ACE INHIBITORS

Drugs : captopril, enalapril

Mainly used in CHF and hypertension
Basis of use;
Angiotensinogen( 2 globulin)
Renin from JG cells of kidney
Angiotensin I
ACE inhibitor - ACE
Decreased Angiotensin II

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Decreased preload and afterload

Increasd cardiac output

Relieves CHF

Indications
HTN
CHF
MI
Angina pectoris
Left ventricular hypertrophy
Diabetic nephropathy

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Decreased blood pressure i.e

relieves HTN

 Adverse effects
HTN
Hyperkalemia
Dry cough
Loss of taste sensation
Rashes, fever,urticaria
Angioedema
Foetopathic
Headache,dizziness,nausea
Acute renal failure
Contraindications
Pregnancy
Hyperkalemic patients,patients on potassium sparing diuretics
Bilateral renal artery stenosis
Difference among ACE inhibitors

Chemical name
Activity status
bioavailability
Time to pick action
Elimination t-half
Mode of excretion
Duration of action
Daily dose (mg)

captopril
sulfhydryl
active
70%
1 hr
2 hr
renal
6-12 hr
25-150

enalapril
carboxyl
prodrug
50%
4-6hr
11 hr
renal
24 hr
2.5-40

Linsopril
Carboxyl
Active
25%
6-8hr
12 hr
renal
24 hr
5-40

perindopril
carboxyl
prodrug
20%
6hr
25-30 hr
renal
24 hr
2-8

ramipril
carboxyl
prodrug
60%
3-6 hr
8-48 hr
renal
24 hr
1.25-10

ANGIOTENSIN ANTAGONISTS
Drugs: losartan
Uses: HTN and CHF
Basis of use:
Acts as competitive antagonists of angiotensin II

Blocks all actions of angiotensin II

1. decreased outflow from sympathetic nervous system
2. Increased vasodilatation of vascular smooth muscle
3. Decreased sodium and water retention
4. Decreasd ADH release and promotion of growth of blood vessels
and heart

Decreases B.P. that lasts

Decreased preload and afterload
,relieves HTN.

Increased cardiac output

for 24 hrs

 Differences between ACE inhibitors and angiotensin II antagonists.

ACE Inhibitors
1.interfere with degradation of bradykininincreases
bradykinin level
2.alternative pathway of A-II production and AT-I
receptor activation remain intact with them
3.causes inactivation of AT-1 and AT-2 receptor
4.has more potential to cause cough and dysguesia

Angiotensin II antagonists
1.no such interference
2.causes complete
inhibition of AT-I receptor
3.causes indirect AT-2
receptor activation
4.has very less potential to
cause

BLOCKER
CLASSIFICATION
1)non selective (1 and 2)
a)without intrinsic sympathomimetic action: propranolol , timolol
b)with intrinsic sympathomimetic activity: pindolol
c)with additional blocking property:labetalol
2)cardioselective (1)
Metoprolol, atenolol
3)selective 2
Butonamide
Basis of use of blocker in
1)HTN

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2)Arrythmia
blockers causes diminision of phase 4 depolarisation

1)Decreased automatic firing of SA node

2)prolongation of AV conduction
3) decreased heart rate and contractility

Helps in the treatment of :

a)tachyarrythmia due to sympathetic overactivity
b)atrial flutter
c)digoxin induced dysrhythmia
d)WPW syndrome
3)Angina pectoris
Bloackade of 1 receptor on heart

Decreased heart rate, force of contraction and cardiac output

Decreased cardiac work and oxygen demand

Relieves stable angina by reducing its frequency and severity

NOTE: Propranolol is used in the chronic management of stable angina and not in an
acute attack
Q)Why blockers are contraindicated in variant angina ?
Ans) Variant angina is due to spasm of coronary artery. Use of blockers leads to
unopposed receptor
mediated constriction of coronary artery.This leads to the
aggravation of variant angina.
Indications of blocker:
Angina pectoris
Hypertension
Cardiac arrhythmias
Acute MI
Migraine prophylaxis
Anxiety neurosis
Chronic open angle glaucoma
Chronic open angle glaucoma
Pheochromocytoma

 Thyrotoxicosis
Tetralogy of fallot
Essential tremor
Adverse effects of blockers:
CCF
Bradycardia
Aggravates AV conduction defects
Bronchoconstriction
Hypoglycaemia
Nausea vomiting and constipation
Uterine hypomotility and prolonged labour
Fatigue depression and hallucination
Cold extremities
Nightmares
Impotency
Contraindications of blockers
Bronchial asthma
CCF
Heart block
Cardiogenic shock
Bradycardia
Patients on oral hypoglycaemic agents
NITRATES
Classification:
Short acting: Glyceryl trinitrate (nitroglycerin)
Long acting : Isosorbide dinitrate,Isosorbide mononitrate
Main action:relaxation of vascular smooth muscle
Basis of use in Angina and CHF.
Nitrates administered

Increased nitrates

Increased nitric oxide(NO).

GTP
cGMP.

Inactive protein kinase GActive protein kinase G

Dephosphorylation of myosin light chain kinase

No activation of myosin

No actin myosin interaction

Vascular smooth muscle relaxes

a)great dilation of large veins

coronary artery dilation

Peripheral pooling of blood

blood and Oxygen supply

To heart

b)small dilation of arterioles

Decreased venous return

c)increased

decreased T.P.R

Increased

decreased afterload

Decreased preload

Indications:
Angina pectoris
CHF and acute LVF
MI
Pulmonary HTN
Biliary colic
Esophageal spasm
Cyanide poisoning
Adverse effects:
Fullness of head, throbbing headache
Flushing
Weakness
Sweating
Palpitation
Dizziness
Fainting
Methenoglobenemia
Rashes
Contraindication:
Glaucoma
Hypertrophic cardiomyopathyss
Hypotension
CALCIUM CHANNEL BLOCKERS
Drugs:
Phenylalkylamine: Verapamil
Benzothiazepine:Diltiazem
Dihydropyridine: Nifedipine, Amlodipine
Differences between nifedipine and amlodipine:
1
2
3

AMLODIPINE
Slow oral absorption
Complete absorption
No early adverse effects like flushing

NIFEDIPINE
Fast oral absorption
Incomplete absorption
Early adverse effects seen

4
5

,palpitation seen
Low first pass metabolism
High volume of distribution and t-2

Long duration of action

High first pass metabolism

Low volume of distribution and
t-2
Short duration of action

Basis of use of CCB:

Blockade of L-type Ca2+ channel in heart and vascular smooth muscle

Blockade of inward movement of Ca2+

No triggering of release of Ca2+ from sarcoplasmic reticulum and

mitochondria

No/low availability of Ca2+ in cytosol

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Indications

Angina pectoris
HTN
Hypertrophic cardiomyopathy
Arrhythmias

 Others: premature labour

Adverse effects:
Tachycardia
Ankle edema
Flushing
Hyperplasia of gums
Hyperkalemia
Headache
Constipation
Lethargy
Bradycardia
Contraindications:
Hypotension
Cardiogenic shock
Acute MI
2nd and 3rd degree heart block
Differences among CCBs
Properties
1 Channel blocking power
2 Frequency dependence
of channel blockade
3 Channel recovery rate
4 Cardiac effects
Heart rate
AV conduction velocity
Contractility
Output
5 Vascular smooth
muscle relaxation
6 Uses

Diltiazem
+
+

Verapamil
++
++

Nifedipine
+++
_

delayed

Much delayed

,_

,
_,
+

_,
_,
++

+++

Angina,HTN,
(Arrythmia)

Angina,arrhythmias,
(HTN)

Angina,H
TN

CARDIAC GLYCOSIDES(DIGOXIN)
Drugs: Digoxin, Digitoxin
Use: Mainly used in CHF
Basis of use in CHF:
Binds reversibly with Na+K+ATPase enzyme of cardiac cell membrane

Inhibition of Na+K+ATPase pump

Increased intracellular concentration of Na+

Increased intracellular Na+ leads to increased Ca++ influx via Na+Ca++

exchange pump

Increased contraction of heart

Increased cardiac output of filling pressure that doesnot produce congestive

symptoms

Improved circulation decreases sympathetic tone and hence total peripheral

resistance

Decreased heart rate and oxygen demand

Provides relief in CHF

Indications:
Congestive cardiac failure
Left ventricular failure
Atrial fibrillation &flutter
Premature beat
Supraventricular tachycardia
Contraindication:
Hypokalemia
Renal&hepatic disease
M.I
Thyrotoxicosis
Myxoedema
Ventricular tachycardia
Partial A-Vblock
Acute myocarditis
Wolf-parkinsons white syndrome
Adverse effects:
I)Cardiac effects
Premature beats
Atrial and ventricular tachycardia
Heart block
Sinus bradycardia
II)GI effects
Anorexia
Nausea
Vomiting
III)Neurological
Vertigo
Headache
Visual hallucination
IV)Others:
Skin rashes
Eosinophilia
Gynaecomastia
DIURETICS
High ceiling diuretics/loop diuretics: Furosemide
Medium efficacy diuretics: Thiazides
Basis of use of diuretics:
THIAZIDES
Drug of choice in uncomplicated HTN

FUROSEMIDE
Drug of choice in complicated

Inhibition of Na+Cl- symport in early DCT

plasma and ECF volume

cardiac output

Compensatory mechanism almost restores

C.O.,but slight Na+ and volume deficit persists

Na+ level in vascular smooth muscle

stiffness,compliance,and response to
constrictive effects of NA

TPR

BP

VASODILATORS
Drugs:
I)Arteriolar dilators(afterload)
Hydralazine,minoxidil
CCBs:Nifedipine
K+ channel opener:Nicorandil
II)Venodilators(preload)
Nitrates:Glyceryl trinitrate, glyceryl dinitrate
III)Mixed dilators(preload and afterload)
ACE inhibitors: enalapril
AT-1 antagonist:losartan
-1 blocker:prazosin
Na nitropruside
Basis of use:

HTN with chronic renal failure,CHF

Inhibition of Na+K+2Clcotransport in thick ascending
loop of henle

plasma and ECF

volume

Decreased C.O.

Decreased BP

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CENTRAL SYMPATHOLYTICS
Drugs: clonidine and methyldopa
Use: HTN
Basis of use:
clonidine
Acts on 2a- receptor agonist in
vasomotor centre in medulla

sympathetic activity

Decrease BP

Dopamine in therapy: cardiogenic shock

Methyldopa
Acts on 2a-receptor agonist in vasomotor
centre in medulla

sympathetic outflow

Decreased TPR

Decreased BP

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RESPIRATORY SYSTEM
DRUGS FOR COUGH
Classification:
Pharyngeal demulcents:logenges, cough drops
Expectorants(mucokinetics)
a)Directly acting:citrate of Na+/K+,KI
b)Reflexly acting:ammonium chloride/carbonate,KI
c)Mucolytics:bromhexine
Antitussives (cough suppressants)
a)opiods:codeine,morphine
b)non opiods:Noscapine,dextromethorphan
c)antihistaminics:promethzine,chlorpheniramine
Basis of use of mucolytics in therapy:
Bromhexine

a)by direct action

b)by liberation of lysosomal enzymes

Dissolves the mucopolysaccaride fibers

Liquefaction of tenacious sputum occurs

Liquid sputum is easily removed out of tract

Short note :cough supressant/antitussives
Mention classification from above
Mode of action:
Cough suppressants

1) Acts on CNS to raise threshold of cough centre

2) Acts on respiratory tract to reduce production of cough

impulse

Controles cough of types

1)dry ,unproductive
2)tiring and sleep disturbing
DRUGS FOR BRONCHIAL ASTHMA

I)Bronchodilators
a)sympathomimetics:salbutamol,terbutalin
b)methylxanthines:aminophylline,theophylline
c)anticholinergics:ipratropium bromide
II)leukotriene antagonists:monteleukast,zafirleukast
III)Mast cell stabilisers:sodium cromoglycate
IV)Corticosteroids:
a)systemic:hydrocortisone,prednisolone
b)inhalational:beclomethasone dipropionate
V)Anti IgE-Antibody:omalizumab
a)sympathomimetics
Drugs: salbutamol, terbutalin(selective 2 agonists)
Basis for use in bronchial asthma:

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Note:when inhaled produce bronchodilation within 5 min. And action lasts for 2-4 hrs
only.so it is used for terminating an attack of asthma instead of round the clock
prophylaxis
Adverse effects of salbutamol MARcH PANT

ALYN,1BMOVE3DUTP0G2S:C5HIF

Muscle tremor
Ankle edema
Restlessness
Hypokalemia
Palpitation
Arrhythmia
Nervousness
Tachycardia

b)methylxanthines
drugs:aminophylline,theophylline
Basis of use:

Adverse effects of aminophylline ,theophylline:(g/ml)

c)anticholinergics

drug:ipratropium bromide
basis of use in asthma:

blockage of cholinergic receptor in large airways

Bronchodilation occurs

Provides relieve in asthma

Note:more suitable for regular prophylactic use,not for acute symptomatic relief
Preferred because it has no effect on mucociliary clearance and respiratory
secretions
II)Mast cell stabilisers
Drug: sodium cromoglycate,ketotifen

Basis of use:

p ro v id e s
re lie f in
a s th m a

d e c r e a s e d i n fl a m m a t o r y
re s p o n s e o f b ro n c h ia l m u s c le .

in h ib it d e g r a n u la t io n
o f m a s s c e lls
c a u s e d b y t r ig g e r in g s t im u lu s

Mainly used for prophylactic purpose.

III)corticosteroids
Systemic:hydrocortisone,prednisolone
Inhalational:beclomethasone dipropionate
Basis of use:
NASAL DECONGESTANTS:
These are agonists which when applied as a dilute solution produce local
vasoconstriction
Drugs:naphazoline,xylometazoline,oxymetazoline,phenylephrine,pseudoephedrine
MOA:
Acts as agonist

Produce vasoconstriction and shrinkage of nasal mucosa

Provides relief from nasal obstruction

Adverse effectsSAARC
Stinging sensation
Atrophic rhinitis
Anosmia
CNS depression
Rise in BP
Uses:common cold ,allergic rhinitis

Contraindication:HTN,patients on MAO inhibitors

DRUGS FOR TUBERCULOSIS:

First line drugs
Isoniazid(H)
Rifampin(R)
Pyrazinamide(Z)
Ethambutol(E)
Streptomycin(S)

Second line drug

Thiacetazone
PAS
Ethionamide
Cycloserine
Kanamycin
Amikacin

Newer drugs
Ciprofloxacin
Ofloxacin
Clarithromycin
azithromycin

Basis for use of Isoniazid:

Sensitive bacteria concentrates isoniazid and convert it into
active metabolite by catalase peroxidise enzyme.

Active metabolites binds with INH-A gene and inhibit synthesis of fatty acid synthase
enzyme

Inhibition of mycolic acid synthesis responsible for cell wall formation

Produce bacteriocidal effect both extracellularly and intracellularly

Basis for use of rifampicin:
Inhibits DNA dependent RNA polymerase

Stoppage of expression of bacterial gene

Tuberculocidal effect is exerted

Adverse effects of anti-tubercular drug
ISONIAZID

RIFAMPIN

PYRAZINAMIDE

ETHAMBUTOL

Peripheral
neuritis
Psychosis

Liver damage

Hepatitis

Influenza like
rxn
Orange red
urine
Fever,skin rash

Hyperuricemia,g
out
Arthralgia

Optic nerve
damage
Anaphylactic rxn

Hepatitis
Rashes,fever

photosensitivity

Nausea,vomiting
Confusion,heada
che

STREPTOMYC
IN
Ototoxicity
Nephrotoxici
ty
Anaphylaxis
eosinophilia

DOTS regimen for TB

DOTS strategy:emphasize on the use of all first line anti-tubercular drugs in single daily
dosing
Basis of combination of anti-tubercular drugs:
To prevent the emergence of resistant organisms and relapse of TB
Use of H and R reduces duration from more than 12 months to less than 9
months whereas addition of Z reduces it to 6 months
GASTRO INTESTINAL SYSTEM

DRUGS USED FOR PEPTIC ULCER

I)H2 antihistaminics:cimetidine, ranitidine
II)proton pump inhibitor:omeprazole ,pantoprazole, lansoprazole
Basis for use in peptic ulcer:
At acidic pH of canaliculi of parietal cell it get converted into active
cationic forms

Binds to cysteine residue of H+K+ATPase by stable covalent

bond

Inhibits H+K+ATPase pump irreversibly

Inhibition of secretion of H+ ion into lumen

No gastric acid secretion

Note: both basal and stimulated gastric acid secretion are inhibited
Also inhibit gastric mucosal case enzyme.
III)Basis for use of sucralfate in peptic ulcer
Acquire -ve charge at acidic pH due to seperstion of Al

Binds to protein molecule tranducing from damage to ulcer base

A viscous paste is formed that adheres to the ulcer base

Protects ulcer base from actions of HCl ,pepsin and bile salts
Note: acts by inactivating bile acids and pepsin
Activate mucosal PG synthesis
IV) basis for use of bismuth chelate in peptic ulcer
es PG synthesis leads to ed mucous and bicarbonate secretion

 Forms glycoprotein bi complex with mucous which coats ulcer and prevent
action of HCl
Removes H.pylori from mucosal surface and kills it .so it prevents cause and
relapse of ulcer
Heals 60% ulcer in 4 wks and 90% ulcer in 8 wks.

Drugs
H2
antihistami
nics

Uses
Duodenal ulcer,gastric ulcer, stress
ulcer,gastritis,ZEsyndrome,GERD,Prophylax
is of aspiration pneumonia

PPI

Peptic ulcer,bleeding peptic ulcer,stress

ulcer,GERD,ZE syndrome

sucralfate
Peptic ulcer
ANTIEMETICS

Adverse effects
Dry mouth, headache,
dizziness,bowel
upset,rashes;CNS effects
like confusional state
,convulsion coma
Abdominal pain, muscle
and joint pain,atrophic
gastritis
constipation

5HT-3 ANTAGONISTS( ondansetron)

Basis of use:

Prokinetic drug (metoclopramide,domperidone,cisapride)

----------Bisacodyl in laxative.
net accumulation of water
and elecrolyte in lumen

motili
ty

stimulation of adenyl
cyclase

Note: bisacodyl is an stimulant purgative

inhibition of Na+K+ATPase at basolateral membrane of

villous cells

Dose:5-15 mg :one to two semiformed motionafter 6-8 hrs

Given as suppository it irritates rectal and anal mucosa

Reflex increase in GI motility

Evacuation in 20-40 hrs

LACTULOSE IN THERAPY:
Semisynthetic dissaccaride of fructose and lactose
Neither digested nor absorbed in small intestine ,so retains water
Changes to more osmotically active substance in colon and absorbs water due
to bacterial action
Dose:10mg BD with plenty of water produces soft stool
ammonia level in hepatic encephalopathy patients
ALBENDAZOLE IN THERAPY

B in
d s
w it
h

im m o b i
liz a t io n
a n d
d e a t h
o f
w o r m s

DIFFERERENCES AMONG/BETWEEN:
I)ACE inhibitors and Ang-II antagonists
ACE INHIBITORS
Interfere with the degradation of
bradykinin which leads to ed
bradykinin level
Alternative path of A-II production
and AT-1 receptor activation
remains intact
Causes inactivation of AT-1 and AT-2
receptor
Has more potential to cause cough
and dysguesia

ANG-II ANTAGONIST
Has no any such interference

Causes complete inhibition of AT-1

receptor
Causes indirect AT-2 receptor
activation
Has very less potential to cause
cough and dysguesia

II) Amlodipine and Nifedipine

AMLODIPINE
Slow oral absorption
Complete absorption
No early adverse effects flushing
,palpitation
Low 1st pass metabolism
High volume of distribution and t2
value
long duration of action

NIFEDIPINE
Fast oral absorption
Incomplete absorption
Early adverse effects seen
High 1st pass metabolism
low
short duration of action

III) TETRACYCLINES

Potency
Plasma protein
binding
t2
Alteration of normal
flora
Diarrhoea
Phototoxicity

Tetracycline
Low
Low

Domecycline
Intermediate
High

Doxycycline
High
High

6-10hr
Marked

16-18hr
Moderate

18-24hr
Least

High
Low

Intermediate
Highest

Low
High

IV)Proton punp inhibitors

Inhibition of
H+K+ATPase
pump
Effect on
H.pylori
infection
Oral
bioavailability
and t2
Onset and
duration of
action
Route

Omeprazole
irreversible

Lansoprazole
Partly
reversible

Pantoprazole
Irreversible

Esmoprazole
Irreversible

Less

More

Less

Less

Relatively slow

Fast

Slow

Slow

Oral

Oral

i.v

Oral

V) BLOCKERS

Drug type

Propranolo
l
1+2

Timolol
1+2

Metoprolo
l
1

Atenolo
l
1

Labetal
ol
+

Potency on 1
Partial agonists
Membrane stabilising
action
Lipid solubility
1st pass metabolism
Route of excretion

1
++

6
+-

1
+-

1
-

++
Yes
Hepatic

+
Yes
hepatic

No
renal

+
Yes
Hepatic

Oral bioavailability

30

+
Partial
Hepatic
+renal
50-75

40-50

50-60

20

VI)CEPHALOSPORINS
1st generation
parenteral:
cefazoline,cephalot
hin.
Oral:cephalexin
Gram +ve /gm-ve
cocci except E.coli,
proteus,K.pneumoni
ae
None enters CNS

2nd generation
Parenteral
:cefuroxime,cefoxiti
n.
Oral:cefaclor
Gm-ve coverage
with some
anaerobes

3rd generation
Parenteral
:ceftriaxone
Oral : cefixime

4th generation
Parenteral:cefepime

Gm+ve/gm-ve cocci
with gm-ve rods

Broad spectrum

Only cefuroxime
enters CNS

None

None

VII)Macrolides
Erythromycin
1 Metabolised by liver,excreted
through bile
2 Inhibits cytochrome P450
3 Unsafe in pregnancy
4 Destroyed by gastric acid so
tab. Is coated
5 Food interfere with absorption
VIII)Aminoglycosides
Streptomycin
narrow
spectrum:gm-ve
bacilli and few
gm+ve cocci

ineffective against
pseudomonas and

Clarithromycin
Metabolised by liver, excreted
through bile
inhibits
unsafe
Not effected

Azithromycin
Excreted by
kidney
No inhibition
Safe
Not effected

es absorption

interferes

Gentamycin
broad spectrum

Tobramycin
like
gentamycin
but 2-4
times more
potent
against
pseudomona
s and
proteus

effective against
pseudomonas,and

lownephroto
xicity and

Amikacin
wide
spectrum
due to
resistance
to
bacterial
aminoglyc
oside
inactivatin
g enzyme
Use like
gentamyci

Neomycin
Wide

Not
effective

proteus and
effective against
only only few
strains of
E.coli,klebsiella and
enterobacter
effective against
M.TB.,staphylococc
us
pneumonia,strept.p
yogenes
less potent

proteus and also

against most strains
of
E.coli,klebsiella,ente
robacter

ototoxicity
than
gentamycin

not effective

n but less
potent
against
pseudomo
nas and
proteus
Mainly in
hospital
infection

against
pseudom
onas and
streptoco
ccal
pyogenes
Systemic
toxicity is
high
,used
topically

more potent
high
low
nephrotoxicit
nephrotoxicity
y
IX)FLUROQUINOLONES/QUINOLONES

1st
generation
Ciprofloxac
in
Norfloxacin
Ofloxacin
Pefloxacin

Oral
bioavailability
%

PPB
%

60-80

2035
15
25

35-45
85-95
90-100

2nd
generation
Lomefloxac 90
in
sparfloxaci 90
n
X)Cough suppressant drugs:
Pharyngeal demulcents
Acts peripherally,soothes
the throat and reduce
afferent impulse from
pharyngeal mucosa

Route

Indications

Oral/i
.v
Oral
Oral/i
v
20-30 Oral/i
.v

UTI,gonorrhoea,chanchoroid,MDRTB

10

Oral

40

oral

Like ciprofloxacin but increases activity

of gm ve bacteria
Pneumonia,exacerbation of acute
bronchitis,sinusitis

Opoids
1)acts on CNS
to raise
threshold of
cough centre
2)has abuse
liability
3)more
constipating
effect.
4)action
blocked by

UTI,GI Infection
Alternate drug for NSV,cervicitis
Meningitis,UTI,GI INFECTION

Non opoids
1)acts on CNS
to raise
threshold of
cough centre
2)no abuse
3)no
constipating
effect
4)no such
blockade
occurs

Antihistaminics
Suppresses cough
by sedative and
anticholinergic
action

naloxone.
SHORT NOTE
1)bioavailability
measure of fraction of administered dose of drug that reaches systemic
circulation in unchanged form
bioavailability of different routes:
i.v.=100%
s.c/i.m =less than 100% due to local PPB
oral=much less due to first pass metabolism
factors affecting bioavailability are:
a)route of administration
b)physical properties of drugs
c)chemical properties of drugs
d)individual variation
e)first pass metabolism
2)first pass metabolism
refers to the metabolism of drug during its passage from site of absorption into
the systemic circulation
all orally administered drugs are expsosed to metabolising enzymes in liver and
intestine.
Occurs even in skin and lungs
Different for different drugs and it determines oral bioavailability
Degree of first pass metabolism ;
a)low:phenobarbitone
b)intermediate:aspirin
c)high:propranolol
3)metabolism of drugs(biotransformation)
Chemical alteration of drug in the body
Lipid soluble drug is converted into lipid insoluble drug which is not reabsorbed
and is excreted
Sites:mainly liver,also in kidney ,intestine,lung
It leads to
a)inactivation of drugs;morphine
b)activation of inactive drug:levodopa is converted into dopamine
c)active metabolite production from active drug:digitoxin is converted to digoxin
Classification of metabolism
Nonsynthetic/phase I/
Functionalization rxn
1.oxidation
2.reduction
3.hydrolysis
4.cyclization
5.decyclization

Synthetic/conjugation/
Phase II reactions
1.glucuronide conjugation
2.acetylation
3.methylation
4.sulfate conjugation
5.glycine conjugation
6.glutathione conjugation

4)phase II metabolism/synthetic rxn

Involves conjugation of drug or phase I metabolite with endogeneous substance to
form highly ionised organic acid so that it is excreted in urine or bile
It requires very high energy

 Involves following reactions

a)glucuronide conjugation:conjugated by glucoronic acid
eg:aspirin ,morphine
b)glutathione conjugation
eg:paracetamol
c)glycine conjugation:conjugated by glycine
eg:salicylates
d)methylation:conjugated by methionine
eg:adrenaline
e)acetylation:conjugated by acetyl coA
f)ribonucleoside synthesis:for purine and pyrimidine antimetabolite used in cancer
therapy
g)sulphate conjugation: conjugated by sulfokinase
eg:sex steroids
5)criterias for essential drug selections
Adequate data regarding efficacy and safety of drug should be available through
clinical studies
In case of two or more similar drug choice should be based on their relative
efficacy,safety, quality,price and availability
Choice should be based on pharmacokinetic properties
Should be single compound
6)disadvantages of antimicrobial combination therapy
It prevents proper diagonis of infection and choice of AMA
Increased incidence of side effects as toxicity of one agent can be enhanced by
another
Increased chances of superinfection
Inadequate dose of drug may lead to emergence of resistance
Increases cost of therapy
7)low dose aspirin
ii

a
r
a
c
h
i
d
o
n
i
c

en
n

dp
ol

ha
et

ie

l
a

ll

ce
et

ls

a
c
i
d

l
s

Balance between the above two helps in the maintainance of circulation

When low dose aspirin is used

Inhibition of cycloxygenase enzyme occurs in platelets by acetylation to

great extent as compared to endothelial cells

Failure of platelet to resynthesize cox enzyme results in decreased TXA2

and ed PGI2 level

No platelet sticking and thrombus formation occurs

Helps in prevantion of attack of MI

8)drugs used to decrease platelet aggregation
NSAIDs:aspirin
Dipyridamole
Clopidogrel
Ticlopidine
Abciximab
9)uses of vitamin K preparations
Adult vitamin K deficiency(malabsorption,obstruction,jaundice)
Vitamin K deficiency in infant following acute diarrhoea
Neonatal vitamin K deficiency
Bleeding state during oral coagulant therapy
10)oral rehydration solution
Used for mild (5-7%BW) or moderate (7.5-10%BW) type of dehydration
Composition of ORS(WHO)
NaCl
KCl
Trisodium citrate
Glucose
Water

OLD
3.5g
1.5g
2.9g
20g
1litre
310mosm/i

NEW
2.6g
1.5g
2.9g
13.5g
1litre
245mosm/l

The old ORS formulation was mainly effective for cholera diarrhoea,but when
used in non cholera diarrhoea it causes periorbital edema due to excess Na+
reabsorption
So in new ORS formulation the concentration of sodium and glucose is reduced
but it has the disadvantage of causing hyponatremia if used in cholera diarrhoea
in adults
Rational of components used
a)Na and water facilitates each others absorption in GIT
b)KCl :to compensate acute diarrhoeal K+ loss
c)bicarbonate,citrate, lactate:to correct acidosis
Uses:
a)diarrhoea
b)non diarrhoeal reasons: heat stroke,post burn/post surgical maintainance of
hydration and nutrition.