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First Aid Chs Part 2 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is the first enzyme activated in acute pancreatitis?

A

Trypsinogen –> trypsin

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2
Q

What 2 types of necrosis is seen in acute pancreatitis?

A

Fat necrosis seen in peri-pancreatic fat. Liquefactive necrosis of the pancreas itself

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3
Q

How does alcohol cause acute pancreatitis?

A

Creates contraction of sphincter of Oddi, decreasing drainage of pancreas

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4
Q

Where does pain from pancreatitis typically refer?

A

Back

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5
Q

What is Cullen’s sign?

A

Peri-umbilical brusing seen with acute pancreatitis

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6
Q

What is Grey-Turner’s sign?

A

Flank hemorrhage seen with acute pancreatitis

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7
Q

What two enzymes are increased as a result of pancreatitis?

A

Lipase and amylase. Lipase is more specific, because amylase can be increased with damage to the salivary gland

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8
Q

What are the two most common causes of chronic pancreatitis?

A

Alcohol (repeated bouts of acute pancreatitis) and cystic fibrosis (kids)

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9
Q

What are the two major risk factors for pancreatic adenocarcinoma?

A

Smoking and chronic pancreatitis

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10
Q

Thin, 85 year old female presents with new-onset DM. What should you think about?

A

Pancreatic adenocarcinoma in the body or tail of the pancreas

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11
Q

What is the serum tumor marker for pancreatic adenocarcinoma?

A

CA-19-9

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12
Q

Why do bile acid binding resins (cholestyramine) lead to gallstones?

A

Decreased bile acids leads to ineffective solublizing of cholesterol, which can cause stones

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13
Q

What color are cholesterol gallstones?

A

Yellow

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14
Q

Why are women at greater risk for gallstones?

A

Estrogen increases HMG-CoA reductase, which increases cholesterol, which can precipitate and cause gallstones

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15
Q

Which gallstones are typically radiopaque?

A

Bilirubin stones

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16
Q

Where does pain from cholecystitis typically radiate?

A

Right scapula

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17
Q

What is a Rokitansky-Aschoff sinus?

A

Outpouching of gallbladder mucosa into the smooth muscle of the GB wall with CHRONIC cholecystitis

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18
Q

What is porcelain gallbladder and how is it treated?

A

Calcified gallbladder due to chronic cholecystitis. Treated by cholecystectomy, because it is considered a pre-cancerous condition.

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19
Q

85 year old woman presents with acute cholecystitis, what are you thinking?

A

GB carcinoma

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20
Q

What causes black pigment stones?

A

Hemolysis

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21
Q

What causes brown pigment stones?

A

Infection

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22
Q

How do gallstones cause ascending cholangitis?

A

When stones block the bile duct, bile can’t flow and wash away bacteria, which can then ascend and cause infection/inflammation.

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23
Q

How can gallstones cause air in the biliary tree?

A

Gallstone ileus - gallstone erodes through GB wall, into duodenum and blocks the ileocecal valve, causing backup of air all the way to the biliary tree

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24
Q

What two drugs given for hyperlipidemia cause cholesterol gallstones?

A

Fibric acid derivatives and cholestyramine

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25
Q

What is Charcot’s triad for ascending cholangitis?

A

Fever, RUQ pain, Jaundice

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26
Q

What is Reynold’s pentad?

A

Fever, RUQ pain, Jaundice, hypotension, mental status changes

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27
Q

What is the result of a pregnant woman being infected with HEV?

A

Fulminant hepatitis with massive liver necrosis

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28
Q

How is HEV typically acquired?

A

Contaminated water or undercooked seafood

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29
Q

What defines chronic HBV infection?

A

Presence of HBsAG for more than 6 months

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30
Q

What is the first serologic marker to rise in HBV infection?

A

HBsAG

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31
Q

What HBV antigen indicates infectivity?

A

HBeAG

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32
Q

What is the only DNA hepatitis virus?

A

HBV

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33
Q

What are the two naked hepatitis viruses?

A

A and E (nAkEd)

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34
Q

Which hepatitis viruses are RNA?

A

HAV, HCV, HDV, HEV

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35
Q

What type of vaccine is HAV?

A

Killed

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36
Q

What type of DNA polymerase does HBV use?

A

RNA dependent DNA polymerase (reverse transcriptase- can treat with RTI’s)

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37
Q

What is a Dane particle?

A

Hepatitis B surface antigen with DNA in it - refers to an infectious HBV particle

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38
Q

Where does HBV replicate its DNA?

A

Cytoplasm

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39
Q

What causes symptoms in HAV/HBV/HCV?

A

Patient’s CD8 cells attacking infected hepatocytes

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40
Q

Which patients are at a higher risk for progression to cancer/cirrhosis from HBV?

A

Those with reduced CMI (AIDS/DiGeorge/kids)

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41
Q

What is the first antibody to appear in HBV?

A

HBcAb - presence indicates recent infection

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42
Q

What does HBeAg positivity indicate?

A

Actively replicating (infective) virus

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43
Q

What type of vaccine is HBV?

A

Recombinant

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44
Q

What family of virus is HCV in?

A

Flavivirus

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45
Q

What does HCV do that makes the liver take it into hepatocytes?

A

Coats itself with LDL or VLDL

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46
Q

What 2 drugs are used to treat HCV?

A

Ribavirin and IFN-alpha. These can CURE HCV!

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47
Q

Explain HDV superinfection

A

A person previously infected with HBV acquires HDV. HBV surface antigen exists in great quantities in this patient’s blood, and it coats the HDV very rapidly, causing fulminant hepatitis.

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48
Q

Explain HDV/HBV co-infection

A

A person acquires HDV and HBV at the same time. Once enough HBV surface antigen is made, HDV coats itself with the surface antigen, and can destroy hepatocytes

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49
Q

What does HDV need from HBV to cause infection?

A

Needs HBV surface antigen - coats itself with it

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50
Q

What can a patient do to protect themselves from HDV?

A

Get vaccinated for HBV!

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51
Q

What is the only population we are concerned about with respect to HEV?

A

Pregnant women

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52
Q

What family is HEV a part of?

A

Hepevirus (HepEvirus)

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53
Q

What two things fail to fuse in cleft lip?

A

The maxillary and nasal processes

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54
Q

What fails to fuse in cleft palate?

A

The lateral palatine processes, the nasal septum, and/or the medial palatine processes.

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55
Q

What 3 things are seen in Bechet syndrome?

A

Recurrent aphthous ulcers, genital ulcers, and uveitis. Due to vasculitis in vessels of all sizes. Also, injury to an area results in a sterile pustule at the site of pinprick. Associated with HLA B-51

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56
Q

What are two risk factors for squamous cell CA of the mouth?

A

Tobacco and alcohol use

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57
Q

Where on the tongue does hairy leukoplakia typically occur?

A

Lateral tongue (due to EBV in immunocompromised).

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58
Q

What 3 sequelae can be seen with mumps infection?

A

Orchitis, pancreatitis, aseptic meningitis.

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59
Q

What is seen on biopsy of a pleiomorphic adenoma of the salivary gland?

A

Benign tumor with stroma (cartilage) and epithelial tissue (glands). It is a mixed tumor.

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60
Q

Why does a pleiomorphic adenoma of the salivary gland recur frequently?

A

It has irregular margins and is tough to remove completely.

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61
Q

What is seen on biopsy of a Warthin’s tumor of the parotid?

A

Cystic tumor with abundant lymphocytes and germinal centers.

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62
Q

What is seen on biopsy of a mucoepidermoid carcinoma of the salivary gland?

A

Malignant tumor composed of mucinous and squamous cells. It invades the facial nerve.

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63
Q

Describe the most common form of TE fistula.

A

Proximal esophagus ends in a blind pouch (atresia) and distal esophagus is attached to the trachea.

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64
Q

What is an esophageal web?

A

Thin protrusion of esophageal mucosa, most often in upper esophagus.

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65
Q

Describe the triad seen in Plummer-Vinson syndrome.

A

Iron deficiency anemia, Glossitis, Esophageal webs

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66
Q

What is a Zenker diverticulum?

A

Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall.

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67
Q

Where does a Zenker diverticulum commonly occur?

A

Above the upper esophageal sphincter at the junction of the esophagus and the pharynx.

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68
Q

What is Mallory-Weiss syndrome?

A

Linear laceration of the mucosa at the GE junction driven by vomiting (alcoholism, bulimia). Presents as painful hematemesis.

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69
Q

What is Boerhave syndrome?

A

Esophageal rupture due to violent retching. Can lead to subcutaneous emphysema.

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70
Q

What are the two abnormalities that occur in achalasia?

A

Decreased peristalsis (due to loss of myenteric plexus) and inability to relax LES (thought to be due to loss of NO/VIP).

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71
Q

List two common causes of secondary achalasia.

A

Chagas disease, CREST syndrome.

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72
Q

Bird’s beak sign

A

Achalasia

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73
Q

Dysphagia for solids and liquids

A

Achalasia

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74
Q

What is seen on esophageal manometry in achalasia?

A

High LES pressure.

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75
Q

Hourglass appearance of stomach

A

Hiatal hernia

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76
Q

What is a common GI cause of adult-onset asthma?

A

GERD

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77
Q

Describe the “new” cells seen in Barrett’s esophagus.

A

Non-ciliated columnar epithelium with goblet cells.

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78
Q

What is the most common esophageal cancer in the USA? Worldwide? Where is each type commonly located?

A

USA - adenocarcinoma (lower 1/3) Worldwide - squamous cell carcinoma (Upper 2/3).

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79
Q

List some risk factors for squamous cell carcinoma of the esophagus.

A

Alcohol, tobacco, hot tea, achalasia, esophageal web, esophageal injury (IRRITATION).

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80
Q

What is the major risk factor for adenocarcioma of the esophagus?

A

Barrett’s esophagus (lower 1/3 of esophagus).

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81
Q

Through which nodes does esophageal cancer from the upper, middle, and lower 1/3 of the esophagus spread?

A

Upper 1/3 - cervical nodes; Middle 1/3 - mediastinal or tracheobronchial nodes; Lower 1/3 - Celiac and gastric nodes

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82
Q

What is the most common benign esophageal tumor? How should you biopsy it?

A

Leiomyoma. Do NOT biopsy it.

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83
Q

How can you differentiate an omphalocele from a gastroschisis?

A

Omphalocele will be covered in peritoneum and amnion, gastroschisis won’t.

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84
Q

Palpable “olive” in the epigastric region of a newborn.

A

Pyloric stenosis.

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85
Q

Are babies with pyloric stenosis born with the disorder?

A

No, they acquire it 2-3 weeks after birth (takes time for the pyloris to become hypertrophic)

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86
Q

Describe the vomiting seen in pyloric stenosis

A

Nonbilous, because the stenosis is proximal to the duodenum.

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87
Q

What is the underlying cause of acute gastritis?

A

Imbalance between mucosal defenses and acidic environment.

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88
Q

What is a Curling ulcer?

A

Acute gastritis following a severe burn (due to decreased bloodflow to the mucosa).

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89
Q

What is a Cushing ulcer?

A

Ulcer caused by increased intracranial pressure, which results in increased vagal tone.

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90
Q

What causes type A chronic gastritis and where in the stomach does it occur?

A

Autoimmune attack of parietal cells or intrinsic factor. It is seen in the body and fundus of the stomach.

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91
Q

What causes type B chronic gastritis and where in the stomach is it commonly seen?

A

H. pylori infection. It is commonly seen in the antrum of the stomach.

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92
Q

What type of hypersensitivity is type A chronic gastritis?

A

Type IV (T cell mediated. As a result, the patient develops parietal cell antibodies, but they aren’t the cause of the damage, they are a result of it).

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93
Q

Describe some clinical features seen with type A chronic gastritis.

A

Atrophy of mucosa; Achlorhydria (decreased acid) with increased gastrin and antral G cell hyperplasia; Megaloblastic anemia; Increased risk for gastric adenocarcinoma (secondary to metaplasia)

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94
Q

H. pylor increases the risk for which two cancers?

A

Gastric adenocarcinoma and MALT lymphoma

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95
Q

What is the #1 cause of duodenal ulcers?

A

H. pylori.

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96
Q

Describe the pain with gastric vs. duodenal ulcers.

A

Gastric ulcer pain - worse with meals. VS Duodenal ulcer pain - better with meals.

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97
Q

Are gastric or duodenal ulcers more likely maignant?

A

Gastric (duodenal ulcers are almost never malignant).

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98
Q

What blood type increases risk for intestinal-type stomach cancer?

A

A

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99
Q

Describe the findings in intestinal-type stomach cancer.

A

Commonly on lesser curvature, looks like an ulcer with raised margins. Associated with H. pylori infection, nitrosamines increase risk.

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100
Q

What is linitis plastica and with what disorder is it associated?

A

Thickening of the stomach wall seen in diffuse type stomach cancer.

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101
Q

What is a signet ring cell and what disorder is it associated with?

A

A cell with its nucleus pushed to the edge. The nucleus is pushed to the edge by mucin in diffuse-type stomach cancer.

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102
Q

Linitis plastica is associated with what disorder?

A

Diffuse-type (signet ring cell) stomach cancer.

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103
Q

H. pylori is associated with what type of stomach cancer?

A

Intestinal-type

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104
Q

Nitrosamines are associated with what type of stomach cancer?

A

Intestinal-type

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105
Q

Signet ring cells are associated with what type of stomach cancer?

A

Diffuse-type stomach cancer.

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106
Q

What are the two types of stomach cancer?

A

Intestinal-type (Ulcerated, H. pylori, nitrosamines, lesser curvature). Diffuse type (signet ring cells, linitis plastica, Krukenburg tumor).

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107
Q

Acanthosis nigricans is associated with what neoplasm?

A

Gastric cancer

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108
Q

What is Leser-Trelat sign?

A

Sudden development of multiple seborrheic keratoses, often on the back. Associated with gastric carcinoma.

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109
Q

What is Virchow’s node?

A

Spread of stomach cancer to the left supraclavicular node.

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110
Q

What is a Sister Mary Joseph nodule?

A

Spread of stomach cancer to superficial umbilical nodes. Seen with intestinal type.

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111
Q

What is Krukenburg tumor?

A

Spread of gastric carcinoma to ovaries. Seen with diffuse type (signet ring).

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112
Q

What is Menetrier’s disease?

A

Gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucus cells. It is a precancerous lesion.

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113
Q

Duodenal atresia is associated with what developmental disorder?

A

Down syndrome.

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114
Q

What is the “double bubble” sign?

A

Distension of stomach and blind loop of duodenum seen with duodenal atresia. The “bubbles” are separated by the pyloric sphincter.

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115
Q

What causes a Meckel diverticulum?

A

Persistence of the vitelline duct.

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116
Q

What is the rule of 2’s in Meckels diverticulum?

A

2% of the population; 2 ft from ileocecal valve; 2 inches long; 2 types of tissue (pancreatic/gastric); 2 year olds

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117
Q

What causes bleeding in a Meckel diverticulum?

A

Gastric tissue secretes acid that destroys surrounding tissue.

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118
Q

How do you diagnose a Meckel diverticulum?

A

Pertechnitate scan

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119
Q

Passage of “currant jelly” stool.

A

Intussusception

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120
Q

Which two HLA subtypes is celiac disease associated with?

A

HLA DQ2 and DQ8

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121
Q

What is the most pathogenic component of gluten?

A

Gliadin

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122
Q

What is seen on duodenal biopsy of a patient with Celiac disease?

A

Flattening of vili, hyperplasia of crypts, and increased intraepithelial lymphocytes.

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123
Q

In what part of the small intestine is celiac disease most prominent?

A

Duodenum

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124
Q

What is the best assay for diagnosis of celiac disease?

A

IgA or IgG (in IgA deficient patients) against tissue transglutaminase.

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125
Q

Celiac disease increases the risk for which two neoplasms?

A

Small bowel CA and T cell lymphoma

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126
Q

What 3 antibodies are found in celiac sprue?

A

Anti-endomysial, anti-gliadin, anti-tissue transglutaminase.

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127
Q

What is tropical sprue?

A

Malabsorption arising after infectious diarrhea caused by an unknown organism.

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128
Q

In what part of the small intestine is tropical sprue most prominent?

A

Jejunum and ileum (NOT duodenum like in Celiac)

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129
Q

Why does tropical sprue cause a folic acid and B12 deficiency?

A

Because it damages the jejunum (where folic acid is reabsorbed) and the ileum (where B12 is reabsorbed).

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130
Q

What will be seen upon biopsy in Whipple disease?

A

Foamy macrophages that are PAS positive, diastase resistant.

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131
Q

What type of malabsorption is caused by Whipple disease?

A

Fat malabsorption (damage to the lamina propria).

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132
Q

What are some non-GI symptoms seen with Whipple disease?

A

Cardiac valve abnormalities, arthralgias, neurologic symptoms.`

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133
Q

Apo-B48 is needed for…

A

Chylomicron formation

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134
Q

Apo-B100 is needed for…

A

VLDL and LDL formation

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135
Q

What will be seen in abetalipoproteinemia?

A

Inability to generate chylomicrons (apo B 48), LDL and VLDL (apo B 100).

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136
Q

What can be used to stain carcinoid tumor?

A

Chromogranin

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137
Q

Carcinoid tumors secrete…

A

Serotonin

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138
Q

What metabolite is excreted in the urine in carcinoid tumor?

A

5-HIAA (metabolite of serotonin)

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139
Q

<p>What is the difference between carcinoid tumor and carcinoid syndrome?</p>

A

<p>Carcinoid syndrome requires serotonin in the systemic circuit.
Serotonin is metabolized by the liver if the lesion is solely in the GI system (carcinoid tumor).
If the tumor metastasizes to the liver, it can then be dumped into the hepatic vein (systemic circuit), and cause serotonin syndrome.</p>

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140
Q

Why don’t you see carcinoid heart disease on the left side of the heart?

A

Because the lung has monoamine oxidase.

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141
Q

Why don’t you see carcinoid syndrome if a carcinoid tumor is localized to the GI system only?

A

Because the liver metabolizes 5-HT into 5-HIAA.

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142
Q

What obstructs the appendiceal lumen to cause appendicitis in children?

A

Lymphoid hyperplasia

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143
Q

What is the key histologic hallmark of ulcerative colitis?

A

Crypt abscess with neutrophils

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144
Q

What two factors determine the risk for carcinoma in a patient with ulcerative colitis?

A

Amount of colon involved and duration of disease (> 10 years = higher risk for dysplasia).

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145
Q

What autoantibody can be seen in association with ulcerative colitis?

A

p-ANCA

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146
Q

Is smoking protective for ulcerative colitis or Crohn disease?

A

Ulcerative colitis

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147
Q

Describe the portion of the gut involved in ulcerative colitis.

A

Always begins in rectum and extends proximally up to the cecum. Only the colon is affected.

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148
Q

Is the involvement continuous or skipped in ulcerative colitis?

A

Continuous

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149
Q

Lead pipe colon

A

Ulcerative colitis

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150
Q

Full thickness colonic inflammation with knife-like fissures

A

Crohn disease

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151
Q

Skip lesions

A

Crohn disease

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152
Q

What is the most common site of Crohn disease?

A

Terminal ileum (can cause a B12 deficiency)

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153
Q

What is always spared in Crohn disease?

A

Rectum

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154
Q

TH2 mediated IBD

A

UC

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155
Q

TH1 mediated IBD

A

Crohn disease

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156
Q

Where is the pain typically localized in UC vs. Crohn disease?

A

LLQ in UC (rectum most commonly involved); RLQ in CD (terminal ileum most commonly involved).

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157
Q

Bowel inflammation with granulomas

A

Crohn disease

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158
Q

Cobblestone mucosa

A

Crohn disease

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159
Q

String sign

A

Crohn disease (narowing of the colonic lumen due to transmural inflammation causing myofibroblast deposition and contraction).

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160
Q

IBD with mouth to anus involvement

A

CD

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161
Q

Why does CD increase the risk for nephrolithiasis?

A

With inflammation of the bowel, absorption of oxalate in the gut is increased.

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162
Q

Which IBD increases the risk of fistula?

A

CD

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163
Q

Does smoking increase or decrease the risk for Crohn disease?

A

Increase

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164
Q

What are some extra-intestinal manifestations of Crohn disease?

A

Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, calcium oxalate kidney stones.

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165
Q

What are some extra-intestinal manifestations of ulcerative colitis?

A

Pyoderma gangrenosum, primary sclerosing cholangitis, anyklosing spondylitis, uveitis, urate kidney stones.

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166
Q

Hirschsprung disease is associated with what developmental disorder?

A

Down syndrome

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167
Q

What is the underlying pathology in Hirschsprung disease?

A

Failure of migration of neural crest cells results in absent myenteric (Auerbach’s) and submucosal (Meissner’s) plexuses in the rectum and distal colon.

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168
Q

How is biopsy performed in patients with Hirschsprung disease?

A

Rectal suction biopsy

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169
Q

Anatomically, what is the most common location of colonic diverticula?

A

Sigmoid colon

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170
Q

Histologically, where do colonic diverticula occur?

A

Where the vasa recta traverses the muscularis propria (weak point in colonic wall).

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171
Q

What parts of the colonic wall form the diverticulum in diverticulosis?

A

Only mucosa and submucosa (false diverticulum).

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172
Q

What is angiodysplasia?

A

Tortuous dilation of mucosal and submucosal capillary beds leading to hematochezia in an older adult.

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173
Q

What is Osler-Weber-Rendu syndrome also known as?

A

Hereditary hemorrhagic telangiectasia

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174
Q

What are the findings in hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)?

A

Telangiectasias, recurrent epistaxis, GI bleeds, skin discoloration. Autosomal dominant.

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175
Q

Where does ischemic colitis most commonly occur?

A

Splenic flexure (SMA/IMA watershed area)

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176
Q

T/F - hyperplastic colonic polyps have a possibility of becoming malignant.

A

False - hyperplastic polyps have no malignant potential.

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177
Q

Colonic polyp with serrated appearance.

A

Hyperplastic polyp. No malignant potential.

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178
Q

T/F - adenomatous colonic polyps have a possibility of becoming malignant.

A

True - they are benign masses, but they are pre-malignant.

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179
Q

What are the two types of colonic polyps?

A

Adenomatous (pre-malignant), hyperplastic (no malignant potential)

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180
Q

What does colonic APC mutation cause?

A

Increased RISK for formation of a polyp (doesn’t cause the polyp to form)

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181
Q

What does colonic K-RAS mutation cause?

A

Formation of a polyp (adenoma) - after an APC mutation increased the risk for polyp formation.

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182
Q

What does colonic p53 mutation cause?

A

Progression of an adenomatous polyp to carcinoma (after APC increased the risk for a polyp, which was formed with K-RAS mutation).

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183
Q

Why is aspirin protective for colorectal carcinoma?

A

Because COX is necessary to form colon cancer.

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184
Q

List the steps in the colon adenoma-carcinoma sequence.

A
  1. APC mutation increases RISK for formation of a polyp. 2. K-RAS mutation causes formation of an adenomatous polyp. 3. p53 mutation and increased COX expression causes adenoma progression to carcinoma.
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185
Q

Mutation of what TSG increases the risk of colonic polyp formation?

A

APC

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186
Q

Mutation of what oncogene causes colonic polyp formation?

A

K-RAS

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187
Q

The APC tumor suppressor gene is located on which chromosome?

A

5 (5 letters in polyp)

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188
Q

Mutation of what tumor suppressor gene allows colonic adenoma to progress to carcinoma?

A

p53

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189
Q

Colon adenomas of what gross and histologic morphology increase the risk of progression to cancer?

A

Gross - sessile (not pedunculated); Histologic - Villous

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190
Q

Formation of hundreds to thousands of colonic polyps

A

Familial adenomatous polyposis

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191
Q

What gene is mutated in FAP?

A

APC

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192
Q

What is Gardner syndrome?

A

FAP (thousands of polyps) with fibromatosis and osteomas.

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193
Q

What is Turcot syndrome?

A

FAP (thousands of polyps) with CNS tumors.

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194
Q

Thousands of colonic polyps with CNS tumors. Dx?

A

Turcot syndrome

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195
Q

Thousands of colonic polyps with fibromatosis and osteomas. Dx?

A

Gardner syndrome

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196
Q

What is a juvenile polyp?

A

A sporadic hamartoma (benign) polyp arising in children. Presents as a solitary rectal polyp that prolapses and bleeds.

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197
Q

What is juvenile polyposis?

A

Multiple juvenile polyps (hamartomas) in the stomach and colon. Large numbers increase the risk of progression to cancer.

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198
Q

Patient has hamartomatous polyps throughout the GI tract with hyperpigmentation on lips. Dx?

A

Peutz-Jeghers syndrome

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199
Q

What is the inheritance pattern of Peutz-Jeghers syndrome?

A

Autosomal dominant

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200
Q

What type of polyps are seen in juvenile polyposis and Peutz-Jeghers syndrome?

A

Hamartomas (benign)

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201
Q

What is the second most common molecular mechanism for formation of colorectal cancer?

A

Microsatellite instability - DNA mismatch repair mutations (hMSH2, hMLH1) leads to sporadic cancer and HNPCC.

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202
Q

What is mutated in HNPCC?

A

DNA mismatch repair enzymes hMSH-2 and hMLH1 (microsatellite instability).

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203
Q

Besides colon, which two other malignancies are patients with HNPCC at increased risk for?

A

Ovarian and endometrial carcinoma

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204
Q

What tumor marker is useful in detecting recurrence of colorectal carcinoma?

A

CEA (good for monitoring response to treatment, NOT good for screening).

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205
Q

What is the use of CEA in colorectal cancer?

A

Good for monitoring recurrence and treatment response, NOT good for screening.

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206
Q

What is the inheritance pattern of HNPCC and FAP?

A

Both are autosomal dominant.

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207
Q

How does right sided colon cancer commonly present?

A

Manifestations of iron deficiency anemia due to blood loss

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208
Q

How does left sided colon cancer commonly present?

A

Changes in stool caliber (usually thin stools), constipation, “napkin ring” lesions.

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209
Q

What is toxic megacolon and what disease increases the risk for it?

A

Rapid colonic distension following complete cessation of neuromuscular activity in the large intestine seen in ulcerative colitis.

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210
Q

A non-compliant patient with known ulcerative colitis presents hypotensive, tachycardic with a distended abdomen. What should be done next? What should be avoided?

A

The patient likely has toxic megacolon. A flat plain x-ray should be done to diagnose the condition. Avoid colonoscopy or barium enema as they increase the risk for rupture.

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211
Q

What is the most common form of appendiceal tumor?

A

Carcinoid

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212
Q

HNPCC is also known as…

A

Lynch syndrome

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213
Q

What is the first step in screening for malabsorption?

A

Sudan III stool stain to look for fat in the stool

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214
Q

What is Courvoisier sign?

A

Palpable but nontender gallbladder, suggestive of adenocarcinoma of the head of the pancreas

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215
Q

Where are anal fissures most commonly located?

A

Posterior midline, distal to the dentate line (painful).

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216
Q

What happens to serum calcium levels in acute pancreatitis and why does this happen?

A

Patients get hypocalcemia, because of calcium depositing on foci of fat necrosis in the damaged peri-pancreatic fat.

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217
Q

What lines pancreatic pseudocysts?

A

Granulation tissue

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218
Q

Why are stools pale with pancreatic adenocarcinoma?

A

Blockage of the bile duct. Bilirubin gives stool its color.

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219
Q

What are the 3 different types of gallstones?

A

Cholesterol; Black pigment - hemolysis, Brown pigment - infection

220
Q

What is biliary colic?

A

Waxing and waning RUQ pain caused by gallbladder contracting against a cystic duct that is blocked by a stone.

221
Q

What makes stool brown?

A

Stercobilin

222
Q

What causes darkening of the urine in excessive extravascular hemolysis?

A

Increased urine urobilinogen (not unconjugated bilirubin, because it is not water soluble).

223
Q

What is kernicterus and what causes it?

A

Deposition of fat soluble unconjugated bilirubin in the basal nuclei leads to neurological deficits and death in newborns.

224
Q

What is the treatment for physiologic jaundice of the newborn and why does it work?

A

Phototherapy - makes unconjugated bilirubin water soluble.

225
Q

Describe the findings in Gilbert syndrome.

A

Mild decrease in the liver’s ability to conjugate bilirubin only causes jaundice in the face of excess stress. Benign.

226
Q

What is decreased in Gilbert syndrome?

A

UDP-glucuronyl transferase is mildly decreased. Causes benign hyperbilirubinemia with stress/fasting.

227
Q

What form of bilirubin is increased in the blood in Gilbert syndrome?

A

Unconjugated (mild decrease in the ability of the liver to conjugate bilirubin in times of stress due to decreased UDP-glucuronyl transferase).

228
Q

What form of bilirubin is increased in the blood in extravascular hemolysis?

A

Unconjugated

229
Q

What form of bilirubin is increased in the blood in physiologic jaundice of the newborn?

A

Unconjugated (liver can’t conjugate it well enough yet).

230
Q

What form of bilirubin is increased in the blood in Crigler-Najjar syndrome?

A

Unconjugated (absence of UGT)

231
Q

Explain the cause of Crigler-Najjar syndrome.

A

Absent UDP-glucoronyl transferase = liver can’t conjugate bilirubin. Leads to unconjugated hyperbilirubinemia, death at a young age.

232
Q

What is defective in Dubin-Johnson syndrome?

A

Bilirubin canalicular transport. The liver can conjugate bilirubin, it just can’t transport it into bile canaliculi.

233
Q

What form of bilirubin is increased in the serum of patients with Dubin-Johnson syndrome?

A

Conjugated

234
Q

Describe the appearance of the liver in patients with Dubin-Johnson syndrome.

A

Grossly black

235
Q

What is the difference between Dubin-Johnson and Rotor syndromes?

A

Both result from a decrease in the liver’s ability to transport conjugated bilirubin into the bile canaliculus. The liver of a patient with DJ syndrome will be grossly black, the liver of a patient with Rotor syndrome won’t.

236
Q

What form of bilirubin is increased in the serum of patients with Rotor syndrome?

A

Conjugated

237
Q

What form of bilirubin is increased in the serum of patients with gallstones?

A

Conjugated (blockage of the bile duct causes leakage of bilirubin into the blood - could also be unconjugated if gallstones are black pigment stones due to hemolysis).

238
Q

What form of bilirubin is increased in the serum of patients with viral hepatitis?

A

Both conjugated (damaging bile ductules = conjugated bilirubin leaks out) AND unconjugated (damaging hepatocytes = decreased conjugating ability)

239
Q

Where does the inflammation primarily occur in chronic hepatitis?

A

In the portal tract (not as much in the lobules)

240
Q

What is the only thing positive during the HBV window phase?

A

HBcAB IgM

241
Q

What mediates fibrosis in cirrhosis?

A

Stellate cell - secretes TGF-beta

242
Q

What are Mallory Bodies?

A

Damaged intermediate filaments in hepatocytes seen in alcoholic hepatitis.

243
Q

What causes damage in hemochromatosis?

A

Generation of free radicals by iron

244
Q

What gene is most commonly mutated in primary hemochromatosis?

A

HFE gene

245
Q

<p>What are the two most common mutations seen in primary hemochromatosis?</p>

A

<p>C282Y or H63D on the HFE gene</p>

Associated with HLA-A3

246
Q

Describe the changes seen in ferritin, TIBC, serum iron, and transferrin saturation in hemochromatosis.

A

Increased ferritin, Decreased TIBC (measure of transferrin), Increased serum iron, Increased transferrin saturation

247
Q

What stain can be used to distinguish iron in the liver from lipofuscin?

A

Prussian blue (will stain iron blue, won’t stain lipofuscin, which is a brown wear and tear pigment derived from oxidized lipids).

248
Q

What gene is mutated in Wilson’s disease?

A

ATP7B gene (normally transports copper into bile)

249
Q

What happens to serum ceruloplasmin in patients with Wilson’s disease?

A

Decreases

250
Q

Antimitochondrial antibody

A

Primary biliary cirrhosis

251
Q

What is the pathophysiology of primary biliary cirrhosis?

A

Autoimmune attack of intralobular bile ducts results in lymphocytic infiltrate and granulomas.

252
Q

Ulcerative colitis increases the risk for what biliary disease?

A

Primary sclerosing cholangitis

253
Q

Periductal fibrosis with “onion skin” appearance.

A

Primary sclerosing cholangitis

254
Q

String of pearl appearance on ECRP.

A

Primary sclerosing cholangitis

255
Q

Describe the findings on imaging in a patient with primary sclerosing cholangitis.

A

Alternating strictures and dilation with “beading” of intra and extra-hepatic ducts. Leads to a “string of pearls” appearance.

256
Q

What is Caroli syndrome?

A

Cystic dilation of intrahepatic bile ducts seen in kids. Associated with renal cystic disease.

257
Q

What is damaged in liver cells in Reye syndrome?

A

Mitochondria

258
Q

What is the only disease that aspirin is indicated in children?

A

Kawasaki disease

259
Q

Hepatic adenoma is associated with use of..

A

Oral contraceptives

260
Q

Aflatoxins increase risk of…

A

Hepatocellular carcinoma (through p53 mutations).

261
Q

What is Budd-Chiari syndrome?

A

Hepatic vein obstruction. Can be caused by polycythemia or liver carcinoma invasion of the hepatic vein.

262
Q

What is the serum tumor marker for hepatocellular carcinoma?

A

Alpha-fetoprotein

263
Q

Polyvinyl chloride increases the risk for what malignancy?

A

Angiosarcoma of the liver

264
Q

What is seen on biopsy of a liver of a child with Reye syndrome?

A

Microvesicular steatosis

265
Q

What are Councilman bodies?

A

Eosinophilic apoptotic hepatocytes seen on liver biopsy in hepatitis

266
Q

What is seen in biopsy of a patient with acute viral hepatitis?

A

Ballooning degeneration

267
Q

hMSH2 mutations lead to…

A

Microsatellite instability, defective mismatch repair, and HNPCC (Lynch syndrome)

268
Q

hMLH1 mutations lead to…

A

Microsatellite instability, defective mismatch repair, and HNPCC (Lynch syndrome)

269
Q

What is alpha-amanitin, what does it cause, and how does it cause it?

A

Alpha amanitin is a toxin produced by some mushrooms that causes massive hepatic failure through inhibition of eukaryotic RNA polymerase II (which synthesizes mRNA).

270
Q

<p>Anti-saccharomyces cerevisiae antibodies</p>

A

<p>Crohn disease</p>

271
Q

What makes up the foregut, midgut and hindgut?

A

Foregut - pharynx to duodenum
Midgut - duodenum to transverse colon
hindgut - distal transverse colon to rectum

272
Q

What occurs if you have a developmental defect of the anterior abdominal wall due to failure of the rostral fold closing?

A

Sternal defects

273
Q

What occurs if you have a developmental defect of the anterior abdominal wall due to failure of the caudal fold closing?

A

Bladder exstrophy

274
Q

What occurs if you have a developmental defect of the anterior abdominal wall due to failure of the lateral fold closing?

A

Omphalocele, gastroschisis

275
Q

what chromosomal abnormality is associated with duodenal atresia?

A

Trisomy 21

276
Q

When the midgut returns to the abdominal cavity during week 10 of development, what does it rotate around?

A

SMA

277
Q

Does a gastroschisis or omphalocele typically include the liver in its contents?

A

Omphalocele

278
Q

Why does an infant with an esophageal atresia with a distal tracheoesophageal fistula develop cyanosis?

A

The cyanosis is secondary to laryngospasm (to avoid reflux-related aspiration)

279
Q

A patient presents with a palpable “olive” mass in the epigastric region and nonbilious projectile vomiting at about 2 weeks old - what is wrong with the baby?

A

Congenital pyloric stenosis

occurs more often in the firstborn males

280
Q

if a patient has PROLONGED vomiting (days to week) how would they present?

A

Decreased HCL will lead to hypochloremia, metabolic alkalosis and hypokalemia (due to H/K pump on cells pushing H into the serum and K into the cells to try to correct for the alkalosis)

281
Q

What is the pancreas derived from?

A

Foregut (endoderm)

282
Q

What do the ventral and dorsal pancreatic buds become?

A

Ventral pancreatic bud - contributes tot he pancreatic head and main pancreatic duct
Doral pancreatic bud - becomes every thing else (body, tail, isthmus and accessory pancreatic duct)

note that the uncinate process is formed by the ventral bud alone

283
Q

What is pancreas divisum?

A

Ventral and dorsal parts of the pancreas fail to fuse at 8 weeks

284
Q

Where does the spleen arise from?

A

spleen arises in the mesentery of the stomach (mesodermal) but it’s supplied by the foregut celiac A

285
Q

Name the retroperitoneal structures

A 
A DUCK PEAR
Aorta and IVC
Duodenum 2-4
Ureters
Colon (descending and ascending)
Kidneys
Pancreas
Esophagus below the diaphragm (lower 2/3)
Adrenals
Rectum
286
Q

what is contained in the falciform ligament?

A

Ligamentum teres hepatis (derivative of the fetal umbilical vein)

it connects the liver to the anterior abdominal wall

287
Q

What is the falciform ligament of derivative of?

A

Ventral mesentery

288
Q

What does the hepatoduodenal ligament contain?

A

Portal triad (hepatic artery, portal vein and common bile duct

289
Q

What is the pringle maneuver?

A

Ligament may be compressed between thumb and index finger placed in the omental foramen to control bleeding (hepatoduodenal ligament)

290
Q

Which ligament connects the greater and lesser sacs?

A

Hepatoduodenal ligament

291
Q

What does the gastrohepatic ligament connect?

A

Liver to the lesser curvature of the stomach

292
Q

What is contained within the gastrohepatic ligament?

A

Gastric arteries

293
Q

What separates the greater and lesser omental sacs on the right?

A

Gastrohepatic ligament - this can be cut during surgery to access the lesser sac

294
Q

What does the gastrocolic ligament connect?

A

The greater curvature and transverse colon

295
Q

What does the gastrocolic ligament contain?

A

Gastroepiploic artreries

296
Q

What does the gastrospenic ligament connect?

A

Greater curvature and spleen

297
Q

What is contained in the gastrosplenic ligament?

A

Short gastrics, left gastroepiploic vessels

298
Q

What ligament separates the greater and lesser omental sacs on the left?

A

Gastrosplenic ligament

299
Q

What does the splenorenal ligament connect?

A

The spleen to the posterior abdominal wall

300
Q

What structures are contained in the splenorenal ligament?

A

Splenic artery and vein, tail of pancreas

301
Q

What are the layers of the gut wall from the inside to the outside?

A

MSMS

Mucosa, Submucosa, Muscularis externa, Serosa

302
Q

Where is the Meissner’s plexus located?

A

In the submucosa

303
Q

Where is the Auerbach’s plexus located?

A

Muscularis externa

304
Q

Where are ulcers vs erosions located in the digestive tract?

A

Ulcers - into submucosa, inner or outer muscular layer

erosions - into mucsoa only

305
Q

what is the histology of the esophagus?

A

nonkeratinized stratified squamous epithelium

306
Q

What is the histology of the stomach?

A

Gastric glands

307
Q

What is the histology of the Duodenum?

A

Villi and microvilli increase absorptive surface. Brunner’s glands (submucosa) and crypts of Lieberkuhn

308
Q

What is the histology of the jejunum?

A

Plicase circulares and crypts of Lieberkuhn

309
Q

What is the histology of the ileum?

A

Peyer’s patches (lamina propria, submucosa), plicae circulares (proximal ilium), and crypts of Lieberkuhn

Has the largest number of goblet cells in the small intestine

310
Q

Colon

A

Colon has crypts but no villi, numerous goblet cells

311
Q

List the branches of the celiac trunk

A

Common hepatic, splenic, and left gastric arteries

312
Q

List the 4 arterial anastomoses that exist if the abdominal aorta were to be blocked

A
  1. Superior epigastric (internal thoracic/mammary) and inferior epigastric (external iliac)
  2. Superior pancreaticoduodenal (celiac trunk) and inferior pancraeticoduodenal (SMA)
  3. Middle colic (SMA) and left colic (IMA)
  4. superior rectal (IMA) and middle + inferior rectal (internal iliac)
313
Q

What is the portal/systemic anastomosis for esophageal varices?

A

Left gastric vein (portal) with esophageal vein/Azygous vein (systemic)

314
Q

What is the portal/systemic anastomosis for caput medusa?

A

Paraumbilical vein with superficial and inferior epigastric veins below the umbilicus and superior epigastric and lateral thoracic veins above the umbilicus

315
Q

What is the portal/systemic anastomosis for Internal hemorrhoids?

A

Superior rectal vein (portal) with middle and inferior rectal (systemic)

316
Q

What is the pectinate (dentate) line?

A

Formed where endoderm (hindgut) meets ectoderm

317
Q

What type of hemorrhoids and cancer can occur above the pectinate line?

A

Internal hemorrhoids and adenocarcinoma

318
Q

What is the blood supply above the pectinate line?

A

Superior rectal artery (IMA)

319
Q

What is the venous drainage above the pectinate line?

A

Superior rectal vein to the inferior mesenteric vein to the portal system

320
Q

What is the lymphatic drainage of the area above vs the area below the pecinate line?

A

Above the pectinate line - deep nodes

Below the pectinate line - superficial inguinal nodes

321
Q

What type of hemorrhoris and cancer can occur blow the pectinate line?

A

External hemorrhoids and squmouas cell carcinoma

322
Q

What is the blood supply below the pectinate line?

A

inferior rectal artery (from the internal pudendal artery)

323
Q

WHat is the venous drainage below the pectinate line?

A

inferior rectal vein to the internal pudendal vein to the internal iliac vein to the IVC

324
Q

Where does blood from hemorrhoids come from?

A

VENOUS

325
Q

What are the three zones of the liver?

A

zone 1 - periportal zone - affected first by viral hepatitis
zone 2 - intermediate
zone 3 - pericentral vein (centrilobular) zone - affected first by ischemia or hypotension

326
Q

Which zone of the liver contains the P450 system?

A

Zone 3 - therefore this is the most sensitive zone to toxic injury and also is the site of alcoholic hepatitis

327
Q

What are the two sources of blood coming into the liver?

A
  1. hepatic artery (oxygenated)

2. portal vein - blood that’s been drained from the GI tract (contains the nutrients, drugs, toxins, etc.

328
Q

What is the ligament of treitz?

A

Demarcation between an upper and lower GI bleed

It arises from CT around the celiac trunk - inserts into the 3rd and 4th portions of the duodenum

329
Q

What makes up the femoral triangle?

A

Contains the femoral vein, artery and nerve

330
Q

What is contained in the femoral sheath?

A

Fascial tube 3-4 cm below the inguinal ligament that contains the femoral vein, artery and canal (deep inguinal lymph nodes) but NOT the formal nerve

331
Q

From lateral to medial describe the organization of the femoral region?

A

lateral to medial to find your NAVL

Nerve - artery - vein - Lymph

332
Q

What protrudes through the internal inguinal ring?

A

Indirect hernia

333
Q

What protrudes through the abdominal wall?

A

Direct hernia

334
Q

Name the layers of the spermatic cord

A

External spermatic fascia (external oblique)
Cremasteric muscle and fascia (internal oblique)
Internal spermatic fascia (transversalis fascia)

335
Q

Which hernia occurs laterally to the inferior epigastric artery?

A

Indirect inguinal hernia

336
Q

Which hernia goes through the internal inguinal ring, external inguinal ring and into the scrotum?

A

Indirect inguinal hernia

337
Q

Which hernia occurs in infants due to a failure of the processus vaginalis to close?

A

indirect inguinal hernia

can form a hydrocele

338
Q

Which hernia is more common in women?

A

femoral hernia

339
Q

Which hernia is the leading cause of bowel incarceration?

A

Femoral hernia

340
Q

Which hernia protrudes through the inguinal triangle (Hesselbach’s triangle)

A

Direct inguinal hernia

341
Q

Which hernia bulges directly though the abdominal wall medial to the inferior epigastric artery?

A

Direct inguinal hernia

342
Q

Which hernia goes through the external (superficial) inguinal ring only and is covered by external spermatic fascia?

A

Direct inguinal hernia

343
Q

Which hernia protrudes below the inguinal ligament through the femoral canal below and lateral to the pubic tubercle?

A

Femoral hernia

344
Q

What is the most common form of diaphragmatic hernia?

A

Sliding hiatal hernia

GE junction gets displaced superiorly and makes an hour glass stomach

345
Q

Which type of diaphragmatic hernia has the fundus of the stomach protruding into the thorax?

A

Paraesophageal hernia

346
Q

How do the parasympathetics regulate gastric acid secretion?

A

via M3 with Ach
stimulates g cells to indirectly increase gastric acid - the Vagus also uses gastrin releasing peptide to indirectly stimulate increased gastric acid
so if you treat a person with anti-muscarinics like atropine, it’ll only work in one area - it won’t complete block acid production from the parasympathetics

347
Q

What is the source of gastrin?

A

G cells in the antrum of the stomach

348
Q

How do you increase gastrin secretion?

A

Increased stomach distension/alkalinization, amino acids like phenylalanine or tryptophan, peptides, or vagal stimulation. also calcium

349
Q

How do you decrease gastrin release?

A

decreasing the stomach pH to less than 1.5

350
Q

What is the function of gastrin?

A

Increases gastric acid secretion, increases growth of gastric mucosa, increases gastric motility

note that chronic PPI use can also lead to increased gastrin

351
Q

What hormone is increased in zollinger Ellison syndrome?

A

Gastrin

352
Q

What is the source of CCK?

A

I cells in the duodenum and jejunum

353
Q

How is CCK regulated?

A

CCK is increased by fatty acids and amino acids

354
Q

What is the action of CCK?

A

Increases pancreatic secretion, increases gallbladder contraction, increases relaxation of the sphincter of oddi
decrease gastric emptying

355
Q

What is the source of Secretin?

A

S cells in the duodenum

356
Q

How does CCK have its effect?

A

CCK acts on neural muscarinic pathways to cause pancreatic secretion

357
Q

How is secretin regulated?

A

Secretin is increased by acid and fatty acids in the lumen of the duodenum

358
Q

What is the action of secretin

A

Increases pancreatic bicarb secretion, decreases gastric acid secretion (by inhibiting gastric parietal cells) and increase bile secretion

359
Q

What is the source of somatostatin?

A

D cells in the pancreatic islets and the GI mucosa

360
Q

What regulates somatostatin release?

A

Increased by acid and decreased by vagal stimulation

361
Q

What is the action of somatostatin?

A

Decreases gastric acid and pepsinogen secretion, degreases pancreatic and small intestine fluid secretion, degreases GB contraction and decreases insulin and glucagon release

362
Q

What is the source of Glucose dependent insulinotropic peptide?

A

K cells in the duodenum and jejunum

363
Q

What is the action of Glucose dependent insulinotropic peptide?

A

Exocrine - decreases gastric acid secretion

Endocrine - increases insulin release

364
Q

How is Glucose dependent insulinotropic peptide regulated?

A

Increaesd by fatty acids,, amino acids and oral glucose

365
Q

What is the other name for Glucose dependent insulinotropic peptide?

A

Gastric inhibitory peptide

366
Q

What hormone is responsible for the fact that an oral glucose load is used more rapidly than the equivalent given by IV?

A

Glucose dependent insulinotropic peptide AKA gastric inhibitory peptide

367
Q

What is the source of vasoactive intestinal polypeptide (VIP)?

A

Parasympathetic ganglia in sphincters, gallbladder and small intestine smooth muscle

368
Q

What is the function of VIP?

A

Increases intestinal water and electrolyte secretion and increases the relaxation of intestinal smooth muscle and sphincters (relaxes LES)

369
Q

How is VIP regulated?

A

Increased by distension and vagal stimulation

decreased by adrenergic input

370
Q

What is a VIPoma?

A

A non-alpha, non-beta islet cell pancreatic tumor that secretes VIP
causes copious watery diarrhea, hypokalemia, and achlorhydria

371
Q

What is WDHA syndrome?

A

Used to describe the effects of a VIPoma

Watery diarrhea, hypokalemia and achlorhydria

372
Q

What is the function of nitric oxide in the GI tract?

A

Increases smooth muscle relaxation, including the lower esophageal sphincter

note that loss of NO secretion is implicated in increased LES tone of achalasia

373
Q

What is the source of motilin?

A

Small intestine

374
Q

What is the action of motilin?

A

Produces migrating motor complexes (MMCs)

375
Q

How is Motilin regulated?

A

Increased during the fasting state

Note that the motilin receptor agonists (like erythromycin) are used to stimulate intestinal peristalsis

376
Q

where are parietal cells located and what do they contain?

A

Stomach

contain intrinsic factor and gastric acid

377
Q

How is gastric acid secretion regulated?

A

Increased by histamine, Ach and gastrin

Decreased by somatostatin, GIP, prostaglandin and secretin

378
Q

What is a gastrinoma?

A

Gastrin secreting tumor that causes continuous high levels of acid secretion and ulcers

379
Q

Where is iron absorbed?

A

duodenum

380
Q

Where is B 12 absorbed?

A

terminal ileum

381
Q

Where is folate absorbed?

A

Jejunum

382
Q

Whats the mnemonic for remember where iron, B12 and folate are absorbed?

A

I’D Be Totally Insane For Jesus

Iron - duodenum
B12 - terminal ileum
Folate - jejunum

383
Q

what is the source of pepsin? What is its function?

A

Chief cells in the stomach (body)

It’s function is to digest proteins

384
Q

What converts pepsinogen to pepsin?

A

H+

385
Q

How is pepsin regulated?

A

Increased by vagal stimulation and local acid

386
Q

What is the source of bicarb in the GI tract?

A

Mucosal cells in the stomach, duodenum, salivary glands and the pancreas
and the Brunner’s glands in the duodenum

387
Q

How is bicarb regulated?

A

Increased by pancreatic and biliary secretion with secretin

388
Q

What is the osmotic state of saliva?

A

Normally hypotonic because of absorption but it’s more isotonic with higher flow rates because there’s less time for absorption

389
Q

What cells are located in the antrum of the stomach?

A

D cells, mucous cells and G cells

390
Q

What cells are located in the body of the stomach?

A

Parietal cells and Chief cells

391
Q

How does Gastrin increase acid secretion?

A

Through its effects on enterochromaffin like cells leading to histamine release (H2 receptors in the parietal cells use Gs to increased cAMP to increase gastric acid)

392
Q

Where are Brunner glands located?

A

Submucosa of the duodenum - secrete alkaline mucus

Hypertrophy of these glands is seen in peptic ulcer disease

393
Q

What can activate trypsinogen into trypsin?

A

Enterokinase/enteropeptidase which is an enzyme secreted from the duodenal mucosa

394
Q

What starts digestion by hydrolyzing alpha 1,4 linkages to yield disaccharides ?

A

Salivary amylase

395
Q

what can you use to assess brush border absorptive function independent of pancreatic function?

A

Use D-xylose

This is a good way to determine if malabsorption is due to pancreatic or intestinal pathology

396
Q

How are monosaccharides absorbed?

A

Glucose and galactose - sodium dependent transport

Fructose - facilitated diffusion

397
Q

what is unencapsulated lymphoid tissue that’s found in the lamina propria and submucosa of the ileum?

A

Peyer’s patches

contain M cells that take up the antigen

398
Q

What are bile salts?

A

Bile acids conjugated to glycine or taurine to make them water soluble

399
Q

What catalyzes the rate limiting step of bile synthesis?

A

Cholesterol 7 alpha hydroxylase

400
Q

can unconjugated bilirubin be found in the urine?

A

No, it is insoluble in water

401
Q

What is direct bilirubin?

A

Conjugated with glucuronic acid - water soluble

402
Q

What is the salivary gland tumor: benign mixed tumor that is the most common salivary gland tumor

A

Pleomorphic adenoma

403
Q

What is the salivary gland tumor: Presents as a painless mobile mass. it’s composed of cartilage and epithelium and recurs frequently

A

Pleomorphic adenoma

404
Q

What is the salivary gland tumor: Papillary cystadenoma lymphomatosum

A

Warthin’s tumor

405
Q

What is the salivary gland tumor: benign cystic tumor with germinal centers

A

Warthin’s tumor

406
Q

What is the salivary gland tumor: Second most common benign tumor

A

Warthin’s tumor

407
Q

What is the salivary gland tumor: The most common malignant tumor

A

Mucoepidermoid carcinoma

408
Q

What is the salivary gland tumor: Has mucinous and squamous components - it presents as a painful mass because of common involvement of the facial nerve

A

Mucoepidermoid carcinoma

409
Q

What is Achalasia?

A

Failure of relaxation of the lower esophageal sphincter due to loss of myenteric (Auerbach’s) plexus

410
Q

What cancer is achalasia associated with?

A

Increased risk of esophageal squamous cell carcinoma

411
Q

How is scleroderma different from achalasia?

A

CREST syndrome is associated with esophageal dysmotility involving LOW pressure proximal to the LES

412
Q

Commonly presents as heartburn and regurgitation upon lying down. May also present with nocturnal cough and dyspnea, adult onset asthma. Has a decreased in LES tone

A

GERD

413
Q

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

A

Esophageal varices

414
Q

Associated with reflux, infection, or chemical ingestion

A

Esophagitis

infections:
- candida: white pseudomembrane;
- HSV-1: punched out ulcers;
- CMV: linear ulcers

415
Q

Mucosal lacerations at the GE junction due to severe vomiting. Leads to hematemesis - usually found in alcoholics and bulimics.

A

Mallory-Weiss tears

Partial thickness tears

416
Q

Transmural esophageal rupture due to violent retching

A

BoerHaave-Syndrome

Full thickness tear
usually occurs in distal esophagus

417
Q

Associated with lye ingestion and acid reflux

A

Esophageal strictures

418
Q

Dysphagia due to webs, glossitis, iron deficiency anemia

A

Plummer Vinson syndrome

419
Q

What metaplasia occurs in Barrett’s esophagus?

A

Glandular metaplasia - replacement of nonkeratinzed (stratified) squamous epithelium with intestinal (nonciliated columnar) epithelium

420
Q

What causes Barretts esophagus? What would a patient have increased risk for?

A

Due to chronic GERD

can lead to adenocarcinoma

421
Q

what type of esophageal cancer is more common in the US? worldwide?

A

US: adenocarcinoma (whites - lower 1/3)
World: squamous cell carcinoma (blacks - upper 1/3)

422
Q

Name 6 malabsorption syndromes?

A

These Will Cause Devastatin Absorption Problems

Tropical Sprue
Whipple's disease
Celiac Sprue
Disaccharidase deficiency
Abetalipoproteinemia
Pancreatic insufficiency
423
Q

what is tropical sprue?

A

Unknown cause but it responds to antibotics. Can affect entire small bowel

424
Q

What disease causes PAS-positive foamy macrophages in the intestinal lamina propria and mesenteric nodes?

A

Whipple’s disease

425
Q

What bug causes Whipples disease?

A

Gram positive tropheryma whipplei

426
Q

What are some of the non-GI symptoms you can see in Whipple’s disease?

A

Cardiac symptoms, Arthralgias, Neurologic symptoms

427
Q

Where does Celiac sprue most often occur?

A

Primarily affects the distal duodenum or proximal jejunum

428
Q

What will you see on histology of a patient with celiac sprue?

A

Loss of villi

429
Q

What causes celiac sprue?

A

Autoantibodies to gluten (gliadin) in wheat and other grains

associated with HLA-DQ2 and HLA-DQ8

430
Q

what do the villi look like in a patient with disaccharidase deficiency?

A

normal

431
Q

What is the lactose tolerance test?

A

Positive for lactose deficiency if:

  • administration of lactose produces symptoms, and
  • glucose rises <20 mg/dL
432
Q

What is Abetalipoproteinemia?

A

Decreased synthesis of apolipoprotein B leading to inability to generate chylomicrons which leads to decreased secretion of cholesterol and VLDL into the blood stream so fat accumulates in enterocytes

433
Q

What are the 3 antibodies you can see in a patient with celiac sprue?

A

Anti-endomysial, anti-tissue transglutaminase, and anti-gliadin

serum levels of tissue transglutaminase are used for screening

434
Q

What is a Curling’s ulcer?

A

a burn

leads to decreased plasma volume and sloughing of the gastric mucosa

435
Q

What is a Cushing’s ulcer?

A

Brain injury

leads to increased vagal stimulation which increased ACH leading to increased acid production

436
Q

Why do NSAIDs lead to acute gastritis?

A

NSAIDs decrease PGE2 which leads to decreased bicarb and therefore decreased gastric mucosa protection

437
Q

What is the difference between acute and chronic gastritis?

A

Acute is erosive and chronic is non-erosive

438
Q

What is type A chronic gastritis?

A

Occurs in the fundus/body; autoimmune disorder characterized by autoantibodies to parietal cells, pernicious anemia and achlorhydria

439
Q

What is type B chronic gastritis?

A

Occurs in the antrum; most common type, caused by H pylori

leads to increased risk of MALT lymphoma

440
Q

Gastric hypertrophy with protein loss, parietal cell atrophy and increased mucus cells. Pre cancerous. Rugae of the stomach are so hypertrophied that they look like brain gyri

A

Menetrier’s disease

441
Q

What commonly occurs with stomach cancer?

A

Acanthosis nigricans

442
Q

What is Virchows node?

A

involvement of the left supraclavicular node by metastasis from the stomach

443
Q

What is a Krukenberg’s tumor?

A

Bilateral mets to the ovaries. Has abundant mucus and signet ring cells

444
Q

What is sister mary joseph’s nodules?

A

subcutaneous periumbilical metastasis

445
Q

Describe intestinal stomach cancer?

A

Associated with H. pylori infection, dietary nitrosamines, achlorhydria, chronic gastritis, TYPE A BLOOD, commonly occurs on the lesser curvature
Looks like an ulcer with raised margins

446
Q

Describe Diffuse stomach cancer?

A

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

447
Q

What is the risk of carcinoma in gastric vs duodenal ulcer?

A

Gastric - increased risk

duodenal - generally benign

448
Q

if a patient has a ruptured gastric ulcer on the lesser curvature of the stomach - where does bleeding occur from?

A

Left gastric artery

449
Q

If a patient has a ruptured ulcer on the posterior wall of the duodenum - where does bleeding occur from?

A

Gastroduodenal ulcer

450
Q

A patient has a NOD2 gene mutation - what are they at increased risk for?

A

Crohn’s disease

451
Q

what is the etiology in Crohn’s vs Ulcerative colitis?

A

Crohn’s - disordered response to intestinal bacteria

UC - autoimmune

452
Q

where does Crohn’s usuallt occur?

A

Ileum and colon

453
Q

What is the microscopic morphology of Crohn’s disease?

A

Noncaseating granuloma and lymphoid aggregates - Th1 medated

454
Q

What is the microscopic morphology of ulcerative colitis?

A

Crypt abscesses and ulcers, bleeding, NO granulomas

Th2 mediated

455
Q

what are some extraintestinal manifestations of Crohn’s disease?

A

Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, kidney stones

456
Q

what are some extraintestinal manifestations of Ulcerative colitis?

A

Pyoderma gangrenosum, primary sclerosing cholangitis, ankylosing spondylitis, uveitis

457
Q

Name 5 drugs you can use to treat Crohn’s disease

A

Corticosteroids, azathioprine, methotrexate, infliximab, adalimumab

458
Q

Name 4 treatments you can use for Ulcerative colitis

A

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

459
Q

what is irritable bowel syndrome?

A

Recurrent abdominal pain associated with 2 or more of the following:

  • pain improves with defecation
  • change in stool frequency
  • change in appearance of stool
460
Q

what can cause acute appendicitis in adults vs kids?

A

Obstruction due to:
adults - fecalith
kids - lymphoid hyperplasia (viral infection)

461
Q

what are the chapman points for appendicitis?

A

tip of 12th rib on the R or posterior is TP of T11

462
Q

Where do diverticulum most commonly occur?

A

Sigmoid colon

463
Q

What can cause diverticulosis?

A

Caused by increased intraluminal pressure and focal weakness in the colonic wall - associated with low fiber diets

464
Q

A patient presents with LLQ pain, fever and leukocytosis - what might this be?

A

Diverticulitis
“left sided appendicitis”
stool occult blood is common with or without hematochezia

465
Q

What is a Zenkers diverticulum?

A

Most commonly above UES
false diverticulum
herniation of mucosal tissue at Killian’striangle - between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor

can occur due to weakness in the cricopharyngeus muscle

466
Q

what is the most common congenital anomaly of the GI tract?

A

Meckle’s diverticulum

467
Q

how do you DX meckles diverticulum?

A

Pertechnetate study for ectopic uptake - shows ectopic gastric tissue

468
Q

Where does intussusception most commonly occur?

A

Ileocecal junction

469
Q

What causes intussusception in children and adults?

A

Children - usually idiopathic, may be viral like adenovirus

Adults - rare can be due to intraluminal mass or tumor

470
Q

how would an infant present with an intussusception?

A

6 mo male with vomiting, blood in stools, intermittent periods of abdominal pain, fussy and kicks legs up in the air

471
Q

What is seen on US in a patient with intussusception?

A

Bulls eye coil spring appearance

472
Q

Where are common places for volvulus to occur?

A

In areas where there is redundant mesentery like the cecum and sigmoid colon

473
Q

Birds beak or ace of spades sign with abdominal distension and vomiting

A

volvulus

474
Q

What causes Hirschsprung’s disease?

A

Congenital megacolon - characterized by lack of ganglion cells/enteric nervous plexuses ( auerbach’s and mmeissner’s plexuses)
due to failure of neural crest cell migration

475
Q

how do you diagnose Hirschsprung’s diease?

A

Rectal suction biopsy

476
Q

double bubble sign on X ray

A

Duodenal atresia

due to failure of recanalization of small bowel

477
Q

Necrosis of intestinal mucosa and possible perforation. Colon is usually involved but can involve the entire GI tract

A

Necrotizing enterocolitis

In neonates, more common in preemies
may have pneumatosis - gas in the wall

478
Q

Where does ischemic colitis often occur?

A

Splenic flexure and distal colon

479
Q

What is ischemic colitis?

A

reduction in intestinal blood flow causing ischemia (pain is out of proportion with physical findings)
patients get pain after they eat so they end up with weight loss. Typically affects the elderly

480
Q

What is an adhesion?

A

Fibrous band of scar tissue; commonly forms after surgery; most common cause of small bowel obstruction. can have well-demarcated necrotic zones

481
Q

What is Angiodysplasia?

A

Tortuous dilation of vessels leading to hematochezia. Most often found In cecum, terminal ileum and ascending colon. more common in older patients.
Confirmed by angiography

482
Q

What types of polyps are precancerous?

A

Adenomatous polyps

malignant risk is associated with increased size, villous (villainous) histology, increased epithelial dysplasia

483
Q

What is the most common non-neoplastic polyp in the colon?

A

Hyperplastic

484
Q

What is juvenile polyps?

A

Mostly sporadic lesions in children younger than 5yo, 80% occur in rectum. if single - has no malignant potential

485
Q

What is juvenile polyposis syndrome?

A

Multiple juvenile polyps in the GI tract

Has increased risk of adenocarcinoma

486
Q

Describe Peutz-Jeghers syndrome

A

AD syndrome featuring multiple nonmalignant hamartomas throughout the GI tract along with hyperpigmented mouth, lips, hands, genitalia
Associated with increased risk of CRC and other visceral malignancies

487
Q

List 4 syndromes that progress to colorectal cancer

A

FAP, Gardner’s syndrome, Turcot’s syndrome, Heretidary nonpolyposis colorectal cancer (lynch syndrome)

488
Q

Describe Familial adenomatous polyposis

A

AT mutation of APC gene on chromosome 5q - 2 hit hypothesis, thousands of polpys, pancolonic, always involves the rectum

489
Q

Describe Gardner’s syndrome

A

FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium

490
Q

Describe Turcot’s syndrome

A

FAP + Malignant CNS tumor like medulloblastoma

491
Q

Describe HNPSS/Lynch syndrome

A

AG mutation of DNA mismatch repair genes - proximal colon is always involved

492
Q

Where does colorectal cancer occur?

A

Rectosigmoid > Ascending > Descending

493
Q

How does ascending colorectal cancer present?

A

exophytic mass, iron deficiency anemia, weight loss

494
Q

How does descending colorectal cancer present?

A

Infiltrating mass, partial obstruction, colicky pain, hematochezia

495
Q

What is the tumor maker for colorectal cancer?

A

CEA - good for monitoring recurrence but not useful for screenign

496
Q

what are the symptoms of carcinoid syndrome?

A

B-FDR

Bronchospasm, Flushing, Diarrhea, Right sided heart problems

497
Q

what are the most common sites of carcinoid tumor?

A

Appendix, ileum, rectum

most common malignancy of the small intestine

498
Q

Dense core bodies seen on electron microscopy

A

Carcinoid tumor

499
Q

What is the treatment for carcinoid tumor?

A

Resection, octreotide, somatostatin

500
Q

what are diagnostic uses for gamma-glutamyl transpeptidase?

A

increased in various liver and biliary diseases like ALP, but NON in bone disease - also a marker for alcohol use

501
Q

What is amylase a marker for?

A

acute pancreatitis, mumps

502
Q

What is lipase a marker for?

A

acute pancreatitis

503
Q

rare often fatal childhood hepatoencephalopathy

A

Reye syndrome

504
Q

what is the mechanism of reye syndrome?

A

Aspirin metabolits decrease beta oxidation by reversible inhibition of mitochondrial enzyme

505
Q

swollen and necrotic hepatocytes with neutrophilic infiltration.

A

Alcoholic hepatitis

506
Q

What are Mallory bodies?

A

intracytoplasmic eosinophilic inclusions - seen in alcoholic hepatitis

507
Q

What does alcoholic cirrhosis look like?

A

micronodular irregularly shrunked liver with hobnail appearance. Sclerosis around central vein in zone 3

508
Q

what are common findings in hepatocellular carcinoma?

A

jaundice, tender hepatomegaly, ascites, polycythemia, and hypoglycemia

509
Q

Common, benign liver tumor; typically occurs at age 30-50yo

A

Cavernous hemangioma

biopsy is contraindicated because of risk of hemorrhage

510
Q

Benign liver tumor, often related to oral contraceptive or steroid use. can regress spontaneously

A

Hepatic adenoma

511
Q

What is an angiosarcoma?

A

Malignant tumor of endothelial origin; associated with exposure to arsenic, PVC

512
Q

What is nutmeg liver and what are some things that can cause it?

A

Backup of blood into the liver. Commonly caused by R sided heart failure and Budd chiari syndrome

513
Q

What can occur with persistent congested liver?

A

centrilobular congestion and necrosis can result in cardiac cirrhosis

514
Q

what is Buff chiari syndrome?

A

Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease (hepatomegaly, ascites, abdominal pain and eventual liver failure) ABSENCE OF JVD

515
Q

What is Budd chiari syndrome associated with?

A

hypercoagulable state, polycythemia vera, pregnancy and hepatocellular carcinoma

516
Q

Misfolded gene product protein aggregates in hepatocellular ER leading to cirrhosis with PAS positive globules in the liver

A

alpha 1 antitrypsin deficiency

AR

517
Q

What’s the inheritance pattern of Gilbert syndrome?

A

AR

518
Q

which is more severe? Crigler Najjar type 1 or type 2?

A

Type 1 is more severe

you can treat type 2 with phenobarbital which will increase liver enzyme synthesis

519
Q

what is another name for Wilson’s disease?

A

hepatolenticular degeneration

leads to basal ganglia degeneration –> parkinsonian symptoms

520
Q

What is the inheritance pattern of Wilson’s disease?

A

AR, chromosome 13; copper is normally excreted into bile by hepatocyte copper transporting ATPase (ATP7B gene)

521
Q

triad of cirrhosis, diabetes mellitus and skin pigmentation (Bronze diabetes)

A

Hemochromatosis

522
Q

What is secondary biliary cirrhosis complicated by?

A

Ascending cholangitis

523
Q

increased serum mitochondrial antibodies, including IgM

A

primary biliary cirrhosis

524
Q

Most commonly see in Women with other autoimmune conditions like REST or rheumatoid arthritis

A

Primary biliary cirrhosis

525
Q

Most commonly seen in men, p-ANCA positive, associated with ulcerative colitis, hypergammaglobulinemia (IgM)

A

Primary sclerosing cholangitis

526
Q

what’s the pathophysiology of primary biliary cirrhosis?

A

autoimmune reaction leading to lymphocytic infiltrate and granulomas

527
Q

What’s the pathophysiology of primary sclerosis cholangitis

A

unknown cause of concentric “onion skin” bile duct fibrosis leading to alternating strictures and dilation with beading of intra and extrahepatic bild ducts on ERCP

528
Q

which gallstones are radiolucent?

A

Cholesterol stones are radiolucent most of the time

pigment stones are radiopaque

529
Q

what is the liver fluke that infects the biliary tree and is associated with pigmented gallstones and cholangiocarcinoma?

A

Clonorchis sinensis

530
Q

What are black and brown gallstones due to?

A

brown are infection

black are hemolysis

531
Q

what is charcot’s triad of cholangitis?

A

jaundice, fever, RUQ pain

532
Q

how do you diagnose gallstones?

A

ultrasound, radionuclide biliary scan (HIDA)

TX with cholecystectomy

533
Q

if a patient has infectious cholcystitis what is a common cause?

A

CMV

534
Q

what are the number 1 and 2 causes of acute pancreatitis?

A

Gallstones (1) alcohol (2)

check CT for pancreatitis

535
Q

What are the major causes of CHRONIC pancreatitis?

A

alcohol abuse and idiopathic

536
Q

What does pancreatic adenocarcinoma arise from?

A

pancreatic ducts

537
Q

What’s the tumor marker for pancreatitis

A

CA-19-9

check CT scan

538
Q

What are the risk factors for adenocarcinoma?

A

Tobacco use (but not ethanol!)
chronic pancreatitis
Jewish and African American
Age older than 50

539
Q

How does pancreatic adenocarcinoma present?

A

abdominal pain radiating to the back, weight loss, migratory thrombophlebitis, obstructive jaundice

540
Q

What is Trousseau’s sign?

A

Migratory thrombophlebitis - redness and tenderness on palpation of extremities

associated with pancreatic adenocarcinoma

541
Q

What is Courvoisier’s sign?

A

Obstructive jaundice with palpable, nontender gallbladder

542
Q

What is the treatment for pancreatic adenocarcinoma?

A

Whipple procedure, chemotherapy, radiation therapy

543
Q

Name 4 H2 blockers

A

Cimetidine, ranitidine, famotidine, nizatidine

544
Q

Why would you use H2 blockers?

A

reversible block of histamine H2 receptors leads to decreased acid secretion by parietal cells for peptic ulcer disease, gastritis, mild esophageal reflux

545
Q

What does cimetidine do to the Cyp450 system?

A

potent INHIBITOR

First Aid Chs Part 2 (6 decks)

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