N. Marus. Prescott College.

Sickle cell anemia Diffuse sclerosis with coarsening of the trabe- Initially purchase lamisil discount, generalized osteoporosis due to marrow cular pattern may be a late manifestation hyperplasia order lamisil 250mg line. Uniform sclerosis of the spine and pelvis seen on a film from an excretory urogram 250mg lamisil amex. Varies in severity and age of clinical presen- body) and “sandwich” vertebrae (increased den- tation from a fulminant, often fatal condition at sity at the end plates). In the extremities, lack of birth to an essentially asymptomatic form that is modeling causes widening of the metaphyseal an incidental radiographic finding. Extensive extramedullary hematopoiesis (hepato- splenomegaly and lymphadenopathy). Picture-frame vertebral body with pelvis, and hips in a 74-year-old woman with the tarda form of condensation of bone along its peripheral margins (ar- this condition. There is straightening of the anterior surface of the bone (arrowhead) and involvement of the pedicles. Patients have short there is mandibular hypoplasia with loss of the stature, but hepatosplenomegaly is infrequent. Unlike osteopetrosis, in the long bones the medullary cavities are preserved, and there is no metaphyseal widening. Obliteration of individual with a high concentration of fluorides, industrial trabeculae may cause affected bones to appear exposure (mining, smelting), or excessive thera- chalky white. There is often calcification of inter- peutic intake of fluoride (treatment of myeloma or osseous membranes and ligaments (paraspinal, Paget’s disease). Areas of increased scle- rosis subjacent to the cartilaginous plates produce the characteristic “rugger jersey” spine in this pa- tient with chronic renal failure. Hyper- trophy of cartilage widens the intervertebral disk spaces, whereas hypertrophy of soft tissue may lead to an increased concavity (scalloping) of the pos- terior aspects of the vertebral bodies. Increased trabeculation, which is most prominent at the periphery of the bone, produces a rim of thickened cortex and a picture-frame appearance. Dense sclerosis of one or more ver- tebral bodies (ivory vertebrae) may present a pattern simulating osteoblastic metastases or Hodgkin’s disease, though in Paget’s disease the vertebrae are also enlarged. Congeni- tal fusion can usually be differentiated from that resulting from disease because the total height of the combined fused bodies is equal to the normal height of two vertebrae less the intervertebral disk space. Enlargement of all vertebral bod- 4 of a vertebral body, producing an ivory vertebra. Benign bone tumor Expansion of a vertebral body may result from hemangioma, aneurysmal bone cyst, osteoblas- toma, or giant cell tumor. Fibrous dysplasia Proliferation of fibrous tissue in the medullary cavity may infrequently involve the spine and cause one or more vertebral bodies to expand. Essentially complete fusion of the cervical spine into a solid mass in a patient with Klippel-Feil deformity. Primarily the bone density of the vertebral body decreases the involves the lumbar and lower thoracic spine cortex appears as a thin line that is relatively dense (where weight-bearing stress is directed toward and prominent, producing a picture-frame pattern. In addition to the typical “fish vertebrae” appear- ance, osteoporotic vertebral bodies may demon- strate anterior wedging and compression fractures. The characteristic concave contours of the superior and inferior disk surfaces result from expansion of the nucleus pulposus into the weakened vertebral bodies. Hyperparathyroidism Generalized demineralization of the vertebral Subchondral resorption at the diskovertebral bodies produces arch-like contour defects of junctions produces areas of structural weakening the superior and inferior vertebral surfaces, that allow herniation of disk material into the simulating osteoporosis. In patients with hyperparathyroidism secondary to renal failure, thick bands of increased density adjacent to the superior and inferior margins of vertebral bodies produce the characteristic “rugger jersey” spine. This results in a striking thickening of the cortices and increased trabeculation of spongy bone. Nevertheless, the bony architecture is abnormal and is prone to fracture with relatively minimal trauma. Severe loss of bone substance in the the pedicles (lacking red marrow) that are fre- spine often results in multiple vertebral com- quently destroyed by metastatic disease. Metastases Destructive process involving not only the Destruction of one or more pedicles may be the vertebral bodies but also the pedicles and neural earliest sign of metastatic disease and aids in arches. Pathologic collapse of vertebral bodies differentiating this process from multiple myeloma frequently occurs in advanced disease. Because cartilage is resistant to invasion by metastases, preservation of the intervertebral disk space may help to distinguish metastases from an inflamma- tory process. Osteomyelitis Pyogenic Various radiographic patterns, including disk Rapid involvement of the intervertebral disks space narrowing, loss of the normally sharp (loss of disk spaces and destruction of adjacent adjacent subchondral plates, areas of cortical end plates), in contrast to the vertebral body demineralization, vertebral body destruction involvement and preservation of disk spaces in and even collapse, and sclerotic new bone metastatic disease. The diffuse myelomatous infiltration causes generalized demineralization of the vertebral bodies and a compression fracture of L2. Unlike pyo- genic infection, tuberculous osteomyelitis is rarely associated with periosteal reaction or bone sclero- sis. In the untreated patient, progressive vertebral collapse and anterior wedging lead to the develop- ment of a characteristic sharp kyphotic angulation and gibbous deformity. Healed lesions may demon- strate mottled calcific deposits in a paravertebral abscess and moderate recalcification and sclerosis of the affected bones. Fungal infections Generally produce spinal involvement mimick- Infrequent manifestation of actinomycosis, blasto- ing tuberculosis. Severe compressive patients, it may be difficult to distinguish an acute forces may drive the nucleus pulposus into the spinal fracture from the vertebral compression that vertebral body, resulting in a burst fracture with is frequently associated with osteoporosis. In the posterosuperior fragment often driven into acute trauma, there is often evidence of cortical the spinal canal. In patients who have jumped disruption, a paraspinal soft-tissue mass, or an ill- from great heights, compression fractures of defined increase in density beneath the end plate the thoracolumbar junction are frequently of an involved vertebra, indicating bone impaction. In osteoporosis, vertebral compression is often associated with osteophytic spurs arising from the apposing margins of the involved and adjacent vertebral bodies. An acute spinal fracture may be difficult to distinguish from a pathologic fracture caused by metastases or multiple myeloma. The affected vertebrae tend to become produces a dorsal kyphosis, which persists even wedge shaped (they decrease in height ante- after the disease has healed.

Combination therapy of statin plus another drug such as a fibrate or niacin may be necessary to achieve ideal lipid control lamisil 250 mg low price, but monitor patients closely for possible adverse reaction to therapy buy lamisil 250mg lowest price. Coronary artery bypass should be performed in a diabetic patient even if there is only 2-vessel coronary disease buy cheap lamisil 250mg on-line. The pathology can be diffuse, which is more common, and lead to widening of glomerular basement membrane and mesangial thickening. Nodular pathology can occur and results in hyalinization of afferent glomerular arterioles (Kimmelstiel-Wilson syndrome). Proteinuria is detectable on a standard dipstick when the level >300 mg per 24 hours. Diabetes is the most common cause of end-stage renal disease in the United States. The retina is affected, and diabetes is the leading cause of blindness in middle-aged patients. Simple/background, or proliferative (microaneurysms, hemorrhages, exudates, retinal edema) damage can occur. For type 1 diabetes, the first screening should take place 5 years after diagnosis, then annually. Proliferative retinopathy is defined as the presence of vitreous hemorrhages or neovascularization; treatment is with laser photocoagulation. Nonproliferative or background retinopathy can only be prevented with tight control of glucose levels. Peripheral neuropathy (most common) is symmetrical, with symptoms of numbness, paresthesia, and pain being prevalent. Podiatric exam (monofilament testing) should occur annually to look for early signs of neuropathy since it leads to increased injury from trauma. Diabetes is responsible for 50% of all nontraumatic amputations in the United States. Autonomic neuropathy can be devastating; patients will have orthostatic hypotension and syncope as main manifestations. Gastrointestinally, patients may have difficulty swallowing, delayed gastric emptying (gastroparesis), constipation, or diarrhea. The diagnostic test of choice for gastroparesis is the gastric emptying scintigraphy study. Impotence and retrograde ejaculation can occur; the prevalence of erectile dysfunction is as high as 50% in patients with 10 years of diabetes. Diabetic Foot Ulcer Wikimedia, Jonathan Moore As with other microvascular complications, prevention of neuropathy in diabetes is by tight glycemic control. For peripheral neuropathy, analgesics, gabapentin, pregabalin, amitriptyline, and carbamazepine are used (gabapentin and pregabalin are the best). Presumably stress-induced epinephrine release blocks insulin secretion, causing the syndrome. In normal individuals insulin reserve is such that hormone release is adequate even in the face of stress. The Somogyi effect is rebound hyperglycemia in the morning because of counterregulatory hormone release after an episode of hypoglycemia in the middle of the night. Symptoms of hypoglycemia are divided into 2 groups and can occur because of excessive secretion of epinephrine, leading to sweating, tremor, tachycardia, anxiety, and hunger. There is no uniform correlation between a given level of blood sugar and symptoms. Postprandial hypoglycemia (reactive) can be secondary to alimentary hyperinsulinism (after gastrectomy, gastrojejunostomy, pyloroplasty, or vagotomy), idiopathic, and galactosemia. Fasting hypoglycemia can result from conditions in which there is an underproduction of glucose, such as hormone deficiencies (panhypopituitarism, adrenal insufficiency), enzyme defects, substrate deficiency (severe malnutrition, late pregnancy), acquired liver disease, or drugs (alcohol, propanolol, salicylates). Fasting hypoglycemia can also occur in conditions related to overutilization of glucose such as hyperinsulinism. Hyperinsulinism can occur secondary to insulinoma, exogenous insulin, sulfonylureas, drugs (quinine), endotoxic shock, and immune disease with insulin receptor antibodies. Overutilization of glucose can also occur in states in which there are appropriate insulin levels, such as extrapancreatic tumors and rare enzyme deficiencies. Clinical findings include symptoms of subacute or chronic hypoglycemia such as blurred vision, headache, feelings of detachment, slurred speech, and weakness. Symptoms occur in the early morning or late afternoon or after fasting or exercise. This is made by finding a serum insulin level ≥8 mg/mL in the presence of blood glucose <40 mg/dL (i. Factitious hyperinsulinism is caused by self-administration of insulin or ingestion of Equal or oral sulfonylureas. Most often, these patients are associated with the health professions or have access to these drugs by a diabetic member of the family. A triad of hypoglycemia, high immunoreactivity, insulin, and suppressed plasma C-peptide is pathognomonic of exogenous insulin administration. Ethanol-induced hypoglycemia can also occur with prolonged starvation, when glycogen reserves become depleted in 18–24 hours and hepatic glucose output depends completely on gluconeogenesis. Ethanol at a concentration of 45 mg/dL can induce hypoglycemia by blocking gluconeogenesis. Test Insulinoma Exogenous Insulin Sulfonylureas Plasma insulin High (usually <200 Very high (usually High µU/mL) >1,000 µU/mL) Proinsulin Increased Normal or low Normal C peptide (insulin connective Increased Normal or low Increased peptide) 1:1 Insulin antibodies Absent +/– Present Absent Plasma or urine sulfonylurea Absent Absent Present Table 2-6. Differential Diagnosis of Insulinoma and Factitious Hyperinsulinism Clinical Recall Which of the following medications is contraindicated in patients with acute pulmonary edema with an ejection fraction of 25%? The cortex is divided into 3 areas, the outer zone (glomerulosa), which is the site of aldosterone synthesis; the central zone (fasciculata), which is the site of cortisol synthesis; and the inner zone (reticularis), which is the site of androgen biosynthesis. The disorders of hyperfunction of the gland are associated with specific hormones: increased cortisol is seen in Cushing syndrome, increased aldosterone is seen in hyperaldosteronism, and increased adrenal androgens is seen with virilization in women. The most common causes are exogenous, iatrogenic, and those secondary to prolonged use of glucocorticoids. Adrenal neoplasia, such as adenoma or carcinoma, and adrenal nodular hyperplasia account for about 30% of Cushing cases. The clinical findings of Cushing syndrome include deposition of adipose tissue in characteristic sites such as upper fat, moon facies; interscapular buffalo hump; and mesenteric bed, truncal obesity. Other clinical findings include hypertension, muscle weakness, and fatigability related to mobilization of peripheral supportive tissue; osteoporosis caused by increased bone catabolism; cutaneous striae; and easy bruisability.

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Insert the first fundoplication suture by taking a bite of the fundus on the patient’s left using 2-0 atraumatic Tevdek generic lamisil 250 mg online. Attach a hemostat to A number of surgeons place sutures fixing the upper tag this stitch but do not tie it 250 mg lamisil. Each bite should contain margin of the Nissen wrap to the esophagus to prevent the 5–6 mm of tissue including submucosa buy lamisil master card, but it should not entire wrap from sliding downward and constricting the penetrate the lumen. To perform a fundoplication without tension, it after considerable experience, advocated a Nissen wrap is necessary to insert the gastric sutures a sufficient distance measuring only 1 cm in length, claiming that longer wraps lateral to the esophagogastric junction. Each suture should contain one bite of fundus, then wrap has effectuated excellent control of reflux. No structed this wrap employing one horizontal mattress suture more than 2–3 cm of esophagus should be encircled by the of 2-0 Prolene buttressed with Teflon pledgets (Figs. If this cannot be plication sutures by inserting a continuous seromuscular done, the wrap is too tight. If a satisfactory repair has been accomplished, 3–4 cm of distal esophagus becomes progressively narrower, tapering to a point at the gastroesophageal junction. If this taper- ing effect is not noted, it suggests that the wrap may be too loose. Successful antireflux procedures, whether by the Nissen, Hill, Belsey, or Collis-Nissen technique, show similar narrowing of Fig. Complications Testing Antireflux Valve Dysphagia, usually transient “gas bloat” (rare) Disruption of fundoplication Ask the anesthesiologist to inject 300–400 ml saline solution Slipping downward of fundoplication with obstruction into the nasogastric tube and then withdraw the tube into the Postoperative paraesophageal hernia if hiatal defect was not esophagus. If the saline cannot be forced into the esophagus by Herniation of fundoplication into thorax moderate manual compression of the stomach, the fundopli- Esophageal or gastric perforation by deep necrosing sutures cation has indeed created a competent antireflux valve. Randomized trial to study the effect of fundic mobilization on long-term results of Nissen fundoplication. Meta-analysis of randomized clinical trials comparing open and laparoscopic anti-reflux surgery. Comparison of long-term outcome of laparoscopic and conventional Nissen fundo- plication: a prospective randomized study with an 11-year follow- up. Scott-Conner Indications necessarily a bit different from those for the open procedure, and several additional features should be noted. Symptomatic reflux esophagitis refractory to medical therapy First, the hiatus is accessed by elevating the left lobe of Barrett’s esophagus (consider mucosal ablation) the liver without dividing its attachments. Second, the esoph- agus is exposed and mobilized by dissecting the crura with minimal manipulation of the esophagus. The resulting exten- Preoperative Preparation sive mediastinal dissection that accompanies esophageal mobilization makes approximation of the crura mandatory. Finally, several short gastric vessels must be divided to ensure creating a floppy wrap. See references at the end for this and other adaptations to newer Injury to the esophagus. We Operative Technique prefer the laparoscopic Nissen fundoplication because it is intended to be virtually identical to a well-established open Room Setup and Trocar Placement procedure when completed. The steps in the dissection are Position the patient with the legs slightly spread and sup- ported on padded stirrups (Fig. We place the primary monitor at the patient’s left shoulder, with a secondary monitor at the C. Scott-Conner shape by tightening the cable in the commodious right sub- phrenic space and is then passed underneath the liver. The liver retractor is properly placed when stable expo- sure is obtained, and the diaphragmatic surface is seen behind the left lobe of the liver. This exposure gen- erally requires that the retractor be “toed in” so the part of the retractor closest to the hiatus has maximal lift applied. The laparoscope and instruments are then insinuated under- neath the left lobe of the liver in the working space thus created. Generally, the stomach and some omentum partially or completely obscure the hiatus even with the liver retracted. Therefore the second part of obtaining exposure entails plac- ing an endoscopic Babcock clamp on the stomach and pull- ing toward the left lower quadrant (Fig. Dissecting the Hiatus The esophagus is dissected by clearing the peritoneum off the hiatus and carefully exposing the muscular crura. Properly performed, this maneuver automatically exposes the esophagus and creates a posterior window. A grasper is used to elevate the flimsy lesser omentum close New York: Springer; 1999) to the hiatus, and ultrasonic dissecting scissors are used to divide the omentum (Fig. It is tempting to begin this dissection by opening the directly facing the hiatus (Fig. If you tial puncture site (to be used for the laparoscope), recall that begin your omental window high, however, near the hiatus, the hiatus is quite high and deep. A trocar pattern must be indi- additional advantage of keeping the window in the lesser vidualized according to the patient’s body habitus. A 30° omentum relatively small, which helps anchor the wrap and angled laparoscope is mandatory for easy visualization. A far safer approach is to Exposure of the Hiatus dissect and clearly define the muscular hiatus and both crura. A Next carry the dissection up over the arch of the crura, con- variety of liver retractors are available, and which one is cho- centrating on exposing the muscle fibers of the diaphragm. We prefer During this dissection, the esophagus becomes obvious by a flexible retractor that becomes rigid and assumes the shape its orientation, longitudinal muscle, and overlying vagus shown in Fig. When the tension on the cable is released, the color and characteristic longitudinal striations. If there is retractor becomes limp and may be straightened out to pass uncertainty as to the location of the esophagus, the nasogas- it through a trocar. Once the retractor is inside the abdomen, tric tube may be palpable to light touch with a grasper, or an the cable is tightened by twisting a knob on the handle. This grasper is introduced parallel to the esophagus through one of the left-sided trocars and is used to probe into the mediastinum by gently pushing the esophagus down. When the upper part of the hiatus has been cleaned thor- oughly, elevate the esophagus gently with a closed grasper and clean the lower part of the left crus from the right side by working underneath the esophagus (Fig.

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Large cheap lamisil 250mg with visa, smooth filling de- fect (arrows) in the medial portion of the duode- num representing a well-differentiated malignant neoplasm discount 250mg lamisil fast delivery. Annular pancreas In infants purchase lamisil online pills, double bubble sign with some gas in Incomplete obstruction with gas in the bowel distal the distal bowel. Duodenal diaphragm Thin lucent line across the lumen, often with Usually involves the second part of the duodenum. The presence of arrow) represents air in the stomach; the right bubble (solid arrow) small amounts of gas distal to the obstruction indi- reflects duodenal gas. There is no gas in the small or large bowel cates that the stenosis is incomplete. The presence of gas in the bowel dis- tal to the diaphragm indicates that the high-grade obstruction is not complete. Often appears similar to annular pancreas, though granular mucosa in the narrowed segment suggests healed ulceration. Crohn’s disease Fusiform and concentric narrowing of the duo- Usually evidence of Crohn’s disease elsewhere. Crohn’s disease of the duodenal bulb and antrum produces tubular narrowing (pseudo–Billroth-I ap- pearance). Obstruction of the third portion of the duodenum (arrow) in a newborn infant, due to dense fibrous bands. Strongyloidiasis/sprue Single or multiple areas of stenosis of the duo- Strongyloidiasis is indistinguishable from Crohn’s denum. Duodenal carcinoma Annular constricting lesion with overhanging Approximately 90% are adenocarcinomas, which edges, nodular mucosal destruction, and ulcer- usually arise at or distal to the ampulla of ation. May be impossible to differentiate from sec- ondary neoplastic invasion of the duodenum due to extension of tumors of the pancreas, gallbladder, or colon. Although there Carcinoma of the pancreas pro- second portion of the duodenum and is narrowing of the second portion of the ducing an annular constricting causes marked mucosal edema and spicu- duodenum with widening of the duode- lesion (arrow). Intramural duodenal Tumor-like intramural mass causing narrowing Secondary to anticoagulant therapy, abnormal hematoma of the duodenal lumen. Aorticoduodenal fistula Extrinsic mass compressing and displacing the Often fatal complication of an abdominal aortic third portion of the duodenum. Radiation injury Smooth stricture, primarily involving the sec- Infrequent complication after radiation therapy to ond portion of the duodenum. Superior mesenteric artery Narrowing or obstruction of the third portion of Controversial entity referring to compression of the syndrome the duodenum with proximal dilatation. Thickening of Duodenal Folds Condition Imaging Findings Comments Peptic ulcer disease Diffuse fold thickening, primarily involving the Most common cause. Uremia (chronic dialysis) Nodular fold thickening, primarily involving the Simulates the appearance of pancreatitis, which bulb and second portion. Crohn’s disease/ Diffuse fold thickening, often with ulceration In Crohn’s disease, usually involvement of the tuberculosis and luminal narrowing. Diffuse thickening of denal sweep, double-contour effect, and sharp spic- folds in the proximal duodenal sweep is associated ulations. Infiltrative disorders Diffuse fold thickening (usually generalized in- Whipple’s disease; amyloidosis; mastocytosis; volvement of the small bowel). Especially in an obese patient with a high trans- verse stomach and a long vertical course of the descending duodenum. Chronic pancreatitis Generalized widening with fold effacement and History of alcoholism in more than half the pa- spiculation. Pancreatic pseudocyst Generalized widening and compression of the Common complication of pancreatitis. Lymphadenopathy due to lymphoma, metastases to lymph nodes, or inflammatory disease. Severe inflammation causes widening of the sweep and a high-grade duodenal obstruction. Peritonitis Generalized ileus, often with blurring of the mu- Suggestive findings include free peritoneal fluid, re- cosal pattern and intestinal edema. Gastroenteritis or enterocolitis without peritonitis can also present as generalized ady- namic ileus. Drugs with atropine-like effects (morphine, Lo- motil, L-dopa, barbiturates, and other sympath- omimetic agents). Most commonly hypokalemia, but also occurs with metabolic disorder hypochloremia, calcium or magnesium abnormal- ities, and hormonal deficits (hypothyroidism, hy- poparathyroidism). Abdominal trauma; retroperitoneal hemorrhage; chest conditions spinal or pelvic fractures; generalized gram-nega- tive sepsis; shock; acute pulmonary disease; mesen- teric vascular occlusion. The clinical presentation simulates tention of the cecum (often horizontally ori- mechanical obstruction. Chronic idiopathic intestinal Distention of the small bowel mimicking intes- Episodic symptoms of intestinal obstruction. Develops between the second and fifth postopera- tive days, especially if there was manipulation of the small bowel. The Colonic ileus in a patient with severe diabetes and diffuse small bowel dilatation simulates mechanical hypokalemia. Diffuse accumulation of a brown lipofuscin pig- ment in the muscularis due to long-standing mal- absorption and prolonged depletion of vitamin E. Causes include septicemia, hormonal or chemical deficits, hypoxia-induced vasculitis, respiratory dis- tress syndrome, intestinal infection, peritonitis, and mesenteric thrombosis. Adynamic ileus simulating mechanical obstruction on (A) supine and (B) upright views. External hernias May have gas or excessive soft-tissue density on External hernias (inguinal, femoral, umbilical, and the affected side. There is pronounced dilatation demonstrates the obstructing stone (white ar- of the duodenum and proximal jejunum to the rows) and barium in the biliary tree (black level of the annular constricting tumor (arrow). Congenital intestinal Double bubble (duodenal atresia) or triple bub- Barium enema may be required to distinguish atresia or stenosis ble (proximal jejunal atresia) signs, or a typical small from large bowel in a low ileal obstruction.