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Pharm > GERD and PUD > Flashcards

GERD and PUD Flashcards

1
Q

when does gastroesophageal reflux become a disease?

A

when it either causes macroscopic damage to the esophagus or casues sxs that reduce QOL.

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2
Q

How does lifestyle affect sxs related in GERD?

A

high fat meals: inc. frequency of sxs; calorically dense meals cause inc. in esophageal acid exposure. Tobacco: inc. in freq of sxs; alcohol: no change; caffeine; no change

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3
Q

How is GERD classified?

A

Based off appearance of esophageal mucosa on upper endoscopy. Erosive esophagitis: visible breaks in distal esophageal mucosa w/or w/o sxs; nonerosvie: presence of sxs w/o evidence of mucosal damage

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4
Q

What are the indications for a scope?

A

To r/o complications ie pts w/alarm feature; dystonia, odynophagia, GI bleed, anemia, weight loss, recurrent vomiting -or-
men >50 w/sx >5 yrs and additional risk factors for Barretts esophagus and esophageal adenocarcinoma (nocturnal reflux sxs, hiatal hernia, elevated BMI, tobacco use and intra-abdo distribution of fat -or-
pt w/ typical sxs that persist despite therapeutic trail of 4-8 weeks PPI twice daily

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5
Q

What are the mechanisms of GERD?

A

dec. lower esophageal sphincter pressure; prolonged esophageal clearance; mucosal resistance; delayed gastric emptying time

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6
Q

What is the normal function of the LES pressure (lower esophageal sphincter) in GERD? and what goes wrong?

A

tonic, contracted state, relaxing to permit free passage of food into stomach. Transient LES relaxations are not associated with swallowing, mechanism unclear, possible causes: esophageal distention, V, belching, retching. responsible for 65% of pts w/GERD.

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7
Q

What are some medication causes of decreased LES

A

anticholinergics, barbituates, benzodiazepines, caffeine, dihydropyridine Ca++ channel blockers, DA, estrogen, ethanol, isoproterenol, narcotics, nitrates, phentolamine, progesterone, theophylline

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8
Q

What are some food causes of decreased LES?

A

fatty meals, peppermint/spearmint, chocolate, caffeinated drinks (coffee, cola, teas), garlic, onions, chili peppers

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9
Q

How are esophageal clearance and GERD related?

A

50% GERD pts have prolonged acid clearance. esophagus normally cleared by peristalsis. Inc. saliva (stimulated by swallowing) provides bicarbonate buffer. Saliva produciton dec. w/ages, Sjogren’s syndrome, Xerostomia, sleep

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10
Q

What are some mucosal irritants?

A

food: spicy food, citrus juice, tomato juice, coffee; medications: alendronate (for osteoporosis), ASA, Fe, NSAIDs, Quinidine, KCl

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11
Q

How does mucosal resistance affect GERD?

A

mucus secreting glands may function to protect esophagus, bicarbonate neutralized acidic reflux. after repeat exposure, H+ ions diffuse into mucosa causing cellular acidicicaiton and necrosis.

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12
Q

How does gastic emptying affect GERD?

A

delayed gastric emptying. Factors inc. gastric V/dec. gastric emptying (smoking and high fat meals); post-prandial reflux, infants (defects in antral motility - complications=failure to thrive, pulmonary aspiration)

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13
Q

What the some lifestyle factors contributing to GERD?

A

exercise (weight lifting, cycling, sit-ups), smoking, obesity, high fat meals, supine body position, tight clothing, pregnancy, stress

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14
Q

What are some sx of GERD?

A

typical: heartburn (pyrosis), hypersalivation, belching, regurgitation
Atypical: non-allergic asthma, chronic cough, hoarseness, pharyngitis, chest pain, dental erosion

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15
Q

What are some complications of GERD?

A

esophagitis; esophageal strictures (complicated by ASA/NSAID use); Barrett’s esophagus; adenocarcinoma (risk inc. if barretts esophagus or long standing reflux);

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16
Q

What are the symptoms of adenocarcinoma of the esophagus

A

continual pain, dysphagia, odynophagia, bleeding, unexplained weight loss, choking

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17
Q

What is the step-up/step-down treatment of GERD?

A

step up for mild and intermittent sx (fewer than 2 episodes/week) with no evidene of mucosal damage if scope done (lifestyle changes = 1st step!!, add meds as needed)
Step down for severe sx, frequent sx (>2 episodes per week) or erosive esophagitis – start w/med and lifestly and dietary changes (if you see damages)

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18
Q

What is the step up treatment of GERD?

A

lifestlye/dietary mods, weight loss, elevate head of bed, avoid dietary triggers (fatty foods, caffeine, chocolate, spicy food, carbonated beverages, peppermint)

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19
Q

What are some other lifestyle changes?

A

physiologic basis but not consistently shown to improve sx (avoid tight fitting clothing, promote salivation throgh oral lozenges/gum, stop smoking/avoid ETOH - both reduce esophageal sphinter pressure relaxation, discontinue drugs that contribute to reflux – Ca++ channel blockers, beta blockers, nitrates, theophylline, caffeine (only if can!), drink lots of water w/meds!

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20
Q

What are some step-up medication choices?

A

suppression of gastric acid production: PRN low dose histamine 2 receptor antagonists w/antacids (if sx occur

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21
Q

What is the step-down treatment?

A

Start w/standard dose PPI x8 weeks w/lifestyle and dietary mods; subsequently dec. to low dose PPI, then H2RA then to no meds if no sx. Exception severe erosive esophagitis or Barrett’s esophagus maintenance PPI therapy

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22
Q

How are antacids used in GERD?

A

20% effective; MOA: neutralize acid to raise intragastric pH, decreased activation of pepsinogen, increased LES pressure. Benefits: rapid onset w/in 5 min; disadvantage: contain combo of magnesium trisilcate, aluminum hydroxie or Ca carbonate

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23
Q

What are side effects of antacids?

A

GI: D or C (D - Magnesium, C- aluminum, gas-Ca, sodium bicarbonate). Sodium bicarbonate products can cause fluid overload in pts with CHF, renal failure, cirrhosis, pregnancy or any salt-restricted diet. avoid in anyone taking Ca++ supplementation or w/renal dysfunciton. DI: alter gastric pH, inc. urinary pH, adsoribing meds, physical barrier to absorption, form insoluble complexes – clinically significant: quinolone, isoniazie, TCN, ferrous sulface, quinidine, sulfonylurea

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24
Q

What precautions should be taken with antacids

A

pts using for >14 days should be evaluated for barrett’s esophagus and risk of upper GI pathology. Patients excessively using antacids: frequent use should be tx w/prescription drugs, freq. use considered more significant dz

25
Q

What is some antacid counseling?

A

dose is product-specific; take at onset of sx; if potential for DI separate dosages by at least 2 hrs; use shouldn’t exceed 14 days; pts should be evaluated if using >14 days

26
Q

what is sucralfate (Carafate)?

A

a surface agent, adheres to mucosal surface promoting healing and protecting from petpic injury. Short duration and limited efficacy compared to other txs limits use to pregnancy!

27
Q

How does Sucralfate (Carafate) work?

A

when the pH is below 5 and extensvie polymerization and cross-linking of sucralfate to form a sticky, viscid yellow-white gel, the gel adheres to epithelial cells and adheres very strongly to the base of ulcer craters

28
Q

What is the clinical utility of Sucralfate?

A

effective at promoting healing in PUD, as maintenance therapy (more efficacious in duodenal than gastric ulcers), used to prevent stress ulcers, more effective when administer prior to meals than after since acid is needed for activation.

29
Q

What are some ADRs and drug interactions of Sucralfate?

A

ADRs: consdipation (Al+++), dry mouth, abdo discomfort
DI: phenytoin, TCN, fluorquinolone abx, Digoxin, Ketoconazole..therefore better to admit these meds 2 hours PRIOR to sucralfate, do NOT administer w/agents that dec. acid.

30
Q

How are H2 receptor antagonists used?

A

MOA: reversibly inhibit histamine-2 receptors or parietal cels, dec. secretion of acid. Use: on-demand therapy for intermittent mild-mod GERD sx, preventative dosig before exercise/meals, prescription strengths needed for more severe sx or for maintenance dosing. LESS effective than PPIs in healing erosive esophagitis.
(FIRST choice if you are stepping up therapy!)

31
Q

What are some H2 receptor Antagonists?

A

Ranitidine (Zantac) OTC and RX, Cimetidine (Tagamet) OTC and RX, Nizatidine (Axid OTC and RX), Famotidine (Pepcid) OTC and RX, Pepcid Complete OTC only??

32
Q

Absorption, Fate and Excretion of H2 receptor antagonists?

A

H2 receptor antagonists are rapidly and well absorbed after PO admin, peak conc 1-2 hours, duration 4-10 hours. Oral bioavailability of Nizatidine ~90% (b/c undergoes 1st pass metaboism, so limits bioavailability of other compounts to 50%). They may need adjustment w/renal impairement b/c large part of these excreted unchaged in urine.

33
Q

What are some side effects and DI of H2 receptor antagonists?

A

well tolerated generally, HA, somnolence, fatigue, dizziness, thrombocytopenia is rare and reversible
DI: Cimetidine - inhibition of metabolism of warfarin, phenytoin, nifedipine, propranolol; acidic enviro required for absorption: ketoconazole, itraconazole, ferrous sulfate (you’re changing the acidic enviro, so theses drugs wont be absorbed as well)

34
Q

Antacids vs. H2 receptor antagonits?

A

combination is MORE effective than antacid therapy alone!

35
Q

How do PPIs work (proton pump inhibitors)?

A

most potent inhibitors of gastric acid secretion, eliminate sx and heal esophagitis more frequently and rapidly than other drugs!! Shown to normalize impaired QOF caused by GERD

36
Q

What is the MOA of PPIs?

A

inhibit the action of the H+, K+ -ATPase (proton pump), all considered prodrugs in that they need to be activated to be effective . They need the acidic enviro (H+) to work! Requires 18 hours to synthesize new H+, K+, -ATPase molecules

37
Q

How are PPIs most effectively used?

A

30 min prior to meal. Qday should be taken before breakfast, some data supports evening meal in nighttime acid is issue. IF higher dose given, should be divided doses w/second dose before evening meal, not bed time. administer daily PRN. Compared to H2RA provide FASTER relief of sx and heal esophagitis in up to 86% of pts!

38
Q

What are the different types of PPIs?

A

Omeprazoel (Prilosec), Lansoprazole (Prevacid), Esomeprazole (Nexium), Pantoprazole (Protonix), Rabeprazole (Aciphex) they are all comparable in activity/effectiveness so selection is based on cost!

39
Q

What are ADRs of PPIs?

A

generally uncommon w/8 week therapy - N/D/C, HA, dizziness, somnolence. Chronic use: prolonged hypochlorhydria and hypergastrinemia (clin sig not established) and poss assoc. w/gastric atrophy (most at risk if H. pylor infectio w/PPI). Hypochlorhydria may predispose to infections and malabsorption

40
Q

What are some chronic PPI concerns?

A

inc. risk of enteric infections (C. diff), dec. acid secretion permits pathogens to colonize upper GI tract which may predispose to PNA (pneumonia) - CAP and HCAP.

41
Q

Malabsorption concern with PPI?

A

Malabsorption: concern w/Fe, Vit B12 (can be addressed w/supplements though), more concerning is Mg and Ca malabsorption (substitution of these may not be enough but should still add). FDA recommends baseline Mg levels prior to initiation of PPI in pts expected to be on long term or who take in conjunction w/ other meds that cause (diuretics, digoxin) and periodic levels while on PPI. Hypochlorhydria can reduce Ca absorption, inhibit osteoclastic activity, dec. bone density! concern for hip fxs in pts >50

42
Q

What are some DI with PPIs?

A

P450s - so there are a lot!!! Omeprazole, Iansoprazole, Esomeprazole, and pantoprazoel metabolized by P450 enzymes (Rabeprazoel metabolized through nonenzymatic reduction pathway). Omeprazole and Esomeprazole reduce metabolism of: Diazepam, Phenytoin, Warfarin

43
Q

When to use maintenance therapy for GERD?

A

fail to respond refer to GI doc, trial off tx if sx completely resovle (exception Barretts esophagitis and severe esophagitis), recurrent sx within 3 mos. (indefinite tx), recurrent after 3 mos. or more trail another course of successful tx

44
Q

What is PUD (peptic ulcer disease)?

A

ulcers extending deep into the muscularis mucosa. 2 most common forms: H. pylori assoc, NSAID induced, stress related mucosal damage

45
Q

What are the sx of PUD?

A

~70% asymptomatic, may not recognized ulcer until complications begin. most common sx is dyspepsia

46
Q

What are the causes and sx of duodenal ulcers?

A

causes: H. pylori (95%), NSAIDs
sx: epigastric pain often worse at night, pain typically 1-3 hrs after meal and may be relieved by eating, pain can be episodic

47
Q

What are the causes and sx of gastric ulcers?

A

caues: NSAIDs, H. pylori
sx: epigastric pain often worse WITH food, assoc sx are heartburn, belching, bloating, N, anorexia

48
Q

What are some complications of PUD?

A
  • Bleeding: upper GI bleed - peptic ulcer, erosion of ulcer into artery, presentation is occult and insidious, melena or hematemesis. Fatal is uncontrolled bleeding, rebleeding
  • Gastric outlet obstruction: ulcers in duodenum, sx are early satiety, bloating, indigesion, anorexia, epigastric pain shortly after eating
  • Penetration and fistulization: change of symptoms
  • Perforation
49
Q

How do you diagnose PUD?

A

direct visualization of ulcer on upper endoscopy. All pts w/PUD dx should be tested for H. pylori, hx of NSAD use obtained!!

50
Q

What is Helicobacter pylori

A

gram-neg rod that colonized mucus of luminal surface of gastric epithelium, causes inflammatory gastritis, may be linked to PUD, gastric lymphoma and adenocarcinoma. 50% of world pop may be colonized. Transmission is fecal-oral, oral-oral, Iatrogenic. To document infection: usually blood test or breath test for urea. tx w/goal or eradication, eradication of infxn should be confirmed 4 weeks (or more) after completion of tx.

51
Q

What is the treatment PUD?

A

withdrawal of contributing factors (avoid NSAIDs and any triggers), antisecretory therapy (choice based on location of ulcer and any complications), antibiotic therapy (if H. pylori)

52
Q

What is the 3-drug regimen treatment for PUD?

A

PAC: PPI (BID x1-2 wk), Amoxicillin (1gm BID x1-2 wk), Clarithromycin (500mg BID x1-2 wk) for patients not allergic to PCN
PMC: PPI (BID x1-2 wk), Metronidazole (500mg x1-2 wk), Clarithromycin (500mg BID x1-2 wk) for patients allergic to PCN w/no recent macrolide or metronidazole use.

PPI: Prevacid, Prilosec, Protonix, Nexium, or Aciphex

53
Q

What is the 4-drug regimen treatment for PUD?

A

PBMT: PPI (BID x1-2 wk), Pepto-Bismol (2 tabs QID x1-2 wk), Metronidazole (250 mg QID x1-2 wk), Tetracycline (500mg QID x1-2 wk) – or amoxi 500 mg QID or Clarithromycin 250-500 mg QID

PPI: Prevacid, Prilosec, Protonix, Nexium, Aciphex

54
Q

What is the treatment if pt is H. pylori positive?

A

uncomplicated duodenal: PPI x10-14 days as listed along with antibiotic regimen
Complicated duodenal and in pts with gastric ulcers: PPI x4-8 weeks (duodenal) and 8-12 weeks (gastric) with antibiotic regimen

55
Q 
What are bismuth compounds use for in PUD?
Bismuth subsalicylate (Pepto-Bismol)
A

beneficial effects include: cytoprotection through enhanced secretion of mucus and HCO3-, inhibit pepsin activity, accumulate bismuth subcitrate in craters of gastric ulcers. Antibacterial effects: reduce bacterial adherence to mucosal cells and damage to bacterial cell walls. Promote healing of both gastric and duodenal ulcers.

56
Q

What are some ADRs of Bismuth Subsalicylate (pepto-bismol)

A

reaction of bismuth w/bacterial H2S leads to bismuth sulfide causing a black color to the oral cavity and feces.
Aspirin ADRs!

57
Q

How do you treat an NSAID induced ulcer?

A

PPI for minimum of 8 weeks, if must remain on NSAID or ASA, maintenance with PPI indicated (so dont need an abx obviously)

58
Q

How to Prostaglanding Analogs work?

A

MOA: Misoprostol is a synthetic analouge of prostaglandin E. Imitates the action of endogenous prostaglandins (PGE2 and PGI2) in maintaining the integrity of the gastroduodenal mucosal barrier. Promotes healing.

59
Q

What are the indications, CI and ADRs of Prostaglandin Analogs?

A

Indications: ulcer healing, ulcer prophylaxis w/NSAID use
CI: HPOTN, breastfeeding, pregnant (don’t give early in preg, can give later???)
ADRs: D/C

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