Dyspepsia / GERD / PUD / IBD Flashcards
Define what functional dyspepsia is.
Epigastric pain or discomfort originating from Upper GIT in which NO STRUCTURAL ABNORMALITIES ARE FOUND.
What can cause functional dyspepsia?
-Altered gastric motility
-H. pylori infection
-Altered gut microbiome
-Inflamed Duodenum
-Psych
-Hypersensitive Viscerae
Between GERD & Functional Dyspepsia, which is more common in terms of dyspepsia causation?
Functional Dyspepsia (70% vs. 15% with GERD).
Dyspepsia risk factors?
-Overeating
-H. pylori
-Meds
-Anxious
-IBS
Does smoking or chronic drinking contribute to the development of dyspepsia?
Nope… But worsens pre-existing dyspepsia.
Highlighted drugs that can induce dyspepsia?
-Bisphosphonates
-Fe2+ / K+ Supplements
-NSAIDs
What symptoms qualify as dyspepsia?
-Epigastric Pain / Discomfort
-Fullness / Early Satiety
-Nausea
-Upper Abdominal Bloating
-Excessive Belching / Burping
-Heartburn & Regurgitation
For what length of time must dyspepsia symptoms persist for before it’s considered true dyspepsia?
> 1mth
How to remember alarm symptoms of Dyspepsia?
VBAD
V - Vomiting
B - Bleeding / Anemia
A - Abdominal Mass / Wt Loss
D - Dysphagia (difficulty swallowing) / Odynophagia (pain swallowing)
What symptom (in isolation to others) would warrant a GERD diagnosis (over a dyspepsia diagnosis)?
Heartburn & Regurgitation
Does dyspepsia impact older adults more than younger adults?
Nope… All age groups impacted equally.
What can cause GERD?
-Lower Esophageal Sphincter = Dysfunctional
-Increase IA Pressure
-Hiatal Hernia (upper stomach bulging through diaphragm)
-Esophageal Peristaltic Impairments
-Slowed Gastric Emptying
-Increased Acid Production
GERD risk factors?
-Obese / Preggo
-Fam Hx
-Smoker
-Old
-Stressed
-Meds / Diet
Three highlighted drug classes that can induce GERD?
Anti-Cholinergics
Benzos
Opioids
Dyspepsic-Causing Drugs work by altering GI motility / induction of mucosal damage… How do GERD-Causing Drugs work?
Slow esophageal peristalsis / induction of lower esophageal sphincter relaxation.
Biggest GERD contributor (in terms of diet)?
Eating too much Adam fucking fatty stop putting down Randy’s.
Aside from primary symptoms (ie. Heartburn & Regurgitation), what other secondary symptoms present with GERD?
-Belching
-Hypersalivation
-Chest Pain
-Chronic Cough
-Excessive Throat Clearing
-SOB / Wheeze
In terms of presentation, what would warrant diagnosis of moderate - severe GERD?
- > /= 3d / wk frequency
- > /= 6mths duration
-Nocturnal Symptoms
-Additional Complications
What can GERD complicate into?
-Esophageal Strictures / Esophagitis / Erosions / Cancer
-Barrett’s Esophagus
What is Barrett’s Esophagus?
Cell types turn into cell types normally found in SI… Extremely high cell turnover rate = Preceding Esophageal Cancer Risk (40 - 60 fold increase).
Is the correlation between GERD severity and presence of complications good?
NOOO… Poor correlation.
What is the most useful diagnostic tool for somebody you suspect has GERD?
PPI Trial (NNT = 1.3)… If drug does not resolve symptoms, likely something else.
Define Refractory GERD.
Failed adequate PPI course, typically 4-8wks in length.
What makes somebody at risk for developing Barrett’s Esophagus?
1) Male with >/= 5yrs GERD
OR
2) More than 1d / wk GERD Symptoms
AND 2 OR MORE:
-Over 50yrs
-White
-Obese
-Smoking / Fam Hx
What contrast agent is used in the GERD Swallowing Diagnostic Test?
Barium
GERD most commonly affects people over what age?
> 40yrs
Of the following lifestyle mods, which ones demonstrate evidence of reducing GERD symptoms?
Small meals
Stop smoking
Stand Up 2-3hrs after eat
Elevate head of the bed
Lose & maintain IBW
No food 3hrs before bed
1) Stop smoking
2) Elevate head of bed
3) Lose & maintain IBW
Of the following drugs, which one(s) work fastest:
H2RAs
Alginates
PPIs
Antacids
Alginates & Antacids… As soon as they enter the stomach.
If Alginates & Antacids work fastest of the drug treatment agents for GERD, what limits their usefulness?
Potency… Weak agents relative to H2RAs / PPIs.
Which work faster in GERD treatment: PPIs or H2RAs?
H2RAs (PPIs slowest option take sev days reg use to see effect).
What are the adjunctive GERD pharmacotherapies we can use?
Domperidone
Metoclopramide
Sodium Alginate’s MOA for treating GERD?
Form viscous rafts that float within stomach (makes it way harder for acid to come back up).
Side effects of Sodium Alginate (in spite of no C/Is being demonstrated)?
Bloating, Flatulence, Belching
Is Sodium Alginate useful as a monotherapy for GERD?
Nope… Only ever used as adjunctive therapy.
T or F: Antacids are C/I in all cases of renal impairment.
FALSE… Would avoid use altogether in severe renal impairment, but has an indication in dialysis patients (to help with Phosphate removal).
How do Antacids work?
Neutralize stomach acid & inhibit Pepsin generation.
When should Antacids be taken in order to work most optimally?
20-30mins after eating… If taken too early before meals, will be cleared from stomach & won’t have adequate acid neutralization.
Common side effects of the following Antacid types:
Aluminum
Magnesium
Calcium
Aluminum - Constipation
Magnesium - Laxation
Calcium - None (very well tolerated)
Serious side effects of following Antacid types:
Aluminum
Magnesium
Calcium
Aluminum - Neurotoxic, Reduced BMD, Low Phosphate in blood
Magnesium - High Mg2+ in blood
Calcium - High Ca2+ in blood, Alkalosis
Serious side effects of Antacids are only of particular worry in what patient population?
Renal Impaired + Overusers
Which drugs demonstrate chelative effects due to co-administration of an Antacid?
Bisphosphonates
Sotalol
Digoxin
Phenytoin
Levothyroxine
Tetracyclines
Fluoroquinolones
Which pH-sensitive drugs demonstrate impaired absorption with Antacid co-administration?
Dabigatran
HIV Meds
Aspirin
Which of the traditional H2RAs is the least tolerated?
Cimetidine
Which of the traditional H2RAs is available OTC?
Famotidine
MOA of H2RAs?
Blockade of H2 Receptors = No H+ Pump activity, so parietal cells cannot pump hydrogen ions into the gastric lumen.
T or F: H2RAs only inhibit stimulated gastric acid secretion.
False… Both basal & stimulated acid secretion is inhibited.
Relative to meal times, when should H2RAs be administered?
30 - 60mins before a meal
Common s/e’s of H2RAs include headache, vomiting, diarrhea, drowsiness… What s/e is unique to Cimetidine?
Gynecomastia (& rates of prev. stated s/e’s higher)
What particular drugs demonstrate reduced absorption with co-admin of an H2RA?
Dabigatran, HIV Meds
Reason why we advise against LTU of H2RAs?
Significant tachyphylaxis demonstrated (sometimes as early as 8wks).
Which of the following drugs would be an appropriate therapy for treating Zollinger-Ellison Syndrome?
PPI
H2RA
Antacid
PPI… Condition = Hypersecretor patients (so PPI is best choice).
What indications do PPIs have?
-GERD Sx
-Sx relief / healing esophagitis & ulcers
-Preventing NSAID ulcers
-H. pylori
-ZES (prev. card)
How must PPIs be continually used for in order to get maximal proton pump inhibition?
At least 3 - 5d
Within how many hours after d/c of a PPI is proton pump activity recovered?
24 - 48hrs
Counseling point for PPI administration?
30mins b/4 breakfast
What patients are indicated for “PPI Double Dosing”?
-Standard dose not working after 4 to 8wk trial
-Presenting Erosive Esophagitis
-Ulcers / GI Bleed
-H. pylori eradication
Side effects of PPIs?
-Bitter / Metallic Taste
-ND / Constipation (sometimes)
-Headache / Dizzy
-Rash
Generally very well tolerated!
Serious s/e’s of PPIs?
-Increased C. difficile
-Microscopic Colitis
-Low Mg2+ in blood
-Fracture increases
-Fundic Gland Polyps (>5yrs)
-Reduced B12 Absorption
-Gastric Cancer
Which of the following drugs demonstrates lower levels when co-admin with Omeprazole or Esomeprazole?
Warfarin
Carbamazepine
Phenytoin
Clopidogrel
Citalopram
Diazepam
Clopidogrel (all others increased levels)
Dopamine Antagonist drugs such as Domperidone & Metoclopramide should be administered __ - __ mins before meals and bedtime.
15 - 30mins
In somebody with Parkinson’s, which Prokinetic GERD drug would be an outright C/I?
Domperidone
Metoclopramide
Metoclopramide (induces Pseudo-Parkinson symptoms)… Domperidone would = DOC!
In a patient with QT Prolongation, which Prokinetic agent would be most suitable to use for GERD management:
Domperidone
Metoclopramide
Metoclopramide… Domperidone = C/I!
In patients with a GI Perforation or Hemorrhage, which Prokinetic agent can be used for GERD management:
Domperidone
Metoclopramide
NEITHER!!! Both drugs are outright C/I!
Metoclopramide common s/e’s?
Drowsy, Headache / Dizzy, Muscle Weakness
Domperidone common s/e’s?
Dry Mouth, Headache
Which of the following drugs have significant interactions with Metoclopramide?
Metformin
Ramipril
Paroxetine
Levodopa
-Paroxetine (CYP2D6i & effects potentiated by Metoclopramide)
-Levodopa (anti-Parkinson drug so Metoclopramide opposes its actions)
Which of the following drugs on JA’s PIP profile warrant you considering a therapy switch off of Domperidone (due to the significant DDI)?
Metoprolol
Fluoxetine
Quetiapine
Amiodarone
Quetiapine & Amiodarone (both drugs prolong QT interval).
GERD is considered to be “Refractory” in nature in what two circumstances?
1) Failure 2mth course on a OD PPI
2) Recurrent Sx within 3mths of PPI stoppage
Good things to assess in a Refractory GERD patient?
-VBAD Sx!
-Tried 8wks?
-Ensure adherence / admin of meds is proper!
-Eating too much? Smoking? Elevating head of bed?
-Adjuncts added on!
-Optimize dose… BID regimen!
Provide suitable candidates for PPI deprescribing.
-H. pylori gone!
-No Sx >/= 3 days in a row!
-Treated PUD.
-Mild to Mod GERD but responding to therapy.
Why is abrupt PPI discontinuation not advisable?
Rebound Hypersecretion (can take place even up to 2wks after stopping PPI).
Four cases in which somebody has a valid indication for chronic PPI usage?
1) Barrett’s Esophagus
2) Chronic NSAID / Low Dose ASA & Elevated Bleed Risks
3) Severe Esophagitis
4) Hx Bleeding GI Ulcers
Are H2RAs & PPIs safe to use during pregnancy / while breastfeeding?
Yep! Very safe.
Antacids with what particular bases should be avoided in pregnancy / lactation?
1) Sodium Bicarb (excess fluid retention)
2) Magnesium Trisilicate (cases of fetal bone development abnormalities)
Provide some examples of drugs that are common culprits for causing Drug-Induced Esophagitis.
-Doxy / Tetracycline / Clindamycin
-K+ Tabs
-ASA / NSAIDs
-Bisphosphonates
Provide the most common Aggressive Factors that induce Peptic Ulcers.
H. pylori
NSAIDs
What other Aggressive Factors can induce Peptic Ulcers?
Pepsin
Acid
Alc
Smoking can worsen pre-existing ulcers but does not outright cause.
Mucosal damage due to NSAID usage leads to what?
-Increased acid permeability
-Tissue injury
-Epithelial cells longer to regenerate
-Formation of erosions / ulcers / perforations
COX-1 inhibition is typically associated with the development of Peptic Ulcers… Would utilizing a COX-2 drug like Celecoxib get us off the hook?
Nope… Recent data suggests that COX-2 may provide some degree of stomach protection so Celecoxib technically has some PU formation risk!
Is GI risk in terms of ulcer development strongly correlated with the extent of COX-1 / COX-2 inhibition?
Nope… Doesn’t tell full story (Diclofenac high COX-2 selectivity but RR for PUD is higher than other less COX-2 selective NSAIDs).
Celecoxib’s COX-2 enzyme selectivity is reduced above daily intakes of > ___ mg.
400mg
Provide factors for determining NSAID-induced ulcer risk.
-Hx Uncomplicated Ulcers
-Over 60yrs
-HD / Multiple NSAIDs
-ASA / GCs / SSRI / Anti-Clot drugs on board
-Hx CVD
H. pylori goes undetected by the immune system due to the production of what two metabolites?
Phospholipase
Catalase
When assessing risk factors for NSAID-Induced PUD, one needs >/= __ risk factors to be considered at high risk. __ - __ risk factors would be considered moderate risk.
HR: >/= 3
MR: 1-2
How does H. pylori invoke toxic effects on mucosa?
-Makes mucosal tissue more susceptive to acid damage
-High Ammonia levels (toxic to Epithelial Cells & prevent acidic detection)
-Promote inflammatory response in GIT
What percentage of Peptic Ulcers are asymptomatic in nature?
70%
Dr. suspects you have a Peptic Ulcer… He asks probing questions about pain due to eating, and you tell him that pain goes away after eating, then returns around two hours after eating. Where does your ulcer likely originate?
Duodenum
Dr. suspects you have a Peptic Ulcer… He asks probing questions about pain due to eating, and you tell him that pain gets worse as soon as you put down a meal. Where does your ulcer likely originate?
Stomach (Gastric origin)
Sudden changes in symptom presentation, bad breath, diarrhea post-meals, & unexplained weight loss are potential signs of what?
Perforation / Fistula Development
Which gender do Peptic Ulcers more commonly affect?
Equal…
_______ is the gold standard for diagnosing PUD.
Endoscopy
Endoscopy is indicated for potential PUD patients presenting with what signs and symptoms?
-New onset & over 50
-Alarm Features (VBAD)
-Refractory GERD
-Barrett’s Esophagus Risk
If one is to undergo an Endoscopic exam to rule in or out H. pylori presence, what drugs (& for what length) must be discontinued?
PPIs (for 2wks)
Bismuth / ABs (for 4wks)
Provide risk recurrence factors for PUD.
-NSAID use
-Suboptimal H. pylori eradication
-Smoker
-Alc
-Long Standing PUD
Which of these two Peptic Ulcers (Duodenal or Gastric) take longer to heal?
Gastric (8-12wks)… Duodenal Ulcers take 4-8wks typically.
Rank the following Secondary PU prevention strategies by increasing efficacy:
NSAID + Misoprostol
NSAID + PPI
NSAID + H2RA
Celecoxib + PPI
NSAID + H2RA (least effective)
NSAID + Misoprostol
Celecoxib Monotherapy
NSAID + PPI (equal to each other)
Celecoxib + PPI (most effective)
When should primary prevention strategies for NSAID-induced PUD be initiated?
When one is at high risk (>/= 3 risk factors seen earlier)
How does Misoprostol work in Primary Prevention of NSAID-Induced Peptic Ulcers?
PG analogue; increases gastric mucous production, bicarbonate secretion, inhibits basal / nocturnal gastric acid secretion.
What is the indicated Misoprostol dose for NSAID-Induced Ulcer prevention?
200mcg QID
1st line H. pylori eradication regimens?
PBMT x 2wks
PAMC x 2wks
2nd line H. pylori eradication regimens?
PAL
PABL
Provide the two week dosing schedules for PBMT.
PPI - Stan. Dose BID
Bismuth - 524mg QID
Metro - 500mg TID-QID
Tetra - 500mg QID
Recent prescribing of what AB class warrants picking PBMC over PAMC for H. pylori eradication?
Macrolides (ie. Erythromycin, Azithromycin, Clarithromycin).
What benefit does the PAMC regimen have over PBMC?
Patient adherence easier (all meds dosed BID instead of QID)
You work at a community pharmacy and see the following scripts come through. What is your next course of action?
1) Pantoprazole 40mg BID x 14d
2) Amoxicillin 1000mg BID x 14d
3) Clarithromycin 500mg BID x 14d
For H. pylori eradication
Contact physician & discuss switch to Quad Regimens… Much more effective & reduced bacterial resistance rates in comparison to Triple Therapy regimens!
If PAMC fails, can I jump ship & use the PBMT therapy strategy to eradicate H. pylori infection?
Yes… However, PBMT to PAMC appears to be ineffective.
Once H. pylori is eradicated, how long do we continue PPI maintenance therapies?
Duodenal Ulcer
Gastric Ulcer
Duodenal: Not indicated (generally)… Possibly 2wks.
Gastric: Continue PPI for 8wks.
In cases of continuing PPI, drop to OD use!
With patients who have non-H. pylori, non-NSAID induced ulcers, what is the only treatment option?
PPI x 4-8wks
Preferred PPIs in pregnancy & lactation for PUD management?
Pregnancy: POL
Lactation: Pantoprazole
In cases of pregnant women with severe H. pylori-Induced PUD, which of the two first-line regimens would you recommend?
PBMT
PAMC
PAMC… Avoid Tetracycline & Bismuth!
Are ‘skip lesions’ common with Ulcerative Colitis?
No… Crohn’s yes.
Is rectal sparing common in Crohn’s Disease?
Yes… With Ulcerative Colitis we never see rectal sparing (is always rectal involvement)!
Between Ulcerative Colitis & Crohn’s, which disease state do we see Fistulas being commonplace?
Crohn’s… Never see Fistulas with UC!
Are Strictures & Granulomas common with UC? Crohn’s?
UCs: Occasional (but not common).
Crohn’s: Common!
Peak onset of Irritable Bowel Disease (IBD) occurs between __ - __ years of age.
15 - 40yrs
T or F: IBD generally has a defined trigger.
False… Initial trigger generally of idiopathic or unknown cause.
Ulcerative Colitis begins in the ____, spreading proximally.
rectum
Crohn’s Disease begins most commonly in the ____ / _____ ____ & spreads in any direction.
Ileum / Proximal Colon
T or F: Nicotine consumption helps protect against the development of UC.
True! Relaxes SM in the Colon, which appears to help with symptoms or disease development.
What are some predisposing risk factors for the development of IBD?
-Age 15 to 40
-Genetics
-Poor Diet
-Sedentary
-Obesity (pro-inflammatory state)
Which Omega Fatty Acid can help with IBD?
Omega 3s… 6 & 9 pro-inflammatory & bad.
Which two drug classes serve to be a risk factor for IBD exacerbation / development?
Broad Spectrum ABs
NSAIDs
Between UC & CD, which one has the higher relapse rate?
UC (»> CD)
Between UC & CD, which one has the higher mortality rate?
CD (1.4 - 5x higher)
Complications of IBD?
-Colon Removal
-Osteoporosis
-VTE
-Anemia
-Gall / Bladder / Kidney Stones
Sx of IBD?
-Abdominal Pain
-Diarrhea
-Constipation (if Strictures develop)
-Mucousy / Bloody Stool
-Wt Loss
-Fever / Sweaty
-Malaise
-Joint Pain
What would be examples of monitoring parameters in IBD treated patients?
-Hemoglobin / Iron
-Nutrition Status
-BMD
-Colonoscopy (within 8yrs onset of disease)
Non-Pharm suggestions to someone who has IBD?
-Increase Fiber
-Lower Fat Intake
-ID “Trigger Foods”
-Supplementation (Zinc, Mg2+, Ca2+, Fe2+, B12, Folic Acid, Vit. ADEK)
Smoking Cessation ____ risk & relapse rates in Crohn’s Disease, whereas it ____ risk & relapse rates in Ulcerative Colitis.
Crohn’s: Reduces risk & relapse rates for IBD.
UC: Increases risk & relapse rates for IBD.
What does true IBD remission look like?
1) Sx Free
2) No Inflammatory Consequences
3) Not Steroid Dependent
Patient has the following presentation of Ulcerative Colitis:
-Passes 6 stools daily (5 over usual baseline)
-Bloody Stool
-Accompanying Fever, HR = 130 BPM, Low Fe2+
Would a topical corticosteroid be appropriate to use?
Nope… Severe UC in this case, so only Oral CS’s should be used (need stronger systemic effects)!
Patient has the following presentation of Ulcerative Colitis:
-Passes 3 stools daily (2 over baseline)
-Blood streaks in stool
-Body Temp = 37 Celsius, HR = 65 BPM
Would a topical corticosteroid be appropriate to use?
Yes… Mild presentation of UC so would be appropriate in this case!
Can topical corticosteroids be used to manage Crohn’s?
Only oral agents… No rectal involvement like in UC so no sense using topicals.
In cases of Severe UC / Crohn’s, what corticosteroid would be ideal for use?
Budesonide
Prednisone
Prednisone… Stronger option.
In cases of Mild - Mod UC / Crohn’s where we can localize which GIT segments are being affected, what corticosteroid would be ideal for use?
Budesonide (as it has targeted effects & way less systemic side effects)
Counseling point to mention to a patient taking topical corticosteroids for UC / Crohn’s management?
Lie on your left side & do your best to retain drug contents for > 30mins.
What is the target dose of Prednisone for those with UC / Crohn’s?
40 - 60mg Daily
Describe the Budesonide tapering strategy for those on it for IBD management.
9-6-3-0 (over 4wks)
Symptom improvement for those initiating IBD CS courses can be seen as early as __ - __ days.
2 - 3 days
On average, it takes __ - __ weeks to see remission of an IBD flare with those on corticosteroids.
2 - 4wks
Common corticosteroid s/e’s (come on you better know these by now).
-GI Intolerance
-Increase Eating
-Nervous / Anxious
-Insomnia
-Tremors
-BG Increases
-GI Bleeds
-Cushingoid Features
-Osteoporosis
-Cataracts
Is Mesalamine (ie. 5-ASA) an effective agent for acute Crohn’s flares or as a maintenance therapy for Crohn’s?
Nope… Indications of Aminosalicylates such as SSZ, Olsalazine, & Mesalamine is in Ulcerative Colitis!
Can we use Mesalamine as a monotherapy in Mod - Severe Ulcerative Colitis (ie. As Induction Therapy)?
Nope… Must be in combination with Prednisone. However, in mild UC, can use 5-ASA as a monotherapy!
Can 5-ASA be used for Mild - Moderate UC as a remission monotherapy?
Yep! Just at Induction should be used in combination with a steroid. As maintenance therapy, is fine as a monotherapy.
A patient previously demonstrated an allergic reaction to TMP / SMX (dermatitis rash). They are being initiated on Mesalamine (in combination with Prednisone) for Induction of Ulcerative Colitis. Is this okay to fill?
Yep… Hypersensitivities to Sulfonamides sees Sulfasalazine being the only outright contraindication to the potential Sulfamethoxazole allergy. 5-ASA & Olsalazine are okay to fill!
JA has mild hepatic impairment, eGFR of 28, and a diagnosis of Ulcerative Colitis. Her doctor wants to initiate Sulfasalazine for disease management. Is this okay?
Nope (C/I)… Due to eGFR being < 30. Mild Hepatic Impairment would have been fine (only outright C/I in Severe Hepatic Impairment).
Which of the three Aminosalicylate drugs for treating UC (Mesalamine, Sulfasalazine, Olsalazine) is a prodrug that gets converted to active drug in the Colon?
SSZ… Converted into 5-ASA in Colon. Mesalamine already exists as 5-ASA.
Mezavant dose for UC Induction?
2.4 - 4.8g OD
If I require a topical dosage form for treating UC, which would be ideal if I need it to reach the Distal Colon?
Enema… Suppository only reaches the Rectum.
Aside from typical GI side effects (NVD / Abdom Pain), what unique side effect to SSZ exists?
Lowered Sperm Count (reversible upon d/c drug)
Serious side effects of Aminosalicylate drugs?
-Hepatotoxic
-Photosensitive (SSZ)
-Bone Marrow Toxicity (SSZ)
-Blood Abnormalities
Significant DDIs with Mesalamine?
Azathioprine / Mercaptopurine (increases the toxicity of both these agents)
Which brand name oral Aminosalicylate product is able to reach all locations in the Small & Large Intestines, as well as the Rectum?
Pentasa (form of Mesalamine)
Is Mezavant able to act at proximal segments of the Small Intestine (ie. Duodenum & Jejunum)?
Nope… Only at the Ileum (distal segment of the SI) & Large Intestine.
Can oral Methotrexate be used to treat IBD?
Nope… Must be the Sc dosage form in order to get benefits.
Name of the Integrin Receptor Blocker that can be used to treat IBD?
Vedolizumab
Name of the IL-12 / 23 Inhibitor that can be used to treat IBD?
Ustekinumab
Primary indication in IBD for Immunomodulator usage (ie. Azathioprine / Mercaptopurine)?
Steroid Dependent Patients
Define what a “Steroid-Dependent” patient is in the context of IBD-indicated Immunomodulator use.
Two or more courses of steroids in past year
OR
More than 12wks use of steroids per year
Can Azathioprine / Mercaptopurine be used as monotherapies in Crohn’s Induction?
Nope… Must be part of a multi-therapy regimen (work waaaaaay too slow 3-6mth OOA).
How do we titrate Purine Antagonist drugs in IBD treatment regimens?
Start empirically at 50mg daily, increase by 25mg every 1-2wks until weight based dosing targets are met!
Although it has a much slower OOA compared to other biologics, what benefit does Vedolizumab have over other therapies?
Lower Infection Rates (as it’s gut selective in nature).
Significant DDIs of the Purine Antagonist drugs (ie. Azathioprine / Mercaptopurine)?
Allopurinol / Febuxostat (their toxic effects greatly increased with co-admin of Purine Antagonist drugs).
Which biologic option appears to have the most efficacy in treating IBD?
Infliximab (slightly better than others in the TNF-alpha class).
Combo Therapy trends in UC management?
-Induction rates greater with combo steroid + Aminosalicylate
-Combo oral Aminosalicylate with Enema greater induction
-Combo of biologic with Azathioprine improves induction & maintenance
-Little evidence for Mesalamine & Immunomodulator combo
Combo Therapy trends in Crohn’s management?
-Pred + SSZ better than monotherapy
-Pred + AZA = Faster time to induction
-Biologic + AZA / MP = Better induction / maintenance, greater steroid sparing, & less AB formation (but increased toxicity)
What is the go-to combination AB regimen used to prevent sepsis in Crohn’s patients?
Metronidazole + or - Ciprofloxacin
Favored class of anti-depressant used to treat co-morbid IBD & depression / anxiety?
TCAs (appear to lower relapse rates, increase QOL, reduce need for steroids).
