Brainscape's Knowledge GenomeTM

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


See full index

Phoebe's GI > Pathology > Flashcards

Pathology Flashcards

1
Q

Acute oesophagitis

A

Rare
Corrosive following chemical ingestion
Infective in immunocompromised (candidas, herpes)

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

Chronic oesophagitis

A

Common

Reflux disease

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

Reflux oesophagitis

A

Inflammation of oesophagus due to refluxed low pH gastric content
May be due to defective sphincter, hiatus hernia, increased intra-abdominal pressure (pregnancy)

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

Microscopic appearance of reflux oesophagitis

A

Basal zone epithelial expansion

Intraepithelial neutrophils, lymphocytes and eosinophils

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

Barret’s Oesophagus

A

Replacement of stratified squamous epithelium by columnar epithelium
Unstable mucosa
Increased risk of developing dysplasia and carcinoma

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

Allergic oesophagitis

A

Eosinophilic oesophagitis
Family history of allergy
Asthma, young, males more

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

Benign Oesophageal Tumours

A 
Squamous Papilloma
Rare
Papilliary 
Asymptomatic 
HPV related
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Malignant Oesophageal Tumours

A

Squamous Cell Carcinoma

Adenocarcinoma

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

Adenocarcinoma of Oesophagus Pathogenesis

A
  1. Genetic factors, reflux disease
  2. Chronic reflux oesophagitis
  3. Barret’s oesophagus
  4. Low grade dysplasia
  5. High grade dysplasia
  6. Adenocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mechanism of metastases

A

Direct invasion
Lymphatic permeation
Vascular invasion

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

Acute gastritis

A

Irritant chemical injury

Severe trauma

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

Chronic gastritis

A

Autoimmune
Bacterial (H. pylori)
Chemical

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

Autoimmune chronic gastritis

A

Anti-parietal and anti-intrinsic factor antibodies
Atrophy and intestinal metaplasia in stomach
Increased risk of malignancy

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

H. Pylori gastritis

A

Bacteria inhabits a niche between epithelial cell surface and mucous barrier
Gram -ve rod
Early inflammatory response
Lamina propria cells produce anti H. Pylori antibodies

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

Chemical gastritis

A

Due to NSAIDS, alcohol, bile reflux
Direct injury to mucous layer by fat solvents
Marked epithelial regeneration, hyperplasia, congestion and little inflammation

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

Peptic Ulceration

A

Breach into GI mucosa as a result of acid and pepsin attack

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

Chronic peptic ulcer sites

A

Duodenum (first part)
Stomach (junction of body and antrum)
Oesophago-gastric junction
Stomal ulcers

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

Peptic ulcers microscopically

A

Layered appearance
Floor of necrotic fibrinopurulent debris
Base of inflamed granulomation tissue
Deepest layer is fibrotic scar tissue

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

Complications of peptic ulcers

A 
Perforation
Penetration
Haemorrhage 
Stenosis
Intractable pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Benign gastric tumours

A

Polyps
Hyperplastic polyps
Cystic fundic gland polyps

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

Malignant gastric tumours

A

Carcinomas
Lymphomas
GI stromal tumours

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

Gastric adenocarcinoma pathogenesis

A
  1. H. Pylori infection
  2. Chronic gastritis
  3. Inestinal metaplasia
  4. Dysplasia
  5. Carcinoma
23
Q

2 types of gastric adenocarcinoma

A

Intestinal type

Diffuse type

24
Q

Intestinal Gastric adenocarcinoma

A

Exophytic/polypoid mass

25
Q

Diffuse gastric adenocarcinoma

A

Expands/infiltrates stomach wall

26
Q

Ischaemia of small bowel

A

Mesenteric arterial occlusion

Non-occlusive perfusion insufficiency

27
Q

Mesenteric arterial occlusion

A
  1. Mesenteric artery atherosclerosis

2. Thromboembolism from heart

28
Q

Non occlusive perfusion insufficiency

A
  1. Shock
  2. Strangulation obstructing venous return
  3. Drugs eg.cocaine
  4. Hyperviscosity
29
Q

Complications of ischaemia of the small bowel

A

Resolution
Fibrosis, stricture, chronic ischaemia, mesenteric angina and obstruction
Gangrene, perforation, peritonitis, sepsis and death

30
Q

Meckel’s Diverticulum

A

Result of incomplete regression of vitello-intestinal duct

Tubular structure, 2 inches long, 2 foot above IC valve

31
Q

Carcinoid tumours of small bowel

A 
Common in appendix
Small, yellow growing tumours
Locally invasive
Produce hormone like substances
Flushing and diarrhoea
32
Q

Appendicitis pathology

A

Acute inflammation
Mucosal ulceration
Serosal congestion, exudate
Pus in lumen

33
Q

Complications of appendicitis

A 
Peritonitis
Rupture
Abscess
Fistula 
Sepsis
34
Q

Polyp

A

Protrusion above an epithelial surface

Tumour (swelling)

35
Q

Why must all adenomas be removed?

A

They are all pre-malignant

36
Q

Primary treatment for adenocarcinoma

A

Surgery

37
Q

Dukes A

A

Confined by muscularis propria

38
Q

Dukes B

A

Through muscularis propria

39
Q

Dukes C

A

Metastatic to lymph nodes

40
Q

Colorectal carcinoma

A

75% left sided (rectum, sigmoid, descending)

25% right sided (caecum, ascending)

41
Q

Adenoma of colon

A

Benign tumour

Not invasive, do not metastasise

42
Q

HNPCC

A

Hereditary Nonpolyposis Colorectal Cancer

43
Q

Hereditary Nonpolyposis Colorectal Cancer

A 
Defect in DNA mismatch repair
Right sided tumour
<100 polyps
Mucinous tumours
Inflammatory response
Associated with gastric and endometrial carcinoma
44
Q

FAP

A

Familial Adenomatous Polyposis

45
Q

Familial Adenomatous Polyposis

A 
Defect in tumour suppression 
Throughout colon
>100 polyps
Adenocarcinoma NOS
Associated with desmoid tumours and thyroid carcinoma
46
Q

Liver injury

A
  1. Insult to hepatocytes (viral, drug, toxin, antibody)
  2. Grading (degree of inflammation)
  3. Staging (degree of fibrosis)
  4. Cirrhosis
47
Q

Pre-hepatic jaundice

A

Too much haem to breakdown
Haemolysis of all causes
Haemolytic anaemias
Unconjugated bilirubin

48
Q

Post-hepatic jaundice

A 
Bile cannot escape into bowel
Congenital biliary atresia
Gallstones block CBDuct
Strictures of CBDuct
Tumours at head of pancreas
49
Q

Non-alcoholic Steatohepatits

A

Non-drinkers
Identical to alcoholic liver disease
Occurs in pts with diabetes, obesity, hyperlipidaemia

50
Q

HALO

A

Haemorrhoidal artery ligation

51
Q

Haemorrhoid

A

Enlarged vascular cushions in lower rectum and anal canal

52
Q

Rectal prolapse

A 
Partial = anterior mucosal prolapse
Complete = full thickness
53
Q

Anal fissure

A

Tear in anal margin due to passage of constipated stool

Phoebe's GI (24 decks)

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