Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3A mine > Neuro > Flashcards

Neuro Flashcards

1
Q

Name the causes of epilepsy

A

Idiopathic
Genetics
Brain trauma
Strokes
Infectious diseases
Developmental disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name the types of focal seizures

A

Simple-no LOC
Complex-Impaired consciousness
Secondary generalised-evolves into generalised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the types of generalised seizures

A

Absence-<10 seconds
Tonic clonic-stiffening and jerkin of limbs
Myoclonic-sudden jerking of lib, trunk or face
Atonic-sudden loss of muscle tone, patient falls but no LOC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name some differentials for epilepsy

A

Syncope
TIA
Migraines
Panic disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name some investigations used to diagnose epilepsy

A

Clinical history
Neuro exam
EEG
CT/MRI
Video EEG telemetry may be used in some cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When are anti-epileptics generally started

A

Following second epileptic seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Under what circumstances might antiepileptics be started after the first seizure

A

Neurological deficit
Brain imaging shows a structural abnormality
EEG shows unequivocal epileptic activity
Patient/family or carers consider risk of having further seizure unacceptable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the treatment for generalised tonic clonic seizures in males

A

Sodium valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the treatment for generalised tonic clonic seizures in females

A

Lamotrigine or levetiracetam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the first line treatment for focal seizures?

A

Lamotrigine or levetiracetam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the second line treatment for focal seizures

A

Carbamazepine
Oxcarbazepine
Zonisamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the first line treatment for absence seizures?

A

Ethosuximide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the second line treatment for absence seizures

A

Male-sodium valproate
Female-Lamotrigine or levetiracetam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which medication can exacerbate absence seizures?

A

Carbamazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the treatment for myoclonus seizures in men?

A

Sodium valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for myoclonic seizures in females

A

Levetiracetam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment for tonic/a tonic seizures in males?

A

Sodium valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment for tonic/atomic seizures in females

A

Lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name some complications of epilepsy

A

Status epilepticus-lasts >5 minutes
Psychiatric conditions
Sudden unexpected death in epilepsy(SUDEP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the side effect of topiramate

A

Abdo pain
Cognitive impairment
Confusion
Mood changes
Muscle spasm
Nausea and vomiting
Neohrolithiasis
Tremor
Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Name some side effects of lamotrigine

A

Blurred vision
Arthralgia
Ataxia
Diarrhoea
Dizziness
Headache
Insomnia
Rash
Tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the side effects of carbamazepine

A

Ataxia
Blood disorders
Blurred vision
Fatigue
Hypo stream is
Skin problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the side effects of sodium valproate

A

Ataxia
Anaemia
Confusion
Gastric irritation
Haemorrhage
Hyponatraemia
Tremor
Weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How long do you have to wait to drive after a one off seizure?

A

6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the side effects of phenytoin

A

Acne
Anorexia
Constipation
Dizziness
Gingival hypertrophy
Hirsutism
Insomnia
Rash
Tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How long do you have to wait to drive after more than one seizure?

A

1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How long doo you have to wait to drive after a change in anti-epileptic medication?

A

6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How long do you have to wait to drive a bus/coach/lorry after a one off seizure?

A

5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How long do you have to wait to drive a bus/coach/lorry for multiple seizures

A

10 seizure free yearss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Define essential tremor

A

Chronic neurological condition that typically manifests as an involuntary shaking or trembling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the epidemiology of essential tremor

A

Highly prevalent
Incidence increases with age
Age of onset earlier in those with a family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the aetiology of essential tremor?

A

Genetic and environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the inheritance pattern in the majority of essential tremor cases

A

Autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What effect does alcohol have on the symptoms of essential tremor?

A

Alcohol can temporarily improve the tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the symptoms of essential tremor

A

Main: postural or kinetic tremor which predominantly effects the upper limbs distally
Less commonly effects the head, lower limbs, voice, tongue, face and trunk
Increased tremor amplitude over time-difficulty with ADL’s
Exacerbation of tremor during ties of stress, anxiety and social interaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Name some differentials for essential tremor

A

Parkinson’s
Hyperthyroidism associated tremor
Dystonic tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What investigations should be done in someone presenting with essential tremor?

A

Mainly clinical diagnosis
Rule out other causes e.g. with Neuro imaging or TFT’s
Evaluation of functional and psychosocial disabilities performed to determine need for pharmacotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the pharmacological management of essential tremor

A

Propranolol
Primidone
Topiramate
Gabapentin
Clonazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the surgical management of essential tremor

A

DBS
Focused ultrasound thalamtomy
Radiosurgical (gamma knife) thalamotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the epidemiology of Parkinson’s disease

A

Second most common Neuro degenerative disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the aetiology and pathophysiology of Parkinson’s

A

Accumulation of Lewy bodies that lead to neuronal death of the dopaminergic cells of the substantia nigra of the basal ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are Lewy bodies?

A

Intracellular inclusions primarily composed of misfolded alpha synuclein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the triad of Parkinson’s?

A

Bradykinesia
Tremor
Lead pipe rigidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the tremor associated with Parkinson’s

A

Asymmetric 3-5Hz ‘pill-rolling’ tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Describe a Parkinsonian gait

A

Small shuffling steps, slow movement especially on initiating and turning, flexed posture
Asymmetric tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is cogwheeling?

A

Jerkiness felt when testing a patient’s muscle tone
Seen in Parkinson’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Name some non-motor features of Parkinson’s disease?

A

Autonomic dysfunction (constipation, postural hypotension erectile dysfunction)
Olfactory loss
Sleep disorders like REM behavioural disorders
Psychiatric features-depression anxiety, hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is hypomimic facies and what condition is it seen in?

A

Reduced facial expression
Parkinson’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

In a patient with features of Parkinson’s and early and prominent autonomic dysfunction what condition should be considered

A

Multiple System Atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

In a patient with features of Parkinson’s an early and prominent cognitive dysfunction what condition should b considered?

A

Dementia with Lewy bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Name some key differentials of Parkinson’s disease

A

Multiple System Atrophy
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasilar degeneration
Wilsson’s disease
Dementia pugilistica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How is Parkinson’s disease diagnosed?

A

Clinical diagnosis, supported by positive response to treatment trials
MRI head/dopamine transporter scan(DaT scan) in atypical cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What can exclude a diagnosis of idiopathic Parkinson’s disease?

A

Absolute failure to respond to 1-1.5g of levodopa daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the main medications used to treat Parkinson’s disease?

A

Levodopa
Dopamine agonists
MAO-B Inhibitors
COMT inhibitors
Amantadine
Anticholinergic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Name the peripheral side effects of levodopa

A

Postural hypotension
Nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How can peripheral side effects from levodopa treatment be reduced?

A

Co-administration of a peripheral dopa decarboxylase inhibitor like
CARBIDOPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What can be used to treat nausea from levodopa therapy?

A

Domperidone
Acts as a peripheral dopamine antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Name the central side effects of levodopa therapy

A

Hallucinations
Confusion
Dyskinesia
Psychosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Why is levodopa treatment for parkinson’s problematic?

A

Can become less effective
End-of-dose effects: motor activity progressively declines as previous dose wear off
On-off phenomenon: random fluctuations in drug effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Name some dopamine agonists

A

Ropinirole
Rotigotine
Apomorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How long does it typically take to develop complete loss of response too levodopa

A

2-5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Why is cabergoline less commonly used now?

A

Associated with lung fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What needs to be monitored for in patients on dopamine agonists?

A

Autoimmune haemolytic anaemia-regular FBC’s and DAT scans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the most potent dopamine agonist and how is it given?

A

Apomorphine
Given subcutaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Name some examples of MAO-B inhibitors

A

Selegiline
Rasagiline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How do MAO-B inhibitors work for patients with Parkinson’s disease?

A

Reduce dopamine breakdown peripherally so increase the central uptake of levodopa-often used in conjunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What should you be cautious of in patients on MAO-B inhibitors?

A

Serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Name some COMT inhibitors

A

Entacapone
Tolcapone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How do COMT inhibitors work for patients with Parkinson’s

A

Extend the use of levodopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What drug class is amantadine

A

NMDA receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Give some examples of anticholinergic agents

A

Procyclidine
Trihexyphenydil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe the surgical management of parkinson’s

A

DBS: typically done by implanting a stimulating device into a target area of the brain, often thalamus or subthalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe the prognosis of those with Parkinson’s

A

Little to no change in life expectancy
Some will have significant disability, others will not progress as fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are motor neurone diseases?

A

Groups of progressive neurological disorders that destroy motor neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Describe the epidemiology of MND

A

Slight 2:1 mile predominance
Mean onset: 50-60 years
90% of cases are sporadic, 10% familial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What condition has a notable overlap in genetics with MND?

A

Frontotemporal dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Name some upper motor neurone signs

A

Spasticity
Hypereflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the aetiology of MND

A

Misfolding of TDP-43 protein in many cases
Can be an inherited condition
2% of cases associated with a mutation in the SOD-1 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Name some lower motor neurone signs

A

Fasciculations
Muscle atrophy
Hyporeflexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the main features of ALS

A

Typically LMN signs in arms and UMN signs in legs
Familial cases: gene lies on chromosome 21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the types of MND?

A

Amyotrophic lateral sclerosis
Primary lateral sclerosis
Progressive multiple atrophy
Progressive bulbar palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the features of progressive bulbar palsy

A

Palsy of the tongue, uncles of chewing/swallowing and facial muscles due to loss of function f brain stem motor nuclei
Carries the worst prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Are eye and sphincter muscles typically involved in MND?

A

No-usually spared until late in disease course

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the most common type of MND

A

ALS-50% of patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Name some differentials of MND

A

Thyrotoxicosis syndrome
Paraprotinemias
Brain stem lesions
Cervical spondylopathy
Myasthenic syndromes
Chronic inflammatory demyelinations polyneuropathy
Multi focal mononeuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the features of primary lateral sclerosis

A

UMN signs only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe thee features of progressive muscular atrophy

A

LMN signs only
Affects distal muscles before proximal
Carries best prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Name some investigations for MND

A

TFT’s
Protein electrophoresis: rule out paraproteinaemias
MRI of brain/spinal cord-rule out brain stem lesions or cervical spondylopathy
EMG and nerve conduction studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Describe the management of MND

A

Riluzole-only disease modifying drug but only extends life expectancy by 3 months
Non invasive ventilation in patients with type 2 reps failure
Anticholinergics for drooling
Supporting feeding via NG/PEG feeding for bulbar diseaseAdvanced care plan in advance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe the prognosis for MND

A

Poor-life expectancy from diagnosis less than 5 years
Most patients die from respiratory complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is an extradural haematoma?

A

Collection of blood between the dura mater(outermost meningeal layer) and the inner surface of the skull

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Which blood vessel is most commonly involved in an extradural haematoma and why?

A

Middle meningeal artery->thin skull at the pterion overlies the middle meningeal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Describe the epidemiology of an extradural haematoma?

A

Young patients
Head injury e.g. from sports or road traffic accident

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Describe the characteristic clinical presentation/history of an extradural haematoma

A

1)Initial, brief loss of consciousness post initial trauma
2)Lucid interval(regained consciousness and apparent recovery)
3)Subsequent deterioration of consciousness and headache onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the pathology behind the lucid interval in an extradural haematoma?

A

The dura mater underneath tears, the pressure falls temporarily & the patient regains consciousness. The pressure then rebuilds = LOC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Describe the pathophysiology behind what happens after the lucid interval of an extradural haematoma

A

Haematoma expands->uncus of temporal lobe herniates around the tentorium cerebelli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What finding may be seen on physical examination of a patient with an extradural haematoma and why?

A

Fixed dilated pupil
Parasympathetic fibres of CN3 compressed by herniation of the uncus of the temporal lobe around the tentorium cerebelli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Name some differentials of an extradural haemorrhage

A

Subdural haematoma
SAH
Intracerebral haemorrhage
Cerebral contusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What investigations should be carried out to diagnose an extradural haematoma?

A

CT scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What would you expect to see on a CT head of a patient with an extradural haematoma

A

Biconvex/lentiform, hyperdense collection limited by the suture lines of the skull
Most commonly unilateral and supratentorial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe the management of a patient with an extradural haemorrhage

A

No neurological deficit: conservative management->supportive therapy, radiological observation
Definitive: craniotomy and evacuation of haematoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is a subdural haemorrhage?

A

Accumulation of venous blood in the potential space between the dura mater and the arachnoid mater of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What percentage of subdural haemorrhages are bilateral?

A

Adults: 15%
Infants: 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Describe the difference in time frame of acute, subacute and chronic subdural haemorrhages

A

Acute: symptoms develop within 48 hour post injury-rapid neurological deterioration
Subacute: Days-weeks post injury-gradual progression
Chronic: Weeks to months-may not remember specific head injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Describe the epidemiology of a subdural haematoma

A

Mostly elderly individuals :>65 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Name some risk factors for developing a subdural haemorrhage

A

> 65 years
Anticoagulants
Chronic alcohol use
Young infants-shaken baby syndrome
Recent trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Why are the elderly and alcoholics more at risk of a subdural haemorrhage?

A

Brain atrophy-> fragile, taut bridging veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the pathological process that causes a subdural heamorrhage?

A

Rupture of bridging veins within the subdural space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Describe the classical history of a patient presenting with a subdural haemorrhage

A

History of head trauma-> lucid interval-> fluctuation and eventual decline in consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What neurological signs/symptoms might a patient with a subdural haemorrhage have?

A

Altered/fluctuating mental status
Focal neurological deficits
Headaches
Memory loss
Seizures
Personality changes
Cognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What examination findings might be present in a patient with a subdural haematoma?

A

Signs of increased ICP:
-Papilloedema
-Cushing’s triad: bradycardia, widened pulse pressure, irregular respirations
Others:
-Gait abnormalities
-Hemiparesis/hemiplegia-midline shift and mass effect
-Pupillary changes-unilateral dilated pupil-CNS compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What investigation should be used to diagnose a subdural haemorrhage?

A

CT scan head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What would you expect to see on a CT scan of a patient with a subdural haemorrhage?

A

Crescent shaped, not restricted by suture lines
Hyperacute(<1hour)-isodense
Acute(<3 days)-hyperdense
Subacute(3 days-3 weeks)-isodense
Chronic(>3 weeks)-hypodense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Describe the management of a subdural haemorrhage?

A

Conservative-monitor ICP
Acute: decompressive craniotomy
Chronic: burr holes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is a subarachnoid haemorrhage?

A

Blood within the subarachnoid space(under arachnoid mater)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Describe the epidemiology of subarachnoid haemorrhage

A

Mc in females
Peak incidence: 40-50 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the most common cause of subarachnoid haemorrhage?

A

Head injury

109
Q

What is the most common cause of spontaneous subarachnoid haemorrhage?

A

Berry aneurysm-85%

110
Q

Name some risk factors for a Berry aneurysm

A

Hypertension
Adult polycystic kidney disease
EDS
Coarctation of aorta

111
Q

Name some causes of a SAH besides a Berry aneurysm

A

AVM’s
Pituitary apoplexy
Mycocytic(infective) aneurysms

112
Q

Describe the symptoms of a SAH

A

Sudden onset ‘thunderclap’ headache
History of previous less severe sentinel headache
Altered consciousness
Nausea and vomiting
Seizures
Meningism: photophobia, neck stiffness

113
Q

Name some signs that may be seen on physical examination of a patient with a SAH

A

Fundoscopy-> retinal haemorrhage
Positive Kernig’s/Brudzinski’s sign
Focal neurological deficits (CN3, 4, 6 compression-diplopia, visual disturbances, aphasia, hemiparesis/plagia)

114
Q

What is the first line investigation used to diagnose a SAH?

A

Non contrast head CT

115
Q

What would you expect to see on a CT scan of a patient with a SAH?

A

Hyperdense blood in basal cisterns/sulci

116
Q

Name some other investigations used to diagnose a SAH besides CT head

A

LP: done >12 hours post symptoms onset if CT done >6hrs symptoms onset was normal
Will show xanthochromia(RBC breakdown), may have high opening pressure
CT angiogram to diagnose aneurysm or vascular abnormalities

117
Q

What is the treatment for a SAH?

A

Oral nimodipine to prevent vasospasm and prevent ischaemic damage
Coiling, stenting, clipping of aneurysm by neurosurgeons/neuroradiologists

118
Q

Name some complications of a SAH

A

Re bleeding
Hydrocephalus
Vasospasm
Hyponatraemia from SIADH
Seizures

119
Q

Describe the prognosis of untreated SAH

A

50% mortality if untreated
Of those who survive past the 1st month-50% will be dependent on others for activities of daily living

120
Q

Name some predictive factors of prognosis for patients with a SAH

A

Age
Consciousness level on admission
Amount of blood visible on CT head

121
Q

Name some ECG changes that may be seen in a SAH

A

Transient ST elevation
Secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines

122
Q

Define a TIA

A

Sudden on set focal neurological deficit with a vascular aetiology typically lasting less than 1 hour, completely resolves within 24 hours

123
Q

Describe the epidemiology of a TIA

A

230/100,000
Peak: 70 years
More common in males

124
Q

Describe the pathology of a TIA

A

Transient disruption of blood flow to a specific region of the CNS resulting in ischaemia and focal neurological deficit

125
Q

Name some causes of a TIA and which is the most common

A

Mc: Embolism-mostly atherosclerotic plaques from the heart
Lacunar
Haemodynamic compromise(often stenosis of major artery)

126
Q

Describe the presentation of a patient presenting with a TIA

A

Any focal neurological deficits that completely resolve in <24 hours, most commonly lasting <1 hour
Aphasia/dysarthria
Unilateral weakness/sensory loss
Ataxia, vertigo, balance issues
Visual: amaurosis fugax, diplopia, homonymous hemianopia

127
Q

What is the main investigation done when investigation a TIA

A

MRI-ischaemia, haemorrhage, vascular abnormalities, any other pathologies

128
Q

Name the investigations done to diagnose a TIA

A

MRI-ischaemia, haemorrhage, vascular abnormalities
Carotid doppler US-atherosclerosis
Echocardiogram-cardiac thrombus
24 hour ECG-A fib
Bloods-glucose, lipid profile, clotting

129
Q

Describe the immediate management of a patient with a TIA

A

Immediate antithrombotic therapy-aspirin 300mg unless CI
Specialist review
<24 hour if TIA in last 7 days
<7 days if TIA in over 7 days
Admission considered if crescendo TIA or cardioembolic source

130
Q

Describe the secondary management of a patient with a TIA

A

Risk factor modification
Antiplatelet therapy-clopidogrel
Lipid modification-atorvastatin 20-80mg daily
Carotid endartectomy if severe carotid stenosis

131
Q

When should you not give aspirin to a patient with a suspected TIA

A

If any contraindications:
-Already on low dose daily aspirin
-Haemorrhagic stroke not ruled out
-Bleeding disorders

132
Q

Describe the driving rules post a TIA

A

Can’t drive until seen by specialist
Once seen by specialist, dr is happy, and no lasting effects:
-1 month for cars
-1 year for bus/lorries

133
Q

Where do Berry aneurysms most commonly occur?

A

Bifurcation points in the Circle of Willis
Anterior circle of Willis
Anterior communicating artery
Middle cerebral artery

134
Q

Which area of the brain does the anterior cerebral artery supply?

A

Middle of the brain-middle cerebral cortex

135
Q

How would an anterior cerebral artery occlusion present?

A

Contralateral loss of sensation and motor control to LOWER body

136
Q

Which area of the brain does the middle cerebral artery supply?

A

Sides-lateral cerebral cortex

137
Q

How would a middle cerebral artery occlusion present?

A

Contralateral loss of sensation and motor control to face and upper limbs
Broca’s aphasia

138
Q

Which area of the brain is supplied by the posterior cerebral artery?

A

Back-posterior cerebral cortex
Occipital lobe, thalamus etc

139
Q

How would a posterior cerebral artery occlusion present?

A

Contralateral homonymous hemianopia

140
Q

How would a basilar artery occlusion present and why?

A

Locked in syndrome
Bilateral loss of corticospinal tracts

141
Q

How would an anterior inferior cerebellar artery occlusion present?

A

Lateral pontine syndrome:
-Ipsilateral CN3 palsy
-Ipsilateral vertigo/nystagmus/deafness
-Ipsilateral poor coordination/tone/balance
Contralateral loss of pain and temperature sensation

142
Q

What is posterior inferior cerebellar stroke also known as?

A

Wallenberg’s syndrome

143
Q

How would a posterior inferior cerebellar artery occlusion present?

A

Horner’s syndrome:
-Ipsilateral ptosis, miosis, anhidrosis
Ipsilateral loss of pain and temp sensation in face
Contralateral loss of pain and temp sensation in trunk and limbs
Ipsilateral cerebellar signs: nystagmus, vertigo
Ipsilateral bulbar muscle weakness: dysphagia, dysarthria
Diplopia

144
Q

Which arteries are involved in a total anterior circulation stroke?

A

Middle cerebral/anterior cerebral

145
Q

What is the criteria for diagnosing a total anterior circulation stroke?

A

3/3 of:
-Unilateral weakness and/or sensory deficit of face, arm, leg
-Homonymous hemianopia
-Higher cerebral dysfunction(dysphagia, visuospatial disorder)

146
Q

What arteries are involved in a partial anterior circulation stroke?

A

Only part of the anterior circulation: Anterior cerebral/middle cerebral

147
Q

What is the criteria to diagnose a partial anterior circulation stroke?

A

2/3 of:
-Unilateral weakness and/or sensory deficit of face, arm ,leg
-Homonymous hemianopia
-Higher cerebral dysfunction(dysphasia, visuospatial disorder)

OR
Higher cerebral dysfunction on its own

148
Q

Which arteries are involved in a posterior circulation stroke?

A

Vertebrobasilar arteries

149
Q

Which parts of the brain are affected by posterior circulation strokes?

A

Cortical
Brainstem
Cerebellum

150
Q

What criteria can be used to diagnose a posterior circulation stroke?

A

1/5 of:
-Cranial nerve palsy and contralateral motor/sensory deficit
-Bilateral motor/sensory deficit
-Conjugate eye movement disorder(like horizontal gaze palsy)
-Cerebellar dysfunction (vertigo, nystagmus, ataxia etc)
-Isolated homonymous hemianopia

151
Q

Describe the pathology of a lacunar stroke

A

Subcortical damage secondary to small vessel disease

152
Q

What distinguishes a lacunar stroke from other strokes?

A

NO loss of higher cerebral function e.g. dysphagia

153
Q

What criteria can be used to diagnose a lacunar stroke?

A

1/4 of:
-Pure sensory stroke
-Pure motor stroke
-Sensori-motor stroke
-Ataxic hemiparesis

154
Q

What is Weber’s syndrome?

A

Stroke: upper basilar and proximal posterior cerebral
Causes ipsilateral CN3 palsy and contralateral hemiparesis

155
Q

Define a stroke

A

Sudden onset focal neurological deficit of vascular aetiology with symptoms lasting over 24 hours

156
Q

What are the 2 types of ischaemic stroke?

A

Thrombotic
Embolic

157
Q

What percentage of strokes are ischaemic and haemorrhagic?

A

Ischaemic: 85%
Haemorrhagic: 15%

158
Q

Describe the pathology behind ischaemic strokes

A

Decrease in blood flow->decreased delivery of oxygen and glucose-> energy failure and disruption of cellular ion haemostasis->excitotoxicity, oxidative stress, inflammation and apoptosis-> irreversible neuronal damage

Can also lead to cerebral oedema-> increased ICP-> secondary neuronal damage

159
Q

Name the strong risk factors fro having a stroke

A

Age
Male
Family history of stroke
Hypertension
Smoking
Diabetes
Afib

160
Q

Name the weak risk factors for having a stroke

A

Hypercholesterolaemia
obesity
poor diet
oestrogen containing therapy
migraines

161
Q

What investigations are done to diagnose a stroke?

A

ROSIER score
Non contrast CT head-areas of low density-takes longer to appear, and hyperdense artery sign visible immediately

162
Q

Describe the ROSIER score

A

-LOC/syncope: -1
-Seizure activity: -1
New, acute onset of:
-Asymmetric facial weakness: +1
-Asymmetric arm weakness: +1
-Asymmetric leg weakness: +1
-Speech disturbance: +1
-Visual field defect:+1

Stroke likely if >0

163
Q

Describe the acute management of a stroke

A

Once haemorrhagic stroke ruled out:
-Aspirin 300mg orally/rectally
-Thrombolysis
-Mechanical thrombectomy

164
Q

What is used for stroke thrombolysis?

A

IV alteplase-tissue plasminogen activator

165
Q

In what time frame can thrombolysis be done?

A

<4.5 hours from symptoms onset

166
Q

Name some contraindications to thrombolysis for stroke

A

Previous haemorrhage/current bleeding, GI bleed, recent surgery, hypertension, increased INR etc

167
Q

When can mechanical thrombectomy be done?

A

Offered within 6 hours of symptoms onset for patients with proximal anterior circulation occlusion seen on CTA/MRA
Done in conjunction with thrombolysis if <4.5 hours
Can be done on certain patients with proximal posterior circulation

168
Q

Describe the long term treatment of strokes

A

Clopidogrel 75mg (If AF was cause-warfarin/rivaroxaban)
Atorvastatin 20-80mg daily
Hypertension management
Diabetes management
Smoking cessation
Surgery-carotid endartectomy

169
Q

What surgery may be offered in some patients post stroke with carotid stenosis?

A

Carotid endartectomy

170
Q

Define Bell’s Palsy

A

Acute, unilateral, idiopathic facial nerve paralysis

171
Q

Describe the epidemiology of Bell’s palsy

A

Peak incidence: 15-45 years
More common in pregnant women

172
Q

Describe the aetiology of Bell’s Palsy

A

Unknown
Linked to HSV1
Also linked to EBV, VZV

173
Q

Describe the presentation of a patient with Bell’s Palsy

A

Acute onset of unilateral LMN facial weakness-no forehead sparing
Post-auricular otalgia
Hyperacusis
Nervus intermedius-altered taste, dry eyes/mouth

174
Q

Is there forehead sparing in patients with Bell’s Palsy? Why?/Why not?

A

NO forehead sparing
Bilateral supply to forehead from both sides of the brain

175
Q

Name some differentials for Bell’s Palsy

A

Ramsay-Hunt-prominent otalgia, vesicular rash
Stroke-forehead sparing
Guillain-Barre
Acute otitis media
Herpes zoster
Lyme disease

176
Q

How is Bell’s palsy diagnosed?

A

Mostly clinical-investigations to rule out other causes/assess extent of damage
FB, CRP, ESR
Viral serology-HSV, VZV etc
Lyme serology
Otoscopy
EG
MIR/CT

177
Q

Describe the management of Bell’s Palsy

A

50mg oral prednisolone once daily for 10 days, then taper
Aciclovir for attempted patients
Supportive therapy-artificial tears/ocular lubricants, eye tape
PT, Psychological support

178
Q

Describe what referrals should be made if a patient with Bell’s palsy isn’t improving

A

3 weeks: Urgent ENT referral
If long standing weakness(months)-plastic surgery referral

179
Q

Describe the prognosis for a patient with Bell’s palsy

A

Complete recovery in 70-80% of adults in a few weeks- months
If untreated, 15% of patients have permanent moderate-severe weakness

180
Q

What are some risk factors for poorer prognosis in a patient with Bell’s palsy?

A

Older
More severe initial facial weakness

181
Q

Describe the epidemiology of essential tremor

A

Common
Peak 40-50 years

182
Q

Describe the aetiology of essential tremor

A

50% of cases are autosomal dominant inheritance

183
Q

Describe the pathophysiology of essential tremor

A

GABA-ergic dysfunction->increased activity in cerebellar-thalamic-cortical circuit

184
Q

What are some of the symptoms of essential tremor plus?

A

Difficulty with tandem gait
Mild cognitive impairment
Slight resting tremor alongside action tremor

185
Q

How is essential tremor diagnosed?

A

Clinical diagnosis
-Bilateral upper lib action tremor
->3 years
-No other tremor elsewhere or other neurological signs

186
Q

Name some differentials for essential tremor

A

Parkinson’s disease
Hyperthyroidism associated tremor
Dystonic tremor
Spasmodic dysphonia

187
Q

What can exacerbate essential tremor?

A

Anxiety, excitement etc

188
Q

What can improve essential tremor?

A

Alcohol-temporarily

189
Q

What happens to the amplitude of essential tremor over time?

A

Increases

190
Q

Describe the 1st line pharmacological management of essential tremor

A

Propranolol
Primidone

191
Q

Describe the 2nd line pharmacological management of essential tremor

A

Gabapentin
Topiramate
Nimodipine

192
Q

Describe the surgical management of essential tremor?

A

DBS
Botulinum toxin type A injections

193
Q

Describe the prognosis of essential tremor

A

Typically worsens with increasing age
Can remain isolated or can spread, e.g. to head, voice over years
Can cause major disability

194
Q

What is myasthenia gravis?

A

Autoimmune disease affecting the NMJ causing muscle weakness the progressively worsens with activity and improves with rest

195
Q

Describe the epidemiology of myasthenia gravis

A

Affects males and females equally
Bimodal distribution: highest prevalence in F<40yrs and M>60 yrs

196
Q

Name some risk factors for myasthenia gravis

A

Thymomas
Thymic hyperplasia
Other autoimmune disorders

197
Q

What are the autoantibodies in myasthenia gravis?

A

AChR antibodies(nicotinic acetylcholine receptor antibodies)
MuSk(muscle specific kinase)
LRP4(low-density lipoprotein receptor related protein)

198
Q

What are MuSK and LRP4 antibodies responsible for?

A

Creation and organisation of AChR-inadequate AChR

199
Q

Describe the normal action of ACh at the NMJ

A

Axons release ACh from the presynaptic membrane->travels across the synapse->attaches to ACh receptors on postsynaptic membrane, stimulating muscle contraction

200
Q

Describe the pathophysiology of myasthenia gravis

A

AChR antibodies bind to postsynaptic AChR, blocked them and preventing stimulation by ACh

201
Q

Why does muscle weakness worsen with activity in patients with myasthenia gravis?

A

The more the ACh receptors are used during muscle activity, the more they become blocked-> less effective stimulation of the muscle with increased activity.
With rest, receptors are clears and symptoms improve

202
Q

Which muscles are most commonly affected by myasthenia gravis? What symptoms can these cause?

A

Ocular-ptosis, diplopia
Bulbar-dysarthria, dysphagia
Limb-proximal limb weakness weakness

203
Q

Name some drugs that can exacerbate myasthenia gravis

A

Beta blockers
lithium
phenytoin
Antibiotics

204
Q

Name some bedside tests that can be used to indicate myasthenia gravis

A

Ice pack test-ice will reduce ptosis
Encourage lots of blinking-> ptosis will worsen
Prolonged upward gazing will exacerbate diplopia
Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

205
Q

How is myasthenia gravis diagnosed?

A

Serology: AChR antibodies(85%), MuSK and LRP4 antibodies in small proportion
CT/MRI chest->thymoma/thymic hyperplasia
Edrophonium test-ACh inhibitor-> rapid, transient increase in muscle strength indicates MG

206
Q

Name some differentials for myasthenia gravis

A

Lambert-Eaton syndrome
MS
Polymyosits/dermatomyositis
Graves ophthalmoplegia
Botulism
Brainstem gliomas

207
Q

Describe the management o myasthenia gravis

A

ACh Inhibitors-pyridostigmine, neostigmine
Immunosuppression-steroids, azathioprine
Thymectomy
Rituximab if severe
In crisis: plasma exchange and IVIG

208
Q

Name some prognostic factors for myasthenia gravis

A

Age of onset
Antibody subtype
Thymus histology
response to treatment

209
Q

What is a myasthenic crisis?

A

Life threatening, acute worsening of symptoms, often triggered by another illness/infection like a URTI

210
Q

What is the main danger when someone has a myasthenic crisis?

A

Respiratory muscle failure

211
Q

When should patients with myasthenia gravis be considered for mechanical ventilation?

A

When FVC<15mL/kg

212
Q

What is the treatment for someone in a myasthenic crisis?

A

IVIG and plasmapheresis
Usual meds

213
Q

Define chronic fatigue syndrome

A

Chronic, disabling condition characterised by profound fatigue and impairment following minimal physical/cognitive effort

214
Q

Describe the epidemiology of chronic fatigue syndrome

A

Peak: 30-40 years
2:1 ratio-more common in females

215
Q

Describe the aetiology of chronic fatigue syndrome

A

Unknown
Triggers like EBV, psychological stress

216
Q

Describe the signs and symptoms of chronic fatigue syndrome

A

Extreme fatigue
Post exertional malaise
Sleep disturbances and unrefreshing sleep
Cognitive impairment
Orthostatic intolerance
Immune, neurological, autonomic, psychiatric manifestations

217
Q

Name some differentials for chronic fatigue syndrome

A

Fibromyalgia
Depression
Hypothyroidism
AI disorders

218
Q

How is chronic fatigue syndrome diagnosed?

A

Mostly clinical-rule out other causes
Bloods-
TFT’s
inflammation
infection
blood cell abnormalities
Present >3 months AND significant decrease in ability to engage in activities from before

219
Q

Describe the management for chronic fatigue syndrome

A

Refer to CFS service if >3 months
Energy conservation
Physical activity and exercise(graded exercise therapy no longer recommended)
Symptom control (pain, sleep etc)
CBT

220
Q

What is encephalitis?

A

Inflammation of the brain parenchyma

221
Q

Describe the epidemiology of encephalitis

A

Peak in >70years, <1 year
Affects males and females equally

222
Q

What is the most common cause of encephalitis?

A

HSV1

223
Q

Name some causes of encephalitis

A

HSV1/2
CMV
EBV
VZV
HIV
Autoimmune

224
Q

Describe the pathophysiology of autoimmune encephalitis

A

NMDA receptor antibody associated encaphilitis

225
Q

Which part of the brain is typically affected by HSV1 encephalitis

A

Temporal and inferior frontal lobes

226
Q

Describe the presentation of a patient with encephalitis

A

Fever
Headache
Psychiatric symptoms
Seizures
Vomiting
Focal features like aphasia
Flu-like prodromal illness

227
Q

Name some differentials for encephalitis

A

Hypoglycaemia
DKA
HE
Uremic/drug induced encephalopathy

228
Q

What investigations should be done to diagnose encephalitis?

A

Routine blood
CSF testing and PCR analysis
CT
MRI-better than CT
EEG

229
Q

What would be seen on a CSF sample of a patient with encephalitis

A

Lymphocytosis
Increased protein
Viral PCR analysis

230
Q

What could be seen on a CT of a patient with encephalitis?

A

medial temporal and inferior frontal changes
-Most commonly bilateral multifocal petechial haemorrhages

231
Q

What might be seen in the EEG of a patient with encephalitis?

A

Lateralised periodic charges at 2Hz

232
Q

Describe the treatment of encephalitis

A

10mg/kg acyclovir TDS for 2 weeks
Broad spectrum antimicrobial cover, eg ceftriaxone 2g
Supportive treatment-such as seizure treatment

233
Q

Name some side effects of acyclovir

A

GI changes
Photosensitivity
Rash
Acute renal failure
Hepatitis

234
Q

Describe the prognosis of encephalitis

A

If treatment started promptly: 10-20% mortality
Untreated: 80% mortality

235
Q

Define meningitis

A

Inflammation of the meninges(dura, arachnoid, pia). Infective and non infective causes

236
Q

Describe the epidemiology of meningitis

A

Viral(enteroviruses) most common and least severe
Bacterial: high morbidity and mortality
Fungal/parasitic-> rare except in immunosuppressed

237
Q

Name some non infective causes of meningitis

A

Malignancies-leukaemia, lymphoma
Drugs-NSAIDs, trimethoprim
Systemic inflammatory diseases-sarcoidosis, SLE, Bechet’s

238
Q

Name some symptoms of meningitis

A

Headache
Fever
nausea and vomiting
seizures
photophobia
neck stiffness
decreased consciousness

239
Q

Name some signs that might be seen in meningitis

A

Non-blanching petechial/purpuric rash->impending DIC
Kernig’s sign-?pain and resistance on knee extension
Brudzinski’s sign-passive neck flexion results in involuntary hip and knee flexion

240
Q

Name some differentials for meningitis

A

Encephalitis
SAH
Brian abscess
Sinusitis
Migraines

241
Q

When might typical signs of meningitis be absent

A

In infants with bacterial meningitis

242
Q

Name some investigations used to diagnose meningitis

A

Bloods-FBC,CRP, coag screen, cultures, PCR, glucose
ABG
CT head
lP for CSF analysis

243
Q

When should an LP not be done?

A

If there are signs of raised ICP

244
Q

Where in the spine is an LP done

A

L3/L4

245
Q

What would you expect in CSF analysis of a patient with bacterial meningitis?

A

High opening pressure
Cloudy/yellow
Low glucose vs serum(<50%)
High protein (>1g/L)
Neutrophilia

246
Q

What would you expect in CSF analysis of a patient with viral meningitis?

A

Normal opening pressure
Clear/cloudy
High glucose vs serum(>60%)
Normal protein
Lymphocytosis

247
Q

What would you expect in CSF analysis of a patient with fungal/TB meningitis?

A

High opening pressure
Cloudy and fibrous
Low glucose vs serum (<50%)
High protein (>1g/L)
Lymphocytosis

248
Q

Describe the treatment in primary care of a patient with suspected meningitis

A

IM benzylpenicillin and urgent hospital transfer

249
Q

Describe the treatment for bacterial meningitis

A

IV cefotaxime/ceftriaxone (3rd gen cephalosporin) and IV dexamethasone

250
Q

What antibiotic should be added in in patients at age extremes with suspected meningitis and why?

A

Amoxicillin-covers for listeria

251
Q

Describe the treatment for viral meningitis

A

Nothing if enteroviruses
Acyclovir if HSV/VZV

252
Q

What prophylaxis should be given to close contacts of someone with bacterial meningitis

A

One off oral ciprofloxacin -if in close contact up to 7 days before

253
Q

Name some complications of meningitis

A

Sepsis
DIC
Coma
SIADH
Seizures
Death

254
Q

Name some delayed complications of meningitis

A

Hearing loss, cranial nerve dysfunction, hydrocephalus, intellectual deficits, ataxia, blindness

255
Q

What is Waterhouse Friedrichsen Syndrome and what can cause it?

A

Adrenal insufficiency caused by intraadrenal haemorrhage from DIC

256
Q

What are the most common bacteria that can cause meningitis in neonates?

A

Group B strep
E.Coli
Gram negative bacilli
Listeria
S.pneumoniae

257
Q

What are the most common bacteria that can cause meningitis in 3month-6years ols?

A

S. pneumonia
n.meningitidis
H.influenzae

258
Q

What are the most common bacteria that can cause meningitis 6-60 year olds?

A

S.pneumonia
N.meningitidis

259
Q

What are the most common bacteria that can cause meningitis in those over 60 years?

A

S.pneumoniae
N.meningitidis
Listeria
Gram negative bacili

260
Q

What kind of bacteria is n.meningitidis?

A

Gram negative diplococcus

261
Q

Which meningitis causing bacteria is there a vaccine for?

A

N.meningitidis

262
Q

Which meningitis causing bacteria causes a non-blanching purpuric rash?

A

N.meningitidis

263
Q

What kind of bacteria is S.pneumoniae?

A

Gram positive diplococcus in chains

264
Q

What kind of bacteria is Group B strep?

A

Gram positive coccus in chains

265
Q

What age group is group B strep most common in and why?

A

Neonates
Colonises in the maternal vagina

266
Q

What kind of bacteria is listeria monocytogenes?

A

Gram positive bacillus

267
Q

What groups are most likely to get meningitis cause by listeria monocytogenes?

A

Extremes of age
pregnancy

268
Q

What is neurofibromatosis?

A

Genetic condition that causes nerve tumours(neuromas) to develop in the nervous system. Benign but can cause structural and neurological problems

269
Q

Which type of neurofibromatosis is more common?

A

neurofibromatosis type 1

270
Q

What is neurofibromatosis type 1 also called?

A

von Recklinghausen’s syndrome

271
Q

HOW IS neurofibromatosis inherited?

A

autosomal dominant

272
Q

Describe the aetiology of neurofibromatosis type 1

A

Mutation on chromosome 17 which codes for neurofibrin->tumour suppressor protein

273
Q

Name the symptoms of neurofibromatosis type 1

A

CABBING
CAFE AU LAit spots
Relative with nf1
bony dysplasia, bowing of long bone or sphenoid wing dysplasia
iris hamartomas(lisch nodules)
neurofibromas(>2 is singificant, or >1 plexiform)
glioma of optic pathway

274
Q

How is nf type 1 treated?

A

monitor and manage complications

275
Q

What are the 2 most significant complications of nf type 1?

A

malignant peripheral nerve sheath tumours(MPNST)
Gastrointestinal stronal tumour(GIST)

276
Q

Name some complications of nft1

A

migraines
epilepsy
hypertension from renal artery stenosis
learnign disability
scoliosis
brain tumours
spinal tumours
increased cancer risk

277
Q

Describe the aetiology of neurofibromatosis type 2

A

mutation on chromosome 22-> merlin-> tumour suppressor protein important in schwann cells->schwannomas

278
Q

What is the main complication of neurofibromatosis type 2

A

Acoustic neuromas
BILATERAL ACOUSTIC NEUROMAS->THINK NF2

279
Q

What is giant cell arteritis also known as?

A

Temporal arteritis

280
Q

What is temporal arteritis?

A

Vasculitis of unknown cause that affects medium to large size of vessel arteries, particularly at the temmples

281
Q

What condition overlaps with temporal arteritis?

A

polymyalgia rheumatica

282
Q

Describe the epidemiology of temporal arteritis

A

most common primary vasculitis
>50 years, peak in 70s
M:F-1:3

283
Q

Describe the aetiology of temporal arteritis

A

genetics
environmental
age
sex
ethnicity(caucasian-scandinavian)

284
Q

describe the presentation of a patient with temporal arteritis

A

temporal headache
jaw claudication
amaurosis fugax
tender, palpable temporal artery, scalp tenderness
50% have PMR features-morning, proximal muscle weakness

285
Q

What investigations shoud be done to diagnose temporal arteritis

A

Inflammatory markers-ESR and CRP raised
LFTs and FBC
Temporal artery biopsy
Doppler ultrasound

286
Q
A

3A mine (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions