MINGGU 3

19 D
ANNISA DANIA JULIANA
BERLIAN NAUFAL
FUKA PRIESLEY
MIRANDA MARDHATILLAH R
RAHMAT AKBAR
RAHMEYDIA AUDYA
RIKO JANUKADRI
ULFAH LATHIFAH
VIRLY TIFFANY

SKENARIO 3 : PERIH ULU HATIKU, LEBIH PEDIH HATIKU

ibu Aci 30 tahun, telah menikah selama 10 tahun belum dikarunia anak. Ia
mengeluh nyeri ulu hati yang bertambah sering sejak satu minggu ini,
sebenarnya keluhan tersebut telah dirasakan sejak enam bulan yang lalu. Ia
sering terlambat makan dan suka makan yang pedas. Selain itu, ibu Aci merasa
cemas karena belum punya anak, ia takut ditinggal suaminya. Apalagi akhir-
akhir ini suaminya sering marah jika tidak cepat dilayani. Bila penyakit maag
kambuh, ia merasa pusing dan nyeri di punggung.
Akhirnya ibu aci berobat ke puskesmas. Dokter menanyakan kepada ibu
Aci adanya nyeri yang bertambah setelah makan, rasa mual, kembung, dan
rasa terbakar di dada. Selanjutnya dokter juga menanyakan riwayat minum obat
penghilang sakit dan BAB yang berwarna hitam. Dokter menjelaskan secara
rinci mengenai kemungkinan diagnosis penyakit lambung ini, dan menyarankan
dilakukan endoskopi di Instalasi Diagnostik Terpadu (IDT) RSUP dr. M. Djamil
Padang.
ibu Aci Penasaran sampai di rumah ia mencari di internet perihal
penyakitnya. Ditemukan bermacam diagnosis, antara lain : gastritis, gastropati
NSAID, ulkus lambung, GERD, dan masalah psikosomatis. Ia bingung sendiri
memikirkan penyakit yang dialaminya.
bagaimana anda menjelaskan kemungkinan penyakit yang dapat terjadi
pada ibu Aci?

TERMINOLOGI
1. Maag -> latin : lambung, gejala gangguan pada
lambung
2. Ulu hati -> epigastrium, daerah perut bagian tengah
atas yang terletak di antara angulus sterni
3. Endoskopi -> pemeriksaan visual untuk melihat bagain
dalam tubuh menggunakan tabung fleksibel yang
memakai kamera kecil diujungnya
4. Gastritis -> perandangan pada lapisan lambung
(mukosa dan submukosa)

Gasropati NSAID -> gangguan pada lambug karena penggunaan obat non steroid 6. Ulkus lambung -> luka akibat terkikisnya pada lapisan dinding lambung 7.TERMINOLOGI 5. refluxnya isi gaster akibat gangguan pada lower esophageal spincter (LES) . GERD -> gastroeshophageal reflux disease.

Apa perbedaan penyakit gastritis. Mengapa bila maag ibu Aci kambuh ia sering merasa pusing dan nyeri di punggung? 7. Apa yang menyebab nyeri ulu hati ibu Aci bertambah sering sejak satu minggu ini? 2. Apakah ada hubungan belum dikarunia anak dengan penyakitnya sekarang? 3. GERD? Dan bagaimana membedakannya dalam mendiagnosis? . rasa mual. Apa alasan dokter menanyakan riwayat minum obat penghilang sakit dan BAB yang berwarna hitam? 9.IDENTIFIKASI MASLAH 1. Apa alasan dokter menyarankan dilakukannya endoskopi pada ibu Aci? 10. ulkus lambung. Mengapa dokter menanyakan adanya nyeri yang bertambah setelah makan. Apakah hubungan suka makanan pedas dan terlambat makan dengan keadaan ibu Aci sekarang? 4. kembung dan rasa terbakar di dada? 8. Apakah kemungkinan diagnosis penyakit ibu Aci? 11. gastropati NSAID. Apakah hubungan rasa cemas ibu Aci dengan keadaanya sekarang? 6. Apakah ada hubungan usia dan jenis kelamin dengan penyakit ibu Aci? 5.

HIPOTESA MASALAH .

obat2 NSAID. faktor stree -> terus menerus -> merangsang sekresi HCL yang berlebihan -> iritasi pada lambung makin bertmbah -> ketidakseimbangan faktor defensif dan agresif -> nyeri . APA YANG MENYEBAB NYERI ULU HATI IBU ACI BERTAMBAH SERING SEJAK SATU MINGGU INI? Nyeli ulu hati -> faktor pencetus : makan tidak teratur. suka makanan pedas. zat kimia.

APAKAH ADA HUBUNGAN BELUM DIKARUNIA ANAK DENGAN PENYAKITNYA SEKARANG? Kontraktilitas lambung menurun -> nafsu makan berkurang -> gizi ibu rendah Stress pada ibu -> meningkatkan saraf simpatis -> adrenalin meningkat -> menekan sistem imun -> ibu mudah sakit Ibu yang terlalu kuras dan terlalu gemuk juga bisa mempengaruhi hormon estrogen .

APAKAH HUBUNGAN SUKA MAKANAN PEDAS DAN TERLAMBAT MAKAN DENGAN KEADAAN IBU ACI SEKARANG? Sebagai faktor pencetus -> meningkatkan asam lambung Makanan pedas dan terlambat makan -> lambung sulit beradaptasi -> ketidakseimbangan faktor defensif dan agresiv -> asam lambung meningkat -> .

JENIS KELAMIN DENGAN PENYAKIT IBU ACI? Usia dan jenis kelamin tidak begitu mempengaruhi. namu jika ada faktor pencetus resikonya akan lebih meningkat Dilihat dari segi stress -> wanita lebih tinggi angka stress dibanding pria -> wanita lebih berisiko Dilihat dari segi gaya hidup seperti mengonsumis alkohol dan roko -> meningkat resiko pada pria dibanding wanita Seiring bertambahnya usia mukosa gaster cendrung menjadi tipis -> lebih cendrung terinfeksi helicobacter pylori Usia produktif -> dengan berbagai kesibukan -> makan tidak teratur/sehat -> meningkat resiko kejadian Semakin meningkatnya usia -> prognosi semakin buruk .

APAKAH HUBUNGAN RASA CEMAS IBU ACI DENGAN KEADAANYA SEKARANG? Stress -> rangsangan saraf simpatis IV (nervus vagus) -> meningkatkan produksi asam lambung -> mual dan muntah .

terutama pada anemia pernisiosa yang bisa menyebabkan gastritis Nyeri punggung -> reffer paint -> saraf otonom .MENGAPA BILA MAAG IBU ACI KAMBUH IA SERING MERASA PUSING DAN NYERI DI PUNGGUNG? Pusing -> multifaktor. seperti :  stress  kurangnya asupan  anemia -> karena perdarahan.

KEMBUNG DAN RASA TERBAKAR DI DADA? Mencari penyebab pasti dan perjalanan penyakit dari ibu Aci Bertambah setelah makan -> sebagai differential diagnosis Rasa mual dan kembung -> memastikan terjadinya peningkatan asam lambung Rasa terbakar di dada -> apakah ada refluks gaster .MENGAPA DOKTER MENANYAKAN ADANYA NYERI YANG BERTAMBAH SETELAH MAKAN. RASA MUAL.

apakah karena obat (NSAID) atau tidak Pemakaian obat penghilang rasa nyeri -> bisa menyebabkan peradangan pada lambung karena menurunnya prostaglandin (sbagi proteksi lambung) BAB yang berwarna hitam -> untuk melihat adanya perdarahan saluran cerna atas .APA ALASAN DOKTER MENANYAKAN RIWAYAT MINUM OBAT PENGHILANG SAKIT DAN BAB YANG BERWARNA HITAM? Riwayat minum obat -> melihat kausal.

APA ALASAN DOKTER MENYARANKAN DILAKUKANNYA ENDOSKOPI PADA IBU ACI? Untuk memastikan apakah tejadi kelainan organik atau non organik (masalah psikosomatis) Pada kelainan organik -> untuk menilai mukos break (derajat penyakit) .

APAKAH KEMUNGKINAN DIAGNOSIS PENYAKIT IBU ACI? Belum dapat dipastikan karena belum adanya kepastian diagnosis seperti melakukan endoskopi -> apakah kelainan organik atau organik Tapi kemungkinan ibu Aci mengalami sindroma dispepsia .

biasanya ada nyeri abdomen yang sering terjadi di malam hari GERD -> adanya rasa terbakar di dada (heartburn) . APA PERBEDAAN PENYAKIT GASTRITIS. ULKUS LAMBUNG. GASTROPATI NSAID. GERD? Gastritis -> peradangan pada lapisan mukosa dan submukosa Gastropati NSAID -> lesi mukosa gaster yang berhubungan dengan penggunaan OAINS Ulkus lambung -> perandangan dari lapisan dinding lambung yang ditandai dengan adanya luka pada dinding lambung.

SKEMA .

LEARNING OBJECTIVE 1. GASTRITIS 2. GASTROPATI NSAID 3. GERD 4. ULKUS PEPTIKUM .

GASTRITIS .

Berdasarkan endoskopi ditemukan eritema mukosa. . Gambaran klinis yang ditemukan berupa dyspepsia atau indigesti. sedangkan hasil foto memperlihatkan iregularitas mukosa . Gastritis adalah inflamasi dari mukosa lambung.

KLASIFIKASI Gastritis akut Merupakan kelainan klinis akut yang jelas penyebabnya dengan tanda dan gejala yang khas. . sering bersifat multifaktor dengan perjalanan klinik yang bervariasi. Biasanya ditemukan sel inflamasi akut dan neutrofil. Kelainan ini berkaitan erat dengan infeksi H. pylori. Gastritis kronik Penyebabnya tidak jelas.

PATOFISIOLOGI

Terdapat gangguan keseimbangan faktor agresif
dan faktor defensive yang berperan dalam
menimbulkan lesi pada mukosa. Faktor-faktor
tersebut dapat dilihat pada tabel berikut.

Dalam keadaan normal, faktor defensif dapat
mengatasi faktor agresif sehingga tidak terjadi
kerusakan atau kelainan patologi.

aktor agresif dan protektif

Faktor Agresif Faktor Defensif
Asam lambung Mukus
Pepsin Bikarbonas mukosa
AINS Prostaglandin
mikrosirkulasi
Empedu
Infeksi virus
Infeksi bakteri : H. Pylory
Bahan korosif : asam & basa
kuat

Gastritis Akut

Lesi mukosa akut berupa erosi dan perdarahan akibat
faktor-faktor agresif atau akibat gangguan sirkulasi
akut mukosa lambung.

Etiologi
Penyebab penyakit ini, antara lain :
Obat-obatan : Aspirin, obat antiinflamasi nonsteroid
(AINS)

namun dapat juga menyeluruh. terutama ditemukan di darah antrum. luka bakar. Sedangkan secara mikroskopik. biasanya disebabkan stress. Jika disebabkan karena obat-obatan AINS. GASTRITIS AKUT Alkohol Gangguan mikrosirkulasi mukosa lambung : trauma. . Jika ditemukan pada korpus dan fundus. Secara makroskopik terdapat lesi erosi mukosa dengan lokasi berbeda. terdapat erosi dengan regenerasi epite. sepsis. dan ditemukan reaksi sel inflamasi neutrofil yang minimal.

terdapat riwayat penggunaan obat- obatan atau bahan kimia tertentu. mual. kemudian disusul dengan tanda-tanda anemia pasca perdarahan. muntah. merupakan salah satu keluhan yang sering muncul.MANIFESTASI KLINIS Sindrom dyspepsia berupa nyeri epigastrium. . kembung. Biasanya. Ditemukan pula perdarahan saluran cerna berupa hematemesis dan melena. jika dilakukan anamnesis lebih dalam.

. Secara umum peranan endoskopi saluran cerna bagian atas lebih sensitif dan spesifik untuk diagnosis kelainan akut lambung. dan gambaran radiologi. yaitu gambaran klinis.DIAGNOSIS Tiga cara dalam menegakkan diagnosis. gambaran lesi mukosa akut di mukosa lambung berupa erosi atau ulkus dangkal dengan tepi rata pada endoskopi.

KOMPLIKASI Perdarahan saluran cerna bagian atas (SCBA) berupa hematemesis dan melena. Namun pada tukak peptik penyebab utamanya adalah infeksi Helicobacter pylori. perlu dibedakan dengan tukak peptik. Diagnosis pasti dapat ditegakkan dengan endoskopi. Khusus untuk perdarahan SCBA. . sebesar 100% pada tukak duodenum dan 60-90% pada tukak lambung. Gambaran klinik yang diperlihatkan hampir sama. dapat berakhir sebagai syok hemoragik.

Diet lambung. berupa antagonis reseptor H 2. inhibitor pompa proton. dengan porsi kecil dan sering. Obat-obatan ditujukan untuk mengatur sekresi asam lambung. Juga ditujukan sebagai sitoprotektor. dan antasid.PENATALAKSANAAN Faktor utama adalah dengan menghilangkan etiologinya. antikolinergik. . berupa sukralfat dan prostaglandin.

apalagi jika ditemukan ulkus pada pemeriksaan penunjang.GASTRITIS KRONIK Jenis berhubungan dengan Helicobacter pylori. Patofisiologi Belum diketahui dengan pasti. .

. anoreksia. nausea. dan pada pemeriksaan fisik tidak dijumpai kelainan. Hanya sebagian kecil mengeluh nyeri ulu hati.MANIFESTASI KLINIS Kebanyakan pasien tidak mempunyai keuhan.

dan anemia karena gangguan absorpsi vitamin B12. perforasi. ulkus.KOMPLIKASI Perdarahan saluran cerna bagian atas. .

Perlu pula dilakukan kultur untuk membuktikan adanya infeksi Helicobacter pylori apalagi jika ditemukan ulkus baik pada lambung ataupun pada duodenum. .DIAGNOSIS Diagnosis gastritis kronik ditegakkan berdasarkan pemeriksaan endoskopi dan dilanjutkan dengan pemeriksaan histopatologi biopsy mukosa lambung. mengingat angka kejadian yang cukup tinggi yaitu hampir mencapai 100%.

GERD .

DEFINITION • Symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus Classic symptom is frequent and persistent heartburn 44 % of Americans experience heartburn at least once per month 7 % have daily symptoms .

2004) -Endoscopic "-" GERD (without esophagitis) -Endoscopic "+" GERD (with esophagitis) . CLASSIFICATION (According to unified clinical and statistical classification of diseases of the digestive system (HCD of Ukraine.

found in 37% of patients).Clinical forms of GERD • Nonerosive GERD (is defined as those who have typical reflux symptoms without evidence of erosive changes in their lower esophageal mucosa. observed in approximately 60% of patients with GERD). • Erosive GERD (erosive changes of esophageal epithelium in varying degree. .

.• Grade A . peptic esophageal ulcer. stricture. but involving less than 75% of the esophageal circumference • Grade D .mucosal breaks continuous between > 2 mucosal folds.one or more mucosal breaks < 5 mm in maximal length • Grade B .one or more mucosal breaks > 5mm. bleeding) (defined in 3% of patients).mucosal breaks involving more than 75% of esophageal circumference • Complications of GERD (Barrett's esophagus. but without continuity across mucosal folds • Grade C .

daily experience of 7 to 11% of the adult population.40-50%.Heartburn . at least 1 time per week .EPIDEMIOLOGY The main symptom (GERD) . .12% at least 1 time per month . In this pregnancy symptom is observed in 48% of women.

to allow food to enter stomach and then contracts to prevent reflux Normal to have some amount of reflux multiple times each day (transient relaxation of LES – not associated with swallowing) . on swallowing.NORMAL FUNCTION Esophagus • Transports food from mouth to stomach through peristaltic contractions Lower esophageal sphincter (LES) • Relaxes.

htm .com/intro/noframe/grossovw.http://www.gerd.

PATHOGENESIS 3 lines of defense must be impaired for GERD to develop • LES barrier impairment • Relaxation of LES • Low resting LES pressure • Increased gastric pressure • Decreased clearance of refluxed materials from esophagus • Decreased esophageal mucosal resistance .

tea Stimulate acid secretions • Garlic • Soda • Onions • Beer • Smoking • Smoking . cola.CONTRIBUTING FACTORS Directly irritate the gastric Decrease LES mucosa pressure • Tomato-based products • Coffee • Chocolate • Spicy foods • Alcohol • Citrus juices • Fatty meals • Meds: NSAIDS. iron. aspirin. alendronate • Coffee. KCl.

g. antihistamines) • Beta-adrenergic agonists • Calcium channel antagonists (nifedipine most reduction) • Diazepam • Dopamine • Meperidine • Nitrates/Other vasodilators • Estrogens/progesterones (including oral contraceptives) • Prostaglandins • Theophylline . TCA’s.CONTRIBUTING FACTORS Drugs that decrease LES pressure • Alpha-adrenergic agonists • Anti-cholinergic agents (e.

LINES OF DEFENSE Clearance of refluxed materials from esophagus • Primary peristalsis from swallowing – increases salivary flow • Secondary peristalsis from esophageal distension • Gravitational effects Esophageal mucosal resistance • Mucus production in esophagus • Bicarbonate movement from blood to mucosa .

PATHOGENESIS Amount of esophageal damage seen dependent on: • Composition of refluxed material • Which is worse: acid or alkaline refluxed material? • Volume of refluxed material • Length of contact time • Natural sensitivity of esophageal mucosa • Rate of gastric emptying .

TYPICAL SYMPTOMS Common symptoms most common when pH<4 • Heartburn • Belching and regurgitation • Hypersalivation May be episodic or nocturnal May be aggravated by meals and reclining position .

ATYPICAL SYMPTOMS • Nonallergic asthma • Chronic cough • Hoarseness • Pharyngitis • Chest pain (mimics angina) May be only symptoms – “omeprazole test” .

COMPLICATIONS • Esophagitis • Esophageal strictures and ulcers • Hemorrhage • Perforation • Aspiration • Development of Barrett’s esophagus • Precipitation of an asthma attack .

0 • Patients with GERD > 10 years – 6.) • Patients with GERD 1-5 years – 3. the > the risk of cancer .4 More frequent. and longer-lasting the symptoms of reflux.BARRETT’S ESOPHAGUS Highest prevalence in adult Caucasian males Histologic change • Lower esophageal tissue begins to resemble the epithelium in the stomach lining Predisposes to esophageal cancer (30-60x) and esophageal strictures (30-80% increased risk) Odds ratio for development (compared with GERD < 1 yr. more severe.

WARNING SIGNS If present. consider an endoscopy: • Dysphagia • Odynophagia • Bleeding • Unexplained weight loss • Choking • Chest pain .

DIAGNOSIS Clinical symptoms and history • Presenting symptoms and associated risk factors Give empiric therapy and look for improvement Endoscopy if warning signs present .

REFER Chest pain Heartburn while taking H2RAs or PPIs • Or heartburn that continues after 2 weeks of treatment Nocturnal heartburn symptoms Frequent heartburn for > 3 months GI bleeding and other warning signs Concurrent use of NSAIDS Pregnant or nursing Children < 12 years old .

THERAPY GOALS Alleviate or eliminate symptoms Diminish the frequency of recurrence and duration of esophageal reflux Promote healing – if mucosa is injured Prevent complications .

THERAPY Therapy is directed at: • Increasing LES pressure • Enhancing esophageal acid clearance • Improving gastric emptying • Protecting esophageal mucosa • Decreasing acidity of reflux • Decreasing gastric volume available to be refluxed .

TREATMENT Three phases in treatment • Phase I: Lifestyle changes – 2 weeks • Lifestyle modifications • Patient-directed therapy with OTC medications • Phase II: Pharmacologic intervention • Standard/high-dose antisecretory therapy • Phase III: Surgical intervention • Patients who fail pharmacologic treatment or have severe complications of GERD • LES positioned within the abdomen where it is under positive pressure .

TREATMENT SELECTION Mild intermittent heartburn (Phase I) • Treat with lifestyle changes plus antacids AND/OR low dose OTC H2-receptor antagonists (H2RA’s) as needed Symptomatic relief of mild to moderate GERD (Phase II) • Treat with lifestyle changes plus standard doses of H2RA’s for 6-12 weeks OR proton pump inhibitors (PPI’s) for 4-8 weeks .

TREATMENT SELECTION Healing of erosive esophagitis or treatment of moderate to severe GERD (Phase II) • Lifestyle modifications plus PPI’s for 8-16 weeks OR high dose H2RA’s for 8-12 weeks • PPI’s preferred as initial choice due to more rapid symptom relief and higher rate of healing • May also add a prokinetic/promotility agent .

nonerosive GERD • May be more expensive and use is limited by side effects .TREATMENT CONSIDERATIONS Prokinetic agents are an alternative to H2RA’s • Efficacy similar to prescription dose H2RA’s • Used as a single agent only in mild to moderate.

PPI most effective .TREATMENT CONSIDERATIONS Maintenance therapy may be needed • Large % of patients experience recurrence within 6-12 months after D’C of therapy • Goal is to control symptoms and prevent complications • May use antacids. PPIs or H2RAs • In patients with more severe symptoms.

LIFESTYLE MODIFICATIONS • Elevate the head of the bed 6-8 inches • Decrease fat intake • Smoking cessation • Avoid recumbency for at least 3 hours post- prandial • Weight loss • Limit alcohol intake • Wear loose-fitting clothing • Avoidance of aggravating foods • These changes alone may not control .

causing alkalinization • Alginic acid (in Gaviscon) forms a highly viscous solution that floats on top of the gastric contents • Dose as needed – typical action – 1-3 hours • Not best choice for nocturnal symptoms because pH suppression cannot be maintained .DRUG THERAPY - ANTACIDS Antacids with or without alginic acid • Antacids increase LES pressure and do not promote esophageal healing • Neutralize gastric acid.

and sodium bicarbonate • Dosing: Initially 40-80 mEq prn (no more than 500-600 mEq per 24 hours) • Maalox/Mylanta 30 ml prn or PC & HS • Maalox TC/Mylanta II 15 ml prn or PC & HS • Gaviscon 2 tabs PC & HS • Tums 0.DRUG THERAPY - ANTACIDS • Products: Magnesium salts.5-1 gm prn . aluminum salts. calcium carbonate.

safety profile and cost Timing • Give in divided doses for constant gastric acid suppression • May give at night if only nocturnal symptoms • Give before an activity that may result in reflux symptoms .DRUG THERAPY – H2RA’S H2RA’s Mainstay of treatment for mild to moderate GERD H2RA’s equally efficacious • Select based on pharmacokinetics.

DRUG THERAPY – H2RA’S Cimetidine Famotidine Nizatidine Ranitidine Low dose 200 mg 10 mg 75 mg 75 mg (qd to bid) Standard 400 mg 20 mg 150 mg 150 mg dose (bid) High 400 mg 40 mg bid 150 mg 150 mg dose qid or 800 qid qid mg bid .

DRUG THERAPY – H2RA’S Response to H2RA’s dependent upon: 1) Severity of disease 2) Duration of therapy 3) Dosage regimen used Tolerance to effect develops .

choose based on cost Prilosec released OTC 2003 • Use for heartburn that occurs ≥ 2 days/week • Label .DRUG THERAPY - PPI’S Proton Pump Inhibitors Used to treat moderate to severe GERD More effective and faster healing than H2RA’s • May be used to treat esophagitis refractory to H2RA’s All agents effective .Don’t use for more than 14 days .

DRUG THERAPY - PPI’S Standard dosing • Esomeprazole 20 mg qd • May 2006: FDA approved Nexium for adolescents 12-17 years for the short-term (up to 8 weeks) treatment of GERD • Lansoprazole 15-30 mg qd • Omeprazole 20 mg qd • Pantoprazole 40 mg qd • Rabeprazole 20 mg qd Timing • Best is 30 minutes prior to breakfast .

DRUG THERAPY - PPI’S May give higher doses bid for • Patients with a partial response to standard therapy • Patients with breakthrough symptoms • Patients with severe esophageal dysmotility • Patients with Barrett’s esophagus Always give second dose 30 minutes prior to evening meal .

MOA • Enhances motility of smooth muscle from esophagus through the proximal small bowel • Accelerates gastric emptying and transit of intestinal contents from duodenum to ileocecal valve .DRUG THERAPY - PROKINETICS Prokinetic Agents -.

DRUG THERAPY - PROKINETICS Prokinetic Agents • Results of therapy • Improved gastric emptying • Enhanced tone of the lower esophageal sphincter • Stimulated esophageal peristalsis (cisapride only) .

10 to 15 mg AC and HS • Adverse Effects – limit use • diarrhea • CNS . • breast tenderness .PRODUCTS Metoclopramide (Reglan) • Dopamine antagonist • Only use if motility dysfunction documented • Administer at least 30 minutes prior to meals • Dose .drowsiness.PROKINETIC AGENTS . motor restlessness. restlessness. etc. depression • extrapyramidal reactions – dystonia.

e. ventricular arrhythmias) Available only through an investigational limited access program for patients who have failed all other treatment options .PRODUCTS Cisapride Was removed from the market July 14.PROKINETIC AGENTS . 2000 due to adverse cardiovascular effects (i.

DRUG THERAPY – MUCOSAL PROTECTANTS Sucralfate • Very limited value in treatment of GERD • Comparisons • Similar healing rate to H2RA in treatment of mild esophagitis • Less effective than H2RAs in refractory esophagitis • Only use in mildest form of GERD .

thickened feedings • Postural management • H2RA’s have been used (e.SPECIAL POPULATIONS Infants can experience a form of GERD • Postmeal regurgitation or small volume vomiting • Occurs due to a poorly functioning sphincter • Treatment • Supportive therapy • Diet adjustments – smaller.g. more frequent feedings. ranitidine 2 mg/kg) and antacids .

SPECIAL POPULATIONS Pregnancy • Common. due to decreased LES pressure and increased abdominal pressure • Nearly half of all pregnant women experience • Antacids other than sodium bicarbonate generally considered safe. but avoid chronic high doses .

GERD IN THE
ELDERLY
In the US, 20% report acid reflux
Worldwide, 3X prevalence in > 70 yo of patients younger than
39 yo
More likely to develop severe disease
More likely to be poorly diagnosed or underdiagnosed
• Due to atypical symptoms
Always look for medication causes

GERD IN THE
ELDERLY
Symptoms
• Dysphagia
• Vomiting
• Weight loss
• Anemia
• Anorexia
Typical symptoms are less frequent

GERD IN THE
ELDERLY
Diagnosis should always include endoscopy
Prokinetic agents should be avoided
PPI’s are medications of choice for acute episodes and
prevention of recurrence due to efficacy, safety, and tolerability
• Step down approach is preferred – more clinically effective and
more cost effective

lansoprazole.PPIS IN THE ELDERLY Decreased clearance with omeprazole. rabeprazole Little effect on clearance with pantoprazole Dosage adjustments not necessary Pantoprazole – lower affinity for CYP450 .

COUNSELING QUESTIONS Before recommending a therapy. ask: • Duration and frequency of symptoms • Quality and timing of symptoms • Use of alcohol and tobacco • Dietary choices • Medications already tried to treat symptoms • Other disease states present and medications being used .

GASTROPATHY OAINS .

and is usually caused by long-term use of NSAIDs gastropathy NSAID. DEFINITION was symptomatic gastropathy refers to the spectrum of the upper gastrointestinal tract complications linked by the use of non-steroidal anti- inflammatory drugs with a duration of time. .

. • and bleeding where these symptoms are not found before using NSAID. ulceration . Called when there is a collection of symptoms gastropathy as varied as • dyspepsia • abdominal pain • up to fatal complications such as perforation .

70% of elderly take NSAIDs at least weekly. Over 110 million NSAID Rx filled yearly .EPIDEMIOLOGY Nearly 20. NSAID Use in the U.S.000 patients die each year as a result of serious gastrointestinal complications from NSAID use .

and alcohol consumption . pylori . . the use of some NSAIDs . the use of high doses of NSAIDs . Risk factors that may be included is an infection by H. and serious systemic disease .ETIOLOGY It is also influenced by other factors such as age . history of previous ulceration . use of anticoagulants . smoking. corticosteroid use .

Systemic effects of NSAIDs are more important that mucosal damage caused by prostaglandin production decreased significantly . Mucosal damage in tropical occur because NSAIDs are acidic and lipofili .PATOFISIOLOGY NSAIDs damage the gastric mucosa through two mechanisms: topical and systemic . . making it easier for trapping hydrogen ions enter the mucosa and cause kerusakan.

.

Prostaglandin • Regulate the release of mucosal bicarbonate and mucus • Inhibit parietal cell secretion • Important in maintaining mucosal blood flow • Epithelial cell restitution .

.

RISK FACTOR • Advanced age • History of ulcer • Concomitant use of glucocorticoids • High dose or multiple NSAIDS • Concomitant of use anticoagulants • Serious or multisystem disease • H. . pylori infection as well can trigger side effects of the NSAIDs • history of smoking and alcohol consumption .

CLINICAL MANIFESTATION • most common manifestation of dyspepsia • Heartburn • abdominal discomfort • nausea • severe symptoms such as peptic ulcer bleeding and perforation . .

• vomiting and belching . Another common complaint felt by patients is impaired in the upper digestive tract . If there has been a active bleeding can manifest hematemesis and melena . nausea . . such as • decreased appetite. • abdominal bloating and • a feeling of fullness in the abdomen .

nausea . Investigations to be performed examinations EGD ( Esofagogastroduedenoscopy ) and histopathologic examination . abdominal discomfort . abdominal bloating and a feeling of fullness in the abdomen . heartburn . investigation.DIAGNOSIS Based on history . . vomiting and belching . On history can be found gastrointestinal symptoms such as dyspepsia. and nausea decreased appetite. physical examination . On physical examination can be found tenderness in the epigastric region and can be found in the abdominal distention severe symptoms .

discontinuation of NSAIDs is not always possible due to the severity of the underlying disease . NSAIDs were discontinued as a first step ulcer therapy . However . . The use of protein pump inhibitors ( PPIs ) are associated with ulcer healing and prevent relapse in patients who used NSAIDs long term .TREATMENT Ideally . in patients given the drug inhibiting acid secretion ( H2 blockers . PPIs ) . Furthermore .

Goals of therapy -Treatment of active ulcer -Prevention of future injury .

RECOMMENDATION FOR TREATMENT OF NSAID RELATED MUCOSAL INJURY Clinical Setting Recommendation Active ulcer NSAID discontinued H2 receptor antagonist or PPI NSAID continued PPI Prophylactic therapy Misoprostol PPI Selective COX-2 inhibitor H. Pylori infection Eradication if active ulcer is present or there is a past history of peptic ulcer disease Harrison's Principles of Internal Medicine .

GUIDE TO NSAID THERAPY No/ Low NSAID GI Risk NSAID GI Risk No CV risk Traditional NSAID Coxib or Traditional (no Aspirin) NSAID + PPI Consider non-NSAID therapy CV risk Traditional NSAID + PPI if A gastroprotective (consider GI risk warrants agent must be gastroprotection added if a traditional Aspirin) Consider non-NSAID NSAID is prescribed therapy Consider non-NSAID therapy Harrison's Principles of Internal Medicine .

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PEPTIC ULCER .

Approximately 10% of the US population has evidence of a duodenal ulcer at some time. PUD affects approximately 4. (United States statistics) . Only about 10% of young persons have H pylori infection.5 million people annually. the lifetime prevalence is approximately 20%. the proportion of people with the infection increases steadily with age. Of those infected with H pylori.EPIDEMIOLOGY In the United States.

ETIOLOGY Peptic ulcer disease (PUD) may be due to any of the following: • H pylori infection • Drugs • Lifestyle factors • Severe physiologic stress • Hypersecretory states (uncommon) • Genetic factors .

The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. PATOPHYSIOLOGY Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. .

which is impermeable to acid and pepsin. . The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer. Prostaglandins of the E type (PGE) have an important protective role. which aids in buffering acid that lies near the mucosa. Other gastric and duodenal cells secrete bicarbonate. because PGE increases the production of both bicarbonate and the mucous layer.

additional mechanisms are in place to reduce injury. ion pumps in the basolateral cell membrane help to regulate intracellular pH by removing excess hydrogen ions. Mucosal blood flow removes acid that diffuses through the injured mucosa and provides bicarbonate to the surface epithelial cells. . healthy cells migrate to the site of injury. Through the process of restitution. In the event of acid and pepsin entering the epithelial cells. Within the epithelial cells.

• NSAID-induced gastritis or ulcers may be silent. especially in elderly patients. dyspnea) may be present • Sudden onset of symptoms may indicate perforation.• Symptoms consistent with anemia (eg. fatigue. • Only 20-25% of patients with symptoms suggestive of peptic ulceration are found on investigation to have a peptic ulcer .

Melena may be intermittent over several days or multiple episodes in a single day. and fatty food intolerance • Heartburn • Chest discomfort • Hematemesis or melena resulting from gastrointestinal bleeding. . • Rarely. distention. bloating.MANIFESTATIONS • Dyspepsia. including belching. a briskly bleeding ulcer can present as hematochezia.

PUD. the clinical findings are few and nonspecific and include the following: • Epigastric tenderness (usually mild) • Right upper quadrant tenderness may suggest a biliary etiology or. PHYSICAL EXAMINATION • In uncomplicated PUD. less frequently. .

• Guaiac-positive stool resulting from occult blood loss • Melena resulting from acute or subacute gastrointestinal bleeding • Succussion splash resulting from partial or complete gastric outlet obstruction .

MEDICATION Proton Pump Inhibitors • Omeprazole (Prilosec) • Lansoprazole (Prevacid) • Rabeprazole (Aciphex) • Esomeprazole (Nexium) • Pantoprazole (Protonix) .

Flagyl ER) .H2 Receptor Blockers • Cimetidine (Tagamet) • Famotidine (Pepcid) • Nizatidine (Axid) • Ranitidine (Zantac) Antimicrobials • Amoxicillin (Amoxil. Biomox. Trimox) • Clarithromycin (Biaxin) • Tetracycline (Sumycin) • Metronidazole (Flagyl.

and the appropriate use of antisecretory therapy. Most patients are treated successfully with eradication of H pylori infection. avoidance of NSAIDs. the prognosis is excellent. this is a higher recurrence rate than previously reported. However. Eradication of H pylori infection changes the natural history of the disease. with a decrease in the ulcer recurrence rate from 60-90% to approximately 10-20%. suggesting an increased number of ulcers not caused by H pylori infection. . PROGNOSIS When the underlying cause is addressed.