The ANS Flashcards

1
Q

State 5 functions of the sympathetic system

A

Increases HR

Increases BP

Decreases gut motility

Relaxes bronchi

Dilates pupils

Relaxes sphincters

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2
Q

State 5 actions of the parasympathetic system

A

Decreases HR

Increases GI motility

Contracts bronchi

Constricts sphincters

Stimulates tears and salivation

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3
Q

Name the visceral afferents to the ANS

A

Visceral afferents arise from:
thermoreceptors (skin)
Mechanoreceptors (gut, bladder, blood vessels)
Chemoreceptors (carotid body)
Pain receptors (respond to damage, stretch, anoxia)

Afferents ascend bilaterally in multisynaptic pathways. Sensation is poorly localised. Afferents involved in reflex control travel with parasympathetic nerves, pain afferents travel with sympathetic nerves.

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4
Q

What are the 3 pathways the hypothalamus is involved with?

A

HPA axis - response to stress

HPT axis - regulates metabolism

HPG axis - controls reproduction

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5
Q

Where are the two groups of respiratory neurons located?

A

Respiratory neurons are located in the medulla. There are two groups:

Rostral medullary group - formed by nucleus of the solitary tract and contains inspiratory neurons.

Ventral medullary group - contains inspiratory and expiratory neurons. In also contains the main CPG for respiration. (Expiratory neurons are only used for forced expiration).

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6
Q

Describe the neuronal control of respiration

A

Pattern generated within the spinal cord and brainstem generate the rhythmic, paced activity of respiration.

The drive for inspiration and forced expiration is locard in the pontine and medullary respiratory centres. The pons controls timing between inspiration and expiration, which impacts the inspiratory and expiratory neurons in the medulla.

Activation of inspiratory neurons by afferent input from CNIX and CNX signals to C3-C5 and the phrenic nerve to move the diaphragm, and to T3-T6 to control the intercostals. This causes inspiration, stretching the lungs which triggers stretch receptors.

Information from stretch receptors is carried back to the medulla via the vagus nerve.

During forced expiration, expiratory neurons are excited and inspiratory neurons are inhibited.

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7
Q

pre-Botzinger complex

A

Main pattern generator for respiration driving the inspiratory neurons.

Lesions in this complex cause Cheyne-stokes respiratory pattern (cycles of respiration that are deep then get progressively shallower with periods of apnoea)

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8
Q

Biots respiration

A

Abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea

Can be caused by damage to respiratory neurons in the medulla.

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9
Q

Impact of the ANS on respiration

A

Sympathetics to the lungs arise in T1-T4 and activation leads to bronchodilation and reduction in secretions

Parasympathetic innervation arises in the Dorsal motor nucleus of the vagus and is carried by the Vagus nerve. Stimulation results in bronchoconstriction and increased glandular secretion.

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10
Q

Effect of a peripheral nerve lesion on respiration

A

can affect respiratory rate and secretions

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11
Q

Effect of a lesion in the thoracic region of the spinal cord on respiration

A

Damage to motor outflow to abdominal wall may result in alteration during forced respiration.

Damage to sympathetic neurons leaves parasympathetic effects dominant. Increases bronchoconstriction and secretions.

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12
Q

Effect of damage to the cervical spinal cord on respiration

A

Will affect the phrenic nerve. Effect depends on the size of the lesion. Sympathetic reflexes are intact but may not be under higher control, resulting in hyperreflexia.

May affect all muscles of respiration, ventilation will be required.

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13
Q

How can UMN lesions affect bladder control?

A

Causes hyperreflexia because the descending control to the sacral spinal reflex has been damaged. Results in a spastic bladder and dyssynergia because the reflex cycles cannot be co-ordinated.

This means the bladder doesn’t fill fully before urination, so there is increased frequency of micturition and urge incontinence.

Normally due to lesions between T11-S4 which damages both sympathetic and parasympathetic input.

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14
Q

How do LMN lesions affect bladder control?

A

There is no control of the bladder because there is no sensory input from the bladder to the spinal cord and no outflow to control the bladder.

This results in a completely areflexic bladder which lacks contractility and tone. This causes the bladder to accumulate large volumes of urine resulting in overflow incontinence and stress incontinence.

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15
Q

What effect does damage to the spinal cord have on bladder control?

A

Following major trauma to the spinal cord at any level, all activity below the level of the lesion is lost (spinal shock) and you get paralysis of the bladder.

The bladder becomes acontractile and there is overflow incontinence as a result of urinary retention and bladder distension.

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16
Q

When might you perform a sympathectomy?

A

Useful for treating severe hyperhidrosis, ischemic leg pain, reynaud’s syndrome

17
Q

Drugs which target the ANS

A
  • Adrenergics (SNS) – α and β blockers
  • Cholinergics (PNS) – nicotinic and muscarinic
  • Uptake inhibitors – Noradrenergic Reuptake Inhibitors (NRI) - antidepressant
  • Breakdown inhibitors – Monoamine oxidase inhibitors (MAOs) – antidepressants and Parkinson’s
18
Q

Describe the features of neurogenic shock

A

Neurogenic shock is caused by the loss of sympathetic control (tone) of resistance vessels, resulting in the massive dilatation of arterioles and venules.

Can be caused by general or spinal anesthesia, spinal cord injury, pain, and anxiety. Insult to the nervous system means the sympathetic system maintain normal vascular control or stimulate vasoconstriciton. Causes large arterial and venous dilation, resulting in reduced SV, CO and BP.

Loss of descending control results in hypothermia.

19
Q

ANS control of erection and ejactulation

A
  1. Higher control (mainly psychogenic) activates parasympathetic outflow in S2-4
  2. Parasympathetic activation leads to vasodilation of the internal pudendal artery, which floods the cavernous tissue with blood (erection) and also increases secretion in the prostate and seminal vesicles.
  3. Sympathetic activation from higher centres causes contraction of the smooth muscle in the vas deferens, prostate gland and seminal vesicles to move the sperm and secretions into the urethra. At the same time the sympathetics also act to contract the internal urethral sphincter to stop backflow into the bladder.
  4. Movement of fluid into the urethra activates sensory pathways, information travels up the pudendal nerve to the S2-4 region and activates the somatic motor outflow to cause rhythmic contractions~ejaculation.
  5. Following ejaculation sympathetic activation causes vasoconstriction resulting in detumescence.
20
Q

ANS control of the genital tracts

A

Males:
Sympathetic (L1-2) Controls emission and ejaculation
Parasympathetic (S2-4) Controls erection, and secretion

Females:
Sympathetic (T12-L1) Controls contraction and vasoconstriction
Parasympathetic (S2-4) Controls glandular secretions and clitoral engorgement