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pharm exam 2 > GI > Flashcards

GI Flashcards

1
Q

patho of GERD

A
  • Lower esophageal sphincter relaxes
  • Alteration in epithelium of esophagus
  • This may create hiatal hernia (secondary to poor esophageal motility)
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2
Q

s/s of GERD

A
  • Heartburn
  • Epigastric pain
  • Belching
  • Acid regurgitation
  • Water brash (excessive saliva production)
  • Atypical symptoms:
    -Non-cardiac chest pain
  • Often from chronic untreated GERD (burning, gnawing sensation and dry non-productive cough is good way to differentiate)
    -Cough, asthma, pneumonia
    -Hoarseness
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3
Q

red flags of GERD

A

o Dysphagia
o Odynophagia (painful swallowing)
o Anemia
o Bleeding
o Weight loss
o Vomiting blood

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4
Q

drugs that lower LES tone

A

(Lower tone–> increased likelihood of hiatal hernia)
* Anticholinergics
* Benzodiazepines
* Caffeine
* Calcium channel blockers (dihydropyridines)
* Estrogen/progesterone
* Nicotine
* Nitrates
* Theophylline
* Tricyclic antidepressants

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5
Q

GERD non pharm tx

A
  • Diet (most common cause): Limit caffeine, ETOH, citrus, tomato products, chocolate, spicy foods, peppermint, fatty foods, onions, garlic
  • Physical: ↑ HOB, avoid lying down for 30 min after eating, avoid tight clothing, avoid bending over
  • Misc:
    o Small frequent meals
    o Stop smoking
    o Weight loss
    o Avoid bisphosphonates
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6
Q

pharm tx:

A

antacids
histamine 2 receptor antagonist
PPIs

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7
Q

what is the MOA of antacids?

A

Neutralize gastric HCl – increases pH of the stomach and duodenum

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8
Q

what are some antacids examples?

A
  • Calcium Carbonate (TUMS, ROLAIDS)
  • Sodium Bicarbonate (ALKA-SELTZER)
  • Aluminum hydroxide (AMPHOGEL)
  • Aluminum carbonate (BASALJEL)
  • Magnesium hydroxide (M.O.M.)
  • Combination products:
    -Aluminum hydroxide and magnesium hydroxide (MAALOX, MYLANTA)
    -Alginic acid, Magnesium trisilicate, calcium stearate (GAVISCON)*
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9
Q

admin instructions of antacids?

A

o Best if taken 1 hour after meals
* Stays in stomach only 20 min if taken before a meal, up to 3 hours after
o Preparations: liquid, tablet (take tablet with full glass of water)

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10
Q

adverse effects of antacids?

A

o Calcium Carbonate - constipation
o Aluminums - constipation
o Magnesium hydroxide – diarrhea
o Sodium bicarbonate - ↑ Na+ levels, fluid retention
o Avoid Mg-based antacids with renal disease due to impaired excretion

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11
Q

drug interactions of antacids: potential interactions

A
  • ASA (Aspirin)
  • Benzodiazepines
  • Anticoagulants
  • Phenytoin
  • Digoxin
  • Nitrofurantoin
  • Tetracycline
  • Phenothiazines
  • Synthroid
  • Histamine receptor antagonists
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12
Q

drug interactions of antacids: mechanisms

A
  • Increase gastric pH – changes the solubility and disintegration of other drugs
  • Bind to drug (increased with Mg-containing antacids)
  • Increase urinary pH (inhibits excretion of weakly basic drugs, enhances elimination of weakly acidic drugs)
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13
Q

sodium bicarbonate: onset of action

A

rapid

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14
Q

sodium bicarbonate: duration of action

A

short

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15
Q

sodium bicarbonate: systemic alkalosis

A

yes

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16
Q

sodium bicarbonate: effect on stool?

A

none

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17
Q

calcium carbonate: onset of action

A

intermediate

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18
Q

calcium carbonate: duration of action

A

moderate

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19
Q

calcium carbonate: systemic alkalosis

A

not really

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20
Q

calcium carbonate: effect on stool?

A

constipating

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21
Q

magnesium hydroxide: onset of action

A

rapid

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22
Q

magnesium hydroxide: duration of action

A

moderate

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23
Q

magnesium hydroxide: systemic alkalosis

A

no

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24
Q

magnesium hydroxide: effect on stool?

A

laxative

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25
Q

aluminum: onset of action

A

slow

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26
Q

aluminum: duration of action

A

moderate

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27
Q

aluminum: systemic alkalosis

A

no

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28
Q

aluminum: effect on stool?

A

constipating

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29
Q

antacid neutralizing capacity

A
  • Amount of 1mEq HCl brought to pH 3.5 by an antacid solution within 15 min.
  • ANC = amount of acid that it can neutralize
  • FDA requires a Min=5 mEq/dose
  • As the ANC number increases the neutralizing capacity of an antacid increases.
  • Suspensions have greater ANC than powders or tablets
  • Greatest neutralizing capacity: Na+ bicarbonate, Ca+ carbonate
  • Ca+ carbonate
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30
Q

histamine 2 recepor antagnoist: MOA

A

bind to histamine-2 receptors on gastric parietal cells to reduce gastric acid secretion

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31
Q

histamine 2 recepor antagnoist: drug examples

A

o Ranitidine (ZANTAC) (150 vs 75mg)
o Cimetidine (TAGAMET)
o Famotidine (PEPCID)
o Nizatidine (AXID)

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32
Q

use of histamine 2 receptor antagonist

A
  • Suppress gastric acid secretion by 70%
  • Slower onset of action than antacids but better at decreasing severity/frequency of heartburn symptoms
  • Not as effective to tx erosive esophagitis
  • First line tx in those with more than occasional symptoms
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33
Q

contraindications: histamine 2 receptor antagonist

A

o Avoid in patients with delirium/at risk for delirium (Beers Criteria)

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34
Q

admin of histamine 2 receptor antagonist

A

o Twice-daily dosing
o Make sure patient has a good physical exam and appropriate labs to rule out gastric malignancy!

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35
Q

side effects of histamine 2 receptor blockers

A

very few

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36
Q

histamine 2 receptor antagonist: drug interactions

A

Ranitidine (ZANTAC) interacts with Warfarin
* H2 blockers prolong PTT

Cimetidine (TAGAMET) interacts with more than 100 medications on the cytochrome P450, 1A2, 2C9 and 2D6 systems
* Beta-blockers, calcium channel blockers, phenytoin, lidocaine, oral hypoglycemics, OCPs, metronidazole, etc.

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37
Q

Ramitidine: recall

A

FDA recalled this bc of large amounts of NDMA which is classified as a possible human carcinogen. AVOID GIVING THIS TO PTS!

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38
Q

Ramitidine: recall

A

FDA recalled this bc of large amounts of NDMA which is classified as a possible human carcinogen. AVOID GIVING THIS TO PTS!

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39
Q

Proton Pump Inhibitors (PPIs): MOA

A

Block acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump in the parietal cell membrane
* Strong inhibitors of gastric acid secretion through inhibition of proton pump, preventing “pumping” or release of gastric acid (24 hr action)
* Decrease acid secretion by up to 95% for up to 48 hours (work well!)

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40
Q

examples of PPIs

A

o Esomeprazole (NEXIUM)
o Lansoprazole (PREVACID)
o Omeprazole (PRILOSEC)
o Pantoprazole (PROTONIX)
o Rabeprazole (ACIPHEX)

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41
Q

use of PPIs

A

o PUD
o GERD
o H. Pylori
o NSAID associated ulcers
o Zollinger-Ellison syndrome

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42
Q

admin/pt teaching of PPIs

A

o 4–8-week course of treatment
-Avoid long-term treatment for most patients
-Long term use increases side effects of PPIs and interactions w/ other meds
o Take 30-60 min before breakfast (in morning on empty stomach)
o Do not crush or chew capsules
o Long-term users (>6 months) must taper off (prevent rebound gastric hypersecretion)
o PPI deprescribing algorithm

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43
Q

Contraindications of PPIs

A

o Hypersensitivity Precautions – metabolized by CYP 450 system
o Can result in malabsorption of nutrients (long term therapy)
-B12, Iron, Magnesium
o Do not administer at the same time as H2RAs – can be given at different times during the day if necessary (space out)
o Avoid in the elderly for longer than 8 weeks (Beers Criteria)

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44
Q

warnings of PPIs

A

o PPIs linked to the increase of enteric bacterial infections especially C. diff.
o Associated with 20 – 50% increased likelihood of chronic kidney disease
o Increased rate of pneumonia (30% increased risk of HAP, CAP)
- Refuted in re-analysis 2019, thought to be minimal risk
o Increased risk of fractures (hip, wrist, spine)
o ? Increased risk of MI – controversial
o Regular users of PPIs (>8 weeks) had a 44% increased risk of dementia– refuted in subsequent study 2017
o Excess risk of death among PPI users, increases with LT use important to limit duration/use

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45
Q

drug interaction of PPIs

A

o Changes absorption of drugs sensitive to gastric pH
o Inhibits cytochrome P450 1A2, 2C, and 3A4 systems
- Warfarin
- Diazepam
- Phenytoin
o Pantoprazole (Protonix) interacts less with CP 450 system

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46
Q

omeprazole

A

blocks gastric acid secretion by irreversing binding to H+/K+ pump –> blockage of gastric acid from parietal cell membrane

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47
Q

Robert Warren and Barry Marshall

A

discovered a link between the bacteria H. pylori and PUD–> won Nobel Prize in 2005

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48
Q

s/s of peptic ulcer disease

A

o ~70% asymptomatic in initial symptoms
-Present late in disease course with complications
o Common Sx= Epigastric/abdominal pain
-Gastric = pain worse with eating
-Duodenal (peptic)= pain worse 2-5 hours after eating
o Belching, early satiety, nausea, vomiting, bloating, heartburn, hematemesis, anorexia
-Hematemesis= pt may have upper GI bleed, fine on occasion but frequent and large volumes= concerning (monitor closely)

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49
Q

peptic ulcer disease: etiologies

A

o Most common: H. Pylori, NSAIDS (including aspirin)
o Less common: post-surgical (gastric sleeve, weight loss surgeries), infections, tumors
o Disruption of normal gastric mucosal defense and healing mechanisms
o Normally epithelial cells of the stomach can produce a protective mucus layer – prostaglandins play an important role in this
-H. Pylori can alkalinize the stomach environment allowing it to survive for long periods of time  irritation of the gastric mucosa and eventually ulcers
-NSAIDs inhibit prostaglandins  impaired gastric mucosal protection

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50
Q

tx of peptic ulcer disease

A

o Decrease acid secretion (PPI)
o Treat infection (if present)
-Antibiotics, Bismuth for H. Pylori
o Protect gastric lining (Cytoprotective Agents)
-Sucralfate
-Misoprostol
-Bismuth
o Limit/eliminate contributing/exacerbating factors
-NSAIDs- teach pts to use Tylenol or take NSAIDs with food

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51
Q

NSAID induced ulcers

A
  • Role of prostaglandins in the body:
    -Thermoregulatory center of the hypothalamus
    -Parietal cells of the stomach to decrease gastric acid
    -Regulate the inflammatory process (stimulation)
    -Decrease intraocular pressure
    -Contraction of uterine smooth muscle
  • Prostaglandins decrease acid secretion and increase mucus production –> gastric protection
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52
Q

cyclooxygenase (COX) pathway

A
  • COX 1 & COX 2= enzymes responsible for formation of prostaglandins and thromboxane
  • Prostaglandins are unsaturated carboxylic acid, synthesized by fatty acid precursors (arachidonic acid)
  • To be converted prostaglandins: COX 1 must be expressed by GI epithelial cells
    -During chronic NSAID treatment, COX 1 are inhibited prostaglandin production decreased
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53
Q

H. pylori

A
  • Associated with up to 90% of duodenal ulcers and 70-75% of gastric ulcers
  • Weakens the protective mucous coating of the stomach and duodenum, which allows acid to get through to the sensitive lining beneath
  • 1st line treatment: H. pylori with or without macrolide resistance
    -Tx differs depending on if pt has macrolide resistance
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54
Q

cytoprotective agents: sucralfate
MOA

A

Covers ulcers creating a barrier and promoting healing of the mucosa
**Does not neutralize acid

55
Q

admin of Sucralfate

A

o Should be taken on an empty stomach
o Typical course 4-8 weeks for acute ulcers
o Tablet or suspension
o May decrease absorption of many other drugs
-Separate admin time by at least 2 hours
-Do not take with antacids (interfere with the binding capacity to the mucosa)

56
Q

side effects/warnings of sucralfate

A

o Constipation most common side effect
o Caution in renal failure due to aluminum content

57
Q

cytoprotective agents: Misoprostol
MOA

A

o Prostaglandin (PGE2) analog
o Stimulates GI pathway decreased gastric acid release

58
Q

misoprostol: use

A

NSAID induced injury

59
Q

misoprostol: side effects

A

diarrhea, pain, and cramps (30%)

60
Q

warnings: misoprostol

A

o Do not give to women of childbearing years unless a reliable method of birth control can be DOCUMENTED
-Can cause birth defects, and premature birth
-Abortifacient

61
Q

Anti- H. pylori therapy

A
  • > 85% PUD caused by H. pylori
  • Antibiotic Ulcer Therapy - Used in Combinations
    o Bismuth – bactericidal, anti-inflammatory, binds toxins
    o Clarithromycin - Inhibits protein synthesis
    o Amoxicillin - Disrupts cell wall
    o Tetracycline - Inhibits protein synthesis
    o Metronidazole – disrupts DNA in bacterial cells
  • Penicillin allergy- treat w/ metronidazole
  • No penicillin allergy- treat w/ clarithromycin??
  • Bismuth Quadruple Therapy “combo pack”
    o Bismuth subsalicylate +
    o PPI (omeprazole 20mg bid or pantoprazole 40mg bid) +
    o Metronidazole 250-500mg tid-qid +
    o Tetracycline 500mg qid
    o Treat for 10-14 days
    o Bismuth + metronidazole + tetracycline available as combination capsule = Pylera
    -~$1000 for 10-day course
    o Sequential therapy not generally recommended
62
Q

pharm tx for Nausea & Vomiting

A
  • Antihistamine-anticholinergics*
  • Dopamine antagonists*
    -Phenothiazines
    -Metoclopramide
    Selective Serotonin antagonists*
  • Other Agents:
    -Antacids
    -Cannaboids (may make N/V worse)
    -Butyrophenones
    -Corticosteroids
    -Benzodiazepines
    -Substance P/neurokinin 1 receptor antagonist
    -Trimethobenzamide
63
Q

vestibular apparatus

A

common trigger of motion sickness or lesions in CNS
* opioids cause most nausea of 3 areas

64
Q

chemoreceptor zone

A

induced by certain meds (chemo meds)

65
Q

GI system

A

ingesting a toxin triggers vomiting reflex

66
Q

emesis

A
  • areas of the brain responsible for triggering vomiting reflex
  • can be triggered by cortex of brain (sensory triggers– seeing, smelling)
67
Q

nausea & vomiting

A
  • N/V are biologic defense mechanisms in response to toxic stimuli
  • Pharm therapy for N/V focuses on manipulating the neurotransmitters that caused it depending on area of brain stimulated
68
Q

neurotransmitters involved

A

o Histamine/Acetylcholine: vestibular nausea/motion sickness
o Dopamine: migraine-associated N/V, gastroenteritis
o Serotonin: gastroenteritis

69
Q

antihistamines/anticholinergics: MOA

A

Block the physiologic action of histamine (H1)/acetylcholine at the receptor site
* Interrupts visceral afferent pathways that are responsible for stimulating nausea and vomiting reflex

70
Q

Antihistamines/ anticholinergics: uses

A

o Motion sickness—common (give 30-60 min before event)
o Vertigo, nausea in pregnancy and general mild nausea (2nd line)

71
Q

examples of antihistamines/anticholingergiccs

A
  • Dimenhydrinate (DRAMAMINE)
  • Hydroxyzine (VISTARIL)
    o Antihistamine effect – also used for severe itching
    o Sedating
    o Can also be anxiety PRN
  • Meclizine (ANTIVERT)
    o 1st line treatment for BPPV
    o Less sedating than hydroxyzine but still use caution
  • Promethazine (PHENERGAN)
    o Commonly prescribed with codeine as a cough syrup to prevent nausea
  • Scopolamine (SCOPODERM)
    o Commonly used for motion sickness prevention and post-operative nausea
    o Also at end of life to dry secretions
72
Q

dopamine (D2 receptor) antagonists: MOA

A

o Primarily work on dopamine receptors but some effect on histamine and muscarinic receptors
* Centrally-acting: inhibiting the dopamine receptors in the medullary chemoreceptor trigger zone
* Peripherally-Acting: block the vagus nerve in the gastrointestinal tract resulting in stimulation of GI motility

73
Q

dopamine (D2 receptor) antagonist: example

A

Phenothiazines

74
Q

dopamine (D2 receptor) antagonists: drug interactions

A
  • Potentiates alcohol, CNS depressants, B-Blockers, Alpha blockers
  • Hypotension with thiazide diuretics
  • Monitor digoxin, lithium, and anticoagulants closely
75
Q

Centrally acting Phenothiazines: examples

A
  • Promethazine (Phenergan) & Prochlorperazine (Compazine) are commonly used as antiemetics as they are least sedating and require lower dosing for antiemetic effect
  • Compazine= most used in class, well tolerated
    -Monitor for extrapyramidal effects
  • Other drugs in this class are used as antipsychotics
    -Chlorpromazine (THORAZINE)
    -Fluphenazine (PROLIXIN)
76
Q

centrally acting phenothiazines
(Promethazin & Prochlorperazine): side effects

A

Blurred vision, Dry mouth, Dizziness, Restlessness, Seizures, Extrapyramidal effects - Tardive dyskinesia (long term treatment)

77
Q

centrally acting phenothiazines
(Promethazin & Prochlorperazine): contraindications

A

o Allergy to phenothiazines
o Glaucoma (increased IOP)
o Liver disease
o Prostate / bladder problems

78
Q

Peripherally Acting Phenothiazines: example

A
  • Metoclopramide (REGLAN) – has both central and peripheral activity
    -Inhibits dopamine receptors in the CTZ
    -Enhances GI motility and gastric emptying
79
Q

Peripherally Acting Phenothiazines (Metoclopramide): uses

A

o Gastroparesis (common use)
o Chemotherapy-associated N/V

80
Q

Peripherally Acting Phenothiazines (Metoclopramide): warnings

A

o Can have extrapyramidal side effects
-Concomitant diphenhydramine administration can prevent/treat these symptoms
o Avoid in the elderly (BEERS criteria

81
Q

Peripherally Acting Phenothiazines (Metoclopramide): side effects

A

diarrhea, fatigue, QT prolongation

82
Q

Peripherally Acting Phenothiazines (Metoclopramide): interactions

A

Avoid alpha and beta blockers
o Avoid ETOH

83
Q

Serotonin (5HT3) Antagonists: examples

A

Ondansetron (Zofran) most common – available generically

84
Q

Serotonin (5HT3) Antagonists (Ondansetron): MOA

A

inhibit emesis mediated through 5-HT(3) receptors both in periphery (small bowel, vagus nerve) and CNS (CTZ), with primary effects in the GI tract (which contains more than 80% of the total body serotonin)

85
Q

Serotonin (5HT3) Antagonists (Ondansetron): indications

A

chemotherapy induced N/V, prevention of post-op n/v
* Often used off label for severe n/v, pregnancy related n/v

86
Q

Serotonin (5HT3) Antagonists (Ondanestron): side effects

A
  • Headache
  • Constipation
  • Monitor LFTs if regular use
  • Can prolong QT interval and cause QRS widening
  • On Beers List for elderly
87
Q

Pregnancy Induced Nausea/Vomiting

A
  • Pathogenesis not completely understood
  • Multifactorial with hormones playing a key role
88
Q

Pregnancy Induced Nausea/Vomiting: tx

A
  • First line: pyridoxine (Vitamin B6) with or without doxylamine (antihistamine)
  • Second line: ondansetron
  • Ginger also found to be effective
  • Try OTC methods before zofran
89
Q

diarrhea patho

A

o Fluid shifts from small intestine which is not absorbed into the body–> large amount of water stays in intestines–>diarrhea
o Lack of segmenting contractions in diarrhea–>increased flow

90
Q

goal of antidiarrheal therapy

A

o Eliminate cause
o Decrease fluid accumulation in lumen
o Decrease propulsive contractions
o Increase mixing contractions.

91
Q

antidiarrheals

A
  • Absorbents
    o Bismuth subsalicylate
  • Opiates
    o Loperamide [IMMODIUM]
    o Diphenoxylate & atropine [LOMOTIL]
92
Q

antidirrheal agents- Subalicyclate
examples

A

Bismuth Subsalicylate (Pepto-Bismol)

93
Q

Bismuth Subsalicylate (Pepto-Bismol): MOA

A

o Stimulates absorption of fluids by the intestine (antisecretory)
o Reduces hypermotility of the stomach
o Reduces inflammation/irritation of the stomach
o Binds bacterial toxins
o Bactericidal action
o Weak antacid properties

94
Q

Bismuth subsalicylate: side effects

A

Can cause black stools and tongue and tinnitus (sign of toxicity)

95
Q

bismuth subsalicylate: indications

A

diarrhea, nausea, GERD, H. Pylori

96
Q

caution: bismuth subsalicylate

A

Caution if also taking aspirin (salicylate toxicity)

97
Q

antidiarrheal agents: opioids

A
  • Agonist at mu opioid receptors
    o Decreases fluid secretion
    o Increases fluid absorption
    o Decreases propulsive contractions
    o Increases segmenting contractions
    o Delays gastric emptying
98
Q

opioids side effects

A

constipation, CNS effects

99
Q

Analgesics that can be used as antidiarrheals:

A

morphine, codeine

100
Q

Antidiarrheal Agents - Loperamide (Imodium)

A
  • Mu opioid agonist
  • Very little distribution into CNS since does not cross BBB (use before Lomotil)
    -Low addiction risk
    -Lower risk of CNS depression
101
Q

Loperamide: side effects

A

fatigue, dizziness, nausea, vomiting, dry mouth, abdominal cramps, anorexia, paralytic ileus, urinary retention, rash
* Constipating

102
Q

loperamide: avoid in pts with

A

Avoid in patients with fever, bloody stools

103
Q

Antidiarrheal Agents - Lomotil

A
  • Diphenoxylate = Mu opioid agonist
    -High doses can cause euphoria and physical dependence = abuse potential
    -Schedule II drug alone, Schedule V with atropine
  • Atropine = anticholinergic
    -Decreases secretion in the bowel and slows peristalsis‡ bulks stool
  • Avoid in patients with fever, bloody stools
  • Available only in prescription
  • Some Opioid Drugs Act Both in the CNS and on Enteric Nerves, Others Act Only on Enteric Nerves
104
Q

constipation: assessment

A

o Subjective: based on change in patient’s normal bowel routine
o Objective: 2BM’s/week or less or straining with > ¼ of BMs

105
Q

constipation: causes

A

o Often a symptom of something else
o Treat the root cause

106
Q

risk factors: constipation

A

o More common in females
o Sedentary lifestyle, low fiber diet, polypharmacy, elderly (decreased intestinal motility)

107
Q

pharm tx of constipation

A

o Bulk Laxatives (1st line)
o Emollients
o Stimulants
o Saline laxatives
o Hyperosmolar laxatives
o Enemas

108
Q

Bulk laxatives

A
  • Psyllium (METAMUCIL, FIBERALL)
  • Methylcellulose (CITRUCEL)
  • Calcium polycarbophil (FIBERCON)
  • Bran
    -Bran Slurry Recipe
    o 3 cups applesauce
    o 2 cups wheat or oat bran
    o 1½ cups unsweetened prune juice
    o Start with one tablespoon per day and titrate up as needed
  • Must drink plenty of water!! (risk of rebound constipation)
  • Not systemically absorbed
109
Q

emollients/surfactants

A
  • Docusate sodium (COLACE)
    -1st line if issue is hard/dry stools
  • Docusate calcium (SURFAK)
110
Q

emollients/surfactants: MOA

A

Soften stool by allowing fecal mass to be penetrated by intestinal fluids
* Generally well tolerated
* Not systemically absorbed

111
Q

admin of emollients/surfactants

A

o Prophylactically prescribe these with meds that may cause constipation
o Use Colace for this over stimulant laxative (since it is more mild)

112
Q

stimulants laxatives: MOA

A

Act directly on intestinal mucosa to stimulate peristalsis (most powerful laxatives)

113
Q

stimulate laxatives: examples

A

o Bisacodyl (DULCOLAX)
o Senna (SENOKOT)
o Castor Oil

114
Q

stimulant laxative: side effects

A
  • Useful in treating constipation related to decreased mobility, neurogenic bowel, constipating drugs
  • Not recommended for long term treatment – can lead to dependency
  • Can cause cramping
115
Q

stimulant laxatives: duration

A
  • Work quickly
    -Dulcolax oral: 6-12 hours
    -Dulcolax suppository: 15-60 minutes
116
Q

saline laxatives: examples

A
  • Magnesium hydroxide (MILK OF MAGNESIA)
  • Magnesium sulfate (EPSOM SALTS)
  • Magnesium citrate
    -Often used for bowel prep
  • Sodium phosphate (FLEET’S PHOSPHOSODA)
  • PO formulation no longer available over the counter
117
Q

saline laxative: adverse effects

A

Risk of dehydration, renal failure, electrolyte imbalance, hypermagnesemia

118
Q

Hyperosmolar/osmotic laxatives: MOA

A

Draw water from extravascular spaces into the intestinal lumen

119
Q

Hyperosmolar/osmotic laxatives: meds

A

o Lactulose (CHRONULAC)
o Sorbitol
o Glycerol (GLYCERIN)
o Polyethylene glycol (GOLYTELY, MIRALAX)
Does not contain electrolytes like the Saline laxatives

120
Q

admin: hyperosmolar/osmotic laxatives

A

o Drink plenty of fluids
o In peds: neuro/psych effects
o Lactulose also used in ETOH use (releases ammonia)

121
Q

enemas: MOA

A

Work primarily by inducing evacuation as a response to colonic distention and by lavage

122
Q

enemas: meds

A

o Sodium phosphate (FLEET’S ENEMA)
o Soap suds
o Tap water
o Oil retention
o Saline
*Enemas should not be given prior to disimpaction (risk of rectal wall perforation)
*Electrolyte imbalances are a risk of all enemas: phosphate (Fleet’s), sodium (water), and potassium (soap)
*Fleet enemas are only by prescription

123
Q

opioid-induced constipation

A
  • 1st line is conventional laxative therapy as just discussed
  • if symptoms refractory, consider a peripherally acting mu-opioid receptor antagonist (PAMORA) or lubiprostone
124
Q

constipation

A
  • Use laxatives with caution if patient has abdominal pain, nausea and/or vomiting
  • Generally good to take with a full glass of water on an empty stomach
  • Suppositories work more quickly than oral formulations
    -Remember to educate on how to insert
  • Lifestyle management is key
  • Disimpact prior to giving laxatives
125
Q

probiotics: MOA

A
  • Live microorganisms
  • MOA: secrete bacteriocins/defensins, competitive inhibition, inhibit bacterial adhesion/translocation, reduce luminal pH, increase mucous layer
    o Immune effect:
    -Stimulates phagocytes
    -Increases IgA
    -Activates CD4 and T-helper cells
126
Q

probiotics: clinical uses

A

Level 1 Evidence:
o Infectious diarrhea
o Treatment of H. Pylori
o Prevention of traveler’s diarrhea
o Prevention of VAP
o Prevention of necrotizing fasciitis in neonates
o Prevention of antibiotic assoc. diarrhea

Level 2 Evidence:
o S.boulardii (with vancomycin) for prevention of recurrent C. diff
o Prevention of post op infections in liver transplants
o Prevention of post-op infections GI surgery

127
Q

probiotics admin

A

o Monostrain or multistrain—one vs. multiple strains of bacteria
o Quantity and quality needed:
-5-10 billion for kids; 10-20 million for adults

128
Q

resistance probiotics

A

o Sometimes gut absorbs well

129
Q

contraindications probiotics

A

ABX and PBX interactions- take apart

130
Q

probiotics: avoid in….

A

immunocompromised (limited benefits)

131
Q

Probiotics that maintain viability in the GI tract=

A

probiotics that survive stomach acid (Acidophilus, B. breve)

132
Q

prebiotics

A
  • Enhance the growth of microorganisms (tomato, artichoke, onion, garlic, berries, banana, flax seeds, legumes)
  • Can do a mix of pro and prebiotics (synbiotics)
133
Q

Probitoic Protocols: OSHU Protocol for Synbiotic Use in Hospitalized Adult Pts

A
  • Indications: patients at risk of AAD, CDI (broad spectrum ABX such as fluoroquinones)
  • Contraindications: Immunosuppressed patients (I.e.: BMT) (neutrophil count <500)
  • Route & Dosage
    o PO: 4 oz Nancy’s yogurt or kefir BID, 1 pack benefiber QID
    o Feeding tube: 80 mL Nancy’s Kefir + 1 pack Benefiber + 60 mL sterile water TID
134
Q

OSHU VAP Prevention Protocol for Adults

A
  • Indications: ventilated patients
  • Contraindications: immunosuppressed patients (neutrophil <500)
  • Route & Dosage
    o Oropharyngeal: Swabbed w/ Nancy’s Kefir BID (following oral care)
    o Feeding tube: 80 mL Nancy’s Kefir + 1 pack Benefiber + 60 mL sterile water TID

pharm exam 2 (3 decks)

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