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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
What are the main ANS locations, cellular response and functional ANS response of α1?
Cardiovascular GI tract Genitourinary ↑ IP3, DAG Vasoconstriction Smooth muscle contraction (GI sphincters and genitourinary)
26
What are the main ANS locations, cellular response and functional ANS response of α2?
Neuronal ↓ cAMP ↓transmi er release
27
What are the main ANS locations, cellular response and functional ANS response of β1?
Heart Kidneys ↑ cAMP ↑ cardiac rate ↑ cardiac force Renin release
28
What are the main ANS locations, cellular response and functional ANS response of β2?
Lungs Smooth muscle Skeletal muscle ↑ cAMP Bronchodilation Relaxation of visceral smooth muscle Vasodilation (sk. muscle) Tremor
29
What is used to treat nasal congestion due to upper respiratory tract infection?
Phenylephrine | Constriction of airway blood vessels (α1)
30
What is used to treat coughing, wheezing, shortness of breath and tightness of the chest due to asthma?
Salbutamol or Salmeterol Also terbutaline All cause bronchodilation (Beta 2 agonist)
31
What are the side effects and differences of Salbutamol and Salmeterol?
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
When does premature labour occur?
Premature labour between 24 and 33 weeks of gestation | Need to delay delivery to prepare treatment or transfer
33
What drug is used to delay delivery in premature labour?
Salbutamol Also terbutaline Relaxation of uterine smooth muscle (β2)
34
What is cariogenic shock?
Damaged heart, unable to supply enough blood to the organs of the body
35
What drug is used to treat cariogenic shock?
Dobutamine | ↑ heart rate and force (β1)
36
What is hypertension?
Elevated blood pressure
37
What drugs are used to treat hypertension?
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
What does prazosin do?
Vasodilation by blocking α1 receptors
39
What does propranolol do?
↓ heart rate and force by blocking β1 receptors | ↓renin release by kidneys (β1)
40
What does atenolol do?
↓ heart rate and force by blocking β1 receptors | ↓renin release by kidneys (β1)
41
What does clonidine do?
Stimulation of pre-synaptic α2 receptors to ↓ NA release. Also has central effect.
42
What are cardiac dysrhythmias?
Atrial fibrillations, with palpitations, rapid heart rate and inefficient cardiac output
43
What drugs treat cardiac dysrhythmias?
``` 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
What is cardiac arrest?
Cessation fo normal cardiac function
45
What drug is used to treat cardiac arrest?
Adrenaline Vasoconstriction (α1) ↑ heart rate and force (β1) Also known as epinephrine
46
What is anaphylaxis?
``` A distributive shock Narrowing of airways Sudden drop in blood pressure Red raised itchy skin rash Swelling of eyes, lips, hands and feet ```
47
What is used to treat anaphylaxis?
Adrenaline Vasoconstriction (α1) ↑ heart rate and force (β1) Bronchodilation (β2) ↓ histamine release by mast cells (β2)
48
What factors constitute the mean arterial blood pressure?
Cardiac output from the heart x total peripheral resistance of the blood vessels
49
Describe the control of blood pressure by the sympathetic nervous system
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
What are the categories of beta blockers?
“cardioselective” or “non-cardioselective”.
51
Describe beta blockers
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
What is benign prostatic hyperplasia?
Swollen prostate causing problems with passing urine
53
What drugs are used to treat benign prostatic hyperplasia?
Prazosin Relax bladder neck and prostate capsule by blocking α1 receptors Tamsulosin Is more prostate-specific also blocker for alpha 1
54
What useful revision tool is in this lecture?
The agonist/antagonist selectivity tables
55
What things should be considered when thinking about adrenoreceptors as therapeutic targets?
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
Summarise the use of drugs in the ANS
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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