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GASTROINTESTINAL > GASTROINTESTINAL- Pathology > Flashcards

GASTROINTESTINAL- Pathology Flashcards

1
Q

Normaly how is the prognosis of salivary gland tumors?

A

Generally benign

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2
Q

Which glands are often affected by cancer?

A

Parotid glands

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3
Q

Salivary gland tumors

A

Pleomorphic adenoma
Warthin tumor
Mucoepidermic carcinoma

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4
Q

Most common salivary gland tumor

A

Pleomorphic adenoma

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5
Q

How is Pleomorphic adenoma consider?

A

Benign mixed tumor

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6
Q

How is pleomorphic adenoma presented?

A

As a painless, mobile mass

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7
Q

Histological characteristics of Pleomorphic adenoma

A

Chondromyxoid stroma and epithelium

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8
Q

Which is the expected evolution of Pleomorphic adenoma?

A

Recurs if incompletely excised or ruptured intraoperatively

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9
Q

What is Warthin tumor?

A

Papillary cystadenoma lymohomatosum

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10
Q

How is Warthin tumor classified?

A

Benign cystic tumor with germinal centers

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11
Q

Most common malignant tumor of Salivary glands

A

Mucoepidermoid carcinoma

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12
Q

Which are the components of Mucoepidermoid carcinoma?

A

Mucinous and squamous components

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13
Q

How is mucoepidermoid carcinoma manifested?

A

Painless, slow growing mass

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14
Q

What is Achalasia?

A

Failure of relaxation of LES due to loss of myenteric (Auerbach) plexus

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15
Q

Main Characteristics of Achalasia

A

High LES opening pressure and uncordinated peristalsis

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16
Q

Findings of Achalasia

A

Progressive dysphagia to solids and liquids

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17
Q

How is dysphagia when caused by obstructive processes?

A

Dysphagia to solids only

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18
Q

Which imaging study helps to diagnose Achalasia? and what does it shows?

A

Barium swallow shows dilated esophagus with an area of distal stenosis

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19
Q

With which disease is Achalasia related to?

A

Associated with ↑ risk of esophageal squamous cell carcinoma

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20
Q

What does Achalasia means?

A

A- chalasia= absence of relaxation

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21
Q

Finding of Achalasia in barium swallow

A

Bird’s beak

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22
Q

Which is the most common cause of secondary achalasia?

A

Chagas disease

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23
Q

Which is the most common cause of secondary achalasia?

A

Chagas disease

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24
Q

What is Boerhaave syndrome?

A

Transmural, usually distal esophageal rupture due to violent retching

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25
Q

Which is the treatment for Boerhaave syndrome?

A

Surgical emergency

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26
Q

In which patients is more common to see Eosinophilic esophagitis?

A

Atopic patients

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27
Q

What is the detonant of Eosinophilic esophagitis?

A

Food allergens → dysphagia, heartburn, strictures

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28
Q

How is the benefict of GERD therapy in Eosinophilic esophagitis?

A

Unresponsive to GERD therapy

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29
Q

What is associated to esophageal strictures?

A

Lye ingestion and acid reflux

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30
Q

What are the Esophageal varices? what cause them?

A

Painless bleeding of dilated submucosal veins in lower 1/3 of esophagus secondary to portal hypertension

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31
Q

Which are agents associated to Esophagitis?

A

Reflux
Infection in immunocompromised
Chemical ingestion

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32
Q

Most common causing agents of Esophatitis in immunodepressed

A

Candida- white pseudomembrane
HSV-1: punched out ulcers
CMV: linear ulcers

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33
Q

How is gastroesophageal reflux disease manifested?

A

Commonly presents as heartburn and regurgitation upon lying down
Nocturnal cough and dyspnea, adult onset asthma

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34
Q

What is affected in gastroesophageal reflux disease?

A

Decrease in LES tone

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35
Q

Mucosal lacerations at the gastroesphageal junction due to severe vomiting

A

Mallory Weiss syndrome

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36
Q

What does Mallory Weiss syndrome leads to?

A

Hematemesis

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37
Q

In which patients is more often to see Mallory Weiss syndrome?

A

In alcoholics and bulimics

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38
Q

In which patients is more often to see Mallory Weiss syndrome?

A

In alcoholics and bulimics

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39
Q

Characteristics of Plummer Vinson syndrome

A

Triad of dysphagia, Iron deficicency anemia, and Glossitis

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40
Q

Why is the reason of dysphagia in Plummer Vinson syndrome?

A

Due to esophageal webs

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41
Q

Which is the result of Sclerodermal esophageal dysmotility?

A

Esophageal smooth muscle atrophy → ↓ LES pressure and dysmotility → acid reflux and dysphagia → stricture, Barret esophagus and aspiration

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42
Q

When do we see Sclerodermal esophageal dysmotility?

A

CREST syndrome

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43
Q

What is Barret esophagus?

A

Glandular Metaplasia

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44
Q

What changes of epithelium is seen in Barret esophagus?

A

Replacement of nonkeratinized (stratified) squamous epithelium with intestinal epithelium (nonciliated columnar with Goblet cells) in distal esophagus

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45
Q

Main reason of Barret esophagus

A

Chronic acid Reflux (GERD)

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46
Q

With which diseases is Barret esophagus associated?

A

Esophagitis, esophageal ulcers, and increased risk of esophageal adenocarcinoma

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47
Q

Where is squamocolumnar junction found?

A

SCJ of Z line of esophagus

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48
Q

Where is squamocolumnar junction found?

A

SCJ of Z line of esophagus

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49
Q

Types of Esophageal cancer

A

Squamous cell carcinoma

Adenocarcinoma

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50
Q

How is the evolution of symptoms ans signs in Esophageal cancer?

A

Typically Presents with progressive dysphagia (first solids, then liquids) and weight loss

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51
Q

How is the prognosis of esophageal cancer?

A

Poor prognosis

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52
Q

Risk factors for Esophageal cancer

A 
AABCDEFFGH
Achalasia
Alcohol
Barret esophagus
Cigarettes
Civerticula (eg Zenker)
Esophageal web
Familial
Fat (obesity)
GERD
Hot liquids
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53
Q

Which risk factors are related to Adenocarcinoma of Esophagus?

A

Barret esophagus
Cigarettes
Fat (obesity)
GERD

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54
Q

Risk factors related to Squamus cell carcinoma of esophagus

A 
Alcohol
Cigartte
Diverticula
Esophageal web
Hot liquids
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55
Q

World wide which is the most common type of esophageal cancer?

A

Squamous cell

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56
Q

In United states which is the most common type of esophageal cancer?

A

Adenocarcinoma

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57
Q

Where does Squamous cell carcinoma of Esophagus affects more?

A

Upper 2/3

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58
Q

Where does Adenocarcinoma of Esophagus affects more?

A

Lower 1/3

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59
Q

Erosive Gastritis

A

Acute Gastritis

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60
Q

In acute gastritis what causes inflmmation?

A

Disruption of mucosal barrier

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61
Q

Reasons of Acute Gastritis

A 
Stress
NSAIDs
Alcohol
Uremia
Burns 
Brain injury
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62
Q

Reasons of Acute Gastritis

A 
Stress
NSAIDs
Alcohol
Uremia
Burns 
Brain injury
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63
Q

How do NSAIDs cause Acute Gastritis?

A

↓ PGE2 → ↓ gastric mucosa protection

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64
Q

What causes Curling Ulcer?

A

↓ plasma volume → sloughing of gastric mucosa

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65
Q

How does a brain injury causes Acute Gastritis?

A

↑ vagal stimulation → ↑ ACh → ↑ H+ production

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66
Q

What is the Cushing Ulcer?

A

↑ vagal stimulation → ↑ ACh → ↑ H+ production

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67
Q

In which patients is more common to see Erosive gastritis?

A

Especially common among alcoholics and patients taking daily NSAIDs

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68
Q

Which patients are propense to acute Gastritis which take daily NSAIDs?

A

Patiens with Rheumatoid Arthritis

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69
Q

Also known as nonerosive gastritis

A

Chronic gastritis

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70
Q

How is Chronic gastritis classified?

A

Type A

Type B

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71
Q

Where does Type A chronic Gastritis affect?

A

Fundus/body

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72
Q

Where does Type B chronic Gastritis affect?

A

Antrum

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73
Q

What is the cause of Type A chronic Gastritis?

A

Autoimmune

Autoantibodies to parietal cells

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74
Q

What could be the results of type A chronic gastritis?

A

pernicious Anemia and Achrolrhydia

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75
Q

Most common type of Chronic gastritis

A

Type B

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76
Q

What causes type B chronic Gastritis?

A

By H. pylori infection

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77
Q

What risks are increased with type B Chronic Gastritis?

A

↑ risk of MALT lymphoma and gastric adenocarcinoma

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78
Q

What is Menetrier disease?

A

Gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucous cells

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79
Q

How risky is Menetrier disease?

A

Precancerous

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80
Q

In which disease rugae of stomach are so hypertrophied that they look like brain gyri

A

Menetrier disease

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81
Q

Most common type of Gastric cancer

A

Almost always Adenocarcinoma

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82
Q

How is the prognosis of Gastric cancer?

A

Early agressive local spread and node/liver metastases

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83
Q

Which is the often finding of Gastric cancer?

A

Acantosis nigricans

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84
Q

Pathological variants of Stomach cancer

A

Intestinal

Diffuse

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85
Q

What causes Intestinal variant of Stomach cancer?

A

Associated with H. pylori infection, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, chronic gastritis

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86
Q

What has dietary nitrosamines?

A

Smoked foods

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87
Q

Where does Intestinal variant of Stomach cancer affect more?

A

Lesser curvature

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88
Q

Macroscopically how does Intestinal variant of Stomach cancer looks like?

A

Ulcer with raised margins

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89
Q

Is diffuse Stomach cancer associated to H. pylori?

A

No

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90
Q

Histological findings of Diffuse stomach cancer

A

Signet ring cells

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91
Q

Characteristic of Diffuse Stomach cancer

A

Stomach wall grossly thickened and leathery (linitis plastica)

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92
Q

When do we see linitis plastica?

A

In diffuse Stomach cancer

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93
Q

What is Linitis plastica?

A

Stomach wall grossly thickened and leathery

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94
Q

What is Virchow node?

A

Involvement of left supracavicular node by metastasis from stomach

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95
Q

What is Krukenberg tumor?

A

Bilateral metastases to ovaries

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96
Q

Histological findings of Krukenberg tumor

A

Abundant mucus, signet ring cells

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97
Q

What is Sister Mary Joseph nodule?

A

Subcutaneous periumbilical metastasis

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98
Q

This peptic ulcer pain decreases with meals

A

Duodenal ulcer

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99
Q

Which peptic ulcer loses weight?

A

Gastric ulcer

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100
Q

How is the pain in Gastric ulcer?

A

Can be greated with meals

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101
Q

In how many cases of Gastric Ulcer is H. pylori infection involved?

A

70%

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102
Q

In how many cases of Duodenal Ulcer is H. pylori infection involved?

A

In almost 100%

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103
Q

What is the mechanism of cause of Gastric ulcer?

A

↓ mucosal protection against gastric acid

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104
Q

How is Duodenal ulcer formed?

A

↓ mucosal protection or ↑ gastric secretion

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105
Q

Other causes for Gastric ulcer

A

NSAIDs

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106
Q

Another cause related to Duodenal ulcer

A

Zollinger Ellison syndrome

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107
Q

Which peptic ulcer is related with increased risk of carcinoma?

A

Gastric ulcer

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108
Q

How risky can Duodenal ulcer be related to carcinoma?

A

Ganerally benign

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109
Q

In which group of age is Gastric ulcer more often?

A

Older patients

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110
Q

Histological findings in Duodenal ulcer

A

Hypertrophy of Brunner glands

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111
Q

Possible ulcer complications

A

Hemorrhage

Perforation

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112
Q

Which peptic ulcer can complicate with hemorrhage?

A

Gastric, duodenal

posterior> anterior

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113
Q

How is hemorrhage produced by gastric ulcer?

A

Ruptured gastric ulcer on the lesser curvature of the stomach → bleeding form left gastric artery

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114
Q

How is hemorrhage produced by duodenal ulcer?

A

An ulcer of the posterior wall of the duodenum → bleeding from gastroduodenal artery

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115
Q

Which peptic ulcer can complicate with perforation?

A

Duodenal ulcer

anterior> posterior

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116
Q

What could be the finding on perforation of duodenal ulcer?

A

May see free air under diaphragm

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117
Q

Clinical findings in perforation of duodenal ulcer

A

With refered pain to the shoulder

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118
Q

Malabsorption syndromes

A 
These Will Cause Devastating Absorption Problems
Tropical sprue
Whipple disease
Celiac sprue
Disaccharidase deficiency
Abetalopoproteinemia
Pancreatic insufficiency
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119
Q

Which are the complications of Malabsorption syndromes?

A

Diarrhea, steatorrhea, weight loss, weakness, and vitamin and mineral deficiencies

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120
Q

Which Malabsorption syndrome has similar findings to Celiac sprue?

A

Tropical sprue

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121
Q

What is the difference of treating Tropical sprue and celiac sprue?

A

Tropical sprue Responds to antibiotics

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122
Q

What is the cause of Tropical sprue?

A

Cause is unknown, but seen in residents of ot recent visitors to tropics

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123
Q

Who causes Whipple disease?

A

Infection with Tropheryma whipplei (gram positive)

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124
Q

Findings in Whipple disease

A

PAS+ foamy macrophages in intestinal lamina propria, mesenteric nodes

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125
Q

Which clinical findings could be found in Whipple disease?

A

Cardiac symptoms, Arthralgias, and Neurologic symptoms are common

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126
Q

Which group of age is more affected by Whipple disease?

A

Most often occurs in Older men

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127
Q

What is the cause of Celiac sprue?

A

Autoimmune mediated intolerace of gliadin (wheat) leading to malabsorption and steatorrhea

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128
Q

What factors are associated to Celiac sprue?

A

HLA-DQ2
HLA-DQ8
northern descent

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129
Q

Main findings of Celiac sprue

A

Anti endomysial, anti tissue transglutaminase, and anti gliadin antibodies

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130
Q

Histological findings of Celiac sprue

A

Blunting of villi and lymphocytes in the lamina propria

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131
Q

Pathophysiology of Celiac sprue

A

↓ mucosal absorption that primarily affects distal duodenum and/or proximal jejunum

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132
Q

What is used in diagnosis of Celiac sprue?

A

Serum levels of tissue transglutaminase antibodies

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133
Q

Which dermatologic finding is associated to Celiac sprue?

A

Dermatitis herpetiformis

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134
Q

What risk does Celiac sprue has?

A

Moderately ↑ risk for malignancy (eg. T cell lymphoma)

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135
Q

What is the treatment for Celiac sprue?

A

Gluten free diet

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136
Q

Most common disaccharidase deficiency

A

Lactase deficiency- —> Milk intolerance

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137
Q

Characteristics of villi in Lactase deficiency

A

Normal villi

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138
Q

How is the diarrhea in disaccharidase deficiency?

A

Osmotic diarrhea

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139
Q

What is the explanation of self limited lactase deficiency can occur following injury (eg. viral diarrhea)?

A

Since lactase is located at tips of intestinal villi, self limited lactase deficiency can occur following injury

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140
Q

How is lactose tolerance test done?

A

Administration of lactose produces symptoms, and Blucose rises

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141
Q

Pathophysiology of Abetalipoproteinemia

A

↓ synthesis of apolipoprotein B → inability to generate chylomicrons →↓ secretion of cholesterol, VLDL into bloodstream → fat accumulation in enterocytes

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142
Q

How is abetalipoproteinemia presented?

A

Presents in early childhood with failure to thrive, steatorrhea, acanthocytosis, ataxia, night blindness

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143
Q

Causes of pancreatic insufficiency

A

Due to cystic fibrosis, obstructing cancer, and chronic pancreatitis

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144
Q

What does pancreatic insufficiency causes?

A

Malabsorption of fat and fat soluble vitamins (Vitamins A, D, E, K)

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145
Q

What is found in stools in Pancreatic insuficiency?

A

↑ neutral fat in stool

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146
Q

What test helps in diagnosing Pancreatic insufficiency?

A

D xylose absorption test

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147
Q

How is D-xylose absorption test in Pancreatic insuficiency?

A

Normal urinary excretion in pancreatic insufficiency

↓ excretion with intestinal mucosa defects or bacterial overgrowth

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148
Q

Name inflammatory bowel diseases

A

Chron Disease

Ulcerative Colitis

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149
Q

Possible etiology of Crohn disease

A

Disordered response to intestinal bacteria

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150
Q

Possible etiology of Crohn disease

A

Disordered response to intestinal bacteria

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151
Q

Ulcerative possible etiology

A

Autoimmune

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152
Q

Where can Crohn disease be localized?

A

Any portion of GI tract, ussually termina ileum and colon

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153
Q

How are the lesion known in Crohn Disease?

A

Skip lesions, rectal sparing

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154
Q

How are the lesions in Ulcerative Colitis?

A

Colitis= Colon inflammation

Continouns colonic lesions, always with rectal involvement

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155
Q

Gross morphology on Crohn Disease

A

Transmural inflammation → Fistulas
Cobblestone mucosa, creeping fat, bowel wall thickening
Linear ulcers
Fissures

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156
Q

What imaging study helps in diagnosis of Crohn disease? What could be found?

A

“Sting sign” on barium swallow X ray

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157
Q

Gross findings in Ulcerative colitis

A

Mucosal and submucosal inflammation only
Friable mucosal pseudopolyps with freely hanging mesentery
Loss of Haustra

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158
Q

What is seen in imaging studies in Ulcerative Colitis?

A

“Lead pipe” aperance on imaging

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159
Q

Microscopic findings of Crohn disease

A

Noncaseating granulomas and lymphoid aggregates

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160
Q

Who mediates inflammatory response in Crohn disease?

A

Th1 mediated

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161
Q

Microscopic findings of Ulcerative Colitis

A

Crypt abscesses and ulcer, bleeding, no granulomas

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162
Q

Who mediates inflammatory response in Ulcerative Colitis?

A

Th2 mediated

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163
Q

Complications of Crohn disease

A

Strictures (leading to obstruction), fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer, gallstones

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164
Q

Complications of Ulcerative Colitis

A

Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma

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165
Q

When is worst the prognosis of Colorectal Cancer related to Ulcerative Colitis?

A

With right sided colitis or pancolitis

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166
Q

Intestinal manifestations of Crohn disease

A

Diarrhea that may or may not be bloody

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167
Q

Intestinal manifestation of Ulcerative Colitis

A

Bloody Diarrhea

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168
Q

Extraintestinal manifestations of Crohn disease

A

Migratory polyathritis, erythema nodosum, ankylosing spondylitis, pyoderma gangrenosum, aphthous ulcers, uveitis, kidney stones

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169
Q

Extraintestinal manifestations of Ulcerative Colitis

A

Pyoderma gangrenosum, erythema nodosum, prymary sclerosing cholangitis, ankylosing spondylitis, apthous ulcers, uveitis

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170
Q

Treatment for Crohn disease

A

Corticosteroids, azathioprine, methotrexate, infliximab, adalimumab

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171
Q

Treatment for Ulcerative Colitis

A

ASA preparations (sulfasalazine), 6- mercaptopurine, ifliximab, colectomy

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172
Q

How is Irritable Bowel syndrome is suspected?

A

Recurrent abdominal pain associated with > 2 of the following:

  • Pain improves with defecation
  • Change in stool frequency
  • Change in apperance of stool
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173
Q

Which are the structural abnormalities seen in irritable Bowel syndrome?

A

No structural abnormalities

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174
Q

In which patients is more common to see irritbale Bowel syndrome?

A

In middle aged women

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175
Q

Which are the posible symptoms of Irritable Bowel syndrome?

A

Diarrhea, constipation, or alternating symptoms

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176
Q

Pathophysiology of Irritable Bowel syndrome

A

Multifaceted

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177
Q

How is Irritable bowel syndrome treated?

A

Treat symptoms

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178
Q

Which is the possible cause of Appendicitis in adults?

A

Inflammation due to obstruction by fecalith

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179
Q

Possible cause of Appendicitis in children

A

Lymphoid hyperplasia

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180
Q

How is the progression of pain in Appendicitis?

A

Initial difusse periumbilical pain migrates to McBurney point

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181
Q

Where is McBurney point?

A

1/3 the distance from anterior superior iliac spine to umbilicus

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182
Q

Common symptoms seen in Appendicitis

A

Nausea, fever

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183
Q

Possible risk of Appendicitis

A

May perforate → peritonitis

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184
Q

Other possible findings in Appendicitis

A

May see psoas, obturador, Rovsing signs

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185
Q

Differential diagnosis of Appendicitis in elderly

A

Diverticulitis

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186
Q

What helps to rule out ectopic preganancy from Apendicits?

A

β-hCG

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187
Q

Treatment for Appendicitis?

A

Appendectomy

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188
Q

What is Diverticulum?

A

Blind pounch protrunding from the alimentary tract that communicates with lumen of the gut

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189
Q

Structures that might present with diverticulum

A

Esophagus, Stomach, duodenum, Colon

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190
Q

How is possible a Diverticulum?

A

They are acquired

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191
Q

Why are Diverticulum called false?

A

In that they lack or have and attenuated muscularis externa

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192
Q

Where are Diverticulum most often found?

A

Sigmoid colon

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193
Q

What is a True Diverticulum?

A

All 3 gut wall layers outpuch

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194
Q

Example of True diverticulum

A

Meckel

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195
Q

This diverticulum only presents with mucosa and submucosa outpuch

A

Flase diverticulum or pseudodiverticulum

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196
Q

Where does Flase diverticulum especially occurs?

A

Where vasa recta perforate muscularis externa

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197
Q

What is Diverticulosis?

A

Many false diverticula of the colon

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198
Q

Common site of apperance of Diverticulosis

A

Sigmid colon

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199
Q

How common is Diverticulosis?

A

Common (in 50% of >60 years old)

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200
Q

Which is the reason Diverticulosis is formed?

A

Caused ↑ intraluminal pressure and focalweakness in colonic wall

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201
Q

Which factor is associated to Diverticulosis?

A

Low fiber diets

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202
Q

Clinical findings of Diverticulosis

A

Often asymptomatic or associated with vague discomfort

A common cause of hematochezia

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203
Q

Complications of Diverticulosis

A

Include Diverticulitis, fistulas

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204
Q

What is Diverticulitis?

A

Inflammation of Divericula

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205
Q

Classical manifestation of Diverticulitis

A

LLQ pain, fever, leukocytosis

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206
Q

Possible complications of Diverticulitis

A 
May perforate → peritonitis, abscess formation, or bowek stenosis
Colovesical fistula (fistula with bladder)
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207
Q

Treatment for Diverticulosis?

A

Antibiotics

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208
Q

What findings can we see in Colovesical fistula?

A

Pneumatura

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209
Q

Lift sided apendicitis

A

Diverticulitis

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210
Q

Pharyngoesophageal flase diverticulum

A

Zenker diverticulum

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211
Q

Pathophysilogy of Zenker diverticulum

A

Herniation of mucosal tissue at KIllian triangle between the thyropharingeal and cricopharyngeal parts of tje inferior pharyngeal constrictor

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212
Q

Presenting symptoms of Zenker diverticulum

A

Dysphagia, obstruction, foul breath from trapped food particles (halitosis)

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213
Q

Who are more propense to Zenker Diverticulum?

A

Elderly males

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214
Q

Which imaging studie helps to diagnose Zenker diverticulum?

A

Barium swallow shows content filling flase diverticulim

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215
Q

Example of false Diverticulum

A

Zenker Diverticulum

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216
Q

Example of True diverticulum

A

Mekel diverticulum

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217
Q

Explanation of Mekel diverticulum

A

Persistence of Vitelline duct

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218
Q

What can Mekel diverticulum may contain?

A

Ectopic acid secreting gastric mucosa and/or pancreatic tissue

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219
Q

Most common congenital anomaly of GI tract

A

Mekel diverticulum

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220
Q

Complications of Meckel diverticulum

A

Melena, RLQ pain, intussusception, volvulus, or obstruction near the terminal ileum

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221
Q

With which disease Meckel diverticulum has contrast?

A

Omphalomesenteric cyst

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222
Q

What is Omphalomesenteric cyst?

A

Cystic dilation of vitelline duct

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223
Q

How is Meckel diverticulum diagnose?

A

Pertechnetate study for uptake by ectopic gastric mucosa

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224
Q

Which are the five 2’s rule in Meckel diverticulum?

A

2 inches long
2 feet from ileocecal valve
2% of population
Commonly presents in first 2 years of life
May have 2 types of epithelia (gastric/ pancreatic)

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225
Q

What is Intussusception?

A

“Telescoping” of 1 bowel segment into distal segment

226
Q

Where is the most common site of Intussusception?

A

Ileocecal junction

227
Q

Presentation of Intussusception

A

Compromised blood supply → intermittent abdominal pain often with “currant jelly” stools

228
Q

How common is Intussusception in adults?

A

Unsual in adults

229
Q

When can we see Intussusception in adults?

A

Associated with intraluminal mass or tumor that acts as lead point that is pulled into the lumen

230
Q

In whom is more common to see Intussusception?

A

Majority of cases occur in children

231
Q

What might be the causes of Intussusception in children?

A

Idiopathic; may be associated with recent enteric or respiratory viral infection

232
Q

How is Intussusception consider?

A

Abdominal emergency in early childhood

233
Q

What is Volvulus?

A

Twisting of portion of bowel around its mesentery

234
Q

What could be the results of volvulus?

A

Can lead to obstruction and infarction

235
Q

Where can Volvulus occur?

A

Throughout the GI tract

236
Q

Which is the most common volvulus in infants and children?

A

Midgut volvulus

237
Q

Which is the most common volvulus in eldery?

A

Sigmoid volvulus

238
Q

Which is the most common volvulus in eldery?

A

Sigmoid volvulus

239
Q

What is Hirschsprung disease?

A

Congenital megacolon characterized by lack of ganglion cells/ enteric nervous plexuses (Auerbach and Meissner plexuses) in segment of intestinal biopsy

240
Q

Which is the cause of Hirschsprung disease?

A

Due to failure of Neural crest cell migration

241
Q

What gene mutation is associated to Hischsprung disease?

A

RET gene

242
Q

How is Hischsprung disease presented?

A

Presents with bilious emesis, abdominal distension, and failure to pass meconium in the first 48 hours of life, ultimately manifesting as chronic constipation

243
Q

In imaging studies what is seen in Hirschsprung disease? Why?

A

Dilated portion of the colon proximal to the aganglionic segment, resulting in a “transition zone”

244
Q

Can Hischsprung disease involve rectum?

A

Yes

245
Q

Which disease has increased risk of Hirschsprung disease?

A

Down syndrome

246
Q

How is Hirschsprun disease diagnosis made?

A

Rectal suction biopsy

247
Q

Which is the treaatment for Hirschsprung disease?

A

Resection

248
Q

What are intestinal adhesions?

A

Fibrous band of scar tissue

249
Q

When are adhesions formed?

A

Commonly formed after surgery

250
Q

Most common cause of bowel obstruction

A

Adhesion

251
Q

What else can be seen in Adhesion?

A

Can have well demarcated necrotic zones

252
Q

Tortous dilation of vessels in GI tract

A

Angiodysplasia

253
Q

Clinical finding of angiodysplasia

A

Hematochezia

254
Q

Where is more often found angiodysplasia?

A

Cecum, terminal ileum and ascending colon

255
Q

In which patiens is more common angiodysplasia?

A

In older patients

256
Q

How is angiodysplasia confirmed?

A

By angiography

257
Q

What does Duodenal atresia causes?

A

Early bilious vomiting with proximal stomach distention

258
Q

What is seen in Duodenal atresia in Imamging studies?

A

“Double bubble” on X-ray

259
Q

Why is proximal stomach distention seen in Duodenal atresia?

A

Because of failure of small bowel recanalization

260
Q

Which disease is associated to Duodenal atresia?

A

Down syndrome

261
Q

What is Ileus?

A

Intestinal hipomotility without obstruction

262
Q

Findings of Ileus

A

Constipation and Decreased Flatulus; distened/ tympanic abdomen with ↓ bowel sounds

263
Q

Which factor are associated to Ileus?

A

Abdominal surgeries, opiates, hypokalemia, and sepsis

264
Q

Reduction in intestinal blood flow causes ischemia

A

Ischemic colitis

265
Q

Clinical findings of Ischemic colitis

A

Pain after eating → weight loss

266
Q

Where is commonly to see inschemic colitis?

A

Splenic flexure and distal colon

267
Q

Who are mainly affected by ischemic colitis?

A

Elderly

268
Q

When is meconium ileus seen?

A

In cystic fibrosis

269
Q

What happens in meconium ileus?

A

Moconium plug obstructs intestine, preventing stool passage at birth

270
Q

Necrosis of intestinal mucosa and possilbe perforation

A

Necrotizing enterocolitis

271
Q

What is mainly affected by Necrotizing enterocolitis?

A

Colon is usually involved, but can involve entire GI tract

272
Q

Who are mainly affected by Necrotizing enterocolitis?

A

In neonates, more common in preemies (↓ immunity)

273
Q

What are Colonic polyps?

A

Masses protruding into gut lumen

274
Q

What apperance do colonic polyps have?

A

Sawtooth apperance

275
Q

Which are the most common Colonic polyps?

A

90% are non neoplastic

276
Q

Where are more common to see Colonic polyps?

A

Rectosigmoid

277
Q

How are Colonic polyps classified?

A

Tubular

Villous

278
Q

Colonic polyps types

A

Adenomatous
Hyperplastic
Juvenile
Hamartomatous

279
Q

How are adenomatous polyps consider?

A

Precancerous

280
Q

With which characteristics is adenomatous polyp associated with malignant risk?

A

↑ size, villous hystology

↑ epithelial dysplasia

281
Q

Precursor to Colorectal cancer

A

Adenomatous polyps

282
Q

Which characteristic of Adenomatous polyps has increased tendency to be malignant?

A

The more villous the polyp, the more likely it is to be malignant (Villous= Villainous)

283
Q

Polyp symptoms

A

Often asymptomatic, lower GI bleed, partia; obstruction, secretopry diarrhea (villous adenomas)

284
Q

Most common non neoplastic polyp in colon

A

Hyperplastic

285
Q

Where are Hyperplastic polyps more often found?

A

> 50% found in rectosigmoid colon

286
Q

Characteristic of Juvenile polyps

A

Mostly sporadic lesions in children

287
Q

Where areJuvenile polyps commonly found ?

A

80% in Rectum

288
Q

When do Juvenile polyps have increased risk for Adenocarcinoma?

A

Multiple Juvenile polyps in GI tract

289
Q

What is the Juvenile Polyposis syndrome?

A

Multiple Juvenile polyps in GI tract

290
Q

What cancer is associated to Juvenile Polyposis syndrome?

A

Adenocarcinoma

291
Q

How risky is having a single Juvenile polyp?

A

No malignant potential

292
Q

Which kind of polyps do Peutz Jeghers syndrome has?

A

Hammartomatous

293
Q

Inheritance mode of Peutz Jeghers syndrome

A

Autosomal dominant

294
Q

Findings of Peutz Jeghers syndrome

A

Multiple nonmalignant hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, genitalia

295
Q

What is associated to Peutz Jeghers syndrome?

A

Increase risk of Colorectal cancer and other malignancies

296
Q

What is associated to Peutz Jeghers syndrome?

A

Increase risk of Colorectal cancer and other malignancies

297
Q

Which group of age is more propense to be affected by Colorectal Cancer?

A

> 50 years old

298
Q

Which percentage of patients with colorectal cancer have a family history?

A

25%

299
Q

Syndromes associated to Colorectal cancer

A

Familial adenomatous polyposis (FAP)
Gardner syndrome
Turcot syndrome
Hereditary nonpolyposis colorectal cancer (HNPCC/Lynch syndrome)

300
Q

Inheritance mode of Familial Adenomatous polyposis

A

Autosomal dominant

301
Q

Which gene is affected in Familial adenomatous polyposis?

A

APC gene on chromosome 5q. 2 hit hypothesis

302
Q

Which percentage of Familial adenomatous polyposis progress to Colorectal cancer?

A

100%

303
Q

How do you stop Familial adenomatous polyposis progresses to Colorectal Cancer?

A

Colon resection

304
Q

How many polyps arise in Familial adenomatous polyposis?

A

Thousans of polyps arise starting at a young age

305
Q

Which structures are involved in Familial adenomatous polyposis?

A

Pancolonic, always involve rectum

306
Q

Findings of Gardener Sydrome

A

Familial adenomatous polyposis+ osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium

307
Q

What does Turcot syndrome includes?

A

Familial adenomatous polyposis+ malignant CNS tumor

308
Q

How else is Hereditary nonpolyposis colorectal cancer known?

A

Lynch syndrome

309
Q

Mode of inheritance of Hereditary nonpolyposis colorectal cancer

A

Autosomal dominant mutation of mutation of DNA mismatch repair genes

310
Q

Which percentage of Hereditary nonpolyposis colorectal cancer progresses to Colorectal Cancer?

A

80%

311
Q

Which structure is always involved in Hereditary nonpolyposis colorectal cancer ?

A

Proximal colon

312
Q

Additional risk factors for Colorectal cancer

A 
Inflammatory bowel disease
Tobaco use 
Large villous adenomas
Juvenile polyposis syndrome
Peutz Jeghers syndrome
313
Q

In order, which structures suffer more colorectal cancer?

A

Rectosigmoid> ascending> descending

314
Q

Findings of Colorectal cancer in Ascending colon

A

Exophytic mass
Iron deficiency anemia
Weight loss

315
Q

Presentation of Colorectal cancer in descending colon

A

Infiltrating mass, partial obstruction, colicky pain, hematochezia

316
Q

Rare presentation of Colorectal cancer

A

Presents as Streptococcus bocis bacteremia

317
Q

Mnemonic of side presentation of Colorectal cancer

A

Right side bleeds

Left obstructs

318
Q

When do you suspect of Colorectal cancer?

A

Iron deficiency anemia in males (especially > 50 years old) and postmenopausal females raises suspicion

319
Q

When and how do you screen patiens from Colorectal cancer?

A

> 50 years old with colonoscopy or stool occult blood test

320
Q

What imaging study made us suspect of Colorectal cancer? and What might be seen?

A

“Apple core” lesions seen on barium enema x ray

321
Q

Good for monitoring recurrence of Colorectal cancer, not useful for screening

A

CEA tumor marker

322
Q

What utility does CEA tumor marker has in Colorectal cancer?

A

Good for monitoring recurrence, not useful for screening

323
Q

Which are the 2 molecular pathways that lead to Colorectal cancer?

A

Microsatelite instability pathway

APC/ β catenin pathway

324
Q

How common is Microsatelite instability pathway causing Colorectal cancer?

A

15%

325
Q

How common is APC/ β catenin pathway causing Colorectal cancer?

A

85%

326
Q

Which is genetic cause of Microsatelite instability pathway in Colorectal cancer?

A

Mismatch repair gene mutations

327
Q

Which Colorectal cancer is related to Microsatelite instability pathway?

A

Sporadic and HNPCC syndrome

328
Q

Characteristic of Microsatelite instability pathway

A

Mutations accumulate, but not defined morphologic correlates

329
Q

Chromosomalinstability of Colon cancer

A

APC/ β catenin pathway

330
Q

What is the result of APC/ β catenin pathway in Colon cancer?

A

Sporadic cancer

331
Q

Order of gene events

A

AK-53

Loss of APC → K-RAS mutation → Loss of gene suppresor gene (p53, DCC)

332
Q

From a normal colon to Colon at risk, what is affected?

A

Loss of APC

333
Q

Celular changes of Colon ephitelia when loss of APC

A

Decreassed intercellular adhesion and increased proliferation

334
Q

From colon at risk to Adenoma, which gene is affected?

A

K-RAS mutation

335
Q

What happens when K-RAS mutation?

A

Unregulated intracellular signal transduction

336
Q

What is affected form the conversion from adenoma to Carcinoma?

A

Loss of tumor supressor gene (p53, DCC)

Increased Tumorogenesis

337
Q

Effects of portal hypertension

A 
Esophageal varices
Melena
Splenomegaly
Caput medusae, ascites
Portal hypertensive gastropathy
Anorectal varices
338
Q

How is Melena produced in Portal hypertension?

A

Esophageal varices→ Melena

Peptic ulcer → Melena

339
Q

Clinical findings of Esophageal varices

A

Melena

Hematemesis

340
Q

Effects of liver cell failure

A 
Hepatic encephalopathy
Scleral icterus
Fetor hepaticus (breath smells musty)
Spider nevi
Gynecomastia 
Jaundice
Testicular atrophy
Liver "flap"= asterixis (coarse hand tremor)
Bledding tendency (↓ clotting factors, ↑ prothrombin time)
Anemia
Ankle edema
341
Q

Why is it possible to see a patient feminized in liver cell failure?

A

Due to ↑ estrogen

342
Q

What happens during cirrhosis?

A

Diffuse fibrosis and nodular regeneration destroys normal architecture of liver

343
Q

What risk is increased with Cirrhosis?

A

Hepatocellular carcinoma

344
Q

Etiologies of Cirrhosis

A

Alcohol
Viral hepatitis
Biliary disease
Hemochromatosis

345
Q

How many cases of Cirrhosis are related to Alcohol?

A

60-70%

346
Q

Benefit of Portosytemic shunts

A

Partially alleviate portal hypertension:
Esophageal varices
Caput medusae

347
Q

Benefit of Portosytemic shunts

A

Partially alleviate portal hypertension:
Esophageal varices
Caput medusae

348
Q

Major diagnostic use for Alkaline phosphatase

A

Obstructive hepatobiliary disease
Hepatocellular carcinoma
Bone disease

349
Q

When are aminotransferases (AST and ALT) elevated?

A 
Viral hepatitis (ALT> AST)
Alcoholic hepatitis (AST> ALT)
350
Q

Wehn do we see Amylase elevated?

A

Acute pancreatitis, mumps

351
Q

Serum marker decreased in Wilson disease

A

Ceruloplasmin

352
Q

γ glutamil transpeptidase (GGT) is elevated in these situations

A

Increased in various liver and biliary diseases (just as ALP can), but not in bone disease; asociated with alcohol with alcohol use

353
Q

Serum marker in acute pancreatitis (most specific)

A

Lipase

354
Q

What is Reye syndrome?

A

Rare, often fatal childhood encephalopathy

355
Q

Findings in Reye syndrome

A 
Mitochondrial abnormalities
Fatty liver (microvesicular fatty change)
Hypoglycemia
Vomiting
Hepatomegaly
Coma
356
Q

When do we see Reye syndrome?

A

Associated with viral infection (especially VZV and influenza B) that has been treated with aspirin

357
Q

Which is the patophysiology of Reye syndrome?

A

Aspirin metabolites ↓ β oxidation by reversible inhibition of mithocondrial enzyme

358
Q

What precautions are made in order to avoid Reye syndrome?

A

Avoid aspirin in children

359
Q

When is necesary to use aspirin in children?

A

In those with Kawasaki disease

360
Q

Phases of Alcoholic liver disease

A

Hepatic steatosis
Alcoholic hepatitis
Alcoholic hepatitis

361
Q

How is the progression of Hepatic steatosis?

A

Reversible with moderate alcohol intake

362
Q

Hystological findings in Hepatic Steatosis

A

Macrovesicular fatty change that may be reversible with alcohol cessation

363
Q

What is needed to get Alcoholic Hepatitis?

A

Requires sustained, long term consuption

364
Q

Hystologic findings of Alcoholic hepatitis

A

Swollen and necrotic hepatocytes with neutrophilic infiltration
Mallory bodies are present

365
Q

What are Mallory bodies?

A

intracytoplasmatic eosinophilic inclusiones in hepatocytes

366
Q

What is increased in Alcoholic hepatotitis?

A

AST> ALT (ratio usually >1.5)

367
Q

How is Alcoholic cirrhosis consider?

A

Final and irreversible form

368
Q

Gross findings of Alcoholic cirrhosis

A

Micronodular, irregular shrunken liver with “hobnail” aperance

369
Q

Microscopic findings in alcoholic cirrhosis

A

Scleoris around central vein (zone III)

370
Q

Manifestation of Alcoholic cirrhosis

A

Of chronic liver diasease:

eg. jaundice, hypoalbuminemia

371
Q

Pathophysiology of Non alcoholic fatty liver disease

A

Metabolic syndrome (insulin resistance) → fatty infiltration of hepatocytes → cellular “ballooning” and eventual necrosis

372
Q

What could be the results of Non alcoholic fatty liver disease?

A

Cirrhosis

Hepatocellular carcinoma

373
Q

Which labs are modified in Non alcoholic fatty liver disease?

A

ALT > AST

374
Q

Pathophysiology of Hepatic encephalopathy

A

Cirrhosis → portosystemic shunts → ↓ NH3 metabolism → neuropsychiatric dysfunction

375
Q

How could Hepatic encephalopathy be manifested?

A

Spectrum from disorientation/asterixis (mild) to difficult arousal or coma (severe)

376
Q

Which are the triggers of Hepatic encephalopathy?

A

↑ NH3 production

↓ NH3 removal

377
Q

Which situations have ↑ NH3 production?

A

Dietary protein
GI bleed
Constipation
Infection

378
Q

Which situations have ↓ NH3 removal?

A

Renal failure
Diuretics
Post-TIPS

379
Q

Which is the treatment for Hepatic encephalopathy?

A

Lactulose (↑ NH4+ generation), low protein diet, and rifaxim (kills intestinal bacteria)

380
Q

Most common primary malignant tumor of the liver in adults

A

Hepatocellular carcinoma

381
Q

Alternative name for Hepatocellular carcinoma

A

Hepatoma

382
Q

Diseases associated to Hepatocellular carcinoma

A 
Hepatitis B and C
Wilson disease
Hemochromatosis
α1 antitrypsin deficiency
Alcoholic cirrhosis
Carcinogens
383
Q

Examples of Carcinogens related to Hepatocellular carcinoma

A

Aflatoxins from Aspergillus

384
Q

What can Hepatocelular Carcinoma lead to?

A

Budd Chiari syndrome

385
Q

Other liver tumors

A

Cavernous hemangioma
Hepatic adenoma
Angiosarcoma

386
Q

How is Cavernous hemangioma classified?

A

Common, benign liver tumor

387
Q

When does Cavernous hemangioma commonly occurs?

A

At age 30-50 years

388
Q

What is contraindicated in Cavernous hemangioma if suspected? Why?

A

Biopsy, because of risk of hemorrhage

389
Q

How is Hepatic adenoma classified?

A

Rare benign liver tumor

390
Q

What is related to Hepatic adenoma?

A

To oral contraceptive or anabolic steroid use

391
Q

How is the progression of Hepatic adenoma?

A

May regress spontaneously or rupture (abdominal pain and shock)

392
Q

Malignant tumor of endothelial origin in liver

A

Angiosarcoma

393
Q

Which factors are associated to Angiosarcoma?

A

Exposure to Arsenic, vinyl chloride

394
Q

Reason of Nutmeg liver

A

Due to backup of blood into liver

395
Q

Causes of Nutmeg liver

A

By right sided heart failure and Budd Chiari syndrome

396
Q

Which is the apperance of Nutmeg liver?

A

Mottled like nutmeg

397
Q

If the Nutmeg liver persists, what is the risk?

A

Centrilobular congestion and necrosis can result in cardiac cirrhosis

398
Q

Pathophysiology of Budd Chiari syndrome

A

Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease

399
Q

Signos of Congestive liver disease

A

Hepatomegaly
Ascites
Abdominal pain
Eventual liver failure

400
Q

Findings of Budd Chiari syndrome

A

May develop varices and have visible abdominal and back veins
Absence of JVD

401
Q

Which disease are associated to Budd Chiari syndrome?

A

Hypercoagulabel states
Polycythemia vera
Pregnancy
Hepatocelular carcinoma

402
Q

Which disease are associated to Budd Chiari syndrome?

A

Hypercoagulabel states
Polycythemia vera
Pregnancy
Hepatocelular carcinoma

403
Q

Pathophysiology of α1 antitrypsin deficiency

A

Misfolded gene product protein aggregates in hepatocellular ER→ cirrhosis with PAS + globules in liver

404
Q

Genetic characterisitic of α1 antitrypsin deficiency

A

Codominant trait

405
Q

What other disease is associated to α1 antitrypsin deficiency?

A

Panacinar emphysema

406
Q

Pathophysiology of Panacinar emphysema

A

In lungs, ↓ α1 antitrypsin deficiency → uninhibited elastase in alveoli→ ↓ elastic tissue → panacinar emphysema

407
Q

What is Jaundice?

A

Abnormal yellowing of the skin and/ or sclera due to bilirubin deposition

408
Q

When does jaundice occurs?

A

At high levels of Bilirubin (>2.5 mg/dL) in the blood secondary to ↑ production or defective metabolism

409
Q

How is Urine Urobilinogen in unconjugated (indirect) hyperbilirubinemia?

A

↑

410
Q

Diseases that have unconjugated hyperbilirubinema

A

Hemolytic physiologic (newborns), Crigler Najjar, Gilbert syndrome

411
Q

How is Urine Urobilinogen in conjugated (direct) hyperbilirubinemia?

A

↓

412
Q

Diseases that present with unconjugated hyperbilirubinema

A

Biliary tract obstruction
Biliary tract disease
Excretion defect

413
Q

Examples of biliary tract obstruction

A

Gallstones, pancreatic liver cancer, liver fluke

414
Q

Examples of Biliary tract disease

A

Primary sclerosing cholangitis, Primary biliary cirrhosis

415
Q

Excretion defects

A

Dubin- Johnson syndrome, Rotor syndrome

416
Q

How is Urine urobilinogen in Mixed (direct and indirect) hyperbilirubinemia?

A

Normal/ ↑

417
Q

Diseases that present with Mixed (direct and indirect) hyperbilirubinemia

A

Hepatitis

Cirrhosis

418
Q

Explanation of physiologic neonatal jaundice leading to kernicterus

A

At birth, immature UDP- glucoronosyltransferase → Unconjugated hyperbilirubinemia → jaundice/ kernicterus

419
Q

Which is the treatment for physiologic neonatal jaundice

A

Phototherapy

420
Q

How does phototherapy helps treating physiologic neonatal jaundice

A

Converts unconjugated bilirubin to water soluble form

421
Q

How does phototherapy helps treating physiologic neonatal jaundice

A

Converts unconjugated bilirubin to water soluble form

422
Q

Pathophysiology of Gilbert syndrome

A

Mildly ↓ UDP- glucoronyltransferanse conjugation activity→ ↓ bilirubin uptake by hepatocytes

423
Q

Clinical findings of Gilbert syndrome

A

Asymptomatic or mild jaundice

424
Q

Labs found in Gilbert syndrome

A

Elevated unconjugated bilirubin without overt hemolysis

425
Q

When is bilirubin during Gilbert syndrome?

A

With fasting and stress

426
Q

How common is Gilbert syndrome?

A

Very common. clinical consequences

427
Q

Pathophysiology of Crigler Najjar syndrome

A

Absent UPD glucoronosyltransferase

428
Q

How is the prognosis of Crigler Najjar syndrome?

A

Presents early in life; patients die within a few years

429
Q

Clinical findings in Crigler Najjar syndrome

A

Jaundice, Kernicterus (bilirubin depositions in brain)

430
Q

Which labs are affected in Crigler Najjar syndrome?

A

↑ unconjugated bilirubin

431
Q

Treatment for Crigler Najjar syndrome?

A

Plasmapheresis, Phototherapy

432
Q

Which Crigler Najjar syndrome type is less severe?

A

Type II

433
Q

Which drug helps in Crigler Najjar syndrome type II?

A

Phenobarbital, Which ↑ liver enzyme synthesis

434
Q

Pathophysiology of Dubin Johnson syndorme

A

Conjugated hyperbilirubinemia due to defective liver excretion

435
Q

How is the liver in Dubin Jonhson syndrome?

A

Grossly black

436
Q

How is Dubin Johnson sindrome consider?

A

Benign

437
Q

Which disease is similar to Dubin Johnson syndrome? What is the difference?

A

Rotor syndrome is similar but even milder and does not cause black liver

438
Q

Where is Space of Disease ubicated?

A

Between endothelial cell and Hepatocyte

439
Q

What circulates in Hepatic sinusoid?

A

Circulating bilirubin, comes from hemoglobin

440
Q

From the bilirubin uptake in hepatocytes what is formed?

A

Unconjugated bilirubin

441
Q

Which enzyme is needed for bilirubin conjugation?

A

Glucuronyl transferase

442
Q

Characteristic of Conjugated bilirubin

A

Bilirubin diglucorinida, water soluble

443
Q

Once Conjugated Bilirubin is formed what happens next?

A

Intracellular transport, and then to Bile flow

444
Q

What is the problem in Gilbert syndrome?

A

With bilirubin uptake

445
Q

What kind of hyperbilirubinemia is Gilbert syndrome?

A

Unconjugated hyperbilirubinemia

446
Q

What is the problem in Crigler Najjar syndrome?

A

With bilirubin conjugation

447
Q

What kind of hyperbilirubinemia in Crigler Najjar syndrome?

A

Unconjugated hyperbilirubinemia

448
Q

What problem is seen in Dublin Johnson syndrome?

A

With excretion of conjugated bilirubin

449
Q

What kind of hyperbilirubinemia is Dublin Johnson?

A

Conjugated hyperbilirubinemia

450
Q

What kind of hyperbilirubinemia is Rotor syndrome?

A

Mild conjugated hyperbilirubinemia

451
Q

Alternative name for Wilson disease

A

Hepatolenticular degeneration

452
Q

Pathophysiology of Wilson disease

A

Inadequate hepatic cooper excretion and failure of cooper to enter circulation as ceruloplasmin

453
Q

What is the result of Wilson disease?

A

Leads to cooper accumulation

454
Q

Where does cooper accumulates primarily in Wilson disease?

A

Liver, brain, cornea, kidneys and joints

455
Q

Characteristics of Wilson disease

A

Cooper is Hella BAD
↓ Ceruloplasmin, Cirrhosis, Corneal deposits, Cooper accumulation, Carcinoma (hepatocellular)
Hemolytic anemia
Basal ganglia degeneration (parkinsonian symptoms)
Asterixis
Dementia, dyskinesia, dysarthria

456
Q

What is the treatment for Wilson disease?

A

Penicillamine or trientine

457
Q

Mode of inheritance of Wilson disease

A

Autosomal recessive inheritance

458
Q

Which chromosome is related to Wilson disease?

A

Chromosome 13

459
Q

How is Cooper normally excreted?

A

Excreted into bile by hepatocyte cooper transporting ATPase

460
Q

Which gene is related to cooper transporting ATPase ?

A

ATP7B gene

461
Q

Kayser Fleisher ring

A

Golden brown corneal ring (Corneal cooper deposits)

462
Q

Deposition of hemosiderin (iron)

A

Hemosiderosis

463
Q

Disease caused by iron deposition (hemosiderin)

A

Hemochromatosis

464
Q

How else is Hemochromatosis known?

A

Bronze diabetes

465
Q

Classic triad of Hemochromatosis

A

Micronodular Cirhosis
Diabetes Mellitus
Skin pigmentation

466
Q

Classic triad of Hemochromatosis

A

Micronodular Cirhosis
Diabetes Mellitus
Skin pigmentation

467
Q

What could be the complications of Hemochromatosis?

A

Congestive Heart failure
Testicular atrophy
Increased risk of Hepatocelular Carcinoma

468
Q

How can Hemochromatosis be acquired?

A

Primary

Secondary

469
Q

How is primary hemochromatosis acquired?

A

Autosomal recessive

470
Q

How is secondary hemochromatosis acquired?

A

To chronic transfusion therapy (eg. β-thalassemia major)

471
Q

Lab alterations in hemochromatosis

A

↑ ferritin, ↑ iron, ↓ TIBC (Total Iron Binding Capacity)→ ↑ tranferrin saturation

472
Q

How much total iron can the body reach?

A

50g

473
Q

Which levels of iron in the human body can be detected with metal detectors at airports?

A

50g

474
Q

Genes that cause Primary hemochromatosis

A

Due to C282Y or H63D mutation on HFE gene

Associated with HLA-A3

475
Q

What factor in women slows the progression of hemochromatosis?

A

Iron loss through menstruation

476
Q

Which is the treatment for hereditary hemochromatosis?

A

Repeated phlebotomy, deferasirox, deferoxamine

477
Q

Which is the treatment for hereditary hemochromatosis?

A

Repeated phlebotomy, deferasirox, deferoxamine

478
Q

Main biliary tract diseases

A

Secondary biliary cirrhosis
Primary biliary cirrhosis
Primary sclerosng cholangitis

479
Q

Pathophysiology of Secondary biliary crirhosis

A

Extrahepatic biliary obstruction→ ↑ pressure in intrahepatic ducts → injury/fibrosis and bile stasis

480
Q

Examples of extraheptaic biliary obstructions

A

Gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head

481
Q

How is the Presentation of all biliary tract diseases?

A

Pruritus, jaundice, dark urine, light stools, hepatosplenomegaly

482
Q

Labs found in all biliary tract diseases

A

↑ conjugated bilirrubin, ↑ cholesterol, ↑ ALP

483
Q

What complicates Secondary biliary cirhosis?

A

By ascending cholangitis

484
Q

Pathophysiology of Primary biliary cirrhosis

A

Auroimmune reaction → lymphocytic infiltrate + granulomas → destruction of infralobular bile ducts

485
Q

Which other special labs are alterated in Primary biliary cirrhosis?

A

↑ serum mitochondrial antibodies, including IgM

486
Q

Which diseases are associated to primary biliary cirrhosis?

A

Other autoimmune conditions (eg. CREST, Sjogren syndrome, rheumatoid arthritis, celiac disease)

487
Q

Pathophysiology of primary sclerosing cholangitis

A

Unknown cause of concentric “onion skin” bile duct fibrosis → alternating strictures and dilation with beading of intra ans extra hepatic bile ducts on ERCP

488
Q

What special lab is found in primary sclerosing cholangitis?

A

Hypergammaglobulinemia (IgM)

489
Q

Pathology associated to Primary sclerosing cholangitis

A

Ulcerative colitis

490
Q

What can Primary sclerosing cholangitis lead to?

A

Secondary cirrhosis and cholangiocarcinoma

491
Q

What can Primary sclerosing cholangitis lead to?

A

Secondary cirrhosis and cholangiocarcinoma

492
Q

Reasons that cause Gallstone?

A

↑ cholesterol and/or bilirubin, ↓ bile salts, and gallblader stasis

493
Q

Types of stones in cholelithiasis

A

Cholesterol stones

Pigemented stones

494
Q

80% of stones in cholelithiasis

A

Cholesterol stones

495
Q

Which percentage of Cholesterol stones are identified in Gallstones?

A

80%

496
Q

In image studies how are cholesterol stones seen?

A

Radiolucent with 10-20% opaque due to calcifications

497
Q

Which factors are associated to Cholesterol stones?

A

Obesity, Chron disease, cystic fibrosis, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss , Native american origins

498
Q

In image studies how are pigmented stones seen?

A 
Black= radiopaque, hemolysis
Brown= radiolucent, infection
499
Q

Causes of pigemented stones in Cholelithiasis

A

Seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection

500
Q

Possible Consequences of Cholelithiasis

A

Most common cholecystitis, also ascending cholangitis, acute pancreatitis, bile statis

501
Q

Which factors are associated to Cholesterol stones?

A

Obesity, Crohn disease, cystic fibrosis, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss , Native american origins

502
Q

Possible Consequences of Cholelithiasis

A

Most common cholecystitis, also ascending cholangitis, acute pancreatitis, bile statis

503
Q

Possible and common effect of Cholelithiasis

A

Biliary colic

504
Q

What is Biliary colic?

A

Neurohormonal activation triggers contraction of the gallbladder, forcing a stone into the cystic duct

505
Q

In which patients is possible to see painless biliary colic?

A

Diabetics

506
Q

What activates neurohormonal biliary colic?

A

by CCK after a fatty meal

507
Q

What other risk does cholelitiasis has?

A

Can cause fistula between gallbladder and small intestine, leading to air in the biliary tree

508
Q

What is gallstone ileus?

A

When gallstone obstruct ileocecal valve

509
Q

How is Cholelithiasis diagnose?

A

Ultrasound

510
Q

Treatment for Cholelithiasis

A

Cholecystectomy if symptomatic

511
Q

Name the 4 F’s risk factors for cholelithiasis

A

Female
Fat
Fertile (pregnant)
Forty

512
Q

Charcot triad of cholangitis

A

Jaundice
Fever
RUQ pain

513
Q

Acute or chronic inflammation of gallbladder

A

Cholecystitis

514
Q

Pathophysiology of Cholecystitis

A

Usually from cholelithiasis; most commonly blocking the cystic duct → secondary infection

515
Q

Possible complications of Cholecystitis

A

Rarely ischemia or primary infection

516
Q

Primary infection related to cholecystitis

A

CMV

517
Q

Which sign helps in the diagnosis of Cholecystitis?

A

Murphy sign

518
Q

In what consists Murphy sign?

A

Inspiratory arrest on RUQ palapation to pain due to pain

519
Q

When does ALP increases during Cholecystitis?

A

If bile duct becomes involved (eg. ascending cholangitis)

520
Q

How is cholecystitis diagnose?

A

With ultrasound or HIDA (hepatobiliary iminodiacetic acid)

521
Q

What is porcelain gallbladder?

A

Calcified gallbladder due to chronic cholecystitis

522
Q

How is porcelain gallbladder found?

A

Usually found uncudentally on imaging

523
Q

What is the treatment for porcelain gallbladder?

A

Prophylactic cholecystectomy

524
Q

Why is recommended prophylactic cholecystectomy in porcelain gallbladder?

A

Due to high rates of gallbladder carcinoma

525
Q

What happens in acute pancreatitis?

A

Autodigestion of pancreas by pancreatic enzymes

526
Q

Causes of acute pancreatitis

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune disease
Scorpion sting
Hypercalcemia/ Hypertriglyceridemia 
ERCP
Drugs
idipathic
527
Q

Which Triglycerides levels are consider to cause risk of Acute pancreatitis?

A

> 1000 mg/ dL

528
Q

Example of drug that can cause acute pancreatitis

A

Sulfa drugs

529
Q

Clinical presentation of Acute pancreatitis

A

Epigastric abdominal pain radiating to back, anorexia, nausea

530
Q

Labs that help in the diagnosis of acute pancreatitis? Which one is more specific?

A

Amylase, lipase (more specific)

531
Q

What can Acute pancreatitis lead to?

A

DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst formation , hemorrhage, infection, and multiorgan failure

532
Q

Explanation of hypocalcemia due to acute pancreatitis

A

Ca2+ collects in pancreatic cakcium soap deposits

533
Q

Possible complication of Acute pancreatitis

A

Pancreatic pseudocyst

534
Q

Characteristics of pancreatic pseudocyst

A

Lined by granulation tissue, not epithelium; can rupture and hemorrhage

535
Q

What happens in chronic pancreatitis?

A

Chronic onflammation, athrophy, calcification of the pancreas

536
Q

Major causes of Chronic pancreatitis

A

Alcohol abuse and idiopathic

537
Q

What can Chronic pancreatits lead to?

A

Pancreatic insufficiency

538
Q

Findings of pancreatic insufficiency

A

Steatorrhea, fat soluble vitamin deficiency, diabetes mellitus

539
Q

What could be the final result of Pancreatic insuffiency?

A

Increase risk of pancreatic adenocarcinoma

540
Q

How is amylase and lypase in Chronic pancreatitis?

A

May or may not be elevated (almost always elevated in acute pancreatitis)

541
Q

Which image study helps in diagnosis of Porcelain gallbladder? what is seen?

A

X ray of the abdomen shows calcified gallblader wall

542
Q

What image study helps in acute pancreatitis diagnosis? What is seen?

A

Axial CT shows acute exudative pancreatitis with extensive fluid collections surrounding the pancreas

543
Q

What is seen in CT in chronic pancreatitis?

A

Near complete atrophy of the pancreas with residual coarse calfication

544
Q

What is seen in CT in chronic pancreatitis?

A

Near complete atrophy of the pancreas with residual coarse calfication

545
Q

How is the prognosis of Pancreatic adenocarcinoma?

A

Averages 1 year

546
Q

How is Pancreatic adenocarcinoma consider?

A

Very agressive tumor arising from pancreatic ducts

547
Q

Histologic findings in Pancreatic adenocarcinoma

A

Disorganized glandular structure with cellular infiltration

548
Q

From where does pancreatic adenocarcinoma arise from?

A

From pancreatic ducts

549
Q

When is commonly found pancreatic adenocarcinoma?

A

Already metastasized at presentation

550
Q

Where is more common to see pancreatic adenocarcinoma? What does it cause?

A

Pancreatic head (causing obstructive jaundice)

551
Q

Which tumor markers are associated to pancreatic adenocarcinoma?

A

Ca-19-9 tumor marker (also CEA, less specific)

552
Q

Risk factors for pancreatic adenocarcinoma

A 
Tobacco use
Chronic pancreatitis 
Diabetes
Age > 50 years
Jewish and african american males
553
Q

When does chronic pancreatitis increases the risk of pancreatic adenocarcinoma?

A

Especially > 20 years

554
Q

How does Pancreatic adenocarcinoma often presents?

A

Abdominal pain radiating to back
Weight loss
Migratory thrombophlebitis
Obstructive jaundice with palpable, nontender galbladder

555
Q

What explains weight loss in Pancreatic adenocarcinoma?

A

Due to malabsorption and anorexia

556
Q

Characteristics of Migratory thrombophlebitis

A

Redness and tenderness on palpation of extremities

557
Q

What is Trousseau syndrome?

A

Redness and tenderness on palpation of extremities

Seen in migratory thrombophlebitis

558
Q

What is Courvoisier sign?

A

Obstructive jaundice with palpable, nontender gallblader

559
Q

Which is the treatment for Pancreatic adenocarcinoma?

A

Whipple procedure, chemotherapy, radiation therapy

560
Q

How could Pancreatic adenocarcinoma be seen in CT scan?

A

Large lobulated low density mass in the head if the pancreas

561
Q

Possible signs found in Pancreatic adenocarcinoma

A

Trousseau syndrome

Courvoisier sign

562
Q

Possible signs found in Pancreatic adenocarcinoma

A

Trousseau syndrome

Courvoisier sign

GASTROINTESTINAL (5 decks)

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