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Phase 2a - Jemima > Neurology > Flashcards

Neurology Flashcards

1
Q

what is a transient ischemic attack

A

sudden onset focal neurological deficit - temporary

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2
Q

what are the two types of transient ischemic attack

A

Internal carotid artery (anterior)- 90%
Vertebral (posterior) - 10%

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3
Q

what are causes of transient ischemic attack

A

Carotid thrombo-emboli
- thrombosis
- Emboli (AF)

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4
Q

what is the CHA2DS2 - VASc score

A

A way of assessing stroke risk from AF in AF patients

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5
Q

what are risk factors for transient ischemic attack

A

same as ischemic heart disease
- smoking
- diabetes T2
- hypertension
- Atrial fibrillation
- obesity/hypercholesterolemia
- VSD

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6
Q

what are the symptoms of anterior cerebral artery syndrome (transient ischemic attack)

A

weak numb contralateral leg

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7
Q

what are the symptoms of middle cerebral artery syndrome (transient ischemic attack)

A

weak numb contralateral side of body, face drooping w/forehead spared, dysphasia (temporal)

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8
Q

what is amaurosis fugax

A

this is when there is occlusion or reduced blood flow to the retina through the ophthalmic/retinal/ciliary artery
- sign that stroke is impending

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9
Q

what are the signs of a posterior coronary artery attack

A

vision loss

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10
Q

what is seen with occipital artery attack

A

contralateral homonymous hemianopia with macular sparing

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11
Q

what is seen in vertebral artery attack (transient ischemic attack)

A

cerebellar syndrome: DANISH
brainstem infarct
cranial nerve lesions 3-12

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12
Q

when can you differentiate between a stroke and a transient ischemic attack

A

after the recovery

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13
Q

how do you tell the difference between a transient ischemic attack and a stroke

A

TIA: resolve within minutes usually and always <24 hours with no infarct
Stroke: last 24 hours with infarct

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14
Q

how do you diagnose transient ischemic attack

A

clinically made
FAST scoring system = face, arms, speech, time
ABCD2 - age (>60), BP (>140/90). Clinical sx, duration, DMT2

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15
Q

how do you treat a transient ischemic attack

A

Acutely = 300mg of aspirin
prophylaxis long term = clopidogrel 75mg + atorvastatin 80mg

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16
Q

what is a stroke

A

a focal neurological defect lasting 24 hours with infarction

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17
Q

what are the two types of stroke

A

ischemic and haemorrhagic

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18
Q

what are the features of an ischemic stroke

A

mc - 85%
caused by carotid-thrombo-emboli

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19
Q

what are the features of haemorrhagic stroke

A

15% of strokes
caused by ruptured blood vessel

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20
Q

what can cause a haemorrhagic stroke

A

trauma
hypertension
berry aneurysm rupture

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21
Q

where are haemorrhagic strokes more common

A

intraendural
subarachnoid

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22
Q

what a specific sign of a stroke

A

the pronator drift

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23
Q

what is the pronator drift and what does it show

A

ask the patient to lift their arms to the ceiling and the arm affected will pronate and the palm faces down
- sign of a stroke

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24
Q

what are risk factors for stroke

A

hypertension
smoking
obesity
type 2 diabetes
atrial fibrillation
transient ischemic attack
hypercoagulability

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25
Q

what are symptoms of a stroke

A

focal neurology - like TIA
haemorrhagic strokes show an increase in intracranial pressure

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26
Q

what are lacunar strokes

A

they are a very common types of ischemic stroke of lenticulostriate arteries (support deep brain structures) which causes ischemia in the basial ganglia, internal capsule, thalamus and pons

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27
Q

what kind of stroke do you suspect is a patient is on oral anticoagulants

A

haemorrhagic stroke until proven otherwise

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28
Q

how do you diagnose stroke

A

NCCT head
ischemic - mostly normal
haemorrhagic - hyperdense blood

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29
Q

how do you treat ischemic stroke

A
  1. if it presents within 4.5 hours use a thrombolytic (alteplase IV)
  2. aspirin 300mg for two weeks
  3. lifelong clopidogrel 75mg
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30
Q

how do you treat a haemorrhagic stroke

A

neurosurgery referral
IV mannitol for increased intracranial pressure

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31
Q

what is the prophylaxis for both ischemic and haemorrhagic stroke

A

atorvastatin
ramipril

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32
Q

what spaces can haemorrhages occur within

A
  1. subarachnoid
  2. subdural
  3. extradural
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33
Q

what can cause a subarachnoid haemorrhage

A

berry aneurysm in the circle of willis rupturing
trauma

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34
Q

what can cause subdural haemorrhage

A

bringing vein rupture

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35
Q

what can cause extradural haemorrhage

A

middle meningeal artery trauma

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36
Q

what are the most common arteries subarachnoid haemorrhage occurs in

A

anterior communicating
anterior cerebral junction

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37
Q

what are the risk factors of a subarachnoid haemorrhage

A

hypertension
polycystic kidney disease
trauma
increased age
family history
male

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38
Q

what are symptoms of a subarachnoid haemorrhage

A

occipital thunderclap headache
suddenly onset
may have sentinel headache - throbbing pain which preceded berry aneurysm rupture
very severe
meningism - kernig and brudzinski signs
low GCS (consciousness)
Fixed dilated pupils
Non specific signs of raised intracranial pressure

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39
Q

what is the Kernig sign

A

Cant extent the leg properly when the knee is flexed

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40
Q

what is the Brudzinski sign

A

when neck elevated, knees automatically flex

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41
Q

what is the Glasgow coma scale

A

coma score out of 15
eyes - 4, Verbal - 5, motor - 6
15 = normal
8 = comatose
3 = unresponsive

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42
Q

what are differential diagnosis for subarachnoid haemorrhage

A

meningitis
migrane

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43
Q

how do you diagnose subarachnoid haemorrhage

A

diagnostic = CT head (expect a star shape)
+ve CT angiogram
-ve Lumbar puncture

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44
Q

what is the first line treatment for subarachnoid haemorrhage

A

neurosurgery: endovascular coiling
also give Nimodipine

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45
Q

why do you give Nimodipine in subarachnoid haemorrhage

A

because it reduced vasospasm and blood pressure
- its a calcium channel blocker

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46
Q

what is a subdural haemorrhage

A

rupture of a bridging vein due to shearing
- deceleration injuries and abused children

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47
Q

what are risk factors of subdural haemorrhage

A

trauma
child abuse
cortical atrophy - dementia

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48
Q

what are symptoms of subdural haemorrhage

A

gradual onset with latent period
bleeding is small: accumulation and autolysis of blood (symptoms after days/weeks/months)
signs of intracranial pressure

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49
Q

what are the signs of increased cranial pressure

A

Cushings triad:
bradycardia
increased pulse pressure
irregular breathing
plus fluctuating GCS and papillodema

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50
Q

how do you diagnose subdural haemorrhage

A

NCCT head - banana or crescent shaped haematoma not confused to suture tines, midline shift

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51
Q

what do
a. acute
b. subacute
c. chronic
subdural haemorrhage look like on a CT

A

a. hyper dense (bright)
b. isodense
c. hypodense - darker than the brain

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52
Q

how do you treat subdural haemorrhage

A

Burr hole and craniotomy
IV mannitol to decrease intracranial pressure

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53
Q

what is an extradural haemorrhage

A

caused by trauma to the middle meningeal artery, due to damage to the lateral pterygoid bone

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54
Q

when is extradural haemorrhage more common

A

in young adults - 20-30
as you age there is a decreased risk as the dura becomes more firmly adhered to the skull

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55
Q

what are the risk factors of extradural haemorrhage

A

head trauma

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56
Q

what are the symptoms of extradural haemorrhage

A

after the initial event there is a lucid interval and then there will be a rapid deterioration due to an increased cranial pressure

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57
Q

why is there a delayed increased inter cranial pressure in extradural haemorrhage

A

because of old blood clots, these clots become haemolysed and takes up water and will therefore increase the volume in the skull

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58
Q

what symptoms are seen in extradural haemorrhage

A

decreased GCS score - comatose and confusion
Increased intracranial pressure signs
death from respiratory arrest

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59
Q

why do you have respiratory arrest in extradural haemorrhage

A

tonsillar hemiation and coning of brain causes a compressed respiration centre

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60
Q

how do you diagnose extradural haemorrhage

A

NCCT the head
- lens shaped hyperdense bleed confined to suture lines
- midline shift

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61
Q

what is the treatment for extradural haemorrhage

A

urgent surgery
mannitol IV to reduce inter cranial pressure

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62
Q

what are primary causes of headaches

A

migrane
cluster
tension
drug overdose

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63
Q

what are secondary causes for headaches

A

due to an underlying condition
GCA
infection
SAH
trauma
cerebrovascular disease
eye, ear, sinus pathology

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64
Q

what is a migraine

A

it is recurrent episodes of throbbing headache plus or minus aura
often with vision changes

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65
Q

what is the most common cause of recurrent headache

A

migraine

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66
Q

In who is migraine most common

A

in women under 40

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67
Q

what are triggers of migraine

A

chocolate
hangovers
orgasms
cheese
bral contraceptives
lie ins
alcohol
tumult
exercise

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68
Q

how does a migraine come on

A

prodrome - days before attack see mood changes
Aura - part of the attack, minutes before headache
Throbbing headache lasting 4-72 hours

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69
Q

what are symptoms of a migraine

A

2 or more of
- unilateral pain
- throbbing
- motion sickness
- mod-severely intense
plus one of
- nausea and vomiting
- photophobia

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70
Q

how do you diagnose migraine

A

clinical
- unless other pathology is suspected

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71
Q

how do you treat migraine

A

Acute: oral triptan or aspirin (900mg)
Prophylaxis: propranolol or TCA (2nd line)

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72
Q

what is a cluster headache

A

a unilateral periorbital pain with autonomic features
10-15 minutes

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73
Q

what is the most disabling primary headache

A

cluster headaches

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74
Q

what are risk factors for cluster headaches

A

male
smoking
genetics - autodom link?

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75
Q

what are symptoms of cluster headaches

A

crescendo unilateral periorbital excruciating pain (may affect temples too)
autonomic features
- face flushing
- conjunctival injection and lacrimation
- ptosis
- miosis
- rhinorrhoea

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76
Q

how do you diagnose cluster headaches

A

clinically
5 or more similar attacks confirm diagnosis

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77
Q

how do you treat cluster headaches

A

acute = Triptans - sumatriptan
Prophylaxis = Verapamil (CCB)

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78
Q

what are tension headaches

A

bilateral generalised headache which can radiate to the neck

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79
Q

what is the most common type of primary headache

A

tension headache

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80
Q

what is the trigger for tension headaches

A

stress

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81
Q

what are symptoms of tension headache

A

rubber band tight around the head
bilateral pain
feel it in the trapezius too
mold-moderate severity
no motion sickness, photophobia or aura

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82
Q

how do you diagnose tension headaches

A

clinically from the history

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83
Q

how do you treat tension headaches

A

simple analgesia
- aspirin
- paracetamol

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84
Q

what is primary trigeminal neuralgia

A

unilateral pain in one or more trigeminal branches

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85
Q

what are risk factors for trigeminal neuralgia

A

MS (20X more likely)
increased age
female

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86
Q

what is trigeminal neuralgia triggered by

A

eating
shaving
talking
brushing teeth

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87
Q

what are symptoms of trigeminal neuralgia

A

electric shock pain (seconds to minutes)
in V1/2/3

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88
Q

how do you diagnose trigeminal neuralgia

A

clinical
three or more attacks with symptoms

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89
Q

what is the treatment for trigeminal neuralgia

A

carbamazepine - anticonvulsant

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90
Q

what is giant cell arteritis

A

it is large vessel vasculitis

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91
Q

how does giant cell arteritis normally present

A

50 y/old caucasian woman presents with unilateral tender scalp, intermittent jay claudication
- worst case is amaurosis fugax which is transient vision loss in one eye

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92
Q

how do you diagnose giant cell arteritis

A

temporal artery biopsy - large region as you can get skip lesions
increased ESR and CRP
normocytic normochromic anaemia of chronic disease

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93
Q

what is seen on a temporal artery biopsy in giant cell arteritis

A

granulomatous non caseating inflammation of the intima and media with skip lesions

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94
Q

how do you treat giant cell ateritis

A

corticosteroids = prednisolone
if there is any sign of vision changes then give high dose IV methylprednisolone quickly

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95
Q

what are causes of seizures

A

VITAMIN DE
vascular
Infection
trauma
autoimmune - SLE
metabolic - hypocalcaemia
Idiopathic - epilepsy
neoplasms
dementia +drugs (cocaine)
eclampsia

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96
Q

what is epilepsy

A

idiopathic cause of seizures with two or more episodes more than 24 hours apart

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97
Q

what are risk factors for epilepsy

A

familial inherited
dementia

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98
Q

what is the pathophysiology behind seizures

A

the normal balance between GABA (-) and glutamate (+) shifts towards glutamate therefore making it more excitatory

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99
Q

how long do epileptic seizures usually last for

A

about 2 minutes

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100
Q

what are the phases of a epileptic fit

A

prodrome
aura
ictal event - seizure
postictal period

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101
Q

what happens in the prodrome stage of a fit

A

this is changes in someones mood days before the event

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102
Q

what happens in the aura stage of a fit

A

minutes before the fit
Deja vu ad automatisms (lip smacking/rapid blinking)
- not always present

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103
Q

what happens in the postictal period of a fit

A

headache
confusion and decreased GCS score
TODD’S paralysis - temporary paralysis and muscle weakness of the motor cortex is affected
dysphagia
amnesia
sore throat - in epileptic seizures

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104
Q

what are different classifications of epileptic seizures

A

generalised - tonic clonic and absence
focal - simple and complex focal

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105
Q

what is a Tonic Clonic generalised seizure

A

GRANDMAL
- no aura
- tonic phase - rigidity, fall to floor
- clonic phase - jerking of limbs
ungazing open eyes, incontinence, tongue bitten

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106
Q

what is an absence generalised seizure

A

Often in childhood
characterised by moments of staring blankly into space
lasts seconds to minutes
3HZ spike on ECG

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107
Q

what does tonic mean

A

when someone is rigid

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108
Q

what does myoclonic mean

A

when someone is jerking limbs

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109
Q

what does atonic mean

A

when someone is suddenly floppy (limbs and muscles)

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110
Q

what generally happens during general seizures

A

all the cortex and deep brain structures bilaterally are affected
- always have a loss of consciousness

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111
Q

what are general features of focal seizures

A

confined to one region of the brain
- temporal may progress to secondary generalised

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112
Q

what is a simple focal seizure

A

where there is no basal ganglia or thalamic involvement

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113
Q

what is a complex focal seizure

A

where there is basal ganglia and thalamic involvement

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114
Q

what are features of a simple focal seizure

A

there is no loss of consciousness
patient is awake and aware
uncontrollable muscle jerking

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115
Q

what are features of a complex focal seizure

A

loss of consciousness
patient is unaware
postictal period positive

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116
Q

what symptoms would you get with a temporal focal seizure

A

AURA
dysphagia
post ictal period

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117
Q

what symptoms would you get with a frontal focal seizure

A

Jacksonian march
todd’s palsy

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118
Q

what symptoms would you get with a parietal seizure

A

paresthesia

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119
Q

what symptoms would you get with an occipital seizure

A

vision changes

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120
Q

how do you diagnose seizures

A

Must have had over 2 24 hours apart to consider epilepsy
CT head and MRI
ECG
Bloods

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121
Q

what do you need to examine on head CT and MRI in seizure diagnosis

A

hippocampus
check for bleeds
check for tumours

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122
Q

what is seen on an ECG in an absence seizure

A

3 HZ wave

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123
Q

how do you treat seizures

A

sodium valproate to all

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124
Q

who cant have sodium valproate for seizures

A

females in childbearing age as its teratogenic

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125
Q

what is given instead of sodium valproate in pregnancy for seizures

A

lamotrigine

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126
Q

what is a complication of seizures

A

status epilepticus = epileptic seizures without a break back to back OR
seizures lasting longer than 5 minutes

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127
Q

how do you treat status epilepticus

A

Benzodiazepines: lorazepam 4mg IV
if its not working then Lorazepam again and then phenytoin

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128
Q

what is parkinsons

A

when there is a loss of dopaminergic neurons from the substantia nigra pars compacta

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129
Q

what are risk factors for developing parkinsons

A

family history
increased age
smoking seems to be protective ?

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130
Q

what is the pathophysiology of parkinsons

A

normally to initiate movement the nigrostriatal pathway signals to the striatum to stop firing to substantia nigra and therefore stops movement inhibition
in Parkinson’s there is degeneration of the substantia nigra so that its harder to initiate movement

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131
Q

what are symptoms of parkinsons’s

A

cardinal Sx = bradycardia, resting tremor, rigidity, postural instability
anosmia seen early
constipation
shuffling gait
pill rolling thumb
cogwheel/lead pipe forearm
typically asymmetrical

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132
Q

How do you diagnose parkinsons

A

clinical
bradykinesia and more than one other cardinal sign

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133
Q

how do you treat parkinsons

A

LDOPA and a decarboxylase inhibitor

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134
Q

what is the problem that can occur with LDOPA

A

the body becomes resistant to it and the effects can wear off and therefore you dont want to give LDOPA too early

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135
Q

what are some differential diagnosis for parkinsons

A

lewy body dementia
parkinsons Sx then dementia = perkinsons dementia
Parkinsons Sx after dementia = lewy body dementia

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136
Q

what is dementia

A

a neurodegenerative disorder with a reduced in cognition (memory, judgement, language) over time

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137
Q

what is the most common type of dementia

A

alzheimers

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138
Q

what is alzheimers disease

A

it is when you have B amyloid plaques and tau neurofibrillary tangles in the cerebral cortex
- increases cortical scarring
- brain atrophy
- decreased Ach

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139
Q

what are risk factors for Alzheimers

A

Down’s syndrome (inevitable)
ApoE4 allele in familial alzheimers

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140
Q

what are symptoms of alzheimers

A

agnosia - cant recognise things
apraxia - cant do basic motor skills
aphasia - cant talk as well as normal

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141
Q

what is vascular dementia

A

it is due to cerebrovascular damage such as a stroke or trauma
history of TIA/stroke, UMN signs and general decrease in cognition

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142
Q

what is Lewy body dementia

A

it is when alpha synuclein and ubiquitin aggregates in the cortex (lewy bodies)

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143
Q

what are symptoms of lewy body dementia

A

cognitive decline
parkinsonism

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144
Q

what is frontotemporal dementia

A

it is when there is frontotemporal atrophy causing speech, language, thinking and memory problems

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145
Q

how do you diagnose dementia

A

mini mental state exam (out of 30)
over 25 is normal
18-25 is impaired
<17 is severely impaired
Brain MRI will show atrophy

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146
Q

what is the treatment for dementia

A

conservative
social stimulation
exercise
for alzheimers - achase i (donepazil)
for vascular - antihypertensives (ramipril)

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147
Q

what is huntingtons chorea

A

it is an autosomal dominant disease with full penetrance
there is a lack of GABA and an excessive nigrostriatal pathway

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148
Q

what is huntingtons disease due to

A

due to trinucleotide expansions repeats - more repeats the earlier it presents

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149
Q

what are the ranges for trinucleotide repeats in huntingtons

A

<35 repeats - no huntingtons
35-55 - huntingtons
60+ - severe huntingtons

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150
Q

what are symptoms of Huntingtons chorea

A

Chorea - excessive limb jerking
dementia
psychiatric issues
depression

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151
Q

how do you treat huntingtons

A

extensive counselling - inevitable Sx
dopamine antagonists for chorea
tetrabenazine

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152
Q

what is multiple sclerosis

A

T4 hypersensitivity against myelin basic protein of oligodendrocytes causing demyelination of the CNS neurons

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153
Q

what are risk factors for multiple sclerosis

A

females
20-40
autoimmune disease
family history
EBV

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154
Q

what are types of multiple sclerosis

A

Relapsing remitting - incomplete recovery
Primary progressive - gradual deterioration
secondary progressive - relapsing-remitting

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155
Q

what is the first presentation of multiple sclerosis

A

blurred vision
- due to optic nerve damage

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156
Q

what are the symptoms of multiple sclerosis

A

paresthesia
blurred vision
Uthoff’s phenomenon (exacerbated in heat)

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157
Q

what are signs of multiple sclerosis

A

optic neuritis - inflamed optic nerve
internuclear ophthalmoplegia - lateral gaze impaired
brainstem signs
sensory signs
UMN signs
Lhermitte phenomenon
charcot neurological triad

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158
Q

what is the Charcot neurological triad

A

dysarthria
nystagmus
intention tremor

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159
Q

what is Lhermitte phenomenon

A

electric shock sensation with neck on flexion

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160
Q

how do you diagnose multiple sclerosis

A

the McDonald criteria = 2 or more attacks disseminated in time and space
MRI brainstem and cord
delayed conduction speeds
LP may show digoclonal igG bands

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161
Q

how do you treat multiple sclerosis

A

Acutely (episodes) = IV methylprednisolone
Prophylaxis = b interferon (DMARD; biologic)

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162
Q

what is motor neuron disease

A

neurodegenerative disease causing lower and upper motor neuron signs

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163
Q

what is the main motor neuron tract affected in motor neuron disease

A

the corticospinal tract

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164
Q

what is the corticospinal tract

A

it has an upper motor neuron from the precentral gyrus which has
- No decussation (anterior 10%)
- decussation (lateral 90%)

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165
Q

what are symptoms of upper motor neuron lesions

A

hypertonia: rigidity + spasticity
hyperreflexia
no fasciculation
Babinski positive
power:
arms - flexors more than extensors
legs - extensors more than flexors

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166
Q

what are symptoms of a lower motor neuron lesion

A

hypotonia - flaccid and muscle wasting
hyporeflexia
fasciculations
Babinski -ve
generally low power

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167
Q

what is an UMN lesion

A

lesion from the pre-central gyrus to the anterior spinal cord
- everything goes UP

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168
Q

what is a LMN lesion

A

Lesion from the anterior spinal cord to the muscles innervated
everything goes DOWN

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169
Q

what happens if you see mixed upper and lower motor neuron signs

A

then it is motor neuron disease

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170
Q

what is organisation of movement

A
  1. idea of movement - association cortexes, pre-motor cortex
  2. Activation of UMNs in motor cortex
  3. Impulse via corticospinal tract
  4. modulation by cerebellum and basal ganglia
  5. movement and somatosensory information
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171
Q

what are risk factors for motor neuron disease

A

male
family history
SOD-1 mutation
increased age

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172
Q

in what diseases are eye muscles affected

A

MS
Myasthenia gravis

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173
Q

in what diseases is sensory function and sphincters affected

A

MS
polyneuropathies

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174
Q

what is amyotrophic lateral sclerosis

A

a neurodegenerative disease that results in the progressive loss of motor neurons that control voluntary muscles

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175
Q

what is the most common motor neuron disease

A

ALS

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176
Q

what can ALS progress to

A

Bulbar palsy

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177
Q

what is progressive bulbar palsy

A

it is where cranial nerves 9-12 are damaged
- worse prognosis and can increase the chance of respiratory failure

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178
Q

what are different kinds of motor neuron disease

A

Amyotrophic lateral sclerosis
progressive muscular atrophy - LMN only
Primary lateral sclerosis - UMNs only
progressive bulbar palsy

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179
Q

what are symptoms of motor neuron disease

A

mixed upper and lower motor neuron signs
- no eye, sensory, cerebellar or parkinson signs

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180
Q

how do you diagnose motor neuron disease

A

mainly clinical - from mixed picture
ECG shown fibrillation potentials
(due to muscle degeneration with LMN)

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181
Q

how do you treat motor neuron disease

A

MDT management
Riluzole - antiglutaminergic
Supportive - physiotherapy and breathing support if necessary

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182
Q

what is a complication of motor neuron disease

A

respiratory failure
aspiration pneumonia
swallowing failure

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183
Q

what is meningitis

A

an infection of the meninges of the brain
- notifiable to PHE

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184
Q

what are the viral causes of meningitis

A

Enteroviruses - coxsackie
HSV-2
V2V

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185
Q

what are bacterial causes of meningitis

A

mainly S.pneumonae
N.meningitidis

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186
Q

what are risk factors for meningitis

A

extremes of age
immunocompromised
crowded environment
non-vaccinated

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187
Q

what bacteria is the most common in meningitis of 0-3 months

A

group B alpha haemolytic strep (S.agalectiae)
listeria
E.coli
S.pneumoniae

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188
Q

what is the most common bacteria in meningitis of 3m-6yrs

A

Strep. Pneumonae
N. meningitidis
H. influenzae

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189
Q

what is the most common bacteria in meningitis 6-60yrs

A

S. pneuminae
N. meningitidis

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190
Q

what is the most common bacteria in meningitis 60+yrs

A

S. pneuminae
N. meningitidis
Listeria

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191
Q

what is N. meningitidis

A

Gram negative diplococcus
vaccine available: men B+C
10% mortality

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192
Q

what is seen in N.meningitidis meningitis

A

non blanching purpuric rash
10% mortality
can cause meningococcal septicemia

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193
Q

what is S. pneumoniae

A

gram positive diplococcus in chains

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194
Q

what is mortality rate of meningitis caused by S. pneumoniae

A

25% mortality

195
Q

why is group B strep most common cause of neonatal meningitis

A

because it colonises the maternal vagina

196
Q

what type of bacteria is Group B strep

A

Gram positive coccus in chains

197
Q

what type of bacteria is listeria monocytogenes

A

gram positive bacilli

198
Q

what meningitis does listeria monocytogenes cause

A

affects the extremes of age and maternal (pregnant ladies)

199
Q

what are symptoms of meningitis

A

meningism: headache, neck stiffness, photophobia

200
Q

what are signs of meningitis

A

Kernig - cant extend knee when hip is flexed (without pain)
Brudzinksi - when neck is flexed, knees and hips automatically flex

201
Q

how do you diagnose meningitis

A

Lumbar puncture and CSF analysis
- sample taken form L3/4

202
Q

when is a lumbar puncture contraindicated in meningitis

A

in increased intercranial pressure

203
Q

what will be seen in a lumbar puncture in bacterial meningitis

A

increased opening pressure
cloudy yellow in appearance
increased WBC - neutrophilia
increased Ig/L
decreased glucose (less than 50% serum level)

204
Q

what will be seen in a lumbar puncture in viral meningitis

A

equal opening pressure
clear normal appearance
increased WBC - lymphocytosis
equal protein (<Ig/L)
glucose is higher than 60% serum level

205
Q

what is seen in a lumbar puncture in fungal/TB meningitis

A

increased opening pressure
cloudy and fibrous appearance
increased WBC - lymphocytosis
increased protein - !g/L
reduced glucose = <50% serum level

206
Q

how do you treat bacterial meningitis

A

In hospital
Ceftriaxone/cefotaxime (3rd gen cephalosporin)
Steroids - dexamethasone
amoxicillin covers listeria

207
Q

what is the treatment for viral menintigis

A

Nothing if enterovirus
Acyclovir if HSV or V2V

208
Q

what is important to do when you have a meningitis diagnosis

A

contact tracing - prophylaxis to contacts with 7 days of more prolonged exposure proceeding the symptoms - i.e live in the same house
- give a one off dose of ciprofloxacin

209
Q

what are complications of meningitis

A

Meningococcal septicemia (DIC)
Waterhouse Friedrichsen syndrome - adrenal insufficiency caused by intradrenal haemorrhage as a result of meningococcal DIC

210
Q

in a GP if someone presents with a non blanching rash and suspected meningococcal septicemia what do you do

A

IM BENZYLPENELICCIN and an immediate hospital referral

211
Q

what is encephalitis

A

viral infection of the brain parenchyma

212
Q

what are most cases of encephalitis caused by

A

95% of cases are caused by HSV-1

213
Q

what are other causes of encephalitis other than HSV-1

A

CMV
EBV
HBV
Toxoplasmosis
HIV

214
Q

what are risk factors for encephalitis

A

immunocompromised
extremes of age

215
Q

what are symptoms of encephalitis

A

fever
headache
encephalopathy
focal neurology (temporal lobe MC affected)

216
Q

how do you diagnose encephalitis

A

CSF may show Viremia (increased lymphocytes)
MRI of the head - unilateral usually temporal encephalitis
Non specific ECG firing of 2Hz periodically

217
Q

how do you treat encephalitis

A

Acyclovir

218
Q

what are examples of primary brain tumours

A

Astrocytoma (90%)
oligodendrocytoma
Meningioma
Schwannoma

219
Q

What types of cancer metastasis cause brain cancer

A

Non-small cell lung cancer (MC)
small cell lung cancer
Breast cancer
Melanoma
renal cell carcinoma
gastric cancer

220
Q

what are the grades of astrocytoma’s

A

graded 1-4 by WHO
1 = benign
4 = glioblastoma (very bad prognosis)

221
Q

what are symptoms of primary brain tumours

A

increased intercranial pressure
Cushings triad
Papilloedema
CN6 palsy
Focal neurology
Epileptic seizures
Lethargy
Weight loss

222
Q

what is Cushings triad of symptoms in primary brain tumours

A

Increased pulse pressure
bradycardia
irregular breathing

223
Q

how do you diagnose primary brain tumours

A

MRI the head - locate the tumour
Biopsy the tumour - grade
NO LUMBAR PUNCTURE (due to increased intercranial pressure it can cause a massive CI)

224
Q

how do you treat primary brain tumour

A

Surgery - remove tumour if possible and reduce intercranial pressure
Chemotherapy - before/during/after surgery
Steroids, dexamethasone, may help

225
Q

what is Hemiplegia

A

Paralysis on one side of the body
- caused by a brain lesion

226
Q

what is Paraplegia

A

paralysis of both legs
- caused by a cord lesion

227
Q

what level does the spinal cord run between

A

C1 - L1/2

228
Q

what is found past L3 of the spine

A

the conus medullaris and the cauda equina

229
Q

What type of tract is the DCML

A

it is an ascending tract

230
Q

what is the pathway of the DCML

A

From the dorsal root to the medulla and then decussates

231
Q

what is the DCML tract used for

A

sensing fine touch
two point discrimination
proprioception

232
Q

Is DCML a sensory or motor nerve

A

A sensory nerve

233
Q

what type of tract is the spinothalamic tract

A

Ascending tract
sensory

234
Q

what is the pathway the spinothalamic tract takes

A

Decussates 1-2 spinal levels above where it enters and then ascends to the medulla

235
Q

what does the spinothalamic tract detect

A

pain
temperature

236
Q

what type of tract is the corticospinal tract

A

A descending tract
Motor

237
Q

What is the pathway taken by the corticospinal tract

A

UMN which then decussates at the medulla
then has its ventral roots down

238
Q

what happens when you have a spinal cord lesion

A

you have ipsilateral sensory signs remaining
you have contralateral motor signs remaining

239
Q

what is the L3/4 reflex

A

the knee jerk reflex

240
Q

what is the L5 reflex

A

the big toe jerk reflex

241
Q

what is the S1 reflex

A

ankle jerk reflex

242
Q

what are causes of spinal cord compressions

A

Vertebral body neoplasms
spinal pathology - disc prolapse/herniation

243
Q

metastasis from what can develop into vertebral body neoplasms

A

breast
lung
renal cell carcinoma
melanoma

244
Q

what is Brown sequard syndrome

A

Incomplete spinal cord injury leading to:
ipsilateral motor weakness
ipsilateral DCML dysfunction
Contralateral spinothalamic dysfunction

245
Q

what are symptoms of spinal cord compression

A

Progressive leg weakness with UMN signs
- contralateral hyperreflexia
- Babinski +ve
- spasticity
sensory loss below the lesion
sphincter involvement is uncommon (v. bad sign)

246
Q

how do you diagnose spinal cord compression

A

MRI spinal cord ASAP - can risk permanent damage if not
Chest X ray if malignancy is suspected

247
Q

what is the treatment for spinal cord compression

A

Neurosurgery
- laminectomy
- microdisectomy

248
Q

what causes cauda equina syndrome

A

lumbar herniation - L4/5 or L5/S1

249
Q

what is cauda equina syndrome

A

Compression below the conus medullaris - emergency

250
Q

what are symptoms of cauda equina syndrome

A

Leg weakness with lower motor neuron signs
- ipsilateral hypotonia
- fasciculations
- hyporeflexia
Saddle anaesthesia
Bladder/bowel dysfunction
Sphincter involvement common

251
Q

how do you treat cauda equina syndrome

A

Neurosurgery ASAP
- microdiscectomy
- spinal fixation

252
Q

how do you diagnose cauda equina syndrome

A

MRI cord
test nerve roots
test reflexes

253
Q

what are mechanisms of peripheral neuropathy

A

demyelination
axonal damage
nerve compression
vasavenosum infarction
Wallerian degeneration - nerve cut and dies

254
Q

what are causes of peripheral neuropathy

A

Demyelination
Diabetes mellitus T2
Surgery
pathology - infection, endocrine. RA

255
Q

what is mononeuropathy

A

Single nerve damage

256
Q

what is mononeuritis multiplex

A

when there is several individual nerves damaged

257
Q

what is polyneuropathy

A

diffuse and often symmetrical pathology

258
Q

what are causes of mononeuritis multiplex

A

WARDS PLC
Wegeners
AIDs/amyloidosis
RA
DMT2
Sarcoidosis
Polyarteriosis nordosa
Leprosy
Carcinomas

259
Q

what nerve roots are affected in carpal tunnel syndrome

A

C6-T1

260
Q

what is carpal tunnel syndrome

A

when there is pressure on the median nerve passing through the carpal tunnel

261
Q

what are risk factors/causes of carpal tunnel syndrome

A

female more likely than male
Hypothyroidism
Acromegaly
Pregnancy
Rheumatoid arthritis
Obesity

262
Q

what are symptoms of carpal tunnel syndrome

A

Gradual onset
- weakness of grip and aching hand/forearm
- paresthesia of the hand
- wasting of the thenar eminence

263
Q

how do you diagnose carpal tunnel syndrome

A

Phalen test
Tinel test
EMG if tests are uncertain

264
Q

what is the Phalen test

A

flex the wrist for one minute and if they have carpel tunnel they will have paresthesia and pain at the wrist

265
Q

what is the Tinel test

A

Tapping of the wrist causes tingling

266
Q

how do you treat carpel tunnel syndrome

A

Wrist splint at night
steroid injection
last resort = surgical decompression

267
Q

what nerve roots are affected in radial palsy

A

C5-T1

268
Q

How does radial palsy present

A

Wrist drop

269
Q

how do you treat radial nerve palsy

A

Splint and simple analgesia

270
Q

what nerve roots are affected in ulnar nerve palsy

A

C8-T1

271
Q

how does ulnar nerve palsy present

A

classic claw hand - 4th and 5th fingers claw up

272
Q

what is sciatica

A

it is a L5/S1 lesion due to
SPINAL: IV disc herniation/prolapse
NON SPINAL: Piriformis syndrome, tumours, pregnancy

273
Q

what are symptoms of sciatica

A

pain from buttock down the lateral leg to pinky toe
weak plantarflexion and absent ankle jerk

274
Q

how do you diagnose sciatica

A

Exam: cant do straight leg raise without pain
MRI the cord to confirm

275
Q

how do you treat sciatica

A

Analgesia and physiotherapy
Neurosurgery

276
Q

how do you treat ulnar nerve palsy

A

Splints and simple analgesia

277
Q

how does polyneuropathy present

A

Glove and stocking distribution
mostly peripheries are affected

278
Q

What are causes of polyneuropathy

A

Motor - guillian barre
sensory - diabetic neuropathy
vasculitis
malignancy
B-12 deficiency
rheumatoid arthritis

279
Q

how do you treat polyneuropathy

A

analgesia and treat the underlying cause

280
Q

how do you diagnose polyneuropathy

A

Find the underlying cause
- bloods
- serology
- ESR/CRP

281
Q

what are common causes of cranial nerve lesions

A

Trauma
MS
tumours

282
Q

what occurs in cranial nerve 3 lesions

A

ptosis
down and out eye
fixed dilated pupil
LEW nuclei dysfunction

283
Q

What happens in cranial nerve 4 lesions

A

Diplopia when looking down
- this is rare and always due to trauma

284
Q

What happens in cranial nerve 6 lesion

A

Adducted eye
a sign of increased intercranial pressure

285
Q

What happens in cranial nerve 5 lesion

A

Jaw deviates towards the affected side
loss of corneal reflex
trigeminal neuralgia including sensory/motor jaw pain in V1/2/3

286
Q

what happens in cranial nerve 7 lesion

A

facial droop with no forehead sparing
Bells palsy
Parotid inflammation

287
Q

what happens in cranial nerve 8 lesion

A

hearing loss
loss of balance
skull changes
compression
middle ear disease

288
Q

what happens in cranial nerve 9+10 lesions

A

Impaired gag reflex
issues with swallowing, respiration and vocal issues
- jugular foramen lesions

289
Q

what happens in cranial nerve 11 lesion

A

cant shrug shoulders
cant turn head against resistance

290
Q

what happens in cranial nerve 12 lesions

A

tongue deviation towards the side of the lesion

291
Q

what is myasthenia gravis

A

AN autoimmune response against the neuromuscular junction post synaptic receptors
- Nicotinic Ach R
- MusK
TYPE 2 HYPERSENSITIVITY

292
Q

what are common causes of myasthenia gravis in
a. men
b. women

A

a. thymoma - thymus tumour (60y/old)
b. autoimmune disease (40y/old)

293
Q

what is the pathophysiology of myasthenia gravis

A

85% Anti Ach-R: bind to post synaptic receptor and inhibit it competitively. Active complement causes NMJ destruction. More binding with exertion
15% Anti MuSK: this helps to synthesise AchR so you have reduced receptor expression

294
Q

what are symptoms of myasthenia gravis

A

Weak eye muscles - diplopia
Ptosis
Myasthenic snarl
Jaw fatiguability
swallowing difficulty
speech fatiguability

295
Q

what is the progression of myasthenia gravis symptoms like?

A

it is worse later on and with excursion
it starts at the head and neck and moves to the lower body
it is better with rest

296
Q

What is a differential diagnosis for myasthenia gravis

A

Lumbar Eaton syndrome

297
Q

What is lambert Eaton syndrome

A

Auto antibodies against presynaptic calcium channels

298
Q

What are symptoms of lambert Eaton syndrome

A

Similar to MG but they start at the extremities and them move to the head and neck
There is also autonomic involvement

299
Q

How do you treat lambert Eaton syndrome

A

Prednisone (steroids)
Immunosuppression

300
Q

How do you diagnose MG

A

Serology anti AchR and anti MusK
Tension/edrotropium test

301
Q

What is the Edrotropium test

A

It is where you administer edrotropium which is a rapidly acting Ach ase inhibitor. If positive then there is an increase in muscle power for a few seconds

302
Q

How do you treat Myasthenia gravis

A

1st line is Ach ase inhibitor (neostigmine/pyrdostigmine)
2nd line immunosuppression (steroid)

303
Q

What is a complication of myasthenia gravis

A

A myasthenic crisis
Acute symptom worsening with a severe respiratory weakness

304
Q

How do you treat a myasthenic crisis

A

Plasma exchange and IV ig

305
Q

What is Guillian Barr syndrome

A

Post infection there is a demyelination response against the peripheral nervous system myelinating oligodendrocytes

306
Q

Who is Guillian Barr syndrome most common in

A

Males 15-30 and 50-70

307
Q

What are causes of Guillian Barr syndrome

A

C.jejuni
CMV
EBV
H2V

308
Q

What is the pathophysiology of guillain Barr syndrome

A

Disease of mimicking
Organism antigens against those on the schwaan cells resulting in antibodies made against the schwaan cells causing demyelination and acute polyneuropathy

309
Q

What are symptoms of guillian Barr syndrome

A

Post infection you present with
Ascending symmetrical muscle weakness
Loss of deep tendon reflexes
Autonomic involvement in 50%
Respiratory failure in about 35%

310
Q

How do you diagnose Guillian Barr syndrome

A

Nerve conduction studies
Lumbar puncture- raised protein and normal WBC (inflammation no infection)

311
Q

How do you treat Guillian Barr syndrome

A

IVIg for 5 days plus plasma exchange
If FVC is less than 0.8 then consider intubation

312
Q

What is wernikes encephalopathy

A

Reversible acute emergency due to a severe B1 (thiamine) deficiency

313
Q

What are causes of Werinkes encephalopathy

A

Mostly high Alcohol

314
Q

What are symptoms of Wernickes encephalopathy

A

Ataxia
Confusion
Opthalmoplegia

315
Q

How do you diagnose Wernickes encephalopathy

A

Clinically recognised supported with microcytic anaemia and deranged LFTs

316
Q

How do you treat Wernickes encephalopathy

A

Parentral pabrinex for 5 days acutely
Oral thymine prophylactically

317
Q

What is a complication of wernickes encephalopathy

A

Korsakoff syndrome

318
Q

what is Korsakoff syndrome

A

when wernickes is left too long without treatment leading to severe thiamine deficiency. Same symptoms with as disproportionate increase in memory loss
= irreversible damage

319
Q

what is Duchenne muscular dystrophy

A

X linked recessive mutated dystrophin gene

320
Q

what is the pathophysiology of Duchenne muscular dystrophy

A

the muscle is replaced with adipose tissue

321
Q

what gender is duchenne muscular dystrophy found in

A

Boys exclusively

322
Q

what are symptoms of Duchenne muscular dystrophy

A

difficulty getting up from lying down - Gowers sign
skeletal deformities
scoliosis
hyperlordosis

323
Q

how do you diagnose Duchenne muscular dystrophy

A

prenatal tests
DNA genetic tests

324
Q

How do you treat Duchenne muscular dystrophy

A

purely supportive treatment

325
Q

what is Charcot marie tooth

A

an inherited sensory and motor PNS polyneuropathy caused by an autonomic dominant mutation of PUP22 gene (chromosome 17)

326
Q

what are symptoms of Charcot marie tooth

A

foot drop - peroneal palsy
stork legs - v.thin calves
hammer toes - curled up
Pes planus - flat feet
Pes cavus - high arched feet
reduced DTRs

327
Q

how do you diagnose Charcot marie tooth

A

Nerve biopsy
nerve conduction study
genetic testing

328
Q

how do you treat Charcot Marie tooth

A

supportive treatment
orthotics
physiotherapy

329
Q

what is tetanus

A

Tetanus is an infection caused by bacteria called Clostridium tetani. When these bacteria enter the body, they produce a toxin that causes painful muscle contractions.

330
Q

what bacteria causes tetanus

A

clostridium tetani

331
Q

what type of bacteria is clostridium tetani

A

gram positive bacilli

332
Q

what is the pathophysiology of tetanus

A

tetanospasmin toxin is produced by the clostridium tetani bacteria, and causes involuntary muscle spasms by targeting VAMP, which is necessary for the release of neurotransmitter from nerve endings

333
Q

how do you treat tetanus

A

PRIMARY - vaccinate

334
Q

what is herpes zoster

A

chicken pox or shingles

335
Q

what percentage of under 16s have varicella zoster virus

A

90% !!!

336
Q

what does reactivation of varicella zoster virus cause

A

Shingles
- peripheral nerves attacked via the dorsal root

337
Q

what is the symptoms of shingles

A

painful rash confined to a dermatome

338
Q

how do you treat shingles

A

oral acyclovir (antiviral)

339
Q

what is Prion/creutzveld-jakub disease

A

‘mad cow disease’
Prion diseases are transmissible, untreatable, and fatal brain diseases of mammals

340
Q

what is the pathophysiology of prions disease

A

the idiopathic misfold proteus is deposited in the cerebrum and cerebellum causing severe cerebellar dysfunction

341
Q

can you treat prions disease

A

no there is no treatment

342
Q

What is a transient ischaemic attack

A

Acute loss of cerebral or ocular function with symptoms lasting less than 24 hours due to an arteriothromboembolism from an artery

343
Q

How long does a transient ischemic attack last for

A

Between 5-15 minutes

344
Q

What presentation do you get with a transient ischemic attack in the carotid artery

A

Amaurosis fugax
Aphasia
Hemiparesis
Hemisensory loss
Hemianopia

345
Q

What presentation do you get with a transient ischemic attack in the vertebrobulbar artery

A

Diplopia
Vomiting
Choking
Vertigo
Ataxia
Hemisensory loss

346
Q

How does an ischemic anterior carotid artery stroke present

A

Contralateral weakness and sensory loss of lower limb
Incontinence
Drowsiness
Thinking and personality changes
Truncal ataxia

347
Q

How does an ischemic middle cerebral artery stroke present

A

Contralateral motor weakness and sensory loss
hemiparesis
Speach changes
Facial dropping

348
Q

how does a posterior carotid artery ischemic stroke present

A

perception
homonymous hemianopia

349
Q

what is seen in a vertebrobasilar artery ischemic attack

A

coordination and balance problems

350
Q

what is seen in lateral medullary syndrome

A

sudden vomiting and vertigo
ipsilateral Horners syndrome - reduced sweating, facial numbness, dysarthria, limb ataxia, dysphagia

351
Q

How does a brainstem infarction present

A

Quadriplegia
facial paralysis and numbness
gaze and vision problems
coma
locked in syndrome
altered consciousness
vertigo
vomiting

352
Q

what is an extradural haematoma

A

it is a bleed between the skull and the dura mater-usually die to a fracture of the skull affecting the middle meningeal artery

353
Q

what skull fracture do you suspect if there is a lemon shaped lesion on a CT

A

Temporal or parietal bone fracture

354
Q

what must you not give in the cause of an extradural haematoma

A

Aspirin

355
Q

what is a subarachnoid haemorrhage

A

it is bleeding between the arachnoid mater and the pia mater

356
Q

what is seen on a CT when a patient has a subarachnoid haematoma

A

a star shapes lesion on CT

357
Q

what is a subdural haematoma

A

it is bleeding between the dura mater and arachnoid mater

358
Q

what is seen on CT when someone has suffered from a subdural haematoma

A

a banana shaped lesion on CT - clot turs from white to grey over time

359
Q

what investigation is done to diagnose a subdural haematoma

A

midline shift of the brain

360
Q

what risk factors increase chances of epilepsy

A

family history
premature babies - abnormal cerebral blood vessels
drugs - cocaine

361
Q

what is the diagnosis criteria for epilepsy

A

need to have 2 unprovoked seizures occurring over 24 hours apart
need to have one unprovoked seizure and probability of future seizures
epileptic syndrome diagnosis

362
Q

when is dysphagia present in epilepsy

A

after a temporal love seizure

363
Q

what is a primary generalised seizure

A

involves the whole cortex
bilateral and symmetrical motor manifestations
loss of consciousness and awareness

364
Q

what is an atonic seizure

A

it is loss of muscle tone - floppy

365
Q

what is seen in temporal lobe focal seizure

A

speech comprehension, memory and emotion are affected
anxiety
lip smacking - automatisms

366
Q

what is seen in a frontal lobe focal seizure

A

motor disturbances
Jacksonian march 0 up and down the motor homunculus
Postical Todds palsy

367
Q

What is seen in a parietal lobe focal seizure

A

sensation changes
occipital - spots, flashes, lines

368
Q

what medication is given in myoclonic seizures

A

Levetiracetam or topiramate

369
Q

what medication is given in absence seizures

A

ethosuximide

370
Q

what is given in partial seizures

A

Lamotrigine or carbamazepine

371
Q

what are features of non epileptic seizures

A

Metabolic disturbances
longer
dont occur in sleep
no incontinence or tongue biting
pre-ictal anxiety signs
no muscle pain

372
Q

what medication is given in parkinsons if the patient is young and biologically fit

A
  1. DA agonist
  2. MOA-B inhibitor
  3. L-DOPA
373
Q

what is given in parkinsons if the patient is biologically frail with comorbidities

A
  1. L-DOPA
  2. MOA-B inhibitor
374
Q

what is the pathophysiology behind huntingtons

A

there is less GABA causing less regulation of dopamine to the striatum. This causes an increase in dopamine levels resulting in excessive thalamic stimulation and subsequent increased movement (chorea)

375
Q

what is the treatment for Huntingtons

A

Benzodiazepines or valproic acid for chorea
SSRI for depression
Haloperidol or risperidone for psychosis

376
Q

what is a differential diagnosis for Huntingtons

A

Sydenham’s chorea - rheumatic fever

377
Q

how do you treat alzheimers

A

can use cholinesterase inhibitors to help slow progression

378
Q

what sort of decline is seen in vascular dementia

A

a stepwise deterioration

379
Q

how do you manage vascular dementia

A

manage predisposing factors

380
Q

How do you manage lewy body dementia

A

cholinesterase inhibitors

381
Q

what are symptoms of lewy body dementia

A

disinhibition
personality change
early memory preservation
progressive aphasia

382
Q

what are other diseases can cause dementia

A

infection
chronic haematoma
SLE
sarcoidosis
neoplasia
hypothyroid
hypoadrenalism
hypercalcaemia
hydrocephalus

383
Q

what are symptoms of frontotemoral (picks) dementia

A

disinhibition
personality change
early memory preservation
progressive aphasia

384
Q

what are secondary causes for headache

A

giant cell/temporal arteritis
sentinel headache
thunderclap headache
trauma
medication overdose
trigeminal neuralgia
systemic infection
meningitis or encephalitis

385
Q

what are red flags in headaches

A

worst headache ever
epilepsy
onset is over 50
severe and rapid onset
abnormal pattern of migraine

386
Q

how does a migraine clinically present

A

unliteral pain
motion sensitivity
throbbing pain
moderate to severe intensity
nausea and vomiting
photophobia and phonophobia

387
Q

what can be given as prophylaxis for migraine

A

beta blockers
acupuncture
TCAs - amitriptyline
Anticonvulsant - topiramate

388
Q

what are causes of tension headache

A

missed meals
conflict
stress
clenched jaw
overexertion
fatigue
depression
bad posture
hunger
noise

389
Q

what are differential diagnosis for tension headache

A

migraine
cluster headaches
GCA
drug induced headache - worsens with analgesia

390
Q

how long can a cluster headache last for

A

15-160 minutes

391
Q

what is the definition of motor neurone disease

A

a group of neurodegenerative disorders that are characterized by the selective loss of neurons in the motor cortex, the cranial nerve nuclei and the anterior horn cells. there is no effect on sensory neurones
it is a progressive and ultimately fatal condition

392
Q

What is ALS

A

type of motor neurone disease where you see loss of neurons in the motor cortex and the anterior horn

393
Q

What are features of ALS

A

Have LMN and UMN signs
Positive babinski response
Asymmetric
Corticobulbar signs indicate a worse prognosis

394
Q

what type of motor neurone disease is the most common

A

ALS

395
Q

what gene is associated with ALS

A

SOD1 gene

396
Q

what is progressive bulbar palsy

A

a type of motor neurone disease affecting cranial nerves 9-12

397
Q

what are features of progressive bulbar palsy

A

UMN and LMN
Dysphagia and chewing difficulties
Flaccid tongue
Speech is hoarse, quiet and nasal
normal or absent jaw jerk

398
Q

What motor neurone disease has the worse prognosis

A

Progressive bulbar palsy

399
Q

what is progressive muscular atrophy

A

A motor neurone disease where the Anterior horn cells are affected

400
Q

what are features of progressive muscular atrophy

A

Only the lower motor neurone is affected, distal muscles are affected first then the proximal ones

401
Q

what is primary lateral sclerosis

A

a rare neuromuscular disease with slowly progressive weakness in voluntary muscle movement. PLS affects the upper motor neurons (also called corticospinal neurons) in the arms, legs, and face

402
Q

what fungi can cause meningitis

A

Cryptococcus
Candida - immunocompromised patients

403
Q

what bacteria can cause meningococcal septicaemia

A

Neisseria meningitidis

404
Q

What would the glass test show in someone with meningitis

A

blanching or non blanching rash

405
Q

what empirical therapy would you give for meningitis before you know whats causing it

A

IV benzylpenicillin

406
Q

what medication would you give to a patient with meningitis if they had a penicillin allergy

A

Chloramphenicol

407
Q

what are differential diagnosis for meningitis

A

SAH
migraine
Encephalitis
Flu

408
Q

what are the clinical presentations of Guillian-Barr syndrome

A

Breathing problems
Back pain
Sensory disturbance
Sweating
Urinary retention

409
Q

what is syncope

A

it is the event of temporarily loosing consciousness due to disruption of blood flow to the brain, often leading to a fall.

410
Q

what can cause primary syncope

A

Dehydration
Missed meals
Extended standing in a warm environment
A vasovagal response to a stimuli such as a sudden surprise

411
Q

What are secondary causes of syncope

A

Hypoglycaemia
dehydration
anaemia
infection
anaphylaxis
arrhythmias
valvular heart disease
hypertrophic obstructive cardiomyopathy

412
Q

what are signs of syncope

A

Hot or clammy symptoms
sweaty
heavy
dizzy or lightheaded
vision going blurry or dark
headache

413
Q

what investigations are done for syncope

A

Full history and examination
ECG - arrhythmias or long QT
24 hour EGC
Echocardiogram
Bloods - FBC, U+E and blood glucose

414
Q

what are the three broad pathologies that can lead to ischaemic stroke

A

primary vascular pathologies
cardiac pathologies
haematological pathologies

415
Q

what are signs and symptoms of an ischaemic stroke

A

Vision loss/vision field deficit
Muscle weakness
Aphasia
Ataxia
Sensory loss
Headache
Diplopia (double vision)
Dysarthria (slurred words)
Gaze paresis (can’t move eyes in same direction)
Arrhythmias, murmurs, pulmonary oedema

416
Q

what are possible complications of ischaemic stroke

A

DVT
haemorrhagic transformation of an ischaemic stroke
depression
aspiration pneumonia

417
Q

what are signs and symptoms of a haemorrhagic stroke

A

Unilateral weakness
Sensory loss (numbness)
Dysphasia
Dysarthria
Visual disturbance
Photophobia
Headache
Ataxia
Vertigo
N+V
Decreased level of
consciousness/coma
Confusion
Gaze paresis

418
Q

what drugs can be given to manage a haemorrhagic stroke

A

Manitol

419
Q

what is the pathophysiology behinds a transient ischaemic attack

A

combination of
- degree of obstruction
- area and function of tissue supplied
- length of time obstruction occurs over
- ability of collateral vessel to provide supplemental perfusion

420
Q

where do the majority of subarachnoid haemorrhages occur

A

anterior communicating/anterior cerebral artery junction
Distal internal carotid artery/posterior communicating artery junction
middle cerebral artery bifurcation

421
Q

what are differential diagnosis for subarachnoid haemorrhage

A

Non-aneurysmal perimesencephalic SAH
Aortic dissection
Cerebral and cervical arteriovenous malformation
Dural arteriovenous fistulae
Vasculitis
Saccular aneurysms of spinal
arteries
Cardiac myxoma
Septic (mycotic) aneurysm
Pituitary apoplexy
Cocaine abuse
Anticoagulants
Sickle cell disease

422
Q

what are complications of subdural haemorrhage

A

Neurological defects
coma
stroke
epilepsy

423
Q

what is the presentation of extradural haemorrhages

A

Drowsiness
Pupil asymmetry (IIIrd cranial nerve compression)
Impaired consciousness
Headache (severe)
Vomiting
Seizures
Confusion
Hemiparesis
Upgoing plantars
Coma

424
Q

what triggers can push neurones past the seizure threshold

A

sleep withdrawal
alcohol intake or withdrawal
drug misuse
physical or mental exhaustion
flickering lights
infection or metabolic disturbance

425
Q

what are tonic symptoms of epilepsy

A

Rigidity
Epileptic cry
Tongue biting
Incontinence
Hypoxia/cyanosis (no breathing during this phase)

426
Q

what are clonic seizure symptoms

A

Convulsions/limb jerking
Eye rolling
Tachycardia
No breathing/random or uncontrolled breaths

427
Q

what is the pathophysiology of parkinsons disease

A

Progressive loss of dopaminergic neurones in the basal ganglia
- mostly substantia nigra

428
Q

what are differential diagnosis for parkinsons disease

A

Alzheimer’s
Multi-infarct dementia
Repeated head injuries
VODKA signs:
Vascular events (stroke/MI)
Orthostatic hypotension with atonic bladder
Dementia with vertical gaze paralysis
Kayser-Fleisher rings
Apraxic gait

429
Q

what can cause drug overuse headache

A

Analgesics - aspirin
Combination pain killers -caffeine and aspirin
Migraine medications
Opiates

430
Q

what are risk factors for drug overuse headaches

A

History of chronic headaches
frequent use of headache medications

431
Q

what are symptoms of drug overdose headache

A

Chronic headache occurring > 15 days a month

Develops/worsens with frequent use of any drug treatment for pain in people with tension headache/migraine

Resolves with withdrawal of symptomatic treatment

432
Q

how do you manage drug overdose headache

A

analgesia withdrawal
no more than 6 days a month on analgesia
log acting anti inflammatories can ease headaches
antiemetics can help withdrawal

433
Q

what is the pathophysiology of multiple sclerosis

A

Demyelination due to CD4 attacking oligodendrocytes, and macrophages digest the myelin sheathe

434
Q

what is the progression of multiple sclerosis

A

relapse -remission disease
relapse - inflammation and damage to myelin
remission - inflammation subsides and some remyelination of damaged areas

435
Q

what are differential diagnosis of multiple sclerosis

A

Migraine
Cerebral neoplasms
Nutritional deficiencies (B12 and copper)
Infections (syphillis/HIV)
MND
Psychiatric disease/functional
Vascular causes
Other progressive diseases
MRI lesions (sarcoidosis, SLE, Bechet’s syndrome)

436
Q

what are complications of multiple sclerosis

A

UTI
Osteopenia and osteoperosis
depression
visual impairment
erectile dysfunction
cognitive impairment
impaired motility

437
Q

what is the pathophysiology behind motor neurone disease

A

there is oxidative neuronal damage with internal cell damage leading to apoptosis, as well as prolonged caspase activity, promoting apoptosis

438
Q

what are causes of parasitic meningitis

A

P. Falciparum

439
Q

what are complications of meningitis

A

hearing loss
epilepsy
memory loss and concentration problems
coordination problems
learning difficulties
vision loss
loss of limbs
bone and joint problems
kidney problems

440
Q

what is the pathophysiology of encephalitis

A

there is an intracranial infection causing an inflammatory response in the
- cortex
- white mater
- basal ganglia
- brain stem

441
Q

what medication can be given to treat high intracranial pressure

A

dexamethasone

442
Q

what are possible complications of encephalitis

A

death
hypothalamic and autonomic dysfunction
ischaemic stroke
neurological sequelae
seizures
cerebral haemorrhage
cerebral vasculitis
hydrocephalus
post viral chronic fatiuge syndrome

443
Q

what are three types of gliomas

A

astrocytoma
oligodendroglioma
ependymoma

444
Q

what are acoustic neuromas

A

Schwann cell tumour of the auditory nerve that innervates the inner ear

445
Q

what is the classic triad seen in acoustic neuromas

A

hearing loss
tinitus
balance problems

446
Q

what are risk factors for primary brain tumours

A

affluent groups
ionising radiation
vinyl chloride
immunosuppression
family history - genetics

447
Q

what are possible complication of primary brain tumours

A

Hydrocephalus
Midline shift and herniations through the foramen magnum

448
Q

what are signs and symptoms of giant cell arteritis

A

Rare under 50
Generalised headaches
Scalp tenderness
Claudication of jaw
Painless temporary or permanent visual loss
Generalised malaise
Fever
Tiredness
Superficial temporal artery tenderness, thickening or nodularity
Absent temporal artery pulse
Abnormal fundoscopy
Associated with polymyalgia rheumatica symptoms

449
Q

what are causes of spinal cord compression

A

degenerative disc lesions
degenerative vertebral lesions
TB
Epidural abscess
vertebral neoplasm
epidural haemorrhage
Paget’s disease

450
Q

what are possible complications of spinal cord compression

A

pressure ulcers
cardiovascular dysfunction
heterotopic ossification
deep vein thrombosis
UTI
PE
MRSA infection

451
Q

what are possible complications for cauda equina syndrome

A

permanent leg weakness
sexual dysfunction
urinary dysfunction
chronic pain
DVT

452
Q

on what level is the common peroneal nerve

A

L4-S1

453
Q

where does the common peroneal nerve originate

A

sciatic nerve, just above the knee

454
Q

ow can the common peroneal nerve be damaged

A

trauma
sitting crossed legged

455
Q

what are signs of common peroneal nerve lesions

A

foot drop
weak ankle dorsiflexion
sensory loss over the dorsum of foot

456
Q

on what level is the median nerve

A

C6-T1

457
Q

on what level is the ulnar nerve

A

C7-T1

458
Q

on what level is the radial nerve

A

C5-T1

459
Q

what are the signs of a lesion in the brachial plexus

A

pain
weakness
variable distribution

460
Q

on what level is the phrenic nerve

A

c3-5

461
Q

what is the lateral cutaneous nerve of the thigh

A

L2-3

462
Q

on what level is the sciatic nerve

A

L4-S3

463
Q

where does the tibial nerve originate

A

L4-S3

464
Q

what does a lesion of the tibial nerve lead to

A

inability to
stand on tiptoes
invert the foot
flex the toe
sensory loss over the sole

465
Q

what are differential diagnosis for myasthenia gravis

A

Lambert-eaton myasthenic syndrome

466
Q

what are differential diagnosis for myasthenia gravis

A

Lambert-eaton myasthenic syndrome
botulism
penicillamine induced myasthenia gravis
primary mypoathies

467
Q

what are complications of myasthenia gravis

A

respiratory failure
impaired swallowing
acute aspiration
secondary pneumonia

468
Q

what causes peripheral neuropathy

A

DAVID
diabetes
alcoholism
vitamin deficiency - B12
infective/inherited - Guillaine-barre/charcot-marie-tooth
drugs - isoniazid

469
Q

what are signs of peripheral neuropathy

A

Numbness/tingling in feet and hands
Burning/stabbing/shooting pain in affected areas
Loss of balance/co-ordination
Muscle weakness (especially in feet)

470
Q

How do you assess depression in clinic

A

The PHQ-9 is the depression tool used by patients, which scores each of the nine DSM-IV criteria as “0” (not at all) to “3” (nearly every day). It has been validated for use in primary care.

471
Q

what are different treatments for depression

A

Selective serotonin reuptake inhibitors
Serotonin-noradrenaline reuptake inhibitors
TCAs
MAOIs

472
Q

what is the mode of action of SSRIS

A

this stop the reuptake of serotonin from the synaptic cleft

473
Q

what are examples of SSRIs

A

SERTRALINE, CITALOPRAM, DAPOXETINE, PAROZETINE

474
Q

what are side effects of SSRIs

A

They can cause nausea, anorexia, insomnia, loss of libido, failure to orgasm, serotonin syndrome where you have too much serotonin which causes tremor hyperthermia and cardiovascular collapse
CONTRAINDICATED WITH NDAIDS

475
Q

what is the mode of action of SNRIs

A

they bloc re-uptake of noradrenaline and serotonin from the synaptic cleft

476
Q

what are examples of SNRIs

A

DULOXETINE AND VENLAFAXINE

477
Q

what are side effects of SNRIs

A

these can cause nausea, dry mouth, dizziness, headache, excessive sweating

478
Q

what is the mode of action of TCAs

A

they block re-uptake of amines by nerve terminals and cause them to be in the synapse longer
- act as a competitive antagonist

479
Q

what are examples of TCAs

A

AMYTRYPTILINE, CLOMPRIMINE, IMIPRAMINE, DOSULEPIN

480
Q

what are side effects of TCAs

A

their side effects are sedation, confusion, dry mouth, blurred vision, constipation, urinary retention, postural hypertension

481
Q

what is the mode of action of MAOIs

A

they inhibit the breakdown of monoamines in the synaptic cleft

482
Q

What are some examples of MAOIs

A

PHENELZINE, ISOCARBOXAZID, SELEGILINE

483
Q

what are side effects of MAOIs

A

side effects are dry mouth, nausea, diarrhoea, constipation, headache, drowsiness, insomnia, dizziness and lightheadedness

Phase 2a - Jemima (11 decks)

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