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Clinical Pharm Exam 3 > GERD & PUD > Flashcards

GERD & PUD Flashcards

1
Q

What type of cell secretes HCl

A

Parietal cells

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2
Q

HCl is secreted in response to what 3 physiologic stimuli?

A
  • ACh
  • Histamine
  • Gastrin
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3
Q

Which of the 3 physiologic stimuli is most important clinically?

A

Histamine

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4
Q

What type of transmitter is histamine?

A

Paracrine

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5
Q

What does histamine bind?

A

H2 receptors on basolateral membrane of parietal cells

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6
Q

H+ ions are actively secreted in exchange for….

A

K+ (by Na+/K+ pump on surface of parietal cells)

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7
Q

Acid secretion is driven by what nerve

A

Vagus n.

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8
Q

What is the most frequent GI condition encountered in outpt. setting

A

GERD (20% of population)

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9
Q

Sx of GERD

A
  • Heartburn & regurg (classic sx)
  • Dyspepsia (early satiety, gutt rot)
  • Chest pain
  • Belching
  • Dysphagia
  • Voice changes
  • Chronic cough
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10
Q

Complications of GERD

A
  • Barrett’s esophagus
  • Strictures
  • Bleeding
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11
Q

What are examples of alarm symptoms?

A

Dysphagia, GI bleed, anemia, wt. loss, persistent vomiting

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12
Q

What diagnostic tool is used to evaluate alarm symptoms?

A

Endoscopy

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13
Q

What other patient population is endoscopy recommended for?

A

Pts at high risk for complications

  • Those who do not respond to 4-8 wk trial of PPI
  • Men >50 w/ chronic GERD (>5yr) who have additional RF for Barrett’s (e.g. obesity, hiatal hernia)
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14
Q

What are examples of lifestyle modifications used in GERD mgmt?

A
  • Avoid lying down for at least 2 hours after eating or drinking
  • Elevating HOB
  • Wt. loss
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15
Q

What lifestyle modification is no longer recommended for GERD pt?

A

Avoiding foods thought to trigger reflux e.g. chocolate, caffeine, alcohol, spicy foods

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16
Q

Tx regimen for mild, infrequent GERD

A

Antacid or H2RA

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17
Q

Tx regimen for severe, frequent GERD OR those whose sx are inadequately controlled on antacid or H2RA

A

PPI

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18
Q

How many weeks of PPI therapy is recommended prior to de-escalation?

A

8 wks

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19
Q

In what populations is PPI de-escalation not recommended?

A
  • Pt. on chronic ASA therapy

- Barrett’s esophagus

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20
Q

Pts. on a PPI (PO QD) who continue to have sx, may benefit from what alteration to their tx regimen?

A
  • BID therapy

- Switching to another PPI

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21
Q

What is recommended for pt. who still have noctural sx despite BID PPI therapy?

A

Addition of H2RA therapy

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22
Q

Pts who have recurrent sx ater stopping a PPI may respond to what?

A
  • Another course of tx

- On-demand PPI tx

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23
Q

What type of tx regimen is recommended for the healing of erosive esophagitis?

A

PPI x8wks (almost all pt. will have relapse within 6mo of stopping tx, most will require indefinite tx)

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24
Q

Most antacids are comprised of various salts including:

A
  • Al(OH)3
  • CaCO3
  • Mg(OH)2
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25
Q

Common antacid preparations

A
  • Aluminum hydroxide + magnesium hydroxide
  • Calcium carbonate + magnesium hydroxide
  • Calcium carbonate
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26
Q

Antacid MOA

A
  • Neutralizes gastric acidity (↑ gastric pH)

- Inhibits proteolytic activity of pepsin when gastric pH >4

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27
Q

Clinical indications for antacids

A

PRN for dyspepsia/GERD

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28
Q

Drug interactions with antacids

A
  • ↓ TCC & FQ absorption (form nonabsorbable complexes)

- ↓ absorption of various agents (itra/ketoconazole, Fe2+, digoxin, phenytoin) d/t “alkalization” of stomach

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29
Q

Al(OH)3 ADRs

A
  • Hypophosphatemia
  • Aluminum intoxication
  • Constipation
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30
Q

Aluminum intoxication could cause what in CKD pts.?

A

Encephalopathy, seizure, coma

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31
Q

CaCO3 ADRs

A
  • Constipation

- Milk-Alkali syndrome

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32
Q

What is Milk-Alkali syndrome?

A

HA, nausea, irritability, weakness, hypercalcemia, metabolic alkalosis, & hypophosphatemia w/ large doses or in CKD pts.

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33
Q

Mg(OH)2 ADRs

A
  • Hypermagnesemia

- Laxative effects

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34
Q

What is sucralfate?

A

Aluminum hydroxide complex of sucrose

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35
Q

Sucralfate MOA

A

Forms a complex by binding with positively charged proteins in exudates; viscous paste-like/adhesive provides protective coating

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36
Q

Clinical indications for sucralfate

A
  • GERD/PUD (minimally used)
  • NSAID-induced mucosal damage
  • Prevention of stress ulcers
  • Suspension used topically for tx of stomatitis d/t CA chemo/other causes
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37
Q

Interactions for sucralfate

A

↓ absorption of itra/ketoconazole, digoxin, phenytoin, warfarin, theophylline, TTC, FQ
- Take other meds 2 hrs before

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38
Q

Why is taking medications 2 hrs before sucralfate difficult?

A

Sucralfate is a QID drug

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39
Q

Sucralfate ADRs

A
  • Constipation

- Aluminum toxicity in CKD pts

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40
Q

Examples of 1st gen H2RAs

A
  • Cimetidine

- Ranitidine

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41
Q

Examples of 2nd gen H2RAs

A
  • Famotidine

- Nizatidine

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42
Q

What H2RA is the FDA investigating in regards to NMDA content?

A

Ranitidine

- Products have been pulled from the market

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43
Q

H2RA MOA

A

Inhibit gastric secretion by blocking histamine receptors on parietal cells
- Reduction in basal gastric acid secretion > food-stimulated after a single dose

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44
Q

Are H2RAs good for regular use or prn use

A

PRN

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45
Q

What H2RA should we encourage the use of?

A

Famotidine

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46
Q

Clinical indications for H2RAs

A
  • Dyspepsia/GERD/PUD
  • SUP in critically ill pt.
  • Gastric hypersecretory states (PPI >)
47
Q

Decreased GI acidity with H2RAs may lead to what?

A

HAP/VAP & CDI

48
Q

Drug interaction with H2RAs

A

↓ absorption of itra/ketoconazole, digoxin, phenytoin, Fe2+

49
Q

Which H2RA is a weak/moderate inhibitor of almost every isoenzyme?

A

Cimetidine

- Use discouraged because of this

50
Q

H2RA ADRs

A
  • Acid rebound (stopping med leads to a surge; mitigated with taper, antacids for breakthrough)
  • Confusion in cognitively impaired/demented elderly pt.
51
Q

Cimetidine ADRs

A
  • ED (libido)/gynecomastia (chronic use)
  • Drug fever
  • Agranulocytosis
52
Q

Examples of PPIs

A
  • Omeprazole*
  • Esomeprazole
  • Pantoprazole*
  • Rabeprazole
  • Lansoprazole*
  • Dexlansoprazole
  • what we use for the most part
53
Q

What PPIs are available IV>

A
  • Esomeprazole

- Pantoprazole

54
Q

Why don’t we use the IR formulation of omeprazole that’s buffered by NaHCO3?

A

Too much Na+

55
Q

PPI MOA

A

Suppresses gastric basal & food-stimulated secretion by inhibiting parietal cell H+/K+ ATP pump

56
Q

When should PPIs be taken/administered?

A

30-60 minutes before 1st meal

57
Q

Why should PPIs be taken/administered after a prolonged fast?

A

Amount of H-K-ATPase present in parietal cell is greatest after a prolonged fast

58
Q

Clinical indications for PPIs

A
  • GERD ( role for chronic dz w/ mild-mod sx; intermittent vs. “on-demand” vs continuous)
  • PUD +/- bleeding - standard of care!
  • SUP in critically ill pt.
  • Gastric hypersecretory states - standard of care!
  • H. pylori infection
59
Q

Indications for intermittent PPI dosing for GERD pt.?

A

Occasionally heart burn sx (every 3rd day)

60
Q

Indications for “on-demand” PPI dosing for GERD pt.?

A

For new change in disease course

61
Q

Indications for continuous PPI dosing for GERD pt.?

A

Pt. w/ complications (e.g. Barrett’s, strictures)

62
Q

Concerns with PPI use that contribute to decision making

A
  • ↑ CDI
  • CAP/HAP
  • ↑ fx risk in PM women & pt. >50yo OR pts. on high dose for >1yr -> ↓ Ca+ absorption
  • Hypomagnesia, iron or B12 deficiency (anemia?) r/t long-term use (>1yr)
63
Q

What is our goal if we put a PPI on board?

A

Use the lowest effective dose for the shortest duration possible

64
Q

Which PPIs are available OTC?

A
  • Omeprazole
  • Esomeprazole
  • Lansoprazole
65
Q

Do PPIs differ clinical for sx relief, esophagitis/ulcer healing etc?

A

nah

66
Q

There is a risk of tolerance developing with H2RAs or PPIs?

A

H2RAs

67
Q

What can we considering monitoring in a pt. on a PPI?

A

Mg+! @ baseline AND periodically in pt. on long-term therapy (>2wks) or those on diuretics, digoxin

68
Q

PPI use should be avoided in what two populations?

A
  1. Pt. on drugs that carry a known risk of TdP

2. Pt. with long QT syndrome

69
Q

Do PPIs cause QT prolongation?

A

NO! The drug itself does not BUT it manipulates the absorption of cations

70
Q

If extended drug therapy is indicated in a pt. that is taking a QT prolonging drug, what should monitor?

A
  • Mg+

- QT interval

71
Q

PPIs are substrates of CYP___ & CYP___

A

CYP2C19; CYP3A4

72
Q

Most PPIs are moderate inhibitors of CYP___

A

CYP2C19

73
Q

What PPIs should we use concomitantly with CYP2C19 substrates, such as phenytoin & clopidogrel?

A
  • Pantoprazole*, lansoprazole, dexlansoprazole

- Omeprazole & esomeprazole may be problematic

74
Q

Omeprazole moderately inhibits CYP___

A

CYP2C9 (caution w/ warfarin, phenytoin)

75
Q

Other drug interactions w/ PPIs

A
  • ↓ absorption of itra/ketoconazole, digoxin, phenytoin, Fe2+/Ca+/Mg+/B12
  • ↓ MTX clearance
76
Q

PPI ADRs (generally)

A
  • Nosocomial inf
  • Anemia
  • Fx
  • AIN -> CKD w/ long term use
77
Q

What drug is a synthetic analog of prostaglandin E1?

A

Misoprostol

78
Q

Misoprostol MOA

A

Gastric antisecretory agent w/ protective effects on GI mucosa

79
Q

Use of misoprostol is CONTRAINDICATED in what pt. population?

A

Pregnant women (stimulates expulsion of ~products of conception~)

  • Category X
  • r/o possibility prior to use + contraception during use
80
Q

Clinical indications fro misoprostol

A
  • Prevention of NSAID-induced ulcers
  • Treatment of PUD
  • Various obstetric indications
81
Q

Why os misoprostol not 1st line for tx of PUD?

A

Requires multiple daily doses & ADRs

82
Q

Misoprostol ADRs

A

Diarrhea & abd pain

83
Q

Why is heartburn so common in pregnancy? (up to 80%)

A

Prostaglandin mediated ↓ in LES tone

84
Q

5 steps to treating GERD/PUD in pregnancy

A 
Step 1: lifestyle modifications 
Step 2: antacids
Step 3: sucralfate (if antacids fail)
Step 4: H2RA
Step 5: PPI considered (persistent sx on H2RA)
85
Q

“Recommended” antacids in pregnancy

A
  • Aluminum hydroxide + magnesium hydroxide
  • Calcium carbonate
  • regarded as safe, but watch for ADRs
86
Q

Antacids to avoid in pregnancy

A
  • Mg+ trisilicates

- Sodium bicarb

87
Q

What harm might Mg+ trisilicates cause to a fetus?

A

Nephrolithiasis, hypotonia, respiratory distress (chronic use/high doses)

88
Q

What harm might sodium bicarb cause in pregnancy?

A

Materal/fetal metabolic alkalosis & fluid overload

89
Q

What drugs/classes are category B?

A
  • Aluminum hydroxide + magnesium hydroxide
  • Sucralfate
  • H2RA (ranitidine > *most data)
  • PPIs (except omeprazole - C)
90
Q

Examples of supplemental iron

A
  • Ferrous sulfate (65-100 elemental iron/tab)
  • Ferrous fumarate (65-100 elemental iron/tab)
  • Ferrous gluconate (35 elemental iron/tab)
91
Q

When should iron supplement be taken?

A

Best absorbed on empty stomach, but may be better tolerated w/ food (if GI upset occurs)

92
Q

Iron supplements may cause ↓ absorption of….

A
  • Bisphosphonates
  • Levodopa
  • LT4
  • FQs
  • TTCs
93
Q

What other meds ↓ absorption of iron supplements?

A
  • Ca+/Al/Mg+ containing antacids
  • H2RAs
  • PPis
94
Q

Dosing of iron:

A

100-200mg/day of ferrous sulfate or ferrous fumarate

- Start 1 tab/d, titrate up to BID or TID over 1-2 wks if tolerated

95
Q

What do we monitor 1x/mo in iron-deficient pt. on supplements?

A

Hgb

96
Q

H. pylori can cause gastric inflammation & has been associated with what other pathologies

A

Gasritis, PUD, gastric adenocarcinoma, MALT

97
Q

Eradication of H. pylori….

A
  • Promote gastric healing
  • Prevents recurrence of ulcers
  • ↓ incidence of gastric CA
98
Q

Testing for H. pylori

A
  • Noninvasive: urea breath, stool antigen, serology

- Invasive: endoscopy w/ bx

99
Q

How to choose a regimen for tx of H. pylori

A
  • Prior macrolide exposure?
  • Allergies?
  • Dosing convenience
  • Cost?
100
Q

What does TRIPLE therapy for H. pylori consist of?

A

PPI + clarithromycin + amox or metronidazole

101
Q

Why is triple therapy falling out of favor?

A

Clarithromycin resistance

102
Q

At what parameter of clarithromycin resistance would be an indication to move to quadruple therapy?

A

Clarithromycin resistance >15%

- Local resistance patters, ABX resistance testing NOT widely available -> make the switch to quadruple therapy anyway

103
Q

What does concomitant QUADRUPLE therapy for H. pylori consist of?

A

PPI + clarithromycin + amox + metronidazole or tinidazole

104
Q

How often is concomitant QUADRUPLE therapy dosed?

A

BID

105
Q

What does bismuth QUADRUPLE therapy for H. pylori consist of?

A

PPI + bismuth + TTC + metronidazole or tinidazole

106
Q

How often is bismuth QUADRUPLE therapy dosed?

A

QID

107
Q

How long do we treat w/ quAdruple therapy?

A

10-14d

108
Q

What do we do post-quadruple therapy treatment?

A

“Cure documentation”

109
Q

What can be used sometimes for dyspepsia or to distinguish GERD & CP in the ED?

A

GI cocktails

- Do NOT rely on to r/o CP

110
Q

What constitutes a GI cocktail?

A

Liquid antacid + viscous lidocaine +/- antispasmodic (e.g. Donnatal)

111
Q

Adding Donnatal), lidocaine, or both to an antacid….

A

Does NOT seem work better for dyspepsia than an antacid alone (liquid antacid alone is recommended)

112
Q

No good evidence that magic mouthwash is better than….

A

Homemade salt & sodium bicarb rinse

113
Q

Two magic mouthwash recipes

A
  1. Viscous lidocaine + diphenhydramine + liquid antacid (1:1:1)
  2. BLM kit: Benadryl + Licocaine + Maalox (Al + Mg hydroxide) + simethicone ($$$)
114
Q

Pt. ed for magic mouthwash

A
  • Swish & SPIT for oral ulcers
  • Swish & SWALLOW for pharyngeal or esophageal ulcers
  • Use q4-6hrs PRN
  • Hold in mouth for 1-2min
  • Don’t eat or drink for 30 min after

Clinical Pharm Exam 3 (4 decks)

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