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MPharm2 SL22105 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is IBS?

A

Most common disorder of the digestive system
Affects 10% of the global adult population
Different classifications IBS-D, IBS-C and IBS-M

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2
Q

What are the 4 options to treat IBS?

A

Targeted towardssymptoms rather than cause
Disease classification defines treatment options
- Antispasmodics
- Laxatives
- Anti-diarrhoeals
- Antidepressants

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3
Q

What are antispasmodics, and what are the three most common?

A

Smooth muscle relaxants

Alverine citrate
- 5-HT antagonist

Hyoscine butylbromide (Buscopan®)
- Muscarinic antagonist

Mebeverine hydrochloride(Colefac®)
- Unknown mechanism of action

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4
Q

What are the 3 types of antidiarrhoeals?

A

Anti-motility
- Loperamide
- µ- opioid receptor agonist
- Increase transit time

Oral-rehydration therapy

Anti-secretory
- Bismuth subsalicylate

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5
Q

How do anti-depressants work against IBS?

A

Can block signals to the GI tract so have effect on
- Gut motility
- Visceral hypersensitivity
- GI transit speed

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6
Q

What are the 3 other approaches to treating IBS?

A
  • Low FODMAP diet
  • Cognitive behavioural therapy (CBT)
  • Drug treatment (Asimadoline or Elobixibat)
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7
Q

What is IBD and the 4 common symptoms?

A

Disorders involving chronic inflammation of the GI tract
- Crohn’s disease
- Ulcerative colitis

Symptoms include
- Diarrhoea
- Abdominal pain
- Fatigue
- Weight loss

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8
Q

What is Crohns and the 5 most common symptoms?

A

Inflammation of entire GI tract in patches
Ulcers that penetrate entire width of abdominal lining

  • blood in poo
  • stomach cramps
  • fatigue
  • weight loss
  • diarrhoea
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9
Q

What is Ulcerative Colitis and the 4 most common symptoms?

A

Inflammation contained to large intestine and rectum, ulcers penetrate inner lining only
- diarrhoea that may contain blood, mucus or pus
- fatigue
- weight loss
- frequent need to poo

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10
Q

What is the order of IBD treatment incresing in severity?

A
  1. Aminosalicylates
  2. Corticosteroids
  3. Immunomodulators
  4. Biologic therapies (JAK inhibitors)
  5. Surgery
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11
Q

What are the 4 most common aminosalicylates and what is the MoA?

A

Mesalamine
Sulfasalazine
Olsalazine
Balsalazide
Anti-inflammatory effects through
- InhibitingCOX

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12
Q

What are the 2 most common corticosteroids and how do they work?

A

Prednisolone
Budesonide
- Alter immune cell function
- Inhibit inflammation

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13
Q

What are the 2 most common immunomodulators and how do they work?

A

Mercaptopurine
Azathioprine

Suppresses genes associated with intestinal inflammation and leukocyte trafficking to the gut

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14
Q

What are biologic therapies and the two MoAs??

A

Monoclonal antibodies that target specific aspects of the immune response that either:
Inhibit TNF-α
or
Inhibit adhesion molecule expression

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15
Q

Which JAK inhibitor is available and what does it do?

A

Tofacitinib
JAK activation stimulates cell proliferation, differentiation, apoptosis.

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16
Q

What is coeliac disease and how is it diagnosed?

A

Chronic autoimmune disorder
Triggered by gluten ingestion in genetically susceptible individuals
Damages the small intestine
Diagnosed by blood test to look for presence of antibodies

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17
Q

What are the 6 symptoms of coeliac disease?

A
  • Mouth - ulcers and tooth enalmel erosion
  • GI - diarrhoea, bloating and constipation
  • weight loss
  • infertility, miscarriage
  • joint and muscle pain
  • skin - brittle nails, acne and eczema
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18
Q

What is the auto immune response in coeliac disease?

A

Pro-inflammatory and pathogenic immune response towards certain parts of gluten and the intestinal tissue itself, resulting in structural changes

Th1 cells that produce high levels of pro-inflammatory cytokines

Cytotoxic effects on epithelial cells

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19
Q

How is coeliac treated?

A

Gluten free diet

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20
Q

What are the 5 main causes vomiting?

A
  • Ingestion of irritants, toxins, bacteria, virus
  • Motion sickness (Disconnect between visual stimuli and proprioception)
  • Distention of stomach (large volumes)
  • Opioid therapy
  • Early pregnancy
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21
Q

What are emetics?

A

NOT recommended in humans
Risk of acid aspiration & oesophagitis

Used in veterinary medicine for non-corrosive poisons
Emetics not safe in rodents, rabbits, horses, birds…

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22
Q

What is chemo induced vomiting both central and peripheral mechanidm?

A

Central Mechanism:
Agent activates the Chemoreceptor Trigger Zone,
which causes release ofneurotransmitters that activate the vomiting centre

Peripheral Mechanism:
Agent causes irritation to gastrointestinal mucosa resulting in neurotransmitter release, which sends signals to vomiting centre

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23
Q

What is post operative N+V and what are the 5 most common causes?

A

Any nausea, retching or vomiting occurring 24-48 hr after surgery
PONV can be triggered by opioids, volatile anaesthetics, anxiety, adverse drug reactions and motion.

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24
Q

What is morning sickness?

A

Several theories about cause
- Increasing levels of HCG or oestrogen overstimulate the CTZ
- Increased production of stomach acid and hypoglycaemia may irritate the stomach and trigger vomiting

Dehydration - severe cases now managed with intravenous infusion
Usually resolves at 16-20 weeks

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25
What are muscarinic receptor antagonists, what are they used for and what are the 3 common side fx?
Anti-cholinergic Cross BBB Action in vestibular system Blocks parasympathetic nerve transmission Useful in motion sickness Can be administered by transdermal patch Side effects – dry mouth, blurred vision, drowsiness
26
What are anti-histamines (as anti-emetics), what are they used for and what are the 2 common side fx?
Act at vestibular nerve Likely some anti-muscarinic activity Useful in motion sickness Promethazine sometimes used in severe morning sickness Side effects – drowsiness, sedation
27
Where do 5-HT3 antagonists act and what are they used for?
Action in the CTZ and GI tract Useful in PONV, and CINV Not effective for motion sickness
28
What are Dopamine receptor antagonists, what are they used for and how?
Many have anti-muscarinic properties Action in the CTZ and GI tract Administered as suppositories Useful in PONV
29
What are neurokinin antagonists and what are they used for?
Target CTZ, emetic centre and GI tract Usually as adjunct Treatment of CINV
30
How do corticosteroids work as anti-emetics and what are they used for?
Direct action on emetic centre Interaction with 5-HT and NK1 receptors Reduce inflammation and stress Treatment of CINV
31
How do prokinetics work as anti-emetics and what are they used for?
Promote gastrointestinal transit Speed up gastric emptying Likely target CB1 in GI tract Used when vomiting induced by gastric stasis
32
How do Phosphorylated carbohydrate solutions work as anti-emetics?
Contain dextrose/fructose Reduce smooth muscle contractions
33
Which herbal remedies are suggested for N+V and when are they reccomended?
Ginger, camomile, lemon oil, mint Suggested by NICE and NHS in pregnancy & postoperative nausea
34
How much gastric acid per day, what pH? Where produced, why?
- ~ 2.5 litres per day - Stomach pH between 2 and 3 - Produced by the parietal cells - Defense mechanism against pathogens – bactericidal and digestion
35
How is secretion of gastric acid controlled?
Histamine involved in the control of gastric acid secretion Histamine released from enterochromaffin-like cells (ECL) Acid secretion driven by activation of parietal cell
36
How is gastric acid secretion enabled and inhibited?
Enabled by consumption of food Inhibited by neural and hormonal reflexes
37
What is the mucus barrier in the stomach?
Gel polymer of hydrated mucin glycoproteins Secreted by surface mucous epithelial cells Protects stomach lining from acid and pepsin
38
What are peptic ulcers, what are the 4 common symptoms and what are the 4 main causes?
Ulceration of stomach or duodenum Symptoms - abdominal pain, bloating - nausea, vomiting - bloody vomit - melena (black stool) Associated with - Helicobacter pylori infection - Chronic NSAID use - Smoking - Stress
39
What is GORD and what are the 4 main symptoms?
Gastro-oesophageal reflux disease Symptoms - heartburn, acid reflux - oesophagitis - bloating and belching - nausea
40
How do antacids treat peptic ulcers and what are the 4 most common?
Neutralisation of stomach acid  - Sodium bicarbonate (Alka Seltzer) - HCO3- buffers H+ - Calcium carbonate (Tums, Rolaids) - CO32- buffers H+ - Aluminium hydroxide (Gaviscon) - OH-  binds H+ - Magnesium hydroxide (Milk of Magnesia) - OH-  binds H+
41
Which 3 drug types can be used to inhibit gastric acid secretion?
H2 antagonists Cholecystokinin receptor antagonists Proton pump inhibitors
42
What are H2 receptor antagonists?
Histamine released from ECL H2 receptors on parietal cells are inhibited so less GA released
43
What are proton pump inhibitors?
Irreversibly block H+/K+ ATPase  (proton pump) in parietal cell Oral dosage in enteric capsules as pro-drugs, pass through stomach, absorbed in small intestine and into blood Accumulate in acid environment of parietal cell canaliculi selectively activated Increasing activity over 5-7 days, irreversibly block the proton pump
44
What are cytoprotective drugs?
Enhance mucosal barrier Alginates naturally occurring, increase viscosity and tenacity of mucus, keeps the gastric contents in place eg. Gaviscon Sucralfate  complex of aluminium hydroxide and a sulphate derivative of sucrose reacts with hydrochloric acid in the stomach to form a viscous paste barrier at the ulcer surface
45
What are prostaglandin agonists?
Reduces gastric acid and pepsin secretion via inhibition of ECL cell Stimulates mucus and bicarbonate secretion by epithelium Increases mucosal blood flow by dilator action on arterioles
46
What are NSAID induced gastric ulcers?
NSAIDs can exacerbate or lead to gastric ulceration Direct irritation of stomach lining Inhibit prostaglandin production via action on COX Removes cytoprotective effects Decreases platelet aggregation – increased bleeding
47
What is achlorhydria and what are the 4 main causes?
No HCl production in stomach Increased stomach pH Caused by - medication - gastric bypass surgery - H. pylori infection - stomach cancer
48
What is primary constipation?
The most common cause of constipation The bowel is healthy but not working properly
49
What are 6 causes of secondary constipation?
- Endocrine/metabolic diseases - Systemic diseases - Myopathy  - Neurologic disease - Structural abnormalities - Iatrogenic (drug-related)
50
What are the 4 types of laxative?
- Bulk-forming (incr. size and fluid) - stool softening (incr. fluid) - osmotic (incr fluid retention) - Stimulant (incr. peristalsis)
51
What are the 4 mechanisms of diarrhoea?
- osmotic - secretory - inflammatory - abnormal motility
52
What is osmotic diarrhoea?
Excessive amounts of insoluble material in the lumen,  water not reabsorbed Ingested solutes poorly absorbed Malabsorption eg. lactose intolerance
53
What is secretory diarrhoea?
Abnormal ion transport, decrease in electrolyte absorption Excessive secretion and/or absorption across the intestinal epithelium Exposure to toxins = prolonged opening of Ca channel
54
What is inflammatory diarrhoea?
Mucosal destruction Defective absorption of fluid and electrolytes Associated with both fluid and blood loss Caused by infection or disease
55
How does abnormal motility causes diarrhoea?
Increased motility leads to decreased absorption of fluid/electrolytes Increased or decreased contact time between luminal    contents and mucosal surface A problem within the muscles that controls     peristalsis A problem with the nerves or hormones that  govern muscle contraction
56
What are the 3 causes of diarrhoea?
Viruses Rotavirus and small round structured virus (SRSV; e.g., norovirus) Bacteria  Including Campylobacter , E. coli, Salmonella & Shigella  Antibiotics  Any form of antibiotic treatment, but generally ‘broad-spectrum’
57
What is oral rehydration therapy?
prevents or reverses dehydration combination of sugars and salts, specifically sodium and potassium stimulates water and electrolyte absorption from the GI tract
58
Which three chemicals promote release of gastric acid?
- acetylcholine - gastrin - histamine
59
What are the 6 stages of drug development?
- choose target - validate biology - lead discovery - refinement (SAR + QSAR) - final optimisation - drug to market
60
What is SAR?
Structure Activity Relationship (SAR) Synthesise a range of compounds related to the lead compound to allow one to see how structural variations affect activity
61
How can you turn agonists into antagonists?
e.g. Histamine binding as an agonist. Change of shape is stabilised, “switching on” the H2 receptor. Histamine analogue binding as an antagonist. Add extra structural units/functional groups to find extra binding interactions (what types??). Block receptor activation. e.g. extra hydrophobic/philic units
62
What was the chain extention theory used for?
elongating the length of the flexible chain pushes polar groups further apart and increases antagonist interaction
63
What is QSAR?
Quantitative Structure Activity Relationship approach Principle: attempt to identify and quantify the physicochemical properties of a drug and investigate whether they affect its biological activity. Aim: derive a mathematical formula relating the biological activity of a series of compounds to particular physicochemical properties (hydrophobicity, electronic effects, sterics).
64
What are proton pumps?
H+/K+-ATPase (pumps protons out of the parietal cell at the same time as it pumps potassium ions back in). Energy required for the process is provided by hydrolysis of ATP to ADP The final stage of the acid secretion process
65
What are the three reasons why PPIs have so few side effects?
The target enzyme (proton pump) is only present in parietal cells. Canaliculi of parietal cells are the only compartments in the body with sufficiently low pH to activate PPIs Protonation prevents the drugs from returning to general circulation and leads to concentration at the target site. Once activated, PPIs react rapidly with the target
66
Why are PPIs irreversible inhibitors?
Inactivation of the proton pump is irreversible. Gastric acid secretion is halted until new pumps are generated by the cell = long duration of action.
67
How do PPIs work?
The PPIs are weak bases and so are not ionised at pH of the intestinal fluid (6.5) or blood (7.4). After crossing the membrane of parietal cells into acidic conditions of canaliculi (pH < 2), PPIs are ionised and cannot cross back into cell. PPIs are prodrugs so are activated at strongly acidic pH.
68
What are the 5 steps to separate a drug from COOH metabolite?
- Add water to the drug and COOH metabolite (aqueous phase) - Add base to take the pH up to 12-13, so the COOH metabolite is in the COO- form (and water soluble) - Add to a separating funnel and extract with a suitable organic solvent (usually x3), remove the organic layer and dry. - Keep the aqueous layer and acidify it, taking the pH down to 2-3, so the COOH metabolite is in the COOH form. - Extract with suitable solvent (x3) and dry.
69
What is LC-MS?
HPLC combined with MS

MPharm2 SL22105 (8 decks)

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