Gastroenterology Flashcards
1
Q
What are the indications for an EGD?
A
Evaluation of GI bleeding, evaluation of dyspepsia. Placement of PEG tube.
2
Q
What is a potential severe complication of ERCP?
A
Pancreatitis occurs in 2-5% of patients (severe in <0.2%)
3
Q
What is the first test usually performed in the workup of dysphagia?
A
EGD is generally done first. Barium swallow may be done first in those with hx of radiation, strictures, lye ingestion
4
Q
What is the preferred treatment for achalasia?
A
Endoscopic balloon myotomy. Surgical myotomy or Botox are alternative treatments.
5
Q
Esophageal neurologic dysfunction presents with what symptoms?
A
Equal solid and liquid dysphagia from the beginning of symptoms
6
Q
What is the most important part of therapy for diffuse esophageal spasm?
A
Reassurance. First line drug treatments include diltiazem or imipramine.
7
Q
What type of problem causes slowly progressive for solids and then liquids?
A
Anatomic narrowing of esophagus from stricture or mass (intrinsic or extrinsic)
8
Q
What is the likely cause of anatomic obstruction of the esophagus in younger patients? In older patients?
A
Schatzki ring in younger. Malignancy in older.
9
Q
What anatomic problem causes slowly progressive, intermittent dysphagia to solid food?
A
Schatzki ring. Esophageal stricture may be slowly progressive and affect solid foods, but it is less likely to be intermittent.
10
Q
What is the LES pressure in patients with dysphagia due to systemic sclerosis?
A
LES pressure is low in SSc leading to GERD which combines with dysmotility to cause symptoms.
11
Q
Which drugs interact with PPIs?
A
Levothyroxine, ketoconazole, itraconazole - effectiveness may be reduced. Digoxin effect may be increased.
12
Q
What is the clinical presentation of GERD?
A
Esophageal – heartburn, dyspepsia
Extra-esophageal – cough, vocal cord dysfunction, asthma, hoarseness
13
Q
What are alarm signals in a patient with GERD symptoms? These indicate the need for what?
A
Alarm symptoms including weight loss, GI bleeding, nausea, dysphagia, elderly age, prolonged symptoms. These make EGD necessary.
14
Q
Which diagnostic test may be helpful for atypical GERD?
A
pH probe with esophageal impedence
15
Q
For how long is severe GERD treated? And with what?
A
Severe GERD should be treated indefinitely with a PPI
16
Q
In patients with GERD which study must be done before anti-reflux surgery?
A
Esophageal manometry is needed before anti-reflux surgery
17
Q
What is the pathologic definition of Barrett esophagus?
A
Change in esophageal epithelium from columnar to intestinal metaplasia
18
Q
What cancer is associated with Barrett esophagus?
A
Adenocarcinoma of esophagus is associated with Barrett esophagus
19
Q
What followup is indicated in patients with non-dysplastic Barrett esophagus?
A
Non-dysplastic Barrett esophagus should be followed with EGD every 3-5 years. Low-grade dysplasia should be followed in 6-12 months High-grade dysplasia requires 3 month follow up
20
Q
What are the treatment options for Barrett esophagus with high-grade dysplasia?
A
Endoscopic mucosal resection, surgery
21
Q
Discuss the differences between adeno- and squamous-cell carcinoma of the esophagus.
A
Squamous - proximal esophagus, associated with smoking and alcohol.
Adenocarcinoma – distal esophagus, associated with Barrett esophagus, more common than squamous cell.
22
Q
Name the risk factors for esophageal cancer.
A
Smoking, alcohol, Barrett esophagus
23
Q
What is the clinical presentation of dyspepsia?
A
Recurrent epigastric pain typically associated with eating. Types include: GERD-like Ulcer-like Dysmotility-like
24
Q
What is the diagnostic/treatment approach to dyspepsia?
A
Stop NSAIDs
Test and treat H. pylori if present
Conduct PPI trial
EGD if alarm symptoms or failure of treatment
25
When do you test for H. pylori?
1. prior history of PUD
2. Current ulcer
3. MALT lymphoma
4. family history of gastric cancer
5. “test and treat” those <55 even without alarm symptoms
26
What type of H. pylori test is not good for checking effectiveness of treatment?
Serology cannot determine eradication of H. pylori. It also has a baseline low PPV so is not currently recommended.
27
Is the CLOtest accurate is a patient is taking a PPI? What other H. pylori tests are affected by PPIs?
PPIs can interfere with all urease based testing including CLOTest and urea breath test. PPIs can also lower the sensitivity of fecal antigen testing. Antibiotics can also affect sensitivity of ureasebased testing.
Test characteristics:
Gold standard is histology evaluation of biopsy specimens
Urease based testing has sensitivity and sensativity of ~95/95%
Fecal antigen testing has sensitivity of 95% and specificity of 98%
Serologic testing is not recommended due to PPV <50%
28
What is the first line treatment regimen for H. pylori infection?
OCLAM - omeprazole, clarithromycin, and amoxicillin for 14 days.
29
What is the most common cause of peptic ulcer disease?
H. pylori accounts for the majority of PUD
30
What is the relationship between NSAIDs and PUD?
NSAIDs increase the risk of PUD and bleeding. ~25% of patients taking NSAIDs have evidence of erosions or superficial ulcers though most of these are asymptomatic.
31
How does smoking affect PUD?
Smoking increases risk of PUD and is synergistic with NSAIDs in causing ulcers.
32
What is the relationship of steroids to PUD? Alcohol?
Steroids do not cause ulcers but increase the risk of NSAID induced ulcers 10-fold. Alcohol intake does not cause ulcers.
33
How are peptic ulcers diagnosed? If perforated?
Via EGD. IF perforation is suspected upright CXR should be done to look for free air.
34
Name at least 3 indications for surgery in a patient with PUD.
Persistent bleeding, gastric outlet obstruction, perforation, recurrent or refractory ulcers,
Zollinger-Ellison syndrome.
35
What is the main cause of bleeding ulcers in the U.S.?
NSAIDs
36
Name 3 EGD findings that indicate increased risk for rebleed of a peptic ulcer.
Active bleeding at time of EGD, visible vessel, visible clot.
37
What is the most common presentation of ZES?
Diarrhea due to hypersecretion of gastric juice causing acidification of duodenum and inactivation of pancreatic enzymes as well as villous damage.
38
What is the usual cause of gastric carcinoid?
Excessive gastrin secretion
39
What are the 3 types of gastric carcinoid?
Type 1 - autoimmune gastritis/pernicious anemia
Type 2 - Zollinger-Ellison Syndrome associated with MEN
Type 3 - Sporadic (most aggressive type)
40
Carcinoids may be associated with which skin condition?
Vitiligo
41
What are the clinical and environmental risk factors for gastric cancer?
```
Clinical:
Chronic H. pylori infection
Metaplastic (chronic) atrophic gastritis
Menetrier disease
Adenomatous gastric polyps (rare)
Environmental:
Diet low in fruits and vegetables and high in dried foods, salty foods, and smoked foods
Food low in nitrites and nitrates
```
42
What is the relationship of alcohol to gastric cancer?
Alcohol intake is not associated with a higher risk of gastric cancer
43
How do you rule out gastric cancer in a patient with a nonhealing ulcer?
Endoscopic biopsy
44
What are the symptoms of dumping syndrome?
Sympathetic symptoms after eating - sweating, palpitations, flushing, lightheadedness, diarrhea, abdominal pain.
45
What is the diagnostic workup of suspected gastroparesis?
Should start with ruling out gastric outlet obstruction then evaluate with gastric emptying study
46
What are the recommended treatments of gastroparesis?
Diet change to low fat, low fiber diet. Good glucose control. Frequent, small volume meals. Metoclopramide (may have long-term side effects). Domperidol commonly used outside of US. Erythromycin is not recommended for long-term use
47
When is colonoscopy contraindicated in IBD?
Colonoscopy in the presence of severe colitis increases risk of toxic megacolon.
48
Sulfasalazine is ineffective in what type of CD?
Sulfasalazine is ineffective in CD of the small bowel because it needs to be split in the colon into mesalamine (active metabolite) and sulfapyridine.
49
What is the most concerning side effect of prolonged metronidazole therapy?
Peripheral neuropathy may complicate prolonged use of metronidazole.
50
When is budesonide used for CD? For UC?
Budesonide is used in CD of the ileum or ileocecal region. A delayed-release form is useful for UC.
51
What are the indications for monoclonal antibodies in patients with IBD?
mAbs are indicated for moderate-to-severe CD, fistulous CD, or refractory UC
52
What is the relationship of CD to cancer?
There is an increased risk of cancer in prolonged CD and especially colonic CD. Anyone with CD >8 years should undergo colonoscopy every other year.
53
What are the colonoscopy and biopsy findings in CD?
Focal, skip, and deep lesions are the hallmark of CD. Granulomas, though pathognomonic, are uncommonly seen.
54
What is the significance of an “Apple core” lesion? How does it differ from the “string sign”?
The “string sign” is narrowing of the distal ileum from CD. If this happens elsewhere in the GI tract it would be called an “apple core” lesion and is more likely associated with
malignancy.
55
What GU complications of the terminal ileum can arise in a patient with Crohn’s?
Rectovaginal or rectovesicular fistula can complicate CD.
56
What is the usual etiology of diarrhea in CD patients with <100cm of the distal ileum removed? With >100cm of the distal ileum removed? What is the treatment for each?
Diarrhea in patients with <100cm of resected distal ileum is usually due to failure to absorb bile acids. This is treated with bile acid binders like cholestyramine and colestipol.
Diarrhea in those with >100cm of distal ileum resection is usually due to steatorrhea. This is treated with low-fat diet. If extra calories are needed these can be supplemented
with medium chain fatty acids.
57
What additional screening should be done in CD patients who have been treated with chronic steroids?
CD patients, especially on steroids, are at high risk for osteoporosis. Bone density screening is indicated annually.
58
What are the findings of UC on colonoscopy?
Uniform, contiguous, and shallow ulcers are seen on colonoscopy in UC.
59
What serologic marker may be found in 70-80% of patients with UC?
70-80% of patient with UC have positive p-ANCA
60
Describe the extra-intestinal manifestations of UC.
Arthritis, aphthous ulcers, ankylosing spondylitis (HLA B27), iritis/episcleritis/uveitis (HLA B27), primary sclerosing cholangitis (HLA 8), erythema nodosum, pyoderma
gangrenosum, venous thrombosis, pericholangitis
61
What is the relationship of UC to cancer?
There is a high risk of cancer in UC patients after 8 years of disease - 5-10% at 20 years and 12-20% at 50 years.
62
What is the treatment of UC with high-grade dysplagia?
Colectomy is indicated for dysplasia in a mass lesion and for high-grade dysplasia in a flat lesion.
63
What is the treatment of moderate-to-severe UC?
The optimal treatment for moderate-to-severe UC is oral steroids. For fulminant UC patient should be treated with IV steroids, infliximab, or cyclosporine. If fulminant UC
persists >48 hours colectomy may be needed.
64
Associate these buzzwords with UC or CD: a) tenesmus, b) rectal bleeding, c) fecal soiling,
and d) pneumaturia.
tenesmus = UC
rectal bleeding = UC
fecal soiling = CD (think fistula)
pneumaturia = CD
65
What are the 2 main categories of diarrhea?
Secretory and osmotic
66
What tests are done in the workup of acute diarrhea?
Stool culture, O&P, C. diff toxin, fecal WBCs or lactoferrin
67
What antibiotic is generally used for invasive diarrhea? Name 2 important exceptions.
Cipro is generally used. Use a macrolide for Campylobacter. Use metronidazole for amebiasis. Don’t treat salmonella as it may prolong infection. Antibiotics are
contraindicated in E. coli O157:H7.
68
Which cause of invasive diarrhea should not be treated with antibiotics?
E. coli O157:H7 (EHEC) should not be treated because this increases risk of HUS/TTP. Treatment of Salmonella with antibiotics may prolong infection.
69
What is the osmotic gap in patients with osmotic diarrhea?
Osmotic gap = stool osm – 2[stool Na + stool K]
Stool osm should always be ~290. If it is lower, suspect dilution of stool with water or urine.
Osmotic gap >50 is consistent with osmotic diarrhea.
70
How does a 24 hour fast affect osmotic diarrhea?
24 hour fast should reduce diarrhea by >50% in osmotic diarrhea.
71
In an AIDS patient with fever and diarrhea, what organisms are on your differential list?
In AIDS patient with diarrhea and fever think of mycobacterium, campylobacter, salmonella, cryptococcus, histoplasma, and CMV.
72
What tumor causes the majority of carcinoid syndrome cases?
Mid-gut carcinoids cause the majority of carcinoid syndrome.
73
What is the clinical presentation of carcinoid syndrome?
Diarrhea, flushing, hypotension are the main symptoms of carcinoid syndrome.
74
How do you diagnose carcinoid?
24 hour urine for 5-HIAA is main test for carcinoid syndrome. Localization can be done with nuclear imaging (MIBG scan).
75
Explain each of the 3 stages used in the workup of chronic diarrhea.
Stage 1 – Stool O&P, fecal WBCs, Serum chemistry, thyroid, C. diff, stool pH, stool weight, Quantitative 3 day fecal fat, trial of lactose-free diet.
Stage 2 – Giardia, if steatorrhea then EUS or CT, lactulose breath test for SIBO, if >1000cc/day of stool check for VIPoma, check for laxative abuse, stool osmolality
Stage 3 – EGD and colonoscopy
76
What lab tests are done in the workup of malabsorption?
Calcium, albumin, cholesterol, carotene, iron, PT
77
What are the extra-intestinal manifestations of celiac disease?
Extraintestinal manifestations of celiac disease include dermatitis herpetiformis, iron deficiency anemia, abnormal transaminases, Osteoporosis, neuropsych symptoms, dental enamel defects
78
How do you diagnose celiac disease?
Use tTG and anti-endomysial antibodies to diagnose celiac disease. EGD with duodenal Biopsy will show flattened villi though these are not specific to celiac disease.
79
What is the clinical presentation of Whipple disease?
Whipple disease presents with arthralgias, abdominal pain, weight loss, and diarrhea.
80
What must be ruled out in a patient >55 years of age with pancreatic insufficiency?
Pancreatic cancer must be ruled out in a patient >55 with new onset pancreatic insufficiency.
81
Steatorrhea is the best indicator of ____?
Steatorrhea is the best indicator of malabsorption.
82
What is the “gold standard” test? What is the best screening test for steatorrhea?
3-day quantitative fecal fat is the gold standard for diagnosing steatorrhea.
83
What is the significance of a normal D-xylose absorption test in a patient with steatorrhea? Low D-xylose?
A normal D-xylose test in a patient with steatorrhea means that mucosal transport is normal and is usually due to pancreatic insufficiency.. A low D-xylose result is nonspecific but suggests small bowel disease, SIBO, gastroparesis, ascites, renal insufficiency, and old age.
84
What are some important causes of bacterial overgrowth?
Causes of SIBO include structural abnormalities (diverticula, fistulae, strictures, prior ileocecal resection), motility disorders (diabetes, scleroderma), achlorhydria, immune disorders (because Igs in the small bowel can decrease bacterial growth).
85
Bacterial overgrowth is associated with which dermatologic condition?
Rosacea is associated with bacterial overgrowth.
86
How do you diagnose bacterial overgrowth as a cause of diarrhea?
SIBO is diagnosed with a lactulose hydrogen breath test.
87
Most cases of constipation are due to what?
Most cases of constipation are idiopathic.
88
What common gynecologic surgery leads to constipation in 5% of patients?
Hysterectomy leads to constipation in 5% of patients.
89
Which demographic groups are more likely to experience fecal incontinence?
Fecal incontinence is most common in the elderly and women who have had childbirth related pelvic floor injuries.
90
What is the clinical presentation of fecal impaction?
Fecal impaction presents as sudden onset of watery stools/incontinence in a person with chronic constipation.
91
Which other diagnoses do you exclude prior to diagnosing a patient with irritable bowel
syndrome?
Celiac disease, lactose intolerance, SIBO, and sorbitol ingestion should be excluded before diagnosis of IBS.
92
What are the Rome III Criteria for IBS?
At least 3 months of continuous or recurrent (at least 3 days per month) with >2 of the following:
- improvement with defecation
- onset associated with a change in stool frequency
- onset associated with a change in appearance, form, or consistency of stool
93
What are the available treatment options for IBS?
Reassurance is paramount
Avoid “sugar-free” foods
Fiber supplementation
Probiotics
Anti-spasmotic can be used short-term
Tricyclic antidepressants
Motility drugs (Lomotil)
Lubiprostone for constipation-predominant IBS
Linaclotide for constipation-predominant IBS
Low FODMAP diet (fermentable, oligo-,di-, mono-saccharides, and polyols
94
Endocarditis due to _____ or _____ (organisms) warrants a colonoscopy to search for colon
cancer?
Bacteremia with Strep bovis or Clostridium septicum should lead one to perform colonoscopy.
95
What size and histologic features of colon adenomas are considered “advanced features” with increased malignant potential?
Size >1cm, villous adenoma, and presence of dysplasia signal increased risk of cancer.
96
What is the relationship between hyperplastic polyps and colon cancer?
There is no association between hyperplastic polyps and malignancy.
97
Know the 2008 ACS guidelines for recommendations on follow-up colonoscopy intervals.
```
Normal or hyperplastic polyps - 10years
1-2 small adenomas - 5 years
3-10 adenomas - 3 years
>10 adenomas - <3 years
Piecemeal resection - 2-6 months
```
98
Which 2 familial polyposis syndromes have the highest risk of carcinoma? Which has no risk of colon cancer?
FAP and Gardner syndrome have 100% cancer risk. Peutz-Jeghers has a 50% cancer risk. Juvenile polyposis is associated with hamartomas but not carcinomas.
99
What is the risk of cancer in Peutz-Jeghers syndrome?
Peutz-Jeghers has a 50% risk of cancer.
100
At what age does screening begin for HNPCC?
Start screening for those with HNPCC risk at age 25.
101
Under what circumstances should periodic colonoscopy be started at 40 years of age?
Those with a family history of colon cancer should begin colonoscopy at age 40 or 10 years before the age of index case.
102
What common colon problem in at-risk patients is an indication for colonoscopy?
Diverticulitis should be followed by colonoscopy after resolution to ensure no cancer.
103
Are CEA levels useful for primary diagnosis, recurrence, or both in colon cancer? Why?
CEA is not useful for screening. It is useful for surveillance of recurrence if it was elevated before resection and goes down with resection of cancer.
104
Surgery for cure is the rule in colon cancer. When is adjuvant chemotherapy used? When is radiation used?
Adjuvant chemo is used for stage III and locally advanced stage II colon cancer. Radiation is indicated only for rectal cancer.
105
What may be seen on abdominal CT scan in a patient with diverticulitis?
CT shows bowel wall thickening and pericolic fluid in diverticulitis.
106
What is the treatment of moderate-to-severe diverticulitis?
Inpatient parenteral antibiotics are indicated for moderate-to-severe diverticulitis.
107
What hereditary condition is associated with AVMs?
Hereditary hemorrhagic telangiectasia is associated with GI AVMs as well as AVMs of other mucous membranes.
108
What are the symptoms of bowel obstruction?
SBO presents with vomiting, obstipation, and constipation.
109
What is the initial treatment for bowel obstruction?
Initial treatment for SBO include IV fluids and NG suction. Failure of initial treatment should prompt surgical intervention.
110
What is the clinical presentation of acute mesenteric ischemia?
Acute mesenteric ischemia presents with abdominal pain, vomiting, diarrhea, and rectal
bleeding. The pain is often described as out of proportion to exam
111
What is “thumbprinting” and when is it seen?
Thumbprinting is due to mucosal bleeding and edema seen in ischemic colitis.
112
What is the clinical presentation of chronic mesenteric ischemia?
Chronic mesenteric ischemia presents with abdominal pain after meals (abdominal angina), abdominal bruit, and weight loss.
113
What are the most common causes of pancreatitis in the U.S.?
Gallstones and alcohol are the two most common. If these are not present think meds
114
What happens to serum amylase and lipase levels over time with acute pancreatitis?
Amylase rises earlier, but lipase stays up longer
115
What 2 relationships do high triglyceride levels have with acute pancreatitis?
Elevated TG levels may artificially lower amylase concentration. Also, highly elevated TG can lead to pancreatitis.
116
Know the Atlanta classification of acute pancreatitis.
The Atlanta criteria include (need at least 2):
1. upper abdominal pain radiating through to back
2. Serum amylase or lipase 3x ULN
3. Cross sectional imaging consistent with acute pancreatitis
117
What physical findings are seen with severe pancreatic necrosis with multiple organ failure?
In severe pancreatitis with multi-organ failure you will see hemoconcentration, hypotension, tachycardia, hypoxemia, renal failure, altered sensorium, hypocalcemia, hypoalbuminemia.
118
What is Cullen sign? What is Turner sign?
Cullen sign is periumbilical blue discoloration due to hemoperitoneum. Turner sign is flank discoloration due to retroperitoneal bleeding.
119
What APACHE II score is used as a cutoff for severe acute pancreatitis?
APACHE II score >8 is cutoff for severe pancreatitis.
120
How is pancreatic necrosis best confirmed?
Pancreatic necrosis is best seen on dynamic CT or MRI.
121
What masses may develop due to acute pancreatitis? What is their timeline and what is their treatment?
Peripancreatic fluid - at onset
Necrotic tissue - 1-2 weeks
Pseudocyst - >4 weeks
Abscess - 4-6 weeks
122
Symptomatic pseudocysts persisting for >3-6 months generally require what interventions?
Symptomatic pseudocysts lasting >3-6 months should be treated with radiologic, surgical, or endoscopic drainage.
123
What is the 1st test in evaluating the etiology of acute pancreatitis?
Gallbladder ultrasound is the first test to evaluate cause of pancreatitis.
124
What is the clinical presentation of chronic pancreatitis?
Initially, there is an asymptomatic phase. Then one gets recurrent bouts of abdominal pain. Late in the disease steatorrhea and diabetes develop.
125
What is the classic diagnostic triad for chronic pancreatitis?
1. pancreatic calcification
2. diabetes
3. steatorrhea
126
What is the preferred initial test used in the workup of chronic pancreatitis?
Abdominal CT is the initial test of choice in chronic pancreatitis.
127
When is ERCP preferred over MRCP as a 2nd level test in the workup of chronic pancreatitis?
ERCP is preferred for the removal of calcific stones in the bile duct.
128
What are the classic symptoms of pancreatic cancer?
The classic presenting symptoms of pancreatic cancer are jaundice, unexplained upper abdominal pain, and weight loss.
129
How is pancreatic cancer treated if there are no metastases? With metastases?
Surgery is indicated for pancreatic cancer without mets. With mets treatment is supportive care and possibly chemo.
130
When is ERCP indicated in pancreatic cancer?
ERCP is used in pancreatic cancer only to place a stent to palliate biliary obstruction.
131
What are 3 causative factors for cholelithiasis?
1) Abnormal bile secretion by the liver
2) Accelerated nucleation of microcrytals to macrocrystals.
3) Defective gallbladder emptying
132
What should you investigate in the patient who has persistent RUQ pain after cholecystectomy or with symptoms of cholangitis?
You should investigate for common bile duct stones in patients with persistent RUQ pain after cholecystectomy or with cholangitis.
133
What is the hallmark test for primary biliary cirrhosis? How do you confirm the diagnosis?
Anti-mitochondrial Ab is the hallmark test for PBC. Diagnosis is confirmed with liver biopsy.
134
PBC: What is the best, proven treatment for early disease? For late disease?
The best treatment for early PBC is ursodeoxycholic acid (Urso). For late disease liver transplant may be needed.
135
List the similarities and differences between PBC and PSC. These are commonly confused diagnoses. (Know!) What are the alk phos, bilirubin, hepatic copper, and antimitochondrial antibody test values in PBC and PSC?
Both affect the bile ducts. PBC is more common in women, and PSC is more common in men. PSC is associated with IBD. Alk phos, bilirubin and liver copper are all elevated in both. Anti-mitochondrial Ab is associated with PBC.
136
A patient presents with cholestatic jaundice and a history of IBD (or history of chronic diarrhea). Which of the following do you include in your differential – PBC or PSC? Why?
PSC is associated with IBD.
137
What are the possible causes of hyperbilirubinemia when bilirubin is found in the urine?
Only conjugated bilirubin (which is less tightly bound to albumin) makes it into the urine. Therefore, bilirubinuria indicated biliary obstruction.
138
What is the usual cause of jaundice in persons <30 years of age? 40-60? 60-80?
>30 - acute viral hepatitis
40-60 - chronic cirrhosis
60-80 - obstrucitve jaundice from tumor or stone
139
With which coinfections can hepatitis A become fulminant?
HBV and HCV can cause HAV to become fulminant. Patients with these infections should receive vaccination against HAV.
140
Regarding HBsAg, HBcAg, HBeAg and associated antibodies: What is the best marker for past infection? What is the best marker for infectivity?
HBcAb is the best marker for past infection. HBeAg is the best marker for infectivity.
141
What antibody test is positive during the “window” period?
HBcAb is positive during the “window” period of HBV infection.
142
Polyarteritis nodosa is associated with which viral hepatitis?
PAN is associated with HBV.
143
Are HepB vaccines safe for pregnant patients?
Hep B vaccines are safe and effective in pregnant patients.
144
How do you confirm that a HepB vaccine was immunogenic?
Positive HBsAb confirmed response to HepB vaccination.
145
Which test confirms that a previous hepatitis C infection did not become chronic?
Absence of hepatitis C RNA confirms that previous hepatitis C infection did not become chronic.
146
With which infection is mixed cryoglobulinemia strongly associated? How does it present?
Mixed cryoglobulinemia is strongly associated with HCV (55% of those with HCV) . It presents with palpable purpura.
147
In order for hepatitis D virus replication to occur, co-infection with which other virus is necessary?
Hepatitis D requires co-infection with HBV to occur.
148
Hepatitis E is associated with what risk factor?
Hepatitis E is associated with pregnancy and has a 20% mortality rate in pregnancy.
149
Which test is positive in 80% of those with autoimmune hepatitis?
Anti-smooth muscle antibody is positive in 80% of autoimmune hepatitis.
150
What is the treatment for autoimmune hepatitis?
Prednisone and azathioprine are the preferred treatments for autoimmune hepatitis.
151
Which drugs are commonly associated with drug-induced hepatitis?
Drug induced hepatitis is associated with methyldopa, nitrofurantoin, acetaminophen, trazodone, phenytoin, methotrexate, OCPs, and INH.
152
How does alcohol intake affect liver toxicity from acetaminophen?
Alcohol induces cytochrome P450 system producing more NAPQI. It also leads to lower levels of glutathione, the agent needed to reduce the NAPQI.
153
What is nonalcoholic fatty liver disease and what are the risk factors?
Risk factors for NAFLD include obesity, T2DM, protein malnutrition, hyperlipidemia, amiodarone, corticosteroids, metabolic syndrome, prolonged TPN.
154
What are the treatment recommendations for NAFLD?
Weight loss and control of diabetes and hyperlipidemia are the mainstays of treatment of NAFLD.
155
What is the most likely diagnosis in a patient with tender hepatomegaly, an RUQ bruit, bloody ascites, a high alk phos, and a very elevated alpha-fetoprotein level?
HCC is the most likely diagnosis in a patient with tender hepatomegaly, RUQ bruit, bloody ascites, high alk phos, and elevated AFP.
156
Name the causes of cirrhosis.
In U.S. - Hep C > Hep B > alcohol.
157
Bleeding risk of esophageal varices is best correlated with what aspects of the varices?
Size of varices correlates best with risk of rebleeding.
158
Which drug class is used for prophylaxis against bleeding with large esophageal varices?
Beta-blockers may prevent rebleeding and prevent or delay initial bleeding in medium to large varices.
159
What drugs and which endoscopic therapies are used for active variceal hemorrhage?
Octreotide is used in acute variceal bleeding. Endoscopic banding or sclerotherapy is used acutely. Beta-blockers decrease risk of rebleeding. Antibiotics decrease risk of SBP and kidney failure.
160
Why are antibiotics given to cirrhotics with GI bleed? What antibiotics are used?
Antibiotics are given to cirrhotics with GI bleed to prevent SBP. 3rd generation cephalosporins or quinolones are generally used.
161
What do you do with small esophageal varices?
Small varices can be monitored endoscopically.
162
Which drug is given to a cirrhotic patient with a history of variceal hemorrhage to decrease the chance of rebleeds?
Beta-blockers, propranolol and nadolol, decrease the risk of variceal rebleed.
163
If the PT is prolonged in an alcoholic and is easily corrected with vitamin K, what does that indicate?
This indicates that the elevated PT is due to nutritional deficiency rather than liver dysfunction.
164
What is chylous ascites due to?
Chylous ascites is due to lymphatic obstruction due to tumors, trauma, TB, or filariasis.
165
How does SBP differs from neutrocytic ascites?
Neutrocytic ascites has elevated PMNs (>250) with no evidence of SBP and negative cultures.
166
How does SBP differ from PBP?
SBP needs to be differentiated from secondary bacterial peritonitis. Secondary BP often has a protein >1, low glucose, very high WBC, and ascites LDH>serum LDH.
Secondary bacterial peritonitis not treated with surgery has a 100% mortality rate. SBP treated with surgery has an 80% mortality rate.
167
Why is albumin given in the treatment of SBP?
Albumin is given in the treatment of SBP to help maintain blood volume and decrease the risk of irreversible renal impairment and mortality.
168
Which hereditary liver disease has increased unconjugated bilirubin?
Gilbert syndrome is a common autosomal recessive disorder characterized by elevated unconjugated (indirect) bilirubin.
169
When does jaundice in Gilbert syndrome typically occur?
Jaundice typically occurs in Gilbert syndrome with exercise, fasting, and infection.
170
What is the risk of hepatocellular cancer in a patient with cirrhosis caused by hemochromatosis?
There is a 25-30% risk of HCC in patients with cirrhosis due to hemochromatosis.
171
What lab findings are common in Wilson disease?
Low ceruloplasmin and high urine copper are seen in Wilson. Hemolytic anemia is also commonly present.
172
What is the pathognomonic finding in Wilson disease?
Keyser-Fleisher rings are pathognomonic for Wilson disease.
173
Know which patients should be considered for liver transplant.
Patient with high bilirubin (>10), low albumin (<2.5), and elevated PT should be considered for transplant. May consider earlier in the setting of HCC.
174
What MELD score indicates that the patient is a candidate for liver transplantation?
MELD >20 is an indication for liver transplant.
175
What is the timeline for development of vitamin deficiency for each of these: a) water-soluble vitamins, b) vitamins A and D, c) iron and cobalt, d) B12?
a) water soluble - weeks
b) vitamins A and D - year
c) iron and cobalt - several years
d) B12 - many years
176
What are the symptoms of wet beriberi? Dry beriberi?
Wet beriberi - CHF, ascites, and peripheral edema
| Dry beriberi - nervous system (neuropathy, Wernicke, Korsakoff)
177
What is the classic presentation of a patient with Wernicke encephalopathy?
Wernicke encephalopathy presents with vomiting, ataxia, ophthalmoplegia, and mental deterioration.
178
What are the findings associated with excessive continuous ingestion of vitamin B6?
Excess B6 presents with peripheral neuropathy with intact motor and sensory function but absent proprioception and vibration sensation.
179
Petechiae are associated with which vitamin deficiency?
Petechiae are associated with vitamin C deficiency - scruvy.
180
Explain how vitamin D is produced and then converted to the active form in the body.
Vitamin D is made from a provitamin D in the skin which is activated by sunlight and to a lesser extent absorbed in the GI tract. It is converted to 25(OH)-vitamin D in the liver and then to the active form (1,25(OH)-vitamin D) by the kidney.
181
What does vitamin D deficiency cause in adults?
Vitamin D deficiency causes rickets in children and osteomalacia in adults. It decreases calcium absorption in the gut and decreased calcium resorption in the kidney. This triggers rise in PTH levels. Think about vitamin D deficiency in elderly patient with muscle weakness or pain.
