Pharm GI Exam 1 Flashcards
Treatment for acute cholecystitis
Initial treatment is supportive care IV fluids Electrolyte correction pain meds (NSAIDS) (can use opioids) Ketorolac (NSAID) Morphine, diluadid, Demerol (no longer meperidine)
Acute calculous cholecystitis Tx
Admit Initial treatment is supportive care IV fluids Electrolyte correction pain meds IV ABX Fasting NG tube if vomiting
Acute cholecystitis IV ABX
Continue IV ABX until gallbladder removed
or cholecystitis resolves
Empiric abx for Acute cholecystitis
Cover most pathogens of
Enterobacteriaceae family
including gram negative rods
and anaerobes
The most frequent isolates from the gall bladder and common bile duct are…
Ecoli 41%
Enterococcus 12%
Klebsiella 11%
Enterobacter 9%
Single agent regimens of low risk, and hospital-acquired intra-abdominal infections
Ertapenem 1 G IV QD
Piper Taz 3.375 G IV Q6h
Single agent regimens of high risk, and hospital-acquired intra-abdominal infections
Imipenem 550mg IV Q6h
Meropenem 1 G IV Q8h
Doripenem 500mg IV Q8H
Piper Taz 4.5 G IV Q6H
Health care acquired intra abdominal infections
Empiric therapy coverage for Streptococci Enterococci Enterobacteriaceae resistant to 3rd gen cef Pseudomonas Anaerobes
Cholangitis S/S Charcot
Charcot’s triad
Fever
Jaundice
RUQ pain
50-75% of patients have all 3
Most common is fever and abdominal pain
Cholangitis S/S Reynolds
Reynolds
Fever
Jaundice
RUQ pain
Plus
Hypotension
AMS
Other misc symptoms can include: Hepatic abscess, MSOD, shock, sepsis,
Acute cholangitis in elderly on glucocorticoids
Hypotension may be only symptom
Charcot’s triad
Fever
Abdominal pain
Jaundice
Should suspect Acute cholangitis
Acute cholangitis treatment
Biliary drainage is required
Infectious Esophagitis CMV
treatment
Ganciclovir
Infectious Esophagitis HSV
treatment
Acyclovir
Infectious Esophagitis Candida
treatment
Fluconazole or ketoconazole
Medication induce esophagitis
meds that can cause it
ABX eg tetracycline Aspirin NSAIDS potassium chloride quinidine iron bisphosphonates
Medication induce esophagitis
factors that affect it
size of med position of patient amount of fluid ingested with it rate of esophageal transit prolonged caustic contact altered esophagus anatomy increased age
GERD treatment criteria
frequency
severity
presence or absence of erosive esophagus
or Barrett’s esophagus on upper gi
GERD Tx
mild/intermittent
with no previous treatments
and no evidence of Barrett’s or erosion
lifestyle and diet changes
low dose histamine 2 receptor antagonists
(H2 blockers)
Antacids or sodium alginate
(for symptoms less than once a week)
If more than once a week
Increase to standard dose H2blockers
BID for minimum of 2 weeks
GERD Tx
Persistent GERD
lifestyle and diet changes
Stop H2 blockers
Start PPI once a day at low dose
increase to standard dose if symptoms persist
once controlled,
should be continued for minimum of 8 weeks
GERD tx
with erosive esophagitis
lifestyle and diet changes
Initial acid suppression therapy with
Standard dose PPI
Once a day
GERD in Pregnancy
lifestyle and diet changes
TX with
antacids
sucralfate
Avoid antacids with sodium bicarb
and
mag trisilicate
move on to H2 blockers
and PPI’s
if antacids don’t work
Systemic antacids
Sodium bicarbonate
sodium citrate
Non systemic antacids
Magnesium hydroxide Mag trisilicate aluminum hydroxide gel magaldrate calcium carbonate
Antacid MOA
Usually contain combination of
Magnesium hydroxide
Mag trisilicate
calcium carbonate
this neutralizes gastric pH
This decreases exposure of esophageal mucosa to acid during reflux
Antacid onset/duration
Usually work within 5 minutes
short duration of
30-60 minutes
Calcium carbonate
Tums
Warning
Hypoparathyroidism
interactions
Calcium blocks absorption of tetracyclines
Antacid misc info
NSAIDS should be taken with antacids
MOA - neutralizes gastric HCL
should not lower pH below 5 due to rebound hyperacidity
Foam is produce which can result in esophageal burning
give with simethicone (anti foam)
sucralfate
Carafate (aluminum sucrose sulfate)
for short term tx of active duodenal ulcers and maintenance of healed ulcers
up to 8 weeks (tabs only)
Interactions
avoid antacids with 30 mins of taking
may reduce absorption
(cimetidine, ranitidine)
A surface agent that promotes healing protects form injury and adheres to mucosal surface
limited to GERD in pregnancy due to short acting compared to PPI
sucralfate MOA
thought to form ulcer adherent complex at the ulcer site protecting it from further injury from stomach acid
sodium alginate
a poly saccharide derived from seaweed that forms a viscous gum that floats in the stomach and neutralizes the post prandial acid pocket in the proximal stomach
Histamine 2 receptor antagonists
decrease the secretion of acid by inhibiting the histamine 2 receptor on the gastric parietal cells
Cimetidine
Tagamet (H2 blocker)
Warnings
impaired renal/hepatic function, elderly, debilitated, immunocompromised,
Preg Cat B,
not recommended for nursing mothers
interactions
Antacids within 1 hour of taking
Adverse
HA, diarrhea, dizziness, somnolence
Proton pump inhibitors
To be used in patients who fail twice daily H2 blockers
Patients with erosive esophagitis
frequent or sever GERD (2 or more times per week)
PPIs are the most potent inhibitors of gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium (H-K) ATPase pump
PPIs should be administered daily rather than on-demand because continuous therapy provided better symptom control, quality of life, and higher endoscopic remission rates
PPI Onset
PPIs are most effective when taken 30 minutes before the first meal of the day because the amount of H-K-ATPase present in the parietal cell is greatest after a prolonged fast
Omeprazole indications
Prilosec
Used in triple therapy or dual therapy for H. Pylori in duodenal ulcer disease Short term active benign gastric ulcer active duodenal ulcer erosive esophagitis maintenance of erosive esophagitis Symptomatic GERD pathologic hypersecretory conditions
Omeprazole
Prilosec
PPI
Warnings
Gastric malignancy
Adverse
HA, abdominal pain, N/V/D, flatulence
Omeprazole dosage (low)
10mg QD
Cimetidine dosage (low)
200mg BID
Foods that worsen GERD by lowering LES pressure
Fatty meals Mints Chocolate coffee tea garlic onions chili peppers
Meds that worsen GERD by lowering LES pressure
Anticholinergics Barbs Caffeine Dihydropyridine CCB Dopamine Estrogen Ethanol Nicotine Nitrates Progesterone Tetracycline Theophylline
Foods that worsen GERD by direct irritation
Spicy foods
Juices (tomato, orange)
Coffee
Meds that worsen GERD by direct irritation
Alendronate Aspirin NSAIDS Iron Quinidine Potassium chloride
Mallory Weiss syndrome tx
IV PPI BID (initial)
(for all patients suspected of upper GI bleed)
prior to endoscopy
Continue standard therapy for 2 weeks
Omeprazole 20mg QD
after endoscopy
These promote hemostasis by neutralizing gastric acid and stabilizing blood clots
PPI and antiemetics
Antiemetics are for persistent nausea and vomiting
For patients with disorders of esophageal hyperperistalsis and GERD symptoms
PPI BID
For patients with no GERD (or well controlled GERD) but have dysphagia
tx
Peppermint oil (2 altoids taken sublingually before each meal)
if no improvement, CCB (diltiazem 60-90 mg QID
If CCB not effective, low dose TCA
(imipramine 25mg at bed time)
Esophageal strictures
tx
After esophageal dilation
PPI
Omeprazole 20mg BID x 1 year
Esophageal varices
vasoactive meds tx
Med to be started at time of presentation and not held pending diagnosis
Vasoactive meds decrease portal blood flow and have shown to decrease mortality and improve hemostasis with acute variceal bleeding
(octreotide, terlipressin, somatostatin)
Esophageal varices
BB Tx
Goal of treatment is to decrease portal venous inflow
Non selective beta blockers block the adrenergic dilatory tone in mesenteric arterioles
This results in unopposed alpha adrenergic mediated vasoconstriction and therefore decrease venous inflow
Propranolol and nadolol
Esophageal varices
Acute management
Hemodynamic resuscitation Octreotide Banding Sclerotherapy Prophylactic ABX (ceftriaxone)
Esophageal varices
Chronic management
Beta blockers
Endoscopic variceal ligation
Hep A vaccine
Havrix (inactivated)
Contraindications
Neomycin allergy
Interactions
immunosuppressives may reduce efficacy
Hep B Diagnoses
Based on detection of Hep B surface antigen (HBsAG)
and IgM antibody to hepatitis B core antigen
Treatment is mainly supportive
The decision to start treatment is based on presence of cirrhosis, ALT and HBV DNA level
Hep B Tx
Treatment is mainly supportive
The decision to start treatment is based on presence of cirrhosis, ALT and HBV DNA level
for treatment naïve patients
nucleotide analogue
we recommend tenofir or entecavir
Tenofovir alafenamide 25mg QD
tenofovir disoproxil fumarate 300mg QD
tenofovir alafenamide
Vemlidy 25mg
Nucleoside analogue (reverse transcriptase inhibitor)
Chronic Hep B Virus in patients with compensated liver disease
Warning
Post treatment severe acute exacerbation of Hep B
tenofovir MOA
Nucleotide analogue of AMP
Inhibits HBV polymerase
First approved for treatment of HIV
emtricitabine MOA
Nucleoside analog of cytosine active against HIV and ABV
Hep B Vaccine
Recombivax HB
Contra
yeast hypersensitivity
HCV infected patient education
HCV-infected patients should be counseled on measures to decrease the risk of transmission and correcting factors associated with accelerated liver disease, including alcohol use, obesity and insulin resistance, and marijuana use.
Substance use treatment is also an important element of care in patients who have ongoing illicit drug use.
Protease inhibitors Meds
Telaprevir boceprevir asunaprevir simeprevir faldaprevir MK-5172r
Translation and polyprotein processing
NNPI Meds
Deleobuvir filibuvir setrobuvir tegobuvir VX-222
RNA replication
Hep D tx
Optimal treatment is uncertain
Treatment of choice for chronic Hep D is interferon Alfa (IFNa)
Mainstay of treatment for Hep D is vaccination against Hep B
Hep E Tx
12 week course of ribavirin monotherapy to certain non pregnant patients with chronic Hep E
Ribavirin
Copegus (nucleoside analogue)
Contraindications:
Hemoglobinopathies
(thalassemia, sickle cell)
Preg Cat X
Male partners of pregnant women
Lactulose
Cephulac (colonic acidifier)
Prevention and treatment of portal systemic encephalopathy
including stages of hepatic pre-coma and coma
Contra
Patients who require a low galactose diet
Adverse
Gas, cramping, diarrhea, nausea, vomiting
Lactulose MOA
Synthetic disaccharide of galactose and fructose
Resists intestinal disaccharidase activity
MOA
Hydrolyzed in the colon to short chain fatty acids
Stimulate colonic propulsive motility
Which of the below is the most common low dosage of omeprazole?
10 mg once a day by mouth
20 mg once a day by mouth
30 mg once a day by mouth
40 mg once a day by mouth
10 mg once a day by mouth
Which of the following medications is would be used for the pharmacologic treatment is to decrease portal venous inflow secondary to esophageal varices?
atenolol
propranolol
acetabutol
metoprolol
propranolol
Which of the below medications is considered a histamine-2 antagonist?
Sucralfate
Omeprazole
Cimetidine
Calcium carbonate
Cimetidine
Which of the below medications is considered a proton pump inhibitor?
Sucralfate
Omeprazole
Cimetidine
Calcium carbonate
Omeprazole
Which of the following is not one of the most frequent isolates from the gallbladder or common bile duct
Escherichia coli
Enterococcus
Klebsiella
Streptococci
Streptococci
Antacid
Gastric acid neutralizers
Systemic
Sodium bicarbonate
Sodium citrate
Nonsystemic Magnesium hydroxide Magnesium trisilicate Aluminum hydroxide gel magaldrate calcium carbonate
GI anticholinergics
Chloridiazepoxide / clidinnium (Librax)
for IBS and PUD
Dicyclomine (Bentyl) for IBS
Gastrointestinal drugs
Antispasmodics
Used to treat symptoms such as pain and spasm in irritable bowel syndrome
Antimuscarinics and anticholinergics Hyoscine Butylbromide Atropine Dicyclomine Propantheline
Smooth muscle relaxants Drotaverine Alverine Mebeverine Peppermint oil
Causes of gastritis
autoimmune pernicious anemia H Pylori NSAIDS ETOH Stress from CNS injury, burns, sepsis, surgery
Peptic ulcer disease
A defect in the gastric or duodenal wall that extends through the muscularis mucosa into the deeper layers of the wall
Tx is based on etiology, ulcer characteristics and anticipated natural history
PUD and H. Pylori
Patients with peptic ulcer disease should be tested forHelicobacter pylori(H. pylori).
Patients withH. pylorishould be treated with a goal of eradication ofH. pyloriinfection.
In patients treated forH. pylori,eradication of infection should be confirmed four or more weeks after the completion of eradication therapy.
PUD and NSAIDS
Patients with peptic ulcers should be advised to avoid nonsteroidal anti-inflammatory drugs (NSAIDs).
Contributing factors should be addressed and treated (eg, treating medical comorbidities, poor nutritional status, ischemia).
PUD anti-secretory therapy
All patients with peptic ulcer disease should receive anti-secretory therapy to facilitate ulcer healing.
The choice and duration of therapy varies based on the etiology, ulcer location (eg, gastric or duodenal), and the presence of ulcer complications (eg, bleeding, perforation, penetration, or gastric outlet obstruction).
All patients with peptic ulcers should receive anti-secretory therapy with a proton pump inhibitor (PPI) (eg,omeprazole20 to 40 mg daily or equivalent) to facilitate ulcer healing
PUD and duodenal ulcers
Patients with duodenal ulcers who have been treated do not need further endoscopy unless symptoms persist at four weeks or recur.
PUD and PPI
PPI use results in faster control of peptic ulcer disease symptoms and higher ulcer healing rates as compared with H2RA (eg, famotidine) as a consequence of stronger acid suppression.
PPIs also heal NSAID-related ulcers more effectively as compared with H2RAs
PUD and H2 blockers with PPI
Combining PPIs and H2RAs adds to cost without enhancing healing.
Although antacids andsucralfatecan heal duodenal ulcers, they are not routinely recommended to treat peptic ulcers as PPIs heal ulcers more rapidly and to a greater extent.
H. pylori tx
Bismuth quad therapy
Bismuth, metronidazole, tetracycline, PPI
Clarithromycin Triple therapy
Amoxicillin, clarithromycin, PPI
Clarithromycin/metronidazole triple therapy
Clarithromycin, metronidazole, PPI
bismuth subsalicylate
Pepto bismol OTC (262mg)
Antidiarrheal
Contra
Varicella or influenza in peds and teenagers
Warnings
Coagulation disorders, diabetes, reyes, pregnancy, nursing mothers (not recommended)
Interactions
Potentiates anticoagulants
Adverse
Darkened tongue and stool
Antidiarrheal MOA
Adsorbents
Coats the walls of the GI tract
Bind to the causative bacteria or toxin which are then eliminated through stool
Pepto bismol
Kaopectate
Prophylactic treatment with PPI
Should be considered in patients with a history of ulcer who require daily NSAIDs use,
as well a history of complications like bleeds, need for chronic steroid use or anticoagulant use.
Pyloric stenosis
IHPS is typically treated with surgical pyloromyotomy.
If the child is well hydrated with normal electrolytes, and if surgeons with expertise in the procedure are available, surgery may take place on the day of diagnosis.
Surgery should be delayed in the setting of dehydration and/or electrolyte derangements until these abnormalities are corrected with appropriate fluid and electrolyte therapy.
Mild regurgitation after pyloromyotomy is common and should not delay the initiation of feeding.
Acute pancreatitis types
Edematous
Necrotizing
Causes of pancreatitis
Heavy alcohol use 40%
Gallstones 40%
Other 20% Trauma meds infection, tumor High calcium High TGL Genetic
Acute pancreatitis treatment
Supportive care
Lots of fluids in first 24 hours
pain control
Electrolyte and metabolic corrections
The majority of patients with mild pancreatitis require no further therapy, and recover within three to seven days.
Patients with moderately severe and severe pancreatitis require more intensive monitoring as they have transient (<48 hours) or persistent (>48 hours) organ failure and local or systemic complications.
Acute pancreatitis most common symptom
Abdominal pain is often the predominant symptom in patients with acute pancreatitis.
Adequate pain control requires the use of intravenous opiates, such asmorphineandfentanyl, usually in the form of a patient-controlled analgesia pump.
Chronic pancreatitis
Presents with chronic unrelenting pain with episodic flares
The goal of treatment in chronic pancreatitis
The goals of treatment include pain management, correction of pancreatic insufficiency, and management of complications.
Pain management in chronic pancreatitis
Pain management should proceed in a stepwise approach.
Initial treatment begins with recommendations to stop alcohol and tobacco and to eat small meals that are low in fat.
We suggest the use of pancreatic enzyme supplements in patients with pain persisting after the above interventions. These relieve pain in some patients and are generally safe.
Treatment with acid suppression (either with an H2 receptor blocker or a proton pump inhibitor) should be given along with pancreatic enzyme supplements to reduce inactivation from gastric acid.
Analgesics with opiates and/or nonsteroidal anti-inflammatory agents can be considered if pancreatic enzyme therapy fails to control pain.
Adjuvant therapy withpregabalincan be considered in patients whose pain is not adequately controlled with opiates and/or nonsteroidal anti-inflammatory agents.
Chronic pancreatitis and diet
Steatorrhea (fat malabsorption) may develop in patients with severe pancreatic exocrine dysfunction. Treatment depends upon the severity of disease.
Dietary modification should begin with restriction of fat intake (to less than 20 g per day).
For patients who do not respond to dietary restriction, we suggest lipase supplementation.
As a general rule, 30,000 international units (IU) of pancreatic lipase (90,000 United States Pharmacopeia units [USP]) swallowed during each meal should suffice in reducing steatorrhea and preventing weight loss. Fat soluble vitamin replacement may be required.
Medium chain triglycerides(MCTs) can provide extra calories in patients with weight loss and a poor response to diet and pancreatic enzyme therapy.
lipase
Ku-zyme (digestive enzyme)
supplement in digestive enzyme deficiency
Contra
Acute pancreatic exacerbations, pork allergy
Interactions
Avoid antacids
Adverse
diarrhea
Digestive enzymes
Amylase
Breaks down carbohydrates to sugars
Digestive enzymes
protease
Breaks down proteins to amino acids
Digestive enzymes
lipase
Breaks down fats to fatty acids
Anorectal abscess treatment
Surgical drainage is primary treatment
should be drained promptly;
lack of fluctuance should not be a reason to delay treatment.
Any undrained anorectal abscess can continue to expand into adjacent spaces as well as progress to generalized systemic infection.
Give empiric abx
4-5 days of Augmentin or cipro + flagyl
Anorectal abscess wound culture
Not necessary unless suspicion or immunosuppression
Anorectal abscess WASH
Warm water sitz bath
Analgesics
Stool softener
High fiber diet
Stool Softners
Docusate sodium
Docusate calcium
Docusate sodium
Colace (stool softener)
interactions
may increase systemic absorption of mineral oil
MOA
Increases penetration of fluid into stool
Softens stool to facilitate passage
Anal fissure treatment
initial therapy with a combination of supportive measures
(fiber, stool softener, sitz bath, topical analgesic)
and one of the topical vasodilators (nifedipineornitroglycerin) for one month,
rather than surgery.
For patients who have access to a compounding pharmacy, we suggestnifedipineointment rather thannitroglycerinointment as the topical vasodilator.
Nifedipine ointment has fewer side effects and potential drug interactions compared with nitroglycerin and may be more effective.
Constipation
Chronic
Tx
Patient education Lifestyle modifications Diet Laxatives Enema
Constipation in patients over 70
Warm water enema
rather than sodium phosphate
Sodium phosphate complications in elderly
associated with complications including hypotension and volume depletion, hyperphosphatemia, hypo- or hyperkalemia, metabolic acidosis, severe hypocalcemia, renal failure, and electrocardiogram changes (prolonged QT interval).
Idiopathic constipation
tx
dietary fiber
bulk-forming laxatives such aspsylliumormethylcellulose,
together with adequate fluids.
Constipation
cant tolerate fiber or bulk laxatives
Osmotic laxatives
Stool, softeners
Stimulant laxatives
Secretory laxatives
Constipation drugs
Bulk forming laxatives
Psyllium
Methylcellulose
Side effects
Impaction above strictures
Fluid overload
Gas and bloating
Psyllium
Metmucil (OTC)
Contra
S/S of appendicitis
Obstruction, impaction, dysphagia
Warnings
Rectal bleeding, esophageal narrowing, Diabetes
Adverse
Obstruction
Constipation drugs
Surfactants (softeners)
Docusate sodium
Docusate calcium
Adverse
Well tolerated
use lower dos if given with another laxative
contact dermatitis
Constipation drugs
Osmotic laxatives
Lactulose Sorbitol Glycerin Magnesium sulfate Magnesium citrate Polyethylene glycol
polyethylene glycol
Miralax (OTC) (osmotic laxative)
Contra
Obstruction
Adverse
Loose watery frequent stools
Constipation drugs
Stimulant laxatives
Bisacodyl
Senna
Bisacodyl
Dulcolax 10mg (Stimulant laxative)
Interactions
Do not take within 1 hour after antacids or milk (TABS)
Adverse
Abdominal discomfort, faintness, cramps
Suppositories: Rectal burning
Bulk forming laxatives (fiber)
MOA
Retention of water in the stool
must be taken with adequate fluid intake
Stool softeners
MOA
Detergent, traps water in the stool
Osmotic laxatives
osmotically pulls water into the stool
Stimulant laxatives
increases contraction of intestinal muscle and increase peristalsis
Fecal impaction tx
Digital disimpaction
warm water enema with mineral oil to soften and assist passage
Mineral oil enema
Fleet enema
Lubricant laxative
Hydorcortisone acetate 25mg
Anusol (steroid)
Adverse
Dermal and epidermal atrophy
poor wound healing
local irritation
IBD
Crohn’s
Choice of therapy depends on location of disease, severity of disease and whether goal is to induce remission or maintain remission
5-ASA (sufasalazine, mesalamine)
Glucocorticoids (prednisone, budesonide)
Immunomodulators (azathioprine, methotrexate)
Biologics (-mabs, certolizuma, pegol , etc)
5 types of meds used to treat IBD
Amino salicylates (anti-inflammatory)
Corticosteroids (anti-inflammatory)
Immunomodulators (suppress the immune system)
ABX (infection)
Biologics (blocks protein Tumor necrosis factor)
Oral 5 -amino salicylates MOA
Mesalamine
Sulfasalazine
Balsalazide
MOA
interfere with the production of arachidonic acid by affecting the thromboxane and lipoxygenase synthesis pathway
Used mainly for UC and less for Crohn’s
Oral 5-amino salicylates-sulfasalazine
Azulfidine
For moderate to severe UC
Adjunct in severe UC
Prolong remission between attacks
Contra
intestinal or urinary obstruction, porphyria
Interactions
Reduces absorption of digoxin and folic acid
Sulfasalazine MOA
Reaches the colon intact
Then metabolized into 5-ASA and sulfa-pyridine
Used for UC and Crohn’s as initial therapy or to maintain remission
0.5g PO BID
increase to 0.5-1.055g PO QID if tolerated
Remission 1g PO BID-QID
mesalamine
Lialda (amino salicylate)
Interactions
Increased toxicity with nephrotoxic drugs (ie NSAID)
Adverse
UC, HA, flatulence, LFT’s, Abdominal pain, acute intolerance syndrome
Glucocorticoids MOA
Treats inflammation
Immunomodulators
Azathioprine
6 mercaptopurine
methotrexate
Purine analogues (prodrugs)
MOA
impair purine biosynthesis and inhibit cell proliferation
Treatment of steroid dependent/resistant disease
UC, Crohn’s
Recurrence
Fistulas
infliximab
Remicade (tumor necrosis factor blocker)
Contra
Moderate or sever heart failure (dose over 5mg)
allergy to murine proteins
Warning
Serious infections
Malignancy
IBS
Lifestyle mods
Diet (limit gas producing foods FODMAPS)
Limit lactose and gluten
Trial of psyllium in patients with IBS constipation
If Psyllium fails, polyethylene glycol
If laxatives fail
Trial of lubiprostone or linaclotide
FODMAPS
Fermentable oligosaccharides disaccharides monosaccharides and polyols
Constipation meds
Non Laxatives
Lubiprostone
Linaclotide
Plecanatide
lubiprostone
Amitiza
IBS with constipation in women
Contra
Obstruction
Adverse
NVD, abdominal pain, hypotension, dyspnea
lubiprostone MOA
opening of chloride channels locally in the GI luminal epithelium, which stimulates chloride rich intestinal fluid secretion and shortens GI transit times
Diarrhea meds with IBS
Lopermide
diphenoxylate / atropine (Lomotil)
Lopermide
Imodium (antidiarrheal)
Warnings
Acute UC or pseudo colitis, discontinue if distention, If taking too much, serious cardiac events or death, abnormal heart rhythm, Hepatic dysfunction, CNS Toxicity
Adverse
Abdominal pain, distention, constipation, dry mouth, nausea, drowsiness, dizziness, fatigue, rash
diphenoxylate / atropine
Lomotil 2.5mg/0.025mg (Opioid anticholinergic)
Diarrhea
Contra
<6yrs resp/CNS depression, Sepsis, jaundice, pseudomembranous colitis, bacteria
Warnings
Dehydration, electrolyte imbalance, acute UC
Hepatic/renal impairment, drug users
Interactions
ETOH
Adverse
NVD, Abdominal pain, paralytic ileus, toxic mega colon
diphenoxylate / atropine
Lomotil
controlled substance category
Category 5
Intestinal ischemia
Abdominal pain is most common symptom of intestinal ischemia
Pain out of proportion to exam
Colonic ischemia
Colonoscopy or sigmoidoscopy
used to diagnose colonic ischemia
Goal of treatment for acute intestinal ischemia
restore blood flow as rapidly as possible after initial supportive management
Ischemic bowel
Initial management
GI decompression Fluid resuscitation hemodynamic support electrolytes pain control anti coagulation Broad spectrum ABX
Ischemic bowel
Pain control
Judiciously controlled
use parenteral opioids
Ischemic bowel
Anticoagulation
systemic anticoagulation to prevent thrombus formation
unless patients are actively bleeding
If abdominal exploration is required, continue anticoagulant after surgery
Ischemic bowel
ABX
Broad spectrum ABX
Obstruction Tx
NPO NG suction / decompression IV fluids Pain meds Surgery
Toxic megacolon
Contraindicated:
Bowel prep
barium enema
colonoscopy
Due to risk of perforation
122
122
Vancomycin
non-severe C Diff
WBC <15,000 / serum Cr <1.5
125mg PO QID x 10 days
Fidaxomicin
non-severe C Diff
WBC <15,000 / serum Cr <1.5
200mg PO BID x 10 days
Vancomycin
severe C Diff
WBC >15,000 / serum Cr >1.5
125mg PO QID x 10 days
Fidaxomicin
severe C Diff
WBC >15,000 / serum Cr >1.5
200mg PO BID x 10 days
Fidaxomicin
Dificid (macrolide)
N/D, Abdominal pain, GI hemorrhage, anemia, neutropenia
Diverticulitis tx
Outpatient
Found on CT, can be out patient
Outpatient tx is ABX for 7 to 10 days
reassess 2-3 days after ABX started
Patients who fail outpatient should be admitted
Diverticulitis
Inpatient
Inpatient treatment of acute colonic diverticulitis typically begins with administration of intravenous antibiotics, intravenous fluids, and parenteral pain medications.
Patients can be made nil per os (NPO) to allow for bowel rest or be offered a clear liquid diet depending upon their clinical status.
Patients without complications typically show clinical response within two to three days, at which point their diet can be further advanced.
Patients who continue to improve are discharged with oral antibiotics to complete a total of 10 to 14 days of antibiotic therapy.
Patients who fail inpatient treatment require surgery.
Anti emetics for Mallory Weiss
Metoclopramide
Prochlorperazine
Smooth muscle relaxants
-verine
peppermint oil
anticholinergic / antimuscarinic
Hyo
buytl
atropine
