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GI System > Session 4- Gastric disease > Flashcards

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
Q

where are H pylori normally found in the stomach

A

antrum

26
Q

how do we diagnosis H pylori

A

urease breath test
stool antigen test
endoscopy with biopsy

27
Q

eradication of H pylori

A

proton pump inhibitor- PPI

2 x antibiotics - clarithromycin and metronidazole

28
Q

what are the stomac defences

A 
mucus layer 
HCO3- secretion 
mucosal blood flow
prostagandins
epithelial renewal
29
Q

what are the effects of NSAIDS

A

they prevent the release of prostaglandins which are needed to stimulate mucosal blood flow

30
Q

risk factors for peptic ulcer disease

A

H pylori
NSAIDS
smoking
massive physiological stress- burn

31
Q

what is teh difference beween acute and chronic ulcers

A

acute ulcers develop as a part of acute gastritis

chronic ulcers occur at the mucosal junctions

32
Q

morphology of Peptic ulcer disease

A

erosion to yhe muscularis externa which is replaced by scar tissue

this narrows the stomach lumen causes pyloric stenosis

33
Q

what artery can stomach ulcers erode into

A

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
Q

symptoms of PUD

A

epigastric pain leading to back pain

pain at night- duodenal ulcers

early satiety

weight loss

35
Q

management of PUD if H pylori is involved and there is no active bleeding

A

eradicate H pylori through PPI and 2 antibiotics which promotes ulcer healing

36
Q

management of PUD if H pylori isnt involved and there osnt active bleeding

A

stop NSAIDS

37
Q

if there is active bleeding how do we manage a PUD

A

adrenaline injected

cauteru

clip application

38
Q

What basic factors (related to the stomach and abdomen) contribute to Gastro Oesophageal Reflux Disease (GORD)?

A

Incompetent LOS raised intraabdominal pressure (after meals, obesity, pregnancy) and
delayed gastric emptying.

39
Q

State three lifestyle changes that can improve symptoms associated with GORD

A

Weight loss, avoid trigger foods, smaller meals, eating earlier in the evening, propping up in
bed with pillows etc

40
Q

Briefly describe the components of the lower oesophageal sphincter mechanism and how
they prevent reflux

A

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

GI System (16 decks)

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