PUD Flashcards
pepsinogen secretion is increased by
- gastrin
- histamine
- vagal stimulation
pepsin activation
- maximally active at pH 1-3 and are rapidly inactivated at pH above 4.5
two forms of gastrin
- G-34: about 2/3 of gastrin in fasting subjects, half life about 30 minutes
- G-17: increases during meal time, half life about 7 minutes
basal secretion of gastric acid
- takes place during fasting
- high rates in the evening and low in the morning
- dependent on the vagus nerve
3 phases of gastric acid secretion
- cephalic phase: secretion in response to senses
- gastric phase: secretion triggered by food in the stomach
- intestinal phase: secretion triggered by entry of food into the duodenum
stimulation of parietal cells
- vagal stimulation
- ACh
- histamine
- gastrin
inhibition of parietal cell secreiton
- luminal acid
- prostaglandins
- endogenous peptides (secretin, somatostatin, glucagon, GIP, peptide Y)
- drugs
pernicious anemia
- decrease of intrinsic factor due to antibodies against parietal cells
diseases associated with increased acid-pepsin secretion
- duodenal ulcer
- ZES: uncontrolled acid secretion due to higher levels of gastrin, islet cell tumor in pancreas, can be associated with multiple endocrine neoplasia type I (MEN1) syndrome
erosive and hemorrhagic gastritis
- seen seriously ill patients as stress lesions
- can be caused by drugs or trauma and physical agents such as NG tubes, reflux injury
H. pylori associations
- healthy adults
- duodenal ulcer
- gastric ulcer
type A gastritis
- autoimmune/genetic
- found in fundus and body
- mucosal damage is progressive
- onset at old age (above 60)
- associated with cancer
- achlorhydria, parietal cell antibodies, mucosal gastric biopsy
- treat with lifelong B12 and cancer surveillance
type B gastritis
- H. pylori infection
- found in antrum
- damage may regress with treatment
- onset at early or middle age
- associated with ulcers
- urea breath positive, H. pylori antibodies and present on biopsy
- treatment usually not required
chronic atrophic gastritis (autoimmune corpus gastritis)
- involves the gastric fundus and body
- histologic damage is progressive
- final expression is pernicious anemia
- associated with B12 deficiency, long term parental B12 required
common forms of peptic ulcer
- H- pylori: associated
- NSAIDs: associated
- stress ulcer
genetics of PUD
- DU clusters in families
- inheritance of blood group O is associated with 1-3 fold increase in DU incidence
presenting symptoms of PUD
- burning epigastric pain, episodes of bleeding, perforations, delayed gastric emptying, nausea, vomiting, early satiety
CI of prostaglandins (misoprostol)
- female of child bearing ages, could lead to miscarriages because it causes smooth muscle contractions
bleeding ulcers
- no parental drugs has been shown to be effective in stopping bleeding
- PPIs can prevent recurrence but do not stop bleeding
- patients with prior bleeding episodes should be considered for long-term maintenance therapy with H2RA/ PPI
decreased efficacy of rapid urease testing
- in patients treated with bismuth, antibiotics, high dose H2 blockers, or PPIs
treatment of H. pylori
- PPI, amoxicillin, and clarithromycin
- 10-14 day regiments favored over 7 day
cancers associated with H. pylori
- non-Hodgkins lymphoma and MALT lymphoma of the stomach
ZES triad
- gastric acid hypersecretion
- severe peptic ulcer disease
- non-beta islet cell tumors of pancrease
gastrinoma
- hyper gastrin state leading to gastric acid hypersecretion leading to PUD, diarrhear or GERD
- may be a part of multiple endocrine neoplasia syndrome (MEN 1)
- very high gastrin levels
