Learning Objectives
Pemicu 1By Stevan Pagar405090268Learning ObjectivesAnatomiHistologiFisiologiBiokimiaGangguan saluran cerna bagian atasMuntahDisfagiaGERGastritisEsofagitis Anatomy - Digestive System
HistologiPhysiology - Digestive SystemThe functions of the digestive system are:Ingestion - eating foodDigestion - breakdown of the foodAbsorption - extraction of nutrients from the foodDefecation - removal of waste products
SourceEnzimActivatorSubstratFunction or katalitik productSaliva gland@-Amilase SalivaCl-Flour essenceHidrolisis bond 1:4 @; produce dextrin @limit, maltotriosa, and maltosaLingual glandLingual lipaseTrigliseridaLipid acid plus 1,2 - diasilgliserolGasterPepsin (pepsinogen)
Gaster lipase
Hcl-Protein and polipeptida
TrigliseridaDecompose peptida chain which closer with aromatic amino acid
Lipid acid and gliserolSourceEnzimActivatorSubstratFunction and katalitik producePancreas eksocrineTripsin (tripsinogen)EnteropeptidaseProein and polipeptidaDecompose peptida bond to karboksil various amino acid basic (arginin or lisin)KemotripsinTripsinProein and polipeptida
Decompose peptida chain to karboksil aromatic acid aminoElastaseTripsinElastin other protein
Decompose karboksil amino acid alifatik chainKarboksipeptidase ATripsinProein and polipeptida
Decompose karboksil teminal acid amino chain which aromatic chain or bifurcate alifatikKarboksipeptidase BTripsinProein and polipeptida
Decompose karboksil terminal acid amino chain which alkali chainKolipaseTripsinLipid itemsTo open a part of active lipase pancreasPancreas LipaseTrigliseridaMonogiserida and fatty acidLipase Choesteril esterCholesterolEster Kolesteril hidrolaseCholesteril esterCholesterol Panckreas @-amilaseCl-Starch@-amilase salivaRibonukleaseRNANukleotidaDeoksiribonukleaseDNANukleotidaFosfolipase A2TripsinPhosfolipidFatty acid and lisophosfolipidSourceEnzimActivatorSubstratFunction and katalitik produceSmall intest mucousEnteropeptidaseTripsinogenTripsinAminopeptidasePolipeptidaDecompose to amino chain acid amino terminal from peptide KarboksipeptidasePolipeptidaDecompose to amino chain acid amino terminal from peptide
EndopeptidasePolipeptidaDecompose to residue between middle of peptideDipeptidaseDipeptida2 amino acidMaltaseMaltosa, maltotriosa, @-dekstrinGlucoseSourceEnzimActivatorSubstratFunction and katalitik produceSmall intest mucousLaktaseLaktosaGalaktosa and glucoseSukrase*Sukosa; maltotriosa and maltosaFruktosa and glucose@-Dekstrinase*@-dekstrin, maltosa, maltotriosaGlucoseThrehalaseTrehalosaGlucoseNuklease and other enzimsNukleat acidPentosa,purin and pirimidin Cytoplasma cell mucousVarious peptidaseDi,tri, and tetrapeptidaAmino acidOrgan
HormonSasaranFungsiStomachGastrinExocrine glands and smooth muscleMotility control, support absorption and digestion process
DuodenumSekretin, kolesistokinin, gastric inhibitor, peptideDigestive tract, pancreas, liver, vesica veleaMotility control, support absorption and digestion process
LiverSomatomedinBones, Soft TissuesGrowth triggerPancreas; langerhans island-Insulin (B cell)
-Glukagon (sel A)
-Somastatine (sel D)
Almost all cell
Almost all cell
Digestive system Pancreatic cell; langerhans islandSupporting absorption, using and saving nutrients by cell for maintain nutrient level after absorption phaseInhibit digestion and absorption
Inhibit all pancreatic hormones secretionBiokimia Dysphagia Dysphagia iscommon symptom thats usually easy to localize.It may be constant or intermittent and is classified by the phase of swallowing it affects. Among the factors that interfere with swallowing are severe pain, obstruction, abnormal peristalsis, impaired gag reflex, and excessive, scanty, or thick oral secretions.Dysphagia is the most commonand sometimes the onlysymptom of esophageal disorders.However, it may also result from oropharyngeal, respiratory, neurologic, and collagen disorders or from the effects of toxins and treatments Dysphagia increases the risk of choking and aspiration and may lead to malnutrition and dehydration.
epidDiseases of the esophagus are among the top 50 reasons that patients seek medical care in frequency, rank alongside problems such as pneumonia, bronchitis and otitis media.Conditions that cause dysphagia can produce esophageal rupture, nutritional deficits and aspiration pneumonia.Elderly patients are at the highest risk of dysphagia and its subsequent complications, especially silent aspiration.Sign of dysphagiaYou swallow repeatedlyYou cough and splutter frequentlyYour voice is unusually husky and you often need to clear your throatWhen you try to eat you dribble. Food and saliva escape from your mouth or even your noseYou find it easier to eat slowlyYou quite often keep old food in your mouth, particularly when you have not had a chance to get rid of it unseenYou feel tired and lose weight
Medical causesAchalasiaAirway obstructionAmyotrophic lateral sclerosisBotulismBulbar paralysisDysphagia lusoriaEsophageal cancerEsophagitisHypocalcemiaLaryngeal cancer (extrinsic)Laryngeal nerve damagePharyngitis (chronic)Plummer-Vinson syndromeScleroderma (progressive systemic sclerosis)Tetanus
Esophageal compression (external)Esophageal diverticulumEsophageal leiomyomaEsophageal obstruction by foreign bodyEsophageal spasmEsophageal strictureGastric carcinomaLower esophageal ringMediastinitisMyasthenia gravisOral cavity tumorParkinsons diseaseRabiesSyphilisSystemic lupus erythematosus
Other causesLead poisoningProcedures: A recent tracheostomy or repeated or prolonged intubation may cause temporary dysphagia.Radiation therapy: When use to treat oral cancerSpecial considerations
Treatment Surgery/switching medical prescriptionPhysical modificationSwallow modificationFood modification
Differential diagnosisOropharyngeal dysphagiaEsophageal dysphagiaNeuromuscular diseaseDiseases of the central nervous system Cerebrovascular accident Parkinson's disease Brain stem tumors Degenerative diseases Amyotrophic lateral sclerosis Multiple sclerosisHuntington's diseasePostinfectious Poliomyelitis Syphilis Peripheral nervous system Peripheral neuropathy Motor end-plate dysfunction Myasthenia gravis Skeletal muscle disease (myopathies) Polymyositis Dermatomyositis Muscular dystrophy (myotonic dystrophy, oculopharyngeal dystrophy)Cricopharyngeal (upper esophageal sphincter), achalasiaObstructive lesionsTumorsInflammatory massesTrauma/surgical resectionZenker's diverticulumEsophageal websExtrinsic structural lesionsAnterior mediastinal massesCervical spondylosisNeuromuscular disorders Achalasia Spastic motor disorders Diffuse esophageal spasm Hypertensive lower esophageal sphincter Nutcracker esophagus Scleroderma Obstructive lesions Intrinsic structural lesions Tumors Strictures Peptic Radiation-induced Chemical-induced Medication-induced Lower esophageal rings (Schatzki's ring) Esophageal webs Foreign bodies Extrinsic structural lesions Vascular compression Enlarged aorta or left atrium Aberrant vessels Mediastinal masses Lymphadenopathy Substernal thyroidregurgitationDefinitionEffortless movement of stomach into the oesophagus and mouth.In distal oesophageal obstrucion and stasis, as in achalasia or the presence of a large diverticulum.The material consist of tasteless mucoid fluid or undigested foodRegurgitation may occur in children who are normal and do nothave complications of gastroesophangeal reflux (GER), such asnutritional deficits, oesophangitis, blood loss, strictures, apneaor airway manifestationepidemiologyRegurgitation, or spitting up has been reported in up to two thirds (65%) of healthy infants,but decreases to 1% by one year of age.Babies with GER regurgitate without secondary signs or symptoms of inadequate weight gain, esophagitis, or respiratory disease.pathophysiologyAvalve between the esophagus and the stomach helps prevent food from coming back up and out of the stomach. In infants, this valve is not well developed and can more easily allow food to go back up the feeding tube and cause spitting up. Because the infants stomach is small, feeding too much or swallowing too much air can help push food past the valve. As the infant grows and the valve develops, food is less likely to pass this valve and travel up the esophagus. Also, as the infant begins to take solid foods, the spitting up usually decreases.Regurgitation overviewSpitting up is very common among normal infants. About 40% of infantsspit up on a regular basis, and almost all infantsspit up at least once in a while.Spitting upusually occurs right after feeding or burping. The spit up fluid may look just like the formula or milk that was just fed or may appear slightly curdled. The amount of fluid spit up is usually just a small portion of the feeding, but it often appears to be much more.The infantseems otherwisewell anddoes not seem hungry until the next feeding.
When to seek doctorIf baby show sign of dehydrationIf weight loss is a concernIf the spitting up is forceful and shoots out of the mouthIf other worrisome signs of illness appear, includingfever,diarrhea, difficulty breathing, or abnormal fussiness
Exam and testsUsually the physician can diagnose normal spitting upbased on adetailed history and physical examination.X-raysor blood tests are required only in rare cases to exclude other more serious causes of the spitting upMinimize regurgitationBurp the infant frequently (after every 1-2 ounces) to prevent the build-up of air in the stomach.Feed slower to allow the stomach contents more time to empty into the intestines.Be careful not to feed too much at a time and to stop feeding when the infant seems full.Keep the infant upright after feeding for at least 15 minutes. This allows gravity to help prevent the stomach contents from coming up.
Minimize regurgitationHandle baby gently and burp often.Try to keep baby in an upright position during and after feedings. Nurse frequently. Smaller, more frequent feedings are easier to digest.Try offering only one breast per feedingIf your baby wants to nurse constantly, and seems to spit up after every feeding, try offering a pacifier.After feedings, try holding baby upright for a half hour or let baby lie upright on your chestTry to identify foods or vitamins in the mother or baby's diet that might be causing a reaction. Avoid foods that exacerbate refluxThere is also ahomeopathic medicinecalled ColicCalm that is very promising in controlling reflux and the accompanying discomfort.vomitingDefinition Forcefull constraction of the stomach that propels its contents up the esophagus and out through the mouthOr oodinate motor response of Gitract, abdominal an thoracic muscles that results in forceful expulsion of stomatch contentsfew tips to help an infant who vomit:Avoid overfeeding.Smaller and frequent feedings will empty the stomach faster.Minimize intake of air during feeding.If the bottle is too low, the baby can swallow air, causing gas and crying.Don't jiggle the baby during and after feeding.Too much movement may cause reflux.Sit her in an upright position after feeding.Sitting and lying on the back makes reflux worse. Hold the baby in your arms as much as you can.Elevate the crib at a 30-degree angle.I suggest using a book under the legs at the head of the crib. Do not use pillows since this can cause suffocation.With your pediatrician's approval, put a baby with severe GERD to sleep on her tummy.
GERDefinitionJust a symptom not a diseaseThe effortless retrograde movement of gastric contents upward into the oesophagus or oropharynxoccurs when the lower esophageal sphincter (LES) opens spontaneously, for varying periods of time, or does not close properly and stomach contents rise up into the esophagusPathophysiology Normally, when an infant feeds, swallowing pushes the milk back into their throat and down into their esophagus. At the bottom of the esophagus there is a muscle that opens to let nourishment pass into the stomach. The muscle then closes when the stomach squeezes to push the food into the small intestine. In children with gastroesophageal reflux, this muscle opens as the stomach squeezes, so food and stomach acid come up their esophagus and out of their mouth. Other times, the acid and food may only come part way up, causing the infant to have abdominal pain or gas similar to when an adult experiences heartburn.Infants with gastroesophageal reflux are good eaters. Many of them are "guzzlers" and can not be put off when hungry, finishing their milk very quicklyIn most cases, gastroesophageal reflux is self-limiting, which means the problem will resolve itself by the time the infant is able to sit up (around six months).Even if the child does not develop problems from their reflux, the condition can sometimes be difficult to care for and stressful on the family.
epidThe prevalence of GER peaks between 1 to 4 months of age, and usually resolves by 6 to 12 months.babies usually outgrow GER by their first birthday, reflux that continues past 1 year of age may be GERDComplication Failure to thriveOesophangitisPulmonary aspirationGERDDefinition A condition in which the liquid content of the stomatch regurgitates(backs up or refluxes) into tje oesophagus.The liquid can inflame and damage the lining of th esophagus although visible signs of inflamation occur in a minitory of patients
epidStudies show GERD is common and may be overlooked in infants and children
GERD symptomburning-type pain in the lower part of the mid-chest, behind the breast bone, and in the mid-abdomen.Most children under 12 years with GERD, and some adults, have GERD without heartburn.Instead, they may experience a dry cough, asthma symptoms, or trouble swallowing.treateningMedication Antacids,such as Alka-Seltzer, Maalox, Mylanta, Rolaids, and Riopan, are usually the first drugs recommended to relieve heartburn and other mild GERD symptomsCalcium carbonate antacids, such as Tums, Titralac, and Alka-2, can also be a supplemental source of calciumFoaming agents,such as Gaviscon (to prevent reflux)H2 blockers,such as cimetidine (Tagamet HB), famotidine (Pepcid AC), nizatidine (Axid AR), and ranitidine (Zantac 75), decrease acid production, provide short-term relief and are effective for about half of those who have GERD symptoms.Proton pump inhibitorsinclude omeprazole (Prilosec, Zegerid), lansoprazole (Prevacid), pantoprazole (Protonix), rabeprazole (Aciphex), and esomeprazole (Nexium). Effective than H2 blockerProkineticshelp strengthen the LES and make the stomach empty faster. Such as bethanechol (Urecholine) and metoclopramide (Reglan). Metoclopramide also improves muscle action in the digestive tract
Diagnostic Barium swallow radiographuses x rays to help spot abnormalities such as a hiatal hernia and other structural or anatomical problems of the esophagusUpper endoscopyThe doctor also may perform a biopsy. Tiny tweezers, called forceps, are passed through the endoscope and allow the doctor to remove small pieces of tissue from your esophaguspH monitoring examination
Treatment SurgeryFundoplicationis the standard surgical treatment for GERD. Usually a specific type of this procedure, called Nissen fundoplication, is performed.Endoscopic techniquesused to treat chronic heartburn include the Bard EndoCinch system, NDO Plicator, and the Stretta system. These techniques require the use of an endoscope to perform the anti-reflux operationComplication Baretts esophagus ( metaplastic collumnar epithelial replaces the normal esophangeal squamous epithelial)Gastritis Definition: inflammation of the gastric mucosaAcute GastritisChronic Gastritis
Acute GastritisAcute gastritis is a term covering a broad spectrum of entities that induce inflammatory changes in the gastric mucosa. Acute gastritis can be broken down into 2 categories:erosive (e.g, superficial erosions, deep erosions, hemorrhagic erosions)non-erosive (generally caused by Helicobacter pylori)Symptoms include nausea, vomiting, loss of appetite, belching, and bloating. Occasionally, acute abdominal pain can be a presenting symptom.52One or more of the following influences are thought to be operative in these varied settings:Disruption of the adherent mucous layerStimulation of acid secretion with hydrogen ion back diffusion into the superficial epitheliumDecreased production of bicarbonate buffer by superficial epithelial cellsReduced mucosal blood flowDirect damage to the epithelium53Satu atau lebih dari pengaruh berikut dianggap beroperasi dalam pengaturan bervariasi ini: Gangguan dari lapisan mukosa pemeluk Stimulasi sekresi asam dengan difusi kembali ion hidrogen ke epitel dangkal Penurunan produksi penyangga bikarbonat oleh sel epitel superfisial Mengurangi aliran darah mukosa Langsung kerusakan pada epitel Risk FactorsAcute gastritis is frequently associated with:Heavy use NSAID, particularly aspirinExcessive alcohol consumptionHeavy smokingTreatment with cancer chemotherapeutic drugsSystemic infections (eg. Salmonellosis)Severe stress (eg. Trauma, burns, surgery)Ischemia and shockSuicide attempts with acids and alkaliMechanical trauma (eg. Nasogastric intubation)Reflux of bilious material after distal gastrectomySign and SymptomsAcute gastritis may be entirely asymptomaticEpigastric painNausea VomitingHematemesisMelenaPotentially fatal blood loss25% of persons who take daily aspirin for rheumatoid arthritis develop acute gastritis at some time in their course, many with occult or overt bleedingThe risk of gastric bleeding from NSAID induced gastritis is dose related, thus increasing the likelihood of this complication in persons requiring longterm use of such drugsChronic GastritisDefinition: the presence of chronic inflammatory changes in the mucosa leading eventually to mucosal atrophy and epithelial metaplasiaMost individuals with the infection also have the associated gastritis but are asymptomaticEpidemiology: american adults older than age 50 show prevalence rates approaching 50%. In areas where the infection is endemic, it seems to be acquired in childhood and persists for decades
Pathophisiology Most important etiologic association is chronic infection by the bacillus H. pyloriGastritis develops as a result of the combined influence of bacterial enzymes and toxins and release of noxious chemicals by the recruited neutrophilsCharacterized by mononuclear cell infiltration in the lamina propia with intestinal metaplasia and frequently proliferation of lymphoid tissue
58Gastritis berkembang sebagai akibat dari pengaruh gabungan enzim bakteri dan racun dan pelepasan bahan kimia berbahaya oleh neutrofil direkrut After initial exposure to H. pylori, gastritis may develop in 2 patterns:An antral-type with high acid production and higher risk for the development of duodenal ulcerA pangastritis with multifocal mucosal atrophy, with low acid secretion and increased risk for adenocarcinomaSign and SymptomsUsually causes few or no symptomsUpper abdominal discomfortNauseaVomiting Most important is the relationship of chronic gastritis to the development of peptic ulcer and gastric carcinomaMost individuals with a peptic ulcers, whether duodenal or gastric, have H. pylori infection
