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SA ICPP > S8) The Autonomic Nervous System > Flashcards

S8) The Autonomic Nervous System Flashcards

1
Q

What does the Autonomic Nervous System control specifically?

A

involuntary functions

  • Smooth muscle (vascular and visceral)
  • Exocrine (and some endocrine) secretions
  • Rate and force of the heart
  • Certain metabolic pathways
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2
Q

Describe the layout and functioning of the ANS

A
  • ANS conveys information from the CNS to the neuro-effector junction via the pre-ganglionic and post-ganglionic neurones
  • The ANS consists of two divisions, the sympathetic and parasympathetic systems
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3
Q

What is a neuro-effector junction?

A

A neuro-effector junction is the point at which the target cell/tissue is innervated

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4
Q

Describe the dual parasympathetic and sympathetic (both divisions of ANS) innervation of tissues

A

Whereever this occurs, sympathetic and parasympathetic systems often have opposing effects e.g. in control of heart rate; smooth muscle in GI motility, etc.

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5
Q

What are the main neurotransmitters in the ANS?

A
  • Acetylcholine (ACh)
  • Noradrenaline (NA)
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6
Q

Describe the nature of pre-ganglionic neurons

A

All pre-ganglionic neurons are cholinergic (ACh is principal transmitter) recieving signal is a nictonic ACh receptor

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7
Q

Describe the nature of post-ganglionic neurons

A
  • Parasympathetic post-ganglionic neurons are also cholinergic uses ACh
  • Most sympathetic post-ganglionic neurons are noradrenergic

- muscarinic receptors

some sympathetic post ganglionic neurones are cholinergic and use ACh eg those innervating sweat glands

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8
Q

In five steps, describe the basic processes that take place at a typical synapse

A

⇒ Synthesis and storage of transmitter

⇒ Depolarisation by action potential and resultant influx of Ca2+

⇒ Exocytotic release of transmitter

⇒ Diffusion to post-synaptic membrane

⇒ Interaction with post-synaptic receptors

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9
Q

Describe the synthesis of noradrenaline

A
  • Noradrenaline is synthesised from tyrosine
  • The presence of phenylethanolamine N-methyltransferase in the chromaffin cells of the adrenal medulla allows adrenaline to be synthesised
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10
Q

Describe the synthesis of acetylcholine

A

Acetylcholine is synthesised by the enzyme choline acetyltransferase from choline and acetyl CoA in the cytoplasm of cholinergic terminals

acted on by cholineesterase which will break down acetylcholine to acetate and choline

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11
Q

Describe cholinergic transmission

A
  • Cholinergic terminals possess numerous vesicles containing ACh released by Ca2+-mediated exocytosis
  • Released ACh interacts with post-synaptic cholinoceptors
  • Cholinesterase rapidly degrades ACh in the synaptic cleft to choline and acetate

(you would find this in the sympathetic and the parasympathetic ganglia - know because of target nicotinic receptor )

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12
Q

Describe adrenergic transmission

A
  • Noradrenaline is released by Ca2+-mediated exocytosis
  • Released noradrenaline interacts with post-synaptic adrenoceptors -> signals effector tissue
  • A high affinity reuptake system (Uptake 1) rapidly removes noradrenaline from the synaptic cleft
  • within seconds its terminated via noradrenaline transport protein (NET)
  • quickly repackaged using MAO and COMT enzymes
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13
Q

Identify some drugs which act on cholinergic nerve terminals

A
  • Nicotinic cholinoceptor antagonists
  • Muscarinic cholinoceptor agonists
  • Muscarinic cholinoceptor antagonists
  • Cholinesterase inhibitors

muscarinic are the best

normally side effects can limit the use of these drugs eg:

  • decrease heart rate
  • mild bronchoconstriction
  • sweating
  • salivation
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14
Q

Identify some drugs acting on adrenergic nerve terminals

A
  • α-Methyl-tyrosine
  • α-Methyl-DOPA
  • CarbiDOPA
  • Uptake 1 inhibitors
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15
Q

Describe the use of selective β1 adrenoceptor agonists (benefits & side effects)

A
  • β1 adrenoceptor agonists cause positive inotropic and chronotropic effects, thus are useful in treating circulatory shock
  • Side effect: cardiac dysrhythmias
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16
Q

Describe the use of selective β2 adrenoceptor agonists and provide an example

A

β2 adrenoceptor agonists are highly effective in reversing bronchoconstriction in asthmatics e.g. salbutamol

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17
Q

Describe the use of selective α1 adrenoceptor agonists

A

α1 adrenoceptor agonists are used as nasal decongestants and may be given with a local anaesthetic injection to cause local vasoconstriction

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18
Q

Describe the use of selective α2 adrenoreceptor agonists

A

Selective α2-agonists can be used as antihypertensive agents

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19
Q

Describe the use of selective α1-adrenoceptor antagonists (benefits & side effects)

A
  • α1-adrenoceptor antagonists are used in the treatment of hypertension
  • Side effects: postural hypotension and impotence
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20
Q

Describe the use of α-adrenoceptor antagonists (benefits and side effects)

A
  • α-adrenoceptor antagonists cause peripheral vasodilatation in the treatment of peripheral vascular disease
  • Side effects: postural hypotension and reflex tachycardia (not used for hypertension treatment)
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21
Q

Describe the use of β-adrenoceptor antagonists (side effects & benefits)

A
  • β-adrenoceptor antagonists are used to treat hypertension, cardiac dysrhythmias, angina and myocardial infarction
  • Side effects: bronchoconstriction (in asthmatics), bradycardia, cold extremities, insomnia and depression
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22
Q

What is asthma?

A

Asthma is a long-term inflammatory disorder of the lungs characterised by airway hyper-responsiveness which causes variable and reversible airflow obstruction

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23
Q

Identify 5 trigger factors for asthma

A
  • Infection
  • Allergens (pollen, dust, mould)
  • Air pollution (cigarette smoke, chemicals)
  • Cold air
  • Exercise
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24
Q

In 4 steps, describe how the pathological abnormalities seen in asthma occur

A

⇒ Eosinophils accumulate and infiltrate bronchial smooth muscle causing mucosal oedema

⇒ Released cytotoxic mediators damage the respiratory epithelial layer

⇒ Exposed sensory nerves result in bronchial hyper-responsiveness

⇒ Hyper-secretion of mucus blocks airways

25
Q

What are the symptoms of a patient with asthma?

A
  • Dyspnoea
  • Chest tightness
  • Chronic cough
  • Wheeze
26
Q

Explain the action of the parasympathetic nervous system

A

On stimulation, parasympathetic nerves release ACh which acts on post-synaptic muscarinic ACh receptors on smooth muscle cells, causing airways to contract

27
Q

In three steps, explain the consequences of increased parasympathetic drive

A

⇒ Increased smooth muscle contraction (bronchoconstriction)

⇒ Lumen narrows

⇒ Increased resistance to air flow

28
Q

Although there is little sympathetic innervation of the human airways there is a large population of adrenoceptors in the smooth muscle cells of the airway.

What subtype are these?

A

β2-adrenoceptors

29
Q

In the airways, what are the consequences of increased sympathetic drive (circulating catecholamines in blood)?

A

Smooth muscle relaxes (bronchodilation)

30
Q

In 7 steps, describe the cellular mechanisms that lead to bronchodilation

A

⇒ Catecholamines stimulate β2 adrenoreceptors in the airways (GS GPCRs)

⇒ Activation of adenylyl cyclase

⇒ Formation of cAMP

⇒ Activation of PKA

⇒ Decreased [Ca2+]i

⇒ Bronchodilation

31
Q

What are the main categories of drugs that are used to treat asthma?

A
  • Bronchodilators:

I. β2 adrenoreceptor agonists

II. Muscarinic receptor antagonists

  • Anti-inflammatory drugs
  • Leukotriene receptor antagonists
32
Q

Describe how the drugs used to treat asthma mimic the functions of the ANS at a cellular level?

A
  • β2-adrenoreceptor agonists increase cAMP resulting in SM relaxation
  • Xanthine drugs increase cAMP resulting in SM relaxation
  • Muscarinic receptor antagonists block ACh-induced bronchospasms
33
Q

Discuss the advantages of using highly selective agents which display either short or long durations of action in treating asthma

A
  • Short acting β2 agonists used acutely to counteract bronchoconstriction during an asthma attack e.g. salbutamol
  • Long acting β2 agonists used at night to try and prevent a fall in peak flow in the morning e.g. salmeterol
34
Q

What advantage does adrenoceptor agonist therapy confer over the use of muscarinic cholinoceptor antagonists?

A
  • Adrenoreceptor agonists cause bronchodilation irrespective of the reason behind the bronchoconstriction
  • Muscarinic receptor antagonists only inhibits the action of the PNS – not usually the cause of an asthma attack
35
Q

What physiological reflexes are involved in the normal control of blood pressure?

A
  • Sympathetic nervous system
  • Renin angiotensin aldosterone system (RAAS)
36
Q

Identify the structures the SNS acts on to control blood pressure and describe its effects

A
  • Systemic vasculature: increases peripheral resistance
  • Heart: increases cardiac output
  • Kidney: reduces Na+ / H2O loss
37
Q

Identify and describe the main classes of drugs used in the treatment of hypertension

A
  • Angiotensin Converting Enzyme Inhibitors (ACEi) – inhibit the production of Angiotensin II
  • Angiotensin II inhibitors (ARBs) – inhibit the action of AII
  • Calcium Channel Blockers – smooth muscle vasodilators
  • Beta-blockers – reduce cardiac output and decrease renin production
  • Alpha-blockers – vasodilators
38
Q

What are the major population of adrenoceptors that mediate vasoconstriction of the vasculature?

A

α1-adrenoceptor

39
Q

Identify the 3 mechanisms through which β-adrenoceptor antagonists exert their anti-hypertensive actions

A
  • Reduced ionotropy (force) of heart beats
  • Reduced chronotropy (frequency) of heart beats
  • Reducing renin release from the kidneys
40
Q

Why should so much consideration be given to side-effect profiles when treating hypertension?

A
  • Hypertension is generally asymptomatic
  • Tablets that treat hypertension all have side effects
  • Patients don’t like side effects
  • This can cause poor compliance to treatment
41
Q

The thyroid gland produces hormones that regulate our metabolic rate.

Identify them and describe their actions

A
  • Triiodothyronine (T3) – active hormone, increases basal metabolic rate
  • Thyroxine (T4) – relatively inactive, reduces levels of T3
42
Q

In six steps, outline the negative feedback loop in the HPT axis

A

⇒ Hypothalamus releases TRH in response to low levels of T3/T4

⇒ TRH acts on the pituitary gland

⇒ Anterior pituitary gland releases TSH

⇒ TSH acts on the thyroid gland

⇒ Thyroid gland releses thyroid hormones

⇒ High levels of T3/T4 prevent further release of TRH and TSH

43
Q

Identify and describe three clinical conditions wherein the thyroid malfunctions

A
  • Hypothyroidism refers to an underactive thyroid gland
  • Hyperthyroidism refers to an overactive thyroid gland
  • Thyrotoxicosis refers to the clinical symptoms due to high levels of thyroid hormone in the bloodstream
44
Q

Compare and contrast the symptoms of thyrotoxicosis with those of anxiety

A
  • Similarities: palpitations, restlessness, increased bowel movements, tremour
  • Differences: goitre, increased appetite, vasodilation, weight loss in anxiety
45
Q

Which drug targeted to the ANS can be used for the treatment for thyrotoxicosis?

A
  • Non-selective β-adrenoceptor antagonists e.g. propanolol
  • Thyroid hormones upregulate the number of adrenoceptors in the body
46
Q

where does the sympathetic nervous system orginates from

A

thorasic and lumbar regions

47
Q

where does the parasytmpathetic system orginate from

A

medullary (cranial) and sacral outflow

it also involves the use of the vagus nerve

48
Q

diagram of nerves involved in ANS

A
49
Q

summary of ACh and noradrenaline

A

ACh acts on muscarinic receptors

noradrenaline acts on adrenoreceptors

50
Q

somatic system

A

voluntary peripheral nervous system

51
Q

parasympathetic release of ACh

A
52
Q

sympathetic release of noradrenaline

A
53
Q

enteric nervous system

A

also known as the gastrointestinal system that can operate independently without the CNS

54
Q

common sites of drug action

A
55
Q

sludge syndrome

A

cant break down acetylcholine (permenant) => stimulates muscurinic receptors

found;

drug overdose

magic mushrooms

treatment:

atropine and pralidoxime

56
Q

mACh receptor agonists and antagonists

A
57
Q

noradrenergic varicosity

A

axon swells to form variscosity

this is where noradrenaline is synthesised, stored and released

58
Q

steps for noradrenaline

A

SA ICPP (11 decks)

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