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PHAR 230 > M6 L4 Drugs for Ulcers > Flashcards

M6 L4 Drugs for Ulcers Flashcards

1
Q

how are parietal cells stimulated to secrete acid during gastric acid secretion

A
  1. gastrin hormone (acts on G/CCK-B-R)
  2. acetylcholine (acts on M3-R)
  3. histamine (acts on H2-R)
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2
Q

how is HCL secreted during gastric acid secretion

A

by H+/K+-ATPase proton pump into the gastric lumen

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3
Q

what is gastrin hormone and how is it secreted during gastric acid secretion

A
  • secreted by G cells in response to: intraluminal dietary peptides, Ach through vagal stim
    -passes from blood vessels to submucosal tissue of fundic glands
  • binds to G/CCK-B-R on parietal cells and ECL cells
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4
Q

what does the vagus nerve stimulate during gastric acid secretion

A
  • stim release of Ach
  • binds to M3-R on parietal and ECL cells
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5
Q

what does gastrin and Ach stimulate ECL cells to release during gastric acid secretion

A

histamine

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6
Q

how is acid secretion turned off

A

increased [H+] + passing of proteins and fats into duodenum -> stim antral D cells to release somatostatin which further gastrin release which inhibits further gastrin release

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7
Q

ex of acid-peptic diseases

A

GERD, peptic ulcer, stress-related mucosal injury, zollinger-ellison syndrome

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8
Q

what is the infection that most commonly causes peptic ulcer

A

helicobacter pylori (>90%)

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9
Q

what is the drug-induced most common causes of peptic ulcer

A
  • NSAIDs
  • steroids
  • antineoplastics
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10
Q

what is a liquid that is the most common cause of peptic ulcer

A

alcohol

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11
Q

what are drugs that reduce intragastric acidity when a pt has a peptic ulcer

A
  • antacids
  • muscarinic receptor antagonists (anticholinergics)
  • histamine-2 receptor antagonists (H2 blockers)
  • PPI’s
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12
Q

drugs that promote mucosal defence in pt w peptic ulcer

A
  • sucralfate
  • prostaglandin analogs
  • bismuth compounds
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13
Q

what are antacids

A
  • widely used OTC drug
  • weak bases (alkaline substance): Na, Ca, Al, Mg salts
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14
Q

how do antacids work?

A

by neutralizing the gastric acid

2HCL (ACID) + Mg(OH)2 (ALKALI) -> MgCl2 (NEUTRAL SALT) + H2O

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15
Q

Systemic Antacids

A

ex: NaHCO3 & CaCO3
- releases CO2 and gastric distension
- has absorption into the body
- can cause metabolic alkalosis, hypercalcemia, renal insufficiency
- adverse effects: NaHCO3 (fluid retention), CaCO3 (constipation)
- less safe

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16
Q

Non-systemic Antacids

A

ex: Mg(OH)2 & Al(OH)3
- no effects, no absorption, no release and gastric distension
- adverse effects: Mg salts (diarrhea), Al salts (constipation)
- more safe
- combo of Mg and Al is useful to avoid the side effects!!

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17
Q

what are muscarinic receptor antagonists like in real life

A
  • less effective w more adverse effects
  • limited use nowadays
18
Q

H2 blockers half life, metabolization, and excretion

A
  • half life: 1.1-4 hrs
  • metabolized by the liver
  • excreted through the kidney
19
Q

what is the mech of action for H2 blockers

A
  • selectively block H2 receptors on the parietal cells
  • decrease gastric acidity (+/- 70%) mainly at night
20
Q

H2 blocker adverse effects

A

<3% so pretty safe
- diarrhea, headache, fatigue, myalgias, and constipation
- impotence and gynecomastia - cimetidine

21
Q

H2 blocker drug interactions

A
  • cimetidine decrease hepatic microsomal enzymes (cytochrome P450s)
  • decrease other drug metabolism -> increase drug levels and toxic response
22
Q

administration of H2 blockers

A
  • oral (twice daily 0.5 h b4 meals)
  • IV (limited use)
23
Q

H2 blocker drug names

A

…tidine
- cimetidine
- ranitidine
- nizatidine
- famotidine

24
Q

what are proton pump inhibitors

A
  • most potent acid suppressors
  • all contain benzimidazole ring
25
Q

absorption + half life of PPI’s

A
  • thru intestine
  • delayed by food intake
  • inactive prodrugs -> activated in the parietal cells
  • half life: 0.5-2 hrs
26
Q

PPIs mech of action

A
  • irreversible decrease H+/K+-ATPase proton pump
  • prevents acid secretion into gastric lumen
27
Q

PPI’s adverse effects

A

1-5% so pretty safe
- diarrhea, headache, abdominal pain
- low gastric acidity: interfere w vitamin B12 absorption, bacterial colonization

28
Q

administration of PPI’s

A

oral
once a day 1 hr b4 meal

29
Q

PPI availability

A

Rx, OTC (some)

30
Q

PPI drug names

A

…prazole
- omeprazole OTC
- esomeprazole (nexium) OTC
- lansoprazole
- dexlansoprazole
- pantoprazole

31
Q

sucralfate

A
  • made of sucrose + Al(OH)3
  • acts locally in stomach
  • reacts w gastric HCL to protect mucosa
  • minimal absorption (<3%) -> no systemic adverse effects
  • use is limited nowadays
32
Q

sucralfate administration

A
  • oral
  • QID
  • 1 hr b4 meals
33
Q

Misoprostol mech of action

A

PGE1 analog
- increases mucus secretion and HCO3 -> protects gastric mucosa -> decrease NSAID-induced ulcers
- decreases HCl secretion

34
Q

misoprostol half life + absorption

A

short half life: <0.5 hr
- rapidly absorbed and metabolized

35
Q

administration of misoprostol

A
  • oral - QID
36
Q

bismuth compounds

A

2 compounds
- bismuth subsalicylate
- bismuth subcitrate potassium

37
Q

bismuth compounds frequently used in combination w…

A
  • PPI’s and antibiotics - treatment of helicobacter pylori
  • w Kaopectate - treatment of dyspepsia and acute diarrhea
38
Q

what can bismuth compunds cause

A

very safe
- can cause harmless black tongue, and black poo

39
Q

what is helicobacter pylori

A
  • gram -‘ve bacilli
  • responsible for >90% of peptic ulcer disease
40
Q

treatment for helicobacter pylori

A
  • quadruple therapy: PPI + tetracycline + metronidazole + bismuth
  • triple therapy: PPI + clarithromycin + amoxicillin (or metronidazole)
    10-14 days for eradication of bacteria
41
Q

what is an ex of a H2 blocker

A

ranitidine

PHAR 230 (31 decks)

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