UWorld 1

Question 1

Dysphagia, coughing, regurgitation, halitosis and a neck mass

Answer 1

Zenker

Question 2

Zenker (pharyngoesophageal) diverticulum

Answer 2

Clinical

1) Usually at least 60 years old
2) More common in males
3) Dysphagia
4) Halitosis
5) Regurgitation and aspiration
6) Variable neck mass

Dx

1) Barium esophagram
2) Esophageal manometry

Management

1) Open/endoscopic surgery
2) Cricopharyngeal myotomy

Potential complications - tracheal compression, ulceration with bleeding, regurgitation, pulmonary aspiration

Question 3

What is thought to cause ZD?

Answer 3

Upper esophageal sphincter dysfunction and esophageal dysmotility

It’s above the upper esophageal sphincter. Caused by posterior herniation btw fibers of the cricopharyngeal muscle.

Question 4

Precipitating factors for hepatic encephalopathy

Answer 4

1) Drugs (sedatives, narcotics)
2) Hypovolemia (diarrhea, vomiting, diuretics, high volume paracentesis)
3) Excessive nitrogen load (GI bleeding, constipation, high protein diet)
4) HypoK and metabolic alkalosis
5) Hypoxia and hypoglycemia
6) Infection (pneumonia, UTI, spontaneous bacterial peritonitis)
7) Portosystemic shunting (surgical shunts)

Question 5

Clinical presentation of hepatic encephalopathy

Answer 5

Stage 1

1) Hypersomnia, insomnia, or inverted sleep cycle
2) Slightly impaired cognition
3) Mild confusion
4) Tremor, possible asterixis

Stage 2

1) Lethargy with slow response to stimuli
2) Moderate confusion
3) Difficulty with writing, slurred speech

Stage 3

1) Marked confusion
2) Sleeping but arousable

Stage 4 - stupor or coma

Question 6

What test can help support a clinical suspicion of hepatic encephalopathy?

Answer 6

Ammonia level, thought it is fairly nonspecific and may be elevated in ASx patients

Question 7

When should you give ABx ppx in a patient with GI bleed?

Answer 7

Cirrhotics - decreases infectious complications, recurrent bleeding and mortality

Question 8

Somatostatin analogs

Answer 8

Octreotide. Inhibits the release of vasodilator hormones, which leads indirectly to splanchnic vasoconstriction and decreased portal flow.

Question 9

Hemoglobin goal in a variceal bleed

Answer 9

Keep above 9. Get serial blood counts.

Platelet transfusion below 50k.

Question 10

Common complications of an esophageal variceal bleed

Answer 10

Coagulopathy, anemia, thrombocytopenia

Question 11

Clinical features of chronic Hep C

Answer 11

Clinical
1) Can be asymptomatic or develop fatigue (most common)***

2) Serum LFTS can be elevated or normal (up to a third of patients)
3) Can progress to cirrhosis in up to 20% of cases
4) Increased risk of HCC

Extrahepatic manifestations

1) Heme - Essential mixed cryoglobulinemia
2) Renal - Membranoproliferative glomerulonephritis
3) Skin - porphyria cutanea tarda, lichen planus
4) Endocrine - Increased risk of diabetes

Question 12

Intermittent elevations of transaminases with fragile skin, photsensitivity, and vesicles /erosions on dorsum of the hands.

Answer 12

Hep C with porphyria cutanea tarda (all patients with PCT should be screened for Hep C)

Question 13

Essential mixed cryoglobulinemia

Answer 13

Half of Hep C patients have cryoglobulinemia

Due to circulating immune complexes that deposit in small to medium vessels and may be associated with low serum complement levels. Patients can develop palpable purpura, arthralgias, renal complications (usually membranoproliferative glomerulonephritis)

Question 14

Pathophys of hepatic encephalopathy

Answer 14

CNS complication of cirrhosis due to liver’s inability to convert ammonia to urea

Question 15

Tx of hepatic encephalopathy

Answer 15

Involves supportive care, treating the underlying precipitant, and lowering the serum ammonia.

Nonabsorbable disaccharides (lactulose, lacitol) are preffered for lowering serum ammonia.

Colonic bacteria metabolize lactulose to short chain fatty acids (lactic acid, acetic acid). This acidifies the colon to stimulate conversion of the absorbable ammonia to the nonabsorbable ammonium (an ammonia trap) and also causes a catharsis

ABx (rifaximin) can decrease the number of ammonia-producing bacteria in the colon. They are usually added to lactulose if patient does not improve within 48h

Catharsis using any laxative may help as well.

Question 16

Spontaneous Bacterial Peritonitis

Answer 16

Clinical

1) Temp of at least 37.8C (100F) - patients with cirrhosis are usually relatively hypothermic so any temp of 100 should be investigated
2) Abdominal pain/tenderness
3) AMS (abnormal connect-the numbers test - Reitan trail test)
4) Hypotension, hypothermia, paralytic ileus (dilated loops of bowel on XR) with severe infection

Diagnosis from ascitic fluid

1) PMNs of at least 250
2) Positive culture, often gram negative organisms (E Coli, Kleb)
3) Protein less than 1
4) SAAG of at least 1.1

Tx

1) Embiric ABx - third generation cephalosporins (cefotaxime)
2) Fluoroquins for SBP ppx

Question 17

What exactly IS spontaneous bacterial peritonitis?

Answer 17

Ascitic fluid infection without an obvious intraabdominal surgical etiology

Most likely due to either intestinal bacterial translocation directly into the ascitic fluid or hematogenous spread to the liver and ascitic fluid (due to other bacterial infections)

Question 18

Major risk factors for pancreatic cancer

Answer 18

Hereditary

1) First degree relative with pancreatic cancer
2) Hereditary pancreatitis
3) Germline mutations (BRCA1, BRCA2, Peutz-Jeghers Syndrome)

Environmental

1) Cigarette smoking (most significant)
2) Obesity, low physical activity
3) Nonhereditary chronic pancreatitis

Long standing diabetes is also a risk factor

Question 19

Common causes of steatorrhea

Answer 19

Pancreatic insufficiency

1) Chronic pancreatitis due to alcohol abuse, cystic fibrosis, or autoimmune/hereditary pancreatitis
2) Pancreatic cancer

Bile salt related

1) Small bowel Crohn’s
2) Bacterial overgrowth
3) Primary biliary cirrhosis
4) Primary sclerosing cholangitis
5) Surgical resection of ileum (at least 60-100cm)

Impaired intestinal surface epithelium

1) Celiac disease
2) AIDS enteropathy
3) Giardiasis

Other rare causes

1) Whipple Disease
2) ZE Syndrome
3) Medication - induced

Question 20

Presentation of steatorrhea

Answer 20

Patients typically develop loose, greasy, malodorous stools that float in the toilet (occasionally with oil droplets) and are difficult to flush

Other symptoms include abdominal distension and borborygmi

Nutritional deficiencies (fat soluble vitamins, vitamin B12) may occur and lead to clinical symptoms and weight loss despite a good appetite

Confirmed by fecal fat tests (Sudan stain on spot stool specimen or 72h collection).

Question 21

Very basic chronic pancreatitis presentation

Answer 21

Long term alcohol use can cause it. Progressive inflammation results in permanent damage to endocrine AND exocrine pancreas. After 90% functional loss, patients develop fat and protein malabsorption

They typically develop postprandial epigastric pain (15-30 minutes after a meal) that is intermittent early in the disease and becomes persistent with disease progression

Question 22

Primary sclerosing cholangitis

Answer 22

Clinical

1) Fatigue and pruritus
2) Majority of patients asymptomatic at time of dx
3) About 90% of patients have underlying IBD, mainly UC

Lab/imaging

1) Cholestatic liver function test pattern (serum aminotransferases usually less than 300)
2) Multifocal stricturing/dilation of intrahepatic and/or extrahepatic bile ducts on cholangiography

Liver bx
1) Fibrous obliteration of small bile ducts with concentric replacement by connective tissue in an “onion skin” pattern

Complications

1) Intrahepatic and/or extrahepatic biliary stricture
2) Cholangitis and cholelithiasis (cholesterol and/or pigment stones)
3) Cholangiocarcinoma (10-15% lifetime risk)
4) Cholestasis (low fat soluble vitamins, osteoporosis)
5) Colon cancer

Question 23

Dx of PSC

Answer 23

US is usually nondiagnostic. Cholangiogram (either endoscopic retrograde or magnetic resonance) usually confirms the dx by showing multifocal narrowing with intrahepatic and extrahepatic duct dilation (beading)

Liver bx can determine stage and prognosis. Usually shows onion skin pattern.

Question 24

Prognosis of PSC

Answer 24

It’s a progressive condition. Disease course includes cholestatic complications (fatigue, pruritus, steatorrhea, fat soluble vitamin deficiencies, metabolic bone disease) and hepatic failure

Patients who do not get a liver transplant have a mean survival of 12 years after dx.

Question 25

Cirrhosis, neuropsych symptoms, and brownish/gray-green rings in eye in young adult. What disease? Background info.

Answer 25

Hepatolenticular Degeneration (WIlson Disease)

Kayser-Fleisher Rings are the eye rings - granular copper deposits in cornea

Rare, autosomal recessive disease most often identified in younger people ages 5-40.

The genetic mutations involved hinder Cu metabolism by reducing the formation and secretion of ceruloplasmin and by decreasing the secretion of Cu into the biliary system.

Cu is pro-oxidant, and as it accumulates in greater quantities within the liver, it causes damage to hepatic tissue through the generation of free radicals. Eventually, Cu leaks from injured hepatocytes into the blood to be deposited in various tissues, including the basal ganglia (hepatolenticular degeneration) and cornea

Question 26

Presentation and dx of Wilson Disease

Answer 26

ASx liver function abnormalities, chronic hepatitis, fulminant hepatitis, portal HTN, or macronodular cirrhosis.

Neuropsych - Parkinson-like tremor, rigidity, ataxia, slurred speech, drooling, personality changes, depression, paranoia, catatonia.

Wilson’s is also associated with Fanconi Anemia, hemolytic anemia, and neuropathy

Gold standard for dx is Liver Bx that shows hepatic copper greater than 250 dry weight.

More commonly, dx is confirmed by low serum ceruloplasmin (particularly less than 20) in conjunction with increased urinary copper excretion or Kayser-Fleishcer rings

Question 27

Tx of Wilson’s Disease

Answer 27

Must be adhered to for the patient’s lifetime and focuses on removing accumulated copper in the tissues and preventing re-accumulation

First line meds - copper chelators like D-penicillamine or trientine

Oral Zinc is also recommended as it prevents copper absorption

Liver transplant may be only option of those with fulminant hepatitis or decompensated liver disease that does not respond to pharm

Question 28

Ascites fluid characteristics

Answer 28

Color

1) Bloody - trauma, malignancy, TB (rarely)
2) Milky - Chylous, pancreatic
3) Turbid - Possible infection
4) Straw color - likely more benign causes

Neutrophils

1) Less than 250 - no peritonitis
2) 250 and up - Peritonitis (secondary or spontaneous bacterial)

Total protein
1) 2.5 and up (high protein ascites) - CHF, constrictive pancreatitis, peritoneal carcinomatosis, TB, Budd-Chiari Syndrome, Fungal (coccidiomycosis)

2) Less than 2.5 - Cirrhosis, nephrotic syndrome

SAAG
1) 1.1 and up (indicates portal HTN) - cardiac ascites, cirrhosis, Budd-Chiari

2) Less than 1.1 (absence of portal HTN) - TB, peritoneal carcinomatosis, pancreatic ascites, nephrotic syndrome

Question 29

SAAG

Answer 29

Serum-to-Ascites Albumin Gradient. Subtract the peritoneal albumin from the serum albumin

Above 1.1 - possible portal HTN etiology, therefore the ascites may be due to increased hydrostatic pressure within hepatic capillary beds

Less than 1.1 - Increased capillary permeability (eg malignant ascites, pancreatitis, nephrotic, TB)

Question 30

Crohn’s vs UC - granulomas

Answer 30

Crohn’s

Question 31

Features of malabsorption in celiac disease

Answer 31

1) General - Bulky, foul smelling, floating stools
2) Fat and protein - Loss of muscle mass, loss of subq fat, fatigue
3) Iron - Pallor (anemia), fatigue
4) Calcium and Vit D - Bone pain (osteomalacia), fracture (osteoporosis)
5) Vit K - Easy bruising
6) Vit A - Hyperkeratosis

Question 32

Dx of Celiac

Answer 32

IgA anti-tissue transglutaminase and IgA anti-endomysial antibodies

BUT, many patients with bx-confirmed (villous atrophy) disease will have negative antibody results since IgA deficiency is fairly common in Celiac

If suspicious for Celiac is high but IgA serology is negative, measure total IgA (or get IgG based serology)

Question 33

Collagenous Colitis

Answer 33

Uncommon disorder producing chronic watery diarrhea. Colon is frequently involved, but colonoscopy shows normal mucosa.

Bx shows mucosal subepithelial collagen deposition

Question 34

ZE Syndrome

Answer 34

Epi

1) Age 20-50
2) 80% Sporadic/20% MEN1

Clinical

1) Multiple and refractory peptic ulcers
2) Ulcers distal to duodenum
3) Chronic diarrhea

Dx
1) Markedly elevated serum gastrin (more than 1000) in the presence of normal gastric acid (pH less than 4)

Workup

1) Endoscopy
2) CT/MRI and somatostatin receptor scintigraphy for tumor localization

Question 35

Diagnosis of ZES

Answer 35

Gastrinoma is usually in pancreas or duodenum

Dx is suggested by marked elevation in serum gastrin (above 1000) in presence of acidic gastric pH (less than 4).

Endoscopy reveals ulcers usually (90%) and sometimes will ID a primary duodenal gastronoma

CT, MRI and somatostatin receptor scintigraphy can be used to ID pancreatic tumors and metastatic disease

If gastrinoma is confirmed, patients should be screened for MEN with assays for PTH, ionized Ca, and Prolactin

Question 36

Compensated vs uncompensated cirrhosis

Answer 36

Patients with compensated cirrhosis typically are either ASx or complain of vague symptoms (anorexia, weakness, fatigue)

Those with decompensated cirrhosis may present with jaundice, pruritus, upper GI bleeding, abdominal distention due to ascites, or confusion due to hepatic encephalopathy

Question 37

Major cause of morbidity and mortality in cirrhosis

Answer 37

Esophageal varices. They can occur in half of patients.

Question 38

Gold standard for diagnosis of cirrhosis

Answer 38

Liver biopsy, though clinical impression and history is usually enough

Question 39

ASx patient with elevated Alk Phos with normal hepatic enzymes, normal RUQ US, and positive anti-mitochondrial antibody assay

Answer 39

Early Primary biliary cholangitis (formerly primary biliary cirrhosis)

Chronic, progressive liver disease characterized by cholestasis with autoimmune destruction of intrahepatic bile ducts

Most common in middle aged women and has insidious onset. Pruritus and fatigue are usually first symptoms.

As it progresses, jaundice, steatorrhea, HSM, eyelid xanthelasma, portal HTN, and osteopenia may develop

Drug of choice - ursodeoxycholic acid. Less effective in advanced disease that may require liver transplant.

Question 40

Ursodeoxycholic acid

Answer 40

used in a number of cholestatic disorders. It is a hydrophilic bile acid that decreases biliary injury by the more hydrophobic endogenous bile acids.

Also increases biliary secretion and may have additional anti-inflammatory effects. It delays progression in PBC and may improve symptoms and possibly survival.

Start it in PBC as soon as dx is made, even if patient is asymptomatic

Liver transplant is definitive treatment but only indicated in those with severe liver damage or cirrhosis

Question 41

Solid liver masses

Answer 41

Focal nodular hyperplasia

1) Associated with anomalous arteries
2) Arterial flow and central scar on imaging

Hepatic adenoma

1) Women on long term OCPs
2) Possible hemorrhage or malignant transformation

Regenerative nodules
1) Acute or chronic liver injury (cirrhosis)

HCC

1) Systemic symptoms
2) Chronic hepatitis or cirrhosis
3) Elevated AFP

Liver mets

1) Single/multiple lesions
2) Known extrahepatic malignancy

Question 42

Dx of hepatic adenoma

Answer 42

It’s benign!

US shows well-demarcated, hyperechoic lesions

Contrast CT can show early peripheral enhancement.

Needle bx is not recommended for suspected hepatic adenoma due to risk of bleeding. Surgical excision is preferred.

Long term complications are progressive growth, rupture, and malignant transformation

Question 43

HCC (brief)

Answer 43

Characterized by rapidly enlarging liver mass, often with satellite lesions. It usually occurs in patients with cirrhosis or chronic hepatitis (esp B)

Question 44

Hydatid cyst

Answer 44

Caused by echinococcus tapeworm. In USA, most cases are seen in immigrants, although occasional cases may be seen in individuals from the southwest who have been exposed to sheep and dogs

It causes cystic not solid liver lesions

Question 45

Nonalcoholic fatty liver disease

Answer 45

Definition

1) Hepatic steatosis on imaging or biopsy
2) Exclusion of significant alcohol use
3) Exclusion of other causes of fatty liver

Clinical

1) Mostly ASx
2) Metabolic Syndrome
3) With or without steatohepatitis (AST/ALT less than 1)
4) Hyperechoic texture on US

Tx

1) Diet and exercise
2) Consider bariatric surgery if BMI is at least 35

Question 46

Typical patient with NAFLD

Answer 46

Middle aged, obese, with features of the metabolic syndrome

Question 47

Histology of NAFLD

Answer 47

Can range from bland steatosis to inflammation and necrosis (steatohepatitis) to fibrosis and cirrhosis

Can resemble alcohol-induced fatty liver (macrovesicular fat deposition, peripheral displacement of nuclei) but occurs in patients with minimal or no alcohol history

Question 48

pathophys of NAFLD

Answer 48

Can be due to increased transport of free fatty acids from adipose tissue to the liver, decreased oxidation of FFA in the liver, or decreased clearance of FFA from the liver (due to decreased VLDL production)

Frequently related to peripheral insulin resistance leading to increased peripheral lipolysis, triglyceride synthesis, and hepatic uptake of fatty acids

Hepatic FFA increases oxidative stress and production of proinflammatory cytokines (tumor necrosis factory alpha)

Question 49

Acute erosive gastritis

Answer 49

Characterized by the development of severe hemorrhagic erosive lesions after exposure to gastric mucosa to various injurious agents or after a substantial reduction in blood flow

Aspirin decreases the protective prostaglandin production. In addition, aspirin and alcohol cause direct mucosal injury

Acute mucosal injury decreases the normal protective barriers (decreased levels of secreted mucins and bicarb and decreased integrity of the epithelium), thus permitting acid and other luminal substances (proteases and bile acids) to penetrate into the lamina propria, thereby causing additional injury to vasculature and subsequent hemorrhage.

Patients may manifest with hematemesis and abdominal pain

***NSAIDs and aspirin cause acute erosive gastritis and upper GI bleeding. Alcohol can make it worse. It is NOT the platelet dysfunction that NSAIDs cause. It is direct injury.

Question 50

Etiologies of acute pancreatitis

Answer 50

1) Chronic alcohol use
2) Gallstones
3) Hyperlipidemia (types 1, 4, and 5)
4) Drugs (didanosine, azathioprine, valproic acid)
5) Infections (CMV, Legionella, Aspergillus)
6) Trauma
7) Iatrogenic (post-ERCP)

Question 51

Clinical presentation of acute pancreatitis

Answer 51

Diagnosis requires 2 of the following

1) Acute epigastric abd pain often radiating to the back
2) Increased amylase, lipase (more than 3 times normal limit)
3) Abdominal imaging showing focal or diffuse pancreatic enlargement with heterogeneous enhancement with IV contrast (CT) or diffusely enlarged and hypoechoic pancreas (US)

Other findings

1) n/v, leukocytosis
2) Severe disease with possible abdominal tenderness, fever, tachypnea, hypoxemia and hypotension
3) ALT level above 150 - biliary pancreatitis

Question 52

Complications of acute pancreatitis

Answer 52

1) Pleural effusion
2) Ileus
3) Pancreatic pseudocyst/abscess/necrosis
4) ARDS

Question 53

Pathophys of acute pancreatitis

Answer 53

Early in pancreatitis, the pancreas synthesizes digestive enzymes but cannot secrete them. These enzymes leak out of the acinar cells into the systemic circulation.

Amylase rises within 6-12h of symptom onset and may remain elevated for 3-5 days.

Lipase rises within 4-8h of symptom onset but remains elevated longer than amylase (8-14d)

As a result, lipase is more useful and sensitive than amylase for dx (esp in alcoholics and patients presenting later in disease course)

Question 54

When is imaging needed for acute pancreatitis

Answer 54

If diagnosis is unclear, or patient does not improve with conservative management (to ID infection or necrosis)

Once diagnosis is made, US can be done to find cause (gallstones)

Early ERCP for suspected biliary pancreatitis may decrease morbidity and mortality.

ERCP is also useful for evaluating patients with recurrent pancreatitis or draining pancreatic pseudocysts

Question 55

Lab values consistent with Fe deficiency anemia

Answer 55

Low serum Fe and ferritin with high TIBC

Question 56

New Fe def anemia in elderly patient

Answer 56

Should be considered to be from GI blood loss (polyps, cancer, angiodysplasia) until proven otherwise

A positive FOBT without lab values is enough to guide management to colonoscopy and endoscopy

A negative FOBT is not enough to rule out occult GI bleed.

Elderly patients with IDA should get colonoscopy and endoscopy despite a single negative FOBT, esp if no other obvious source of chronic blood loss is identified.

Question 57

Isotope-labeled erythrocytes scintigraphy

Answer 57

Radioisotope scan that is useful in determining the source of active bleeding but not diagnostic in absence of active bleed

Typically used in acute (NOT chronic) GI blood loss when source of bleeding remains unidentified on colonoscopy and endoscopy

Question 58

Clinical clues for common etiologies of cirrhosis (11)

Answer 58

More common
1) Chronic hepatitis B or C infections - IV drug use, blood transfusions, multiple sexual contacts

2) Alcoholic liver disease - excessive alcohol intake
3) Nonalcoholic fatty liver disease - Diabetes, obesity and/or metabolic syndrome
4) Hemochromatosis - FHx of cirrhosis; history of diabetes, bronze skin, high transferrin saturation

Less common
1) Autoimmune - FHx of cirrhosis, history of other coexisting autoimmune disorders (thyroiditis), anti-smooth muscle/liver kidney microsomal type 1 antibodies

2) PBC - more common in women, fatigue, pruritus, elevated alk phos, positive antimitochondrial antibody
3) PSC - Associated with IBD
4) Alpha 1 antitrypsin deficiency - coexisting lung involvement. FHx of cirrhosis
5) Cardiac cirrhosis - coexisting R-sided HF
6) Meds - Methotrexate, isoniazid
7) Wilson Disease - FHx of cirrhosis at young age, KF rings in eyes

Question 59

Most likely cause of cirrhosis

Answer 59

Alcohol or hepatitis or NAFLD. Pick one of these 3 if the question is about “most likely” in USA

Question 60

Mallory-Weiss tear

Answer 60

Etiology

1) Sudden increase in abdominal pressure (forceful retching, blunt abdominal trauma)
2) Mucosal tear in esophagus or stomach (submucosal arterial or venous plexus bleeding)
3) Risk - hiatal hernia, alcoholism***

Clinical

1) Vomiting, retching
2) Hematemesis
3) Epigastric pain

Dx
1) Longitudinal laceration on endoscopy near GEJ

Tx

1) Most heal spontaneously
2) Endoscopy therapy for persistent bleeding (electrocoagulation or local injection of epinephrine)

Question 61

Toxic megacolon

Answer 61

Typically presents with total or segmental nonobstructive colonic dilation, severe bloody diarrhea and systemic findings (fever, tachy)

IBD patients are at the highest risk of developing it early in the disease, within 3 years of dx.

Other causes of toxic megacolon:

1) Ischemic colitis
2) Volvulus
3) Diverticulitis
4) Infections (C Dif)
5) Obstructive colon cancer (less common)

Dx is confirmed on plain abdominal XR and at least of the following:

1) Fever above 38C
2) Pulse over 120
3) WBC over 10,500
4) Anemia

May also see volume depletion, AMS, hypotension, lyte issues. Plain XR shows dilated Right or Transverse Colon (greater than 6cm), possible multiple air-fluid levels, and thick haustral markings that do not extend across the entire lumen

Tx - it’s an emergency! Can cause perforation. Give IV fluids, broad spectrum ABX, NG decompression, and bowel rest.

IV steroids are preferred for treating IBD-induced toxic megacolon

Emergency surgery (subtotal colectomy with end ileostomy as procedure of choice) may be needed if it does not resolve

Question 62

D-xylose

Answer 62

monosccharide that can be absorbed in the proximal small intestine WITHOUT degradation by pancreatic or brush border enzymes

It is then excreted in the urine.

In the D-xylose test, patient is given an oral dose with subsequent assay of urine and venous blood.

Patients with proximal intestine mucosal disease (Celiac) cannot absorb D-xylose in the intestine, and urinary and venous D-xylose levels will be low. Fecal levels will be high.

Patients with malabsorption due to enzyme deficiencies (chronic pancreatitis) will have normal absorption of D-xylose.

Question 63

False positive D-xylose test

Answer 63

False positive is decreased urinary excretion of xylose even though they have normal mucosal absorption.

Can be seen in patients with delayed gastric emptying or impaired glomerular filtration.

Question 64

Small intestinal bacterial overgrowth (SIBO)

Answer 64

Characterized by alterations in the flora of the SI, usually due to abnormal intestinal anatomy or motility,

A false positive D-xylose test can be seen in SIBO due to bacterial fermentation of the ingested d-xylose dose before it can be absorbed.

Treatment with Rifaximin will improve this condition (if D-xylose is still positive on rifaximin, the prob is most likely Celiac)

Question 65

Intestinal lactase deficiency

Answer 65

Causes diarrhea, abdominal pain, and flatulence after consuming milk or milk-containing products. Normal D-xylose.

Question 66

Gallbladder stasis

Answer 66

Presence of proteins and fatty acids in the duodenum acts as a stimulus for release of CCK, which in turn stimulates the contraction of the gallbladder. In patients on TPN or prolonged fasting, the normal stimulus for CCK release and GB contraction is absent.

This leads to biliary stasis and promotes the formation of bile sludge and gallstones.

Small bowel (ileal) resection (or Crohn’s) also contributes to formation of gallstones via DECREASED enterohepatic circulation of bile acids that results in altered hepatic bile composition, which becomes supersaturated with cholesterol and promotes gallstone formation

Question 67

Mechanism for gallstone formation during pregnancy and in women on OCPs

Answer 67

Estrogen-induced increase in cholesterol secretion.

Estrogen causes an increase in cholesterol secretion and progesterone causes a reduction in bile acid secretion, causing increased cholesterol saturation of bile.

Progesterone also slows GB emptying and facilitates formation of cholesterol gallstones.

Question 68

Diffuse esophageal spasm

Answer 68

Pathophys - Uncoordinated, simultaneous contractions of esophageal body

Symptoms - intermittent Chest pain, dysphagia for solids and liquids

Dx - Esophagram shows “corkscrew pattern.” Manometry - intermittent peristalsis, multiple simultaneous contractions

Tx - CCBs. Alternative is nitrates or TCAs

Endoscopy is often normal.

Question 69

Prinzmetal angina

Answer 69

Angina due to coronary artery spasm. Typical symptoms include episodic chest pain at rest. Patients may have normal ECG findings btw attacks, with variable ST abnormalities during acute events.

Dysphagia rules this out.

Question 70

Globus sensation

Answer 70

Functional disorder of esophagus characterized by sensation of foreign body in throat. Often worse when swallowing saliva and is frequently associated with anxiety.

Pain, dysphagia, dysphonia or systemic symptoms are NOT TYPICAL and would suggest something else.

Question 71

Shock Liver (Ischemic hepatic injury)

Answer 71

Occurs in setting of hypotension (septic shock, heart failure) and manifests as acute, massive increases in AST and ALT with milder associated increases in total bili and alk phos.

In patients who survive the inciting condition, liver enzymes typically return to normal within a few weeks.

Look for a patient who comes in in shock and develops massive liver enzyme elevations like a day later.

Question 72

Unexplained leukocytosis in hospitalized patient

Answer 72

Should raise suspicion for C dif, even without diarrhea

Question 73

Risk factors for C Diff

Answer 73

Recent hospitalization, advanced age, antibiotic use (fluoroquinolones, penicillins, cephalosporins, clindamycin)

Question 74

Asymptomatic funguria

Answer 74

Common in patients with longstanding indwelling urinary catheters

Actual symptomatic fungal UTIs are rare. In cases of uncomplicated symptomatic fungal UTIs, antifungals arent needed.

Question 75

Treatment of patient with suspected C Dif colitis

Answer 75

empiric metronidazole while awaiting stool studies

Question 76

Most frequent sources for liver mets

Answer 76

GI malignancies like colorectal or pancreatic cancers since venous drainage is through the portal system directly to liver

Lung, breast, skin also spread to liver often.

Liver is common site for mets bc of its dual blood supply (systemic and portal) and hepatic sinusoidal fenestrations allow for easier met deposition

Question 77

Management of hepatic encephalopathy

Answer 77

1) Supportive care (volume repletion [albumin] if needed, restraints if agitated, correct lytes)
2) Adequate nutrition without protein-restricted diet unless patient is unable to tolerate protein intake
3) Treat precipitating cause (GI bleed, hypovolemia, infection, lyte abnormalities)

4) Lower serum ammonia.
4a) Lactulose orally or enema if unable to take oral
4b) Rifaximin orally if no improvement in 48h with lactulose or unable to take lactulose

Question 78

HE and K - whats the connection?

Answer 78

Hypokalemia increases renal ammonia production. Metabolic alkalosis (from intravascular volume depletion, poor oral intake) stimulates conversion of ammonium (can’t cross BBB) to ammonia (can cross BBB).

This is why patients with HE and hypoK require intravascular volume repletion (albumin) and K repletion.

Disaccharides (lactulose or lacitol) convert ammonia to ammonium (ammonia trap).

Question 79

Burning, localized pain and regional hyperesthesia/allodynia in context of recent cancer treatment

Answer 79

Shingles - consider it when patients have regional pain and no conclusive evidence of disease in the local internal organs

Question 80

Shingles

Answer 80

Can occur at any age. Most common after age 50. Risk goes up with age.

Frequently triggered by severe physical stress (cancer tx) or immunosuppressed states, but many cases are spontaneous

Reactivation of varicella zoster in DRG where it was dormant since last chickenpox infection

Pain may precede rash by several days

Question 81

Post-herpetic neuralgia

Answer 81

Patients may develop persistent hypersensitivity of afferent pain fibers after shingles infection.

Question 82

Tx of shingles

Answer 82

Antivirals (acyclovir, valacyclovir, famciclovir) in first few days of outbreak can shorten the duration of symptoms and decrease the risk of post-herpetic neuralgia

Question 83

MEN syndromes

Answer 83

Type 1

1) Primary hyperparathyroidism (more than 90%)
2) Enteropancreatic tumors (60-70%)
3) Pituitary tumors (10-20%)

Type 2A

1) MTC (More than 90%)
2) Pheochromocytoma (40-50%)
3) Parathyroid hyperplasia (10-20%)

Type 2B

1) MTC
2) Pheo
3) Other - mucosal and intestinal neuromas, marfanoid habitus

Question 84

Signs of liver mets

Answer 84

Abdominal pain, microcytic anemia, positive FOBT, and hepatomegaly with a hard edge

Moderate abnormalities in LFTs (high alk phos with mild elevations in AST and ALT) - this makes a liver injury less likely (more likely to be infiltrative or cholestatic in the case described)

Pleural effusion on Left (hepatic hydrothorax from cirrhosis is on the right usually)

Question 85

Alcoholic cirrhosis on PE and Labs

Answer 85

Liver is often shrunken and edge is not palpable. AST usually greater than ALT by factor of 1.5-2

Question 86

Underlying causes of oropharyngeal dysphasia

Answer 86

Presents with difficulty initiating swallowing due to inability to properly transfer food from mouth to pharynx

Etiologies include stroke, advanced dementia, oropharyngeal malignancy, neuromuscular disorders (MG)

Question 87

Complications of oropharyngeal dysphagia

Answer 87

Coughing, choking, nasal regurgitation on swallowing.

Aspiration pneumonia and weight loss** (look for recurrent RLL pneumonias)

Question 88

Initial evaluation in patient with oropharyngeal dysphagia

Answer 88

Videofluoroscopic modified barium swallow

Question 89

Colon cancer screening in high risk patients

Answer 89

FHx of adenomatous polyps or CRC - 1st degree relative at age younger than 60

1) Colonoscopy at age 40 OR 10 years before the age of dx in the relative (whichever comes first)
2) Repeat every 3-5y

IBD - UC or Crohn

1) Begin 8 years post diagnosis (12-15 years if disease only in L colon)
2) Colonoscopy with biopsies every 1-2 years

Familial adenomatous polyposis

1) Begin at age 10-12
2) Colonoscopy every year

Hereditary nonpolyposis CRC (Lynch Syndrome)

1) Begin at age 20-25
2) Colonoscopy every 1-2 years

Question 90

Management of gallstones

Answer 90

Gallstones without symptoms - No tx needed in most patients (only 20% of ASx gallstones will develop symptoms within 15y) - exception is patients at higher risk of developing gallbladder cancer (like if they have a porcelain gallbladder)

Gallstones with typical biliary colic symptoms - elective lap chole, possible ursodeoxycholic acid in poor surgical candidates

Complicated gallstone disease (acute cholecystitis, choledocholithiasis, gallstone pancreatitis) - chole within 72h

Question 91

Overview of chronic pancreatitis

Answer 91

Etiology

1) ***Alcohol use (even prolonged use of socially acceptable amounts)
2) Cystic fibrosis (common in kids)
3) Ductal obstruction (malignancy, stones)
4) Autoimmune

Clinical presentation

1) Chronic epigastric pain with intermittent pain-free intervals
2) Malabsorption - steatorrhea, weight loss (from reduced exocrine function like less amylase, protease, lipase)
3) Diabetes mellitus

Lab results/imaging

1) Amylase/lipase can be normal and nondiagnositc
2) CT scan or MRCP can show calcifications, dilated ducts and enlarged pancreas

Tx

1) Pain management
2) Alcohol and smoking cessation
3) Frequent, small meals
4) Pancreatic enzyme supplements

Question 92

What marker is elevated in pancreatic cancer?

Answer 92

CA 19-9

Question 93

Chronic mesenteric ischemia

Answer 93

Can present with dull abdominal pain (usually after eating) and unintentional weight loss due to avoidance of food.

Mood cases due to atherosclerosis

Dx with mesenteric angiogram

Question 94

Achalasia vs pseudoachalasia

Answer 94

Patient presents with dysphagia to solids and liquids and a dilated esophagus with smooth tapering of distal esophagus. Primary achalasia is loss of peristalsis in distal esophagus with lack of LES relaxation. Pseudo is due to esophageal cancer (narrowing of distal esophagus NOT due to denervation)

So what clues point you to pseudo?

1) Tobacco and alcohol use are major risk factors for esophageal cancer
2) Significant weight loss
3) rapid symptom onset (less than 6 months)
4) Presentation at age greater than 60

Moral of the story: In all patients with suspected achalasia, get an endoscopy to rule out malignancy

In primary achalasia, it is usually easy to pass scope through LES and scope will show normal mucosa and dilated esophagus

If endoscopy shows malignancy, do CT for staging

Question 95

Tx for achalasia

Answer 95

Low surgical risk - Lap myotomy, pneumatic balloon dilatation

High surgical risk - BoTox, nitrates, CCBs

ONLY consider treatment after malignancy is excluded by endoscopy

Question 96

Esophageal cancer

Answer 96

Subtypes

1) Adeno - distal esophagus, arises from Barret esophagus
2) SCC - anywhere in esophagus

Risk

1) Acid reflux, obesity, also smoking (adeno)
2) Smoking, alcohol, caustic injury (SCC)

Symptoms

1) CP
2) Weight loss
3) Dysphagia (solids)

Dx

1) Endoscopy with bx
2) CT (PET/CT) for staging

Question 97

Dx of esophageal cancer

Answer 97

Young, low risk patients with undetermined esophageal symptoms may start with Barium esophagram

Those over 55 OR who have alarm symptoms (weight loss, gross or occult bleeding, early satiety) will usually go straight to endoscopy