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Gastrointestinal System > PUD > Flashcards

PUD Flashcards

1
Q

pepsinogen secretion is increased by

A
  • gastrin
  • histamine
  • vagal stimulation
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2
Q

pepsin activation

A
  • maximally active at pH 1-3 and are rapidly inactivated at pH above 4.5
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3
Q

two forms of gastrin

A
  • 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
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4
Q

basal secretion of gastric acid

A
  • takes place during fasting
  • high rates in the evening and low in the morning
  • dependent on the vagus nerve
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5
Q

3 phases of gastric acid secretion

A
  • 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
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6
Q

stimulation of parietal cells

A
  • vagal stimulation
  • ACh
  • histamine
  • gastrin
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7
Q

inhibition of parietal cell secreiton

A
  • luminal acid
  • prostaglandins
  • endogenous peptides (secretin, somatostatin, glucagon, GIP, peptide Y)
  • drugs
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8
Q

pernicious anemia

A
  • decrease of intrinsic factor due to antibodies against parietal cells
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9
Q

diseases associated with increased acid-pepsin secretion

A
  • 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
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10
Q

erosive and hemorrhagic gastritis

A
  • seen seriously ill patients as stress lesions

- can be caused by drugs or trauma and physical agents such as NG tubes, reflux injury

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11
Q

H. pylori associations

A
  • healthy adults
  • duodenal ulcer
  • gastric ulcer
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12
Q

type A gastritis

A
  • 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
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13
Q

type B gastritis

A
  • 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
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14
Q

chronic atrophic gastritis (autoimmune corpus gastritis)

A
  • involves the gastric fundus and body
  • histologic damage is progressive
  • final expression is pernicious anemia
  • associated with B12 deficiency, long term parental B12 required
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15
Q

common forms of peptic ulcer

A
  • H- pylori: associated
  • NSAIDs: associated
  • stress ulcer
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16
Q

genetics of PUD

A
  • DU clusters in families

- inheritance of blood group O is associated with 1-3 fold increase in DU incidence

17
Q

presenting symptoms of PUD

A
  • burning epigastric pain, episodes of bleeding, perforations, delayed gastric emptying, nausea, vomiting, early satiety
18
Q

CI of prostaglandins (misoprostol)

A
  • female of child bearing ages, could lead to miscarriages because it causes smooth muscle contractions
19
Q

bleeding ulcers

A
  • 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
20
Q

decreased efficacy of rapid urease testing

A
  • in patients treated with bismuth, antibiotics, high dose H2 blockers, or PPIs
21
Q

treatment of H. pylori

A
  • PPI, amoxicillin, and clarithromycin

- 10-14 day regiments favored over 7 day

22
Q

cancers associated with H. pylori

A
  • non-Hodgkins lymphoma and MALT lymphoma of the stomach
23
Q

ZES triad

A
  • gastric acid hypersecretion
  • severe peptic ulcer disease
  • non-beta islet cell tumors of pancrease
24
Q

gastrinoma

A
  • 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
25
Q

Menetriers disease

A
  • frequent in men over 50
  • vague epigastric discomfort, diarrhea, weakness, anemia, weight loss, edema secondary to protein loss (hypoalbuminemia)
  • treatment includes H2RAs, prednisone, and PPIs

Gastrointestinal System (12 decks)

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