Nothing Special   »   [go: up one dir, main page]
Scribd Logo
Upload

Welcome to Scribd!

  • 5 views

    5 - Pharmacodynamics I

    Uploaded by

    Chidera Emmanuel
    Vvb

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd

    5 - Pharmacodynamics I

    Uploaded by

    Chidera Emmanuel
    5 views11 pages
    Vvb

    Original Title

    5- Pharmacodynamics I

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    Vvb

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    5 views11 pages

    5 - Pharmacodynamics I

    Uploaded by

    Chidera Emmanuel
    Vvb

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    of 11

    Lecture (5)

    Pharmacodynamics I

    • Red : important
    • Black : in male / female slides
    • Pink : in girls slides only
    • Blue : in male slides only
    • Green : notes, Extra
    Editing File:
    https://docs.google.com/document/d/1W
    vdeC1atp7J-
    ZKWOUSukSLsEcosjZ0AqV4z2VcH2TA0/edi
    t?usp=sharing
    Objectives:

    • Identify different targets of drug


    action
    • Differentiate between their patterns
    of action ; agonism vs antagonism
    • Elaborate on drug binding to
    receptors
    What is Pharmacodynamics?
    Study of biochemical and physiological effects of drugs and
    their mechanism of action.

    Mechanism
    The mechanism of action Based on the drug target site:

    Receptor-mediated
    Non receptor-
    mechanism
    mediated
    (binding with
    mechanism:
    biomolecule):

    - Receptors=
    By chemical action: By physical action: E.g.
    Osmosis, purgative Biomolecules
    E.g. Neutralization of effect of MgSO4 =Target
    gastric acidity by (treatment of
    - Targets are mostly
    constipation)
    Antacids. protein in nature

    Where are receptors


    Receptor: a special target
    located?
    macromolecule that binds to
    • Cell membrane
    the drug to produce
    • Cytoplasm
    pharmacological actions.
    • Nucleus
    Receptor-mediated
    mechanism:
    Target = Receptor = protein
    Biomolecules = Site of action

    Structural
    Regulatory

    Binding forces between Drugs


    and Receptors:
    Receptors
    1. Ionic Bond
    2. Van-Dar-Waal
    3. Hydrogen Bond
    4. Covalent Bond
    Ion Channel
    1- STRUCTRAL:
    Tubulin: is target for drugs such as anticancer drugs and anti gout
    drugs. Tubulin is required for microtubules formation
    (cytoskeleton). Carrier molecule
    target for :
    Vincristine : Anticancer drug that kills cancerous cells by
    inhibiting microtubule formation and cell division.
    Colchicine : Anti gout drug binds to tubulin and inhibit Enzyme
    microtubule formation preventing neutrophil motility and
    decreasing inflammation
    2- REGULATORY: 1-ENZYMES:
    The drug competes with the natural substrate for the enzyme.
    E.g. Anticholinesterases inhibit acetyl cholinesterase thus producing cholinomimetic action.

    A- Reversible: Neostigmine reversibly B- Irreversible: Organophosphates


    competes with ACH for acetyl irreversibly competes with ACH for acetyl
    cholinesterase at motor end plate cholinesterase.
    (Effect lasts forever)
    (neuromuscular junction). (Effect lasts for
    short duration of time)

    2-ION CHANNEL:
    • Responsible for influx or out-flux of ions through cell membranes.
    • They are activated by alteration in action potential.
    • Drugs bind to alter channel function (opening or blockade) E.g.:

    A-Local Anesthetics: B-Sulfonylurea drugs (Antidiabetic drug):


    block sodium Na# influx through Block potassium K # channel in pancreatic
    # #
    Na channel in nerve fibers. (Na channel beta cells, resulting in depolarization and
    Blockers) opening of calcium channels and insulin
    secretion.
    3-CARRIER MOLECULES:
    Responsible for transport of ions and small organic molecules between intracellular
    compartments, through cell membranes or in extracellular fluids. The drug binds to such
    molecules altering their transport ability.

    A- Digoxin: B- Cocaine:
    blocks efflux of !"# via !"# /$ # pump blocks transport or reuptake of
    (Na# /K # -ATPase). catecholamines mainly Dopamine at
    Used in the treatment of heart failure. synaptic cleft. The dopamine transporter
    (drugs used for treatment of heart Failure can’t perform its reuptake function therefore
    increase the contraction of the heart) dopamine accumulates in the synaptic cleft
    producing Euphoria.
    Agonist Antagonist

    Is a drug that combines with the receptor and Is a drug that combines with the receptor
    elicit a response without producing a response (0) .
    E.g. Ach acts upon muscarinic receptors It blocks the action of the agonist.
    E.g. Atropine block the action of Ach on
    muscarinic receptors.
    Efficacy (intrinsic It has similar chemical structure to the Agonist.
    Affinity
    activity)

    Affinity BUT Efficacy (intrinsic


    Ability of the drug -Capacity of a drug receptor NO activity) = 0
    to combine with complex to produce action
    the receptor - Is the maximal response
    D+R -> D-R produced by a drug (E max)
    complex - The value ranges from 0 to 1

    Extra definitions found on girl’s slides only :

    Affinity is the capacity of a drug Efficacy(Intrinsic activity) the ability Antagonist having full affinity
    to form a complex with the of the drug once bound to the to the receptor but no
    receptor(DR complex) receptor to trigger response intrinsic activity
    Types of Agonist:
    Full Agonist Partial Agonist

    A drug that combines with its specific Combines with its receptor & evokes a
    receptor to produce maximal effect (1) response that’s submaximal effect (< 1)
    by increasing its concentration regardless of its concentration
    E.g. Ach E.g. pindolol
    Is a beta blocker which is a partial
    agonist, produces less decrease in heart Partial Agonist: Even though the
    Affinity HIGH Efficacy rate than pure antagonist such as drugs may combine with the same
    propranolol. number of receptors, the
    magnitude they can produce may
    Affinity PARTIAL Efficacy differ

    Extra definitions found on girl’s slides only :

    Full agonist having a full Partial agonist having a full


    affinity to the receptor affinity to the receptor but with
    and a maximal intrinsic low intrinsic activity
    activity
    SUMMARY
    Drug mechanism of action
    antiacids Neutralization of gastric acidity
    Neostigmine (cholinesterase inhibitor) competes with ACh for acetyl cholinesterase
    enzyme at motor end plate (neuromuscular
    junction).
    Sulphunylurea (anti diabetic) block K+ outflux via the K channels in pancreatic
    beta cells resulting in opening of calcium channels
    and insulin secretion.
    Digoxine ( drug of heart failure) blocks Na efflux via Na pump
    Cocaine blocks transport or reuptake of catecholamines
    (dopamine) at synaptic cleft
    vincristine Anticancer agent
    colchicine Drug for gout treatment
    Atropine (anticholinergic) a drug that combines with a receptor without
    producing responses. It blocks the action of the
    agonist
    Propranolol (Beta blocker) a partial agonist, produces less decrease in heart
    rate than pure antagonists
    QUIZ

    Q1/ Receptors are located on all of the following except:


    A- nucleus B- cell membrane C- ribosomes D- cytoplasm

    Q2/ Digoxin is a drug used for treatment of heart failure , its mechanism of action is:
    A- blocking Ca efflux B-Blocking K efflux C-Blocking Na efflux

    Q3/ Tubulin is a target for which of these drugs?

    A-Cocaine B- Colchicine C- Propranolol D- Digoxin

    Q4/ dopamine accumulation in the synaptic cleft produces:

    A- Heart contraction B-Euphoria C- Decreased heart rate

    Q5/ Efficacy = 1 when the drug is:

    A- Full Agonist B- Antagonist C- Partial Agonist

    1-C 2-C 3-B 4-B 5-A


    Good luck Thanks to the pharma team 435

    Girls team leader Boys team leader


    Nouf Alshammari Omar Alghadir
    Girls team members Boys team members
    Reema Almutawa Abdulaziz Alghamdi
    Njoud Almutairi Alwaleed Alzunaidi
    Najla Alkilani Abdulrahman Bedaiwi
    Shahad Althaqeb Mohsen Almutairi
    Shahad Alsahil Bader Aldhafeeri
    Deana Awartani Abdullah Alassaf
    Joud Alkhalifah Bassem Alkhuwaitir
    Reema Alserhani Nasser Almutawa
    Noura Almazrou Ziyad Alshareef
    Mohammed Alshehri

    You might also like