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STUDENT DIGITAL NEWSLETTER ALAGAPPA INSTITUTIONS |
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Alfonso Casta, MD
Share information with the patient is cholesterol in shrimp bad for you generic 160mg fenofibrate overnight delivery, especially at transition points during the visit cholesterol fried foods order 160mg fenofibrate free shipping. It often provides valuable information about past diagnoses and treatments; however cholesterol ratio 5 purchase 160 mg fenofibrate, data may be incomplete or even disagree with what you learn from the patient how much cholesterol in eggs benedict buy fenofibrate 160 mg, so be open to developing new approaches or ideas. Posture, gestures, eye contact, and tone of voice all can express interest, attention, acceptance, and understanding. Reactions that betray disapproval, embarrassment, impatience, or boredom block communication. Patients find cleanliness, neatness, conservative dress, and a name tag reassuring. Suggest moving to an empty room rather than having a conversation that can be overheard. Look for signs of discomfort, such as frequent changes of position or facial expressions that show pain or anxiety. Move any physical barriers between you and the patient, such as desks or bedside tables, out of the way. If necessary, jot down short phrases, specific dates, or words rather than trying to put them into a final format. Maintain good eye contact, and whenever the patient is talking about sensitive or disturbing material, put down your pen. Often, you may need to focus the interview by asking the patient which problem is most pressing. Use verbal and nonverbal cues that prompt patients to recount their stories spontaneously. Use continuers, especially at the outset, such as nodding your head and using phrases such as "Uh huh," "Go on," and "I see. In this model, disease is the explanation that the clinician brings to the symptoms. It is the way that the clinician organizes what he or she learns from the patient into a coherent picture that leads to a clinical diagnosis and treatment plan. This is crucial to patient satisfaction, effective health care, and patient follow-through. Patients offer various clues to their concerns that may be direct or indirect, verbal or nonverbal; they may express them as ideas or emotions. Each symptom has attributes that must be clarified, including context, associations, and chronology, especially for pain. Include environmental factors, personal activities, emotional reactions, or other circumstances that may have contributed to the illness. In general, the patient interview moves back and forth from an open-ended question to a directed question and then on to another open-ended question. Learning about the disease and conceptualizing the illness give you and the patient the basis for planning further evaluation (physical examination, laboratory tests, consultations, etc. Motivational interviewing techniques may help the patient achieve desired behavior changes. Because we bring our own values, assumptions, and biases to every encounter, we must look inward to clarify how our expectations and reactions may affect what we hear and how we behave. Self-reflection brings a deepening personal awareness to our work with patients and is one of the most rewarding aspects of providing patient care. Culture is a system of shared ideas, rules, and meanings that influences how we view the world, experience it emotionally, and behave in relation to other people. The influence of culture is not limited to minority groups-it is relevant to everyone, including the culture of clinicians and their training. Cultural competence commonly is viewed as "a set of attitudes, skills, behaviors, and policies that enable organizations and staff to work effectively in cross-cultural situations. It reflects the ability to acquire and use knowledge of the health-related benefits, attitudes, practices, and communication patterns of clients and their families to improve services, strengthen programs, increase community participation, and close the gaps in health status among diverse population groups. As clinicians, we face the task of bringing our own values and biases to a conscious level. Biases are the attitudes or feelings that we attach to perceived differences, for example, the way an individual relates to time, which can be a culturally determined phenomenon. Communication based on trust, respect, and a willingness to re-examine assumptions helps allow patients to express concerns that run counter to the dominant culture. You, the clinician, must be willing to listen to and validate these emotions, and not let your own feelings prevent you from exploring painful areas. You may need to shift your inquiry to symptoms of depression or begin an exploratory mental status examination. Focus on the context of the symptoms and guide the interview into a psychosocial assessment. The history is vague and difficult to understand, and patients may describe symptoms in bizarre terms. Watch for delirium in acutely ill or intoxicated patients and for dementia in the elderly. When you suspect a psychiatric or neurologic disorder, shift to a mental status examination, focusing on level of consciousness, orientation, and memory. Some patients cannot provide their own histories because of delirium, dementia, or other conditions. In such cases, determine whether the patient has decision-making capacity, or the ability to understand information related to health, to make medical choices based on reason and a consistent set of values, and to declare preferences about treatments. Many patients with psychiatric or cognitive deficits still retain the ability to make decisions. For patients with capacity, obtain their consent before talking about their health with others. Consider dividing the interview into two segments-one with the patient and the other with both the patient and a second informant. For patients with impaired capacity, find a surrogate informant or decision maker to assist with the history. Check whether the patient has a durable power of attorney for health care or a health care proxy. Many patients have reasons to be angry: they are ill, they have suffered a loss, they lack accustomed control over their own lives, and they feel relatively powerless. Accept angry feelings from patients and allow them to express such emotions without getting angry in return. The ideal interpreter is a neutral, objective person trained in both languages and cultures. Avoid using family members or friends as interpreters: confidentiality may be violated. As you begin working with the interpreter, make questions clear, short, and simple. During the introduction, include information as to the roles individuals will play. Transparency: Let the patient know that everything said will be interpreted throughout the session. Ethics: Use qualified interpreters (not family members or children) when conducting an interview. Qualified interpreters allow the patient to maintain autonomy and make informed decisions about his or her care. The interpreter may be able to serve as a cultural broker and help explain any cultural beliefs that may exist. Make sure to ask and address any questions the patient may have prior to ending the encounter. Retain Control: It is important as the provider that you remain in control of the interaction and not let the patient or the interpreter take over the conversation. Explain: Use simple language and short sentences when working with an interpreter. This will ensure that comparable words can be found in the second language and that all the information can be conveyed clearly. On the chart, note that the patient needs an interpreter and who served as an interpreter this time. Simply handing the patient written material upside-down to see if the patient turns it around may settle the question. Assess health literacy, or the skills to function effectively in the health care system: interpreting documents, reading labels and medication instructions, and speaking and listening effectively.
If three fingers are placed side by side from the midline of the forehead outwards cholesterol medication lawsuit buy fenofibrate 160 mg overnight delivery, the second finger lies on the orbit where this is crossed by the supratrochlear nerve cholesterol test during pregnancy discount fenofibrate 160 mg visa, and the third finger lies over the supra-orbital nerve cholesterol test kit ebay fenofibrate 160 mg cheap. The latter point may often be identified by palpation of the supra-orbital notch cholesterol levels chart in south africa discount fenofibrate 160mg without prescription, pressure on which is unpleasantly painful. The nasociliary nerve enters the superior orbital fissure within the tendinous ring of origin of the recti. Here it becomes the anterior ethmoidal nerve, which runs along the anterior cranial fossa on the cribriform plate to enter the nasal cavity, through an aperture near the crista galli, where it splits into septal and lateral branches. The septal branch supplies the mucosa over the anterior 252 the Cranial Nerves part of the nasal septum; the lateral branch supplies the anterior part of the lateral wall, then emerges as the external nasal nerve between the lower border of the nasal bone and the lateral nasal cartilage to supply the skin over the ala and the tip of the nose (the nasociliary nerve thus supplies the cartilaginous tip of the nose on both its inner and outer aspects). It leaves the orbit, as its name implies, below the trochlea and innervates the skin of the side of the nose and the conjunctiva near the inner canthus. It is a tiny structure, about 1 mm in diameter, which receives parasympathetic, sympathetic and sensory fibres. Relay takes place in the ciliary ganglion and postganglionic fibres then pass in the short ciliary nerves, about six in number, to the eyeball, where they supply the sphincter pupillae and the ciliary muscle. Sympathetic fibres reach the ganglion from the superior cervical ganglion via the internal carotid plexus. Both the sympathetic and sensory components pass through the ciliary ganglion without synapse to reach the eye via the short ciliary nerves, where they are respectively vasoconstrictor and sensory to the globe of the eye. Its course is through four anatomical zones: skull base, pterygopalatine fossa, infra-orbital canal and finally the subcutaneous tissues of the cheek. The Trigeminal Nerve (V) 255 the maxillary nerve arises from the anterior border of the trigeminal ganglion, and then runs along the lower lateral wall of the cavernous sinus below the ophthalmic nerve. It then leaves the skull base through the foramen rotundum and traverses the pterygopalatine fossa. The nerve is now named the infra-orbital nerve and lies, in turn, in the infra-orbital groove and then the infra-orbital canal of the orbital aspect of the maxilla. The nerve emerges from the infra-orbital foramen, where it lies beneath levator labii superioris, then divides into branches that are distributed to the lower eyelid, the side of the nose, the cheek and the upper lip. The zygomatic nerve arises from the maxillary nerve as this traverses the pterygopalatine fossa. It passes through the inferior orbital fissure to run on the lateral wall of the orbit, where it divides into two branches: 1 the zygomaticotemporal nerve traverses the zygomaticotemporal canal in the zygomatic bone to enter the temporal fossa; thence it ascends to supply the skin of the temporal region. While still within the orbit, this nerve gives a twig to the lacrimal nerve, along which parasympathetic secretomotor fibres from the pterygopalatine ganglion are conveyed to the lacrimal gland. The ganglionic branches (two in number) comprise the sensory roots of the pterygopalatine ganglion (see below). The posterior superior alveolar nerve, which may be double, descends over the posterior surface of the maxilla, then enters the posterior dental canal (which again may be double) on the posterior aspect of the maxilla, and gives branches to each molar tooth. The middle superior alveolar nerve originates in the posterior part of the infra-orbital canal, then runs downwards in the lateral wall of the maxilla to supply the two upper premolars. The anterior superior alveolar nerve arises at the anterior end of the infraorbital canal and descends in the anterior maxillary wall to innervate the upper canine and incisor teeth. A tiny branch pierces the lateral wall of the inferior 256 the Cranial Nerves meatus to supply the mucous membrane of the lower anterior part of the lateral wall and the floor of the nasal cavity. As the infra-orbital nerve emerges from the infra-orbital foramen, it breaks up into a spray of branches: 1 the palpebral branches supply the skin of the lower eyelid and the conjunctiva; 2 the nasal branches supply the skin of the side of the nose; 3 the labial branches supply the skin and mucous membrane of the upper lip and the anterior part of the cheek. This nerve traverses the petrous temporal bone then runs in a groove on the anterior surface of the bone deep to the trigeminal ganglion to enter the foramen lacerum. Here, it is joined by the deep petrosal nerve to form the nerve of the pterygoid canal (the Vidian nerve), which passes through the pterygoid canal to reach the pterygopalatine ganglion. These parasympathetic fibres, having arrived at the ganglion, have not completed their complicated journey. They are transmitted via the zygomaticotemporal branch of the maxillary nerve to the lacrimal branch of the ophthalmic nerve, by which they arrive at their final destination as secretomotor fibres to the lacrimal gland. Sympathetic fibres, derived from the internal carotid plexus, form the deep petrosal nerve which, as described above, reaches the ganglion via the nerve of the pterygoid canal. The sensory component is derived from the two sphenopalatine branches of the maxillary nerve. The sensory and sympathetic (vasoconstrictor) branches of the ganglion are distributed to the nose, nasopharynx, palate and orbit via the following branches (Figs 171 & 172): 1 the nasopalatine (long sphenapalatine) nerve passes medially through the sphenopalatine foramen, crosses the roof of the nasal cavity, then passes downwards and forwards along the nasal septum, grooving the vomer as it does so, to reach the incisive foramen and thence the mucous membrane of the roof of the mouth. It supplies filaments to the posterior part of the nasal roof, to the nasal septum, and to those parts of the gums and anterior part of the hard palate that are in relation to the incisor teeth. The Trigeminal Nerve (V) 257 Incisors Canine Premolars Incisive foramen Greater and lesser palatine foramina Molars Medial pterygoid plate Pterygoid hamulus Lateral pterygoid plate. It innervates the mucosa of the gums and hard palate as far forward as the level of the canine teeth. Other fibres pass backwards to serve both aspects of the soft palate, and nasal branches pierce openings in the perpendicular plate of the palatine bone to supply the region of the inferior nasal concha. A digression on the pterygopalatine fossa It might be wise here to consider briefly the anatomy of the pterygopalatine fossa, through whose openings pass the numerous branches of the second part of the maxillary nerve and of the pterygopalatine ganglion. The fossa is an elongated, narrow, pyramidal interval below the apex of the orbit, lying between the upper part of the posterior surface of the maxilla in front and the greater wing and the root of the pterygoid process of the sphenoid 258 the Cranial Nerves behind. The roof is formed by the inferior surface of the body of the sphenoid medially, but laterally the roof is deficient and the fossa opens freely into the orbit via the posterior part of the superior orbital fissure. Medially, the space is closed by the vertical plate of the palatine bone but laterally the fossa is wide open and communicates with the infratemporal fossa through the pterygomaxillary fissure. Inferiorly, the anterior and posterior walls come into apposition, thus sealing off the base of the fossa. The entrances into and exits from the pterygopalatine fossa: 1 Medialathe sphenopalatine foramen is the gap in the upper end of the vertical plate of the palatine bone between its orbital and sphenoidal processes; it transmits into the nasal cavity, the nasopalatine and the medial and lateral posterior superior nasal nerves and the accompanying branches from the maxillary vessels. It transmits the maxillary nerve, zygomatic nerve, orbital branches of the pterygopalatine ganglion and the infra-orbital vessels. The posterior superior alveolar branch of the maxillary nerve emerges through this fissure to enter the posterior dental canal on the posterior aspect of the maxilla. Maxillary nerve block Maxillary nerve block is performed for acute or chronic herpetic neuralgia, trigeminal neuralgia and cancer pain. Injection is performed as the nerve lies in the pterygopalatine fossa after emerging from the foramen rotundum. It is reached by inserting a needle through the mid-point of the coronoid notch beneath the zygomatic arch. The needle is withdrawn a little and advanced in an antero-superior direction to enter the pterygopalatine fossa. The presence of a plexus of veins in this area means that haematoma formation occasionally occurs. It is occasionally useful to perform a localized nerve block of the infra-orbital nerve. The infra-orbital foramen can usually be palpated midway between the outer canthus of the eye and the alar process of the nose. The supra-orbital notch (or foramen), infra-orbital foramen and the mental foramen all lie in the same sagittal plane. The mandibular nerve (V) the mandibular nerve (Figs 177 & 178), the third division of the Vth nerve, is the largest, has the widest distribution and is the only one with a motor component. It is the sensory nerve to the temporal region, the tragus and front of the helix, to the skin over the mandible and the lower lip, and to the mucosa of the anterior two-thirds of the tongue and floor of the mouth. Its motor fibres supply the muscles of mastication, tensor tympani, tensor palati, the mylohyoid and the anterior belly of digastric. The sensory and motor roots of the nerve pass individually through the foramen ovale and unite immediately beyond it into a short trunk that lies deep to the lateral pterygoid muscle and upon the tensor palati, the latter separating it from the Eustachian (auditory) tube. Mandibular nerve block the technique is similar to that for a maxillary nerve block: a needle is inserted through the mid-point of the coronoid notch beneath the zygomatic arch. The needle is withdrawn and directed postero-superiorly so that it moves off the posterior surface of the lateral pterygoid plate to meet the mandibular nerve as this emerges from the foramen ovale. At this point, the nerve lies in close relationship to the middle meningeal artery, the maxillary artery and the pterygoid plexus of veins.
Coinciding with the fall in pulmonary vascular resistance cholesterol jokes generic fenofibrate 160 mg without a prescription, the volume of pulmonary blood flow increases and thus the volume of blood returning to the left atrium increases proportionately cholesterol and triglycerides order fenofibrate 160 mg online. The left atrial pressure rises cholesterol medication in canada order 160 mg fenofibrate with mastercard, exceeds the right atrial pressure cholesterol levels after menopause discount 160 mg fenofibrate with amex, and closes the foramen ovale functionally. In most infants for up to several months, a small left-to-right shunt occurs via the incompetent flap of the foramen ovale. Anatomically, the atrial septum ultimately seals in 75% of children and remains "probe-patent" in 25%. The ductus narrows by muscular contraction within 24 hours of birth, although anatomic closure may take several days. The closure of the ductus is associated with a lowering of pulmonary arterial pressure to normal levels. When the ductus and foramen ovale close, the pulmonary blood flow equals systemic blood flow, and the circulations are in series. In the neonatal period, the changes that occur in the ductus, foramen ovale, and pulmonary arterioles are reversible. The pulmonary arterioles and the ductus 248 Pediatric cardiology arteriosus are responsive to oxygen levels and acidosis. An increase in the vascular resistance occurs in conditions associated with hypoxia. Although minor changes occur at a PaO2 of 50 mmHg, large increases in pulmonary vascular resistance occur at PaO2 levels less than 25 mmHg. If acidosis coexists with hypoxia, the increase in pulmonary resistance is far greater than at comparable levels of PaO2 occurring at normal pH. Persistent pulmonary hypertension of the newborn Neonates with pulmonary parenchymal disease, such as respiratory distress syndrome, develop increased pulmonary vascular resistance and increased pulmonary arterial pressure because of hypoxia. Because of the elevation of right ventricular systolic pressure, right atrial pressure increases, causing a right-to-left shunt at the foramen ovale. In a similar way, the ductus arteriosus of a neonate is also responsive to oxygen. With hypoxia, the ductus may reopen and, should the pulmonary resistance be simultaneously elevated, a right-to-left shunt could occur through the ductus arteriosus. Clinically, this is recognized by a lower PaO2 (or pulse oximetry saturation) in the legs than arms. Thus, cyanosis in the neonate with pulmonary parenchymal disease can result from right-to-left shunting of blood, as well as from intrapulmonary shunting and diffusion defects. Administration of 100% oxygen improves both of these abnormalities, but often the improvement is not great enough to exclude cyanotic cardiac malformations. Administration of oxygen to cyanotic patients with a cardiac anomaly generally also lessens the degree of cyanosis. With the development of echocardiography, the ability to distinguish these has been greatly enhanced. However, during the transition to the normal circulatory pattern, particularly as the ductus arteriosus is closing and then closes, certain malformations become evident. These malformations have one of three circulatory patterns in which the ductus played an important role during fetal life, and as it closes postnatally the neonatal circulatory pattern is disrupted. The three types of malformations dependent upon ductal blood flow following birth are as follows: (1) Transposition of the great arteries. In this condition, the blood flow from the aorta through the ductus into the pulmonary artery provides an important pathway for mixing of blood. In these conditions, the ductus provides the sole or major flow into the lung and therefore the pulmonary circulation. As the ductus closes in the first 2 days of life, the neonate becomes increasingly cyanotic. In hypoplastic left heart syndrome, the blood flow through the ductus from right to left provides the entire systemic circulation and in interruption of the aortic arch it provides the entire blood flow to the descending aorta. In neonates with a coarctation, the aortic obstruction does not become evident until the ductus closes completely. Prior to closure, blood can pass from the ascending to descending aorta through the aortic orifice of the ductus as it closes from the pulmonary artery toward the descending aorta. Because of cardiovascular problems which result from ductal closure, the severity of the neonatal condition and the potential for correction or palliation in the first days of life, guidelines for screening of all neonates by peripheral oximetry are being incorporated in newborn nurseries as a method of identifying such neonates. Pulse oximetry is used to measure oxygen saturations of the right hand and one lower extremity to detect the presence of hypoxia or a clinically important difference between upper and lower extremity saturations. When done after 24 hours of age, the specificity of the test is maximized (false-positive readings are minimized). The test is highly sensitive for detecting most cyanotic malformations and some left heart obstructive lesions with a right-to-left ductal shunt. Cardiac malformations may lead to severe cardiac symptoms and death in the neonatal period. The types of cardiac malformations causing symptoms in this age group generally differ from those leading to symptoms later in infancy. Other conditions, such as tetralogy of Fallot, await the development of sufficient stenosis before becoming symptomatic. In the neonate, hypoxia and congestive cardiac failure are the major cardiac symptom complexes. This approach begins with the prompt recognition of cardiac disease in the newborn nursery. If no other etiology is found, immediate echocardiogram interpreted by a pediatric cardiologist is indicated. If no other etiology is found, consultation with pediatric cardiology or neonatology is indicated to arrange for a diagnostic echocardiogram to be interpreted by a pediatric cardiologist. This screening algorithm should not take the place of clinical judgment or customary clinical practice. Reprinted with the kind permission of the Alabama Department of Public Health ( Hypoxia Severe cardiac symptoms also occur in neonates because of hypoxia from conditions discussed in Chapter 6. Two circulatory patterns can be the cause: inadequate mixing as in complete transposition of the great arteries, or severe obstruction to pulmonary blood flow coexisting with an intracardiac shunt. In neonates, tetralogy of Fallot, often with pulmonary atresia, pulmonary atresia with intact ventricular septum (hypoplastic right ventricle), and tricuspid atresia are the most common conditions in this category. Critical pulmonary stenosis is valvar pulmonary stenosis with a large right-to-left shunt through a foramen ovale and with various degrees of right ventricular hypoplasia and abnormal compliance; the physiology is similar to that of pulmonary atresia with intact ventricular septum. Rapid, difficult respiration occurs from metabolic acidosis, which can develop quickly because of the hypoxia; cardiac failure is usually not a major problem. Malformations with inadequate pulmonary blood flow are improved by prostaglandin administration followed by a corrective operation if possible, an aorticopulmonary shunt to improve oxygenation, or catheter intervention. Neonates with complete transposition of the great arteries require prostaglandins to keep the ductus patent and a Rashkind atrial septostomy to improve intracardiac mixing. Thus, a diverse group of cardiac conditions cause symptoms in the neonatal period. Because of the potential for correction or palliation, any neonate with severe cardiac symptoms should be stabilized. Then echocardiography and, in many neonates, cardiac catheterization and angiocardiography are used to define 252 Pediatric cardiology the anatomic and physiologic details of the cardiac malformation. Although there is some risk (1% mortality) when performing a cardiac catheterization in neonates, it is outweighed by the benefits of the data obtained or the therapeutic interventions performed. Following definition of the malformation, appropriate decisions are made concerning an operation; and in some malformations. Congestive cardiac failure In the neonatal period, congestive cardiac failure results most commonly from (1) anomalies that cause severe outflow obstruction, particularly to the left side of the heart, and often associated with a hypoplastic left ventricle, (2) volume overload from an insufficient cardiac valve or systemic arteriovenous fistula, and (3) cardiomyopathy or myocarditis. Occasionally, in prematurely born infants, a patent ductus arteriosus may lead to signs of cardiac failure. Presumably, the pulmonary vasculature approaches normal levels more quickly than in full-term infants. The resultant large volume of pulmonary blood flow causes overload of the left ventricle. The term encompasses several cardiac malformations, each associated with a diminutive left ventricle and similar clinical and physiologic features, and include aortic atresia, mitral atresia, and severe ("critical") aortic stenosis. In each, severe obstruction to both left ventricular inflow and outflow is present. Whether from an atretic mitral valve or from a small left ventricle, filling of the left ventricle is impeded or impossible.
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