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3a > Geratology > Flashcards

Geratology Flashcards

1
Q

Describe the presentation of a stroke

A
  • Sudden onset
  • limb weakness
    -Facial weakness
    -Dysphasia
    -Visual field defect
    -Sensory loss
    -Ataxia and vertigo
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2
Q

In stroke what does ataxia and vertigo indicate?

A

The posterior circulation is affected

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3
Q

List the risk factors for stroke

A

-Previous TIA
-AF
-carotid artery stenosis
-Hypertension
-Diabetes
-High cholesterol
-Family history
-Smoking
-Obesity
-Vasculitis
-Thrombophilia
-Combined oral contraceptive

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4
Q

In which people does the combined oral contraception increase the risk of stroke?

A

The risk is higher if the person has migraines, is over 34, smokes or has a history of a stroke/TIA

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5
Q

What is important to do before treating someone for a stroke?

A

Exclude hypoglycaemia

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6
Q

When using the ROSIER tool to assess for stroke what score indicates a stroke being likely?

A

Above 1

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7
Q

Which symptoms on the ROSIER tool give a -1 score?

A

-Loss of consciousness
-Seizure activity

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8
Q

Which symptoms of the ROSIER tool give a +1 score?

A

-Asymmetrical facial weakness
-Asymmetrical arm weakness
-Asymmetrical leg weakness
-Speech disturbance
-Visual field defect

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9
Q

Describe the findings of a non contrast CT head with an ischaemic stroke.

A

-Low density grey and white matter in 1 area which may take time to show up
-Hyperdense artery, visible immediately with a visible clot

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10
Q

Describe the findings of a non contrast CT head with a haemorrhagic stroke.

A

Areas of hyper density (blood), surrounded by low density (oedema)

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11
Q

Describe the management of an ischaemic stroke

A

-Exclude hypoglycaemia
-Immediate non contrast CT brain
-300mg aspirin
-Admission to specialist stroke centre
-Thrombolysis with alteplase (within 4.5 hours of onset)
-Thrombectomy (within 24 hours)
- Investigate for carotid artery stenosis and AF

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12
Q

What is the mechanism by which alteplase works?

A

It’s a tissue plasminogen activator

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13
Q

What are the absolute contraindications of alteplase?

A

-Previous intracranial haemorrhage
-Seizure at onset of stroke
- intracranial neoplasm
-Suspected subarachnoid haemorrhage
-Stroke caused by traumatic brain injury preceding 7 days
-Gi bleed preceding 3 weeks
-active bleeding
-pregnancy
-oesophageal varices
-Uncontrolled hypertension (2oo/120hg)

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14
Q

What are the relative contraindications of alteplase?

A

-concurrent anticoagulation, INR above 1.7
-Haemorrhagic diatheses (tendency to bleed)
-diabetic haemorrhagic retinopathy
-suspected intracardiac thrombus
-major surgery preceding 2 weeks

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15
Q

Why shouldn’t lowering BP be done generally in ischaemic stroke?

A

It will worsen the ischaemia

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16
Q

In ischaemic stroke when can hypertension be treated?

A
  • In hypertensive emergency
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17
Q

Which areas of circulation can a thrombectomy be used?

A

Proximal anterior circulation or proximal posterior circulation (basilar or posterior cerebral artery)

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18
Q

What can be used to identify the area where a clot is in circulation?

A

Computed tomographic angiography or magnetic resonance angiography

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19
Q

How are haemorrhagic stroked treated?

A
  • exclude hypoglycaemia
  • lower blood pressure
  • reverse effects of anticoagulant medicines
    -emergency craniotomy
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20
Q

In patients with AF when is anticoagulation resumed after a stroke?

A

14 days after

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21
Q

How is carotid stenosis investigated and treated?

A

-carotid ultrasound
-carotid artery endarterectomy/ angioplasty/ stenting

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22
Q

Describe secondary stroke prevention

A
  • Clopidogrel 75mg/day
    -Atorvastatin 20-80mg delayed 24 hours
    -Bp and diabetes control
    -altering modifiable RF
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23
Q

Define a TIA

A

Temporary neurological dysfunction lasting less than 24 hours (usually less than 1hour)

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24
Q

In a TIA which areas are ischaemic?

A

could be:
-focal brain
-spinal
-retinal

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25
Q

What is a crescendo TIA and what does it indicate?

A

2 or more TIA’s within a week, high risk of stroke

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26
Q

What is the management of TIA?

A

-3oomg/day aspirin
-referral for specialist assessment within 24 hours if it happened within the past week
-referral for specialist assessment within a week if it happened more than a week ago
- diffusion weighted MRI
-carotid imaging

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27
Q

Describe the mechanism of aspirin

A

-NSAID
-blocks cyclooxygenase-1 and 2, cyclooxygenase-1/2 is responsible for thromboxane synthesis
- stops platelet aggregation

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28
Q

Describe the mechanism of clopidogrel

A

-It’s a thienopyridine
-Inhibits platelet activation by being a P2Y12 adenosine diphosphate receptor antagonist

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29
Q

What drug is 1st line in an ischaemic stroke?

A

Clopidogrel

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30
Q

What can make clopidogrel less effective?

A

Repeated PPI use

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31
Q

Describe benign paroxysmal positional vertigo

A

-triggered by head movement
-peripheral cause
settles after 20-60 seconds
-no hearing loss or tinnitus

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32
Q

Describe the pathophysiology of benign paroxysmal positional vertigo

A

-Calcium carbonate crystals (otoconia) displaced in the semi-circular canals
-Disrupts normal flow of endolymph, disrupts the vestibular system= vertigo

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33
Q

Which semi-circular canal are the calcium carbonate crystals usually displaced into?

A

posterior semi-circular canal

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34
Q

What can displace the calcium carbonate crystals?

A

Viral infection, head trauma, ageing, idiopathic

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35
Q

describe the dix-hallpike manoeuvre

A

-Move head to initiate vertigo
-check pain in the neck
-check for rotational nystagmus towards affected ear

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36
Q

What is the main treatment for benign paroxysmal positional vertigo?

A

The Epley manoeuvre, effective in 80% of patients

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37
Q

What are brandt-daroff exercises?

A

Exercises performed at home to improve paroxysmal benign positional vertigo symptoms at home.

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38
Q

what is delirium?

A

Impaired mental state

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39
Q

What causes delirium? (PINCH ME)

A

Pain/post surgery
Infection
Nutrition
Confusion/ constipation
Hydration/ hypoxia
Medication
Environment / electrolyte disturbances

and renal failure

40
Q

What makes someone more likely to be experiencing delirium than dementia?

A

-Acute
-Impaired consciousness
-fluctuating symptoms (worse at night)
-abnormal perception
- agitation and fear
-delusions

41
Q

What are the types of delirium?

A

Hyperactive, hypoactive and mixed state

42
Q

Describe hypoactive delirium

A

sluggish
drowsy
less reactive
sullen
looks withdrawn

43
Q

List risk factors for delirium

A
  • recent surgery (narcotic pain relief, benzodiazepines, hypnotics, anticholinergics)
    -underlying disease
    -chronic fatigue
    -co-morbities (dementia, constipation, pneumonia, UTI
44
Q

How to de- escalate a situation with delirium?

A

Provide routine
glasses
hearing aids
constipation
sleep

45
Q

In ICU what is used to sedate people?

A

dexmetomide

46
Q

What is the most common type of dementia in the UK?

A

Alzheimer’s

47
Q

What is the peak incidence of Alzheimer’s?

A

70

48
Q

Describe the genetic factors involved in Alzheimer’s disease.

A
  • 5% inherited autosomal dominant
    -mutations in the amyloid precursor gene (chromosome 21), presenilin 1(chromosome 14), presenilin 2(chromosome 1)
    -apoprotein E, allele E4
    -down syndrome
49
Q

What is apoprotein E?

A

Cholesterol transport protein

50
Q

Describe the macroscopic pathological changes in Alzheimer’s

A

Cerebral atrophy (particularly in the cortex and hippocampus)

51
Q

Describe the microscopic pathological changes in Alzheimer’s

A

-cortical plaques
-deposition of A-beta- amyloid
-Intraneuronal neurofibrillary tangles

52
Q

What causes neurofibrillary tangles in Alzheimer’s?

A

abnormal aggregation of tau protein, hyperphosphorylation also linked

53
Q

What is the roll of tau protein?

A

Interacts with tubulin to stabilise microtubules

54
Q

what is there a deficit of in AD?

A

acetylcholine

55
Q

Describe the general features of AD

A

-occurs over months/ years
-difficulty with daily living

56
Q

Describe the cognitive impairment associated with AD

A

-memory loss
-difficulty learning new information
-vague with dates
-reasoning and communication
-difficulty making decisions
-dysphasia

57
Q

Describe the behavioural and psychological features associated with AD

A

-depression
-agitation
-psychosis
-apathy
-disinhibition

58
Q

Describe the non-pharmacological treatments for AD

A

-social prescribing
-group cognitive stimulation therapy (mild and moderate)
-group reminiscence therapy

59
Q

describe the pharmacological treatment for AD

A
  • 3 acetylcholinesterase inhibitors
    -memantine
60
Q

When are acetylcholinesterase inhibitors used in AD?

A

in mild- moderate Alzheimer’s

61
Q

Name 3 acetylcholinesterase inhibitors

A

-Donepezil
-galantamine
-rivastigmine

62
Q

What is contraindicative of acetylcholinesterase inhibitors?

A

bradycardia

63
Q

What is a common side effect of anticholinesterases?

A

insomnia

64
Q

What class of drug is memantine?

A

NMDA receptor antagonist

65
Q

When is memantine used?

A

-moderate Alzheimer’s where acetylcholinesterase’s aren’t tolerated
- add on in moderate/severe Alzheimer’s
-monotherapy in severe Alzheimer’s

66
Q

Are antidepressants used to treat low mode is AD?

A

no

67
Q

What are used to treat patients at risk of hurting themselves or other who have AD?

A

antipsychotics

68
Q

How common is vascular dementia?

A

2nd most common type of dementia

69
Q

List risk factors of vascular dementia

A

-TIA history
-AF
-Hypertension
-DM
-hyperlipidaemia
-smoking
-obesity
-CHD
-FH stroke or CVD
-

70
Q

Can vascular dementia be inherited?

A

-yes
-cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

71
Q

How can vascular dementia be sub categorised?

A

-Stroke related (multi infarct or single infarct dementia)
-subcortical (small vessel disease)
-mixed (VD+ AD)

72
Q

What is the timescale for the presentation of vascular dementia?

A

-Stepwise progression
-months/years

73
Q

List the symptoms of vascular dementia

A

-Focal neurological symptoms
-Difficulty with attention / focusing
-seizures
-memory disturbances
-gait disturbances
-speech disturbances
-emotional disturbance

74
Q

How would vascular dementia be diagnosed?

A

-History and examination
-Formal screen for cognitive impairment
-Medical review to exclude prolonged medication as a cause
-MRI- infarcts in the white matter

75
Q

Describe the non pharmacological treatment for vascular dementia

A

-Cognitive stimulation
-Multisensory stimulation
-music and art therapy
-animal assisted therapy

76
Q

Describe the pharmacological treatment for vascular dementia

A

-Treat symptoms
-Address and treat cardiac risk factors
- No pharmacological treatment specifically for vascular dementia

77
Q

Describe the pathophysiology of Parkinson’s disease.

A
  • Basal ganglia coordinate habitual movements, control voluntary movements and specific learning patterns
    -Dopamine is essential to basal ganglia functioning
    -There’s a progressive reduction in dopamine which results in movement disorders
78
Q

Describe the classic triad of Parkinson’s

A

-Resting tremor
-Cogwheel rigidity ( resisting passive movement)
-Bradykinesia

79
Q

Describe the features of the tremor associated with Parkinson’s disease

A
  • worse on one side
    -4-6 hertz
    -pill rolling tremor
    -more noticeable at rest
    -better with voluntary movement
    -worse when the patient is distracted
    -using the other hand exaggerates the tremor
80
Q

Describe the features of the bradykinesia associated with Parkinson’s disease

A

-Micrographia
-shuffling gait
-festinating gait
-difficulty initiating movements
-Lots of small steps when turning
-hypomimia

81
Q

List some features of Parkinson’s disease

A

-depression
-sleep disturbance
-insomnia
-anosmia
-postural instability
-cognitive impairment and memory problems

82
Q

How can we differentiate between a Parkinson’s tremor and a benign essential tremor

A

Benign essential tremor:
- symmetrical
-6-12 hertz
-improves at rest
-worse with intentional movement
-no other Parkinson’s features
-Improves with alcohol

Parkinson’s:
-asymmetrical
-4-6 hertz
-worse at rest
-improves with intentional movement
-other Parkinson’s features
-No change with alcohol

83
Q

What has a similar presentation to Parkinson’s disease?

A

Multiple system atrophy
Dementia with lewy bodies

84
Q

Describe multiple system atrophy

A

-Various systems in the brain degenerate (including the basal ganglia) which can lead to a Parkinson’s presentation
-Cerebellar dysfunction (ataxia)
-Other area degeneration, autonomic dysfunction

85
Q

Which type of dementia is associated with Parkinson’s?

A

Dementia with Lewy bodies

86
Q

How is Parkinson’s diagnosed?

A
  • History and examination
    -UK Parkinson’s disease society brain bank clinical diagnostic criteria
87
Q

What is the approach to treating Parkinson’s?

A

Treating for symptomatic relief not for a cure

88
Q

What is the most effective treatment for Parkinson’s disease and what is it’s main issue?

A

-Levodopa
-less effective over time

89
Q

What are the side effects of Levodopa?

A

-Dystonia
-chorea (involuntary irregular movements)
-athetosis (slow continuous involuntary writhing movement)

90
Q

what is levodopa combined with when treating Parkinson’s disease and why?

A

-Peripheral decarboxylase inhibitors
-Stops L-dopa being metabolised peripherally before it reaches the brain

91
Q

What is levodopa?

A

synthetic dopamine

92
Q

Name 2 peripheral carboxylase inhibitors

A

-carbidopa
-benserazide

93
Q

name 2 combination drug names for l-dopa and a peripheral carboxylase inhibitor

A

-Co-beledopa (madopa)
-Co-carledopa (sinemet)

94
Q

What does COMPT stand for?

A

catechol-o-methyl transferase

95
Q

What does the COMPT enzyme do?

A

metabolises levodopa peripherally

96
Q

Name a COMPT inhibitor and what it’s used for

A

-Entacopone
-taken with levodopa to slow down it’s break down

97
Q
A

3a (3 decks)

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