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pharm > peptic ulcer disease (acid) > Flashcards

peptic ulcer disease (acid) Flashcards

1
Q

stomach secretions

A
  • hydrochloric acid (parietal cells)
  • pepsinogen (chief cells)
  • mucus
  • bicarbonate
  • prostaglandins
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2
Q

parietal cells

A

produce and secrete HCl to keep stomach pH at 1-2
- primary site of action for many acid-controller drugs

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3
Q

ECL cells

A

secrete histamine
- stimulate parietal cells

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4
Q

stomach acid related diseases

A

action of acidity of digestive tract integrity
lay terms for stomach problems (indigestion, sour stomach, heartburn, acid stomach)
- PUD: peptic ulcer disease
- GERD: gastroesophageal reflux disease

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5
Q

aggressive factors against stomach (makes ulcers)

A
  • h. pylori
  • NSAIDs
  • acid
  • pepsin
  • smoking
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6
Q

defensive factors for stomach (protect from ulcers)

A
  • mucus
  • bicarbonate (neutralize)
  • blood flow
  • prostaglandins
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7
Q

what do PUD drug therapies do?

A
  • eradicate h.pylori if present in stomach
  • reduce gastric acidity
  • enhance mucosal defences

treat ulcer but also prevent it from happening in the future

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8
Q

h pylori

A

helicobacter pylori
- 90% duodenal ulcers, 70% gastric ulcers
- antibacterials eradicate it
- recurrence rates much less with eradication
- releases its own chemicals to protect from acid

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9
Q

inhibitors of gastric acid secretion/action

A
  • H2 antagonists
  • Proton pump inhibitors
  • antacids (Mg, Ca, Al salts)
  • other agents: protect. mucosa
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10
Q

H2 antagonists

A

histamine 2 receptors: inhibit production of acid
- reduce acid secretion
- OTC in low dose
- most popular

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11
Q

H2 antagonist examples

A
  • cimetidine (adverse effects)
  • famotidine
  • ranitidine
  • nizatidine
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12
Q

H2 antagonist mechanism of action

A

block h2 receptors of acid-producing parietal cells
- decreased HCl production
- allows ulcer to heal due to less acidity

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13
Q

H2 antagonist indications

A
  • GERD - erosive esophagitis
  • PUD
  • adjunct therapy in control of upper GI bleeding
  • pathological gastric hypersecretory conditions
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14
Q

H2 antagonists adverse effects

A

low incidence of AE
- cimetidine may induce impotence and gynecomastia (antiandrogenic effect - sex hormones)
- in elderly may see CNS depression (lethargy), confusion because of renal/hepatic impairment

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15
Q

H2 antagonists drug interactions

A

Cimetidine
- inhibits liver cytochrome p-450
- affect metabolism of other drugs causing increased drug levels (warfarin - increased bleeding)

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16
Q

H2 antagonist client implications

A

cimetidine:
- care in pt with impaired renal/liver function (metabolism and excretion)
- caution with pt who are confused, disoriented, elderly
- do not take with antacids, affects absorption (take at least an hour apart)

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17
Q

proton pump inhibitors (PPI)

A

inhibit production of acid
- inhibition of the pump that moves H+ ions into stomach lumen (acidity)
- more effective than H2 antagonists

18
Q

PPI mechanism of action

A
  • irreversibly bind to H+/K+ ATPase enzyme pump
  • normal acid secretion now requires parietal cell to make new atpase
19
Q

PPI examples

A
  • omeprazole
  • lansoprazole
  • rabeprazole
  • pantoprazole
  • esomeprazole
20
Q

omeprazole

A

enteric coated (avoid being broken down by acid in stomach to it can be absorbed in small intestine)
- broken down by acid
- absorbed in small intestine into circulation then brought to stomach

21
Q

PPI indications

A
  • GERD maintenance therapy
  • erosive esophagitis
  • short term treatment of active and benign gastric ulcers
  • gastric-producing tumour (zollinger-ellison syndrome)
22
Q

PPI adverse effects

A

safe for short term therapy (4-8 weeks)
- incidence low and uncommon
- headaches, GI (n&v, diarrhea)
- caution in pt with liver disease

23
Q

PPI drug interactions

A

may inhibit absorption of drugs that require an acidic GI environment for absorption
- pH levels raised to drugs that need a low pH to be absorbed can’t be, pass through stomach
- ketoconazole (antifungal)

24
Q

treatment for h pylori infection

A

triple therapy
- 2 antibacterials: amoxicillin + clarithromycin
- PPI: omeprazole
- 7-14 days
- 2 antibacterials reduce resistance development

25
Q

client care: PPI

A

omeprazole:
- capsule swallowed whole (enteric coated - not crushed, opened or chewed)
- may be given with antacids
- short term treatment

26
Q

antacids mechanism of action

A

chemically neutralize acid
- do not prevent acid production
- no absorbed into circulation, works in the lumen
- add on for PUD, not as good on its own

27
Q

antacids examples

A

alone or in combination:
- aluminum salts
- magnesium salts
- calcium salts
- sodium bicarbonate

28
Q

aluminum salts

A
  • may cause constipation
  • often used with magnesium salts to counteract constipation (cause diarrhea)

aluminum hydroxide
aluminum carbonate

29
Q

magnesium salts

A
  • commonly cause diarrhea
  • used with other agents to counteract
  • dangerous when used with renal failure (accumulation and kidneys not getting rid of it)
  • magnesium carbonate, hydroxide, oxide, trisilicate
30
Q

calcium salts

A
  • may cause constipation
  • possible kidney stones
  • calcium carbonate
  • often advertised as dietary carbonate
31
Q

sodium bicarbonate

A

rare use
- highly soluble
- quick onset, short duration
- may cause metabolic alkalosis
- sodium content may cause problems in clients with HF, hypertension, or renal insufficiency

32
Q

antacids adverse effects

A

minimal and depend of the compound used
- aluminum and calcium: constipation
- magnesium: diarrhea
- calcium carbonate: constipation, gas, belching (often combined with simethicone)

33
Q

antacids drug interactions

A

absorption of other drugs:
- may reduce absorption of other drugs given at same time (H2)

chelation (binding together)
- chemical binding or inactivation of another drug
- produces insoluble complezes
- reduce absorption
- eg tetracycline

34
Q

care implications antacids

A

assess for allergies and preexisting conditions that may restrict the use of antacids
- fluid imbalances, renal disease, HF, pregnancy, GI obstruction

client with HR or hypertension should use low-sodium antacids

35
Q

client implications antacids cont

A
  • root cause of many drug interactions
  • give meds 1-2 hours after antacid
  • antacids may cause premature dissolving of EC meds
  • administer with 240 ml h20 to enhance dispersion
  • caffeine, alcohol, harsh spices, and black pepper may aggravate underlying GI condition
36
Q

other agents: protect mucosa

A
  • sucralfate: bind directly to ulcer surface
  • misoprostol: prostaglandin agent
37
Q

sucralfate

A
  • cytoprotective agent
  • used for intestinal erosions
  • forms gel with mucus in low pH
  • attracted to and binds to base of ulcers and erosions forming a protective barrier
  • protects cells and allows recovery
  • inhibits pepsin
  • do not administer with antacids
38
Q

sucralfate cont

A
  • little absorption from the gut
  • may cause constipation, nausea, and dry mouth
  • may impair absorption of other drugs (tetracycline, digoxin), sticks to drugs and makes them less effective
  • binds with phosphate (may be used in chronic renal failure to reduce phosphate levels)
39
Q

misoprostol

A

synthetic prostaglandin
- does job of PGI2 and PGE2

prostaglandins have cytoprotective activity
- produce mucus and bicarbonate (neutralize)
- reduce acid secretion
- promote local cell regeneration
- help to maintain mucosal blood flow

40
Q

misoprostol cont.

A

reduce gastric effects of NSAIDs (ASA, diclofenac)
- combination tablets (arthrotec = diclofenac + misoprostol)

not in pregnancy
- used to terminate pregnancy (smooth muscle constriction - medical abortion)

41
Q

misoprostol adverse effects

A

abdominal cramps, diarrhea
- contraction of smooth muscle

pharm (28 decks)

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