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Physiology 1 : GI > Pharmacological basis of GI treatment > Flashcards

Pharmacological basis of GI treatment Flashcards

1
Q

What are 4 examples of H2 receptor antagonists?

A

→ranitidine
→cimetidine,
→ famotidine
→nizartidine

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2
Q

What are clinical uses of H2 receptor antagonists?

A

→ Peptic ulcer reflex oesophagitis

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3
Q

What do H2 receptor antagonists inhibit and promote ?

A

→Inhibits histamine, ACh and gastrin stimulated acid secretion on parietal cells
→Promotes healing of duodenal ulcers

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4
Q

What does stopping treatment of H2 receptor antagonists do?

A

→Stopping treatment means relapse

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5
Q

How is the H+/K+ pump activated by action of gastrin?

A

→Gastrin can activate ECL cells to release histamine

→ it binds to H2 receptors on parietal cells

→activates the H+/K+ ATPase pump

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6
Q

What do H2 receptor antagonists reduce?

A

→Reduces gastric acid secretion and as a consequence reduces pepsin secretion

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7
Q

What can H2 receptor antagonists decrease?

A

→Can decrease basal and food stimulated acid secretion by 90%

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8
Q

What can 4 side effects of H2 receptor antagonists be?

A

→diarrhoea
→muscle cramps
→transient rashes
→hypergastrinaemia

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9
Q

What is a side effect of cimetidine?

A

→ Gynecomastia

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10
Q

What does cimetidine inhibit?

A

→ P450 enzymes

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11
Q

What does a low IC50 mean?

A

→ Drug is more powerful

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12
Q

What does IC50 mean?

A

→ Inhibitory concentration

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13
Q

What are 4 examples of proton pump inhibitors?

A

→ omeprazole
→ lanzoprazole
→ pantoprazole
→ rabeprazole

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14
Q

What are clinical uses of proton pump inhibitors?

A 
→Peptic ulcer
→ reflux oesophagitis
→therapy for H. Pylori
→ treatment for Zollinger-Ellison 
→Drugs of choice if hyper-secretion occurs
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15
Q

What is the mechanism of action of proton pump inhibitors?

A

→ Weak bases - inactive at neutral pH and irreversibly inhibit the H+/K+ ATPase pump
→ Decrease basal and food stimulated gastric acid secretion

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16
Q

What are side effects of proton pump inhibitors?

A 
→Headache
→diarrhoea
→ mental confusion
→rashes
→somnolence
→ impotence
→ gynecomastia
→ dizziness
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17
Q

What protects the gastric mucosa?

A

→ PGE1

→ PGE2

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18
Q

What drugs protect the gastric mucosa?

A

→ misoprostol - stable analogue of PGE1

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19
Q

What does misoprostol inhibit?

A

→Inhibits basal and food stimulates gastric acid secretion
→Inhibits histamine and caffeine induced gastric secretion
→Inhibits the activity of parietal cells

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20
Q

What does misoprostol increase and induce?

A

→Increases mucosal blood flow and can augment the secretion of HCO3- and mucus
→Induces labour/abortion

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21
Q

What does metoclopramide do?

A

→inhibits pre and postsynaptic dopamine (inhibits ACh) receptors as well as 5HT3

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22
Q

What do 5HT3 receptors do?

A

→receptors which inhibits vomiting

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23
Q

What does dopamine inhibit?

A

→ ACh release

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24
Q

How does dopamine inhibit ACh?

A

→inhibits the release of ACh from intrinsic myenteric cholinergic neurons by activating prejunctional D2 receptors

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25
Q

What kind of effects does dopamine have on the gut and where?

A

→relaxant effects on the gut by activating D2 receptors in the lower oesophageal sphincter and stomach

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26
Q

What does dopamine do in the distal and proximal areas of the gut?

A

→can induce contraction in the proximal

→relaxation in the distal

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27
Q

What does increased ACh mean?

A

→Increased ACh means increased intragastric pressure →due to increased LOS tone
→ increased tone of gastric contractions

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28
Q

What does an increase of ACh do to contraction and emptying?

A

→These improve antral duodenal contraction which →accelerates gastric emptying
→relaxes the pyloric sphincter

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29
Q

What two properties does metoclopramide have?

A

→ antiemetic properties via central effects

→relieves headache via central effects

30
Q

What is metoclopramide useful for?

A

→GI reflux

31
Q

What does metoclopramide stimulate and accelerate?

A

→ S: gastric motility

→ A: gastric emptying

32
Q

What neurons does metoclopramide stimulate?

A

→inhibitory nitregic neurons

→mediate NO release

33
Q

What are the 6 effects of metoclopramide?

A

→Inhibits presynaptic and postsynaptic D2 receptors

→Stimulates the release of ACh / SP from enteric neurons

→Elicits mixed 5-HT agonist and antagonist effects, e.g., stimulates excitatory 5-HT4 receptors (ENS), but inhibits 5-HT3 receptors (CNS);

→Stimulates inhibitory nitregic neurons – mediate NO release

→Increases intragastric pressure -↑ LOS and gastric tones

→Motility stimulant - improves antro-duodenal coordination and accelerated gastric emptying

34
Q

What are 3 examples of antispasmodic agents?

A

→Propantheline
→ dicloxerine
→ mebeverine

35
Q

What do antispasmodic agents do?

A

→Decrease spasm in bowel, they have relaxant action on GIT (smooth muscle in GIT)

36
Q

What is propantheline?

A

→antimuscarinic agent

37
Q

What do muscarinic receptor antagonists do?

A

→inhibit parasympathetic activity which reduces spasm in the bowel

38
Q

What is the goal in pharmacological intervention in gastric ulcer?

A

→Reduce acid secretion with H2 receptor antagonists
→Neutralise secreted acid with antacids
→Attempt to eradicate H. pylori

39
Q

What kind of bacteria is H.Pylori?

A

→H.Pylori is a gram negative bacillus

40
Q

What is the mechanism of action of antacids?

A

→Neutralize gastric acid

→increase the pH of gastric acid

41
Q

What does bismuth chelate do?

A 
→Protects gastric mucosa 
→Forms a base over crater of ulcer 
→Adsorbs pepsin 
→Increased HCO3- and PG secretion 
→Toxic against H. Pylori - used as part of a triple therapy to eradicate it 
→Blackens stool and tongue
42
Q

What can bismuth chelate cause?

A

→Can cause encephalopathy

43
Q

How do prostaglandins protect the mucosal layer?

A

→Stimulating bicarbonate secretion
→Reducing H+ secretion
→Promotes vasodilation

44
Q

Why do NSAIDS (e.g. aspirin) cause gastric bleeding?

A

→ Inhibit PG synthesis

45
Q

What reduces bleeding from NSAIDs?

A

→Celecoxib

→ rofecoxib

46
Q

What is H.Pylori a risk factor for?

A

→ gastric cancer

47
Q

What is a 3 combination therapy for H.Pylori?

A

Omeprazole, amoxicillin and metronidazole

48
Q

What cytoprotective effects does bismuth chelate have?

A

→Provide a physical barrier (coat) over the surface/base of the ulcer
→Enhances local synthesis of PGs
→Promote bicarbonate secretion

49
Q

What reaction happens if metronidazole is taken with alcohol?

A

→Disulfiram like reaction

50
Q

What does disulfiram do to alcohol?

A

→ Inhibits acetaldehyde dehydrogenase so acetaldehyde builds up

51
Q

What are consequences of constipation?

A 
→Headache
→Loss of appetite 
→Nausea 
→Abdominal distension and stomach pain 
→Holding of fecal matter → Water loss and drier feces → painful and harder to defecate
52
Q

What are 3 causes of constipation?

A

→Decreased motility of large intestine
→Old age
→Damage to enteric nervous system of colon

53
Q

What are factors that can increase colonic motility?

A

→Increased fibre, cellulose and complex polysaccharides
→Bran, fruits, vegetables with high fibre
→Laxatives but excessive use - decrease in responsiveness
→Mineral oil - lubricates feces
→Castor oil - stimulates motility of colon

54
Q

What are alarm signs for people with chronic constipation?

A 
→Acute onset in older individuals 
→Weight loss 
→Blood 
→Anaemia 
→Family history of colon cancer or inflammatory bowel disease
55
Q

What can purgatives do?

A

→modulate/hasten food transit in the intestine

56
Q

What are bulk laxatives?

A

→Bulk laxatives - methylcellulose

→Plant gums (sterculia, agar, linseed, bran)

57
Q

What do bulk laxatives do?

A

→They retain water in the gut lumen → promote peristalsis but take a few days to work
→Increase the stools solid content /Bloating and flatulence

58
Q

What do osmotic laxatives do?

A

→Increases and maintains the volume of fluid in the lumen of the bowel by osmosis

59
Q

What do high doses of osmotic laxatives cause?

A 
→flatulence
→ cramps
→diarrhoea
→ vomiting 
→tolerance
60
Q

What do anti-diarrheal agents do?

A

→Maintain body fluids and electrolytes

61
Q

What are 4 causes of diarrhoea?

A

→Infectious agents
→Toxins
→Anxiety
→Drugs

62
Q

What does oral rehydration therapy do?

A

→maintain fluid and electrolyte balance

63
Q

What does loperamide do?

A

→Selective on GIT
→Decreases passage of feces
→Decreases duration of illness

64
Q

What does bismuth subsalicylate do?

A

→Decreases fluid secretion in bowel
→Safe for young children
→Tinnitus and blackening of stool

65
Q

What type of drug is loperamide?

A

→Opioid receptor agonist

66
Q

Where does loperamide exert its effects?

A

→Exerts effects on mu opioid receptor of the myenteric plexus of the large intestine

67
Q

What does loperamide do to the GIT?

A

→reduces smooth muscle activity in the GIT

→reduces passage of feces

68
Q

What does loperamide increase?

A

→Increases haustral mixing of proximal colon

69
Q

What does loperamide inhibit?

A

→Inhibits propulsive mass movement of the distal colon

70
Q

Why does loperamide not have CNS effects?

A

→ Does not cross the blood brain barrier

71
Q

What does loperamide reduce?

A

→ Force and speed of colonic movements

Physiology 1 : GI (15 decks)

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