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BCS Lectures > Colin Dale > Flashcards

Colin Dale Flashcards

1
Q

FAB classification

A

slide 12 of haem malignancies lecture

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2
Q

Disorders associated with ALL

A
  • Down’s Syndrome
  • Klinefelter’s Syndrome
  • Fanconi’s anaemia
  • Ataxia-Telangectasia
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3
Q

know all haem malignancy stuff in USMLE notebook

A

know all haem malignancy stuff in USMLE notebook

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4
Q

Infectious causes of NHL

A
  • HTLV1 in adult T-cell leukaemia-lymphoma

- EBV in mature B-cell ALL and Burkitt’s lymphoma.`

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5
Q

ALL clinical characteristics

A

Nonspecific Symptoms

  • Fatigue
  • Anorexia / Weight Loss
  • Fever / Infection
  • Easy & excessive bruising
  • Bleeding (nosebleeds and bleedings from gums)
  • Dyspnoea

Bone /Joint pain

CNS involvement

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6
Q

morphological subtypes of ALL (FAB)

A

Subtype Morphology

Occurrence (%)

L1 - 75%

Small round blasts clumped chromatin

L2 - 20%

Pleomorphic larger blasts clefted nuclei, fine chromatin

L3 - 5%

Large blasts, nucleoli,
vacuolated cytoplasm

Peroxidase or sudan black - L1, L2 and L3 negative

Non specific esterase - L1, L2 , L3 all positive

Periodic acid Schiff - no reaction in any

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7
Q

B Lineage ALL MARKERS

A

B lineage accounts for 80% of ALL

Pro-B
CD19(+),Tdt(+),CD10(-),CyIg(-)

Common
CD19(+),Tdt(+),CD10(+),CyIg(-)

Pre-B
CD19(+),Tdt(+),CD10(+),CyIg(+),SmIg(-)

Mature-B
cD19(+),Tdt(+),CD10(±),CyIg(±),SmIg(+)

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8
Q

T lineage ALL marker

A

T lineage accounts for 20% of ALL

Pre-T
CD7(+), CD2(-), Tdt(+)

Mature-T
CD7(+), CD2(+), Tdt(+)

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9
Q

FavourabLe prognostic factors in ALL

A
  • normal karyotype

-hyperdiploidy
>50 chromosomes

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10
Q

Poor prognostic factors in ALL

A
  • t (8;14)
  • t (4;11)

Very poor

9:22 BCR:ABL

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11
Q

High risk ALL

A
  1. Pre-T cell ALL
  2. Pro-B cell ALL
  3. Age > 35 years
  4. WBC >30,000 in B-ALL
    >100,000 in T-ALL
  5. No remission after 4 weeks of induction
    therapy
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12
Q

Tx of ALL

A

Combination chemotherapy:

  • Induction (4-8 weeks):
  • Goals: restore normal haematopoiesis, induce a

complete remission rapidly

-4 or 5 drugs: vincristine, prednisone, anthracycline,
L-asparaginase, +/- cyclophosphamide

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13
Q

Tx of tumour lysis syndrome?

A

Allopurinol, aggressive hydration

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14
Q

Post remission in high and very high risk ALL

A

Allogeneic stem cell transplantation (SCT)

  • Eradicates patient’s hematopoietic stem cells
  • Replaced with those of an HLA-matched (Human Leucocyte Antigen) sibling donor or a matched unrelated donor
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15
Q

Survival rates in ALL

A

Children - 80%

Adults 30-40%

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16
Q

Recall that, embryologically, the colon is derived from both the mid-gut & hind gut. Where is the division and which arteries supply them?

A

Midgut extended to the proximal ⅔ of the transcending colon and the hind gut begins after this
Midgut supplied by SMA
Hindgut supplied by IMA

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17
Q

Retroperitoneal organs

A 
Suprarenal glands (adrenal)
Aorta (desc)
Duodenum (2nd to 4th part)
Pancreas (except tail)
Ureters
Colon (asc. and desc.)
Kidneys
Esophagus
Rectum
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18
Q

Lymph drainage of the GI

A

lymph vessels – along arteries

lymph nodes - roots of the three

gut arteries in front of the aorta,
(inferior mesenteric, superior
mesenteric, coeliac nodes)

coeliac nodes => cisterna chyli

NOTE:
mucous membrane - ly mphoid follicles

Mesentery - paracolic nodes,
intermediate nodes.

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19
Q

Innervation of the foregut

A

(Coeliac plexus):
Sympathetic: Greater (T5-9) and
lesser (T10-11) splanchnic nerves

Parasympathetic: Vagus

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20
Q

Innervation of the midgut

A

(Superior Mesenteric Plexus):
Sympathetic: Coeliac and lesser
(T10-11) splanchnic nerves

Parasympathetic: Vagus

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21
Q

Innervation of the hindgut

A

(Inferior mesenteric and inferior
hypogastric plexuses):

Sympathetic: Intermesenteric
plexus, and lumbar sympathetic
trunk.

Parasympathetic: Pelvic Splanchnic
nerves (S2, S3, S4).

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22
Q

Features of the sympathetic fibres of the gut

A
  • SEE NOTEBOOK
  • Synapse in preaortic ganglia
  • Travel along arterial supply
  • Result in contriction of the gut and antagonise the PNS
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23
Q

Features of PNS

A

Vagus nerve follows arterial supply - see notebook

Pelvic splanchnic does not follow arterial supply as uniformly see notebook

Sensation of gut follow parasympathetic fibres

Pain afferents are proximal to mid sigmoid and follow sympathetic fibres

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24
Q

Fx of large colon

A
  1. Water absorption

2. Conversion of liquid chyme to solid stool/faeces

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25
Q

Extra features of the colon

A

Teniae coli from base of appendix to rectosigmoid junction

Haustra: sacculation of wall between the teniae

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26
Q

Features of the appendix

A

Blind intestinal diverticulum 6-10 cm

Contains lymphoid tissue

Mesoappendix

Usually retrocoecal

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27
Q

Features of the colon

A

Ascending -

  • Secondarily retroperitoneal
  • In 25% of people is has a short mesentery
  • Right paracolic gutter

Transverse –
- intraperitoneal
- Attaches to the diaphragm through the
phrenicocolic ligament

Descending - 
- Secondarily
retroperitoneal
- In 33% of people is has a short mesentery
especially in the iliac fossa
- Left paracolic gutter

Sigmoid
- From the left iliac fossa to the S3 vertebra
- Rectosigmoid junction – termination of
teniae coli

Sigmoid mesocolon
- inverted “V” shaped attachment
- Posterior to the apex – left ureter and
the division of the left common iliac
artery
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28
Q

Where do the sigmoid and rectum differntiate

A

s3

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29
Q

Features of the rectum

A

RECTUM
- Primarily retroperitoneal and subperitoneal

  • Peritoneal cover:

Superior third - anterior and lateral

Middle third - only anterior

Lower third - none

Continuous with sigmoid at S3

Ends near the tip of the coccyx just before the
anorectal flexure of the anal canal – where the gut
perforates the pelvic diaphragm (levator ani) - 80
degrees

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30
Q

Significance of the angle of the pelvic diaphragm

A

The angle at the pelvic diaphragm is maintained
by the puborectalis muscle and is an important
mechanism for maintaining continence

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31
Q

What is the dilated terminal part of the rectum called and what is its function

A

The dilated terminal part is called the ampulla
of the rectum – holds and accommodates faecal
material until defaecation

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32
Q

Pouches of the rectal area

A

In males, the reflection of peritoneum from the rectum to the posterior bladder wall forms the rectovesical pouch.

In females, the peritoneum reflects to the posterior vagina and cervix, forming the rectouterine pouch (pouch of Douglas)

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33
Q

Blood supply of the rectum

A

See notebook too

SUPERIOR RECTAL ARTERY (& VEIN)
- Continuation of Inferior Mesenteric – proximal part of
rectum

MIDDLE RECTAL ARTERIES (& VEIN)
- From anterior divisions of internal iliac – middle and
inferior part

INFERIOR RECTAL ARTERIES (& VEIN)
- From internal pudendal – anorectal junction and anal canal

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34
Q

Features of the anal canal

A

From the superior aspect of the pelvic diaphragm (puborectalis)
to the anus

2.5 – 3.5 cm long

Surrounded by the external and internal anal sphincters

Except during defecation, the anal canal is collapsed by the internal and external anal sphincters to prevent the passage of faecal material.

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35
Q

Features of the internal anal sphincter

A

Internal anal sphincter – surrounds the upper 2/3 of the anal canal. It is formed from a thickening of the involuntary circular smooth muscle in the bowel wall.

Contraction stimulated and maintained by
sympathetic fibers (superior rectal and hypogastric
plexuses)

Contraction inhibited by parasympathetic fibers
(pelvic splanchnic nerves)

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36
Q

Features of external anal sphincter

A

External anal sphincter – voluntary muscle that surrounds the lower 2/3 of the anal canal (and so overlaps with the internal sphincter). It blends superiorly with the puborectalis muscle of the pelvic floor.

  • Attached anteriorly to perineal body and poster to
    coccyx via the anococcygeal ligament

Superiorly it blends with the puborectalis muscle

Supplied by S4

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37
Q

What is at the junction of the internal and external sphincter and what are their functions

A

anorectal ring. It is formed by the fusion of the internal anal sphincter, external anal sphincter and puborectalis muscle, and is palpable on digital rectal examination.

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38
Q

What is the levator ani made up of

A

From closest to the anus to furthest away

Puborectalis, Pubococcygeus, Iliococcygeus
Coccygeus

Note: These muscles are contracted at normal times and their relaxation allows
urination and defaecation

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39
Q

Difference in the anal canal above and below the pectinate line

A

he anal valves collectively form an irregular circle – known as the pectinate line (or dentate line). This line divides the anal canal into upper and lower parts, which differ in both structure and neurovascular supply. This is a result of their different embryological origins:

Above the pectinate line – derived from the embryonic hindgut.
Below the pectinate line – derived from the ectoderm of the proctodeum.

Superior = columnar epithelium

Below = non keratinised stratified squamous epithelium (known as the anal pecten).

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40
Q

What prevents reflux of colonic contents into the terminal ileum?

A

ileocecal valve

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41
Q

What causes appendicitis? Why does it frequently become gangrenous?

A

Obstruction of the lumen of the appendix is the main cause of acute appendicitis. Faecolith (a hard mass of faecal matter), normal stool, or lymphoid hyperplasia are the main causes for obstruction. Faecolith alone causes simple appendicitis in 40%, gangrenous non-perforated appendicitis in 65%, and perforated appendicitis in 90% of cases.

Becomes gangrenous due to lack of blood supply

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42
Q

Signs and symptoms of appendicitis

A
  1. Constant mid-abdominal pain that later shifts to right lower quadrant. Usually worse on movement.
  2. Anorexia
  3. Classic sign is right lower quadrant abdominal tenderness (McBurney’s sign). There may be localized rebound tenderness, especially if the appendix is anterior. Compressing the left lower quadrant may also elicit pain in the right lower quadrant (Rovsing’s sign). Pain may also be elicited with the patient lying on their left side and slowly extending the right thigh to cause a stretch in the iliopsoas muscle (psoas sign) or by internal rotation of the flexed right thigh (obturator sign).
  4. Nausea, fever
  5. Diminished bowel sounds
  6. Tachycardia (especially in perforation
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43
Q

Characteristics and Fx of the small intestine

A
  • Is divided anatomically into three regions:
    Duodenum: 25 cm long
    Jejunum: 2.5m long
    Ileum: 3.5m long
  • Principal site of disgestion and absorption of food
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44
Q

What is the role of enterocytes

A

secrete enzymes

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45
Q

what are plicae circularis

A 
Plicae circularis (circular folds):
Permanent transverse folds of the
intestinal surface.
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46
Q

Which surface are microvilli found

A

apical surface

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47
Q

Histological features of the duodenum

A 
- Brunner’s glands in the submucosa
(tubuloacinar mucous glands
producing alkaline secretion, pH 8.8
to 9.3, that neutralises the acidic
chime from the stomach)
  • Villi are short and broad (leaflike)
  • Surrounded by incomplete serosa
    and extensive adventitia
  • Base of the crypts of Lieberkuhn may
    contain Paneth cells
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48
Q

do tubular, villous or tubulovillous adenomas have hughest risk of becoming cancerous

A

villous

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49
Q

Histological features of jejunum

A
  • Long finger like villi
  • Well-developed lacteal in the core (central
    lymphatic vessel)
  • No Brunner’s glands in submucosa
  • Paneth cells are found in the crypts of
    Lieberkuhn
  • Some Peyer’s patches in the lamina propria
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50
Q

Histological features of the ileum

A
  • Peyer’s patches: lymphoid follicles
    (nodules) in the mucosa and part of the
    submucosa (GALT: gut-associated
    lymphoid tissue)
  • Lack of Brunner’s glands
  • Shorter finger-like villi
  • Paneth cells at the base of Lieberkuhn’s
    crypts
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51
Q

Components of the small intestinal villi

A
  • Villi consists of a core of loose connective tissue covered by simple columnar epithelium.
  • The lamina propria of the villus contains a central lymphatic
    capillary called the lacteal.
  • Lieberkuhn’s crypts: intestinal simple tubular glands originate from
    the muscularis mucosa, covered with simple columnar epithelium
    that is continuous with the villi epithelium.
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52
Q

Fx goblet cells

A

mucus secretion

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53
Q

Fx of paneth cells

A

Secrete antimicrobial
substances. Easily identified by H&E
due to pink staining of the secreting
granules.

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54
Q

Fx of M cells (microfold cells)

A

modified

enterocytes that cover the lymphoid

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55
Q

Histological features of the large intestine

A
  • Circular folds and villi are NOT present.
  • It contains numerous straight tubular glands that extent through the
    full thickness of the mucosa.
  • The mucosa is covered by simple columnar epithelium.
  • The principal function of the large intestine is the reabsorption of water
    and electrolytes and the elimination of undigested food.
  • The mucosa contains the same cell types (Goblet cells, enterocytes), as
    the small intestine except Paneth cells that are absent in humans.
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56
Q

Histology of rectum

A
  • Can be distinquished by the presence of transverse rectal folds.
  • The mucosa is similar to the distal colon.
  • Straight tubular glands with numerous goblet
    cells
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57
Q

Histology of the anal canal

A

Divide into three zones:

Colorectal zone: simple columnar epithelium

Anal Transitional Zone: Transition between simple
columnar to stratified squamous epithelium.

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58
Q

Types of polyps

A

Sessile: No Stalk, Pedunculated: Stalked

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59
Q

Are polypscancerious

A

no

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60
Q

Types of adenommas

A

Tubular adenomas: Tubular glands

Villous adenomas: Vilous Projections

Tubulovillous adenoma: A mixture of the previous two

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61
Q

Histology of a polyp

A

serration of the luminal epithelial surface.

Delayed shedding of the epithelial cells leads to infolding and fission of the crypts

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62
Q

What are juvenile polyps

A 
Juvenile polyps are
hamartomatous lesions that
consist of a lamina propria
and dilated cystic glands
rather than increased
numbers of epithelial cells
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63
Q

What are peutz-jeghers polyps

A 
hamartomatous
lesion of glandular
epithelium supported by
smooth muscle cells that
is contiguous with the
muscularis mucosa
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64
Q

Features of tubular adenoma

A

the glands resemble normal colonic
tubules; these are often small and pedunculated, with low grade
dysplasia

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65
Q

Features of villous adenoma

A

sessile up to 10cm in diameter. Their histology is
characterized by villiform extensions of the mucosa, covered by
dysplastic and disordered columnar epithelium. All degrees of
dysplasia may be encountered.

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66
Q

Features of tubulovillous a

A

the glands resemble normal colonic
tubules but are thrown up into villous folds in many areas; these are
often large and may be sessile or pedunculated . Variable dysplasia.

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67
Q

Describe the adenoma carcinoma sequence

A

see slide 30 of colon cancer histology lecture

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68
Q

Tumour markers in the blood

A
  1. AFP : (hepatocellular Ca),
  2. Ca19.9 (pancreas),
  3. Ca125 - (ovary)
  4. CEA (colorectum –more often used in
    follow-up)
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69
Q

Describe familial polyposis coli

A
  • Germline mutation of APC gene

- Offered colectomy as soon as first adenomas appear

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70
Q

Describe TNM staging

A

T1: confined to submucosa

T2: confined to muscle

T3: through muscle into fat

T4: exposed on serosal surface or
invades adjacent organ/structure

N0: no nodes involved

N1: <4 nodes involved

N2: >4 nodes involved

M0/1: metastases -/+

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71
Q

Staging of cancer

A

Stage 0:
Tis N0 M0
~100% 5YS

Stage I:
T1/2 N0 M0
94% 5YS

Stage II:
T3/4 N0 M0
83% 5YS

Stage III:
Any T N1/2 M0
56% 5YS

Stage IV:
Any T Any N M1
27% 5YS

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72
Q

Dukes staging (not used practically)

A 
A – Tumour infiltrating to
muscularis propria
• B – Tumour infiltrating
through bowel wall
• C – Tumour with lymph
node involvement
• ‘D’ – Distant Metastases
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73
Q

Tumour gradin

A
  • Refers to how much the tumor
    cells resemble normal cells of the same tissue type
  • G 1, 2, 3, and 4.
  • Grade 1 tumors resemble normal cells, and tend to grow and multiply
    slowly. Grade 1 tumors are generally considered the least aggressive in
    behavior.
  • Grade 3 or Grade 4 tumors do not look like normal cells of the same type.
    Grade 3 and 4 tumors tend to grow rapidly and spread faster than tumors
    with a lower grade. There are different grading systems for each type of
    cancer.
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74
Q

5YS Dukes

A

A = 85-90+%

B = 60-80%

C = 15-45%

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75
Q

Oncogene inheritence

A

usually autosomal dominant

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76
Q

TSG inheritance

A

usually autosomal recessive

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77
Q

Describe hypermethylation of CPG islands

A

repeated C-G-C-G-C-G- etc sequences found in many commonly
‘silenced’ tumour-related genes is often the way the 2nd
copy of a gene is ‘knocked out’, eg APC or RB-1

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78
Q

Featuresof growth factor oncogenes

A

Increased growth factor (autocrine
or paracrine effects) or abnormal growth factor production (eg c-sis
encodes FGF). Many other growth factor mutations are linked to tumours,
eg PDGF, EGF.

79
Q

Features of cell-surface growth factor receptors

A

Increased growth factor receptor
expression or abnormal growth factor receptors (eg Her-2-neu gene
encodes EGFR – gene amplification due to mutation indicates that the
drug Herceptin will be clinically effective.)

80
Q

Featrures of signal transduction oncogenes

A

Permanent activation of intracellular
signalling mechanisms cause continuous signal transduction (eg v-src
encodes a protein tyrosine kinase, c-ras encodes a
membrane-associated G-protein receptor). Ras gene point mutations are
the commonest oncogene mutations, eg colon, breast and lung cancers.

81
Q

Features of nuclear protein oncogenes

A

Mutations of the messenger molecules which initiate
DNA transcription produce oncoproetins which continually stimulate cell
division. Translocation of c-myc to lie beside the Ig gene occurs in
Burkitt’s lymphoma (t8:14); amplification of myc is seen in breast and
lung cancer.

82
Q

Resistance to apoptosis oncogene

A

(eg BCl-2 mutation prevents caspase

activation)

83
Q

Featuresof TSG

A

gene mutations are

“recessive”, ie both alleles must be mutated).

84
Q

TSGs that act on intermediate messengers

A

beta catenin acts in the cytoplasm, on
microtubules or cell-cell adhesion mechanisms
(APC acts at all these points).

85
Q

TSGs affecting cell cycl

A

(The APC gene is a bit confusing, with bothdominant effects (AD inheritance in FAP) and a
TSG effect. This is probably due to effects on
both beta and gamma catenin .)

86
Q

Featuresof p53, p21, p16-INK4:

A

P53 - a ‘caretaker gene’. P53
protein is produced if there is DNA damage. If DNA
repair is possible, p53 activates transcription of p21
protein. This inhibits CDKs, arresting the cell cycle
while DNA repair enzymes work. If repair is
impossible the cell is consigned to apoptotic death.
P53 mutation permits further mutations to occur.

87
Q

Features of retinoblastoma gene

A

RB binds
transcription factor E2F, preventing it from driving
the cell cycle from G1 to S phase. Phosphorylation
of RB by CDK causes it to dissociate from E2F.
TFE2F activates DNA transcription genes, allowing
progression from G1 to S phase. P16-INK4 binds
CDK4/CyD, preventing phosphorylation of RB, thus
inhibiting progression.

88
Q 
Features of Cyclin kinases (eg CyB, D,E) and cyclin
dependent kinases (eg CDK1,2,4))
A

suppressed by p53, p21 or p16, or

non-phosphorylated RB protein.

89
Q

Features DNA mismatch repair enzymes,

A

eg MLH-1 and
MSH-2. MMR remove mismatched DNA segments
and install accurate replacements. These genes
protect against spontaneous replicative errors
during mitosis.

90
Q

Microscopic features of malignancy

A

high N:C ratio
and their nuclei usually
show a variety of shapes
and much size variation.

Nuclear chromatin is coarse
in malignant tumours and
nucleoli are often prominent
and strange shapes.

Mitoses tend to be easily
visible on microscopy of
malignant tumours and are
often bizarre in shape.

91
Q

definition of metaplasia

A

alteration of one mature

cell type for another

92
Q

Are there precursors to cancer (ie can

we predict that a cancer will develop)?

A

Inherited mutations in key cancer-related
genes predispose to cancer development, eg:

  • APC gene mutation (Ca colon)
  • Mismatch repair (MMR) enzyme mutation (Lynch
    syndrome /HNPCC)
  • BRCA-1 or 2 (Ca breast and elsewhere)
  • RB-1 (retinoblastoma)
  • NF-1 (neurofibromatosis, some sarcomas)
93
Q

Where is squamous epithelium found

A

Covers skin, oropharynx, oesophagus,
anal canal, vagina, external auditory canal

  • Benign and malignant tumours may arise
    as a result of viral infection (eg HPV)
94
Q

Definition of koilocytosis

A

term for warty
changes in the epithelium: spiky
nuclei and perinuclear haloes

95
Q

Where is glandular epithelium found

A 
-Covers entire GI tract from stomach to
rectum
Lines ducts and acini of glands
Forms tubular structures, such as renal
tubules
  • Glandular tumours may arise at
    ‘inappropriate’ sites following
    metaplasia, eg Barrett’s metaplasia in
    gastro-oesophageal reflux disease
96
Q

Where is urothelium (transitional epithelium)

A

Covers urothelial tract, ie renal pelvis,

ureter, bladder and urethra

97
Q

Festures of tumours of renal parenchyma

A

Tumours of the renal parenchyma itself are a subtype of
adenocarcinoma, but because of their distinctive clear cells are
usually known as ‘clear cell carcinoma’

98
Q

Germ cell tumours

A

Testicular tumours, eg:
Teratoma
Seminoma

Ovarian germ cell tumours, eg:
Teratoma
Dysgerminoma

99
Q

which tumours do not spread

A

brain - BBBW

100
Q

Which cells to GI stromal cell tumours arise from

A

Interstitial Cells of

Cajal – the pacemaker cells in the gut.

101
Q

How do we predict GIST

A

Predicting their behaviour is made by assessing size and
mitotic activity and evidence of metastatic disease.
Tumours <2cm diameter are almost always benign.

102
Q

tX OF gist

A
  • surgical – the stomach is the commonest site and wedge resection is sufficient.
  • Most inoperable GISTs respond well initially to Imatinib
    (Glivec), a ‘designer drug’ which blocks TK receptors.

Mutational analysis is important in determining

103
Q

What is transcoelomic spread

A

across peritoneal cavity

eg ovarian metastases from colorectal or
gastric primary (krukenberg tumours)
104
Q

Implanation spread of tumour

A

laparotomy wound or laparoscopic trocar ports.

105
Q

Pre operative staging of colorectal cancer

A

Best estimate of the extent of disease at the time of diagnosis, based
on the results of the physical examination, colonoscopic biopsy, pre
op US, CT, MRI etc.

106
Q

Tis tumour

A

Tis: (in situ). Tumour

involves only the mucosa.

107
Q

Tx of T1- T2, N0, M0

Tumour is localized within the bowel

A
  • Surgical Resection is usually adequate treatment
  • No additional pre operative (neoadjuvant) or post-operative (adjuvant)
    therapy (Chemo or radiotherapy) is necessary
108
Q

Tx of T3, T4, N0
Any T with Nodal or M involvement
Tumour has breached the wall of the bowel

A
  • Surgical Resection alone is inadequate treatment
  • Additional pre operative (neoadjuvant) or post-operative (adjuvant) is
    necessary
109
Q

Types of bowel polyps

A
  • Pseudopolyps – ( UC, crohns disease)
  • Hyperplastic
  • Hamartomatous - (Peutz Jeghers Syndrome) - malignant
  • Adenomatous - (Familial Adenomatous Polyposis) - malignant
110
Q

What does the risk of malignant transformation depend on?

A
  • Number of polyps
  • Their size (>2cm)

• The histological characteristics of
the polyp
• Tubular
• Villous

111
Q

Defining high risk cancerous polyps

A

Positive resection margin

and / or

Poorly differentiated

and / or

Vascular or lymphatic invasion

112
Q

Pros of surgical resection

A
  • Certainty of local control
  • Relevant lymph node clearance
  • Accurate staging
113
Q

Cons of surgical resection

A

• Morbidity and mortality of surgery

114
Q

What are the symptoms of advanced disease

A

Abdominal distension
• Fatigue due to chronic anaemia
• Weight loss
• Sx of obstruction or perforation

115
Q

Main diagnostic investigations

A
  • Blood tests
  • FBC, U&E , LFTS, Serum Proteins, INR
  • Tumour markers
  • CEA, CA 19-9
  • Proctoscopy / Sigmoidoscopy (rigid / flexible)
  • Barium enema
  • Colonoscopy & definitive biopsy - GOLD STANDARD
116
Q

Significance of CEA

A

• If elevated at time of diagnosis, may be a useful marker
of active disease
• Levels fall after surgery / adjuvant treatment
• Rising levels during follow-up may be the first sign of
recurrent disease
• Low levels at initial diagnosis may indicate high grade,
undifferentiated tumour with a poor prognosis

117
Q

Staging investigations

A

Abdominal Ultrasound

CT Chest & Abdomen - GOLD STANDARD

Pelvic MRI

Endorectal Ultrasound

118
Q

Use of CT in CRC

A
  • Gold standard

• Accurately identifies
site of primary

• Detects invasion
into neighbouring
organs

119
Q

Use of chest and abdominal CT

A

• Detects enlarged
lymph nodes

• Detects metastases

• Detects any
co-existent disease

120
Q

Use of pelvic MRI

A
  • eXTREMELY USEFUL

• Detailed images
of pelvic anatomy

• Accurate pre op
local staging of
rectal tumours

  • Can determine size and shape and invasion of bowel wall
  • nodal involvement
121
Q

Use of endoanal unltrasound

A

• Position
• invasion of
bowel wall
• nodal involvement

122
Q

Advantage of surgical resection

A

provides the most rapid relief of symptoms,
including those arising due to:

  • Bleeding
  • Obstruction
  • perforation and
  • fistulation into surrounding organs.
123
Q

Use of combo of chemo and surgery

A

locally
advanced lesions (those that have penetrated the
muscular wall of the bowel) will benefit from adjuvant
chemotherapy and in the case of rectal tumours,

neoadjuvant chemoradiotherapy

124
Q

Tx options

A

• Surgery only

• Surgery+ Adjuvant (post op) chemotherapy
(colonic tumours)

Neoadjuvant (pre-op) chemo /radiotherapy + Surgery
(rectal tumours)

125
Q

Preparation for surgery

A

• ? neoadjuvant treatment
- On basis of pre-op staging – locally advanced rectal tumours
• Informed consent
• Preparation for stoma, counselling (if applicable)
- Low rectal cancers where sphincters cannot be saved
• Cross match blood
• Bowel preparation
- improves wound infection
- minimises septic consequences of anastomotic leak
• Antibiotic prophylaxis
- Cefuroxime / Metronidazole
- improves wound infection
• Thrombo-embolism prophylaxis

126
Q

Bowel prep

A

2 days pre-op : Low fibre diet

I day pre-op : Cathartics (Kleen Prep, SennaPlus), Enemas

127
Q

Principles of recetion

A
  • Any surgical resection
    requires 5 cm clearance
    for colonic lesions
- 1 cm distal clearance of
rectal lesions is adequate
if mesorectum
resected.(Total mesorectal
excision) - if involves sphincter within 1cm you need to remove them 
- Radial margin or
circumferential resection
margin (CRM) should be
histopathologically free of tumour - This applies especially for
rectal tumours – the CRM
must be >1mm for a
curative resection.
- For a segmental colectomy
lymph node resection
should be performed to the
origin of the feeding vessel
on the SMA or IMA
  • En Bloc resection of
    adherent tumours
    should be performed

ie, removal of portion of
adherent neighbouring
organ in continuity with
resected bowel.

128
Q

Benefit of adjuvant chemo

A
  • T1 T2 N0 – No benefit
  • T3-4, N0 – 2-5% absolute benefit
  • T3-4, N1-3 – 5-10% absolute benefit
129
Q

Poor prognostic factors for colon cancer

A
  • T4 tumours
  • Poorly differentiated
  • Venous invasion
  • Mucinous adenocarcinomas
130
Q

Where to rectal recurrences tend to occur

A

Initial recurrences tend to be local
rather than distant, whereas in
colonic cancer initial recurrence is
usually to distant organs

  • local recurrences are extremely difficult to treat
131
Q

What has improved local recurrence

A 
total mesorectal excision (entire mesorectal
compartment including the rectum,
surrounding mesorectal fat, perirectal
lymph nodes and its envelope, i.e. the
mesorectal fascia is completely
removed.)
132
Q

Types of rectal excision

A
  • LOW ANTERIOR RESECTION

-

133
Q

When is low anterior resecetion indication

A

• Low anastomosis
(usually <5 cm from anus)
• Preop radiotherapy
• Technically difficult anastomosis

134
Q

What needsto be done with a low anatamoses

A

Diverting (defunctioning) stoma:
• diverts the faecal stream from the anastomosis
• protects it in the immediate postoperative period.

Usually closed 8-12 weeks later, after contrast or endoscopic study
demonstrating anastomotic integrity

135
Q

Use of neoadjuvant Tx in rectal cancer

A

Proven to be of value in tumours that have breached the
muscular wall of the rectum T3,4, N0, T1T2 N+ as
indicated by pre-operative staging MRI
• Reduced toxicity as compared to post op (adjuvant)
treatment

136
Q

Role of neo adjuvant therapy

A

• Reduces local recurrence rates (RXT alone)
- Convincing & large evidence base

• Shrinks locally advanced tumours (RXT & chemo)
- Facilitates ‘curative resection’ with clear margins

• Increases chance of sphincter preservation
- Controversial, not evidence based

• Definitive treatment in its own right
- In patients unfit for surgery

137
Q

Indication for ABDOMINOPERINEAL RESECTION OF THE RECTUM

A

• Indicated only for very distal rectal tumours involving
sphincter or for advanced squamous cell tumours of the anus.

• Attempted anastomosis would result in poor function or
inadequate tumour clearance.

138
Q

Method of abdominoperineal resection

A

• Recto-sigmoid, & anal sphincter complex excised and perineal
opening closed

• Permanent left iliac fossa stoma

• APR has increased local recurrence rates and poorer survival
than anterior resection.

139
Q

Indication for local resection of rectal tumours

A

•Poor risk patients
•Benign polyps
•T1 N0 M0 tumours
Well / moderately well differentiated

140
Q

Indication for transanal resection

A

Suitable for lesions which have their
upper margins lying within 5 cm from the
anal verge.

Can be done under epidural / spinal

Access to the lesion is by dilating the
anus by means of anal retractors, and
applying traction on the lesion.

Benign polyps (TVA’s) - submucosal excision

For T1 cancers - full thickness excision of the rectal wall, which is closed
with sutures.

141
Q

Difference between open and laproscopic methods of surgery

A

no difference in

  • overall survival
  • disease-free survival
  • and local and distant recurrence
142
Q

Pros of laproscopic colorectal surgery

A
  • Shorter hospital stay
  • Quicker return to normal activities
  • Avoidance of incisional hernias

• Fewer intra-abdominal adhesions
• Equivalent surgical resection
margins and lymph node retrieval
rates

• Probably no oncological
disadvantage

143
Q

Complications of colorectal surgery

A 
General:
• Post op pneumonia
• Deep venous thrombosis
• Pulmonary embolus
• Myocardial infarction
Specific:
• Wound infection
• Anastomotic leakage
• Visceral injury (spleen, ureter)
• Incisional hernias
• Abdominal adhesions
• Urinary / sexual dysfunction
• Defaecatory disturbances
• Local recurrence
144
Q

Common emergency presentation of colorectal cancer

A

• Obstruction
clinical picture of small or large bowel obstruction

• Perforation
Peritonitis / paracolic abscess

  • Fistulation
  • Bleeding
145
Q

Presentation of obstruction

A 
Colicky abdominal pain
Abdominal distension
Constipation
Nausea, Vomiting
PR Bleeding, anaemia
146
Q

Presentation of perforation

A

Faecal Peritonitis / localized abscess

Generalized abdominal pain

Localized mass (abscess)

Abdominal guarding, rigidity

Abdominal distension due to ileus

Fever, shock

147
Q

Diagnostic investigations in emergency presentation

A
  • Plain Chest / Abdominal Xrays
  • Contrast studies
  • CT Scanning
  • Allows identification of site
  • Stages the cancer
148
Q

Use of CT in colorectal emergency

A
  • Confirms diagnosis
  • Identifies the site of obstruction
  • Identifies the underlying cause
  • Stages malignant disease (detects metastases)
  • Detects perforation
  • Detects any co-existent disease
149
Q

Pre operative preparation

A
  • Resuscitation
  • O2 & fluids
  • Fluid loss may be considerable ( >5 litres)
  • Correct electrolyte abnormalities
  • Correct anaemia
  • Commence broad spectrum antibiotics
  • main concern is that there is no bowel preparation

-This is less of a problem with right sided large bowel tumours
since an emergency right sided resection leaves no faecally
loaded large bowel proximal to the ileocolic anastomosis.

150
Q

Options for left sided obstructed lesions

A

 Defunction with proximal stoma - 1st stage of a 3 stage procedure

 Hartmann’s procedure
 Resection (+/- on-table lavage) and primary anastomosis
 Subtotal colectomy

151
Q

Use of Defunctioning proximal colostomy

A
  • Very sick patient
  • Inexperienced operator
  • 1st stage of a 3 stage procedure
152
Q

use of subtotal colectomy

A

• Multiple (synchronous) cancers
• Grossly dilated, ischaemic proximal
bowel

MAKE SURE YOU LOOK AT KECTURE SLIDES PICTURES OF THESE SURGIES

153
Q

Outcome of elective vs emergency surgery

A

Elective Surgery
Mortality: 0.9 - 6%
Morbidity: 5 -15%

Emergency Surgery
Mortality: 5 - 20%
Morbidity: 10 - 50%
Stoma rate: 41%
(only 60% reversed)
154
Q

Follow up of colorectal cancer

A

• Three monthly for first 1-2 years, then six monthly
and discharge after 5 years.
• 3-6 monthly CEA.
• 6m -Yearly CT / MRI for first three years.
• Colonoscopy – within six months (or Pre-op),
thereafter 5 yearly.
- Very rare for metastasis to occur after 5 years

155
Q

Treatment of local recurrence

A
  • Curative - Salvage surgery
  • Sacrectomy,
  • Pelvic exenteration

• Palliative
– Radiotherapy
- Chemotherapy

156
Q

Tx of anal carcinoma

A
  • Usually chemo/radiotherapyis sufficient

• Surgery only for:
• Tumours that fail to respond to radiotherapy
• Large tumours causing gastrointestinal obstruction
• Small anal margin tumours without sphincter
involvement

157
Q

Phases of wound healing

A
  1. INFLAMMATORY PHASE
  2. PROLIFERATIVE PHASE
  3. REMODELLING PHASE
158
Q

Describe the inflammatory phase of wound healing

A 
I. INFLAMMATORY PHASE (Immediate to 2-5 days)
• A. Haemostasis
• Vasoconstriction
• Platelet aggregation
• Thromboplastin forms clot
  • B. Inflammation
  • Vasodilation
  • PMN and Macrophage migration – Phagocytosis of debris
159
Q

Describe the proliferative phase

A

II. PROLIFERATIVE PHASE ( 2 days to 3 weeks)
• A) Granulation
• Fibroblasts lay bed of collagen
• Fills defect and produces new capillaries (angiogenesis)
• B) Contraction
• Myofibroblasts pull wound edges together to reduce defect
• D) Epithelialization
• Replication by mitosis & migration of epithelial cells

160
Q

Describe remodelling phase

A

III. REMODELLING PHASE ( 3 weeks to 2 years)
• Type II collagen replaced by Type I collagen which increases
tensile strength to wounds
• Blood vessels that are no longer needed are removed
by apoptosis
• Scar tissue is only 80 percent as strong as original tissue

161
Q

Categories of wound healing

A

Primary wound healing (Healing by first intention)
• Occurs within hours of repairing by approximation
• eg suturing the edges of a full thickness surgical wound.
• Minimal scarring

Delayed primary healing
• If wound edges are not approximated immediately.eg
contaminated wounds
• Wound may be sutured 4-5th day. Scarring inevitable

Secondary healing (Healing by secondary intention)
• Full thickness wound allowed to heal without surgical
intervention
• More intense inflammatory response, pronounced wound
contracture

162
Q

What must you always consider in an older patient presenting with appendicitis?

A

Cancer and diverticulitis (usually on the left instead of the right)

163
Q

What can appendicitis be confused with in children and teenagers?

A

Mesenteric adentitis

164
Q

To what does the transverse meso-colon attach? At which vertebral level? Branches of which artery does it contain?

A

Transverse mesocolon is the broad fold of peritoneum connecting the transverse colon to the posterior wall of the abdominal cavity.
Fuses with greater omentum to form gastrocolic ligament
Contains middle colic vessels, nerves and lymphatics

165
Q

Embryologically, which structure does it fuse with? Therefore, how many layers constitute this structure?

A

Posterior wall of lesser sac - 4 layers

166
Q

During which commonly performed surgical procedure is the transverse colon at risk of being injured?

A

Laproscopy

167
Q

What is the white line of toldt

A

Lateral reflection of posterior parietal peritoneum of abdomen over the mesentery of the ascending and descending colon.

168
Q

What is the ‘marginal artery of Drummond’? Clinical significance?

A

an artery that connects the inferior mesenteric arterywith the superior mesenteric artery. It is sometimes absent, as an anatomical variant.

169
Q

Describe the lymphatic drainage of the colon and what is its clinical significance?

A

The lymphatic drainage of the ascending and transverse colon is into the superior mesenteric nodes. The descending colon and sigmoid drain into the inferior mesenteric nodes

170
Q

What are ‘appendices epiploicae’?

A

a.k.a omental appendices - small pouches of the peritoneum filled with fat and situated along the colon, but are absent in the rectum.

171
Q

Which parts of the colon are commonly used for ‘stoma’ formation?

A

Transverse and sigmoid

172
Q

What are the ‘rectal valves’ (of Houston)?

A

lateral flexures of the rectum

173
Q

What is ‘Denonvillier’s fascia’? Into which structure does it insert, inferiorly?

A

is a membranous partition at the lowest part of the rectovesical pouch. It separates the prostate and urinary bladder from the rectum. It consists of a single fibromuscular structure with several layers that are fused together and covering the seminal vesicles

174
Q

What is the mesorectum and what is its surgical significance

A

Fatty tissue surrounding the rectum - Needs to be removed in rectal cancer to prevent metastasis

175
Q

Why is the rectum not affected by diverticular disease?

A

Does not have omental bursae

176
Q

What is the venous drainage of the rectum and what is the clinical significance of this

A

In the settin gof rectal cancer

IMA and SMA drain to the portal vein - metastasis to the liver
Pudendal drains to the IVC metastasis to the lung

177
Q

Innervation of the rectum

A

See notebook

178
Q

What is the lymphatic drainage of the rectum

A

pararectal lymph nodes, which drain into the inferior mesenteric nodes.

Additionally, the lymph from the lower aspect of the rectum drains directly into the internal iliac lymph nodes.

179
Q

What constitutes the ‘internal anal sphincter?

A

Thickening of the circular smooth muscle layer. COntinuation of SM of the rectum

180
Q

What is the inter-sphincteric groove and what marks this level?

A

a.k.a. hiltons white line - marks separation between the smooth and skeletal muscle

181
Q

Describe the molecular pathogenesis of adenocarcinoma

A

SEE DISEASE LOB

- Must do this is an official lob

182
Q

Histopathology of colon polyps

A

Must do see Despina lecture

183
Q

Advice on wound care

A
  1. Paracetamol for pain - avoid aspirin, brufen or voltarol as this can prolong bleeding
  2. Rest and avoid strain
  3. Look for signs of infection
  4. Keep the dressing clean and dry for 48 hours avoiding baths and showers.
    5.Avoid dirty water in baths and swimming
    pools while the stitches are in place
184
Q

What to do if a wound bleeds?

A

Very occasionally the wound may bleed. Do not remove the dressing but apply
continuous pressure with a clean handkerchief or towel for 15 minutes. Slowly
release pressure and if the wound is still bleeding re-apply firm pressure for
another 15 minutes.

185
Q

What to do after stitches are removed

A

After
the stitches are removed ensure the wound is secured with steristrips for 1
week on the face or 6-8 weeks on the body or limbs. Avoid strenuous exercise
that will put tension on the wound for another 4-6 of weeks depending on the
site of surgery.

186
Q

Long term management of wound?

A

massage the scar with vaseline or moisturiser for about 1
minute, 3 times a day for a year. This will help soften the scar and improve the
cosmetic result

187
Q

Signs of wound infection?

A

Become more swollen Is hot or painful to touch or child is experiencing increasing pain Oozes pus or smells or change in discharge colour Bleeds Your child develops a fever and generally feels unwell

188
Q

NICE guidelines for follow up after curative CRC surgery

A
  1. Clinic visits every 4-6 weeks
  2. a minimum of two CTs of the chest, abdomen, and pelvis in the first 3 years
  3. regular serum carcinoembryonic antigen tests (at least every 6 months in the first 3 years)
  4. Surveillance colonoscopy at 1 year after initial treatment. If this investigation is normal consider further colonoscopic follow‑up after 5 years, and thereafter as determined by cancer networks.
189
Q

Principles of radiation

A

Generally normal cells have excellent repair
mechanisms but cancer cells are have diminished
ability to repair the damages and hence continue to
produce cells with the damage.

These cells, which have the damaged DNA, will either
die or reproduce slowly

190
Q

Limitations of radiotherapy

A

Tumours outgrow their blood supply and
tissues become relatively hypoxic.

The more hypoxic the tumour is the greater the
resistance to radiotherapy.

Fixation of oxygen plays a very important role
in causing permanent damage to the DNA.

191
Q

Indication for radiotherapy

A

Line of excision includes mesorectum

192
Q

Side effects of radiotherapy

A

Acute:
- damage to epithelial surfaces of the skin, mouth, pharynx
and bowel mucosa cause soreness, diarrhoea and nausea.

Oedema and erythema:
swelling of the soft tissues is encountered during
radiotherapy. Red rashes are seen in the area of treatment.
The patient is given steroids to reduce swelling

Infertility

Fibrosis and skin problems: inflammation, desquamation,
hyperpigmentation, pruritus

Hair loss: radiotherapy to the head and neck region causes
permanent hair loss

Dryness: Dry mouth (xerostomia) and dry eyes (xerophthalmia)

Secondary malignancies: are seen in a small minority of patients,
generally >15 years after they have received a curative course of
radiation treatment.

Fetal damage is seen in case of pregnant woman

Radiotherapy lowers the immunity status of the patient and increases
the susceptibility of infection.

193
Q

MOA of bevacizumab

A

Bevacizumab

Anti v-EGF antibody

Targets
neovascularization of
solid tumours

Survival benefit in
metastatic colon and
breast cancer

causing regression of existing microvasculature

within 24 hours of VEGF inhibition: loss of lumen patency,
cessation of blood flow in some vessels, endothelial cell
apoptosis

194
Q

Role of cetuximab in colon cancer

A

EGFR over-expressed
in colon cancer

Monoclonal antibody
binds to EGFR

Clinical responses and
improved survival seen
in chemo-refractory
metastatic colon cancer

BCS Lectures (8 decks)

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