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A Comprehensive Review for the Certification and Recertification Examination for Physician Asistants > GI > Flashcards

GI Flashcards

1
Q

What is Barrett’s esophagitis?

A

Replacement of normal squamous epithelium with metastatic columnar epithelium, which can predispose to malignancy

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2
Q

What medications can worsen symptoms of GERD?

A

Antibiotics (tetracycline), bisphosphonates, iron, NSAIDs, anticholinergics, CCBs, narcotics, benzodiazepines, and others

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3
Q

When is endoscopy warranted in GERD?

A
  1. Patients older than 45 years of age with a new onset of symptoms
  2. Long-standing or frequently recurring symptoms
  3. Failure to respond to therapy or symptoms indicating more severe conditions such as anemia, dysphagia, or recurrent vomiting
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4
Q

Appropriate lifestyle modifications for GERD

A
  1. Cessation of smoking
  2. Avoidance of eating at bedtime
  3. Avoidance of large meals
  4. Avoidance of alcohol and foods that cause irritation (tomatoes, fried foods, caffeine, etc.)
  5. Elevate the head of the bed
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5
Q

What is the most powerful anti-GERD medication?

A

PPIs

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6
Q

What treatment combination may be used in a patient with significant nighttime symptoms of GERD?

A

A combination of an H2 blocker at nighttime and a PPI in the daytime

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7
Q

What some fungal causes of infectious esophagitis?

A

Candida sp. should be considered, especially if oral thrush is present

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8
Q

What are some viral causes of infectious esophagitis?

A

CMV and HSV are common causes

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9
Q

Besides viral and fungal causes, what are other causes of infectious esophagitis?

A

HIV, mycobacterium tuberculosis, Epstein-Barr virus, and mycobacterium avium intracellulare

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10
Q

Treatment of fungal infectious esophagitis

A

Fluconazole or ketoconazole

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11
Q

Treatment of HSV infectious esophagitis

A

Acyclovir

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12
Q

Treatment of CMV infectious esophagitis

A

IV ganciclovir; forscarnet is indicated in cases of poor tolerability or poor response

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13
Q

What are disorders of esophageal motility?

A

Neurogenic dysphagia, Zenker diverticulum, esophageal stenosis, achalasia, diffuse esophageal spasm, and scleroderma

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14
Q

Dysmotility of the esophagus can be caused by what?

A

Neurologic factors, intrinsic or extrinsic blockage, or malfunction of esophageal peristalsis

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15
Q

What is Zenker diverticulum?

A

Outpouching of the posterior hypo pharynx that can cause regurgitation of undigested food and liquid into the pharynx several hours after eating

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16
Q

What is achalasia?

A

Global esophageal motor disorder in which peristalsis is decreased and lower esophageal sphincter tone is increased, causing slowly progressive dysphagia with episodic regurgitation and chest pain

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17
Q

What are the barium swallow findings in achalasia?

A

“Parrot beak” appearance (i.e., a dilated esophagus tapering to the distal obstruction)

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18
Q

Treatment of strictures in esophageal dysmotility

A
  1. Most benign strictures can be managed by dilation

2. Malignant strictures must be resected

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19
Q

What are the most common esophageal neoplasms?

A

Squamous cell carcinomas and adenocarcinomas

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20
Q

Why is is common to have esophageal neoplasms spread to the mediastinum?

A

Because the esophagus has no serosa

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21
Q

What are some other causes to esophageal cancers?

A
  1. Cigarette smoking*
  2. Chronic alcohol use
  3. Exposure to other caustic agents (e.g., nitrosamines, fungal toxins, and other carcinogens)
  4. Hot foods
  5. Mucosal abnormalities
  6. Poor oral hygiene
  7. HPV
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22
Q

What is the best initial test for esophageal CA?

A

Biphasic barium esophagram

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23
Q

Treatment of esophageal CA

A

Generally surgical. Radiotherapy and adjunctive chemotherapy have been used in various combinations with or without surgery

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24
Q

What is a Mallory-Weiss tear?

A

Linear mucosal tear in the esophagus, generally at the gastroesophageal junction, that occurs with forceful vomiting or retching, causing hematemesis

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25
Q

A Mallory-Weiss tear is often associated with what?

A

Alcohol use, but it should be considered in all cases of upper GI bleed

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26
Q

Diagnosis of Mallory-Weiss tear

A

Endoscopy

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27
Q

Treatment of Mallory-Weiss tear

A

Most resolve without treatment. A PPI may be used if the active bleed is resolved. Endoscopic injection of epinephrine or thermal coagulation may be required if bleeding does not resolve on its own

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28
Q

What are esophageal varices?

A

Dilations of the veins of the esophagus, generally at the distal end

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29
Q

What is the underlying causes of esophageal varices?

A

Portal HTN, most commonly caused by cirrhosis from either alcohol abuse or from chronic viral hepatitis. Use of NSAIDs can exacerbate bleeding

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30
Q

Budd-Chiari syndrome and esophagal varices

A

Budd-Chiari syndrome may cause thrombosis of the portal vein, leading to esophageal varices

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31
Q

Prevention of variceal bleeding in cirrhotic patients

A

Beta blockers with or without isosorbide mononitrate, along with discontinuation of hepatotoxic agents

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32
Q

What treatment may be used for esophageal varices if medical treatment is insufficient?

A

Endoscopic band ligation

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33
Q

Hemodynamic support in bleeding esophageal varices?

A

Support with high-volume fluid replacement and vasopressors and immediate control of bleeding

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34
Q

What is the preferred therapy for acute bleeds of esophageal varices?

A

Endoscopic band ligation. Endoscopic pharmacologic vasoconstriction (e.g., octreotide) in conjunction is highly effective as well

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35
Q

Autoimmune disorders (e.g., pernicious anemia) and other noninfectious factors cause what type of gastritis?

A

Type A gastritis, which involves the body of the stomach

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36
Q

H. pylori causes what type of gastritis?

A

Type B gastritis, which involves the antrum and body of the stomach

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37
Q

Besides gastritis, H. pylori is associated with what other conditions?

A

Peptic ulcer, gastric adenocarcinoma, and gastric lymphoma

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38
Q

Treatment of delayed gastric emptying

A

Prokinetic medications (e.g., cisapride, metoclopramide) can sometimes help to speed the movement of food through the stomach

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39
Q

What is the most common cause of PUD?

A

H. pylori

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40
Q

Does food help or worsen symptoms of a gastric ulcer?

A

It worsens, which leads to anorexia and weight loss (compared to helping with duodenal ulcers)

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41
Q

What is the most common cause of nonhemorrhagic GI bleeds?

A

PUD

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42
Q

Combination therapy for H. pylori regimen should be taken for 2-4 weeks. What are the treatment options?

A
  1. PPI with clarithromycin and amoxicillin or clarithromycin and addition of metronidazole
  2. Bismuth subsalicylate plus tetracycline, metronidazole, and PPI
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43
Q

Prophylactic treatment for patients with a history of ulcer who require daily NSAID use; a history of complications, such as a bleed; a need for chronic steroids or anticoagulants; or significant other cormorbidities

A

Misoprostol or a PPI

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44
Q

What occurs in Zollinger-Ellison syndrome (ZES)?

A

A gastrin-secreting tumor (gastrinoma) causes hypergastrinemia, which results in refractory PUD

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45
Q

Where are most gastrinoma found?

A

In the pancreas or duodenum

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46
Q

About 1/3 of gastrinoma are part of a syndrome known as what?

A

Multiple endocrine neoplasia type I (MEN1), an autosomal dominant condition

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47
Q

Abdominal pain in ZES may be accompanied by a secretory diarrhea that improves with what?

A

H2 blockers (ranitidine, cimetidine) or PPIs (omeprazole, lansoprazole)

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48
Q

Diagnostic studies in ZES

A
  1. Fasting gastrin level
  2. A secretin test
  3. Endoscopy, CT, or MRI to help localize the tumor
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49
Q

Fasting gastrin level in ZES

A

A level greater than 150 pg/mL indicates hypergastrinemia

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50
Q

Secretin test in ZES

A
  1. Patients are given secretin 2 U/kg IV

2. In most patients with ZES, the gastrin level will increase by more than 200 pg/mL

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51
Q

Treatment of ZES

A
  1. Use of PPIs control gastrin secretion

2. Surgical resection of the gastrinoma should be attempted when possible

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52
Q

Signs of metastatic spread of gastric adenocarcinomas includes what?

A

Left supraclavicular lymphadenopathy (virchow node) and an umbilical node (Sister Mary Joseph nodule)

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53
Q

What is the most common lab finding in gastric adenocarcinoma?

A

Iron deficiency anemia

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54
Q

What is the most common extranodal site for non-Hodgkin lymphoma?

A

The stomach

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55
Q

Treatment of gastric lymphoma

A

Treatment is resection with or without radiation or chemotherapy

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56
Q

Norovirus source

A

Food, water, person to person

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57
Q

Norovirus onset of symptoms

A

1-3 days

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58
Q

Norovirus nausea and vomiting?

A

Yes

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59
Q

Norovirus diarrhea

A

Watery

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60
Q

Norovirus fever

A

Low grade

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61
Q

Norovirus duration

A

1-2 days

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62
Q

Norovirus therapy

A

Hydration (prevention: hand washing)

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63
Q

Rotavirus source

A

Person to person

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64
Q

Rotavirus onset of symptoms

A

1-3 days

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65
Q

Rotavirus nausea and vomiting?

A

Yes

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66
Q

Rotavirus diarrhea

A

Watery

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67
Q

Rotavirus fever

A

Low grade

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68
Q

Rotavirus duration

A

5-8 days

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69
Q

Rotavirus therapy

A

Hydration (prevention: hand washing)

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70
Q

Staphylococcus aureus (toxin) source

A

Food, after cooking

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71
Q

Staphylococcus aureus (toxin) onset of symptoms

A

1-7 hours

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72
Q

Staphylococcus aureus (toxin) nausea and vomiting?

A

Yes, rapid onset

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73
Q

Staphylococcus aureus (toxin) diarrhea

A

Cramping, some diarrhea

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74
Q

Staphylococcus aureus (toxin) fever

A

Uncommon

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75
Q

Staphylococcus aureus (toxin) duration

A

Acute (4-6 hours); total (1-2 days)

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76
Q

Staphylococcus aureus (toxin) therapy

A

Supportive

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77
Q

Clostridum perfringens (toxin) source

A

Food, before cooking

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78
Q

Clostridum perfringens (toxin) onset of symptoms

A

8-14 hours

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79
Q

Clostridum perfringens (toxin) nausea and vomiting?

A

Uncommon

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80
Q

Clostridum perfringens (toxin) diarrhea

A

Cramping, watery

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81
Q

Clostridum perfringens (toxin) fever

A

Rare

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82
Q

Clostridum perfringens (toxin) duration

A

24 hr.

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83
Q

Clostridum perfringens (toxin) therapy

A

Supportive

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84
Q

Vibrio spp. (cholera) source

A

Water

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85
Q

Vibrio spp. (cholera) onset of symptoms

A

2-3 days

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86
Q

Vibrio spp. (cholera) nausea and vomiting?

A

Some

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87
Q

Vibrio spp. (cholera) diarrhea

A

Profuse, watery

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88
Q

Vibrio spp. (cholera) fever

A

Rare

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89
Q

Vibrio spp. (cholera) duration

A

Days

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90
Q

Vibrio spp. (cholera) therapy

A

hydration

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91
Q

Enterotoxic escherichia coli source

A

Food

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92
Q

Enterotoxic escherichia coli onset of symptoms

A

5-15 days

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93
Q

Enterotoxic escherichia coli nausea and vomiting?

A

Some

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94
Q

Enterotoxic escherichia coli diarrhea

A

Cramping, watery

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95
Q

Enterotoxic escherichia coli fever

A

Low grade

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96
Q

Enterotoxic escherichia coli duration

A

1-5 days

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97
Q

Enterotoxic escherichia coli therapy

A

hydration, bismuth/loperamide

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98
Q

Giardia lamblia source

A

Water, person to person

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99
Q

Giardia lamblia onset of symptoms

A

5-25 days

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100
Q

Giardia lamblia nausea and vomiting?

A

Nausea

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101
Q

Giardia lamblia diarrhea

A

Diarrhea, bloating

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102
Q

Giardia lamblia fever

A

None possible

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103
Q

Giardia lamblia duration

A

Until treated

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104
Q

Giardia lamblia therapy

A

Metronidazole, 250mg twice a day for 10 days

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105
Q

Cryptosporidium source

A

Water, outbreaks

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106
Q

Cryptosporidium onset of symptoms

A

2-10 days

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107
Q

Cryptosporidium nausea and vomiting?

A

Yes

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108
Q

Cryptosporidium diarrhea

A

Watery

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109
Q

Cryptosporidium fever

A

Possible

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110
Q

Cryptosporidium duration

A

30 days (unless HIV)

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111
Q

Cryptosporidium therapy

A

Supportive, HIV treatment

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112
Q

Cyclospora source

A

Imported, uncooked foods

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113
Q

Cyclospora onset of symptoms

A

7 days

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114
Q

Cyclospora nausea and vomiting?

A

Nausea, anorexia

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115
Q

Cyclospora diarrhea

A

Watery

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116
Q

Cyclospora fever

A

low grade

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117
Q

Cyclospora duration

A

Weeks

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118
Q

Cyclospora therapy

A

Trimethoprim-sulfamethoxazole BID for 7 days

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119
Q

Salmonella (invasive) source

A

Poultry

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120
Q

Salmonella (invasive) onset of symptoms

A

6-72 hours

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121
Q

Salmonella (invasive) nausea and vomiting?

A

Nausea, some vomiting

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122
Q

Salmonella (invasive) diarrhea

A

Purulent

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123
Q

Salmonella (invasive) fever

A

Yes, septicemia common

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124
Q

Salmonella (invasive) duration

A

4-7 days

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125
Q

Salmonella (invasive) therapy

A

Hydration

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126
Q

Enterohemorrhagic E. coli (invasive) source

A

Undercooked ground beef

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127
Q

Enterohemorrhagic E. coli (invasive) onset of symptoms

A

12-60 hours

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128
Q

Enterohemorrhagic E. coli (invasive) nausea and vomiting?

A

No

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129
Q

Enterohemorrhagic E. coli (invasive) diarrhea

A

Purulent, bloody, cramping

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130
Q

Enterohemorrhagic E. coli (invasive) fever

A

Yes

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131
Q

Enterohemorrhagic E. coli (invasive) duration

A

5-10 days

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132
Q

Enterohemorrhagic E. coli (invasive) therapy

A

Supportive unless severe

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133
Q

Shigella (invasive) source

A

Fecal-oral

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134
Q

Shigella (invasive) onset of symptoms

A

1-6 days

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135
Q

Shigella (invasive) nausea and vomiting?

A

No

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136
Q

Shigella (invasive) diarrhea

A

Purulent, bloody, cramping

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137
Q

Shigella (invasive) fever

A

Yes

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138
Q

Shigella (invasive) duration

A

1-7 days

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139
Q

Shigella (invasive) therapy

A

Supportive

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140
Q

Campylobacter (invasive) source

A

Undercooked poultry

141
Q

Campylobacter (invasive) onset of symptoms

A

2-5 days

142
Q

Campylobacter (invasive) nausea and vomiting?

A

Some

143
Q

Campylobacter (invasive) diarrhea

A

Purulent, bloody, cramping

144
Q

Campylobacter (invasive) fever

A

Yes

145
Q

Campylobacter (invasive) duration

A

2-5 days

146
Q

Campylobacter (invasive) therapy

A

Supportive

147
Q

Treatment of a bowel obstruction

A
  1. NPO, nasogastric suctioning, IV fluids, monitoring
  2. Partial obstruction in a hemodynamically stable patient may be managed with IV hydration and nasogastric decompression
  3. Urgent surgical consultation is necessary when mechanical obstruction is suspected, especially of the large bowel
  4. Pain management is necessary for patients with bowel obstruction
148
Q

Diagnostic studies in malabsorption

A
  1. If a 72-hour fecal fat test is normal, specific defects, such as pancreatic insufficiency and abnormal bile salt metabolism, should be considered
  2. A D-xylose test will distinguish maldigestion (e.g., pancreatic insufficiency, bile salt deficiency) from malabsorption. A normal test r/o malabsorption
  3. Specific tests may be used to detect vitamin B12, calcium, or albumin deficiency
149
Q

Diagnostic studies in Celiac disease

A
  1. IgA antiendomysial (EMA) and antitissue translutaminase (anti-tTG) antibodies are the serologic screening tests
  2. Small bowel biopsy is needed to confirm the diagnosis
150
Q

What medication may be given for refractory cases of Celiac disease?

A

Prednisone

151
Q

Distribution of Crohn’s disease

A

Mouth to anus, predominately right sided; skip areas

152
Q

Complications of Crohn’s disease

A

Fistulas (common), toxic megacolon, colon CA

153
Q

Onset of Crohn’s disease

A

Gradual

154
Q

Depth of lesions in Crohn’s disease

A

transmural

155
Q

Symptoms of Crohn’s disease

A

Diarrhea and pain

156
Q

For acute attacks of Crohn’s disease, what is the treatment?

A

-Oral corticosteroids (prednisone) are used with or without aminosalicylates.

157
Q

What is added to the treatment regimen of Crohn’s disease for perianal disease, fissures, or fistulae?

A

Metronidazole or ciprofloxacin

158
Q

What may be added to the treatment regimen of Crohn’s disease in refractory cases?

A

Infliximab

159
Q

In Crohn’s disease, what is the best option for maintenance therapy?

A

Mesalamine

160
Q

Does smoking alleviate or aggravate the symptoms of Crohn’s disease?

A

Aggravate

161
Q

Ulcerative colitis onset

A

Sudden or gradual

162
Q

Ulcerative colitis distribution

A

Distal to proximal, continuous

163
Q

Ulcerative colitis depth of lesions

A

Mucosal surface

164
Q

Ulcerative colitis symptoms

A

Bloody, pus-filled diarrhea; tenesmus

165
Q

Ulcerative colitis complications

A

Toxic megacolon, colon CA

166
Q

What are the mainstays of medical treatment in Ulcerative Colitis?

A

Topical or oral aminosalicylates and corticosteroids

167
Q

What treatment is indicated for refractory disease of ulcerative colitis?

A

Immunomodulators

168
Q

In which IBD disease is surgery curative?

A

UC. Segmental resection is possible, but total proctocolectomy is the most common surgical cure

169
Q

In adults, intussusception is almost always due to what?

A

Neoplasm

170
Q

Diagnostic studies of intussusception in children

A

Barium or air enema (it may be both diagnostic and therapeutic)

171
Q

Diagnostic studies of intussusception in adults

A

CT is best means of establishing the diagnosis, but many cases are diagnosed only at surgery
-DO NOT use barium enema

172
Q

What study should be avoided in patients with an acute episode of diverticulitis?

A

Barium enema (it ma lead to perforation and peritonitis)

173
Q

Treatment of diverticulitis

A
  1. Low-residue diet and broad-spectrum antibiotics are appropriate for patients with mild diverticulitis
  2. Hospitalization for IV administration of abx, bowel rest, and analgesic often is required. An NG tube is inserted if ileus develops
174
Q

When is surgery needed in diverticulitis?

A

It may be necessary in severe cases, including peritonitis, large abscesses, fistulae, or obstruction

175
Q

Diet for patients with diverticulitis

A

Patients should maintain a high-fiber diet to prevent diverticulitis. Evidence has negated the need to recommend avoidance of nuts, seeds, and popcorn

176
Q

For both acute mesenteric ischemia and chronic mesenteric ischemia, what is the typical patient population?

A

Older than 50 years of age and have other signs of cardiovascular or collagen vascular disease

177
Q

Acute mesenteric ischemia causes

A

May be caused by arterial embolus, arterial thrombosis, or venous thrombosis

178
Q

Intestinal infarction is more common in the small bowel or large bowel?

A

Small bowel

179
Q

Chronic mesenteric ischemia clinical features

A

Presents as abdominal angina, with pain occurring 10-30 minutes after eating, which is relieved somewhat by squatting or lying down. Physical exam is normal

180
Q

Acute mesenteric ischemia clinical features

A

Presents with sudden onset of severe abdominal pain out of proportion to examination findings. Later in the process, involuntary guarding, rebound, and heme-positive stool may develop

181
Q

All patients with ischemic bowel disease should have what study done?

A

Duplex u/s of the mesenteric arteries, which may be confirmed by angiography

182
Q

Treatment for acute mesenteric ischemia or chronic mesenteric ischemia

A

Surgical revascularization. Hydration is also a critical factor

183
Q

What is toxic megacolon?

A

It is extreme dilation and immobility of the colon and represents a true emergency.

184
Q

Toxic megacolon can be caused by Hirschsprung disease. What is this disease?

A

It is a congenital aganglionosis of the colon, leading to functional obstruction in the newborn

185
Q

In adults, toxic megacolon occurs as a complication of what?

A

UC, Crohn colitis, pseudomembranous colitis, and specific infectious causes (particularly amebiasis, Shigella sp., Campylobacter sp., and Clostridium difficile)

186
Q

Toxic megacolon treatment

A
  1. Decompression of the colon is required. In some cases, colostomy or even complete colonic resection may be required
  2. Careful attention must be paid to fluid and electrolyte balance
187
Q

Which type of colonic polyps carry the lowest risk of dysplasia?

A

Hyperplastic polyps

188
Q

Which type of colonic polyps carry the highest risk of malignancy?

A

Villous polyps

189
Q

Family members of those with familial polyposis syndrome should be evaluated how often?

A

Every 1-2 years beginning at 10-12 years of age. Elective colectomy may be an option for high-risk individuals

190
Q

Having a single distal hyperplastic poly requires follow-ups how often?

A

Every 10 years

191
Q

Having multiple hyperplastic polyps, hyperplastic polyps at sites rather than distal, or tubular polyps requires follow-ups how often?

A

Every 5 years

192
Q

Villous polyps requires follow-ups how often?

A

Every 3 years

193
Q

Clinical features of right-sided colon CA lesions

A

They typically cause chronic blood loss and iron deficiency anemia. Obstruction is uncommon

194
Q

Clinical features of left-sided colon CA lesions

A

Circumferential, causing change in bowel habits and obstructive symptoms

195
Q

Treatment of colon CA

A
  1. Treatment is by surgical resection, which is accompanied by chemotherapy in patients with stage III (Dukes C or higher) or higher (and sometimes in stage II [Dukes B]) lesions
  2. Radiation may be used for rectal tumors
196
Q

An anorectal abscess is a result of what?

A

Infection

197
Q

A fistula is a result of what?

A

Chronic complication of abscess

198
Q

What is a anorectal fistula?

A

An open tract between two epithelium-lined areas and most commonly is associated with deeper anorectal abscesses

199
Q

Treatment of an anorectal abscess

A

Requires surgical drainage, followed by warm-water cleansing, analgesics, stool softeners, and high-fiber diet (WASH regimen)

200
Q

Treatment of anorectal fistuale

A

Treated surgically

201
Q

What are anal fissures?

A

Linear lesions in the rectal wall most commonly found on the posterior midline

202
Q

Treatment of anal fissure

A

Treatment includes bulking agents and increased fluids to avoid straining. Sitz baths will relieve acute pain.

203
Q

What medications may help with healing of an anal fissure?

A

Topical nitroglycerin ointment or topical styptic, such as silver nitrate (1-2%) or gentian violet solution (1%)

204
Q

Stage I internal hemorrhoids

A

Confined to the anal canal and may bleed with defecation

205
Q

Stage II internal hemorrhoids

A

Protrude from the anal opening but reduce spontaneously. Bleeding and mucoid discharge may occur

206
Q

Stage III internal hemorrhoids

A

Require manual reduction after bowel movements. Patients may develop pain and discomfort

207
Q

Stage IV internal hemorrhoids

A

Chronically protruding and risk strangulation

208
Q

Stages I and II internal hemorrhoids can be managed how?

A

With a high-fiber diet and increased fluids. Bulk laxatives may be helpful

209
Q

Higher stage hemorrhoidal disease may benefit from what treatment?

A

From suppositories with anesthetic and astringent properties

210
Q

Surgical treatment of hemorrhoids is indicated for whom?

A

Those unresponsive to conservative treatment and all stage IV hemorrhoids

211
Q

What are the surgical options for hemorrhoids?

A

Injection, rubber band ligation, or sclerotherapy

212
Q

Treatment of pilonidal disease

A
  1. Treatment is surgical drainage, which may be supplemented with antibiotics
  2. Follicle removal may be required, with unroofing of sinus tracts
213
Q

What are complications of fecal impaction?

A

Urinary tract obstruction and infection, spontaneous perforation of the colon, and stercoral ulcer where the mass has pressed on the colon

214
Q

Fecaliths may cause and develop what?

A

Appendicitis

215
Q

More proximal fecal impaction generally indicates what?

A

neoplasm

216
Q

Anal cancer is caused by what?

A

HPV and is a common finding among women with HPV and people with HIV infection, particularly men who have sex with men (MSM)

217
Q

Treatment of anal cancer

A

Surgical

218
Q

What is the most common cause of appendicitis?

A

Fecalith

219
Q

What are the most common causes of pancreatitis?

A

Cholelithiasis or alcohol abuse

220
Q

What are some indications of a grave prognosis?

A

Severe hypovolemia, adult respiratory distress syndrome, and tachycardia of greater than 130 bpm

221
Q

Hemorrhagic pancreatitis may cause bleeding where?

A

Into the flanks (Grey Turner sign) or umbilical area (Cullen sign)

222
Q

Which is the most sensitive and specific test for acute pancreatitis?

A

Serum lipase (but only with elevations of threefold or greater)

223
Q

Ranson criteria for poor prognosis for pancreatitis: leukocyte count

A

> 16,000/µL

224
Q

Ranson criteria for poor prognosis for pancreatitis: blood glucose level

A

> 200 mg/dL

225
Q

Ranson criteria for poor prognosis for pancreatitis: lactate dehydrogenase

A

> 350 IU/dL (normal <20-50 IU/dL)

226
Q

Ranson criteria for poor prognosis for pancreatitis: AST

A

> 250 IU/dL (normal <120 IU/dL)

227
Q

Ranson criteria for poor prognosis for pancreatitis: Arterial PO2

A

<60 mm Hg

228
Q

Ranson criteria for poor prognosis for pancreatitis: Base deficit

A

> 4 mEq/L

229
Q

Ranson criteria for poor prognosis for pancreatitis: Calcium

A

Falling

230
Q

Ranson criteria for poor prognosis for pancreatitis: BUN

A

Rising

231
Q

Treatment for acute pancreatitis

A
  1. Oral intake must be stopped to prevent continued secretion of pancreatic juices
  2. Fluid volume must be restored and maintained. Parenteral hyperalimentation should be started early to prevent nutritional depletion
  3. Pain is managed with an opioid. Antibiotics should be considered
  4. The patient must be monitored closely for complications
232
Q

Complications of acute pancreatitis

A

Pancreatic pseudocyst, renal failure, pleural effusion, hypocalcemia, and pancreatic abscess

233
Q

What is the classic triad of chronic pancreatitis?

A

Pancreatic calcification, steatorrhea, and DM

234
Q

Treatment of chronic pancreatitis

A
  1. Treatment is as for acute pancreatitis. A low-fat diet should be recommended at discharge
  2. Surgical removal of part of the pancreas can control pain
  3. The only definitive treatment for chronic pancreatitis is to address the underlying cause, which most commonly is alcohol
235
Q

What is Courvoisier sign?

A

It is a palpable gallbladder that may be seen in pancreatic CA

236
Q

Treatment of pancreatic CA

A
  1. Treatment is surgical resection (modified Whipple procedure) in those w/o metastases
  2. Subsequent radiation and chemotherapy are controversial
237
Q

What are complications of choledocholithiasis?

A

Cholecystitis, pancreatitis, and acute cholangitis

238
Q

What is the Charcot triad?

A

RUQ tenderness, jaundice, and fever that is found in acute cholangitis

239
Q

What is Reynolds pentad?

A

RUQ tenderness, jaundice, fever, altered mental status, and hypotension

240
Q

What is the optimal procedure both for diagnosis and treatment of acute cholangitis?

A

ERCP (however it should not be done until the patient is stable)

241
Q

What is the initial treatment of acute cholangitis?

A

Antibiotics (generally a fluoroquinolone, a cephalosporin, ampicillin, or gentamicin with metronidazole), fluid and electrolyte replacement, and analgesia are the initial treatment

242
Q

What is primary sclerosing cholangitis (PSC)?

A

Chronic thickening of the bile duct walls of unknown etiology, although 80% are associated with inflammatory bowel disease, generally UC

243
Q

PSC is strongly associated with what?

A

Cholangiocarcinoma as well as with an increased risk of pancreatic and colorectal carcinoma

244
Q

What is the most common presenting features of PSC?

A

Jaundice and pruritus

245
Q

Treatment of PSC

A
  1. Localized strictures may be relieved with balloon dilation and stent placement. Long-term stenting increases the risk of cholangitis
  2. Liver transplant is the only treatment with a known survival benefit
246
Q

What is the most common cause of acute hepatitis?

A

Viral; toxins (e.g., alcohol) are the second most common cause

247
Q

How is hepatitis A and E transmitted?

A

Fecal-oral contamination and can be prevented by maintaining a sanitary water supply and hand washing

248
Q

How is hepatitis B, C, and D transmitted?

A

Parenterally or by mucous membrane contact

249
Q

Hepatitis D is seen only in conjunction with what?

A

hepatitis B

250
Q

Immunoglobulin M antibody to hepatitis A virus (anti-HAV) can be detect with what?

A

the onset of clinical disease but it disappears after several months.

251
Q

What does HAV IgG indicate?

A

Resolved hepatitis A

252
Q

What does hepatitis B surface antigen (HBsAg) indicate?

A

Ongoing infection of any duration

253
Q

What does antibody against hepatitis B surface antigen (anti-HBs) indicate?

A

immunity by past infection or vaccination

254
Q

When is hepatitis B core antibody (anti-HBc) present and what does it indicate?

A

It is present between the disappearance of HBsAg and the appearance of anti-HBs, indicating acute hepatitis

255
Q

What does hepatitis B envelope antigen (HBeAg) indicate?

A

Active infection that is highly contagious

256
Q

What does hepatitis B envelope antigen antibody (anti-HBe) indicate?

A

A lower viral titer

257
Q

What medication regimen will cover hepatitis B and the additional antiretroviral medication that will cover the HIV infection?

A

Tenofovir with either emtricitabine or lamivudine

258
Q

What is the goal of therapy with hepatitis C?

A

Reduction of viral RNA to undetctable at 6 months posttherapy

259
Q

What is the maximum daily dose of acetaminophen in adults?

A

4 g

260
Q

What can be given for acetaminophen toxicity?

A

Acetylcysteine

261
Q

What does spontaneous bacterial peritonitis present with?

A

Fevers, chills, worsening ascites, and abdominal pain

262
Q

What diuretic may be given in cirrhosis?

A

Spironolactone, 100 mg daily

263
Q

How is spontaneous bacterial peritonitis treated?

A

With antibiotics (cefotaxime 2 g IV q 8 hours)

264
Q

Liver abscess is generally caused by what organisms?

A

Entamoeba histolytica or the coliform bacteria

265
Q

Treatment of liver abscess

A

Antibiotics (ampicillin-sulbactam) and percutaneous drainage or surgical excision

266
Q

Benign liver neoplasms include what?

A

Cavernous hemangioma, hepatocellular adenoma, and infantile hemangioendothelioma

267
Q

The liver is a common site of metastasis for other primary cancers, especially which ones?

A

lung and breast cancers.

268
Q

Primary hepatocellular carcinoma is associated with what?

A

hepatitis B, hepatitis C, aflatoxin B1 exposure, and cirrhosis

269
Q

Alpha-fetoprotein may be elevated in what conditions?

A

hepatic carcinoma, chronic hepatitis C, and cirrhosis

270
Q

Should needle biopsy be performed in liver neoplasm?

A

It should not be perfomred if the tumor is resectable for fear of seeding

271
Q

Indirect hernias

A

Most common; passage of intestine through the internal inguinal ring down the inguinal canal, may pass into the scrotum

272
Q

Direct hernias

A

Passage of intestine through external inguinal ring at Hesselbach triangle, rarely enters the scrotum

273
Q

Femoral hernia

A

Least common; passage through femoral ring

274
Q

Ventral hernia occurs when?

A

When there is a weakening in the anterior abdominal wall and may be either incisional or umbilical

275
Q

Esophageal atresia presents in newborns as what?

A

As excessive saliva and choking or cough with attempts to feed

276
Q

What will establish the diagnosis of esophageal atresia?

A

Inability to pass a nasogastric tube

277
Q

Treatment of esophageal atresia

A

Surgical; pulmonary aspiration should be prevented in the interim by suction and withholding of oral feedings

278
Q

Why does a diaphragmatic hernia cause immediate respiratory distress in the newborn?

A

Because the affected lung is compressed by pressure from abdominal contents

279
Q

A diagnosis of a diaphragmatic hernia can be made how?

A

If bowel sounds are heard in the chest

280
Q

Radiography of a diaphragmatic hernia shows what?

A

Loops of bowel in the involved hemithorax, with displacement of the heart and mediastinal structures

281
Q

Treatment of a diaphragmatic hernia

A

Surgical

282
Q

Lab findings in pyloric stenosis

A

U/S will generally demonstrate the lesion (olive-shaped mass) while barium swallow will show delayed emptying and a “string sign”

283
Q

Hirschsprung disease (congenital megacolon) is caused by what?

A

Congenital absence of Meissner and Auerbach autonomic plexuses enervating the bowel wall

284
Q

Symptoms of Hirschsprung disease

A

Constipation or obstipation, vomiting, and failure to thrive

285
Q

Treatment of Hirschsprung disease

A

Surgical resection of the affected bowel

286
Q

Vitamin A sources

A

Liver, fish oils, fortified milk, eggs

287
Q

Vitamin A function(s)

A

Vision, epithelial cell maturity, resistance to infection, antioxidant

288
Q

Vitamin A at-risk groups

A

Elderly, alcoholics, liver disease

289
Q

Vitamin A deficiency

A

Night blindness, dry skin

290
Q

Vitamin A toxicity

A

Skin disorders, hair loss, teratogenicity

291
Q

Vitamin D sources

A

Fortified mild

292
Q

Vitamin D function

A

Calcium regulation, cell differentiation

293
Q

Vitamin D at-risk groups

A

Elderly, shut-ins with low sun exposure

294
Q

Vitamin D deficiency

A

Rickets, osteomalacia

295
Q

Vitamin D toxicity

A

Hypercalcemia, kidney stones, soft-tissue deposits

296
Q

Vitamin E sources

A

Plant oils, wheat germ, asparagus, peanuts, margarine

297
Q

Vitamin E function(s)

A

Retard cell aging, vascular and red cell wall integrity, antioxidant

298
Q

Vitamin E at-risk groups

A

Rare

299
Q

Vitamin E deficiency

A

Hemolytic anemia, degenerative nerve changes

300
Q

Vitamin E toxicity

A

Inhibition of vitamin K, myalgia, HA, weakness

301
Q

Vitamin K sources

A

Liver, green leafy vegetables, broccoli, peas, green beans

302
Q

Vitamin K function(s)

A

clotting

303
Q

Vitamin K at-risk groups

A

Rare

304
Q

Vitamin K deficiency

A

Bleeding

305
Q

Vitamin K toxicity

A

Anemia, jaundice

306
Q

Thiamin sources

A

Pork, grains, dried beans, peas, brewer’s yeast

307
Q

Thiamin function(s)

A

Carbohydrate metabolism, nerve function

308
Q

Thiamin at-risk groups

A

Alcoholism, poverty

309
Q

Thiamin deficiency

A

Beriberi (nervous tingling, poor coordination, edema, weakness, cardiac dysfunction)

310
Q

Thiamin toxicity

A

N/A

311
Q

Riboflavin sources

A

Milk, spinach, liver, grains

312
Q

Riboflavin function(s)

A

Energy

313
Q

Riboflavin at-risk groups

A

N/A

314
Q

Riboflavin deficiency

A

Oral inflammation, eye disorders

315
Q

Riboflavin toxicity

A

N/A

316
Q

Niacin sources

A

Bran, tuna, salmon, chicken, beef, liver, peanuts, grains

317
Q

Niacin function(s)

A

Energy, fat metabolism

318
Q

Niacin at-risk groups

A

Poverty, alcoholism

319
Q

Niacin deficiency

A

Flushing

320
Q

Niacin toxicity

A

N/A

321
Q

Pantothenic acid sources

A

Liver, broccoli, eggs

322
Q

Pantothenic acid function(s)

A

Energy, fat metabolism

323
Q

Pantothenic acid at-risk groups

A

Alcoholism

324
Q

Pantothenic acid deficiency

A

Tingling, fatigue, HA

325
Q

Biotin sources

A

Cheese, eggs, cauliflower, peanut butter, liver

326
Q

Biotin function(s)

A

Glucose production, fat synthesis

327
Q

Biotin at-risk groups

A

Alcoholism

328
Q

Biotin deficiency

A

Dermatitis, tongue pain, anemia, depression

329
Q

Biotin toxicity

A

N/A

330
Q

Vitamin B6 (pyridoxine) sources

A

Animal protein, spinach, broccoli, bananas, salmon

331
Q

Vitamin B6 (pyridoxine) function(s)

A

Protein metabolism, neurotransmitter synthesis, hemoglobin

332
Q

Vitamin B6 (pyridoxine) at-risk groups

A

Adolescents, alcoholism

333
Q

Vitamin B6 (pyridoxine) deficiency

A

HA, anemia, seizures, flaky skin, sore tongue

334
Q

Vitamin B6 (pyridoxine) toxicity

A

Nerve destruction

335
Q

Folate sources

A

Green leafy vegetables, orange juice, grains, organ meats

336
Q

Folate function(s)

A

DNA synthesis

337
Q

Folate at-risk groups

A

Alcoholism, pregnancy

338
Q

Folate deficiency

A

Megaloblastic anemia, sore tongue, diarrhea, mental disorders

339
Q

Folate toxicity

A

N/A

340
Q

Vitamin B12 (cobalamin) sources

A

Animal foods

341
Q

Vitamin B12 (cobalamin) function(s)

A

Folate metabolism, nerve function

342
Q

Vitamin B12 (cobalamin) at-risk groups

A

Elderly, vegans

343
Q

Vitamin B12 (cobalamin) deficiency

A

Megaloblastic anemia, poor nerve function

344
Q

Vitamin B12 (cobalamin) toxicity

A

N/A

345
Q

Vitamin C sources

A

Citrus fruits, strawberries, broccoli, greens

346
Q

Vitamin C function(s)

A

Collagen synthesis, hormone function, neurotransmitter synthesis

347
Q

Vitamin C at-risk groups

A

Alcoholism, elderly men

348
Q

Vitamin C deficiency

A

Scurvy (poor wound healing, petechiae, bleeding gums)

349
Q

Vitamin C toxicity

A

Diarrhea

A Comprehensive Review for the Certification and Recertification Examination for Physician Asistants (8 decks)

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