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learning outcomes Flashcards

1
Q

the fibrous layer of the eye contains

A

contains the cornea and sclera.

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2
Q

function of the cornea and sclera

A

The cornea is transparent and allows light to enter, the sclera provides attachment for the muscles moving the eye.

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3
Q

vascular layer of the eye contains

A

contains the ciliary body, iris and choroid.

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4
Q

function of the ciliary body, iris and choroid

A

The ciliary body suspends the lens and produces aqueous humor, the iris which controls the entry of light through the diameter and the choroid which supplies blood to the outer layers of the retina.

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5
Q

the sensory layer contains and function

A

with the retina which contains the light sensitive rods and cones which enable sight.

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6
Q

anterior segment contains

A

a watery fluid called aqueous humour

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7
Q

posterior segment contains

A

transparent gel called vitreous humour

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8
Q

structure and function of the conjunctiva

A

the conjunctiva is the mucous membrane on the inside with a thin vascular membrane. its function is to generate moisture for the eye

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9
Q

the structure of eyelids

A

The hard plate known as the tarsal plate that help keeps its shape and contains the meibomian glands, and oily secretory glands for tear film. There is a muscle levator palpebrae superioris and orbicularis oculi

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10
Q

structure and innervation of the lacrimal system

A

The lacrimal gland is situated in the orbit laterally innervated parasympathetically by the facial nerve, its duct opens into the conjunctival sac via the punctae. Through the lacrimal duct it then empties into the inferior meatus of the nasal cavity.

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11
Q

the posterior chamber is behind the

A

iris

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12
Q

the function of vitreous humour

A

maintains posterior segment pressure

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13
Q

posterior segment is behind the

A

lens

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14
Q

function of the aqueous humour

A

fluid that maintains the intraocular pressure

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15
Q

anterior chamber is in front of the

A

iris

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16
Q

anterior segment is in front of the

A

lens

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17
Q

6 extraocular muscles

A

there are 6 extrinsic ocular muscle that move the eye such as the medial, lateral, inferior, and superior rectus and 2 oblique such as the superior and inferior.

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18
Q

bones of the orbit

A

frontal bone, sphenoid, lacrimal, ethmoid, maxillary, zygomatic, palatine

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19
Q

fissures of the eye

A

There is the optic foramen, superior orbital fissure and inferior orbital fissure.

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20
Q

intrinsic eye muscles and inner

A

The intrinsic eye muscles are the ciliaris muscle and constrictor pupillae innervated by the parasympathetic 3 cranial nerve. Dilator pupillae which is innervated by the sympathetic plexus around blood vessels.

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21
Q

histological features of the cornea

A

there is the surface epithelium with stratified squamous non-keratinised. The basement membrane is called the bowman’s membrane. Then there is the avascular stroma, which is regularly arranged collagen. Then there is the descemet’s layer which is the basement membrane of the endothelium.

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22
Q

tear film function and physiology

A

tear film washes the cornea, maintains moisture. Contains lysozymes and provides a smooth layer for refraction. It consists of three layers a mucinous layer, aqueous, and oily. The aqueous layer evaporates and once it the mucinous and oily layers come into contact the tear film disintegrates and stimulates a blink.

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23
Q

cornea transparency physiology

A

the Cornea is avascular which aids in transparency, the main form of transparency is from the stroma and the parallel collagen fibres.

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24
Q

aqueous humour outflow

A

the aqueous humour is produced in the ciliary body, flows into the anterior segment in front of the lens, towards the angle of the anterior chamber through the trabecular meshwork, into the schlemm’s canal then into venous drainage.

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25
Q

Describe how the functional anatomy of the eye serves to project a sharp image onto the retina

A

light waves bend at the cornea and at the lens through refraction the image is projected onto the retina. As object moves close, the lens thickens to allows for a clear image to still be formed.

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26
Q

accommodation means

A

refers to the ability of the eye to allow focus to change.

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27
Q

ciliary muscles of our eyes to accommodate

A

ciliary muscles can contract, causing the ciliary body to bulge which results in the suspensory ligaments relaxing and the lens becoming thicker as it is no longer stretched

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28
Q

pupils and their function in accommodation

A

pupils can constrict to limit the entry of light through the sphincter pupillae via parasympathetic innervation to enable close focus.

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29
Q

medial rectus and its role in accommodation

A

the medial rectus muscle of our eyes stimulated by the third cranial nerve can allow our eyes to converge to enable close work to be performed.

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30
Q

myopic refers to

A

myopic refers to the eyeball being too long, the image is formed in front of the retina so far off objects cannot be seen. The bending power of the cornea and lens is too much.

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31
Q

myopic symptoms

A

Symptoms include headaches, divergent squint, and easy loss of interest.

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32
Q

treatment of myopia

A

biconcave

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33
Q

hyperopia refers to

A

hyperopia is farsightedness meaning close objects are hazy. The eyeball is too short or the cornea/lens is too flat resulting in the image being formed behind the retina. The individual uses their accommodative power to thicken the lens for distant objects and thus cannot see close objects

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34
Q

symptoms of hyperopia

A

Symptoms of eye strain, convergent squint

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35
Q

treatment of hyperopia

A

biconvex

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36
Q

astigmatism refers to and requires

A

when close and distant objects appear hazy as the surface of the cornea has different curvatures. It requires cylindrical glasses to cancel out the incorrect medians called toric glasses.

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37
Q

presbyopia refers to

A

is old age long sightedness in which ciliary muscles contractions don’t stimulate the ciliary body and ligaments as well. Close objects become difficult to see and thus require biconvex reading glasses.

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38
Q

photo transduction mechanism

A

light particle enters the eye and goes to a rod cell. it hits a integral transmembrane helical protein complex called rhodopsin on the many lamellae, stimulating a chromophore retinal derived from vitamin A to alter shape from a cis to a trans. This chromophore can no longer fit into opsin and causes rhodopsin to split resulting in bleaching. This then stimulates a cascade event that culminates in sodium channels closing and less sodium entering the cell which stimulates hyperpolarisation of the rod cell and a rush of calcium ions to the bipolar cell synapse. Vitamin A is then essential for regeneration of this process in the pigment epithelial cell.

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39
Q

constrictor papillae innervation

A

parasympathetic 3rd cranial nerve

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40
Q

dilator papillae innervation

A

sympathetic fibres from blood vessels

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41
Q

optic neural pathway

A

fibres pass through optic nerve to optic chiasma in which the nasal fibres cross to the opposite side. Optic tract contains fibres from the lateral temporal half of the ipsilateral eye and crossed over nasal fibres from the contralateral eye. Fibres from optic tract finally synapse at the lateral geniculate body of the thalamus, then optic radiation passes to reach the primary visual cortex.

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42
Q

lateral rectus abducts causing

A

; SR elevates, IR depresses

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43
Q

medial rectus adducts causing

A

SR intorsion, IR extorsion

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44
Q

superior rectus function

A

elevates, adducts, intorsion

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45
Q

inferior rectus functions

A

depresses, adducts, extorsion

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46
Q

superior oblique functions

A

intorsion, depression and abduction

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47
Q

inferior oblique functions

A

extorsion, elevation, abduction

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48
Q

esotropia refers to

A

convergent squint

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49
Q

exotropia refers to

A

divergent squint

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50
Q

amblyopia refers to

A

brain supressing eye leading to poor image

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51
Q

diplopia refers to

A

double vision

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52
Q

visual field explained from the left eye

A

In the eyes the temporal side of the left eye will take in light from the right visual field and in the nasal side from the left visual field.

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53
Q

primary visual cortex in terms of visual fields

A

the right side of the primary visual cortex in the occipital will process only from the right visual field, and the left PVC of the occipital will process only the light from the left visual field.

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54
Q

visual field explained from the right eye

A

n a right eye the temporal side will take light in from the left visual field and the nasal will take in light from the right visual field.

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55
Q

damage to the right optic nerve will cause

A

right eye blindness

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56
Q

damage to the optic chiasma will cause

A

bitemporal hemianopia

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57
Q

left optic tract damage will cause

A

contralateral homonymous hemianopia

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58
Q

if optic radiation damaged then

A

contralateral homonymous hemianopia

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59
Q

damage to the left optic nerve will cause

A

left eye blindness

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60
Q

pupillary light reflex afferent fibres

A

impulses from light travel from the retina along the optic nerve to the chiasma and to the optic tract. The activation of the pupillary reflex arise from the midbrain to the nucleus of the oculomotor nerve known as the Edinger-Westphal nucleus

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61
Q

efferent limb of pupillary light reflex

A

pupillary reflex arise from the midbrain to the nucleus of the oculomotor nerve known as the Edinger-Westphal nucleus for parasympathetic innervation to stimulate the pupillary reflex fibres on both sides. this travels along the preganglionic fibre via the oculomotor nerve to synapse in the ciliary ganglion then travel along the short ciliary nerves to constrictor pupillae.

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62
Q

why does disruption to sympathetic innervation produces horner’s syndrome

A

Horner’s syndrome symptoms are anisocoria due to sympathetic innervation damage, ptosis, anhidrosis and miosis. Sympathetic innervation arises from the thoracolumbar outflow from the sympathetic chain to the cervical ganglion and that post ganglionic fibres travel along the blood vessels. Something like a tumour compression such as Pancoast will cause Horner’s syndrome

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63
Q

if pupillary reflex is absent during oculomotor nerve palsy you have to assume

A

cerebral artery aneurysm

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64
Q

explain a cataract formation

A

since the lens is a avascular structure produced by parallel collagen fibres, damage in the from of UV rays result in damage, and more collagen fibres being produced causing an increase in density and thus becoming gradually more opaque.

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65
Q

aetiology of conjunctivitis

A

; viral or bacterial infection

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66
Q

features of conjunctivitis

A

red, watery eyes, discharge. Vision unaffected unless corneal spread.

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67
Q

management of conjunctivitis

A

antibiotic eye drops

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68
Q

corneal ulcer aetiology

A

viral/bacterial or from trauma and degeneration

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69
Q

features of corneal ulcer

A

opacification of the cornea

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70
Q

management of corneal ulcer

A

keratoplasty

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71
Q

non inflammatory corneal dystrophy aetiology

A

; genetic, accumulation of lipids

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72
Q

features of non inflammatory corneal dystrophy

A

bilateral, opacification commonly in first to fourth decade

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73
Q

management of non-inflammatory corneal dystrophy

A

keratoplasty

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74
Q

cataracts aetiology

A

UV rays and damage to lens

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75
Q

features of cataracts

A

opacification of lens

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76
Q

management of cataracts

A

cataract surgery

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77
Q

aetiology of glaucoma primary open angle

A

raised intra ocular pressure due to drainage through trabecular meshwork blockage

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78
Q

features of glaucoma primary open angle

A

asymptomatic, bilateral, altered field of vision, gradual

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79
Q

treatment of glaucoma primary open angle

A

eyedrops such as beta blockers, carbonic anhydrase inhibitors, prostaglandin analogues and trabeculoplasty or trabeculectomy.

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80
Q

glaucoma closed angle features

A

sudden onset, painful, blurry vision, headaches, red eye, opaque cornea

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81
Q

glaucoma closed angle aetiology

A

; intra ocular pressure severely raised due to peripheral iris blocking the angle preventing aqueous humour from draining

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82
Q

management of glaucoma closed angle

A

; steroid eye drops, IV carbonic anhydrase inhibitors, analgesics, antiemetics, constrictor eye drops pilocarpine and iridotomy to bypass blockage

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83
Q

uveitis aetiology

A

illness, autoimmune, infectious disease TB, or systemic disease

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84
Q

features of uveitis

A

red, painful, visual loss, floaters in vision, blurred vision

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85
Q

describe the main components of nervous system (general)

A

central nervous system with the brain and spinal cord
the peripheral nervous system with the cranial and spinal nerves, which further sub divides into the sensory afferent division and motor efferent division, the motor efferent division divides into the somatic motor and autonomic with the sympathetic and parasympathetic divisions.

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86
Q

describe neurones

A

there are neurons which are excitable cells that carry nerve impulses. They have multiple dendrites and one axon and transmit impulses from cell body to the synaptic terminal typically. They have a high metabolic rate, long living and amitotic. They may be myelinated and conduct via saltatory conduction.

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87
Q

different types of neurones

A

There are interneurons for motor transmission, bipolar found in the olfactory mucosa or retinal fibres and pseudo-unipolar sensory neurons.

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88
Q

schwann cells are for

A

in the peripheral nervous system there are satellite cells for surrounding cell bodies, and schwann cells for myelination.

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89
Q

ependymal cells are for

A

lining ventricles

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90
Q

astrocytes are for

A

form the blood-brain barrier, surrounding synapses and potassium buffering,

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91
Q

oligodendrocytes are for

A

myelination and microglia for phagocytosis.

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92
Q

compare grey matter and white matter

A

grey matter is collections of cell bodies such as ganglion or nuclei in the brain and in the spinal cord. White matter is axons, white due to the myelination and forms tracts for specific signals.

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93
Q

CSF purpose

A

CSF maintains intracranial pressure and protecting the brain to some degree from crushing itself

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94
Q

CSF presence and circulation and production

A

weight between the pia and arachnoid and its also present within the ventricles, being produced by a choroid plexus in each ventricle, it then circulate around the brain being eventually reabsorbed by the arachnoid villi into the sagittal sinus a venous channel in the brain

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95
Q

blood brain barrier description

A

it’s a protective mechanism to prevent harmful amino acids and ions transferring from the blood to the brain consisting of tight junctions between endothelium, a thick basal lamina and the foot processes of astrocytes.

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96
Q

drug therapy and the brain barrier

A

There are a few circumventricular organs such as the hypothalamus, and posterior pituitary that enables the delivery of lipid soluble drugs or certain vectors.

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97
Q

describe the lateral ventricle

A

lateral ‘C’ ventricles in the cerebral hemisphere

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98
Q

3rd ventricle is within

A

diencephalon

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99
Q

lateral and 3rd ventricle are connected by the

A

interventricular foramen

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100
Q

4rth and 3rd ventricles are connected by

A

the cerebral aqueduct in the midbrain

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101
Q

the 4rth ventricles is within

A

diamond shaped in the hindbrain

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102
Q

describe the meninges

A

the dura mater is a tough fibrous layer with fold then there is the arachnoid mater and the subarachnoid space which contains the cerebrospinal fluid and the pia mater which is vascularised and dips into the folds of the brain.

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103
Q

sensory cells in the bony canals are called

A

ampulla

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104
Q

the ampulla contains

A

flexible jelly like cupula organs that respond to endolymph movement.

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105
Q

movement is detected by in the ampulla

A

The embedded cilia synapse with the vestibular nerve and detect rotational acceleration, the movement of the ampulla then the delayed movement of the endolymph due to its inertia generates drag.

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106
Q

hyperpolarisation of the kinocilium are generated by

A

movement away from the kinocilium

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107
Q

depolarisation of the kinocilium is generated by

A

movement towards the kinocilium

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108
Q

sensory receptors within the utricle and saccule are called

A

the maculae

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109
Q

the maculae are

A

sensory receptors within the utricle and saccule

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110
Q

the ampulla Is

A

sensory cells within the base of the bony canals

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111
Q

the utricle detects

A

the horizontal plane

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112
Q

the saccule detects the

A

vertical plane

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113
Q

cilia detecting movement in the macula

A

The cilia protrude into a mass called the otolith membrane which is embedded also with CaCO3 crystals called otoliths which move in response to gravity. Tilted the head stimulates the crystals greater then the endolymph and distorts the membrane moving the cilia, tilting backwards causes the kinocilium to depolarise and tilting forward causes hyperpolarisation

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114
Q

otoliths are

A

CaCO3 crystals

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115
Q

projections from the vestibular nuclei lead to the

A

descending motor pathways

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116
Q

what is vestibular nystagmus

A

saccadic eye movements that rotate the eye against body rotation to maintain focus on original intention, eye movement is restricted and when at its range it will flick back to a neutral position and this will repeat as long as rotation occurs.

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117
Q

how can vestibular nystagmus test vestibular function

A

post rotary nystagmus in experiments involves rotation in a barany chair the rotation to the left generates left nystagmus, then deceleration generates right nystagmus due to the endolymph overcoming the initial inertia and drag and pushing the cupula in an opposite direction.

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118
Q

COW caloric stimulation

A

Cold Opposite, Warm Same COWS).

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119
Q

caloric stimulation explanation

A

caloric stimulation, when washing the ear with hot or cold water it can generate conventional current altering the flow of endolymph, either towards the affected side if >37C or away if cold <37

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120
Q

labyrinthitis acute infection may cause

A

nausea, pallor, vertigo, dizziness, vomiting and sweating

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121
Q

Meniere’s disease may cause

A

vertigo, nausea, nystagmus and tinnitus due to an overproduction of endolymph increasing the pressure

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122
Q

nystagmus at rest may be pathologically caused by

A

brain stem lesions

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123
Q

tonic labyrinthine reflexes

A

there are tonic labyrinthine reflexes which is the relationship between the head and the body which depends on the maculae and neck proprioceptors.

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124
Q

dynamic righting reflexes

A

there is the dynamic righting reflex which allows for rapid positional movement to aid in balance, it’s a long reflex depending on extension of all limbs to prevent falling when tripping.

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125
Q

vestibo-ocular reflexes

A

which follows afferent fibres from the semi circular canals to the extraocular nuclei to influence eye movement and the visual system aids in posture control.

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126
Q

vestibo-ocular static reflex

A

static reflex which is the ability of the eyes to compensate for head movement to maintain focus on an image and dynamic vestibular nystagmus which is saccadic eye movements that enable the eye to work against rotation of the body and head to that the gaze is preserved.

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127
Q

the medulla landmarks

A

it contains the fourth ventricle and is a continuation of the spinal cord through the foramen magnum. It contains the pyramids and their decussation, olives laterally, and connects to the cerebellum by the inferior cerebellar peduncle. It is associated with the cranial nerves 9-12.

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128
Q

pons landmarks

A

pons; it has the fourth ventricle posterior to it, and on the surface has the middle cerebellar peduncle and the cranial nerves 5-8.

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129
Q

midbrain landmarks

A

; it contains the cerebral aqueduct as well as the cerebral peduncle, superior cerebellar peduncle, the superior and inferior colliculus and the origins of the oculomotor nerve anteriorly and the trochlear nerve posteriorly

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130
Q

cerebellum landmarks

A

there is a right and left hemisphere separated by a vermis. Each hemisphere has an a small anterior lobe, large posterior lobe and tiny flocculonodular lobe as well as a small posterior section called the cerebellar tonsil. The surface is marked by sulci and folia and through three peduncles connects to the brainstem.

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131
Q

cerebellum function

A

its function is to receive motor information from the pyramidal tracts, ipsilateral peripheral proprioceptors and from the vestibular nuclei regarding balance and posture. It then coordinates force and direction of muscle for contraction to fine tune motor activity and posture and sends this to the cerebral cortex via the superior cerebellar peduncle.

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132
Q

diencephalon located

A

diencephalon lies deep within the cerebral hemispheres around the third ventricle

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133
Q

thalamus location

A

within the diencephalon. which is a dense collection of grey matter just lateral to the third ventricle and operates as a sensory relay station.

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134
Q

hypothalamus location

A

part of the diencephalon. There is the hypothalamus separated by the hypothalamic sulcus for controlling homeostasis and visceral organs, from the hypothalamus is the pituitary stalk.

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135
Q

internal carotids route

A

Two internal carotid arteries enter the skull through the foramen lacerum

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136
Q

vertebral artery route

A

then two vertebral arteries arise from the subclavian artery through the foramen magnum.

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137
Q

circle of Willis consists of

A

the circle of Willis is made up of the vertebral arteries joining to form the basilar artery, which then leads into the posterior cerebral artery, then the posterior communicating artery, then the internal carotid feeds in forming the ophthalmic artery, the middle cerebral artery and the anterior cerebral arteries which are joined by a anterior communicating artery.

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138
Q

ventrobasilar system supplies

A

brainstem and cerebellum

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139
Q

clinical significance of circle of willis

A

all branches are end arteries

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140
Q

anterior cerebral artery supplies

A

medial aspects but the occipital

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141
Q

middle cerebral artery supplies the

A

lateral aspects

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142
Q

the posterior cerebral artery supplies the

A

inferior cerebrum and occipital lobe

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143
Q

venous drainage of the brain is through

A

venous sinuses between 2 layers of dura mater such as the inferior sagittal sinus, superior sagittal sinus, the cavernous sinus, transverse sinus, and the petrosal superior and inferior sinuses all eventually feeding into the jugular veins.

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144
Q

frontal and parietal lobes are separated by

A

central sulcus

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145
Q

temporal lobe is separated from the frontal lobe by a

A

lateral sulcus

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146
Q

parietal lobe consists of

A

superior and inferior lobule

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147
Q

the occipital lobe is divided by

A

calcarine fissure

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148
Q

the corpus callosum and limbic lobe is separated from the cerebrum

A

cingulate sulcus

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149
Q

within the lateral fold of the temporal lobes is the

A

insula

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150
Q

frontal lobe is for

A

motor function and intellect

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151
Q

parietal lobe is for

A

somatosensory

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152
Q

temporal lobe is for

A

hearing and smell

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153
Q

occipital lobe for

A

vision

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154
Q

the frontal lobe contains

A

area 4 the precentral gyrus which the is primary motor cortex for somatotopic representation of the contralateral half of the body.
the inferior frontal gyrus known as Broca’s area of motor speech are 44,45.
then there is the prefrontal cortex which is involved in cognitive functions.

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155
Q

are 4/precentral gyrus is for

A

primary motor cortex

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156
Q

inferior frontal gyrus is for

A

broca’s area of motor speech 44,45

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157
Q

area’s 3,1,2 Is the

A

primary sensory area receives somatotopic representation of general sensation from contralateral half of the body.

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158
Q

post central gyrus contains

A

areas 3,1,2 known as the primary sensory area which receives somatotopic representation of general sensation from contralateral half of the body.

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159
Q

superior parietal lobe function

A

processes general sensory data and conscious sensation of contralateral half of the body making it an association area

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160
Q

inferior parietal lobule is for

A

interface between the somatosensory cortex and visual/auditory areas, in the dominant sphere it contributes to language function.

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161
Q

temporal lobe contains

A

the superior temporal gyrus which is the primary auditory cortex areas 41, 42.
Then there is the Wernicke’s area, the auditory association area in the dominant sphere crucial for spoken word understanding.
the inferior surface receives fibres form the olfactory tract for conscious appreciation of smell.

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162
Q

superior temporal gyrus is the

A

which is the primary auditory cortex areas 41, 42.

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163
Q

areas 41, 42 are the

A

superior temporal gyrus in the primary auditory cortex

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164
Q

Wernicke’s are is for

A

the auditory association area in the dominant sphere crucial for spoken word understanding.

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165
Q

the auditory association area in the dominant sphere crucial for spoken word understanding is called

A

Wernicke’s area

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166
Q

inferior surface of the temporal lobe is for

A

receiving fibres from the olfactory tract

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167
Q

occipital lobe contains

A

responsible for vision, on the medial surface either side of the calcarine sulcus is the primary vision cortex 17. Areas 18, 19 is responsible for interpretation of visual images.

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168
Q

the calcarine sulcus is the

A

primary vision cortex 17

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169
Q

primary vision cortex 17 is located in the occipital lobe at the

A

calcarine sulcus

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170
Q

areas 18, 19 Is for

A

interpretation of visual images

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171
Q

interpretation of the visual images occurs in the

A

area 18, 19 of the occipital lobes

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172
Q

association area is for

A

integration and processing of information

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173
Q

premotor cortex function is

A

planning, control and execution of voluntary movements

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174
Q

primary motor cortex is for

A

sending signals to generate movements

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175
Q

language centres of the forebrain

A

Broca’s area (44,45) is the motor speech area, Wernicke’s area if auditory association area for recognition of spoken word in the dominant hemisphere, the auditory cortex (41,42) and motor control of mouth and lips in the precentral gyrus are also essential

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176
Q

what fibres connect the two hemispheres through the corpus callosum is

A

commissural fibres

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177
Q

the parts of the cortex is connected through

A

association fibres

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178
Q

connections between the cerebral cortex and subcortical centres pass through the corona radiata and internal capsule fibres

A

projection fibres

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179
Q

projection fibres

A

Then finally is the projection fibres which run between the cerebral cortex and various subcortical centres though the corona radiata and internal capsule.

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180
Q

basal ganglia consist of

A

deep grey matter

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181
Q

basal ganglia are the

A

There is the caudate, globus pallidus and the putamen which form the lentiform nucleus and the substantia nigra.

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182
Q

the caudate and putamen receive information from and this then goes to

A

the motor cortex, premotor cortex and thalamus, it then sends this to the output regions which are the globus pallidus and substantia nigra and then projects this to the thalamus

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183
Q

the purpose of the basal ganglia are

A

The purpose of this system is regulate movement through initiating or terminating movement making it extrapyramidal system.

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184
Q

gross anatomy of the spinal cord

A

on a cross section there is a dorsal and ventral side. On the dorsal side there is the dorsal root ganglion and the dorsal root feeding into a dorsal horn. on the ventral side is the ventral root, both roots arising from a spinal nerve into the ventral horn. The horns consist of grey matter and surrounded by white matter which form tracts.

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185
Q

ascending corticospinal tract carries

A

the corticospinal tract carries motor impulses from the motor cortex to the skeletal muscle. The pathway starts in area 4 the motor cortex, passing through the internal capsule and along the cerebral peduncle, before travelling along the pons pyramids and then decussating to the contralateral corticospinal tract where is will then leave through the ventral horn to the root, then into the spinal nerve to the muscle.

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186
Q

the ascending posterior dorsal column

A

the posterior dorsal column carries touch, vibration, tactile localisation and proprioception. The signal travels from the dorsal root ganglion to the dorsal horn and along the tract, synapsing in the gracile and cuneate nucleii in the medulla and decussating across into the contralateral half of the medial lemniscus of the pons before synapsing again in the VPL nucleus of the thalamus which sends the signal to the post central gyrus of the parietal lobe.

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187
Q

the lateral spinothalamic tract

A

the lateral spinothalamic tract is responsible for pain and temperature. The sensory neuron enters through the dorsal root ganglion, synapsing at its spinal segment, crossing over contralaterally to the tract before heading to the VPL of the thalamus, synapsing again before heading to the post central gyrus of the parietal lobe.

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188
Q

posterior dorsal column carries

A

touch, vibration, tactile localisation and proprioception.

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189
Q

the corticospinal tract carries

A

motor impulses from the motor cortex to the skeletal muscle.

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190
Q

lateral spinothalamic tract carries

A

pain and temperature

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191
Q

corticospinal tract decussates in the

A

pons pyramids

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192
Q

posterior dorsal column decussates

A

medial lemniscus of the pons

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193
Q

lateral spinothalamic tract decussates

A

at its spinal segment

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194
Q

what is lower motor neurone disease

A

affects the ventral horn of the spinal cord resulting in neurone death and muscle atrophy. It is a progressive incurable disease.

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195
Q

lower motor neurones mediates

A

reflexes and muscle tone, they link upper motor neurones to the muscle and mediate control.

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196
Q

upper motor neurones mediates

A

carry the information from the brain down the spinal cord.

197
Q

upper motor neurone lesion

A

cause spasticity paralysis and hyperreflexia,

198
Q

lower motor neurone lesion causes

A

LMN caused flaccidity paralysis and areflexia.

199
Q

stretch reflex explained

A

tendon stretched then leads to intrafusal muscle fibre stimulation, which results in sensory neurone activation. This signal travels along a monosynaptic arc, whilst a polysynaptic reflex arc to an inhibitory interneuron to the antagonist muscle. The agonist muscle contract and the antagonist muscle receive reciprocal inhibitory innervation.

200
Q

flexor reflex arc explain

A

involves a pain stimulus, sensory neurone activation, a polysynaptic arc with flexion and withdrawal unilaterally, and contralateral extensor response.

201
Q

left upper motor neuron lesion within the internal capsule for the corticospinal tract yields

A

right sided paralysis, hyper reflexia, and increased tone.

202
Q

left upper motor neurone lesion at upper cervical spinal cord results in

A

left sided paralysis, hyper flexia and increased tone.

203
Q

left lower motor neurone lesion results in

A

left sided paralysis, absent reflexes and flaccidity.

204
Q

in the posterior dorsal column lesions above the decussation result

A

in contralateral sensory loss,

205
Q

in the posterior dorsal column lesions below the decussation result

A

the decussation is ipsilateral sensory loss for fine touch, tactile localisation, vibration and proprioception.

206
Q

stage 1 sleep

A

slow wave, slow eye movements. Easily roused. High amplitude and low frequency theta waves associated with sleep or stress

207
Q

stage 2 sleep

A

cessation of eye movements, frequency reduced with sleep spindle clusters of high frequency bursts

208
Q

stage 3 sleep

A

; increasing amplitude, slow delta waves associated with deep sleep. Presence of spindle activity declining.

209
Q

stage 4 sleep

A

; exclusively delta waves associated with deep sleep.

210
Q

REM sleep

A

rapid eye movements, paradoxical sleep associated with alpha and beta waves. High frequency and low fast asynchronous amplitude waves.

211
Q

typical night pattern of sleep

A

it cycles from awake, eyes closed in alpha waves, progressing to the short-lasting stage one REM, then to the transition states of stage 2 and 3, before entering a deep sleep stage. This cycle repeats again but REM gradually increases and deep sleep stages will only occur once more before being replaced by REM.

212
Q

describe the characteristic of deep slow wave sleep

A

deep slow wave sleep allows for dreams, deep restful sleep and decreased vascular tone and blood pressure, and reduced respiratory and basal metabolic rate.

213
Q

without sleep there is

A

is impaired cognitive function, physical performance, fatigue, and irritability as well as increased risk of psychosis.

214
Q

sleep is important for

A

for neuronal plasticity, learning and memory, cognition, clearance of waste from the CNs, conservation of energy and immune function.

215
Q

dreams occur in

A

REM sleep

216
Q

REM sleep description/physiology

A

eyes have burst of rapid activity whilst skeletal muscle is inhibited by the pons. This stage depends on cholinergic pathwats within the reticular formation projecting to the thalamus, hypothalamus and cortex. Heart rate and brain metabolism irregularly increases and brain waves resemble beta waves. We are difficult to arouse in this stage and it appears to be of some clinical importance.

217
Q

falling asleep process physiological process

A

sleep centres in within the mid-pons take over when the active excitatory cells for wakefulness become fatigued resulting in inhibition of the cortex and this inhibitory process is likely serotonergic as well as being supported by sleep inducing peptides in the CSF. There is also support from suprachiasmatic nuclei in the hypothalamus for generating a circadian rhythm that induces the release of melatonin from the pineal gland for stimulating sleepiness.

218
Q

waking process physiology

A

On the contrary wakefulness is stimulated by a hypothalamus neurotransmitter orexin which stimulate excitatory neurons in the ascending reticular activating system are released from inhibition by sleep centres in the reticular formation generating a feedback loop.

219
Q

insomnia description

A

chronically unable to have quality sleep to maintain normal behaviour.

220
Q

night terrors occur during

A

delta sleep

221
Q

somnambulism refers to

A

sleepwalking during non REM sleep

222
Q

narcolepsy description

A

individual enters REM sleep suddenly and is linked to dysfunctional orexin release from the hypothalamus.

223
Q

role of suprachiasmatic nucleus in circadian rhythm

A

suprachiasmatic nucleus of the hypothalamus above the optic chiasma have an inherent 24hr cycle imbued by external cues such as light via the optic nerve. If destroyed there is likely the loss of melatonin signalling and orexin signalling in the hypothalamus.

224
Q

describe the different components of voluntary motor system

A

voluntary brain control of muscles or reflexive control is via the common pathway which is alpha motor neurones in the spinal cord, particularly for reflexes it’s at a segmental level. the cerebral cortex, basal ganglia and cerebellum influence the brainstem nuclei to integrate and control reflexes through descending tracts such as the vestibulospinal and reticulospinal.

225
Q

basal ganglia function in voluntary movement

A

initiates movement stimulating the cortex in regard to planning and initiating movement

226
Q

the brainstem in the voluntary movement

A

brainstem centers for basic movements and posture which are influenced by the cerebellum in regards to sensory information about coordination of movement.

227
Q

sensory inputs stimulate for voluntary movement

A

, sensory inputs stimulate local circuit neurons to integrate information and travel then along the common path for both system the alpha motor neurone which ultimately influences skeletal muscle.

228
Q

how can descending inputs interact with segmental reflexes

A

descending input from the brainstem and direct cortical input travels along the corticospinal pyramidal tract. Descending voluntary excitation of alpha motor neurones can override the inhibition from the golgi tendon organs to maintain contraction if the cause is deemed worthy. This is the same for stretch reflex. The descending inputs are the result of the motor cortex planning, initiating and directing voluntary movements and the brainstem controlling basic movements and posture control.

229
Q

how are muscles mapped in the spinal cord

A

there is a spatial map of body musculature that is mediolaterally mapped. Proximal muscles to medial motor neurones and distal to lateral motor neurones. This then travels along the axis of the spinal cord generating a 3D image essentially of functional motor neurones.

230
Q

inverse stretch reflex is mediated by and physiology

A

mediated by golgi tendon organs monitoring muscle tension, contraction pulls the tendon and an impulse is sent along a 1b sensory neurone stimulating activation of inhibitory interneurons to the agonist muscle, and excitatory interneurons to the antagonist muscle, as well as informing the somatosensory cortex via the dorsal columns. This is a polysynaptic and protective process.

231
Q

readiness potential refers to

A

Readiness potential refers to the increase in electrical cortical activity prior to voluntary movement in which the duration of the manifestation reflects the complexity.

232
Q

readiness potential influence with the basal ganglia

A

The basal ganglia then process this to initiate the voluntary movement

233
Q

readiness potential within the cerebellum

A

the cerebellum processes this and modulates timing, coordination and automatic voluntary movements, known as reflexes

234
Q

Parkinson’s disease explanation

A

Parkinson’s disease results in hypokinesia which is slowness characterised by rigidity and tremors. It is due to atrophy of neurones in the substantia nigra and their dopaminergic inputs to the striatum.

235
Q

huntington’s disease explanation

A

Huntington’s unlike Parkinson’s disease reflects hyperkinesia. Often characterised by spontaneous movements. It is due to atrophy of caudate, putamen and globus pallidus, preventing the inhibitory effects of the basal ganglia.

236
Q

cerebellum for motor learning

A

gathers previous experiences to modulate motor processes with calculations to compare intention with action and then compensates to ensure success. Information from the somatosensory cortex, layer 5, and areas 4 and 6 are all projected to the cerebellum via the cortico-ponto-cerebellar projection. This connects the cortex, pontine nuclei and cerebellum. The cerebellum then feeds back to the cortex via the ventrolateral thalamus. Essentially this process is a feedback loop of voluntary movement.

237
Q

lesions to the cerebellum cause

A

uncoordinated movements, ataxia, failure to touch the nose with the eyes shut, similar to the effects of alcohol.

238
Q

presentation of multiple sclerosis

A

gradual onset over days
stabilises day to weeks
optic neuritis presents with subacute visual loss, painful eye movement, colour vision loss and relative afferent pupillary defect.
brainstem relapsed involve internuclear ophthalmoplegia, cranial nerve involvement, vertigo, nystagmus, ataxia and upper motor neurone signs in the limbs and sensory involvement.
myelitis often involves a hyperaesthesia, weakness, and bladder/bowel involvement.
gradual resolution to complete or partial recovery, often has relapses however.

239
Q

MS relapse

A

a relapse results in optic neuritis, sensory symptoms, limb weakness. With vertigo, diplopia, vertigo and ataxia. Often with spinal cord bilateral symptoms and signs of bladder involvement. As well as limb weakness and sphincter disturbance.

240
Q

MS clinically isolated syndrome

A

syndrome will be just a on off episode or is may be episodes of demyelination disseminated in space and time.

241
Q

progressive phase MS

A

phase involves an accumulation of symptoms and signs with fatigue, sensory, stiffness, spasms, slurred speech, swallowing, bladder and bowel, diplopia, oscillopsia, and cognitive dementia.

242
Q

progressive MS

A

. Primary progressive presents in their 50’s to 60’s with no relapses, poor prognosis and bladder/spinal symptoms.

243
Q

MS Pathology

A

multiple sclerosis is a central nervous disease affecting the central nervous system, particularly the white matter through demyelination. This is through an auto-immune disease as T cells cross the blood brain barrier and inflame the myelin sheath.

244
Q

MS diagnosis

A

diagnosis often depends on stage but signs involve sensory, cerebellar, hyperreflexia, plantar extensor, afferent pupillary defect, weakness, nystagmus and spasticity.
For a formal diagnosis it requires evidence of demyelination over a period of time and space. Often may be clinical through macdonald criteria or MRI. On an MRI you are looking for lesions. Other investigations involve lumbar puncture, visual/somatosensory responses, bloods and CXR.

245
Q

general treatment for MS

A

involves general health, diet, vaccines, treatment of relapse

246
Q

MS relapse treatment

A

looking for infection, treat with oral prednisolone, rehabilitation and SYMPTOMATIC TREATMENT

247
Q

disease modifying treatment

A

treatment are intramuscular or subcutaneous injections of beta interferons or glatiramer acetate. Oral treatment includes teriflunomide and dimethyl fumarate. Second line treatments are natalizumab, fingolimod, and alemtuzumab.

248
Q

symptomatic treatment is

A

anti-spasmodic medication, physiotherapy, for the dysesthesia amitriptyline or gabapentin, for urinary symptoms anticholinergics or catheters, constipation use laxatives and sexual dysfunction sildenafil is recommended. Cognitive behavioural therapy for depression, aids for the tremors, vision carbamazepine, SALT for speech/swallowing. Treat the patient’s symptoms not the general.

249
Q

sensory transduction

A

the ability of sensory receptors to transduce adequate stimulus into a local detrimental depolarising generator potential, if significant enough the generator potential will overcome the threshold and reach the trigger zone activating action potentials. The frequency of which will be translated to reflect the intensity of stimulus. The receptive field encodes the location of the stimulus.

250
Q

the major pathway by which information from the body about pain and temperature reaches consciousness

A

transported by A delta small myelinated and C unmyelinated fibres to synapse in the dorsal horn, then decussate in the segmental level to then project through the contralateral spinothalamic tract to the reticular formation, thalamus and ending in the somatosensory cortex of the post central gyrus S1.

251
Q

pain and temperature are transported fibres by

A

small myelinated A delta and C unmyelinated

252
Q

Describe the major pathway by which information from the body about touch and limb position reaches consciousness

A

touch is transported by A beta large myelinated fibres which project up through ipsilateral dorsal columns, synapsing in the cuneate and gracile nuclei. The 2nd order fibres decussate in the brain stem and project to the reticular formation, thalamus and ending into the somatosensory cortex S1 in the post central gyrus.

253
Q

nociceptors are activated by

A

low pH by ASIC receptors, TRPV for heat, or through noxious stimuli channel activated by bradykinin which is stimulated by prostaglandins via G protein cascade. This results in depolarisation.

254
Q

Pain pathway

A

This then travels along A delta and C fibres via the dorsal root ganglion, synapsing in the dorsal horn then decussating across at the segmental level to travel along the spinothalamic tract to the reticular formation, thalamus and finally terminating in the somatosensory cortex of the post central gyrus S1.

255
Q

Explain why pain originating from the viscera can often result in sensation being referred to a somatic structure from the same dermatomes

A

this is due to convergence. The system enables to reduce the number of necessary neurones but results in specific ascending pathways where two touch receptors may synapse to the same second order neurone. There are also nonspecific ascending pathways in which a touch receptor and temperature receptor may synapse at the same second order neurone. This is often seen as resulting in referred pain.

256
Q

explain convergence in neurone pathways

A

this is due to convergence. The system enables to reduce the number of necessary neurones but results in specific ascending pathways where two touch receptors may synapse to the same second order neurone.

257
Q

non-specific ascending pathways in pain neurone pathways

A

pathways in which a touch receptor and temperature receptor may synapse at the same second order neurone. This is often seen as resulting in referred pain.

258
Q

gate control hypothesis for pain modulation

A

Segmental control arises from faster fibres for touch and pressure, A alpha and A beta which activate inhibitory interneurons which release opioid peptides called endorphins that “close the gate”

259
Q

Describe how pain can be controlled by descending pathway in the CNS

A

descending controls from the peri-aqueductal grey matter PAG and the nucleus Raphe Magnus NRM stimulate the same inhibitory interneurons that release endorphins closing the gate.

260
Q

non-steroidal anti-inflammatory drugs pharmacological process

A

they inhibit cyclo-oxygenase which normally converts arachidonic acid to prostaglandins. Thus, preventing the sensation of nociceptors to bradykinin.

261
Q

local anaesthetics process pharmacological process

A

blocks sodium action potentials and therefore all axonal transmission

262
Q

trans cutaneous electric nerve stimulation pharmacological process

A

electrically stimulating the skin to stimulate A beta neurones to stimulate inhibitory interneurons to close the gate.

263
Q

opiates pharmacological process

A

reduce the sensitivity of nociceptors. They block transmitter release in the dorsal horn and activate descending inhibitory pathways.

264
Q

limbic system relevance in memory

A

emotional significance for memory

265
Q

cingulate gyrus and amygdala association for in memory

A

emotion

266
Q

hypothalamus is associated with

A

autonomic nervous system

267
Q

immediate memory

A

experiences held for seconds, visual decaying fastest then auditory slowest.

268
Q

what decays faster auditory or visual memory?

A

visual

269
Q

short term memory

A

seconds to hours as a working memory associated with reverberating circuits.

270
Q

intermediate long term memory

A

hours to weeks associated with chemical adaptation at the presynaptic terminal. Often associated with increased calcium entry stimulating greater neurotransmitter release.

271
Q

long term memory

A

ifelong, associated with structural changes in the synaptic connections.
There is also an increased amplitude in graded membrane potential in the post synaptic cell called long term potential allowing a well-established pattern associated with a memory.

272
Q

long term memory types

A

. Long term memory can be declarative, abstract recall of rules, events and language requiring the hippocampus or procedural acquired through repetition “motor memory”, it is independent of the hippocampus and based in the cerebellum.

273
Q

reverberating circuit significance in memory

A

reverberating circuit is the idea a memory is initially electrical, circulating around neurones that needs to be continually excited. It’s essentially the first step to consolidating memory from short term to long term. This activity is through the papez circuit which is the hippocampus, mamillary bodies, anterior thalamus and cingulate gyrus.

274
Q

retrograde amnesia explain

A

cannot access old memories. Cannot remember leading up to the injury. Long term memories are unaffected, often presents with anterograde amnesia, however if the thalamus is damaged and hippocampus spared then it is only retrograde amnesia as its essential for accessing memories.

275
Q

antergrade amnesia explain

A

cannot form new memories. Cannot recall events after an injury, often associated with injury to the hippocampus.

276
Q

short term memory into long term memory

A

continually activating a reverberating circuit will provide time for the memory to be deemed significant, allowing for consolidation. This requires converting an electrical memory into a chemical, and structural change. This is through selective strengthening of the synaptic connections. Memory is eventually stored in various parts of the cortex with visual in the visual cortex

277
Q

importance for sleep for memory processing

A

consolidation requires attention. Subjects deprived of REM sleep show impairment of memory consolidation for complex cognitive tasks, dreaming may enable consolidation and reinforce weaker circuits

278
Q

Acute angle closure Glaucoma symptoms

A

very painful, redness, blurred vision, nausea and vomiting, hazy cornea, fixed mid-dilated pupil and hard eyeball

279
Q

scleritis symptoms

A

; very painful, redness, nodules, very tender

280
Q

acute anterior uveitis symptoms

A

pain, watering, photophobia, blurred vision, floaters, red, cells in anterior chamber, hypopyon, small irregular pupil, prior history.

281
Q

corneal abrasion symptoms

A

; pain, watering, blurred vision, epithelial defects

282
Q

allergic conjunctivitis symptoms

A

itchy, red, discharge, acute, lid swelling, conjunctival swelling

283
Q

infective conjunctivitis symptoms

A

gritty, red, discharge

284
Q

symptoms and signs of cellulitis

A

symptoms and signs include painful, redness, blurred vision, malaise, proptosis, reduced eye movement.

285
Q

management of cellulitis

A

involves admittance to hospital, Ct scan and drainage of pus.

286
Q

FFA – Fluorescein angiography - method

A

rapid fundal photography following injection of fluorescein dye to examine flow of the vessels, pigment epithelium detail and retinal circulation and assessment of retinal vessel integrity.

287
Q

OCT- optical coherence tomography method

A

use of infrared light to capture 3D images from optical scattering media.

288
Q

ERG Electroretinography method

A

is an eye test for detecting the function of the retina. It picks up the electrical signals from photoreceptors. It uses an electrode on the cornea to measure electrical response.

289
Q

EOG electrooculography

A

recording eye movements and position by measuring the difference in electrical potential between two electrodes on either side of the eye. There is a dark phase and a light phase. If its ratio is less than 1.8 it indicates a malfunction of the structure form which the potential originates.

290
Q

VEP – visual evoked potential

A

visual evoked potential is a test using a visual stimulus such as a alternating checkerboard on a computer screen, responses are recorded using electrodes on the back of the head and presented as an EEG reading. It highlights the receiving and interpreting of visual signals.

291
Q

non-arteritic painless anterior ischaemic optic neuropathy description

A

infarct within the short posterior ciliary arteries resulting In compartment syndrome from the oedema resulting In retinal ganglion cell death

292
Q

signs of non-arteritic painless anterior ischaemic optic neuropathy;

A

Normal signs of decreased visual acuity, dyschromatopisa acquired loss of colour vision), and a swollen optic nerve.

293
Q

non-arteritic painless anterior ischaemic optic neuropathy; symptoms

A

acute, painless unilateral vision loss commonly described as blurring/cloudiness.

294
Q

Central retinal artery occlusion; description

A

obstruction of the retinal vascular lumen by embolus, thrombosis or inflammation, damage or spasm, associated with giant cell arteritis. Ischaemia of the inner retina occurs and oedema, this resolves by choroidal circulation with mild recovery.

295
Q

central retinal artery occlusion signs

A

include normal fundus, relative afferent pupillary defect, retinal whitening and cherry red spot. Chronic signs include pale optic disc, thin retinal tissue, attenuated vessels and altered retinal pigment

296
Q

symptoms of central retinal artery occlusion

A

acute painless vision loss

297
Q

central vein occlusion description

A

gradual loss or sudden loss of vision due to a blocked vein and fluid leakage into the retina, swelling altering vision and nerve cell death.

298
Q

symptoms of central retinal vein occlusion

A

Symptoms are floaters/dark spots in vision, in severe cases pain and pressure. Normally unilateral.

299
Q

cataracts explanation

A

gradual opacification of the lens with symptoms of loss of vision, dazzle and glare

300
Q

glaucoma explanation

A

raised intraocular pressure with optic neuropathy associated with visual field changes.

301
Q

diabetic retinopathy explanation

A

high blood sugar blocks of the small blood vessels for supplying the retina, new vessels develop but will be weaker and leak blood into the eye.

302
Q

signs of diabetic retinopathy

A

signs of microaneurysms, retinal exudate and neovascularisation.

303
Q

symptoms of diabetic retinopathy

A

loss of central vision, inability to see colours and black spots in vision.

304
Q

central retinal artery occlusion retinal appearance

A

retina pale except in the macular area in which the choroidal circulation causes a cherry red spot to form resulting in sudden, painless and complete loss of vision in one eye.

305
Q

central retinal vein occlusion retinal appearance

A

gives the appearance of a stormy sunset with engorged veins, and haemorrhages alongside them.

306
Q

optic neuritis pathology

A

Develops as a result of demyelination of the optic nerve resulting in visual loss. It’s often associated with multiple sclerosis. Due to the autoimmune processes of systemic T cell targeting of myelin.

307
Q

ischaemic optic neuropathy pathology

A

often develops due to giant cell arteritis or atherosclerosis in non-arteritis. The acute ischaemia then causes nerve oedema, causing swelling to the optic disk and retina dysfunction.

308
Q

optic neuritis signs

A

associated with multiple sclerosis, commonly affects young adults in one eye

309
Q

optic neuritis symptoms

A

vision loss, reduced colour vision, pain on eye movement

310
Q

ischaemic optic neuropathy signs

A

unilateral, reduced visual acuity, afferent pupillary defect. Splinter haemorrhage optic disk and swollen. Pale if arteritis or non-arteritis then hyperaemic, defect often in the inferior and central visual fields.

311
Q

symptoms of ischaemic optic neuropathy

A

vision loss, painless, rapid. Malaise, muscle aches and pains, headaches, jaw claudication

312
Q

retinitis pigmentosa pathology

A

progressive inherited disease that results in retinal degeneration.

313
Q

symptoms retinitis pigmentosa

A

Often symptoms include peripheral and night vision. Then as it progresses colour perception, visual acuity and central vision are diminished

314
Q

signs of age related macular degeneration

A

symptoms of progressive distortion of central vision. It has signs of distortion on an amsler chart, drusen and pigmental changes

315
Q

pathology of age related macular degeneration DRY

A

It may be dry due to atrophy, or wet due to choroidal angiogenesis. either way it results in damage to the macula, made noticeable by pigment changes in the retina. Late stage dry AMD is due to the gradual breakdown of light sensitive cells in the macula and supporting tissue

316
Q

Wet Age related macular degeneration pathology

A

is due to abnormal vessel growth leaking fluid into the macula causing it to swell and degrade. It may be rapid or long term.

317
Q

symptoms of muscle disorders

A

weakness of skeletal muscle, shortness of breath, poor swallow, cardiomyopathy, cramp, pain, stiffness and myoglobinuria.

318
Q

signs of muscle disorders

A

wasting, hypertrophy, reduced tone and reflex and no sensory signs purely motor weakness.

319
Q

congenital classifications of muscle disease

A

structural muscular dystrophy, contractile congenital myopathies, coupling channelopathies, and energy with enzyme and mitochondria dysfunction

320
Q

acquired diseases of muscles classifications

A

metabolic, endocrine, inflammatory and iatrogenic

321
Q

investigations of muscle diseases

A

creatine kinase, EMG, muscle biopsy of structure, biochemistry, and inflammation. As well as genetic testing.

322
Q

myasthenia gravis presentation

A

fatigable weakness of limbs, eyelids, muscles of mastication resulting in difficulty or fatigue in talking, breathing and diplopia

323
Q

investigations of myasthenia gravis

A

investigations involve an AChR ab, anti MuSK ab, neurophysiology of repetitive stimulation and jitter, and a CT scan of the chest to check for a thymoma.

324
Q

treatment for myasthenia gravis

A

involves acetylcholinesterase inhibitor, and immunosuppression through prednisolone, and steroid saving agent. Immunoglobulins/plasma exchange and a thymectomy.

325
Q

causes of peripheral neuropathy

A

lesion of an individual nerve through compression or vasculitis or through a general peripheral neuropathy.

326
Q

general neuropathy causes

A

General neuropathy causes are though hereditary, metabolic particularly alcohol or diabetes, toxic drugs, infection, malignancy as a paraneoplastic syndrome or inflammation causing demyelination as acute Gullian Barre syndrome or chronic polyneuropathy.

327
Q

nerve root symptoms

A

nerve root symptoms include myotomal wasting and weakness, reflex changes, and dermatomal sensory change.

328
Q

generalised peripheral neuropathy symptoms

A

include sensory and motor symptoms stating distally and moving proximally.

329
Q

individual nerve symptoms pathology

A

There is individual nerve symptoms of specific sensory changes, and wasting/weakness of innervated muscle

330
Q

LMN

A

muscle fasciculation, wasting and weakness, reduced tone, reflexes, flexor planter

331
Q

UMN

A

increased tone, brisk reflexes, no wasting, and pyramidal pattern of weakness, extensor plantar

332
Q

clinical presentation of motor neurone disease

A

muscle fasciculations, wasting and weakness associated with lower motor neurones lesions, and upper motor neurones signs of increased tone and brisk reflexes. No sensory involvement and cognitive decline in 10%. Starts with limb, progressing to bulbar and then respiratory

333
Q

treatment of motor neurone disease

A

Treatment is supportive through PEG feed, non-invasive ventilation, physio, OT, SALT, care. Riluzole, and anticipatory care/palliation.

334
Q

investigations of motor neurone disease

A

signs and EMG

335
Q

spinal cord stroke symptoms

A

back pain, visceral referred pain, weakness, vascular risk factors. Onset over several hours or sudden, paraesthesia, and urinary symptoms with urinary retention and incontinence.

336
Q

symptoms prior to a migraine

A

Prior to an attack there is fatigue, mood swings, cognitive changes, muscle pains and food cravings

337
Q

early migraine headaches are characterized

A

characterized by dull headaches, nasal congestion and muscle pain.

338
Q

advanced migraines are characterised

A

Advanced headaches are unilateral throbbing with nausea, photophobia, osmophobia, and phonophobia.

339
Q

Aura is a

A

transient cortical dysfunction affecting visual, sensory, motor or speech in a slow wave.

340
Q

postdrome migraine characteristics

A

fatigue, cognitive changes and muscle pain

341
Q

percentage of migraines that originate from medication

A

60%

342
Q

chronic migraine is a migraine that lasts longer than

A

15 days taking a symptomatic drugs

343
Q

causes of a medication migraine

A

Triptans, ergots, opioids (>10 per month), analgesics, or caffeine overuse

344
Q

cluster head description and symptoms

A

mainly orbital and temporal, 15 minute to 3 hours of pain with a rapid onset and cessation. Extremely excruciating with prominent autonomic symptoms and typical aura. It occurs in clusters with 1 to 8 in a day over a bout of time.

345
Q

paroxysmal hemicrania symptoms ad description

A

can occur up to 1 to 40 times a day for 2-3 minutes resulting in restlessness unlike migraines, precipitated by bending or rotating the head and normally chronic.

346
Q

SUNCT description/ symptoms

A

SUNCT lasts only 240 seconds characterised by stabbing or pulsatile pain, with frequency of 3-200 a day accompanied by conjunctival injection and lacrimation

347
Q

tension headache description

A

headaches are rarely disabling, with a bilateral tightening but with no associated features.

348
Q

migraine treatment

A

abortive use of aspirin, Triptans, limit to 10 days a month. Prophylactic use of propranolol, anti-epileptics, tricyclic anti-depressants, venlafaxine.

349
Q

cluster headache treatment

A

abortive use of nasal spray, oxygen and subcutaneous injection of sumatriptan as it needs to be rapid. Abortive for a bout requires depomedrone injection, or oral prednisone. Preventative; verapamil high dose, or lithium.

350
Q

paroxysmal hemicrania prophylaxis

A

indomethacin

351
Q

SUNCT/SUNA prophylaxis

A

gabapentin or carbamazepine

352
Q

trigeminal neuralgia treatment

A

carbamazepine or surgical intervention with glycerol ganglion injection, decompression surgery or stereotactic radiosurgery.

353
Q

red flags for headaches

A 
thunderclap
persisting
>50
immunosuppression
cancer
neuro symptoms
fever
neck stiffness
exertional
morning headaches
standing up trigger
jaw claudication
visual
354
Q

thunderclap presentation

A

high intensity within a minute

355
Q

raised ICP presentation

A

worse in morning, worse lying flat, focal symptoms, cognitive/ personality changes, seizures and visual obscuration and pulsatile tinnitus.

356
Q

intracranial hypotension presentation

A

worse standing upright

357
Q

giant cell arteritis presentation

A

diffuse, persistent, systematic unwellness, scalp tenderness, jaw claudication and visual disturbance with prominent temporal arteries.

358
Q

trigeminal neuralgia features

A

maxillary or mandibular sensory area with unilateral stabbing pain with similar SUNCT triggers and frequency but with no autonomic features

359
Q

treatment for trigeminal neuralgia

A

treatment; prophylaxis with carbamazepine or surgical intervention with a glycerol ganglion injection, stereotactic radiosurgery or decompression surgery.

360
Q

thunderclap management

A

hospital assessment, CT, angiography an LP in case of subarachnoid haemorrhage.

361
Q

meningitis features

A

headache and fever, nausea, vomiting, photo/phonophobia, stiff neck

362
Q

raised ICP features

A

progressive headache that’s worse lying down or in the morning, focal symptoms and signs, cognitive changes, seizures, visual obscuration’s and pulsatile tinnitus.

363
Q

intracranial hypotension treatment

A

MRI, bed rest, fluids, analgesia, caffeine, epidural blood patch.

364
Q

giant cell arteritis features

A

diffuse, persistent, severe, systemic unwellness, scalp tenderness, jaw claudication, visual disturbance and prominent temporal arteries

365
Q

treatment of giant cell arteritis

A

elevated ESR >50, raised CRP then high dose prednisolone and biopsy.

366
Q

pain fibres

A

Alpha delta fibres and C fibres

367
Q

the second order neurone pain pathway

A

spinothalamic tract, decussating at that segmental level along the lateral side of the tract in rexed lamina 2 & 5. It is then transmitted to the brain via the ventroposterior thalamic nuclei within the medial thalamus. Next the signal is sent to the limbic system and cortex via the pain matrix as pain is perceived in the somatosensory cortex.

368
Q

descending pathway of pain

A

The medial part of the pain matrix feedback information and forward it to the brainstem PAG for emotional and affective components and control of pain. Finally, the descending pathway if from the brain to the dorsal horn via a noradrenergic periaqueductal grey matter and usually decreases the pain.

369
Q

allodynia

A

inflammatory markers from an injury that decreases the threshold for a response causing hyperalgesia

370
Q

hyperalgesia

A

increased perception of noxious stimuli

371
Q

secondary hyperalgesia

A

increased perception of noxious stimuli in uninjured tissue

372
Q

wind up modulation of pain pathways

A

to the activated homo synaptic synapses that depend on progressive increase of neurones to increases the response, growing over the course of the stimuli and terminating with the stimuli.

373
Q

classical sensitization of pain pathways

A

new (hetero) synapses in the dorsal horn will start transmitting once the threshold has ben met and begins immediately, outlasting the initial stimuli and maintain at low levels of stimuli if they are ongoing and it is this process responsible for secondary hyperalgesia.

374
Q

neuropathic pain

A

often chronic pain, initiated by a primary lesion or dysfunction in somatosensory nervous system. May be referred pain due to the neurological territory and responds poorly to analgesics.

375
Q

differentials of blackouts

A

syncope, first seizure, hypoxic seizure, concussive seizure, cardiac arrhythmia, non-epileptic attack.

376
Q

features of partial seizures

A

characterised according to aura, motor features, autonomic features and degree of awareness, may even into a generalised convulsive seizure. Occurs at any age, focal abnormality on EEG and MRI may show the cause.

377
Q

history of the epilepsy

A

what were they doing at the time, any warning, what they were doing the night before, how did they feel, incontinence, tongue biting.

378
Q

investigation of epilepsy

A

blood sugar, ECG, consider alcohol and drugs, CT head. Video telemetry may be recommended and a EEG, with stimulation.

379
Q

first line therapy for epilepsy

A

first line; sodium valproate
levetiracetam for primary general
carbamazepine for partial and secondary

380
Q

treatment of status epilepticus

A

requires midazolam, lorazepam and diazepam. Second line is phenytoin or valproate and third line being anaesthesia

381
Q

after 1 seizure normal patient must wait before driving

A

6 month s

382
Q

patients with seizures must wait

A

1 year free on medication

383
Q

features for viral encephalitis

A

flu like prodrome, progressive headache, +/- meningism, gradually progressive cerebral dysfunction with confusion, abnormal behaviour, memory disturbance, depressed consciousness, seizures, focal symptoms and signs.

384
Q

autoimmune encephalitis causes

A

anti VGKC

anti NMDA

385
Q

investigations for encephalitis

A

blood cultures, CT +/- MRI, lumbar puncture (unless signs of a lesion, or raised intracranial pressure), EEG

386
Q

microbiology for encephalitis

A

herpes simplex virus, enteroviruses, arbovirus,

387
Q

Anti-VGKC epilepsy symptoms

A

seizures, amnesia, altered mental state

388
Q

Anti-NMDA symptoms

A

prodrome, psychiatric features, seizures and altered mental states, progresses to movement disorder and coma.

389
Q

cerebral abscess features

A

; fever, headache, focal symptoms, papilledema, depressed consciousness, +/- meningism.

390
Q

cerebral abscess of microbiology

A

spread from adjacent infection, blood borne infection or from neurosurgical procedure. Often polymicrobial, often streptococci and anaerobes such as bacteriodes or prevotella

391
Q

treatment for cerebral abscess

A

; surgical drainage, high doses of penicillin or ceftriaxone for streps or metronidazole for anaerobes.

392
Q

meningitis clinical features

A

; neck stiffness, altered mental state, fever. Short history or progressive headache, photophobia, nausea, vomiting, cerebral dysfunction, cranial nerve palsy, and petechial skin rash.

393
Q

microbiology of meningitis

A

bacterial meningococcal meningitis or streptococcus pneumonia, or viral from enteroviruses

394
Q

investigations of meningitis

A

blood cultures, CSF lumbar puncture (unless lesion or raised intracranial pressure)

395
Q

lyme disease features

A

features; vector borne, multi system rheumatological, neurological, ophthalmological, cardiac.
Local infection with erythema migrans with flu symptoms, fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness. Stage 2 multi system, Peripheral nervous system affected more. Stage 3 subacute encephalopathy and encephalomyelitis.

396
Q

investigations for lyme disease

A

serology, CSF lymphocytosis, MRI brain/spine, nerve conduction studies

397
Q

treatment for lyme disease

A

I.V. ceftriaxone, oral doxycycline

398
Q

microbiology for lyme disease

A

borrelia burgdorferi

399
Q

neurosyphilis investigations

A

treponema antibody tests, CSF lymphocytes

400
Q

microbiology of neurosyphilis

A

treponema pallidum

401
Q

treatment of neurosyphilis

A

high dose penicillin

402
Q

a prion is

A

transmissible proteinaceous particle

403
Q

CJD affect on nervous system

A

rapid onset dementia, myoclonus, neurological decline, cerebellar ataxia, cortical blindness and seizures, extrapyramidal with tremors, rigidity, bradykinesias, dystonia, pyramidal with weakness, spasticity and hyper-reflexes and pyramidal with weakness, spasticity and hyper reflexes

404
Q

rabies immunisation

A

to those at risk, post exposure given passive immunisation and active immunisation.

405
Q

tetanus immunisation

A

toxoid immunisation and passive immunisation for those at high risk.
botulism given anti toxin

406
Q

longstanding ischaemia pathological appearance

A

results in localised brain death due to death of neurones from oxygen starvation. The wedge shaped is a result of the arterial perfusion territory, it then becomes soft and then cystic. Foamy macrophages move in to repair the damage resulting in fibrosis and there is yellowing of tissue.

407
Q

watershed zones reason for in ischaemia

A

prolonged period of hypotension with oxygenated blood results in watershed zones (areas between cerebral artery territories) being poorly perfused. Often symmetrical

408
Q

pathological appearance of cardiac arrest ischaemia

A

cardiac arrest, brain deprived of oxygen results in large grey matter areas thinning, necrosis and laminar lines.

409
Q

primary brain tumours

A

neuroepithelial tissue and can be pituitary adenomas, gliomas and meningioma

410
Q

secondary brain tumours

A

metastatic spread

411
Q

glioma description

A

Glioma’s arise from astrocytes, therefore are aggressive, and spread through the white matter and CSF pathways but unlikely to spread systematically.

412
Q

meningioma description

A

slow growing, extra axial benign tumours arising from the arachnoid. Often along the falx, convexity or sphenoid bone.

413
Q

pituitary tumours often causes

A

often cause visual disturbance and hormone imbalances

414
Q

CSF production

A

400-450cc

415
Q

CSF function

A

CSF; bathes brain and spinal cord from the subarachnoid space. Main function is to act as a shock absorber, removes some waste products and provides some immunological support.

416
Q

foramina of the 4rth ventricle

A

foramen of magendie (medial 1 ) and foramen of Luschka (lateral 2)

417
Q

flow of CSF

A

choroid plexus to flow is from lateral, foramina of munro, 3rd, aqueduct of sylvius, 4rth, foramen of magendie and foramen of Luschka2 then into the subarachnoid space, to the granulations and uptake by the villi into the dural venous sinuses.

418
Q

hydrocephalus is the

A

blockage of CSF

419
Q

obstructive hydrocephalus is

A

blockage of ventricle outflow

420
Q

communicating obstructive hydrocephalus

A

level of arachnoid granulations

421
Q

features of hydrocephalus

A

features; asymptomatic, increased ICP, headaches worse in the morning or on coughing, papilledema, visual disturbances, gait abnormality, loss of up gaze or abducens palsy, impaired consciousness.

422
Q

treatment of hydrocephalus

A

carbonic anhydrase inhibitor, extraventricular drain in emergencies, CSF diversion through 3rd ventriculostomy for non- communicating or shunt insertion.

423
Q

indications for a lumbar puncture

A

; CSF for analysis for blood, protein, viral, bacterial infections, measurement of pressure, and diagnostic tests as well as therapeutic for raised pressure.

424
Q

normal pressure hydrocephalus features

A

reversible dementia, gait disturbance (magnetic), urinary incontinence, over age of 60

425
Q

idiopathic hydrocephalus features

A

raised ICP without cause, headaches an visual disturbances, often young obese females

426
Q

management post lumbar puncture

A

bed rest for 2-4 hours, warn for low pressure headaches. Stop if patient becomes unconscious or develops neurological deficit.

427
Q

normal CSF stats

A

normal CSF should be clear, colourless, pH of 7.33 to 7.35, WBC 0-5, 0 RBC’s, Protein of 300 mg/l and glucose around 40-80mg/dl. Total volume should be 150ml.

428
Q

meningitis CSF

A

cloudy, lots of polymorphs, protein >1g and low glucose.

429
Q

CSF blood

A

trauma

430
Q

yellow CSF

A

breakdown of blood products

431
Q

stroke epidemiology

A

2nd - 3rd leading cause of death

432
Q

ACA occlusion symptoms

A

contralateral paralysis of foot and leg with sensory loss. Impairment of gait and stance.

433
Q

MCA occlusion symptoms

A

contralateral paralysis of arm, face leg, sensory loss and homonymous hemianopia. Gaze paralysis to opposite side, aphasia if on dominant side, unilateral neglect and agnosia for half of external space in non-dominant stroke.

434
Q

lacunar stroke symptoms

A

can be pure motor, pure sensory, dysarthria and ataxic hemiparesis.

435
Q

PCA circulation symptoms

A

; coma, vertigo, vomiting, nerve palsies, ataxia, hemiparesis, hemisensory loss, crossed sensori-motor deficits visual field deficits

436
Q

stroke acute treatment

A

thrombectomy has the highest rate of preventing death. Then it is a IV TPA within 3 hours, then stroke units and IV TPA within 3-5 hours. Aspirin has the lowest number needed to prevent 1 death or dependency.

437
Q

secondary prevention for a stroke

A

a carotid endarterectomy for internal carotid stenosis. However there are anti hypertensives, anti-platelets, lipid lowering agents, warfarin for AF all reduce risk.

438
Q

stroke investigation

A

investigations; routine blood tests, CT for infarct, haemorrhage then MRI, ECG, echocardiogram, carotid doppler, cerebral angiogram, hyper coagulability screen.

439
Q

TPA contraindications

A

It cannot be used if blood is present, recent surgery or bleeding episodes, coagulation problems, BP >185 or diastolic >110, or if glucose is less than <2.8 or >22mmol/L.

440
Q

depressed respiration

A

drug overdose, metabolic disturbance

441
Q

increased respiration

A

hypoxia, hypercapnia, acidosis

442
Q

fluctuating respiration

A

brainstem lesion

443
Q

investigations for a coma

A

blood sample for biochemistry, haematology, blood gas, toxicology, glucose. Establish baseline pressure, pulse, temperature.
temperature, skin, breath, abdomen, meningism, fundal examination, respiration, heart rate, blood pressure, CVs.

444
Q

coma without focal or lateralising signs or without meningism - investigations

A

toxicology, blood sugar and electrolytes, hepatic and renal function, acid-base and arterial blood gases, blood pressure and carbon monoxide poisoning.

445
Q

coma without focal or lateralising signs but with meningism; - investigations

A

; CT scan, lumbar puncture

446
Q

coma with focal brainstem or lateralising cerebral signs - investigations

A

CT/MRI with metabolic screens, lumbar puncture or EEG if necessary

447
Q

prognosis of coma

A

15% of patient in non-traumatic coma >6 hours make a recovery.

448
Q

management of coma

A

maintenance of vital functions, skin care and avoidance of pressure sores, management of bladder and bowel function, control of seizures, prophylaxis of DVT and peptic ulcers, prevention of contractures.

449
Q

coma definition

A

state of unarousable psychological unresponsiveness with not psychological response to stimulus or needs”

450
Q

consciousness requires

A

an intact ascending reticular activating system for alertness, and a functioning cerebral cortex for interpretation of consciousness. Therefore, consciousness is arousal and awareness of environment

451
Q

persistent vegetative state definition

A

brain stem recovery but with no cortical function. There is arousal but no awareness of the state.

452
Q

coma without focal or lateralising signs or without meningism causes

A

ischaemia, metabolic, intoxication, systemic infection, hyperthermia or hypothermia, epilepsy are all possible causes.

453
Q

coma without focal or lateralising signs but with meningism

A

subarachnoid haemorrhage, meningitis, encephalitis

454
Q

coma with focal brainstem or lateralising cerebral signs

A

tumour, haemorrhage, infraction or abscesses in the cerebrum

455
Q

locked in syndrome definition

A

head injuries such as diffuse axonal injury, contusion, intracerebral haematoma, extracerebral haematoma (sub/extradural).

456
Q

management of increases intracranial pressure

A

surgery to relieve pressure via a haematoma, or ventricular shunt. Osmotic agents such as mannitol, analgesics, maintain PO2 whilst reducing PCO2 and reduce metabolism through temperature reduction and barbiturates.

457
Q

subdural CT appearance haemorrhage

A

convex ellipse

458
Q

extradural CT haemorrhage appearance

A

concave, convex lens

459
Q

test for CN2

A

– visual acuity, pupillary reactions, fundoscopy, colour vision, visual fields

460
Q

tests for CN 3,5,6

A

ptosis, pupil size, pupillary reaction, eye movements.

461
Q

CN 5 tests

A

sensation, power of mastication, corneal reflex, jaw reflex.

462
Q

CN 7 tests

A

expression, corneal reflex, taste

463
Q

CN 8 tests

A

Rhinne’s and Weber tests, Dix Hallpike test and Untenberger’s test

464
Q

9,10CN tests

A

movement of palate, gag reflex, quality of speech, quality of cough

465
Q

CN 11 tests

A

shoulder shrugging and head turning

466
Q

CN 12 tests

A

appearance, movement and power of tongue

467
Q

pupillary light reaction afferent and efferent

A

2 afferent, efferent 3

468
Q

corneal reflex afferent and efferent

A

afferent 5, efferent 7

469
Q

jaw jerk reflex afferent and efferent

A

afferent and efferent 5

470
Q

gag reflex afferent and efferent

A

afferent 9, efferent 10 #

471
Q

causes for dilated pupils

A

third nerve palsy results in dilated pupils. As well as youth, dim lighting, mydriatic eye drops, amphetamine or cocaine, brain death, anxiety.

472
Q

constricted pupil reasons

A

pathway results in a constricted pupil. Other causes include old age, bright lights, miotic eye drops, opiate overdose, horner’s syndrome.

473
Q

trigeminal neuralgia features

A

paroxysmal attacks of lancinating pain, middle aged and older, caused by a vascular loop compression.

474
Q

ball’s palsy features

A

unilateral facial weakness, LMN, pain behind ear, risk of corneal damage due to eye closure disruption.

475
Q

vestibular neuronitis features

A

sudden onset, disabling vertigo, vomiting, gradual recovery, may be viral.

476
Q

pseudobulbar palsy features

A

difficulty swallowing and disorder articulation/slurring occurs in bulbar and pseudobulbar palsy.
pseudobulbar palsy is a UMN lesion of both internal capsules resulting in dysarthria, dysphonia, dysphagia, spastic mobile tongue, brisk jaw reflex, brisk gag reflex.

477
Q

bulbar reflex feature

A

bulbar reflex is a bilateral LMN lesion affecting 9-12th cranial nerves resulting in a wasted fasciculation tongue, dysarthria, dysphonia, and dysphagia.

478
Q

cranial nerve midbrain nuclei

A

3 + 4

479
Q

pons CN nuclei

A

5+6+7

480
Q

pontomedullary junction CN nuclei

A

8

481
Q

medulla CN nuclei

A

9 +10+11+12

482
Q

dementia clinical syndrome

A

progressive impairment of multiple domains of cognitive function in alert patient leading to loss of acquired skills and interference in occupational and social roles.

483
Q

Parkinson’s syndrome

A

dopamine loss within the basal ganglia resulting in bradykinesia, rigidity, tremor, postural instability.

484
Q

dementia diagnosis + inv

A

history, family history, progression, risk factors and deficits. Investigations involve routine bloods, CT/MRI others include CSF, EEG, functional imaging and genetics. Cognitive function may be measured with the MMSE on montreal screening tests.

485
Q

Parkinson’s diagnosis

A

bradykinesia with tremor, rigidity, postural instability and slowly progressive. Responsive to dopamine replacement treatment. May use a dopamine transporter SPECT to diagnose

486
Q

alzheimer’s treatment

A

cholinesterase inhibitors with donepezil, or NMDA antagonist.

487
Q

Parkinson’s treatment

A

dopamine replacement treatment through dopamine agonists, MOA-B inhibitor, COMT inhibitor. Followed on by Levodopa increased half life, continuous infusions, functional neurosurgery (deep brain stimulation) and allied health care professionals.

488
Q

features of temporo-parietal features

A

early memory disturbance, language and visuospatial problems, personality preserved until later.

489
Q

frontotemporal dementia features

A

early change in personality, behaviour, change in eating habits, early dysphasia, memory and visuospatial relatively preserved

neurology (6 decks)

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