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Year Level 8: Clerkship

Generic Name: Pantoprazole

Drug Class: Proton-pump inhibitor
Drug Structure:

Drug Database
Brand Names: Antaxid, Pantoprix, Pantoloc
Dosage Forms: Oral, intravenous
Drug Appearance:

Indications: Indicated for the treatment of duodenal ulcers, benign gastric ulcers, gastroesophageal reflux disease
(GERD), heartburn and other symptoms associated with GERD, erosive esophagitis, and long-term treatment of
pathological hypersecretory conditions like Zollinger-Ellison syndrome, multiple endocrine adenomas, and systemic
mastocytosis.
Dosing:
ORAL
GERD: 20-40 mg for 4 weeks, up to 8 weeks if needed; Maintenance: 20-40 mg/day
Erosive esophagitis: 20-40 mg for up to 16 weeks if needed
Peptic ulcer: 40 mg for 2-4 weeks (duodenal ulcer) or 4-8 weeks for (benign gastric ulceration)
Prophylaxis of NSAID-induced ulcers: 20 mg
Zollinger-Ellison syndrome: Initial: 80 mg; Max: 240 mg/day; Daily doses > 80 mg should be given in 2 divided
doses
H. pylori infection: 40 mg BID with clarithromycin and either amoxicillin or metronidazole.
INTRAVENOUS
Zollinger-Ellison syndrome: 80 mg once or twice daily until PO can be resumed; Max: 240 mg/day in divided
doses
GERD, peptic ulcer: 40 mg/day until PO can be resumed
Adverse Effects: PPIs are safe. Diarrhea, headache, and abdominal pain are reported in 1-5% of patients.
Increasing cases of acute interstitial nephritis have been reported. Moreover, since acid is important in releasing
vitamin B12, there is a minor reduction in its absorption.
Drug Interactions: Increased risk of digoxin-induced cardiotoxic effects. Increased risk of hypomagnesaemia w/
diuretics. May increase INR and prothrombin time of warfarin. May increase serum concentration of methotrexate
and saquinavir. Delayed absorption and decreased bioavailability w/ sucralfate. Decreased absorption of
ketoconazole, itraconazole. Potentially fatal for the following: may decrease serum levels and pharmacological
effects of rilpivirine, atazanavir and nelfinavir.
Mechanism of Action: Suppresses gastric acid secretion, both fasting and Half Life: 1.0-1.9 hours
meal-stimulated, by irreversible inhibition of the H+/K+-ATPase in the gastric
parietal cell by blocking the final common pathway of acid secretion, the
proton pump.
Metabolism/Excretion: Proton pump inhibitors undergo rapid first-pass and Onset of Action: Occurs within
systemic hepatic metabolism. Clearance is through the kidney but is one hour and maximum effect
negligible. Dose reduction is not needed for patients with renal insufficiency occurring within two hours
or mild to moderate liver disease.
Bioavailability: 77%
Metabolites: Two were identified
as hydroxyomeprazole and the
corresponding carboxylic acid.
Patient Correlation
Pantoprazole is used for gastric protection to prevent stress-induced gastritis.

Generic Name: Paracetamol

Drug Class: Analgesics and Antipyretics

Drug Database
Brand Names: Calpol, Panadol, Tipol, Tylenol
Dosage Forms:
Tablet: 250 mg, 500 mg
Oral Powder: 500 mg, 600 mg, 1000 mg
Oral Liquid: 24 mg/mL, 48 mg/mL, 100 mg/mL

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Drug Structure:

Drug Appearance:

Indications: headaches, dental pain, postoperative pain, pain in connection with colds, post-traumatic muscle pain
Dosing:
Adult: PO 0.5-1 g 4-6 hrly. Max: 4 g/day. Rectal As supp: 0.5-1 g 4-6 hrly. Max: 4 g/day. IV 33-50 kg: 15 mg/kg as a
single dose, at least 4 hrly. Max: 60 mg/kg/day up to 3 g/day; >50 kg: 1 g as a single dose, at least 4 hrly. Max: 4
g/day. Admin by infusion over 15 min.
Adverse Effects: rashes, itching, swelling, severe dizziness, trouble breathing
Drug Interactions: Potentiate effects of L-dopa andmeclofenoxate (clophenoxate)
Mechanism of Action: Paracetamol exhibits analgesic Half Life: 1-3 hours
action by peripheral blockage of pain impulse generation.
It produces antipyresis by inhibiting the hypothalamic
heat-regulating centre. Its weak anti-inflammatory
activity is related to inhibition of prostaglandin synthesis
in the CNS.
Metabolism/ Excretion: Hepatic via glucuronic and Onset of Action: Oral: <1 hr. IV: 5-10 min (analgesia);
sulfuric acid conjugation; mainly via urine
w/in 30 min (antipyretic)
Bioavailability: 70 90 %
Metabolites: N-acetyl-p-benzoquinoneimine
Patient Correlation
Given to the patient as needed for fever

Generic Name: Metaclopramide

Drug Class: GIT Regulators, Antiflatulents, AntiInflammatories, Antiemetics

Drug Structure:

Drug Database
Brand Names: Reglan, Maxolon, Metozolv
Dosage Forms:
Injectable solution: 5 mg/mL
Syrup: 5 mg/5 mL, 10 mg/10mL
Tablet: 5 mg, 10 mg
Drug Appearance:

Indications: diabetes, gastroparesis, chemotherapy, radiotherapy, nausea

Dosing:
Adult: PO GERD 10-15 mg 4 times/day. If symptoms are intermittent, may give single doses of 20 mg prior to
provoking situation. Max duration: 12 wk. Diabetic gastric stasis 10 mg 4 times/day for 2-8 wk. Nausea and
vomiting associated w/ cancer chemotherapy or radiotherapy 10 mg, up to tid. Max duration: 5
days. IM/IV Diabetic gastric stasis 10 mg 4 times/day by IM inj or slow IV inj over 1-2 min for up to 10 days. Convert
to oral admin when symptoms subside sufficiently. Prophylaxis of post-op nausea and vomiting 10 mg as a single
dose by IM or slow IV inj over at least 3 min. IV Prophylaxis of chemotherapy-induced nausea and vomiting For
highly emetogenic drugs/regimens: Initial: 2 mg/kg by slow inj over at least 15 min, 30 min before chemotherapy.
Repeat 2 hrly for 2 doses, then 3 hrly for 3 doses. For less emetogenic drugs/regimens: 1 mg/kg may be used. Max
duration: 5 days. Intubation of the small intestine; Premedication for radiologic examination of the upper
GI tract 10 mg as a single dose by slow inj over 1-2 min.

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Adverse Effects: decreased energy, tiredness, diarrhea, dizziness, drowsiness, headache, nausea, vomiting,
restlessness, malaise, insomnia, swelling, urinating more than usual
Drug Interactions: Antagonistic effect w/ anticholinergics and morphine derivatives. Potentiation of sedative effects
w/ CNS depressants. Additive effect w/ other neuroleptics on the occurrence of extrapyramydal disorders. May
increase the risk of serotonin syndrome w/ serotonergic drugs (e.g. SSRIs). May decrease digoxin bioavailability. May
increase ciclosporin bioavailability. May prolong the neuromuscular blocking effect of mivacurium and suxamethonium.
Increased exposure levels w/ strong CYP2D6 inhibitors (e.g. fluoxetine). May reduce plasma concentration of
atovaquone.
Mechanism
of
Action:
Metoclopramide
blocks Half Life: 1-2 hours
dopamine receptors and in higher doses, it also blocks
serotonin receptors in chemoreceptor trigger zone of the
CNS. It enhances the response to acetylcholine of tissue
in upper GI tract causing enhanced motility and
accelerated gastric emptying without stimulating gastric,
biliary, or pancreatic secretions. It also increases lower
esophageal sphincter tone.
Metabolism/ Excretion: Undergoes hepatic first-pass Onset of Action: 6-12 hours
metabolism; Via urine, 85% (20% as unchanged drug and
the remainder as sulfate or glucuronide conjugates or as
metabolites); feces via the bile (approx 5%)
Bioavailability: 80 %
Metabolites: N-hydroxylation and N-deethylation
Patient Correlation
Given to the patient to treat symptom of nausea
Drug Database
Generic Name: Amlodipine
Brand Names: Norvasc, Tekamlo, Amturnide, Caduet,
Lotrel, Ambulenz, Tribenzor, Exforge, Azor, Prestalia,
Twynsta
Drug Class: Anti-Anginal Drugs /Calcium Antagonists
Dosage Forms: tablet: 2.5 mg, 5 mg, 10 mg
Drug Structure:
Drug Appearance:

Indications: Hypertension, Coronary Artery Disease, Angina

Dosing:
Adult: PO Stable angina; HTN; Prinzmetal's angina Initial: 5 mg once daily. Max: 10 mg once daily.
Adverse Effects: Swelling of feet, difficult breathing, dizziness, feeling of warmth, redness of face, neck, arms and
upper chest, shortness of breath, tightness in chest
Drug Interactions: Plasma concentrations may be elevated w/ CYP3A4 inhibitors (e.g. azole antifungals, ritonavir).
Concomitant therapy w/ simvastatin may increase risk of myopathy including rhabdomyolysis. May increase
ciclosporin plasma levels and conivaptan.
Mechanism of Action: Amlodipine relaxes peripheral Half Life: 35-50 hours
and coronary vascular smooth muscle. It produces
coronary vasodilation by inhibiting the entry of Ca ions
into the slow channels or select voltage-sensitive
channels of the vascular smooth muscle and myocardium
during depolarisation. It also increases myocardial oxygen
delivery in patients w/ vasospastic angina.
Metabolism/Excretion: Hepatically metabolized to Onset of Action: 6-12 hours
inactive metabolites; Via urine (mainly as metabolites,
<10% as unchanged drug)
Bioavailability: 60-65 %
Metabolites: inactive

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Year Level 8: Clerkship
Patient Correlation
Given to the patient for hypertension

Generic Name: Atorvastatin

Drug Class: Dyslipidemic Agents
Drug Structure:

Drug Database
Brand Names: Iovstatin, Simvastatin, Fluvastatin,
Pravastatin, Rosuvastatin
Dosage Forms: 10 mg, 20 mg, 40 mg, 80 mg tablets
Drug Appearance:

Indications: Hypercholesterolemia, Mixed Dyslipidemia, Hyperlipidemia, Hypertriglyceridemia

Dosing:
Adult: PO Mixed
dyslipidaemia;
Heterozygous
familial
hypercholesterolaemia;
Nonfamilial
hypercholesterolaemia Initial: 10 or 20 mg once daily, may be adjusted at 4-wk interval. May initiate 40 mg once
daily in patients who require >45% reduction in LDL-cholesterol. Max: 80 mg/day.
Adverse Effects: cough, weight gain, dizziness, fever, nausea, itching, muscle cramps, skin rash, unusual weakness,
swelling
Drug Interactions: May increase risk of myopathy and rhabdomyolysis w/ CYP3A4 potent inhibitor (e.g. HIV or HCV
protease inhibitors, itraconazole, clarithromycin), fenofibrate, colchicines, fixed combination of lopinavir/ritonavir. May
decrease plasma concentration w/ CYP3A4 inducer (e.g. rifampicin, efavirenz). May significantly increase AUC and
peak plasma concentration of digoxin. Increased AUC for norethindrone and ethinyl estradiol.
Mechanism of Action: Atorvastatin competitively Half Life: approximately 14 hours
inhibits HMG-CoA reductase, the enzyme that catalyses
the conversion of HMG-CoA to mevalonate. This results in
the induction of the LDL receptors and stimulation of LDL
catabolism, leading to lowered LDL-cholesterol levels.
Metabolism/Excretion:
Metabolised
by
CYP3A4 Onset of Action: Readily absorbed from the GI tract
isoenzyme; Via faeces (as metabolites); urine (<2% as
unchanged drug)
Bioavailability: 12 %
Metabolites: feces
Patient Correlation
Given to the patient for dyslipidemia

Generic Name: Omeprazole

Drug Class: Proton-pump inhibitor

Drug Structure:

Drug Database
Brand Names: Prilosec, Omesec, Omepron
Dosage Forms:
Packet: 2.5 mg, 10 mg
Suspension: 2 mg/mL
Tablet: 20 mg
Capsule: 10 mg, 20 mg, 40 mg
Drug Appearance:

Indications: Indicated for the treatment of duodenal ulcers, benign gastric ulcers, gastroesophageal reflux disease

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Year Level 8: Clerkship
(GERD), heartburn and other symptoms associated with GERD, erosive esophagitis, and long-term treatment of
pathological hypersecretory conditions like Zollinger-Ellison syndrome, multiple endocrine adenomas, and systemic
mastocytosis.
Dosing:
Adult: PO Duodenal ulcer 20 mg once/day for 4-8 weeks. Helicobacter pylori infection dual therapy: 40 mg
once/day in the morning plus clarithromycin 500 mg 3x/day on days 1-14, 20 mg once/day in the morning on days 1528. triple therapy: 20 mg 2x/day for 10 days plus clarithromycin 500 mg 2x/day for 10 days plus amoxicillin 1000 mg
2x/day for 10 days. If an ulcer is present at the initiation of therapy, continue 20 mg once/day for an additional 18
days. Gastric ulcer 40 mg once.day before a meal for 4-8 weeks. Erosive Esophagitis 20 mg once/day before a
meal. Zollinger-Ellison Syndrome Initial: 60 mg once/day, Maintenance: up to 120 mg 3x/day. GERD Initial: 20 mg
once/day before a meal for 4-8 weeks, Maintenance: 10-20 mg once/day. Multiple Endocrine Adenomas Initial: 60
mg once/day before a meal, Maintenance: up to 120 mg 3x/day. Systemic Mastocytosis Initial: 60 mg once/day
before a meal, Maintenance: up to 120 mg 3x/day. Dyspepsia Prevention of frequent heartburn: 20 mg once/day
before a meal for 14 days.
Adverse Effects: Constipation, diarrhea, flatulence, nausea, vomiting and acid regurgitation, abdominal pain,
asthenia, headache, dizziness and rash
Drug Interactions: Increased gastric pH during omperazole treatment may change the absorption of some
antiretroviral drugs. Other possible interaction mechanisms are via CYP2C19. Co-administration of digoxin with
omeprazole is expected to increase systemic exposure of digoxin. Omeprazole can prolong the elimination of
diazepam, warfarin, and phenytoin (drugs that are metabolized by oxidation in the liver). Co-administration with
warfarin may increase INR and prothrombin time of patient, which may lead to abnormal bleeding and even death.
Mechanism of Action: Suppresses gastric acid secretion Half Life: 0.5-1 hour (healthy subjects, delayed-release
by specific inhibition of the H+/K+-ATPase in the gastric
capsule); 3 hours (hepatic impairment)
parietal cell. By acting specifically on the proton pump,
omeprazole blocks the final step in acid production, thus
reducing gastric acidity.
Metabolism/ Excretion: Urinary excretion is a primary
Onset of Action: Occurs within one hour and maximum
route of excretion of omeprazole metabolites. The
effect occurring within two hours
majority of the dose (about 77%) was eliminated in urine
as at least six metabolites. Little, if any unchanged drug
was excreted in the urine. The remainder of the dose was
recovered in the feces.
Bioavailability: 76%
Metabolites: Two were identified as hydroxyomeprazole
and the corresponding carboxylic acid.
Patient Correlation
Omeprazole is used for gastric protection to prevent stress induced gastritis.

Generic Name: Lactulose

Drug Class: Hyperosmotic Laxative

Drug Structure:

Drug Database
Brand Names: Cephulac, Chronulac, Movelax, Lilac
Dosage Forms:
Oral/Rectal Solution: 10 g/15 mL
Packet: 10 g, 20 g
Drug Appearance:

Indications: Indicated for the treatment of constipation and prevention and treatment of portal systemic
encephalopathy
Dosing:
Adult: PO Portal Systemic Encephalopathy 30-45 mL 3-4x/day adjusted to produce 2-3 soft stools/day. Chronic
Constipation 30-60 mL once/day as needed.

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Adverse Effects: Flatulence, borborygmi, belching, abdominal cramps, pain, and distention (initial dose); diarrhea
(excessive dose); nausea, vomiting, colon accumulation of hydrogen gas; hypernatremia.
Drug Interactions: The elimination of certain colonic bacteria by neomycin use and possibly other anti-infective
agents may interfere with the desired degradation of lactulose and thus prevent the acidification of colonic contents.
Nonabsorbable antacids given concurrently with lactulose may inhibit the desired lactulose-induced drop in colonic pH.
Other laxatives should not be used.
Mechanism of Action: Constipation: Increases stool
Half Life: 1.7-2 hours
water contents, softens stool, promotes peristalsis, and
reduced blood ammonia concentration
Portal systemic encephalopathy: Breakdown of lactulose
to organic acids by colonic bacteria acidifies colonic
contents, thereby subsequently inhibiting diffusion of
ammonia back to blood; agent also enhances diffusion of
NH3 from blood into gut, where it is converted to NH4+
Metabolism/ Excretion: Absorbed lactulose is not
Onset of Action: Occurs within 8-48 hours
metabolized; unabsorbed lactulose is extensively
metabolized to organic acids by colonic bacteria.
Absorbed lactulose is excreted via the urine; Unabsorbed
lactulose and metabolites are excreted via feces and bile.
Bioavailability: <3% absorbed
Metabolites: Lactic acid (main), formic acid, acetic acid
(all active)
Patient Correlation
Lactulose is used to maintain regular bowel movements.

Generic Name: Furosemide

Drug Class: Loop diuretic

Drug Structure:

Drug Database
Brand Names: Lasix, Diaqua-2, Lo-Aqua
Dosage Forms: oral tablet, injectable solution, oral
liquid, oral solution, compounding powder, intravenous
solution
Drug Appearance:

Indications: For the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal
disease, including the nephrotic syndrome. Also for the treatment of hypertension alone or in combination with other
antihypertensive agents.
Dosing:
Adverse Effects: Hyponatraemia, hypochloraemic alkalosis, hypokalaemia, headache, drowsiness, muscle cramps,
hypotension, dry mouth, thirst, weakness, lethargy, restlessness, oliguria, GI disturbances, hypovolaemia,
dehydration, hyperuricaemia, acute generalised exanthematous pustulosis, drug rash w/ eosinophilia and systemic
symptoms, reversible or irreversible hearing impairment, deafness, tinnitus, severe anaphylactic or anaphylactoid
reactions (e.g. w/ shock), Stevens-Johnson syndrome, toxic epidermal necrolysis; increased liver enzyme, cholesterol
and triglyceride serum levels.
Drug Interactions: May increase nephrotoxicity of cephalosporins (e.g. cefalotin), NSAIDs. May increase ototoxicity
of aminoglycoside, ethacrynic acid, other ototoxic drugs. Reduced serum level w/ aliskiren. May increase hypotensive
effect of ACE inhibitors or angiotensin II receptor antagonists. Increased risk of hyperkalaemia w/ K-sparing diuretics.
Increased risk of cardiotoxicity w/ cardiac glycosides, antihistamines. May reduce serum level of lithium. May
antagonise hypoglycaemic effect of antidiabetics. Increased hypotensive effect w/ MAOIs. Increased hyponatraemia w/
carbamazepine. Reduced natriuretic and hypotensive effect w/ indometacin. Diminished diuretic effect w/ salicylates.
Mechanism of Action: inhibits water reabsorption in the nephron by blocking the Half Life: 2 hours
sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the

Ateneo School of Medicine and Public Health

Year Level 8: Clerkship
loop of Henle. This is achieved through competitive inhibition at the chloride binding
site on the cotransporter, thus preventing the transport of sodium from the lumen of
the loop of Henle into the basolateral interstitium. Consequently, the lumen becomes
more hypertonic while the interstitium becomes less hypertonic, which in turn
diminishes the osmotic gradient for water reabsorption throughout the nephron.
Because the thick ascending limb is responsible for 25% of sodium reabsorption in
the nephron, furosemide is a very potent diuretic.
Metabolism/ Excretion: Undergoes minimal hepatic metabolism; excreted in urine
Bioavalability: Approx 60-70%.

Onset of Action: Unknown

Metabolites: Only a small
amount is hepatically
metabolized to the
defurfurylated derivative, 4chloro-5-sulfamoylanthranilic
acid.

Patient Correlation
Blood transfusions are often complicated by water retention, which may worsen lung function, heart function and/or
kidney function. Loop diuretics, like furosemide, that reduce body water by making the kidneys excrete more urine, are
thought to prevent water retention.
Drug Database
Generic Name: Deferiprone
Drug Class: iron chelator
Drug Structure:

Brand Names: Ferriprox, Kelfer-500

Dosage Forms: oral tablet, oral liquid
Drug Appearance:

Indications: Indicated in thalassemia syndromes when first line chelation agents are not adequate to treat
transfusional iron overload.
Dosing:

Initial dose: 25 mg/kg, orally, 3 times a day (total daily dose: 75 mg/kg)

Maximum dose: 33 mg/kg, orally, 3 times a day (total daily dose: 99 mg/kg)
Adverse Effects: Black, tarry stools, chills, cough, fever, lower back or side pain, painful or difficult urination, pale
skin, shortness of breath, sore throat, ulcers, sores, or white spots in the mouth, unusual bleeding or bruising, unusual
tiredness or weakness
Drug Interactions: Avoid using deferiprone with aluminium-containing antacids as it can chelates trivalent metal
ions.
Mechanism of Action: Binds to ferric ions (iron III) and
Half Life: 1.9 hours
forms a 3:1 (deferiprone:iron) stable complex and is then
eliminated in the urine. Deferiprone is more selective for
iron in which other metals such as zinc, copper, and
aluminum have a lower affinity for deferiprone.
Metabolism/ Excretion: Rapidly absorbed from the GI
Onset of Action: Unknown
tract after oral admin. Excreted mainly in the urine
Bioavailability:
Metabolites: Deferiprone is mainly metabolized by
UGT1A6 to the 3-O-glucuronide metabolite.
Patient Correlation
Since the patient is a diagnosed case of thalassemia, deferiprone is used to prevent transfusional iron overload.

Ateneo School of Medicine and Public Health

Year Level 8: Clerkship

Ateneo School of Medicine and Public Health

Year Level 8: Clerkship

1
Lactulose
Pen g
1
Citicoline
Aspirin
Lactulose
1
Meropenem
Acetylcysteine
Doxofylline
Aspirin
Enalapril
Isosothide mononitrate
Phenytoin
Hydrocortisone
Human albumin
lactulose
2
omep
lactulose