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Year 2 - Pharmacology and Therapeutics > SNS Antagonist > Flashcards

SNS Antagonist Flashcards

1
Q

4 main types of adrenoceptors in the SNS?

A

Alpha 1

Alpha 2

Beta 1

Beta 2

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2
Q

Are the 4 main adrenoceptors pre- or post-synaptic?

A

Alpha 2 - PRE-synaptic

Other 3 are POST-synaptic

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3
Q

Alpha-1 function?

A

o VasoCONSTRICTION

o RELAXATION of GIT

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4
Q

Alpha-2 function?

A

o INHIBITION of NT release
- -VE feedback on NE release

o CONTRACTION of VSMC, CNS

(pre-synaptic!)

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5
Q

Beta-1 function?

A

o Cardiac STIMULATION

o RELAXATION of GIT

o RENIN release

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6
Q

Beta-2 function?

A

o BronchoDILATION

o VasoDILATION

o RELAXATION of VSMCs

o Hepatic Glycogenolysis

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7
Q

Beta-3 function?

A

Lipolysis

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8
Q

Some adrenoceptor antagonists?

A

Non-selective (a1 & b1) = Labetalol

a1 + b2 = Phentolamine

a1 = Prazosin

b1 + b2 = Propranolol

b1 = Atenolol

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9
Q

Hypertension physiology?

Clue - equation

A

CO x TPR = BP

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10
Q

Pathophysiology of hypertension?

A

Constantly >140/90mmHg

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11
Q

Main contributors towards hypertension?

A

o Blood volume
o CO
o Vascular tone

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12
Q

What are the main tissue targets for anti-hypertensives?

A

o SNS nerves
- that release the vasoconstrictor NA

o Heart
- CO

o Kidney
- blood volume/vasocontriction

o Arterioles
- control/determine TPR

o CNS

  • determine BP set-point
  • regulate some systems involved in BP control & autonomic NS
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13
Q

Quick way to decipher is a drug is a beta-blocker?

A

Ends in -OLOL

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14
Q

Beta-blockers associated with the different tissue targets of anti-hypertensives?

A

o The heart

  • B1
  • reduce ionotropic & chronotropic effects

o SNS nerves
- B1/B2

o The kidney

  • B1
  • reduce renin production
  • common long-term feature is reduction in TPR

o Arterioles

  • NONE
  • if block the A1 receptors, would get dilation = do NOT want this

o CNS

  • B1/B2
  • reduce sympathetic tone
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15
Q

How can blockade of B1 receptors also help in anti-hypertensive effects?

A

On the pre-synaptic membrane
SO
blockade of this reduces the +ve feedback on NE release = contribute to anti-hypertensive effects

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16
Q

4 broad types of beta-blockers?

A
  1. NON-SELECTIVE
    o equal affinity for B1 & B2 receptors
    o e.g. Propranolol
  2. B1-SELECTIVE
    o more selective for B1
    o e.g. Atenolol
  3. MIXED A & B-BLOCKERS
    o A1 blockade gives additional vasodilator properties
    o e.g. Carvedilol
  4. OTHER
    o e.g. Nebivolol - also potentiates NO
    o e.g. Sotalol - also inhibits K+ channels
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17
Q

Unwanted effects that can rise due to the use of beta-blockers?

A
  1. Bronchoconstriction
    o of little importance unless patient has an airway disease (B2)
  2. Cardiac Failure
    o need some SNS drive to the heart
    o may be problem is have heart disease
  3. Hypoglycaemia
    o B-blockers may mask symptoms (e.g. tremors)
    o NON-SELECTIVE B-blockers will also block hepatic glycogenolysis (B2)
  4. Fatigue
    o CO falls = muscle perfusion falls (B2)
  5. Cold extremities
    o loss of B-receptor mediated vasodilation in cutaneous vessels
  6. Bad dreams

4,5,6 = LESS SERIOUS

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18
Q

Propranolol?

A

B1 & B2 NON-SELECTIVE

During rest = very little effect
During exercise = can REDUCE HR, CO & ABP

As non-selective, produces ALL typical adverse effects

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19
Q

Atenolol?

A

B1-SELECTIVE

Antagonises the effects of NE on the heart
o BUT also affects any other organ with B1 receptors (e.g. kidneys)

Selectivity is CONCENTRATION-DEPENDANT
o too much and it becomes non-selective

20
Q

What is the advantage of atenolol over propranolol?

A

As selective, LESS EFFECT on airways that non-selective drugs
o (and also the liver!)

BUT still not safe with asthmatic patients!
- as could become non-selective!

21
Q

Carvedilol?

A

MIXED A & B-BLOCKERS

A1 blockade gives additional vasodilator properties

22
Q

What advantage does carvediolol have other atenolol & propranolol?

A

Get a more powerful HYPOTENSIVE EFFECT (as not just affecting cardioselective B1)

o Heart - B1 effect
o Kidneys - B2 effect
o ALSO blocking vasoconstriction of arteries

23
Q

Labetalol?

A

A1 & B1 dual-action antagonist
(higher ratio of B1:A1)

o lowers BP via. reduction in TPR
o induces a reduction in HR or CO (this effect wanes after chronic use)

24
Q

Receptors linked with A1 & A2 receptors?

A

A1 - linked to STIMULATORY proteins

o Gq-linked
o POST-synaptic on VSMCs

A2 - linked to INHIBITORY proteins

o Gi-linked
o PRE-synaptic autoreceptors inhibiting NE release

25
Q

2 main Alpha-blocker drugs?

A

Phentolamine - NON-SELECTIVE

Prazosin - A1 specific

26
Q

What is an issue associated with A-receptor antagonists?

A

REFLEX TACHYCARDIA!

  1. There is a fall in arterial pressure
    o as A-receptors are the main TPR mediators
  2. As TPR falls, get reflex tachycardia
    o increase in HR & CO as BETA-receptor mediated
  3. Blood flow in cutaneous & splanchnic vascular beds increase

This is problem with postural hypotension!

27
Q

Phentolamine?

A

NON-SELECTIVE ALPHA-ANTAGONIST

Causes
 o vasoDILATION = fall in BP
BUT also
 o increase in NE release due to simultaneous blockade of A2 receptors
  - this enhances the reflex tachycardia

Also increases GIT motility & diarrhoea
o so no longer clinically used

28
Q

Why do A2-receptors and baroreceptors reduce the effectiveness of phentolamine?

A

Alpha-2 = non-selective so will block this as well so reduce -ve feedback = MORE NA being released
• This means more NA will compete with phentolamine at the alpha-1 receptors causing it to bind = which mean more alpha-1 stimulation

Baroreceptors = if block alpha-receptors, cause dilation of blood vessels impacting pressure
• Baroreceptors respond to this so a reduced in pressure causes REDUCTION in FIRING which causes an INCREASE in SN activity which compenstates by increasing SV

29
Q

Prazosin?

A

A1-ANTAGONIST

Causes
o vasoDILATION = fall in BP
- CO decreases due to fall in venous pressure as a result of dilation of capacitance vessels

o LESS reflex tachycardia
- as do NOT block A2 to increase NE release

o Also causes a modest decrease in LDL & increase in HDL

30
Q

Example of a false transmitter and how is it formed?

A

Alpha-methyl-noradrenaline

Methyldopa is take up by noradrenergic neurones
• it is then decarboxylated & hydroxylated to form the false NT

31
Q

Why is the false transmitter useful?

A

NOT broken down within the neuron by MAO
• tends to accumulate in larger quantities than NA
• therefore displaces NA from vesicles

32
Q

MOA of the false transmitter?

A

LESS active than NA on A1-receptors
• less effective in causing vasoconstriction

MORE active on A2-receptors
• more -VE feedback on NE release
• this is as not metabolised by MAO = reduced [gradient] = uptake is slower = binds to A2 more

Some minor effects on CNS
• stimulated vasopressor centre

33
Q

Name of the false transmitter as the antihypertensive medication?

A

Methyldopa

34
Q

Benefits on methyldopa?

A

Renal & CNS blood flow well maintained
• so used in patient with renal insufficiency OR CNS disease

Recommended in hypertensive pregnant women as no adverse effects of foetus
• DOES cross the placenta however

35
Q

Adverse effects of methyldopa?

A

Dry mouth
Sedation
Orthostatic hypotension
Male sex dysfunction

As impacting the SN across the whole system!

36
Q

Define arrhythmias and what is the main cause of it?

A

Abnormal or irregular heart beats

Main cause if myocardial ischaemia

37
Q

What can aggravate arrhythmias?

A

Class 2 anti-arrhythmics

An increase in SNS drive to the heart via. B1-receptors
• can aggravate arrhythmias, particularly after MI

AV-conductance also dependant on SNS activity
• as the refractory period is increased by B-adrenoceptor antagonists

38
Q

What can be given to people with arrhythmias?

A

Propranolol (non-selective, class II drug)

  • reduces mortality of patients with an MI
  • partially successful in arrhythmias that occur during exercise or mental stress
39
Q

Define angina and where is it felt?

A

Pain that occurs when the O2 supply to the myocardium is insufficient for its needs

Pain spread down dermatome T1
• chest, arm and neck
• brought upon by exertion or excitement

40
Q

Type of angina?

A

STABLE
• pain on EXERTION
• due to fixed narrowing of coronary vessels

UNSTABLE
• pain with LESS EXERTION & at REST
• thrombus but without complete occlusion of vessel (risk of infarction)

VARIABLE
• occurs at REST
• caused by coronary artery spasm (associated with atheromatous disease)

41
Q

How do beta-blockers help with angina?

A

B-adrenoceptor antagonists

Reduce myocardial demand by
• decrease ionotropic & chronotropic effect

At low doses, does NOT affect
• bronchial SM, systolic BP, reduce O2 demand

42
Q

What are some adverse effects beta-blockers can have on those with angina?

A 
Fatigue
Insomnia
Dizziness
Sexual dysfunction
Bronchospasm
Bradycardia
Heart block
Hypotension

i.e. not used in patients that these are exacerbated in e.g. people w. congestive HF

43
Q

What is glaucoma characterised by?

A

Increase in IOP

44
Q

What causes glaucoma?

A

Poor drainage of aqueous humour
AND
Can permanently damage the optic nerve (CN II)

45
Q

How is the aqueous humour produced?

A

Produced by blood vessels in ciliary body
• via. actions of carbonic anhydrase

Production is INDIRECTLY related to BP

Flow
• posterior chamber –> through pupil –> to anterior chamber –> trabecular meshwork –> into veins –> canal of Schlemm

46
Q

How can glaucoma be treated?

A

Beta-adrenoceptor antagonists

• Non-selective B1 & B2

  • reduce rate of aqueous humour formation by blocking receptors on ciliary body
  • e.g. levobunolol

• Selective B1

  • been shown to be effective
  • e.g. betaxolol hydrochloride

Year 2 - Pharmacology and Therapeutics (9 decks)

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