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Year 2- GIT > Gastrointestinal Pharmacology > Flashcards

Gastrointestinal Pharmacology Flashcards

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1
Q

What can excess acid secretion lead to?

A

Ulceration of mucosa

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2
Q

List the drug types which can help reduce acid secretion in the GIT.

A

Antacids
H2 receptor (histamine) antagonists
PPI’s

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3
Q

List some drugs which can affect motility in the GIT.

A

Anti-emetics
Anti-muscarinic
Anti-spasmodic
Anti-molility

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4
Q

List some drugs that can be used in treatment of IBD.

A

Corticosteroids
Immunosuppressants
Aminosalicyclates
Biologics

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5
Q

List some drugs which can affect the biliary secretions.

A

Bile acid sequestrants
Ursodeoxycholic acid

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6
Q

Name the two plexus’ of the enteric NS.

A

Myenteric plexus
Submucosal plexus

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7
Q

Where would you find the myenteric plexus?

A

Between the circular muscle layer and longitudal muscle layer

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8
Q

Where would you find the submucosal plexus?

A

Between the circular muscle layer and the submucosa

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9
Q

Where do the two plexuses of the enteric NS receive their pre-ganglionic parasympathetic fibres from?

A

Vagus nerve

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10
Q

What do the pre-ganglionic parasympathetic fibres for the enteric NS cause to happen?

A

Mostly excitatory so increase muscle contraction

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11
Q

What is the main neurotransmitter for the pre-ganglionic parasympathetic fibres of the ENS?

A

Acetylcholine

->substance P is also released and has a similar excitatory response.

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12
Q

What do acetylcholine Vasoactive intestinal peptide do?

A

Excitatory neurotransmitters which evoke secretion from intestinal crypts.

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13
Q

Are the parasympathetic fibres in the ENS mainly preganglionic or postganglionic?

A

Preganglionic

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14
Q

Are the sympathetic fibres in the ENS mainly preganglionic or postganglionic?

A

Postganglionic

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15
Q

Do the parasympathetic nerve fibres inhibit or stimulate the nerve plexuses of the GIT?

A

Stimulate

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16
Q

Do the sympathetic nerve fibres inhibit or stimulate the nerve plexuses of the GIT?

A

Inhibit

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17
Q

What role do sensory neurons play in the ENS?

A

Form part of the reflex pathways which respond to mucosal stroking and distension.
This means that they contract muscle above the bolus and relax muscle underneath to allow bolus to move through the GIT.

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18
Q

Which paracrine cells are released from cells throughout the GIT and act on nearby cells and have an important role in regulation of acid secretion?

A

Histamine
Somatostatin

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19
Q

Which receptors does gastrin bind to?

A

CCK2 receptors

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20
Q

What happens when gastrin binds to CCK2 receptors?

A

Mobilisation and exocytosis of histamine

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21
Q

Which type of receptor is CCK2?

A

G-protein coupled receptor

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22
Q

Which receptors can histamine bind to and which one specifically in related to the GIT?

A

H1- allergy related
H2- GI related

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23
Q

Which type of receptor is H2?

A

G-protein coupled receptor

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24
Q

What happens when histamine binds to the H2 receptor?

A

Increase in cAMP which then promotes gastric acid secretion.

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25
Q

What is the function of the membrane folds called canaliculi?

A

Increase surface area available for the secretion.

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26
Q

Vagal stimulation releases acetylcholine. What will acetylcholine bind to?

A

M3 receptors

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27
Q

As well as binding to M3, what can acetylcholine cause the release of?

A

Histamine

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28
Q

List some conditions which can cause damage to the GIT because of acid secretion.

A

Barrett’s oesophagus
GORD
Peptic ulcer disease

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29
Q

Physiologically, what causes reflux problems?

A
  1. Abnormalities in the neural or myogenic control of lower oesophageal sphincter
  2. High abdominal pressure due to lesions which occupy space
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30
Q

Given some examples of space-occupying-lesions which can lead to high abdominal pressure which can cause reflux.

A

Tumours
Ascites fluid
Pregnancy- baby taking up space

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31
Q

Which prostaglandins inhibit the production of acid and increase mucous secretion?

A

Prostaglandin E2 and I2

->if there is not the correct balance between the release of acid and mucous, damage and ulceration might occur.

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32
Q

How can nitric oxide help with ulceration?

A

Promotes healing blood flow to areas of ulceration

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33
Q

As well as acid production, what else can cause damage to the gut mucosa?

A

H.pylori infection

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34
Q

How can H.pylori cause damage to the mucosa?

A

Organism causes inflammation putting epithelial cells in direct contact with acid

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35
Q

What should be tested for in those with GORD or ulceration?

A

Test for H.pylori

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36
Q

What is the treatment if the patient is positive for H.pylori?

A

Triple therapy- PPI and 2 antibacterials

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37
Q

Which antibacterials should be given in the treatment of H.hylori infections?

A

Amoxicillin and metronidazole/clarithromycin

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38
Q

What do PPI’s do?

A

Reduce the secretion of gastric acid

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39
Q

What is the treatment for GORD or ulceration if the patient is negative for H.pylori?

A

Acid suppression using -
-Antacids
-Alginates

May want to use PPI’s or H2-receptor antagonists
Other mucosal protectors

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40
Q

Give an example of a common alginate that can be purchased over the counter.

A

Gaviscon

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41
Q

How do antacids and alginates help with acid suppression?

A

Neutralise acid

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42
Q

What can happen if over the counter medication for acid suppression is used excessively?

A

May be masking something more serious.
May get excess rebound acid production when stopping taking the medication.

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43
Q

What is Sucralfate ?

A

Medication which is used in treatment against ulcers

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44
Q

How does Sucralfate work?

A

In an acidic environment, it hydrolyses and turns into a thick paste which coats the mucosa.

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45
Q

Name some of the mucosal protecting drugs.

A

Sucralfate
Bismuth
Misoprostol

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46
Q

Give an example of a H2 receptor antagonist.

A

Ranitidine

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47
Q

What is the mechanism of action for Ranitidine?

A

Blocks histamine receptors and blocks acid secretion

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48
Q

When may H2 receptor antagonists, like Ranitidine be given?

A

GORD
Peptic Ulcer Disease

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49
Q

Give an example of a PPI.

A

Omeprazole

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50
Q

What is the mechanism of action for PPI’s, like omeprazole?

A

Irreversible inhibitor of the proton pump

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51
Q

When may PPI’s, like omeprazole, be given?

A

GORD
Peptic Ulcer Disease

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52
Q

What are some of the adverse effects of PPI’s, like omeprazole?

A

More likely to have C.difficile infection
B12 deficiency
ECL tumours
AIN (type of kidney disease)

53
Q

Describe the reaction of vomiting.

A

Defensive reaction to get rid of toxic or irritant components of the gut

54
Q

Describe the motor involvement of the gut in vomiting.

A

Contraction of diaphragm and abdominal muscles to squeeze the stomach

55
Q

Describe the autonomic activity during the process of vomiting.

A

Increased salivation
Relaxation of smooth muscle and superior end of GIT, and contraction at inferior end to create pressure gradient to push vomit up!

56
Q

Where in the brain is the vomiting centre?

A

Medulla

57
Q

What does the vomiting centre in the medulla do?

A

Receives input from chemoreceptor trigger zone which detects toxins in the blood

58
Q

Why might you be sick after being dizzy?

A

Being dizzy creates the same affects as being poisoned so if dizzy, the brain thinks that there is poison that the body needs to eject, hence the vomiting

59
Q

Which system is reliable for the whole vomiting while dizzy thing?

A

Vestibular system

60
Q

Which receptors is the Vestibular system mediated by?

A

Muscarinic receptors
H1 receptors

61
Q

What can activation of NK1 and CB1 receptors cause to happen?

A

Vomiting

62
Q

Which receptors are associated with the integration of signalling within the medulla?

A

D2 receptor
M1 receptor

63
Q

When may you give a NK1 antagonist?

A

Late phase of cytotoxic emesis (nausea and vomiting caused by chemo or radiotherapy).

64
Q

When may you give CB1 drugs?

A

If patient has cytotoxic drugs

65
Q

USEFUL

A

Look at the slide on the powerpoint when going over drugs so you can visualize what is happening pls xx

66
Q

When may you give H1 receptor antagonist drugs?

A

Motion sickness

67
Q

When may you give anti-muscurinic drugs?

A

Motion sickness

68
Q

When may you give a D2 (dopamine) antagonist?

A

During pregnancy

69
Q

When may you give 5-HT receptor antagonist drugs?

A

Cytotoxic drugs
Post surgery
Radiation

70
Q

What are some side effects of D2 (dopamine) receptor antagonists?

A

Sedation
Movement
Prolactin release

gal idk either, this is what she put on the slide and did not explain

71
Q

What are some of the side effects of CB1 drugs?

A

Drowsiness
Dizziness
Dry mouth

Triple D idk

72
Q

What are some of the side effects of anti-muscarinic drugs?

A

Dry mouth
Blurred vision

73
Q

It can be difficult to treat nausea, but which drugs can work?

A

Low dose antidepressants, especially tricyclics

74
Q

Which groups of drugs can be used in the treatment of constipation?

A

Purgatives
Agents that increase drug motility as aim of treatment is to move food through the gut more quickly

75
Q

Which groups of drugs can be used in treatment of diarrhoea?

A

Anti-diarrhoeal drugs- agents that slow down transit of food through the gut
Anti-spasmodic drugs which decrease smooth muscle tone

76
Q

What do bulk and osmotic laxatives do?

A

Increase volume and water content of stools

77
Q

Give an example of a bulk laxative.

A

Methylcellulose

->might be worth remembering that cellulose is associated with fibre

78
Q

What is the mechanism of action for osmotic laxatives?

A

They contain poorly-absorbed solutes that increase the osmotic load of the gut contents, drawing water into the stool.

79
Q

What are the pros and cons of bulk laxatives.

A

No adverse effects
Take a few days to work

80
Q

What are the pros and cons of osmotic laxatives?

A

Quick to work
May cause electrolyte disturbances.

81
Q

Give an example of a faecal softener.

A

Docusate sodium

82
Q

What do stimulant purgatives/laxatives do?

A

Increase electrolyte secretion by gut mucosa

83
Q

What are some side effects of stimulant purgatives/laxatives?

A

Cramping

84
Q

When are stimulant purgatives/laxatives contraindicated?

A

In cases of bowel obstruction.

85
Q

Given an example of a stimulant purgative/laxative which is taken orally.

A

Sodium picosulphate

86
Q

Give an example of a stimulant purgative/laxative which is taken suppository*.

*cone placed, usually up bottom. It dissolves to release mediciation

A

Biscodyl

87
Q

How does domperidone, a type of D2 antagonist, affect motility?

A

Increases motility

This is because it increases lower oesophageal sphincter pressure, increasing gastric emptying and duodenal peristalsis.

88
Q

How does metraclopramide affect motility?

A

Increases motility.

Increases gastric motility and emptying.

89
Q

Which types of drugs reduce motility?

A

Anti-diarrhoeal

90
Q

List some of the drug groups used in the treatment of diarrhoea.

A

Anti-infective drugs
Anti-diarrhoeal drugs
Anti-spasmatic drugs

91
Q

Which type of drug is often used to reduce motility?

A

Opiates e.g. loperamide

92
Q

Describe the treatment of IBS

A

Symptomatic treatment, may include anti-motility agents, antidepressants.
High residue diet, lots of fibre

93
Q

Which type of drug are used in the treatment of flare ups of IBD?

A

Corticosteroids, usually prednisolone

94
Q

What are some of the side effects of corticosteroids?

A

Osteoporosis
Cushingoid symptoms (moon-face appearance).
Thinning of skin
Increased risk of infection

95
Q

Which drugs are usually used in the treatment of chronic IBD?

A

Aminosalicyclates

96
Q

Give some examples of aminosalicyclates.

A

Mesalazine
Olsalazine

97
Q

What are some of the adverse effects of aminosalicyclates?

A

GI upset
Renal impairment
Blood dyscrasias

98
Q

Give some examples of immunosuppressants that can be used in the treatment of IBD.

A

Azathioprine
Cyclosporin
56-mercaptopurine.

99
Q

Describe the mechanism of action of immunosuppressants

A

Prevents the formation of purines which are required for DNA synthesis so reduces immune cell proliferation

100
Q

What are some of the adverse effects of immunosuppressants like azathioprine, cyclosporin, etc.?

A

Targets any rapidly dividing cells.
May cause bone marrow suppression
Organ damage. lungs, liver
Pancreatitis due to pancreatic damage

101
Q

Why are biologics only used for severe cases of CD?

A

Expensive
Blocks body’s response to infection

102
Q

What are some of the adverse effects of biologics?

A

Higher risk of infection
Infusion reaction causing fever and itch
Anaemia
Malignancy

103
Q

When can anti-spasmatic drugs be used?

A

Treatment of diarrhoea e.g. IBS

104
Q

Which receptors can acetylcholine bind to to cause smooth muscle contraction?

A

M2
M3

105
Q

What do antimuscarinic drugs do?

A

Inhibit the binding of acetylcholine to M2/M3 causing muscle relaxation and reduces spasm

106
Q

Give an example of a antimuscarinic.

A

Buscopan

107
Q

Which natural oil is an antimuscarinic?

A

Peppermint oil

108
Q

How does peppermint oil act as an antimuscarinic?

A

Contains calcium channel blockers which reduce calcium required for smooth muscle contraction

109
Q

What is the preferred treatment for gallstones?

A

Surgery

110
Q

Which drugs can be used to dissolve gallstones?

A

Usodeoxycholic acid

111
Q

How do bile acid sequestrants, like cholestyramine, lower cholesterol levels?

A

Cholesterol gets converted into bile acids, which are then excreted in bile. Bile acids sequestrants hold the bile in the gut, hence lowering cholesterol levels.

112
Q

What is one disadvantage of bile acid sequestrants?

A

May interfere with vitamin absorption

113
Q

How do a lot of drugs get distributed around the body?

A

Bind to plasma proteins

114
Q

Why may liver disease effect the distribution of drugs?

A

Less albumin in liver disease, affecting protein binding

115
Q

Where is the main site of drug metabolism?

A

Liver

116
Q

What is the effect of damaged gut wall in metabolism of drugs?

A

Less first-pass metabolism

117
Q

How can GI disease affect absorption of drugs?

A

pH
Gut length
Transit time

118
Q

What happens if drugs are excreted via the biliary system?

A

Drugs may build up

119
Q

What may happen to the liver due to the metabolism of drugs primarily taking place here?

A

May accumulate and have a hepatotoxic effect

120
Q

Which receptors do NSAIDs block?

A

COX1, COX2

121
Q

What are the adverse effects of NSAIDs?

A

Can cause mucosa bleeding

122
Q

How does inhibition of COX1 cause bleeding?

A

Reduced mucus and bicarbonate secretion
Reduced mucosa blood flow
Impaired platelet aggregation

All of this causes impaired defence and can lead to mucosa damage and bleeding

123
Q

How does inhibition of COX2 cause bleeding

A

Reduced angiogenesis causing impaired healing
Activation of leukocytes due to leukocyte adhesion.

Both cause mucosal damage and bleeding

124
Q

Which drug may cause acute hepatitis?

A

Paracetamol
Isoniazid
Ritonavir
Troglotazone

125
Q

Which drug may cause chronic hepatitis?

A

Diclofenec
Methyldopa
Minocycline
Nitrofurantoin

126
Q

Which drug may cause acute cholestasis?

A

ACEi
Co-amoxiclav
Chlorpromazine
Erythromycins

127
Q

Which drug may cause fibrosis or cirrhosis?

A

Methotrexate

128
Q

Which drug may cause NAFLD?

A

Amiodarone
Tamoxifen

129
Q
A

Year 2- GIT (37 decks)

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