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gi exam 3 > Inflammatory Bowel Disease > Flashcards

Inflammatory Bowel Disease Flashcards

1
Q

Overlap in sxs between different inflammatory conditions of the colon

A
  • Abdominal pain
  • Changes in bowel
    movements
  • Bleeding
  • Fever
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2
Q

Dysregulation of these three things = chronic inflammation

A

Gut bacteria
Mucosal cells
Immune system

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3
Q

Pathophysiology of Inflammatory bowel disease

A
  • Abnormal levels of
    immunoregulatory and inflammatory
    cytokines
  • Excessive immune cell recruitment
    and activation
  • Changes in the epithelial barrier
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4
Q

Ulcerative Colitis (UC)

A
  • Inflammation, diffuse friability and erosions of mucosal layer of the colon. Usually bleeding
  • Almost always involves the rectum
  • May extend in a proximal and continuous fashion to involve other parts of the
    colon
  • Relapsing and remitting episodes
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5
Q

Hallmark of Ulcerative colitis

A

Relapsing and remitting episodes

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6
Q

Ulcerative Colitis- Epidemiology

A

○ Ulcerative Colitis is 3x more common than Crohn’s Disease
○ Bimodal pattern of onset:
■ Large peak at 15-25 years of age
■ Smaller peak at 55-65 years of age

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7
Q

Ulcerative Colitis- Pathophysiology

A

○ Subsets of T Cells accumulate in the
lamina propria (mucosa)
○ In UC patients, these T Cells are cytotoxic to the colonic epithelium, leading to ulceration.
○ This starts distally, at the rectum, and progresses proximally.
○ Disease spread is continuous WITHOUT: skip area, fistulas, or severe perianal disease.

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8
Q

Ulcerative Colitis- Signs and Sxs

A

○ Onset: usually gradual and progressive, can be abrupt onset
○ Course: relapsing and remitting
○ Chronic (over 4 weeks) of frequently
bloody diarrhea
○ Mucus may also be present in stools
○ Commonly colicky abdominal pain
○ Tenesmus
○ Fecal urgency

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9
Q

Complications and Extracolonic Manifestations of Ulcerative colitis include:

A

■ Erythema Nodosum
○ Toxic Megacolon and malignancy are
more common for UC than Crohn’s.
■ Pyoderma Gangrenosum

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10
Q

Definitive diagnosis of UC requires _____

A

Endoscopy with Biopsy
● Erythematous mucosa with ulcerations extending
from the rectum to all or part of the colon.
● Uniform inflammation without intervening areas of normal mucosa (no skipping).

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11
Q

T/F Abdominal imaging is not required for the diagnosis of ulcerative colitis

A

T

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12
Q

What imaging should be avoided in significant acute UC?

A

Colonoscopy and Barium Enema should be avoided in significant acute disease (until inflammation calms down) because of the increased risk of perforation or Toxic
Megacolon

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13
Q

Two main objectives of UC management

A
  • Terminate the acute, symptomatic attack/flare up.
  • Induction and maintenance of remission
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14
Q

UC Treatment - for acute attack

A

Depends on severity of attack
* Mild acute disease: 1st Mild acute disease : topical (suppository)- Mesalamine (a 5-ASA) x 4-6 wks
* Moderate to severe: * Topical steroids, Oral 5-ASA agents (Mesalamine or Sulfasalazine ), Oral steroids- budesonide or prednisone
* Very severe or refractory: * TNF inhibitor (such as Infliximab or Adalimumab) with or without immunomodulator (Azothioprine), Can add PO steroid (prednisone)

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15
Q

UC treatment - Maintenance of remission

A
  • Preferred: Aminosalicylates (oral or topical)
  • Severe, refractory cases: 1 st: biologic agents- Infliximab (with or without an immunomodulator)
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16
Q

T/F Surgery can be curative for UC

A

T

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17
Q

T/F all patients with UC should get surgery

A

F - Surgery is generally only performed in those with severe disease (25%)

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18
Q

Patients with Ulcerative Colitis should be followed long-term by a
Gastroenterology provider with _____

A

colonoscopy every 1-2 years

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19
Q

The most common cause of death in patients with UC is _____

A

Toxic Megacolon

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20
Q

Crohn’s disease

A

● idiopathic, chronic inflammatory disease
● can affect any part of the gastrointestinal
tract from the mouth to the anus (which is
different than Ulcerative Colitis).
● inheritable risk
● Often waxing and waning of sxs, experiencing periods of symptomatic relapse between periods of remission.

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21
Q

“J Pouch”

A

Surgical option in UC
- Ileal pouch-anal anastomosis

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22
Q

Crohn’s Disease- Epidemiology

A

○ The age of onset has a bimodal distribution
■ Large peak at 15-30 years of age; slightly F>M
■ Smaller peak at 60-70 years of age
○ Most cases begin before the age of 30
○ Smoking increases the risk of developing Crohn’s, and those who smoke have a more severe disease process (more relapses).

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23
Q

Crohn’s Disease- Pathophysiology

A

○ Intestinal inflammation secondary to activation of Type 1 Helper T cells.
○ The inflammatory response – causes non-caseating granulomas throughout the walls of the intestine. Histological finding
○ Ulceration and hypertrophy of the smooth muscles, coupled with inflammation leads to a “Cobblestone” appearance, as well as “skip lesions.”
○ Strictures and fistulas are a common finding in Crohn’s as well, with fistulas forming anywhere in the GI tract.

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24
Q

Crohn’s Disease- Signs and Sxs

A
  1. abdominal pain
  2. diarrhea (with or without gross bleeding)
  3. fatigue
  4. weight loss
25
Q

Crohn’s Disease- Lab findings

A

■ Elevated ESR and CRP (correlates with active flare)
■ Anti- Saccharomyces Cerevisiae Antibody (ASCA) may be positive and may predict earlier need for surgery-
(Yeast found in the GI tract)
○ Stool studies to r/o infectious causes of diarrhea.
○ Fecal Leukocyte testing may be positive.

26
Q

Crohn’s Disease- Diagnosis

A

○ Definitive diagnosis of requires Endoscopy with Biopsy.
■ Colonoscopy is most valuable tool
■ EGD for upper GI lesions

27
Q

Endoscopic characteristics of Chrons:

A

● Erythematous and inflamed intestinal walls
● Ulcerations and fissures
● Most commonly involving the terminal ileum & cecum (beg. of
large intest.) (but can be anywhere)
● Rectum is commonly spared and skip lesions are common
■ Histology of the biopsy reveals transmural (full thickness) disease, often with the presence of non-caseating granulomas.

28
Q

Imaging to avoid in crohns

A

Avoid Colonoscopy and Barium Enema in significant acute disease
(until inflammation calms down) because of the increased risk of
perforation or Toxic Megacolon

29
Q

Mild Crohn disease

A

ambulatory, tolerating an oral diet; <10 percent weight loss, and no
symptoms of systemic disease such as fever, tachycardia, abdominal tenderness, and no
signs or symptoms of obstruction

30
Q

Moderate to severe Crohns disease

A

failed tx for mild to moderate disease; prominent symptoms such
as fever, weight loss, abdominal pain and tenderness, intermittent nausea or vomiting,
or anemia

31
Q

Severe-fulminant disease of crohns disease

A

Patients with persistent symptoms despite glucocorticoids or
biologic agents (infliximab, adalimumab, certolizumab pegol, natalizumab, vedolizumab,
or ustekinumab) as outpatients, or individuals presenting with high fever, persistent
vomiting, intestinal obstruction, peritoneal signs, cachexia, or evidence of an abscess.

32
Q

Crohn’s Disease- Treatment

A
  • Oral 5-aminosalicylates (5-ASAs) (eg, sulfasalazine, mesalamine)
  • Glucocorticoids (eg, prednisone, budesonide)
  • Immunomodulators
    (eg, azathioprine, 6-mercaptopurine, methotrexate)
  • Biologic therapies (eg, infliximab, adalimumab, certolizumab pegol, natalizumab, vedolizumab, ustekinumab)
33
Q

Crohn’s Disease- Treatment of acute attacks

A
  • oral corticosteroids (budesonide x 12 wks,
    prednisone x 8 weeks) taper
  • with or without the addition of aminosalicylates
    (mesalamine)
34
Q

Crohn’s Disease- Treatment of severe refractory cases

A
  • TNF Inhibitor (Infliximab or Adalimumab)
  • May combine with immunomodulator
    (azathioprine or methotrexate)
35
Q

Crohn’s Disease- Maintenance therapy

A
  • Taper steroid and observe
  • May stay on mesalamine long-term
  • If achieve remission on TNF inhibitor- may continue
36
Q

Is surgery curative for crohns?

A

No

37
Q

Smoking cessation is critical for reducing the severity/frequency of
relapses of

A

Crohns

38
Q

Crohn’s Disease- Prognosis

A

○ Chronic relapsing-remitting course
○ Prognosis is generally good
○ In the first year after diagnosis, relapse rate approaches 50%.
○ Most patients will eventually develop complications that require surgical intervention

39
Q

IBD - Lifestyle change

A

● Low FODMAP diet

40
Q

Aminosalicylates:

A

○ Mesalamine (Pentasa)
○ Sulfasalazine (Azulfidine)
○ Olsalazine (Dipentum)

41
Q

Corticosteroid

A

○ Prednisone
○ Methylprednisolone

42
Q

TNF Alpha Inhibitors:

A

○ Infliximab (Remicade)
○ Adalimumab (Humira)
○ Golimumab (Simponi)

43
Q

Aminosalicylates- Mechanism of Action

A

○ Inhibit inflammatory cytokines by
inhibiting Nuclear Factor Kappa B (NF-KB),
a transcription factor for inflammatory
cytokines.
○ Although these are structurally related to salicylates (such as Aspirin), MOA is slightly different.

44
Q

Oral Mesalamine special feature

A

○ Time released to dissolve at pH 6.0-7.0
○ This allows for release into the small
bowel and colon

45
Q

Oral Sulfasalazine special feature

A

○ Minimal absorption by small intestine
○ Requires cleavage to colonic bacteria
→ colonic action

46
Q

Aminosalicylates Indications

A

○ Ulcerative Colitis
○ Crohn’s Disease
○ Sulfasalazine only- Rheumatoid Arthritis

47
Q

Aminosalicylates contraindications

A

○ Febrile viral illness, such as influenza or varicella
○ Caution with hepatic or renal impairments
○ Sulfasalazine should be used with caution with G6PD deficiency
■ Worsening Hemolytic Anemia
○ Can trigger allergic reaction in those with Sulfa allergy

48
Q

Aminosalicylates

A

○ Sulfasalazine has been associated with
Stevens-Johnson Syndrome and Toxic
Epidermal Necrolysis
○ Blood dyscrasias

49
Q

Aminosalicylates follow up/monitoring

A

○ Mesalamine and Sulfasalazine and pregnancy - “Risk of fetal harm is low based on human data”
○ For Sulfasalazine, CBC with diff and LFTs should be checked every 2 weeks for the first 3 months of therapy, and then periodically after that.

50
Q

Corticosteroids MOA

A

○ Anti-inflammatory
○ Inducing clinical remission
○ Not effective in maintaining remission
○ Oral and IV preparations

51
Q

Corticosteroids side effects/adverse effects

A

○ Mood change, insomnia, weight gain, dyspepsia, hyperglycemia
○ Serious potential side effects occur with long-term use.
■ Osteoporosis
■ Osteonecrosis of femoral head
■ Immunosuppression
■ Myopathy

52
Q

Tumor Necrosis Factor Alpha Inhibitors MOA

A

○ TNF-alpha is an important pro-inflammatory cytokine, especially in
diseases like IBD and Rheumatism.
○ TNF-alpha has been called the master regulator of the immune
system.
○ Monoclonal antibodies to TNF-alpha
Epocrates Online. Medscape.
○ These medications bind to and inhibit TNF-alpha, preventing it from
binding to cytokine receptors and promoting inflammation.

53
Q

TNF Alpha Inhibitors Indications

A

○ Autoimmune-driven disease conditions:
■ Crohn’s Disease and Ulcerative Colitis
■ Rheumatoid Arthritis
■ Psoriasis and Psoriatic arthritis
■ Ankylosing Spondylitis

54
Q

TNF Alpha Inhibitors contraindications

A

○ Patients with Latent Tuberculosis infection (can trigger reactivation)
○ Patients who are already immunocompromised
○ Patients with significant active infections

55
Q

TNF Alpha Inhibitors- Side Effects (BBW)

A

○ Risk of Serious Infection- These medications modulate the immune system
significantly through inhibition of TNF-alpha, which places the patient at
increased risk of developing a serious, life-threatening infection.
○ Risk of Malignancy- Again, these medications modulate the immune
system significantly, opening up the possibility of the development of
malignancies.

56
Q

TNF Alpha Inhibitors- Minor Side Effects

A

○ Acute inflammatory reaction- Can occur within 24 hours (usually within 6
hours) of the first dose.

57
Q

TNF Alpha Inhibitors- Major Adverse Reactions

A

○ Serious infection (new, opportunistic, etc)
○ Cancer- melanoma (2x higher) and non-Hodgkin’s lymphoma
○ Reactivation of Hepatitis B Virus Infection

○ Heart failure
○ Liver failure
○ Demyelinating disorders of the Central Nervous System

58
Q

TNF Alpha Inhibitors Follow up

A

○ Immunogenicity: The medication can generate an immune response and antibody
formation against the drug. Leads to loss of response to the drug

gi exam 3 (5 decks)

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