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Phase 2 Mine > Revision List Neurology > Flashcards

Revision List Neurology Flashcards

1
Q

Depression

A

It is characterized by persistent sadness and a lack of interest or pleasure in previously rewarding or enjoyable activities. It can also disturb sleep and appetite; tiredness and poor concentration are common.

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2
Q

What are the risk factors for depression?

A
  1. Stressful events - bereavement/ relationship breakdown
  2. Personality - low self esteem/ overly self critical and other certain personality traits
  3. Family history
  4. Giving birth - hormonal and physical changes and added responsibility
  5. Loneliness
  6. Alcohol and drugs - too much alcohol and drugs affect chemistry of brain
  7. Illness - higher risk of depression if physically limited
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3
Q

Diagnostic criteria of depression?

A

2 main and at least 3/4 minor symptoms.

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4
Q

What are the 2 main symptoms of depression?

A
  1. Persistent sadness or low mood nearly every day

2. Loss of interest or pleasure in most activities

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5
Q

Other symptoms of depression

A
  1. Fatigue/loss of energy
  2. Worthlessness, excessive or inappropriate guilt
  3. Recurrent thoughts of death, suicidal thoughts or actual suicide attempts
  4. Diminished ability to think/ concentrate or increased indecision
  5. Insomnia/hypersomnia
  6. Psychomotor agitation or retardation
  7. Change in appetite and or weight loss
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6
Q

What test is used to assess depression in GP settings?

A

PHQ9 or GAD7

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7
Q

Lifestyle modifications to treat depression?

A
  1. Drink less alcohol
  2. Eat healthily
  3. Exercise more
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8
Q

Non pharmacological management of depression?

A
  1. CBT
  2. Interpersonal therapy
  3. Electroconvulsive therapy
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9
Q

Pharmacological management of depression?

A

SSRI?

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10
Q

What are SSRI? How do they work?

A

Selective serotonin reuptake inhibitor

Limiting its reabsorption (reuptake) into the presynaptic cell, increasing the level of serotonin in the synaptic cleft

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11
Q

Example of an SSRI?

A

Sertraline

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12
Q

Risk factors for subarachnoid haemorrhage?

A
  1. Smoking
  2. Hypertension
  3. Bleeding disorders
  4. Polycystic kidney disease
  5. Ehler Danlos
  6. Coarctation of aorta
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13
Q

Clinical presentation of subarachnoid haemorrhage?

A
  1. Thunderclap headache
  2. Vomiting, collapse, seizure, coma
  3. Neck stiffness
  4. Papilloedema/vision loss/ diplopia
  5. Kernig’s and Brudzinki’s sign
  6. Focal neurological: fixed dilated pupil - CN3 palsy in posterior communicating artery
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14
Q

What is Kernig’s sign?

A

When thigh flexed - knee extension is painful/stiff

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15
Q

What is Brudzinki’s sign?

A

When neck is flexed, hip and knee flex

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16
Q

Diagnosis of subarachnoid haemorrhage?

A
  1. ABG - exclude hypoxia
  2. CT Head - star shape lesion
  3. CT angiography
  4. Lumbar puncture - blood initially then xanthochromic
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17
Q

Treatment of subarachnoid haemorrhage?

A
  1. Refer to neurosurgeon
  2. Maintain cerebral perfusion - IV fluid if BP <160
  3. Calcium channel blocker - nimodipine IV
  4. Endovascular coiling - preferred to surgical clip promote thrombosis and aneurysm ablation
  5. Surgery - intracranial stents and balloon remodelling for wide necked aneurysms
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18
Q

What are nimodipine used for?

A

Decreased vasospasm and morbidity from cerebral ischaemia

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19
Q

Complications of SAH?

A
  1. Rebleeding
  2. Cerebral ischaemia due to vasospasm
  3. Hydrocephalus
  4. Hyponatraemia
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20
Q

How long do trigeminal neuralgia last?

A

1-180s

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21
Q

Triggers for trigeminal neuralgia?

A
  1. Washing affected area
  2. Shaving
  3. Eating/talking
  4. Dental prostheses
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22
Q

Treatments for trigeminal neuralgia?

A
  1. Carbamazepine

2. TCA - amitriptyline

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23
Q

Define Parkinson’s disease?

A

Degenerative movement disorder characterised by decrease in dopamine in the susbtantia nigra

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24
Q

What is Parkinson’s disease characterised by?

A
  1. Bradykinesia/Akinesia
  2. Resting tremor
  3. Rigidity
25
Q

Epidemiology of parkinson’s?

A
  1. M>F and prevalence increase with age - 55-65 years
26
Q

What can Parkinson’s present as before developing motor symptoms?

A
  1. Anosmia
  2. Depression/anxiety
  3. Ache and pain
  4. REM sleep disorders
  5. Hypotension and constipation/ urinary urgency
27
Q

Describe Parkinson’s tremor in more detail?

A
  1. Worse at rest
  2. Unilateral/asymmetrical
  3. Pill rolling thumbs
  4. Writing smaller
  5. 4/6 cycles per sec - slower than cerebellar
  6. Improved by voluntary movements/ anxiety worsens
28
Q

Describe Parkinson’s rigidity in more detail?

A
  1. Extrapyramidal lesions - increase tone in limbs and trunk
  2. Limbs resist passive extension throughout movement
  3. Can cause pain and problems when turning in bed
29
Q

Describe Parkinson’s brady/akinesia in more detail?

A
  1. Difficulty initiating movement and slow and low amplitude
  2. Problems doing fine movements
  3. Monotonous hyphonic speech micrographia
30
Q

Name two hardware problems:

A
  1. Huntington’s

2. Parkinson’

31
Q

Name 3 software problems:

A
  1. Dystonia
    Essential tremor
  2. Tourette
32
Q

Describe the gait in Parkinson’s?

A
  1. Shuffling gait - small steps
  2. Reduced arm swing - asymmetrical
  3. Drag foot with flexed trunk - stooped posture
  4. Difficulty initiating movement and turning
33
Q

What are some non motor symptoms of Parkinson’s?

A
  1. Difficulty swallowing –> late presentation as aspiration pneumonia
  2. Depression/constipation/increased urinary frequency
  3. Psychiatric problems: phobia, anxiety disorder
34
Q

Aetiology of Parkinson’s disorders?

A
  1. Environment - pesticides, MPTP
  2. Genetics: mutations in the alpha synuclein gene, parkin gene
  3. Oxidative stress and mitochondrial dysfunction
35
Q

Pathophysiology of Parkinson’s?

A
  1. Decrease dopaminergic neurones in substantia nigra pars compacts
  2. Decreased striatal dopamine levels
  3. Neuronal inclusions of Lewy bodies - contains tangles of alpha synuclein and ubiquitin
    - -> gradually more widespread
36
Q

Treatment of Parkinson’s?

A
  1. Levodopa oral + decarboxylase inhibitor e.g. co-beneldopa
  2. Dopamine agonists - ropinirole, pramiprexole
  3. Monoamine oxidase B inhibitors - rasigiline/seligiline
  4. Catechol-O-methyl transferase - entacapone, tolcapone
  5. SSRI Tx depression etc…
37
Q

How do Levodopa work?

A

Dopamine precursor that can cross BBB to increase dopamine levels in SN

38
Q

How do decarboxylase inhibitors work?

A

Decreasse peripheral conversion of L-Dopa to dopamine - maximise dose and decrease SE peripherally

39
Q

SE of Levodopa+decarboxylase inhibitors?

A

Nausea/vomiting, hallucination, compulsive behaviour

40
Q

How do dopamine agonists work?

A

Stimulates dopamine receptors in the SN

41
Q

SE of dopamine agonists?

A

Drowsy, nausea/vomiting, hallucinations, compulsive behaviour

42
Q

How do MAO/COMT inhibitors work?

A

Decrease breakdown of catecholamines

43
Q

SE of MAO inhibitors?

A

Postural hypotension

AF

44
Q

SE of COMT inhibitors?

A

Esp tolcapone = liver damage

45
Q

Late stage PD motor complications?

A
  1. Wearing off: decrease efficacy over time even when dose is increased
  2. On-dyskinesia: hyperkinetic, choreiform movement whenever drugs work
  3. Off-dyskinesia: fixed, painful dystonic posture
  4. Freezing - unpredictable loss of motility
46
Q

Factors that indicate that it is not Parkinson’s?

A
  1. Incontinence
  2. Dementia
  3. Symmetry
47
Q

Definition of motor neurone disease

A

Cluster of major degenerative diseases characterised by selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells.

48
Q

Pathophysiology of MND?

A
  1. Mainly affects anterior horn cells.
  2. Relentless unexplained destruction of UMN and anterior horn cells in brain and spinal cord.
  3. Production of ROS –> damage DNA, lipids, proteins
49
Q

Difference between MND and myasthenia gravis?

A

Eye movements affected in myasthenia gravis

50
Q

MND vs MS/polyneuropathy?

A

No sensory loss or sphincter dysfunction in MND.

51
Q

4 types of MND

A
  1. Amyotrophic lateral sclerosis
  2. Progressive muscular atrophy
  3. Progressive bulbar palsy
  4. Progressive lateral sclerosis
52
Q

Clinical presentation of amyotrophic lateral sclerosis?

A
  1. Loss of motor neurones in motor cortex and anterior horn of spinal cord
  2. UMN signs: Plantar upping, spastic gait
  3. LMN signs: wasting/fasciculation/ foot drop/wrist drop +/- proximal myopathy, weak grip
  4. Split hand signs: thenar wasting, hypothenar wasting = less
  5. Cramps - common but not specific
53
Q

Clinical presentation of progressive muscular atrophy?

A
  1. Weakness, muscle wasting, fasciculation - start in one limb and spread
  2. Distal muscles first
54
Q

Clinical presentation of progressive bulbar palsy?

A
  1. Lower cranial nerves 9-12, dysarthria, dysphagia, nasal regurgitation of fluids and choking
  2. LMN lesion of tongue + swallow + talk muscles –> flaccid, fasciculating tongue. speech - hoarse quiet nasal
55
Q

Clinical presentation of progressive lateral sclerosis?

A
  1. Loss of Betz cells in motor cortex
  2. Spastic weakness of leg
  3. Progressive tetraparesis amd pseudobulbar palsy.
56
Q

Differential diagnosis of MND?

A
  1. MS or polyneuropathy
  2. Myasthenia gravis
  3. Diabetuc amytrophy
  4. Guillan Barre syndrome
  5. Spinal cord tumour
57
Q

Diagnostic criteria for MND?

A
  1. LMN + UMN signs in 3 regions
  2. LMN + UMN signs in 2 regions = probable
  3. LMN +UMN in 1 region/UMN in >1 region + EMG acute denervation needs labs support
58
Q

Investigations used to identify MND?

A

Brain/cord MRI - exclude structural causes

  1. Lumbar puncture - exclude inflammatory causes
  2. Nerve conductions studies and electromyography –> denervation of muscle due to degeneration of LMN’s - EMG confirmation
59
Q

Treating MND?

A
  1. Antiglutamergic drugs: oral riluzole
    Na+ channel blocker inhibits glutamate release
  2. Drool due to bulbar palsy - oral propantheline/ amytriptilline
  3. Dysphagia - blend food, NG tube, PEG
  4. Spasm - oral baclofen

Phase 2 Mine (12 decks)

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