SNS Antagonists Flashcards
(72 cards)
1
Q
Difference between metabolism of NT in PSNS and SNS?
A
NA is reuptaken into tissue for metabolism, whereas ACh is broken down in the synapse
2
Q
Which adrenoceptor is primarily responsible for increased cardiac rate and force
A
B1
3
Q
Which adrenoceptor is primarily responsible for relaxation of the GIT
A
A1 and B1
4
Q
Which adrenoceptor is primarily responsible for renin release from the kidney
A
B1
5
Q
Which adrenoceptor is primarily responsible for bronchodilation
A
B2
6
Q
Which adrenoceptor is primarily responsible for vasodilation
A
B2
7
Q
Which adrenoceptor is primarily responsible for relaxation of visceral smooth muscle
A
B2
8
Q
Which adrenoceptor is primarily responsible for hepatic glycogenolysis
A
B2
9
Q
Which adrenoceptor is primarily responsible for lipolysis
A
B3
10
Q
Which adrenoceptor is primarily responsible for CNS actions
A
A2
11
Q
Which adrenoceptor is primarily responsible for contraction of vascular smooth muscle
A
A2
12
Q
Which adrenoceptor is primarily responsible for inhibition of NT release
A
A2
13
Q
Which adrenoceptor is primarily responsible for vasoconstriction
A
A1
14
Q
What selectivity does this drug have: carvedilol
A
A1 and B1 antagonism
15
Q
What selectivity does this drug have: phentolamine
A
A1 and A2 antagonism
16
Q
What selectivity does this drug have: prazosin
A
A1 antagonism
17
Q
What selectivity does this drug have: propranolol
A
B1 and B2 antagonism
18
Q
What selectivity does this drug have: atenolol
A
B1 antagonism
19
Q
Drug that has antagonistic selectivity for: A1 and B1
A
carvedilol
20
Q
Drug that has antagonistic selectivity for: A1
A
prazosin
21
Q
Drug that has antagonistic selectivity for: A1 and A2
A
phentolamine
22
Q
Drug that has antagonistic selectivity for: B1
A
atenolol
23
Q
name 5 adrenoceptor antagonists
A
carvedilol, phentolamine, prazosin, propranolol, atenolol
24
Q
Main uses of SNS antagonists?
A
- Hypertension
- Cardiac Arrhythmias
- Angina
- Glaucoma
25
What adrenoceptor controls the heart sympathetically
B1
26
What adrenoceptor controls renin release sympathetically
B1
27
Tissue Targets for Anti-hypertensives (5)
Sympa nerves, kidneys, heart, arterioles, and CNS
28
How is the CNS involved in BP
baroreceptors setting BP
29
which receptor blockade has positive and which has negative of B1 and 2
most of the POSITIVE effects are from Beta 1 blockade and most of the NEGATIVE effects are from Beta 2 blockade
30
Which adrenoceptors are found in Sympa nerves, kidneys, heart, arterioles, and CNS
The heart has B1 receptors, sympa nerves have B1 and B2, kidney has B1 and CNS has B1 and B2. Arterioles have no B receptor
31
Blockade of what where has the biggest impact on reducing BP and why
B1 in the kidneys as renin secretion falls reducing TPR
32
How do BB's work to reduce BP (30
* Act in the CNS to reduce sympathetic drive
* Act on the beta 1 receptors in the heart to reduce heart rate and reduce cardiac output but this effect disappears with chronic treatment - the heart resets itself
* Acts on the KIDNEYS on the beta 1 receptors to REDUCE RENIN PRODUCTION
33
`What are Presynaptic Beta 1/2 Receptors, how common are they?
These presynaptic beta receptors have a positive facilitation effect on the synthesis and release of a neurotransmitter. These receptors are not found in all nerve endings but they can have a major effect.
34
What effect does interfering with Presynaptic Beta 1/2 Receptors have
If you block the beta 1 then you remove this positive facilitation effect and reduce the amount of noradrenaline coming from the nerve terminal.
35
What has superseded BB as antihypertensives and why
ACE inhibitors have superceded beta blockers as there are less side effects.
36
Unwanted effects of Beta blockers? (6)
BRONCHOCONSTRICTION, CARDIAC FAILURE, HYPOGLYCAEMIA, FATIGUE, COLD EXTREMITIES, BAD DREAMS
37
Which preexisting conditions mean you do not prescribe BBs (4)
o ASTHMA
o COPD
o CARDIAC FAILURE
o DIABETES
38
Drug that is beta non-selective?
Propranolol
39
when is the effect of propranolol particularly evident
when exercising
40
What is a cardioselective BB
Atenolol
41
Main areas that atenolol affects?
Heart and kidneys beta1 receptors
42
Carvedilol is most selective for, and then followed by?
B1 and then A1
43
How does carvedilol lower BP
This lowers blood pressure by blocking the alpha1 receptors in the arterioles to lower the total peripheral resistance
44
Main adrenoceptor linked to TPR?
A1
45
What can cause postural hypotension?
Alpha antagonists blocking sympathetic drive
46
a non-selective alpha antagonist ?
Phentolamine
47
What does phentolamine do
non-selective alpha antagonist.
Causes vasodilation and a fall in blood pressure due to blockade of alpha-1 adrenoceptors
However, blockade of presynaptic alpha-2 receptors removes the inhibitory effect of the alpha-2 receptors on noradrenaline release and so you get an increase in noradrenaline release which leads to competitive drug-receptor interactions.
Phentolamine is outcompeted by NA as there is more of NA.
This makes reflex tachycardia stronger
48
Special effect of prazosin?
• Unlike other anti-hypertensives, alpha-1 antagonists cause a decrease in LDL and an increase in HDL cholesterol.
49
What does prazosin antagonise
A1 selective
50
A1 selective antagonist?
Prazosin
51
Why is an A1 selective antagonist less tachycardic?
There is less tachycardia than non-selective antagonists since they do NOT increase noradrenaline release from nerve terminals (no alpha-2 actions
52
methyldopa synthesis and metabolism?
taken up by the noradrenergic neurons
form the false transmitter - alpha-methyl noradrenaline
It is NOT well metabolised within the neuron by MAO and tends to accumulate in larger quantities than noradrenaline.
It displaces noradrenaline from the synaptic vesicles when taken up
53
MOA methyldopa?
(alpha-methyl noradrenaline) is released in the same way as noradrenaline into the synapse.
It is less active than noradrenaline on alpha-1, beta-1, and beta-2 receptors - LESS EFFECTIVE AT CAUSING VASOCONSTRICTION (as it is shit on alpha 1) so there will be a fall in BP.
it is more active on presynaptic alpha-2 receptors (the ones that mediate the negative feedback and release of NA shut down the synthesis and release).
• This means that the auto-inhibitory feedback mechanism operates more strongly and reduces noradrenaline release below normal levels
• It also has some CNS effects, it stimulates the vasopressor centre in the brainstem to inhibit sympathetic outflow
54
What is the active form of methyldopa
alpha-methyl noradrenaline
55
Other benefits to methyldopa? (3)
o Improves blood flow greatly.
o Renal and CNS blood flow is well maintained so it is widely used in patients with renal insufficiency or cerebrovascular disease
o It is also the recommended anti-hypertensive in pregnant women because it has no adverse effects on the foetus despite crossing the blood-placenta barrier
56
Adverse effects of methyldopa (4)
dry mouth, sedation, orthostatic/postural hypotension (problem in the elderly), male sexual dysfunction
57
Class II antiarrhythmics AKA ...
BB
58
Why are BB used as antiarrhythmics
sympathetic drive and b1 receptors controls the pacemaker current so beta blockers are a good way of controlling arrhythmias in patients
59
main cause of arrhythmias?
Myocardial ischaemia
60
How does a BB help control arrhythmias
The refractory period of the AV node is increased by beta antagonists
This interferes with AV conduction in atrial tachycardias and slows down ventricular rate
61
Drug that is used antiarrhythmically?
Propranolol
62
What is angina
Pain that occurs when the oxygen supply to the myocardium is insufficient for its needs
63
Types of angina?
Stable, unstable, variable
64
Stable angina, pain when? Why? Heart effect?
o Pain on exertion
o Due to a fixed narrowing of the coronary vessels e.g. atheroma
o There is increased demand on the heart
65
Unstable angina, pain when? Peak pain? Why? Risks of?
o Pain with less and less exertion
o Culminates with pain at rest
o The atheromatous plaque is starting to rupture and breaks away.
o You get a platelet-fibrin thrombus associated with the ruptured atheromatous plaque but without complete occlusion of the vessel
o High risk of infarction
66
Variable angina, when? why? association?
o Occurs at rest
o Caused by coronary artery spasm not so much atherosclerosis
o It is associated with atheromatous disease
67
How do BB help angina? (brief)
• Beta blockers do nothing about the cause of the angina (atherosclerosis) they simply lower the work the heart has to do
68
How do BB help angina? (specific, 3)
* Decrease heart rate
* Decrease systolic blood pressure
* Decrease cardiac contractile activity
69
BB should not be used to treat patients with angina if they have:
Bradycardia, bronchospasm, hypotension, AV block
70
Where is aqueous humour produced and how
Ciliary body by carbonic anhydrase
71
What is the amount of humour produced in the eye directly related to
Blood flow in the ciliary body
72
What SNS antagonists can be used to treat glaucoma
o Adrenaline can act on the alpha-1 receptors to cause vasoconstriction and reduce blood flow through the ciliary body --> this reduces the amount of aqueous humour.
There are also drugs that can act on the beta-1 receptors which drives the action of carbonic anhydrase to produce bicarbonate, , blocking these receptors reduces carbonic anhydrase activity
