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Oncology > GI malignancy > Flashcards

GI malignancy Flashcards

1
Q

2 histologic subtypes of oesophageal ca

A

Squamous (mid-proximal)

Adenocarcinoma (distal, GEJ) *Western countries more common

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2
Q

Risk factors for oesphageal ca

A

SCC
Smoking
Excess ETOH
HPV (weak)

Adenocarcinoma
Barrett's 
Obesity
Smoking
Absence of H.pylori
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3
Q

Gastric cancer 2 main subtypes

A

95% adenocarcinomas

Diffuse - undifferentiated (30% of cases)

  • Proximal stomach
  • Associated with linitus plastica
  • Inferior prognosis

Intestinal - well differentiated (reducing but still more common ~50%)

  • Evolves from chronic gastritis
  • Elderly male
  • More favourable prognosis
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4
Q

Risk factors gastric ca

A

H pylori, smoking, high salt intake, obesity, EBV

CDH1 mutation (hereditary diffuse gastric ca)
Lynch syndrome
Polyposis syndrome - FAP, Peutz-Jeugers

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5
Q

Hereditary diffuse gastric ca

A

Autosomal dominant
CDH1 mutation

Prophylactic total gastroectomy recommended between 18-40 years

Women with CDH1 mutation increased risk of breast ca

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6
Q

How to stage gastric cancer?

A

TNM

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7
Q

Rx localised oesophageal/gastric ca

A

Resectable
- Neoadjuvant chemo (docetaxel/5FU/oxaliplatin) –> surgery

Unresectable
- Definitive chemoradiotherapy

Asian population benefit from chemo post resection

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8
Q

Rx advanced/metastatic oesophageal/gastric ca

A

HER2 neg
1st line: platinum + fluoropyrimidine

HER2 positive (poor prognosis)
1st line: platinum + fluoropyrimidine + trastuzumab
Many anti-HER2 agents have shown NEGATIVE results

If no response to first line, generally poor prognosis

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9
Q

Dumping syndrome post gastrectomy

A

GI and vasomotor symptoms due to rapid emptying of gastric contents into small bowel

Can be early or late dumping
Early (10-30 min after): abdo discomfort, nausea, diarrhoea, bloating
Late (4 hours after): hypoglycaemia (excess insulin release)

Management: mainly lifestyle modification

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10
Q

Vitamin deficiencies after upper GI surgery

A

Vitamin B, iron deficiency –> anaemia

Fat soluble vitamins A, D, E, K

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11
Q

Majority of pancreatic ca is located where?

A

70% pancreatic head

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12
Q

Risk factors pancreatic ca

A

Smoking
ETOH +++
High BMI
Chronic DM (especially with weight loss)

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13
Q

Genetic predisposition pancreatic ca

A

Familial component 10% of cases
Peutz-Jeghers syndrome
Lynch syndrome
BRCA 1/2

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14
Q

staging pancreatic ca

A

TNM

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15
Q

Treatment pancreatic ca

1) Resectable
2) Borderline resectable
3) Metastasis/unresectable

A

Depends on resectability

10-15% resectable –> surgery + adjuvant chemo

30-40% borderline resectable –> consider neoadjuvant chemotherapy (not mainstream) –> surgery

50-60% metastasis/unresectable - -> chemotherapy + systemic therapy +/- radiotherapy

Chemo: doublet or triple regimen e.g. Nab-paclitaxel/gemcitabine, FOLFIRINOX (5FU/oxaliplatin/irinotecan)

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16
Q

PARP and BRCA mutation

Explain pathophysiology in pancreatic ca

A

BRCA repairs double strand DNA breaks = homologous recombination repair

PARP repairs single strand DNA breaks

If one strand breaks, and we inhibit PARP, it is unable to be repaired. Single strand breaks eventually turn into double strand breaks –> mutated BRCA is unable to undergo homologous recombination repair –> cell death

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17
Q

PARP inhibitor toxicity

A

Fatigue
nausea
anaemia
GI symptoms - abdo pain, diarrhoea

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18
Q

Rx BRCA mutated metastatic pancreatic ca

A

PARP inhibitor - olaparib

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19
Q

Complications of pancreatic ca

A

Biliary obstruction 75%
- Biliary stenting/percutaneous drainage

Gastric outlet obstruction 25%
- Enteric stent/PEG, duodenal bypass

Abdo pain (invade into coeliac plexus)
- Consider coeliac plexus neurolysis/radiotherapy

Pancreatic exocrine insufficiency - steatorrhoea, abdo cramps
- Creon replacement therapy

Thromboembolic disease

GI bleed due to invasion into adjacent structures (poorer prognosis)
- Endoscopic, radiotherapy, angiographic embolisation

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20
Q

Which factor is the most important in determining suitability to commence chemotherapy?

A

ECOG performance status

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21
Q

GIST features

A 
Mesenchymal tumour related to CT/SM
Spindle shaped cells
95% express c-kit mutation
Rare ca, but most common sarcoma of the GIT
Stomach > small intestine
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22
Q

Prognostic factors GIST

A

Large tumour size
High mitotic count
Non-gastric locations

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23
Q

Rx GIST

A

TK inhibitors

Imatinib –> dose escalation –> sunitinib –> Regorafenib

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24
Q

GIST histology

A

Spindle shaped cells, 95% express C-KIT mutation

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25
Q

HCC risk factors

A

HBV, HCV
Chronic ETOH
NAFLD, NASH
Genetic haemochromatosis

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26
Q

HCC screening involves

A

All liver cirrhotic patients

Abdo USS + AFP every 6/12

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27
Q

Diagnosis of HCC

A

Arterial hypervascularity and ‘wash out’ on portal venous phases (multi-phase CT)
Rising AFP
Biopsy in selected cases - increasingly done now due to better techniques(due to risk of seeding)

28
Q

Management HCC

1) BCLC A+B
2) BCLC C
3) BCLC D

A

Depends on resectability

1) BCLC A+B
Resection, transplant = best cure
- Resection is difficult in portal HTN. Transplant preferred.

Locoregional therapies (TACE, ablation, RT) = not curative but can be a bridge to curative therapies

2) BCLC C
Systemic therapy in advanced disease
- Child pugh A (good liver function) only
- PDL1 inhibitor (Atezolizumab) + Anti-VEGF (bevacizumab) 1st line

3) BCLC D
Best supportive care

29
Q

HCC and liver transplant follow which criteria?

A

Milan criteria
- Single tumour ≤5cm or ≤3 nodules ≤3cm

Expanded criteria (UCSF criteria)

  • Single lesion ≤6.5cm
  • ≤3 nodules, each ≤4.5cm
  • Total tumour diameter ≤8cm
30
Q

CRC most common histology is….

A

> 90% adenocarcinoma

Histologic variants include mucinous and signet ring cell carcinoma = inferior prognosis

31
Q

3 main types of CRC

A

3 main types

  • Sporadic 65%
  • FHx but no associated gene identified 25%
  • Hereditary 5% - HNPCC ie Lynch syndrome, FAP
32
Q

Features of Chromosomal instability (CIN) in CRC

A

Something wrong with the actual chromosome/gene

APC gene - FAP
KRAS gene
TP53 gene

Lt sided colon
Younger male

33
Q

Features of CpG island methylator phenotype (CIMP) in CRC

A

MLH1 promoter hypermethylation

Rt sided colon + transverse colon up to splenic flexure
Can be associated with MSI high, BRAF mutation
Older females

34
Q

Features of MSI high in CRC

A

Loss of MMR protein (most due to MLH1 methylation)

CIMP and MSI are correlated. 70% of MSI-high CRC are also CIMP-high
Key differentiation is BRAF mutation which is strongly associated with sporadic origin i.e. CIMP

35
Q

What are the 3 carcinogenic pathways in CRC?

A

1) Adenoma-carcinoma sequence
- Small adenoma –> large adenoma –> cancer
- CIN-high
- 90% of sporadic CRC

2) Serrated pathway
- Hyperplastic polyp –> sessile serrated adenoma –> cancer
- CIMP-high
- 10% of sporadic CRC

3) Inflammatory pathway
- <2% of all CRC

36
Q

Lynch syndrome/HNPCC

How common?
What is it?
Where is the mutation?

A

3% of CRC

Genetic syndrome
Autosomal dominant with high penetrance

Rt sided colon cancer (early onset), endometrial ca, ovarian ca

Mutation in mismatch repair genes (MMR): MLH1, MSH2, EPCAM, MSH6, PMS2
[From high to low risk]

MMR usually goes and repair genes –> when it doesn’t work, small genetic mutations accumulate –> ‘microsatellite instability’

Often poorly differentiated, mucinous and infiltrating lymphocytes

37
Q

Diagnosis lynch syndrome

A

Amsterdam criteria “3-2-1’ rule

At least 3 relatives with associated lynch syndrome cancer (CRC, endometrial, small bowel, ureter, or renal pelvis)
2 successful generations should be affected
1 should be diagnosed before age 50

38
Q

Surveillance and surgical management of lynch syndrome

A

Surveillance colonmoscpy every 1-2 years
Commence at age 25 or 5 years younger than the youngest affected family members if <30 years

Extended resection generally favoured. Annual surveillance required for residual colon.

High dose Aspirin prophylaxis 600mg daily for 2 years reduce Lynch-syndrome associated cancers

39
Q

FAP features

How common?
Cause?
Clinical features
Risk of CRC
Associated cancers
A

<1%

Germline APC mutation
Autosomal dominant with high penetrance

Polyps ++++
Distal left sided colon, beginning from adolescence

Risk of CRC 100% by age 40

Other associated ca: papillary thyroid, gastric ca, ileal carcinoid

40
Q

Surveillance and surgical management for FAP

A

Colonoscopy from age 10-15
In classical FAP, sigmoidoscopy is adequate since adenoma occur simultaneously throughout the colorectum
Once an adenoma is identified, annual colonoscopy until colectomy
Colectomy at age 15-25

NSAID chemoprophylaxis if surgery inappropriate

41
Q

Population screening CRC

A

Immunochemical FOBT
Age 50-74
Every 2 years
Current screening participation 40%

Cost effective
Improve CRC mortality
Diagnose at earlier stage

42
Q

Screening for people with FHx CRC

A

3 categories

1 - near average risk
- iFOBT every 2 years from age 50-74 (same as general population)

2 - moderately increased risk

  • iFOBT every 2 years from age 40-49
  • Colonoscopy every 5 years from age 50-74

3 - potentially high risk

  • iFOBT every 2 years from 35-44
  • Colonoscopy every 5 years from age 45-74
43
Q

Fluoropyrimidine toxicities

A

Includes 5-FU infusion, oral capecitabine

Diarrhoea, hand-foot syndrome, coronary artery spasm
DPD enzyme - exaggerated toxicities which can be life threatening - diarrhoea, mucositis, myelosuppression

44
Q

Irinotecan toxicities

A

Diarrhoea, neutropenia, myelosuppression
Acute cholinergic syndrome (early onset diarrhoea) Rx atropine

UGT1A enzyme deficiency - toxicities

45
Q

Oxaliplatin toxicities

A

Diarrhoea, neutropenia

Acute neurotoxicity - aggravated by exposure to cold, sensory and motor. Cold induced pharyngolaryngeal dysethesia 1-2%

Chronic neurotoxicity mainly sensory, usually reversible

46
Q

Advanced/metastatic CRC KRAS mutation

A

40% mCRC

Ligand binds to EGFR receptor –> downstream signalling K-RAS –> RAF –> MEK –> ERK —> DNA transcription –> cell proliferation, survival, cancer

If you have a KRAS mutation, blocking EGFR (cetuximab/panitumumab) is not sufficient to block downstream pathways

47
Q

EGFRi - cetuximab/panitumumab toxicities

A

Acneiform rash
Diarrhoea
Electrolyte derangement
Skin and nail toxicities

48
Q

Bevacizumab in CRC

MOA
Toxicities

A

Monoclonal ab against VEGF-A
Inhibits new vessel growth, normalises tumour blood flow and allows chemo to be delivered to the tumour

Used in conjunction with chemo

Toxicities: HTN, proteinuria, GI perforation, VTE, delayed wound healing

49
Q

BRAF V600 mutation in mCRC management

A

Aggressive
Poor prognosis
Single BRAFi is not good enough

Encorafenib (BRAFi) + cetuximab (EGFRi) + Binimetinib (MEK inhibitor) - not standard of care at the moment but great results in 2nd line and beyond

50
Q

MSI-h in mCRC management

A

PD1 inhibitor with pembrolizumab

1st line

51
Q

Types of pancreatic ca

A

Adenocarcinoma (95%)
Neuroendocrine
Lymphoma
Sarcoma

52
Q

Clinical presentation of pancreatic ca

A

Head of pancreas (70%)
- Obstructive jaundice

Others

  • Epigastric/back pain
  • LOW, LOA
  • Fatigue
  • Malabsorption

Often vague sx leading to late presentation

53
Q

Tumour marker for pancreatic Ca

A

CA19-9 (also for other GI ca)

54
Q

Role of PARP inhibitors in pancreatic ca with BRCA mutation

A

Increased PFS but not overall survival

Hence not currently PBS funded

55
Q

How to stage HCC?

A

Barcelona clinic liver cancer staging

Combines tumour stage, liver function and ECOG

56
Q

Risk factors for CRC

A

IBD
- Especially those with PSC (UC)

Previous abdominopelvic radiation

Obesity

Diabetes/insulin resistance

Processed meats

57
Q

How does mutation in mismatch repair gene cause CRC?

A

Mismatch repair gene mutation –> deficient mismatch repair –> large increases in DNA sequences referred to as ‘microsatellites’ –> frameshift mutation –> CRC

58
Q

Treatment of T3/T4 rectal cancer

A

Neoadjuvant chemotherapy (to reduce risk of recurrence given proximity to other organs) –> wait 10 weeks –> surgery –> adjuvant chemotherapy

59
Q

How to follow up curatively treated CRC?

A

Those who haven’t had a full colonoscopy at diagnosis require one at the conclusion of treatment, then at 3 years, then 5 yearly

Physical exam with CEA 3 monthly for 3 years, then 6 monthly

CTCAP annually for 3 years

60
Q

Compare right sided and left sided CRC

A

Right sided

  • More aggressive, worse prognosis
  • BRAF mutations
  • More active immune cells promoting immunogenicity

Left sided
- RAS/RAF mutations

61
Q

Treatment of early stage CRC (stage 1 and 2)

A

Curative surgery +/- adjuvant chemotherapy (benefit is ~5% in stage 2 high risk patients)

If MSI high, no need for adjuvant chemotherapy

62
Q

Treatment of stage 3 CRC (lymph node positive)

A

Surgery + adjuvant chemotherapy (5FU/capecitabine + oxaliplatin) for 3-6/12

63
Q

Treatment of stage 4 CRC

Oligometastatic and resectable

A

Surgery +/- adjuvant chemotherapy (5FU/capecitabine + oxaliplatin)

64
Q

Treatment of stage 4 CRC

Oligometastatic and partially resectable

A

Neoadjuvant chemo –> surgery –> adjuvant chemo

65
Q

Treatment of stage 4 CRC

Unresectable disease

A

Doublet chemotherapy (5FU/capecitabine PLUS oxaliplatin or irinotecan)

If RAS/RAF wildtype: add EGFR inhibitor (panitumumab or cetuximab)

If RAS/RAF mutation: add VEGF inhibitor (bevacizumab)

If MSI high (not yet PBS approved): immunotherapy (pembrolizumab or nivolumab or ipilimumab with nivolumab)

66
Q

Cancer genetic testing is now available for 3 conditions. What are they?

A

1) All high grade serous ovarian ca (non-mucinous) <70 years
2) All triple neg breast ca <50 years
3) Breast ca with manchester score >15 (>10% pre test probability of BRCA1/2 mutation)

Oncology (7 decks)

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