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PDA > PDA Exam 5 > Flashcards

PDA Exam 5 Flashcards

1
Q
  • What’s a catecholamine?

- What are some important chatelaines?

A
  • Compounds containing a catechol moiety and an amide side chain
  • Norepinephrine, Epinephrine, Dopamine, and Isoprenaline
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2
Q
  • What are the steps of the biosynthesis of catecholamines?
A

Tyrosine –> (tyrosine hydroxylase) DOPA –> (aromatic L-amino acid decarboxylase) Dopamine –> (dopamine beta hydroxylase) Norepinephrine –> (phenylethanolamine-N-methyltransferase) Epinephrine

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3
Q
  • What triggers the release of NE and co-transmitters by exocytosis?
A
  • Calcium influx
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4
Q
  • Where is dopamine converted to norepinephrine?
A
  • Dopamine is transported into vesicles through vesicle monoamine transporters (VMAT) and converted to norepinephrine
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5
Q
  • In what uptake is NE taken back up into the presynaptic nueron?
  • What is Uptake I?
  • What is Uptake II?
  • What transporter does coke inhibit?
A
  • NE is taken back up by Uptake I mostly
  • Uptake I is where NE is taken back up into the presynaptic neuron by norpinephrine transporters (NET)
  • Uptake II is where the remaining NE is captured by non-neuronal cells by OCT transporters
  • Coke inhibits the NET transporter
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6
Q
  • Once inside the neuronal cytoplasm, what metabolizes NE?
A
  • Monoamine oxidase (MAO)
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7
Q
  • Which uptake has a higher transport capacity (Vmax)?
A
  • Uptake II/non-neuronal (OCT)
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8
Q
  • Which uptake has a higher affinity (Km) for NE?
A
  • Uptake I/neuronal (NET)
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9
Q
  • What drugs inhibit Uptake I?
A
  • Cocaine

- Tricyclic antidepressants (desipramine)

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10
Q
  • What drugs inhibit Uptake II?
A
  • Steroid hormones (cortisone)
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11
Q
  • At what sites does metabolism of catecholamines occur?
A
  • Presynaptic sympathetic nerve terminal, liver, kidney, and GIT
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12
Q
  • In the liver, adrenal medulla, and GIT what enzymes metabolize catecholamines?
  • Which enzyme is more specific?
A
  • COMT (catechol-o-methyl transferase)
  • MAO (monoamine oxidase)
  • COMT is more specific
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13
Q
  • In the neuron what enzymes metabolize catecholamines?
A
  • MAO (monoamine oxidase)
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14
Q
  • What do COMT (catechol-o-methyl transferase) do?
A
  • COMT catalyzes O-methylation of the meta-hydroxyl group on the catechol nucleus
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15
Q
  • What does MAO do?
A
  • MAO catalyzes the removal of an amine group from a variety of substrates
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16
Q
  • What is the end product of catecholamine metabolism?
A
  • Vanillylmandelic acid (VMA), which is excreted in the urine
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17
Q
  • What is the MOA of amphetamine?
A
  • It enters nerve terminals via NET and is transported to synaptic vesicles via VMAT, in exchange for NE
  • Some NE escapes in exchange for amphetamine via the NET
  • NE reuptake is reduced
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18
Q
  • What is the MOA of cocaine and TCAs?
A
  • Coke binds the NET transporters preventing the reuptake of NE
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19
Q
  • What is the rate limiting step of catecholamine biosynthesis?
A
  • Tyrosine hydroxylase is the rate limiting enzyme
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20
Q
  • What is the distribution of alpha 1 receptors?
  • What is their G protein class?
  • What is their response?
A
  • Blood vessels to skin and viscera and visceral smooth muscle, eye - iris/radical muscle
  • Gq
  • Smooth muscle contraction, vasoconstriction, increased blood pressure
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21
Q
  • What is the distribution of alpha 2 receptors?
  • What is their G protein class?
  • What is their response?
A
  • Presynaptic nerve terminal, platelet, pancreas (beta cells)
  • Gi
  • Decreases NE release from noradrenergic nerves, platelet aggregation, and decreased insulin release
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22
Q
  • What is the distribution of beta 1 receptors?
  • What is their G protein class?
  • What is their response?
A
  • Heart and kidneys
  • Gs
  • Increased heart rate, increased force of contraction, increased renin release
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23
Q
  • What is the distribution of beta 2 receptors?
  • What is their G protein class?
  • What is their response?
A
  • Blood vessels of skeletal muscle, lung, smooth muscle of GIT, and liver
  • Gs
  • Vasodilation, bronchodilation, relaxation, and increased glycogenolysis
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24
Q
  • What is the distribution of beta 3 receptors?
  • What is their G protein class?
  • What is their response?
A
  • Adipose tissue
  • Gs
  • Increased lipolysis
25
Q
  • What is the SAR correlation with alkyl substitution on the amine?
A
  • As the size of the substituting group increases, beta agonist activity is increased
26
Q
  • What happens to the SAR if the OH group is removed from the phenyl ring on the catechol ring structure?
A
  • The molecule is protected from COMT metabolism and the drug is more lipophilic
27
Q
  • What happens to the SAR on catecholamines when there’s ALPHA carbon substitution?
A
  • Blocks MAO metabolism which prolongs duration of action
28
Q
  • What happens to the SAR on catecholamines when there’s BETA carbon substitution?
A
  • It promotes alpha and beta receptor agonist activity

- Also promotes storage in pre-synaptic neuron vesicles

29
Q
  • These drugs act directly on alpha or beta receptors
A
  • Direct-acting agonists
30
Q
  • These agents may block the reuptake of NE or cause the release of NE from the vesicles of the adrenergic neuron
  • e.g. coke, amphetamine
A
  • Indirect-acting agonists
31
Q
  • Stimulate adrenoceptors directly and release NE from the adrenergic neuron
  • e.g. Ephedrine, pseudophedrine
A
  • Mixed-acting agonists
32
Q
  • What kind of agonists are these drugs?
  • epinephrine: act on all receptors (a1, a2, b1, b2 )
  • isoprenaline (b1 and b2)
A
  • Non-selective agonists - drugs that act on more than one adrenoceptor
33
Q
  • What kind of agonists are these drugs?
  • phenylephrine (a1)
  • clonidine (a2)
  • dobutamine (b1>b2)
  • salmeterol, albuterol, and terbutaline (b2)
A
  • Selective agonists

- drugs that act on single receptor subtype

34
Q
  • Name the drug:
  • a1 agonist, vasoconstriction
  • nasal decongestant (nasal spray)
A
  • Phenylephrine
35
Q

Name the drug:

  • b1 agonist, increases force of contraction
  • heart failure, circulatory/cardiogenic shock (IV infusion)
  • selective agonist
A
  • Dobutamine
36
Q

Name the drug:

  • b2 agonist, bronchodilation
  • asthma (inhaler)
  • selective agonist
A
  • Salmeterol, albuterol, and terbutaline
37
Q

Name the drug:

  • a1, a2, b1, b2 agonist
  • anaphylactic shock, emergency treatment of asthma, adjunct to local anesthesia to decrease blood flow and bleeding
  • nonselective agonist
A
  • epinephrine
38
Q

Name the drug:

  • d1 (low dose, causes renal vasodilation and increases GFR), b1 (medium dose), a1 (high dose)
  • circulatory/cariogenic shock
A
  • dopamine
39
Q
  • What are antagonists of NE and E?
A
  • Alpha-blockers
40
Q
  • What is the main pharmacological effect of alpha blockers?
A
  • Relaxes vascular smooth muscles
41
Q

Name the drug:

  • non selective alpha blocker
  • decreases blood pressure
  • long duration of action
A

Phenoxybenzamine

42
Q

Name the drug:

  • Selective alpha 1 antagonist
  • Causes vasodilation
A
  • Prazosin

- Doxazosin

43
Q

Name the drug:

  • Selective alpha 1 antagonist
  • Relaxes smooth muscle of ureter
A
  • Terazosin

- Tamsulosin

44
Q
  • These drugs antagonize the effects of EPI and NE
A
  • Beta blockers
45
Q

What kind of beta blocker is this?

- decreases heart rate, force of contraction, impulse conduction, and renin release

A
  • Beta 1 blockade
46
Q

What kind of beta blocker is this?

  • Causes bronchospasm
  • Blocks glycogenolysis
A
  • Beta 2 blockade
47
Q
  • What kind of drugs are propranolol, timolol, and ndaolol?
A
  • Non selective beta blockers
48
Q
  • What are the selective beta 1 blockers that are safe for diabetics and asthmatics?
A
  • Mnemonic: New Beta Blockers Acting Exclusively At Myocardium
  • Nebivolol
  • Betaxalol
  • Bisoprolol
  • Acebutolol
  • Esmolol
  • Atenolol
  • Metoprolol
49
Q

How are prostaglandins degraded?

A
  • Rapid metabolism (first pass) in the lung
  • Intracellular uptake via organic anion transporter (OATP 2A1)
  • Oxidation by PG-specific 15-OH dehydrogenase
  • Further oxidative steps
50
Q
  • Housekeeping function in many tissues

- Protection of gastric mucosa

A
  • Cox-1
51
Q
  • Inducible and involved in inflammatory response and carcinogenesis
  • Cytokines, shear stress, tumor promoters
A
  • Cox -2
52
Q
  • Cox inhibitors

- Spectrum of selectivity for cox-1 and cox-2

A

NSAIDS

53
Q
  • What do non cox-2 selective NSAIDs inhibit?
A
  • Inhibit platelet aggregation

- Aspirin covalently and irreversible inhibits cox at low dose selectivity

54
Q
  • What is the benefit of cox 2 inhibitors

- What is the problem with cox 2 inhibitors?

A
  • Benefit: less GI ulcers

- Problem: increases cardiovascular thrombotic events

55
Q
  • What are some uses of prostaglandin derived drugs?
A
  • Induction of labor
  • Pulmonary hypertension
  • Peptic ulcer prophylaxis
  • Induction of early abortion
  • Open angle glaucoma
  • Post partum hemorhage
  • Abortion induction
56
Q
  • What are potent mediators in bronchoconstriction and anaphylactic reactions?
A
  • Leukotrienes
57
Q
  • Astma drugs that inhibit leukotriene receptors and lipoxygenases.
A
  • Montelukast

- Zileuton

58
Q

CysLT1:

  • What endogenous ligand does it work on?
  • What secondary ligand does it work on?
  • What G protein; seconds messenger is it?
  • What are the major phenotypes in knockout mice?
A
  • LTD4
  • LTC4/LTE4
  • Gq; Increased PLC, Increased Ca2+i
  • Decreased innate and adaptive immune vascular permeability response and increased pulmonary inflammatory and fibrotic response

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