I. Jaundice
II. Drugs for Reducing bilirubin levels
III. Causes of Isolated Hyperbilirubinemia
a. G-6PD deficiency
b. Drug-induced Liver Injury
IV. Acute Cholecystitis
a. Antibiotics
b. Pain Management
V. Vaccines for Liver Diseases
a. Hepatitis A vaccine
b. Hepatits A Immune Globulin
c. Hepatitis B vaccine
d. Hepatitis B Immune Globulin
VI. Recommendations for Post-exposure prophylaxis for contact
with patients positive for HbsAg
VII. Drugs for Chronic Active Hepatitis
VIII. Treatment for Hepatitis C Infection
IX. Self-test
Methyl salicylate, the major constituent of the essental oil
of wintergreen
Jaundice, or icterus : results from the deposition of bilirubin.
• An anticonvulsant
• Used to reduce serum bilirubin levels by at least 25%
• MOA: Increases conjugation and excretion of bilirubin.
• documented hypersensitivity
• severe respiratory disease
• marked impairment of liver function
• patients with nephritis
Drug interactions:
• decreases effects of Chloramphenicol, Digitoxin,
corticosteroids, carbamazepine, theophylline, verapamil,
metronidazole, anticoagulants
• coadministration with alcohol may produce additive CNS
effects and death
• toxicity may be increased by chloramphenicol, valproic acid
and monoamine oxidase inhibitors (MAOIs)
• Rifampicin may decrease effects
• induction of microsomal enzymes may result in decreased
effects of oral contraceptives in women
Hyperbilirubinemia may result from:
1. overproduction of bilirubin
2. impaired uptake, conjugation, or excretion of bilirubin; or
3. regurgitation of unconjugated or conjugated bilirubin from
damaged hepatocytes or bile ducts.
• Reduces serum bilirubin levels
• MOA: unknown.
• Lowers serum triglycerides and very low-density lipoprotein
(VLDL) levels
Differential diagnosis for the yellowing of the skin:
1. jaundice
2. carotenoderma
3. the use of the drug quinacrine, and
4. excessive exposure to phenols.
Examples of Phenolic compounds
• Phenol, the parent compound, used as a disinfectant
• Salicylic acid
• Cannabinoids, the active constituents of cannabis
• Capsaicin, the pungent compound of chilli peppers
• Tyrosine, an amino acid.
• The neurotransmitters serotonin, dopamine, adrenaline,
and noradrenaline.
• L-DOPA, a drug for Parkinson's disease.
• Chavibetol from betel
Estradiol and other estrogens
• Diethylstilbestrol
• The pH indicator phenolphthalein
• Thymol, an antiseptic that is used in mouthwashes
Causes of Isolated Hyperbilirubinemia
I. Indirect hyperbilirubinemia
A. Hemolytic disorders
1. Inherited
Spherocytosis, elliptocytosis
G-6-PD and pyruvate kinase deficiencies
Sickle cell anemia
2. Acquired
Microangiopathic hemolytic anemias
Paroxysmal nocturnal hemoglobinuria
Immune hemolysis
B. Ineffective erythropoiesis
Cobalamin, folate, & iron deficiencies
C. Drugs
Rifampicin, probenecid, ribavirin
D. Inherited conditions
Crigler-Najjar types I and II
Gilbert's syndrome
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II. Direct hyperbilirubinemia
Inherited conditions
Dubin-Johnson syndrome
Rotor's syndrome
To decrease likelihood of hemolysis, AVOID:
• Antimalarials: Primaquine, Chloroquine, Dapsone (antileprosy drug), Pamaquine, Pentaquine
• Antimicrobials
urinary antiseptic (nitrofurantoin)
quinolones (nalidixic acid, ciprofloxacin,
antiparasitic (antischistosomal niridazole)
anti-TB (isoniazid)
• Antimethemoglobinemic dye (methylene blue)
• Urinary analgesic (phenazopyridine)
• Vitamin K analogs
• Certain chemicals such as those in mothballs
• Analgesic (acetanilid)
• Antineoplastic antibiotic (doxorubicin)
• Isobutyl nitrite
• Ineffective erythropoiesis occurs in cobalamin, folate, and
iron deficiencies
** These are at increased risk due to depletion of glutathione stores.
FOR JAUNDICE in patients with chronic hemolysis, high incidence of
pigmented (calcium bilirubinate) gallstones increases the likelihood of
choleducholithiasis as an alternative explanation for
Classification of Drug-induced hepatocellular injury:
1. Predictable : dose-dependent & affects all patients who
ingest a toxic dose of the drug in question.
Classic example: paracetamol hepatotoxicity
2. Unpredictable or idiosyncratic : not dose-dependent &
occur in minority
Isoniazid hepatotoxicity (not very common)
Environmental toxins - important cause of hepatocellular injury
• industrial chemicals
vinyl chloride
• herbal preparations containing…
pyrrolizidine alkaloids (Jamaica bush tea)
the mushrooms Amanita phalloides or verna
(contain hepatotoxic amatoxins)
Risk factors for drug-induced liver injury
1. Race
• blacks & Hispanics
more susceptible to isoniazid (INH) toxicity
rate of metabolism under the control of P-450
• Elderly persons are at increased risk
• More common in women for unknown reasons
Alcohol Ingestion
• induces liver injury & cirrhotic changes
• causes depletion of glutathione (hepatoprotective)
stores that make the person more susceptible to
toxicity by drugs
Liver Disease
Genetic Factors
• Genetic factors affecting P450 enzymes
Other comorbidities
• Malnutrition
• Fasting
Drug Formulation
• Long-acting drugs may cause more injuries
Host factors that may enhance susceptibility to drugs,
possibly inducing liver disease
• Female: Halothane, nitrofurantoin, sulindac
• Male: Amoxicillin-clavulanic acid (Augmentin)
• Old age: paracetamol, halothane, INH, co-amoxiclav
• Young age: valproic acid, salicylates (We don’t give
Aspilet, a salicylate, to children now since they are
very prone to Reye’s Syndrome; which can also make
children more prone to viral infection like chicken pox
and croup)
• Fasting or malnutrition: paracetamol
• Large body mass index/obesity: halothane (binding to
fat cells)
• Diabetes mellitus: methotrexate, niacin
• Renal failure: tetracycline, allopurinol
• AIDS: dapsone, cotrimoxazole (used for treating
Pneumocystis carinii)
• Hepatitis C: ibuprofen, ritonavir, flutamide
• Pre-existing liver disease: niacin, tetracycline,
Signature Effects of Drugs on the Liver
• Paracetamol (Acetaminophen): hepatotoxicity due to the
toxic metabolite N-acetyl-p-benzoquinone (NAPQI) causing
centrilobular necrosis
• Amoxicillin: moderate rise in SGOT or SGPT levels, or both
• Amiodarone: abnormal liver function test results in 15-50%
of patients
• Chlorpromazine: resembles that of infectious hepatitis with
laboratory features of obstructive jaundice
• Quinolones; cholestatic jaundice with repeated use
• Diclofenac: induced liver injury with elderly female more
susceptible; elevation of one or more liver tests
• Erythromycin: may cause hepatic dysfunction; increased
liver enzyme levels and hepatocellular and/or cholestatic
• Fluconazole: mild transient elevations in transaminase
levels to hepatitis, cholestasis, and fulminant hepatic failure
• Isoniazid: severe and fatal hepatitis
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Methyldopa: contraindicated in patients with active liver
Oral contraceptives: can lead to intrahepatic cholestasis
without portal inflammation and vascular lesions; with
pruritus and jaundice
Statins: biochemical abnormalities of liver function like
moderate elevations of serum transaminase levels
Rifampicin: mild hepatitis, usually a general hypersensitivity
Valproic acid and Divalproex sodium: microvesicular
Cocaine: abuse associated with acute elevation of hepatic
enzymes with necrosis and microvascular changes.
Ecstasy: an amphetamine used as a stimulant which may
cause hepatitis and cirrhosis.
Inducers of the Hepatic P-450 enzymes:
• Phenobarbital
• Phenytoin
• Carbamazepine
• Primidone
• Ethanol
• Glucocorticoids
• Rifampin
• Griseofulvin
• Quinine
• Omeprazole - Induces CYP 1A2
Inhibitors of the Hepatic P-450 Enzymes
• Amiodarone
• Cimetidine
• Erythromycin
• Grape fruit
• Isoniazid
• Ketoconazole
• Metronidazole
• Sulfonamides
• Quinidine
• Omeprazole - Inhibits CYP2C8
Initial empiric anti-microbial therapy:
• Must be comprehensive
• Should cover both aerobic and anaerobic gram-negative
• Most commonly indicated for Cholangitis and
Initial Treatment of Acute Cholecystitis
• bowel rest
• intravenous hydration
• analgesia
• intravenous antibiotics
• For mild cases: antibiotic therapy with a single broadspectrum antibiotic is adequate
Acute Cholecystitis
• Current antibiotic recommendations include:
ampicillin/sulbactam, or
• For severe cases of acute cholecystitis:
gentamicin with clindamycin or
metronidazole with a third-generation cephalosporin
• Bacteria that are commonly associated with cholecystitis
E coli
Bacteroides fragilis
Pseudomonas species.
Ampicillin and Sulbactam (Unasyn)
• Drug combination of beta-lactamase inhibitor with ampicillin
• Covers epidermal and enteric flora and anaerobes.
• Not ideal for nosocomial pathogens
• Bactericidal activity against susceptible organisms (against
G(+), G(-) (improved activity) and non-β-lactamase
producing anaerobes)
• Effective for shigellosis
• Not active against agents of nosocomial infections
(Klebsiella, Enterobacter, Pseudomonas, Citrobacter,
Serratia, indole (+) Proteus and G(-) aerobes
• MOA: inhibit bacterial growth by interfering with the
transpeptidation reaction of cell wall synthesis
• Kinetics:
good distribution in gall bladder
Acid-stable; well absorbed after oral administration
Intake of food prior to ingestion diminishes absorption
T ½: 80 minutes
Ampicillin appears in the bile, undergoes
enterohepatic circulation, and is excreted in
appreciable quantities in the feces
• Important ADR: hypersensitivity
• Drug Interactions:
Probenecid and disulfiram elevate levels
Allopurinol decreases effects and has
additive effects on ampicillin rash
may decrease effects of oral contraceptives
Piperacillin and Tazobactam
• Antipseudomonal penicillin plus beta-lactamase inhibitor.
• MOA: Inhibits biosynthesis of cell wall mucopeptide and is
effective during stage of active multiplication
• has anti-pseudomonal activity
• Excellent antimicrobial activity against Pseudomonas,
Klebsiella, and certain other G(-) microorganisms; retains
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the activity of ampicillin against G(+) cocci and L.
In combination with a β-lactamase inhibitor (piperacillintazobactam, ZOSYN) it has the broadest antibacterial
spectrum of the penicillin
Kinetics: good distribution in gall bladder; high biliary
concentrations are achieved
Important ADR: hypersensitivity
Drug Interactions:
Tetracyclines may decrease effects
Coadministration with aminoglycosides has synergistic
effects (however, high concentrations may physically
inactivate aminoglycosides)
probenecid may increase levels
• a lincosamide
• for treatment of serious skin and soft tissue staphylococcal
• also effective against aerobic and anaerobic streptococci
(except enterococci)
• MOA: Inhibits bacterial growth, possibly by blocking
dissociation of peptidyl tRNA from ribosomes, causing
RNA-dependent protein synthesis to arrest.
• adjust dose in severe hepatic dysfunction
• associated with severe and possibly fatal colitis by allowing
overgrowth of C difficile
Ceftazidime (Fortum)
• Third-generation cephalosporin with broad-spectrum,
gram-negative activity
• lower efficacy against gram-positive organisms
• higher efficacy against resistant organisms.
• MOA: arrests bacterial growth by binding to one or more
penicillin-binding proteins
• Kinetics: distributed in most tissues including the gall
• Important ADR: hypersensitivity
• Drug Interactions:
nephrotoxicity may increase with concomitant use of
aminoglycosides, furosemide, & ethacrynic acid
probenecid may increase levels
 For pseudomonal infections and infections due to
multidrug-resistant gram-negative organisms.
 Contraindicated in pediatric age group (18 years and
• Aminoglycoside antibiotic for gram-negative coverage.
• Used in combination with both an agent against grampositive organisms and one that covers anaerobes.
• Kinetics: poorly absorbed
• Drug Interactions:
Coadministration with other aminoglycosides,
cephalosporins, penicillins, and amphotericin B may
increase nephrotoxicity
aminoglycosides enhance effects of neuromuscular
blocking agents - prolonged respiratory depression may
coadministration with loop diuretics may increase
auditory toxicity of aminoglycosides
possible irreversible hearing loss of varying degrees
may occur (monitor regularly)
Imipenem and Cilastatin (Tienem)
• For treatment of multiple organism infections in which other
agents do not have wide spectrum coverage or are
contraindicated because of potential for toxicity.
• imidazole ring-based antibiotic active against various
anaerobic bacteria and protozoa
• often used in combination with other antimicrobial agents
(except Clostridium difficile enterocolitis)
• Fluoroquinolone with activity against Pseudomonas
species, streptococci, MRSA, Staphylococcus epidermidis,
and most gram-negative organisms
• No activity against anaerobes.
• MOA: Inhibits bacterial DNA synthesis through inhibition of
DNA gyrase enzyme.
• Important ADR: hypersensitivity
Contraindicated in pediatric age group (18 years and
Drug Interactions:
Antacids, iron salts, and zinc salts may reduce serum
Cimetidine may interfere with metabolism of
Reduces therapeutic effects of phenytoin
Probenecid may increase ciprofloxacin serum
May increase toxicity of theophylline, caffeine,
cyclosporine, and digoxin (monitor digoxin levels)
May increase effects of anticoagulants (monitor PT)
Pain is a prominent feature of cholecystitis
Classic teaching:
Morphine is NOT the agent of choice because of the
possibility of increasing tone at the sphincter of Oddi
Meperidine – provides adequate analgesia without
affecting the sphincter of Oddi and DOC for cholecystitis
pain relief
Meperidine (Demerol)
• Agonist activity at opioid receptors
• analgesic with multiple actions similar to those of morphine.
• Exerts its chief pharmacological action on the CNS and the
neural elements in the bowel
• Kinetics
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Greater ability to enter the CNS, thereby producing
analgesia at lower systemic concentrations
Metabolized chiefly in the liver, t ½ of about 3 hours.
Significant antimuscarinic effects, may be a
contrainidication if tachycardia would be a problem
Negative inotropic action on the heart produce less
constipation, smooth muscle spasm, and depression of
cough reflex than similar analgesic doses of morphine
Other ADR: Upper airway obstruction or significant
respiratory depression.
Accumulation of its metabolite, normeperidine 
excitatory symptoms (hallucinations, tremors, muscle
twitches, dilated pupils, hyperactive reflexes, convulsions,
Pancreatic enzyme supplements
• For treatment of pancreatic enzyme insufficiency which
causes steatorrhea, azotorrhea, vitamin malabsorption and
weight loss
• 2 major preparations: pancreatin (no longer common) and
• Pancrelipase: enriched preparation of amylase, lipase and
Available in enteric-coated and non-enteric coated
preparations (should be given with acid suppression
Dosing individualized to age and weight
• Well-tolerated
• Excessive doses: abdominal pain and diarrhea;
hyperuricosuria and renal stones
o The most widely used oral bile salt compound is
ursodeoxycholate, which is effective only for small, pure
cholesterol stones located in a functioning gallbladder.
o Despite maintenance therapy, recurrence rates are high,
averaging 50-60% in most published series.
Also effective for prevention of gall stones in obese
patients undergoing rapid weight loss therapy
Dosage: 10 mg/kg/d for 12-24 months  dissolution
occurs in up to half of patients with small (<5-10mm)
noncalcified gall stones
documented hypersensitivity
calcified cholesterol stones
radiopaque stones
bile pigment stones
Practically free of serious adverse effects. Bile-salt induced
diarrhea is uncommon. Not associated with hepatotoxicity.
Patients with steatorrhea may benefit from:
pancreatic enzyme supplements and
fat-soluble vitamins A, D, E, and K
Gallstone dissolution agents –
Ursodeoxycholic acid - a naturally occurring bile acid
used in the dissolution of gallstones, microlithiasis,
and in primary biliary cirrhosis.
• Naturally occurring bile acid
• MOA: decreases cholesterol content of bile and bile
stones probably by reducing secretion of cholesterol from
the liver and the amount reabsorbed by intestines. Also
appears to stabilize hepatocyte canalicular membranes,
possibly through a reduction in the concentration of other
endogenous bile acids or through the inhibition of immunemediated hepatocyte destruction.
• Kinetics
After oral administration, it is absorbed, conjugated in
the liver with glycine or taurine and excreted in the
Conjugated ursodiol undergoes extensive
enterohepatic recirculation
t ½: 100 hours
Unabsorbed or unconjugated ursodiol  colon where
it is either excreted or dehydroxylated by bacteria to
lithocolic acid (potentially hepatotoxic)
• Indication
dissolution of small cholesterol gall stones with
symptomatic gall bladder disease who refuse
cholecystectomy or who are poor surgical candidates.
Drug-induced Intrahepatic Cholestasis
• usually reversible
• Associated with:
- anabolic & contraceptive steroids - most common
- chlorpromazine, imipramine, tolbutamide, sulindac,
- antibiotics as: erythromycin estolate, co-trimoxazole, &
penicillins (such as ampicillin, dicloxacillin, &
clavulanic acid)
• Chronic cholestasis has been associated with:
- chlorpromazine
- prochlorperazine
Vaccines are used for active immunization while immune globulins
are for passive immunization.
Hepatitis A Vaccine
• Inactivated vaccine
• Used for active immunization against disease caused by
• Route: Intra-muscular
• May be administered with immunoglobulin injections
without affecting its efficacy
• Efficacy: used for active immunization (efficacy >85%)
1˚ immunization: One dose (administered 2-4 weeks
before travel to endemic areas)
Booster: At 6-12 months for long-term immunity
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Indications: Travelers to HepA endemic areas; homosexual
and bisexual men; illicit drug users; chronic liver disease or
clotting factor disorders; persons with occupation risk for
infection; persons living in, or relocating to endemic areas;
and household and sexual contacts of individuals with
acute HepA
Precautions: Caution in individuals taking anticoagulant
Drug Interactions: May decrease effects of
immunosuppressive agents
Hepatitis B Immune Globulin (HBIG)
• For post-exposure prophylaxis in nonimmune persons
following percutaneous, mucosal, sexual or perinatal
• Efficacy
derived from plasma
passive immunization for individuals who describe
recent exposure to a patient infected with HBV
• Hepatitis B vaccine should also be administered
Immune globulins
• Purified preparation of gamma globulin.
• Derived from large pools of human plasma and is
composed of 4 subclasses of antibodies, approximating the
distribution of human serum.
• Used for postexposure prophylaxis or when inadequate
time is available for immunization to be effective before
potential exposure
• Efficacy: Effective when administered within 14 days of
Hepatitis A Immune Globulin(HAIG)
• Mechanisms of Action
neutralizes circulating myelin antibodies through antiidiotypic antibodies
down-regulates proinflammatory cytokines, including
blocks Fc receptors on macrophages
may increase CSF IgG (10%).
Perinatal exposure - HBIG plus vaccination at time of birth
(90% effective)
Sexual contact with an acutely infected patient - HBIG plus
Sexual contact with a chronic carrier - Vaccination
Household contact with an acutely infected patient - None
Household contact with an acutely infected person
resulting in known exposure – HBIG with or without
Infant ( <12 mo) primarily cared for by an acutely infected
patient - HBIG with or without vaccination
Inadvertent percutaneous or permucosal exposure - HBIG
with or without vaccination
Hepatitis B Vaccine
• Inactivated viral antigen, recombinant
• Intramuscular route (subcutaneous if with bleeding
1˚ immunization: 3 doses (0, 1 and 6 months)
Booster: Not routinely recommended
• Efficacy
consists of recombinant HBsAg produced in yeast
low response rates have been associated with
obesity, smoking, immunosuppression, and advanced
approximately 25-50% of persons who initially do not
respond to the vaccine will respond to one additional
vaccine dose, and 50-75% of persons will respond to
a second 3-dose series
• Safety
HBV vaccine seems to be safe, although some
questions exist regarding neurological complications
For infants born to mothers with active HBV infection,
a passive-active (immunoglobulin and vaccination)
approach is recommended
Indications: All infants; Preadolescents, adolescents and
young adults; persons with occupational, lifestyle or
environmental risk; hemophiliacs; hemodialysis patients;
and postexposure prophylaxis
Therapy is currently recommended for patients with
evidence of chronic active disease (ie, high levels of the
aminotransferases, positive HBV DNA findings, HBeAg).
Currently, interferon alfa (IFN-a), lamivudine, and adefovir
dipivoxil are the main drugs approved globally.
Interferon alfa
• Protein product manufactured by recombinant DNA
• Efficacy
Published reports show that after IFN-a treatment for
4 months, the HBV DNA levels and HBeAg
become undetectable in 30-40% of patients.
dose: with 5 million U/d or 10 million units 3 times per
week subcutaneously
MOA: not understood
modulation of host immune responses
enhances cytolytic T-cell activity
stimulates natural killer cell activity and
amplifies HLA class I protein on infected cells.
• High levels of aminotransferases, a low viral load, and
infection with the wild type are good prognostic factors for
response to IFN-a treatment.
• Special attention for patients with HBV-decompensated
cirrhosis (eg, ascites, encephalopathy) who are taking IFNα because they either respond or can deteriorate further.
• Elimination: mainly renal; liver metabolism and biliary
excretion are minor pathways
• ADRs: can be severe, even devastating:
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Transient hepatic enzyme elevations may occur
in the first 8-12 weeks
flulike syndrome
myelosuppression (eg, leukopenia,
nausea, diarrhea,
irritability, depression,
thyroid dysfunction,
Contraindications: hepatic decompensation, autoimmune
disease and hx of cardiac arrhythmia
Abortifacient  Do not give to pregnant patients!
Drug interaction: increased theophylline and methadone
levels; Combination with NRTI agents  hepatic failure;
Co-administration with zidovudine  exacerbate cytopenia
• A thymidine nucleoside analogue
• Prolonged intracellular half-life on HBV cell lines  lower
dose and less frequent administration
• Safely administered to patients with hepatic
• MOA: inhibits the viral polymerase; inhibits HBV DNA
polymerase and HIV reverse transcriptase by competing
with dCTP for incorporation into the viral DNA resulting in
chain termination
• Efficacy:
associated with a 4-log reduction of the viral load
appears to be effective for patients who do not
respond to IFN-α treatment
Suppression of HBV DNA to undetectable levels
in 44% of patients
Seroconversion of HBeAg from positive to
negative in 17% of patients
shown to dramatically improve the condition of
patients with decompensated disease due to
HBV reactivation.
Major complication: the emergence of viral variants
Safety: At therapeutic doses, excellent safety profile
Adefovir dipivoxil
• a nucleoside analogue
• Diester prodrug of adefovir (acyclic phosphonated adenine
nucleotide analog)
• MOA: phosphorylated by cellular kinases to active
disphosphate metabolite and then competitively inhibits
HBV DNA polymerase  chain termination (a potent
inhibitor of the viral polymerase)
• Kinetics
Oral BA: 59%, unaffected by meals; t ½ : 7.5 hrs
Renal elimination  may be given to patients with
decompensated liver disease
• Efficacy
has been tested in HbeAg-positive, HbeAg-negative,
and lamivudine-resistant patients with encouraging
3.5 logs reduction of HBV DNA
Normalization of aspartate aminotransferase in 4872%
Improvement in liver histology and fibrosis in 53-64%
of patients at 48 wks
Prolonged therapy  higher response rates
Optimal dose seems to be 10 mg/d. Higher doses are
Safety: well-tolerated; may cause dose-dependent
Other ADRs: headache, diarrhea, asthenia, abdominal pain
• Oral guanosine nucleoside analog
• Competitively inhibits all 3 functions of DNA polymerase:
base priming, reverse transcription and synthesis of
positive strand
• Oral BA approaches 100% but decreased by food
• T ½: 15 hours; renal elimination
• Efficacy compared to lamivudine
Similar rates of HBeAg seroconversion
Higher rates of viral DNA suppression, normalization
of aspartate aminotransferase and improvement in
liver histology
• No primary resistance after 48 weeks of use
• Safety: Well tolerated. Common ADRs: headache, fatigue,
dizziness and nausea
Primary goal: viral eradication
Current standard of treatment: once-weekly pegylated
interferon alfa and daily oral ribavirin
• Guanosine analog
• Phosphorylated intracellularly by host cell enzymes
• MOA: appears to interfere with synthesis of guanosine
triphosphate  inhibit capping of viral mRNA; inhibit viral
RNA-dependent polymerase
• Oral BA: 64%, increases with high fat meals and decreases
with antacids
• Elimination through urine
• Improved response if in combination with interferon alfa but
should be balanced with increased risk for toxicity
• ADR: dose-dependent hemolytic anemia (10-20%),
depression, fatigue, irritability, rash, cough, insomnia,
nausea and pruritus
• Tetatogenic and embryotoxic in animals, as well as
mutagenic in mammals
• Contraindications: uncorrected anemia, end-stage renal
disease, ischemic vascular disease and pregnancy
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A type of phenolic compounds used as pungent compounds of
chili peppers
a. Cannabinoids
b. Capsaicin
c. Chavibetol
d. Phenol
2. An anticonvulsant that is used for the treatment of jaundice by
increasing conjugation and excretion of bilirubin
a. Carbamezepine
b. Phenytoin
c. Phenobarbital
d. All of the above
3. Co administration of this substance together with you answer on
number 2 will produce additive CNS effects and death.
a. Theophylline
b. Alcohols
c. Verapamil
d. Carbamezepine
4. Drugs to be avoided with G6-PD deficiency patients
a. Primaquine
b. Pamaquine
c. Quinolones
d. Only A and B
e. All of the above
5. TRUE of the risk factors for drug-induced liver injury, except.
a. Black and Hispanics are more susceptible to isoniazid
b. More common in women
c. Male patient taking Augmentin
d. Female patient taking nitrofurantoin
e. None of the above
6. Correct pair on signature effects of drugs in the liver, EXCEPT
a. Amoxicillin – moderate rise in SGOT or SGPT levels
b. Quinolones – cholestatic jaundice reported with
repeated use
c. Diclofenac – elevation of one or more liver test results
d. Oral contraceptives - can lead to intrahepatic
e. None of the above
7. Drug that both induces CYP 1A2 and inhibits CYP2C8
a. Quinidine
b. Sulfonamide
c. Omeprazole
d. Cimetidine
8. Initial treatment for acute cholecystitis
a. Single broad spectrum antibiotic
b. Narrow spectrum antibiotic
c. Intermediate spectrum antibiotic
d. A and C
9. TRUE on treating pain from cholecystitis, EXCEPT
a. Meperidine provides analgesia
b. Morphine provides analgesia
c. Morphine increases the tone of sphincter of Oddi
d. Meperidine has no effect on the tone of sphincter of
10. Recommendations for postexposure prophylaxis for contacts of
patients positive for HBsAg, EXCEPT
a. Perinatal exposure
b. Sexual contact with an acutely infected patient
c. Sexual contact with a chronic carrier
d. Household contact with an acutely infected patient
e. None of the above
Answers: 1.B 2.C 3. B 4.E 5.E 6.E 7.C 8.A 9.B 10.D
Faye Bautista | Ralph Bautista | Paul Bejosa | Berry Beriña | Alex Bondoc | Mafe Bonifacio | Mau Borja
Jei Chan | Ivan de Guzman | Lance Domingo | Ram Enerio | Joy Esguerra | Lea Esquivel | Nice Gelvosa
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OUTLINE Jaundice Drugs for Reducing bilirubin levels Causes of