1Pharmacodynamics
what the drug does to the body
-related to the mechanisms of action of a drug
-related to how a drug interacts with a target tissue
; altering the activity of a cell through interactions with receptor
; altering the activity of an enzyme
2What targets do drugs bind to?
-Some drugs directly to/in bacterial viruses
-Anticancer (to dna)
*most targets are protein structures: receptors on cell membranes*
-specifity (lock and key= fewer side effects)
-Endogenous substances (hormones, neurotransmitters)
-Receptor binding triggers a change within the cell or blocks receptor
36 major receptor types
-G protein (GPCR)
-Ion channels
-Nuclear receptors
-Enzymes (x2)
-Non enzyme JAK STAT
4G protein
eg: epinephrine
-stimulates g protein and second messenger systems= sypathominnetic stimulation
location: cell membrane
examples: NE, Ach, muscarinic receptor
*all water soluble!
5Ion channel
-inhibits depolarization+ no pain transduction
-most bind to voltage gated channels
Location: cell membrane
Drug examples: Ach on nicotine receptor, lidocane
6Nuclear Receptors
-Aka steroid receptors
-most bind in cytoplasm- charge cell
-function via DNA
location: cytoplasm, nucleus
drug examples:
-estrogen, corticosteroids, thryroid hormone
7Enzyme binding
2 types:
Intracellular enxymes
Transmembrane enzymes
8Intracellular enzymes
work inside the cell where they control cell metabolism (eg respiration).
9Transmembrane enzyes
eg: insulin membrane receptor- stimulates tyrosine lenase, activate cellular glucose uptake
10JAK-STAT signaling pathway
Signaling pathway activated by cytokines and some hormones, it provides one of the most direct routes from cell-surface receptors to gene regulation. In this pathway, cytosolic tyrosine kinases (JAKs) phosphorylate gene regulatory proteins (STATs)
*involves immunity, cell division, cell death and tumour formation
11Cytokine mediated signal
-interferons
-interleukins
-growth factors
12Intracellular transcription factors mediate
-cellular immunity
-proligeration
-apoptosis
-differentiation
14Stat-protein
Signal transducer and activator of transcription protein
15Drug response depends on:
- Receptor affinity
-Efficiancy= effectiveness
-Potency=strength
16Receptor affinity
-strength of binding/length of binding
-specific, saturable, reversible
17Efficiacy=effectiveness
-degree to which a drug induces maximum therapeutic effect
-how well it works
18Potency= strength
how much drug is required!
eg: drug a needs 20 mg
drug b needs 10 mg
drug b has a higher potency!
19Groundings:
-receptors
-ion channels
-enzymes
-transporters
20Receptors
-agonists
-antagonists
21Ion channels
-agonists
-antagonists
-allosteric modulators
-blockers
22Enzymes
-inhibitors
-inducers
23Transporters
-inhibitors
-relesors
24Agonists
-drug mimmics endogenous substance
-binds to receptors readily and produces very good effects
*Primary agonist*: extensively and successfully binds to existing receptor
25Partial agonist
-maximum response is smaller than that of a primary, even if all receptors are occupied
-lower efficacy
*In presence of a full agonist, partial acts as an antagonist!*
26Antagonist
-drug blocks receptor site to prevent endogenous or endogenous like substances from binding
-no effect other than to block others from binding!
*no effiacy*
27Receptor agonist
a drug that binds to a receptor and activates it
-sumatriptan
-miranes
serotonin
28Receptor antagonist
a drug that binds to a receptor and inhibits its function
-prpranolol: non selective
Ranitidine: histamine r. antagonist
29Transport inhibitor blocler
Fluoxetine: ssri, prozac transport blocker
Omeprozole: proton pump inhibitor for GED
30Channel agonist/opener
Flupritine: K+ channel opener, pain killer
Retigabin: K+ channel opener, antimusculant, epilepsy
31Channel antagonistlocker
Nifedipine: Ca_ channel blocker, use in BV dialation
Lidocaine: NA+ channel blocker, local anethesia (nerve)
32Enzyme activation
RO28-1675: glucose kinase activator
AICAR: protein lenase stimulatory; protects from cardiac ischemia
33Enzyme inhibitor
Atovastatin: competitive inhibitor for reductase
Aspirin: inactivates COX enzyme for prostaglandin and thrombosine synthesis
34allosteric modulators
Substances that bind to a cell receptor and alter the receptor's affinity for specific drugs; common allosteric modulators include guanine nucleotides, ammonium ions, calcium, and other divalent cations.
*many neurocognitive problems!*
35positive allosteric modulator
-parkinsons, dopamine agonists
-schizophrenia
36Negative allosteric modulators
-cns disorders, depression, cognitive, memory
37Pharmacodynamic variability
-median effective dose
-therapeutic index/window
-graded dose response relationship
-potency and efficiacy
38Interpatient variability- ED50
-dose where 50 percent of a population has desired therapeutic ranges
39Therapeutic index
the ratio between the toxic and therapeutic concentrations of a drug
40therapeutic index equation
LD50/ED50
41Graded dose-response relationship
Graphically visualizes differences in responses to medications in a single patient. Obtained by observing and measuring patient's response at different doses of the drug.
42Phase 1 GD response relationship
low doses, little change in response as dose increases- few receptors or enzymes affected; response minimal
43Phase 2 GD response relationship
Linear phase- sharp increase in response as dose is increased: more enzymeseceptors affected
*desired- achieves safe, therapeutic effect!*
44Phase 3 GD response relationship
-plateau phase- no change in response as dose increases: drug is bound to all receptors or enzymes or symptoms have all been alleviated: dose has no further effect
45Therapeutic window
-effective range of a drug (and the dose) without unacceptable toxicity
46Efficacy
-maximum intensity of response produces by a particular dose of drug
-drug with the greatest intensity of response has highest efficacy
47Potency
Amount of drug necessary to elicit a biologic effect; refers to the drug's strength