drug list Flashcards
what’s the first antisense drug to be approved by FDA?
vitravene
what’s used in the treatment of CMV retinitis?
vitravene
what is only effective in about 20% of patients that overexposes HER2 receptor?
Herceptin
Herceptin aka
trastuzamab
what is a metastatic breast cancer treatment ?
Herceptin
what drug may lead to cardio toxicity and ADRs?
Herceptin
following patient testing what’s one of the first drugs to be prescribed for patients with breast cancer?
Herceptin
what are the two MOA of Herceptin?
1 prevent HER2 receptor from releasing growth signals
2 it will tell your immune cells to target cells with HER@ receptor
what happens in the absence of Herceptin?
HER2 cancer cells release excess growth signals for proliferation
what drug is metabolized by isoenzyme CYP2D6?
debrisoquine
what kind of drug is debrisoquine?
antihypertensive
what alter metabolism of debrisoquine?
SNPs in the isoenzyme
what drugs follow zero order kinetics?
ethanol and aspirin
ethanol is excreted in …
sweat
what’s penicillin?
an acidic antibiotic
how are penicillin and aspirin excreted?
via proximal tubular secretion (renal excretion)
what is used in the excretion of penicillin and aspirin?
anion transport system
what may prolong effects of penicillin?
competition for secretion with probenecid
what is aspirin?
acidic salicylate
what is given to prevent gout?
aspirin is given to compete with uric acid during distal tubular active reabsorption
what drugs are alkylating agents ?
cyclophosphamide and thio-TEPA
cyclophosphamide and thio-TEPA MOA
creates highly reactive carbonium ion which alkylates guanine at N-7 position
what prodrug is acts on S/G2 phase and G2/M phase?
cyclophosphamide
what activates cyclophosphamide?
CYTP450
what drug is used for treatment of chronic lymphatic leukemia?
cyclophosphamide
what drug is used for treatment of breast and ovarian cancer?
cyclophosphamide
what drug is used in the management of rheumatic disorders and autoimmune nephritis?
cyclophosphamide
what are the adverse effects associated with cyclophosphamide and thio-TEPA ?
myelosuppression
nausea and vomitting
teratogenesis
gonadal atrophy
what drugs carry risk of leukomegenesis and resistance?
cyclophosphamide and thio-TEPA
what drug is aka as ethyleneammonium?
thio-TEPA
how is thio-TEPA activated?
its converted into its active metabolite try ethylene phosphor amide by liver MFO
what’s used in the treatment of bladder cancer?
thio-TEPA
what are antimetabolites used to treat cancer?
methotrexate (MTX) and 5-fluorouracil (5-FU)
what drug is a folic acid antagonist?
methotrexate (MTX)
what does methotrexate (MTX) do?
irreversibly inhibits DHFR which is needed for thymidine and purine synthesis
what drug is a prymidine antagonist?
5-fluorouracil (5-FU)
what drug is a thymine analogue that has a fluorine group instead of a methyl group?
5-fluorouracil (5-FU)
what does 5-fluorouracil (5-FU) do?
its active metabolite 5-dUMP inhibits DNA synthesis and 5-dUTP when incorporated into RNA prevents its function
what’s used in treatment of solid tumors?
5-fluorouracil (5-FU)
what’s used in treatment of breast tumors?
5-fluorouracil (5-FU)
what’s used in collateral tumors and gastric tumors?
5-fluorouracil (5-FU)
what’s used in the treatment of squamous cell tumors of the head and neck?
5-fluorouracil (5-FU)
what are adverse effects of methotrexate (MTX) and 5-fluorouracil (5-FU)?
myelosuppresion severe leukopenia bone marrow aplasia hepatotoxicity thrombocytopenia gi disturbances crystal urea
what drugs are G1/S and S/G2 specific?
methotrexate (MTX) and 5-fluorouracil (5-FU)
what drugs intercalate btwn bps –> topoismoerase ii inhibited and free radicals fare formed –> inhibition of. dna synthesis and cause strand incision?
Doxorubicin and Actinomycin D
what drug is an anthracycline?
Doxorubicin
how does Doxorubicin work?
It gets reduced by CYTP450 reductase into a reduced metabolite and a superoxide ion hydrogen peroxide, which breaks the strands in DNA
what drugs may lead to severe cardiac toxicity and serious pulmonary and mucocutaneous reactions because of their free radical formation?
Doxorubicin and Actinomycin D
what are the adverse effects of Doxorubicin and Actinomycin D?
Cardiac toxicity
Severe pulmonary and mucocutaneous reactions
Bone marrow depression
Severe and prolonged Myelosuppression
Total alopecia
It is a cell cycle specific
drug: G1/S and G2/M
Actinomycin D
It’s used to treat
gestational and pediatric
tumors (Ewing Sarcoma
and Wilms Tumor)
Actinomycin D
It intercalates DNA and
inhibits DNA and mRNA
synthesis.
Actinomycin D
what drug causes excess hypotension in poor metabolizers ?
Debrisoquine
what drug is an antidepressant?
paroxetine
what affects response of paroxetine?
Its response is affected by
SNPs in the Serotonin 2A
receptor.
whats the purpose of paroxetine?
It is a serotonin reuptake
inhibitor.
what was found in patients taking paroxetine?
They found that depressed patients with the C/C genotype for the serotonin 2A receptor were more likely to discontinue the use of Paroxetine then the T/C and T/T genotype.
name an endogenous adrenergic
agonist
nora
what are the Direct-acting adrenergic
agonist?
Nora phenylephrine clonidine isoprenaline dobutamine salbutamol
what receptors does NA act on?
alpha 1 and alpha 2
NA is a catecholamine what does that mean?
can’t be ingested orally bc it will be digested by MAO and COMT before it reaches systemic circulation ( short DOA)
cannot pass the BBB so minimal effect on CNS
what blocks release of NA from presynaptic neuron?
guanthedine
what direct acting adrenergic agonists are sympathomimetic?
phenylephrine
clonidine
dobutamine
salbutamol
true or false phenylephrine can be given orally.
true
what drug is a selective alpha 1 adrenergic agonist?
phenylephrine
what drug causes vasoconstriction?
phenylephrine
what drug is used as a nasal decongestant?
phenylephrine
why is phenylephrine used as a nasal decongestant?
acts on alpha 1 receptors on bvs of nasal mucosa to relieve congestion by inducing vasoconstriction
what is a selective alpha 2 adrenergic agonist ?
clonidine
what is used to treat hypertension by inhibiting sympathetic outflow leading to decreased blood pressure?
clonidine
what inhibits NA release ?
clonidine
what drugs are catecholamines ?
NA
isoprenaline
what drug is a nonselective beta agonist?
isoprenaline
what is the effect when isoprenaline acts on B1 receptors?
increase renin release and contractility and rate of heart
what is the effect when isoprenaline acts on B2 receptors?
bronchodilation and peripheral vasodilation
what drug is a selective b1 adrenergic agonist?
dobutamine
what drug increases cardiac output and contractility of heart?
dobutamine
whats useful in Tx of CHF by increasing cardiac output?
dobutamine
how does dobutamine indirectly increase heart rate?
increase release of renin from kidneys promoting release of angiotensin II which brings up heart rate
what drug is a selective B2 adrenergic agonist?
salbutamol
whats used in the treatment of asthma for its bronchodilator effect?
salbutamol
whats used in the treatment of premature labor because it relaxes the smooth muscles of the uterus?
salbutamol
what drug is a nonselective alpha adrenergic blocker?
phentolamine
whats used to treat hypertensive crisis cause by phaeochromocytoma?
phentolamine
phentolamine …… until tumor ( phaeochromocytoma) is removed.
release of catecholamines
whats a selective alpha 1 adrenergic antagonist ?
prazosin
whats used in treatment of primary hypertension?
prazosin
what is used to treat benign symptoms of prostatic hyperplasia?
prazosin
how does prazosin treat benign symptoms of prostatic hyperplasia?
prevents contraction of urinary smooth muscles and bladder neck allowing urine to pass easily and reducing lower UT symptoms
what drug is a nonselective beta antagonists?
propranolol
It is a selective B1
adrenergic agonist
Dobutamine
It increases the cardiac
output and contractility of
the heart.
Dobutamine
• It is useful in the
treatment of CHF by
increasing the CO.
Dobutamine
It also can increase the release of renin from the kidneys promoting the release of angiotensin II which brings up the heart rate.
Dobutamine
It is a selective B2
adrenergic agonist
Salbutamol
Used in the treatment of Asthma for its bronchodilator effect and in the treatment of premature labor (relaxes the smooth muscles of the uterus).
Salbutamol
Non -selective alpha - adrenergic blocker (Acts on both alpha 1 and alpha 2)
Phentolamine
It is used to treat hypertensive crises caused by phaeochromocytoma (which is a tumor of the adrenal glands that secretes excess catecholamines)
Phentolamine
__________ prevents
the release of
catecholamines until the
tumor is removed.
Phentolamine
Selective alpha 1
adrenergic antagonist
Prazosin
It is useful in the
treatment of primary
hypertension.
Prazosin
It is used to treat symptoms of benign prostatic hyperplasia. It prevents contractions of the urinary smooth muscles and bladder neck allowing the urine to pass easily and reducing lower UT symptoms.
Prazosin
Non -selective beta - adrenergic antagonist (blocks beta 1 and beta 2).
Propranolol
• It blocks the effects of
catecholamines on the
heart and blood vessels.
Propranolol
Is used to treat angina pectoris - chest pain caused by lack of O2 to the heart (because of increased blood flow). \_\_\_\_\_\_\_\_\_ decreases the CO and BP allowing time for the blood to pass through the heart.
Propranolol
Considered as a first line treatment for hypertension and can be used in combination with other blood pressure lowering drugs to maximize the affect.
Propranolol
It is also proven to have a protective affect in patients who have had a MI (prevents them from getting it a second time so its protective on the heart)
Propranolol
It is also used in the treatment of hyperthyroidism (which can cause tachycardia and anxiety)
Propranolol
It can also decrease the bp
by decreasing the CO and
renin release.
Propranolol
AE: Since it is non
-selective
it may cause
bronchospasm in patients
who have asthma.
Propranolol
AE: It may also lead to
cardiac depression and
signs of HF.
Propranolol
It is used in the treatment of hypertension and may be used in combo with other blood pressure lowering drugs.
Atenolol
used in the
treatment of angina
pectoris.
Atenolol
It is used to treat MI
protective effect
Atenolol
used to treat
hyperthyroidism
Atenolol
AE : cardiac depression and HF
Atenolol
• It also decreases bp by
decreasing the CO and
renin release.
Atenolol
It blocks the effect of
catecholamines on the
heart and blood vessels.
Atenolol
Indirect acting adrenergic agonists
cocaine tricyclic antidepressants amphetamine tyramine MAO inhibitors
direct acting adrenergic agonists
dopamine
epinephrine
isoproterenol
mixed action adrenergic agonists
ephedrine
It inhibits neuronal uptake
uptake 1
cocaine
tricyclic antidepressant
It increases the amount of NA in synaptic gap and thus promotes increased activation of adrenergic receptors (both
cocaine
tricyclic antidepressant
tricyclic antidepressant
Imiprimane
It blocks the release of NA
into synaptic space.
Guanethidine
Noradrenergic neuron
blocking drug
Guanethidine
Drugs that act on
noradrenergic nerve
terminals
Reserpine
It blocks the transport of
NA into synaptic vesicles,
thus depleting the stores.
Reserpine
It is not used clinically.
Reserpine
It does not bind to a receptor instead it displaces NA from the vesicles to cause NA release.
Amphetamine
MOA: it enters the nerve terminal via uptake 1 and enters the synaptic vesicle in exchange for NA. This causes NA to accumulate presynaptically and some of it will be broken down by MAO, while the rest of it will be released into the synaptic cleft to act on adrenergic receptors.
Amphetamine
It acts in a similar way to
amphetamine (ya3ny it
displaces NA from its
vesicle)
Tyramine
It can cause severe
hypertension in patients
who take MAO inhibitors.
Tyramine
It is naturally broken down
by MAO (you can see why
MAO inhibitors are a
problem)
Tyramine
A protein found in cheese
products
Tyramine
It is involved in the cheese
reaction.
Tyramine
Mixed acting adrenergic agonist (ya3ny it can increase the amount of NA released or it can bind to the receptors and activate them directly)
Ephedrine
Non-catecholamine
Ephedrine
It is the major
neurotransmitter of the
PSNS
Acetylcholine
It is an endogenous and direct acting
cholinergic agonist
Acetylcholine
It is involved in the PSNS and
acts on nicotinic or
muscarinic receptors.
Acetylcholine
Typically acts on skeletal
muscles in the somatic
efferent pathway
Acetylcholine
It is the major neurotransmitter in all presynaptic neurons of the PNS and is only active in the PSNS post-synaptically.
Acetylcholine
Heart: decreases CO
and rate of the heart
Blood vessels:
vasodilation and
decreased blood
pressure
Acetylcholine
GI: stimulates
salivary and
intestinal secretion
and gastric motility
Acetylcholine
Lungs: it induces
bronchiolar
secretion and
bronchoconstriction.
Acetylcholine
Genitourinary tract: it increases the detrusor urinae muscle tone for expulsion of urine.
Acetylcholine
Eye: muscle
contraction for near
vision and pupil
constriction (miosis)
Acetylcholine
It is broken down by
acetylcholinesterase
Acetylcholine
It activates all cholinergic
receptors (muscarinic and
nicotinic receptors)
Acetylcholine
It is not used therapeutically because of its multiplicity of action and its rapid degradation by acetylcholinesterase.
Acetylcholine
It is a type of choline ester
(direct
-acting cholinergic
agonist)
Acetylcholine
It is only clinically used for its
miotic effects in cataract
surgery.
Acetylcholine
It is contraindicated in: People with coronary
insufficiency because it causes hypotension
and people with Hyperthyroidism
(atrial arrythmias)
Acetylcholine
It is contraindicated in: People with Asthma or Peptic ulcers
Acetylcholine
It is an alkaloid found in
Atropa Belladona
Atropine
It blocks all types of muscarinic receptors (It does not affect nicotinic receptors)
Atropine
At low doses it has no effect
on the CNS
Atropine
At high doses it causes excitation effects on the CNS (hallucinations, disorientation, and restlessness)
Atropine
It is a cholinergic
antagonist –> binds competitively and
reversibly
Atropine
Eye: mydriasis (persistent) Antispasmodic: relaxes GIT and bladder
Atropine
Antisecretory: it prevents secretion from upper and lower respiratory tract prior to surgery
Atropine
surgery
o Used to treat
anticholinesterase
Atropine
Adverse effects: Dry mouth Blurred vision Tachycardia Constipation Confusion (CNS)
Atropine
in surgery its used as a pre anesthetic to prevent salivary and bronchiolar secretions
Atropine
Ophthalmology: It is used to induce mydriasis, to dilate the pupil, and paralyze the eye lens for examination (long -lasting effects)
Atropine
Antidote: treatment
of
anticholinesterase
poisoning
Atropine
Treatment of GIT
cramps
Atropine
Treatment of
Parkinson’s disease
and tardive
dyskinesia
Atropine
Treatment of sinus
bradycardia after an
MI
Atropine
Its use is contraindicated in
children because it increases
their body temperature.
Atropine
It can be used in conjunction
with pralidoxime to treat
organophosphate poisoning.
Atropine
It is used in the treatment of
Parkinsonism and tardive
dyskinesia
Benztropine
It is a cholinergic
antagonist that only acts on muscarinic
receptors
Benztropine
It blocks the release of
acetylcholine from the
presynaptic cholinergic
neurons.
Botulinum Toxin
A bacterial toxin
Botulinum Toxin
It is an indirect
-acting cholinergic agonist and anticholinesterase
Echothiophate
It is an organophosphate
Echothiophate
It is irreversible and long
-acting
Echothiophate
Typically used in the
preparation of war gases and
pesticides
Echothiophate
It may be used to treat
glaucoma (but not as a first
choice).
Echothiophate
what causes these side effects? Respiratory depression (very dangerous) Agitation Confusion Vomiting, colic, and diarrhea
Echothiophate
what causes these side effects? Constricted pupils that are unresponsive to light Sweating and salivation Bronchoconstriction
Echothiophate
what causes this side effects? CNS: It may cause demyelination, which causes sensory loss and respiratory paralysis.
Echothiophate
When used in combo with a
NMB it may lead to
prolonged and excessive
muscular (skeletal) paralysis
Gentamicin
It prevents the release of
acetylcholine
Gentamicin
It may be used in combo with
vecuronium= blocks nicotinic
receptors
Gentamicin
its an Aminoglycoside
Gentamicin
Blocks the choline uptake (rate limiting step) (prevents the entry of choline to the presynaptic membrane via choline carrier) → inhibits acetylcholine synthesis → Blocks cholinergic transmission.
Hemicholinum
Blocker of Cholinergic
transmission
Hemicholinum
Cholinergic antagonist acts on muscarinic
receptors
Ipratropium
It is a quaternary nitrogen
compound
Ipratropium
Used to treat chronic
bronchitis and asthma; it
relaxes smooth muscles.
Ipratropium
It binds competitively and
reversibly
It is inhaled
Ipratropium
It inhibits plasma cholinesterases from metabolizing another NMB= Suxamethonium (prolonging its duration of action)
Neostigmine
Reversible and long
-acting
anticholinesterase
Neostigmine
It is used to reverse
competitive NMB
Neostigmine
Used in the treatment of
paralytic ileus and bladder
atony
Neostigmine
It is also used in the
treatment of myasthenia
gravis
Neostigmine
It leads to the AE mentioned earlier for anticholinesterases (all except confusion, agitation, and respiratory depression)
Neostigmine
Used to treat glaucoma
because it’s only
administered on the eyes
Physostigmine
Used as an antidote for
atropine poisoning
Physostigmine
Used in the treatment of
Alzheimer’s disease
Physostigmine
It may cause agitation, confusion and respiratory depression (along with the other side effects on anticholinesterases)
Physostigmine
It is a naturally occurring
alkaloid
Pilocarpine
It has a longer DOA than
acetylcholine
It specifically acts on
muscarinic receptors
Pilocarpine
used to treat glaucoma
Pilocarpine
contraindicated in the following : - Coronary insufficiency (hypotension) Hyperthyroidism (atrial arrythmias) Peptic ulcer Asthma
Pilocarpine
At therapeutic dose it is a
depressant in the CNS: it
leads to sedation, drowsiness
and amnesia
Scopolamine
It is also an antiemetic • It has a longer DOA than
acetylcholine
Scopolamine
It also has a greater overall
effect on the CNS than
acetylcholine
Scopolamine
AKA: Hyoscine It’s another type of plant product It is a muscarinic antagonist
Scopolamine
It is used in the treatment of motion sickness
Scopolamine
It is uses as a
adjunct with
anesthesia
Scopolamine
It also blocks short term memory (useful so that the patient can’t remember the surgery)
Scopolamine
AE: very similar to Atropine
dry mouth blurred vusuin constipation tachycardia confusion
Scopolamine
in Surgery: it is used as a pre-anesthetic to prevent salivary and bronchiolar secretions
Scopolamine
It is also used in the
treatment of GIT
cramps.
Scopolamine
Blocks the storage of
acetylcholine
Vesamicol
Blocker of cholinergic
transmission
Vesamicol
It has a longer DOA than acetylcholine It is selective to muscarinic receptors It is used to treat paralytic ileus and urinary retention
Bethanechol
Direct-acting cholinergic agonist
It is a choline ester
(synthetic ester of
choline)
Bethanechol
It increases the release of
acetylcholine from
presynaptic cholinergic
neurons
Latrotoxin
It is also found in spider
venom
• Typically known as Black
Widow Toxin
Latrotoxin
It is used in the treatment of
organophosphate poisoning
Pralidoxime
May be used in conjugation
with Atropine
• It reactivates cholinesterases
Pralidoxime
• Oxime compound
Pralidoxime
Reactivates enzymes
inactivated by
phosphorylation.
Pralidoxime
It is a competitive NMB
It is non-depolarizing
Suxamethonium Rocuronium Mivacurium Tubocurarine Vecuronium
It competes with acetylcholine to bind to nicotinic receptors • It is clinically important • It is an active drug
Mivacurium
It is useful in patients
suffering from kidney
disease because it cannot
be excreted by the kidneys
Mivacurium
It is rapidly hydrolyzed by
plasma cholinesterase
(short acting)
Mivacurium
Only causes mild or transient histamine release and hypotension No effect on muscarinic receptors
Mivacurium
It is of clinically important use • It has an intermediate duration of action (30-40 minutes).
Rocuronium
It has no ganglionic block
or histamine release
• It does not act on
muscarinic receptors
Rocuronium
No tachycardia
• Its onset is rapid (1 -2 minutes)
Rocuronium
It is used in electroconvulsive therapy to reduce trauma • It is also used in rapid endotracheal intubation.
Suxamethonium
It is used in electroconvulsive therapy to reduce trauma • It is also used in rapid endotracheal intubation.
Suxamethonium
It is the only depolarizing
NMB used clinically.
Its onset of action is rapid
(1 minute).
Suxamethonium
MOA: It behaves like acetylcholine; it binds to the nicotinic receptor and induces contraction. However, it is not susceptible to acetylcholinesterases. This means that it persists for a longer period of time on the receptor leading to sustained muscular contraction and depolarization that leads to inactivation of the receptor and relaxation of the muscle. It actually produces transient twitching (fasciculation) before causing the block.
Suxamethonium
It is short acting in its nature (5 minutes) as it is digested rapidly by plasma cholinesterases. However, at the NMJ it must be redistributed to the plasma (no plasma cholinesterases at the NMJ)
Suxamethonium
Its use is contraindicated in people with a deficiency or defective plasma cholinesterases because its duration of action is prolonged (prolonged neuromuscular paralysis)
Suxamethonium
AE associated with o Depression of respiration o Post -operative pain o Hyperkalemia which can cause cardiac arrythmias o Malignant hyperthermia o Prolonged muscle paralysis and apnea (in plasma cholinesterase deficient patients= paralyzes diaphragm)
Suxamethonium
side effects = Bradycardia (muscarinic agonist effect) o Increased intraocular pressure (nicotinic agonist effect on extraocular muscles)
Suxamethonium
Its effect can be enhanced by neostigmine blocking the plasma cholinesterases as it is a an anticholinesterase
Suxamethonium
Non -competitive NMB
• It is depolarizing in its
nature
• AKA: succinylcholine
Suxamethonium
Competitive NMB • Non-depolarizing • Alkaloid
Tubocurarine
It is a prototype • It is not clinically used
because of its lack of
selectivity and multiple
side effects
Tubocurarine
It leads to histamine release, which causes bronchoconstriction and and hypotension • It also leads to ganglionic block
Tubocurarine
It is only important
because it was one of the
first NMB to ever be
introduced to medicine
Tubocurarine
It is clinically important
It has an intermediate duration of action (30-40 minutes)
It has a rapid onset ( 1-2 minutes)
Vecuronium
It does not promote
histamine release
It does not cause ganglionic block (so it doesn’t act on muscarinic receptors= no tachycardia)
Vecuronium
It may lead to prolonged
muscle paralysis when
administered with
gentamicin.
Vecuronium
It is used against gram -ve bacteria. It is bactericidal against streptococci but bacteriostatic against enterococci.
Penicillins
Some bacteria produce B-
lactamase and are
resistant to it
Penicillins
Closely related to penicillin
• Some bacteria that
produce B-lactamase are
also resistant
Cephalosporins
If a patient has an allergy
towards penicillin= he
should not take it
Cephalosporins
It may cause kidney
damage.
Cephalosporins
They inhibit folic acid
synthesis
They cause kernicterus in
neonates
Sulfonamides
During pregnancy, they
lead to neonatal jaundice
and hemolytic anemia
Sulfonamides
They prevent bacterial
DNA synthesis (since they
need folic acid for
synthesis)
Sulfonamides
It interferes with cell
division (selective toxicity
to bacteria and not
humans)
Sulfonamides
It is prototypic of
Sulfonamides
• It is active against gram \+ve and -ve bacteria • It helped overcome an outbreak of meningitis • It also inhibits folic acid synthesis in bacteria
Sulfanilamide
Prototypic of an aminoglycoside • It was especially designed against the penicillin resistant gram-ve bacteria
Streptomycin
It inhibits the 30s
ribosomal subunit in
bacterial species= inhibits
protein synthesis
Streptomycin
Since its an aminoglycoside, it requires an oxygen dependent transport mechanism= anaerobes are inherently resistant to it
Streptomycin
Some bacteria, becomes resistant to it because their DNA is altered= Ribosome altered. • It may lead to kidney damage in the fetus and hearing problems.
Streptomycin
Their uptake may be reduced by bacterial mechanisms which promote the outflux of antibiotics. • They are used as a bacteriostatic agent in pneumococcal infections
Tetracyclines
In pregnancy and
breastfeeding= weak bone
and teeth formation
Tetracyclines
Isolated from streptomyces organism • It is active against gram \+ve and -ve bacteria, ricketssia, and some protozoa
Chlortetracycline
It is active against gram -ve and gram +ve bacteria • It was found to cause aplastic anemia, so it is not widely used anymore (unless person is resistant to other drugs)
Chloramphenicol
It inhibits the 50s ribosomal subunit of bacteria (inhibiting protein synthesis) • It may cause gray baby syndrome • It is metabolized by the liver (may lead to toxicity in those patients who have liver damage)
Chloramphenicol
Metabolized by liver
enzymes and may lead to
toxicity if liver function is
impaired
Erythromycin
Clarithromycin
Rifampin
Leads to kidney damage and hearing problems when taken in pregnancy and breast feeding • Anaerobes are resistant to it because it requires an oxygen dependent transport mechanism
Aminoglycosides
Vinka Alkaloids (Taxens= have the
same MOA= prevent polymerization) MOA: They are tubulin -binding agents - arrest the cell in G2/M phase by preventing the formation of the mitotic filament for nuclear and cell division
Vinblastine
It is obtained from the
Vinca Rosa
• It’s mostly used in combo
with other drugs
Vinblastine
It’s used with cisplatin and
bleomycin = to treat
metastatic testicular and
prostate cancer.
Vinblastine
AE:
Severe neurotoxicity
Foot drop
Ataxia
Vinblastine
Vincristine
It is obtained from the Vinca Rosa • It is often used in combo with other drugs • It is used with prednisone= treats childhood leukemia
Vincristine
It is used against a wide
range of neoplasms.
• It’s a cell cycle non-specific drug
Cisplatin
MOA: They bind to guanine in DNA
and RNA and the interaction is stabilized by hydrogen bonding, which causes unwinding and shortening of the DNA helix.
Cisplatin
Carboplatin
It is given intravenously as a first line treatment for: o Testicular cancer o Ovarian cancer o Bladder cancer o Melanoma o And a number of other solid tumors
Cisplatin
AE: o Severe nausea o Nephrotoxicity o Vomiting o Little myelosuppression.
Cisplatin
Carboplatin
Used in the treatment of a wide variety of neoplasms • It has a similar spectrum of action to cisplatin. However, it is only used as a second-line drug for ovarian cancer.
Carboplatin
Estrogen • It inhibits the effects of endogenous androgens • It is used in the treatment of androgen-dependent metastatic prostatic carcinoma
Diethylstilbestrol
Hormone
MOA: Several types of hormone-
dependent cancers respond to their antagonist hormones as treatment.
Diethylstilbestrol
Fluoxymesterone
Tamoxifen
Anastrozole
AE: o CVD= cerebrovascular and cardiac complications o Male breast carcinoma
Diethylstilbestrol
Androgen • It’s MOA in breast cancer is very similar to estrogens • AE: o Hepatic toxicity o Virilizing effects
Fluoxymesterone
Sex hormone antagonist
• It antagonizes the ERs of
estrogen sensitive cancer
cells
Tamoxifen
It is used in the treatment of ER sensitive breast carcinomas and progestin resistant endometrial cancer
Tamoxifen
AE: o Hot flushes o Venous thrombosis o Vaginal bleeding
Tamoxifen
Aromatase inhibitor • The aromatase reaction is responsible for the extra- adrenal estrogen synthesis from androstenedione in post-menstrual women.
Anastrozole
It is used as a first line treatment for breast cancer in post-menopausal women to decrease estrogen production.
Anastrozole
AE:
o Bone pain
o Peripheral edema
Anastrozole
There are many neoplastic cells that require asparagine to grow faster. • L-asparaginase catalyzes the deamination of Asparagine to aspartate and ammonia.
Asparaginase
It is used in the treatment of childhood acute lymphatic leukemia (in combo therapy) • AE: Acute Pancreatitis
Asparaginase
It is used as an inhibitor of the tyrosine kinase activity of the protein product produced by the BCR-Abl oncogene. • Used in the treatment of chronic myeloid leukemia.
Imatinib
Half life in neonates= 2.2-5
hours
• Half life in adults= 0.9-2.2 hrs • Due to the lack of development in fetal liver metabolizing enzymes, its half life is prolonged.
Acetaminophen
Its hazardous in cases of low blood flow because its distribution relies on increased blood flow • Its elimination is slower in neonates because their GFR and tubular secretion is very low.
Gentamicin
It is a hydrophilic drug, so its volume of distribution is high in neonates (because neonates have a greater water: body fat ratio)
Gentamicin
Its renal clearance is low • Its half life is prolonged in geriatric age due to impaired renal function and clearance= could be very toxic if not adjusted.
Gentamicin
It is highly bound to plasma proteins • It should bind to serum albumin, but because of lower serum concentrations of albumin= its free fraction in plasma will go up (in old age) • The loading dose= decreases in elderly
Warfarin
It is less effective in old
people because of the
reduced number of
receptors and affinity.
B1- agonists
Uses: o In the treatment of anaphylactic shock o Severe hypertension o Atrioventricular blockage o Refractory HF
B1- agonists
It increases the myocardial O2 demand= Elderly may suffer from cardiac arrythmias and angina, especially if they have CAD.
B1- agonists
These are substances which activate receptors on the heart and kidney to allow increased heart rate and contractility and increased secretion of renin.
B1- agonists
These drugs are used in the treatment of: o Cardiac arrythmias o CHF o Angina o HTN o MI
B- blockers
In elderly, it may lead to an undue-blockade of sympathetic influences on the heart= bradycardia, hypotension, and Heat failure • In elderly, it may also lead to an AV-nodule conduction block
B- blockers
They are CVS drugs that can lead to (especially in those patients suffering from arryythmia, type 2 DM, and gout): o Hyperglycemia o Hyperuricemia o Hypokalemia
B- blockers
It should not be used in elderly patients suffering from any obstructive airway disease (it will lead to bronchoconstriction)
B- blockers
These substances block the actions of adrenergic agonists on the heart,
smooth muscles of the lungs, and fat cells.
B- blockers
It is hazardous in neonates because of decreased blood flow to the site of administration • Half life in neonates= 60- 70 hrs • Half life in adults= 30-60 hrs
Digoxin
It is rapidly eliminated in toddlerhood because of increased GFR • Absorption of it is delayed by increased gastric emptying • It’s renal clearance is low
Digoxin
Its vd in geriatrics is low
because of decreased lean
body mass in old age (this
is because digoxin needs to bind to the muscles in order to exert its action). • Digoxin’s half -life is prolonged in elderly patients because of decreased renal clearance= dose needs to be adjusted.
Digoxin
It is a CVS drug and it can lead to toxic arrhythmogenic action= you need to decrease the dose to decrease the effect in elderly.
Digoxin
It’s ability to bind to plasma proteins in neonates is low. • Reduced by MFO (mixed function oxidases) and has a long elimination half life in neonates (their liver enzymes are not as developed) • Half-life in neonates: 25-100 hrs • Half-life in adults= 40-50hrs
Diazepam
It’s a hydrophobic drug so its vd is decreased in neonates (because they have a high water: body fat ratio) • In elderly, due to increased fat stores, its volume of distribution is high (because it’s a lipophilic drug)
Diazepam
Due to decreased amount of albumin in elderly, the percentage of unbound or free drugs increase (its Vd is increased and so is its action) • Because of decreased liver enzyme function in the elderly, their half life is prolonged (phase I reactions are altered)
Diazepam
Because it’s a CNS drug=
ataxia (especially in elderly
because its half life is
prolonged)
Diazepam
Can only be given as a treatment if the toxicant was ingested less than an hour ago • It works against hydrophobic toxicants
Activated charcoal
Can only be given as a treatment if the toxicant was ingested less than an hour ago • It works against hydrophobic toxicants
Activated charcoal
It is not used for corrosives MDAC can be used to enhance the elimination of a toxicant, but this is mainly used if the patient took a life threatening amount of drug that can be removed well by charcoal.
Activated charcoal
Used in decontamination from a toxicant • Used in enhancing the elimination of a toxicant by metabolism
Activated charcoal
Toxicodynamic effect: It causes antimuscarinic syndrome, which is characterized by hypertension, tachycardia, hyperthermia, and mydriasis, and urinary retention (toxic syndrome).
Atropine
It can be used as an antidote in anticholinesterase poisoning. It acts as this by blocking the receptors preventing acetylcholine from binding (if there’s too much of it).
Atropine
It is also used as an
antidote for OP’s.
Atropine
It produces a very toxic metabolite that is metabolized by N-acetylcysteine • Its antidote is N -acetylcysteine.
Acetaminophen
Since it is an alcohol, the general agreement is that as its dosage increase, its response increases and causes an elevated anion gap.
Ethanol
Methanol
It completes with methanol to bind to ADH. It does this to prevent the formation of methanol’s toxic metabolite.
Ethanol
The mechanism is competitive inhibition • It acts as an antidote against methanol and ethylene glycol
Ethanol
It produces a toxic metabolite when it binds to ADH • Its actions are terminated by ethanol (its antidote)
Methanol
Given to comatose patients mainly Used in stabilization and supportive care of the intoxicated patient
Dextrose
In its poisoning state it causes an elevated anion gap • It is treated using sodium bicarbonate, which enhances its elimination through the kidneys
Salicylates
Hemodialysis may also
enhance its elimination
Salicylates
It induces emesis
(although apomorphine is
parenterally preferred)
It is used to
decontaminate the GI
Syrup of Ipecac
It is contraindicated in
people who are:
o Unconscious patients or experiencing convulsions o Corrosives o Drugs that induce
Syrup of Ipecac
It treats patients suffering
from poisoning by
acetaminophen’s toxic
N-acetylcystine
It enhances urinary excretion of acidic drugs mainly by altering the pH of the urine (makes it more alkaline to ionize acidic drugs like aspirin, enhancing its excretion).
Sodium bicarbonate
AKA: NaHCO3
• It is used as a measure to
enhance drug elimination
Sodium bicarbonate
It leads to an augmented adverse drug reaction • Leads to bradycardia • It can also lead to chest pain if abruptly stopped.
Atenolol
It causes an augmented adverse drug reaction • It causes dry skin and constipation and tachycardia.
Atropine
It leads to an immunogenic bizarre adverse drug reaction • Immunogenic= allergic reactions • It causes pulmonary reactions • It causes skin reactions
aspirin
It can lead to an augmented adverse drug reaction when given in the form of an injection • Hypoglycemia (since it brings down blood glucose)
Insulin
Result in bizarre adverse
drug reactions
• These reactions are immunogenic in nature. • They bind to tissue proteins forming immunogens • They also cause allergic reactions: skin reactions and anaphylactic shock.
Pencillins
It leads to a bizarre adverse drug reaction • The reaction is genetic in nature. • It leads to prolonged paralysis and apnea in patients who are deficient in plasma cholinesterases.
Suxamethonium
It results in a bizarre adverse drug reaction • The reaction is genetic in nature • It’s been shown that it may lead to hemolytic anemia in those patients who are deficient in G6PD. • It typically affects black males (10%) and Mediterraneans.
Primiquine
It leads to bizarre adverse drug reactions • These reactions are also genetic in their nature • It tends to affect people who are slow-acetylators (so they have a polymorphism in metabolism of acetyaltors)
Isoniazid
It induces peripheral
neuropathy in people who
are deficient in N-acetyltransferase
Isoniazid
It causes delayed adverse drug reactions • These reactions are typically congenital in nature and can be severe
Warfarin
It causes a craniofacial
abnormality- nasal hypoplasia
Warfarin
It causes delayed adverse
drug reactions
• It is mainly congenital in
nature and is very severe
• It causes deformed limbs
in the infant
Thalidomide
It is susceptible to drug interactions
because it has a low therapeutic
range.
Digoxin
Its absorption is altered by an increase in the gastric pH caused by
antacids.
Ketoconazole
If the antacids contain aluminum or calcium, they can chelate tetracycline and reduce its absorption and effectiveness.
Antacids
It can be displaced from plasma
binding proteins causing an
increase in its effect= you would
see excess bleeding.
Aspirin
In cases of aspirin toxicity, you would want to increase the renal excretion. To prevent tubular reabsorption, you make the urine more alkaline to increase the chances of aspirin being ionized.
Aspirin
When administered with Warfarin, it poses an increased risk of bleeding (additivism= pharmacodynamic affect) • When administered with garlic or ginkgo will cause increased bleeding.
Aspirin
It can be displaced from the plasma
binding protein leading to an
increase in its effect= you would
see excess bleeding.
Warfarin
In the presence of
phenobarbital, it becomes
rapidly metabolized
reducing its effectiveness.
Warfarin
When administered with aspirin, it increases the risk of bleeding (pharmacodynamic effect=additivism) • When administered with garlic or ginkgo may lead to increased bleeding.
Warfarin
In the presence of
phenobarbital, it becomes
rapidly metabolized
reducing its effectiveness.
Cimetidine
Cytochrome p450 isoenzyme
inhibitor
Cimetidine
Cytochrome p450 isoenzyme inhibitor
Cimetidine
If iron contains aluminum or
calcium it will form a complex with
tetracycline reducing its
Iron
It is an inducer of the cytochrome p450 phase 1 reaction enzymes • When administered it accelerates the metabolism of many other drugs. • Warfarin’s effectiveness is reduced in the presence of phenobarbital because of its increased metabolism.
Phenobarbital
When administered with Penicillin,
it inhibits its active secretion
allowing it to stay longer in the
circulation (beneficial)
Probenecid
Normally administered to treat asthma by relaxing the smooth muscles in the bronchioles • When administered with a b-blocker (antagonist), its effects are reduced.
Salbutamol
Its excretion is increased by making the urine more alkaline • Aspirin is an example of a salicylate
• When administered with
garlic and ginkgo it may
lead to excess bleeding
Salicylates
Drugs like iron and antacids that contain calcium or aluminum can form chelates with tetracycline reducing its absorption and effectiveness.
Tetracyclines
When administered with milk products, which are high in calcium, it results in decreased absorption of tetracycline (because it is chelated)
Tetracyclines
When administered with aminoglycosides it will inhibit cell wall synthesis allowing for increased penetration of the cell wall by aminoglycosides. (syngergistic) • Administered to treat against Staph. Aureus infections.
Penicillin
When administered with NA, it
inhibits the reuptake of NA allowing
NA to persist longer in the synaptic
cleft (potentiating its affect)
Cocaine
When administered with
acetylcholinesterases, its affect is
potentiated, as it will persist longer
in the synaptic cleft.
Acetylcholine
Tyramine is an important dietary protein that is needed for the formation of NA • When a person consumes a tyramine rich diet and is taking monoamine oxidase inhibitors (phenelzine), the chances of developing hypertensive crisis are high.
Tyramine
It is involved in dietary drug interactions • It is very important in those patients who consume high amounts of cheese, particularly because of the presence of
Tyramine within these
cheese products
Phenelzine
When tyramine is
consumed in the presence
of phenelzine it may lead
to a hypertensive crisis.
Phenelzine
It has a pharmacodynamic drug interaction affect • The effect is potentiation • It allows for prolonged action of acetylcholine by inhibition of acetylcholinesterases.
Physostigmine
It causes increased gastric emptying= increased absorption of drugs (not sure about this). • Thus, it can lead to pharmacokinetic drug interactions • It does so by altering the gastrointestinal absorption of drugs.
Bethanecol
It inhibits the metabolism of some drugs like calcium channel blockers (antihypertensives). • This leads to hypotension because the calcium channel blockers cannot be metabolized due to the blockage of the intestinal CYP3A4.
Grapefruit juice
