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222 Cards in this Set

  • Front
  • Back
What are the 3 types of drug names?
1. chemical
2. generic
3. trade
why is it important to know the generic names of drugs?
Generic names are the same everywhere.
Define pharmacokinetics
The study of the movement of drugs through the body
(i.e. what the body does to the drug)
Define pharmacodynamics
The study of the mechanisms of action & physiological effects of drugs
(i.e. what the drug does to the body)
Where do drugs come from?
1. A naturally-occuring substance
2. a modification of a naturally-occuring chemical
What does ADME stand for?
A-absorption
D-distribution
M-metabolism
E-excretion
What does ADME describe?
the processes affecting the movement of drugs through the body. PHARMACOKINETICS
Following administration, a drug must reach _______
systemic circulation
To be effective, drugs must _________ before reaching the target tissue
not be inactivated
What is bioavailability?
The FRACTION of administered dose of drug that reaches the SYSTEMIC circulation UNCHANGED
What is enteral administration?
"via the intestine"
usually oral
What is parenteral administration?
Routes that involve absorption of drug from sites other that the stomach or intestine.
what are the advantages of oral administration?
- simple; most convenient for self-administration
- usually safer than injection
What are the disadvantages of oral administration
- erratic absorption
- patient complience
- not for unconscious patients
- "first pass" effect
- too slow for some emergency situations
What is the first pass effect?
Drugs administered orally are absorbed into the portal vein and delivered first to the liver where metabolism my inactivate a percentage of the drug.
What is subligual administration?
Drugs placed inder the tongue. Absorption is across oral mucosa
what are the advantages of sublingual administration?
- no first-pass metabolism
Disadvantages of subligual administration?
- patient must cooperate (not swallow the drug)
- significant proportion of dose may be swallowed dispite efforts not to swallow
What is subcutaneous injection?
an injection of a drug uner the skin
Advantages of subcutaneous injection?
- suitable for solid pellets, insoluble suspensions, oily vehicles ("depot" formulations)
- easier the IV
- absorption slower than by IV or IM routes (may also be a disadvantage)
Disadvantages of subcutaneous injection?
- not for large volumes
- pain or necrosis with irritating drugs
- absorption can be very slow
- possible infection
What is intramuscular injection?
injection of a drug into the muscle of a patient.
Advantages of intramuscular injection?
- suitable for moderate volumes and oily vehicles ('depot" formulas)
- safer and easier that IV
Disadvantages of intramuscular injection?
- local pain, swelling, possibe infection
- avoid during anticoagulant treatment (extensive hemorrhage/bruising may occur)
What is intravenous administration?
- injection directly into the vein of a patient
advantages of IV?
- emergency use, rapid drug availability
- large volumes (slowly)
- irritating drugs (when diluted)
disadvantages of IV?
- higher risk o adverse effects
often must inject slowly due to cardiax toxicity risk
- not for oily or insoluble drugs
- requires more skill
what is topical administration?
drugs placed on the suface
- eye, ear, skin, mucous membranes (conjuctiva, nasopharynx, oropharynx, vagina, colon, urethra)
advantages of topical administration?
- drug delivered to site of need
- can achieve very high concentrations
disadvantages of topical administration?
-may be absobed systemically
- may not remain in place/messy
what is drug "formulation"?
the physical form of a medication as well as its chemical ingredients
what do the inactive ingredients in drugs do?
- balance pH
- alter flavour
- produce the desireable physical form
most drug are found as _____
weak acids or weak bases
non-ionized form = more _______ solube
lipid
ionized form = more _______ soluble
water
________ molecules can diffuse accross membranes
non-ionized
diffusion rate depends on _______
lipid solubility
what determines the ionization state of a drug?
the pKa
what is the pKa?
pH when 50% of drug is ionized
pKa is usually between ___ and ____
pH 3 and pH 11
what is the pKa of acetaminophen?
9.5
what is the pKa of aspirin?
3.5
what is "ion trapping"?
when drug accumulates on side of membrane where ionization is highest
(basic accumulate in acidic and acidic accumulate in basic)
distibution usually begins _______ absorption is finished
before
most drugs goes where it is not needed, only a small fraction reaches ________
receptor sites
what 3 factors effect drug distribution?
1. Physicochemical properties of drug
2. anatomy and physiology of patient (tissue perfusion, blood brain barrier)
3. plasma protein binding
examples of physicochemical properties of drug
- lipid solubility
- degree of ionization
- size, molecular weight
once drug enters blood, it distributes to entire blood volume in _____
1-2 min
organs with ______ blood flow get more drug
higher
what organs have higher blood flow? (20% of cardiac output)
- brain, kidney, heart, liver
what is the blood brain barrier?
- capillaries in the brain are much less permeable to som water-soluble substances due to glial cells
the blood brain barrier is totally impermeable to ________
plasma proteins
water soluble substances will enter the CNS ______
very slowly
_______ administration is useless if intended site of action is the CNS
systermic
which drugs cross the blood brain barrier well?
high lipid soluble, low protein drugs
what is the main plasma binding protein?
albumin
what percentage of the total plasma protein is albumin?
50%
_______ drugs connot enter tissues and cannot be eliminated via kidneys
protein-bound
infected tissue is more _____ than healthy tissue
acidic
is lidocane a weak acid or a weak base?
weak base
true/false: drugs distribute equally to all tissues
false
-some remain almost exclusively in blood (~7% of body volume)
- some distribute readily to other tissues
what is volume of distribution ?
a rough estimate of th extent to which the drug leaves the bloodstream and enters other tissues
what factors effect the volume of distribution?
- ion trapping
- highly lipid-soluble drug
- irreversilble receptor binding
- incorporation into tissue
what is biotransformation or metabolism?
a change in the chemical structure of an absorbed drug within a living organism, usually by nzyme-catalyzed reaction
why is drug metabolism important?
-enzymes play a pivotal role in terminating drug action
- metabolism makes drugs more excretable and inactivates many drugs
why are lipid soluble drugs not readily excreted?
- cross out of urine through membranes back into the blood
where are drug metabolized?
- in the liver
- but also in lungs, GI tract, skin, kidneys, brain
the enzymes resonsible for biotransformation are located in______________
- *endoplasmic reticulum
- * cytoplasm
- mitocondria
- nuclear or cell membrane
- lysosomes
following differential centrifugation of cell homogenates, drug metabolizing enzymes are present mainly in _______ and _______
microsomes and cytosol
what are microsomes?
- visicle consisting of membranes of ER which contain membrane-bound P450 enzymes (mediate Phase l metabolism)
what is the cytosol?
supernatant consisting of cytoplamic fluid and soluble Phase ll enzymes
how are drugs metabolized?
phase l and phase ll reactions
what is a phase l reaction?
- drugs are converted to more polar metabolites
- then they are either excreted or they go to phase ll reactions
what is a phase ll reaction?
conjugation or synthesis reactions in which endogenous sustance combines with the functional group derived from phase 1 reaction
- polar = excretable
what are the characteristics of phase l reactions?
1. makes drugs moore reactive, capable of combining with polar conjugate bodies
2. substrates are lipid soluble, of widely varied chemical structure
3. metabolites are more water-soluble, either excreted or go to phase ll reactions
4. involve one or more cytochrome P450 enzyme found in smooth ER
what are P450 enzymes called P450 enzymes?
they are heme-containing proteins (P) that maximally absorb light at 450 nm
what are the other names for P450 enzymes?
- microsomal
- CYP enzymes system
- mixed-function oxidases (MFOs)
what are the different types o Phase l reactions?
1. oxidation
2. reduction
3. hydrolysis
what is the most common type of phase l reaction?
oxidation
what is an oxidation reaction?
involves the addition of oxygen or removal of hydrogen from the drug
- involves P450 enzymes
what are the characteristics of phase ll reactions?
1. couple drug (or phase l metabolite) with substrates from diet to produce conjugates
2. conjugates are often polar, inactive and readily excretable
what are some conjugating substances?
- glucuronic acid
- sulfate
- glutathione
- methl groups
- glycine
- cysteine
- methionine
- acetic acid
what are the different types of phase ll reactions?
1. glucuronic acid conjugation
2. sulphate conjugation
3. acetylation
4. glutathione conjugation
what are the features of glucuronic acid conjugation?
- very important
- enterohepatic recirculation
- individuals deficient in glucuronide synthesis are slow to metabolize certain drugs (e.g. neonates, cats)
what is enterohepatic recirculation?
large drugs (>500 MW) are excreted in bile for elimination in feces, but glucuronidases in gut bacteria can hydrolyze conjugate and free drug, which can be reabsorbed
what drugs are metabolized using glucuronic acid conjugation?
- morphiine
- acetaminophen
- salicylic acid
- chloramphenicol
what types of drugs are metabolized using sulphate conjugation?
- phenol and alcohol
- e.g. acepaminophen, morphine
what types of drugs are metabolized by acetylation?
- occurs in drugs with -NH2 group conjugated to COCH3
- e.g. most sulfonamide antimicrobial drugs
whaat types of drugs are metabolized using glutathione conjugation?
- epoxides, arene oxides conjugated to glutathione (GSH)
- e..g. some anticancer drugs (alkylating agents)
in the metabolism of acetaminophen (Ac), what three pathway does it follow?
1. Ac to Ac-glucuronide
2. Ac to Ac-sulfate
3. Ac to reactive electrophilic compound (Ac*) - uses P450
what happens in acetaminophen overdose?
1. acetaminophen gets turned into a reactive electrophilic compound by P450 enzyme
2. this then gets turned into acetaminophen bound to protein by cell macromolecules
3. this causes cell death
4. leading to liver failure
what factors effect drug metabolism?
1. enzyme induction and inhibition
2. multidrug therapy
3. distribution
4. age
5. genetics
6. disease
what is induction?
- many drug metabolizing enzymes can increase in amount and activity in response to chemical inducers
- induction can increase drug metabolism and decrease drug action
- can increase drug-related toxicity depending on whether phase l or ll enzymes are induced
what is inhibition?
- certain drugs may inhibit P450 activity mostly by competing for the same isozyme
what is multi-drug therapy?
- there is a finite number of hepatic enzymes
- systems can be saturated
- most comon when multiple drugs requiring the same metabolic enzyme are taken at once
- drugs compete for, or inhibit, metabolizing enzymes
what is distribution?
- drugs bound to plasma proteins or stored in fat not available for metabolism
how does age effect metabolism?
- neonates, geriatric patients deficient in metabolc capacity
how does genetic effect drug metabolism?
- drug metabolizing enzyme levels may vary between individuals due to genetic polymorphisms
how does health and disease effect drug metabolism?
- poor nutrition can lead to deficiency in substances needed for conjugation
- endocrine diseases, liver diseases, infectious/inflammatory diseases can inhibit drug metabolism
- heart disease can cause impaired blood flow to liver
how can acetaminophen overdose be treated?
- glutathione conjugation can inactivate the reactive intermediate (NAPQI)
- a physician will administer a source of glutathione (n-acetyllcysteine), which minimizes hepatic damage
what is elimination?
the tranfer for drugs to the external environment
what organs are involved in elimination?
- *kidney
- * liver
- lungs (volatile drugs)
- intestinal tract
- other (milk, sweat, tears, etc.)
what can be used to describe elimination?
half life
how many half lives does it take for 99.9% of a dose to be eliminated?
10 half lives
for practical purposes, drug is essentially eliminated after________
4-5 half lives
what is a loading dose?
an initial dose that is larger then subsequent doeses
if excretion decreases, drug half-life ________
increases
hte most benificial way to administer drugs is?
small doses more frequently
what are the mechanisms of renal elimination?
1. glomerular filtration
2. tubular secretion
3. tubular reabsorption (passive) - working against excretion
what are the characteristics of glomerular filtration?
- passive
- non-selective
- non-saturable
- drug with MW< 68 000 goes into urine
- drugs bound to albumin dont get filtered (slow elimination)
what are the characteristics of tubular secretion?
- active transport and passive diffusion
non-specific secretory mechanism for acids (e.g. penicillin) and bases (e.g. morphine)
- may saturate if [drug] is high
- competition by different drugs for same active transport mechanism, individual excretion rates may decrease (longer T1/2)
what are the characteristics of tubular reabsorption?
- works against excretion
- follows filtration or secretion
- many lipid-soluble drugs simply diffuse from tubule back into plasma
- aided by continuous re-absorption of water
mainly passive (rare active processes)
what is tubular reabsorption affected by?
a) physiochemical properties of drug
b) rate of urine flow
what are the physiochemical properties of a drug?
- degree of ionization (affected by diet: pH 5.5 - 8.0; can alkalinize for weak acid OD e.g. aspirin)
- acid vs. base
- molecular size
-
how does the rate os urine flow effect elimination?
- increased flow means increased elimination
can use fluids, diuretics to increase elimination
what is hepatic elimination?
- only drug not bound to plasma proteins
metabolism in hepatocytes
- excretion into bile (ative transport to gut to feces
what is enertohepatic recycling?
-drug reabsorbed in small intestine gets returned to liver in portal blood
gut microbes may ________
reactivate drug
drugs that are conjugated get excreted into ____
bile
what are the characteristics of hepatic elimination?
- active process, against conc gradient
- once in bile drug moves to intestine then to feces
- some conjugated drugs can be deconjugated and reabsorbed into blood
- important if recycling prolongs drug action
what is the therapeutic margin?
- drug response is essentially proportional to the concentration of free drug at the target organ
what is drug clearance?
a concept used to compare rates of elimination of drugs
what is pharmacodynamics?
what drugs do to the body
what are the 2 sub-sections of pharmacodynamics?
1. what the drug does to individual cells
2. what the drug does to the entire body
most drugs exert their effects by binding to _______ proteins in the plasma membrane of cells
receptor
drugs can _____ or ______ receptors
stimulate or block
receptors are normally modulated by ______________
endogenous ligands
examples of endogenous ligands
neurotransmitters, hormones, endorphines, leukotrienes and other intra-cellular signalling chemicals produced by the body
the fracion o drug receptors occupied by drug is dependent on _________
drug concentration in extracellular fluid
drug effect is generally proportional to the __________ by drug
percentage of receptors occupied
where are drug receptors located?
cell membranes
lipid soluble drugs can have receptors located in_______
the nuclear membrane
most drugs are receptor ______ or ______
agonists or antagonists
what is a agonist?
- activates receptor
what is an antagonist?
- bind to but do not activate the receptor
- blocks physiological response
most receptors are ______
proteins
many receptors have ______ binding sites
several
advantages of multiple binding sites on a receptor ?
- different abilities to dissociate
- critical for response
- continued response requires repeated binding and unbinding
irreversible binding generally produces _________
toxicity
what are the different types of bond for receptor-drug complexes.
1. covalent bonds
2. ionic or electrostatic bonds
3. hydrogen bond
4. van der waal's forces
5. hydrophobic bond
what are the characteristics of a covalent bond?
- high energy
- cannot be broken
- recovery from drug depends on new receptor production
- e.g. phenoxybenamine (irreversable blocker of alpha receptors)
what are the characteristics of a ionic bond?
- medium energy
- occurs between opposite charges
- reversible
- may attract drug to receptor over a distance
what are the characteristics of hydrogen bonds?
- medium energy
- e.g. between amino acids
what are the characteristics of van der waals forces?
- low energy
- drug and receptor close together, increases dipole
- may be many dipoles, increases drug receptor selectivity
what are the chracteristics of a hydrophobic bond?
- low energy
between fat soluble (hydrophobic) regions
- usually very selective D-R binding
what effect can drugs have on a receptor?
- initiate
- enhance
- diminish
- terminate (block)
the magnitude of response depends on ______?
the percentage os receptors occupied bu the drug
what are the 5 important signal transduction mechanisms?
1. lipid-soluble drug binds intracellular receptor (enzyme, gene regulator)
2. D-R complex activates cytoplasmic enzymatic activity
3.D-R complex activates tyrosine kinase
4. Drug binds to and opens or block ion channel
5. D-R acts through G-protein to activate effector enzyme
what is an effector?
- molecule that translate D-R interaction into a change in cellular activity
- drug R usually extracellular and effector intracellular
- therefore signal crosses cell membrane
what important signal transduction mechanisms are essential for action of drugs?
- ion channels
- second messengers
- DNA/RNA synthesis
what are the characteristics of intracellular receptors?
- lipid soluble of diffusible ligands (e.g. steriod hormones, nitric oxide)
- cross membrane and bind to intracellular R that affects an intracellular effector molecule
- no specialized transmembrane signaling device required
- ultimately increases transcription and expression of regulator genes (e.g. estrogen, glucocorticoids, Vit D)
what are the characteristics of receptors that activate cytoplasmic enzymatic activity?
- R have extrcellular and intracellular domains
- membrane-spanning Rs bind separate kinase molecules
what are the chracteristics of receptors with membrane-spanning enzymes?
- drugs bind R on extrcellular portion os enzyme and modify intracellular activity
- when activated, Rs dimerize and kinases phosphorylate tyrosine residues on the cytoplasmic domain (e.g. insulin or EGF acts on receptor tyrosine kinase located in membrane which increases glucose uptake)
what are the characteristsics of receptors that act as ion channels?
- receptors regulate pore-forming transmembrane proteins causing the opening of an ion channel
- regulate ion flow across membrane producing depolarization or hyperpolarization
what is a ion channel?
- type on ligand-gated ion channel (e.g. nicotinic acetylcholine R NAChR)
where are ion channels located?
- motor end plates of NMJ
- CNS
- autonomic ganglia
what is the structure of an ion channel?
- 5 subunits: 2 alpha, 1 beta, 1 gamma, 1 delta
what are the characteristics of receptors linked to G proteins?
- R linked by coupling proteins (G proteins) to intracellular or membrane effectors
- guanosine triphosphate (GTP) proteins amplify signal
- activated G protein the changes the activity of an effector element (e.g. enzyme or ion channel)
- this element then changes the concentration of second messenger
what does a does response curve show?
response is related to drug concentration and affinity of drug for receptor
when on a drug response curve does a drug produce half-maximal effect?
at EC50
when does a drug produce half maximal receptor occupancy?
at KD
Competitive antagonists can be completely overcome by ________
increasing the concentration of the agonist
irreversible antagonists reduce_____
Emax
what is allosteric antagonism?
results from the binding of a chemical (antagonsist) to a site on the receptor different from the agonist binging site ( the antagonist reduces the receptors affinity for the drug)
what is potency?
the relative ability to different drugs that are agonists at the same receptor to produce half-maximal effect
the drug that produces ______ at the lowest concentration is the most potent drug
Emax/2
what is efficacy?
the magnitude of the maximum response that a drug produces
the most efficacious drug produces quantitatively the ______ response
largest
what is tachyphylaxis?
the rapid loss of response of an organ to receptor activation by a drug e.g. after a few days or weeks
what is desenitization?
refers to tachyphylaxis at the receptor level
what is receptor down-regulation?
occurs when a receptor type has been excessively stimulated for an exended period of time - the number of receptor (and therefore the response tot he drug) is decreased
what is up-regulation?
occurs when a drug has been restricted for an extended period of time and the response to the drug increasses due to increases receptor numbers
what are inert receptors?
do not produce a pharmacological responce when drug binds e.g. plasma protein binding sites
"rest and digest"
parasympathetic nervous system
"fight or flight"
sympathetic nervous system
what organs do not receive input from both PSNS and the SNS
- adrenal gland, sweat gland, pilomotor muscles, blood vessels
in general, the PSNS and SNS mediate _______ responses in effector organ
opposing
what is ganglia?
aggregation of cell bodies of postganglionic neurons
what are preganglionic fibers?
brain and spinal cord to ganglia
what are postganglionic fibers?
axons from ganglia to effector organs
what are the characteristics of the PSNS?
- leaves CNS via cranial an sacral nerves
- ganglia close to or within end organ
- long preganglionic and short postganglionic fibers
- one preganglionic to one postganglionic fiber
what are the characteristics of the SNS?
- cell bodies in thoracic and lumbar spinal cord
- ganglia near spinal cord
- short preganglionic and long postganglionic fibers
one preganglionic to many post ganglionic fibers
what are the main neurotransmitters in the ANS?
- acetylcholine (ACh)
- norepinepherine (NE)
- epinepherine (EP)
what are the 2 types of cholinergic receptors?
1. muscarinic (M1-M5)
2. Nicotinic (Nn, Nm)
what are the characteristics of muscarinic receptors?
- found in organs innervated by PSNS (M1-M3)
- found on endothelial cells (M3 and M5)
- found in sweat glands innervate by cholinergic SNS fibers (M3)
what are the characteristics of nicotinic receptors?
-Nn found in all ganglia (PSNS and SNS)
- Nm found on skeletal muscle (somatic nervous system innervation)
what are the characteristics of adrenergic receptors?
- found in organs innervaated by SNS
- location and subtype determine tissue response
what are the 2 types of adrenergic receptors?
1 alpha (1 and 2)
- activated by NE and EP
2. beta (1,2,3)
- activation of B2: EP>>>>>NE
acteylcholine is synthesized by the enzyme ________
choline acetyltransferase (ChAT)
acetylcholine is degraded by the enzyme _____________
acetylcholinesterase (AChE)
muscarinic receptors activate ________
second messengers (G proteins)
in muscarinic receptors increasing IP3 and DAG =
stimulatory
in muscarinic receptors, decreasing cAMP =
inhibitory
nicotinic receptors open _____
ion channels
where are M1 receptors located and what is there action?
- gastric mucosa
- increase secretion
where are M2 receptors located and what is there action?
- heart
- decrease rate/force of contraction
AND
- adrenergic nerve
- decrease NE release
where are M3 receptors located and what is there action?
- smooth muscle glands
- contracts
AND
- endothelial cells
- increase EDRF release
where are M5 receptors located and what is there action?
- endothelial cells
- increase EDRF release
what is EDRF?
- endothelial derived relaxing factor (nitric oxide)
where are Nn receptors and what is there action?
- postganglionic neurons
- opens Na+ and K+ channels
AND
- CNS
- excitation
where are the Nm receptors located and what is there action?
- skeletal muscles
- opens Na+ and K+ channels
what does ion influx cause?
depolarization / contraction
what are the 3 steps in norepinepherine synthesis?
1. tyrosine hydroxylase
2. dopa decarboxylase
3. dopamine beta-hydroxylase
what are the 2 steps in the termination of NE?
1. re-uptake
2. diffusion away from synapse
- metabolized by: monoamine oxidase (MAO) or catechol-O-methyltransferase (COMT)
dopamine transported into synaptic vescles and converted to NE by ________
beta-hydroxylase
all adrenoreceptors are linked to _____________
G-protein second messenger systems
where are a1 receptors located and what is there action?
- smooth muscles cells (eye, vascular (organs and skin), pilomotor, GI and urinary sphincters)
- contraction
where are a2 receptors located and what is there action?
- SNS nerve terminals
- decrease NE
AND
- PSNS nerve terminals in GI tract
- decrease ACh
AND
- Platelets
- aggregation
-
where are B1 receptors located and what is their action?
- heart
- increase rate/force of contraction
where are B2 receptors located and what is their action?
- smooth muscle cells (skeletal muscle vessels, bronchial tree, uterine, GI and bladder walls)
- relaxation
where are B3 receptors located and what is their function?
- fat cells
- increase lipolysis
what are the effects of the direct acting receptor agonists have on the heart?
M2 - decrease heart rate
B1 - increase heart rate
what are the effects of the direct acting receptor agonists have on the blood vessels?
M3 - vasodilation
a1 - vasoconstriction
what are the effects of the direct acting receptor agonists have on the blood vessels in skeletal muscles?
B2 - vasodilation
what are the effects of the direct acting receptor agonists have on most organ sysems/glands?
M3 - contraction - increase activity - increase secretion
B2 - relaxation of smooth muscle
a1 - constriction of sphincters
autonomic transmission can be inhibited or stimulated by chemicals that affect?
- neurotransmitter synthesis
- neurotransmitter storage
- neurotransmitter release
- receptor activation
- neurotransmitter re-uptake or inactivation
what are cholinomimetics?
mimic action of ACh
- direct (receptor agonists)
- indirect (AChE inhibitors)
what are the 2 types of cholinergic antagonists?
1. antimuscarinic
2. antinicotinic
what are th examples of direct acting cholinergic agonists?
1. acetylcholine
2. bethanechol
3. muscarinic
4. pilocarpine
5. nicotine
what agonists are AChE susceptible?
acetylcholine
what are the examples of indirect acting cholinergic agonists (AChE inhibitors)
- physostigmine
- echothiophate
- carbamate
- organophosphate
what are the examples of cholinergic antagonists?
- atropine (M-)
- trimethaphan (Nn-)
- D-tubocurarine (Nm-)