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Pharmacy School 2016-17 > COPD and PUD Therapeutics > Flashcards

COPD and PUD Therapeutics Flashcards

1
Q

GERD Description

A

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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2
Q

GERD Symptoms

A

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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3
Q

Heartburn vs Angina

A

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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4
Q

Foods that decrease LES tone

A

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

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5
Q

Medications that decrease LES tone

A

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

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6
Q

Foods that are direct irritants

A

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

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7
Q

Medications that are direct irritants

A

ASA, bisphosphonates, NSAIDs, Quinine, KCl

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8
Q

GERD treatment goals

A

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

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9
Q

GERD lifestyle modifications

A

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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10
Q

Antacids

A

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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11
Q

H2RAs

A

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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12
Q

PPIs

A

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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13
Q

Long term ADRs of PPIs

A

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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14
Q

Which PPIs can be given IV

A

Esomeprazole, Pantoprazole

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15
Q

Which PPI is available in a kit

A

Omeprazole

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16
Q

Which PPIs can you take without regard to food?

A

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

17
Q

Sucralfate

A

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

18
Q

Misoprostol

A

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…

  1. negative pregnancy test within 2 weeks of starting therapy
  2. capable of complying with contractions
  3. oral and written warnings
  4. begin misoprostol on 2nd or 3rd day of next normal menstrual period
19
Q

Bismuth subsalicylate

A

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

20
Q

GERD in pregnancy/lactation

A
  1. lifestyle modifications
  2. antacids (calcium carbonate, then aluminum hydroxide/magnesium hydroxide)
  3. Sucralfate
  4. Ranitidine/famotidine
  5. PPIs
21
Q

Acute vs Chronic PUD

A

Chronic results from NSAID use or H. pylori

Acute results from stress related mucosal damage (SRMD)

22
Q

PUD (NSAID induced)

A

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

23
Q

PUD (specifically H. pylori)

A

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

24
Q

PUD presentation

A

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

25
Q

PUD Lab tests and Diagnosis

A

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

26
Q

PUD Treatment

A

Goals (relieve pain, heal ulcer, prevent recurrence, reduce ulcer-related complications)

Non-pharm (reduce stress, smoking cessation, discontinue NSAIDs,l including ASA, if appropriate)

27
Q

H. pylori treatment First Line

A

Bismuth quadruple (PBMT):

PPI + bismuth* + metronidazole** + tetracycline* (or doxycycline)

Concomitant non-bismuth quadruple (PAMC):

PPI + amoxicillin + metronidazole + clarithromycin

28
Q

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

A

PPI Triple (PAC, PMC, or PAM):

PPI + amox + clarithromycin
PPI + metro + clarithromycin
PPI + amox + metro

29
Q

H. pylor treatment if treatment failure

A 
Levofloxacin containing (PAL): 
PPI + amox + levo

Rifabutin containing therapy (usually if failed 3) (PAR):
PPI + amox + rifabutin

30
Q

Describe an Antibiogram

A

Contain commonly treated organisms and commonly used antimicrobials

Useful for empiric therapy and resistance trends

Compiled annually

31
Q

Amoxicillin counseling points

A

Hypersensitivity reaction

32
Q

Metronidazole counseling points

A

Disulfuram reaction

Metallic taste

33
Q

Tetracycline counseling points

A

Photosensitivity, pregnancy/pediatrics (tooth discoloration)

34
Q

Clarithromcyin counseling points

A

NVD, HA, taste disturbances

Major 3A4 substrate and inhibitor

35
Q

Bismuth counseling points

A

Black stools/black tongue

36
Q

Stress Related Mucosal Damage (SRMD)

A

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

37
Q

SRMD risk factors

A

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

38
Q

SRMD recommendations

A

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)

39
Q

SRMD considerations

A

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

Pharmacy School 2016-17 (22 decks)

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