Fisiologi Gastrointestinall PDF

Summary

This document provides an overview of gastrointestinal physiology, covering the anatomy, basic functions, and various aspects of the digestive system. It includes learning objectives and detailed information about digestion, secretion, motility, and control mechanisms.

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The Digestive System 1 Nurfitri Bustamam, SSi, MKes, MPdKed. 2 Nurfitri Bustamam Learning Objectives 3 Describe the anatomy & basic function of digestive system Describe the composition & functions of saliva, & exp...

The Digestive System 1 Nurfitri Bustamam, SSi, MKes, MPdKed. 2 Nurfitri Bustamam Learning Objectives 3 Describe the anatomy & basic function of digestive system Describe the composition & functions of saliva, & explain how saliva is regulated Describe the mechanism of chewing & swallowing Identify structure of the wall of stomach that enhance the digestive process Describe the composition of gastric juice Explain regulations of gastric secretion & stomach motility Nurfitri Bustamam Alimentary canal & Accessory digestive organ Gastrointestinal Activity 5 Nurfitri Bustamam Digesti Proses pencernaan mekanik & kimia molekul besar mjd molekul kecil sehingga dapat diserap sal. GI 6 Sekresi Kelenjar yg terkait sal. GI, mensekresi air, elektrolit, or zat yg penting lain utk pencernaan, misalnya enzim, empedu, atau mucus. Motilitas Tone: a constant low level of contraction Pacesetter cells:  in m. mucosae & m. externa  spontan & ritmis  Basic Electrical Rhythm (BER)/slow wave potential Nurfitri Bustamam 7 It is believed that slow waves originate in the interstitial cells of Cajal, which are abundant in the myenteric plexus. Slow wave: depolarization (Ca2+ inward) & repolarization (K+ outward) Even without the occurrence of action potentials, the smooth muscle is not completely relaxed but exhibits basal contractions, or tonic contractions. If slow wave  threshold  action potential  phasic contraction (Constanzo 5th ed.) Peristalsis: propels materials along the length of digestive tract. 8 Segmentation: small intestine & large intestine churn & fragment the chyme, mixing the content with intestinal secretion do not push materials along the tract in any direction Absorpsi penyerapan hasil pencernaan dari lumen saluran GI, menembus lapisan epitel masuk ke dalam darah atau cairan limfe Nurfitri Bustamam Layers of digestive tract wall 9 Mucosa Submucosa Muscularis externa Serosa Nurfitri Bustamam Histology of The Alimentary Canal 10 Nurfitri Bustamam Mukosa Sel epitel tdd sel yg mensekresi mucus, sel kelenjar 11 endokrin, & sel kelenjar eksokrin yg menghasilkan enzim, asam, air & ion ke dalam lumen GI. Di bawah epitel tdpt lamina propria yg dilalui pembuluh darah, saraf, & saluran limfe. Di bawah lamina propria terdapat muskularis mukosa. Submukosa Jar. ikat yg dilalui pembuluh darah & terdapat jala saraf (pleksus) submukosa/Meissner Nurfitri Bustamam Epithelial Renewal & Repair 12 Nurfitri Bustamam Muskularis Eksterna 13 Otot sirkuler (di sebelah dalam & tebal), pleksus meinterikus (Auerbach), otot longitudinal (di sebelah luar & tipis) Pl. submukosa & Pl.mienterikus (Pl. intramural) serta neuron lain di saluran GI membentuk sistem saraf enterik. Serosa Selapis sel-sel mesotel yg mensekresikan cairan serous utk membasahi & mencegah gesekan antara organ pencernaan & organ dalam sekitarnya Nurfitri Bustamam Control of Digestive Function 14 Di dlm lumen GI diciptakan lingk. khusus agar proses digesti & absorpsi optimal via pengendalian sekresi kelenjar & kontraksi otot. Pengendalian tsb bergantung pada volume & komposisi kandungan lumen GI. Rangsang: regangan dinding lumen, osmolaritas kimus, keasaman kimus, hasil pencernaan KH, lemak, & protein Reseptor: mekanoreseptor, osmoreseptor, kemoreseptor Efektor: kel eksokrin, kel endokrin or otot dinding GI Nurfitri Bustamam Control of Digestive Function 15 (Sherwood , 2016) Nervous control 16 Extrinsic/autonomic Intrinsic Sympathetic (decreases Submucous or Meissner’s motor and secretory plexus (controls secretory activity, contraction of function) sphincters) Myenteric or Auerbach’s Parasympathetic plexus (controls motor (stimulatory) activity) Nurfitri Bustamam Pengaturan Saraf 17 Sistem saraf intrinsik dibentuk oleh pleksus mienterikus dan submukosa sehingga refleks GI tdk bergantung pd SSP Sistem saraf ekstrinsik: SSO (simpatis dan parasimpatis) yg bersinaps dg neuron di pleksus Ada dua jalur refleks, yaitu refleks pendek & panjang Tdk semua refleks pengendalian di mulai dari dlm saluran GI, jika dimulai dari reseptor lain, misalnya melihat makanan, pasti SSP terlibat dalam responsnya Nurfitri Bustamam Pengaturan Saraf 18 Hormonal control 19 Nurfitri Bustamam Oral / Buccal Cavity 20 Nurfitri Bustamam Mengunyah 21  Pemecahan partikel besar makanan mjd partikel kecil & mencampurnya dg saliva sehingga terbentuk bolus  Mengunyah melibatkan kerjasama otot pengunyah, lidah, dan pipi  Mengunyah mrpkan gerakan ritmis yg dikendalikan oleh ss somatik yg menuju otot2 pengunyah  Disamping pengendalian volunter, gerakan mengunyah yg ritmis ini dikendalikan secara refleks yg diaktifkan oleh tek. makanan terhadap gusi, gigi, palatum durum, dan lidah Nurfitri Bustamam Kelenjar Saliva 22 volume 1-1,5 L/hari, pH  7,0 99,4% H2O: - submandibular 70% - parotis 25% - sublingual 5% 0,6% tdd: - enzim: lingual lipase ptyalin -amylase - glikoprotein (mucin) utk lubrikasi. Nurfitri Bustamam 23 Functions of saliva 24 Digestive functions: Amylase breaks down starch, and lingual lipase breaks down triglycerides (active in the stomach). It dissolves food materials so it can be sensed by taste buds. Lubrication: Keeps mouth moist and thus facilitates movements of lips and tongue during speech. Moistens food and thus facilitates swallowing. Protection: Keeps mouth and teeth clean by dissolving and washing food particles from between the teeth. Has an anti-bacterial action. Buffers acidic gastric secretions. Fungsi Saliva 25 26 Sjögren’s syndrome  immune disorder in which many different exocrine glands are rendered nonfunctional by the infiltration of white blood cells and immune complexes. loss of salivary gland function  impaired sense of taste, difficulty chewing, and even ulcers (holes) in the mucosa of the mouth 27 (Constanzo 5th ed) Pengendalian Sekresi Saliva 28 Refleks tidak bersyarat: dari lidah/mulut & esofagus bawah/lambung/usus halus sebelah atas Refleks bersyarat: dari daerah korteks serebri (melihat, menghidu, mendengar, memikirkan makanan) Ivan Pavlov Nurfitri Bustamam 29 Nurfitri Bustamam 30 Nurfitri Bustamam 31 (Constanzo 5th ed) 32 Fase sekresi saliva - sefalik - bukal - esofago/gastro/intestinal (rangsang iritasi sekresi saliva yg berperan sbg pelarut & buffer rangsang iritan tsb) Perangsangan parasimpatis: saliva encer, kaya enzim, banyak, & sedikit mengandung bahan organik Perangsangan simpatis: saliva kental (banyak mucus), sedikit, dan banyak mengandung bahan organik Nurfitri Bustamam Esofagus Esofagus (25 cm) tdd: 33 - 1/3 bag atas: otot rangka - 1/3 bag tengah: otot rangka & otot polos - 1/3 bag bwh: otot polos Esofagus mensekresi mucus sbg pelumas sewaktu menelan & proteksi dinding esofagus dari asam & enzim jika tjd reflux Esophagus 34 Function: Swallowing or deglutition, which is the process of moving food from the mouth through the esophagus into the stomach No digestion or absorption Secretions: mucus Nurfitri Bustamam Menelan 35 Pharynx & esofagus tdk ikut dlm proses pencernaan, tetapi hanya mrpkan jalur masuknya makanan ke lambung (6-10 detik) Proses ini mrpkan refleks majemuk yg ditimbulkan oleh perangsangan reseptor di dinding farings oleh bolus. Impuls aferen disalurkan mll n.V, VII, XII, dan X. Nurfitri Bustamam Swallowing 36 Swallowing can be initiated voluntarily but then it is under reflex control. Swallowing reflex Receptors: touch receptors in pharynx Afferent: sensory impulses from receptors Centre: swallowing centre in brain stem Efferent: parasympathetic nerves to muscles of pharynx and esophagus Nurfitri Bustamam Fase Menelan 37 1. Fase Oral volunter; bolus didorong ke orofarings oleh lidah (kontraksi m. miohioid dan stiloglosus), merangsang reseptor taktil yg akan memulai refleks menelan 2. Fase Faringeal uvula terangkat ke atas mencegah bolus masuk ke nasal epiglotis ke bawah, pita suara bergerak saling mendekati mencegah bolus masuk ke trakea sfingter oesofagus atas (UOS) melemas, otot konstriktor farings superior berkontraksi kuat mendorong bolus 3. Fase Esofageal Nurfitri Bustamam 38 Fase Buccal Fase Faringeal Nurfitri Bustamam Fase Protective reflexes during pharyngeal phase of swallowing: 39 a) Elevation of the soft palate: closes posterior nasal openings, thus preventing food reflux into the nasal cavities.Elevation of the larynx against the epiglottis: closes the superior laryngeal orifice (glottis), thus preventing food entrance into the trachea. b) Approximation of the vocal cords: This also closes the glottis, but its role is much more important than that of the epiglottis d) Temporary apnea: stoppage of breathing for few seconds which also prevents food entrance into the trachea Nurfitri Bustamam 40 Nurfitri Bustamam 41 Fase Esofageal 42 Nurfitri Bustamam Receptive Relaxation 43 Distention of lower esophagus by food  relaxation of LOS & relaxation of orad stomach, called receptive relaxation Receptive relaxation reduces the pressure & increases the volume of the orad stomach, which, in its relaxed state, can accommodate as much as 1.5 L of food Receptive relaxation is a vagovagal reflex (Constanzo 5th ed.) 44 Setelah bolus melewati UOS, secara refleks UOS konstriksi. Tepat di bwh UOS dimulai gelombang peristaltik primer yg dikendalikan oleh pusat menelan di medulla oblongata Jika gelombang peristaltik primer tidak cukup menyapu bolus, tjd peregangan esofagus yg merangsang gelombang peristaltik sekunder yg dikendalikan oleh pleksus. Upside down or zero gravity? Nurfitri Bustamam the last portion of the esophagus lies below the diaphragm and is subject to the same abdominal 45 pressures as the stomach During cycles of respiration or contraction of the abdominal muscles, the pressures on both the gastric contents and the terminal segment of the esophagus are increased together  prevents the formation of a pressure gradient between the stomach and esophagus that could force the stomach’s contents into the esophagus Smoking, alcohol & caffeine  gastroesophageal reflux  heartburn (because the pain appears to be located in the area of the heart) & can also cause coughing and irritation of the larynx tek esofagus < atmosfir, tek lambung > esofagus 46 UOS cegah udara masuk ke esofagus + LOS cegah reflux gastric content LOS tetap tertutup meskipun terjadi peningkatan tek abdomen, misal pada ekspirasi paksa, karena letak LOS dibwh diafragma Pada kehamilan: janin + peningkatan tek abdominal mendorong LOS ke rongga torax  LOS terbuka & isi lambung terdorong ke esofagus Esophagitis/Gastro Esophageal Reflux Disease (GERD): HCl mengiritasi esofagus timbul spasme otot & nyeri (heart burn). Pd akhir kehamilan heart burn subside Achalasia 47 Food accumulation in esophagus & the organ becomes massively dilated. It is due to increased resting LOS tension, incomplete relaxing of LOS, & weak esophageal peristalsis. Secondary peristaltic wave repeatedly discomfort. Th/ cutting the circular muscle layer at the base of esophagus Aphagia: in ability to swallow Dysphagia: difficulty in swallowing Aerophagia  burping (sendawa) Gaster 48 Nurfitri Bustamam 49 50 51 Motilitas Gaster 52 Lambung kosong mempunyai vol. 50 ml. Pada saat menelan makanan, otot polos di fundus & korpus secara refleks melemas sebelum makanan sampai di lambung shg volumenya meningkat mjd 1,5 L tanpa peningkatan tekanan yg nyata (receptive relaxation ini berlangsung mll perangsangan n. vagus & dikendalikan oleh pusat menelan). Setelah lambung terisi, mulailah kontraksi lemah di daerah fundus & korpus yg menekan isi lambung. Kontraksi ini berlangsung beberapa waktu, tetapi tdk mencampur isi lambung dg liur lambung. Oleh karena itu amilase saliva masih dpt bekerja. Kontraksi lemah akan menekan isi lambung shg 53 meningkatkan tek lambung. Kontraksi akan menjalar ke antrum dan mjd semakin kuat (frekuensi 3X per menit). Isi lambung yg didorong oleh peristaltik antrum sebagian dipantulkan kembali ke korpus krn belum dpt melewati pilorus yg hanya dpt dilalui partikel berukuran < 1 mm) Nurfitri Bustamam 54 55 Kontraksi antrum akan diikuti kontraksi pilorus & duodenum atas. Aliran balik duodenum tdk akan tjd krn kontraksi pilorus berlangsung sedikit lbh lama dari kontraksi duodenum. 56 Keaktifan di antrum akan: 1.Mencampur & mengaduk isi lambung dg cepat dan cermat dengan sekret lambung 2.Memecah makanan menjadi partikel yg lbh kecil 3.Mencurahkan isi lambung yg sdh berbentuk kimus sedikit demi sedikit ke duodenum (pompa antrum/pilorus) 57 Kontraksi peristaltik dikoordinasi oleh gastric slow wave yg dimulai dr fundus ke pilorus tiap 20 detik Kecepatan Pengosongan Lambung 58 1. Keadaan di lambung a. jenis makanan; KH > protein > lipid lebih cepat meninggalkan lambung b. volume isi lambung; makin teregang  sekresi gastrin  motilitas 2. Keadaan di duonenum yg menghambat pengosongan lambung - volume/peregangan dinding - hiperosmolaritas kimus - keasaman (pH < 3,5) - hasil pencernaan protein - lemak Keadaan di Duodenum 59 60 (Sherwood , 2016) 61 (Vander , 2019) Keaktifan Lambung Kosong (Fasting Motor Activity) 62 Bersifat siklik (tiap 90’- 120’), tdd Fase I (periode tenang) Fase II (periode kontraksi yg intermitten) Fase III (hamburan kontraksi kuat yg singkat); keaktifan ini dpt menyapu isi lambung proksimal hingga ke ileum terminal kemudian mendorongnya hingga ke sekum. Fase ini berperan membersihkan lambung & usus dari sisa-sisa sampah dan sekret; mungkin juga penting dlm mencegah pertumbuhan kuman yg berlebihan. Keaktifan kuat lambung yg kosong dpt dirasakan. Oleh karena disertai rasa lapar, disebut kontraksi lapar. Migrating Myoelectric Complexes 63 During fasting, there are periodic gastric contractions, called the migrating myoelectric complexes, which are mediated by motilin. These contractions occur at 90-minute intervals and function to clear the stomach of any residue remaining from the previous meal. Nurfitri Bustamam Kelenjar di Lambung 64 Pilorus Sel mucus  mukus Sel G (pilorus/antrum)  gastrin Korpus & Fundus Sel parietal/oksintik  HCl & faktor intrinsik Chief cells/zimogen  pepsinogen Mucus Neck cells  mukus Nurfitri Bustamam 65 Sekresi Liur Lambung 66 2500 ml/hari pH  1 Na+ , K +, Mg + +, H + Cl- , HPO4- - , SO4 - - pepsinogen, mukus, faktor intrinsik, air faktor intrinsik utk absorpsi vit. B12 di ileum. Defisiensi vit B12  anemia pernisiosa Sekresi HCl 67 Sel Parietal Setelah makan, sekresi HCl naik dan kadar bikarbonat darah yg berasal dari lambung naik, pH darah naik (postprandial alkaline tide) 68 69 Enteric nerve endings release gastrin releasing peptide (GRP) or bombesin  G cells  gastrin  bloodstream  parietal cells (HCl) & enterochromaffin-like cells/ECL (histamin). Histamin binds to H2 receptors at Parietal cells HCl. Parietal, Chief & ECL cells can also stimulated by ACh release from enteric nerve ending. 70 Cephalic phase  predominantly activated by vagal input  GRP & ACh. Meal in the stomach  strecth receptor  vago-vagal (local reflexes)  amplify secretion of gastrin. Meal  buffer gastric acidity  somatostatin secretion  inhibit G, ECL cells & Parietal cells secretion. A key mechanism whereby gastric secretion is terminated after meal moves from stomach. Nurfitri Bustamam Fungsi HCl 71 memecah partikel makanan & membentuk larutan molekul yg disebut kimus denaturasi protein & inaktivasi enzim dlm makanan aktivasi pepsin membunuh mikroorganisme dalam makanan merangsang sekresi empedu & liur pankreas Regulasi Sekresi HCl 72 73 (Constanzo 5th ed) 74 Nurfitri Bustamam 75 Nurfitri Bustamam Abar Bikarbonat-Mukosa 76 Terbentuk dari mukus dan bikarbonat yg disekresi oleh mukosa lambung dan hubungan antar sel-sel mukosa yg bersifat tight junction Melindungi sel mukosa lambung dari pengrusakan oleh HCl dan pepsin Bahan yg merusak abar: etanol, cuka, aspirin, obat antiinflamasi non steroid (NSAID), garam empedu Sekresi mukus dirangsang oleh iritasi mukosa, nervus vagus, dan prostaglandin Nurfitri Bustamam 77 Nurfitri Bustamam Tukak Lambung 78 Nurfitri Bustamam 79 (Constanzo 5th ed) 80 Nurfitri Bustamam When Bugs Break The Barrier 81 1990s Helicobacter pylori – 80% peptic ulcer Punya 4-6 flagella Habitat di antrum  acid-producing parietal cells Menghslkan urease yg menghidrolisis urea mjd amonia (berfungsi sbg buffer) H. pylori is an extremely common pathogen; rates of infection are highest in the world’s poorest countries, where sanitation facilities and standards of personal hygiene are low. The most likely route of spread from person to person is fecal–oral. Helicobacter pylori 82 Nurfitri Bustamam 83 Absorpsi di lambung tdk tjd sebab 1. Sel-sel epitel diselimuti oleh mucus alkalin shg secara tdk lgs terpapar kimus 2. Sel-sel epitel tdk mempunyai mekanisme transpor spt yg tdpt pd usus halus 3. Sel-sel epitel lambung relatif impermeabel thd air 4. Partikel makanan di lambung masih berukuran besar (pencernaan blm sempurna) Note: alcohol dpt diabsorpsi di lambung Nurfitri Bustamam Nurfitri Bustamam

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