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Subcutaneous Fat Necrosis

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861. Conventional Lateral Internal Sphincterotomy, V-Y Anoplasty and Tailored Lateral Internal Sphincterotomy With V-YF in Treatment of Chronic Anal Fissure(CAF)

. The V-shaped flap formed of skin and subcutaneous fat was mobilized sufficiently to allow advancement into the anal canal to cover the fissure defect. Care was taken to preserve enough pedicles to ensure adequate blood supply. The base of flap was sutured to the lower anal mucosa with interrupted 000 Vicryl Rapide. Figures 1, 2, 3 and 4 illustrate the procedure. GroupIII: Tailored lateral internal sphincterotomy with V-Y advancement flap: Tailored lateral sphincterotomy was performed (...) of skin and subcutaneous fat was mobilized sufficiently to allow advancement into the anal canal to cover the fissure defect. Care was taken to preserve enough pedicles to ensure adequate blood supply. The base of flap was sutured to the lower anal mucosa with interrupted 000 Vicryl Rapide. Figures 1, 2, 3 and 4 illustrate the procedure. Procedure: GroupII: V-Y advancement flap GroupII: V-Y advancement flap: The V-Y advancement flap was performed by making a V-shaped incision from the edges

2011 Clinical Trials

862. Breast Cancer and Exercise Trial in Alberta

[ Time Frame: 36 Months ] Body composition (including weight, hip circumference, waist circumference, waist-hip ratio, total body fat, subcutaneous fat, intra-abdominal fat, lean body mass, body mass index) Secondary Outcome Measures : Insulin resistance [ Time Frame: 36 months ] Measurements taken of Insulin Levels, Glucose Levels, Insulin Resistance (HOMA Score) Sex Hormone Levels [ Time Frame: 36 months ] Measure levels of Estrone, Estradiol, Androstenedione and Testosterone Inflammation [ Time (...) to an exercise facility, body composition assessment. Other: High Volume Participate in one-year high volume (300 minutes per week)aerobic exercise. Active Comparator: Moderate Volume Participate in one year of moderate volume (150 minutes per week) aerobic exercise with free provision of a personal trainer, membership to an exercise facility, body composition assessment. Other: Moderate Volume Moderate volume (150 minutes per week) aerobic exercise Outcome Measures Go to Primary Outcome Measures : Body Fat

2011 Clinical Trials

863. Epithelioid rhabdomyosarcoma: clinicopathologic analysis of 16 cases of a morphologically distinct variant of rhabdomyosarcoma. (PubMed)

, 10 were intramuscular, and 2 were subcutaneous. Tumor size ranged from 3 to 8.5 cm; the tumors had nodular fleshy cut surfaces, grossly appreciable necrosis, and infiltrative edges. Microscopically, tumors showed sheet-like growth of uniformly sized epithelioid cells with abundant amphophilic-to-eosinophilic cytoplasm, large vesicular nuclei, and frequently prominent nucleoli. Necrosis and infiltration into adjacent structures (such as skeletal muscle or fat) were present in all cases

2011 American Journal of Surgical Pathology


PASSAGE OF COXSACKIE VIRUS (CONNECTICUT-5 STRAIN) IN ADULT MICE WITH PRODUCTION OF PANCREATIC DISEASE 1. With Conn.-5 strain of Coxsackie virus, pancreatic disease can be regularly produced in adult mice. 2. The lesions consist of widespread necrosis, followed by repair; there occurs more or less complete loss of glandular acini, with fatty or fibrous replacement. The islands of Langerhans and pancreatic ducts persist. 3. Injection of virus suspensions by the intraperitoneal, subcutaneous (...) , intramuscular, or intracerebral route is followed by selective necrosis of the pancreas. 4. The liver, in the earlier stages of the disease, is the seat of fat infiltration. There may be necrosis of individual hepatic cells, but the diffuse hepatitis described in suckling mice does not occur. In the later stages of the disease, the liver is not significantly altered. 5. Localized areas of fat necrosis, scattered through intra-abdominal adipose tissue, are usually present in the acute phase of the disease

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1951 The Journal of experimental medicine


which varies greatly in character. The duodenum and upper jejunum may also be involved in the inflammatory process. 4. Intraperitoneal injections of formalin cause peritonitis of a fibrino-haemorrhagic character. A definite reaction is obtained when very dilute formalin (1-1000) is employed. In the peritoneal cavity formalin exercises a destructive action upon all organs (pancreas, liver, peritoneal fat, Fallopian tubes, etc.) with which it comes in contact and causes inflammation in these organs. 5 (...) . The lethal dose of formalin when injected intraperitoneally into guinea pigs is approximately 2 cc. of 1-1000 formalin for each 100 grm. of body weight. 6. The injection of formalin into the lungs is followed by pneumonia and bronchitis. 7. The inflammation which follows subcutaneous injections of formalin is characterized by intense exudation. 8. The injection of formalin into the muscles produces myositis. 9. The injection of formalin into the anterior chamber of the eye causes the accumulation

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1905 The Journal of experimental medicine

866. Revolade - eltrombopag

degeneration/ necrosis in the kidney (not considered treatment related) Toxicokinetics: For a 10-fold increase in dose, AUC 0-24 and C max values increased 32- and 36-fold, with no marked difference between sexes. Rat (Sprague- Dawley) 10/sex/group Toxicokinetics: additional 3/sex/group 0, 3, 10, 40/ p.o.(gavage) once daily 14 days 10 mg/kg/day (C max = 79.9 µg/mL, AUC 0- 24 =650 µg.h/mL (on Day 14)) Body weight and food consumption: ? food consumption and body weight gain at 40 mg/kg/day (M) during (...) and necrosis, and periportal and 15/79 Species/Sex/ Number/Group Dose (mg/kg/day)/ Route Duration NOEL/ NOAEL Major findings midzonal hepatocellular vacuolation. Adrenal cortex: vacuolation and necrosis. Pituitary: vacuolation in the par distalis. Eye: cataracts. Endosteal hyperostosis in the femur (2 M) and tibia (1 M) at 60 mg/kg/day. Depletion on lymphoid cells in the spleen, lymph nodes and thymus at 60 mg/kg/day. Toxicokinetics: Plasma concentrations increased with increasing dose. T max ~ 1-4 h post

2010 European Medicines Agency - EPARs

867. Possia - ticagrelor

studies were performed on possible drug-drug interactions of ticagrelor with aspirin. However, this was investigated in the clinical trials and no interactions on plasma protein binding or on metabolism were observed. Ingestion of a high-fat meal resulted in a 21% increase in ticagrelor AUC and 22% decrease in the active metabolite Cmax, indicating a possible interaction with P-gp and/or CYP3A4/5. The Applicant concluded that these changes are considered of minimal clinical significance. The in vivo (...) change in the liver. In the 24-month rat carcinogenicity study, focal necrosis in the liver was seen in males at all dose groups, albeit at low incidence and without a dose response. No liver effects were seen in marmosets and signals of liver toxicity in clinical trials are questionable, therefore this effect is likely a rodent specific response to increased liver load. Nevertheless, from these results, it cannot be completely ruled out that ticagrelor treatment induces liver toxicity, and liver

2010 European Medicines Agency - EPARs

868. Cachexia in Cancer

tumor necrosis factor-alpha, IL-1b, and IL-6, which are produced by tumor cells and host cells in the tissue mass. The ATP-ubiquitin-protease pathway plays a role as well. Cachexia is easy to recognize, primarily by weight loss, which is most apparent with loss of temporalis muscle mass in the face (Hippocratic facies). The loss of subcutaneous fat increases the risk of pressure ulcers over bony prominences. Treatment Treatment involves treatment of the cancer. If the cancer can be controlled

2013 Merck Manual (19th Edition)

869. Amyloidosis

. Aspiration of subcutaneous abdominal fat is positive in about 80% of patients with AL, 50% in AF, but less than 25% of patients with ATTRwt. If the fat biopsy result is negative, a clinically involved organ should be biopsied. The diagnostic sensitivity of kidney and heart biopsies is nearly 100% when these organs are clinically involved. Tissue sections are stained with Congo red dye and examined with a polarizing microscope for characteristic birefringence. Nonbranching 10-nm fibrils can also (...) (secondary amyloidosis) This form can occur secondary to several infectious, inflammatory, and malignant conditions and is caused by aggregation of isoforms of the acute-phase reactant serum amyloid A. Common causative infections include Predisposing inflammatory conditions include Inherited periodic fever syndromes such as Castleman disease Inflammatory cytokines (eg, IL-1, tumor necrosis factor [TNF], IL-6) that are produced in these disorders or ectopically by tumor cells cause increased hepatic

2013 Merck Manual (19th Edition)

870. Diabetes Mellitus (DM)

adults, plasma glucose levels reach higher levels after eating than in younger adults, especially after meals with high carbohydrate loads. Glucose levels also take longer to return to normal, in part because of increased accumulation of visceral and abdominal fat and decreased muscle mass. Type 2 DM is becoming increasingly common among children as childhood obesity has become epidemic. Over 90% of adults with DM have type 2 disease. There are clear genetic determinants, as evidenced by the high (...) and muscle glycogen synthase activity. Adipose tissue also appears to function as an endocrine organ, releasing multiple factors (adipocytokines) that favorably (adiponectin) and adversely (tumor necrosis factor-alpha, IL-6, leptin, resistin) influence glucose metabolism. Intrauterine growth restriction and low birth weight have also been associated with insulin resistance in later life and may reflect adverse prenatal environmental influences on glucose metabolism. Miscellaneous types of diabetes

2013 Merck Manual (19th Edition)

871. Male Hypogonadism

Male Hypogonadism Male Hypogonadism - Genitourinary Disorders - MSD Manual Professional Edition Brought to you by The trusted provider of medical information since 1899 SEARCH SEARCH MEDICAL TOPICS Common Health Topics Resources QUIZZES & CASES Quizzes Cases The trusted provider of medical information since 1899 SEARCH SEARCH MEDICAL TOPICS Common Health Topics Resources QUIZZES & CASES Quizzes Cases / / / / IN THIS TOPIC OTHER TOPICS IN THIS CHAPTER Test your knowledge Acute Tubular Necrosis (...) Which of the following is a more common cause of acute tubular necrosis (ATN)? Ethylene glycol poisoning Burns Renal hypoperfusion Rhabdomyolysis NEWS & VIDEOS Adjuvant Tx for Early Testicular Cancer Does Not Harm Sperm WEDNESDAY, Feb. 27, 2019 (HealthDay News) -- For clinical stage I testicular cancer (TC) patients, adjuvant treatment after orchiectomy has no long-term significant effect on sperm production... 3D Model Male Reproductive System Video How to Catheterize the Urethra in Women SOCIAL

2013 Merck Manual (19th Edition)

872. Pressure Ulcers

%, a rate over 5 times the increase of hospital admissions overall. The rate increased most in patients who developed PUs during hospitalization. Today, an estimated 1.3 to 3 million patients in the US have PUs, resulting in a significant financial burden to patients and health care institutions. Etiology Risk factors for PUs include the following: Age > 65 (possibly due to reduced subcutaneous fat and capillary blood flow) Decreased mobility (eg, due to prolonged hospital stay, bed rest, spinal cord (...) PU, subcutaneous tissue can become necrotic before the epidermis erodes. Thus, a small ulcer may in fact represent extensive subcutaneous necrosis and damage. Pearls & Pitfalls Suspect deeper tissue damage than is clinically evident in patients who have PUs. Complications PUs are a reservoir for hospital-acquired antibiotic-resistant organisms. High bacteria counts within the wound can hinder tissue healing. If wound healing is delayed despite proper treatment, underlying (present in up to 32

2013 Merck Manual (19th Edition)

873. Specific Poisons

generally Ingestion: Salty or soapy taste With large doses: Tremors, seizures, CNS depression, shock, renal failure Skin and mucosal contact: Painful superficial or deep burns Inhalation: Intense eye and nasal irritation, headache, dyspnea, sense of suffocation, glottal edema, pulmonary edema, bronchitis, pneumonia, mediastinal and subcutaneous emphysema due to bleb rupture Ingestion: Dilution with milk or water, IV glucose and saline, 10% Ca gluconate 30 mL IV (in children, 0.6 mL/kg) or 10% CaCl 2 10 (...) — Formaldehyde Formalin (may contain methyl alcohol) Ingestion: Oral and gastric pain, nausea, vomiting, hematemesis, shock, hematuria, anuria, coma, respiratory failure Skin contact: Irritation, coagulation necrosis (with high concentrations), dermatitis, hypersensitivity Inhalation: Eye, nose, and respiratory tract irritation; laryngeal spasm and edema; dysphagia; bronchitis; pneumonia Ingestion: Dilution with water or milk; treatment of shock, NaHCO 3 to correct acidosis, respiratory support, observation

2013 Merck Manual (19th Edition)

874. Neonatal Hypercalcemia

causes of neonatal hypercalcemia include Maternal hypoparathyroidism Subcutaneous fat necrosis Parathyroid hyperplasia Abnormal renal function Williams syndrome Idiopathic Maternal hypoparathyroidism or maternal hypocalcemia may cause secondary fetal hyperparathyroidism, with changes in fetal mineralization (eg, osteopenia). Subcutaneous fat necrosis may occur after major trauma and causes hypercalcemia that usually resolves spontaneously. Neonatal hyperparathyroidism is very rare. Williams (...) hypercalcemia may be noted when total serum calcium is > 12 mg/dL ( > 3 mmol/L). These signs can include anorexia, , nausea, vomiting, lethargy or seizures or generalized irritability, and hypertension. Other symptoms and signs include constipation, abdominal pain, dehydration, feeding intolerance, and failure to thrive. Some neonates have weakness. With subcutaneous fat necrosis, firm purple nodules may be observed on trunk, buttocks, or legs. Diagnosis Total or ionized serum calcium level Diagnosis

2013 Merck Manual (19th Edition)

875. Overview of Lysosomal Storage Disorders

with bone pain, avascular necrosis of the femoral head, vertebral compression, thrombocytopenia, anemia Increased frequency in Ashkenazi Jews Treatment: Supportive care Splenectomy Enzyme replacement (imiglucerase) Substrate reduction ( eliglustat , miglustat ) Bone marrow or stem cell transplantation Type II (infantile form; 230900) Onset: Infancy Urine metabolites: None Clinical features: Infantile hydrops, hepatosplenomegaly, dysphagia, bone lesions, hypertonicity, pseudobulbar palsy, laryngeal spasm (...) , ichthyosis, developmental delay, hypersplenism, death by age 2 yr Treatment: Supportive care Type III (juvenile form, Norrbottnian type; 231000) Onset: 4–8 yr Urine metabolites: None Clinical features: Similar to type II except milder, possible survival into adulthood Treatment: Supportive care Farber disease (lipogranulomatosis; 228000) Ceramidase ASAH (8p22-p21.3)* Onset: First weeks of life Urine metabolites: Ceramide Clinical features: Lipogranulomatosis, periarticular subcutaneous nodules

2013 Merck Manual (19th Edition)

876. Adipose tissue

or abdominal fat (also known as organ fat or intra-abdominal fat) is located inside the , packed between the organs (stomach, liver, intestines, kidneys, etc.). Visceral fat is different from underneath the , and interspersed in . Fat in the lower body, as in thighs and buttocks, is subcutaneous and is not consistently spaced tissue, whereas fat in the is mostly visceral and semi-fluid. Visceral fat is composed of several adipose depots, including , (EWAT), and depots. Visceral fat is often expressed (...) . Subcutaneous fat [ ] See also: Micro-anatomy of subcutaneous fat Most of the remaining nonvisceral fat is found just below the skin in a region called the . This subcutaneous fat is not related to many of the classic obesity-related pathologies, such as , cancer, and , and some evidence even suggests it might be protective. The typically female (or gynecoid) pattern of body fat distribution around the hips, thighs, and buttocks is subcutaneous fat, and therefore poses less of a health risk compared

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2012 Wikipedia

877. Acute pancreatitis

Miscellaneous Subcutaneous fat necrosis Arthalgia Causes [ ] Most common [ ] Biliary Pancreatitis due to gallstones or constriction of in 40% of cases in 30% of cases Idiopathic in 15-25% of cases Metabolic disorders: , , , Post- Abdominal trauma Penetrating ulcers of the , and other Drugs: (e.g., , ), (e.g., , , , ), , , , and , , , , [ ] Infections: , , , , , Structural abnormalities: , Less common [ ] from other than mumps, including Hyperparathyroidism or reaction Pathology [ ] Pathogenesis [ ] Acute (...) . The inflammatory response leads to the secondary manifestations of pancreatitis: hypovolemia from capillary permeability, acute respiratory distress syndrome, disseminated intravascular coagulations, renal failure, cardiovascular failure, and gastrointestinal hemorrhage. Histopathology [ ] The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas , focal enzymic necrosis of pancreatic fat and vessel necrosis ( ). These are produced

2012 Wikipedia

878. Polycystic ovary syndrome

. Approximately three-quarters of women with PCOS (by the diagnostic criteria of NIH/NICHD 1990) have evidence of . : This appears as a tendency towards and other symptoms associated with . Serum , insulin resistance, and levels are higher in women with PCOS. Asians affected by PCOS are less likely to develop hirsutism than those of other ethnic backgrounds. Women with PCOS tend to have central obesity, but studies are conflicting as to whether visceral and subcutaneous abdominal fat is increased, unchanged (...) , or decreased in women with PCOS relative to reproductively normal women with the same . In any case, androgens, such as , (dihydrotestosterone), and , have been found to increase visceral fat deposition in both female animals and women. Cause [ ] PCOS is a of uncertain cause. There is some evidence that it is a . Such evidence includes the familial clustering of cases, greater in compared with twins and heritability of endocrine and metabolic features of PCOS. There is some evidence that exposure to higher

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2012 Wikipedia

879. Resistin

, chemicals such as , , and pro-inflammatory . As cited, it has recently been discovered that resistin also participates in the inflammatory response. In further support of its inflammatory profile, resistin has been shown to increase transcriptional events, leading to an increased expression of several pro-inflammatory cytokines including (but not limited to) (IL-1), (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-α ( ) in an -mediated (nuclear factor kappa-light-chain-enhancer of activated B (...) is increased in obese humans". J. Clin. Endocrinol. Metab . 88 (11): 5452–5. : . . ^ Gabriely I, Ma XH, Yang XM, Atzmon G, Rajala MW, Berg AH, Scherer P, Rossetti L, Barzilai N (October 2002). "Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process?". Diabetes . 51 (10): 2951–8. : . . Levy JR, Davenport B, Clore JN, Stevens W (March 2002). "Lipid metabolism and resistin gene expression in insulin-resistant Fischer 344 rats". Am. J. Physiol

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2012 Wikipedia

880. Hepatitis

in the liver cells in a process called . This initially reversible process overwhelms the 's ability to maintain lipid homeostasis leading to a toxic effect as fat molecules accumulate and are broken down in the setting of an . Over time, this abnormal lipid deposition triggers the via (TLR4) resulting in the production of inflammatory such as TNF that cause liver cell injury and death. These events mark the transition to and in the setting of chronic injury, eventually develops setting up events that lead (...) to cirrhosis and hepatocellular carcinoma. Microscopically, changes that can be seen include steatosis with large and swollen hepatocytes ( ), evidence of cellular injury and cell death (apoptosis, necrosis), evidence of inflammation in particular in , variable degrees of fibrosis and . Diagnosis [ ] Predominantly elevated aminotransferase Cause ALT Chronic hepatitis B, C, and D Nonalcoholic liver disease Acute viral hepatitis Medications/toxins Autoimmune hepatitis Wilson's disease Alpha-1-antitrypsin

2012 Wikipedia

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