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OS5 > GI Pathoma > Flashcards

GI Pathoma Flashcards

1
Q

Aphthous ulcer

A

Painful, superficial ulceration of the oral mucosa

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2
Q

An aphthous ulcer arises in relation to _______ and resolves spontenously, but often recurs.

A

Stress

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3
Q

Gross appearance of apthous ulcer

A

Grayish base surrounded by erthema

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4
Q

Behcet syndrome

A

Recurrent apthous ulcers, genital ulcers, and uveitis

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5
Q

Cause of behcet syndrome

A

Due to immune complex vasculitis involving small vessels

NOTE: Can be seen after viral infection, but etiology is unknown

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6
Q

oral herpes

A

Vesicles inbolving oral mucosa that rupture, resulting in shallow, painful, red ulcers

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7
Q

Where does oral herpes remain dormant?

A

Ganglia of the trigeminal nerve

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8
Q

_______ and _____ cause reactivation of HSV1.

A

Sunlight; stress

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9
Q

Risk factors for squamous cell carcinoma of the oral mucosa

A

Tobacco; alcohol

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10
Q

Common location for squamous cell carcinoma of the oral mucosa

A

Floor of mouth

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11
Q

Precursor lesions for squamous cell carcinoma of the oral mucosa

A

Leukoplakia and erythroplakia

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12
Q

Leukoplakia

A

White plaque that cannot be scraped away

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13
Q

Is hairly leukoplakia pre-malignant?

A

No

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14
Q

Erythroplakia

A

Vacularized leukoplakia; highly suggestive of squamous cell dysplasia

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15
Q

Major salivary glands

A

Parotid, submandibular, and sublingual

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16
Q

Symptoms of mumps

A

Bilateral inflamed parotid glands

Orchitis

Pancreatitis

Aseptic meningitis

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17
Q

Mumps virus causes the increase in which enzyme?

A

Serum amylase; due to salivary gland or pancreatic involvement

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18
Q

Sialadenitis

A

Inflammation of the salivary gland

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19
Q

Cause of sialadenitis

A

An obstructing stone leading to S. Aureus infections; usaully unilateral

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20
Q

Most common tumor of the salivary gland

A

Pleomorphic adenoma

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21
Q

Pleomorphic adenoma

A

Benign tumor composed of stromal and epithelial tissue

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22
Q

Pleomorphic adenoma usually arises in ________.

A

Parotid

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23
Q

How does pleomorphic adenoma present?

A

Mobile, painless, circumscribed mass at the angle of the jaw

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24
Q

Pleomorphic adenoma has a high rate of recurrence. Why may this be?

A

Extension of smalll islands of tumor through tumor capsule opten leads to incomplete resection

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25
Q

Pleomorphic adenoma carcinoma rarely may transform into carcinoma. How does this present?

A

Signs of facial nerve damage

REMEMBER:Facial nerve runs through parotid gland

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26
Q

Warthin tumor

A

Benign cystic tumor with abundant lymphocytes and germinal centers

*Alwats arises in the parotid gland

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27
Q

Mucoepidermoid carcinoma

A

Malignatn tumor composed of mucinous and squamous cells

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28
Q

Most common tumor of the salivary gland

A

Mucoepidermoid carcinoma

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29
Q

Congenital defect resulting in a connection betweeen the esophagus and trachea

A

Tracheoesophageal fistula

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30
Q

What is the most common variat of tracheoesophageal fistula?

A

Proximal esophageal atresia with the distal esophagus arising from the trachea

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31
Q

How does a tracheoesophageal fistula present?

A

Vomiting, polyhydramnios, abdominal distension, and aspiration

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32
Q

Thin protrusion of esophageal mucosa

A

Esophageal web

*Most often in the upper esophagus

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33
Q
A
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34
Q

How does esophageal web present?

A

Dysphagia for poorly chewed food

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35
Q

Esophogeal web presents an increased risk for _________.

A

Esophogeal squamous cell carcinoma

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36
Q

Plummer-Vinson syndrome

A

Esophageal web

Severe iron deficiency anemia

Beefy-red tongue due to atrophic glottitis

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37
Q

Zenker diverticulum

A

Outpouching mucosa through an acquired defect in the musclular wall

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38
Q

Where does a zenker diverticulum arise?

A

Above the upper esophogeal sphincter at the junction of the esophagus and pharynx

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39
Q

How does zenker diverticulum presnent?

A

Dysphagia

Obstruction

Halitosis

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40
Q

Mallory-Weiss syndrome

A

Longitudinal laceration of mucosa at the gastroesophageal junction

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41
Q

Causes of mallory-weiss syndrome

A

Severe vomiting, usually due to alcoholism or bulimia

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42
Q

How does mallory-weiss syndrome present?

A

Painful hematemesis

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43
Q

Mallory-weiss syndrome presents a risk for_____

A

Boerhaave syndrome

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44
Q

Boerhaave syndrome

A

Rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema

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45
Q

Esophageal varices

A

Dilated submucosal veins in the lower esophagus

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46
Q

Esophageal varises arise secondary to __________.

A

Portal HTN

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47
Q

Distal esophageal vein normally drains into the portal vein via the _________.

A

Left gastric vein

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48
Q

In portal HTN, the _________ backs up into the esophageal vein, result in dilation.

A

Left gastric vein

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49
Q

Most common cause of death in cirrhosis

A

Esophageal varices

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50
Q

Achalasia

A

Disordered esophageal motility with inability to relax the lower esophageal sphincter

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51
Q

What bug can damage ganglion cells of myenteric plexus?

A

Trypanosoma cruzi

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52
Q

Cause of achalasia

A

Due to damaged ganglion cells in the myenteric plexus

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53
Q

Functions of the ganglion cells in the myenteric plexus

A

Regulate bowel motility and relaxing the LES

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54
Q

Clinical features of achalasia

A
  • Dysphagia for solids and liquids
  • Putrid breath
  • High LES pressure on esophageal manometry
  • “Bird-beak” sign on barium swallow study
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55
Q

Achalasia presents an increased risk for ________

A

esophageal squamous cell carcinoma

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56
Q

GERD

A

Reflux of acid from stomach due to reduced LES tone

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57
Q

Risk factors for GERD

A

Alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia

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58
Q

Clinical features of GERD

A
  • Heartburn
  • Asthma (adult-onset) and cough
  • Damage to enamel of teeth
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59
Q

Complications of GERD

A

Ulceration with stricture and Barret esophagus

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60
Q

Barret esophagus

A

Metaplasia of the lower esophageal mucosa from strtified squamous epithelium to nonciliated columnar epithium with goblet cells

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61
Q

Barret esophagus is seen in _______% of patients with GERD.

A

10

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62
Q

Most common type of esophageal carcinoma in the West

A

Adenocarcinoma

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63
Q
A
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64
Q

Esophageal adenocarcinoma

A
  • Arises from preexisting Barrett esophagus
  • Usually involves the lower one-thrid of the esophagus
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65
Q

Most common esophageal cancer worldwide

A

Squamous cell carcinoma

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66
Q

In which part of the esophagus does squamous cell carcinoma usually arise?

A

Upper or mild third of esophagus

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67
Q

What are the risk factors for squamous cell carcinoma of the esophagus?

A
  • Alcohol and tobacco
  • Very hot tea
  • Achalasia
  • Esophageal web
  • Esophageal injury
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68
Q

Symptoms of esophageal carcinom

A

Progressive dysphagia

Weight loss

Pain

Hematemesis

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69
Q

What are the additiona symptoms of squamous cell carcinoma of the esophagus?

A

Hoarse voice (recurrent layngeal nerve involvement)

Cough (tracheal involvement)

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70
Q

What lymph node does the upper 1/3 of esophagus go to?

A

Cervical

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71
Q

What lymph node does the middle 1/3 of esophagus go to?

A

Mediastinal or tracheobronchial nodes

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72
Q

What lymph node does the lower 1/3 of esophagus go to?

A

Celiac and gastric nodes

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73
Q

Gastroschisis

A

Congenital malformation of the anterior abdominal wall leading to exposure of abdominal contents

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74
Q

Omphalocele

A

Persistant herniation of bowel into umbilical cord

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75
Q

Cause of omphalocele

A

Due to failure of herniated intestines to return to the body during development

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76
Q

In an omphalocele, contents are covered by _______ and ____________.

A

Peritoneum; amnion of the umbilical cord

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77
Q

Congenital hypertrophy of pyloric smooth muscle

A

Pyloric stenosi

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78
Q

True or false. Pyloric stenosis is more common in males.

A

True

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79
Q

How does pyloric stenosis present?

A

Projectile nonbilious vomiting

Visible peristalsis

Olive-like mass in the abdomen

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80
Q

Treatment for pyloric stenosis

A

Myotomy

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81
Q

Acute gastritis is due to

A

Imbalance between mucosal defenses and acidic environment

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82
Q

Mucosal defenses

A

Mucin layer produced by foveolar cells

Bicarbonate secretion by surface epithelium

Normal blood supply

PGE

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83
Q

Risk factors for acture gastritis

A

Severe burn (curling ulcer)

NSAIDs

Heavy alcohol consumption

Increased intracranial pressure (Cushing ulcer)

Shock

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84
Q

Curling ulcer vs Cushing ulcer

A

Curling ulcer: Severe burn

Cushing ulcer: Increased intracranial pressure

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85
Q

By what mechanism does severe burns causes acute gastritis?

A

Hypovolemia leads to decreased blood supply, whcih decreased mucousal defenses

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86
Q

By what mechanism, do NSAIDs causes acute gastritis?

A

Decrease PGE2

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87
Q

By what mechanism does increased intracranial pressure cause actue gastritis?

A

Increased stimulation of vagus nerve leads to increased acid production

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88
Q

Erosion vs ulcer

A

Erosion: Loss of superficial epithelium

Ulcer: Loss of mucousal layer

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89
Q

Two types of chronic gastritis

A
  • Chronic autoimmune gastritis
  • Chronic H. pylori gastritis
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90
Q

Chronic autoimmune gastritis is due to …

A

Autoimmune destruction of gastric parietal cells, which are located in the stomach body and fundus

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91
Q

Pathogenesis of chronic autoimmune gastritis

A

Mediated by T cells (Type IV hypersensity)

NOTE: Also associated with antibodies against parietal cells and/ or intrinsic factor

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92
Q

Clinical features of chronic autoimmune gastritis

A
  • Atrophy of mucosa with intestial metaplasia
  • Achlorhydria with increased gastrin levels and antral G-cell hyperplasia
  • Megaloblasic (pernicious) anemia due to lack of intrinsic factor
  • increased risk for gastric adenocarcinoma (intestinal type)
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93
Q

Most common site of chronic H pylori gastritis

A

Antrum

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94
Q

How does chronic H. pylori gastritis present?

A

Epigastric abdominal pain

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95
Q

What tests confirm eradication of H pylori?

A

Negative urea breath test

Lack of stool antigen

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96
Q

Peptic ulcer disease

A

Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%)

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97
Q

How does a duodenal ulcer present?

A

Epigastric pain that improves with meals

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98
Q

How is a duodenal ulcer diagnosed?

A

Endoscopic biopsy shows ulcer with hypertrophy of Brunner galnds

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99
Q

Duodenal ulcer usually arrises in the anterior duodenum. When it arises in the posterior duodenum, what are the complications?

A

Rupture, which may lead to bleeding from the gastroduodenal artery or acute pancreatitis

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100
Q

Causes of duodenal ulcer?

A
  • H. pylori (>99%)
  • ZE syndrome (rarely)
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101
Q

Causes of gastric ulcers

A

H.pylori (75%)

NSAIDs

Bile reflux

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102
Q

How does a gastric ulcer present?

A

Epigastric pain that worsens with meals

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103
Q

Where are gastric ulcers usually located?

A

Lesser curvature of the antru,

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104
Q
A
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105
Q

Gastric ulcer rupture carries risk of bleeding from _________.

A

Left gastric artery

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106
Q

_________ulcers are almost never malignant.

A

Duodenal

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107
Q

Gross of benign peptic ulcers

A

Small, sharply demarcated (“puched-out”) and surrounded by radiating folds of mucosa

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108
Q

Gross of malignant peptic ulcers

A

Large and irregular with heaped up margins

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109
Q

Subclasses of gastric carcinoma

A

Intestinal and diffuse

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110
Q
A
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111
Q

How does the intestinal type of gastric carcinoma present?

A

Large, irregular ulcer with heaped up margins; most commonly involves the lesser curvature of the antrum

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112
Q

Risk factors for the intestinal type of gastric carcinoma

A

Intestinal metaplasia

Nitrosamines in smoked foods

Blood type A

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113
Q

How does the diffuse type of gastic carcinoma present?

A

Signet ring cells that diffusely infiltrate the gastric wall

Desmoplasia results in thickening of stomach wall

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114
Q

How does gastric carcinoma present?

A

Weight loss

Abdominal pain

Anemia

Early satiety

*Rarely presents as Acanthosis nigricans or Leser Trelat sign

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115
Q

Gastric spread to the lymph nodes can involve the _________

A

Left supraclavicular node (Virchow node)

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116
Q

Where does gastric carcinoma metastizes to?

A

Liver (most common)

Periumbilical region (Sister Marey Joseph nodule)- Intestinal type

Bilateral ovaries (Krukenburg tumor)- Diffuse type

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117
Q

When does pyloric stenosis present?

A

About 2 weeks after birth

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118
Q

Duodeal atresia

A

Congenital failure of duodenum to canalize

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119
Q

Clinical features of duodenal atresia

A

polyhydramnios

Distension of stomach and blind looop of duodenum (“double bubble sign”)

Bilious vomiting

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120
Q

Double bubble sign

A

Duodenal atresia

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121
Q

Meckel Diverticulum

A

Outpouching of all three layers of the bowel wall

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122
Q

Meckel diverticulum arises due to failure of the ________ to involute.

A

Vitelline duct

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123
Q

Rule of 2s Meckel Diverticulum

A

Seen in 2% of the population

2 inches ling and located in the small bowel within 2 feet of the ileocecal valve

Can present during the first 2 years of life

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124
Q

Clinical presentation of meckel diverticulum

A

Bleeding

Volvulus

Intussusception

obstruction

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125
Q

Volvulus

A

Twisting of bowel along its mesentery

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126
Q

Results of volvulus

A

Obstruction and disruption of the blood supply with infarction

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127
Q

Most common locations of a volvulus

A

Sigmoid colon (elderly)

Cecum (young adults)

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128
Q

intussusception

A

Telescoping of proximal segment of bowel forward into distal segement

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129
Q

Cause of intussusception

A

Telescoped segment is pulled forward by peristalsis, resulting in obstruction and disruption of blood supply with infarction

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130
Q

intussusception is associated with ________

A

A leading edge (focus of traction)

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131
Q

Most common cause of intrussusception in children

A

Lymphoid hyperplasia; usually arises in the terminal ileum, leading to intussusception into the cecum

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132
Q

Most common cause of intrussusception in adults

A

Tumor

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133
Q

Two types of small bowel infarction

A

Transmural

Mucosal

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134
Q

Causes of Transmural small bowel infarction

A

Occurs with thrombosis/embolism of the superior mesenteric artery or thrombosis of the mesenteric vein

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135
Q

Causes of mucosal small bowel infarction

A

Occurs with marked hypotension

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136
Q

Clinical features of small bowel infarction

A

Abdominal pain

Bloody diarrhea

Decreased bowel sounds

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137
Q

Where is the lactase enzyme found?

A

In the brush border of enterocytes

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138
Q

How does lactose intolerance present?

A

Abdominal distension

Diarrhea

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139
Q

When is lactose intolerance seen?

A

Congenital

Acquired

Temorary (after small bowel infection)

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140
Q

HLA associated with celiac disease

A

HLA-DQ2 and DQ8

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141
Q

Celiac disease

A

Immune-mediated damge of small bowel villi due to gluten exposure

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142
Q

Most pathogenic component of gluten

A

Gliadin

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143
Q

Pathogenesis of celiac disease

A
  • Once absorbed, gliadin is deamidated by tissue translutaminase
  • Deamidated dliadin is presented by antigen presenting cells via MHC class II
  • Helper T cells mediate tissue damage
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144
Q

Clinical presentation of celiac disease

A
  • Children
    • Abdominal distension, diarrhea, and failure to thrive
  • Adults
    • Chronic diarrhea and bloating
  • Small, herpes-like vesicles may arise on skin (dermatitis herpetiformis)
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145
Q

Dermatitis herpetiformis

A

Due to IgA deposition at the tips of dermal papillae; resolves with gluten-free diet

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146
Q

Late complications of celiac disease

A

Small bowel carcinoma and T-cell lymphoma

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147
Q

Laboratory findings of cleiac disease

A
  • IdA antibodies against endomysium, tTG or gliadin
  • IgG antibodies- useful for diagnosis of individuals with IgA defiency
  • Duodenal biopsy- flattening of villi, hyperplasia of crypts, and increased intraepithelial lymphocytes
148
Q

In celiac disease where is the damage most prominent?

149
Q

Tropical sprue

A

Damage to small bowel villi due to an unknown organism resulting in malabsorption

150
Q

Tropical sprue arises after ________.

A

Infectious diarrhea

151
Q

Tropical sprue is most prominent in the _______

A

Jejunum and ileum

152
Q

Whipple disease

A

Systemic tissue damage characterized by macrophages loaded with Tropheryma whippelii organisms; partially destroyed organisms are present in macrophage lysosomes

153
Q

Classic site of involvement for Whipple disease

A

Small bowel lamina propria

154
Q

Pathogenesis of whipple disease

A
  • Marcrophages loaded with organisms
  • Macrophages compress lacteals
  • Chylomicrons cannot be transferred from enterocytes to lymphatics
  • Results in fat malabsorption and steatorrhea
155
Q

Aside from small bowel lamina propria, what are other sites of involvement in Whipple disease?

A

Synovium of joints (arthritis)

Cardiac valves

Lymph nodes

CNS

156
Q

Abetalipoproteinemia

A

Autosomal recessive deficiency of apolipoprotein B-48 and B-100

157
Q

Clinical features of abetalipoproteinemia

A
  • malabsorption- due to defective chylomicron firmation (requires B-48)
  • Absent plasma VLDL and LDL (requires B-100)
158
Q

Most common site of carcinoid tumors

A

Small bowel

NOTE: it can arrises anywhere along the gut

159
Q

Gross of carcinoid tumor

A

grows as a submucosal poly-like nodule

160
Q

What allows for the formation of carcinoid syndrome and carcinoid heart disease?

A
  • Metastatis of carnoid tumor to the liver allows serotonin to bypass liver metabolism (by MAO).
  • Serotonin is released into the hepatic vein and leaks into systemic circulation bia hepato-systemic shunts
161
Q

Carcinoid syndrome

A

Brochospasm

DiarrheaFlshing of skin

162
Q

Triggers for symptoms of carcinoid syndrome

A

Alcohol or motional stress, which stimulate serotonin release from the tumor

163
Q

Carcinoid heart disease

A

Characterized by right-sided valvular fibrosis leading to tricupsid regurgitation and pulmonary valve stenosis

164
Q

Are left-sided valvular leasions seen in carcinoid heart disease?

A

No becuase of the presence of MAO in the lungs

165
Q

Clinical features of acute appendicitis

A
  • Periumbilical pain, fever and nausea; pain eventually localizes to right lower quadrant (McBurney point)
166
Q

Appendix rupture results in ________.

A

Peritonitis that presents with guarding and rebound tenderness

167
Q

Common complication of acute appendicitis

A

Periappendiceal abscess

168
Q

Location:Ulcerative colitis

A

Begins in rectum and can extend proximally up to cecum (involvement is continuous)

169
Q

inflammatory bowel disease

A

Chronic, relapsing inflammation of bowel

170
Q

Clasical presentation of IBD

A

Young women, as recurrent bouts of bloody diarhea and abdominal pain

171
Q

Wall involvement ulcerative colitits

A

Mucosal and submucosal

172
Q

Wall involvement Chrons disease

A

Full-thickness inflammation with knife-like fissures

173
Q

Location:Chrons disease

A

Anywhere from mouth to anus with skip lesionsl terminal ileum is the most common site, rectum is least common

174
Q

Symptoms :Chrons disease

A

Right lower quadrant pain (ileum) with non-bloody diarrhea

175
Q

Symptoms :Ulcerative colitis

A

Left lower quadrant pain (rectum) with bloody diarrhea

176
Q

Inflammation:Chrons disease

A

Lymphoid aggregates with granuloms

177
Q

Inflammation:Ulcerative colitis

A

Crypt abscess with neutrophils

178
Q

Gross apperance:Chrons disease

A

Cobblestone mucosa, creeping fat and strictures (string sign on imaging)

179
Q

String sign of imaging

A

Chrons diasese

180
Q

Gross apperance: Ulcerative colitis

A

Psudopolyps; loss of haustra (“lead pipe” sign on imaging

181
Q

Lead pipe sign on imaging

A

Ulcerative colitits

182
Q

Complications:Chrons disease

A

Malabsoprtion with nutritional deficiency, calcium oxalate nephrolithiasis, fistula formation, and carcinoma, if colonic disease is present

183
Q

Complications:Ulcerative colitits

A

Toxic megacolon and carcinoma (risk is based on extent of colonic involvement and duration of disease; generally not a concern until >10 yrs of disease)

184
Q

Smoking:Chrons disease

A

Increases risk for Chrons disease

185
Q

Smoking:Ulcerative colitis

A

Protects against UC

186
Q

Extraintestinal manifestations of both ulcerative colitis and chrohn disease

A

Arthritis (peripheral joints, ankylosing spondylitis, sacroilitis, magratory polyartritis)

Uveitis

Erythema nodosum

Pyoderma gangrenosum

Primary sclerosing cholangitis

p-ANCA

187
Q

Types of IBD

A

Ulcerative colitis

Chrohn disease

188
Q

Hirschsprung disease

A

Defective relaxation and peristalsis of rectum and distal sigmoid colon

189
Q

Hirschsprung disease is associated with _________.

A

Down syndrome

190
Q

Cause of hirschsprung disease

A

Congenital failure of ganglion cells (neural crest-derived) to descend into myenteric and submucosal plexus

191
Q

Clinical features of hirschsprung disease

A

Failure to pass meconium

Empty rectal vault on DRE

Massive dilatation (megacolon) of bowel proximal to obstruction with risk for rupture

192
Q

Rectal suction biopsy in hirschsprung disease

A

lack of ganglion cells

193
Q

Treatment of hirschsprung disease

A

Resection of the involved bowel; ganglion cells are present in the bowel proximal to the diseased segment

194
Q

Colonic diverticula

A

Outpouchings of mucosa and submucosa through the muscularis propria

195
Q

Colonic diverticula are associated with …

A

Constipation, straining, and low-fiber diet

196
Q

Colonic diverticula arise where?

A

Where the vasa recta traverse the muscularis propria; sigmoid colon is the most common location

197
Q

Complications of colonic diverticula

A
  • Rectal bleeding
  • Diverticulitis
  • Fistula
198
Q

Cause of diverticulits complications seen in colonic diverticula

A

Due to obstructing fecal material; presents with appendicitis-like symptoms in the left lower quadrant

199
Q

Cause of fistula complications seen in colonic diverticula

A

Inflamed diverticulum ruptures and attaches to a local structure

200
Q

How does a colovesicular fistula present?

A

With air (or stool) in urine

201
Q

Angiodysplasia

A

Acquired malformation of mucosal and submucosal capillary beds

202
Q

Where does angiodysplasia usually arise?

A

Cecum and right colon due to high wall tension

203
Q

Hereditary hemorrhagic telangiectasia

A

Autosomal dominat disorder resulting in thin-walled blood vessels, especially in the mouth and GI Tract

204
Q

Ischemic colitis

A

Ischemic damage to the colon, usually at the splenic flexure (watershed area of superior mesenteric artery)

205
Q

Most common caus of ischemic colitits

A

Atherosclerosis of SMA

206
Q

How does ischemic colitis present?

A

Postprandial pain and weight loss; infarction results in pain and bloody diarrhea

207
Q

irritable bowel syndrome

A

Relapsing abdominal pain with bloating, flatulence, and change in bowel habits that improves with defecation

208
Q

Irritable bowel syndrome is related to…

A

Disturbed intestinal motility

209
Q

Most common types of colonic polyps

A

Hyperplastic and adenomatous polyps

210
Q

Microscopy of hyperplastic colonic polypics

211
Q

Where does a hyperplastic poly usually arise?

A

Left colon (rectosigmoid)

212
Q

Adenoma-carcinoma sequence

A
  • APC mutations increase risk for formation of polyp
  • K-ras mutation leads to formation of polyp
  • p53 mutation and increased expression of COX allow for progression to carcinoma
213
Q

______ impedes progression from adenoma to carcinoma.

214
Q

Greatest risk for progression from adenoma to carcinoma is related to..

A

size >2 cm

Sessile growth

Villous histology

215
Q

Is FAP autosomal recessive or autosomal dominant?

A

Autosomal dominant

216
Q

Cause of FAP

A

Due to inherited AP mutation on chromosome 5

217
Q

_________ is FAP with fibromatosis and ostomas.

A

Gardner syndrome

218
Q

Fibromatosis

A

non-neoplastic proliferation of fibroblasts; arises in retroperitoneum and locally destroys tissue

219
Q

Benign tumor of bone that usually arises in the skill

220
Q

FAP with CNS tumors (medulloblastoma and glial tumors)

A

Turcot syndrome

221
Q

How is juvenile poypsis characterized?

A

Multiple juvenile polps in the stomach and colon; large numbers of juvenile polps increase the risk of progression to carcinoma

222
Q

Peutz-Jeghers syndrome

A

Hamartomatous polps throught GI tract and mucocutaneous hyperpigmentation on lips, oral mucosa, and genital skin

223
Q

True or false. Peutz-jeghers syndrome is an autosomal dominant disorder.

224
Q

Peutz-Jeghers syndrome increases risk for…

A

Colorectal, breast, and gynecologic cancer

225
Q

peak incidence of colorectal carcinoma

226
Q

Microsattelite instability

A

DNA mismatch repair enzymes

227
Q

_____________ colorectal carcinoma is due to inherited mutations in DNA mismatch repair enzymes.

A

Hereditary nonpolyposis

228
Q

Clinical features of left-sided colorectal carcinoma

A
  • Grows as a “napkin-ring” lesion
  • Decreased stool caliber
  • Left lower quadrant pain
  • Blood-streaked stool
229
Q

Clinical features of right-sided colorectal carcinoma

A
  • Grows as a raised lesion
  • Presents with irondeficiency anemia
  • Vague pain
230
Q

Colonic carcinoma is associated with an increased risk for ______ endocarditis.

A

Strep bovis

231
Q

Annular Pancreas

A

Developmental malformation in which the pancreas forms a ring aroung the duodenum; risk of duodenal obstruction

232
Q

Pathogenesis of acture pancreatitis

A
  • Due to autodigestion of pancreatic parenchyma by pancreatic enzymes
    • Premature activation of trypsin leads to activation of other pancreatic enzymes
233
Q

Acute pancreatitis results in …

A

Liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat

234
Q

Causes of acute pancreatitis

A

Alcohol and gallstones

Traue

Hypercalcemia

Hyperlipidemia

Drugs

Scorpion stings

Mumps

Rupture of a posterior duodenal ulcer

235
Q

Clinical features of acute pancreatitis

A

Epigastric abdominal pain that radiates to the back

Nausea and vomiting

Periumbilical and flank hemorrhage

Elevated serum lipase and amylase

Hypocalcemia

236
Q

Complications of acute pancreatitis

A
  • Shock
  • Pancreatic pseudocyst
  • Pancreatic abscess
  • DIC and ARDS
237
Q

Pathogenesis of shock complication seen in acute pancreatitis

A

Due to perpancreatic hemorrhage and fluid sequestration

238
Q

Pathogenesis of pancreatic pseudocyst complication seen in acute pancreatitis

A

Formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes

239
Q

Pathogenesis of pancreatic abscess complication seen in acute pancreatitis

A

Often due to E. Coli

240
Q

How does a pancreatic abscess present?

A

Abdominal pain

High fever

Persistently elevated amylase

241
Q

Chronic pancreatitis

A

Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis

242
Q

Causes of chronic pancreatitis

A

Alcohol

Cystic fibrosis

243
Q

Clinical features of chronic pancreatitis

A
  • Epigastric abdominal pain that radiates to the back
  • Pancreatic insufficiency
  • Dystrophic calcification of pancreatic parenchyma on imaging
  • Secondary diabetes mellitus
  • Increased risk for pancreatic carcinoma
244
Q

Contrast studies of chronic pancreatitis

A

“Chain of lakes” pattern due to dilatation of pancreatic ducts

245
Q

Average age for pancreatic carcinoma

246
Q

Risk factors for pancreatic carcinoma

A

Smoking and chronic pancreatitis

247
Q

Serum marker for pancreatic carcinoma

248
Q

Clinical features of pancreatic carcinoma

A
  • Epigastric abdominal pain and weight loss
  • Obstructive jaundice with pale stools and palpable gallblader
  • Secondary diabetes mellitus
  • Pancreatitis
  • Migratory thrombophlebitis (Trousseau syndrome)
249
Q

How does migratory thrombophelbitis (Trusseau syndrome) present?

A

Swelling, erythma, and tenderness in the extremities

250
Q

Whipple procedule

A

En bloc removal of the head and neck of pancreas, proximal duodenum, and gallbladder

251
Q

How does a pancreatic psudocyst present?

A

Abdominal mass with persistenly evelated serum amylase

NOTE: Rupture is associated with release of enzymes into the abdominal cavity and hemorrhage

252
Q

Biliary atresia

A

Failure to form or early destructionof extrahepatic biliary tree

253
Q

________ leads to biliary obstruction within the first 2 months of life.

A

Biliary atresia

254
Q

How does biliary atresia present?

A

Jaundice and progresses to cirrhosis

255
Q

What factors precipitate gallstone formation?

A
  • Supersaturation of cholesterol or bilirubin
  • Decreased phospholipids or bile acids
  • Stasis
256
Q

________ gallstones are usually radiolucent.

A

Cholesterol

257
Q

Risk factors for cholesterol gallstones

A

Age (40s)

Estrogen

Clofibrate

Native American ethnicity

Crohn disease

Cirrhosis

258
Q

_________ gallstones are radiopaque.

259
Q

Risk factors for bilirubin gallstones

A

Extravascular hemolysis

Biliary tract ingections

260
Q

Which bugs cause biliary tract infections?

A

E. Coli

Ascaris lumbricoides

Clonorchis sinesis

261
Q

How is ascaris lumbricoides transmitted?

A

Fecal-oral

262
Q

In which areas is clonorchis sinensis endemic?

A

China, Korea, and Vietnam

263
Q

Chonorchis sinensis increases the risk for _________, _________, and __________.

A

Gallstones

Cholangitis

Cholangiocarcinoma

264
Q

Complications of gallstones

A

Biliary colic

Acute and chronic cholecystitis

Ascending cholangitis

Gallstone ileaus

Gallbladder cancer

265
Q

Biliary colic

A

Waxing and waning right upper quadrant pain

266
Q

Cause of biliary colic

A

Due to the gallbladder contracting against a stone lodged in the cystic duct

267
Q

Common bile duct obstruction may result in _________ or ____________.

A

Acute pancreatitis; obstructive jaundice

268
Q

Acute cholecystitis

A

Acute inflammation of the gallbladder wall

269
Q

How does acute cholecystitis present?

A
  • Right upper quadrant pain, often radiating to right scapula
  • Fever with increased WBC count
  • Nausea
  • Increased alkaline phosphatase (from duct damage)
270
Q

Chronic cholecystitis is due to…

A

Chemical irritation from longstanding cholelithiasis, with or without superimposed bouts of acute cholecystitis

271
Q

How is chronic cholecystitis characterized?

A

Herniation of gallbladder mucosa into the muscular wall (Rokitansky-Aschoff sinus)

272
Q

How does chronic cholecystitis present?

A

Vague right upper quadrant pain, especially after eating

273
Q

Late complication of chronic cholecystitis

A

Porcelain gallbladder (shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification)

274
Q

Treatment for chronic cholecystisis?

A

Cholecystectomy, especially if porcelain gallbladder is present

275
Q

Ascending cholangitis

A

Bacterial infection of the bile ducts

276
Q

Ascending cholangitis is usually due to ascending infection with ________ bacteria.

A

Enteric gram-negative

277
Q

How does ascending cholangitis present?

A

Sepsis (high fever and chiils)

Jaundice

Abdominal pain

278
Q

Gallbladder carcinoma

A

Adenocarcinoma arising from the glandular epithelium that lines the gallbladder wall

279
Q

How does gallbladder carcinoma present?

A

Cholecystitis in an elderly woman

280
Q

Role of phospholipds and bile acids in production of bile

A

Increase solubility

281
Q

Scleral icterus

A

Yellow discoloration of the sclera

282
Q

Jaundice is due to..

A

Increased serum biliubin, usaully >2.5mg/dL

283
Q

Noraml bilirubin metabolism

A
  • RBCs are consumed by macrophages of the reticuloendothelial system
  • Protoporphyrin is converted to unconjugated bilirubin
  • Albumin carries UCB to the liver
  • Uridine glucuronyl transferase in hepatocytes conjugates bilirubin
  • Conjugated bilirubin is transferred to bile canaliculi to form bile, which is stored in the gallbladder
  • Bile is released into the small bowel to aid in digestion
284
Q

___________ convert CB to urobilinogen.

A

Intestinal flora

285
Q

Urobilinogen is oxidized to __________ and _________.

A

Stercobilin: makes stool brown

Urobilin: Partially reabsorbed into blood and filtered by kidney, making urine yellow

286
Q

How does extravascular hemolysis or ineffective erythropoiesis cause jaundice?

A

High levels of UCB overwhelm the conjucating ability of the liver

287
Q

How does physiolgic jaundic of the newborn cause jaundice?

A

Newborn liver has transiently low UGT

288
Q

How does Gilbert Syndrome cause jaundice?

A

Mildly low UGT activity; autosomal recessive

289
Q

How does Crigler-Najjar Syndrome cause jaundice?

A

Absence of UGT

290
Q

How does Dubin- Johnson Syndrome cause jaundice?

A

Deficency of bilirubin canalicular transport protein; autosomal recessive

291
Q

How does bilary tract obstruction cause jaundice?

A

Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and lver fluke (Clonorchis sinensis)

292
Q

How does viral hepatitis cause jaundice?

A

Inflammation disrupts hepatocytes and small bile ductules

293
Q

What are the lab findings for extravascular hemolysis or ineffective erythropoiesis?

A

Elevated UCB

294
Q

What are the lab findings for physiologic jaundice of the newborn?

A

Elevated ICB

295
Q

What are the lab findings for Gilbert Syndrome?

A

Elevated UCB

296
Q

What are the lab findings for Cringler-Najjar Syndrome?

A

Elevated UCB

297
Q

What are the lab findings for Dubin-Johnson Syndrome?

A

Elevated CB

298
Q

What are the lab findings for biliary tract obstruction?

A

Elevated CB

Decreased urine urobilinogen

Increased alkaline phosphatase

299
Q

What are the lab findings for viral hepatitis?

A

Elevated CB and UCB

300
Q

What are the clinical features of extravascular hemolysis or ineffective erythropoiesis?

A
  • Dark urine due to elevated urine uroblinogen
  • Increased risk for pigmented bilirubin gallstones
301
Q

What are the clinical features of physiologic jaundice of the newborn

A
  • UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neurological defictis and death
302
Q

Treatment for physiologic jaundice of the newborn?

A

Phototherapy (makes UCB water soluble)

303
Q

What are the clinical features of gilbert syndrome?

A

Jaundice during stress

304
Q

What are the clinical features of Cringler-Najjar syndrome?

A

Kernicterus; usually fatal

305
Q

What are the clinical features of Dubin-Johnson syndrome?

A
  • Liver is dark
306
Q

_____________ is similar to Dubin-Johnson syndrome, but lacks liver discoloration.

A

Rotor syndrome

307
Q

What are the clinical features of biliary tract obstruction?

A
  • Dark urine (due to bilirubinuria)
  • Pale stool
  • Pruitis due to increased plasma bile acids
  • Hypercholesterolemia with xanthomas
  • Steatorrhea with malabsoption of fat-soluble vitamins
308
Q

What are the clinical features of viral hepatitis?

A

Dark urine due to increased urine bilirubin; urine urobilinogen is normal or increased

309
Q

Which two forms of hepatitis are transmitted via the fecal-oral route?

310
Q

Hep A is commonly acquired by ________.

311
Q

Hep E is commonly acquired from ___________

A

Contaminated water or undercooked seafood

312
Q

Which type of hep is commonly seen in pregnant women? What is the result?

A

Hep E. Associated with gulminant hepatitis (liver failure with massive liver necrosis)

313
Q

How is Hep B transmitted?

A

Parenteral transmission (childbirth, unprotected sexual intercourse, IV drug abuse, and needle stick)

314
Q

How is hep C transmitted?

A

Parenteral (intravenous drug abuse)

315
Q

___________test confirms Hep C infection.

A

HCV-RNA

NOTE: Decreased RNA levels indicate recovery; persistence indicates chronic disease

316
Q

Hep D is dependent on ________ for infection.

A

HBV

NOTE: Superinfection upon existing HBV is more severe than coinfection

317
Q

Additional causes of viral hepatitis

A

EBV and CMV

318
Q

How does acute hepatitis present?

A

Jaundice with dark urine

Fever, malaise, nausea

Elevated liver enzymes

319
Q

How long do viral hepatitis symptoms last?

A

Acute: Less than 6 months

Chronic: More than 6 months

320
Q

Inflammation (acute hepatitis) involves _________ and ____________ and is characterized by _________.

A

Lobules of liver; portal tracts; apoptosis of hepatocytes

321
Q

inflammation (chronic hepatitis) predominently involves the __________.

A

Portal tract

NOTE: Risk of progression to cirrhosis

322
Q

Cirrhosis

A

End-stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocyte

323
Q

What mediates fibrosis seen in cirrhosis?

A

Fibrosis is mediated by TGF-B from stellate cells which lie beneath the endothelial cells that line the sinusoids

324
Q

Clinical features of cirrhosis

A
  • Ascites
  • Congestive splenomegaly/hyerplenism
  • Portosystemic shunts
  • Hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)
325
Q

Results of decreased detoxification due to cirrhosis

A
  • Mental status changes, asterixis, and eventual coma
  • Gynecomastia, spider angiomata, and palmar erythema due to hyperestrinism
  • Jaundice
326
Q

Results of decreased protein synthesis due to cirrhosis

A
  • Hypoalbuminemia with edema
  • Coagulopathy
327
Q

Pathogenesis of alcoholic hepatitis?

A
  • Results from chemical injury to hepatocytes
    • Acetaldehyde mediates damage
328
Q

Alcoholic hepatitis is characterized by …

A
  • Swelling of hepatocytes with formation of Mallory bodies
  • Necrosis
  • Acute inflammation
329
Q

Mallory bodies

A

Damaged cytokeratin filaments

330
Q

How does alcoholic hepatitis present?

A
  • Painful hepatomegaly
  • Elevated liver enzymes (AST>ALT)
331
Q

Nonalcoholic fatty liver disease is associated with ______.

332
Q

Causes of hemochromatosis

A
  • Autosomal recessive defect in iron absorption
  • Chronic transfusions
333
Q

Primary hemochromatosis is due to mutations if the _______ gene.

A

HFE

NOTE: Usually cysteine is replaced by tyrosine at amino acid 282

334
Q

How does hemochromatosis present?

A
  • late in adulthood with:
    • Cirrhosis, secondary diabetes mellitus, and bronze skin
    • Dilated cardiomyopathy, cardiac arrythmias and gonadal dysfunction (due to testicular atrophy)
335
Q

Lab findings of hemochromatosis

A
  • Elevated ferritin
  • Decreased TIBC
  • Increased serum iron
  • Increased % saturation
336
Q

What does a liver biopsy in a pateint with hemochromatosis reveal?

A
  • Accumulation of brown pigment in hepatocytes
    • prussian blue stain distinguishes iron from lipofuscin
337
Q

Hemochromatosis increases the risk for _____________.

A

Hepatocellular carcinoma

338
Q

Hemochromatosis treatment

A

Phlebotomy

339
Q

Wilson disease

A

Autosomal recessive defect in ATP-mediated hepatocyte copper transport

340
Q

Wilson disease results in lack of copper transport into bile and lack of copper incorporation into ___________.

A

Ceruplasmin

341
Q

Pathogenesis of Wilson disease

A
  • Copper builds up in hepatocytes, leaks into serum, and deposits in tissues
    • Copper-mediated production of hydroxyl free radicals leads to tissue damage
342
Q

How does Wilson disease present?

A
  • Cirrhosis
  • Neurologic manifestations (behavioral changes, dementia, chorea, and Parkinsonian symptoms)
  • Kayer-Fleisher rings in cornea
343
Q

Lab findings: Wilson Disease

A
  • Elevated urinary copper
  • Decreased serum ceruloplasmina
  • Elevated copper on liver biopsy
344
Q

Treatment for Wilson disease

A

D-penicillamine (chelates copper)

345
Q

Wilson disease increases risk of _________.

A

Hepatocelllar carcinoma

346
Q

Primary biliary cirrhosis

A
  • Autoimmune granulomatous destruction of intrahepatic bile ducts
347
Q

________________ antibody is present in primary biliary cirrhosis.

A

Antimitochondrial antibody

348
Q

How does primary biliary cirrhosis present?

A

Obstructive jaundice

349
Q

Primary sclerosing cholangitis

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts

350
Q

How is primary sclerosing cholangitis characterized?

A
  • periductal fibrosis with an “onion skin” appearance
  • Uninvolved regions are dilated resuting in a “beaded appearance on contrast imaging
351
Q

Primary sclerosing cholangitis is associated with __________ and _______ is often positive.

A

Ulterative colitis; p-ANCA

352
Q

How does primary sclerosing cholangitis present?

A

Obstructive jaundice

NOTE: Cirrhosis is a late complication

353
Q

Primary sclerosing cholangitis increases risk for __________.

A

Cholangiocarcinoma

354
Q

Reye syndrome

A

Fulminant liver failure and encephalopathy in children wth viral illness who take aspirin

355
Q

How does reye syndrome present?

A
  • Hypoglycemia
  • Elevated liver enzymes
  • Nausea with vomiting
356
Q

Hepatic adenoma is associated with _________.

A

Oral contraceptive use

357
Q

Hepatic adenomas grow with exposure to ______.

358
Q

Risk associated with hepatic adenoma

A

Risk of rupture and intraperitoneal bleeding, especially during pregnancy

NOTE: Tumors are subcapsular and grow with exposure to estrogen

359
Q

Risk factors for hepatocellular carcinoma

A
  • Chronic hepatitis
  • Cirrhosis
  • Aflatoxins derived from Aspergillus
360
Q

Aflatoxins derived from Aspergillus induce ______ mutation.

361
Q

Hepatocellular carcinoma increases risk for _________ syndrome.

A

Budd-Chiari

362
Q

Budd-Chiari syndrome

A

Liver infarction secondary to hepatic vein obstruction

363
Q

How does Budd-Chiari syndrome present?

A

Painful hepatomegaly and ascites

364
Q

Serum tumor maker for hepatocellular carcinoma

A

Alpha-fetoprotein

365
Q

What tumors metastasize to the liver?

A

Colon

Pancrease

Lung

Breast carcinoma

OS5 (4 decks)

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