4. Stomach And Pathology Flashcards

(37 cards)

1
Q

Epithelium above and below pyloric sphincter

A

Oesophagus- stratified squamous
Stomach- simple columnar

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2
Q

What causes receptive relaxation of proximal stomach?

A

Peristalsis in oesophagus, alerts stomach somethings entering

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3
Q

Which part of diaphragm contributes to pyloric sphincter?

A

Crural part

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4
Q

In receptive relaxation, what distends?

A

Fundus

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5
Q

Is upper stomach more muscular than lower?

A

No

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6
Q

What are gastric pits made from?

A

Invaginations of stomach epithelia

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7
Q

How many gastric glands per gastric pit?

A

1 or multiple

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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

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9
Q

What receptor does gastrin stimulate on parietal cells? How?

A

CCK, similar structures

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10
Q

Stimulation of entero-chromaffin like cells (ECL)

A

-vagal by ACh
-gastrin from G cells

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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

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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

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13
Q

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

A

Sustained increased pressure overcomes the lower oesophageal sphincter

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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

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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
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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?

20
Q

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

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
Whats meant by H pylori being microaerophilic?
Needs some O2 but less than atmospheric, so stomach is perfe t level
26
Features of H pylori that enable its survival
-flagellae -chemotaxis - under mucous layer of epithelium -adhesins - fix to epithelium and resists peristalsis
27
Explain different products made by H pylori causing gatsritis
-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
Compare effects of H pylori in antrum vs body/fundus
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
Is colonisation of antrum and body by H pylori asymptomatic?
Yes
30
Explain process of diagnosing H pylori
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
Treatment for eradication of H pylori
-PPI -2x antibiotics (clarithromycin and metronidazole) 7 days
32
Compare the following characteristics for gastric and duodenal ulcers -incidence -age -blood group -acid levels -H pylori
- 1:3 -increase/up to 35 -A vs O -could be low/ could be high -70% vs 95-100%
33
Where do chronic ulcers develop?
Mucosal junctions e.g. antrum meets body, antrum meets small intestine
34
Effects of scar tissue formed from peptic ulcer disease
Narrows stomach lumen, pyloric stenosis so vomiting
35
How does haematemesis happen with ulcers of duodenum?
-ulcer can erode into gastroduodenal artery -blood fills stomach, vomit it -or could be partly digested and excreted as malaena
36
Management of PUD if active bleeding
Endoscopy inject adrenaline and cautery
37
Management of PUD with no active bleeding
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