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(LUSUMA) Introduction to Cell Physiology and Pharmacology > S8) The Autonomic Nervous System > Flashcards

S8) The Autonomic Nervous System Flashcards

1
Q

What does the Autonomic Nervous System control specifically?

A
  • 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)

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7
Q

Describe the nature of post-ganglionic neurons

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

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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
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12
Q

Describe adrenergic transmission

A
  • Noradrenaline is released by Ca2+-mediated exocytosis
  • Released noradrenaline interacts with post-synaptic adrenoceptors
  • A high affinity reuptake system (Uptake 1) rapidly removes noradrenaline from the synaptic cleft
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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
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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
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)
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
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

23
Q

Identify 5 trigger factors for asthma

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

(LUSUMA) Introduction to Cell Physiology and Pharmacology (13 decks)

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