COPD and PUD Therapeutics Flashcards
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
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)
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
Foods that decrease LES tone
Fatty meals, peppermint, spearmint, chocolate, coffee, soda, tea, garlic, onions, chili peppers, alcohol
Medications that decrease LES tone
Anticholinergics, barbiturates, caffeine, DHP calcium channel blockers, estrogen, progesterone, nicotine, nitrates, tetracycline, theophylline
Foods that are direct irritants
Spicy foods, citrus, tomato juice, coffee, tobacco, alcohol
Medications that are direct irritants
ASA, bisphosphonates, NSAIDs, Quinine, KCl
GERD treatment goals
Improve quality of life, prevent further damage, prevent progression to complications
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
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)
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)
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)
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)
Which PPIs can be given IV
Esomeprazole, Pantoprazole
Which PPI is available in a kit
Omeprazole
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
