The ANS Flashcards
State 5 functions of the sympathetic system
Increases HR
Increases BP
Decreases gut motility
Relaxes bronchi
Dilates pupils
Relaxes sphincters
State 5 actions of the parasympathetic system
Decreases HR
Increases GI motility
Contracts bronchi
Constricts sphincters
Stimulates tears and salivation
Name the visceral afferents to the ANS
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.
What are the 3 pathways the hypothalamus is involved with?
HPA axis - response to stress
HPT axis - regulates metabolism
HPG axis - controls reproduction
Where are the two groups of respiratory neurons located?
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).
Describe the neuronal control of respiration
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.
pre-Botzinger complex
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)
Biots respiration
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.
Impact of the ANS on respiration
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.
Effect of a peripheral nerve lesion on respiration
can affect respiratory rate and secretions
Effect of a lesion in the thoracic region of the spinal cord on respiration
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.
Effect of damage to the cervical spinal cord on respiration
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.
How can UMN lesions affect bladder control?
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.
How do LMN lesions affect bladder control?
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.
What effect does damage to the spinal cord have on bladder control?
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.