Metacain 2% Jelly

Country: Malasía

Tungumál: enska

Heimild: NPRA (National Pharmaceutical Regulatory Agency, Bahagian Regulatori Farmasi Negara)

Virkt innihaldsefni:

LIDOCAINE HYDROCHLORIDE

Fáanlegur frá:

UNIMED SDN BHD

INN (Alþjóðlegt nafn):

LIDOCAINE HYDROCHLORIDE

Einingar í pakka:

1 x 30gm gm

Framleitt af:

Galentic Pharma (India) Pvt. Ltd.

Vara einkenni

METACAIN 2% JELLY (LIDOCAINE HYDROCHLORIDE USP 20MG)
DESCRIPTION
Transparent colourless gel, free from foreign particles.
PHARMACODYNAMICS
Lidocaine like other local anaesthetics, causes a reversible blockade
of impulse propagation
along nerve fibres by preventing the inward movement of sodium ions
through the nerve
membrane. Local anaesthetics of the amide type are thought to act
within the sodium channels
of the nerve membrane.
Local anaesthetic drugs may also have similar effects on excitable
membranes in the brain and
myocardium. If excessive amounts of drug reach the systemic
circulation rapidly, symptoms
and signs of toxicity will appear, emanating from the central nervous
and cardiovascular
systems.
Central nervous system toxicity (Over dosage) usually precedes the
cardiovascular effects as it
occurs at lower plasma concentrations. Direct effects of local
anaesthetics on the heart include
slow conduction, negative inotropism and possibly cardiac arrest.
PHARMACOKINETICS
Lidocaine is absorbed following topical administration to mucous
membranes, its rate and
extent of absorption being dependent upon concentration and the total
dose administered, the
specific site of application, and the duration of exposure. In
general, the rate of absorption of
local anaesthetic agents following topical application is most rapid
after intratracheal and
bronchial administration. Lidocaine is also well-absorbed from the
gastrointestinal tract,
although little intact drug appears in the circulation because of
biotransformation in the liver.
Normally about 65% of the lidocaine is bound to plasma proteins. Amide
local anaesthetics are
mainly bound to alpha-1-acid glycoprotein but also to albumin.
Lidocaine crosses the blood-
brain and placental barriers, presumably by passive diffusion.
The main elimination pathway of lidocaine is by liver metabolism. The
primary route of
lidocaine in human is N-dealkylation to monoethylglycine xylidine
(MEGX), followed by
hydrolysis to 2,6-xylidine and hydroxylation to
4-hydroxy-2,6-xylidine.