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Flashcards in Alimentary Pharmacology Deck (34)
1

List some of the drugs used for Acid suppression

Antacids (e.g. Maalox)
Alginates (e.g. Gaviscon)
Mucosal Protectors (bismuth, sucralfate, misoprostol)
H2 Receptor Antagonists (e.g. Ranitidine)
Proton Pump Inhibitors (e.g. Omeprazole)

2

Briefly describe antacids giving an example

Maalox

Contain Magnesium or aluminium
Neutralise gastric acid
Taken when symptoms occur

Patients commonly take these for reflux. Ask them if they do. If they take a lot and its not helping GORD may be severe

3

Briefly describe alginates giving an example

Gaviscon

Forms a viscous gell that floats on stomach contents and reduces reflux

4

Give an example of mucosal protectors

Bismuth
Sucralfate
Misoprostol

Not commonly used

5

Name and describe H2 Receptor Antagonists

Ranitidine

Block histamine receptor thereby reducing acid secretion
Indicated in GORD/ Peptic Ulcer disease
Given orally or IV
Has some GI side effects

Other drugs more effective so not hugely common

6

Name and describe Proton Pump Inhibitors

Omeprazole

Block proton pump and thereby reduce acid secretion
Indicated in GORD/Peptic ulcer disease
Oral or IV administration
Widely used because its so damn effective
Problems with upper GI upset and C. diff infection in the long term

7

Compare the main 3 treatments for excess stomach acid in terms pf where they act

Acid secretion stimulated by Gastrin, Histamine and ACh.

H2 antagonists work on H2 receptor.
Gastrin and ACh can still stimulate acid production
Reduced acid secretion therefore

PPI act on Proton Pump so no protons are transported into lumen. HIGHLY effective

Antacids act after all this and target the acid itself

8

Give a brief description of drugs that increase GI motility.

Metoclopromide and Domperidone

Laxatives and anti-emetics (increase gastric emptying)

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

Domperidone probably acts by blocking dopamine receptors which inhibit post synaptic cholinergic neurones

9

Give a brief description of drugs that decrease GI motility

Loperamide (immodium), Opioids

Mechanism of action is via opiate receptors in GI tract to decrease ACh release and thereby muscle contraction

Loperamide has few central opiate effects as it is not absorbed across the blood brain barrier

10

What should you keep in mind when prescribing drugs for diarrhoea?

Infective diarrhoea is there for a reason. Let it run its course and provide supportive treatment.

Overflow diarrhoea (children and elderly) diarrhoea may actually be due to constipation. You want to give laxatives for this!

11

Give a description of anti-splasmotics

Can be used to decrease diarrhoea symptoms

Work by 3 mechanisms:
-Anti-cholinergic muscarinic antagonists (buscopan, mebeverine) inhibit smooth muscle constriction in the gut wall, producing muscle contraction and muscle spasm
-Smooth muscle relaxants
-CCB's reduce calcium required for smooth muscle contraction
-Drugs tend to have mixed pharmacological properties

12

What renal condition are anti-spasmodics used to treat?

Renal colic pain
Kidney stone moves into ureter
Buscopan is great for this

13

You prescribe a hypertensive patient CCB's.
They later come back with heartburn.
Whats happened?

CCB's reduce muscle contraction
Gastric motility and emptying slows
Increases chance of GORD like symptoms

14

What are the 4 types of laxatives

Bulk (isphagula)
Osmotic (e.g. Lactulose)
Stimulant (e.g. senna)
Softeners (e.g. Arachis oil)

Work by increasing bulk or drawing fluid into gut

15

What are some of the issues with laxatives?

Obstruction
Route of administration (oral or rectal)
Need for other measures (osmotic laxatives will not work without adequate fluid intake)
Misuse

16

Name the types of drugs used to treat IBD

Aminosalicylates
Steroids
Immunosuppressants
Biologics

17

Give examples and a description of aminosalicylates

e.g. Mesalazine and Olsalazine

Mechanism unclear but anti-inflammatory
Oral or rectal administration
Chemically related to salicylates so avoid if allergic
Caution in renal impairment
Adverse effects - GI upset, blood dyscrasia, renal impairment

18

Give a description corticosteroids

Anti-inflammatory effects
Given orally, IV or rectally

Usual concerns and contraindications
-Osteoperosis
-Cushing's syndrome features including weight gain
-Increased susceptibility to infection
-ADDISONIAN CRISIS IN ABRUPT WITHDRAWAL

19

Give an example and description of immunosuppressants

Azathioprine

Cytotoxic.
Prevents the formation of purines required for DNA synthesis so reduces immune cell proliferation.
Adverse effects mainly relate to bone marrow suppression but also azathioprine hypersensitivity and organ damage (lung, liver and pancreatitis).
Numerous drug interactions
Specialist use and close monitoring required

20

Give an example and description of biologics

Biologics (anti TNF-a antibodies)

e.g. Infliximab
Prevents action of TNFa (key cytokine in inflammatory response)
Also used in psoriasis, rheumatoid arthritis
Addresses inflammatory response but not underlying disease process

21

What are the contraindications and adverse effects of Infliximab?

Contraindications:
-Current TB or other serious infections
-Multiple Sclerosis
-Pregnancy/Breastfeeding

Adverse Effects:
-Risk of infection, particularly TB so all patients should be screened
-Infusion reaction (itch, fever)
-Anaemia, thrombocytopenia, neutropenia
-?Demyelination
-Malignancy

22

Name two drugs affecting biliary secretions

Cholestyramine and Ursodeoxycholic Acid

23

Give a description of Cholestyramine

Pruritis from biliary cause
Reduces bile salts by binding with them in the gut and then secreting as an insoluble complex
May affect absorption of other drugs so should be taken separately
May affect fat soluble vitamin absorption so may decrease vitamin K levels (affecting clotting and warfarin)

24

Give a description of Ursodeoxycholic Acid

Used in gallstones and primary biliary cirrhosis

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

25

Why should ADME be considered in alimentary disease?

GI or liver disease can affect the process of drug absorption, distribution, metabolism and excretion

GI symptoms may also necessitate a change in route of administration.

26

Why must absorption of drugs be considered in GI disease?

pH may be changed in GI disease and treatment. Many drugs need acid to react

Gut length (how much area there to absorb drug)

Transit time (breakdown in stomach. absorption in small intestine)

27

Why must distribution of drugs be considered in GI disease?

Low albumin
Decreased binding and increased free drug concentration
e.g. phenytoin

28

Why must metabolism of drugs be considered in GI disease?

Increased gut bacteria -> metabolise drugs so increased dose needed
Gut wall metabolism (disease may reduce first pass metabolism) e.g. morphine
Liver enzymes
Liver blood flow

29

Why must secretion of drugs be considered in GI disease?

Biliary excretion (increased toxicity if hepatobiliary disease)
e.g. spironolactone

30

Describe adverse drug reaction causing Diarrhoea/Constipation

May be acute or chronic

e.g. cholinergics, NSAIDs, antimicrobials
Opioids, anticholinergics

Multiple mechanisms
25% of drug induced diarrhoea is due to antimicrobials

31

Describe adverse drug reactions causing GI bleeding/ Ulceration

Aspirin/NSAIDs are the 1st and warfarin 3rd most common cause
Mechanisms include ulcer causation and increased bleeding tendency

32

Describe ADRs causing changes to gut bacteria

Mainly antibiotics
Reduced vitamin K absorption (increased prothrombin time)
Overgrowth of pathogenic bacteria (e.g. C. Diff)

33

Describe drug induced liver injury

Intrinsic hepatotoxicity (predictable, dose-dependent, acute) type A ADR
Idiosyncratic hepatotoxicity (unpredictable, non dose dependent, and may occur at any time- may be part of a hypersensitivity reaction) Type B ADR

May be due to drug itself or active metabolite
Can range from asymptomatic increase in LFTs or fulminant liver failure and death
Generally hepatitis and cholestasis, but can mimic any pattern of acute or chronic liver disease

34

What are the risk factors for GI side effects?

Age (elderly and young)
Sex (females at risk)
Alcohol consumption
Genetic factors
Malnourishment