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► Med Notes > Gastrointestinal Pathology_1 > Flashcards

Gastrointestinal Pathology_1 Flashcards

1
Q

What is dysphagia?

A

difficulty in swallowing

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2
Q

what causes dysphagia?

A

diseases that narrow or obstruct the lumen

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3
Q

what causes pain and hematemesis?

A

inflammation or ulceration of the esophageal mucosa

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4
Q

what is heartburn?

A

retrosternal burning pain

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5
Q

what causes heartburn?

A

regurgitation of gastric contents

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6
Q

what is the most frequent GI complaint?

A

gas

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7
Q

what are esophageal sinuses?

A

blind tubes

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8
Q

what are esophageal fistulas?

A

tunnels

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9
Q

what is an esophageal perforation?

A

hollow viscous open up into hollow cavity (usually peritoneal cavity)

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10
Q

what are the 2 types of esophageal herniations?

A

internal or external

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11
Q

what is the most common anemia of GI bleeding?

A

IDA

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12
Q

what are the disorders of the esophagus?

A
  1. dysphagia • 2. pain and hematemesis • 3. heartburn • 4. gas • 5. inflammation and ulcers • 6. sinuses • 7. fistulas • 8. perforation • 9. herniation • 10. bleeding • 11. tumors
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13
Q

what are the important structures in the esophagus?

A
  1. UES= Upper Esophageal Sphincter • 2. LES= Lower Esophageal Sphincter
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14
Q

UES is made up of what?

A

skeletal muscle • - cricopharyngeus muscle

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15
Q

which esophageal structure is involved in scleroderma?

A

UES

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16
Q

where does the LES open up?

A

into the stomach

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17
Q

what size is the gastro-esophageal junction?

A

3 cm

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18
Q

what is a gastro-esophageal junction >3 cm called?

A

Barrett’s esophagus

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19
Q

what is the cell type of the LES transitional zone?

A

columnar

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20
Q

what do congenital anomalies of the esophagus do?

A

produce choking on breast feeding

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21
Q

what are the congenital anomalies of the esophagus?

A

atresia • fistulas • webs • Schatzki’s rings • Stenosis

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22
Q

what is esophageal atresia?

A

noncanalzed segment

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23
Q

what are esophageal fistulas?

A

connection/opening between esophagus trachea • - several types

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24
Q

how do esophageal webs present?

A

dysphagia to solids

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25
Q

what are the clinical features of Plummer-Vinson/Paterson-Kelly syndrome?

A

post cricoid web • IDA • glossitis • cheilosis in perimenopausal female • risk of postcricoid squamous cell carcinoma

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26
Q

What is a type I Tracheoesophageal fistula?

A

Esophageal agenesis. Very rare

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27
Q

What is a type A/2 TEF?

A

Proximal and distal esophageal bud- a normal esophagus with a missing mid-segment

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28
Q

what is a type B/3A TEF?

A

Proximal esophageal termination on the lower trachea with distal esophageal bud

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29
Q

what is a type C/3B TEF?

A

proximal esophageal atresia (esophagus continuous with the mouth ending in a blind loop superior to the sternal angle) with a distal esophagus arising from the lower trachea or carina

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30
Q

what is the most common type of TEF?

A

Type C/3B

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31
Q

what is a type D/3C TEF?

A

proximal esophageal termination on the lower trachea or carina with distal esophagus arising from the carina

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32
Q

what is a type E TEF?

A

a variant of type D: if the 2 segments of the esophagus communicate, this is sometimes termed an H type fistula due to its resemblance of to the letter H.

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33
Q

which fistula is TEF without EA?

A

Type E/H

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34
Q

where do Schatzki’s rings present?

A

LES

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35
Q

what do Schatzki’s rings cause?

A

narrowing (stenosis) of esophagus

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36
Q

what is the most common cause of esophageal stenosis?

A

gastro-esophageal reflux

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37
Q

is esophageal stenosis more commonly inherited or acquired?

A

acquired (corrosives, radiation, Scleroderma CREST syndrome)

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38
Q

what is the major symptoms associated with esophageal stenosis?

A

dysphagia

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39
Q

what are the esophageal lesions with motor dysfunction?

A

Achalasia cardia • Hiatal Hernia • True Diverticula • Zenker’s (pharyngeal diverticulum) • Epiphrenic diverticulum

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40
Q

what age group is affected by achalasia cardia?

A

adults

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41
Q

what is the nature of achalasia cardia?

A

‘failure to relax’

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42
Q

what are the clinical features of achalasia cardia?

A
  1. aperistalsis • 2. complete or partial relaxation of LES with swallowing • 3. Increased resting tone of LES
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43
Q

what are the complications associated with achalasia cardia?

A
  • aspiration pneumonia • - candidal esophagitis (due to stagnation of food) • - diverticulae • - squamous cell carcinoma (2-5%)
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44
Q

achalasia cardia can also be caused by what?

A

Chaga’s disease (Trypanosoma cruzi) • Diabetic autonomic neuropathy

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45
Q

what is Hiatal Hernia?

A

Upward protrusion of part of stomach through the diaphragmatic esophageal foramen

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46
Q

what is a true diverticulum?

A

out-pouching of the esophageal wall (contains all visceral layers)

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47
Q

what is a false diverticulum?

A

out-pouching of mucosa and submucosa only

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48
Q

Zenker’s (pharyngeal) diverticulum is seen as what?

A

mass in neck of elderly patient above UES

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49
Q

Zenker’s diverticulum is due to what?

A

disordered cricopharyngeal motor dysfunction

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50
Q

Zenker’s diverticula produce what problems?

A

food regurgitation and dysphagia

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51
Q

what are the features of traction diverticulum?

A

asymptomatic and located near midpoint of esophagus

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52
Q

where is an epiphrenic diverticulum located?

A

just above the LES

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53
Q

epiphrenic diverticulum is caused by what?

A

dyscoordinated peristalsis and motor dysfuction of LES

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54
Q

epiphrenic diverticulum causes what?

A

regurgitation of food and aspiration pneumonia

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55
Q

what is the most common TEF?

A

C

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56
Q

what is the most life threatening TEF?

A

B: • cough, sputter, suffocate

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57
Q

TEF are associated with what?

A

heart and other GIT anomalies

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58
Q

90% of hiatal hernias are which type?

A

sliding

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59
Q

10% of hiatal hernias are which type?

A

rolling

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60
Q

what are the features of sliding hiatal hernia?

A

shortened esophagus dragging part of the stomach into the thoracic cavity (stomach continuous with the esophagus)

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61
Q

what are the features of rolling hiatal hernia?

A

(para-esophageal hernia) • - part of the stomach (fundus) herniates alongside esophagus into the thorax

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62
Q

which hiatal hernia is vulnerable to serious strangulation?

A

rolling

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63
Q

hiatal hernias are prone to what?

A

ulceration • bleeding • dysphagia

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64
Q

what is the site of Mallory-Weiss syndrome?

A

gastro-esophageal junction (GEJ)

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65
Q

what is Mallory-Weiss syndrome caused by?

A

excessive vomiting in the presence of LES spasm

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66
Q

when is Mallory-Weiss syndrome most common?

A

alcoholics and pregnancy

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67
Q

what is the morphology of Mallory-Weiss syndrome?

A

irregular longitudinal tear in the GEJ involve only the mucosa

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68
Q

what is the morphological difference between Boerhaave’s syndrome and Mallory-Weiss syndrome?

A

in Boerhaave’s tear penetrates all layers of esophagus

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69
Q

what is the clinical presentation of Mallory Weiss tear?

A

severe hematemesis

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70
Q

what is the clinical presentation of Boerhaave’s syndrome?

A

produces mediastinitis or peritonitis

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71
Q

what are esophageal varices?

A

dilated tortuous submucosal veins

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72
Q

when are esophageal varices seen?

A

long-standing cirrhosis with portal HTN

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73
Q

how many patients with cirrhosis bleed and die of varices?

A

50% • MCC of death

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74
Q

what are the causes of esophagitis?

A
  1. reflux of gastric contents • 2. Barrett’s esophagus
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75
Q

what is the most common cause of esophagitis?

A

reflux esophagitis

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76
Q

what part of the esophagus is affected by reflux esophagitis?

A

distal part

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77
Q

what is the clinical presentation of reflux esophagitis?

A

dysphagia • heartburn • regurgitation • develop Barrett’s esophagus in long standing cases

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78
Q

Barrett’s esophagus is a complication of what?

A

long-standing gastroesophageal reflux

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79
Q

what is Barrett’s esophagus?

A

columnar metaplasia of distal esophagus

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80
Q

what is the cancer risk associated with Barrett’s?

A

30 times more risk of adenocarcinoma in the lower esophagus

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81
Q

what is the histological presentation of Barrett’s esophagus?

A

gastric type mucosa above the gastroesophageal junction

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82
Q

metaplasia in Barrett’s results from what?

A

chronic GERD

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83
Q

what is typical barrett’s mucosa?

A

gastric mucosa with intestinalization • - goblet cells in columnar mucosa

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84
Q

what is the most common benign tumor of esophagus?

A

leiomyoma

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85
Q

from what does esophageal leiomyoma arise?

A

smooth muscle cells

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86
Q

what is the incidence of squamous cell carcinoma of the esophagus?

A

common in China • Rare in US (Adenocarcinoma- MC in USA) • M>F • >50yo

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87
Q

what are the risk factors for esophageal squamous cell carcinoma?

A

cigarette smoking • alcohol • nitrosamines in preserved foods • fungus contaminated foods

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88
Q

what is the site of squamous cell carcinoma of the esophagus?

A

50% are in the middle 1/3

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89
Q

what is early carcinoma in SCC of esophagus?

A

up to submucosa

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90
Q

what is the prognosis for early carcinoma in SCC of esophagus?

A

5 yr= 90% even with lymph node involvement

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91
Q

to where does esophageal SCC spread?

A

locally into mediastinal structures and to lymph nodes

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92
Q

what are the clinical features of esophageal SCC?

A

insidious dysphagia • weight loss • hemorrhage • esophago-tracheal fistula

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93
Q

what is the overall survival for SCC of esophagus?

A

5 yr=5%

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94
Q

what is the incidence of esophageal adenocarcinoma?

A

<25% of esophageal cancers world wide • ** up to 50% of esophageal cancer in USA

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95
Q

what is the primary risk factor for esophageal adenocarcinoma?

A

Barrett’s esophagus

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96
Q

what is site of esophageal adenocarcinoma?

A

most arise in the distal 1/3rd of the esophagus

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97
Q

what is the histology of esophageal adenocarcinoma?

A

mucin producing tubular (intestinal), or signet cell/ring (gastric/infiltrative) carcinoma, undifferentiated

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98
Q

how does esophageal adenocarcinoma present?

A

dysphagia

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99
Q

what is the overall survival of esophageal adenocarcinoma?

A

15%

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100
Q

what is the typical morphology of esophageal SCC?

A

irregular reddish, ulcerated, exophytic • MC in midesophageal mass seen on mucosal surface

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101
Q

what is the typical histological presentation of esophageal SCC?

A

NAME?

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102
Q

what is the incidence of the malignant esophageal tumors?

A

squamous= 75% • adenocarcinoma=25%

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103
Q

what are the geographic regions most commonly associated with the malignant esophageal tumors?

A

Squamous= asia • adeno= usa

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104
Q

what is the age group MC affected by the malignant esophageal tumors?

A

squamous >50yo • adeno >40yo

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105
Q

what are the sites of the malignant tumors of the esophagus?

A

squamous= middle 1/3 • adeno= lower 1/3

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106
Q

what are the risk factors associated with the malignant tumors of the esophagus?

A

SCC- smoking, EtOH, foods • adeno- Reflux esophagitis (Barrett’s)

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107
Q

what is the prognosis for the malignant tumors of the esophagus?

A

SCC= 5yr= 5% • adeno= 5yr= 15%

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108
Q

What are the cells associated with stomach glands and where are they found?

A
  • parietal cells found in the fundus and body • - chief cells are more at fundus and body
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109
Q

what do stomach parietal cells secrete?

A

HCl and IF

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110
Q

what do stomach chief cells secrete?

A

pepsinogen I and II

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111
Q

what are the congenital abnormalities of the stomach?

A
  1. diaphragmatic hernia • 2. congenital hypertrophic pyloric stenosis
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112
Q

what causes diaphragmatic hernia?

A

defect in the diaphragm–> away from the hiatal orifice

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113
Q

what herniates in a diaphragmatic hernia?

A

portions of the stomach and small intestines

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114
Q

diaphragmatic hernia results in what?

A

respiratory impairment • pulmonary hypoplasia

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115
Q

what is the problem in congenital hypertrophic pyloric stenosis?

A

hypertrophy of the circular muscle of the pylorus results in regurgitation and vomiting in the neonatal period

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116
Q

what is the classic PE finding in congenital hypertrophic pyloric stenosis?

A

VGP= visible gastric peristalsis • + • palpable mass in the epigastrium

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117
Q

what is the inheritance of congenital hypertrophic pyloric stenosis?

A

males • multifactorial inheritance

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118
Q

what is the treatment for congenital hypertrophic pyloric stenosis?

A

full thickness muscle splitting incision (pyloromyotomy) is curative (Heller’s operation)

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119
Q

what is acute gastritis?

A

inflammation of gastric mucosa

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120
Q

what cells are associated with acute gastritis?

A

presence of neutrophils

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121
Q

what cells are associated with chronic gastritis?

A

lymphocytes and plasma cells

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122
Q

what is acute gastritis caused by?

A

ingestion of strong acids or alkalies, • NSAIDs, • cancer chemotherapy, • irradiation, • alcohol, • uremia, • severe stress and shock states

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123
Q

what are the proposed mechanisms of acute gastritis?

A

increased acid production with decreased surface bicarb buffer

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124
Q

what is the morphology associated with acute gastritis?

A

mucosal edema • hyperemia • PML infiltration • erosions (not deeper than muscularis mucosa) • hemorrhages

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125
Q

how deep do erosions in acute gastritis penetrate?

A

not deeper than muscularis mucosa

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126
Q

what is the histologic presentation of acute gastritis?

A

gastric mucosa infiltration by neutrophils

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127
Q

what is the gross morphologic presentation of acute gastritis?

A

diffusely hyperemic gastric mucosa

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128
Q

what are the common causes for acute gastritis?

A

alcoholism • drugs • infections etc

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129
Q

what is chronic gastritis?

A

chronic mucosal inflammation leading to mucosal atrophy, intestinal metaplasia, and dysplasia

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130
Q

what is the MCC of chronic gastritis?

A

chronic infection by H. pylori

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131
Q

what is the mechanism of chronic gastritis caused by H. pylori?

A

elaboration of urease produces ammonia that buffers gastric acid, protecting organism from acid

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132
Q

what are the other diseases (besides chronic gastritis) associated with H. pylori infection?

A

peptic ulcer disease • gastric carcinoma • gastric lymphoma

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133
Q

what causes 10% of chronic gastritis?

A

autoimmunity: • Ab to parietal cells cause parietal cell destruction (HCl +IF)

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134
Q

what is the histological presentation of H. pylori that causes chronic gastritis?

A

NAME?

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135
Q

how is H pylori in chronic gastritis visualized?

A

stain with methylene blue

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136
Q

what is the problem associated with autoimmune gastritis?

A

pernicious anemia

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137
Q

chronic atrophic gastritis is associated with antibodies against what?

A

IF • parietal cell

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138
Q

what is a gastric ulcer?

A

a breach in mucosa and extends through muscularis mucosae into submucosa or deeper

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139
Q

what is acute erosive gastritis?

A

erosions above the muscularis mucosa

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140
Q

acute gastric ulcers are caused by what?

A

severe stress • shock/extensive burns • severe head injury • patients in ICU

141
Q

what is the name for acute erosive gastritis caused by severe stress?

A

stress uclers

142
Q

what is the name for acute erosive gastritis caused by shock, extensive burns?

A

Curling’s ulcers

143
Q

what is the name for acute erosive gastritis caused by severe head injuries?

A

Cushing’s ulcers

144
Q

what is the cause of acute erosive gastritis in patients in ICU?

A

use of NSAIDs

145
Q

what is the morphology of acute gastric ulcers?

A

multiple, small (<1cm ulcers) normal adjacent mucosa

146
Q

what is the clinical presentation of acute gastric ulcers?

A

upper GIT hemorrhage

147
Q

what is the Tx for acute gastric ulcers?

A

treat underlying cause

148
Q

what do stress ulcers look like?

A

small, shallow gastric ulcerations

149
Q

chronic peptic ulcers are characterized by what?

A

solitary, chronic ulcers

150
Q

what is the ratio of duodenal to gastric chronic peptic ulcers?

A

4:01

151
Q

what is the more common chronic peptic ulcer?

A

duodenal

152
Q

what is the morphology of chronic peptic ulcer?

A

sharply punched out mucosal defect with sharp borders and clean ulcer base • - surrounding mucosa shows chronic gastritis & radial convergence of rugal folds towards the ulcer niche (unlike malignant ulcer)

153
Q

how do chronic peptic ulcers present clinically?

A

epigastric pain 1-3h after meals and worse at night; nausea; vomiting; belching; occult blood in the stool

154
Q

what are the complications of chronic peptic ulcers?

A

perforation • hemorrhage • obstruction • malignant transformation

155
Q

perforation accounts for how many ulcer deaths?

A

03-Feb

156
Q

hemorrhage accounts for how many ulcer death?

A

25%

157
Q

what does obstruction caused by peptic ulcer cause?

A

severe crampy abdominal pain

158
Q

how common is malignant transformation in peptic ulcer?

A

extremely rare

159
Q

what are the normal damaging forces in the stomach?

A

gastric acidity • peptic enzymes

160
Q

what are the normal defensive forces in the stomach?

A
  1. surface mucus secretion • 2. bicarbonate secretion into mucus • 3. mucosal blood flow • 4. apical surface membrane transport • 5. epithelial regenerative capacity • 6. elaboration of prostaglandins
161
Q

what are the forces that lead to increased damage in the stomach and can produce ulcer?

A

H pylori infection • NSAID • ASA • Cigs • EtOH • gastric hyperacidity • too rapid gastric emptying • psych stress

162
Q

what are the impaired defensive forces in the stomach that can lead to peptic ulcer?

A
  1. decreased mucus secretion • 2. decreased PG synth • 3. delayed gastric emptying
163
Q

what are the microscopic features of gastric ulcer?

A

sharply demarcated • normal gastric mucosa falling away into deep ulcer whose base contrains inflamed necrotic debris

164
Q

hypertrophic gastropathy is characterized by what?

A

giant enlargement of the gastric rugal folds

165
Q

hypertrophic gastropathy is caused by what?

A

hyperplasia of epithelial cells (not due to inflammation)

166
Q

what is the malignant risk associated with hypertrophic gastropathy?

A

increased risk of cancer

167
Q

what are the 3 variants of hypertrophic gastropathy?

A
  • Menetrier’s disease • - Hypersecretory Gastropathy • - Zollinger-Ellison syndrome
168
Q

what is another name for Menetrier’s disease?

A

protein losing gastropathy

169
Q

what are the features of Menetier’s disease?

A
  • hyperplasia of surface mucus cells • - glandular atrophy • - excessive loss of proteins in gastric secretion
170
Q

what are the features of hypersecretory gastropathy?

A
  • hyperplasia of parietal and chief cells • - secondary to excessive gastrin stimulaton
171
Q

what is the cause of Zollinger-Ellison syndrome?

A

gastrinoma of the pancreas secreting gastrin–> elevated serum gastrin levels

172
Q

what are the features of Zollinger-Ellison syndrome?

A
  • multiple peptic ulcerations in stomach, duodenum, jejunum • - hypertrophic rugal folds and parietal cell hyperplasia–> excessive gastric acid production
173
Q

what are the benign tumors of the stomach?

A

gastric polyps • adenomatous polyps

174
Q

how many gastric polyps are neoplastic?

A

90% non-neoplastic= • hyperplastic or inflammatory

175
Q

do non-neoplastic gastric polyps have malignant potential?

A

no

176
Q

what is the tx for gastric polyps?

A

biopsy

177
Q

what are adenomatous polyps in the stomach?

A

true neoplasms with proliferative dysplastic epithelium

178
Q

do adenomatous polyps of the stomach have malignant potential?

A

yes, common in old age

179
Q

adenomatous polyps of the stomach are MC associated with what?

A

chronic gastritis or familial polyposis syndromes

180
Q

what are the malignant tumors of the stomach?

A
  1. Gastric carcinoma • 2. Gastrointestinal Stromal Tumor • 3. carcinoid (neuroendocrine) tumors • 4. gastric lymphoma
181
Q

what is the incidence of gastric carcinoma?

A

4 fold decline in incidence over the last 70 years for unknown reasons

182
Q

what are the dietary risk factors for gastric carcinoma?

A

nitrites (from food preservatives), smoked and salted foods, deficiency of fresh fruits and vegetables

183
Q

what are the host factor risk factors for gastric carcinoma?

A

chronic gastritis (autoimmune & H. pylori), adenomatous polyps, partial gastrectomy pt

184
Q

what are the genetic risk factors for gastric carcinoma?

A

blood group A • close relatives of stomach cancer patients • certain racial groups (Japanese)

185
Q

what are the classifications of Gastric Carcinoma?

A
  1. early gastric carcinoma • 2. advanced gastric carcinoma
186
Q

what is early gastric carcinoma?

A

confined to the mucosa & submucosa, despite lymph node spread

187
Q

what is the prognosis for early gastric carcinoma?

A

associated with very good prognosis >90% 5yr

188
Q

what is advanced gastric carcinoma?

A

has extended beyond the submucosa & spread is by local invasion, lymphatics, blood (to liver and lungs)

189
Q

what is Krukenberg tumor?

A

bilateral ovarian metastases (stomach, breast, pancreas, even gallbladder)

190
Q

what is Virchow node?

A

left supraclavicular node with mets

191
Q

what is the sister Mary Joseph nodule?

A

metastasize to the periumbilical region (subQ malignant nodule)

192
Q

what are the histologic types of gastric carcinoma?

A

intestinal type • gastric type

193
Q

what are the features of intestinal type gastric carcinoma?

A

glandular, expansile growth pattern

194
Q

what are the features of gastric type gastric carcinoma?

A

diffuse ‘signet ring’ infiltrating pattern

195
Q

what is the most important prognostic indicator in gastric carcinoma?

A

pathologic stage

196
Q

from what do GISTs arise?

A

interstitial cells of Cajal

197
Q

what are the markers of GISTs?

A

c-KIT (CD117) & CD34 positive

198
Q

what are carcinoid (neuroendocrine) tumors of the stomach made of?

A

made of ECL cell tumors

199
Q

carcinoid neuroendocrine tumors of the stomach are associated with what diseases?

A

MEN1 • Zollinger-Ellison Syndrome

200
Q

what is the most common site for extranodal lymphoma?

A

gastric lymphoma

201
Q

majority of gastric lymphoma are associated with what?

A

80% associated with H pylori chronic gastritis

202
Q

when are most gastric adenocarcinomas in the US found?

A

at a late stage when the neoplasm has invaded and/or metastasized

203
Q

what is a cautious approach for early detection of gastric carcinoma?

A

all gastric ulcers and all gastric masses must be biopsied

204
Q

what is the level of malignancy of duodenal peptic ulcers?

A

virtually all are benign

205
Q

what is linitis plastica?

A

diffuse infiltrative gastric adenocarcinoma

206
Q

what are the features of linitis plastica?

A
  • stomach looks like shrunken leather bottle • - markedly thickened gastric wall • - very poor prognosis
207
Q

which type of gastric carcinoma typically produces krukenberg tumor?

A

gastric type

208
Q

what structures make up the small intestine?

A

duodenum • jejunum • ileum

209
Q

what is the purpose of the villi and microvilli in the small intestine?

A

increase surface area of the mucosa

210
Q

what are the crypts of Lieberkuhn

A

pits between the bases of the villi in small intestine

211
Q

what is the normal villus:crypt height ratio?

A

4:01

212
Q

where are the digestive enzymes in small intestines located?

A

in the membranes of microvilli

213
Q

how do bile ducts connect to the small intestine?

A

common bile duct and pancreatic duct empty into the 2nd part of the duodenum

214
Q

what types of glands are found in the duodenum?

A

Brunner’s glands

215
Q

what are the lymphoid structures in the ileum?

A

Peyer’s patches

216
Q

what are the structures of the large intestine?

A
  1. cecum & its appendix • 2. colon • - ascending • - transverse • - descending • - sigmoid • 3. rectum • 4. anal canal
217
Q

are there villi and microvilli in the large intestine?

A

large intestine lacks villi and microvilli

218
Q

does the large intestine have goblet cells?

A

has numerous goblet cells in the mucosa

219
Q

what is the function of the large intestine?

A

absorption of fluids, electrolytes and secretion of mucus

220
Q

what is the arterial supply of the intestines up to the hepatic flexure of the colon?

A

SMA

221
Q

what is the arterial supply to the intestine from the hepatic flexure to the rectum?

A

IMA

222
Q

what are the arterial interconnections in that supply the intestines called?

A

mesenteric arcades

223
Q

what is the artery that supplies the upper rectum?

A

superior hemorrhoidal artery from IMA

224
Q

what is the artery that supplies the lower rectum?

A

hemorrhoidal artery from internal iliac or internal pudendal artery

225
Q

what is the distribution of venous drainage of the intestines?

A

same as the arterial supply

226
Q

which intestinal vessels connect to form portal and systemic connections?

A

anastomotic capillary beds between superior and inferior hemorrhoidal veins

227
Q

are the ascending and descending colon intra- or retroperitoneal?

A

retroperitoneal

228
Q

where does the accessory blood supply and lymphatic drainage of the ascending and descending colon come from?

A

posterior abdominal wall

229
Q

do lymphatics have arcades?

A

no • run as parallel vessels without arcades

230
Q

what is the lymphoid tissue in the intestines?

A

MALT • mucosa associated lymphoid tissue

231
Q

what is the grossly visible lymphoid structure associated with the ileum?

A

Peyer’s patches

232
Q

what is the function of immune M cells in the intestines?

A

M (membranous cells) transport Ag to APC in SI and LI

233
Q

what is the direction of small intestinal peristalsis?

A

anterograde and retrograde

234
Q

what is peristalsis in the intestines mediated by?

A

intrinsic (myenteric plexus) and extrinsic (autonomic innervation) neural control

235
Q

what are the parts of the myenteric plexus?

A

meissner plexus (in submucosa) • auerbach plexs (muscle wall layers)

236
Q

what differentiates large from small intestine?

A

large intestine lacks villi and has numerous goblet cells

237
Q

what are the general symptoms associated with intestinal pathology?

A
  1. anorexia • 2. nausea • 3. vomiting • 4. flatulence • 5. bloating • 6. abdominal discomfort • 7. weight loss • 8. malaise
238
Q

what are the esophagus-specific symptoms of GI pathology?

A

dysphagia • odynophagia • heartburn • regurgitation • retrosternal pain

239
Q

what are the gastric-specific symptoms of GI pathology?

A

early satiety • hematemesis • upper abdominal pain/discomfort

240
Q

what are the small intestine specific symptoms of GI pathology?

A

diarrhea • steatorrhea • anemia • abdominal colic

241
Q

what are the large intestine specific symptoms of GI pathology?

A

diarrhea • constipation • blood and mucus per rectum • tenesmus • proctalgia • anemia

242
Q

what are the congenital anomalies of the intestines?

A
  • atresia and stenosis • - meckel diverticulum • - Hirschsprung disease
243
Q

what is atresia?

A

complete obstruction

244
Q

what is the most common site of intestinal atresia?

A

duodenum

245
Q

what is the common cause of neonatal intestinal obstruction?

A

duodenal atresia

246
Q

what is the frequency of jejunum and ileum atresia?

A

jejunum and ileum are equally involved, less so than the duodenum, but more so than the colon

247
Q

how often does atresia of the colon happen?

A

never

248
Q

what is stenosis?

A

incomplete obstruction

249
Q

what is more common, intestinal atresia or stenosis?

A

atresia

250
Q

what is imperforate anus?

A

failure of cloacal diaphragm to rupture–> • neonatal intestinal obstruction

251
Q

what type of diverticulum is Meckel’s diverticulum?

A

true diverticulum

252
Q

what is the 2% rule of Meckel’s diverticulum?

A

2 feet from ileocecal valve, seen i 2% of people, 2” in size

253
Q

what are the symptoms of Meckel’s diverticulum?

A

asymptomatic

254
Q

what is in Meckel’s diverticulum?

A

may contain gastric or pancreatic tissues &(peptic ulcers, diverticulitis, intestinal obstruction, intussusception)

255
Q

what is the cause of Meckel’s diverticulum?

A

persistent segment of the vitelline duct (h connects the yolk sac + gut lumen)

256
Q

what is another name for Hirschsprung’s disease?

A

aganglionic megacolon

257
Q

what causes Hirchsprung’s disease?

A

arrested migration of nerve elemets into distal part of gut

258
Q

what is Hirschsprung’s disease?

A

absence of ganglion cells in the large bowel (Aurbach’s and Meissner’s plexus)

259
Q

50% of familial and 15% of sporadic cases of Hirschsprung’s disease are due to what?

A

mutations in the RET gene

260
Q

what does the RET gene do?

A

promote survival and growth of neurite and direction to migrating neural crest cells

261
Q

Hirschsprung’s disease is characterized by what?

A

aganglionic (aperistaltic) segment–> narrow unaffected proximal colon–> dilation and hypertrophy (megacolon)

262
Q

there is an increased risk of Hirschsprung’s disease with what condition?

A

down syndrome

263
Q

what is the incidence of Hirschsprung’s disease?

A

1:8000 live births • M:F=4:1

264
Q

how does Hirschsprung’s disease present?

A

meconium ileus • abdominal distention • constipation • diarrhea (enterocolitis) • perforation (rare)

265
Q

what is involved in the diagnosis of hirschsprung’s disease?

A

histological demonstration of absence of ganglion cells in intestinal submucosa

266
Q

how is a biopsy suspicious for Hirschsprung’s treated for lab dx?

A

stained for acetyl cholinesterase

267
Q

what are the conditions important in the differential diagnosis of Hirschsprung’s disease?

A

any acquired megacolon: • 1. Chagas disease • 2. Obstruction (neoplastic) or inflammatory stricture of the bowel • 3. toxic megacolon- ulcerative colitis or Crohn disease • 4. functional causes

268
Q

what is diarrhea?

A

frequent passage of loose watery stools

269
Q

what is secretory diarrhea?

A

passage of >500ml/day of watery stools, isotonic with plasma (intestinal secretion)

270
Q

what is osmotic diarrhea?

A

> 500mL/d stools, the osmolality of which exceeds that of plasma by >50 mOsm

271
Q

what is exudative diarrhea?

A

frequent passage of loose, purulent, bloody stools

272
Q

what is dysentery?

A

painful bloody diarrhea (tenesmus)

273
Q

what does malabsorption look like?

A

bulky stools with excess fat (floats on water) and increased osmolality

274
Q

what is the volvume/day of secretory diarrhea?

A

> 500mL

275
Q

what is the volume/day of osmotic diarrhea?

A

> 500mL

276
Q

what is the volume of stool in malabsorption?

A

large volume

277
Q

what is the osmolarity of stool with respect to plasma in secretory diarrhea?

A

isotonic

278
Q

what is the osmolarity of stool with respect to plasma in osmotic diarrhea?

A

> 50mOsm hypertonic

279
Q

what is the osmolarity of stool with respect to plasma in malabsorption?

A

hypertonic

280
Q

does secretory diarrhea persist on fasting/

A

yes

281
Q

does osmotic diarrhea persist on fasting?

A

no

282
Q

does exudative diarrhea persist on fasting?

A

yes

283
Q

does malabsorption diarrhea persist on fasting?

A

no

284
Q

is there steatorrhea in secretory diarrhea?

A

no

285
Q

is there steatorrhea in osmotic diarrhea?

A

no

286
Q

is there steatorrhea in exudative diarrhea?

A

no

287
Q

is there steatorrhea in malabsorption diarrhea?

A

yes

288
Q

is there blood/pus in secretory diarrhea?

A

no

289
Q

is there blood/pus in osmotic diarrhea?

A

no

290
Q

is there blood/pus in exudative diarrhea?

A

yes

291
Q

is there blood/pus in malabsorption diarrhea?

A

no

292
Q

what are the types of infective enterocolitis?

A
  1. viral • 2. bacterial • 3. bacterial overgrowth syndrome • 4. parasitic EC • 5. necrotizing EC • 6. collagen & lymphocytic EC
293
Q

what is infective enterocolitis?

A

acute, self limited infectious diarrhea

294
Q

infective enterocolitis is a major cause of morbidity among which population?

A

children

295
Q

what is the most common cause of infective enterocolitis?

A

enteric viruses

296
Q

viral enterocolitis is characterized by what?

A

food and water infections that cause damage of small intestinal epithelium with shortening of villi • - diarrhea for 1-7 days

297
Q

what are the most common causes of viral enterocolitis?

A
  1. Rotavirus (Group A) • 2. Norwalk Virus • 3. Adenovirus
298
Q

who is affected by Rotavirus Group A infections?

A

outbreaks in children 6-24 months

299
Q

what happens in rotavirus group A EC?

A

selectively infects and destroys mature enterocytes in the small intestine, without infecting crypt cells

300
Q

what are the features of Norwalk virus EC?

A

food borne nonbacterial outbreaks in school children and adults

301
Q

adenovirus EC outbreaks affect which populations?

A

infants

302
Q

what do the morphologic changes in bacterial EC depend on?

A

the causative agent

303
Q

what are the pathogenic mechanisms underlying bacterial EC?

A
  1. ingestion of preformed toxins • 2. infection by toxigenic orgnisms
304
Q

Bacterial EC can be caused by ingestion of preformed toxins present in contaminated food by what organisms?

A

Staph. aureus • Clost. perfringens • Virbrios

305
Q

what are the 2 ways that bacterial EC caused by infection by toxigenic organisms proliferate?

A
  1. proliferate within gut lumen and elaborate an enterotoxin • 2. proliferate, invade, and destroy mucosal epithelial cells
306
Q

which organisms that cause bacterial EC proliferate within the gut lumen and elaborate an enterotoxin?

A

enteroinvasive organisms: • - E coli • - Shigella • - Salmonella

307
Q

what are the 2 types of enterotoxins associated with bacterial EC?

A

secretagogues (cholera toxin) • cytotoxins (Shiga toxin)

308
Q

what are the clinical features of bacterial EC caused by ingestion of preformed toxins?

A
  • develop within a matter of hours • - explosive diarrhea • - actue abdominal distress • - passes in a day or so
309
Q

what are the clinical features of bacterial EC caused by infection with enteric pathogen?

A
  • incubation period of several hours to days • - followed by diarrhea and dehydration
310
Q

what are the complications associated with bacterial EC?

A
  • massive fluid loss or destruction of intestinal mucosal barrier • - dehydration, sepsis, perforation
311
Q

what are the major sources Salmonella in the USA?

A

Feces contaminated beef and chicken

312
Q

what is the more common organism that causes bacterial EC from chicken?

A

Campylobacter jejuni • - more common than Shigella and Salmonella

313
Q

how does cholera toxin cause secretory diarrhea?

A
  1. permanently activate GTP–> persistent activation of adenylate cyclase–> high levels of intracellular cAMP–> stimulates secretion of chloride and bicarb • 2. chloride and sodium reabsorption is inhibited
314
Q

what is another name for pseudomembranous colitis?

A

antibiotic associated colitis (EC)

315
Q

what type of colitis is pseudo-membranous colitis?

A

acute colitis

316
Q

what is pseudo-membranous colitis caused by?

A

enterotoxins of Clostridium dificile

317
Q

what is the role of the enterotoxins of Colstridium dificile in pseudomembranous colitis?

A

due to toxins A and B–> cytokine production–> cell apoptosis

318
Q

antibiotic associated colitis is characterized by what?

A

the formation of an adherent necrotic membrane (pseudomembrane) overlying extensive mucosal inflammation

319
Q

what makes up the pseudomembrane associated with pseudomembranous colitis?

A

mucus, fibrin, and inflammatory debris

320
Q

similarly to pseudomembranous colitis, fibrinopurulent necrotic pseudomembrane forms in what?

A

enteroinvasive infections • ischemic EC

321
Q

what are the clinical features of pseudomembranous colitis?

A
  • presents as acute diarrhea while on antibiotic therapy • - toxin detectable in stools • - responds to appropriate antibiotics
322
Q

what is the cause of bacterial overgrowth syndrome?

A

surgical procedures- decreasing the time for exposure of ingested bacteria to gastric acid • - bacterial overgrowth in the small intestine

323
Q

how does bacterial overgrowth syndrome present clinically?

A

chronic diarrhea • abdominal pain • malabsorption • weight loss

324
Q

what is involved in the diagnosis of bacterial overgrowth syndrome?

A
  • breath tests for volatile bacterial byproducts • - clinical history • - demonstration of bacteria in the proximal small intestine by direct culture
325
Q

what are the nematodes that cause parasitic EC?

A
  1. ascaris lumbricoides • 2. strongyloides • 3. hookworm • - necator duodenale • - ancylostoma duodenale • 4. enterobius vermicularis (pinworm) • 5. trichuris trichiuria (whipworm)
326
Q

what is the most common nematode cause of parasitic EC?

A

ascaris lumbricoides

327
Q

what are the features of parasitic EC caused by ascaris lumbricoides?

A
  • obstruct the intestine or biliary tree • - pneumonitis • - hepatic abscess
328
Q

how is ascaris lumbricoides diagnosed?

A

detection of eggs in the feces

329
Q

what are the features of parasitic EC caused by strongyloides?

A
  • pulmonary infiltrates with eosinophilia • - autoinfection in immnosuppressed
330
Q

what are the features of parasitic EC caused by the hookworms necator duodenale or ancylostoma duodenale?

A
  • intestinal mucosa erosions, focal hemorrhage • - long term infection lead to IDA
331
Q

what are the features of parasitic EC caused by pinworm enterobius vermicularis?

A

perianal pruritus

332
Q

what causes perianal pruritus in parasitic EC caused by enterobius vermicularis?

A

worms migrate to the anal orifice and deposit eggs

333
Q

how is enterobius vermicularis diagnosed?

A

perianal skin tape

334
Q

what are the features of parasitic EC caused by trichuris trichiura?

A
  • Heavy infections- cause bloody diarrhea and rectal prolapse • - in young children
335
Q

what are the features of parasitic EC caused by cestodes?

A
  • never invade beyond the intestinal mucosa • - no eosinophilia
336
Q

what are the cestodes that cause parasitic EC?

A

Diphyllobothrium latum (fish tapeworm) • Taenia solium (pork tapeworm) • Hymenolepsis nana (dwarf tapeworm)

337
Q

what are the protozal infections that cause parasitic EC?

A
  1. Amebiasis (Entamoeba histolytica) • 2. Giardiasis
338
Q

what is the site of infection in parasitic EC caused by Amebiasis vs. Giardiasis?

A

Amebiasis= LI (cecum and ascending colon) • Giardiasis= SI (duodenum)

339
Q

what is the difference in the stool caused by parasitic EC from amebiasis vs giardiasis?

A

Amebiasis= dysentery • Giardiasis= diarrhea

340
Q

what type of ulcers are present in parasitic EC caused by amebiasis vs giardiasis?

A

amebiasis= flask shaped ulcer • giardiasis= no ulcers

341
Q

what is the difference between trophozoites in amebiasis vs giardiasis?

A

amebiasis= 1 nucleus • giardiasis= 2 nuclei

342
Q

what is the difference between the flagella of the organisms that cause amebiasis vs giardiasis?

A

amebiasis= no flagella • giardiasis= flagellated

343
Q

what is the difference between the treatment for amebiasis vs giardiasis?

A

rx is same for both

344
Q

what is the most common acquired gastrointestinal emergency?

A

necrotizing enterocolitis

345
Q

which babies are at highest risk for necrotizing enterocolitis?

A

premature • low birth weight

346
Q

what causes necrotizing enterocolitis?

A

immaturity of the gut immune system

347
Q

necrotizing enterocolitis is characterized by what?

A

necrotizing inflammation of the small and large intestine

348
Q

what happens in necrotizing enterocolitis?

A

initiation of oral feeding–> release of cytokines (PAF)–> inflammatory response • –> gut colonization with bacteria • –> mucosal injury

► Med Notes (62 decks)

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