Brainscape's Knowledge GenomeTM

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


See full index

Semester 3 > GI Session 10 > Flashcards

GI Session 10 Flashcards

1
Q

What are the clinical features of oesophageal carcinoma?

A

Progressive worsening dysphasia from dry solids –> liquids and weightloss

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

What are the pathological features of oesophageal carcinoma?

A

Squamous cell can occur anywhere in the oesophagus

Adenocarcinoma occurs in the lower 1/3 where Barrett’s is seen

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

What is the pathogensis of SCC of the oesophagus?

A

HPV/tannin/vitamin A deficiency/riboflavin deficiency –> dysplasia –> neoplasia

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

What is the pathogensis of adenocarcinoma of the oesophagus?

A

Metaplaetic epithelium –> dysplasia –> neoplasia

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

What is the prognosis for oesophageal carcinoma?

A

Most pts present with advanced disease where there is direct spread through the oesophageal wall –> 5% 5-year survival rate

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

Describe the epidemiology of gastric cancer.

A

Accounts for 15% of cancer deaths worldwide
More common in men
High incidence in Japan, Columbia and Finland
Associated with gastritis and blood group A

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

What are the clinical features of gastric cancer?

A

Vague symptoms –> epigastric pain, vomiting and weight loss in advanced disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the macroscopic pathological features of gastric cancer?

A

Early is confined to submucosa/mucosa

Late appears fungating, ulcerating, infiltrative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the microscopic features of gastric cancer?

A

Intestinal cancers are all adenocarcinomas with variable degrees of gland formation
Diffuse disease –> single cells, small cells, signet ring cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the pathogenesis of gastric lymphoma?

A

H.pylori –> low grade lesion –> neoplasia of B lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pathogenesis of gastric cancer?

A

H.pylori –> early confined to mucosa/submucosa –> advanced spreads direct/lymph/liver/trans-coelomic to peritoneum +/- ovaries

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

What is the pathogensis of GI stromal tumours?

A

Intestinal cells of rajal (gastric pacemaker) become neoplastic –> C-kit serum marker release

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

What is used to assess the risk of unpredictable GI stromal tumours?

A

Site and size of lesion

Degree of pleomorphism, mitoses and necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the commonest GI lymphoma?

A

Gastric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the prognosis of gastric cancer?

A

Early gastric = good
Advanced gastric = 10% 5-year survival rate
Lymphoma = good
Stromal = unpredictable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are gastric cancers treated?

A

Surgery
Chemotherapy
Herceptin
Imatinib for stromal

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

Describe the epidemiology of oesophageal carcinoma.

A

Accounts for 2% of malignancies in the UK
Higher incidence in men
Highest incidence in China
SCC more common but incidence decreasing, opposite for adenocarcinoma

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

Describe the epidemiology of large intestine adenomas.

A

Increased incidence with age in western population and increased incidence with genetic syndromes

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

Describe the epidemiology of large intestine adenocarcinomas.

A

Peak at 60-70 y.o. In UK

Higher incidence in polyposis syndromes, UC and Crohn’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Are carcinoid tumour, lymphoma and smooth muscle tumours of the large intestine common?

A

No, they are rare

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

What are the clinical features of large intestinal adenocarcinomas?

A

R side rectosigmoid –> anaemia

L side rectosigmoid –> obstructive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the pathological features of large intestinal adenomas?

A

Variable degree of dysplasia microscopically and sessile/pedunculated mascroscopically

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

What are the pathological features of large intestine adenocarcinomas?

A

60-70% rectosigmoid –> fungating on R, stenotic on L

See microscopically with moderately differentiated adenocarcinoma or occasionally mucinous or signet ring cell type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What provides evidence for the adenoma-carcinoma sequence?

A

Geographical and anatomical distributions very similar
Synchronous lesions
Metachronous lesions
Adenomas with invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the aetiology of large intestine adenomas?

A

FAP

Gardeners syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the pathogensis of large intestine adenocarcinoma?

A

+/- previous Adenoma

Low residue diet/slow transit time/high fat intake/genetics –> neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does large intestine adenocarcinoma spread?

A

Directly
Lymph
Portal venous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is FAP?

A

Autosomal dominant in chromosome 5 –> 1000s of adenomas by 20 y.o.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is Gardener’s syndrome?

A

Similar to FAP –> nine and soft tissue tumours

30
Q

Where are carcinoid tumours usually found in the large intestine?

A

Appendix but can be anywhere

31
Q

Why do carcinoid large ins testing tumours have a normal mortality rate despite being hard to predict?

A

Rarely metastasise

32
Q

How is the prognosis of large insets tonal adenocarcinoma assessed?

A

Duke’s staging then TNM

33
Q

What is commonly seen in advanced large intestine adenocarcinoma?

A

Liver metastases

34
Q

What are the Tx options for adenocarcinoma of the large intestine?

A

Palliative chemotherapy
Resection of liver deposits
Local radiotherapy for rectal cancer

35
Q

What are the primary malignant tumours of the liver?

A

Hepatocellular carcinoma
Cholangiocarcinoma
Helatiblastoma

36
Q

What are the clinical features of carcinoma of the pancreas?

A

Early symptoms vague –> diagnosis delayed until weight loss, jaundice or Trossaeu’s sign seen

37
Q

What is Trosseau’s sign?

A

Trypsin release –> fleeting thrombophlebitis

38
Q

What can imagine allow in carcinoma of the pancreas?

A

Radiological diagnosis from small lesions

39
Q

What are the pathological features of carcinoma of the pancreas?

A

2/3 in head –> firm pale mass which on cutting appears necrotic/haemorrhagic/cystic
80% ductal with well formed glands +/- mucin
Some acinar tumours contain zymogen granules

40
Q

What is the aetiology of carcinoma of the pancreas?

A 
Islet cell tumours (rare)
Gastrinoma --> Z-E syndrome
Insulinoma --> hypoglycaemia
Glucagonoma --> definitive skin rash
(Vasoactive intestinal peptide) VIPoma -->Werner Morrison syndrome
41
Q

What is the prognosis for any type of carcinoma of the pancreas?

A

Poor

42
Q

What methods can be used to image the GI tract?

A 
Plain X-rays
Contrast studies: barium swallow/enema/meal/follow through or water-soluble contrasts
US
CT for emergency pts
MRI
Angiography
43
Q

When should an AXR be requested?

A

Small/large bowel obstruction
Acute IBD exacerbation
?toxic megacolon

44
Q

When should an AXR not be requested?

A

Acute abdominal pain (most causes not visible)
Renal colic
Constipation

45
Q

What projection are all AXR?

A

AP

46
Q

What should be included in an AXR?

A

Public tubercle
T5
Properitoneal fat stripes

47
Q

When might properitoneal fat stripes not be visible?

A

Lost on pathology e.g. appendicitis

48
Q

What contents should be seen in the bowel due to its transit time?

A 
Stomach (medium t.t.) = fluid and lots of gas
Small bowel (fast t.t.) = fluid
Large bowel (slow t.t.) = faeces +/- gas
49
Q

How can the small bowel and colon be distinguished on AXR?

A

Small bowel is central with valvulae conniventes

Colon is peripheral with haustra

50
Q

How is the rule of 3s used to assess abnormal gas patterns?

A

> 3 cm = small bowel obstruction
6 cm = large bowel obstruction with incompetent iliocaecal valve
9cm = large bowel with competent iliocaecal valve

51
Q

What soft tissues should be identifiable on a normal AXR?

A 
Liver
Spleen
L+R kidneys
Bladder
Psoas muscle
52
Q

What can be used as an approximate measure of 3 cm on radiograph?

A

Vertebral body height

53
Q

What causes small bowel obstructions?

A

Adhesions from surgery
Hernias esp inguinal
Tumours
Inflammation

54
Q

What are the progressive S/S of small bowel obstruction?

A

Vomiting –> mild distension –> absolute constipation –> colicky pain

55
Q

What causes large bowel obstruction?

A 
Colorectal carcinoma
Diverticular stricture
Hernia
Volvulus
Pseudo-obstruction
56
Q

What are the S/S of large bowel obstruction?

A

Vomiting (faeculant when late)
Significant distension
Pain
Early absolute constipation

57
Q

What is the pathogenesis of volvulus?

A

Twisting around mesentery–> enclosed bowel loop –> dilation –> perforation and ischaemia

58
Q

Why causes volvulus in the caecum?

A

Lack of mesentery

59
Q

How does sigmoid volvulus appear on AXR?

A

Starts in LIF –> coffee bean sign to RUQ –> proximal bowel obstruction

60
Q

What is the pathogenesis of toxic megacolon?

A

Acute deterioration of UC –> colonic dilatation –> oedema and pseudopolyps

61
Q

What is the pathogenesis of lead pipe colon?

A

UC causes chronic inflammation –> loss of haustra so featureless colon

62
Q

What is thumbprinting on AXR?

A

Active inflammation often in UC but also oedematous processes –> oedematous thickened haustra –> thickened wall

63
Q

What extra-GI abnormalities are visible on AXR?

A 
Renal calculi
Chronic pancreatitis
Vascular calcification
AAA
Foreign bodies
64
Q

What is the pathogensis of pneumoperitoneum?

A

Peptic ulcer/diverticular/tumour/obstruction/trauma/iatrogenic –> air under diaphragm

65
Q

What is used to identify pneumoperitoneum?

A

Erect CXR after sitting for 10-20 mins

CT

66
Q

What is visible on CT taken at T12?

A 
Loves of liver
Curves of stomach
Coeliac trunk
AA
IVC
Hepatic veins
67
Q

What is seen on CT taken at L1?

A 
(Transpyloric plane of Addison)
Lobes of liver
Pancreatic head
Renal hila
Spleen
Transverse colon
68
Q

What are the advantages of using CT to image the abdomen?

A

Gives good spatial resolution
Reformatting can be used to identify mechanisms of injury
Can be used to build virtual colonoscopy instead of barium enema

69
Q

What are the applications of MRI in imagine the abdomen?

A

Good spatial and contrast resolution
Moving object cause blurring but this can be used with fluid to examine peristalsis in Crohn’s (absent in active disease)

70
Q

What is the clinical application of abdominal US?

A

Cheap and portable but highly user dependent
Gallstones
Dilated CBD
Examine bowel wall layers e.g. In appendix
Combine with endoscopy

Semester 3 (50 decks)

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