Module 3: Crohns Disease Dr. Covert Flashcards
Dr. Covert EXAM V
IBD Etiology
-not fully understood
-a combination of:
Immunology factors: autoimmune activity against the linage of the GI tract -> Immunosuppressants
Infection
Genetics: tends to run in the family, some genes discovered
Infection: pro-inflammatory microflora in patients with IBD (theory)
Differences Crohn’s Disease vs. Ulcerative Colitis
-Crohn’s disease: patchy areas of inflammation (Cobblestone appearance) in the Gi (also from mouth to anus), Illeal involvement more common, transmural involvement (deep in the layer of the GI mucosa)
-Ulcerative colitis:
continuous area of inflammation primarily in the colon (large intestine), rectal involvement more common
Which symptoms are more common in Crohn’s disease?
-Fatigue, malaise
-abdominal pain
-rectal bleeding (also seen sometimes)
Which symptoms are more common in Ulcerative Colitis?
-rectal bleeding
-abdominal (also seen sometimes)
Common Complications in Crohn’s Disease
-Strictures (narrowing of the affected GI organ e.g small intestine)
-Fistulas (e.g. tunnel between small and large intestinal loop)
-Ulcers
-Malnutrition (bc of a higher percentage of inflammation in Crohn’s disease)
Common Complications in Ulcerative Colitis
-Crypt Abscesses
-Toxic Megacolon
-Colon cancer
Staging of Crohn’s disease
Mild: is the patient ambulatory?, able to take PO, afebrile?
Moderate: failed mild therapy or more fever, weight loss, abdominal pain, tenderness
Severe: failed corticosteroids and biologics (mABs), high fever, persistent N/V, obstruction, abscess
Which drug to use in Mild to moderate IBD?
Aminosalicylates (induction or maintenance of remission)
-more in UC than in CD (oral and rectal depending on the area of inflammation - endoscopy or colonoscopy check)
Counseling points/ Caution in 5-ASA
-allergies to Salicylates and Sulfasalazine/Sulfonamides
-take after a meal (better absorption)
-do not crush (bc they are XR, DR and it would release too early)
-may initially worsen IBD
-may take 4-6 weeks for symptom resolution
ADR of 5-ASA
-headache
-rash
-N/VD
-severe ADR: hepatoxicity (not common)
How to identify the area of inflammation
-Endoscopy
-Colonoscopy
-important bc different drugs work in SPECIFIC parts of the GI
Which drugs work where
Which drug to use to induce remission?
Steroids
systemic steroids: 40-60 mg PO or IV Prednisone daily
-taper when on for > 10 days
-no response after 3-7: poor prognosis
-high dose hydrocortisone for severe disease: 100 mg IV 3-4x daily
Topical steroid
Budesonide for mild Chrohns disease, less side effects since topical
-Entocort EC: capsule released only in the distal part of the GI tract
-Uceris: rectal form
Which agents can be used for Induction and Maintenance
Biologics
-take almost 2 weeks -> consider steroids to “bridge”
-Infliximab (Remicade), Infliximab-dyyb (Inflectra)
-Adalimumab (Humira), Adalimumab-atto (Amjevita)
-Certolizumab (Cimzia)
-Natalizumab (Tysabri)
-Vedolizumab (Entyvio)
-Ustekinumab (Stelara)
Which Anti-TNF agents (bilogics) are commonly used when oral agents failed in UC and CD?
-Adalimumab (SC)
-> when failed:
-Infliximab (IV) + thiopurine
Which biologic is reserved for Crohn’s disease?
Certolizumab (SQ)
What are the side effects of anti-TNF agents?
Black box warnings:
-Tuberculosis infection (they need a negative Tb test)
-Hepatic malignancy (HSTCL)
-also for:
anaphylaxis
worsening of HF
Hep B reactivation
Pancytopenia
What are the second-line biologics
-Integrin receptor antagonists (for patients who failed anti-TNF)
-Vedolizumab (Entyvio) -> more often used
CD and UC
IV infusion
Minimal PML risk (crosses the brain less)
-Natalizumab (Tysabri) - crosses the brain more
CD only
IV infusion
Progressive multifocal leukoencephalopathy (PML)
-> brain damage in those who had a John Cunningham virus
What to screen for when using Natalizumab?
John Cunningham virus (JC virus)
Last line antibitotic
Ustekinumab (Stelara®): Maintenance of
Remission
-MOA: IL-12 and IL-23 antagonist
-SubQ q 4-12 weeks
-used when other biologics fail
-ADR: infections, malignancy
Immunomodulators
Monotherapy or Combination with biologic, Thiopurines preferred
-Thiopurines (Azathioprine, 6-Mercaptopurine)
CD and UC
PO
ADR: Bone marrow suppression, hepatotoxicity
-Methotrexate
CD
IM, SQ
ADR: Bone marrow suppression
Which Immunomodulator should be avoided?
Methotrexate, especially in combination with TNF inhibitor -> HSTCL cancer
Which antibiotic should only be used in Fistulizing Crohn’s disease?
-Fistula: connection between parts of bowels that are normally not connected -> bacteria moving in areas where they are not supposed to be
-gram-negative and anaerobe coverage
-Metronidazile 500 mg IV q8h +
Cipro 400 mg IV q 12h
How to induce remission
-5-ASA +/- Budesonide PO
-continue Budesonide for 8-12 weeks then taper
-Maintenance: 5-ASA
What to do if the patient does not respond/ or moderate/ severe Crohn’s disease?
-5-ASA with 60 mg Prednisone/equivalent (higher steroid dose)
-if they respond: taper the steroid -> continue 5-ASA
What if they still don’t respond?
-add steroid back OR
-add immunomodulator OR
-add TNF inhibitor OR
vedolizumab (integrin receptor antagonist) +/- immunomodulator (thiopurine)
-> Remove 5-ASA
if response: taper steroid after 2-4 weeks, continue biologic +/- immunomodulator (thiopurine)
What if they still don’t respond?
add immunomodulator (thiopurine) if not already OR
consider Ustekimumab
What agent to consider in severe or Fistula Crohns disease?
-Hydrocortisone IV 100 mg q 6-8h
-consider infliximab (TNF-inhibitor) + immunomodulator (thiopurine)
Fistula: same + antibiotics (gram negative + anaerobe coverage)
-Hydrocortisone IV 100 mg q 6-8h
-consider infliximab (TNF-inhibitor) + immunomodulator (thiopurine) + antibiotics
Non-pharmacologic therapies
Nutrition:
-Elimination of exacerbating foods
-Probiotic use
-Nutrition support (gain and maintain weight)
Fecal microbiota transplants: more data needed
