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1
Q

How much gastric acid secreted daily?

A

2.5L

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2
Q

What do endocrine secretions release?

A

substances into GIT (peptides eg gastrin).

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3
Q

Which areas of GIT are of pharmalogical importance + why?

A
  • Gastric secretion - vomiting –> damage –> ulcer
  • Gut motility - stasis of gut increases likelihood of reflux + reduces ability of clearance of acid from oesophagus, in intestine –> constipation
  • Bile formation + excretion - gallstones or malnutrition
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4
Q

What are paracrine secretions?

A

regulatory peptides released by cells GIT wall (eg histamine) + function as NT (eg CCK)

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5
Q

Describe what happens when parietal cell stimulated

A
  • parietal cell stimulated
  • H-K pumps H+into lumen of gastric gland in exchange for K+
  • K+recycles back into lumen via K+channels
  • carbonic anhydrase provides H+ extruded by H-K pump,
  • exits via basolateral anion exchanger (AE2)
  • Cl−enters basolateral membrane via AE2
  • Na/K/Cl cotransporter NKCC1 + electrogenic SLC26A7
  • Cl−exits via apical CFTR (+ ClC) channels
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6
Q

Stimuli that act on parietal cell?

A

gastrin, ACh, histamine, PGE2 + PGI2

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7
Q

How gastrin acts on parietal cell?

A
  • peptide hormone secreted by gastric mucosa + duodenum
  • stimulates gastric secretion, BF, gastric motility
  • parietal cells express gastrin receptors
  • release of gastrin controlled by NT, other mediators eg milk + Ca2+ solutions stimulate gastrin release in stomach
  • so don’t use Ca2+-containing salts to control acid secretion

PGE2 & PGI2: Inhibit acid secretion

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8
Q

How ACh acts on parietal cell?

A

NT stimulates muscarinic ACh receptors on parietal cells + on histamine-containing cells

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9
Q

How histamine acts on parietal cell?

A
  • local hormone
  • acts on H2 receptors on parietal + mast cells
  • release increased by gastrin + ACh
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10
Q

How PGE2 + PGI2 acts on parietal cell?

A

inhibit acid secretion

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11
Q

Role of proglutamide?

A

drug blocks CCK2 receptors

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12
Q

Effect of metoclopromide?

A
  • Inhibits pre- + post-synaptic dopamine (D2), 5-HT3 receptors (CNS) – inhibiting vomiting
  • Stimulates 5-HT receptors (ENS) – prokinetic
  • Stimulates inhibitory nitregeric (NO) neurons → coordinated gastric motility
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13
Q

Role of dopamine?

A
  • Inhibits ACh release from intrinsic myenteric cholinergic neurons by activating prejunctional D2 receptors which leads to indirect inhibition of musculature
  • Relaxant effect on gut by activating D2 receptors in LOS, stomach (fundus + antrum)
  • Mixed effects on gut – induce contraction in proximal but relaxation in distal small intestine
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14
Q

Describe features of all dopamine receptors

A
  • 2 D1-like receptor subtypes : D1 + D5 couple to Gs
  • activate adenylyl cyclase
  • other receptor subtypes belong to D2-like subfamily : D2, D3, D4 + prototypic of G receptors
  • inhibit adenylyl cyclase
  • activate K+ channels
  • genes for D1 + D5 receptors are intronless, but pseudogenes of D5 exist
  • D2 + D3 receptors vary in tissues, species due to alternative splicing
  • D4 receptor gene exhibits extensive polymorphic variation
  • in CNS dopamine receptors expressed since they’re involved in control of locomotion, cognition, emotion + neuroendocrine secretion
  • in periphery dopamine receptors in kidney, vasculature, pituitary to affect sodium homeostasis, vascular tone, hormone secretion
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15
Q

Antagonistic activity of metoclopramide at dopamine (D2) receptors?

A

↑ACh release :

  • (↑ peristalsis of duodenum, jejunum, ileum)
  • ↑intragastric pressure (due ↑LOS tone + ↑tone of gastric contractions)
  • -> improve antroduodenal coordination which accelerates gastric emptying, relaxes pyloric sphincter
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16
Q

Prokinetic effects of metoclopramide?

A

Stimulates presynaptic excitatory 5-HT receptors + inhibitory nitregeric neurons –> coordinated gastric motility

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17
Q

Major roles of 5-HT receptors in GIT?

A
  • Stimulates 5-HT3 or 5-HT4 receptors on enteric cholinergic neurons to release ACh –> smooth muscle contraction
  • Stimulate 5-HT4, 5-HT1A or 5-HT1D receptors on inhibitory enteric or nitrergic neurons to release NO –>smooth muscle relaxation.
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18
Q

Role of Prochlorperazine?

A

(a phenothyziane, very potent antipsychotic agent)

D2 receptor antagonist for nausea/vertigo.

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19
Q

Feaures of dopamine receptor antagonist metoclopramide?

A
  • Increasing LOS pressure + gastric emptying rate
  • Treatment of diabetic gastroparesis, severe gastroesophageal reflux, postoperative situations involving visceral atony
  • Useful adjunctive drug for intestinal intubation + radiologic examination
  • Intravenously controls headache, nausea, vomiting of intensive cancer chemotherapy eg with cisplatin
  • Antiemetic due to actions on chemoreceptor trigger zone + intestinal motility
  • Not long-term use
  • Oral preparations 4-12 weeks of therapy
  • Parenteral metoclopramide 1-2 days
  • Adverse reactions : restlessness, drowsiness, fatigue, lassitude
  • Extrapyramidal symptoms rare + only with high dosage or prolonged use
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20
Q

Role of metoclopramide?

A
  • For gastrointestinal reflux (but useless in paralytic ileus since causes moderate to diffuse abdominal discomfort eg abdominal distension, nausea/vomiting after meals, lack of bowel movement/flatulence)
  • Stimulates gastric motility
  • Accelerates gastric emptying
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21
Q

Clinical utility of metoclopromide?

A

Symptoms of gastroparesis
Promotes gastric emptying
Anti-emetic effects via central pathways

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22
Q

What’s paralytic ileus?

A

= postoperative adynamic ileus

  • Ileus/obstruction persisting for > 3 days following surgery
  • Obstruction of intestine due to paralysis of intestinal muscles
  • Intestinal muscles so inactive preventing passage of food –> functional blockage of intestine
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23
Q

Summary of metoclopromide effects :

A

Promotes gut motility by:

  • Inhibits presynaptic + postsynaptic D2 receptors
  • Stimulates ACh release/SP from enteric neurons
  • Mixed 5-HT agonist + antagonist effects :
  • stimulates excitatory 5-HT4 receptors (ENS)
  • inhibits 5-HT3 receptors (CNS antiemitic)
  • Stimulates inhibitory nitregic neurons for NO release
  • Increases intragastric pressure -↑LOS + gastric tones
  • Motility stimulant - improves antro-duodenal coordination + accelerated gastric emptying

-GORD; nausea due to surgery or cancer; symptoms of gastroparesis

  • Increases gastric emptying by enhancing antral contractions + decreasing postprandial fundus relaxation
  • Prokinetic effects limited to proximal gut
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24
Q

Features of antispasmodic agents + eg?

A

eg propantheline, dicycloverine (dicyclomine), mebeverine

  • ↓Spasm in bowel
  • Relax smooth muscle in GIT)
  • Propantheline = antimuscarinic agent
  • Useful in IBS + diverticular disease – congenital lesion, source of bacterial overgrowth
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25
Q

Role of muscarinic receptor antagonists + eg?

A

inhibit parasympathetic activity - reduces spasm in bowel eg Propantheline

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26
Q

Role of Dicycloverine?

A

=dicyclomine

  • For intestinal hypermotility + symptoms of IBS (spastic colon)
  • Relieves muscle spasms – non-selective smooth muscle relaxant
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27
Q

What’s kolanticon?

A

Anti-flatulent simethicone added + antacid

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28
Q

Role of Mebeverine?

A
  • Eases bloaty/crampy/colicky-type pain associated with IBS

- Musculotropic that potently blocks intestinal peristalsis.

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29
Q

Goals of pharmacological intervention in gastric ulcer?

A
  • Reduce acid secretion with H2 receptor antagonists
  • Neutralise secreted acid with antacids
  • Eradicate H. pylori

Drugs can be used to inhibit or neutralise gastric acid secretion for the following conditions:
Peptic ulcer
Reflux oesophagitis: gastric acid secretion can damage oesophagus
Zollinger-Ellison syndrome: gastrin-producing tumour

It is unclear why gastric ulcer develop

But H. pylori infection is a risk factor.
H. pylori: a Gram negative bacillus→ chronic gastritis → duodenal ulcer.

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30
Q

Goals of pharmacological intervention in gastric ulcer?

A
  • Reduce acid secretion with H2 receptor antagonists
  • Neutralise secreted acid with antacids
  • Eradicate H. pylori
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31
Q

When to use drugs to inhibit or neutralise gastric acid secretion?

A
  • Peptic ulcer
  • Reflux oesophagitis: gastric acid secretion damage oesophagus
  • Zollinger-Ellison syndrome: gastrin-producing tumour
32
Q

Why remove H. Pylori to treat gastric ulcer?

A
  • Risk factor.

- H. pylori: gram negative bacillus→ chronic gastritis → duodenal ulcer

33
Q

Describe action of antacids

A
  • neutralise gastric acid
  • ↑pH of gastric acid
  • (peptic activity stops at pH 5)
34
Q

Describe action of antacids

A
  • neutralise gastric acid
  • ↑pH of gastric acid
  • (peptic activity stops at pH 5)
  • relieves heartburn
35
Q

Features of sodium alginate or algin?

A
  • Anionic polysaccharide in cell walls of brown algae
  • Natural polysaccharide extracted from brown seaweed -Ingredient in gaviscon
  • Combines with bicarbonate for reflux as it forms a viscous gum : a component of biofilms produced by pseudomonas aeruginosa (pathogen in CF) so confers high antibacterial resistance + killing by macrophages
36
Q

Effect of bismuth chelate?

A
  • protects gastric mucosa
  • forms a base over crater of ulcer
  • adsorbs pepsin
  • ↑HCO3- + PG secretion
  • toxic against H. pylori – part of triple therapy to eradicate it
  • Blackens stool + tongue
37
Q

Effect of H2 receptor antagonists?

A

eg ranitidine, cimetidine, famotidine, nizatidine

  • Inhibit histamine-, ACh-, gastrin-stimulated acid secretion
  • Reduce gastric acid secretion (also reduces pepsin secretion)
  • Decrease basal + food-stimulated acid secretion by 90%
  • Promote healing of duodenal ulcers
  • Peptic ulcer
  • Reflex oesophagitis

In clinical trials: Promote the healing of duodenal ulcers
But if you stop treatment, you get relapse

38
Q

Effect of H2 receptor antagonists + eg?

A

eg ranitidine, cimetidine, famotidine, nizatidine

  • Inhibit histamine-, ACh-, gastrin-stimulated acid secretion
  • Reduce gastric acid secretion (also reduces pepsin secretion)
  • Decrease basal + food-stimulated acid secretion by 90%
  • Promote healing of duodenal ulcers but if stop treatment –> relapse
  • Peptic ulcer
  • Reflex oesophagitis
39
Q

Diff between Ranitidine vs Cimetidine?

A

Ranitidine has lower IC 50 so at lower conc produces 50% response so more potent than Cimetidine

40
Q

How do prostaglandins protect stomach mucus against damage?

A
  • Stimulating bicarbonate secretion
  • Reducing H+ secretion
  • Promoting vasodilation
41
Q

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

A
  • Inhibits PG synthesis (less protection) + Thromboxane A2 (involved in healing)
  • Use selective COX-2 inhibitors causing less bleeding eg Celecoxib, rofecoxib
42
Q

How does H. Pylori cause mucosal damage?

A

Causes crater, exposing epithelium to HCl, pepsin +

cytotoxins

43
Q

Combination therapy for H. Pylori infection?

A
  • Omeprazole, amoxicillin, metronidazole
  • Omeprazole, clarythromycin and amoxicillin or tetracycline, metronidazole, bismuth chelates
  • Lansoprazole, clarithromycin, tinidazole, bismuth chelates
44
Q

Drugs that protect gastric mucosa?

A

eg bismuth chelate (colloidal bismuth subcitrate, tripotassium dicitratobismuthate) - cytoprotective effects

45
Q

Describe how drugs protect gastric mucosa (bismuth chelate)

A
  • physical barrier (coat) over surface/base of ulcer
  • enhances local synthesis of PGs
  • promote bicarbonate secretion
  • bismuth chelate has toxic effects on bacillus:
  • prevents adherence of H. pylori to mucosa
  • or inhibit its proteolytic activity - stimulates bicarbonate secretion to ↑PG synthesis + adsorbs pepsin
46
Q

Unwanted effects of bismuth chelate?

A

nausea, vomiting, blackening of tongue + faeces

47
Q

Warning of bismuth chelate?

A

If patient has renal impairment, [bismuth chelate]plasma rises causing encephalopathy
DO NOT EXCEED RECOMMENDED DOSE

48
Q

Effect of diff does of bismuth chelate?

A
  • Minor ingestions: nausea, epigastric discomfort only
  • Moderate/substantial ingestions: nausea, vomiting, abdominal pain within hrs, precede features of nephrotoxicity + neurotoxicity delayed for days eg renal glomerular, tubular failure, muscle cramps, weakness, blurred vision, hyperreflexia. Liver transaminase activities increased
  • Chronic excess ingestion (excess daily ingestion or exceeding advised duration) : bismuth encephalopathy with insidious onset of incoordination, behavioural changes, memory deterioration, psychiatric symptoms progressing to fulminant encephalopathy with myoclonic jerks, confusion, dysarthria, coma, convulsions
  • Chronic bismuth poisoning : erythematous rashes, renal failure, thrombocytopenia, bone demineralisation, spontaneous fractures of thoracic vertebrae, paralytic ileus-like syndrome.
49
Q

Patient advice when taking metronidazole for treatment of H. pylori infection?

A
  • Adhere to treatment
  • Resistance to metronidazole
  • Disulfiram-like reaction if metronidazole taken with alcohol :
  • If severely ill stop taking drug
  • Disulfiram inhibits acetaldehyde dehydrogenase, build up of acetaldehyde → unpleasant flushing + nausea
  • Don’t give in 1st trimester or else –> midline facial defects (cleft lip/palate, holotelencephaly)

Holoprosencephaly (arhinencephaly) = cephalic disorder where prosencephalon (forebrain of embryo) fails to develop into 2 hemispheres

50
Q

Clinical uses of proton pump inhibitors + eg?

A

eg omeprazole, lanzoprazole, rabeprazole

  • Peptic ulcer, reflux oesophagitis, component therapy for H. pylori
  • Treatment of Zollinger-Ellison syndrome
  • If hyper-secretion occurs eg Zollinger-Ellison syndrome
51
Q

Describe how proton pump inhibitors work

A
  • Weak bases; inactive at neutral pH + irreversibly inhibit H+/K+-ATPase pump
  • Decreases basal + food-stimulated gastric acid secretion
52
Q

Role of Omeprazole + Ranitidine?

A

lower acid production
Omeprazole = proton pump inhibitor
Ranitidine = H2 receptor agonist

53
Q

Constipation :

A
  • Subjective complaint
  • Obstruction? → constipation so investigate
  • Is freq of bowel movement normal?
  • Normal/regular bowel opening = 1-3x daily
  • Doesn’t have to be regular to be physiologically adequate
  • No toxic substances accumulate upon prolonged constipation
54
Q

Consequences of constipation from rectal distension?

A 
Headache from low blood sugar
Loss of appetite
Nausea
Abdominal distension and stomach pain
Holding of faecal matter → ↑water loss + dryer faeces (painful + harder to defecate)
55
Q

Causes of constipation?

A 
Diet
↓ motility of large intestine
Damage to enteric nervous system of the colon?
Disease?
Old age
Drugs?

In elderly
Diet
Inactivity
Drugs (polypharmacy)

56
Q

Alarm signs + symptoms of patients with chronic constipation?

A

Acute onset constipation in older individuals
Weight loss (10lb)
Blood in the stool
Anaemia
Family history of colon cancer or inflammatory bowel disease

57
Q

Factors that can increase colonic motility?

A

↑Distension of large intestine to improve symptoms :

  • ↑Fibre, cellulose, complex polysaccharides
  • Bran, fruits + vege with high fibre
  • Laxatives, but excessive → ↓responsiveness
  • Mineral oil – lubricates faeces
  • Castor oil – stimulates motility of colon
58
Q

Management of constipation?

A

Lifestyle changes
Diet, fluid intake, exercise and their effects on constipation (appealing?)
↑ fibre intake → bloating and flatulence (not appealing)
↑ water intake??

59
Q

Features of bulk-forming + osmotic laxatives?

A
  • Bulk laxatives: methylcellulose,
  • Plant gums (eg sterculia, agar, linseed, bran, ispaghula husk- are polysaccharide polymers)
  • Retain water in gut lumen → promotion of peristalsis few days to work
  • Increase stool’s solid content
  • Bloating + flatulence
60
Q

What are purgatives?

A

laxatives, faecal softeners, stimulant purgatives can modulate/hasten food transit in intestine

61
Q

What are laxatives?

A

=(purgatives, aperients)
-Loosen stools + increase bowel movements
-Treat + prevent constipation
Psyllium husks = isphaghula

62
Q

What’s sterculia?

A

Natural dietary fibre to treat constipation or to regulate passage of food via digestive system in people with certain long-term bowel disorders

63
Q

Describe effect of osmotic laxatives: lactulose

A
  • ↑+maintain volume of fluid in bowel lumen by osmosis
  • ↑ transfer of gut contents into intestine
  • ↑ volume of gut content entering colon
  • distension + purgation (evacuation of the bowels)in 1hr
  • High doses → flatulence, cramps, diarrhoea, vomiting, tolerance
64
Q

Why does lactulose increase growth of colonic bacteria?

A

carbohydrate source for lactobacilli + bifidobacteria

65
Q

Describe lactulose mode of action

A
  • unchanged lactulose reaches colon
  • colonic bacteria breaks it down -> short chain FA (isobutyrate, butyrate, isovalerate, valerate, isocaproate, caproate)
  • osmotic p + biomass increases
  • softening of faeces
  • volume of stool increases
  • stimulates peristalsis
  • colon transit time decreased
66
Q

Role of antidiarrhoeal agents?

A
  • Maintain body fluids + electrolytes
  • Identify causal organism + if possible treat with antibiotics eg. erythromycin for Campylobacter jejuni
  • Modify secretion/absorption balance
67
Q

Features of Campylobacter jejuni?

A
  • Gram-negative slender, curved, motile rod
  • Microaerophilic organism so needs reduced levels of oxygen
  • Fragile, sensitive to environmental stresses (eg 21% oxygen, drying, heating, disinfectants, acidic conditions)
  • Cause of gastroenteritis in developed countries
68
Q

Causes of diarrhoea?

A

Infectious agents
Toxins
Anxiety
Drugs: antidepressants (amitriptyline, doxepin), antihypertensives (clonidine); pain medication (codeine, tramadol, methadone), opioid –containing cough medicines hydrocodone butyrate; aluminium antacids, calcium supplements; antibiotics

69
Q

Acute diarrhoeal diseases:?

A
  • Diarrhoea → ↑motility of GIT, with ↑secretion +↓ absorption of fluid → ↓electrolyte (Na+) +H2O
  • Malnutrition
  • Cholera toxins → loss of gut contents
70
Q

Therapeutic strategies to diarrhoea treatment?

A
  • Maintain fluid + electrolyte balance: Oral rehydration therapy
  • Anti-infectives: Bacterial infections may resolve with time :
  • Campylobacter sp: cause of gastroenteritis in UK
  • Use erythromycin or ciprofloxacin in severe infections
  • If viral no anti-infectives
  • Non-microbial anti-diarrhoeal agents
  • Anti-motility drugs: adsorbents + agents that modify fluid, electrolyte transport
71
Q

Movement of substances modulated by?

A

Purgatives: ↑passage of food via intestine

72
Q

Agents that ↑motility without → purgation?

A

Antidiarrhoeal drugs → ↓movement

Antispasmodic drugs → ↓movement; relax smooth muscles in GIT

73
Q

Features of traveller’s diarrhoea?

A
  • Gorbach, 1987: Travelling broadens the mind + loosens the bowel
  • 3 million people travel abroad/yr + experience it
  • But some infections may be self-limiting
74
Q

Effect of Loperamide?

A

Selective on GIT, decreases passage of faeces;

Decreases duration of illness

75
Q

Effect of Codeine + loperamide

A

Anti-secretory action;
↓ intestinal motility
↓ stomach cramps

76
Q

Effect of Bismuth subsalicylate?

A

Decreases fluid secretion in bowel;
Safe for young children;
May cause tinnitus + blackening of stool

77
Q

Effects of loperamide?

A

-μ-opioid receptor agonist of the myenteric plexus (controls motility + secretion of GIT) of large intestine
Inhibits gastric emptying
-Increases sphincter tone
-Induces stationary motor patterns
-Blocks peristalsis
-Spasmolytic (antispasmodic) agent which reduces smooth muscle activity in GIT –> reduces passage of faeces
-Reduces force + speed of colonic movement
-Increases haustral mixing of proximal colon
-Inhibits propulsive mass movement of distal colon
-Doesn’t cross BBB – no CNS effects

GI (15 decks)

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