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GI Pharm Flashcards

1
Q

PONV Risk Factors

A
  • Patient
  • Surgical
  • Anesthetic
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2
Q

PONV Risk Factors:

Patient

A
  • Patient:
    1. female
    2. age <50
    3. non-smokers
    4. hx PONV/motion sickness
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3
Q

PONV Risk Factors:

Surgical

A
  • Surgical:
    1. length of surgery
    2. laparotomies
    3. laparoscopic procedures
    4. ENT
    5. breast
    6. OBGYN
    7. plastic surgeries
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4
Q

PONV Risk Factors:

Anesthetic

A
  • Anesthetic:
    1. inhalational agents
    2. N2O
    3. neostigmine
    4. etomidate
    5. opioids
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5
Q

PONV is associated with…

A
  1. increased morbidity
  2. dehydration
  3. electrolyte imbalances
  4. wound dehiscence
  5. bleeding
  6. esophageal rupture
  7. airway compromise
  8. low pt satisfaction
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6
Q

Areas that our Antiemetics focus on

A
  • Emesis is a complex reflex involving multiple NT’s triggered by activating the vomiting center in the medulla oblongata
  • Direct stimuli—noxious odors, pain, motion sickness
  • Indirect—first activate chemoreceptor trigger zone (CTZ) in area postrema/floor of 4th ventricle which then activates vomiting center
    • CTZ is stimulated by signals in stomach/small intestine or by direct stimulation (ex. opioids, chemotherapy)
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7
Q

Emesis Treatment

A
  • Multimodal approach is best
  • Modulate activity in vomiting center and CRTZ
  • Treatment Options not discussed in detail in this lecture:
    • Midazolam (benzo) → may work to decrease synthesis and release of DA in CRTZ and decrease anxiety related signaling to vomiting center
    • Dexamethasone (corticosteroid) → discussed in steroids lecture; unclear antiemetic mechanism; typically given post induction for antiemetic effect. 4-8 mg
      • ​synergistic with zofran
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8
Q

Scopolamine:

MOA/Dose

A
  • “antimuscarinic of choice”
  • Anticholinergic at muscarinic receptor
    • Competitively and reversibly binds to muscarinic receptors to inhibit binding of Ach
    • Tertiary amine = crosses BBB
  • Most often used transdermal
    • 5 mcg/hr for 72 hrs
    • Best when placed at least 4 hrs prior to noxious stimuli for prophylaxis
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9
Q

Scopolamine:

Side Effects

A
  • Pupillary dilation, ↑ IOP → avoid in glaucoma (esp narrow angle)
  • Bronchodilation
  • Antisialogogue, Dry mouth
  • Sedation
  • Moderate ↑ HR/CO
  • Anticholinergic syndrome: restlessness, hallucinations, somnolence, unconsciousness
    • Tx: physostigmine
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10
Q

Metoclopramide (Reglan)

MOA

A
  • Benzamide (PABA derivative); prokinetic
    • DA-2 receptor antagonist acting centrally on CRTZ (crosses BBB) and peripherally to ↑ mobility of esophagus, stomach, and intestine
    • ↑Ach release via 5-HT4 receptor stimulation = ↑GI tract mobility
      • Contraction of LES and gastric fundus, ↑ gastric and small intestine motility, ↓ muscle activity in pylorus and duodenum
  • 5HT-4 agonist to ↑cAMP to ↑peristaltic activity
  • Weak 5-HT3 receptor antagonist (at high doses might enhance anti-emetic effects)
  • Kinetic only NO change in gastric pH
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11
Q

Metoclopramide (Reglan)

Pk

A
  • PB = 30%
  • Onset = 1-3 min
  • DOA = 1-2 hrs
  • E½t = 2-4 hrs
  • Renal excretion, 40% unchanged (“not goof for renal failure and dialysis pts”)
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12
Q

Metoclopramide (Reglan)

Side Effects

A
  • Extrapyramidal effects (contraindicated in Parkinson’s, caution in restless leg syndrome or other movement dxs)
  • Restlessness/Akathesia
  • Cramping → give slowly over 3-5 min
  • ↑ lactation
  • ↑ HR / ↓BP
  • Dysrhythmias if used in conjunction w/ ondansetron (case reports)
  • CONTRAINDICATED IN BOWEL OBSTRUCTION
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13
Q

Metoclopramide (Reglan)

Dosage

A
  • Dose 10-20 mg IV slowly; 15-30 min before induction (for pro-kinetic benefit)
    • 0.15 mg/kg to children post T&A to reduce PONV in PACU
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14
Q

**Droperidol** and Haloperidol

MOA/Pk/Dose

A
  • Butyrophenone; DA-2 receptor antagonists at CRTZ (antiemetic properties)
  • Pk:
    • Highly PB
    • Peak = 30 min
    • DOA = 12 hrs (“long half life good for post op”)
  • Antiemetic dose = droperidol 0.625 mg – 1.25 mg IV
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15
Q

**Droperidol** and Haloperidol

Side Effects

A
  • Extrapyramidal symptoms (avoid in Parkinson’s)… DO NOT give w/ metoclopramide
  • Additive w/ CNS depressants
  • Drowsiness (higher doses)
  • Hallucinations
  • Slow HR
  • QT prolongation and torsades (black box warning)
  • Malignant neuroleptic syndrome (tachycardia, alterations BP, fluctuating LOC, muscle rigidity, hyperthermia, rhabdomyolysis, autonomic instability = mirror MH)
    • Tx: Amantadine- DA-agonist w/ mild anticholinergic effects
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16
Q

Amisulpride (Barhemsys®)

A
  • Dopamine (D2/D3) antagonist FDA approved 2020 for PONV
    • Replacement for droperidol in multimodal PONV mgt.
    • Dose-dependent QT prolongation warning on insert
      • Avoid doses >10mg. Avoid in known prolonged QT. Avoid w/ other drugs w/ prolonged QT as SE.
  • Minimal drug interactions
    • neither inhibits nor promotes liver enzyme activity
    • exhibits limited protein binding (25-30%)
    • AVOID w/ Parkinson’s pts
  • Adverse effects similar to placebo group
  • Well-tolerated in elderly pts
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17
Q

Amisulpride (Barhemsys®)

Pk

A
  • Vd in surgical pts: 127-144 L
  • Rapid onset (1-2 min)
  • E½t: 4-5 hrs
  • Minimal metabolism/no CYP450 metabolism (excreted unchanged in urine 58%/feces 23%)
  • Avoid in renal failure (OK in mild to mod renal dz GFR >30 mL/min)
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18
Q

Amisulpride (Barhemsys®)

Use

A
  • Prevention of PONV (either alone or in combination):
    • 5 mg as single IV dose infused over 1-2 min at anesthesia induction.
  • Treatment of PONV
    • 10 mg as single IV dose infused over 1-2 min post-op.
    • Photodegradation an issue: administer w/in 12 hrs of removal from protective carton.
    • Infusion site pain reported
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19
Q

Ondansetron (Zofran)

A
  • 5-HT3 Receptor antagonist, antiemetic
    • Primarily works at CRTZ centrally and vagal nerve terminals peripherally
    • Not effective in motion sickness or PONV caused by vestibular stimulation
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20
Q

Ondansetron (Zofran)

Pk

A
  • PB 70%
  • Vd: 2 L/kg
  • Onset: 30 min
  • DOA: 4-8 hrs
  • E½t: 3-4 hrs
  • Liver metabolism
  • Cross BBB
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21
Q

Ondansetron (Zofran)

Dose

A
  • Dose: 4- 8 mg IV over 2 min
    • Pediatric 0.05-0.15 mg/kg IV
  • Debate over beginning of surgery vs. end of surgery
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22
Q

Ondansetron (Zofran)

Side Effects

A
  • Headache w/ rapid admin
  • Sedation
  • Constipation
  • Slight QT prolongation
  • AV block (w/ co-admin of metoclopramide)
  • Caution in liver dz
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23
Q

Additional 5-HT3 Antagonists

A

Dolasetron

Grainsetron

Palonosetron

Ramosetron

Tropisetron

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24
Q

Aprepitant (emend):

MOA/dose

A
  • Neurokinin- 1(NK1) antagonist
    • Serves to antagonize substance P
    • Little/no affinity for serotonin, DA, and corticosteroid receptors
  • PONV and N/V r/t CA chemo (typically combo w/ other antiemetics)
    • Moderate effectiveness- usually part of multimodal approach
  • Dose PONV: 40 mg IV prior to induction
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25
Q

Aprepitant (emend):

Pk

A
  • PB >95%
  • Vd = 70 L
  • E½t = 9-13 hrs
  • Primary metabolism by liver, CYP3A4
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26
Q

Antiemetics: NK1 Antagonists

Side Effects

A
  • Neutropenia, Anemia, Leukopenia (concern in CA pts)
  • Fatigue
  • Peripheral neuropathy
  • Dyspepsia
  • Diarrhea
  • UTI
  • Injection site pain
  • CYP3A4 metabolism inhibition: many drug interactions including many chemo drugs and corticosteroids… adjusted doses important).
  • CYP2D6 inducer: warfarin, oral contraceptives (“r/f unwanted pregnancy”), codeine (“r/f overdose”)
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27
Q

Promethazine, Chlorpromazine, Prochlorperazine

Action/Use/Pk/Dose

A
  • Phenothiazines
    • Exert antiemetic effects by interaction w/ DA receptors in CRTZ
    • H1 antagonist- to be covered later
  • Use: blood transfusion reaction, allergic reaction, sedation, PONV
  • Following IV admin, clinical effects in 5 min
  • DOA 4-6 hrs
  • E½t = 9-16 hrs
  • Liver metabolism
  • Contraindicated under 2 yrs old (fatal resp depression)/comatose state
  • Sedation common concern
  • Dose: Promethazine 6.25-12 mg IV, up to 25 mg
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28
Q

Antiemetics: Cannabinoids

A
  • Agents: Dronabinol [Marinol], Nabilone [Cesamet] both chemically related to active ingredient in marijuana
  • Unknown MOA: activation of cannabinoid receptors adjacent and within vomiting center
  • Improves chemotherapy induced nausea
  • Improves appetite in HIV pts
  • NOT currently FDA approved PONV use
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29
Q

Antiemetics: Cannabinoids

Adverse Effects

A
  • AE: same as marijuana –
    1. Dysphoria
    2. Sedation (additive w/ other sedatives)
    3. Temporal disintegration
    4. Personality changes
    5. Tachycardia
    6. Hypotension
  • Abuse potential (Schedule III DEA controlled substance)
30
Q

Aspiration precaution/prevention

A
  • 1/3 aspiration cases occur w/ laryngoscopy, ​1/3 w/ extubation, ​1/3 during procedure
  • Volume and acidity of aspirated gastric contents are primary determinants of pulmonary complications
  • Drugs that ↓volume or ↑pH of gastric contents decrease severity of aspiration sequelae
31
Q

What is GERD

A
  • Disorder characterized by mucosal damage d/t abnormal reflux of gastric contents into esophagus
  • LES resting tone below normal = gastric contents to regurgitate into esophagus
  • Most common symptom is heartburn
32
Q

GERD Treatment:

Lifestyle

A
  • Lifestyle modification essential
  • Eat smaller meals throughout day
  • Sleep w/ HOB elevated
  • Avoid foods that precipitate effects:
    • Alcohol, Caffeine
    • Fatty meals, Chocolate
    • Acidic foods, Citrus
    • Smoking
33
Q

GERD Treatment:

Pharmacologic

A
  • Pharmacologic management:
    • PPIs - ↓ acid secretion
    • H2 blockers - ↓ acid secretion
    • Antacids - ↑ gastric pH
    • Metoclopramide - prokinetic functions
    • Sucralfate/misoprostol – cytoprotective (not used in aspiration prophylaxis)
34
Q

Gastric Acid Production:
Drug Targets

A

Final step of gastric acid secretion is stimulation of the

H+/K+ ATPase pump

aka: the “Proton Pump”

35
Q

Antacids:
Action

A
  • Neutralize H+ ions in gastric contents or ↓ secretion of hydrogen chloride into stomach
  • Al, Ca, Mg salts
    • H+ ions in stomach acid react w/ the base, forming a stable compound- consuming the H+ ions and ↑pH >5.
  • Relieves symptoms of gastritis, improves rate of gastric ulcer healing and duodenal ulcer pain relief, ↑ gastric motility (neutralized pH increases gastrin release and gastric motility).
  • pH too high = impaired food digestion
  • Electrolyte abnormalities
36
Q

Antacids:

Drug Interactions

A
  • ↑ rate of absorption for:
    • salicylates
    • indomethacin
    • naproxen
  • decreased bioavailability of PO cimetidine
37
Q

Anatacids:

Meds

A
  • Sodium Bicarbonate
  • Calcium carbonate
  • Aluminum hydroxide
  • Magnesiums hydroxide (milk of magnesia)
38
Q

Anatacids

Sodium Bicarbonate

A
  • Rapidly neuralizes stomach pH, may result in acid rebound
  • Pts w/ HTN, CV dz may not tolerate Na+ load
39
Q

Anatacids

Magnesium hydroxide

A
  • Milk of magnesia
  • Prominent laxative, osmotic diarrhea
  • Caution in renal impairment- results in met. alk., neurologic, neuromuscular and cv impairments
40
Q

Anatacids

Calcium Carbonate

A
  • Met alk w/ chronic therapy
  • Symptomatic hypercalcemia in renal disease, hypophosphatemia, acid rebound
41
Q

Anatacids

Aluminum Hydroxide

A
  • Renal dz, excessive aluminum concentration→ encephalopathy
  • SLOWS gastric emptying, constipation
  • Phosphorous depletion leading to anorexia, muscle weakness, osteoporosis
42
Q

Sodium Citrate (Bicitra)

A
  • Non-particulate (clear) antacid of choice when increasing gastric pH is desired prior to induction.
  • Less likely to cause inflammatory reaction if aspirated than other antacids.
  • More complete mixing w/ gastric fluid
  • More rapid onset
  • ↑ intragastric volume
  • pH 8.4, very unpleasant taste
43
Q

Sodium Citrate (Bicitra dose)

A
  • 15-30 mL of 0.3 M solution 15-30 min before induction is effective in increasing gastric pH in preg and non-preg pts.
44
Q

Histamine Review

A
  • Naturally occurring endogenous amine
  • Synthesized in tissues –decarboxylation of histadine
  • Stored in vesicles- mast cells (skin, lung, gastric mucosa) & circulating basophils
  • Released in response to antigen-antibody reaction/ certain drugs
  • Induces contraction of smooth muscle in airways, ↑secretion of acid in stomach, and stimulates release of neurotransmitters in CNS
  • Effects mediated by H1, H2 and H3 receptors
45
Q

HISTAMINE RECEPTOR- H1

A
  • H1 (smooth muscle-contraction lung & GI, vascular endothelium- release of NO, sensory nerve stimulation)
    • Lungs - bronchoconstriction – asthma/bronchitis-> increased airway resistance
    • Vascular smooth muscle – predominant effect of histamine = dilation – hypotension/erythema
    • Vascular endothelium – ↑ capillary permeability - edema
    • Peripheral nerves - sensitization - itching, pain, sneezing
    • Heart-found in A-V node-slow HR by slowing conduction
46
Q

HISTAMINE RECEPTOR- H2

A
  • H2 (gastric parietal cells, cardiac muscle, mast cells)
    • Heart – Positive inotropic and chronotropic effects → ↑ in HR and contractility
    • Coronary vasculature- vasodilation (offsets H1 constriction)
    • Airways-relaxes bronchial smooth muscle
    • Stomach
      • Activation of cAMP → activates proton pump of parietal cells to secrete H+ ions
      • Effects d/t direct stimulation of gastric parietal cells- ↑gastric acid secretion – ↑ r/f PUD, GERD
47
Q

HISTAMINE RECEPTOR- H3

A
  • Location- Heart & Presynaptic postganglionic SNS fibers
  • Stimulation causes inhibition of synthesis and release of histamine
  • Activity impaired by H2 antagonists > enhanced histamine release. AVOID rapid administration of these agents esp when in combo w/ a histamine releaser (eg. Atracurium)
48
Q

H1 or H2 antagonists

A
  • Competitive and reversible inhibition.
    • The drugs occupy receptors on effector cell membranes.
    • Histamine receptors are seven-transmembrane G protein-coupled receptors.
  • H1 antagonists: Allergic rhinitis treatment
  • H2 antagonists: Inhibit acid gastric fluid secretion
  • H1 and H2 antagonists do not inhibit release of histamine- they block response to histamine!
49
Q

H1 Antagonists: Antihistamines

A
  • Used to treat: mild allergy (rhinitis, conjunctivitis, urticaria, pruritis), motion sickness, chemo induced NV/PONV, insomnia
  • Block the following actions of histamine at the H1 receptor:
    • Vasodilation
    • Increased capillary permeability
    • Bronchoconstriction
    • CNS effects
    • Itching
    • Pain
  • Do not block H2 receptors
  • Some bind to muscarinic receptors
50
Q

Acute anaphylaxis

A
  • Diphenhydramine use is directed at blocking further histamine-mediated vasodilation and hemodynamic instability and respiratory compromise. Used in conjunction with epinephrine (adjunct only….not adequate treatment by itself .
51
Q

H1 antihistamines

First generation

A
  • First-generation: sedation, activate muscarinic, serotonin and alpha receptors
    • Lipophilic
    • Nonionized at physiologic pH
    • Cross BBB
  • Diphenhydramine
  • Hydroxyzine
  • Chlorpheniramine
  • Promethazine (Phenergan)
  • Doxepin
52
Q

H1 antihistamines

Second generation

A
  • Second generation: generation-non-drowsy, more selective for H1 + less crosses BBB→ ↓ CNS toxicity
    • Ionized at physiologic pH
  • Loratidine
  • Desloratidine
  • Acrivastine
  • Fexofenadine
53
Q

H1- Antihistamines

Pk

A
  • Excellent absorption
  • Cmax in 2-3 hrs
  • Protein binding 78-99%
  • Hepatically metabolized by CYP450
  • Variable E1/2t
    • Chlorpheniramine >24 hrs
    • Acrivastine- 2 hrs
54
Q

H1- Antihistamines

Adverse Effects

A
  • CNS toxicity
    • Sedative effects (primarily 1st gen)
  • Cardiac toxicity
    • QT prolong
    • Withdrawal from market- terfinadine and astemizole
  • Anticholinergic effects
    • Pupillary dilation, dry eyes, dry mouth, urinary hesitancy
55
Q

H2 Antagonists

A
  • Competitive antagonism of H2 receptors to suppress gastric acid secretion by parietal cells
  • Agents Available
    • Cimetidine
    • Nizatidine
    • Ranitidine
    • Famotidine
  • Inhibit binding of histamine to H2 receptors → ↓ intracellular cAMP and secretion H+ ions
  • Cimetidine least potent
  • Famotidine most potent
  • No effect LES tone or gastric emptying
56
Q

H2 antagonists: clinical uses

A
  • Treatment of duodenal ulcer disease, GERD
  • Chemoprophylaxis prior to induction of GA:
    • Cimetidine 300 mg p.o. 1-2 hours preop
    • Famotidine 20-40 mg p.o. or 20 mg IV am of surgery
    • Ranitidine 150mg p.o. or 50 mg IV
  • Gastric pH of fluid already present in stomach- NO Effect
    • Risk of aspiration! Often combined with Metoclopramide (Reglan) to reduce volume of gastric fluid in stomach
  • Effect on gastric volume = very unpredictable
57
Q

H2 Antagonists

Pk

A
  • Rapid absorption oral- first pass hepatic metabolism- only 50% bioavailability
  • Cmax 1-3 hrs w/ oral administration
  • 13-35% protein binding
  • All 4 drugs cross BBB
  • Elimination 1.5-4 hrs
  • Nizatidine-renal excretion
  • Hepatic metabolism- principle method clearance-
    • Cimetidine
    • Ranitidine
    • Famotidine
58
Q

H2 Antagonists

Adverse Events

A
  • Generally well tolerated (ranitidine and famotidine have very few AE)
    • Cimetidine associated with the most adverse effects
      • Gynecomastia, impotence, CNS toxicity (confusion, restlessness, agitation, headaches, dizziness)
    • Idiosyncratic cases of myelosuppression, thrombocytopenia, neutropenia, anemia
    • May have transient ↑ in LFTs (transaminases)
    • Serum B12 deficiency w/ long term use
    • Association with pneumonia
      • ↓ gastric acidity = more bacterial colonization in stomach and secondary in lungs
59
Q

H2 Antagonists: Side Effects

A
  • Rapid IV administration of Cimetidine & Ranitidine may cause bradycardia, hypotension – GIVE OVER 15-30 MINUTES!
    • Famotidine may be given over 2 min
  • Drug Interactions:
    • decreases metabolism of drugs that undergo extensive hepatic extraction: PROPRANOLOL, DIAZEPAM
    • By altering gastric pH, may change rates of absorption of other drugs
    • Cimetidine may slow metabolism of Lidocaine & many other drugs (Refer to Table 21-6 p. 439- Stoelting’s pharm)
60
Q

Proton Pump Inhibitors

MOA/Use

A
  • Suppress gastric acid secretion by irreversibly inhibiting the H+/K+-ATPase pump (final common pathway)
    • Acid suppression lasts 3-5 days after each dose
      • New enzyme must by synthesized – can take weeks to return to baseline
  • Preferred treatment
    • PUD with H. pylori
    • Hemorrhagic ulcers
    • PUD in patient who requires NSAID use
    • Can also be used pre-operatively for aspiration prophylaxis
61
Q

PPI’s: Agents Available

A
  • Agents available
    • Pantoprazole
    • Omeprazole
    • Lansoprazole
    • Esomeprazole
    • Rabeprazole
62
Q

PPIs

Pk

A
  • Rapid absorption
  • Omeprazole: Prodrug converted to active drug in parietal cell canaliculus
    • Hepatically metabolized by CYP2C19, 3A4
    • Most effective after 2-3 doses (decreases acid production by 90%)
  • Short half-life
  • Cross placenta
63
Q

PPI’s

Adverse Effects

A
  • Well tolerated short term (<4-8 weeks)
    • “Take lowest possible dose for shortest possible time”
  • Fractures/osteoporosis (long term use)
  • Acid rebound
  • Low mag
  • Associated w/ pneumonia (caution COPD pts.), C. diff infections
  • Gastric CA/carcinoid tumor (rats only- FDA concluded NOT in humans)
  • Headache, dizziness, drowsiness, abdominal pain, constipation, diarrhea, flatulence
64
Q

Anticholinergics

A
  • Dicyclomine
    • Muscarinic ACh receptor antagonist
    • Decreases acid secretion
    • Primarily used to treat IBS
  • Less effective than H2 antagonists and PPIs
  • Adverse effects
    • Dry mouth, constipation, blurred vision, cardiac arrhythmia, urinary retention
65
Q

Peptic Ulcer Disease (PUD)

A
  • Ulcer in lining of stomach d/t increased acid and pepsin secretion and impaired mucosal cytoprotection
  • Common causes:
    • Helicobacter pylori (Majority of cases)
    • Chronic NSAID use
    • Smoking
66
Q

Peptic Ulcer Disease (PUD) Treatment

Non-pharm

A
  • Avoid NSAIDs
  • Avoid smoking
  • Avoid alcohol, precipitating foods, and stress???? (No strong evidence to support these recommendations)
67
Q

Peptic Ulcer Disease (PUD) Treatment

Pharmacologic

A
  • Antisecretory Agents (PPIs, H2RAs)
    • Reduce gastric acid production
    • *Should be used in all patients
  • Antacids
    • Neutralize gastric acid
  • Antibiotics
    • Eradicate H. pylori infection
    • *All patients should be tested for infection
  • Sucralfate
    • Protect gastric mucosa
  • Misoprostol
    • Protect gastric mucosa
68
Q

Cytoprotective Agents

A
  • Agents
    • Sucralfate (Carafate®)
    • Misoprostol (Cytotec®)
69
Q

Misoprostol

A
  • Methyl analog of prostaglandin E1
    • In US, only indicated in prevention of NSAID-induced ulcers
  • MOA
    • Inhibits gastric acid secretion by inhibiting histamine-stimulated cAMP production
    • Mucosa-protective; binds to prostaglandin E receptors, facilitates production of mucus and bicarbonate
  • Pregnancy category X
    • Stimulates uterine contraction
    • Used in combo w/ mifepristone to induce pregnancy termination
  • ADE
    • Diarrhea (up to 40%)
    • Abdominal cramps (7 – 20%)
70
Q

Sucralfate

A
  • Aluminum salt of a sulfated disaccharide
  • Used for acute/maintenance tx of duodenal ulcers
  • MOA: In acidic environment (pH < 4), forms gel-like substance that selectively binds to mucosa; forms protective barrier against acid, pepsin etc…No acid-neutralizing activity
    • Does not treat cause of ulcer, just coats/protects it
  • Minimal systemic absorption; > 90% excreted in feces
  • ADE: Constipation (2%), Aluminum toxicity
  • Separate administration of other drugs by 2 hrs before or 4 hrs after
    • This prevents 1) changes in pH 2) inhibition of absorption of other drugs (common with co-administration)
  • Pills difficult to swallow for many pts

Pharm-Spring (7 decks)

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