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Oncology > GIT Malignancy > Flashcards

GIT Malignancy Flashcards

1
Q

Oesophageal Cancer subtypes and associated distribution?

A

Squamous cell carcinoma (proximal third)
Adenocarcinoma (distal, GEJ)

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2
Q

Oesophageal cancer subtypes and associated risk factors?

A

SCC:
- Smoking
- Excvessive etoh
- HPV (weak)

Adeno
- Barrett’s
- Obesity
- Smoking
- Absence of H pylori

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3
Q

Hereditary Oesophageal cancer syndromes?

A

Howel Evans Syndrome
- AD, RHBDF2 gene

NEPPK (non-epidermolytic palmoplantar keratosis)
- Essentially howel-Evans syndrome without the palmoplantar keratosis
- AD, RHBDF2 gene

Familial Barretts oesophagus
- AD

Bloom Syndrome
- AR, BLM/RECQL3 gene

Fanconi Anaemia
- AR
- BRCA2, FANCD1, FANCN gene

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4
Q

Main type of gastric cancer and subtypes?

A

95% Gastric Ca are adenocarinomas
2 main subtypes:
- Intestinal - most common, well differentiated. Chronic inflammatory process fro chronic gastritis -> cancer. Elderly male. Good prognosis
- Diffuse - Undifferentiated, located in proximal stomach. Associated with lichen plastica. Poor prognosis

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5
Q

Hereditary gastric cancer syndromes (some also associated with other forms of cancers ie CRC)?

A

Hereditary diffuse gastric cancer
- AD
- CDH1 gene
- Need prophylactic gatrectomy

Lynch Syndrome (aka HNPCC)
- AD
- EPCAM, MLH1, MSH2, MSH 6, PMS2

Juvenile possibly syndrome (JPS)
- AD
- SMAD4, BMPR1A

Peutz Jegher syndrome (PJS):
- AD
- STK11

Familial Adenomatous Polyposis (FAP)
- AD
- APC gene

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6
Q

Treatment for Resectable oesophageal and gastric cancers?

A

Oesophageal / GEJ:
- neoadjuvant carboplatin/paclitaxel, resection, adjuvant immunotherapy

GEJ / gastric:
- Perioperative chemo (FLOT4)

Gastric:
- Adjuvant capecitabine plus oxaliplatin (CAPOX) chemo

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7
Q

Treatment for unresectable oesophageal cancers?

A

Definitive chemotherapy with platinum + flurouracil

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8
Q

Treatment for advanced / metastatic esophageal / gastric cancers?

A

HER2 Negative ~80%
- 1st line - a platinum + fluropyrimidine + immunotherapy

HER2 amplified - IHC 3+, or IHC 2+ / ISH +ve (~20%)
- 1st line - a platinum + fluropyrimidine + trantuzumab

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9
Q

Two types of dumping syndrome and their associated symptoms?

A

Early Dumping - occurs 30 mins post meal
- Cause - hyperosmolar content into small bowel draws water in
- GIT Sx - abdo discomfort, nausea, dia, bloating
- Vasomotor symptoms - Flushing, palp / tachycardia, sweating

Late Dumping - occurs after several hours
- Cause - carb dump leading to hyper insulin state and hypoglycemia
- GIT Sx: - Hypoglycemia
Vasomotor Symptoms - tired, faint, hunger, sweatign (low BSL Sx)

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10
Q

Dumping syndrome management?

A

Lifestyle and diet modification:
- small regular meals, rather than big meals
- delay fluid intake until at least 30 mins following meal
- Avoid high GI carbs
- Lie down after meal - avoids hypovolaemia symptoms

Pharm
- Short acting somatostatin anologues (ie octreotide)
- Acarbose in late dumping (nil effect in early dumping)

Surgical
- Nil

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11
Q

Pancreatic cancer most common location?

A

70% located in panc head

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12
Q

Pancreatic cancer subtypes?

A

Adenocarcinoma (95%)
NET (5%)

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13
Q

Pancreatic cancer risk factors?

A

Smoking
heavy etoh
high BMI
Long term DM

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14
Q

Inherited GIT cancer syndromes that increase risk of pancreatic cancer?

A

Familial component in 10% of cases of pancreatic cancer cases
- Peutz-Jegher syndrome
- Lynch syndrome
- BRCA1/2 mutation - more so BRCA2 mutation

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15
Q

Explain the role of BRCA genes and PARP proteins and the MOA of PARP inhibitors?

A

BRCA1/2 are tumor suppressor genes that play a fundamental role in a DNA repair pathway called homologous recombination repair
Mutations can be germline or somatic (tumor only) variants

PARPs are a large family of proteins which facilitate DNA repair in pathways involving single strand breaks.
Inhibition of PARPs with a PARP inhibitor leads to accumulation of single strand breaks which eventually results in double strand breaks (synthetic lethality)
- therefore PARP inhibitors are only good in pts with BRCA mutations

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16
Q

What is synthetic lethality?

A

Synthetic lethality is a type of genetic interaction where the combination of two genetic events results in cell death or death of an organism
For example, combination of BRCA1/2 mutation and PARP inhibition leads to cell death

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17
Q

Pancreatic cancer prognosis and treatment?

A

Very poor prognosis even if early Dx

Treatment:
- resectable - upfront surgery followed by adjuvant chemo
- Boarderline resectable - consider neoadjuvant chemo followed by surgery (emerging)
- Locally advance / metastatic - chemoradiotherapy / systemic therapy

Olaparib is associated with significant increase in PFS in metastatic pancreatic cancer compared to placebo

18
Q

Pancreatic cancer complications?

A

Biliary obstruction (common, 70%)
- Biliary stenting or PTC insertion

Gastric outlet obstruction (10-25%)
- Enteric stenting, PEJ tube insertion
- Duodenal bypass surgery if prognosis >3-6 months

Tumor associated abdo pain
- usually due to coeliac plexus involvment
- Consider coeliac plexus neurolysis (block that results in damage to nerves) / radiotherapy

Thromboembolic disease
- very thrombotic cancer. currently no need for prophylactic anticoagulation

GI bleeding

19
Q

Gastro intestinal stromal tumours (GIST) basic details?

A

Mesenchymal tumour related to connective tissue / smooth muscle

Rare cancer, but most common form of GI sarcoma
Occurs in stomach (50-60%), small intestines (30-40%), but can arise anywhere in GI tract

Characterized by spindle shaped cells

20
Q

Genetic mutation associated with GIST?

A

95% express KIT
- activating mutation in KIT or PDGFRA gene

21
Q

Treatment of GIST?

A

Imatinib -> dose escalation -> sunitinib -> regorafenib -> ripretinib

22
Q

Risk factors for HCC?

A

Major risk factor is chronic liver disease:
- HBV
- HCV
- Chronic etoh consumption
- NAFLD (including NASH)
- genetic haemochromatosis

23
Q

What does HCC screening involve and who should be screened?

A

HCC screening in at risk individuals (ie pts with CLD)
Screening involves 6 monthly AFP and liver USS

24
Q

Diagnosis of HCC?

A

HCC is one of the only cancers that can be Dx based on imaging (nil tissue required)
- Quad phase CT - single lesion with arterial hypervascularity and wash out on portal venous phase

Other components of Dx include:
- rising AFP
- Biopsy in selected cases

25
Q

Treatment of HCC?

A

Resection or transplantation (curative potential)

Locoregional therapies (nil curative but can be bridge to curative therapies)
- TACE, ablation, RT

Systemic therapies in pts with unresectable metastatic HCC (advanced disease)
- Atezolizumab (PDL1) + bevacizumab (VEGF). Otherwise Lenvatinib (VEGFR1,2,3) or sorafenib
- Not much benefit with systemic cytotoxic chemo
- Systemic therapy only offered to CPA cirrhosis pts (not decompensated disease)

26
Q

Transplant criteria for HCC?

A

Milan criteria or UCSF criteria

UCSF criteria:
- single nodule <6.5cm diameter
- </=3 modules, each </= 4.5cm each. Total dia </= 8cm

27
Q

Colorectal Cancer histological variants?

A

Adenocarcinoma (>90%)
Mucinous
signet ring carcinoma

28
Q

Classification / main types of CRC?

A

Sporadic (60-65%)

Familial (25%)
- familial association however nil identified gene defects

Hereditary
- HNPCC
- FAP

29
Q

Main features in CRC carcinogenesis?

A

Chromosomal instability (CIN)
- errors during mitosis leading to abnormalities in chromosomal number and structure

CpG island Methylator Phenotype (CIMP)
- MLH1 promotor hypermethylation

Microsatelite instability (MSI)
- Loss of MMR genes (MLH1, MSH2
- CIMP and MSI are strongly corrolated
- BRAF mutation strongly associated with sporadic CRC (ie BRAF mut = sporadic)

30
Q

Gene defects in HNPCC / Lynch syndrome?

A

Mutations in MMR genes: MLH1, MSH2, MSH6, PMS2
- MSH2 and MLH1 are in >90% of cases

31
Q

Basic details of HNPCC / lynch syndrome?

A

AD inheritance, high penetrance
Results in right sided colon cancer
Often poorly differentiated, mucinous and infiltrating lymphocytes
MMR gene defects: MLH1, MSH2, MSH6, PMS2

32
Q

Diagnostic criteria for HNPCC / Lynch Syndrome?

A

Amsterdam criteria (3-2-1 rule)
- at least 3 relative with any lynch syndrome associated cancer
- at least 2 consecutive generations affected
- at least one relative Dx before age of 50yrs

33
Q

Surveillance and surgery in HNPCC / Lynch syndrome?

A

Surveillance from age of 25yrs, or 5 years younger than youngest affected family member
Surveillance C scope every 1-2 years

Surgical management with extended colectomy (subtotal or total colectomy preferred)
Annual survailence of residual colon
NSIAD chemoporphylaxis (aspirin 600mg daily)

34
Q

Basic details of FAP? Associated cancers?

A

AD inheritance, high penetrance
Results in 100s of distal left sided polyps from adolescence
Risk of CRC is 100% at age >40yrs

Other associated cancers
- papiliary thyroid
- Gastric
- Ileal Carcinoid

35
Q

Gene defect in FAP?

A

Germline APC mutation

36
Q

Surveillance and surgery in FAP?

A

Endoscopic survailence from age 10-15yrs (or earlier if GI symptoms)
Sigmoidoscpy sufficient due to predominate left sided polyps

Colectomy usually between age 15 and 25yrs
NSAID chemoprophylaxis when surgery inappropriate

37
Q

Population screening for CRC?

A

FOBT every 2 years from age 50 - 74yrs
Low participation 40% of population currently

38
Q

Treatment of CRC?

A

Locally advanced (stage II or III) disease
- Neoadjuvant chemoradiotherapy, followed by surgery (total mesorectal excision) +/- adjuvant chemotherapy
- Total neoadjuvant therapy involves systemic chemo and chemoradiation before surgery (ie systemic chemo with Folfirinox, then cRT, then surgery)

Folfirinox = folinic acid, furouricil, irinotecan, oxaliplatin

Locally advances (stage II or III) disease with “high risk” features
- High risk features include: T4 disease, poorly differentiated, presence of obstruction, perforation etc
- Neoadjuvant chemoradiotherapy, followed by surgery (total mesorectal excision) + adjuvant chemotherapy
- Adjuvant chemo with 3-6/12 fluropyrimidine (5-FU/capecitabine) + oxaliplatin
- limited role for irinotecan / bevacizumab / EGFRi in adjuvant setting

Advanced / metastatic CRC - targeted therapies
- mCRC with KRAS mutation (KRAS found in 70% of mCRC) -> KRASi (Divarasib) +/- EGFRi
- mCRC with EGFR mutation -> first line chemo + EGFRi (cetuximab, panitumumab)
- mCRC with VEGF mutation -> first line chemo + VEGFi (Bevacizumab)
- mCRC with BRAF mutation -> BRAFi (encorafenib) + EGFRi (cetuximab) + MEKi (Binimetinib)
- mCRC with MSI-h -> 1st line PD-1 inhibitor (pembrilizumab)

39
Q

Common GIT chemotherapy agents related toxicities?

A

Fluropyrimidines (5-FU, capecitibine, etc)
- Diarrhoea, hand foot syndrome, coronary artery vasospasm

Oxaplatin
- Acute neurotoxicity agrevated by exposure to cold
- cold induced pharyngolaryngeal dysesthesia

40
Q

EGFR cancer pathway downstream components?

A

EGFR (cell surface receptor)
KRAS
BRAF V600E
MEK
ERK

Activation leading to stimulation of cell growth and cancer

Oncology (6 decks)

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