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Gastrointestinal 2 > Clinical Presentation of IBD > Flashcards

Clinical Presentation of IBD Flashcards

1
Q

What is important regarding the pathophysiology as it relates to treatment for IBD?

A
  • there is increased permeability within the tight junctions allowing pro-inflammatory cytokines to be activated (mainly TNF-a).
  • circulating T cells with integrin-a4B7 bind to endothelial cells increasing entry of gut specific T cells.
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2
Q

Does decreased physical activity and obesity increase your risk for Crohn’s disease?

A

YES

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3
Q

How does ulcerative colitis present clinically?

A
  • diarrhea (often bloody), frequent but small volume
  • urgency
  • colicky abdominal pain
  • gradual and progressive onset
  • in moderate to severe disease= fever, pallor, tenderness, and muscle wasting
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4
Q

Do most patients with ulcerative colitis present with mild disease?

A

YES= less than 5 stools/day, no systemic toxicity, and mild crampy pain.

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5
Q

What are the lab/imaging findings for acute ulcerative colitis?

A
  • anemia
  • elevated sed rate (always elevated for inflammation)
  • low albumin
  • electrolyte abnormalities
  • elevated fecal calprotectin (BEST)
  • p-ANCA
  • thickened bowel wall on CT
  • loss of haustra on barium swallow
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6
Q

How do you basically diagnose ulcerative colitis?

A
  • exclude other causes (history, labs…)

- diarrhea greater than 4 weeks + active inflammation on colonoscopy + chronic changes on biopsy

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7
Q

What will you see on a colonoscopy for ulcerative colitis?

A
  • loss of vascular markings (engorgement)
  • erythema, granularity
  • petechiae, exudates, edema, erosions, friability
  • pseudopolyps
  • profuse bleeding
  • ALWAYS involves RECTUM and proceeds proximally in a circumferential pattern.
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8
Q

Do we always biopsy the ileum in IBD?

A

YES to help us discern whether it is Ulcerative colitis or Crohn’s disease

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9
Q

Do patients with just proctitis (inflammation of the rectum) have a more benign course in ulcerative colitis?

A

YES

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10
Q

What is the goal with treatment of ulcerative colitis?

A

heal the mucosa, thus decreasing the risk of colectomy (removal of colon).

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11
Q

What are the complications of ulcerative colitis?

A
  • toxic megacolon (greater than 5 cm)= increased colonic diameter with systemic toxicity. This can lead to perforation (50% mortality).
  • benign strictures (MALIGNANT mass until proven otherwise).
  • dysplasia/colorectal cancer (highest risk in pancolitis).
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12
Q

What are the extraintestinal manifestations of ulcerative colitis? (see printout)

A
  • PRIMARY SCLEROSING CHOLANGITIS= inflammation of intra and extra hepatic bile ducts leading to cholestasis (look for beaded strictures of bile ducts on ERCP). Independent of disease activity.
  • ankylosing spondylitis (more in Crohn’s; independent of disease activity)
  • peripheral arthritis (independent of disease activity)
  • osteopenia/osteoporosis
  • pyoderma gangrenosum (independent of disease activity).
  • aphthous stomatitis (canker sores)
  • sweets syndrome=sudden onset of fever, leukocytosis, and tender, red, well-demarcated papules and plaques (not specific to IBD).
  • increased risk of venous thromboembolism
  • hemolytic anemia
  • uveitis (independent of disease activity)
  • episcleritits
  • erythema nodosum (more in Crohn’s)
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13
Q

Does treatment of IBD affect the course of primary sclerosing cholangitis?

A

NO

*you could take out the entire colon and you would still have primary sclerosing cholangitis.

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14
Q

Does primary sclerosing cholangitis increase your risk for colon cancer?

A

YES. Therefore you must get a colonoscopy every 1-2 years when you have this.

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15
Q

Is there a cure for IBD?

A

NO

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16
Q

What are the 2 goals for managing IBD?

A
  1. induce remission

2. maintain remission

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17
Q

What is mesalamine (5-ASA)?

A
  • oral medication used ONLY for IBD, developed to prevent proximal absorption via ph and time dependence along with a colonic bacteria requirement for activation. Works by inhibitings pro-inflammatory cytokines, cause immunosuppression, free radial scavenger, and impairs leukocyte function.
  • topical formulation via enema exists as well.
  • used only for mild-moderate ULCERATIVE COLITIS (sometimes for crohn’s).
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18
Q

Does mesalamine reach past the splenic flexure?

A

NO

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19
Q

What is Azathioprine?

A
  • rapidly metabolized to 6-mercaptopurine (6-MP), which inhibits proliferation of B and T cells, and causes apoptosis of T cells.
  • TPMT (thiopurine S-methyltransferase) will convert 6-MP to an inactive metabolite. Thus TPMT must be measured in all pts prior to starting this drug.
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20
Q

If a pt has homozygous non-functional alleles for TPMT, can you use azathioprine?

A

NO

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21
Q

If a pt has heterozygous non-functional alleles for TPMT, can you use azathioprine?

A

YES but decrease the dose

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22
Q

What do we use to monitor drug levels of azathioprine?

A

6-thioguanine (6-TGN) to measure for toxic effects.

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23
Q

When is azathioprine used?

A

in pts who have steroid refractory UC and Crohn’s disease

*takes 6 months to take effect (usually used in combination with other drugs)

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24
Q

** What is a side effect of azathioprine? (TEST QUESTION)

A

hepatosplenic T cell lymphoma

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25
Q

What is Methotrexate?

A

folic acid analogue that inhibits dihydrofolate reductase. It somehow helps with maintenance of remission in Crohn’s disease but we don’t know how.

26
Q

What is Cyclosporine A?

A
  • inhibits calcineurin to block transcription of cytokine genes in T cells. Induces remission in ACUTE SEVERE STEROID REFRACTORY ULCERATIVE COLITIS.
  • rapid onset (1-2 weeks) but only used short-term.
27
Q

What are the side effects of cyclosporine A?

A

infections, seizures, low cholesterol, nephrotoxicity, and neuropathy

28
Q

What are the biologics?

A

inhibitors of TNF-alpha (this is the new craze)

  • infliximab (used for both UC and crohn’s)= chimeric (mouse/human) and therefore we can mount an antibody response to it; IV infusion every 8 weeks.
  • adalimumab (used for both UC and crohn’s)= fully human and less likely to form antibodies agains it; SQ injection every 2 weeks.
29
Q

What are the side effects of the biologics (TNF-alpha inhibitors)?

A
  • infections (latent TB or hepatitis B)
  • malignancies (RARE)
  • heart failure
  • cutaneous (viral or bacterial infection)
  • demyelinating disease
30
Q

What is Vedolizumab?

A
  • newest integrin receptor antagonist that is a humanized immunoglobulin against alpha-4-beta 7 integrin. This inhibits trafficking of lymphocytes and its action is confined to the GI tract.
  • used for induction/maintenance of remission in REFRACTORY UC and CROHN’S.
31
Q

What is the advantage of Vedolizumab over the TNF-alpha inhibitors?

A

no known risk of major infection or malignancy

32
Q

What is oral prednisone or IV solumedrol or topical rectal hydrocortisone?

A
  • corticosteroids used ONLY to INDUCE REMISSION in UC and Crohn’s.
  • safe to use in pregnancy
33
Q

What are the side effects of corticosteroids?

A

psychosis, anxiety, HTN, salt retention, muscle wasting, weight gain, hyperglycemia, osteoporosis, and infection risk.

34
Q

** What steroids do we use more now?

A

intraluminal steroids that remain longer in the GI tract.

  • Budesonide is used for mild-moderate CROHN’S in the ileum and proximal colon
  • Budesonide-MMX is for delivery to the entire colon in mild-moderate UC.
  • side effects are rare due to 90% first past metabolism.
35
Q

Can antibiotics be used in Crohn’s?

A

rarely but can sometimes be used (bacterial overgrowth or Clostridum difficile).

36
Q

What are the basic principles for managing acute IBD symptoms? (remember IBD is a chronic disease with acute flare ups)

A
  • determine if symptoms are really from IBD
  • determine outpatient vs impatient
  • rule out complications (not everyone needs imaging)
  • bowel rest if severe symptoms (NPO then clears, then low fiber).
  • IV fluid if hospitalized
  • determine if colonoscopy will change management
  • continue maintenance medication
  • add medication for induction (steroids most common)
37
Q

What is the first line INDUCTIVE treatment for mild-moderate ulcerative proctitis/proctosigmoiditis (aka ULCERATIVE COLITIS)?

A
  • topical 5-aminosalicylic acid (5-ASA) or suppository or enema depending on location.
  • if this doesn’t work, add a rectal steroid, followed by an oral steroid if that doesn’t work.
38
Q

What is the MAINTENANCE treatment for mild-moderate ulcerative proctitis/proctosigmoiditis (aka ULCERATIVE COLITIS)

A
  • nothing if 1st episode and you had a prompt response to inductive therapy.
  • if you relapse, then 5-ASA (mesalamine) and/or rectal 5-ASA.
39
Q

What is the INDUCTION therapy for mild-moderate left-sided/extensive colitis, pancolitis (aka ULCERATIVE COLITIS)?

A

oral + topical 5-ASA

*if no response add rectal steroid, followed by oral budesonide-MMX if that fails.

40
Q

What is the MAINTENANCE treatment for mild-moderate left-sided/extensive colitis, pancolitis (aka ULCERATIVE COLITIS)?

A
  • oral 5-ASA +/- topical 5-ASA

* can’t do rectal steroids long term

41
Q

What is important to remember about oral steroids (prednisone)?

A

must taper gradually

42
Q

What is steroid DEPENDENT UC?

A
  • unable to taper prednisone below 10 mg or they relapse within 3 months
43
Q

What is the initial management for severe/fulminant colitis (aka ULCERATIVE COLITIS)?

A
  • oral prednisone + high dose oral 5-ASA + topical 5-ASA/steroid
  • discontinue anticholinergics, antidiarrheals, NSAIDS, and opiates
  • if they don’t respond, hospitalize and give them IV steroids.
44
Q

How do you treat severe/fulminant UC that is steroid REFRACTORY in the hospital?

A
  • anti-TNF (infliximab)
  • cyclosporine to transition to azathioprine (similar to steroid dependent).
  • colectomy
45
Q

Are corticosteroids for short term use only?

A

YES

46
Q

How do you treat steroid DEPENDENT (can’t taper steroids to less than 10 mg) UC patients?

A
  • azathioprine/6-MP for maintenance
  • OR- add IV cyclosporine to transition more quickly to azathioprine.
  • if they do not respond, go to colectomy.
47
Q

What surgery can be done for pts who do not respond to medical therapy for UC?

A
  • proctocolectomy with ileal pouch-anal anastomosis
48
Q

What is chromoendoscopy?

A
  • stains or pigments (blue) sprayed during colonoscopy to improve tissue location when looking for dysplasia/colorectal cancer
49
Q

How is CROHN’S DISEASE classified (vienna classification)?

A
  • inflammatory= just inflammation
  • stricturing= inflammation with narrowed lumen (either inflammatory; can treat medically, -OR- fibrotic; requires surgery).
  • penetrating (fistulizing)= inflammation with abnormal communication between bowel and other structures.
50
Q

What is a phlegmon/abscess that occurs due to CROHN’S DISEASE?

A
  • phlegmon= walled off inflammatory mass w/o infection.

- abscess= + infection, localized peritonitis.

51
Q

What is perianal disease (associate with CROHN’S DISEASE)?

A
  • pain and drainage from large skin tags, anal fissures, perirectal abscesses, or anorectal fistulas.
52
Q

** What are the unique extraintestinal manifestations for CROHN’S DISEASE?

A
  • renal stones (calcium oxalate)
  • bone loss/osteoporosis
  • B12 deficiency
53
Q

Will you see perianal disease in crohn’s or UC?

A

ONLY CROHN’S

54
Q

How do we diagnose CROHN’S?

A
  • if abdominal pain= imaging
  • if diarrhea= colonoscopy
  • anti-saccharomyces cerevisiae antibody (ASCA), CRP, and fecal calprotectin are also used.
55
Q

Why is management of CROHN’S DISEASE so much different than management of UC?

A

bc we use the BIG GUNS first for CROHN’S, whereas we start lightly with UC and work our way up.

56
Q

What is the management for mild-moderate CROHN’S DISEASE?

A
  • oral 5-ASA
  • antibiotics if no response
  • oral steroids if no response.
57
Q

What is the management for refractory/severe CROHN’S DISEASE?

A
  • azathioprine/6-MP
  • methotrexate
  • biologics (vedolizumab)
58
Q

Should you give steroids to a pt with fistulas or localized peritonitis from CROHN’S?

A

NO bc these are infectious and steroids will make it worse.

*treat with antibiotics instead.

59
Q

How do you treat an abscess due to CROHN’S?

A

antibiotics and drain.

60
Q

Is the risk of colorectal cancer higher or lower in Crohn’s vs UC?

A

lower than UC

Gastrointestinal 2 (18 decks)

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