Brainscape's Knowledge GenomeTM

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


See full index

GI Week 2 > Lecture 7: Esophagus and Stomach Histology > Flashcards

Lecture 7: Esophagus and Stomach Histology Flashcards

1
Q

What is the first part of the GI tract according to Furth?

A

The brain

Thinking about the eating activates shit

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

What is the function of stomach and function?

A
  1. motility
  2. barrier
    Stomach = breakdown, hormone production and intrinsic factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the epithelium of esophagus?

A

Stratified squamous

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

What type of epithelium lines the FETAL esophagus? Significance?

A

Ciliated COLUMNAR
Same epithelium as the trachea so it shows the common derivation of trachea and esophagus
Tracheo-esophageal fistulas then can occur

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

Where is the last place that you can find salivary glands?

A

Esophagus

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

What types of glands can be found in esophagus?

A

Salivary glands

Provides lubrication and enzymes like amylase

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

What are developmental abnormalities of esophagus?

A
  1. atresia
  2. fistula (tracheal-esophageal)
  3. Duplication cyst
  4. Inlet Patch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a duplicatioin cyst?

A

Rare congenital malformations of GI tract
Duplication of the segment to which it is adjacent
Can compress the airweay

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

What is an inlet patch?

A

A congenital anomaly when gastric mucosa is present at the end of what should be the esophagus
Can lead to esophagitis when acid is secreted by the gastric mucosa
Can actually be any type of mucosa
No biologic significance in patient

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

What is esophagitis?

A

Injury to the mucosal lining of the esophagus
Neutrophils and eosinophils are there
Lymphocytes are NORMAL

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

Why are there lymphocytes normally there in esophagus?

A

Because it is part of the mucosal associated lymphoid tissue (MALT)

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

What are the etiologies for esophagitis?

A 
Allergy
Pill
Crohns
Trauma
REFLUX
And a shitload more
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes reflux esophagitis?

A

Failure of gastro-esophageal sphincter and gastric contents come up (bile and HCl)

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

Why does it matter as to the “type” or etiology of esophagitis a person may have?

A

Because it helps with treatment
Viral inclusions vs. neutrophils vs. fungus
Such as CMV

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

What are the histological/gross characteristics of eosinophillic esophagitis?

A 
Histology = eosinophils 
Gross = striped tiger like appearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are skin disorders that present as esophagitis?

A
  1. Pemphigus
  2. Pemphigoid
  3. Lichenoid reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why does skin shit affect esophagus?

A

Because skin and esophagus have the same epithelium

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

What is pemphigus?

A

A skin disease in which watery blisters form on the skin

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

What is one of the most common causes of dysphagia?

A

A Schatzki Ring

Ingrowth of the squamous epithelium that blocks shit

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

What is achalasia?

A

HYPERmotility disorder
Lower esophageal sphincter is tight and won’t open or relax
Leads to squamous cell carcinoma progression
Esophagus will enlarge due to the blockage

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

What happens in connective tissue disorders like scleroderma?

A

Selective atrophy of inner circular muscle layer

Presents with Raynaud’s

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

What is a Mallory Weiss tear?

A

When you rip the distal esophagus causing massive bleeding

Happens after wrenching vomiting

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

How do you know if it is striated

vs. smooth muscle problem?

A

If you have trouble swallowing it is striated

24
Q

What are the types of malignant tumors of the esophagus?

A
  1. adenocarcinoma
  2. squamous cell carcinoma
  3. sarcoma
  4. lymphoma
  5. melanoma
  6. metastatic
    Can also be benign
25
Q

What is number 1 in cancer deaths among GI organs?

A

Colo-rectal

Colo-rectal is most common of GI

26
Q

In esophagus, what is most common malignant tumors?

A

Carcinomas
Squamous cell carcinoma is most common in world
Adenocarcinoma is most common in western countries

27
Q

What is the pathogenesis of adenocarcinoma?

A

Reflux of acid leads to metaplasia of the esophagus

Metaplasia then leads to formation of adenocarcinoma

28
Q

What is Barrett esophagus?

A

Glandular metaplastic mucosa (goblet cells) INSTEAD OF squamous mucosa
Patients with Barrett’s have an increased risk of progressing to esophageal adenocarcinoma
Due to reflux
10%
Over 50% of patients with barrett’s has no symptoms
i. the length of intestinal metaplasia is determined at initiation of injury (doesn’t change)
ii. short segments do not convert to long segments (so length of metaplasia is static)
iii. the risk of cancer is greater in long segment than short segment

29
Q

Where should you have goblet cells in GI?

A

Small intestine

So if you see that somewhere else, you are fucked

30
Q

Does the esophagus have a serosa?

A

NO, it only has an adventitia

31
Q

What are the etiologic factors for squamous cell carcinoma?

A
  1. smoking
  2. lye digestion
  3. achalasia
  4. diverticulum
  5. not caused by HPV
32
Q

What is the timeline of cancer diagnosis?

A

Squamous mucosa  intestinal metaplasia  Dysplasia  invasion = cancer
Dysplasia only occurs in EPITHELIUM not in endothelium (so you don’t see that shit with HCC)

33
Q

What is dysplasia?

A

Neoplastic epithelium that remains confined within basement membrane of epithelial surface
Nuclei = large, hyperchromatic, irregular contours)

34
Q

What are the three glandular regions of stomach and what are their functions?

A
  1. cardia
    -are of reactive changes
  2. Corpus
    -oxyntic mucosa (acid producing)
  3. Antrum
    -mucous glands predominate
    NO OXYNTIC glands
    Gastrin producing endocrine cells
35
Q

What are the normal architecture of normal antrum?

A

DEVOID of MALT (because acid is all you neeed)
Flat
Makes gastrin
Motility function

36
Q

What is acute gastritis?

A

Acute inflammation and/or erosion of gastric mucosa
Breakdown of mucosal barrier can allow luminal contents (HCL) to diffuse to lamina propia
Done by NSAIDs, EtOH, pills

37
Q

What is chronic gastritis?

A

Chronic inflammation (lymphocytes and plasma cells) in gastric mucosa

38
Q

What are the two causes of chronic gastritis?

A
  1. H. pylori

2. autoimmune gastritis

39
Q

What pills can cause gastritis?

A

Iron pill

40
Q

What does it mean to have “activity” with acute gastritis? Significance?

A

Activity = presence of neutrophils

Gastritis with activity suggests presence of H. pylori or bacteria

41
Q

What does ATROPHIC chronic gastritis?

A

Loss of parietal and chief cells

How you lose them is not necessary for label

42
Q

What is the significance of atrophic chronic gastritis?

A
  1. carcinoma/lymphoma evolution

2. AUTOIMMUNE etiology

43
Q

What does it mean for something to be antralized?

A

It means your parietal and chief cells of your OXYNTIC (corpus) mucosa is killed so the histology slide looks more like the antrum than the corpus

44
Q

What are antibodies attacking in autoimmune gastritis?

A

They attack H+ pump

45
Q

What happens when you have autoimmune gastritis?

A 
No parietal cells
Hypergastrin secretion
Proliferation of ECL cells
“carcinoid tumors”
Benign and wont kill your shit
46
Q

What is the difference between H pylori and autoimmune gastritis?

A

H pylori starts in the antrum and moves up to corpus

Autoimmune gastritis starts from corpus (because it is where the chief cells) and moves down to antrum

47
Q

What is the significance of fundic gland polyp?

A

It is benign with no clinical consequences
Dilatation of oxyntic and chief cells
Bigger oxyntic and chief cells

48
Q

What are the key characteristics of hyperplastic gastric polyp?

A

Benign
Located in the antrum
Arise on some form of underlying gastritis

49
Q

How can you have enlarged gastric folds?

A
  1. lymphoma
  2. gastric cancer
  3. metastatic breast lobular carcinoma
  4. diffuse gastritis
  5. true increase in gastric epithelium (hypertrophic gastrophies)
50
Q

What is Menetriers Disease?

A

Error in TGF alpha signaling
Induces epithelial (foveolar) cell proliferation
Inhibits parietal cell acid secretion
Increases mucin production
Too much mucin = less protein available which will lead to lower serum albumin
Lower serum albumin = diarrhea

51
Q

What are the two types of gastric cancer?

A
  1. Intestinal

2. Signet Ring

52
Q

What are the key characteristics of intestinal type gastric cancer?

A

Gland formation

Repeated injury/chronic gastritis

53
Q

What are the key characteristics of signet ring type?

A

E-cadherin
No injury/gastritis
Sporadic, so no geographic variation

54
Q

What does gastric signet ring carcinoma present as?

A

Linitus plastic (leather bottle stomach)

55
Q

What happens when you lose E-cadherin?

A

Loss of cell to cell adhesion

Makes cell bunch up into signet ring type shape

GI Week 2 (15 decks)

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