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Pharmacology > GI: Peptic Ulcers & GERD > Flashcards

GI: Peptic Ulcers & GERD Flashcards

1
Q

Peptic Ulcer is a result of?

A

Imbalance between acid-pepsin secretion and mucosal defense factors

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2
Q

Gastric Acid Secretion is Regulated by which chemicals and what are their receptors?

A

Acetylcholine: M1 Receptor
Gastrin: G Receptor
Histamine (Released by enterochromaffin cells under influence of Ach and G): H2 Receptors

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3
Q

H. pylori is associated with which disease?

A

Helicobacter pylori : Chronic gastritis, Peptic Ulcers, and their recurrence.

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4
Q

Classification of Drugs used in Peptic Ulcer:

A

1) Drugs for neutralization of Acid
2) Drugs that reduce gastric acid secretion
3) Ulcer Protectives

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5
Q

Antacids pH, how are they given, MOA

A

Antacids are Basic Substances, which are given orally and raise the pH of the gastric contents.

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6
Q

Types of Antacids, with examples; Basis of classification

A

1) Systemic Antacids: Eg Sodium Bicarbonate
2) Nonsystemic Antacids: Eg: Aluminium hydroxide, Magnesium trisilicate, Magnesium hydroxide, calcium carbonate.
3) Others: Simethicone

Based on absorption in circulation.

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7
Q

Systemic Antacid: Sodium Bicarbonate, Its Onset of Action, Duration of Action , MOA.

A

Fast Acting,
Short-Acting,
Neutralizes HCl to form Nacl and CO2

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8
Q

Systemic Antacid: Sodium Bicarbonate, Its Uses, ADRs

A

Uses: In Peptic Ulcers and Hyperacidity, To Alkanise urine in treatment of poisoning due to acidic drugs, Metabolic Acidosis

ADRs: NaHCO3 gets absorbed from intestines-> Systemic Alkalosis. Rebound Hyperacidity due to increase gastrin levels. Increase sodium load -> Troublesome to Patients w/ Cardiovascular Diseases
In high doses may cause MILK-ALKALI SYNDROME: Hypercalcaemia, metabolic Alkalosis & Renal Dysfunction.

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9
Q

Systemic Antacids examples?

A

Sodium Bicarbonate
Sodium Citrate

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10
Q

Nonsystemic Antacids: Examples, MOA

A

Examples: Aluminium hydroxide, Magnesium salts and Calcium carbonate

MOA: They are insoluble substances which react with HCl to form Chloride Salts (Non absorbable) & H2O

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11
Q

Nonsystemic Antacids: AL(OH)3. MOA & ADRs

A

It is a slow acting neutralizing substance which also forms a protective layer over the ulcers.

ADRs: Relaxes smooth muscles which leads to constipation
Binds with phosphate which leads to hypophosphataemia on prolonged use.

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12
Q

Nonsystemic Antacids: Mg Salts, MOA & ADRs

A

Mg(OH)2, MgTrisilicate, MgO, MgCO3.
Neutralizes the acid to form MgCl2.
Quick action and prolonged action.

ADRs: MgCl2 is purgative and may cause diarrhoea
MgTrisilicate may get absorbed in small amounts.
It may lead to hypermagnesaemia in renal dysfunction.

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13
Q

What is Magaldrate?

A

Hydrated complex of hydroxymagnesium aluminate, it reacts with acid to release Al(OH)3. which has prolonged effect.

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14
Q

Nonsystemic Antacids: CaCO3 MOA,ADRs

A

Quick and prolonged action.
Liberates CO2 which may cause discomfort.

ADRs: May cause constipation
Hypercalcaemia which may cause rebound acidity.
Long term use may cause Renal stones and Milk Alkali Syndrome.

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15
Q

Antacid Combinations: Examples and reasons.

A

Examples: GELUSIL Liquid, GELUSIL Tablet, DIGENE Gel & Tablet.

Advantages:
1) Quick and prolonged Effect: Mg(OH)2 :Fast acting, Al(OH)3 long acting.
2)Canceling out side effects: Mg:Laxative, Al: Constipation
3) Additive Effect: Cancels out side effects but increases the effect without increasing the individual doses..

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16
Q

Antacid Drug Interaction:

A

They form complexes with Iron, tetracyclines, digoxin, ranitidine, sulfonamides and antimuscarinic drugs.
Antacids should be taken 2 hours before or after these drugs

17
Q

Drugs that reduce gastric acid secretion: H2 Receptor Blockers. MOA And Pharmacokinetics.

A

They Bind to H2 Receptor and competitively inhibit action of histamine. Both Volume and acidity are reduced. Single dose can cause 60-70% reduction in secretion.

Rapidly absorbed but undergoes first pass meta.

18
Q

Gastric acid secretion: H2 Receptor Blockers: ADRs

A

Diarrhoea, Dizziness, Muscle Pain, headache. Crosses placenta and +nt in milk ergo should be avoided in pregnancy and lactation.

19
Q

Examples of gastric acid secretion: H2 Receptor Blockers (CENFRR)

A

Cimetidine
Ebrotidine
Nizatidine
Famotidine
Ranitidine
Roxatidine

20
Q

ADRs of Cimetidine

A

It is antiandrogenic, increases prolactin levels and inhibits estrogen metabolism in liver.
Results in Gynaecomastia, dec. sperm count, impotence, loss of libido and galactorrhoea in women.

CNS effects: Confusion, restlessness, delirium and hallucinations.
Headache, dizziness, rashes, diarrhoea

CVS Effects: Bradycardia, AV block, C.Arrest, A Fribli.

Interferes with metabolism of many drugs (Cyt.)

Ergo not preferred.

21
Q

Advs and ADR of Ranitidine

A

Preferred over cimetidine cause:
More potent and long acting.
No ADRs like in Cimetidine

Only ADR : Dizziness and headache

22
Q

Advs and ADR of Famotidine

A

Similar to Ranitidine but more potent.

ADRs: Headache, Dizziness, Bowel disturbances and rashes, QT Prolongation

23
Q

Advs and ADR of Roxatidine

A

Similar to Ranitidine but twice as potent; Same ADRs

24
Q

Advs and ADR of Nizatidine

A

Same as Ranitidine:

More potent and long acting.
No ADRs like in Cimetidine
90% Excreted thru kidney
Only ADR : Dizziness and headache

25
Q

Uses of H2 Blockers wrt GIT

A

1) Peptic ulcer: Rapid relief from pain and ulcers heal in 80-90% patients within 6-8 weeks.
2) Gastritis: First line drugs for non ulcer dyspepsia
3) Prevention of Stress induced Ulcers
4) Zollinger Elison Syndrone: Gastrin Secreting Tumor
5) GERD
6) Preanaesthetic: Ranitidine

26
Q

Gastric acid secretion: M1 Receptor Blockers.
Which drugs are used and why is atropine not used.

A

Pirenzepine and Telenzepine are used as they have no CNS side effects like atropine as they cannot cross BBB and is specific to gastric M1 Receptors
ADRs: Dryness of Mouth and Blurring of Vision

27
Q

Gastric acid secretion: Proton Pump Inhibitors: Examples (OPREDL)

A

Omeprazole (Prototype)
Pantoprazole (Most acid stable, Oral And IV)
Rabeprazole (Fastest onset of action)
Esomeprazole (S enantiomer of ome.)
Dexlansoprazole (Higher oral bioavailability than Ome.)
Lansoprazole (Higher oral bioavailability than Ome.)

28
Q

Gastric acid secretion: PPI: MOA

A

They are prodrugs which get activated in parietal cells in acidic environment to Sulfenamide. Sulfenamide binds with the proton pump inactivating it irreversibly.
Single dose can decrease upto 90-95% secretion.
It takes 3-4 days for the onset of action.

29
Q

Gastric acid secretion: PPI: Pharmacokinetics

A

They are acid labile. Ergo are enteric coated. They are lipid soluble and are absorbed in intestines rapidly. It reaches parietal cells due to its acidic nature. Conc of the drug is 1000 times more as its trapped.

Pantoprazole and Esomeprazole can be used as IV

T1/2 is 1-2 hours but the action is for 2-3 days.

Metabolised in Liver CytP450

Food interferes therefore PPI should be taken 1hr before.

30
Q

Gastric acid secretion: PPI: ADRs

A

Well Tolerated
1) Prolonged acid suppression : Infections
2) Dizziness headache diarrhoea abd. pain nausea
3) Long term use: VitB12 Def., Decreased Iron, magnesium and calcium absorption (Osteoporosis)
Atrophic changes in stomach after 3-4 years of use

31
Q

Gastric acid secretion: PPI:Uses

A

1)Peptic Ulcers
2)GERD
3) Dyspepsia
4)Drug induced ulcers
5) H. pylori regimen
6) Zollinger Ellison Syndrome
7) Gastrinoma
8) Preanesthetic Medication

32
Q

Gastric acid secretion: PPI: Drug Interactions

A

1) PPI decrease drug absorption of drugs which need acid environment
2) Enzyme inhibition by Omeprazole and Esomeprazole
which inhibit meta. of diazepam, phenytoin and warfarin.

33
Q

Ulcer Protectives: Sucralfate: MOA and Uses

A

Salt of Sucrose and Sulfated aluminium hydroxide. In acidic medium it polymerizes to form viscid layer over the ulcer. Negative charged sucralfate is attracted to positively charged proteins in ulcer. Remains for 6 hours. Also stimulates PG syn. to secrete Mucus.

Uses: Peptic Ulcer healing, Prevent Stress Induced
ulcer

ADR: Dryness of mouth and constipation (Al)

34
Q

Ulcer Protectives: Bismuth Salts: MOA and Uses

A

Colloidal Salts of Bismuth subcitrate and subsalicylate.
Chelates and forms a layer on ulcer base. Also inhibits H. pylori growth. And stimulates Mucus sec. and PG syn.

Uses: P. Ulcer healing, Prevents Travellers diarrhoea

ADRs: Constipation, Black stools, darkening of tongue and dizziness.

35
Q

Other P. Ulcer Drugs: Prostaglandins: Examples and MOA

A

MOA : Decrease gastric secretion and stimulates mucus secretion

Examples: Misoprostol, enprostil, rioprostil

Also Prevents NSAID induced gastric ulcers.

36
Q

What is Simethicone:

A

Aka Dimethylpolysiloxane, silicone polymer.
Pharmacologically inert. Helps in proper dispersion of antacids. Also decreases flatulence as it reduces surface tension (Prevents bubbles).

Pharmacology (2 decks)

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