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PM2C: Therapeutics and Patient Care: Autumn > Physiological systems to Molecular drug targets Part 2 > Flashcards

Physiological systems to Molecular drug targets Part 2 Flashcards

1
Q

Where do the vast majority of postganglionic sympathetic fibres release noradrenaline to act on?

A
  1. Alpha adrenoceptors

2. Beta adrenoceptors

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2
Q

Where is noradrenaline release regulated?

A

Inhibitory presynaptic alpha 2 adrenoceptors

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3
Q

Where is noradrenaline released and how can you identify it compared to other catacholamine/biogenic amine structure?

A
  1. Released by post ganglionic sympathetic nerves

2. Benzenediol and methyl amine group attached

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4
Q

What is produced during the negative feedback on noradrenaline? Why is this good?

A
  1. Tyrosine hydroxylase

2. Can easily restart the change and go back unlike adrenaline

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5
Q

What are some examples of catacholamine/biogenic amine groups?

A
  1. Noradrenaline
  2. Adrenaline
  3. Dopamine
  4. Isoproterenol
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6
Q

Why is tyrosine hydroxylase such an important enzyme?

A

It’s the starting point to producing DOPA, dopamine, Noradrenaline and adrenaline

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7
Q

What is the location and function of the B1, B2 (most important) and B3 receptors?

A
  1. B1 - heart - increases cardiac rate and force
  2. B2- Smooth muscle heart, skeletal muscle and nerve terminals - vasodilation and bronchodilation
  3. B3- Skeletal fat muscle- Thermogenesis and Lipolysis
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8
Q

What G protein and response do beta 1, 2 and 3 represent?

A
  1. They all are G alpha S

2. They all Increase in cyclic AMP

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9
Q

Explain how the GPCRS in G alpha S (beta 1,2,3) stimulate adenylate cyclase?

A
  1. The addition of G alpha S and GTP leads to the stimulation of adenylate cyclase
  2. Leads to ATP converting to cAMP
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10
Q

What effects can cAMP have and what can this lead to in the beta 1 and 2 receptors?

A
  1. cAMP can increase protein phosphorylation
  2. Beta 1:
    Increased cardiac muscle contraction
    cAMP activates protein kinase A
  3. Beta 2:
    Decreased smooth muscle contraction
    cAMP inhibits myosin light chain kinase
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11
Q

What is the three agonist potents in beta 1, 2 and 3?

A

Isoprenaline
Noradrenaline
Adrenaline

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12
Q

What is the main selective agonists for B2 receptors?

A
  1. Salbutamol
  2. ritodrine
  3. terbutaline
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13
Q

What is the main selective agonists for B1 receptors? and antagonists?

A
  1. dobutamine
  2. xamoterol
  3. Atenolol
  4. bisprolol
  5. propranolol
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14
Q

Explain the main cardiovascular effects the noradrenaline can have?

A
  1. Alpha selective which causes vasoconstriction (alpha 1)
  2. Leads to reflex of bradycardia (baroreceptor response) due to ACh action at the vagal nerve
  3. Overall increase in blood pressure
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15
Q

Explain the main cardiovascular effects the isoprenaline can have?

A
  1. Beta selective which predominantly causes vasodilation (beta 2) and tachycardia (beta 1)
  2. Overall decrease in blood pressure
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16
Q

Explain the main cardiovascular effects adrenaline can have?

A
  1. Immediate action and low concentration

2. Leads to an increase in blood pressure

17
Q

Explain how the adrenergic transmission occurs in the synapse?

A
  1. Thousands of varacosities (means swelling)
  2. Tyrosine hydroxylase is converted to noradrenaline
  3. Alpha 2 receptor causes a negative response and is uptaken in the “1” transport system
18
Q

How do we block the “1” and “2” transport systems?

A
  1. Sympathomimetics:
    - psuedoephedrine amphetamine
  2. Blockers:
    - Tricyclic antidepressants (blocks build up of noradrenaline)
19
Q

How does psuedoepherdrine work?

A
  1. Selectively effects the uptake “1” transport system as it mimics the structure of noradrenaline
  2. Takes up psuedoepherdrine instead of noradrenaline which causes a build up in the synaptic cleft
  3. Noradrenaline causes vasoconstriction which reduces oedema in the nose so acts as a nasal decongestant
20
Q

Where is the location of the alpha 1 adrenoceptor and the function of it?

A
  1. Location: smooth muscle
  2. Function:
    - Vasoconstriction
    - Contraction (relaxes GI tract)
    - Glycogenolysis
21
Q

Where is the location of the alpha 2 adrenoceptor and the function of it?

A
  1. Location:
    - smooth muscle
    - nerve terminals
  2. Function:
    - Contraction
    - inhibition of transmitter release
22
Q

What is the G protein in alpha 1 and 2 adrenoceptor? And the response each give?

A

Alpha 1 adrenoceptor:

  • G alpha Q
  • Increase in IP3

Alpha 2 adrenoceptor:

  • G alpha I/O
  • Decrease in cAMP

PM2C: Therapeutics and Patient Care: Autumn (24 decks)

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