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Year 1 Neurology > Neurology Phisyology > Flashcards

Neurology Phisyology Flashcards

1
Q

What are the 3 functions of the nervous system? How are these functions achieved?

A

Sensation - Receptors detect changes in the environment and provide information to the CNS Integration - Input from environment is processed and integrated by the CNS. Decisions are made and responses formulated Activation - Response forwarded to the appropriate muscles and glands

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2
Q

What is the function of the nervous system dependent on?

A

Anatomical relationships between neurons (Axon length, type of neuron, amount of neurons in circuit) Interactions between neurons (Mode of communication, receptor density, number of transmitters)

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3
Q

Give 5 reasons why there may be dysfunction of the nervous system

A

Damage by trauma or disease Neurons loose the ability to produce transmitters Neurons over or under produce transmitters Neurons fail to recognise transmitters Effector organs fail to respond

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4
Q

How can dysfunction of the nervous system manifest in a patient?

A

Loss of sensation or function Gain of a new feature Change in behaviour, personality or perception

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5
Q

What are the two main cell types in the nervous system?

A

Neurons Glia

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6
Q

Give two examples of neurons

A

Principle cells Inter-neurons

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7
Q

Give 5 examples of Glia

A

Astrocytes Ependymal cells Microglia Oliodendroglia Schwann cells

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8
Q

Which cell type in the nervous system commonly malfunctions and forms tumours?

A

Glia cells

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9
Q

What are the three main groups of neurons, and why are they classified in this way?

A

Multipolar Bipolar Unipolar Classified according to the number of processes in and out of the neuron

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10
Q

What is the function of a dendrite?

A

Receptive field of the neurons. Sensitive to neurotransmitter input

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11
Q

What is the Soma of a neuron?

A

The metabolic and integrating centre. Also may be called the cell body

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12
Q

What is the function of an axon?

A

Rapid one way communication between the cell body and the axon terminals

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13
Q

What is the function of synaptic terminals?

A

Releases transmitters and communicates with other cells in a pathway or circuit

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14
Q

Name 4 common features of all neurons?

A

Dendrites, Soma, Axon, Synaptic terminals

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15
Q

What are the functions and features of an Astrocyte?

A

Form a bridge between the neuron and blood vessels. Structure, homeostasis and neuro-vascular communication. Large star shaped cell with multiple dendritic processes.

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16
Q

What are the functions and features of an Ependymal cell?

A

Form the lining of the ventricular system. Production and movement of CSF. Simple ciliated cuboidal epithelial cells.

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17
Q

What are the functions and features of Microglia?

A

Immune response (WBC’s of the CNS). Activated on trauma. Small glial cells with multiple processes. Over activation can cause problems in the CNS.

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18
Q

What are the functions and features of Oligodendroglia?

A

Myelin producing cells found in the CNS. Myelination and insulation of the axons. Large with broad processes.

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19
Q

What are the functions and features of Schwann cells?

A

Mylein producing cells in the PNS. Myelination and insulation of the axons. Large with broad processes.

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20
Q

What is the resting membrane potential in a neuron?

A

-70mV

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21
Q

What is the threshold potential in a neuron and what happens at this point?

A

-55mV All sodium channels open and there is a surge of sodium into the cell

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22
Q

The balance of what ions cause a action potential to fire in a neuron. How does this differ to a cardiac or a muscle cell?

A

Sodium and Potassium In a muscle or Cardiac cell there is also Calcium involved

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23
Q

Name the 6 phases in action potential firing

A

Rest Depolarisation AP firing Repolarisation Refractory period After-hyperpolarisation

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24
Q

What is Saltatory conduction?

A

The propagation of an action potential along a mylenated axon, from one node of Ranvier to another. This allows for faster transmission of the action potential, and therefore speeds up communication.

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25
Q

Name two Myelination disorders and what causes them

A

Multiple Sclerosis - Dysfunction in Oligodendrocytes in the CNS Guillian Barre - Dysfunction in Schwann cells in the PNS

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26
Q

What age is Myelination completed in the spinal cord and what is this important for?

A

Completed at 18 months. Essential in the spinal cord for control of motor function

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27
Q

What are the two types of synaptic transmission?

A

Chemical Electrical

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28
Q

How do chemical synapses work?

A

Action potential reaches the axon terminal and depolarises the membrane causing voltage gaited sodium channels to open Sodium ions enter the cell, causing the pre-synaptic membrane to further depolarise This causes voltage gaited calcium channels to open and calcium to enter the cell This initiates a signalling sequence that causes the vesicle and pre-synaptic membrane to fuse Neurotransmitters released across the synaptic junction Neurotransmitters act on receptors in the postsynaptic terminal MAJOR DRUG TARGET

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29
Q

How do electrical synapses work?

A

Pre-synaptic and Post-synaptic terminal join via channel proteins to form gap junction, resulting in a narrow gap between the membranes Allows currents to pass directly through the synapse and also allows molecules carrying the current through Can be bi-directional

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30
Q

How do chemical and electrical synapses differ in transmission times?

A

Chemical = Fast transmission, slower cell to cell transmission but can cope with a higher frequency of activity Electrical = Slower transmission, faster cell to cell contact, but more effective at lower frequencies

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31
Q

How is communication achieved between the nervous system and muscles?

A

Communication is achieved via the neuromuscular junction. Propergation of an action potential triggers exocyosis of Ach from the synaptic terminal Ach crosses the cleft and acts on cholinergic receptors in the motor end plate This initiates muscle contraction Impulse is carried through the muscle via T-tubules and sarcoplasmic reticulium

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32
Q

What is the cause of Myaesthenia Gravis? How is it investigated?

A

Autoimmune disease that affects the neuromuscular junction Circulating anti-bodies block Ach receptors, causing them to not work properly; thereby stopping communication Slows muscle activity and reduces tone investigated using nerve conduction tests and electromyography

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33
Q

What are the two main chemical transmitters used in the CNS? Are they excitatory or inhibitory?

A

Glutamate = Major excitatory trasmitter GABA = Major inhibitory transmitter

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34
Q

Why is inhibition essential in communication of the nervous system? Name the 3 types of inhibition in the CNS

A

Key for coding of signal and activity in order to get a pattern Direct inhibition Lateral inhibition Dis-inhibition

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35
Q

What factors does communication of the nervous system rely on? How do these factors help communication?

A

Inhibition = coding Synchrony = co-ordinates activity Plasticity = changes the strength of the signal

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36
Q

How does direct inhibition aid in communication in the CNS? Give a example of a drug that can alter this

A

Excitatory neurons have regular firing in the absence of inhibition Inhibition produces patterns of activity (coding) Coding carries the information and can be read by the brain LSD increases firing of excitatory neurons, making it a good drug for depression Drugs that increase firing can lead to loss of coding and therefore can decrease the effectiveness of the brain and lead to psychological side effects

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37
Q

How does lateral inhibition aid in communication in the CNS? What pathways is this type of inhibition normally found in?

A

Activation of excitatory cells also activates associated inhibitory cells Inhibition acts on neighbouring cells to reduce activity This strengthens the response of the cell directly stimulated Lateral inhibition can be seen in sensory pathways: Vision Touch Olfaction

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38
Q

How does Dis-inhibition aid in communication in the CNS? Where is this process key in the CNS?

A

Activation of a inhibitory circuit leads to excitation Inhibition of a inhibitory cell results in excitation of the excitatory cell (2 negatives make a positive) This types of inhibition plays a vital role in the basal ganglia, as it shapes motor function

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39
Q

How does synchrony modify communication in the CNS?

A

It changes strength at a network level This occurs cell to cell via gap junctions

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40
Q

How is synchrony investigated?

A

Using a Electroencephalography (EEG)

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41
Q

How does plasticity modify communication in the CNS?

A

Plasticity changes strength at a neuronal level It is the up or down regulation of synaptic strength, thereby making neurons change their behaviour

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42
Q

What is the benefit of plasticity occurring at the level of a synapse? Name 3 ways this can occur

A

When changes occurring at the level of the synapse in order to regulate synaptic strength, this allows east reactivation of a circuit should a event ever happen again Changes in size (no of neurotransmitters receptors/vesicles etc) Changes in perforation (increase in receptor recycling/transmission) Change in independent synaptic release sites

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43
Q

What is the difference between Neurotransmitters and Neuromodulators?

A

Neurotransmitters act directly to alter neuronal activity Neuromodultors act on receptors or membranes to indirectly alter neuronal activity

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44
Q

Describe the role and function of neurotransmitters in cell to cell communication. Indicate the difference between inhibitory and excitatory propagation

A

Neurotransmitters are used by neurons for rapid cell to cell communication. They are stored in the vesicles in the presynaptic terminal Nerve impulse arrives and calcium channels open Terminal is depolarised Calcium binds to the synaptic vesicle Synaptic vesicle fuses with pre-synaptic membrane Neurotransmitter is released into the synaptic cleft Neurotransmitter binds to receptors on the ligand-gaited channel on the post-synaptic terminal Sodium enters the channel Action potential is generated Excitatory neurons propagate the signal onward, whereas inhibitory neurons block onwards propagation

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45
Q

How do neuromodulators alter neuronal activity? What do neuromodulators act on?

A

Neuromodulators are co-localised with neurotransmitters. Found in vesicles. They act on receptors or membranes to indirectly alter neuronal activity by changing the sensitivity or kinetics of a neurotransmitter receptor Neuromodulators can also act on glial cells

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46
Q

Name 2 excitatory neurotransmitters

A

Glutamate Aspartate

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47
Q

Name 2 inhibitory neurotransmitters

A

GABA Glycine

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48
Q

What is the main role of Adrenaline and Nora-adrenaline?

A

Stress and arousal

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49
Q

What is the main role of dopamine?

A

Motivation/motor function

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50
Q

Give 2 examples of neuromodulators and their roles

A

Vasopressin = osmoregualtion Somatostatin = Growth

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51
Q

Give 3 examples of modulatory transmitters

A

NO CO ATP

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52
Q

What are most neurological disorders linked to?

A

A change transmitter efficacy. Some can result for a single transmitter alteration, however in the majority of cases multiple pathways will be affected

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53
Q

Name 3 disorders associated with 5HT

A

Migraine Fibromyaligia Depression

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54
Q

What disease is associated with GABA?

A

Huntington’s

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55
Q

What neurotransmitter is associated with Alzheimer’s?

A

Acetylcholine

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56
Q

Name 2 disorders associated with Dopamine

A

Parkinson’s Schizophrenia

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57
Q

If activation of one class of neuron can have knock on effects on other pathways, explain how Noradrenaline levels can indirectly affect GABA activity

A

Noradrenaline alters 5HT activity 5HT levels alter Dopamine activity Dopamine levels alter Acetlycholine activity Acetylcholine levels alter GABA activity

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58
Q

Name 2 types of general receptors in the nervous system

A

Ionotropic G-protein linked receptors

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59
Q

What are the roles of specialised receptors in the nervous system?

A

General and sensory sensation Responsive to particular stimuli Transduce physical to electrical energy

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60
Q

Give 4 types of specialised receptors in the nervous system and their functions.

A

Mechanoreceptors = tactile sensation Thermoreceptors = temperature changes Nociceptors = painful/noxious stimuli Proprioceptors = detect changes in head and boy position

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61
Q

What is a channelopathy?

A

Mutations in channel sub-units that cause a change in kinetics or sensitivity

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62
Q

Give an example of a disorder caused by channelopathies, and a disorder that can cause channelopathies.

A

Developmental forms of epilepsy are caused Autoimmune disorders can cause

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63
Q

How many types of subtype receptor is a drug normally targeted at?

A

One

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64
Q

What is a polyvalent drug? Name a benefit of them

A

A non-selective drug, that can have effects on multiple sub-type receptors Have fewer side effects in the CNS

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65
Q

What mechanisms are involved in pathogenesis of neuronal and psychological disorders?

A

Altered neuronal activity Altered synchrony Cellular changes Subcellular changes Genetic/Epigenetic changes

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66
Q

What is the aim when treating neuronal and psychological disorders?

A

To restore balance leading to a good quality of life

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67
Q

What is neuroendocrinology?

A

A branch of life sciences dealing with neurosecretion and the physiological interaction between the CNS and endocrine system

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68
Q

What are the basic components of the neuroendocrine system?

A

Parvocellular neurones and Magnocellular neurones in the hypothalamus act on the anterior and posterior pituitary in the pituitary gland, which act on target tissue, adrenal glands, thyroid gland and the gonads.

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69
Q

What is the function of the hypothalamus in neuroendocrinology?

A

To integrate autonomic responses and endocrine function with behaviour

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70
Q

Give 3 ways the hypothalamus controls homeostasis

A

Behaviour concerned with everyday homeostatic requirements of life Neuronal control through the autonomic nervous system Hormonal control through hormone release from the pituitary gland

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71
Q

What are the six homeostatic functions controlled by the hypothalamus and how is this achieved?

A

1) Blood pressure and electrolyte composition 2) Body temperature 3) Energy metabolism 4) Reproduction 5) Stress response 6) Growth 1) Control of drinking salt appetite and control of blood osmolarity and vasomotor tone 2) Metabolic thermoregulation and behaviours like seeing an appropriate environment 3) Feeding, digestion and metabolic rate 4) Hormonal control of mating, pregnancy, lactation 5) Adrenal stress hormones 6) Growth hormone

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72
Q

Which hypothalamic nuclei is responsible for: Stress Energy balance Osmoregulation Maternal Control Blood pressure

A

Paraventricular nucleus

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73
Q

Which hypothalamic nuclei is responsible for: Osmoregulation Maternal control

A

Supraoptic nucleus

74
Q

Which hypothalamic nuclei is responsible for: Reproduction Growth Lactation

A

Arcuate nucleus

75
Q

What is associated with a loss of Hypothalamic Orexin Neurones?

A

Narcolepsy

76
Q

Where is the pituitary gland located?

A

In a bony cavity at the base of the brain called the Sella Turcica

77
Q

How is the pituitary gland connected to the hypothalamus?

A

Via the pituitary stalk

78
Q

Respectively, where do the anterior and posterior pituitary glands develop from?

A

A = Pharyngeal Epithelium P = Neuronal

79
Q

Respectively, what cells do the anterior and posterior pituitary glands contain?

A

A = Glandular cells P = Axon terminals

80
Q

Respectively, which neurons act on the anterior and posterior pituitary glands?

A

A = Parvocellular neurons P = Magnocellular neurons

81
Q

Respectively, what is the neuroendocrinological action of the anterior and posterior pituitary gland?

A

A = Releasing/inhibiting factors via hypophysial portal system P = Hormones directly released from magnocellular axons

82
Q

Which hormone is responsible for long bone growth?

A

Growth hormone

83
Q

Which hormone is responsible for Thyroid stimulation and regulation? (T3 and T4 release)

A

Thyroid stimulating hormone

84
Q

Which hormone is responsible for stimulation of the adrenal cortex? What is released on stimulation?

A

ACTH Corticosteroids

85
Q

Which hormones are responsible for stimulation of the ovaries and testies? What is released on stimulation?

A

FSH and LH Oestrogen and progesterone are released by the ovaries Testosterone is released by the testis

86
Q

What hormone is responsible for milk production in lactating women?

A

Prolactin

87
Q

What does the hormone oxytocin do? Where is it released from?

A

Milk letdown in lactating women and uterine contractions in pregnant women Released from the posterior pituitary gland

88
Q

What does the hormone ADH do? Where is it released from?

A

Kidney water retention Posterior pituitary gland

89
Q

What is the feedback mechanism of prolactin?

A

Prolactin secretion causes the Parvocellular neurons in the anterior pituitary gland to reduce dopamine secretion, which in turn causes increased prolactin secretion and therfore more milk production Dopamine secretion and therefore milk production can also be regulated by a suckling stimulus

90
Q

Describe the HPT axis (Hypothalamic-pituitary-thyroid axis) feedback loop What type of feedback loop is this?

A

Hypothalamus senses low levels of T3/T4 and responds by releasing TRH (thyrotropin-releasing hormone). TRH stimulates the anterior pituitary to produce TSH which in turn stimulates the thyroid to produce thyroid hormone until blood levels return to normal. This is a negative feedback look

91
Q

Describe the HPA axis (Hypothalmic-pituitary- adrenal axis) feedback loop

A

HPA axis is responsible for the stress response. Hypothalamus releases CRH (corticotropin-releasing factor) which binds to receptors on the anterior pituitary gland causing CTH to be released. ACTH binds to receptors on the adrenal cortex and stimulates the release of cortisol. At a certain blood level of cortisol , the cortisol exerts negative feedback on to the release of CRH and ACTH

92
Q

What are the 3 major neuroendocrine systems through whch the hypothalamus and anterior pituitary gland direct neuroendocrine function?

A

HPT axis HPA axis HPG axis

93
Q

Describe the HPG axis (Hypothalmic-pituitary-gonadal axis) feedback loop

A
94
Q

Describe the feedback loop in which vasopressin is released as a result of low blood pressure

A

Major restriction in blood volume is detected by baroreceptors

CN IX and CN X carry this information to the NTS in the brainstem

This either stimulates or inhibits the release of Vasporessin from the hypothalamus

Vasopressin acts of the V1 receptors on blood vessels, causing vasoconstriction and therefore an increase in blood pressure

95
Q

What is schizophrenia and how is it charecterized?

A

A psychotic disorder that at a miniumum consitists of dellusions and hallucinations

Charecterised by distortions of thinking and perception. It affects the emotionial response to stimuli/situations, becoming inapproprite or blunted

96
Q

What are the 5 diensions of symptoms shown by Schizophrenic sufferers?

A

Posititve symptoms

Negitive symptoms

Cognitive symptoms

Agressive symptoms

Depression and anxiety

97
Q

What is required for a diagnosis of Schizophrenia to be reached?

A

Disturbance lasting for 6 months or longer with at least one of the classical symptoms, delusions, hallucinations, disorganised or catatonic behavior or negitive symptoms

98
Q

Name 5 classical symptoms of Schizophrenia

A

Thought echo/instertion/withdrawal

Delusional perception and control

Hallucinatory voices that comment or discuss the patient in the third person

Though disorders

Influence or passivity

99
Q

Give 4 ‘negitive’ symptoms of Schozophrenia

A

Affective blunting = reduced emotional reactivity

Ahedonia = loss of enjoyment or intrest in previously enjoyed activites

Alogia = Loss of the ability to speak

Apathy = Absence or supression of emotion feeling, concern or passion

100
Q

Give 5 positive symptoms of Schizophrenia

A

Delusions

Hallucinations

Agitation

Exaggerated/disorganised speech

Exaggerated/disorganised bizzare behavior

101
Q

What anatomical alreations can be see in Schizophrenia?

A

Imbalance in transmitter levels are thought to underpin schizophrena (dopamine)

Degeneration occurs within the grey matter - particularly within the medial temporal lobes

Enlarged ventricles and sulci are apparent on scanning as a result

Cerebral blood flow is reduced in the basal ganglia and frontal lobes

102
Q

What is the target for antipsycotics?

A

Dopamine receptors

Dopamine antagonists have been proven to calm Schizophrenic patients

103
Q

What is the major problem with antipsychotics?

A

Less effect on negitive symptoms

60% of patients still suffer these even when the negitive symptoms are under control

104
Q

What are the two groups of antipsychotics?

A

First generation - Classical

Second generation - Atypical

105
Q

What receptors do first generation antipsychotics act on?

A

Primarily potent antagonists at the D2 receptor

Also act on Muscaranic, Histamine, and Adrengic receptors

Low efficacy and 30% of patients are non-responders

106
Q

What are the 4 main groups of first generation antipsychotics?

A

Phenothiazines

Butyrophenones

Thioxanthines

Dibenzoiazenes

107
Q

Second generation antipsychotics were initially delveloped to around 5HT and dopamine antagonism, however they have been found to act on other receptors. What are these receptors?

A

Multiple receptor subtypes of 5HT and Dopamine

Muscarinic, histminergic and aderenergic receptors

May also inhibit reuptake mechanisms

108
Q

What is the gold standard second generation Antipsychotic?

A

Clozapine

High efficancy but has the most associated side effects (cardiovascular)

Also causes Agranulocytosis

Generally only used after at least 2 second generation antipsychotics have been shown to be ineffective

109
Q

Which two second generation antipsychotic drugs are the most effective at tacking negitive symptoms?

A

Risperidone and Olanzapine

110
Q

Risaperidone can be classed as both a first and second generation antipsychotic. Why is this?

What other uses/benfits does this drug have?

A

Shows biphasic activity. Atypical at low doses and more conventional at higher doses.

Used to treat dementia

Can be used in children and adolescents

111
Q

Name first (2), second (3) and third generation (1) antipsychotics

A

1st = Chlorpromazine, Haloperidol

2nd = Amisulpride, Risperidone, Clozapine

3rd = Aripiprazole

112
Q

What are the majority of side effects seen with antipsychotics called?

What are they a result of?

A

Extrapyramidal symptoms

As a result of altering activity within the nigrostrital pathway

113
Q

Give examples of 3 extrapyramidal symptoms caused as a side effect of antipsychotics

A

Dystonias

Akathisia

Parkinsonisms

114
Q

What are the side effects of antipsychotics?

A

Extrapyramidal symptoms

Sedation

Seizures

Hypotension

Hypothermia

Hypersensitvity

Weight gain

115
Q

Why are second generation antipsychotics associated with seeing reduced side effects?

A

2nd generation antipsychotics have a higher affinity for the mesolimbic and cortical pathways than the nigrostriatal dopaminergic pathways.

116
Q

What is neuroleptic malignant syndrome?

A

Describes the side effects associated with the use of antipsychotics in patients with a genetic polymorphism of the D2 receptor

High fever, autonomic problems, and altered consciousness

117
Q

Where a patient presents with neuroleptic malignant syndrome, how can the side effects caused by the use of antipsychotics be treated?

A

Dopamine agonists and benzodiazepines can be used following immedate withdrawal of the antipsychotic

118
Q

What is Tardive dyskinesia?

A

Disabling invoulentary movements of the face and limbs: tounge protruding, grimacing and twisting of the face and limbs

Only side effect that is irrevesible - spontanelously remitts in 30% of presentations

119
Q

What causes Tardive dyskinesia?

A

A result of oxidative neurodegneration caused by increased glutamatergic transmission wich results from a down-regulation of the dopamine system

Caused by prolonged use of classical antipsychotics

120
Q

What would be the action you would take on presentation of Tardive dyskinesia?

A

Withdraw the classical antipsychotic

Switch to a atypical antipsychotic

Immediately stop any anticholinergics being used

121
Q

What dopamine pathway is involved in the pathogenesis of schizophrenia?

A

Mesolimbic and Mesocortical

122
Q

Which of the dopamine pathways are used in parkinsonism?

A

Striatongral

123
Q

What substances can induce iatrogenic parkinsonism?

A

Antiemetics

Antiepileptics

Cardiovascular agents

Vestibular Seditives

124
Q

What are the three main effects of anaesthetic drugs?

A

Unconsciousness

(action on the reticular dormationa nd ARAS)

Loss of reflex’s

(Affects the sensory input to the reflex arc)

Analgesia

(reduced transmission of conscious sensation)

125
Q

What are the two main groups of anaesthetics, and how do they differ in administration?

A

General

(Intravenous eg. propofol)

(Inhilation eg. isofluorane)

Local

(same as general but administered in low doses to affect small localised regions)

126
Q

How are local anaesthetics grouped?

A

Split into 2 groups according to structure (normally have a ‘caine ending)

Amino-esters = metabolised in the plasma

Amino-amides = metabolised in the liver

127
Q

What is the mechanism of local anaesthetics?

A

Via sodium channel block which dampens down neuronal activity and reduces sensory transmission to the cortex

2 ways:

Directly entering the channel when its open (more channels open the bigger the effect = use dependence)

Accessing channel by crossing the axonal membrane and binding from the inside

128
Q

Give a clinical example of when local anaesthetics wouldnt work and why.

A

When the tissue is inflamed.

Local anaesthetics ability to work is pH-dependent - inflammatory soup in damaged tissue tends to be acidic

Local anaesthetics ionise in acidic pH = reduces their ability to cross the neuronal membrane and attach to the sodium channel

129
Q

How is sensation affected by administration of local anaesthetics?

A

Local anaesthetics work more easily on smaller or un-myelinated nociceptive sensory fibres (A-delta and C-fibres) and unmyelinated autonomic fibers.

This is because the access to the sodium channels via the membrane is easier than across the larger and highly myelinated proprioceptive fibres

130
Q

What 3 factors need to be taken into consideraton when selecting a local anaesthetic?

A

Needs to be:

Agent with low irritant effect and toxicity

Rapid onset of action

Half-life to allow adequate time to do a procedure

131
Q

Name 3 commonly used local anaesthetics and their uses and half lives

A

Lidocane (amide) = 1-2 hours

(Local infiltratioin, nerve block, dental and topical)

Bupivacaine (amide) = 1-3 hours

(Local infiltration, peripheral nerve block, epidural, and sympathetic nerve block)

Benzocaine (ester) = <1 minuite

(Throat lozenges)

132
Q

What are the main side effects of local anaesthetics?

A

Local irritation and inflammation occuring at the site of administration

Can be exasberated by the use of local vasoconstrictors or trauma to tissue on administration

133
Q

Rarely there can be systemic side effects on the use of local anaesthetics.

What causes this and what are the systemic side effects?

A

Caused by overadministration of of the agent, leading to increased plasma levels of the drug

Cardiovasuclar changes

(Caused by local vasodialation or cardiotoxicity through binding in the heart)

CNS chnages

(Light-headedness, sedation, loss of consciousness)

Anaphylaxis

(Rare and only found with ester drugs)

134
Q

What do general anaesthetics do?

A

Induce a loss of sensation, altered state of consciousness and a loss of memory for what happens under its influence

135
Q

Name and explain the 6 steps in the process of anaesthesia

A

Premedicaion

Benzodiazepine to reduce anxiety and help with memory loss

Induction

Inhalation of IV administration of the anaesthetic

Muscle relaxation and intubation

Uses a neuromuscular blocking agent to relax the muscles during long surgical procedures

Maintenance

Inhilation or IV administration

Analgesia

Administration of agents to reduce pain on recovery from surgery

Reversal

Of both neuromuscular blocking agent and anaesthetic

Results in return of consciousness

136
Q

What are some benifits of Inhilation anaesthetics?

A

Very potent and readily mixed with oxygen for administation (25% to prevent hypoxia)

Low blood solubility = rapid induction and recovery with fewer lingering effects

The speed of effect means anaesthetic levels can be quickly adjusted

137
Q

Nitrous oxide (simple gas) can be used in combination with volitile liquids when administering inhilation anaesthetics.

Give an example of a volitile liquid and explain why NO is used.

A

Isoflurane

NO is not very potent but can be used in combiation with other inhilarion agents.

It provides some analgesia, so when used in combination it can mean reductions in the required doses of other drugs

138
Q

What are the 4 factors that depth and speed of recovery from inhilation anaesthetics are linked to?

A

Rate of alveolar absorption

(depends on depth of inspiration and the concentration of the concentration of the agent administered)

Speed of equilibration

(balance of anaesthetic concentration in the air, blood and fats, which depends on solubility of the agent)

The relative concentations at equlibrium

Cardiac output

(controls delivery of drug o the brain)

139
Q

Regarding inhilation anaesthetics, what is the activity of the agent linked to?

A

The blood:gas partition coefficent

Indicates solubility

The oil:gas partition coefficent

Indicates the relationship between concentration of inhaled ages and that in the fat (brain/lipid membranes)

140
Q

What is the potency of an inhilation anaesthetic calculated as?

A

Minimum alveolar concentration (MAC) required to immoilise 50% of patients during noxious stimulation

141
Q

What is the Meyer-Overton theory based on?

A

The correlation between lipid solubility of inhaled anaesthetics and minimum alvelolar concentration.

States that anaesthesia occured when a sufficent number of inhilational anaesthetic molecules had accumulated in the lipid cell membrane, regardless of the drug type

142
Q

What are the main side effects of inhilation anaesthetic agents?

A

Reduce activity throughout the body, via depression of cardiac output and blood pressure

Cause respiritory depression through an action on teh brainstem respiritory centres

Cause irritation of the respiritory tract, resuting in bronchospasm and laryngospasm

143
Q

Why are IV anaesthetics not used alone for long term anaesthesia?

A

IV is used to induce anaesthesia and maintainace is provided by inhilation or a combination of inhilation and IV

This is due to accumulation affects and slow redistribution

144
Q

What are the 5 most commonly used IV anaesthetics?

A

Thiopental

Propofol

Etomidate

Ketamine (slower acting)

Midazolam (slower acting)

There is not just one mechanism of action for all the drugs

145
Q

In general, how do IV anaesthetics work?

A

Supress consciousness through a reduction of activity within the CNS with agents acting on both the inhibitory and excitatory pathways

Thiopental and Midazolam increase activity at the GABA receptor (inhibitory)

Ketamine blocks glutamatergic NMDA receptors (excitatory)

146
Q

What are the side effects of general anaesthetics?

A

Vary according to the concentration, duration and drug used

Decreased cardiac contractitlity

Respiritory depression (in overdose, leading to respiritory failure and death)

Decreased CNS fucntion

Reduced sympathetic activity

147
Q

Why might opiods be given alongside anaesthetics?

A

When given at induction, opoids can provide analgesia and reduce the dose of antibiotic required to have a seditive effect

Their effect on the CV and respiritory system can also help counteract the effects of invasive treatments, reducing HR, BP and resp rate increases that are caused by the stress

148
Q

Name 3 fast acting opiods used in combination with anaesthetics

A

Fentanyl

Alfentanil

Remifentanil

149
Q

What are epidural anaesthetics used for?

A

Use general or local anaesthetics and sedatives to remove sensation

Use analgesics to block pain sensation specifically

150
Q

Why does epidural anaesthetic have more of a effect on sensory rather than motor functions?

A

Sensory neurons are significantly more sensitive to the effects of local anaesthetics than motor neurons

Linked to the levels of myelination and the ease of entry of the anaesthetic

Epidurals do have an effect on the motor system but it is drug and concentration dependent

Midazolam = seditive and muscle relaxant effects

151
Q

What sensation is removed during labour when a epidural is used?

A

Pain is removed, but pressure sensation is not

152
Q

Whar are the most commonly used anaesthetics?

A

Bupivacaine and Lidocaine

153
Q

Why may other agents be added to an epidural?

A

To prolong the duration of the block and decrease bleeding and toxicity

Adrenaine is the most commonly added

Opoids (fentanyl and morphine) can be added for muscle relaxing and analgesica properties

154
Q

What is the Bromage scale?

A

A scale used to determine the level of epiduaral block.

Asseses and grades the patients ability to move their legs following induction - 4 levels:

1) Complete block

Patient is unable to move the knees or feet

2) Almost complete block

Patient demonstrates an inability to flex the knees but has the ability to flex the feet

3) Partial block

Patient can partially flex the knees and resist gravity and has movemnt of the feet

4) No block

Patient can flex the knees and feet fully

155
Q

What are the two groups of neuromuscular blockers?

A

Depolarising

Non-depolarising

Both groups are used to relax muscle by blocking the activity at the neuromuscular junction

156
Q

What is the mechanism of depolarising neuromuscular blockers?

A

Non-competitive/agonist neuromuscular blockers

Also includes anticholinesterases

Depolarising NMB binds to the Ach receptor causing prolonged depolarisation (receptor closes and repolarises even though agonist is still bound) and the site to be blocked = prevents depolarisation and muscle contraction

Initial depolariation causes fasciculation of the muscles prior to relaxation occuring = increases likelihood of post-operative muscle pain

157
Q

What is the most common neuromuscular blocker used?

A

Suxamethonium

Only administered IV

Rapid acting = muscle relaxation within 1 min

Rapidly metabolised by plasma cholinesterase (5-10 mins) so requires a constant infusion to maintain the blockade

158
Q

What group of neuromuscular blockers do anticholinesterases fit into?

Give and example of one

A

Depolarising neuromuscular blockers

Neostigmine

159
Q

How do anticholinesterases work when used as neuromuscular blockers?

(Acetylcholinesterase)

A

Work non-competitivly to increase the levels of Ach in the junctional cleft by blocking acetylcholinesterase breakdown of Ach

Cause muscle paralysis by overloading the system = activating all Ach receptors at maxiumum and leaving no room for additional movement

(similar to neuromuscular blockers)

160
Q

What are the issuses associated with acetylcholinesterase inhibitors?

A

They increase activity in the PNS causing bradycardia, increased secretion and increased peristalsis

161
Q

Give an example of a neurotoxin that works in a similar way to anticholinesterases

A

Botulinum toxin A ( botox)

Works to reduce muscle activity by blocking pre-synaptic release of Ach

Used clinicnally to treat muscle spazams and tic

Also known for its cosmetic uses

162
Q

What is the mechanism of non-depolarising neuromuscular blockers?

A

Known as competitive or antagonist neuromuscular blockers

Compete with Ach to bind to the Ach receptors

Once bound they prevent depolarisation thereby blocking the effect of Ach

Also act pre-synaptically to reduce calcium entry = reduces the release of transmitter from presynaptic vesicles

Do not cross theh blood brain barrier = no effect on teh CNS

163
Q

Name 2 common non-depolarising neuromuscular blockers

A

Atracurium

Vecuronium

164
Q

Other than their direct mechanisms how do depolarising and non-depolarising neuromuscular blockers differ?

A

Non-depolarising have a slower onset time (2-5 mins) with a duration between 15-90 mins

Non-depolarising are also water soluble and show no accumulation with repeated doses = more suitible for long term use

165
Q

What can happen is neuromuscular blockers and inhilation anaesthetics are taken together?

A

Inhilation anaesthetics can increase the effects of neuromuscular blockers

Must talior the cocentrations used by correlating teh effects of multiple drugs

Need a balanced level of anaesthesia, analgesia and muscle relaxation

166
Q

Which group of neuromuscular blockers is always chemically reversed prior to recovery?

What are the drugs used to do this?

A

Non-depolarising

Neostigmine (anticholinesterase)

  • Specific for a non-depolarising blockade
  • Rapid (1 min)
  • Effects last for 20-30 mins

Sugammadex (Selective relaxant binding agent)

167
Q

Anticholinesterases work as a depolarising neuromuscular blocker (acetylcholineseterase inhibitors).

What other function can they have?

A

Also work to reverse the effects of some non-depolarising neuromuscular blockers eg. atracurium

But they can prolong the action of depolarising neuromuscular drugs eg. suxamethonium

168
Q

In the event that anticholinesterases must be given, what else can be given to counteract the side effects?

A

Bradycardia and increased secretions as a result of the muscuranic effects on the PNS are the side effects

Give Glycopyrronium or Atropine prior to, or with a reversing agent

169
Q

How do selective binding agents work to undo the blockade caused by neuromuscular blockers?

Give an example of one

A

Sugammadex

Selective relaxant binding agent used for raid reversal of NMB blockade and acts by forming a complex with the drug by encapsulating it to inactivate it

Well tollerated, no effect on the cholinergic nervous system, minimises the risk of residual paralysis and is rapidly cleared form the plasma and excreted within 24 hours

170
Q

What is addiction defined as?

A

Relapsing remitting disorder comprising behaviors that are performed in a compulsive manner in spite of the potential for self harm

171
Q

Define dependency

A

Comprised of two components

Psychological dependence

Describe the effects of the compulsive behaviors and is charecterised by emotional distress caused by withdrawal of the drug

Physical dependence

The functional effect of the drug on the body itself. It is charecterised by physical symptoms of withdrawal of the drug

172
Q

What is required for a definate diagnosis of dependence?

Name the 6 boundaries used

A

Can only be made if 3 or more of the following have been present together at some point in the last year:

1) Stong desire or sense of compulsion to take the substance
2) Difficulties in controlling substance taking behavior (onset, termination, or amount)
3) A physiological withdrawal state (negitive behaviors associated with being unable to achive intoxication state)
4) Evidence of tolerance (the need to increase the amount of drug needed to achieve the same high/positive elements
5) Progressive neglect of alternative pleasure or increased intrest in the amount of time taking the drug or recovering from its effects
6) Persisting with substance abuse despite clear evidence of harmful consequences

173
Q

What are the 3 general defining components for drug dependence?

A

Psychological tollerance

Physical dependence

Tolerance

174
Q

What are the main pathways thought to be associated with controlling reward?

A

Mesolimbic and mesocortical dopamine pathways = changes in doperminergic activity

Drugs of abuse target many of the main transmitter systems also

175
Q

What are the neuroreceptors targeted by the following drugs? What are the actions of these drugs?

  1. Codeine/Heroin
  2. MDMA/Ecstasy
  3. Ketamine/PCP
  4. Alcohol
  5. Cocaine
  6. Valium
  7. Cannabis
A
  1. Opiod receptor = Agonist
  2. 5HT receptor = Increases release
  3. Glutamate receptor = Antagonist
  4. Potassium channel = Increases opening time
  5. 5HT/DA/NA = inhibits reuptake
  6. GABA receptor = co-agonist
  7. Cannabinoid receptor = agonist
176
Q

What are the 4 main dopamine containing pathways within the CNS?

A

Nigrostriatal

Mesocortical

Mesolimbic

Tuberoinfundibular

177
Q

How does the Nigrostriatal dopamine pathway work?

A

Projections from the substantia nigra pars compacta (midbrain) release dopamine in the striatum (caudate and putamen), part of the basal ganglia, which modulates motor and impacts cognitive and function

178
Q

How does the Mesocortical dopamine pathway work?

A

Projections from the ventral tegmental area (midbrain) release dopamine in the frontal cortex (particularly the pre-frontal cortex) to modulate reward, motivation and attention

179
Q

How does the Mesolimbic dopamine pathway work?

A

Projections from the ventral tegmental area (midbrain) release dopamine into the limbic system structures and are involved in cognition, learning and memory

180
Q

How does the Tuberoinfundibular dopamine pathway work?

A

Connects the hypothalamus to the median eminence. Dopamine released from these cells control prolactin secretions from the pituitary

Year 1 Neurology (26 decks)

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