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Gastroenterology Flashcards

1
Q

What’s the first study that should be ordered to evaluate dysphagia of unknown cause?

A

Barium study

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2
Q

What is the pre-cancerous histologic change that affects the esophagus called?

A

Barrett esophagus

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3
Q

Describe the presentation of achalasia.

A

Young nonsmoker w/ dysphagia to both solids and liquids
- may also have regurgitation of food and aspiration
- may be progressive

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4
Q

What is the best initial test for achalasia? Most accurate?

A

First: Barium swallow or CXR
Most accurate: esophageal manometry

  • endoscopy can be ordered to exclude malignancy but isn’t needed for dx of achalasia
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5
Q

How does manometry assist in making the diagnosis of achalasia?

A

Shows an absence of normal esophageal peristalsis
- abnormally high pressure at lower esophageal sphincter (pathophysiology involves failure of gastroesophageal sphincter to relax)
- no mucosal abnormality

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6
Q

How is achalasia treated? What are the associated risks?

A

Pneumatic dilation of the esophageal sphincter (risk of perforation) or surgical myotomy

Severe dz treated by per oral endoscopic myotomy (POEM)
- uses upper endoscopy to reach the surgical site

  • a botulinum toxin injection may be used as an alternative if pt declines the above txs *
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7
Q

What combinations of symptoms can you use to help distinguish between esophageal pathologies and cancer in a patient w/ dysphagia and weight loss?

A

Dysphagia + wt loss = esophageal pathology

Dysphagia + wt loss + heme-positive stool/anemia = cancer

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8
Q

How does esophageal cancer present?

A

Dysphagia (first to solids, then liquids)
+ possible heme-positive stool/anemia
+ pt >50yo w/ smoking/EtOH hx

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9
Q

What’s the best initial test if you suspect esophageal cancer?

A

Endoscopy; next option would be barium swallow

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10
Q

How is esophageal cancer treated?

A

Surgical resection (if there are no local or distant mets) followed by 5-fluorouracil chemo

Palliative stenting can be performed to relieve obstruction

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11
Q

What is the common underlying cause for esophageal webs and rings (aka “peptic strictures”)?

A

Repeated exposure of esophagus to stomach acid –> scarring and stricture formation

  • previous use of sclerosing agents for variceal bleeding can also cause these problems, which is why variceal banding is preferred
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12
Q

What constellation of symptoms is suggestive of eosinophilic esophagitis? How do you diagnose and treat it?

A
  • Dysphagia
  • Hx of allergies

Dx: Scope + biopsy
Tx: PPIs and budesonide

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13
Q

What is Plummer-Vinson syndrome? How is it treated?

A

A proximal stricture a/w iron deficiency anemia and squamous cell esophageal cancer common in middle-aged women

Tx: iron replacement

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14
Q

What is Schatzki ring? How do you treat it?

A

Peptic stricture of the distal ring of the esophagus that presents w/ intermittent dysphagia

Tx: pneumatic dilation

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15
Q

How is peptic stricture from acid reflux treated?

A

Pneumatic dilation

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16
Q

What procedures should be avoided in a patient w/ Zenker diverticulum?

A

Endoscopy and nasogastric tube placement

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17
Q

What is a Zenker diverticulum? How does it present, and how do you treat it?

A

Dilation of posterior pharyngeal constrictor muscles diagnosed via barium study
- pt presents w/ dysphagia and very bad breath due to decomposing food retained in the diverticulum

Tx: surgical resection

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18
Q

How does a case of diffuse esophageal spasm or nutcracker esophagus present? What test is best? How do you treat?

A

Sx: severe chest pain w/o risk factors for ischemic heart disease +/- dysphagia
- normal EKG, stress test, angiography

Dx: manometry
- barium swallow could show corkscrew pattern if it was performed during an acute attack

Tx: CCBs and nitrates (same as Prinzmetal angina)
- TCAs can be tried if CCBs aren’t an option

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19
Q

How is Prinzmetal angina distinguished from diffuse esophageal spasm?

A

Prinzmetal angina will give ST elevation on EKG and abnormality on stimulation of coronary arteries

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20
Q

How does scleroderma (progressive systemic sclerosis) present and how is it treated?

A

Presents as reflux w/ colonic dysmotility

Tx: PPIs

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21
Q

How does esophagitis present?

A

Odynophagia, NOT dysphagia

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22
Q

What is the most common cause of esophagitis in HIV-positive patients? What’s another less common cause?

A

In pts w/ <100 CD4 cells, candida esophagitis causes >90% of cases
- less commonly pill esophagitis from doxycycline, bisphosphonate, alendronate, etc.

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23
Q

What advice should be given to patients experiencing pill esophagitis?

A
  • Sit up and drink more water with pills
  • Remain upright for >30 minutes after taking pill
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24
Q

How does eosinophilic esophagitis present? What’s the relevant exam finding on endoscopy? What’s the relevant lab test?

A

Swallowing difficulty, food impaction, and heartburn in a pt w/ hx of asthma and allergic diseases
- multiple concentric rings on endoscopy
- biopsy finding w/ eosinophils (most accurate test)

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25
Q

How do you treat eosinophilic esophagitis? What’s the single most effective treatment?

A

PPIs and elimination of allergenic foods
- most effective: swallowing steroid inhalers

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26
Q

How does treatment differ between patients with and without HIV in cases of esophagitis?

A

HIV-positive, <100 CD4s: fluconazole, then endoscopy if there’s no response (**remember most cases are Candida)
HIV-negative: endoscopy before initiating treatment

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27
Q

What is a Mallory-Weiss tear?

A

A tear in the esophageal wall that presents w/ sudden upper GI bleeding w/ violent retching and vomiting
- may or may not have hematemesis or black stool

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28
Q

How do you diagnose and treat Mallory-Weiss tear?

A

Diagnose w/ endoscopy (barium swallow shows nothing)
* subcutaneous air seen only in perforation of the esophagus

Most cases resolve spontaneously
- if bleeding persists, inject epinephrine

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29
Q

Describe the symptoms of GERD.

A
  • substernal chest pain
  • epigastric pain
  • sore throat
  • metallic or bitter taste
  • hoarseness
  • chronic cough (20-25% of cases of chronic cough can also be diagnosed w/ GERD)
  • wheezing
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30
Q

PPIs are both diagnostic and therapeutic for GERD. If there is no response to PPI therapy, what’s your next step to make the diagnosis?

A

24-hour pH monitor

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31
Q

What is the initial treatment for mild GERD?

A

Lifestyle modification
- weight loss
- not eating within 3hrs of sleep
- elevating head of bed
- quit smoking
- limit EtOH, caffeine, chocolate, mint

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32
Q

If lifestyle modifications don’t work to treat GERD, what are the other options?

A
  • PPIs achieve control in 95% of cases (all options are equal in efficacy)
  • H2 blockers (cimetidine, famotidine, nizatidine) have a 70% success rate
  • promotility agents (metoclopramide) are equal to H2 blockers in efficacy but less effective than PPIs
  • surgical or endoscopic procedure to narrow distal esophagus and re-constrict lower esophageal sphincter (Nissen fundoplication)
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33
Q

How does high calcium cause ulcers?

A

Stimulates gastrin release

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34
Q

When is reflux an alarming symptom that warrants endoscopy?

A

When associated w/ weight loss, anemia, blood in the stool, and dysphagia

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35
Q

What is Barrett esophagus?

A

A precancerous lesion (0.5% of cases per year develop into cancer) diagnosed by endoscopy and biopsy that confirms change of squamous epithelium to columnar epithelium w/ metaplasia

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36
Q

How is Barrett esophagus treated? Low-grade dysplasia? High-grade dysplasia?

A

Barrett: PPI and repeat endoscopy q3-5 years
Low-grade dysplasia: PPI, ablation, repeat endoscopy in 3-6mo
High-grade dysplasia: endoscopic mucosal resection, ablative removal, or distal esophagectomy

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37
Q

What is the most common cause of epigastric discomfort?

A

Functional (nonulcer) dyspepsia, which is a diagnosis of exclusion
- diagnosed after endoscopy has ruled out ulcers, cancer, and gastritis

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38
Q

How do you treat functional dyspepsia?

A

Symptomatic treatment w/ H2 blockers, liquid antacids, or PPIs
- you can treat for Helicobacter in refractory disease

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39
Q

Can you distinguish between duodenal ulcer and gastric ulcer without endoscopy?

A

No, though generally food makes gastric ulcer pain worse and duodenal ulcer pain better.

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40
Q

What MUST be done in a patient over 60yo with epigastric pain?

A

Scope to rule out gastric cancer

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41
Q

How do you treat Helicobacter pylori?

A

PPI + clarithromycin + amoxicillin
- increasing macrolide resistance is increasing the use of metronidazole and bismuth as adjunct

  • only treat H. pylori when a/w gastritis; there’s no benefit in GERD
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42
Q

What do you do if PPI + clarithromycin + amoxicillin doesn’t successfully treat H pylori?

A

Repeat treatment w/ metronidazole and tetracycline + PPI; consider adding bismuth
- if repeat course fails, evaluate for Zollinger-Ellison

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43
Q

What are the adverse effects of PPIs?

A
  • impaired calcium absorption (may lead to fractures)
  • impaired magnesium absorption
  • impaired vitamin B12 absorption
  • impaired iron absorption
  • impaired resistance to bacterial invasion (reduced acid barrier –> increased risk of pna and C. Diff)
  • impaired kidney function leading to interstitial nephritis (eosinophils in urine)
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44
Q

What are the primary conditions that lead to stress peptic ulcers?

A

Head trauma, intubation/ventilation, burns, coagulopathy + steroid use

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45
Q

Which medications are most effective at preventing stress ulcers?

A

PPI&raquo_space; H2 blocker, sulcrafate

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46
Q

What is Zollinger-Ellison syndrome? How is it diagnosed?

A

aka gastrinoma

  • elevated gastrin level
  • elevated gastric acid output
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47
Q

What are the characteristics of a normal peptic ulcer? What are the characteristics of ulcers suspicious for Zollinger-Ellison syndrome?

A

Normal: single ulcer near pylorus, <1cm, resolves easily w/ tx
ZES: multiple large ulcers, >1cm, distally located near ligament of Treitz, recurrent or resistance despite adequate treatment

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48
Q

If hypercalcemia is present along w/ multiple large distally-located, treatment-resistant gastric ulcers, what do you suspect?

A

Parathyroid problem + Zollinger-Ellison syndrome, which together raise the suspicion for multiple endocrine neoplasia (MEN) syndrome

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49
Q

Which medications cause elevated gastrin levels?

A

H2 blockers and PPIs

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50
Q

Which tests are appropriate for Zollinger-Ellison syndrome? Which is most accurate?

A
  • endoscopic ultrasound
  • nuclear somatostatin scan (very sensitive b/c ZES causes huge increase in # of somatostatin receptors)
  • secretin suppression (most accurate!!)
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51
Q

What is the treatment for Zollinger-Ellison?

A

Surgical resection for local disease and lifelong PPIs for metastatic dz

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52
Q

How does secretin suppression test for Zollinger-Ellison syndrome?

A

Infusion of IV secretin causes healthy people to decrease gastrin level and acid output

ZES pts will show increased or unchanged gastrin level and no decrease in acid output

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53
Q

What are the extra-intestinal manifestations of IBD?

A
  • joint pain
  • iritis/uveitis
  • pyoderma gangrenosum, erythema nodosum
  • sclerosing cholangitis
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54
Q

Which features are more common in Crohn disease than ulcerative colitis?

A
  • masses
  • skip lesions
  • upper GI tract involvement
  • perianal disease
  • transmural granulomas
  • fistulae
  • hypocalcemia from fat malabsorption
  • obstruction
  • calcium oxalate kidney stones
  • cholesterol gallstones
  • vitamin B12 malabsorption
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55
Q

What tests are used in diagnosis of IBD?

A
  • endoscopy
  • barium study
  • blood tests (if diagnosis is not clear)
  • fecal calprotectin (made by WBCs) to track disease activity
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56
Q

How are fecal calprotectin levels interpreted in cases of possible IBD?

A

High in IBD and bowel infection
Low in absence of infection/inflammation

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57
Q

Which blood tests can be used to assist in the diagnosis of IBD?

A

ASCA (positive in Crohn’s, negative in UC)
ANCA (negative in Crohn’s, positive in UC)

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58
Q

How does IBD impact the need for colon cancer screening?

A

CD w/ colonic involvement and UC can lead to colon cancer

After 8-10 years of colonic involvement, colonoscopies should be completed every 1-2 years

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59
Q

What is the best initial treatment for both Crohn’s and ulcerative colitis?

A

Mesalamine
- not sulfasalazine due to side effects (rash, hemolytic anemia, interstitial nephritis)

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60
Q

What are the treatments for IBD?

A

Mesalamine (best initial)

Steroids
- budesonide (glucocorticoid) for control of acute exacerbations has limited systemic adverse effects

Azathioprine and 6-mercaptopurine
-for severe disease w/ recurrent symptoms after steroid cessation
- can help pts wean off steroids
- thiopurine methyltransferase (TPMT) testing can help ensure pts can metabolize potentially toxic metabolites of these drugs

TNF inhibitors
- for CD a/w fistula formation
- test for and start treatment for latent TB before initiating infliximab bc it can reactivate TB by releasing it from granulomas
- you don’t have to complete tx before starting infliximab or JAK inhibitor, just start it

Metronidazole + ciprofloxacin
- for perianal involvement in Crohns

Vedolizumab (IV integrin receptor antagonist)
- for severe IBD not controlled by other txs
- induces and maintains remission w/o risk of PML

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61
Q

What role does surgery play in IBD treatment?

A

Can be curative in UC by removing colon, but CD will still recur at surgical site
*surgery may still be necessary in Crohns in the event of stricture or obstruction

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62
Q

Which TNF inhibitors may be used in IBD? How can you monitor and adjust for effectiveness?

A

Adalimumab, certolizumab, etanercept, golimumab, and infliximab

If ineffective, check TNF level and antibodies and switch TNF drugs.
If level is normal but there are no antibodies, switch drug class.

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63
Q

What is the most important feature of infectious diarrhea presentation in regards to diagnosis and management?

A

Presence or absence of blood; blood indicates presence of invasive bacteria

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64
Q

Which bacteria is the most common cause of food poisoning?

A

Campylobacter (may be associated w/ Guillain-Barre and reactive arthritis)

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65
Q

Which bacteria is transmitted by chickens/eggs? Associated w/ seafood?

A

Chickens: salmonella
Seafood: vibrio

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66
Q

Which bacteria is most commonly associated w/ hemolytic uremic syndrome (HUS)?

A

E. coli 0157:H7, which secretes verotoxin and is associated w/ undercooked beef

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67
Q

What common treatments can worsen HUS?

A

Platelet transfusions and antibiotics

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68
Q

Which infectious diarrhea patient makes you suspicious for Vibrio vulnificus?

A

Shellfish consumption in a person w/ liver disease and skin lesions

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69
Q

Which bacteria responsible for infectious diarrhea are associated w/ reactive arthritis?

A

Campylobacter and Shigella (shiga toxin)

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70
Q

What defines severe disease in a patient with infectious diarrhea?

A

Presence of blood, fever, abdominal pain, hypotension/tachycardia

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71
Q

How do you treat mild vs severe cases of infectious diarrhea?

A

Mild: hydration only; dz is time-limited
Severe: fluroquinolones (ciprofloxacin or azithromycin)

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72
Q

Which pathogens cause exclusively non-bloody diarrhea?

A

Viruses: rotavirus, norovirus, hepatitis A/E
Giardia
Staph aureus
Bacillus cereus
Cryptosporidiosis
Scombroid (histamine fish poisoning)

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73
Q

What history should raise suspicion for Giardia infection? What’s the testing and treatment?

A

Camping, hiking, and contact w/ feces (changing diapers, sexual contact, etc.)

Test: stool ELISA antigen >90% sensitive/specific (better than O&P)
Tx: metronidazole or tinidazole

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74
Q

How does staph aureus diarrhea present and what’s the disease course?

A

Vomiting + diarrhea; resolves spontaneously

75
Q

What exposure is associated w/ Bacillus cereus? What’s the disease course?

A

A/w refried/reheated Chinese rice and vomiting; resolves spontaneously

76
Q

Which patient w/ non-bloody diarrhea should make you suspicious for Cryptosporidiosis?

A

HIV-positive pt w/ CD4 <100

77
Q

How do you diagnose cryptosporidiosis? How do you treat it?

A

Dx: modified acid-fast stain
Tx: antiretrovirals to raise CD4 levels (nitazoxanide and paromycin)

78
Q

Describe the presentation and treatment of scombroid diarrhea.

A

Histamine fish poisoning (toxic levels of histamine present in improperly stored fish like tuna, mackerel, or mahi-mahi)
- rapid onset of diarrhea and wheezing within ten minutes of eating fish
- Tx: antihistamines like diphendyramine

79
Q

Which antibiotic is most commonly associated w/ C. Diff?

A

Clindamycin (but can be caused by ANY abx)

80
Q

Which is the best initial test for C. diff? Most accurate?

A

Initial: stool toxin assay
Most accurate: stool PCR

81
Q

What is the treatment for C. diff?

A

PO vancomycin (PO fidaxomicin as alternative) ** IV is not useful!

  • if diarrhea resolves then recurs, retreat w/ PO vanc
  • add metronidazole if dz is severe
  • stool transplant after multiple recurrences
82
Q

What are indications for surgery in C. diff? What agent can be used to prevent recurrence?

A

Surgery for severe dz: toxic megacolon, elevated lactate, leukocytosis, elevated creatinine
Prevent recurrence: bezlotoxumab

83
Q

What is the most common cause of chronic diarrhea and flatulence?

A

Lactose intolerance

84
Q

What is carcinoid syndrome? How is it diagnosed? How do you treat?

A

Chronic secretory diarrhea a/w flushing and episodes of hypotension

Dx: urinary 5-HIAA level
** not pre-malignant, not an indication for additional surveillance **

Tx: octreotide (somatostatin analog)

85
Q

What are the causes of fat malabsorption?

A

Celiac disease
Non-tropical or tropical spure
Chronic pancreatitis
Whipple disease

86
Q

All forms of fat malabsorption are associated w/ what features?

A
  • hypocalcemia from vitamin D deficiency (may lead to osteoporosis)
  • oxalate overabsorption –> oxalate kidney stones
  • vitamin K malabsorption –> easy bruising, elevated prothrombin time/INR
  • vitamin B12 malabsorption from destruction of terminal ileum or loss of pancreatic enzymes necessary for B12 absorption
87
Q

What is the diagnostic testing for fat malabsorption?

A

Sudan black stain of stool to test for presence of fat (initial test)

72-hour fecal fat (most sensitive)

88
Q

In addition to fat, what other malabsorption(s) and resulting condition(s) is associated w/ celiac disease?

A

Malabsorption of Fe ==> microcytic anemia
* this fact differentiates it from pancreatic insufficiency

Malabsorption of folate from destruction of villi

89
Q

What skin lesion is associated w/ celiac disease?

A

Vesicular skin lesion not present on mucosal surfaces called dermatitis herpetiformis

90
Q

What are the diagnostic tests for celiac disesase?

A
  • Antigliadin, anti-endomysial, and anti-tissue transglutaminase Abs (best initial)
  • small bowel biopsy (most accurate)
  • D-xylose (also abnormal in Whipple disease and tropical sprue) usually not necessary

*biopsy is necessary to exclude bowel wall lymphoma

91
Q

How does tropical sprue present? What are the diagnostic tests and treatment?

A

Presents like celiac disease but w/ history of being in the tropics

  • serologic tests (anti-tissue transglutaminase) will be negative
  • most accurate test is small bowel biopsy showing microorganisms

Tx: doxycycline or TMP/SMX 3-6 months

92
Q

What findings on presentation help distinguish Whipple disease from celiac/sprue?

A

Arthralgia, neurological abnormalities, ocular findings

93
Q

What testing is needed to diagnose Whipple disease? Treatment?

A

Small bowel bx w/ PAS-positive organisms (most accurate)
- alternately: PCR of stool for tropheryma whippeli

Tx: TMP/SMX or doxy for 12 months

94
Q

What is the presentation of chronic pancreatitis?

A

Fat malabsorption w/ history of alcoholism and/or multiple episodes of pancreatitis
- amylase + lipase likely normal
- malabsorption of vit K/D less common than with celiac disease
- Fe and folate levels normal
- B12 may be low
- D-xylose testing normal

95
Q

What are the best initial and most accurate tests for chronic pancreatitis? What’s the treatment?

A

Initial: Abdominal x-ray (50-60% sensitive for detection of pancreatic calcifications), abdominal CT w/o contrast (60-80% sensitive)

Most accurate: secretin stimulation testing

Tx: long-term PO replacement of pancreatic enzymes (amylase, lipase, trypsin)

96
Q

What are three key factors in the history that help differentiate IBS from IBD?

A

IBS w/ have no fever, weight loss, or bloody stool

97
Q

How does IBS present?

A
  • abdominal pain relieved by bowel movement
  • abdominal pain which is better at night
  • abdominal pain with diarrhea alternating w/ constipation

Normal diagnostic tests: stool guaiac, stool leukocytes, culture, O&P, colonoscopy, abdominal CT

98
Q

How do you treat IBS?

A

Fiber (increased stool bulk helps relieve pain)
- if fiber doesn’t help pain, add antispasmodic/anticholinergic agents (dicyclomine, hyoscyamine)
- if no response, add tricyclic antidepressant (amitriptyline)

99
Q

What medications can be helpful for diarrhea-prominent IBS?

A

Rifaximin, Alosetron, Eluxadoline, Tenapenor

100
Q

What are some key principles for treating constipation-prominent IBS?

A

Start w/ fiber, then try miralax, then chloride-channel activator (lubiprostone) or guanylate cyclase agonist (linaclotide or plecanatide)

101
Q

What are the screening guidelines for general population colon cancer?

A

General population: 45yo, colonoscopy q10 years (OR sigmoidoscopy q5 years, fecal immunochemistry and stool DNA q3 years)
- FOBT and scope yearly if colonoscopy (+)

102
Q

What are the screening guidelines for pts w/ one family member w/ colon cancer?

A

One family member w/ colon Ca: 40yo OR 10yrs before age at which family member was diagnosed

103
Q

What are the colon cancer screening guidelines for pts w/ three family members, two generations, or one family member diagnosed <50yo?

A

Colonoscopy starting at age 25, repeat q1-2 years (suspect Lynch syndrome or hereditary nonpolyposis colon cancer)

104
Q

What are the colon cancer screening guidelines for patients w/ familial adenomatous polyposis?

A

Begin screening sigmoidoscopy at 12yo at perform colectomy when polyps are found

105
Q

What is Gardner syndrome?

A

Subvariant of FAP that presents w/ benign bone tumors (osteomas) and other soft tissue tumors
- long-term risk of colon cancer plus thyroid, pancreas, and small bowel cancer

*screen w/ sigmoidoscopy starting at 12yo same as FAP

106
Q

How does Peutz-Jeghers present? How does it impact cancer screening?

A

Melanotic spots on the lips + hamartomatous polyps throughout small bowel and colon
- risk of cancer VERY high
- screening w/ sigmoidoscopy at 8yo

107
Q

What is juvenile polyposis? How does it impact cancer risk?

A

Multiple extra hamartomas in bowel
- risk of cancer and premature cancer is high
- screen upper and lower GI tract starting at 12yo

108
Q

How does colon cancer screening change when a dysplastic polyp is found?

A

Repeat colonoscopy in 3-5 years

109
Q

Is carcinoembryonic antigen a screening test?

A

NO. It is used to monitor response to therapy.

110
Q

What causes diverticulosis and how does it present? How do you manage it?

A

Caused by low-fiber, high-fat, low-residue diet

Sx: LLQ pain + lower GI bleed
Dx: colonoscopy
Tx: high-fiber diet

111
Q

What is diverticulitis and how does it present? How do you manage it?

A

Complication of diverticulosis that presents with LLQ pain, tenderness, fever and leukocytosis
- Dx: CT abdomen/pelvis
- Tx: abx w/ gram (-) and anaerobic coverage (ex: quinolone/cephalosporine [usually cipro] + metronidazole)

** colonoscopy/barium swallow are contraindicated bc of increased risk of perforation

112
Q

What do you order on CCS for large-volume GI bleeding?

A
  • Bolus NS or LR
  • CBC
  • PT/INR
  • type and cross
  • consult GI
  • EKG
113
Q

Unnecessary use of prophylactic PPIs increases risk of what two conditions?

A

PNA and C. diff

114
Q

Which type of GI bleed has the highest mortality?

115
Q

What features should raise your suspicion for variceal bleeds?

A

Pt w/ EtOH use and hematemesis and/or liver disease
- splenomegaly
- low platelets
- spider angiomata
- gynecomastia

116
Q

How do you treat variceal bleeding?

A
  • octreotide (somatostatin analog to decrease portal HTN)
  • ceftriaxone if ascites is present (for SBP prophylaxis)
  • stat EGD
  • TIPS procedure if bleeding persists

*propranolol can be used to prevent future episodes

117
Q

What is the role of Blakemore gastric tamponade balloon in management of variceal bleeding?

A

(rarely used)

will temporarily stop bleeding to allow shunt to be placed

118
Q

What is the most common complication of TIPS procedure?

A

Hepatic encephalopathy

119
Q

What is the goal INR in a patient w/ variceal bleeding?

120
Q

What are the common causes of upper GI bleeds?

A
  • ulcer disease
  • esophagitis, gastritis, duodenitis
  • varices
  • cancer
121
Q

What are the common causes of lower GI bleeds?

A
  • angiodysplasia
  • diverticular dz
  • polyps
  • ischemic colitis
  • IBD
  • cancer
122
Q

What diagnostic procedures can you use to identify the location of GI bleeding if endoscopy does not?

A
  • technetium bleeding scan (tagged RBC scan)
  • angiography (can be done pre-op to target resection)
  • capsule endoscopy (for small bowel)
123
Q

When do you transfuse packed RBCs?

A

Hematocrit <30 in older patient or <20-25 in younger patient w/o heart disease

124
Q

When do you transfuse FFP?

A

When PT/INR is elevated and vitamin K is too slow

125
Q

When do you transfuse platelets?

A

When patient is bleeding or scheduled for surgery and platelets are <50K

126
Q

What is the most common cause of death in pts w/ GI bleeding?

A

Myocardial ischemia
- myocytes of LV cannot distinguish b/tw ischemia, anemia, carbon monoxide poisoning, or coronary artery stenosis ==> all lead to MI

  • order EKG in older pts w/ GI bleed
127
Q

When do patients w/ GI bleeds need an NG tube?

A

When it’s unclear whether bleeding is from upper or lower GI, but this offers limited info and doesn’t change anything if the patient is going to be scoped anyway

*iced saline lavage is never the right answer

128
Q

What are some possible causes of constipation?

A
  • dehydration
  • CCBs
  • narcotics
  • hypothyroidism
  • DM (loss of sensation in bowel)
  • Fe sulfate
  • Anticholinergics and TCAs
129
Q

What is dumping syndrome?

A

Relatively rare downstream effect of gastric surgery (ex: Roux-en-Y) that presents w/ shaking, sweating, and weakness
- may involve hypotension
- tx: frequent small meals

130
Q

What is diabetic gastroparesis and how do you treat it?

A

Impaired neural supply to the bowel 2/2 longstanding diabetes which impairs normal motility
- Tx: erythromycin or metoclopramide (erythromycin increases motilin levels in the gut)

131
Q

How does acute pancreatitis present? What are the common causes?

A

Severe mid-epigastric pain and tenderness in an alcoholic pt or someone w/ gallstones
- non-bloody vomiting, anorexia, tenderness
- (severe cases) hypotension, metabolic acidosis, leukocytosis, hemoconcentration, hyperglycemia, hypocalcemia 2/2 fat malabsorption, hypoxia

Causes: hypertriglyceridemia, trauma, infection, ERCP, meds (thiazides, didanosine, stavudine, azathioprine)

132
Q

What are the diagnostic tests for acute pancreatitis?

A
  • Amylase and lipase (best initial)
  • CT abdomen (dilated common bile ducts; most accurate)
  • MRCP
  • ERCP (predominantly therapeutic)
133
Q

How do you treat acute pancreatitis?

A
  • bowel rest
  • hydration
  • pain management
134
Q

What are Ranson criteria?

A

Operative criteria to see which patient’s need pancreatic debridement (severity is mostly determined by CT now)

135
Q

What is the treatment for necrotic pancreatitis?

A

If CT shows >30% necrosis of the pancreas: abx (imipenem) + CT-guided bx

If bx shows infection: necrotic pancreatitis ==> surgical debridement

136
Q

How do patients with acute hepatitis present?

A
  • jaundice
  • fatigue
  • weight loss
  • dark urine (bilirubin)
  • serum sickness phenomena (joint pain, urticaria, fever –> Hep B/C)
  • polyarteritis nodosa (hep B)
  • cryoglobulinemia (hep C)
137
Q

Which hepatitis is most severe in pregnancy?

A

Hep E (can be fatal)

138
Q

What are the diagnostic tests for acute hepatitis?

A
  • elevated conjugated (direct) bilirubin
  • bilirubin in urine
  • unconjugated bilirubin does not pass into urine
139
Q

What are the diagnostic test findings for viral hepatitis?

A

Elevated ALT

140
Q

What are the diagnostic test findings for drug-induced hepatitis?

A

Elevated AST

141
Q

What are the diagnostic test findings for hepatitis A, C, D, E?

A

Serology for antibodies (most accurate)

142
Q

What are the diagnostic test findings for hepatitis B?

A

surface antigen, core antibody, e-antigen, or surface antibodies (most accurate)

143
Q

What is the first test to become abnormal in acute hep B?

A

Surface antigen
- elevation of ALT, e-antigen and symptoms occur afterward

144
Q

What lab abnormalities differentiate chronic hep B from acute?

A

Chronic has the same serologic pattern but surface antigen persists >6mo

145
Q

What is the status of surface antigen, e-antigen, core antibody, and surface antibody in acute hep B, window period, vaccinated individuals, and healed/recovered hep B?

A

Acute dz: surface (+), e (+), core (+), surface (-)
Window period: surface (-), e (-), core (+), surface (-)
Vaccinated: surface (-), e (-), core (-), surface (+)
Recovered: surface (-), e (-), core (+), surface (+)

146
Q

Is there a treatment for acute hep B?

147
Q

Which lab tests indicate active viral replication?

A

Hep B DNA polymerase = e-antigen = Hep B PCR for DNA

(all equivalent tests)

148
Q

Which is the only acute hepatitis that has a treatment available?

149
Q

What is the best initial test for acute Hep C?

A

Hep C ab (cannot tell activity level of virus and stays positive after treatment)

150
Q

What is the most accurate test to tell the activity level of the Hep C virus and degree of viral replication?

A

Hep C PCR for RNA (also most accurate to determine response to therapy)

151
Q

What is the most accurate test to determine the seriousness of acute hep c?

A

Liver biopsy
- pt can have up to 10yrs of viral replication w/ relatively little liver damage
- bx can determine extent of liver damage but isn’t necessary to determine need for tx

152
Q

Which patient with chronic Hep B is most likely to benefit from antiviral therapy? (serologic results)

A

Pt w/ surface antigen, e-antigen and DNA polymerase or PCR for DNA
- look for >6mo positive serology

153
Q

What is the treatment for chronic hep B?

A

ONE of the following
- tenofovir
- lamivudine
- adefovir
- entecavir
- telbivudine
- interferon (ONLY when pt has hep D co-infection)

154
Q

What are the side effects of tenofovir?

A

Bone demineralization and renal tubular acidosis (affects proximal convoluted tubule)

155
Q

What are the side effects of interferon?

A
  • flu-like sxs
  • arthralgia/myalgia
  • fatigue
  • depression
  • thrombocytopenia
156
Q

Who should be tested for Hep C?

A

Everyone 18yo+

157
Q

How can you assess for cirrhosis in chronic hep C pts w/o biopsy?

A

Liver elastography (non-invasive) to assess liver fibrosis
- can determine who may need EGD and beta-blockers to prevent bleeding

158
Q

What is the treatment for chronic hep C? What is required prior to initiating tx?

A

FIRST: genotype of virus determines which treatment combo is ideal

  • PO tx for 12wks
  • all genotypes can be treated w/ sofosbuvir/velpatasvir or glecaprevir/pibrentasvir
159
Q

How do you assess the cure success in chronic hep C?

A

Suppressed PCR-RNA viral load 12 and 24 weeks after therapy stops

160
Q

When is Hep A/B vaccination given? What are specific indications for it?

A

Given in childhood to all patients

Special considerations:
Hep A –> travelers and homeless
Hep B –> healthcare workers, pts on dialysis, diabetes

161
Q

What are the strongest indications for vaccination against both Hep A and B in adults?

A
  • chronic liver dz (greater risk of fulminant hepatitis if infected)
  • household contacts w/ hep A or B
  • men who have sex w/ men
  • chronic recipients of blood products
  • injection drug users
162
Q

How is Hep E acquired? What population is at highest risk and what’s the disease course?

A

Fecal-oral transmission (greater in poor countries)
- worse in pregnant women
- can progress to chronic disease in immunosuppressed pts
- usually resolves spontanteously (ribavirin/interferon in immunosuppressed pts)

163
Q

What is the post-exposure prophylaxis for Hep A?

A

Hep A vaccine is enough
- single dose for pts over 12mo
- if immunocompromised or has chronic liver disease –> immune globulin

164
Q

What are the key features of cirrhosis?

A
  • edema (from low oncotic pressure)
  • gynecomastia
  • palmar erythema
  • splenomegaly
  • thrombocytopenia (2/2 splenic sequestration)
  • encephalopathy
  • ascites
  • esophageal varices
165
Q

How do you treat edema associated w/ cirrhosis?

A

Spironolactone and diuretics

166
Q

How do you treat encephalopathy associated w/ cirrhosis?

A

Lactulose and/or rifaximin

167
Q

What are the HCC screening guidelines for pts w/ cirrhosis?

A

US every 6mos
- 95% sensitive at detecting cancer

168
Q

Which pts w/ ascites need paracentesis?

A

New ascites or old ascites w/ pain, fever, or tenderness

169
Q

What tests should be performed on ascitic fluid from paracentesis? What do they indicate?

A

Fluid albumin level
- serum-to-ascites albumin gradient (SAAG) >1.1 ==> portal HTN from cirrhosis or congestive failure is present

Fluid cell count
- >250 neutrophils ==> SBP

170
Q

What is the treatment of SBP?

A

Cefotaxime or ceftriaxone
- any pt who has had SBP needs lifelong prophylaxis w/ TMP/SMX or norfloxacin

171
Q

What is primary biliary cholangitis?

A

Cause of cirrhosis which presents in middle-aged women complaining of itching
- increases risk of osteoporosis
- xanthelasmas (cholesterol deposits) on exam
- may have hx of immune disorders

172
Q

What are the best initial and most accurate tests for primary biliary cholangitis?

A

Initial: elevated alk phos w/ normal bilirubin, elevated IgM
Most accurate: antimitochondrial antibody (AMA), liver bx

173
Q

What is the treatment for primary biliary cholangitis?

A

Ursodeoxycholic acid
- if no response, add obeticholic acid (suppresses bile acid synthesis)
- if itching, add antihistamine

Cholestyramine can improve symptoms

174
Q

What is primary sclerosing cholangitis? What’s the most accurate test?

A

Sequela of IBD in 80% of cases and cause of cirrhosis
- presents w/ itching, elevated bilirubin and elevated alk phos

ERCP: beading of biliary system
anti-smooth muscle antibody (ASMA) and ANCA positive

175
Q

What is the treatment for primary sclerosing cholangitis?

A

Ursoeoxycholic acid

176
Q

What is Wilson disease? How is it diagnosed?

A

Cirrhosis and liver dz in a pt w/ choreiform movement d/o and neuropsychiatric abnormalities and hemolysis

Best initial test: slit lamp for Kayser-Fleischer rings > ceruloplasmin level (low)
Most accurate: liver bx

177
Q

What is the treatment for Wilson disease?

A

Penicillamine or trientine +/- zinc

178
Q

What is hemochromatosis?

A

Cause of cirrhosis due to genetic disorder causing overabsorption of Fe
- Fe deposits throughout body, mostly in liver
- restrictive cardiomyopathy
- skin darkening
- joint pain (pseudogout or calcium pyrophosphate deposition dz)
- pancreas damage (leads to diabetes)
- pituitary accumulation w/ panhypopituitarism
- infertility
- hepatoma

179
Q

What are the diagnostic tests for hemochromatosis?

A

Best Initial: elevated serum Fe and ferritin w/ low TIBC; iron saturation >45%
Most Accurate: liver biopsy
- MRI + HFe gene mutation test can be used to avoid biopsy

180
Q

What is the treatment of hemochromatosis?

A

Phlebotomy

  • Fe chelators (deferasirox/deferiprone used only for overtransfusion, not genetic overabsorption)
181
Q

What is the classic presentation of autoimmune hepatitis?

A

Young woman w/ autoimmune diseases like Coombs positive hemolytic anemia, thyroiditis, and ITP

182
Q

What are the diagnostic tests and treatment for autoimmune hepatitis?

A

Best initial: ANA (+), antismooth muscle antibody, serum protein electrophoresis (hypergammaglobulinemia)
Most accurate: liver biopsy

Tx: prednisone
- immunosuppressants like azathioprine may be needed to help wean pt off steroids

183
Q

What are the two degrees of NAFLD?

A

Nonalcoholic fatty liver (NAFL): milder; doesn’t cause cirrhosis

Nonalcoholic steatohepatitis (NASH): more severe; leads to cirrhosis and possibly cancer
- strongly associated w/ T2DM, obesity, HLD

184
Q

What are the tests and treatments for NAFLD?

A

Best initial: ALT > AST
Most accurate: liver bx w/ fatty liver infiltration (looks like alcoholic liver dz)

Tx: control underlying causes
- if diabetes, pioglitazone is best initial therapy

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