colorectal cancer + pancreatic cancer Flashcards

1
Q

how common is colorectal cancer. what types of cancer is colorectal cancer usually

A

3rd most common cancer in UK (lung, breast)
2nd most deadly.

majority are adenocarcinoma
1 in 20 will develop bowel ca during their lifetime.

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2
Q

risk factors for colorectal cancer

A

neoplastic polyps, imflammatory bowel disease, genetic predisposition, diet (low fibre high red/ processed meat), the classics (alcohol, smoking, prev cancer)

its a disease of older age –> aquired ginetic mutations.

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3
Q

clincial signs and symptoms for CRC

A

can be asympomatic–> detected through screening program.

Right sided/ Caecal: non-specific- wt loss, melena, RIF mass/pain, fatigue, weakness due to iron deficiency anaemia (Any Iron def anaemia in older man/ post menopausal women is Ca unless ruled out) - in keeping with slow bleeding.

left sided/ Sigmoid: altered bowel habit, blood per rectum, bowel obstruction, masss. tenesmus.

RED FLAGS: malaise, wt loss, abdo pain.

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4
Q

investigations for CRC

A

FBC (testing for microcytic / anaemia)
foecal occult blood
sigmoidoscopy/ colonoscopy is ultimate requirement for tissue biopsy.
If family history of famlilal adenomatous polyps then DNA test @15.

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5
Q

where does it spread to, how is it graded

A

liver, lungs, bone.

T(tumor differentiation- Well,moderately, poorly)
N-nodes
M-metastases

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6
Q

what is the treatment of CRC

A

Surgical intervention is the primary method or Rx.
Right hemicolleectomy (cecal, ascending or prox transverse)
left hemi- (dist transverse or desc)
sigmoid collectomy- sigmoid
AP resection (in rectum)
heartmans for emergency obstruction.

stenting in obstruction for palliation is an option.
Radiotherapy can be used in palliation
chaemo- in stage 3 can be used alongside surg.

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7
Q

prognosis of bowel ca

A

stage 1- 5yr survival 75%.
stage 4- 5%

highlights importance of screening.

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8
Q

physiology of adenoma carcinoma CRC pathway

A

70% of CRC via this path.

mutation in K-RAS and C-myc, + inactivation of tumour suppressor genes (TP53) and APC.

acquired through lifetime mutations.

Leads to polyps forming which progress to cancer

(APC- binds to beta-catenin, metabolises it, when WNT binds to the WNT receptor, this causes APC to disassociate from beta-catenin –> BC goes to nucleus and causes proliferation.)
If APC don’t work unstoppable BC.

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9
Q

what is a FAP

A

Germline mutation in one allele of the APC gene

Inherited in an autosomal dominant way

De-novo germline mutations account for up to 25% of the cases

Affects 1 in 10,000

Every single cell in the body has the mutation, so every cell is already one step further along the above pathway than in non-FAP patients

They get loads of adenomatous polyps throughout their large intestine during teens and 20s => risk of development to ca is almost 100% by the age of 40 => need to do prophylactic pan proctocolectomy

LOADS OF POLYPS!

FAP is less common than Lynch syndrome

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10
Q

what is the serrated pathway

A

more of a BRAF gene process.

polys become big and have jagged/ serrated edges.

further mutations (MLH1, MSH2) cause silencing of suppressing genes.

mutations accumulate and cancer develops

30% of CRC, more aggressive than normal polyps and harder to detect.

villous is worse, tubulo-villous then tubular is least bad

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11
Q

what is Lynch syndrome

A

Autosomal dominant disease BRCA mutation

when 2nd copy is lost through mutation tumours develop.

get less polyps than FAP. Right sided mostly

Endometrial, pancreatic cancers are also common.

Avg age of CRC Dx in LS mutation carriers = 45-50 years old

microsatelite pathway. 80% progress to CRC

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12
Q

discuss the bowel cancer screening program on the nhs

A

faecal immunochemical test (FIT) every 2 years

there is an ab to human globin inside kit.

sensitive, 80%
specific, 95%

looks for bleeding into the rectum- which would come from a polyp

PPV 15-30%.

would get colonospcopy

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13
Q

risk factors for pancreatic cancer, tissue type, cell type.

A

60-80 y/o, smoker, booze, diabetes, chronic pancreatitis, hereditary non-polyposis colorectal cancer.

adenocarcinoma (like CRC)

glandular duct cells, commonly in the head of the pancreas. - tumor will compress the CBD so bile cannot drain.

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14
Q

signs and symptoms of pancreatic cancer

A

courvoisiers law= painless jaundice, palpable gallbladder –> pancreatic cancer.

(pancras obstructs common bile duct- post hepatic jaundice)

weight loss + steatorrhea, diabetes, epigastric mass, abdopain radiating to back.

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15
Q

investigations of pancreatic cancer + management

A

FBC- anaemia
LFT- raised ALP

abdo ultrasound.

CT-CAP- double duct sign visible

Rx: whipples procedure–> remove head of pancras, antrum of stomach, 1+2nd parts of duodenum, CBD and gallbladder.

5 year survival post whipples 20-40%

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16
Q

what is metaplasia + dysplasia + neoplasia

A

a reversable replacement of one mature tissue with another.

dysplasia can happen as a result or independently. - it is premalignant.- includes DNA damage. may/not be reversable.

neoplasia- growth has become autonomous- not sensitive to feedback mechanisms. (can be benign or malignant)