Brainscape's Knowledge GenomeTM

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


See full index

Clinical Pathology G > GI Pathology > Flashcards

GI Pathology Flashcards

1
Q

How long should a normal oesophagus be?

A

25 cm long muscular tube mostly lined by squamous epithelium

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

What are the two oesophageal sphincters?

A

Sphincter at upper end (cricopharyngeal) and lower end (gastro-oesophageal junction)

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

What is distinct about the distal 1.5-2cm of the oesophagus?

A

Distal 1.5-2 cm are situated below the diaphragm and lined by glandular (columnar) mucosa.

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

Where is the squamo-columnar junction?

A

The squamo-columnar junction is usually located at 40 cm from the incisor teeth.

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

What are the causes of oesophageal inflammation?

A 
Infectious
Bacterial, viral (HSV1, CMV), fungal (candida)
Chemical
Ingestion of corrosive substances
Reflux of gastric contents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the reflux of bile called?

A

duodeno-gastric reflux

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

What are the risk factors for reflux oesophagitis?

A

Defective lower oesophageal sphincter
Hiatus hernia
Increased intra-abdominal pressure
Increased gastric fluid volume due to gastric outflow stenosis

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

What is a hiatus hernia?

A

Abnormal bulging of a portion of the stomach through the diaphragm

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

Histologically, what would be seen in reflux oesophagitis?

A

Squamous epithelium
Basal cell hyperplasia, elongation of papillae, increased cell desquamation

Lamina propria
Inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)

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

What can be the complications from reflux oesophagitis?

A

Ulceration

Haemorrhage

Perforation

Benign stricture (segmental narrowing)

Barrett’s oesophagus

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

What is Barrett’s oesophagus?

A

Cause:
Longstanding reflux

Risk factors:
Same as for reflux (male, Caucasian, overweight)

Macroscopy:
Proximal extension of the squamo-columnar junction

Histology:
Squamous mucosa replaced by columnar mucosa > “glandular metaplasia”

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

What are the types of columnar mucosa?

A

Gastric cardia type

Gastric body type

Intestinal type = “specialised Barrett’s mucosa”

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

Why is Barrett’s oesophagus concerning?

A

Premalignant condition with an increased risk of developing adenocarcinoma

Regular endoscopic surveillance is recommended for early detection of neoplasia

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

How common is oesophageal carcinoma?

A

8th most common cancer in the world

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

What are the 2 histological types of oesophageal carcinoma?

A

Squamous cell carcinoma

Adenocarcinoma

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

Which gender is oesophageal adenocarcinoma more common in?

A

Male 7:1

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

What is the aetiology for oesophageal adenocarcinoma?

A

Barrett’s oesophagus

tobacco, obesity

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

Where are oesophageal adenocarcinomas usually found?

A

lower oesophagus

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

What does an oesophageal adenocarcinoma look like?

A

Plaque-like, nodular, fungating, ulcerated, depressed, infiltrating

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

What are the risk factors for squamous carcinoma?

A 
Tobacco and alcohol
Nutrition (potential sources of nitrosamines)
Thermal injury (hot beverages)
HPV
Male
Ethnicity (black)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are squamous carcinomas most common?

A

Iran, China, South Africa, Southern Brazil

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

How are oesophageal cancers staged?

A

TNM system

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

How is the depth of invasion of the primary tumour scored?

A 
pT1: tumour invades lamina propria, muscularis mucosae or 
        submucosa
pT2: tumour invades muscularis propria
pT3: tumour invades adventitia
pT4: tumour invades adjacent structures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How are the regional lymph node involvements scored?

A

pN0: no regional lymph node metastasis
pN1: regional lymph node metastasis in 1 or 2 nodes
pN2: regional lymph node metastasis in 3 to 6 nodes
pN3: regional lymph node metastasis in 7 or more nodes

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

What are the 4 anatomical regions of the stomach?

A

Cardia
Fundus
Body
Antrum

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

What features normally protect the stomach from gastritis>?

A
  • Balance of aggressive
    (acid) and defensive
    forces
  • Surface mucous
  • Bicarbonate secretion
  • Mucosal blood flow
  • Regenerative capacity
  • Prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What factors can cause increased aggression of gastritis?

A

Excessive alcohol

  • Drugs
  • Heavy smoking
  • Corrosive
  • Radiation
  • Chemotherapy
  • Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What factors can impair defences against gastritis?

A
  • Ischaemia
  • Shock
  • Delayed emptying
  • Duodenal reflux
  • Impaired regulation of
    pepsin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the pathogenic mechanisms of autoimmune gastritis?

A

Anti-parietal cell and anti-intrinsic factor antibodies

Sensitised T-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the pathogenic mechanisms of bacterial gastritis? (H.Pylori)

A 
Cytotoxins
Liberation of chemokines
Mucolytic enzymes
?Ammonia production by bacterial urease
Tissue damage by immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the pathogenic mechanisms of NSAID gastritis?

A

Disruption of the mucus layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the pathogenic mechanisms of bile reflux gastritis?

A

Degranulation of mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is Helicobacter Pylori?

A

Gram negative spiral shaped bacterium
2.5-5.0 micrometres long
4 to 6 flagellae
Lives on the epithelial surface protected by the overlying mucus barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where in the stomach is H.pylori most common?

A

the antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does h.pylori result in?

A

glandular atrophy, replacement fibrosis and intestinal metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What can be the complications of h.pylori infection?

A 
Gastric ulcer
gastric cancer
MALT lymphoma
pre-pyloric gastric ulcer
duodenal ulcer

(however 85% patients have no complications)

37
Q

What is peptic ulcer disease?

A

Localised defect extending at least into submucosa

38
Q

What are the major sites of peptic ulcer disease?

A 
First part of duodenum
Junction of antral and body mucosa
Distal oesophagus (GOJ)
39
Q

What are the main etiological factors of peptic ulcer disease?

A 
Hyperacidity
H. pylori infection
Duodeno-gastric reflux
Drugs (NSAIDs)
Smoking
40
Q

What is the histology of an acute gastric ulcer?

A

Full-thickness coagulative necrosis of mucosa (or deeper layers)

Covered with ulcer slough (necrotic debris + fibrin + neutrophils)

Granulation tissue at ulcer floor

41
Q

What is the histology of a chronic gastric ulcer?

A

Clear-cut edges overhanging the base
Extensive granulation and scar tissue at ulcer floor
Scarring often throughout the entire gastric wall with breaching of the muscularis propria
Bleeding

42
Q

What are the complications possible with peptic ulcers?

A

Haemorrhage (acute and/or chronic anaemia)
Perforation peritonitis
Penetration into an adjacent organ (liver, pancreas)
Stricturing  hour-glass deformity

43
Q

What are the main causes of gastric cancer?

A

Most frequently:
Adenocarcinoma

Less frequently:
Endocrine tumours
MALT lymphomas
Stromal tumours (GIST)

44
Q

What is the incidence of gastric adenocarcinoma?

A

5th most common cancer in the World
(951,594 new cases/year)
Wide geographical variation (high rates in Eastern Asia, Andean regions of South America, Eastern Europe)
Steady decline over the past decades

45
Q

What is the aetiology of gastric adenocarcinoma?

A

Diet (smoked/cured meat or fish, pickled vegetables)
Helicobacter pylori infection
Bile reflux (e.g. post Billroth II operation)
Hypochlorhydria (allows bacterial growth)
~1% hereditary

46
Q

What are the features of carcinoma of GOJ?

A
  • White males
  • Association with GO reflux
  • No association with H. pylori / diet
  • Increased incidence in recent years
47
Q

What are the risk features of carcinoma of gastric body/antrum?

A
  • Association with H. pylori
  • Association with diet (salt, low fruit
    & vegetables)
  • No association with GO reflux
  • Decreased incidence in recent years
48
Q

What are the 2 main histological subtypes of gastric adenocarcinoma?

A

Scattered growth

  • Diffuse type
  • (signet ring cell ca)

Non-scattered growth
Intestinal type
(tubular adenocarcinoma)

49
Q

What is coeliac disease?

A

Also known as Coeliac sprueorgluten sensitive enteropathy

Immune mediated enteropathy

50
Q

How common is coeliac disease?

A

Fairly common, estimated prevalence of 0.5% to 1%

51
Q

What is GLIADIN?

A

Alcohol soluble component of gluten
Contains most of the disease-producing components
Induces epithelial cells to express IL-15

52
Q

What are CD8+ Intraepithelial lymphocytes (IELs)?

A

IL15 produced by the epithelium activation / proliferation of CD8+ IELs
These are cytotoxic and kill enterocytes
CD8+ IELs do not recognise gliadin directly
Gliadin-induced IL15 secretion by epithelium is the mechanism

53
Q

Why is diagnosis of coeliac disease often difficult?

A

Atypical presentations / non specific symptoms
Silentdisease
Positive serology / villous atrophy but no symptoms
Latentdisease
Positive serology but no villous atrophy
Symptomatic patients
Anaemia, chronic diarrhoea, bloating, or chronic fatigue

54
Q

What are the clinical features and associations of coeliac disease?

A

No gender preference

Other disease associations
Dermatitis herpetiformis - 10% of patients
Lymphocytic gastritisandlymphocytic colitis

Coeliac disease and cancer
Enteropathy-associated T-cell lymphoma
Small intestinal adenocarcinoma
BEWARE!!!! Symptoms despite GFD

55
Q

How is coeliac disease diagnosed?

A

Non-invasive serologic tests usually performed before biopsy
The most sensitive tests
IgA antibodies to tissue transglutaminase (TTG)
IgA or IgG antibodies to deamidated gliadin
Anti-endomysial antibodies - highly specific but less sensitive
Tissue biopsy is diagnostic (2nd biopsy after GFD)

56
Q

How is coeliac disease treated?

A

Gluten-free diet symptomatic improvement for most patients
Reduces risk of long-term complications including anaemia, female infertility, osteoporosis, and cancer

57
Q

What are the types of IDIOPATHIC INFLAMMATORY BOWEL DISEASE?

A

ULCERATIVE COLITIS
CROHN’S DISEASE
INDETERMINATE COLITIS ( 10 – 15 % )

58
Q

What is the epidemiology of IBD?

A

UC 5 – 15 cases per 100,000 p.a.
CD 5 – 10 cases per 100,000 p.a.

Incidence highest in Scandinavia, UK, Northern Europe, USA
Lower in Japan, Southern Europe, Africa

Peak age incidence 20 – 40 years of age

CD more common in females 1.3 : 1

UC equally common in males and females

Incidence of UC is increased in urban areas

59
Q

What are other risk factors for IBD?

A 
Cigarette smoking      UC  0.5 x
                                     CD  2 x
Oral Contraceptive     UC  1.4 x
                                     CD  1.6 x
Others eg. Childhood infections
                       MMR
                       domestic hygeine
                       appendicectomy
60
Q

What is the clinical presentation of ulcerative colitis?

A

Diarrhoea ( > 66 % ) with urgency/tenesmus

Constipation (2 %)

Rectal bleeding (> 90%)

Abdominal pain (30 – 60 %)

Anorexia

Weight loss (15 – 40 %)

anaemia

61
Q

What are the complications of ulcerative colitis?

A

Toxic megacolon and perforation
Haemorrhage
Stricture ( rare )
Carcinoma

62
Q

What are the clinical features of Chrohn’s disease?

A 
Chronic relapsing disease
Affects all levels of GIT from mouth to anus
Diarrhoea ( may be bloody )
Colicky abdominal pain 
Palpable abdominal mass
Weight loss / failure to thrive
Anorexia
Fever
Oral ulcers
Peri – anal disease
anaemia
63
Q

What is the distribution of Crohn’s disease throughout the GI tract?

A

Ileocolic 30 – 55 %
Small bowel 25 – 35 %
Colonic 15 – 25 %
Peri-anal / ano-rectal 2 – 3 %
Gastro – duodenal 1 – 2 %

64
Q

What complications can arise from Crohn’s disease?

A 
Toxic megacolon
Perforation
Fistula
Stricture (common)
Haemorrhage
Carcinoma
Short bowel syndrome (repeated resection)
65
Q

What are some hepatic manifestations of IBD?

A

Fatty change
Granulomas
PSC
Bile duct carcinoma

66
Q

What are some skeletal manifestations of IBD?

A

Polyarthritis
Sacro-ileitis
Ankylosing spondylitis

67
Q

What are some muco-cutaneous manifestations of IBD?

A 
Oral apthoid ulcers
Pyoderma gangrenosum
Erythema nodosum
Ocular
Iritis/uveitis
Episcleritis
retinitis
68
Q

What are some haematological manifestations of IBD?

A

Anaemia
Leucocytosis
Thrombocytosis
Thrombo-embolic disease

69
Q

What are some renal and systemic manifestations of IBD?

A

kidney and bladder stones

amyloid and vasculitis

70
Q

Risk factors for colo-rectal cancer in ulcerative colitis?

A 
Early age of onset
Duration of disease  > 8-10 years
Total or extensive colitis
PSC
Family History of CRC
? Severity of inflammation ( pseudopolyps )
Presence of dysplasia
71
Q

What are colorectal polyps?

A 
A  “mucosal protrusion”
Solitary or multiple ( polyposis )
Pedunculated , sessile or “flat”
Small or large
Due to mucosal or submucosal pathology or a lesion deeper in the bowel wall
72
Q

What are the types of colorectal polyps?

A

Neoplastic , hamartomatous , inflammatory or reactive
Benign or Malignant
Epithelial or Mesenchymal

73
Q

What are the features of a hyperplastic polyp?

A 
Common 
1 – 5 mm in size
often multiple
located in rectum and sigmoid colon
small distal HPs have NO malignant potential

NB some large right sided “hyperplastic polyps” ( sessile serrated lesions ) may give rise to microsatellite unstable carcinoma ( 10 – 15 % all colorectal cancer )

74
Q

What are the features of a juvenile polyp?

A

often spherical and pedunculated
10 – 30 mm
commonest type of polyp in children
typically occur in rectum & distal colon
sporadic polyps have no malignant potential

NB juvenile polyposis associated with increased risk of colorectal and gastric cancer

75
Q

What is PEUTZ-JEGHERS SYNDROME?

A

Autosomal dominant condition ( mutation in STK11 gene on chromosome 19 )

Prevalence : 1 in 50,000 – 1 in 120,000 births

Present clinically in teens or 20s with abdominal pain ( intussusception ), gastro-intestinal bleeding & anaemia

Multiple gastro-intestinal tract polyps ( predominantly small bowel )

Muco-cutaneous pigmentation
( 1 – 5mm macules peri-oral , lips , buccal mucosa , fingers and toes )

76
Q

What is the distribution of polyps in Peutz-Jeghers Syndrome?

A

Small bowel 96 %
Colon 27 %
Rectum 24 %
Stomach 24 %

NB polyps also described in gallbladder, urinary bladder and nasopharynx

77
Q

What are some examples of benign neoplastic polyps?

A 
Adenoma
Lipoma
Leiomyoma
Haemangioma
Neurofibroma
78
Q

What are some examples of malignant neoplastic polyps?

A 
Carcinoma
Carcinoid
Leiomyosarcoma
GIST
Lymphoma
Metastatic tumour
79
Q

What are the features of colorectal adenomas?

A

Benign epithelial tumours
Commonly polypoid but may be “flat”
Precursor of colorectal cancer (at least 80%)
Present 25% - 35% population > 50 years
Multiple in 20 – 30 % patients
Evenly distributed around colon BUT larger in recto-sigmoid and caecum

80
Q

A small % of adenomas progress to adenocarcinoma over an average of 10 – 15 years. What are some specific risk factors for this?

A 
“flat” adenomas
Size ( most malignant polyps > 10 mm )
Villous & Tubulo-Villous 
Severe ( high grade ) dysplasia
HNPCC associated adenomas
81
Q

What are the statistics of colorectal cancer in the UK?

A

2nd or 3rd commonest cancer (mortality) after bronchus, breast and prostate

Lifetime risk 1 in 18 to 1 in 20

Estimated prevalence in UK 77,000

Incidence in UK 35,300

Mortality in UK 16,220

82
Q

What are the risk factors for colorectal cancer?

A

Diet
- Dietary fibre, fat, red meat, folate, calcium

Obesity / Physical Activity

Alcohol

NSAIDs

HRT and oral contraceptives

Schistosomiasis

Pelvic radiation

Ulcerative colitis and Crohns disease

83
Q

What is FAP?

A

inherited gene that increases susceptibility to colorectal cancer

84
Q

What is HNPCC?

A

inherited gene that increases susceptibility to colorectal cancer

1 – 2 % all colorectal cancer
Autosomal dominant
50 - 70 % lifetime risk of large bowel cancer
Increased risk of endometrial, ovarian, gastric, small bowel, urinary tract and biliary tract cancer
Due to mutations in DNA mismatch repair genes

85
Q

What is the most common type of colorectal cancer?

A

Adenocarcinoma (>95%)

86
Q

What are the ways colorectal cancer can spread?

A

Direct invasion of adjacent tissues

Lymphatic metastasis (lymph nodes)

Haematogenous metastasis (liver & lung)

Transcoelomic ( peritoneal ) metastasis

Iatrogenic spread eg. needle track recurrence or port site recurrence

87
Q

How are colorectal cancers staged?

A

Dukes stage
TNM stage

May be clinical ( imaging ) or pathological
Describes extent of local and distant tumour spread

88
Q

What are Duke’s stages?

A

Stage A : adenocarcinoma confined to the bowel wall with no lymph node metastasis

Stage B : adenocarcinoma invading through the bowel wall with no lymph node metastasis

Stage C : adenocarcinoma with regional lymph node metastasis regardless of depth of invasion

Stage D : distant metastasis present

89
Q

What are the frequency and 5yr survival rates of the different Duke’s stages?

A

A, 10 – 20 %, > 90 %

B, 30 – 40 %, 60 – 80 %

C, 40 – 50 %, 40 – 50 %

D, 15 – 25 %,

Clinical Pathology G (23 decks)

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