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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

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

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

A

inhibits K+/H+ ATPase pump of parietal cell

22
Q

MoA of proton pump inhibitor

A

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

23
Q

omeprazole MoA

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

A
  • dyspepsia
  • PUD
  • reflux oesophagitis (GORD)
25
Q

common ADRs of PPI

A
  • GI disturbance

- headache

26
Q

important ADRs of PPI

A
  • increased risk of C. diff.
  • hyponatraemia, hypomagnesaemia
  • hepatitis, interstitial nephritis, blood disorders
  • risk of community acquired pneumonia
  • risk of developing CKD
27
Q

interactions of PPI

A

(slight variation between diff PPIs)

  • Warfarin –> weak CYP450 enz inhibitors –> increase anticoagulant effect
  • clopidogrel (hepatic pro drug) –> reduce anti platelet effect
28
Q

why should you not take PPIs for more than 8 weeks

A

rebound acid hypertension syndrome (RAHS)

29
Q

how can you typically recognise H2 receptor antagonists

A

end in -tidine e.g. cimetidine

30
Q

role of H2 receptor antagonists in PUD treatment

A

competitive antagonist at H2 receptor thus reducing gastric acid secretion
- reduce basal and stimulated acid output (90%)

31
Q

clinical indications of cimetidine

A

2nd line agent for PUD and reflux oesophagitis

32
Q

cimetidine ADRs

A
  • diarrhoea
  • confusion
  • gynaecomastia
33
Q

cimetidine interactions

A

potent inhibitor of cytochrome p450 dependent metabolism

  • any other drugs being hepatically processed would produce side-effects
34
Q

MoA for ranitidine

A

competitive antagonist at H2 receptor in gastric parietal cells

35
Q

clinical indications for ranitidine

A

2nd line agent for PUD and reflux oesophagitis

36
Q

ranitidine ARDs

A

diarrhoea

fewer than cimetidine

37
Q

what type of bacteria is helicobacter pylori

A

gram negative bacillus

38
Q

what bacteria is a common cause of ulcer disease

A

helicobacter pylori

39
Q

what other conditions can helicobacter pylori be assc w/

A
  • mucosa-assc lymphoid tissue (MALT) lymphoma

- gastric cancer

40
Q

why is ranitidine not really used anymore

A

carcinogenic effects

41
Q

how does helicobacter pylori cause PUD

A
  • secretes inflammatory proteins and toxins in mucus layer

- urease producing –> urea to NH4+ and CO2- –> undermines mucosal protection system

42
Q

describe the helicobacter pylori eradication regimen

A
  • 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
Q

how is helicobacter pylori initially detected

A
  • Carbon-13 urea breath test
  • upper GI endoscopy with biopsy and rapid urease test
  • serology (IgG) though inadequate performance so not recommended
44
Q

when is an urgent upper GI endoscopy required

A
  • acute bleeding suspected
  • chronic bleeding/ Fe def anaemia
  • weight loss
  • dysphagia
  • persistent vomiting
  • unexplained, persistent dyspepsia (especially if elderly)
45
Q

how is constipation most commonly treated

A

non-pharmalogical interventions:

  • ^ fluid uptake
  • improve mobility
  • ^ fibre uptake (unless d/t opioids)
  • stop constipating drugs
  • exclude underlying pathology
46
Q

causes of constipation

A
  • 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
Q

name some types of laxatives and MoA for each

A
  • 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
Q

constipation management

A
  • 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
Q

constipation management for patient with opined-induced constipation

A
  • AVOID bulking laxatives

- use osmotic laxative AND stimulant

GERR (46 decks)

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