Lecture 1 (GI)-Exam 1

Question 1

Gall bladder disease: Risk factors
* Why are females at higher risk?
* Why does fat incease risk?

Answer 1

Female
* Increase estrogen-> increased HMG-caA reductase-> increase cholesterol synthesis
* Increased progesterone-> decreased bil acid production

Fat:
* Increased cholesterol

Question 2

Gall bladder disease:
What are the overall risk factors ? (5)

Answer 2

Female, fat, forty, fertile and fair (5 Fs)

Question 3

Gall bladder disease-risk factors
* Why does fertile matter?
* What about fairness?

Answer 3

Question 4

Cholelithiasis
* What is it?
* What is asymptomatic choletlithiasis? What is the treatment?

Answer 4

Gallstones in gall bladder

Asymptomatic
* No symptoms=no treatment needed

Question 5

Cholelithiasis
* What are the sxs for symptomatic (3)?

Answer 5

• Biliary cholic – gall stone stuck in cystic duct
• Dull RUQ pain when gall bladder contracts after meals
• Subsides when gall stone dislodges

Question 6

Symptomatic cholelithiasis
* What is first line?
* What are the alternative treatments?

Answer 6

First-line: elective cholecystectomy

Alternative: Medical treatment
* Patients refusing surgery
* Nonsurgical candidates (high risk patients)

Question 7

Non-surgical symptomatic cholelithiasis
* What is the medication?
* What is the MOA? (decreases and increases)?

Answer 7

Ursodeoxycholic acid [ursidiol (Actigall)]

MOA:
* Decreases biliary cholesterol secretion
* Increases biliary bile salt concentration
* Increased cholesterol solubility

Question 8

Symptomatic cholelithiasis (U-acid)
* What are the indication?
* What is the efficacy?

Answer 8

• Indication:Gall stone resolution / prevention
• Efficacy:50% reduction in stone size at one year

Question 9

Acute cholecystitis
* What is it?
* what is the cause?

Answer 9

Inflammation of the cystic duct
* Blocked stone does not dislodge
* Bile stasis
* Inflammation, distention, increased pressure

Question 10

Acute cholecystitis
* When bile statsis occurs, what does it create?
* MC bacteria?

Answer 10

• Creates good environment for bacterial growth
• MC E. coli; Klebsiella

Question 11

acute cholecysitis:
* What are the sxs? (5)

Answer 11

• RUQ pain
• Radiation to right scapula
• • Murphy’s sign
• Fever
• Nausea / vomiting

Question 12

Acute cholecystitis
* How do you dx it? What do you see?

Answer 12

Ultrasound
* Gallbladder wall thickening
* Pericholecystic fluid
* ± Gallbladder stones

Question 13

Acute cholecystitis
* What do you do if US is not diagnosistic?

Answer 13

Hepatobiliary iminodiacetic acid (HIDA)
* If US not diagnostic
* MOST SENSITIVE AND SPECIFIC TEST

Question 14

Answer 14

Question 15

What is the supportive care for acute cholecystitis? (7)

Answer 15

• Hospitalization
• Intravenous fluids
• Correct electrolyte abnormalities from vomitting
• Pain control (options: ketorlac-> opioids if cannot)
• Nausea control
• NPO
• Antibiotics before and at time of surgery->Not postoperatively

Question 16

Cholecystectomy (laparoscopic vs open)
* Recommended when? Why? (3)

Answer 16

Recommended within 1-3 days
* Decreased complications
* Decreased hospital LOS
* Improved outcomes

Question 17

Cholecystectomy (laparoscopic vs open)
* Emergent if what?
* Also recommended for who?

Answer 17

• Emergent if perforation/necrosis
• Also recommended for elderly (>65 yr) and pregnant women

Question 18

Acute cholecystitis treatment
* What is the MC organisms? (5)

Answer 18

Empiric coverage of MC organisms:
* Escherichia coli (41%)
* Enterococcus spp (12%)
* Klebsiella (11%)
* Enterobacter (9%)
* Misc (Bacteroides, Clostridium)

Question 19

Acute cholecystitis treatment
* What is first line for antibiotics? (2)

Answer 19

• Piperacillin-tazobactam
• Ertapenem

Question 20

Acute cholecystitis treatment
* What are the alternative antibiotics? (3)
* What does hosptial infections need to cover?

Answer 20

Alternative:
* Meropenem or imipenem
* Cefotetan or ceftriaxone or ceftazidime or cefepime plus metronidazole
* Fluoroquinolone plus metronidazole

Hospital acquired infections:
* Empiric coverage should include Pseudomonas and Enterococcus

Question 21

Acute cholangitis:
* Complication of what?
* What are the cause?

Answer 21

Complication of choledocholithiasis
* Gallstone blockage of common bile duct
* Allows enteric bacteria to slowly move up the duct and colonize the biliary system
* Patients present with fever, RUQ pain and jaundice
* Sepsis may result in hypotension and confusion (AMS)

Question 22

Acute cholangitis
* What is reynold’s pentad
* What is charcot’s triad?

Answer 22

Question 23

Acute cholangitis treatment
* What is the supportive care? (7)

Answer 23

• Hospitalization
• Intravenous fluids ± vasopressors
• Correct electrolyte abnormalities
• Pain control
• Nausea control
• NPO
• Empiric antibiotics

Question 24

Acute cholangitis treatment
* What is the dx test and txt?

Answer 24

Endoscopic retrograde cholangiopancreatography (ERCP) - emergently
* Diagnostic and therapeutic

Cholecystectomy once recovered

Question 25

Acute cholangitis treatment * What the first line anx (2) * What are the alternatives? (3)

Answer 25

First-line: * Piperacillin-tazobactam * Ertapenem Alternative: * Meropenem or imipenem * Cefotetan or ceftriaxone or ceftazidime or cefepime plus metronidazole * Fluoroquinolone plus metronidazole

Question 26

Acute cholangitis treatment * What should be given for hospital accquired infections? * What is the txt duration?

Answer 26

Hospital acquired infections: * Empiric coverage should include Pseudomonas and Enterococcus Treatment duration 7 to 10 days (cont post-op)

Question 27

Esophagus inflammation - esophagitis What are the causes? (5)

Answer 27

* Pill-induced * Caustic induced * Infectious * Eosinophilic * GERD

Question 28

Pill-induced esophagitis * What is it? * what is the cause? (2) * First reported when and with what?

Answer 28

Esophageal mucosal injury caused by the medications * Direct toxic effect on esophageal mucosa * Highly acidic or alkaline medications * First reported in 1970 – potassium chloride

Question 29

Pill-induced esophagitis * What are the sxs?

Answer 29

* Retrosternal pain * Dysphagia * Odynophagia

Question 30

Pill-induced esophagitis * What are the risk factors? (3)

Answer 30

* Specific medications * Inadequate water intake * Taking while laying down

Question 31

Pill-induced esophagitis * What are the medications?

Answer 31

* Antibiotics (MC tetracyclines) * NSAIDS * Bisphosphonates * Potassium chloride * Ferrous sulfate * Acetaminophen | FAB NAP

Question 32

Pill induced esophagitis * What is the prevention? (4)

Answer 32

* Take medications while standing * Do not lay down for 30 minutes * Take medications with a minimum of 8 oz of water * Eat a meal after taking medication

Question 33

Pill induced esophagitis * What is the treatment?

Answer 33

* DC caustic agent if possible * ± change to liquid formulation

Question 34

Pill induced esophagitis * What is the supportive care?(4)

Answer 34

Supportive care (most resolve in 7-10d) * Pain control * Sucralfate * Oral lidocaine / compounded numbing agents * Avoiding extremes of hot, cold, spicy foods

Question 35

Caustic esophagitis * What are the causes? What happens with kids and adults?

Answer 35

Ingestion of highly acidic or alkali substance * Bleach or ammonia * MC children (80%) - accidental * Adults – intentional

Question 36

Caustic esophagitis * What happens with acids?

Answer 36

Acids – pH < 2 * Coagulative necrosis * Hypoxic and ischemic tissue * Less damage compared to alkali

Question 37

Caustic esophagitis * What happens with alkali?

Answer 37

Alkali – pH > 11 * Liquefaction necrosis * Cell lysis -> digestive enzymes released * Dissolution of tissue -> deeper penetration of exposed mucosa- more injury

Question 38

Caustic ingestion What is the general treatment? (3)

Answer 38

A,B,C’s * 50% of adults require intubation * CXR – pneumomediastinum * Vomiting should NOT be induced

Question 39

Caustic ingestion general treatment * What do you do for unintentional alkali asymptomatic and sxs?

Answer 39

* Asymptomatic -> observe * Vomiting or drooling or not tolerating PO-> NPO overnight with PO challenge * Multiple symptoms or stridor alone -> endoscopy

Question 40

Caustic ingestion general treatment * What is the dx Intentional alkali / any acid?

Answer 40

Endoscopy

Question 41

Intentional alkali / any acid * What is the txt for Grade 0, I and IIA? * What is the txt for Grade IIB?

Answer 41

Grade 0, I and IIA * Supportive care with PO challenge Grade IIB * Supportive care with NG feeding / TPN * ± Usta protocol (alkali ingestion)

Question 42

Casustic ingestion * What is the txt for Grade III and IV?

Answer 42

* Surgical emergency for tissue debridement * Significant morbidity

Question 43

Infectious esophagitis * MC in who? * How do you dx

Answer 43

MC in immunocompromised patients * HIV, cancer, transplant patients Diagnosis * Symptoms + endoscopy with biopsy

Question 44

Candida: * * What does it look like? * What does it appear like on EDG? * What is the txt?

Answer 44

Question 45

HSV: * What does it look like? * What does it appear like on EDG? * What is the txt?

Answer 45

Question 46

CMV: * What does it look like? * What does it appear like on EDG? * What is the txt?

Answer 46

Question 47

Eosinophilic esophagitis * Allergic rxns to what? * What is in the esophagus? Most patients have what? * What are the triggers (enviroment and foods)

Answer 47

Allergic reaction to food or environment Inflammation and eosinophils in esophagus * Most patients atopic Triggers * Environment: pollen, animals, dust mites, molds * Foods: MC dairy, egg, wheat, soy

Question 48

Eosinophilic esophagitis * What are the sxs with infants/ toddlers?(4) What are the sxs of teens/adults?(6)

Answer 48

Infants/toddlers * Decreased appetite, abdominal pain, trouble swallowing or vomiting Teens/ adults * Same symptoms + dysphagia * Esophageal food impaction

Question 49

Eosinophilic esophagitis * What is the dx and what does it show?

Answer 49

Diagnostics – upper endoscopy * Bx positive for eosinophils * Corrugated esophagus

Question 50

First-line Treatments-EoE * What is the two, four, six food elimination diet?

Answer 50

Induce histopathologic / symptomatic remission in 40 to 60% of patient

Question 51

What is the Two and four food elimination diets ?

Answer 51

* Dairy and gluten MCC EOE * Less restrictive * Increased compliance ## Footnote MC!!!

Question 52

What is the first line treatment of EOE?(3)

Answer 52

Diet, Proton pump inhibitors, swallowed topical corticosteroids

Question 53

First-line Treatments-EoE * What is the MOA of PPI?

Answer 53

* Decreases expression of interleukins and decrease inflammatory response * Restores the integrity of damaged mucosa * Reverses fibrous remodeling

Question 54

First-line Treatments-EoE-> PPI * _ effect * Similar what? * induction therapy when? * What is required?

Answer 54

* Class effect * Similar remission rates compared to STC * (> 70%) * Induction therapy 6 to 12 weeks * Maintenance therapy required

Question 55

Answer 55

Question 56

First-line Treatments-EoE: Swallowed topical corticosteroids (STC) * High what? * Low what? * What is recommended? * Maintence therapy? * What is the MC SE?

Answer 56

* High remission rates (> 70%) * Low adverse effects compared to systemic steroids * Multiple formulations * 6 to 12 weeks of induction therapy recommended * Maintenance therapy generally 50% of induction dose * MC adverse effect = candida esophagitis

Question 57

EOE treatment approach * What can be used? * No evidence of what? * What is recommended as f/u * What is recommended for all patients after txt? * What does Patients with strictures need?

Answer 57

* Any first-line therapy may be used * No evidence that combination therapy is better that single therapy * Follow up endoscopy recommended 6 to 12 weeks after therapy initiation to verify response * Maintenance therapy recommended for all patients * Patients with strictures require surgical dilation

Question 58

Answer 58

Question 59

GERD symptoms * What are they?

Answer 59

Question 60

GERD symptoms * What are the alarm sxs? (9)

Answer 60

* Odynophagia * Dysphagia * Unintentional weight loss * Anemia * Anorexia * Vomiting * Bleeding * New onset ≥ 60 years * First-degree relative with GI cancer

Question 61

GERD - treatment * What are the treatment goals? (4)

Answer 61

* Alleviate or eliminate symptoms * Decreased reoccurrence and duration of symptoms * Promote mucosal healing * Prevent complications

Question 62

GERD - treatment * What is the therapy is aaimed at what? (6)

Answer 62

* Decreasing the acidity of refluxate * Decreasing gastric volume available for reflux * Improve gastric emptying * Increase LES pressure * Enhance esophageal acid clearance * Protect esophageal mucosa

Question 63

Answer 63

Question 64

Answer 64

Question 65

Treatment - Mild GERD * What is it considered? * What is the txt? (3) * Reasses when?

Answer 65

* Symptoms < 2 times per week * Lifestyle modifications * Low dose H2RA prn * Antacids if symptoms < 1 time per week * Reassess in 4 weeks

Question 66

Answer 66

Question 67

Answer 67

Question 68

Mild intermittent sxs * What do you need to do if sxs cont after the first round of txt? * What do you do for sxs improvement? * What do you do if sxs do not improve after the second round of failure txt?

Answer 68

Question 69

Recurrent sxs: * What do you do if more than 3 months from discontinuing acid suppresion? * What do you do if less than 3 months from discontinuing acid suppresion?

Answer 69

Question 70

What do you do for severe or frequent sxs? (overview)

Answer 70

Question 71

Treatment-severe symptoms of GERD * What do you do for inital therapy? * What do you do if txt failure at 2 months?

Answer 71

Question 72

Treatment-severe symptoms mild GERD * What do you do after two failed rounds of treatement?

Answer 72

Question 73

Answer 73

Question 74

Refractory GERD * What are additional therapies (3)

Answer 74

* H2 antagonist at bedtime * Sodium alginate * Sucralfate

Question 75

Refractory GERD: Antireflux surgeries * What type of option? * Not generally recommended in what? * What are the three options?

Answer 75

Question 76

Gerd – maintenance therapy * Who is it recommended for? (3)

Answer 76

* Patients with continued symptoms after PPI discontinuation * Patient with complications including erosive esophagitis and Barrett’s esophagitis->Use lowest effective PPI dose * H2 receptor antagonists may be used as maintenance in patient without erosive disease

Question 77

Gerd and pregnancy * What is first line? (2) * What are the alternatives? (2)

Answer 77

First-line: * Calcium carbonate * H2 receptor antagonists Alternatives: * Sucralfate * PPI

Question 78

Answer 78

Question 79

Answer 79

Question 80

Esophageal varices * MC associated with what? * patients usually have what? * What is the patho behind it? * Rupture can cause what?

Answer 80

* Most commonly associated with portal hypertension * Patients with cirrhosis (chronic hepatitis / alcoholics /nonalcoholic fatty liver disease) * Esophageal vein and left gastric vein drain into the portal vein; can’t drain if high portal pressures * Rupture can cause life-threatening bleeding

Question 81

Esophageal varices * What does the txt include?

Answer 81

* Primary prophylaxis * Treatment of acute variceal hemorrhage * Secondary prophylaxis

Question 82

Hemodynamic changes in cirrhosis * What are all the changes? (overview)

Answer 82

* Decreased albumin * Increased NO production * Portal HTN * Portal vein back up * Splanhic VD

Question 83

Hemodynamic changes in cirrhosis * What happens with the decreased albumin?

Answer 83

* Fall in oncotic pressure -> decreased effective circulating volume * Activation of the RAAS ->sodium and water retention

Question 84

Hemodynamic changes in cirrhosis * What happens with the increased NO production?

Answer 84

* Increased nitric oxide production -> splanchnic vasodilation * Fall in BP ->activation of the RAAS -> sodium and water retention

Question 85

Hemodynamic changes in cirrhosis * What happens with the portal hypertension?

Answer 85

Cirrhosis -> abnormal architecture of the liver -> obstruction of blood flow through the liver

Question 86

Hemodynamic changes in cirrhosis * Portal vein drains from where? to where? What happens though in patients with cirrhosis? * What happens with splanchnic VD?

Answer 86

Question 87

Primary prophylaxis * When are patients screened for varies? * What happens when there is no varices * What happens when there is varices and high risk of bleeding?

Answer 87

Patients diagnosed with cirrhosis are screened for varies at diagnosis * Patient without varices –> no treatment * Patients with small varices and high risk of bleeding (e.g., Child Pugh C, red whale marks)-> Non-selective beta blockers (NSBB)- propranolol, nadolol, carvedilol

Question 88

Primary prophylaxis: Non-selective beta blockers (NSBB)- propranolol, nadolol, carvedilol * What does is decrease? * How does it work? * Titrate dose to what?

Answer 88

Question 90

Seen before, so i placed it all together

Answer 90

Question 91

Child-Pugh score * What does it quantify? * Used to what? * baed on what? * Somewhat _

Answer 91

* Quantifies effects of cirrhosis * Used to dose adjust medications in patients with liver disease when data available * Based on physical and laboratory findings * Somewhat subjective

Question 92

Model for end-stage liver disease (MELD) score * less what? * What is it used for?

Answer 92

* less subjective * Used for organ procurement / transplantation

Question 93

Primary prophylaxis * What do you do for patients with medium to large varices? (2)

Answer 93

Question 94

What do you have to do for acute variceal hemorrhage?

Answer 94

Question 95

Answer 95

Question 96

Acute variceal hemorrhage * How do we control the bleeding? (4)

Answer 96

* Octreotide – while awaiting endoscopy * Endoscopy within 12 hours - EVL vs sclerotherapy * Balloon tamponade * TIPS

Question 97

Acute variceal hemorrhage * What do you prophylaxis with for Spontaneous bacterial peritonitis (SBP)

Answer 97

First-line: ceftriaxone

Question 98

Octreotide * What is the MOA? * What are the SE? (4)

Answer 98

MOA: * Inhibition of vasodilatory peptides (glucagon) -> splanchnic vasoconstriction Adverse effects * Hyperglycemia * Vomiting / abdominal pain * Bradycardia, hypertension * Arrythmias

Question 99

Acute variceal hemorrhage-Octreotide * What is the dose? * May be discont when? * May be cont when?

Answer 99

* 50mcg IV x 1 dose; followed by 50 mcg/hr IV * May be discontinued once bleeding stopped x 24 hours * May be continued 2 to 5 days after bleeding stopped to prevent rebleeding

Question 100

Acute variceal hemorrhage-Spontaneous bacterial peritonitis (SBP) prophylaxis * Who is at high risk? * Decreases risk of what? * What are the options?

Answer 100

* Spontaneous bacterial peritonitis (SBP) prophylaxis * Cirrhotic patients with active bleeding at high risk * Decreases risk of infection and rebleeding; increases survival * Ciprofloxacin or ceftriaxone (5 to 7 days)

Question 101

Acute variceal hemorrhage-Prevent re-bleeding (secondary prophylaxis) * What do you give in terms of meds? * What do you do in terms of dx?

Answer 101

Beta-blockers Surveillance endoscopy and EVL * Every 3 to 4 weeks until variceal obliteration, then at 1 to 3 months, then every 6 to 12 months

Question 102

Acute variceal hemorrhage * Perserve what? (2)

Answer 102

* Preserve liver function * Prevent acute kidney injury

Question 103

Cirrhosis * What are the complications of cirrhosis? (9)

Answer 103

* Variceal hemorrhage * Ascites - is typically treated with a combination of diuretics and sodium restriction * Spontaneous bacterial peritonitis-early antibiotic treatment with ascitic fluid * Hepatic encephalopathy * Hepatocellular carcinoma * Hepatorenal syndrome * Hepatopulmonary syndrome * Portal vein thrombosis * Cardiomyopathy

Question 104

Ascites * Accumulation of what? Why does this happen?(3)

Answer 104

Question 105

What is the txt for ascites? (3)

Answer 105

Alcohol cessation – improves ETOH associated ascites more than other causes Sodium restriction – 2000 mg/day Diuretics – spironolactone alone or furosemide plus spironolactone (100:40mg daily)

Question 106

Ascites * Early disease? * What happens in early progressive disease?

Answer 106

Early disease – minimal renal effects Early progressive disease * Activation of the RAAS – hyperaldosteronism * Increased aldosterone leads to increased Na reabsorption in DCT and CD * Aldosterone antagonists = first-line treatment

Question 107

Ascites * What happens in late progressive disease?

Answer 107

* Activation of the sympathetic nervous system * More proximal Na reabsorption – Loop of Henle * Loop diuretics used as add on therapy

Question 108

SBP * What is this? * What are the MC organisms? * What are the sxs? * How do you dx it?

Answer 108

Bacteria from gut gain access to ascitic fluid MC organisms * E. coli, K. pneumoniae, Streptococcus spp sx: Fever, abdominal pain, ± encephalopathy Diagnosis: Ascitic fluid PMN (neutrophils) ≥ 250 cells/uL

Question 109

SBP * What is first line txt? * What is secondary prophylaxis?

Answer 109

Question 110

Hepatic encephalopathy * What causes this?

Answer 110

* Ammonia (NH3) build up in the systemic circulation secondary to porto-systemic shunting * Ammonia build up in central nervous system * High ammonia level ≠ hepatic encephalopathy

Question 111

Hepatic encephalopathy * High ammonia level with CNS symptoms is often precipitated by what? Can be what?

Answer 111

High ammonia level with CNS symptoms * Often precipitated by a trigger * Can be persistent or intermittent

Question 112

Hepatic encephalopathy * Do not treat what?

Answer 112

Do not treat isolated high ammonia level aka no sxs

Question 113

Hepatic encephalopathy * What is the txt?

Answer 113

* Diet therapy: 1.2 to 1.5 g/kg/day protein intake * Lactulose – nonabsorbable disaccaride * Rifaximin

Question 114

Lactulose – nonabsorbable disaccaride * Metabolized by what? * What does it lower? * Decreases what? what does that promote? * Dose titrated to what?

Answer 114

Metabolized by gut flora to acetic acid and lactic acid Lower GI pH – cathartic ->increases elimination of nitrogen wastes Decreases the survival of urease producing gut flora * Promotes conversion of ammonia to ammonium (not readily absorbed) Dose titrated to 2 to 3 stools per day

Question 115

What does Rifaximin do?

Answer 115

Reduces the production of ammonia in the gut

Question 116

What are the SE of laxative?

Answer 116

Laxative: gas, abdominal cramping, diarrhea, nausea, diarrhea

Question 117

Hepatitis A * What is key? why?

Answer 117

Prevention and prophylaxis key * No specific treatment * Supportive care mainstay

Question 118

Hepatitis A * What is the prevention?

Answer 118

Good hand hygiene Hepatitis A vaccine * Approved in 1995 * Recommended routine vaccination

Question 119

Interpret the Hepatitis A Serologies

Answer 119

Question 120

Hepatitis A vaccine * What type of prevention? * When is the first dose? * When is the second dose?

Answer 120

Question 121

Hepatitis A pre / post exposure prophylaxis * What is first line? when? * Who should get this? (3)

Answer 121

* Hep A vaccine * ASAP (within 2 weeks of exposure) * All patients ≥ 12 months * All patients without contraindications

Question 122

Hepatitis A pre / post exposure prophylaxis * Preferred? * Concomitant treatment with what?

Answer 122

* **Preferred – long term immunity if second dose added** * Concomitant treatment with hepatitis A immunoglobulin for patients > 40 years with underlying medical conditions

Question 123

Hepatitis A pre / post exposure prophylaxis * What is the alternative? * When do you give this? * Who should get this? (2)

Answer 123

Immunoglobulin * ASAP (within 2 weeks of exposure) * Infants < 12 months * Patients traveling to high-risk areas in < 2 weeks * Older patients, immunocompromised, liver disease or other comorbidities

Question 124

Answer 124

Question 125

Hepatitis B Virus Risk Transmission * What is the acute vs chronic situation? * What can happen in the chronic state?

Answer 125

90% will get through symptoms and will recover 10% will become chronic * Most likely in patients with vertical transmission. Chronic patients may develop HCC without going through cirrhosis

Question 125

Hepatitis B Virus Risk Transmission * How does it spread? What is the incubation period?

Answer 125

Question 126

Hepatitis B Virus Risk Transmission * What is the acute vs chronic situation? * Chronic patients may develop what?

Answer 126

Question 127

Prevention-Hep B Vaccination * Recommended for who? * First vaccine against what? * Vaccination remains what? Why? (2)

Answer 127

Recommended for all individuals First vaccine against a major human cancer Vaccination remains below target levels * Less than 85% target for birth dose vaccination for infants born to HBsAg positive women * Many adults do not complete 3 dose series

Question 128

Prevention-Hep B Vaccination * not as effective as what? * Hepatitis b immune globulin (HBIg): Given in what?

Answer 128

Not as effective as HAV; may require greater than 3 doses for full immunity Hepatitis b immune globulin (HBIg): Given in addition to hep b vaccine for infants born to HBsAg positive mothers

Question 129

What if a person does not develop a protective concentration of anti-HBs (<10 mIU/mL) after receiving the hepatitis B vaccine series ?

Answer 129

Repeat the 3 vaccine doses & repeat anti-HBs 1-2 months after completion

Question 130

* Persons who do not have a protective concentration of anti-HBs after revaccination should be tested for what? * What happens if it positive or negative?

Answer 130

Persons who do not have a protective concentration of anti-HBs after revaccination should be tested for HBsAg. * If the HBsAg test result is positive, the person should receive appropriate management, and any household, sex, or needle-sharing contacts should be identified and vaccinated . * Persons who test negative for HBsAg should be considered susceptible to HBV infection and should be counseled about precautions to prevent HBV infection and the need to obtain HBIG postexposure prophylaxis for any known or likely parenteral exposure to HBsAg-positive blood.

Question 131

Management of Chronic Hepatitis B * Vaccinate against what? * Avoid what? * Screen for what? * What do you need to manage?

Answer 131

* Vaccinate against Hepatitis A to prevent liver failure * Avoid hepatotoxic medications & alcohol * Screen for Hepatocellular Carcinoma: AFP + RUQ US * If Portal HTN is present, manage complications

Question 132

Management of chronic hepatitis B * What are the goals?

Answer 132

Suppress hepatitis virus B replication Prevent disease progression to cirrhosis and HCC Surrogate markers * Normalization of ALT * HBV DNA PCR undetectable * Loss of HBeAg and HBsAg ± anti-HBs / antiHBe seroconversion

Question 133

Non viral suppressive pharmacotherapy * Vaccination of what? * Barrier contraception for what? * What increases risk of HCC? * Alchol and smoking may do what?

Answer 133

* Vaccination of sexual and household contacts * Barrier contraception for casual sex partners or partners that are not completely vaccinated * Concomitant metabolic syndrome and insulin resistance increase risk of HCC * Alcohol and smoking may potentiate liver disease

Question 134

Candidates for pharmacotherapy * Who? (4)

Answer 134

* > 6 months since diagnosis * Any patient with cirrhosis * HBV DNA > 2000 IU/mL * AST > 2x upper limit of normal

Question 135

Answer 135

Question 136

Answer 136

Question 137

Fill in covered part

Answer 137

Question 138

Hepatitis C Virus (HCV) * Most commoncause of what? * What are the biral properties?

Answer 138

* Most common cause of liver transplant and chronic hepatitis in the US * Caused by flavi-like virus with RNA genome of > 9,000 nucleotides(similar to yellow fever virus, dengue virus)

Question 139

Hepatitis C Virus (HCV) * What is the incubation period ? what most devlop into? * CDC recommendation to screen who?

Answer 139

Incubation Period * 2-8 weeks * 85-90% will develop chronic hepatitis CDC recommendation to screen all baby boomers, because that is the highest risk group, and 75 % does not know they have it.

Question 140

Answer 140

Question 141

HCV * Who gets screened? * What are the txt goals? (3)

Answer 141

Screening: * USPSTF – all adults 18 to 79 years * One-time for most Treatment goals * Eradicate HCV * Cure = undetectable HCV RNA 12 weeks after treatment complete * All patients

Question 142

HCV: general approach * Quanitative what? For what? (2) * Obtain what? * Verify what? * Screen for what? Vaccinate for what?

Answer 142

Question 143

HCV treatment combinations * What has changed the approach to HCV? What has been reported? * Early treatment included what?

Answer 143

Direct acting agents (DAAs) changed the approach to HCV treatment * 2010 to 2015 * Reactivation of HBV has been reported Early treatment included interferon ± ribavirin * Less effective * Lower cure rates

Question 144

HCV treatment combinations * What is first line agent? * Duration? * Cure rates?

Answer 144

* First-line agent: depends on genotype * Duration: depends on extent of disease * Cure rates: > 90%

Question 145

Hepatitis D Virus * It requires what? * Coinfection with what? * No specific what?

Answer 145

* It requires the hepatitis B virus to survive and replicate * Coinfection with Hepatitis B * No specific treatment or vaccine available for Hepatitis D. Vaccinate patients for Hepatitis B