GASTRITIS -

1. acute
1. erosive (nsaid/aspirin);
2. nonerosive (h.pylori);
3. ingestion of strong acid/alkali (gangrene ->scarring -> stenosis);
4. stress-related (trauma, burn

1. chronic -
1. h.pylori
2. long term drug therapy
3. reflux of duodenal contents after gastric surgery

PATHO -
1. destroyed mucosal barrier (protects stomach from digestive juices -hcl & pepsin)
2. inflammation
3. edematous and hyperemic gastric mucosa & erosion
4. [chronic] atrophy

diminished production of intrinsic factor -> cant absorb b12 (cobalamine)-> pernicious anemia
-> B12 injection

PROHIBIT
1. COFFEE - cns stimulant >inc. gastric activity * pepsin secretion
2. SMOKING - nicotine dec. bicarb secretion

MEDS
1. antibiotics - eradicating h.pylori
2. antidiarrheal - bismuth subsalicylate - suppress h pylori & ulcer healing
3. H2 receptor antagonist (-tidine) - dec. Hcl
4. ppi (prazole) - dec. gastric acid sec. by slowing
5. prostaglandin e analog (misoprostol / sucralfate) - protects gastric mucosa& inc. mucus

PEPTIC ULCER DISEASE - excavation of mucosa (can extend to muscles layers and
peritoneum)
1. gastric (in lesser curvature)
2. duodenal (more likely)
3. esophageal (GERD)

causes
 h. pylori
 nsaid use
 blood type o

Zollinger–Ellison syndrome
1. a condition in which a gastrin-secreting tumor or hyperplasia of the islet cells in the pancreas
causes overproduction of gastric acid, resulting in recurrent peptic ulcers.
PATHO
1. EROSION (due to inc. pepsin & dec. resistance of protective mucosal barrier)
 2. DUODENAL - secrete more acid
3. GASTRIC - normal/decreased acid pero masakit pa rin kasi impaired na mucosal barrier

fiberoptic endoscopy - reveals shallow erosions

stress ulcer:
1. curling - burns (antrum of stomach or duodenum)
2. cushing - head injury, iICP>overstimulation of vagus>increased gastric acid secretion
CLINICAL MANI
 duodenal - 2-3 hrs after eating, relief after eating & antacid
 gastric - immediately after (inc acid production to digest food)
diagnostic
 physical exam
 upper GI endoscopy (visualize inflam)
 histology (h pylori)

pharmaco
 antibiotics + PPI + bismuth salts
o metronidazole, amoxicillin, clarithromycin, tetracyline
o omeprazole
o pepto bismoL
 dual – 1 antibiiotic +PPI
 triple therapy – 2 antibiotics + PPI
 quadruple – 2 antibitoics + PPI + bismuth salts

surgery
pyroplasty – opening pylorus
antrectomy – removal of pyloric (antrum) of stomach with anastomosis
o billroth I: stomach  duodenum (gastroduodenostomy)
o billroth II: stomach  jejunum (gastrojejunostomy)
 vagotomy – cutting vagus nerve (diminsihing cholinergic stimulation  less responsive to
gastrin)
o truncal v – severs right and left, used to dec. acid secretion
o selective v – severs vagal innetration to stomach but maintain to other organs
o parietal cell v – denervates acid-secreting parieta cells but preserves vagal inn to
gastrci anrum and pylorus
 SUBTITAL GASTROECTOMY WITH BILLROTH I/II
COMPLICATIONS
i. HEMORRHAGE
 Symptoms: melena, hematemesis
 Assess: faintness, dizziness, nausea, SHOCK (tachy, hypo, tachypnea),
 Management
o Endoscopy for dx and treatment
1) Injecting epinephrine/ alcohol
2) Cauterizing
3) Cipping ulcer
o Surgery
1) Removal of ulcer
2) ligating bood vessels
 3) vagotomy, pyroplasty, gastrectomy
o Transcatheter Arterial Embilization (TAE) – catheter in skin  embolic agent to
occlude blood flow  stop bleeding
1) Embolic agents: mettalic coils, polyvinyl alcohol particles, gelfoam
o TRANEXAMIC ACID
ii. PERFORATION AND PENETRATION
a. Perforation: erosion of ulcer into peritoneal cavity. Most lethal
b. Penetration: erosion thorugh adjacent structures
iii. GASTRIC OUTLET OBSRUCTION
 Area near pyloric sphincter becomes scarred and stenosed due to alternate healing and
breaking down
 Management:
o NGT decompression
o Balloon dilation of pylorus

GASTRIC CANCER
 CAUSES:
o DIET: smoked, salted, pickled, low fruits and veggies
o H.pylori
o Can be familial
 PATHO
o Adenocarcinoma  arise from mucus-producing cells of inner most lining of stomach
o Lesion on top later of mucosa lesion penetrates cells in deeper mucosa  inflitrates
stomach  extends to othe rorgans
 ASSESSMENT AND DX
o Physical exam is not helpful bc gastric tumors are not palpable
o Ascites and hepatomegaly only if metasitizied
o Sister mary joseph’s nodules  gi malignancy
o DIAGNOSTICS
1) ESOPHAGOGASTRODUODONESCOPY
2) BARIUM XRAY
3) ENDOSCOPY
4) CT SCAN (assess resectability)
5) CBC
 Anemia assessment
 Tumor markers: carcinoembryonic antigen (CEA), carbohydrate antigen
(CA-19-9), CA 50
 SURGICAL MNGMT
o Total gastrectomy
o Esophagojejunostomy
o Billroth  lower cure rate than billroth II due to limited resection, b2 dec possibility of
lymph node spread an metastasis
 COMPLICATIONS OF GASTRIC SURGERY
o Dumping syndrome – rapid gastric emptying
1) Rapid dumping – 10-30 mins; triggers body to move fluid from bloodstream to
intestine to “dilute food”  boloated, nausea, abdominal cramps & dec. blood
volume  rapid HR, dizzi faiinting
 2) Late – 1-3 hrs. rapid increase of suagr absorption tirggers pancreas to more
insulin to prevent hyperglycemia  may overract and cause hypoglycemia
3) TREATMENT:
 Diet: small meals, avoid sugary, eat more complex carbs, fiber, d not
drink liquid with meals,thickennn food
 Meds: ocreotide, acarbose
o BILE REFLUX – bile acts as barrier to prevent duodenal conetns back into stomach
1) Cholestyramine – binds w/ bile acids to eliminate to stool
o GASTRIC OUTLET OBSTRUCTION – narrowing, stenosis
 CHEMOTHERAPY
o Flourouracil, carboplatin,

INFLAMMATORY BOWEL DISEASE

 Women 10-30 y.o
ULCERATIVE COLITIS CROHN’S DISEASE
men women
15-30 20-29
Stopped smoking smokers
Chronic, remissions and Remission& exacerbation
exacerbatins
Mucosal and submucosal layers All layers
Rectum and colon Occur anywhere in GI tract but
common in distal ileum and
ascending colon
Blood and pus diarrhea Cobble-stone appearance
Ulcers  Bleeding Fistula, fissure, abcess
Bowel narrowing and
shortening
Skip lesions  “regional”
enteritis
LLQ pain RLQ pain
Intermittent tenesmus
Diarreha with blood and pus Diarrhea unrelived by
6 or more liquid stools per day defecation
Hypoalbuminemia, electrolyte Eating  peristalsis  pain
imabalnce, anemia after eating (malnutrition)
Abdominal xray BARIUM XRAY
Colonoscopy – can distinguish UGIS
from other diseases CT SCAN  more sensitive
Blood positive for blood, low
hematocrit and hemoglobin
levels
Toxic megacolon – infla extends Enterocutanoeus fistula -- small
to muscularis  cannot bowel contents leak to skin due
contract  DILATED COLON to a formed channel between
perforation them
Subtotal colectomy
 Proctolectomy and ilesotomy Total colectomy and ileostomy
Strictureplasty
SULFONAMIDES – antibiotic of choice
Criteria for surgery in IBD
1. Intractable disease
2. Poor quality of life
3. Complications form disease/ medical management
TYPES OF SURGERY
 Total colectomy with ileostomy
 Total colectomy with continent ileostoy (kock pouch = no ostomy bag)
 Total colectomy with ileonala anastomosis

DIVERTICULITIS
Hirschsprung disease – ribbon-like stool
SURGERY
 One-stage resection. HARTMANN PROCEDURE
 Multiple-stage procedures. Double barrel colostomy
Laxative – psyllium

GUIDEINES FOR EA;RY DETECTION OF COLORECTAL CANCER

1. Digital rectal examination yearly after age 40
2. Occult blood test yearly after age 50
3. Proctosigmoidiscopy every 5 years after age 50
Ibd
Sufalazine

COLORECTAL CANCER
LYNCH SYDNROME – hereditary colorectal cancer
Carcinoembryonic antigen (CEA)

STAGES OF APPENDICITIS
1. Early/Suppurative – there is inflammation in the appendix.
2. Congestive – Really inflamed, more painful. The area is being compromised to receive oxygenated
blood.
3. Gangrenous – Due to no blood supply, the area loses its function and dies as it becomes gangrenous.
4. Perforative – this is when rupture of appendix happens.

1. Female
2. Forty
3. Fertile
4. Fat
5. Fair complexion