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M.T.B > Internal Med- Gastroenterology > Flashcards

Internal Med- Gastroenterology Flashcards

1
Q

What is a Hiatal Hernia?

A

Hiatal hernia is a protrusion on the upper part of the stomach into the chest, generally caused by obesity weakening the diaphragm.

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2
Q

What is the best way to Dx a Hiatal Hernia?

A

endoscopy or barium studies

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3
Q

What is the best initial therapy for a Hiatal Hernia?

A

Weight loss and PPIs

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4
Q

What are some of the alarm symptoms indicating endoscopy?

A

Weight loss
Blood in stool
Anemia

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5
Q

What is Achalasia?

A

is the inability of the lower esophageal sphincter (LES) to relax due to a loss of the nerve plexus within the lower esophagus.

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6
Q

What clinical picture would make Achalasia the most likely diagnosis?

A

Progressive dysphagia to both solids and liquids at the same time

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7
Q

What is the best initial test for Achalasia?

What is the most accurate test?

A

Barium esophagram will show a “bird’s beak” as the esophagus comes down to a point.

Manometry is the “most accurate test” and will show a failure of the lower
esophageal sphincter to relax.

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8
Q

What are some of the ways that Achalasia can be Mgx?

A
  1. Pneumatic dilation
  2. Surgical sectioning / myotomy
  3. Botulinum toxin injection (effects will wear off in about 3 to 6 months, requiring reinjection)
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9
Q

What set of clinival features would make Esophageal Cancer the most likely Dx?

A
  • Age 50 or older.
  • Dysphagia first for solids, followed later (progressing) to dysphagia for liquids.
  • Association with prolonged alcohol and tobacco use.
  • More than 5–10 years of GERD symptoms.
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10
Q

What is the best initial test when suspecting esophageal cancer?

What is the most accurate

A

Barium swallow

Biopsy (through Endoscopy)

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11
Q

What is the main use of a PET Scan?

A

It is often used to determine whether a cancer is resectable. Local disease is resectable, and widely metastatic disease is not.

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12
Q

How is esophageal cancer Mgx?

A
  1. No resection = no cure. Surgical resection is always the thing to try.
  2. Chemotherapy and radiation are used in addition to surgical removal.
  3. Stent placement is used for lesions that cannot be resected surgically just to keep the esophagus open for palliation and to improve dysphagia.
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13
Q

What are the 2 main forms of Esophageal Spasm?

What is the clinical difference between them?

A

Diffuse esophageal spasm (DES) and nutcracker esophagus

They are clinically indistinguishable. Both present with the sudden onset of chest pain that is not related to exertion.

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14
Q

What can precipitate Esophageal Spasm?

A

Drinking cold liquids

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15
Q

How can you distinguish between Diffuse esophageal spasm (DES) and nutcracker esophagus?

A

manometry- will show a different pattern of abnormal contraction in each of them.

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16
Q

How would you Mgx Esophageal Spasm?

A

calcium channel blockers and nitrates.

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17
Q

What is the relationship between Esophageal Spasm and Prinzmetal Angina in terms of Tx?

A

The Tx is similar

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18
Q

What clinical picture would make Eosinophilic Esophagitis the most likely Dx?

A

Swallowing difficulty, food impaction, and heartburn + a history of asthma and allergic diseases.

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19
Q

What is the best initial test for Eosinophilic Esophagitis?

What is the most accurate?

A

Endoscopy- showing multiple concentric rings.

A biopsy finding eosinophils

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20
Q

A 43-year-old man recently diagnosed with AIDS comes to the emergency department with pain on swallowing that has become progressively worse over the last several weeks. There is no pain when not swallowing. His CD4 count is 43 mm3. The patient is not currently taking any medications.

What is the most appropriate next step in management?

a. Esophagram.
b. Upper endoscopy.
c. Oral nystatin swish and swallow.
d. Intravenous amphotericin.
e. Oral fluconazole.

A

Oral candidiasis (thrush) need not be present in esophageal candidiasis. One does not automatically follow from the other. Although other infections such as CMV and herpes can also cause esophageal infection, over 90% of esophageal infections in patients with AIDS are caused by Candida. Empiric therapy with fluconazole is the best course of action. If fluconazole does not improve symptoms, then endoscopy is performed. Intravenous amphotericin is used for confirmed candidiasis not responding to fluconazole. Oral nystatin swish and swallow is not sufficient to control esophageal candidiasis. Nystatin treats oral candidiasis.

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21
Q

If a Pt presents with dysphagia and HIV CD4 <100, What is the next best step?

A

Empirically start with Fluconazole for candida.

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22
Q

If a Pt presents with dysphagia and HIV CD4 <100 and fails to respond to empirical therapy with Fluconazole What is the next best step?

A

Perform upper endoscopy;
1) If Large ulcerations=> CMV- Ganciclovir or Foscarnet

2) If Small ulcerations=> HSV- Acyclovir

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23
Q

What is the common factor between Schatzki ring and Plummer-Vinson syndrome?

A

Both give dysphagia.

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24
Q

What is Schatzki ring?

A

This is a type tightening (also called peptic stricture) of the distal esophagus (squamocolumnar junction).

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25
Q

What is the best initial diagnostic test for Schatzki ring?

A

Barium swallow

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26
Q

What is the best initial Tx for Schatzki ring?

A

Bougie dilator/ Ballon dilation + a PPI

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27
Q

What clinical features would make Plummer-Vinson syndrome the most likely Dx?

A

A triad of Dysphagia, Upper esophageal webs and Fe-deficiency anemia.

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28
Q

Between Pts with Schatzki ring and Pts with Plummer-Vinson syndrome, which group will have an increased risk of developing squamous cell carcinoma?

A

Plummer-Vinson syndrome Pts

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29
Q

Between Pts with Schatzki ring and Pts with Plummer-Vinson syndrome, which group is associated with acid reflux and hiatal hernia?

A

Schatzki ring Pts

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30
Q

What is Steakhouse syndrome?

A

Dysphagia from solid food associated with

Schatzki ring

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31
Q

What is Zenker Diverticulum?

A

It is an outpocketing of the posterior pharyngeal constrictor muscles.

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32
Q

What are some of the clinical features of Zenkers Diverticulum?

A

Dysphagia, severe halitosis, and regurgitation of food particles. Some
patients suffer from aspiration pneumonia

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33
Q

What is the best initial Dx test for Zenkers Diverticulum?

A

Barium swallow (lateral projection- dorsal protruding pouch at level C5/C6

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34
Q

What is the best initial Tx test for Zenkers Diverticulum?

A

Surgery. There is no medical therapy.

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35
Q

Which 2 procedures are contraindicated in Zenkers Diverticulum? Why?

A

Nasogastric tube placement and Upper endoscopy.

They may cause perforation

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36
Q

When would Scleroderma be the likely cause of reflux?

A

A patient who presents with symptoms of reflux and have a clear history of scleroderma, or progressive systemic sclerosis.

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37
Q

What would be the best initial Dx test to show that reflux in a Pt is caused by Scleroderma?

A

Manometry would show decreased lower esophageal sphincter pressure from an inability to close the LES.

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38
Q

How would you Mgx reflux in a Pt caused by Scleroderma?

A

PPIs as it would be for any person with reflux symptoms

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39
Q

What clinical scenario would make a Mallory-Weiss Tear the most likely Dx?

A

Upper gastrointestinal bleeding after prolonged or severe vomiting or retching. Repeated retching is followed by hematemesis of bright red blood, or by black stool.

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40
Q

How would you Mgx a Pt with a Mallory-Weiss Tear?

A

There is no specific therapy, and it will resolve spontaneously. Severe cases with persistent bleeding are managed with an injection of epinephrine to stop bleeding or the use of electrocautery.

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41
Q

What is the difference between Boerhaave syndrome and a Mallory-Weiss Tear?

A

Boerhaave syndrome is full penetration of the esophagus.

Mallory-Weiss is a nonpenetrating tear of only the mucosa.

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42
Q

A 44-year-old woman comes to see you because of pain in her epigastric area for the last several months. She denies nausea, vomiting, weight loss, or blood in her stool. On physical examination, you find no abnormalities.

What is the most likely diagnosis?

a. Duodenal ulcer disease.
b. Gastric ulcer disease.
c. Gastritis.
d. Pancreatitis.
e. Non-ulcer dyspepsia.
f. Pancreatic cancer.

A

E. This is often a very hard question for the average medical student. This is because of the selection bias of which cases you, as a student, see admitted to the hospital. Non-ulcer dyspepsia is, by far, the most common cause of epigastric pain and at a minimum accounts for 50% to 90% of all cases of epigastric pain. This is particularly true in patients under the age of 50.
In the hospital, you will see far more patients with ulcer disease, pancreatic disorders, or cancer because those are the ones who are admitted. Non-ulcer dyspepsia is virtually never a reason to be admitted to hospital.

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43
Q

What would be the most likely Dx in a Pt with epigastric pain presenting with one of the following;

  1. Pain worse with food
  2. Pain better with food
  3. Weight loss
  4. Tenderness
A
  1. Gastric ulcer
  2. Duodenal ulcer
  3. Cancer, gastric ulcer
  4. Pancreatitis
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44
Q

What would be the most likely Dx in a Pt with epigastric pain presenting with one of the following;

  1. Bad taste, cough, hoarse
  2. Diabetes, bloating
  3. Nothing
A
  1. Gastroesophageal reflux
  2. Gastroparesis
  3. Non-ulcer dyspepsia
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45
Q

Which diagnostic test would help best understand the etiology of epigastric pain from ulcer disease?

A

Endoscopy

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46
Q

What could be some of the causes of Right Upper Quadrant (RUQ) pain?

A

Cholecystitis
Biliary colic
Cholangitis
Perforated duodenal ulcer

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47
Q

What could be some of the causes of Left Upper Quadrant (LUQ) pain?

A

Splenic rupture

Splenic flexure syndrome

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48
Q

What could be some of the causes of Right Lower Quadrant (RLQ) pain?

A

Appendicitis
Ovarian torsion
Ectopic Pregnancy
Cecal diverticulitis

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49
Q

What could be some of the causes of Left Lower Quadrant (LLQ) pain?

A

Sigmoid volvulus
Sigmoid diverticulitis
Ovarian torsion
Ectopic Pregnancy

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50
Q

What could be some of the causes of Midepigastrium pain?

A

Pancreatitis
Aortic dissection
Peptic ulcer disease

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51
Q

What is the best initial empiric therapy for epigastric pain? What other medications can be used?

A 
Proton pump inhibitors (PPIs) are always a good place to start in the therapy of epigastric pain. There is no difference in the efficacy of different PPIs.
H2 blockers (ranitidine, nizatidine, cimetidine, famotidine) are not as effective, but will work in about 70% of patients. Liquid antacids have roughly the same efficacy as H2 blockers.
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52
Q

What clinical features will make GERD the most likely Dx?

A
  • Epigastric burning pain
  • Sore throat
  • Bad taste in the mouth (metallic)
  • Hoarseness
  • Cough
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53
Q

A 42-year-old man comes to the office with several weeks of epigastric pain radiating up under his chest which becomes worse after lying flat for an hour. He also has a “brackish” taste in his mouth and a sore throat.

What is the most appropriate next step in the management of this patient?

a. Ranitidine.
b. Liquid antacid.
c. Lansoprazole.
d. Endoscopy.
e. Barium swallow.
f. 24-hour pH monitoring.

A

*C.
Lansoprazole is a PPI that should be used to control the symptoms of GERD. When the diagnosis is very clear (such as in this case), with epigastric pain going under the sternum, bad taste, and sore throat, confirmatory testing is not necessary. H2 blockers such as ranitidine are effective in about 70% of patients, but are clearly inferior to PPIs. Endoscopy does not diagnose GERD and is certainly not necessary when the diagnosis is so clear. Barium swallow shows major anatomic abnormalities of the esophagus and is worthless in GERD.

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54
Q

When is a 24-hour pH monitor indicated in GERD?

A

Pt with an unclear Dx

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55
Q

How would you Mgx GERD?

A

Lifestyle modifications + :

1) Mild or Intermittent Symptoms- liquid antacids or H2 blockers.
2) Persistent Symptoms or Erosive Esophagitis- PPIs

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56
Q

When is surgery indicated in GERD and what types of surgical interventions can be performed in GERD?

A

Patients who do not respond to medical therapy.

  1. Nissen fundoplication: wrapping the stomach around the lower esophageal sphincter
  2. Endocinch: using a scope to place a suture around the LES to tighten it
  3. Local heat or radiation of LES: causes scarring
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57
Q

Briefly explain how Barrett Esophagus occurs

A

Long-standing GERD leads to histologic changes in the lower esophagus with columnar metaplasia. Columnar metaplasia usually needs at least 5 years of reflux to develop.

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58
Q

How is Barrett Esophagus Dx?

Why is this diagnostic measure indispensable?

A

Endoscopic biopsy

This is indispensable because the biopsy drives therapy

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59
Q

How is Barrett Esophagus Mgx according to the biopsy findings?

A

1) Metaplasia- PPIs and rescope every 2–3 years
2) Low-grade
dysplasia- PPIs and rescope every 6–12 months
3) High-grade
dysplasia- Ablation with endoscopy: photodynamic therapy, radiofrequency ablation, endoscopic mucosal resection

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60
Q

Which clinical features and history findings will make Gastritis the most likely Dx?

A

Gastrointestinal bleeding without pain. Pain if severe erosive gastritis.
NSAIDs or alcoholism in the history

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61
Q

What on the CBC can indicate Atrophic Gastritis?

A

Anemia (Vitamin B12 deficiency)

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62
Q

How is Gastritis Dx?

A

Upper endoscopy

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63
Q

What is the next best step after Dx Gastritis?

A

Testing for Helicobacter pylori

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64
Q

When testing for H.pylori, what is(are) the main advantage(s) and disadvantage(s) of:

1) Endoscopic biopsy
2) Serology

A

1) Adv: The most accurate of all the tests
Dis: Requires an invasive procedure such as endoscopy

2) Adv: Inexpensive, easily excludes infection if it is negative; no complications or
procedures required
Dis: Lacks specificity; a positive test does not easily tell the difference between current and previous infection

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65
Q

When testing for H.pylori, what is(are) the main advantage(s) and disadvantage(s) of:

1) Urea C13 or C14 breath testing
2) H. pylori stool antigen

A

1) Adv: Positive only in active infection; noninvasive
Dis: Requires expensive equipment in office

2) Adv: Positive only in active infection; noninvasive
Dis: Requires stool sample

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66
Q

What are the indications for stress ulcer prophylaxis?

A

Mechanical ventilation
Burns
Head trauma
Coagulopathy

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67
Q

What is peptic ulcer disease (PUD)?

A

The term peptic ulcer disease (PUD) refers to both duodenal ulcer and gastric ulcer disease.
The name is a misnomer based on the mistaken belief that they were caused by the protein-digesting enzyme pepsin.

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68
Q

What are the 2 most common etiologies of peptic ulcer disease (PUD)?

A

PUD is most commonly caused by Helicobacter pylori. NSAIDs are the second most common cause.
NSAIDs inhibit prostaglandins and prostaglandins produce the mucus.

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69
Q

What is the relationship between peptic ulcer disease (PUD) and eating?

A

Duodenal ulcer (DU) disease is more often improved with eating, whereas gastric ulcer (GU) disease is more often worsened by eating. Hence, GU is associated with weight loss.

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70
Q

What are the chances of a Pt having gastric cancer in a Pt with a Gastric ulcer (GU) or Duodenal ulcer (DU)?

A

Cancer is present in 4% of those with GU but in none of those with DU.

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71
Q

What the best initial therapy for peptic ulcer disease (PUD)?

A

a PPI combined with clarithromycin and

amoxicillin.

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72
Q

Which drugs can be used in peptic ulcer disease (PUD) if the Pt does not respond to the Tx?

A

Metronidazole and Tetracycline can be used as alternate antibiotics. Adding Bismuth to a change of antibiotics may aid in resolution of treatment-resistant ulcers.

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73
Q

After how long and how can we test if the therapy has cured H. pylori in peptic ulcer disease (PUD)?

A

30-60days post-therapy.

Retest with stool antigen or breath test

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74
Q

A 56-year-old woman comes to the clinic because her symptoms of epigastric pain from an endoscopically confirmed duodenal ulcer that has not responded to several weeks of a PPI, clarithromycin, and amoxicillin.

What is the most appropriate next step in the management of this patient?

a. Refer for surgery.
b. Switch the PPI to ranitidine.
c. Abdominal CT scan.
d. Capsule endoscopy.
e. Urea breath testing.
f. Vagotomy.
g. Add sucralfate.

A

*E.
If there is no response to DU therapy with PPIs, clarithromycin, and amoxicillin, the first thought should be antibiotic resistance of the organism. Persistent H. pylori infection can be detected with several methods such as urea breath testing, stool antigen detection, or a repeat endoscopy for biopsy. It would be very hard to choose between these, and that is why they are not all given as choices in this question
Capsule endoscopy cannot detect H. pylori. Vagotomy and surgery were done more frequently in the past before we knew that H. pylori was the cause of most ulcers and we did not routinely eradicate it. H2 blockers and sucralfate add nothing to a PPI and have less efficacy, not more

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75
Q

What is the most common cause of epigastric pain?

A

Non-Ulcer Dyspepsia (NUD)

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76
Q

How is the age of the patient important when considering the next best step in a Pt you suspect to have Non-Ulcer Dyspepsia (NUD)?

A

If the patient is under 45 years old, treat empirically with antisecretory therapy such as PPIs and scope only if symptoms do not resolve.
For those over 55, endoscopy is definitely indicated to exclude cancer.
If “Alarm” symptoms are present (dysphagia, weight loss, anemia), scope

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77
Q

What features of the ulcers would make a Gastrinoma (Zollinger-Ellison Syndrome) the most likely diagnosis?

A 
A patient with ulcers that are:
Large (>1–2 cm)
Recurrent after Helicobacter eradication
Distal in the duodenum
Multiple
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78
Q

Why are Gastronomas often associated with diarrhea?

A

Acid Inactivates lipase.

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79
Q

How is a Gastrinoma (Zollinger-Ellison Syndrome) Dx?

A

After endoscopy confirms the presence of an ulcer, the most accurate diagnostic test is:
High gastrin levels despite antisecretory therapy (PPIs or H2 blockers) with high gastric acidity.
Or, Persistent high gastrin levels despite injecting secretin

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80
Q

What in the chemical metabolic profile will make multiple endocrine neoplasia from
hyperparathyroidism the most likely diagnosis?

A

Hypercalcemia

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81
Q

Once a gastrinoma is confirmed, what is the next best step?

A

Exclude metastatic disease with CT and or MRI (though not very accurate).
Somatostatin receptor scintigraphy (nuclear octreotide scan) is combined with endoscopic ultrasound to exclude metastatic disease if the CT and MRI are normal.

82
Q

How is a Gastrinoma (Zollinger-Ellison Syndrome) Mgx?

A

Local disease is removed surgically.

Metastatic disease is unresectable and is Tx with lifelong PPIs to block acid production.

83
Q

Describe Diabetic Gastroparesis

A

Gastroparesis is an autonomic neuropathy leading to dysmotility. Dysmotility is from the inability to sense stretch in the GI tract.

84
Q

What clinical features would make Diabetic Gastroparesis the most likely Dx?

A

A diabetic patient with chronic abdominal discomfort, “bloating,” and constipation.

There is also anorexia, nausea, vomiting, and early satiety.

85
Q

A 64-year-old patient with diabetes for 20 years comes to the office with several months of abdominal fullness, intermittent nausea, constipation, and a sense of “bloating.” On physical examination, a “splash” is heard over the stomach on auscultation of the
stomach when moving the patient.

What is the most appropriate next step in the management of this patient?

a. Abdominal CT scan.
b. Colonoscopy.
c. Erythromycin.
d. Upper endoscopy.
e. Nuclear gastric emptying study.

A

*C.
When the diagnosis of diabetic gastroparesis seems clear, there is no need to do diagnostic testing unless there is a failure of therapy. Erythromycin and metoclopramide increase gastrointestinal motility. The most accurate test for diabetic gastroparesis is the nuclear gastric emptying study, although it is rarely needed.

86
Q

A 69-year-old woman comes to the emergency department with multiple red/black stools over the last day. Her past medical history is significant for aortic stenosis. Her pulse is 115 per minute and her blood pressure is 94/62 mm Hg. The physical examination is otherwise normal.

What is the most appropriate next step in the management of this patient?

a. Colonoscopy.
b. Nasogastric tube placement.
c. Upper endoscopy.
d. Bolus of normal saline.
e. CBC.
f. Bolus of 5% dextrose in water.
g. Consult gastroenterology.
h. Check for orthostasis.

A

*D.
The precise etiology of severe GI bleeding is not as important as a fluid resuscitation. There is no point in checking for orthostasis with the person’s systolic blood pressure under 100 mm Hg or when there is a tachycardia at rest. Endoscopy should be performed, but it is not as important to do first as fluid resuscitation. When blood pressure is low, normal saline (NS) or Ringer lactate are better fluids to give than 5% dextrose in water (D5W). D5W does not stay in the vascular space to raise blood pressure as well as NS.

87
Q

What are some of the causes of upper GI bleeding? What is the most common cause?

A

ulcer disease is the most common, but it can also be caused by: gastritis, esophagitis, duodenitis, cancer, and varices.

88
Q

What are some of the causes of lower GI bleeding? What is the most common cause?

A

diverticulosis is the most common, but it can also be caused by:
Angiodysplasia (arteriovenous malformation, or AVM)
Polyps or cancer
Inflammatory bowel disease
Hemorrhoids
Upper GI bleeding with rapid transit due to high volume

89
Q

What is the best initial step when suspecting GI bleed?

A

Assessing blood pressure

90
Q

How would you define Orthostasis?

A

More than a 10-point rise in pulse when going from lying down to sitting or standing up

or

Systolic blood pressure drop of 20 points or more when sitting up

91
Q

In acute bleeding or severe bleeding, what is the order of Mgx?

A

it is far more important to replace fluids and check the hematocrit, platelet count, and coagulation tests such as the prothrombin time (PT) or INR than it is to do an endoscopy.

92
Q

Why do we do fluid

resuscitation first instead of trying to stop the GI bleed?

A

Eighty percent of GI bleeding will stop spontaneously if the fluid resuscitation is adequate. Most patients die of inadequate fluid replacement.

93
Q

What are some of the other (3) diagnostic tests for GI Bleeding and what are their indications?

A

1) Nuclear bleeding scan- Endoscopy unrevealing in a massive acute hemorrhage; lacks accuracy
2) Angiography- Specific vessel or site of bleeding needs to be identified prior to surgery or embolization of the vessel; used only in massive, nonresponsive bleeding
3) Capsule endoscopy- Small bowel bleeding; upper and lower endoscopy do not show the etiology

94
Q

What are the 8 different ways of Mgx GI Bleeds?

A
  1. Fluid replacement with high volumes (1 to 2 liters an hour) of saline or Ringer lactate in those with acute, severe bleeding.
  2. Packed red blood cells if the hematocrit is below 30 in those who are older or suffer from coronary artery disease; if the patient is young, transfusion may not be needed until the hematocrit is very low (under 20-25).
  3. Fresh frozen plasma if the PT or INR is elevated and active bleeding is occurring.
  4. Platelets if the count is below 50,000 and there is bleeding.
  5. Octreotide for variceal bleeding.
  6. Endoscopy to determine the diagnosis and administer some treatment (band varices, cauterize ulcers, inject epinephrine into bleeding gastric vessels).
  7. IV PPI for upper GI bleeding.
  8. Surgery to remove the site of bleeding if fluids, blood, platelets, and plasma will not control the bleeding.
95
Q

If Platelets are transfused when the count is under 50,000/μl when there is active bleeding, is it possible to transfuse platelets to prevent a spontaneous bleed?

A

Yes, if the count is much lower (below 10,000–20,000).

96
Q

In case of Esophageal and Gastric Varices, what do you do in addition to fluids, blood, platelets, plasma?

A
  1. Octreotide (somatostatin) decreases portal pressure.
  2. Banding performed by endoscopy obliterates esophageal varices.
  3. Transjugular intrahepatic portosystemic shunting (TIPS) is used to decrease portal pressure in those who are not controlled by octreotide and banding.
  4. Propranolol or nadolol is used to prevent subsequent episodes of bleeding. Beta blockers such as propranolol will not do anything for the current episode of bleeding.
  5. Antibiotics to prevent SBP with ascites.
97
Q

The relationship between Clostridium difficile (C. diff) and Antibiotic-Associated Diarrhea

A

Colonization with C. difficile occurs following antibiotictreatment of other diseases, as the bacteria is particularly resistant to antibiotics. The resulting damage to the intestinal flora promotes infection

98
Q

What is the best initial test for Antibiotic-Associated Diarrhea?

A

Stool C. diff toxin test or PCR

99
Q

What is the best initial therapy for Antibiotic-Associated Diarrhea?

What is the next best step in management if the best initial therapy does not respond?

A

Metronidazole

oral vancomycin

100
Q

A 75-year-old man is admitted to the hospital with pneumonia. Several days after the start of antibiotics, he begins to have diarrhea. The stool C. diff toxin is positive and he is started on metronidazole, which leads to resolution of diarrhea over a few days. Two weeks later the diarrhea recurs and the C. diff toxin is again positive.

What is the most appropriate next step in the management of this patient?

a. Retreat with metronidazole orally.
b. Use vancomycin orally.
c. Sigmoidoscopy and treat only if pseudomembranes are found.
d. Intravenous metronidazole.
e. Wait for stool culture.
f. Intravenous vancomycin.

A

*A.
Recurrent episodes of C. diff-associated diarrhea are best treated with another course of metronidazole. Intravenous metronidazole is used only if oral therapy cannot be used, such as in a patient with an adynamic ileus. Stool is never cultured for C. diff because it simply will not grow in culture. The difficulty in culturing C. diff is the source of the name of the organism. Endoscopy looking for pseudomembranes will diagnose antibiotic-associated diarrhea, but is not a necessary step given the availability of stool toxin assay.
Switching to oral vancomycin is the answer when the case does not respond to metronidazole.

101
Q

What is the most common cause of Malabsorption?

What are the 2 rare causes?

A

Celiac disease

Tropical sprue and
Whipple disease

102
Q

What kind of manifestations can we expect in malabsorption resulting in deficiencies of vitamins D, K and B12?

A

Vit D- Hypocalcemia, osteoporosis
Vit K- Bleeding, easy bruising
Vit B12- Anemia, hypersegmented neutrophils, neuropathy

103
Q

What clinical feature can Celiac disease give in 10% of cases?

A

Dermatitis herpetiformis

104
Q

How is Whipple Disease Tx?

A

Ceftriaxone followed by TMP/SMZ

105
Q

What is the main distinction between chronic pancreatitis and gluten sensitive enteropathy (Celiac disease)?

A

the presence of iron deficiency. This is because iron needs an intact bowel wall to be absorbed, but does not need pancreatic enzymes to be absorbed.

106
Q

What is the most accurate diagnostic test for celiac disease?

A

A small bowel biopsy

that shows flattening of the villi.

107
Q

What is the most accurate diagnostic test for Whipple disease?

A

A bowel wall biopsy showing the specific

organism.

108
Q

What is the most accurate diagnostic test for Tropical sprue?

A

A bowel wall biopsy showing the specific

organism.

109
Q

Why is a biopsy necessary in celiac disease?

A

to exclude lymphoma

110
Q

What are the 3 ways of diagnosing Chronic Pancreatitis in order of accuracy or sensitivity?

A
  1. Secretin stimulation testing: Is the most accurate diagnostic test
  2. Abdominal CT scan: 80% to 90% sensitive for pancreatic calcification
  3. Abdominal x-ray: 50% to 60% sensitive for calcification of the pancreas
111
Q

How is Secretin stimulation testing done?

A

Place a nasogastric tube; an unaffected pancreas will release a large volume of bicarbonate-rich fluids after the intravenous injection of secretin

112
Q

What is the specific treatment for Chronic Pancreatitis?

A

Enzyme Replacement

113
Q

What is the specific treatment for Celiac Disease?

A

Avoid gluten-containing foods such as wheat, oats rye, or, barley

*rice and wine are safe

114
Q

Briefly describe the pathophysiology and clinical features of Carcinoid syndrome.

A

Carcinoids are small, slow-growingneuroendocrine tumors. They are most commonly located in the gastrointestinal tract and can synthesize a variety of hormones (especially serotonin). Most carcinoids are asymptomatic because most of the hormones they produce are metabolized by the first-pass effect in the liver. Carcinoid syndrome – characterized by diarrhea, flushing, dyspnea, and wheezing – may occur if a serotonin-producing tumor has metastasized to the liver, bypassing first-pass metabolism.

115
Q

What is the best initial diagnostic test when suspecting Carcinoid syndrome?

A

Elevated Urinary 5-hydroxyindoleacetic acid (5-HIAA) test.

116
Q

If a carcinoid tumor is inoperable, what is the best initial therapy?

A

A somatostatin analog to control diarrhea (octreotide)

117
Q

Why is there no weight loss in diarrhea caused by Lactose Intolerance?

A

Because lactose is only one of several sugars to absorb. Lactose intolerance does not alter the absorption of any other nutrient such as fat so there is no deficiency in calories. Vitamins are absorbed normally.

118
Q

How would you Dx Lactose Intolerance?

A

The stool osmolality is increased, but the usual way to make the diagnosis is simply to remove all milk-containing products from the diet and wait a single day for resolution of symptoms.

119
Q

How would you Mgx Lactose Intolerance?

A

Avoiding milk products except yogurt is the therapy. Using oral
lactase replacement is also good therapy

120
Q

Briefly describe Irritable Bowel Syndrome.

A

Irritable bowel syndrome (IBS) is a pain syndrome that can have diarrhea or constipation, or both. It is a diagnosis of exclusion in association with a complex of symptoms. IBS is not associated with weight loss.

121
Q

What is the standard therapy for Irritable bowel syndrome (IBS)?

A
  1. Fiber in the diet
  2. Antispasmodic agents such as:
    - Hyoscyamine
    - Dicyclomine
  3. Tricyclic antidepressants (e.g., amitriptyline or SSRIs)
122
Q

What is the additional therapy for Irritable bowel syndrome (diarrhea-predominant IBS)?

A
  • Rifaximin: nonabsorbed antibiotic with modest effect in diarrhea predominant IBS
  • Alosetron: inhibitor of serotonin with modest effect in IBS; needs special permissions to use
  • Eluxadoline: mu-opioid receptor agonist for diarrhea IBS; relieves pain/slows bowel
123
Q

What is the additional therapy for Irritable bowel syndrome (constipation-predominant IBS)?

A
  • Polyethylene glycol (PEG): nonabsorbed bowel lubricant

- Lubiprostone (chloride channel activator): use if PEG doesn’t work

124
Q

What are the general clinical features of Inflammatory bowel disease (IBD)?

A

Diarrhea, blood in the stool, weight loss, and fever.

125
Q

What are the extraintestinal manifestations that are present in both Crohn’s Disease (CD) and Ulcerative Colitis (UC)?

A
  • Arthralgias
  • Uveitis, iritis
  • Skin manifestation (erythema nodosum, pyoderma gangrenosum)
  • Sclerosing cholangitis (more frequent in UC)
126
Q

Which has a higher risk of colon cancer, Crohn’s Disease (CD) or Ulcerative Colitis (UC)?

A

Both forms of IBD can lead to colon cancer. The risk of colon cancer is related to the duration of involvement of the colon. CD that involves the colon has the same risk of colon cancer as UC.

127
Q

What are some of the differences between Crohn’s Disease (CD) and Ulcerative Colitis (UC)?

A

1)

  • Crohn’s Disease (CD)=> Skip lesions
  • Ulcerative Colitis (UC)=> Continuous lesions

2)

  • Crohn’s Disease (CD)=> Transmural granulomas (inflammation)
  • Ulcerative Colitis (UC)=> Entirely mucosal inflammation

3)

  • Crohn’s Disease (CD)=> Fistulas and abscesses
  • Ulcerative Colitis (UC)=> No fistulas, no abscesses

4)

  • Crohn’s Disease (CD)=> Masses and obstruction
  • Ulcerative Colitis (UC)=> No obstruction

5)

  • Crohn’s Disease (CD)=> Perianal disease
  • Ulcerative Colitis (UC)=> No perianal disease
128
Q

When and how often should screening occur in a Pt with Crohn’s Disease (CD) or Ulcerative Colitis (UC)?

A

After 8 to 10 years of colonic involvement, with colonoscopy every 1 to 2 years.

129
Q

What is the most accurate way to Dx Inflammatory bowel disease (IBD)?

A

Endoscopy is the most accurate test when the disease can be reached by a scope.

130
Q

If endoscopy cannot reach or is inconclusive, what is the next best step?

A

serologic testing:
Antineutrophil cytoplasmic antibody (ANCA)- for UC
Anti-Saccharomyces cerevisiae antibody (ASCA)- for CD

U See ANCA, Aska for a CD

131
Q

How would you Tx Inflammatory bowel disease (IBD)?

A

1) Acute exacerbations of disease are treated with steroids (prednisone or budesonide) in both CD and UC.

2) Chronic maintenance of remission is with 5-ASA derivatives such as
mesalamine.
For CD=> Pentasa (mesalamine)
For UC=> Asacol (mesalamine)
Rowasa (mesalamine) is for UC largely limited to the rectum.

3) Everyone gets calcium and vitamin D.

132
Q

How would you Tx Perianal CD?

A

ciprofloxacin and metronidazole

133
Q

How would you Tx Fistulae and severe IBD unresponsive to other agents?

A

Antitumor necrosis factor (TNF) agents such as infliximab

134
Q

What is the most accurate test to Dx Diverticulosis?

A

Colonoscopy. Barium studies are acceptable, but not as accurate.

135
Q

What set of clinical features would make Diverticulitis the most likely diagnosis?

A
  • Left lower quadrant pain and tenderness
  • Fever
  • Leukocytosis
  • Palpable mass sometimes occurs.
136
Q

What is the best initial test when suspecting Diverticulitis?

A

CT scan. Colonoscopy and barium enema are contraindicated.

137
Q

Why are Colonoscopy and barium enema are contraindicated when suspecting Diverticulitis?

A

because of increased risk of perforation. Infection weakens the colonic
wall.

138
Q

What is the Tx for Diverticulitis?

A

Ciprofloxacin combined with metronidazole or Amoxicillin/clavulanate.
Patients with acute diverticulitis should not be fed.

139
Q

What percentage of colon cancer deaths are preventable with screening?

A

95%

140
Q

Which of the following is the most effective method of screening for colon cancer?

a. Colonoscopy.
b. Sigmoidoscopy.
c. Fecal occult blood testing (FOBT).
d. Barium enema.
e. Virtual colonoscopy with CT scanning.
f. Capsule endoscopy

A

*A.
Since 40% of colon cancer occurs proximal to the rectum and sigmoid colon, sigmoidoscopy is not nearly as sensitive in detecting lesions as colonoscopy. Barium studies, CT colonoscopy, and capsule endoscopy do not allow for biopsy. FOBT has more false positives and false negatives than colonoscopy. In addition, a positive FOBT must be followed up with colonoscopy.

141
Q

In which situation is Capsule endoscopy used?

A

It is used to detect sources of bleeding in the small bowel not reachable by endoscopy.

142
Q

In a patient with no family history of Colon Cancer, when should routine screening start, and how often should it be?

A

Every 10 years beginning at age 50.

143
Q

What clinical features would make Pancreatitis the most likely diagnosis?

A

Acute epigastric pain + tenderness + nausea/vomiting

In severe cases there is hypotension and fever.

144
Q

What is the characteristic difference between the pain in Pancreatitis and Cholecystitis?

A

The pain of pancreatitis goes straight through to the back “like a spear” stabbed into the abdomen. Cholecystitis pain goes around the side to the back.

145
Q

Which of the following is associated with the worst prognosis in pancreatitis?

a. Elevated amylase.
b. Elevated lipase.
c. Intensity of the pain.
d. Low calcium.
e. C-reactive protein (CRP) rising.

A

*D.
Severe pancreatic damage decreases lipase production and release leading to fat malabsorption in the gut. Calcium binds with fat (saponifies) in the bowel, leading to calcium malabsorption. Although amylase and lipase are elevated in pancreatitis, there is no correlation between the height of these enzyme levels and disease severity.
Pain intensity is subjective and does not correlate with the degree of organ damage.
CRP has never shown definite correlation with severity in any disease.

146
Q

What is the best initial test when suspecting Pancreatitis?

What is the most accurate test?

A

Amylase and lipase.

CT scan.

147
Q

What is the Tx for Acute Pancreatitis?

A
  • NPO (no food)
  • IV hydration at very high volume
  • Analgesia
  • PPIs decrease pancreatic stimulation from acid entering the duodenum
148
Q
  1. What percentage of necrosis is deemed Severe/Extensive necrosis?
  2. What is the next best step?
A
  1. 30% necrosis on CT or MRI
  2. adding antibiotics such as imipenem or meropenem may decrease mortality by decreasing the development of infected, necrotic pancreatitis. + needle biopsy to determine the presence of infection.
149
Q

What is the Tx for Infected, necrotic pancreatitis?

A

Resection with surgical

debridement to prevent ARDS and death.

150
Q

What are some of the stigmata of Liver Disease?

A
  • Ascites
  • Coagulopathy (all clotting factors except VIII are made in liver)
  • Asterixis and encephalopathy
  • Hypoalbuminemia and edema
  • Spider angiomata and palmar erythema
  • Portal hypertension leading to varices
  • Thrombocytopenia from splenic sequestration
  • Renal insufficiency (hepatorenal syndrome)
  • Hepatopulmonary syndrome
151
Q

What are the possible etiologies of a serum ascites albumin gradient (SAAG) >1.1 g/dL?

A
  • Portal hypertension
  • CHF
  • Hepatic vein thrombosis
  • Constrictive pericarditis
152
Q

What are the possible etiologies of a serum ascites albumin gradient (SAAG) <1.1 g/dL?

A
  • Infections (except SBP)
  • Cancer
  • Nephrotic syndrome
153
Q

Give a brief background of Spontaneous bacterial peritonitis (SBP) and its etiology.

A

It is an infection without a perforation of the bowel. We don’t actually know how the bacteria gets there. E coli is the most common organism. Anaerobes are rarely the cause of SBP. Pneumococcus, a respiratory pathogen, causes SBP for unknown reasons.

154
Q

What is the best initial test when suspecting Spontaneous bacterial peritonitis (SBP)?

A

Cell count with more than 250 neutrophils is the basis upon which we start therapy.

155
Q

How useful are Gram staining and Culturing when suspecting Spontaneous bacterial peritonitis (SBP)?

A

Gram stain is almost always negative. Fluid culture is the most accurate test, but the results are never available at the time we have to make a treatment decision.

156
Q

what is the Tx for Spontaneous bacterial peritonitis (SBP)?

A

Cefotaxime or ceftriaxone.

157
Q

What is the specific Tx for Ascites and edema in Cirrhosis?

A

Spironolactone and other diuretics. Serial paracenteses for large-volume ascites.

158
Q

What is the specific Tx for Ascites and edema in Cirrhosis?

A

FFP and/platelets only if bleeding occurs

159
Q

What is the specific Tx for Encephalopathy in Cirrhosis?

A

Lactulose and rifaximin

160
Q

What is the specific Tx for Varices in Cirrhosis?

A

Propranolol and banding via endoscopy

161
Q

What is the specific Tx for Hepatorenal syndrome in Cirrhosis?

A

Somatostatin (octreotide), midodrine

162
Q

In Cirrhosis, what clinical feature would point to Hepatopulmonary Syndrome?

A

Orthodeoxia, which is hypoxia upon sitting upright.

163
Q

Binge drinking

gives a sudden rise in which marker?

A

GGTP

164
Q

What clinical features would make Primary Biliary Cholangitis (PBC) the most likely Dx?

A
  • Woman in 40s or 50s
  • Fatigue and itching
  • Normal bilirubin with an elevated alkaline phosphatase
  • **Xanthelasma/xanthoma
  • **Osteoporosis
165
Q

What is the most accurate test to Dx Primary Biliary Cholangitis (PBC)?

A

A liver biopsy is the most accurate test. The most accurate blood test is the antimitochondrial antibody.

166
Q

What is the Tx for Primary Biliary Cholangitis (PBC)?

A

Ursodeoxycholic acid or obeticholic acid. Obeticholic acid decreases fibrosis.

167
Q

What clinical features would make Primary Sclerosing Cholangitis (PSC) the most likely Dx?

A
  • Pruritus
  • Elevated alkaline phosphatase and GGTP as well as elevated bilirubin level
  • Over 80% of primary sclerosing cholangitis (PSC) occurs in association with inflammatory bowel disease.
168
Q

What is the most accurate test to Dx Primary Sclerosing Cholangitis (PSC)?

A

MRCP or ERCP that shows beading, narrowing, or strictures in the biliary system. MRCP is generally done because there is no therapeutic need for ERCP.

169
Q

What is the Tx for Primary Sclerosing Cholangitis (PSC)?

A

Cholestyramine or ursodeoxycholic acid, the same as PBC.

170
Q

Does Primary Sclerosing Cholangitis (PSC) improve or resolve with resolution of the IBD?

A

No, the patient may still progress to needing a

liver transplantation.

171
Q

What clinical features would make Alpha 1-Antitrypsin Deficiency the most likely Dx?

A

A combination of liver disease and emphysema (COPD) in a young patient (under 40) who is a nonsmoker.

172
Q

What is the Tx for Alpha 1-Antitrypsin Deficiency?

A

Replacing the enzyme

173
Q

What clinical features would make Hemochromatosis the most likely Dx?

A

A patient in his 50s with mild increases in AST and alkaline
phosphatase and:
-Fatigue and joint pain (pseudogout)
-Erectile dysfunction in men, and amenorrhea in women (from pituitary involvement)
-Skin darkening
-Diabetes
-Cardiomyopathy

174
Q

Which infections are common in a Pt with Hemochromatosis?

A

Vibrio vulnificus, Yersinia, and Listeria infections occur because these organisms feed on iron.

175
Q

What best initial test for Hemochromatosis?

A
  • Increased serum iron and ferritin

- Decreased iron binding capacity

176
Q

What is the most accurate test to Dx Hemochromatosis?

A

A liver biopsy for increased iron.

177
Q

A 54-year-old man has been evaluated in the office for fatigue, erectile dysfunction, and skin darkening. He is found to have transferrin saturation (iron divided by TIBC) above 50%. His AST is 2 times the upper limit of normal.

What would you do next to confirm the diagnosis?

a. Echocardiography.
b. Glucose level.
c. Abdominal MRI and HFE (C282y) gene testing.
d. Liver biopsy.
e. Prussian blue stain of the bone marrow.
f. Deferoxamine.
g. Deferasirox.

A

*C.
MRI will show increased iron deposition in the liver. An abnormal MRI combined with an abnormal genetic test for hemochromatosis can spare the patient the need for a liver biopsy. There is an association with diabetes; however, glucose levels will not confirm a diagnosis of hemochromatosis. Prussian blue is the stain of blood cells for iron. Prussian blue is also used to diagnose sideroblastic anemia.
Iron chelation therapy is used in hemochromatosis for those who:
1. Cannot be managed with phlebotomy
2. Are anemic and have hemochromatosis from overtransfusion such as thalassemia

Deferoxamine, deferasirox, or deferiprone should not be started until the diagnosis is confirmed. Deferasirox and deferiprone are huge breakthrough medications because they are effective orally. Deferoxamine has to be given lifelong by injection.

178
Q

What is the best initial therapy for Hemochromatosis?

A

Phlebotomy is clearly the best therapy for those with overabsorption of iron.

179
Q

What is the Tx for Acute hepatitis C?

A

interferon, ribavirin, and either telaprevir

180
Q

What is the Tx for Chronic hepatitis B?

A 
Any one of the following agents:
Adefovir
Lamivudine
Entecavir
Tenofovir
Interferon
181
Q

What is the Tx for Chronic hepatitis C?

A
  • Sofosbuvir-velpatasvir (for all genotypes)

- Sofosbuvir-ledipasvir (Genotype 1)

182
Q

How long should the Tx for hepatitis be, and how can we assess the cure?

A

12 weeks, PCR-RNA viral load 12 and

24 weeks after therapy.

183
Q

In hepatitis, what predicts the response to therapy?

A

Genotype.

184
Q

In hepatitis, what tells the extent of liver damage?

A

Liver biopsy, but rarely needed.

185
Q

What are some of the adverse effects of Interferon?

A

Arthralgias, thrombocytopenia, depression, leukopenia

186
Q

What is the main adverse effect of Ribavirin?

A

Anemia

187
Q

What is the main adverse effect of Adefovir?

A

Renal dysfunction

188
Q

What are some of the adverse effects of Lamivudine?

A

None

189
Q

What is the pathophysiology behind Wilson Disease?

A

Because of a decrease in ceruloplasmin, copper is not excreted and it builds up in the body in the liver, kidney, red blood cells, and the nervous system.

190
Q

What clinical features would make Wilson Disease the most likely Dx?

A

In addition to the features of cirrhosis and hepatic insufficiency;

  • Neurological symptoms: psychosis, tremor, dysarthria, ataxia, or seizures
  • Coombs negative hemolytic anemia
  • Renal tubular acidosis or nephrolithiasis
191
Q

What is the difference in terms of neurological manifestations of Wilson Disease compared to those of from any other form of liver failure?

A

Wilson disease gives psychosis and delusions, not the encephalopathic features or delirium that you would get with any form of liver failure.

192
Q

What is the best initial test for Wilson disease?

What other test can be used to confirm the Dx?

A

Slit-lamp examination

Ceruloplasmin levels=>
usually low

193
Q

What is the most accurate way to Dx Wilson disease?

A

Biopsy or looking for an abnormally increased amount of copper excretion into the urine after giving penicillamine.

194
Q

Why is looking for a Decreased ceruloplasmin level not the most accurate test when Dx Wilson disease?

A

Because all plasma proteins can be decreased in those with liver dysfunction and cirrhosis.

195
Q

How would you Tx Wilson disease?

A

Penicillamine - will chelate copper and remove it from the body. Additional therapy:
-Zinc: interferes with intestinal copper absorption

196
Q

What clinical features would make Autoimmune Hepatitis the most likely Dx?

A

A young woman with signs of liver inflammation with a positive ANA. More specific tests are liver-kidney microsomal antibodies, high gamma globulin (IgG), anti-smooth muscle antibodies, and anti-liver/kidney microsomal antibodies.

197
Q

How would you Tx Autoimmune Hepatitis?

A

Prednisone and or Azathioprine.

198
Q

What is the most accurate way to Dx Nonalcoholic Steatohepatitis (NASH) or Nonalcoholic Fatty
Liver Disease?

A

Biopsy is the most accurate test and shows the microvesicular fatty deposits you would find in alcoholic liver disease, but without the history of alcohol use.

199
Q

What are some of the things associated with Nonalcoholic Steatohepatitis (NASH) or Nonalcoholic Fatty
Liver Disease?

A

Obesity
Diabetes
Hyperlipidemia
Corticosteroid use

200
Q

How would you Mgx Nonalcoholic Steatohepatitis (NASH) or Nonalcoholic Fatty
Liver Disease?

A

Management is with correcting the underlying cause. There is no specific drug therapy to reverse it.

M.T.B (9 decks)

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