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GI II > GI Tract > Flashcards

GI Tract Flashcards

1
Q

VATER association

A

congenital anomalies that occur simultaneously-vertebral, anal anomalies, cardia, TE fistula, renal anomalies, limb anomalies

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2
Q

Most common form of intestinal atresia

A

imperforate anus

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3
Q

Most common site of fistulization

A

esophagus

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4
Q

What other congenital anomalies are TE fistulas associated with?

A

cardiac

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5
Q

Occurrance of TE fistula

A

1/3500 births

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6
Q

Most common TE fistula

A

esophageal atresia with distal TEF

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7
Q

Cause of TE fistulas

A

abnormal septation of caudal foregut during fourth and fifth weeks

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8
Q

Clinical presentation of TE fistula

A

aspiration, suffocation, pneumonia, severe fluid and electrolyte imbalances

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9
Q

Stenosis

A

incomplete atresia in which lumen is reduced in caliber as a result of fibrous thickening of the wall

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10
Q

Most common true diverticulum

A

Meckel diverticulum

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11
Q

Cause of meckel diverticulum

A

persistence of vitelline duct, which connects lumen of gut to yolk sac

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12
Q

Rule of 2s for Meckel diverticulum

A

2% population, 2 ft from ileocecal valve, 2x more likely in men, 2 inches long, symptomatic by age 2

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13
Q

Ectopic tissues that may be present in Meckel diverticulum

A

gastric or pancreatic tissue

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14
Q

Presentation of Meckel diverticulum

A

abdominal pain, intussusception, GI bleed, ulceration, inflammation/adhesions

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15
Q

Occurrence of pyloric stenosis

A

M>F, monozygotic twins have a high rate of concordance, common in Turner and Edward syndrome, correlation with women who use erythromycin or azithromycin during pregnancy

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16
Q

Clinical presentation pyloric stenosis

A

regurgitation, projectile, nonbilious vomiting after feeding, olive sized mass

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17
Q

Occurrence of Hirschsprung disease

A

1 of 5000 births

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18
Q

Cause of Hirschsprung dz

A

abnormal migration of premature death of entire ganglion cells, failure of NCC migration

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19
Q

Hirschsprung obstruction

A

functional

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20
Q

Gene mutation often linked to Hirschsprung dz

A

RET mutation

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21
Q

Portions of bowel involved inHirschsprung

A

rectum is always involved, will have varying degrees of colonic involvement

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22
Q

Diagnosis of Hirschsprung

A

absence of ganglion cells within the affected bowel segment

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23
Q

Clinical presentation of Hirschsprung

A

failure to pass meconium, obstruction or constipation, abd distension, bilious vomiting

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24
Q

Treatment of Hirschsprung dz

A

surgical removal of aganglionic segment

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25
Q

Causes of acquired megacolon

A

Chagas disease, obstruction by neoplasm, ulcerative colitis, visceral myopathy, etc.

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26
Q

Embryonic development of esophagus

A

develops from cranial portion of foregut, recognizable by third week of gestation

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27
Q

Nutcracker esophagus

A

high amplitude contractions of the distal esophagus due to loss of coordination between the inner and outer circular layers

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28
Q

Diffuse esophageal spasm

A

repetitive, simultaneous contractions of the entire esophagus; completely uncoordinated contractions

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29
Q

Zenker diverticulum

A

outpouching of the esophagus that occurs at Killian’s triangle, immediately above UES

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30
Q

Cause of Zenker diverticulum

A

failure of cricopharyngeus muscle to result after swallowing

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31
Q

Esophageal webs

A

ledge-like protrusions of mucosa that may cause obstruction

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32
Q

Disease associations of esophageal webs

A

GERD, C-GVHD, Celiac, Paterson-Brown-Kelly or Plummer-Vinson syndrome

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33
Q

Presentation of esophageal webs

A

nonprogressive dysphagia associated with incompletely chewed food

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34
Q

Schatzki ring

A

circumferential, thicker esophageal strictures

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35
Q

Presentation of schatzki ring

A

progressive dysphagia

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36
Q

Achalasia triad

A

incomplete LES relaxation, increased LES tone, aperistalsis of esophagus

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37
Q

Sxs of achalasia

A

dysphagia for solids and liquids, difficulty in belching, chest pain

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38
Q

Cause of primary achalasia

A

degeneration of ganglion cells

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39
Q

Causes of secondary achalasia

A

Chagas disease, failure of peristalsis, esophageal dilation, achalasia-like diseases, infiltrative disorders, lesions of DMN, HSV1, autoimmune diseases

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40
Q

Tx of achalsia

A

laparoscopic myotomy, pneumatic balloon dilation, Botox injection

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41
Q

Characteristics of Mallory-Weiss tear

A

longitudinal laceration near gastroesophageal junction

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42
Q

Cause of Mallory-Weiss tear

A

binge drinking and severe retching

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43
Q

Characteristics of Boerhaave’s syndrome

A

transmural tearing and rupture of distal esophagus

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44
Q

Sxs of Boerhaave’s syndrome

A

chest pain, shock, subcutaneous emphysema, mediastinitis

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45
Q

Hamman’s sign

A

crunching sound upon auscultation of heart due to pneumomediastinum

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46
Q

Tx of variceal hemorrhage

A

splanchnic vasoconstriction, sclerotherapy, balloon tamponade, variceal ligation

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47
Q

Pathogenesis of esophageal varices

A

collateral vessel channels (due to portal hypertension) become congested; hepatic schistosomiasis

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48
Q

Location of upper GI bleed

A

proximal to ligament of Treitz

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49
Q

GE varices clinical features

A

may be asymptomatic but can hemorrhage and result in hypovolemic shock, hepatic coma, and other life-threatening complications

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50
Q

Radiation induced esophagitis is characterized by…

A

fibrosis, mutagenesis, carcinogenesis, and teratogenesis

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51
Q

Pill-induced esophagitis

A

medicinal pills are lodged in the esophagus and dissolve in the esophagus

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52
Q

Sxs of esophagitis

A

self-limited pain on swallowing, hemorrhage, stricture, perforation

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53
Q

Infectious causes of esophagitis

A

HSV, CMV, fungi (candidiasis, mucormycosis, aspergillosis)

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54
Q

Morphological changes of radiation esophagitis

A

intimal proliferation and luminal narrowing

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55
Q

Morphological changes of HSV induced esophagitis

A

punched-out ulcers, nuclear viral inclusions in squamous cells

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56
Q

Morphological changes of CMV induced esophagitis

A

shallow ulcers, nuclear viral inclusions in capillary endothelium and stromal cells

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57
Q

Morphological changes of GVHD esophagitis

A

basal epithelial apoptosis, mucosal atrophy, submucosal fibrosis

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58
Q

Eosinophilic esophagitis sxs

A

food impaction, dysphagia, or feeding intolerance in infants; food or seasonal allergies that present as asthma, allergic rhinitis, atopic dermatitis

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59
Q

Morphological changes of eosinophilic esophagitis

A

trachealization of esophagus, >25 eosinophils per hpf

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60
Q

Atopy

A

genetic tendency to develop allergic diseases such as allergic rhinitis, asthma, atopic dermatis

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61
Q

Most frequent cause of esophagitis

A

reflux of gastric contents into lower esophagus

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62
Q

Pathogenesis of LES relaxation

A

may be due to vagal mediated pathways, increased intra-abdominal pressure, alcohol and tobacco, obesity, hiatal hernia, delayed gastric emptying idiopathic

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63
Q

Clinical features of GERD

A

heartburn, dysphagia, regurgitation of sour-tasting gastric contents; may be punctuated by attacks of sever chest pain

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64
Q

Morphological changes in GERD

A

hyperemia, histology often unremarkable; eosinophils may be recruited with more significant disease

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65
Q

Complications of GERD

A

ulceration, hematemesis, melena, stricture development; often see metaplasia (squamous-to-columnar) in severe, prolonged cases

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66
Q

Barrett esophagus

A

complication of chronic GERD characterized by intestinal metaplasia in esophageal squamous mucosa

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67
Q

Barrett esophagus and CA association

A

increased risk of esophageal adenocarcnioma

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68
Q

Endoscopic examination of Barrett esophagus

A

tongues or patches of red, velvety mucosa extending upward from GE junction

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69
Q

Diagnostic appearance of Barrett esophagus

A

endoscopic evidence of metaplastic columnar mucosa above GE junction

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70
Q

Characteristics of dysplasia

A

atypical mitoses, nuclear hyperchromasia, irregularly clumped chromatin, increased N:C ratio, failure of epithelial cell maturation

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71
Q

Tissue derivative of benign esophageal tumors

A

mesenchymal, grow in submucosa layer

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72
Q

Esophageal adenocarcinomas arise from…

A

Barrett esophagus

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73
Q

Geographic distribution of adenocarcinoma of the esophagus

A

highest rates in the US, UK, Canada, Australia

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74
Q

Highest risk group for esophageal adenocarcinomas

A

Caucasian men

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75
Q

Risk factors for esophageal adenocarcinoma

A

Barrett esophagus, tobacco, radiation, reduced H. pylori

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76
Q

Morphological changes of esophageal adenocarcinoma

A

flat or raised patches in intact mucosa, large masses of 5cm or more in diameter may develop, can infiltrate diffusely or ulcerate and invade deeply

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77
Q

Location of esophageal adenocarcinomas

A

distal third of esophagus

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78
Q

Histological appearance of esophageal adenocarcinoma

A

mucinous, form gland structures, may be composed of diffusely infiltrative signet-ring cells

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79
Q

Clinical features esophageal adenocarcinoma

A

pain or difficulty in swallowing, progressive weight loss, hematemesis, chest pain, vomiting

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80
Q

Geographic distribution squamous cell carcinoma

A

Iran, central China, Hong Kong

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81
Q

Highest risk group for squamous cell carcinoma

A

> 45, males 4:1, african americans are 8x more likely

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82
Q

Risk factors for SCC

A

alcohol, tobacco, poverty, caustic esophageal injury, achalasia, tylosis, radiation, Plummer-Vinson syndrome, diets deficient in fruits or vegetables, frequent consumption of very hot beverages

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83
Q

Morphological appearance of esophageal SCC

A

small, gray-white, plaque-like thickenings

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84
Q

Tylosis mutation and sxs

A

RHBDF2 mutation, squamous hyperplasia of hands and feet

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85
Q

Presentation of esophageal SCC

A

dysphagia, odynophagia, obstruction, weight loss and debilitation, hemorrhage and sepsis may occur

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86
Q

Cells that secrete HCl and IF

A

parietal cells

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87
Q

Cells that secrete pepsinogen

A

chief cells

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88
Q

Cells that secrete gastrin

A

G cells

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89
Q

Cells that secrete mucin

A

mucous cells

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90
Q

Actions of gastrin

A

enhance gastric mucosal growth, motility and secretion of HCl

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91
Q

Which part of the stomach is most often involved in gastric adenocarcinomas?

A

gastric antrum, lymph flow to lesser curvature

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92
Q

Ectopia

A

ectopic tissues in GI tract; pancreatic tissue, if present in the pylorus, may lead to inflammation and scarring/obstruction

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93
Q

Gastritis

A

mucosal inflammatory process

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94
Q

Acute gastritis

A

mucosal inflammatory process when neutrophils are present

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95
Q

Gastropathy

A

mucosal inflammatory process when inflammatory cells are rare or absent

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96
Q

Actions of exogenous prostaglandins

A

inhibit acid secretion, stimulate mucus and bicarb secretion, alter mucosal blood flow

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97
Q

Stress ulcers are common in individuals with…

A

shock, sepsis, severe trauma

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98
Q

Curling ulcers

A

proximal duodenal ulcers associated with severe burns or trauma

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99
Q

Cushing ulcers

A

gastric, duodenal, esophageal ulcers arising in persons with intracranial disease

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100
Q

Pathogenesis of stress-related mucosal injury

A

local ischemia due to systemic hypotension or reduced blood flow

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101
Q

Dieulafoy lesion

A

submucosal artery that does not branch properly in stomach, resulting in a large mucosal artery; often found in lesser curvature, if overlying epithelium erodes, bleeding will occur

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102
Q

Gastric antral vascular ectasia

A

longitudinal stripes of edematous erythematous mucosal created by ectatic mucosal vessels; antral mucosa shows gastropathy with dilated capillaries containing fibrin thrombi

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103
Q

Most common cause of chronic gastritis

A

H. pylori infection

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104
Q

Long-standing chronic gastritis that involves the body and fundus may lead to…

A

mucosal atrophy and intestinal metaplasia

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105
Q

H. pylori is most common in which area of the stomach

A

antrum

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106
Q

H. pylori infection most commonly affects which populations?

A

impoverished, crowded housing, those with limited education, AA or Mexican American, those who live in rural areas or were born outside US

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107
Q

multifocal atrophic gastritis causes what morphological changes

A

patchy mucosal atrophy, reduced parietal cell mass and acid secretion, intestinal metaplasia and increased risk of gastric adenocarcinoma

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108
Q

Virulence factors of H. pylori

A

flagella, urease, adhesins, toxins (CagA)

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109
Q

Endoscopic appearance of H. pylori infection

A

erythematous, nodular appearance of gastric mucosa

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110
Q

Histologic appearance of H. pylori infection

A

inflammatory infiltrate generally involves neutrophils, plasma cells, macrophages, lymphocytes; can increase rugal folds and create areas of lymphoid aggregates

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111
Q

diagnostic tests for H. pylori

A

noninvasive serologic test for abs, fecal bacterial detection, urea breath test, gastric biopsy

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112
Q

effective tx for H. pylori

A

2 abx and 1 PPI

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113
Q

Common location of autoimmune gastritis

A

body of the stomach

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114
Q

Characteristics of autoimmune gastritis

A

abs to parietal cells and intrinsic factor, reduced pepsinogen I concentration, endocrine cell hyperplasia, vitamin B12 deficiency, achlorydia

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115
Q

Pathogenesis of autoimmune gastritis

A

loss of parietal cells, CD4+ T cells against parietal cell components and autoabs to parietal cells

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116
Q

Morphological changes in autoimmune gastritis

A

diffuse mucosal damage of oxyntic mucosa within body and fundus, inflammatory infiltrate is composed of lymphocytes and macrophages, rxn centered around glands

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117
Q

Clinical presentation of autoimmune gastritis

A

pernicious anemia, other autoimmune dz, atrophic glossitis, megaloblastosis of RBCs and epithelial cells, peripheral neuropathies

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118
Q

Eosinophilic gastritis

A

tissue damage associated with dense infiltrates of eosinophils in mucosa and muscularis; occurs in association with allergies, immune disorders, parasites, H. pylori ifx

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119
Q

Lymphocytic gastritis

A

often associated with celiac and most common in women; endoscopic appearance of thickened folds covered by small nodules with aphthous ulceration, increase in T cells

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120
Q

Granulomatous gastritis

A

well-formed granulomas or aggregates of macrophages

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121
Q

Peptic ulcer disease

A

chronic mucosal ulceration affecting the stomach or duodenum

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122
Q

Causes of PUD

A

H. pylori, NSAIDs, cigarette smoking

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123
Q

What GI secretions change in response to chronic H. pylori infection in antrum and duodenum

A

increased gastric acid secretion, decreased bicarb

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124
Q

Endoscopic appearance of peptic ulcer

A

round to oval, sharply punched-out defect

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125
Q

Clinical features of PUD

A

epigastric burning or aching pain (1-3 hrs after meals, referred to back, LUQ or chest; complications include bleeding, perforation, obstruction, dysplasia, mucosal atrophy and intestinal metaplasia

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126
Q

Gastritis cystics

A

epithelial proliferation associated with entrapment of epithelial-lined cysts

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127
Q

Hypertrophic gastropathies are characterized by…

A

“cerebriform” enlargement of rugal folds due to epithelial hyperplasia without inflammation

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128
Q

Menetrier Disease

A

excess secretion of TGFa, diffuse hyperplasia of mucosal cells and hypoproteinemia

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129
Q

Inflammatory infiltrate of menetrier disease

A

lymphocytes

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130
Q

Sxs of Menetrier Disease

A

hypoproteinemia, weight loss, diarrhea

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131
Q

What CA is Menetrier Dz associated with?

A

adenocarcinoma

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132
Q

Zollinger Ellison syndrome

A

caused by gastrin-secreting tumors often found in the small intestine or pancreas, increase in parietal cells

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133
Q

Inflammatory infiltrate of ZE syndrome

A

neutrophils

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134
Q

Risk factors for development of ZE syndrome

A

MEN (multiple endocrine neoplasia)

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135
Q

Is ZE associated with adenocarcinoma?

A

No

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136
Q

Percentage of UGI endoscopies that reveal a polyp

A

5%

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137
Q

Most common gastric polyp

A

inflammatory or hyperplastic polyps

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138
Q

Hyperplastic polyps are most common in what population?

A

50-60 yo with chronic gastritis

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139
Q

Morphological changes of hyperplastic polyps

A

irregular, cystically dilated foveolar glands; edematous lamina propria, may have surface ulceration

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140
Q

Fundic gland polyps are associated with what genetic syndrome?

A

familial adenomatous polyposis

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141
Q

Patho of fundic gland polyps due to PPI use

A

inhibition of acid production increases gastrin being secreted and increases oxyntic gland growth

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142
Q

Gastric adenomas occur in association with…

A

chronic gastritis with atrophy and intestinal metaplasia

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143
Q

Most common malignancy in stomach

A

adenocarcinoma

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144
Q

Gastric adenocarcinoma is most common in which countries?

A

Japan, Chile, Costa Rica, Eastern Europe

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145
Q

Sites most commonly involved in gastric adenocarcinoma metastasis

A

Virchow node, Sister Mary Joseph nodule, left axillary LN, krukenberg tumor, pouch of douglas

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146
Q

Precursor lesions associated with gastric adenocarcinoma

A

gastric dysplasia and adenomas

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147
Q

Genetic mutation in the development of diffuse gastric adenocarcinoma

A

CDH1 LOF mutation; loss of E-cadherin is a key step

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148
Q

Genetic mutation in development of sporadic intestinal-type gastric cancers

A

increased signaling via WNT, loss-of-function of adenomatous polyposis coli, 5q21 tumor suppressor, gain-of function in B-catenin

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149
Q

Precursor lesions for intestinal-type gastric CA

A

metaplasia, atrophy, dysplasia, adenoma, Menetrier

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150
Q

Population most at risk for intestinal-type gastric CA

A

high risk geographic areas, M>F, mean age 55

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151
Q

Area of stomach most commonly affected by gastric adenocarcinomas

A

gastric antrum and lesser curvature

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152
Q

Histological morphology of intestinal-type gastric CA

A

glandular structures, form exophytic mass or ulcerated tumor, apical mucin vacuoles

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153
Q

Histological morphology of diffuse type gastric adenocarcionoma

A

singet ring cells (large mucin vacuoles), discohesive cells

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154
Q

Lintis plastica

A

rugal flattening and rigid, thickened wall give the stomach a leather bottle appearance

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155
Q

Most powerful tool for prognosis of gastric CA

A

depth of invasion and extent of nodal and distant metastases

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156
Q

Most common extranodal site of marginal zone B-cell lymphomas

A

GI tract

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157
Q

Translocation most commonly associated with MALToma

A

t(11;18)

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158
Q

MALT is most commonly induced as a result of what

A

chronic gastritis - H. pylori

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159
Q

Histological appearance of gastric MALToma

A

dense lymphocytic infiltrate in lamina propria, create diagnostic lymphoepithelial lesions, reactive appearing B cell follicles

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160
Q

Most common presenting symptoms of MALToma

A

dyspepsia and epigastric pain, hematemesis, melena, and constitutional sxs

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161
Q

Most important prognostic factor for carcinoid tumor

A

location

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162
Q

Location of GI tract in which carcinoid tumors are most aggressive

A

jejunum and ileum

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163
Q

Gastric carcinoid tumors are most commonly associated with what diseases

A

endocrine cell hyperplasia, autoimmune chronic gastritis,

MEN-I, ZE syndrome

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164
Q

Histological appearance of carcinoid tumor

A

salt and pepper chromatin, positive synaptophysin and chromographin, neurosecretory granules, uniform cells with granular cytoplasm

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165
Q

Morphological appearance of carcinoid tumor

A

circumscribed yellow mass

166
Q

Clinical features of carcinoid tumors

A

cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, right-sided cardiac valve fibrosis

167
Q

Most common mesenchymal tumor of the abdomen

A

Gastrointestinal stromal tumor

168
Q

From which cells does GIST arise from

A

interstitial cells of Cajal

169
Q

Peak age of GIST

A

approx 60 yrs

170
Q

Carney syndrome triad

A

GIST, paraganglioma, pulmonary chondroma

171
Q

Mutation in GIST

A

gain-of-function tyrosine kinase KIT or PDGFRA

172
Q

Symptoms of GISTs

A

mass effects, blood loss, anemia

173
Q

Prognosis of GIST is related to…

A

size, mitotic index, and location

174
Q

Most common site of GI neoplasia in Western populations

A

colon

175
Q

When, during embryologic development do the intestines grow and form?

A

Weeks 4 and 5, NCC enter foregut wk 4 and hindgut wk 5

176
Q

Omphalocele

A

abdominal viscera herniating into base of umbilicus, covered by membrane

177
Q

Gastroschicis

A

uncovered bowel protruding through abdominal wall without a membrane covering

178
Q

Two main purposes of GI tract

A

transport of food and absorption of nutrients

179
Q

Main causes of mechanical obstruction in intestines

A

hernias, intestinal adhesions, intussusception, volvulus

180
Q

Clinical manifestations of intestinal obstruction

A

abdominal pain and distention, vomiting, and constipation

181
Q

Functional bowel obstruction

A

paralytic ileus, temporary disturbance of peristalsis in absence of mechanical obstruction, may be caused by metabolic disturbances, endocrinopathies, certain drugs

182
Q

Hernia

A

weakness or defect in abdominal wall that permits protrusion of a serosa-lined pouch of the peritoneum

183
Q

Most common cause of intestinal obstruction worldwide

A

hernia

184
Q

Progression of hernia if not treated

A

pressure at the neck of the pouch may impair venous draining resulting in stasis and edema, leading to permanent incarceration, strangulation, and infarction

185
Q

Cause of adhesions

A

surgical procedures, infection, peritoneal inflammation

186
Q

Most common cause of intestinal obstruction in the US

A

adhesions

187
Q

Volvulus

A

twisting of loop of bowel about its mesenteric point of attachment

188
Q

Clinical presentation of volvulus

A

obstruction and infarction of bowel

189
Q

Most common location of volvulus

A

sigmoid colon

190
Q

Intussusception

A

segment of intestine telescopes into an immediately distal segment

191
Q

Most common cause of intestinal obstruction in children <2

A

intussusception

192
Q

Potential causes of intussusception in children

A

idiopathic, viral infection, rotavirus vaccine

193
Q

Potential cause of intussusception in adults

A

intraluminal mass or tumor

194
Q

How are the intestines able to tolerate a slowly progressive loss of blood supply?

A

Collateral circulation and interconnections between arcades

195
Q

Acute vascular compromise of the intestines affects what layers

A

mucosal, submucosal, muscularis; may be mucosal, non-transmural, or transmural

196
Q

Obstruction of what artery causes the worst outcome for ischemic bowel disease

A

superior mesenteric artery

197
Q

Etiologies of acute obstruction of blood flow

A

sever atherosclerosis, cardiac mural thrombi, hypercoagulable states, tumors, trauma, cirrhosis

198
Q

Etiologies of chronic obstruction of blood flow

A

cardiac failure, shock, dehydration, drugs (vasoconstrictors - cocaine)

199
Q

Hypoxic injury in vascular compromise

A

epithelial cells are mostly resistant to transient hypoxia

200
Q

Reperfusion injury in vascular compromise

A

may trigger multiorgan failure; free radical formation, neutrophil infiltration, release of inflammatory mediators

201
Q

Variables that determine severity of ischemic bowel disease

A

severity of compromise, time frame, vessels affected

202
Q

Microscopic appearance of ischemic intestine

A

atrophy or sloughing of epithelium, hyperproliferative crypts, fibrous scarring due to chronic ischemia, pseudomembrane formation

203
Q

Most common population to have ischemic bowel disease

A

females >70

204
Q

Presentation of acute colonic ischemia

A

sudden onset of cramping, left lower abdominal pain, desire to defecate, passage of blood or bloody diarrhea

205
Q

Pain on which side of the abdomen is associated with a worse outcome in ischemic bowel disease

A

right

206
Q

CMV induced ischemic GI disease

A

viral tropism for endothelial cells

207
Q

Radiation enteritis

A

epithelial damage and vascular injury may cause changes similar to ischemic disease

208
Q

Angiodysplasia

A

lesion characterized by malformed submucosal and mucosal blood vessels that are thin walled

209
Q

Angiodysplasia is most common where in the GI tract and in what population?

A

most common in cecum or right colon, usually becomes clinically significant in 6th decade of life

210
Q

Presentation of angiodysplasia

A

can range from chronic, intermittent to acute, massive hemorrhage

211
Q

Malabsorption is characterized by defection absorption of what?

A

fats, fat- and water-soluble vitamins, proteins, carbs, electrolytes, minerals and water

212
Q

Common clinical presentation of malabsorption

A

chronic diarrhea, weight loss, anaorexia, abdominal distention, borborygmi, muscle wasting, steatorrhea

213
Q

Most common chronic malabsorptive disorders in the US

A

pancreatic insufficiency, celiac disease, Crohn disease

214
Q

Phases of nutrient absorption

A

intraluminal digestion, terminal digestion, transepithelial transport, lymphatic transport of fats

215
Q

Definition of diarrhea

A

increase in stool mass, frequency, fluidity greater than 200 gm per day

216
Q

Dysentery

A

Painful, bloody, small-volume diarrhea

217
Q

Secretory diarrhea

A

isotonic stool that persists during fasting

218
Q

Osmotic diarrhea

A

excessive osmotic forces exerted by unabsorbed luminal solutes, fluid is more than 50 mOsm more concentrated than plasma, subsides with fasting

219
Q

Malabsorptive diarrhea

A

failure of nutrient absorption, often associated with steatorrhea, relieved by fasting

220
Q

Exudative diarrhea

A

purulent, bloody stools that continue during fasting

221
Q

Phases of nutrient absorption affected in cystic fibrosis

A

intraluminal digestion

222
Q

Patho of malabsorption in CF

A

pancreatic abnormalities cause an accumulation of mucus in exocrine glands, impaired fat absorption, avitaminosis A and formation of viscid plugs

223
Q

Clinical manifestations of avitaminosis A

A

bitot spots (Xerophthalmia), derm manifestations, poor bone growth

224
Q

Celiac disease

A

immune-mediated enteropathy triggered by gluten-containing foods

225
Q

Autoimmunity in celiac disease occurs due to…

A

inherited gene susceptibility and environmental triggers

226
Q

Disease producing component of gluten

A

gliadin

227
Q

Gliadin triggers the release of what inflammatory mediator and what are the downstream effects?

A

IL-15, triggers activation and proliferation of CD8 intrapeithelial lymphocytes

228
Q

Receptor interaction of CD8 and enterocytes

A

MIC-A on epithelial cells, NKG2D on CD8 T cells

229
Q

Enzyme that deaminates gliadin

A

tissue transglutaminase

230
Q

HLA susceptibility for celiad disease

A

HLA DQ2 or DQ8

231
Q

Adaptive response to gliadin in celiac disease

A

sensitization of CD4 Tcells and B cells

232
Q

Morphologic changes of intestinal biopsy in patients with celiac disease

A

increased CD8 cells, crypt hyperplasia, villous atrophy, increased crypt mitotic activity

233
Q

Diagnostic serology for patients with celiac disease

A

IgA endomysial antibodies, IgA tTG abs

234
Q

Clinical features of Celiac Disease in adults

A

F>M 30-60 yo, bloating, diarrhea, fatigue, malabsorption, dermatitis herpetiformis

235
Q

Clinical features of Celiac Disease in children

A

typically presents between 6-24 mo with irritability, abdominal distension, chronic diarrhea, weight loss, muscle loss, FTT

236
Q

Extraintestinal manifestations of CD in children

A

arthritis/joint pain, aphthous ulcers, stomatitis, anemia, delayed puberty, short stature

237
Q

Environmental enteropathy is commonly seen in which populations

A

populations with poor sanitation and hygiene, parts of sub-Saharan Africa and aboriginal populations in northern Australia

238
Q

Clinical manifestations of environmental enteropathy

A

malabsorption, malnutrition, stunted growth, defective intestinal mucosal immune function

239
Q

Phases of nutrient absorption that are defective in celiac disease and environmental enteropathy

A

terminal digestion, transepithelial transport

240
Q

Autoimmune enteropathy

A

X-linked disorder characterized by severe persistent diarrhea and autoimmune disease that occurs most often in young children

241
Q

IPEX

A

immune dysregulation, polyendocrinopathy, X-linkage, enteropathy

242
Q

Germline mutation in IPEX

A

germline loss of FOXP3 function

243
Q

Autoantibodies to what are common in autoimmune enteropathy?

A

enterocytes and goblet cells, may have abs to parietal or islet cells

244
Q

Tx of autoimmune enteropathy

A

immunosupressive drugs like cyclosporine and HSC transplant

245
Q

Phases of nutrient absorption disrupted in autoimmune enteropathy

A

terminal digestion and transepithelial transport

246
Q

Lactase deficiency

A

absence of lactase results in the inability to breakdown lactose, cannot be absorbed and exerts an osmotic force causing osmotic diarrhea

247
Q

Congenital lactase deficiency

A

mutation in gene encoding lactase, autosomal recessive; presents as explosive diarrhea with watery, frothy stools and abdominal distention upon milk ingestion

248
Q

Acquired lactase deficiency

A

downregulation of lactase gene expression; presents as abdominal fullness, diarrhea, and flatulence

249
Q

Microvillus Inclusion disease

A

rare autosomal disorder of vesicular transport that leads to deficient brush-border assembly

250
Q

Microvillus inclusion disease mutation

A

MYO5B gene, motor protein

251
Q

Abetalipoproteinemia

A

rare autosomal recessive disease characterized by inability to assemble triglyceride-rich lipoproteins

252
Q

Mutated protein in abetalipoproteinemia

A

microsomal triglyceride transfer protein

253
Q

Absence of MTP causes what to accumulate

A

lipids in enterocytes

254
Q

Clinical presentation of abetalipoproteinemia

A

presents in infancy as FTT, diarrhea, steatorrhea, no apolipoprotein B, lipid membrane defects causes acanthocytic RBC

255
Q

Phase of nutrition disrupted in abetalipoproteinemia

A

transepithelial transport

256
Q

Clinical presentation of infectious enterocolitis

A

diarrhea, abdominal pain, urgency, perianal discomfort, incontinence, and hemorrhage

257
Q

Diagnostic tests for infectious enterocolitis

A

selective serologic testing, fecal leukocytes and lactoferrin assay, stool culture, assays for toxins, stool for ova and parasites

258
Q

Vibrio cholerae characteristics

A

comma-shaped, G- bacteria that cause cholera; endemic in Ganges Valley of India and Bangladesh

259
Q

What does the cholera toxin bind to on intestinal epithelial cells?

A

GM1 ganglioside

260
Q

Actions of A subunit of cholera toxin

A

activate Gsalpha to stimulate cAMP production and pump Cl- out of the cell

261
Q

Clinical features of V. cholerae

A

may be asymptomatic or have mild diarrhea; severe disease results in watery diarrhea and vomiting

262
Q

Stool in Cholera

A

rice water with a fishy odor

263
Q

Most common bacterial enteric pathogen in common countries

A

Campylobacter jejuni

264
Q

C. jejuni infections are associated with ingestion of…

A

improperly cooked chicken, unpasteurized milk, contaminated water

265
Q

Virulence of C. jejuni is due to

A

motility, adherence, toxin production, invasion

266
Q

Clinical presentation of C. jejuni infection

A

watery or bloody diarrhea, enteric fever, reactive arthritis (HLA-B27), Guillain-Barre and erythema nodosum

267
Q

Guillain-Barre syndrome

A

acute inflammatory demyelinating polyneuropathy that causes paresthesias in hands and feet, symmetrical and ascending muscle weakness

268
Q

Erythema Nodosum

A

skin inflammation located in fatty layer of skin, reddish, painful, tender lumps commonly located in front of legs or below knees

269
Q

Shigella characteristics

A

G- unencapsulated, nonmotile, facultative anaerobes that belong to Enterobacteriaceae family

270
Q

Stool in Shigellosis

A

bloody diarrhea

271
Q

Populations commonly effected by Shigellosis in US and Europe

A

children in daycare centers, migrant workers, travelers to low resource countries, individuals in nursing homes

272
Q

Where in the GI tract are shigella infections most common?

A

left colon

273
Q

Morphologic appearance of shigellosis

A

hemorrhagic and ulcerated mucosa with pseudomembranes

274
Q

Clinical presentation of Shigellosis

A

7-10 days of diarrhea, fever, and abdominal pain; watery diarrhea that progresses to dysentery

275
Q

Shigellosis may mimic what disease?

A

new-onset ulcerative colitis

276
Q

Complications of shigellosis

A

extra-intestinal manifestations (reactive arthropathy), HUS, toxic megacolon

277
Q

Causes of salmonella infection

A

contaminated meat, poultry, eggs, milk

278
Q

Populations commonly affected by salmonella infection

A

young children and older adults, especially during summer and fall

279
Q

Population commonly affected by S. typhi in endemic areas

A

children and adolescents

280
Q

Areas of the world where S. typhi is endemic

A

India, Mexico, Philippines, Pakistan, El Salvador, Haiti

281
Q

Clinical manifestations of Salmonella infection

A

fever, diarrhea

282
Q

Morphological changes due to Salmonella infection

A

Peyer patches in terminal ileum enlarge into delineated, plateau-like elevations, neutrophils accumulate in lamina propria with macrophages, oval ulcers

283
Q

Morphological changes due to disseminated S. typhi infection

A

enlarged, soft spleen, phagocyte hyperplasia, liver is punctated by foci of parenchymal necrosis in which hepatocytes are replaced by macrophage aggregates (typhoid nodules)

284
Q

S. typhi acute infection

A

anorexia, abdominal pain, bloating, nausea, vomiting, bloody diarrhea

285
Q

S. typhi disseminated infection

A

encephalopathy meningitis, seizures, endocarditis, myocarditis, pneumonia, cholecystitis

286
Q

At risk groups for salmonella infection

A

CA patients, immunosuppressed, EtOH, CV, sickle cell, hemolytic anemia

287
Q

Three species of yersinia that are human pathogens

A

Y. enterocolitica, Y. pseudotuberculosis, Y. pestis

288
Q

Yersinia infections are commonly linked to ingestion of ;…

A

pork, raw milk, contaminated water

289
Q

What molecule in the body can enhance the virulence of Yersinia?

A

Iron

290
Q

Where do Yersinia infections commonly occur in the GI tract?

A

ileum, appendix, right colon

291
Q

Morphological changes associated with Yersinia infections

A

regional LN and peyer patch hyperplasia, overlying lymphoid tissue may be hemorrhagic with apthous erosions and ulcers

292
Q

Post infectious complications due to Yersinia

A

reactive arthritis with urethritis and conjunctivitis, myocarditis, erythema nodosum, and kidney disease

293
Q

E. coli subset that is the principle cause of traveler’s diarrhea

A

ETEC, enterotoxigenic

294
Q

E. coli subset prevalent in developing countries as an important cause of endemic diarrhea

A

enteropathogenic, EPEC

295
Q

important type of EHEC E. coli

A

O157:H7

296
Q

E. coli subset biologically similar similar to shigella

A

EIEC, enteroinvasive

297
Q

E. coli with “stacked brick” morphology

A

EAEC, enteroaggregative

298
Q

Pathologic organism responsible for pseudomembranous colitis

A

C. difficile

299
Q

Risk factors of pseudomembranous colitis

A

antibiotic treatment, advanced age, hospitalization, immunosuppression

300
Q

Pseudomembrane morphology

A

adherent layer of inflammatory cells and debris

301
Q

Pathognomic histology of C. difficile colitis

A

denuded surface epithelium, dense infiltrate of neutrophils in lamina propria, damaged crypts become distended by mucopurulent exudate

302
Q

Clinical presentation of pseudomembranous colitis

A

fever, leukocytosis, abdominal pain, cramps, watery diarrhea, dehydration, hypoalbuminemia

303
Q

Common therapies for pseudomembranous colitis

A

metronidazole, vancomycin

304
Q

Whipple disease most commonly affects…

A

Caucasian men, particularly farmers or others with occupational exposures to animals or soil

305
Q

Clinical presentation of Whipple disease

A

diarrhea, weight loss, arthralgia, fever, LAD, neuro, cardio, pulm dz

306
Q

Morphologic hallmark of Whipple disease

A

dense accumulation of distended, foamy macrophages in small intestinal lamina propria

307
Q

Organism responsible for whipple disease

A

Topheryma whippelii

308
Q

Malabsorptive diarrhea of Whipple disease is due to

A

lymphatic obstruction

309
Q

Macrophage appearance in whipple disease

A

macrophages are PAS positive with diastase-resistant granules, NOT acid-fast

310
Q

Most common cause of viral gastroenteritis

A

norovirus

311
Q

Population most commonly affected by rotavirus

A

6-24mo, outbreaks commonly occur in hospitals and daycare centers

312
Q

Life cycle of Ascaris lumbricoides

A

soil contamination -> ingestion of eggs -> larvae penetrate intestines and migrate to lungs where tehy are coughed and swallowed

313
Q

Life cycle of Strongyloides stercoralis

A

soil and dog infection -> larvae penetrate skin -> migrate to small intestines

314
Q

Life cycle of Intestinal hookworm

A

larvae penetrate skin, enter lungs, coughed up and swallowed

315
Q

Life cycle of enterobius vermicularis

A

eggs in perianal folds are ingested by humans where they hatch in the small intestine

316
Q

Life cycle of Schistosoma

A

penetrate skin in water, enter circulation and migrate to portal blood and mature; can cause cirrhosis

317
Q

Life cycle of Taenia

A

infected meat is consumed, attach to intestines

318
Q

Life cycle of Diphyllobothriid tapeworms

A

ingestion of infected fish, adults live in small intestine

319
Q

Life cycle of amebiasis

A

mature cysts ingested, common in India, Mexico, and columbia; development of hepatic and pulmonary abscesses

320
Q

Life cycle of Giardia

A

contamination of water or food with cysts, mature in small intestine

321
Q

Life cycle of Cryptosporidium

A

thick walled oocyst, contaminated water is ingested, mature and develop in small intestine

322
Q

Irritable bowel syndrome

A

chronic, relapsing abdominal pain, bloating, changes in bowel habits without obvious gross or histo pathology

323
Q

Epidemiological impact of IBS

A

prevalence 5-10%, female predominance in high income countries

324
Q

Populations most commonly impacted by IBD

A

teens/early 20s, Caucasians, 3-5x more likely in Ashkenazi Jews, most common in developed countries

325
Q

Common causes of increased bacterial exposure in patients with intestinal inflammation

A

disruption of mucus layer, dysregulation of epithelial tight junctions, increased intestinal permeability, increased bacterial adherence to epithelial cells

326
Q

Characteristics of Crohn disease

A

commonly occurs in ileum, ileocecal valve, cecum; transmural inflammation, deep ulcers, malabsorption; skip lesions

327
Q

Morphological characteristics of CD

A

thickened and rubbery intestinal wall, stricture formation, creeping fat

328
Q

Ulcer appearance in CD

A

aphthous ulcers coalesce into elongated, serpentine ulcers, fissures and fistulas can develop, cobblestone appearance of the mucosa

329
Q

Characteristics of ulcerative colitis

A

always involves rectum and extends proximally; inflammation limited to mucosa, thin walls without stricture

330
Q

Gross appearance of colonic mucosa in UC

A

red and granular or extensive, broad-based ulcers; mucosal atrophy with smooth mucosal surface

331
Q

Extra-intestinal manifestations of IBD

A

uveitis, nephrolithiasis, fistulae, UTI, erythema nodosum, stomatitis, steatosis, gallstones, spondylitis

332
Q

Neoplasia in IBD is related to…

A

duration of disease, extent of disease, neutrophilic response

333
Q

Diversion colitis

A

blind colon segment as result of surgical treatment that results in ostomy

334
Q

Microscopic collagenous colitis

A

collagen layer below epithelium, watery diarrhea without weight loss in middle aged women

335
Q

Microscopic lymphocytic colitis

A

watery diarrhea without weight loss in setting of celiac and autoimmune disease

336
Q

Graft-versus-host disease in intestine occurs following…

A

allogenic hematopoietic stem cell transplant, crypts may be completely destroyed; presents as watery diarrhea that may become bloody

337
Q

Diverticular disease occurs due to…

A

pseudodivderticular outpouchings of colonic mucosa and submucosa

338
Q

Prevalence of diverticular disease

A

rare under 30 but common after age 60

339
Q

Pathgenesis of diverticular disease

A

result from unique structure of colonic muscularis propria and elevated intraluminal pressure in sigmoid colon; focal musclar discontinuities

340
Q

Clinical manifestations of diverticulitis

A

intermittent cramping, continuous lower abdominal discomfort, constipation, distention

341
Q

Where in the GI tract are polyps most common?

A

colon and rectum

342
Q

sessile polyp

A

small elevation without a stalk

343
Q

pedunculated polyp

A

polyp with stalks

344
Q

Four types of polyps

A

hyperplastic, inflammatory, hamartomoatous, adenoma

345
Q

Hyperplastic polyps result from…

A

decreased epithelial cell turnover and delayed shedding of surface epithelial cells, leading to a “piling up” of goblet cells and absorptive cells

346
Q

When and where are hyperplastic polyps typically found?

A

Left colon in the 6th-7th decade of life

347
Q

Hyperplastic polyps must be differentiated from what malignant growth?

A

sessile serrated adenomas

348
Q

Triad of solitary rectal ulcer syndrome

A

rectal bleeding, mucus discharge, anterior rectal wall

349
Q

What causes the formation of inflammatory polyps?

A

chronic cycles of injury and healing

350
Q

Histologic features of inflammatory polyps?

A

mixed inflammatory infiltrates, erosion, and epithelial hyperplasia with prolapse-induced lamina propria fibromusclar hyperplasia

351
Q

Most hamartomatous polyps are caused by what?

A

germline mutation of tumor suppressor genes or protooncogenes

352
Q

When and where do juvenile polyps typically occur?

A

typically occur under 5 years of age, rectal location

353
Q

Complications of juvenile polyps

A

rectal bleeding, intussusception, intestinal obstruction, polyp prolapse

354
Q

Extraintestinal manifestations of juvenile polyposis

A

pulmonary AV malformation and other congenital malforamations, digital clubbing

355
Q

Mutated genes of Juvenile polyposis

A

SMAD4, BMPR1A

356
Q

Peutz-Jeghers syndrome

A

autosomal dominant syndrome that presents around 11 yo with multiple GI hamartomatous polyps and mucocutaneous hyperpigmentation

357
Q

Common locations of Peutz-Jeghers polyps

A

small intestine, stomach and colon, bladder and lungs

358
Q

LOF mutation in what gene is responsible for Peutz-Jeghers

A

STK11, a tumor suppressor enzyme

359
Q

Histologic appearance of Peutz-Jeghers polyp

A

arborizing network of CT, smooth muscle, lamina propria, and glands lined by normal-appearing intestinal epithelium

360
Q

What types of CA are at a greater risk for development in Peutz-Jeghers syndrome?

A

colon, breast, lung, pancreatic, thyroid

361
Q

Most common neoplastic polyps

A

adenomatous polyp

362
Q

Sex predominance of adenomatous polyps

A

male

363
Q

Colorectal adenomas are characterized by what histological feature?

A

presence of epithelial dysplasia; nuclear hyperchromasia, elongation, stratification

364
Q

Most important characteristic of a polyp that correlates with malignancy risk

A

size

365
Q

Familial adenomatous polyposis

A

autosomal dominant disorder in which patients develop colorectal adenomas as teenagers

366
Q

Genetic mutation that causes FAP

A

somatic mutation in APC gene

367
Q

Extraintestinal manifestations of FAP

A

congenital hypertrophy of retinal pigment epithelium

368
Q

Risk of CA in patients with FAP

A

Colorectal adenocarcinoma develops in 100% of untreated FAP patients

369
Q

Most common cause of malignancy of GI tract

A

adenocarcinoma of the colon

370
Q

Where does colonic adenocarcinoma most commonly occur in the world?

A

North America

371
Q

Peak age of colonic adenocarcinoma

A

60-70 yo

372
Q

Dietary factors that contribute to colonic adenocarcinoma

A

low fiber, high fat and refined carbs

373
Q

Pharmacologic chemoprevention of colonic adenocarcinoma

A

ASA and NSAIDs can contribute to polyp regression

374
Q

Two genetic pathways that contribute to pathogenesis of Colonic Adenocarcinoma

A

APC/B-catenin/Wnt pathway and Microsatellite instability pathway

375
Q

What gene must be mutated for adenomas to develop

A

both copies of APC at 5q21

376
Q

Function of APC

A

negative regulator of B-catenin (involved in Wnt signaling

377
Q

Function of B-catenin

A

binds to DNA and upregulates gene transcription that promote cell growth

378
Q

Mutations in KRAS promote what?

A

12p12, promotes cell growth and prevent apoptosis

379
Q

SMAD2/SMAD 4 mutation result

A

uncontrolled cell growth

380
Q

Microsatellite instability

A

mutations accumulate in microsatellite repeats

381
Q

Hereditary non polyposis colorectal cancer mutation

A

inherited mutations in mismatch repair genes

382
Q

What CAs have the highest risk in HNPCC?

A

Colon, endometrium, stomach

383
Q

Morphology of GI tract adenocarcinoma in colon

A

tumors in proximal colon grow as polypoid, exophytic masses that extend along wall of cecum and colon; tumors in distal colon tend to be annular, narrowing lumen

384
Q

Histology of adenocarcinomas

A

tall columnar cells, signet-ring cells, stromal desmoplastic response

385
Q

Clinical features of GI adenocarcinoma (R vs. L)

A

R will present with fatigue and weakness due to IDA, L will present with occult bleeding, changes in bowel habits, cramping and LLQ discomfort

386
Q

Most important prognostic factors for GI adenocarcinoma

A

depth of invasion and LN metastases

387
Q

5 year prognosis for colon adenocarcinoma

A

65% at five years

388
Q

Epithelium in upper anal canal

A

columnar rectal

389
Q

Epithelium in middle anal canal

A

transitional epithelium

390
Q

Epithelium in lower anal canal

A

stratified squamous epithelium

391
Q

CAs below pectinate line are usually

A

squamous cell carcinomas

392
Q

CAs above pectinate line are usually

A

adenocarcinoma

393
Q

What LN do anal canal cancers spread to?

A

inguinal lymphnodes

394
Q

Most common viral cause of SCC of anal canal

A

HPV

395
Q

Hemorrhoids develop secondary to…

A

elevated venous pressure in hemorrhoidal plexus–due to pregnancy, straining, constipation, portal hypertension

396
Q

External hemorrhoids are located…

A

below anorectal line

397
Q

Histological presentation of hemorrhoids

A

thin-walled, dilated, submucosal vessels that protrude beneath the anal or rectal mucosa

398
Q

Clinical presentation of hemorrhoids

A

pain and rectal bleeding

399
Q

Acute appendicitis is most common in what age groups?

A

adolescents and young adults, males are slightly more affected

400
Q

DDx for acute appendicitis

A

Meckel diverticulum, mesenteric lymphadenitis, acute salpingitis, ectopic pregnancy, mittelschmirtz

401
Q

Pathogenesis of acute appendicitis

A

overt luminal obstruction–fecalith, gallstone, tumor, mass of worms

402
Q

Clinical presentation of acute appendicitis

A

periumbilical pain that localizes to RLQ followed by N/V and fever

403
Q

most common tumor of the appendix

A

well-differentiated neuroendocrine tumor

404
Q

Pseudomyxoma peritonei

A

syndrome of progressive intraperitoneal accumulation of mucinous ascites related to a mucin-producing neoplasm

405
Q

Cause of sterile peritonitis

A

leakage of bile or pancreatic enzymes

406
Q

Causes of peritonitis

A

perforation of biliary system, acute hemorrhagic pancreatitis, foreign material, endometriosis, ruptured dermoid cysts

407
Q

Sclerosing retroperitonitis is characterized by…

A

dense fibrosis that may extend to involve the mesentery, often surrounds abdominal aorta and ureters

408
Q

Most common presenting symptom of sclerosing retroperitonitis

A

back and abdominal pain

409
Q

Peritoneal mesotheliomas are almost always associated with what kind of environmental exposure?

A

asbestos

410
Q

Most common soft tissue tumor of peritoneum

A

desmoplastic small round cell tumor

411
Q

Peritoneal carcinomatosis

A

secondary tumors that involve peritoneum by direct spread or metastatic seeding

GI II (8 decks)

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