Exact mechanism unknown but thought the be a combination of factors including: - damage to epithelial mucin proteins and tight junctions - breakdown of homeostatic balance between host's mucosal immunity and enteric microflora - genetic polymorphisms in toll-like receptors - disrupted homeostatic balance between regulatory and effector T cells - Host immune response to own gut flora - imbalance and deregulation between regulatory and effector T cells

- symptoms wax and wane - rectal bleeding - bloody diarrhea - fecal urgency - tenesmus - abdominal pain LLQ and suprapubic pain - abdominal tenderness - aphthous oral ulcers - iritis- severe eye pain and photophobia - seronegative arthritis with flares - erythema nodosum on lower extrem. and extensors - autoimmune hemolytic anemia - primary sclerosing cholangitis

- gradual onset of diarrhea less than 4 days and intermittent bloody mucoid stool - urgency and tenesmus - LLQ cramping relieved by bowel movement - mild fever, anemia, hypoalbunemia

- gradual onset of diarrhea less than 6 days and intermittent bloody mucoid stool - urgency and tenesmus - LLQ cramping relieved by bowel movement - mild fever, anemia, hypoalbunemia

- more than 6 bloody diarrhea stools/day - severe anemia, hypovolemia, hypoalbunemia with nutritional deficit - abdominal pain and tenderness - fulminant colitis - pulse over 90 - fever over 37.5C - ESR over 30

- based on clinical symptoms and confirmed by sigmoidoscopic and colonoscopic and histologic examination

IBD Flashcards by Kristin Shaw

Patho of IBD

Exact mechanism unknown but thought the be a combination of factors including:

damage to epithelial mucin proteins and tight junctions
breakdown of homeostatic balance between host’s mucosal immunity and enteric microflora
genetic polymorphisms in toll-like receptors
disrupted homeostatic balance between regulatory and effector T cells
Host immune response to own gut flora
imbalance and deregulation between regulatory and effector T cells

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Where is IBD prevalent and why?

W. world due to diet and environment

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Two types of IBD

ulcerative colitis and Crohn’s disease

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Which IBD disease has a higher incidence

ulcerative colitis

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Age for Ulcerative colitis

15-30 and 50-70 (bimodal)

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What is most important in ulcerative colitis

family history

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Who has the highest risk factor of ulcerative colitis

Ashkenazi jews

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What environmental factors affect ulcerative colitis?

smoking decreases risk of flares
history of prior GI infections (shigella, salmonella, campylobacter) changes gut flora–> chronic inflammatory process
weak association btw NSAID/OCP and UC
stress is not a trigger

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Clinical UC

symptoms wax and wane
rectal bleeding
bloody diarrhea
fecal urgency
tenesmus
abdominal pain LLQ and suprapubic pain
abdominal tenderness
aphthous oral ulcers
iritis- severe eye pain and photophobia
seronegative arthritis with flares
erythema nodosum on lower extrem. and extensors
autoimmune hemolytic anemia
primary sclerosing cholangitis

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Clinical Mild UC

gradual onset of diarrhea less than 4 days and intermittent bloody mucoid stool
urgency and tenesmus
LLQ cramping relieved by bowel movement
mild fever, anemia, hypoalbunemia

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Clinical Moderate UC

gradual onset of diarrhea less than 6 days and intermittent bloody mucoid stool
urgency and tenesmus
LLQ cramping relieved by bowel movement
mild fever, anemia, hypoalbunemia

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Clinical Severe UC

more than 6 bloody diarrhea stools/day
severe anemia, hypovolemia, hypoalbunemia with nutritional deficit
abdominal pain and tenderness
fulminant colitis
pulse over 90
fever over 37.5C
ESR over 30

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What is fulminant colitis

subset of severe dz which is rapidly worsening symptoms with toxicity
distended abdomen, tender leukocytosis, severe diarrhea, fever

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Primary sclerosing cholangitis

life long chronic disease or scarring anti-inflammation of the bile ducts
bile ducts scar and narrow

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Which UC extraintestinal symptoms improve after colectomy

arthritis
ankylosin spondylitis
erythema nodosum
pyoderma gangrenosum

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Which UC extraintestinal symptoms do not improve after colectomy

primary sclerosing cholangitis

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Who is more likely to develop primary sclerosing cholangitis

HLA-B8 or HLA-DR3

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What is increased risk with primary sclerosing cholangitis? What is cure for primary sclerosing cholangitis?

colon cancer

liver transplant

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Classification of UC

E= extent/location
1- inflammation of rectum (proctitis)
2- inflammation of splenic flexure (left side; distal)
3- inflammation extendes to proximal splenic flexture (pancolitis)
S= severity
0- remision, no sx
1- mild
2- moderate
3- severe

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UC and CD dx

based on clinical symptoms and confirmed by sigmoidoscopic and colonoscopic and histologic examination

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If severe pancolitis use what for dx?

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flex sig

UC colonoscopy results

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diffuse confluent disease from dentate line proximal
edema, friability of mucosa, mucous, erythema, erosions, ulcerations, and spontaneous bleed
only found in the colon

Histology UC

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distortion of crypt architecture
crypt abscee
infiltration of lamina propria with plasma cells
eosinophils
lymphocytes
lymphoid aggregates
mucin depletion

Tx Mild UC

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5-ASA drugs (aminosalicylates)- release only in colon
(Mesalazine PR suppository or budesonide rectal foam if rectal proctitis)
Distal colon inflammation- rectal/oral 5-ASA (PO sulfasalazine and PR mesalazine)
long term maintenance with 5-ASA

Tx Mild/Moderate UC

- Fail of 5-ASA - PO Budesonide - Prednisone - Taper over 60 days

Tx Severe UC

- hospitalization and IV steroids with IVF (methylprednisone 60mg/d) - Anti-biologics if fail steroid tx (TNF alpha- infliximab, adalimumab, golimumab) or (VGEF blocker if fail TNF- vedolizumab) - cyclosporine is last resort

Maintenence TX UC

- once in remission - 5-ASA - Budesonide - Immunosuppressant- golimumab or 6-MP - Induct with infliximab, then continue use - probiotics

Only curative tx for UC

colectomy

Surgery TX UC

Emergency- toxic megacolon Urgent- severe dz and not responding to tx in hospital Elective - refractory: intolerant to long term maintenance tx - colorectal dysplasia or adenocarcinoma found - dz more than 7-10yrs

UC patients at increased risk of?

colorectal cancer

Screening UC

- colonoscopy begins 8yrs after dz onset - if L. sided colitis/pancolitis: every 1-2 yrs - UC with PSC: every yr from PSC dx

Def Crohn Dz

insidious variable presentation of lifelong idiopathic inflammatory dz that affects anywhere in GI system

What type of inflammation in crohn dz and what does it cause?

transmural inflammation in skip distribution that causes strictures, fistulas, ulcerations, abscess

MC area affected in Crohn dz

small bowel and colon (terminal ileum and ascending colon)

Strongest risk factor for CD

family hx

Environmental factors for CD

tobacco sedentary lifestyle exposure to air pollution consumption of western diet

When does CD commonly begin?

after infectious gastroenteritis

Clinical CD

- RLQ, periumbilical pain - watery diarrhea - incontinence - low grade fever - weight loss/anorexia/ malnutrition - weak, fatigue, malaise - bone loss - SBO presentation - rectal abscess or anal fistula - arthralgia - iritis - erythema nodosum

6 complication of CD

``` abscess obstruction fistula perianal dz colon cancer dysplasia/malignancy--> malabsorption ```

Treat fistulas in patient with CD

TPN/ oral elemental diet Antibiologics for 10 weeks Surgery is medication fails

Treat perianal dz in patient with CD

ABX (flagyl or cipro) Mesalamine suppository or tacrolimus ointment if refractory fissure Antibiologics

Classification of CD

``` L= extent 1- terminal ileum 2- colon 3- ileum and colon 4- upper GI L3+L4= upper GI and distal B= phenotype 1- no stricture and non-penetrating 2- stricture 3- penetrating 3p- perianal penetrating ```

Colonoscopy results for CD

aphthoid, stellate, linear ulcers strictures segmental involvement with skip lesions

General TX CD

- stop smoking | - diarrhea: loperamide, BAS (terminal ileal disease), low fat diet if short gut

Tx mild CD

Mesalamine (colon and small bowel)

Tx moderate to severe

- Steroid short term to control sx, use until remission and then a slow 60day taper - immunosuppressants (azathioprine or methotrexate)

When to use TNF alpha in CD

- steroid dependent and no taper - fistula tx no responding to ABX refractory cases - can do an induction and maintenance - infliximab, adalimumab, certolizumab pegol

When to use anti-integrins in CD

- no response to TNF | - vedolizumab (gut leukocyte trafficking)

Screen CD

- Regular screen TB, hepatitis, CMV, HIV, and C. diff - more than 1/3 colon affected (L3) colonoscopy 8 yrs after onset and repeat every 1-2yrs and 1-3 once normal - PSC= annual screening

PSC and CD have a risk of? Screen with?

cholangiocarcinoma (cancer of bile ducts) | screen with MRCP

IBD Flashcards

(50 cards)