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Uterine activity needs to be monitored accurately in order to classify the diferent decelerations buy 20mg nifedipine free shipping blood pressure quadriplegic, as management would depend on the type of the deceleration generic nifedipine 30 mg otc blood pressure scale. The causes of early decelerations are physiological – head compression resulting in Box 4 Causes of late decelerations increased vagal tone – not pathological purchase nifedipine 20mg online heart attack 5 year survival rate. Late Postterm pregnancy decelerations are thought to be caused by a decreased blood fow (associated with a uterine contraction) Maternal condition beyond the capacity of the fetus to extract oxygen buy nifedipine 20mg amex blood pressure 65. Here the baseline rate is 130 beats/ minute, with a baseline variability of 10–15 beats/minute and there are accelerations. There is includes: however a baseline tachycardia and a reduced baseline variability. If repeated accelerations are present with reduced vari- This would be then classifed as atypical variable decelerations. True early uniform decelerations are rare and benign, and stage of labour, and substantial head compression therefore they are not signifcant. This could include features described, variable decelerations are said moving the woman to theatre if the fetal heart has not to be atypical if they have any of the following recovered by 9 minutes. If the fetal heart recovers within 9 minutes, the decision to deliver should be reconsidered in characteristics (Fig. However, an tion; increase in the baseline heart rate, even within the normal prolonged secondary rise in baseline rate (exaggerated range, with other non-reassuring or abnormal features shouldering); should increase concern about the well being of the fetus. A full history of the presenting complaint is extremely important, as are any associated symp- If the pH is 7. If a third sample is to the gestational age, as aetiologies change through- required, a consultant should be involved in further out pregnancy. Routine Clinical fndings may be less obvious and more diffcult electronic monitoring of fetal heart rate and to elicit in pregnancy than in non-pregnant women with uterine activity during labor. Fetal heart rate mon- result of lifting and stretching of the anterior abdominal wall. This means that any underlying infammation is itoring during labour: too frequent inter- not in direct contact with the peritoneum, thus reducing vention, too little beneft? National Collaborating Centre for Women’s decubitus position to help distinguish between uterine and Children’s Health. This manoeuvre displaces the care of healthy women and their babies uterus to one side. It may be worthwhile carrying out a vaginal examination if a gynaecological cause is suspected. In patients presenting early in pregnancy, it is import- ant to rule out ectopic pregnancy although it should be emphasised that this tends to cause pain in the lower abdomen. Laboratory investigations Commonly used laboratory tests have diferent ranges in pregnancy (see Appendix), and therefore may be of limited use in aiding diagnosis. It is due to an increased intra- rad) have not been associated with fetal abnormalities abdominal pressure from a gravid uterus and leads or pregnancy loss. However, there is a possible associa- to dysfunction of the lower oesophageal sphincter tion between prenatal radiation exposure and childhood cancer. Tere is also delayed clearance medically and other imaging options have been consid- of the refux leading to increased acid exposure times. It has been used in later waterbrash (excess salivation, especially during an epi- pregnancy to exclude morbidly adherent placentae. It sode of pain); must be remembered that the duty of care of any attend- regurgitation of acid and bile, which can, rarely, give rise ing doctor is primarily to the mother, as the fetus has no to nocturnal sore throat or indeed asthma. Treatment Conditions with increased frequency in General measures include elevation of the head of pregnancy the bed, small, frequent meals, and avoiding anything The following conditions causing epigastric pain that obviously exacerbates the symptoms. Patients occur more frequently when a woman is pregnant: should be advised to avoid eating just prior to lying down. Although there is no con- biliary colic; clusive evidence for the safety of H2-receptor antag- acute cholecystitis (due to decreased gallbladder motility and increased cholesterol saturation of bile in pregnancy). The following conditions can occur as a result of Biliary colic and acute cholecystitis pregnancy: Asymptomatic gallbladder disease (seen on imag- rupture of the rectus abdominis muscles; ing) occurs in 3–4 per cent of pregnant women. Stomach Delayed Conditions incidental to pregnancy gastric Conditions incidental to pregnancy are: emptying non-ulcer dyspepsia; Uterus Increasing gastric and duodenal ulceration; uterine size gastritis and duodenitis; irritable bowel syndrome; acute and chronic pancreatitis. It is most commonly be avoided, as both bismuth and tetracycline are felt in the right upper quadrant but can be epigastric teratogenic. Tere is a decreasing incidence of this condition in Blood tests are of limited value as both leucocytosis the Western world owing to the declining incidence of and raised alkaline phosphatase levels are observed in H. Transient increases in amylase can occur in 30 percent of The clinical features in this condition include epigas- those with biliary colic but markedly raised levels suggest tric pain before meals. However, amylase may not be elevated in patients with acute on chronic pancreatitis. Gastritis, duodenitis and non-ulcer Treatment dyspepsia Conservative treatment with intravenous fuids Tese conditions can present with dyspeptic symp- and analgesia, particularly pethidine, is the ini- toms of mild to moderate epigastric discomfort and a tial approach. Ideally this should be undertaken dur- ing the second trimester, which minimises the risks irritable bowel syndrome for premature delivery. Changes in bowel habit occur as a result of the increasing levels of serum progesterone, which acts to relax smooth muscle in the gut wall. Acute pancreatitis Initial management involves optimisation of lifestyle Tis occurs most commonly secondary to gallstones through dietary changes. Endoscopic retrograde cholangiopancreaticogram Eosinophilic oesophagitis (Eo) and sphincterotomy can be performed safely in patients found to have common bile duct stones as Eosinophilic oesophagitis is a chronic infamma- a cause for the pancreatitis. While epigastric pain and refux symptoms are features, patients typically present with dysphagia and food regurgitation. Treatment usually involves swallowing sents with epigastric pain afer eating, and is ofen inhaled corticosteroids, and this is considered to be associated with anorexia and weight loss. It is com- appropriate in pregnancy, provided a careful risk/ monly caused by Helicobacter pylori and diagnosed beneft assessment is performed. Probhodana Ranaweera 3 Radiological investigations are generally contraindicated during pregnancy unless there are extremely good introduction indications for using them. Ultrasound is widely used Postoperative fever is a common sign encountered in and is safe in pregnancy. Evaluating and managing 4 Gastro-oesophageal refux disease is very common in pregnancy and is consequently the commonest cause of a patient with a postoperative fever requires a sound epigastric pain. Many pancreatitis, and peptic ulceration, which may need a patients develop fever in the frst few days afer different management plan in pregnancy. Childhood and adult cancer after intrauterine exposure to ionizing Manifestation of fever is due to cytokine release in response to various stimuli. Medical versus surgical management cytokine most closely correlated with postopera- tive fever. For example, laparoscopic oopho- Gastrointest Endosc 2009; 69(3 Part 1): rectomy is associated with less tissue trauma and 453–61.

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The energy costs and relative demands of some familiar activities are listed in Table 29 nifedipine 30mg generic blood pressure quitting drinking. Exhaustion is predictable on the basis of relative demand on the maximal oxygen uptake buy nifedipine 30mg mastercard blood pressure 3rd trimester. Historically order nifedipine 30 mg on line arrhythmia kamaliya download, many arguments claim primacy for either cardiac output (oxygen delivery) or muscle metabolic capacity (oxygen use) limitations cheap nifedipine 20 mg otc heart attack risk assessment. However, it may be that every link in the chain taking oxygen from the atmosphere to the mitochondrion reaches its capacity at about the same time. In practical terms, this means that any lung, heart, vascular, or musculoskeletal illness that reduces oxygen flow capacity will diminish a patient’s functional capacity. It has been shown that in untrained subjects, the oxygen consumption dominates, whereas in endurance-trained athletes, oxygen supply is the main limiting factor. In isometric exercise, force is generated at constant muscle length and without rhythmic episodes of relaxation. For prolonged work, the oxidation of foodstuff supplies this energy, with the cardiovascular system carrying the oxygen to working muscles. Local control of blood flow ensures that only working muscles with increased metabolic demands receive increased blood and oxygen delivery. If the legs alone are active, leg muscle blood flow should increase, whereas arm muscle blood flow remains unchanged or is reduced. In dynamic exercise, both total cardiac output and relative and absolute output directed to working skeletal muscle increase dramatically (Table 29. For millennia, our ancestors successfully used exercise both to escape being eaten and to catch food; therefore, it is no surprise that cardiovascular control in exercise is complex and unique. It is as if a brain software program titled “Exercise” was inserted into the brain as work begins. Initially, the motor cortex is activated; the total neural activity is roughly proportional to the muscle mass and its work intensity. This neural activity communicates with the cardiovascular control centers, reducing vagal tone on the heart (which raises heart rate) and resetting the arterial baroreceptors to a higher level. As work rate is increased further, lactic acid is formed in actively contracting muscles, which stimulates muscle afferent nerves to send information to the cardiovascular center that increases sympathetic outflow to the heart and systemic resistance vessels. Increased sympathetic drive does elevate heart rate and cardiac contractility, resulting in increased cardiac output; local factors in the coronary vessels mediate coronary vasodilation. Increased sympathetic vasoconstrictor tone in the renal and splanchnic vascular beds and in inactive muscle reduces blood flow to these tissues. Increased vascular resistance and decreased blood volume in these tissues help maintain blood pressure during dynamic exercise. In contrast to blood flow reductions in the viscera and in inactive muscle, the brain autoregulates blood flow at constant levels independent of exercise. During strenuous exercise, sympathetic drive can begin to limit vasodilation in active muscle. When exercise is prolonged in the heat, increased skin blood flow and sweating-induced reduction in plasma volume both contribute to the risk of hyperthermia and hypotension (heat exhaustion). Although chronic exercise provides some heat acclimatization, even highly trained athletes are at risk of hyperthermia and hypotension if work is prolonged and water is withheld in demanding environmental conditions. Muscle blood flow increases relative to the resting condition, as does cardiac output, but the higher mean intramuscular pressure limits these flow increases much more than when exercise is rhythmic. These percentages are much less than the equivalent for dynamic work, as defined in terms of. Rhythmic exercise requiring 70% of the can be maintained in healthy subjects for about an hour, whereas work at 50% of the may be prolonged for several hours (see Fig. The reliance on anaerobic metabolism in isometric exercise triggers muscle ischemic chemoreflex responses that raise blood pressure more and cardiac output and heart rate less than that in dynamic work. Oddly, for dynamic exercise, the elevation of blood pressure is most pronounced when a medium muscle mass is working. This response results from the combination of a small, dilated active muscle mass with powerful central sympathetic vasoconstrictor drive. Typically, the arms exemplify a medium muscle mass; shoveling snow is a good example of primarily arm and heavily isometric exercise. Shoveling snow can be risky for those in danger of stroke or heart attack because it substantially raises systemic arterial pressure. The elevated pressure places already-compromised cerebral arteries at risk and presents an ischemic or failing heart with a greatly increased afterload. In acute dynamic exercise, vagal withdrawal and increases in sympathetic outflow elevate heart rate and contractility in proportion to exercise intensity (Table 29. These include the “muscle pump,” which compresses veins as muscles rhythmically contract, and the “respiratory pump,” which increases breath-by-breath oscillations in intrathoracic pressure (see Chapter 17). The importance of these factors is clear in patients with heart transplants who lack extrinsic cardiac innervation. Stroke volume rises in cardiac transplant patients with increasing exercise intensity as a result of increased venous return that enhances cardiac preload. In addition, circulating epinephrine and norepinephrine from the adrenal medulla and norepinephrine from sympathetic nerve spillover augment heart rate and contractility. Stroke volume, in contrast, reaches a plateau in moderate work and is unchanged as exercise reaches its maximum intensity (see Table 29. This plateau occurs in the face of ever-shortening ventricular filling time, testimony to the increasing effectiveness of the mechanisms that enhance venous return and those that promote cardiac contractility. Sympathetic stimulation decreases left ventricular volume and pressure at the onset of cardiac relaxation (as a result of increased ejection fraction), leading to more rapid ventricular filling early in diastole. Even in untrained subjects, the ejection fraction (stroke volume as a percentage of end-diastolic volume) reaches 80% in strenuous exercise. The increased blood pressure, heart rate, stroke volume, and cardiac contractility seen in exercise all increase myocardial oxygen demands. A linear increase in coronary blood flow during exercise that can reach a value five times the basal level meets these demands. Coronary oxygen extraction, high at rest, increases further with exercise (up to 80% of delivered oxygen). In healthy subjects, there is no evidence of myocardial ischemia under any exercise condition, and there may be a coronary vasodilator reserve in even the most intense exercise (Clinical Focus 29. In many patients, coronary blood flow is adequate at rest but, because of coronary arterial blockage, cannot rise sufficiently to meet the increased demands of exercise. With proper supervision, the stress test is a safe method for detecting coronary artery disease. Because the exercise load is gradually increased, the test can be stopped at the first sign of problems. The heart adapts to chronic exercise overload much as it does to high-demand pathologic states: by increasing left ventricular volume when exercise requires high blood flow and by left ventricular hypertrophy when exercise creates high systemic arterial pressure (high afterload). Consequently, the hearts of subjects adapted to prolonged, rhythmic exercise that involves relatively low arterial pressure exhibit large left ventricular volumes with normal wall thickness, whereas wall thickness is increased at normal volume in those adapted to activities involving isometric contraction and greatly elevated arterial pressure such as lifting weights. The larger left ventricular volume in subjects chronically active in dynamic exercise leads directly to larger resting and exercise stroke volume. A simultaneous increase in vagal tone and decrease in β- adrenergic sensitivity enhance the resting and exercise bradycardia seen after training, so that in effect the trained heart operates further up the ascending limb of its length–tension relationship.

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Because H O absorption is determined by the osmolality difference of the lumen and the blood 30mg nifedipine with visa arteria interossea communis, H O can2 2 move both ways in the intestinal tract (i buy discount nifedipine 30mg on-line blood pressure medication one kidney. The2 water of a hypertonic meal is therefore absorbed mainly in the ileum and colon buy cheap nifedipine 20 mg on-line hypertension quality improvement. These two communities are not the same and the genera of microbes living in the mucosa vary from those residing in the lumen cheap 20 mg nifedipine visa pulse pressure widening. It is well established that the species composition and relative abundance of the gut microbiota are impacted by the diet, lifestyle, and overall health of an individual. Humans, like many other animals, have developed a commensalistic relationship with the gut microbiota. Over time, this relationship has evolved to become a mutualistic and interdependent one, in which the physiological activity of the microbiota has a significant impact on the host and the activity of the host impacts the genera comprising the microbiota. In support of life, gut microbial metabolism supplies the host with short- chain fatty acids, essential vitamins (i. The interactions do not end with digestion as microbial chemical signals influence other systems such as the activity of the host’s immune cells and immunologic homeostasis. In a normal, healthy individual, the interactions between the host and microbiota are primarily beneficial. However, dysbiosis can lead to, or be a contributing factor in, a number of maladies including inflammatory bowel disease (e. Clues to the development of the intestinal microbiota have emerged from many different studies. It has long been held that fetuses develop in a sterile environment within the amniotic sac. However, recent studies have shown that certain bacteria are able to cross the placental barrier. When investigators orally administered a genetically labeled species of bacteria to pregnant mice, they noted the appearance of the bacteria in both the amniotic fluid and the meconium of the pups. Others have shown that the oral microbiota is also capable of reaching, and becoming established at, the level of the placenta. Regardless, as indicated by microbial analysis of meconium, infants are born with relatively few microbes colonizing the intestinal lumen. All indications are that the major microbial colonization of the gut occurs following birth. These colonizers will generally reflect the microbial diversity present in the environment to which the infant is first exposed. For example, a vaginal birth versus one that occurs by cesarean section exposes the infant to very different microbes. Microbial recovery back to homeostasis after antibiotic treatment may take up to several months. Given the many factors that have an impact on the microbial community, there is a wide range of potential microbiota that can ultimately colonize an infant’s gut. Immediately after birth, the environment in a newborn’s gut is favorable for supporting the growth of facultative anaerobic microbes. Later, the environment favors growth of anaerobes, particularly in the distal regions of the gut with aerobes favoring the more proximal regions. By 5 years of age, the child’s gut microbial community has changed to be similar to the adult gut. The health of the host and the composition of the gut microbiota are intimately linked through the interactions that occur between the gut microbiome and the host’s innate and adaptive immune systems. These interactions have a large impact on the development of the immune system early in life and on the possibility of the host developing certain diseases in later life. Examples include local inflammatory responses in the gut (mentioned previously) and systemic autoimmune disorders such as rheumatoid arthritis, multiple sclerosis, and type 1 diabetes. Beyond the immune system, the intestinal microbiota is felt to play a role in systemic events outside the digestive tract (e. Secreted antimicrobial proteins and IgA play a role in maintaining the effectiveness of that barrier. Microbes have been implicated in other interactions that occur between the body systems. Such interactions generally result in a healthy individual with a normal body mass index. However, it is known that obese individuals do not have the same genera in their gut microbiota as that of more lean individuals. These differences lead to noticeable imbalances in energy metabolism and fat storage along with insulin resistance and have led to such extreme treatments as fecal transplants to treat obesity. However, the cause and effect may be hard to fully ascertain as the composition of the diet also influences the mixture of genera that comprise the gut microbiota. Recent data on patients who have undergone Roux-en-Y gastric bypass surgery indicate that following the procedure, the patient’s gut microbiota changed significantly enough that it contributed to the weight loss observed in these patients, most likely by way of altered fatty acid metabolism and fat storage. Students are encouraged to consult the literature to learn more about other aspects of the host–microbiota interaction in health and disease. The major function of the gastrointestinal tract is storage, mixing, digestion, and absorption of nutrients. The stomach prepares chyme to aid in the digestion of food in the small intestine. Parietal cells secrete hydrochloric acid and intrinsic factor, and chief cells secrete pepsinogen. The acidity of gastric secretion provides a barrier to microbial invasion of the gastrointestinal tract. Gastric secretion is under neural and hormonal control and consists of three phases: cephalic, gastric, and intestinal. Gastric inhibitory peptide, secreted by K cells, is a potent inhibitor of gastric acid secretion and enhances insulin release in elevated concentrations of plasma glucose. Pancreatic secretion neutralizes the acids in chyme and contains enzymes involved in the digestion of carbohydrates, fat, and protein. Secretin stimulates the pancreas to secrete a bicarbonate-rich fluid, thereby neutralizing acidic chyme. Pancreatic secretion is under neural and hormonal control and consists of three phases: cephalic, gastric, and intestinal. Proteins are digested to form amino acids, dipeptides, and tripeptides before being taken up by enterocytes and transported in the blood. The gastrointestinal tract absorbs water-soluble vitamins and ions by different mechanisms. Most of the salt and water entering the intestinal tract, whether in the diet or in gastrointestinal secretions, is absorbed in the small intestine. Lipids absorbed by enterocytes are packaged and secreted as chylomicrons into the lymph. Carbohydrates, when digested, form maltose, maltotriose, and α-limit dextrins, which are cleaved to brush border enzymes to monosaccharides and taken up by enterocytes.

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The amount of water lost from the body by sweating depends on both the environment and the body fluid composition before exercise order nifedipine 20mg amex blood pressure medication inderal. The early effects of dehydration are to increase heart rate order nifedipine 30 mg amex blood pressure chart with age and height, and this impairs heat transfer from muscle contraction to skin where it is dissipated for cooling buy cheap nifedipine 30 mg on line pulse pressure normal rate. Sweating is the body’s way of getting rid of heat that is produced by muscle exercise purchase 30 mg nifedipine with mastercard arteria circumflexa femoris lateralis. Sweat glands produce a fluid that is derived from the interstitial spaces and capillaries in the skin and is similar to plasma in that it is composed principally of water and sodium ions. As sweat evaporates, it dissipates the excess heat to cool the body; the dryer the air, the quicker evaporation and cooling occur to help maintain homeostasis. The water lost by sweating comes from the fluid compartments of the body, thus there is a net increase in the concentration of the electrolytes (ions) in the body fluid creating hypertonicity (having a higher concentration of electrolytes inside the fluid compartments than outside). If the water lost due to exercise and sweating is not replaced, dehydration can occur. The solution to the problem is to drink plenty of fluids before and during exercise. Without adequate water replacement, the water and electrolyte imbalance can lead to heat stroke and even death. Rarely is there a necessity to replace lost sodium, although many sports drinks contain both sodium and potassium. The reason for this is that ingested water, which is rapidly absorbed through the gut, results in adequate salt replacement by absorption from the contents of the digestive tract. Explain the specialized functions of the different cell types of the nervous system. Explain the mechanism by which components are transported between the soma and neuronal terminals. Explain how movement of ions through ion channels can produce an action potential. Explain why an action potential is unidirectional and how it propagates without decrement. Explain how the specializations of the synapse contribute to synaptic transmission. Describe different synaptic transmitters in terms of their signaling, function, and role in disease. The efferent function consists of communicating with organ systems to maintain or adjust function as well as controlling motor function. Together, these effectively restrict transepithelial permeability and serve to protect the brain from infection and toxins. In the periphery, capillary endothelial cells have gaps (termed fenestrae) between them and use intracellular pinocytotic vesicles to facilitate the transcapillary transport of fluid and soluble molecules. The cells have fewer pinocytotic vesicles and are surrounded by pericytes and astroglial processes. The primary cell types in the nervous system, neurons and glia, differ in function and morphology. Glia support this function and can be divided into multiple cell groups based on morphology and function. They serve an immune function in that they phagocytose damaged cells, invade microorganisms, and secrete immune mediators. This myelin sheath can be disrupted, as happens with multiple sclerosis, resulting in abnormalities in signal conduction. Glial cells are more numerous than neurons and can proliferate particularly in response to injury or infection. This ability to proliferate can also go awry and result in gliomas: tumors derived from glial cells. Neurons are less numerous than glial cells and, like glia, can be classified into different types based on morphology and function (Fig. All neurons have a soma (cell body) containing the nucleus and primary organelles such as the endoplasmic reticulum and Golgi apparatus. In the case of unipolar cells, there is only one process that extends from the soma, whereas bipolar cells have two processes and multipolar cells have multiple processes. The portion of the axon that extends from the cell body, the axon hillock, is generally a thickened area. These myelin sheaths are made of lipids and proteins and are wound around the axon at regular intervals. In between myelin sheaths are the nodes of Ranvier: short segments of the axon that are unmyelinated. At the end of the axon is a specialized segment referred to as the presynaptic terminal or bouton. The axon functions to transmit information in the form of an action potential and to transport materials to the presynaptic terminal. The axon has an efferent function in that it releases signaling molecules to transmit information. The neuron may have one process sharing dendritic and axonal function (unipolar), one process that is a dendrite (bipolar), or multiple dendritic processes (multipolar). In the case of multipolar neurons, each dendritic branch can have branches off of it producing extensive arborization. Dendrites serve an afferent function in that they gather information and transmit it to the soma. They form postsynaptic terminals receiving information released from the axon’s presynaptic terminal. The specialized region in which molecules are released from the axon and interact with dendrites is referred to as the synapse. A simplified schematic of a synapse consists of a presynaptic terminal at the end of an axon adjacent to a postsynaptic terminal at the end of a dendrite. The presynaptic terminal contains vesicles that release chemical messengers into the synaptic cleft where they can then interact with receptors that are located on the postsynaptic terminal. These are relatively rare but are utilized in some regions such as the retina and other special senses. These are the most common neuronal type and are found in the brain, spinal cord, and autonomic ganglia. Some individuals do not fully recover between episodes but demonstrate continued deterioration such that progressive attacks are more severe. A small percentage of individuals experience a progressive disease without remission. The etiology of the disease is not well understood but may be influenced by exposure to the Epstein-Barr virus and vitamin D deficiency. Common symptoms experienced in the early phases of the disease include visual disturbances, tingling sensations, and motor disturbances. This leads to their inability to fully myelinate axons and can result in damage to axonal processes. Other immune cells also infiltrate the damaged area along with astrocytes, which can result in scarring around the damaged axon.

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