Stomach Flashcards

1
Q

what are the 4 areas of the stomach

A

fundus
body
antrum
pylorus

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2
Q

where does the oesophagus meet the stomach

A

cardia

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3
Q

what is the main function of the stomach

A

mixing of gastric secretions into chyme

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4
Q

what happens in the orad region of the stomach

A

no slow wave activity

weak tonic contractions move gastric contents into the caudad region

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5
Q

what happens in the caudad region of the stomach

A

slow wave activity occurs

peristalsis pushes chyme along pylorus then retropulsion occurs

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6
Q

what is retropulsion

A

rebound of chyme against distal antrum into the body to allow further mixing of chyme into small particles

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7
Q

where in the stomach does most of the mixing of chyme take place

A

antrum

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8
Q

what factors promote the emptying of the stomach (gastric factors)

A

large volume of chyme

thin consistency of chyme

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9
Q

what factors delay the release of chyme (duodenal factors)

A

enterogastric reflexes

hormonal response - CCK and secretin

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10
Q

what is the enterogastric reflex

A

duodenum signals to the stomach that it has enough chyme causing peristalsis to slow down

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11
Q

where are the pyloric gland and oxyntic glands located

A

pyloric - antrum

oxyntic - fundus and body

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12
Q

what cells are within pyloric gland and what do they secrete

A

D cells - somatostatin

G cells - gastrin

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13
Q

what cells are within oxyntic gland and what do they secrete

A

parietal cells - HCl and intrinsic factor
enterochromaffin like cells - histamine
chief cells - pepsinogen

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14
Q

what does intrinsic factor do

A

binds to vitamin B12 to help with digestion

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15
Q

what do gastrin and histamine do

A

stimulate secretion of HCl

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16
Q

what does somatostatin do

A

inhibit secretion of HCl

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17
Q

how is HCl secreted from gastrin and histamine

A

CO2 and H2O form carbonic anhydrase - dissociates into H+ and HCO3
HCO3 is pumped out via antiporter exchanged for Cl-
Cl- is pumped out via CFTR channel
H+ leaves via proton pump and H+ and Cl- bind

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18
Q

what are secretagogues and give examples

A

substances that stimulate production of HCl

eg histamine, gastrin and ACh

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19
Q

what are the 3 phases of gastric secretions

A

cephalic phase
gastric phase
intestinal phase

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20
Q

describe the cephalic phase

A

stomach prepared for good. conditioned by chewing/swallowing, causes increased gastric secretions from secretagogues

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21
Q

describe the gastric phase

A

when food is in the stomach

distension of stomach causes mechanoceptors to increase secretions

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22
Q

describe the intestinal phase

A

once the food has left the stomach

gastric secretions stopped through the release of CCK and somatostatin

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23
Q

name groups of drugs that influence gastric acid secretion

A

PPIs
H2 receptor antagonists
Muscarinic receptor antagonists
NSAIDs

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24
Q

what is contained within normal gastric mucosa to prevent irritation

A

contains mucus as physical barrier

contains HCO3 to buffer the mucosa

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25
Q

what effect does prostaglandin have on mucosa

A

increases mucus and HCO3 production and increases blood flow therefore preventing gastric irritation

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26
Q

what effect do NSAIDs have on gastric mucosa

A

inhibit prostaglandin production though COX1 causing less mucus and decreased blood flow - increases change of developing peptic ulcer and bleeding

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27
Q

give an example of a PPI and when/route of administration

A

omeprazole

orally before breakfast

28
Q

how to PPIs work

A

inhibit the proton pump preventing secretion of acid

only active at low pH

29
Q

give an example of a H2 receptor antagonist and when to administer

A

ranitidine or cimetidine

take orally once/twice daily

30
Q

how do H2 receptor antagonists work

A

competitive antagonist of H2 receptor which reduces acid secretion from ACh

31
Q

what are the causes of acute gastritis

A

irritants/chemicals
trauma
severe burns

32
Q

what are the symptoms of acute gastritis

A

sudden onset of epigastric pain

vomiting (possibly with blood)

33
Q

what are the causes of chronic gastritis

A

autoimmune
bacterial - H. Pylori
chemical - NSAIDs alcohol

34
Q

what autoimmune conditions are associated with chronic gastritis

A

anti-parietal and anti-intrinsic factor antibodies - increased risk of malignancy with these conditions

35
Q

what are the symptoms of chronic gastritis

A

epigastric pain
reflux
vomiting
feeling full after eating

36
Q

what are 4 complications of chronic gastritis

A

ulceration
perforation
bleeding
stenosis

37
Q

what investigations are recommended for chronic gastritis

A

endoscopy

test for H. pylori

38
Q

what is the treatment for chronic gastritis

A

antacids, PPIs
antibiotics if H. Pylori
eat smaller more frequent meals

39
Q

what are benign gastric tumours known as

A

polyps - most common is adenoma

40
Q

what are the symptoms of polyps

A

usually asymptomatic but if perforate may cause bleeding

41
Q

what causes gastric polyps

A

chronic gastritis
familial adenomatous polyposis (FAP genetic condition)
drugs triggers typically PPIs

42
Q

do polyps need removed and why

A

yes - metastatic tissue that does have malignant potenial

removed at endoscopy on biopsy

43
Q

what types of malignant gastric cancers can arise

A

adenocarcinoma

lymphomas from MALT - mucosal associated gut lymphoid tissue

44
Q

what are the main symptoms of gastric cancer

A

weight loss
anaemia
haematemesis
palpable mass

45
Q

how does H. pylori increase risk of developing cancer

A

H pylori - chronic gastritis - metaplasia - dysplasia - adenocarcinoma

46
Q

how and where is gastric adenocarcinoma likely to spread to

A

lymph nodes
haematogenous - liver metastases
direct invasion - ovaries and peritoneal cavity

47
Q

what is the treatment for gastric cancer

A

no mets - curative surgery

mets - palliation as chemo has little success

48
Q

what is gastroparesis

A

delayed gastric emptying

49
Q

what causes gastroparesis

A
idiopathic 
diabetes 
cannabis 
drugs eg opiates 
systemic disease (sclerosis)
50
Q

what are the classical symptoms of gastroparesis

A

feeling full easily
nausea/vomiting
upper abdominal pain
weight loss

51
Q

what is the main treatment for gastroparesis

A

remove precipitating factor
liquid diet/small portion
pro-motility drug

52
Q

define peptic ulcer disease

A

breach in gastric mucosa by acid/pepsin due to imbalance of gastro-protective factors and mucosal injurious substances

53
Q

what are the main causes of peptic ulcer disease

A

H. Pylori infection
NSAIDs
idiopathic associated with IBS

54
Q

what are the symptoms of peptic ulcer disease

A

epigastric pain (radiates to back)
relapsing/remitting symptoms
pain relieved by eating - gastric ulcer
pain on eating - duodenal ulcer

55
Q

what sort of bacterium is H. Pylori and how does it cause peptic ulcer disease

A

grame -ve flagellated bacillus

increases acid secretion causing erosion of the stomach

56
Q

how is H. Pylori spread

A

faecal-oral or oral-oral

acquired in infancy but doesnt cause disease until later life

57
Q

what investigations are required for diagnosing H. Pylori

A

urease breath test
serology for IgA
stool sample for FAT (faecal antigen test)
possible endoscopy and biopsy

58
Q

if someone has H. pylori -ve peptic ulcer disease what is the treatment

A

anti-secretory therapy eg PPI and antacid

remove NSAIDs

59
Q

if someone has H. pylori +ve peptic ulcer disease what is the treatment

A

triple therapy

PPI + amoxicillin + clarythromycin for 1 week

60
Q

what are the main complications of peptic ulcer disease

A

bleeding
perforation
anaemia

61
Q

where in the GI tract is a peptic ulcer more likely to arise

A

duodenum followed by stomach

62
Q

functional dyspepsia is more common than organic dyspepsia true/false

A

true

63
Q

which individuals are at risk of developing GI infections

A
malnutrition deficiencies 
immunocompromised individuals 
closed communities eg ward 
extremes of age 
gastric acid secretion suppression
64
Q

what is dysentry

A

inflammation of the intestine esp colon

causes bloody diarrhoea with mucus and associated with gastroenteritis

65
Q

name some organisms causing gastroenteritis that have short incubation times (1-6 hours)

A

staph aureus

bacillus cereus

66
Q

name some organisms causing gastroenteritis that have medium incubation times (12-48 hours)

A

salmonella

C. perfringes

67
Q

name some organisms causing gastroenteritis that have long incubation times

A

campylobacter

E. Coli 0157