Session 4- Gastric disease Flashcards

1
Q

how do most pathological conditions of tbe stomach arise

A

inability of the stomach to protect itself from it acidic contents

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2
Q

what is dyspepsia

A

complex of upper GI symptoms which are typically present for 4 or more weeks

  • upper abdominal pain or discomfort
  • heartburn
  • acid reflux
  • nausea
  • vomiting
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3
Q

common triggers for GORD

A
Altered LOS function
delayed gastric emptying 
obesity 
pregnancy
smoking
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4
Q

treatment for GORD

A

lifestyle modidications

pharmacological interventions

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5
Q

what is GORD

A

gastro-oesophageal reflux disease

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6
Q

what are the consequences of GORD

A

reflux of the acidic stomach contents into the oesophagus can lead to metaplasia of the loweer oesophageal epithelia- Barret’s oesophagus

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7
Q

gastritis

A

inflammatory process in the stomach mucosal layer

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8
Q

what causes acute gastritis

A

heavy NSAID use or excessive alchohol consumption

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9
Q

what causes chronic gastritis

A

H-pylori infection

autoimmune- antibodies against gastic parietal cells

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10
Q

what is H pylori

A

a gram negative bacterium well adapted to the acidic environment of the stomach.
It produces ureases which allow it to produce ammonium from the urea present in the stomach- withstand acidic conditions in the stomach

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11
Q

what effect does H pylori have

A

damages the epithelia of stomach an dis pro-inflammatory

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12
Q

what is peptic ulcer disease

A

breach in the gastric or duodenal mucosa that EXTENFS THROUGH THE MUSCULARIS MUCOSA

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13
Q

treatment of chronic ulcer disease

A

removing the exacerbating factors - H pylori, NSAIDS, reducing acus

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14
Q

pharmalogical intervention to gastric diseases

A

they are a result of acid damage to teh mucosa

therefore they target the parietal cell at either the proton pumo or the H2 receptor

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15
Q

Hiatus hernia

A

herniation of the stomach through the diaphragm into the thorax when the LOS herniates through the diaphragm and ends up in the thorax it looses its function

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16
Q

mechanism of the LOS

A

muscular element- intrinsic muscles that contract to close it

as the oesophagus pierces the diaphragm it comes through the crural part - right crus- muscular element that helps to contract the sphincter - when pressure increases it closes the LOS off

travels obliquely into the stomach

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17
Q

what is the normal state of teh LOS

A

normally contracted

only relaxes when it detects food moving through the oesophagus

18
Q

what epithelial change occur in barrets oesophagus

A

repeated exposure to gastric elements causes the reversible change of stratified squamous to become columnar cells w

19
Q

adenocarcinoma

A

glandular cancer in oesophagus

20
Q

how is GORD treated surgically

A

fundoplication

-fundus of stomach wrapped around the oesophagus to help with sphincter mechanism

21
Q

pathological changes that occur in gastrtis

A

epithelial damage
epithelial hyperplasia
vasodilataion
neutrophil response

OR

lymphocyte respinse
glandular atrophy
fibrotic changes

22
Q

automimmune cause of gastritis

A
  1. antibodies to parietal cells
  2. lose parietal cells
  3. reduction in acid and intrinsic factor production
  4. atrophy of body of stomach
23
Q

what is intrinsic factor essential for

A

absorption of b12 in the ileum

24
Q

symptoms of gastritis

A

megaloblastic anaemia
neurological symptoms
anorexia
glositis

25
where are H pylori normally found in the stomach
antrum
26
how do we diagnosis H pylori
urease breath test stool antigen test endoscopy with biopsy
27
eradication of H pylori
proton pump inhibitor- PPI | 2 x antibiotics - clarithromycin and metronidazole
28
what are the stomac defences
``` mucus layer HCO3- secretion mucosal blood flow prostagandins epithelial renewal ```
29
what are the effects of NSAIDS
they prevent the release of prostaglandins which are needed to stimulate mucosal blood flow
30
risk factors for peptic ulcer disease
H pylori NSAIDS smoking massive physiological stress- burn
31
what is teh difference beween acute and chronic ulcers
acute ulcers develop as a part of acute gastritis chronic ulcers occur at the mucosal junctions
32
morphology of Peptic ulcer disease
erosion to yhe muscularis externa which is replaced by scar tissue this narrows the stomach lumen causes pyloric stenosis
33
what artery can stomach ulcers erode into
gastro-duodenal artery causing the stomach to fill with blood this causes malaena as the haem component is oxidised by passing through GI tract which causes black faeces
34
symptoms of PUD
epigastric pain leading to back pain pain at night- duodenal ulcers early satiety weight loss
35
management of PUD if H pylori is involved and there is no active bleeding
eradicate H pylori through PPI and 2 antibiotics which promotes ulcer healing
36
management of PUD if H pylori isnt involved and there osnt active bleeding
stop NSAIDS
37
if there is active bleeding how do we manage a PUD
adrenaline injected cauteru clip application
38
What basic factors (related to the stomach and abdomen) contribute to Gastro Oesophageal Reflux Disease (GORD)?
Incompetent LOS raised intraabdominal pressure (after meals, obesity, pregnancy) and delayed gastric emptying.
39
State three lifestyle changes that can improve symptoms associated with GORD
Weight loss, avoid trigger foods, smaller meals, eating earlier in the evening, propping up in bed with pillows etc
40
Briefly describe the components of the lower oesophageal sphincter mechanism and how they prevent reflux
The acute angle of entry of the oesophagus into the stomach Intrinsic smooth muscle of the LOS Crural part of the diaphragm has smooth muscle that is distinct from the rest of the diaphragm. The right crus forms a sling around the lower oesophagus which tightens when intraabdominal pressure rises. The smooth muscle elements of the LOS contract when pressure in the stomach rises