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FCM Matrix > Neurology > Flashcards

Neurology Flashcards

1
Q

What is shingles also known as?

A

Herpes Zoster Infection

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2
Q

What causes shingles?

A

reactivation of varicella zoster virus

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3
Q

Key risk factors for shingles

A

increasing age, immunosuppressive conditions, HIV

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4
Q

typical presentation of shingles

A

acute, unilateral, painful blistering rash

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5
Q

Which dermatomes are commonly affected in shingles

A

T1- L2

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6
Q

Features of shingles

A

prodromal period

  • 2-3day hx of burning pain over the dermatomes affected
  • may have fever, headache, lethargy

Rash

  • erythematous, macular rash which becomes vesicular
  • demarcated by dermatome and doesnt cross the midline
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7
Q

How is shingles diagnosed?

A

clinical diagnosis

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8
Q

What is the medical management of shingles?

A

Analgesia

  • paracetemol and NSAIDs
  • amitriptyline if first line insufficient
  • oral corticosteroids if not responding to the above

Antivirals within 72hrs unless <50yo and mild rash/pain with no risk factors

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9
Q

Advice given to patient with shingles

A

remind them they are infectious until vesicles have crusted over usually 5-7 days following onset (avoid pregnant and immunosuppressed people)

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10
Q

What are the complications of shingles

A
  • post- herpetic neuralgia
  • herpes zoster ophthalmicus
  • herpes zoster oticus (Ramsay Hunt syndrome):
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11
Q

What is syncope?

A

transient loss of consciousness with spontaneous complete recovery

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12
Q

What are the main causes of syncope?

A
  • Reflex mediated (neurally mediated)
  • Cardiac (arrhythmias and structural causes)
  • Orthostatic (iatrogenic, dementia, volume depletion)
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13
Q

Which investigations should be carried out in syncope?

A
  • ECG (?prolonged QT)
  • lying standing BP / tilt table test
  • Glucose
  • Electrolytes
  • FBC
  • Underlying illness (CXR, CT, LP, ECHO etc)
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14
Q

Causes of cardiac syncope

A 
arrhythmias 
- bradycardia / tachycardia 
structural
- valvular
- MI
- HOCM
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15
Q

Treatment of cardiac syncope

A

treat the problem

  • medicine (beta blockers, atropine)
  • electrical cardioversion
  • catheter ablation
  • pacemaker
  • implantable cardioverter defibrillator (ICD)
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16
Q

What is vasovagal syncope?

A

triggered by emotion, pain or stress. Often referred to as ‘fainting’

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17
Q

What is subarachnoid haemorrhage?

A

presence of blood in the subarachnoid space

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18
Q

What are the causes of SAH?

A

head injury (traumatic SAH) is the most common cause

spontaneous SAH (non-traumatic)

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19
Q

Causes of spontaneous SAH

A
  • Intracranial aneurysm( ruptured ‘berry’ aneurysms)

- Arterial dissection

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20
Q

Which conditions are associated with berry aneurysms?

A
  • Adult Polycystic Kidney Disease

- coarctation of the aorta

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21
Q

Classical presentation of SAH

A
  • Thunderclap headache
  • N&V
  • Meningism (photophobia, stiff neck)
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22
Q

How can a SAH be confirmed?

A

CT head
LP if CT Head if negative
Neuro referral

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23
Q

Which findings on an LP are indicative of SAH

A

xanthochromia (result of RBC breakdown) and normal or raised opening pressure

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24
Q

After SAH is confirmed, which investigations can be carried out to identify a causative pathology?

A

CT inter-cranial angiogram (vascular lesion e.g aneurysm)

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25
Q

What is Multiple sclerosis?

A

autoimmune disorder characterised by demyelination in the central nervous system

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26
Q

Who is at higher risk of MS

A

women ages 20-40 living at higher latitude

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27
Q

How can MS be diagnosed

A

refer to neuro and bloods to exclude other causes

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28
Q

What are the most common initial presentations of MS

A
  • optic neuritis
  • transverse myelitis (inflammation within spinal cord)
  • cerebellar sx ( dysmetria, ataxia, vertigo)

sx disseminated in time and space

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29
Q

Which investigations should be carried out for MS?

A

MRI

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30
Q

How is an acute relapse of MS treated?

A

High dose steroids (methylprednisolone) to shorten duration of relapse

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31
Q

What is a venous sinus thrombosis?

A

occurs when a blood clot forms in the brain’s venous sinuses. This prevents blood from draining out of the brain. As a result, blood cells may break and leak blood into the brain tissues, forming a hemorrhage.

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32
Q

What are the symptoms of venous sinus thrombosis?

A
  • headaches
  • n&v
  • blurred vision
  • LOC
  • seizures
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33
Q

How is venous sinus thrombosis diagnosed?

A

MRI venography

CT venography

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34
Q

Treatment of venous sinus thrombosis

A

Heparin

Warfarin for long term

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35
Q

What is a Cavernous sinus thrombosis

A

the formation of a clot within the cavernous sinus

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36
Q

What is the most common cause of CST

A

infection

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37
Q

Common clinical features of CST

A

headache, unilateral periorbital oedema, proptosis (eye bulging), photophobia and cranial nerve palsies

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38
Q

Which nerve is most commonly affected in CST

A

abducens nerve (CN VI)

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39
Q

Complication of CST

A

Where the cause is infection, thrombosis of the cavernous sinus can rapidly progress to meningitis.

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40
Q

Investigations requested in suspected CST

A

CT Head/ MRI
FBC
Blood culture
?LP

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41
Q

How is CST treated

A

Abx for causative infection

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42
Q

Which seizures last a few seconds and are associated with a quick recovery

A

Absence

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43
Q

What may provoke an absence seizure

A

hyperventilation or stress

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44
Q

Who is most commonly affected by absence seizures?

A

3-10 years old and girls are affected twice as commonly as boys

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45
Q

How are absence seizures managed?

A

sodium valproate and ethosuximide are first-line treatment

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46
Q

Prognosis of absence seizures

A

good prognosis - most become seizure free in adolescence

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47
Q

Status epilepticus is defined as…

A

a single seizure lasting >5 minutes OR

>= 2 seizures within a 5-minute period without the person returning to normal between them

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48
Q

Why is the priority in Status epilepticus to terminate seizure activity

A

can lead to irreversible brain damage

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49
Q

What is the immediate management of Status epilepticus?

A

ABC

IV benzodiazepines

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50
Q

What may be used in management if there is ongoing status epilepticus

A

phenytoin or phenobarbital infusion

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51
Q

What is a febrile convulsion?

A

seizures provoked by fever in otherwise normal children

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52
Q

clinical features of febrile convulsion

A

usually occur early in a viral infection
usually lasting less than 5 minutes
most commonly tonic-clonic

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53
Q

How can a generalise seizure be further classified

A

Motor- e.g tonic-clonic

Non-motor - e.g absence

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54
Q

Sx of epilepsy

A

bite their tongue
incontinence of urine
post-ictal phase

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55
Q

Which investigations are ordered following a patients first seizure?

A

EEG and MRI

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56
Q

First line tx for generalised seizure

A

sodium valproate

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57
Q

First line tx for focal seizure

A

carbamazepine

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58
Q

What are the guidelines for driving post seizure?

A
  • Generally patients cannot drive for 6 months following a seizure.
  • For patients with established epilepsy they must be fit free for 12 months before being able to drive
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59
Q

What is the difference between a generalised and focal seizure?

A

Focal onset seizures start in one area and can spread across the brain and cause mild or severe symptoms, depending on how the electrical discharges spread. Generalized seizures can start as focal seizures that spread to both sides of the brain.

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60
Q

What happens in tonic-clonic seizure?

A 
Tonic 
- muscles stiffen
- LOC
- tongue biting
Clonic 
- rhythmical jerking
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61
Q

What is Bell’s palsy?

A

Acute, unilateral facial nerve (CN VII) paralysis

- rapid onset ( < 72 hours)

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62
Q

Features of Bell’s palsy

A
  • Lower motor neuron facial nerve : forehead affected
  • Post-auricular pain (preceding paralysis)
  • Altered taste
  • Dry eyes

Facial muscle weakness (unilateral):

  • drooping of the eyebrows
  • corner of the mouth
  • loss of the nasolabial fold
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63
Q

What is the bell’s phenomenon?

A

The eye can’t be closed- eyeball rotates upwards and outwards

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64
Q

What is the management of bell’s palsy?

A
  • oral prednisolone within 72 hours
  • Seek specialist advice
  • Eyecare: prescription of artificial tear + eye lubricants
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65
Q

What is the follow-up for bell’s palsy?

A

If paralysis shows no improvement after 3 week, refer to ENT urgently

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66
Q

What is the prognosis for bell’s palsy?

A

Full recovery within 3-4 months

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67
Q

What dose of prednisolone is given in bell’s palsy?

A

50 mg for 10 days

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68
Q

What are the two main ascending tracts of the spinal cord and what information do they carry?

A

Dorsal - fine touch, proprioception, vibration sense

Spinothalamic - pain and temperature

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69
Q

What is the descending tract of the spinal cord called and what does it carry?

A

corticospinal tract carries motor information

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70
Q

Which signs indicate there is a problem with the spinal cord rather than with the other parts of the nervous system?

A

often bilateral and asymmetrical

mixed upper and lower motor neuron signs as the spinal cord is part of both the CNS and PNS

  • upper signs : increased tone, clonus, hyperreflexia
  • lower signs: muscle wasting, flaccid paralysis, reduced reflexes

sphincter involvement (e.g urinary retention/constipation)

autonomic dysfunction indicates lesion is above T6

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71
Q

How to tell where in the spinal cord the problem is

A

cervical if all 4 limbs affected
thoracic if only lower limbs affected

above C3 if resp difficulties and diaphragm affected

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72
Q

What is Amyotrophic lateral sclerosis

A

(motor neuron disease)
affects both upper (corticospinal tracts) and lower motor neurons
results in a combination of upper and lower motor neuron signs

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73
Q

What features are seen in neoplastic spinal cord decompression?

A

back pain, may be worse on coughing or lying down

  • lower limb weakness
  • sensory loss or numbness
  • neuro signs dependent on level of lesion
  • -above L1 usually UMN in legs and sensory
    • below L1 usually LMN in legs and perianal numbness
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74
Q

Which investigation should be requested following suspected neoplastic spinal cord decompression?

A

urgent whole MRI spine within 24hrs of presentation

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75
Q

Management of neoplastic spinal cord decompression

A

high-dose oral dexamethasone

urgent oncological assessment for consideration of radiotherapy or surgery

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76
Q

What are the symptoms of diabetic peripheral neuropathy?

A

Sensory loss:

  • Tingling
  • Numbness - unable to feel light touch
  • Cannot feel pain
  • Unable to detect change in temperature
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77
Q

Management of diabetic peripheral neuropathy

A

1st line = amitriptyline, duloxetine, gabapentin or pregabalin

  • glycaemic control
  • referral to podiatry
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78
Q

What are the presentations of diabetic foot disease?

A
  1. neuropathy: loss of sensation

2. ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication

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79
Q

What is involved in annual diabetic foot check?

A
  1. screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse
  2. screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot
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80
Q

What is guillain-barre syndrome?

A

immune-mediated demyelination of the peripheral nervous system often triggered by an infection

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81
Q

What infection triggers guillain-barre syndrome?

A

campylobacter jejuni

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82
Q

What are the characteristic features of guillain-barre syndrome?

A

Progressive, symmetrical weakness of all limbs

  • usually ascending (leg first)
  • reflexes reduced or absent
  • mild sensory symptoms
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83
Q

What are the other features for guillain-barre syndrome?

A
  1. Weakness
    - Maximum severity at 2 weeks after initial onset , stops progressing after 5 weeks
    - Facial weakness, dysphasia, dysarthria
    - May lead to resp failure
  2. Pain – neuropathic pain esp in legs, possible back pain
  3. Reflexes – may be reduced or absent
  4. Sensory symptoms – paraesthesia & sensory loss starting in the lower extremities
  5. Autonomic symptoms – reduced sweating, heat tolerance, urinary hesitancy
84
Q

How do you diagnose GBS?

A

Clinical assessment

85
Q

What investigations may be helpful in diagnosing GBS?

A
  1. Nerve conduction studies – most useful confirmatory test, if initially normal should be repeated after 2 weeks.
  2. Lumbar puncture – elevated level of CSF protein with normal white cell count, week 1 after symptom onset
86
Q

Management of GBS

A
  1. Admission to hospital, preferably hospital with Neuro Critical Care capabilities
  2. Intravenous Immunoglobulin or Plasmapheresis.
    - -> IVIG - contraindicated in IgA deficiency or renal impairment
  3. DVT prophylaxis – until able to walk independently
  4. Watch pt. closely for need of intubation
  5. Initiate cardiac monitoring –
  6. HTN management
  7. Pain control – gabapentin, opiates, carbamazepine
  8. Physical Therapy to avoid contractures, maintain flexibility
  9. Rehabilitation MDT approach
    Psychological support for pt. and family
87
Q

What does Chronic IDP stand for?

A

chronic inflammatory demyelinating polyneuropathy

88
Q

Symptoms of Chronic IDP

A
  1. Initially present with some limb weakness which will slowly progress to symmetrical weakness in muscles of the hands, feet, shoulder and hip.
  2. Symptoms may be progressive, episodic or monophasic (1-3 years).
  3. Symptoms should last > 8 weeks
  4. Loss of sensation, numbness, tingling, pins and needles
89
Q

Clinical features of Chronic IDP

A
  1. Muscle atrophy in hands, feet, shoulders and hips
  2. Absent or diminished deep tendon reflexes
  3. Impaired responses to sensory stimulation
  4. Ataxic gait
  5. Some cranial nerve involvement such as dysphagia or diplopia
90
Q

Investigations of Chronic IDP

A
  • NCS
  • Lumbar Puncture
  • Peripheral nerve biopsy
91
Q

Management of Chronic IDP

A

Conservative:
- Physical and occupational therapy to prevent accumulating disability over time and encouraging active lifestyle.

Medical :
1st line:
- Intravenous Immunoglobulin (IVIG)
- Plasma exchange – may only be effective for several weeks and therefore may require an intermittent treatment schedule. - Corticosteroids – used in with immunosuppressants.

  1. Long term immunosuppression :
    Takes the attack off the peripheral nerves
  2. Pharmacotherapy for neuropathic pain : e.g. gabapentin & pregabalin
92
Q

Features of migraine

A
  1. a severe, unilateral, throbbing headache
    - -> attacks may last up to 72 hours
  2. associated with nausea, photophobia and phonophobia
  3. patients characteristically go to a darkened, quiet room during an attack
  4. ‘classic’ migraine attacks are precipitated by an aura.
  5. typical aura are visual, progressive, last 5-60 minutes and are characterised by transient hemianopic disturbance or a spreading scintillating scotoma
93
Q

Management of migraine

A

Headache diary, avoid triggers – sleep, stress, hydrate, regular meals

  1. Acute:
    - -> 1st line: triptan and NSAID
    - -> simple analgesia – ibuprofen, aspirin, paracetamol before onset
    - -> Anti-emetic: metoclopramide
    - -> Follow-up within 2-8 weeks
  2. Preventative: propranolol, topiramate or amitriptyline
  3. Refer: migraine > 72 hours, typical aura: motor weakness, poor balance, headache changes
94
Q

What medication is contraindicated in migraine with aura?

A

COCP

95
Q

Symptoms of tension headache

A
  • often described as a ‘tight band’ around the head or a pressure sensation.
  • bilateral
  • tends to be of a lower intensity than migraine
  • may be related to stress
96
Q

Management of tension headache

A
  • Acute: 1st line (aspirin, paracetamol or an NSAID)
  • Prophylaxis: 10 sessions of acupuncture over 5-8 weeks
  • -> Low dose amitriptyline (10-75mg)
  • —–>Not responsive – stop and discuss neuro
  • —–>Responsive – attempt withdrawal 4-6 months
97
Q

Symptoms of cluster headache

A
  1. Unilateral periorbital pain
  2. Ipsilateral autonomic symptoms: eyelid oedema, facial sweating or flushing, nasal congestion, conjunctival injection, lacrimation
  3. Brief attacks of < 3 hours duration
  4. pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
  5. clusters typically last 4-12 weeks
98
Q

Management of cluster headache

A
  1. acute: 100% oxygen, subcutaneous triptan
  2. prophylaxis: verapamil is the drug of choice.
  3. Seek specialist advice from a neurologist if a patient develops cluster headaches with respect to neuroimaging
99
Q

What is essential tremor?

A

Autosomal dominant condition which usually affects both upper limbs

100
Q

Features of essential tremor

A
  • postural tremor: worse if arms outstretched

- improved by alcohol and rest

101
Q

Management of essential tremor

A

1st line = propanolol at low dose

102
Q

What is parkinson’s disease?

A

Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra

103
Q

What is the classic triad of features of parkinson’s disease?

A
  1. Bradykinesia
    - short, shuffling steps
    - difficulty initiating movement
  2. Tremor
    - worse when stessed or tired
    - ‘pill-rolling’
  3. Rigidity
    - lead pipe
104
Q

How is parkinson’s diagnosed?

A

usually clinical

105
Q

What investigation can distinguish between essential tremor and parkinson’s?

A
  • Single-photon emission computed tomography
106
Q

How do you differentiate between parkinson’s disease and drug-induced parkinsonism?

A

In drug-induced parkisonism:
- motor symptoms are generally rapid onset and bilateral

  • rigidity and rest tremor are uncommon
107
Q

Management of parkinson’s disease

A

Only specialist should initiate treatment:

1st line:
Levodopa - if motor symptoms affecting QOL
Dopamine agonist - if motor symptoms not affecting QOL

108
Q

What is huntington’s disease?

A
  • inherited neurodegenerative condition.

- progressive and incurable condition that typically results in death 20 years after the initial symptoms develop.

109
Q

Features of huntington’s disease

A

Typically develop after 35 years of age:

  • chorea
  • personality changes (e.g. irritability, apathy, depression) and intellectual impairment
  • dystonia
  • saccadic eye movements
110
Q

What can peripheral neuropathy conditions be divided into?

A
  1. Motor loss

2. Sensory loss

111
Q

What conditions cause motor loss in peripheral. neuropathy?

A
  1. Guillain-Barre syndrome
  2. lead poisoning
  3. chronic inflammatory demyelinating polyneuropathy (CIDP)
  4. diphtheria
112
Q

What conditions cause sensory loss in peripheral. neuropathy?

A
  1. diabetes
  2. uraemia
  3. leprosy
  4. alcoholism
  5. vitamin B12 deficiency
  6. amyloidosis
113
Q

What nerve damage causes a foot drop?

A

Peroneal nerve (L4-L5, S1-S2)

114
Q

What nerve damage causes a wrist drop?

A

Radial nerve

115
Q

What is carpel tunnel syndrome?

A

When carpel tunnel is swollen/inflammed - the median nerve is affected

116
Q

Symptoms of carpel tunnel syndrome

A
  • Aching, tingling, pins & needles
  • Symptoms can spread up the arm
  • Worse on movement
  • temporary relief by hanging had out of bed at night or shaking vigorously
117
Q

What examination tests do you carry out for carpel tunnel syndrome?

A

Phalens

  • hold wrist fully palmarflexed
  • tap on wrist reproduces symtpoms

Tinel’s sign
- tapping over dorsum of the wrist percipitates pain

118
Q

What does wasting of the thenar eminence indicate?

A

Median nerve affected

119
Q

What investigation can be carried out for carpel tunnel syndrome?

A

NCS

120
Q

Management of carpel tunnel syndrome

A
  • Spontaneously resolves 3-6 months < 30 y/o
  • Splint
  • Steroid injection?
  • Referral for surgical decompression
121
Q

What do you not prescribe for carpel tunnel syndrome?

A

NSAIDs

122
Q

What is myasthenia gravis?

A

Autoimmune disorder from insufficient functioning ACh receptors

Affect women > men

123
Q

What is the key feature of myasthenia gravis?

A

muscle fatigability

  • worsens with activity
  • improves after rest
124
Q

What other features can you get with myasthenia gravis?

A
  • extraocular muscle weakness: diplopia
  • proximal muscle weakness: face, neck, limb girdle
  • ptosis
  • dysphagia
125
Q

What is the diagnostic test for myasthenia gravis?

A
  • Serological testing for ACh receptor antibodies

- Repetitive EMG

126
Q

Management of myasthenia gravis

A

1st line = pyridostigmine
(long-acting acetylcholinesterase inhibitors)

  • Eventually immunosuppression : prednisolone
127
Q

Management of myasthenic crisis

A
  • plasmapheresis

- IV immunoglobulins

128
Q

What is cerebral palsy?

A

disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain

129
Q

What is the classification of cerebral palsy?

A
  1. Spastic
  2. dyskinetic
  3. ataxic
  4. mixed
130
Q

What non-motor problems can children with cerebral palsy develop?

A
  1. learning difficulties (60%)
  2. epilepsy (30%)
  3. squints (30%)
  4. hearing impairment (20%)
131
Q

What are the possible manifestations of cerebral palsy?

A
  1. abnormal tone early infancy
  2. delayed motor milestones
  3. abnormal gait
  4. feeding difficulties.
132
Q

Management of cerebral palsy?

A
  1. MDT approach
  2. Oral diazepam - for spasticity
  3. Anticonvulsant , analgesia
133
Q

What is stroke?

A

sudden interruption in the vascular supply of the brain

134
Q

What are the types of stoke?

A
  1. Ischaemic
    - subtype: TIA
    - ‘ blockage in blood vessel’
  2. Haemorrhagic
    - blood vessel burst leading to reduction in blood
135
Q

What are the symptoms of a stroke?

A
  1. Motor weakness
  2. speech problems (dysphasia)
  3. swallowing problems
  4. visual field defects
  5. balance problems
136
Q

What are some symptoms more common with haemorrhagic stroke than ischaemic?

A
  • decrease in consciousness
  • headache
  • N & V
  • Seizures
137
Q

What is the FAST campaign?

A
  1. Face - ‘Has their face fallen on one side? Can they smile?’
  2. Arms - ‘Can they raise both arms and keep them there?’
  3. Speech - ‘Is their speech slurred?’

4, Time - ‘Time to call 999 if you see any single one of these signs.’

138
Q

What are the 2 types of imaging used in stroke?

A

CT
MRI

1st line = non-contrast CT head

139
Q

What criteria needs to be met for immediate treatment of ischaemic stroke?

A

Criteria
1. patients present with 4.5 hours of onset of stroke symptoms

  1. the patient has not had a previous intracranial haemorrhage, uncontrolled hypertension, pregnant etc
140
Q

What is the immediate management of ischaemic stroke?

A

Alteplase (< 4.5 hours)

Aspirin 300mg within 24 hours

141
Q

What is the management of confirmed haemorrhagic stroke?

A

Neurosurgical consultation

Those not suitable for surgery:

  1. Supportive: stop anticoag + antithrombotic meds
  2. ? lower BP acutely
142
Q

What is the surgical option for acute ischaemic stroke?

A

Thrombectomy

143
Q

Secondary prevention for stroke

A

1st line = Clopidogrel

2nd line = aspirin + modified-release (MR) dipyridamole

144
Q

What other factors need to be treated in stroke?

A
  1. fluid management
  2. Glycaemic control
  3. BP
  4. Feeding assessment + management
145
Q

What is TIA?

A

a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction. (<24 hours)

146
Q

Clinical features of TIA

A
  • unilateral weakness or sensory loss.
  • aphasia or dysarthria
  • ataxia, vertigo, or loss of balance

symptoms typically resolve within 1 hour

147
Q

Immediate management of TIA

Contraindications

A

Aspirin 300 mg immediately, unless

  1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
  2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
  3. Aspirin is contraindicated: discuss management urgently with the specialist team
148
Q

What is the advice on driving for TIA?

A

Do not drive until seen by specialist

149
Q

What investigation should be carried out for TIA?

A
  1. MRI - to detect territory of ischaemia
  2. Urgent carotid doppler

CT should be done unless alternative diagnosis

150
Q

Management of TIA

A

1st line = Clopidogrel

151
Q

What is raised intracranial pressure?

A

Additional volume in the brain + ventricles

152
Q

Features of raised ICP

A
  1. headache
  2. vomiting
  3. reduced levels of consciousness
  4. papilloedema
  5. Cushing’s triad
    - widening pulse pressure
    - bradycardia
    - irregular breathing
153
Q

What investigations should be carried out for raised ICP?

A
  1. Neuroimaging = underlying causes

2. Invasive ICP monitoring

154
Q

Management of raised ICP

A
  1. Head elevation to 30 degrees
  2. IV mannitol
  3. Controlled hyperventilation
  4. Removal of CSF
155
Q

What is temporal arteritis?

A

Large vessel vasculitis which overlaps with polymyalgia rheumatica (PMR).

156
Q

Features of temporal arteritis

A
  1. Jaw claudication
  2. temporal headache
  3. eventually leads to vision loss as optic nerve loses blood supply as large to medium vessels becomes narrowed.
  4. Can be systemically unwell.
  5. Hard, non-pulsating temporal artery (normal = pulsating, able to palpate and doesn’t feel hard)
157
Q

What is the gold standard investigation for temporal arteritis?

A

USS and biopsy

  • raised ESR > 50mm/hr
158
Q

Management of temporal arteritis

A

Urgent steroid course = high dose glucocorticoids
- as soon as diagnosis is suspected before biopsy

  1. no visual loss = high dose prednisolone
  2. visual loss = IV methylprednisolone before high-dose prednisolone
159
Q

What is vasculitis?

A

Inflammation of small vessels

- May be drug reaction

160
Q

Symptoms of vasculitis

A
  • Itching, burning purpuritic rash

- 1-3mm lesions, often on legs

161
Q

Treatment of vasculitis

A
  1. Treat underlying cause, if known
  2. Compression stockings, elevation
  3. Sedating antihistamine
  4. Colchicine/Dapsone if no systemic involvement
  5. High-dose steroid if systemic involvement, +/- methotrexate, azathioprine
162
Q

What is Alzheimers?

A

progressive degenerative disease of the brain

163
Q

Non-pharmacological management of Alzheimers

A

offer wellbeing services and group cognitive stimulation therapy

164
Q

pharmacological management of Alzheimers

A

First line: acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine)

Second line: memantine (an NMDA receptor antagonist)

165
Q

When should antipsychotics be given to patients with Alzheimers?

A

when pt is at risk of harming themselves or others or has delusions/hallucinations causing them severe distress

166
Q

What is the most common causative pathogen in enchephalitis?

A

HSV-1

167
Q

Symptoms of enchephalitis

A 
confusion or disorientation.
seizures or fits.
changes in personality and behaviour.
difficulty speaking.
weakness or loss of movement in some parts of the body.
loss of consciousness.
168
Q

Which investigations should be requested in ?encephalitis

A

CSF
PCR for HSV
MRI
EEG

169
Q

What might you see in CSF of encephalitic patient

A

lymphocytosis, elevated protein

170
Q

What is the tx of all cases of suspected encephalitis?

A

IV Aciclovir

171
Q

Life threatening complication of meningitis

A

septicaemia resulting in permanent damage of nerves or brain

172
Q

Symptoms of meningitis

A

headache, neck stiffness, photophobia, confusion, fevers, non-blanching rash

173
Q

Gold standard investigation for meningitis

A

lumbar puncture

174
Q

Characteristic CSF findings in bacterial meningitis

A

cloudy, low glucose, high protein

175
Q

What should be given to patients with suspected meningococcal disease in a pre-hospital setting?

A

IM benzylpenicillin

176
Q

When should you suspect hiv ?

A
  • unusually severe/prolonged symptoms that are recurrent or unexplained
  • conditions related to immunosuppression (shingles/oral candidiasis)
  • lymphadenopathy
  • pyrexia
  • weight loss
177
Q

HIV risk factors

A
  • coming from high prevalence area
  • sex between men and men
  • injecting drug use
178
Q

When should asymptomatic patients with HIV be tested after possible exposure?

A

at 4 weeks

179
Q

How is HIV monitored

A

HIV viral load and CD4 lymphocyte cell count

180
Q

What are people with CD4 count <200 at a higher risk of?

A

HIV-related opportunistic infections and cancers

181
Q

How is HIV treated

A

antiretrovirals - suppresses viral replication but does not eliminate HIV therefore treatment is lifelong

182
Q

The causative pathogen of tuberculosis

A

Mycobacterium tuberculosis

183
Q

Which vaccine offers protection against TB

A

BCG

184
Q

What are the 2 types of TB

A

PRIMARY
infection occurring in previously uninfected host , usually asymptomatic

SECONDARY
If the host becomes immunocompromised the initial infection may become reactivated.

185
Q

Gold standard investigation for active TB

A

Sputum culture

186
Q

What investigations may be requested in ?active TB

A

Sputum culture -GOLD STANDARD
CXR
NAAT

187
Q

What is a classical finding in CXRs in active TB

A

Upper lobe cavitation and hilar lymphadenopathy

188
Q

What is the standard therapy for treating active TB and how long should they be given

A 
first 2 months:
Rifampicin 
Isoniazid 
Pyrazinamide
Ethambutol

continue for further 4 months:
Rifampicin
Isoniazid

189
Q

How is latent TB treated

A

3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)

pyridoxine reduces the occurence of isoniazid side effects

190
Q

Give key side effects for TB drugs

A

Rifampicin : red/orange secretions

Isoniazid: peripheral neuropathy

Pyrazinamide: hyperuricaemia=gout

Ethambutol : optic neuritis

191
Q

Primary and secondary features of syphilis

A

Primary features

  • chancre
  • lymphadenopathy

Secondary features - occurs 6-10 weeks after primary infection

  • systemic symptoms: fevers, lymphadenopathy
  • rash on trunk, palms and soles
  • condylomata lata (painless, warty lesions on the genitalia )
192
Q

Investigations for ?syphilis

A

clinical diagnosis and GUM referral for serology and microscopic

193
Q

Management of syphilis

A

IM Benzathine penicillin

194
Q

How is lyme disease spread

A

ticks

195
Q

key features of lyme disease

A 
erythema migrans (bulls eye rash)
systemic features (headaches, lethargy, fever)
196
Q

How is lyme disease diagnosed

A

clinical if erythema migrans is present

ELISA antibodies to Borrelia burgdorferi

197
Q

Management of lyme disease

A

doxycyline/amox (pregnancy)

198
Q

What is a prion disease and what is the most common

A

A prion is a type of protein that can trigger normal proteins in the brain to fold abnormally.

Creutzfeldt-Jakob disease

199
Q

features of prion disease

A

rapid onset dementia and myoclonus

200
Q

What is Whipples disease

A

Whipple disease is a rare bacterial infection that most often affects your joints and digestive system. Whipple disease interferes with normal digestion by impairing the breakdown of foods, and hampering your body’s ability to absorb nutrients, such as fats and carbohydrates.

201
Q

If no response in status epilepticus within 45 minutes, what is the next step?

A

Induction of general anaesthesia

202
Q

2nd line for generalised tonic-clonic seizures

A

Lamotrigine

Carbamzepine

203
Q

2nd line for focal seizures

A

levetiracetam

204
Q

Specific types of generalised seziures

A 
tonic-clonic (grand mal)
tonic
clonic
typical absence (petit mal)
atonic
205
Q

Classifications of seizures

A

Focal
Generalised
Unknown onset

FCM Matrix (17 decks)

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