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EXAM 1 > LOWER GI DISEASE- IBD > Flashcards

LOWER GI DISEASE- IBD Flashcards

1
Q

What is the definition of IBD?

A

*2 inflammatory disorders of the GI tract- Crohn’s D and Ulcerative C

*Chronic disease that follows unpredictable relapsing and remitting.

*10-15% of UC & CD= Difficult to distinguish

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2
Q

Where does CD and UC affect?

A

Crohn’s Disease:
-Affects ANY part of GI M-R
-Inflammation extends through all layers of the gut wall
-Inflammation = PATCHY in distribution

Ulcerative Colitis:
-Affects only COLON and RECTUM
-Affects ONLY Mucosa and Submucosa
-Inflammation is diffuse in Distribution

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3
Q

What is the Epidemiology of IBD?

A

Common=Industrialised countries, all races and both sex

Peak incidence= 10-40yrs, 15% = over 60yrs, Occur any age

1/250 = affected in UK

Rapid increase incidence bet 1955-75 (CD)= now stabilised

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4
Q

What is the Incidence rate in terms of population in UC & CD?

A

CD:
-5-10 per 100,000 population per year
-Prevalence of 50-100 cases per 100,000 population
-More common = FEMALES, occurs in younger age + mean age of onset = 26 years!! M:F = 1:1.2

UC:
-10-20 per 100,000 population per year
- Prevalence of 100-200 cases per 100,000 population
- Common = Males, Occurs = Older age, Mean age = 35 years. M:F = 1:2.1

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5
Q

What is the Aetiology of IBD in terms of Environmental factors?

A
  • Causative agent = Unknown

-Diet (fat, fast food indigestion, milk, fibre, R carbs)

-Smoking (Increase risk of relapse and need for surgery)

-Infection (Mycobacterium Paratuberculosis = CD
Associated with measles & mumps infection

  • Enteric Microflora ( IBD patients- Loss of immunological tolerance to intestinal microflora). Manipulated by antibiotics

Drugs ( NSAIDs can exacerbate IBD , Antibiotics, Oral contraceptive pill- increase risk of CD, Isotretinoin-acne)

Appendectomy: protective effect in UC and UC

Stress: can trigger relapse in IBD, Activate inflammatory mediators at enteric nerve ends in guy wall

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6
Q

What is the Aetiology of IBD in terms of Genetic factors?

A
  • Mutations of the gene CARD15/NOD2 located on chromosome 16
    – Associated with small intestine CD in white populations
  • The genes OCTNI on chromosome 5 and DLG5 on chromosome 10 have also been linked to CD
  • 70% of UC patients – Have anti-neutrophil cytoplasmic antibodies (pANCA)
  • ? Autoimmune component – Association between IBD, ankylosing spondylitis & histocompatibility antigen HLA-B27
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7
Q

What is the Aetiology of IBD in terms of Ethical and Familial factors?

A
  • Ethical factors:
    – Jews are more prone than non-Jews
    – IBD incidence is lower in non-white races
  • Familial factors:
    – First-degree relatives of those with IBD have up to 20-fold increase in developing the disease
    – 15-fold greater concordance for IBD in identical twins than non-identical twins
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8
Q

Genetic factors influence the risk of IBD by causing?

A

– Disruption of epithelial barrier integrity
– Deficits in autophagy
– Deficiencies in innate pattern recognition receptors
– Problems with lymphocyte differentiation, especially CD

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9
Q

What % of UC and CD patients are smoker?

A

-40% of CD patients are smokers (10% UC)

  • Smoking may help to prevent the onset of UC
    – Chemicals affect colon smooth muscle
  • Alters gut motility & transit time
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10
Q

What is the Pathogenesis of IBD?

A

– Increased activity of effector lymphocytes & proinflammatory cytokines that override normal control mechanisms
– Primary failure of regulatory lymphocytes &
cytokines
– In CD, T cells are resistant to apoptosis after inactivation

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11
Q

What is the Pathophysiology of Crohn’s Disease?

A

One or multiple areas ( affected areas are thickened, oedematous and narrow)
-Deep ulcers can appear
– Mucous membrane between fissures has a
cobblestone appearance
– Can progress to deep fissuring ulcers, fibrosis &
strictures
-Can lead to bowel obstructions, abscesses and guy perforations

Usually Terminal ileum & ascending colon
Discontinuous

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12
Q

What is the Pathophysiology of Crohn’s Disease Microscopically?

A

– Non-specific granulomatous inflammation
– Inflammation extends throughout all layers of the bowel (transmural)
– Inflammatory cells are seen throughout –
lymphocytes and plasma cells
– Th1-associated

Chronic inflammation leads to an increased risk of cancer

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13
Q

What is the Pathophysiology of Ulcerative Colitis?

A
  • At first presentation:
    – 40%- rectum (proctitis)
    – 40% - sigmoid & descending colon (left-sided colitis)
    – 20% - whole colon
  • Only the mucosa & submucosa are affected
  • Continuous, starting in rectum
  • Formation of crypt abscesses & mucosal ulceration
  • Mucosa looks red, inflamed & bleeds easily
    – Purulent & granular with superficial ulceration
    – Pseudo polyps in severe inflammation
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14
Q

What is the Pathophysiology of Ulcerative Colitis Microscopically?

A

Microscopically:

– Inflammatory cells infiltrate the lamina propria & crypts
– Th2-associated
– Dysplasia can be seen from biopsies
* Can progress to carcinomas

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15
Q

What does IBD depend on in terms of clinical features?

A

IBD – depends on site, extent & severity of active disease

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16
Q

What are the Clinical symptoms of IBD (BOTH)?

A

– Diarrhoea
– Fever
– Abdominal pain
– Nausea & vomiting(more common in CD)
– Malaise
– Lethargy
– Weight loss (more common in CD)
– Malabsorption
– Growth retardation in children

17
Q

What are the Clinical symptoms of of CD?

A
  • Tends to be more disabling than UC
  • Onset can be acute or insidious
  • Other symptoms can include:
    – Pain (particularly LRQ)
    – Anaemia
    – Palpable masses
    – Small bowel obstructions
    – Abscesses
    – Fistulas
    – Gut perforation
18
Q

What are the Clinical symptoms of of CD?

A
  • Symptoms
    – Diarrhoea – possibly with blood/mucus
  • Up to 10-20 liquid stools a day
    – Abdominal pain (cramps) with fever
    – Constipation
  • 50% of UC patients have a relapse each year
    – Severe attacks can be life-threatening
19
Q

What are the Complications of IBD? 10-20%

A
  • Joints and Bones
    – Arthropathies & Osteopenia
  • Skin
    – Erythema nodosum (Tender, hot, red nodules – subside over a few days to leave brown skin discolouration)
    – Pyoderma gangrenosum (Pustule–develops into an ulcer)
  • Ocular
    – Episcleritis (Intense burning & itching of blood vessels involved)
    – Uveitis ( Headache, burning red eye, blurred vision
  • Sclerosing Cholangitis
    – Chronic inflammation of the biliary tree
    – Leads to progressive fibrosis & biliary
    strictures
20
Q

What are you at increased risk of in CD than in UC?

A
  • Quality of life generally lower in CD vs UC, especially because of recurrences after surgery
  • Increased risk of peritonitis and malignancy
  • Malnutrition and chronic anaemia common in long-standing CD
21
Q

How do you Diagnose IBD?

A
  • Confirmed by clinical evaluation & a combination of investigations:

– Biochemical
– Endoscopic
– Radiological
– Histological
– Nuclear medicine based

22
Q

How do you Diagnose IBD using the History of Disease?

A
  • Full history including:
    – Recent travel
    – Medication
    – Smoking
    – Family history
  • Details of symptoms including:
    – Stool frequency & consistency
    – Urgency
    – Rectal bleeding
    – Abdominal pain
    – Fever
23
Q

What Examinations should you carry out in order to Diagnose IBD?

A

Physical signs:
– General well-being
– Pulse
– Blood pressure
– Temperature
– Weight loss
– Abdomen tenderness or distension
* Right iliac fossa mass
– Anus
*Oedematous anal tags, fissures or perianal abscesses

24
Q

What Initial Investigations should be carried out in order to Diagnose IBD?

A
  • Blood tests
    – Anaemia is common
    – Deficiency of iron and/or folate also occurs
    – Raised ESR & CRP & a raised WCC
    – Hypoalbuminaemia
    – LFTs may be abnormal
  • Microbiological testing for infectious diarrhoea
  • Serological tests
    – Saccharomyces cerevisae antibody usually present in CD
    – p-ANCA antibody
    • -ve in CD & +ve in UC
25
Q

What happens in Abdominal Radiography?

A
  • Essential in the initial assessment of suspected severe IBD
  • Excludes colonic dilatation
  • Helps assess disease extent in UC
  • Identifies proximal constipation
  • Gives an impression of right iliac fossa mass in
    CD
  • Can show evidence of small bowel dilation
26
Q

What Investigations are carried out in terms of …scopys?

A
  • SIGMOIDOSCOPY
    – Internal examination of the colon (lower third) using a sigmoidoscope.
    – Used for all patients presenting with diarrhoea
    – Used to confirm diagnosis of UC
  • RECTAL BIOPSY
    – Detects non-specific histological changes in the mucosa
  • COLONSCOPY
    – Internal examination of the colon (entire length) using a colonoscope
    – Used for mild or moderate disease to assess extent of disease
    – Biopsy can be performed as well
27
Q

What is the difference between Colonoscopy and Sigmoidoscopy?

A

Colonoscopy examines the ENTIRE length of the Colon; Sigmoidoscopy examines ONLY the lower Colon

28
Q

What other investigations Should be carried out when Diagnosing IBD?

A

Double contrast barium enema
– Inferior to colonoscopy
– Can detect early mucosal changes

Small bowel radiology
– Current standard for assessing small intestine

Ultrasound
– Sensitive & non-invasive
– Identifies thickened small bowel loops in CD

Computer tomography & magnetic resonance imaging
– Evaluates activity & complications of the disease

EXAM 1 (14 decks)

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