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Elderly Care > Elderly Care > Flashcards

Elderly Care Flashcards

1
Q

what type of lesion in occurs in MS

A

typically, a plaque of demyelination in the CNS or optic nerve

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2
Q

why does MS lead to loss of conduction through a nerve

A

loss of myelin sheath means inefficient/loss of saltatory conduction therefore neurotransmission is duly impaired to the size of the lesion

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3
Q

how does the MS lesion present itself clinically

A

evolves over a few days, and last for a few weeks or days, and gradually settles. vision in one eye may deteriorate if the optic nerve is affected, or there is weakness in limb

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4
Q

what does the nature of the neurological deficit in MS depend on

A

site of the plaque of demyelination

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5
Q

what are the two classifications for dissemination of MS

A

dissemination in time and place

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6
Q

what is the clinical presentation of MS if it affects the optic nerve

A 
optic neuritis. 
reduced acuity, blurring
most commonly central vision
colour vision and density faded
the optic disk may be red and swollen, with exudates and haemorrhages
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7
Q

how many weeks doe sit usually take for vision to recover in MS episode

A

4-8weeks

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8
Q

what are the clinical presentations of MS if it affects the midbrain, pons, medulla

A
  • cranial nerve dysfunction
  • cerebellar dysfunction e.g. nystagmua, ataxia
  • motor deficits for UMN in any of the four limbs
  • sensory deficits, spinothalamic or post column in type in any of four limbs
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9
Q

what are the clinical presentations of MS if it affects the spine

A

symptoms of tracts, UMN, autonomic in spine - below the level of the lesion.

  • heaviness/dragging weakness
  • loss of pain and temp sensation
  • tingling/numbness/in arms/legs
  • clumsiness of hand
  • bladder/bowel/sexual dysfunction
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10
Q

what are the accumulated ongoing neurological deficits in a patient who has had MS for a long time?

A
  • asymmetric optic pallor, w/o major deficit in visual acuity
  • cerebellar deficit causing nystagmus, dysarthria and arm ataxia
  • UMN deficit mild in arms, mod in trunk, sev in legs
  • impaired sexual/bladder/bowel dysfunction
  • sensory loss most evident in trunk and lower limbs
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11
Q

where does MS have more evident effects - arms or legs

A

legs (more distal?)

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12
Q

how is MS diagnosed

A
  • MR brain reveals multiple lesions
  • neurophysiology - measure CNS nerve conduction
  • inflammatory nature of demyelinating lesion may lead to increased lymphocyte and globulin content in CSF
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13
Q

what is the management for mild/early MS?

A
  • inform family and patient of diagnosis and education
  • encourage normal attitudes to life, activities
  • counselling
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14
Q

what is the management of more serious cases of MS

A
  • continued education and support
  • attention to vision, cerebellar deficit, pain (gabapentin/anitryptylline), paraplegia, fatigue
  • MDT
  • respite care arrangements if required
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15
Q

what is the management ( inc pharmacological ) in all cases of MS

A

1) immunomodulatory drugs
2) high dose IV cotricosteroids (usually methylprednisolone) over 3 days reducing individual episodes
3) avoid obesity and sedentary lifestyle

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16
Q

list some of the immunomodulatory drugs used in the treatment of MS

A 
azathioprine
B-interferon
copaxone
mitoxantrone
natalizumab
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17
Q

what are the DIS and DIT MS criteria

A

at least 2 episodes of symtpoms

  • occur at different points in time
  • result from involvement of different areas of the CNS
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18
Q

what are the typical scan feature of MS lesions in the CNS

A

oval, well defined, enhancement
3-6mm
ring or semi-ring

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19
Q

what are the two main types of stroke

A

ischaemic and haemorrhagic

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20
Q

what is the usual cause of a cerebellar infarct

A

emblous from carotid artery atheromatous plaque, but can come from anywehre between aorta and cerebral artery itself.
beware can come from dissecting carotid/vertebral a

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21
Q

patients with which conditions usually get stroke from small vessels disease

A

those with HTN or diabetes

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22
Q

list some of the cardiac diseases associated with tia/stroke

A
  • af
  • mural thrombosis after mi
  • aortic or mitral valve disease
  • bacterial endocarditis
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23
Q

what is the likely pattern of symptoms in MCA ischaemia?

A
  • loss of contralat face/arm use
  • loss of contralat face/arm sensation
  • dysphasia
  • dyslexia, dysgraphia, dyscalculia
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24
Q

what is the likely pattern of symptoms in ACA ischaemia?

A
  • loss of use or feeling/use in contralat leg
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25
Q

what is the likely pattern of symptoms in PCA ischaemia?

A
  • contralateral homonymous hemionopia
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26
Q

what is the likely pattern of symptoms in opthalmic artery occlusion (from MCA)

A

monocular loss of vision

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27
Q

what is the likely pattern of symptoms in vertebrobasilar artery occlusion

A
  • double vision
  • facial numbness
  • facial weakness
  • vertigo
  • dysphagia
    (CN lesions)
  • dysarthria
  • ataxia
  • loss of feeling in both of arms/legs
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28
Q

what type of vessels usually occlude to cause a lacunar stroke?

A

small vessels

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29
Q

what is the likely pattern of symptoms in lacunar stroke?

A
  • pure loss of use of contralat arm and leg

- pure loss of sensation of contralat arm and leg

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30
Q

what must be excluded before you give thrombolysis to a patient with stroke?

A

haemorrhagic stroke

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31
Q

how are patients assessed and looked after when they come into a&e with suspected stroke?

A
  • rap on call team assess
  • determined if they are having a stroke therefore if they need a ct
  • stroke unit
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32
Q

what is the importance of the SALT team in patients with stroke

A
  • assess patient’s swallowing to determine need for NBM/NGT if they are at risk from aspiration pneumonia
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33
Q

which other mdt professionals are involved in looking after patients with stroke, apart from doctors and nurses

A

early involvement of - pt/ot/salt

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34
Q

what meds should be given to a patient with stroke/tia to prevent furhter strokes and manage cardiovascular risk?

A

aspirin

statin

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35
Q

what is needed to be arranged for the patient after they leave hospital with a stroke?

A

further care and rehabilitation
community liaison e.g nurses
physical and psychological support

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36
Q

what investigations should be done in the patient’s bloods when they present with stroke

A

fbc/u&e/esr

lipids and blood glucose

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37
Q

what investigations apart from bloods should be done on patients presenting with stroke

A
  • ecg
  • cxr
  • echo
  • Carotid USS
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38
Q

why is it important to do a CUSS in a patient who presents with stroke

A

-investigate the patient as they may still benefit from carotid endarterectomy

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39
Q

what is usually the origin of SAH?

A

berry aneurysm, usually from circle of willis

sometimes rarely av malformations

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40
Q

what is the usual presentation of a SAH

A

sudden onset thundercalp, very severe, headache
sudden rise in icp can cause haedache, vomiting, reduced consciousness and eventually papilloedema
often brief loc with initial bleed

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41
Q

what may be the presentation of a patient who has an intracranial bleed into the region of the internal capsule

A

severe motor/sensory/visual problems in contralat side of the body

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42
Q

what is the management of SAH

A
  • CT scan confirmation
  • CCB
  • manage HTN (not over-vigorously)
  • neurosurgery (clips/embolism/packing)
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43
Q

what is the most reliable way to prevent SAH’s

A

keep BP under control

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44
Q

what should be avoided in a patient with haemorrhagic stroke?

A

thrombolysis should be AVOIDED!

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45
Q

how do people with olfactory nerve dysfunction present?

A

loss of sense of smell

inability to taste different foods

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46
Q

list some of the cause of monocular blindness

A
  • prodrome of migraine
  • thromboembolism of opthalmic artery (from ICA) - curtain like
  • infarction of optic nerve or retina
  • GCA
  • optic neuritis as part of MS
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47
Q

what is the usual cause of bitemporal hemionopia

A

optic chiasm compression by pituitary adenoma growing upwards from sella tursica/pituitary fossa

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48
Q

what are some of the causes of homonymous hemionopia

A
  • POCS
  • infarct/haematoma in internal capsule
  • lesions
  • abscesses
  • tumurs affecting optic radiations
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49
Q

which condition is often the cause of visual inattention/neglect

A

stroke

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50
Q

which muscles does myasthenia gravis often affect in the upper body

A

ocular

bulbar

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51
Q

what is the effect of grave’s disease on ocular muscles

A

inflammatory swelling o the external ocular muscles within the orbit eventually leads to fibrosis - proptosis, lid retraction, lid lag

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52
Q

what is bulbar palsy and how does it present?

A

bilateral impairment of CN IX, X and XII causing:

  • dysarthria
  • dysphagia
  • dysphonia and poor cough (vocal cords)
  • susceptibility to aspiration pneumonia
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53
Q

list some of the ways in which the recurrent laryngeal nerve can become damaged

A
  • aortic aneurysm
  • tumours (esp in mediastinum)
  • malignant nodes
  • surgery
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54
Q

what is the difference between dysphasia and dysarthria

A

dysarthria is purely mechanical, whereas dysphasia is an impairment in language

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55
Q

what is the characteristic speech in patients with cerebellar dysfunction?

A

scanning/staccato dysarthria

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56
Q

where do the spinal nerves exit the spinal column

A

intervertebral foramina

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57
Q

which anatomical structures herniate to cause prolapse disc

A

nucleus pulposus protrudes through annulus fibrosus of the intervertebral disc to cause disc prolapse

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58
Q

how does herpes zoster of nerve roots present

A

painful vesicular eruption of shingles in demraome distrbution.

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59
Q

what is post herpetic neuralgia

A

pain that follows herpes zoster of nerve roots, even after the rash has disappeared

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60
Q

what may be given to immunocompromised patients who have herpes zoster of nerve roots

A

systemic aciclovir

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61
Q

what is MND

A

selective loss of lower motor neurones from the pons, medulla and spinal cord, together with loss of UMNs from the motor cortex of the brain

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62
Q

which functions are left intact in MND

A

special senses, cerebellar, sensory and autonomic functions are left intact

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63
Q

how may MND first present

A

as problem in the bulbar muscles or limbs, tends to be either UMN or LMN in nature

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64
Q

list the key features of MND

A
  • muscle weakness
  • muscle wasting
  • muscle fasciculation
  • exaggerated reflexes
  • no loss of sensation
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65
Q

what does a limb look like on examination of a patient with MND

A
  • weak, wasted, fasciculating

- deep tendon reflexes very brisk

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66
Q

is there sensory loss in MND?

A

no

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67
Q

what are most deaths in MND caused by?

A

Inanition (exhaustion by lack of nourishment) and chest infections due to involvement of bulbar and respiratory muscles account for most deaths

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68
Q

what is Amyotrophic Lateral Sclerosis (ALS)

A

specific disease that causes death of neurones which control voluntary muscles
a.k.a MND

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69
Q

how does bulbar palsy present in patients with MND

A
  • weakness/wasting

- fasciculation of lower facial muscles and muscles moving in the palate, pharynx, larynx and tongue

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70
Q

how does MND affect muscles of the limb (s+s)

A
  • progressive muscle atrophy
  • weakness, wasting and fasciculation of any of the limbs or trunk muscles
  • muscle cramps
  • small muscles of hand involved
  • ALS
  • spasticity, clonus
  • increased deep tendon reflexes
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71
Q

what is riluzole used to treat and how does it work?

A

MND - glutamate antagonist which blocks a specific channel associated with damaged neurones to slow the progression and prolong survival from MND

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72
Q

give the ways in which MND can be managed

A
  • physio and drugs for cramps (e.g. quining)
  • drooling - hyoscine hydrobromide, glycopyrolate
  • depression management
  • stiffness - baclofen
  • speech therapy, dietetic review
  • PEG feeding
  • portable NIV
  • aids around house e.g. lift, wheelchair, ramp etc
  • nursing help and respite care
  • discussion re end of life care
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73
Q

what are the common causes of peripheral neuropathy

A

commonest - alcohol and diabetes mellitus
vitamin deficiency
leprosy is rare cause

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74
Q

how does diabetic neuropathy present

A

predominantly sensory neuropathy
painful weakness and wasting
autonomic ns involvement causes postural hypotension, impaired bladder/bowel/sexual dysfunction, loss of normal sweating

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75
Q

what is charcot marie tooth

A

hereditary condition where there are LMN signs in feet, legs and small muscles of the hand - distal weakness and wasting
due to demyelination and remyelination of peripheral nerves

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76
Q

what is the presentation of Guillain Barre syndrome

A 
peripheral neuropathy (affects nerve roots and peripheries) which evolves rapidly over days and produce severe weakness, paralysis and sensory loss. this worsens day by day until 1-2 weeks, then stops advancing.
commonly occurs 1-2 weeks after infection e.g. campylobacter enteritis
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77
Q

why does a patient with GBS need to be hospitalised until the disease has run its course

A

chest and bulbar involvement may require ventilation and NGT to prevent death

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78
Q

are steroids of any benefit in GBS

A

no - if needed, may manage with IV Immunoglobulin transfusion or plasma exchange to prevent deterioration

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79
Q

what is the pathology behind GBS

A

thought to be inflammatory/autoimmune - there is demyelination of peripheral nerves (including nerve roots too). Is a peripheral neuropathy

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80
Q

what would be found in LP investigations of a patient with GBS

A

increased protein in CSF

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81
Q

what are the common causes of death in a patient with GBS

A
  • aspiration pneumonia
  • DVT/PE
  • cardiac arrhythmia (autonomic involvement of neurones)
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82
Q

what is Myasthenia Gravis

A

disease that results from impaired neurotransmission neuromuscular synapse - caused by autoantibody whcih attacks ACh receptors on post synaptic membrane

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83
Q

is myasthenia gravis more common in men or women

A

women

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84
Q

list the s + s of myasthenia gravis

A

muscle weakness and fatiguability which improves after rest, and is usually worse at the end of the day/ after repetitive use of muscle.

  • extraocular involvement causes double vision and ptosis
  • bulbar involvement causes dysphagia and dysarthria
  • proximal limb weakness - difficulty in lifting arms, standing up etc
  • trunk - breathing problems and difficulty sitting from lying position
  • distal limb weakness - weak hand grip, ankle and foot weakness
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85
Q

list the tests you would do to confirm diagnosis of myasthenia gravis

A
  • tensilon test - anticholinesterase should produce sudden elevation of weakness
  • detection of serum ACh-R antibodies
  • EMG studies
  • chest radiography/CT for enlargement of thymus identified (uncertain cause why this is assoicated with myasthenia)
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86
Q

list the management options for myasthenia gravis

A
  • oral anticholinesterase drugs e.g. prostigmine and pyridostigmine
  • immunosuppression by prednisolone or azathioprine for those not sufficiently managed on anticholinesterases alone
  • thymectomy
  • plasma exchange to remove circulating antibodies
  • hospital admission for myasthenic/cholinergic crisis
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87
Q

what is the inheritance pattern of DMD

A

X linked recessive

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88
Q

how do patients with DMD present

A

usually <5 yo, gower’s sign, muscle weakness, pseudohypertrophy of calf muscles

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89
Q

what do patients with DMD die of

A

profound muscle weakness - predisposes to chest infections, associated cardiomyopathy,

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90
Q

what is found of serology tests of patients with DMD

A

elevated CK

genetic testing for dystrophin gene

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91
Q

what is myotonic dystrophy

A

inherited condition where there are dystrophic changes in muscle, associated with myotonic contraction

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92
Q

how does myotonic dystrophy present

A

difficulty in rapidly relaxing tightly contracted muscle
muscle contracts when hit by tendon hammer/ percussion
(associated cardiomyopathy)

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93
Q

what are polymyositis and dermatomyositis

A

autoimmune conditions where there is inflammatory cell infiltration into muscle and muscle fibre necrosis.
however, in dermatomyositis, there is additional involvement of skin - especially face and hands
(managed by immunosuppression)

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94
Q

list some of the ways in which the data from death certificates is used in public health

A
  • monitor health of population
  • public health interventions
  • health services
  • medical research
  • international comparisons of health and healthcare services
  • monitor quality of clinical care in clinical governance programmes
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95
Q

describe death certification in terms of foetal age

A

<24 wks - non viable foetus, no certification

>24 wks - still birth certificate

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96
Q

does the doctor have to be present at the time of death or see the body after death in order to be able to fill out a death certificate?

A

no to both (has to have seen patient within 14days of death however)

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97
Q

what are the different sections on the “cause of death” section on the death certificate of a patient

A

1 a) disease leading directly to death
1 b) other disease or condition (if any) leading to 1a)
1 c) other disease or condition (if any) leading to 1c)
2) other significant conditions, contributing to the death but NOT relating to the disease/condition leading to death

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98
Q

can old age be used as a cause of death on death certificates?

A

only if no other cause is found

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99
Q

list some unacceptable terms to avoid in death certificates

A 
asphyxia
arrhytmia
cachexia
cardiac arrest
coma
debility
exhaustion
HF
Liver/renal failure
respiratory arrest
shock syncope
uraemia
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100
Q

what are the rules for describing cancers when filling out death certificates

A 
histopathology of tumour
benign or malignant
anatomical site
primary or secondary
date of previous removal if any
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101
Q

list some of the cases you must report to a coroner when dealing with death and death certificates

A

1) no doctor has treated the deceased within the last 24hours
2) when doctor attending patient didn’t see him or her within the last 14 days before death or after death
3) when death occurred during operation
4) death sudden/unexplained/suspicious
5) due to industrial injury or disease
6) due to accident/violence/neglect/abortion/any kind of poisoning
7) occurred in prison or in police custody or under section of MHA

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102
Q

what drug is given to treat focal epilepsy

A

carbamazepine

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103
Q

which drug is very teratogenic

A

child bearing

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104
Q

what is epilepsy

A

the tendency to suffer from seizures

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105
Q

what are the two main types of epilepsy

A

generalised and focal

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106
Q

what is the difference between generalised and focal seizures

A 
generalised = electrical discharges start in deep midline structures of the brain and spread rapidly and simultaneously to all parts of the brain - affecting the whole brain
focal = electrical discharges start in one part of the cerebral cortex and dont spread to both hemispheres
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107
Q

what is a complex partial seizures

A

seizure starts off as focal but spread to all of the cerebral cortex, resulting in generalised seizure

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108
Q

list the types of generalised seizure

A
  • primary generalised tonic-clonic
  • absence
  • myoclonic
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109
Q

list the different phases in a primary tonic-clonic seizure with a brief description

A

1) tonic phase - LOC and sudden muscle stiffening, limb and neck extension, cyanosis
2) clonic phase - sustained muscle contraction and a series of disorganised jerks and jitters. jaw closes, causing tongue biting, breathing disorganised
3) coma phase - after convulsive movements - breathing becomes regular and regular, colour returns to normal
4) postictal phase - state of confusion, headache, restlessness, drowsiness before final recovery. limb pain, sore tongue

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110
Q

how do absence seizures present

A

sudden onset and offset, does not usually last more than 10 seconds
few moments pass when patient notices they’ve been unaware of what has happened - suddenly stop what they’re doing, with eyes open and staring blankly. may be rhythmic movements of eyelids
remains standing or sitting
no response to any stimuli

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111
Q

is there usually an aura assoc with generalised otnic clonic seizure

A

no -aura is usually for partial

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112
Q

what is a myoclonic seizure

A

take form abrupt muscle jerks, typically causing upper limbs to flex
patient drops anything they are holding
jerks may occur singly or in brief run
consciousness not usually affected
(often coexists with tonic clonic or absence seizures)

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113
Q

how does focal epilepsy present

A

depends on the part of the brain where the electrical discharge is coming from - can be focal motor, sensory, frontal lobe, temporal etc.

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114
Q

how does frontal lobe partial seizure present

A

strong convulsive turning of eyes, head and neck towards contralat side; or complex posturing with one arm flexed and the other extended

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115
Q

list some of the subjective symptoms in temporal lobe seizures

A
  • de ja vu
  • memories rushing through brain
  • loss of memory during attack
  • hallucination of smell/taste
  • sensation rising in body
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116
Q

list some of the objective symptoms in temporal lobe seizures

A
  • diminished contact with environment
  • slow, confused
  • lip smacking and sniffing movements
  • repetitive utterances/movements
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117
Q

what are febrile convulsions

A

tonic clonic transient attacks occurring at time of febrile illness in children - especially common in <5years

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118
Q

what is the prognosis for children who have a febrile convulsion

A

usually very good - a very small percentage of children with febrile convulsions then go on to suffer from epileptic attacks later in life - and these children ususlly have other factors such as FHx, abnormal neuro signs etc.

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119
Q

what is juvenile myoclonic epilepsy

A

tonic clonic seizures starting in teenagers - primarily generalised, and may not continue into adult yeats

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120
Q

what is status epilepticus

A

occurence of tonic clonic seizures without recovery in between episodes, or one that lasts >30 mins

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121
Q

what are the steps in managing status epilepticus

A

1) diazepam PR/buccal midazolam –> repeat in 15 mins
2) lorazepam IV bolus
3) phenytoin infusion
4) refractory status - anaesthetic - propofol/midazolam/thiopental etc.

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122
Q

think of some secondary causes for epilepsy

A
  • brith trauma to brain
  • trauma to skull and brain
  • meningitis, encephalitis, brain abscess
  • infarct/haemorrhage/sah
  • trauma/neurosurgery
  • alcohol/drug withdrawal
  • hepatic/uraemic
  • hypo
  • tranquilisers/antidepressants
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123
Q

list some of the restrictions that must be advised in the daily life of a patient with epilepsy

A
  • awareness of bathing/driving/riding/bicycle/heights/water sports
  • refrain from driving for 1 year
  • avoid flashing lights if photosensitive epilepsy
  • occupations e.g. HGV or police that are impossible career paths
  • other jobs such as working with machinery, nursing, children that may be more difficult if epilepsy is uncontrolled
  • pregnancy and teratogenecity counselling in women of child bearing age
  • psych factors and support groups
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124
Q

when is surgical treatment used in epilepsy

A

last line in intractable cases

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125
Q

define delirium

A

global impairment fo cognitive function, with disturbances of attention and conscious level. abnormal psychomotor, behaviour and affect, disturbed sleep-wake cycle

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126
Q

what is the pattern of symptoms in delirium

A

fluctuating symptoms, typically worse at night

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127
Q

list some of the risk factors for delirium

A
  • age extremes
  • pre-existing dementia
  • fracture (esp hip)
  • certain prescribed drugs
  • recreational drug intoxication and wtihdrawal
  • sensory impairment
  • surgery
  • sleep deprivation
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128
Q

list some of the drugs that are high risks for delirium

A
  • psychogenic drugs e.g. antidepressants, antipsychotics, bzd’s
  • antiparkinsonian drugs
  • opiates
  • diuretics
  • anticholinergic drugs
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129
Q

list the different sections of the AMT

A

1) age
2) time to nearest hr
3) address for recall e.g. 43 west st
4) year
5) name of hospital
6) recognise two persons e.g. nurse, doc
7) DOB
8) year of WW1/WW2
9) name of monarch/prime minister
10) count backwards from 20 to 1

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130
Q

list some of the ways in which you can manage a patient with delirirum

A
  • underlying condition management
  • drug review
  • maintain hydration and nutrition
  • physical and human envt - clock, near window, photos of family
  • hearing/visual aids
  • avoid unnecessary procedures and changes
  • promote regular sleep patterns and routines
  • if patient is unsafe to themselves or others - haloperidol for sedation (sometimes olanzapine 2nd line?)
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131
Q

describe the types of delirium

A

1) hyperactive/agitated: psychomotor agitation, increased arousal, inappropriate behaviour
2) hypoactive delirium: psychoactive retardation, lethargy, excessive somnolence
3) mixed

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132
Q

list the non-reversible types of dementia

A
  • alzeihmers
  • vascular
  • lewy body
  • frontotemporal
  • others e.g. CJD, HIV
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133
Q

list the reversible types of dementia

A
  • chronic alcohol abuse
  • vitamin deficiencies e.g. thiamine, B12, T4
  • normal pressure hydrocephalus
  • infection e.g. syphilis
  • metabolic.endocrine
  • neoplastic frontal lobe tumours
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134
Q

what are the risk factors for dementia

A
  • genetic: Apo E4 allele
  • vascular risk factors
  • nutritional, social, educational
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135
Q

what are the protective factors for dementia

A
  • diet - vitamins etc
  • physical activity
  • mentally challenging/complex work
  • mental activity - reading, cultural involvement etc
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136
Q

list some fo the symptoms associated with frontal lobe alzeihmers

A

irritable, disinhibited, personality changes, behaviour changes

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137
Q

list some of the symptoms associated with temporal lobe alzeihmers

A

apraxia, agnosia, apathy

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138
Q

what are the features of mild alzeihmers

A
  • forgetfulness
  • recent memory deficit
  • normal ADLs
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139
Q

what are the features of moderate alzeihmers

A
  • significant memory loss
  • personality and behaviour changes
  • language problems
  • impaired ADLs
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140
Q

what are the features of severe alzeihmers

A
  • dysphasia
  • aggression
  • restlessness, wandering
  • delusions
  • hallucinations
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141
Q

what does lewy body dementia tend to affect the most

A

memory, praxis, language, reasoning

visual hallucinations, parkinsonism

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142
Q

what is the clinical course in alzeihmers dementia

A

gradual onset, slow progression

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143
Q

what is the clinical course in vascular dementia

A

stepwise deterioration - first deficit plateus before worsening

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144
Q

what is the clinical course of frontotemporal dementia

A

insidious - slow symptom progression

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145
Q

what are the features of alzeihmers dementia

A
  • memory loss
  • personality changes
  • behaviour changes
  • ADL impairment
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146
Q

what are the features of vascular dementia

A
  • memory and congition impairment
  • uneven deficit distribution
  • UMN signs
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147
Q

what are the features of lewy body dementia

A
  • visual hallucinations
  • repeated falls
  • parkinsonism
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148
Q

what are the features of frontotemporal dementia

A
  • slowly progressive frontal lobe symptoms
  • language and speech problems
  • RARE to have memory problems
  • behaviour changes
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149
Q

what are the pathological features of alzeihmers dementia

A
  • shrunken brain, wide sulci, ventricular atrophy, temporal lobe atrophy,
  • B amyloid plaques
  • neurofibrillary Tau tangles
  • neurone loss and neuronal tract decay
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150
Q

what are the pathological features of vascular dementia

A
  • arteriosclerosis
  • thrombus/embolus
  • neuronal death
  • vasculitis
  • haemorrhage
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151
Q

what are the pathological features of lewy body dementia

A
  • lewy bodies
  • a synuclein
  • ubiquitin
  • cerebral and substantia nigra
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152
Q

list some of the differences between delirium and dementia

A
  • delirium is acute onset, dementia chronic
  • attention decreased more in delirium
  • hallucinations more common in delirium
  • tremor/myoclonus more common in delirium
  • physical illness signs more common in delirium
  • fluctuating signs and symptoms in delirium, whereas dementia is more consistent
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153
Q

describe how someone with a tension headache would present

A

pain feels like a tight band around head

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154
Q

what is thought to be the cause of tension headaches

A

excess contraction of head and neck muscles

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155
Q

how is tension headache managed

A

reassurance - and also explain why a scan would not be beneficial if they are asking for one
midification of lifestyle, relaxing therapies
small night time doses of amitryptilline
treat underlying depression

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156
Q

how would someone with migraine present

A

<40y/o for first presentation, usually FHx
episodes of headache lasting few hours-days and feeling normal between attacks
prodrome
aura - e.g. blurred vision, tingling, unilat weakness rarely etc
headache is throbbing, severe, at front of head, worse on one side
nausea, vomiting, pallor, photophobia may be associated

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157
Q

list some of the possible triggers for migraine

A
  • stress/fatigue/relaxation after stress
  • skipping meals/binge eating
  • menstruation/ovulation/menopause/cocp/early post partum
  • head injury
  • htn
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158
Q

what are some of the ways in which patients with migraine can be managed

A
  • encourage avoiding triggers e.g. stress
  • individual attacks may respond to simple analgesia +/- dopamine antagonist e.g. aspirin and metoclopramide
  • failing that, serotonin angonists e.g. ergotamine and triptans
  • sublingual meds if ptt is vomiting
  • preventative - regular b blockers, amitryptilline, sodium valproate
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159
Q

how may a patient with cluster headache present

A

occur repetitively once/twice a day for several weeks, with long intervals in between (hence clusters)
attacks last between 1/2 hour to 2 hours
severe, around eye, ipsilateral signs of autonomic dysfunction - redness, swelling, nasal congestion, horner’s syndrome

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160
Q

what can be given to help a cluster headache

A

o2
injection of sumitriptan
steroids and verapamil as preventative
anticonvulsants may be tried later on

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161
Q

what is analgesic-depedant headache

A

overuse of analgesia can lead to headaches daily, often throbbing in nature

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162
Q

which drugs are more likely to give you analgesic-dependant headache

A

weak opioids such as codeine

ergotamine, triptans

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163
Q

how is analgesic dependant headache treated

A

discontinuing causative drug

gradual amitryptilline introduction for prophyalxis

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164
Q

describe the headaches found in those with increased ICP

A

worse when lying flat, in morning, may be woken from sleep

other neuro signs e.g. vomiting, papilloedema

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165
Q

describe the headaches found in those with decreased ICP

A

relieved by lying flat, rapidly resume when ptt upright

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166
Q

describe how a patient with GCA headache would present

A

headache and tenderness of scalp

superficial temporal artery may appear red, swollen, non pulsatile and feel tender

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167
Q

who is most prone to subdural haematomas

A

elderly people, alcoholics, people on anticoags who bang their heads

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168
Q

how may people with subdural haematomas present

A

cognitive decline, subacute headache and increased ICP signs

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169
Q

how does sah and meningitis headache present

A

neck stiffness

felt throughout head, and especially occcipitally

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170
Q

how does trigeminal neuralgia present

A 
sudden, momentary pains, like electric shocks (lacinating pain) in the distribution of the trigeminal nerve
waxes and wanes
unilat - usually maxillary or mandibular
severe stabs of pain
triggered by contact with skin
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171
Q

list some of the triggers for trigeminal neuralgia

A 
cold on face
washing
shaving
cleaning teeth
talking
eating
drinking
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172
Q

what drugs are given to patients to treat trigeminal neuralgia

A

anticovulsants like carbamazepine, lamotrigine and gabapetin

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173
Q

describe how someone with post herpetic neuralgia presents

A

after a painful vesicular phase, the pain persists in affected patients.
causes constant burning pain in the area affected by shingles

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174
Q

how is post herpetic neuralgia managed

A

TCA’s
gabapentin
topical capsaicin cream

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175
Q

how may someone with post concussion syndrome present

A

symptoms of headache, poor conc, dizziness, irritability, for months-years after head trauma/concussion episode

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176
Q

define malnutrition

A

deficiency or excess of energy, protein or other nutrients that cause adverse effects on tissue body form, body function and clinical outcome

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177
Q

what are some of the causes of malnutrition

A
  • unbalanced or insufficient diet
  • increased nutritional demand e.g. surgery, infection
  • impaired absorption of foods e.g. N&V, diarrhoea
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178
Q

list some of the consequences of malnutrition

A
  • impaired immune system
  • increased risk of pressure sores
  • decreased wound healing
  • muscle wasting/weakness, including resp and cardiac muscle
  • impaired mental function
  • increased length of hospital stay
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179
Q

list the steps of achieving adequate nutrition

A
  • oral nutrition first
  • enriched oral nutrition
  • oral nutritional supplements
  • alternative route of feeding e.g. NGT/PEG
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180
Q

list some of the factors taken into account when assessing nutritional status

A
  • medical - vomiting/diarrhoea/pressure sores
  • physical - appearance, loose clothes, feeding difficulties
  • dietary
  • nutritional screening tool, score
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181
Q

explain what an NG tube is used for

A

short term feeding directly into stomach, for <14days

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182
Q

explain what Gastrostomy is for

A

long term feeding, directly into stomach from abdominal surface

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183
Q

list the different regimens for enteral feeding

A
  • continuous pump feeding
  • intermittent pump feeding
  • bolus feeding
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184
Q

what are some of the indications for use of oral nutritional supplements

A

poor appetite, regardless of BMI
low BMI
difficulties in meeting nutritional requirements

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185
Q

what should be monitored in patients in terms of feeding

A
  • nutritional intake
  • tolerance
  • weight
  • oral intake
  • fluid balance
  • biochem (electrolytes, refeeding bloods)
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186
Q

which electrolytes should be monitored in patients who are receiving enteral feeding

A

serum K+, PO4 3-, Mg2+ every 12-24 hours when feeding started

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187
Q

which patients are at risk of refeeding

A

those ho have had very little/ no food intake for >5 days, especially if already undernourished or weight loss

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188
Q

define refeeding syndrome

A

severe fluid and electrolyte shifts, and related metabolic complications in malnourished patients undergoing refeeding

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189
Q

list some of the physiological mechanisms involved in refeeding sydnrome

A
  • increased carbohydrate metabolism, using thiamine
  • increased uptake of glucose, PO3 4-, and K+ into cells
  • Mg2+, Na+ and K+ used for cellular pumps
  • increased protein synthesis
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190
Q

list the consequences of refeeding syndrome

A
  • decreased phosphate
  • decreased potassium
  • decreased magnesium
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191
Q

how is refeeding managed

A
  • lower rate of feeding
  • during first few days of feeding: oral thiamine supplements, vitamin B, multivitamins, trace element supplements
  • monitor fluid balance
  • monitor biochem
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192
Q

what are the steps in the MUST score

A

1- measure BMI
2- not percentage of unplanned weight loss and score
3- establish acute disease effect/no nutritional intake>5 days and score
4- add scores from steps 1-3 and obtain overall risk of malnutrition
5- use management guidelines/stepwise policy

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193
Q

list some of the risk factors for pressure sores

A
  • immobility
  • reduced sensation/awareness
  • poor circulation
  • moisture
  • poor nutrition
  • previous pressure ulcers
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194
Q

which score is used to predict risk of developing pressure sore in a patient

A

waterlow score

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195
Q

what is the management of pressure sores

A 
look for infection signs
exacerbating factors
debride and dress
issue viability input, plastics,
photographs, documentation, datix
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196
Q

describe Myasthenia Gravis

A

autoimmune disease of the NMJ characterised by fluctuating weakness in certain skeletal muscle groups

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197
Q

list the muscle groups commonly affected by MG

A
  • extraocular
  • bulbar
  • limbs (proximally)
  • resp muscles
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198
Q

what are the ages commonly affected by MG

A

20-30 F

60-80 M

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199
Q

what is the pathophysiology of MG

A

Autoimmune destruction of Ach-R sites at the NMJ by antibodies, means that there are less Ach receptors for muscle contraction

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200
Q

what is the difference between MG and Lambert Eaton syndrome

A

failure presynapse to release acetylcholine in L-E, whereas MG is the destruction of Ach-R in the postsynapse

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201
Q

what are the features of MG

A
  • easy fatiguability of certain muscle groups
  • fluctuating, painless
  • weaker in the evening or with repetitive use/activity
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202
Q

list some of the precipitants of MG becoming worse

A

stress, activity, menses, illness, thyroid dysfunction, trauma, temperature extremes, drugs

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203
Q

list some of the drugs affecting neuromuscular transmission, therefore could have an effect on MG

A
  • aminoglycosides e.g. streptomycin
  • B blockers
  • CCBs
  • procainamide
  • succinylcholine
  • chloroquinine, penicillamine
  • magnesium
  • ACEi
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204
Q

list some of the complications of MG

A
  • resp failure
  • aspiration
  • resp infection
  • acute exacerbation
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205
Q

describe a myasthenic crisis

A

severe exacerbation of MG, where facial muscles slack, unable to support head, jaw slack, voice has nasal quality, body limp, gag reflex absent (can lead to aspiration)

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206
Q

what is the most important thing to do in a patient with myasthenic crisis

A

secure airway and monitor breathing with regular FVC measurements - may require intubation if deteriorating

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207
Q

describe a cholinergic crisis

A

excess use of cholinesterase inhibitors can lead to excessive Ach stimulation. produces flaccid muscle paralysis, weakness (similar to myasthenic crisis), urinary retention, bradycardia, small pupils, SSLUDGE syndrome

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208
Q

list the components of SSLUDGE in cholinergic crisis

A
  • Salivation
  • Sweating
  • Lacrimation
  • Urinary incontinence
  • Diarrhoea
  • GI upset
  • Emesis/hypermotility
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209
Q

list some of the diagnostic studies for MG

A
  • ACh-R antibodies
  • Tensilon test
  • EMG
  • CT thorax (thymus)
  • ice test
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210
Q

describe the Tensilon test

A

performed in patients with MG - IV anticholinesterase (edrophonium chloride) causes markedly improved symptoms

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211
Q

why is a ct thorax sometimes performed in patients with MG

A

may show enlarged thymus - association, unknown reason. abnormal thymus often present, and thymectomy can help improve symptoms

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212
Q

what is the ice test in MG

A

placing ice over fatigues (esp extraocular) muscles helps rest them and restore their function after fatiguing

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213
Q

what are the cautions in in patients undertaking tensilon test

A

those with heart problems - may case bradycardia (therefore have atropine drawn up ready)
should only be performed by a neurologist, with cardiac monitoring

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214
Q

what is the therapeutic management for MG

A
  • anticholinesterase inihibitors e.g. neostigmine, pyridostigmine
  • corticosteroids to reduce immune response start LOW dose; azathioprine is steroid-sparing option
  • IV Ig
  • plasmaphoresis - removes Ach-R antibodies and can cause a short term improvement
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215
Q

what is the most common subtype of GBSin the western world

A

AIDP - acute inflammatory demyelinating polyradiculopathy

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216
Q

what other condition overlaps with GBS

A

miller-fischer syndrome

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217
Q

describe Guillain Barre Syndrome

A

acute rapidly-progressing polyneuritis/polyenuropathy, usually post infectious, affecting the peripheral nervous system

218
Q

what is the pathophysiology of GBS

A

unknown aetiology, frequently preceded by infeciton/trauma/immune system stimulation etc. with cross reaction between schwann cells causing loss of myelin. this disrupts nerve impulses

219
Q

list the main infectious organisms causing GBS

A 
Campylobacter jejuni is main 
CMV
EBV
HIV
VZV
shigella
M. pneumoniae
220
Q

what are the clinical manifestations of GBS

A

usually develops 1-3 weeks post infection, often complaining of backache, pain, muscle cramps, weakness, hyperaesthesia, tingling in feet extending up
this becomes worse and then plateus at around 4 weeks, after which recovery occurs

221
Q

what are the required features for diagnosing GBS

A

1) progressive weakness in both arms and legs

2) areflexia/hyporeflexia

222
Q

list some features supportive of diagnosis of GBS

A
  • progression over weeks
  • relatively symmetric
  • mild sensory s+s
  • CN involvement
  • recovery begining at 2-4wks
  • autonomic dysfunction
  • typical CSF/EMG/NCS features
223
Q

what are the CSF changes in GBS

A

initialyl may be none, however, increased protein with normal cells in CSF is typical

224
Q

list some of the complications of GBS

A
  • autonomic NS dysfunction causing arrhythmias, postural hypotension, HTN, urinary retention, ileus etc.
  • respiratory - monitor FVC
  • dvt/pe, siadh, pain, renal failure, hyperCa2+
225
Q

what is the therapeutic management for GBS

A 
close observation, bedside spirometry, ventilatory support, ecg and cardiac montioring
nutritional support
dvt prophylaxis
urinary cath may be needed
laxatives and bowel care
pain control with opiates

specifically:

  • IV immunoglobin
  • plasmaphoresis within first 2 weeks of onset for severe cases
  • STEROIDS NOT EFFECTIVE
226
Q

list some differentials for acute flaccid paralysis

A
  • mass in brainstem/sc
  • trauma
  • GBS, miller fischer, lyme, diptheria
  • MG, lambert eaton
  • neurotoxins e.g. botulinum
  • myopathies, steroids, thyrotoxicosis, muscular dystrophies
227
Q

list some stroke mimics

A
  • migraine aura
  • epilepsy
  • transient global amnesia
  • intracranial lesion/SOL
  • MS
  • Labyrinthine disorders
  • metabolic disorders e.g.. hypercalceamia, hypoglycaemia, , hyponatreamia
  • peripheral nerve lesions
  • MG
  • psychological
228
Q

list some of the drugs/substances that can cause intracerebral haemorrhage

A

cocaine
amphetamines
alcohol

229
Q

list some of the questions to ask about the onset of symptoms in patients with ?stroke

A
  • day and time
  • what they were doing
  • sudden?
230
Q

list some of the associated symptoms to ask about in patients presenting with ?stroke

A
  • headache
  • focal or global symptoms
  • vomiting
  • altered conscious level
  • cardiac symptoms
231
Q

list some of the major modifiable risk factors in stroke

A

hypertension, heart disease, af(?), diabetes mellitus, smoking, hypercholesterolaemia

232
Q

what is 5 and 4 on the MRC scale of power

A 
5 = normal power against resistance and gravity
4 = reduced power, but still some against gravity/resistance
233
Q

what is 3 and 2 on the MRC scale of power

A 
3 = reduced power, can overcome gravity but not resistance
2 = muscle can move with gravity/resistance removed
234
Q

what is 1 and 0 on the MRC scale of power

A 
1 = flicker of movement
0 = no movement
235
Q

list some of the causes of weakness at the anterior horn cell level

A

MND/ALS
poliomyelitis
syringomyelia, tumours (mass)

236
Q

list some of the features of myopathic weakness

A

proximal, symmetrical
no sensory loss or fasciculation
no reflex change or wasting

237
Q

list some of the conditions causing neuromuscular weakness

A

myasthenia gravis
myasthenic syndrome (LEMS)
neurotoxins

238
Q

what is lambert eaton syndrome associated with

A

paraneoplastic

239
Q

define adverse drug reaction

A

any response to a drug which is noxious or unintended

240
Q

list some of the factors that can affect compliance in the elderly population

A
  • complexity of regimes
  • manual dexterity - cannot open containers etc
  • poor vision, tremor etc
241
Q

what is the probem of NSAIDs in the elderly population

A 
reduce prostaglandins (gastroprotective - therefore GI bleeds can occur
renally-cleared therefore can be nephrotoxic and cause renal failure
therefore aim to keep doses for under 1 week
242
Q

list some of the common se of BZDs

A

sedation, confusion, ataxia

243
Q

list some of the common se of antipsychotics

A

sedation, epse, neuroleptic malignant syndrome, postural hypotension

244
Q

list some of the common se of opioids

A

sedation, confusion, constipation, resp depression

245
Q

list some of the common se of antihypertensives

A

postural hypotension, syncope, falls, u and e disturbance in thiazides and acei, arf

246
Q

list some of the drugs with anticholinergic activity (associated with increased confusion in elderly)

A
  • tca’s

- drugs for overactive bladder e.g. oxybutinin

247
Q

list the stimulant laxatives

A

senna
bisacodyl
picosulphate
glycerol suppository

248
Q

list the bulk laxatives

A

fybogel

movicol

249
Q

list the osmotic laxatives

A

lactulose

enemas

250
Q

list a lubricant laxative

A

arachis oil

251
Q

what are 1 and 2 on the bristol stool chart

A

1 - separate hard lumps

2 - lumpy, sausage-shaped

252
Q

what are 3 and 4 on the bristol stool chart

A

3 - like sausage but with cracks on surface

4 - smooth, soft, sausage shaped

253
Q

what are 5 and 6 and 7 on bristol stool chart

A

5 - soft blobs, clear cut edges
6 - fluffy pices, ragged edges, mushy
7 - watery, no solid pieces

254
Q

how do you manage risk in a patient post-TIA

A

as there is high risk of another stroke in next 24-48hrs, refer to TIA clinic in 24hours, tell them not to drive, aspirin cover

255
Q

what are the components of the ABCD2 score, and what does the score tell us

A 
A - age >60
B - BP >140/90
C - clinical ipsilat weakness/speech
D - diabetes
D - duration (different intervals)
score of 4 or more means they need to be seen in TIA clinic within 24hrs; <4 - within 7 days
256
Q

what should be commenced in patients who present with a TIA

A
  • aspirin 300mg
  • simvastatin 40mg
    (thrombolysis within 4.5 hours if not getting any better, refer to neurosurgeons for thrombectomy etc)
257
Q

what are the two main categories of headache

A

primary e.g. tension, cluster, migraine

secondary e.g. infection, trauma, metabolic, neoplasia

258
Q

list the red flag symptoms of headache

A
  • thunderclap
  • neck stiffness
  • rash
  • photophobia
  • focal neurology
  • nausea/vomiting
  • present on waking/worse when lying down
  • valsalva/bending down exacerbates
  • papilloedema
  • fever
  • recent onset of change in character
259
Q

list some acute headache types

A
  • meningitis
  • encephalitis
  • other infections
  • sah
  • post ictal
  • migraine
  • cluster
260
Q

list some chronic headache types

A
  • temporal arteritis
  • migraine
  • analgesic abuse
  • tension
  • paget’s
  • increased icp/bih
261
Q

list the symptoms in subarachnoid haemorrhage

A 
thunderclap headache
neck stiffness, photophobia
focal neurology
N and V
altered conscious level
subhyaloid heaemorrhage
262
Q

what is the underlying pathology in sah

A

berry aneurysms, av malformations, htn, idiopathic

263
Q

what are the ways to diagnose a sah

A

CT - most sensitive in first 24 hours
LP 12 hours after onset showing xanthochromia; measure opening pressure (protect sample from light)
cerebral angiography if fit for neurosurgery (neurosurgeon involvement)

264
Q

list some of the complications of sah

A

rebleed, vasospasm, poor cerebral perfusion, hydrocephalus,

265
Q

how is sah treated

A

neurosurgeons - clipping of aneurysm, embolisation of aneurysm w/ coils

266
Q

what is positive kernigs sign

A

in meningitis - when thigh is flexed at hip and knee flexed at 90 deg, the subsequent extension of the knee is painful - leading to resistance

267
Q

how is meningitis treated immediately

A

1.2g benzylpenicillin, +/- steroids
iv fluids, O2, cultures (meningococcal PCR)
isolate for 24hours

then give 2g ceftriaxone iv

268
Q

should you do LP in meningitis

A

no if increased icp signs or drowsiness

269
Q

what is the white cell count like in LP of bacterial meningitis

A

increased polymorphs

270
Q

what is the white cell count like in LP of viral meningitis

A

increased lymphocytes

271
Q

what is the white cell count like in LP of TB

A

elevated mixed

272
Q

what is the protein content like in LP of bacterial meningitis

A

increased

273
Q

what is the protein content like in LP of viral meningitis

A

increased

274
Q

what is the protein content like in LP of TB meningitis

A

usually increased

275
Q

what is the glucose content like in LP of bacterial meningitis

A

reduced to less than 50% of serum level

276
Q

what is the glucose content like in LP of viral meningitis

A

normal

277
Q

what is the glucose content like in LP of TB meningitis

A

reduced to 50% of serum level

278
Q

what is the appearance like in LP of bacterial, viral and TB meningitis

A

bacterial - cloudy
viral - can be clear or cloudy
TB - slightly cloudy, fibrin webs

279
Q

list some of the causes of bacterial meningitis

A
  • N meningitides in adolescents
  • S pneumoniae in older populations
  • listeria monocytogenes in >50y/o
  • H influenzae
  • S aureus
  • E.coli, klebsiella, proteus, pseudomonas
  • group B strep
  • mycobacterium
280
Q

when should you consider an urgent CT with someone who has meningitis

A
  • reduced conscious level
  • signs of increased ICP
  • suspicion of SAH
281
Q

what is the clinical presentation of TB meningitis

A

insidious onset 1-9 months

mild headache + constitutional upset

282
Q

what is the treatment for Tb meningitis

A
  • RIPE therapy for 2 months + steroids
  • double therapy (isoniazid, rifampicin + pyridoxine) for 12 months at least
  • may require shunt insertion
283
Q

what is the characteristic pain of SOL headache

A

deep, aching, dull pain

284
Q

who is most affected by temporal arteritis

A

> 50 y/o

female

285
Q

how does temporal arteritis present

A

tender red scalp
visible tortuous artery
constitutional symptoms e.g. weight loss, night sweat, fever, joint aching, jaw claudication
(assoc with PMR)

286
Q

what tests would you carry out to diagnose temporal arteritis

A
  • raised plasma viscosity/ESR

- temporal artery biopsy >1 cm to account for skip lesions

287
Q

list some of the causes of raised ICP

A

sol - tumour, abscess
venous sinus thrombosis
hydrocephalus
benign intracranial HTN

288
Q

list the symptoms of raised ICP

A
  • headache on waking, worse when lying down
  • papilloedema
  • nausea and vomiting
  • bradycardia if severe
  • periodic breathing aponea (cyclical changes in breathing)
  • false localising signs
289
Q

who is especially at risk of venous sinus thrombosis

A

cancer patients, pregnant

290
Q

what is the treatment for venous sinus thrombosis

A

anticoagulation

291
Q

describe cushings reflex

A

bradycardia and increased hr, irregular breathing due to effects of raised ICP affecting the brainstem

292
Q

what are the features of migraine headache

A

unilateral, throbbing
photo and phonophobia
aura may be associated

293
Q

how is migraine headache treated

A

analgesics,
antiemetics,
triptans
can use prophylactic treatment like propanolol, amitryptilline, topiramate

294
Q

list some of the symptoms of cluster headache

A
  • severe short-lived, unilateral headache
  • around the eye
  • nasal congestion/rhinorrhoea/conjunctival infection
  • episodic - daily for weeks, then nothing in between
295
Q

what is the treatment for cluster headache

A
  • high dose O2
  • triptans
  • analgesics
  • steroids
  • lithium
  • verapamil
296
Q

what is the typical patient who presents with benign intracranial htn

A

usually young, overweight woman

297
Q

how is benign intracranial hypertension diagnosed

A
  • ct scan and venous scan of brain
  • LP with manometry (once imaging is normal - dont want coning!!)
  • papilloedema usually present
298
Q

what is the normal pressure in the brain, and what is it in BIH

A

normal - 15-20mmhg

bih - 25 mmhg

299
Q

what is the management for BIH

A

weight loss is effective
relieve pressure immediately - send to neurosurgeons
may be able to insert shunt

300
Q

what is the management of tension headaches

A
  • reassurance
  • stress/anxiety relief and relaxation
  • mamagement of depression
  • small night time doses of amitryptilline
301
Q

what is the management of migraine

A

encourage patient to avoid triggers
analgesia and dopamine antagonist e.g. aspirin + metoclopramide
serotonin agonists such as ergotamie and triptan family of drugs failing that
(sublingual if vomiting persistent problem)

302
Q

what are some of the preventative drugs that can be given in migraine

A

b blockers, amitryptilline, sodium valproate

303
Q

how is analgesic-dependant headache treated

A

stop offending drug - gradual amitryptilline prophylaxis

304
Q

which patients are most susceptible to subdural haematoma

A

elderly, alcoholic, on anticoags

305
Q

how does trigeminal neuralgia present

A

sudden momentary pains like electric shocks (lancinating pain) in the distribution of the trigeminal nerve

306
Q

which drugs may be given to control trigeminal neuralgia

A

gabapentin, amitryptilline

anticonvulsants like carbamazepine, lamotrigine etc

307
Q

how does post herpetic neuralgia present

A

following acute painful vesicular stage, pain persists in small percentage of patients, causing constant burning pain in thin area affected by shingles.
may not be able to sleep properly, depressed

308
Q

what is the management for post herpetic neuralgia

A

TCA’s
gabapentin
topical capsaicin

309
Q

what is post concussion syndrome

A

following concussion, patient may suffer from symptoms for months/years after - headaches, poor conc, memory problems, irritability etc

310
Q

describe the arteries that make up the circle of willis

A
  • 2 vertebral arteries -> basilar artery
  • 2 internal carotids -> circle of willis
  • basilar artery -> circle of willis
  • circle of willis : ACA, MCA, PCA
311
Q

when is surgery performed in carotid artery stenosis

A

> 50% occlusion, symptomatic

312
Q

define stroke

A

sudden onset of focal neurological deficit attributable to vascular cause i.e. in a vascular territory
either haemorrhagic or embolic/thrombotic

313
Q

would you usually expect symptoms such as headache, loc etc in stroke patients

A

no -these are generalised, not focal neurological deficits. however, there are some exceptions

314
Q

what other risk factors, apart from vascular ones, should be considered in patients who have had a stroke

A
  • cocp
  • trauma
  • hiv
  • cannabis
  • legal highs
  • cocaine
  • …other elicit drugs
315
Q

list some of the lobar symptoms of stroke affecting the frontal lobe

A
  • motor problems, especially leg movements
  • broca’s - dysphasia
  • urinary incontinence
  • disinhibition
  • heigher mental function impairment
  • memory
  • personality change
316
Q

list some of the lobar symptoms of stroke affecting the parietal lobe

A
  • problems with facial/object recognition - agnosia
  • sensory disturbance
  • quadrantonopias (optic radiations pass here)
  • nominal aphasia, dysphasia
  • language problems
  • inattention
317
Q

list some of the lobar symptoms of stroke affecting the temporal lobe

A
  • auditory/vestibular
  • wernicke’s area - dyphasia
  • memory problems
  • quadrantonopias (optic radiations)
318
Q

list some of the lobar symptoms of stroke affecting the occipital lobe

A
  • visual symptoms (homonymous hemianopias)
319
Q

list some of the lobar symptoms of stroke affecting the cerebellum/brainstem

A
  • cranial nerve disturbance
  • ataxia
  • past pointing
  • vertigo
  • unsteady
  • nausea and vomiting
320
Q

why is important to ask if patient woke up with stroke symptoms

A

gives indication about whether it occurred during sleep

321
Q

what is the usual pathophysiology of ischaemic stroke?

A

often carotid artery thrombus being thrown off and an embolus, causing occlusion and ischaemia in brain
can also come from arch of aorta
venous thrombosis more rare - this can happen in the cerebral venous sinuses or dvt going through a patent foramen ovale

322
Q

how do the acute symptoms in stroke differ from the ones that emerge later

A

acutely - hypotonic, loss of reflexes

later - more umn signs - hypertonic, upgoing plantars etc

323
Q

list some post stroke complications

A

1) infections
2) metabolic upset
3) malnutrition
4) seizures
5) contractures
6) incontinence, disability
7) depression, anxiety, cognitive decline
8) pneumonia
9) shoulder/hip subluxation

324
Q

list some of the red flag symptoms in someone who presents with a stroke

A
  • falls
  • headache preceding neurology
  • progressive neurology
  • fluctuating/deteriorating consciousness
  • systemicatically unwell
  • no vascular risk factors
  • inconsistent
325
Q

list the bloods that should be done in a patient with stroke

A
  • platelets, fbc
  • u+e
  • LFT
  • glucose, lipids
  • crp/plasma viscosity (vasculitic disease)
326
Q

what is the NIHSS

A

scale/score looking at many domains in a stroke patient - dictating use of thrombolysis in a clinical setting
can look at whether people are improving or getting worse

327
Q

list two disability outcome scores following stroke

A

barthel index

ranken

328
Q

which vessels are usually affected in TACS

A

prox - ICA/MCA

329
Q

which vessels are usually affected in PACS

A

MCA (more distal)

330
Q

which vessels are usually affected in LACS

A

single perforating - small vessel disease

331
Q

which vessels are usually affected in POCS

A

PCA, posterior circulation arteries

332
Q

which symptoms must be present for a TACS in the oxford classification of stroke

A
  • contralat hemiparesis/hemianaesthesia
  • contralat hemianopia
  • higher cerebral dysfunction
333
Q

which symptoms must be present for a PACS in the oxford classification of stroke

A

2/3 of those of TACS or motor deficits restricted to face/leg/arm only or restricted cortical signs

334
Q

which symptoms must be present for a LACS in the oxford classification of stroke

A
  • pure motor
  • pure sensory
  • sensorimotor
  • ataxic hemiparesis
335
Q

which symptoms must be present for a POCS in the oxford classification of stroke

A

brainstem/cerebellar/occipital involvement/signs

336
Q

what are the NICE guidelines on the pharmacological management of ischaemic stroke

A

thrombolysis with alteplase if no CI
aspirin 300mg
may initiate statins

337
Q

list some of the secondary causes for haemorrhagic stroke

A
  • haemorrhagic transformation of infarct
  • tumours
  • vascular
  • coagulopaty
  • cocaine, alcohol
338
Q

what are some of the predictors of poor outcome in patients with haemorrhagic stroke

A
  • ?30mls
  • intraventricular
  • deep locations e.g. thalamus
  • elderly
  • GCS <9
339
Q

what are the locations for a head bleed

A
  • intraparenchymal
  • intraventricular
  • subarachnoid
  • subdural
  • extradural
340
Q

how is a haemorrhagic stroke diagnosed

A

CT - acute bleed seen as white
MRI for hyperacute, subacute, chronic bleeds
may want to do angiogram if venous infarct transformed to bleed

341
Q

what is the management for haemorrhagic stroke

A
  • neurosurgery for clot reduction, decompression, craniotomy
  • intraventricular shunt insertion
  • medical supportive measures e.g. obs, seizures,
342
Q

how many months after a heamorrhagic stroke should a follow up scan take place

A

2 months

343
Q

go through the stages of appearance of a CT in haemorrhagic stroke, according to progression of time

A
  • hyperacute - high density, white
  • acute - perilesional oedema appears as lower density than that of surrounding brain
  • subacute - globin molecule breaks down starting from periphery and going inwards (appears darker at edges)
  • chronic - dark
344
Q

list some of the “mass effects” of haemorrhagic stroke

A
  • effacement of ventricles
  • displacement of ventricles
  • midline shift
  • twisted ventricle
  • hydrocephalus
  • cerebral herniation (subfalcine, uncal, tentorial, coning)
345
Q

what is the equation for calculating the cerebral perfusion pressure (CPP)

A

CPP = MAP - ICP

if CPP becomes <70mmhg, brain suffers ischaemic injury

346
Q

where does blood collect in an extradural haematoma, and how does it look on CT

A
  • collects between naked bone and layer of dura

- appears as biconcave, hyperdense, “lentate’ lesion

347
Q

where does blood collec tin subdural haematoma and what does it look like on ct

A

collects between arachnoid and dura

crescent shaped, sulcal markings often present

348
Q

which veins are usually torn in subdurals

A

bridging veins

349
Q

how are MRIs useful in head imaging

A

good for finding underlying pathology, aged bleeds, subacute and chronic bleeds (bad at acute)

350
Q

what do late/subacute bleeds look like on MRI as compared to acute bleeds

A

late ones tend to show up as bright (depends on weighting), whereas earlier bleeds are much harder to detect on MRI and may even appear normal

351
Q

what pattern of symptoms do you expect to see in an MCA ischaemia

A
  • loss of use/sensation of contralat face, arm
  • dysphasia
  • dyslexia, dysgraphia, dyscalculia
352
Q

what pattern of symptoms do you expect to see in an ACA ischaemia

A
  • loss of use/feeling in contralat leg
353
Q

what pattern of symptoms do you expect to see in an PCA ischaemia

A
  • contralateral homonymous hemionopia
354
Q

what pattern of symptoms do you expect to see in an ICA ischaemia

A

arm, face and leg

hemionopia?

355
Q

what pattern of symptoms do you expect to see in an opthalmic artery ischaemia

A

monocular loss of vision

356
Q

what does the chadsvasc score predict

A

stroke risk for patients with AF

357
Q

what are the components of the chadsvasc score

A
  • ccf
  • htn
  • age
  • diabetes mellitus
  • sex
  • stroke
358
Q

list some of the clinical problems following stroke

A
  • dysphasia, dysarthria
  • delirium
  • dysphagia
  • dyspraxia
  • sensory neglect
  • visuospatial perception
  • executive function difficulties
  • weakness of limbs
  • sensory loss
  • hemianopia
  • depression
  • thalamic pain
  • shoulder pain
359
Q

list some ddx for cerebellar infarct

A
  • bppv
  • meniere’s disease
  • migrainous vertigo
  • vestibular neuritis
  • labyrinthitis
360
Q

list some symptoms/ signs of cerebellar infarct

A
  • vertigo
  • max intensity at onset
  • severe ataxia
  • difficulty walking
  • direction-changing nystagmus
  • focal neurology signs
361
Q

what is the advice re driving in patients who have had a stroke

A
  • do not drive for 1 month

- tell dvla and insurance company

362
Q

what is the rosier score for

A

quick assessment as to whether patients presenting in a and e are likely to have had a stroke
includes parameters such as loc, seizures, asymmetrical facial/arm/leg weakness, speech disturbance, visual field defect

363
Q

what are some of the ways in which complications of stroke can be managed

A
  • early as possible involvement of PT/OT/SALT
  • mobile as soon as possible, heparin, turning, comfortable position
  • antiepileptics if seizures
  • surgery for contractures.neurosurgery
  • neuropathic pain management
  • antidepressants
    • treat any uti/other infections that may develop
364
Q

list some of the risk factors for delirium

A
  • icreasing age
  • comorbidities/ severe illness
  • infections
  • malnutrition
  • particular medications, polypharmacy
  • immobility
  • decreased ADLs; superimprosed on dementia
  • urinary catheter
  • u and e imbalance
  • constipation
365
Q

define delirium

A

acute confusional state, characterised by disturbed consciousness, cognitive function or perception. Has an acute onset and fluctuating course

366
Q

list the 4 criteria for diagnosing delirium with the DSMIV criteria

A
  • disturbance of consciousness
  • change in cognition
  • acute
  • due to medical condition/intoxication/substance withdrawal/multiple aetiologies
367
Q

what are the negative effects on recovery, from delirium

A
  • increased mortality
  • risk of falls increased
  • prolonged hospital admission
  • higher complication rates
  • institutionalisation
  • increased risk of developing dementia
368
Q

list some of the precipitating factors for delirium

A
  • immobility
  • medication
  • physical/medical
  • iatrogenic
  • surgery
  • malnutrition
  • intercurrent illness
  • dehydration
369
Q

list some of the features of hypoactive delirium

A
  • lethargy and reduced motor activity
  • excess somnolence
  • depression-like symptoms
370
Q

list some of the features of hyperactive delirium

A
  • increased motor activity and agitation
  • hallucinations
  • inappropriate behaviour, aggression
371
Q

what are the 10 domains in the AMT test

A

1) age
2) time to nearest hour
3) address to recall at end of test e.g. 42 west street
4) year
5) name of hospital/where they are presently
6) recognise two persons e.g. nurse/doctor
7) dob
8) name of monarch/prime minister
9) start date of ww1/ww2
10) count backwards from 20-1

372
Q

why is it useful to be mindful when treating elderly patients with drugs which have anticholinergic properties

A

increased risk of delirium

373
Q

what investigations should you order in a patient with delirium

A
  • bloods e.g. fbc, renal/liver function etc
  • ecg
  • cxr/urinalysis to to and find source of infection
  • regular obs
  • may need cultures, ct, eeg, lp, abg (specific situations)
374
Q

what are the rules for sedation in delirium

A
  • try and avoid, but if required then use the minimum amount of time/dose, least restrictive
  • sedative drugs themselves can often precipitate delirium
  • when all else has failed
  • patient danger to themselves/others, lacking capacity
  • use of haloperidol first line; lorazepam 2nd
375
Q

list some of the non-pharmacological measures in the management of delirium

A
  • hearing aids and glasses available
  • reduce change in staff and ward transfers
  • familiar objects, clock, near window, photos of relatives
376
Q

list some of the pharmo-related management options in delirium

A
  • drug review
  • treat underlying condition
  • sedatives - try to avoid unless very necessary
377
Q

what is the management of delirium

A
  • try and find precipitating factor and manage this!
  • drug review is essential
  • nutrition, hydration, control distressing physical symptoms
  • attention to physical and human environment, hearing and visual aids
  • avoid unnecessary procedures e.g. catherisation
  • promote regular sleep patterns, routines
  • sedation as last resort
378
Q

list the non-reversible types of dementia

A

1) AD
2) vascular
3) lewy body
4) fronto temporal
5) cjd, aids dementia etc

379
Q

list the reversible types of dementia

A
  • chronic alcohol abuse
  • thiamine/b12/t4 deficiency
  • normal pressure hydrocephalus
  • infections e.g. syphillis
  • metabolic/endocrine
  • neoplastic e.g. frontal lobe tumours
380
Q

list some fo the risk factors for dementia

A
  • apoE4 gene
  • vasc factors for vasc dementia
  • nutritional, social, engagement, education
381
Q

list some of the protective factors for dementia

A
  • diet - veg, fruit, antioxidants
  • physical activity
  • mentally challenging/complex work
  • mental activity e.g. reading, cultural
382
Q

list some of the symptoms of AD affecting mainly the frontal lobe

A

irritability, disinhibited, change in behaviour

383
Q

list some of the symptoms of AD affecting mainly the parietal lobe

A

agnosia, apraxia, apathy

384
Q

what are the features of mild dementia

A
  • forgetful
  • recent memory deficit
  • adl’s not impaired
385
Q

what are the features of moderate dementia

A
  • significant memory loss
  • personality and behaviour changes
  • difficulties in orientation and language
  • impaired adl’s
386
Q

what are the features of severe dementia

A
  • dysphasia
  • aggression
  • restlessness, wandering
  • delusions, hallucination
387
Q

what is the clinical course of AD

A

gradual onset, slow progression

388
Q

what is the clinical course of vascular dementia

A

stepwise deterioration (first deficit plateus before next one commences)

389
Q

what is the clinical course of lewy body dementia

A

fluctuating memory and cognitive function

390
Q

what is the clinical course of frontotemporal dementia

A

insidious - slow symptom progression

391
Q

what are the features of AD

A

memory loss
personality changes
behaviour changes
adl impairment

392
Q

what are the features of vascular dementia

A

memory and cognition impaired
uneven deficit distribution
umn signs

393
Q

what are the features of lewy body dementia

A

visual hallucinations
repeated falls
parkinsonism

394
Q

what are the features of frontotemporal dementia

A

slowly progressive frontal lobe symptoms
language and speech problems
memory problems RARE
behaviour changes

395
Q

list the pathological features of AD

A

shrunken brain, wide sulci, ventircular atrophy, median temporal lobe atrophy (esp hippocampus)
B amyloid plaques
neurofibrillary tau tangle
neuronal loss, neuronal tract decay

396
Q

list the pathological features of vascular dementia

A 
arteriosclerosis
thrombus/embolus
neuronal death
vasculitis
haemorrhage
397
Q

list the pathological features of lewy body dementia

A

lewy bodies
alpha synuclein
ubiquitin
cerebral and substantia nigra

398
Q

list some of the differences between delirium and dementia

A
  • delirium is acute, dementia is chronic
  • attention is decreased more in delirium
  • hallucinations more common in delirium
  • psychomotor activity more likely to be affected in delirium
  • physical illness symptoms more likely in delirium
  • signs and symptoms are fluctuating/worse during night in delirium, whereas in dementia they are consistent
399
Q

how would you assess insight in a patient

A

1) does patient believe theyre suffering from illness at all?
2) do they believe they have a mental illness
3) do they believe they will benefit from treatment
4) will they accept the treatment

400
Q

list the bloods that may be undertaken in the confusion screen

A
  • fbc
  • b12/folate/haemotinics
  • u and e
  • lft
  • inr
  • tft
  • calcium
  • glucose
401
Q

list some causes of non-syncopal attacks

A
  • metabolic e.g. hypoglycaemia, hypoxia..
  • epilepsy
  • intoxication
  • tias - vertebro-basal
  • psychogenic syncope
402
Q

what are the categories of causes for syncopal attacks

A

1) neurally-mediated reflex syncope
2) orthostatic
3) arrhythmia (cardiac)
4) structural cardiac/cardiopulm disease
5) cerebrovascular (vascular steal syndrome)

403
Q

list some of the causes for neurally-mediated reflex syncope

A
  • vasovagal
  • carotid sinus syncope
  • situational faint e.g. post micutrition
  • glossopharyngeal/trigeminal neuralgia
404
Q

list some causes of orthostatic syncope

A
  • volume depletion
  • autonomic failure - primary or secondary
  • drugs, alcohol
405
Q

list some causes of cardiac arrhythmia syncope

A
  • sinus node dysfunction
  • av conduction disease
  • svt/vt
  • inherited e.g. long qt
  • implanted device malfunction
406
Q

list some causes of structural/cardiac/cardiopulm syncope

A
  • valvular disease
  • acute MI/ischaemia
  • obstructive cardiomyopathy
  • atrial myxoma
  • acute aortic dissection
  • pericardial disease/tamponade
  • pe/pulm hypotension
407
Q

define syncope

A

symptom defined as transient, self limited LOC associated with loss of voluntary muscle tone. Onset relatively rapid and subsequent recovery spontaneous, usually prompt. underlying cause is transient global hypoperfusion

408
Q

what is a poor prognostic factor in syncope

A

structural heart disease

409
Q

list some of the features suggesting a neurally-mediated syncope

A
  • after sudden unexpected stimulus
  • standing in warm crowded places
  • N and V associated with syncope
  • post prandial <1 hour
  • after exertion
  • syncope with throat/facial pain (glossopharyngeal/trigeminal neuralgia)
410
Q

list some of the circumstances where you would hospitalise a patient with syncope

A
  • suspected/known significant heart disease
  • ecg abnormality suggesting arrhythmia
  • syncope during exercise
  • syncope when supine
  • fhx of sudden death
  • sudden onset palpitations in absence of heart disease
  • frequent, recurrent episodes
  • arrhythmia causing syncope
  • cardiac ischemia
  • structural heart/cardiopulm disease
  • stroke/focal neurology
411
Q

what should be assessed when a patient presents with syncope

A
  • obs
  • gait/balance
  • joints
  • cns
  • cvs, ecg - lying and standing
  • vision
  • medications
  • cognition
  • continence history
  • referral for tilt-table test in some cases
412
Q

list the circumstances in which you would refer a patient with syncope to a specialist falls service

A 
- previous fragility fracture
-
attended a and e/call 999 with fall?
- 2 + intrinsic factors in fall
- frequent unexplained falls
- falls in nursing/residential home
- unsafe housing
- very afraid of falling
413
Q

what are the factors that should be considered when trying to work out the aetiology of falls

A
  • intrinsic (to do with patient)

- extrinsic(to do with surroundings/envt)

414
Q

list some of the multidisciplinary interventions for patients with falls

A
  • strength and balance training
  • home hazards assessment and intervention
  • vision assessment and referral
  • meds review/modification/withdrawal
  • also assess future risk, interventions to prevent future falls
415
Q

what are the suggestions for drivers who have had a syncopal event

A

if simple e.g. vasovagal, then can continue
others- domestic drivers shouldnt drive for 1 month, depending on cause
professional drivers - longer

416
Q

in order to rule out other causes of tloc, what questions should be asked to the patient/ in the collateral history

A
  • tongue biting
  • limb jerking - duration
  • duration of episode
  • presence of confusion during recovery period
  • weakness down one side during recovery period/before
417
Q

if, after taking full history, examination and investigations, you are still unsure of the cause of a patient’s syncope, what should be considered next

A

does the patient have cardiac history/structural heart disease

  • if no and normal ecg - no further evaluation usually required
  • if yes/abnormal ecg - cardiac evaluation, and manage as per diagnosis
418
Q

list the three categories of causes for cardiac syncope

A
  • arrhythmia
  • structure
  • vascular
419
Q

list some of the structural disease that may cause cardiac syncope

A
  • cardiomyopathy e..g obstructive
  • atrial myxoma
  • pericardial disease/tamponade
  • valvular
420
Q

how do you test for neuronally-mediated syncope

A
  • tilt table test
  • carotid sinus massage
  • ?implantable loop recorder/24 ecg
421
Q

what is the criteria for diagnosing orthostatic hypotension

A

systolic BP fall >20mmHg or diastolic >10mmHg in first 10 mins of standing

422
Q

how would you manage orthostatic hypotension

A
  • treat underlying cause e.g. hypovolaemia, drugs, addisson’s etc
  • increased salt intake
  • fludocortison or midrodine are pharmacological treatments
423
Q

how do you manage vasovagal syncope

A
  • education and reassurance
  • physical counter pressure
  • action when recognising prodrome symtpoms
  • drug/polypharmacy alteration
  • (midodrine)
424
Q

how do you manage carotid sinus sensitivity syndrome

A
  • dual-chamber pacing for cardioinhibitory-type CSSS
  • prevention and abortive measures
  • reassurance
  • physical counter pressure manoeuvres
  • polypharmacy alteration
425
Q

what investigations should be done in patients who experiences blackouts

A
  • blood glucose
  • blood gases
  • ecg
  • eeg
  • cario evaluation
426
Q

list some personal safety advice that you may give a patient who suffers with blackouts

A
  • do not drive motor vehicles if subject to sudden episodes of LOC
  • consider showers instead of baths
  • job considerations - machinery, heights
  • care with some recreational activities e.g. swimming
427
Q

list some changes in elderly patients, which would lead to them being at increased risk of falls

A
  • decreased visual acuity
  • balance impairment
  • sarcopenia
  • kyphotic posture
  • increased body sway
  • irregular gait pattern, small steps
  • cerebrovascular changes, contributing to cognitive changes
  • sensory impairment
428
Q

describe how the apley manouvre is performed

A

1) lie patient on back, neck extended 30deg and turned to one side at 45deg - nystagmus will occur if BPPV is present
2) after 30-60 seconds, turn head 90deg to face the other side
3) after 30-60 seconds, turn them on their side, and turn their head another 90deg so that their face is against the pillow (at 45 deg from horizontal)
4) after 30-60 seconds, the patient should sit up

429
Q

list the drugs associated with high risk of falls

A

1) antihypertensives
2) opiates and analgesics
3) long acting hypoglycaemic drugs
4) hypnotics, long lasting BZDs
5) antidepressants esp TCAs
6) antiepileptics
7) anticholinergics (anticholinergic burden)

430
Q

list some of the extrinsic features for falls

A
  • older housing
  • poor lighting
  • clutter, pets underfoot, cables
  • inappropriate footwear, esp slippers
  • incorrect use of walking aids
  • lack of grab rails in bath/shower
  • unfamiliar envt e.g. care home
  • uneven/icy/wet pavements
431
Q

list some of the sequelae after a long lie on floor following fall

A
  • pressure sores
  • rhabdomyolysis
  • hypothermia
  • hypostatic pneumonia
432
Q

list some of the steps you can take to reduce the cosnequences of falls

A
  • pt/ot involvement to increase confidence with mobilising
  • vit d and calcium prescription
  • maintain good environment temp
  • carpeting, remove obstacles and dangers
  • place emergency bedding where it can be reached from floor
  • personally worn alarm system
  • education about safety in home - family and patient
433
Q

list some of the physical complications of immobility

A
  • muscle wasting
  • contractures
  • osteoporosis
  • pressure sores
  • hypothermia
  • hypostatic pneumonia
  • costipation
  • incontinence
  • dvt
434
Q

list some of the psychological complication of immoblilty

A
  • depression

- loss of confidence

435
Q

what is the definition of ataxia

A

loss of coordination

436
Q

what is the definition of apraxia

A

inability to execute voluntary purposeful movement despite demonstrating normal muscle function

437
Q

what is the definition of agnosia

A

inability to recognise sensory input even when the specific pathway is not defective

438
Q

what are some of the gait signs which indicate incoordination on examination

A
  • inability ot stand on narrow base
  • broad based gait
  • romberg sign
  • inability to stand on one leg
  • impaired tandem gait
  • positive unterberger signs
  • impaired hell-shin test
  • impaired foot tapping
439
Q

list some of the upper limb signs which indicate incoordination on examination

A
  • difficulty with rapid alternating movements
  • dysdiadokokinesis
  • impaired finger-nose test
  • past-pointing
  • intention tremor
  • rebound test
440
Q

list some of the causes for sensory ataxia

A
  • sensory neuropathy
  • ms
  • subacute combined degeneration
  • tabes dorsalis
  • cervical myelopathy
  • cord tumours
441
Q

list some of the forms of agnosia

A
  • alexia (dyslexia)
  • auditory, visual
  • prosopagnosia (faces)
  • amusia (music)
  • astereogenesis (shapes)
442
Q

list some of the signs of parietal lesion

A
  • apraxia
  • parietal drift
  • sensory inattention
  • 2 point discrimination
  • astereogenesis
  • dysgrafisthesia
  • visual field defect - quadrantonopia
443
Q

what is a seizure

A

the clinical manifestation of abnormal and excessive excitation of a population of neurones

444
Q

what is epilepsy

A

a tendency towards recurrent seizure unprovoked by systemic or neurological insults

445
Q

what is important to elicit in terms of a patient’s childhood history if they present with seizures

A
  • birth trauma
  • meningitis
  • childhood illness
446
Q

list some of the specialist tests in epilepsy

A
  • EEG - sleep deprived/non sleep deprive
  • video telemetry
  • MEG
447
Q

list the different types of seizure

A

generalised: tonic, clonic, tonic-clonic, atonic, myoclonic, absence
focal: simple partial - simple partial can become a secondary generalised seizure

448
Q

list some of the impacts of epilepsy

A
  • unable to drive/do certain jobs or activities
  • social embarassment
  • risk of injury
  • risk of sudden death
  • comorbidities e.g. neuro disability, drug s/e, depression
449
Q

what is the definition of status epilepticus

A

seizure activity continuous for >30 minutes or recurrent seizures w/o 5 minute breaks in between attacks

450
Q

what is the management of status epilepticus

A
  • buccal midazolam or PR diazepam
  • ambulance can administer: IV diazepam or lorazepam
  • if lorazepam fails: phenytoin, ITU admission (may give midazolam)
451
Q

what is important to remember about phenytoin

A

zero-order metabolism

452
Q

state some of the different mechanisms of action for antiepileptic drugs

A
  • enhance GABA
  • suppress Glutamate
  • acts on Na+/K+ channels
  • Na/Ca dependent action potentials
  • direct effect on neuronal firing
453
Q

which drugs are usually used to treat generalised seizures

A

sodium valproate
lamotrigine
keppra

454
Q

which drugs are used to treat complex partial seizures

A

carbamazepine
lamotrigine
keppra

455
Q

how do absence seizures present

A

tend to occur in children, with multiple attacks, where patient may not be aware. speech stops, look blank, stop what theyre doing. eyelids may flutter.

456
Q

what should not be used to treat absence seizures

A

carbamazepine

457
Q

what is neurofibromatosis

A

several genetically-inherited conditions that carry a high possibility of tumour formation - nf1 and nf2 type

458
Q

what are the features of nf1

A
  • cutaneous conditions
  • 6 or more cafe au lait spots
  • 2 of more neurofibromas
  • 2 or more growth on iris
  • behaviour and learning problems
  • scoliosis
  • optic gliomas
  • growths in sc?
459
Q

what are the features of nf2

A
  • bilateral acoustic neuromas often leading to hearing loss
  • prenatally - may have bilat cestibular schwanommas
  • skin neurofibromas
  • eye lesions
  • spinal lesions
460
Q

what are some of the investigations that may be done to diagnose neurofibromatosis

A 
radiography
ct
mri
eeg
slit lamp examination
genetic testing
histology
461
Q

what is the treatment for neurofibromatosis

A
  • surgical removal of tumours e.g. acoustic neuromas
  • chemo for optic pathway gliomas
  • specialist team
  • management of hearing loss
462
Q

what is multiple sclerosis

A

an inflammatory demyelinating condition of the cns which eventually leads to axonal loss, neurodegeneration

463
Q

what is the epidemiology of ms

A

affects f more than m
f 25-35
more frequent in populations further away from equator

464
Q

list some of the presentations of ms

A
  • optic nerve inflammation - visual changes
  • diplopia
  • if affecting brainstem - can cause cranial nerve deficits
  • ataxia
  • vertigo
  • weakness, clumsiness
  • bladder, bowel dysfunction
  • pain
  • sensory loss
465
Q

what do the lesions of ms look like on imaging

A

round/oval shaped, well defined, 3-6mm enhancement

466
Q

how is ms diagnosed

A

at least 2 episodes of symptoms occuring at two different points in time and involving different areas of the cns (lesions)
MR brain revealing lesions

467
Q

what are the different patterns of ms presentation/progression

A
  • relapsing-remitting
  • relapsing-remitting with persistent deficit
  • primary progressive
  • progressive relapsing
468
Q

what is the treatment and management of MS

A
  • education, mdt
  • treat exacerbations with corticosteroids, iv Ig, plasma exchange
  • pain control, anitspasmodics
  • mamaneg impaired bladder/bowel function
  • immune-modulating drugs - B interferon, capoxone 1st line; natalizumab/mitoxantron/fingolimod 2nd line
  • physio
  • psychological support, counselling
  • avoid obesity and sedentary state
469
Q

what is the presenation of cn1 disorder

A

anosmia, all foods taste the same

470
Q

what is the presentation for cn2 disorder, depending on anatomical position of lesion

A
  • ipsilateral monocular blindness (migraine, embolism of opthalmic artery, GCA, infarction of optic nerve/retina)
  • bitemporal hemionopia (pituitary gland tumour)
  • contralateral homonymous hemionopnia (POCS, SOL in post part of brain…)
471
Q

what are the functions of the cn3

A
  • looking up (superior rectus)
  • looking down (inferior rectus)
  • adduction (medial rectus)
  • looking up in adducted position (inferior oblique)
472
Q

what is the function of cn4

A
  • looking down in adducted position (superior oblique)
473
Q

what is the function of cn6

A
  • abduction (lateral rectus) - aka abducens nerve
474
Q

what is the presentation of cn3 palsy

A

dilated pupil, down and out, weakness of eye movement

475
Q

what is the presentation of cn4 palsy

A

incomplete depression of the eye in the adducted position

476
Q

what is the presentation of cn6 palsy

A

unable to abduct eye

477
Q

what is the presentation of horner’s syndrome

A

minor ptosis (due to small innervation of LPS), constricted pupil, enophthalmos, loss of sweating on affected side of face

478
Q

what is the innervation of the LPS

A

CNIII mostly, with very small proportion supplied by sns

479
Q

what autonomic supply does the facial nerve supply

A

lacrimal and salivary gland

480
Q

what does the facial nerve supply

A

muscles of face
autonomic supply
afferent taste fibres for ant 2/3 tongue
muscles of inner ear

481
Q

hows does bells palsy present

A

usually, after some aching around the ear, facial weakness develops quite quickly, causing facial droop on one side (including the forehead muscles)
usually proximal enough to affect hearing and taste
drainage of tears from eye may be affected

482
Q

list some of the symptoms of cnviii dysfunction

A

deafness, tinnitus, vertigo, loss of balance, nystagmus, ataxia

483
Q

what does the cnxi supply

A

scm and part of trapezius

484
Q

what do cnix and x supply

A

mouth and throat for normal speech and swallowing.
glossopharyngeal - taste perception in post 1/3 tongue
autonomic functions
vagus - reucrrent laryngeal nerve

485
Q

what is bulbar palsy

A

where there is bilat impairment of cnix, x, xii, causing syarthria, dysphagia, dysphonia

486
Q

where is the recurrent laryngeal nerve vulnerable

A

neck and mediastinum e.g. aortic aneurysm, tumours, malignant nodes, surgery

487
Q

list some of the common pathologies affecting the nerve root

A
  • prolapsed intervertebral disc
  • herpes zoster
  • metastatic disease
  • primary tumours/neurofibromas causing compression
488
Q

what are the symptom of a prolapsed disc

A
  • pain
  • reduced rom
  • reduced slr
  • sensory loss in affected dermatome
  • weakness, wasting with time
  • loss of tendon reflexes in appropriate segmental value
489
Q

list some of the different intervertebral disc diseases

A
  • acute disc prolapse
  • gradual multiple disc hermiation
  • cervical myelopathy
  • cauda equina
490
Q

which diseases tend to affect the sacral plexus of nerves

A

gynaecological - as plexus runs down iliopsoas, and over pelvic brim

491
Q

what is meralgia paraesthesia

A

chronic entrapment of lateral cutaneous nerve of thigh as it penetrated the inguinal ligament of deep fascia around asis
paraesthesia and partial numbness over anterolateral aspect of the thigh

492
Q

what is mnd

A

disease where there is selective loss of lower motor neurones from brainstem together with upper motor neurones from motor cortex of brain.
special senses, cerebellar and sensory functions are left INTACT

493
Q

where does mnd first tend to present

A

bulbar muscles or the limbs

initially either umn or lmn,

494
Q

what are the key features of mnd

A
  • muscle weakness
  • muscle wasting
  • fasciculation
  • bulbar muscles affected
  • exaggerated reflexes
  • no loss of sensation
495
Q

what happens as mnd progresses

A

becomes more generalised and tends to affect but umn and lmn
inanition (exhaustion by lack of nourishment) or chest infections (due to involvement of bulbar/resp muscles)account for most deaths

496
Q

what is the main drug treatment for mnd

A

Riluzole - a glutamate antagonist which blocks a specific channel associated with damaged neurones, slows progression and increases survival

497
Q

list some of the ways to improve QOL in patients who have mnd

A
  • explanation and education
  • self help groups
  • drugs for cramps, drooling (hyoscine hydrobromate), depression, stiffness
  • salt, dietician, peg?
  • communication aids for dysarthria
  • non invasive protable ventilators for resp muscle weakness
  • ot - alterations to house e.g. rails, ramps
  • nursing help and respite care
  • timely discussion about terminal care
498
Q

is it ul or ll that tends to be affected more in peripheral neuropathy

A

legs and feet

499
Q

list some of the causes of peripheral neuropathy

A
  • commonly diabetes mellitus and alcohol
  • vitamin deficiency B1, B12
  • leprosy
500
Q

list osme of the neural effects of diabetes mellitus

A
  • sensory neuropathy
  • if affects autonomic ns - abnormal pupils, postural hypotension, impaired bladder/bowel/sexual function
  • dry feet
501
Q

what is charcot marie tooth

A

inherited condition where there is demyelination and remyelination of nerves - causing pes cavus, muscles weakness and wasting

502
Q

what does romberg’s test look for

A

proprioception

503
Q

what is duchenne muscular dystrophy/how it presents

A

inherited x linked condition, which usually presents with muscular weakness, gower’s signs (prox myopathy), pesudohypertrophy of calf muscles, before the age of five

504
Q

what are some of the complications of dmd

A

chest infections
cardiomyopathy
profound muscle weakness

505
Q

what tests can be done to diagnosis dmd

A
  • prenatal detection
  • genetic
  • elevated level of ck in blood
506
Q

what are the hallmark features of parkinsons

A
  • bradykinesia
  • rigidity
  • resting tremor
  • postural instability
507
Q

list some of the non-motor problems associated with parkinsons disease

A
  • salivation
  • sweating
  • pain
  • sphincter problems
  • sleep disorders
  • smell
  • mood
  • psychosis
  • dementia
508
Q

list the different classes of agents used to treat parkinsons disease

A
  • levodopa
  • dopamine receptor agonists
  • MAOB inhibitors
  • COMT inhibitors
  • anticholinergics
509
Q

what is the main use of anticholinergics in parkinsons

A

tremor

510
Q

list some of the features of psychosis in Parkinsons

A

complex visual hallucinations

paranoid ideation

511
Q

list some of the hyperkinetic movements disorders

A
  • huntingtons
  • chorea
  • dystonia
  • hemiballismus
  • tremor
  • myoclonus
  • tic
512
Q

tardive dyskinesia is a side effect from which drugs

A

antipsychotics

513
Q

what are the features of tremor in parkinsons patients

A

resting tremor, suppressed by purposeful movement

514
Q

what is the typical tremor in cerebellar disease

A

mainly on movement or sustained posture

515
Q

what is the pathophysiology of parkinsons disease

A

damage of the dopamine-producing neurones in the substantia nigra, affecting the nigrostriatal pathways

516
Q

list some of the early symptoms of parkinsons disease

A
  • aches and pains
  • disturbed sleep
  • anxiety and depression
  • slower dressing
  • slower walking
517
Q

list some of the later symptoms of parkinsons disease

A
  • tremor
  • difficulty turning in bed
  • stooping or shuffling
  • softer speech
  • spidery handwritting, micrographia
518
Q

list some of the signs that may be observed when seeing a parkinsons patient

A 
reduced arm swing when walking
slowing of movements
stooping
pedestal turning
hypomimia
increased tone throughout range of movement
constant resistance (lead pipe)
519
Q

why are patients with PD likely to have falls

A

posture and movement changes

orthostatic hypotension more likely - due both to PD and the drugs PD patients take

520
Q

describe how dementia in PD presents

A

patients start to lose thread of conversation, memory loss, confusion, visual hallucinations
may even have sleep and behavioural disturbance

521
Q

list some levodopa drugs

A

duodopa, caramet, madopar and sinemet

522
Q

list the MOAB inhibitor drug

A

selegiline

523
Q

list the COMT inhibitor drug

A

entacapone

524
Q

list the glutamate antagonist used in pd

A

amantadine

525
Q

list the cholinergics used in pd

A

rivastigmine, donepezil

526
Q

list some dopamine agonists

A

aripiprazole, bromocriptine, rotigoxine, mirapexin

527
Q

what are some of the cautions/advice that should be given to patients who are prescribe Levodopa drugs for PD

A

may work very well initially, but effects can wear off after a few years.
May give dyskinetic effects when first administered, and wear off by the time of the next dose

528
Q

give a caution given to patients started on dopamine agonists

A

may experience compulsive/impulsive behaviour

529
Q

how are COMT inhibitors, and glutamate agonists used

A

in conjunction with Levodopa drugs

530
Q

list some of the non-oral treatments for PD

A
  • deep brain stimulation
  • apomorphine
  • transdermal patch (if problem with PO use)
  • duodopa - intestinal gel (for severe fluctuations)
531
Q

how is apomorphine used in PD

A

used as subcut injection in patients who experience a loss of body movements, slow movements of loss of control of body movements

532
Q

list some of the different types and causes for dementia

A
  • alzeihmer’s
  • lewy body
  • vascular
  • intracranial pathology
  • alcohol and drugs
  • hiv-aids, syphillis, cjd, vit B deficiency
533
Q

list some of the memory-related symptoms of dementia

A
  • disorientation, especially to time
  • impaired knowledge of recent events
  • forgetfulness, repeating self, loses things around house
  • increasing dependence on familiar surroundings and daily routine
534
Q

list some of the symptoms relating to thinking/understanding/reasoning of dementia

A
  • poor organisation
  • ordinary jobs poorly executed
  • slow, inaccurate, circumstantial conversation
  • poor comprehension
  • difficulty in making decisions or judgements
  • increasing dependence on relatives
535
Q

list some of the dominant hemisphere functions of dementia

A
  • decreased vocabulary, overuse of simple phrases
  • difficulty naming and word finding
  • occassional misuse of words
  • reading, writing, spelling problems
  • difficulties in calculation and inability to handle money
536
Q

do patients with dementia usually have insight

A

no

537
Q

what is the cause of vascular dementia

A

usually widespread small vessels disease - due to htn, dm etc. diffuse damage

538
Q

what are the investigations of someone with dementia

A

accurate history and collateral history
full physical examination
test memory ,language, spatial orientation, reasoning
carefully examine mental state, mmse
explore s and s of anxiety and depression
ct/mri scanning may be needed

539
Q

how may someone with a chronic subdural present

A

may not recall causative head injury, but can become drowsy and intellectually impaired over a few days
focal neuro signs appear late

540
Q

list some of the routine bloods that should be done for dementia

A
  • fbc
  • esr
  • u and e, glucose, calcium, lfts, tfts
  • syphillis serology
  • vit b12
  • antinuclear ab
541
Q

list some of the ways in which dementia may be managed

A
  • careful explanation
  • assess social situation and family’s ability to provide support
  • old age psychiatry and community services
  • voluntary care organisations, support groups e.g. alzeihmer’s society
  • careful trial of cholinesterase inhibitor e.g. donepezil
  • seeking power of attorney and legal advice
  • treat coexisting anxiety and depression

Elderly Care (1 decks)

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