Gastrointestinal Flashcards

0
Q

Senna

A

Herbal STIMULANT laxative

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1
Q

Lactulose

A

Semi synthetic fructose/galactose osmotic laxative

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2
Q

Loperamide

A

Opioid agonist (GIT selective) anti-diarrheal agent.

Activation of predominantly mu-opioid receptors located in the myenteric plexus and intestines results in increased smooth muscle tone, decreased peristalsis and decreased secretions.

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3
Q

Metoclopramide

A

•D2, dopamine antagonist.
•Antiemetic effects predominantly due to inhibition of D2 receptors in the chemo trigger zone CTZ.
•Weak seretonin antagonist.
Contraindicated by Parkinsoniam patients.

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4
Q

Ondansetron

A

Anti emetic. Ondansetron is a 5HT3 antagonist and is thought to produce its anti-emetic effect by blocking 5HT3 receptors located on vagal afferents and in the CTZ.

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5
Q

Orlistat

A

Anti obesity drug.

Orlistat binds to lipases irreversibly inhibiting them from breaking down triglycerides.

  • Flatulence
  • Faecal urgency
  • Increased fatty stools

Can reduce fat soluble vitamins. Bit k deficiency may have anti coagulant effects.

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6
Q

Rifampicin

A
  • Effective against gram + bacteria TB
  • Frequently used in combination with other antimycobacterials (isoniazid) to treat tuberculosis.
  • MOA?
  • Binds to the Beta subunit of bacterial DNA dependent RNA-polymerase resulting in suppresion of RNA synthesis in susceptible bacteria.
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7
Q

Ranitidine

A
  • Competitive H2 antagonist
  • Blocks the action of Histamine at H2 receptors and as a result inhibits histamine-induced gastric acid secretion.
  • SIDE EFFECTS?
  • Generally well tolerated.
  • Dose?
  • variable
  • Interactions?
  • Gastric pH is increased in patients taking H2 antagonists, which can lead to decreased absorption of antiretrovrials, antifungals, and tyrosine kinase inhibitors.
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8
Q

Where is gastric acid produced- and name three ways of regulating acid secretion.

A
  • Gastric acid is produced by parietal cells located in the glands of the fundus mucosa.
  • The regulation of acid secretion is a complex with:
  • Neuronal: (ACETYLCHOLINE) factors
  • Hormonal: (GASTRIN) factors
  • Paracrine (HISTAMINE) factors
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9
Q

Esomeprazole

A
  • After systemic absorption, proton pump inhibitors diffuse into the parietal cells and in this acidic environment they are converted from a pro-drug into an active drug that reduces gastric acid secretion by irreversibly inhibiting the H+/K+/ATPase
  • AE?
  • Headache
  • GI disturbances (nausea, vomiting, diarrhoea)
  • DOSE? variable
  • INTERACTIONS?
  • CYP450 enzymes drugs that either induce or inhibit these isoenzymes may cause either a decrease or increase in PPI concentrations respectively.
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10
Q

Name four defensive actions against the acidity of the stomach.

A
  • Mucus:Continually secreted, protective factor
  • Bicarbonate:Secreted from endothelial cells. Maintains mucosal surfacepH 6-7, despite acidic environment of lumen (pH1-2)
  • Blood flow:Good blood flow maintains mucosal integrity
  • PGs: Suppress secretion of gastric acid. Promote blood flow. Stimulate secretion of bicarbonate and mucus
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11
Q

Gastric ulcer vs duodenal ulcer. Name 5 differences

A
  • Common in late middle age incidence increases with age
  • More male
  • NSAID uses
  • Less related to H.pylori than duodenal ulcers
  • 10-20% of patients with a gastric ulcer have a concomittant duodenal ulcer

Vs

  • 4*more common than gastric
  • Most common in middle age
  • Male to female ratio
  • Genetic link: 3* more common in first degree relatives
  • H. Pylori
  • Smoking twice as common
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12
Q

Name the three treatment groups for gastric ulcers.

A
  • Non-phamalogical
  • Anti-secretory agents
  • H2-receptor antagonists
  • Proton pump inhibitors
  • anticholinergics
  • Cytoprotective agents and mucosal strengtheners:
  • Sucralfate
  • Prostaglandins
  • Bismuth
  • antacids
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13
Q

What is sulfacrate?

A
  • Mucosal strengthener: mucosal protective agents
  • Complex of aluminium hydroxide and sulfated sucrose
  • Viscous at acid pH and adheres to surface of ulcers, to act as a barrier the aggressive luminal factors (eg. Acid, pepsin, bile salts)
  • Stimulates mucosal protecting mechanisms (mucus, bicarbonate, pGs)
  • Taken on an empty stomach, 1 hr before meal.
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14
Q

What is misoprotosol?

A
Prostaglandin analogues
•Misoprotosol. 
•Mucosal protective agents: prostaglandin analogues
•Produced in response to COX
•Inhibit acid secretion
•Increase mucosal blood flow and mucus
•Cytoprotective on gastric mucosa
  • P.O
  • Only in patients using NSAIDS with high risk of ulcer
  • Comparable ulcer healing efficacy with H2 receptor antagonists.
  • SE:
  • Pain endings sensitised so pain often worsens initially.
  • Diarrhoea, nausea, headache, dizziness
  • Uterine contractions; contraindicated in pregnancy.
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15
Q

What is bismuth chelate?

A

Cytoprotective agent and mucosal strengtheners

•Not first line; used in combination therapy
•Coats ulcer base
•Forms precipitate which binds to proteins on surface of ulcers at acidic pH providing barrier to aggressive factors in gastric juice.
•Enhances PG synthesis, stimulates mucus and bicarbonate secretion.
Black stools and tongue

16
Q

What is carbenoxolon?

A

CYTOPROTECTIVE AGENTS AND MUCOSAL STRENGTHENERS
•CARBENOXOLONE
•Derived from liquorice roots
•Appears to accelerate the healing of gastric ulcers
•Promotes the production of mucus

17
Q

What are antacids?

A

•Weakest bases that neutralise acid (raise gastric pH)
•Also inhibit formation of pepsin (as pepsinogen converted to pepsin in formation of acidic pH)
•More effective against duodenal ulcers (than gastric)
•OTC drug for symptomatic relief of dyspepsia (indigestion)
•Presents day antacids:
•Aluminium hydroxide- constipation
•Magnesium hydroxide- diarrhoea
Both renal toxicity. Less common Na or Ca salts

  • Duration of action:
  • 30 min on empty stomach
  • 2 hr taken after a meal.
18
Q

What is H. Pylori?

A
  • Gram –ve bacteria
  • Major cause of gastric and duodenal ulcers
  • Classified as class 1 carcinogenic for gastric cancer.
19
Q

What is the triple therapy?

A

•PPI+metronidazole+amoxycillin or clarithromycin (bismuth)

Extra info: 
•Bismuth:Disrupts cell wall of H.pylori
•Clarithromycin:Inhibits protein synth
•Amoxicilin:Disrupts cell wall
•Tetracycline:Inhibits protein synthesis
•Metronidazole:Bacterial resistance to amoxicillin/tetracycline
20
Q

Definition of GORD

A
  • Gastro-oesophageal reflux disease:
  • Backflow of acidic stomach/duodenal contents into the oesophagus
  • Can lead to inflamed esophageal mucosa (esophagitis)
  • Symptom: heart burn/chest pain
  • Incidence: 1:10
21
Q

Name three drugs promoting GORD.

A
  • Anticholinergics
  • Nitrites
  • Calcium channel blockers
  • Dopamine agonists
  • Phosphodieterase inhibitors

•Patient factors also important (alcohol, smoking, stress, coffee, rich/greasy foods, overeating)

22
Q

GORD treatment?

A
  • Drugs of choice: PPI

* OTHERs: antacids, H2 receptor antagonists, sucralfate