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O cc: pain at upper tummy for 14 hours localized, sharp,continous pain and ↑ in severity HT vomit several times abdomen distended still have bowel movement no history of abnormal micturation ,defecation, normal appetite,constant weight gain, no problem of swallowing deny any fever before pain episodic epigastric pain (2 mon ago)esp came after had a heavy mealnot relieved after meal and taking some medication took piroxicam for knee pain (3 mon ago) ↓ seen Dr for several times and was advised to take stomach pills including antacids and ranitidine ↓no improvement undergo barium meal x-ray exam and esophagogastro-duodenoscopy[1 mon ago] histopatho result:+ve H.pylori got duodenal ulcer ↓ PE still conscious pale, get perspirated BP 100/60Normal tachycardia and tachypnea high fever [38.60] heart, lung exm :normal Abdomen: distended but still symmetry perilstatic scarce, nearly normal no vascular murmur diffuse tenderness in upper abdomen liver dullnesss present with varying tympany palpation: muscular rigidity, rebound tenderness Digital Rectal exm weak sphincter tone intact mucosal layer oxygen mask and IV line was establish to the pt urinary catheter inserted, and hoursly production observed LAB Hb ↓ , Ht ↓= anemia WBC ↑ = leukocytosis amylase, ureum , creatinine ↑ Lipase : normal IMAGING abdominal x-ray: supine position↑ bowel gas distribution, with dilatation small bowel erect position: no air-fluid level appearance, dubious free gas chest x-ray: Subphrenic air +ve
diagnosis – diffuse peritonitis due to suspected perforated peptic ulcer **decide to perform acute laparotomy after administration of fluid resuscitation histopatho finding: no sign of malignant ulcer and prophylactic antibiotics to pt +ve H.pylori LAPAROTOMY treatment peritoneal fluid with gastric content apprx 500 cc --amoxicilin , clarithromycin, st perforated ulcerat anterior wall of 1 part of duodenum [approx 1 cm distal omeprazole [for 2 wks] to the pyloric region] Omentum covers the perforated region and adhesions is easy to release TREATMENT Surgical treatmentsuturing the perforation with omental patch ulcer is biopsied hospitalization for 1 week Omeprazole, Sucralfate ↓ laparotomy wound heal well and condition pt improved
prognosis: GOOD 7th postoperative daydischarged
CC: pain at upper tummy/epigastric pain ↓ organ probably involved 1. esophagus esophagitis, GERDno problem swallowing
Abdomen portion of trunk[between thorax and pelvic] start from diaphragm and extend until pelvic inlet division4 quadrants, 9 regions
2. 3. 4. 5.
heart and its pericardiuminf. MIHeart Normal on PE liverliver normal on PE and liver enzyme also Normal pancreaspancreatitislipase Normal Great vessels [aneurysm of aorta]no masses with pulsation or vascular murmur on PE stomach
R hypochrondri ac R lumbar R inguinal
L hypochondri ac L lumbar
DUODENUM anatomy 1st part and the shortest part of small intestine, C-shaped structure 12 fingers length=25 cm starting from pyloric sphincterduodenojejunal flexure at sharp bend hv 4 part : superiordescendinginferior/horizontalascending major and minor papilla ↓ receive pancreatic secretion and bile from liver blood supply : celiac trunk , SMA Histology----same as other GIT Mucosa Epithelium [simple columnar].contain
Hypogastri L inguinal c covered by peritoneum [more specific description of position of organ in abdomen] thin, transparent membrane [histologically composed of mesothelium] consist of 2 layer [similar to pericardium , pleural membrane]
intraperitoneal =stomach, spleen, liver, gallbladder Extraperitoneal = pancreas,kidney, duodenum,IVC, aorta
PARIETAL P Line the internal surface of abd. wall Its BV, LD, nerves continuous with those in abd. wall Innervated by somatic nerve[spinal nerve] Sharp, severe, persistent and well localized pain
VISCERAL P. Line the internal surface of abd. viscera Its BV, LD, nerves continuous with those in abd. viscera Innervated by autonomic nerve[sympathetic and parasympathetic nerve] Dull, crampy, poorly localized pain
Submucosa Duodenal/brunner’s glands serosa alkaline mucus STOMACH Goblet cellsmucus 1. BV 2. absorptive cells Anatomy 3. intestinal glands J-shaped structure, mobile Lymphatic nodules 4. obliquely in left portion ofnerves peneath lie abdomen [left hypochondriac, epigastric, cellslysozyme, umbilical] phospholipase; bacterial protection btwn esophagus and duodenum[ gastroesophageal pyloric sphincter] LP anterior : diaphragm, left lobe liver, anterior abd wall Muscularis mucosa posterior : omental bursa hv 2 curvature Physiology 1. lesser C= constitute its R and superior margin food digestion and absorption 2. Greater C=constitue its L and inferior margin cells villi, microvilli, brush border enzyme, absorptive hvfat being emulsified by bile into smaller unit 4 regions pancreatic enzymechemical digestion of CHO, protein and fat 1. cardiacsmall area inside cardiac orifice neutralize stomach acidalkaline bile and pancreatic secretion 2. fundusdilated superior portion of stomach, its superior part at level 5th ICS
peritoneal cavity no organ, sterile area contain peritoneal fluid50ml, composed of water, electrolyte and other substance that derived from intestitial fluids in adjacent tissue also contain ABfight against infection
bodymajor part 4. pyloric antrum canal : narrower, thick ring of SM there create pyloric sphincterregulate passage of stomach chyme into duodenum
Abdominal pain Parietal pain arise from parietal peritoneum pain is more localized, intense, severe, sharp and persistent somatic innervtn[spinal nerve]
Visceral pain arise from visceral peritoneum pain poorly localized, dull , crampy, involved sweating and nausea autonomic innervtn [parasymphttc n symphttc]
Referred pain visceral pain felt at some distance from affected organ due to they share a central afferent pathway with affected organ
Mucosa Epithelium =simple columnar invaginate into LPform pitreceive secretion from tubular glands cardiac glands pyloric glands 3. gastric glandskt fundus and body ↓ Collectively they hv several cells type Parietal cell mostly in upper part of gastric glands, few in pyloric glands secrete HCl and intrinsic factor Chief cells most numerous cellin lower half of gastric glands secrete rennin and lipase during infancy, enteroendocri ne cell pepsinosinogen throughout life most in lower end of glands found throughout stomach type G cellssecrete hormone gastrinstimulate parietal and chief cell secretion D cellssomatostatininhibit release of other hormone icl, gastrin Mucous cell located in upper part of cardiac and pyloric glands fx: secrete mucusprotective barrier Stem cells submucos a Musculari s external found at base of glands divide rapidly for replacing cell dies BV, nerve, lymphoid cells 1. 2.
Smooth muscle fibers arranged in 3 direction
longitudinaloutercontain pacemaker cells [greater curvature of pyloric regionsecrete mainly mucus cardiac, fundus region] thin
1. 2. 3.
fundus ,bodysecrete mainly acid and enzyme
Physiology of stomach
4 aspectsfilling, storage, mixing and emptying presence of pacemaker cells in longitudinal muscle in greater curvature in region of fundusgenerate APperilstatic contraction
From fundus[ muscle thin, weak]weak perilstatic contractionnot enough to mix food with gastric def : CHRONIC, most often solitary lesions, that occur in any portion of GIt that exposed to aggressive action of peptic juice juice until pyloric [muscle stronger, thick]string and powerful perilstatic contractionenable mixing with gastric juice, later on empyting st most common 1 portion of duodenum, stomach[usually antrum] foodmouthesophagusstomach etiology NSAID use, H.pylori infection [most common], also can be cause by alcohol, ↑ caffeine intake
↓ Filling Storage Mixing Emptying mech: it will cause imbalance btwn damaging forces and protective forces [damaging forces ↑ ] Stomach stretch, ruggae In body In antrum Usually after 3-4 hoursdepends on type of foods and volume flattento accommodate food [periltatic contraction too weak to Controlled by hormonal [eg gastrin], nervous [eg vagus nerve] Damaging forces Protective forces [in stomach] can hold food up to 4 L mix food with gastric juice ↑ acid secretion Mucous coatthick, highly alkaline [presence of Secretion Regulation bicarbonate] mucus resist the action of acid and enzyme Cephalic phase [20%] Gastric phase [70%] Intestinal phase ↑ enzyme secretion Rapid Epithelial cell replacementlie only food reaches stomach Vagus nerve stimulate gastric secretion Ingested for 3-6 duodenum initially enhance eventhoughdays then slough off and replace by new cells before food is swallowedin gastric secretion, but soon it response to Presence of tight jx btwn epithelial cellsprevent sight, smell, though of food will inhibit it ↑ pH of stretching of stomach stomach gastric juice from leakage inside ↓ ↓ ↓ Send inhibitory signal by way enteric Sight, smell, taste, though of food Gastric ulcer Duodenal ulcerwill activate both short and long reflex stimulate ECL G nervous system and send signals to ↓ Send these sensory and mental signal to more common release ↓ medulla that cell to than GU EPIDEMIO 4 times stimulate gastric secretion through medulla oblongata 1. inhibit vagus nuclei gastrin elaboration of 3 chemicals AGE ONSET Older population [50-70y.o] 20-50 y.o ↓ 2. stimulate symphatetic ↓ 1. ACH PAIN Intermittent epigastric pain Parasympathetetic AP carried by vagus neuron stimulate chief 2. histamine PATTERN nerve to stimulate postganglionic cell3. min-2 hours and parietal gastrin Pain occur immediately after stomach Pain occur after 30 neurons in enteric plexus in **the chyme also stimulate cells ↓ eating after eating [when food pass ↓ duodenum ECL to secrete secretin, 3 of them hv receptor Stimulate secretion from chief duodenum] cells, CCK, gastric inhibitory peptide Pain-antacid-relief patternECL cells parietal cells and also Pain-antacid-relief pattern on parietal ↓ Food-pain pattern Pain-food-relief pattern cellstimulate them to Suppress gastric secretion and Nocturnal pain common secrete HCl n intrinsic motility factor H.PYLORI May be present [60-80%] Often present[95%-100%] Cause more anorexia, Ach, gastrinstimulate omitting and weight loss function HCL gastric juice [2-3 L/day] 1. bactericidal as pH low as 0.8 1. HCL produce by parietal cells[posses carbonic anyhydrase] 2. convert ingested ferric ionsferrous ions [absorbable CO2 + H2O CAH > H2CO3 HCO3 + H+ form] 3. activate enzyme pepsin
breakdown plant and
mucus protective barrier endocrine and paracrine regulatory factorsgastrin, somatostatin, histamine, etc Digestion CHOcontinue in body of stomach due to presence of salivary amylase Proteinby pepsin , in antrum ↓ Digestion continue in small intestine no nutrient absorption here
enzyme pepsinsecrete by chief cellspepsinogen[inactive form]HCL will remove some of it’s a.aconvert into pepsin[activated form water intrinsic factorssecrete by parietal cellsit will bind avidly to vit B12enable intestinal cells to absorp this compleximportant for Hb synthesis
Ulcer defined histologically as breach of mucosa of GIT that extend thru muscularis mucosa into submucosa or deeper ↓ significant bleeding, scarring and perforation
Erosion small, superficial mucosal lesion [<5mm in diameter] ↓ Juz mild bleeding [superficial mucosa only contain capillary]
H.PYLORI spiral,Gram –ve bacteria, have multiple fragella at 1 pole optimal pH to grow= pH 6-7 [kat epithelial side of stomach] considered as normal flora in human gastric80% of pt hvg this bacteria remain asymptomatic but may associated with occurrence of peptic disease and gastritis colonization factors hv fragellahighly motile and move quickly from stomach lumen mucus layer and lastly lies on the epithelial side of mucus layer [pH suitable for its growth] 2. produce ureasewill split urea into CO2 and HCO3- buffer acid from kill them 3. adherence factor towards gastric epithelium protect and prevent them from being shed during epithelial shedding diagnosis
termittent epigastric pain, which esp occur after had heavy meal
↑ acid secretion to digest large fooddat y pain at ulcer site PERITONITIS= inflammation/infection of peritoneum d after meal, taking some medication type f RF: use of piroxicam to relieve knee pain 1. primary/spontaneous P due to underlying dsz [usually due to chronic liver dsz] we confirm barium meal x-ray exam and endoscopy : show duodenal ulcer,; histopatho result found H.pylori 2. secondary Pspillage of stomach, intestinal content, appendix content into peritoneal cavity due to perforation or ruptureinitiate inflammation and infection to peritoneum
tertiary Pdvlp in those who undergoing CAPD [continous ambulatory peritoneal dialysis]
diagnosis [20 peritonitis] peptic ulcer + H.pylori present most effective treatment combination of 1 PPI + 2 antibiotics case : omeprazole,1. SSpain increasing once infection spread to peritoneal cavity, continuously, tenderness, fever, hypotension [bleeding], vomit clarithromycin, amoxicillin 2. in absence of H.pylori longabdominal exam: abdominal distended, muscle guarding. muscle rigidity, rebound tenderness term higher doses of PPI
Digital rectal exam : weak sphincter tone,filled ampulla [weak contraction for defecation],tenderness upon upward thrust Lab : leukocytosis [sign infection], anemia [bleeding], amylase , ureum , creatinine ↑
5. confirm the diagnosis abdominal X-ray: ↑ bowel gas distribution with dilation of small bowel complications chest x-ray subphrenic air +ve GI bleeding[melena, hematemesis], obstruction[scarring and swelling due to ulcer cause narrowing in duodenum and gastric outlet perforationspillage it content into abd.cavity peritonitis, pancreatitis
[indicate that organ are torn/perforate]
treatment 1. fluid resuscitation antibiotic administrationto prevent bacteremiaamoxicilin, clarithromycin laparotomy/surgical debridement
laparotomy • peritoneal fluid with gastric content apprx 500 cc • perforated ulcerat anterior wall of 1st part of duodenum [approx 1 cm distal to the pyloric region] • Omentum covers the perforated region and adhesions is easy to release • histo : H.pylori +ve Drugs in this case MOA Piroxicam =NSAID inhibit synthesis of prostaglandin via blockage of COX enzymeanalgesic effect!! [take for knee pain] SE=renal toxicity, GI ulcer, bleeding, Antacids =weak base [given for epigastric pain] SE=gastric distnsion,blenching, diarrhea[MgOH], constipation [ALOH] Ranitidine =H2 receptor antagonist SE= heache, myalgia, diarrhea, fatigue Omeprazole =Proton pump inhibitor SE= Exteremely safediarrhea, headche Sucralfate= Mucosa protective agent SE=heache, flatus, dry mouth Amoxicillin = beta lactam antibiotic SE=allergic, nausea, vomit Clarithromycin = antibiotic, macrolides SE=muscle pain, dizziness, headache , GI upest
will react with gastric acidform water and saltreduce intragastric acidity also posses mucosal protective action by stimulate production of prostaglandin
competitive inhibition at parietal cell H2 receptorHistamine from ECL cells can’t bind to H2 receptor ↓ diminish acid secretion ← decreased intracellular [ ] of cAMP Inhibit proton pumpSuppress secretion H+ ions into gastric lumenInhibit gastric acid secretion 1. -ve charge sucrose sulfate bind to +ve ly charged protein in the base of ulcer or erosion ↓ Form physical barrier/coat that prevent further damage
2. also binds to epithelial growth factorenhance tissue repair** Inhibit cell wall synthesis of bacteria
Bind to 50S bacterial ribosomeInhibit protein synthesis of bacteria ****important role of prostaglandin stimulate secretion of protective mucus and acid-neutralizing bicarbonate**** case : piroxicam[NSAID] ↓inhibit COX-2 suppress synthesis prostaglandin ↓ no protective mucous coat ↓bicarbonate secretion to buffer H+ will result in ↑HCL formation in lumen↑HCL will promote conversion of inactive pepsinogen to active pepsin + case :H.pylori infection, acid resistant bacteria ↓ invade mucosa of stomach and duodenumopen way for gastric juice to damage the tissue secrete urease split urea into CO2 and ammoniaammonia will increase lumen pH↑ acid secretion [physiology adaptation] release cytokines, lipopolysaccharides, heat shock protein,vacuolating cytotoxin [VacA]mediate inflammatory cascadefurther tissue injury has adherence factors that enable H.pylori to bind specifically to gastrictype epitheliumprotect and prevent them from being shed during epithelial shedding
has adherence factors that enable H.pylori to bind specifically to gastric-type epithelium ↓ protect and prevent them from being shed during epithelial shedding
BHP 4 ethical principle -beneficence -Non maleficence -autonomy -justice
CHOP Prevention primary: avoid risk factor secondary : early diagnosis n prompt treatment tertiary:prevent from getting worse
CRP Epidemiology Case study : prevalence of peptic ulcer cases among teenagers in jatinangor
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