Peptic Ulcer Disease Flashcards
PUD
etiology
pathophysiology
Peptic Ulcer Disease (PUD)
- a break in the gastric OR duodenal mucosa creating an ulcer
- ulcer = a lesion (cut) which extends through the muscularis mucosae layer that is greater than 5mm in diameter
Causes
the two major caues of PUD are NSAID use and H. pylori infection
- Zollinger-Ellison syndrome
- CMV
- chrons
- lymphoma
- medications
- cirrhosis
- CKD
Pathophysiology of H. Pylori infections & PUD
- majority of the h pylori uclers are within the duodenum (70-90%)
- in duodenum: metaplasia in small islands occurs at the doudenal bulb due to increase acid exposure; these islands is wehre h pylori makes its uclers
- in stomach: majority of causes at the antrum of the stomach
Pathophysiology of NSAIDS & PUD
- 10-20% gastric uclers & 2-5% duodenal ulcers (so think gastric)
- more common in those who…
1. are in the first 3 months of using the NSAID
2. those over 60
3. a prior history of ulcer disease
- those who take NSAIDS + asprin/steroids/anticoags are at increased risk
How NSAIDS create PUD
- NSAIDS act on inhibition of prostaglandins at both COX-1 and COX-2
- COX-1: within the gastirc mucosa (to help protect from the gastric acidity)
- COX-2: at sites of inflammation only
- thus, NSAIDS block COX-1 & 2 therefore the uclers happen in the stomach
- coxibs (specifically celecoxib) only inhibit COX-2 therefore can help decrease the risk of PUD for pts.
those with…
1. increaes risk of bleeding due to NSAIDS
2. those with history of ulcers and GI bleeding
3. aspring + NSAID use
4. those with NSAID use and H pylori infection
all at increased risk of PUD
Signs and Symptoms of PUD
Labs & Imaging
tests specifically for H pylori
Symptoms
- epigastric pain (dyspepsia) described as : gnawing, dull, achy or hunger-like pain
- relief of pain with food or antacids seen in 50% of pts (but symptoms return hours later)
- some are asymptomatic
- nocturnal pain
- naseua & anorexia (gastric ulcers)
Signs
- pts. will have epigastric tenderness on palpation
- FOBT: postive in 1/3 of pts.
Labs
- CBC with diff = for anemia
- amylase = check pancreas function (if its infiltrating the pancreas = see evidence)
- fasting gastrin = screen for ZE syndrome
Imaging
- abdominal CT: for those with complicatsion due to the PUD
- diagnosis of choice: upper GI endoscopy to visualize the uclerations & obtain bx. to confirm presence of h pylori
H Pylori Specific Test
1. fecal antigen assay
2. urea breath test (to see h pylori convert urea into hydrogen)
if pt. has a history of PUD = use these test to see if treatment was successful or if the have a recurrent infection
always hold PPI for 14 days prior to these test if they are on one
Treatment of PUD
- H Pylori
H Pylori Treatment
1. acid antisectrtory agent = proton pump inhibitor
- PPIs =”-prazole”
-
H-2 Receptor Antagonists
- “-tidine” (cimetidine, faomtadine, nizatidine) -
Mucosal Enhacing Agents
- can be add on thearpy with a PPI
- Bismuth sucralfate, misoprostol
Treatment Combos
-
Standard Bismuth Quadruple Thearpy
- PPI + Bismuth + tetracycline + metronidazole -
Rifabutin- Based Triple Thearpy
- Omeprazole + Rifabutin + amoxicillin -
standard triple thearpy only if low resistance to clairthromycin
- PPI + Clairthromycin + Amoxicllin
After Inital Treatment
ulcer size & dictaing the continuation of PpI
- if the ucler is > 1 cm = continue PPI for…
- 2-4 weeks if it is a duodenal ulcer
- 4-6 weeks if it is a gastric ulcer
2-4 weeks after the PPI and more then 4 weeks after completing abx. test to confirm H pylori infection is gone
- tests can be the urea breath test, fecal antigen test or endoscopy
Treatment of PUD due to NSAIDS
- stop NSAID use
-
PPI use preferred
- uncomplicated duodenal ucler: 4 weeks
- uncomplicated gastric ucler: 8 weeks
OR
-
H-2 Receptor Antagonists
- 6 weeks for duodenal
- 8 weeks for gastric
Treatment of Recurrence Ulcers
- H pylori
- NSAIDS
H Pylori
- some pts. may need long term PPI
NSAIDS
- use the NSAID at the lowest dose possible
- if they ahve hx. of PUD with NSAID/antiplatlet = test for h pylori
- PPI daily
- misoprostol
- celecoxib + PPI
those with CVD risk: dont use NSAIDS
those with GI bleeding risk factors: use celecoxib
Complications of PUD
- GI Hemorrhage
approx. 50% of upper GI bleeding is due to an ulcer
Symptoms
- some pts. are asymptomatic
- melena (black tarry stool)
- hematemesis or coffee ground emesis
- massive GI bleed: hematochezia (fresh blood in stools)
Labs
- CBC with diff
- BMP
Imaging
- endoscopy
Treatment
- IV PPI (NOT PO)
Complications of PUD
Ulcer Performation
- An ulceration performation can put an individual at risk for chemical peritonitis (the contents and chemcials from stoamch/duodenum can spill out)
Symptoms
- sudden and severe general abdominal pain
- ill, rigid quite abdomen and rebound tenderness
Labs
- CBC with diff
- amylase
Imaging
- CT
Treatment
- surgery (laproscopic closure)
post-op treatment
- H pylori tests
- avoiding NSAIDS
- PPI to help reduce bleed
PUD Complication
Ulcer Penetration
- penetration to the pancreas, liver, biliary tree (the ulcer is erroding into another organ, not the peritoneum)
Symptoms
- change in intensity or rythmicity of their ulcer symptoms
- severe, constant pain (raidating to the back)
- not responsive to antacids or food
- Labs and PE will be nonspecific
Imaging
- Endoscopy (to see the ulcerations)
- CT (to see the penetration)
Treatment
- IV PPIs, then surgery if no improvement
PUD Complication
Gastric Outlet Obstruction
- less common with H pylori
- mostly causes by gastic cancers or extrinsic duodenal obstructions due to intraabdominal neoplasms
- edema and scarring that narrows the pylorus or the duodenal bulb leading to the obstruction
Symptoms
- early satiety
- vomiting
- weight loss
- epigastric fullness/heaviness after meals
Signs
- succusion splash in epigastrium (heard with stethescope)
- foul smelling fluid on NG aspiration
- metabolic acidosis
- hypokalemia
Imaging
- upper endscopy
Treatment
- IV isotonic fluids or KCL to correct electrolytes
- IV PPIs
- NG decompression
- hydrostatic balloons (dilated stomach)
- surgical treatment (vagotomy, pylorplasty, antrecetomy)
PUD Complication
Gastric Outlet Obstruction
- less common with H pylori
- mostly causes by gastic cancers or extrinsic duodenal obstructions due to intraabdominal neoplasms
- edema and scarring that narrows the pylorus or the duodenal bulb leading to the obstruction
Symptoms
- early satiety
- vomiting
- weight loss
- epigastric fullness/heaviness after meals
Signs
- succusion splash in epigastrium (heard with stethescope)
- foul smelling fluid on NG aspiration
- metabolic acidosis
- hypokalemia
Imaging
- upper endscopy
Treatment
- IV isotonic fluids or KCL to correct electrolytes
- IV PPIs
- NG decompression
- hydrostatic balloons (dilated stomach)
- surgical treatment (vagotomy, pylorplasty, antrecetomy)
Zollinger-Ellison Syndrome (ZES)
etiology
patho
symptoms
Etiology
- gastrin secreting gut neuroendocrine tumor (gastrinomas)
Patho
- increased gastrin = increase acid secretion
- risk of the inc. acid causing ulcerations (ruining the lining of the stomach) PUD < 1%
majority of the tumors arise in the gastrinomas triangle
- porta hepatis
- neck of pancreas
- 3rd part of the duodenum
Symptoms
- can be asymptomatic
- GERD is commong
- diarrhea is commong
- steatorrhea and weight loss
increased risk of ZES if
- history of multiple ulcers
- giant ulcers
- H pylori absent and not using NSAIDS
- family hisotry
screen for ZES with fasting gastrin levels
Labs
- if gastrin > 1000 and gastric pH < 2 = diagnosis
- giving secretin: triggers increase in gastrin levels
determine if hyperparathyroidism and MEN I syndrome v ZES
- serum parathyroid hormone
- prolactin
- FSH
- growth hormone levels
Imaging
- for determination of metastasis or identify primary tumor
- CT or MRI scan
- PET scan or CT best sensitivity
Treatment
- initial = PPI PO
- if hepatic mass isolated (surgical resection )
- systemic therapy : long acting somatostatin anaolg (to supress the gastrin)
- TKI and Peptide receptor radionucleotide thearpy
Loaclized Disease
- rescete before hepatic spread
- laparotomy, duodenotomy
surgery not recommened for those with MEN I
Gastropathy V Gastritis
Erosive Hemorrhagic Gastritis
Gastropathy = epithelial damage WITHOUT inflammation
Gastritis = evidence of inflammation with th epithelial damage
Erosive & Hemorrhagic Gastritis
Etiology
- NSAIDS, alcohol, stress, portal HTN
Symptoms
- asymptomatic
- anorexia
- epigastric pain
- N/V
Labs
- low Hgb/Hct due to iron defiency because of the bleed
Stress- INduced: Treatment
- (TBI, sepsis, shock, burns)
- use H2 blocks or PPIs IV
- sucralfate (to protect mucosal lining)
NSAIDS: Treatment
- (severe pain, GI bleeding or anemia)
- discontinue med, use PPI to help
Alcohol: Treatment
- (dyspepsia, nausea, emesis, hematemisis)
- use H2 blockers, PPis or sucralfate
Portal HTN: Treatment
- (usually asymptomatic) bleeding
- propranolol or nadolol to lower HTN of the portal vein
Non-errosive Non specific Gastritis
two classes
H pylori Class
- gastritis due to H pylori under the gastric mucosal layer
- causes muocasal inflammation
- can lead to ulcers
- dx. with endoscopy (upper GI)
- obtain fecal antigen and urea breath test
Pernicious Anemia Gastritis
- rare autoimmune disorder
- fundic glands with resulting lack of HCL, decreased intrinsic factor, and vitB12 malabsorbtion
- histology = severe gland atrophy and intestinal metaplasis
- see anti-intrinsic factor antiboides on labs
Specific Types of Gastritis
1. Infections
2. Eosinophilic Gastritis
3. Menetrier Disease
Infections
- acute bacterial infections
- viral infections (CMV)
- bone marrow or solid organ transplation
- funcal infections
- parasitic infections
Eosinophilic
- rare, eosiniphilic infiltrtated anturm (in the mucosa, muscularis or serosa)
Menetrier Disease
- a hypertrophic gastropathy with unknown cases
- giant thinkened gastric folds in teh body of the stomach
