GERD/PUD Flashcards

1
Q

List a few Paxton lifestyle interventions for GERD.

A
  • do not lie down for at least 2hr after eating/drinking
  • elevate head of bed
  • weight loss
  • routine avoidance of foods that have been thought to trigger reflux (chocolate, caffeine, alcohol, spicy) is no longer recommended **
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2
Q

Describe the general pharm management of GERD (based on severity)

A

Mild, infrequent: antacid or H2RA PRN

Inadequate control or severe, frequent sxs: PPI qd x 8wk

Continued sxs: BID PPI or switch to different PPI

Nocturnal sxs despite BID PPI: add H2RA

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3
Q

What are the 3 main salts used as antacids?

A
  1. Al (OH)3 - aluminum hydroxide
  2. CaCO3 - calcium carbonate
  3. Mg (OH)3 - magnesium hydroxide
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4
Q

What is the MOA of antacids? Clinical use?

A

MOA:

  • neutralize gastric acidity by increasing pH
  • inhibit proteolytic activity of pepsin when gastric pH > 4

Clinical indication: dyspepsia, GERD prn

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5
Q

What are two different drug interactions related to antacids?

A
  1. DEC TTC/FQ absorption (cations)

2. DEC absorption d/t “alkalization” of stomach - Fe***
also - ketoconazole, digoxin, phenytoin

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6
Q

List the three ADRs associated with Al(OH)3.

A
  • hypophosphatemia
  • aluminum intoxication (encephalopathy, seizure, coma in CKD pt)
  • constipation**
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7
Q

List the two ADRs associated with CaCO3.

A
  • Constipation**

- Milk-alkali syndrome (HA, Nausea, irritability, weakness, hypercalcemia, metabolic alkalosis, hypophosphatemia)

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8
Q

What are two ADRs associated with Mg(OH)2.

A
  • hyperMg

- laxative effects **

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9
Q

Reiteration - which two antacids cause constipation? Which causes laxative effects?

A

Constipation: aluminum hydroxide, calcium carbonate

Laxative: magnesium hydroxide

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10
Q

What is the MOA of Sucralfate (Carafate) and clinical indications?

A

Aluminum hydroxide complex of sucrose

MOA: forms a “protective coating” by binding with positively charged proteins in exudates

Indications:

  • GERD/PUD
  • Tx NSAID-induced mucosal damage
  • prevent stress ulcer

** suspension - topical tx of stomatitis d/t chemo **

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11
Q

What drug interaction should you be aware of with sucralfate? What are two ADRs?

A

Interaction: DEC absorption of digoxin, phenytoin, warfarin, ketoconazole, theophylline, TTC, FQ

ADRs: constipation, aluminum tox in CKD pt

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12
Q

Name two first gen and two second gen H2RAs.

A

First gen: cimetidine & ranitidine*

Second gen: famotidine* & nizatidine

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13
Q

Why was ranitidine pulled off the shelves?

A

Concern for NDMA in the drug

Currently being investigated by the FDA

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14
Q

Describe the MOA of H2RAs.

A
  • inhibit gastric secretion by blocking H2
  • reduces basal acid secretion primarily (some food stimulated secretion)
    • good for PRN use
    • less potent at reducing nocturnal secretion
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15
Q

What are the clinical indications of H2RAs?

A
  • dyspepsia / GERD / PUD
  • SUP in critically ill pt [may lead to more pneumonia and CDI**]
  • gastric hypersecretory states (ZES, MEN) but PPIs often more effective
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16
Q

What is a class drug effect of H2RAs? What CYP ish should you know?

A
  • DEC absorption Fe*** (ketoconazole, digoxin, phenytoin)… these require acidic environment to be absorbed

CYP

  • Cimetidine: inhibits all isoenzymes, don’t use*
  • Ranitidine, famotidine*, nizatidine - fairly clean
17
Q

What are two class ADRs related to H2RAs?

A
  • acid rebound possible

- confusion in cognitive impairment / demented* elderly pt

18
Q

What are three ADRs related to cimetidine specifically?

A
  • anti-androgen effects w/chronic use
  • drug fever
  • agranulocytosis
19
Q

What is the PPI suffix? Which two are IV?

A

-prazole

IV: Esomeprazole, Pantoprazole

20
Q

What is the MOA of PPIs?

A

Inhibit parietal cell H+/K+ ATP pump
- suppress gastric basal and food stimulated acid secretion

** PPIs should be administered 30-60 min before first meal

21
Q

What are the clinical indications for PPIs?

A
  1. GERD
    - intermittent vs. on-demand vs. continuous
  2. PUD* +/- bleeding (commonly H. pylori)
  3. SUP in critically ill pt
    - not routine hospitalized pt**
    - larger doses for more than 2d increase risk of CDI**
  4. Gastric hypersecretory states (ZES, MEN)
  5. H. pylori infection
22
Q

There are 4 main concerns related to PPI use, what are they?

A
  1. INC CDI
  2. CAP / HAP d/t DEC gastric acid allowing bacterial overgrowth
  3. INC fracture risk in PMP
    - recommend Ca citrate* and Vit D
  4. Other deficiencies
    - hypoMg d/t DEC absorption
    - DEC absorption of iron and Vit B12
23
Q

Who truly needs a PPI?

A

Those at high risk for ulcers or GI bleeding d/t severe GERD, erosive esophagitis, NSAIDs, etc.

Use lowest effective dose for shortest possible duration**

Consider Fe, Ca, Vit B12 supplementation

24
Q

Is there any clinical difference b/t PPIs for symptom relief, esophagitis / ulcer healing? *

A

No

Pt may respond to one and not another

25
Q

What should you monitor with your pt taking a PPI?

A

Mg - baseline and periodically in pt on long-term therapy (> 2wk) or who take diuretics or digoxin

26
Q

Who should you avoid extended PPI therapy (> 2wk) in?

A

Pt w/risk of TdP and those w/long QT syndrome

TdP secondary to altered Mg levels

27
Q

Which CYP interactions are important to know regarding PPIs?

A

Substrates: 2C19, 3A4

Most agents inhibit 2C19
** Clopidogrel - remember, use PANTOPRAZOLE** instead of omeprazole

2C9 inhibitor - Omeprazole
- careful with Warfarin**

28
Q

What are three other important drug interactions to be aware of with PPIs?

A
  • all DEC absorption of ketoconazole, Mg, Fe, Ca, Vit B12, digoxin, phenytoin
  • DEC MTX clearance
  • PPI + diuretic –> DEC Mg –> TdP
29
Q

Old thinking says PPIs are fairly well tolerated. What must you remember when discontinuing these meds?

A

Taper!!

Acid rebound may occur with d/c

Consider H2RAs or antacids for breakthrough

30
Q

What are some newer ADRs to be aware of with PPIs?

A
  • nosocomial infections (HAP/VAP, CDI)
  • anemia (Fe def, pernicious)
  • fractures (hip, wrist, spine)
  • CKD with long-term use?