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imed3004 > Non-neoplastic Disease of the Colon > Flashcards

Non-neoplastic Disease of the Colon Flashcards

1
Q

What are the most important functions of the colon?

A

Water and electrolyte absorption

Transport, storage and evacuation of faeces

Nutrient/vitamin absorption

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2
Q

What are the types of diseases that affect the colon?

A

VITAMIN C DEF

Vascular
Infective/Inflammatory
Traumatic
Autoimmune
Metabolic
Iatrogenic/Idiopathic
Neoplastic
Congenital
Degenerative/Developmental
Endocrine/Environmental
Functional
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3
Q

What is Inflammatory Bowel Disease? What are the major groups of IBD?

A

A chronic inflammatory condition arising from inappropriate immunological activation.

It is chronic and punctuated by relapses and remission.

Composed of 2 major disorders: Ulcerative colitis and Crohn’s disease

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4
Q

Where is Inflammatory Bowel Disease most common?

A

Most common among industrialised nations and less common in Asia, Africa, and South America

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5
Q

How common is IBD in countries that it affects most commonly?

A
  1. 5million americans
  2. 2 million Europeans

Several hundred thousand more worldwide

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6
Q

What is the incidence of Ulcerative Colitis IBD?

A

UC 2.2 - 19.2 per 100k person years

CD 3.1 - 20.2 per 100k person-years

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7
Q

What is the prevalence of Ulcerative colitis and Crohn’s disease IBD?

A

UC 238 per 100k population

CD 201 per 100k population

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8
Q

What conditions seem to have a higher correlation with IBD?

A

Jews > non-jew; caucasians > African-American / Hispanics

Urban > Rural

Colder climate regions > Warmer climate regions

North - South gradient.

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9
Q

What age and gender is most affected by IBD?

A

Bimodal age incidence: 2nd to 4th decade then 6th to 7th decade’

Affects both males and females. (CD has slight female predominance)

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10
Q

What are the risk factors for IBD?

A

Risk factors span spectrum of life: mode of childbirth and early life exposure in adulthood.

Lifestyle and behaviour (Exercise, smoking, and diet)

Family history is a strong risk factor: RR of IBD in first degree relative is 5 - 8% CD and 2 - 5% UC, if both parents are affected there is a 1/3 risk for IBD <30 years in offspring

Smokers have reduced risk of ulcerative colitis but higher risk of crohn’s disease

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11
Q

What is the aetiopathogenesis of IBD?

A

Genetics

Environment

Microbiota

Immune response

These factors have a complex interaction resulting in dysregulated immune response and development of chronic inflammatory change.

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12
Q

What are the clinical features of ulcerative colitis?

A

Ulcerative colitis:

Diarrhoea, rectal bleeding, passage of mucous (affects colon and rectum usually)

Tenesmus (feeling of constant need to pass faeces) and urgency

Abdominal pain, fever, and weight loss

Initial presentation (pancolitis, left-sided colitis, proctitis/rectosigmoiditis)

Thin wall, no fat wrapping, normal ileum, deep fissuring/linear ulcers are not a feature.

Extraintestinal manifestations.

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13
Q

What are the clinical features of crohn’s disease?

A

Abdominal pain (Can affect whole GI tract or parts other than colon)

Constitutional symptoms, weight loss, fever, growth retardation, anal fissure/perianal disease.

Diarrhoea +/- blood

Predilection for distal Small Intestine and proximal colon (1/3rd have ileocolonic disease, 1/3rd confined to SI, mainly ileum, and up to 1/3rd colonic disease)

Extraintestinal manifestations.

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14
Q

What extra-intestinal manifestations can be caused by IBD?

A

Skin (erythema nodosum or pyoderma gangrenosum)

Sclerosing cholangitis

Eyes and mucous membranes

These effects can occur before during and after

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15
Q

What features of ulcerative colitis make it easy to confuse with crohn’s disease?

A

Skip lesions (Peri-appendicieal inflammation and caecal patch)

ileitis

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16
Q

What does ulcerative colitis look like microscopically?

A

Confined to mucosa architectural distortion and mucosal metaplasia (paneth cell metaplasia)

Cryptitis and crypt abscesses

Erosions, ulcers

Lamina propria shows chronic inflammation

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17
Q

What are the pathological features of Crohn’s disease?

A

It is characteristically mouth to anus

Predilection for distal small intestine and proximal colon

Focal inflammation; skip lesions

Rectal sparing

Aphthous ulcers, fissuring, lineal ulcers

Sinuses / fistulas

Anal fissure / perianal disease

Cobblestone mucosa

Thickening of the wall

Creeping fat

Strictures

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18
Q

What are the microscopic features of Crohn’s disease?

A

Patchy/focal inflammation

Transmural inflammation and lymphoid aggregates

Aphthous ulcers, fissuring ulcers

Architectural distortion and metaplasia (pyloric, Paneth cell metaplasia); active (cryptitis, crypt abscesses) and chronic inflammation

Granulomas

Connective tissue changes

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19
Q

How can ulcerative colitis be differentiated from Crohn’s disease?

A

Distribution:

UC is seen in colon/rectum and extends proximally

UC is seen anywhere from mouth to anus and is typically seen in distal small bowel or proximal colon

Mucosa:

UC is continuous; granular, erythematous

CD has cobblestone and skip lesions.

Ulceration:

UC forms shallow, broad-based ulcers, CD forms deep, fissuring, knife-like, linear ulceration.

Wall:

UC results in thinner wall whereas CD results in thicker wall

Strictures:

UC = rare. CD = yes

Pseudopolyps:

UC = marked. CD = moderate

Fistulas/sinuses:

UC = NO, CD = Yes

Fat creeping:

UC - NO, CD = Yes

Inflammation:

UC = superficial
CD = Transmural

Lymphoid reaction:

UC = Moderate
CD = Marked

Fibrosis:

UC = none/mild
CD = marked

Serositis:

UC = None or mild
CD = Marked

Granulomas:

UC = No
CD = Yes in ~30%
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20
Q

What are potential complications of UC?

A

Toxic megacolon, perforation

Dysplacia and colorectal adenocarcinoma

Pouchitis

Extraintestinal manifestations

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21
Q

What are potentail complications of CD?

A

Fistula or sinuses

Stenosis / stricture

Abscesses

Malabsorption and nutritional deficiency

Toxic megacolon, perforation

Dysplasia and adenocarcinoma

Extraintestinal manifestations.

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22
Q

What is microscopic colitis?

A

Macroscopically normal colonic mucosa with microscopic inflammation.

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23
Q

What are the types of microscopic colitis?

A

2 entities:

Collagenous colitis

Lymphocytic colitis

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24
Q

Who gets microscopic collitis?

A

Typically seen in older people (50 - 70 years of age)

Children may be affected

Female predominance

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25
Q

What is the incidence of microscopic colitis?

A

Previously 1 - 12 / 100k person-years; recent studies suggest increase to 12 - 19 / 100k person - years

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26
Q

What are associated diseases with microscopic colitis?

A

Rheumatoid arthritis

Thyroid disorders

Coeliac’s disease

Diabetes

Autoimmune or lymphocytic gastritis

Drug use (NSAIDs for example)

27
Q

What causes microscopic colitis? (aetiopathogenesis)

A

Inflammatory disorder arising from epithelial immune responses to intraluminal antigens.

Inciting antigens are uncertain and include medications (NSAIDs), bile salts, toxins, infectious agents have been postulated

28
Q

How do patients with microscopic colitis present macroscopically?

A

Chronic non-bloody diarrhoea

Radiology and colonoscopy come back normally.

Some patients present with abdominal pain, fatigue, weight loss, and arthralgia.

29
Q

What are the microscopic features of microscopic colitis?

A

Normal architecture

Increased intraepithelial lymphocytes

Epithelial injury

Lamina propria chronic inflammation

Thickening of subepithelial collagen distinguishes collagenous colitis from lymphocytic colitis.

30
Q

How is collagenous colitis different from lymphocytic colitis?

A

Subepithelial collagen is thickened in collagenous colitis.

31
Q

What is the prognosis like in microscopic collitis?

A

Prognosis is excellent.

Most patients respond to cessation of potential risk factors like NSAIDs and symptomatic measures.

> 70% experience long-term cessation of diarrhoea and the remaining people respond to anti-inflammatory therapy or surgery.

32
Q

Who most commonly suffers from infectious colitis? How are these infections transmitted?

A

Extremities of age: Children and elderly

More than 2000 deaths/day among children in developing countries and >10% of all deaths <5 years old worldwide.

Many infections are transmitted through contaminated food and water.

33
Q

What infectious agents most commonly cause infectious colitis?

A

Mostly bacteria (campylobacter, salmonella, shigella, E. Coli, Clostridia, Yersinia, Aeromonas)

Most common cause is viral

Fungal, or parasitic causes also exist.

34
Q

How does the host prevent infection? How does the bacteria get past these defences?

A

Host defenses:

Gastric acidity

Intestinal motility

Mucous

Intestinal microflora

Systemic and local immune mechanisms

Bacterial virulence:

Adherence

Enterotoxins

Cytotoxic production

Mucosal invasion

Others (Evasion of phagocytosis, mucolytic enzymes, etc)

35
Q

What are the clinical features of infectious colitis?

A

Diarrhoea, nausea, vomiting

Abdominal pain, tenesmus, urgency

Fevers/chills, malaise, arthralgia/myalgia

In general non-invasive organisms that produce toxins tend to cause less severe morphological changes / symptoms and non-inflammatory diarrhoea

Invasive organisms are more severe.

36
Q

What are gross pathological features of infective colitis?

A

redness, swelling, bleeding, erosions, ulcerations, etc.

37
Q

What are the microscopic features of infectious colitis?

A

Mucosal and intraepithelial neutrophilic infiltrates

Cryptitis and crypt abscesses.

Minimal change in not so severe organisms.

If it is viral there will be viral inclusions in stromal and endothelial cells.

If caused by entamoeba histolytica there are amoebic organisms in ulcer slough

38
Q

What is the prognosis of infectious colitis?

A

It is self-limiting in a majority of cases. However:

Dehydration

Sepsis and shock

Toxic megacolon

Extraintestinal manifestations (guillan barre, HUS)

39
Q

How is infectious colitis treated?

A

Supportive treatment

Specific antimicrobial therapy

40
Q

What are antibiotic associated diarrhoea (AAD) and pseudomembranous colitis (PMC) caused by?

A

Use of antibiotics.

Pseudomembranous colitis results in formation of pseudomembranes and associated with toxin producing C. Difficile

41
Q

How common is AAD/PMC?

A

Complication seen in 2 - 25% of antibiotic treatment courses.

42
Q

What are the risk factors for PMC?

A

Age

Antibiotics

Hospitalisation

NGT

GI procedures

Chemotherapy

Acid suppression therapy

Surgery

IBD

Immunosuppression

Others

43
Q

What causes AAD and PMC?

A

Disruption of colonic flora causing overgrowth of pathogenic bacteria.

44
Q

What are the characteristic appearances of AAD and PMC?

A

AAD: normal or minor change with colitis. (normal to minimal changes and features resemble acute infectious colitis)

PMC: Yellowish white pseudomembranes that bleed when scraped off (Pseudomembranes composed of fibrin, mucin and neutrophils)

45
Q

What is the prognosis like in AAD?

A

Mild and self limiting. Can be treated by withdrawal of implicated antibiotic.

46
Q

What is the prognosis like in PMC?

A

Fulminant colitis with toxic megacolon or perforation.

Dehydration, hypoalbuminaemia, ascites, electrolyte disturbances.

Extraintestinal manifestations

47
Q

How is PMC treated?

A

Cessation of culprit antibiotics

Supportive or symptomatic treatment

Specific therapy

Blinding resins, probiotics

Microbiota transplantation; IV immune globulin.

48
Q

What causes ischaemic colitis?

A

Loss of blood supply to the gut resulting in secondary inflammation.

49
Q

Who most commonly gets ischaemic colitis?

A

Most common in females ages 70 - 79 years

50
Q

What is the incidence of ischaemic colitis?

A

4.5 to 44 cases per 100k person-years

51
Q

What are the causes of ischaemic colitis?

A

Occlusive: Arterial and venous occlusion due to thrombosis/embolism or cholesterolemboli.

Non-occlusive: Hypotension, haemorrhagic shock, heart failure, sepsis, and medications.

52
Q

What are the clinical features of ischaemic colitis?

A

Acute: Sudden onset abdominal pain and tenderness, urgent desire to defecate, nausea + vomiting, bloody diarrhoea, loss of bowel sounds, abdominal rigidity, shock, vascular collapse.

Subacute / Chronic: Non-specific symptoms, episodes of bloody diarrhoea, blood loss, sepsis, symptomatic strictures, weight loss

53
Q

What is the prognosis like in ischaemic colitis?

A

Reversible in more than 50% of cases. Symptoms resolve as a result in 2 - 3 days.

Colon heals in 1 - 2 weeks (up to 6 months if severe)

54
Q

What are the potential complications of bowel ischaemia?

A

Perforation

Massive haemorrhage

Sepsis

Stricture

55
Q

How can ischaemic colitis be treated?

A

Medical and surgical treatments

56
Q

What is diverticular disease?

A

Diverticulum is acquired pseudodiverticular outpouching of mucosa and submucosa.

Diverticulosis presence of multiple diverticula and generally implies absence of symptoms

Any clinical state caused by colonic diverticula (eg haemorrhage, inflammation, complications, etc)

57
Q

What is diverticulitis?

A

An inflammatory process associated with diverticula.

58
Q

Where is diverticular disease most common and what part of the body is most commonly affected?

A

Prevalence increases with age (60% over age of 70)

Sigmoid colon affected in 95% of cases

Geographic variation. (Western nations > Asia, Africa, and other developing countries)

59
Q

What are the aetiopathogenic factors that results in diverticular disease?

A

Genetic factors

Environmental factors:

Low-fiber diet, obesity, decreased physical activity, Corticosteroids, NSAIDs, alcohol, caffeine intake, Cigarette smoking, Polycystic kidney disease

Epidemiologica factors:

Age, geography, lifestyle, ethnicity.

60
Q

What are the clinical features of diverticulitis?

A

Asymptomatic

Alternating constipation and diarrhoea mimic IBS.

Intermittent cramping, continuous lower abdominal discomgort, diarrhoea, tenesmus.

Fever

Chronic or intermittent blood loss

Inflammatory mass

Massive haemorrhage.

61
Q

Where in the colon do diverticula form?

A

Tend to form in 2 rows between anti-mesenteric taenia and mesenteric taenia.

Forms at points of weakness - vessels and nerves penetrate the muscular wall.

62
Q

How is diverticulitis managed?

A

Can be managed medically and surgically.

63
Q

What are the iatrogenic causes of colitis?

A

Diversion colitis: inflammation in diverted segment of bowel

Radiation proctitis: following radiation injury to rectum

Graft versus host disease

Drug-induced (eg NSAID ulcers/strictures, focal active colitis, microscopic colitis)

imed3004 (50 decks)

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