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A: The operation is performed utilizing hypothermic cardiopulmonary bypass with cannulation of the superior and inferior vena cavae discount 0.5mg cabergoline amex menstrual gas. The aorta is cross-clamped and the myocardium is protected with intermittent doses of cold cardioplegic solution generic 0.25mg cabergoline otc womens health 7 day eating plan. B: The atrial septum and majority of the limbus are resected to create a large atrial septal defect that extends to the superior and inferior vena cava generic cabergoline 0.25 mg line women's health center doylestown. C: The large interatrial communication has been created exposing the pulmonary veins buy cabergoline 0.25 mg breast cancer poems. Note that there is atrioventricular concordance so that the mitral valve is left sided and the tricuspid valve right sided. D: An intra-atrial baffle (shaded), usually of pericardium, is constructed to direct the vena caval flow to the mitral valve. The suture line is begun anterior to the left-sided pulmonary veins between the veins and the orifice of the left atrial appendage. E: The baffle suture line is then brought inferior to the pulmonary veins and laterally to the right atrial–inferior vena caval junction, anteriorly around the inferior vena caval orifice, and to the retained anterior portion of the atrial septum. In a similar fashion, the superior edge of the baffle is brought superior to the pulmonary veins and laterally to the right atrial–superior vena caval junction, anteriorly around the superior vena caval orifice, and onto the anterior portion of the atrial septum to complete the suture line. Pulmonary venous return is directed around the baffle to the aorta via the tricuspid valve and right ventricle (red arrow), and systemic venous return is directed under the baffle to the pulmonary artery via the mitral valve and left ventricle (blue arrows) leading to a physiologic correction at the atrial level. This leaves the morphologic right ventricle as the systemic ventricle and the tricuspid valve as the systemic atrioventricular valve. A: External anatomy with the aorta arising from the right ventricle (situs solitus with atrioventricular concordance and ventriculoarterial discordance). B: The operation is performed utilizing hypothermic cardiopulmonary bypass with aortic and bicaval cannulation. The aorta is cross-clamped and the myocardium is protected with intermittent doses of cold cardioplegic solution. If a ventricular septal defect is present it can be repaired at this time via a right atriotomy incision. The aorta is then transected several millimeters above the aortic valve commissures. Note that the ductus arteriosus has been ligated and divided to allow for later mobilization of the pulmonary artery bifurcation anterior to the aorta (Lecompte maneuver). D: The coronary arteries are harvested on buttons of aortic sinus tissue and mobilized to allow for translocation to the pulmonary artery (neo-aortic root). Medially based trap-door incisions are created in the pulmonary root at the translocation sites. These trap-door incisions prevent rotation of the coronaries and allow for the coronaries to sit in a natural orientation when translocated. E, F: The coronary buttons are translocated to the pulmonary root and sutured in place. G: The pulmonary artery bifurcation is brought anterior to the ascending aorta (Lecompte maneuver) and an end-to-end anastomosis is performed between the neo-aortic root and the ascending aorta. The Lecompte maneuver allows for a direct pulmonary artery anastomosis and avoids the need for prosthetic conduit reconstruction of the pulmonary outflow tract (61). H: The coronary artery harvest sites are reconstructed with autologous pericardial patches. This can be performed with the heart beating after the aortic cross-clamp has been removed. Pulmonary venous return is directed to the aorta via the left ventricle ( red arrow) and systemic venous return is directed to the pulmonary artery via the right ventricle ( blue arrow) leading to an anatomic correction at the arterial level. This leaves the morphologic left ventricle as the systemic ventricle and the mitral valve as the systemic atrioventricular valve. Overall survival for the arterial switch operation in the current era can be accomplished P. Thus, anatomic details of the coronary arteries prior to the operation is an important finding for many centers. However, in experienced surgical hands, complex coronary anatomy does not adversely affect the short- or long-term outcomes of the arterial switch operation (56,57,58,59,60). First described by Rastelli in 1969 (62,63), operative mortality in the current era (64) for transposition of the great arteries with ventricular septal defect and left ventricular outflow tract obstruction now approaches 0% with the Rastelli procedure (Fig. A: The operation is performed utilizing hypothermic cardiopulmonary bypass with ascending aortic and bicaval cannulation. The aorta is cross- clamped and the myocardium is protected with intermittent doses of cold cardioplegic solution. B: A right ventriculotomy is used to expose the ventricular septal defect (shaded grey) and create the intracardiac baffle. The pulmonary artery is divided and the pulmonary valve and proximal main pulmonary artery stump are closed. Right ventricle-to-pulmonary artery continuity is established with placement of a valved conduit. Pulmonary venous return is directed from the left ventricle across the ventricular septal defect to the aorta via the intracardiac baffle (Insert: red arrow). Systemic venous return is directed from the right ventricle to the pulmonary arteries via the right ventricle-to-pulmonary artery conduit (blue arrow). This redirects the ventricular outflows and bypasses the left ventricular outflow tract obstruction leaving the morphologic left ventricle as the systemic ventricle and the mitral valve as the systemic atrioventricular valve. Administration of 100% oxygen and performing the hyperoxia test can readily distinguish pulmonary from cardiac pathology due to mixing. Little or no increase in the partial pressure of oxygen on 100% oxygen is seen in patients with transposition of the great arteries and other significant congenital cyanotic heart lesions. Supplemental oxygen should be administered and correction of metabolic derangements and acidosis should be performed. Prostaglandin E1 infusion is critical for adequate mixing in these patients, particularly prior to a balloon atrial septostomy. This allows adequate patency of the duct while at the same time enabling a natural airway to be maintained without apnea and resultant intubation, in most patients. Higher doses of prostaglandin may be needed in some patients if adequate mixing does not occur. Ultimately, most patients will require a balloon atrial septostomy soon after diagnosis for adequate mixing to occur. In many centers, this is performed judiciously on a case-by-case basis, depending on amount of mixing present and timing of surgery. In other centers, most patients undergo a balloon atrial septostomy, which is our preferred approach as well.

Capillaries generic cabergoline 0.5mg with visa menopause natural supplements, The output of the hypothalamus is also neural derived from the superior hypophysial artery and humoral cabergoline 0.5 mg line menstrual quotes. The two major targets of neural and located in the median eminence and infun- output are as follows: dibulum purchase cabergoline 0.5 mg fast delivery women's health common issues, form portal vessels that pass down the 1 buy 0.25mg cabergoline amex women's health center greensboro nc. The cerebral cortex directly from the hypo- pituitary stalk to a second capillary bed in the thalamus and indirectly via (1) the anterior anterior pituitary. It is through this route that thalamic nucleus, a component of Papez cir- the hypothalamus regulatory hormones reach the cuit, which receives the mamillothalamic anterior pituitary. Brainstem and spinal cord motor and auto- best described by considering the manifestations nomic centers, which receive direct and of a hypothalamic lesion as given in the clinical indirect input from the lateral and poste- illustration at the beginning of this chapter. The rior hypothalamus and the paraventricular hypothalamic syndrome is manifested chiefy nucleus via the dorsal longitudinal fasciculus by (a) diabetes insipidus, (b) endocrine imbal- and mamillotegmental tract (Fig. Lesions in the of hypothalamic regulatory hormones that infu- posterior hypothalamus may result in a decrease ence the anterior pituitary or adenohypophysis. But, particularly in the arcuate nucleus, but also in the most frequently, posterior hypothalamic lesions paraventricular nucleus. The regulatory hormones result in poikilothermy, the condition in which are transported via the axons of the tuberoinfun- body temperature varies with the environment. Within the pituitary shivering is no longer functional and the impulses gland, these hormones regulate the production from the anterior hypothalamic heat loss center, and release of the adrenocorticotropic, growth, which normally elicit sweating and vasodilation, thyrotropic, follicle-stimulating, and luteinizing are interrupted en route to the brainstem reticu- hormones. Glucose or hypoadrenalism, hypothyroidism, and abnormali- fat-sensitive neurons in these areas infuence the ties in the reproductive system cycles. Body temperature is regulated in the hypo- Bilateral lesions of the “satiety center” in the thalamus by a heat loss center located anteriorly ventromedial nuclei result in increased appetite and a heat gain center located posteriorly. Bilateral lesions of the Chapter 18 The Hypothalamus: Vegetative and Endocrine Imbalance 241 “feeding center” in the lateral hypothalamus at Animals with such lesions fy into a rage and the tuberal level result in decreased food and attack repeatedly without provocation. Patients with these lesions enced by the preoptic, anterior, and ventromedial exhibit violent, aggressive behavior toward any- nuclei. It seems prob- neurons in these areas elicit the production of able, therefore, that the ventromedial area of the appropriate hormones that regulate the production hypothalamus normally exerts a regulatory effect and release of the anterior pituitary gonadotropins. Such mechanisms include Sleep and the sleep-wake cycle are infuenced increased heart rate, elevated blood pressure, by several areas of the hypothalamus. The supra- increased respiration, pupillary dilation, piloerec- chiasmatic nucleus, which receives input from tion, etc. It is nuclei including the dorsomedial, is the biologic generally accepted that the posterior hypothala- clock that plays a role in the circadian rhythm of mus controls sympathetic activity. The anterior and preop- the anterior hypothalamus controls parasympa- tic nuclei can induce sleep, and the posterolateral thetic events (Table 18-1). It is well known that hypothalamic lesions result in abnormalities of sleep patterns. Lesions Chapter Review in the anterior hypothalamus, particularly the Questions preoptic nuclei, result in insomnia. What are the anteroposterior subdivisions fulness that varies from drowsiness to permanent of the hypothalamus? The posterior hypothalamus lateral to the mamillary bodies appears to be associated with 18-2. What is the chief neural output of the this abnormality; lesions here may result in nar- hypothalamus? The autonomic or involuntary system regulates The basic anatomic features of the two parts visceral activity throughout the body. First, sympathetic activity nomic system is divided into efferent and afferent enters the peripheral nervous system only via parts, both of which innervate the involuntary the thoracolumbar spinal nerves, whereas para- musculature (as smooth and cardiac) and glan- sympathetic activity enters the peripheral ner- dular tissue. The autonomic efferent system is vous system only via cranial nerves and sacral composed of two divisions: sympathetic and spinal nerves (Table 19-1). The autonomic afferent system of its short postganglionic fbers and the small consists of visceral afferent fbers that travel in ratio of preganglionic fbers to postganglionic the nerves making up the sympathetic and para- neurons (1:2; Fig. The para- plied by both sympathetic and parasympathetic sympathetic division, with its very localized nerves, all visceral organs are innervated by four infuence, is associated with the protection, types of fbers: sympathetic efferents and afferents rest, and recuperation of individual organs and and parasympathetic efferents and afferents. Because of these somatic efferent systems differ considerably: two anatomic features, sympathetic system activity efferent neurons exist in the autonomic path, results in diffuse phenomena associated with whereas only a single neuron exists in the somatic emergency situations such as “fght or fight,” that path (Fig. Parasympathetic Division from the oculomotor nerve; the pterygopalatine and submandibular ganglia, which receive pre- All activity in parasympathetic nerve fbers origi- ganglionic fbers from the facial nerve; and the nates in the brainstem or spinal cord (Fig. The pregan- neurons are found in four locations: glionic fbers in the vagus nerve synapse in ter- 1. The Edinger-Westphal nucleus, the viscero- minal ganglia both extrinsic and intrinsic to the motor component of the oculomotor nuclear thoracic, abdominal, and pelvic viscera that are complex vagally innervated (Fig. The superior salivatory nucleus, the viscerose- The sacral preganglionic parasympathetic cretory component of the facial nuclear neurons are in and near the intermediolateral complex nucleus in spinal cord segments S2, S3, and S4. The inferior salivatory nucleus, found near The preganglionic fbers emerge from the spinal the rostral part of the nucleus ambiguus and cord and pass to the terminal ganglia of the colon contributing viscerosecretory fbers to the and rectum, urinary bladder, prostate and vagi- glossopharyngeal nerve nal glands, and erectile tissues of the penis and 4. The sacral parasympathetic nerves con- neurons scattered near the caudal part of the trol defecation, urination, and erection. The visceromotor and vis- cerosecretory axons of these neurons emerge Sympathetic Division in the vagus nerve. All activity in sympathetic nerve fbers origi- The cranial ganglia that give rise to the post- nates in the spinal cord (Fig. These sympathetic columns are an also scattered in the lateral funiculus near the intermediolateral nucleus in the lateral horn, lateral horn. Chapter 19 The Autonomic Nervous System: Visceral Abnormalities 245 sympathetic trunk ganglia comprise 20 to 25 effects. However, in most instances, the two pairs along the vertebral column, whereas the divisions collaborate, both of them regulating autonomic plexus ganglia are found along the and adjusting visceral functions. Most visceral abdominal aorta, especially around the origins of organs are innervated by both divisions. One the celiac, superior mesenteric, and inferior mes- division usually produces effects opposite those enteric arteries. The primary The basic circuitry of the sympathetic system postganglionic neurotransmitters are acetylcho- (Fig. All preganglionic sympathetic fbers emerge sweat glands are an exception because they are from the spinal cord in spinal nerves T1 innervated by cholinergic (acetylcholine) sym- through L2. Within the sympathetic trunk, the pregangli- The importance of impulses arising from visceral onic sympathetic fbers may: organs and blood vessels is mainly the initiation a. Those auto- cranial sympathetic trunk ganglion; nomic afferent impulses that do reach levels of c. The sympathetic trunk neurons give rise to three types of postganglionic fbers: Primary Visceral Afferents a. These are sels, sweat glands, and piloerector muscles; the autonomic afferents responsible for visceral c.

However buy cheap cabergoline 0.5mg online women's health center in grants pass or, these two tests are not routinely available in our center buy generic cabergoline 0.5 mg online women's health center memorial city; therefore discount 0.5mg cabergoline womens health va, midnight awake serum cortisol was performed as a second screening test buy cabergoline 0.5mg amex 8 menopause myths. High midnight serum cortisol of 667 nmol/L (normal <207 nmol/L) confirmed the loss of circadian rhythm of cortisol secretion and endogenous hypercortisolemia. Further, even a pituitary adenoma of size >6 mm has a sensitivity of only 40% to be a corticotropinoma, with a specificity of 98%. High-dose dexamethasone suppression test not required in this patient, but it was performed as a part of Liddle’s protocol followed at our institute. Osteoporosis in Cushing’s syndrome is reversible with cura- tive treatment particularly in children and young adults. After optimal blood pres- sure and glycemic control, she underwent transsphenoidal surgery uneventfully. She was monitored for signs and symptoms of adrenal insufficiency along with daily 0800h serum cortisol. She had desquamation of skin in immediate postoperative period with progressive regression of features of protein catabolism, resolution of diabetes, and reduction in doses of antihypertensive drugs. Cushing’s syndrome is a disorder of chronic glucocorticoid excess and is char- acterized by features of protein catabolism along with varying signs and symp- toms. The most common cause of Cushing’s syndrome is exogenous administration of glucocorticoids. The clinical features that best discriminate Cushing’s syndrome are prototype manifestations of protein catabolism and include easy bruisibility, proximal muscle weakness, striae (especially if purplish and >1 cm wide), facial pleth- ora, and cuticular/pulp atrophy. Features like obesity, hypertension, and diabe- tes are not discriminatory as they are highly prevalent in general population. However, onset of hypertension, diabetes, or vertebral osteoporosis at a younger age should raise a suspicion of Cushing’s syndrome. The etiology of endogenous Cushing’s syndrome is summarized in the figure given below. Approximately 90% of patients with Cushing’s disease have microadenoma, while macroadenoma contributes to the rest. What are the conditions associated with hypercortisolemia in the absence of clinical features of Cushing ’ s syndrome? Pseudo-Cushing’s syndrome is a group of reversible disorders with subtle symptoms and signs of Cushing’s syndrome and hypercortisolism with anomalous response to dexamethasone suppression tests. Morbid obesity, depression, alcoholism, metabolic syndrome, poorly controlled diabetes, and polycystic ovarian disease are associated with pseudo-Cushing’s syndrome. Resolution of the underlying disorder leads to amelioration of pseudo-Cushing’s syndrome. Obesity is a pseudo-Cushing’s state and is associated with loss of circadian rhythm of cortisol, normal total serum cortisol, mildly increased urinary free cortisol, and variability in response to overnight dexamethasone suppression test. Obesity is associated with increased cortisol turnover, with augmented synthesis as well as clearance of cortisol, resulting in a normal circulating level of cortisol. The augmented clear- ance of cortisol is due to enhanced A-ring reduction of cortisol leading to increased urinary excretion. Cyclical Cushing’s syndrome is characterized by periods of waxing and wan- ing symptoms and signs of hypercortisolemia and anomalous results of corti- sol dynamic tests. It is biochemically defined as presence of three peaks and two troughs of cortisol secretion over a period of time (usually weeks to months). These patients require frequent monitoring with urine free cortisol or late-night salivary cortisol to establish the diagnosis, as cycle length varies from days to months. Spot urine cortisol to creatinine ratio and measurement of scalp hair cortisol may also be useful. Cyclical Cushing’s syndrome can occur with pituitary (54%), ectopic (26%), or even with adrenal Cushing’s (11%). The mechanism of cyclicity are elusive; however, periodic hormono- genesis is a commonly purported mechanism; periodicity in hormone biosyn- thesis may be due to recurrent hemorrhage in the tumor or early programmed tumoral cell death. Subclinical Cushing’s syndrome is characterized by lack of specific symptoms and signs of Cushing’s syndrome, but with evidence of autonomous glucocor- ticoid secretion. However, majority of these patients have obesity, hyperten- sion, and type 2 diabetes. Causes of weight gain in a patient with Cushing’s syndrome are increased appetite, enhanced adipogenesis, fluid retention, and decreased physical activity. Increased appetite is because of stimulatory effect of cortisol on feeding center through aug- mented adenosine monophosphate kinase activity, insulin resistance, decreased corticotrophin-releasing hormone, and increased neuropeptide Y. Enhanced adipo- genesis is attributed to cortisol-mediated diversion of primitive mesenchymal stem cells to adipocytes and increased activity of lipoprotein lipase and glycerol- 3-phosphate dehydrogenase. Fluid retention also contributes to weight gain and is due to action of excess cortisol on mineralocorticoid receptor (specificity spill- over). Decreased physical activity resulting from proximal muscle weakness or neuropsychiatric manifestations is also a cause of weight gain. Nearly 45% of patients with Cushing’s syndrome have central obesity as against 55% with generalized obesity. However, children with Cushing’s syn- drome usually have generalized obesity, probably due to lesser omental fat. Weight gain is a hallmark feature of Cushing’s syndrome; however, some patients may present with weight loss. The causes include adrenocortical carci- noma, ectopic Cushing’s syndrome, uncontrolled diabetes, concurrent infec- tions like tuberculosis, and endogenous depression. Headache in patients with Cushing’s syndrome can be due to adenoma per se, sinusitis, cor- tical vein thrombosis, benign intracranial hypertension, and glaucoma. Striae are one of the classical features of Cushing’s syndrome and are present in 60–70% of patients. Striae in Cushing’s syndrome are violaceous-purple, dehis- cent, >1 cm wide and are commonly present over abdomen, thighs, buttocks, arms, and inframammary region. Wide and purplish striae are due to venular dila- tation and thinned out dermis, which in turn occurs as a result of loss of perivas- cular collagen support and dermal collagen breakdown, respectively. Striae may be absent in patients with childhood Cushing’s syndrome, adrenocortical carci- noma, ectopic Cushing’s syndrome, and hypercortisolemia associated with androgen excess. Causes of striae in the absence of Cushing’s syndrome include rapid weight gain during puberty, pregnancy, and pseudo-Cushing’s states. Cutaneous manifestations of Cushing’s syndrome are bruise, striae, plethora, cutic- ular atrophy (“cigarette paper” appearance – Liddle’s sign), and fungal infections. Bruise, striae, and plethora are due to loss of dermal collagen, while cuticular atro- phy is a result of atrophy of stratum corneum. Rarely, purpura can be associated with Cushing’s syndrome due to qualitative abnormalities in platelet function. Proximal myopathy in patients with Cushing’s syndrome is due to decreased muscle protein synthesis, increased muscle protein catabolism, and myocyte apoptosis. Concurrent hypokale- mia, hypophosphatemia, hypomagnesemia, vitamin D deficiency, and hypogo- nadism further contribute to muscle weakness in patients with Cushing’s syndrome. Why do some patients with Cushing ’ s syndrome lack features of protein catabolism?

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