Clinical Pharmacology of Alimentary Flashcards

1
Q

What are the drugs of the alimentary system for?

A

Acid suppression

Drugs affecting GI motility

Laxitives

Drugs for inflammatory bowel disease

Drugs affecting intestinal secretions

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2
Q

What are the ways to reduce acidity?

A

Antacids

Alginates

H2 receptor antagonists

Proton pump inhibitors

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3
Q

What do antacids contain?

A

Magnesium or aluminium - neutralises gastric acid

Taken when symptoms occur

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4
Q

Give an example of an antacid

A

Example: Maalox

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5
Q

How do alginates work?

A

–Form a viscous gel that floats on stomach contents and reduces reflux

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6
Q

Give an example of an alginate

A

Gaviscon

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7
Q

What does the H2 receptor antagonist block?

A

The effects of histamine: Increases the rate of the hydrogen potassium carrier

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8
Q

Give an example of a H2 receptor antagonist and when you would use it

A

Ranitidine

Indicated in GORD/Peptic Ulcer disease

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9
Q

What are the routes of administration for ranitidine?

A

Orally or intravenously

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10
Q

Name a proton pump inhibitor

A

Omeprazole

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11
Q

How do proton pump inhibitors reduce acid secretion?

A

Block the proton pump

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12
Q

When are proton pump inhibitors indicated?

A

–GORD/peptic ulcer disease

–Triple therapy for treatment of PU/DU associated with H pylori

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13
Q

What is the route of administration for omeprazole?

A

Oral or IV

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14
Q

What is the effect of prokinetics?

A

Increase gut motility and gastric emptying

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15
Q

What is the effect of an anti-emitic drug?

A

Effective against vomiting and nausea

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16
Q

What are Prokinetics used for?

A

Gastroparesis

GORD?

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17
Q

Give examples of prokinetic agents

A

Metoclopramide

Domperidone

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18
Q

What is the mechanism of prokinetics?

A

•Mechanism of action is not clear but involves parasympathetic nervous system control of smooth muscle and sphincter tone (via ACh)

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19
Q

What is the action of domperidone?

A

Probably acts by blocking dopamine receptors which inhibit post-synaptic cholinergic neurones

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20
Q

What is the purpose of drugs which decrease motility?

A

Anti- diarrhoea

Can cause constipation

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21
Q

Give examples of drugs which decrease GI motility

A

Loperamide (immodium) and Opioids

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22
Q

What is the mechanism of action in drugs which decrease motility?

A

•Mechanism of action is via opiate receptors in GI tract to decrease ACh release

Reduced smooth muscle contraction

Increased anal sphincter tone

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23
Q

What are antispasmotics used for?

A

Reduce symptoms of IBS, renal colic

24
Q

Define what is meant by colic pain

A

Starts and stops abruptly

25
Q

What are the three mechanisms of anti-spasmodics

A

–Anti-cholinergic muscarinic antagonists (hyoscine buscopan, mebeverine)

•inhibit smooth muscle constriction in the gut wall, producing muscle relaxation and reduction spasm.

–Direct smooth muscle relaxants

–Calcium-channel blockers (peppermint oil) reduce calcium required for smooth muscle contraction

26
Q

What are the 4 types of laxitives?

How do they work?

A

–Bulk (e.g. Isphagula)

–Osmotic (e.g. Lactulose)

–Stimulant (e.g. Senna)

–Softeners (e.g. Arachis oil)

–Work by increasing bulk or drawing fluid into gut

27
Q

What is the route of administration for laxitives?

A

Oral or rectal

28
Q

What is the prerequisite for osmotic laxitives?

A

Water, they will ont work without adequate fluid intake

29
Q

What are the drugs for IBD?

A

Aminosalicylates

Corticosteroids

Immunosuppressants

Biologics

30
Q

Give an example of an aminosalicylate

A

Mesalazine, Olsalazine

31
Q

What is the method of action of aminosalicylates?

A

Anti - inflammatory

32
Q

What is the route of admission of aminosalicylates?

A

Oral

Rectal

33
Q

What are the adverse effects of aminosalicylates?

A

GI upset, blood dyscrasias, renal impairment

34
Q

What are the effects of corticosteroids on IBD?

A

Anti - inflammatory

35
Q

What are the long term effects of steroids?

A

Osteoporosis

Cushingoid features including weight gain

Increased susceptibility to infection

Addisonian crisis with abrupt withdrawal

36
Q

What is the effect of immuno suppressants on IBD?

A

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

37
Q

Name an immunosuppressant drug

A

Azathioprine

38
Q

What are the adverse effects of immunosuppressants?

A

–Adverse effects mainly relate to bone marrow suppression but also azathioprine hypersensitivity and organ damage (lung, liver, pancreatitis)

–Numerous drug interactions

39
Q

What is the mechanism of action for bioloics in inflammatory bowel disease?

A

Prevents action of TNF alpha - major cytokine in inflammatory response

40
Q

Give an example of a biologic agent

A

Infliximab

41
Q

What other conditions are biologic agents used for?

A

Psoriasis, Rheumatoid Arthritis

42
Q

What are the cautions / contraindications for infliximab?

A

–Current TB or other serious infection

–Multiple sclerosis

–Pregnancy/breast feeding

43
Q

What are the adverse effects of infliximab?

A

–Risk of infection, particularly TB so all patients should be screened

–Infusion reaction (fever, itch)

–Anaemia, thrombocytopenia, neutropenia

–?Demyelination

–Malignancy

44
Q

What is the effect of cholestyramine?

A

Reduces bile salts by binding with them in the gut and then excreting as insoluble complexe

45
Q

What is ursodeoxycholic acid used for?

A

To treat gallstones and primary biliary cirrhosis

46
Q

What is the mechanism of action of ursodeoxycholic acid?

A

–Inhibits an enzyme involved in the formation of cholesterol, altering the amount of cholesterol in bile and slowly dissolving non-calcified stones

47
Q

What is the action of drugs affected in the case of GI or liver disease

A

Can affect the processes of drug:

–Absorption,

–Distribution,

–Metabolism

–Excretion

GI symptoms may also necessitate a change in route of administration

48
Q

Why might absorption be affected?

A

Change in pH

Change in gut length

Change in transit time (Digoxin, warfarin)

49
Q

Why might distribution be affected?

A

–Low albumin (decreased binding and increased free drug concentration)

•e.g. Phenytoin

50
Q

Why might metabolism be affected?

A

–Liver enzymes (variability in effects but generally toxicity)

–Increased gut bacteria (metabolise drugs so increased dose needed)

–Gut wall metabolism (disease may reduce first pass metabolism)

•e.g. Morphine

–Liver blood flow (drugs with a high extraction ratio)

51
Q

What are GI adverse effects?

A

Diarrhoea / constipation (–25% of drug-induced diarrhoea is due to antimicrobials)

GI Bleed / Ulceration - Low dose aspirin is the most common cause, warfarin is the third most common cause (newer agent to warfarin is called NOAC’s - lower incidence of intracranial haemorrhage)

Warfarin is used to treat DVT and PE

Changes to gut bacteria - antibiotics, reduced vitamin K absorption (increased prothrombin time), c.Diff overgrowth

Type A adverse reaction - intrinsic hepatotoxicity (predictable - dose related)

Tybe B adverse reaction - as a result of drug / active metabolite, asymptomatic increase in LFT’s, liver failure, hepatitis, cholestasis, may mimic any pattern of acute or chronic liver disease

52
Q

Why is the oral contraceptive affected by antibiotics?

A

Relies on metablism and recirculation by gut bacteria – antibiotic stops the circulation and metabolism of the drug

53
Q

When should you take care when prescribing with the context of liver disease?

A

care with / avoidance of

–Drugs which can be toxic due to changes in pharmacokinetics

–Drugs which are hepatotoxic (azathioprine, methotrexate) (statins?)

–Drugs which may worsen the non-liver aspects of liver disease (e.g. encephalopathy) (benzodiazapines)

54
Q

What is the risk attached to warfarin / anticoagulants?

A

–In liver disease, clotting factors are already low

55
Q

What is the risk attached to using Aspirin / NSAIDS?

A

–Can increase bleeding time, in combination with deficiency in clotting factors;

–NSAIDs can worsen ascites due to fluid retention

56
Q

What is the risk assoicated with opiates / benzodiazepines?

A

–May precipitate encephalopathy by increasing sedation

57
Q
A