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BCS Flashcards

1
Q

Drugs that cause issues with hearing - most common?

A

Gentamicin (and other with aminoglycosides), antidepressents, high dose NSAIDs, others

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2
Q

What is considered normal volume?

A

60dB

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3
Q

Myopia

A

nearsightedness, can’t see things that are far away

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4
Q

Hypermetropia

A

Longsightedness, can’t see things that are close up

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5
Q

Astigmatism

A

Astigmatism is a type of refractive error caused by the irregularities in the shape of a person’s cornea. In this condition, the eye fails to focus the light equally on the retina leading to blurred or distorted vision. It can be present at the time of birth, or can develop gradually in life.

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6
Q

REVIEW - What does ophthalmology look at?

A

Eyes, structures around the eyes, vision, eye movements

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7
Q

What is the role of the cornea?

A

It is the major refractive surface of the eye Goal is for light to meet at a point on the back Snell’s law - when light moves between surfaces of different density, the rays bend

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8
Q

What are the layers of tear film?

A

On top of cornea, air to tear journey bends the light

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9
Q

What is the role of the lens? Near or far?

A
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10
Q

Describe the defects that make people near or farsighted? What are the proper names for these conditions? What kind of lenses do they require?

A

Near - myopic

Far - hypermetropic

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11
Q

Define presbyopia

A

long-sightedness caused by loss of elasticity of the lens of the eye, occurring typically in middle and old age.

Weakening of accommodation

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12
Q

How is the pupi innervated? What controls constriction? dilation?

A

Sym - dilates the pupil (arousal / fear, need wider vision), starts in hypothalamus and has long journey

Para - constricts to focus (like for reading), runs along 3rd cranial nerve

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13
Q

Describe the pupil light reflex

A

If you shine light in one eye, both will constrict

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14
Q

Describe th pupil near reflex

A

If you hold something near the nose, pupils get small (miosis), accommodate (flattening of lens) and converge (look towards nose)

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15
Q

Why are pupils clinically important?

A
  • Window into the pre-chiasmal afferent visual pathway (retina and optic nerve)
  • Window into the III nerve function
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16
Q

REVIEW overview on pupils

A
  • •Two separate innervation: symp and parasymp
  • •Symp goes via down the spinal cord, then up the neck, internal CA
  • •Symp dilates pupil – fear and arousal
  • •Parasymp travels from the midbrain with III
  • •Parasymp for light reflex and near reflex
  • •Pupil reflex tested as part of neuro exam
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17
Q

What is the aqueous humour? Where is it produced? What path does it follow? What does it do (3)? What issue can it cause?

A
  • Produced by: ciliary body
  • Fills the anterior chamber of the eye and hydrates the vitreous
  • Supplies oxygen and nutrients to the posterior cornea
  • Maintains intra-ocular pressure and therefore eyeball shape
  • ISSUE: Disorders of drainage cause glaucoma

PATH: •Drains through angle structures (trabecular meshwork, canal of Schlemm)

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18
Q

What is glaucoma? What are the key diagnostic signs? (3) Patient usually presents with what symptoms? What is the main risk factor?

A
  • Disease of the optic nerve/retinal ganglion cells
  • Potentially blinding
  • Symptoms: generally none
  • 3 key signs:
    • Raised intra-ocular pressure
    • Optic disc cupping
    • Visual field loss
  • Main risk factor is AGE
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19
Q

What is normal intraocular pressure? How high can it be in glaucoma?

A

10-21mmHg

In glaucoma can be 25, 30, 35…

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20
Q

Potential treatments for glaucoma

A
  • •Medication (drops)
    • Reduce aqueous production (B blockers)
    • Increase outflow (prostaglandin analogues)
  • Surgery
    • trabeculectomy
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21
Q

What is the most common eye disease worldwide? What is the top eye disease in UK?

A

Cataracts worldwide

In UK< age-related macular degeneration

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22
Q

What is cataracts? WHat are the risk factors? Symptoms? Signs? Treatment

A
  • •Loss of clarity of the lens
  • •Risk factors: age, smoking, diabetes, steroids, Few congenital
  • •Symptoms: blurring, glare, monoc double vision
  • •Signs: reduced acuity, normal fields, normal pupils, dim red reflex, hazy view of fundus

Treatment: suck out lens and put in synthetic

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23
Q

What is the neurotransmittor associated with parkinson’s disease?

A

A drop in dopamine

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24
Q

What is the neurotransmittor associated with psychosis and schizophrenia?

A

Increase in dopamine

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25
Q

What is the neurotransmittor associated with depression?

A

Drop in serotonin (5-HT)

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26
Q

What is the neurotransmittor associated with sedation and anxiety?

A

Increase in GABA

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27
Q

What are criteria for a neurotransmitter? (5)

A
  1. Synthesised in nerves – genes present in nucleus of cell body
  2. Released from nerves – Present in vesicles
  3. Identity of action – stimulate nerves, same effect as applying NT
  4. Receptors for NT – use of agonists, antagonists
  5. Mechanism present to terminate action of NT - uptake transporters and / or enzymes
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28
Q

What are the 3 types of neurotransmitter in the CNS?

A

Amino acids, amines and neuromodulators / neurotrophic agents

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29
Q

Describe the synthesis of glutamate and GABA. What kind of neurotransmitters are they?

A

Amino acid neurotransmitters

Synthesis of Glutamate and GABA are interconnected

Glutamate

  • From glutamine released from glia cells which enters neurones
  • From glucose – via Krebs cycle

GABA

  • From glutamate via glutamic acid decarboxylase
  • (this enzyme is required in GABAergic neurones)
  • So changes in glutamate will also potentially alter GABA
  • Tricky to study and predict effects……
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30
Q

What is glutamate? What kind of receptors does it work at (2)? What is it crucial for? But risks? Example of a drug that interacts with it

A
  • Major excitatory neurotransmitter in CNS
  • Distributed throughout CNS
  • Ligand-gated receptors – AMPA, kainate, NMDA – Na/Ca influx
  • G-protein coupled receptors – mGlu
  • Stimulation of these postsynaptic receptors: activate nerve cells – induce firing
  • Synaptic plasticity – basis for learning/memory
    • High frequency stimulation of nerve cell enhances synaptic activity in that cell lasting for hours, days, weeks – Memory forming?
  • Excitotoxicity – Glutamate is actually toxic to nerves?
    • Needs to be quickly taken up by glia cells
    • Excess release of glutamate, e.g. Stroke, is highly toxic

Huge pharmacological potential, e.g. neurodegeneration

But: potential for huge side effects

Ketamine: non-competitive block at NMDA, used in anaesthesia, recreational

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31
Q

What is GABA? Which receptors do they act at? What drugs act at these receptors?

A
  • GABA is major inhibitory neurotransmitter in CNS
  • Mainly found in interneurones – 30% of all synapses are GABAergic
  • Receptors
    • Ligand-gated receptor-channels complexes – GABA-A (Cl channel)

G-protein coupled receptors – GABA-B (inhibit Ca channels, activate K channels)

  • Drugs that act at GABA-A
    • Benzodiazepines - UP­ channel activity, UP­ GABA effect, used for sedation, anxiety
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32
Q

What is glycine? What receptor does it act at? Which drugs act at this receptor (2)?

A
  • Glycine - important in spinal cord
  • Ligand-gate receptor (Cl channel)
  • Drugs that act at glycine receptors
    • Strychnine – DOWN Cl channel activity, DOWN glycine effect, DOWN inhibitory neurotransmission, muscle spasm, very toxic, asphyxiation
    • Tetanus toxin - DOWN Glycine release, less inhibition, muscle spasms, ‘lock-jaw’
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33
Q

Describe dopamine - why is it important? (in what conditions?) What processes does it contribute to (3)? Which receptors does it act at (2 types)?

A
  • Important neurotransmitter – strong link to– Parkinson’s disease, schizophrenia/psychotic episodes, attention-deficit disorder, drug dependence, endocrine issues
  • Processes
    • Control of pituitary gland - e.g. drop in prolactin
    • Movement
    • Addiction, reward, dependence
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34
Q

How is dopamine synthesised and broken down?

A
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35
Q

Outline the pharmacology in Parkinson’s disease - what are the drugs that may be uased (3) - what are their roles and important side effects?

A
  • Levodopa – oral dose - Precursor to dopamine, used as a dopamine replacement agent
  • Prescribed with peripheral DDC inhibitor
    • Carbidopa (does not cross BBB)
      • Prevent synthesis of dopamine in periphery
      • Diminishes periphery effects
      • Maximises DA synthesis in brain
  • Also, prescribed with COMT inhibitor entacapone
    • Prevent dopamine metabolism
  • 80% of patients improve
    • BUT only 3rd still have improvements after 5 years
  • Important side effects
    • Dyskinesia – involuntary movements
    • Fluctuations in clinical state – good to bad to good – Use of entacapone stabilises DA levels
    • Schizophrenic-like syndromes
    • Nausea, vomiting, anorexia, hypotension
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36
Q

Describe (2) dopamine agonists in addition to levodopa - why would you use them?

A
  • Bromocriptine (D1/D2 selective)
    • Fewer motor adverse effects but not as effective as L-dopa
    • Often 1st drug used
    • Can cause excessive vomiting, sleepiness (somnolence)
  • New drugs – Ropinirole (D2/D3 selective) less side effects
    • But evidence of changes in behaviour patterns
    • Excessive gambling, over-eating, sexual activity
    • Increased reward functions of DA system?
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37
Q

Why would you prescribe Selegiline? Can you use alongside other medications?

A
  • Used in treatment of parkinson’s
  • MAO-B found in CNS not periphery – blocking it does not cause cheese reaction (­ BP)
  • Levodopa and selegiline better than levodopa alone
  • in relieving symptoms and prolonging life
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38
Q

In what cases may you have to use dopamine antagonists? What are their side effects?

A
  • Strong correlation between raised DA levels and schizophrenia, psychotic-like symptoms
  • Typical anti-psychotics - Haliperidol (selective D2 receptor antagonist)
    • Significant side effects
      • Extrapyramidal effects such as:
      • Acute dystonia – involuntary movement, PD-like
      • Akathisia- inner restlessness
      • Tardive dyskinesia – late occurring, irreversible?, pointless random movements, , e.g. Lip-smacking
      • Also: Hyperprolactin secretion (Breast swelling/pain, including men) and weight gain
  • Atypical anti-psychotics, e.g. Olanzapine (D2 and 5-HT2 receptor antagonist)
    • Less EP effects
    • But metabolic issues (weigh gain, diabetes, lipid changes)
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39
Q

What is the role of serotonin (5-ht)? What are it’s functions? Which receptors does it work at (3 types)?

A
  • Important neurotransmitter – strong link to – mood disorders (depression, anxiety)
  • Multiple functions: Behaviour, mood, sleep, feeding
  • 14 5-HT receptors!, 13 GPCRs, 1 ligand-gated
  • Descending pathway: linked to ‘endogenous analgesic pathway’
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40
Q

How is serotonin (5-HT) synthesised and broken down?

A
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41
Q

Describe the common types of serotonin (5-HT) related drugs? (7 types)

A
  • Strong correlation between lowered 5-HT levels and mood (affective) disorders
  • Anti-depressants
    • Selective serotonin reuptake inhibitors, e.g. Fluoxetine
      • Moderate-severe depression, panic disorder, OCD
      • DOWN 5-HT reuptake into pre-synaptic terminals, ­UP synaptic cleft 5-HT levels
      • Safer in overdose
  • Tricyclics, e.g. Amitriptyline
    • Moderate-severe depression, neuropathic pain (at lower doses)
    • 5-HT and neuroadrenaline reuptake inhibitor
  • Other 5-HT acting drugs
    • MAO inhibitors – phenelzine, anti-depressant, cheese reaction, rarely used
    • Sumatriptan – 5-HT1B/D agonist, vasoconstriction, treatment for migraine
    • Buspirone – 5-HT1A agonist, used to treat anxiety
    • Onansetron – 5-HT3 antagonist, anti-emetic agent
    • Atypical anti-psychotics – also block 5-HT2 receptors
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42
Q

Review the parts of the eye responsible for focus (3), image capture (2) and support (3)

A
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43
Q

Desribe the difference between rods and cones - location, optimal light conditions, acuity, colour sensitivity, type of vision, relative number

A
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44
Q

What ions are incolved in response to light in rods/cones? What happens in LOW light conditions?

A

Sodium and Potassium

Sodium rushes in to membrane discs

Potassium leaves inner segment

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45
Q

Describe the process of light transduction - where does it occur? How is it initiated?

A

Photorecetpor cells in retina (membrane discs), sodium cells are moving into cells in the dark (channel stimulated by cycle GMP) - the cell in this state is depolarised and gultamate is being produced and released

When light hits the rhodopsin (made up of retinal and opsin), the retinal changes to trans retinol, and transducin is stimulate - this turns on phosphodiesterase which breaks down the cGMP, stopping sodium influx and glutamate production

LACK of glutamate tells system that there is a light stimulus, and then arrestin moves in to stop the process

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46
Q

What is Retinitis pigmentosa?

A

Retinitis pigmentosa (RP) is a group of rare, genetic disorders that involve a breakdown and loss of cells in the retina — which is the light sensitive tissue that lines the back of the eye. Common symptoms include difficulty seeing at night and a loss of side (peripheral) vision

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47
Q

How rapid can our vision response be? What does this require?

A

We can see a stimulus that is flickering 70 times per second

Requires a high metabolic rate, oxygen and nutrients

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48
Q

What is the role of the peripheral retina? What does this require? Describe the layers of the peripheral retina (5)

A

Photoreceptor outer segments support high resolution sampling of the visual image:

  • For this they need to be packed into a neatly arranged hexagonal array. . .
  • . . . which would be badly disrupted by the presence of a normal capillary bed.
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49
Q

What sits between the photoreceptos and the choroid? What is occurring here?

A

retinal pigment epithelium (RPE)

Transfer of nutrients / waste and 11-cis retinol / all-trans retinol

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50
Q

What happens to the retinal pigment epithelium (RPE) with age?

A

With age RPE tends to become clogged with intracellular debris (“lipofuscin”)

& fatty plaques (“drusen”)

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51
Q

What is the role of the retinal pigment epithelium? (4)

A
  • It holds the retina in place.
  • It acts as the blood-retinal barrier between the outer segments and the choroid.
  • It regenerates 11-cis retinal.
  • It helps to renew the outer segment membranes.

Dysfunction of the RPE is a feature of many retinal diseases

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52
Q

What determines your ability to see the fine detail in an image?

A
  1. precise focus
  2. detailed sampling
  3. small pixels
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53
Q

What happens to an image as it passes through the retina?

A

it blurs

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54
Q

What part of the eye is specialised for high resolution?

A

The centre of the retina, Image is well-focused in the foveal pit

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55
Q

Describe the role of the retinal ganglion cells in changes in illumination?

A
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56
Q

What are on vs off cells?

A
  • “off” cells are excited by decreased illumination of their photoreceptors.
  • “on” cells are excited by increased illumination of their photoreceptors.
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57
Q

What are parcocellular vs magnocellular ganglion cells specialised for?

A
  • “parvocellular” GCs are specialised for high resolution & colour.
  • “magnocellular” GCs are specialised to detect fast moving & low contrast objects.
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58
Q

Describe Parvocellular cells, what they do and what damage to them causes

A
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59
Q

Describe Magnocellular cells, what they do and what damage to them causes

A
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60
Q

Describe the primary visual pathway

A
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61
Q

What do retina and lateral geniculate cells encode? (2) What do primary visual cortical cells encode? (4)

A

Retina and lateral geniculate cells encode:

  • • contrast - i.e. the edges of things
  • • wavelength

Primary visual cortical cells also encode:

  • • orientation of edges
  • • continuity of edges (ie corners etc)
  • • direction of motion
  • • binocular disparity (depth)
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62
Q

Higher visual cortical areas - What do location tasks activate? What about facial recognition tasks?

A
  • Location tasks activate parietal cortex
  • Facial recognition tasks activate ventral occipital & inferior temporal cortex

Parietal areas are associated with control of self-movement, Movement also activates inferior parietal cortex

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63
Q

What do Occipito-temporal lesions produce?

A

Occipito-temporal lesions produce associative agnosia –

“a normal percept stripped of meaning”

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64
Q

What do Occipito-parietal lesions produce?

A

Occipito-parietal lesions produce problems with spatial vision and visuo-spatial co-ordination

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65
Q

What are the 4 type sof primary afferent fibres? What are each for? Which ones carry pain?

A
  • A-alpha nerve fibers carry information related to proprioception (muscle sense).
  • A-beta nerve fibers carry information related to touch.
  • A-delta nerve fibers carry information related to pain and temperature.
  • C-nerve fibers carry information related to pain, temperature and itch.
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66
Q

What are the parts of the outer, middle and inner ear? What nerves enter the ear?

A
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67
Q

Describe he parts of the tympanic membrane

A
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68
Q

What are the three types of earing loss?

A
  • Conductive hearing loss
  • Sensorineural hearing loss
  • Mixed hearing loss
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69
Q

What parts of the ear are implicated in conductive hearing loss? In sensorineural hearing loss?

A

Conductive is outer and middle

SN is inner

70
Q

What are the tuning fork tests you can perform on the ear? What do they tell you? What kind of tuning fork?

A
  • Tuning Fork Tests: Rinne’s and Weber’s test
  • •Bedside test to determine if it is conductive or sensorineural deafness (if you don’t have access to audiometry)
  • •512Hz tuning fork
71
Q

Rinne’s test - what do the potential findings mean?

A

Louder in front or behind? Testing air (front) or bone (behind) conduction

  • •If louder in front i.e. AC > BC =
    • Rinne’s positive = normal or mild/mod SNHL* on that side
  • •If louder behind i.e. AC < BC =
    • Rinne’s negative =
      • conductive hearing loss on that side,
      • or severe/profound SNHL* that side
72
Q

Weber’s test - what do the potential findings mean?

A

Tuning fork on forehead, Ask patient where they hear the sound - ‘Do you hear it loudest in the left, right, or in the centre?’

  • Does not lateralise
    • = normal (or symmetrical mild/mod hearing loss)
  • Lateralises
    • = either conductive hearing loss same side or SNHL other ear
73
Q

What is pure tone audiometry? What does it measure?

A
  • Subjective test
  • Measures the quietest sounds a person can hear at different frequencies (pitch) in each ear separately
  • Results are plotted in a pure tone audiogram
74
Q

What is a pure tone audiogram? What does it show? How do you describe the findings?

A

You can plot the quietst sounds a person can hear at different frequencies - each ear plotted separately

  • •Unilateral / bilateral hearing loss
  • •Bilateral symmetric, asymmetric
  • •Degree of hearing loss:
    • mild, moderate, severe , profound
  • •Type of hearing loss:
    • conductive, sensorineural or mixed
  • •Configuration of hearing loss:
    • flat, downward/upward sloping,
    • u shaped, notched, cookie bite, etc
75
Q

What are the ranges for mild, moderate, devere and profound hearing loss?

A
  • mild (21–40 dB)
  • moderate (41–70 dB)
  • severe (71–95 dB)
  • profound (95 dB).
76
Q

What is tympanometry?

A
  • Tympanometry is an examination used to test the condition of the middle ear and mobility of the eardrum (tympanic membrane) and the conduction bones by creating variations of air pressure in the ear canal.
  • Tympanometry is an objective test of middle-ear function.
77
Q

REVIEW the epidemiology of hearing loss

A
  • •Currently >11 million people in UK have deafness
  • •By 2035 this is estimated to rise to 15.6 million
  • •>900 000 are severely or profoundly deaf
  • •>45 000 deaf children in UK (plus many more who have temporary deafness)
  • •Dual sensory loss (sight and hearing loss) affects ~250 000 in UK
  • •6.7 million could benefit from hearing aids
  • •On average it takes 10 years for people to address their hearing loss
78
Q

Outline the outer, middle, inner and central causes of adult hearing impairment

A

Exostosis, also called osteoma, is a benign growth of new bone on top of existing bone

79
Q

What is presbycusis? Who does it commonly affect? What factors make it more likely? Symptoms? Treatments?

A
  • Common cause of hearing loss, affecting more than half of all adults by age 75.
  • Multiple factors influence the onset and severity, including: genetic predisposition; low socioeconomic status; noise exposure; smoking; hypertension; diabetes; vascular disease
  • Hallmark is progressive, symmetric loss of high-frequency hearing loss over many years.
  • Treatment: hearing aids, hearing tactics
80
Q

REVIEW classes of drugs that cause ototoxicity

A
81
Q

What is a Vestibular Schwannoma (Acoustic Neuroma)? How does it present? How do you diagnose it? How do you manage it?

A
  • •Benign, usually slow growing tumour from an overproduction of Schwann cells.
  • •Annual incidence ~1 per 100 000.
  • •Presentation: asymmetrical hearing loss, tinnitus and dizziness. CN VII symptoms if large.
  • •Diagnosis: MRI of Internal acoustic meatus
  • •Management:
    • –Dependent on size & symptoms
      • •Monitoring – national database
      • •Radiotherapy
      • •Surgery
82
Q

xREVIEW the epidemiology of tinnitus

A
  • •30-40% adults experience tinnitus during their lives (and many children) i.e. ~6 million people
  • •1 in 10 adults have persistent tinnitus of whom ~10% will experience significant impact on life quality i.e. ~600,000 people
  • •2/3 of patients with tinnitus have associated hearing loss
  • •Cause not fully understood
83
Q

REVIEW - History taking of someone with hearing loss - questions to ask

A
  • •Nature – pulsatile? unilateral/bilateral? worse in particular situations?
  • •Associated symptoms? Imbalance, tinnitus, hearing loss, dysacusis, otalgia, stress
  • •Other medical history? Hypertension, infection, head injury
  • •Drug history
  • •Family history?
  • •Occupational or leisure noise exposure?
  • •Recent upset/life event or particularly demanding hearing needs?
84
Q

Examination in adult with hearing loss and/tinnitus

A
  • •Otoscopy
  • •Blood pressure
  • •Consider
    • •Tuning fork tests
    • •Auscultation of ears head and neck if there is pulsatile tinnitus
    • •Cranial nerves
    • •Audiometry
    • •(Referral to audiology)
85
Q

What is tinnitus? How can you manage it?

A
  • Tinnitus is the perception of noise or ringing in the ears. A common problem, tinnitus affects about 15 to 20 percent of people. Tinnitus isn’t a condition itself — it’s a symptom of an underlying condition, such as age-related hearing loss, ear injury or a circulatory system disorder
  • Management:
    • •Investigation where indicated and treatment as indicated
    • •Advice and reassurance
    • •Sound enrichment
    • •Relaxation/Stress reduction techniques
    • •Consider referral to audiology/hearing therapy
    • •Hearing aids
86
Q

What are the common types of hearing aids?

A
  • Behind the ear hearing aids. Behind the ear (BTE) hearing aids are the most common type.
  • Receiver in the ear hearing aids.
  • In the ear hearing aids.
  • In the canal hearing aids.
  • Completely in the canal and invisible in the canal hearing aids.
  • CROS/BiCROS hearing aids.
  • Body worn hearing aids.
87
Q

Describe the process of NT sythesis, movement, breakdown (7 steps) - where are they traveling? What ion is the process dependent on?

A
88
Q

Describe how action potentials are generally generated & ions

A
  1. Neurotransmitter binds to post-synaptic membrane which can open channel to either let sodium or chloride through - if Na+, excitatory post-synaptic potential - enough of this creates an ACTION POTENTIAL
  2. The action potential causes increased membrane permeablity to Na+ (coming in to axon) and K+ (going out of axon) - these two moving causes message to move down axon towards terminal buttons
  3. This process allows Ca2+ channels to open in terminal buttons, signal to vesicles to move to left and release NT
  4. START AT #1 AND GO AGAIN
89
Q

How can drugs affect the propogation of action potentials? What are the principles behind this and what are 3 examples of classes

A

Principle - the movement of Na in and K out allows the message to pass down the axon. If you block the voltage-dependent Na channels, you prevent prevent AP generation and propagation along axon, stop pre-synaptic terminal depolarisation and inhibit synaptic transmission

  1. Local anaesthetics e.g. Lignocaine : Prevent AP conduction and synaptic transmission in sensory nerves – stops inputs to brain that code for pain – no pain sensation
  2. Anti-epileptic e.g. phenytoin : Prevent excess synaptic transmission during high-frequency firing in CNS associated with seizures
  3. Tricyclic anti-depressants e.g. amitriptyline : Used for neuropathic pain
90
Q

What are three classes of drugs that block voltage-dependent Na+ channels and what are their therapeutic purposes?

A
  1. Local anaesthetics e.g. Lignocaine : Prevent AP conduction and synaptic transmission in sensory nerves – stops inputs to brain that code for pain – no pain sensation
  2. Anti-epileptic e.g. phenytoin : Prevent excess synaptic transmission during high-frequency firing in CNS associated with seizures
  3. Tricyclic anti-depressants e.g. amitriptyline : Used for neuropathic pain
91
Q

What is the effect of inhibiting voltage-dependent Ca2+ channels (VDCCs)?

A

The inhibition of VDCCs causes potent block of synaptic transmission (you prevent Ca2+ influx, which prevents release of neurotransmitter, which inhibits synaptic transmission

E.g. Analgesics

92
Q

What is a drug that works to inhibit voltage-dependent calcium channels?

A
  • Analgesics e.g. Ziconotide (Prialt)
  • Synthetic form of w-conotoxin (marine cone snail) potent blocker of VGCCs
  • 100-100x more potent than morphine
  • Prevents synaptic release of transmitters involved in conduction of pain signals
  • Used for severe chronic pain
  • Intrathecal injection (CSF)
93
Q

Describe how acetylcholine is synthesised? Where do you get the components for it? Where does synthesis occur?

A
  • Where you get components from:
    • Choline : From diet (liver, fish) - Taken up by choline carrier at pre-synaptic terminal
    • Acetyl CoA : Produced by cellular respiration
  • Where does synthesis happen?
    • Occurs in NMJ, ganglia, parasym post-ganglionic fibres, CNS
94
Q

What classes of drugs can interrupt the synthesis (1) of acetylcholine?

A
  • SYNTHESIS:
    • ChaT inhibitors (e.g. fa64a) are potentially v dangerous biological weapons
95
Q

What classes of drugs/toxins can interrupt the release (4) of acetylcholine?

A
  • RELEASE:
    • Clostridium botulinum
      • Bacteria produces toxin (highly dangerous, 1kg enough to kill worldwide population) – causes botulism
      • Toxin enters terminals and degrades Ach-containing vesicles
      • ANS and motor fibres are inhibited – paralysis (respiratory collapse)
    • Botox
      • Very low levels of botulinum toxin are used to produce local paralysis (cosmetic, clinical uses)
      • Also, used to prevent excess sweating
    • b-bungarotoxin
      • Snake (Many-banded Krait) venom, prevents Ach release
    • Latrotoxin
      • Black widow spider venom, causes massive release of Ach
96
Q

What classes of drugs/toxins can interrupt the in-activation and re-uptake of acetylcholine? (1, with three types)

A
  • Anti-cholinesterases
    • Enhance / prolong cholinergic transmission
    • Increased parasympathetic actions – bradycardia, bronchoconstriction
    • Increased NMJ actions - muscle twitches, paralysis
  • Classified by duration / mode of action
  • Short acting (Edrophonium) – diagnostic, improves myasthenia gravis
  • Medium acting (neostigmine) – reverse neuromuscular block and atonic states of GI tract/bladder after surgery
  • Long acting (Organophosphorus insecticides, VX agent (Kim Jong-Nam), Sarin) – irreversible, need new AchE synthesis, hence very dangerous due to muscle paralysis, asphyxiation
97
Q

Describe the process if in-activation and re-uptake of Ach

A
  • Released Ach is rapidly in-activated by acetylcholinesterase (AchE) located at the post-synaptic membrane
  • Very important for regulating cholinergic transmission

Ach –> choline + acetate (mediated by acetylcholinesterase)

98
Q

Describe activity and types of Anti-cholinesterases? What process do they interrupt? What kind should you avoid therapeutically?

A
  • Anti-cholinesterases enhance / prolong cholinergic transmission to cause increased parasympathetic actions – bradycardia, bronchoconstriction BUT also increased NMJ actions - muscle twitches, paralysis
  • Classified by duration / mode of action
    • Short acting (Edrophonium) – diagnostic, improves myasthenia gravis
    • Medium acting (neostigmine) – reverse neuromuscular block and atonic states of GI tract/bladder after surgery
    • Long acting (Organophosphorus insecticides, VX agent (Kim Jong-Nam), Sarin) – irreversible, need new AchE synthesis, hence very dangerous due to muscle paralysis, asphyxiation
99
Q

REVIEW drugs that act on cholinergic transmission

A

Consider drugs that action on NIC and MUS receptors generally

100
Q

Describe how adrenaline is synthesised - where? Prcoess and enzymes involved

A

Where: Occurs at sympathetic post-ganglionic fibres, CNS, adrenal medulla

101
Q

Where is noradrenaline stored? In a complex with what? What drug inhibits this storage process?

A

Stored in vesicles in a complex with ATP (ATP is also neurotransmitter at noradrenergic synapses)

  • Reserpine
    • Inhibits vesicular monoamine transporter (VMAT)
    • Reduces ability of vesicles to take-up NA
    • Progressively depletes NA available for release and causes reduction of adrenergic transmission
    • Early treatment for hypertension
102
Q

Which drugs facilitate adrenergic transmission? (three classes) What do each of them do?

A

Facilitation – Indirect Sympathomimetics (­ HR, ­TPR, ­CO, ­BP)

  • Tyramine
    • Dietary constituent (meats, cheeses, chocolate)
    • Enter terminal to displace NA into synaptic cleft
    • Inactivated by monoamine oxidase inhibitors (MAO) in GI tract
    • Can cause marked hypertension in patients treated with MAO inhibitors (MAO-I) for depression – called the ‘cheese effect’
  • Amphetamine
    • Binds to, and reverses action of monoamine uptake transporters causing release of NA into cleft
    • Un-couples NA from vesicles - more NA in cytosol released by transporter
  • Ephedrine
    • Derivative of amphetamine
    • Used as decongestant – vasoconstriction of nasal blood vessels
103
Q

Describe the activity of tyramine? What does it do? What is it inactivated by? But what do you need to watch out for?

A
  • Dietary constituent (meats, cheeses, chocolate)
  • Helps regulate blood pressure
  • Enter terminal to displace NA into synaptic cleft
  • Inactivated by monoamine oxidase inhibitors (MAO) in GI tract (so if these are blocked, there is too much of it)
  • Can cause marked hypertension in patients treated with MAO inhibitors (MAO-I) for depression – called the ‘cheese effect’
104
Q

Which clases fo drugs inhibit adrenergic transmission? One type, two examples of drugs

A

Inhibition – adrenergic neurone blockers (¯BP)

  • Guanethidine
    • Transported by uptake 1 into vesicle
    • Compete with NA for inclusion into vesicles
    • Prevents conversion of impulses into release of NA from vesicle
  • Clonidine
    • Stimulate pre-synaptic a2 receptors
    • Reduces NA release
    • Stimulates a2 receptors in CNS which reduce sympathetic nerve activity
  • These drugs still can be used in UK for hypertensive emergencies when other mediations are ineffective
105
Q

Describe the process of adrenergic in-activation and re-uptake - how does it differ from Ach? What are the two types of carriers? What is it metabolised by and where?

A
  • Different to Ach – not enzymatic
  • Carriers
    • High affinity carrier: Uptake1 (neuronal sites, ANS, CNS)
    • Low affinity carrier: Uptake2 (non-neuronal sites)
  1. NA is terminated by re-uptake unchanged into pre-synaptic terminal
  2. NA is then,
  3. recycled back into vesicles
  4. Metabolised by monoamine oxidase (MAO) in neurones or catechol-O-=methyltransferase (COMT) in non-neuronal sites (e.g. adrenal medulla)
106
Q

What drugs inhibit the in-activation and re-updake of NA? What is the ultimate effect of these drugs?

A
  • The ultimate effect: strengthen the power of NA by not letting it up inactivated/recycled
  • Cocaine / tricyclic anti-depressants (imipramine)
    • Inhibit Uptake1
    • Potentiate adrenergic transmission
  • MAO inhibitor e.g. Moclobemide
    • Potentiate adrenergic transmission
    • Anti-depressant
107
Q

REVIEW drugs acting on adrenergic transmission

A
108
Q

REVIEW Common drugs acting on chemical transmission in the central nervous system

A
109
Q

What are nociceptors? Where do they synapse? Where is their cell body?

A
  • somatosensory primary afferents
  • synapses in the dorsal horn (laminae I, II & V)
  • cell body in the dorsal root ganglion
110
Q

What are the two broad classes on nociceptor? What NTs are associated?

A

A-delta - axon is thin and myelinated, FAST, NT is glutamate, sharp immediate pain

C fibres - axon is thin and myelinated, DELAYED, NTs inclu glutamate and substance P, delayed aching pain

111
Q

Describe the process of activating A-delta and C fibres. What stimulates them and what are the actions/reflexes they cause?

A

FYI Bacteria release chemicals that recruit immune cells and cause inflammation, but also (recent evidence suggests) directly depolarise nociceptors which then release chemicals that recruit immune cells and cause inflammation.

112
Q

Describe the process of sensation and perception? Which ain pathway is involved?

A
  • SENSATION
    • awareness that an event has occurred
  • PERCEPTION
    • what is it?
    • where is it?
    • what does it mean?
    • what should I do

LATERAL PAIN PATHWAY

113
Q

Describe the path of the dorsal column pathways

A
114
Q

Describe the path of the lateral pain pathway

A
115
Q

Describe the subconscious response to pain stimuli. What pain pathway is involved?

A
  • CONTROL OF MOVEMENT
    • proprioceptor and vestibular input to motor pathways
    • nociceptors trigger withdrawal and immobilization of injury
  • AUTONOMIC RESPONSES
    • olfactory input - salivation and gastric motility
    • nociceptors activate sympathetic ANS (flight / fight)
  • EMOTIONAL & BEHAVIOURAL RESPONSES
    • sight/smell of food - feeding behaviour
    • nociceptors trigger a variety of affective, preventative and recuperative responses

MEDIAL PAIN PATHWAY

116
Q

REVIEW pain pathways (two)

A
117
Q

Describe the process of ‘arousal’ in pain - what is the pain pathway involved?

A

DESCENDING PAIN CONTROL

  • MODULATORY PATHWAYS
    • sleep and wakefulness .
    • sensory input can wake a sleeper
    • pain can ruin sleep
  • focusing attention .
    • concentration on one sensory modality can suppress awareness of the others . . .
    • pain disrupts concentration on other modalities
  • switching attention .
    • . . . but a salient stimulus can recapture awareness
    • INJURY (threatened or actual) is a powerfully salient stimulus
118
Q

Describe the descending pain pathway and the neurotransmitters involved

A
119
Q

What is nociceptive vs inflammatory vs

A

Nociceptive pain - “normal” pain due to tissue damage, which stimulates nociceptor nerve endings

Inflammatory pain - inflammation and “central sensitisation” may lead to: hyperalgesia (nociceptor activation becomes more painful) and allodynia (touch becomes painful)

120
Q

What is central sensitisation?

A

“central sensitisation” encompasses a variety of mechanisms that can amplify signalling in the pain pathways, making the response to a given nociceptor input higher and hence the pain sensation stronger. For example, changes in the balance of the descending systems, potentiation of excitatory synapses, loss of inhibition, promoted / maintained by changes in the function of glial cells, microglial activation and release of cytokines.

121
Q
A
122
Q

What is the role of nociceptors in innflammation

A

The respond AND contribute to inflammation

•Neurogenic inflammation is mediated mainly by the release of the neuropeptides calcitonin gene related peptide (CGRP) and substance P from nociceptors, which act directly on vascular endothelial and smooth muscle cells2–5. CGRP produces vasodilation effects2,3, whereas substance P increases capillary permeability, which leads to plasma extravasation and edema4,5, contributing to the rubor, calor and tumor of Celsus. However, besides these, nociceptors release many more neuropeptides (for a database, see http://www.neuropeptides.nl/), including adrenomedullin, neurokinins A and B, vasoactive intestinal peptide, neuropeptide Y and gastrin releasing peptide, as well as other molecular mediators such as glutamate, nitric oxide and cytokines such as eotaxin6.

123
Q

What is pathological pain? (3)

A
  1. pain can result from nociceptor response to pathological conditions (e.g. diabetic neuropathy)
  2. abnormal activity can trigger centrally-mediated hypersensitivity
  3. Abnormal processing in CNS can lead to pain without apparent cause (neurogenic pain)
124
Q

Describe the role of the inhibitory interneurones - normal and pathological

A

It is a descending control system to manage the amount of nociceptor signal being passed up

may become chronically shifted to favour facilitation of activity in the pain pathways (instead of fine balance between pain, touch, etc)

125
Q

What is the role of antidepressents in reducing pain?

A
  1. improving mood and coping ability
  2. ALSO increase transmission in the descending anti-nociceptive pathways
126
Q

What is the role of benzodiazepines in reducing pain?

A
  1. act as anxiolytics (also antipanic or antianxiety agent) is a medication, or other intervention, that inhibits anxiety
  2. ALSO reduce activity in the pain pathways by enhancing spinal cord inhibition
127
Q

What is the role of anticonvulsants in reducing pain?

A
  1. normally used to block high frequency AP firing during seizures
  2. AND reduce transmitter release, specifically at potentiated synapses
128
Q

Outline some of the mechanisms thought to contribute to neurogenic pain (3)

A
  • Inhibitory interneurones start prioritising pain messages
  • Dysfunction of spinal inhibitory systems is seen in models of neuropathic pain
  • Long-term potentiation of excitatory synapses occurs after:
    • High level / persistent activation (eg diabetic neuropathy) OR injury discharges (trauma to nerve)
129
Q

What symptoms may require imaging of the brain?

A
  • •Loss of consciousness
  • •Seizure
  • •Headache
  • •Focal neurological deficit
  • •Psychiatric – hallucination, personality change
  • •Slow neurological development
  • •Cranial nerve palsies
130
Q

What are the uses of plain film? When is it good? When is it not so good?

A
  • •Plain film
    • good bone detail
    • little information about soft tissue/ brain
    • few indications now:
  • foreign bodies (particularly good for metal), facial views,
  • shunt series, skeletal survey
  • •No longer used for head injuries – CT head (NICE guidelines)
131
Q

How does an MRI scanner work?

A
  • •Spinning protons act like little magnets
  • •Strong magnetic field they all align
  • •Apply a radiofrequency pulse to aligned protons and they ‘wobble’ or recess
  • •Remove RF pulse, protons emit RF signal and return to aligned state
132
Q

What are the advantages of MRI?

A
  • •Good soft tissue definition
  • •More sensitive than CT
  • •Better anatomical detail
  • •More information – imaging features help distinguish between different diseases
133
Q

What are the limitations of MRI? (4)

A
  • •Long scan times – 30-90 mins
  • •Movement artefact
  • Claustrophobia, unstable
  • •Ferromagnetic metal equipment and implants
    • cardiac pacemakers
    • metal valves
    • metal foreign bodies
134
Q

What is Diffusion tensor imaging (DTI) - how does it work? what is it used for?

A
  • •Brownian motion of water molecules
  • •Water diffusion/transport along fibres (water moves around so you can see where tracts are)
  • •Normal variation of signal due white matter tract orientation – anisotropy
  • •DTI collects multidirectional diffusion information
  • •Map white matter tracts (tractography)
    • –Tumours
    • –MS, epilepsy, cognitive problems etc
135
Q

What is functional MRI? What does it look at? What is it used for?

A
  • •Image oxygen levels in brain
  • •Increased oxygen levels indicate active areas
  • •Brain mapping –
    • mainly research
    • preoperative assessment
136
Q

What is MR Spectroscopy - how does it work? what is it used for?

A
  • •Non-invasive chemical analysis of brain
  • •Patterns of changes in chemical spectrum occur with certain diseases – eg tumour, demyelination, infection
  • •Problem solving tool, not usually definitive or diagnostic on its own
137
Q

What imaging should you use in head trauma? What are you looking for (primary and secondary objectives)?

A
  • •NICE guidelines - 2007
  • •CT – first line
  • •MRI
  • •Objectives:
    • primary traumatic brain injury
    • secondary ↑ICP, oedema, ischaemia, hydrocephalus

LOOKING FOR ON THE CT:

  • •Haemorrhage
  • •Brain injury – contusion, ischaemia, diffuse axonal injury, assess oedema
  • •Ischaemia – systemic
    • vascular injury - dissection
  • •Fractures

LOOKING FOR ON THE MRI (later stage):

  • •Problem solving tool, not usually used in acute setting
  • •Advantages – more sensitive for parenchymal damage, DAI,
  • •Disadvantages – longer scan times, can’t take equipment into scanner, not as readily available as CT, patients find it more difficult to tolerate
138
Q

What are the 12 cranial nerves and are they motor or sensory?

A

Oh oh oh to touch and feel very good velvet such heaven

Some say marry money but my brother says big brains matter more

I - olfactory (sensory)

II - optic (sensory)

III - oculomotor (motor)

IV - trochlear (motor)

V - trigenminal (both)

VI - Abducens (motor)

VII - Facial (both)

VIII - vestibulocochlear (sensory)

IX - glossopharyngeal (both)

X - vagus (both)

XI - spinal accessory nerve (motor)

XII - hypoglossal (motor)

139
Q

What is the examination of ‘doll’s eye’ movements looking at in comatose patients?

A

examination of cranial nerves 3, 6, and 8, the reflex arc including brainstem nuclei, and overall gross brainstem function

140
Q

What is Cushing’s triad?

A

Hypertension, bradycardia, irregular breathing

physiological nervous system response to acute elevations of intracranial pressure (ICP)

141
Q

What is the CHASVASC score?

A

risk of patient with AF having a stroke

142
Q

What are movement disorders?

A

neurologic syndromes in which there is either:

  1. an excess of movement or,
  2. a paucity of voluntary and automatic movements

unrelated to weakness or spasticity

143
Q

What are the four categories/classes of movement?

A
  • Automatic - learned motor behaviors that are performed without conscious effort
    • walking an accustomed route, and tapping of the fingers when thinking about something else
  • Voluntary - Intentional or externally triggered
    • external stimulus, turning the head toward a loud noise or withdrawing a hand from a hot plate
    • Intentional voluntary movements are preceded by the Bereitschaftspotential (or readiness potential), a slow negative potential recorded over the supplementary motor area and contralateral premotor and motor cortex appearing 1–1.5 seconds prior to the movement. The Bereitschaftspotential does not appear with other movements, including the externally triggered voluntary movements.
  • Semi-voluntary - induced by an inner sensory stimulus
    • Scratching an itch, The restless legs syndrome can be considered semi-voluntary because the movements are usually the result of an action to nullify an unwanted, unpleasant sensation.
    • Semivoluntary movements are suppressible
    • Tics can be semivoluntary.
  • Involuntary – most non-suppressible
    • Tremors and myoclonus
    • Some can be partially suppressible (e.g., some tremors, chorea, dystonia, stereotypies and some tics).
144
Q

What is the most common movement disorder?

A

Restless leg syndrome

(then tourette, then essential tremor)

  • •Prevalence of movement disorders /100,000
  • •Restless legs 9800
  • •Essential tremor 415
  • •Parkinson disease 187
  • •Tourette syndrome 29–1052
  • •Primary torsion dystonia 33
  • •Hemifacial spasm 7.4–14.5
  • •Blepharospasm 13.3
  • •Hereditary ataxia 6
  • •Huntington disease 2–12
  • •Wilson disease 3
  • •Progressive supranuclear palsy 2-6.4
  • •Multiple system atrophy 4.4
145
Q

What is a tremor?

A

•an oscillatory, typically rhythmic and regular, movement that affects one or more body parts

146
Q

What is dystonia?

A

sustained, twisting and frequently repetitive with prolonged abnormal postures. dystonic movements repeatedly involve the same group of muscles – that is, they are patterned.

147
Q

What is chorea?

A

•involuntary, irregular, purposeless, nonrhythmic, abrupt, rapid, unsustained movements that seem to flow from one body part to another.

148
Q

What is myoclonus?

A

•Myoclonic jerks are sudden, brief, shocklike involuntary movements caused by muscular contractions (positive myoclonus) or inhibitions (negative myoclonus – e.g asterixis seen in hepatic disease)

149
Q

What are tics?

A

•abrupt sudden isolated movements. Tics consist of abnormal movements (motor tics) or abnormal sounds (phonic tics).

150
Q

What are the 4 types of causes of parkinsonism? And examples of each type

A
  • PD is the commonest cause of parkinsonism and is “primary”
  • Primary – Parkinson’s Disease
  • Secondary - Drug induced
  • Parkinsonism-plus syndromes – Multiple System Atrophy / Progressive Supranuclear Palsy / Corticobasal Degeneration
  • Heredo-degenerative disorders – Spinocerebellar Ataxia / Wilsons Disease (excess copper) etc.
151
Q

What are the main symptoms associated with parkinsonism

A
  • Tremor
    • •Pill rolling tremor
    • •Tremor at rest
  • Rigidity
  • Akinesia / bradykinesia / hypokinesia
  • Posture - Loss of postural reflexes
    • Flexed posture of neck, trunk and limbs
  • Dementia

TRAPD

152
Q

Review genes associated with Parkinson’s - which one is most commonly associated?

A
  • SNCA – rare – usually families with multiple affected individuals
  • LRRK2 – 5-15% of apparently familial PD, 1-3% of sporadic PD (esp. Ashkenazi and North African Arab and Basque region) variable penetrance
  • PARKIN (PARK2) – AR – 50% of young onset with recessive FHx will have mutn - ~15% of those<45 with sporadic disease
  • PINK1 and DJ-1 more uncommon
153
Q

What does a positive pronator drift test mean?

A

If a forearm pronates, with or without downward motion, then the person is said to have pronator drift on that side reflecting a contralateral pyramidal tract lesion. In the presence of an upper motor neuron lesion, the supinator muscles in the upper limb are weaker than the pronator muscles, and as a result, the arm drifts downward and the palm turns toward the floor. A lesion in the ipsilateral cerebellum or ipsilateral dorsal column usually produces a drift upward, along with slow pronation of the wrist and elbow.

154
Q

Is it damage to the cerebellum or basal ganglia? How can you tell from movement?

A

vCerebellum: Movements jerky, uncoordinated and inaccurate (ataxia)

vBasal ganglia: Uncontrolled movements at rest, e.g. Parkinson’s, Huntington’s, Hemiballism

155
Q

Define bradykinesia

How do we test it?

A

Bradykinesia - slower movements AND often slower (less amplitude)

Repetitive movements on each side

156
Q

What is delirium? (5) Why is it dangerous? (5)

A
  1. Disturbance in attention and awareness
  2. Develops over a short period of time
  3. Disturbance in cognition
  4. 1&3 are not explained by pre-existing neuro / cognitive disorder
  5. Evidence that it is a physiological consequence of something (but not neuro - see above)
  • –High mortality
    • •Patients with delirium in ED have 70% increased risk of death in next 6 months
    • •Patients with delirium on medical/geriatric wards have 50% increased risk of death in next year
  • –Risk of institutionalisation
  • –Medical complications
  • –Increased length of stay
  • –Increased risk of dementia
157
Q

What are the features of delerium? (4 categories)

A
  • •Cognitive function:
    • –worsened concentration, slow responses, confusion
  • •Perception:
    • –visual or auditory hallucinations
  • •Physical function:
    • –reduced mobility, reduced movement, restlessness, agitation, changes in appetite, sleep disturbance
  • •Social behaviour:
    • –lack of cooperation with reasonable requests, withdrawal, or alterations in communication, mood and/or attitude
158
Q

How can patients present with delirium? How long does it last?

A
  • •Patients may just present with acute cognitive impairment
  • •But drowsiness to the point that the patient is not speaking, severe agitation, or psychotic features such as hallucinations or delusions may be the most prominent features
  • •Can be described using hyperactive, hypoactive or mixed labels depending on the level of arousal
  • •Most delirium has a duration of a small number of days, but in around 20% of cases, it can persist for weeks or months
159
Q

Wht are the risk and precipitating factors for delirium? (11)

A
  • •Age > 70
  • •Physical frailty
  • •Severe illness
  • •Dementia (increases risk 5x)
  • •Visual/hearing impairment
  • •Polypharmacy (sedatives, analgesics, tricyclics, steroids)
  • •Urinary catheterisation
  • •Alcohol excess
  • •Renal impairment, other metabolic derangements
  • •Admission with infection, dehydration, hip #
  • •Surgery
160
Q

What can cause delirium? (6)

A
  • •Head injury
  • •Stroke
  • •Subdural or extradural haematoma
  • •Seizures, post-ictal confusion
  • •Brain tumour or abscess
  • •Viral or auto-immune encephalitis
161
Q

Outline some possible physiological mechanisms of delirium

A
  • •Drugs, hypercortisolism, electrolyte disturbance, hypoxia, impaired glucose oxidation
  • •Sepsis releases inflammatory cytokines (IL-6, IL-8), leading to brain inflammation, impaired blood flow, and neuronal apoptosis
  • •Neuroinflammation causes microglial over-activation, resulting in neurotoxic response and neuronal injury
  • •Peripheral inflammation can activate CNS via several routes including vagal afferents, pro-inflammatory cytokines, endothelial activation with bbb disruption, microglial over-activation
  • •Increased CSF IL-8, S100b
  • •Loss of cerebral autoregulation
  • •Increased brain dopamine
  • •Decreased brain acetylcholine
162
Q

Outline the DDX for delirium (5)

A
  • •Non-acute cognitive dysfunction e.g. Dementia, Learning Disability
  • •Cognitive fluctuations of Dementia with Lewy bodies
  • •Psychiatric illness
    • –Depression, Mania, Psychosis
  • •Dissociative disorder/Factitious disorder
  • •Normal mentation but inability to communicate
    • –e.g. dysphasia secondary to stroke
163
Q

Outline the clinical assessment of mental state in delirium (6)

A
  • •Assessment of conscious level
    • –Ensure patient is not in coma
  • •Rousable but alertness is altered and fluctuating
    • –Be aware of hypo- and hyper-active forms
  • •Impaired attention
    • –Observe for distractibility
    • –Test digit span, months of the year
  • •Disorientation in time, place, person
  • •“Disorganised thinking”
    • –Ask patient why they’re in hospital
  • •Other cognitive tests as needed
164
Q

Outlined the simplified way to assess whether patients are delirous? What is the scoring method?

A

4AT

Weight is on alertness and acuteness

165
Q

How do you manage delirium? What do you need to rule out first?

A
  • •First consider acute, life-threatening causes of delirium, including low oxygen level, low blood pressure, low glucose level, and drug intoxication or withdrawal
  • •Systematically identify and treat potential causes (medications, acute illness, etc), noting that multiple causes are common
  • •Optimise physiology, management of concurrent conditions, environment (reduce noise), medications, and natural sleep, to promote brain recovery
  • •Communicate the diagnosis to patients and carers, encourage involvement of carers and provide ongoing engagement and support.
  • •Aim to prevent complications of delirium such as immobility, falls, pressure sores, dehydration, malnourishment, isolation.
  • •Monitor for recovery and consider specialist referral if not recovering.
  • •Promote cognitive engagement, mobilisation, and other rehabilitation strategies
  • •Specifically detect, assess causes of, and treat agitation and/or distress, using nonpharmacological means only if possible
166
Q

Outline the investigations in suspected delirium - what is normal and what are the exceptions?

A
  • •No diagnostic changes on CT or MRI
  • •Blocks access to scanner for urgent patients
  • •CT brain scan should not be used routinely but should be considered in the presence of:
    • –new focal neurological signs
    • –reduced level of consciousness (not adequately explained by another cause)
    • –history of recent falls
    • –head injury (patients of any age)
    • –anticoagulation therapy
  • •If delirium does not resolve rapidly, brain imaging might have a role in:
    • –Ruling out a “missed” neurological illness e.g. subdural haematoma
    • –Providing information on brain health e.g. presence of brain atrophy or vascular disease
167
Q

How could you prevent delirium? (9)

A
  • •Orientation and ensuring patients have their glasses and hearing aids
  • •Promoting sleep hygiene
  • •Early mobilisation
  • •Pain control
    • Appropriate use of anesthesia (local instead of general if possible)
  • •Prevention, early identification and treatment of postoperative complications
  • •Maintaining optimal hydration and nutrition
  • •Regulation of bladder and bowel function
  • •Provision of supplementary oxygen, if appropriate.
  • •Medication review by an experienced healthcare professional
168
Q

What are the long term consequences of delirium?

A

Dementia (new cases or worsening), functional worsening, motality

169
Q

Outline the relationship between delirium and dementia

A

They appear to go together -

  • •Delirium fundamentally alters trajectory of AD
    • –2-fold acceleration in rate of decline in the year following hospitalisation, effects persist at 5 years
  • •Most older people with delirium triggered by a relatively trivial insult either
    • –Have underlying dementia
    • –Or will develop it within 5 years
  • •Doesn’t mean that delirium initiates dementia
    • –Pathological changes of AD start >10 years prior to clinical onset
170
Q

Outline the theory of delirium as a form of brain injury

A
  • –Accelerates the neurodegenerative or vascular processes leading to dementia
  • –Mechanism is unknown
  • –Not obviously related to acceleration in Alzheimer, alpha-synuclein or vascular pathology
  • –Reduces brain reserve through neurotoxic or neurotransmitter-mediated brain injury?
171
Q

Describe the difference between onset, course, conscious level, deficits, hallucinations, delusions and psychomotor activity is DELIRIUM VS DEMENTIA

A

Life Control (1 decks)

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