4. Stomach And Pathology Flashcards Preview

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Flashcards in 4. Stomach And Pathology Deck (37)
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1
Q

Epithelium above and below pyloric sphincter

A

Oesophagus- stratified squamous
Stomach- simple columnar

2
Q

What causes receptive relaxation of proximal stomach?

A

Peristalsis in oesophagus, alerts stomach somethings entering

3
Q

Which part of diaphragm contributes to pyloric sphincter?

A

Crural part

4
Q

In receptive relaxation, what distends?

A

Fundus

5
Q

Is upper stomach more muscular than lower?

A

No

6
Q

What are gastric pits made from?

A

Invaginations of stomach epithelia

7
Q

How many gastric glands per gastric pit?

A

1 or multiple

8
Q

Compare the resting and active states of parietal cells

A

Resting
-tubulovesicles containing proton pumps not associated with apical membrane
-lack K+ permeability

Active
-tubulovesicles in contact with apical membrane
-K+ channelsand proton pumps brough together
-cannaliculi and microvilli on apical membrane increase SA

9
Q

What receptor does gastrin stimulate on parietal cells? How?

A

CCK, similar structures

10
Q

Stimulation of entero-chromaffin like cells (ECL)

A

-vagal by ACh
-gastrin from G cells

11
Q

Explain histamine stimulation in parietal cells

A

-Either vagal or gastrin acting on CCK receptors stimaultes ECL cells to produce histamine
-Histamine acts on H2 receptors of parietal cells to increase acid production

12
Q

Describe alkaline tide in relation to HCl production in parietal cells

A

-HCO3- is transported out of parietal cell into blood via anion anti-port protein, whilst Cl- goes into parietal cells
-this creates an alkaline tide in blood
-Cl- combines with H+ from parietal cell in the lumen of stomach

13
Q

How is delayed gastric emptying a risk factor for gastro-oesophageal reflux disease?

A

Sustained increased pressure overcomes the lower oesophageal sphincter

14
Q

What is a hiatus hernia? How does it form?

A

In people with GORD, part of stomach can herniate through diaphragm into thorax, so LOS now in thorax
-loses crural muscle action on sphincter, so reflux a lot

15
Q

Name 3 things that help the LOS

A
  1. Muscles: intrinsic and diaphragm
  2. Right crus, pulls tighter when pressure higher
  3. Acute angke of oesophageal entry to stomach, orevents reflux straight back up
16
Q

What must an ulcer pass through to class as an ulcer?

A

Muscularis mucosae

17
Q

Name 6 lifestyle changes to manage GORD

A
  1. Weight loss
  2. Avoid trigger foods
  3. Eat smaller meals
  4. Dont eat then sleep
  5. Decrease alcohol and caffeine
  6. Stop smoking
18
Q

Describe the surgery for GORD

A

Fundoplication
-fundus wrapped round back of oesophagus, anchors it below diaphragm to help sphincter mechanism

19
Q

What layer of stomach is inflamed in gastritis?

A

Mucosa

20
Q

In gastritis, what cells could be seen in lamina propria on histology?

A

Neutrophils

21
Q

Pathological changes in acute gastritis

A

-epihtelial damage
-epithelial hyperplasia
-vasodilation = angry looking
-neutrophil response

22
Q

Pathological changes in chronic gastritis

A

-lymphocytes invade lamina propria
-glandular atrophy
-Fibrotic changes
-Metaplastic changes

23
Q

Explain how autoimmune chronic gastritis can cause pernicious anaemia

A

-autoimmune antibodies to parietal cells, lose parietal cells
-less acid and intrinsic factor
-less absoroption of B12
-can cause megaloblastic anaemia as DnA synthesis halted in RBCs, so abnormally large cytoplasm

24
Q

Symptoms of autoimmune chronic gastritis take time. What are they?

A

-anaemia
-neurological
-anorexia
-glossitis

25
Q

Whats meant by H pylori being microaerophilic?

A

Needs some O2 but less than atmospheric, so stomach is perfe t level

26
Q

Features of H pylori that enable its survival

A

-flagellae
-chemotaxis - under mucous layer of epithelium
-adhesins - fix to epithelium and resists peristalsis

27
Q

Explain different products made by H pylori causing gatsritis

A

-urease: converts Urea and H2O to CO2 and ammonia, ammonia damages stomach epithelium

-cytotoxin associated gene A gets into epithelia and stimulates IL-8 = inflammation

-Vacuolating toxin A is toxic to epithelium

28
Q

Compare effects of H pylori in antrum vs body/fundus

A

Antrum:
-G cells overactive so parietal cells increase number and acid
- hyme leaving stomach is more acidic

Body/fundus
-atrophy of parietal cells
-precursor to dysplasia

29
Q

Is colonisation of antrum and body by H pylori asymptomatic?

A

Yes

30
Q

Explain process of diagnosing H pylori

A

Urease breath test
-patient ingests urea enriched with C13
-if urease oressnt, C13 converted to COW
-CO2 excreted in breath and would comtain isotope C13

31
Q

Treatment for eradication of H pylori

A

-PPI
-2x antibiotics (clarithromycin and metronidazole)
7 days

32
Q

Compare the following characteristics for gastric and duodenal ulcers
-incidence
-age
-blood group
-acid levels
-H pylori

A
  • 1:3
    -increase/up to 35
    -A vs O
    -could be low/ could be high
    -70% vs 95-100%
33
Q

Where do chronic ulcers develop?

A

Mucosal junctions e.g. antrum meets body, antrum meets small intestine

34
Q

Effects of scar tissue formed from peptic ulcer disease

A

Narrows stomach lumen, pyloric stenosis so vomiting

35
Q

How does haematemesis happen with ulcers of duodenum?

A

-ulcer can erode into gastroduodenal artery
-blood fills stomach, vomit it
-or could be partly digested and excreted as malaena

36
Q

Management of PUD if active bleeding

A

Endoscopy inject adrenaline and cautery

37
Q

Management of PUD with no active bleeding

A

H pylori positive
-eradicate H pylori first via PPI and 2 antibiotics

H pylroi negative
-stop exacerbating meds
-can add in PPIs to offset meds if cant stop them