info from slides Flashcards
vasotec
enalapril maleate. ace inhibitor used to treat high BP
trandate
labetalol hydrochloride. beta 1 and 2 blocker. also blocks alpha 1. reduces heart strain and bp
albuterol sulfate
proventil HFA
additive interactions
1+1=2 sum of two effects is equal to each of them given separately but at the same time
Synergistic Interactions:
The summation of each individual drug’s activity exceeds the sum of the two individual drugs”
Potentiation:
One drug (which has no direct effect) increases the response of the other drug, which normally has a lesser effect”
law of mass action drug receptor inter actions
reversible because drug receptor complex is reversible. effects are proportional to # of receptors occupied. effects plateau because of limitation of total # of receptors. drug effects are proportional to dose
intrinsic activity
measure of drugs effectiveness of causing a response (efficacy) An antagonistic drug’s intrinsic activity is 0, meaning it would bind but have no response. An intrinsic activity of 1 would be a full agonist, and 0.5 would equal a partial agonist.
tolerance
increased amount of drug needed to produce same effect
desensitization
longterm exposure makes tissues/cells less responsive over time
down regulation
ccurs over a longer period than desensitization (hours to days to weeks)
- Receptors are internalized and eliminated
- Consequently, the effects of down- regulation are longer-lasting
potency
The amount of drug necessary to produce an effect of a given magnitude”
- Potencies are compared by the amount of drug required to produce 50% of the maximal effect (EC50)
- Differences in potency can be overcome by simply giving more drug.
efficacy
he ability of a drug to elicit a response when it interacts with a receptor”
- Think of fentanyl being more potent than morphine and both are more effica- cious for pain than aspirin.
- Efficacy is generally more important than potency.
therapeutic index
herapeutic Index = The TD50/ED50 -The ratio of the drug doses that produces a specified toxic effect in 50% of the population vs. the dose that produces a specified therapeutic effect in 50% of the population. 2 or lower is not safe
signal amplification
One drug molecule interacts with many receptors.
2) The activated receptors can persist for longer than the original drug ligand/receptor complex existed.
three aspects of drug receptor function
Receptors determine the nature and characteristics of the “Drug Concentration-Effect Curve”.
2) Receptors function as regulatory proteins and part of chemical signaling mechanisms that provide targets for drugs.
3) Receptors determine the therapeutic and toxic effects of drugs on a critter.
types of receptors
regulatory proteins such as
neurotransmittors or hormones
2) Enzymes
3) Transport proteins such as Na+/K+ ATPase
4) Structural proteins such as tubulin, the receptor for colchicine
spare receptor concept
1) Maximal response can be achieved by an agonist even if only a fraction of the receptors are occupied.
2) Sensitivity of the cell to an agonist concentration depends on affinity of receptors for the drug and total receptor concentration.
bioavailability
The fraction of an
administered drug that reaches the systemic circulation”
Factors affecting Bioavailability
Solubility characteristics of the drug. Chemical Stability in the GI tract. Drug formulation
Volume of Distribution
• This distribution is mostly dependent on three things:
Blood flow, fat/water solubility, and protein binding.
This half-life assumption assumes “First Order Kinetics”
First Order Kinetics: “The rate of drug metabolism and elimination is directly proportional to the concentration of free drug”
clearance rate=
(.693 x Vd)/T(1/2/)
Zero-Order Kinetics
ome drugs are administered in such high quantities (dosages) that they are eliminated by a constant AMOUNT (not proportion) over time because they’ve overwhelmed clearance mechanisms
earance, half-life, and volume of distribution are all related to
drug dosing. Sooooo….it means that repeated dosing of a drug won’t allow for the drug to “accumulate” in the critter unless the dosing interval is < 4 half- lives.
• ….and accumulation of a drug is necessary in order for the drug to reach a “steady-state” in the critter’s plasma.
Target Concentration”
The drug concentration that will produce the desired therapeutic effect.”
Loading Dose=
(Vd)x(Target plasma concentration)/ Bioavailability %
Maintenance Dosing=
(Cl)x(Target plasma concentration)/bioavailability%. Dosing rate X Dosing interval
What does Biotransformation accomplish?
Biotransformation can shorten a drug’s biological half-life: if an anesthetic is very non-polar (and thus enters the brain easily) biotransforming it into a polar molecule can greatly decrease its activity (and biological half-life.) Alternatively, biotransformation can turn non- biologically active chemicals into active drugs or convert drugs into even more active forms.
two types of biotransformation
Phase I Biotransformation:Metabolizes the drug into a more polar form. Phase II Biotransformation:Conjugates the drug with another chemical (such as acetylation)
induced vs inhibited cytochrome p450
Induced P450 enzymes metabolize drugs faster.
Inihibited P450 enzymes metabolize drugs slower.
Semiautonomouspart of ANS in the GI tract
Twocomponents: 1) Myenteric plexus
(plexus of Auerbach)
2) Submucous plexus (plexus of Meissner)
These neurons send sensory input to the parasympathetic and sympathetic nervous systems and receives motor output from them
FEEDBACK OF NOREPINEPHRINE
BARORECEPTORS SENSE INCREASED PRESSURE. They begin to fire and cause vagal stimulation which slows HR. So net effect is increase in SVR through alpha receptors and decrease in HR even though it has direct chronotropic effects
autoreceptor
If the presynaptic neuron is inhibited by the chemical it produces (such as norepinephine) i
heteroreceptor
f the presynaptic neuron is inhibited by chemicals that are released by neurons with which it has a synapse (and which that presynaptic neuron doesn’t produce)
Six Steps of Cholinergic Neurotransmission
- )synthesis of ACH (INHIBITED BY HEMICHOLINIUM) rate limiting and has to be actively transported
- ) uptake into storage vesicles where it is protected from degradation
- )release of ACH
- )binds to postsynaptic receptor
- )deagradtion of ACH by ACHe in synaptic cleft
- )recycling of choline by Na transport which allows it to get into membrane
