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165 Cards in this Set
- Front
- Back
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Receptor
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protein molecule designed to bind small molecules and transduce that information into an effector.
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Ligand
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binds a receptor
drugs |
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Kd
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equilibrium,dissociation constant
describes how well a receptor and ligand "fit" together. inversely related to the affinity of the ligand for a receptor Kd= k2/k1 Kd= L*R/ LR |
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Affinity
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how tightly a ligand wants to bind to a receptor.
Due to either ionic bonds, H-bonds or Van De Waals interactions. |
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Rt
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the total number of receptors
Rt= LR +R |
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intrinsic activity
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the ability of a ligand to activate a Receptor
sometimes called efficacy |
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Agonist
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intrinsic activity = 1
binds to receptor and completely activates it |
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antagonist
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intrinsic activity=0
can bind to a receptor but does not activate it |
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Partial agonist
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intrinsic activity is btwn. 0 and 1.
can bind to receptor and partially activate it |
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spare receptors
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function is to increase sensitivity of the cell to a low concentration of ligand.
do not need all the receptors occupied in order to have maximum effect. EC50 does not always = Kd |
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Potency
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the relationship btwn. the amount of drug and its effect.
depends on the affinity for the site of action and the ability to reach the site of action. mirrored by the position of the curve on the x-axis. |
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ED50
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The dose at which 50% of people respond to the drug
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LD50
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the lethal dose for 50% of ppl
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TD50
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Toxic dose for 50% of ppl
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Therapeutic index
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the ratio of TD:ED
want these to be far apart so they are safe to give. |
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hyporeactive
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respond at higher doses
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hyper-reactive
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respond at lower doses
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hypersensitivity
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allergic or inflammatory response
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bioavailability
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fraction of the dose that reaches the systemic circulation
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First pass effect
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the liver inactivates the drug administered, mainly drugs that are given orally.
reduces the bioavailability |
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bioequivalence
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2 drug preparations with the same active ingredients at the same amount and delivered by the same route of administration are bioequivalent if the extent and rate of drug delivery into the circulation are the same
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redistribution
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when a drug is absorbed into its site of action and then once is it cleared from the circulation the drug leaves its site of action and goes into other tissues
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therapeutic window
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the range of concentrations of a drug that are high enough to produce a therapeutic effect miniminal toxic effects
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volume of distribution
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a measure of the apparent space in the body available to contain the drug
Vd= concentration *Dose |
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Clearance
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the amount of plasma that can be cleared of a drug per unit time.
Cl= rate of elimination/concentration units= L/min |
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rate of elimination
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is how fast a drug is eliminated from the body
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1/2 life
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the amount of time it takes to reduce the drug concentration by 1/2
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loading dose
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a larger dose of the drug that allows for therapeutic levels to be achieved more quickly.
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maintenance dose
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the dose which needs to keep getting administered in order to keep the drug levels in the therapeutic window.
MD= (Css*Cl)/F |
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Prodrug
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a drug that is converted into its active form by metabolic enzymes
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Phase I metabolism
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Oxidation, reduction, dealkylation or hydrolysis reactions
enzymes are found in the SER Require- CYP450, P450 reductase, NADPH, 02 Drug |
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Phase II Metabolism
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conjugation reactions
most of these enzymes are cytosolic board specifcities inducible can work on endogenous molecules |
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CytochromeP450
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hemeproteins that are major catalysts of phase I biotransformation reactions
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monooxygenase
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Phase I type reactions
reduce a dioxgyen molecules into a OH group |
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Flavin-containing monooxygenase (FMO)
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Flavoprotein localized in SER
Catalyze monooxygenase reactions of soft nueclophiles Not a heme protein |
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Enzyme induction
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exposure to some drugs and environmental chemicals can markedly regulate enzyme amount and/or activity
usually transcriptional increase more enzyme=faster metabolism can increase or decrease drug effects |
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Enzyme inhibition
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drug or environmental chemical may inhibit the metabolism of several drugs
can have competitive or non-competitive ex: grapefruit juice |
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Pharmacogenetics
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genetically controlled variations in drug response
genetic factors that alter an individual's response to a drug |
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genotype
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an individual's composition at the gene level
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phenotype
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an individual's expression of their genotype
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genetic polymorphisms
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mendelian trait that exists in the population in at least two phenotypes neither of which is rare
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Single nuecleotide polymorphism
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a change in one single base pair in the DNA sequence that differs from the wild type or predominant sequence
may or may not result un an altered phenotype |
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haplotype
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refers to closely linked genetic markers on a chromosome that tend to be inherited together
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Halotype
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refers to a cluster of SNPs that occur together in an individual
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Autosomal co-dominance
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each allele contributes to the phenotype
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autosomal recessive
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wild-type allele has predominant effect
its takes 2 recessive alleles to see the effect |
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autosomal dominant
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a single allele predominates over the presence of other possible alleles
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x-linked inheritance
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genes inherited on X chromosome; all males will express these traits
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homozygous
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have 2 identical alleles
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heterozygous
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have 2 different alleles
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pharmacogenomics
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whole genome variation
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NAT-2 polymorphism
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N-acetyltransferase-2 is responsible for metabolism of the isoniazid
ppl with this see an increase in neurological side effects if given isoniazid, also see increase in bladder cancer, hypersensitivity to sulfonamides AR- for slow acetylators |
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CYP2D6 polymorphism
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ppl given debrisoquine experience severe hypotension
autosomal gene mutant allele in about 30% of patients 2-10% of patients are homozygous for slow metabolizer ultra fast metabolizers have a lot more normal gene CYP2D6 metabolizes 25% of prescription drugs- antidepressants |
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CYP2C19 polymorphism
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present in 3-20% of the population
affects anitconvulsants proton-pump inhibitors anti-platelets drugs |
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Phenytoin
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anticonvulsant affected by CYP2C19 polymorphism
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Omeprazole
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proton-pump inhibitor
patients with CYP2C19 polymorphism have better outcomes with this drug decreases the effectiveness of clopidogrel |
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Clopidogrel
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anti-platelet drugs
pts with one slow allele have less active drug and >50% increase in MI and stroke |
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CYP2C9 polymorphism
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2 predominant variants
metabolizes about 15% of drugs affects Warfarin metabolism *3 allele has a larger impact on warfarin clearance than *2 both decrease warfarin clearance, increase warfarin 1/2 life, increased risk of serious bleeding, need lower maintenance doses |
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Warfarin
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anticoagulant
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VKORCI polymorphism
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10 SNPs common
subunit of the vit. K epoxide reductase complez Warfarin blocks this complex FDA update prescribing info sheets to include this |
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A Clade
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haplotypes H1,2 require lower warfarin doses
associated with lower expression of VKORCI |
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B Clade
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need more drug
haplotypes H7,8,9 associated with higher expression of VKORCI more protein which binds more Warfarin |
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Pseudocholinesterase polymorphism
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causes a variant response to succinycholine
30-90% decrease in cholinesterase activity 1-6% of the population |
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succinylcholine
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depolarizing muscle relaxant used during surgery
usually cleared very quickly |
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TPMT polymorphism
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increased risk for life-threatening bone marrow suppression in cancer patients treated with thiopurine
low activity allele has 2 SNPs in the TPMT gene DNA testing recommended by the FDA 11% heterozygous |
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6-mercaptopurine
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thiopurine drug used in cancer treatment
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P-glycoprotein polymorphism
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result in increased net uptake of the cardiac glycoside digoxin
low expression alleles found in 16-57% of pts. Also affects: other drugs has positive effects for HIV drugs |
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digoxin
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drug that was used for heart failure
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Intracellular steroid Receptors
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AKA: nuclear receptors
receptors for small hydrophobic signaling molecules (steroid hormones, thyroid hormones) these receptors are intracellular and bind ligands in the cytoplasm of nucleus the receptors are ligand-activated transcriptional factors Have a hormone binding site, DNA binding domain and a transcription-activating domain. |
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Example of intracellular steroid receptor
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Activation of glucocorticoid receptor
1. cortisol is solublized by reversible binding to a carrier protein in blood 2. after release from the carrier protein, the hydrophobic signaling molecules diffuse through the plasma membrane 3. the signaling molecules bind to a specific receptor 4. subcellular localization of the receptors in the basal state is unclear hormone binding activates receptor by inducing conformational change 5. this conformation change releases the inhibitory proteins from the receptor 6. active receptor binds with high affinity to hormone response element 7. GRE located near the promoter of target gene |
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Membrane Receptors
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ion-channel
G-protein coupled enzyme linked |
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Ion channel linked receptors
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composed of multiple subunits
receptor directly gates ion channel major target for drugs rapid signaling ex: Nicotinic acetylcholine receptor and GABA Receptor gated Cl channels |
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Nicotinic acetylcholine receptor
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consists of 5 subunits
cation selective, excitatory located on NMJ,PNS,CNS converts acteylcholine binding into an electrical signal in the post-synpatic cell |
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GABA- receptor gated Cl channels
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main post-synaptic inhibitory neurotransmitter in CNS
regulate flux of Cl ex: Benzodiazepines, barbiturates,hypnotics, anesthesia |
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G-protein coupled receptors
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multi-component system
mediate the effects of neurotransmitters, light, odorants, hormones and other extracellular messengers is a single protein that passes through the membrane 7 times |
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Heterotrimeric G-proteins
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guanine nucleotide binding proteins
link the ligand-activated G-protein coupled receptor to effector enzymes the receptor provides specificity, it is a transduces and provides the catalytic component to generate the 2nd messenger cycles btwn. 2 states, GDP-bound inactive and GTP-bound active |
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Enzyme-linked receptors
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diverse group of receptors with different enzymatic activity
ex: tyrosine kinase, serine/threonine, protein phosphatase, and guanlyl cyclase |
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tyrosine kinase linked-receptors
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single protein with one transmembrane domain which dimerizes upon ligand binding or a tetramer composed of 2 extracellular subunits and 2 transmembrane subunits
the extracellular domain/subunits bind the ligand cytoplasmic domain has tyrosine-specific protein kinase activity, but can also bind tyrosine- specific protein kinases or proteins with other enzymatic activities Ligand binding leads to dimerization, activation by autophosphorylation, binding of intracellular signaling molecules regulate cell proliferation and differentiation in response to hormones and growth factors play an important role in onocogenesis |
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Intracellular signaling molecules
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Transcription factors
protein kinases protein phosphatases second messengers |
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Transcription factors
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DNA binding proteins that regulate transcription.
signal transduction cascades regulate many properties of transcription factors activated transcription factors induce transcription by activating RNA polymerase, resulting in transcription of mRNA from the target gene some transcription factors are activated when they are phosphorylated by protein kinase and inactivated when they are dephoshphorylated |
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Protein kinases
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catalyze the addition of phosphate group to side chain of a.a or proteins and peptides
classified according to the type of aa modified. |
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Protein phosphatases
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catalyze the cleavage of phosphate group from side chain of aa of protein and peptides
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second messengers
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small diffusible signaling molecules that are generated in response to ligand-receptor binding and activated other downstream signaling molecules
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cAMP
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2nd messenger
generated by adenyl cyclase which is activated by Galphas protein activates cAMP-dependent kinases |
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Diacylglycerol
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generated when phosphilpase C cleaves phosphatidylinsitol 4,5-bisphosphate into diacylglycerol and inositol triphosphate
activates protein kinase C |
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inositol triphosphate
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generated when phospholipase C cleaves PIP2 into DAG and IP3
binds IP3 receptors on the ER, causing release of calcium from the ER |
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Calcium
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generated by the opening of ion channesl
activate PKC and other protein kinases |
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Cyclic nucleotide pathways- Gaplha s
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cAMP regulated by GPCRs coupled to Gaplhas
1. ligand binds to receptor 2. Galphas binds GTP and dissociates from BetaGamma subunits of the G protein complex 3. Galphas-GTP activates adenylyl cyclase 4. adenyl cyclase converts ATP to cAMP 5.cAMP activates Protein kinase A 6. the C subunit of PKA phosphorylates specific proteins on serine and threonine residues 7. this phosphorylation results in activation or inactivation of of the phosphorylated protein 8. AMPLIFICATION OF THE SIGNAL |
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cAMP pathway regulated by Gaplhai
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opposite function of the stimulatory pathway and results in a decrease of cAMP and a decrease in PKA activity
GPCRs are different than the Gaplhas receptors |
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Phospholipid hydrolysis pathway- inositol-lipid pathway
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1. ligand binds and activates GPCR
2. G aphlaq binds CTP and dissociates from betagamma subunits 3.Gaq-GTP activates PLC 4.PLC cleaves PIP2 to generate IP3 and DAG 5. IP3 diffuses into the cytoplasms and releases Ca from the ER 6. Ca binds to calmodulin and activates Ca/calmodulin dependent kinase 7. DAG remains at the plasma membrane and together with Ca activates PKC |
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Monomeric G proteins
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AKA: small G proteins
are recruited to receptor- linked tyrosine kinases and turned on by GEF and turned off by GAP activated by direct interation with a GEF important in the MAP Kinase signaling pathway |
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GEF
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nucelotide exchange factor
EX: Sos |
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Sos
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a GEF
activates Ras, causes Ras to release its bound GDP and bind GTP |
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GAP
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GTPase-activating protein
turns off monomeric G-proteins |
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MAP Kinase signaling cascade
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A Map kinase kinase kinase phosphorylates a MAP kinase kinase, which then phosporylates a MAP kinase
the last MAP kinase then usually phosphorylates a transcription factor, leading to increased gene transcription |
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Ras
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a monomeric G protein
couples tyrosine-kinase linked receptors to the MAP kinase signaling cascade. |
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Pathway for Ras coupling the tyrosine-kinase linked receptors to the MAP kinase pathway
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1. ligand binds to tyrosine-linked receptor, which dimerizes and undergoes cross-autophosphorylation
2.receptor bind GRB2 3. GBR2 binds both the receptor and the guanine nucleotide exchange factor 3. SOS activates Ras by inducing Ras to release GDP and bind GTP 4.Ras-GTP activates the MAPKKK called Raf 5. Raf phoshphorylates Mkk1 6.MKK1 phosphorylates the MAPK, ERK 7. ERK phosphorylates several transcription factors, resulting in increased transcription of specific gene factors, resulting in increased gene transcription |
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Tyrosine kinase inhibitors
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Gefitinib and erlotinib
target the kinase domain of the epidermal growth factor receptor and inhibit signaling of the EGF receptor. decrease tumor burden in 80% of pts. |
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Adaptation
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modulation of signals is possible by adaptation in response to the intensity and frequency of stimulation
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Receptor mediated endocytosis
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regulates the number of receptors and may promote degradation of both the receptor and the ligand
1. in absence of ligands, receptors are not localized specifically 2. upon binding of ligands, receptors migrate to coated pits 3. vesicle pinches off and fuses with tubular-reticular structures termed CURL 4. most of the dissociated ligands incorporate into vesicles which fuse with lysozmes 5. free receptor in CURL may recirculate to cell membrane or be sequestered or degraded 6. internalized ligand never enters cytoplasm |
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Acetylcholine
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a neurotransmitter in both the PNS and CNS
Decreases HR, contractility, and conduction stimulates contraction of bronchiole sm and stimulates bronchial glands increase motility and tone in the GI, relaxes sphincters and increases secretions in the eye it causes ciliary muscle and sphincter muscle contraction and increases secretions from the lacrimal glands in the bladder it stimulates contraction of the detrusor and relaxes the sphincter and trigone causes an erection increases secretions from the pancreas |
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acetycholine synthesis storage and release
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choline is taken up into the nerve terminals via Na-dependent carrier (rate limiting step, blocked by hemicholinium)
choline acetyl transferase synthesizes acetylcholine from acteyl-coA and choline in nerve terminals aceylcholine is transported into vesicle by another transporter acteycholine is released into the synaptic cleft by exocytosis ( this is inhibited by botulinum toxin) |
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Norepinephrine
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is a catecholamine
increases HR,contractility, conduction and velocity in the heart constricts arterioles and blood vessels in the skeletal muscle (some dilation d/t Beta 2 receptors) and veins. bronch. smooth muscle relaxation decreases motility and tone in the gi, increases sphincter contraction and decreases secretions contracts the iris increases renin secretion relaxes the detrusor muscle and contracts the spincter increases ureter tone and motility causes ejaculation increases glycogenolysis and gluconeogenesis in liver and skeletal muscle |
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norepinephrine synthesis and release
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tyrosine-->dopa by tyrosine kinase (rate-limiting step blocked by alpha-methyltyrosine)-->dopamine-->norepinephrine
dopamine synthesized in the nerve terminals is transported into storage vesicles via the vesicular monoamine transporter where it is converted to norepinephrine, (blocked by reserpine) upon depolarization, granules fuse with the nerve terminal membrane and release NE into the synaptic cleft removed from the cleft by: reuptake by NET (87%) (blocked by cocaine), diffusion and uptake by the extraneuronal transporter |
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epinephrine
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another catecholamine
synthesized in the adrenal medulla |
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alpha-methyltryosine
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blocks tyrosine kinase
decreases the amount of NE and EPI releases |
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Resperine
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blocks the transport of dopamine into the vesicle by the VMAT2
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cocaine
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blocks the reuptake of NE
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hemicholinum
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blocks the rate-limiting step in acetylcholine synthesis
doesn't allow choline to be taken-up into the nerve terminals |
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botulinum toxin
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blocks vesicle fusion at the presynaptic cleft blocking acetylcholine release.
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Norepinephrine
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sympathetic NT
α1,α2,β1 Mainly α1 affects- peripheral vasoconstriction--> increases TPR to increase BP can cause reflex bradycardia used for shock |
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Epinephrine
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naturally occurring, synthesized in adrenal medulla
α1,α2,β1,β2 increases HR, contractility,CO increase systolic and decrease diastolic BP (dose-dependent) constriction of most vascular beds but dilation of skeletal muscle blood vessels (dose-dependent) net effect is to decrease TPR Bronchodilation - beta 2 receptor hyperglycemia lipolysis used for anaphylaxis, administered with local anesthetics to increase duration of action, bradyarrhythmias decreases conjunctival decongestion decrease hemorrhage |
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isoproterenol
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synthetic
beta1 (heart) and beta2 (skeletal muscle) receptors decreases peripheral resistance --> decreases diastolic P increases HR,contractility, CO--> increases systolic P decreases mean BP bronchodilation used to stimulate HR during bradycardia or heart block |
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dopamine
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naturally occurring NT
DA, beta and alpha1 low dose- vasodilation of renal and mesenteric arteries -->decrease peripheral resist (DA, alpha 1 R) medium dose-increase HR, Contractility and CO (Beta1) high dose- vasoconstriction and increase peripheral resistance (alpha1) used for acute heart failure, shock (cardiogenic or septic) |
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dobutamine
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synthetic catecholamine
fxns as beta 1 agonist b/c of large amine group increase cardiac rate, contractility and output minimal change in peripheral resistance and BP b/c not affecting Beta 2 or alpha receptor used for acute heart failure and cardiac stress testing |
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methyldopa
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pro-drug- metabolized in adrenergic nerve terminals to alphamethylnorephinephrine, which is stored in nerve terminal and released with stimulation
potent alpha 2 agonist, reduces sympathetic out-flow from the CNS used as an anti-hypertensive |
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phenylephrine
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acts only on alpha receptors
increases systolic and diastolic BP decreases HR decreases blood flow longer 1/2 life can be given orally tx: ophthalmic- mydriatic, decrease hemorrhage, conjuctival decongestion nasal decongestant used with local anesthetics to increase duration of action increase BP |
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Clonidine
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orally active
alpha2 adrenergic agonist used as anti-HTN (reduces BP by activation alpha 2 R in the CNS suppressing outflow of the sympathetic nervous system of the brain. |
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albuterol and terbutaline
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act mainly on beta2 adrenergic R
used for asthma- bronchodilator mainly used by inhalation but can be given orally side effect is increased HR |
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tyramine
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pure indirect-acting agent
not used as a drug releases NE from sympathetic nerves causing sympathomimetic actions found at high levels in certain foods (wines, beer, cheese) normally metabolized to inactive products by MAO. pts. already taking MAO inhibitors (anti-depressants) and this drug can have HTN crisis |
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amphetamine
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potent CNS stimulant
release NE from adrenergic neurons weak direct alpha and beta R agonist weakly blocks NET depresses appetite used for narcolepsy, ADD d-isomer is 3-4x more potent as CNS stimulant not degraded by MAO or catecholamine |
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ephedrine
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direct beta2 agonist and releases NE that activates alpha1 and beta1 R
used to treat asthma, but has been replaced b/c of its central effects some herbal preparation contain this, FDA has banned the sal of dietary supplement contain ephedra has 4 isomers |
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pseudoephedrine
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direct alpha1 agonist with beta 2 agonist activity (not effective for asthma)
less CNS stimulant used as nasal decongestant used as a precusor to illegally synthesize methamphetamine |
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side effects of ephedrine and pseudoephedrine
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throbbing headahce due to potent vasoconstriction- alpha
increased HR- beta pericardial pain -beta cardiac arrhythmias-beta cerebral hemorrhage- d/t increased systemic BP- alpha restlessness, anxiety- beta and alpha |
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guanadrel
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anti-hypertensive agent
taken into adrenergic nerves by NET only effects PNS, not the CNS major side effects- orthostatic hypotension interacts with cocaine, tricyclic anti-depressants |
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reserpine
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diffuses into adrenergic nerves
depletes nerves of NT by inhibiting vesicular monoamine transporter 2 responsible for sequestering dopamine into storage vesicles penetrates the CNS b/c its lipophilic historically used fro HTN side effects similar to guanethidine and also produce CNS depression and suicidal tendencies |
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Phenoxybenzamine
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a competitive irreversible antagonist
long duration of action produces vasodilation proportional to the degree of sympathetic tone |
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phentolamine
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shorter duration of action
block can be overcome by using agonist |
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clinical uses and side effects of phenoxybenzamine and phentolamine
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HTN (phentolamine- in combination with other agents)
peripheral vascular disorders- Reynaud's disease phenochromocytoma (tumor of adrenal gland) side effects: tachycardia and salt/water retention, orhtostatic hypotension |
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prazosin
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selective competitive blocker of alpha 1 R, reverisble
little blockade of pre-synaptic alpha2 R (therefore reflex tachycardia is less problematic) decreases vascular tone in resistance (arterioles) and capacitance (veins) produces favorable lipid profile, decrease LDH and increase HDL Major uses: hypertension, short term treatment for CHF,BPH side effects: first dose phenomenon- hypotension and syncope 30-90 mintues after first dose, persistent orthostatic hypotension and salt and water retention |
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propranolol
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competitive reversible blockade of beta1 and beta 2 R.
used for: HTN,angina, arrthymias d/t excessive catecholamines, acute MI,pheochromocytoma and migraine prophylaxis side effects: can induce heart failure, heart block, bronchospasm, blunt recognition of hypoglycemia and may delay recovery from insulin-induced hypoglycemia, withdrawal syndrome if stopped suddenly |
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timolol
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non-selective beta R antagonist
used for HTN and migraine prophylaxis and for wide angle glaucoma by decreasing aqueous humor formation by ciliary epithelium leading to decreased intraocular pressure. |
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metoprolol
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competitive, reversible beta R blocker
at low doses it is more selective for Bet1 R used for: HTN, angina, MI and CHF side effects similar to propranolol, less bronchodilation in lower lobes |
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esmolol
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moderately selective beta1 R antagonist
ultra-short acting, T 1/2= 10-20 minutes, quickly metabolized by plasma esterases in RBC used for emergency treatment of sinus tachycardia and atrial flutter. used when intubating patients. |
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labetalol
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competitive antagonist of alpha1 R and both beta R
used to treat essential HTN (oral) and hypertensive emergencies (IV) |
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carvedilol
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competitive antagonist of alpha1 R and beta R.
has anti-oxidant properties blocks L-type calcium channels at higher doses (vasodilator) used for chronic heart failure and hypertension reduces cardiovascular morality in pts. after MI |
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Adrenergic agonists-catecholamines
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NE
EPI ISOPROTERENOL DOPAMINE DOBUTAMINE METHYLDOPA |
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Adrenergic agonists-non-catecholamines
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phenylephrine
clonidine albuterol terbutaline |
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indirect acting adrengeric agonist only
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tyramine
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indirect acting adrengeric agonist- mixed
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amphetamine
ephedrine pseudoephedrine |
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Adrenergic antagonist-neuron blockers
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guanadrel
reserpine |
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Adrenergic antagonist- alpha receptor blockers
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phenoxybenzamine
phentolamine prazosin |
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Adrenergic antagonist- beta receptor blockers (non-selective)
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propranolol
timolol |
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adrenergic antagonist- beta receptor blockers (selective/ 2nd generation)
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metoprolol
esmolol |
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adrenergic antagonist- beta receptor blockers with additional CV effects (3rd generation)
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labetalol
carvedilol |
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location and effects of alpha 1 R
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eye-contraction of the radial muscle of iris
arteries-constriction veins-constriction GU smooth muscle (male)- constriction Vas Deferens- ejaculation |
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location of alpha 2 R and effects
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pre-synaptic nerve terminals- inhibition of NT release
CNS- inhibition of sympathetic outflow |
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location of beta 1 R and effects
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heart- increase HR, contractility and increase AV conduction
kidney-renin release |
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location of beta 2 R and effects
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arteries-dilation
bronchi-dilation skeletal muscle- glycogenolysis liver-glycogeneolysis and glucaneogenesis |
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location and effects of dopamine R
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kideny-dilation of kidney vasculature
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Lysergic Acid diethylamide (LSD)
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Potent hallucinogen
full or partial agonist at 5-HT2 receptors |
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Buspirone
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partial agonist at HT-1AR
used as antianxiety |
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Sumatriptan
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agonist at 5-HT1D receptor
used in treatment of migraine headaches, stops existing headaches. side effects include nausea, vomiting,angina,dizziness and flushing |
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Fluoxetine
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serotonin specific re-uptake inhibitor
used for affective disorders, OCD and panic attacks |
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Cyproheptadine
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5-HT2 R and Histamine antagonist
used for skin allergies (pruritis and urticaria) and carcinoid |
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Ondansetron
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dolasetron and granisetron 5-HT3R antagonists
very effective in treatment of chemotherapy induced nausea and vomitting acts on both GI and brain receptors IV an oral forms available |
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Alosetron
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selective 5-HT3 antagonist used to treat women with diarrhea predominant IBS who have failed to respond to conventional therapy. Can produce severe GI adverse effects. Restricted prescribing program must be followed.
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Bethanechol
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prototype muscarinic receptor agonist used for tx of postperative atony of gut or bladder and for xerostomia following head and neck radiation treatment; resistant to degradation by acteylcholinesterase
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pilocarpine
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tertiary amine with predominantly muscarinic effects
available orally to treat xerostomia used topically to treat wide angle glaucoma as well as emergency treatment for narrow angle glaucoma |
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Atropine
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blocks pilocarpine and bethanechol
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edrophonium
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reversible competitive enzyme inhibitor
rapid onset and short duration of action useful for the diagnosis of myasthenia gravis and for distinguishing myastehnic vs. cholinergic crisis used for reversal of paralysis by competitive neuromuscular blocking drugs |
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physostigmine
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alkaloid from calabar or ordeal bean
slowly reversible tertiary amine which can penetrate all cell membranes and this can have CNS effects used in the treatment of chronic wide angle glaucoma useful in the treating CNS effects of anitmuscarinic drug poisonings |
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sarin
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nerve gas
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malathion
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insecticide
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echothiophate
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organophosphate irreversible inhibitor to treat glaucoma
used topically with along duration of action long term used may be associated with formation of cataracts |
