Stomach Flashcards
Explain what shall omphalocele?
How does a Dr distinguish gastroschisis from omphalocele?
Congenital malformation of ant. abdominal wall with
persistence of herniation of ab-contents/bowel into umbilical cord
sealed by peritoneum
due to lateral fold closure problem
The contents are covered by
peritoneum and amnion
of the umbilical cord
therefore distinguishing gastroschisis
Explain gastroschisis
Congenital malformation of abdominal wall -> extrusion of AB contents
through AB folds
not covered by Peritoneum
It’s a lateral fold closure defect
What is pyloric stenosis due to?
When does pyloric stenosis occur?
As a result Pressure in the stomach what does the patient presents with?
Treatment?
Smooth-muscle hypertrophy @pylorus
Two weeks after birth
Builder pressure + stomach – >
(non-bilious projectile vomiting) +
(strong peristalsis = visible) +
(feel olive like mass = pylorus)
Give a global summary of gastritis (Acute + chronic)
Acute = surface of stomach burning by acid i.e.
Increased acid production/degrees protection from mucosa = Erosive
Chronic = Nonerosive
chronic AutoImm gastritis /Chronic H. pylori gastritis
What cell produces the mucus and the HCO3 layer?
Give 5 reasons why we can get the acute gastritis
Foveolar cells - I CAN BS
- brain injury – >
increased ICP = Cushing also – >
increased vagal stimulation – >increased ACh –>
increased parietal cell acid produce= ACID damage - chemotherapy – >knock out fast turning oversells – >can’t regenerate cells @ stomach mucosa
– >decreased mucosal protection - alcohol heavy = toxin – >damage mucosa – >acid damages stomach
- NSAIDs – >decreased PGE2 – >decreased acid production, mucus, bicarb, bloodflow to mucosal barrier – >decreased protection = sluff gastric mucosa
- burns/curling ulcer + shock – >
Hypovolaemia – > Decreased blood flow to stomach – > mucosa does not receive enough oxygen +
blood not removing enough acid
As a result of acid damage what three things Happen to the mucosal layer
Superficial inflammation = damaged epithelium
Erosion = lose epithelium
Ulcer = not out entire mucosal layer
What is type A chronic gastritis due to?
Where in the stomach does it occur?
What cell affect?
Pathogenesis of type a autoimmune chronic gastritis?
Type 4 HSR Autoimmune destruction = T-cell mediated damage @Fundus + body of Parietal cell
– >
side-effect of damage = auto AB against parietal cell + intrinsic factor – >
– Knockout thickness of mucosa = mucosal atrophy
– achlorhydria = decreased acid production – > increased gastrin = G cell hyperplasia
No intrinsic factor –> can’t absorb vitamin B12 – > megaloblastic/pernicious anaemia
How does the chronic inflammation lead to gastric carcinoma?
CI – >lots of inflammatory cells @stomach – > form peyers patch @ stomach = intestinal metaplasia– >Increased risk of gastric carcinoma
Explain type B chronic gastritis?
Where in the stomach does it occur?
Explain pathogenesis
Due to age pylori
Induces a + C inflammation – >gastritis = Not in bed mucosa only sit at mucosa
H pylori makes urease + proteases – > NH3
– > Inflammation + weakening of mucosal defences
– >
MALT lymphoma, ULCER, Gastric adenocarcinoma
What’s three things do triple therapy resolve?
Ulceration – it was gastritis
Cancer – resolve intestinal metaplasia
Lymphoma – resolve inflammatory infiltrate
If you want to check for H pylori what two things can you check for?
Check for urea in breath
Check for H. pylori antigen @stool
Explain Menetrier disease
What is the risk of occurring ?
Gastric hyperplasia of mucosa – >hypertrophied ruggae – >
(XS new production – >protein loss) +
(parietal cell atrophy – >decreased acid production)
Precancerous = ruggae of stomach = hypertrophy = look like brain Gyri
In peptic Ulcer disease what do you get and what are their respective percentages?
Solitary mucosal also involving
– Proximal duodenum = 90%
– distal stomach = 10%
Explain Zollinger-Ellison syndrome
Gastronoma Tumour produces XS gastrin
– >increased serum gastrin – >parietal cells secrete more H+ – >
peptic ulcer disease with duodenal ulcer
Comparing gastric ulcers with duodenal ulcers
Look at book and pic in phone date 3/3/15
What is a gastric carcinoma
Malignant proliferation of surface epithelial cells = columnar
What are the two types of gastric adenocarcinomas
Intestinal gastric carcinoma
Diffuse type gastric carcinoma
Explain intestinal gastric carcinoma
Large and itregular ulcers with heaped up margins
@Lesser curvature of antrum
What are the risk factors for intestinal gastric carcinoma
Chronic autoimmune gastritis H pylori Achlorhydria + type A blood Nitrosamines Smoking
How is diffuse type gastric carcinoma different from intestinal gastric carcinoma
Not associated with nitrosamines
No intestinal metaplasia
No H. pylori involved
Histologically what do you see in diffuse type gastric carcinoma
Signet ring cell diffusely infiltrated
(Mucin production ⬆️-> pushes nucleus to the edge)
In the gastric wall we see:
cancer
+
desmoplasia (thickening of stomach wall = linitis plastica = in response to tumour have reactive response to stroma and get fibrous tissue + blood vessels)
How does a person with this type gastric carcinoma present
Weight loss, abdominal pain, anaemia
early satiety - thickening + fibrosis of wall -> stomach cannot expand with food
What are clinical signs of gastric carcinoma
Acanthosis nigricans – thick dark skin @ axilla
Leser Trélat + – dozens of seborrhoeic keratosis
What node does gastric carcinoma Spread to
Left supra clavicular node - Virchow node
