GI Flashcards
(134 cards)
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)
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
3
Q
red flags of GERD
A
o Dysphagia
o Odynophagia (painful swallowing)
o Anemia
o Bleeding
o Weight loss
o Vomiting blood
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
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
6
Q
pharm tx:
A
antacids
histamine 2 receptor antagonist
PPIs
7
Q
what is the MOA of antacids?
A
Neutralize gastric HCl – increases pH of the stomach and duodenum
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)*
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)
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
11
Q
drug interactions of antacids: potential interactions
A
- ASA (Aspirin)
- Benzodiazepines
- Anticoagulants
- Phenytoin
- Digoxin
- Nitrofurantoin
- Tetracycline
- Phenothiazines
- Synthroid
- Histamine receptor antagonists
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)
13
Q
sodium bicarbonate: onset of action
A
rapid
14
Q
sodium bicarbonate: duration of action
A
short
15
Q
sodium bicarbonate: systemic alkalosis
A
yes
16
Q
sodium bicarbonate: effect on stool?
A
none
17
Q
calcium carbonate: onset of action
A
intermediate
18
Q
calcium carbonate: duration of action
A
moderate
19
Q
calcium carbonate: systemic alkalosis
A
not really
20
Q
calcium carbonate: effect on stool?
A
constipating
21
Q
magnesium hydroxide: onset of action
A
rapid
22
Q
magnesium hydroxide: duration of action
A
moderate
23
Q
magnesium hydroxide: systemic alkalosis
A
no
24
Q
magnesium hydroxide: effect on stool?
A
laxative
25
aluminum: onset of action
slow
26
aluminum: duration of action
moderate
27
aluminum: systemic alkalosis
no
28
aluminum: effect on stool?
constipating
29
antacid neutralizing capacity
* 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
30
histamine 2 recepor antagnoist: MOA
bind to histamine-2 receptors on gastric parietal cells to reduce gastric acid secretion
31
histamine 2 recepor antagnoist: drug examples
o Ranitidine (ZANTAC) (150 vs 75mg)
o Cimetidine (TAGAMET)
o Famotidine (PEPCID)
o Nizatidine (AXID)
32
use of histamine 2 receptor antagonist
* 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
33
contraindications: histamine 2 receptor antagonist
o Avoid in patients with delirium/at risk for delirium (Beers Criteria)
34
admin of histamine 2 receptor antagonist
o Twice-daily dosing
o Make sure patient has a good physical exam and appropriate labs to rule out gastric malignancy!
35
side effects of histamine 2 receptor blockers
very few
36
histamine 2 receptor antagonist: drug interactions
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.**
37
Ramitidine: recall
FDA recalled this bc of large amounts of NDMA which is classified as a possible human carcinogen. AVOID GIVING THIS TO PTS!
38
Ramitidine: recall
FDA recalled this bc of large amounts of NDMA which is classified as a possible human carcinogen. AVOID GIVING THIS TO PTS!
39
Proton Pump Inhibitors (PPIs): MOA
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!)
40
examples of PPIs
o Esomeprazole (NEXIUM)
o Lansoprazole (PREVACID)
o Omeprazole (PRILOSEC)
o Pantoprazole (PROTONIX)
o Rabeprazole (ACIPHEX)
41
use of PPIs
o PUD
o GERD
o H. Pylori
o NSAID associated ulcers
o Zollinger-Ellison syndrome
42
admin/pt teaching of PPIs
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
43
Contraindications of PPIs
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)
44
warnings of PPIs
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
45
drug interaction of PPIs
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
46
omeprazole
blocks gastric acid secretion by irreversing binding to H+/K+ pump --> blockage of gastric acid from parietal cell membrane
47
Robert Warren and Barry Marshall
discovered a link between the bacteria H. pylori and PUD--> won Nobel Prize in 2005
48
s/s of peptic ulcer disease
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)
49
peptic ulcer disease: etiologies
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
50
tx of peptic ulcer disease
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
51
NSAID induced ulcers
* 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
52
cyclooxygenase (COX) pathway
* 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
53
H. pylori
* 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
54
cytoprotective agents: sucralfate
MOA
Covers ulcers creating a barrier and promoting healing of the mucosa
****Does not neutralize acid
55
admin of Sucralfate
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
side effects/warnings of sucralfate
o Constipation most common side effect
o Caution in renal failure due to aluminum content
57
cytoprotective agents: Misoprostol
MOA
o Prostaglandin (PGE2) analog
o Stimulates GI pathway decreased gastric acid release
58
misoprostol: use
NSAID induced injury
59
misoprostol: side effects
diarrhea, pain, and cramps (30%)
60
warnings: misoprostol
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
Anti- H. pylori therapy
* >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
pharm tx for Nausea & Vomiting
* 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
vestibular apparatus
common trigger of motion sickness or lesions in CNS
* opioids cause most nausea of 3 areas
64
chemoreceptor zone
induced by certain meds (chemo meds)
65
GI system
ingesting a toxin triggers vomiting reflex
66
emesis
* areas of the brain responsible for triggering vomiting reflex
* can be triggered by cortex of brain (sensory triggers-- seeing, smelling)
67
nausea & vomiting
* 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
neurotransmitters involved
o Histamine/Acetylcholine: vestibular nausea/motion sickness
o Dopamine: migraine-associated N/V, gastroenteritis
o Serotonin: gastroenteritis
69
antihistamines/anticholinergics: MOA
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
Antihistamines/ anticholinergics: uses
o Motion sickness—common (give 30-60 min before event)
o Vertigo, nausea in pregnancy and general mild nausea (2nd line)
71
examples of antihistamines/anticholingergiccs
* 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
dopamine (D2 receptor) antagonists: MOA
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
dopamine (D2 receptor) antagonist: example
Phenothiazines
74
dopamine (D2 receptor) antagonists: drug interactions
* Potentiates alcohol, CNS depressants, B-Blockers, Alpha blockers
* Hypotension with thiazide diuretics
* Monitor digoxin, lithium, and anticoagulants closely
75
Centrally acting Phenothiazines: examples
* 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
centrally acting phenothiazines
(Promethazin & Prochlorperazine): side effects
Blurred vision, Dry mouth, Dizziness, Restlessness, Seizures, Extrapyramidal effects - Tardive dyskinesia (long term treatment)
77
centrally acting phenothiazines
(Promethazin & Prochlorperazine): contraindications
o Allergy to phenothiazines
o Glaucoma (increased IOP)
o Liver disease
o Prostate / bladder problems
78
Peripherally Acting Phenothiazines: example
* Metoclopramide (REGLAN) – has both central and peripheral activity
-Inhibits dopamine receptors in the CTZ
-Enhances GI motility and gastric emptying
79
Peripherally Acting Phenothiazines (Metoclopramide): uses
o Gastroparesis (common use)
o Chemotherapy-associated N/V
80
Peripherally Acting Phenothiazines (Metoclopramide): warnings
o Can have extrapyramidal side effects
-Concomitant diphenhydramine administration can prevent/treat these symptoms
o Avoid in the elderly (BEERS criteria
81
Peripherally Acting Phenothiazines (Metoclopramide): side effects
diarrhea, fatigue, QT prolongation
82
Peripherally Acting Phenothiazines (Metoclopramide): interactions
Avoid alpha and beta blockers
o Avoid ETOH
83
Serotonin (5HT3) Antagonists: examples
Ondansetron (Zofran) most common – available generically
84
Serotonin (5HT3) Antagonists (Ondansetron): MOA
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
Serotonin (5HT3) Antagonists (Ondansetron): indications
chemotherapy induced N/V, prevention of post-op n/v
* Often used off label for severe n/v, pregnancy related n/v
86
Serotonin (5HT3) Antagonists (Ondanestron): side effects
* Headache
* Constipation
* Monitor LFTs if regular use
* Can prolong QT interval and cause QRS widening
* On Beers List for elderly
87
Pregnancy Induced Nausea/Vomiting
* Pathogenesis not completely understood
* Multifactorial with hormones playing a key role
88
Pregnancy Induced Nausea/Vomiting: tx
* 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
diarrhea patho
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
goal of antidiarrheal therapy
o Eliminate cause
o Decrease fluid accumulation in lumen
o Decrease propulsive contractions
o Increase mixing contractions.
91
antidiarrheals
* Absorbents
o Bismuth subsalicylate
* Opiates
o Loperamide [IMMODIUM]
o Diphenoxylate & atropine [LOMOTIL]
92
antidirrheal agents- Subalicyclate
examples
Bismuth Subsalicylate (Pepto-Bismol)
93
Bismuth Subsalicylate (Pepto-Bismol): MOA
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
Bismuth subsalicylate: side effects
Can cause black stools and tongue and tinnitus (sign of toxicity)
95
bismuth subsalicylate: indications
diarrhea, nausea, GERD, H. Pylori
96
caution: bismuth subsalicylate
Caution if also taking aspirin (salicylate toxicity)
97
antidiarrheal agents: opioids
* 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
opioids side effects
constipation, CNS effects
99
Analgesics that can be used as antidiarrheals:
morphine, codeine
100
Antidiarrheal Agents - Loperamide (Imodium)
* 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
Loperamide: side effects
fatigue, dizziness, nausea, vomiting, dry mouth, abdominal cramps, anorexia, paralytic ileus, urinary retention, rash
* Constipating
102
loperamide: avoid in pts with
Avoid in patients with fever, bloody stools
103
Antidiarrheal Agents - Lomotil
* 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
constipation: assessment
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
constipation: causes
o Often a symptom of something else
o Treat the root cause
106
risk factors: constipation
o More common in females
o Sedentary lifestyle, low fiber diet, polypharmacy, elderly (decreased intestinal motility)
107
pharm tx of constipation
o Bulk Laxatives (1st line)
o Emollients
o Stimulants
o Saline laxatives
o Hyperosmolar laxatives
o Enemas
108
Bulk laxatives
* 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
emollients/surfactants
* Docusate sodium (COLACE)
-1st line if issue is hard/dry stools
* Docusate calcium (SURFAK)
110
emollients/surfactants: MOA
Soften stool by allowing fecal mass to be penetrated by intestinal fluids
* Generally well tolerated
* Not systemically absorbed
111
admin of emollients/surfactants
o Prophylactically prescribe these with meds that may cause constipation
o Use Colace for this over stimulant laxative (since it is more mild)
112
stimulants laxatives: MOA
Act directly on intestinal mucosa to stimulate peristalsis (most powerful laxatives)
113
stimulate laxatives: examples
o Bisacodyl (DULCOLAX)
o Senna (SENOKOT)
o Castor Oil
114
stimulant laxative: side effects
* 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
stimulant laxatives: duration
* Work quickly
-Dulcolax oral: 6-12 hours
-Dulcolax suppository: 15-60 minutes
116
saline laxatives: examples
* 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
saline laxative: adverse effects
Risk of dehydration, renal failure, electrolyte imbalance, hypermagnesemia
118
Hyperosmolar/osmotic laxatives: MOA
Draw water from extravascular spaces into the intestinal lumen
119
Hyperosmolar/osmotic laxatives: meds
o Lactulose (CHRONULAC)
o Sorbitol
o Glycerol (GLYCERIN)
o Polyethylene glycol (GOLYTELY, MIRALAX)
Does not contain electrolytes like the Saline laxatives
120
admin: hyperosmolar/osmotic laxatives
o Drink plenty of fluids
o In peds: neuro/psych effects
o Lactulose also used in ETOH use (releases ammonia)
121
enemas: MOA
Work primarily by inducing evacuation as a response to colonic distention and by lavage
122
enemas: meds
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
opioid-induced constipation
* 1st line is conventional laxative therapy as just discussed
* if symptoms refractory, consider a peripherally acting mu-opioid receptor antagonist (PAMORA) or lubiprostone
124
constipation
* 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
probiotics: MOA
* 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
probiotics: clinical uses
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
probiotics admin
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
resistance probiotics
o Sometimes gut absorbs well
129
contraindications probiotics
ABX and PBX interactions- take apart
130
probiotics: avoid in....
immunocompromised (limited benefits)
131
Probiotics that maintain viability in the GI tract=
probiotics that survive stomach acid (Acidophilus, B. breve)
132
prebiotics
* Enhance the growth of microorganisms (tomato, artichoke, onion, garlic, berries, banana, flax seeds, legumes)
* Can do a mix of pro and prebiotics (synbiotics)
133
Probitoic Protocols: OSHU Protocol for Synbiotic Use in Hospitalized Adult Pts
* 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
OSHU VAP Prevention Protocol for Adults
* 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
