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COLORECTAL > COLORECTAL > Flashcards

COLORECTAL Flashcards

1
Q

What is the difference between a hyperplastic, traditional serrated adenoma (TSA) and a sessile serrated adenoma (SSA)?

A

all 3 are serrated polyps which have varying malignant potential

hyperplastic = normal cell architecture, no dysplasia, rectosigmoid

TSA = have dysplasia, rectosigmoid

SSA = lack classic dysplasia but may have mild cytologic atypia. Located more proximally.

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2
Q

How do you do diagnose sessile serrated polyposis syndrome?

A

Use WHO criteria (number and/or size of polyps)

Number

  • >20 + any location

or

  • >5 + proximal to sigmoid
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3
Q

what is the cause of adenomatous polyps?

A

genetic mutations = MMR pathway, APC pathway

enviromental = reduced fibre, increased fat (more associative rather than causative

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4
Q

what is the Vogelstein hypothesis?

A
  • mutations are required for malignant transformation,
  • the accumulation of multiple genetic mutations rather than their sequence determines the biological behavior of the tumor
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5
Q

What are the mismatch repair genes?

A

MLH1, MSH2, MSH6, PMS2

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6
Q

what is meant by RAS? (e.g. K-RAS)

A

Types

  • RAS = oncogene with 3 subtypes (K-RAS, H-RAS, N-RAS)
  • K-RAS most frequently mutated

Function

  • one-way switch for the transmission of extracellular growth signals to the nucleus

K-RAS mutations

  • constitutively active GTP-bound protein and a continuous growth stimulus
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7
Q

How is finding a K-RAS mutation clinically relevant?

A

epidermal growth factor receptor (EGFR) such as cetuximab less effective

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8
Q

What is meant by CIMP?

A

CpG Island hyperMethylation Phenotype pathway (CIMP+)

  • Methylation of CpG islands inactivates genes
  • May result in hypermethylation of the promoter region of MMR enzymes such as MLH1 and silencing of gene expression (­ accumulation of errors similar to MMR pathway)
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9
Q

what is the Amsterdam criteria?

A

(Modified) Amsterdam criteria (3,2,1 rule)

  • 3 relatives with a HNPCC cancer (colorectal, endometrium, small bowel, urothelium)
  • 2 successive generations
  • 1 affected individual is <50
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10
Q

what is the Bethesda criteria?

A

Bethesda criteria

  • BET
  • Histopathology – resembles MSI pathology in patients <60 years (LAMPS)
  • Extracolonic cancers – endometrium, small bowel, urothelium
  • Single – 1st degree relative < 50
  • Double 1st/2nd degree relative HNPCC cancer
  • Age < 50
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11
Q

What are the pathological features that suggest Lynch?

A

LAMPS

Tumour infiltrating lymphocytes, Crohn’s like lymphocytic reaction

associted extracolonic features (endometrium, stomach, ovary, small bowel)

Metachranous, mucinous

Proximal (right sided), poorly differentiated

signet ring,

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12
Q

Pathophysiology of C diff

A

Anerobic Gram-positive spore forming and toxin producing organism

Antibiotics = disruption of colonic flora = C difficile spores ingested = toxins released

TOXINS

Toxin A (enterotoxin)

  • Neutrophil chemotaxis causes inflammation, mucosal injury, fluid secretion mediated by cytokines IL-1, TNF-a

Toxin B (cytotoxin)

  • 10 times more virulent than toxin A
  • is the clinically important toxin; no CDAD due to toxin A alone has been reported.

Once intracellular, toxins A + B inhibit regulatory pathways leading to apoptosis and disrupt intercellular tight junctions.

A minority of C. difficile strains (10 to 30 percent) are non-toxigenic and do not produce toxins; these strains can colonize the gastrointestinal tract and grow normally in culture media but are not pathogenic

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13
Q

What are the risk factors for anal cancer?

A

immunosuppressed - HIV, transplant, steroids

MSM -

AIN (especially high grade)

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14
Q

what HPV subtypes cause anal warts and anal intra-epithelial neoplasia (AIN)

A

AIN = HPV 16 + 18

warts = HPV 6 + 11

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15
Q

What is the Nigro protocol?

A

Definitive chemodradiation using Nigro protocol

  • Infusion of 5-FU (days 1-4 and 29-32)
  • Mitomycin C (Day 1)
  • 30 Gy radiotherapy over 3 weeks
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16
Q

Managment principles

A

“CARESS”

Cause

  • primary (cryptoglandular)
  • secondary (crohn’s, cancer, radiation, trauma)

Anatomy

  • define anatomy. Park’s classification.

Risk (simple vs. complex)

  • Simple = intersphincteric/low transphincteric.
  • Complex = recurrent, high, horshoe, Crohn’s, anterior in women)

Eradicate

  • eradicate as much fistula tract as possible
  • identify both ends (internal and external)

Sepsis

  • Drain sepsis
  • obvious internal opening = seton
  • if not obvious = leave alone as can cause iatrogenic fistula

Sphincters

  • preserve as much as possible
  • document
17
Q

What is the cryptoglandular theory?

A

blocked anal gland becomes infected. pus follows the path of least resistance and results in fistula formation

18
Q

What is the difference between internal and external haemorrhoids?

A

internal

  • above dentate line
  • superior haemorrhoidal cushion
  • epithelium = columnar
  • visecerally innervated – insensitive to pain/touch/temperature

external

  • below dentate line
  • inferior haemorrhoidal plexus
  • epithelium = modified squamous
  • somatically innervated - painful
19
Q

Pathogenesis

A

Primary – usually posterior midline

  • Trauma – forceful tearing of anal canal (hard formed stools/constipation, anal sex)
  • Anodermal ischaemia (of posterior midline anal canal) – end arteries susceptible to ischaemia
  • Hypertonicity of IAS - Increased resting anal pressures from sustained resting hypertonia

Secondary - Usually lateral

  • AIDS/HIV
  • TB
  • Crohn’s disease, Cancer
  • STDiseases (sexually transmitted) – syphilis
20
Q

What are the theories of pilonidal disease development?

A

Simple = hairs either block or cause trauma/foreign body reaction

Bascom’s theory (Blockage theory)

  • Hair follicles become distended with keratin causing obstruction and secondary abscess formation.
  • Abscess ruptures into subcutaneous tissue causing sinus

Karydarkis’ theory (foreign body reaction)

  • Hair roots with chisel like ends insert into the natal cleft causing foreign body tissue reaction and infection.
21
Q

what are the microscopic features of UC?

A
  • Submucosal/mucosal layer only
  • crypt abscess
  • goblet cell depletion
  • no (non-caseating) granulomas
22
Q

What are the findings of UC on colonscopy?

A
  • Loss of vascularity
  • mucosal oedema
  • contact bleeding
  • ulceration
  • pseudopolyps
23
Q

What is the Truelove and Witts criteria for determining the severity of UC?

A

HITTS

Severe UC

  • Haemoglobin <105
  • Inflammatory markers - CRP>30
  • Tachycardia - >90
  • Temperature >37.8
  • Stools (bloody) - >6/day
24
Q

What are the key components of medically managing acute UC?

A

Resuscitation

  • fluids, electrolytes
  • nutrition
  • Hb > 100

Medications

  • stop - ones that increase toxic dilatation (NSAIDs, antidirrahoeal, anti-cholinergic)
  • start - hydrocortisone 100 mg TDS (maximum 5 days)

If fails, then 2 options

  • surgery (3 stage - subtotal colectomy + ileostomy, completion proctectomy, ileostomy reversal)

or

  • immune therapy (infliximab, tacrolimus)
25
Q

What medications are not safe in pregant IBD patients?

A

Methotrexate

  • stop before (ie trying to conceive)
  • during pregnancy (teratogenic)

Sulfasalazine

  • can be used but impairs folic acid synthesis
  • must be given with folate

remainder (steroids, biologics, antibiotics, immunomodulators) safe in low doses

26
Q

What is the mechanism of stone formation (gallstones, kidney stones) in IBD?

A

Gallstones:

  • Common in Crohn’s because TI disease → ↓ bile salt pool → lack of enough bile salts to solubilize the cholesterol in bile

Kidney stones:

  • oxalate stones mechanism: due to ileal disease, non-absorbed fatty acids bind to calcium in the intestinal lumen, allowing free oxalate (which would usu bind to Ca) to be absorbed from the colon
27
Q

Which type of antibodies are found in IBD?

A

Crohn’s = ASCA

UC = P-ANCA

28
Q

What are the indications for TEMS?

A
  • T1 if Haggit 1-3
  • mobile tumour < 3cm in diameter
  • well differentiated
  • no LVI
  • no nodal metastasis
29
Q

When do you offere surveillance colonoscopy for patients with

  1. adenomas
  2. genetic syndromes
  3. IBD
A

Adenomas

  • high risk adenoma (> 3 adenomas, villous/TV/HGD, measuring >1 cm) = 3 yearly
  • low risk adenoma = 5 yearly

Genetic syndromes

  • FAP = 1-2 yearly colonoscopy at 12-15 (gastroscopy at 30). Prophylactic colectomy in teens
  • Lynch = 2 yearly from 25

IBD

yearly if

  • active disease
  • complicated disease (stricture, inflammatory polyps)
  • DALMs (LGD)
  • PSC
  • FHx of CRC in first degree relative <50

3 yearly if

  • stable disease (ie none of above factors)

5 yearly if

  • last two scopes were normal macroscopically and histologically
30
Q

How do you manage dysplasia in UC?

A

confirm diagnosis with 2nd pathologist

HGD or multifocal LGD or DALM in raised lesion = colectomy

not above = surveillance (preferably with chromendoscopy. If not possible then random 4 quadrant biopsies every 10 cm)

31
Q

Which patients with CRC do you give chemotherapy to?

A

Stage I

  • none

Stage II

  • Controversial but consider if high risk features (T4, LNC>12, obstructing/perforating cancer, LVI, positive/close margins)

Stage III

  • FOLFOX (based on MOSAIC trial - NEJM 2004) for 6 months

Stage IV

  • Multiple protocols but main are either FOLFOX, FOLFIRI or FOLFOXIRI
  • Add cetuximab if K-RAS wild-type
  • Consider adding bevacizumab
32
Q

How do you treat neutropenic enterocolitis?

A

Management is primarily medical

  • bowel rest
  • broad-spectrum antimicrobials for hospital-acquired infections (including fungal pathogens)
  • intravenous fluid resuscitation
  • correction of neutropenia with granulocyte colony stimulating factors.
  • Colonoscopy has no role in the diagnosis or treatment of NE.

Surgical intervention if

  • gastrointestinal bleeding not responsive to blood component therapy
  • free intra-abdominal perforation
  • clinical deterioration with uncontrolled sepsis
  • other intra-abdominal pathology not associated with neutropenia.
33
Q

When does neutropenic enterocolitis typically occur clinically?

A
  • It typically occurs with the nadir in neutrophil count 10–14 days after chemotherapy.
34
Q

What is the typical CT finding of neutropenic enterocolitis?

A
  • The radiographic finding of pneumatosis intestinalis lacks sensitivity but is very specific for NE.
35
Q

What are the clinical manifestations of FAP?

A

Intestinal

  • Colonic = multiple polyps (>100)
  • UGI = duodenal polyps

Gardner’s syndrome

  • sebaceous cyst
  • desmoid
  • osteomas
  • thyroid cancers
  • CHRPE (congenital hypertrophy of retinal pigment epithelium)

Other

UGI = duodenal/gastric polyps

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