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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
What are some late complications of a stoma?
``` prolapse stenosis parastomal hernia fistula formation gas odor parastomal varices dermatoses cancer skin manifestations bowel obstruction ```
26
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
27
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
28
What are some complications of chronic gastritis?
ulceration gastric carcinoma primary gastric lymphoma
29
What is Peptic Ulceration Disease?
= ulceration from peptic juices on GI mucosa common sites inc: duodenum, oesophagus, stomach, Meckel's diverticulum
30
What are the RFs for PUD?
``` M>F H.pylori gastrinoma alcohol blood group NSAIDs genes smoking + tobacco ```
31
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
32
What are some complications of PUD?
haemorrhage obstruction from oedema + scarring perforation peritonitis
33
Where are the most common sites of gastric carcinoma?
antrum - 50% body - 25% GOJ - 25%
34
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
35
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 ```
36
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
37
What are hyperplastic polyps?
``` serrated not dysplastic asymptomatic <5mm in size most common found L side ```
38
What is a traditional serrated adenoma?
tubulovillous architecture | L sided
39
What are sessile serrated lesions?
inc polyps + adenomas neoplastic w/ premalignant features >10mm in size BRAF mutation microsatellite instability
40
What are hamartomatous polyps?
rare seen in children + YA normal colonic tissue in an abnormal place
41
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
42
What are Peutz-Jeghers polyps?
hamartomatous polyps with an arborising appearance | can be dysplastic or adenocarcinoma
43
What are juvenile polyps?
sessile or pedunculated 5-50mm in size typically young polyps eg benign growth, not adenoma
44
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
45
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
46
Which genes are associated with CRC?
APC B-catenin KRAS TP53 ``` (HNPCC FAP BMPR1A SMAD1A STK11) ```
47
What are the common sites of metastasis for CRC?
lungs ovaries (Krookenberg) liver peritoneum
48
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.
49
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
50
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
51
What are the complications of fistulae?
spasm of internal anal sphincter --> impaired blood supply --> non-healing ulcer --> infection
52
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
53
What is a Mallory-Weiss Tear?
mucosal tear in the oesophagus | caused by forceful vomiting
54
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
55
Where is the ligament of Treitz?
duodenojejunal junction
56
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 ```
57
What is the ratio required when giving a full blood transfusion?
1 : 1 : 1 | FFP : Blood : Platelets
58
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
59
What are the risks associated with a massive blood transfusion?
fluid overload electrolyte/acid-base disturbance low clotting factors hypothermia if repeated --> iron overload
60
What are the transfusion targets for ___? a. average population b. ischaemic HD c. CLD
a. Hb >80 b. Hb >100 c. Hb >70
61
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
62
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
63
What is the Blatchford score?
determines how urgent an endoscopy is <2 --> low risk UGIB --> OP endoscopy >6 --> urgent endoscopy
64
How can adrenaline help treat ulcers?
1:10,000 5-40mls vasoconstriction + local tamponade
65
How do you treat ulcers?
Adrenaline clip ulcer edges diathermine haemospray
66
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
67
How do you treat H.Pylori?
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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