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GI II > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is upper endoscopy (esophagogastroduodenoscopy) the study of choice for

A

Evaluating persistent heartburn, dysphagia, odynophagia and structural abnormalities detected on barium esophagography

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2
Q

What is video esophagogography (videofluoorscopy) the study of choice to evaluate

A

Uses barium; oropharyngeal dysphagia

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3
Q

What is barium esophagography used to evaluate

A

Esophageal dysphasia *first evaluation is with a Radiographic barium study -> differentiates between mechanical lesions and motility disorders; barium study is more sensitive for detecting subtle esophageal narrowing due to rings, achalasia and proximal esophageal lesions

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4
Q

When do you use esophageal manometry

A

Establish etiology of dysphagia in patients in whom a mechanical obstruction cannot be found *especially if achalasia is suspected

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5
Q

What are the two systems used for esophageal pH recording

A
  • catheter based: long trans nasal catheter connected to a recording device
  • wireless: capsule attached to esophageal mucosa under endoscopic visualization and data transmitted via radiotelemetry to recording device
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6
Q

When do you use pH recording

A

In patients with atypical reflux symptoms or persistent sx despite PPI

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7
Q

What are some neuro differentials for dysphagia

A

Brainstem CVA, ALS, MS, pseudobulbar palsy, post polio, guillain barre, Parkinson’s, Huntington, dementia, tardive dyskinesia

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8
Q

What are some metabolic disorders that can cause dysphagia

A

Thyrotoxicosis, amyloidosis, Cushing, Wilson, med side effects

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9
Q

How does mechanical obstruction present

A

Solid foods worse than liquids

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10
Q

How does schatzki ring present

A

Intermittent dysphagia; not progressive

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11
Q

How does peptic stricture present

A

Chronic heartburn; progressive dysphagia

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12
Q

How does esophageal cancer present

A

Progressive dysphagia; age over 50

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13
Q

How does eosinophilic esophagitis present

A

Young adults; small caliber lumen, proximal stricture, corrugated. Rings, or white papules

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14
Q

How do motility disorders present

A

Solid AND liquids hard to swallow

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15
Q

How does achalasia present

A

Progressive dysphagia

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16
Q

How does diffuse esophageal spasm present

A

Intermittent not progressive; may have chest pain

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17
Q

How does scleroderma present

A

Chronic heartburn, raynaud

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18
Q

What are the sx of oropharyngeal dysphasia vs esophageal dysphasia

A

Oropharyngeal: localized to neck, nasal regurgitation, aspiration, assoc ENT sx
Esophageal: localized to chest or neck; food impaction

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19
Q

What would you use to dx GERD

A

PH testing; *if alarm sx -> EGD

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20
Q

How do you treat GERD

A

If no red flags, acid suppression and lifestyle modifications -> decrease ETOH and caffeine, small low fat meals, bed at an incline, assess psychosocial situation, PPI first line; H pylori eradication if indicated

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21
Q

What are the alarm features for GERD sx.

A

Weight loss, persistent vomiting, constant or severe pain, dysphagia/odynophagia, hematemesis, melena, anemia

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22
Q

What are the atypical or extraesophageal manifestations of GERD

A

Asthma, chronic cough, chronic laryngitis (laryngopharyngeal reflux), sore throat, non-cardiac chest pain, sleep disturbances

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23
Q

What is the treatment of extraesophageal reflux manifestations occur for GERD

A

Twice daily PPI for 2-3 months; improvement of extraesophageal manifestations suggests but does not prove that reflux is cause

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24
Q

What is killians triangle

A

Where zenker occurs

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25
Q

What are the risk factors for Barrett

A

Chronic reflux; truncates obesity independent of GERD

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26
Q

Does Barrett product specific sx

A

No

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27
Q

Do PPIs cause regression of Barrett

A

No but can reduct risk of cancer

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28
Q

When do you do preventative screening for esophageal adenocarcinoma

A

Patients with GERD WITH multiple risk factors (hiatal hernia, obesity, white Rae, male, age over 50)

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29
Q

What is the surveillance of those with Barrett

A

Endoscopy every 3-5 years

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30
Q

What are the sx of peptic stricture

A

Gradual development of solid food dysphagia over months to years; reduction in heartburn b cause stricture acts as a barrier to reflux

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31
Q

How do you dx peptic stricture

A

Endoscopy with biopsy is mandatory in all cases

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32
Q

What is the treatment for peptic stricture

A

Dilation at time of endoscopy; long term therapy with PPI required to decrease risk of stricture recurrence

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33
Q

What are the risks for development of squamous cell carcinoma of the esophagus

A

Smoking, alcohol, achalasia, Plummer Vinson, tylosis, lye ingestion, hot beverages

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34
Q

What are the most commonly implicated causes of pill induced esophagitis

A

NSAIDs, potassium chloride, quinidine, zalcitabine, zidovudine, biphsophate meds (*alendronate and risedronate), emperonium bromide, iron, vit C< and *abx

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35
Q

What can you do to prevent pill induced esophagitis

A

Take pills w/ 4 oz of water and remain upright for 30 min after ingestion; known offending agents should not be given to ppl with esophageal dysmotility, dysphagia or strictures

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36
Q

What are the risk factors for candida esophagitis

A

Diabetes, systemic corticosteroids, radiation, systemic abx

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37
Q

Which infection of the esophagus can infect normal hosts

A

HSV

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38
Q

How do you treat CMV esophagitis

A

Ganciclovir; side effect: neutropenia

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39
Q

How do you treat candida esophagitis

A

Systemic fluconazole

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40
Q

What should you look at first if someone has just ingested toxins (caustic esophageal injuries)

A

Circulatory status and assessment of airways and oropharyngeal mucosa (laryngoscopy); chest and ab radiographs to look for pneumonitis or free perforation

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41
Q

What is the treatment for caustic esophageal injury

A

ICU; initial: supportive with IVF, IV PPI to prevent gastric stress ulceration and analgesics; nasogastric lovage and oral antidotes are dangerous and should NOT*** be given; laryngoscopy should be performed in pts with ARDS to assess need for trach; endoscopy within first 24 hours; if signs of severe injury -> NPO, nasogastric feeding tube, oral feeding after 2-3 days, *no oral corticosteroids or abs; esophageal strictures occur in many with severe injury; warrants endoscopic surveillance 15-20 yrs after incidence for evaluation of SCC

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42
Q

Who is eosinophilic esophagitis more common in

A

Men

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43
Q

How do you dx eosinophilic esophagitis

A

Barium swallow: will show multiple concentric rings

  • trial of PPI for 2 months to exclude GERD
  • endoscopy with esophageal bx required for dx
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44
Q

What does eosinophilic esophagitis look like

A

White exudates or papules, red furrow,s corrugated concentric rings and strictures

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45
Q

What are the risk factors for esopageal webs

A

Congenital, Plummer Vinson, eosinophilic esophagitis, graft vs host, pemphigoid, epidermolysis bullosa, pemphigus vulgaris

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46
Q

What is used for dx of esophageal webs and rings

A

Barium esophagography

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47
Q

What are esophageal rings usually associated with

A

Hiatal hernia

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48
Q

What is used to dx zenker

A

Video esophagography

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49
Q

What is kollonychia

A

Spoon nails

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50
Q

What is feline esophagus a feature of

A

Eosinophilic esophagitis

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51
Q

What are the risks of bleeding of esophageal varices

A

Size, presence of red wale markings (dilated longitudinal vessels on variceal surface), severity of liver dz, active alcohol abuse

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52
Q

What is the treatment for esophageal variceal bleeding

A

Fresh frozen plasma or platelets, vitamin K IV; abx prophylaxis (increased risk of gram neg infection) *fluoroquinolones or 3rd gen cephalosporins preferred; somatostatin and octreotide to reduce portal HTN and lactulose for encephalopathy

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53
Q

What is the goal of beta blocker therapy to prevent variceal bleeding

A

HR falls by 25% or reaches 55-60 bpm; as long as systolic BP >90 and no side effects

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54
Q

What is balloon tube tamponade

A

Used for esophageal varices; complications: esoph and oral ulceration, perforation, aspiration and airway obstruction; used for temporizing measure only in patients with bleeding that cannot be controlled until TIPS procedure can be provided

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55
Q

What is TIPS procedure

A

Transvenous intrahepatic portosystemic shunts; wire passed through jugular v and mesh stent is passed through liver parenchyma creating portosystemic shunt from portal to hepatic v; can control acute hem but has increased risk of encephalopathy; lowers risk of rebleeding but does not decrease mortality *reserved for ppl with 2 or more episodes of bleeding that have failed other therapies

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56
Q

What is required for the dx of achalasia

A

Barium esophagography followed by EGD to evaluate distal esophagus to exude distal stricture or carcinoma; esophageal manometry confirms dx

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57
Q

What is the tx for achalasia

A

Botulinum toxin injection, pneumatic dilation, surgery; all rx once daily PPI

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58
Q

What is nutcracker esophagus

A

Hypertensive peristalsis; LES relaxes normally but elevated pressure at baseline; dysphasia to solid and liquids; intermittent; dx via manometry and video fluoroscopy

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59
Q

What is diffuse esophageal spasm

A

Uncoordinated esophageal contraction; corkscrew esophagus, rosary bead esophagus on barium x ray; LES is normal; dysphasia to solids and liquids, intermittent; dx via manometry, EGD, barium swallow

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60
Q

How do you confirm esophageal perforation

A

Contrast swallow usually gastrografin followed by thin barium

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61
Q

How do you treat esophageal perforation

A

NGT suction, NPO, parenteral abx and surgery

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62
Q

What are the signs of pneumomediastinum

A
  • subcutaneous emphysema in neck or precordial area
  • hammans sign: crunching rasping sound heard over precordium mainly during systole and in L lateral decubitus position
  • dyspnea * do not measure peak exploratory flow rate because can exacerbate sx -> use pulse oximetry
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63
Q

What are the causes of gastroparesis

A

DM, postviral, postvagotomy

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64
Q

What are the causes of hemorrhagic gastritis

A
  • aspirin
  • stress ulcers
  • alcoholic, portal HTN gastropathy
  • uncommon causes; ischemia, ingestion of damaging agent, radiation
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65
Q

What are the risk factors for stress gastritis

A

-mechanical ventilation, coagulopathy, trauma, surgery, burns, shock, sepsis, CNS injury, liver failure, kidney dz, multiorgan failure

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66
Q

What reduces the risk of stress related bleeding

A

Enteral nutrition

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67
Q

What reduces the incidence of stress ulcer

A

PPI or H2 blocker

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68
Q

What is the most common clinical manifestation of erosive gastritis

A

Upper GI bleeding; presents as hematemesis, coffee ground emesis or bloody aspirate in patient receiving nasogastric suction, or melena

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69
Q

How do you dx erosive gastritis

A

Upper endoscopy -> no significant inflammation on histo

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70
Q

How do you prevent stress ulcers in critically ill patients

A

Hourly oral administration of liquid antacids, sucralfate or IV PPI

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71
Q

What is Type A gastritis

A

FUNDIC type; body-predominant and less common form; asymptomatic; common in elderly; AI mech assoc with achlorhydria, pernicious anemia and increased risk of gastric cancer *autoimmune gastritis

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72
Q

What is type B gastritis

A

Antral type (h pylori); infection early in life or in setting of malnutrition or low gastric acid output is associated with gastritis of entire stomach and increased risk of gastric CA

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73
Q

What part of the stomach does menetrier dz affect

A

Body

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74
Q

What is anasarca

A

Generalized edema

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75
Q

What can be used to treat menetrier dz

A

Cetuximab (ab to EGFR)

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76
Q

What ages are duodenal vs stomach ulcers more prominent

A

Duodenal: 30-55
Gastric: 55-70

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77
Q

What are descriptions used for epigastric pain caused by PUD

A

Gnawing, dull, aching, hunger like ; many experience periodicity (periods with no symptoms)

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78
Q

Does nasogastric lavage negative for blood exclude active bleeding from duodenal ulcer

A

No

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79
Q

Where does h pylori infect to cause duodenal vs gastric ulcers

A

Duodenal: gastric antrum
Gastric: gastric body (decreases acid)

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80
Q

What do you do after eradicating H pylori

A

If ulcer is large or complicated, continue tx with PPI q day for 4-6 wks

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81
Q

When do you confirm eradication of h pylori

A

At least 4 wks after completion of abx thx and 1-2 wks after PPI thx

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82
Q

When are the risk of NSAID complications greater

A

People over 60, people with previous ulcer, ppl who take NSAIDs + aspirin, corticosteroids, or anticoagulants; within first 3 months of therapy

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83
Q

What are other causes of PUD

A

Smoking, hypercalcemia, mast oxytocin’s, blood group O (antigens bind h pylori), corticosteroids, alcohol

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84
Q

What is the most sensitive and specific test for h pylori

A

Stool antigen; urea breath test (false negative with recent therapy)

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85
Q

What do you test for on histo when testing for h pylori

A

Warthin silver stain or rapid CLO (clofaximine test); false negative with recent PPI, abx, or bismuth compounds

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86
Q

Is serology helpful to show eradication of h pylori

A

No; shows IgA abs (takes months to go away)

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87
Q

What does leukocytosis suggest in the setting of PUD

A

Penetration or perforation

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88
Q

Why may the BUN rise in PUD

A

Absorption of nitrogen from small intestine and presently azotemia

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89
Q

What is the treatment for active GIB

A

Continuous infusion of PPI IV starting with a bonus; once stable needs EGD

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90
Q

What is dumping syndrome

A

Rapid gastric emptying, abdominal distress and postprandial vasomotor sx as a result of gastric surgery for PUD

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91
Q

What is bezoar

A

Small mass of undigested material that accumulates in Gi tract

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92
Q

What ddx should you consider for upper GIB

A

PUD, erosive gastritis, AV malformation, Mallory Weiss tear, esophageal varices

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93
Q

What ddx should you consider for epigastric pain (dyspepsia)

A

PUD (severe is uncommon unless perforated), functional dyspepsia (no organic explanation), typical GERD, gastric cancer, food poisoning, viral gastroenteritis, biliary tract dz,

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94
Q

What complications do COX-2 inhibitors cause

A

CV complications; decreases vascular prostacyclin; Celebrex is equal risk to NSAIDs (usually greater risk)

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95
Q

What are the clinical features of duodenal vs gastric ulcers

A

Duodenal: pain 1-3 hours after meals; often nocturnal; relieved by food
Gastric: made worse by food (within 30 min of eating); N/anorexia, food aversion, rarely weight loss

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96
Q

What is important in the dx of GASTRIC ulcer

A

*exclude malignancy

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97
Q

What is the treatment for both duodenal and gastric ulcers

A

Eradicate h pylor, PPI or H2 blocker for 4-6wks (duodenal) or 6-8 wks (gastric)

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98
Q

What kind of ulcers have a risk factor of smoking

A

Gastric

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99
Q

What diet factors are risks for gastric adenocarcinoma

A

Smoked meats and fish, pickled vegetables, nitrosamines, benzpyrene, reduced intake of fruits and veggies

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100
Q

Which blood type is assoc with higher risk of gastric adenocarcinoma

A

A

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101
Q

When should you consider ZE

A

When ulcer dz is refractory to therapy, ulcers in weird places, assoc with diarrhea (NG tube can fix this), steatorrhea, weight loss

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102
Q

What is MEN 1

A

Gastrinoma, hyperparathyroidism (increased calcium) and pituitary neoplasm

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103
Q

What is the confirmatory test for diagnosis of ZE

A

Gastrin > 1000 ng/L drawn fasting and on acid suppression meds; secretin stimulation test is positive

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104
Q

What is the most sensitive test for detecting primary tumors and Mets of ZE

A

Radiolabeled octreotide scanning; somatostatin receptor scintigraphy with single photon emission CT allows total body imaging for detection of primary gastrinomas

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105
Q

What should you do in all patients with ZE

A

Draw: serum PTH, prolactin, LH and FSH, and GH to exclude MEN 1

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106
Q

How do you treat patients with MEN 1

A

Treat hyperparathryoidism first (may improve hypergastrinemia); for unresectable tumors -> parietal cell vagotomy; chemo

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107
Q

What is the inheritance pattern of MEN 1

A

AD

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108
Q

What imaging do you do for gastroparesis

A

Gastric scintigraphy with low fat solid meal; assesses gastric emptying; gastric retention of 60% after 2 hrs or more than 10% after 4 hrs is abnormal

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109
Q

How do you treat gastroparesis

A

No specific therapy; for acute exacerbation -> NG suction and IV fluid; eat small frequent meals low in fiber, milk, gas forming foods and fat; avoid opioids and anticholinergic; *in DM maintain glucose below 200 mg/dL (can cause gastroparesis even without neuropathy); metoclopramide and erythromycin beneficial (meto -> tardive dyskinesia)

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110
Q

What are the true liver function tests

A

PT/INR, albumin, cholesterol

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111
Q

What can cause severe (vs mild) elevations of aminotransferases

A

Acute viral hep, medications, ischemic hep, autoimmune hep, Wilson, acute bile duct obstruction, acute budd chiari syndrome, hepatic artery ligation

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112
Q

What are some nonhepatic causes of aminotransferase elevation

A

Strenuous exercise, hemolysis, myopathy, thyroid dz, macro-AST

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113
Q

What are nonhepatic sources of AST

A

Skeletal m, cardiac m, RBCs

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114
Q

What are nonhepatic sources for ALT

A

Skeletal m, cardiac m, kidneys

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115
Q

What are nonhepatic sources for LDH

A

Heart, RBC

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116
Q

What are nonhepatic sources for alk phosphatase

A

Bone, first trimester placenta, kidneys, intestines

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117
Q

What can cause drug induced cholestasis

A
  • non-inflammatory: anabolic steroids, azathiprine, cyclosporine, diclofenac, estrogens, Indinavir, tamoxifen
  • inflammatory: amoxicillin-clavulanic acid, azathriprine, azithromycin, celecoxib, cephalosporins, erythromycin, penicillamine
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118
Q

What would be in your ddx for someone who is immunocompromised with acute hep

A

CMV, EBV, HSV

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119
Q

What is the prodrome of hep A

A

Anorexia, N/V, malaise, aversion to smoking

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120
Q

What does IgG anti-HAV in absence of IgM anti-HAV indicate

A

Previous exposure to HAV, non-infectious and immunity

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121
Q

What is the prodrome of Hep B

A

N/V, anorexia, malaise, aversion to smoking

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122
Q

What can HBV be associated with

A

Glomerulonephritis, serum sickness, polyarteritis nodosa

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123
Q

Is cholestasis a feature of Hep A or B

A

A *elevated alk and bilirubin

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124
Q

What do you give to someone who has been exposed to HBV

A

Hep B immune globulin (hbig) 14 days after exposure plus the vaccine

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125
Q

What is detected during the window period for HBV

A

Anti-HBc

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126
Q

What is detected during acute infxn of HBV

A

HBsAg, anti-HBc, HBeAg, HBV DNA

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127
Q

What is detected in someone who was previously infected with HBV

A

Anti-HBs, Anti-HBc (IgG only)

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128
Q

What indicates a chronic infxn of HBV

A

HBsAg, anti-HBc (IgM and IgG), HBeAg, HBV DNA

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129
Q

What does someone who is immune to HBV have

A

Anti-HBs

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130
Q

Besides pregnant women, who has an increased chance of progressing to chronic HEV infection

A

Transplant patients treated with tacrolimus

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131
Q

What does anti-HCV without HCV RNA indicate

A

Recovery; rare

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132
Q

What vaccinations should be given to someone with chronic liver dz

A

HAV and HBV

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133
Q

What are complications of HCV

A

HCC, cirrhosis, mixed cryoglobulinemia and membranoproliferative glomerulonephritis, lichen planus, AI thyroiditis, lymphocytic sialadenitis, idiopathic pulm fibrosis, sporadic porphyria cutanea , monoclonal gammopathies ; increased risk of non-Hodgkin lymphoma

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134
Q

What does chronic HCV do to cholesterol

A

Decreases serum level

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135
Q

What is the histo classification of chronic hep

A

Grade: histo assessment of necrosis and inflammation activity
Stage: level of dz progression; based on degree of fibrosis

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136
Q

What are the extrahepatic manifestations of HBV

A

Urticaria, arthritis, polyarteritis nodosa vascuitis, polyneuropathy, glomerulonephritis

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137
Q

What are the extrahepatic manifestations of HCV

A

Mixed cryooblobulinemia, porphyria cutanea tarda, membranoproliferative glommerulonephritis, lymphocytic sialadenitis

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138
Q

What test can ID presence or absence of fibrosis in chronic hep

A

Serum fibrosure or US elastography

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139
Q

What are idiosyncratic drugs

A

Variable doses and time of onset for drug induced hep; eg: isoniazid, halothane, phenytoin, methyldopa, carbamazepine, diclofenac, sulfonamides

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140
Q

What do you do for acetominophen OD

A

Sulfhydryl compounds (N-acetylcysteine) within 8 hrs; measure levels and plot on rumak Matthew chart

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141
Q

What is fulminant hep

A

Massive hep necrosis with impaired consciousness occurring within 8 wks of onset

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142
Q

What is the treatment for fulminant hep

A

Supportive: maintain fluid balance, support circulation and resp, control bleeding, restrict protein intake, oral lactulose or neomycin administered; prophylactic abx *one factor that improves survival; liver transplant

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143
Q

What is maddrey’s discriminating function

A

Calculates PT and serum bilirubin; values >32 poor prognosis for alcoholic liver dz

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144
Q

What is Glasgow alcoholic hep score

A

Predicts mortality based on age, serum bilirubin, BUN, prothrombin time, and peripheral WBC count; >9 who receive glucocorticoids have higher survival rates

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145
Q

How do you treat alcoholic hepatitis

A

Low protein diet, daily multivitamin, thiamine, folic acid, zinc, glucose administration increases thiamine requirement and can precipitate korsakoff if thiamine not coadministered, if severe -> corticosteroids; pentoxifylline improves survival (decreases chance of hepatorenal syndrome)

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146
Q

What are ppl with metabolic syndrome at risk fo

A

CV dz, kidney dz, and colorectal cancer

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147
Q

People with what condition are at increased risk for NAFLD

A

Psoriasis

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148
Q

What protects against NAFLD

A

Coffee and physical activity v

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149
Q

What imaging would you do for NAFLD

A

US, CT or MRI to see microvascular steatosis

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150
Q

People with PBC may have a history of _____-

A

UTI, smoking, use of hormone replacement therapy, hair dye

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151
Q

What dz are associated with PBC

A

Sjogren, collagen vascular z, thyroiditis, glomerulonephritis, pernicious anemia, renal tubular acidosis

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152
Q

What is cholestyramine used for

A

Itching

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153
Q

What abs are present for type I AI hep

A

Anti smooth muscle and antinuclear

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154
Q

What are the extrahepatic manifestations of autoimmune hep

A

Rash, arthralgias, keratoconjunctivitis sicca, thyroiditis, hemolytic anemia, nephritis, UC

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155
Q

What is the tx for autoimmune hep

A

Glucocorticoids, azathioprine, monitor liver functions

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156
Q

What infections are people with hemochromatosis at increased risk for

A

Vibrio vulnificus, listeria, yersinia and siderophilic organisms

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157
Q

What imaging would you do for hemochromatosis

A

MRI to assess degree of fibrosis and hepatic iron stores

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158
Q

When would you do a live bx for someone with hemochromatosis

A

If homozygous; dont do if serum ferritin less than 1000 and ast is Normal

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159
Q

What food should you avoid if you have hemochromatosis

A

Red meat, alcohol, vitamin C, raw shellfish and supplemental iron

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160
Q

What is the tx for hemochromatosis

A

Weekly phlebotomy until deplete iron stores, then maintain with phlebotomy every 2-4 months; PPI to reduce iron absorption; chelating agent deferoxamine for pts with anemia or secondary iron overload that cannot tolerate phlebotomies

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161
Q

What is hepatolenticualr degeneration

A

Wilson

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162
Q

When should you consider Wilson’s

A

In any child or young adults with hep, splenomegaly with hypersplenism, negative Coombs test for hemolytic anemia, portal HTN and neuro abnormalities

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163
Q

What conditions are associated with Wilson

A

Renal calculi, aminoaciduria, renal tubular acidosis, hypoparathyroidism, infertility, hemolytic anemia, subcutaneous lipomas

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164
Q

What would you see on imaging for hepatic vein obstruction (budd chiari)

A

Prominent caudate liver lobe *screening test of choice is contrast enhanced CEUS; can use color or pulsed Doppler US; MRI will show obstructed vessels; direct venom rapid will show cavalry webs and occluded veins (spider web pattern)

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165
Q

What lobes do people with antitrypsin deficiency have emphysema in

A

Lower lobes (smokers are upper)

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166
Q

What can protect against ischemic hep

A

Statin

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167
Q

What is the hallmark of ischemic hep

A

Elevation of aminotransferases often greater than 5000 units/L

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168
Q

What is hepatojugular reflux

A

When you press on the liver, causes jugular distention; seen in right sided heart failure

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169
Q

What are the causes of noncirrhotic portal HTN

A

Portal v thrombosis, splenic v obstruction, schisto

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170
Q

How does splenic v obstruction present

A

Gastric varices without esophageal varices

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171
Q

What imaging should you use for noncirrhotic causes of portal HTN

A

Color Doppler US and contrast CT

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172
Q

What is the treatment for splenic v thrombosis

A

Splenectomy

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173
Q

What is charcot’s triad

A

Fever, RUQ pain, jaundice

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174
Q

What risk is pyogenic liver abscess associated with

A

GI malignancy

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175
Q

What is the most common cause of hepatic abscess in the US

A

Ascending cholangitis

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176
Q

What are the most frequently identified organisms causing hepatic abscesses

A

E. coli, klebsiella pneumoniae, proteus vulgaris, enterobacter aerogenes, strep angiosus (microaerophilic and anaerobic species)

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177
Q

What imaging would you use for a pyogenic liver abscess

A
  • Chest radiograph show elevation of diaphragm if in right lobe
  • US, CT, MRI can show intrahepatic lesions
  • MRI: characteristic finding is high signal intensity on T2-weighted image
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178
Q

What causes cavernous hemangioma to enlarge

A

Women taking hormonal therapy

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179
Q

Is focal nodular hyperplasia a true neoplasm

A

No; proliferation of hepatocytes in response to altered blood flow; stain for glutamine syntahse

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180
Q

What is the difference between focal nodular hyperplasia and hepatocellular adenoma

A

Hepatocellular adenoma is hypovascular and focal nodular hyperplasia is hypervascular

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181
Q

How can you distinguish focal nodular hyperplasia from hepatocellular adnoma

A

Arterial phase helical Ct and multiphase dynamic MRI with contrast

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182
Q

What is the treatment for focal nodular hyperplasia

A

Affected women undergo annual us for 2-3 yrs

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183
Q

What lab findings would you see with cirrhosis

A

CBC: anemia (microcytic, macrocytic or hemolytic); pancytopenia - Low wbc, platelets and hb
Prolonged Pt
-Chemistry: hyponatremia, hypokalemic alkalosis, glucose disturbances, hypoalbuminemia

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184
Q

Consumption of what reduces the risk of cirrhosis

A

Coffee and tea

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185
Q

What is cardiac cirrhosis

A

Caused by constrictive pericarditis or heart failure

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186
Q

What do you order for the child Pugh scoring system

A

CMP or hepatic function panel (bilirubin, albumin, PT/INR); PE for ascites and encephalopathy

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187
Q

What pressure is increased with portal HTN

A

Hydrostatic

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188
Q

When do you give beta blockers to patients with varices

A

Large; small if have variceal red wale marks and advanced cirrhosis (B or C)

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189
Q

Do varices themselves cause any sx

A

No

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190
Q

If you need to do an emergent endoscopy on someone with active variceal bleeding, what must you also do

A

Endotracheal intubation

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191
Q

What are Minnesota and sengstaken-blakemore tubes?

A

Balloon tamponade used for esophageal varices; provides control of hemorrhage

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192
Q

What are complications of balloon tamponade

A

Esophageal and oral ulceration, perforation, aspiration and airway obstruction

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193
Q

What are the stages of encephalopathy

A

Mild confusion, drowsiness, stupor and coma

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194
Q

What test is used to detect hepatic encephalopathy

A

EncephalApp or stroop test

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195
Q

Do serum ammonia levels tell you the progression of encephalopathy

A

No

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196
Q

What are precipitants of hepatic encephalopathy

A

Gi bleed, azotemia, consolation, high protein meal, hypokalemic alkalosis, CNS depressants, hypoxia, hypercarbia, sepsis

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197
Q

What is the treatment for hepatic encephalopathy

A

Lactulose (nonabsorbable disaccharide) results in colonic acidification and diarrhea -> goal to produce 2-3 stools per day; poorly absorbed abx used if cant tolerate lactulose

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198
Q

When should tuberculous peritonitis be considered

A

In immigrants, immunocompromised, or severely malnourished

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199
Q

What is the test of choice for establishing a dx of ascites

A

Ab ultrasound

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200
Q

When is abdominal paracentesis performed

A

All patients with new onset ascites or when patients with known ascites deteriorate clinically to exclude spontaneous bacterial peritonitis

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201
Q

What do you always test ascitic fluid for

A

Cell count (WBC w/ diff), albumin and total protein, culture and gram stain

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202
Q

What is suggestive of spontaneous bacterial peritonitis

A

PMN count of greater than 250/mcL (neutrocytic ascites)

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203
Q

What is the best single test for classification of ascites

A

Serum ascites albumin gradient (SAAG)

  • portal HTN (SAAG of 1.1 or more)
  • nonportal HTN (SAAG of less than 1.1)
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204
Q

How do you calculate SAAG

A

Subtracting ascitic fluid albumin from serum albumin

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205
Q

What are optional tests of ascitic fluid

A

Amylase (pancreatic ascites; perforation of GI tract), bilirubin (perforation of biliary tree), creatinine (leakage of urine), cytology (for carcinomatosis), adenosine delaminates (tuberculous)

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206
Q

What causes of ascites would fall under an SAAG for >1.1

A

Hepatic congestion (heart failure, tricuspid insufficiency, budd chiari, Veno occlusive dz), liver dz, portal v occlusion, myxedema

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207
Q

What causes of ascites would fall under SAAG <1.1

A

Hypoalbuminemia (nephrotic syndrome, protein losing enteropathy, severe malnutrition with anasarca), chylous ascites, pancreatic, bile, nephrogenic, urine, ovarian dz, infections, malignant conditions, familial Mediterranean fever, Vasculitis, granulomatous peritonitis, eosinophilic peritonitis

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208
Q

What are the most common pathogens that cause spontaneous bacterial peritonitis

A

Gram negative (e coli, klebsiella), gram positive bacteria (strep pneumoniae and viridans, enterococcus) ***no anaerobic

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209
Q

What are the sx of spontaneous bacterial peritonitis

A

Fever and ab pain; can present with change in mental status, worsening of renal fxn

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210
Q

What must you distinguish spontaneous bacterial peritonitis from

A

Secondary bacterial peritonitis (from other source like appendicitis) **presence of multiple organisms on ascitis fluid gram stain is diagnostic of secondary

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211
Q

How do you prevent spontaneous bacterial peritonitis

A

Oral once daily norfloxacin, ciprofloxacin or trimethoprim sulfamethoxazole

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212
Q

How do you treat spontaneous bacterial peritonitis

A

Third gen cephalosporins or combination of beta lactam/beta lactamase agent (ampicillin/sulbactam); DO NOT use aminoglycosides (b/c renal failure); IV albumin to reduce risk of kidney failure

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213
Q

How do you treat secondary bacterial peritonitis

A

Broad spectrum coverage

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214
Q

How do you treat recurrent spontaneous bacterial peritonitis

A

Liver transplant

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215
Q

What causes carinomatosis

A

Adenocarcinoma of the ovary, uterus, pancreas, stomach, colon, lung

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216
Q

Do malignant ascites respond to diuretics

A

No

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217
Q

What is familial Mediterranean fever

A

AR; lack protease in serosal fluids; present before age 20; episodic bouts of acute peritontisis associated with serositis of joints and pleura *attacks resolve in 24-48 hrs without treatment; colchicine reduces severity of attacks; main COD -> amyloidosis with renal or hep involvement

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218
Q

What will chest radiograph reveal in half of patients with mesothelioma

A

Pulmonary asbestosis

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219
Q

What does the ascitic fluid look like in primary mesothelioma

A

Hemorrhagic; cytology negative; ab CT reveals sheet like masses

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220
Q

How is dx of mesothelioma made

A

Laparotomy or laparoscopy; prognosis is extremely poor

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221
Q

What is chylous ascites

A

Accumulation of lipid rich lymph; milky appearance; triglyceride level greater than 1000 mg/dL; usual cause is lymph obstruction or leakage by malignancy (lymphoma)

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222
Q

What does pancreatic ascites look like

A

High protein level; amylase in excess

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223
Q

What does paracentesis of bile ascites show

A

Yellow fluid; bilirubin: serum bilirubin > 1

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224
Q

Which vaccine should people with cirrhosis receive

A

HAV, HBV, pneumococcal, and yearly influenza

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225
Q

Which drugs are contraindicated in people with cirrhosis

A

NSAIDs, angiotensin-converting enzyme inhibitors, angiotensin II. Antagonists

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226
Q

What do you need to monitor in someone on spironolactone

A

Hyperkalemia

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227
Q

What is associated with mortality after TIPS

A

Chronic kidney dz, diastolic cardiac dysfunction, refractory encephalopathy, hyperbilirubinemia

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228
Q

What are the complications of TIPS

A

Hepatic encephalopathy, infection, shunt stenosis, shunt occlusion

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229
Q

What is the difference between fulminant and subfulminant hepatic failure

A

Fulminant: encephalopathy and coagulopathy within 8 wks
Sub: later

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230
Q

How is liver transplant prioritization established

A

MELD score

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231
Q

What do you order for a MELD score

A

CMP (bilirubin and creatinine) and PT/INR; measures mortality risk in patients with ESLD; *MELD score > 14 required for liver transplant listing

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232
Q

What are clinical predictors of re-bleeding and death in a GI emergency

A

Age > 60, comborbid illnesses, systoli BP <90, HR >90 and bright red blood in NG aspirate or rectal exam

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233
Q

What are the signs of shock

A

Hypotension, tachycardia, oliguria (decreased urine output), altered mental status, tachypnea (>24 breaths/min), met acidosis, elevated lactate

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234
Q

How do you stabilize someone in shock

A

2 large bore (18 gauge or larger) IV lines; give NS or lactated ringers

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235
Q

What does octreotide do

A

Reduces splanchnic blood flow and portal BP; effective in initial control of bleeding related to portal HTN; administered to all patients with active upper GIB and evidence of over dz or portal HTN

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236
Q

What should be considered if hypotension presents early with ab pain

A

Ruptured AAA, mesenteric infarction, acute pancreatitis

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237
Q

Where does ulcer penetration occur

A

Posterior wall -> penetrates into other structures; pain radiates to back and is unresponsive to antacids; treat with PPI and monitored; if no improvement -> surgery

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238
Q

What is gastric outlet obstruction

A

More commonly caused by gastric neoplasms -> obstructs pylorus; upper endoscopy performed

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239
Q

What should be in your ddx from someone under 50 with lower GIB

A

Infectious colitis, anorectal dz, IBD; younger than 40 -> neoplasms , crohn, celiac and meckel

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240
Q

What is the most common cause of lower tract bleeding

A

Diverticulosis; painless

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241
Q

What should be included in your ddx of someone over 50 with lower GIB

A

Diverticulosis, angiectasias, malignancy, ischemia

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242
Q

Who are angectasias more common in

A

Over 70 with chronic renal failure

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243
Q

What do maroon stools imply

A

Lesion in right colon or small intestine

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244
Q

What do black tarry stools suggest

A

Source proximal to lig of treitz

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245
Q

What does bloody diarrhea with cramping suggest

A

IBD, infectious colitis or ischemic colitis

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246
Q

What is a therapeutic colonoscopy for lower bleed

A

Epi injection, cautery, or application of metallic clips or bands

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247
Q

How do you treat hemorrhage from diverticulosis

A

Self limited

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248
Q

What are the characteristics of acute mesenteric ischemia

A

Periumbilical pain out of proportion to tenderness; writhing in pain but PE unremarkable; food fear; N/V/distention; ab x-ray shows air fluid levels, thumb-printing (submucosal edema) *CT angiography study of choice; anticoagulation for mesenteric venous thrombosis but not arterial

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249
Q

What does ischemic colitis imaging show

A

Ab X-ray shows colonic dilation and thumb printing

Sigmoidoscopy shows submucosal hemorrhage, friability, ulceration

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250
Q

What is anoscopic exam used to visualize

A

Hemorrhoids

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251
Q

What should be performed in ALL patients with hematochezia

A

Proctosigmoidoscopy or colonoscopy

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252
Q

How do you treat the pain of hemorrhoids

A

Stool softeners, sitz baths, witch hazel and analgesics

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253
Q

What are characteristics of anal fissures

A

Due to straining or trauma; tearing pain during defecation followed by throbbing discomfort that can lead to constipation due to fear of recurrent pain; confirmed by looking at anal verge (look like cracks in epithelium); chronic results in fibrosis and development of skin tag

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254
Q

What are treatments for anal fissures

A

Relaxation of anal canal with nitroglycerin ointment or botulinum toxin; surgical if very severe: internal anal sphincterotomy

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255
Q

How is occult GIB detected

A

Positive fecal occult blood test, fecal immunochemical test (FIT) or by iron deficiency anemia in absence of visible blood loss

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256
Q

What should patients with iron deficiency anemia be evaluated for

A

Celiac dz

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257
Q

What is the most useful diagnostic tool for dx of meckel’s

A

Technetium-99m scan

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258
Q

What are some causes of toxic megacolon

A

UC, C diff, Ogilvie syndrome

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259
Q

What are the atypical presentations of appendicitis

A
  • retrocecal: less intense and poorly localized pain; Psoas positive
  • pelvic: pain in lower ab with urge to urinate or dedicate; ab tenderness absent; obturator sign present
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260
Q

What imaging is used to dx appendicitis

A

Ultrasound and CT

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261
Q

What is appendectomy before age 21 protective for

A

UC

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262
Q

How do you treat intestinal obstruction

A

NG tube decompression and fluid resuscitation; urgent laparotomy for lysis of adhesions must be performed before bowel ischemia develops

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263
Q

What is acute paralytic ileus

A

Neurogenic failure or loss of peristalsis in intestine in the absence of any mechanical obstruction

264
Q

How is postoperative ileus reduced

A

Use of epidural analgesia, avoidance of IV opioids, early ambulation, gum chewing, and initiation of a clear liquid diet

265
Q

What is ogilvie syndrome

A

Acute colonic pseudo obstruction; arises in post op state or with severe medical illness; minimal pain and tenderness, severe ab distention; massive dilation of cecum or right colon

266
Q

What is reynod’s pentad

A

Charcots triad plus hypotension and confusion -> can result from acute suppurative cholangitis

267
Q

What do you use to monitor AAA

A

US

268
Q

What are risk factors for ectopic pregnancy

A

PID, infertility, ruptured appendix, prior tubal surgery

269
Q

Where do most ovarian torsions occur

A

Right side because increased length of utero-ovarian ligament on the right

270
Q

What are the risk factors for ovarian torsion

A

Pregnancy due to enlarged corpus luteum, presence of large ovarian cysts, chemical induction of ovulation, tubal ligation

271
Q

What is the presentation of ovarian torsion

A

Unilateral lower ab pain upon exertion

272
Q

Is the testicle of neonates with prenatal torsion salvageable

A

No

273
Q

What imaging is used to dx scrotal torsion

A

Doppler US

274
Q

Which ethnicities are IBD more prevalent in

A

Jewish then non-Jewish whites

275
Q

What are the extraintestinal manifestations of IBD

A

Peripheral arthritis, erythema nodosum, aphthous ulcers, pyoderma gangrenosum, conjunctivitis, fatty liver, PSC, thromboembolic events (DVT), nephrolithiasis with irate or calcium oxalate stones

276
Q

How do you distinguish between UC and infectious enterocolitis

A

Stool studies and biopsy

277
Q

Do erythema nodosum and pyoderma gangrenosum occur more commonly with UC or CD

A

UC

278
Q

How do you decrease the risk of colon CA with UC

A

Long term 5 ASA therapy and ingestion of folic acid

279
Q

Is hypokalemia seen in UC or CD

A

UC

280
Q

Would you see hypoalbuminemia in UC or CD

A

CD

281
Q

What lab findings would you see in both CD and UC

A

Anemia, leukocytosis, increased sedimentation rate and CRP level; fecal calprotein levesl increased

282
Q

What dx studies should b e used for UC

A

Sigmoidoscopy study of choice; do not do colonoscopy in ppl with bad UC; plan X ray to assess colonic dilation; *lead pipe -. Loss of haustra

283
Q

What is Prometheus IBD serology 7

A

Used when cannot decide if UC or CD: includes abs to pANCA, abs to saccharomyes cerevisiae,

284
Q

How do you dx and treat an abscess caused by crohns

A

Emergent CT; broad spectrum abx; drainage usually required

285
Q

How do you treat intestinal obstruction caused by CD

A

IV fluids with nasogastric suction; placed on low-roughage diet (no raw fruits or veggies, popcorn, nuts)

286
Q

What is the best noninvasive study for evaluating perianal fistula

A

Pelvic MRI

287
Q

What is the treatment for perianal lesions

A

Oral abx (metronidzole or ciprofloxacin)

288
Q

What is recommended in patients who have had 100 cm or more of their terminal ileum resected due to crohns

A

Low fat diet bc fat malabsorption; parenteral vit B 12

289
Q

When do you give bile salt binding agents (cholestyramine or colesevelam)

A

Patients with crohns with involvement of terminal ileum -> prevents secretory diarrhea; NOT in patients with extensive ileal dz

290
Q

How do oxalate kidney stones develop in crohns

A

Unabsorbed fA bind with calcium, decreasing its absorption and increasing the absorption of oxalate therefore give calcium supplements

291
Q

What are the adverse effects of glucocorticoids

A

Mood changes, insomnia, buffalo hump, weight gain (striae), edema, increased glucose, acne and moon fancies

292
Q

What are the long term side effects of corticosteroids

A

Osteoporosis, osteonecrosis of femoral head, myopathy, cataracts, calcium and vit D supplementation

293
Q

What are the side effects of 5-ASA

A

Acute interstitial nephritis

294
Q

What is sulfasalazine always administered with

A

Folate

295
Q

What should you test for prior to use of TNF abs

A

Latent tubercuosis with PPD testing and CXR

296
Q

What do anti-TNF therapies increase the risk for

A

Non-melanoma skin cA and non-Hodgkin lymphoma

297
Q

Can the GB be visualized in dubin Johnson syndrome

A

NO; but can be in rotor

298
Q

What increases the risk of occurrence of intrahepatic cholestasis of pregnancy

A

Another pregnancy or use of OCP

299
Q

What further work up needs to be done if conjugated bilirubin found to be elevated

A

Viral hep, AMA, ceruloplasmin, ferritin, iron saturation, lipase/amylase

300
Q

What is the dx test for obstructive jaundice

A

US; followed by cholangiography

301
Q

What most commonly occurs persistent mild elevations of ALT and AST

A

NAFLD

302
Q

How would biliary dyskinesia present

A

RUQ pain, normal US, pain longer than 30 min, recurrent sx, not received by BM or antacids; normal liver enzymes, conjugated bilirubin and amylase/lipase; *HIDA scan -> normal (GB visualized within 1 hour)

303
Q

What is a CCK-HIDA

A

Tests ejection fraction of GB; less than 35-38% is abnormal -> cholecystectomy

304
Q

What is protective against gallstones

A

Low carb diet, physical activity, caffeine in women, high intake of Mg and polyunsaturated fat in men, high fiber diet and statin, ASA and NSAIDs

305
Q

What are findings of acute cholecystitis on US

A

GB wall thickening, pericholecystic fluid, and sonographic Murphy sign

306
Q

What is the procedure of choice for choledocholithiasis

A

ERCP with sphincterotomy and stone extraction or stent placement

307
Q

How can you visualize porcelain GB

A

KUB

308
Q

When should you do a cholecystectomy in someone with gallstones

A

Symptomatic, previous complications, underlying condition predisposing to increased risk of complications, pt with gallstones >3 cm

309
Q

How do you treat acute cholecystitis

A

NPO, NG suction, IV fluids and electrolytes, analgesia, abx,

310
Q

What would be the test of choice for ischemic colitis

A

CT angiography

311
Q

What do you need to do before an ERCP

A

Measure INR, pregnancy test, kidney fxn

312
Q

What needs to be done before a HIDA scan (PIPIDA)

A

NPO 4-6 hrs before testing; no opiates for 4 half lives of the drug or 6 hrs prior to study, withhold calcium channel blockers, octreotide, progesterone, indomethacin, theophylline, bento, H2 blockers

313
Q

What is an oral cholecystogram/ography

A

OCG; contrast tablets swallowed night before exam, X-RAY taken, evaluate GB

314
Q

What is cholangiography

A

Uses iodine; percutaneous transheptic

315
Q

What is the criteria for dx of acute pancreatitis

A

Two of three: ab pain in epigastric that may radiate to back, threefold or greater elevation in serum lipase and/or amylase, confirmatory findings of acute pancreatitis on cross sectional ab imaging

316
Q

What are risk factors for acute pancreatitis

A

Smoking, high dietary glycemic load, ab adiposity, increased age and obesity

317
Q

What are protective factors against acute pancreatitis

A

Eating vegetables, use of statins

318
Q

What is the pain of pancreatitis described as

A

Boring

319
Q

What must you rule out if amylase is 3x the upper limit

A

Salivary gland dz and intestinal perforation

320
Q

What conditions can also have elevated amylase

A

High intestinal obstruction, gastroenteritis, mumps, ectopic pregnancy, administration of opioids, after ab surgery

321
Q

What are associated with an increase in mortality rate of pancreatitis

A

Hypoalbunemia and elevated serum LDH

322
Q

What is a sentinel loop

A

Segment of air filled SI most commonly in LUQ; seen on imagine for pancreatitis

323
Q

What is the colon cutoff sign

A

Gas filled segment of transverse colon abruptly ending at the area of pancreatic inflammation (absence of gas distal to splenic flexure caused by colonic spasm rom pancreatic inflammation)

324
Q

What is used to confirm presence of acute pancreatitis

A

CT WITHOUT contrast

325
Q

When is rapid bonus IV contrast enhanced CT used for pancreatitis

A

Following volume resuscitation after 3 days of severe acute pancreatitis; avoid if serum Cr >1/5

326
Q

Seeing what on perfusion CT is associate with higher mortality rate of pancreatitis

A

Fluid collection

327
Q

What can be used to drain a pseudocyst

A

Endoscopic ultrasound

328
Q

What is a complication of ERCP

A

Pancreatitis

329
Q

When would you do an ERCP for pancreatitis

A

Not after first attack unless associated cholangitis, jaundice, or bile duct stone

330
Q

What is the most important treatment for pancreatitis

A

Aggressive IV fluid resuscitation

331
Q

What are the risk factors for 3rd spacing with pancreatitis

A

Younger age, alcohol etiology, higher hematocrit value, higher serum glucose, systemic inflammatory response syndrome in first 48 hours of hospital admission

332
Q

If you have hypocalcemia with pancreatitis, what must you give

A

Calcium gluconate

333
Q

What does administration of fresh frozen plasma or serum albumin increase the risk of

A

ARDS

334
Q

If fluids and RBC replacement doesn’t improve shock in pancreatitis patients, what do you do

A

Pressers

335
Q

What are complications of SAP

A

Necrotizing pancreatitis, multi organ failure, volume depletion, ileus

336
Q

How do you assess severity of pancreatitis

A

APACHE II (for all ICU patients), Beside index for severity in acute pancreatitis (BISAP) = BUN >25, impaired mental status, SIRS, age >60, pleural effusion; HAPS (harmless acute pancreatitis score) predicts non-severe course (no ab tenderness, rebound or guarding, normal hematocrit, normal Cr)

337
Q

What is the ransom criteria pneumonic

A

GA-LAW; C & HOBBS; stands for: glucose >200, age >55, LDH >350, AST >250, WBC > 16k; calcium <8, hematocrit drop >10%, oxygen <60mmHg, base deficit >4, BUN increase >5, squesteration of fluid >6L

338
Q

What is the class of pancreatitis using Atlanta criteria

A

Mild: no organ failure; no local complications
Moderate: transient organ failure <48 hrs; plus or minus local complications
Severe: persistent organ failure >48 hrs

339
Q

What is autoimmune pancreatitis associated with

A

Hypergammaglobulinemia (IgG4)

340
Q

Is there a specific lab test for chronic pancreatitis

A

No; amylase and lipase often normal

341
Q

What test would you run on someone with suspected pancreatic steatorrhea

A

Fecal elastase 1 and small bowel bx

342
Q

What should be given for pain with chronic pancreatitis

A

Acetominophen, NSAIDs, tramadol along with tricyclic antidepressants, SSRI and gabapentin or pregabalin (can lower pain med requirement)

343
Q

Addiction to what is common with chronic pancreatitis

A

Opioids or narcotics

344
Q

What is MEN 1

A

Two or more of the following: parathyroid -> hypercalcemia increased PTH; pancreas (gastrinoma or insulinoma), pituitary

345
Q

What is men 2A

A

Thyroid: medullary thyroid CA; elevated calcitonin -> low calcium
Adrenal: pheochromocytoma
Parathyroid: hyeprcalcemia
*can have normal calcium b/c balances out; 5% develop hirschsprung

346
Q

What is MEN 2B

A

Marfanoid body habitus, medullary thyroid CA, pheocrhomocytomas, neuromas (on lips, tongue, mouth eyelids)

347
Q

What is the difference between GER and GERD in a baby

A

GER: passage of gastric contents into esophagus; happy spitter
GERD: sx or complications as a result of GER; hard to feed, cry a lot, arch and scream, hard to gain weight

348
Q

When should a child have surgery for GERD

A

Only if puts nutrition or respiratory status at risk; more common in developmentally delayed children; fundoplication

349
Q

Where do most cases of intussusception occur

A

Ileocolic; ileum invaginates into colon at ileocecal valve

350
Q

What does air enema show with intusseception

A

Coiled spring appearance

351
Q

What is the treatment for intusseception

A

In first 48 hrs -> hydrostatic reduction with contrast enema or pneumatic reduction with air enema *DONT DO EITHER IF PERITONEAL SIGNS

352
Q

What is the classic metabolic picture of a child with pyloric stenosis

A

Hypochloremic, hypokalemic, metabolic alkalosis; lose HCl via emesis; kidney holds on to hydrogen at expense of potassium

353
Q

How do you treat hirschsprung

A

2 stages: diverting colostomy with bowel that contains ganglion cells; then aganglionic portion removed

354
Q

What is unconjugated bilirubin usually bound to

A

Albumin; can be displaced by meds like ceftriaxone

355
Q

What are examples of non-path causes of neonatal jaundice

A

Physiologic jaundice, breast milk and breast feeding jaundice

356
Q

What is the difference between breast feeding and breast milk jaundice

A

Feeding: function of dehydration and decreased excretion of bilirubin in stool
Milk: deconjugating enzymes

357
Q

Is conjugated hyperbilirubinemia ever non pathologic

A

No

358
Q

What are the path causes off unconjugated hyperbilirubinemia

A
  • increased bilirubin production: erythrocytes enzyme deficiencies, blood group incompatibility, G6PD def
  • impaired conjugation
  • increased enterohepatic circulation: decreased intake, decreased passage of stool
359
Q

When should the infant’s cord blood be evaluated

A

When mom is type O or Rh negative; test for direct ab (Coombs), blood type, and Rh

360
Q

What are some causes of conjugated hyperbilirubinemia

A

UTI, biliary atresia/cholestasis, hypothyroidism, galactosemia

361
Q

What are the phases of acute bilirubin toxicity (with high unconjugated hyperbilirubinemia)

A
  • phase 1: first 1-2 days; poor suck, high pitched cry, stupor, hypotonia, seizures
  • phase 2: middle of first week; hypertonic of extensor mm, opisthotonus, retrocollis, fever
  • phase 3: after first week; hypertonic
362
Q

What is BIND

A

Bilirubin induced neurological dysfunction

363
Q

How does jaundice progress

A

Cephalad -> caudad

364
Q

During what gestational weeks are infants most at risk for developing hyperbilirubinemia

A

35-36

365
Q

What labs should you order if the conjugated bilirubin is elevated

A

Urine culture, blood cultures

366
Q

How do you treat mild jaundice

A

No phototherapy; increase frequency of feedings; continue breast feeding but if inadequent give supplemental breast milk or formula

367
Q

When is exchange transfusion considered

A

When bili > 25 of sx of encephalopathy

368
Q

What are the sx of biliary atresia

A

Cholestatic jaundice, hepatomegaly, acholic stools

369
Q

What causes idiopathic neonatal hepatitis

A

Aka giant cell hepatitis; prolonged cholestatis jaundice; liver bx shows disrupted hepatic structure

370
Q

What is alagille syndrome

A

Bile duct paucity or arteriohepatic dysplasia; AD; reduction of intrahepatic bile duct

371
Q

Which crigler najar does bilirubin decrease with phenobarbital

A

II

372
Q

What are the different types of stool according to the chart

A

1: separate hard lumps (hard to pass)
2: sausage shaped but lumpy
3: like a sausage but with cracks
4: soft and smooth sausage
5: soft blobs
6: fluffy mushy
7: pure liquid

373
Q

What are the reasons to not do a digital rectal exam

A

The patient has leukopenia

374
Q

What is melanosis coli

A

Hyperpigmentation of the colon caused by chronic use of laxatives

375
Q

What is the definition of acute diarrhea

A

Less than 2. Wks

376
Q

What are the most common causes of chronic diarrhea

A

IBS, meds, lactose intolerance; *presence of nocturnal diarrhea, weight loss, anemia, or positive FOBT warrants further testing

377
Q

What lab tests should you order for chronic diarrhea

A

CBC, serum electrolytes, liver fxn, calcium, phosphorous, albumin, TSH, vit A and D, INR, ESR, CRP

378
Q

What does increased ESR or CRP suggest

A

IBD

379
Q

What should you analyze stool for for chronic diarrhea

A

Electrolytes to calculate osmotic gap (high in osmotic diarrhea or disorder of malabsorption), fat (Sudan stain), leukocytes, calprotectin, lactoferrin (IBD), fecal antigen for giardia and e histolytics, acid fast for cryptosporidium and cyclosporine

380
Q

When would patients with chronic diarrhea undergo colonoscopy vs endoscopy

A

Colon: exclude IBD, colonic neoplasia
Endo: small intestine malabsorption disorder (celiac, whipple); in AIDS patients for cryptosporidium and M Avium intracellular

381
Q

When should neuroendocrine tumors be considered for cause of chronic diarrhea

A

High volume watery diarrhea that persists during fasting with a normal osmotic gap

382
Q

What can you test for for a neuroendocrine tumor

A

VIP (VIPoma), calcitonin, gastrin, urinary 5-hydroxyindoleacetic acid (carcinoid)

383
Q

What does the hydrogen breath test test for

A

Carb malabsorption and lactase deficiency

384
Q

What meds cause microscopic colitis

A

NSAIDs PPI, ACE inhibitors, SSRI, beta blockers

385
Q

How do you treat microscopic colitis

A

Loperamide

386
Q

What is characteristic of bile salt malabsorption

A

No weight loss, but deficiencies in ADEK

387
Q

What are the extrainestinal manifestations of Celiac

A

Iron deficiency anemia, dermatitis herpetiformis, osteoporosis, depression, fatigue, delayed puberty, amenorrhea, reduced fertility

388
Q

What is dermatitis herpetiformis

A

Purification papulovesicles over extensor surfaces of extremities and trunk, scalp and neck

389
Q

What GI dz can be suggested with elevated alkaline phosphatase but normal GGT

A

Celiac (malabsorption of calcium)

390
Q

What would you look for when testing for celiac in someone with IgA def

A

IgG ab to deamidated gliadin peptides (antiDGP)

391
Q

When will abs show up when testing for celiac

A

Only if actually eating gluten

392
Q

What else are celiac patients also likely to have an intolerance to

A

Lactose

393
Q

What are the characteristics of t whipple I

A

PAS positive, gram positive

394
Q

What does whipple look like on EM

A

Trilammellar wall

395
Q

How do you confirm a dx of bacterial overgrowth

A

Jejunal aspiration with quantititative bacterial culture

396
Q

What are causes of bacterial overgrowth

A

Gastric achlorhydria (PPI therapy), stagnation, motility disorders (DM, vagotomy), gastrocolic or coloenteric fistula

397
Q

What is short bowel syndrome

A

Malabsorptive condition caused by removal of small intestine parts; most common causes: crohn, mesenteric infarct, radiation enteritis, volvulus, tumor resection, trauma; depends on length and despite of removal

398
Q

What is needed to maintain oral nutrition when resecting bowel

A

At least 200 cm of proximal jejunum

399
Q

What will be malabsorbed if you remove the duodenum

A

Folate, iron or calcium; use antidiarrheal agents; octreotide reduces intestinal transit time

400
Q

What complications SI resection

A

Gastric hypersecretion; use PPI

401
Q

What is the most common GI dz in clinical practice

A

IBS

402
Q

What is Rome Criteria

A

Recurrent ab pain or discomfort for at least 3 days per month in last 3 months associated with 2 or more of: improvement with defecation, onset assoc with change in frequency in stool, onset associated with change in appareance of stool

403
Q

What dietary therapy can help IBS

A

Low FODMAP diet

404
Q

What is ogilvie syndrome

A

Aka acute colonic pseudo-obstruction; spontaneous massive dilation of cecum or right colon w/o mech obstruction; can usually still pass stool; cecal diameter >10-12 risk of colonic perforation

405
Q

How do you treat ogilvie syndrome

A

Conservative in patients with smaller than 12 cm dilation, no fever, no leukocytosis; NG and rectal tube placed; ambulated periodically; no oral laxatives *assess cecal size every 12 hours; intervention if *no improvement within 48 hrs, cecal dilation >10 for prolonged period, >12 cm -> neostigmine, colonoscopic decompression

406
Q

What is the difference between abx assoc diarrhea andd colitis

A

Diarrhea: occurs during period of abx exposure
Colitis: C diff; TcdA and B toxins *most common after use of ampicillin, clindamycin, 3rd gen cephalosporins, and fluoroquinolones

407
Q

What should be considered in all hospital patients with unexplained leukocytosis

A

C diff

408
Q

What test should you use to test for c diff toxins

A

PCR - more sensitive than EIA and are able to detect NAP1 hypervirulent strain

409
Q

What is the presentation of diverticulitis

A

Constipation -> loose stools because inflammation only allows this to pass

410
Q

How do you confirm diverticulitis

A

CT with contrast

411
Q

What is complicated during an acute attack of diverticulitis

A

Colonoscopy

412
Q

What can cause anorectal infections

A

Gonorhea, syphylis, chlamydia, herpes 2

413
Q

How do you test for gonorhea

A

Rectal swabs

414
Q

What causes condylomata acuminata vs condyloma Lata

A

Acuminata: HPV
Lata:syphilis

415
Q

When should you screen for colorectal cancer

A

45-75

416
Q

What mutation is common in adenomas vs serrated polyps

A

Adenomas: APC
Serrated: BRAF activation, MLH-1/MSH-2, or Kras mutation

417
Q

What is FIT

A

Fecal immunochemical test - used for colon ca detection

418
Q

What other kind of cancer are you at risk for with lynch syndrome

A

Endometrial, ovarian, renal or bladder, Hepatobiliary, gastric, and SI at a young age

419
Q

What are the extraintestinal manifestations of FAP

A

Soft tissue tumors of skin, desmoid tumors, osteomas, congenital hypertrophy of the retinal pigment

420
Q

What other mutation can cause FAP

A

MuTYH (AR) APC is AD

421
Q

What should be done to treat ppl with lynch syndrome

A

Subtotal colectomy with ileorectal anastomoses and surveillance of stump; women undergo pelvic exam, Transvag US, and endometrial sampling (hysterectomy recommended after child bearing years); screening for gastric cA with upper endoscopy beginning at 30

422
Q

What do you see with cowden syndrome

A

Hamartomatous polyps and lipomas throughout GI tract, trichilemmomas, and cerebellar lesions

423
Q

What causes pseudo diarrhea

A

IBS or proctitis

424
Q

What is the difference between enterotoxin and entero-adherent pathogens

A

Entero-adherent: not as much vomiting, but more ab cramping and fever

425
Q

What food sweetener causes diarrhea

A

Sorbitol

426
Q

When do you need to work up acute diarrhea

A

Dysentery, hypotension, tachycardia, profuse diarrhea (6> per day), fever >101 (38.5), recent abx use, severe ab pain, elderly, immunocompromised, Cr >1.5 times normal, peripheral leukocytes

427
Q

Which organisms need special cultures

A

EHEC, vibrio, yersinia, C diff toxin, ova parasites, stool antigen

428
Q

What organism is found in lunch meat

A

Listeria

429
Q

What are the features of staph aureus

A

Gram positive cocci, clusters, preformed enterotoxins

430
Q

What are the characteristics of shigella

A

Gram negative rods; non-motile; enterotoxin shiga toxin; lettuce, raw veggies, fever; fecal leukocytes

431
Q

What are the characteristics of typhimurium

A

Gram negative rod; fever; fecal leukocytes; self limited; exposure to reptiles (turtles), ducks and birds *no ab

432
Q

What are the features of campylobacter

A

Gram negative spiral shaped rod; fecal leukocytes; self limited; no abx; need campy blood agar to culture; oxidase positive, motile with cork-screw motion

433
Q

What is vibrio parahemolyticus

A

Gram negative bacilli; causes seafood associated diarrhea; cytotoxic production; watery or bloody diarrhea

434
Q

What is vibrio vulnificus

A

Gram negative; salt water; open would can cause bullous skin lesions; life threatening in immunocompromised especially in cirrhosis and hemochromatosis patients

435
Q

What is aeromonas hydrophila

A

Grade negative non spore forming rod shaped faculative anaerobes with flagellum; fresh water; eating fish; necrotizing fasciitis

436
Q

What is the most common pathogen for travelers diarrhea

A

ETEC

437
Q

Does EHEC typically produce a fever

A

No

438
Q

What are the characteristics of listeria

A

Gram positive rod; predilection for pregnant women and hemochromatosis; dx via blood culture

439
Q

What does rotavirus look like on EM

A

Wagon wheel appearance

440
Q

What does adenovirus cause

A

Fever, chills, myalgia, sore throat, conjunctivitis (most common cause in kids), pharyngitis; prolonged course

441
Q

What is the most common cause of dysentery in the world

A

E histolytica

442
Q

How do you dx E histolytics

A

Stool ova and parasite or stool antigen; will have fecal leukocytes; treat with metronidazole

443
Q

Will you see fecal leukocytes with G lamblia

A

No; check stool for ova parasites and stool antigen

444
Q

What would you see on micro for cryptosporidium

A

Acid fast staining, direct fluorescent ab; no fecal leukocytes

445
Q

Those infected with what are at greater risk for strongyloides stercoralis infection

A

Human T cell lymphotropic virus

446
Q

How do you dx strongyloides

A

Rhabditiform larvae in stool; eosinophils in stool

447
Q

Where do you get cyclospora cayetanesis

A

Produce from endemic areas or travel; watery diarrhea; fecal leukocytes negative; resistant to chloride and iodine; dx via oocysts in stool sample

448
Q

What is cystoisospora belli

A

Causes acute non bloody watery diarrhea; can last for weeks; severe in immunosuppressed; need repeated stool examinations, if negative do a duodenal biopsy; stain modified acid fast

449
Q

What can schistoma Mansoni cause

A

Bloody stools, bladder cancer, liver cysts

450
Q

What can taenia solium cause

A

Seizures

451
Q

In general, when will you see fecal leukocytes

A

Inflammatory - bloody diarrhea; with the exception of listeria and c diff

452
Q

When can you use anti motility agents

A

No fever, no blood; but NOT in EHEC or c diff

453
Q

What diet should ppl with infectious diarrhea be on

A

BRAT; bananas, rice, applesauce, toast

454
Q

What are alcohol gels ineffective against

A

Norovirus and c diff

455
Q

What are side effects of bismuth subsalicylate

A

Darkening of tongue and stools

456
Q

What can yersiniosis lead to

A

Autoimmune thyroiditis, pericarditis, and glomerulonephritis

457
Q

What is the difference in presentation of a pathogen that affects the small vs large bowel

A

Small: large volume watery stools, ab cramps, weight loss; no WBCs in stool; dehydration
Large:frequent small volume stools; assoc with fever, blood or WBCs in stool

458
Q

What are the types of antacids and supplements

A
  • low systemic: aluminum, calcium, magnesium
  • high systemic: sodium
  • supplemental: simethicone
459
Q

What is the MOA of antacids

A

Combine with hydrogen ions; increases LES tone; DO NOT reduce acid secretion or production -> rebound acid production possible

460
Q

Which antacids have a rapid onset

A

Calcium, magnesium, and sodium

461
Q

Which antacids have a long duration of action

A

Calcium and magnesium

462
Q

Which antacid has the best aid neutralizing capability

A

Calcium

463
Q

What is simethicone

A

Aids in expulsion of gas

464
Q

What are the side effects of aluminum

A

Constipation, hypophosphatemia (acute treatment for hyperphosphatemia)

465
Q

What are the side effects of magnesium

A

Diarrhea, hypermagnesemia

466
Q

What are the adverse effects of calcium

A

Consolation, hypercalcemia (milk alkali syndrome -> nephropathy and metabolic alkalosis), hypophosphatemia, calcium based kidney stones

467
Q

What are the side effects of sodium anatacids

A

Gas, hypernatremia, metabolic alkalosis

468
Q

What are important patient factors to consider when giving antacids

A

Dosage form, presence of renal or heart dz, electrolyte status, diseases assoc with diarrhea and constipation

469
Q

When should you take antacids if you are on other medications

A

1-2 hours before other mediations or 2-4 hours after

470
Q

What is the surface acting anti ulcer agent

A

Sucralfate

471
Q

What is the only histamine blocker that is PO only

A

Nizatidine

472
Q

What is the onset of action for H2 blockers

A

Longer than antacids but shorter than PPI

473
Q

How long does it take an ulcer to heal on H2 blockers

A

4-8 wks

474
Q

What are the more rare side effects of H2 blockers

A

More likely with long term use; cimetidine: decreases testosterone binding to androgen receptor (gynecomastia in men, galactorrhea in women); neutropenia or thrombocytopenia

475
Q

What drug interactions exist with H2 blockers

A

Cimetidine inhibitor of CYP450; ranitidine also weak CYP450 inhibitor

476
Q

What are the contraindications for H2 blockers

A

Pregnancy; only if necessary - ranitidine

477
Q

Which PPIs can only be given PO

A

Ompeprazole, lansoprazole, deslansoprazole, rabeprazole

478
Q

What are the side effects of PPI

A

C diff, kidney dz, bone fractures, MI

479
Q

What drug interactions exist with PPI

A

Omeprazole is CYP450 inhibitor

480
Q

What are the contraindications for PPI

A

Pregnancy; only if necessary - lansoprazole

481
Q

What dose sucralfate do

A

Band aid; can also stimulate prostaglandin and mucus production

482
Q

What are the side effects of sucralfate

A

Constipation

483
Q

What are the contraindications to use of sucralfate

A

Severe renal failure (contains aluminum)

484
Q

What is the dosing for sucralfate

A

4 times a day

485
Q

What does misoprostol do

A

Increases mucosal blood flow, stimulates bicarbonate and mucus production; reduces acid output

486
Q

What is the indication for use of misoprostol

A

Prevention of NSAID induced ulceration in patients at high risk

487
Q

What else can misoprostol be used for

A

With mifepristone for pregnancy termination, alone for cervical ripening, postpartum hemorrhaging

488
Q

What are the contraindications for misoprostol

A

Pregnancy, IBD

489
Q

What do bismuth compounds do

A

Anti bacterial; OTC for heartburn, indigestion and diarrhea; Rx: in combo with abx for h pylori

490
Q

What are the adverse effects of bismuth compounds

A

Consipation, black dark regularly formed stools

491
Q

What are the contraindications for bismuth compounds

A

Relative: pt on anti platelets or anticoagulants, severe renal failure
Absolute: allergy, GI bleed

492
Q

What do you need for treatment of h pylori

A

At least 2 abx and PPI or H2 blocker

493
Q

What is the first line therapy for h pylori

A

10-14 days of a PPI, clarithromycin, and either amoxicillin or metronidazole *all BID

494
Q

What is the quadruple therapy for h pylori

A

PPI (BID), metronidazole, tetracycline and bismuth subsalicylate (QID)

495
Q

What is Prevpac and omeclamox

A

Both given BID

  • prevpac:amoxicillin, clarithromycin, lansoprazole
  • Omeclamox: amoxicillin, clarithromycin, omeprazole
496
Q

What is holiday

A

QID

Bismuth subsalicylate, metronidazole, tetracycline Plus a PPI

497
Q

What is pylera

A

3 capsules QID

Bismuth, metronidazole, tetracycline, PPI

498
Q

When do you discontinue PPI after eradicatin of h pylori

A

2-3 wks after

499
Q

How do you treat someone with h pylori with a penicillin allergy

A

Metronidazole substitution

500
Q

How do you treat metronidazole resistant h pylori

A

Substitute tetracycline; consider quadruple

501
Q

How do you treat clarithromycin resistant h pylori

A

Substitute amoxicillin or tetracycline; consider quadruple

502
Q

How should you treat a pregnant patient with PUD without h pylori

A

Short course of antacids or sucralfate; moderate: ranitidine; severe: lansoprazole

503
Q

If someone is at NSAID risk for ulcer what should you do

A

Change to acetominophen or if NSAID required, COX-2 NSAID and PPI or misoprostol

504
Q

Which receptors are targeted for anti nausea therapy

A

5HT3, H1, M1, D2, NK1 (neurokinin)

505
Q

What do all the serotonin antagonists end in

A

-setron

506
Q

Which serotonin antagonist has a SQ injection form

A

Granisetron

507
Q

What is alosetron indicated for

A

IBS-D; PO

508
Q

What are serotonin antagonists used for

A

Chemo induced NV, radiation induced, post operative, pregnancy

509
Q

What is the worst side effect of serotonin antagonists

A

QT prolongation and torsade’s; dolasetron high risk - no longer used for chemo prophylaxis

510
Q

Which serotonin receptor antagonists have longer half lives

A

Palonosetron and granisetron; used for delayed-chemo induced as a single dose

511
Q

What do the neurokinin antagonists end in

A

-pitant

512
Q

When are netupitant and fosnetupitant given

A

Only in combo with palonosetron; fos is prodrug

513
Q

Which neurokinin antagonists are PO

A

Aprepitant, netupitant

514
Q

What are neurokinin antagonists used for

A

Chemo induced (most effective with serotonin antagonists combo); prophylaxis of post op *only aprepitant

515
Q

What are the histamine 1 antagonists

A

Diphenhydramine, dimenhydrinate, hydroxyzine, promethazine, meclizine, cyclizine

516
Q

What is doxylamine used for

A

Used with B6 as inital therapy for NVP

517
Q

How strong are the antiemetic activity of histamine 1 blockers

A

Weak; have anticholinergic properties

518
Q

What is the only indication for meclizine and cylizine

A

Motion sickness/vertigo

519
Q

How is hydroxzine administered

A

IM

520
Q

What are the D2 antagonists

A

Phenothiazines: chlorpromazine, perphenazine, prochlorperazine

521
Q

Which D2 antagonists is PO only

A

Perphenazine

522
Q

What is metoclopramide used to treat

A

Dysmotility; stimulates Ach in gut and increases LES tone

523
Q

Are dopamine antagonists used for chemo induced vomiting

A

Yes but in combo with other agents

524
Q

What are the side effects of dopamine antagonist

A

Anticholinergic effects, arrhythmia

525
Q

What is scopolamine

A

Muscarinic antagonist; patch for 72 hrs; weak antiemetic for motion sickness end of life care;

526
Q

What are the canniboid agonists

A

Dronabinol, nabilone

527
Q

What kind of antiemetic properties do cannabinoids have

A

Strong; reserved fro treatment of chemo induced *IF treatment resistant; decreases excitation of neurons and minimizes serotonin release; also used for appetite stimulation in anorexic patients

528
Q

What drug interactions do cannabinoids have

A

Caution use with other CNS depressants and CV agents and sympathomimetics

529
Q

What is the high emetogenic regimen for chemo induced nausea

A

NK receptor antagonist, serotonin antagonist, corticosteroid; give day before for acute and 3 days after for delayed

530
Q

What is the moderate emetogenic regimen for chemo induced nausea

A

Serotonin antagonist (palonosetron,granisetron SQ), corticosteroid; give day before and 3 days after; can add NK antagonist or olanzapine or cannabinoid after going up to 3 drug regimen

531
Q

What is the low emetogenic regimen

A

One drug of the following: corticosteroid, serotonin antagonist, metoclopramide, prochlorperazine; give day of

532
Q

What is given for minimal emetogenic regimen

A

NOTHING

533
Q

How do you treat breakthrough nausea

A

One agent from different class to current regimen

534
Q

What can you use for pregnancy induced nausea

A

Vit B6 or histamine antagonist with B6 or serotonin antagonist; dopamine antagonist, steroid or different dopamine antagonist

535
Q

What can be given for motion sickness

A

Scopolamine, dimenhydrinate, meclizine

536
Q

Which classes of drugs are used for diarrhea

A

Prostaglandin inhibitors, opioid agonists, serotonin antagonists, chloride channel inhibitors

537
Q

What is loperamide

A

Related to opioids but does not produce opiate like effects; slows motility; side effects: fatigue, urinary retention

538
Q

What is diphenoxylate

A

Opiate agonist (C-V); opioid effects seen at high doses; has small quantity of atropine; antipropulsive

539
Q

What is eluxadoline

A

Agonist at opioid mu and kappa; anti propulsive; antagonist at delta receptor - decreases secretions; indicated for IBS-D

540
Q

What are the side effects of eluxadoline (C-IV)

A

Hepatic/pancreatic toxicity; pancreatitis high risk in patients without a gallbladder

541
Q

What are the contraindications of eluxadoline

A

Biliary duct obstruction, sphincter of oddi dysfunction, alcoholism, history of pancreatitis, severe hepatic impairment; *stop therapy if severe constipation lasts 4 or more days

542
Q

What is alosetron indicated for

A

Chronic severe IBS-D not responsive to other treatment

543
Q

What is the major side effect of alosetron

A

Ischemic colitis; *no refills without follow up exam, physician must enroll in prescribing program, must sign risk-benefit, must sign a statement adhering to therapy plan, self training and testing by physicians to learn to appropriatedly dx IBS required

544
Q

What are the contraindications of alosetron

A

History of GI obstruction, perforation, toxic megacolon, diverticulitis, crohns, UC, impaired circulation, severe consipation -> DC immediately

545
Q

What is crofelemer

A

Cl channel inhibitor; derived from sap; MOA: blocks CFTR and calcium chloride channels; indicated for non infectious diarrhea in HIV AIDs patients on anti retroviral therapy; side effects: infections of resp/urinary

546
Q

Which class of drugs is used for ab pain

A

Antimuscarininc -> hyoscyamine, dicyclomine, clidinium/chlordiazepoxide

547
Q

Which drug classes are used for constipation

A

Laxative and cathartic agents, peripheral opioid antagonists, guanylate Cyclase c agonist, selective chloride channel activators

548
Q

What is linaclotide

A

Guanylate Cyclase c agonist; increases cGMP; stimulates secretion of chloride/bicarbonate into lumen via CFTR -> increased fluid and accelerated transit; indicated for IBS-C and chronic idiopathic consipation

549
Q

What is lubiprostone

A

Prostaglandin derivative; increases intestinal fluid secretion by activated chloride channels; indicated for IBS-C, chronic idiopathic constipation, opioid induced constipation in non-cancer/past cancer adults

550
Q

What is methylnaltrexone

A
  • relistor: IV/PO, naloxegol: PO, alvimopan PO *Hospital use only
  • peripheral mu opioid antagonist; indicated for opioid induced constipation (non-cancer/past cancer); alvimpoan only for accelerating time to GI recovering following bowel resection with anastomoses (prevents post op ileus)
551
Q

What are the side effects of alvimopan

A

MI; max 15 doses

552
Q

What are the classifications of laxatives and cathartic

A
  • stimulants: bisacodyl, castor oil, glycerin, senna, Na picosulfate
  • osmotic: lactulose, mag citrate, PEG, sorbitol
  • saline’s: mag hydroxide, Na phosphate
  • bulk form: dietary fiber, psyllium, methylcellulose, calcium polycarbophil
  • stool softeners: docusate, mineral oil
553
Q

What are the adverse effects of bulk forming agents

A

Bloating/obstruction (drink fluids - caution in renal failure); lots of drug interactions

554
Q

What are stool softeners also called

A

Surfactant and emollient agents

555
Q

Which stimulant is also osmotic

A

Sodium picosulfate; also glycerin

556
Q

What is castor oil hydrolyzed to

A

Ricinoleic acid

557
Q

Which laxative has a pretty quick onset of action compared to others

A

Stimulants

558
Q

What are the adverse effects of stimulants

A

Urine discoloration (senna), fluid/electrolyte disturbances with long use

559
Q

What are the contraindications/cautions of stimulants

A

GI obstruction, ileus; passed through breast milk

560
Q

What route can bisacodyl and glycerin be given

A

PR; faster onset

561
Q

When is prepopik and large dose PEG used

A

Pre colonoscopy ONLY

562
Q

How do saline agents work

A

They are poorly absorbed so make hyperosmolar solutions and pulls in water; greater volume shortens transit time

563
Q

What drug interactions/cautions need to be taken with saline agents

A

Interact with diuretics; cautions: renal dz, CHF/HTN

564
Q

Besides constipation, what else is lactulose used for

A

Liver dz (hyperammonia); change in pH traps ammonia in GI

565
Q

What is the treatment for c diff

A

Severe: vancomycin
Mild: metronidazole or if oral administration doesn’t work for patient
Recurrent: fidaxomicin; spares anaerobic colonic flora

566
Q

What are the classes of vancomycin, metronidazole and fidaxomicin

A

Vancomycin: glycopeptide
Fidaxomicin: macrolide

567
Q

What do you use to treat h pylori

A

Bismuth subsalicylate, metronidazole, tetracycline, omeprazole

568
Q

What is the life cycle of e histolytica

A

Trophozoite -> binucleated precyst -> tetranucleated cyst

569
Q

What are the therapeutic goals of treating e histolytica

A
  • eliminate invading trophozoites: metronidazole or tinidazole
  • eradicate intestinal carriage of organism - paramomycin or iodoquinol
570
Q

How do you treat asymptomatic carriage of e histolytica

A

(Cysts or trophozoites w/o internalized RBC); treat with luminal amebicide agents (paromomycin or iodoquinol)

571
Q

What is the MOA of iodoquinol

A

Unknown; most retained in intestine and excreted in feces; adverse effects: diarrhea, nausea, ab pain, HA, rash, itching

572
Q

What drug class are paromomycin and iodoquinol

A

Paromomycin: aminoglycoside

Iodoquinol: 8-hydroxyquinolines

573
Q

What is the first line agent for treatment of giardia

A

Tinidazole; *metronidazole NOT approved for this indication; can also use nitazoxanide

574
Q

What is the MOA of nitazoxanide

A

Inhibits pyruvate ferredoxin oxioreductase; * prodrug -> active is tizaxanide; rapidly absorbed; adverse effects: increased appetite, Flatus, enlarged salivary glands, yellow eyes, dysuria, bright yellow urine

575
Q

What are the characteristics of cryptosprodium parvum

A

Oocysts with 4 motile sporozoites; life cycle occurs within intestinal cells

576
Q

What is the treatment for cryptosporidium parvum

A

Antidiarrheal agent -> loperamide

Antimicrobial agents: nitazoxanide (preferred), paromomycin

577
Q

What does cryptosprodium parvum treatment depend on

A

Immune status

  • HIV: antiretroviral therapy with nitazoxanide
  • other: reduce immunosuppressant and add nitazoxanide
578
Q

How do you dx nematodes

A

Eggs in feces; round worms; immune response is to dead worms and eggs

579
Q

Are eggs passed in the stool with strongyloides

A

No; dx with larvae in feces

580
Q

What are the characteristics of trichuris trichuria

A

Whip worm; ingestion of eggs -> eggs hatch -> produce more eggs; * no larvae, no transit through intestinal wall, no lung involvement, no eosinophilia, no auto infection; dx: football shaped egg in feces

581
Q

What is the treatment for nematodes (necator, ancylostoma, strongyloides, ascaris, trichuris, enterobius)

A

Albendazole, Mebendazole, ivermectin, thiabendazole, Pyrantel pamoate

582
Q

What is the MOA of albendazole and mebendazole

A

Inhibits microtubule synthesis, paralyzes worms, worms pass in stool; *prodrug

583
Q

What is the MOA of thiabendazole

A

Same as albendzaole; but a lot of side effects: dizziness, anorexia, vomiting, irreversible liver failure and fatal Stevens Johnson syndrome

584
Q

What is the MOA of ivermectin

A

Intensifies GABA mediated transmission in peripheral n of nematodes; dont combine with other GABA drugs (benzo, barbiturates, valproic acid)

585
Q

What is the MOA of pyrantel pamoate

A

Neuromuscular blocking agent causes release of Ach and inbhition of cholineterase -» paralysis of nematodes; poorly absorbed

586
Q

Which nematodes does albendazole cover

A

N Americanus, a duodenale, a lumbricoides, e vermicularis

Alternative therapy for strongyloides and trichuris

587
Q

What nematodes does mebendazole cover

A

Ascaris, trichuria, e vermicularis

Alternative for americanus and duodenale

588
Q

What nematodes does ivermectin cover

A

Strongyloides*

Alternative for ascaris, second alternative for trichuria, poor against americanus and duodenale

589
Q

What nematodes does pyrantel pamoate cover

A

E vermicularis; alternative for americanus and duodenale

590
Q

What are the types of schistoma and where does each reside

A

Japonicum and mansoni (intestines); haematobium (bladder)

591
Q

What are the clinical manifestations of schistoma

A

Dermatitis, katayma fever, chronic fibrosis

592
Q

What is the treatment for schistoma

A

Praziquantel

593
Q

What is the MOA of praziquantel

A

Increases permeability of worm cell membranes to calcium -> paralysis and death; excreted by kidneys; side effects: headache, lassitude; low grade fever, itching

594
Q

What do solium vs saginata attach via

A

Solium: hooks
Saginata: suckers

595
Q

What do you use to treat cestodes

A

Praziquantel, Niclosamide, albendazole

596
Q

What is the MOA of niclosamide

A

Not effective against hydatid cyst; inhibition of oxidative phosphorylation or stimulation of ATPase activity; oral administration; use limited by side effects; need long duration of therapy

597
Q

What drug classes are used to treat UC

A

5-ASA, Jack stat inhibitors, TNF alpha inhibitors, alpha 4 integrity inhibitors

598
Q

What drug classes are used to treat crohn dz

A

IL-12/23 inhibitors, TNF alpha inhibitors, alpha integrity inhibitors

599
Q

What do all ASA meds have in their names

A

Sala

600
Q

What is the MOA Of 5-ASA agents

A

Reduction in PMN and macrophage recruitment; can also inhibit NFkB pathway

601
Q

What is sulfasalazine

A

Sulfapyridine + 5-ASA

602
Q

What is mesalamine

A

Single 5-ASA

603
Q

What is olsalazine

A

2 molecules of 5-ASA

604
Q

What is balsalazide

A

Inert carrier and 5-ASA

605
Q

What are the diff distributions of ASA tx

A

Oral: throughout GI tract
Rectal: splenic flexure
Suppositories: reach upper rectum

606
Q

Which ASA agents have fewer side effects

A

The ones without sulfa

607
Q

What are the indications for use of 5ASA

A

Active and maintenance of mild-moderate UC; except olsalazine only for maintenance and balsalazide only for active dz in males

608
Q

What is the MOA of TNF alpha inhibitors

A

Blocks leukocyte migraition to site of inflammation

609
Q

What are the TNF alpha inhibitors

A

Adalimumab, infliximab, golimumab, certolizumab (recombinant ab fragment (Fab)); all IgG abs

610
Q

Which TNF alpha inhibitor is used for UC ONLY

A

Golimumab

611
Q

Which TNF alpha inhibitor is used for CD ONLY

A

Certolizumab

612
Q

What are the side effects of TNF alpha inhibitors

A

Infections; need TB testing, liver toxicity, dermatologic, malignancies

613
Q

What are the indications of TNF alpha inhibitors

A

Active and maintenance; used only after inadequate response to conventional or immunosuppressant therapy

614
Q

What are the maintenance doses for each of the TNF alpha inhibitors

A
  • adalimumab: SQ every 2 weeks
  • infliximab: IV every 8 weeks
  • golimumab: SQ every 4 weeks
  • certolizumab: SQ every 4 weeks
615
Q

What are the alpha 4 integrin inhibitors

A

Natalizumab and vedolizumab; both IgG

616
Q

Which alpha 4 integrin inhibitor is only for CD

A

Natalizumab

617
Q

What are the side effects of alpha 4 integrin inhibitors (natalizumab)

A

PML; treatment >2 yrs, prior immunosuppressant treatment, anti-JC virus abs are risk factors

618
Q

What are the indications for alpha 4 integrin inhibitors

A

Active and maintenance; used after failed immunosuppressant or TNF alpha inhibitor therapy

619
Q

What is the maintenance dose for each of the alpha 4 integrin inhibitors

A
  • natalizumab: IV every 4 weeks

- vedolizumab: IV every 8 weeks

620
Q

What is the IL-12/23 inhibitor

A

Ustekinumab: IgG ab; also indicated for plaque psoriasis and psoriatic arthritis

621
Q

What are the side effects of IL-12/23 inhibitors

A

Infections *TB testing, increased risk of malignancy

622
Q

What are the indications for IL-12/23 inhibitors

A

Active and maintenance for CD for patients intolerant to immunosuppressants, steroids, or TNF alpha therapy

623
Q

What is the dosing for ustekinumab

A

IV as single infusion and SQ every 8 weeks for maintenance

624
Q

What is the jak stat inhibitor

A

Tofacitinib; oral; indicated for psoriatic and RA; side effects: lymphopenia/lymphocytosis, neutropenia, anemia, increased LDL and HDL, increased malignancy

625
Q

What are the indications for jak stat inhibitors

A

Active and maintenance of UC *do not use in combo with anything else

626
Q

What is the dosing for tofacitinib

A

PO BID

627
Q

What are the indications for steroids

A

Acute and or sever UC and CD OR steroid dependent; use lowest dose for shortest amount of time

628
Q

When are IFN alpha use

A

Treatment of patients with well compensated liver dz; not long term treatment or planning to be pregnant within next 2-3 yrs

629
Q

What are the cons of IFN alpha treatment for HBV

A

Parenteral administration; expensive; side effect: flue like syndrome, dangerous in decompensated cirrhosis

630
Q

What is the MOA of IFN

A

Protect nearby healthy cells by allowing them to mount defense; signal macrophage and NK to clear infected cell; act in auto rinse fashion to stimulate lysosome lysis

631
Q

How does IFN alpha work

A

Binds to type 1 IFN receptor and activates JAK1 and tyrosine kinase 2 -> phosphorylation of type 1 IFN receptor -> recruitment of STAT1/2 -> transcribe genes

632
Q

What are the mechanisms of IFN stimulated genes (ISGs)

A

Inhibit steps of viral replication; ZAP, IFIT, OAS-RNAseL pathway, PKR

633
Q

What does PEGylated IFN alpha increase levels of during treatment

A

ALT; but means its working

634
Q

What toxicities are IFN treatment assoc with

A

Bone marrow suppression; neurotoxicity (behavioral changes)

635
Q

What are the characteristics of nucleosides/tides for HBV treatment

A

HBV DNA RT/DNApol inhibitors; oral*; better tolerated than IFN treatment and higher response; *can be used in patients with decompensated cirrhosis

636
Q

What is are examples of nucleoside drugs

A

Lamivudine, telbivudine, entecavine

637
Q

How can HBV become resistant to nucleoside/tide treatment

A

Impaired purine/pyramiding kinase activity

638
Q

What is an example of a nucleotide drug

A

Tenofovir and adefovir

639
Q

What is the first line treatment for wild type HBV

A

Tenofovir (analog of adenosine); used in patients with lamivudine, telbbivudine or entecivir resistance; side effects: proximal renal tubule nephrotoxicity

640
Q

What is entecavir

A

Guanosine nucleoside; first line HBV agent; low rate of resistance (except in those who are also resistant to lamivudine); better choice than adefovir or tenofovir in patients with renal insufficiency

641
Q

Does lamivudine have long term efficacy

A

No; resistance

642
Q

What is the treatment for HCV

A

24-48 wk course of PEGylated IFN plus ribavirin

643
Q

What is ribavirin

A

Nucleoside analogs of guanosine; interferes with synthesis of GTP, inhibits capping of viral mRNA, inhibits viral RNA pol; potentiates action of PEGylated IFN; contraindicated in patients with anemia or pregnant*

644
Q

What is simeprevir

A

Second gen protease inhibitor; administer in combo with PEG IFN and ribavirin or sofosbuvir +/- ribavirin (chronic genotype 1 infxn)

645
Q

What are telaprevir and boceprevir

A

First gen protease inhibitors; administered with PEGylated IFN and ribavirin (chronic genotype 1 infxn); simeprevir has diminished importance of these drugs

646
Q

What is sofosbuvir

A

NS5B (RNA dep RNA pol needed for HCV replication) inhibitor; nucleotide analog; use in combo with other antivirals (ledipasvir); used for all genotypes of HCV

647
Q

What are the NS5A inhibitors

A

Ledipasvir, elbasvir, velpatasvir; effective for all genotypes; not given as monotherapy b/c resistance; traditionally given with ribavirin and PEg IFN

648
Q

What is the standard regimen for genotype 1 HCV

A

Ledipasvir + sofosbuvir

649
Q

What is the standard treatment for HCV genotype 1,2,3

A

Velpatasvir + sofosbuvir

Elbasvir + grazoprevir

650
Q

What abx causes red man syndrome

A

Vancomycin

651
Q

What is iodoquinol contraindicated in

A

Iodine allergies

652
Q

What are long term side effects of albendazole and mebendazole

A

Alopecia and GI dz

653
Q

What are the important characteristics of PEGeylated IFN

A

Slower clearance, longer 1/2 life, less frequent dose

654
Q

What is the relationship between IFN and ribavirin

A

Synergistic

655
Q

What is the side effect if bisphophatase

A

Pill esophagitis

GI II (2 decks)

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