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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
Q

What are muscarinic receptor antagonists, what are they used for and what are the 3 common side fx?

A

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

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26
Q

What are anti-histamines (as anti-emetics), what are they used for and what are the 2 common side fx?

A

Act at vestibular nerve
Likely some anti-muscarinic activity

Useful in motion sickness
Promethazine sometimes used in severe morning sickness

Side effects – drowsiness, sedation

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27
Q

Where do 5-HT3 antagonists act and what are they used for?

A

Action in the CTZ and GI tract

Useful in PONV, and CINV
Not effective for motion sickness

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28
Q

What are Dopamine receptor antagonists, what are they used for and how?

A

Many have anti-muscarinic properties
Action in the CTZ and GI tract
Administered as suppositories
Useful in PONV

29
Q

What are neurokinin antagonists and what are they used for?

A

TargetCTZ, emetic centre and GI tract
Usually as adjunct

Treatment of CINV

30
Q

How do corticosteroids work as anti-emetics and what are they used for?

A

Direct action on emetic centre
Interaction with 5-HT and NK1 receptors
Reduce inflammation and stress
Treatment of CINV

31
Q

How do prokinetics work as anti-emetics and what are they used for?

A

Promote gastrointestinal transit
Speed up gastric emptying
Likely target CB1 in GI tract

Used when vomiting induced by gastric stasis

32
Q

How do Phosphorylated carbohydrate solutions work as anti-emetics?

A

Contain dextrose/fructose
Reduce smooth muscle contractions

33
Q

Which herbal remedies are suggested for N+V and when are they reccomended?

A

Ginger, camomile, lemon oil, mint

Suggested by NICE and NHS in pregnancy & postoperative nausea

34
Q

How much gastric acid per day, what pH?
Where produced, why?

A
  • ~ 2.5 litres per day
  • Stomach pH between 2 and 3
  • Produced by the parietal cells
  • Defense mechanism against pathogens – bactericidal and digestion
35
Q

How is secretion of gastric acid controlled?

A

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
Q

How is gastric acid secretion enabled and inhibited?

A

Enabled by consumption of food
Inhibited by neural and hormonalreflexes

37
Q

What is the mucus barrier in the stomach?

A

Gel polymer of hydrated mucin glycoproteins
Secreted by surface mucous epithelial cells
Protects stomach lining from acid and pepsin

38
Q

What are peptic ulcers, what are the 4 common symptoms and what are the 4 main causes?

A

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
Q

What is GORD and what are the 4 main symptoms?

A

Gastro-oesophageal reflux disease
Symptoms
- heartburn, acid reflux
- oesophagitis
- bloating and belching
- nausea

40
Q

How do antacids treat peptic ulcers and what are the 4 most common?

A

Neutralisation of stomach acid

  • Sodium bicarbonate (Alka Seltzer)
    • HCO3- buffers H+
  • Calcium carbonate (Tums, Rolaids)
    • CO32- buffers H+
  • Aluminiumhydroxide (Gaviscon)
    • OH-binds H+
  • Magnesium hydroxide(Milk of Magnesia)
    • OH-binds H+
41
Q

Which 3 drug types can be used to inhibit gastric acid secretion?

A

H2 antagonists
Cholecystokinin receptor antagonists
Proton pump inhibitors

42
Q

What are H2 receptor antagonists?

A

Histamine released from ECL
H2 receptors on parietal cells are inhibited so less GA released

43
Q

What are proton pump inhibitors?

A

Irreversibly block H+/K+ ATPase (proton pump) inparietal cell

Oral dosage in enteric capsules as pro-drugs, pass through stomach, absorbed in small intestine and into blood

Accumulate in acid environment of parietalcell canaliculi
selectively activated

Increasing activity over 5-7 days, irreversibly block the proton pump

44
Q

What are cytoprotective drugs?

A

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
Q

What are prostaglandin agonists?

A

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
Q

What are NSAID induced gastric ulcers?

A

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
Q

What is achlorhydria and what are the 4 main causes?

A

No HCl production in stomach
Increased stomach pH
Caused by
- medication
- gastric bypass surgery
- H. pylori infection
- stomach cancer

48
Q

What is primary constipation?

A

The most common cause of constipation
The bowel is healthy but not working properly

49
Q

What are 6 causes of secondary constipation?

A
  • Endocrine/metabolic diseases
  • Systemic diseases
  • Myopathy
  • Neurologic disease
  • Structural abnormalities
  • Iatrogenic (drug-related)
50
Q

What are the 4 types of laxative?

A
  • Bulk-forming (incr. size and fluid)
  • stool softening (incr. fluid)
  • osmotic (incr fluid retention)
  • Stimulant (incr. peristalsis)
51
Q

What are the 4 mechanisms of diarrhoea?

A
  • osmotic
  • secretory
  • inflammatory
  • abnormal motility
52
Q

What is osmotic diarrhoea?

A

Excessive amounts of insoluble material in the lumen, water not reabsorbed
Ingested solutespoorly absorbed
Malabsorption eg. lactose intolerance

53
Q

What is secretory diarrhoea?

A

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
Q

What is inflammatory diarrhoea?

A

Mucosal destruction
Defective absorption of fluid and electrolytes
Associated with both fluid and blood loss
Caused by infection or disease

55
Q

How does abnormal motility causes diarrhoea?

A

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
Q

What are the 3 causes of diarrhoea?

A

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
Q

What is oral rehydration therapy?

A

prevents or reverses dehydration
combination of sugars and salts, specificallysodium and potassium
stimulates waterand electrolyte absorptionfrom the GI tract

58
Q

Which three chemicals promote release of gastric acid?

A
  • acetylcholine
  • gastrin
  • histamine
59
Q

What are the 6 stages of drug development?

A
  • choose target
  • validate biology
  • lead discovery
  • refinement (SAR + QSAR)
  • final optimisation
  • drug to market
60
Q

What is SAR?

A

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
Q

How can you turn agonists into antagonists?

A

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
Q

What was the chain extention theory used for?

A

elongating the length of the flexible chain pushes polar groups further apart and increases antagonist interaction

63
Q

What is QSAR?

A

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
Q

What are proton pumps?

A

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
Q

What are the three reasons why PPIs have so few side effects?

A

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
Q

Why are PPIs irreversible inhibitors?

A

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
Q

How do PPIs work?

A

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
Q

What are the 5 steps to separate a drug from COOH metabolite?

A
  • 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
Q

What is LC-MS?

A

HPLC combined with MS

MPharm2 SL22105 (8 decks)

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