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Digestive System Module > Drugs and GI tract > Flashcards

Drugs and GI tract Flashcards

1
Q

Histamine Receptor Antagonists

A

Burimamide first H2 receptor antagonist (James Black)
Cimetidine but problems with drug interactions (1st Clinical)
Ranitidine for peptic ulcer disease (caused by H.pylori, but now H. pylori treatment)
-now prescribed for Reflux

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2
Q

Drugs for GI conditions

A

generally inhibit Gastric acid secretion

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3
Q

Histamine

A
  1. Allergic reactions
    - H1 receptor: smooth muscle + Endothelial cells
    - receptor antagonist: anti-histamines
  2. Acid secretion
    - H2 receptor: Parietal cells
    - ECH cells release the histamine)
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4
Q

H2 receptor antagonists

A

Rinitadine

  • Competitive Antagonist. competes with agonistic histamine for binding site
  • Histamine can have a strong agonist effect and “overcome” rinitadine (breakthrough symptoms)
  • Not dose effective (not accumulative)
  • Rapid but short action (6-8 hrs)
  • Tolerance (tachyphylaxis) –first dose is most effective (efficacy starts to fall)
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5
Q

H2 antagonist Problems

A

Not effective for Heart burn/ moderate-severe GORD (not mucosal healing)
Multiple doses daily (4x /day if severe)
50% max acid suppression
Single Night-time dose Okay for Peptic ulcer-but will Reoccur if stopping
-more effective at healing PU>heart burn control

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6
Q

Proton Pump

A

Proton pumps on Gastric Parietal cells

Secrete Acid

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7
Q

Proton pump inhibitor pathway

A

Omeprazole
Orally-Must be absorbed by blood
Circulation –> Parietal cell –> Canaliculi –acid conv. O to SULPHonamide(active)–> Proton pump –> reactions occur leading to PP inactivation
Most effective at inhibiting HCL secretion

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8
Q

Localisation of Proton pumps

A

Canaliculi (of parietal cell)

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9
Q

Proton pump inhibitors

A

Irreversible blockage of activated Proton pump

  • Long duration (once daily/pot. twice daily as is 16-18hrs (90% acid suppression in most people (effective at treating heartburn from GORD and healing peptic ulcers)
  • does treat Hpylori (triple theory (2x AB Clarithomisin, Amoxiccilin (penicillin antibiotic))
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10
Q

Potential problems with long-term acid suppression

A
  • patients not worried. be aware and make sure not prolong if not needed
    1. Bacterial overgrowth of the stomach (everything except h.pylori)
    2. Malabsorption (no acid for B12, Fe and Ca absorption)
    3. Potential formation of carcinogenic??? compounds (gastric cancer)
    4. Acid required to STERILISE food
  • small risk, probably insignificant, or enteric infections
    5. ECL hyperplasia secondary to high gastrin (compensatory response)
  • rebound level in stomach, stomach senses insufficient acid, hyperplasia of ECH cells, increase Gastric acid secretion
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11
Q

H. Pylori treatment and Omeprazole

A 
H. pylori --> Peptic Ulcers (PU)
1. Proton pump inhibitor: Omeprazole
-helps to decrease gastric acid secretion = AB antibiotics work better at higher ph enviro
2x AB anitibiotics
-Clarithromysin
-Amoxicyillin (Penicillin antibiotic)
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12
Q

Practical tips re H2 receptor antagonists

A

H2 receptors good “if required” dosing because of rapid onset and good first dose effect

  • most effective in reducing Nocturnal acid secretion
  • Not as good for food stimulated acid secretion
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13
Q

Practical tips re Proton Pump inhibitors

A

PP inhibitors require
-Several days for maximal effect
-Good for maintenance treatment
-Prevention of degradation by stomach- enteric coated
-A meal to stimulate proton pumps (give 30 mins before meal)
(if with food = high HCl levels= decreased efficacy of drug)

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14
Q

Use of proton pump inhibitors

A

Mostly used not for GORD
Not required as much for ulcer disease as in the era for effective H.pylori treatment
Required in the ulcer disease caused by non-steroidal anti-inflammatory drugs (NSAIDS)
Useful for acute ulcer bleeding
-Possible mechanism (decreases activity of pepsin when the pH is >5)
-Pepsin may dissolve fibrin clot in vessel in the ulcer base (allows clot to form and stabilise over ulcer)

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15
Q

Effect of normal gut physiology on drug delivery

A
  1. Acid degradation
    - drugs may need to be enteric coated/delayed release
  2. Acid enhanced absorption
    - Intraconazole
  3. Effect of rate of gastric emptying
    - Matching insulin and meals
  4. Hepatic enzyme function (cytochrome p450 pathway)
  5. Enterohepatic circulation / biliary secretion
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16
Q

Case 1
50-year-old man with chronic pancreatitis from long history of excessive alcohol
Develops steatorrhoea
-Diagnosis: Fat malabsorption from pancreatic exocrine insufficiency
-Plan: Supplement pancreatic enzymes

A

Large volume of enzymes required to replace normal pancreatic enzyme function
Degradation by gastric acid
Need for neutral pH in the duodenum
Release in the proximal small bowel
Possible solutions
Enteric coated capsules - protect from acid but release will be delayed
Non-enteric coated but give with proton pump inhibitor

17
Q

Case 2
20-year-old man with bloody diarrhoea for 6 months presents for colonoscopy
-Diagnosis: Mild ulcerative colitis affecting left and transverse colon
-Plan: Start 5-aminosalicylic acid

A

5-ASA is the active drug used to treat IBD but is degraded by gastric acid

5-ASA needs to be delivered in highest concentration to areas of inflammation
Mostly colon and terminal ileum

Possible solutions
Join two 5-ASA molecules together with an azo bond
Needs colonic bacteria to cleave bond
Enteric coated
Resists gastric breakdown
pH-dependent release (neutral/alkaline pH)
Time-dependent release

-Sulphasalazine
Consists of 5-ASA linked to sulphapyridine
Uses colonic bacteria to provide release at appropriate site

18
Q

Sulphasalazine

+ Limitations

A

Consists of 5-ASA linked to sulphapyridine
Uses colonic bacteria to provide release at appropriate site
-Adverse effects (hypersensitivity or intolerance in 20% of patients)
Caused by “sulphur” part – sulphapyridine
Only acts in colonic disease
Higher doses may be more effective but cause severe adverse effects in most patients

19
Q

Case 3:

A

36-year-old woman takes ibuprofen for 6 weeks for sprained ankle
Presents with melaena and has gastroscopy
Diagnosis: Gastric ulcers
Plan: Stop ibuprofen, start omeprazole

20
Q

Anti-inflammatory drugs

A

NSAIDs very common treatment for arthritis and musculoskeletal pain
Frequent cause of hospital admission even though risk per prescription is low
NSAIDs can cause gastrointestinal bleeding from gastric ulceration
-widespread ulcers and erosions (not solitary)

21
Q

NSAIDs effect on gastric mucosa

A

NSAIDs and aspirin causes mucosal injury mainly via systemic (rather than topical) effects
-take with food to reduce non-specific GI symptoms/ side effects
Main mechanism: inhibition of COX-1
COX-1 is an enzyme that is important in synthesis of prostaglandins
These prostaglandins include those with inflammatory activity and cytoprotective activity (coat stomach lining with mucus and aid platelet aggregation)

22
Q

Reducing risk of GI bleeding from NSAIDs

A 
Possible solutions
Stop NSAIDs – is the drug required?
Are there alternatives to NSAIDs?
Use lowest possible dose
Use a “protective” drug:
Proton pump inhibitor
COX2 inhibitors
23
Q

Cox2 inhibitors

A

Newer
COX2 only catalyses formation of inflammatory prostaglandins
Inhibition of COX2 has reduced effect on cytoprotective prostagladins
Reduced risk of bleeding (50%) but more expensive and increased risk of myocardial infarction

Digestive System Module (38 decks)

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