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Physiology: GI > Dyspepsia and GORD > Flashcards

Dyspepsia and GORD Flashcards

1
Q

Which age groups does Peptic Ulcer Disease (PUD)?

A

Occurs in children (rare)
Peak in population 55 and 65 years
Duodenal ulcers 25 and 75 years

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2
Q

Which gender has a higher risk of PUD?

A

Twice as more risky for males

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3
Q

What are risk factors of PUD?

A 
Caffeine
Smoking
Alcohol
NSAIDs
Stress
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4
Q

What are some causes of PUD?

A

H.Pylori
Long term use of NSAIDs
Stress Ulcers

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5
Q

Which ulceration is associated with normal/decreased acid secretion?

A

Gastric Ulceration

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6
Q

Which ulceration is associated with normal/increased acid secretion?

A

Duodenal Ulceration

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7
Q

What is the development of a peptic ulcer normally assosicated with?

A

Disruption of mucosal-damaging and mucosal-protecting mechanisms

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8
Q

What is an example of an NSAID which reduces prostaglanding formation (COX 1 inhibition)?

A

Aspirin

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9
Q

What can COX1 inhibition trigger?

A

Gastric ulceration

Bleeding

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10
Q

How can gastric damage be prevented (NSAID)?

A

Stable PGE1 analogue

Misoprostol

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11
Q

What are the two ways we can treat dyspepsia and GI disorders?

A

Neutralisation

Reduction of Acid Secretion

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12
Q

What are the medications used for Neutralisation?

A

Antacids
Alginates
Sucralfate (mucosal protectants)

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13
Q

What are the medications used for Reduction of acid secretion?

A

PPIs
Histamine H2 Receptor Antagonists
Prokinetics

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14
Q

What are antacids?

A

Weak bases which NEUTRALISE xs stomach acid

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15
Q

How do antacids neutralise acid?

A

Buffer the gastric acid, neutralising gastric acid.

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16
Q

What are they combined with to achieve a higher pH?

A

Alginates with anti-foaming agents, anti-foaming agents reduce surface tension of stomach acid to prevent bubbles, producing a defoaming action.

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17
Q

What are the two types of antacids?

A

Systemic and Non-systemic

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18
Q

What are the advantages of Systemic Antacids?

A

Useful in short-term therapy

Rapid onset

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19
Q

What is the disadvantage of Systemic Antacids?

A

Prolonged use causes an overload on kidneys

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20
Q

What are the advantages of Non-Systemic Antacids?

A

Remain in GI tract

Useful in long-term therapy

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21
Q

What are examples of Non-systemic Antacids?

A

Calcium-based antacids
Magnesium antacids
Aluminium-based antacids
Bicarbonate based antacids

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22
Q

What are the pharmacokinetic interactions and pharamacodynamic interactions?

A

Binding of other drugs to the antacid causing reduced bioavailiability
Chemical inactivation of drugs
Increased gastric pH

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23
Q

What are the adverse effects of Antacids?

A

Relatively minor contraindications

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24
Q

What side effects does Magnesium hydroxide have?

A

Laxative properties

25
Q

What side effects does Aluminium hydroxide have?

A

Causes constipation

26
Q

What side effects does Calcium carbonate?

A

May cause renal calculi (stones) and constipation

27
Q

What side effects can Carbonates have?

A

Generation of CO2 leading to bloating and flatulence

28
Q

What side effects can Sodium bicarbonate have?

A

Metabolic alkalosis

29
Q

What is an Alginate?

A

Polysaccharide found in cell walls of brown algae

30
Q

What is Gaviscon composed of?

A

Antacids and Alginate

31
Q

How does Gaviscon react?

A

Reacts rapidly with acid to form alginic-acid gel, near neutral pH

32
Q

How are PPIs delivered?

A

Via the systemic circulation to the secretory gastric canaliculi

33
Q

What are prodrugs?

A

They are inactive at a neutral pH, but activated at a strongly acidic environment

34
Q

What happens when a prodrug binds to a cysteine of the H+/K+pump?

A

An irreversible reaction takes place and inhibits the active proton pump, preventing movement of H+ into the stomach

35
Q

What is the result of the prodrug binding irreversibly?

A

Achlorhydria “ALL gastric acid secretion blocked”

36
Q

Give an example of a common PPI?

A

Omeprazole

37
Q

Describe Omeprazole Activation and Activity

A

Diffuses into the parietal cells of stomach and accumulates
Activated by proton-catalyzed formation of sulfenic acid
Active drug binds to sulfhydryl groups of cysteines of H+/K+ pump
Charged drug molecule cannot diffuse out of parietal cells
Irreversible activation of proton pump

38
Q

Which is the best time to take a PPI?

A

At a time when the PPIs are effective

39
Q

How does Histamine stimulate acid production?

A

Histamine binds to H2 receptors on parietal cells

40
Q

Which other hormone stimulates high levels of histamine?

A

Gastrin which is stimulated by ECL cells

41
Q

What are examples of H2 receptor blocks?

A

Cimetidine

Ranitidine

42
Q

What is the mechanism of a H2 receptor antagonist?

A

1) Acts as a competitive antagonist on basolateral membrane of parietal cells
2) Block the histamine H2 receptor and reduces secretion evoked by gastrin and ACh

43
Q

How is it usually administered and how often should it be taken?

A

OAD/BOD via oral administration

44
Q

What are the side effects of Histamine H2 anatagonists?

A

Overall, less than 3% incidence of side effects.

45
Q

What are the pharmacokinetics of Histamine H2 receptors?

  • absorption?
  • serum concentrations?
  • therapeutic levels?
A

Rapid absorption
Serum concentrations peak in 1-3 hour
Therapeutic levels maintained upto 12 hours

46
Q

What are the drug interactions of Histamine H2 receptors?

A

Cimetedine inhibits P450s

Inhibits absorption of drugs

47
Q

Which prostaglandins are synthesized by the gastric mucosa?

A

PGE2 and PGI2

48
Q

Which receptors do PGE2 and PGI2 bind to?

A

EP3 receptor

49
Q

What are the cytoprotective effects of prostaglandins?

A

Stimulate mucin and bicarbonate production

50
Q

What are the pharmacokinetics effects of Prostaglandins?

  • absorption?
  • therapeutic effects?
A

Rapidly absorbed

Effects peak at 60-90 minutes and lasts 3 hours (4x a day does)

51
Q

What are the adverse effects of Prostaglandins?

A

Diarrhoea
Can excaerbate inflammatory bowel disease
Contraindicated during pregnancy

52
Q

What is Sucralfate used for?

A

Treatment of Benign gastric and duodenal ulceration

53
Q

What is Sucralfate composed of?

A

Aluminium hydroxide and sucrose octasulphate

54
Q

How does Sucralfate work?

A

Dissociates in gastric acidic environment to anionic form
Forms complex gel with mucus and forms cross-linked viscous polymer
Acts as an acid buffer and impairs diffusion of H+

55
Q

What is the mechanism of Sucralfate?

A

Acts as acid buffer and impairs diffusion of H

Stimulates PG-sythesis and bicarbonate secretion

56
Q

What are the pharmacokinetics of Sucralfate?

-side effects

A

Only slightly absorbed in the gut
Free if side effects
May cause constipation

57
Q

What are prokinetics?

A

Dopamine receptor antagonist

58
Q

What do prokinetics do?

A

Enhances gastric motility
Increases rate of gastric emptying
Increases gastro-oesophageal tone

59
Q

What are the severe side effects of prokinetics?

A 
Fatigue
Tremors
Parkinsonism
Tardive Dyskinesia
Severe cardiac events

Physiology: GI (6 decks)

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