Drug Name Scientific name Brand Name Indications Drug Mechanism NMDA - receptor ADR's - Adverse Drug Reaction
Drug Mechanism NMDA - receptor
Aspirin is a nonsteroidal anti-inflammatory drug (NSAIDs). Aspirin
contains salicylate, a compound found in plants such as the willow tree and
myrtle. It was the first of this class of drug to be discovered. These agents
reduce the signs and symptoms of inflammation and exhibit a broad range of
pharmacologic activities, including analgesic, antipyretic, and
Ecosprin, Sprin, antiplatelet properties. Aspirin and the other NSAIDs do not generally
2-Acetoxybenzoic
Aspirin Aspro, Eprin and change the course of the disease process in those conditions where they are
acid
Delisprin used for symptomatic relief.
Aspirin has many uses including - Relieving pain and swelling - Aspirin can
relieve mild to moderate pain, swelling, or both associated with many health
issues, such as: headaches, a cold or flu, sprains and strains, menstrual
cramps, long-term conditions, such as arthritis and migraine
Reducing the risk of cardiovascular events in people with a high risk.
Paracetamol has a central analgesic effect that is mediated through
Paracetamol is a mild analgesic and antipyretic, and is recommended for the
Tylenol, Excedrin, activation of descending serotonergic pathways. Debate exists about
treatment of most painful and febrile conditions, for example, headache
Paracetmol Acetaminophen Calpol, and its primary site of action, which may be inhibition of prostaglandin
including migraine, toothache, neuralgia, colds and influenza, sore throat,
Panadol. (PG) synthesis or through an active metabolite influencing
backache, rheumatic pain and dysmenorrhoea.
cannabinoid receptors.
Anelgesic-antipyretic with poor antiinflamnatory action. It is a derivative of
Amidopyrine and belongs to the category of non-steroidal antiinflammatory
Dipyrone, analgin,
drugs. It is used in the treatment of pain caused by a toothache, headache,
Novalgin Metamizole algocalmine,
arthralgia (joint pain), neuralgia (nerve pain), myalgia (muscle pain), colicky
melubrin
pain, and severe pain after surgeries, traumas (injuries), etc. It is also used as
a fever reducer.
Ibuprofen is a commonly used nonsteroidal antiinflammatory (NSAID) drug
which is available both by prescription and over-the-counter. Ibuprofen
reduces pain, fever, swelling, and inflammation by blocking the
production of cyclooxygenase (COX)-1 and COX-2. The body releases these
substances in response to illness and injury. ibuprofen is used to relieve
(RS)-2-(4-(2-
responses of the body to an infection/disease but is not used to cure the
methylpropyl) Advil, Brufen,
Ibuprofen disease itslef.
phenyl)propanoic Motrin and Nurofen
Non prescription doses: to relieve minor pain and inflammation, including
acid
headache, muscular aches, toothache, fever, backache, and
dysmenorrhea.
prescription doses: used for the long-term treatment of rheumatoid
arthritis, osteoarthritis, ankylosing spondylitis, and other chronic
conditions.
antibiotics having beta-lactam ring. most potent pencillin for Gram (+)
Bicillin C-R,
organisms. uses- otitis media, meningitis, sore throat, pneumonia &
Bicillin LA,
respiratory infections, septicemia, peritonitis, gonorrhea UTIs. known issues-
Crystapen, Pen Vee
resistance(beta-lactamase and other mechanisms), allergic rxns, cross
Pencillin - G Benzylpenicillin K pencillin inhibits the cell wall of bacteria by blocking transpeptidase
hypersensitivity(1-3% w/ cephalosporins). therapeutic uses- Streptococcus
penicillin G
pneumoniae infections, S. Pyogenes infections, Viridans strep endocarditis
aqueous, Permapen,
(also given prophylactically), anaerobes except Bacteroides fragilis group,
Pfizerpen,Veetids
Meningococcal infections, Syphilis and other diseases caused by spirochetes.
Antibiotic which is used against gram positive bacterias. Acute infections,
Penicillin beta- Zydus Cadila, Meningitis(infection in meninges), Urinary tract infections, Gonnorrhoea,
Ampicillin
lactam Principen Typhoid fever, Subacuta Bacterial endocarditis (infection in the vavlves of
heart), Cholecystitis (inflammation of the gallbladder)
Amoxicillin is used to treat a wide variety of bacterial infections. This
medication is a penicillin-type antibiotic. It works by stopping the growth of
bacteria.This antibiotic treats only bacterial infections. It will not work for
Amoxil, Moxatag,
Amoxicillin Amoxicillin viral infections (such as common cold, flu). Using any antibiotic when it is
and Trimox.
not needed can cause it to not work for future infections.Amoxicillin is also
used with other medications to treat stomach/intestinal ulcers caused by the
bacteria H. pylori and to prevent the ulcers from returning.
Chloramphenicol
It has a role as a H1-receptor antagonist, an anti-allergic agent, a sedative
and a carcinogenic agent. They act in the bronchi, capillaries, and some other
methapyrilene smooth muscles, and are used to prevent or allay motion sickness, seasonal
Paradormalene,
thenylpyramine rhinitis. It has relatively strong sedative effects, to the extent that its primary
Methapyrilene Pyrathyn,
Paradormalene use was as a medication for insomnia rather than for its antihistamine action.
Pyrinistab
Lullamin For symptomatic traetement of seasonal and perennial allergic rhinitis,
allergic conjuctivitis dur to inhalant allegrgens and foods, mild
uncompllicated allergic skin manifestaion of Urticaria and angioedema.
Chlorpheniramine Antihistamine used to treat the symptoms of allergic conditions such as
Chlorpheniaramine Cadistin Exp
maleate. allergic rhinitis. It is taken by mouth.
Acyclovir is used to treat infections caused by certain types of viruses. It
treats cold sores around the mouth (caused by herpes simplex), shingles
(caused by herpes zoster), and chickenpox.This medication is also used to
treat outbreaks of genital herpes. In people with frequent outbreaks,
acyclovir is used to help reduce the number of future episodes.Acyclovir is
an antiviral drug. However, it is not a cure for these infections. The viruses
Acyclovir Aciclovir (ACV) Zovirax that cause these infections continue to live in the body even between
outbreaks. Acyclovir decreases the severity and length of these outbreaks. It
helps the sores heal faster, keeps new sores from forming, and decreases
pain/itching. This medication may also help reduce how long pain remains
after the sores heal. In addition, in people with a weakened immune system,
acyclovir can decrease the risk of the virus spreading to other parts of the
body and causing serious infections
For the chemoprophylaxis, prophylaxis, and treatment of signs and
symptoms of infection caused by various strains of influenza A virus. Also
Symmetrel, for the treatment of parkinsonism and drug-induced extrapyramidal
Amantadine
Osmolex reactions.
Chloramphenicol is a semisynthetic, broad-spectrum antibiotic derived from
Streptomyces venequelae with primarily bacteriostatic activity.
Chloramphenicol diffuses through the bacterial cell wall and reversibly binds
to the bacterial 50S ribosomal subunit. Chloramphenicol is a medication
used in the management and treatment of superficial eye infections such as
bacterial conjunctivitis, and otitis externa. It has also been used for the
treatment of typhoid and cholera. Chloramphenicol is an antibiotic and is in
chloromycetin, the class of antimicrobials that inhibits protein synthesis. Indications for its
Chloramphenicol
chloramphenicol IV use include superficial eye infections (bacterial conjunctivitis), and otitis
externa. It is also reserved for severe infections, such as rickettsial diseases,
meningitis caused by Haemophilus Influenza, Neisseria meningitidis, or
Streptococcus pneumoniae, or in typhoid fever caused by Salmonella
enterica serotype Typhi. It can also be used for the treatment of cholera.
Chloramphenicol ointments are also used perioperatively as prophylaxis for
surgical wound infections. This therapy is often necessary for plastic surgery
and eye surgery
ADR's - Adverse Drug Reaction PK - Pharmacokinetics
It blocks prostaglandin synthesis. It is non-selective for COX-1 and
COX-2 enzymes 9,10,11. Inhibition of COX-1 results in the inhibition
of platelet aggregation for about 7-10 days (average platelet lifespan).
The acetyl group of acetylsalicylic acid binds with a serine residue of
the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible
inhibition. This prevents the production of pain-causing
prostaglandins. This process also stops the conversion of arachidonic
acid to thromboxane A2 (TXA2), which is a potent inducer of platelet
aggregation Label. Platelet aggregation can result in clots and harmful
aspirin is an allosteric inhibitor of the B2 receptor, a property
venous and arterial thromboembolism, leading to conditions such as
that may be involved in its therapeutic actions.
pulmonary embolism and stroke.
The active site of COX-2 is, however, slightly larger than the active
site of COX-1, so that arachidonic acid (which later becomes
prostaglandins) manages to bypass the aspirin molecule inactivating
COX-2 11,12. Hence it exerts more action on the COX-1 receptor
rather than on the COX-2 receptor 14.
Metamizole is a pro-drug, which spontaneously breaks down after
oral administration to structurally related pyrazolone compounds.
Apart from its analgesic effect, the medication is an antipyretic and
spasmolytic agent. The mechanism responsible for the analgesic
effect is a complex one, and most probably rests on the inhibition of a
central cyclooxygenase-3 and activation of the opioidergic system and
cannabinoid system. The mechanism responsible for the spasmolytic
effect of metamizole is associated with the inhibited release of
intracellular Ca2+ as a result of the reduced synthesis of inositol
phosphate.
Ibuprofen exerts its anti-inflammatory and analgesic effects through
inhibition of both COX isoforms. The main mechanism of action of
ibuprofen is the non-selective, reversible inhibition of the
cyclooxygenase enzymes COX-1 and COX-2. COX-1 and COX-2
catalyze the first committed step in the synthesis of prostanoids –
prostaglandin (PG) E2, PGD2, PGF2α, PGI2 (also known as
prostacyclin), and thromboxane (Tx) A2 – from arachidonic acid.
penicillin covalently binds to PBP4 receptors within various
pencillins are bactericidal antibiotics as they kill the microorganisms
microbes, including S. aureus and E. coli, which leads to
when used at therapeutic dose. the synthesis of cell wall of bacteria is
weakened cell walls and, ultimately, autolysis.Penicillin and
completely depended upon an enzyme named as transpeptidase.
other antibiotics in the beta-lactam family contain a
characteristic four-membered beta-lactam ring. Penicillin kills
after binding to pencillin-binding protein(PBP) and prevents its
bacteria through binding of the beta-lactam ring to DD-
synthesis. result- bacteria cells die from cell lysis. pencillins do not
transpeptidase, inhibiting its cross-linking activity and
kill other cells in the body.
preventing new cell wall formation.
Ampicillin binds to specific penicillin-binding proteins (PBPs) (like
transpeptidases, carboxypeptidases, and endopeptidases) located
inside the bacterial cell wall, Ampicillin 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 Ampicillin interferes with an autolysin inhibitor.
Amoxicillin is similar to penicillin in its bactericidal action against
susceptible bacteria during the stage of active multiplication. It acts
through the inhibition of cell wall biosynthesis that leads to the death
of the bacteria.
A central nervous system depressant used to induce drowsiness or
sleep or to reduce psychological excitement or anxiety. H 1 -receptor
antagonists are the drugs that selectively bind to but do not activate
histamine H 1 receptors, thereby blocking the actions of endogenous
histamine.
Chloropheniaramine works by blocking histamine synthesis in our
binds to the histamine H1 receptor. This blocks the action of symptoms include rash, watery eyes,
body during allergic reactions. It also blocks another substance in out
endogenous histamine, which subsequently leads to temporary itchy eyes/nose/throat/skin, cough, runny nose,
body called acetylcholine which helps dry up bodily fluids to relieve
symptoks such as watery eyes and runny nose.
Acyclovir is becomes acyclovir monophosphate due to the action of
viral thymidine kinase.5 Acyclovir monophosphate is converted to the
diphosphate form by guanylate kinase.1 Acyclovir diphosphate is
converted to acyclovir triphosphate by nucleoside diphosphate kinase,
pyruvate kinase, creatine kinase, phosphoglycerate kinase, succinyl-
CoA synthetase, phosphoenolpyruvate carboxykinase and
adenylosuccinate synthetase.1,7 Acyclovir triphosphate has higher
affinity for viral DNA polymerase than cellular DNA polymerase and
incorporates into the DNA where the missing 2' and 3' carbons causes
DNA chain termination.5 In other cases acyclovir triphosphate
competes so strongly for viral DNA polymerase that other bases
cannot associate with the enzyme, inactivating it.
The mechanism of its antiparkinsonic effect is not fully understood,
but it appears to be releasing dopamine from the nerve endings of the
brain cells, together with stimulation of norepinephrine response. It
also has NMDA receptor antagonistic effects. The antiviral
mechanism seems to be unrelated. The drug interferes with a viral
protein, M2 (an ion channel), which is needed for the viral particle to
become "uncoated" once it is taken inside the cell by endocytosis.
. It is a broad-spectrum antibiotic be used against Gram-positive,
Gram-negative, and anaerobic bacteria.[9][10] Chloramphenicol
works by inhibiting protein synthesis by binding to the 50S ribosomal
subunit and directly preventing the formation of bacterial protein. On
a molecular level, chloramphenicol inhibits the attachment of transfer
RNA to the A site on the 50S ribosome. It specifically binds to A2451
and A2452 residues[36] in the 23S rRNA of the 50S ribosomal
subunit, preventing peptide bond formation
Dosage
p-Aminophenol is conjugated with arachidonic acid by fatty
acid amide hydrolase to form AM404. AM404 exerts effect
through cannabinoid receptors. It may also work through
PGHS, particularly in areas of the brain with high
concentrations of fatty acid amide hydrolase.
It is primarily a kappa-opiate receptor agonist and also has
local anesthetic effects. It has more affinity for the kappa-
receptor than morphine. Opiate receptors are coupled with G-
protein receptors and function as both positive and negative
regulators of synaptic transmission via G-proteins that activate
effector proteins. Binding of the opiate stimulates the
exchange of GTP for GDP on the G-protein complex. As the
effector system is adenylate cyclase and cAMP located at the
inner surface of the plasma membrane, opioids decrease
intracellular cAMP by inhibiting adenylate cyclase.
Subsequently, the release of nociceptive neurotransmitters
such as substance P, GABA, dopamine, acetylcholine and
noradrenaline is inhibited. Opioids also inhibit the release of
vasopressin, somatostatin, insulin and glucagon. It's analgesic
activity is, most likely, due to its conversion to morphine. This
results in hyperpolarization and reduced neuronal excitability
Ibuprofen may activate the antinociceptive axis(ie is the
action or process of blocking the detection of a painful or
injurious stimulus by sensory neurons) through binding to the
cannabinoid receptors(Cannabinoid receptors have been
implicated in diverse physiological and pathophysiological
roles in the body, including regulation of mood, appetite, pain-
sensation, vascular and nonvascular smooth muscle tone, and
immune function) and through inhibition of fatty acid amide
hydrolase (FAAH), which metabolizes the endocannabinoid
anandamide.
Ampicillin binds to and inactivates penicillin-binding proteins multiforme)
(PBP) located on the inner membrane of the bacterial cell
wall.
Amoxicillin competitively inhibits penicillin-binding protein 1
and other high molecular weight penicillin binding proteins.
Penicillin bind proteins are responsible for glycosyltransferase distress, Abdominal or stomach cramps or tenderness,
and transpeptidase reactions that lead to cross-linking of D-
alanine and D-aspartic acid in bacterial cell walls. Without the blistering, peeling, or loosening of the skin; bloating;
action of penicillin binding proteins, bacteria upregulate
autolytic enzymes and are unable to build and repair the cell
wall, leading to bacteriocidal action.
Not much information is available regarding the receptor.
relief of the negative symptoms brought on by histamine. and sneezing.
amantadine binding inhibits current flow through NMDA
receptor channels but show that its main inhibitory action at
pharmaceutically relevant concentrations results from
stabilization of closed states of the channel.
T 1/2
signs of an allergic reaction to aspirin: hives; difficult
breathing; swelling of your face, lips, tongue, or
throat.
Ringing in your ears, confusion, hallucinations, rapid
breathing, seizure (convulsions);
severe nausea, vomiting, or stomach pain;
bloody or tarry stools, coughing up blood or vomit
that looks like coffee grounds;
fever lasting longer than 3 days; or
swelling, or pain lasting longer than 10 days.
low fever with nausea, stomach pain, and loss of
appetite; dark urine, clay-colored stools; or. jaundice
(yellowing of the skin or eyes).
Some common side effects of novalgin are increased
heart rate, insomnia, restlessness, and irritation, etc.
Blood: Reduced white blood cell counts
(agranulocytosis), reduced red blood cell counts due These effects occur even before acetylsalicylic acid is detectable in the
to reduced production of the cells (aplastic anemia).
May trigger acute porphyria. Severe skin reactions
like toxic epidermal necrolysis. Kidney damage, Low absorption.
blood pressure, Allergic reaction which may include a
rash, low blood pressure, and breathing difficulty
The short plasma half-life, a wide therapeutic
window, and the lack of prolonged retention in
specific body compartments make ibuprofen a
relatively safe drug. Like other NSAIDs, ibuprofen
can cause serious gastrointestinal and possibly
cardiovascular adverse events, especially at high
doses. Most observational studies with ibuprofen have administration and is not subject to significant first-pass metabolism.
reported no increased risk for cardiovascular events, Ibuprofen is almost completely metabolized, with little to no unchanged
such as myocardial infarction and sudden cardiac
death. Although serious skin diseases, such as the
Stevens-Johnson syndrome and toxic epidermal
necrolysis, have been reported in patients with
ibuprofen use, these are exceedingly rare, at a rate of
less than 1 per 1 million users per week for most
NSAIDs.
common-Diarrhea, Nausea, Vomiting, Sore or
irritation in the mouth, Change of color of the tongue,
Irritation at injection site, heandache. adverse- severe
allergic shock(might lead to death), rash, hives,
itching, red swollen blistered or peeling skin, fever,
wheezing, tightness in the chest or throat, breathing
problems, trouble swallowing, hoarse voice, swelling
in mouth, face,lips, tongue ot throat.
acute inflammatory skin eruption (erythema
Although it may take 10 days for the total platelet population to be
renewed, and thus restore normal COX activity, it has been shown that if
redness and peeling of the skin (exfoliative dermatitis)
as little as 20% of platelets have normal COX activity, hemostasis may
rash, hives, fever, seizure, black hairy tongue,
be normal.
diarrhea.
diarrhea, rash, vomiting, and nausea, gastrointestinal
back, leg, or stomach pains; black, tarry stools;
blood in the urine; bloody nose; chest pain.
The most frequent reactions with short-term use of
oral acyclovir are nausea and vomiting and with 6
months' use headache, diarrhea, nausea, and vomiting.
These symptoms are also seen frequently with
placebos. The most frequent adverse reaction to
intravenous use has been inflammation and phlebitis
at the injection site. The two most important serious
adverse effects are (1) encephalopathic changes with
abnormal electroencephalograms and lethargy,
tremors, confusion, and seizures and (2) renal
precipitation of the drug because of a rapid bolus of
drug administered parenterally
Over doses produce excutement, convulsions,
Hyperpyrexia, cerebral edema, depression and
ocassionally renal tubular necrosis. Death has also
been resported from overdosing. Cases of central
anticholingeric toxicity: Hallucinations, delirium and
confusion. Methapyrilene has ... been shown to
enhance liver tumor development when administered
either before or after a genotoxic liver carcinogen.
Side Effects
Nausea, diarrhea, headache, or vomiting may occur. If Biopharmaceutical Classification System (BCS), aciclovir falls under the
any of these effects persist or worsen, tell your doctor BCS Class III drug i.e. soluble with low intestinal permeability.[47]
or pharmacist promptly.
Blurred vision, nausea, loss of appetite, drowsiness,
dizziness, lightheadedness, headache, dry mouth,
constipation, or trouble sleeping may occur. If any of
these effects last or get worse, tell your doctor or
pharmacist promptly. Dizziness and lightheadedness
can increase the risk of falling.
chloramphenicol has reportedly caused fatal aplastic
anemia, with possible increased risk when taken
together with cimetidine.Besides causing fatal aplastic
anemia and bone marrow suppression, other side
effects of chloramphenicol include ototoxicity with
the use of topical ear drops, gastrointestinal reactions
such as oesophagitis with oral use, neurotoxicity, and
severe metabolic acidosis.Optic neuritis is the most
commonly associated neurotoxic complication that
can arise from chloramphenicol use. takes more than 3
weeks to manifest presenting with either acute or
subacute vision loss, with possible fundal changes. It
may also present with peripheral neuropathy, which
may present as numbness or tingling. If optic
neuropathy occurs, the drug should be withdrawn
immediately, which will usually lead to partial or
complete recovery of vision
Route of Administartion Metabolism Elimination
Aspirin is rapidly absorbed in the upper gastrointestinal (GI) tract and It is available in different doses, the
results in a measurable inhibition of platelet function within 60 minutes. lowest being 81 mg, also called a
This antiplatelet effect is associated with prolongation of the bleeding baby aspirin. Incase of pain and
time and inhibition of TXA2-dependent platelet aggregation. fever -
These effects occur even before acetylsalicylic acid is detectable in the Adults: 325-650 mg orally/rectally
peripheral blood, owing to the exposure of platelets to aspirin in the
portal circulation.34 Enteric coating of aspirin significantly delays its Children under 12 years:
absorption. 10-15 mg/kg orally once every 4
The plasma half-life of aspirin is only 20 minutes; however, because hours, up to 60-80 mg/kg/day
platelets cannot generate new COX, the effects of aspirin last for the
duration of the life of the platelet (≈10 days). Children 12 years and older:
After a single dose of aspirin, platelet COX activity recovers by ≈10% 325-650 mg orally/rectally once
per day as a function of platelet turnover. every 4-6 hours as needed
Although it may take 10 days for the total platelet population to be
renewed, and thus restore normal COX activity, it has been shown that if Controlled/extended/delayed-release
as little as 20% of platelets have normal COX activity, hemostasis may products (enteric-coated): 650-1300
be normal. mg orally once every 8 hours; not to
exceed 3.9 g/day
- dose for adults is one or two
This antiplatelet effect is associated with prolongation of the bleeding 500mg tablets up to 4 times in 24
time and inhibition of TXA2-dependent platelet aggregation. hours. least 4 hours between each
doses.
The oral adult dose for metamizole
is 500 mg 3-4 times. The injection is 14 minutes (parent
peripheral blood, owing to the exposure of platelets to aspirin in the
administered in a dose of 250-500
portal circulation.34 Enteric coating of aspirin significantly delays its
mg three times into a muscle or a
vein
Ibuprofen is rapidly
Ibuprofen is rapidly and completely absorbed following oral Over-the-counter doses (800–1200
absorbed, reaching peak
mg/day); Prescription doses of
serum levels one to two
Ibuprofen (adult: 200–800 mg every
hours after administration,
drug found in the urine. The primary route of elimination is oxidative 6–8 h; pediatric: 5–10 mg/kg every
and has a half-life of 1.8 to
metabolism by CYP enzymes to inactive metabolites. 6–8 h).
two hours.
Adults and teenagers—200,000 to
500,000 Units (125 to 312
milligrams [mg]) every four to six
Rapidly absorbed following both intramuscular and subcutaneous hours.
half life-
injection. Initial blood levels following parenteral administration are high Infants and children less than 12
In adults with normal renal
but transient. Oral absorption in fasting, healthy humans is only about 15- years of age—Dose is based on
function is reportedly 0.4–
30% as it is very susceptible to acid-catalyzed hydrolysis. volume of body weight. The usual dose is 4167 0.9 hours
distribution- 0.53–0.67 L/kg in adults with normal renal function to 30,000 Units per kilogram (kg) of
body weight every four to eight
hours.
Orally: 250-500 mg every 6 hours,
approximately 60-90
Intravenously/intramuscularly: 1-2 g
minutes.
every 4-6 hours
Amoxicillin is stable in the presence of gastric acid and is rapidly
absorbed after oral administration. Orally administered doses of 250-mg
and 500-mg amoxicillin capsules result in average peak blood levels 1 to
Typical dosage is 500 mg every 12
2 hours after administration in the range of 3.5 mcg/mL to 5.0 mcg/mL
hours, or 250 mg every 8 hours.
and 5.5 mcg/mL to 7.5 mcg/mL, respectively. Orally administered doses
Child dosage (ages 3 months–17
of amoxicillin suspension, 125 mg/5 mL and 250 mg/5 mL, result in
years).
average peak blood levels 1 to 2 hours after administration in the range of
1.5 mcg/mL to 3.0 mcg/mL and 3.5 mcg/mL to 5.0 mcg/mL,
respectively.
A death has been reported from an
Drugs that selectively bind to but do not activate histamine H1 receptors,
oral dose as small as 12 mg/kg, but
thereby blocking the actions of endogenous histamine. Included here are Not been confirmed and not
others have survived after 80 mg/kg.
the classical antihistaminics that antagonize or prevent the action of much information available.
Hence not much information about
histamine mainly in immediate hypersensitivity.
dosge have been confirmed.
Orally - 4mg, 8mg, 12mg. Syrup -
Chlorpheniramine has a serum half-life of approximately 20 hours in 2mcg/5mL. Tablets or syrup: 4 mg
adults, and elimination from the body is primarily by metabolism to orally every 4-6 hours; not to exceed
20 hours in adults
monodesmethyl and didesmethyl compounds. The half-life is increased in 24 mg/day
the presence of renal dysfunction and decreased in children.
injectable solution
50mg/mL
Aciclovir is poorly water-soluble and has poor oral bioavailability (15–
injection, lyophilized powder for
30%), hence intravenous administration is necessary if high
reconstitution
concentrations are required. When orally administered, peak plasma
500mg/vial
concentration occurs after 1–2 hours. According to the
1000mg/vial
oral suspension
200mg/5mL
Aciclovir has a high distribution rate; protein binding is reported to range
tablet
from 9 to 33%.[48] The elimination half-life (t1/2) of aciclovir depends
400mg
according to age group; neonates have a t1/2 of 4 hours, children 1–12
800mg
years have a t1/2 of 2–3 hours whereas adults have a t1/2 of 3 hours
capsule
200mg
The adult daily dosage of
Amantadine is well absorbed orally. The onset of action is usually within
SYMMETREL (amantadine
48 hours when used for parkinsonian syndromes, including dyskinesia.
hydrochloride) is 200 mg; two 100
As plasma concentrations of amantadine increase, there is a greater risk
mg tablets (or four teaspoonfuls of The half-life was 17 ± 4
for toxicity. Half-life elimination averages eight days in patients with
syrup) as a single daily dose. The
end-stage kidney disease. Amantadine is only minimally removed by
children's total daily dose is 200 mg hours).
hemodialysis. Amantadine is metabolized to a small extent (5-15%) by
given as one tablet of 100 mg (or
acetylation. It is mainly excreted (90%) unchanged in urine by kidney
two teaspoonfuls of syrup) twice a
excretion.
day.
Chloramphenicol is extremely lipid-soluble; it remains relatively
unbound to protein and is a small molecule. It has a large apparent
50 mg/kg/day intravenously divided
volume of distribution and penetrates effectively into all tissues of the
every 6 hours; in exceptional cases,
body, including the brain. Distribution is not uniform, with highest
patients with moderately resistant
concentrations found in the liver and kidney, with lowest in the brain and
organisms or severe infections may
cerebrospinal fluid.[26] The concentration achieved in brain and
require increased dosage up to 100
cerebrospinal fluid is around 30 to 50% of the overall average body
mg/kg/day; decrease these high
concentration, even when the meninges are not inflamed; this increases to
doses as soon as possible
as high as 89% when the meninges are inflamed. it also increases
absorption of iron.
The half-life is 13 - 19
minutes. Blood
concentrations drop rapidly
after complete absorption.
The half-life of the salicylate
ranges between 3.5 and 4.5
hours
Concentration of the drug in route of administration can lead
plasma reaches a peak in 30- to different levels of
60 minutes and the plasma effectiveness because of the
half-life is 1-4 hours.
compound; parenteral);
metabolites: 2–4 hours
one hour
Oral Capsule, Topical Lotion
Oral acyclovir has an
average plasma half-life of
three hours and is eliminated
primarily by renal
mechanisms. Peak plasma
concentrations occur 1.5 to intravenous.
2.5 hours after
administration and the oral
bioavailability is 15 to 30
percent.
hours (range: 10 to 25
Half-life in adults with
normal hepatic and renal
function is 1.5 - 3.5 hours.
In patients with impaired
renal function half-life is 3 -
4 hours. In patients with
severely impaired hepatic
function half-life is 4.6 -
11.6 hours. Half-life in
children 1 month to 16 years
old is 3 - 6.5 hours, while
half-life in infants 1 to 2
days old is 24 hours or
longer and is highly
variable, especially in low
birth-weight infant
Aspirin can be administered via
the oral, rectal, and intravenous
(IV) route.
paracetamol can be given as a
rectal, oral, or intravenous. the
differences in absorption and
the time to reach peak plasma
levels.
The tablet should be
administered orally with food. and cases of potential metamizole-associated
The intravenous dose should be hepatotoxicity have been described. Howvever not much Urine (96%, IV; 85%, oral), faeces (4%, IV).
administered through a slow
infusion into a vein
Ibuprofen is most commonly
administered orally, but can
also be administered in an
intravenous formulation. Other
formulations, most notably
topical and rectal, can be
prepared.
taken in oral form or through I.
V urine of patients on penicillin G. A small percentage of
orally as capsules or pills,
intravenous as injections
capsule, a tablet, a chewable
tablet, and as a suspension
(liquid) to take by mouth.
Orally - the tablet, capsule, or
liquid form by mouth with or
without food.The injection may elimination from the body is primarily by metabolism to
be given by the subcutaneous,
intramuscular or intravenous
route
administration may be oral or
For oral dosage forms (capsules,
syrup, and tablets).
Chloramphenicol can be
administered topically as eye or
ear drops, or as an eye ointment.
It can also be given parenterally
as intravenous injection or
infusion or taken as oral
capsules
Acetylsalicylic acid is hydrolyzed in the plasma to Excretion of salicylates occurs mainly through the
salicylic acid. Plasma concentrations of aspirin following kidney, by the processes of glomerular filtration
after administration of the extended-release form are and tubular excretion, in the form of free salicylic
mostly undetectable 4-8 hours after ingestion of a single acid, salicyluric acid, and, additionally, phenolic
dose. Salicylic acid was measured at 24 hours following and acyl glucuronides .
a single dose of extended-release acetylsalicylic acid 21.
Salicylate can be found in the urine soon after
Salicylate is mainly metabolized in the liver, although administration, however, the entire dose takes
other tissues may also be involved in this process. The about 48 hours to be completely eliminated. The
major metabolites of acetylsalicylic acid are salicylic rate of salicylate is often variable, ranging from
acid, salicyluric acid, the ether or phenolic glucuronide 10% to 85% in the urine, and heavily depends on
and the ester or acyl glucuronide. A small portion is urinary pH. Acidic urine generally aids in
converted to gentisic acid and other hydroxybenzoic reabsorption of salicylate by the renal tubules,
acids. while alkaline urine increases excretion
Paracetamol is metabolized primarily in the liver by
enzymes of phase I and II. Phase I reaction for It is metabolised in the liver and excreted in the
paracetamol may occur by oxidation, reduction, and urine mainly as the glucuronide and sulphate
hydrolysis: It results in polar metabolites of the original conjugates. Less than 5% is excreted as unchanged
chemicals and leads either to activation or inactivation of paracetamol.
the drug.
Metamizole undergoes extensive metabolism in the liver
information is provided due to being banned in some
countries.
Ibuprofen is rapidly metabolized and biotransformed in
the liver to the formation of major metabolites which are
the hydroxylated and carboxylated derivatives. Ibuprofen
metabolism can be divided into phase I which is
represented by the hydroxylation of the isobutyl chains Ibuprofen is rapidly metabolized and eliminated in
for the formation of 2 or 3-hydroxy derivatives followed the urine thus, this accounts for more than 90% of
by oxidation to 2-carboxy-ibuprofen and p-carboxy-2- the administered dose. It is completely eliminated
propionate. These oxidative reactions are performed by 24 hours after the last dose and almost all the
the activity of the cytochrome P450 isoforms CYP 2C9, administered dose goes through metabolism,
CYP 2C19, and CYP 2C8. Therefore, these enzymes representing about 99% of the eliminated dose.
participate in the oxidation of the alkyl side chain to The biliary excretion of unchanged drug and
hydroxyl and carboxyl derivatives. From these enzymes, active phase II metabolites represents 1% of the
the major catalyst in the formation of oxidative administered dose.
metabolites is the isoform CYP 2C9.23. The metabolic
phase I is followed by a phase II in which the oxidative
metabolites may be conjugated to glucuronide prior to
excretion. This activity forms phenolic and acyl
glucuronides.
About 16-30% of an intramuscular dose is metabolized to
penicilloic acid, an inactive metabolite. Small amounts of
6-aminopenicillanic acid have been recovered in the
the drug appears to be hydroxylated into one or more
active metabolites, which are also excreted via urine.
Some ampicillin is metabolized by hydrolyzing the beta-
lactam ring to penicilloic acid, though most of it is In summary, ibuprofen is excreted as metabolites
excreted unchanged. In the kidneys, it is filtered out or their conjugates. The elimination of ibuprofen
mostly by tubular secretion; some also undergoes is not impaired by old age or the presence of renal
glomerular filtration, and the rest is excreted in the feces impairment
and bile.
It is metabolized by the live. Clavulanic acid appears to
be metabolized extensively, with metabolites eliminated
via the urine, bile, feces and lungs. Variation in Approximately 60% of an orally administered
bioavailability may be related to differences in first-pass dose of amoxicillin is excreted in the urine within
effects through those organs.
6 to 8 hours. Detectable serum levels are observed
Approximately 50–70% of the administered amoxicillin up to 8 hours after an orally administered dose of
and 25–40% of clavulanic acid are recovered intact from amoxicillin.
the urine. Most renal excretion occurs in the first 6 h and
is unaffected by probenecid, although probenecid
prolongs the renal excretion of amoxicillin. In renal
failure, the volume of distribution and systemic
availability are unaffected after oral or intravenous
administration, but clearance is progressively depressed
with renal function.
Approximately 40% and 35% of the administered
The metabolism of methapyrilene (I), was examined in
dose was excreted in the urine in the first 24 hr in
vivo by g.l.c. and g.l.c.-mass spectrometric analysis of rat
the low and high dose groups, respectively, as
urinary extracts. After 4 weeks of treatment with I, rats
determined by liquid scintillation
also excrete detectable amounts of the 3- and (6-
spectrophotometry. Fecal excretion accounted for
hydroxylpyridyl)-methapyrilene metabolites suggesting
38% and 44% of the administered dose in the first
that pretreatment with I alters the metabolism of the
24 hr in the low and high dose groups,
pyridine ring. Metabolic removal of the 2-
respectively, as confirmed via combustion
thienylmethylene moiety is also facile, as large amounts
analysis. The terminal plasma elimination t1/2 of
of N'-(2-pyridyl)-N,N-dimethylethylenediamine and its
methapyrilene did not increase with increasing
metabolite N'-[2(5-hydroxylpyridyl)]-N,N-
doses (2.75 hr, 0.7 mg/kg; 2.81 hr, 3.5 mg/kg);
dimethylethylenediamine are excreted under all dosing
thus, methapyrilene does not exhibit dose-
regimens.
dependent elimination over this 5-fold dose range.
Chlorpheniramine was extensively metabolized
and excreted in the urine. The greatest portion of
monodesmethyl and didesmethyl compounds the drug was excreted as an unidentified polar
metabolite.
Acyclovir is <15% oxidized to 9-
carboxymethoxymethylguanine by alcohol
dehydrogenase and aldehyde dehydrogenase and 1% 8-
hydroxylated to 8-hydroxy-acyclovir by aldehyde
oxidase.4 The majority of acyclovir is excreted in the urine
Acyclovir is becomes acyclovir monophosphate due to as unchanged drug.4,14 90-92% of the drug can be
the action of viral thymidine kinase.5 Acyclovir excreted unchanged through glomerular filtration
monophosphate is converted to the diphosphate form by and tubular secretion.5 <2% of the drug is
guanylate kinase.1 Acyclovir diphosphate is converted to recovered in feces and <0.1% is expired as CO2
acyclovir triphosphate by nucleoside diphosphate kinase,
pyruvate kinase, creatine kinase, phosphoglycerate
kinase, succinyl-CoA synthetase, phosphoenolpyruvate
carboxykinase and adenylosuccinate synthetase
Amantadine is metabolized to a small extent (5-15%) by
acetylation. It is mainly excreted (90%) unchanged in
It is primarily excreted unchanged in the urine by
urine by kidney excretion.[28]
glomerular filtration and tubular secretion.
Chloramphenicol is eliminated primarily by
biotransformation. In humans, as much as 90% is
eliminated as the chloramphenicol glucuronide
conjugate. The majority of the remaining 10% is
eliminated in the kidney by glomerular filtration.
This is sufficient to produce therapeutic
concentrations in the urine. Conditions associated
with decreased liver function may slow
Chloramphenicol is metabolized by the liver to
elimination and must be taken into account during
chloramphenicol glucuronate (which is inactive
therapy. Approximately 80% of the conjugated
chloramphenicol is eliminated in the urine by
active tubular secretion. Both hepatic
biotransformation to form the conjugate and active
transport in the kidney are poorly developed in
neonates. As a result, chloramphenicol and its
metabolites may accumulate to toxic
concentrations if adult dose regimens are used.
Gray baby syndrome is the shock-like condition
produced by this accumulation.