Generic name: FUROSEMIDE

Trade Name(s): Lasix

Ther. Class.: diuretics
Pharm. Class. loop diuretics

Action

 Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule.

 Increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium.

 Effectiveness persists in impaired renal function.

Pharmacokinetics
Absorption: 60–67% absorbed after oral administration (↓ in acute HF and in renal failure); also
absorbed from IM sites.
Distribution: Crosses placenta, enters breast milk.
Protein Binding: 91–99%.
Metabolism and Excretion: Minimally metabolized by liver, some nonhepatic metabolism,
some renal excretion as unchanged drug.
Half-life: 30–60 min (↑ in renal impairment).
TIME/ACTION PROFILE (diuretic effect)
ROUTE ONSET PEAK DURATION
PO 30–60 min 1–2 hr 6–8 hr
IM 10–30 min unknown 4–8 hr
IV 5 min 30 min 2 hr

Indications

 Edema due to heart failure, hepatic impairment, or renal disease.

 Hypertension.

Contraindication/Precautions
Contraindicated in:
 Hypersensitivity;

 Cross-sensitivity with thiazides and sulfonamides may occur;

 Hepatic coma or anuria;

 Some liquid products may contain alcohol, avoid in patients with alcohol intolerance.
Use Cautiously in:
 Severe liver disease (may precipitate hepatic coma; concurrent use with potassium-sparing diuretics may be necessary);

 Electrolyte depletion;

 Diabetes mellitus;

 Hypoproteinemia (↑ risk of ototoxicity);

 Severe renal impairment (↑ risk of ototoxicity);

 OB: Lactation: Safety not established;

 Pedi: ↑ risk for renal calculi and patent ductus arteriosis in premature neonates;

 Geri: May have ↑ risk of side effects, especially hypotension and electrolyte imbalance, at usual doses.

Adverse Reactions/Side Effects

CNS: blurred vision, dizziness, headache, vertigo
EENT: hearing loss, tinnitus
CV: hypotension
GI: anorexia, constipation, diarrhea, dry mouth, dyspepsia, ↑ liver enzymes, nausea, pancreatitis,
vomiting
GU: ↑ BUN, excessive urination, nephrocalcinosis
Derm: ERYTHEMA MULTIFORME, STEVENS-JOHNSON SYNDROME, TOXIC
EPIDERMAL NECROLYSIS, photosensitivity, pruritis, rash, urticaria
Endo: hypercholesterolemia, hyperglycemia, hypertriglyceridemia, hyperuricemia
F and
E: dehydration, hypocalcemia, hypochloremia, hypokalemia, hypomagnesemia, hyponatremia, h
ypovolemia, metabolic alkalosis
Hemat: APLASTIC ANEMIA, AGRANULOCYTOSIS, hemolytic anemia, leukopenia,
thrombocytopenia
MS: muscle cramps
Neuro: paresthesia
Misc: fever
* CAPITALS indicate life-threatening.
Underline indicate most frequent.

Route/Dosage
Edema
PO: (Adults) 20–80 mg/day as a single dose initially, may repeat in 6–8 hr; may ↑ dose by 20–
40 mg q 6–8 hr until desired response. Maintenance doses may be given once or twice daily
(doses up to 2.5 g/day have been used in patients with HF or renal disease). Hypertension– 40
twice daily initially (when added to regimen, ↓ dose of other antihypertensives by 50%); adjust
further dosing based on response; Hypercalcemia– 120 mg/day in 1–3 doses.
PO: (Children >1 mo): 2 mg/kg as a single dose; may be ↑ by 1–2 mg/kg q 6–8 hr (maximum
dose = 6 mg/kg).
PO: Neonates 1–4 mg/kg/dose 1–2 times/day.
IM: IV: (Adults) 20–40 mg, may repeat in 1–2 hr and ↑ by 20 mg every 1–2 hr until response is
obtained, maintenance dose may be given q 6–12 hr; Continuous infusion– Bolus 0.1 mg/kg
followed by 0.1 mg/kg/hr, double q 2 hr to a maximum of 0.4 mg/kg/hr.
IM: IV: Children 1–2 mg/kg/dose q 6–12 hr; Continuous infusion– 0.05 mg/kg/hr, titrate to
clinical effect.
IM: IV: Neonates 1–2 mg/kg/dose q 12–24 hr.
Hypertension
PO: (Adults) 40 twice daily initially (when added to regimen, ↓ dose of other antihypertensives
by 50%); adjust further dosing based on response.
General: Felodipine

Trade Name(s): Plendil 

Ther. Class.
antianginals
antihypertensives
Pharm. Class.
calcium channel blocker

Mechanism of action
Felodipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the
influx of calcium ions through voltage-gated L-type calcium channels. It reversibly competes against
nitrendipine and other DHP CCBs for DHP binding sites in vascular smooth muscle and cultured rabbit atrial
cells

Absorption
Is completely absorbed from the gastrointestinal tract; however, extensive first-pass metabolism through the
portal circulation results in a low systemic availability of 15%. Bioavailability is unaffected by food.
Volume of distribution

 10 L/kg
Protein binding
99%, primarily to the albumin fraction.
Metabolism
Hepatic metabolism primarily via cytochrome P450 3A4. Six metabolites with no appreciable vasodilatory
effects have been identified.

 Felodipine 

 dehydrofelodipine
Route of elimination
Although higher concentrations of the metabolites are present in the plasma due to decreased urinary
excretion, these are inactive. Animal studies have demonstrated that felodipine crosses the blood-brain
barrier and the placenta.
Half life
17.5-31.5 hours in hypertensive patients; 19.1-35.9 hours in elderly hypertensive patients; 8.5-19.7 in
healthy volunteers.
Clearance

 0.8 L/min [Young healthy subjects]

Toxicity
Symptoms of overdose include excessive peripheral vasodilation with marked hypotension and possibly
bradycardia. Oral rat LD50 is 1050 mg/kg.

INDICATIONS

PLENDIL is indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure lowers the
risk of fatal and non-fatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have
been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including
felodipine

DOSAGE AND ADMINISTRATION

The recommended starting dose is 5 mg once a day. Depending on the patient's response, the dosage can be
decreased to 2.5 mg or increased to 10 mg once a day. These adjustments should occur generally at intervals of not
less than 2 weeks. The recommended dosage range is 2.5–10 mg once daily. In clinical trials, doses above 10 mg
daily showed an increased blood pressure response but a large increase in the rate of peripheral edema and other
vasodilatory adverse events (see ADVERSE REACTIONS). Modification of the recommended dosage is usually not
required in patients with renal impairment.

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Drug Description

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PLENDIL® 
(felodipine) Extended-Release Tablets

DESCRIPTION

PLENDIL (felodipine) is a calcium antagonist (calcium channel blocker). Felodipine is a

dihydropyridine derivative that is chemically described as ± ethyl methyl 4-(2,3-
dichlorophenyl)1,4-dihydro-2,6-dimethyl-3,5-pyridinedicarboxylate. Its empirical formula is
C H Cl NO  and its structural formula is:
18 19 2 4

Felodipine is a slightly yellowish, crystalline powder with a molecular weight of 384.26. It is

insoluble in water and is freely soluble in dichloromethane and ethanol. Felodipine is a racemic
mixture.

Tablets PLENDIL provide extended release of felodipine. They are available as tablets
containing 2.5 mg, 5 mg, or 10 mg of felodipine for oral administration. In addition to the active
ingredient felodipine, the tablets contain the following inactive ingredients: Tablets PLENDIL
2.5 mg — hydroxypropyl cellulose, lactose, FD&C Blue 2, sodium stearyl fumarate, titanium
dioxide, yellow iron oxide, and other ingredients. Tablets PLENDIL 5 mg and 10 mg —
cellulose, red and yellow oxide, lactose, polyethylene glycol, sodium stearyl fumarate, titanium
dioxide, and other ingredients.

Indications

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INDICATIONS

PLENDIL is indicated for the treatment of hypertension, to lower blood pressure. Lowering
blood pressure lowers the risk of fatal and non-fatal cardiovascular events, primarily strokes and
myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive
drugs from a wide variety of pharmacologic classes including felodipine.

Control of high blood pressure should be part of comprehensive cardiovascular risk

management, including, as appropriate, lipid control, diabetes management, antithrombotic
therapy, smoking cessation, exercise, and limited sodium intake. Many patients will require more
than 1 drug to achieve blood pressure goals. For specific advice on goals and management, see
published guidelines, such as those of the National High Blood Pressure Education Program's
Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure (JNC).

Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different
mechanisms of action, have been shown in randomized controlled trials to reduce
cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure
reduction, and not some other pharmacologic property of the drugs, that is largely responsible for
those benefits. The largest and most consistent cardiovascular outcome benefit has been a
reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular
mortality also have been seen regularly.

Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk

increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe
hypertension can provide substantial benefit. Relative risk reduction from blood pressure
reduction is similar across populations with varying absolute risk, so the absolute benefit is
greater in patients who are at higher risk independent of their hypertension (for example, patients
with diabetes or hyperlipidemia), and such patients would be expected to benefit from more
aggressive treatment to a lower blood pressure goal.

Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black
patients, and many antihypertensive drugs have additional approved indications and effects (eg,
on angina, heart failure, or diabetic kidney disease). These considerations may guide selection of
therapy.

PLENDIL may be administered with other antihypertensive agents.

CONTRAINDICATIONS

PLENDIL is contraindicated in patients who are hypersensitive to this product.

DOSAGE AND ADMINISTRATION

The recommended starting dose is 5 mg once a day. Depending on the patient's response, the
dosage can be decreased to 2.5 mg or increased to 10 mg once a day. These adjustments should
occur generally at intervals of not less than 2 weeks. The recommended dosage range is 2.5–10
mg once daily. In clinical trials, doses above 10 mg daily showed an increased blood pressure
response but a large increase in the rate of peripheral edema and other vasodilatory adverse
events (see ADVERSE REACTIONS). Modification of the recommended dosage is usually not
required in patients with renal impairment.

SIDE EFFECTS
Body as a Whole: Chest pain, facial edema, flu-like illness; Cardiovascular: Myocardial
infarction, hypotension, syncope, angina pectoris, arrhythmia, tachycardia, premature beats; Digestive:Abdominal
pain, diarrhea, vomiting, dry mouth, flatulence, acid regurgitation; Endocrine:Gynecomastia;
Hematologic: Anemia; Metabolic: ALT (SGPT) increased; Musculoskeletal:Arthralgia, back pain, leg pain, foot
pain, muscle cramps, myalgia, arm pain, knee pain, hip pain; Nervous/Psychiatric: Insomnia, depression, anxiety
disorders, irritability, nervousness, somnolence,
decreased libido; Respiratory: Dyspnea, pharyngitis, bronchitis, influenza, sinusitis, epistaxis, respiratory infection; Sk
in: Angioedema, contusion, erythema, urticaria, leukocytoclastic vasculitis; Special Senses: Visual
disturbances; Urogenital: Impotence, urinary frequency, urinary urgency, dysuria, polyuria.

hydralazine (Apresoline)
Class
Diazanaphthalenes
Sub Class
Benzodiazines

Mechanism of action
Although the precise mechanism of action of hydralazine is not fully understood, the major effects are on the
cardiovascular system. Hydralazine apparently lowers blood pressure by exerting a peripheral vasodilating
effect through a direct relaxation of vascular smooth muscle. It has also been suggested that cyclic 3',5'-
adenosine monophosphate (cyclic AMP) mediates, at least partly, the relaxation of arterial smooth muscle
by altering cellular calcium metabolism, which interferes with the calcium movements within the vascular
smooth muscle that are responsible for initiating or maintaining the contractile state. 

Absorption
Hydralazine is rapidly and extensively absorbed (up to 90%) from the gastrointestinal tract and undergoes
extensive first-pass metabolism by genetic polymorphic acetylation. Oral bioavailability of hydralazine is
dependent upon acetylator phenotype. Bioavailability is approximately 31% in slow acetylators and 10% in
fast acetylators.
Volume of distribution
Not Available
Protein binding
87%
Metabolism
Hydralazine, when administered orally, undergoes extensive first-pass metabolism by genetic polymorphic
acetylation, which is responsible for a threefold range of oral bioavailability. Intravenously administered
hydralazine does not undergo first-pass metabolism and, therefore, is not affected by acetylator phenotype.
After the drug reaches the systemic circulation, it is combined with endogenous aldehydes and ketones,
including pyruvic acid, to form hydrazone metabolites. The active metabolites, hydralazine acetonide
hydrazone and hydralazine pyruvate hydrazone, are equipotent with the parent, hydralazine.

 Hydralazine 

 Hydralazine acetone hydrazone

 Hydralazine 

 Hydralazine pyruvate hydrazone

Route of elimination
Hydralazine undergoes extensive hepatic metabolism; it is excreted mainly in the form of metabolites in the
urine.
Half life
3 to 7 hours
Clearance
Not Available
Indications and dosages 
 Moderate to severe hypertension. Adults:  Initially, 10 mg P.O. q.i.d. for 2 to 4 days; then increased to 25 mg q.i.d.
for remainder of week. If needed, increase dosage to 50 mg q.i.d. Maximum recommended dose is 200 mg daily, but some
patients may require 300 to 400 mg daily. 
 For severe hypertension, 10 to 50 mg I.M. or 10 to 20 mg I.V. repeated, p.r.n. Switch to oral antihypertensives as soon as
possible. 
 For hypertensive crisis caused by pregnancy, initially 5 mg I.V., followed by 5 to 10 mg I.V. q 20 to 30 minutes until
adequate reduction in blood pressure is achieved (usual range, 5 to 20 mg). 
Children: Initially, 0.75 mg/kg P.O. daily in four divided doses (25 mg/m2 daily); may increase gradually to 7.5 mg/kg
daily. 
 I.M. or I.V. dosage is 0.4 to 1.2 mg/kg or 50 to 100 mg/m2 daily in four to six divided doses. Initial parenteral dose
shouldn’t exceed 20 mg. 
Adverse reactions
CNS: peripheral neuritis, headache,  dizziness. 
CV: orthostatic hypotension, tachycardia,  edema, angina, palpitations,  flushing. 
EENT: lacrimation, nasal congestion. 
GI: nausea, vomiting, diarrhea, anorexia,  constipation. 
Hematologic: neutropenia, leukopenia, agranulocytosis. 
Musculoskeletal: muscle cramps. 
Skin: rash. 
Other: lupus-like syndrome. 

CEFALEXIN (Cefovit)

Class
Lactams
Sub Class
Beta lactams
Direct Parent
Cephalosporins
MOA

Cephalexin, like the penicillins, is a beta-lactam antibiotic. By binding to specific penicillin-binding proteins (PBPs)
located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then
mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cephalexin interferes with an
autolysin inhibitor

Absorption
Well absorbed from the gastrointestinal tract
Volume of distribution
Not Available
Protein binding
14%
Metabolism
No appreciable biotransformation in the liver (90% of the drug is excreted unchanged in the urine).

Route of elimination
Cephalexin is excreted in the urine by glomerular filtration and tubular secretion. Studies showed that over
90% of the drug was excreted unchanged in the urine within 8 hours.
Half life
1 hour
Clearance
Not Available
Toxicity
Symptoms of overdose include blood in the urine, diarrhea, nausea, upper abdominal pain, and vomiting.
The oral median lethal dose of cephalexin in rats is >5000 mg/kg.
Indication
For the treatment of respiratory tract infections caused by Streptococcus pneumoniae and Streptococcus
pyogenes; otitis media due to Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus
aureus, Streptococcus pyogenes, and Moraxella catarrhalis; skin and skin structure infections caused
by Staphylococcus aureus and/or Streptococcus pyogenes; bone infections caused by Staphylococcus
aureus and/or Proteus mirabilis; genitourinary tract infections, including acute prostatitis, caused
by Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae.
ADVERSE EFFECFT

More Common

 Diarrhea
Rare

 Abdominal or stomach pain

 blistering, peeling, or loosening of the skin
 chills
 clay-colored stools
 cough
 dark urine
 diarrhea
 dizziness
 fever
 general tiredness and weakness
 headache
 itching or rash
 joint or muscle pain
 light-colored stools
 loss of appetite
 nausea and vomiting
 red skin lesions, often with a purple center
 red, irritated eyes
 sore throat
 sores, ulcers, or white spots in the mouth or on the lips
 unpleasant breath odor
 unusual tiredness or weakness
 upper right abdominal or stomach pain
 vomiting of blood
 yellow eyes or skin

Usual Adult Dose for Pharyngitis

250 to 333 mg orally every 6 hours OR 500 mg orally every 12 hours
-Maximum dose: 4 g per day
-Duration of therapy: 7 to 14 days

Usual Pediatric Dose for Upper Respiratory Tract Infection

1 to 15 years:
Mild to moderate infections: 25 to 50 mg/kg orally per day, given in equally divided doses
Severe infections: 50 to 100 mg/kg orally per day, given in equally divided doses
Duration of therapy: 7 to 14 days

15 years and older: 250 to 333 mg orally every 6 hours OR 500 mg orally every 12 hours
-Maximum dose: 4 g per day
-Duration of therapy: 7 to 14 days
Losartan

Generic Name: losartan (loe SAR tan)

Brand Names: Cozaar

Class
Benzene and substituted derivatives (ANGIOTENSIN-II BLOCKERS)
Sub Class
Biphenyls and derivatives
Mechanism of action
Losartan competitively inhibits the binding of angiotensin II to AT1 in many tissues including vascular
smooth muscle and the adrenal glands. Losartan is metabolized to its active metabolite, E-3174, which is 10
to 40 times more potent than losartan and acts as a non-competitive AT1 antagonist. Inhibition of
angiotensin II binding to AT1 inhibits its AT1-mediated vasoconstrictive and aldosterone-secreting effects
and results in decreased vascular resistance and blood pressure. Losartan is 1,000 times more selective for
AT1 than AT2. Inhibition of aldosterone secretion may increase sodium and water excretion while
decreasing potassium excretion. Losartan is effective for reducing blood pressure and may be used to treat
essential hypertension, left ventricular hypertrophy and diabetic nephropathy.

Absorption
Losartan is well absorbed and undergoes substantial first-pass metabolism; the systemic bioavailability of
losartan is approximately 33%. Mean peak concentrations of losartan and its active metabolite are reached
in 1 hour and in 3-4 hours, respectively. While maximum plasma concentrations of losartan and its active
metabolite are approximately equal, the AUC of the metabolite is about 4 times as great as that of losartan.
When given with a meal, absorption is slows down and Cmax decreases.
Volume of distribution

 34 L [losartan, healthy subjects]

 12 L [active metabolite, healthy subjects]
Protein binding
99.7% protein bound, primarily to albumin
Metabolism
Hepatic. Losartan is metabolized to a 5-carboxylic acid derivative (E-3174) via an aldehyde intermediate (E-
3179) primarily by cytochrome P450 (CYP) 2C9 and CYP3A4. E-3174 is an active metabolite with 10- to 40-
fold higher potency than its parent compound, losartan. Approxiamtely 14% of losartan is converted to E-
3174; however, the AUC of E-3174 was found to be 4- to 8-fold higher than losartan and E-3174 is
considered the main contributor to the pharmacologic effects of this medication.

 Losartan 

 E-3179

o E-3179 

 E-3174

 Losartan 

 Losartan N2-glucuronide

 Losartan 

 E-3174
Route of elimination
 Following oral administration of losartan, 35% of the dose is recovered in the urine and about 60% in the
feces. Following an intravenous dose, 45% is recovered in the urine and 50% in the feces.
Half life
The terminal t1/2 of losartan is 2 hours. The active metabolite has a half-life of 6-9 hours.
Clearance

 Total plasma clearance = 600 mL/min losartan

 Total plasma clearance = 50 mL/min [active metabolite]
 Renal clearance = 75 mL/min losartan
 Renal clearance = 25 mL/min [active metabolite]
Toxicity
Hypotension and tachycardia; Bradycardia could occur from parasympathetic (vagal) stimulation, LD50= 1000
mg/kg (orally in rat)
Indication
May be used as a first line agent to treat uncomplicated hypertension, isolated systolic hypertension and left
ventricular hypertrophy. May be used as a first line agent to delay progression of diabetic nephropathy.
Losartan may be also used as a second line agent in the treatment of congestive heart failure, systolic
dysfunction, myocardial infarction and coronary artery disease in those intolerant of ACE inhibitors.
Commonly reported side effects of losartan include: asthenia, chest pain, diarrhea, fatigue, and
hypoglycemia. Other side effects include: hyperkalemia, hypotension, and orthostatic hypotension

Usual Adult Dose for Hypertension

Initial dose: 50 mg orally once a day
Maximum dose: 100 mg orally once a day

Usual Pediatric Dose for Hypertension

6 Years or Older:
Initial dose: 0.7 mg/kg orally once a day (up to 50 mg total)