MED CHEM 5TH SEM NOTES

1. What is Angina Pe,
croris....:l
c:.~ ~ .....
► It is chest pain or discr1m1·11rl due l.o co.ronary heart
disease
► It occurs ·w.b1
en the heart .muscl.
e 1
d.
oes1
n't gl
et as ·mucb
.
BLOOD & O.
XYGEN as It n.eeds
► This, usually happens because one or more of the
heart's arte·
ries are .narrowed or blocked, also called
. .
b ,
.,
ISC: ·em1a
q/21/70 l~ P,. die il-Of Be lcdJe111

2. Types ,
ofAngina Pectoris
► Sta:
ble·Anlina I Anli,
na Pec;
toris
► Unstable.
An1ioa1
► Varl1
an.
t (Prlnzmeta'I) Angina
► Microv·ascularAngina
9/B/]fJ19

3. Tests,:
► EK1
G (Electrocardiogra:
m)
~ 1
s··· trnc,s ..,esu
··no
r _.·'-...a ,_· It ·- -
111
► Blood,Tests
► 1
Cbesl,X-Rays
► 1
C1
0.
ronary AnlJi,
ograpby,and Cardiac Catllete:
rization
► Computed Tomo&raplly Angio~aphy
Treatment i1
n1
cl
ludes:
► Lifestyle chan1esl
► Medicines
► 1
C1
ardiac p~edures
► 1
Ca.
nliac Rehab1
~/l'l/2{] 19

4. Anti..anginal Agents
As pe.
r PC1
l 1
SJ·llahus
, VasodilBt1
ors :
Nilrates & Nitrites: Amyl nilrite, Nitn11Jycerio, Penta1
erylbrilol
tetranitrate, 'lsosorb1
i.
d1
e dinitrlte, Dipyridamole
, Calcium channel bl1
ockers:
, ,. ·1,
- a
-- ·m1 h ~1
--.-1.1 ·d oo
·ti
.. h d. cbl1 - ·d
.erapam1~ ...epr1 1
Juruua_
on· e, . . azem , .. ro· o·n·1 e.
Nifedipine, Aml.
odip·ine, Felodipine, Nlcardip·
ine, Nimodlp.lne
, Anti-hyperrensi-we Agents:
Timolol, Capto·
prll, Llsinop.rll, Enal,
a·pril,, Bena1'eprl1
hyd.rochloride, 1
01
11iDBpril bydrm:'blaride, Me~yldop,ate
hydmcbloride, Clonldlne hydrochloride, Guanelhldlne
mo,nosolpb,■te, Guanabenz acetate, Sod'lum nitroprusside•
.D,
iazoxid.
e, .Minoxidil, :
Reserpine,]Hydralazioe h.
y1
drochloride
~ 113/201~
Ii

5. ~ Diure1ics:
• Carbonic anhydrase inhibitors: .Acetazolamide, Metbazolam·
ide,
Dichlorphena,mld:
e
• 'Thiazid1
es: Chlo1
.rt'hiazid1
e, Hydrocblerotlriazide,
HydroD11111ethiazide, Cyclotldadd,
e
L di t.. Fu ··11e B et •d
' Etha ., ·
•d
• ot)p ure 1cs: ..1 n1Jem1 , .. ··11m _ an1 e, .. · ·11crymc ac1 _.
• Polass.
ium sparing Diuretic..~: Splronolactone, 'Trlamterene,
AmiJorid.
e
•
1
0sm1
otic Diuretics: Mannito1
l
~nJ/Z019 rr-atcuor Bl.'.! UEtvu

6. 1
Vasodilators
Nitrates & Nitrites:
1
• Organic nlen,RC1
00R' are nten 01
'f 1
0rgj
a11lc ■cld1 RC001
,
H wllh a,aanlc:
111£ol101
l1R1
-o·n
• 0rga'nlc nllr■tes(R11
0NOJ1 &,1
0 1
rpnl1 nllrilt1(R
1
'0N-O) ■N esten 0.1
f nl1
t111u1
add (HNOJ) 1
ar nJlrlc acid (HNOJ) with 1n1organic alcohol R' O,
H where
altacbmenl ,
r6 NO1 ls on,Osy1m I.e.
RO.H
Alcohol
'RO-H ·+·
,
Alcollol
9/B/1019
HO-N=O
N. A "d
llrolll · ,Cl··
0
0
e/
I
MO N
~ . -
~
N1mc act 1
0
Pra:,re1S.Or &1ut1e-t1l
.. RO-N=O +
I ~ ' l1
tnte
Alkyl N~ ,
.
0
1
0
.._
@
/ +·
AO N
~
Alkyl N"tr tc
~.,_ 1 ,a ·o
1

7. Mr
echanism ofAclion:
• Nilric oxide (NO) sliimulates the for.matioo of cGMP~
• Nitmdilaton are 'lhe dru1s~ that mimic the actio1
DS1 1
Df endOGCD.
OUS N1
0 by
r-elcasiog N·
o or forming NO widun li&-sues~
1
• These drugs acl directly on the vscular smooth muscle 101
cause relaxalim an.d
th.
ereforc serve as endothel-i~eJ-indqMmdem vasodilatcn..
•
1
There an: two basic lypcs of oiDucHlalOrs: dtose tbal. n:lcasc NO spontaneously
1
(e~
,g.., sodi.um oilJ7oprusside) r
and organic'nitrates th.al require ,
am enzymatic process
1
·
01
form N01
..
•
1
0i:ganic·nitrates do ·not dimcdy mlea1
SC NO, h,
OYJCYCr, tt.:ir nitrate sroups i.oteracl
with enzyrnes and inttacel'lwlar ,
sulfhydryl grou.ps tlu1.reduce the nitrate groups lo
N011
Dr to S·-llitmscthiol, wbicb then is reduced to NO.
• Nitric 0 1
xide activates smooth muscle soluble ,guan,ylyl cyclase tOC1
) to Jam
cO~
• Increased inncdlular cGMP1
inbilliJ
II cakium entry inl.
o lb£ ,
a:·
11. lhcn:by
decreasing intrace1·
1uls mdcium CODCColndioos and
·. cm1,i!!in-c- . ~•1... . )
__·:. - -- -- __ .... I li ■ uu·ulU muse .
C
relaxation.
~/.B/101.9 PrO'h.~·:uo,r Be u11rn.i.

8. • .NO al,o a~livale.s ·
K• channc~ which h:ads. lu hyperpo]arization and.relaxatiDn.
• Finally.
" N·o aciing 1hmu.gh cGMP can s1hnula1e a cGMP-d-ependmt protein
kina'ie Lbat activates m;
yosin lighl chain pbosphalase·, the 1
cnzym.
e that
dephosp..horylatcs myos·in li,ght mains,. which leads to rreho:ntion~
rllechanism o,f .
Action of Nitr,
ovas.,
odilators
hef l.111 t {)f'I C
_
I.
Ml( fit.
•d ffl p-otcm lu.fl!l:IE

9. CHs
I
H:1C ·
,
Amy.
I Nitrile
•
o
-· o
."- ✓ .
~ ''N'
u
0
0
11
1
- -+
,,.N,
1
Q o-
01 O
'"
- I I
. ' . .
•N
I;'
Ill
0
N"dm&IYmrille
9/B/1019
0 a~~-
Dlpv . . L I
_ . • ~ I .
. I • ~ - Peataery111r1to1 telraallrate,
,..._
_.
.....
Sodium Nlr.apnalde
Qr
~ --o
lsosarlllde1
dlnllnle
10

10. Cal!
cium ch•nnel bla,kers
• Cuneolly approved ,calcimn-dlanoel hlackers (CCBs) bind to L..type
1
caleium f!b,annels located on die lfascu1
ear woatb muscle, cardiac myocytes,
a11d ranliar nodal tluue (llnoalrlal and ■lrlavenlriadar oodes),
.
• Th.
ae, tbanoels ,
are respomd1
ble lor .
Rpllatlng lbe Influx of raltium mlo
muscle cells,1 whicll la 'tum stimulates smooth :
m111tle conlraclion alld
,
canlM myoryte 1
"tllll:n1:·tlon1
• In e_
ardiac nactal tiaae, L-lype ralemm eunoe.11 play an loqt0rtanl 111le
in pacemaller C?urr-entl,anti in rh■w 1
81
oflhe artlon palenlials.
■ Therefom, by blodmlg cal.dam entry into1
the tell,. CCBs cause YBKDlm:
.sm,
eoth musde· rrluation 1
(~81odUa,tmn), dea-eased myocardial Force
generation (neptiwe iaatropy),,decnased heart rate tneptive dlronolrop,
y).
and decreased comlacdon 1111od1J wl1
t'bln Ille. 'heart (aepllte dmmotnJp,
y),
partirularly at 'tbe 1
atrioventrlcular node.,
9/2l/XH9

11. Structural Activity Relationship
1,4-dihydropyridines(l,4-DHP)
Alk,
yl group •• C2 & R
2
C6 lncttases ••e
antagonistic activity
9!11/XJl'J
o/m-sub posscssN
optimum acti,·ity
Sub phen,·I ring at
iacrea1n th~ acth in,
X ho"e,·er Ub "itb small no~
planer alkyl or c,·cloalkyl
aroup decrea.~l~
~the acti, it)
.,,...Rs

12. a..04.
Nil, adipine
0
H,C..;1'0 .
H
Fcludipinc
lsradipine
9/ll/201!>
Structures
~o
1
.mlodipine
Diltian:m
r
NICedipln'.C
u