Brainscape's Knowledge GenomeTM

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


See full index

GI > Pathology: Lecture 1 = Mouth & oesophagus and Lecture 2 = Stomach > Flashcards

Pathology: Lecture 1 = Mouth & oesophagus and Lecture 2 = Stomach Flashcards

1
Q

look at photo of normal oesophagus - slide 7.

What is an important line in the oesophagus?

A

look at photo of normal oesophagus - slide 7

= Z line

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

look at histological slide of oesophagus - slide 9.

A

look at histological slide of oesophagus - slide 0

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

what are some inflammatory disorders of the oesophagus?

A

1) acute oesophagitis (rare)

2) chronic oesophagus (common)

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

what is acute oesophagitis?

A

= corrosive following chemical ingestion

- infective in immunocompromised patiens. e.g. cadidiasis, herpes, CMV

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

what is chronic oesophagittis also known as?

A

= reflux diseases “reflex oesophagitis”

- rare causes include Crohn’s disease

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

what is reflux oesophagitis?

A

= inflammation of oesophagus due to reflex low pH gastric contents

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

what might reflux oesophagitis be due to?

A

= defective sphincter mechanism +/- hiatus hernia

= abnormal oesophageal motility

= increased intra-abdominal pressure (pregnancy and obese people)

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

how would reflux oesophagus show microscopically?

A

1) basal zone epithelial expansion
& lengthening of papillae

2) intra-epithelial neutrophils, lymphocytes and eosinophils

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

what are complications of reflux?

A

1) ulceration (bleeding)
2) stricture
3) Barrett’s Oesophagus

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

what is Barrett’s oesophagus in pathological terms?

A

= replacement of stratified squamous epithelium by columnar epithelium

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

when does Barrett’s oesopjaus occur?

A

= due to persistent reflux of acid or bile

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

what may cause Barrett’s oesophagus?

A

= due to expansion of columnar epithelium from gastric glands or from sub-mucosal glands
- may be due to differentiation rom oesophageal stem cells

  • protective response, faster regeneration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what macroscopically would you see in Barrett’s oesophagus?

A

= red velvety mucosa in lower oesophagus

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

what would you see under a microscope, hidtrologically, in Barrett’s oesophagus?

A

1) columnar lined mucosa with intestinal metaplasia

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

describe eh mucosa in barrette’s oesophagus and what does this cause an increased risk of developing?

A

= unstable mucosa (contains damage)

+ increased risk of developing dysplasia & carcinoma and adenocarcinoma of oesophagus
+ requires surveillance although value of this is disputed

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

what is allergic oeosphagitis?

A

= eosinophilic oesophagitis

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

what do people with allergic oeosphagitis present with?

A
  • personal/family history of allergy
  • asthma
  • young
  • males > females
  • pH probe negative for reflux
  • increased eosinophils in blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what would the oesophagus look like in allergic oeosphagitis?

A
  • corrugated (feline) or spotty’ oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe the histological appearance in allergic oeosphagtiis?

A

= large numbers of intra-epithelial eosinophils

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

what could you treat allergic oeosphagitis with?

A

= steroids
= chromoglycate
= montelukast

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

what is a common type of benign oesophageal tumour?

A

= squamous cell papilloma

  • rare
  • papillary
  • asymptomatic
  • HPV related
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are 4 other benign oesophageal tumours?

A
  • Leiomyomas
  • Lipomas
  • Fibrovascular polyps
  • Granular cell tumours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are 2 examples of malignant oesophageal tumours?

A

1) squamous cell carcinoma

2) adenocarcinoma

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

describe the epidemiology and causes of squamous cell carcinoma?

A

= commoner in males

Causes;

  • vit A/zinc deficiency
  • tannic acid/strong tea
  • smoking, alcohol
  • HPV
  • oesophagitis
  • genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe the histological appearance of squamous cell carcinoma?

A

= Severe dysplasia a in squamous layer

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

what does squamous cell carcinoma cause?

A

= obstruction and dysphagia

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

what would you see macroscopically in squamous cell carcinoma?

A
  • keratin formation

- invasive type squamous cells

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

where is adenocarcinoma of oesophagus most common?

A
  • in lower 1/3 of oesophagus

- commoner in males/obese individuals

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

describe the pathogenesis of adenocarcinoma of oesophagus?

A

1) genetic factors, reflux diseases, others
2) chronic reflux oeosphagitis
3) Barret’s oesophagus (intestinal metaplasia)
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
30
Q

similarly to squamous cell carcinoma, what does adenocarcinoma cause?

A

= obstruction and dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the 3 mechanisms for metastases of carcinoma of oesophagus?

A

1) direct invasion
2) lymphatic permutation
3) vascular invasion

32
Q

what may you present with if there is a carcinoma of oesophagus?

A

Dysphagia;
- due to tumour obstruction

General symptoms;

  • anaemia
  • weigh loss
  • loss energy

= due to effects of metastases

33
Q

what are 2 other oesophageal pathology?

A

1) mallory Weiss tear

2) oesophageal varices

34
Q

what is the cancer most common to oral cavity ?

A

oral squamous cell carcinoma

35
Q

what do oral squamous cell carcinomas present with and what are high risk and low risk sites?

A
  • white, red, speckled, ulcers or lumps

High risk sites;

  • floor of mouth
  • lateral border of venture tongue
  • soft palate
  • retromolar pad
  • tonsils pillars

RARE;

  • on hard palate
  • dorsum of tongue
36
Q

what are the causes of oral squamous cell carcinomas?

A

1) Tobacco
2) Alcohol
3) Betel quid
4) Viral - HPV (p16)
5) Chronic infections
6) Nutritional deficiencies
7) Genetics
8) Post Transplant
9) Pt with history of primary oral SCC, increased risk of developing new second primary

37
Q

what do ALL malignant squamous epithelium show?

A

= invasion and destruction of local tissues

38
Q

what are variants of malignant squamous epithelium?

A
  • verrucous and acantholytic
39
Q

describe the differentiation of malignancy?

A
  • Well-differentiated tumour cells very obviously squamous with ‘prickles’ and keratinization
  • Moderately differentiated
  • Poorly differentiated, may be difficult to identify tumour cells as epithelial
40
Q

what are the features relating to prognosis of squamous cell carcinoma?

A

1) Tumour diameter
2) Depth of invasion
3) Pattern of invasion- cohesive versus non-cohesive front
4) Lymphovascular invasion
5) Neural invasion by tumour
6) Involvement of surgical margins
7) Metastatic disease
8) Extracapsular spread of lymph node metastases

41
Q

what are the tumour stages of cancers?

A

= TNM system

T= greatest diameter of tumour, structures invaded
N= lymph node status
M= metastasis

Eg pT2N1MX

42
Q

how do you treat it?

A

1) surgery

2) adjuvant therapy

43
Q

LECTURE 2 - pathology of stomach

A

LECTURE 2 - pathology of stomach

44
Q

what are 2 inflammatory disorders of the stomach?

A

1) acute gastritis

2) chronic gastritis

45
Q

what is acute gastritis and what are 4 possible causes?

A

= irritant chemical injury

caused by;

  • severe burns
  • shock
  • severe trauma
  • head injury
46
Q

what is chronic gastritis and what are 3 possible causes?

A
  • auto-immune
  • bacterial
  • chemical
47
Q

what are 3 rare inflammatory disorders of the stomach?

A
  • lymphocytic
  • eosinophilic
  • granulomatous
48
Q

what bacteria is associated with chronic gastritis?

A

= H. pylori

49
Q

how would you identify chronic gastritis?

A

red, inflamed stomach

50
Q

what happens in auto-immune chronic gastritis and what does it result in? (rare)

A

= anti-parietal and anti-intrinsic factor antibodies attack causing atrophy and intestinal metaplasia in body of stomach

Resulting in;
= pernicious anaemia, microcytic, due to B12 deficiency

+ increased risk of malignancy
- SACDC

51
Q

what happens in H. pylori associated chronic gastritis? (most common)

A

= bacteria inhabits a niche between epithelial cell surface and mucous barrier
- excites early acute inflammatory response

  • if not cleared, then a chronic active inflammation ensures
52
Q

what is critical in H. pylori associated chronic gastritis?

A

IL8

53
Q

what type of bacteria is H. pylori involved in chronic gastritis?

A

= gram negative curvilinear rod like.

54
Q

what produces anti- H. pylori antibodies and what does it increase the risk of?

A

= lamina propria plasma cells

Increasing risk of;

  • of duodenal ulcers
  • of gastric ulcers
  • of gastric carcinoma
  • of gastric lymphoma
55
Q

what is chemical gastritis due to?

A
  • NSAIIDS
  • alcohol
  • bile regluc
56
Q

what happens in chemical gastritis?

A

= direct injury to mucus layer by fat solvents

57
Q

what is chemical gastritis marked by?

A

= epithelial regeneration, hyperplasia, congestion and little inflammation

  • may produce erosion and ulcers
58
Q

what is peptic ulceration?

A

a breach in gastro-intestinal mucosa as a result of acid and pepsin attack

59
Q

what are chronic peptic ulcers and what are 4 common sites for them?

A

= ulceration which is longstanding and deep

Common sites;

  • duodenum (1st part)
  • stomach (junction of body and antrum)
  • oesophagi-gastric junction
  • stomal ulcers
60
Q

describe the pathogenesis of chronic duodenal ulcers?

A

= increased attack and failure of defence

  • increased acid in duodenum produces gastric metaplasia, and leads to H. pylori infection, inflammation, epithelial damage and ulceration
    ALSO
  • failure of mucosal defence
61
Q

describe the morphology of peptic ulcers?

A

2-10cm across

- edges clear cut, punched out

62
Q

describe the microscopic appearance of peptic ulcers?

A
  • layered appearance
  • Floor of necrotic fibrinopurulent debris
  • Base of inflamed Granulation tissue
  • Deepest layer is fibrotic scar tissue
63
Q

what are 5 complications of peptic ulcers?

A

1) perforation
2) penetration
3) haemorrhage
4) stenosis
5) intractable pain

64
Q

what are 2 examples of benign (polyps) gastric tumours?

A

1) hyperplastic polyps

2) cystic fundic gland polyps

65
Q

what are 3 examples of malignant (tumour) gastric tumours?

A

1) carcinomas - adenocarcinomas
2) lymphomas
3) gastrointestinal stromal tumours (GISTs)

66
Q

what is the major cause of gastric adenocarcinomas?

A

= H. pylori

patients with H. pylori infections/anti-bodies have higher risk of cancer

67
Q

describe the pathogenesis of gastric adenocarcinomas?

A

1) H. pylori infection
2) chronic gastris
3) intestinal metaplasia/atrophy
4) dysplasia
5) carcinoma

68
Q

what are 4 other pre-malignant conditions associated with gastric adenocarcinoma?

A

1) pernicious anaemia
2) partial gastrectomy
3) HNPC/Lynch syndrome
4) menetrier’s disease

69
Q

what are 2 sub-types of gastric adenocarcinomas?

A

1) intestinal type
- exophytic/polypoid mass

2) diffuse type
- expands/infiltrates stomach wall

70
Q

describe the appearance of gastric adenocarcinomas?

A

= raised rolled edges

71
Q

what does benign peptic ulcers mimic?

A

= cancer but is more punched out and lacks raised rolled edges

72
Q

describe the histological appearance of adenocarcinomas intestinal type?

A

= gland formation

73
Q

describe histological appearance of gastric adenocarcinomas - diffuse type?

A

= red and bloody

74
Q

what are 3 possible histological appearance of gastric adenocarinnomas - in diffuse form?

A

1) linitis plastica
2) signed ring type
3) sclerosis

75
Q

what is the difference between intestinal and diffuse gastric adenocarcinoma?

A

Intestinal = slightly better prognosis

76
Q

where does gastric adenocarcinoma spread to locally?

A

= into other organs and peritoneal cavity and ovaries … Kruckenberg
= lymph nodes
= haematogenous (liver)

77
Q

describe gastric lymphoma?

A

= maltoma

  • associated with H. pylori infection
  • continuous inflammation inducing an evolution into a clonal B cell proliferation… low grade lymphoma
  • if unchecked into evolves into a high grade B cell lymphoma

GI (43 decks)

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