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autumn amy L pm2c (copied) > From Physiological Systems To Molecular Drug Targets II > Flashcards

From Physiological Systems To Molecular Drug Targets II Flashcards

1
Q

Name the 3 locations where nicotinic ACh receptors are found

A
  1. Muscle (neuromuscular junctions)
  2. Ganglion
  3. CNS
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2
Q

What is the function of nicotinic ACh receptors?

A

Excitation

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3
Q

Name an agonist for nicotinic ACh receptors

A

Acetyl Choline

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4
Q

How many transmembrane domains does a subunit of a nAChR have?

A

4

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5
Q

How many subunits does a nicotinic receptor have?

A

5: alpha, alpha, beta, delta, gamma

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6
Q

What do the nicotinic receptor subunits come together to form?

A

An ion channel

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7
Q

What is a nicotinic receptor’s ion channel permeable to?

A

Na+

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8
Q

How do nicotinic receptors cause excitation?

A
  1. 2 ACh molecules bind to the nAChR
  2. Conformational change occurs
  3. Ion channel opens
  4. Na+ enters the cell causing an increase in positive charge inside of the cell
  5. This causes excitation
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9
Q

What acts as the receptor gate in a nicotinic receptor?

A
  • 2 alpha helices, 1 in each alpha subunit
  • Conformational change when ACh binds causes them to open the ion channel
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10
Q

What is an issue when synthesising drugs targeted at the ANS ganglia nAChRs?

A

The drugs do not discriminate between sympathetic and parasympathetic nerves

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11
Q

Where do neuromuscular blocking agents work?

A

Neuromuscular junction

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12
Q

Name 2 types of neuromuscular blocking agents

A
  1. Competitive blockers
  2. Depolarising blockers
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13
Q

What are competitive blockers?

A

Competitive antagonists of nAChRs

(Increase concentration of agonist = decrease power of antagonist)

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14
Q

What are depolarising blockers?

A

Agonists which cause a depolarising block of the muscle fibre endplate

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15
Q

How do depolarising blockers work?

A
  1. Switch the receptor on = increase in Na+ entering the cell
  2. Blocker stops channel from closing so sodium keeps coming into the cell
  3. Eventually too much sodium enters the cell and prevents further excitation
  4. Activation of receptor switched off
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16
Q

Give a use of competitive blockers

A
  • Muscle relaxants as an adjunct to anaesthesia
  • In particular in obstetrics as they do not cross into the placenta
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17
Q

Name 3 examples of a competitive blocker

A
  1. Tubocurarine
  2. Pancuronium
  3. Vecuronium
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18
Q

Why are competitive blockers used as muscle relaxants?

A

They selectively work on the nAChRs at the neuromuscular junction, rather than at the ganglia and the brain/CNS

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19
Q

Why are different competitive blockers used for minor vs major surgeries

A

Some have shorter half lives than others therefore work for shorter periods of time

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20
Q

Give an example of a use of depolarising blockers

A

Cause paralysis during anaesthesia

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21
Q

How do depolarising blockers cause paralysis?

A
  1. The muscle contracts due to maintained depolarisation
  2. Muscle cannot repolarise (relax)
  3. This causes loss of excitability (sodium channels cannot inactivate)
  4. Therefore the continual stimulation of the NMJ by DB’s causes muscle paralysis
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22
Q

Name an example of a depolarising blocker

A

Succinylcholine (Suxamethonium)

Works on nAChRs

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23
Q

What is succinylcholine used for?

A

To cause paralysis during anaesthesia

Minor surgery

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24
Q

Why is suxamethonium so short acting? (10 mins)

A

Because it is rapidly hydrolysed by cholinesterases

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25
What is the **indication** for **Donepezil**?
For the **treatment** of mild-moderate **Alzheimer's Disease**
26
What is the **mechanism of action** of **Donepezil**?
**Anticholinesterase** = inhibits ACh-esterase
27
**How** does **botulinum toxin type A work**?
It **blocks vesicle docking/release** and therefore **prevents** the **release of ACh**
28
How can **botulinum toxin type A be deadly**?
Can cause **respiratory paralysis**
29
**Why** is **botulinum toxin type A** so **toxic**?
It has a very **low LD50 value** LD50 = **10ng/kg**
30
List **3 therapeutic indications** for **botulinum toxin**
1. Excessive **muscle spasm** - can result from stroke, brain or spinal cord injury, CP 2. **Migraine/headache** treatment - facial muscle contraction stimulates headaches 3. **Excessive secretion** - severe underarm sweating or salivation
31
What **receptors** does **noradrenaline act** on?
**α** or **β-adrenoceptors**
32
What is **noradrenaline release regulated by**?
**Inhibitory presynaptic α2-adrenoceptors**
33
What are **β​-blockers**?
**Blockers** of the **β-adrenoceptors**
34
How is **adrenaline released** into the **bloodstream**?
It is **secreted** from the **adrenal gland**
35
What is **dopamine**?
A **precursor** for noradrenaline and adrenaline And a **CNS transmitter**
36
Which amino acid are adrenaline, noradrenaline and dopamine **generated from**?
**Tyrosine**
37
Describe the **biogenic amine synthesis process**
**Tyrosine** --\> **DOPA** --\> **Dopamine** --\> **Noradrenaline** --\> **Adrenaline**
38
How can one of the substances in **biogenic amine synthesis build up**?
If the **enzyme** which converts the substance into something else becomes **inhibited**
39
What acts as **negative feedback** in **biogenic amine synthesis?**
* Build up of **noradrenaline** * **Negative feedback** on to **tyrosine hydroxylase** (converts Tyrosine to DOPA)
40
How many **subtypes** of **adrenoceptor** are there?
**5**: α1 α2 β1 β2 β3
41
Where is the **β1-adrenoceptor located**?
**Heart**
42
Where is the **β2-adrenoceptor located**?
**Smooth muscle**
43
Where is the **α1-adrenoceptor located**?
**Smooth muscle**
44
Where is the **α2-adrenoceptor located**?
**Smooth muscle**
45
What type of **G protein** is the **α1-adrenoceptor** coupled to?
Gαq
46
What type of **G protein** does the **α2-adrenoceptor** couple to?
**Gα​i/o**
47
What type of **G protein** do the **β-adrenoceptors** couple to?
**Gαs**
48
What **response** does the **α1-adrenoceptor** cause when its G protein is bound?
**Increase in IP3**
49
What **response** does the **α2-adrenoceptor** cause when bound to its G protein?
**Decrease in cAMP**
50
What **response** do the **β-adrenoceptors** cause when their G protein is bound?
**Increase in cAMP**
51
Name the **enzyme** that **Gαs** (with **β​1/2/3** adrenoceptors) **stimulates**
**Adenylate cyclase**
52
What **process** does **adenylate cyclase** carry out?
Converts **ATP --\> cAMP**
53
What **effect** does **increased cAMP** have?
**Increased protein phosphorylation**
54
What would be the **agonist** of choice to **activate** the **α1-adrenoceptor**
**Noradrenaline**
55
What would be the **agonist** of choice to activate the **α2-adrenoceptor**
**Adrenaline**
56
What would be the **agonist** of choice to **activate** the **β-adrenoceptors**
**Isoprenaline**
57
What **effect** does **NA** cause when **bound** to an **α1 receptor** (α selective)
* **Vasoconstriction** * This causes reflex **bradycardia** due to **baroreceptor response** * **ACh** release = slows **vagal nerve** * Overall **increase in BP**
58
What **effect** does **isoprenaline** have when it binds to **β adrenoceptors**? (β- selective)
Causes **vasodilation** (β2) and **tachycardia** (β1) Overall **decrease in BP**
59
What **effect** does **adrenaline** have when it binds to a **β** or **α-adenoceptor**?
**Higher affinity** for **β** receptor but can still bind to α Slight **increase in BP**
60
What are **adrenergic synapses** also known as?
**Varicosities** (= swelling)
61
How do **sympathomimetics work**?
**Mimic CNS**
62
What is the **indication** for **salbutamol**?
**Asthma** treatment
63
What is the **mechanism of action** for **salbutamol**?
Selective **β2 adrenoceptor agonist** Causes **bronchodilation**
64
What is the **indication** for **atenolol**?
**Hypertension**
65
What is the **mechanism of action** of **atenolol**?
Cardioselective **β1 adrenoceptor antagonist** (= **β​ blocker**)
66
What is the **indication** of **pseudoephedrine**?
**Nasal decongestion**
67
What is the **mechanism of action** of **pseudoephedrine**? (Sudafed)
Substrate for biogenic amine uptake system = **sympathomimetic** 1. **Mimics NA** and gets **taken up** by uptake system 2. Therefore **NA displaced** from vesicles 3. **Released NA** builds up in synapatic cleft = **vasoconstriction** of mucosal blood vessels (**α1 adrenoceptors**) 4. This **reduces fluid build up** in the nose

autumn amy L pm2c (copied) (16 decks)

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