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Nurse Anesthesia Pharm I > Receptors > Flashcards

Receptors Flashcards

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1
Q

What is a receptor?

A

It is a specific protein that is the site for binding of a signaling molecule.

  • Can also be: Enzymes, Na+, K+ ATPase pump, nucleic acids
  • Two types
    • Transmembrane
    • Intracellular (some nucleic)
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2
Q

Ligand

A

Is a compound that is specific fo each receptor

  • Activates the receptor causing biological response
  • Endogenous substances
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3
Q

Agonist

A

A compound that binds to a receptor causing activation and EXPECTED effect

  • Effect can be natural or synthetic
  • Two main types:
    • Full
    • Partial
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4
Q

Partial Agonist

A

A drug that binds to a receptor (usually at agonist site) that activates the receptor, but not as much as a full agonist.

  • When a partial agonist is administered with a full agonist, drug effect of full agonist is decreased
  • Partial agonist can have antagonistic activity: agonist- antagonist
  • Occupy the same number of receptors as full agonist, but effect is decreased
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5
Q

Inverse Agonist

A

A compound that binds to the receptor creating OPPOSITE of expected effect

  • Binds to same sites as agonist (competing with it)
  • “Turns off” activity of the receptor

*It is NOT an ANTAGONIST

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6
Q

Antagonist

A

A compound that when bound to a receptor causes INACTIVATION, preventing expected (normal) response.

  • Usually reversible
  • Two Types:
    • Competitive
    • Noncompetitive
      • When ligand is bound
  • Interact with receptor but DO NOT CHANGE receptor
  • Have affinity but NO EFFICACY
  • Block the action of other drugs
  • Effect observed ONLY IN THE PRESENCE OF AGONIST
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7
Q

Competitive Antagonist

A

COMPETES with AGONIST for receptor binding sites

  • Concentration and receptor affinity affect response
  • Can reverse the effects of ANtagonist with large dose of AGONIST
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8
Q

Noncompetitive Antagonist

A

Binds to receptor at DISCRETE SITES [allosteric] (different from Agonist) and alters maximal response

  • Partial Response: Decreases maximum efficacy of drug
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9
Q

Receptor States

A

Multiple receptors in the cell and they change in number

  • Not all receptors are active or inactive
  1. Agonist–Fully Active
  2. Partial Agonist–Some Active
  3. Antagonist–Changes balance so receptor is inactive
    • “active” but blocked
  4. Inverse Agonist–Favors inverse of full agonist
    • acts as antagonist
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10
Q

Agonists

vs

Antagonists

A

AGONIST:

Enzyme activation/Inhibition

Ion channel modulation

DNA transcription

ANTAGONIST:

Effect of Agonist blocked

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11
Q

Non-Polar Molecule

A

A molecule that has a neutral charge; no net positive or negative charge

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12
Q

Polar Molecule

A
  • Do not have a net charge, but certain regions have partial negative and positive charge
    • Soluable in H2O–water is polar
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13
Q

Occurs in the absence of a ligand. Cell will increase the number of receptors in an attempt to sense missing ligand

A

Up-Regulation

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14
Q

Occurs with increase stimulation by a ligand. Cell will reduce the number of receptors specific to that ligand.

A

Down-Regulation

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15
Q

Name the four types of cell receptors.

A
  1. Ion channel linked
  2. G-protein coupled
  3. Intrinsic enzyme linked
  4. Intracellular
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16
Q
  • Respond to fast neurotransmitters such as Ach.
  • Nicotinic and glutamate receptors (Excitatory)
  • GABAa and glycine receptors (Inhibitory)
A

Ligand-gated Ion Channel

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17
Q
  • Present in the membranes of excitable nerves, cardiac, and skeletal muscle cells
  • Open/Close in response to voltage changes in cell
  • Named for ion permeability
  • Play an important role in muscle contraction/propagation of action potentials
  • Some excitatory, some inhibitory
  • Local anesthetics bind to the intracellular domain of this receptor
A

Voltage-gated ion Channel

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18
Q
  • Cellular response illicited with these receptors through protein that stimulates an increase or decrease in protein synthesis. (Ex: Catecholamines)
  • Most numerous receptor type
  • Contains three subunits that influence enzyme activity and ion channels
A

G-Protein Coupled Receptors

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19
Q
  • Subunit that stimulates, increases adenylcyclase, makes cAMP from ATP.
    • cAMP is important 2nd messenger
A

Gs

Protein Subunit

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20
Q
  • Subunit that inhibits Adenylcyclase
A

G<span>i</span>

Protein Subunit

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21
Q
  • Activates phospholipase C, increasing DAG and IP3, which increases Ca2+ from cells
A

Gq

Protein Subunit

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22
Q

Prolonged exposure of a receptor to an agonist causing subsequent dosing with agonist to produce reduced maximal effects.

–Barash Chpt 11, pg 254

A

Desensitization

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23
Q

Prolonged exposure of receptors to antagonist.

Can occur with long term use of beta-blockers and abrupt discontinuation.

A

Hypersensitization

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24
Q
  • Associated with sypathetic response of the autonomic nervous system (ANS)
  • Located in CNS and peripheral tissues
  • Characterized by neurotransmitter response
    • Epi, Norepi, Dopamine
  • Largely excitatory response; Fight or Flight
A

Adrenergic Receptor

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25
Q

Name the three major subtypes of Adrenergic Receptors.

A
  1. Alpha
  2. Beta (ß)
  3. Dopaminergic (D or DA)
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26
Q
  • Receptors located in vascular smooth mm, GU smooth mm, the liver, and CNS post-synaptically (excitatory)
  • Activation causes contsriction of smooth mm (vasoconstriction) and positive inotropism in the myocardium
  • GPCR
    • Gq subunit - activates phospolipase C, increasing DAG and IP3
A

Alpha-1

Adrenergic Receptors

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27
Q

Alpha-1 Adrenergic

Agonists

A
  • Phenylepherine, Norepinepherine, Epinepherine, Dopamine
  • Causes smooth mm contraction, vasoconstriction, antidiuresis; increases IP3 and DAG
28
Q

Alpha-1 Adrenergic ANtagonists

A
  • Phenoxybenzamine, phentolamine (Regitine-used as a “reversal” for Epi, NE infiltration in PIV), Labetalol, Doxazosin (Cardura), Prazosin (Minipress)
  • Vasodilation, relaxation of smooth mm
29
Q
  • Receptors located in pancreatic islet (ß) cells, platelets, nerve terminals, CNS, and vascular smooth mm
  • Presynaptic activation decreases cAMP which inhibits NE release, resulting in decreased SVR, decreased CO, decreased inotropism, and decreased HR
  • Postsynaptic activation causes vasoconstriction and platelet aggregation
  • GPCR
    • Gi subunit - Inhibits adenylate cyclase, Ca+ and K<span>+</span> ion channels.
A

Alpha-2

Adrenergic Receptors

30
Q

Alpha-2 Adrenergic

Agonists

A
  • Clonidine, NorEpi, Epi, Phenylepherine
  • Presynaptically: Clonidine; dexmedetomidine (Precedex)
    • Reduced Peripheral Vascular Resistance (PVR)
    • Inhibit release of NorEpi
    • CNS depression, Sedation
  • Postsynaptically: NorEpi, Phenylepherine, Epi
    • Vasoconstriction
    • Inhibition of insulin release, decreased GI motility, inhibition of ADH, platelet aggregation
31
Q

Alpha-2 Adrenergic

Antagonists

A
  • Rarely used medically
  • Similar to Alpha-1 Antagonists-inhibit release of NE
32
Q
  • Receptors located in the heart (SA node, myocardium, ventricular conduction system) and renal juxtaglomerular cells
  • Activation increases cAMP
    • Increased HR, positive inotropic and chronotropic effects, renal renin release, relaxed coronaries
  • Postsynaptic, sensitive to NE and Epi equally
  • GPCR
    • Gs subunit - stimulates adenylate cyclase and Ca+ ion channels
A

Beta (ß)-1

Adrenergic Receptors

33
Q

Beta (ß)-1 Adrenergic Agonists

A
  • Isoproterenol, Epi, NorEpi, Dopamine, Dobutamine
  • Increased HR, Increase contractility
34
Q

Beta (ß)-1 Adrenergic Antagonists

A
  • Commonly called “Beta-Blockers”
    • Sudden cessation can elicit rebound tachycardia and myocardial ischemia r/t upregluation of B-1 receptors
  • Metoprolol, Propanolol, Esmolol
  • Postsynaptic: Vasodilation, decreased HR, decrease inotropy
35
Q
  • Receptor located:
    • presynaptically in the myocardium and SA node
    • postsynaptically in vascular, bronchial, GI, and GU smooth mm
  • Activation increases cAMP:
    • Sensitive to NE presynaptically:
      • ​ constriction, accelerated NE release
    • Epi postsynaptically:
      • ​Positive inotropism, chronotriopism, dialation of smooth mm
  • Gs subunit - Stimulates adenylate cyclase and Ca+ ion channels
A

Beta (ß)-2 Adrenergic Receptor

36
Q

Beta (ß)-2 Adrenergic Agonists

A
  • Commonly used for bronchodilatory effects
  • Isoproterenol (used for bronchospasm during anesthesia), Albuterol (SABA), Epi, NE, Dopamine
    • Presynaptic: Increased HR, accelerates NE release
      ​
    • Postsynaptic: Vasodilation, bronchodilation, Gi and GU relaxation, uterine relaxation, insulin secretion, amylase secretion
37
Q

Beta (ß)-2 Adrenergic Antagonists

A
  • ß2 receptors are typically antagonized with nonselective ß1 Blockers
  • Butoxamine (selective–used primarly in experimentation to identify ß2 receptors), Propanolol, Alprenolol (antihypertensive/angina med; older med), Esmolol, Nadolol, Timolol, Labetolol
  • small degree of peripheral vascular bed vasoconstriction occurs with selective antagonism
38
Q
  • Receptors located within the CNS, vascular smooth mm, kidneys, and postganglionic sympathetic nerves
  • Has 5 subtypes, two of which are predominant
  • GPCR
A

Dopaminergic Receptors

39
Q
  • Receptors located in vascular smooth mm, renal and mesentery BV, rental tubules, juxtaglomerular cells, and sypathetic ganglia
    • Similar in structure to subtype 5, but located in different areas.
  • Activation increases cAMP:
    • Postsynaptic:
      • Vasodilation, diuresis, renin release, sodium excretion, minor inhibition of sypathetic ganglial nerves
  • GPCR
    • Gs subunit - stimulates adenylate cyclase and Ca+ ion channels
A

Dopamine (DA,D)1

Receptor

40
Q

DA1

Agonists

A
  • Fenoldopam, Dopamine, Epi
  • Vasodilation, diuresis, nausea, vomiting, dizziness
41
Q

DA1

Antagonist

A
  • Haloperidol, Droperidol, Phenothiazines (Thorazine), Metoclopramide (Reglan)
  • Relief of n/v (Reglan, Haloperidol, Droperidol), increased gastric motility (Reglan), mesenteric smooth mm constriction,
42
Q
  • Receptor located in presynaptic postganglionic sympathetic nerves and postsynaptic renal and mesenteric vascular smooth mm.
    • Similar in structure to subtypes 3 and 4
  • Activation decreases cAMP
    • Presynaptic: inhibition of NE, secondary vasodilation
    • Postsynaptic: vasoconstriction, inhibition of aldosterone relase from adrenal cortex
  • GPCR
    • Gi subunit - inhibits adenylate cyclase, Ca+ and K+ ion channels
A

Dopamine (DA,D)2

Receptor

43
Q

DA2

Agonists

A
  • Dopamine, Bromocriptine
  • Presynaptic:
    • Inhibition of NE release, secondary vasodilation
  • Postsynaptic:
    • Vasoconstriction of renal and mesenteric vasculature
44
Q

DA2

Antagonists

A
  • Domperidone
  • GI prokinesis, prolactin release, antiemetic effects
45
Q
  • Associated with the parasympathetic region of the CNS, Rest and Digest
  • Has excitatory and inbitory,
  • Two main types:
    • Nicotinic
    • Muscarinic
A

Cholinergic Receptors

46
Q
  • Ligand-gated ion channel receptors
  • Two subtypes
    • ​m - found in postsynaptic skeletal neuromuscular junction
    • n - found in the autonomic ganglia (postganglionic; ANS) and adrenal medulla
  • Activated by Acetycholine, opening Na+ and K+ depolarizing ion channel
    • ​action mediated by ion
A

Nicotinic Cholinergic Receptor

47
Q

Nicotinic

Agonists

A
  • Acetycholine, Nicotine
    • Nn and Nm
  • Succinylcholine
    • Nm : depolarizing NMB, opens ligand ion channel, depolarizing and inhibiting neurotranmission
48
Q

Nicotinic

Antagonists

A
  • Nn
    • Dextromethorphan
    • Trimethaphan - inhibits sympathetic and parasympathetic autonomic activity, used for BP control in aortic dissection
      • vasodilation
  • Nm
    • Vecuronium - competitive antagonist, blocks Ach at the NM junction; muscle relaxation, paralysis.
    • Rocuronium, Cisatracurium (Nimbex)
49
Q
  • G-protein coupled receptor
  • Has 5 subtypes
    • 1,3,5 - Gq subunit: activates Phospholipase C, increasing DAG and IP3
      • 1 - present in CNS, autonomic ganglia, glands (salivary, gastric), enteric GI nerves
      • 3 - present in CNS, smooth mm, and glands
      • 5 - low levels in CNS, associated with Dopamine neurons
    • 2, 4 - Gi subunit: inhibits adenylate cyclase
      • 2 - present in CNS, heart, smooth mm, and autonomic nerve terminals
      • 4 - present in CNS, forebrain
A

Muscarinic Cholinergic Receptors

50
Q

Muscarinic

Agonists

A
  • Acetycholine
  • Muscarine
    • Toxic compound in mushrooms
  • Increased salivation, gastric secretions (M1), decreased HR and atrial contractility (M2), smooth mm contraction, emesis (M3)
51
Q

Muscarinic

Antagonists

A
  • Scopolamine
    • antiemetic properties, reduces secretions
  • Atropine
    • broad antagonist
    • reduces secretions, increases HR and atrial contractility
52
Q
  • Two main types of these receptors
    • A type - found primarily in the CNS
    • B type - found mainly in peripheral tissue
  • Postsynaptic inhibitory receptor
    • ​A type - CNS depression
    • B type - skeletal muscle relaxation
  • GPCR
A

GABA receptors

53
Q

GABAA

Agonists

A
  • Act on GABAA receptor through potentiation, direct gating and inhibition
    • Benzodiazepines
    • Propofol
    • Etomidate
    • volitile anesthetics
    • anesthetic steroids
54
Q

GABAA

Antagonists

A
  • Flumazenil (Romazicon) - competative antagonist
55
Q

GABAB

Agonists

A
  • Baclofen
    • antispasmotic
    • peripheral smooth mm relaxant
56
Q

GABAB

Antagonists

A
  • Saclofen
    • competative antagonist
    • used in research
57
Q
  • a member of the Serotonin receptor family
  • ligand gated ion channel receptor
  • targeted for the management of drug induced n/v
    • antiemetics (Zofran) antagonize
      • can potentiate a midgraine; migraine meds are serotonin receptor agonists
    • agonized response n/v
A

5-HT3 Serotonin Receptor

58
Q
  • Receptors located on nerve endings of sensory neurons in spinal cord and in the brain on descending neurons
  • Three types
    • Mu
    • Kappa
    • Delta
  • When activated, decending neurons release NE and 5HT, the release of Substance P and glutamate is reduced creating less neurotranmission to brain = brain interprets less pain
  • GPCR
    • Gi subunit - inhibition of adenylate cyclase, reduction of cAMP
A

Opioid Receptors

59
Q
  • Has different subtypes
    • subtype 2 associated with physical dependence
  • Responsible for analgesia in spinal and supraspinal areas
    • specifically substantia gelatinosa in posterior horn of spinal cord
    • brain areas responsible for pain interpretation
  • Most lipophilic receptor
  • Activation elicits:
    • Analgesia, euphoria, miosis, bradycardia, hypothermia, urinary retention, depression of ventilation, constipation
A

Mu

Opioid Receptor

(MOR)

60
Q

Mu

Agonists

A
  • Endorphins, Morphine, Synthetic opioids
  • Analgesic effect, euphoria, miosis, bradycardia, hypothermia, urinary retention, decreased GI motility (Mu2), respiratory depression (Mu2), physical dependence (Mu2)
61
Q
  • Responsible for analgesia spinal and supraspinal
    • dorsal horn of spinal cord
    • same areas as Mu
  • Activation results in inhibition of neurotransmitter release via N-type Ca+ ion channels.
    • Analgesia, sedation, dysphoria, miosis, diuresis, low abuse potential
  • Opioid agonist-antagonists act principally on this receptor
  • Extensive research conducted on antagonists to combat addiction
A

Kappa

Opioid Receptor

(KOR)

62
Q

Kappa

Agonists

A
  • Dynorphins
    • endogenous opioid peptide
  • Analgesic effect spinal, supraspinal, dysphoria, sedation, pupillary constriction, diuresis, low abuse potential
63
Q
  • Responsible for supraspinal and spinal analgesia
  • No current drugs on the market targeting receptor
  • Respond to endogenous ligands: enkephalins
  • May modulate activity of Mu receptors
  • Activation causes modulation of hormone and neurotransmitter release:
    • Analgesia, respiratory depression, physical dependence, mild constipation, urinary retention
A

Delta

Opioid Receptor

(DOR)

64
Q

Delta

Agonists

A
  • Enkephalins
    • No drugs on market
  • Spinal and supraspinal analgesia, moderation of Mu receptors, respiratory depression, mild constipation, urinary retention, physical dependence
65
Q

Opioid Receptor

(MOR, KOR, DOR)

Antagonists

A
  • Naloxone (Narcan)
    • Competative antagonist
    • increases sympathetic nervous system activity
      • tachypnea, tachycardia, hypertension, nausea, vomiting, sudden perception of pain
  • Naltrexone
    • similar to Naloxone, but has sustained antagonism up to 24h
    • reduces euphoric effect
    • highly effective orally
  • Nalmefene
    • pure opioid antagonist
    • analogue of naltrexone
    • same potency as Naloxone
  • Methylnaltrexone
    • active at peripheral opioid receptors
    • ionized, does not cross blood-brain barrier

Nurse Anesthesia Pharm I (1 decks)

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