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NS > Noradrenaline > Flashcards

Noradrenaline Flashcards

1
Q

Cardiovascular effects of sympathetic stimulation

A
  • increased heart rate

- increased force of contraction

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2
Q

Pulmonary effects of sympathetic stimulation

A

bronchodilatation (expansion of bronchial airways)

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3
Q

Gastrointestinal effects

A
  • decreased peristalsis
  • decreased luminal secretions
  • increased vasoconstriction in GI organs
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4
Q

Other effects of sympathetic stimulation

A
  • pupil dilation (mydriasis)
  • glycogenolysis (conversion of glycogen to glucose)
  • lipolysis (breakdown of fats and other lipids by hydrolysis to release fatty acids)
  • renin secretion (enzyme secreted and stored in the kidneys which promotes the production of angiotensin)
  • vasodilatation of skeletal muscles
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5
Q

what type of drug is used to treat asthma?

A

salbutamol, salmeterol
beta2 adrenergic agonist

increased bronchodilation for enhanced gas exchange

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6
Q

type of drug used in premature labour

A

intravenous salbutamol
beta 2 adrenergic agonist

to stimulate uterine relaxation

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7
Q

type of drug used in HTN

A

propranolol
non-selective beta adrenergic antagonist

to decrease blood pressure

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8
Q

type of drug used in angina

A

propranolol
non-selective beta adrenergic antagonist

to decrease heart rate and force of contraction

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9
Q

type of drugs used in benign prostatic hypertrophy

A

prazosin, tamusolin
alpha adrenoreceptor antagonist

to decrease size of prostate gland

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10
Q

where are the sites of drug intervention in the sympathetic nervous system

A

in CNS- drugs would need to penetrate BBB so effects are widespread

in sympathetic ganglion, transmission is similar (ACh mediated) at all autonomic ganglia (sympathetic and parasympathetic), widespread and non-specific effects

BUT at the neuroeffector junction, allows for specific targeting of function e.g. heart, lungs, minimal off-target effects

WANT A DRUG THAT HAS SPECIFIC ACTIONS BUT LIMITED TARGET EFFECTS

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11
Q

what is a ganglion

A

a structure containing a number of cell bodies, typically linked by synapses and often forming a swelling in the nerve fibre

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12
Q

Draw out the synthesis of noradrenaline

A 
tyrosine
    tyrosine hydroxyase
DOPA
    DOPA decarboxylase
dopamine
     dopamine beta hydroxylase 
noradrenaline
     phenylethanolamine- N-methyl transferase
adrenaline
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13
Q

how does alpha-methyl tyrosine interfere with NA synthesis

A

FALSE SUBSTRATE
alpha-methyl tyrosine inhibits the action of tyrosine hydroxylase

blocks formation of DOPA
decrease amount of noradrenaline formed

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14
Q

what are the uses of alpha methyl tyrosine

A
  • decreases blood pressure in pheochromocytoma

benign tumour in adrenal gland causing persistant high blood pressure

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15
Q

side effects of alpha-methyl tyrosine

SPD

A
  • sedation
  • parkinsonism
  • diarrhoea
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16
Q

how does methyldopa intefere with noradrenaline synthesis

A
  • a competitive inhibitor of DOPA decarboxylase, decreases amount of dopamine and noradrenaline synthesis, decreasing sympathetic nervous activity
  • results in the production of alpha-methylnoradrenaline instead
  • lower blood pressure by stimulating inhibitory alpha 2 adrenoceptors in the brainste, decreasing sympathetic nervous activity
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17
Q

how does reserpine intefere with noradrenaline synthesis

A
  • unprotected monoamines (NA, dopamine, serotonin) are metabolised by monoamine oxidase
  • under normal conditions, NA is taken into vesicles via the vesicular monoamine transporter VMAT
  • reserpine blocks VMAT, preventing NA uptake into vesicles leading to its metabolism by MAO to DOPAC- 3,4-dihydroxymandelic acid
  • ## within 24 hours of treatment, the nerve is depleted of NA
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18
Q

what is reserpine used for

A

historical drug
no longer used in the clinic
wide range of effects that leads to depression of the CNS signal

used as antihypertensives

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19
Q

side effects of reserpine

A
  • profound CNS depression
  • diarrhoea
  • nasal congestion
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20
Q

what drugs inhibit NA release

A

guanethidine and debrisoquine

and clonidine

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21
Q

how do guanethidine and debrisoquine inhibit NA release

A
  • after release, NA can be transported back into the varicosity through uptake 1 channels
  • drugs can inhibit NA release by entering the varicosity through these channels and displacing NA in the vesicles
  • this leads to metabolism of NA by MAO and the gradual depletion of NA within the nerve terminal
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22
Q

how does clonidine inhibit NA release?

A

by activation of the alpha 2- adrenergic receptor (AR) on the presynaptic terminal in a negative feedback mechanism

is a alpha- 2 adrenoreceptor specific agonist

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23
Q

uses of clonidine?

A

in hypertension and tachycardia

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24
Q

side effects of clonidine

A
  • postural hypotension
  • headaches
  • diarrhoea
  • fluid retention
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25
Q

what drug promotes NA release

A

amphetamine, tyramine, ephedrine

26
Q

how does amphetamine promote drug release?

A
  • enter the varicosity through uptake 1 channels NET
  • drugs can compete with NA to enter the vesicles through the VMAT
  • drug displaces NA from its storage sites leading to NA leakage into the synaptic gap where it can activate receptors
  • amphetamine also has secondary effects by inhibiting MAO, increasing the concentration of free NA for release into the synaptic gap
27
Q

what is ephedrine used as?

A

nasal congestant and bronchodilator

28
Q

what is amphetamine used for?

A

ADHD

29
Q

side effects of amphetamine, tyramine, ephedrine

A
  • tachycardia
  • restlesness
  • insomnia
  • dry mouth
  • tolerance
  • rebound effects
30
Q

what are adrenergic receptors

A

a class of G protein coupled receptors that are targets of catecholamines

31
Q

what receptors does vascular smooth muscle contain and which drug as the greatest activity?

A

alpha adrenergic receptors

noradrenaline > adrenaline > isoprenaline

32
Q

what receptors does cardiac smooth muscle contain and which drug has the greatest activity ?

A

beta adrenergic receptors

isoprenaline > adrenaline > noradrenaline

33
Q

subunits of alpha 1, alpha 2 and beta adrenergic receptors?

A

A1: a1A, a1B, a1D
A2: a2A, a2B, a2C

B: B1, B2, B3

34
Q

effect of activating alpha 1 postsynaptic receptors

A
  • vascular smooth muscle contraction —> vasoconstriction, reduced blood flow, increased blood pressure
  • relaxation of longitudinal muscle in GI tract
  • anal sphincter contraction
  • reduced GI motility —> constipation
  • bladder relaxation —> sphincter contraction- urinary retention
  • pregnant uterine muscle contraction
  • radial muscle contraction
  • increased secretion from salivary glands
  • increased glycogen mobilisation from the liver
  • vas deferens circulation (ejaculation)
35
Q

effect of activating alpha 2 presynaptic receptors

A
  • widespread distribution
  • inhibition of neurotransmitter release
    negative feedback mechanism
36
Q

effect of activating beta 1 postsynaptic receptors

A
  • predominantly located in the cardiac muscles
  • increased heart rate
  • increased force of contraction
  • increased cAMP production in pacemaker tissue
37
Q

effect of stimulating beta 2 receptors

not at synaptic sites

A
  • relaxation of bronchial smooth muscle
    (dilation of airways, greater gas exchange, greater absorption of O2 from the blood)
  • vascular smooth muscle relaxation
  • skeletal muscle, coronary and hepatic arteriole vasodilation
  • uterine smooth muscle contraction
  • glycogen mobilisation in the liver
38
Q

what are sympathomimetics

A

drugs which mimic the action of endogenous sympathetic nervous agents

39
Q

name some non selective sympathomimetics

A

noradrenaline and adrenaline

40
Q

action of noradrenaline

A

potent agonist at alpha 1, alpha 2 receptors
moderate agonist at beta 1
weak agonist at beta 2

  • emergency treatment of acute hypotension
  • cardiac arrest
41
Q

action of noradrenaline

A
  • potent agonist at beta 2 and beta 1 receptors
  • moderate agonist at alpha 1 and 2 receptors
  • emergency treatment of acute hypotension
  • cardiac arrest
  • anaphalyactic shock
  • given with local anaesthetics
42
Q

name some alpha selective sympathomimetics

A

phenylephrine and clonidine

43
Q

action of phenylephrine

A

moderate agonist at alpha 1 receptors

  • acute hypotension
  • nasal congestion
44
Q

action of clonidine

A
  • potent agonist at alpha 2 receptors
  • hypertension
  • migraine
45
Q

name some beta selective sympathomimetics

A

isoprenaline
salbutamok
dobutamine

46
Q

action of isoprenaline

A

potent agonist at beta 1 and 2 receptors

  • heart block
47
Q

action of salbutamol

A
  • potent agonist at beta receptors
  • asthma
  • premature labour (uterine relaxation)
48
Q

action of dobutamine

A

potent agonist at beta 2 receptors

  • cardiogenic shock
49
Q

how do adrenergic receptor antagonists work?

A

block sympathetic vasoconstrictor tone

resulting in decreased blood pressure

50
Q

name some non selective blockers

A

phenoxybenzamine (irreversible competitive antagonist)

phentolamine (reversible competitve antagonist
can cause severe reflex tachycardia)

51
Q

name some selective alpha blockers

A

prazosin (in benign prostatic hypertrophy)

doxasozin

  • decreased risk of reflex tachycardia
  • antihypertensive agents
  • used in benign prostatic hyperplasia
52
Q

side effects of alpha blockers?

A
  • postural hypotension
  • nasal congestion
  • importance
  • priapism
  • diarrhoea
53
Q

how do beta blockers work

A

beta adrenergic antagonists

  • directly block sympathetic nervous input into the heart
  • decreased force of contraction
  • decreased frequency of contraction
  • decreased vascular tone
  • leads to decreased cardiac output and decreased blood pressure
54
Q

what drugs are non selective to alpha and beta blockers?

A

labetalol and carvedilol block both alpha 1 and beta receptors

  • reduce arterial blood pressure
  • used in stable congestive heart failure
55
Q

what drugs are beta selective (block both beta 1 and beta 2 receptors)?

A
  • propranolol
  • timolol
  • used to treat disturbances in cardiac rhythm, myocardial infarction and angina
56
Q

what drug is beta 1 selective

A

metoprolol
atenolol

  • used to treat disturbances in cardiac rhythm, myocardial infarction and angina
57
Q

6 adverse effects of beta blockers?

A
  • fatigue
    reduced cardiac output contributes to decreased muscle perfusion leading to poor response to exercise
  • reduced peripheral blood flow
    reynauds syndrome
  • bronchoconstriction
    BETA BLOCKERS CONTRAINDICATED IN ASTHMATIC PATIENTS
  • increased risk of cardiac failure
    in extreme heart failure, sympathetic tone is important for the maintenance of function
  • risk of hypoglycaemia
  • rebound effects
58
Q

Which two enzymes are endogenous and exogenous catecholamines metabolised by?

A
  • monoamine oxidase (within cells bound to surface membrane of mitochondria)
  • catechol- O- methyl transferase (COMT)- widespread enzyme found in both neuronal and non-neuronal tissues
59
Q

action of MAO

A

(abundant in noradrenergic nerve terminals but also live in intestinal epithelium)

MAO converts catecholamines into their corresponding aldehydes and then by aldehyde dehydrogenase (ADH) to DOMA

dihydroxymandelic acid

60
Q

two isoforms of MAO?

A

MAOa in CNS, pulmonary vascular endothelium, GI tract and placenta

MAOb in CNS and platelets

61
Q

examples of MAO inhibitors

A

phenylzine (irreversible non-selective inhibitor of both isoforms)

moclobemide- short acting MAOa selective inhibitor

selegiline- irreversible MAOb selective inhibitor
— selective for dopamine and used in PD

62
Q

side effects of MAO-i

A
  • urinary retention
  • headache
  • insomnia
  • postural hypotension
  • diarrhoea

NS (7 decks)

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