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Met 3A > Upper & Lower GI Pathology > Flashcards

Upper & Lower GI Pathology Flashcards

1
Q

How common are oesophageal cancers? Who do they most affect and where?

A

5-10% of GI cancers in the western world
M>F
>50yrs

upper third - 20%
middle third - 50%
lower third - 30%

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2
Q

What RFs predisposes someone to oesophageal carcinoma?

A 
diet
oesophageal disorders
genetic
race
smoking
alcohol
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3
Q

Describe the macro/microscopic features of oesophageal cancers

A 
macro:
polypoid
ulcerating
annular constricting
diffuse infiltrating

micro:
85% squamous cell carcinoma
10% adenocarcinoma
5% undifferentiated

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4
Q

What is the typical presentation of a patient with oesophageal cancer?

A 
progressive dysphagia
anorexia
weight loss
aspiration pneumonia
fistula formation
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5
Q

How is oesophageal cancer treated?

A

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)

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6
Q

How common is gastric cancer? What is the most common cause?

A

2nd most common in the world

H pylori –> chronic gastritis –> intestinal metaplasia –> dysplasia –> carcinoma

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7
Q

Describe the macro/microscopic appearance of gastric cancer

A

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

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8
Q

How can oesophageal/gastric/colonic cancers spread?

A

O = direct, lymphatics

G = direct, lymphatics, haematogenous, transcoelomic

C = direct, lymphatics, haematogenous, transcoelomic

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9
Q

How might a patient with gastric cancer present?

A 
anorexia, weight loss
dyspepsia
abdominal pain
haemorrhage
anaemia
metastatic disease eg bone ache, lymphadenopathy
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10
Q

What is the prognosis like for gastric cancer patients?

A 
early = >90% 5 year survival
late = 5-15% 5 year survival
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11
Q

How can gastric cancer be treated?

A

cure = surgical resection (sub/distal/total gastrectomy)

neoadjuvant chemo
peri/post-op chemo
radio

fluoropyrimidine, oxaliplatin –> advanced cancers

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12
Q

What is the prevalence of colorectal cancer? Where are they most likely to arise?

A 
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

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13
Q

What are the RFs for colorectal cancer?

A 
CRC tends to arise from pre-existing adenomas
polyposis syndrome - FAP, HNPCC, JP
IBD 
diet
urban environment
physical inactivity
age
overweight
excess alcohol
FHx
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14
Q

What types of CRC can you get?

A

tubular - irregular outlines, cystic dilatations, low-grade dysplasia

villous - finger-like projections

tubulovillous

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15
Q

What does a CR adenocarcinoma look like microscopically?

A

incomplete glands
loss of polarity of nuclei
necrosis in middle
lymphatic invasion

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16
Q

How is CRC staged?

A

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

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17
Q

How can FAP lead to CRC?

A

= familial adenomatous polyposis

APC mutation

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18
Q

How can HNPCC lead to CRC?

A

= hereditary non-polyposis colon cancer syndrome

mismatch repair genes mutated
eg hMLH1, hMSH2, hMSH6
deficient mismatch

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19
Q

What would you expect to find on examination for a patient suspected of having CRC?

A 
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

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20
Q

What lab test would you send off for and how would they diagnose CRC?

A

FBC - iron deficiency anaemia

LFTs + Renal Function for baseline and assess for future treatment

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21
Q

What imaging and investigations would you order for CRC?

A

Colonoscopy - to visualise + bx
Double-contrast barium enema - mass or apple core lesion
CT colonography - an exophytic lesion that may be narrowing lumen

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22
Q

What surgical options are available to CRC patients?

A

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

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23
Q

What is the role of palliative care?

A 
provide pain relief
keep patient active
provide emotional and spiritual support
retain dignity and QoL
offer support to the family
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24
Q

What are some early complications of a stoma?

A 
poor location
retraction
ischaemic necrosis
detachment
abscess formation
opening wrong end
excoriation
dermatitis
high output
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25
Q

What are some late complications of a stoma?

A 
prolapse
stenosis
parastomal hernia
fistula formation
gas
odor
parastomal varices 
dermatoses
cancer
skin manifestations
bowel obstruction
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26
Q

What is Barrett’s Oesophagus?

A

= metaplasia due to injury usually from excess acid

white epithelial stratified squamous –> red glandular tissue

30x risk of developing oesophageal cancer
monitored via OGD

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27
Q

What is Chronic Gastritis?

A

= 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

28
Q

What are some complications of chronic gastritis?

A

ulceration
gastric carcinoma
primary gastric lymphoma

29
Q

What is Peptic Ulceration Disease?

A

= ulceration from peptic juices on GI mucosa

common sites inc: duodenum, oesophagus, stomach, Meckel’s diverticulum

30
Q

What are the RFs for PUD?

A 
M>F 
H.pylori
gastrinoma
alcohol
blood group
NSAIDs
genes
smoking + tobacco
31
Q

How does PUD look macroscopically?

A

80% of the time it is a single lesion
usually <3cm
has a ‘punched out’ appearance
fibrosis at the base

32
Q

What are some complications of PUD?

A

haemorrhage
obstruction from oedema + scarring
perforation
peritonitis

33
Q

Where are the most common sites of gastric carcinoma?

A

antrum - 50%
body - 25%
GOJ - 25%

34
Q

What are polyps?

A

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

35
Q

What are the S&S of polyps?

A 
depends on site
R side:
less overt blood 
intussusception
constipation
diarrhoea
obstruction
L side:
frank blood
constipation
diarrhoea
obstruction
36
Q

What are inflammatory polyps?

A

non-neoplastic
epithelial and stromal
typically associated with IBD (especially UC), surgical anastomosis

may have a polypoid outline, ulceration, erosion and distortion

37
Q

What are hyperplastic polyps?

A 
serrated not dysplastic
asymptomatic 
<5mm in size
most common 
found L side
38
Q

What is a traditional serrated adenoma?

A

tubulovillous architecture

L sided

39
Q

What are sessile serrated lesions?

A

inc polyps + adenomas

neoplastic w/ premalignant features
>10mm in size
BRAF mutation
microsatellite instability

40
Q

What are hamartomatous polyps?

A

rare
seen in children + YA
normal colonic tissue in an abnormal place

41
Q

What is Peutz-Jeghers Syndrome?

A

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

42
Q

What are Peutz-Jeghers polyps?

A

hamartomatous polyps with an arborising appearance

can be dysplastic or adenocarcinoma

43
Q

What are juvenile polyps?

A

sessile or pedunculated
5-50mm in size typically
young polyps eg benign growth, not adenoma

44
Q

What is juvenile polyposis syndrome?

A

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

45
Q

What are adenomas?

A

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

46
Q

Which genes are associated with CRC?

A

APC
B-catenin
KRAS
TP53

(HNPCC
FAP
BMPR1A
SMAD1A
STK11)
47
Q

What are the common sites of metastasis for CRC?

A

lungs
ovaries (Krookenberg)
liver
peritoneum

48
Q

What is the screening process for CRC?

A

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.

49
Q

What are anal fissures?

A

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

50
Q

What are fistulas?

A

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

51
Q

What are the complications of fistulae?

A

spasm of internal anal sphincter –> impaired blood supply –> non-healing ulcer –> infection

52
Q

How do you medically treat a fissure?

A

relieve constipation to break the cycle - fibre and stool softeners

nictoglycerin 0.4% intra-anal application

botulinum toxin injection

53
Q

What is a Mallory-Weiss Tear?

A

mucosal tear in the oesophagus

caused by forceful vomiting

54
Q

What are the signs of Upper and Lower GI bleeds?

A

Upper = bleeding proximal to the ligament of Treitz
haematemesis
malaena
haematochezia

Lower = bleeding distal to the ligament of Treitz
malaena
haematochezia

55
Q

Where is the ligament of Treitz?

A

duodenojejunal junction

56
Q

What are the 4 stages of haemorrhoids?

A 
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
57
Q

What is the ratio required when giving a full blood transfusion?

A

1 : 1 : 1

FFP : Blood : Platelets

58
Q

What are the 4 classes of hypovolaemic shock?

A

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

59
Q

What are the risks associated with a massive blood transfusion?

A

fluid overload
electrolyte/acid-base disturbance
low clotting factors
hypothermia

if repeated –> iron overload

60
Q

What are the transfusion targets for ___?

a. average population
b. ischaemic HD
c. CLD

A

a. Hb >80
b. Hb >100
c. Hb >70

61
Q

What can you give to reverse the effect of anticoagulants?

A

nothing can truly reverse anticoagulant effects so you promote coagulation instead:
vit K
FFP
Pro-thrombin complex

62
Q

What is the immediate management of a patient with a variceal bleed?

A

ABCDE

Terlipressin = mesenteric/splanchnic constrictor
1-2mg QDS

Prophylactic Abx = cephalosporin, quinolone, augmentin

63
Q

What is the Blatchford score?

A

determines how urgent an endoscopy is

<2 –> low risk UGIB –> OP endoscopy
>6 –> urgent endoscopy

64
Q

How can adrenaline help treat ulcers?

A

1:10,000
5-40mls
vasoconstriction + local tamponade

65
Q

How do you treat ulcers?

A

Adrenaline
clip ulcer edges
diathermine
haemospray

66
Q

How do you surgically treat varices?

A

band ligation - scarring prevents bleeding
injection scleropathy - scarring prevents bleeding
sengstaken Blakemore tube - balloon to cease bleeding when intubated

67
Q

How do you treat H.Pylori?

A

Triple therapy - for 7/14 days
PPI + amoxicillin + clarithromycin/metronidazole

or if allergic to penicillin:
PPI + clarithromycin + metronidazole

Met 3A (19 decks)

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