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Physiology 1 > 38) Pharmacological basis for the treatment of GI disorders > Flashcards

38) Pharmacological basis for the treatment of GI disorders Flashcards

1
Q

What area of the GI tract are of pharmological importance?

A
  • Gastric secretions
  • Vomiting
  • Gut motility
  • Bile formation and excretion
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2
Q

What are the anti-secretory agents?

A
  • Chemicals that reduce the secretion of gastric acid
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3
Q

What are H2 receptors antagonists used to treat?

A
  • They are used to treat peptic ulcers and reflux oesophagitis
  • They promote the healing of duodenal ulcers but if treatment stops relapse may occur
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4
Q

How do H2 receptor antagonists work?

A
  • The act on H2 receptors (the receptors histamine bind to) to prevent the secretion of gastric acid
  • They inhibit histamine, ACh and gastrin stimulated acid secretions of the parietal cells
  • This reduces gastric acid secretion and as a result reduces pepsin secretion
  • This is because acid secretion is crucial for the conversion of pepsinogen (inactive) to pepsin (active)
  • This results in a huge decrease in basal and food stimulated acid secretions
  • Two examples are ranitidine and cimetidine
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5
Q

What are some unwanted effects of H2 receptor antagonists?

A
  • They may cause diarrhoea, muscle cramps, transient rashes and hypergastrinaemia (too much gastrin secretion)
  • Cimetidine may cause gynaecomastia in men which can decrease sexual function
  • Cimetidine may also inhibit P450 enzymes which decreases metabolism of many drugs metabolised by P450 (e.g. anticoagulants and antidepressants)
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6
Q

Which H2 receptor antagonist is more active?

A
  • Ranitidine is more potent than cimetidine as on a dose response curve ranitidine had a lower IC50 (less drug was needed to illicit half the response of the drug)
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7
Q

What are proton pump inhibitors used for?

A
  • To treat peptic ulcers
  • To treat reflux oesophagitis
  • As a component of therapy for H.pylori
  • Can be used in the treatment for Zollinger-Ellison Syndrome
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8
Q

How do proton pump inhibitors work?

A
  • They are weak bases and so has the potential to accumulate in acidic components (e.g. stomach)
  • It will concentrate in these areas and so will inhibit the H+/K+ ATPase pump
  • Therefore there is decreased basal and food-stimulated gastric acid secretion
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9
Q

What are some unwanted effects of proton pump inhibitors?

A
  • Headache
  • Diarrhoea
  • Mental confusion
  • Rashes
  • Somnolence
  • Impotence
  • Gynaecomastia
  • Dizziness
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10
Q

What protects the gastric mucosa?

A
  • Prostaglandins protect the gastric mucosa and are said to be gastroprotective
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11
Q

How does prostaglandin protect the mucosa?

A
  • If there is too much acid secretion prostaglandin will inhibit basal and food stimulated gastric acid secretion
  • It will also inhibit histamine and caffeine induced gastric acid secretion
  • As a result it inhibits the activity of parietal cells
  • It also promotes the secretion of mucus and HCO3- as well as increases blood flow to the mucosa
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12
Q

What gastroprotective agent (drug) is given to patients?

A
  • Misoprostol (a stable analogue of prostaglandin)
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13
Q

What gastroprotective agent (drug) is given to patients?

A
  • Misoprostol (a stable analogue of prostaglandin)
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14
Q

What is an unwanted effect of prostaglandin?

A
  • Induces labour/ labour
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15
Q

What gastroprotective agent (drug) is given to patients?

A
  • Misoprostol (a stable analogue of prostaglandin)
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16
Q

What is the effect of metoclopramide on gastric emptying and motility?

A
  • It inhibits pre sympathetic dopamine receptors and post sympathetic dopamine receptors.
  • It also inhibits 5-HT3 receptors in the CNS to inhibit vomiting
  • They stimulate 5-HT4 receptors in the ENS and so promotes gut motility
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17
Q

What are the effects of dopamine on the body?

A
  • Dopamine acts on dopamine receptors
  • It has relaxant effects n the gut by activating D2 receptors in the lower oesophageal sphincter and stomach
  • Overall dopamine can induce contractions in proximal regions but can induce relaxations in the distal areas of the small intestines
  • Dopamine can also inhibit the release of ACh which inhibits peristalsis (and decreases gut motility) and also inhibits some secretions
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18
Q

How does metoclopramide promote gastric motility and emptying?

A
  • Metoclopramide inhibit dopamine at D2 receptors
  • This causes an increase in the release of ACh
  • An increase in ACh increases the peristalsis which takes place (and thus increasing gastric motility)
  • Increased ACh also increases intragastric pressure as the tone of the lower oesophageal sphincter increases and so the tone of gastric contractions also increases
  • This improves the antroduodenal coordination which accelerates gastric emptying and relaxes the pyloric sphincter
  • It also stimulates 5-HT receptors and inhibitory nitregeric neurones which causes coordinated gut motility
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19
Q

What is another effect of metoclopramide?

A
  • It is able to inhibit nausea and so has antiemetic properties via central effects
  • It also relieves headaches via central effects
20
Q

What are the conditions in which metoclopramide is used?

A
  • Antiemetic effects via central pathways
  • Gastro-oesophageal reflux disease (GORD)
  • Relief symptoms of gastroparesis as it promotes gastric emptying to stimulate gastric motility and accelerate gastric emptying
21
Q

What are antispasmodic agents?

A
  • Drugs that decrease spasms in the bowel whilst also having a relaxant action on the smooth muscles of the GI tract
  • They are useful in irritable bowel syndrome and diverticular disease (a congenital lesion which can be a source of bacterial overgrowth)
  • Muscarinic receptor antagonists inhibit parasympathetic activity which reduces spasms of the bowel by inhibiting peristalsis
  • Examples include propantheline (antimuscarinic), dicloxerine and mebverine
22
Q

What are the main goals in pharmacological intervention in gastric ulcers?

A
  • Reduce acid secretion with H2 receptor agonist
  • Neutralise secreted acids with antacids
  • Attempt to eradicate H. pylori
  • Inhibition of acid secretion removes the constant irritation and allows the ulcer to heal
23
Q

When can drugs be used to combat excess gastric acid secretion?

A
  • In peptic ulcers
  • Reflux oesophagitis (as gastric acid can damage the oesophagus)
  • Zollinger- Ellison syndrome (gastrin producing tumour)
24
Q

Why do ulcers develop?

A
  • It is unclear as to why they develop although H. pylori is a risk factor
  • H. pylori is a gram negative bacteria which causes chronic gastritis which can lead to a duodenal ulcer
25
Q

How do antacids work?

A
  • They neutralise gastric acid by increasing the pH of the gastric acid which inhibits the activity of peptic acid (as peptic activity stops at pH 5)
  • Prolonged dosage can lead to healing of duodenal ulcers however it is less effective against gastric ulcers
26
Q

How does Bismuth chelate help with heartburn?

A
  • It protects the gastric mucosa by forming a base over the crater of the ulcer
  • It also absorbs pepsin while increasing HCO3- and prostaglandin
  • It is also toxic against H. pylori and can be used as part of triple therapy to eradicate it
27
Q

What are some side effects of Bismuth chelate?

A
  • It blackens tongue and stool
  • It can cause Reye’s syndrome in children with chicken pox or flu-like symptoms
  • Nausea
  • Vomiting
  • Can cause encephalopathy if renal impairment is present
28
Q

How does prostaglandin protect the stomach from damage?

A
  • They stimulate the secretion of HCO3- which neutralises gastric acid
  • They reduce H+ secretions
  • They stimulate mucus production
  • They promote vasodilation
29
Q

Why do NSAIDS cause gastric bleeding?

A
  • They inhibit COX which inhibits synthesis of prostaglandin and as a result we loose the gastroprotective effects of prostaglandin resulting in gastric bleeding
30
Q

How is H. pylori treated?

A
  • Antibiotics are required as it is a bacteria

- Protein pump inhibitors are also used to deal with the increased gastric secretion

31
Q

What advice is given to patients that are treating a H. pylori infection?

A
  • Adhere to treatment
  • Watch for resistance to metronidazole
  • Alcohol must not be taken when under metronidazole as a disulfiram reaction can occur where patients may feel severely ill and stop taking the drug. Disulfiram inhibits acetaldehyde dehydrogenase causing a build up of acetaldehyde leading to unpleasant flushing and nausea.
  • Do not give to pregnant women in the first trimester
32
Q

What is constipation?

A
  • A subjective complaint where there is an obstruction causing bowel movement to be less frequent than normal
  • Prolonged constipation does not cause harmful material to build up but rather causes hardening of the stool which is painful
33
Q

What are the consequences of constipation as a result of rectal distension?

A
  • Headache
  • Loss of appetite
  • Nausea
  • Abdominal distension and stomach pain
  • Holding faecal matter leads to increased water loss and dryer faeces making it harder to defecate
34
Q

What are the causes of constipation?

A
  • Decreased motility of the large intestine due to old age
  • Damage to enteric nervous system of the colon as this may affect the vago-vagal reflex
  • Poor diet
  • Drugs
35
Q

What are factors that can increase colonic motility and prevent constipation?

A
  • Increased fibre, cellulose and complex polysaccharides in diets
  • Bran and some fruits and vegetables with high fibre
  • Laxative however excessive use can decrease responsiveness
  • Mineral oil which lubricates faeces
  • Castor oil which stimulates motility of the colon
  • Increase water intake
  • Lifestyle changes
36
Q

What are the alarm signs and symptoms of chronic constipation?

A
  • Acute onset of constipation in older individuals
  • Weight loss
  • Blood in stool
  • Anaemia
  • Family history of colon cancer or inflammatory bowl disease
37
Q

How can we treat constipation using purgatives?

A
  • We use purgatives which modulate/hasten food transit through the intestines
  • These include laxative, faecal softeners and stimulants
  • Plant gums are polysaccharide polymers that retain water in the gut lumen (causing distension and promoting peristalsis) and they also increase the stool’s solid content
38
Q

How can we treat constipation using osmotic laxatives?

A
  • They increase and maintain volume of fluid in the lumen of the bowel through osmosis
  • They increase transfer of gut content into the intestine
  • They increase the volume of gut content entering the colon leading to distention and purgation
  • High doses can lead to flatulence, cramps, diarrhoea, vomiting and tolerance
39
Q

How do osmotic laxatives work?

A
  • Lactulose reaches the colon unchanged where the colonic bacteria break it down into fatty acids
  • These fatty acids cause osmotic pressure and biomass to increase
  • These factors soften the faeces and increase the volume of the stool causing peristalsis to be stimulated
  • As a result colonic transit time is shortened
40
Q

What is diarrhoea?

A
  • The frequent passage of liquid faeces
41
Q

How do we deal with diarrhoea?

A
  • Maintain body fluid and electrolytes
  • Identify cause and treat with antibiotics if possible
  • Modify secretions/absorbance balance
  • Use anti-motility drugs
  • Use anti-diarrhoeal agents
42
Q

What are the causes of diarrhoea?

A
  • Infectious agents (e.g. cholera toxins)
  • Toxins
  • Anxiety
  • Drugs
43
Q

How does acute diarrhoeal disease lead to electrolyte imbalance?

A
  • Diarrhoea causes increased motility of the GI tract with increased secretions and decreased absorption of fluids
  • This causes a decrease in electrolytes leading to electrolyte imbalance
44
Q

How do anti-diarrhoeal agents work?

A
  • Loperamide is selective to the GI tract and decreases passage of faeces. This decreases the duration of the illness
  • Loperamide also has anti-secretory actions as it decreases intestinal motility
  • Bismuth subsalicylate decreases fluid secretions in the bowel
45
Q

What is the mechanism of action of loperamide?

A
  • It is an opioid receptor agonist which binds to the (mu)-opioid receptor of the myenteric plexus of the large intestines
  • This causes inhibition of the bowel function as it inhibits gastric emptying, increases sphincter tone, induces stationary motor patterns and blocks peristalsis
  • It contains spasmolytic agents which reduce smooth muscle activity n the GI tract and hence reduces passage of the faeces
  • It reduces the force and speed of colonic movement by increasing haustral mixing of the proximal colon while also inhibiting propulsive mass movement in the distal colon
  • There is no CNS effect as they do not cross the blood-brain barrier

Physiology 1 (64 decks)

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