COPD and PUD Therapeutics Flashcards by John White

GERD Description

Decreased resting tone of lower esophageal sphincter

Delayed gastric emptying

Transient LES relaxation

Impaired peristalsis

Decreased salivation

Impaired tissue resistances

No change in acid production

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GERD Symptoms

Typical (heartburn, acid brash, regurgitation/belching, chest pain)

Extra-esophogeal, present with typical symptoms (chronic cough, laryngitis, asthma, dental enamel erosion)

Alarming (dysphagia, odynophagia, bleeding, anemia, weight loss)

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Heartburn vs Angina

Heartburn: due to acid reflux; burning, squeezing; spontaneous or after meals, sleep or may be stress induced; relieved by antacids or food; worse with recumbence; substernal

Angina: due to myocardial ischemia; pressure, heaviness; exertional/stress induced; relieved by rest or nitroglycerin; radiates to neck, jaw or shoulder; dyspnea, N/V, diaphoresis, presyncope, palpitations

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Foods that decrease LES tone

Fatty meals, peppermint, spearmint, chocolate, coffee, soda, tea, garlic, onions, chili peppers, alcohol

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Medications that decrease LES tone

Anticholinergics, barbiturates, caffeine, DHP calcium channel blockers, estrogen, progesterone, nicotine, nitrates, tetracycline, theophylline

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Foods that are direct irritants

Spicy foods, citrus, tomato juice, coffee, tobacco, alcohol

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Medications that are direct irritants

ASA, bisphosphonates, NSAIDs, Quinine, KCl

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GERD treatment goals

Improve quality of life, prevent further damage, prevent progression to complications

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GERD lifestyle modifications

Weight loss, elevation of head of bed, dietary modification if trigger foods (use a diary), avoid tight-fitting clothing, avoid tobacco and alcohol

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Antacids

Aluminum hydroxide (constipation, aluminum toxicity in those with renal impairment), Calcium Carbonate (less effective; hypercalcemia in renal impairment), Magnesium hydroxide (diarrhea), Sodium bicarbonate (belching; possible alkalosis; hypercalcemia in renal impairment)

Onset 30 minutes (duration 45 minutes)

Chew tablets to help distribute medication and to increase saliva production

DONT RELY ON BRAND NAMES

Calcium carbonate = 1st line in pregnancy (after lifestyle modifications)

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H2RAs

Famotidine, Nizatidine, Ranitidine, Cimetidine (lots of SEs)

Onset 1 hour PO, 30 minutes IV; 10-12 hour duration

ADRs include headache, dizzines, confusion, B12 deficiency with long term use, cardiac effects if rapidly infused

DDIs: drugs requiring acid for absorptio (-azole, -nib, -antivirals)

Clinical pearls: can administer with antacids, all renally adjusted (Famotidine dose 50% if CrCl <50mL/minute); tolerance can develop

Cimetidine has most ADRs, many DDIs (moderate 2C19 inhibitor, weak 3A4, 2D6)

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PPIs

Omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole, rabeprazole

Irreversibly and selectively inhibit the proton pump

Onset 1 hour, full effect can take 3-4 days; duration 24 hours

ADRs include HA, diarrhea

DDISs (drugs requiring acid for absorption; omeprazole and esomeprazole have moderate 2C19 inhibition which metabolizes clopidogrel to active drug)

Long term use may cause bacterial overgrowth/infection; poor absorption of B12 , Mg, Ca, Fe; risk of gastric cancer but only in animals

Give 30-60 minutes before food; OTC vs Rx (14 days, repeat in 4 months)

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Long term ADRs of PPIs

Hypomagnesaemia (long-term use)

B12 deficiency (conflicting evidence)

CAP (short-term and high-dose PPI use)

PPIs can change concentration of methotrexate (which has a narrow therapeutic window)

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Which PPIs can be given IV

Esomeprazole, Pantoprazole

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Which PPI is available in a kit

Omeprazole

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Which PPIs can you take without regard to food?

Dexlansoprazole capsule, rebeprazole tablets (rebaprazole capsule can be sprinkled in food but still needs to be taken 30 minutes prior to meal)

Sucralfate

Provides physical barrier in stomach

Onset 1-2 hours; duration 6 hours

Given QID

ADRs include constipation, Aluminum accumulation in renal failure

DDIs (many oral interactions including warfarin)

Currently still a brand name only medication; second line in pregnancy after antacids; must give 2 hours before or 6 hours after interacting medications

Misoprostol

Prostaglandin analogue

Onset 30-60 minutes; duration 3 hours

Given QID

Indicated for NSAID-induced ulcers

ADRs (diarrhea, abdominal pain - do not administer with Mg antacids; uterine contractions)

Pearls (wear gloves)

Black box for women of childbearing age unless…

negative pregnancy test within 2 weeks of starting therapy
capable of complying with contractions
oral and written warnings
begin misoprostol on 2nd or 3rd day of next normal menstrual period

Bismuth subsalicylate

Has barrier and antibiotic effect

Onset 30 minutes; duration 3 hours

ADRs: (rare) neurotoxicity, tinnitus/hearing loss, fecal or tongue discoloration

Increased levels with: warfarin, valproic acid, methotrexate

Decreased levels with: tetracyclines, quinolones, probenecid

*watch for Reye’s syndrome q

GERD in pregnancy/lactation

lifestyle modifications
antacids (calcium carbonate, then aluminum hydroxide/magnesium hydroxide)
Sucralfate
Ranitidine/famotidine
PPIs

Acute vs Chronic PUD

Chronic results from NSAID use or H. pylori

Acute results from stress related mucosal damage (SRMD)

PUD (NSAID induced)

Includes low dose aspirin

Ulcers in 25%, bleeding/perforation (2-4% of those with ulcers)

Risk factors (>65 yo, history of ulcer, NSAID-related dyspepsia, high dose/multiple NSAIDS [COX1 greater risk than COX2], aspirin use, chronic conditions, H. pylori, smoking or alcohol use)

NSAID with aspirin, oral bisphosphonate, corticosteroid, anticoagulant, antiplatelet or SSRI also increases risk

PUD (specifically H. pylori)

Gram negative rod

~60% of ulcers have concomitant H. pylori infection

Prevalence varies depending on socioeconomic status, region, etc.

Consequences include PUD, MALT (mucosal associated lymphoid tissue) and gastric cancer

Transmission: gastro-oral/fecal-oral in childhood; contaminated endoscopes

PUD presentation

Epigastric pain (burning, fullness, cramping; nocturnal, causes awakenings; may occur seasonally or in clusters)

Relieved by antacids

Warning signs include: N/V, anorexia, weight loss, changes in type of pain, dark or tarry stool

PUD Lab tests and Diagnosis

Tests: H/H, Fecal occult blood test H. pylori: endoscopy required - histology is gold standard, culture usually only after treatment failure, biopsy H. pylori: endoscopy not required - antibody test (historical, not affected by PPI or bismuth), urea breath test or fecal antigen

PUD Treatment

Goals (relieve pain, heal ulcer, prevent recurrence, reduce ulcer-related complications) Non-pharm (reduce stress, smoking cessation, discontinue NSAIDs,l including ASA, if appropriate)

H. pylori treatment First Line

Bismuth quadruple (PBMT): PPI + bismuth* + metronidazole** + tetracycline* (or doxycycline) Concomitant non-bismuth quadruple (PAMC): PPI + amoxicillin + metronidazole + clarithromycin

H. pylori first line if clarithromycin resistance is <15%

PPI Triple (PAC, PMC, or PAM): PPI + amox + clarithromycin PPI + metro + clarithromycin PPI + amox + metro

H. pylor treatment if treatment failure

``` Levofloxacin containing (PAL): PPI + amox + levo ``` Rifabutin containing therapy (usually if failed 3) (PAR): PPI + amox + rifabutin

Describe an Antibiogram

Contain commonly treated organisms and commonly used antimicrobials Useful for empiric therapy and resistance trends Compiled annually

Amoxicillin counseling points

Hypersensitivity reaction

Metronidazole counseling points

Disulfuram reaction Metallic taste

Tetracycline counseling points

Photosensitivity, pregnancy/pediatrics (tooth discoloration)

Clarithromcyin counseling points

NVD, HA, taste disturbances Major 3A4 substrate and inhibitor

Bismuth counseling points

Black stools/black tongue

Stress Related Mucosal Damage (SRMD)

Mucous layer normally is physical barrier and traps bicarbonate In ICU patients, SRMD in up to 100% of them; clinical bleeding in up to 25% of ICU patients due to refluxed bile salts, uremic toxins and poor gut perfusion

SRMD risk factors

Mechanical ventilation (>48 hours) Coagulopathy (INR >1.5, platelet <50,000/microL) Others include sepsis, HF, renal failure, trauma, burns over 35% BSA, organ transplant, history of peptic ulcer disease or upper GI bleeding, glucocorticoid therapy, ASA or NSAIDs

SRMD recommendations

Surviving sepsis guidelines: >stress ulcer prophylaxis with H2RA or PPI in all patients with sepsis with bleeding risk factors (PPI preferred) >patients without risk factors do NOT receive prophylaxis Indications: Coagulopathy (INR >1.5, platelet < 50,000), mechanical ventilation >48 hours, history of GI ulceration or bleeding within 1 year of admission, at least 2 of the following (sepsis, ICU stay > 1 week, occult bleeding lasting 6 days or longer, >250 mg hydrocortisone or equivalent)

SRMD considerations

PPI overuse in hospital, transitions of care, tolerance with H2RAs, sucralfate, cost