Tugas Dr Kamal 1

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<p>TUGAS dari Dr KAMAL BASRI SIREGAR, Sp.B(K) Onk</p> <p>DISUSUN OLEH :</p> <p>JOS BRIYAN R. H. SIBARANI(110100302)</p> <p>PROGRAM PENDIDIKAN PROFESI DOKTERDEPARTEMEN ILMU BEDAH UMUMFAKULTAS KEDOKTERAN UNIVERSITAS SUMATERA UTARARSUP HAJI ADAM MALIKMEDAN4</p> <p>2016I. Teori Genetik pada Karsinogenesis Kolorektal oleh Eric R. Fearon dan Bert Vogelstein 1.1 Tahapan perubahan adenoma menjadi karsinoma Colorectal cancerdevelopmentKanker kolorektal berkembang dari adenoma menjadi karsinoma melalui beberapa tahapan yang disertai akumulasi dari sejumlah mutasi genetik dan epigenetik (Morson 1968; Fearon dan Vogelstein 1990). Mutasi akumulasi bervariasi dalam kanker keturunan tergantung pada mutasi memulai. Dalam keadaan normal mereka, gen supresor tumor menghambat proliferasi sel. hambatan pertumbuhan hilang ketika kedua alel dinonaktifkan dengan mutasi dan / atau perubahan epigenetik, seperti promotor metilasi yang menghambat ekspresi gen. gen supresor tumor secara luas sesuai dengan hipotesis Knudson klasik dua hit, di mana inaktivasi kedua alel diperlukan untuk gen supresor tumor kehilangan fungsi normal mereka (Knudson 1971). Sebaliknya, proto-onkogen tindakan dengan mempromosikan proliferasi sel. Mutasi gen ini menyebabkan onkogenik yang abnormal over-ekspresi atau peningkatan aktivitas dari protein.Colorectal cancer develops via an adenoma to carcinoma sequence with the accumulation of a number of genetic and epigenetic mutations (Figure 13) (Morson 1968; Fearon and Vogelstein 1990). The mutations accumulated vary in hereditary cancer depending on the initiating mutation. In their normal state,tumour suppressor genesinhibit cell proliferation. Growth inhibition is lost when both alleles are inactivated by mutation and/or epigenetic changes, such as promoter methylation which stifles expression of the gene. Tumour suppressor genes broadly conform to Knudsons classic two-hit hypothesis, where inactivation of both alleles is required for tumour suppressor genes to lose their normal function (Knudson 1971). In contrast, proto-oncogenes act by promoting cell proliferation. Mutation of these genes leads to abnormal oncogenic over-expression or increased activity of the protein.The adenoma-to-carcinoma sequence for colorectal cancer is probably most commonly initiated by bi-allelic mutation of theAPCtumour suppressor gene.APCmutations have been found in microadenomas (Otori et al. 1998), the earliest lesion on the pathway (also called aberrant crypt foci (Roncucci et al. 1991)), and in ~60-80% of early sporadic adenomas and carcinomas (Cottrell et al. 1992; Miyoshi et al. 1992; Nakamura et al. 1992).APCis a key member of the canonicalWnt signalling pathway, and the key mechanism by which mutation of this gene contributes to carcinogenesis is by activation of this pathway. However, further accumulated mutations in additional genes are required for progression of the early lesions to cancer.</p> <p>The adenomacarcinoma sequence. The initial step in colorectal carcinogenesis is thought to be the formation of aberrant crypt foci (ACF). Activation of the Wnt pathway occurs during this step as a result of inactivating mutations in the APC gene. Progression to adenoma and carcinoma is usually mediated by activating mutations in KRAS and loss of TP53 expression, respectively. A subset of advanced adenomas may progress due to mutations in PIK3CA and lossof 18q. Reproduced with permission from: Pino MS, Chung DC (2010) The chromosomal instability pathway (CIN) in colon cancer. Gastroenterology 138(6):20592072</p> <p>It has long been observed that luminal environmental conditions alter from the distal ileum to the rectum, and that these conditions are associated with changes in the physical chemistry of the lumen contents including pH, proportions of short- and branched-chain fatty acids and the products of protein fermentation,32 as well as those of the microbiota. Colorectal bacterial populations are responsible for important aspects of both health (synthesis of micronutrients such as Vitamin K, protection of the intestine from pathogenic species) and disease (inflammatory reactions and production of carcinogenic metabolites). In relatively recent publications, authors have described associations between species of bacteria, such as Streptococcus bovis subtypes,33 and Fusobacterium spp.34 and colorectal neoplasia. Importantly, the composition of the gut microbiota also varies with gender,34 and this may be reflected in the distinct distributions of molecular colorectal carcinoma subtypes seen in male and female subjects. A possible explanation for the bimodal distribution of colorectal carcinoma, we observed is that the contact of the large bowel mucosa with luminal contents may last longer in both extremities of the colon than in the mid-colon.</p> <p>Terapi Cairan pada luka bakar</p> <p>Formula yang terkenal untuk resusitasi cairan adalah formula Parkland :24 jam pertama.Cairan Kristaloid (Ringer laktat) : 4ml/kgBB/%luka bakar contohnya pria dengan berat 80 kg dengan luas luka bakar 25 % membutuhkan cairan : (25) X (80 kg) X (4 ml) = 8000 ml dalam 24 jam pertama jumlah cairan (4000 ml) diberikan dalam 8 jam jumlah cairan sisanya (4000 ml) diberikan dalam 16 jam berikutnya.</p> <p>Cara lain adalah cara Evans : l. Luas luka bakar dalam % x berat badan dalam kg = jumlah NaCl / 24 jam2. Luas luka bakar dalam % x berat badan dalam kg =jumah plasma / 24 jam(no 1 dan 2 pengganti cairan yang hilang. Plasma untuk mengganti plasma yang keluar dari pembuluh dan meningkatkan tekanan osmosis hingga mengurangi perembesan keluar dan menarik kembali cairan yang telah keluar).3. 2000 cc Dextrose 5% / 24 jam (untuk mengganti cairan yang hilang akibat penguapan)Separuh dari jumlah cairan 1+2+3 diberikan dalam 8 jam pertama, sisanya diberikan dalam 16 jam berikutnya. Pada hari kedua diberikan setengah jumlah cairan pada hari pertama. Dan hari ketiga diberikan setengah jumlah cairan hari kedua. Formula Cairan 24 jam pertama Kristaloid Pada 24 jam kedua Koloid Pada 24 jam kedua </p> <p>Parkland Kristaloid 4 ml / kg / %LB20-60% estimate plasma volume Pemantauan output urine 30 ml/jam </p> <p>Evans Larutan saline 1 ml/kg/%LB, 2000 ml D5W*, dan koloid 1 ml/ kg / %LB 50% volume cairan 24 jam pertama + 2000 ml D5W 50% volume cairan 24 jam pertama </p> <p>Slater Kristaloid 2 L/24 jam + fresh frozen plasma 75 ml/kg/24 jam </p> <p>Brooke (Yowler, 2000) RL 1.5 ml / kg / %LB, koloid 0.5 ml / kg/ %LB, dan 2000 ml D5W 50% volume cairan 24 jam pertama + 2000 ml D5W 50% volume cairan 24 jam pertama </p> <p>Modified Brooke RL 2 ml / kg / %LB </p> <p>MetroHealth (Cleveland) RL + 50 mEq sodium bicarbonate per liter, 4 ml / kg / %LB lar. Saline, pantau output urine1 U fresh frozen plasma untuk tiap liter dari lar. saline yg digunakan + D5W dibutuhkan utk hipoglikemia.</p> <p>Monafo hypertonic Demling 250 mEq/L saline pantau output urine 30 ml/jam, dextran 40 dalam lar. saline 2 ml/kg/jam untuk 8 jam, RL pantau output urine 30 ml/jam, dan fresh frozen plasma 0.5 ml/jam untuk 18 jam dimulai 8 jam setelah terbakar. 1/3 lar. Saline, pantau output urine </p> <p>Sumber lainTabel Resusitasi cairan pada luka bakar dalam 24 jam pertama berdasarkan usia</p> <p>Rujukan : Pham T. N., Leopoldo C. C., Nicole S. G. 2008. American Burn Association Practice Guidelines Burn Shock Resuscitation. Journal of Burn Care &amp; Research January/February </p>