GIT disorders drugs

Question 1

why peptic ulcer occur?

Answer 1

imbalance (aggresive factor & defensive)

Question 2

Molecule stimulate acid secretion?

Answer 2

1. Acetylcholine
   (from nerve ending -> stimulate M3 receptor on:
   - parietal cell (HCI)
   -Enterochromaffin cells & mast cell (produce histamine)
   -G cell (produce gatsrin)

Histamine:
stimulate parietal cell -> produce HCL (hydrochloric acid)

Gastrin:
by chemical substances in food

Question 3

Medication (reduce gastrict acid) ?

Answer 3

1. proton pump inhibators:
(Zantac, prevacid, nexium, prilosec)
- H2 receptor antagonist
-muscarine receptor antagonist
-antacids

2. Mucosal protective agents:
   - sucralfate
   - PGE1 agonists (misoprostol)
   - colloidal bismuth compunds
   - Carbenoxolone

Question 4

Proton pump inhibator=

Answer 4

Most potent suppressor gastric acid secretion

1. omeprazole
2. esomeprazole
3. lansoprazole
4. rabeprazole
5. pantoprazole

Action:
inhibit HCI secretion -> inactivate proton pump @wall of parietal cell c acid secretion.

Adverse effect:

• vit b12 deficiency (prolong use)
• hypomagnesemia
• osteoporosis
• diarrhea, constipate, nausea
• myopathy(muscle weakness), arthralgia(joint pain), headeache
• hypergastrinemia (>gastrin @blood, due to rebound upon stop meds)

Therapeutic use?

• GERD
• gastric, duodenal ulcer
• Prevent NSAID associate gastric
• reduce risk duodenal ulcer w H.pyloric infection

Question 5

PPI: H2 receptor antagonist

Answer 5

Ranitidine, famotidine, nizatidine

MOA:
-suppress HCI, inhibit H2 receptor @parietal cell

• LESS POTENT than PPI
• suppress basal gastric acid more than meal stimulate secretion

uses:
GERD (uncomplicated)
gastric, duodenal
prevent stress ulcer

Question 6

PPI: muscarie receptor antagonist

Answer 6

Pirenzepine, telenzepine

Question 7

PPI: Antacid

Answer 7

MOA:
1. reduce intragastric acidity react w gastrict HCI to form salt&water

2. stimulate mucosal PG production

Types & effects of antacid:

1. sodium bicarbonate
   - rapid neutralize gastrict HCL

• sodium -> fluid retention, HPT
• CO2 (gastrict distent, high gastrin)
• dairy ->hypercalcemia & renal insufficiency (milk-alkali syndrome)

2. calcium carbonate
   - effect react part: less rapid neutralize gastric HCL
3. Aluminium hydroxide
   - x metabolic alkalosis
   - unabsorb aluminium slats -> constipation
4. Magnesium hydroxide
   - unabsorb magnesium salts -> osmotic diarrhea
   - excrete thru kidney(x gv pt w kidney disease)

effects:
(neutralize excess HCI)
-raise PH 1.3 to 1.6 (50%)
-raise PH 1.3 to 2.3 (90%)

Question 8

Mucosal protective agents

Answer 8

1. Sucralfate
   = complex aluminium hydroxide + sulfate + sucrose

MOA:
- form viscous paste bind ulcer 6hr -> form barrier against hydrolysis of mucosal protein by pepsin

• stimlate mucosal PG & bicarbonate production
• bind w bile salt (TX biliary gatritis
  2. PGE1 agonists (misoprostol) produce by gatric mucosa

PGE1 MOA:
inhibit histamine -> reduce gatric

stimulate mucin & bicarbonate secretion

increase mucosa blood flow

PGI2 (prostacyclin):
inhibit histamin

3. Colloidal bismuth compunds
4. Carbenoxolone

Question 9

Specific acid dyspeptic disorder & therapeutic startegies?

Answer 9

GERD:
1. mild: H2 receptor antagonist (ranitidine BD)

2. severe: PPI 8wks
3. antacid (mild, heart burn)
4. severe noctural acid: PPI + H2 receptor antagonist

H.pylori:
14day tx
-PPI + clarithromycin 500mg + metronidazole 500mg/amoxicillin 1g) BD

NSAID ulcer
PPI, H2, misoprostil

peptic ulcer - PPI