Colorectal Flashcards
82 How are anal fissures treated?
Conservative
- High fibre diet
- Adequate fluid intake
- Sitz bath (bathing perianal area in water/saline)
- Stool softeners
Medical
- Topical analgesia
- Topical muscle relaxants (PR GTN, topical diltiazem, topical nifedipine) to target internal anal sphincter
- Botulinum toxin injection
Surgical (very rarely done)
- Partial lateral internal sphincterotomy (risk of faecal incontinence)
- Anal advancement flap (less effective but less risk)
83 What is an anal fissure?
How does if develop?
What causes it to persist?
Longitudinal tear in the skin and mucosa of the anal canal, distal to the dendate line
Primary causes = trauma (hard stool, prolonged diarrhoea, vaginal delivery, anal sex)
Secondary causes = previous anal surgical procedures, IBD, malignancy, communicable diseases (HIV, syphilis, chlamydia)
In chronic anal fissure, persistent IAS spasm prevents healing and causes repeated tearing open of the fissure
84 How would you go about investigating a previously well 63 yoa man who presented to you with a short history of rectal bleeding?
All rectal bleeding is assumed to be due to a rectal tumour until proven otherwise
History:
- Characterise bleeding (duration, frequency, volume, colour, relationship to stool)
- PMH pain, constipation, weight loss, diarrhoea
- Fx colorectal cancer
- Medications (esp. anticoagulants)
- Prev colonoscopy findings
- Smoking
Examination
- Vitals
- Abdominal exam incl. PR
- Signs of chronic anaemia (conjunctival pallor, SOB)
Investigation
- Bloods: FBC, iron studies
- Stool MCS OCP
- Sigmoidoscopy/colonoscopy
Ddx
- Anorectal: haemorrhoids, acute anal fissure, distal proctitis, rectal prolapse
- Rectosigmoid: rectal tumour, proctocolitis, diverticular disease
- Proximal colon: colonic tumour, colitis, angiodysplasia, NSAID- induced ulceration
85 How would you go about investigating a previously well 63 yoa man who presented to you with a short history of anaemia?
History
Dizziness, SOB, chest pain
Constitutional symptoms
PR bleeding, change in bowel habits
PMHx
PUD, GORD, malignancy, haematology, IBD, liver disease, coeliac
Dietary, smoking, EtOH
iFOBT, colonoscopies
Medications
NSAIDs, anticoagulants
Ix
FBC, iron, B12, folate, DAT
ECG
iFOBT
86 How would you go about investigating a previously well 63 yoa man who presented to you with a short history of a change in bowel habit to more frequent evacuation of loose stools with mucus?
Mucus is suggestive of an inflammatory diarrhoea
Causes
- Irritable bowel syndrome
- Villous adenoma
- Inflammatory bowel disorders
- Diverticular disease (occasionally)
- Haemorrhoids (maybe)
History
- Change in bowel habits (duration, frequency)
- Associated symptoms: PR bleeding, abdo pain, weight loss, fatigue
- Constitutional symptoms
- PMH: IBD
- Fx IBD, colorectal cancer
- Social: smoking, EtOH, recent gastro contacts, change in diet
Examination
- General inspection and vitals
- Abdo exam incl. PR
Investigation
- FBC, iron studies, serum B12 and folate
- Faecal calprotectin (released into the intestines in excess when there is any inflammation)
- Colonoscopy
87 What are the major risk factors for colorectal cancer?
There are non-modifiable, medical and lifestyle risk factors for colorectal cancer
Colorectal adeonomas are the most significant risk factor as cancer is thought to progress from them
Non-modifiable
Family history
Increasing age
Hereditary syndromes (FAP, HNPCC, SPS)
Medical comorbidities
IBD
Diet and lifestyle
Smoking
Alcohol
Obesity
Processed meat, high fat, low-fibre diet
88 What method is used for population screening for Colorectal cancer in Australia?
FOBT - used in asymptomatic average risk population 2-yearly between the ages of 50 and 75. It will be fully implemented by 2020
Average risk (no personal hx/fx/polyps/IBD, 1 x 1st/2nd degree relative with CRC \>55yo) - FOBT 2-yearly from age 50 to 75
Moderate risk (1 x 1st degree relative with CRC >55yo OR 2 x 1st degree on same side of family with CRC at any age OR 1 1st 1 2nd same side any age)
- Colonoscopy/sigmoidoscopy+CT colonography 5-yearly from age 50 (or 10 years younger than dx age in relative)
- FOBT every non-colonoscopy year
High risk (3+ 1st or 2nd same side with CRC/Lynch syndrome OR 2+ with CRC + high risk features OR suspected FAP OR confirmed fx of APC mutation)
- Genetic screening
- Flexi sig (FAP) or colonoscopy (attentuated FAP)every year between ages 12-35, 3-yearly after 35yo
- Colonoscopy + prophylactic aspirin (Lynch syndrome) 1-2 yearly from age 25 or 5 years younger than earliest family dx
89 What is neoadjuvant therapy for rectal cancer?
Neo-adjuvant therapy is the administration of therapeutic agents prior to the main surgical treatment. Surgical resection is the mainstay curative treatment of rectal adenocarcinomas.
Benefits:
- Improvement in resectability
- Tumour regression
- Higher rate of sphincter preservation
Indications:
- Usually only for T3 or T4
- Clinically node-positive T1 or T2 staged by MRI or trans-rectal USS (relative)
- Distal rectal tumour requiring abdominoperineal resection (relative)
- Tumour appears to invade mesorectal fascia on pre-op imaging (relative, decreased likelihood of achieving clear margins)
No established best regimen
- “Long course” = conventional fractionation RT + long-course concurrent chemo (5-FU)
- “Short course” = short-course RT only
90 Where are the common sites that metastatic disease from a colorectal primary are found?
Common:
- Liver (venous drainage via portal system)
- Lungs (next organ in the venous pathway)
- Peritoneum (proximity)
- Regional lymph nodes
Less common:
- Bone
- Brain
- Adrenal glands
- Kidneys
91 What are the treatment options for liver metastases from a colorectal primary?
Different from the normal approach to metastasis - 1/3 of CRC patients with mets have isolation to the liver, therefore curative treatment can still actively be pursued
Some general rules:
1) Resect where possible
2) RFA where surgically resectable lesion but patient not fit for surgery
3) Neo-adjuvant chemo or palliative chemo where surgically unresectable
Pre-op management
1) Neo-adjuvant chemo (unresectable -> resectable) - 5-FU, leucovorin, oxaliplatin (by HIA)
2) Portal vein branch embolisation (block flow to diseased portions, increases remnant liver volume due to post-embolisation regeneration, enabling hepatectomy while reducing risk of post-op liver failure)
Surgical resection
- Only treatment with definitive survival benefit
- MRI and PET to identify hepatic lesions and occult mets
- Procedure: segmentectomy/lobectomy OR wedge resection (smaller, non-anatomical)
- Can be done at same time as resection of CRC primary
Resection eligibility:
1) Primary cancer is being resected for cure
2) No extra-hepatic mets
3) Adequate post-resection hepatic function (at least 2 of 8 segments)
4) No involvement of major structures (portal vein, hepatic artery)
Radiofrequency ablation (RFA)
- Insertion of image-guided probe percutaneously into the tumour which produces high energy current into the tumour bed to effectively burn cancer cells
- Limited evidence (no RCT assessing efficacy)
Selective Internal Radiation Therapy (SIRT)
- Catheter-guided injection of small radioactive particles into the hepatic blood vessels and the blocking of hepatic vessels to trap beads in the tumour bed
- Targeted approach minimises damage to healthy parenchyma
- BUT, lack of evidence (no RCT)
92 What is the adenoma-carcinoma sequence?
The adenoma-carcinoma sequence is the progressive accumulation of mutations in oncogenes (e.g., KRAS) and tumour suppressor genes (e.g., APC, TP53) that results in the slow transformation of adenomas into carcinomas
It is based on the hypothesis that CRCs develop from intermediate pre-cancerous precursors such as adenomas/adenomatous polyps that become dysplastic over the course of 5-10 years.
During the normal growth process, epithelial cell proliferation occurs at the crypt base. As the cells migrate luminally they cease proliferating and then terminally differentiate.
In the adenoma-carcinoma sequence, the normal growth pattern becomes increasingly disrupted, with normal epithelium transforming into dysplastic aberrant crypt foci into adenoma as the tissue increases in size. This may be due to genetic predisposition (e.g. APC gene) or inactivation of DNA repair mechanisms.
Eventually, sufficient changes to oncogenes and tumour suppressor genes cause progression to a carcinoma which gains invasive potential
93 What is Crohn’s disease?
Crohn’s disease is an incurable chronic inflammatory bowel disease that can affect any part of the GIT from mouth to anus, characterised by unpredictable flares and remissions.
Epidemiology
- Males = females
- Peak age of symptom onset is teens to early 20s (with a second smaller peak 60-80yo)
- 4-10 per 100,000 annually
Aetiology is unclear but genetic factors and environmental factors are thought to play a role. These include familial histories of the disease, smoking, NSAIDs, and nutritional factors.
Pathology:
- Most commonly involves TERMINAL ILEUM and CAECUM (hence RLQ pain)
- Transmural inflammation
- Skip lesions, luminal stricturing, fistulation
- Deep ulceration creating cobblestone appearance
- Mesenteric “fat creeping” on small bowel
Clinical features: diarrhoea (non-bloody), malabsorption/weight loss, abdominal pain (usually RLQ), N/V, extra-intestinal manifestations (e.g. arthritis, skin disorders, vitamin B12 deficiency)
Investigations: colonoscopy + biopsy, CT/MRI enterography, exclusion of other inflammatory diarrhoea causes (stool MCS & OCP, c. diff toxin assay)
Management:
- Conservative: nutrition supplementation/elimination diet/low carb + symptomatic therapy (loperamide, paracetamol)
- Medical: prednisone, oral corticosteroids (budesonide), IV corticosteroids (hydrocortisone. methylprednisone), immunosuppression (azathioprine, methotrexate, mercaptopurine), immunomodulators (TNF-a inhibitors e.g. infliximab)
- Surgical: resection of obstructed areas (but NOT curative)
Antibiotics (metronidazole and ciprofloxacin) should only be used in perianal and fistulising disease.
94 What is diverticular disease?
Acquired outpouchings of colonic mucosa and overlying connective tissue through colonic wall
Mostly asymptomatic, but may present as diverticulitis or bleeding diverticular disease
Diverticulitis: LIF pain, nausea, fever, loose stools
Bleeding: large volume dark red, clotted blood. Due to rupture of a peridiverticular submucosal blood vessel
Environmental factors: chronic lack of dietary fibre, decreased physical activity, obesity, red meat consumption, excess alcohol/caffeine
Genetic factors: altered colonic wall structure (e.g. increased collagen synthesis and elastin deposition), connective tissue abnormalities
Commonly affected areas are sites of potential defect between teniae coli where mucosal blood vessels penetrate the wall. The sigmoid colon is most commonly affected.
Right-sided diverticular disease commonly affects Japanese, Chinese, Polynesian, and Hawaiian patients.
Isolated caecal diverticula are common in westernised countries and are susceptible to perforation.
95 What is diverticulitis?
How does it present clinically?
Diverticulitis is the inflammation of one or more diverticulum. It can be acute or chronic, uncomplicated or complicated by diverticular abscess, fistula, bowel obstruction, or free perforation.
Incidence increases with age and is increasing with low-fibre diets being prevalent in westernised society.
Signs and symptoms: LLQ pain (70%), change in bowel habits, N/V, flatulence, bloating
On examination: fever, localised tenderness, tender palpable mass (where diverticular abscess present), signs of perforation (peritonism, distension, absent/reduced bowel sounds), signs of fistula (PV discharge, UTI)
96 What are the major complications that can result from diverticulitis?
- Abscess
- Perforation (frank or contained/micro)
- Fistula (between bladder, vagina, uterus, other bowel segments, and the abdominal wall
- Obstruction