PANCREAS.pptx
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PANKREAS
DR. RESTI ARANIA Sp.PA
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Lokasi fungsi
• kuadran kanan atas• retroperitoneal• Caput, corpus , tail
• endokrin• eksokrin
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anatomi- - histologi
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• ENDOKRIN• Pulau Langerhans (>tail)• hx hormon• Diabetes Melitus• Hiperfungsi pulau2
(hiperplasia, neoplasma)• Hormon hx : insulin,
glukagon, gastrin, PP, somatostatin, VIP/dll
• EKSOKRIN• sel-sel asiner pankreas• hx enzim2 pencernaan• duktus _-- papila
duodenum dan CBD• Tripsin, kemotripsin,
lipase, fosfolipase, amilase
• kongenital, radang, kista, neoplasma
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Anomali kongenital
• Gangguan perkembangan : Agenesis, pankreas divisum (sering),
caput– annular pankreas—gejala obstruksi duodenum
• Ektopik / aberans: gaster, duodenum, jejunum, divertikulum Meckel
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• AKUT• serius• mortalitas tinggi• dewasa• kausa : obstruksi duktus
oleh batu empedu, alkohol, inf virus mumps, hiperkalsemi, syok, trauma
• patologi : enzime release• gejala
Radang : PANKREATITIS
• KRONIK• relaps pankreatitis akut• kausa: alkohol, cystic
fibrosis• patologi : fibrosis, atrofi
kelenjar• Dewasa > anak• gejala : nyeri, steatorea,
berat badan turun: • Klinik : ro kalsifikasi
pankreas, serum amilase
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Pankreatitis akut
• tripsin kemotripsin aktivasi : mediator kimia---radang
• aktivasi lipase—nekrosis lemak
• Amilase, lipase ---darah—marker
• Aktivasi kaskade koagulasi—DIC
Gejala : -Emergensi- nyeri mendadak, terus menerus-- muntah- perdarahan—syok- Radang,perdarahan– Cullen`s sign---Turner sign-DIC- ikterus
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Pankreatitis akut– Nyeri perut mendadak, necrosis + enzymatic +
keradangan– Enzym amilase (+) dalam urine & darah– Lipase fat nekrosis acute hemorrhage
Morfologi :1. Kerusakan proteolitik pankreas2. Nekrosis vaskular perdarahan interstitial3. Enzim lipolitik nekrosis lemak4. Reaksi radang akut
Bila sembuh pseudokista pankreas
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Gejala/ Komplikasi
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PANKREAS
• Eksokrin (85-90%)1. Pankreatitis - akut
- khronik2. karsinoma
• Endokrin (10-15%)– Diabetes Mellitus
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Pankreatitis kronik– Faktor alkohol penting– Penyakit traktus biliaris– Hiperkalsemia, hiperlipoproteinemia– Malnutrisi kalori protein pankreatitis tropik– Mutasi cystic fibrosis transmembrane conductance
regulator gene pankreatitis idiopatik
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Morfologi– Pankreas fibrotik, padat atrofi– Infiltrasi radang kronik– Protein plug obstruksi duktus– Kelenjar keras, duktus lebar, kalsifikasi– Sering ada pseudokista
Gambaran klinik :– Abdominal pain berulang-ulang– Menjalar ke punggung– Timbul insuffisiensi pankreas diabetes– Serum amilase dan lipase tinggi– CT Scan / USG kalsifikasi, pseudokista
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KISTA PANKREAS
• KISTA DEFINITIF• DIBATASI EPITEL• KONGENITAL
• PSEUDOKISTA• TANPA EPITEL PELAPIS• BIASANYA AKIBAT
PANKREATITIS AKUT YANG SEMBUH
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KISTA NEOPLASTIK
• KISTADENOMA : serosa, musinosa• jarang• Soliter• serosa : jarang jadi ganas, tanpa gejala• musinosa : tumbuh lambat– potensial ganas
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NEOPLASMA
• HIPERPLASIA• KISTADENOMA - serosum - musinosum
• KARSINOMA• 60% : CAPUT• 15% corpus• 20% difus• jenis adenokarsinoma
tersering, sangat invasif• khas : respon
desmoplastik
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KARSINOMA PANKREAS
– Tumor dari eksokrin– Banyak pada perokok– Umur 60 – 80 tahun– Lebih banyak pada herediter pankreatitis– Terdapat mutasi K.RAS gene, dan tumor suppresor gene
CDKN2A (P16) 90% kasus– TP53 (dulu P53) mutasi 50% kasus– Deleted in pancreatic cancer (DPC4) hilang pada 50%
kasus– ERBB2 (HER2/NEU) 50% kasus– BRCA2 dan MLHI juga ada
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Morfologi :
60 – 70 % caput50 – 60 % corpus10 – 15 % tail20 % seluruhnya– Adeno Ca membentuk mucin– Tumor head ampulary obstruksi empedu 50 %– Metastasis : syaraf, lien, adrenal vertebra, colon,
gaster, kelenjar getah bening, dll
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Gambaran klinik
- Tergantung lokasi tumor, di caput gejala cepat- corpus/ tail –gejala lambat, meluas ke sekitar–Bila menembus kapsul ke syaraf nyeri–Ca caput IKTERUS OBSTRUKTIF–Ca body/tail flebotrombosis (Trousseau
Sign)– karsinoembrionik Ag, CA 19-9 Ag (+)
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ENDOKRINDIABETES MELITUS
• DEFISIENSI absolut /relatif insulin• Absolut : juvenile/ IDDM• relatif : adult tipe/ NIDDM
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ENDOKRINDiperankan oleh PULAU LANGERHANS• Tipe sel pulau Langerhans :- Sel Beta ( 1 juta sel,1 pulau sekitar 1.000 sel)- sel alpha• Jenis Hormon yang penting :- Insulin- glukagon• Jenis hormon lain yang di hx :- PP (polipeptida pankreas)- VIP (vasoactive intestinal polypeptide)
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Endokrin Pankreas
– Pulau Langerhans, sekitar 1 juta– Jenis sel
• Beta 70 % hx : insulin• Alpha 5 – 20 % hx: glukagon• Delta 5 – 10 % hx: somatostatin• DD (pancreatic polypeptide) juga ada pada exocrine 1 –
2 %
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insulin
• Fungsi biokimia : mengatur transfer glukosa dari plasma darah ke sitoplasma sel target
• sel target al : hati, otot, lemak.• Susunan kimia : rantai A tda 21 as. amino dan
rantai B tda 30 as. amino
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DIABETES MELLITUS
• Penyakit kronis krn defisiensi insulin absolut atau relatif
• Defisiensi insulin metabolisme karbohidrat hyperglicemia/ intoleransi glukosa
Klasifikasi & Insidens1. Primer kelainan produksi/aksi insulin2. Sekunder kelainan pankreas
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Perbandingan tipe2 DM primer• Tabel 1. Sumber : Concise Pathology. Chandrasoma.
Tipe I (juvenilis) Tipe II (dewasa)
insiden 15% 85%
Terapi insulin Selalu perlu Kadang-kadang
Usia (pada umumnya) Di bawah 30 tahun Di atas 30 tahun
Hubungan dengan obesitas tidak ya
Predisposisi genetik Lemah, poligenik Kuat, poligenik
Hub dg sistem HLA ya tidak
Intoleransi glukosa berat Ringan
ketoasidosis Sering jarang
Jumlah sel beta pada pulau berkurang bervariasi
Kadar Insulin serum menurun bervariasi
Gejala klasik 3P, BB turun sering jarang
Penyebab klasik Viral? Otoimun? Resistensi insulin
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Komplikasi jangka panjang DM
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1. Type I Diabetes
• Insulin dependent DM / juvenile onset DM 5 – 10 %–Type IA Beta sel rusak karena
otoimun–Type IB Beta sel rusak bukan karena
otoimun
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2. Type II Diabetes• Non insulin DM / adult onset DM 80 %
• 10 %
3. DM jenis lain
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Patogenesis
Fisiologi insulin normal :– Gen insulin berada pada sel beta, insulin
disintesa dan disimpan dlm granule– Stimuli penting yang mengeluarkan insulin
adalah glukosa– Insulin adalah hormon anabolik major, ini
untuk:1. Transport transmembran glukosa & asam
amino
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2. Pembentukan glikogen pada liver dan otot
3. konversi glukosa menjadi trigliserida4. Sintesa asam nukleat5. Sintesa protein
– Insulin bekerja pada sel targetnya ikatan dengan reseptor
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Kriteria DM
1. Puasa semalam glukosa darah ≥126 mg/dl
2. Gejala diabetes glukosa darah sewaktu/ GDS ≥200 mg/dl
3. Pemberian 75 gr glukosa, 2 jam ≥200 mg/dl
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Patogenesa type IA
• Kerusakan sel Beta karena otoimun• Mekanisme kerusakan islet sel
a. Genetic susceptibility – allele class II Major Histocompatibility Complex (MHC)
b. Reaksi otoimunc. Pengaruh lingkungan
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Genetic susceptibility
• Sering orang Eropa Utara• Jarang pada orang-orang hitam, Hispanic,
Amerika pribumi, Asia• Family 6 % anak• Kembar 40 %• Chromosome 6p21 ( termasuk MHC class II
gene )
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Reaksi otoimun
• T cell membrane, autoimmune• Cytotoxic CD8 + lymphocyte membunuh islet
sel dengan pelepasan granule• Antigen intracellular yang bereaksi dg
autoantibodi adalah glutamic acid decarboxylase, insulin
• 10-20% type IA sering punya penyakit lain-lain : Hashimoto, Celiac disease, Graves, Addison, Pernicious anemia