Mr.Amir, 66 y.

O
cc: pain at upper tummy
for 14 hours
localized, sharp,continous pain and ↑ in
severity

HT PE
vomit several times still conscious oxygen mask and IV line was establish to
abdomen distended pale, get perspirated the pt
still have bowel movement BP 100/60Normal urinary catheter inserted, and hoursly
production observed
no history of abnormal micturation ,defecation, tachycardia and tachypnea
LAB
normal appetite,constant weight gain, no problem of high fever [38.60] Hb ↓ , Ht ↓= anemia
swallowing heart, lung exm :normal WBC ↑ = leukocytosis
deny any fever before pain
Abdomen: amylase, ureum , creatinine ↑
episodic epigastric pain (2 mon ago)esp  distended but still symmetry Lipase : normal
came after had a heavy mealnot relieved  perilstatic scarce, nearly
after meal and taking some medication normal IMAGING
took piroxicam for knee pain (3 mon ago)  no vascular murmur abdominal x-ray:
 diffuse tenderness in supine position↑ bowel gas
↓
seen Dr for several times and was advised to take upper abdomen distribution, with dilatation
stomach pills including antacids and ranitidine  liver dullnesss present small bowel
↓no improvement with varying tympany erect position: no air-fluid level
undergo barium meal x-ray exam and esophago-  palpation: muscular appearance, dubious free gas
gastro-duodenoscopy[1 mon ago] rigidity, rebound chest x-ray: Subphrenic air +ve
histopatho result:+ve H.pylori tenderness
Digital Rectal exm
got duodenal ulcer
weak sphincter tone
↓
intact mucosal layer
diagnosis
– diffuse peritonitis due to suspected perforated peptic ulcer
**decide to perform acute laparotomy after administration of fluid resuscitation histopatho finding:
and prophylactic antibiotics to pt no sign of malignant ulcer
LAPAROTOMY  +ve H.pylori
peritoneal fluid with gastric content apprx 500 cc treatment
st --amoxicilin , clarithromycin,
perforated ulcerat 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 treatmentsuturing the perforation with omental
patch
ulcer is biopsied
prognosis: GOOD
hospitalization for 1 week
7th postoperative
Omeprazole, Sucralfate
↓ daydischarged
laparotomy wound heal well
and condition pt improved
 CC: pain at upper tummy/epigastric pain Abdomen
↓ portion of trunk[between thorax and pelvic]
organ probably involved start from diaphragm and extend until pelvic inlet
1. esophagus esophagitis, GERDno problem swallowing division4 quadrants, 9 regions
2. heart and its pericardiuminf. MIHeart Normal on PE
3. liverliver normal on PE and liver enzyme also Normal
4. pancreaspancreatitislipase Normal R L
5. Great vessels [aneurysm of aorta]no masses with pulsation or RUQ LUQ hypochrondri epigastric hypochondri
vascular murmur on PE ac ac
6. stomach RLQ LLQ R lumbar umbilical L lumbar
R inguinal Hypogastri L inguinal
c
covered by peritoneum [more specific description of position of
DUODENUM organ
thin, transparent in abdomen]
membrane [histologically composed of mesothelium]
anatomy consist of 2 layer [similar to pericardium , pleural membrane]
1st part and the shortest part of small intestine, C-shaped structure
12 fingers length=25 cm
starting from pyloric sphincterduodenojejunal flexure at sharp bend PARIETAL P VISCERAL P.
hv 4 part : superiordescendinginferior/horizontalascending Line the internal surface Line the internal surface of abd.
intraperitoneal
of abd. wall viscera
major and minor papilla =stomach, spleen,
liver, gallbladder Its BV, LD, nerves Its BV, LD, nerves continuous
↓ continuous with those in with those in abd. viscera
receive pancreatic secretion and bile from liver abd. wall
Extraperitoneal
blood supply : celiac trunk , SMA Innervated by somatic Innervated by autonomic
=
nerve[spinal nerve] nerve[sympathetic and
muscularis pancreas,kidney, parasympathetic nerve]
Histology----same as other GIT duodenum,IVC, Sharp, severe, persistent Dull, crampy, poorly localized
external
Mucosa Submucosa aorta and well localized pain pain
Epithelium [simple Duodenal/brunner’s
columnar].contain glands
serosa peritoneal cavity
STOMACH1. Goblet cellsmucus alkaline mucus
 no organ, sterile area
Anatomy2. absorptive cells BV
 contain peritoneal fluid50ml, composed of water,
3. intestinal
J-shaped glandsmobile Lymphatic nodules
structure, electrolyte and other substance that derived from
4. peneath nerves
lie obliquely in left portion of abdomen [left hypochondriac, epigastric, intestitial fluids in adjacent tissue
cellslysozyme,  also contain ABfight against infection
umbilical]
phospholipase;
btwnbacterial
esophagusprotection
and duodenum[ gastroesophageal pyloric sphincter]
LP
anteriormucosa
Muscularis : diaphragm, left lobe liver, anterior abd wall Abdominal pain
posterior : omental bursa Parietal pain Visceral pain Referred pain
 arise from  arise from visceral  visceral pain
hv 2 curvature parietal peritoneum felt at some
Physiology
 1.foodlesser C= constitute
digestion its R and superior margin
and absorption peritoneum  pain poorly distance from
2.villi,
Greater C=constitue
microvilli, its L and
brush border inferior
enzyme, margin cells
absorptive  pain is more localized, dull , affected
localized, crampy, involved organ
hvfat
4 regions
being emulsified by bile into smaller unit
intense, severe, sweating and  due to they
enzymechemical digestion of CHO, protein and fat
1.pancreatic
cardiacsmall area inside cardiac orifice sharp and nausea share a
 neutralize stomach acidalkaline bile and pancreatic secretion persistent  autonomic central
2. fundusdilated superior portion of stomach, its superior part at level  somatic innervtn afferent
5th ICS innervtn[spinal [parasymphttc n pathway with
nerve] symphttc] affected
3. bodymajor part
organ
4. pyloric
antrum
canal : narrower, thick ring of SM there create pyloric
sphincterregulate passage of stomach chyme into duodenum
 Histology
Mucosa Epithelium =simple columnar
 invaginate into LPform pitreceive secretion from tubular
glands

1. cardiac glands
2. pyloric glands
3. gastric glandskt 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 cellin lower half of gastric
glands
secrete rennin and lipase during infancy,
pepsinosinogen throughout life
enteroendocri most in lower end of glands
ne cell found throughout stomach
type
G cellssecrete hormone gastrinstimulate
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protective barrier

Stem cells found at base of glands

divide rapidly for replacing cell dies

submucos  BV, nerve, lymphoid cells

a
Musculari Smooth muscle fibers arranged in 3 direction
s 1. obliqueinner
external
2. circularmiddle
3. longitudinaloutercontain pacemaker cells [greater curvature
of fundus
cardiac, pyloricregion]
regionsecrete mainly mucus
Serosa thin
fundus ,bodysecrete mainly acid and enzyme

Physiology of stomach
 Motility 4 aspectsfilling, storage, mixing and emptying
presence of pacemaker cells in longitudinal muscle in greater curvature in region of fundusgenerate APperilstatic contraction
PEPTIC ULCER
def : CHRONIC, mostoften
From fundus[
solitary muscle
lesions, thin,
that weak]weak
occur perilstatic
in any portion contractionnot
of GIt that enough to action
exposed to aggressive mix food with gastric
of peptic juice juice
 until pyloric [muscle stronger, thick]string and powerful perilstatic contractionenable mixing with gastric juice, later on empyting
most common 1 portion
st
of duodenum, stomach[usually antrum]
foodmouthesophagusstomach
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 hoursdepends on type of foods and volume
flattento 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 coatthick, highly alkaline [presence of
Secretion Regulation
bicarbonate] mucus resist the action of acid and
Cephalic phase enzyme
[20%] Gastric phase [70%] Intestinal phase
↑ enzyme secretion
Vagus nerveRapid Epithelial
stimulate cell
gastric replacementlie
secretion only food
Ingested for 3-6
reaches stomach  duodenum initially enhance
eventhoughdays beforethen
foodslough off and replace by new cells
is swallowedin gastric secretion, but soon it
response to Presence of tight
sight, smell, jx btwn
though epithelial cellsprevent
of food will inhibit it
gastric juice from leakage inside ↑ pH of stretching
stomach of stomach ↓
Sight, smell, taste, though of food ↓ ↓ Send inhibitory signal by way enteric
Gastric ulcer ↓ will activate
Duodenal ulcerstimulate ECLboth
G short and long reflex nervous system and send signals to
Send these sensory and mental signal cell to release
to more common ↓ medulla that
EPIDEMIO 4 times than GU
medulla oblongata stimulate gastric secretion through 1. inhibit vagus nuclei
gastrin
AGE ONSET Older population [50-70y.o]
↓ 20-50 y.o elaboration of 3 chemicals 2. stimulate symphatetic
1. ACH↓
PAIN Intermittent epigastric
Parasympathetetic pain by vagus
AP carried neuron
PATTERN stimulate chief
2. histamine
nerve to stimulate postganglionic
Pain occurinimmediately
neurons enteric plexus after cell
Pain occur after 30
in stomach and
3. min-2parietal
gastrin
hours **the chyme also stimulate
eating ↓ after eating [when food cells
↓ pass duodenum ECL to secrete secretin,
Stimulate secretion from chief duodenum]
cells,  3 of them hv receptor CCK, gastric inhibitory peptide
Pain-antacid-relief
parietal cells and
pattern
also ECL cellsPain-antacid-relief pattern on parietal ↓
Food-pain pattern Pain-food-relief pattern cellstimulate them to Suppress gastric secretion and
Nocturnal pain common secrete HCl n intrinsic motility
H.PYLORI May be present [60-80%] Often present[95%-100%] factor
Cause more anorexia,  Ach, gastrinstimulate
omitting and weight loss
gastric juice [2-3 L/day] function HCL
1. bactericidal as pH low as 0.8
1. HCL produce by parietal cells[posses carbonic anyhydrase]
2. convert ingested ferric
CO2 + H2O CAH > H2CO3  HCO3 + H+ ionsferrous ions [absorbable
form]
3. activate enzyme pepsin
4. breakdown plant and

2. enzyme pepsinsecrete by chief cellspepsinogen[inactive form]HCL will remove some of it’s a.aconvert into pepsin[activated form
3. water
4. intrinsic factorssecrete by parietal cellsit will bind avidly to vit B12enable intestinal cells to absorp this compleximportant for Hb synthesis
5. mucus protective barrier
endocrine and paracrine regulatory factorsgastrin, somatostatin, histamine, etc
Digestion CHOcontinue in body of stomach due to presence of salivary amylase
Proteinby pepsin , in antrum
↓
Digestion continue in small intestine
Absorption no nutrient absorption here
 Ulcer Erosion
defined histologically as breach of small, superficial
mucosa of GIT that extend thru mucosal lesion [<5mm
muscularis mucosa into submucosa or in diameter]
deeper ↓
↓ Juz mild bleeding
significant bleeding, scarring and [superficial mucosa only
perforation 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 and gastritis
colonization factors
1. hv fragellahighly 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
termittent epigastric pain, which esp occur after had heavy meal 3. adherence factor towards gastric epithelium protect and
prevent them from being shed during epithelial shedding
↑ acid secretion to digest
PERITONITIS= large fooddat y pain
inflammation/infection at ulcer site
of peritoneum diagnosis
d after meal, taking some
type medication
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 Pspillage of stomach, intestinal content, appendix content into peritoneal cavity due to perforation or ruptureinitiate inflammation and
infection to peritoneum
3. tertiary Pdvlp in those who undergoing CAPD [continous ambulatory peritoneal dialysis]
treatment
diagnosis [20 peritonitis]
peptic ulcer + H.pylori present most effective treatment combination of 1 PPI + 2 antibiotics
case : omeprazole,1. SSpain increasing
clarithromycin, once infection spread to peritoneal cavity, continuously, tenderness, fever, hypotension [bleeding], vomit
amoxicillin
2. abdominal exam: abdominal
in absence of H.pylori long term higher doses of PPI distended, muscle guarding. muscle rigidity, rebound tenderness
3. Digital rectal exam : weak sphincter tone,filled ampulla [weak contraction for defecation],tenderness upon upward thrust
4. 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 [indicate that organ are torn/perforate]
GI bleeding[melena, hematemesis],
obstruction[scarring and swelling due to ulcer cause narrowing in duodenum and gastric outlet
perforationspillage it content into abd.cavity peritonitis, pancreatitis

treatment
1. fluid resuscitation
2. antibiotic administrationto prevent bacteremiaamoxicilin, clarithromycin
3. laparotomy/surgical debridement
 laparotomy
• peritoneal fluid with gastric content apprx 500 cc
• perforated ulcerat 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
Piroxicam =NSAID
[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 safediarrhea, 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
MOA
inhibit synthesis of prostaglandin via blockage of COX enzymeanalgesic effect!!
1. will react with gastric acidform water and saltreduce intragastric acidity
2. also posses mucosal protective action by stimulate production of prostaglandin
competitive inhibition at parietal cell H2 receptorHistamine from ECL cells can’t bind to H2 receptor
↓
diminish acid secretion ← decreased intracellular [ ] of cAMP
Inhibit proton pumpSuppress secretion H+ ions into gastric lumenInhibit 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 factorenhance tissue repair**
Inhibit cell wall synthesis of bacteria
Bind to 50S bacterial ribosomeInhibit 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 duodenumopen way for gastric juice to
damage the tissue
secrete urease split urea into CO2 and ammoniaammonia will increase
lumen pH↑ acid secretion [physiology adaptation]
release cytokines, lipopolysaccharides, heat shock protein,vacuolating
cytotoxin [VacA]mediate inflammatory cascadefurther tissue injury
has adherence factors that enable H.pylori to bind specifically to gastric-
type epitheliumprotect 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 CHOP CRP

4 ethical principle Prevention Epidemiology
-beneficence primary: avoid risk factor Case study : prevalence of peptic
-Non maleficence secondary : early diagnosis n prompt ulcer cases among teenagers in
-autonomy treatment jatinangor
-justice tertiary:prevent from getting worse