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Pathology > Chapter 17 > Flashcards

Chapter 17 Flashcards

1
Q

Presentation of congenital abnormalities in the GI tract

A

Regurgitation during feeding

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2
Q

How treat congenital abnormalities

A

Surgery

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3
Q

Globus

A

Feeling of something stuck int he back of the throat that cant be swallowed

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4
Q

Developmental abnormalities of the esophagus are often associated with what

A

Congenital heart defectsGU malformations

Neurological disorders

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5
Q

What is esophageal atresia

A

Thin, noncanalized cord replaces a segment of the structure creating a mechanical obstruction

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6
Q

Where is esophageal atresia common

A

Tracheal bifurcation

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7
Q

What is esophageal atresia associated with

A

A fistula connecting the upper and lower esophageal pouches to a bronchus or the trachea

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8
Q

Most commonly a clindamycin upper segment in esophageal atresia is associated with a fistula connecting what

A

The lower segment to the trachea

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9
Q

Immperforate anus: intestinal atresia is less common than esophageal atresia but frequently involves the ___

A

Duodenum

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10
Q

__ __ is the most common form of congenital intestinal atresia

A

Imperforate anus

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11
Q

What causes imperforate anus

A

Failure of cloacal membrane to involuted during development

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12
Q

Fistula

A

Connection between the esophagus and the trachea/bronchi

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13
Q

What happens when u have a fistula

A

Swallowed material or gastric fluids can enter the respiratory tract

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14
Q

Clinical fistula

A

Aspiration, suffocation, pneumonia, severe fluid/electrolyte imbalance

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15
Q

Stenosis

A

Incompeteform of atresia in which the lumen is markedly reduced in caliber via a fibrous thickening of the wall causing partial of complete obstruction

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16
Q

Causes of stenosis

A

Congenital or acquired as a consequence of inflammatory scarring int he setting of GERD, irradiation, systemic sclerosis (scleroderma), or caustic injury

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17
Q

Where is stenosis msot common

A

Esophagus and small intestine

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18
Q

Diaphragmatic hernia

A

Incomplete formation of the diaphragm allows cephalad displacement of the abdominal viscera

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19
Q

What can diaphragmatic hernia cause

A

Pulmonary hypoplasia which is incompatible with postnatal life

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20
Q

Omphalocele

A

Abdominal musculatureis incomplete and viscera herniate into the ventral membranous sac

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21
Q

How can you fix omphalocele

A

Surgery

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22
Q

_% of infants with omphalocele have another birth defect

A

40

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23
Q

Gastroschisis

A

Similar to an omphalocele but all layers of the abdominal wall fail to develop, from the peritoneum to the skin

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24
Q

What are ectopic tissues

A

Developmental rests

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25
Q

Where is most common gastric mucosa

A

Upper 1/3 of the esophagus (referred as an inlet patch)

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26
Q

Clinical ectopic pancreatic tissue

A

Asymptomatic, but can release gastric acid and lead to dysphagia, esophagitis, Barrett’s esophagus, or rarely adenocarcinoma

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27
Q

Where is ectopic pancreatic tissue found

A

Stomach or esophagus

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28
Q

Clinical ectopic pancreatic tissue

A

Nodules are usually asymptomatic, but can produce local damage and inflammation in some instances

If present in the pylorus->inflammation and scarring may lead to obstruction

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29
Q

What is gastric heteropia and how does it present

A

Small patches of ectopic gastric mucosa in the small bowel or colon can present with occult blood loss due to peptic ulceration of adjacent mucosa

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30
Q

True diverticulum

A

Blind pouch leading of the alimentary tract that communicates with the lumen
*lined by mucosa and ALL THREE LAYERS OF THE BOWEL WALL ARE PRESENT: MUCOSA, SUBMUCOSA, MUSCULARIS PROPORIA

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31
Q

What is the most common true diverticulum

A

Meckel diverticulum

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32
Q

Where does meckel diverticulum occur

A

Ileum

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33
Q

Why get meckel diverticulum

A

Persistence of the vitelline duct which connects lumen of the developing gut to the yolk sac

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34
Q

Meckel diverticulum extends from the __-__ side of the bowel

A

Anti mesenteric

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35
Q

Issues with meckel diverticulum

A

Mucosal lining may resemble normal small intestine but ectopic pancreatic or gastric tissue may be present (and functional)

Acid secretion can cause ulceration of adjacent mucosa can lead to occult bleeding or abdominal pain that looks like appendicitis

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36
Q

What is the rule of 2s for meckels diverticulum

A

2% of population
Occur within 2 feet of the ileocecal valve
2 inches long
2x more common in males
Symptomatic be age 2 (only4% are ever symptomatic)

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37
Q

Acquired diverticula most commonly occur in the __ __

A

Sigmoid colon

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38
Q

Acquired diverticula lack __ __ or have an attenuated __ ___

A

Muscularis propria

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39
Q

What causes congenital hypertrophic pyloric stenosis

A

Hyperplasia of the pylorus muscularis propria which obstructs the gastric outflow tract

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40
Q

What is congenital hypertrophic pyloric stenosis associated with

A

3-5x more likely in males

Turner syndrome and trisomy 18(Edward)

Erythromycin/azithromycin exposure (either orally or through maternal milk) in the first 2 weeks of like

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41
Q

Genetic component of congenital hypertrophic pyloric stenosis

A

Yup high concordance in monozygotic twins

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42
Q

Clinical congenital hypertrophic pyloric ctenosis

A

Regurgitation and new onset regurgitation, projectile, nonbillous vomiting after feeding with frequent demands for refeeding

Antecedent visible hyperperistalsis

Palpable firm, 1-2 cm ovoid abdominal mass

Signs and symptoms onset: between 3rd and 6th weeks of life

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43
Q

Treatment of congenital hypertrophic pyloric stenosis

A

Surgical splitting of the muscularis (myotome) is curative

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44
Q

Why do people get acquired pyloric stenonosis

A

Adults as a result of antral gastritis or peptic ulcers near the pylorus
Or
Carcinomas of the distal stomach and pancreas may also narrow the pyloric channel due to fibrosis or malignant infiltration

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45
Q

Hirschsprung disease

A

Congenital anganglionic megacolon (both plexuses are absent “anglionosis”

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46
Q

What causes hirschsprung disease

A

Arrested migration of NCC into the gut (neurocristopathy)

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47
Q

In hirschsprung disease NCC fail to migrate from the _ to the _ or ganglion cells undergo __ __

A

Cecum
Rectum

Premature death

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48
Q

In hirschsprung, what is absent in distal segments

A

Submucosal plexus (miessner) and myenteric plexus (of auerbach)

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49
Q

Describe the effect of having an aganglionic segment in hirschsprung disease

A

It lacks coordinating peristaltic contractions

Get functional obstruction

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50
Q

What happens to the normally innervated proximal colon in hirschsprung

A

Undergo progressive dilation and become massively distended-> may stretch and thin the colonic wall to the point of rupture (occurs most frequently near the cecum)

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51
Q

In hirschsprung the rectum is always affected, but what happens if only a few cm of the rectum is involved

A

Occasional passage of stool may occur and obscure the diagnosis

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52
Q

10% of hirschsprung disease cases occur in kid with __ __

A

Down syndrome

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53
Q

In 5% of hirschsprung disease 5% present with __ ___

A

Neurologic abnormalities

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54
Q

Genetics of hirschsprung disease

A

Mainly heterozygous loss-of-function mutations in RET (RTK) accounts for majority of familial causes and 15% of sporadic

Or

Sex linked factors -more likely in males, when present in females have longer aganlionic segments

Genetic and environmental modifiers

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55
Q

Clinical presentation of hirschsprung disease

A

Failure to pass meconium in the immediate post natal period

Obstruction or constipation, with visible, ineffective peristalsis

May progress to bilious vomiting or abdominal distension

At risk for perforation, peritonitis, and enterocolitis with fluid/electrolyte imbalance/ derangement

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56
Q

How diagnose hirschsprung

A

Requires documentation of the absence of ganglion cells in the affected segment

Confirm via intraoperative frozen section analysis

Can stain for the ganglion cells with H/E and immune staining for acetylcholinesterase

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57
Q

Treat hirschsprung

A

Surgical resection of aganglionic segment with anastomoses of the noramal proximal colon to the rectum

May require years to attain normal bowel function and continence

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58
Q

Acquired megacolon can occur at any age due to what

A

Associated with loss of ganglion cells (chagas disease)

Or not associated with loss of ganglion cells

  • obstruction by neoplasm or inflammatory stricture
  • toxic megacolon complicating ulcerative colitis
  • visceral myopathy
  • psychosomatic disorders
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59
Q

The upper 12 of the esophagus is supplied by what

A

Inferior thyroid artery

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60
Q

What supplies the middle 1/3 of the esophagus

A

Thoracic aorta branches

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61
Q

What supplies the lower 1.3 of the esophagus

A

Left gastric artery

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62
Q

Normal histology esophagus

A

Stratified squamous epithelium

Inner circular muscle+ outer longitudinal muscle

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63
Q

What does the esophagus develop from

A

Cranial portion of the foregut

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64
Q

Esophageal dysmotility

A

Structural obstruction

Functional obstruction:disruption of coordinated peristaltic contractions following swallowing

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65
Q

What are the three principle forms of esophageal dysmotility

A

Nutcracker esophagus
Diffuse esophageal spasm
Hypertensive lower esophageal sphincter

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66
Q

Esophageal dysmotility mimics __ pain

A

MI

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67
Q

Clinical esophageal dysmotility

A

Dysphagia+odynophagia+globus (feels like something’s is stuck in the back of the throat)

Regurgitation

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68
Q

Nutcracker esophagus (jackhammer esophagus)

A

High amplitude contractions of the distal esophagus

Due to loss of normal coordination between the inner circulat and outer longitudinal smooth muscle contractions

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69
Q

Diffuse esophageal spasm

A

Repetitive, simultaneous contractions of the distal esophageal smooth muscle

When swallowing cold food=chest pain

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70
Q

Hypertensive lower esophageal sphincter

A

Lower esophageal sphincter abnormality int he absence of altered contraction patterns -achalasia includes reduced esophageal peristaltic contractions
-achlasia is not a hypertensive lower esophageal sphincter

High resting pressure or incomplete relaxation is absent -seen in nutcracker esophagus and diffuse esophageal spasm

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71
Q

CREST syndrome

A 
Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia
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72
Q

Zenker diverticulum (pharyngoesophageal diverticulum)

A

Functional obstruction==maintain weight and appetite

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73
Q

Sequelae of zenker diverticulum

A

Increased pressure within the distal pharynx due to impaired relaxation and spasm of the cricopharyngeus muscle after swallowing

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74
Q

Location of zenker diverticulum

A

Immediately above the upper esophageal sphincter

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75
Q

Who gets zenker diverticulum

A

Patients after 50

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76
Q

Clinical zenker diverticulum

A

Accumulate significant amounts of food

Can lead to regurgitation and halitosis

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77
Q

Mechanical esophageal obstruction cause

A

Strictures or cancer

Benign stricture-maintain weight and appetite
Malignant stricture-weight loss

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78
Q

Clinical mechanical esophageal obstruction

A

Progressive dysphagia
Initial onset of inability to swallow solids which then progresses to inability to swallow liquids

Patients may subconsciously modify their diet to favor soft food and liquid until the obstruction is nearly complete

Generally maintain their weight

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79
Q

Benign esophageal stenosis cause

A

Generally caused by fibrous thickening of the submucosa due to inflammation and scarring from chronic GERD, irradiation, or caustic injury

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80
Q

What is benign esophageal stenosis associated with

A

Atrophy of the muscularis proporia as well as secondary epithelial damage

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81
Q

What are esophageal mucosal webs

A

Uncommon, idiopathic ledge-like protrusions of mucosa that may cause obstruction

Semi circumferential lesions that protrude less than 5 mm are 2-4 mm thick, and are composed of a fibrovascular connective tissue and overlying epithelium

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82
Q

Who gets esophageal mucosal webs

A

Females over 40

Seen in paterson-brown-Kelly or Plummer-Vinson syndrome

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83
Q

What is esophageal mucosal web associated with

A

GERD, chronic graft-versus host disease, or blistering skin diseases

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84
Q

Main symptoms esophageal mucosal webs

A

Nonprogressive dysphagia with incompletely chewed food

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85
Q

Patterson brown Kelly (Plummer vinson) syndrome

A

Upper esophageal mucosal webs associated with

  • iron deficient anemia
  • glossitis(inflammation of the tongue)
  • Cheilosis (corners of the mouth cracked)
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86
Q

Esophageal rings (schatzki rings)

A

Circumferential, including the mucosa, submucosa and (sometimes) hypertrophic muscularis proporia

Webs are semi-circumferential, thinner, and do not include the mucosa and submucosa

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87
Q

Esophageal rings involve what layers of the esophagus

A

All layers, usually distal

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88
Q

Esophageal rings: A rings

A

In distal esophagus above the gastro-esophageal jucntion; covered with squamous mucosa

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89
Q

Esophageal rings : B rings

A

At the squamocolumnar jucntion of the lower esophagus; may have gastric cardia-type mucosa

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90
Q

Diagnose esophageal rings

A

Barium swallow

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91
Q

Achalasia

A

Increased tone fo the lower esophageal sphincter as a result of impaired smooth muscle relaxation and an important cause of esophageal obstruction

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92
Q

Triad of achlasia

A

Incomplete lower esophageal sphincter (LES) relaxation (lack of NO and vasoactive intestinal polypeptide)

Increased LES tone tone (cholinergic signaling)

Lack of peristalsis of the esophagus

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93
Q

Signs and symptoms of achalasia

A

Dysphagia for solids and liquids

Difficulty belching

Chest pain

Bird beak sign on barium swallow

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94
Q

Should u do surveillance endoscopy for achlasia patients

A

Nah risk of esophageal cancer is too low

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95
Q

Primary achalasia causes

A

Idiopathic

Result of distal esophageal inhibitory neuronal degeneration-hirschsprung of the esophagus(failure of distal esophageal neurons to induce LES relaxation during swallowing

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96
Q

Signs of primary achalasia

A

Increase in tone, inability to relax LES and esophageal aperistalsis

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97
Q

Secondary achalasia cause

A

Chagas’ disease (trypanosoma cruzi)

  • cause estruction of the myenteric plexus of auerbach, failure of peristalsis and esophageal dilation
  • duodenal, colonic and ureteric myenteric plexuses may also be effected
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98
Q

Other systemic disease that can lead to achlasia-like disease

A 
Diabetic autonomic neuropathy
Malignancy
Amyloidosis
Sarcoidosis
Sarcoidosis
Lesions of dorsal motor nuclei (polio, surgical ablation)
Down syndrome 
Allgrove (triple A) syndrome
Immune mediated destruction of inhibitory esophageal neurons
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99
Q

Allgrove (triple A) syndrome

A

AR
Achalasia
Alacrima
Adrenocorticocotrophic hormone-resistant adrenal insufficiency

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100
Q

Immune mediated destruction of inhibitory esophageal neurons

A

Associated with HSV1

Occasionally coexistence with Sjögren’s syndrome or autoimmune thyroid disease

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101
Q

Achlasia treatment

A

Need to overcome the mechanical obstruction
Laparoscopic myotome
Pneumatic balloon dilation
Botox injections to inhibit LES cholinergic neurons

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102
Q

Mallory Weiss tears

A

Longitudinal lacerations of the mucosa near the gastroesophageal junction that usually cross the gastroesophageal function

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103
Q

What are Mallory Weiss tears associated with

A

Severe retching secondary to acute alcohol intoxication

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104
Q

What happens when you have Mallory Weiss tears

A

Prolonged vomiting

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105
Q

Why is there prolonged vomiting with Mallory Weiss tears

A

Reflex fails and allows for refluxing gastric contents to overwhelm the gastric inlet which leads to esophageal stretching and tearing ->hematemesis

Normally reflex relaxation of the LES usually precedes anti-peristaltic waves

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106
Q

Are Mallory Weiss tears fatal

A

No you get prompt healing without surgical intervention

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107
Q

Boerhaave syndrome

A

Much less common but much more severe

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108
Q

Characterization of Mallory Weiss tears

A

Transmural tearing and rupture of the distal esophagus

Severe mediastinitis

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109
Q

Presentation of boerhaave syndrome

A

Presents like a heart attack-severe chest pain , tachypnea and shock

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110
Q

Boerhaave causes __ sign: due to pneumoperitoneum in the mediastinum

A

Hamman

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111
Q

Treatment boerhaave syndrome

A

Surgical intervention

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112
Q

What is chemical and infectious esophagitis

A

Stratified squamous epithelial damage leading to dysphagia and pain+/- hemorrhage, stricture, or perforation

Odynophagia=pain on swallowing

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113
Q

Causes of chemical and infectious esophagitis

A

Induced by alcohol, corrosive acids/askalisis, hot fluids, heavy smoking or pharmalogical agents

Kids:accidental ingestion of household cleaning products

Adults: more severe damage following attempted suicide

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114
Q

Pill induced esophagitis

A

Less severe chemical injury to the esophageal mucosa can occur when medicinal pills lodge and dissolve int he esophagus rather than passing into the stomach intact

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115
Q

Iatrogenic chemical and infectious esophagitis

A

Irradiation, chemotherapy, graft vs host disease

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116
Q

What systemic desquamative disorders can cause chemical and infectious esophagitis

A

Bullous pemphigoid

Epidermolysis bullosa

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117
Q

Can crohns cause chemical and infectious esophagitis

A

Yup

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118
Q

Infectious causes of chemical and infectious esophagitis

A

Healthy: HSV
Immunosuppressed: HSV, CMV, or fungal (candida, mucormycosis, or aspergillosis)

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119
Q

Morphology chemical and infectious esophagitis

A

Commonly with dense neutrophilic infiltrates +/- necrosis

Granulation tissue leads to fibrosis

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120
Q

How does radiation causechemical and infectious esophagitis

A

Intimate proliferation and luminal narrowing of submucosal and mural blooms vessels which takes years to develop interstitial fibrosis following radiation therapy

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121
Q

How do pathogenic bugs causechemical and infectious esophagitis

A

Invade the laminae propria and cause necrosis of overlying mucosa

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122
Q

Candidiasis morphology in esophagitis

A

Grey white pseudomembranes of hyphae and inflammatory cells

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123
Q

HSV morphology esophagitis

A

Punched out ulcers with viral inclusions and a rim of epithelial cells

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124
Q

CMV morphology esophagitis

A

Shallow ulceration with nuclear and cytoplasmic inclusions

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125
Q

GVHD morphology esophagitis

A

Basal epithelial apoptosis, mucosal atrophy and submucosal fibrosis without significant acute inflammatory infiltrates

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126
Q

Reflux esophagitis GERD

A

Mucosal injury due to reflux of gastric juices-stratified squamous epithelium is resistant to abrasion from foods, but is sensitive to acid (gastric juice)

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127
Q

Most common cause of esophagitis and most common outpatient GI diagnosis

A

Reflux esophagitis GERD

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128
Q

Most common cause of GERD

A

Transient lower esophageal sphincter relaxation mediated by vagal pathways and can be triggered by gastric distension

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129
Q

What do submucosalglands in proximal and distal esophagus secrete

A

Mucin and HCO3

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130
Q

What does LES tone normally do

A

Prevent reflux of acidic gastric contents and decreased LES tone

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131
Q

What does decreased LES tone and/or increased abdominal pressure cause (GERD)

A

Reflux

  • abdominal contents are under positive pressure
  • thoracic contents are under negative pressure
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132
Q

What may exacerbate reflux disease GERD

A

Alcohol, tobacco, obesity, CNS depressants, pregnancy, hiatal hernia, delayed gastric emptying or increasedgastric volume

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133
Q

Reflux of gastric juices is central to the development of __ injury

A

Mucosal

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134
Q

Severe cases of GERD

A

Reflux of bile from the duodenum may exacerbate the damage

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135
Q

Morphology GERD

A

Hyperemia(redness)+edema

Basal zone hyperplasia

Thinning of superficial epithelial layers

Neutrophil and/or eosinophils infiltration

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136
Q

Clinical GERD who gets is

A

Most common in patients over 40

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137
Q

Symptoms of GERD

A

Heartburn, dysphagia, regurgitation of sour tasting contents, increased saliva

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138
Q

Is severity of GERD related to the histological damage

A

Nope histological damage does increase with disease duration

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139
Q

Kids with GERD symptoms

A

Fail to eat, failure to thrive, recurrent pneumonia’s

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140
Q

Complications GERD

A

Ulceration, hematemesis, melena, stricture, or barret esophagus

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141
Q

Treat GERD

A

Symptomatic relief with PPIs (omeprazole)

Which have replaced H2 histamine receptor blockers (cimetidine) to reduce gastric acidity

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142
Q

Hiatal hernia

A

Characterized by separation of the diaphragmatic courage and protrusion of the stomach into the thorax

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143
Q

Hiatal hernia symptoms

A

Symptomatic in fewer than 10%

Heartburn and regurgitation of gastric juices

May cause lower esophageal sphincter incompetence

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144
Q

Eosinophilia esophagitis

A

Incidence has increased

Large numbers of intraepithelial eosinophils, particularly superficially

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145
Q

What differentiates eosinophilia esophagitis from GERD, crohns and other causes of esophagitis

A

Large numbers of intraepithelial eosinophils , particularly superficially

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146
Q

Symptoms of eosinophilic esophagitis

A

Adults:food impaction+dysphagia
Children: feeding intolerance+GERD like signs and symptoms
-acid reflux is not prominent **

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147
Q

Eosinophilic esophagitis is associated with what

A

Atopic disorders-atopic dermatitis, allergic rhinitis, asthma, peripheral eosinophilia

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148
Q

Treat eosinophilic esophagitis

A

Dietary resection +/- topical or systemic corticosteroids

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149
Q

Do PPI help with eosinophilic esophagitis

A

Not provide relief nope nope

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150
Q

Esophageal varicose

A

Distention of subepithelial and submucosal venous vessels within the distal esophagus and proximal stomach

Varices=tortuous dilated veins within the submucosa

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151
Q

What causes esophageal varices

A

Portal HTN can result in the development of collateral channels at sites where the portal and canal system communicate->portal canal anastomoses

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152
Q

_% of patients with cirrhosis livers have __ __

A

Esophageal varices

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153
Q

What is the second most common cause of esophageal varices

A

Hepatic schistosomiasis (snail liver) is the second most common cause of varices worldwide

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154
Q

Pathogenesis esophageal varices

A
  • collateral channel between the portal and canal circulations is established in severe portal HTN
  • subepithelial and submucosal veins in the distal esophagus become congested
  • most commonly associated with alcoholic cirrhosis and schistomiasis
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155
Q

Morphology esophageal varices

A

Tortuous, dilated veins in the distal esophageal and proximal gastric submucosa
Irregular luminal protrusion of overlying mucosa with superficial ulceration, inflammation or adherent blood clots

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156
Q

Clinical esophageal varices

A

Clinically silent until they rupture with catastrophic hematemesis (30% or more patients with varices hemorrhage die as a direct consequence of hemorrhage such as hypokalemia shock, hepatic coma, or other complications

Rupture may be due to inflammatory erosion, increased venous pressure, or increased hydrostatic pressure from vomiting

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157
Q

Treat esophageal varices

A

Splanchnic vasoconstriction, sclerotherapy (injection of thrombotic drugs), balloon tamponade, or band ligation

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158
Q

50% of people with esophageal varices die when

A

The first bleed (exsanguination or hepatic coma)

But also >50% chance of recurrence within 1 year with the same mortality rate

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159
Q

Patients with esophageal varices have a high risk of ____ (lage varices, elevated hepatic venous presssure gradient, previous bleeding, and advanced liver disease)

A

Hemorrhage

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160
Q

How treat esophageal varices propholactically

A

Treated prophylactically with beta blockers to reduce portal blood flow and with endoscopic varices ligation

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161
Q

Barret esophagus

A

Complication of chronic GERD

Intestinal metaplasia within the esophageal squamous mucosa

Stratified squamous epithelium->columnar epithelium
-columnar metaplasia of the esophageal squamous mucosa(names for what it turns into)

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162
Q

What percent of people with GERD have barret esophagus

A

10%

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163
Q

What color is mucous in Barrett’s esophagus

A

Salmon

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164
Q

Who gets Barrett esophagus

A

White males 40-60

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165
Q

People with Barrett’s esophagus have an increased risk of what

A

Esophageal adenocarcinoma
S-barrettt esophagus is a precursor lesion

Most don’t bet esophageal tumours

Shared mutations common when dysplasia is present

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166
Q

Morphology Barrett

A

Patches of red, velvety mucosa extend cephalad from the gastroesophageal jucntion

Metaplastic mucosa alternates with residual smooth, pale squamous (esophageal) mucosa and interfaces with light brown columnar (gastric) mucosa distally-obliterates the Z line

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167
Q

Subclassifications of Barrett esophagus

A

Long segment >_3cm

Short segment <3cm

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168
Q

Risk of dysplasia in barrett correlates with what

A

Length of esophagus affected

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169
Q

Gland architecture in barrett

A

Abnormal and characterized by budding, irregular shapes and cellular crowding

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170
Q

What can Barrett’s progress to

A

Intramucosal carcinoma, if there is neoplastic cel invasion of the lamina propria

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171
Q

Diagnosis Barrett’s

A
  • identified only with endoscopy and biopsy, prompted by GERC signs and symptoms
  • diagnosis requires intestinal-type columnar epithelium (mucin secreting goblet cells)
  • there are mucous vacuoles that stain light blue in the shape of a wine-goblet with H/E
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172
Q

Clinical barrett

A

Esophagitis like heartburn, regurgitation, dysphagia

Not all patients will develop cancer, but no way to predict

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173
Q

Treatment barrett

A

Periodic endoscopy with biopsy for dysplasia surveillance

Therapeutic intervention with carcinoma including surgical resection, esophagectomy, photodynamic therapy, laser ablation and endoscopic mucosectomy

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174
Q

Esophageal tumors

A

Most are squamous cell carcinoma or adenocarcinoma

Other esophageal malignancies are less common

Benign:mesenchymal origin (leiomyomas are most common)

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175
Q

Risk factors for esophageal adenocarcinoma

A 
Most arise from barretts or obesity related GERD
Tobacco, radiation exposure
H pylori
Caucasian 
Males 7x more likely
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176
Q

How does helicobacter cause esophageal adenocarcinoma

A

H pylori-.gastric atrophy->decrease acid secretion->decreased GERD->decreased barret esophagus
Reduced rates of H pylori may also be a factor in the increasing indecency of esophageal adenocarcinoma

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177
Q

Esophageal adenocarcinoma accounts for _% of all esophageal cancers in the USA

A

> 50

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178
Q

Genetics esophageal adenocarcinoma

A

Stepwise accu,Latino of genetic and epigenetic alterations from barret esophagus

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179
Q

Early mutations of esophageal adenocarcinoma

A

TP53, CDKN2A (p16/INK4a)

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180
Q

Late mutations that cause esophageal adenocarcinoma

A

EGFR, ERBB2, met, cyclin D1, cyclin E

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181
Q

Morphology esophageal adenocarcinoma

A

Range from exophytic nodules to excavated, deeply infiltrating masses

Mostly in distal 1/3 of esophagus and can invade the adjacent cardia

Tumors produce mucin and form glands

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182
Q

Clinical esophageal adenocarcinoma-how discovered

A

In evaluation of GERD or surveillance of barrett

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183
Q

Presentation symptoms of clinical esophageal adenocarcinoma

A

Dysphagia, progressive weight loss, hematemesis, chest pain and vomiting

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184
Q

Prognosis esophageal adenocarcinoma

A

By the time symptoms appear, the tumor has likely spread to submucosal lymphatic vessels-advanced stage

5 year survival <35%, 80% if limited to the mucosa or submucosa

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185
Q

Risk factors for esophageal squamous call carcinoma

A

Patients greater than 45
Males 4:1
8x increased risk in african American vs white
Alcohol and tobacco synergy, caustic esophageal injury, achalasia, Plummer Vinson syndrome, scalding beverages, tylosis (AKA howel-Evans syndrome) (RHBDF2 mutation)
Nutritional defiency (poverty), polycyclic hydrocarbons, nitrosamines, other mutagens

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186
Q

What geographies have increased incidence os esophageal squamous cell carcinoma

A

Iran, central china, Hong Kong, Brazil, South Africa, and western Kenya (consumption of a fermented milk, called mursik, which contains acetaldehyde)

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187
Q

Genetics of esophageal squamous cell carcinoma

A

HPV infection in high risk areas

SOX2 amplification-believed to be involved in cancer stem cell self renewal and survival

Cyclin D1 overexpression

Tumor suppressor TP53, E cadherine, NOTch1 loss of function

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188
Q

How does squamous cell carcinoma begin

A

Begins as a squamous dysplasia (in situation lesion same as intraepithelial neoplasia or carcinoma in situation elsewhere)

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189
Q

Morphology of early squamous cell carcinoma esophagus

A

Small, gray white plaque like mucosal thickening

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190
Q

Lesions of squamous cell carcinoma esophagus may expand as __ ___, ulcerate, or become diffusely infiltrating with wall thickening and luminal stenosis/obstruction

A

Exophytic lesions

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191
Q

___ network allows circumferential and longitudinal spread in squamous cellcarcinoma

A

Lymphatic

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192
Q

What happens when there is deep invasion of squamous cell carcinoma into adjacent structures

A

Can lead to PNA or exsanguination form invasion into the aorta

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193
Q

Most squamous cell carcinoma esophagus are moderately well differentiated-prognosis implication

A

Not terrible

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194
Q

Half of squamous cell carcinoma occur in the ___ of the esophagus in contract to adenocarcinoma

A

Middle 1/3

195
Q

Where does esophageal squamous cell carcinoma spread from the upper third (poor prognosis0

A

Cervical lymph nodes

196
Q

Where does esophageal squamous cell carcinoma spread from the middle third of the esophagus (poor prognosis)

A

Mediastinal, paratracheal, and tracheobronchial lymph nodes

197
Q

Where does esophageal squamous cell carcinoma spread from the lower third of the esophagus (poor prognosis)

A

Gastric and celiac lymph nodes

198
Q

Clinical esophageal squamous cell carcinoma

A

Insidious onset of dysphagia, odynophagia (painful swallowing) or obstruction

Diet is subconsciously altered to soft food and liquid which contributes to nutritional defiency and weight loss in addition to the systemic effects of the tumor itself

Hemorrhage, iron defiency, sepsis due to ulceration

Tracheoesophageal fistula (risk for aspiration)

199
Q

Prognosis esophageal squamous cell carcinoma

A

Early detection (still superficial) : 75% 5 year survival

USA prognosis<20% 5 year survival

Variable based on tumor stage and and patient age, race, and gender

200
Q

What does the cardia/antrum of stomach consist of

A

Lined with mucin secreting foveolar cells that form small glands

Endocrine cells (G cells) that relase gastrin and stimulate luminal acid secretion via parietal cells in the fundus and body

201
Q

What does the body and fundus of the stomach consist of

A

Well-developed glands and chief cells that produce and secrete digestive enzymes (pepsinogen)

Parietal cells secrete HCL

202
Q

Gastritis

A

Mucosal inflammatory process

203
Q

Acute gastritis

A

When neutrophils are present

204
Q

Gastroparesis

A

When inflammatory cells are rare or absent

205
Q

Gastritis symptoms

A

May be asymptomatic or have persistent epigastric pain

Billious vomiting is possible with bile reflux

206
Q

Gastritis respond to PPI

A

Maybe maybe not

207
Q

Can you distinguish gastrophy from gastritis based on clinical grounds

A

No

208
Q

Gatropathy

A

When inflammatory cells are rare or absent

209
Q

Acute gastritis

A

Transient mucosal inflammatory process involving neutrophils

Self limiting with neutrophils on biopsy

Hyperemia and no blood loss

May be transient or cause variable degrees of epigastric pain, nausea, and vomiting

210
Q

What can severe acute gastritis lead to

A

Mucosal erosion, ulceration, hemorrhage, hemtemesis, melena, and massive blood loss

211
Q

Gastropathy

A

Mucosal inflammation with scant inflammatory cells

212
Q

What may cause gastropathy

A

NSAIDS, alcohol, bile, stress induced injury, portal HTN

213
Q

Symptoms gastropathy

A

May be transient or cause variable degrees of epigastric pain, nausea, and vomiting

214
Q

What can severe gastropathy lead to

A

Mucosal erosion, ulceration, hemorrhage, hematemesis, melena, and massive blood loss

215
Q

How do NSAIDS damage gastric mucosa

A

NSAIDS reduce bicarbonate production and interfere with muco/cyto-protective prostagladins which inhibit acid production, promote mucin synthesis and increase vascular perfusion

216
Q

How is gastric mucosa damaged by h pylori and in uremic patients

A

Inhibition of gastric bicarbonate transporters by ammonium ions in urease secreting h pylori and uremic patients

217
Q

How do damaged gastric mucosal cells damage in old people

A

Reduce secretion of mucin and bicarbonate

218
Q

How else can gastric mucosa be damaged

A

Decreased O2 at high altitudes

Ingestion of harsh chemicals (alcohol smoking)
Ischemia and shock

219
Q

Gastric mucosa protection by foveolar cells

A

Mucin secretion prevents food from directly touching the epithelium

220
Q

How often is the gastric mucosa replaced

A

3-7 days

221
Q

Gastric mucosa protection epithelial cell

A

Physician barrier; beneath the mucus

222
Q

Gastric mucosa protectionL limits back diffusion of acid and luminal materials (pepsin) into the __ __

A

Lamina propria

223
Q

Gastric mucosa protection: any back diffused material is washed away by ____ ___

A

Mucosal vasculature

224
Q

In acid secreting parts of the stomach, a capillary ____ is generated as parietal cells secrete hydrochloride acid into the gastric lumen and bicarbonate into the vessels

A

Alkaline tide

225
Q

__ Into the lumen, __ into the vessels

A

Acid

Bicarbonate

226
Q

COX dependent synthesis of ___

A

Prostagladins E2 and I2

227
Q

__ plays a larger role that __, but both isoenzymes contribute to mucosal protection

A

COX1 COX2

228
Q

Gastrophy and acute gastritis morphology

A

Moderate edema and slight vascular congestion

Surface epithelium is intact

Foveolar cell hyperplasia and characteristic corkscrew profiles and epithelial proliferation
Presence of neutrophils above the basement membrane in direct contact with epithelial cells is abnormal in all parts of the GI tract and signifies active inflammation (gastritis not gastropathy)

Erosion==loss of epithelium; superficial mucosal defect
-accompanied by a pronounced neutrophilic infiltrate and a fibrincontaining pursuant exudate in the lumen, hemorrhage may occur and cause dark, punctae in hyperemic mucosa

Concurrent erosion and hemorrhage==acute erosive hemorrhagic gastritis

When erosions extend deeply, they may progress to ulcers

229
Q

Stress related mucosal disease cause

A

Due to severe trauma, extensive burns, intracranial disease, major surgery, physiologic stress

Often related to localized ischemia

230
Q

For stress related mucosal disease, endoscopically visibile lesions tend to appear in the first _ days of illness

A

3

231
Q

Stress ulcers

A

Occur in individuals with shock, sepsis or severe trauma
-1-4% of critically ill patients admitted to intensive care units show histological evidence of gastric mucosal damage and will require transfusion

232
Q

Curling ulcer

A

Occur in the proximal duodenum; associated with severe burns or trauma (like from a curling iron0

233
Q

Cushing ulcers

A

Associated with increased intracranial pressure (Cushing reflex)

  • direct stimulation of vagal nuclei leads to hypersecretion of gastric acid
  • damage to parasympathetic component of vagus nerve
  • may occur in several GI regions: gastric, duodenal and esophageal
  • high incidence of perforation
234
Q

Pathogenesis stress related mucosal disease

A
  • often related to local ischemia (hypotension or reduced flow from splanchnic vasoconstriction)
  • upregulation of inducing BO synthase
  • increased release of endothelin1 (vasoconstrictor)
  • COX2 upregulation is protective (nonselective NSAIDS will block COX1 and COX2)
  • intracranial injury->direct stimulation of vagal nuclei->hypersecretion of gastric acid
  • systemic acidosis->lowers intracellular pH of mucosal cells->mucosal injury
235
Q

Morphology stress related mucosal disease

A

Multiple shallow ulcers found anywhere int he stomach

Base is brown (blood)

Adjacent mucosa is normal

There is no scarring and blood vessel thickening that characteristic chronic peptic ulcers

236
Q

Clinical stress related mucosal disease

A

Healing takes days to weeks once the stimulus has ended

Most important determinant of prognosis: ability to correct underlying conditions

237
Q

Stress related mucosal disease if corrected , ___ is normal

A

Re-epithelialization

238
Q

1-4% of critically ill patients with stress related gastric mucosa admitted to the ICU show histological evidence of what

A

Gastric mucosal damage and will require transfusion

239
Q

_% of stress related gastric mucosa perforate

A

5%

240
Q

Dieulafoy lesion

A

Rare, improperly branched submucosal artery within the wall of the stomach

241
Q

Diameter of dieulafoy lesion

A

10x greater than a mucosal capillary

242
Q

Where are dieulafoy lesions found

A

Along lesser curvature , near gastroesophageal junction

243
Q

Why do dieulafoy lesions bleed

A

Gastric bleeding can occur secondary to erosion of overlying epithelium

244
Q

Treat dieulafoy lesion

A

Self limited, but can be copious

245
Q

What are dieulfaoy lesions associated with

A

NSAIDS, often recurrent

246
Q

Gastric antral ectasia (GAVE)

A

Longitudinal stripes of edematous erythematous mucosa alternating with less severely injured, paler mucosa

247
Q

What causes gastric antral vascular ecstasia

A

Due to ecstatic mucosal vessels producing stripes of edematous erythematous mucosa alternating with less severely injured pale mucosa

248
Q

Why get erythematous stripes with gastric antral vascular ecstasia

A

Ecstatic mucosal vessels

249
Q

Nickname for gastric antral vascular ectasia

A

Watermelon stomach

250
Q

Gastric antral vascular ecstasia morphology

A

Antral mucosa has reactive gastropathy with dilated capillaries containing fibrin thrombi

251
Q

Cause of gastric antral vascular ecstasia

A

Idiopathic or associated with cirrhosis or systemic sclerosis

252
Q

Presentation gastric antral vascular ecstasia

A

May present with occult fecal blood or iron deficient anemia

253
Q

Chronic gastritis

A

Ongoing mucosal inflammation with mucosal atrophy

254
Q

What is the most common cause of chronic gastritis

A

Helicobacter pylori

255
Q

Most common cause of diffuse atrophic gastritis

A

Autoimmune

256
Q

Autoimmune etiologies make up less than 10% of chronic gastritis cases but is the most common form of chronic gastritis in patients without _____

A

H pylori

257
Q

Symptoms chronic gastritis

A

Nausea, vomiting, upper abdominal pain

258
Q

Prognosis chronic gastritis

A

Less severe than acute gastritis, but more persistent signs and symptoms

Hematemesis is rare

259
Q

Helicobacter pylori

A

Spiral or curved bacilli

260
Q

Almost all patients with duodenal ulcers, gastric ulcers, or chronic gastritis have __

A

H pylori

261
Q

Most patients with H pylori are asymptomatic. When do they seek help

A

When chronic gastritis is causing problems

262
Q

What is h pylori associated with

A

Poverty, household crowding, decreased education, rural, mexican

263
Q

Spreading of h pylori

A

Fecal oral

264
Q

How does h pylori present

A

Antral gastritis with normal or increased acid production

265
Q

H pylori causes increased __ production, but ___ is uncommon

A

Gastrin

Hypergastrinemia

266
Q

Pathogenesis h pylori

A

Interplay of gastroduodenal mucosal defenses, inflammatory responses and bacteria virluence factors

267
Q

Multifocal atrophic gastritis

A

Gastritis that progresses to involve the gastric body and fundus: associated with patchy mucosal atrophy , reduced parietal cell mass and acid secretion, intestinal metaplasia, and increased risk of adenocarcinoma

268
Q

Inverse relationship between duodenal peptic ulcer and gastric adenocarcinoma that correlated with pattern of gastritis

A

?

269
Q

What are the virluence factors of H pylori

A

Flagella: motility

Urease: generates ammonia from endogenous urea and elevates local gastric pH; enhances bacterial survival

Adhesions:bind surface of foveolar cells

CagA associated with increased risk of gastric gander

270
Q

CagA expressing strains of h pylori can effectively colonize the gastric body and cause __ ___ ___

A

Multifocal atrophic gastritis

271
Q

Risk factors associated with pangastritis, atrophy and gastric cancer with h pylori

A

Overexpression of TNF, IL-1B

Decreased IL10

Iron defiency

272
Q

H pylori are concentrated where

A

Superficial mucus overlying surface and neck epithelium ant typically infect the antrum

273
Q

Morphology H pylori infection

A

Infected mucosa is erythematous and coarse to nodular

Variable numbers of intra epithelium and luminal neutrophils forming pit abscesses

Lamina propria with abundant plasma cells, macrophages and lymphocytes

274
Q

Chronic h pylori morphology

A

Diffuse mucosal atrophy with prominent lymphoid aggregates (occasional germinal centers) and is associated with increased risk of gastric adenocarcinoma

275
Q

Look for helicobacter pylori with a _____ stain

A

Warthrin starry

276
Q

How diagnose h pylori

A

Serologic test for antibodies

Fecal bacteria detection

Urea breath test (ammonia production)

Biopsies *GOLD STANDARD

277
Q

Treat h pylori

A

Antibiotic+PPI

Patients usually improve after treat but relapses can occur after incomplete eradication or reinfection

Prophylactic and therapeutic vaccines are still at an early stage non development

278
Q

Location of h pylori vs autoimmune

A

H p-antrum

Autoimmune -body

279
Q

Inflammatory infiltrate h pylori vs autoimmune

A

Hp-neutrophils, subepithelial plasma cells

Autoimmune-lymphocytes,macrophages

280
Q

Acid production h pylori vs autoimmune

A

Hp-increased to slightly decreased

Autoimmmune-decreased

281
Q

Gastrin h pylori vs autoimmune

A

Hp-normal to decreased

Autoimmune-increased

282
Q

Other lesions h pylori vs autoimmunes

A

Hp-hyperplastic/inflammatory polyps

Autoimmune-neuroendocrine hyperplasia

283
Q

Serology h pylori vs autoimmune

A

Hp-antibodies to h pylori

Autoimmune-antibodies to parietal cells (H, K-ATPase, IF)

284
Q

Associations h pylori vs autoimmune

A

Hp-peptic ulcer, adenocarcinoma, MALToma

Autoimmune0autoimmune disease, thyroiditis, DM, Graves’ disease

285
Q

Distribution h pylori vs autoimmune

A

Hp-multifocal, leaves patches of residual parietal and chief cells (hypochlorhydria)

Autoimmune-diffuse, knocks out all the parietal cells and alt he chief cells (achlorhydria)

286
Q

Autoimmune gastritis

A

Antibodies to parietal cells and IF leading to loss of gastrin and IF in serum and gastric acid secretions

287
Q

What is spared in autoimmune gastritis

A

Antrum

288
Q

Autoimmune gastritis is associated with hyper____

A

Gastrinemia

289
Q

Why get hypergastrinemia with autoimmune gastritis

A

Loss of negative feedback

290
Q

Symptoms of autoimmune gastritis

A

Antibodies to parietal cells and intrinsic factors detectable in serum and gastric secretions

Decreased serum pepsinogen I concentration—chief cells are collateral damage

B12 (cobalmin) defiency and associated megaloblastaic pernicious anemia
-also see hyper-segmented neutrophils

Defective gastric acid (achlorhydria)
-h pylori may cause hypochlorhydria, but not achlorhydria

291
Q

In autoimmune gastritis, __T cells destroy patietal cells, including H/K ATPase

A

CD4

292
Q

In autoimmune gastritis, what does loss of parietal cells result in

A

Loss of gastric acid (HCL and IF) production

293
Q

Chief cells and autoimmune gastritis

A

They are collateral damage

294
Q

Can you get repopulation in autoimmune gastritis

A

If immunosuppression is sufficient, gastric stem cells survive and differentiate

295
Q

Diagnosis autoimmune gastritis

A

Autoantibodies important but not pathogenic bc they cant access the target

296
Q

Morphology autoimmune gastritis

A

Diffuse atrophy

Rugal folds lost

Diffuse mucosal damage of oxyntic (acid producing) mucosa in the body and fundus, but there may be regions of oxyntic mucosa that is still intact that looks like polyps or nodules

  • inflammatory infiltrate of lymphocytes, macrophages, and plasma cells
  • CAN SEE THE BLOOD VESSELS BECASEU THE MUCOSA IS SO THIN
297
Q

What do we see with lost of rugal folds in autoimmune gastritis

A

Smooth appearance seen in autoimmune gastritis

298
Q

Are rugal folds lost in h pylori

A

Nope

299
Q

Presentation autoimmune gastritis

A

Early detection of autoantibodies to parietal cells and IF

Anemia in a few

20% of individuals with pernicious anemia have autoimmune gastritis, although may be asymptomatic

300
Q

Autoimmune gastritis progresses to __ _ over 20-30 years

A

Gastric atrophy

301
Q

Age of diagnosis of autoimmune gastritis

A

60

302
Q

Autoimmune gastritis is associated with _ defiency

A

B12

303
Q

Genetics autoimmune gastritis

A

Familial/genetic predisposition

-little evidence of linkage to specific HLA alleles

304
Q

What happens to the spinal cord with B12 defiency

A

Subacute degeneration!

305
Q

B12 defiency: spinal cord lesion

A

Demyelination of dorsal and lateral spinal tracts

306
Q

B12 defiency: peripheral neuropathy

A

Paresthesia and numbness

307
Q

B12 defiency cerebral dysfunction

A

Personality changes

308
Q

B12 defiency: cerebral dysfunction

A

Persaonality changes

309
Q

B12 defiency: memory

A

Memory loss to psychosis

310
Q

Are neurological symptoms reversed with b12 replacement therapy

A

Nope

311
Q

B12 defiency atrophic glossitis

A

Tongue becomes smooth and beefy red

312
Q

B12 megaloblastisis of RBC and epithelial cells (rarely: pernicious anemia)

A

Ok

313
Q

Diarrhea b12 defiency

A

Yup

314
Q

Eosinophilic gastritis

A

Heavy eosinophilic infiltration of mucosa and muscularis in the antral or pyloric region

315
Q

Eosinophilic gastritis has elevated ig_

A

E

316
Q

Eosinophilic gastritis

A

May be infectious, due to allergy to ingested material (cows milk and soy protein are the most common in children), systemic sclerosis (scleroderma), polymyositis, parasitic infections and H pylori

317
Q

Lymphocytic (varioliform) gastritis

A

Idiopathic, affecting females

318
Q

40% of lymphocytic (varioliform) gastritis cases are associated with __ __ (implies immune mediated pathogenesis)

A

Celiac disase

319
Q

Lymphocytic (varioform) gastritis has marked increase in the number of the intraepithelial DC_ T cells

A

8

320
Q

Morphology lymphocytic (varioliform) gastritis

A

Distinctive endoscopic appearance: thickened folds covered by small nodules with central aphthous ulceration

321
Q

What part of the stomach does lymphocytic (varioform) gastritis effect

A

Entire stomach

322
Q

Granulomatous gastritis

A

Any gastritis that contains well formed granulomas or aggregates of epithelioid macrophages

Many idiopathic

323
Q

Most common specific cause of granulomatous gastritis

A

Gastric involvement by Crohn’s disease

Also associated with sarcoidosis and infection (mycobacteria, fungi, CMV, H pylori)

324
Q

In granulomatous gastritis, what mar occur secondary to transmural granulomatous inflammation

A

Narrowing and rigidity of the gastric antrum

325
Q

Peptic ulcer disease

A

Chronic mucosal ulceration of the lesser curve of the stomach at junction of body and antrum (gastric peptic ulcers) or proximal duodenum

326
Q

What is peptic ulcer disease associated with

A

H pylori infection, NSAIDS< or cigarette smoking

Increased gastric acid secretion and decreased duodenal bicarbonate secretion

327
Q

Why has incidence of peptic ulcer disease decreased in developed countries

A

H pylori control

328
Q

New group of patients getting PUD??

A

Older than 60 years has emerged with PUD due to prolonged NSAID

329
Q

Pathogenesis peptic ulcer disease

A

Imbalance in mucosal defense mechanisms and damaging factors causing chronic gastritis

Decreased mucosal blood flow, oxygenation and healing

Develops on a background of chronic gastritis

330
Q

What is peptic ulcer disease associated

A

Cigarettes and CV

331
Q

Where are peptic ulcers most common

A

Proximal duodenum-usually solitary

332
Q

Morphology peptic ulcer disease

A

Sharply punched out defect with over hanging mucosal borders and smooth, clean ulcer bases
-HEAPED UP PERIPHERAL MARGINS==MALIGNANC

Vessel walls within the affected area are commonly thickened and sometimes thrombosed. Bleeding can lead to life threatening hemorrhage

333
Q

Does peptic ulcer disase transform to cancer

A

Not really

334
Q

If peptic ulcer does transform to cancer, what is the sign

A

Heaped up peripheral margins=malignancy

335
Q

Surrounding mucosa in peptic ulcer disease

A

Chronic gastritis, intestinal metaplasia develops in both forms of chronic gastritis and is a risk factor for gastric adenocarcinoma

336
Q

Clinical presentation peptic ulcer disease

A

Epigastric burning or aching pain, which is worse at night and 1-3 hours after meals since food buffers the acid

Nausea, vomiting, bloating, belching and weight loss often occur

337
Q

Pain of penetrating peptic ulcers may be referrred where

A

Back, LUQ or chest (misinterpret origin of pain)

338
Q

What causes relief of peptic ulcer disease

A

Milk, alkali agents or food

339
Q

Is peptic ulcer disease is perforation the first indication

A

No rarely the first indication

340
Q

Treat peptic ulcer disease

A

H pylori eradication, neutralization of acid via PPI

Discontinue NSAIDS

Surgery is relegated for bleeding or perforated peptic ulcers because antibiotics are so effective

341
Q

Mucosal atrophy and intestinal metaplasia

A

Long standing chronic gastritis of body and fundus leads to loss of parietal cell mass (oxyntic atrophy)

342
Q

How do we recognize mucosal atrophy and intestinal metaplasia

A

Presence of goblet cells

343
Q

Risk of mucosal atrophy and intestinal metaplasia

A

Risk of adenocarcinoma is greatest in autoimmune gastritis possibly because achlorhydria of gastric mucosal atrophy allows overgrowth go bacteria that produce nitrosamines

344
Q

Mucosal atrophy and metaplasia h pylori

A

Less commonly occurs in chronic h pylori gastritis, but regresses after clearance of organism

345
Q

Dysplasia

A

Pre invasive in situ lesion

Chronic gastritis exposes epithelium to inflammation related free radical damage and proliferate stimuli

346
Q

Pathogenesis dysplasia

A

Chronic gastritis leads to accumulation of genetic alterations-> pre invasive in situ lesions->carcinoma

347
Q

Morphology dysplasia

A

Variable epithelial size, shape and orientation with coarse chromatin texture, hyperchromasia and nuclear enlargement

Remain cytologically immature (vs regenerating epithelial cells which mature at surface)
-reactive epithelial cells mature as they reach the mucosal surface, while dysplastic lesions remain cytologically immature

348
Q

Gastritis cystica

A

Exuberant epithelial proliferation with entrapment of epithelium lined cysts

349
Q

Gastritis cystica submucosa

A

Gastritis cystica polyposa

350
Q

Gastritis cysticadeep layers of gastric wall

A

Gastritis cystica profunda

351
Q

What is gastritis cystica associated with

A

Chronic gastritis and partial gastrectomy

-presumed that gastritis cystica i trauma induced

352
Q

Gastritis cystica may mimic what

A

Invasive adenocarcinoma

-regenerative epithelial changes can be prominent the entrapped epithelium

353
Q

Hypertrophic gastropathies

A

Uncommon diseases characterized by giant cerebriform enlargement of the rugal folds due to epithelial hyperplasia without inflammation

Get excessive growth factor release

354
Q

Examples of hypertrophic gastropathies

A

Menetrier disease

Zollinger Ellison syndrome

355
Q

Menetrier disease

A

Rare, diffuse foveolar cell hyperplasia of the body and fundus

356
Q

Pathology menetrier disease

A

Protein losing enteropathy leads to systemic hypoproteinemia

Due to overexpression of TGFa

357
Q

Morphology menetrier disease

A

Irregular enlargement of gastric rugae in body and fundus

Hyperplasia of foveolar mucous cells

Glands are elongated with a corkscrew like appearance with cystic dilation

Only modest inflammation

Diffuse patchy hypoplasia of parietal and chief cells is common

358
Q

Menetrier disease presentation

A

Weight loss, diarrhea, peripheral edema (hypoproteinemia)

359
Q

Menetrier disease kids

A

Self limiting

Ofte follows a respiratory infection in children

360
Q

Adults with menetrier disease have an increased risk of what

A

Increased risk of gastric adenocarcinoma in adults

361
Q

Treat menetrier disease

A

IV albumin+parenteral nutrition (supportive)

TGFa blocking agents show promise

Severe:gastrctomy

362
Q

Zollinger Ellison

A

Rare gastrinoma (gastrin secreting tumors) of the small intestine or pancreas

363
Q

Increased gastrin levels in zollinger ellison

A

Proliferation of gastric parietal cells (up to 5x)

364
Q

In zollinger ellison, there is hyperplasia of what

A

Mucus and neck cells

365
Q

In zollinger ellison there is __ hyperproduction

A

Mucin

366
Q

Characterization zollinger ellison

A

Doubling of the oxyntic mucosal thickness due to

  • a fivefold increase in the number of parietal cells
  • hyperplasia of mucous neck cells
  • mucin hyperproduction-proliferation of endocrine cells within oxyntic mucosa
367
Q

Presentation of zollinger ellison

A

Duodenal ulcers (excess aid production) and/or chronic diarrhea

368
Q

Zollinger ellison increased risk of

A

Proliferation of gastric endocrine cells (may form small nodules or true carcinoid tumors)

369
Q

Treat zollinger ellison

A

Block hypersecretion of acid via PPI

Allows peptic ulcers to heal

Prevents gastric perforation

Then begins to focus on the tumor, the main determinant of long term survival

370
Q

Gastrinomas-what percent malignant

A

60-90% though slow growing

371
Q

Gastrinomas-what percent sporadic

A

75%

372
Q

Gastrinomas: what percent have MEN I (multiple endocrine neoplasia) aka warmer syndrome

A

25%

373
Q

Treat gastrinomas

A

Somatostatin analogues

374
Q

Menetrier disease-age, location, predominent cell, inflammatory infiltrate, signs and symptoms, risk factors, malignant transformation

A

30-69

Body and fundus

Mucosa

Limited, lymphocytic

Hypoproteinemia, weight loss, diarrhea, peripheral edema

None

Yes

375
Q

Zollinger ellison - age, location, predominant cell, inflammatory infiltrate, sign and symptoms, risk factors, malignant transformation

A

50

Fundus

Parietal cells > mucous, endocrine

Neutrophilic

Peptic ulcers (duodenal)

MEN 1

No

376
Q

Inflammatory and hyperplastic polyps-age, location, predominant cell, inflammatory infiltrate, signs and symptoms, risk factors, malignant transformation

A

50-60

Antrum>body

Mucous

Neutrophils and lymphocytes

Similar to chronic gastritis

Chronic gastritis, H pylori

Occasional

377
Q

Gastrica cystica - age, location, predominent cell, inflammatory infiltrate, signs and symptoms , risk factors, malignant transformation to adenocarcinoma

A

Variable

Body

Mucous, cyst-lining

Neutrophils and lymphocytes

Similar to chronic gastritis

Trauma, prior surgery

No

378
Q

Fundus gland polyps-age, location, predominent cell, inflammatory infiltrate, signs and symptoms, risk factors, malignant transformation to adenocarcinoma

A

50

Body and fundus

Parietal and chief

None

None, nausea

PPIs, FAP

Syndromic (FAP)

379
Q

Gastric adenomas-age, location, predominent cell, inflammatory infiltrate, signs and symptoms, risk factors, malignant transformation to adenocarcinomas

A

50-60

Antrum>body

Dysplastic intestinal

Variable

Similar to chronic gastritis

Chronic gastritis, atrophy, intestinal metaplasia

Frequent

380
Q

What is the most common gastric polyp and tumor

A

Hyperplastic (inflammatory) polyp

75% of all gastric polyps

381
Q

What are hyperplastic (inflammatory ) polyps associated with

A

Chronic gastritis (indicated the injury that leads to reactive hyperplasia and polyp growth)

382
Q

Who gets hyperplastic polyps

A

50-60

383
Q

In hyperplastic polyps, dysplasia is correlated with what

A

Polyp size

384
Q

Morphology hyperplastic polyps

A

Multiple
Ovoid in shape with a smooth surface, though there may be superficial erosions/ulceration

Irregular, dilated, elongated foveolar glands

Lamina proporia is edematous with variable acute/chronic inflammation

385
Q

Fundic gland polyps

A

Polyps that develop in the gastric body and fundus , can be single or multiple

386
Q

Why get fundic gland polyps

A

Sporadically and in individuals with familial adenomatous polyposis (FAP)

387
Q

Fundic gland polyps have increasaed incidence associated with what

A

With increased PPI use

388
Q

Why do PPI cause fundic gland polyps

A

PPI inhibit acid production->increased gastrin secretion->tropic effect of oxyntic glands

389
Q

Presentation of fundic gland polyps

A

Asymptomatic OR nausea, vomiting or epigastric pain

390
Q

Morphology fundic gland polyps

A

Well circumscribed lesions with a smooth surface

Cystically dilated, irregular glands lined by flattened parietal and chief cells

Inflammation absent or minimal

391
Q

Genetic fundic gland polyps

A

FAP mutation

392
Q

Cancer risk of sporadic fundic gland polyps

A

Sporadic fundic polyps carry zero cancer risk

393
Q

Cancer risk familial adenomatous polyposis (FAP) associated polyps

A

Dysplasia and cancer can follow

394
Q

Gastric adenoma represent _% of gastric polyps

A

10

395
Q

What are gastric adenoma associated with

A

FAP and chronic gastritis with atrophy and intestinal metaplasia (gastric adenomas are pre malignant neoplastic lesions)

396
Q

Gastric adenoma risk of transformation

A

Risk of transformation to invasive cancer is much higher in gastric adenomas than intestinal adenomas

397
Q

Males or females gastric adenoma

A

Males 3:1

398
Q

Who gets gastric adenoma

A

50-60

399
Q

Gastric adenoma single or multiple

A

Solitary

400
Q

Where are gastric adenomas

A

<2cm, if greater be concerned

Antrum

401
Q

Morphology gastric adenomas

A

Some degree of dysplasia of the intestinal type columnar epithelium

Enlargement, elongation, pseudostratification, hyperchormasia of nuclei, epithelial crowding

High grade: more atypia, glandular budding, gland within gland, or cribiform structures

402
Q

Most common malignant of the stomach 905

A

Gastric adenocarcinoma

403
Q

Where are gastric adenocarcinoma

A

Antrum

404
Q

Who gets gastric adenocarcinoma

A

Japan, china, Costa Rica, Eastern Europe

405
Q

Where should we use mass endoscopic screening for gastric adenocarcinoma

A

Effective in areas where incidence is high

Not cost effective in areas where incidence is low

406
Q

Socioeconomic status and gastric adenocarcinoma

A

Most common in lower socioeconomic groups and individuals with multifocal mucosal atrophy and intestinal metaplasia—gastric dysplasia and adenomas are recognizable precursor lesion associated with gastric adenocarcinoma

407
Q

Environmental factors gastric adenocarcinoma

A

H pylori cause of overall reduction in gastric cancer is most closely linked to decrease in h pylori prevelance

408
Q

Dietary factors and gastric adenocarcinoma

A

Gastric cancer rates in second generation immigrants similar to those in their new country of residence

Nitroso compounds, benzoapyrene=increased

Antioxidants of fruit/vegetables, leafy greens=decreased

Partial gastrectomy (for PUD) allows bile reflux and development of chronic gastritis

409
Q

Gastric adenocarcinoma precursor lesion

A

Gastric dysplasia and adenomas

410
Q

Why is overall incidence of adenocarcinoma falling

A

Likely due to barrett esophagus , reflecting increased GERD and obesity

-gastric cardia cancer on the rise

411
Q

Genetics gastric adenocarcinoma

A

TP53 mutation in both diffuse and intestinal gastric cancers

412
Q

Metastases of gastric adenocarcinoma goes to where

A
  • left supraclavicular sentinel lymph node (virchow node)
  • periumbilical lymph nodes (sister Mary Joseph nodule)
  • left axillary lymph node (Irish node)
  • ovary (krukenberg tumor)
  • pouch of Douglas (blunder shelf)
413
Q

Diffuse type gastric adenocarcinoma

A

Infiltrates the wall diffuses, thickens it and is typically composed of signet ring cells

414
Q

Genetics diffuse gastric adenocarcinomas

A

CDH1(tumor suppressor gene that encodes E cadherin) mutation, BRCA1

-loss of e cadherin is a key step in the development of diffuse gastric cancer

415
Q

Diffuse type gastric adenocarcinoma morphology

A
  • signet ring cells that are discohesive and do not form glands-discohesive as a result of loss of e cadherin
  • large intracellular mucin vacuoles that push nucleus to the periphery=signet ring
  • induce fibrous desmoplastic response
  • no identified precursor lesion
  • linitis plastica (leather bottle): appearance when there are large areas of infiltration, diffuse rugal flattening, and a rigid , thickened wall
416
Q

Diffuse type gastric adenocarcinomas: epidemiology

A

Occurs uniformly across the globe

No gender preference

417
Q

Clinical diffuse type gastric adenocarcinoma

A
  • incidence is uniform across countries
  • no identified precursor lesions
  • no gender preference
  • early satiety=gastric wall cant expand
418
Q

Intestinal type gastric adenocarcinoma

A

Forms bulky masses

419
Q

Intestinal type gastric adenocarcinoma genetics

A

Increased Wnt signaling

Loss of function mutations: APC, TGFb, BAX, CDKN2A (tumour suppressor genes…FAP patients carry germline APC mutations->increased risk of intestinal type gastric cancer)

-gain of function B catenin

Genetic variants of pro inflammatory and immune response genes, including those that encode IL-1B, TNF, IL10, IL8, and TLR4 are associated with elevated risk of gastric cancer when accompanied by H pylori infection (chronic inflammation accompanies gastric neoplasia)

420
Q

Morphology intestinal type gastric adenocarcinoma

A

Tend to grow along broad cohesive fronts to form either an exophytic mass of an ulcerated tumor

Apical mucin vacuoles, abundant mucin may be present in gland lumina

Develop from precursor lesions including flat dysplasia and adenomas

421
Q

Epidiomiology intestinal type gastric adenocarcinoma

A

55 years
Males 2:1
Occurs mostly in high risk areas

Decrease in gastric cancer incidence applies only to the intestinal type because intestinal type is more closely associated with atrophic gastritis and intestinal metaplasia

422
Q

Clinical gastric adenocarcinoma

A

Early signs and symptoms resemble chronic gastritis and PUD

Dyspepsia, dysphagia, nausea

Often discovered locate with weight loss, anorexia, early satiety, anemia, and hemorrhage

423
Q

Prognosis gastric adenocarcinoma

A

Depth of invasion and extend of nodal and distant metastases at time of diagnosis==most important

Local invasion of duodenum, pancreas and retoperitoneum

Metastases to virchow node , periumbilical nodes, axillary nodes, or pouch of Douglas

424
Q

Treatment gastric adenocarcinoma

A

Surgical resection remains preferred

425
Q

Survival gastric adenocarcinoma (local lymph node metastases)

A

5 year survival >90% even with lymph node metastases

426
Q

Survival gastric adenocarcinoma (advanced)

A

<20% 5 year survival

427
Q

Overall survival gastric adenocarcinoma

A

30% 5 year survival

428
Q

Why is prognosis for gastric adenocarcinoma not great

A

Advanced stage that most gastric cancers are discovered

429
Q

MALToma

A

Extranodal lymphoma that arises anywhere in the GI tract, but espicially in the stomach

430
Q

What is the most common site of extranodal lymphoma

A

Stomach

431
Q

What is the msot common site of EBV-positive B cell lymphoproliferations in allergenic hematopoietic stem cell and organ transplant recipients

A

Bowel

432
Q

What percent of gastric malignancies are primary lymphomas

A

5

433
Q

Induction of MALToma

A

Induced as a result of chronic inflammation (chronic gastritis: H pylori)

434
Q

Most commonly raised sites of MALToma

A

Arises in sites normally devoid of organized lymphoid tissue

435
Q

Induction of stomach MALT

A

Result of chronic gastritis

436
Q

Most common induction of MALToma in stomach

A

H pylori most common inducer in the stomach

437
Q

H pylori eradication results in durable remission with low rates of recurrence for MALToma. How treat h pylori

A

Combination antibiotic therapy results in long term remission—treat the underlying condition and cure the cancer

438
Q

Peters patches MALToma

A

May also occur in areas of preexisting malt (Peyers patches)

439
Q

Antibiotics MALToma

A

Induces tumor regression

440
Q

Recurrence rate MALToma

A

Low rate of recurrence

441
Q

Genetics MALToma-what are the three translocations?

A

T(11;18)(q21;q21) most common

T(1;4)(p22;q32)

T(14;18)(q32;q21)

Also h pylori can activate MLT/BCL10 pathway in MALTomas that lack these translocations

442
Q

What do the translocations of MALTomas cause

A

Constitutive activation of NFKB-> B cell growth and proliferation

443
Q

T(11;18)(q21;q21)

A

API2 (apoptosis inhibitor)-MLT (mutated in MALT lymphoma) fusion protein

444
Q

T(1;4)(p22;q32)

A

Increased BCL-10

445
Q

T(14;18)(q32;q21)

A

Increased expression of intact MALT1

446
Q

Prognosis MALToma

A

Failure to eradicate leads to invasion of muscularis proporia and lymph node involvement

May transform to more aggressive diffuse, large B cell lymphomas

Associated with p53+/p16 mutations which makes them unresponsive to H pylori eradication

447
Q

Morphology MALTomas

A

Dense infiltrate of atypical lymphocytes in lamina proporia

Neoplastic lymphocytes infiltrate the gastric glands vocally to create lymphoepithelial lesion (diagnostic)

May have B cell follicles or plasmacytic differentiation

Express CD19, 20-B cell markers

25% CD43+ve-unusual feature that may be diagnostic

Monoclonality may be demonstrated by restricted expression of either kappa or gamma light chains

448
Q

Presentation MALToma

A

Dyspepsia+epigastric pain

Possible hematemesis, melena and constitutional signs and symptoms (weight loss)

449
Q

MALToma may be difficult to distinguish from

A

H pylori gastritis

450
Q

H pylori gastric and MALTOma may __

A

Coexist or have overlapping signs and symptoms and appearances on endoscopy

451
Q

Treat MALToma

A

Combination antibiotic therapy results in long term remission

452
Q

Carcinoid tumor (well differentiated neruoendocrine tumors)

A

More indolent course than a GI carcinoma

453
Q

What are carcinoid tumors associated with

A

Endocrine cell hyperplasia, autoimmune chronic atrophic gastritis, MEN-I and zollinger ellison syndrome

  • gastric endocrine cell hyperplasia has been linked to proton pump inhibitor therapy
  • progression to a neuroendocrine neoplasm is extremely low
454
Q

Where are carcinoid tumor

A

40% in the small intestine

Tracheobronchial tree and lungs-2nd most common

455
Q

Carcinoid tumor morphology

A

Yellow-tan intramural or submucosal masses that create smal polypoid lesions
-typically arise within oxyntic mucosa when in the stomach

Firm due to intense desmoplastic response which can cause bowel obstruction

Range from islands to sheets of uniform cohesive cells with scant granular cytoplasm

Oval, stippled nuclei

456
Q

Carcinoid tumors are are + for what

A

Neuroendocrine markers

457
Q

When does carcinoid tumor present

A

Peak incidence in 6th decade

458
Q

Signs and symptoms carcinoid tumors

A

Based on type of hormone being produced

459
Q

Prognosis carcinoid tumor

A

Based on location

460
Q

Prognosis foregut carcinoid tumor

A

Rarely metastasize and are generally cured by resection

461
Q

Carcinoid midgut prognosis

A

Multiple and tend to be aggressive

462
Q

Hindgut carcinoid prognosis

A

Almost always benign

463
Q

Stomach -prevelance, secretory products, signs and symptoms, behavior, associations

A

<10%

Histamine, somatostatin, serotonin

Gastritis and ulcers

Variable

Atrophic gastritis, MEN-1

464
Q

Proximal duodenum-prevelance, secretory products, signs and symptoms, behavior , associations

A

<10%

Gastrin, somatostatin, CCK
Peptic ulcers, biliary obstruction, abdominal pain

Variable

Zollinger ellison syndrome , NF-1

465
Q

Jejunum and ileum -prevelance, secretory products, signs and symptoms , behavior,associations

A

> 40%

Serotonin, substance P, polypeptide YY

Obstruction, metastatic disease

Aggressive

466
Q

Appendix-prevelance, secretory products,signs and symptoms, behavior, associations

A

<25%

Serotonin, polypeptide YY

Asymptomatic

Benign

467
Q

Colorectal -prevelance, secretory products, signs and symptoms, behavior, associations

A

<25%

Serotonin, polypeptide YY

Abdominal pain, weight loss

Variable

468
Q

Carcinoid syndrome

A

Ileal tumors that lead to cutaneous flushing+sweating
Bronchospasm
Diarrhea+colicky abdominal pain
Right sided cardiac valvular fibrosis
Due to vasoactive secretion of 5HT into systemic circulation
Associated with metastatic liver disease
Intestinal tumors that produce vasoactive substances have significant ‘first pass’ effect
—-no first pass if liver is burdened with disease

469
Q

Gastrointestinal stromal tumor

A

Most common mesenchymal tumor of the abdomen

Mesenchymal tumor that arises from intestitial cells of cajal (pacemaker cells for gut peristalsis) or the GI muscularis propria

470
Q

Where do gastrointestinal stromal tumor

A

1/2 in stomach

471
Q

Precursor lesions gastrointestinal stromal tumor

A

Clinically silent with low mitosis index, lack pleomorphism

472
Q

Age of gastrointestinal stromal tumor

A

60 years

473
Q

Kids gastrointestinal stromal tumor

A

Carney triad (non hereditary syndrome of unknown etiology seen primary in young females that includes GIST, paraganglioma, and pulmonary chondroma)

474
Q

Increased risk of gastrointestinal stromal tumors in who

A

Increased risk in patients with NF1

475
Q

GIST genetics

A

KIT tyrosine kinase gain of function 80%

PDGFRA activating mutation 8%(overexpressed in stomach)

Deletion of chromosome 9p (CDKN2A), 14, and 22

Alterations in chromosome #

Mitochondrial succinate dehydrogenase complex (SDH-A, SDH-B, SDH-C, SDH-D) mutation

  • loss of function of SDH inherited germline
  • Carey-stratakis syndrome :increased for GIST and paraganglioma
476
Q

Mutation of _ or _ (mutually exclusive) is an early even in sporadic GIST

A

KIT

PDGFRA

477
Q

Morphology GIST

A

Solitary, well-circumscribed fleshy masses

Cut surface shows whorled appearance

Epithelioid: epithelial appearing cells

Spindle type:the elongated cells

478
Q

Diagnostic markers for GIST

A

KIT in interstitial cells of cajal and 95% of gastric GIST

479
Q

Clinical GIST

A

Signs and symptoms related to mass effects or blood loss (anemia)

480
Q

Treat GIST

A

Surgical resection

481
Q

KIT, PDGFRA GIST treat

A

Imatinib treatment (resistance due to secondary mutations)

482
Q

What determines prognosis GIST

A

Tumor size, mitosis index, location

483
Q

Gastric GIST are _ aggressive than intestinal GIST

A

Less

484
Q

Recurrence is _ for GIST smaller than 5 cm but ___ for mitotically active tumors larger than 10 cm

A

Rare

Common

Pathology (36 decks)

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