Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Z YEAR 1 BRS Gastroentology > Gastrointestinal cancer > Flashcards

Gastrointestinal cancer Flashcards

1
Q

What is cancer?

A

•A disease caused by an uncontrolled division of abnormal cells in a part of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is primary?

A

•Arising directly from the cells in an organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is secondary/metastasis?

A

•Spread from another organ, directly or by other means (blood or lymph)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are epithelial cells and cancers of GI tract?

A

squamous - squamous cell carcinoma (SCC)

“glandular epithelium” - adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are neuroendocrine cells and cancers of GI tract?

A

enterocendocrine cells - neuroendocrine tumours (NETs)

Intersittial cells of Canal - gastrointestinal stroll tumours (GISTs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are connective tissue and cancers of GI tract?

A

smooth muscle - leiomyoma/leiomyosarcomas

adipose tissue - liposarcomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is squamous cell carcinoma?

A
  • From normal oesophageal squamous epithelium
  • Upper 2/3
  • Acetaldehyde pathway
  • Less developed world
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is adenocarcinoma?

A
  • From metaplastic columnar epithelium
  • Lower 1/3 of oesophagus
  • Related to acid reflux
  • More developed world
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the progress from reflux to cancer?

A
  1. Oesphagitis (inflammation) 30% of uk (GORD)
  2. Barretts (metaplasia) 5% of 30%
  3. Adenocarcinoma 0.5-1% barretta lifetime risk of cancer
    - 30-100 fold risk of cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the progression to adenocarcinoma?

A
  1. Barrett’s oesophagus
  2. Dysplasia (low grade)
  3. Dysplasia (high grade)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Barrett’s surveillance?

A

BSG guidelines
• No dysplasia → Every 2-3 years
• LGD → every 6 months
• HGD → intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is oesophageal cancer occurrence?

A

•Squamous- adenocarcinoma
•9th most common cancer
•Affects the elderly
Male/female (adeno 10:1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is survival of oesophageal cancer?

A
  • Late presentation
  • 65% palliative
  • High morbidity & complex surgery
  • Poor 5-year survival <20%
  • Palliation- difficult
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the management pathway for oesophageal cancer?

A
  1. Diagnosis: endoscopy-> biopsy
  2. Staging: Ct scan, Laparscopy, EUS< PET scan
  3. Treatment:
    - Curative: Neo-ajuvant chemo -> radical surgery
    - Palliative: chemo, DXT, Stent
    - Oesophagectomy
    - Two-stage Ivor Lewis approach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the prevalence of colorectal cancer?

A
  • Most common GI cancer in Western Societies
  • Third most common cancer death in men & women
  • Lifetime risk
  • 1 in 10 for men
  • 1 in 14 for women
  • Appendicitis is 8.6% M vs. 6.7% F
  • Generally affect patients > 50 years (>90% of cases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is sporadic form of colorectal cancer?

A

•Absence of family history, older population, isolated lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is familial form of colorectal cancer?

A

•Family history, higher risk if index case is young (<50years) and the relative is close (1st degree)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is hereditary syndrome form of colorectal cancer?

A

•Family history, younger age of onset, specific gene defects
•e.g. Familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome)
-Hispathology: adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the development?

A
  1. normal epithelium: APC mutation
  2. Hyper proliferative epithelium, aberramt cryptic foci (COX-2 over expression)
  3. Small adenoma (Kras mutation)
  4. Large adenoma (p53 mutation) (loss of 18q)
  5. Colon carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the history risk factors of colorectal cancer?

A

-Past history:
•Colorectal cancer
•Adenoma, ulcerative colitis, radiotherapy
-Family history:
•1st degree relative < 55 yrs
•Relatives with identified genetic predisposition
•(e.g. FAP, HNPCC, Peutz-Jegher’s syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the diet/environmental risk factors of colorectal cancer?

A
  • ?carcinogenic foods
  • Smoking
  • Obesity
  • Socioeconomic status
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the locations of the colorectal cancer?

A
  • ⅔ in descending colon and rectum

* ½ in sigmoid colon and rectum (i.e. within reach of flexible sigmoidoscopy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens in caecal and right sided cancer clinical presentation?

A
  • Iron deficiency anaemia (most common)
  • Change of bowel habit (diarrhoea)
  • Distal ileum obstruction (late)
  • Palpable mass (late)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a clinical presentation for left sided & sigmoid carcinoma?

A
  • PR bleeding, mucus
  • Thin stool (late)
  • Bowel obstruction (late)
25
Q

What is clinical presentation for Rectal carcinoma?

A
  • PR bleeding, mucus
  • Tenesmus
  • Anal, perineal, sacral pain (late)
26
Q

What is the clinical presentation for a late local invasion?

A
  • Bladder symptoms

* Female genital tract symptoms

27
Q

What is clinical presentation for late metastasis?

A
  • Liver (hepatic pain, jaundice)
  • Lung (cough)
  • Regional lymph nodes
  • Peritoneum
  • Sister Marie Joseph nodule
28
Q

What are signs of primary cancer?

A
  • Abdominal mass
  • DRE: most <12cm dentate and reached by examining finger
  • Rigid sigmoidoscopy
  • Abdominal tenderness and distension – large bowel obstruction
29
Q

What are signs of metastasis and complications?

A
  • Hepatomegaly (mets)
  • Monophonic wheeze
  • Bone pain
30
Q

What is a faecal occult blood test?

A
  • Guaiac test (Hemoccult) – based on pseudoperoxidase activity of haematin
  • Sensitivity of 40-80%; Specificity of 98%
  • Dietary restrictions – avoid red meat, melons, horse-radish, vitamin C & NSAIDs for 3 days before test
31
Q

What blood test do you do?

A
  • FBC: anaemia, haematinics – low ferritin
  • Tumour markers: CEA which is useful for monitoring
  • NOT diagnostic tool
32
Q

What is a Double contrast barium enema

for an investigation for colorectal cancer?

A
  • Does not require sedation
  • Decreased risk of perforation
  • More limited in detecting small lesions
  • All lesions need to be confirmed by colonoscopy and biopsy
  • Historic interest only
33
Q

What is colonoscopy for investigation of colorectal cancer?

A
  • Can visualize lesions < 5mm
  • Small polyps can be removed
  • Reduced cancer incidence
  • Usually performed under sedation
34
Q

How is CT colonoscopy/colonography used for investigation of colorectal cancer?

A
  • Can visualize lesions > 5mm
  • No need for sedation
  • Less invasive, better tolerated
  • If lesions identified patient needs colonoscopy for diagnosis
35
Q

How is an MRI of pelvis used for colorectal cancer?

A

MRI pelvis – Rectal Cancer
•Depth of invasion, mesorectal lymph node involvement
•No bowel prep or sedation required
•Help choose between preoperative chemoradiotherapy or straight to surgery
•Is the CRM threatened?

36
Q

Why is CT used in colorectal cancer?

A

CT Chest/Abdo/Pelvis

•Staging prior to treatment

37
Q

How would you manage colorectal cancer?

A
  1. Colon cancer is primarily managed by surgery
  2. ? Stent/Radiotherapy/Chemotherapy
  3. Obstructing colon carcinoma
    •Right & transverse colon – resection and primary anastomosis
    •Left sided obstruction
    •Hartmann’s procedure
    •Proximal end colostomy (LIF)
    •+/- Reversal in 6 months
    •Primary anastomosis
    •Intraoperative bowel lavage with primary anastomosis (10% leak)
    •Defunctioning ileostomy
    •Palliative stent
38
Q

What is the epideimeology of pancreatic caner?

A

-Commonest form of panc CA is pancreatic ductal adenocarcinoma (PDA)
-80-85% have late presentation
•Overall median survival <6 months
•5-year survival 0.4 - 5%
-15-20% have resectable disease
•Median survival 11-20 months
•5-year survival 20–25%
•Virtually all pts dead within 7 years of surgery

39
Q

What is the incidence of pancreatic cancer like?

A

•Incidence ↑er in Western/industrialised countries
•Rare before 45 years, 80% occur between 60 & 80 years of age
•Men > women (1.5 - 2:1)
•UK & USA annual incidence panc CA 100 per million popn
•4th commonest cause of cancer death
•Incidence & mortality roughly equivalent – UK in 2015
-9,921 new cases of PDA
-9263 deaths from PDA
•2nd commonest cause of cancer death – in USA 2030
- 48,000 deaths

40
Q

What are risk factors for pancreatic cancer?

A
  1. Chronic pancreatitis → 18-fold ↑er risk
  2. Type II diabetes mellitus → relative risk 1.8
  3. Cholelithiasis, previous gastric surgery & pernicious anaemia – WEAK
  4. Diet (↑fat & protein, ↓fruit & veg, coffee & EtOH) - WEAK
  5. Occupation (insecticides, aluminium, nickel & acrylamide)
  6. Cigarette smoking → causes 25-30% PDAs
  7. 7-10% have a family history
    - Relative risk of PDA increased by: 2, 6 & 30-fold with: 1, 2 & 3 affected first degree relatives
41
Q

What inherited syndromes increase your risk for pancreatic cancer?

A
  1. Hereditary pancreatitis
  2. Familial atypical multiple mole melanoma
  3. Familial breast-ovarian syndrome
  4. Peutz-Jegers syndrome
  5. HNPCC (Lynch syndrome)
  6. FAP
42
Q

Describe the pathogenesis of pancreatic cancer?

A

-Pancreatic Intraepithelial Neoplasias (PanIN)
•PDAs evolve through non-invasive neoplastic precursor lesions
•PanINs are microscopic (<5 mm diameter) & not visible by pancreatic imaging
•Acquire clonally selected genetic & epigenetic alterations along the way
-Normal, PannIN 1A, 1B, , 3

43
Q

Where do PDAs usually arrive?

A

Carcinoma of the head of the pancreas

•At least two-thirds of PDAs arise in the head

44
Q

When is jaundice a clinical presentation of pancreatic cancer?

A

Jaundice >90% due to either invasion or compression of CBD
- often painless
- palpable gallbladder (Courvoisier’s sign)

45
Q

When is weight loss a clinical presentation of pancreatic cancer?

A

Weight loss
- anorexia
- malabsorption (secondary to exocrine insufficiency)
- diabetes.

46
Q

When is pain a clinical presentation of pancreatic cancer?

A

Pain 70% at the time of diagnosis
- epigastrium
- radiates to back in 25%
- back pain usually indicates posterior capsule invasion and irresectability.

47
Q

What are other clinical presentations of pancreatic cancers?

A

• 5% atypical attack of acute pancreatitis.
• In advanced cases, duodenal obstruction results in persistent vomiting.
• Gastrointestinal bleeding
- duodenal invasion or varices secondary to portal or splenic vein occlusion

48
Q

What is the clinical presentation for Carcinoma of the body & tail of pancreas

A
  • Develop insidiously and are asymptomatic in early stages
  • At diagnosis they are often more advanced than lesions located in the head
  • There is marked weight loss with back pain in 60% of patients.
  • Jaundice is uncommon
  • Vomiting sometimes occurs at a late stage from invasion of the DJ flexure
  • Most unresectable at the time of diagnosis
49
Q

What tumour marker investigations can be done for pancreatic cancer?

A

•Tumour marker CA19-9
- falsely elevated in pancreatitis, hepatic dysfunction & obstructive jaundice.
- concentrations > 200 U/ml confer 90% sensitivity
- concentrations in the thousands associated with high specificity\

50
Q

What ultrasonography for pancreatic cancer?

A

-Ultrasonography
- can identify pancreatic tumours
- dilated bile ducts
- liver metastases

51
Q

How is dual phase CT used in pancreatic cancer?

A

-Dual-phase CT accurately predicts resectability in 80–90% of cases
- contiguous organ invasion
- vascular invasion (coeliac axis & SMA)
- distant metastases

52
Q

What investigations can be done with pancreatic cancer?

A

•MRI imaging detects and predicts resectability with accuracies similar to CT
•MRCP provides ductal images without complications of ERCP
• ERCP
- confirms the typical ‘double duct’ sign
- aspiration/brushing of the bile-duct system
- therapeutic modality → biliary stenting to relieve jaundice

53
Q

What other investigations can be done with pancreatic cancer?

A

•EUS
- highly sensitive in the detection of small tumours
- assessing vascular invasion
- FNA

• Laparoscopy & laparoscopic ultrasound
- detect radiologically occult metastatic lesions of liver & peritoneal cavity

•PET mainly used for demonstrating occult metastases

54
Q

What are different liver cancers?

A
  • HCC
  • ChCA
  • CRC
  • GB CA
55
Q

What is HCC?

A

Primary Liver Cancer (Hepatocellular Carcinoma [HCC])
•Aetiology
- 70-90% have underlying cirrhosis
- Aflatoxin
• Median survival without Rx 4-6 m
• 5yr survival <5%
• Systemic chemotherapy ineffective (RR <20%)
• Other effective Rx options
- OLTx
- TACE
- RFA
• Optimal Rx surgical excision with curative intent
- 5yr survival >30%
• 5-15% suitable for surgery

56
Q

What is gallbladder cancer?

A 
•Aetiology unknown 
 - GS
 - porcelain GB
 - chronic typhoid infection
• Median survival without Rx 5-8 m
• 5yr survival <5% 
• Systemic chemotherapy ineffective 
• No other effective Rx options
• Optimal Rx surgical excision with curative intent
 - 5yr survival: stage II 64%; stage III 44%; stage IV 8% 
• <15% suitable for surgery
57
Q

What is ChCA?

A

Cholangiocarcinoma (ChCA)

•Aetiology
- PSC & UC
- liver fluke (clonorchis sinesis)
- choledochal cyst
• Median survival (depends on site) without Rx <6 m
• 5yr survival <5%
• Systemic chemotherapy ineffective
• GEMCIS - median overall survival 11.7 months*
• No other effective Rx options (OLTx)
• Optimal Rx surgical excision with curative intent
- 5yr survival 20-40%
• 20-30% suitable for surgery

58
Q

What is CRC?

A 
Secondary liver metastases (CRC) 
•15-20% synchronous, 25% metachronous
• median survival without Rx <1yr
• 5yr survival 0% 
• Systemic chemotherapy improving
• Other effective Rx options (RFA &amp; SIRT) 
• Optimal Rx surgical excision with curative intent
 - 5yr survival rates of 25-50%
• 25% suitable for surgery

Z YEAR 1 BRS Gastroentology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions