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GI > Comprehensive review (1) > Flashcards

Comprehensive review (1) Flashcards

1
Q

Secretion is accomplished by glands located:

  1. MUCOSA :
  2. SUBMUCOSA :
  3. EXTRAMURAL GLANDS :
A

glands located:

  1. MUCOSA (stomach, small + large intestine)
  2. SUBMUCOSA (only in esophagus, duodenum)
  3. EXTRAMURAL GLANDS (Outside of the tubular gut
    - e.g., liver, pancreas)
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2
Q

Glands in esophagus

A 
• Mostly in submucosa
• Primarily mucous secretion
• Note: upper and lower
esophagus also has
MUCOSAL glands (called
“cardiac” due to similarity to
cardiac glands of the
stomach)
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3
Q

Name of glands located in upper and lower esophagus

A

cardiac glands

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4
Q

Function of: Muscularis externa & Myenteric plexus (Auerbach’s plexus)

A

Controls contraction of muscularis externa; wave-like

contractions that move contents = peristalsis

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5
Q

heart burn, dysphagia, achalasia, Barrets and esophageal cancer are common place in what region?

A

the Gastroesophageal junction

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6
Q

Lack of peristalsis in the lower esophagus due to loss of myenteric neurons
(chalasis = relaxation)

A

achalasia

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7
Q

Change in esophageal mucosa from squamous to “intestinal” (i.e. columnar)
Result of prolonged injury: e.g. chronic reflux, noxious agents (smoking, etc.)
“pre-cancerous:” 10% risk of progression to adenocarcinoma

A

Barrets esophagus

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8
Q

Esophageal cancer: Squamous cell carcinoma –carcinogenesis of____ cells

A

basal

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9
Q

–progression of Barrett’s esophagus into cancer or (rarely)

from submucosal glands

A

Adenocarcinoma

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10
Q

inflammation and ulceration of mucosa

A

odynophagia

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11
Q

difficulty swallowing) –

obstruction, deranged motor function

A

dysphagia

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12
Q

Types of congenital anomailes in espohagus

A
  1. Ectopic tissue – gastric, pancreatic
  2. Duplication cysts
  3. Atresias and fistulas
    aspiration, suffocation from food
    fluid and electrolyte imbalance
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13
Q

Atresia occurs most commonly at or near the tracheal bifurcation and is usually associated with a_____ connecting the upper or lower esophageal pouches to a bronchus or the trachea

A

fistula

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14
Q

Esophageal webs are Congenital or acquired
• GERD
• Occur in_____ esophagus
• Produce dysphagia

A

upper

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15
Q

• Schatzki ring from esophageal rins:
 A ring____ the GE junction
 B ring ___the GE junction

A

above

at

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16
Q

result of esophageal rings

A
  • Produces dysphagia

* Similar to a web but thicker and circumferential

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17
Q

fibrious thickening of esophageal wall most often due to
inflammation and scarring that may be caused by chronic gastroesophageal reflux, irradiation, scleroderma, or caustic injury

A

Esophageal stenosis

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18
Q

Symptoms and features of esophateal stenosis

A

Symptoms: dysphagia –>total obstruction
Features:
• Inflammatory scarring
• Atrophy and Fibrosis of muscularis propria and secondary epithelial damage

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19
Q
  1. Incomplete LES relaxation
  2. Increased LES tone
  3. Aperistalsis of the esophagus
A

features of achalasia

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20
Q

Primary cause of achalasia

A

Idiopathic nerve abnormality

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21
Q

Complications of achalasia

A
  1. Squamous cell carcinoma (5%)
  2. Candida esophagitis
  3. Diverticula
  4. Aspiration pneumonia
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22
Q

What cancer can achalasia cause?

A

squamous cell carcinoma

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23
Q 
The following are all responsible for:
Nerve damage to
1. Trypanosoma cruzi
2. metastatic tumor
3. amyloidosis
4. sarcoidosis
A

Pseudoacalasia

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24
Q

MOre common hiatal hernia

symptoms?S

A

Sliding esophageal, etiology often unknown, often asymptomatic

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25
Q

Complications of hiatal hernia

A
  • Ulceration
  • Bleeding
  • Perforation
  • Strangulation (paraesophagus)
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26
Q

Diverticulum just above the UES

A

Zenker diverticulum

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27
Q

etiology of Zenker diverticulum

A

Motor dysfunction
Increased stress on wall
GERD

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28
Q

Symptoms of Zenker diverticulm

A

Dysphagia
Regurgitation
Mass in neck
Aspiration of contents

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29
Q

Diverticulum that occurs near midpoint of esophagus

A

Traction; scarring from mediastinal lyphadenitis, see motor dysfunx, increased stress on wall and GERD; IG asymptomatic

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30
Q

Diverticulum Occurs just above LES

A

Epiphrenic diverticulum

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31
Q

Etiology and symptoms of Epiphrenic Diverticulum

A 
Etiology
– Dyscoordination of peristalsis
– LES relaxation
• Symptoms
– Massive nocturnal regurgitation
32
Q 
Longitudinal tears at the
GE junction from severe
wretching and/or vomiting
• Seen in alcoholics
• Hemorrhage
• Accounts for 5-10% of UGI bleeding episodes
A

Mallory Weiss Syndrome

33
Q

Occur secondary to portal hypertension most often d/t Alcoholism

A

Esophageal varices

34
Q

What is the concerning part of esophageal varices?

A

Asymptomatic until they bleed –

massive hemorrhage

35
Q

Veins involved in esophageal varices and mortality rate

A

Lower esophageal veins, mortality is 40-50%

36
Q

Inflammation of the esophageal mucosa

A

Esophagitis

37
Q

Etiology of esophagitis

A

 Reflux (GERD)
 Mucosal irritants, alcohol, acid, alkalis
 Infections, especially in immunosuppressed
patients
 Post radiation therapy
 GVHD
 Allergies (eosinophilic esophagitis)

38
Q 
All of the following can lead to:
• Decrease LES tone
• Sliding hiatal hernia
• Delayed gastric emptying
• Decreased reparative capacity ofesophageal mucosa
A

Gastroesophageal Reflux

Disease (GERD)

39
Q

What are the sypmtoms of GERD

A
  • Heartburn
  • Dysphagia
  • Regurgitation
  • Hematemesis or melana
40
Q

What do we see with the lamina propria papillae in reflux

A

elongation of lamina propria papillae

41
Q

What happens to the basal and supra-basal cells in reflux esophagiits

A

hyperplasia; shouldn’t extend more then 15% of mucosa

42
Q

What kind of chages do we see in the cells in reflux esophatitis?

A

reactive epithelial changes and mixed acute and chronic inflammatory cells in epithelium and lamina propria

43
Q

Consequences of reflux

A
  • Bleeding
  • Ulceration – perforation
  • Stricture development
  • Barrett’s esophagus
44
Q

Pt presents with all the symptoms of GERD but don’t respond to GERG therapy. ON endoscopy, you see rings in the esophgus.

A

Eosinophilic Esophagitis

45
Q

If you see basal cell hyperplasia with over 20 eosinophils per field dx is

A

eosinophilic esophagitis

46
Q 
scattered intraepithelial
eosinophils. Although mild
basal zone expansion can be
appreciated, squamous cell
maturation is relatively normal.
A

reflux esophagits

47
Q 
Endoscopic evidence (velvet mucosa) at GE junction
• “Intestinal metaplasia” of mucosa
Single most important risk factor for esophageal adenocarcinoma
A

Barrets Esophagus

48
Q

What type of cells are seen in intestinal metaplasia of Barrets

A

Goblet cells ~ should only be in intestine!!

49
Q

Syptoms of esophageal carcinoma and prognostic factors

A

• Symptoms include dysphagia, weight loss
• Prognostic factors
– Depth of tumor
– Nodal metastasis

50
Q

Adenocarcinoma of esophagus are located near:

mean age?

A

arise near GE junction in Barrett’s esophagus

occurs after age 40, mean age 60

51
Q

progression from normal esophagus to adenocarcinoma (w/ BE)

A

normal–> esophagitis–> Barrets–> Dysplasia in Barrets–> adenocarcinoma

52
Q

Age and gender of sq cell carcinoma of esophagus

A

after 50 and male predominance from (2:1 to 20:1)

53
Q

Histologic features of sq.cell carcinoma

A

keritanized nests!

54
Q

FActors associated with devo os sq cell carcinoma

A
  • Dietary
  • Lifestyle
  • Predisposing esophageal disorder
  • Genetics
55
Q

Fundus has what cell types that secreate what?

A

Cheif cells–> pepsin

parietal cells–> acid

56
Q

The cardia of the stomach secreaetes?

A

mucous via mucous cells

57
Q

The antrum of stomach has what type of cells?

A

Mucous cells and G cells–> gastrin

58
Q

Progressive hypertrophy of pyloric sphincter
Presentation at 2-4 weeks of age
male predominant and seen in 1:500 live births

A

Congenital Hypertrophic Pyloric

Stenosis

59
Q

baby born with regurg and projective vomiting and dx with Congenital Hypertrophic Pyloric
Stenosis. What would this look like grossly and what is in the vomit?

A

vomit has NO bile

grossly there would be a palpable mass and there would be visible peristalsis

60
Q

Symptoms of gastritis

A

epigastric pain
nausea
vomiting
hemorrhage

61
Q

Hemorrage from gastritis could result in

A
  • chronic anemia
  • melana
  • massive life threatening
62
Q

Inflammation of the gastric mucosa

63
Q

What is responsible for acute gastritis?

A 
 NSAIDS
 Excessive ethanol
 Heavy smoking
 Cancer chemotherapy agents
 Ischemia and shock
 Stress (severe, e.g. trauma, burns, surgery)
 Uremia
 Systemic infections
 Suicide attempts (acid, alkali)
 Mechanical trauma (NG tube “hickeys
64
Q

Cell type seen in acute gastritis?

A

neutrophils

65
Q

Stomach has Punctate erosions with dark adherent blood (acid

exposure); this is seen with

A

acute gastritis

66
Q

What do we see on low power micrograph with acute gastritis?

A

– focal mucosal disruption with

hemorrhage

67
Q

What happens with chronic gastritis, what can happen eventually?

A

mucosal inflammatory changes
leading to atrophy and metaplasia
• A set-up for dysplasia and neoplasia

68
Q

Cell type seen in chronic gastritis?

A

Lymphocytes

69
Q

Causes of Chronic gastritis

A
  • Chronic infection (Helicobacter pylori) – most important (Type B)
  • Immunologic (in association with pernicious anemia) (Type A)
  • Toxic (ethanol, tobacco)
  • Post-surgery (e.g., partial gastrectomy)
70
Q

Morphology of chronic gastritis

A 
• Lymphocytic mucosal infiltrate
 Neutrophils in epithelium, and gastric pits
• Regenerative change
• Metaplasia (intestinal)
• Atrophy
• Dysplasia
71
Q
  • Accounts for < 10% of chronic gastritis
  • Occurs in pernicious anemia
  • Autoantibodies
A

Autoimmune gastritis

72
Q

AutoantiB in autoimmune gastritis are made against what?

A

 Parietal cells
 Achlorhydria, hypergastrinemia
 Intrinsic factor (pernicious anemia develops due to lack
of absorption of vitamin B12)

73
Q

Where in the stomach do we see autoimmune gastritis?

A

In the body-fundic mucosa, not antrum

74
Q

What factors in H.Pylori set it to cause chronic gastritis?

A

urease, toxins, gastric acidity, peptic enZ d/t infection

75
Q

What happens overtime with chrnoic gastritis from H.pylori

A

intestinal metaplasia, lymphoid aggregates, neurtophil infiltratres

76
Q

How can we Dx H.Pylori infection?

A
  • Detect urease in gastric biopsy
  • Radiolabeled urea breath test
  • Store antigen
  • Serologic tests
  • Demonstrate organism in gastricmucosa
77
Q

Diseases associated with H.pylori

A

• Gastric MALT lymphoma: Definite etiologic role
• Chronic gastritis:Strong causal
association
• Peptic ulcer disease: Strong causal association
• Gastric carcinoma: Strong causal association

GI (14 decks)

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