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First Aid 2014 > GI: 349 - 353 > Flashcards

GI: 349 - 353 Flashcards

1
Q

Bilirubin is a product of the metabolism of what?

A

Heme

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2
Q

What is another name for unconjugated bilirubin?

A

Indirect

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3
Q

Direct vs. indirect bilirubin - which one is water soluble?

A

Conjugated - water soluble; Unconjugated - water insoluble

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4
Q

What is bilirubin conjugated with to make it water soluble?

A

Glucuronic acid

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5
Q

What organ removes bilirubin from the blood?

A

Liver

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6
Q

Where is heme broken down into bilirubin?

A

Macrophages

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7
Q

How does bilirubin get to the liver?

A

Travels in the bloodstream bound to albumin

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8
Q

Where does bilirubin get conjugated?

A

Liver

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9
Q

What enzyme conjugates bilirubin?

A

UDP-glucuronosyl-transferase

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10
Q

Where does conjugated bilirubin go and what does it become?

A

To the gut where it becomes urobilinogen

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11
Q

80% of urobilinogen does what?

A

Excreted into the feces as stercobilin which gives feces its brown color

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12
Q

20% of urobilinogen does what (2 possible fates)?

A
  1. 90% (of this 20%) reenters enterohepatic circulation and goes back to the liver.
  2. 10% (of this 20%) is excreted in urine which gives urine its yellow color
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13
Q

Are salivary gland tumors generallly benign or malignant?

A

Benign

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14
Q

Which salivary gland is most likely to have a tumor?

A

Parotid gland

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15
Q

What are 3 types of salivary gland tumors?

A
  1. Pleomorphic adenoma
  2. Warthrin tumor
  3. Mucoepidermoid carcinoma
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16
Q

Which is the most common salivary gland tumor?

A

Pleomorphic adenoma

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17
Q

What is a pleomorphic adenoma composed of?

A

Benign mixed tumor - made of chondromyxoid stroma and epithelium

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18
Q

How does pleomorphic adenoma present?

A

Painless mobile mass

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19
Q

When does pleomorphic adenoma recur?

A

Incomplete excision or intraoperative rupture

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20
Q

Describe a warthrin tumor.

A

Papillary cystadenoma lymphomatosum - a benign cystic tumor with germinal centers

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21
Q

What is the most common malignant salivary gland tumor?

A

Mucoepidermoid carcinoma

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22
Q

Describe a mucoepidermoid carcinoma

A

Has mucinous and squamous components that typically presents as a painless slow-growing mass

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23
Q

What is achalasia?

A

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

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24
Q

What happens in achalasia?

A

High LES opening pressure and uncoordinated peristalsis leads to progressive dysphagia to solids and liquids

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25
Q

How is achalasia different from obstruction?

A

Achalasia is dysphagia of solids and liquids while obstruction is just dysphagia of solids

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26
Q

What test can we use to check for achalasia and what will it show?

A

Barium swallow shows dilated esophagus with an area of distal stenosis - “Bird’s beak”

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27
Q

Achalasia is associated with an increased risk of what cancer?

A

Esophageal squamous cell carcinoma

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28
Q

Achalasia maybe be secondary to what other disease?

A

Chagas

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29
Q

What is Boerhaave syndrome?

A

Transmural, usually distal esophageal rupture due to violent retching

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30
Q

How should Boerhaave syndrome be treated?

A

Surgical emergency

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31
Q

What is eosinophilic esophagitis?

A

Infiltration of eosinophils in the esophagus in atopic patients (food allergy)

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32
Q

What are 3 characteristics of eosinophilic esophagitis?

A

Dysphagia, heartburn, strictures

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33
Q

Can eosinophilic esophagitis be treated with GERD therapy?

A

No

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34
Q

Characterize esophageal varices.

A

Painless bleeding of dilated submucosal veins in the lower 1/3 of esophagus

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35
Q

What are esophageal varices secondary to?

A

Portal hypertension

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36
Q

What are 3 associations of esophagitis?

A
  1. Reflux
  2. Infection in immunocompromised
  3. Chemical ingestion
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37
Q

What are 3 infections that are associated with esophagitis and how do you differentiate between them?

A
  1. Candida - white pseudomembrane
  2. HSV-1 - punched out ulcers
  3. CMV - linear ulcers
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38
Q

How does GERD typically present?

A

Heartburn, regurgitation upon lying down, nocturnal cough and dyspnea, adult-onset asthma

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39
Q

GERD involves decreased tone of which sphincter?

A

LES

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40
Q

What is Mallory-Weiss syndrome?

A

Mucosal lacerations at the GE junction due to severe vomiting

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41
Q

What is a key presenting symptom of Mallory-Weiss syndrome?

A

Hematemesis

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42
Q

What 2 groups are especially prone to Mallory-Weiss syndrome?

A

Bulimics and alcoholics

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43
Q

What is the triad of Plummer-Vinson syndrome?

A

Mnemonic: DIG

Dysphagia (due to esophageal webs), Iron deficiency anemia, Glossitis

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44
Q

Describe the pathophysiology of sclerodermal esophageal dysmotility.

A

Esophageal smooth muscle atrophy leads to decreased LES pressure and dysmotility leads to acid reflux and dysphagia leads to stricture, Barrett esophagus, and aspiration

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45
Q

What syndrome is sclerodermal esophageal dysmotility a part of?

A

CREST

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46
Q

What is Barrett esophagus?

A

Glandular metaplasia - replacement of nonkeratinized (stratifeid) squamous epithelium with intestinal epithelium (nonciliated columnar with goblet cells) in the distal esophagus

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47
Q

What causes Barrett esophagus?

A

Chronic GERD

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48
Q

What are 3 things associated with Barrett esophagus?

A

Esophagitis, esophageal ulcers, and increased risk of esophageal adenocarcinoma

49
Q

What are the 2 types of esophageal cancer?

A

Squamous cell and adenocarcinoma

50
Q

How does esophageal cancer typically present?

A

Progressive dysphagia and weight loss

51
Q

Does esophageal cancer have a good prognosis?

52
Q

Contrast the incidence of the 2 types of esophageal cancer as well as where they tend to occur in the esophagus.

A
  1. Squamous cell - more common worldwide (makes sense since this is the one linked to EtOH and Asian flush), upper 2/3 of esophagus
  2. Adenocarcinoma - more common in the U.S., lower 1/3
53
Q

What are the risk factors for esophageal cancer?

A 
Mnemonic: AABCDEFFGH
Achalasia
Alcohol - squamous
Barrett esophagus - adeno
Cigarettes - both
Diverticula (e.g. Zenker) - squamous
Esophageal web - squamous
Familial
Fat (obesity) - adeno
GERD - adeno
Hot liquids - squamous
54
Q

Gastritis can broadly be broken up into what 2 groups?

A

Acute (erosive) vs. chronic (nonerosive)

55
Q

Describe what happens in acute gastritis.

A

Disruption of mucosal barrier leads to inflammation

56
Q

What can cause acute gastritis?

A

Stress, NSAIDs, EtOH, uremia, burns, brain injury

57
Q

Why do NSAIDs cause acute gastritis?

A

Decreased PGE2 leads to decreased gastric mucosa production

58
Q

What’s the difference between a curling ulcer vs. cushing ulcer?

A

Mnemonic: Burned by the curling iron and always cushion the brain

  1. Curling ulcer is associated with burns - decreased plasma volume causes sloughing of gastric mucosa
  2. Cushing ulcer is associated with brain injury - increased vagal stimulation causes increased ACh causes increased H+ production
59
Q

What are the 2 types of chronic gastritis?

A

Mnemonic: A before B

Type A - fundus/body vs. Type B - antrum

60
Q

Which is more common Type A or Type B chronic gastritis?

61
Q

What causes Type A chronic gastritis?

A

Autoimmune disorder characterized by autoantibodies to parietal cells, pernicious anemia, achlorhydia

62
Q

What causes Type B chronic gastritis?

A

H. pylori infection

63
Q

Type B chronic gastritis is associated with increased risk of?

A

MALT lymphoma and gastric adenocarcinoma

64
Q

What is Menetrier disease?

A

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

65
Q

What does gross inspection of Menetrier disease reveal?

A

Rugae of stomach are so hypertrophied that they look like brain gyri

66
Q

How does Menetrier disease relate to cancer?

A

It is a precancerous condition

67
Q

Stomach cancer is almost always what type?

A

Adenocarcinoma

68
Q

What paraneoplastic syndrome often presents with stomach cancer?

A

Acanthosis nigricans

69
Q

Describe the course of stomach cancer.

A

Early aggressive local spread and node/liver metastases

70
Q

How can you break down the different presentations of stomach cancer?

A

Intestinal vs. diffuse

71
Q

Is intestinal or diffuse stomach cancer associated with H. pylori?

A

Intestinal

72
Q

Aside from H. pylori what are other causes of intestinal stomach cancer?

A

Dietary nitrosamines, tobacco smoking, achlorhydia, chronic gastritis

73
Q

Describe what you would see with intestinal stomach cancer.

A

Commonly on the lesser curvature - looks like ulcer with raised margins

74
Q

Describe what you would see with diffuse stomach cancer.

A

Signet ring cells and the stomach wall is grossly thickened and leathery (linitis plastica)

75
Q

What is Virchow node?

A

Involvement of left supraclavicular node by metastasis from the stomach

76
Q

What is a Krukenberg tumor?

A

Bilateral metastases to ovaries of stomach cancer; marked by abundant mucus and signet ring cells

77
Q

Subcutaneous periumbilical metastasis from stomach cancer is called what?

A

Sister Mary Joseph nodule

78
Q

Pain decreasing with meals - gastric or duodenal ulcer?

79
Q

Weight gain - gastric or duodenal ulcer?

80
Q

Which one is more strongly associated with H. pylori infection - gastric or duodenal ulcer?

A

Duodenal (almost 100%) vs. gastric (70%)

81
Q

Aside from H. pylori infection what are other causes of ulcers?

A

NSAIDs - gastric, Zollinger-Ellison - duodenal

82
Q

Are gastric or duodenal ulcers associated with increased risk of carcinoma?

83
Q

Which ulcer often occurs in older patients?

84
Q

What do we see histologically for duodenal ulcers?

A

Hypertrophy of Brunner glands

85
Q

What are 2 complications of ulcers?

A

Hemorrhage and perforation

86
Q

Where do we tend to see hemorrhage as a complication of ulcer?

A
  1. Ruptured gastric ulcer on the lesser curvature of the stomach - bleeding from the left gastric artery
  2. Ulcer on the posterior wall of the duodenum - bleeding from gastroduodenal artery
87
Q

Where do we tend to see perforation as a complication of ulcer?

A

Anterior wall of the duodenum

88
Q

Chest radiograph shows what with perforation of an ulcer?

A

Free air under the diaphragm

89
Q

A patient with a perforated ulcer may have referred pain to where?

90
Q

Tropical sprue, whipple disease, celiac sprue, disaccharidase deficiency, abetalipoproteinemia, pancreatic insufficiency are all examples of what?

A

Malabsorption syndromes

91
Q

Malabsorption syndromes can cause what symptoms?

A

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

92
Q

What is the difference between tropical and celiac sprue?

A

Tropical sprue responds to antibiotics - cause is unknown but tropical sprue is seen in residents of or recent visitors to the tropics

93
Q

What causes Whipple disease?

A

Tropheryma whipplei infection

94
Q

Is tropheryma whipplei gram positive or negative?

A

Gram positive

95
Q

What do you see on histology with Whipple disease?

A

PAS + foamy macrophages in intestinal lamina propria, mesenteric nodes

96
Q

What demographic tends to get Whipple disease more often?

97
Q

What are 3 characteristic symptoms (aside from GI) of Whipple disease?

A

Mnemonic: Whipped cream in a CAN

Cardiac symptoms, Athralgia, Neurological symptoms

98
Q

What is celiac sprue?

A

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

99
Q

What are three things (2 genetic, 1 demographic) associated with celiac sprue?

A
  1. HLA-DQ2
  2. HLA-DQ8
  3. Northern European descent
100
Q

Name 3 antibodies found in celiac sprue.

A
  1. Antiendomysial
  2. Anti-tissue transglutaminase
  3. Anti-gliadin
101
Q

What happens to villi in celiac sprue?

102
Q

Where do you see lymphocytes in celiac sprue?

A

Lamina propria

103
Q

Decreased mucosal absorption in celiac sprue primarily affects what parts of the GI tract?

A

Distal duodenum and/or proximal jejunum

104
Q

What is used to diagnose celiac sprue?

A

Serum levels of tissue transglutaminase antibodies

105
Q

What other condition is celiac sprue associated with?

A

Dermatitis herpetiformis

106
Q

Does celiac sprue increase your risk of cancer?

A

Moderately (e.g. T cell lymphoma)

107
Q

How is celiac sprue treated?

A

Gluten-free diet

108
Q

What is the most common disaccharidase deficiency?

A

Lactase deficiency

109
Q

What happens to the villi in disaccharidase deficiency?

A

Nothing - they look normal

110
Q

What symptoms characterizes disaccharidase deficiency?

A

Osmotic diarrhea

111
Q

When do you see self-limited lactase deficiency and why?

A

Following injury (e.g. virus) to the tips of the villi which is where lactase is located

112
Q

What marks a positive lactose tolerance test for deficiency of lactase?

A
  1. Administration of lactose produces symptoms

2. Glucose rises < 20 mg/dL

113
Q

Describe the pathophysiology in abetalipoproteinemia.

A

Decreased synthesis of apolipoprotein B leads to inability to generate chylomicrons leads to decreased secretion of cholesterol and VLDL into the bloodstream leads to fat accumulation in enterocytes

114
Q

When does abetalipoproteinemia present?

A

Early childhood

115
Q

What are 5 symptoms in abetalipoproteinemia?

A
  1. Failure to thrive
  2. Steatorrhea
  3. Acanthocytosis
  4. Ataxia
  5. Night blindness
116
Q

What are 3 causes of pancreatic insufficiency?

A
  1. Cystic fibrosis
  2. Obstructing cancer
  3. Chronic pancreatitis
117
Q

Pancreatic insufficiency causes malabsorption of what?

A

Fat and fat-soluble vitamins (A, D, E, K)

118
Q

What happens to stool in pancreatic insufficiency?

A

Increase in neutral fat

119
Q

Describe what we use a D-xylose absorption test for.

A

Normal urinary excretion in pancreatic insufficiency vs. decreased excretion with intestinal mucosa defects or bacterial overgrowth

First Aid 2014 (24 decks)

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