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Pharma 2 > Drugs used in the Treatment of Peptic Ulcer > Flashcards

Drugs used in the Treatment of Peptic Ulcer Flashcards

1
Q

GIT Control

A 
Neuronal
   Myenteric Plexus 
   Meissner Plexus
   Receive PS fibers from N.X
   Symp. fiber innervations: blood vessels, SM, some 
      glandular cells

Neurons within Plexus = Enteric NS
Secretion of neuropeptides: ACh, NE, purines, 5HT

Hormonal
Endocrine Secretion-> Gastrin
Paracrine Secretion-> Histamine

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2
Q

Cells of Stomach

A

Mucous Neck Cells
Secrete mucous and bicarbonate

Parietal Cells
Secrete HCl and IF for absorption of B12, Ca2

Enterochromaffin Like Cells
Secrete histamine-> stimulate HCl secretion

Chief Cells
Secrete pepsinogen and gastric lipase

D Cells
Secrete somatostatin-> inhibits HCl secretion

G Cells
Secrete gastrin -> stimulate HCl secretion

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3
Q

Physiology of Gastric Acid Secretion

A

Around 2.5l/day

Phases:
Cephalic: taste and smell
Gastric: mechanical and chemical
Intestinal

Mechanism
   Neuronal control: N. X--> ACh
   Paracrine control: Enterochromaffin- like and mast cells: 
         histamine 
   Endocrine control: G cells-> gastrin

Regulation
Gastric contents increase secretion
protein, peptides, AA, milk, Ca salts

Neuronal factors
Increase: N.X and intramural plexi
Decrease: ACh-> decrease pH-> decrease HCl secre.

Hormonal Factors
Epinephrine: via b R-> increase gastric acid secretion
Somatostatin: reduce gastric acid secretion

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4
Q

Mechanism of Gastric Acid Secretion

Transporters req.

A

1) Cl/HCl antiporter
Cl into cell; HCl from cell-> plasma

2) Cl/K Cotransporter
Cl and K from cell into lumen

3) K/H ATPase
H from cell into lumen (created by carbonic anhydrase)
K from lumen into cell

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5
Q

Pathological Conditions

A

Erosive and ulcerative disease of upper GIT

GERD
Acute peptic ulcer: due to drugs (NSAIDs, steroids,
alcohol)
Chronic peptic ulcer: disturbance between aggressive
factors and protective factors
Zollinger Ellison Syndrome (ZES)
Gastrin producing tumor

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6
Q

Therapy of Acid Related GIT Diseases

Basic Principles

A

Inhibition of pain
Helping ulcer heal
Prevent ulcer recurrence

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7
Q

Drug Categories

A

Inhibition of Acid Secretion
Neutralising Gastric Acid
Increasing Resistance of Mucosa

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8
Q

Neutralising Gastric Acid

Antacids
   Definition
   Factors on which effects depend on
   Categorisation
   Clinical use
   Formulations
A

Are weak bases
Form salts with HCl-> decrease acidity
At pH>4 pepsin activity decreases
Mucosal PG and Bicarbonate secretion increases

Effects depend on
   Solubility in stomach
   Physiological effect 
   Chemical activity
   Time of presence in stomach

Categorisation
Systemic: also water soluble at alkali pH-> absorbed
from intestines; can cause metabolic alkalosis

Non Systemic: formation of non water soluble salts in
intestine-> no absorption and influence on blood pH

Clinical Use
Good effect on duodenal ulcer
Poor effect on gastric ulcer
GERD: adjuvant th

Formulation
Tablet
Solution
Gel

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9
Q

Neutralising Gastric Acid

Antacids: Drug Names

A

NaHCO3 (Na Citrate)
CaCO3
MgO, Mg(OH)2, MgCO3
Al(OH)2

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10
Q

Neutralising Gastric Acid

Antacids: NaHCO3

A

(SYSTEMIC)
Fast effect
CO2 producing : decreases pyloric spasms-> faster
gastric emptying; but abdominal discomfort

SE in high doses
Na can cause oedema and hypertension
Milk alkali syndrome: when combo with milk: headache
dizziness, vomiting, constipation, Ca stones

Drug Interactions
Increase pH and motility in GIT-> decrease absorption
of Iron, Digoxin, Oral Anticoagulants, ABs

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11
Q

Neutralising Gastric Acid

Antacids: CaCO3

A

DON’T admin long term

Ca increases gastrin secretion and directly stimulates parietal cells-> increased acid production

Combo with a lot of milk-> milk alkali syndrome

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12
Q

Neutralising Gastric Acid

Antacids: MgO, Mg(OH)2, MgCO3

A

MgO and Mg(OH)2: fast neutralising action

NaCO3: slower, not freq. used

SE
laxative (osmotic): combo with Al(OH)3
Hypermagnesia in renal dysfunction: bradycardia

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13
Q

Neutralising Gastric Acid

Antacids: Al(OH)3

A

Weak neutralising-> slow onset and weak effect

AlCl3 salt forms gel like protective layer on injured mucosa

–> Neutralising + direct protection

SE
   Obstipation (combo with Mg compound antacid)
   Hyperphosphatemia in renal failure (forms insoluble 
      phosphate salt in bowels)
   Weakness
   Osteomalacia
   Absorbed AI--> encephalopathy
   Chelates of drugs
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14
Q

Inhibition of Acid Secretion

Drug Groups

A

Competitive Antagonist H2

Muscarine R Antagonist

PPI

Other Anti Secretory Agents

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15
Q

Inhibition of Acid Secretion

Competitive Antagonist H2
   MoA
   SE
   Pharmacokinetics
   Clinical Uses
A

MoA
Inhibits HCl secretion in stomach (parietal cells)
Reduces histamine and partially ACh induced gastrin
secretion
Decrease volume of gastric juice, H+ and pepsin
secretion

SE (minimal)
Diarrhoea, muscle pain, skin rash
Cimetidine reduces androgens–> reduces sex.
function, gynecomastia
Also is a major CYP450 inhibitor!

Pharmacokinetics
Good oral absorption
T1/2: 1-3 hrs; once a day enough as can use high dose
Renal elimination

Clinical Uses
Duodenal ulcer: healing and post healed ulcer:
preventative dose at 1/2 th dose
Gastric ulcer: healing and post healed ulcer:
preventative dose at 1/2 th dose
GERD and ZES: high dose
H. Pylori disease

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16
Q

Inhibition of Acid Secretion

Competitive Antagonist H2
Drug Names

A

Cimetidine
Ranitidine
Famotidine
Nizatidine

17
Q

Inhibition of Acid Secretion

Muscarinic R Antagonist

Nonselective

A

Atropine and Dicyclomine

MoA
On Mast and Enterochromaffin Like Cells:
Inhibits histamine secretion (M1 block)

On Parietal cells: inhibit gastric acid secretion(M3 block)

SE
Many parasympatholytic
dry mouth, obstipation, blurred vision

Also used as
Spasmolytic (relaxation of SM)
in Inflammatory BD

18
Q

Inhibition of Acid Secretion

Muscarinic R Antagonist

M1 Selective

A

Pirenzepine and Telezepine

MoA
Inhibition of histamine release: Mast and Enterochro.
Cells

SE
Minimal parasympatholytic
No CNS SE

Medical Use
Ulcers not responding to H2 Blockers
Prevention of ulcer relapses

19
Q

Inhibition of Acid Secretion

Proton Pump Inhibitors

A

Omeprazole, Pantoprazole, Rabeprazole, Esomeprazole

MoA
Irreversibly inhibit H/K ATPase (covalent binding SH
group)

Pharmacokinetics:
Good oral absorption, lipid soluble

Weak base, inactivation in stomach-> need special prep
enterosolvent capsules)

SE
Nausea, rashes, headache
Danger: long term hypoacidity: sensitive to H. Pylori

Increased tendency for hip fractures in elderly: osetoclasts have similar H+ pump. Can inhibit resolving function of osteoclasts; remodelling balance disturbed-> increase in fractures

Possible increased risk of gastric cc, carcinoid tumor

Medical Uses
   Severe GERD
   Refractory ulcer
   Short treatment of active duodenal ulcer
   ZES
20
Q

Inhibition of Acid Secretion

Other

A

Somatostatin-> Octeotride
decrease: HCl, pepsin, secretin prod, endocrine and
exocrine functions of pancreas, splanchnic blood flow

Medical Uses
Decrease ulcer and esophageal varix bleeding
Decrease portal hypertension
Decrease pancreatic secretion
Decrease tumor growth and meta. from ZES

TCA: Trimipramine
H2R antagonist effect

Prostaglandin Antagonist: Misoprostol
Deceases parietal cell histamine stim. activity
–> decrease gastric secretion
CI in pregnancy

Gastrin antagonist: Proglumide

Ca Antagonist

21
Q

Increase Resistance of Gastric Mucosa

Sucralfate

A

MoA
Polymerises in stomach
AL component removed from sucrose part
- charged molecule binds to + part of necrotic mucosal
peptides
Also absorbs pepsin and bile

DO NOT COMBO with secretion inhibitors or antacids

SE
Absorption of Al: encephalopathy
rarely obstipation

22
Q

Increase Resistance of Gastric Mucosa

Colloidal Bismuth Compound

A

Bi-Chelate, Bi-Subcitrate

MoA
Bi chelates with glycoproteins of necrotic mucosa->
creates barrier on ulcer surface
Decreases pepsin activity
Increases prostaglandin production
Combo with Metronidazole and Tetracycline: H. Pylori

SE
dark discolouration of tongue and teeth
encephalopathy in renal failure

23
Q

Increase Resistance of Gastric Mucosa

Carbenoxolone

A

MoA
Increases amount and viscosity of gastic mucus
Decreases H+ diffusion from lumen to mucosa

SE
Mineralocorticoid like due to steroid structure
–> good to combo with thiazine

24
Q

Increase Resistance of Gastric Mucosa

PGE

A

Misoprostol
Synthetic PGE1 analogue

MoA
   decrease acid secretion
   cytoprotective of gastic mucosa
   Increase mucus and bicarbonate secretion
   Increases mucosal blood flow
   Decreases H+ diffusion to mucosa

SE
Dose dep. diarrhoea
Abdominal cramps
CI in pregnancy (uterus contractions)

Used in NSAID treated patients

25
Q

Eradication of H.Pylori

A

PPI
Metronidazole
Clarythromycin

26
Q

Agents Increasing Gastric Acid Production

A

Amara
Caffeine
Alcohol

Can be used in gastric acid replacement

Pharma 2 (19 decks)

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