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Pharmacology II > GERD/Peptic Ulcer Disease > Flashcards

GERD/Peptic Ulcer Disease Flashcards

1
Q

The physiology of gastric acid secretion is modulated by which pathways?

A

Paracrine (histmaine)
Neuroendocrine (Ach)
Endocrine (Gastrin)

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2
Q

Which receptors are activated by the pathways in the physiology of gastric acid secretion?

A

H2, M3, CCK2

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3
Q

What limit the extent of acid secretion in gastric acid secretion?

A

Somatostatin-secreting D cells and prostaglandins

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4
Q

Is GERD more common in men or women?

A

Women- common is pregnancy

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5
Q

What are the lifestyles and sx associated with GERD?

A

High fat meals- increase frequency of sx, calorically dense meals
Tabacco- increases the frequency of sx
Alcohol- no change
Caffeine-no change

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6
Q

What are the four mechanisms associated with GERD?

A
  • Decreased lower esophageal sphincter pressure
  • Prolonged esophageal clearance
  • Mucosal resistance
  • Delayed gastric emptying
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7
Q

What is the normal function of the Lower esophageal sphincter?

A

tonic, contracted state, relaxing to permit free passage of food into the stomach

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8
Q

What is involved in transient LES relaxations?

A

Not associated w/ swallowing
Mechanism unclear, possible causes- esophageal distention, vomiting, belching, retching
Responsible for 65% of reflux episodes in GERD pts

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9
Q

What are the medication causes of decreased LES?

A 
Anticholinergics
Barbituates
Benzodiazepines
Caffeine
Dihydropyridine Ca2+ channel blockers
Dopamine
Estrogen
Ethanol
Isoproterenol
Narcotics
Nicotine
Nitrates
Phentolamine
Progesterone
Theophylline
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10
Q

What are the food causes of decreased LES?

A 
Fatty meals
Peppermint/spearmint
Chocolate
Caffeinated Drinks- coffee, cola, tea
Garlic, onions, and chili peppers
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11
Q

What is involved in esophageal clearance?

A

50% GERD pts have prolonged acid clearance.
Esophagus is normally cleared by peristalsis
Increased salivia provided bicarbonate buffer

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12
Q

What does saliva production decrease with?

A

Age
Sjogren’s syndrome
Xerostomia
Sleep

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13
Q

What is involved in mucosal resistance?

A

Mucus secreting glands may function to protect the esophagus

After repeat exposure, H+ ions diffuse into mucosa causing cellular acidification and necrosis

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14
Q

What foods are mucosal irritants?

A

Spicy foods
Citrus foods
Tomato juice
Coffee

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15
Q

What medications are mucosal irritants?

A 
Aledronate (take w/ full glass water then upright 30 min to avoid ulcerations)
Aspirin
Iron
NSAIDS
Quinidine
Potassium chloride
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16
Q

What is involved in gastric emptying?

A

Problem- delayed gastric emptying time. Factors increasing gastric volume/decreasing gastric emptying- smoking and high fat meals
Post-prandial reflux
Infants- defects in antral motility resulting in failure to thrive and pulmonary aspiration

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17
Q

What life style factors are associated with reducing the sx of GERD?

A 
Exercise- weigh lifting, cycling, sit-ups
Smoking cessation
Obesity
Avoid high-fat meals
Avoid supine body position
Avoid tight fitting clothing
Avoid pregnancy 
Avoid stress
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18
Q

What are typical symptoms of GERD?

A

Heartburn (pyrosis)
Hypersalivations
Belching
Regurgitation

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19
Q

What are the atypical symptoms of GERD?

A 
Non-allergic astham
Chronic cough
Hoarseness
Pharyngitis
Chest Pain 
Dental Erosion
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20
Q

How is GERD diagnosed?

A

History
Endoscopy
24 hr ambulatory pH monitoring
Pre-emptively treating with standard or double dose omeprazoel

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21
Q

When is 24 hr ambulatory pH monitoring used to diagnose GERD?

A

Unusual sx or failure to respond

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22
Q

What are the complications of GERD?

A

Esophagitis
Esophageal strictures (Complicated by ASA/NSAIDS)
Barretts esophagus
Adenocarcinoma of esophagus

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23
Q

What increases the risk of adenocarcinoma of the esophagus?

A

30-60x increase if barretts esophagus

Long standing frequent reflux

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24
Q

What are the symptoms of adenocarcinoma esophagus?

A 
Continual pain
Dysphagia
Odynophagia
Bleeding
Unexplained weight loss
Choking
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25
Q

What are the goals of therapy of GERD?

A
  • Alleviate or eliminate symptoms
  • Decrease the frequency or recurrence and duration of the reflux
  • Promote healing of the mucosa
  • Prevent development of complications
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26
Q

What are the treatments of GERD?

A

Lifestyle modification
Suppression of Gastric acid production
Promotility therapy
Surgery

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27
Q

What is used for suppression of gastric acid production in the treatment of GERD?

A

Antacids after meals and at bedtime
H2 histamine receptor antagonist
Covalent inhibitors of the H+, K+ -ATPase of the parietal cell (PPIs)

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28
Q

What is used for promotility therapy in the treatment of GERD?

A

Metoclopramide (domapine antagonist)

Bethanechol (Cholinergic agent)

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29
Q

What are the lifestyle modifications that can be made to help GERD?

A

Elevate the head of the bed (increases esophageal clearance)
Make dietary changes
Smoking cessation (decreases spontaneous esophageal sphincter relaxation)
Avoid ETOH
Avoid tight fitting flothing
Discontinue drugs that contribute to reflux
Take medications with plenty of water

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30
Q

What medications contribute to reflux in GERD?

A 
Ca++ channel blockers
Beta blockers
Nitrates
Theophylline
Caffeine
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31
Q

What are the dietary changes that should be made to help GERD?

A

Avoid foods that lower esophageal sphincter pressure (fats, chocolate, ETOH, peppermint & spearmint)
Avoids foods that have instant effect on the esophageal mucosa (spicy foods, OJ, tomato juice, coffee)
Include protein-rich foods, augments lower esophageal sphincter pressure
Eat small meals and avoid eating prior to sleeping-decrease gastric volume.
Loose weight-reduces symptoms.

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32
Q

What are the two therapeutic approaches to GERD?

A

Patient-directed therapy, progressing to pharmacologic management or interventional therapies
OR
Proton pump inhibitor 1-2x daily then reducing to lowest degree of acid suppression for symptom control

Lifestyle modifications are started initially and continued throughout treatment

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33
Q

What are considered patient directed therapy?

A

Antacids and OTC acid suppressants
Both shown to be effective in symptom relief induced by heartburn promoting meal
Combination of both superior to antacids alone
OTC H2-blockers considered interchangeable

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34
Q

Antacids- MOA

A 
Neutralize acid to raise intragastric pH
Decrease activation of pepsinogen
Increased LES pressure
Benefit- rapid onset
Disadvantage- short duration
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35
Q

Antacid- Side effects

A 
GI- diarrhea or constipiation
- diarrhea: magnesium
-constipation: aluminum
-Gas: calcium, 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 supplemental calcium or with renal dysfunction
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36
Q

Antacid- Drug interactions

A

alter gastric pH, increase urinary pH, adsorbing medications, physical barrier to absorption, form insoluble complexes
Clinically significant- abx- quinolone, isoniazid, tetracycline, ferrous sulfate, quinidine, sulfonylurea

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37
Q

Antacids- Precautions

A

Use of med >14 days needs evaluation for barrett’s esophagus and upper GI pathology due to increased risk
Pts excessively using antavids should be treated w/ rx drugs, and is considered more significant disease.

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38
Q

What is involved in antacid counseling?

A

Dose is product-specific…follow manufacturer’s recommendations

Take at onset of symptoms

If potential for drug interactions, separate dosages by at least 2 hours

Use should not exceed 14 days

Pts should be evaluated if using >2x week

39
Q

H2 receptor antagonists- MOA

A

Reversibly inhibit histamine-2 receptors on parietal cells

40
Q

H2 receptor antagonists- USE

A

On-demand therapy for intermittent mild to moderate GERD symptoms
Preventive dosing before exercise/meals
Prescription strengths needed for more severe symptoms or for maintenance dosing
Less effective than PPIs in healing erosive esophagitis

41
Q

What drugs are H2 receptor antagonists?

A 
Ranitidine (Zantac)
Cimetidine (tagamet)
Nixatidine (Axid)
Famotidine (Pepcid)
Pepcid Complete
These resemble histamines
42
Q

H2- receptor antagonist- Absorption, fate, and excretion

A

H2 receptor antagonists are rapidly & well absorbed after oral admin.
Peak conc. 1-2 hours
Oral bioavailability of nizatidine ~ 90%
-Whereas first-pass metabolism limits bioavailability of the other compounds to ~50%,
A large part of these drugs are excreted unchanged in the urine and therefore may need a reduction in dosage w/renal impairment.

43
Q

H2- receptor antagonist- side effects

A

Well tolerated
HA, somnolence, fatigue, dizziness, constipation or diarrhea
Thrombocytopenia: rare, reversible

44
Q

H2- receptor antagonist- Drug interactions

A

Cimetidine
-Inhibition of metabolism of warfarin, phenytoin, nifedipine, propranolol
Acidic environment required for absorption
-Ketoconazole, itraconazole, ferrous sulfate

45
Q

Antacids vs H2-receptor antagonist

A

Combination more effective than antacid therapy alone

46
Q

What is used in acid suppression?

A

Proton pump inhibitors (PPIs)- eliminate symptoms and heal esophagitis more frequently and rapidly than other drugs

47
Q

When should PPIs be given?

A

Prior to meals

48
Q

What are the names of the PPIs?

A

Prototypes- omeprazole (prilosec)

Other agents- Lansoprazole (prevacid), esomeprazole (nexium), pantoprazole (Protonix), rabeprazole (aciphex)

49
Q

Proton pump inhibitor- MOA

A
  • Inhibit the action of the H+,K+ -ATPase.
  • All considered prodrugs in that they need to be activated to be effective. They need the acidic environment (H+) to work.
  • Requires 18 hours to synthesize new H+,K+ -ATPase molecules
50
Q

Proton pump inhibitor- ADRs

A

Generally uncommon
N/D/C
HA, dizziness, somnolence
May have higher incidence of community-acquired pneumonia
-Clinical significance unclear
-Pts with asthma, COPD, immunocompromised, young or elderly may be at risk

51
Q

Proton pump inhibitors- Drug interactions

A

P450s
Omeprazole, lansoprazole, esomeprazole and pantoprazole metabolized by P450 enzymes (rabeprazole metabolized thru nonenzymatic reduction pathway)
Omeprazole and esomeprazole reduce metabolism of: Diazepam, Phenytoin, warfarin

52
Q

When are promotility agents used?

A

LES incompetence
Decreased esophageal clearance
Delayed gastric emptying

53
Q

Promotility agents- Side effects

A

Limited side effect profile:
CNS effects: drowsiness, irritability, extrapyramidal effects
–Metoclopramide (Reglan): contraindicated in Parkinson’s Dz, mechanical obstruction, concomitant use of other dopamine antagonists, anticholinergics, and pheochromocytoma
–Bethanechol (Urecholine): may increase acid production, not well tolerated due to cholinergic side-effects (usually used for the bladder and not intestines)
–Fatal cardiac dysrhythmia: cisapride

54
Q

Sulcralfate- MOA

A

Mucosal protectant
Non-absorbable aluminum salt
Compared to H2-receptor antagonist for mild esophagitis
Less effective in refractory esophagitis

55
Q

Are mucosal protectants (sucralfate) recommended for use in mild cases of GERD?

A

Yes

Not recommended for used EXCEPT FOR VERY MILD CASES OF GERD

56
Q

Sulcralfate (Carafate)- Chemistry and effects

A
  • When the pH is below 4, an extensive polymerization & 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.
57
Q

Sulcralfate (Carafate)- Clinical utility

A
  • Effective at promoting healing in PUD
  • As a 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.
58
Q

Sulcralfate (Carafate)- ADRs

A

Constipation - A3+
Dry mouth
Abdominal discomfort

59
Q

Sulcralfate (Carafate)- drug interactions

A

Phenytoin
Tetracycline
Fluroquinolone Antibiotics
Digoxin
Ketocanazole
Better to administer these meds 2 hrs before sucralfate
DO NOT administer w/ agents that decrease acid

60
Q

What is maintenance therapy?

A

Improvement of symptoms with full dose PPIs usually reverses with discontinuation of therapy
Effective maintenance therapy controls symptoms and prevents complications
Some pts require chronic PPI therapy

61
Q

What is ineffective maintenance therapy?

A

Full dose H2-receptor antagonist once daily not appropriate
Reduced dose PPIs
Alternate day dosing
“Weekend” therapy
Dose needed to control symptoms is appropriate dose for maintenance

62
Q

What are the effects of therapy on complications in GERD?

A

Acid suppression decreases recurrence of esophageal strictures
Full dose PPIs lengthen time between symptomatic relapses
No data on prevention of prevention of progression of Barrett’s esophagus
–May be some reappearance of squamous epithelium but significance unclear

63
Q

What can you give to a phase 1 intermittent, mild heart burn patient?

A

Lifestyle changes
and antacids
and/or low dose OTC H2 receptor antagonist
Or OTC PPI

64
Q

What can you give to a Phase 2 patient for symptomatic relief of GERD?

A

Lifestyle cahnges
And standard doses of H2-receptor antagonist for 6-12 wks
Or PPI for 4-8 weeks

65
Q

What can you give to a phase 3 patient- healing of erosive esophagitis, moderate to severe symptoms, or complications of GERD?

A

Lifestyle changes
And PPI for 4-1 weeks (up to BID)
Or high doses of H2-receptor antagonist for 8-12 weeks

66
Q

What are the phase 3 interventional therapies?

A

Antireflux surgery

Endoluminal therapy

67
Q

What is peptic ulcer dz?

A

Ulcers extending deep into the muscularis mucosa

68
Q

What are the two most common forms of peptic ulcer disease?

A

H. Pylori associated
NSAID induced
Stress related mucosal damage (3rd)

69
Q

What does the incidence vary on for peptic ulcer disease?

A

Ulcer type-duodenal, gastric
Age
Gender
Societal factors- H. pylori, NSAID use, smoking

70
Q

What are the two main causes of duodenal ulcers?

A

H. pylori and NSAIDS

71
Q

What are the sx of duodenal ulcers?

A

Epigastric pain, often worse at night
Pain typically 1-3 hrs after meal and may be relieved by eating
Pain can be episodic

72
Q

What are the two most common causes of gastric ulcers?

A

NSAID use and h. pylori

73
Q

What are the sx of gastric ulcers?

A

Epigastric pain, often worse with food

Associated symptoms: heartburn, belching, bloating, nausea, anorexia

74
Q

What is involved in the etiology of peptic ulcer dz?

A

H. Pylor
NSAIDS
Psychological stress
Diet- In high concentrations, alcohol associated with acute gastric mucosal damage, upper GI bleed
Smoking: unclear mechanism, impairs healing, higher death rates

75
Q

Helicobacter pylori

A

Gram negative rode that colonized the mucus on the luminal surface of the gastric epithelium
Causes inflammatory gastritis

76
Q

How is H. pylori transmitted?

A

Fecal-oral
Oral-oral
Iatrogenic

77
Q

How do you document an H. pylori infection?

A

Usually a blood test

Breath test for urea

78
Q

What are the complications of peptic ulcer dz?

A

Zollinger-Ellison Syndrome
Upper GI bleed
Perforation
Obstructions

79
Q

Zollinger-Ellison Syndrome

A
  • -Gastric acid hypersecretion and recurring ulceration from a gastrin-secreting tumor
  • -Appox. 1% of patients
  • -Can metastasize
  • -Treatment: PPIs
80
Q

Upper GI bleed

A
  • -Erosion of ulcer into artery
  • -10-15% pts
  • -Presentation: Occult and insidious, Melena or hematemesis
  • -Fatal- Uncontrolled bleed, Rebleeding
81
Q

Perforation

A
  • -Ulceration into a cavity
  • -7% of patients
  • -Increases with NSAID use
  • -Mortality higher in perforated gastric ulcer vs duodenal ulcer
82
Q

Obstruction

A
  • -2% of patients
  • -Typically in chronic PUD
  • -Caused by scarring or edema of duodenal bulb or pyloric channel land lead to gastric retention
  • -Symptoms:Over several months, Early satiety, bloating, anorexia, nausea, vomiting, weight loss
83
Q

What is the three drug regimen for peptic ulcer dz?

A 
P= PPI
A= Amoxicillin
C= Clarithromycin

OR

P=PPI
M==Metronidazole
C=Clarithromycin

84
Q

what is the drug of choice for PUD?

A

PPIs

85
Q

What is the 4 drug regimen for peptic ulcer dz?

A

P=PPI (or H2 blcoker)
B= Peto bismol
M=Metronidazole
T=tetracycline (or amox, or clarithro)

86
Q

How do you treat treatment failures?

A 
Retreat with different antibiotics
Use Bismuth based regimen
Extended treatment duration
Assess adverse effects
Assess compliance
87
Q

Bismuth Subsalicylate (pepto-bismol)- beneficial effects

A

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, Damage bacterial cell walls.
Promote healing of both gastric and duodenal ulcers

88
Q

Bismuth Subsalicylate (pepto-bismol)- ADRs

A
  • Reaction of bismuth w/bacterial H2S leads to bismuth sulfide causing a black color to the oral cavity and to feces.
  • Aspirin ADRs
89
Q

Prostaglandin Analogs- MOA

A
  • Misoprostol is a synthetic analogue of prostaglandin E.
  • Imitates the action of endogenous prostaglandins (PGE2 and PGI2) in maintaining the integrity of the gastroduodenal mucosal barrier.
  • Promotes healing.
90
Q

Prostaglandin analogs- Indications

A

Ulcer healing

Ulcer prophylaxis w/ NSAID use

91
Q

Prostaglandin Analog- contraindications

A

Hypotension
Breastfeeding
Pregnant

92
Q

Prostaglandin Angalog- ADRs

A

Diarrhea

Constipation

93
Q

What is the nonpharmacologic treatment of PUD?

A 
Eliminate or reduce: 
Psychological stress
Cigarette smoking
The use of NSAIDs including aspirin
-Consider APAP
-Lowering the dose
-Nonacetylated salicylate (salsalate)
-Relatively selective COX-2 inhibitors (nabumetone, etodolac) or highly-selective COX-2 inhibitors (celecoxib)
-Co-administration w/H2 antagonist or PPI
94
Q

What are the diet changes for nonpharmacologic treatment of PUD?

A

Avoid food and beverages that cause dyspepsia or exacerbate ulcer symptoms: spicy foods, caffeine, ETOH

Pharmacology II (23 decks)

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