Pharmacology Chapter 19 Review Quiz Match Medication With Classification
Receptors are macromolecules involved in chemic signaling between and within cells; they may be located on the jail cell surface membrane or within the cytoplasm (meet table Some Types of Physiologic and Drug-Receptor Proteins Effect of Crumbling on Drug Response 
). Activated receptors directly or indirectly regulate cellular biochemical processes (eg, ion conductance, poly peptide phosphorylation, Dna transcription, enzymatic action).
A drug's ability to affect a given receptor is related to the drug'due south affinity (probability of the drug occupying a receptor at whatever given instant) and intrinsic efficacy (intrinsic action—degree to which a ligand activates receptors and leads to cellular response). A drug's affinity and action are adamant past its chemical structure.
The pharmacologic effect is besides determined past the duration of fourth dimension that the drug-receptor complex persists (residence fourth dimension). The lifetime of the drug-receptor circuitous is affected by dynamic processes (conformation changes) that command the rate of drug association and dissociation from the target. A longer residence time explains a prolonged pharmacologic effect. Drugs with long residence times include finasteride and darunavir. A longer residence fourth dimension tin be a potential disadvantage when it prolongs a drug'south toxicity. For some receptors, transient drug occupancy produces the desired pharmacologic event, whereas prolonged occupancy causes toxicity.
Physiologic functions (eg, contraction, secretion) are unremarkably regulated by multiple receptor-mediated mechanisms, and several steps (eg, receptor-coupling, multiple intracellular 2d messenger substances) may be interposed between the initial molecular drug–receptor interaction and ultimate tissue or organ response. Thus, several dissimilar drug molecules can often be used to produce the aforementioned desired response.
Ability to bind to a receptor is influenced by external factors equally well as by intracellular regulatory mechanisms. Baseline receptor density and the efficiency of stimulus-response mechanisms vary from tissue to tissue. Drugs, crumbling, genetic mutations, and disorders can increase (upregulate) or decrease (downregulate) the number and bounden analogousness of receptors. For example, clonidine downregulates alpha 2 receptors; thus, rapid withdrawal of clonidine can cause hypertensive crisis Hypertensive Emergencies A hypertensive emergency is severe hypertension with signs of damage to target organs (primarily the encephalon, cardiovascular system, and kidneys). Diagnosis is past blood pressure level (BP) measurement... read more . Chronic therapy with beta-blockers upregulates beta-receptor density; thus, severe hypertension or tachycardia can result from abrupt withdrawal. Receptor upregulation and downregulation bear upon adaptation to drugs (eg, desensitization, tachyphylaxis, tolerance, acquired resistance, postwithdrawal supersensitivity).
Ligands bind to precise molecular regions, called recognition sites, on receptor macromolecules. The bounden site for a drug may be the aforementioned as or dissimilar from that of an endogenous agonist (hormone or neurotransmitter). Agonists that bind to an adjacent site or a different site on a receptor are sometimes called allosteric agonists. Nonspecific drug bounden also occurs—ie, at molecular sites not designated as receptors (eg, plasma proteins). Drug bounden to such nonspecific sites, such every bit binding to serum proteins, prohibits the drug from binding to the receptor and thus inactivates the drug. Unbound drug is available to bind to receptors and thus accept an effect.
Agonists actuate receptors to produce the desired response. Conventional agonists increase the proportion of activated receptors. Inverse agonists stabilize the receptor in its inactive conformation and act similarly to competitive antagonists. Many hormones, neurotransmitters (eg, acetylcholine, histamine, norepinephrine ), and drugs (eg, morphine, phenylephrine, isoproterenol, benzodiazepines, barbiturates) human action as agonists.
Antagonists forbid receptor activation. Preventing activation has many effects. Antagonists increase cellular function if they block the activity of a substance that normally decreases cellular function. Antagonists decrease cellular function if they block the action of a substance that normally increases cellular office.
Receptor antagonists can be classified every bit reversible or irreversible. Reversible antagonists readily dissociate from their receptor; irreversible antagonists form a stable, permanent or near permanent chemical bond with their receptor (eg, by alkylation). Pseudo-irreversible antagonists slowly dissociate from their receptor.
In competitive antagonism, binding of the adversary to the receptor prevents binding of the agonist to the receptor.
In noncompetitive antagonism, agonist and antagonist can be bound simultaneously, merely antagonist binding reduces or prevents the action of the agonist.
In reversible competitive antagonism, agonist and antagonist form brusk-lasting bonds with the receptor, and a steady country among agonist, antagonist, and receptor is reached. Such antagonism can be overcome by increasing the concentration of the agonist. For instance, naloxone (an opioid receptor adversary that is structurally like to morphine), when given shortly before or later on morphine, blocks morphine'due south effects. Withal, competitive animosity by naloxone can be overcome by giving more than morphine.
Structural analogs of agonist molecules frequently take agonist and adversary properties; such drugs are chosen partial (low-efficacy) agonists, or agonist-antagonists. For example, pentazocine activates opioid receptors but blocks their activation by other opioids. Thus, pentazocine provides opioid effects but blunts the furnishings of another opioid if the opioid is given while pentazocine is still bound. A drug that acts as a fractional agonist in 1 tissue may deed as a total agonist in another.
Source: https://www.msdmanuals.com/professional/clinical-pharmacology/pharmacodynamics/drug%E2%80%93receptor-interactions
0 Response to "Pharmacology Chapter 19 Review Quiz Match Medication With Classification"
Post a Comment