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Pharm III > Lecture 1 (GI)-Exam 1 > Flashcards

Lecture 1 (GI)-Exam 1 Flashcards

1
Q

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

A

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

Fat:
* Increased cholesterol

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2
Q

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

A

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

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3
Q

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

A
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4
Q

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

A

Gallstones in gall bladder

Asymptomatic
* No symptoms=no treatment needed

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5
Q

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

A
  • Biliary cholic – gall stone stuck in cystic duct
  • Dull RUQ pain when gall bladder contracts after meals
  • Subsides when gall stone dislodges
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6
Q

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

A

First-line: elective cholecystectomy

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

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7
Q

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

A

Ursodeoxycholic acid [ursidiol (Actigall)]

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

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8
Q

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

A
  • Indication:Gall stone resolution / prevention
  • Efficacy:50% reduction in stone size at one year
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9
Q

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

A

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

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10
Q

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

A
  • Creates good environment for bacterial growth
  • MC E. coli; Klebsiella
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11
Q

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

A
  • RUQ pain
  • Radiation to right scapula
    • Murphy’s sign
  • Fever
  • Nausea / vomiting
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12
Q

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

A

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

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13
Q

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

A

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

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14
Q
A
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15
Q

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

A
  • 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
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16
Q

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

A

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

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17
Q

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

A
  • Emergent if perforation/necrosis
  • Also recommended for elderly (>65 yr) and pregnant women
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18
Q

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

A

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

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19
Q

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

A
  • Piperacillin-tazobactam
  • Ertapenem
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20
Q

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

A

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

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21
Q

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

A

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)

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22
Q

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

A
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23
Q

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

A
  • Hospitalization
  • Intravenous fluids ± vasopressors
  • Correct electrolyte abnormalities
  • Pain control
  • Nausea control
  • NPO
  • Empiric antibiotics
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24
Q

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

A

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

Cholecystectomy once recovered

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25
Q

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

A

First-line:
* Piperacillin-tazobactam
* Ertapenem

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

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26
Q

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

A

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

Treatment duration 7 to 10 days (cont post-op)

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27
Q

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

A
  • Pill-induced
  • Caustic induced
  • Infectious
  • Eosinophilic
  • GERD
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28
Q

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

A

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

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29
Q

Pill-induced esophagitis
* What are the sxs?

A
  • Retrosternal pain
  • Dysphagia
  • Odynophagia
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30
Q

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

A
  • Specific medications
  • Inadequate water intake
  • Taking while laying down
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31
Q

Pill-induced esophagitis
* What are the medications?

A
  • Antibiotics (MC tetracyclines)
  • NSAIDS
  • Bisphosphonates
  • Potassium chloride
  • Ferrous sulfate
  • Acetaminophen

FAB NAP

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32
Q

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

A
  • 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
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33
Q

Pill induced esophagitis
* What is the treatment?

A
  • DC caustic agent if possible
  • ± change to liquid formulation
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34
Q

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

A

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

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35
Q

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

A

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

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36
Q

Caustic esophagitis
* What happens with acids?

A

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

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37
Q

Caustic esophagitis
* What happens with alkali?

A

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

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38
Q

Caustic ingestion
What is the general treatment? (3)

A

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

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39
Q

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

A
  • Asymptomatic -> observe
  • Vomiting or drooling or not tolerating PO-> NPO overnight with PO challenge
  • Multiple symptoms or stridor alone -> endoscopy
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40
Q

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

A

Endoscopy

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41
Q

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

A

Grade 0, I and IIA
* Supportive care with PO challenge

Grade IIB
* Supportive care with NG feeding / TPN
* ± Usta protocol (alkali ingestion)

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42
Q

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

A
  • Surgical emergency for tissue debridement
  • Significant morbidity
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43
Q

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

A

MC in immunocompromised patients
* HIV, cancer, transplant patients

Diagnosis
* Symptoms + endoscopy with biopsy

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44
Q

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

A
COMMON IN ASTHMA PTS
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45
Q

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

A
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46
Q

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

A
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47
Q

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

A

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

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48
Q

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

A

Infants/toddlers
* Decreased appetite, abdominal pain, trouble swallowing or vomiting

Teens/ adults
* Same symptoms + dysphagia
* Esophageal food impaction

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49
Q

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

A

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

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50
Q

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

A

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

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51
Q

What is the Two and four food elimination diets ?

A
  • Dairy and gluten MCC EOE
  • Less restrictive
  • Increased compliance

MC!!!

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52
Q

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

A

Diet, Proton pump inhibitors, swallowed topical corticosteroids

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53
Q

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

A
  • Decreases expression of interleukins and decrease inflammatory response
  • Restores the integrity of damaged mucosa
  • Reverses fibrous remodeling
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54
Q

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

A
  • Class effect
  • Similar remission rates compared to STC
  • (> 70%)
  • Induction therapy 6 to 12 weeks
  • Maintenance therapy required
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55
Q
A
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56
Q

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

A
  • 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
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57
Q

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?

A
  • 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
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58
Q
A
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59
Q

GERD symptoms
* What are they?

A
60
Q

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

A
  • Odynophagia
  • Dysphagia
  • Unintentional weight loss
  • Anemia
  • Anorexia
  • Vomiting
  • Bleeding
  • New onset ≥ 60 years
  • First-degree relative with GI cancer
61
Q

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

A
  • Alleviate or eliminate symptoms
  • Decreased reoccurrence and duration of symptoms
  • Promote mucosal healing
  • Prevent complications
62
Q

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

A
  • Decreasing the acidity of refluxate
  • Decreasing gastric volume available for reflux
  • Improve gastric emptying
  • Increase LES pressure
  • Enhance esophageal acid clearance
  • Protect esophageal mucosa
63
Q
A
64
Q
A
65
Q

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

A
  • Symptoms < 2 times per week
  • Lifestyle modifications
  • Low dose H2RA prn
  • Antacids if symptoms < 1 time per week
  • Reassess in 4 weeks
66
Q
A
67
Q
A
68
Q

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?

A
69
Q

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?

A
70
Q

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

A
71
Q

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

A
72
Q

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

A
73
Q
A
74
Q

Refractory GERD
* What are additional therapies (3)

A
  • H2 antagonist at bedtime
  • Sodium alginate
  • Sucralfate
75
Q

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

A
76
Q

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

A
  • 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
77
Q

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

A

First-line:
* Calcium carbonate
* H2 receptor antagonists

Alternatives:
* Sucralfate
* PPI

78
Q
A
79
Q
A
80
Q

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

A
  • 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
81
Q

Esophageal varices
* What does the txt include?

A
  • Primary prophylaxis
  • Treatment of acute variceal hemorrhage
  • Secondary prophylaxis
82
Q

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

A
  • Decreased albumin
  • Increased NO production
  • Portal HTN
  • Portal vein back up
  • Splanhic VD
83
Q

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

A
  • Fall in oncotic pressure -> decreased effective circulating volume
  • Activation of the RAAS ->sodium and water retention
84
Q

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

A
  • Increased nitric oxide production -> splanchnic vasodilation
  • Fall in BP ->activation of the RAAS -> sodium and water retention
85
Q

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

A

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

86
Q

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

A
87
Q

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?

A

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

88
Q

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

A
89
Q
A
90
Q

Seen before, so i placed it all together

A
91
Q

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

A
  • 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
92
Q

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

A
  • less subjective
  • Used for organ procurement / transplantation
93
Q

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

A
94
Q

What do you have to do for acute variceal hemorrhage?

A
95
Q
A
96
Q

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

A
  • Octreotide – while awaiting endoscopy
  • Endoscopy within 12 hours - EVL vs sclerotherapy
  • Balloon tamponade
  • TIPS
97
Q

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

A

First-line: ceftriaxone

98
Q

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

A

MOA:
* Inhibition of vasodilatory peptides (glucagon) -> splanchnic vasoconstriction

Adverse effects
* Hyperglycemia
* Vomiting / abdominal pain
* Bradycardia, hypertension
* Arrythmias

99
Q

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

A
  • 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
100
Q

Acute variceal hemorrhage-Spontaneous bacterial peritonitis (SBP) prophylaxis

  • Who is at high risk?
  • Decreases risk of what?
  • What are the options?
A
  • 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)
101
Q

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

A

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

102
Q

Acute variceal hemorrhage
* Perserve what? (2)

A
  • Preserve liver function
  • Prevent acute kidney injury
103
Q

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

A
  • 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
104
Q

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

A
105
Q

What is the txt for ascites? (3)

A

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)

106
Q

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

A

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

107
Q

Ascites
* What happens in late progressive disease?

A
  • Activation of the sympathetic nervous system
  • More proximal Na reabsorption – Loop of Henle
  • Loop diuretics used as add on therapy
108
Q

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

A

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

109
Q

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

A
110
Q

Hepatic encephalopathy
* What causes this?

A
  • 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
111
Q

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

A

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

112
Q

Hepatic encephalopathy
* Do not treat what?

A

Do not treat isolated high ammonia level aka no sxs

113
Q

Hepatic encephalopathy
* What is the txt?

A
  • Diet therapy: 1.2 to 1.5 g/kg/day protein intake
  • Lactulose – nonabsorbable disaccaride
  • Rifaximin
114
Q

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

A

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

115
Q

What does Rifaximin do?

A

Reduces the production of ammonia in the gut

116
Q

What are the SE of laxative?

A

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

117
Q

Hepatitis A
* What is key? why?

A

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

118
Q

Hepatitis A
* What is the prevention?

A

Good hand hygiene

Hepatitis A vaccine
* Approved in 1995
* Recommended routine vaccination

119
Q

Interpret the Hepatitis A Serologies

A
120
Q

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

A
121
Q

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

A
  • Hep A vaccine
  • ASAP (within 2 weeks of exposure)
  • All patients ≥ 12 months
  • All patients without contraindications
122
Q

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

A
  • Preferred – long term immunity if second dose added
  • Concomitant treatment with hepatitis A immunoglobulin for patients > 40 years with underlying medical conditions
123
Q

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

A

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

124
Q
A
125
Q

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

A

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

125
Q

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

A
126
Q

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

A
127
Q

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

A

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

128
Q

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

A

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

129
Q

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

A

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

130
Q
  • 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?
A

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.

131
Q

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

A
  • 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
132
Q

Management of chronic hepatitis B
* What are the goals?

A

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

133
Q

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

A
  • 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
134
Q

Candidates for pharmacotherapy
* Who? (4)

A
  • > 6 months since diagnosis
  • Any patient with cirrhosis
  • HBV DNA > 2000 IU/mL
  • AST > 2x upper limit of normal
135
Q
A
136
Q
A
137
Q

Fill in covered part

A
138
Q

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

A
  • 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)
139
Q

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

A

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.

140
Q
A
141
Q

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

A

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

142
Q

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

A
143
Q

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

A

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

144
Q

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

A
  • First-line agent: depends on genotype
  • Duration: depends on extent of disease
  • Cure rates: > 90%
145
Q

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

A
  • 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

Pharm III (5 decks)

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