Stomach Flashcards

0
Q

Explain what shall omphalocele?

How does a Dr distinguish gastroschisis from omphalocele?

A

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

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1
Q

Explain gastroschisis

A

Congenital malformation of abdominal wall -> extrusion of AB contents
through AB folds
not covered by Peritoneum

It’s a lateral fold closure defect

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2
Q

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?

A

Smooth-muscle hypertrophy @pylorus

Two weeks after birth

Builder pressure + stomach – >
(non-bilious projectile vomiting) +
(strong peristalsis = visible) +
(feel olive like mass = pylorus)

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3
Q

Give a global summary of gastritis (Acute + chronic)

A

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

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4
Q

What cell produces the mucus and the HCO3 layer?

Give 5 reasons why we can get the acute gastritis

A

Foveolar cells - I CAN BS

  1. brain injury – >
    increased ICP = Cushing also – >
    increased vagal stimulation – >increased ACh –>
    increased parietal cell acid produce= ACID damage
  2. chemotherapy – >knock out fast turning oversells – >can’t regenerate cells @ stomach mucosa
    – >decreased mucosal protection
  3. alcohol heavy = toxin – >damage mucosa – >acid damages stomach
  4. NSAIDs – >decreased PGE2 – >decreased acid production, mucus, bicarb, bloodflow to mucosal barrier – >decreased protection = sluff gastric mucosa
  5. burns/curling ulcer + shock – >
    Hypovolaemia – > Decreased blood flow to stomach – > mucosa does not receive enough oxygen +
    blood not removing enough acid
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5
Q

As a result of acid damage what three things Happen to the mucosal layer

A

Superficial inflammation = damaged epithelium

Erosion = lose epithelium

Ulcer = not out entire mucosal layer

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6
Q

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?

A

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

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7
Q

How does the chronic inflammation lead to gastric carcinoma?

A

CI – >lots of inflammatory cells @stomach – > form peyers patch @ stomach = intestinal metaplasia– >Increased risk of gastric carcinoma

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8
Q

Explain type B chronic gastritis?
Where in the stomach does it occur?
Explain pathogenesis

A

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

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9
Q

What’s three things do triple therapy resolve?

A

Ulceration – it was gastritis
Cancer – resolve intestinal metaplasia
Lymphoma – resolve inflammatory infiltrate

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10
Q

If you want to check for H pylori what two things can you check for?

A

Check for urea in breath

Check for H. pylori antigen @stool

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11
Q

Explain Menetrier disease

What is the risk of occurring ?

A

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

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12
Q

In peptic Ulcer disease what do you get and what are their respective percentages?

A

Solitary mucosal also involving
– Proximal duodenum = 90%
– distal stomach = 10%

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13
Q

Explain Zollinger-Ellison syndrome

A

Gastronoma Tumour produces XS gastrin
– >increased serum gastrin – >parietal cells secrete more H+ – >
peptic ulcer disease with duodenal ulcer

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14
Q

Comparing gastric ulcers with duodenal ulcers

A

Look at book and pic in phone date 3/3/15

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15
Q

What is a gastric carcinoma

A

Malignant proliferation of surface epithelial cells = columnar

16
Q

What are the two types of gastric adenocarcinomas

A

Intestinal gastric carcinoma

Diffuse type gastric carcinoma

17
Q

Explain intestinal gastric carcinoma

A

Large and itregular ulcers with heaped up margins

@Lesser curvature of antrum

18
Q

What are the risk factors for intestinal gastric carcinoma

A
Chronic autoimmune gastritis
H pylori
Achlorhydria + type A blood
Nitrosamines
Smoking
19
Q

How is diffuse type gastric carcinoma different from intestinal gastric carcinoma

A

Not associated with nitrosamines

No intestinal metaplasia

No H. pylori involved

20
Q

Histologically what do you see in diffuse type gastric carcinoma

A

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)

21
Q

How does a person with this type gastric carcinoma present

A

Weight loss, abdominal pain, anaemia

early satiety - thickening + fibrosis of wall -> stomach cannot expand with food

22
Q

What are clinical signs of gastric carcinoma

A

Acanthosis nigricans – thick dark skin @ axilla

Leser Trélat + – dozens of seborrhoeic keratosis

23
Q

What node does gastric carcinoma Spread to

A

Left supra clavicular node - Virchow node

24
Q

What organ does distant stomach metastases involve?
Where does the intestinal type metastasised to?
Where does the diffuse type Metastasise to?

A

Liver

Periumbilical region – Sister Mary Joseph not you

Bilateral ovaries – Krukenberg tumour