Stomach Flashcards
(45 cards)
What are acute gastritis and gastropathy?
Acute gastritis:
-inflammation of the gastric mucosa w/ inflammatory cells
Gastropathy:
-inflammation of the gastric mucosa w/o inflammatory cells
What are causes of acute gastritis?
-alcohol
-tobacco
- medications (NSAIDs/steroids)
- shock
- radiation/chemo
- infections (viral/H. pylori)
What are causes of gastropathy?
Chemical irritation:
- NSAIDs
- smoking
- acohol
Systemic effects:
- hypovolemia (burns)
- parasympathetic stimulation (brain lesions)
- DM
- portal HTN
What are the main causes of chronic gastritis?
- H. pylori infection (gastritis type B)
- autoimmune gastritis (gastritis type A)
What is type B gastritis?
(cause and presentation)
Antral-type/H. pylori gastritis:
- most common chronic gastristis (~90%)
- caused by chronic H. pylori infection
- predominantly in antrum of stomach
- typically asymptomatic w/ normal exam
How is type B gastritis diagnosed and treated?
Diagnosis (testing for H. pylori)
- fecal Ag test
- urea breath test (more to confirm eradication)
- endoscopy w/ biosy
Treatment (typically only w/ development of PUD or MALT lymphoma):
-eradication of H. pylori (double abx therapy with PPI)
How does type B gastritis appear on endoscopy?
-nodules between rugae
What complications are associated with type B gastritis?
- gastric adenocarcinoma/intestinal metaplasia
- MALT lymphoma
- PUD
- B12 deficiency/pernicious anemia*
- hypochlorhydria*
*less pronounced/common than in type A
How does acute gastritis due to H. pylori differ from chonic gastritis due to H. pylori?
acute typically will have increased acid production
chronic will typically have decreased acid produciton due to atrophy of gastric glands
What is type A gastritis?
(cause and presentation)
Fundus-type/autoimmune gastritis:
- less common chronic gastristis (~10%)
- caused by cell-mediated destruciton of parietal cells
- anti-parietal cell Abs (>90%)
- anti-intrinsic factor Abs (70%)
- predominantly in fundus (near esophagus) of stomach
- typically asymptomatic w/ normal exam but can present with symptoms of vitamin B12 deficiency (atrophic glossitis, megaloblastosis, and peripheral neruopathy)
How is type A gastritis diagnosed and treated?
Diagnosis (autoimmune/megaloblastic anemia detection)
- test for anti-parietal cell Abs and anti-IF Abs
- CBC (megaloblastic anemia)
- low B12
- elevated methylmalonic acid and homocysteine
- endoscopy w/ biosy
Treatment:
-B12 supplementation
How does type A gastritis appear on endoscopy?
-mucosal atrophy (rugae absent)
What complications are associated with type A gastritis?
- B12 deficiency/pernicious anemia*
- achlorhydria* -> hypergastrinemia (lack of acid inhibition of G cells) -> carcinoid/neuroendocrine tumor (5%)
- gastric adenocarcinoma/intestinal metaplasia
*more pronounced/common than in type B
What complications associated with chronic gastritis are unlikely in acute gastritis?
mucosal atrophy or intestinal metaplasia -> adenocarcinoma
gastric dysplasia (prolonged inflammatory damage/proliferative stimuli) -> carcinoma
How do NSAIDs and steroids cause gastropathy?
prostaglandins protection gastric mucosa by:
- inhibiting acid secretion
- stimulating mucous production
- stimulating bicarbonate secretion
NSAIDs:
-inhibit COX-1/2 preventing prostaglandin formation
Steroids:
-inhibit phospholipases which produce arachadonic acid which is a precursor to prostaglandins
What is an upper GI bleed and how does it present?
Describe the symptoms and what causes them.
GI bleeding from a source proximal to the ligament of Treitz (esophagus, stomach, duodenum)
-4x more common than LGIB
Presentaiton:
- hematemesis (either bright red blood or “coffee ground”)
- melena (dark, tarry stool; as little as 50mL of blood)
- hematochezia; mostly associated with LGIB but occurs with significant UGIB (bright red blood; >1000mL of blood)
frank blood (emesis or per recturm) -> likely more severe bleeing
coagulation and oxidation of heme by gastirc acid -> coffee ground ememsis
oxidation of heme by bacteria in intestine (slow process) -> melena
What are causes of upper GI bleeds?
- PUD
- esophageal varices
- hemorrhagic gastropathy/gastrisits
- Mallory-Weiss tear/Boerhaave syndrome
- Dieulafoy lesion
- GAVE syndrome
What is the difference between an erosion and an ulcer?
Depth:
- erosion is to the lamina propria
- ulcer is to the submucosa
What are peptic ulcers?
(where and why)
ulceration of the gastric mucosa from chronic gastritis
Duodenal ulcers:
- 90% of PUD
- almost entirely caused by H. pylori
- rarely caused by Zollinger-Ellison syndrome
Gastric ulcers:
-10% of PUD, mostly lesser curvature
- largely caused by H. pylori
- also caused by NSAIDs, glucocorticoids, smoking, and alcohol
Can also occur anywhere in the GI tract that gastric ectopia occurs
How do peptic ulcers present?
How does it differ for duodenal and gastric ulcers?
- epigastric gnawing or “hunger-like” pain
- pain is intermittent but occurs for weeks
- signs of UGIB
duodenal ulcer pain acutely IMPROVES with meals but worsens >1 hour after
gastric ulcer pain acutely WORSENS with meals
What do peptic ulcers looks like on endoscopy?
How do they appear different from malignant ulcers?
Ulcers:
-small (<3 cm), round, punched-out lesions
Malignant ulcers:
-large, irregular lesions
How are peptic ulcers treated?
- eradication of H. pylori (double abx therapy with PPI)
- cessation of other irritating factors (ie. NSAIDs, smoking, alcohol consumption)
- intervention for active bleeding
- biospy of gastric ulcers to r/o carcinoma
What are possible complications of peptic ulcers?
- UGIB (gastroduodenal A. and L gastric A.)
- perforation (mostly anterior) -> peritonitis and pneumoperitoneum
-perforation (when posterior) into liver or pancreas -> pancreatitis
- progression to gastric carcinoma (intestinal type); almost exclusively in gastric ulcers
- obstruction (when near pylorus)
What are the different types/causes of stress ulcers?
Medical/surgical stress ulcer:
-present in those with severe illness/shock (common in ICU patients)
Curling ulcer:
- severe burns (decreased plasma volume -> mucosal atrophy)
- “burned with a curling iron”
Cushing’s ulcers:
-brain lesions -> overstimulation of vagus nerve -> excess acid
