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GI Week 2 > ICL 4.2: Disorders of Acid Production, GI Pharmacology & Acid Suppression > Flashcards

ICL 4.2: Disorders of Acid Production, GI Pharmacology & Acid Suppression Flashcards

1
Q

why are antacids used clinically?

A
  1. cheap and easily obtainable
  2. provide quick relief
  3. first-line treatment for mild intermittent (less than twice weekly) or breakthrough symptoms for patients receiving H2RA or PPI therapy
  4. not appropriate for chronic symptoms or for healing esophageal erosions
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2
Q

which medications are antacids?

A
  1. calcium carbonate
  2. aluminum carbonate
  3. magnesium oxide
  4. alginic acid
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3
Q

what is the MOA of antacids?

A

they neutralize gastric acidity, increase pH of the stomach and duodenal bulb

additionally, increasing the gastric pH above 4, inhibits the proteolytic activity of pepsin

alginic acid forms a viscous layer that floats on the surface of gastric contents as a protective barrier

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4
Q

what is the dosing of antacids?

A

short duration of action requires several administrations throughout the day

in a fasting state, antacids reduce acidity for approximately 20 to 40 minutes because of rapid gastric emptying

if ingested 1 hour after meals, they reduce gastric acidity for at least 3 hours so it’s better to take an antacid after eating

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5
Q

what are the side effects of antacids?

A

usually well tolerated with minimal adverse effects when used appropriately

  1. constipation (aluminum)
  2. diarrhea (magnesium)
  3. chalky taste
  4. abdominal cramps
  5. potential to cause acid rebound
  6. don’t use with renal dysfunction due to accumulation/electrolyte disturbances
  7. hypophosphatemia (aluminum)
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6
Q

what are the interactions associated with antacids?

A

take 1–3 hours after other medications to avoid potential drug interactions (gut binding, increased/decreased absorption)

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7
Q

why are histamine 2 receptor antagonists used clinically?

A
  1. cheap and easily obtainable
  2. empiric therapy for mild GERD symptoms
  3. maintenance therapy for those without erosive disease with intermittent symptoms (less effective than PPIs in healing)
  4. add-on therapy to PPI; can use on-demand for intermittent symptoms caused by food, exercise and/or at bedtime (quicker onset; peak in 1–2 hours)
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8
Q

which medications are histamine 2 receptor antagonists?

A
  1. cimetidine
  2. famotidine
  3. ranitidine
  4. nizatidine

“tidine”

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9
Q

what is the MOA of H2RAs?

A

competitive inhibition of histamine at H2 receptors of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentration

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10
Q

what is the dosing of H2RAs?

A

OTC dose is usually one-half the entire prescription dose

dosing varies based on condition, refer to product labelling for specific dosing

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11
Q

what are the side effects of H2RAs?

A
  1. headache
  2. dizziness
  3. fatigue
  4. confusion
  5. constipation
  6. diarrhea

caution with patients with hepatic and renal impairment

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12
Q

what are the drug interactions associated with H2RAs?

A
  1. medications with pH-dependent absorption may be altered
    ex. ketoconazole, itraconazole, protease inhibitors (HIV)
  2. cimetidine inhibits the cytochrome P450 (CYP) enzyme system—specifically 1A2, 2C9, 2C19, 2D6, 2E1, and 3A4

ranitidine is a less potent inhibitor than cimetidine and famotidine; therefore, clinically significant interactions are less

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13
Q

what are proton pump inhibitors used for clinically?

A

empiric therapy for individuals with frequent, continual symptoms: Standard once-daily dosing for 8 weeks

maintenance therapy: administer for persistent symptoms and in patients with complications (erosive esophagitis, Barrett esophagus)

chronic therapy should be administered at the lowest effective dose, including on-demand and intermittent strategies

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14
Q

which medications are proton pump inhibitors?

A
  1. omeprazole (Prilosec)
  2. esomeprazole
  3. lansoprazole
  4. dexlansoprazole
  5. pantoprazole
  6. rabeprazole
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15
Q

what is the MOA of proton pump inhibitors?

A

decrease acid secretion in gastric parietal cells through inhibition of the H-K-ATPase enzyme system reducing gastric acidity

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16
Q

what is the dosing of proton pump inhibitors?

A

should be taken 30-60 minutes before meal, preferably breakfast or first meal of day as H-K-ATPase pump availability is greatest after a fast

dexlansoprazole can be administered without regard to meals

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17
Q

what are the side effects of proton pump inhibitors?

A
  1. headache
  2. dizziness
  3. somnolence
  4. diarrhea/constipation
  5. nausea
  6. rebound hyper secretion after discontinuation; tape dose to ween off
  7. vitamin B12 deficiency
  8. osteoporosis and hip fractures due to decreased calcium absorption
  9. hypomagnesemia
  10. community acquired infections like C. diff and pneumonia

avoid long term use

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18
Q

what are the drug interactions associated with proton pump inhibitors?

A
  1. medications with pH-dependent absorption may be altered
    ex. ketoconazole, itraconazole, protease inhibitors (HIV)
  2. medications metabolized by CYP 2C19 or 3A4 substrates (PPIs inhibit these to varying degrees
  3. clopidogrel
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19
Q

what is sucralfate used for?

A

duodenal ulcers

forms a complex by binding with positively charged proteins in exudates, forming a viscous paste-like, adhesive substance that protects the gastric lining

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20
Q

what is misoprostol used for?

A
  1. NSAID induced gastric ulcer prevention (200 mcg 4 times daily)
  2. termination of intrauterine pregnancy

it’s a synthetic prostaglandin E1 analog that replaces the protective prostaglandins consumed with prostaglandin-inhibiting therapies (ie, NSAIDs)

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21
Q

which antibiotics are used for H. pylori infections?

A
  1. amoxicillin
  2. clarithromycin
  3. levofloxacin
  4. tetracycline
  5. metronidazole
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22
Q

which NSAIDs are primarily COX-1 selective?

A
  1. aspirin
  2. ketoprofen
  3. indomethacin

4 .piroxicam

  1. sulindac
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23
Q

which NSAIDs are slightly COX-1 selective?

A
  1. ibuprofen
  2. naproxen
  3. diclofenac
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24
Q

which NSAIDs are slightly COX-2 selective?

A
  1. etdolac
  2. nabumetone
  3. meloxicam
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25
Q

which NSAIDs are primarily COX-2 selective?

A

celecoxib

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26
Q

what is the MOA of NSAIDs?

A

o Inhibit cyclooxygenase (COX), the enzyme that catalyzes the synthesis of cyclic endoperoxides from arachidonic acid to form prostaglandins

in the gastric mucosa, prostaglandins decrease gastric acid synthesis, stimulate the production of glutathione that scavenges superoxides, promote the generation of a protective barrier of mucus and bicarbonate, and promote adequate blood flow to the gastric mucosal cells

prostaglandin in the kidneys modulates intrarenal plasma flow and electrolyte balance.

COX-1 is constantly produced and important for homeostatic maintenance, such as platelet aggregation, the regulation of blood flow in the kidney and stomach, and the regulation of gastric acid secretion

COX-2 is induced during pain and inflammatory stimuli

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27
Q

what are the side effects of NSAIDs?

A
  1. tinnitus
  2. comprise renal fnction
  3. serious GI bleeding, ulcerations, perforations
  4. cardiovascular thrombotic events
  5. increased bP, edema, water retention
  6. rash
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28
Q

which medication is a Proton Pump Inhibitor (PPI)?

a. Ranitidine
b. Omeprazole
c. Sucralfate
d. Misoprostol

A

b. Omeprazole

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29
Q

which medication is a Histamine 2 Receptor Antagonist (H2RA)?

a. Esomeprazole
b. Bismuth
c. Famotidine
d. Calcium carbonate

A

c. Famotidine

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30
Q

which class of medication inhibits the H-K-ATPase enzyme system in gastric parietal cells to increase gastric pH?

a. H2RA
b. PPI
c. Antacids
d. Selective 5-HT3 Receptor Antagonist

A

b. PPI

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31
Q

which class of medications has a quicker onset of action?

a. H2RA
b. PPI

A

a. H2RA

32
Q

which medication forms a viscous paste-like, adhesive substance that protects the gastric lining?

a. Aluminum hydroxide
b. Bismuth
c. Cimetidine
d. Sucralfate

A

d. Sucralfate

33
Q

which medication has a boxed warning for birth defects and premature birth?

a. Misoprostol
b. Omeprazole
c. Aluminum hydroxide
d. Bismuth

A

a. Misoprostol

34
Q

which medication would be most likely to cause dark stools?

a. Bismuth
b. Aspirin
c. Misoprostol
d. Calcium carbonate

A

a. Bismuth

35
Q

which medication is most effective at decreasing gastric acidity when taken 30 minutes before first meal?

a. Cimetidine
b. Calcium carbonate
c. Sucralfate
d. Lansoprazole

A

d. Lansoprazole

36
Q

which class of medication is most effective at promoting ulcer healing?

a. Antacid
b. H2RA
c. PPI
d. Bismuth

A

c. PPI

37
Q

which class of medication is most likely to affect the absorption of other medications due to binding in the gut if taken together?

a. Antacid
b. H2RA
c. PPI
d. Misoprostol

A

a. Antacid

38
Q

which medication inhibits CYP enzymes to a greater extent?

a. Ranitidine
b. Esomeprazole
c. Cimetidine
d. Sucralfate

A

c. Cimetidine

39
Q

which medication would be best to use for gastric ulcer prevention in a patient at risk?

a. Misoprostol
b. Famotidine
c. Sucralfate
d. Alginic acid

A

a. Misoprostol

40
Q

which medication requires several doses throughout the day due to a short duration of action?

a. Omeprazole
b. Ranitidine
c. Magnesium oxide
d. Famotidine

A

c. Magnesium oxide

41
Q

which class may increase risk of osteoporosis & community acquired infections?

a. NSAID
b. PPI
c. H2RA
d. Antacids

A

b. PPI

42
Q

which NSAID would be less likely to cause GI irritation?

a. primarily COX-1 Selective
b. slightly COX-1 Selective
c. slightly COX-2 Selective
d. primarily COX-2 Selective

A

d. primarily COX-2 Selective

43
Q

wow COX-1/COX-2 selective are ibuprofen and naproxen?

a. Primarily COX-1 Selective
b. Slightly COX-1 Selective
c. Slightly COX-2 Selective
d. Primarily COX-2 Selective

A

b. slightly COX-1 selective

44
Q

what are the symptoms of GERD?

A
  1. heart burn
  2. regurgitation
  3. acid taste
  4. extraesophageal symptoms = asthma, laryngitis, chronic cough
  5. chest pain; rule out cardiac causes

atypical symptoms
1. dyspepsia

  1. epigastric pain
  2. nausea
  3. bloating
  4. belching
45
Q

what are the alarm symptoms of GERD?

A
  1. anemia
  2. chest pain
  3. choking
  4. epigastric mass
  5. GI bleeding
  6. vomiting
  7. unintentional weight loss
  8. unimproved dysphagia
46
Q

what are the non-pharmacologic treatments for GERD?

A
  1. dietary changes
  2. smoking cessation
  3. tight clothing
  4. weight loss
  5. elevate HOB
  6. avoid meals before bed
  7. avoid chocolate, caffeine, alcohol, acidic/spicy foods
  8. medications: anticholinergics, barbiturates, dihydropyridine calcium channel blockers, dopamine, estrogen, GABA agonists, NO inhibitors, progesterone, serotonin, antagonists, tetracycline, theophylline
47
Q

how would you pharmacologically treat GERD?

A

PPI for 4-8 weeks taking 30 minutes before the first meal of the day

then maintenance with H2RAs; do not use PPIs for a prolonged time due to all the side effects

48
Q

what are the symptoms of dyspepsia?

A
  1. epigastric pain lasting at least 1 month
  2. epigastric fullness
  3. nausea/vomiting
  4. heartburn
49
Q

what are the alarm symptoms associated with dyspepsia?

A
  1. weight loss
  2. anemia
  3. dysphagia
  4. persistent vomiting
50
Q

how do you treat dyspepsia?

A

if they’re H. pylori positive, treat with antibiotics

if they’re H. pylori negative or if there’s still symptoms after giving antibiotics, give PPIs

51
Q

what is Barrett’s esophagus?

A

change of the normal squamous epithelium of the distal esophagus to a columnar-lined intestinal metaplasia

52
Q

what are the risk factors for Barret’s esophagus?

A
  1. 50+ years old
  2. male
  3. smokers
  4. obese
  5. caucasian
  6. family history
53
Q

how do you treat Barrett’s esophagus?

A

once daily PPI; 2x daily isn’t recommended unless poor control of reflux symptoms or esophagitis

avoid aspirin or NSAIDs

54
Q

what are the locations of more peptic ulcers?

A
  1. duodenal

2. gastric

55
Q

what are the common causes of peptic ulcers?

A
  1. H. pylori
  2. empiric PPIs
  3. critical illness/stress
56
Q

what are the high risk vs moderate vs low risk factors of peptic ulcers?

A

HIGH RISK
1. history of complicated ulcers

  1. more than 2 risk factors

MODERATE RISK
1. 65+ years old

  1. high dose NSAID use
  2. previous peptic ulcer
  3. aspirin use, corticosteroid use or anticoagulant use

LOW RISK = no risk factors present

H. pylori infection is an independent and additive risk factor which should be addressed separately

57
Q

how do you treat peptic ulcers?

A
  1. risk factor modification
  2. reduce or eliminate NSAID use if possible
  3. PPIs are first line therapy for ulcer healing!!
58
Q

how do you prevent peptic ulcers?

A

LOW CV RISK
low GI risk = NSAIDs alone

moderate GI risk = NSAID + PPI/misoprostol

high GI risk = alternative therapy or COX2 inhibitors + PPI/misoprostol

HIGH CV RISK
low GI risk = naproxen + PPI/misoprostol

moderate GI risk = naproxen + PPI/misoprostol

high GI risk = avoid NSAIDs or COX2 inhibitors

59
Q

how do you treat peptic ulcers?

A
  1. risk factor modification
  2. reduce or eliminate NSAID use
  3. test and treat H. pylori

PPIs are FIRST LINE for ulcer healing and secondary prevention!!!!

other options include misoprostol and H2RAS

60
Q

what are the symptoms of an upper GI bleed?

A
  1. hematemesis
  2. coffee ground emesis
  3. melena (black tarry stools)
  4. hematochezia
61
Q

how o you treat upper GI bleeds?

A

hemodynamic stabilization if needed

pre-endoscopy: IV erythromycin and IV PPI

post-endoscopy: IV PPI for active bleeds or standard PPI for ulcers with clean bases/flat pigmented spots

62
Q

what are the indications to test for an H. pylori infection?

A
  1. active peptic ulcer disease
  2. low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma, or a history of endoscopic resection of early gastric cancer (EGC)
  3. uninvestigated dyspepsia who are under the age of 60 years and without alarm features, non-endoscopic testing
  4. can consider in patients initiating low-dose ASA or chronic NSAID therapy

dont test people who just have symptoms of GERD without a history of PUD

63
Q

how do you treat an H. pylori infection?

A
  1. clarithromycin triple therapy = PPI, clarithromycin and amoxicillin or metronidazole for 14 days
  2. bismuth quadruple therapy = PPI, bismuth, tetracycline and metronidazole for 10-14 days if they have a penicillin allergy or previous macrolide exposure
64
Q

what are the tests to detect for H. pylori infection?

A
  1. urea breath test (expensive and inconvenient)
  2. stool monoclonal antibody test (cheaper but only detects active infections)
  3. serologic tests( good for mass population surveys in patients who can’t stop taking PPIs)
65
Q

which of following should be considered an alarm symptoms in a patient with GERD?

a. Acid taste/regurgitation
b. Chronic cough/nausea
c. Choking/vomiting
d. Epigastric pain/bloating

A

c. Choking/vomiting

66
Q

which of the following is not an appropriate non-pharmacologic intervention to treat GERD?

a. Elevate foot of bed
b. Smoking cessation
c. Avoid alcohol
d. Lose weight

A

a. Elevate foot of bed

67
Q

how long should a patient with GERD be prescribed a PPI?

a. 2-4 weeks
b. 4-8 weeks
c. No more than 4 weeks
d. As long as needed

A

b. 4-8 weeks

68
Q

which condition would be most appropriate to treat with long-term (>8 weeks) PPI therapy?

a. GERD
b. Heartburn
c. H. pylori
d. Berrett’s esophagus

A

d. Berrett’s esophagus

69
Q

which symptom(s) is/are used to distinguish dyspepsia?

a. Epigastric pain >1 month
b. Heartburn and regurgitation
c. Dark stools
d. Acid taste in mouth

A

a. Epigastric pain >1 month

70
Q

how long is a typical H. pylori eradication regimen?

a. 5-7 days
b. 7-10 days
c. 10-14 days
d. 14-21 days

A

c. 10-14 days

71
Q

which H. pylori regimen would be the best choice for a patient allergic to PCN?

a. PMC
b. PAC
c. PAMC
d. Levofloxacin triple therapy

A

a. PMC

PPI, metronidazole and clarithromycin

72
Q

which H. pylori regimen would be the best choice for a patient who previously received a macrolide?

a. PMC
b. PBMT
c. PAMC
d. Hybrid therapy

A

b. PBMT

PPI, bismuth, metronidazole, tetracycline

73
Q

which of the following is NOT a risk factor for Barrett’s esophagus?

a. Age <50 years old
b. Central obesity
c. Smoking
d. Caucasian race

A

a. age <50 years old

74
Q

screening for Barrett’s Esophagus should be considered in which of the following patients?

a. 40 yo white male with weekly GERD symptoms for the last 6 months and positive FH for BE
b. 60 yo black male with weekly GERD symptoms for the last 2 years and current smoker
c. 50 yo white male with weekly GERD symptoms for the last 5 years and central obesity
d. 55 yo white female with weekly GERD symptoms for the last 5 years

A

c. 50 yo white male with weekly GERD symptoms for the last 5 years and central obesity

75
Q

which of the following patients has a moderate risk for developing a PUD?

a. 45 yo black male with a previous uncomplicated peptic ulcer
b. 50 yo white female with a recent complicated ulcer
c. 67 yo white male who received a ketorolac injection, is taking ibuprofen as needed, and takes a daily 81mg aspirin
d. 60 yo black female with symptoms of heartburn

A

a. 45 yo black male with a previous uncomplicated peptic ulcer

76
Q

you would like to start a 50 yo white male with a history of peptic ulcer on an OTC NSAID. Which of the following regimens would be appropriate to minimize his risk of ulceration?

a. NSAID alone
b. Celecoxib
c. NSAID plus PPI
d. NSAID plus misoprostol

A

c. NSAID plus PPI

NSAID alone isn’t appropriate; celecoxib and misoprostol are prescription only

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