Upper & Lower GI Pathology Flashcards
How common are oesophageal cancers? Who do they most affect and where?
5-10% of GI cancers in the western world
M>F
>50yrs
upper third - 20%
middle third - 50%
lower third - 30%
What RFs predisposes someone to oesophageal carcinoma?
diet oesophageal disorders genetic race smoking alcohol
Describe the macro/microscopic features of oesophageal cancers
macro: polypoid ulcerating annular constricting diffuse infiltrating
micro:
85% squamous cell carcinoma
10% adenocarcinoma
5% undifferentiated
What is the typical presentation of a patient with oesophageal cancer?
progressive dysphagia anorexia weight loss aspiration pneumonia fistula formation
How is oesophageal cancer treated?
stage 0-IA = endoscopic resection with or w/o ablation
stage IB, IIA = oesophagectomy
stage IIB, III = oesophagectomy + pre/post-op chemo
stage IV = chemo + radio + palliative surgery (endo ablation + stenting)
How common is gastric cancer? What is the most common cause?
2nd most common in the world
H pylori –> chronic gastritis –> intestinal metaplasia –> dysplasia –> carcinoma
Describe the macro/microscopic appearance of gastric cancer
polypoid fungating –> with ulceration –> ulcerated –> diffuse infiltrating
95% adenocarcinoma
- intestinal - mimics glands, presents as polypoid or ulceration
- diffuse - linitis plastica, single-cell infiltration throughout the gastric wall, originates from mucous nest cells in gastric pits
5% undifferentiated
How can oesophageal/gastric/colonic cancers spread?
O = direct, lymphatics
G = direct, lymphatics, haematogenous, transcoelomic
C = direct, lymphatics, haematogenous, transcoelomic
How might a patient with gastric cancer present?
anorexia, weight loss dyspepsia abdominal pain haemorrhage anaemia metastatic disease eg bone ache, lymphadenopathy
What is the prognosis like for gastric cancer patients?
early = >90% 5 year survival late = 5-15% 5 year survival
How can gastric cancer be treated?
cure = surgical resection (sub/distal/total gastrectomy)
neoadjuvant chemo
peri/post-op chemo
radio
fluoropyrimidine, oxaliplatin –> advanced cancers
What is the prevalence of colorectal cancer? Where are they most likely to arise?
3rd most common cancer in the western world 15% of cancer deaths in the UK peak 60-70 years rare <40 years M>F
71% arise in colon
29% in rectum
What are the RFs for colorectal cancer?
CRC tends to arise from pre-existing adenomas polyposis syndrome - FAP, HNPCC, JP IBD diet urban environment physical inactivity age overweight excess alcohol FHx
What types of CRC can you get?
tubular - irregular outlines, cystic dilatations, low-grade dysplasia
villous - finger-like projections
tubulovillous
What does a CR adenocarcinoma look like microscopically?
incomplete glands
loss of polarity of nuclei
necrosis in middle
lymphatic invasion
How is CRC staged?
TMN
Dukes =
A - tumour does not extend beyond muscularis propria, no nodal involvement, 90% 5 yr survival rate
B - tumour extends beyond muscularis propria, no nodal involvement, 70% 5 yr survival rate
C - any depth, present in nodes, 35% 5 yr survival rate
How can FAP lead to CRC?
= familial adenomatous polyposis
APC mutation
How can HNPCC lead to CRC?
= hereditary non-polyposis colon cancer syndrome
mismatch repair genes mutated
eg hMLH1, hMSH2, hMSH6
deficient mismatch
What would you expect to find on examination for a patient suspected of having CRC?
rectal bleeding rectal mass anaemia abdo distension palpable lymph nodes abdo pain
rectosigmoid tumours:
changes in bowel habit, obstruction
R sided tumours:
changes in bowel habit, weight loss, anorexia
What lab test would you send off for and how would they diagnose CRC?
FBC - iron deficiency anaemia
LFTs + Renal Function for baseline and assess for future treatment
What imaging and investigations would you order for CRC?
Colonoscopy - to visualise + bx
Double-contrast barium enema - mass or apple core lesion
CT colonography - an exophytic lesion that may be narrowing lumen
What surgical options are available to CRC patients?
stage I = T1-2, N0, M0
Complete local removal
stage I - high risk
radical resection
stage II-III
radical resection
pre-op chemo + radio
post-op chemo
stage IV
surgical resection
chemo + radio
What is the role of palliative care?
provide pain relief keep patient active provide emotional and spiritual support retain dignity and QoL offer support to the family
What are some early complications of a stoma?
poor location retraction ischaemic necrosis detachment abscess formation opening wrong end excoriation dermatitis high output
What are some late complications of a stoma?
prolapse stenosis parastomal hernia fistula formation gas odor parastomal varices dermatoses cancer skin manifestations bowel obstruction
What is Barrett’s Oesophagus?
= metaplasia due to injury usually from excess acid
white epithelial stratified squamous –> red glandular tissue
30x risk of developing oesophageal cancer
monitored via OGD
What is Chronic Gastritis?
= inflammation of the stomach progressively worsening and potentially life-long
affects epithelium + lamina propria
usually caused by H.pylori infection but can also be caused by long-term NSAIDs, chemicals, autoimmune
What are some complications of chronic gastritis?
ulceration
gastric carcinoma
primary gastric lymphoma
What is Peptic Ulceration Disease?
= ulceration from peptic juices on GI mucosa
common sites inc: duodenum, oesophagus, stomach, Meckel’s diverticulum
What are the RFs for PUD?
M>F H.pylori gastrinoma alcohol blood group NSAIDs genes smoking + tobacco
How does PUD look macroscopically?
80% of the time it is a single lesion
usually <3cm
has a ‘punched out’ appearance
fibrosis at the base
What are some complications of PUD?
haemorrhage
obstruction from oedema + scarring
perforation
peritonitis
Where are the most common sites of gastric carcinoma?
antrum - 50%
body - 25%
GOJ - 25%
What are polyps?
they are fleshy growths lining the colon and rectum
they are originally benign but can mutate to become cancerous
they can be non-neoplastic or neoplastic
What are the S&S of polyps?
depends on site R side: less overt blood intussusception constipation diarrhoea obstruction
L side: frank blood constipation diarrhoea obstruction
What are inflammatory polyps?
non-neoplastic
epithelial and stromal
typically associated with IBD (especially UC), surgical anastomosis
may have a polypoid outline, ulceration, erosion and distortion
What are hyperplastic polyps?
serrated not dysplastic asymptomatic <5mm in size most common found L side
What is a traditional serrated adenoma?
tubulovillous architecture
L sided
What are sessile serrated lesions?
inc polyps + adenomas
neoplastic w/ premalignant features
>10mm in size
BRAF mutation
microsatellite instability
What are hamartomatous polyps?
rare
seen in children + YA
normal colonic tissue in an abnormal place
What is Peutz-Jeghers Syndrome?
autosomal dominant - STK11 chromosome 19 (tumour suppressor)
characterized by the development of benign hamartomatous polyps in the gastrointestinal tract and hyperpigmented macules on the lips and oral mucosa (melanosis)
to be diagnosed:
>3 PJ polyps
any no of polyps if there is Fhx of PJS
characteristic mucocutaneous pigmentation w/ FHx of PJS
any no. of PJ polyps + mucocutaneous pigmentation
What are Peutz-Jeghers polyps?
hamartomatous polyps with an arborising appearance
can be dysplastic or adenocarcinoma
What are juvenile polyps?
sessile or pedunculated
5-50mm in size typically
young polyps eg benign growth, not adenoma
What is juvenile polyposis syndrome?
autosomal dominant -BMPR1A +/- SMAD4
These usually begin appearing before age 20, but the term juvenile refers to the type of polyp (i.e benign hamartoma, as opposed to adenoma for example), not to the age of the affected person
diagnosis:
>5 JP in colorectum
JP throughout GI tract
any no of JP + FHx
What are adenomas?
dysplastic polyps - a premalignant lesion
tubular is the most common type
there is a risk of invasion if; >1cm, more than 3 lesions, villous appearance, high-grade dysplasia
RFs:
age, FHx, smoking, overweight, red meat in large amounts
Which genes are associated with CRC?
APC
B-catenin
KRAS
TP53
(HNPCC FAP BMPR1A SMAD1A STK11)
What are the common sites of metastasis for CRC?
lungs
ovaries (Krookenberg)
liver
peritoneum
What is the screening process for CRC?
screening every 2 years from 60 -74 yrs
Foecal Occult Blood test:
Normal = No further tests are needed - will
be invited to take part in screening
again in two years
Unclear = Repeat the FOB test.
Abnormal = Offered an appointment
to discuss colonoscopy at a local
screening centre.
What are anal fissures?
A break or tear in the skin of the anal canal
usually, extend from the anal opening and are usually located posteriorly in the midline
Fissure depth may be superficial or sometimes down to the underlying sphincter muscle. Untreated fissures develop a hood like skin tag (sentinel piles)
bright red anal bleeding on toilet paper and undergarments, or sometimes in the toilet
If acute they are painful after defecation
If chronic, pain intensity often reduces.
common causes inc:
childbirth trauma
anal sex
IBD
What are fistulas?
an abnormal connection between two hollow spaces (technically, two epithelialized surfaces), such as blood vessels, intestines, or other hollow organs.
usually from injury or surgery
symptoms depend on where they’re located
What are the complications of fistulae?
spasm of internal anal sphincter –> impaired blood supply –> non-healing ulcer –> infection
How do you medically treat a fissure?
relieve constipation to break the cycle - fibre and stool softeners
nictoglycerin 0.4% intra-anal application
botulinum toxin injection
What is a Mallory-Weiss Tear?
mucosal tear in the oesophagus
caused by forceful vomiting
What are the signs of Upper and Lower GI bleeds?
Upper = bleeding proximal to the ligament of Treitz
haematemesis
malaena
haematochezia
Lower = bleeding distal to the ligament of Treitz
malaena
haematochezia
Where is the ligament of Treitz?
duodenojejunal junction
What are the 4 stages of haemorrhoids?
I = internal II = internal but may come out on defecation, automatically go back in III = external but can be pushed back in IV = external and cannot be pushed back in
What is the ratio required when giving a full blood transfusion?
1 : 1 : 1
FFP : Blood : Platelets
What are the 4 classes of hypovolaemic shock?
I = 10-15% loss (~750ml)
II = 15-30% (~1.5L)
postural hypotension, generalised vasoconstriction
III = 30-40% (~2L)
hypotension, tachycardia, tachypnoeic, confusion
IV = >40% (~3L)
hypotensive, tachycardia, tachpneoic, comatose
What are the risks associated with a massive blood transfusion?
fluid overload
electrolyte/acid-base disturbance
low clotting factors
hypothermia
if repeated –> iron overload
What are the transfusion targets for ___?
a. average population
b. ischaemic HD
c. CLD
a. Hb >80
b. Hb >100
c. Hb >70
What can you give to reverse the effect of anticoagulants?
nothing can truly reverse anticoagulant effects so you promote coagulation instead:
vit K
FFP
Pro-thrombin complex
What is the immediate management of a patient with a variceal bleed?
ABCDE
Terlipressin = mesenteric/splanchnic constrictor
1-2mg QDS
Prophylactic Abx = cephalosporin, quinolone, augmentin
What is the Blatchford score?
determines how urgent an endoscopy is
<2 –> low risk UGIB –> OP endoscopy
>6 –> urgent endoscopy
How can adrenaline help treat ulcers?
1:10,000
5-40mls
vasoconstriction + local tamponade
How do you treat ulcers?
Adrenaline
clip ulcer edges
diathermine
haemospray
How do you surgically treat varices?
band ligation - scarring prevents bleeding
injection scleropathy - scarring prevents bleeding
sengstaken Blakemore tube - balloon to cease bleeding when intubated
How do you treat H.Pylori?
Triple therapy - for 7/14 days
PPI + amoxicillin + clarithromycin/metronidazole
or if allergic to penicillin:
PPI + clarithromycin + metronidazole
