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GERR > Lecture 13: Pharmacology of Upper and Lower GIT Drug Treatment > Flashcards

Lecture 13: Pharmacology of Upper and Lower GIT Drug Treatment Flashcards

(49 cards)

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1
Q

what is dyspepsia

A

indigestion e.g. heartburn, bloating, gas etc

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2
Q

what is dysphagia

A

difficulty swallowing

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3
Q

what is the target cell for drugs treating gastric inflammation/ulceration

A

parietal cell

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4
Q

describe the physiological control of acid secretion in the GIT

A

vagal nerve (parasympathetic system) –> acetylcholine –> +ve signal promoting acid secretion by H+/K+ ATPase dependent (proton) pump

  • histamine also stimulates acid signal through H2 receptor
  • gastrin responds to dietary intake signalling gastric acid secretion
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5
Q

name the 3 main influencers promoting gastric acid secretion via the proton pump

A
  • acetylcholine
  • gastrin
  • histamine
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6
Q

what hormone has a negative signal to acid secretion

A
  • prostaglandin 2 (PGE2)
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7
Q

what is a peptic ulcer

A

defect in the gastric or duodenal mucosa due to imbalance in the peptic acid secretion and gastroduodenal mucosal defence

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8
Q

which patient suffering from peptic ulcer requires investigation

A

those at increased risk of gastric carcinoma

especially older patients

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9
Q

why is it important to investigate patients at increased risk of gastric carcinoma before PUD therapy

A

treatment may mask early symptoms of the gastric carcinoma

  • pain could be that of could be stomach cancer
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10
Q

what type of pain is more typical of a peptic ulcer

A

epigastric pain

  • sometimes no pain experienced in duodenal
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11
Q

what is the first step in PUD treatment

A

remove the irritants

  • especially NSAIDs
  • helicobacter pylori if present
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12
Q

name some of the treatment options for PUD

A
  • antacids
  • proton pump inhibitor
  • H2 receptor antagonist
  • antibiotics
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13
Q

how do NSAIDs affect prostaglandin production

A

inhibitory effect on prostaglandin formation enzymes COX 1 and COX 2

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14
Q

how does COX 1 affect acid secretion

A
  • COX 1 –> PGE2 prostaglandin signal to reduce acid secretion
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15
Q

what other drugs are aetiological factors in PUD

A
  • aspirin/corticosteroids
  • bisphosphonates
  • nicotine
  • alcohol
  • caffeine
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16
Q

how do antacids produce symptomatic relief in PUD

A

alkali based (Al and Mg) salts that raise gastric pH and reduce proteolytic activity

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17
Q

why are aluminium and magnesium salt antacids most commonly used for PUD treatment

A
  • they aren’t as easily absorbed so not as likely to affect blood pH
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18
Q

why is sodium bicarbonate typically not used as an antacid

A

it is easily absorbed into the blood which affects blood pH and can cause…

  • metabolic alkalosis
  • Na and H2O retention
  • renal stone formation
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19
Q

why is antacid use limited (not long term)

A

parietal cells will continue to secrete HCl acid so imbalance between acid over-production and irritation of stomach lining continues after alkali has been absorbed

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20
Q

how can you typically recognise proton pump inhibitors

Study These Flashcards
A

names end with -prazole/-azole e.g. omeprazole

CAUTION -prazole ending can be used for a wide range of drug types

21
Q

MoA of proton pump inhibitor

Study These Flashcards
A

inhibits K+/H+ ATPase pump of parietal cell

22
Q

MoA of proton pump inhibitor

Study These Flashcards
A

inhibits K+/H+ ATPase pump of parietal cell –> irreversible

23
Q

omeprazole MoA

Study These Flashcards
A

targeted irreversible proton pump inhibitor

  • irreversible –> will last a bit longer (until parietal cell replaced)
  • very effective and well tolerated by patients
24
Q

clinical indications of omeprazole

Study These Flashcards
A
  • dyspepsia
  • PUD
  • reflux oesophagitis (GORD)
25
common ADRs of PPI
- GI disturbance | - headache
26
important ADRs of PPI
- increased risk of C. diff. - hyponatraemia, hypomagnesaemia - hepatitis, interstitial nephritis, blood disorders - risk of community acquired pneumonia - risk of developing CKD
27
interactions of PPI
(slight variation between diff PPIs) - Warfarin --> weak CYP450 enz inhibitors --> increase anticoagulant effect - clopidogrel (hepatic pro drug) --> reduce anti platelet effect
28
why should you not take PPIs for more than 8 weeks
rebound acid hypertension syndrome (RAHS)
29
how can you typically recognise H2 receptor antagonists
end in -tidine e.g. cimetidine
30
role of H2 receptor antagonists in PUD treatment
competitive antagonist at H2 receptor thus reducing gastric acid secretion - reduce basal and stimulated acid output (90%)
31
clinical indications of cimetidine
2nd line agent for PUD and reflux oesophagitis
32
cimetidine ADRs
- diarrhoea - confusion - gynaecomastia
33
cimetidine interactions
potent inhibitor of cytochrome p450 dependent metabolism - any other drugs being hepatically processed would produce side-effects
34
MoA for ranitidine
competitive antagonist at H2 receptor in gastric parietal cells
35
clinical indications for ranitidine
2nd line agent for PUD and reflux oesophagitis
36
ranitidine ARDs
diarrhoea | fewer than cimetidine
37
what type of bacteria is helicobacter pylori
gram negative bacillus
38
what bacteria is a common cause of ulcer disease
helicobacter pylori
39
what other conditions can helicobacter pylori be assc w/
- mucosa-assc lymphoid tissue (MALT) lymphoma | - gastric cancer
40
why is ranitidine not really used anymore
carcinogenic effects
41
how does helicobacter pylori cause PUD
- secretes inflammatory proteins and toxins in mucus layer | - urease producing --> urea to NH4+ and CO2- --> undermines mucosal protection system
42
describe the helicobacter pylori eradication regimen
- PPI (or H2RA) - clarithromycin - amoxicillin (or metronidazole if penicillin allergic) - triple therapy 7 days - if ulcer large or complicated (by haemorrhage or perforation) continue PPI (or H2RA) for 3 more weeks - use different antibiotic if needing second treatment course
43
how is helicobacter pylori initially detected
- Carbon-13 urea breath test - upper GI endoscopy with biopsy and rapid urease test - serology (IgG) though inadequate performance so not recommended
44
when is an urgent upper GI endoscopy required
- acute bleeding suspected - chronic bleeding/ Fe def anaemia - weight loss - dysphagia - persistent vomiting - unexplained, persistent dyspepsia (especially if elderly)
45
how is constipation most commonly treated
non-pharmalogical interventions: - ^ fluid uptake - improve mobility - ^ fibre uptake (unless d/t opioids) - stop constipating drugs - exclude underlying pathology
46
causes of constipation
- drugs --> esp opioids and anti-muscarinics --> slow peristaltic movement - local pain e.g. anal fissure, peri-anal access - benign colorectal disease - endocrine/metabolic e.g. hypercalcaemia, hypothyroidism - malignancy
47
name some types of laxatives and MoA for each
- bulk laxatives e.g. fybogel --> binding agent for water to make stools big and easy to pass; swells and distends colon - osmotic laxatives e.g. macrogols --> pulls water into lumen to bind with bulking agent - faecal softener e.g. decussate --> ^ intestinal fluid secretion - stimulant laxatives e.g. bisacodyl, Senna --> stimulate enteric NS to promote peristalsis
48
constipation management
- put everyone at risk (e.g. patients on opioids) on laxatives - treat reversible causes - adjust any constipating medication - advise ^ dietary uptake, ^ fluid uptake, exercise - offer oral laxatives if dietary measure ineffective
49
constipation management for patient with opined-induced constipation
- AVOID bulking laxatives | - use osmotic laxative AND stimulant

GERR (46 decks)

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