PUD Flashcards
Gastroc mucosal Defense 3 Level Barrier
- PREEPITHELIAL
mucus bicarbonate e phospholipid layer surface epithelial cell - EPITHELIAL
- SUBEPITHELIAL
- generates hest shock proteins, trefoil factor family peptides and cathelicidins
- restitution: EGF, TGF, FGF
- has microvascular system that is the key component of subepithelial defense
EPITHELIAL SURFACE
- 2 Principal gastric secretory products; capable of inducing injury
- plays a role on digestion, absorption of iron and Vit B12 as well as killing bacteria
- HCl
- pepsinogen
- occurs in basal and stimulated condition
- the basal acid production occur in circadian rhythm (highest level during night, lowest during morning)
Gastric Secretion
- influence by cholinergic input (vagus nerve) and histaminergic input (local gastric sources)
- somatostatin, cholecystokinin, gherlin, obestatin, secretin, serotonin- plays a role in counterbalancing gastric acid secretion
Basal acid production
3 Phases of Gastric Secretion
- sight, smell, taste of food
- cephalic phase
3 Phases of Gastric Secretion
- activated once food enters the stomach
gastic phase
3 Phases of Gastric Secretion
- initiated as food enters the intestine
intestinal phase
- located in oxyntic gland
- also important in gastric secretory proceess
- secretes intrinsic factor, IL11
- express several stimulants of acid secretions (histamine 2, gastrin, Ach:M3)
- express receptors for ligands that inhibit acid production (prostaglandins, somatostatin, EGF)
Parietal cell
- responsible for generating large conc of H+
- consist of alpha (active catalytic site) and beta subunit
- usses chemical energy of ATP to transfer H+ ions from parietal cell cytoplasm to the secretory canaliculi
H+, K+- ATPase
- found primarily in the gastric fundus
- synthesizes and secretes pepsinogen- inactive precursor of pesin
- pepsin activity significantly diminished at pH 4, irreversibly inactivated and denatured at pH >/=7
Chief cell
break in the mucosal surface >5mm in size w/ depth to the submucosa
Ulcer
most common risk factor
H. pylori & NSAIDs
- often occur in the 1st portion, w/ 90% located w/in 3cm of pylorus
- usually = to 1cm in diameter but occ’l can reach 3-6cm
- sharply demarcated w/ depth at times reaching the muscularis propia
- the base often consist of zone of eosinophilic necrosis w/ surrounding fibrosis
Duodenal Ulcer
account for the majority of DU
H.pylori and NSAID
- attributed to either H.pylori or NSAID induced mucosal damage
- gastric acid output tends to be normal or decreased
- abnormalities in resting and stimulated pyloric sphincter pressure w/ increase in duodenal gastric reflux
Gastric Ulcer
Classification of Gastric Ulcer
-Type I
-Type II
- TYpe III
- Type IV
- Type I: gastric body; ass w/ low gastric acid production
- Type II: antrum; gastric acid vary from low to normal
- Type III: occur w/in 3cm of pylorus; acccompanied by duodenal ulcerl normal -high gastric acid production
- Type IV: found in cardia; low gastric acid secretion
2 factors that predispose to high colonization rate
- poor socioeconomic status
- less education
MOT of PUD
- person-person
- oral-oral
- fecal-oral
Risk Factors for H.pylori Infection
- birth or residence in developing country
- domestic crowding
- unsanitary living condition
- unclean food or water
- exposure to gastric contents of an infected individual
Pathogenic Factors Unrelated to H.pylori and NSAID in Aic Peptic Disease
- cigarette smoking
- genetic
- diet
- systemic mastocytosis
Infection Causes of Ulcers
- CMV
- HSV
- H. heilmannii
Drug/Toxin Causes of Ulcers
- biphosphonates
- chemo
- clopidogrel
- crack cocaine
- glucocorticoids
- mycophenolate mofetil
- KCl
Clinical Features of PUD
- abdominal pain: epigastric (burning or gnowing)
- nausea & weight loss
- tarry stools or coffee ground emesis
Physical Exam in PUD
- epigastric pain
- tachycardia & orthostasis
- presence of a succusion splash
PUD related complications
- GI bleeding: mc
- perforation: 2nd
- gastric ooutlet obstruction
Dx Evaluation of PUD
- Barium study
- endoscopy
Test for Detection of H.pylori
Invasive
- rapid urease
- histology
Test for Detection of H.pylori
Non Invasive
- serology
- urea breath test
- stool antigen
Tx of PUD
- eradication of H. pylori & therapy prevention of NSAID induced dse
- acid suppressing drugs: antacids, H2 receptors antagonists, PPI
- mucosal protectives
Surgery that is performed only in DU
Vagotomy
severe peptic diathesis secondary to gastric acid hypersecretion due to unrerlated gastrni release frm a non-beta cell endocrine tumor
Zollinger ELisson Syndrome
Manifestation of Zollinger Ellison Syndrome
- PUD-mc
- diarrhea
When to obtain fasting serum gastrin?
- multiple ulcers
- ulcers in unsual locations
- ulcer px awaiting surgery
- extensive fam hx for PUD
- post 0- ulcer recurrence
-basal hyperchloridria - unexplained diarrhea/ steathorrea
-hypercalcemia - fam hx of pancreatic islet, pituitary, parathyroid tumor
- prominent gastric/duodenal folds
Tx for Zollinger Ellison Syndrome
- directed at ameliorating the signs and symptoms related to hormone overproduction
- PPI: tx of choice
- surgery
presence of inflammatory cell infiltrates (lympho, plasma cells, neutro)
Chronic Gastritis
Types of Chronic Gastritis
- Superficial
- Atrophic
- Gastric atrophy
- Type A
- type B
- Superficial: early phase
- Atrophic: inflamm infiltrates extends deeper into the mucosa
- Gastric atrophy: glandular structure are lost, there is a paucity of inflamm infiltrates
- Type A: autoimmune, body predominant
- type B: H.pylori related, antrall predominant
Tx for Gastritis
aimed at the sequelea and not the underlying inflamm
Miscellaneous form of gastritis
- lymphocytic:
- Eosinophilic:
- russel body:
- lymphocytic: unknown etiology, described in px w/ celiac sprue
- Eosinophilic: markerd eosinophilic infiltration involving any layer of the stomach
- russel body: mucosal lesion of unknown etiology
- pseudotumural appearance
- presence of numerous plasma cell containing RB that expresses kappa and lambda light chains
Russel body gastritis
- rare entity char. as large, totous gastric mucosal folds
- massive foveolar hyperplasia
- epigastric pain, nausea, vomit, anorexia, wt loss
- gastric acid secretion reduced or absent
- endoscopy w/ deep mucosal biopsy is required to dx
Menietriers dse
Tx foe Menietriers dse
- medical therapy- anticolinergic agents, prostaglandins, PPI, predisone, H2 receptr antagonist
- subtotal gastrectomy
