Presentation on amlodipine baharuddin

presentation

1. PRESENTATION ON DRUG -AMLODIPINE
•PRESENTED BY:
•MD BAHARUDDIN
•PHARM-D FIRST YEAR
•ROLL.NO:07(PB)
PRESENTED TO:
DR SEEMA TABASSUM
ASST.PROFESSOR

2. OUTLINES
•INTRODUCTION
•PREGNANCY CATEGORY AND BREASTFEEDING
•PHARMACOLOGY
•DOSE
•DOSAGE FORM
•CONTRAINDICATION WITH DRUGS
•ADVERSE EFFECTS
•DRUG-DRUG INTERACTION
•DRUG-FOOD INTERACTION
•PATIENT COUNSELLING

3. INTRODUCTION
•Amlodipine, sold under the brand nameNorvascamong others, is a
medication used to treathigh blood pressureandcoronary artery
disease.While not typically recommended inheart failure,it may be
used if other medications are not sufficient for treating high blood
pressure orheart-related chest pain.It is taken by mouth and has an
effect that lasts for at least a day.
•It is an antianginal and antihypertensive agents by decrease in
peripheral resistance and and inhibition of coronary spasm
•It is a dihydropyridine calcium channel blocker that exerts its effect by
blocking the transmembrane influx of calcium ions into cardiac and
vascular smooth muscles.
•It does not affect serum calcium concentrations.
•It was patented in 1982 and approved for medical use in 1990

4. PREGNANCY CATEGORY AND BREAST FEEDING
•US FDA pregnancy category: C
•Use of adequate methods of contraception should be encouraged.
•If this drug is used during pregnancy, or if the patient becomes
pregnant while taking this drug, the patient should be apprised of the
potential harm to the fetus.
•Available evidence is inconclusive or is inadequate for determining
fetal risk when used in pregnant women or women of childbearing
potential. Weigh the potential benefits of drug treatment against
potential risks before prescribing this drug during pregnancy.
•Administer amlodipine during pregnancy only if the potential
maternal benefit outweighs the potential fetal risk.
•Infant risk cannot be ruled out.

5. PHARMACOLOGY
•Amlodipine is an angioselectivecalcium channel blockerand
inhibits the movement of calcium ions intovascular smooth
musclecells andcardiac muscle cellswhich inhibits the contraction
of cardiac muscle and vascular smooth muscle cells. Amlodipine
inhibits calcium ion influx across cell membranes, with a greater
effect on vascular smooth muscle cells. This causes vasodilation and
a reduction inperipheral vascular resistance,thus lowering blood
pressure. Its effects on cardiac muscle also prevent excessive
constriction in thecoronary arteries.
•PHARMACOKINETICS; The terminal half-life of amlodipine is
approximately 30 to 50 hours.
•The plasma elimination half-life of amlodipine is 56 hours in
patients with impaired hepatic function

6. DOSE
Hypertension
1)FDA Dosage
a)Initial dosage: 5 mg orally once a day.
c)Maximum dosage: 10 mg once daily.
•2)Guideline Dosage
a)Initial dosage: 2.5 mg orally once daily.
•b)Target dosage: 10 mg once daily.
•Stable angina, chronic
1)Usual dosage: 5 to 10 mg orally once daily; most patients will require 10
mg for adequate effect.
•Variant angina
1)Usual dosage: 5 to 10 mg orally once daily; most patients will require 10
mg for adequate effect.
•Usual dosage: 5 to 10 mg orally once daily; most patients required the 10 mg
dose in clinical trials.

7. DOSAGE FORM
•ADULT
•Dosage Forms & Strengths
•TABLET
•2.5mg (Norvasc, generic)
•5mg (Norvasc, generic)
•10mg (Norvasc, generic)
•oral suspension
•1mg/mL(Katerzia)
•PEDIATRIC
•2.5mg (Norvasc, generic)
•5mg (Norvasc, generic)
•10mg (Norvasc, generic)
•GERRIATRIC

8. ADVERSE EFFECTS
•Cardiovascular:Edema (1.8% to 10.8% )
•Gastrointestinal:Abdominal pain (1.6% ), Nausea (2.9% )
•Neurologic:Somnolence (1.4% )
•Other:Fatigue (4.5% )
•Palpitations(4.5).

9. DRUG-DRUG INTERACTIONS
CERITINIB
•Probable Mechanism: inhibition of CYP3A-mediated metabolism
of drug by ceritinib
•Interaction Effect: increased exposure of CYP3A substrate
•Severity: major
•Onset: unspecified
•Clinical Management: Concomitant use of ceritinib(a strong CYP3A
inhibitor) and a CYP3A substrate may increase exposure of the substrate.
Avoid use of sensitive CYP3A substrates and if other CYP3A substrates are
coadministered, consider dose reductions of the CYP3A substrate

10. DRUG-DRUG INTERACTIONS
ATAZANAVIR
•Probable Mechanism: inhibition of cytochromeP450 3A-mediated
metabolism of amlodipineby atazanavirand additive PR interval
prolongation
•Interaction Effect: increased amlodipineconcentrations, and an
increased risk of cardiotoxicity(prolonged PR interval)
•Severity: major
•Onset:unspecified
•Clinical Management: Coadministrationof amlodipineand atazanavir
may result in increased amlodipineconcentrations. If coadministration
cannot be avoided, monitor for signs and symptoms of edema,
hypotension,andelectrocardiogram abnormalities especially PR interval
prolongation. Consider dose titration of amlodipine

11. DRUG-DRUG INTERACTIONS
TACROLIMUS
Probable Mechanism: unknown
Interaction Effect: increased tacrolimusexposure
Severity: major
Onset: unspecified
Clinical Management: Concomitant use of amlodipine
and tacrolimusmay result in increased tacrolimus
concentrations. Monitor trough tacrolimusconcentrations
frequently after starting amlodipinetherapy and adjust the
tacrolimusdosage if appropriate.Alsomonitor the patient
for signs of tacrolimustoxicity, including renal dysfunction,
cholestasis, and paresthesias.

12. DRUG-DRUG INTERACTIONS
YOHIMBINE
Probable Mechanism: increased norepinephrinerelease
by yohimbine
Interaction Effect: reduced calcium channel blocker
effectiveness
Severity: moderate
Onset: rapid
Clinical Management: Avoid concomitant use of
yohimbineand calcium channel blockers. Yohimbinemay
counteract the hypotensiveeffect of calcium channel
blockers

13. DRUG-DRUG INTERACTIONS
MA HAUNG(EPHEDRA)
Probable Mechanism: antagonistic effect through
sympathomimeticactivity of ephedrine and pseudoephedrine in Ma
Huang
Interaction Effect: reduced hypotensiveeffect of calcium channel
blockers
Severity: moderate
Clinical Management: Concomitant use of ma huangis not
advised in patients using antihypertensives. The ephedrine content
of Ma Huang may exacerbate hypertension. ma huangis
contraindicated in patients who are ephedrine or pseudoephedrine
sensitive, and those with renal failure or pheochromocytoma.

14. DRUG-DRUG INTERACTIONS
LACOSAMIDE
Probable Mechanism: additive effects on PR interval prolongation
Interaction Effect: increased risk of PR interval prolongation, AV block,
bradycardia, and ventricular tachyarrhythmia.
Severity: major
Onset: unspecified
Clinical Management: Lacosamidehas been associated with PR-interval
prolongation therefore concomitant use of lacosamideand agents that affect
cardiac conduction should be done cautiously due to the risk of AV block,
bradycardia, and ventricular tachyarrhythmia. This includes sodium channel
blockers, beta-blockers, calcium channel blockers, potassium channel blockers,
and other drugs that prolong the PR interval (including sodium channel blocking
antiepileptic agents). Obtain an ECG before beginning lacosamide, and after
lacosamideis titrated to steady-state maintenance dose. In addition, closely
monitor if lacosamideis administered via the IV route

15. DRUG-DRUG INTERACTIONS
DIGOXIN
Probable Mechanism: additive effects on AV node
conduction
Interaction Effect: increased risk of complete heart block
Severity: major
Onset: rapid
Clinical Management: Coadministrationof digoxinand a calcium
channel blocker may have additive effects on AV node conduction
and increase the risk of bradycardiaand advanced or complete
heart block. Caution is recommended if concomitant use is
required.

16. DRUG-DRUG INTERACTIONS
DOMPERIDONE
Probable Mechanism: inhibition of CYP3A4-mediated domperidonemetabolism
Interaction Effect: increased domperidoneexposure and an increased risk of QT
prolongation.
Severity: major
Onset: unspecified
Clinical Management: Use caution with the concomitant administration of
amlodipineand domperidoneas this may result in increased plasma
concentrations of domperidoneand may increase the risk of serious cardiac
effects, including ventricular arrhythmias and sudden cardiac death, particularly
at domperidonedoses greater than 30 mg/day and in patients older than 60
years. Domperidoneshould be initiated at the lowest possible dose and titrated
with caution. Discontinue domperidoneif the patient experiences dizziness,
palpitations, syncope, or seizure.

17. DRUG-FOOD INTERACTIONS
MONITOR.: Calcium-containing products may decrease the
effectiveness of calcium channel blockers by saturating
calcium channels with calcium. Calcium chloride has been
used to manage acute severe verapamiltoxicity.
MANAGEMENT: Management consists of monitoring the
effectiveness of calcium channel blocker therapy during
coadministrationwith calcium products.
The consumption of grapefruit juice may slightly increase
plasma concentrations of amlodipine. The mechanism is
inhibition of CYP450 3A4-mediated first-pass metabolism
in the gut wall by certain compounds present in
grapefruits.

18. PATIENT COUNSELLING
1.Amlodipine is used to treat high blood pressure and chest pain
(angina).
2. The tablets are taken once each day with a glass of water. Try
to take them at the same time each day.
3. Do not stop taking the tablets without speaking to your doctor
first. Your condition could get worse if you stopped suddenly.
4. Like most medicines, amlodipinecan have some unwanted
effects. These include flushing, headache and dizziness. Ankle
swelling may occur, particularly if you sit down for a long time. If
you do sit for much of the day, it is a good idea to rest your feet
on a stool. If you keep taking the tablets these effects may go
away within a week or so, but if any side effects are persistent or
troublesome tell your doctor.