tugas dr kamal 1
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TUGAS dari Dr KAMAL BASRI SIREGAR, Sp.B(K) Onk
DISUSUN OLEH :
JOS BRIYAN R. H. SIBARANI (110100302)
PROGRAM PENDIDIKAN PROFESI DOKTER
DEPARTEMEN ILMU BEDAH UMUM
FAKULTAS KEDOKTERAN UNIVERSITAS SUMATERA UTARA
RSUP HAJI ADAM MALIK
MEDAN
2016
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I. Teori Genetik pada Karsinogenesis Kolorektal oleh Eric R. Fearon dan
Bert Vogelstein 1.1 Tahapan perubahan adenoma menjadi karsinoma – Colorectal cancer development
Kanker 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 1-3) (Morson
1968; Fearon and Vogelstein 1990). The mutations accumulated vary in hereditary
cancer depending on the initiating mutation. In their normal state, tumour suppressor
genes inhibit 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
Knudson’s 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.
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The adenoma-to-carcinoma sequence for colorectal cancer is probably most
commonly initiated by bi-allelic mutation of the APC tumour suppressor
gene. APC mutations 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). APC is a key member of the
canonical Wnt 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.
The adenoma–carcinoma sequence. The initial step in colorectal carcinogenesis is
thought to be the formation of aberrant crypt foci (ACF). Activation of the Wnt
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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 loss
of 18q. Reproduced with permission from: Pino MS, Chung DC (2010) The
chromosomal instability pathway (CIN) in colon cancer. Gastroenterology
138(6):2059–2072
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.
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Terapi Cairan pada luka bakar
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
½ jumlah cairan (4000 ml) diberikan dalam 8 jam
½ jumlah cairan sisanya (4000 ml) diberikan dalam 16 jam berikutnya.
Cara lain adalah cara Evans :
l. Luas luka bakar dalam % x berat badan dalam kg = jumlah NaCl / 24 jam
2. 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
6
Parkland Kristaloid 4 ml /
kg / %LB
20-60% estimate
plasma volume
Pemantauan output
urine 30 ml/jam
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
Slater Kristaloid 2 L/24
jam + fresh
frozen plasma 75
ml/kg/24 jam
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
Modified
Brooke
RL 2 ml / kg /
%LB
MetroHealth
(Cleveland)
RL + 50 mEq
sodium
bicarbonate per
liter, 4 ml / kg /
½ lar. Saline,
pantau output urine
1 U fresh frozen
plasma untuk tiap liter
dari ½ lar. saline yg
digunakan + D5W
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%LB dibutuhkan utk
hipoglikemia.
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
Sumber lain
Tabel Resusitasi cairan pada luka bakar dalam 24 jam pertama berdasarkan usia
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Rujukan : Pham T. N., Leopoldo C. C., Nicole S. G. 2008. American Burn Association Practice Guidelines Burn Shock Resuscitation. Journal of Burn Care & Research January/February