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charlies medicine > NAS > Flashcards

NAS Flashcards

1
Q

What does CN I innervate?

A

Olfactory- sensory: smell

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2
Q

What does CN II innervate?

A

Optic- Sensory: vision

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3
Q

What does CN III innervate?

A

Oculomotor- Motor: Sphincer Pupillae, all external muscles of the eye except those of CN IV and VI

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4
Q

What does CN IV innervate?

A

Trochlear- Motor: Superior Oblique muscle of the eye

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5
Q

What does CN V innervate?

A

Trigeminal- split into opthalmic, maxillary and mandibular
Sensory: face, anterior two thirds of the tongue, teeth, mouth
Motor: Muscles of mastication

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6
Q

What does CN VI innervate?

A

Abducent- Motor: Lateral rectus muscles of the eye

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7
Q

What does CN VII innervate?

A

Facial- Motor: Muscles of facial expression, submandibular, sublingual, nasal and palatine glands
Sensory- Special sensory- taste from anterior two thirds of the tounge

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8
Q

What does CN VIII innervate?

A

Vestibulocochlear- Sensory:
Vestibular Nerve- Motion
Cochlear Nerve- Hearing

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9
Q

What does CN IX innervate?

A

Glossopharyngeal- Motor: Parotid Gland

Sensory: Taste from posterior third of tongue

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10
Q

What does CN X innervate?

A

Vagus- Motor: Palate, pharnyx, larynx, bronchial tree, GI tract to left colonic flexure, heart
Sensory: same as motor

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11
Q

What does CN XI innervate?

A

Accessory- motor: sternocleidomastoid, Trapezius

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12
Q

What does CN XII innervate?

A

Hypoglossal- Motor: muscles of the tongue

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13
Q

Why do most CNS fibres not regenerate?

A

Clean up is slow
Oligodendrocytes inhibit regeneration
environment in not optimal

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14
Q

What is the rate of growth in the PNS during regeneration?

A

1mm/day

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15
Q

what is neurapraxia?

A

Compression of a nerve in the PNS that results in compression of the myelin sheath and a reversible conduction block

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16
Q

what is axonotmesis?

A

When the axon is damaged and lost but the endoneurium is still in tact.

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17
Q

What is neurotmesis

A

When the myelin sheaths and axon and endoneurium layers are damaged

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18
Q

What is the result of damage to the endo, peri or epineurium?

A

endoneurium- fair growth
perineurium- poor growth
epineurium- no growth

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19
Q

What is found in grey matter?

A

Cell bodies
dendrites
axon terminals
unmyelinated axons

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20
Q

What is found in white matter

A 
axons
myelin sheaths (give the white matter its white appearance)
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21
Q

What happens in the grey matter?

A

synapses and integration between the CNS and PNS

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22
Q

What happens in the white matter?

A

As it is myelinated axons it carries information from place to place

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23
Q

What is the small hole in the centre of the spinal cord and what does it contain?

A

It is the central canal and contains CSF

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24
Q

which cells in the CNS myelinate axons?

A

Oligodendrocytes

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25
Q

What glial cells are there in the CNS other than oligodendrocytes, what is their function?

A

Microglial cells- immune function
Astrocytes- responsible for uptake into CNS from blood
star shaped
They wrap around the blood vessels in order to control ion and neurotransmitter uptake into the blood
Help from the BBB

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26
Q

Which Glial cells mylinate the axons of the PNS?

A

Schwaan Cells

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27
Q

What Glial cells surround cell bodies in the PNS and act as astrocytes?

A

Satellite cells

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28
Q

What Sensory (afferent) nerve cell types are found in the PNS?

A

Unipolar cells with cell body in middle but a single long axon
Bipolar cells where the cell body is also in the middle but seperates the axon into a long dendrite and an axon

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29
Q

How do schwaan cells myelinate axons?

A

The cell itself contains myelin and wraps itself around the axon
Hence it can only myelinate one axon at a time

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30
Q

What nerve cell types are found in the CNS?

A

Interneurones:
Anaxonic neurones- only have dendrites and a cell body
Multipolar neurones- have very short axon so appear similar to anaxonic, are also some longer multipolar cells for transmitting information

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31
Q

What motor (efferent) nerve cell types are found in the PNS?

A

Multipolar neurones- they have their cell body at the dendritic end of the neurone.
Are longer than in CNS and can be myelinated or unmyelinated

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32
Q

What is the pre-ganglionic cell body, nerve and ganglion for the pupillary constrictor?

A

pre-ganglionic cell body: edinger westphal
Nerve: CN III Oculomotor
Ganglion: Ciliary

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33
Q

What is the pre-ganglionic cell body, nerve and ganglion for the nose and eyes

A

pre-ganglionic cell body: Superior salivatory
Nerve: CN VII Facial
Ganglion: Pterygopalatine

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34
Q

What is the pre-ganglionic cell body, nerve and ganglion for the salivary glands (sl, sm)

A

Pre-ganglionic cell body: superior salivatory
Nerve: CN VII
Ganglion: Submandibular

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35
Q

What is the pre-ganglionic cell body, nerve and ganglion for the parotid gland?

A

Pre-ganglionic cell body:inferior salivary
Nerve:CN IX glossopharangeal
Ganglion: Otic

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36
Q

What is the pre-ganglionic cell body, nerve and ganglion for the Digestive system?

A

Pre-ganglionic cell body: Dorsal nucleus of X
Nerve: CN X Vagus
Ganglion: Cardiac,pulmonary,enteric

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37
Q

What are the 4 possible courses that pre synaptic sympathetic fibres follow?

A
  • Ascend, synapse with a postsynaptic neuron higher
  • Descend in the sympathetic trunk to synapse with a postsynaptic neuron lower
  • Synapse immediately with a postsynaptic neuron of the paravertebral ganglion at that level
  • Pass through the sympathetic trunk withoutsynapsing, continuing on through an abdominopelvic splanchnic nerve
38
Q

What are the two locations of Post synaptic sympathetic neurones?

A
  • Paravertebral ganglia: Linked to form right and left sympathetic chainson each side of the vertebral column
  • Prevertebral ganglia: In the plexuses that surround the origins of the main branches of the abdominal aorta, such as the large celiac ganglia. Known as Prevertebral/pre-aorticas the post-ganglionic fibresend up coming in front of the vertebrae and aorta.
39
Q

Where do sympathetic nerves emerge from the spinal cord?

A

Anterior roots

40
Q

What are the two locations of presynaptic cell bodies for the parasympathetic nervous system?

A

Grey matter of brainstem

Grey matter of sacral segment (S2-S4)

41
Q

Which cranial nerves constitute the cranial parasympathetic outflow?

A

CN III oculomotor
VII facial
IX glossopharangeal
X vagus

42
Q

What is the sacral parasympathetic outflow?

A

S2-S4

43
Q

What type of receptor is a muscarinic acetylcholine receptor?

A

G-protein coupled receptor

44
Q

What type of receptor is a nicotinic acetylcholine receptor?

A

Ligand gated ion channel

45
Q

How many neuromuscular junctions does each muscle fibre have?

A

1

46
Q

What role do calcium ions play in the pre synaptic terminal of a neuromuscular junction?

A

Arriving action potential causes influx of calcium ions from the synaptic cleft due to the opening of voltage gated ion channels
This promotes ach vesicle fusion to the presynaptic membrane

47
Q

How is the end plate potential generated at a neuromuscular junction?

A

Two ach molecules bind to the nicotinic receptor and cause breakdown of the hydrophobic interactions causing it to open (for Na+ and K+)
Na+ has greater driving force than K+ due to Em of the muscle being further from the Na+ resting potential
This causes generation of the end plate potential

48
Q

What process occurs at the end of generation of an end plate potential?

A

Acetylcholinesterase on the postsynaptic membrane hydrolyse acetylcholine to acetate and choline
Choline can be recycled back into the pre synaptic cell and be combined with acetyl coA to reform acetylcholine

49
Q

What are the electrical properties of en end plate potential?

A

It is very quick due to AP arriving to EPP generation being less than 1ms
It is generated by ligand channels that are quicker to open than voltage gated channels
EPP is very large compared to normal APs
Threshold is easily surpassed due to the large quantity of receptors

50
Q

How does an EPP lead to muscle contraction?

A

The AP passes along the surface of the muscle fibre
It is then propagated down the T-tubules which surround individual muscle fibres (and their contractile proteins)
This causes a release of Ca2+ from the sarcoplasmic reticulum
This allows for muscle contraction

51
Q

How does an action potential in the T tubules cause Ca2+ release?

A

T-tubule voltage sensor is linked to the calcium channels in the sarcoplasmic reticulum
Causes a conformational change in the Ca2+ channel so that ca2+ moves into the sarcoplasm

52
Q

What is Myesthenia Gravis and how is it treated?

A

Muscle weakness during sustained activity
It is an autoimmune disease of nAChR (antibodies generated against it)
This causes a reduction at the NMJ
It is treated via AChE inhibitors (Neostigmine)

53
Q

Give an example of an AChesterase inhibitor?

A

Neostigmine

54
Q

What is suxamethonium and how does it work?

A

A depolorising neuromuscular blocker
it works by binding to nicotinic receptors at the neuromuscular junction and causing Na+ channels to be open continuously
This prevents action potentials from occuring

55
Q

Give an example of a local anaesthetic?

A

Bupivacaine - long lasting

56
Q

How do acidity and alkalinity affect ionisation of drugs?

A

Acidic causes the drug to shift to ionised form
Alkaline causes it to shift to non ionised form
Therefore at natural pH there is more non ionised form

57
Q

What is the mechanism by which local anaesthetics work?

A

Unionised form of the drug is lipid soluble so moves into the axon
The change in pH causes a different equilibrium with some of the ionised form
The ionised form blocks Na+ voltage gated channels so prevents APs

58
Q

What factor affects the effectiveness of local anaesthetics?

A

Tissue pH, Higher acidity means there will be less unionised forms of the drug to diffuse into the axon so the anaesthetic is less effective

59
Q

What are the routes of administration for local anaesthetics?

A 
Topical
Infiltration-ring of injections into tissue
Nerve block-injection close to nerve
Spinal-inject into csf
Epidural
60
Q

What are the side effects of local anaesthetics?

A

CNS can be affected as all Na+ channels affected, causes decreased cardiovascular contraction which leads to low blood pressure
respiratory failure, convulsions and tremors can also occur
Other things in the drug other than the anaesthetic could cause an allergic reaction

61
Q

Which receptor sub-types are affected by propanolol?

A

Beta 1 adrenoreceptors

62
Q

What receptor sub-types are affected by prazosin?

A

Alpha 1 adrenoreceptor

63
Q

What receptor sub-types are affected by phentolamine?

A

Alpha 1 and alpha 2 adrenoreceptors

64
Q

What is the mechanism for the cross-extensor reflex (withdrawal reflex)?

A

Harmful stimuli is transmitted to brain, aware of pain
Causes increase in sensory neurone activity
This has several branches which connect to several interneurones
Some effect are on the same side as sensory, others on the other side
Front foot: Muscle of at back of thigh contract, front of thigh relaxes
Back foot: Muscle at front of thigh contracts, back of thigh relaxes
The cross over occurs as the posture needs to be adjusted to stand on the other

65
Q

What are the two types of refectory period?

A

Absolute-Na+ channels inactivated so no APs can occur

Relative where some of the Na+ channels still inactivated so has a larger threshold potential

66
Q

How do you distinguish between myopathy and neuropathy clinically?

A

Fasciculationstends to imply disease of the motor neuron (thusneuropathy)
Sensory abnormalities also imply neuropathy
Brisk reflexes (faster than usual) imply neuropathy

67
Q

What are the laboratory tests to distinguish myopathy and neuropathy?

A

Muscle enzymes: Creatine kinase levels and lactate dehydrogenase levels high
Electromyography
Muscle biopsy

68
Q

What is electromyography and what are its results for myopathy and neuropathy?

A

This involves inserting a small needle into muscle in order to record motor units (measuring duration and amplitude Aps in each motor unit)
Myopathic disease: No resting activity, shorter and small motor unit potentials
Neurogenic disease: Spontaneousactivity, giant motor unit potentials, reduced interference pattern (no of units under voluntary control)

69
Q

What are the different results of a muscle biopsy?

A

In normal muscle: Fibres of 1 motor unit are interspersed with fibres of other motor units. This leads to a checkerboard staining pattern, with myosin ATPase
In denervated muscle: Fibre type grouping occurs, as axons from neighbouring motor units innervate the denervated fibres.
Muscular dystrophy: Huge variation in fibre size, increased fat and connective tissue, inflammation possible

70
Q

What do muscle enzymes show?

A

Elevated creatine kinase levels shows neuropathy

71
Q

What is Guillian Barre syndrome?

A

Occurs soon after an infection and antibodies attack peripheral nerves
Main symptom is weakness

72
Q

What is peripheral neuropathy?

A

Can be demylinating or axonal variations

73
Q

What causes peripheral neuropathy?

A

Can be inherited or acquired

Acquired: Alcohol, nutritional

74
Q

What are the signs of hereditary peripheral neuropathy?

A 
Inverted champagne bottle legs
Pes Cavus (high arch)
75
Q

Give an example of an inherited and an acquired myopathy?

A

Inherited- DMD (duhenne muscular dystrophy)

Acquired- Dermatomyositis

76
Q

What is DMD?

A

Duchenne muscular dystrophy- proximal muscle weakness and wasting
X-linked recessive disorder so mainly affects boys
Affects genes for dystrophin that acts as an anchoring protein for actin

77
Q

How would you diagnose DMD?

A

Very high serum creatine kinase

78
Q

What is dermatomyositis?

A

Autoimmune disorder of small muscles blood vessels
Acquired peripheral neuropathy characterised by rash on face, chest and hands
Proximal wasting of muscles
Very high serum creatine kinase

79
Q

What is the mechanism for a simple myotatic reflex?

A

A muscle spindle is stretched generating an AP
Monosynaptic so sensory neurone synapses with motor neurone
This causes muscles to contract that returns muscle to original position
This prevents muscle damage

80
Q

What is the mechanism for the reverse myotatic reflex?

A

Golgi tendon organ pulled by increased muscle contraction which causes an AP
Polysynaptic as synapses with INHIBITORY interneurone
Releases an inhibitory neurotransmitter that prevents activation of the motor neurone
This prevents damage due to overwork

81
Q

What happens in the knee jerk reflex?

A

Myotatic reflex in quadriceps causes contraction

Reverse myotatic reflex in hamstrings prevents contraction of hamstring

82
Q

What are the neuronal degeneration events?

A

immediately- conduction stops and cytoplasm is lost into endoneurium then axonal membranes fuse
Degeneration of the synaptic bouton- uncontrolled release of neurotransmitter into synapse
phagocytosis of the axon occurs- schwaan cells become phagocytic and recruit microglia
Proximal segment also degenerates 3 or 4 nodes to allow for regeneration from a clean structure

83
Q

What are nissl bodies?

A

Granules of RER

84
Q

How does neuronal repair occur from the degenerated axon?

A

Axons with swellings sprout from the proximal segment

They are guided along the schwaan cells down the endoneurial sheath

85
Q

What are the requirements for axonal regeneration?

A

Regeneration requires:
Neuronotrophic factors (NF)
Growth associated proteins
Endoneurial sheath

86
Q

Why does neuronal repair not occur in the CNS?

A

Astrocytes form scar tissues that prevent neurones sprouting

87
Q

What affects the likelihood of neurone repair?

A

Location and length: short and further from cell body more likely to repair
Injury: crush more likely to repair than cut
Age:more likely to repair in children

88
Q

What are the consequences of nerve degeneration?

A

Hours
Fasciculation and fibrillation: Uncontrolled muscle spasms, fasciculation is one fascicle, fibrillation is muscle fibre. This is due to the Ach vesicle release
Days-weeks:
Fibrillation: This is due to more receptors being formed to attract any Ach left causing contraction
Paralysis
Weeks-months:
Atrophy: The muscle begins to die as it is not innervated thus is no use. Can be rescued within 6 months
Reduction in bone density: Due to bone decalcification

89
Q

What are the different tissues the adrenoreceptors work on?

A

alpha 1-smooth muscle
alpha 2-platelet aggregation
beta 1-heart rate
beta 2-bronchodilation

90
Q

What are the three junctional points in metabolism?

A

–Junction 1-gluose-6-phosphate
can either go through glycolysis or the pentose phosphate pathway
–Junction 2-pyruvate
Junction between carbohydrate and amino acid metabolism
can be converted to acetyl CoA or lactate, amino acids can also input here by being turned into pyruvate
Pyruvate can also be converted back to glucose-6-phosphate
–Junction 3-acetyl CoA
junction between carbohydrate and fat metabolism
acetyl coa can be created from fatty acids
it can form ketone bodies
can also enter TCA cycle

91
Q

What is formed from neural crest cells?

A 
Melanocytes
Dorsal root ganglion
Schwaan cells
neurons
neuroglial cells
Adrenal medulla

charlies medicine (9 decks)

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