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Semester 2 Year 1 > Autonomic Nervous System 3 > Flashcards

Autonomic Nervous System 3 Flashcards

1
Q

What are some catecholamines?

A

Dopamine, Adrenaline, Noradrenaline, DOPA, all derived from tyrosine

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2
Q

What are some proteins that catecholamines can effect?

A

tyrosine hydroxylase

DOPA decarboxylase – Methyldopa

Dopamine β-hydroxylase (DBH)

PNMT

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3
Q

What is the order of the Tyrosine -> adrenaline pathway?

A

Tyrosine is modified by tyrosine hydroxylase to form DOPA (rate limiting step)

DOPA is modified by DOPA decarboxylase to form dopamine

Dopamine is modified by Dopamine β-hydroxylase (DBH) to form noradrenaline

Noradrenaline is modified by PNMT to form adrenaline

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4
Q

Describe some properties of tyrosine hydroxylase?

A

– Rate limiting step

– Inhibited by catecholamines

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5
Q

Describe some properties of DOPA decarboxylase?

A

– also known as Methyldopa

• used for Hypertension in pregnancy

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6
Q

Describe some properties of dopamine β-hydroxylase (DBH)?

A

– Membrane bound

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7
Q

Describe some properties of PNMT?

A

– Mainly located in adrenal medulla

– Induced by adrenal cortex hormones

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8
Q

What is PNMT?

A

Phenylethanolamine N-methyltransferase

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9
Q

Describe noradrenaline (NA) release

A

Release facilitated by Ca2+
α2 adrenoreceptors on the presynaptic terminal
– ↓Ca2+influx thus ↓NA release

No equivalent to acetylcholinesterases for NA
—-– ~75% recaptured by neurons
—-– Norepinephrine transporter
(NET) is what reuptakes NA
—-– “Repackaged” into vesicles by vesicular monoamine transporter (VMAT)

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10
Q

What do anticholinesterases do?

A

Anticholinesterases are a class of drugs that decrease breakdown of acetylcholine

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11
Q

Describe noradrenaline uptake and degradation

A

– ~75% recaptured by neurons
– Norepinephrine transporter
(NET) is what reuptakes NA
– “Repackaged” into vesicles by vesicular monoamine transporter (VMAT)

Affected by:
Indirectly acting sympathomimetic drugs
Monoamine oxidase (MAO) inhibitors
Uptake inhibitors

Amphetamines displace NA from vesicles and chucks it out into synapse which is baller

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12
Q

What are some drugs that affect the noradrenergic neurons?

A

MAO inhibitors
α2 adrenoreceptor agonists
α2 adrenoreceptor antagonists
NET inhibitors

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13
Q

What do MAO inhibitors do?

A

Inhibit MAO which prevents it from breaking down NA into metabolites

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14
Q

What do α2 adrenoreceptor agonists and α2 adrenoreceptor antagonists do?

A

Support/block the release of noradrenaline

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15
Q

What do NET inhibitors do?

A

Block uptake of NA in cells

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16
Q

What are some drugs that affect catecholamine synthesis?

A

methyldopa

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17
Q

What are some drugs that affect catecholamine release?

A

– Indirectly acting sympathomimetics – e.g. amphetamines

– By acting on α2 adrenoreceptors – e.g. clonidine

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18
Q

What are some inhibitors of catecholamine uptake?

A

– NET inhibitors – e.g. cocaine, tricylic antidepressants

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19
Q

What are some inhibitors of catecholamine metabolic degradation?

A

– Monoamine oxidase inhibitors used in depression

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20
Q

What are the actions of drugs that affect noradrenergic neurons?

A

Drugs that affect catecholamine synthesis
Drugs that affect catecholamine release
Inhibitors of catecholamine uptake
Inhibitors of catecholamine metabolic degradation

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21
Q

What actions do ANS adrenergic receptors take?

A

Adrenergic receptors are metabotropic (G-protein coupled receptors)

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22
Q

What are the two main groups of adrenoreceptors?

A

α1, α2

β1, β2, β3

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23
Q

What is the importance of an understanding of the two main groups of adrenoreceptors?

A

There are exploitable differences in the selectivity of these receptors for catecholamines
There are general patterns of tissue distribution that allow for some specificity of drug action

24
Q

What are the adrenorecpetor subtypes we have to know?

A

All are G-protein coupled (metabotropic) receptors

α1
α2
β1
β2

25
Q

What are the main ANS locations, cellular response and functional ANS response of α1?

A

Cardiovascular GI tract Genitourinary

↑ IP3, DAG

Vasoconstriction
Smooth muscle contraction (GI sphincters and genitourinary)

26
Q

What are the main ANS locations, cellular response and functional ANS response of α2?

A

Neuronal

↓ cAMP

↓transmi er
release

27
Q

What are the main ANS locations, cellular response and functional ANS response of β1?

A

Heart Kidneys

↑ cAMP

↑ cardiac rate ↑ cardiac force
Renin release

28
Q

What are the main ANS locations, cellular response and functional ANS response of β2?

A

Lungs Smooth muscle Skeletal muscle

↑ cAMP

Bronchodilation
Relaxation of visceral smooth muscle
Vasodilation (sk. muscle) Tremor

29
Q

What is used to treat nasal congestion due to upper respiratory tract infection?

A

Phenylephrine

Constriction of airway blood vessels (α1)

30
Q

What is used to treat coughing, wheezing, shortness of breath and tightness of the chest due to asthma?

A

Salbutamol or Salmeterol
Also terbutaline
All cause bronchodilation (Beta 2 agonist)

31
Q

What are the side effects and differences of Salbutamol and Salmeterol?

A

Side effects can include muscle tremor and cardiac arrhythmias
– What does this suggest?
(At high doses these drugs may start to have some Beta 1 agonist effects)
Difference between them is more about their
duration of action than receptor specificity – Short-acting (SABA) = salbutamtol
– Long-acting (LABA) = salmeterol

32
Q

When does premature labour occur?

A

Premature labour between 24 and 33 weeks of gestation

Need to delay delivery to prepare treatment or transfer

33
Q

What drug is used to delay delivery in premature labour?

A

Salbutamol
Also terbutaline
Relaxation of uterine smooth muscle (β2)

34
Q

What is cariogenic shock?

A

Damaged heart, unable to supply enough blood to the organs of the body

35
Q

What drug is used to treat cariogenic shock?

A

Dobutamine

↑ heart rate and force (β1)

36
Q

What is hypertension?

A

Elevated blood pressure

37
Q

What drugs are used to treat hypertension?

A

Prazosin
Vasodilation by blocking α1 receptors Propranolol
↓ heart rate and force by blocking β1 receptors
↓renin release by kidneys (β1)
Atenolol
↓ heart rate and force by blocking β1 receptors
↓renin release by kidneys (β1)
Clonidine
Stimulation of pre-synaptic α2 receptors to ↓ NA release. Also has central effect.

38
Q

What does prazosin do?

A

Vasodilation by blocking α1 receptors

39
Q

What does propranolol do?

A

↓ heart rate and force by blocking β1 receptors

↓renin release by kidneys (β1)

40
Q

What does atenolol do?

A

↓ heart rate and force by blocking β1 receptors

↓renin release by kidneys (β1)

41
Q

What does clonidine do?

A

Stimulation of pre-synaptic α2 receptors to ↓ NA release. Also has central effect.

42
Q

What are cardiac dysrhythmias?

A

Atrial fibrillations, with palpitations, rapid heart rate and inefficient cardiac output

43
Q

What drugs treat cardiac dysrhythmias?

A 
Propranolol
↓ heart rate and force by blocking β1
receptors
↓renin release by kidneys (β1)
Atenolol
↓ heart rate and force by blocking β1
receptors
↓renin release by kidneys (β1)
Beta Blockers
44
Q

What is cardiac arrest?

A

Cessation fo normal cardiac function

45
Q

What drug is used to treat cardiac arrest?

A

Adrenaline
Vasoconstriction (α1)
↑ heart rate and force (β1)

Also known as epinephrine

46
Q

What is anaphylaxis?

A 
A distributive shock
Narrowing of airways
Sudden drop in blood pressure
Red raised itchy skin rash
Swelling of eyes, lips, hands and feet
47
Q

What is used to treat anaphylaxis?

A

Adrenaline
Vasoconstriction (α1)
↑ heart rate and force (β1) Bronchodilation (β2)
↓ histamine release by mast cells (β2)

48
Q

What factors constitute the mean arterial blood pressure?

A

Cardiac output from the heart x total peripheral resistance of the blood vessels

49
Q

Describe the control of blood pressure by the sympathetic nervous system

A

Sympathetic stimulation increases cardiac output – By increasing the heart rate
– By increasing the volume pumped on each stroke
– Both mediated by β1 receptors

Sympathetic stimulation increases total peripheral resistance – By constricting blood vessels (mainly small arteries/arterioles)
– Mediated by α1 receptors

50
Q

What are the categories of beta blockers?

A

“cardioselective” or “non-cardioselective”.

51
Q

Describe beta blockers

A

Often referred to as “cardioselective” or “non-cardioselective”.
Use of non-cardioselective potentially problematic in asthmatics.
– Why? (Contraindicated in patients w asthma)
Sometimes used in anxiety (blockers NA signalling in CNS)

52
Q

What is benign prostatic hyperplasia?

A

Swollen prostate causing problems with passing urine

53
Q

What drugs are used to treat benign prostatic hyperplasia?

A

Prazosin
Relax bladder neck and prostate capsule by blocking α1 receptors
Tamsulosin
Is more prostate-specific also blocker for alpha 1

54
Q

What useful revision tool is in this lecture?

A

The agonist/antagonist selectivity tables

55
Q

What things should be considered when thinking about adrenoreceptors as therapeutic targets?

A

Think of the pattern of distribution of adrenoreceptors on the target organ/tissue
Think of the normal function of sympathetic innervation relating to the target organ/tissue
Think if you’re trying to return to normal function (agonist) or subdue normal function (antagonist)

56
Q

Summarise the use of drugs in the ANS

A

Sympathetic and parasympathetic systems often have opposing effects
– Agonist of one may have same effect as antagonist for the other
Differences in the postganglionic transmitters and target tissue receptors are exploitable
– Between parasympathetic and sympathetic
– Between sub-types of receptors within branches
Other chemical properties of agents can further enhance their specificity of action

Semester 2 Year 1 (82 decks)

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