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Gastrointestinal Flashcards

1
Q

In an immunocompromised person with odynophagia consider-

A

candidiasis

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2
Q

dysphagia

A

difficulty swallowing

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3
Q

odynophagia

A

pain with swallowing

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4
Q

oropharyngeal dysphagia presentation and complications

A

issues initiating swallowing.

can cause aspiration of food into lungs. (coughing, choking, drooling)

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5
Q

Etiology of oropharyngeal dysphagia

A

neurologic or muscular. stroke. parkinson. myesthenia gravis. prolonged intubation. Zenker diverticulum.

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6
Q

oropharyngeal dysphagia is usually more of a problem with ______ than _____

A

liquids than solids

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7
Q

Esophageal dysphagia

etiologies and presentation

A

obstruction caused by stricture, schatzki rings, carcinoma.

motility disorder- achalasia, scleroderma, esophageal spasm

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8
Q

esophageal obstruction causes more of a problem with _____ than _____

A

solids than liquids

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9
Q

Motility disorders cause issues with eating _____ and _____

A

solids AND liquids

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10
Q

Diagnosis/work up for oropharyngeal dysphagia

A
  1. modified barium swallow (video flouroscopic swallow exam) sometimes EGD
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11
Q

Diagnosis/work up for esophageal dysphagia

A

Initially EGD (can do pre EGD barium swallow) **esp if history of esophageal radiation and strictures

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12
Q

Diagnosis of odynophagia?

A

EGD

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13
Q

Should you ever perform manometry before EGD?

A

NO

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14
Q

Candida esophagitis is an ___ defining illness

A

AIDS

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15
Q

Name causes of infectious esophagitis

A
  1. candida albicans
  2. herpes simplex virus
  3. CMV
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16
Q

Exam findings, upper EGD findings, Treatment for Candida albicans

A

Exam: oral thrush. can be scraped off
EGD: yellow, white plaques adherent to mucosa
Treatment: fluconazole PO

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17
Q

Exam findings, upper EGD findings, Treatment for Herpes Simplex Virus

A

Exam: oral ulcers
EGD: small, deep ulcerations. +Tzank smear. multinucleated inclusions on biopsy
Treat: Acyclovir IV

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18
Q

Exam findings, upper EGD findings, Treatment for CMV

A

exam: retinitis, colitis
EGD: large, superficial ulcerations. intranuclear and intracytoplasmic inclusions on biopsy
Treatment: Ganciclovir IV

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19
Q

Diffuse distal esophageal spasm

A

motility disorder where normal peristalsis is interrupted by non-peristaltic contractions

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20
Q

Presentation of esophageal spasms

A

heartburn, chest pain, dysphagia, odynophagia

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21
Q

esophageal spasms are often precipitated by ingestion of? pain relieved by?

A

Hot or cold liquids.

Nitroglycerin provides relief

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22
Q

Diagnosis of esophageal spasm?

A

EGD to rule out structural abnormalities
Barium swallow
Esophageal manometry:(DEFINITIVE TES)

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23
Q

what will barium swallow show for patient with esophageal spasm?

A

Corkscrew-shaped esophagus

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24
Q

What will esophageal manometry show for esophageal spasm?

A

DEFINITIVE TEST. high amplitude, simultaneous contractions in greater than 20% of swallow.

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25
Q

Corkscrew barium swallow

A

esophageal spasm

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26
Q

Birds beak sign on barium swallow

A

achalasia

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27
Q

Nodular mucosa and raised filling defect on barium swallow

A

barret esophagus and adenocarcinoma

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28
Q

musculature in upper 1/3 of esophagus is _____ while lower 2/3 is _______

A

skeletal, smooth

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29
Q

Treatment for esophageal spasm?

A

calcium channel blockers, TCAs, nitrates

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30
Q

treatment for severe incapacitating symptoms of spasm?

A

surgery (esophageal myotomy)

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31
Q

Achalasia

A

motility disorder of esophagus characterized by impaired relaxation of LES and loss of peristalsis in distal 2/3 esophagus

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32
Q

Cause of achalasia

A

degeneration of inhibitory neurons in myenteric (Auerbach) plexus

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33
Q

presentation of achalasia

A

Progressive dysphagia (solids + liquids), chest pain, regurg of undigested food, weight loss, nocturnal cough

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34
Q

what may mimic achalasia?

A

malignancy

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35
Q

Diagnosis of achalasia?

A

EGD to rule out structural disorders (mechanical obstruction)- especially cancer

initial test: barium swallow- dilation with a “bird beak” sign

Definitive test: manometry: increased resting LES pressure, incomplete LES relaxation with swallow, and decrease peristalsis in esophagus

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36
Q

Treatment for achalasia

A

short term: nitrates, ccb, endoscopic injection of botulinum toxin into LES
long term: pneumatic balloon dilation or surgical (Heller) myotomy.

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37
Q

Zenker diverticulum

A

cervical out-pouching through cricopharyngeus muscle (posterior-FALSE diverticulum)

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38
Q

presentation of Zenker diverticulum?

A

chest pain, dysphagia, halitosis, regurg of undigested food

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39
Q

Dx of Zenker:

A

barium swallow with outpouchings

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40
Q

Tx of Zenker:

A

Surgical excision of diverticulum if symptomatic. (myotomy of cricopharyngeus to relieve high pressure)

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41
Q

Most common type of esophageal cancer world-wide?

A

SCC

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42
Q

Most common type of esophageal cancer in U.S, Europe, Australia?

A

Adenocarcinoma

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43
Q

Risk factors for SCC?

A

Alcohol, tobacco use, nitrosamines

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44
Q

Adenocarcinoma risk factors?

A

Barett esophagus (columnar metaplasia of distal esophagus secondary to chronic GERD)

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45
Q

Presentation of esophageal cancer?

A

Progressive dysphagia. initially to solids. then to liquids. weight loss. odynophagia. GERD. GI bleed. Vomiting.

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46
Q

Why does esophageal cancer metastasize early?

A

Esophagus lacks a serosa

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47
Q

SCC occurs in _____ of esophagus. Adeno occurs in _____ of esophagus.

A

SCC- upper and middle thirds. Adeno- lower 3rd

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48
Q

Diagnosis of esophageal cancer

A

Initial test: barium study: narrowing of esophagus with irregular border protruding into lumen

EDG with biopsy makes diagnosis:

CT and endoscopic ultrasound: staging cancer

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49
Q

treatment for esophageal cancer

A

chemo and surgical resection are 1st line treatment

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50
Q

treatment for cases of high grade barrett’s?

A

resection may be required

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51
Q

Etiology of GERD?

A

most often from transient LES relaxation

incompetent LES, gastroparesis, hiatal hernia

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52
Q

sour taste “water brash” or sensation of globus lump in throat?

A

GERD

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53
Q

Diagnosis of GERD

A

clinical diagnosis with empiric treatment first

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54
Q

when is EGD with biopsy performed for GERD patients

A
  1. refractory symptoms to therapy
  2. long standing GERD (rule out barrett and adeno)
  3. blood in stool, weight loss, dysphagia, odynophagia, chest pain
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55
Q

Definitive test for GERD?

A

24 hour pH monitoring with impedance (only for uncertain diagnosis)

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56
Q

Treatment for GERD

A

lifestyle
mild intermittent: antacids
chronic/frequent: H2 antagonists (cimetidine, ranitidine) or PPIs (omeprazole, lansoprazole)

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57
Q

Treatment for severe, erosive GERD

A

PPI first. Nissen fundoplication

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58
Q

Complications of GERD

A

Erosive esophagitis, peptic stricure, aspiration pneumonia, upper GI bleed, Barrett esophagus

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59
Q

Hiatal hernia 3 types

A
  1. sliding hiatal hernia (95%)
  2. paraesophageal hiatal hernia (5%)
  3. mixed hiatal hernia (rare)
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60
Q

Sliding hiatal hernia

A

GE junction and any portion of stomach above diaphragm. usually asymptomatic

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61
Q

Is GERD a result of presence of H.pylori?

A

NO. arises from relaxation of LES

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62
Q

Paraesophageal hiatal hernia

A

GE junction below diaphragm. fundus herniates into thorax. can cause strangulation

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63
Q

Sliding hiatal hernia presentation?

A

can be asymptomatic or GERD

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64
Q

Dx of hiatal hernia?

A

often indidental finding on CXR. barium swallow or EGD diagnosis

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65
Q

Tx sliding hiatal hernia

A

medical therapy and lifestyle mods to decrease GERD

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66
Q

Tx paraesophageal hernia

A

surgical gastropexy (attachment of stomach to rectal sheath and closure of hiatus

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67
Q

Acute gastritis

A

rapidly developing superficial lesions. often due to NSAID use, alcohol, H.pylori, stress from severe illness (burns, CNS injury)

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68
Q

Chronic gastritis Type A and Type B

A

Type A: (10%)- Occurs in fundus. due to autoantibodies to parietal cells (pernicious anemia).
Type B: (90%)- Antrum, caused by NSAIDs or H.pylori. often asymptomatic. but associated with increased risk of peptic ulcer disease and gastric cancer

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69
Q

Pernicious anemia associated with?

A

associated with other autoimmune disorders and increased risk of gastric adenocarcinoma

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70
Q

Type A related gastritis (autoantibodies to parietal cells) occurs in the ____ of stomach?

A

fundus

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71
Q

Does H.pylori infection always cause gastritis?

A

NO

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72
Q

Why is type A gastritis associated with pernicious anemia?

A

Auto-antibodies attack parietal cells. Parietal cells make intrinsic factor. Need intrinsic factor to absorb B12.

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73
Q

Curling ulcers

A

stress ulcers associated with burn injuries

burn with curling iron

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74
Q

cushing ulcer

A

stress ulcer associated with CNS injury (TBI)

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75
Q

Treatment for PUD/Gastritis

A

Stop offending agents (NSAID, alcohol)
Antacids, sucralfate, H2 receptor blockers, PPIs
**Triple therapy (amoxicillin, clarithromycin, omeprazole) for H. Pylori infection

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76
Q

What should triple therapy for H.Pylori include if patient is allergic to penicillin?

A

Metronidazole, clarithromycin, omeprazole

Metro instead of amoxicillin

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77
Q

Are H. pylori antibodies a good measure of infection? why/why not?

A

NO. they stay (+) even when disease is cleared.

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78
Q

How to diagnose H. pylori?

A

Urea breath test

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79
Q

Test of cure for H. pylori?

A

repeat stool antigen

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80
Q

4 different tests for H. pylori

A
  1. serology
  2. urea breath test
  3. stool antigen test
  4. endoscopic biopsy
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81
Q

Who should get prophylactic PPIs?

A

Patients at risk for stress ulcer- ICU patients!

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82
Q

Krukenberg tumor

A

gastric adenocarcinoma that metastasizes to ovary

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83
Q

How does urea breath test work?

A

H.pylori urease converts urea to CO2 and ammonia. Test detect ammonia from urea metabolism.

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84
Q

sensitivity and specificity of serology IgG testing for h.pylori?

A

high sensitivity. lower specificity

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85
Q

sensitivity specificity for for urea breath test?

A

high specificity. lower sensitivity. PPIs can cause false negatives.

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86
Q

stool antigen test for H. pylori

A

detects H. pylori antigen in stool. high specificity and high sensitivity. cost-effective initial test for H.pylori**

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87
Q

Gold standard diagnosis for H.pylori or gastritis?

A

endoscopic biopsy.

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88
Q

Malt Lymphoma

A

rare gastric tumor that presents in patients with chronic H.pylori infection.

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89
Q

how to cure malt lymphoma

A

only malignancy that can be cured with antibiotics. treat with triple therapy. (amox, clarithromycin, omeprazole)

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90
Q

Virchow node.

A

enlargement of left supraclavicular node. often indicative of gastric cancer.

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91
Q

most common GI cancer?

A

adenocarcinoma (common in Korea and Japan)

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92
Q

Risk factors for GI adenocarcinoma

A

Diet high in nitrites, salt, low in fresh veggies (antioxidants). H.pylori. Chronic gastritis

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93
Q

presentation of gastric cancer

A

indigestion, loss of appetite early

late- weight loss, upper GI bleed, abd pain

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94
Q

Dx gastric cancer:

A

upper endoscopy with biopsy (definitive)

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95
Q

Tx: gastric cancer

A

surgical resection. most patients present with late stage, incurable disease.

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96
Q

<90% of duodenal ulcers and 70% of gastric ulcers are caused by?

A

H.pylori

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97
Q

Other risk factors for PUD

A

alcohol, NSAID, tobacco

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98
Q

Presentation of acute perf caused by PUD

A

rigid abdomen, rebound tenderness, guarding (do upright KUB- show free air under diaphragm)

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99
Q

In recurrent or refractory cases of PUD, check serum ______ to screen for?

A

gastrin, Zollinger-Ellison syndrome

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100
Q

if Xray shows no perf, but high clinical suspicion of PUD perf, order?

A

CT

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101
Q

How to rule out/in active bleeding with PUD?

A

serial hematocrits, rectal vault exam, NG lavage. Monitor BP and treat with IV hydration, blood transfusion, IV PPIs. Perform urgent EGD to control suspected bleeding.

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102
Q

Parietal cell vagotomy should be performed

A

with severe cases of PUD refractory to medical therapy

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103
Q

After a meal pain from Gastric ulcer is ________ while pain from Duodenal ulcer is _______

A

Gastric ulcer - Greater

Duodenal ulcer- Decreased

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104
Q

Should all gastric ulcers be biopsied? why/why not?

A

YES. rule out malignancy

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105
Q

What is a major complication of gastric ulcer?

A

Hemorrhage

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106
Q

What gastric ulcers are most likely to cause hemorrhage? why?

A

Posterior gastric ulcers that erode into the gastroduodenal artery

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107
Q

Other complications of gastric ulcer?

A

perforation, gastric outlet obstruction, intractable vomiting

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108
Q

What can you give patients who require NSAID therapy for arthritis to help with PUD? why?

A

Misoprostol- PGE1 analogue -> increases production and secretion of gastric mucous barrier and decreases gastric acid production.

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109
Q

Zollinger-Ellison syndrome?

A

Rare condition characterized by gastrin producing tumor in duodenum or pancreas.

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110
Q

Gastrinomas are associated with what syndrome 20% of the time?

A

MEN 1

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111
Q

how to diagnose ZE syndrome?

A

fasting serum gastrin levels elevated and increased gastrin levels with the administration of secretin. (CT scan to stage the disease)

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112
Q

Tx of ZE:

A

moderate to high dose PPI

Surgical resection of gastrinoma after CT or octreotide scan to identify carcinoid tumors

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113
Q

ZE syndrome components

A
  1. hypercalcemia (MEN 1)
  2. Epigastric pain (peptic ulcer)
  3. Diarrhea (mucosal damage and pancreas enzyme inactivation leading to malabsorption)
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114
Q

Diarrhea definition

A

production of >200g feces/day along with increased frequency or liquidity of stool.

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115
Q

most common subtypes of diarrhea

A
  1. malabsorption/maldigestive/osmotic
  2. secretory
  3. inflammatory/infectious
  4. increased motility
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116
Q

Normal stool osmotic gap?

A

50-100

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117
Q

Stool osmotic gap equation

A

stool osmotic gap = 290 - 2(Stool Na + stool K)

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118
Q

Acute diarrhea definition and common etiology

A

< 2 weeks, usually infectious and self-limited

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119
Q

Common causes of pediatric diarrhea

A

rotavirus, norwalk, enterovirus

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120
Q

Chronic diarrhea definition and common causes

A

> 4 weeks. insidious onset.

Secretory, Malabsorption, Inflammatory/Infectious, Increase motility

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121
Q

Secretory diarrhea examples

A

Carcinoid tumor, VIPoma (VIP increases intestinal water and electrolyte secretion)

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122
Q

Malabsoption diarrhea ex:

A

bacterial overgrowth, pancreatic insufficiency, mucosal damage, lactose intolerance, celiac disease, laxative abuse, post-surgical short bowel

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123
Q

inflammatory diarrhea ex:

A

IBD

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124
Q

Increased motility diarrhea ex:

A

IBS

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125
Q

Cryptosporidium and Isospora are associated with chronic diarrhea in _____ patients

A

HIV/AIDS

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126
Q

Organisms that cause bloody diarrhea include

A
  1. salmonella
  2. shigella
  3. e.coli (EHEC)
  4. campylobacter
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127
Q

Organisms that cause watery diarrhea include

A
  1. vibrio cholera
  2. rotavirus
  3. e.coli (ETEC)
  4. Cryptosporidium
  5. Giardia
  6. Norovirus
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128
Q

When are studies needed for acute diarrhea?

A

high fever, bloody diarrhea, lasting > 4-5 days diarrhea

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129
Q

Additional studies for chronic diarrhea

A
  1. stool analysis (leukocytes, culture, c.diff, ova and parasite)
  2. sigmoidoscopy (only if with bloody diarrhea and unknown cause)
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130
Q

Low osmotic gap diarrhea <50

A

Secretory diarrhea (increase secretion or inhibition of water absorption) (cholera, e.coli, VIPoma, gastrinoma, medullary cancer of thyroid

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131
Q

High osmotic gap diarrhea >100

A

osmotic diarrhea (osmotically active compounds draw in water) (celiac, whipple disease, pancreatic insufficiency, laxative abuse)

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132
Q

Whipple Disease

CAN of Chocolate WHIP cream

A

C-cardiovascular
A-arthralgia
N-neurologic

Chocolate (diarrhea)

AND Osmotic diarrhea

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133
Q

History, Exam, Test Results, Treatment: campylobacter

A

History: most common cause of bacterial diarrhea (ingesting contaminated food/water). affects young kids and young adults. lasts 7-10 days.
Exam/Tests: Bloody diarrhea. Fecal RBC/Fecal WBC
Treatment: rule out IBD, rule out appendicitis. Supportive treatment then ciprofox or azithromycin if needed

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134
Q

History, Exam, Test Results, Treatment: C.diff

A

history: recent treatment with abx (penicillin, quinolone, clinda). hospitalized adult patients.
exam: fecal RBC/WBC. fever, abd pain, systemic tox
Dx: c.diff toxin. sigmoidoscopy with psuedomembrane.
Tx: stop antibiotics. PO metronidazole (mild)
PO vanc (mod-severe)
IV metro +/- rectal vanc if ILEUS

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135
Q

History, Exam, Test Results, Treatment: Entamoeba Histolytica

A

hx: travel in develop countries (food/water)
incubation can be 3 months. severe abd pain and fever.
dx: endoscopy with flask shaped ulcers
Tx: metronidazole

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136
Q

History, Exam, Test Results, Treatment: E.coli O157H7

A

hx: ingestion of raw meat. affects kids and elderly. lasts 5-10 days. severe abd pain, low fever, vomiting.

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137
Q

History, Exam, Test Results, Treatment: Salmonella

A

hx: ingestion of contaminated poultry, egg. young children and elderly. 2-5 days. prodromal HA, fever, myalgia, abd pain
tx: fluids! oral quinolone or TMP-SMX

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138
Q

History, Exam, Test Results, Treatment: Shigella

A

hx: extremely contagious. fecal oral. young children and hospitalized. can cause febrile seizures in the young.
tx: TMP-SMX to decrease person/person spread.

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139
Q

What should you watch for as severe complication of C.diff infection?

A

toxic megacolon

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140
Q

Flask shaped ulcers on endoscopy?

A

entamoeba histolytica

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141
Q

Treating entameoba histolytica with steroids can lead to?

A

fatal perforation

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142
Q

what is a complication of entamoeba histolytica

A

chronic amebic colitis (mimics IBD)

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143
Q

potential complication of E.coli- particularly in children?

A

HUS

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144
Q

What e.coli treatment increases risk of HUS?

A

Antibiotics or antidiarrheal therapy (SO DONT GIVE)

145
Q

What is a major concern for salmonella

A

SEPSIS. 5-10% become bacteremic.

146
Q

What patients are at particular risk if they contract salmonella?

A

sickle cell patients. invasive disease leading to osteomyelitis is more common

147
Q

Antidiarrheal agents

A

loperamide, bismuth salicylate

148
Q

Tropical sprue

A

malabsorption, tropical regions, abnormal flattening of villi, inflammation of lining of small intestine,

(typically 30 degrees north or south of equator)

149
Q

Celiac disease is associated with which rash?

A

dermatitis herpetiformis

150
Q

Carb malabsorption will present with?

A

frequent, loose, watery stool

151
Q

fat mal absorption

A

pale, foul smelling, bulky stool associated with flatus, bloating, weight loss, nutritional deficiency and fatigue

152
Q

Lactase

A

brush border enzyme that metabolizes lactose into glucose and galactose

153
Q

transiet lactose intolerance can occur after

A

acute gastroenteritis

154
Q

presentation of lactose intolerance

A

bloating, flatulence, cramping, watery diarrhea following milk ingestion

155
Q

hydrogen breath test shows ____ in lactose intolerant individuals

A

Increased hydrogen following ingestion of lactose

156
Q

Carcinoid syndrome

A

metastasis of carcinoid tumors- most commonly arise in ileum or appendix and produce serotonin.

157
Q

Why dont carcinoid tumors cause symptoms until they metastasize?

A

because serotonin secreted hormones go first pass through the liver.

158
Q

presentation of carcinoid tumor

A

cutaneous flushing, diarrhea, abd cramp, wheezing, right sided cardiac valve lesions

159
Q

patients with carcinoid syndrome develop _____ deficiency because tryptophan is metabolized into _______

A

niacin

serotonin

160
Q

Dx of carcinoid syndrome

A

high urine levels of 5-HIAA. CT and octreotide scans used to localize tumor

161
Q

Tx for carcinoid tumor

A

octreotide and surgical resection

162
Q

Classic presentation of Pellagra

A 
4 D's: 
Diarrhea
Dementia
Dermatitis 
Death
163
Q

Rome III diagnostic criteria

A

diagnosis of IBS:
At least 3 days in 3 months of episodic abd discomfort that is (1. relieved by defecation) 2. associated with change in stool frequency/consistency 3. associated with change in stool appearance

-exclude organic disorders with CBC, TSH, electrolytes, stool culture, abdominal film, barium contrast, colonoscopy with biopsy

164
Q

Increased incidence of ______ disease in IBS patients

165
Q

Partial SBO

A

continued flatus, no stool

166
Q

Obstipation

A

no flatus or stool. complete SBO

167
Q

most common cause of SBO in adults? kids?

A

adults: stricture/adhesions
kids: hernia

168
Q

presentation of SBO

A

crampy abd pain at 4-5 min intervals. vomiting. distension, tenderness, high pitched tinkles and peristaltic rushes- hyperactive BS on exam.

169
Q

Complications of SBO

A

ischemic necrosis, bowel rupture

170
Q

Fever, hypotension, rebound tenderness, tachy and history of SBO- worry about?

A

ischemic necrosis or bowel rupture

171
Q

Pellagra is deficiency in?

A

vitamin B3- niacin

172
Q

Why niacin deficiency with carcinoid syndrome?

A

Carcinoid tumors produce serotonin. Tryptophan is used to make serotonin and also niacin. So much tryptophan goes into serotonin production that niacin levels fall and cause the 4 D’s of pellagra.

173
Q

Gallstone ileus

A

form of SBO that occurs when gallstone lodges in ileocecal valve

174
Q

Diagnosis of SBO - INITIAL TEST

A

abd films showing stepladder pattern of dilated small bowel loops with air-fluid levels and small amount of gas in colon

175
Q

Definitive test for SBO?

A

CT of abdomen (evaluate for etiology of SBO)

176
Q

leukocytosis may be present with SBO if there is?

A

ischemia or necrosis of bowel

177
Q

Lab test with SBO often show

A

dehydration and metabolic alkalosis

178
Q

Lactic acidosis is a prognostic sign with SBO as it means?

A

ischemic bowel may be present

179
Q

Treatment of SBO

partial obstruction?
complete obstruction?

A
  1. give fluids
    partial: supportive care. NPO status, NG suction, IV hydration, correction of electrolytes, foley cath to monitor fluid status, pain management (avoid opioids and anticholinergics as they slow GI motility)
    complete: exploratory laparotomy indicated in compete SBO, ischemic necrosis, refractory SBO
180
Q

Ileus

A

loss of peristalsis without structural obstruction

181
Q

Risk factors for ileus

A

recent surgery/GI procedures, severe medical illness, immobility, hypokalemia, other electrolyte abnml, hypothyroid, DM, meds slowing GI

182
Q

presentation and PE for Ileus

A

constant abd discomfort, n/v, absence of gas and BM

Exam: hypoactive BS. diffuse tenderness, abd distension. rectal exam needed to rule out fecal impaction

183
Q

Dx of ileus

A

Distended loop of small and large bowel with air in colon and rectum (compared to SBO)

CT- definitive test

184
Q

Tx:

A

stop anti GI motility agents, bowel rest, NG suction/parenteral feeds as needed, hydrate and replete electrolytes as needed

185
Q

Mesenteric Ischemia most common causes

A
  1. embolism
  2. acute arterial occlusion from thrombosis
  3. atherosclerosis
  4. arterial vasospasm
  5. venous thrombosis
  6. shock
186
Q

Emboli as cause of Mes Isch

A

most common to come from heart (afib, stasis due to decreased EF are risk factors)

187
Q

Arterial occlusion from thrombosis as cause of Mes Isch most common to occur where? greatest risk factor?

A

occurs in proximal SMA

atherosclerosis

188
Q

presentation of mesenteric ischemia

A

severe abd pain out of proportion to physical exam (n/v/diarrhea/bloody stool) and prior episodes of abd pain post eating (intestinal angina)

189
Q

Diagnosis of mesenteric ischemia

initial test

A

CXR and CT- reveal bowel wall edema “THUMBPRINTING” and air within bowel wall “PNEUMATOSIS INTESTINALIS”

190
Q

Definitive test for diagnosis mes ischemia

A

Mesenteric/CT angiography: gold standard for diagnosis of arterial occlusive disease

191
Q

Conventional angio allow for ______ for mes ischemia

A

therapeutic intervention of thrombosis/embolism

192
Q 
Treatment of mes ischemia
for all: 
for acute thrombosis/embolism: 
for venous thrombosis: 
for infarcted bowel:
A

for all: fluid resuscitation, broad spectrum abx
acute thrombus/embolism: anticoag and laparotomy or angioplasty
venous thrombosis: anticoag
infarcted bowel: surg resection

193
Q

complications of mes ischemia

A

sepsis/shock, multisystem organ failure, death

194
Q

most common cause of acute lower GI bleeding in patients > 40 years of age?

A

Diverticulosis

195
Q

Diverticula

moist common where?

A

outpouching of mucosa and submucosa (FALSE diverticula)

Sigmoid colon

196
Q

diverticulitis

A

inflammation and generally microperf of diverticula 2ndary to a fecolith impaction

197
Q

should you perform sigmoidoscopy in initial stage of diverticulitis?

A

no! risk of perf

198
Q

iron def in elderly is ____ until proven otherwise

A

colon cancer

199
Q

compare SBO/LBO history

A

SBO-copious emesis!

LBO- pain less intense than SBO. less n/v than SBO but typically feculent

200
Q

compare exam SBO/LBO

A

Both: high-pitched tinkly bowel sounds
and later complete absence of BS

SBO: surgical scars/hernias

201
Q

etiology of SBO/LBO

A

SBO: hernia, adhesions from surg, volvulus, intussuception, gallstone ileus, foreign body, crohn, CF, hematoma, neoplasm

LBO: colon cancer!, diverticulitis, volvulus, fecal impactin, benign tumor (always assume colon cancer until proven otherwise)

202
Q

Ogilvie syndrome

A

pseudo-obstruction

203
Q

Water contrast enema should be done when?

A

to help diagnose LBO- if perf is suspected

204
Q

treatment for LBO

A

obstruction can be relieved with gastrografin enema, colonoscopy, rectal tube but surgery is usually required. ischemic colon requires partial colectomy with diverting colostomy.

205
Q

Patient found to have aortic endocarditis with strep bovis. what is next diagnostic step?

A

colonscopy! association between strep bovis and colon cancer.

206
Q

ulcerative colitis or crohn disease more likely to get colon cancer?

A

ulcerative colitis

207
Q

rank adenomatous polyps from most concerning to least

A

villious > tubular; sessile > pedunculated

208
Q

Treatment for colon cancer

A

surgical resection. adjuvant chemo when lymph node +

209
Q

how do you track colon cancer recurrence?

A

CEA levels, colonoscopy, LFTs, CXR, abdominal CT

210
Q

Ischemic colitis usually affects what location?

A

left colon. watershed area at splenic flexure

211
Q

risk factor for ischemic colitis?

A

atherosclerosis

212
Q

presentation of iscemic colitis

A

crampy lower abd pain followed by bloody diarrhea after meals or exertion in heat. fever and peritoneal signs suggest bowel necrosis

213
Q

Initial test for diagnosis of ischemic colitis

A

CT scan with contrast (thickened bowel wall and atherosclerosis0

214
Q

Colonscopy for ischemic colitis will show

A

pale bowel wall with petechial bleeding

215
Q

If first degree relative with colon cancer, how does screening change?

A

Colonscopy every 5 years starting at age 40 or every 5 years starting 10 year prior to affected family member at their time of diagnosis

216
Q

Screening for colon cancer if you have ulcerative colitis?

A

colonoscopy every 1-2 years starting 8-10 years after diagnosis

217
Q

Tx for ischemic colitis

A

supportive therapy with bowel rest, IV fluids, broad spectrum abx
surgical resection for infarction, fulminant colitis, obstruction

218
Q

One unit of packed RBCs increases Hgb by? Hct by?

A

Hgb by 1. Hct by 3-4.

219
Q

How to diagnose upper GI bleed?

A

NG tube and lavage (can be - in 15% upper GI bleeds)

endoscopy is definitive diagnosis

220
Q

How to diagnose lower GI bleed?

A

Rule out upper GI hemorrhage with NG lavage if brisk.
Anoscopy/Sigmoid for patients < 45 with small amount of bleeding
Colonscopy if stable
Ateriography or ex-lap if unstable

221
Q

Initial management of GI bleed

A

Protect airway (intubation may be needed), stabilize patient with IV fluids and packed RBCs (hct may be normal early on)

222
Q

Inguinal hernia

A

protrusion of abdominal contents (usually small I) into inguinal region through a weakness or defect in abdominal wall (direct or indirect)

223
Q

Direct hernias lie _____ and indirect hernias lie _____ to inferior epigastric vessels

A

MDs Dont LIE

224
Q

Hesselbach triangle is an area bounded by?

A

inguinal ligament, inferior epigastric artery, rectus abdominus

225
Q

Indirect hernia location

A

Lateral to epigastric vessels. through both external and internal rings.

226
Q

indirect hernia etiology

A

patent processus vaginalis

227
Q

what is more common- indirect or direct hernia?

228
Q

direct hernia location

A

medial to epigastric vessels. herniation through floor of hesselbach triangle

229
Q

etiology of direct hernia?

A

mechanical breakdown in transversalis fascia resulting from age

230
Q

femoral hernia location

A

herniation below inguinal ligament through femoral canal, below and lateral to pubic tubercle

231
Q

etiology of femoral hernia

A

increased intra abdominal pressure, weakened pelvic floor (more common in women)

232
Q

primary sclerosing cholangitis is associated with?

A

ulcerative colitis and crohns

233
Q

Pseudopolyps on colonscopy are found in?

A

ulcerative colitis

234
Q

diagnosis of chrons requires

A

upper GI series with small bowel follow through

235
Q

colonoscopy of crohns may show

A

stellate ulcers, strictures, “cobblestoning” and “skip lesions” and “creeping fat” during laparotomy

236
Q

Treatment for UC

A

5-ASA agents (sulfasalazine, mesalamine) topical or oral corticosteroid for flare ups
immunomodulators (azathioprine) or biologics (infliximab) for refractory or mod disase

237
Q

treatment for crohns

A

5 ASA agents (mesalamine sulfasalazine)
steroid for flare
biologics (infliximab)

238
Q

black pigmented gall stones result from

239
Q

brown pigmented gall stones result from

240
Q

most gallstones are precipitations of cholesterol and are not _______

A

radioopaque

241
Q

Labs in cholelithiasis

A

normal total bili, alk phos, serum amylase

242
Q

treatment for symptomatic cholelithiasis

A

elective cholecystecomy

243
Q

Labs in cholecystitis

A

increased WBC, normal t.bili, alk phos, amylase

244
Q

diagnosis of cholecystitis

A

US, HIDA scan

245
Q

If patient is too ill to undergo cholecystectomy when they have cholecystitis what do you do?

A

transcutaneous drainage of gall bladder

246
Q

cholelithiasis

A

transient stone in cystic duct

247
Q

cholecystitis

A

inflammation of gallbladder due to stone occluding cystic duct

248
Q

choledocholithiasis

A

stone in CBD (jaundice, RUQ pain)

249
Q

labs for choledocholithiasis

A

normal or increased WBC.
Increased t.bili
Increased alk phos
possible increased amylase/lipase

250
Q

cholangitis

A

infection of CBD usually due to stone in CBD

251
Q

Presentation of cholangitis

A

charcot triad: RUQ pain, fever, jaundice

Reynolds pentad: shock and altered mental status

252
Q

labs for cholangitis

A

increased WBC, total bili, alk phos

253
Q

diagnosis and management of cholangitis

A

clinical dilation confirmed by biliary dilation on imaging or ERCP (ERCP also therapeutic). surgery if patient toxic

254
Q

choledocolithiasis management

A

ERCP to remove stone followed by cholecystectomy.

255
Q

Findings on ultrasound to diagnose cholecystitis

A

Stone in gall bladder, bile sludge, pericholecystic fluid, thickened gall bladder wall, gas in wall of gall bladder, ultrasonic murphys sign

256
Q

When ultrasound is equivocal for cholecystitis next step?

257
Q

treatment for cholecystitis

A

broad spectrum antibiotics and IV fluids

cholecystectomy

258
Q

Treatment for acute cholangitis

A

patients often need ICU admission for monitoring, hydration, BP support, broad spec abx

259
Q

Patients with acute suppurative cholangitis require emergent _____

A

bile duct decompression via ERCP sphincterotomy, percutaneous transhepatic drainage, open decompression

260
Q

subacute SBO in elderly woman is classic for?

A

gallstone ileus

261
Q

CXR with characteristics of SBO and pneumobilia (gas in biliary tree) is specific for?

A

gallstone ileus

262
Q

In patients with gallstone ileus, upper GI barium contrast images will demonstrate _______

A

no contrast in the colon

263
Q

Tx of gallstone ileus

A

laparotomy with stone extraction. closure of fistula. cholecystectomy

264
Q

What percent of hep C patients will develop chronic Hep C?

265
Q

Most common causes of acute hepatitis?

A

HAV, HBV, HCV, HDV, HEV and drugs (alcohol, acetaminophen, INH, methyldopa)

266
Q

Fulminant hepatitis

A

Acute liver failure. Liver injury with INR > 1.5 and hepatic encephalopathy and patient has no signs of underlying chronic liver disease

267
Q

Most common causes of chronic hepatitis?

A

HCV, HBV (world-wide), alcohol, autoimmue, Wilson disease, Hemochromatosis, A1AT

268
Q

If you have increased alk phos and bili without ducatal dilation of CBD what should you think about?

A

intrahepatic cholestatsis due to medications, post-op complications, sepsis

269
Q

How does acute hepatitis initially present?

A

nonspecific viral prodrome (malaise, fever, joint pain, fatigue, URI, n/v, changes in bowels)

Next jaundice and RUQ tenderness

270
Q

Self-limited acute phase viral hepatitis?

A

HAV and HEV

271
Q

Presentation of chronic hepatitis

A

can be asymptomatic. may also cause fatigue and muscle/joint pain. jaundice and compications of portal htn (hepatic encephalopathy, ascites, esophageal varices)

272
Q

Diagnosis of acute hepatitis

A

Labs reveal markedly elevated ALT and AST and bili/alk phos

273
Q

Diagnosis of chronic hepatitis

A

ALT and AST are mildly elevated or can be normal low.

274
Q

What pathology should you think about with isolated unconjugated hyperbilirubinemia?

A

Overproduction- hemolytic anemia
Defective conjugation - Gilbert (<5)
Crigler-Najjar

275
Q

Pathology for elevated conjugated bili?

A

defective excretion from liver - Dubin Johnson and Rotor syndrome

276
Q

Transmission of HAV and HEV

A

fecal-oral

277
Q

Transmission of HBV, HCV, HDV

A

Body fluid

278
Q

Which hepatitis can cause a more severe co-infection with HBV? And is actually dependent on HBV surface antigens

279
Q

Which type of Hep has a high mortality rate in preg women and may become chronic in immunosuppressed patients?

280
Q

What type of Hep is most likely to lead to fulminant hepatic failure? What type of Hep is most likely to become chronic?

A

Hep B ; Hep C

281
Q

Diagnostic studies for work up of acute hepatitis?

A

Viral hep serologies
Autoimmune hepatitis
Hemochromatosis
Wilson disease

282
Q

Autoimmune hepatitis lab studies

A

(+ ANA and anti-smooth muscle antibodies (type 1). anti liver-kidney microsomal-1 antibodies and anti liver cytosol antibodies (type 2). also elevated serum IgG and p-ANCA

283
Q

Hemochromotosis labs will show

A

elevated ferritin and transferrin saturation > 50%. Liver biopsy with high hepatic iron index.

284
Q

Wilson disease

A

decrease ceruplasmin, increase urine copper, keyser-fleischer rings. liver biopsy if uncertain about diagnosis

285
Q

Sequela of chronic hep?

A

cirrhosis, portal htn, liver failure, hepatocellular carcinoma

286
Q

treatment of acute hep B

A

generally supportive. may require antivirals

287
Q

Chronic hepatitis treatment of HBV

A

Tenofovir and entecavir

288
Q

Chronic HCV treatment

A

meds and treatment vary based on genotype, cirrhosis status, history of prior treatment

(either 2 direct acting antivirals or 1 DAA plus ribavirin) Interferon is used occasionally.

289
Q

Definitive treatment for patients with end stage liver failure?

A

Liver transplant

290
Q

Cirrhosis

A

bridging fibrosis and nodular regeneration resulting from chronic hepatic injury

291
Q

most common causes of liver cirrhosis?

A

alcohol, chronic HCV, non-alcoholic steatohepatitis (causes can be intrahepatic or extrahepatic)

292
Q

Extrahepatic causes of cirrhosis

A

biliary tract disease (primary biliary cirrhosis, primary sclerosing cholangitis)

293
Q

posthepatic causes of cirrhosis

A

right sided heart failure, constrictive pericarditis, budd chiari syndrome

294
Q

budd chiari syndrome

A

hepatic vein thrombosis 2ndary to hypercoagulability

295
Q

How is SBP diagnosed?

A

> 250 PMNs in ascitic fluid

296
Q

Diagnosis of cirrhosis

A

synthetic dysfunction tests: decreased albumin, elevated PT/INR, elevated bili
portal htn: thrombocytopenia (2ndary to hypersplenism sequestration in liver and decreased thrombopoetin production), varices, ascites (paracentesis)

297
Q

Definitive test for cirrhosis?

A

biopsy showing bridging fibrosis and nodular regeneration

298
Q

How do you determine the etiology of ascites?

A

SAAG = serum albumin - ascites albumin

299
Q

Etiologies for SAAG > 1.1

A

Portal htn:
Presinusoidal: splenic or portal vein thrombosis, schistosomiasis, mass effect.
Sinusoidal: cirrhosis
Postsinusoidal: RHF, budd-chiari, constrictive pericarditis

300
Q

Etilogies for SAAG < 1.1

A

Nephrotic syndrome
TB
Malignancy (ovarian cancer)

301
Q

Presentation and treatment of SBP

A

fever, abd pain, chills, nausea, vomiting

tx: IV abx (3rd gen cephalosporin)
IV albumin, prophylaxis with fluoroquinolone to prevent recurrence. SBP- poor 1 year prognosis

302
Q

hepatorenal syndrome

A

acute prerenal failure in setting of severe liver disease. due to splanchinic vasodilation and reduced blood flow to kidneys. Urine Na will be less than 10mEq/L

303
Q

Treatment for hepatorenal syndrome?

A

trial of volume repletion and rule out other causes of renal failure. can use octreotide to decrease splanchnic vasodilation and midodrine to increase blood pressure. may need dialysis. poor prognosis. liver transplant is curative

304
Q

Surveillance and treatment of esophageal varices

A

EGD surveillance in cirrhosis patients
Med prophylaxis with B-blockers or endoscopic band ligation

for acute bleeding: EGD with band ligation or sclerotherapy. Urgent TIPS procedure if refractory

305
Q

For acute bleeding due to coagulopathy what should you give?

306
Q

Will vit K correct coagulopathy?

307
Q

Primary sclerosing cholangitis is strongly associated with?

A

Ulcerative colitis

308
Q

primary sclerosing cholangitis

A

idiopathic disorder- progressive inflammation and fibrosis strictures of extrahepatic and intrahepatic bile ducts. usually presents in young men with UC

309
Q

Primary sclerosing cholangitis patients are at increased risk for?

A

cholangiocarcinoma

310
Q

How do patients with primary sclerosing cholangitis present?

A

Jaundice, prutitis, fatigue

311
Q

diagnosis of primary sclerosing cholangitis?

A

Alk phos, bili elevated. MRCP/ERCP shows bile duct strictures and dilatations “beads on a string”

312
Q

Liver biopsy of primary sclerosing cholangitis reveals?

A

“onion skinning”

313
Q

all newly diagnosed primary sclerosing cholagitis patients should have what other test?

A

colonoscopy to assess for IBD

314
Q

treatment for PSC

A

dilation and stenting of biliary strictures with ERCP

Liver transplant is definitive treatment

315
Q

Primary biliary cirrhosis. presents in?

A

autoimmune disease characterized by destruction of intrahepatic bile ducts. most commonly found in middle-aged women with other autoimmune conditions

316
Q

how do patients with PBC present?

A

progressive jaundice, pruritis, fat soluble vitamin deficiencies (ADEK)

317
Q

Diagnosis of PBC

A

Lab: elevated alk phos, elevated bili, + antimitochondrial antibody, elevated cholesterol

318
Q

Tx of PBC:

A

Ursodeoxycholic acid (slow progression of disease)

Cholestyramine for pruritis

liver transplant- definitive

319
Q

PBC affects _____ ducts while PSC affects _____ and ______ ducts.

A

Intrahepatic ;

Intra and extra hepatic

320
Q

Non-alcoholic fatty liver disease

A

steatosis of hepatocytes -> can progress to NASH -> liver fibrosis -> cirrhosis

321
Q

Non-alc fatty liver disease is associated with?

A

Insulin resistance, metabolic syndrome

322
Q

Tx for non-alc fatty liver?

A

weight loss, diet, exercise.

NASH: vitamin E and pioglitazone

323
Q

Hepatocellular carcinoma Incidence

Risk factors in US/ Worldwide

A

One of most common cancers worldwide. Low incidence in US.

U.S risk factors: cirrhosis (alc, HCV, NASH) and chronic hep B even without cirrhosis.

WW: HBV and aflatoxins (in food sources)

324
Q

Presentation of patients with hepatocellular carcinoma?

A

RUQ tenderness, abd distension, jaundice, easy bruisability, coagulopathy, enlargement of liver

325
Q

Dx of hepatocellular carcinoma

A

mass on US or CT, abnml LFTs, significantly elevated AFP. Biopsy needed if uncertain about diagnosis.

326
Q

Tx for hepatocellular carcinoma

A

Surgical: partial hepatectomy. orthotopic (liver removed and transplant placed in same place in body) liver transplant if only a few small tumors

327
Q

Milan criteria

A

help decide treatment for hepatocellular carcinoma (single lesion <5cm or 3 lesions less than 3cm) - can perform orthotopic transplant

328
Q

hemochromatosis

A

iron overload. hemosiderin accumulates in liver, pancreas islet cells, heart, adrenals, testes, pituitary.

329
Q

primary hemochromatosis vs 2ndary

A

1: autosomal recessive disease characterized by mutations in HFE gene- result in excessive absorption of iron
2: patients receiving chronic transfusion therapy (sickle cell disease or alpha thalassemia)

330
Q

how might patients with hemochromatosis present?

A

abd pain, DM, hypogonadism, arthropathy of MCP joints, heart failure, impotence, cirrhisis, bronze skin pigmentation, CHF, hepatomegaly, testicle atrophy

331
Q

dx of hemochromatosis:

A

increase serum iron, percent saturation of iron and ferritin
decreased transferrin

liver biopsy, MRI, HFE genetic mutation screen

332
Q

A transferrin saturation (serum iron / TIBC) > 45% is suggestive of?

A

iron overload

333
Q

Tx hemochromatosis

A

weekly phlebotomy to normalize serum iron. Then maintenance phlebotomy every 2-4 months

Deferoxamine- iron chelating agent

334
Q

Deferoxamine

A

iron chelating agent useful for iron toxicity or hemochromatosis

335
Q

Wilson disease

A

AR disorder. defective Cu transport. Accumulation of Cu in Liver and brain. Occurs in patients < 30 yoa. 50% symptomatic by 15.

336
Q

Presentation of wilson disease

A

hepatitis/cirrhosis, neuro dysfunction (ataxia, tremor), psych abnormalities (psychosis, anxiety, depression, maina)

337
Q

PE of wilson disease

A

kayser-fleischer rings, jaundice, hepatomegaly, asterixis, choreiform movements, rigidity

338
Q

Dx of wilson disease

A

Liver biopsy for uncertain diagnosis. low ceruloplasmin. elevated 24 hour urine Cu excretion.

339
Q

Tx: wilson disease

A

penicillamine or trientine (copper chelators that increase urinary copper excretion)

dietary copper restriction: no shellfish, liver, legumes

340
Q

hallmark finding in pancreatic cancer

A

non-tender, palpable gall bladder with jaundice

341
Q

Insulinoma is associated with?

A

MEN type 1

342
Q

hx of patient with insulinoma

A

hypoglycemia satisfying Whipple Triad

  1. hypoglycemia on venipuncture
  2. ass symp- sweating, palpitations, anxiety, tremor, HA, confusion
  3. resolution of symp w/ correction of hypoglycemia
343
Q

Dx of insulinoma

A

lab: elevated fasting serum insulin. elevated c-peptide

344
Q

definitve test for insulinoma

A

72 hour fasting (profound or symptomatic hypoglycemia after fast)

345
Q

What screen should you always do in patients presenting with hypoglycemia?

A

sulfonyurea abuse check

346
Q

VIPoma

A

highly malignant tumors

watery diarrhea, dehydration, muscle weakness, flushing

347
Q

dx VIPoma

A

stool sample: low stool osmotic gap (secretory diarrhea)
Lab: high VIP, achlorhydria (gastrin inhibited by VIP), hyperglycemia, hypercacemia, hypokalemia
CT: localize tumor

348
Q

Pancreatic cancer- most common type? most common location?

A

75% are adenocarcinoma in head of pancreas

349
Q

risk factors for pancreatic cancer

A

smoking, chronic pancreatitis, first degree relative with panc cancer

350
Q

presentation of panc cancer

A

abd pain radiating to back, obstructive jaundice, loss of appetite, n/v, weight loss, weakness, fatigue

usually asymptomatic so presents late in disease course

351
Q

Courvoisier sign

A

non-tender palpable gallbladder- PANC CANCER

352
Q

Trousseau sign

A

migratory thrombophlebitis

353
Q

Diagnosis panc cancer

A

CT scan with contrast.

Endoscopic ultrasound plus/minus ERCP if nothing seen on CT

354
Q

Tumor marker for pancreatic cancer that is neither sensitive nor specific?

355
Q

Grey Turner Sign

A

Flank bruising indicative of acute pancreatitis

356
Q

Cullen Sign

A

periumbilical discoloration indicative of acute pancreatitis

357
Q

Diagnosis of acute pancreatitis

A

elevated lipase, amylase. decreased calcium if severe.

358
Q

“sentinel loop” or “colon cutoff sign”

A

signs on CXR- indicative of acute panc

359
Q

Ranson criteria

A

predict mortality secondary to acute pancreatitis

Step 2 CK (26 decks)

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