Mr.Amir, 66 y.O cc: pain at upper tummy for 14 hours localized, sharp,continous pain and ↑ in
HT
PE 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 epigastric pain (2 mon ago) esp came after had a heavy meal not relieved after meal and taking some medication took piroxicam for knee pain (3 mon ago 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 ↓
still conscious pale, get perspirated BP 100/60 Normal 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
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
diagnosis – diffuse diffuse periton peritonitis itis due due to suspe suspected cted perfor perforated ated peptic peptic ulcer 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 --amoxicilin , clarithromycin, perforated ulcerat anterior wall of 1st part of duodenum [approx 1 cm distal omeprazole [for 2 wks] to the pyloric region] Omentum Omentum covers covers the the erforated erforated re ion and adhesions adhesions is eas to release release
TREATMENT Surgical treatment treatmentsuturing the perforation with omental patch ulcer is biopsied hospitalization for 1 week Omeprazole, Sucralfate ↓ laparotomy wound heal well
prognosis: GOOD 7th postoperative
CC: pain at upper tummy/epigastric pain ↓ organ probably involved
1. 2. 3. 4. 5.
Abdomen portion of trunk[between thorax and pelvic] start from diaphragm and extend until pelvic inlet
esophagus esophagitis, GERD no problem swallowing
division4 quadrants, 9 regions
heart and its pericardium inf. MIHeart Normal on PE
liver liver normal on PE and liver enzyme also Normal pancreas pancreatitislipase Normal
R hypochrondri ac R lumbar
Great vessels [aneurysm of aorta]no masses with pulsation or vascular murmur on PE
RUQ
LUQ
RLQ
LLQ
epigastric umbilical
L hypochondri ac L lumbar
R inguinal
DUODENUM anatomy 1st part and the shortest part of small intestine, C-shaped structure
Hypogastri L inguinal c covered by peritoneum [more specific description of position of organ in abdomen] thin, transparent membrane [histologically composed of mesothelium] [histologically consist of 2 layer [similar to pericardium , pleural membrane]
12 fingers length=25 cm starting from pyloric sphincterduodenojejunal flexure at sharp bend hv 4 part : superior descendinginferior/horizontalascending
major and minor papilla ↓
receive pancreatic pancreatic secretion and bile from liver blood supply : celiac trunk , SMA
muscularis external
Histology----same as other GIT Histology----same Mucosa Epithelium [simple columnar].contain
Submucosa Sub mucosa Duodenal/brunner’s glands serosa alkaline mucus STOMACH 1. Goblet cellsmucus BV abso sorp rpti tive ve ce cell lls s Anatomy2. ab 3. in inte test stin inal al gl glan ands ds J-shaped structure, mobile Lymphatic nodules nerves 4. peneath lie obliquely in left portion of abdomen [left hypochondriac, epigastric, cells lysozyme, umbilical] phospholipase; bacterial protection btwn esophagus and duodenum[ gastroesophageal pyloric sphincter] LP anterior : diaphragm, left lobe liver, anterior abd wall Muscularis mucosa
intraperitoneal =stomach, spleen, liver, gallbladder Extraperitoneal = pancreas,kidney, duodenum,IVC, aorta
PARIETAL P Line the internal surface of abd. wall
VISCERAL P. Line the internal surface of abd. viscera
Its BV, LD, nerves continuous with those in abd. wall Innervated by somatic nerve[spinal nerve]
Its BV, LD, nerves continuous with those in abd. viscera
Sharp, severe, persistent and well localized pain
Innervated by autonomic nerve[sympathetic and parasympathetic nerve] Dull, crampy, poorly localized pain
peritoneal cavity no organ, sterile area contain peritoneal fluid 50ml, composed of water, electrolyte electroly te and other substance that derived from intestitial fluids in adjacent tissue also contain AB fight against infection
posterior : omental bursa hv 2 curvature Physiology lesser less er C= const constitute its R and superi superior or margin margin digestion anditute absorption 1.food 2. villi, Greater Grea ter C=con C=constit stitue ueborder its L and its an d inferior inferior margin margi n cells microvilli, brush enzyme, absorptive hv 4fat regions being emulsified by bile into smaller unit pancreatic enzymechemical digestion of CHO, protein and fat 1. cardiac small area inside cardiac orifice neutralize stomach acidalkaline bile and pancreatic secretion 2. fundus dilated superior portion of stomach, its superior part at level 5th ICS
Abdominal pain Parietal pain
3.
bodymajor part
4.
pyloric
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
Histology Mucosa
Epithelium =simple columnar secretion from tubular invaginate into LP form pit receive secretion glands
1. 2.
cardia card iac c gla gland nds s pylo py lori ric c gla gland nds s
3.
gastric glands kt fundus and body ↓ Collectively they hv several cells type Parietal cell mostly in upper part of of gastric glands, few
in pyloric glands secrete HCl and intrinsic factor most numerous cellin lower half of gastric
Chief cells
glands secrete rennin rennin and lipase during infancy, pepsinosinogen throughout life most in lower end of glands
enteroendocri ne cell
found throughout stomach type G cellssecrete hormone gastrinstimulate
parietal and chief cell secretion D cells somatostatin inhibit release of other hormone icl, gastrin
Mucous cell
located in upper part of cardiac and pyloric glands fx: secrete mucus
Stem cells
protective barrier
found at base of glands divide rapidly for replacing cell cell dies
submucos a Musculari s external
Serosa
Physiology of stomach
BV, nerve, lymphoid cells
Smooth muscle fibers arranged in 3 d irection
1. 2. 3.
obliqueinner circular middle
longitudinal outer contain pacemaker cells [greater curvature of fundus cardiac, pyloricregion] regionsecrete mainly mucus thin fundus ,body secrete mainly acid and enzyme
4 aspectsfilling, storage, mixing and emptying
Motility
presence of pacemaker cells in longitudinal muscle in greater greater curvature in region of fundus generate APperilstatic contraction
PEPTIC ULCER
From fundus[ muscle thin, weak] weak perilstatic contractionnot enough to mix food with gastric juice often def : CHRONIC, most solitary lesions, that occur in any portion of GIt that exposed to aggressive action of peptic juice until pyloric [muscle stronger, thick] string and p owerful 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 an antr trum um Usua Us uall lly y aft after er 33-4 4 hou hours rsdepends on type of foods and volume flatten to accommodate food [periltatic contraction too weak to Controlled by hormonal [eg gastrin], nervous [eg vagus nerve] Dama Da magi ging ng fo forc rces es Prot Pr otec ecti tive ve fo forc rce es [in [in sto stoma mach ch]] mix food with gastric juice can hold food up to 4 L ↑ acid secretion Mucous coat thick, highly alkaline [presence of Secretion Regulation bicarbonate] mucus resist the action of acid and enzyme Cephalic pha se [20%] Gastric phase [70%] Intestinal phase ↑ enzyme secretion Epithelial cell replacement lie only food for 3-6 Vagus nerveRapid stimulate gastric secretion Ingested reaches stomach duodenum initially enhance then slough off and replace by new cells eventhoughdays before food is swallowed in gastric secretion, but soon it of tight jx btwn epithelial cells prevent response to Presence sight, smell, though of food will inhibit it ↑ pH of stretching stomach of stomach gastric juice from leakage inside ↓ ↓ ↓ Send inhibitory signal by way enteric Sight, smell, taste, though of food both ECL G short and long reflex Gastric ulc ulcer Duodenal ulcestimulate rwill activate ↓ nervous system and send signals to ↓ Send these sensory and mental signal medulla that EPIDEMIO 4 timeto s more cocell mmto on release than GU stimulate gastric secretion through medulla oblongata 1. in inhi hibi bitt vagu vagus s nucl nuclei ei gastrin elaboration of 3 chemicals AGE AG E ON ONSE SET T Olde Ol derr po popu pula lati tion on [5 [5070y. y.o] o] 20-5 20 -50 0 y. y.o o ↓0-70 2. sti stimul mulate ate sym sympha phatet tetic ic ↓ 1. ACH PAIN Intermittent epigastric pain by vagus Parasympathetetic Parasympathete tic AP carried neuron stimulate chief 2 . h i s t a m i n e PATTERN nerve to stimulate postganglionic cell parietal 3and .min-2 ga sthours rin Pain occurinimmediately after Pain occur after 30 neurons enteric plexus in stomach **the chyme also stimulate ↓ pass eating after eating [when food ↓ duodenum ECL to secrete secretin, 3 of them hv receptor Stimulate secretion from chief duodenum] cells, CCK, gastric inhibitory peptide Pain-antacid-relief Pain-antacid-reli parietal cellsef and pattern also ECL cells Pain-antacid-relief Pain-antacid-rel ief pattern on parietal ↓ Food-pain pattern Pain-food-relieff pattern Pain-food-relie cell stimulate them to Suppress gastric secretion and Nocturnal pain common secrete HCl n intrinsic motility factor H.PYLORI May be be pr presen t [60-80%] Often pr present[95%-100%] Cause more anorexia, omitting and weight loss function HCL gastric juice [2-3 L/day] 1. bac bacte teric ricida idall as pH pH low low as 0. 0.8 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. act activa ivate te enz enzyme yme pep pepsin sin
4. 2. 3.
4. 5.
enzyme pepsinsecrete by chief cells water
pepsinogen[inactive pepsinogen[inacti ve form]HCL will remove some of it’s a.a convert into pepsin[activated form
intrinsic factorssecrete by parietal cells
it will bind avidly to vit B12enable intestinal cells to absorp this compleximportant for Hb synthesis
mucus protective barrier endocrine and paracrine regulatory factorsgastrin, somatostatin, histamine, etc Digestion
CHO continue in body of stomach due to presence of salivary amylase
Proteinby pepsin , in antrum ↓
Absorption
Digestion continue in small intestine no nutrient absorption here
breakdown lant and
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 gastric 80% of pt hvg this
bacteria remain asymptomatic but may associated with occurrence of peptic disease disease and gastritis colonization factors
ermittent epigastric pain, which esp occur after had heavy meal
1.
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 urease will 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 epithelial shedding diagnosis
↑ acid secretion to digest large fooddat y pain at ulcer site PERITONITIS= inflammation/infection inflammation/infection of peritoneum after meal, taking some type medication RF: use of piroxicam to relieve knee pain 1. primary/spontane primary/spontaneous ous P due to underlying dsz [usually due to chronic chronic liver dsz] we confirm barium meal x-ray exam and endoscopy : show duodenal ulcer,; histopatho result found H.pylori 2. secondary P spillage of stomach, intestinal content, appendix content into peritoneal cavity due to perforation or rupture initiate inflammation and infection to peritoneum
3.
tertiary Pdvlp in those who undergoing CAPD [continous ambulatory peritoneal dialysis]
treatment treatme nt
diagnosis [20 peritonitis] peptic ulcer + H.pylori present most effective treatment combination of 1 PP I + 2 antibiotics SSpain increasing once infection spread to peritoneal cavity, continuously, tenderness, fever, hypotension [bleeding], vomit case : omeprazole,1. clarithromycin, amoxicillin exam: abdominal distended, muscle guarding. muscle rigidity, rebound tenderness in absence of H.pylori 2. longabdominal term higher doses of PPI
3. 4.
Digital rectal exam : weak sphincter tone,filled ampulla [weak contraction for defecation],t defecation],tenderness enderness upon upward thrust Lab : leukocytosis [sign infection], infection], anemia [bleeding], amylase , ureum , creatinine creatinine ↑
5. confirm the diagnosis abdominal X-ray: ↑ bowel bowel gas distribution with dilation of small 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
treatment 1.
flui fl uid d resu resusc scit itat atio ion n
[indicate that organ are torn/perforate]
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 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 prostaglandin via blockage of COX enzyme enzymeanalgesic effect!! [take for knee pain] •
• •
SE=renal toxicity, GI ulcer, bleeding, Antacids =weak base [given for epigastric pain] SE=gastric distnsion,blenchi distnsion,blenching, ng, diarrhea[MgOH], constipation [ALOH] Ranitidine =H2 receptor antagonist SE= heache, myalgia, diarrhea, fatigue Omeprazole =Proton =Proton pump inhibitor inhibitor SE= Exteremely safe diarrhea, headche Sucralfate= Mucosa protective agent
1. 2.
will react with gastric acidform water and saltreduce intragastric acidity also posses posses mucosal protecti protective ve action action by stim stimulate ulate producti production on of prostaglandin prostaglandin
competitive competitiv e inhibition at parietal cell H2 receptor
Histamine from ECL cells can’t bind to H2 receptor ↓ diminish acid secretion ← decreased intracellular intracellular [ ] of cAMP Inhibit proton pumpSuppress secretion H+ ions into gastric lumenInhibit gastric acid secretion
SE=heache, flatus, dry mouth Amoxicillin = beta lactam antibiotic SE=allergic, nausea, vomit Clarithromycin = antibiotic, macrolides SE=muscle pain, dizziness, headache , GI upest
1.
-ve charge charge sucrose sulfate bind to +ve ly charged charged protein in the base of ulcer or erosion ↓ Form physical barrier/coat barrier/coat that prevent further damage damage
2. also binds to epithelial growth factor enhance 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[NSA piroxicam[NSAID] ID] ↓inhibit COX-2 suppress synthesis prostaglandin ↓ no protective mucous coat ↓bicarbonate secretion 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,vacuolati protein,vacuolating ng
cytotoxin [VacA]mediate inflammatory cascadefurther tissue injury
has adherence factors that enable H.pylori to bind specifically to gastric-type epithelium ↓ protect and prevent prevent them from being shed during epithelial shedding
BHP
CHOP 4 ethical principle -beneficence -Non maleficence -autonomy -justice
Prevention primary: avoid risk factor secondary : early diagnosis n prompt treatment tertiary:prevent tertiary:prev ent from getting worse
CRP Epidemiology Case study : prevalence of peptic ulcer cases among teenagers in jatinangor
