T11-L2: Lower GI Pathology Flashcards

1
Q

Where are diverticula commonly found?

A

Diverticula are protrusions of mucosa and submucosa through the bowel commonly found at the sigmoid colon. They are located between mesenteric and anti-mesenteric taenia coli.

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2
Q

What is the pathogenesis of diverticular disease?

A
  • They can be due to increased intra-luminal pressure. This can be due to uncoordinated and irregular peristalsis of the sigmoid colon causing closed compartments of increased presser’s. There is also overlapping semi-circular arcs of the bowel.
  • Points of relative weakness in the bowel leads to penetration by nutrient arteries between mesenteric and anti mesenteric Tania coli.

Muscle is thickened and undergoes hypertrophy. The diverticulum can perforate and cause an abscess.

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3
Q

Give acute complications of diverticular disease.

A
  • Diverticulitis / peridiverticular abscess ( 20 – 25 % ) due to the faeces in the diverticulum
  • Perforation - inflamed and weakened diverticulum perforated releasing faeces into the peritoneal cavity
  • Haemorrhage ( 5 % ) - diverticulum erodes into an artery causing gastrointestinal haemorrhage and so they may bleed into the rectum
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4
Q

Give chronic complications of diverticular disease.

A
  • Intestinal obstruction (strictures : 5 – 10 % ) - due to structuring of the bowel
  • Fistula ( urinary bladder, vagina ) - channel developing leading to faecal material in urine or from the vagina due to the diverticulum being coming stuck at these area
  • Diverticular colitis (segmental and granulomatous ) - lining mucosa of the bowel becomes inflamed as well as the diverticulum
  • Polypoid prolapsing mucosal folds - the redundant folds forming in diverticulosis can also prolapse and bleed
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5
Q

Give causes of acute colitis..

A
  • Acute infective colitis e.g. shigella, salmonella, EMV
  • Antibiotic associated colitis
  • Drug induced
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6
Q

What are risk factors for chronic colitis?

A
  • Cigarette smoking especially in CD (incidence is lower in UC)
  • Oral contraceptives
  • Family history
  • Others includes childhood infections, domestic hygiene, appendectomy (protective against UC)
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7
Q

Give the clinical presentation and possible complications of UC.

A

Clinical presentation:

  • Diarrhoea
  • Constipation
  • Bleeding
  • Abdominal pain
  • Anorexia
  • Weight Loss
  • Anaemia

Possible complications:

  • Toxic megacolon and perforation
  • Haemorrhage
  • Stricture is rare
  • Carcinoma
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8
Q

What is the main differences between distribution fo inflammation in UC and CD?

A

In UC the inflammation is continuous; it always involved the rectum and spreads up. Inflammation is limited to the mucosa.

In CD the inflammation is discontinuous and so is known as skip lesions. It can occur from anywhere from the mouth to the anus. The inflammation is transmural leading to the narrowing of the lumen and strictures.

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9
Q

Give the clinical presentation and possible complications of CD.

A

Clinical presentation:

  • Chronic relapsing disease and can effect anywhere from the mouth to the anus
  • Diarrhoea
  • Colicky abdominal pain
  • Palpable abdominal mass
  • Weight loss
  • Anorexia
  • Fever
  • Mouth ulcers
  • peri-anal disease e
  • Anaemia

Complications:

  • Perforation
  • Strictures are more common due to transmural inflammation than in UC
  • Toxic megacolon
  • Haemorrhage
  • Carcinoma - also a risk fo small bowel cancer as well as in the large bowel
  • Short bowel syndrome
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10
Q

What is toxic megacolon?

A

Toxic megacolon is an acute form of colonic distension. It is characterized by a very dilated colon (megacolon), accompanied by abdominal distension (bloating), and sometimes fever, abdominal pain, or shock. This can lead to further complications as pressure builds up in the colon due to relative fecal stasis including sepsis, intestinal hemorrhage or free perforation and spontaneous decompression.

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11
Q

What extra-intestinal manifestations can we see in inflammatory bowel disease?

A
  • Hepatic manifestations - fatty change and granulomas. We can also see PSC and bile duct carcinoma
  • Osteoarticualr - Polyarthritis, sarco-ileitis and spondylitis
  • Muco-cutaneous - oral ulcers, pyoderma grangrenosum and erythema nodosum
  • Ocular - retinitis
  • Systemic - Amyloidosis and thrombi-embolic disease
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12
Q

What is Ischaemic Bowel Disease?

A

This is a “colonic injury secondary to an acute, intermittent or chronic reduction in blood flow.” It may be transient, chronic or a severe acute necrotising form.

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13
Q

What is the aetiology of Ischaemic Bowel Disease?

A
  • Arterial embolism (40-50%) especially in cardiac problems such as MI, AF, endocarditis
  • Arterial thrombosis
  • Non-occulsive mesenteric ischaemia
  • Low cardiac output with mesenteric. vasoconstriction e.g. MI, CCF, major surgery & trauma
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14
Q

Why is the splenic flexure the most likely place for ischaemic bowel to present in?

A

Splenic flexure is a watershed area and so the arterial blood supply is not so good and so more prone to ischaemia.

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15
Q

Give example classifications of colorectal polyps.

A
  • Hyperplasia polyps - commonest type of non-neoplastic polyps. They are often multiple found in the rectum, caecum and sigmoid. They are often unimportant.

Hamartomatous polyps:

  • Peutz-jeghers polys - these are are and seen in AD. they present in adolescences with abdominal pain due to intussusception, gastrointestinal bellying and anaemia. It may also present with a muco-cutaneous pigmentation.
  • Juvenile polyps - seen in the rectum or distal colon. Sporadic polyps have no malignant potential. Juvenile polyposis is associated with increased risk of colorectal cancer and gastric cancer. It is a very uncommon genetic disease. They can occur at any age.
  • Polyps related to mucosal prolapse
  • Prost-inflammatory polyps
  • Inflammatory fibroid polyps
  • Benign lymphoid polyps
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16
Q

What is the most common neoplastic polyp?

A

Adenoma
- May cause diarrhoea, bleeding (if big and ulcerated) and pain. They have the potential to progress to malignant. They are in 30% of the population in the over 50s.

17
Q

What are risk factors for Colorectal cancer?

A
  • Diet
  • Obesity
  • Dietary fibres
  • Alcohol
  • NSAIDs and aspirin (protective)
  • HRT and oral contraceptives
  • Schistosomiasis
  • pelvic radiation
  • UC and Crohn’s disease
  • Family history e.g. Familial adenomatous polyposis - AD due to mutation in the APC tumour suppressor gene (2-3%) and Lynch Syndrome (1-2%) - due to mutations in DNA mismatch repair gene
18
Q

What is the most common colorectal cancer?

A

Adenocarcinoma (95%)

19
Q

How does colorectal cancer spread?

A
  • Direct invasion of adjacent tissues
    • Lymphatic metastasis ( lymph nodes )
    • Haematogenous metastasis ( liver & lung ) - but also brain, skin and bones
    • Transcoelomic ( peritoneal ) metastasis
    • Iatrogenic spread e.g. needle track recurrence, port site recurrence - through seeding
20
Q

How is TNM staging used in colorectal cancer?

A
  • T stage is how far it has spread into the bowel wall - spread to the submucosa T1, T2 invades to the muscular wall but not through it, T3 through the muscular wall and T4 perforates into the abdominal cavity`.
  • Nodal staging is based on the number of nodes involved.
  • M looks at metastasis.

Staging is important in the management of cancer as it tells you how likely the tumour is to be cured by surgery, to recover, lead to mortality and triage which patients need additional treatment.