IBD Of The Colon Flashcards

1
Q

What is the most characteristic feature of crohn disease?

A

“Skip-like” inflammatory lesions involving all layers of the gut wall that can be found anywhere in the alimentary tract, but usually is found in the terminal ileum

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2
Q

Bowel symptoms between CD and UC

A

CD: (usually diagnosed in 20s)

  • intermittent abdominal pain and cramping
  • watery diarrhea that infrequently has blood in it (although it can)

UC: (usually diagnosed in 30s)

  • abdominal pain only when defecating
  • almost always bloody diarrhea
  • urge incontinence and tenesmus
  • increased stool frequency
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3
Q

Systemic symptoms of CD and UC

A

CD:

  • weight loss
  • fever
  • bloating
  • postprandial nausea

UC: (way less common than CD)

  • weight loss
  • fever
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4
Q

Extra manifestations of UC and CD

A

CD:

  • canker sores (aphthous ulcers)**
  • esophageal ulcers and dysphagia
  • waxy skin tags on anus**
  • anal diseases
  • osteopenia
  • arthropathies
  • erythema nodosum/gangrenosum (more common)**

UC:

  • osteopenia
  • arthropathies
  • erythema nodosum/gangrenosum (less common)**
  • primary sclerosing cholangitis**
  • opthalamologic manifestations**
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5
Q

What is “indetermittent colits”?

A

IBD that cant be distinguished between UC or CD
- these cases are exceptionally difficult to determine proper treatment

**also need to know before doing colon resection since UC will be “cured” but CD will not be sure in this

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6
Q

What is the histology findings in CD

A

Non-caseating granulomas
- live cells inside

Crypt atrophy

Transmural ulcers (“bear claw ulcers”)

“Skip areas”

Granulation tissue with monocyte infiltrates

Fistula/abscesses and strictures of all layers (may or may not be found)

Aphthous ulcers in bowel walls

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7
Q

What is the histology findings in UC

A

Ulcers that only affect mucosa layer

Mild crypt branching and abscesses

“Cryptitis” (crypts grow into the goblet cells)

Pa colonic inflammation

Mucosal damage with normal serosa

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8
Q

Gross pathology of CD

A

Bowel will show strictures and ulcers (narrowing lumen)
- will also show “creeping fat” where the mesentery moves to engulf the bowel stricture sections

Thick inflamed transmural bowel
- NEVER effects the rectum and usually not the. Sigmoid colon

Also may show pseudopolyps

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9
Q

Ashkenazi jews and IBD

A

Have the highest documented rates of all subsections of populations.
- also has the highest amongst all Jewish cultures

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10
Q

Gross pathology of UC

A

Shows “pancolitis”

  • the entire colon can be involved in the inflammatory process
  • also is usually chronic

Can show pseudopolyps and hemorrhages

There will be NO creeping fat

Can show “lead pipe” appearance also
- colon loses haustra

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11
Q

Blood testing in CD/UC

A

Both need the following 4 tests

1) CBC
- look for microcytic/microcytic anemia
(Macrocytic is more common in CD patients especially if they have had terminal ileal resection)
- elevated WBC

2) liver function tests
- AST/ALT levels (will especially be high in primary sclerosing cholangitis)
- bilirubin, albumin, transferrin levels

3) inflammatory markers
- CRP (more commonly elevated in CD)
- ESR (more commonly elevated in UC)

4) serum antibodies
- p-ANCA (more commonly elevated in UC)
- ASCA (more commonly elevated in CD)

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12
Q

Imaging for diagnosis of CD/YC

A

CTR enterography with oral contest

MRI enterography
- very useful in pregnancy and children**

Small bowel follow-through (SBFT)

MRI/CT of the abdomen
- MRI is better across the board

Plain film radiography of abdomen
- useful for accessing toxic or perforated colon**

Colonoscopy w/ biopsy
- gold standard for diagnosis for IBD

Capsule endoscopy
- be very careful if structures are suspected (need to use dissolvable potency pill in this case)

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13
Q

Smoking and IBD

A

Smoking increases the odds of getting IBD
- is the #1 environmental risk factor

HOWEVER, it is actually protective against UC, but increases risk of CD

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14
Q

Genetic risk factors for IBD

A
#1 risk factor is a family member has IBD (especially siblings) 
- Chance and risk is increased 17x in this case 

IBD risk of monozygotic twin = 50%

2 affected family members = 30%

Dizygotic twin = 7-10%

Being genetically Jewish = 6.6%

Being white with 1 first degree relative affected = 3.3%

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15
Q

3 most commonly associated genes for IBD

A

NOD2

  • role is defense from bacteri a
  • shows severe CD

ATG16L1

  • role is Autophagy for immune system
  • often shows ileal CD or mild UC

IRGM

  • role is Autophagy
  • shows mild CD and/or UC
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16
Q

Treatments for IBD

A

Mild = topical corticosteroids and 5-ASA is usually first line

Moderate = immunomodulators and oral corticosteroids is first line

Severe surgery = biological antibodies/Natalinzumab (anti-integrin antibody)

Last resort/extreme secondary effects = go surgery
- these people are called “refractory IBD populations”

17
Q

When is surgery usually required for CD?

A

Once transmural thickening occurs = strictures = bowel obstruction = surgery

also needs surgery once fistula/abscess occurs (if it does)

18
Q

What is the general indication for all mainstay medications in IBD?

A

Corticosteroids

  • short-term only
  • reducing inflammation

5-ASA

  • can use long and short term
  • used for maintaining remission

AZA/6-mercaptopurine

  • long term use only
  • steroid reduction and weaning maintenance therapies

TNF antagonists

  • short and long term
  • induction of remission and maintance of remission
  • ** infliximab is the most popular and is very good at fistula treatment. However effectiveness is poor long term

Methotrexate

  • only for long term Crohn’s
  • maintenance for remission
  • **usually only reserved for people who cant use anti-TNF antagonists

Cyclosporine

  • only for short term UC
  • maintenance for remission
  • **used only in failure of IV corticosteroids and is last ditch drug

Natalizumab (anti-integrin drug)

  • monotherapy for Crohn’s only
  • absolutely last resort for severe CD patients
  • **need to check for JC virus antibodies before use (if they have this, it will reactivated JCD)
19
Q

Azathiopurine and 6-MP

A

Usually only used after clinical relapse or corticosteroid dependency develops

Is controversial monotherapy and therefore is usually used together with anti-TNFs

before beginning, must check levels of natural TPMT enzymes (if numbers are low = rapid/severe leukopenia)

20
Q

Can you use antibiotics for CD/UC treatment

A

NO
- doesn’t treat it at all

can still use though, just not for UC/CD treatment, more so for secondary infections

21
Q

Top down vs bottom up treatments

A

Bottom-up
- normal train of thought along treatment pyramid

Top-up
- reverses the pyramid and starts with anti-TNF factors and works back down to safer meds

**surgery is always last resort in both or unless a stricture/secondary complication occurs*

22
Q

Colo-rectal cancer and IBD

A

inflammation is always a risk factor for development of cancer

15% of IBD patients go on to die from colo-rectal cancers

23
Q

Where is the most common recurrence of CD with surgery?

A

At the anastomosis site