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Oxford MRCS Pathology > Inflammatory Bowel Disease [IBD] (21) > Flashcards

Inflammatory Bowel Disease [IBD] (21) Flashcards

1
Q

What is ulcerative colitis?

A

Inflammatory bowel disease affecting the colon.
It is chronic, relapsing-remitting & non-infectious.

It is characterized by diffuse, continuous, superficial inflammation of the large bowel limited to the intestinal mucosa, and usually affects the rectum with a variable length of the colon involved proximally.

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2
Q

What is the pathogenesis of ulcerative colitis?

A

Idiopathic

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3
Q

A Lady known to have ulcerative colitis and on surveillance colonoscopy is found to have a lesion less than 1cm in sigmoid colon

What will you offer the patient with tubular dysplasia and adenocarcinoma in the sigmoid colon on a background of ulcerative colitis?

A
  • Total colectomy
  • Why? The whole colon is susceptible
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4
Q

What are the possible causes of diarrhea in a patient who has had resection of the terminal ileum?

A

-Relapse of Crohn’s (flare of IBD)
-malabsorption

Other:
-Infection (novovirus / C.diff colitis)
-Ischaemic colitis

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4
Q

How does liver metastasis affect TNM staging?

A

M1

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5
Q

Why is endoscopic surveillance necessary?

A

For risk of colon cancer

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6
Q

How does Crohn’s disease lead to renal stone formation?

A

Increased intestinal fat (due to malabsorption) → binds to calcium → leaving oxalates (hyperoxaluria)

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6
Q

What are the reasons for diarrhea in a patient with inflammatory bowel disease?

A
  • Malabsorption
  • Infection
  • Increased motility
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6
Q

What are the complications of inflammatory bowel disease?

A
  • Intestinal obstruction
  • Fistula formation
  • Abscess
  • Toxic megacolon
  • Malabsorption
  • Malignancy
  • Gall stones (due to inhibition of enterohepatic circulation so bile salts will not be absorbed leading to increased amount of cholesterol)
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7
Q

What should be done in case of stoma ischemia?

A

Inform consultant, patient relatives, consider refashioning

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8
Q

What type of vitamin deficiency is common in inflammatory bowel disease?

A

D, A, E, K deficiency
(fat soluble vitamins)

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9
Q

What are other investigations for inflammatory bowel disease?

A
  • Stool analysis
  • Barium follow-through
  • Prothrombin concentration: to detect vit. K def.
  • Calcium oxalate levels
  • Full blood count: macrocytic anemia
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10
Q

Extraintestinal manifestations of IBD?

A
  • Aphthous ulcers
  • Pyoderma gangrenosum
  • Iritis
  • Erythema nodosum
  • Sclerosing cholangitis
  • Arthritis
  • Clubbing
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11
Q

What are the management options for Crohn’s disease?

A
  • Medical management:
    • Advice from gastroenterology
    • Steroids, antibiotics, 5-aminosalicylic acid, immunomodulators
  • Conservative management:
    • Dietary control (low residue diet)
  • Surgical management for:
    • Refractory disease
    • Intestinal obstruction
    • Toxic megacolon
    • Abscess, fistula, perforation, hemorrhage, cancer
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12
Q

What are the differences between Crohn’s & Ulcerative colitis?

A
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13
Q

What is the adenoma carcinoma sequence?

A
  • Stepwise accumulation of mutations of oncogenes and tumor suppressor genes:
    1. Loss of APC (tumor suppressor gene) → hyperplasia
    2. K-RAS (oncogene) mutation → dysplasia
    3. Loss of p53 (tumor suppressor gene) → adenocarcinoma
13
Q

How do proto-oncogenes and tumor suppressor genes act?

A

Proto-oncogenes:
- Normal cellular genes whose products promote cell proliferation

Oncogenes:
- Mutated or overexpressed versions of proto-oncogenes that function autonomously, having lost dependence on normal growth-promoting signals

Tumor suppressor genes (p53, APC):
- Normal genes whose absence can lead to development of cancer
- They act as gatekeepers: inhibit proliferation or promote the death of cells with damaged DNA

14
Q

What is the function of KRAS?

A
  • Provides instructions for making a protein called K-Ras that is part of a signaling pathway known as the RAS/MAPK pathway
  • The protein relays signal from outside the cell to the cell’s nucleus, instructing the cell to grow and divide (proliferate) or to mature and take on specialized functions (differentiate)
  • The K-Ras protein acts like a switch that is turned on and off by the GTP and GDP molecules
15
Q

What are the intrinsic and extrinsic pathways of apoptosis?

A
  • Mechanisms used by tumor cells to evade cell death

Intrinsic pathways:
- Loss of p53, leading to reduced function of pro-apoptotic factors such as BAX
- Reduced egress of cytochrome c from mitochondria as a result of upregulation of anti-apoptotic factors such as BCL2, BCL-XL, and MCL-1
- Loss of apoptotic peptidase activating factor 1 (APAF1)

Extrinsic pathways:
- Upregulation of inhibitors of apoptosis (IAP)
- Reduced CD95 level
- Inactivation of death-induced signaling complex

15
Q

What is the function of APC?

A

Encodes a factor that negatively regulates the WNT pathway in colonic epithelium by promoting the formation of a complex that degrades β-catenin

16
Q

What is the function of p53?

A
  • DNA damage and other stress signals may trigger the increase of p53 proteins, which have three major functions:
    • Growth arrest
    • DNA repair
    • Apoptosis (cell death)
  • The growth arrest stops the progression of cell cycle, preventing replication of damaged DNA
  • During the growth arrest, p53 may activate the transcription of proteins involved in DNA repair
  • Apoptosis is the “last resort” to avoid proliferation of cells containing abnormal DNA
17
Q

What is TNF

A
  • TNF is a cytokine involved in systemic inflammation and in making up the acute phase reaction.
  • In IBD, TNF and other immune-mediated signals direct epithelia to increase tight junctions permeability, which increases the flux of luminal bacterial components that activate innate and adaptive immune responses.
18
Q

Mechanism of action of these drugs?

A

Monoclonal IgG1 antibody to TNF- α

19
Q

What drugs antagonize TNF?

A
  • Infliximab
  • Adalimumab
  • Certolizumab
20
Q

Why are they used in treatment of UC?

A

They are called (biologics), used mainly in steroid refractory UC cases and for
treatment of extra intestinal manifestations

Oxford MRCS Pathology (34 decks)

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