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Pharmacology > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q

What are the major endogenous neurotransmitters of the adrenergic system?

A

Catecholamines: dopamine, epinepherine and norepinepherine

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2
Q

What vital functions do catecholamines modulate?

A
  • rate and force of cardiac contraction
  • peripheral resistance
  • release of insuline
  • breakdown of fat
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3
Q

Why are drugs that target catecholamines clincally relevant?

A

Drugs that target the sythesis, storage, release, and reuptake of catecholamies and their receptors are frequent therapies for treatment of:

-hypertension, shock, depression, asthma, angina

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4
Q

What molecule is the base of catecholamines?

A

Tyrosine

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5
Q

Where is epinepherine primarily synthesized?

A
  • The adrenal medulla
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6
Q

Where is norepinepherine typically found?

A

In the sympathetic neurons. It is used as their typical neurotransmiter.

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7
Q

In the first step of catecholamine synthesis, tyrosine is converted to what compound? What enzyme mediates this transformation?

A

Tyrosine—-> dihydroxyphenylalanine (DOPA)

Tyrosine hydroxylase

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8
Q

What enzyme constitutes the rate limiting step in catecholamie synthesis?

A

Tyrosine hydroylase

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9
Q

In the third step of catecholamine synthesis, after DOPA is converted to dopamine, dopamine-beta-hydroxylase converts dopamine to what product?

A

Norepinepherine

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10
Q

How is norepinepherine converted to epinepherine?

A

It is methylated by phenylethanolamine N-methyltransferase. (PMNT)

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11
Q

How is dopamine transported into the synaptic vessicles to be converted?

A

By Vsicular monoamine transporter (VMAT)

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12
Q

Where o the signals that activate the sympathetic nervous system orriginate?

A

In the CNS, Specifically the limbic system.

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13
Q

What transmitter do preganglionic neurons use to actvate nAChRs?

A

ACh

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14
Q

What trigger vessicle release from the neurons?

A

Ca2+

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15
Q

What are the three (3) ways that catecholamie responses are terminated?

A
  1. reuptake of catechoamine into the presynaptic neuron
  2. metabolism of catecholamine
  3. diffusion of the catcholamine out of the synaptic cleft
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16
Q

What transporter mediates reuptake of catecholamines?

A

**Norepinepherine transporter (NET) **

~90% recycled

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17
Q

What are the two souces of catecholamine for release?

A
  1. Synthesized de novo
  2. recycled molecules
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18
Q

What 2 enzymes are involved in catecholamine metabolism?

A
  1. MAO
  2. Catechol-O-Methyltransferase (COMT)
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19
Q

MAO-A preferentially degrades ____(3)___, while MAO-B degrades ________ more rapidly than other catecholamines.

A
  1. serotonin, norepinepherine, dopamine
  2. dopamine
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20
Q

In which organ is COMT primarily expressed?

A

The liver

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21
Q

Monoamine oxygenases (MAOs) have efficacy in the treatment of what disorder?

A

Depression

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22
Q

What is the name of the receptor that is selective for norepinepherine and epinepherine?

A

Adrenoceptors (adrogenic receptors)

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23
Q

What is the location of Alpha1 recetors and what do they cause there?

A
  • Vascular smooth muscle (contraction)
  • genitourinary smooth muscle (contraction)
  • intestinal smooth muscle (relaxation)
  • heart (increase in excitability)
  • liver (Glycogenolysis and gluconeogenisis)
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24
Q

Alpha1 receptors involve Gq mediated pathways that cause increases in what?

A

IP3/DAG and intracellular Ca2+

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25
Q

When alpha2 receptors are activated, what G protein is activated? What is the result?

A

Inhibitory Gi protein is activated which causes a decrease in cAMP levels.

-inhibition of neuronal Ca2+ channels

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26
Q

Where are alpha2 receptors principally expressed and what does action here cause?

A

Pancreatic B-cells (Decrease insuline release)

Platelets (aggregation)

Nerves (Decrease in norepinepherine release)

Vasuclar smooth muscle (contraction)

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27
Q

What is the priciple treatment target of alpha2-antagonist at the CNS?

A

Hypertension

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28
Q

What are the primary locations and actions of the beta1 receptors?

A

Heart (increase in inotropy and conduction velocity)

Kidney (renin release)

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29
Q

What G protein is activated by all beta adrenoceptors?

A

Stimulatory Gs

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30
Q

What are the sites of the Beta2 adrenoceptor?

A
  • smooth muscle
  • liver
  • skeletal muscle
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31
Q

What is the action of the Beta2 adrenoceptor at the smooth muscle, liver and skeletal muscle?

A
  • SM–>relaxation
  • Liver–> glycogenolysis and gluconeogenisis
  • Skeletal Muscle–> Glycogenolysis and K+ uptake
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32
Q

What is the location of Beta3 adrenoceptors?

A

Adipocytes

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33
Q

What is the action of activation of Beta3 adrenoceptors and what is the significance of this?

A
  • Stimulation leads to an increase in lipolysis
  • may be used to treat obesity, non-insuline dependant diabetes mellitus
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34
Q

How do G protein receptor kinases reguate adrenoceptor responses?

A

-phosphorylates the G protein which can then bind inhibitory proteins

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35
Q

What is the action of B-arrestin?

A

-binds to the phosphorylated G-protein and deactivates it through steric hinderance

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36
Q

What is the process of down regulation?

A

-receptor-b arrestin complexes are endocytosed in a clathrin-dependant manner

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37
Q

What receptors does epinepherine primarily act at in low concentrations?

A

Beta1 and Beta2 adrenoceptors

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38
Q

What are the physiologic effects of epinepherine acting at Beta1 adrenoceptors?

A
  • increases in cardiac contractility and O2 consumption
  • increase in systolic BP
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39
Q

What are the physiologic effect of epinepherine acting at Beta2 adrenoceptors?

A
  • Relaxes bronchial smooth muscle
  • decreases diastolic BP
  • Vasodilitation
  • release of glucose and fatty acids
40
Q

What is the drug of choice for the treatment of anaphylaxis?

A

Epinepherine

41
Q

Why is norepinepherine the drug of choice for treatment of hypotension and shock?

A

Because NE acts at alpha1 and beta1 adrenoceptors but not at Beta2.

-This means that it increase systolic and diastolic BP and increases TPR

42
Q

At which receptors does dopamine act when in low concentrations? What is the result?

A

Acts at D1 Receptors in renal, mesenteric and coronary vascular beds–> Increases cAMP

-vasodilitation

43
Q

Where does dopamine act at an intermediate does?

A

Beta1 adrenoceptors

44
Q

What is the action of dopamine at doses higher than 10micrograms/kg?

A

Acts at alpha1 adrenoceptors where it causes vasoconstriction.

45
Q

What drug is an example of a catecholamine synthesis inhibitor?

A

-alpha-methyltyrosine

46
Q

What is the MOA of alpha-methyltyrosine and why is it not widely used?

A
  • Inhibits tyrosine hydroxylase
  • causes severe orthostatic hypotension and sedation
  • inhibits all catecholamine sythesis
47
Q

What are examples of inhibitors of catecholamine storage?

A
  • Reserpine
  • Tyramine
  • Guanethidine
  • Amphetamine
  • Ephedrine/Pseudoephedrine
  • Methylphenidate
  • Methamphetamine
48
Q

What is the MOA of Reserpine?

A
  • Reserpine binds to and inhibits VMAT.
  • at high concentrations it causes neurotransmitter leakage into the synapse and a trasient Sympathomimetic effect.
  • recovery takes days to weeks–>depression
49
Q

What foods contain lots of Tyramine?

A

-Wine and aged cheese

50
Q

How is Tyramine able to cause acute hypertensive crisis?

A
  • In pateints taking MAOIs, Tyramine builds up in synaptic vesicles, replacing norepinepherine.
  • NE spills over into the cleft causing hypertension
51
Q

What is the long term effect of Tyramine exposure in the presence of an MAOI?

A
  • Replacement of noepinepherine with octopamine
  • Postural hypotension
52
Q

What is the mechaism of Guanethidine?

A
  • Same as tyramine
  • Into vesicles via NET and reduces amount of norepinepherin available
  • postural hypotension and decreased cardiac preload
53
Q

What are the three ways by which amphetamine affects the storage of catecholamines?

A
  1. displaces endogenous catecholamine
  2. inhibits MAO
  3. blocks catecholamine reuptake by NET
54
Q

What is amphetamine used to treat?

A

depression

55
Q

What are the medical uses of ephedrine and pseudoephedrine?

A
  • Ephedrine: persistant hypotension
  • Pseudoephedrine: over the counter decongestant
56
Q

What is the major use of methylphenidate?

A

-treatment of ADHD

57
Q

What is the major use of Methamphetamine?

A

-Drug of abuse

58
Q

What is the major mechanism of action of inhibitors of catecholamine reuptake?

A

-Exert powerful sympathomimetic effects by prolonging the time a neurotransmitter remains in the synaptic cleft.

59
Q

What enzyme does cocain inhibit?

A

NET

60
Q

What is the action of Tricyclic antidepressants (TCAs)?

A

-inhibit NET mediated reuptake of norepinepherine

61
Q

What is the acion of an MAOI and what are they used to treat?

A
  • Inhibits the metabolism of catecholamines in the synaptic cleft
  • elogates their action
  • treats depression
62
Q

What is an example of a selective and non-selective MAOI?

A
  • Phenelzine (non-slelective)
  • Selegiline (selective for MAO-B)
63
Q

What is the primary action of alpha1 agonists?

A

-Maintain or elevate blood pressure

64
Q

What is the clinical use of methoxamine?

A
  • alpha1 agonist
  • treatment of shock
65
Q

What are the uses of phenylepherine and oxymetazoline?

A

-topical use for nasal congestion

66
Q

What receptor does Clonidine act at? What is it’s use?

A
  • Alpha2 receptors
  • used to treat withdrawl from ethanol and opioid drugs
67
Q

What are the clinical effects of guanficine?

A

-Similar to clonidine

68
Q

What is important clinical effect of the alpha2 agonist dexmedetomidine?

A
  • sedates surgical patients while stabilizing their BP
  • does not depress breathing
69
Q

What is the MOA of alpha-methyldopa? What is a noteworthy use?

A
  • alpha2 agonist–> lowers BP
  • Treats hypertension in pregnant women
70
Q

What are the uses of Beta (B1 and B2) receptor agonists?

A

B1- causes increase in heart rate and force of contraction leadin to increased cardiac output

B2- causes relaxtion of vascular, bronchial, and GI smooth muscle

71
Q

How does isoproterenol affect beta1 and beta2 actions?

A
  • Lowers TPR and diastolic BP (beta1)
  • Systolic BP remains unchanged (beta2)
72
Q

What is a use of isoproterenol?

A

-emergency situations to treat prfound bradycardia

73
Q

What is the receptor and action of dobutamine?

A
  • Beta1 agonist
  • increases cardiac contractility and output (treats severe heart failure)
74
Q

What two drugs are beta2 agonists that are used to treat asthma?

A

-Terbutaline and albuterol

75
Q

What is an example of a long acting Beta2 agonist?

A

-Salmeterol

76
Q

What is the result of the use of an Alpha-adrenergic antagonist?

A
  • vasodilitation, decreased blood pressure, decreased periferal resistance.
  • leads in increase in cadiac output reflex
77
Q

What is the significance of phenoxybenzamine?

A

-alkylating agent the blocks both Alpha1 and Alpha2 receptors irreversibly.

78
Q

What is Phentolamine used to treat?

A
  • Hypertension.
  • Non-selective alpha antagonist
79
Q

What are 3 Alpha1 selective antagonists used to treat hypertension?

A
  • Prazosin
  • Terazosin
  • Doxazosin
80
Q

What is different between Terazosin/Doxazosin and prazosin?

A

-Terazosin and Doxazosin are longer acting

81
Q

What is the drug of choice for treatment of genitourinary issues in BPH? What receptor?

A
  • Tamulosin
  • Binds to Alpha1A receptors
82
Q

What is the result of a Beta1 blockade (beta1 receptor antagonist)?

A

-decrease in HR and myocardial contractility

83
Q

What is the net result in an Alpha1 blockade?

A

decreased TPR

84
Q

What is the clincal significant of a Beta2 blockade?

A

-can cause life threstening bronchial constriction in patients with asthma

85
Q

Is Propranolol a B1 or B2 receptor antagonist?

A

-both (nonselective)

86
Q

What is the clinical use of propranolol?

A
  • Treatment of HTN and angina
  • Contraindicated in Asthma patients but not COPD
87
Q

What receptors are blocked by Carvedilol, and what is its clinical use?

A
  • Blocks Alpha1, Beta1, Beta2
  • Management of heart failure with decreased systolic function.
88
Q

What is the name of the partial Beta1 and Beta2 agonist used to treat hypertension?

A

-Pindalol

89
Q

What is the name of a partial Beta1 agonist used to treat HTN?

A

Acebutolol

90
Q

What is the MOA and usage of Esmolol?

A
  • Beta1 selective antagonist
  • short half life—> safer for more unstable patients
91
Q

What is the mechanism of Alpha1 selective agonists?

A

-Activate alpha1 adrenergic receptors to increase peripheral vascular resistance

92
Q

What are some side effects of Alpha1 receptor agonists?

A
  • Bradycardia (vagal relfex), and cadiac arrhythmias
  • hypertension
  • anxiety
93
Q

What is the mechaism of an alpha2 andrenergic receptor?

A

inhibit sympathetic outflow

94
Q

What are common alpha2 agonist side effects?

A

Bradycardia, constipation, xerostomia, seation, hypotension

95
Q

Side effects of beta-adrenergic agonist

A

tremors, bradycardia, asthma attack

96
Q

Side effects of alpa-adrenergic antagonist

A
  • anything with low BP
  • hypotension, dizzyness, sedation, nasal congestion, urnary frequency (Alpha1A)
97
Q

Side effects of Beta-adrenergic antaognists

A

broncospasm, hypoglycemia

Pharmacology (17 decks)

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