Gastroenterology Flashcards

1
Q

Primary sclerosing cholangitis
Presentation

A

Patients are usually asymptomatic but can present with fatigue, pruritus, and a cholestatic pattern of elevations in liver function tests.

Continued bile duct destruction leads to end-stage liver disease and portal hypertension.

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2
Q

Primary sclerosing cholangitis investigation

A

Ultrasound is usually nondiagnostic; a cholangiogram (either endoscopic or magnetic resonance) may show multifocal narrowing and dilation of both intrahepatic and extrahepatic bile ducts.

Liver biopsy is helpful for disease staging and prognosis, and can reveal intrahepatic ductal obliteration with moderate lymphocytic infiltration and periductal “onion skin” fibrosis.

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3
Q

Primary sclerosing cholangitis
Screening colonoscopy

A

colonoscopy with full biopsies in newly diagnosed patients with PSC regardless of the presence of other symptoms.
Patients found to have IBD require yearly follow-up with colonoscopy; those with PSC but without IBD should have colonoscopy every 5 years.

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4
Q

Primary sclerosing cholangitis
Treatment

A

Liver transplantation is the preferred treatment for PSC as medical therapy (eg, cyclosporine) does not appear to slow progression of the disease

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5
Q

Boerhaave syndrome (esophageal rupture) is a medical emergency

A

The classic triad of forceful vomiting, chest pain, and subcutaneous emphysema

Chest x-ray may show mediastinal air and the diagnosis can be confirmed with an esophagram.

Another important clinical clue is the rapid development of pleural effusion (often within hours), usually on the left side. Very acidic effusion with high amylase

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6
Q

H.pylori testing in special setting

A

Patients with acute gastrointestinal hemorrhage due to peptic ulcer should undergo endoscopic sampling for Helicobacter pylori.

However, false-negative results can occur due to active gastrointestinal bleeding or certain medications (eg, proton pump inhibitors, bismuth, antibiotics).

Therefore, a negative biopsy should be confirmed by a second test (urea breath or stool antigen) after the patient can safely stop the proton pump inhibitor for 1-2 weeks

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7
Q

Sigmoid volvulus management
“Uncomplicated”

A

Patients without gangrene or perforation (eg, fever, sepsis, peritonitis) need sigmoidoscopy to untwist the volvulus, restore blood supply, and assess colonic viability.

However, sigmoidoscopy should be stopped if gangrene is present.

Most endoscopists leave a rectal tube beyond the volvulus segment to further decompress the bowel and prevent recurrence.

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8
Q

Sigmoid volvulus surgery indication

A

Surgery is reserved for patients with initial perforation/gangrene or recurrent volvulus despite conservative therapy

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9
Q

Acute hepatitis B presentation

A

Acute HBV infection can present with mild flu-like symptoms or fulminant liver failure.

In some patients, a serum sickness-like reaction (fever, rash, and symmetric polyarthralgias/arthritis) may develop, followed by jaundice and nonspecific systemic complaints.

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10
Q

Corrosive ingestion management

A

In a case of corrosive ingestion after initial stabilization is achieved, endoscopy should be performed to grade the severity of injury (within 24 hrs).
Steroids are not recommended in such cases.

All patients with alkali ingestion should have routine screening for esophageal cancer (15-20 years post ingestion)

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11
Q

Celiac disease
Refractory sprue

A

Type I: No initial response to gluten-free diet for 12 months

Type II: Initial response but symptoms return despite dietary adherence
• Poor prognosis & frequent progression to EATL
• Treatment involves glucocorticoids

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12
Q

Celiac disease complications

Enteropathy associated T cell lymphoma & ulcerative jejunoiletis

A

Due to aberrant T cell populations

Presents with abdominal pain, B symptoms & GI bleeding

Often presents with intestinal obstruction or perforation

No response to glucocorticoids

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13
Q

Triglycerides induced pancreatitis
Risks

A

Triglyceride levels (mg/dL)
• <500: minimal risk
• 500-999: mild risk
• 1,000-1,999: moderate risk
• ≥2,000: high risk

Other risk factors: pregnancy, alcoholism, obesity, uncontrolled diabetes

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14
Q

Triglycerides induced pancreatitis
Treatment

A

• Intravenous fluid hydration, pain control

• Triglycerides ≥500 mg/dL: consider insulin infusion

• Triglycerides >1,000 mg/dL or severe pancreatitis (eg, lactic acidosis, hypocalcemia): consider apheresis (therapeutic plasma exchange)

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15
Q

High risk ulcers in GI bleed

A

• Active arterial bleeding
• Nonbleeding visible vessel
• Adherent clot
• Oozing without visible vessel

Management
Endoscopic hemostasis, IV PPI
Clear liquid diet for 2 days, eradicate h.pylori
Hospitalize for 3 days and discharge on PPI BID for 2 weeks then daily.

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16
Q

Intermediate risk ulcers in GI bleed

A

Flat pogmented spot in endoscopy.

Management
• Once-daily oral PPI
• Clear liquids for 1 day
• Eradicate H pylori
• Risk reduction*
Hospitalize for 1-2 days

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17
Q

Hepato pulmonary syndrome

A

The presence of orthodeoxia and platypnea are quite specific for hepatopulmonary syndrome (HPS).
Hepatopulmonary syndrome is seen in 5%-40% of chronic liver disease patients. It is associated with portal hypertension,
typically present with the classic triad of liver disease, hypoxemia, and intrapulmonary vascular dilatations (IPVDs). IPVDs cause right-to-left shunting, which results in cyanosis and hypoxemia.

The IPVDs can be demonstrated by contrast enhanced echocardiography (eg, with agitated saline; “bubble study”)
There is no effective medical therapy for HPS, and liver transplant is recommended for patients with severe hypoxemia.

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18
Q

Mallory Weiss tear

A

upper gastrointestinal mucosal tear due to a sudden increase of intra-abdominal pressure from forceful retching. Endoscopy is preferred for diagnosis. Most patients have self-limited (24-48 hours) bleeding with spontaneous healing of ulcers. Patients with active bleeding usually require endoscopic treatment with epinephrine injection, cautery, or hemoclip application.

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19
Q

Microscopic colitis
Presentation & Risk factors

A

Presentation
• Chronic watery, nonbloody diarrhea
• Fecal urgency & incontinence
• Variable abdominal pain, weight loss

Risk factors
• Smoking
• Medications (eg, NSAIDs, PPIs, SSRIs)
• Female age ≥45

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20
Q

Microscopic colitis
Diagnosis and treatment

A

Diagnosis
Colonoscopic biopsy: mononuclear infiltrate in lamina propria
• Collagenous: thickened subepithelial collagen band
• Lymphocytic: high concentration of intraepithelial lymphocytes +/- cryptitis

Treatment
• Withdrawal of trigger medications; smoking cessation
• Antidiarrheal medications & oral budesonide

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21
Q

Gastrinoma presentation

A

Which can be sporadic or found in conjunction with multiple endocrine neoplasia type 1 (MEN-1) in 20% of cases.

Gastrinomas usually present in patients age 20-50 with dyspepsia, reflux symptoms, abdominal pain, weight loss, or frank gastrointestinal bleeding.

Endoscopy often shows thickened gastric folds, multiple peptic ulcers, refractory ulcers despite proton pump inhibitor use, or ulcers distal to the duodenum in the jejunum.

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22
Q

Gastrinoma presentation

A

Which can be sporadic or found in conjunction with multiple endocrine neoplasia type 1 (MEN-1) in 20% of cases.

Gastrinomas usually present in patients age 20-50 with dyspepsia, reflux symptoms, abdominal pain, weight loss, or frank gastrointestinal bleeding.

Endoscopy often shows thickened gastric folds, multiple peptic ulcers, refractory ulcers despite proton pump inhibitor use, or ulcers distal to the duodenum in the jejunum.

23
Q

Gastrinoma diagnosis

A

The gastrin level should be checked in suspected gastrinoma; a level < 110pg / mL rules it out.

A gastrin level > 1000pg / mL highly suggestive and requires checking the gastric pH off PPI, with pH > 4 ruling out gastrinoma. ApH <= 4 suggests gastrinoma and requires further testing (eg, endoscopic ultrasound, somatostatin Xeceptor scintigraphy, and CT or MRI) for localization.

A gastrin level of 110 - 1000pg / m L requires a follow-up secretin stimulation test. A negative secretin test rules out gastrinoma; a positive test requires further localization testing.

24
Q

Gastrinoma treatment

A

Gastrinoma associated with MEN-1 syndrome usually responds to proton pump therapy. However, surgery is usually preferred for sporadic gastrinomas or MEN-1 patients with uncontrolled symptoms on medical therapy.

25
Q

Gastrinoma treatment

A

Gastrinoma associated with MEN-1 syndrome usually responds to proton pump therapy. However, surgery is usually preferred for sporadic gastrinomas or MEN-1 patients with uncontrolled symptoms on medical therapy.

26
Q

CMV esophagitis

A

• EGD: Sharply demarcated, linear ulcers in distal 1/3 of esophagus
• Biopsy: Intranuclear inclusions
• IV ganciclovir

27
Q

HSV esophagitis

A

• EGD: Well-circumscribed shallow ulcers
• Biopsy: Stains positive for herpes simplex virus, viral culture
• Tx: Acyclovir

28
Q

Abdominal pain post endoscopy

A

Perforation from routine endoscopic procedures is uncommon and typically occurs from mechanical trauma, barotrauma, electrocautery, or therapeutic interventions.

Immediate abdominal (upright or lateral decubitus) and upright chest radiographs can confirm a perforation. Patients with high clinical suspicion for perforation and negative x-rays should undergo CT scan with a water-soluble contrast agent, which can detect subtle perforation

29
Q

Primary biliary cholangitis diagnostic criteria

A

The diagnosis of primary biliary cholangitis can be established without a liver biopsy in patients with an alkaline phosphatase level elevated more than 1.5 times the upper limit of normal and positive results on testing for antimitochondrial, sp100, or gp210 antibodies.

30
Q

Wilson disease

A

Hepatic
• Asymptomatic liver function abnorma
• Chronic hepatitis
• Acute liver failure
Neuropsychiatric
• Parkinsonian-like tremor, rigidity, clumsiness of gait
• Subtle personality changes to overt depression, paranoia, and catatonia
Other
• Hemolytic anemia
• Fanconi syndrome
• Recurrent nephrolithiasis
• Premature arthropathy & chondrocalcinosis (common in knees)

Diagnosis is supported by increased serum and urine copper levels, and decreased serum ceruloplasmin levels. Early diagnosis and medical therapy with penicillamine or trientine may prevent many of the permanent sequelae.

31
Q

When to do PH monitoring while on PPIs

A

pH monitoring study should be performed during therapy with a PPI when the diagnosis of GERD is certain, but the patient has not had a response to acid-suppressive therapy.

32
Q

GERD defining conditions

A

🔴 Total Acid Exposure time > 6%.
🔴Reflux esophagitis LA B,C&D.
🔴Long segment Barret’s esophagus (>3 cm).
🔴Peptic stricture.

33
Q

Functional heart burn

A

Normal acid exposure + Negative symptom-reflux association

34
Q

Acid hypersensitivity

A

Normal acid exposure + positive acid-reflux symptoms association

35
Q

Barret’s Esophagitis screening caveat

A

Patients with erosive esophagitis (LA grade B, C, or D) should have another endoscopic evaluation after 8 to 12 weeks of PPI therapy to assess for underlying BE and healing of esophagitis

36
Q

Adult with dyspepsia approach

A

Age >60 ⏩ EGD
Age <60 ⏩ test for H.pylori (if negative treat with PPI)

37
Q

Gastric emptying study positive results

A

retained meal value > 60% at 2 hr or > 10% at 4 hr support Dx

38
Q

Vitamin A toxicity

A

🔴portal hypertension
🔴 Rash
🔴 headaches (pseudotumor cerebri)

39
Q

Stool osmotic gap (SOG)

A

= Serum osmolality - 2 *(stool Na + Stool K)

Secretory diarrhea SOG<50
Osmotic diarrhea. SOG >125

In between is indeterminate

40
Q

Whipple’s disease

A

🔴Caused by the bacterium Tropheryma whipplei.

🔴Symptoms: weight loss, arthritis, carditis, neurological manifestation.

🔴Both Tropheryma whipplei and MAC can infect the small bowel and cause macrophages to stain positive with PAS.

🔴Acid-fast staining of biopsy samples will be positive if patients have MAC infection and negative if patients have Whipple disease.

🔴Treatment: at least 1 year of trimethoprim- sulfamethoxazole with 2 weeks of intravenous induction therapy in severe cases or cases of central nervous system involvement with an antibiotic that penetrates the blood- brain barrier, such as ceftriaxone or meropenem.

41
Q

Pyoderma gangrenosum treatment

A

Pyoderma gangrenosum [PG] can be treated with sys- temic corticosteroids, infliximab [EL1b] or adalimumab [EL3b], or topical or oral calcineurin inhibitors [

42
Q

Medications adjustment in cirrhosis

A

• Medications that decrease renal perfusion pressures, such as ACE inhibitors, can worsen ascites in patients with portal hypertension.

•B-Blockers and NSAIDs should be used with caution or discontinued in patients with portal hypertension and ascites.

43
Q

Hepatic abscess management

A

• In patients with pyogenic liver abscess, empiric broad-spectrum parenteral antibiotics that cover streptococci, enteric gram-negative bacilli, and anaer- obes should be initiated.

• Hepatic abscesses 3 cm or greater in diameter typi- cally do not resolve with antibiotic therapy alone, and aspiration of the abscess by percutaneous needle approach is warranted

44
Q

Uncomplicated diverticulitis treatment

A

• Uncomplicated diverticulitis is treated with oral anti- biotics (ciprofloxacin or metronidazole) and a liquid diet.

• Hospitalization and intravenous antibiotics are required to treat acute diverticulitis in patients who cannot tolerate an oral diet; patients with severe comorbidities, advanced age, or immunosuppression; and patients for whom oral antibiotics have been ineffective.

45
Q

Constipation evaluation

A

• Constipation can be secondary or functional (idio- pathic); medications are the most common cause of secondary constipation.

• Colonoscopy is the initial evaluation of constipation in elderly patients with acute constipation and patients with unintentional weight loss, family history of colo- rectal cancer, unexplained anemia, and age older than 50 years with no previous colonoscopy

46
Q

Management of Autoimmune hepatitis

A

• The mainstay of treatment of autoimmune hepatitis is immunosuppression with prednisone or a combination of prednisone and azathioprine.

• Because autoimmune hepatitis has a high rate of relapse, therapy is recommended for at least 2 to 3 years before discontinuation of the medications.

47
Q

HCC management

A

• Patients with hepatocellular carcinoma who have well-compensated cirrhosis, no symptoms referable to liver disease, no evidence of portal hypertension, and normal liver function markers should be referred for surgical resection.

• Liver transplantation for hepatocellular cancer is the best therapy for patients who also have portal hypertension or features of liver dysfunction.

48
Q

Suspect PSC in UC patients with cholestatic liver injury

A

• Primary sclerosing cholangitis is an autoimmune fibroinflammatory disease that most commonly affects the large bile ducts but can also affect the small intrahepatic ducts; it can be diagnosed with magnetic resonance cholangiopancreatography.

• Liver biopsy is needed to diagnose small-duct primary sclerosing cholangitis.

49
Q

Hepatic adenoma management

A

• Factors posing an increased risk for malignant transformation of hepatic adenomas include adenomas greater than 5 cm in diameter, adenomas with B-catenin activation, or adenomas found in men.

Adenoma with high risk of malignant transformation should undergo resection.

• Oral contraceptives should be discontinued in women with hepatic adenomas with follow-up CT or MRI at 6-month intervals to confirm stability or regression in the size of the lesion.

50
Q

When to treat for HBV

A

• Treatment of hepatitis B virus (HBV) infection is advised for patients with acute liver failure, chronic infection in the immune-active phase or reactivation phase, or cirrhosis and for selected immunosuppressed patients.

• Immune-active chronic HBV infection is defined by presence of hepatitis B core antibody, elevated alanine aminotransferase level, and HBV viral load greater than 2000 U/ml. in patients negative for hepatitis B e antigen and greater than 20,000 U/mL in patients positive for hepatitis B e antigen

51
Q

Acute cholecystitis management

A

• Acute cholecystitis can be diagnosed by ultrasonogra- phy showing gallbladder wall thickening and/or edema and a positive Murphy sign elicited during ultrasonography.

• Treatment of acute cholecystitis includes analgesia, intravenous antibiotics with gram-negative and anaerobic coverage, and cholecystectomy before hospital discharge.
Emergency surgery is necessary for suspected gallbladder perforation or emphysematous cholecystitis

52
Q

Lynch syndrome screening

A

Lynch syndrome is caused by germline mutations in the mismatch repair genes MLH1, MSH2, MSH6, and PMS2 or the epithelial cell adhesion molecule gene (EPCAM).

• Patients with Lynch syndrome should be screened for colon cancer with colonoscopy beginning at ages 20 to 25 years (or 2-5 years before the earliest cancer diagnosis in the family) and screened for stomach and small-bowel cancers with upper endoscopy beginning at age 30 to 35 years.

53
Q

Hepato pulmonary syndrome vs Porto pulmonary hypertension

A

• Features of hepatopulmonary syndrome include orth- odeoxia (worsening oxygen saturation while upright) and platypnea (worsening sense of dyspnea when upright); echocardiography with contrast can confirm the diagnosis.

• Patients with cirrhosis and portal hypertension who present with dyspnea on exertion should be suspected of having portopulmonary hypertension; echocardiography is the initial screening test

54
Q

Gallbladder polyps

A

• Gallbladder polyp size greater than 1 cm is a risk factor for malignancy; treatment for such polyps should be cholecystectomy.

• Gallbladder polyps associated with gallbladder stones or primary sclerosing cholangitis are more likely to be neoplastic regardless of the polyp size.