. To establish that the leakage examination of the anterior is extraurethral rather than vagina and apex. To diagnose multiple fstulae vaginal apex and it is therefore diffcult to determine clinically whether the origin of the leakage Biochemistry and is the bladder or ureter. Following pelvic examination, the bladder microbiology should be always catheterized and a urine sample sent for microscopy Initial laboratory investigations and culture. Urine for culture and microscopy diagnosis confrmed by observing to rule out infection the leakage of dye-stained urine 2. Urea and electrolyte – assess ingest 200mg oral phenazopyridine urea and creatinine level which ( pyridium) 3 hours before may be elevated with ureteric 190 injuries fndings are equivocal, contrast 4. If the urea and creatinine level of Retrograde pyelography is a the discharge is greater than reliable way to identify the exact the serum values, it is highly site of a ureterovaginal fstula. It will, Anaesthesia And however, confrm a suspected Cystoscopy vesicouavaginal, vesicouterine or complex fstula.

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Tetralogy of Fallot Named after Etienne-Louis Arthur Fallot (1888) who described it as "la maladie blue" and is a common developmental cardiac defect avanafil 200 mg amex erectile dysfunction treatment uk. The syndrome consists of a number of a number of cardiac defects possibly stemming from abnormal neural crest migration purchase avanafil american express impotence at 16. The long Fetal period (4x the embryonic period) is a time of extensive growth in size and mass as well as ongoing differentiation of organ systems established in the embryonic period and do so at different times. For example, the brain continues to grow and develop extensively during this period (and postnatally), the respiratory system differentiates (and completes only just before birth), the urogenital system further differentiates between male/female, endocrine and gastrointestinal tract begins to function. First Trimester (1 - 12 weeks) - embryonic and early fetal Second Trimester (13 - 24 weeks) - organ development and function, growth Third Trimester (25 - 40 weeks) - organ function and rapid growth Lecture Audio Lecture Date: 13-10-2009 Lecture Time: 12:00 Venue: BioMed E Speaker: Mark Hill Fetal Fetal length and weight (http://lectopia. Fetal Weight See also Fetal origins hypothesis and Normal Development - Birth - Low Birth Weight (http://embryology. Microscopically there is ongoing: cell migration, extension of processes, cell death and glial cell development. Cortical maturation (sulcation and gyration) and vascularization of the lateral surface of the brain starts with the insular cortex (insula, insulary cortex or insular lobe) region during the fetal period. This cerebral cortex region in the adult brain lies deep within the lateral sulcus between the Timeline of events in Human temporal lobe and the parietal lobe. Neural Development sulcation - The process of brain growth in the second to third trimester which forms sulci, grooves or folds visible on fetal brain surface as gyri grow (gyration). A study of 78 premature and mature newborns showed that total brain tissue volume increased linearly over this period at a rate of 22 ml/week. The rapid increase in total grey matter is mainly due to a Human brain at four months (inferior surface) fourfold increase in cortical grey matter. Month 3-6 - lungs appear glandular, end month 6 alveolar cells type 2 appear and begin to secrete surfactant. Gonadal Hormones testosterone - required during fetal development for external genital development and internal genital tract in male. A teratogen (Greek, teraton = monster) is defined as any agent that causes a structural abnormality (congenital abnormalities) following fetal exposure during pregnancy. Absolute risk - the rate of occurrence of an abnormal phenotype among individuals exposed to the agent. Fetotoxicant - is a chemical that adversely affects the developing fetus, resulting in low birth weight, symptoms of poisoning at birth or stillbirth (fetus dies before it is born). Synergism - when the combined effect of exposure to more than one chemical at one time, or to a chemical in combination with other hazards (heat, radiation, infection) results in effects of such exposure to be greater than the sum of the individual effects of each hazard by itself. Cells exposed to a stress, drug or toxicant respond by altering the pattern of expression of genes within their chromosomes. There is also growing evidence that some effects are more subtle and relate to later life health events. The theory was therefore originally called the "Barker Hypothesis" and has recently been renamed as "fetal origins" or "programming". Glossary Links 2009 Lecture 23 From Embryology Contents Birth and Postnatal Development Introduction There are a great number of comprehensive, scientific and general, books and articles that cover Parturition, Birth or Childbirth. Birth or parturition is a critical stage in development, representing in mammals a transition from direct maternal support of fetal development, physical expulsion and establishment of the newborns own respiratory, circulatory and digestive systems. Childbirth Parturition (Latin, parturitio = "childbirth") describes expelling the fetus, placenta and fetal membranes and is probably initiated by fetus not mother. Preterm birth - Risks of preterm birth in abnormal low birth weight (intrauterine growth restriction) and high (large for gestational age) categories are 2- to 3-fold greater than the risk among appropriate- for-gestational-age infants. Respiration Lungs at birth collapsed and fluid-filled - replaced with air by powerful inspiratory movement and absorption through the alveoli Lung epithelia has to rapidly change from its prenatal secretory function to that of fluid absorbtion. Adult rib orientation is oblique (both anterior and lateral views), allows for pump-handle and bucket handle types of inspiration. The adult anatomical remnant of the umbilical vein between the umbilicus and liver is the ligamentum teres. Postnatal closure occurs initially by by smooth muscle contraction and begins at the first breath and is rapid, completed within the first day (about 15 hr after birth). Anatomical closure is much slower occuring by 2–3 weeks after birth (33% of infants), by 2 months (90% of infants) and by 1 year (99% of infants). The adult anatomical remnant of the ductus venosus is the ligamentum venosum (a dorsal fissure on the liver). In recent years there has been some controversy of the relevance and accuracy of some of the criteria used in this test, though many feel it is still an invaluable initial assessment tool particularly where medical services are limited. Different countries and medical services have different policies on not only what will be diagnostically tested, but also how long the test card will be kept following analysis. This incidence is influenced by several factors (diagnostic criteria, gender, genetic and racial factors, and age of the population). However, it is acceptable medical practice not to initiate intensive care if parents so wish, following appropriate counselling. Breech position - occurs in about 3% of fetuses when buttocks or lower limb are presented to the birth canal rather than normal cephalic (head-first) position (presentation). Associated increased - perinatal mortality, perinatal morbidity, recurrence in successive siblings Current research suggests that genetically that both men and women delivered in breech presentation at term could also contribute to an increased risk of breech delivery in their offspring. Normally this meconium is defaecated (passed) postnatally over the first 48 hours and then transitional stools from day 4. Premature discharge into the amniotic sac can lead to mixing with amniotic fluid and be reswallowed by Breech Birth the fetus. Necrotizing Enterocolitis Occurs postnatally in mainly in premature and low birth weight infants (1 in 2,000 - 4,000 births). The underdeveloped gastointestinal tract appears to be susceptible to bacteria, normally found within the tract,to spread widely to other regions where they damage the tract wall and may enter the bloodstream. Stillbirth and Perinatal Death Perinatal period is the early postnatal period relating to the birth, statistically it includes the period up to 7 days after birth. In pregnant women anywhere between 2 - 15% have birth weights of greater than 4000 grams (4 Kg, 8 lb 13 oz). Vertex Presentation (cephalic presentation) where the fetus head is the presenting part, most common and safest birth position. Each topic summary is designed for use in conjunction with the relevant didactic lecture given during the rotation. Original and Review Articles – Original, and review articles are provided for residents who seek a more comprehensive understanding of a topic. We recognize that residency is a busy time, but we hope that you will take the time to read articles relevant to the management of your patients. In order to facilitate learning at many levels, several other educational opportunities are available. Tutorials – These are 20-30 minute sessions offered during the rotation that will provide the resident with hands on experience (e. The goal of morning rounds is to develop treatment plans that can be defended by the best available scientific evidence.