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MD3002 > treatment of peptic ulcers > Flashcards

treatment of peptic ulcers Flashcards

1
Q

what do oxyntic cells produce

A

HCl, pepsinogen, intrinsic factor, mucus

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2
Q

what do pyloric glands secrete

A

mucus to protect the mucosa

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3
Q

how do oxyntic cells form HCl

A

hydrogen pottasium pump in the villus like projections of the oxyntic cells

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4
Q

what do ECL cells produce in response to gastrin

A

histamine

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5
Q

where are ECL cells found

A

deep in the oxyntic gland

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6
Q

where is gastrin formed

A

in the antrum of the stomach

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7
Q

what are the two forms of gastrin

A

G-34 and G-17

17 is more common

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8
Q

what do ECL cells stimulate

A

HCL release

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9
Q

why is gastric secretion inhibited

A
  • distention of the small bowel
  • acid in the upper intesting
  • presence of protein breakdown products
  • irritation of the mucosa
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10
Q

what hormone opposes gastric secretion

A

secretin

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11
Q

what is the pathogenesis of an H.pylori infection

A

H. pylori invades the mucus layer
it secretes urease in order to neutralise the gastric acid
it damages the mucus layer and mucosa leading to inflammation and mucosal cell death

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12
Q

what can H. pylori infection lead to

A

peptic ulcer disease
gastric carcinoma
MALT lymphoma

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13
Q

what is a MALT lymphoma

A

B cells become abnormal and grow in an uncontrolled way

affects mucosa associated lymphoid tissue

usually occurs after long term inflammation
strongly associated with H.pylori

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14
Q

what are the symptoms of H. pylori infection

A

acute infection
nausea, dyspepsia, malaise, halitosis
gastric mucosa is inflammed with neutrophils and inflammatory cells with marked lymphocyte penetration
stomach acid production falls

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15
Q

what affects the outcome of H. pylori infection

A 
pattern of inflammation 
host response
virulence, 
environmental factors
patients age
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16
Q

what are the features of antral predominant gastritis

A 
stimulates G cells
increased gastric acid output 
gastric metaplasia of duodenum
colonisation of duodenum
duodenal ulceration and cancer
17
Q

what are the features of pangastritis

A 
G- cell stimulation 
inflammation prevents acid production 
decreased gastric acid output 
gastric atrophy
gastric ulceration 
adenocarcinoma
18
Q

what are the consequences of helicobacter infection

A 
• Peptic	ulcer	disease
• Distal	gastric	adenocarcinoma
• Primary	gastric	mucosa	associated	lymphoic tissue	
lymphoma	 (MALT)
• Dyspepsia
• Atrophic	gastritis
• Iron	deficiency	anaemia
• Idiopathic	thrombocytopaenic purpura
19
Q

how does the urea breath test work

A

pts swallow urea labelled with an isotope
bacteria will split the urea into carbon dioxide and ammonia
the carbon dioxide isotope is exhaled and detected

20
Q

how is damage to the mucosa reduced

A

diet change
antacids
bismuth salts

21
Q

how is peptic ulcer disease managed

A

antibiotics
proton pump inhibitors
H2 blockers

22
Q

how is H. pylori killed

A

proton pump inhibitor
ampicillin
clarythromycin or metronidazole

23
Q

how are antihistamines 2 used to treat peptic ulcers

A

reduce gastric acid

eg CIMETIDINE
now RANITIDINE is used

24
Q

what are the features of ranitidine

A
  • Similar indication to cimetidine
  • Now available over the counter (OTC)
  • Well absorbed orally (50%0
  • Half like 2-2.5 hours
  • Renal excretion
  • Malaise and dizziness
  • Liver toxicity
  • Increased risk of GI infection
25
Q

what is omeprazole

A

proton pump inhibitor

26
Q

what are the side effects of omeprazole

A

• Central nervous system: headache (7%), dizziness (2%)
• Respiratory: upper respiratory tract infection (2%), cough
• Gastrointestinal: abdominal pain (5%), diarrhea (4%),
nausea (4%), vomiting (3%), flatulence (3%), acid
regurgitation (2%), constipation (2%)
• Neuromuscular and skeletal: back pain (1%), weakness
(1%)
• Dermatologic: rash (2%)

27
Q

how is a previous exposure to and penicillin allergy treated

A 
PPi
bismuth
metronidazole
tetracycline 
alternative antibiotics
28
Q

what is the second line treatment

A

alternative regimen or quadruple treatment

29
Q

how else is infection managed

A

endoscopy
repeat testing
try not to take NSAIDS

30
Q

what is the difference between enterochromaffin cells and enterochromaffin like cells (ECL)

A

enterochromaffin cells release serotonin which causes contraction and is also involved in emesis
ECL cells respond to gastrin released by G-cells by releasing histamine, which will stimulate the parietal cells to produce gastric acid.

31
Q

what type of gastritis causes low gastric pH

A

pangastritis

due to inflammation damaging acid production

MD3002 (56 decks)

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