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PHAR 255 > GI Conditions > Flashcards

GI Conditions Flashcards

1
Q

What is dyspepsia?

A

Epigastic pain or discomfort originating from upper GI tract

It is an umbrella term to describe many possible symptoms and causes

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2
Q

What is GERD?

A

Gastroesophageal reflux disease

It is reflux of gastric contents into the esophagus

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3
Q

What is peptic ulcer disease?

A

An ulcer formed in the gastric or duodenal mucosa

Similar symptoms as dyspepsia or GERD

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4
Q

What is the most common diagnosis of dyspepsia?

A

Uninvestigated dyspepsia (only after endoscopy are patients organized between functional dyspepsia or GERD)

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5
Q

What are some mechanisms by which functional dyspepsia can develop?

A
  • Gastric motility and compliance
  • Visceral hypersensitivity (linked to pH and motility)
  • H. Pylori
  • Altered gut microbiome
  • Duodenal inflammation
  • Psychosocial dysfunction
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6
Q

What are some non-functional causses of dyspepsia?

A
  • GERD (most common)
  • Gastric ulcer
  • Gastric erosions
  • Gastro-esophageal malignancy (rare)
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7
Q

What are some risk factors associated for developing risk factors for dyspepsia?

A
  • No strong association with sex, age, socioeconomic status
  • Dietary indiscretion
  • Medications
  • H. Pylori infection
  • IBS
  • Smoking or alcohol use (can worsen existing dyspepsia)
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8
Q

What are some drugs that can cause drug-induced dyspepsia?

A
  • Bisphosphonates
  • Iron
  • NSAIDs
  • Potassium
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9
Q

What are some symptoms of dyspepsia?

A

Any of the following for more than 1 year
- Epigastric pain or discomfort
- Fullness or early satiety
- Nausea
- Upper abdominal bloating

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10
Q

What are the main “red flag” symptoms for dyspepsia?

A
  • Vomitting
  • Bleeding
  • Abdominal mass or unexplained weight loss
  • Dysphagia or odynophagia
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11
Q

How many Canadians have dyspepsia?

A

About 30% of Canadians have some degree of dyspepsia

All ages impacted equally

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12
Q

What happens in GERD?

A

Reflux of stomach acid contents into esophagus, possibly leading to reflux (non-erosive) esophagitis or erosive esophagitis

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13
Q

How many GERD patients have reflux esophagitis (non-erosive)?

A

About 70% of GERD patients have less severe presentation

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14
Q

How many GERD patients have erosive esophagits?

A

About 30% of patients have the more severe presentation of GERD

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15
Q

What are some causes of GERD specifically?

A
  • Defective lower esophageal sphincter
  • Increased intra-abdominal pressure
  • Hiatal hernia
  • Impaired esophageal peristalsis
  • Delayed gastric emptying
  • Excessive gastric acid production
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16
Q

What are some risk factors for developing GERD?

A
  • Obesity
  • Pregnancy
  • Family history
  • Smoking
  • Increased age (more than 65)
  • Hiatal hernia
  • Stress and anxiety
  • Drugs
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17
Q

What are the most common drugs that cause GERD?

A
  • Anticholinergics
  • Benzodiazepines
  • Opioids

These drugs slow esophageal peristalsis or relaxation of upper esophageal sphincter

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18
Q

What are some dietary contributors to GERD?

A

Over-eating in general

Specific foods:
- Fatty foods
- Chocolate
- Coffee
- Alcohol
- Carbonated drinks
- Acidic juices

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19
Q

Review slide 22 for classifying the severity of GERD symptoms

A
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20
Q

What are some potential complications associated with GERD?

A
  • Esophagitis
  • Esophageal stricture
  • Esophageal erosions
  • Barrett’s esophagus (squamous cells in esophagus are replaced by hardier columnar cells, but 40-60x higher cancer risk)
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21
Q

What are some red flags for physician referral?

A
  • VBAD symptoms
  • Choking
  • Constant pain
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22
Q

How can a trial of pharmacological therapy use used as a diagnostic tool for GERD?

A

PPI treatment will resolve GERD, if issue not resolved then other causes may be present

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23
Q

Who are some people that qualify for a upper endoscopy for GERD diagnosis?

A

New onset of symptoms after the age of 50
- VBAD symptoms
- Refractory GERD
- At risk for Barrett’s esophagus (endoscopy is indicated)

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24
Q

What patient groups are at risk for Barrett’s esophagus?

A

Male, chronic GERD (longer than 5 years or frequent episodes) and 2 more of the following:
- Older than 50
- Caucasian
- Central obesity
- Current or past history of smoking
- Family history of Barrett’s esophagus

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25
Q

Besides upper endoscopy, what are some other diagnostic tests for GERD?

A
  • Barium swallow
  • Esophageal manometry
  • Ambulatory esophageal pH monitoring
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26
Q

Where is GERD the most prevalent?

A

10-20% of people living in the West report having GERD or GERD like symptoms

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27
Q

What are some goals of treatment for GERD?

A
  1. Relieve symptoms
  2. Promote healing of injured mucosa
  3. Prevent and treat complications
  4. Prevent recurrence
  5. Avoid issues with long-term use of pharmacotherapy
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28
Q

What are some lifestyle changes that can demonstrate benefit in GERD treatment?

A
  • Lose and maintain ideal weight
  • Stop smoking
  • Elevate head of bed
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29
Q

What are some commonly used drugs in GERD treatment?

A
  • Alginates and Antacids (used at the onset of symptoms and more for PRN Use)
  • H2RAs and PPIs (prevent symptoms from occuring in the first place)
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30
Q

What is the mechanism of action for alginates?

A

Forms a viscous “raft” that floats within the stomach

Starts working in less than an hour

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31
Q

What is the mechanism of action for antacids?

A
  • Neutralizes stomach acid
  • Inhibits pepsin generation
  • Rapid acting, but short duration of action

Take after a meal for the best effect

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32
Q

What are some contraindications for antacids?

A
  • Avoid in severe renal impairment (unless the patient is on dialysis and calcium carbonate can be also used as a phosphate binder)
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33
Q

How are antacids taken?

A
  • Chew 2-4 tables up to QID
  • 30-60 minutes after a meal and/or bedtime
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34
Q

What are some common side effects associated with antacids?

A

Depends on the metal ion:

Aluminium - constipating

Magnesium - laxative effect

Calcium - well tolerated

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35
Q

What are some serious side effects associated with antacids?

A

Depends on the metal ion:

Aluminium - bone demineralization, neurotoxicity, hypophosphatemia

Magnesium - hypermagnesemia

Calcium - Hypercalcemia, alkalosis

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36
Q

What are the main types of drug interactions with antacids?

A
  • Chelation with many drugs (antibiotics, iron, bisphosphonates, etc.)
  • Impaired absorption of pH sensitive drugs (dabigatran, HIV meds)
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37
Q

What is the efficacy of antacids in GERD treatment?

A
  • Limited evidence
  • Slight reduction in symptom severity and frequency
  • Better than placebo, inferior to other agents (good for mild, infrequent dyspepsia/GERD)
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38
Q

What are some examples of antacids?

A
  • Aluminium hydroxide
  • Magnesium hydroxide
  • Magnesium trisilicate
  • Calcium carbonate
  • Sodium bicarbonate
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39
Q

What are some examples of H2RAs?

A
  • Cimetidine
  • Famotidine
  • Ranitidine
  • Nizatidine
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40
Q

What is the mechanism of action for H2RAs?

A
  • Parietal cells in stomach pump hydrogen ions into gastric lumen
  • Blocking the H2 receptors prevents pump activation
  • Reduction in basal and stimulated gastric acid activation
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41
Q

What are some common side effects associated with H2RAs?

A
  • Extremely well tolerated (except cimetidine)
  • Headache, vomiting, diarrhea, drowsiness (just as potent as other options, but more side effects)
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42
Q

What are some drug interactions associated with H2RAs?

A
  • All drugs that need higher stomach acidity for optimal absorption (Dabigatran and HIV drugs are particularly concering)
  • Cimetidine
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43
Q

What is the efficacy of H2RAs?

A

They are more effective than antacids, less effective than PPIs (tend to be the mainstay of self-care therapy)

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44
Q

Can H2RAs be used long-term?

A

No, patients rapidly develop tolerance against H2RAs (usually within 8 weeks of continuous use)

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45
Q

Are H2RAs combined with PPI to get more benefit?

A

No, the combo is not any more effective

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46
Q

What are some examples of PPIs?

A
  • Rabeprazole
  • Omeprazole
  • Esomeprazole
  • Pantoprazole
  • Lansoprazole
  • Dexlansoprazole
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47
Q

What are the two formulations of pantoprazole, and are they interchangable?

A

Panto sodium and panto magnesium (they are not interchangable)

sodium (older formulation)

magnesium (newer formulation, longer duration of action)

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48
Q

What are the main indications for PPIs?

A
  • Treatment of GERD symptoms
  • Symptomatic relief and healing of duodenal and gastric ulcers
  • Use in H. Pylori eradication regimens
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49
Q

What are some contraindications associated with PPI treatment?

A

None

50
Q

What is the mechanism of action for PPIs?

A
  • Directly inhibits proton pumps (only if they are actively secreting H+) to prevent gastric acid secretion
51
Q

When is the best time to administer a PPI?

A

30 min before breakfast or the first meal of the day (PPIs work best when preceded by a fast)

52
Q

What is the onset of action for PPIs?

A

Daily use for at least 3-5 days results in maximal inhibition (scheduled use is more beneficial)

53
Q

What is the duration of action for PPIs?

A

PPI recovery takes 24-48 hours after discontinuation

54
Q

What are some indications for double-dose PPIs?

A
  • Standard dose is not effective after adequate trial (4-8 weeks)
  • Initial presentation of erosive esophagitis
  • Ulcers or GI bleed indications
  • H. Pylori eradication
55
Q

What are some common side effects associated with PPI use?

A

Overall well tolerated

  • Dysgeusia (altered taste, bitter or metallic)
  • Nausea
  • Headache
  • Dizziness
56
Q

What are some serious side effects of PPIs?

A
  • C. diff infection (rare in healthy patients)
  • Microscopic colitis
  • Hypomagnesemia
  • Fractures (reduced absorption of calcium carbonate due to higher pH)
  • Fundic Gland Polyps
  • B12 deficiency
  • Pneumonia
  • Gastric Cancer (low risk)
  • Increased Mortality (confounding variable, people on PPIs have other conditions)
57
Q

How can the risk associated with PPI use be managed?

A

Understand PPIs tend to be overused (periodically reassess dose and and need for on-going therapy)

58
Q

What are some drug interactions associated with PPI use?

A

Any drug that depends on stomach acidity for absorption (reduced absorption when concurrently administered)

59
Q

What are some drug interactions that are specific to Lansoprazole?

A

Theophylline (rarely used) and mycophenolate

60
Q

What are some drug interactions that are specific to Omeprazole and Esomeprazole?

A

Reduce Clopidogrel

Increase:
- Warfarin
- Phenytoin
- Citalopram

61
Q

What is the relative efficacy of PPIs ?

A

They are equally effective

More effective than H2RAs and antacids

62
Q

What are some pro-kinetic drugs used in GI conditions?

A

Domperidone and Metoclopramide (dopamine antagonists stimulate GI motility)

Used for GI motility disorder, limited use in GERD

63
Q

When should pro-kinetic drugs administered for GI conditions?

A

Give 15-30 minutes before meals and bedtime

64
Q

What are some contraindications associated with Metoclopramide?

A

GI obstruction, perforation, or hemorrhage

Crosses the BBB and can cause CNS effects (seizures, extra-pyramidal symptoms, pseudo-Parkinson’s)

65
Q

What are some contraindications associated with Domperidone?

A
  • GI obstruction, perforation, or hemorrhage
  • Long QT prolongations (with high doses)
  • Electrolyte disorders
66
Q

What is the preferred treatment strategy for GERD?

A

Step down
1. Scheduled course of PPI for specific duration
2. Then find lowest strength options to control symptoms (lower dose on-demand PPI, H2RA prn or scheduled, no therapy)

67
Q

What are some factors that confirm refractory GERD?

A
  • Failure on 2 month course of once daily PPI
  • Symptoms recur within 3 months of PPI discontinuation
  • About 25% of patients will be refractory
68
Q

What are some causes of PPI treatment failure?

A
  • Medication timing and adherence (30 min before meal and take everyday)
  • CYP polymorphisms
  • Weakly acidic or alkaline reflux (acidity is not issue in this patient)
  • Reflux hypersensitivity
  • alternative diagnosis
69
Q

Review slide 73 for management of refractory GERD

A
70
Q

When should PPIs be deprescribed?

A

Should attempt to deprescribe after 4-8 week trial (ensure they do not have chronic needs)

If long-term therapy, attempt deprescribing once per year

71
Q

Who are some ideal candidates for PPI deprescribing?

A
  • Mild-moderate GERD who responded to therapy
  • Peptic ulcer disease treated for proper duration
  • Asymptomatic for 3 consecutive days
  • H. Pylori eradication successful
72
Q

What is the process of PPI deprescribing?

A

Tapering PPI is more successful than abrupt discontinuation
- Decrease dose every other day
- Initiate H2RA may help with taper
- On-demand PPI (used for GERD symptom recurrence)

73
Q

What is the main indication for chronic PPI therapy?

A

Chronic NSAID users can use PPIs to help reduce GI bleed risk

74
Q

Review slide 76 for more details on PPI deprescribing

A
75
Q

What is the treatment strategy for functional dyspepsia?

A
  1. PPIs once daily for 4-8 weeks
  2. H. Pylori testing/eradication
  3. Switch/add-on TCA
  4. Switch/add-on prokinetic agent (domperidone and metoclopramide)
76
Q

When should GERD treatment be considered in infants?

A

Only in the case of complications
- Poor weight gain (failure to thrive)
- Blood in stool or vomitus
- Intense irritability temporally related to food intake

77
Q

What are some red flag associated with GERD in pediatrics?

A
  • Forceful vomiting
  • Abdominal tenderness or distension
  • Fever
  • Systemic signs
78
Q

Review slide 79 for treatment strategy for GERD in pediatrics

A
79
Q

Are PPIs safe in pregnant women?

A

No harm indicated with PPIs and H2RAs

Lansoprazole, Omeprazole, and Pantoprazole are preferred

Panto is preferred in lactating women

80
Q

When can pharmacists prescribe PPIs for GERD?

A

Appropriate for mild-moderate symptoms and no red flags

  • Predominate symptom must be heartburn and regurgitation
  • If mild and infrequent, must be step-up approach
  • If infrequent or moderate, can initiate on a PPI for 4 weeks + 1 refill
  • If a recurrence occurs within 3 months of d/c, considered refractory (then refer)
81
Q

What are some drugs that can cause drug-induced esophagitis?

A

Pills can become lodged in esophagus (take drugs with water and do not lie down for at least 30 minutes)

Common culprits:
- Doxy/tetra
- K+ tablets
- ASA and NSAIDs
- Bisphosphonates
- Clindamycin

82
Q

What patient groups with GI issues qualify for endoscopy?

A
  • New onset symptoms (over 50)
  • Any alarm symptoms (VBAD)
  • Refractory symptoms
  • At risk for Barrett’s esophagus
83
Q

What is the definition of peptic ulcer disease (PUD)?

A

A broad term that encapsulates any breach in the mucosa of the digestive tract

Majority of PUD are gastric or duodenal ulcers (esophaus ulcers are rare)

84
Q

What are gastric erosions?

A

They are less severe forms of ulcers because they do not affect deeper tissues

85
Q

What are some causes of PUD?

A
  • H. Pylori
  • NSAIDs
  • Pepsin (stomach enzymes)
  • Physiologic stress
  • Acid
  • Alcohol
86
Q

What are some protective factors for PUD?

A
  • Gastric mucous
  • HCO3
  • Prostaglandins
  • Mucosal blood flow
  • Epithelial cell regeneration
87
Q

What are the lowest risk NSAIDs for developing PUD?

A

Celecoxib (COX-2 selective)
Ibuprofen

88
Q

What is the risk level of Naproxen to cause PUD?

A

Average risk

89
Q

What is the highest risk NSAID for developing PUD?

A

Ketorolac

90
Q

What patient groups are at elevated risk for developing PUD?

A
  • History of an uncomplicated ulcer
  • Age over 60
  • High dose or multiple NSAID use
  • Concomitant ASA, glucocorticoids, anticoagulants, SSRI
  • History of CVD

High risk (complicated ulcer history to 3 of the above factors)
Moderate risk (1 or 2 risk factors)
Low risk (none)

91
Q

What are some characteristics of H. Pylori?

A

Gram negative rod spread via fecal-oral route (exclusively colonizers gastric epithelium)

Risk factors for colonization:
- Crowded living conditions
- Unclean water
- Raw vegetables

H. Pylori produces phospholipase and catalase (inhibit immune system reaction)

92
Q

What are the pathogenic mechanisms for H. Pylori induced PUD?

A
  • Direct cytotoxic effect
  • Renders underlying mucosa more vulnerable to acid damage
  • High levels of ammonia (prevents detection of acidity, more acid is released, causes more damage)
  • Promotion of cytokines and inflammation
93
Q

What is the primary cause of PUD?

A

H. Pylori is responsible for 80-90% of all PUDs, the remainder are largely caused by NSAIDs

94
Q

What are the clinical symptoms of PUD?

A

70% of peptic ulcers are asymptomatic (especially in elderly and NSAID induced PUD), a GI bleed is often the first sign

Dyspeptic symptoms

Symptoms in relating to food (can provide information about location before endoscopy)

95
Q

What are some complications associated with PUD?

A
  • Quality of life decrease
  • GI bleeds
  • Perforations or fistulations
  • Gastric outlet obstructions
  • Mortality increase
96
Q

What are some signs of PUD related bleeding?

A
  • Nausea and vomitting (coffee ground emesis)
  • Melena (dark, tarry stool)
  • Orthostatic hypotension
  • Red blood in stool if massive bleed (considered emergency if source of bleed is upper GI = lots of undigested blood)
97
Q

What are some signs of PUD related obstruction?

A
  • Nausea and vomiting
  • Early satiety
  • Bloating
  • Indigestion
  • Anorexia and weight loss
98
Q

What are some symptoms of a perforation of a GI ulcer?

A
  • Sudden change in symptom pattern
  • Halitosis
  • Post-prandial diarrhea
  • Weight loss
99
Q

Review slide 110 to 112 for PUD diagnosis

A
100
Q

What is the most common H. Pylori test?

A

Urea Breath Testing (H. Pylori causes more ammonia to develop in the stomach)

101
Q

What are some risk factors for PUD recurrence?

A
  • NSAIDs
  • H. Pylori suboptimal eradication or reinfection
  • Smoking
  • Alcohol use
  • Long-standing PUD
102
Q

What are the goals of therapy for PUD?

A
  • Relieve dyspepsia
  • Heal the ulcer
  • Prevent complications
  • Prevent recurrence
  • Implement lifestyle changes (avoid foods that trigger symptoms, eliminate alcohol, smoking cessation)
103
Q

What is the treatment strategy for NSAID-induced ulcers?

A
  1. d/c the NSAID if possible, consider alternatives
  2. Begin ulcer healing therapy (PPI standard dose, gastic ulcer=8 to 12 weeks, duodenal ulcer=4 to 8 weeks)
  3. H. Pylori testing should be done
  4. Consider on-going secondary prevention for some patients
104
Q

What are some options for secondary prevention of NSAID-induced PUD?

A
  • Lower NSAID dose
  • Switch to Celecoxib
  • Add long-term PPI
  • Add misoprostol
105
Q

What is the mechanism of action of misoprostol in PUD?

A

It is a prostaglandin analogue leading to an increase in:
- Gastric mucous
- Bicarbonate secretion
- Inhibition of basal and nocturnal gastric acid secretion

106
Q

What is the preferred treatment option for H. Pylori induced ulcers?

A

Quadruple therapy (PBMT and PAMC)

PBMT (PPI, Bismuth, Metronidazole, Tetracycline)
PAMC (PPI, Bismuth, Metronidazole, Clarithromycin)

107
Q

What are some second line treatment options for H. Pylori induced ulcers?

A

PAL (PPI, Amox, Levoflox) or PABL (PPI, Amox, Bismuth, Levoflox)

PBMT if not tried already

108
Q

What are some characteristics of PBMT treatment of H. Pylori induced ulcer management?

A

Advantages:
- Highly effective
- Overcomes resistance
- Preferred if penicillin allergy

Disadvantages:
- High pill burden (QID treatment)
- Metronidazole interacts with alcohol

109
Q

What are some characteristics of PAMC treatment of H. Pylori induced ulcer management?

A

Advantages:
- Highly effective (less than PBMT)
- Simplified regimen (BID instead of QID)

Disadvantages:
- More GI ADRs
- Clarithromycin resistance
- Pencillin allergy
- Metronidazole interacts with alcohol

110
Q

Why are triple therapy regimens not recommended for H. pylori-induced ulcer management?

A

They are restricted in use due to high resistance rates, which leads to higher failure rates

111
Q

What is the utility of PAL or PABL treatments in H. Pylori induced ulcers?

A

Used in treatment failure with PMBT or PAMC treatment

112
Q

What are some characteristics of PAL/PABL treatment for H. Pylori induced ulcers?

A

Advantages:
- Important option for previous failure

Disadvantages:
- Lower eradication rates vs. first line
- Penicillin allergy
- Increased risk of increasing resistance to levofloxacin

113
Q

What is the role of PAR treatment in H. Pylori induced ulcers?

A

It is a last-line option if all other regimens have failed

114
Q

What patient factors should be considered when choosing a treatment regimen for H. Pylori induced ulcers?

A
  • Allergy history
  • Recent antibiotic use (esp. metro/clarithro)
  • Alcohol use (avoid metronidazole)
  • DI potential (especially with clarithro)
  • Adherence/pill burden (difficulty especially if patient is already on polypharmacy)
  • Anticoagulant or antiplatelet use if considering bismuth
115
Q

Review slide 135 for H. Pylori induced ulcer treatment algorithm

A
116
Q

What are some common reasons for H. Pylori induced ulcer treatment failure?

A
  • Poor adherence (can help with compliance packaging)
  • Incorrect regimen used (use evidence based treatment combinations only)
  • High local resistance rates
117
Q

How is treatment success for H. Pylori induced ulcers assessed?

A

Fecal stool antigen test four weeks after completion of therapy is optimal

118
Q

What is the role of PPI maintenance therapy after successful H. Pylori eradication?

A

Duodenal ulcer: generally not indicated (possiblity 2 weeks after stopping combo therapy)

Gastric ulcer: continue PPI for 8 weeks

119
Q

What is the utility of probiotics in H. Pylori induced ulcer management?

A

Improves efficacy and tolerability (not harmful to try)

120
Q

For ulcers that are not caused by H. Pylori or NSAID use, what is the treatment strategy?

A
  • Poor prognosis
  • PPI for 4-8 weeks is the only treatment option
  • Increase dose and duration if initial trial fails
  • Reassess and consider alternate diagnosis if little improvement
  • Consider long-term PPI
121
Q
A

PHAR 255 (15 decks)

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